W

MOSES KAZEVU
SURGERY MK

FOREWORD
This review book is designed for use by medical students and the junior medical
doctor in the diagnosis, management and curative care of regional Adult Surgical
conditions.
The book serves as a good guide and revision tool for board/shelf/licentiate
examinations.
Effort has been put in to simplify the literature and make it as practical as possible
while maintaining scientific accuracy.
Despite all efforts, it is possible that certain errors may have been overlooked in this
book. Please inform the authors of any errors detected.
NOTE: Information contained in this publication is copyrighted as such
photocopying of any part of this book without any written permission from the
author is prohibited by Law.
MOSES KAZEVU
(Tel: +260979161345)

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SURGERY MK
COURSE OBJECTIVES (5th year)
KNOWLEDGE OBJECTIVES
1. Explain the physiological, anatomical and pathological basis of surgical disease.
2. Recognize symptoms and signs of the common surgical disease conditions.
3. Analyze symptoms and signs of surgical disease processes to arrive at a
differential diagnosis.
4. Identify and interpret laboratory, imaging and bedside investigations required to
make a diagnosis and/or monitor clinical progress.

SKILLS OBJECTIVES
1. Obtain a detailed clinical history from the surgical patient.
2. Elicit physical signs in a patient with emphasis from the surgical patient.
3. Perform basic procedures.

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TOPICS
Topics Components
Introduction to surgery • History taking in the surgical patient
• Physical examination technique by system
• The operative theatre, sterility, asepsis, aseptic techniques
• Infection prevention
Basic principles of surgery • Hypovolemic and septic shock, fluid and electrolyte balance
• Blood transfusion, blood and blood products
• Monitoring the surgical patient
• The critically injured patient-assessment and management
• Surgical emergencies
• Peri-operative assessment
Gastrointestinal system • Esophageal pathologies
• Stomach pathologies
• Intestinal pathologies
• Anal pathologies
• Liver and biliary tree pathology
• Pancreas
• Hernias
Respiratory system • Signs and symptoms of upper airway obstruction
• Methods of airway access
• Signs and symptoms of traumatic conditions
➢ Fracture ribs
➢ Flail chest
➢ Pneumothorax
➢ Hemothorax
➢ Diaphragmatic trauma
• Chest drainage
• Tumors of the thorax
• Investigations of the respiratory system
Nervous system • Neurological examination and examination of the cranial nerves
• Assessment of head injury patient
• Congenital anomalies of the nervous system
• Urological, gastrointestinal, respiratory and musculoskeletal
problems of the spinal injury patient
• Peripheral neuropathy and nerve injuries
• Investigations of the nervous system

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 SURGERY MK
Cardiovascular system • Surgical anatomy of the cardiovascular system
• History taking and examination of a patient with cardiovascular
pathology
• Signs and symptoms of pathology
• Approaches to investigation of pathology
Endocrine system • Pituitary: tumors and clinical presentation
• Hyperparathyroidism
• Thyroid gland: colloid goiter, thyrotoxicosis, thyroglossal cyst,
tumors, symptoms, signs and investigation. Complications of thyroid
disease.
• The pancreas: diabetes and tumors
• The adrenals: tumors and clinical manifestations, secondary
hypertension in surgical practice
• Breast: anatomy, functions and disorders of the breast, benign and
malignant lesions of the breast, differential diagnosis and
investigations.
Integumentary system • Surgical anatomy and functions of the skin
• Symptoms and signs of infections and other surgical disorders of the
skin
• The burnt patients
➢ Percent surface area estimation
➢ Fluid replacement
➢ Immediate management
➢ Complications in the burns patient
➢ Grafting
• Common ulcers and lumps in skin and sub-dermal structures
• Pigmented lesions of the skin: differential diagnosis and biopsy.
• Ulcers of varying aetiology
Haemopoitic and • Haemopoiesis
lymphoreticular system • Haemolytic disease is surgery
• Bleeding disorders and haemostasis
• Disorders of immunity
• Lymphedema
• Spleen: signs and symptoms of splenic disorders as well as
approaches to investigating disorders of the spleen
Head and neck • Surgical anatomy of the head and neck
• History taking and examination of the patient with head and neck
pathology.

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 SURGERY MK
• Signs and symptoms of head and neck disorders
Urology • Surgical anatomy of genitourinary system
• Congenital anomalies and infections of the urinary tract and genitalia
• Signs and symptoms of disorder of the genitourinary tract
• Physical examination including digital rectal examination
• Laboratory and radiological investigations of the urinary treat
• Trauma to the genitourinary tract
• Common urological emergencies, conditions, malignancies.
• Basic urological procedures (urethral catheterization, suprapubic
cystostomy)
• Basic equipment and materials used in urology
• Catheters of various types: bougies and cystoscopies
Orthopedics • Surgical anatomy of the musculoskeletal system.
• Physical examination of muscles, bones and joints.
• Neurological evaluations including joint motion, reflexes and muscle
power
• Common hand conditions and emergencies
Traumatology • Classification and types of fractures, dislocation, ligamentous and
muscular injuries
• Bone healing
• Spinal trauma, paraplegia, quadriplegia and physiotherapy
• Outline of concomitant injuries to head, thorax abdomen and pelvis
including the gastrointestinal and genitourinary system
• Upper and lower limb injuries, compartment syndrome, fat
embolism, pulmonary embolism
• Plaster technique and complications
• Amputations and rehabilitation
• Infective conditions of bone and joints: septic arthritis, osteomyelitis,
pyomyositis
• Affections of epiphyses and soft tissue

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SURGERY MK
COURSE OBJECTIVES (7th year)
KNOWLEDGE OBJECTIVES
1. Explain the physiological, anatomical and pathological basis of surgical disease.
2. Recognize symptoms and signs of the common surgical disease conditions.
3. Analyze symptoms and signs of surgical disease processes to arrive at a
differential diagnosis.
4. Identify and interpret laboratory, imaging and bedside investigations required to
make a diagnosis and/or monitor clinical progress.

SKILLS OBJECTIVES
1. Obtain a detailed clinical history from the surgical patient.
2. Elicit physical signs in a patient with emphasis from the surgical patient.
3. Perform basic procedures.
4. Resuscitate a critically ill surgical patient.
5. Manage common surgical conditions.
6. Communicate effectively verbally and in writing with patients, relatives and
professional colleagues
7. Exhibit leadership ability

TOPICS
• Topic list essentially the same as fifth year list only addition to each section is:
management of the various pathologies.

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TABLE CONTENTS
COURSE OBJECTIVES (5TH YEAR) ...................................................................3
KNOWLEDGE OBJECTIVES ........................................................................................................................................3
SKILLS OBJECTIVES....................................................................................................................................................3
TOPICS ......................................................................................................................................................................4

COURSE OBJECTIVES (7TH YEAR) ...................................................................7

KNOWLEDGE OBJECTIVES ........................................................................................................................................7
SKILLS OBJECTIVES....................................................................................................................................................7
TOPICS ......................................................................................................................................................................7

INTRODUCTION TO SURGERY ......................................................................13

HISTORY TAKING ....................................................................................................................................................13
PHYSICAL EXAMINATION ........................................................................................................................................17

BASIC SURGICAL EXAMINATION AND EQUIMENT ...............................19

BLOOD COLLECTION BOTTLES ................................................................................................................................19
LUMPS AND MASSES ..............................................................................................................................................20

BASIC PRINCIPLES OF SURGERY .................................................................23

METABOLIC RESPONSE TO TRAUMA AND THE SYSTEMIC INFLAMMATORY RESPONSE SYNDROME .....................23
TRAUMA AND ITS MANAGEMENT ..........................................................................................................................31
FLUIDS, ELECTROLYTE IMBALANCE AND NUTRITION .............................................................................................51
BLOOD PRODUCTS AND BLOOD TRANSFUSION .....................................................................................................70
SHOCK AND HYPOTENSION ....................................................................................................................................88
WOUNDS AND WOUND HEALING ........................................................................................................................106
ULCERS .................................................................................................................................................................118
BURNS ..................................................................................................................................................................129
STOMAS ...............................................................................................................................................................155
PREOPERATIVE AND POST-OPERATIVE MANAGEMENT .......................................................................................162
PAIN AND PAIN RELIEF..........................................................................................................................................163
NEOPLASIA ...........................................................................................................................................................164

STINGS AND BITES ..........................................................................................165

SNAKE BITE ...........................................................................................................................................................165
RABIES AND DOG BITES ........................................................................................................................................170
MAMMALIAN BITE ...............................................................................................................................................176
SPIDER BITE ..........................................................................................................................................................176
BEE STING .............................................................................................................................................................177
SCORPION STING ..................................................................................................................................................177

CHEST SURGICAL CONDITIONS .................................................................179

BASIC SURGICAL PROCEDURES .............................................................................................................................179
CHEST TRAUMA ....................................................................................................................................................182

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ESOPHAGEAL PATHOLOGY .........................................................................192
RELEVANT SURGICAL ANATOMY ..........................................................................................................................192
RELEVANT PHYSIOLOGY .......................................................................................................................................195
DYSPHAGIA...........................................................................................................................................................197
EVALUATION OF THE PATIENT ..............................................................................................................................201
GASTROESOPHAGEAL REFLUX DISEASE................................................................................................................203
ESOPHAGITIS ........................................................................................................................................................203
ESOPHAGEAL STRICTURES ....................................................................................................................................204
BARRETT’S ESOPHAGUS .......................................................................................................................................207
ESOPHAGEAL HERNIA ...........................................................................................................................................207
ESOPHAGEAL DIVERTICULAE ................................................................................................................................207
PLUMMER VINSON ...............................................................................................................................................207
ACHALASIA CARDIA (CARDIOSPASM) ...................................................................................................................208
ESOPHAGEAL PERFORATIONS ..............................................................................................................................213
ESOPHAGEAL CARCINOMA ..................................................................................................................................214

ABDOMINAL SURGICAL CONDITIONS .....................................................225

ABDOMINAL MASSES ...........................................................................................................................................225
ABDOMINAL TRAUMA ..........................................................................................................................................228
GASTRITIS AND PEPTIC ULCER DISEASE ................................................................................................................229
GASTROINTESTINAL BLEEDING ............................................................................................................................229
GASTRIC TUMORS ................................................................................................................................................229
ACUTE ABDOMEN ................................................................................................................................................230
INTESTINAL OBSTRUCTION ..................................................................................................................................240
APPENDICITIS .......................................................................................................................................................269
DIVERTICULAR DISEASE ........................................................................................................................................282
CHRONIC INFLAMMATORY BOWEL DISEASE ........................................................................................................282
COLON POLYPS .....................................................................................................................................................282
CARCINOMA OF THE COLON AND RECTUM .........................................................................................................282
CARCINOMA OF THE ANUS ...................................................................................................................................283

LIVER AND SPLEEN .........................................................................................285

LIVER AND SPLEEN INJURY ...................................................................................................................................285
LIVER TUMORS .....................................................................................................................................................285

PANCREAS ..........................................................................................................291
PANCREATITIS ......................................................................................................................................................295
PANCREATIC TUMORS ..........................................................................................................................................320

GALLBLADDER .................................................................................................329
GALLSTONES/ CHOLELITHIASIS ............................................................................................................................331
CHOLEDOCHOLITHAISIS .......................................................................................................................................340
CHOLECYSTITIS .....................................................................................................................................................341
MUCOCELE OF THE GALLBLADDER .......................................................................................................................351
CHOLANGITIS .......................................................................................................................................................352
TUMORS OF THE BILIARY TRACT...........................................................................................................................352

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OBSTRUCTIVE JAUNDICE .............................................................................353
METABOLISM OF BILIRUBIN .................................................................................................................................353
CAUSES .................................................................................................................................................................354
CLINICAL FEATURES ..............................................................................................................................................356
BENJAMIN’S (1983) CLASSIFICATION OF BILIARY OBSTRUCTION .........................................................................355
INVESTIGATIONS ..................................................................................................................................................357
MANAGEMENT.....................................................................................................................................................359

PAINFUL ANAL CONDITIONS.......................................................................366

HEMORRHOIDS/PILES ..........................................................................................................................................367
ANAL FISTULA (FISTULA IN ANO) ..........................................................................................................................373
ANAL FISSURE .......................................................................................................................................................377
PILONIDAL SINUS..................................................................................................................................................378

HERNIA ................................................................................................................382
PARTS OF A HERNIA ..............................................................................................................................................383
CLASSIFICATION OF HERNIA .................................................................................................................................384
MANAGEMENT OF HERNIA ..................................................................................................................................386
INGUINAL HERNIA ................................................................................................................................................387
FEMORAL HERNIA ................................................................................................................................................402
UMBILICAL HERNIA ..............................................................................................................................................405
PARAUMBILICAL HERNIA......................................................................................................................................406
EPIGASTRIC HERNIA .............................................................................................................................................406
INCISIONAL HERNIA..............................................................................................................................................407

ORTHOPEDICS ..................................................................................................409
GENERAL PRINCIPLES OF FRACTURES...................................................................................................................409
TRACTION .............................................................................................................................................................435
FRACTURES IN CHILDREN .....................................................................................................................................444
FRACTURES IN ADULTS .........................................................................................................................................454
JOINT DISLOCATIONS ...........................................................................................................................................464
AMPUTATIONS .....................................................................................................................................................466
OSTEOARTHRITIS ..................................................................................................................................................469
RHEUMATOID ARTHRITIS .....................................................................................................................................471
SEPTIC ARTHRITIS .................................................................................................................................................471
OSTEOMYELITIS ....................................................................................................................................................471

ENDOCRINE .......................................................................................................478
THYROID ...............................................................................................................................................................478
PARATHYROID GLAND ..........................................................................................................................................513
ADRENAL GLANDS ................................................................................................................................................513
PITUITARY GLAND ................................................................................................................................................514

BREAST ................................................................................................................515
APPROACH TO A BREAST LUMP............................................................................................................................517
BREAST ANATOMY ...............................................................................................................................................524
BREAST PATHOLOGY ............................................................................................................................................528

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UROLOGY ...........................................................................................................559
HEMATURIA .........................................................................................................................................................559
INFECTIONS OF THE UROGENITAL SYSTEM ..........................................................................................................562
INCONTINENCE AND NEUROPATHIC BLADDER DISORDERS .................................................................................562
CYSTIC DISEASES OF KIDNEY .................................................................................................................................562
URINARY STONES .................................................................................................................................................565
URINARY RETENTION ...........................................................................................................................................565
URINARY TRACT OBSTRUCTION ...........................................................................................................................569
BENIGN PROSTATIC HYPERPLASIA........................................................................................................................579
CARCINOMA PROSTATE .......................................................................................................................................589
RENAL CARCINOMA .............................................................................................................................................595
NEPHROBLASTOMA (WILMS TUMOR) .................................................................................................................595
TUMORS OF THE RENAL PELVIS AND URETER ......................................................................................................595
CARCINOMA OF THE BLADDER .............................................................................................................................595
TESTICULAR CANCER ............................................................................................................................................595
CANCER OF THE PENIS ..........................................................................................................................................595
TESTICULAR TORSION...........................................................................................................................................595
TESTICULAR/SCROTAL MASSES AND SWELLINGS .................................................................................................597

NEUROSURGERY..............................................................................................598
HEAD INJURY ........................................................................................................................................................599
INTRACRANIAL HEMORRHAGE .............................................................................................................................612
DEPRESSED SKULL FRACTURE ...............................................................................................................................618
BASILAR FRACTURE ..............................................................................................................................................619
SPINAL TRAUMA ...................................................................................................................................................619
CERVICAL SPINAL INJURY......................................................................................................................................629
CERVICAL SPINE FRACTURES AND DISLOCATION .................................................................................................630
THORACIC SPINE FRACTURES ...............................................................................................................................633
THORACOLUMBAR JUNCTION AND LUMBAR SPINE FRACTURES AND DISLOCATIONS ........................................633
DISTRACTION OR SEAT-BELT INJURY ....................................................................................................................634
THORACIC OUTLET SYNDROME ............................................................................................................................634
CNS TUMORS ........................................................................................................................................................635
HYDROCEPHALUS .................................................................................................................................................635

MISCELLANEOUS.............................................................................................636
HAND INFECTIONS................................................................................................................................................636
ISCHEMIA AND SWELLING OF THE LOWER LIMBS ................................................................................................640
PROCEDURES........................................................................................................................................................642

ANSWERS TO CLINICAL BOX ......................................................................664

A CASE OF EPIGASTRIC PAIN AND VOMITING .......................................................................................................664

END OF BOOK REVISION ...............................................................................667

TRUE/FALSE ..........................................................................................................................................................667
ESSAYS ..................................................................................................................................................................753
ANSWERS TO TRUE/FALSE ....................................................................................................................................762
ANSWERS TO ESSAYS ............................................................................................................................................848

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CHAPTER 1: INTRODUCTION TO SURGERY

INTRODUCTION TO SURGERY
HISTORY TAKING • These should be listed in order of
severity, with a record of precisely
HISTORY TAKING when and how they started.
(Alternatively, some clinicians
DEMOGRAPHICS advocate for them to be listed in
• Make sure you know and always order of chronological presentation
record the patient’s: i.e. from the longest standing
➢ Name complaint to the most recent).
➢ Age • Whenever possible it should be
➢ Sex noted why the patient is more
➢ Ethnic group concerned with one complaint than
➢ Marital status another.
➢ Occupation • Include the duration of each
➢ Address symptom.
• Always record who the informant
was and record the date of the HISTORY OF
examination. PRESENTING
• State whether the case is a self-
COMPLAINT
referral or a hospital referral.
• The full history of the main
PRESENTING complaint or complaints must be
recorded in detail, with precise
COMPLAINT
dates.
• It is customary to ask the patient
• It is important to get right back to
‘what are you complaining of?’ and
the beginning of the problem. For
to record the answer in the patient’s
example, a patient may complain of
own words.
a recent sudden attack of
• If you ask ‘What is the matter?’ the
indigestion, if further questioning
patient will probably tell you their
reveals that similar symptoms
diagnosis.
occurred some years previously,
• It is better not to know the their description should be included
diagnosis made by the patient or in this section.
other doctors because none may be
correct.

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SURGERY MK
• It is essential to exhaust any other
possible questions that involves the
system of the presenting complaint.
• When assessing pain don’t forget SOCRATES:
➢ S-site
➢ O-onset
➢ C-character
➢ R-radiation
➢ A-alleviating factors
➢ T-time course (Duration)
➢ E-exacerbating factors
➢ S-symptoms associated

REVIEW OF SYSTEM
• These are direct questions that every patient should be asked, because the answers
may amplify your knowledge about the main complaint and will often reveal the
presence of other disorders of which the patient was unaware or thought
irrelevant.
• Negative answers are just as important as positive answers.
• All the answers to every question, whether they be positive or negative must be
recorded.

SYSTEM AREA OF INTEREST AND QUESTIONS

Central nervous • Headache
system • Syncopal attacks/Fainting
• Convulsions
• Dizziness, vertigo and lightheadedness
• Tremors
• Memory loss
• Change in vision, smell or hearing
• Muscle weakness, paralysis or sensory disturbances
• Changes in sleep patterns
Respiratory • Cough- nature, productivity, hemoptysis
system • Dyspnea
• Hoarseness
• Wheezing

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SURGERY MK
• Chest pain
• Exercise intolerance and night sweats
Cardiovascular • Dyspnea
system • Paroxysmal nocturnal dyspnea
• Orthopnea
• Chest pain
• Palpitations
Gastrointestinal • Nausea and vomiting
system • Diarrhea or constipation
• Weight loss
• Dysphagia, polyphagia
• Indigestion
• Hematesis
• Melena
• Tenesmus
• Bowel habits and nature of stool
Genitourinary • Hematuria, Dysuria
system • Nocturia
• Polyuria
• Vaginal/ penile discharge
• Urine color
• Urinary hesitancy
• Dribbling
• Urinary stream
Musculoskeletal • Aches or pains in muscles, bones or joints
and skin • Joint swellings
• Limitation of movements
• Locking
• Weakness
• Disturbances of gait
• Skin rash

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SURGERY MK

PAST MEDICAL DRUG HISTORY

HISTORY • Ask if the patient is taking any
• Record the history of those drugs.
conditions which are not directly • Specifically enquire about steroids,
related to the presenting complaint. anti-depressants, insulin, diuretics,
• These include (Remember anti-hypertensive, hormone
“D.E.A.T.H.S”): replacement therapy and the
➢ Diabetes mellitus contraceptive pill.
➢ Epilepsy • Also ask for any drug related
➢ Asthma allergies.
➢ Tuberculosis • For children ask about the
➢ Hypertension immunization history (Diphtheria,
➢ HIV tetanus, whooping cough, measles,
➢ Sickle cell disease mumps, rubella, poliomyelitis,
• Ask about history of similar illness smallpox, typhoid and TB)
in the past
GYNAE HISTORY
• Ask also about previous hospital
admissions and previous history of (WOMEN)
blood transfusion. • Date of menarche or menopause
➢ Ask about the duration of • Frequency, Quantity and duration
admission of menstruation
➢ Date of admission • Last menstrual period
➢ Cause of admission/blood • The use of family planning and oral
transfusion contraceptives
➢ Treatment offered
FAMILY HISTORY
PAST SURGICAL • Enquire about the health and age, or
HISTORY cause of death of the patient’s
• Record any history of surgical parents, grandparents, brothers and
procedures performed on the sisters and ask about any children
patient. who have died.
➢ Including date, procedure and • Also ask for specific diseases in the
any complications associated family such as diabetes mellitus,
with the procedure. epilepsy, asthma, Tuberculosis,
Hypertension, Sickle cell disease.

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SURGERY MK
SOCIAL-ECONOMIC • The impression and differentials
must be accurately related to the
HISTORY
information obtained in the history.
• Record the marital status and type
• Note: you may query somethings
and place of dwelling.
that you suspect e.g. “?
➢ Number of rooms in the house
malignancy”.
➢ Ventilation
➢ Source of water PHYSICAL EXAMINATION
• Ask about their occupation.
• Ask about history of smoking and PHYSICAL
alcohol intake
➢ Type
EXAMINATION
➢ Frequency • The sequence follows a specific
➢ Duration pattern; details will be provided in
the subsequent chapters of this
SUMMARY OF HISTORY literature.
• This is one sentence that
summarizes the important parts of GENERAL EXAMINTION
the history. Include identifying • Mental state- GCS, this is also
information, presenting complaint, assessed as you interact with the
a very brief description of the patient. (assess patients hearing-
history of presenting complaints Vestibulocochlear nerve, rule out
plus essential details from ROS, ear wax)
PMHx, Family and social- • Nutritional status
economic Hx. • Vital signs
• In the summary do not use the name ➢ Blood pressure
(use initials) and use an estimated ➢ Respiratory rate
age range i.e. ➢ Pulse
➢ <45 years: young age ➢ Temperature
➢ 45-65 years: middle age ➢ Oxygen saturation
➢ > 65 years: old age • Important negatives- J.A.C.C.Ln.
D
IMPRESSION ➢ Jaundice: sclera
• These are based on the history ➢ Anemia: pale conjunctiva
given. o At this point you also check
eye movements and
pupillary light reflex

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SURGERY MK
including the facial nerve CHEST
(raising eyebrows) • Inspection
o Sensation on the face- • Palpation
Trigeminal (CN V) • Percussion
➢ Central cyanosis: mouth • Auscultation
o At this point CN IX, X and
XI can be assessed- moving ABDOMEN
tongue around + saying • Inspection
“Ah” and note the elevation • Palpation
of soft palate. • Percussion
o Also assess Olfactory nerve • Auscultation
(rule out common colds • Vaginal examination (when
first) indication), Assess hernia orifices
➢ Clubbing- fingers
MUSCULOSKELETAL
➢ Lymphadenopathy
• Gait
o Submental, submandibular,
• Arms
pre-auricular, subauricular,
post-auricular, sub- • Limbs
occipital, cervical, • Spine
supraclavicular and • After the examination summarize
infraclavicular as well as findings and offer an impression
axillary and epitrochlear with some differentials and suggest
o Check accessory by appropriate investigations.
shrugging shoulders
➢ Dehydration- signs of
dehydration

SYSTEMIC
EXAMINTION
HEAD AND NECK
• Check if neck is supple
(movements)- you already checked
the cranial nerves because it was
incorporated in the general
examination

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SURGERY MK

CHAPTER 2: BASIC PRINCIPLES OF SURGERY

BASIC SURGICAL EXAMINATION AND

EQUIMENT
BLOOD COLLECTION BOTTLES

Figure 1: Blood collection bottles (Adapted from Surgery Magic notes)

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SURGERY MK

LUMPS AND MASSES by ignoring a lump just

because it does not hurt
FOCUSED HISTORY OF them.
A LUMP/MASS ➢ What are the symptoms of the
• Most patient with a lump/mass feel lump?
it frequently and should be able to o It may be painful and if it is,
tell you about the history of its you must take a careful
clinical features. history of the pain.
• The following questions should be o The characteristic feature of
asked: pain associated with acute
➢ When was the lump first infection is its throbbing
noticed? nature.
o It is important to be precise o A lump may be disfiguring
with dates and terminology. or interfere with movement,
o Do not write ‘the lump first respiration or swallowing.
appeared 6 months ago’, Describe the history of each
when you mean ‘the lump symptom carefully.
was first noticed 6 months ➢ Has the lump changed since it
ago’. was first noticed?
o Lumps may exist for o They should be able to tell
months, even years, before you whether the lump has
the patient notices them. got bigger, smaller, or has
➢ What made the patient notice fluctuated in size and when
the lump? they noticed a change in
o The presence or absence of size.
pain is important, o They may also have
particularly if it is the appreciated other changes in
presenting feature. the nature of the lump that
o In very general terms, pain they can tell you about.
is usually associated with o They may also have noticed
inflammation, not tenderness, which may have
neoplastic change. altered in any of the ways
o Most patients expect cancer that a pain may change.
to be painful- and do
themselves irreparable harm

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SURGERY MK
➢ Does the lump ever disappear?
The history of a lump or an ulcer
o A lump may disappear on
lying down or during ➢ Duration: when was it first
exercise and yet be noticed?
irreducible at the time of ➢ First symptom: what brought it to
your examination. the patient’s notice?
o The patient should always
➢ Other symptoms: what symptoms
be asked if the lump ever
does it cause?
goes away, because this
physical characteristic is ➢ Progression: how has it changed
peculiar to only a few types since it was first noticed?
of lumps. ➢ Persistence: has it ever disappeared
➢ Has the patient ever had any or healed?
other lumps? ➢ Multiplicity: has (or had) the
o You must ask this question patient any other lumps or ulcers?
because it might not have
➢ Cause: what does the patient think
occurred to the patient that
caused it?
there could be any
connection between their
present lump and a previous
lump or even a coexisting
one.
➢ What does the patient think
caused the lump?
o Lumps occasionally follow
injuries or systemic illness
known only to the patient.

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SURGERY MK
EXAMINATION OF A PALPATION
• Temperature
LUMP
• Tenderness
GENERAL EXAMINATION
• Surface
• It is often tempting to examine only
• Edge
the lump about which the patient is
• Size
complaining.
• Composition
• This will cause you to make
innumerable misdiagnoses. You • Consistence
must always examine the whole • Fluctuation
patient. • Compressibility
• Do not forget to perform a general • Reducibility
examination and a systemic • Translucence
examination. PERCUSION
LOCAL EXAMINATION OF A • Fluid thrill
LUMP • Resonance
INSPECTION AUSCULATATION
• Site: this must be described in exact • For Bruits
anatomical terms, using distances
measured from bony points. Do not EXTRAS
guess distance, use a tape measure. • Relations to surrounding structures
• Color and texture of overlying skin: • State of the regional lymph glands
The skin over a lump may be • State of the local tissue
discolored and become smooth and
shiny or thick and rough.
• Shape: remember that lumps have 3 • Complete your examination by
dimensions. You cannot have a performing a systemic
circular lump because a circle is a examination.
plane figure. Many lumps are not
regular spheres, or hemispheres but
have an asymmetrical outline. In
these circumstances, it is
permissible to use descriptive terms
such as pear shaped or kidney
shaped.

22
SURGERY MK

CHAPTER 3: BASIC PRINCIPLES OF SURGERY

• Response to injury is graded: the

BASIC PRINCIPLES more severe the injury, the greater
OF SURGERY the response.
• Following elective surgery
METABOLIC RESPONSE
immediate severity, there may be
TO TRAUMA AND SIRS transient and modest rise in
temperature, heart rate, respiratory
METABOLIC rate, energy expenditure and
RESPONSE TO peripheral cell count.
• Following major trauma/sepsis,
TRAUMA AND THE
these physiological functions are
SYSTEMIC accentuated, resulting in a systemic
INFLAMMATORY inflammatory response syndrome
(SIRS), hypermetabolism, marked
RESPONSE catabolism, shock and even
SYNDROME multiple organ dysfunction.
• Homeostasis is the maintenance of • The metabolic response also
a constant internal environment. evolves with time. In particular the
• Complex homeostatic responses immunological sequelae of major
involving the brain, nerves, heart, injury evolve from a pro-
lungs, kidneys and spleen work to inflammatory state driven primarily
maintain body constancy. by the innate immune system
• Response to injury are in general (macrophages, neutrophils,
beneficial to the host and allow dendritic cells) into a compensatory
healing and survival. anti-inflammatory response
(CARS) characterized by
• Understanding of the metabolic
suppressed immunity and
response to injury, provides the
diminished resistance to infection.
basis to seek to reduce the need for
a homeostatic response by • In patients who develop infective
minimizing the primary insult complications, CARS will drive
through elective surgical practice. on-going systemic inflammation,
the acute phase response and
continued catabolism.

23
SURGERY MK
MEDIATORS OF THE • The counter-regulatory hormones
(glucagon, glucocorticoids and
METABOLIC RESPONSE
catecholamines) produce many
TO INJURY aspects of the metabolic response to
• The classical neuroendocrine injury.
pathways of the stress response • There are however many other
consist of afferent nociceptive players including insulin release
neurons, the spinal cord, thalamus and sensitivity, hypersecretion of
and pituitary gland. prolactin and growth hormone
• The neuroendocrine response to (GH) in the presence of low
severe injury/critical illness is circulatory insulin-like growth
biphasic: factor-1 (IGF-1) and inactivation of
➢ Acute phase: due to an actively peripheral thyroid hormones and
secreting pituitary and elevated gonadal function.
counter-regulatory hormones • GH has direct lipolytic, insulin-
(cortisol, glucagon, adrenaline). antagonizing and pro-inflammatory
Changes are thought to be properties.
beneficial for short-term • The innate immune system (mainly
survival. macrophages) interact in a complex
➢ Chronic phase: associated with manner with the adaptive immune
hypothalamic suppression and system (T-cells, B-cells) in co-
low serum levels of the generating the metabolic response
respective target organ to injury.
hormones. Changes contribute • Pro-inflammatory cytokines
to chronic wasting. include:
• Corticotrophin releasing factor ➢ Interleukin-1 (IL1)
(CRF) released from the ➢ Tumor necrosis factor alpha
hypothalamus increases ➢ Interleukin 6 (IL-6)
adrenocorticotrophic hormone ➢ Interleukin 8 (IL-8)
(ACTH) release from the anterior • IL-6 and IL-8 are produced within
pituitary the first 24 hours and act directly on
• ACT acts on the adrenals to the hypothalamus to cause pyrexia.
increase the secretion of cortisol. • Such cytokines also augment the
• Hypothalamic activation of the hypothalamic stress response and
sympathetic nervous system causes act directly on skeletal muscle to
release of adrenaline and also induce proteolysis while inducing
stimulates the release of glucagon.

24
SURGERY MK
acute phase protein production in immunosuppressive at high levels,
the liver. it acts synergistically with IL-6 to
• Pro-inflammatory cytokines also promote the hepatic acute phase
play a complex role in the response. ACTH released is
development of peripheral insulin enhanced by proinflammatory
resistance. cytokines and the noradrenergic
• Other important pro-inflammatory system. The resulting rise in
mediators: cortisol levels may form a weak
➢ Nitric oxide (produced from feedback loop attempting to limit
inducible nitric oxide synthesis) the pro-inflammatory stress
➢ Prostanoids (produced from the response. Finally, hyperglycemia
cyclo-oxygenase-2 enzyme) may aggravate the inflammatory
• Within hours of the upregulation of response via substrate overflow in
pro-inflammatory cytokines, mitochondria, causing the
endogenous cytokine antagonists formation of excess free oxygen
enter the circulation e.g. radicals and also altering gene
interleukin-1 receptor antagonist expression to enhance cytokine
(IL-1Ra) and TNF soluble production
receptors (TNF-sR-55 and 75) act • At molecular level, the changes
to control the pro-inflammatory accompanying systemic
response. inflammation are extremely
• A complex further series of complex and may involve gene
adaptive changes includes the expression/inactivation.
development of a Th2 type counter-
inflammatory response (regulated
by IL-4, 5, 9 and 12 and
transforming growth factor beta)
which if accentuated and prolonged
in critical illness is characterized as
the CARS and result in
immunosuppression and increased
susceptibility to opportunistic
(nosocomial infection).
• There are many complex
interactions between the
neuroendocrine, cytokine and
metabolic axes. E.g. Cortisol is

25
SURGERY MK

Figure 2: The integrated response to surgical injury (first 24-48h): there is a complex interplay
between the neuroendocrine stress response and the pro-inflammatory cytokine response of the
innate immune system (Image from Baily & Love’s Short Practice of Surgery)

EBB AND FLOW MODEL o It may be attenuated by

• The natural response to injury proper resuscitation but not
include: completely abolished
➢ Immobility/rest o It is characterized by
➢ Anorexia hypovolemia, decreased
➢ Catabolism basal metabolic rate, reduce
• The changes are designed to aid cardiac output and lactic
acidosis.
survival of moderate injury in the
absence of medical intervention. o Predominant hormones
regulating the EBB phase
• In 1930, Sir David Cuthbertson
are catecholamines, cortisol
divided the metabolic response to
and aldosterone (following
injury in humans into the ‘EBB’
activation of the renin-
and the ‘Flow’ phase
angiotensin system).
➢ ‘EBB’:
o Magnitude of the
o Starts at the time of injury
neuroendocrine response
and lasts for approximately
depends on degree of blood
24-48 hours.

26
SURGERY MK
loss and stimulation of required following
somatic afferent nerves at serious injury
the site of injury. o During the catabolic phase
o The role of the EBB phase is the increased production of
to conserve both circulating counter-regulatory
volume and energy stores hormones (catecholamines,
for recovery. cortisol, insulin and
➢ ‘Flow’ phases glucagon) and
o Following resuscitation, the inflammatory cytokines
EBB phase evolves into a (IL-1, -6 and TNF-alpha)
hypermetabolic flow phase, results in significant fat and
which corresponds to the protein mobilization leading
SIRS. This phase involves to significant weight loss
the mobilization of body and increased urinary
energy stores for recovery nitrogen excretion. The
and repair and the increased production of
subsequent replacement of insulin at this time is
lost or damaged tissue. associated with significant
o It is characterized by tissue insulin resistance and
edema (from vasodilation therefor injured patients
and increased capillary often exhibit poor glycemic
leakage), increased basal control.
metabolic rate o The combination of
(hypermetabolism), pronounced or prolonged
increased cardiac output, catabolism in association
raised body temperature, with insulin resistance
leukocytosis, increased places patients within this
oxygen consumption and phase at increased risk of
increased gluconeogenesis. complications particularly
o The flow phase may be infections and
divided into: cardiovascular.
- Catabolic phase: lasts o The development of
about 3-10 days complications will further
- Anabolic phase: lasts aggravate the
for weeks if extensive neuroendocrine and
recovery and repair are inflammatory stress

27
SURGERY MK
response thus creating a SYSTEMIC
vicious catabolic cycle.
INFLAMAMTORY
RESPONSE SYNDROME
• Systemic inflammatory response
syndrome is a systemic
inflammatory response
characterized by the presence of 2
or more of the following:
Figure 3: Phases of physiological response ➢ Temperature >38oC
to injury (Image from Baily & Love’s Short
(hyperthermia) or <36oC
Practice of Surgery)
➢ Tachycardia >90 beats/min
• It must be remembered that, during ➢ Tachypnea >20 min or PaCO2-
the response to injury, not all <4.3 kPa
tissues are catabolic. Indeed, the ➢ WBC >12, 000/L or <4, 000/L
essence of this coordinated (with predominant neutrophilia
response is to allow the body to or neutropenia)
reprioritize limited resources away • Sepsis syndrome: a state of SIRS
from peripheral tissue (muscle, with proven infection.
adipose tissue, skin) and towards • Septic shock: sepsis with systemic
key viscera (liver, immune system) shock not responsive to fluids.
and the wound. • Multiple organ dysfunction
• Hypermetabolism following injury syndrome (MODS) is a state of
is mainly caused by an acceleration derangement of physiology such
of futile metabolic cycles. that organ function cannot maintain
• Avoidable factors that compound homeostasis. Several organs may
the response to injury include: be involved:
➢ Continued hemorrhage ➢ Lungs (ARDS)
➢ Hypothermia ➢ Kidneys (Acute renal failure)
➢ Tissue edema ➢ Gastrointestinal tract (liver
➢ Tissue under-perfusion failure, stress ulceration)
➢ Starvation ➢ Central nervous system
➢ Immobility (confusion)
➢ Blood (DIC)
➢ Heart (Cardiac depression)
• When two or more end-organs fail
a diagnosis of MODS is made.

28
SURGERY MK
- Gram-positive bacteria:
exotoxin
o Macrophage cytokine
release
o Microcirculatory injury
o Gut barrier failure
• TNF-alpha released from activated
macrophages and neutrophils is
cytotoxic to endothelial cells and
parenchymal cells of end-organs.
• Lipopolysaccharides (LPS)
released from Gram negative
bacterial cell walls activates
Figure 4: MODS (Image from Clinical macrophages via attachment of
Surgery 2nd Ed)
LPS-binding protein and activation
• Compensatory anti-inflammatory of CD14 molecules on the cell
response syndrome (CARS) is an surface.
anti-inflammatory response that • IL-6 and IL-1 beta cause
counteracts the systemic endothelial cell activation and
inflammation of SIRS. CARS is damage. They promote
characterized by the release of complement and chemokine
potent anti-inflammatory cytokines release.
including IL-4, IL-10 and TGF- • High dose IV steroids have little
beta. It may also be deleterious role in established SIRS (probably
resulting in opportunistic infection because of multiple pathways of
such as systemic candidiasis. activation). Steroids for early SIRS
• The pathophysiology of are unproven.
SIRS/MODS is complex. One or • Platelet activation factor (PAF):
more of many initiating factors implicated particularly in acute
causes a systemic pancreatitis. No proven role for
hyperinflammatory response and it anti-PAF antibody.
is the uncontrolled activity of this • Inducible nitric oxide synthase
response that leads to organ failure. synthesized by leukocytes,
➢ Inciting factors include: macrophages and Kupffer cells is
o Infection active for up to 20h and produces
- Gram-negative bacteria: nitric oxide (NO) a potent
endotoxin vasodilator and a free radical

29
SURGERY MK
scavenger. However, it can also • Common surgical causes of SIRS
form peroxynitrite (ONOO-), a free include:
radical that may cause cellular ➢ Acute pancreatitis
damage. ➢ Perforated viscus with
peritonitis
➢ Fulminant colitis
➢ Multiple trauma
➢ Massive blood transfusion
➢ Aspiration pneumonia
➢ Ischemia-reperfusion injury

Figure 5: Pathophysiology of SIRS (Image

from Clinical surgery 2nd Ed)

Figure 6: Pathophysiology of SIRS (Image from Clinical surgery 2nd Ed)

• Early treatment of SIRS may ➢ Treat infection: removal of

reduce risk of MODS developing. necrotic tissue or drainage of
The role of treatment is to eliminate abscess is essential. Nosocomial
any causative factor and support the infection must be prevented by
cardiovascular and respiratory aggressive physiotherapy,
physiology until the patient can pulmonary toilet and care of
recover. Treatment include: central lines. Wounds must be

30
SURGERY MK
kept clean and debrided if ➢ Inability to increase cardiac
necessary. Antibiotic therapy is output
initiated on the basis of the most ➢ Inability to find septic source
likely infective organisms until ➢ Multiple end-organ failure
the result of blood culture are
available when more specific TRAUMA AND ITS
antibiotic treatment can be MANAGEMENT
initiated.
➢ Ensure adequate tissue TRAUMA AND ITS
oxygenation: adequate IV fluids MANAGEMENT
with constant monitoring of
• Traumatology (Greek “trauma”-
urine output and pulmonary
injury or wound), is a branch of
artery pressure. Diuretics may
medicine that entails the study of
be required to maintain urinary
wounds and injuries caused by
output and should only be used
accidents or violence to a person
when adequate hydration is
and the surgical therapy and repair
achieved. Ventilatory support
of the damage.
may be necessary with
• Traumatology may also be known
supplementary oxygen or
as accident surgery.
mechanical ventilation in severe
• The “Golden Hour” of Trauma is
cases.
the period immediately following
➢ Maintain nutritional support:
trauma in which rapid assessment,
enteral or total parenteral
diagnosis, and stabilization must
nutrition.
occur.
➢ Minimize systemic
• The Advanced Trauma Life
inflammatory response:
Support course (ATLS) has
Corticosteroids
established a standardized
➢ Use of recombinant activated
approach to trauma assessment &
protein C (still under testing)
management.
• Overall mortality for SIRS is 7%,
• The ATLS includes:
14% for sepsis syndrome, 40% for
➢ Primary survey- ABCDE
established septic shock and 90%
o A-airway maintenance with
for 3-system failure.
cervical spine protection.
• Factors predicting poor outcome:
o B- breathing and
➢ Very young and very old
ventilation.
➢ Severe initial insult

31
SURGERY MK
o C-circulation with definitive care management
hemorrhage control plan.
o D-disability/ neurologic
assessment PRIMARY SURVERY AT
o E- Exposure and THE SITE OF EVENT
environmental control (FIRST AID)
o F- fluids • This uses the A, B, C approach
o G- Glucose ➢ A- airway maintenance with
➢ Secondary survey cervical spine protection
o When the primary survey is ➢ B-breathing and ventilation
completed, resuscitation ➢ C-circulation with hemorrhagic
efforts are well established control
and the vital signs are
• This approach is particularly
normalizing, the secondary
important when assessing patients
survey can begin.
with multiple injuries.
o The secondary survey is a
head-to-toe evaluation of AIRWAY
the trauma patient, • Signs of an obstructed airway are
including a complete history cyanosis, apnea (not breathing) and
and physical examination stridor (a high pitched creaking
including the reassessment noise heard especially on
of all vital signs. inspiration).
o Each region of the body • It is essential to protect and secure
must be fully examined. X- an adequate airway.
rays indicated by • Lungs cannot be oxygenated if the
examination are obtained. airway is obstructed for example by
o If at any time during the jaw and tongue falling back,
secondary survey the patient swollen soft tissues, direct damage
deteriorates, another to the upper airway, false teeth,
primary survey is carried vomitus or blood.
out. • The airway of unconscious patients
➢ Tertiary survey: A careful and lying on their back often becomes
complete examination is obstructed by their own soft tissues,
followed by serial assessments but before they are rolled into the
to help recognize missed supine or semi-prone position or
injuries and as well as allow a the neck extended always consider

32
SURGERY MK
and if possible exclude an • Airway obstruction is often
associated cervical spinal injury. relieved by lifting the jaw upwards
• All patients found to be but may only be relieved by
unconscious after an injury must be inserting a finger in the mouth and
assumed to have an associated pulling the jaw or palate forward,
injury of their cervical spine especially when the obstruction is
because abrupt or careless turning associated with a fractured maxilla
may further dislocate or sublux a or mandible.
cervical vertebra and injure the
spinal cord when no injury existed
or turn partial cord damage into a
complete.
• The neck should thus be
immobilized in all unconscious
injured patients by longitudinal
manual support, the application of a
hard collar and the use of
stabilizing sand bags and tape
before turning the patient onto their
side until clinical examination and Figure 8: Jaw maneuvers to clear the airway
radiographs have excluded unstable
• An oropharyngeal or
fractures of the cervical spine.
nasopharyngeal airway should be
inserted as soon as possible and
then in an unconscious patient,
replaced by an endotracheal tube,
inserted by an experienced
anesthetist because the absence of a
gag reflex in an unconscious patient
makes aspiration of saliva, vomitus
or blood into the lungs is a major
hazard.
BREATHING
Figure 7:: Chin lift with longitudinal manual • If the patient remains cyanosed or
support apneic after the airway has been
cleared, mouth-to-mouth

33
SURGERY MK
resuscitation should be started transfer to hospital by experienced
immediately. ambulance staff.
➢ This is easier and safer (from
CIRCULATION
risks of cross-infections) if a
• Severe external bleeding at the
Brook’s airway, a facemask, an
scene of the accident requires
Ambu bag and oxygen are
manual compression directly over
available.
the wound or pressure proximal to
the point of bleeding, where the
feeding artery can be compressed
against an underlying bony point.
• Tourniquets should only be used to
stop distal limb bleeding. They
rarely work efficiently and often
exacerbate bleeding by obstruction
of the venous outflow while failing
to occlude the arterial outflow.
Figure 9: An Ambu bag • An effective tourniquet makes the
whole limb ischemic and will cause
➢ Mouth to mouth ventilation permanent muscle and nerve
combined with external cardiac damage if it is kept in place for
massage may, however be more than 1.5 to 2 hours.
lifesaving in patients who have • Tourniquets theoretically cause
undergone a short period of reperfusion problems/injury when
respiratory arrest. released- metabolic acidosis,
➢ If there is no breathing or a pulse myoglobinuria and hypercalcemia.
within 10 seconds begin chest • Nevertheless, a tourniquet can
compressions. Start CPR with sometimes be lifesaving if it is
30 chest compressions before applied at the correct pressure to a
giving two rescue breaths (30:2) mangled bleeding limb for a short
in children use a 15:2 ratio. period.
• There are few indications for heroic ➢ The time of application must be
attempts at inserting home-made carefully recorded and passed
tracheostomy devices at the scene on to ambulance and medical
of the accident. The patients are stuff.
probably better served by a rapid • Direct manual pressure applied
provided it is achieving its desired

34
SURGERY MK
effect (i.e. stopping or reducing • All patients who are unconscious or
blood loss) is usually preferable to suspected of having multiple or
a tourniquet. serious injuries should be admitted
• This can be very tiring because it directly to the resuscitation area of
must be maintained until the patient the accident and emergency
reaches the hospital. department.
• The clinical assessment (history
GENERAL FIRST-AID ADVICE
and examination) and resuscitation
• First aiders should ensure there is
must occur simultaneously if lives
no immediate danger to themselves
are to be saved.
before approaching a casualty.
• The routine A, B, C, D, E
• Many injured patients are best
assessment must be done despite
served by leaving them where they
whatever happened before the
are until help arrives unless they are
hospital admission.
in any kind of danger or threat e.g.
➢ A- airway maintenance with
inside a burning car.
cervical spine protection
• Provided the patient has a strong
➢ B- breathing and ventilation
pulse, is breathing normally and is
➢ C-circulation with hemorrhage
not overtly bleeding it is best to call
control
for help and wait.
➢ D- disability/ neurologic
• As help is waited for monitor pulse,
assessment
breathing and provide morale
➢ E- exposure and environmental
support.
control
• Under no circumstances should an ➢ F- fluids
injured patient be given anything to ➢ G-glucose
eat or drink.
TRIAGE
PRIMARY SURVERY IN • This is the assignment of degrees of
THE ACCIDENT AND urgency to wounds or illnesses to
EMERGENCY decide the order of treatment of a
large number of patients or
DEPARTMENT casualties.
• The first and key part of the • This should be sorted out according
assessment of patients presenting to their need for treatment and the
with trauma is called the primary resources available.
survey. • It starts at the scene and continues
at the receiving hospital.

35
SURGERY MK
• Priority is given to patients most easily miss blood in his thoracic
likely to deteriorate clinically. cavity or a slowly developing
• It takes into account the vital signs, hemoperitoneum.
pre-hospital clinical course, • More lives are lost from failing to
mechanism of injury, age and other care for the airway than from any
medical conditions. other cause.
• Multiple casualties: the number of AIRWAY
patients and severity of injury do • The neck must be protected by a
not exceed the capacity of
collar and immobilized fully using
treatment center- life threatening sand bags and tape.
injuries and multiple system
• An anesthetist should assess the
injuries are treated first.
need for better control of the
• Mass casualties: the number of
airway.
patients and severity of injury
• Look for the signs of inadequate
exceeds capacity of the treatment
oxygenation, airway obstruction,
center- patients are selected for
foreign bodies, facial, mandibular
treatment according to best chance
or laryngeal fractures:
of survival with least expenditure
of resources (time, personnel,
➢ Respiratory distress, use of
equipment, supplies).
accessory muscles of
INITIAL ASSESSMENT respiration, flaring of the nares
• This comprises of: ➢ Apnea
➢ Resuscitation and primary ➢ Cyanosis
survey ➢ Tracheal tag
➢ Secondary survey ➢ Loss of consciousness and
➢ Definitive treatment or transfer presence of major facial, neck or
for definitive care chest injuries that might
• Many mistakes are caused by not obstruct the airway may all
examining the patient carefully. indicate the need for
• The peripheral injuries are unlikely endotracheal or nasogastric
to kill the patient even if you miss intubation once the neck has
them but you can easily overlook been stabilized.
serious central ones especially • Look for signs of inadequate
injuries to the chest and abdomen. ventilation
• You will not miss a bone sticking
out of a trouser leg but you can

36
SURGERY MK
➢ Chest should be uncovered and
palpated to assess respiratory
movements.
➢ Confirm the presence of air
entry into the lungs with a
stethoscope (though some books
say the primary survey should
not use instruments however do
whatever it takes to save the
patient).
➢ The neck and jaws should be
palpated to check for deformity.
➢ Insert a finger into the mouth to
extract any foreign bodies and to
check for jaw fractures.
Occasionally severe damage to
the upper airways or trachea
makes intubation impossible.
➢ An emergency tracheostomy is
indicated if the patient is deeply
cyanosed or apneic and an
endotracheal tube cannot be
inserted safely.
• Management may involve Figure 10: Endotracheal intubation
➢ Secretion control
➢ Intubation or
➢ Surgical airway e.g.
cricothyroidotomy, emergency
tracheostomy

37
SURGERY MK

Figure 13: : Tracheostomy

• Establish a clear airway (chin lift or

jaw thrust) but protect the cervical
spine at all times.

Figure 11: Endotracheal tube

Figure 14: Jaw maneuvers to clear airway

• If the patient can talk, the airway is

likely to be safe, however, remain
vigilant and recheck.
• An oropharyngeal airway may be
put but in an unconscious patient
with no gag reflex replace with an
endotracheal tube inserted by an
experienced anesthetist.
Figure 12: Tracheostomy
• Definitive airway should be
established if the patient is unable
to maintain integrity of airway.

38
SURGERY MK
mask from the moment of arrival in
the accident and emergency
department.
• An oxygen saturation monitor
placed on an extremity is a valuable
means of assessing the
effectiveness of the patient’s
ventilation.
INSPECTION AND PALPATION
Figure 15: Oropharyngeal airway • Open wounds or flail segments in
• Cervical spine protection is critical the chest indicate the need for chest
throughout the airway management drain and positive-pressure
process. ventilation.
➢ A flail segment occurs when
• Movement of the cervical spine
several ribs are fractured in two
could cause spinal injury so
places. The flail segments sink
movement of the cervical spine
inwards during inspiration
should be avoided unless absolutely
(paradoxical breathing)
necessary for maintaining an
airway. • Bruising over the chest indicates
that rib fractures are likely
BREATHING • Surgical emphysema
• Assess the condition and function (subcutaneous emphysema)
of the thoracic cage. suggests that the pleura has been
• Once you ensure that the airway is breached.
patent, assess the adequacy of ➢ It presents as a crackling
ventilation by: sensation in the subcutaneous
➢ Inspecting: for symmetry and tissues. It is due to air being
chest movements trapped in the subcutaneous
➢ Palpating: for symmetry and tissues.
chest movements ➢ A ‘sucking’ chest wound may
➢ Percussion: for dullness be present.
➢ Auscultation: for breath sounds
PERCUSION
• Patients with multiple injuries or
• A tension pneumothorax must be
chest problems causing hypoxia
suspected if breathing is difficult.
should be given high-flow oxygen
➢ The trachea is deviated to the
through a closed circuit oxygen
contralateral side and there is

39
SURGERY MK
decreased air entry over the ➢ Hemothorax: Will usually
affected lung. require intercostal drain
➢ Although the clinical diagnosis insertion
will have to be confirmed with a ➢ Pneumothorax: may require
chest radiograph, a chest drain intercostal drain insertion
should be inserted on the
TENSION PNEUMOTHORAX
evidence of the clinical signs if
the patient is unstable. • The accumulation of air under
• Bilateral tension pneumothoraces pressure in the pleural space.
are very rare, but cause severe • An imminent danger is that the lung
cardiac and respiratory will collapse under the pressure.
compromise. • In tension pneumothorax, air enters
➢ They present with cyanosis, the pleural cavity and is trapped
severe air hunger, a weak pulse there during expiration so the air
and hypotension. pressure within the thorax mounts
➢ In bilateral pneumothoraces, the higher than atmospheric pressure,
trachea remains central but air compresses the lung, may displace
entry is poor into both lungs. the mediastinum and its structures
➢ The rapid insertion of chest (including the lung) toward the
drains which are connected to opposite side and cause
under-water seal drainage cardiopulmonary impairment. Also
bottles relieves the situation. called pressure pneumothorax.
AUSCULTATION
• Decreasing air entry and breath
sounds indicate the need for chest
drainage.
LESIONS ACUTELY IMPAIRING
VENTILATION
• Lesions acutely impairing
ventilation:
➢ Tension pneumothorax:
requires needle thoracostomy
followed by drainage.
➢ Flail chest: management
involves ventilation.

40
SURGERY MK

Figure 16: A pneumothorax. Note deviation of the trachea away from the affected side.

FLAIL CHEST
• Occurs when a segment of the rib
cage breaks due to trauma and
becomes detached from the rest of
the chest wall.
• It occurs when multiple adjacent
ribs are broken in multiple places,
separating a segment, so a part of
the chest wall moves
independently.
• The flail segment moves in the
opposite direction to the rest of the
chest wall, it goes in while the rest
of the chest is moving out, and vice
versa.
• This so called “paradoxical
breathing” is painful and increases
the work involved in breathing.
Figure 17: A pneumothorax

41
SURGERY MK

Figure 18: A flail chest

Figure 19: A flail chest

42
SURGERY MK

Figure 20: A hemothorax (left) and an intercostal drainage (right)

CIRCULATION • Blood loss is the main preventable

• Restoration of the circulation may cause of death after trauma. To
take precedence over the airway assess blood loss rapidly observe:
and ventilation if the patient is ➢ Level of consciousness
breathing satisfactorily. ➢ Skin color
• It can be assessed simultaneously ➢ Pulse
with the airway and breathing if an ➢ Bleeding- this should be
experienced anesthetist is available assessed and controlled
to manage ventilation. o IV access with 2 large bore
• There are two major causes of cannulae in an upper limb.
circulatory failure: Cardiac Access by cut down or
damage/tamponade and central venous
hemorrhage. catheterization may be done
• Cardiac tamponade is rare but life according to skills
threatening and easily missed. It available.
must therefore be briefly o Fluid therapy should be
considered in all patients with initiated with up to 2L of an
major injuries, especially in those isotonic (either Ringer’s
with penetrating injuries of the lactate or Normal Saline)
chest. crystalloid solution.
Pediatric patients should
receive an IV bolus of
20ml/kg.
o Use warmed fluids
wherever possible

43
SURGERY MK
o At cannula insertion, blood cavity, around the heart and
should be taken for cross- embarrass its action.
match and baseline • This reduces the cardiac output,
investigations. producing a weak pulse and
o IV fluids will need to be hypotension.
given rapidly. Ringer’s • The condition should be suspected
lactate is the preferred initial if the JVP is markedly elevated and
crystalloid solution. rises rather than falls with
o Direct manual pressure inspiration (Kussmaul’s sign),
should be used to stem however jugular venous distention
visible bleeding (not may not occur in a patient who has
tourniquets, except for lost a large quantity of blood.
traumatic amputation, as • Pulsus paradoxus, when the pulse
these cause distal ischemia) volume decreases on inspiration
o Occult bleeding into the rather than increasing, may be
abdominal cavity and present.
around long-bone or pelvic • The heart sounds are usually
fractures is problematic but muffled and poorly heard.
should be suspected in a • Beck’s triad of acute cardiac
patient not responding to tamponade:
fluid resuscitation. ➢ Hypotension (low arterial blood
pressure)
➢ Distended neck veins (raised
JVP)
➢ Muffled/distant heart sound
• Chest X-ray may show an enlarged
cardiac shadow.
• An echocardiogram will confirm
the diagnosis.
• The patient’s condition may be
stabilized by aspirating the blood
Figure 21: An IV line with fluids running
from the pericardial sac using
CARDIAC TAMPONADE echocardiography and
• Occurs when large quantities of electrocardiography to ensure
blood collect within the pericardial correct placement of the needle and

44
SURGERY MK
catheter before definitive surgery is cold extremities, a rapid,
undertaken. thready pulse, tachypnea and
hypotension.
REVEALED HEMORRHAGE
• Visible arterial bleeding presents as DISABILITY/NEUROLOGICAL
a pulsating stream of bright red STATUS
blood coming from an open wound, • After A, B, and C above, rapid
whereas venous bleeding is dark neurological assessment is made to
and continuous. establish:
• Arterial hemorrhage from an open ➢ Level of consciousness, Using
wound can usually be controlled by Glasgow coma scale.
direct digital pressure or proximal (Alternatively the APVU scale
arterial compression as well as use can be used for quick
of sterile vascular clamps before assessment)
definitive surgery. ➢ Pupils: size, symmetry and
• Venous bleeding always responds reaction
to simple pressure and may be ➢ Any lateralizing sign
made worse by the application of a ➢ Level of any spinal cord injury
tourniquet. (limb movements, spontaneous
respiratory effort)
CONCEALED (INTERNAL)
➢ Oxygenation, ventilation,
HEMORRHAGE
perfusion, drugs, alcohol and
• These are much harder to diagnose hypoglycemia may all also
and therefore must be suspected in affect the level of
all patients with multiple or serious consciousness.
injuries.
• It always accompanies major
fractures of long bones and
fractures of the pelvis.
• They must be quickly diagnosed
and treated in order to save lives.
CLINICAL SIGNS OF
HEMORRHAGE
• Diagnosis based on finding signs
of:
➢ Hypovolemic shock- pale,
anxious, sweaty patient with Figure 22: The Glasgow coma scale

45
SURGERY MK

Figure 23: The Glasgow coma scale

Figure 24: The AVPU scale

46
SURGERY MK

• Patients should be re-evaluated dysrhythmias, ischemia, cardiac

frequently at regular intervals. injury.
• Deterioration can occur rapidly and • Urinary catheters: Output of urine
often patient can be lucid following can guide fluid replacement; it
a significant head injury before reflects renal perfusion. (note: prior
worsening. to catheter insertion urethral injury
• Signs such as pupil asymmetry or should be excluded- suspect if there
dilatation, impaired or absent light is blood at meatus, pelvic fracture,
reflexes, and hemiplegia/weakness scrotal blood, perineal bruising.)
all suggest an expanding Per rectum and genital examination
intracranial mass or diffuse edema. are mandatory prior to catheter
• This requires IV mannitol, insertion.
ventilation and urgent
neurosurgical opinion.
EXPOSURE/ ENVIRONMETAL
CONTROL
• Undress the patient, but prevent
hypothermia.
• Clothes may need to be cut off. Figure 25: A urinary catheter
• After examination, attend to
• Gastric catheters are inserted to
prevention of heat loss with
reduce aspiration risk. Suction
warming devices, warmed
should be applied.
blankets, etc.
• Other monitoring: monitoring of
FLUIDS AND GLUCOSE resuscitation by measuring various
• See circulation for fluids. important parameters:
• Check the random blood sugar and ➢ Pulse rate, blood pressure,
give glucose where needed as well ventilator rate, arterial blood
as insulin with potassium chloride. gases, body temperature and
urinary output.
ADDITIONAL MONITORING
• ECG monitoring: this can guide
resuscitation by diagnosing

47
SURGERY MK
➢ Pulse oximetry measure oxygen • The secondary survey thus
saturation comprises of History (AMPLE) and
physical examination.
➢ A- allergies
➢ M- medication currently used
➢ P- past illnesses/ pregnancy
➢ L-last meal
➢ E- events/Environment related
to injury
Figure 26: A pulse Oximeter • The physical examination will
repeat some examinations already
➢ Remember: blood pressure is a undertaken in the primary survey
poor measure of perfusion. and will be further informed by the
• In trauma centers, teamwork should progress of the resuscitation.
ensure critically injured patients are • Examination aims to identify
evaluated as diagnostic procedures serious injuries, occult bleeding etc.
are performed simultaneously, thus
• A review of neurological status
reducing the time to treatment.
including GCS score is also
• A team approach is demanding of undertaken.
personnel and resources and in
• Back and spinal injuries are
smaller institutions, non-hospital
commonly missed and pelvis
settings or with mass casualties,
fractures cause large blood loss
available personnel and resources
which is often underestimated.
can rapidly be overwhelmed.
PHYSICAL EXAMINTION-
SECONDARY SURVEY HEAD TO TOE
• This begins after the “ABCDE” of • Head- head and face fracture, CSF
the primary survey, once leaks from nose and ears.
resuscitation is underway and the • Eyes
patient is responding with ➢ Record the size and reaction to
normalization of vital signs. light (fixed and dilated pupils
• The secondary survey is essentially suggest severe brain damage)
a head-to-toe examination. ➢ Always ask the conscious
• Completion of the history and patient if he can see with both
reassessment of progress, vital eyes.
signs. ➢ Look for eye injury in the
unconscious patient.

48
SURGERY MK
➢ In unconscious patients check ➢ Auscultate for reduced air entry
for the corneal reflex. and added sounds. Coarse
➢ Examine the conjunctiva and crepitations may suggest
tongue for pallor and cyanosis. aspiration of blood or vomit.
You are not looking for signs of • Abdomen
anemia but rather the pale white ➢ The following may suggest
tongue of massive hemorrhage intra-abdominal injury.
or a discolored purplish tongue o Abdominal or shoulder tip
suggestive of hypoxia pain
• Mouth o Reduced movement with
➢ Can a patient open and close his respirations
mouth? o Distension
➢ Do the teeth occlude properly? o Bruising
➢ Failure to do either of these o Rigidity
suggests a fracture or o Tenderness
dislocation of the mandible. o Absent bowel sounds
➢ Is the mandible stable? ➢ If there is major hemorrhage
• Chest within the abdomen, signs of
➢ Is there pain on breathing? hypovolemic shock will be
➢ Watch the breathing pattern, is present. The abdominal organs
there a paradoxical movement prone to trauma are spleen and
or inequality between the sides liver. These organs can rupture
of the chest? and cause massive hemorrhage.
➢ Assess the depth of breathing, • Pelvis
does the patient use accessory ➢ Compress the iliac bones and
muscles for breathing? spring the pubis to determine
➢ Are there bruises or penetrating whether there is a fracture.
wounds? ➢ Look for blood at external
➢ Palpate for fractures and meatus of the urethra or if
surgical emphysema catheterized check for
➢ Is the trachea centrally hematuria, which would suggest
positioned or shifted? a urethral injury or bladder
➢ Percuss the chest, are both sides injury.
equal? Is there any hyper- ➢ Is the bladder full, empty or
resonance suggestive of a ruptured?
pneumothorax, or dullness
suggestive of hemothorax?

49
SURGERY MK
• Limbs after the secondary survey. These
➢ Look for swelling, bruising, include:
rotation or deformity. ➢ X-rays- Skull, lateral cervical
➢ Feel distal pulses e.g. dorsalis spine, Chest, Abdominal/Pelvic
pedis and radials. ➢ Focused abdominal sonogram
➢ Test sensation for trauma (FAST) is used for
➢ Palpate all bones unless there is rapid detection of intra-
severe pain or obvious injury abdominal bleeding that often
➢ Move all joints unless painful occurs early in the resuscitative
➢ Always examine the distal process
pulses when there is a feature or ➢ Ultrasound investigations
soft tissue injury to a limb ➢ Bronchoscopy
➢ Record all injuries and wounds ➢ CT/MRI scans: only done for
carefully in the patient notes. hemodynamically stable
➢ A trauma form with a two patients
figures of a body, one front and ➢ Angiography
one back view will help to
record injuries and it is quicker DEFINITIVE CARE
to draw the site of a laceration • Choosing where definitive care
than to describe it. should continue most appropriately
will depend on results of the
ADDITIONAL INVESTIGATIONS primary and secondary surveys
• A range of further diagnostic tests (what’s the final diagnosis?)
and procedures may be required • Refer to appropriate closest
facilities available.

50
SURGERY MK
FLUID, ELECTROLYTE
IMBALANCE AND NUTRITION

FLUIDS, ELECTROLYTE IMBALANCE AND

NUTRITION
FLUIDS, ELECTROLYTES AND ELECTROLYTE
IMBALANCE
• Surgical illness and operative intervention disrupt homeostasis and lead to
changes in fluid, electrolyte and acid-base balance.
• Total body water constitutes 50-70% of total body weight.
• Total body water is greater in lean individuals because fat contains little water
(60%).
• Total body water is greater in newborns (70%) then decreases with age to around
50%.
➢ Example: an average 70kg man would have 42 litters of water since 1L of
water=1kg.
• The total body water is divided amount 2 compartments:
➢ Intracellular fluid (ICF): 22-30L
➢ Extracellular fluid (ECF): 10-15L
• Intracellular fluid accounts for 2/3 of total body water.
• Intracellular fluid is mostly in skeletal muscle mass thus it is slightly lower in
females (50%) than males (60%).
• The cell wall separates the ICF from the ECF and acts as a semipermeable
membrane.
• Extracellular fluid accounts for 1/3 of total body water. ECF is made up of plasma
(1/4 of ECF)-3L and Interstitial fluid (3/4 of ECF)-10-12L.
• The capillary membrane separates plasma and interstitial fluid and acts as a
semipermeable membrane.

51
SURGERY MK

Figure 27: Body fluids

• Water flows freely between the 3 compartments, shifting compartments to

maintain osmotic equilibrium between them.
• Hydrostatic pressure at the arteriolar end of the capillary and the oncotic pressure
(25mmHg) of plasma at the venular extremity govern the bidirectional movement
of water between the plasma and interstitial fluid across the capillary bed.
• The exchange of fluid across the capillary membranes is essential for supply of
nutrients and oxygen to the tissues and the elimination of waste products of
metabolism.
• Osmolality is the amount of solute dissolved in a solvent like water measured in
weight (Kg) i.e. per Kg of solvent.
• Osmolarity is the amount of solute dissolved in a solvent like water measured in
volume (L) i.e. per L of solution.
• The normal plasma osmolality (total particle concentration) is 280-295
mosmol/Kg H2O.
• The main cation in plasma is sodium.
• The main anions in plasma are chloride and bicarbonate ions.
• In normal state, plasma electrolytes account for the majority of the plasma
osmolality. There is a good correlation between the plasma osmolality and
plasma sodium concentration i.e. a high plasma sodium concentration signifies
hyperosmolality and vice versa.
[𝑔𝑙𝑢𝑐𝑜𝑠𝑒 𝑖𝑛 𝑚𝑔/𝑑𝑙] [𝐵𝑈𝑁]
• Plasma osmolality= 2[𝑁𝑎] + +
18 2.8
• Note [Na] is in mmol/L and [BUN], [glucose] in mg/dl.
• Osmolar gap= measured osmolality- calculated plasma osmolality
• Normal osmolar gap <10mmol/L
• If osmolar gap> 10mmol/l suspect lactic acid, ketones, methanol, ethanol.

52
SURGERY MK
• As a rule of thumb:
➢ Fluid input should match fluid output
➢ The daily (24-h) requirements of an average subject are 100 mmol
(2mmol/Kg) Sodium and 60 mmol (1mmol/Kg) Potassium.

Figure 28: Daily requirements of a normal 70-Kg man

INTRAVENOUS FLUID THERAPY

• Indications:
➢ Preoperative resuscitation e.g. before emergency surgery, elective surgery in
a jaundiced patient
➢ Replacement of abnormal losses e.g. dehydration due to vomiting, diarrhea,
ileostomy bags, shock due to hemorrhage or sepsis or burns
➢ Provision of normal daily requirements if patient is nil by mouth (total
parenteral nutrition).
➢ Postoperative resuscitation
➢ Electrolyte disorders
• Patients not eating or drinking must be provided with their daily requirements i.e.
2.5-3L of water, 100mmol Sodium, 60 mmol Potassium, 5mmol Calcium and
1mmol magnesium.
• Types of fluid:
➢ Crystalloids: used to provide normal daily requirements and replace additional
losses.
o Normal saline (0.9% sodium chloride): 1L contains 154mmol of NaCl.
o Dextrose saline: 1L contains 31 mmol NaCl and 40g dextrose
o 5% Dextrose: 1L 5% dextrose contains 50g dextrose
o Hartmann’s solution (Sodium lactate solution or Ringer’s lactate):
replacement fluid favored by anesthetists because it is a physiological

53
SURGERY MK
mixture of ions and water. It should be avoided in liver failure but since it
does not contain glucose it can be used in diabetics. 1L Hartmann’s
solution contains 3 mmol Calcium, 4mmol Potassium, 28mmol
Bicarbonate ions (lactate), 109 mmol Chloride and 130mmol Sodium
ions.
➢ Colloids:
o Natural e.g. blood, albumin
o Synthetic e.g. gelatin-based infusions
• Potassium can be added to Normal saline and Dextrose saline in the form of
potassium chloride (KCL).
• Calculation of drop rate of IV fluids:
➢ 1ml = 16 drops in usual drip set. For microdrip set 1ml=60 drops.
➢ Drop rate (/min)= Quantity of fluid required in L/day x 10
o E.g. if 2.5 liters is need per day, Drop rate= 2.5 x 10= 25 drops/minute
➢ Number of drops/min= Fluid volume (ml) to be infused divided by 4
o E.g. 100ml/hour means 25 drops/minute
➢ Number of microdrop/min= Volume in ml/hour
o E.g. 50 microdrop/min =50ml/hr
• Complications of fluid therapy:
➢ Fluid overload: pulmonary edema and cardiac failure
➢ Thrombophlebitis, hematoma and cellulitis in local area
➢ Pyogenic reaction and bacteremia
➢ Air embolism
FLUID IMBALANCES
• Fluid status is judged by examination of the patient every day:
➢ Check for signs of dehydration
➢ Check blood pressure and pulse
➢ Examine the abdomen and chest
➢ Check the ankles for edema
• The fluid balance chart should be examined to determine the patient’s fluid input
and output. The hourly urine output is a good guide to fluid status, urine output
should not fall below 30ml/h.
• There 2 major regimens used for fluid replacement. If the patient is also losing
additional fluid (e.g. vomiting, nasogastric tube, ileostomy) then this volume
must also be measured and replaced over and above the normal requirements
using normal saline.

54
SURGERY MK
➢ Regimen one: 1L of Normal saline (over 8 hours plus) and 2L of 5% dextrose
with 20mmol KCL added to each bag (over 8 hours plus)
➢ Regimen two: 3L of dextrose-saline with added 20 mmol KCL to each 1L
over 8 hours plus.
• Assessment of adequacy of resuscitation:
➢ Clinical history and observation: Pulse, blood pressure, skin turgor
➢ Urine output: oliguria is defined as <0.5 ml/kg per h
➢ Central venous pressure (CVP) or pulmonary capillary wedge pressure
➢ Response of urine output or CVP to fluid challenge:
o 200-250ml bolus of colloid is administered as quickly as possible
o Response in CVP or urine output should be seen within minutes
o Size and duration of the CVP response rather than actual value recorded
is more important
WATER EXCESS
• It can be divided into:
➢ Water and salt excess: occurs in CCF, cirrhosis, nephrotic syndrome,
hypoproteinemia, renal failure, excessive saline infusion.
➢ Water intoxication (predominant water excess): occurs in TURP
(transurethral resection of prostate) when irrigating fluid water or glycine is
used, excess infusion of 5% dextrose only, SIADH section (with lobar
pneumonia, empyema, oat cell carcinoma and head injury), psychogenic
polydipsia
• There is an expansion of the intracellular and extracellular fluid compartments
and a low serum sodium.
• Clinical features:
➢ Widespread edema:
o Gain in body weight (most sensitive and consistent sign)
o Circulatory overload: tachycardia, pulmonary edema, hypertension,
distended neck veins
o Bilateral basal crepitations and ascites
o Pedal edema
➢ Irritability, drowsiness, weakness, convulsions and coma
➢ Nausea and vomiting
➢ Passing dilute urine
➢ Raised central venous pressure and pulmonary capillary wedge pressure
• Investigations:

55
SURGERY MK
➢ Full blood count: hematocrit
➢ Urea and Electrolytes: low sodium, low potassium, low blood urea.
• Treatment is by water restriction, observation (preferably in ICU), management
of electrolyte imbalance and sometimes administration of hypertonic saline.
• Administration of diuretic and hypertonic saline should be avoided as it can cause
rapid changes in serum sodium water level which will lead to neuronal
demyelination and fatal outcome.
WATER LOSSE (VOLUME DEFICIT)
• This is the most common fluid disorder.
• Both ECF and ICF are lost but it is usually ECF loss which is more important and
assessed
• It can be:
➢ Isotonic volume depletion: both salt and water are lost and this leads to
hypovolemia. Fluid loss is only of the ECF and so early intravascular volume
reduction occurs causing hypotension.
o Features: hypotension and decreased tissue perfusion. Dry tongue, rapid
pulse, cold clammy extremities, sunken eyes, oliguria, raised blood urea,
decreased urinary sodium. Hypovolemia can be mild (<2L fluid loss),
Moderate (2-3 L fluid loss) or severe (>3 L loss)
➢ Loss of only water with minimal loss of electrolytes which leads into
dehydration with proportionate decrease in total body water. As ECF
including intravascular fluid loss is less, hypotension is less.
o Features: severe thirst, confusion and convulsions due to hypernatremia.
Blood pressure is relatively normal. Dehydration can be mild (weight loss
5%), moderate (10%) and severe (15%)
• Causes include:
➢ Losses that mimic ECF
o Hemorrhage
o Loss of GI fluid- vomiting, NG tube suction, diarrhea, fistula drainage
o Postoperative fluid sequestration (third spacing): intestinal obstruction
o Intra-abdominal and retroperitoneal inflammation (e.g. pancreatitis,
peritonitis)
o Systemic inflammatory response syndrome (SIRS), burns, sepsis,
pancreatitis

56
SURGERY MK

➢ Losses that are principally water

o Fever
o Osmotic diuresis
o Diabetes insipidus
o Prolonged water deprivation
o Inadequate input during procedure
• Management:
➢ Evaluation is done by doing serum sodium, urinary sodium and blood urea
➢ Isotonic volume depletion: give 0.9% normal saline.
➢ Pure water depletion: correct by more water intake/intravenous 5% dextrose
➢ Monitoring fluid therapy by skin and tongue examination, weight gain, pulse,
blood pressure, central venous pressure and pulmonary capillary wedge
pressure.

ELECTROLYTE IMBALANCE
• The concentration of electrolytes is closely maintained in ECF and ICF.

Figure 29: Electrolyte concentrations in ECF and ICF

HYPONATREMIA
• This is the most common acute biochemical disturbance encountered in surgical
practice.
• Normal sodium ECF concentration= 135-145 mEq/L
• Hyponatremia is low serum sodium (<130mmol/L) but treatment warranted with
severe <100mmol/L in the acute type or <115mmol/L in the chronic type.
• Hyponatremia can be
➢ Acute- presents as neurological manifestations
➢ Chronic- causes pontine myelinolysis. It presents as behavioral changes,
progressive weakness, and cranial nerve palsies.
• Causes:
➢ Hypovolemic hyponatremia: due to hypovolemia by the following:
o GI losses (NG tube suctioning, vomiting, diarrhea)

57
SURGERY MK
o Renal losses
o Diuretic therapies e.g. furosemide and thiazide diuretics
➢ Euvolemic hyponatremia: due to
o Hypothyroidism
o SIADH
o Adrenal insufficiency (Addison’s disease)
➢ Hypervolemic hyponatremia: rapid absorption of fluid occurs into
intravascular compartment leading to pulmonary and cerebral edema.
o Congestive heart failure
o Cirrhosis
o Nephrotic syndrome
• Clinical features:
➢ Asymptomatic unless severe or acute
➢ Irritability, disorientation/confusion, coma, seizures, Abdominal cramps,
Nausea, vomiting, and pitting edema over the sternum
➢ When plasma sodium falls below 120mmol/L the patient becomes confused.
There is severe contraction of ECF with hypovolemia, poor venous filling,
dry coated tongue, oliguria with dark scanty urine, dry skin with loss of turgor
(dry wrinkled skin) and sunken eyeball.
➢ If sodium levels decreases below 110mmol/L convulsion and coma may
ensue.
➢ In chronic hyponatremia- hypothermia, reduced tendon reflexes and
pseudobulbar palsy.
• Investigations:
➢ Serum sodium (low)
o Sodium deficit= (125- Present serum sodium) x body weight in Kg x 0.6
➢ Urine sodium (low)
➢ Serum and Urine osmolarity
MANAGEMENT
• Treat underlying cause. Losses of sodium can be replaced by increasing sodium
intake without increasing daily fluid intake (e.g. giving normal saline
continuously), water retention should be treated by fluid restriction.
• CNS manifestations
➢ 200ml 5% NaCl over 6 hours. Monitor serum sodium hourly.
➢ Aim to increase sodium to 120mmol/l at a rate of 0.5-1.0 mmol/l per hour
➢ If no CNS symptoms, do not use hypertonic saline.

58
SURGERY MK
➢ Once serum sodium is around 120 mmol/L, stop active therapy and restrict
fluid intake to approximately 500ml/day.
• Asymptomatic: Can use conservative measure like fluid restriction may be
enough
• SIADH
➢ Restrict fluid intake to 50-60% of estimated maintenance fluid requirements
(+/- 1L/day)
HYPERNATREMIA
• Normal sodium ECF concentration= 135-145 mmol/L
• This is defined as a serum sodium >150 mmol/L
• Excess infusion of normal saline cause overload in circulating salt and water. It
is usually due to water deficit.
• Hypernatremia types include:
➢ Euvolemic hypernatremia (pure water loss): due to failure of water intake
like in comatous patients, bedridden people, postoperative patients and in
patients with high fever leading into extra-renal loss of water. It can occur in
diabetes insipidus or chronic renal failure as renal loss of water.
➢ Hypovolemic hypernatremia (among loss of water and sodium, more water
is lost than sodium): it is due to vomiting, diarrhea, more undue sweating
(extra-renal), osmotic diuresis by glucose/mannitol (Renal)
➢ Hypervolemic hypernatremia (both sodium and water gain but sodium is
more than water gain): seen in more salt intake, excess steroids, sodium
bicarbonate/hypertonic saline infusion (salt gain).
• Causes:
➢ Water loss more than electrolyte
➢ Cardiac failure
➢ GIT losses
➢ Renal losses (Renal dysfunction)
➢ Diabetes insipidus
➢ Diabetes mellitus
➢ Increase in sodium
o Hyperaldosteronism
o Cushing’s
o Excessive saline or Sodium bicarbonate infusion
➢ Drugs: NSAIDs, corticosteroids

59
SURGERY MK
• Clinical features:
➢ Pitting edema
➢ Puffiness of face
➢ Increased urination
➢ Often dilated jugular veins
➢ Features of pulmonary edema
• Investigations:
➢ Serum Sodium
➢ Urine Sodium
➢ Renal function tests
➢ Hematocrit
MANAGEMENT
• Correct water deficit- rehydrate patient if dehydrated then administer half
strength saline (0.45%) and later 5% dextrose i.e. gradual controlled correction
is done. Otherwise cerebral edema and hyperglycemia can develop. There should
be oral and nasogastric administration of water/fluids.
• Stable/asymptomatic patients
➢ Take it easy (hypernatremia should be corrected slowly)
➢ Replace fluids orally
• Unstable/symptomatic patients
➢ IV fluids with NS, DNS
➢ Avoid 5% dextrose as sodium may drop too fast
➢ Rate of lowering serum sodium 0.5-1mmol/hr, aim for 12 mmol/L in 24hours
and not more than this.
➢ Estimate the effect of 1 liter of any infusion on serum sodium
𝐼𝑛𝑓𝑢𝑠𝑖𝑜𝑛 𝑠𝑜𝑑𝑖𝑢𝑚−𝑆𝑒𝑟𝑢𝑚 𝑠𝑜𝑑𝑖𝑢𝑚
➢ Change in serum Sodium=
𝑇𝑜𝑡𝑎𝑙 𝑏𝑜𝑑𝑦 𝑤𝑎𝑡𝑒𝑟+1
➢ The answer is in mmol/L. The formula helps to calculate the infusion rate so
that you do not exceed 1 mmol/min.

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SURGERY MK
HYPERKALEMIA
• Normal potassium ECF concentration= 3.5-5.5 mEq/L
• Hyperkalemia is a serum potassium >5.5 mmol/L.
• Potassium excess is a dangerous condition which can cause sudden cardiac arrest.
• Causes:
➢ Trauma and tissue destruction
➢ Tumor necrosis
➢ Crush injuries
➢ Burns
➢ Renal failure
➢ Excessive intake of potassium rich food and supplements
➢ Metabolic acidosis
➢ Addison’s disease
➢ Diuretic therapy (potassium sparing diuretics), cyclosporine, beta blockers
➢ Transfusion of stored blood
➢ Insulin deficiency
➢ Diabetic ketoacidosis
➢ Familial hyperkalemic periodic paralysis
• Clinical features:
➢ Symptoms: Muscle weakness, diarrhea, colickly abdominal pain
➢ Signs:
o Ascending paralysis with respiratory failure
o Cardiac instability, ventricular fibrillation, cardiac arrest
o May have signs of acute kidney injury or metabolic acidosis
• Investigations:
➢ Serum potassium
o Mild hyperkalemia: 5.5-5.9
o Moderate hyperkalemia: 6.0-6.5
o Severe hyperkalemia: >6.5 and ECG changes
➢ ECG findings:
o Bradycardia
o Flat P waves
o Increased PR interval
o AV block
o Wide QRS complex
o Tall peaked symmetrical T waves (most important to remember)

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SURGERY MK
MANAGEMENT
• Stop source of potassium (Oranges, bananas, ACEI, potassium sparing diuretics,
septrin, heparin, NSAIDs, Beta-blockers)
Mild hyperkalemia (5.5- Moderate hyperkalemia (6.0- Severe hyperkalemia (>6.5)
5.9) 6.5)
• Push Potassium out of • Protect the heart: 10mls • Protect the heart: 10mls
the body 10% Calcium Gluconate 10% Calcium Gluconate
➢ Furosemide over 10 mins. Effect is over 10 mins. Effect is
1mg/kg IV temporary but can be temporary but can be
(hydrate patient repeated after 15 minutes. repeated after 15 minutes.
first if dehydrated) • Push Potassium into cells • Push Potassium into cells
➢ Kayexalate/sodium ➢ 50mls 50% Dextrose ➢ 50mls 50% Dextrose
Resonium 15-30g with 10IU soluble with 10IU soluble
in 50-100ml 20% insulin over 15-20 insulin over 15-20
Sorbitol or with mins. May be given 2-4 mins. May be given 2-
lactulose PO/PR hourly as required. 4 hourly as required.
➢ Consider Monitor serum glucose Monitor serum glucose
hemodialysis if and potassium 2-4 and potassium 2-4
refractory hourly hourly
➢ 10-20mg Nebulized ➢ 10-20mg Nebulized
Salbutamol (or 0.5mg Salbutamol (or 0.5mg
in 100ml of 5% glucose in 100ml of 5%
over 15 min-rarely glucose over 15 min-
used) rarely used)
• Push Potassium out of the • Push Potassium out of the
body body
➢ Furosemide 1mg/kg IV ➢ Furosemide 1mg/kg
(hydrate patient first if IV (hydrate patient
dehydrated) first if dehydrated)
➢ Kayexalate ➢ Kayexalate
(polystyrene (polystyrene
sulphonate) /sodium sulphonate)/sodium
Resonium 15-30g in Resonium 15-30g in
50-100ml 20% Sorbitol 50-100ml 20%
or with lactulose Sorbitol or with
PO/PR lactulose PO/PR
• Consider hemodialysis if ➢ Consider hemodialysis
refractory if refractory

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SURGERY MK
HYPOKALEMIA
• This is a serum potassium <3.5, it may be associated with hypomagnesemia and
hypocalcemia.
• Causes:
➢ GIT losses (NG tube suctioning, vomiting, diarrhea)
➢ After trauma or surgery
➢ Pyloric stenosis with gastric outlet obstruction
➢ Duodenal fistula, ileostomy
➢ After ureterosigmoidostomy
➢ Insulin therapy
➢ Poisoning
➢ Drugs like beta agonists
➢ Renal losses (Renal disease)
➢ Metabolic alkalosis
➢ Potassium wasting diuretics
➢ Cushing’s disease (Sodium retention leads to potassium loss)
➢ Familial periodic paralysis
• Clinical features:
➢ Symptoms:
o Muscle weakness
o Fatigue
o Constipation
o Muscle cramps
o Inability to produce concentrated urine so can cause nocturia and
polyuria
➢ Signs:
o Slurred speech
o Muscle hypotonia
o Paralytic ileus
o Ascending paralysis
o Reduced reflexes
o Tetany when associated with alkalosis (Alkalosis is due to increased
reabsorption of bicarbonate and excretion of hydrogen ions from the
proximal convoluted tubule in the kidneys)
o Arrhythmias

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SURGERY MK
• Investigations:
➢ Check potassium, other electrolytes and serum pH.
➢ ECG
o Flat or inverted T wave
o Prominent U wave
o QT interval prolongation
o Depression of ST segment
MANAGEMENT
• 20mmol KCL in 250-500ml Normal saline over 1 hour. Check Potassium before
repeating dose and ECG monitoring.
• Consider 6-12ml (5-10mml/l) 20% MgSO4 or 2ml 50% diluted in 50ml over 1
hour.
• It cardiac arrhythmia or arrest give 2mmol KCL per minute IV for 5mins. Repeat
once only if necessary
• Oral Potassium supplements if potassium >3.0.
• Hypokalemic alkalosis which occur in pyloric stenosis should be treated carefully
by IV potassium as there will be severe potassium loss.

Figure 30: ECG changes in both hypo and hyperkalemia

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SURGERY MK
HYPERCALCEMIA
• Normal serum calcium: 2.2-2.6mmol/L. Calcium is usually bound to albumin and
the levels of both calcium and albumin should be measured together (to correct
for low serum albumin, 0.025 should be added to the calcium for every 1g/L that
the albumin is lower than 40g/L)
• Corrected serum Calcium >2.65mmol/L
• Causes
➢ Endocrine: Hyperparathyroidism, ectopic PTH production, thyrotoxicosis,
Addison’s disease
➢ Bone disease: secondary tumor deposits, myeloma, lymphoma and paget’s
disease
➢ Malignancy
➢ Sarcoidosis
➢ Drugs e.g thiazides
➢ Vitamin D intoxication especially in renal patients
➢ Milk alkali syndrome
• Clinical features: usually asymptomatic until serum calcium <3.5 mmol/L but
above 3.5mmol/L clinical features include
➢ Muscle weakness
➢ Lassitude
➢ Drowsiness
➢ Hyperreflexia
➢ Anxiety and mania may develop with coma as a terminal event
➢ Polyuria and polydipsia indicate impaired renal concentration
➢ Nausea, vomiting, constipation and peptic ulceration may occur
• Investigations
➢ Serum Calcium, Urea + Electrolytes, Albumin, Magnesium, phosphate, ALP,
serum electrophoresis
➢ PTH
➢ X-rays
➢ ECG
o Short QT interval
o Wide QRS complex
o Flat T waves
o AV block
o May have fatal arrhythmias (frequent association with hypokalemia
increases risk of arrhythmias)

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SURGERY MK
MANAGEMENT
• Treat underlying cause
• Hydrate with normal saline 500ml/hr until urine output >200ml/hr then reduce
100-200ml/hr.
• Furosemide 1mg/kg only when patient has been hydrated or if in cardiac failure
• Hemodialysis or peritoneal dialysis with low calcium dialysate. Hemodialysis is
preferred.
• Prednisolone 40mg daily especially for Vitamin D intoxication, sarcoidosis,
multiple myeloma, metastasis
• Pamidronate 60-90mg in 500-100ml NS infusion.
HYPOCALCEMIA
• This is a serum calcium concentration <2mmol/L in a dramatic clinical picture
characterized by tetany.
• In its mildest form there may be paresthesia and muscle cramps.
• Full-blown picture shows hyperexcitability of the nervous system expressed as
carpopedal spasm (severe tonic contractions of the muscles of the hands: the
fingers are bunched together and flexed at the metacarpophalageal joints and
wrist is acutely flexed- main d’accoucheur, the toes are flexed and the ankle joint
is also acutely plantar flexed).
➢ Latent tetany may be demonstrated by Chovstek’s sign (Tapping over the
facial nerve induces twitching of the facial muscles)
➢ Trousseau’s sign (Carpal spasms induced by inflating a sphygmomanometer
cuff above systolic pressure)
• Causes:
➢ Hypoproteinemia
➢ Vitamin D deficiency
➢ Parathyroidectomy
➢ Acute pancreatitis
➢ Medullary carcinoma of thyroid
➢ Idiopathic
• Acute hypocalcium is treated by slow infusion of calcium gluconate (10%
solution).

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SURGERY MK
HYPERMAGNESEMIA
• It is rare.
• Serum magnesium >2.5 mmol/L (normal serum magnesium= 1.5-2.5 mmol/L
and intracellular magnesium= 26mmol/L)
• Magnesium is mainly deposited in bone (60%). It is a cofactor for many enzymes
necessary in phosphorylation of glucose in the cell and ATP utilization in muscle
fibers.
• Daily required dietary intake is 0.4g. it is reabsorbed well in proximal renal tubule
• Causes:
➢ Advance renal failure: treated with magnesium contain anatacids
➢ Ketoacidosis
➢ Intentionally produced hypermagnesemia while treating pre-eclampsia.
• Clinical features:
➢ Loss of tendon reflexes (most common)
➢ Neuromuscular depression
➢ Flaccid quadriplegia
➢ Respiratory paralysis
➢ Somnolence
➢ Hypotension
HYPOMAGNESEMIA
• Serum magnesium <1.5 mmol/L
• Causes:
➢ Malnutrition
➢ Alcohol
➢ Large GI fluid loss
➢ Patients on total parenteral nutrition
• Clinical features:
➢ Hyper-reflexia
➢ Muscle spasm
➢ Paresthesia
➢ Tetany
➢ It mimics hypocalcemia. It is often associated with hypokalemia and
hypocalcemia
• Treatment: 2g (16 mEq) of magnesium sulphate slow intravenously in 10
minutes. Later maintenance dose of 1mEq/kg/day as slow continuous infusion is
given/oral magnesium as needed.

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SURGERY MK
ACID-BASE BALANCE
• Normal blood pH= 7.35-7.45
• Factors which control the pH:
➢ Buffer systems
o Bicarbonate buffer
o Protein buffer
o Phosphate buffer
➢ Renal control of pH
➢ Respiratory control of pH
• Acidosis is pH of blood less than 7.35
• Alkalosis is pH of blood more than 7.45
• Note: the lungs and kidneys act in concert such that in the presence of mild renal
impairment, increased acid removal is achieved by the lungs and vice versa.
• Certain disease states overwhelm these homeostatic mechanisms and result in
significant accumulation acid or base with corresponding deviations from normal
pH.
METABOLIC ALKASOSIS
• Primary base excess i.e. bicarbonate. A standard bicarbonate above 27 mmol/L.
• Causes:
➢ Repeated vomiting due to any cause. Commonly seen in pyloric stenosis
(hypokalemic alkalosis)
➢ Nasogastric suctioning
➢ Excess alkali ingestion e.g. antacids
➢ Hypokalemia and diuretics, Excess citrate
➢ Cortisol excess either due to over administration or Cushing’s syndrome
• Clinical features:
➢ Cheyne-stokes breathing (irregular breathing- short breaths gradually
increasing to deep breaths then reducing again until breathing appears to
stop) with period of apnea 5-30 seconds
➢ Tetany due to alkalosis. More often latent tetany which is revealed by
Trousseau’s sign
• Investigations:
➢ Serum electrolytes
➢ Arterial blood gas analysis
o pH >7.45 (Hydrogen ion <36nmol/L)
o PaCO2 >6.0 KPa

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SURGERY MK
o Bicarbonate >32mmol/L
o Base excess >+5 mmol/L
• Treatment:
➢ Normal saline or double strength normal saline IV infusion with slow IV
potassium chloride 40 mmol/L in saline slowly under ECG monitoring.
➢ pH more than 7.7 is life threatening and requires rapid correction by infusion
dilute hydrochloric acid or ammonium chloride however with care and
monitoring.
RESPIRATORY ALKALOSIS
• Arterial PCO2 is below normal
• Causes:
➢ Hyperventilation during anesthesia, due to head injury/severe pain
➢ High altitude
➢ Hyperpyrexia
➢ Encephalitis, hypothalamic tumors, drugs like salicyclates, due to cirrhosis
of liver
➢ Apprehension and Hysteria
• Clinical features:
➢ It can be acute or chronic
➢ Headache, tingling, circumoral anesthesia, tightness in chest, tetany,
arrhythmias
• Investigations:
➢ Serum electrolytes
➢ Arterial blood gas analysis
o pH >7.45 (Hydrogen ion <36nmol/L)
o PaCO2 <5.3 KPa
o Bicarbonate 22mmol/L
o Base excess +2 mmol/L
• Management:
➢ Oxygen therapy
➢ Treat underlying cause
➢ Acetazolamide in high altitude
➢ Respiratory suppression due to alkalosis is treated by carbon dioxide

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SURGERY MK
METABOLIC ACIDOSIS
• It is an excess acid or base deficit. A standard bicarbonate below 21 mmol/L
• Causes:
➢ Increase in fixed acid:
o Diabetic ketoacidosis
o Starvation
o Hypoxia
o Renal insufficiency
o Cardiac arrest
o Excessive excessive
o Intestinal strangulation. Here anion gap is increased
➢ Loss of base
o Diarrhea
o Ulcerative colitis
o Gastrocolic fistula
o Intestinal fistula
o Ureterosigmoidostomy causes hyperchloremic hypokalemic acidosis.
Here anion gap is normal
• Clinical features:
➢ Rapid, deep, noisy breathing (air hunger)- Kussmaul’s breathing
➢ Cold clammy skin, tachycardia, right heart strain, altered level of
consciousness
➢ Cardiac arrhythmias, hypotension
➢ Anorexia, muscle weakness, vomiting
➢ pH below 7.2 is dangerous and life-threatening
➢ Capillary stasis
➢ Urine is strongly acidic
• Investigations:
➢ Serum electrolytes
➢ Arterial blood gas analysis
o pH <7.35 (Hydrogen ion >44nmol/L)
o PaCO2 <4.7 KPa
o Bicarbonate <18 mmol/L
o Base excess <-5 mmol/L
• Management:
➢ Correct hypoxia
➢ 50mmol of 8.4% sodium bicarbonate infusion IV

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SURGERY MK
o Sodium bicarbonate required in mEq/L= Body weight (Kg) x Base deficit
x 0.3
➢ Correct electrolyte imbalances
➢ Treat underlying cause
RESPIRATORY ACIDOSIS
• It is a feature of respiratory failure with high arterial PCO2 causing fall in pH.
• Causes:
➢ During and after anesthesia
➢ Chronic bronchitis
➢ Emphysema
➢ Thoracic disease
➢ Upper abdominal surgeries and disease.
➢ Respiratory airway obstruction
➢ Myasthenia gravis
➢ Poliomyelitis
➢ Stroke, infection, obesity and hypoventilation
• Clinical features:
➢ Features of hypercapnia: dyspnea, confusion, psychosis, hallucinations, sleep
disturbances, tremor, jerks and personality changes.
➢ CNS manifestations are more severe in respiratory acidosis than in metabolic
acidosis as lipid soluble Carbon dioxide crosses blood brain barrier easily
than bicarbonate
• Investigations:
➢ Serum electrolytes
➢ Arterial blood gas analysis
o pH <7.38 (Hydrogen ion >44nmol/L)
o PaCO2 >5.7 KPa
o Bicarbonate >22mmol/L
o Base excess <-2 mmol/L
• Management:
➢ Oxygen therapy (should not be used in chronic hypercapnia unless it is really
indicted as hypoxia stimulated respiration may be suppressed), ventilator
support.
➢ Alkali therapy is not usually used unless acidosis is very severe (below 7.15)
or there is severe bronchospasm.

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SURGERY MK

Anion gap: This is the

measurement of the interval
between the sum of “routinely
measured” cations minus the
sum of the “routinely measured
anions in the blood.
The anion gap= (Na+ + K+) –
(Cl- + HCO3-)
The anion gap can be normal (16
± 4mEq/l if the calculation
employs potassium and 12 ±
4mEq/L if the calculation does
not employ potassium), high or
low
The test is commonly performed
in patients who present with
altered mental status, unknown
exposures, acute renal failure
and acute illnesses.
A high anion gap indicates
metabolic acidosis.
A low anion gap is relatively
rare but may occur from the
Figure 31: Acidosis and alkalosis presence of abnormal positively
charged proteins, as in multiple
myeloma.

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SURGERY MK
NUTRITION

NUTRITION
PRINCIPLES OF NUTRITION
• Avoiding of malnutrition is the basic goal in nutrition therapy as malnutrition
increases the morbidity and mortality of the disease process and prevents or
delays recovery.
• Malnutrition increases the chance of sepsis, prevents wound healing, increases
the respiratory complications and decreases the efficacy and tolerance to
radiotherapy or chemotherapy.
• Whenever possible enteral route of nutrition should be used ideally. If that is not
possible then parenteral nutrition is used.
• Overfeeding should be avoided as it leads into hyperglycemia, hepatic steatosis,
raised BUN, and excess CO2 production.
• Timing and type of nutrition is also important.
• Nutrition therapy reduces protein wasting.
• Immunomodulators like glutamine, arginine and omega 3 fatty acids are also very
useful.
• Caloric requirement:
➢ Neonatal: 100 kcal/kg/day
➢ Adult: 40 kcal/kg/day (25-35kcal/kg)
➢ Adult with catabolism: 60 kcal/kg/day
• It is given as:
➢ Carbohydrates: 50%
➢ Fat: 30-40%
➢ Protein: 10-15%
• Caloric values:
➢ Carbohydrate= 4 kcal/g
➢ Fat= 9 Kcal/g
➢ Protein= 4 Kcal/g

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SURGERY MK
INDICATIONS FOR NUTRITIONAL SUPPORT
• Preoperative nutritional depletion
• Postoperative complications: sepsis, ileus, fistula
• Intestinal fistula: High type wherein output is more than 500ml/day. It may be
duodenal, biliary, pancreatic, intestinal.
• Pancreatitis, malabsorption, ulcerative colitis, pyloric stenosis
• Anorexia nervosa and intractable vomiting
• Trauma- multiple fractures, fasciomaxillary injuries, head and neck injuries.
• Burns
• Malignant disease
• Renal and liver failure
• Massive bowel resection causing short bowel syndrome
ASSESSMENT AND NUTRITIONAL REQUIREMENTS
• Clinical findings: history and examination, regular weights, body mass index.
• Anthropometric measurements:
➢ Body weight
➢ Skinfold thickness (e.g. triceps, iliac crest)
➢ Mid-arm circumference
➢ Grip strength
• Blood tests:
➢ Serum albumin
➢ Serum transferrin
➢ Lymphocyte count
• Nutritional requirements: carbohydrates, fats, proteins, vitamins (includes fat
soluble vitamins), minerals, trace elements.
METHODS OF FEEDING
• Methods include:
➢ Enteral: preferred for the patient unable to maintain an adequate oral intake
but who has a functioning GIT that can be used safely. Early enteral nutrition
has been advocated to persevere intestinal structure.
➢ Total parenteral nutrition (TPN): can be given via a large peripheral vein or
central venous channel

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SURGERY MK
ENTERAL
• GIT is the best route to provide nutrition in order to preserve intestinal structure
and the role of the intestine in the immune system.
• Enteral feeding can be delivered by bolus, by gravity or using mechanical pump
through:
➢ Mouth: needs common sense, cleanliness, compassion.
➢ Nasogastric tube: confirmation of the tube in the stomach is made by injecting
5ml of air down the tube and listening through a stethoscope for its bubbling
entry into the stomach. Feeding rate is 30-50ml/hours. 5 hours night time gap
is given to allow gastric pH to return to normal.
➢ Enterostomy: gastrostomy (surgical or endoscopic- percutaneous endoscopic
gastrostomy), Jejunostomy (surgical).
• Enteral feeding can be done initially by providing supplement drinks. If this is
not sufficient, then an elemental diet can be given through a fine-bore nasogastric
tube directly into the stomach or small bowel. These types of feeds (e.g. osmolite)
provide approximately 1912 Kcal (8000 Kj) of energy plus about 70g protein in
2-3L.
• Types of feed:
➢ Polymeric (near-normal composition): contain intact proteins, starch and
long-chain fatty acids. They are useful in patients with functioning stomach
and normal digestive capacity.
➢ Disease specific: they are tailored for requirements of specific diseases e.g.
feeds for patients with liver disease are deficient in branched-chain amino
acids as they can exacerbate encephalopathy.
➢ Elemental: chemically defined feeds that contain simple amino acids,
oligosaccharides and monosaccharides. These require minimal digestion and
are useful in patients with intestinal fistulae but are far from palatable.
• Indications:
➢ Long term feeding
➢ Dysphagia e.g. stricture, stroke
➢ Chronic disease e.g. neoplasia
➢ Malnutrition
➢ Sepsis
➢ Burns
➢ Major surgery
➢ Coma/ICU

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SURGERY MK
Problems with tube feeding Complications of enteral feeding
• Blockage • Aspiration
• Nausea and vomiting, • Wound infection and leak
aspiration • Diarrhea due to rapid feeding
• Hyperosmolarity or hyperosomolarity
• Diarrhea • Hyperglycemia
• Tube discomfort • Electrolyte imbalance:
• Cholestasis Hypokalemia
• Refeeding syndrome due to
severe hypokalemia and
hypophosphataemia

ADVANTAGES OF ENTERAL NUTRITION

• Enteral nutrition preserves mucosal protein, digestive enzymes, IgA secretion,
prevents mucosal atrophy and bacterial translocation.
• It is more physiological as nutrients pass through liver (first filter). Gallstone
formation is prevented (unlike long term TPN) by stimulating gall bladder
motility.
• It has got less serious complications.
• It is cost effective
• It supplies glutamine and short chained fatty acids to gut.
CONTRAINDICATIONS OF ENTERAL NUTRITON
• Intestinal obstruction, GI bleed, paralytic ileus, severe diarrhea, high output
fistula.
• Low cardiac output, hemodynamically unstable patient.
• If safe access to enteral feeding is not present.
• Anticipated complications if thought to be present should be avoided.

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SURGERY MK
GASTROSTOMY
• It is done if feeding is required for more than 1 month.
• Indications:
➢ Severe malnutrition
➢ Major surgeries
➢ Severe sepsis
➢ Trauma
➢ Head and neck surgeries
• Types:
➢ Based on duration of use:
o Temporary
o Permanent
➢ Based on lining:
o Serosal lined (temporary)
o Mucus lined (permanent)
➢ Based on technique
o Stamm temporary gastrostomy: after opening the abdomen, anterior wall
of the stomach is opened. Feeding tube (Malecot’s catheter) is placed in
positon. 2 layers of purse string sutures are put around the tube/ wound is
closed.
o Kader-Senn temporary gastrostomy
o Percutaneous endoscopic gastrostomy (popular)- now becoming common
method
o Janeway’s mucus lined permanent gastrostomy by creating tunnel in
stomach wall.
• Problems in gastrostomy
➢ Leak- gastric fistula
➢ Infection
➢ Aspiration and pneumonia
➢ Diarrhea is common-30%
➢ Bloating, abdominal cramps
➢ Displacement, blockage of the tube
• Contraindications
➢ Previous gastric surgeries
➢ Intestinal obstruction
➢ Gastric outlet obstruction

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SURGERY MK

JEJUNOSTOMY
• These are becoming more popular because of:
➢ Comfort
➢ Easy to do
➢ Can be kept for long time
➢ Lesser complication than gastrostomy
• Indications are the same as gastrostomy
• Types
➢ Witzel jejunostomy: site of placing jejunostomy is 30cm from duodenojejunal
junction.
➢ Needle jejunostomy using catheter of small gauge.

TOTAL PARENTERAL NUTRITION (TPN)

• All nutritional requirements are given only through intravenous route, not
through the GIT.
• It can be through a central catheter through the subclavian/internal jugular vein
where the tip of venous catheter is at distal part of superior vena cava.
• Can also be a peripheral (peripheral parenteral nutrition/ PPN) through a
peripherally inserted central venous catheter (PICC) or through a femoral
peripheral venous line.
• Indications:
➢ Failure or contraindication for any enteral nutrition for 7-10 days.
➢ High output abdominal fistulas, duodenal, biliary, pancreatic fistula.
➢ Major abdominal surgeries of liver, pancreas, biliary, colonic
➢ Septicemia
➢ Multiple trauma
➢ Short bowel syndrome
➢ Severe pancreatitis, bowel ischemia, peritonitis, prolonged ileus
➢ Massive GI bleeding, unstable haemodynamically
➢ High risk of aspiration
➢ Hyperemesis gravidarum
➢ Multiorgan failure, head injury, severe burns where upper GIT is severely
damaged

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SURGERY MK
➢ Severe malnutrition
➢ Severe Crohn’s disease
➢ Inability to swallow e.g. esophageal tumor
• About 5% of hospital admissions require TPN.
• Contraindications:
➢ Cardiac failure
➢ Blood dyscrasias
➢ Altered fat metabolism
• Technique:
➢ Using a needle and guide wire a subclavian vein catheter is passed just below
the clavicle and fixed securely to the skin.
➢ TPN is given through central vein and not through a peripheral vein.
➢ Peripherally inserted central catheter (PICC) is also commonly used (PPN)
• Complications:
➢ Pneumothorax/hemothorax
➢ Cardiac tamponade
➢ Sepsis e.g. Staphylococcus epidermidis, Candida, Pseudomonas
➢ Mineral overload
➢ Reactive hypoglycemia
➢ Vitamin and mineral deficiencies

REFEEDING SYNDROME
• Refeeding syndrome is occurrence of severe fluid and electrolyte imbalance in
severely malnourished individuals while starting the proper feeding enteral or
parenteral nutrition.
• It is common in TPN.
• It causes hypomagnesaemia, hypocalcemia and hypophosphataemia leading into
myocardial dysfunction, respiratory changes, altered liver functions, altered level
of consciousness, convulsions and often death.
• Gradual feeding and correction of magnesium, phosphate and calcium and other
electrolytes is important.
• Condition is common in chronic starvation, severe anorexia and alcoholic
patients.

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SURGERY MK

BLOOD PRODUCTS AND

BLOOD TRANSFUSION

BLOOD PRODUCTS AND BLOOD TRANSFUSION

• Blood is a connective tissue found in fluid form. It consists formed elements and
plasma. Blood is circulated around the body in arteries and veins by the pumping
action of the heart
• Plasma is the fluid component of circulating blood in which the formed elements
(Erythrocytes, leukocytes and platelets) are suspended.
• Blood and plasma products are derived from voluntary non-remunerated donors
aged 18-65 years.
• Donors are carefully selected and all donations are tested for known markers of
disease. These include:
➢ Human immunodeficiency virus (HIV)-1 and 2
➢ Syphilis
➢ Hepatitis B and C viruses
• Modern blood transfusion is based on the intravenous administration of those
components of blood that are deficient in a particular rather than transfusion of
whole blood. This practice ensures the safe economic use of blood products and
increases the therapeutic scope.
• Safe blood transfusion depends on:
➢ Careful selection of donors
➢ Quality assurance testing of blood and blood products prepared and issued by
transfusion centers
➢ Blood grouping, antibody screening and cross-matching
➢ Standardized blood ordering policies
➢ Strict guidelines for administration and monitoring of patients receiving blood
products
➢ Local and central reporting of adverse effects when encountered
• Documentation of the details of any blood component infused is essential and
mandatory including:
➢ Indication
➢ Date/time of issue
➢ Donation number
➢ Ordering physician

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SURGERY MK
➢ Duration of infusion
➢ Who gave the infusion and who checked it prior to administration
➢ Time the infusion was commenced
• The patient’s red cells are grouped for ABO and Rh (D). The antibody screen is
carried out on all the serum samples to detect the presence in the recipient of any
clinically important antibody that would hemolyze the transfused cells.
• Cross-matching entails testing the red cells from the donor units against the
patient’s serum.
• Before transfusing there is a 2 people verification that has to be done to ensure
that the information on the transfusion request form, the labels on the unit of
blood and the patient identification (from patient notes and wrist band) all agree.
This remains the weakest link in the safety chain and most deaths from blood
transfusion are related to misappropriation.
• Note: there is no medical or surgical condition that justifies transfusion of less
than 2 units of blood.
• Type and screen (group and hold, group and save) is done for operations that do
not usually require blood. The patient’s serum is kept in the blood transfusion
laboratory for 7 days. Should blood be required cross-matched red cell units can
be available in 15 minutes.
• Patients do not require a preoperative blood transfusion unless the hemoglobin is
less than 8g/dl. The exceptions to this rule are patients with cardiovascular
disease or those expected to have covert cardiovascular disease (elderly patients
and patients with peripheral vascular disease). These patients are likely to benefit
and thus require a blood transfusion when their hemoglobin falls below 9g/dl.

BLOOD SPARING STRATEGIES

• Blood sparing strategies should be considered in all patient who might require a
blood transfusion, especially:
➢ Jehovah’s Witnesses
➢ Patients with multiple antibodies
➢ Patients with serious anxieties about the transfusion of allogeneic blood.
• Blood sparing strategies include:
➢ Preoperative autologous blood donation (pre-deposit)
➢ Erythropoietin
➢ Acute normovolemic hemodilution
➢ Antifibrinolytic drugs
➢ Cell salvage

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SURGERY MK
PREOPERATIVE AUTOLOGOUS BLOOD DONATION
• The benefit of autologous, as opposed to allogeneic transfusion is the elimination
of disease transmission and allergic and incompatible reactions (other than
procedural errors).
• It should only be offered when it is possible to guarantee admission and operative
dates and is targeted to patients who are to undergo elective surgery where blood
will be lost and whose Hb at presentation is 11.0-14.5g/dl in males and 13.5-
14.5g/dl in females.
• Pre-deposit is more expensive than allogeneic blood transfusion. In addition, the
blood is wasted if the patient does not need perioperative transfusion as it cannot
be administered to other patients.
• If the patient require blood in excess of the predeposited units, all possible
advantage is lost thus a balance must be struck between collecting enough units
to minimize allogeneic exposure and wastage.
ERYTHROPOIETIN
• This is a hormone produced and secreted by the kidneys and regulate
erythropoiesis.
• Recombinant human erythropoietin (alpha and beta) are widely used in anemia
associated with renal failure and as blood sparring strategy in patients undergoing
major surgery.
• It is administered subcutaneously (600 units/kg) 3 times weekly and on the day
of surgery and is preferably accompanied by oral/IV iron therapy.
• EPO is used to counteract blood loss in:
➢ Patients scheduled for major surgery under 70 years of age with a presenting
HB <13g/dl
➢ Patients scheduled for major surgery who refuse allogeneic blood transfusion
➢ Jehovah’s Witnesses.
• The risk of EPO therapy is deep vein thrombosis, especially if the Hb exceed
13g/dl.
• A 500ml venesection is necessary whenever EPO induces the patient’s
hematocrit to rise above 0.5. Patients on EPO should have their hematocrit
checked weekly.

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ACUTE NORMOVOLEMIC HEMODILUTION
• Immediately before surgery usually following induction, 1000ml of blood are
removed with replacement of blood volume by crystalloids (with monitoring of
central venous pressure).
• The blood is given to the patient if and when it is needed during or after surgery.
• Acute normovolemic hemodilution is useful in fit patients if:
➢ A substantial blood loss is anticipated during surgery
➢ The patient’s initial hemoglobin is high
➢ A relatively low target hemoglobin is acceptable
ANTIFIBRINOLYTIC DRUGS
• These include aprotinin (a kallikrein inhibitor) and tranexamic acid.
• They are recommended for patients undergoing cardiac surgery that carries high
risk of transfusion such as:
➢ Repeat cardiac operations
➢ Multiple valve replacements
➢ Thoracic aortic operations
➢ Patients on aspirin therapy
➢ Anticipated long bypass times
• Antifibrinolytic drugs are acceptable to Jehovah’s
Witnesses
INTRAOPERATIVE BLOOD SALVAGE
• This include automated blood salvage using the cell
saver equipment (Haemonetics) and the simpler manual
systems for storage and reinfusion of red cells as
exemplified by the Solcotrans autologous collection
system.
• Both techniques are only applicable to clean operative
sites without bacterial, bowel or tumor cell
contamination.
• The Haemonetics cell saver system is a completely
automated device that aspirates, anticoagulates and
filters the extravasated blood from the operative field.
• The red cells are then washed before being transfused in
a packed volume of 0.5. This system is used extensively Figure 32: Cell saver

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SURGERY MK
during liver transplantation and in Jehovah’s Witnesses undergoing major
surgery.

BLOOD AND PLASMA PRODUCTS

Blood products Examples
Red cell preparations • Whole blood
• Red cell concentrate (Packed cells)
• Leukocyte-poor red cell concentrate
• Frozen red cells (not available generally)
• Autologous blood
Platelets • Random donor pooled
• Single-donor apheresis
• Human leukocyte antigen-matched
• Cross-matched
Plasma components • Fresh frozen plasma (plasma + all clotting factors)- ABO
compatibility is essential
• Cryoprecipitate (Factor VIII, von Willebrand factor,
fibrinogen)- ABO compatibility is essential
• Plasma protein fraction (5% albumin in buffered saline)
• Salt-poor human albumin (25%)
• Factor VIII concentrate
• Factor VIIa
• Factors II, IX, X
• Factor VII
• Von Willebrand factor
• Antithrombin III
• Intravenous IgG
➢ Human normal IgG
➢ Specific hyperimmune IgG (Rh anti-D, tetanus etc.)
• Fibrin sealant (glue)

STORED WHOLE BLOOD

• This is blood from which no constituent has been removed.
• Whole blood is only indicated for treatment of acute hemorrhage, hypovolemia
is accompanied by an acute reduction in red cell mass, resulting in impaired
oxygen carrying capacity at a time when tissue perfusion is compromised.

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SURGERY MK
• It should be reserved for those patients with substantial blood loss and a
hematocrit of 0.3 or less after volume replacement with crystalloids and plasma
expanders.
• Stored blood has a number of unwanted features
➢ Citrate anticoagulant
➢ Acid pH (6.6-6.8)
➢ High level of potassium (from the stored red blood cells)
➢ Ammonia (from erythrocyte adenosine)
➢ Reduced red-cell 2,3 diphosphoglycerate (2,3-DPG) which leads to impaired
release of oxygen from oxyhemoglobin)
• The use of stored whole blood is declining rapidly because of increasing demand
for individual blood products and for economic reasons.
RED CELL CONCENTRATES
• These are solutions of erythrocytes obtained from blood after the plasma has been
removed. They also contain some white cells.
• Pack red cells have the same oxygen carrying capacity of blood but a lower
volume.
• They are ideal for treatment of anemic patients who invariably have a normal
blood volume and are at risk from circulatory overload. Even so, unless the
anemia is severe and symptomatic transfusion is no substitute for hematinic
(promotion of blood production) therapy and is only indicated in patients how:
➢ Do not respond to hematinic treatment (refractory anemia)
➢ Are unable to adapt to the reduced oxygen-carrying capacity of the blood and
exhibit signs of incipient cardiovascular failure.
➢ Require urgent surgery
• Up to 10% of patients develop Alloimmunisation to leukocyte antigens, usually
after repeated red cell infusions.
• The antibodies cause severe febrile reactions, which can only be prevented by the
use of leukocyte-poor red cell concentrates.
FROZEN RED CELLS
• The use of cryoprotective agents such as glycerol or hydroxyethyl starch allows
satisfactory storage of red cells at -80 to -196oC (mechanical freezing or liquid
nitrogen storage) for long periods (up to 10 years),

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• This method of storage removes leukocytes, platelets and any viral particles
thereby reducing the incidence of both transmission of viral disease and
Alloimmunisation to leukocyte and platelet antigens.
• Red cells recovered from a frozen bank are of particular value to patients on renal
dialysis programs, those with refractory anemias and those with rare cell types
and complex antibody mixtures. However, frozen red cells are very expensive
and impractical for most patients.
PLATELET CONCENTRATES
• These are solutions containing platelets that are frequently derived from several
donors
• They can be obtained by centrifugation of blood from several donors or by
platetpheresis of a single donation.
• Because of the variable but significant contamination with red cells, platelets
concentrates have to be obtained from ABO/Rh-compatible donors.
• Some human leukocyte antigens (HLAs) are expressed on platelets and determine
platelet survival after transfusion. These HLAs lead to Alloimmunisation in
patients requiring repeated platelet transfusions.
• The antibodies generated cause rapid destruction of the transfused platelets and
account for the progressive inefficacy of repeated transfusions.
• For these patients, HLA-matched platelet concentrates are needed.
• Indications of platelet:
➢ Surgical
o Bleeding and thrombocytopenia
o Limited cover for operative interventions where platelet count <40 x
109/L
o Platelet dysfunction
o Acute disseminated intravascular coagulation (with fresh frozen plasma)
o Massive blood transfusion (washout thrombocytopenia)
o Post cardiac bypass platelet loss and/or dysfunction
➢ Medical
o Marrow-suppressed patients (intensive chemotherapy)
o Aplastic anemia
• In surgical practice, platelet transfusions are most commonly used to stop
bleeding in thrombocytopenic patients, to cover surgery if the platelet count is
below 40 x 109/L and in patients with platelet dysfunction.

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SURGERY MK
PLASMA PRODUCTS
• They are produced from voluntary donors and are used for a variety of purposes.
➢ As coagulation factors for specific deficiency states, either to stop
spontaneous bleeding or cover an operation/intervention in a patient with such
a deficiency e.g. hemophilia A (congenital factor VIII deficiency).
➢ To provide passive immunity to non-immunized individuals exposed to a
serious infective agent (viral or bacterial) e.g. human tetanus immunoglobulin
➢ In prophylaxis of hemolytic disease of the newborn due to Rhesus
incompatibility and sensitization of Rh (D)-negative women
➢ In management of autoimmune thrombocytopenic purpura. IgG can be used
to treat idiopathic thrombocytopenic purpura requiring surgery including
elective splenectomy
➢ As volume replacement fluid (ALBA 4.5%) and as plasma volume expander
and short-term management in hypoproteinemic patients (human Albumin
solution 20%)
• The most common fraction used in surgical practice is fresh frozen plasma (FFP).
Each unit is obtained from a single donation and consists of 200-300ml of plasma
with 40-60ml of citrate anticoagulant nutrient mixture.
• Fresh frozen plasma is plasma prepared from the supernatant liquid obtained by
centrifugation of one donation of whole blood.
• Indications of FFP:
➢ Correct isolated deficiencies of plasma proteins e.g. factor II, V, VII, X, XI,
XIII, pseudocholinesterase, antithrombin III and C1 esterase inhibitor
➢ Reverse oral anticoagulation with warfarin/coumarin compounds if
prothrombin complex concentrate is not available. Normally, reversal of
anticoagulant is indicated in the presence of bleeding.
➢ Provide hemostatic support and to cover operations/interventions in patients
with liver disease, major hepatic resections and severe liver injuries
➢ Treatment of DIC
➢ In patients who develop a bleeding diathesis after large volume blood
transfusion. However, platelets transfusion is more commonly needed first.
➢ In treatment of thrombotic thrombocytopenic purpura where FFP us usually
combined with plasma exchange
• Cryoprecipitate (factor I-fibrinogen, VII, von Willebrand factor) is used in
hemophilia, von Willebrand’s disease and fibrinogen deficiency. Because of the
risk of transmitted infection, cryoprecipitate is now used much less in

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SURGERY MK
hemophilia. Factor VIII concentrate is now used as it is safer and gives a more
certain dose.
• Factor IX concentrate is indicated to arrest acute bleeding and cover operative
interventions in patients with Christmas disease.
• Factor VIII and IX therapy requires expert guidance.

Figure 33: Blood and plasma products

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SURGERY MK
ADVERSE EFFECTS OF TRANSFSION
• Blood transfusion is nowadays very safe with the overall risk of an adverse
outcome being 1 in 12 000.
• The mechanisms of transfusion reactions are varied, depending on the cause.
• Complications of transfusion are usually classified according to etiology; they
may either be:
➢ Acute
➢ Delayed
• NOTE: It is recommended that every patient is monitored closely during the first
15-30 minutes of the infusion of each unit of blood. This enables early detection
of the clinical manifestations of severe acute reaction due to incompatibility or
bacterial infection at which point the infusion is stopped and the necessary action
taken.
Acute transfusion reactions Delated transfusion reaction
• Acute Hemolytic reaction • Delayed hemolytic
• Non hemolytic reactions • Infective
➢ Pyrogenic (febrile) reactions ➢ Bacterial: brucellosis, syphilis
➢ Hypersensitivity ➢ Helminthic: filariasis
• Metabolic, respirator and hemostatic ➢ Protozoal: babesiosis, Chagas’
complications disease, Kala-azar, malaria,
• Circulatory overload trypanosomiasis, toxoplasmosis
• Septic shock (bacterially infected ➢ Rickettsial: relapsing fever, Rocky
units) Mountain spotted fever
➢ Viral: B19, CMV, EBV, HIV 1, 2,
HTLV-1/2, hepatitis, yellow fever
• Sensitization/Alloimmunisation
➢ Hemolytic disease of the newborn
➢ Immune suppression (increased
infective risk)
➢ Post-transfusion purpura
➢ Platelet refractoriness
• Transfusion iron overload
(hemosiderosis)
• Graft vs host disease

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ACUTE REACTIONS
ACUTE HEMOLYTIC REACTION
• Hemolysis can occur intravascular or extravascular.
INTRAVASCULAR HEMOLYSIS
• This is due ABO incompatibility due to human error at the bedside (blood given
to the wrong patient) or in the lab (faulty cross-matching).
• The transfused cells react with the patient’s own anti-A or anti-B antibodies or
other alloantibodies to red cell antigens.
• It carries a 3% mortality rate but it is higher if more than 200ml of incompatible
blood are administered.
• The reaction is usually most severe if group A red cells are administered to a
group O patient. The syndrome is caused by the release of polypeptide products
of complement in the plasma which causes contraction of smooth muscle and
degranulation of mast cells with release of vasoactive peptides (bradykinin and
serotonin)
• Procoagulant substances are released from the stroma of lysed red cells. Together
with antigen-antibody complexes these initiate DIC.
• Hemolytic transfusion reactions result in:
➢ Hemoglobinemia, hemoglobinuria and renal failure
➢ Disseminated intravascular coagulation
➢ Complement-mediated cardiovascular collapse
• Hemolytic reactions occur after a small amount of blood has been transfused and
almost always before the unit is transfused completely.
• Clinical features in conscious patients:
➢ Pain/burning at the infusion site and along the vein
➢ Facial burning
➢ Chest (tightness) and back pain
➢ Joint pain
➢ Fever
➢ Flushed facies
➢ Chills
➢ Rigors and vomiting
➢ Apprehension, Restlessness and dyspnea
➢ Hypotension
➢ Oozing from vascular access sites and wounds
➢ Physical examination: tachycardia, tachypnea, in severe cases hypotension

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SURGERY MK
• The only manifestation of incompatibility blood transfusion in unconscious or
anesthetized patients are sudden hypotension and bleeding due to DIC.
• Extensive intravascular hemolysis results in hemoglobinemia and
hemoglobinuria. Urine is dark.
• Oliguria rapidly supervenes and progresses to acute When dealing with acute
renal failure. hemolytic transfusion episode:
• The differential diagnosis is between incompatibility 1. Report incident to the blood
and infusion of bacterially contaminated blood. transfusion department
• Management: 2. Establish that the unit of blood
➢ Immediate recognition with cessation of the has been issued to the patient
transfusion and replacement of the giving set. who received it
Inform medical officer on call. 3. Obtain fresh samples of
➢ Adequate hydration by intravenous infusion of patient’s blood (clotted and in
crystalloids (normal saline) EDTA) for repeat cross-
➢ Examine the blood to determine if the patient matching and serological
received the correct blood unit. testing
➢ Catheterize the patient and attempt to force diuresis 4. Send the unit of blood to blood
with IV large dose furosemide (150 mg) transfusion department
o If furosemide fails, 20% solution of mannitol 5. Obtain further blood samples
(100ml) is administered. from the patient for clinical
o If diuresis is obtained, a high urine output (30- chemistry (electrolytes, urea,
100ml/h) is maintained by large volume free hemoglobin) and
crystalloid infusion. If patient progressives to coagulation screen
acute renal failure they will require 6. Discuss any further transfusion
hemodialysis. requirements with blood
➢ Low dose dopamine may be considered to increase transfusion officer
renal blood flow.
➢ Treat DIC (blood component therapy guided by clinical state and coagulation
screen)
➢ Treat hyperkalemia
o 50ml of 50% dextrose + 10 IU of insulin if potassium above 6.0mmol/L
o Followed by 10% glucose infusion containing 10 units of insulin over a
period of 4 hours.
➢ Add acetaminophen for fever
➢ Investigate incident fully (box above)
➢ Also consider endotracheal intubation if in respiratory insufficiency, in severe
hemolytic reactions and patients with hypoxemia. Keep O2 stats >92%.

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EXTRAVASCULAR HEMOLYSIS
• This is due to recipients’ antibodies against Rh or non-ABO antigens.
• Patients are usually exposed to antigen through prior pregnancies, transplantation
or transfusion.
• Antibody titers are too low often to be detected during screening however
production increase with re-exposure to the initial antigen.
• Antibodies do not activate complement (no intravascular hemolysis) instead they
coat RBCs which are removed by splenic macrophages.
ACUTE NON-HEMOLYTIC REACTION
• Quality control in the manufacture of IV fluids and disposable giving sets has
virtually eliminated pyrogenic reactions.
• Pyrexia following blood transfusion is nowadays as a result of Alloimmunisation
to leukocyte and platelet antigens in patients requiring repeated blood
transfusions. This is the commonest cause of severe febrile reaction.
• Although it is usually self-limiting and benign, the transfusion must be stopped
to exclude the possibility of more serious hemolytic reactions.
• Febrile reactions in alloimunized patients can be prevented by using cell
concentrate from which most of other formed elements have been removed
(leukocytes, platelets, soluble histocompatibility antigens).
• Other non-hemolytic reactions include severe immediate hypersensitivity
reactions and mild allergic or anaphylactoid reactions. The causes of these
reactions are rarely established. The reaction results in the release of vasoactive
peptides and activation of complements.
• There is profound hypotension, laryngeal spasm and/or bronchospasm and
cutaneous flushing.
• Anaphylaxis is treated with:
➢ Immediate termination of the transfusion
➢ IV crystalloids
➢ Maintenance of airway and administration of oxygen
➢ Adrenaline (0.5-1.0 mg IM)
o Adrenaline dose is repeated if necessary, every 10 min depending on the
improvement in blood pressure and pulse.
➢ Chlorpheniramine 10-20mg is administered by slow IV injection after the
adrenaline treatment and is continued for 24-48 hours.
➢ Salbutamol is administered by nebulizer.

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• Severe anaphylaxis can only be predicted in patients with low serum IgA. If
possible, transfusion should be avoided in these patients.
TRANSFUSION-RELATIVE ACUTE LUNG INJURY
• This is one cause of acute respiratory distress syndrome (ARDS) and it was
thought to be due to pulmonary microvascular occlusion by microaggregates of
platelets, leukocytes and fibrin (50-200 micrometers) which are known to be
present in stored blood.
• For this reason, microaggregate filters were recommended for transfusion using
in excess of 5 units of blood.
• A more definite cause is donor blood containing antibodies reacting with the
patient’s leukocytes (nearly always donations from multiparous women).
Following transfusion, the patient develops fever, increasing breathlessness, non-
productive cough and hypoxemia.
• The chest X-ray shows the typical features of ARDS with perihilar infiltrates
leading to a whiteout in severe cases.
• Treatment:
➢ Respiratory support as it may need ventilation with positive end-expiratory
pressure (PEEP)
METABOLIC, HEMOSTATIC AND RESPIRATORY COMPLICATIONS
• These are confined to patients who because of severe hemorrhage, receive a
massive blood transfusion.
• Massive blood transfusion is defined as:
➢ Replacement of a volume equivalent to or exceeding the patient’s own blood
transfused within 12 hours.
➢ Replacement of more than one half of the blood volume within 24 hours
➢ Replacement of 10 units of blood over the course of few hours
• Effects of stored whole blood
➢ Cold (4oC)
➢ Acid pH
➢ Citrate anticoagulant
➢ Elevated plasma potassium and ammonia
➢ Reduced 2,3-DPG
• Metabolic consequences:
➢ Hypothermia: may lead to cardiac arrhythmias, including ventricular
fibrillation and asystole. For this reason, blood warming is necessary if the

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transfusion rate exceeds 50ml/min. Unfortunately, heating coils increase the
resistance of the give circuit, nonetheless their use is essential in these
patients.
➢ Acidosis
➢ Increased affinity of oxyhemoglobin for oxygen resulting in defective tissue
oxygen uptake.
➢ Citrate intoxication is due to the chelation of ionized calcium which may result
in prolongation of the QT interval. However, this does not usually affect
cardiac function and ionized calcium levels rapidly return to normal after
transfusion as the excess citrate is metabolized and excreted. Do not give
supplemental calcium as it may give rise to arrhythmias,
➢ Hyperkalemia: this is rarely a problem because the excess plasma potassium
enters the red cells with warming to body temperature. However, it is a
consideration in patients with acidosis and renal failure when calcium is
administered as the physiological antidote.
➢ Stored blood is deficient in platelets and labile clotting factors (V and VIII).
o In massive transfusion of stored blood there is dilution of labile clotting
factors in addition to a moderate thrombocytopenia.
o The deficiency is corrected by transfusing 2 units of FFP for every 8 units
of blood.
o The transfusion-related thrombocytopenia is rarely significant and can
usually be ignored.
• Management:
➢ Hypothermia: transfuse warm blood
➢ Metabolic acidosis: may need NaHCO3
➢ Impaired release of oxygen from RBCs: self-limiting, no therapy needed
➢ Citrate intoxication causing hypocalcemia: Self-limiting, no therapy needed
➢ Hyperkalemia: rarely a serious problem
➢ Platelet and clotting factor deficiency: give 2 units FFP for every 8 units of
blood
CIRCULATORY OVERLOAD
• Circulatory overload is encountered in the transfusion of anemic patients,
particularly those with severe and longstanding anemia.
• These patients must be transfused very slowly and only with packed cells (with
or without concomitant diuretic therapy).

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• In some patients, an exchange transfusion has to be carried out to avoid severe
congestive failure.
TRASNFUSION OF BACTERIALLY CONTAMINATED/INFECTED BLOOD
• This is fortunately rare.
• The majority have been associated with platelet transfusion.
• The pathogens are usually cold-growing strains of Pseudomonas fluorescens or
Yersinia enterocolitica.
• Skin organisms such as Staphylococci can proliferate in platelet concentrates
stored at 20-22oC.
• The clinical picture is similar to that of ABO incompatible blood transfusion
reaction.
• Despite aggressive support therapy (full resuscitation and management in ICU
for septic shock), mortality is high and around 60%.

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Figure 34: Acute transfusion reactions

DELAYED REACTIONS
TRANSMISSION OF INFECTIOUS DISEASE
• A wide spectrum of infectious disease can be transmitted by the transfusion of
blood and blood products, although the modern practice of screening blood
donors and heat treatment of blood protein products means the risk is extremely
small (1 in 105-106).
• Post-transfusion levels of HIV, human T-cell leukemia virus (HTLV), HBV and
HCV are extremely low and the risk of their transmission is minimal compared
with other risks.
• HCV transmission is extremely low compared with other risks.
• Hepatitis A and G can be transmitted by blood products.

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SURGERY MK
IMMUNE SUPPRESION
• There is an immunosuppressive effect of blood transfusion.
• Prior to the introduction of cyclosporine, transfusion before renal transplantation
was employed specifically to improve graft survival. The use of cyclosporine has
made this procedure unnecessary.
• In the context of general surgery, perioperative blood transfusion has undoubted
undesirable consequences because of its immunosuppressive effect (which is
additive to the immunosuppression produced by operative trauma).
• Aside the risk of circulatory overload, perioperative blood transfusion enhances
the risk of infective complications (proven) and may increase recurrence rate and
reduce disease-free survival n patients after extirpative surgery for cancer. The
latter, however remains unproven.
TRANSFUSION HEMOSIDEROSIS
• Iron overload of the monocyte-macrophage system is caused by repeated red cell
transfusion over many years.
• This becomes significant after 100 units have been administered when the liver,
pancreas, myocardium and endocrine glands become damaged.
• It is especially a problem in childhood anemia e.g. thalassemia and in patients
with chronic refractory anemia
• Iron overload is reduced in these patients by iron chelation therapy with
desferrioxamine.
GRAFT VS HOST DISEASE
• Graft vs host disease (GvHD) is a rare but usually fatal complication that occurs
mainly in immunodeficient patients e.g. recipients of allogeneic marrow
transplants and fetuses receiving intrauterine transfusions.
• GvHD has also been documented in immunocompetent patients after transfusion
of blood from a relative.
• The disease is caused by T lymphocytes and starts some 4-30 days after the
transfusion.
• The patient develops a high fever, a diffuse erythematous skin rash progressing
to erythroderma and desquamation, gastrointestinal symptoms, severe hepatic
dysfunction and pancytopenia.
• GvHD is prevented by administering gamma-irradiated cellular components to
immunodeficient patients.
• Similarly, blood donated from relatives should be gamma-irradiated.

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Figure 35: Delayed transfusion reactions

SHOCK AND HYPOTENSION

SHOCK AND HYPOTENSION

• Hypotension is a state of low blood pressure with systolic blood pressure (SBP)
<90mmHg or mean arterial pressure <65.
➢ In relative hypotension the SBP is >30mmHg below baseline
• Shock is a state of cardiovascular failure resulting in impaired tissue perfusion
and disturbed cellular metabolism and function as a result of decreased oxygen
supply.
• Clinically shock can be defined as a 20% sudden blood loss or shift from
peripheral circulation.
• Adequate blood flow to tissues depends on:
➢ Blood volume
➢ Myocardial contractility
➢ Peripheral resistance
• Any disturbance in the above 3 can lead to shock.
➢ Pump failure leads to cardiogenic or obstructive failure
➢ Peripheral circulatory failure leads to hypovolemic (decreased blood volume)
or distributive shock (decreased peripheral resistance).

CLASSIFICATION OF SHOCK
• Shock can be classified into:
➢ Hypovolemic (Oligemic) shock: due to diminished blood volume (loss of
fluid/blood- hemorrhagic shock)

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➢ Cardiogenic shock: due to inefficient myocardial function (decreased cardiac
contractility)
➢ Distributive shock: due to peripheral blood pooling. Can either be
o Septic shock: due to systemic infection
o Neurogenic shock: due to peripheral vasodilation, reduced peripheral
resistance and peripheral pooling of blood.
o Anaphylactic shock: due to antigen-antibody reaction that also leads to
peripheral pooling of blood e.g. injection of anti-tetanic serum
o Endocrinal shock: due to acute severe hormonal imbalance e.g. in adrenal
insufficiency or pituitary failure. It may present with a combination of
any of the above types.
➢ Obstructive shock: due to decreased blood flow to the left ventricle as in
cardiac tamponade, pulmonary embolism, and tension pneumothorax.
• Patients may have more than 1 type of shock e.g. hypovolemic and septic.

PATHOPHYSOLOGY
• This includes cellular changes, microcirculatory changes, acid-base imbalances
and systemic changes.
• Cellular changes:
➢ Tissue hypo-perfusion resulting in a decrease in oxygen delivery to the tissue
and cells undergo anaerobic metabolism producing lactic acid (causing
metabolic acidosis).
➢ This continues until cellular glucose is depleted resulting in stoppage of cell
metabolism release of auto-digestive enzymes and rupture of plasma and
lysosomal membranes.
• Microcirculatory changes:
➢ Under the effect of catecholamines the precapillary sphincters constrict, less
blood enters the capillaries and the capillary circulation becomes sluggish.
➢ Untreated hypovolemia thus leads to hypoxia.
➢ Under normal conditions only one third of the capillary bed is open at a time.
➢ Under ischemic conditions however the body reacts by opening more
capillaries this results in:
o Further slowing of the capillary circulation, the so called slugging of
blood.

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SURGERY MK
o Slugging encourages spontaneous coagulation of blood in these
capillaries.
o If extensive, it is called disseminated intravascular coagulation (DIC).
o This depletes coagulation factors and induces bleeding in the rest of the
body (consumption coagulopathy)
➢ A sluggish circulation and DIC compound tissue hypoxia and affect the
function of capillary endothelium. The result of the latter is leakage of large
protein molecules from the vessels into interstitial space dragging with them
huge amounts of fluid. This third space loss of fluid reduces blood volume.
• Acid-base imbalance: Shock is accompanied by metabolic acidosis which is
caused by accumulation of lactic acid as a result of anaerobic metabolism and
renal failure as a result of prolonged ischemia, aggravates acidosis.
• Systemic changes:
➢ Sympathetic response: release of catecholamines & stress hormones
(Cortisol, glucagon), release of ADH and activation of renin-angiotensin-
aldosterone system.
➢ Cardiovascular: reduced coronary artery perfusion and direct depression of
myocardium by tumor necrosis factor
➢ Respiratory: metabolic acidosis results in tachypnea which causes carbon
dioxide washout and compensatory respiratory alkalosis. Leakage and
swelling can develop in the lungs, causing difficulty in breathing (respiratory
distress- ARDS)
➢ GIT: mucosal hypoperfusion causes mucosa death and stress ulcers. Mucosal
death may also result in bacterial translocation, septicemia and multi-organ
failure.
➢ Liver: ischemic hepatic dysfunction
➢ Renal: renal hypoperfusion decreases GFR, urine output and may lead to pre-
renal failure and acute tubular necrosis.
➢ Ischemic perfusion syndrome:
o It is due to systemic hypoperfusion, tissue hypoxia and local activation
of inflammatory mediators.
o Further injury occurs once normal circulation is restored to tissues:
▪ Myocardial depression
▪ Cellular and humoral elements activated by hypoxia are flushed back
into circulation causing more endothelial injury e.g. acute lung
injury, acute renal injury
o It only can be minimized by decreasing the period of hypoperfusion.

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STAGES OF SHOCK
• Initial: decreased oxygen and increased lactate.
• Compensatory stage:
➢ Increased respiratory rate
➢ Sympathetic response: increased heart rate, fluid retention
➢ Increased renin and ADH secretion
• Progressive/decompensated stage: If compensatory mechanisms and treatment
are unsuccessful.
➢ Worsening hypotension due to vasodilation, blood pooling in capillaries,
and fluid leak from vessels.
➢ Altered mental status
➢ Electrolyte imbalances
• Refractory: irreversible

GENERAL CLINICAL FEATURES OF SHOCK

• Change in mental status: a continuum from agitation, confusion/delirium,
obtundation/coma.
• Hypotension: absolute (systolic blood pressure <90mmHg) or relative (a drop in
systolic blood pressure >40mmHg), which is why a patient may be in shock with
a high or normal blood pressure.
• Increased heart rate, pulse may be thread (barely perceptible). Capillary refill >2s
• Oliguria (<30ml/hr)- from shunting of renal flow to other vital organs,
intravascular volume depletion or both.
• Cool, clammy skin- compensatory peripheral vasoconstriction redirects blood
from the peripheral to the vital organs (heart, brain, splanchnic). However, in
early distributive shock or terminal shock the skin may be flushed or hyperemic
due to failure of compensatory vasoconstriction.
• Metabolic acidosis- increased lactate production from anaerobic respiration when
shock progresses to circulatory failure and tissue hypoxia along with decreased
clearance of lactate by the liver, kidneys and skeletal muscle.

APPROACH TO THE PATIENT WITH SHOCK

HISTORY
• Look for underlying causes, try to classify the type of shock. Often limited due
to confusion or obtundation.
• Ask for any history of:

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➢ Bleeding? Trauma? Hematemesis? Hematochezia? Melena? (if so suspect
hypovolemic shock)
➢ Coronary artery disease? Valvular heart disease? CCF? (if so suspect
cardiogenic shock)
➢ History of fever? Pneumonia? Meningitis? (if so suspect septic shock)
EXAMINATION
• General examination: ill appearing, confused, lethargic, unresponsive and
temperature >38oC or <36oC.
• Neurologic: meningism and focal neurologic deficits
• Cardiac: Tachycardic (HR> 100), hypotensive (SBP <100), Dizziness,
Orthostatic hypotension, S3 heart sound, murmur, Extremities may be warm/well
perfused or cold/blue, Capillary refill brisk or slow, Chest pain
• Pulmonary: Evidence of pneumonia, use of accessory muscles of respirations,
Respiratory rate >30, Oxygen saturation <95%.
• Gastrointestinal: Abdominal pain, Tense/Rigid abdomen (may indicate
perforated viscus, hemorrhage, peritonitis), rebound tenderness, guarding,
melena or blood on rectal exam.
• Renal: Flank tenderness (pyelonephritis), Urine output <0.5ml/kg/hr or <30ml/h
INVESTIGATIONS
• Blood investigations:
➢ Urea and electrolytes (Sodium, potassium, chloride and bicarbonate) +
Creatinine
➢ Liver enzymes
➢ Serum glucose
➢ Full blood count (leukocytes and bandemia in sepsis)
➢ Clotting profile: Bleeding time, Prothrombin time and activated partial
thromboplastin time to rule out bleeding tendencies
➢ Blood culture
➢ Cardiac enzymes
➢ Arterial blood gas/lactate (if available)
• Imaging:
➢ Chest and abdominal X-ray
➢ ECG
➢ Echocardiogram
➢ Ultrasound- Focused assessment with sonography for trauma (FAST)

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• Septic work up: CXR, blood culture, sputum microscopy culture and sensitivity,
urine dipstick, microscopy, culture and sensitivity, lumbar puncture.
MANAGEMENT
• Management depends entirely on the type of shock.
• Shock is always an emergency and must be treated rapidly as it is life threatening.
• Treat the underlying cause
• Management includes:
➢ Frequent monitoring of vital signs
➢ 2 large bore IV cannulas- 18 gauge (green) or greater.
➢ Foley catheter and monitoring of urine output.
➢ Aggressive colloid (normal saline or ringers lactate) fluid resuscitation for
hypotension- especially in hypovolemic + septic shock (may require >10 L)
➢ Intubation if in respiratory distress
➢ Packed red cells if bleeding/hypovolemic
➢ Stop any antihypertensive or diuretics. Give pressors (dopamine,
dobutamine, epinephrine, neosynephrine etc.) if shock is present despite
aggressive fluid resuscitation.
➢ Hypovolemic shock:
o IV fluids
o Check electrolytes
o Fix underlying condition e.g. diabetic ketoacidosis
o Send for X-match for urgent transfusion if hemorrhage (most common
cause of hypovolemic shock)
➢ Cardiogenic shock:
o IV fluids may be harmful
o IV Lasix and or dopamine may help
o Fix underlying cause e.g. valve replacement
➢ Septic shock:
o Search for source and start empiric antibiotics based on likely type of
infection.
o Give IV fluids
➢ Anaphylactic shock:
o IV fluids
o Subcutaneous epinephrine 0.3ml 1: 1000 solution if severe
o Antihistamines and corticosteroids may help
➢ Adrenal insufficiency: give hydrocortisone 100mg TDS x 5/7

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➢ Obstructive shock
o IV fluids
o Urgent ECG
o CXR to confirm
o Thrombolysis for Pulmonary embolism
o Chest tube for tension pneumothorax
o Pericardiocentesis for tamponade.

HYPOVOLEMIC SHOCK
ETIOLOGY
• This is due to diminished blood volume as a result of:
➢ Whole blood loss i.e. hemorrhage which can be traumatic or pathological
o Trauma
o Ruptured abdominal aortic aneurysm
o Aortic dissection
o Upper GI bleeding
o Ruptured ectopic pregnancy
➢ Plasma loss as in burns, heat exhaustion or peritonitis
➢ Water and electrolyte loss (especially Sodium) as in: severe vomiting,
diarrhea, intestinal obstruction and fluid sequestration (as in acute
pancreatitis).
STAGES
• Compensated stage: in this stage the body employs the physiological
mechanisms, in a trial to restore blood volume or at least, preserve the normal
function of the vital organs (brain, kidneys, heart and lung). With loss of >15%
of blood volume, the compensatory mechanisms usually fail.
• Decompensated stage (40% blood loss): if the cause of shock is not treated
successfully and after failure of compensatory mechanisms there will be
progressive poor perfusion and micro-circulatory changes with deterioration of
functions of the brain, kidney, heart and lung.
• Refractory stage: The shock can no longer be reversed. Failure of vital organs
and death occurs imminently.
CLINICAL FEATURES
• Of shock
➢ Symptoms:
o Weakness and fainting

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o The patient feels cold and thirsty
➢ Signs:
o Patient is cold and clammy with a narrow pulse pressure
o Decrease in blood pressure: SBP<90 or 60 below normal
o Orthostatic hypotension can be an early sign of hypovolemia.
o Capillary refill>2s
o Oliguria: <30ml/hr
o Altered mental status (may vary from anxious to drowsy but the patient
usually remains alert).
o Hypotension, tachycardia (increased heart rate, pulse may be thread-
barely perceptible) and decreased pulse pressure (thready pulse)
• Of the cause
➢ Sites of bleeding
➢ Signs of internal hemorrhage
➢ Burns
➢ Intestinal obstruction
➢ In hemorrhagic shock, trauma or signs of GI bleeding (melena, abdominal
pain)
• Of complications:
➢ Anuria
➢ Acute respiratory depress syndrome
INVESTIGATIONS
• Blood investigations:
➢ Full blood count (check Hemoglobin, hematocrit)
➢ Cross match (for blood transfusion) as well as group and save
➢ Urea and electrolytes (Sodium, potassium, chloride and bicarbonate) +
creatinine
➢ Clotting profile: Bleeding time, Prothrombin time and activated partial
thromboplastin time to rule out bleeding tendencies
➢ Liver function tests
➢ Serum glucose
➢ Arterial blood gasses: lactate >2 suggests hypoperfusion
• Imaging:
➢ Chest X-ray and ECG: to exclude cardiogenic causes
➢ Abdominal ultrasound: to rule out internal hemorrhage
➢ Head CT scan: if the patient with head injury or unconscious

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MANAGEMENT
RESUSCITATION
• ABCs
➢ Airway should be patent by: Pulling the tongue forward, aspiration of
secretions, and tracheostomy if needed
➢ Breathing should be maintained by: oxygen mask and ambu bag. Administer
oxygen.
➢ Circulation:
o 2 large bore IV cannula 18G (green) or bigger: one for IV fluids and the
other for sampling (if no veins available/all collapsed)
o Stop any external bleeding by compression.
➢ Drugs: analgesics for any pain
• Insert an NGT to evacuate the stomach (if surgery may be needed)
• Insert a urinary catheter to monitor urine output Recall:
• Elevate legs and head down to restore cerebral blood
60% of the body is fluid. It is
flow (Trendelenburg’s position)
distributed in 3 compartments:
• Give sufficient warmth (but avoid over warmth)
➢ 2/3 is intracellular fluid
FLUID ADMINISTRATION
➢ 1/3 is extracellular fluid
• Crystalloids: may be the only fluid given to patients
o ¾ (75%) of ECF is in
with hypovolemia caused by loss of water and
the interstitium
electrolytes.
o ¼ (25%) of ECF is in
➢ Normal saline: to replenish equivalent loss of both
the intravascular
water and electrolytes.
compartment
➢ Ringer: gives potassium supply (after ensuring good
urine output) in prolonged shock
➢ Lactated Ringer’s solution: also a buffer, in prolonged shock and acidosis
➢ Note: Glucose 5% is not used in shock because glucose is rapidly
redistributed this leads to an increase in the amount of ECF (without
electrolytes) causing dilutional hyponatremia and increased ICF with brain
edema and increased intracranial pressure.
• Fluid therapy:
➢ Resuscitation:
o 500ml crystalloid bolus over <15minutes. 250ml if old or heart failure.
o Reassess and re-give up to 2L
o Don’t wait until SBP is under 90. A SBP of 110 in the presence of
increased heart rate suggests impaired output.

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➢ Replacement:
o Estimate fluid losses, and replace gradually over 2-3 days i.e. in addition
to maintenance fluids.
➢ Maintenance:
o Basic needs:
▪ 25-30ml/kg/day water. 20-25ml/kg/day if old, kidney or heart failure
or malnourished. So just over 1ml/kg/hr
▪ 1mmol/kg/day of sodium, potassium and chloride. In general, don’t
give >10mmol/hr
▪ 50-100g/day of glucose.
o Management:
▪ Usually need around 2-3 liters per day so around 100ml/hr is typical
e.g. 1L over 8-10 hours. 500ml over 8 hours if old or heart failure.
▪ 1L of normal saline contains 154mmol of both sodium and chloride
and 1 L of Hartmann’s solution contains 131 mmol of sodium and
111mmol of chloride (plus 5 mmol of potassium). So 500ml of each
roughly covers daily needs.
▪ Typical daily regimen may be 1L 5% dextrose with 20mmol
potassium, then 500ml normal saline with 20mmol potassium, then
1L 5% dextrose with 20 mmol potassium.
▪ Monitor potassium to determine needs
▪ Monitor increase in chloride daily if on normal saline due to risk of
increased chloride ions.
• Colloids: contain large insoluble molecules increasing oncotic pressure and in
theory keeping the fluid in the intravascular compartment longer. In clinical
trials, however, colloids have shown no benefit (and sometimes harm) relative to
crystalloids.
➢ Plasma substitutes: needs matching and adequate storage
➢ Dextran (polysaccharide polymers): high molecular and low molecular
weight
• Blood and blood products:
➢ Red blood cells
o Indications:
▪ Decreased Hb (Hb<7g/dl)
▪ Hb <8g/dl in patients with ACS
▪ Major hemorrhage (given in combination with FFP and platelets)
o 1 unit of blood increases Hb by 1g/dl

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o 1 unit of whole blood is around 450ml while 1 unit of packed cells is 250-
300ml.
o Prescribe 1 unit at a time, checking response (symptoms and/or Hb) after
each.
o If unused must return to fridge within 30 minutes for reuse.
o RBCs typically given over 2-3 hours but can be up to 4 hours most other
products are given over 30 minutes.
o Assess patient at baseline, 15 minutes and at the end of transfusion.
➢ Fresh frozen plasma (FFP)
o Human plasma which contains clotting factors (II, V, VIII, IX, X, XI and
antithrombin III)
o Indications
▪ Major hemorrhage
▪ Warfarin reversal (INR>1.5)
o Cryoprecipitate is another alternative to FFP, though less used now. It is
the precipitate from human plasma, and contains fibrinogen, factor VIII
(8), vWF and factor XIII (13)
➢ Platelets
o Indications:
▪ Platelet <50K/L and bleeding
▪ Platelet <20 K/L and septic
▪ Platelet <10 K/L
▪ Stop any anti-platelets if giving
Transfusion reaction Signs Management
Mild • <2oC rise in • Pause transfusion and assess
temperature patient
• Rash/Urticaria • Consider paracetamol or
chlorphenamine
• Re-start transfusion with close
observation
Severe • o
>2 C rise in • Stop transfusion and replace
temperature any fluid needs with saline
• Rigors • Call hematology, contact lab to
• Loin or back pain return product, and complete
• Anxiety or angor incident report
animi

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• Unexpected
increased heart rate
• Infusion site pain

• Transfusion associated circulatory overload (TACO):

➢ Commonest cause of transfusion-associated death
➢ Presents with 6 hours of transfusion with acute respiratory distress,
pulmonary edema, increased heart rate and increased BP.
➢ Risk factors: age <3 or >60, low birth weight, heart failure, kidney failure
➢ Blood products are prescribed in mls in neonates to reduce TACO
• Transfusion-related acute lung injury (TRALI)
➢ Very uncommon
➢ Respiratory distress, decreased BP
➢ Usually due to FFP or platelets
• Other complications:
➢ Anaphylaxis
➢ Hemolytic anemia
➢ Increased potassium
➢ Infection
MONITORING
• Monitor:
➢ Pulse and ECG
➢ Blood pressure
➢ Temperature
➢ Urine output (optimum urinary output= 0.5-1ml/kg/hr)
➢ Arterial blood gasses (normal PO2=80-100mmHg, normal PCO2= 35-
45mmHg)
DRUGS
• Drugs that increase BP by increasing cardiac contractility (inotropes) and/or
vasoconstriction (vasopressors). Many also increase heart rate (positive
chronotropy).
• Indicated in shock for which IV fluids are insufficient or inappropriate.
• Delivery is typically as an infusion through a central line.
• Many commonly used agents are synthetic versions of endogenous
catecholamines

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Drug Mechanism of action Dosage Side-effect

Noradrenaline Vasopressor via alpha 1 0.05-1.0mcg/kg/min Peripheral
(norepinephrine) agonism but also administration carries
inotropy via Beta 1 a risk of extravasation
First line agent agonism at higher doses. and hence tissue
for shock in Reflex bradycardia from necrosis via
many ICUs increased BP typically vasoconstriction.
cancels out chronotropic However short term
effect. delivery via a large,
Adrenaline Acts on all adrenergic 0.05-1.0mcg/kg/min proximal peripheral
(epinephrine) receptors. At lower line is sometimes
doses works primarily acceptable.
Most commonly on beta 1 (inotropy and
used for chronotropy) and beta 2 Ischemia especially
anaphylaxis and (airway and vessel to the GIT, kidney
cardiac arrest dilation) and alpha 1 and extremities
(vasoconstriction) at
higher doses (including Atrial and ventricular
cardiac arrest dose) arrhythmias
Dobutamine Inodilator with inotropy Dobutamine 5-10
via beta 1 agonism and microgram/kg/min IV
Used in acute vasodilation via beta 2. infusion
heart failure
Dopamine DA agonist at lower Give dopamine 5-10 Risk of
doses, alpha and beta micrograms/kg/min IV Tachyarrhythmias
effects at higher doses infusion (dilute 400mg in Evidence suggests
500ml of 5% dextrose that dopamine
infusion rate to be inhibits secretion of
calculated according to prolactin and could
body weight) increase lymphocytes
• Start 5mcg/kg/min, apoptosis
titrate to effects. (impairment of
immune response to
sepsis)

TREAMENT OF CAUSE AND COMPLICATIONS

• Treat the underlying cause.

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CARDIOGENIC SHOCK
• This is due to inadequate blood flow to vital organs due to inadequate cardiac
output despite of normal blood volume.
• It is characterized by
➢ SBP <90mmHg
➢ Mean arterial pressure drop >30mmHg
➢ Urine output <0.5ml/kg/hr
➢ Heart rate >60bpm
ETIOLOGY
• Primary pump failure due to:
➢ MI (commonest cause) or its complications e.g. ventricular septal rupture
➢ Severe arrhythmias
➢ Massive pulmonary embolism
➢ Cardiac tamponade
➢ Myocarditis
➢ Severe valve disease
➢ Trauma
➢ High spinal anesthesia
CLINICAL FEATURES
• Of shock:
➢ Clinical picture similar to hypovolemic shock.
➢ Comatose
➢ Patient is cold and clammy and pulse pressure may be narrow
➢ Peripheral cyanosis
➢ Poor urine output
➢ Increased JVP and decreased heart rate
• Of the cause: enlarged liver, chest pain, pulsus alternans, ‘gallop’ rhythm,
murmur, basal crackle, pulmonary edema.
INVESTIGATIONS
• Blood investigations:
➢ Full blood count (check Hemoglobin, hematocrit)
➢ Cross match (for blood transfusion) as well as group and save
➢ Urea and electrolytes (Sodium, potassium, chloride and bicarbonate) +
creatinine

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➢ Clotting profile: Bleeding time, Prothrombin time and activated partial
thromboplastin time to rule out bleeding tendencies
➢ Liver function tests
➢ Serum glucose
➢ Arterial blood gasses: lactate >2 suggests hypoperfusion
• Imaging:
➢ Cardiorespiratory: ECG, CXR (enlarged heart, pulmonary venous
congestion) and echo
➢ Abdominal ultrasound: to rule out internal hemorrhage
➢ Head CT scan: if the patient with head injury or unconscious
MANAGEMENT
• Management aims at:
➢ Improving cardiac output:
o Correct dysrhythmias
o Optimize preload
o Improve contractility
o Reduce afterload
➢ Minimizing cardiac work:
o Maintain normal temperature
o Sedation
o Intubation and mechanical ventilation
o Correct anemia
• ICU care
• Give oxygen
• Regular monitoring of temperature, heart rate, blood pressure and cardiac
monitoring.
• Give dopamine 5-10 micrograms/kg/min IV infusion (dilute 400mg in 500ml of
5% dextrose infusion rate to be calculated according to body weight)
➢ Start 5mcg/kg/min, titrate to effects.
➢ Evidence suggests that dopamine inhibits secretion of prolactin and could
increase lymphocytes apoptosis (impairment of immune response to sepsis).
• Dobutamine 5-10 microgram/kg/min IV infusion
• Prophylactic anticoagulation with ASA 75mg PO OD.
• Treat underlying cause
• If in heart failure and BP goes above 90mmHg treat as class IV.

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➢ Captopril 25mg BD/TDS or Lisinopril 10-20mg OD or Enalapril 5-20mg
OD (if patient develops dry cough Losartan 50mg OD)
➢ Furosemide IV 40-80mg OD or BD (monitor potassium levels)
➢ Digoxin 0.125mg-0.25mg daily
➢ Isosorbide dinitrate 5-10mg BD + hydralazine 25-50mg BD orally if patient
cannot tolerate ACEi.
➢ Spironolactone 25-50mg OD or BD
➢ ASA 75mg OD

DISTRIBUTIVE SHOCK
• Vasodilation leads to a relative (though not absolute) deficiency in volume.
SEPTIC SHOCK (ENDOTOXIC SHOCK)
• Septic shock is a type of distributive shock though it may also include an element
of hypovolemic shock as altered capillary permeability leads to volume loss from
the vasculature.
• It is the most serious type of shock and the most difficult to treat.
ETIOLOGY
• Gram negative bacilli (commonest cause)
• Staphylococci
• Candida
PREDISPOSING FACTORS (IMMUNOSUPPRESION)
• Extremes of age
• Malignancy
• Malnutrition
• Diabetes mellitus
• Chemotherapy, corticosteroids or immunosuppressants
• HIV infection
PATHOPHYSIOLOGY
• Bacterial endotoxins are released when immune cells (i.e. macrophages) kill
gram negative bacteria.
• Immune cells release cytokine, TNF and IL-2 which damage capillary
endothelium leading to edema and vasodilation (rapid shifting of blood bypassing
capillary) and tissue ischemia.

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• Septic shock starts as maldistribution of blood followed by myocardial
depression and hypovolemia.
CLINICAL FEATURES
• Hyper-dynamic (warm) septic shock (early phase): diagnosis is difficult and high
index of suspicion is required to detect it at early stage.
➢ Restless and confusion
➢ Skin: flushed, warm and dry
➢ Vitals:
o Fever >38oC + Chills
o Mild decreased in arterial blood pressure, pulse pressure may be wide
with a low DBP.
o Tachycardia
o Tachypnea
➢ High cardiac output
• Hypo-dynamic “cold” septic shock (Late phase): picture similar to hypovolemic
shock with reduced cardiac output
➢ Skin: cold and clammy
➢ Vitals:
o SBP<90mmHg
o Tachycardia
o Tachypnea
➢ Oliguria
➢ Multi-organ failure starts at this stage.
DIAGNOSIS
• To diagnose septic shock, the following 2 criteria must be met
➢ Evidence of infection, through a positive blood culture
➢ Refractory hypotension (Despite adequate fluid resuscitation and cardiac
output)
• In addition to the 2 criteria above 2 or more of the following must be met (SIRS)
➢ RR >20bpm (high respiratory rate)
➢ WBC <4000 cells/mm3 or > 12 000 cells/mm3
➢ Temperature >38oC or <36oC
➢ HR>90b/min
➢ Arterial blood gasses PaCO2 <32mmHg

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MANAGEMENT
• Give oxygen
• Give fluids:
➢ Ringer’s lactate + Plasma
➢ If low hematocrit packed RBCs or whole blood transfusion
• Drugs
➢ Inotropes and vasopressors: dopamine and dobutamine
➢ Give if patient remains hypotensive despite adequate fluid replacement.
➢ Give dopamine 5-10 micrograms/kg/min IV infusion (dilute 400mg in 500ml
of 5% dextrose infusion rate to be calculated according to body weight)
o Start 5mcg/kg/min, titrate to effects.
o Evidence suggests that dopamine inhibits secretion of prolactin and could
increase lymphocytes apoptosis (impairment of immune response to
sepsis).
➢ Dobutamine 5-10 microgram/kg/min IV infusion
• Antibiotics: parenteral combined broad-spectrum started early without waiting
for culture and sensitivity results (3rd generation cephalosporin e.g. ceftriaxone +
Aminoglycoside e.g. gentamicin + Metronidazole) then changed to culture and
sensitivity.
• Monitor vitals and urine output regularly.
• ASA 75mg OD for DVT prophylaxis
• Proton pump inhibitors to prevent stress ulcers.
• Use of corticosteroids in septic shock remains controversial.

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WOUNDS AND WOUND HEALING

WOUNDS AND • There is no need of antibiotic use in

clean wounds except in
WOUND HEALING immunosuppressed patients or
• A wound is described as a break in patients having a prosthetic heart
the integrity of the skin or tissues valve.
often which may be associated with
CLEAN CONTAMINATED
disruption of the structure and
WOUND
function.
• An ulcer is a disruption or break in • This type of wound has low risk of
the continuity of epithelium- may infection (10% risk).
be skin, mucous membrane or • These wounds include entry into
others associated with microscopic hollow organ that is not inflamed
death of tissue. and entry into abscess cavity, minor
➢ Ulcers are a type of wound. breach in aseptic procedure, mild
spillage of intra-abdominal viscous.
CLASSIFICATION OF ➢ Appendectomy
WOUNDS ➢ Bowel surgeries
CLASSIFIACTION OF ➢ Gallbladder, biliary and
SURGICAL WOUNDS pancreatic surgeries
CLEAN WOUND • Prophylactic treatment with
antibiotics is required.
• This class of wounds have minimal
risk of infection (less than 2%). CONTAMINATED WOUND
• They include surgically incised • These have high rate of infection
wounds with complete adherence (15-30% risk).
of all septic conditions without any • They occur when there is major
breech of any hollow viscera. breach in aseptic condition even
➢ Thyroidectomy without entry into abscess cavity or
➢ Herniorrhaphy hollow viscus.
➢ Herniotomy ➢ Acute abdominal conditions
➢ Lumpectomy ➢ Open fresh accidental wounds
➢ Excisions: lipoma
• Therapeutic antibiotics aimed at
➢ Surgeries of the brain, joints,
treatment and not prophylaxis are
heart, transplant
given.

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DIRTY OR INFECTED WOUND ➢ Repair replaces damaged tissue
with fibrous scar. It occurs when
• These have very high risk of
regenerative stem cells are lost
infection (40-70% risk).
or when tissue lacks
• Dirty wounds appear grossly
regenerative capacity.
infected with pus with entry into an
• Recall that, based on regenerative
abscess cavity such as in
capacity tissues are divided into:
gangrenous bowel.
➢ Labile tissue/continuous
➢ Abscess drainage
dividers:
➢ Pyocele
o Continuously in the cycle to
➢ Empyema gallbladder
regenerate
➢ Fecal peritonitis
o Examples: small and large
Table 3.41: Wound Classification (Courtesy bowel (stem cells in
of SRB's Manual of Surgery 4th Ed) mucosal crypts), skin (stem
cells in basal layer), bone
marrow (hematopoietic
stem cells), Lung tissue
(type II pneumocytes are the
stem cells)
➢ Stable tissue/Facultative
dividers/quiescent cells:
o Are quiescent but can re-
enter the cell cycle.
o Regeneration of liver by
compensatory hyperplasia
after partial resection.
o Each hepatocyte produces
additional cells and then re-
WOUND HEALING enters quiescence.
• Wound healing is a complex o Cells of proximal renal
method to achieve anatomical and tubules are also stable
functional integrity of disrupted ➢ Permanent tissue
tissue. o Lacks significant
• Healing is by regeneration and regenerative potential
repair. o Examples: myocardium,
➢ Regeneration replaces damaged skeletal muscle, neurons.
tissue with natural tissue.

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• Healing involves neutrophils, • Re-epithelialisation occurs from
macrophages, lymphocytes, remaining dermal elements or
fibroblasts and collagen in an wound margins.
organized staged pathway.
HEALING BY THIRD
TYPES OF WOUND CLOSURE INTENTION (TERTIARY
PRIMARY HEALING (FIRST WOUND HEALING OR
INTENTION) DELAYED PRIMARY CLOSURE)
• If staples or sutures close a wound, • After wound debridement and
healing is said to be by primary control of local infection, wound is
intention. closed with sutures or covered
• Occurs in a clean incised wound or using skin graft.
surgical wound. • Primary contaminated or mixed
• Wound edges are approximated tissue wounds heal by tertiary
with sutures. There is more intention (Also known as delayed
epithelial regeneration than primary closure)
fibrosis.
• Wound heals rapidly with complete Note: the average wound
closure. usually achieves
• Scar will be linear, smooth and approximately 4-8% of its
supple. expected tensile strength after
1-2 week.
SECONDARY HEALING
(SECOND INTENTION) When completely healed it has
80% tensile strength as
• Occurs in a wound with extensive
compared to uninjured tissue
soft tissue loss like in major trauma,
burns and wound with sepsis.
• Edges are not approximated with STAGES OF WOUND
sutures; granulation tissue fills the HEALING
defect. • There are 4 distinct stages of
• It heals slowly with fibrosis. It normal wound healing, which are
leads into a wide scar often not mutually exclusive and show
hypertrophied and contracted. It considerable overlap.
may lead into disability • These stages include:
(contracture). ➢ Stage of coagulation/hemostasis
➢ Stage of inflammation

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➢ Stage of fibroplasia/ • Polymorphonuclear leukocytes
Proliferation (PMN leukocytes) appear after 48
➢ Stage of re-modeling hours which secrete inflammatory
mediators and bactericidal oxygen
PHASES OF WOUND derived free radical.
HEALING ➢ They also remove clots, foreign
COAGULATION/ HEMOSTASIS bodies and bacteria.
• Happens almost immediately. • Chemical factors in wound healing:
• Following injury, the clotting ➢ Growth factors
cascade is initiated, local o TGF alpha- epithelial and
vasoconstriction occurs and a fibroblast growth factor
platelet clot forms. o TGF beta- important
• Platelet-derived growth factor fibroblast growth factor,
(PDGF) is released. inhibits inflammation
• After the transient phase of o Platelet derived growth
vasoconstriction there is factor- endothelium, smooth
vasodilatation to initiate the muscle, fibroblast growth
inflammatory phase. factor.
o Fibroblast growth factor-
INFLAMMATORY PHASE angiogenesis, skeletal
• Begins immediately after development
vasodilatation. o Vascular endothelial
• Inflammatory cells are attracted to derived growth factor-
the site of injury, initially angiogenesis
neutrophils then macrophages,
which remove tissue debris. PROLIFERATIVE PHASE
(COLLAGEN/FIBROBLASTIC
• Lymphocytes are recruited later
PHASE)
and persist in chronic
inflammation. • There is formation of granulation
tissue.
• Lasts 0 to about 4/6 days.
• It lasts from 4 days to 3 weeks (4
• Shows the features of inflammation
days to 21 days).
(rubor, calor, tumor, dolor and loss
of function) • Granulation tissue consists of:
➢ Fibroblasts: deposits type III
• Macrophages secrete fibroblastic
collagen
growth factor (FGF)
o Recall Type I collagen is
➢ FGF enhances angiogenesis and
found in bONE, Type II
skeletal development

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SURGERY MK
collagen is found in FACTORS AFFECTING
cartilage (car-two-lage),
Type III collagen is found in
WOUND HEALING
blood vessels, granulation • Local factors:
tissue, and embryonic tissue ➢ Infection (most common cause
e.g. skin because of its of delayed wound healing).
pliability characteristic and ➢ Presence of necrotic tissue and
Type IV collagen is found in foreign body.
the basement membrane. ➢ Poor blood supply
➢ Capillaries: provide nutrients ➢ Venous or lymph stasis
➢ Myofibroblast: contract wound ➢ Tissue tension
➢ Hematoma
REMODELLING PHASE ➢ Large defect or poor apposition
(MATURATION PHASE) ➢ Recurrent trauma
• It is from 3weeks to 18 months. ➢ X-ray irradiated area
• There is maturation of collagen by ➢ Site of wound e.g. wounds over
cross-linking which is responsible the joints and back heal poorly.
for tensile strength of the scar. ➢ Underlying diseases like
• There is differentiation of fibroblast osteomyelitis and malignancy
into myofibroblasts which are ➢ Mechanism and type of wound-
responsible for wound contraction. incised/lacerated/crush/avulsion
• Collagen production is not present ➢ Tissue hypoxia locally reduces
after 42 days of wound healing. macrophage and fibroblast
• Type III collagen is replaced with activity
type I collagen and blood vessels • General factors:
atrophy. ➢ Age, obesity, smoking
• The processes result in wound ➢ Malnutrition, zinc deficiency
healing by an epithelialized white (required for collagenase),
scar. copper deficiency (lysly
• Collagenase removes type III oxidase), manganese deficiency
collagen and requires zinc as a co- ➢ Vitamin deficiency (Vitamin C-
factor. required for the hydroxylation
• Maximal wound tensile strength is of collagen as it is maturing,
achieved at about day 60, when it is Vitamin A)
80% of normal. ➢ Hypoproteinemia
➢ Anemia
➢ Malignancy

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➢ Uremia ➢ The bleeding if present should
➢ Jaundice be controlled
➢ Diabetes, metabolic disease ➢ Intravenous fluids are started
➢ HIV and immunosuppressive ➢ Oxygen if required may be
diseases given
➢ Steroids and cytotoxic drugs ➢ Deeper communicating injuries
➢ Neuropathies of different causes and fractures should be looked
for.
COMPLICATIONS OF • If it is an incised wound then
WOUND HEALING primary suturing is done after
1. Dehiscence thorough cleaning.
➢ Rupture of wound, most ➢ Primary suturing means
commonly seen after abdominal suturing the wound immediately
surgery. within 6 hours. It is done in
2. Hypertrophic scars clean incised wounds.
➢ Excess production of scar tissue ➢ Primary suturing should not be
that is localized to the wound done if there is
3. Keloid edema/infection/devitalized
➢ Excess production of scar tissue tissue/ hematoma.
that is out of proportion to the ➢ Always associated injuries to
wound (exceeds wound deeper structures like
margins). vessels/nerves or tendons
➢ Characterized by excess type III should be looked for before
collagen closure of the wound.
➢ Genetic predisposition (more ➢ Wound should be widened by
common in African American) extending the incision whenever
➢ Classically affects ear lobes, needed to have proper
face and upper extremities evaluation of the deeper
structures-proper exploration
MANAGEMENT OF ➢ Proper cleaning, asepsis, wound
WOUNDS excision/debridement
• Wound is inspected and classified ➢ Any foreign body in the wound
as per the type of wounds. should be removed
• If it is in a vital area (ABCs): ➢ Skin closure if it is possible
➢ The airway should be without tension
maintained ➢ Skin closure by graft/flap-
immediate or delayed

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SURGERY MK
➢ Untidy wound should be made sutured with 6-zero polypropylene
tidy and clean before suturing non-absorbable suture material. If
➢ Proper aseptic precautions the nerves are having clean cut
should be undertaken wounds it can be sutured primarily
➢ Antibiotics/analgesics are with polypropylene 6-zero or 7-
needed zero suture material. If there is
➢ Sutured wound should be difficult in identifying the nerve
inspected in 48 hours. (for ends or if there are crushed cut ends
neurovascular state) of nerves then marker stitches are
➢ Sutures are removed after 7 days placed using silk at the site and later
• If it is a crushed or devitalized secondary repair of the nerve is
wound there will be edema and done.
tension in the wound. So after • Internal injuries (intracranial by
wound debridement or wound craniotomy, intrathoracic by
excision by excising all devitalized intercostal tube drainage, intra-
tissue, the edema is allowed to abdominal by laparotomy) has to be
subside for 2-6 days. Then delayed dealt with accordingly. Fractured
primary suturing is done. bone is also identified and properly
➢ Delayed primary suturing dealt with.
means suturing the wound in • Antibiotics, fluid and electrolyte
48hours to 10 days. It is done in balance, blood transfusion, tetanus
lacerated wounds. This time is toxoid (0.5 ml intramuscular to
allowed for the edema to deltoid muscle) or antitetanus
subside. globulin (ATG) injection.
• If it is deep devitalized wound, after • Wound debridement (wound toilet
wound debridement it is allowed to or wound excision) is liberal
granulate completely. Later if the excision of all devitalized tissue at
wound is small secondary suturing regular intervals (of 48-72 hours)
is done. If the wound is large a split until healthy, bleeding, vascular
skin graft (Thiersch graft) is used to tidy wound is created.
cover the defect ➢ Wound toilet is washing the
• In a wound with tension, wound thoroughly using normal
fasciotomy is done so as to prevent saline-ideal
the development of compartment ➢ Wound debridement is allowing
syndrome. content to come out by release
• Vascular or nerve injuries are dealt incisions or fasciotomies. But
with accordingly. Vessels are

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SURGERY MK
commonly debridement is used fractures, edema, ischemia
for wound excision. injury, hematomas, positioning
➢ Wound excision is actually after trauma, burn injury etc.
correct terminology for excision ➢ High pressure injuries like gun
of devitalized tissues once or injury, oil-based material injury,
serially. extravasation of
➢ Radical wound excision chemotherapeutic drugs, snake
(pesudotumor approach) is bites.
excising entire devitalized • Pathophysiology:
tissues leaving tissues with ➢ Edema is often a sequela of
visible bleeding from all layers. trauma. If it occurs in a limited
anatomical space such as one of
COMPARTMENT the four compartments of the
SYNDROME lower limb, the tissue pressure
• This is a special entity, common in will rise.
leg, forearm, thigh and arms. ➢ As tissue pressure rises, the
• It is a syndrome due to increased pressure on and within the local
intra-compartmental pressure venous system also rises.
within a limited space ➢ Arterial resistance subsequently
compromising the circulation and increases and inflow is reduced.
function of tissues within that ➢ If untreated there is vascular
closed space. compromise and the enclosed
• Compartment syndrome in the muscle becomes ischemic.
lower limb is defined as ➢ Prolonged ischemia results in
intercompartmental pressures necrosis and ultimately, fibrosis
exceeding 30 mmHg. of the muscle and surrounding
• It is characterized by severe, soft-tissue structures.
progressive and persistent pain that ➢ As pressure increases there is
poorly responds to analgesics and is loss of sensation in the
aggravated by passive muscle distribution of the involved
stretching. nerves and ultimately the local
• Causes: pulses are lost, although the
➢ Narrowed space due to tight latter is not necessary to make
dressings/ plaster cast, lying on the diagnosis.
one limb in comatous patient • The “Five Ps” of compartment
➢ Increased content within the syndrome:
compartment due to trauma like

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SURGERY MK
➢ Pain (severe, progressive, • Compartment pressure more than
persistent, poorly localized and 30 mmHg is an indication for
poorly responding to analgesia. fasciotomy.
Exacerbated on passive muscle • Intracompartment pressure can be
stretch) measured using 3 techniques:
➢ Paresthesia: first sign in leg is ➢ Whitesides saline/needle
paresthesia at the first web space technique: an 18G needle
(between great and second toes) connected via a 3-way stop cock
➢ Paralysis: Occurs after ischemia to an air-filled 20ml syringe. Air
is well established filled tubing is connected to a
➢ Pulselessness: Shown to occur mercury manometer and a small
late at times. Pulse may be amount of saline sites in the tube
present connected to the needle.
➢ Pallor: not necessary for Compression of the syringe
diagnosis, may not be present raises the pressure till saline
➢ Poikilothermia flows into the compartment (this
• Tense tender regional lymph node is indicated by meniscus
is typical. Pulse will be usually moving)
normally felt in compartment ➢ Arterial pressure transducer:
syndrome but may become absent this is a device used in ICU to
if there is associated arterial injury. measure arterial blood pressure
• It compromises circulation and and CVP. There is no need to
function of muscles and nerves. inject fluid. Pressure in the
• It often maintains the normal color saline tube equalizes with
and temperature of the fingers and compartment. The transducer is
distal pulses may be obliterated in connected to a Wick or slit
spite of severe muscle ischemia. catheter. Slits have many
• Muscle ischemia more than 4 hours longitudinal slits to equalize
causes muscle death and pressure in the tube with
myoglobinuria. Muscle necrosis compartment
releases myoglobin which is ➢ Stryker device: a variation of the
excreted in urine, damages the arterial pressure transducer
kidneys leading into renal failure.
• Irreversible nerve
• damage develops if ischemia
persists for 8 hours.

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SURGERY MK
fat and deep fascia should be
done until underneath muscle
bulges out properly. The
wounds are left open, allowing
swelling to occur unrestricted
and dressed with appropriate
sterile dressings. The wounds
are closed at a later time once
the acute episode has resolved.
Sometimes this is not possible
directly and split skin grafts are
used.
➢ Antibiotics
➢ Catheterisation
➢ Mannitol or diuretics to causes
diuresis so as to flush the kidney
Figure 36: Whiteside saline/needle technique ➢ Fresh blood transfusion
• It is common in calf and forearm. ➢ Hyperbaric oxygen
• Closed injuries cause hematoma KELOID
leading to increased pressure.
• Keloids (“like a claw”) are
• It is often associated with fracture
common in blacks. They are much
of the underlying bone which in
more common in females and carry
turn compresses the major vessels
a genetic predisposition often
further aggravating the ischemia
familial but can happen
causing pallor, pulselessness, pain,
spontaneously.
paraesthesia, diffuse swelling and
• There is a defect in maturation and
cold limb.
stabilization of collagen fibrils.
• If allowed to progress it may
Normal collagen bundles are
eventually lead to gangrene or
absent.
chronic ischemic contracture with
• Keloids continue to grow even after
deformed, disabled limb.
6 months, maybe for many years.
• Treatment:
They extend into adjacent normal
➢ Fasciotomy (Under general
skin and they are brownish black/
anesthesia): when pressure
Pinkish black (due to vascularity)
exceeds 30 mmHg. Adequate
in color, painful, tender and
length incision involving skin,

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SURGERY MK
sometimes hyperaesthetic, spreads ➢ Intralesional excision retaining
and causes itching. the scar margin may prevent
• Keloids may be associated with recurrence. It is ideal and better
Ehlers-Danlos syndrome or than just excision
scleroderma. ➢ Excision and irradiation or
• When keloids occur following an irradiation alone
unnoticed trauma without scar ➢ Excision and skin grafting may
formation they are called be done.
sponataneous keloids, commonly • Note: excision and primary
seen in Negroes. suturing has got high recurrence
• Some keloids occasionally become rate (more than 50%), hence it is
non-progressive after initial not usually practiced.
growth.
• Pathologically keloid contain
HYPERTROPHIC SCAR
proliferating immature fibroblasts, • Occurs anywhere in the body.
proliferating immature blood • Not genetically predisposed or
vessels and type III thick collagen familial.
stroma. • Growth usually limits up to 6
• Site: common over the sternum. months.
Other sites are upper arm, chest • It is limited to the scar tissue only.
wall, lower neck in front. It will not extend to normal skin.
• Differential diagnosis: • It is pale brown in color, not
hypertrophic scar. painful, non-tender.
• Treatment: controversial • Often self-limiting also. It responds
➢ Steroid injection- intrakeloidal very well to steroid injection
triamcinolone, is injected at • Recurrence is uncommon.
regular intervals, may be once in • It is common in wounds crossing
7-10 days, of 6-8 injections. tension lines, deep dermal burns,
➢ Steroid injection-excision- wounds healed by secondary
steroid injection intension.
➢ Methotrexate and vitamin A • Complications:
therapy into the keloid ➢ Often this scar breaks repeatedly
➢ Silicone gel sheeting, topical and causes infection, pain
retinoids ➢ After repeated breakdown it
➢ Laser therapy may turn into Marjolin’s ulcer.
➢ Vitamin E/ palm oil massage

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• Treatment: it is controlled by SURGICAL WOUND
pressure garments or often revision
INFECTION
excision of scar and closure, if
required with skin graft.

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ULCERS

ULCERS SLOPING EDGE/SHELVING

• This is seen in a healing ulcer.
• An ulcer is a break in the continuity
of the covering epithelium (either • Its inner part is red because of red,
skin/ mucous membrane) healthy granulation tissue.
associated with • Its outer part is white due to scar/
microscopic/molecular death. fibrous part.
• Its middle part is blue due to
PARTS OF AN ULCER epithelial proliferation.
• Ulcers have the following parts:
➢ Margin
➢ Edge
➢ Floor
➢ Base

Figure 38: A healing ulcer (Image Adapted

From SRB's Manual of Surgery)

Figure 37: Parts of an Ulcer (Image

Adapted from SRB's Manual of Surgery).

MARGIN Figure 39: A healing ulcer (Image Adapted

• This may be regular or irregular. from SRB's Manual of Surgery).
• It may be round or oval. UNDERMINED EDGE
EDGE • Seen in a tuberculous ulcer as well
• This connects the floor to the as decubitus ulcers (pressure sores).
margin. • Disease process advances in deeper
• There are different types of edges. planes (in subcutaneous tissue)
• The margin indicates the nature of whereas skin proliferates inwards.
the lesion.

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PUNCHED-OUT EDGE
• Punched-out ulcers have sharp
edges.
• Seen in a gummatous (syphilitic
ulcer) and trophic ulcer (pressure
sores/decubitus ulcers).
Figure 40: Undermined ulcer in TB (Image • It is due to end-arteritis.
Adapted from SRB's Manual of Surgery).

Figure 43: Punched out ulcer (Image

Adapted from SRB's Manual of Surgery).

ELEVATED/EVERTED EDGE
(ROLLED OUT EDGE)
• It is seen in a carcinomatous ulcer
Figure 41: Tuberculous ulcer on Chest wall
(Image Adapted from SRB's Manual of
(basal cell or squamous cell
Surgery). carcinoma of the skin) due to spill
of the proliferating malignant
tissues over the normal skin.

Figure 44: Elevated edge (Image Adapted

from SRB's Manual of Surgery).

Figure 42: Tuberculous ulcer around ankle

(Image Adapted from SRB's Manual of
Surgery).

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SURGERY MK

Figure 47: Basal cell carcinoma of face-

Rodent ulcer. Edge is raised and beaded in
appearance (Image Adapted from SRB's
Manual of Surgery).

FLOOR
Figure 45: Squamous cell carcinoma scalp.
Note the ulceroproliferative lesion with
• It is the one that is seen.
everted edges (Image Adapted from SRB's • It may contain discharges, slough,
Manual of Surgery). or granulation tissue.
RAISED AND BEADED EDGE BASE
(PEARLY WHITE) • This is where the ulcer rests on. It is
• Seen in a rodent ulcer (Basal cell not seen but felt.
carcinoma). • It may rest on bone or soft tissue.
• Beads are due to proliferating • If there is inflammatory
active cells. involvement, the surrounding
tissues feel indurated and the ulcer
appears fixed and is tender.
Fixation and induration may be the
result of neoplastic infiltration of
the deeper tissue if ulcer is
Figure 46: Raised and beaded edge (Image malignant. In this instance fixation
Adapted from SRB's Manual of Surgery).
is not accompanied by tenderness.

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SURGERY MK

INDURATION OF AN WAGNER’S
ULCER CLASSIFICATION OF AN
• Induration is a clinical palpatory ULCER
sign which means a specific type of • Grade 0: pre-ulcerative lesion/
hardness in the diseased tissue. healed ulcer
• It is obvious in well-differentiated • Grade 1: superficial ulcer
carcinomas. • Grade 2: Ulcer deeper to
• It is better felt in squamous cell subcutaneous tissue exposing soft
carcinoma. tissue or bone
• It is also observed in long standing • Grade 3: abscess formation
ulcer with underlying fibrosis. underneath/ osteomyelitis
• It is absent/ less in poorly • Grade 4: Gangrene of part of the
differentiated carcinoma and tissue/ limb foot
malignant melanoma. • Grade 5: Gangrene of entire one
• Less indurated carcinoma is more area/foot
aggressive.
• Specific types of induration are CLASSIFICATION OF
observed in venous diseases and ULCERS
chronic deep venous thrombosis. • Uses two types of classification
• Brawny induration is a feature of an systems:
abscess. ➢ Clinical
• Induration is felt at edge, base and ➢ Pathological
surrounding area of an ulcer.
• Induration at surrounding areas CLINICAL
signifies the extent of disease • Ulcers classified based on:
(tumor) ➢ Location:
• Outer most part of the induration is o Arterial ulcer- lateral
taken as the point from where o Venous- dorsum/ medial
clearance of wide excision is part of foot
planned. ➢ Floor of ulcer: granulation
➢ Discharge:
o Serous (granulation)
o Blood (malignant)
o Purulent (spreading)

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SURGERY MK
➢ Edges o Arterial ulcer:
o Sloping: healing Atherosclerosis, TAO
o Punched out: syphilis and o Venous ulcer, Gravitational
trophic ulcers/pressure ulcer, Post-phlebitic ulcer
ulcers o Trophic/ pressure ulcer
o Undermined- TB o Infective ulcer: pyogenic
o Rolled out/ elevated- o Tropical ulcers: it occurs in
malignant tropical countries. It is
o Raised and beaded- rodent callous type of ulcer e.g.
(malignant) Vincent’s ulcer.
➢ Surrounding area o Ulcers due to chilblains and
o Thick and pigmented skin frostbite (cryopathic ulcers)
(varicose ulcer) o Bazin’s ulcer
o Thick and dark (arterial o Martonell’s hypertensive
ulcer) ulcer
o Diabetic ulcer
PATHOLOGICAL
o Ulcers due to leukemia,
• Ulcers can either be:
polycythemia, jaundice,
➢ Specific ulcers which are
collagen diseases,
associated with a cause
lymphedema.
o Tuberculous ulcer,
o Cortisol ulcers are due to
syphilitic ulcer (punched
long time application of
out, deep. With “wash
cortisol (Steroid) creams to
leather” slough in the floor
certain skin diseases. These
and with indurated base).
ulcers last for long time and
Actinomycosis, meleney’s
require excision and skin
ulcer.
grafting.
➢ Malignant ulcers:
carcinomatous ulcer (marjolin’s GRANULATION TISSUE
ulcer), rodent ulcer, melanotic HEALTHY GRANULATION
ulcer TISSUE
➢ Non-specific ulcers not • Occurs in a healing ulcer.
associated with a specific cause
• It has a slopping edge.
o Traumatic ulcer (common):
• It bleeds on touch and has a serous
may be mechanical,
discharge.
physical, chemical

122
SURGERY MK
• 5Ps of granulation: • The cause of the ulcer should be
➢ Pink found- diabetes/ venous/ arterial/
➢ Punctate hemorrhage (bleeds on infective
touch)
LOCAL EXAMINTION OF AN
➢ Pulsates
ULCER
➢ Painless
INSPECTION
➢ Pin head granulation
• Site of ulcer
• Skin grafting takes up well with
➢ Arterial ulcer: digits
healthy granulation tissue.
o Arterial ulcers are usually
• Streptococci growth in culture
found on the lateral aspect
should be <105/ gram of tissue
of the foot.
before skin grafting.
➢ Venous ulcer: malleoli (medial
UNHEALTHY GRANULATION malleolus- commonly)
TISSUE o Venous ulcers are usually
• It is pale with purulent discharge. found on the medial aspect
• Its floor is covered with slough, its of the foot.
edge is inflamed and edematous. ➢ Trophic ulcer: heel/pressure
• It is a spreading ulcer. points.
• Unhealthy, pale, flat granulation • Size of ulcer
tissue is seen in chronic non- • Shape of ulcer
healing (callous ulcer). • Depth of the ulcer
• Number
EXAMINATION AND • Margin whether regular/irregular/
ASSESMENT OF AN well-defined/ ill-defined
ULCER • Edge of the ulcer
HISTORY ➢ Indurated (fibrosis): squamous
• Mode of onset cell carcinoma and chronic
• Duration ulcers
• Pain- its time of onset, progress, • Floor of the ulcer- floor is what one
severity sees. It rests on the base (base is not
seen; it is only felt).
• Discharge from ulcer
➢ Red color in floor- healing ulcer
• History suggestive of associated
➢ Slough with pale/purulent
disease/ treatment history
discharge- non-healing ulcer or
tubercular

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SURGERY MK
➢ Wash leather slough-syphilitic • Depth of ulcer- trophic ulcer is deep
ulcer with bone as its base- often it is
➢ Proliferative and nodular floor- measured gently in mm.
squamous cell carcinoma • Bleeding on palpation and
➢ Pigmented- melanoma, touching.
Pigmented basal cell carcinoma • Palpation for deeper structures and
• Discharge from ulcer bed its relation to ulcer.
➢ Serous: in healing ulcer • Surrounding skin and tibia/
➢ Purulent: in infected ulcer calcaneum/ other related bones for
o Staphylococci: yellowish thickening.
and creamy • Examination of adjacent joint for
o Streptococci: bloody and mobility.
opalescent • Examination of regional lymph
o Pseudomonas: Greenish nodes is essential- tenderness
color due to pseudocyanin (Acute infection), mobility,
➢ Bloody: malignant ulcer, consistency may be hard
healing ulcer from healthy (Carcinoma metastasis)/ firm/soft
granulation tissue and non-tender (inflammatory),
➢ Seropurulent fixity (malignancy), ulceration or
➢ Seroanguinous: serous and fungation (malignancy), sinus
blood (nonspecific, tuberculosis or
➢ Serous with Sulphur granules: carcinoma)
actinomycosis • Palpation also of arterial pulse,
• Surrounding area to be examined peripherally in relation to ulcer.
for inflammation, edema, eczema,
scarring, pigmentation AUSCULATION
• Inspection of the entire part/ limb • Auscultation of peripheral arteries
for any bruits.
PALPATION
• Tenderness over edge, base and SPECIFIC SYSTEM
surrounding area. • Examination for varicose veins in
• Warmness over surrounding area. standing position.
• Edge palpation for induration • Examination of the abdomen for
• Palpation of base for splenomegaly (sickle cell disease),
induration/fixity hepatomegaly.
➢ Fixed: malignant • Examination of spine (gibbus,
➢ Non-fixed: non malignant paraspinal spasm, movements) and

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SURGERY MK
neurological system like sensation 5. Control infection (antibiotics) and
and muscle power. give rest to the part
6. Care of ulcer by debridement, ulcer
INVESTIGATIONS FOR cleaning and dressing
AN ULCER ➢ Ulcer cleaning
• Study of discharge: culture and o Done using dilute povidone
sensitivity, AFB study, cytology. iodine and normal saline
➢ For skin graft swabs and culture (ideal)
must yield staphylococci of o It should be done daily or 2
<105/ gram times a day depending on
• Edge biopsy: biopsy taken from the the severity.
edge because contains multiplying ➢ Debridement of ulcer
cells. Usually 2 biopsies are taken. o It is removal of devitalized
Biopsy taken from the center may tissue.
be inadequate because of central o Small ulcers are debrided in
necrosis. ward.
• FNAC of the lymph node (fine o Large ulcers are debrided in
needle aspiration cytology) operation theatre under
• X-ray of the part to look for general anesthesia
periostitis/ osteomyelitis o All dead, devitalized,
• CXR, Mantoux test is suspected in necrotic tissue are removed.
cases of a tuberculous ulcer. o Slough should be separated
• Full blood count adequately before
debridement.
• NOTE: ulcer will not granulate if
o Often devitalized tissue
Hb is less than 10g/dl and serum
separates on its own by
albumin is <3gm%
autolysis.
MANAGEMENT OF AN o Enzymes like collagenase
ULCER are used for debridement.
o Hydrotherapy and dressings
1. Investigate and treat underlying
are mechanical non-
cause.
selective method of
2. Correct the deficiencies like
debridement.
anemia, protein and vitamin
o Note: debridement can be
deficiencies.
surgical, mechanical,
3. Transfuse blood if required.
autolytic or enzymatic.
4. Control pain (analgesics)

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SURGERY MK
➢ Dressing of an ulcer aims to: • Causes of formation of chronic
o Keep the ulcer moist ulcers in skin: recurrent infection,
o Keep the surrounding skin trauma, absence of rest, poor blood
dry supply, hypoxia, edema of area,
o Reduce pain loss of sensation, malignancy,
o Soothe the tissue specific causes like tuberculosis,
o Protect the wound fibrosis, periostitis or osteomyelitis
o Absorb any discharge of the underlying bone.
➢ Ulcer dressing:
o Cotton dressing- cheap but
traumatic
o Paraffin dressing
o Polyurethane dressing used
in clean wounds.
o Alginates (Seaweed)
dressing used when there
are heavy exudates
o Type 1 collagen dressing
cause hemostasis,
proliferation of fibroblast
and improves blood supply.
o Foam dressing are highly
absorbent, decrease the
wound maceration and
reduce the frequency of
dressing- hydrophilic foam.
o Hydrocolloid dressing help
in separation of slough and
autolysis of dead tissues.
o Transparent film dressing
are waterproof permit
oxygen and water vapor
across and prevent
contamination.
o Hydrogel dressings used to
clean wounds.

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SURGERY MK
DIABETIC FOOT AND • Diabetic neuropathy: due to
sensory neuropathy minor injuries
DIABETIC GANGRENE
are not noticed and so infection
• A diabetic foot is a foot that
occurs. Due to motor neuropathy,
exhibits any pathology that results
dysfunction of muscles, arches of
directly from diabetes mellitus or
foot and joints occur. And loss of
any long term (or chronic)
reflexes of foot occurs causing
complication of diabetic mellitus.
more prone for trauma and abscess.
• Presence of several characteristic Due to autonomic neuropathy skin
diabetic foot pathologies such as will be dry, causing defective skin
infection, diabetic foot ulcer and barrier and so more prone to
neuropathic osteoarthropathy is infection.
called diabetic foot syndrome.
CLINICAL FEATURES
PATHOGENESIS OF DIABETIC
• Pain in the foot
FOOT/GANGRENE
• Ulceration
• High glucose level in tissues is a
• Absence of sensation
good culture media for bacteria. So
• Absence of pulsations in the foot
infection is common.
(posterior tibial and dorsalis pedis
• Diabetic microangiopathy causes
arteries)
blockade of microcirculation
• Loss of joint movements
leading to hypoxia.
• Abscess formation
• Diabetic atherosclerosis: reduces
blood supply and causes gangrene. • Change in temperature and color
Thrombosis can be precipitated by when gangrene sets in
infection causing infective • Patient may succumb to
gangrene. Blockage occurs at ketoacidosis, septicemia or
plantar, tibial and dorsalis pedis myocardial infarction.
vessels. MEGGITT’S CLASSIFCATION
• Increased glycosylated OF DIABETIC FOOT
hemoglobin: causes defective • Grade 0: foot symptoms like pain,
oxygen dissociation leading to only
more hypoxia. At tissue level there • Grade 1: Superficial ulcers
will be increased glycosylated • Grade 2: deep ulcers
tissue proteins, which prevent • Grade 3: ulcers with bone
proper oxygen utilization and so involvement
aggravates hypoxia. • Grade 4: forefoot gangrene

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• Grade 5: full foot gangrene ➢ Antibiotics- decided by pus C/S
➢ Regular dressing
INVESTIGATIONS
➢ Drugs: vasodilators,
• Blood investigations:
pentoxiphylline, dipyridamole,
➢ Blood sugar and ketones
low dose aspirin.
➢ Glycosylated hemoglobin
➢ Diabetes is controlled by insulin
➢ Blood urea and serum creatinine
only.
• Urine ketones ➢ Diet control, control obesity.
• Imaging: ➢ Surgical debridement of wound
➢ X-ray of part to look for ➢ Amputations of gangrenous
osteomyelitis. area. Level of amputation has to
➢ Doppler study of lower limb to be decided by skin changes and
assess arterial patency. temperature changes or Doppler
➢ Angiogram to look for proximal study.
blockage • Care of feet in diabetes:
➢ Ultrasound of abdomen to see ➢ Any injury has to be avoided.
the status of abdominal aorta ➢ MCR foot wears must be used
• Pus for culture and sensitivity. (microcellular rubber).
TREATMENT ➢ Feet has to be kept clean and dry
• Foot can be saved only if there is especially the toes and clefts.
good blood supply: ➢ Hyperkeratosis has to be
avoided.

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BURNS

BURNS
• Burns are a type of coagulative necrosis causing injury to the skin or other tissues
as a result of flames, friction, radiation, electrical, chemical or heat.
• Recall that the skin consists of:
➢ The epidermis: contains 5 histological layers (Stratum Basale, Stratum
Spinosum, Stratum Granulosum, Stratum Lucidum, and Stratum Corneum)
o The stratum Lucidum is only found in thick skin (palm of hands and soles
of feet) and not in thin skin.
o The stratum Basale and Spinosum are referred collectively as the
Malpighian layer.
➢ The dermis: it is divided into the upper papillary dermis and lower reticular
dermis. It contains blood vessels, nerves and connective tissue.
➢ Subcutaneous tissue (hypodermis): contains adipose.
• The majority of burns in children are scalds caused by accidents with kettles,
pans, hot drinks and bath water.
• Among adolescents patients, the burns are usually caused by young males
experimenting with matches and flammable liquids.
• In adults scalds are not uncommon but are less frequent than flame burns. Most
electrical and chemical injuries occur in adults.

ETIOLOGY AND MECHANISM OF INJURY

• Heat (Thermal injury)
➢ Scald- spillage of hot liquids. Common in children (70%), child abuse
especially if the pattern of the burn does not fit the description of the event
given by the parents e.g. burns of both buttocks typically produced by holding
a small child by arms & legs and dunking them into boiling water. They also
occur in adults and tend to be superficial to dermal burns.
➢ Flame burns: due to fire. Common in adults (50%) and associated with
inhalational injury and other concomitant trauma. They tend to be dermal or
full thickness burns.
➢ Contact burns- contact with hot metals/objects/materials. Commonly seen in
epileptics, alcoholics and drug abusers as well as in the elderly due to loss of
consciousness. They tend to be dermal or full thickness burns.
➢ Flash burns due to exposure of natural gas, alcohol, combustible liquids.

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• Cold (frost bite)
• Sun burns: these are usually superficial burns (they are very painful)
• Electrical injury: these are always deeper and worse than they appear. Massive
debridements or amputations may be required.
➢ Classification of electrical burns:
o Low voltage (<1000 V): deep contact burns at entry and exit sites.
o True high voltage (>1000 V): current goes through body. Extensive soft
tissue and bone necrosis.
o Flash high voltage (> 1000V): current does not pass through the body.
‘Flash’ burn from heat generated by current arc from high-tension source.
Exposed parts of body affected (Face, hands).
➢ Electrical burns may be associated with:
o Myoglobinemia-myoglobinuria and renal failure: give plenty of fluids and
osmotic diuretics like mannitol and alkalinize the urine
o Orthopedic injuries secondary to massive muscle contractions: posterior
dislocation of the shoulder, compression fractures of vertebral bodies and
o Late development of cataracts and demyelination syndromes.
➢ Electrical burns require ECG monitoring.
• Chemicals (acid/alkali): require massive irrigation to remove offending agent.
Alkaline burns (Liquid Plumr, Drano) are worse than acid burns (battery acid).
Alkaline burns are worse because they cause liquefactive necrosis. Irrigation
must begin as soon as possible at the site where the injury occurred (tap water,
shower). Do not “play chemist” and attempt to neutralize the agent. These tend
to be deep burns.
• Ionizing radiation burns and Friction burns.
• Respiratory burns (inhalation injuries): Occur with flame burns in an enclosed
space (e.g. burning building, car, plane).
➢ They are chemical injuries caused by smoke inhalation.
➢ Burns around the mouth or soot inside the throat, burnt/loss of nasal hair,
change in voice and stridor are suggestive clues.
➢ Diagnosis is confirmed with fiberoptic bronchoscopy however the key issue
is whether respiratory support (A respirator) is needed or not, and blood gases
are best to make that determination.
➢ Intubation should be done if there is any concern about adequacy of the
airway. Monitor carboxyhemoglobin and give 100% oxygen for 24 hours to
shorten its half-life if elevated.

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PATHOPHYSIOLOGY
• Burns cause damage in a number of different ways, but by far the most common
organ affected is the skin.
• Burns result in local (Jackson Zones of a burn) and systemic response (affecting
the cardiovascular, respiratory, metabolic, gastrointestinal and immunological
system)
LOCAL RESPONSE
ZONES OF A BURN (JACKSON)
• 3 Zones of a burn were described by Jackson
in 1947. These include:
➢ Zone of coagulation: this is the point of
maximum damage. There is irreversible
tissue loss due to coagulation of constituent
protein.
➢ Zone of stasis: this is characterized by
decreased tissue perfusion. The tissue in
Figure 48: Jackson's burn zones
this zone is potentially salvageable. Additional (Image from Clinical Surgery 2nd Ed)
insults, such as prolonged hypotension, infection or
edema can convert this zone into an area of complete tissue loss.
➢ Zone of hyperemia: tissue perfusion is increased. This zone will invariably
recover.
• In a burn wound, these zones are 3-dimensional, loss of tissue in the zone of stasis
will lead to the burn deepening.
SYSTEMIC RESPONSE
• The release of cytokines and other inflammatory mediators at the site of injury
has a systemic effect once the burn reaches 30%.
➢ Activation and release of various complement factors, histamine and
prostaglandins results in myocardial dysfunction, edema of tissues, reduced
immunoglobulin synthesis.
➢ Catecholamine levels are raised drastically in patients with burns. There will
be lipolysis, proteolysis, increased release of glutamine and alanine from
skeletal muscles.
➢ Urea production is increased due to more proteolysis.

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RESPIRATORY CHANGES
• Hot gasses may physically burn the nose, mouth, tongue, palate and larynx. Once
injured these linings start to swell. After a few hours they may start to interfere
with the larynx and may completely block the airway if action is not taken to
secure the airway.
• Inhaled hot gases, steam, smoke particle, and poisons have different effects on
the respiratory system:
➢ Inhaled hot gases can cause supraglottic airway burns and laryngeal edema
➢ Inhaled steam can cause subglottic burns and loss of respiratory epithelium
➢ Inhaled smoke particles can cause chemical alveolitis and respiratory failure
➢ Inhaled poisons such as carbon monoxide can cause metabolic poisoning
➢ Full thickness burns to the chest can cause mechanical blockage to rib
movement.
• Injury to the airways below the larynx is rare because exchange mechanisms in
the supraglottic airway are usually able to safely absorb the heat from the hot air.
However, steam has a large latent heat of evaporation can cause thermal damage
to the lower airway. In such injuries the respiratory epithelium rapidly swells and
detaches from the bronchial tree. This creates casts which can block the main
upper airway.
• There are many poisonous gases that can be given off in a fire with carbon
monoxide being the most common.
• Recall:
➢ Carbon monoxide is a production of incomplete combustion that is often
produced by fires in enclosed spaces.
➢ CO is the usual cause of a person being found with altered consciousness at
the scene of a fire.
➢ CO binds to hemoglobin with a higher affinity than oxygen (240 times) and
therefore blocks the transport of oxygen.
➢ When CO binds hemoglobin it forms a stable compound carboxyhemoglobin.
Carboxyhemoglobin in the bloodstream can be measured. Concentrations
above 10% are dangerous and need treatment with pure oxygen for more than
24 hours. Death occurs with concentrations around 60%.
• Another metabolic toxin produced in house fires is hydrogen cyanide which
causes a metabolic acidosis by interfering with mitochondrial respiration.
• Inhalational injury is caused by the minute particles within thick smoke, which
because of their small size are not filtered by the upper airway and are carried

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down to the lung parenchyma. They stick to the moist lining causing an intense
reaction in the alveoli. This chemical pneumonitis causes edema within the
alveolar sacs and decreasing exchange over the ensuing 24 hours and often gives
rise to bacterial pneumonia. Its presence has a very significant effect on the
mortality of any burn patient.
• Note also that burned skin is very thick and stiff and this can physically stop the
ribs moving if there is a large full-thickness burn across the chest.

• Pulmonary changes are due to:

➢ Massive edema due to altered pressure gradient because of the injury to
basement membrane and systemic inflammatory response syndrome (SIRS).
➢ Bronchoconstriction which may be seen secondary to inflammatory
mediators.
➢ Air way edema causing adult respiratory distress syndrome (ARDS)
o Note: Pulmonary edema in burns can be due to burn injury, fluid
overload, inhalation injury
➢ Inhaled hot gases leading to supraglottic airway burns and laryngeal edema
➢ Inhaled steam causing subglottic burns and loss of respiratory epithelium
➢ Inhaled smoke particles causing chemical alveolitis (and superadded
bacterial pneumonia) and respiratory failure
➢ Inhaled poisons such as carbon monoxide causing metabolic poisoning
➢ Full thickness burns to the chest can cause mechanical blockage to rib
movement.

CARDIOVASCULAR RESPONSE
• Cardiovascular changes occur because burned skin activates various
inflammatory processes.
• The release of neuropeptides and activation of complement are initiated by the
stimulation of pain fibers and alteration of proteins by heat.
• Activation of Hageman factor initiates a number of protease-driven cascades
altering the arachidonic acid, thrombin and Kallikrein pathways.
• Complement causes degranulation of mast cells and coats the proteins altered by
burn. This attracts neutrophils which also degranulate and release free radicals
and proteases in large amounts causing more damage to the tissue.

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• Additionally, Mast cells also release primary cytokines such as tumor necrosis
factor alpha (TNF-alpha). These act as chemotactic agents to inflammatory cells
and cause release of many secondary cytokine.
• Inflammatory factors:
➢ Alter permeability of blood vessels causing intravascular fluid escape.
➢ Increase permeability such that large proteins can also escape with ease. The
damaged collagen and extravasated proteins increase the oncotic pressure
within the burned tissue further increasing the flow of water from the
intravascular to the extravascular space.
➢ Vasoconstriction raising capillary hydrostatic pressure leading into cellular
aggregation.
• Note: There is a net flow of water, solutes and proteins from the intravascular to
the extravascular space. This flow occurs over the first 36 hours after the injury
but does not include red blood cells. Blockage of lymphatics causes poor
clearance of fluid and proteins from interstitial spaces.
• In small burns, the reaction is small and localized, as the size approaches 10-15%
of total body surface area (TBSA), the loss of intravascular fluid can cause a level
of circulatory shock. Increase to 25% of TBSA causes an inflammatory reaction
that culminates in fluid loss in vessels away from the burn injury. This is why it
is important to measure the TBSA involved in any burn as it dictates the size of
inflammatory reaction and the amount of fluid needed to control shock.
• In full-thickness burns, the collagen fibers are coagulated. The normal elasticity
of skin is lost and therefore a circumferential full-thickness burn to a limb acts as
a tourniquet as the limb swells. If untreated will progress to limb-threatening
ischemia.

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SURGERY MK
• Cardiovascular changes:
➢ Increase in capillary permeability, leading to loss of protein and fluids
from the intravascular into the interstitial compartment (hypovolemia).
➢ Vasoconstriction raising capillary hydrostatic pressure leading into
cellular aggregation.
➢ Blockage of lymphatics causes poor clearance of fluid and proteins from
interstitial spaces.
➢ Release of hormones like catecholamines, vasopressin, angiotensin.
➢ Peripheral and splanchnic vasoconstriction
➢ Decreased myocardial contractility possibly due to tumor necrosis
factor-alpha.
➢ Limb-threatening ischemia in circumferential full thickness burns
affecting the limbs
• These changes coupled with fluid loss from the burn wound result in
systemic hypotension and end-organ damage.

GASTROINTESTINAL RESPONSE
• The inflammatory stimulus and shock can cause microvascular damage and
ischemia to the gut mucosa. This reduces gut motility and can prevent absorption
of food.
• Failure of enteral feeding in large burns is a life-threatening complication.
• This process also increases the translocation of gut bacteria, which can become
an important source of infection in large burns.
• Gut mucosal swelling, gastric stasis and peritoneal edema can also cause
abdominal compartment syndrome which splints the diaphragm and increases the
airway pressures needed for respiration.

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• Gastrointestinal changes:
➢ Microvascular and ischemia to the gut mucosa
causing GIT mucosa ulceration (Curling’s ulcer)
➢ Reduced gut motility and reduced absorption of food
(failure to enteral feed)
➢ Increased translocation of gut bacteria
➢ Gut mucosal swelling, gastric stasis and peritoneal
edema causing abdominal compartment syndrome
which splints the diaphragm increasing the airway
pressures needed for respiration.
➢ Acute gastric dilation (in 2-4 days)
➢ Paralytic ileus
➢ Cholestasis and hepatic damage
➢ Acute acalculous cholecystitis, and acute pancreatitis

RENAL AND METABOLIC RESPONSE

• Due to hypovolemia and shock there is release of ADH from posterior pituitary
to cause maximum water reabsorption and release of aldosterone from adrenals
to cause maximum sodium reabsorption.
• Pre-renal failure (due to hypovolemia and acute tubular necrosis).
• Toxins released from the wound along with sepsis can cause acute tubular
necrosis.
• Myoglobin released from muscles (in case of electric injury or often from eschar)
is most injurious to kidneys. (acute kidney injury)
• Metabolic changes:
➢ Hypermetabolic rate (due to release of catecholamines, glucagon)
➢ Negative nitrogen balance i.e. urinary nitrogen losses are greater than oral
nitrogen intake.
➢ Electrolyte imbalance
o Hyponatremia
o Hyperkalemia
➢ Deficiencies of vitamins and essential elements
➢ Metabolic acidosis due to hypoxia and lactic acid

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• Renal changes:
➢ Pre-renal failure (due to hypovolemia and acute
tubular necrosis)
➢ Acute kidney injury (due to myoglobin)
➢ Release of ADH for water reabsorption
➢ Release of aldosterone for sodium retention.
• Metabolic changes:
➢ Hypermetabolic rate
➢ Negative nitrogen balance
➢ Electrolyte imbalance
o Hyponatremia
o Hyperkalemia
➢ Deficiency of vitamins and essential elements
➢ Metabolic acidosis due to hypoxia and lactic acid

IMMUNOLOGICAL RESPONSE
• Cell mediated immunity is significantly reduced in large burns, leaving an
individual more susceptible to bacterial and fungal infection.
➢ There is a non-specific downregulation of the immune response, affecting
both cell-mediated and humoral pathways.
➢ Loss of immunity, loss of proteins and immunoglobulins, loss of barrier
causes sepsis. Opportunistic infection is also common.
➢ Associated conditions such as DM, HIV, infections, old age, respiratory
diseases worsen the sepsis in burn injury.
• Potential sources of infection include burn wound, lungs (if injured), from central
venous lines, tracheostomies or urinary catheters present.
• Infection commonly due to
➢ Streptococci (Beta hemolytic- most common)
➢ Pseudomonas
➢ Klebsiella
➢ Staphylococci
➢ Other gram-negative organisms
➢ Candida albicans
• Systemic infection like pneumonia, bacteria, septicemia can occur. Sepsis is
identified by fever, lethargy, leukocytosis and thrombocytopenia.

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• Immunological response:
➢ There is a non-specific downregulation of the immune response,
affecting both cell-mediated and humoral pathways.
➢ Loss of immunity, loss of proteins and immunoglobulins, loss of
barrier causes sepsis. Opportunistic infection is also common.
➢ Associated conditions such as DM, HIV, infections, old age,
respiratory diseases worsen the sepsis in burn injury.
• Infection commonly due to
➢ Streptococci (Beta hemolytic- most common)
➢ Pseudomonas
➢ Klebsiella
➢ Staphylococci
➢ Other gram-negative organisms
➢ Candida albicans
• Systemic infection like pneumonia, bacteria, septicemia can occur.

OTHER RESPONSES
• CNS:
➢ Altered mental state (electrolyte imbalance/ shock)
➢ Comatose

CLINICAL FEATURES
• History of burn.
• Pain, burning, anxious status, tachycardia, tachypnea, fluid loss.
• In severe degrees features of shock. Tolerable temperature of human skin is 40 OC
for brief period.

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CLASSIFICATION OF BURNS
• Burns are classified according to:
➢ Thickness of skin involved.
➢ Percentage body surface area involved.
➢ Severity
THICKNESS OF SKIN INVOLVED
• Depending on the thickness of skin involved burns can be classified as:
➢ First degree burns- Also known as superficial burns
➢ Second degree burns include:
o Superficial partial thickness burns
o Deep partial thickness burns
➢ Third degree also known as full thickness burn
➢ Fourth degree burns
FIRST DEGREE (SUPERFICIAL BURNS)
• First degree: Affects only the epidermis (Also known as superficial
thickness burns).
• Here the epidermis looks red and painful, no blisters, heals rapidly in 5-
7 days by epithelialization without scarring. Skin peels.
• Pin-prick test is positive (severe pain to pin prick).
• Example: non-blistering sun burns.
SECOND DEGREE Figure 49: First
• These are divided into: degree/ Superficial
thickness burns
➢ Superficial partial thickness burns (Superficial dermal burns): (Courtesy of SRB's
affecting the epidermis and the papillary dermis Manual of Surgery 4th
➢ Deep partial thickness burns (deep dermal burns): affecting the Ed).
epidermis, the upper dermis and the reticular dermis.
• The affected area is mottled, red, painful with blisters,
and heals by epithelialization in 14-21 days (2-3 weeks)
without scarring.
• Hallmark feature: Blistering.
• Superficial partial thickness (Superficial dermal): Figure 50: Second Degree burns
➢ Heals and causes pigmentation (superficial partial) with blistering
(Courtesy of SRB's Manual of Surgery
➢ They cause blisters. 4th Ed).
➢ Blanches with pressure.
➢ They tend to be pink below blister, moist and very painful.

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• Deep partial thickness (Deep dermal):
➢ They are yellow or white. Deep red below blister from vasodilation, or red
dots (vessels) on white background.
➢ Less blanching and may be blistering.
Blanching: ➢ They may be sensory changes
make white or ➢ They are also fairly dry and heal after 3-8 weeks.
by extracting ➢ Heal by combination of epithelialization, pigmentation, wound
color i.e. when contracture and scarring.
pressure is
THIRD DEGREE
applied to a
burn area it • Third degree (Full thickness burns): Affect the epidermis, dermis and
becomes pale. subcutaneous tissue.
• Affected area is charred, parchment like, painless
(negative pin prick sensation) and insensitive, with
thrombosis of superficial vessels.
• It requires grafting. Charred, denatured, insensitive, contracted
full thickness burn is called as eschar.
• These wounds must heal by re-epithelization from wound edge.
• The skin appears stiff and white/brown. There is no blanching. Figure 51: Third degree
With a leathery texture. burns with charred skin,
thrombosed veins and eschar
• They are painless. (Courtesy of SRB's Manual of
• Healing is prolonged (months) and incomplete. Surgery 4th Ed).

FOURTH DEGREE
• Involves the epidermis, dermis and underlying tissues- muscles,
bones.
➢ They are Black, charred with eschar
➢ They are dry and painless

Char: partially
burn so as to
Figure 52: Face burns in
blacken the an adult - severe third
surface. degree (Courtesy of SRB's
Manual of Surgery 4th Ed).

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 SURGERY MK
Table 1: Classification of burns according to depth/thickness involved

• Note: Circumferential burns of the extremities can lead to cutoff of the blood
supply as edema accumulates underneath eschar. In circumferential burns of the
chest, a similar mechanical problem may interfere with breathing. Escharotomies
(done at the bedside, with no need for anesthesia) will provide immediate relief.
• In reality most burns will be a mixture of different depths. The assessment of
depth is important for planning because the more superficial burns will tend to
heal spontaneously but deeper burns will need surgical intervention.
Feature Superficial Superficial partial Deep partial Full thickness
Appearance Red glistening wound Redness, with Paler (yellow, white), Dry, leathery,
that often blanches blanching and drier, less blanching hard wound
clear blisters and blistering
Bleeding (use Brisk bleeding on Brisk bleeding on Delayed bleeding on No bleeding
21-G needle) superficial prick superficial prick deeper prick
Sensation (use Pain Pain Pin can be felt but no No sensation
21-G needle pain

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SEVERITY
• Depending on the percentage of burns (See Table below):
➢ Mild (minor)
➢ Moderate
➢ Severe
MILD
• Partial thickness burns <10% in adults or <5% in children.
• Full thickness burns less than 2%.
• Can be treated on outpatient basis.
MODERATE
• Second degree (Partial thickness) of 10-20% burns in adults (5-10% in children).
• Third degree (Full thickness) between 2-5% burns.
• Note: burns should not involve eyes, ears, face, hand, feet, perineum.
SEVERE
• Second degree (Partial thickness) burns more than 20% in adults, in children
more than 10%.
• All third-degree burns (Full thickness) of 5% or more.
• Burns involving eyes, ears, feet, hands, perineum.
• All inhalation and electrical burns.
• Burns with fractures or major mechanical trauma.
Table 2: Classification of burns according to severity

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ASSESSMENT OF BURNS
• Note: when calculating the burn wound area,
erythema should not be included. Erythema
may take a few hours to fade so it is inevitable
that some overestimation will occur if the
burn is estimated acutely.
WALLACE’S RULE OF NINE (EARLY
ASSESSMENT)-ADULTS
• A percentage is assigned to each body part:
➢ Head and neck- 9%
➢ Arm-9% each arm
➢ Trunk- 36% (9 + 9 – front chest &
abdomen and 9+ 9- back chest and
abdomen)
➢ Leg- 18% (9% front, 9% back) Figure 53: Wallace rule of 9s
➢ Perineum- 1%
RULE OF 7’S-CHILDREN
• Percentages are as follows:
➢ Head and neck- 28%
➢ Arms- 7% each
➢ Trunk- 28% (14% front, 14% back)
➢ Lower limbs-14% (7% front, 7% back)
each
➢ Perineum- 2%
• This allows the emergency medical provider
to obtain a quick estimate of how much body
surface area is burned. For example, if an
adult patient’s entire back (18%) and entire
left leg (18%) are burned about 36% of the
patient’s body surface area is affected. Figure 54: Rule of 7s
• The body surface area assigned to each body
part refers to the entire body part. So, if half of a patient’s left leg were burned,
it would be assigned a body surface area value of 9% (half of the total surface
area of the leg). Thus, if a patient’s entire back (18%), but only half of their left
leg (9%) was burned, the amount of body surface area affected would be 27%.

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• Some studies have raised concerns about the rule of nines’ accuracy with obese
patients, noting that the proportional contribution of various major body
segments to the total body surface area changes with obesity.
• Note: Babies have bigger heads and smaller legs thus the “rule of 9s” for them
assigns two 9s to the head, and both legs share a total of three 9’s instead of four.
In determining what is third-degree we should remember that in babies those
areas look deep bright red (rather than the leathery dry, gray appearance in adults)

Figure 55: Wallace Rule of 9s in babies

RULE OF THE PALM

• The patient’s entire palm area (i.e. not the fingers) is 1%. (0.8% in males and
0.6% in females of the total body surface area)
• The rule of palms can be used to estimate relatively small burns (<15%) or very
large burns (>85% when unburnt skin is counted). For large burns it is inaccurate.
• A clean piece of paper is cut to the size of hand and through that the percentage
of burns is assessed.
LUND AND BROWDER CHART
• This is a better method for assessing the burn wounds. Here each part of the body
is individually assessed for involvement of burns.

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Figure 56: Lund and Browder Chart

• Note: if used correctly, this is the most accurate method of assessing burn area.

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• Note: Unlike the Wallace rule of nines, the Lund and Browder chart takes into
consideration the age of the person with decreasing percentage body surface area
for head and increasing percentage body surface area for the legs as the child
ages, making it more useful in pediatric burns.
• NOTE: 44OC temperature takes 6 hours to cause deep burns. 65 OC takes 45-60
seconds to cause deep full thickness burn.
• When you are on call, and a patient comes with burns, the 3 things you should
tell the consultant on the phone about the patient:
➢ The % estimate of the burns: this helps with management of the patient
(especially on admission criteria).
➢ Cause of the burn- this helps tell the depth of the burns
o Domestic burns are usually superficial.
o Industrial burns are usually deep.
➢ Time of burn: this will help with fluid replacement therapy.

DIFFERENTIAL DIAGNOSIS
• Necrotizing fasciitis

PATIENT ASSESSMENT
HISTORY
• Time and mechanism of the injury:
➢ Type of burn i.e. scald, flame, electrical, chemical
o Scald injuries
- What was the liquid?
- If tea/coffee, was there milk in it?
- Was there a solute in the liquid? This will raise the boiling
temperature and result in a worse injury.
o Electrocution injuries
- What voltage?
- Was there a flash/arcing?
- Contact time
o Chemical injuries: what chemical?
➢ How was the person put out? How long were they alight for?
➢ What first aid was carried out? If cooling was performed, what with and for
how long?
• Likelihood of concomitant injuries (i.e. fall from height, road traffic accident,
explosion).

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• Likelihood of inhalational injury: did the burn occur in an enclosed space?
• Any suspicion of non-accidental injury?
INVESTIGATIONS
• Blood investigations:
➢ Full blood count: to pick up any cytopenias
o Hematocrit
o Hemoglobin
o Platelet count
o Differential count
➢ Group and save/cross-match
➢ Urea, Electrolytes and creatinine: to assess renal function and electrolyte
imbalances
➢ Liver function tests
• Pus swab
• For electrical burns:
➢ 12 lead ECG
➢ Cardiac enzymes (high-tension injury)
• For inhalation burns: chest X-ray and Arterial blood gases

MANAGEMENT
FIRST AID
• Stop the burning process and keep the patient away from the burning area.
• Cool the area with tap water by continuous irrigation for 20 minutes (not cold
water as it can cause hypothermia).
• Do the ABCs.
DEFINITIVE TREATMENT
INITIAL
• Admit the patient
➢ Admission criteria:
o Any moderate and severe burns.
o Airway burns of any type. Inhalational injury
o Burns in extremes of age.
o All electrical/deep chemical burns.
o All burns affecting joints, face, perineum and all joints with fractures or
multiple injuries.

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o Burns likely to require fluid resuscitation and surgery.
o Patients whose psychiatric or social background
o Suspicion of non-accidental injury
• Maintain airway, breathing, circulation. (ABCs)
➢ Tracheostomy/ endotracheal intubation tube may be required in impending
respiratory failure or upper airway block. The airway should be secure until
the swelling has subsided which is usually after 48 hours.
o Symptoms of laryngeal edema: voice change, stridor, anxiety and
respiratory difficulty are very late symptoms. Intubation at this point is
often difficult or impossible owing to swelling, so acute
cricothyroidotomy equipment must be at hand when intubating patients
with a delayed diagnosis of airway burn.
o The time frame from burn to airway occlusion is usually 4 and 24 hours.
➢ Treat carbon monoxide poisoning with high inspired 100% oxygen for 24
hours.
• Catheterize Patient- monitor urine output (Normal is 0.5-1ml/kg/hr in adults and
1ml/kg/hr in children)
• Assess the percentage, degree and type of burn.
• Keep the patient in a clean warm and isolated environment.
• Sedation and proper analgesia.
• Labs:
➢ Culture of the discharge
➢ FBC at regular intervals
• Fluid resuscitation (discussed later)
• Monitoring the patient vitals hourly:
➢ Pulse
➢ Blood pressure
➢ Respiratory rate
➢ Blood gasses: PO2, PCO2
• Monitor:
➢ Electrolyte analysis
➢ Blood urea
• Give Nasal oxygen
• Patient should be in burns unit (ideally air conditioned) with barrier nursing,
sterile clothes, bed sheets with all aseptic methods.

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INTERMEDIATE
• Daily wound cleaning:
• Principles of dressing for burns:
➢ Full-thickness and deep dermal burns need antibacterial dressings to delay
colonization prior to surgery
➢ Superficial burns will heal and need simple dressings
➢ An optimal healing environment can make a difference to outcome in
borderline depth burns.
• Methods for wound care include:
➢ Open methods:
o Application of silver sulfadiazine (Flamazine cream) without any
dressing, used commonly in burns of face, head and neck.
o For patients allergic to Sulphur drugs use Povidone cream or
Chloherxidine cream
➢ Closed methods:
o Dressings done to soothe and protect the wound, to reduce pain and act as
an absorbent.
o Done for up to 10 days
➢ Mixed: clean and apply wet soaks
• Sloughectomy/ Escharotomy if indicated should be performed.
LONG TERM
• Monitoring:
➢ Mental status
➢ Heart rate- rapid rate may also indicate infection or severe dehydration
➢ Pulse rate
➢ Edema
➢ Temperature- spikes may indicate infection
➢ Fluid replacement
➢ Urine output (0.5-1ml/kg/hr for adults and 1ml/kg/hr for children)
• Check for proper wound healing: healthy granulation tissue (5Ps of granulation
tissue- Pink, Punctate hemorrhages, Pulsating, Painless, Pinhead granulation)
• Nutritional status:
➢ Check weight and Skin fold thickness
➢ High protein diet, total parenteral nutrition

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• Drugs:
➢ Tetanus toxoid should be given. (0.5mls IM-single dose)
➢ IV ranitidine 50 mg TDS.
➢ Antibiotics: penicillins, aminoglycosides, cephalosporins, metronidazole.
➢ Painkillers: IV morphine
FLUID RESUSCITATION
• Fluid needs in the first 48 hours after burn can be estimated by calculations that
take into account the extent of the burn and provide either an estimated total
amount needed or more simply an appropriate initial rate of infusion.
• For children, any burn which is 10% (15% adults) or above is severe and fluid
has to be given IV otherwise give fluids orally in each case.
• There are 2 regimes of fluid:
➢ Fluid replacement: this is given to replace the loss due to burn. Most of the
fluid leaves the circulation and is in the interstitial space.
➢ Maintenance fluid: this is the daily requirement due to insensible losses
through sweat, breathe etc.
• Fluid resuscitation:
➢ In children with burns over 10% TBSA and adults with burns over 15%
TBSA, consider the need for intravenous fluid resuscitation
➢ If oral fluids are to be used, salt must be added.
➢ Fluids needed can be calculated from a standard formula
➢ The key is to monitor urine output
FLUID AND COLLOID REPLACEMENT
• Formulas to calculate the fluid replacement:
➢ Parkland regime (Baxter) this is commonly used (for Expected weight for children:
crystalloids)
For infants (<12 months) =
𝑉 = 4𝑚𝑙 × 𝑚𝑎𝑠𝑠 (𝑘𝑔) × %𝑏𝑢𝑟𝑛 𝐴𝑔𝑒 𝑖𝑛 𝑚𝑜𝑛𝑡ℎ𝑠+9
2
o The parkland formula is used to determine the
amount of replacement fluid required for the first 24 For children 1-5= 2 x (age in
hours of a burn patient. years +5)
o Maximum percentage considered is 50%. For children 5-14= 4 x age in
o Half the volume is given in first 8 hours and the rest years
given in 16 hours.
o When considering time use “time the patient was burned” not time of
admission.

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o Fluid of choice is Ringer’s lactate.
o An additional 2, 000 ml of 5% dextrose in water (D5W) are usually added
on the first day for the fact that the patient is typically NPO, with a
nasogastric (NG) tube in place. (Colloids should not be given on day 1 as
they would leak out into the edema fluid).
o On day two, half of what was given on day 1 should be given, it may
include colloids if so desired though this has some controversies.
o By day 3 there should be no need for further fluid infusion and a brisk
diuresis should be expected.
o The actual amount of fluid infused is eventually provided by “fine-tuning”
based on the patient’s response, aiming for a urine output of 1-2ml/kg/hr.
➢ Muir and Burclay formula (used for colloids)
% 𝐵𝑢𝑟𝑛𝑠 × 𝑏𝑜𝑑𝑦 𝑤𝑒𝑖𝑔ℎ𝑡 𝑖𝑛 𝐾𝑔
= 1 𝑟𝑎𝑡𝑖𝑜𝑛
2
o 3 Rations given in first 12 hours (give 4 hourly)
o 2 rations in second 12 hours (give 6 hourly)
o 1 ration in third 12 hours
• Fluids used are normal saline, ringer lactate (Hartmann fluid), plasma.
• Ringer lactate is the fluid of choice.
• Blood is transfused in later period (after 48 hours) if indicated but recently not
advisable because of increased permeability so there is an increased chance of
concentrating blood and making it more viscus.
• In the first 24 hours only crystalloids should be given (crystalloids can pass
through capillary wall like saline either hypo, iso or hypertronic, dextrose saline,
Ringer lactate).
➢ Sodium is assessed by formula: 0.52mmol x kg body weight x % burns
➢ Given at a rate of 4.0 to 4.4ml/kg/hour
• After 24 hours up to 30-48 hours, colloids should be given to compensate plasma
loss (colloids are one which are retained in intravascular compartment).
• Plasma, haemaccel (gelatin), dextrans, hetastarch are used. Usually at a rate of
0.35-0.5ml/kg/% burns are used in 24 hours.
MAINTENANCE FLUID IN 24 HOURS
• In 24 hours Give:
➢ 100ml/kg for the first 10kg
➢ 50ml/kg for the next 10kg

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➢ 20ml/kg for 24 hours for each kilogram over 20kg body weight
• 5% dextrose (Dextrose-saline) is used for maintenance

• For example, a child weighing 28kg maintenance fluid is calculated as follows:

➢ First 10kg give 10kg x 100ml/kg= 1000ml
➢ Next 10kg give 10kg x 50ml/kg= 500ml
➢ Remaining 8kg give 8kg x 20ml/kg= 160ml
➢ Give a total of 1660ml in 24hours of 5% dextrose IV
OTHER CARE
• Clean the burns thoroughly with soap (lifebuoy) and water,
preferably running water (shower is preferred to tab).
• Slough removed by wet dressings. If thick slough is present in
deep burns, surgical sloughectomy is recommended. Eschar
requires Escharotomy.
• Specific care for burns involves the eyes, mouth, perineum and
joints.
• Burns near the eyes are covered with triple antibiotic ointment
(Silver sulfadiazine is irritating to the eyes).
• In the early period, all pain medication is given intravenously.
• Keep patient warm to avoid hypothermia
• Patient might need blood transfusion
• Physiotherapy of burns involving joints. Rehabilitation starts on
day one.
• Nutritional support- high-calorie/high nitrogen diets, Vitamins.
• After 2 or 3 weeks of wound care and general support, the burned
areas that have not regenerated are grafted.
➢ The concept of early excision and grafting is used whenever Figure 57: Incisions for
Escharotomy.
possible to save costs and minimize pain, suffering and
complications.
➢ It implies removal in the or (on day 1) of the burned areas with immediate
skin grafting.
➢ This can be done only for fairly limited burns (under 20%) that are obviously
third-degree, but the experts are extending the concept to highly selected
patients with more extensive burns.
➢ Deep dermal burns need tangential shaving and split skin grafting
➢ All but the smallest full-thickness burns need surgery

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➢ All burnt tissue needs to be excised

• Types of skin grafts:

➢ Skin Autografts: burned area is covered with the
patient’s own skin. This is done in burn wounds less
than 50% of total body surface area. Split skin grafts
are taken from unburnt areas and are usually meshed
(i.e. have slit perforations placed in them). This
helps any exudate beneath the graft to ooze out and
also allows the graft to be stretched to cover a larger
area. Meshed skin grafts heal with the mesh pattern
visible so tend not to be used on the face. The grafts
are secured with staples or tissue adhesive and then
dressed. It is important to prevent shearing forces
from disrupting the graft so joints may be
temporarily splinted.
➢ Skin Allografts: cadaveric skin can be used as
temporary biological dressing. The storage solution
decreases the antigenicity of the skin and the
Figure 58: Skin grafts
burn patient is relatively immunosuppressed so
the graft is not rejected for a few weeks. This may allow autograft donor sites
time to heal for regrafting.
➢ Skin Xenografts: porcine skin can also be used as a temporary biological
dressing.
• Prognosis
➢ Percentage mortality= Age of patient + % burn
➢ Inhalational injury increases mortality but it is arguable by how much.
➢ A decision should be made about whether resuscitation should be started or
whether the patient should just be kept comfortable.

COMPLICATIONS OF BURNS
EARLY
• Respiratory system:
➢ Airway obstruction: due to pulmonary edema, ARDS, respiratory arrest and
respiratory failure
• Cardiovascular system:

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➢ Edema: due to release of inflammatory mediators to produce vasoconstriction
and vasodilation leading to increased capillary permeability.
➢ Hypovolemia: due to fluid loss as a result of increased capillary permeability
due to SIRS and this may lead to renal failure.
➢ Hypoxia: due to destruction of RBCs because thermal injury causes
coagulative necrosis to the epidermis and underlying tissue.
➢ Shock: due to SIRS or due to an inflammatory response causing release of
inflammatory mediators like cytokines which leads to vasodilatation in burnt
areas.
➢ Toxic shock: bacterial infection and bacteremia.
• Skin
➢ Hypothermia (loss of thermoregulation in skin due to damage)
o Warm fluids that are being given to burns patient.
• Genitourinary system
➢ Electrolyte imbalance and shock
• Metabolic
➢ Metabolic Acidosis
➢ Hypoglycemia- hyper-catabolism & mobilization of glucose as a result of
stress hormones
INTERMEDIATE
• Wound infection (Staph aureus, Beta hemolytic Strep, Pseudomonas, Klebsiella)
• Septicemia
• Septic arthritis
• Stress ulcers (curling ulcer- hypovolemia, ischemia of mucosa, erosive gastritis)
• Paralytic ileus due to electrolyte imbalance
• Compartment syndrome due to eschar (slough produced)
• Hypo-proteinemia
• DVT
LATE
• Contractures: due to fibrosis
➢ May lead to ectropion, microstomia, disability of different joints, defective
hand functions, growth retardation causing shortening.
• Hypertrophic scar or keloids
• Marjolin’s ulcer (malignant)
• Nerve compression

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• Psychological effects-cosmetic effect

STOMAS

STOMAS
• A stoma is an iatrogenic hollow muco-cutaneous fistula used for enteral feeding,
drainage, or to divert feces and flatus.

CLASSIFICATION OF STOMAS
• They are classified as
➢ Temporary
➢ Permanent
TEMPORARY
• Input stomas include:
➢ Gastrostomy
➢ Jejunostomy
• Output stomas include:
➢ Pharyngostomy
➢ Esophagostomy
➢ Caecostomy
➢ Ileostomy
➢ Colostomy Figure 59: Stomas
PERMANENT
• End-ileostomy
• End-colostomy

TEMPORARY INPUT STOMAS

GASTROSTOMY
• This is an opening between the skin and the stomach.
• Indicated usually for feeding following upper GIT surgery, or in caustic (NaOH)
stricture of esophagus before surgery.
• Not indicated for advanced carcinoma of the esophagus.
• May be done as an open procedure or endoscopically.
JEJUNOSTOMY
• Opening between jejunum and skin.

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• Indicated following surgery of the upper GIT especially stomach. This is to allow
surgical wounds to heal while facilitating enteral feeding.
• A small feeding tube is inserted to allow feeds to pass through.
• Feeds should be specialized.

TEMPORARY OUTPUT STOMAS

PHARNGOSTOMY
• Used for diversion of solid and saliva to protect the bronchial tree in neonates
with esophageal atresia or tracheal esophageal fistula (TOF).
• May be used as a stage operation in esophageal replacement surgery.
• It involves diverting the pharynx to the skin.
• Technically difficult operation because of the structures found in the neck.
ESOPHAGOSTOMY
• Used for diversion of solid and saliva to protect the bronchial tree in neonates
with esophageal atresia or TOF.
• May be used as a stage operation in esophageal replacement surgery.
• It usually involves diverting the middle esophagus to the skin.
• Care should be taken not to damage the neck structures (nerves and vessels).
CAECOSTOMY
• Stoma between the skin and caecum.
• Used for decompression purposes of the colon following colonic surgery
especially anastomosis of large bowel where the integrity of the anastomosis is
not guaranteed.
ILEOSTOMY
• Diversion at the level of the ileum
• Effluent mostly fluid feces, water and electrolytes.
• These are high output and may cause electrolyte imbalances.
• May complicate into skin excoriation
• May also complicate into gallstone formation
COLOSTOMY
• This is a mucocutaneous opening between the colon and the skin.
TYPES
• They can either be temporary or permanent.

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TEMPORARY
• Done in conditions wherein diversion is required to facilitate healing distally in
the rectum or distal colon.
• This is closed once the purpose is over.
• Site of temporary colostomy is usually right hypochondrium and left iliac fossa.

Figure 60: Sites of a colostomy

• Temporal colostomies can be

➢ Loop colostomy: usually done on the transverse colon

➢ Devine’s double barrel colostomy: there is a gap between the 2 openings of

the colostomy which prevents spillage into the loop
➢ Spectacle
➢ Hartmann
PERMANENT
• Permanent colostomy is always end colostomy placed in left iliac fossa, 6cm
above and medial to the anterior superior iliac spine.

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INDICATIONS
• Congenital
➢ Congenital megacolon
➢ Anorectal malformations
➢ Imperforate anus
➢ Hirschsprung disease
➢ Anal atresia
➢ Anorectal agenesis
➢ Anal stenosis
• Acquired
➢ Intestinal obstruction e.g. Sigmoid volvulus
➢ Ischemic bowel disease/ gangrene due to strangulation
➢ Penetrating trauma to the bowel (left sided)
➢ Tumors: Anal Ca and Rectal Ca
➢ Perforation of left sided colon
➢ High anal fistula
➢ After Hartmann’s operation

COMPLICATIONS
• Complications can always be divided into specific to the procedure vs general for
any surgical procedure and also into immediate (<24 hours), early (1 month) and
later (>1 month).
• Specific:
➢ Ischemic gangrene
➢ Hemorrhage
➢ Retraction
➢ Prolapse/ intussusception
➢ Parastomal hernia
➢ Stenosis- leads to constipation
➢ Skin excoriation
• General complications- related to underlying disease:
➢ Stoma diarrhea- related to water and electrolyte imbalance, hypokalemia
being the commonest and most important consequence and metabolic acidosis
(due to loss of bicarbonate)
➢ Nutritional disorders
➢ Stones- gallstones and renal stones increase in frequency following an
ileostomy.

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➢ Psychosexual- leading to impotence in men/ loss of libido
➢ Residual disease e.g. Crohn’s and Parastomal fistula

Ileostomy Colostomy
Site Right iliac Left iliac fossa
fossa
Surface Sprout Flush with skin
(contents are
corrosive and
can damage
local skin)
Contents Watery- small Feculent
bowel
contents
Examples Post Abdomino-
of panprocto- peroneal resection
permanent colectomy of rectum (End
stomas colostomy)
Examples Ileostomy Hartmann’s
of loop over low procedure
temporary anastomosis of
stomas anterior
resection abdomen
PREOPERATION PREPARATION
• Psychosocial and physical preparation.
• Explanation of the indications and complications.
• Marking of the site- with the patient standing up as he or she must be able to see
the stoma.
➢ 5cm from the umbilicus
➢ Away from scars/ skin creases
➢ Away from bony points
➢ At a site easily accessible to the patient
• The stoma must be within the rectus sheath.

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PRINCIPLES OF SITING A STOMA
• It should be sited pre-operatively ideally.
• Should be in the most favorable position for the patient:
➢ Away from bony prominences
➢ Should be in a position easy for the patient to change
• An end colostomy is usually sited in the left iliac fossa.
• A transverse loop colostomy usually in the upper quadrants of the abdomen.
• Bowel mucus is usually flush with skin in the colostomy while an ileostomy
usually has a sprout.

EXAMINATION OF A STOMA
• Greet the patient.
• Explain the examination and gain consent.
• Expose the patient.
INSPECTION
• Do not start at the hands as you have a specific direction to inspect the abdomen.
• Start by commenting that you seeing a stoma in Epigastric or right iliac or left
iliac fossa.
➢ Is it covered by a bag and in the bag there is?
o Fecal materials
- Formed stool or semi-formed or liquid stool.
- Watery or urine
➢ It is not covered by the bag?
o The mucosal lining looks healthy/ unhealthy
o There is a sprout or flush and skin
o It has one opening (end) or loop (an afferent and efferent portion of bowel
with common opening or 2 separate openings)
➢ Comment on the rest of the abdomen shows:
o A scar
o Midline transverse incision
o Wound dehiscence or and mass
o Also other drains or healed
o Stoma scar

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PALPATION
• If you are only asked to inspect, then do not touch the patient at any time, even
to move the stoma bag out of the way- there may be a good reason why you
should not touch it.
COMPLETION
• Tell the examiner that you would like to examine the rest of the abdomen to look
for reasons why the stoma may have been formed in the first place.
• Thank the patient and cover them.

REHABILITATION OF A PATIENT FOLLOWING THE

PLACEMENT OF A STOMA
• Diet should be normal.
• Bag should be changed once or twice a day (needs to be emptied more frequently
than this if it is urine or fluid faeces)
• Ileostomies should have the base plate under the bag changed every 5 days and
the bag changed daily.
• Psychological and psychosexual support.

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PREOPERATIVE AND POST-OPERATIVE
MANAGEMENT

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PAIN AND PAIN RELIEF

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NEOPLASIA
GENERAL TERMS
• Aplasia- is an almost complete lack of development of a part, so that proper form
and structure are not acquired.
• Hypoplasia- is a lack of development of a part to full or mature.
• Hyperplasia- an increase in the number of cells of a part. It merges with the
process of neoplasia (tumor formation).
➢ It may occur in response to chronic irritation (as in lymphoid tissue) or
endocrine stimulation or it may be compensatory.
➢ The liver has great powers of compensatory hyperplasia.
➢ The remaining thyroid tissue may become hyperplastic when part of it is
removed.
➢ The bone marrow is hyperplastic when there is increased demand for blood.
➢ The prostate often becomes hyperplastic in men over 45, probably due to a
relative hyperestrinism.
• Hypertrophy- this is increase in the size of individual cells or fibers so that an
organ is enlarged. There is no increase in the number of cells or fibers.
➢ True hypertrophy occurs in response to some demand for increased function.
➢ Physiological hypertrophy occurs apart from disease e.g. pregnant uterus,
muscles of athletes and laborers.
➢ Adaptive hypertrophy occurs in hollow viscera when the outlet is partially
obstructed, the wall becoming thickened from enlargement of muscle fibers
e.g. left ventricle in aortic stenosis, the stomach in pyloric stenosis, the
intestine in chronic obstruction and the urinary bladder in urethral obstruction.
➢ Compensatory hypertrophy is an increase in the size to make up for a loss of
tissue especially in paired organs such as the kidney.
• Atrophy: is an acquired decrease in size of a portion of the body, an organ, tissue
or individual cells.
➢ The term is applied only when full size was once present, so that atrophy must
be distinguished from hypoplasia, aplasia and agenesis.
➢ In atrophy the reduction in size in part may be due to a decrease in the number
of its structural units or in the size of the individual units or both.

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CHAPTER 4: STINGS AND
BITES

STINGS AND BITES

SNAKE BITE
• Snakes belong to Crotalidae,
Elapidae and Viperidae family.
• Common poisonous snakes are
cobra, krait and viper.
• Common snakes are cobra,
Figure 61: Coral snake
Russell’s viper, saw scaled viper,
pit viper, krait. the degree of threat the snake feels
• Snake bites can cause neurological threatened and the size of the prey.
problems, cardiac complications, • The nostril pits respond to the heat
pulmonary edema and renal failure. emission of the prey, which may
• Snake bites do not necessarily enable the snake to vary the amount
result in envenomation, even if the of venom delivered.
snake is poisonous (up to 30% of • Venom is mostly water.
bitten patients are not envenomed).
• Enzymatic proteins in venom
CLINICAL FEATURES impart its destructive properties.
• The most reliable signs of ➢ Proteases, collagenase and
envenomation are severe local pain, arginine ester hydrolase have
swelling and discoloration been identified in pit viper
developing within 30 minutes of venom.
the bite. ➢ Neurotoxins comprise the
majority of coral snake venom.
PATHOPHYSIOLOGY ➢ Hyaluronidase allows rapid
• Venom is produced and stored in spread of venom through
paired glands below the eye. It is subcutaneous tissue by
discharged from hollow fangs disrupting
located in the upper jaw. Fangs can mucopolysaccharides.
grow to 20mm in large rattlesnakes. ➢ Phospholipase A2 plays a major
• Venom dosage per bite depends on role in hemolysis secondary to
the elapsed time since the last bite, the esterolytic effect on red cell

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membranes and promotes • Enzyme concentrations vary
muscle necrosis. among species, thereby causing
➢ Thrombogenic enzymes dissimilar envenomation.
promote the formation of a weak • Copperhead bites generally are
fibrin clot, which in turn, limited to local tissue destruction.
activates plasmin and results in Rattlesnakes can leave impressive
a consumptive coagulopathy wounds and cause systemic
and its hemorrhagic toxicity.
consequences. • Coral snakes may leave small
➢ Protease 1-amino acid oxidases: wounds that later result in
tissue necrosis. respiratory failure from the typical
systemic neuromuscular blockade.

Figure 62: Effects of snake venom

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LOCAL EFFECTS ➢ Obtain a description of the
• Burning pain, edema and erythema snake or capture it, if possible,
• Swelling, ecchymoses and to determine its color, pattern, or
hemorrhagic bullae. the existence of a rattle.
• Local bleeding. ➢ Most snakes remain within 20
• Tissue necrosis, ulceration and feet after biting.
gangrene ➢ Assess the timing of events and
onset of symptoms. Inquire
SYSTEMIC about the time the bite occurred
• Neurological manifestations and details about the onset of
• Weakness, perioral paresthesia, pain. Early and intense pain
muscle twitching implies significant
• Shock envenomation.
• Bleeding tendency ➢ Systemic symptoms include
• Pulmonary edema nausea, syncope and difficult
• Renal failure swallowing or breathing.
• Vipers affect multiple organs and • Determine history of prior exposure
soft tissues. Cobra and coral snakes to antivenin or snakebite.
are neurotoxic. • Determine history of allergies to
medicine because antibiotic may be
HISTORY required.
• History usually can be obtained • Determine history of comorbid
from the patient. conditions (e.g. cardiac pulmonary,
• Most cases result from attempting and renal disease) or medications
to handle snakes, so the genus (e.g. aspirin, beta-blockers)
usually is known.
• Knowledge of indigenous fauna PHYSICAL
also is important. EXAMINATION
• The time elapsed since the bite is a • Follow the established routine for a
necessary component of the complete comprehensive
history. examination.
• This allows assessment of the ➢ Vital signs, airway, breathing,
temporal effects of the bite to circulation.
determine if the process is confined ➢ Fang marks or scratches
locally or if systemic signs have (determine coral snake bite
developed. pattern by expressing blood
from the suspected wound)

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INVESTIGATIONS ➢ All the first aid measures that
• Full Blood count you learned at boy scouts are
• Blood Cross match wrong. Do not make cruciate
cuts, suck out venom, wrap with
• Coagulation studies like bleeding
ice or apply a tourniquet.
time, clotting time and prothrombin
time. • Immediately transfer to definitive
care.
• Blood urea and serum creatinine.
• Serum electrolytes DEFINITIVE TREATMENT
• Urine analysis for RBCs, albumin, • Definitive treatment includes
myoglobin reviewing the ABCs and evaluating
• Liver function tests the patient for signs of shock (e.g.
• Creatinine phosphokinase [CPK] tachypnea, tachycardia, dry pale
• Arterial blood gasses: PO2 and skin, mental status changes,
PCO2 assessment hypotension).
• The site has to be incised and
MANAGEMENT cleaned.
FIRST AID • It is thoroughly cleaned with
• Reassurance of the pain, ensure the debridement.
patient is calm to preclude hysteria. • Fasciotomy is not indicated in
• Immobilization of the patient, keep every bite, only for those patients
walking to a minimum. with objective evidence of elevated
• Implement the ABCs. compartment pressure
• Monitor vital signs and establish at (compartment syndrome)
least 1 large bore intravenous and • Tourniquets are used to occlude
crystalloid infusion. lymphatics only but not venous or
• Administer oxygen therapy. Keep a arterial circulation.
close watch on the airway at all • The snake has to be identified.
times in case intubation becomes • The patient must be transferred to
necessary. proper medical center as early as
• Negative-pressure suctioning possible.
devices offer some benefit if used • The bite wound is identified and
within several minutes of assessed.
envenomation. Again do not make • Envenomation grading determines
an incision or give antivenin in the the need for antivenin in pit viper
field. victims. Grades are defined as mild,
moderate or severe.

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➢ Mild envenomation: local pain, drops/minute as flow rate. If the
edema, no signs of systemic snake has been identified
toxicity and normal lab values. monovalent serum is better and
➢ Moderate envenomation: severe more potent.
local pain, edema larger than ➢ Preferred agent for crotalids is
30cm surrounding the wound CROFAD of which several vials
and systemic toxicity including are usually needed
nausea, vomiting and alteration • Tetanus prophylaxis
in lab values (e.g. fallen • IV fluids, blood transfusion and
hematocrit or platelet value). plasma
➢ Severe envenomation: • Antibiotics (ceftriaxone- third
generalized petechiae, generation cephalosporin broad
ecchymosis, blood-tinged spectrum antibiotic more effective
sputum, hypotension, hypo- on gram negative)
perfusion, renal dysfunction, • Urine output measurement
changes in prothrombin time • Monitoring by regular checking of
and activated partial blood urea, serum creatinine and
thromboplastin time, and other bleeding and clotting time.
abnormal tests defining • In cobra bite, there is
consumptive coagulopathy. neuromuscular blockade and
• Grading envenomation is a paralysis. So neostigmine should be
dynamic process. Over several given 0.5 mg IV every half hourly
hours, an initially mild syndrome and later repeated. It is given along
may progress to a moderate or even with 0.6mg of atropine.
severe reaction. • In viper bite, DIC is common. So
• Polyvalent anti-snake venom heparin is given as 10, 000 to 15,
(against cobra, krait, vipers) should 000 units loading dose and later 5,
be given. 000 units as maintenance dose
➢ It should be given earliest within TDS.
4-24 hours. • Human fibrinogen, whenever
➢ Dose is 20-150ml depending on required.
the type, severity and age of the
individual. Children get the COMPLICATIONS
same dosages as adults. • Local wound complications:
➢ It is dissolved in normal saline infection, skin loss, Cellulitis and
and given as IV infusion in gangrene of the part.
500ml saline with 20

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SURGERY MK
• Compartment syndrome especially • The virus has a marked affinity for
with pit viper snake bites. nervous tissue and the salivary
• Neurological complications glands.
• Cardiovascular and Hematological: • 2 major epidemiological types of
Deep venous thrombosis (DVT), rabies exist:
Pancytopenia, DIC and hemorrhage ➢ Urban rabies (95%): most
• Pulmonary collapse frequently transmitted to
• Septicemia humans through rabid dogs, and
• Renal failure less frequently cats.
• Marjolin’s ulcer ➢ Sylvan (wild) rabies: this is
• Antivenin-associated maintained in the wild by a host
complications: anaphylaxis (Type of animal reservoirs such as
I) and serum sickness (Type III). foxes, skunks, jackals,
mongooses and bats.
RABIES AND DOG • Transmission is usually through the
bite of an infected animal.
BITES However, the percentage of rabid
RABIES bites leading to clinical disease
• Rabies is a major problem in some ranges from 10% (on the legs) to
countries. It is an acute fatal 80% (on the head). Other forms of
encephalomyelitis. transmission if they occur are rare.
• There is no predilection for age or • The virus replicates in the muscle
sex even though it is observed more cells near the entry wound. It
in children and adult males. penetrates the nerve endings and
• Established infection is almost travels in the axoplasm to the spinal
invariably fatal. It is caused by a cord and the brain.
genotype 1 single-stranded RNA • In the CNS the virus again
virus of the Lyssavirus genus. proliferates before spreading to the
• The rabies virus is bullet-shaped salivary glands, lungs, kidneys and
and has spike-like structures arising other organs via the autonomic
from its surface containing nerves.
glycoproteins that cause the host to • In the brain it causes encephalitis
produce neutralizing, and in the spinal cord it causes
hemagglutination-inhibiting transverse myelitis.
antibodies. • Natural occurring rabies virus is
called as street virus which shows

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long incubation period of 20-60 salivation and paralysis may
days. Serial passage of the virus to occur.
brain of rabbits creates fixed virus o Hyperexcitability
which has got a short incubation (Hallmark of this form of
period of 4-6 days which does not rabies) is precipitated by
show Negri bodies. This fixed virus auditory or visual stimuli.
which cannot multiply in o Hydrophobia (fear of water)
extraneural tissues is inactivated to is present in 50% of patients
prepare vaccine. and is due to severe
pharyngeal spasms on
CLINICAL FEATURES
attempting to eat or drink.
• Incubation period is variable and
o Aerophobia (Fear of air) is
ranges from few weeks to several
considered pathognomonic
years (average 1-3 months).
of rabies.
• Bites on the head, face and neck
o Examination reveals
have a shorter incubation period
hyperreflexia, spasticity and
than those elsewhere.
evidence of sympathetic
• In humans, 2 distinct clinical overactivity indicated by
varieties are recognized: pupillary dilation and
➢ Classic variety (Furious rabies): diaphoresis.
the dogs are aggressive like a o The patient goes on to
mad dog. Dog changes its develop convulsions,
behavior with loss of fear of respiratory paralysis and
humans, bites objects, eat, mud cardiac arrhythmias.
etc. running amok, voice o Death usually occurs in 10-
change, inability to bark 14 days.
properly, excessive salivation ➢ Paralytic variety (Dumb rabies):
and foaming paralysis and Dog is paralytic and sleepy.
death. In humans: There is no aggressiveness at all.
o Prodromal period only Dog sleeps for 3 days and dies.
shows pain and tingling at Once symptoms of rabies
the site of the initial wound. develop in a dog it rarely
o 10 days later, marked survives more than a week. In
anxiety and agitation or humans:
depressive features develop. o Presents with a symmetrical
o Hallucinations, bizzare ascending paralysis
behavior, increased

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resembling the Guillain- all patients with rabies, these are
Barre syndrome. esosinophilic, cytoplasmic, ovoid
o This variety of rabies bodies, 2-10 nm in diameter, seen
commonly occurs after bites in greatest numbers in the neurons
from rabid bats. of the hippocampus and
cerebellum.
DIAGNOSIS
• Diagnosis should be made
• Clinical
pathologically on the biting animal
➢ Class I: touching or feeding the
using RT-PCR,
diseased animal, lick over intact
immunofluorescence assay (IFA)
skin or scratches without oozing
or tissue culture of the brain
of blood
➢ Class II: licks on broken skin, MANAGEMENT
scratches with blood ooze and • Once CNS disease is established,
all bites except over head, face, therapy is symptomatic and death is
palms and fingers. Minor virtually inevitable.
wounds less than five in number ➢ Patient should be nursed in a
➢ Class III: all bites over head, quiet, darkened room.
face, palms and fingers, ➢ Nutritional, respiratory and
lacerated wounds, wounds more cardiovascular support may be
than five in number, wild animal necessary.
bites, and contamination of ➢ Drugs such as morphine,
mucous membrane with saliva. diazepam and chlorpromazine
• Skin punch biopsy can be used to should be used liberally in
detect antigen with an patients who are excitable.
immunofluorescent antibody test • Prevention
on frozen section. ➢ Pre-exposure prophylaxis:
• Viral RNA can be isolated using the given to individuals at high risk
reverse transcription polymerase of contracting rabies e.g.
chain reaction (RT-PCR). laboratory workers, animal
• Isolation of viruses from saliva or handlers and veterinarians
the presence of antibodies in blood o 3 doses (1.0 ml) of human
or CSF may establish the diagnosis. diploid (HDCV) or chick
• Corneal smear test is not embryo cell vaccine given
recommended as it is unreliable. by deep subcutaneous or
The classic Negri bodies are intramuscular injection on
detected at post-morterm in 90% of

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SURGERY MK
days 0, 7 and 28 to provide needle method is being
effective immunity. phased out as it is
o A reinforcing dose is given expensive.
after 12 months and o Prophylaxis is effective
additional reinforcing doses when given within 10 days
are given every 3-5 years of exposure.
depending on the risk of o Reaction to the vaccine is
exposure. uncommon.
➢ Post-exposure prophylaxis: • Domestic animals should be
o Wound should be cleaned vaccinated if there is any risk of
carefully and thoroughly rabies in the country otherwise,
with soap and water and left they should be put down if they
open. cannot be vaccinated.
o Povidone-iodine or alcohol ➢ BPL inactivated nervous tissue
is then recommended to vaccine (20 % infected sheep
reduce the virus further. brain suspension): single dose
o Human rabies 5ml to dogs, 3 ml to cats.
immunoglobulin should be Second dose after 6 months.
given immediately (20 Then once a year regularly.
IU/Kg). ➢ Modified live virus vaccine:
o Half should be injected 33% infected chick embryo
around the wound and the suspension. Dose-3ml single
other half should be given dose which is repeated once in 3
intramuscularly. years.
o People that have been ➢ Oral vaccines: used successfully
previous immunized against to control wild foxes in Canada
rabies do not need to receive by placing vaccine in food
the immunoglobulin just the through baits.
post-exposure vaccination
at days 0 and 3. DOG BITES
o Five 1.0 ml doses of HDCV • For all patients presenting, a
should be given thorough history and clinical
intramuscularly as follows examination is a must.
on days 0, 3, 7, 14 and 28. • It is vital that serious or major
o Injection should be given injuries are excluded such as to the
over the deltoid muscle as airway and cervical spine, major
abdominal-based large vessels with life or limb threat or

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specialized structures especially of Delay in presentation and
the head and neck. treatment has been identified as
• Assessment of these patients should a significant risk factor for a
be in accordance with the principles resulting wound infection.
of Advanced Trauma Life Support • Examination: Local
(ATLS)-ABCs. ➢ Wound often comprises of
• Any penetrating bite injury can lead tissue tears and lacerations,
to considerable damage of both punctures, crush injuries with or
hard and soft tissues. without resulting tissue loss.
• History assessment: ➢ Consideration should be given
➢ Where and when the bite to the presence of hard tissue,
occurred. soft tissue or a combination of
➢ How did the bite happen and (if both.
a child) was there supervision of ➢ Typical dog bite results in a
the child and/or animal? ‘hole and tear effect’ with a
➢ Is there any associated relevant combination of a deep puncture
medical history: DM (increased and tissue tearing.
risk of wound infection), ➢ Dog bite wounds at the ‘minor
Chronic liver or lung disease end’ of the scale of severity can
and Immunosuppressive states be a simple abrasion or
(HIV/AIDS, chemotherapy)- superficial penetration of the
can reduce healing rate and skin layers and these are the
increase risk of infection. wounds likely to present to the
➢ What is the patient’s tetanus GP for treatment.
status? ➢ Damage to muscle, vessels,
➢ History of alcohol dependence, nerves, bone or joints
smoking and/or substance abuse constitutes a serious injury and
can also affect wound healing their management requires a
and infection risk and may have thorough examination,
been a precipitant to the bite assessment and will involve
injury. referring the patient to hospital
➢ Consideration should also be to the relevant surgical
given to current medications, specialty.
nutritional states and extremes
of age.
MANAGEMENT
➢ The timing of the injury to the • Wound must be thoroughly cleaned
time of presentation is also vital. with saline.

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• Irrigation and debridement is bacterial colonization and growth
important in preventing subsequent and also leads to infection.
infection and should be instigated • Closure of wound:
at the earliest opportunity. ➢ Primary closure: wound closure
• Local anesthetic should be in the primary care setting is
administered through uninvolved rarely recommended and
adjacent skin and away from the therefore majority of injuries are
damaged tissue and if a distal left open to heal by secondary
periphery is involved, instructing intention. The concern has
the patient to elevate the affected always been that closure of the
limb can reduce subsequent tissue wound could lead to tissue
edema and swelling. necrosis, abscess formation and
• Tetanus immunization as well as systemic sepsis.
rabies vaccine plus rabies ➢ In cases of minor wounds
immunoglobins are given. (superficial lacerations,
➢ Anti-tetanus toxoid (0.5 ml) abrasions) through cleaning and
➢ 20IU/kg of Human rabies wound ‘toilet’ should be
immunoglobulin. Half should undertaken with irrigation.
be injected around the wound These wounds are deemed low
and the other half should be risk. Exceptions are to those
given intramuscularly wounds deemed high risk cases
➢ Five 1.0 ml doses of human for infection or clinically the
diploid (HDCV) should be wound appears infected.
given intramuscularly as • The use of prophylactic antibiotics
follows on days 0, 3, 7, 14 and in high risk wounds (location on the
28. hand, deep puncture wounds or
• Puncture wounds are at higher risk immunocompromised host) should
of infection, as they harbor be strongly considered, together
microorganisms deep within the with those cases presenting late (>9
wound, and have a narrow entry hours since injury).
point making thorough cleaning ➢ Antibiotic of choice is co-
difficult. amoxiclav (amoxicillin and
• Crush injuries can precipitate clavulanic acid)
infections because of the resulting ➢ For patients allergic to penicillin
ischemic damaged tissue. This doxycycline combined with
devitalized tissue predisposes to metronidazole is recommended.

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COMPLICATIONS ➢ Black widow spider bite
• Infection: Pasteurella spp. ➢ Brown recluse spider bite
• Lymphangitis BLACK WIDOW SPIDER
• Local abscess
BITE
• Septic arthritis
• Black widow spiders are black with
• Tenosynovitis
a red hourglass on their belly.
• Osteomyelitis
• Their bite causes neurotoxicity.
• Bite wounds can be complicated by
• It causes muscle spasms, pain and
serous disseminated infection
abdominal rigidity.
leading to septic shock, meningitis
• Nausea, vomiting, Hypertension,
and brain abscess, endocarditis and
tachycardia and diaphoresis are the
other severe sequel including DIC
other features.
(especially in
immunocompromised) • Its effects last for 2-3 days.
• Cleaning the wound, antibiotics,
MAMMALIAN BITE antihistamines, specific antivenims
• It also includes human bites also. are the line of treatment.
• Infection rate is more in • The antidote is IV calcium
mammalian bites. gluconate. Muscle relaxants also
• Human bites are bacteriologically help.
the dirtiest bite one can get. They
require extensive irrigation and
debridement (in the OR).
• Proper wound toileting is very
important.
• Within 12 hours, incised wound is
closed primarily.
• All lacerated wounds and wound
which is seen after 12 hours is left
open. Wound is closed secondarily.
• Antibiotics are must in all Figure 63: Black widow spider
mammalian bites.
• Human bite is very dangerous bite.
BROWN SPIDER BITE
• These are often not recognized at
SPIDER BITE the time, by the next day a skin
• Types of spider bites include: ulcer develops with necrotic center

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and a surrounding halo of ➢ These lancets get attached to
erythema. human skin to release the
• It releases sphingomyelinase-D venom.
which causes necrosis of the skin ➢ Bees die after sting.
and hemolysis. • Yellow jacket wasps are more
• Local effects: skin rash, blister aggressive.
formation, necrosis of the skin and • Bee venom contains dopamine,
extensive ulceration. histamine, neurotoxin and toxic
• Systemic effects: anaphylaxis, peptides.
arthralgia, thrombocytopenia,
hemolysis and renal failure. CLINICAL FEATURES
• Often it can be life-threatening • Allergic reactions
especially in children and elderly. • Anaphylaxis: wheezing and rash
• The effects last for 2-3 weeks. • Pain in the local region, edema,
• Wound debridement (surgical pruritus, flushing
excision may be needed but should • Hypotension (vasomotor shock-
be delayed until the full extent of ‘pink and warm’ shock), laryngeal
the damage is evident-as much as 1 edema, bronchospasm
week), antibiotics, antihistamines, • Muscle spasm, convulsion
steroid therapy, antivenins and • Renal failure in severe cases
management of systemic
complications.
MANAGEMENT
• Dapsone is helpful. • The stingers should be removed
without squeezing them.
• Soda bicarbonate is used to
neutralize the bee venom.
• Antibiotics and antihistamines are
also given.
• Epinephrine is the drug of choice
(0.3 to 0.5ml of 1: 1 000 solution).

SCORPION STING
Figure 64: Brown spider • Scorpion stings are painful but
rarely life-threatening.
BEE STING • Young children and older adults are
• Honey bee has got barbed stinger most at risk of serious
with two lancets. complications.

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• World-wide, only about 30 of
estimated 1500 species of scorpions
produce venom toxic enough to be
fatal.
• A scorpion sting is caused by the
stinger in a scorpion’s tail. When a
scorpion stings, its stinger can
release venom. The venom contains
a complex mix of neurotoxins.

CLINICAL FEATURES
• Symptoms:
➢ Pain which can be intense
➢ Numbness and tingling
➢ Slight swelling
➢ Warmth
• Signs:
➢ Difficult breathing
➢ Muscle twitching or thrashing
➢ Unusual head, neck and eye
movements
➢ Drooling
➢ Sweating
➢ Nausea and vomiting
➢ Hypertension
➢ Tachycardia
➢ Restlessness or excitability or
inconsolable crying in children
➢ Allergic reactions and
anaphylaxis: hives, difficult
breathing, nausea and vomiting

MANAGEMENT
• Analgesia
• Scorpion antivenin

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CHAPTER 5: CHEST SURGICAL
CONDITIONS

➢ A collecting container below

CHEST SURGICAL chest level
CONDITIONS ➢ A one-way mechanism such as
an underwater seal or Heimlich
BASIC SURGICAL valve
PROCEDURES
INDICATIONS
BASIC SURGICAL 1. Recurrent pleural effusion or
massive pleural effusion
PROCEDURES ➢ Chylothorax (lymphatic fluid)
INTERCOSTAL CHEST DRAIN ➢ Empyema thoracis (pus)
➢ Hemothorax (blood)
INTERCOSTAL CHEST ➢ Hydrothorax (Serous fluid)
DRAIN (ICD) 2. Pneumothorax
3. In any hypo-ventilated patient
• Chest drain (also called chest tube,
4. Post-operation:
thoracic catheter, tube
➢ Thoracotomy
thoracostomy or intercostal drain)
➢ Esophagectomy
is a conduit inserted through the
➢ Cardiac surgery
chest wall and into the pleural space
to remove air (pneumothorax) or CONTRAINDICATIONS
fluid from the pleural cavity. 1. Refractory coagulopathy
• The fluid can be blood 2. Diaphragmatic hernia
(hemothorax), pus (empyema), 3. Hepatic hydrothorax
chyle (chylothorax) or a pleural 4. Scarring in the pleural space
effusion. (adhesions)
• For a chest drain to be efficient it MECHANISM OF ACTION
must allow re-expansion of the
• Drainage occurs during expiration
underlying lung and must prevent
when pleural pressure is positive.
entry of air or drained fluid back
➢ Recall when relaxed pleural
into the chest.
pressure is sub-atmospheric (-
• A chest drain must therefore have 3 2.5 mmHg). Normal
components: atmospheric pressure
➢ An unobstructed chest drain 760mmHg

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SURGERY MK
• Fluid within pleural cavity drains • Blunt dissection and insertion of
into an underwater seal. finger should ensure that pleura
• Air bubbles through water seal to cavity is entered.
outside world. • Previous it used to be taught that:
• The length of drain below fluid ➢ To drain fluid, it should be
level is important. If greater than 2- inserted to base of pleural cavity
3 centimeters increases resistance ➢ To drain air, it should be
to air drainage. inserted towards the apex of the
lung
• Probably the position of the tube in
the pleural cavity does not matter
provided there is no loculation of
fluid within pleural cavity.
• A large drain (28 Fr or above)
should be used to drain blood or
pus.
• Drain should be anchored and
purse-string or Z-stitch inserted in
anticipation of removal
Figure 65: Basic concept of an intercostal
chest drain

PRINCIPLES OF CHEST DRAINS

INSERTION
• Unless emergency situation then
pre-procedure chest X-ray should
be performed.
• Drain usually inserted under local
anesthesia using aseptic technique.
• Inserted in 5th intercostal space in
mid-axillary line Figure 66: An Intercostal chest drain
inserted with a Z-string
• Inserted over upper border of rib to
avoid intercostal vessels and EQUIPEMENT
nerves. • Bottles:
➢ Under water vacuum

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SURGERY MK
➢ Under water seal • For a simple pneumothorax it can
➢ One-way valve apparatus often be removed within 24 hours.
ASSESING FUNCTIONALITY OF • To remove drain, ask patient to
CHEST DRAIN perform a Valsalva maneuver.
• Ask the patient to cough and check • Remove drain at the height of
out bubbles in the bottle expiration.
• Check the moving menisci • Tie to pre-inserted purse-string or
Z-stitch.
TRANSFERRING THE PATIENT • Perform a post-procedure chest X-
• Clump the tube with artery forceps ray to exclude a pneumothorax
• Patient should carry it not raised
COMPLICATIONS
above insertion
• When you reach the place, put it • “There is no organ in the thoracic or
abdominal cavity that has not been
down and unclamp
pierced by a chest drain”
DO’S AND DON’TS OF CHEST
EARLY
DRAINS
• Misplacement: Tube displaced,
• Avoid clamping of drain as it can
tube inserted too far, tube placed
result in a tension pneumothorax
subcutaneously.
• Drain should only be clamped
• Subcutaneous surgical emphysema
when changing the bottle or
transferring patient. • Injury to organs and other
• Always keep drain below the level structures:
of the patient. ➢ Diaphragm causing injury to
liver or spleen,
• If lifted above chest level contents
➢ Parenchymal or hilar injuries,
of drain can siphon back into chest.
lung lacerations
• If disconnection occurs reconnect
➢ Injury to the heart
and ask patient to cough.
➢ Phrenic nerve injury
• If persistent air leak consider low
➢ Neurovascular bundle injury
pressure suction.
➢ Esophageal perforation-
• Observe for post-expansion hemorrhage
pulmonary edema. ➢ Bowel injury in the presence of
REMOVAL unrecognized diaphragmatic
• Remove drain as soon as it has hernia
served its purpose. • Contralateral pneumothorax
• Hemorrhage and hemothorax

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INTERMEDIATE • The mechanism of injury is
• Surgical emphysema important as it determines the
• Re-expansion pulmonary edema extent and type of damage
• Tube blockage sustained.
• Infection along the chest tube • The mechanisms that cause injury
• Pain to the chest are identical to those
that cause injuries to the abdomen
LATE and frequently patients with
• Retained hemothorax thoracic injuries also have
• Pneumothorax after removal abdominal involvement. An
• Empyema important example of this is a rib
• Abscess fracture on the left side that leads to
• Fistula-formation splenic laceration.
• The problems caused by thoracic
CHEST TRAUMA
trauma relate to the disruption of
adequate gas exchange, leading to
CHEST TRAUMA hypoxia, hypercapnia and acidosis.
• When considering trauma to the • Other problems relate to shock
chest it is important to remember secondary to disruption of major
the anatomical structures present viscera in the chest.
and how they could be damaged.
• In general trauma to the chest can TYPES OF CHEST
be considered as: INJURY
➢ Blunt • These include:
➢ Penetrating ➢ Chest wall trauma
• Chest injuries may occur secondary o Fractured ribs
to other traumatic processes and o Flail chest
may significantly impair breathing o Fractured sternum
for example severe burns to the ➢ Lungs and pleura
chest can cause encircling eschar o Simple pneumothorax
that impairs the respiratory o Tension pneumothorax
excursions of the thoracic cage. o Hemothorax
• In both blunt and penetrating types o Pulmonary laceration
of chest trauma the forces causing o Tracheobronchial
the trauma can either be: disruption
➢ Low velocity ➢ Cardiovascular injuries
➢ High velocity. o Cardiac trauma

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SURGERY MK
o Aortic disruption • Fractured ribs can also puncture the
➢ Diaphragmatic injuries pleura and even the lung substance
• These injuries can be detected on and cause a pneumothorax.
either primary survey or secondary • In more severe thoracic cage
survey. trauma 2 or more consecutive ribs
• Primary survey injuries: can be fractured in 2 or more places
➢ Fractured ribs this is defined as a flail segment.
➢ Flail chest • The consequences of rib fractures
➢ Fractured sternum are treated individually. A simple
➢ Pneumothorax rib fracture itself requires no
➢ Tension pneumothorax specific treatment other than
➢ Hemothorax analgesia.
➢ Cardiac tamponade
FLAIL SEGMENT
• Secondary survey injuries:
• This happens when 2 or more
➢ Pulmonary contusion
consecutive ribs are fractured in 2
➢ Aortic disruption
or more places.
➢ Diaphragmatic injury
• A flail segment compromises a
➢ Tracheobronchial disruption
patient’s breathing because the
➢ Esophageal disruption
fractured segment undergoes
PRIMARY SURVEY INJURIES paradoxical movement on
FRACTURED RIBS inspiration. The segment moves
• The most common fractures are inwards rather than outwards and
those of the lower ribs usually the hence impedes ventilation of the
5th to the 9th. ipsilateral lung.
• Fractures of the lower ribs have
significance because they can
lacerate upper intra-abdominal
viscera (especially the spleen).
• It is also important to note that
fractures of the upper 4 ribs
particularly the 1st rib are indicative
of extremely high-velocity trauma
as these ribs do not usually fracture
because of their short, stout
anatomy.

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SURGERY MK
• A fractured sternum produces
intense, deep pain.
• The risk of injury to the
mediastinum cause the greatest
concern.
• Patients with sternal fractures
should always be admitted and
observed and ECG performed to
look for electrical abnormalities
• Cardiac enzymes should also be
measured to ensure myocardium
has not sustained significant
damage.
• Management also involves
adequate analgesia.
PNEUMOTHORAX
Figure 67: Rib fractures leading to a flail • This is air in the pleural cavity
segment with paradoxical movement. The secondary to trauma.
paradoxical respiration can lead to
embarrassment of gaseous exchange.

• The degree of trauma causing a flail

segment is likely to lead to
underlying lung contusion and even
laceration.
• A flail segment requires strapping
of the segments and even positive
pressure ventilation to compensate
for poor oxygenation and to aid
healing of the chest.
FRACTURED STERNUM
• The mechanism of injury is usually Figure 68: Chest X-ray showing a simple
a severe impact on a solid structure, pneumothorax on the right and a lung
most common example is where a contusion on the left
driver of a motor vehicle is thrown
onto the steering wheel.

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SURGERY MK
• It is the most common pleural-
related problem that any doctor is
likely to encounter in practice.
• Despite most pneumothoraces
occurring with trauma, they may be
associated with other diseases e.g.
bullous disease of the lung
secondary to emphysema.
• Pneumothoraces may be caused by
fractures of the ribs secondary to
blunt trauma or by a penetrating
injury (e.g. a knife).
• A pneumothorax can either be a:
➢ Tension pneumothorax
➢ Simple pneumothorax
• Tension pneumothorax develops
when a penetrating injury of the
chest allows air from the external Figure 69: The mediastinal shift that occurs
due to a tension pneumothorax. Release of
environment to enter the pleural tension pneumothorax after insertion of a
cavity but not leave the wound cannula into the right second intercostal
acting as a one-way valve. space.
• Eventually the accumulation of air • A tension pneumothorax should be
in the pleural cavity displaces the recognized at the time of the
mediastinum to the opposite side, primary survey.
thereby decreasing venous return
• The patient is typically short of
and leading to cardiac arrest that
breath and the trachea is displaced
shows signs of electromechanical
away from the side injury.
dissociation.
• The chest on the injured side also
fails to expand and is
Hyperresonant to percussion.
• If, together with the above findings,
breath sounds are absent on the
injured side, the patient should not
proceed to chest X-ray.
• Immediate management is to
relieve the build-up air in the

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SURGERY MK
pleural cavity by needle when the re-expanded lung adheres
decompression. to the chest wall due to the secretion
• A large bore needle is inserted into of fibrin.
the 2nd intercostal space in the • A drain tube should only be
midclavicular line on the affected removed if there is cessation of
side. bubbling in the drainage bottle even
• Successful decompression is with suction.
heralded by a rush of air through the • When the lung is fully expanded,
needle after insertion. This converts this lack of bubbling needs to have
a tension pneumothorax into a been present for at least a day.
simple pneumothorax. • It is important to tie a second purse-
• Simple pneumothoraces are those string suture to allow adequate
where there is a defect in the chest closure of the drain site. After drain
wall that allows air to enter and removal, a chest X-ray should be
leave the pleural cavity causing the taken to confirm continued lung
lung to collapse. expansion.
• Air does not accumulate in the HEMOTHORAX
pleural cavity there is no deviation
• This is accumulation of blood in the
of the mediastinum as seen in a
pleural space.
tension pneumothorax.
• Hemothoraces are most commonly
• The initial management of an open
associated with laceration or
pneumothorax is prompt closure of
disruption of the lung parenchyma
the defect with a sterile occlusive
and are obviously more common in
dressing large enough to overlap
penetrating than blunt injuries.
the edges of the wound and taped
• Hemothoraces can either be:
securely on 3 sides. This works as a
➢ Small: these are less than 1L of
flutter valve preventing air from
blood
entering the pleural cavity when the
➢ Massive: rapid accumulation of
patient inhales but allows air to
more than 1L of blood in the
leave when the patient exhale.
chest cavity. This is most
• Definitively both pneumothoraces
commonly caused by disruption
are managed by insertion of a chest
of the hilar vessels of the lung
tube to drain the air from the pleural
and hence the problems
cavity.
experienced by the patient
• The majority of simple would be not only those of
pneumothoraces resolve in days

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SURGERY MK
hypoxia but also those of pericardial sac which restricts the
hypovolemia. filling and contraction of the heart
• Clinically, a massive hemothorax is and leads to shock.
characterized by hypoxia, • If this fluid is blood it can come
hypotension and a chest where from disruption of the great vessels
there may be obvious signs of or the heart itself, most commonly
trauma and on the ipsilateral side as a result of penetrating injuries,
decreased expansion, stony dull although severe blunt trauma can
percussion note and decreased also be a cause.
breath sounds. • As little as 20ml of blood can cause
• Initial management involves symptoms.
insertion of a large bore chest tube • Beck’s triad of cardiac tamponade:
into the 6th intercostal space in the ➢ Elevated JVP
midaxillary line. ➢ Decreasing in blood pressure
• If a massive hemothorax is ➢ Muffled heart sounds
suspected, the blood from the chest • Additionally, the patient may
can be used for auto-transfusion. demonstrate pulsus paradoxus and
• The subsequent management of the a rise in venous pressure with
patient depends on the volume of inspiration (Kussmaul’s sign).
blood loss. • Transthoracic echocardiography
➢ If over 1L is immediately can help in confirming the
drained from the thoracic cavity, diagnosis. However, the diagnosis
the patient requires an early is often made only when
thoracotomy Pericardiocentesis is performed in a
➢ If less than 1L is drained, the last-ditch effort to relieve the
patient can be managed cardiogenic shock.
expectantly with decision for • In this procedure, a long spinal
surgery based on the rate of needle is inserted in the subxiphoid
continuing blood loss. region and blood is evacuated. This
➢ If the rate of blood loss is procedure should always be
200ml/h over the subsequent 2- performed under ECG monitoring.
4 hours, the patient should be • In very extreme situations the
considered for surgery. thorax is opened and the
CARDIAC TAMPONADE pericardium evacuated.
• Cardiac tamponade is the
accumulation of fluid in the

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• More severe pulmonary injuries
can lead to pulmonary laceration.
However, this is most commonly
observed with an associated
fractured rib or secondary to
penetrating trauma.
AORTIC DISRUPTION
• Traumatic disruption of the aorta is
a common cause of death after
trauma that involves very rapid
deceleration from great speeds such
Figure 70: Site of insertion of a as high-velocity road traffic
Pericardiocentesis needle to decompress a
cardiac tamponade accidents and falls from a great
height.
SECONDARY SURVERY CHEST • These patients are initially stable
INJURIES but continue to be hypotensive
• Hemothoraces and despite resuscitation due to failure
pneumothoraces can also cause of hematoma to contain the
death during the secondary survey bleeding.
however, the occurrence and • There are usually few specific signs
discovery of visceral injuries that and symptoms.
were not obvious initially tend to • A high index of suspicion and a
dominant the secondary survey. history of decelerating force will
PULMONARY CONTUSION lead to inspection of chest X-ray for
• This can often display subtle signs, specific signs of mediastinal
where significant portions of the widening.
lung fail to function and cause the • If the patient is stable, angiography
patient to become markedly and even CT scanning will help
hypoxic. confirm the diagnosis.
• The patient’s injuries may often be • Immediate referral to a
sufficiently severe to require cardiothoracic surgeon is
assisted ventilation and may also imperative if the patient is to
contribute to the development of survive.
adult respiratory distress syndrome
(ARDS).

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DIAPHRAGMATIC INJURY ESOPHAGEAL DISRUPTION
• Huge compressional forces can • The esophagus is most commonly
cause the diaphragm to be torn from traumatized by penetrating trauma.
its attachment. • The esophagus can also tear due to
• Diaphragmatic injuries can also be forceful expulsion of contents from
due to penetrating trauma where the stomach during hug impacts.
there is associated abdominal • This causes gastric contents and air
injury. to leak into the mediastinum,
• Diaphragmatic trauma is often resulting in mediastinitis and air in
missed or diagnosed late. the subcutaneous tissue of the neck,
• Some patients may present later recognized as surgical emphysema.
with herniation through previous • Patients may also develop a
diaphragmatic defects caused by pneumothorax usually more
trauma. common on the left than the right.
• On chest X-ray these injuries may • The diagnosis is confirmed when
be recognized by an elevated particulate gastric matter is
diaphragm and confirmed by recovered from the chest tube.
inserting contrast into the • Prompt diagnosis and repair
esophagus and observing a high produce the best results in these
stomach. patients.
TRACHEOBRONCHIAL
DISRUPTION
• This is uncommon and fatal if
overlooked.
• Patients who suffer severe
tracheobronchial disruption usually
die at the scene of the accident.
• Those with minor degree of
disruption are frequently
recognized by the fact that they
have a pneumothorax with
associated emphysema, the
pneumothorax persists despite
chest tube drainage.
• Frequently, definitive surgery is
required to correct the abnormality.

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Anatomical region Clinical features Management

CHEST WALL
Fractured ribs • Usually 6th to 9th ribs. • Adequate analgesia
• Fracture of 1st rib or upper 4 ribs • Breathing exercises
indicates high velocity trauma
Flail chest • Paradoxical chest wall movement on • Adequate analgesia
respiration • Strapping of flail segment
• Positive pressure ventilation
Fractured sternum • Intense deep pain • Adequate analgesia
• Look for cardiac injury • Cardiac monitor
• Check cardiac enzymes
LUNG AND PLEURA
Simple • Dyspnea • Chest X-ray
pneumothorax • Chest wall Hyperresonant • Chest drain if >5-10% lung
collapse (5th-6th intercostal
space midaxillary line)
Tension • Dyspnea • Do not perform chest X-ray to
pneumothorax • Trachea deviated to opposite side confirm diagnosis
• Chest wall Hyperresonant • Insert large-bore needle into the
• Cardiac arrest chest (2nd intercostal space
midclavicular line) then chest
X-ray and chest drain
Open (sucking) • Open defect in chest wall • Cover defect with sterile
pneumothorax occlusive dressing tapped down
on 3 sides.
Hemothorax • Penetrating injury • Insert large-bore chest drain
• Decreased expansion, stony dull • If >1L blood discharges
percussion, reduced breath sounds immediately patient needs
• + hypoxia and shock for massive thoracotomy
hemothorax (>1L) • If <1L blood discharges
• + dyspnea for small hemothorax (<1L) immediately, observe
• If continuing blood loss of
200ml/h patient needs
thoracotomy
Pulmonary • Hypoxia • May need ventilation
contusion or • ARDS
laceration

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Tracheobronchial • Pneumothorax plus subcutaneous • Surgical repair
disruption emphysema
• Persistent air leak from chest drain
CARDIOVASCULAR
Cardiac • Beck’s triad: Elevated JVP, Decreased • Pericardiocentesis
tamponade blood pressure and muffled heart • Sternotomy and drainage of
(cardiac trauma) sounds pericardium (open repair of
• Pulsus paradoxus heart injury)
• Rise in JVP on inspiration (Kussmaul’s
sign)
Aortic disruption • History of rapid deceleration in high- • Chest X-ray shows widened
velocity injury mediastinum
• Hypotensive despite resuscitation • Diagnosis confirmed with
contrast-enhanced CT
• Open surgical repair
Venous injury • Rare • Surgical repair
• History of penetrating injury
MISCELLANEOUS
Esophagus • Mediastinitis • Urgent surgical repair
• Subcutaneous emphysema in neck • Poor prognosis with
sometimes hydropneumothorax (L>R) mediastinitis
Diaphragm • History of compression force on • Often present late with
(rupture or abdomen herniation of stomach into chest
penetration) • History of penetrating trauma • Reduction of stomach into
abdomen and open repair of
diaphragm

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CHAPTER 6: ESOPHAGEAL PATHOLOGY

ESOPHAGEAL PATHOLOGY
RELEVANT SURGICAL ANATOMY
• The esophagus is a hollow muscular tube that transports food from the pharynx
to the stomach.
• It begins at the lower edge of the cricoid cartilage (lower border of C6 vertebra)
and ends at the esophagogastric junction (T12 vertebra).
• It is 25cm long.
• The esophagus lies anterior to the vertebral column and posterior to the trachea
it travels through the thorax in the posterior mediastinum and empties into the
cardia of the stomach. It lacks serosal layer but is surrounded by a layer of loose
fibroareolar adventitia. Because the esophagus does not have a serosal layer,
esophageal anastomoses are prone to leaks.
• The esophageal mucosa is lined by squamous epithelium that becomes columnar
near the gastroesophageal junction. The next layer encountered moving radially
outward is the submucosa which has the submucous (Meissner) plexus. Next are
2 muscular layers, the inner circular muscle layer and the outer longitudinal
muscle. Sandwiched in between these two muscular layers is the myenteric
(Auerbach) plexus.
• The esophagus is divided into 3 parts:
➢ Upper (cervical esophagus):
o Extends from the cricophayngeus (horizontal part of the inferior
constrictor muscle i.e. lower cricoid border and 6th cervical verterba) to
the level of the carina.
o This part lies in the midline. It descends anterior to the vertebral column
through the superior and posterior mediastinum.
o In the groove between the esophagus and trachea is the recurrent laryngeal
nerve on each side.
o Lateral are common carotid arteries and posterior part of the thyroid gland
o In the lower neck the esophagus deviates to the left.
o The thoracic duct ascends on the left side.

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➢ Middle (thoracic esophagus):
o Extends from the level of the carina to halfway between the carina and
esophagogastric junction
o In the superior mediastinum it is between the trachea and the vertebral
column
o It deviates from the left to the midline and then to the right behind the
aortic arch (pulsating constriction) 25cm from incisors.
o It enters the posterior mediastinum and descends on the right of the
thoracic aorta.
o Below the pulmonary roots the vagus nerves descend in contact with the
esophagus. The left trunk lies on the anterior side and right trunk lies on
the posterior side.
o It inclines to the left, crosses the midline to the right as it enters the
diaphragm at 10th thoracic vertebra to enter the abdomen.
➢ Lower (abdominal esophagus):
o This is the remaining segment that joints the stomach
o It emerges from the right diaphragmatic crus
slightly left to the midline and level with 10 th Recall the vertebral levels at
thoracic vertebra which the following structures
o It grooves its posterior surface to left lobe of the traverse the diaphragm:
liver and curves sharply to the left ending at the T8- inferior vena cava (IVC)
gastric cardiac orifice.
T10- esophagus
o This part is the shortest and is 1.25cm long.
• Initially it is striated muscle and progresses to smooth T12- aorta
muscle in the lower half. It is lined by squamous
“I (IVC) ate (T8) ten (T10)
epithelium. The proximal 1/3 of the esophagus contains
eggs (esophagus) at (aorta)
striated muscle only, the middle 1/3 contains both striated
noon (T120”
and smooth muscle whilst the distal 1/3 contains smooth
muscle only. Clinically significant motility disorders involve smooth muscle in
the lower 2/3 only.

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• The cardia is the junction between the esophagus and
stomach. It contains the squamocolumnar junction
which forms the serrated Z-line that marks an abrupt
change from the tough pale squamous epithelium of the
esophagus to the columnar epithelium of the stomach.
• The lower esophagus is the most important site of
communication between the portal and systemic venous
systems in view of the development of varices in patients
with portal hypertension.
• Three areas of narrowing (evident on barium swallow
are seen), the so-called Esophageal constrictions:
➢ Cricopharyngeal constriction- is at the beginning of
the esophagus, it is 15cm from the incisor teeth
Figure 71: Important clinical endoscopic
➢ Aortic/Bronchial constriction- is where the left measurement of the esophagus in adults
mainstem bronchus and aortic arch cross. It is (Image adapted from First Aid for the
25cm from incisor teeth Surgery Clerkship 2nd Edition)
➢ Diaphragmatic constriction: this is at the hiatus. It
is 40cm from the incisor teeth. This distance serves as an important landmark
in upper gastrointestinal endoscopy.
• The esophagus receives its artery blood supply by the inferior thyroid artery,
esophageal branches of the aorta, gastric arteries and inferior phrenic arteries
➢ The superior and inferior thyroid arteries supply the upper esophagus.
➢ The intercostals, left gastric and phrenic arteries supply the lower esophagus.
• Its venomous drainage is by the inferior thyroid vein, brachiocephalic vein, left
hemiazygos vein, azygos vein, coronary vein, splenic vein and inferior phrenic
vein. Veins are longitudinal and they lie in the submucosal plane in the lower
third and in the muscular plane above.
➢ Venous drainage of the upper esophagus is into the inferior thyroid and
vertebral veins, whereas the mid and lower esophagus drains into the azygos,
hemiazygos and left gastric veins.
• The lymphatics forms extensive plexuses such that lymph flows long distances
in the large submucosal plexus before passing through the muscular coat to
draining lymph nodes.
• These are grouped into 3 main tiers:
➢ Para-esophageal (lie alongside the esophagus)
➢ Mediastinal lymph nodes

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➢ Deep cervical, supraclavicular, tracheobronchial and coeliac nodes (from
above downwards)
• In general lymph drainage from the upper 2 thirds of the esophagus proceeds in
a proximal direction whereas the lower third distally to the subdiaphragmatic
region and coeliac lymph nodes.
• The esophagus receives parasympathatic nerve branches of the vagus nerve.
• 2 nerve plexuses in the esophageal wall (Meissner’s plexus in the submucosa and
Auerbach’s plexus in the muscularis) form networks of ganglion cells which
receive axons from the vagus.
• Two sphincters are present which function as control points:
➢ Upper esophageal sphincter (UES, Cricopharyngeus muscle): prevents the
passage of excess air into the stomach during breathing.
➢ Lower esophageal sphincter (LES):
o It is a physiological sphincter with a high physiological pressure zone
located in the lower end of the esophagus in the terminal 4cm with a
resting pressure of 10-25mmHg.
o It relaxes with initiation of pharyngeal phase of swallowing and prevents
reflex of gastric contents when swallowing is not occurring.
o Esophageal peristalsis accompanying swallowing is termed primary
peristalsis. Secondary peristalsis can be initiated by the esophageal
musculature without the pharyngeal phase to clear the esophagus of any
substance left behind from primary peristalsis.
o This LES prevents reflux of gastric and duodenal contents and is
influenced by food, gastric distension, gastric pathology, smoking, GI
hormones and alcohol.

RELEVANT PHYSIOLOGY
• Swallowing or deglutition refers to the passage of food from the oral cavity into
the stomach.
• Swallowing is divided into 3 phases:
➢ Voluntary (oral) phase: initiates swallowing process
➢ Pharyngeal phase: is involuntary and constitutes passage of food through the
pharynx into the esophagus.
➢ Esophageal phase: involuntary phase that transports food from the pharynx to
the stomach.
• During the voluntary (oral) stage the food bolus is voluntarily squeezed or rolled
posteriorly into the pharynx by pressure of the tongue upwards and backwards

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against the palate. From here on swallowing becomes entirely or almost entirely
automatic and ordinarily cannot be stopped.
• The pharyngeal stage of swallowing is caused by a swallowing reflex
➢ Receptors present around the opening of the pharynx (especially over the
tonsillar pillars) are stimulated when the bolus moves from the mouth into the
pharynx and initiate the reflex activity.
➢ Afferents impulses are carried through the trigeminal nerve, glossopharyngeal
and vagus nerve to deglutition centers in the medulla oblongata and lower
pons (i.e. the nucleus of the tractus solitaries and nucleus ambiguous)
➢ Efferent impulses through the trigeminal, glossopharyngeal, vagus and
hypoglossal cause muscular contraction.
➢ The soft palate is pulled upwards to close the posterior nares preventing reflux
of food into the nasal cavities.
➢ The palatopharyngeal folds on each side of the pharynx are pulled medially to
form a sagittal slit through which the food must pass into the posterior pharynx
(the slit performs a selective action allowing food that has been masticated
sufficiently to pass with ease. Because this stage of swallowing lasts less than
1 second, any large object is usually impeded too much to pass into the
esophagus.)
➢ The vocal cords of the larynx are strongly approximated and the larynx is
pulled upwards and anterior by the neck muscles. These actions combined
with the presence of ligaments prevent upward movement of the epiglottis
causing the epiglottis to swing backward over the opening of the larynx. All
these effects acting together prevent passage of food into the nose and trachea.
➢ The upward movement of the larynx also pulls up and enlarges the opening
of the esophagus, at the same time the upper esophageal (pharyngoesophageal
sphincter) relaxing allowing food into the esophagus. Between swallows, the
sphincter remains strongly contracted, thereby preventing air from going into
the esophagus during respiration.
• The pharyngeal phase occurs in less than 6 seconds during which respiration is
inhibited.
• During the esophageal stage food is propelled by 2 types peristalsis:
➢ Primary peristalsis: this is a continuation of the peristaltic wave that begins in
the pharynx and spreads into the esophagus during the pharyngeal phase. This
wave passes all the way from the pharynx to the stomach in 8 to 10 seconds.
➢ Secondary peristalsis: this is a result of distention of the esophagus by retained
food (as primary peristalsis fails to move all the food in the esophagus). It is

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initiated by the intrinsic circuits in the myenteric plexus and partly by reflexes
that begin in the pharynx and are then transmitted upward through the vagal
afferent fibers to the medulla and back to the esophagus via the
glossopharyngeal and vagus.
o The musculature of the pharyngeal wall and upper third of the esophagus
is striated and thus peristaltic waves in this region are controlled by
skeletal nerve impulses from glossopharyngeal and vagus nerves.
o In the lower third of the esophagus the musculature is smooth muscle but
this portion of the esophagus is also strongly controlled by the vagus
through connections within the esophageal myenteric plexus.
o When the esophageal peristaltic wave approaches the stomach, a wave of
relaxation transmitted through myenteric inhibitory neurons precedes the
peristalsis causing the stomach to relax and opening the lower esophageal
(Cardiac) sphincter (receptive relaxation)
o After food enters the stomach the cardiac sphincter contracts to prevent
regurgitation of food in the esophagus. With this the esophageal phase of
deglutition is completed.
• Tertiary esophageal contractions can occur spontaneously and are non-
propulsive. They are encountered in various esophageal motility disorders but
also occur in healthy individual.

DYSPHAGIA
• This is difficulty in swallowing.
• Painful swallowing is known as odynophagia.
• Dysphagia with associated hoarseness of voice may present in advanced
pharyngeal or post cricoid carcinomas. At late stage, laryngeal carcinoma also
causes dysphagia along with hoarseness of voice.
• Dysphagia for solids implies significant disease, whereas dysphagia for liquids
only is more likely to be of functional origin (esophageal motility disorder) in
which case it may be intermittent.
• Persistent and progressive dysphagia indicates mechanical narrowing of the
esophageal lumen and is usually associated with regurgitation. Eventually, the
patient is unable to swallow saliva and exhibits constant drooling.
• Obstructive dysphagia is first experienced when 20-30% of esophageal lumen is
lost, most patients usually present when 50% of the esophageal lumen is
compromised.

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• When there is a problem with swallowing in the voluntary (oral or pharyngeal)
phases, patients will usually say that they cannot swallow properly but they do
not characteristically describe ‘food sticking’. Instead, when they try to initiate a
conscious swallow, food fails to enter the esophagus, stays in the mouth or enters
the airways causing coughing or spluttering.
• Esophageal dysphagia occurs in the involuntary phase and is characterized by a
sensation of food sticking.

CLASSIFICATION
• Dysphagia may be classified by
➢ Onset
o Acute: due to foreign body impaction or acute infection
o Chronic: stricture or carcinoma etc.
➢ Duration
o Intermittent
o Progressive
➢ Location
o Oropharyngeal: Pathology in voluntary/pharyngeal phase of the
swallowing wherein patient also develops cough while swallowing.
o Esophageal: Pathology in esophageal involuntary phase of swallowing
characterized by food getting stuck in the pathway. But site of “food
getting stuck” feeling is not relevant.

CAUSES
• They can be divided into
➢ Extraluminal causes
➢ Intramural causes
➢ Luminal
EXTRALUMINAL CAUSES
• Mediastinal nodes- secondaries/ lymphoma/ TB
• Mediastinitis/ mass
• Aortic aneurysm, Thoracic artery aneurysm
• Rolling hiatus hernia
• Thyroid enlargement- malignant: it is uncommon to develop dysphagia in a
thyroid swelling. There will always be dyspnea when dysphagia develops. Large

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malignant thyroid or anaplastic thyroid can cause dysphagia with dyspnea or
stridor. Retrosternal goiters may also present with dysphagia.
• Dysphagia lusoria: the word Lusoria means “sport of nature” in Latin. Dysphagia
lusoria is a congenital vascular anomaly of aortic root.
➢ Aortic arch anormalies are:
o Double arch (40%)
o Right and left ligamentum arteriosum (25%)
o Anomalous innominate or common carotid artery
o Aberrant right subclavian artery (10%)
➢ All patient having this anomaly (dysphagia lusoria) have got an aberrant right
subclavian artery in a transposed position arising from descending aorta that
courses posterior to esophagus. Often there will be complete vascular ring
around trachea and esophagus.
➢ Commonly they are asymptomatic but may present with dysphagia, chest
pain, stridor, wheeze, recurrent respiratory infection (usually presents after the
age of 40).
➢ Investigation: Chest X-ray, barium swallow (T4 level diagonal impression),
endoscopy (shows pulsating extraluminal compressive mass), MRI, CT chest
➢ Treatment is reconstruction or ligation of aberrant right subclavian artery by
sternotomy/ by neck approach.
• Congenital anomalies
• Pharyngeal pouch (Zenker’s diverticulum)
• Malignancy

INTRAMURAL CAUSES (ESOPHAGUS AND OTHER

AREAS)
• Carcinoma esophagus: here dysphagia is of short duration and progressive. 2/3
of the lumen should be blocked by tumor to develop dysphagia. It is also
associated with weight loss, anorexia and anemia.
• Corrosive/TB/inflammatory/congenital stricture esophagus
• Benign or malignant strictures, GERD (gastroesophageal reflux disease)
• Achalasia cardia: failure of the lower esophageal sphincter to relax. Dysphagia is
more with liquids than solids. There is frequent regurgitation, recurrent chest
infections due to aspiration. It is usually has a long history.

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• Plummer-Vinson syndrome (esophageal web): iron deficiency anemia, glossitis,
cheilosis and esophageal webs. Iron deficiency anemia leads to desquamated
epithelium. It is common in middle-aged women.
• Esophageal diverticulum
• Carcinoma posterior 1/3rd of tongue/pharynx
• Diffuse esophageal spasm: they are in-coordinated contractions of the esophagus
causing chest pain or dysphagia. It is common in distal 2/3 rd of the esophagus.
Hypertrophy of circular muscle fibers with very high persistent pressure of 400-
500mmHg is specific. Treatment is calcium channel blockers, vasodilators,
endoscopic dilation and extended esophageal surgical myotomy up to the aortic
arch (very useful especially for dysphagia, not much for chest pain)
• Esophageal ring (Schatzki ring): ring of mucosal tissue
• Systemic sclerosis
• Congenital anomalies
• Retropharyngeal abscess/ peritonsillar abscess (Quinsy)/ acute tonsillitis/
pharyngitis

LUMINAL CAUSES
• Foreign body in esophagus- coin/ dentures/ fish or meat bone
• Infection: candidiasis, pharyngitis, retropharyngeal abscess
• Esophagitis
• Polyps
• Other causes: Cranial causes (neurological)
➢ Bulbar palsy/pseudobulbar palsy, Infarction/hemiplegia
➢ Vertebro basilar insufficiency
COMMON CAUSES OF DYSPAGIA RARE CAUSES OF DYSPHAGIA
• GERD • Diffuse esophageal spasm
• Carcinoma esophagus • Esophageal diverticula
• Plummer-Vinson syndrome • Chagas’ disease
• Mediastinal swellings-Primary • Dysphagia lusoria
tumors/nodal mass either lymphoma or • Thyroid swelling
secondaries or tuberculosis • Boerhaave’s syndrome: vertical full thickness tear
of lower esophagus due to vomiting with closed
glottis. It is often life threatening and emergency
• Neurological (stroke, bulbar palsy, motor neuron
disease, Parkinson’s disease etc.)

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• Congenital anomalies of esophagus
• Drug induce: KCL, quinine, NSAIDs
• Mediastinal fibrosis
EVALUATION OF THE PATIENT
HISTORY
• Demographics: Name, age, sex, address, occupation, religion
• Symptoms:
➢ When did it start?
➢ Is it new or long standing?
➢ Is it rapidly worsening or relatively constant? (Intermittent- spasms,
constant./worsening- malignant stricture or both-achalasia)
➢ Was there difficult swallowing solids or liquids from the start? (if it started
with liquids, think motility disorders-systemic sclerosis, myasthenia gravis,
bulbar palsy or achalasia or pharyngeal problems. If it started with solids think
mechanical problems e.g. benign or malignant stricture)
➢ Is it worse on solids from the start?
➢ Is there any difficulty in making swallowing movement?
(bulbar/pseudobulbar palsy)
➢ At which level does food stick?
➢ Is swallowing painful? (cancer, ulcer, esophageal spasm- relieved by glyceryl
trinitrate)
➢ Is dysphagia intermittent or is it constant and getting worse?
➢ Can it be relieved by anything e.g. warm drinks?
➢ Is it associated with coughing (tracho-esophageal fistula)?
➢ Does the neck bulge or gurgle on drinking? (Pharyngeal pouch)
➢ Any chest pain? Heart burn? (GERD)
➢ Coughing on lying? (achalasia, pharyngeal pouch)
➢ Regurgitation or substance cramp?
➢ Any significant weight loss? (Consequence of poor intake or sign of
malignancy)
• Predisposing factors:
➢ History of alcohol or smoking
➢ Diet- history of hot foods (chili)
➢ Any gastro-esophageal reflux disease
➢ History of taking corrosive substance (Accidental or intentional suicidal)
➢ History of surgery (strictures)

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➢ History of radiotherapy (Ca esophagus)
➢ Immune suppression

INVESTIGATIONS
• Diagnostic:
➢ Chest X-ray: shows mediastinal mass lesion/foreign body
➢ Barium swallow: may show irregular filling defect or extrinsic compression.
➢ Esophageal manometry: in achalasia cardia/GERD
➢ 24 hours pH monitoring: ideal and most accurate for GERD. Small pH probe
(transnasal catheter) is passed into the distal esophagus 5cm proximal to upper
margin of the LOS under manometry guidance. The probe is connected to a
digital recorder worn by the patient for 2 hours. Record is analysed using a
computer. A pH less than 4 for more than 4% of total 24 hours period (more
than neart to one hour in total in 24 hours) is pathological reflux. It is often
assessed by scoring system. Radio-telemetry pH probes are used not without
any nasal tube. It is passed and placed on the esophageal wall using
endoscope.
➢ Esophagoscopy: once lesion is detected, it is treated accordingly. Biopsy from
lesions, endotherapy if needed should be carried out (like F/B removal,
stricture dilatation, sclerotherapy)
➢ Endosonography: useful in many conditions. It can assess the site, layers of
esophagus, nodes, spread etc. properly. Different layers are seen as alternating
hyperechoic and hypoechoic bands.
➢ Ultrasound: to see abdominal nodes, liver/ascites
➢ CT scan: identifies the anatomical location of the cause
(nodes/tumors/aorta/cardiac causes/congenital). Extent, spread, nodal status,
size and operability of the tumor also well-assessed
➢ MRI
• Full blood count: hematocrit, anemia is common with tumors than reflux
• Liver function test: to exclude hepatic disease

TREATMENT
• Depends on cause- modified Heller’s myotomy, esophageal resection, dilatation,
F/B removal etc.

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GASTROESOPHAGEAL REFLUX DISEASE

ESOPHAGITIS

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ESOPHAGEAL STRICTURES
• This is local, stenotic regions within the lumen of the esophagus.
• They are usually as a result of an inflammatory or neoplastic process.
• Benign strictures arise most commonly secondary to long-standing reflux disease
and less commonly esophageal/gastric resections or ingestion of corrosive
agents.

ETIOLOGY AND RISK FACTORS

• Corrosive/caustic esophagitis (most common):
➢ Mainly due to ingestion of alkali (Lye Stricture-Lye is a strong alkali sodium
hydroxide) sodium hydroxide, occasionally due to acid (sulphuric acid, nitric
acid). Acid commonly damages the stomach.
➢ Ingestion of corrosive substances can be accidental (children) or suicidal
(adults)
➢ It causes extensive inflammation of the mucosa with periesophagitis which if
not treated leads to multiple strictures in the esophagus.
➢ Sometimes it causes severe life-threatening necrotizing lesion which requires
immediate surgical intervention.
➢ Alkali is odorless and tasteless and so large volume is ingested. Alkali causes
liquefaction, saponification and thrombosis of vessels and later leading to
fibrosis and stricture.
➢ Acid causes intense pylorospasm, antral pooling of acid, coagulation necrosis
and eschar formation.
➢ Severity depends on type of agent, its concentration and volume.
• Long standing GERD (peptic stricture/esophagitis induced)
• Radiation esophagitis
• Infectious esophagitis e.g. Tuberculosis
• Foreign body
• Post-surgical
• Congenital
• Drugs like tetracycline, vitamin C
• Sclerotherapy for bleeding varices

CLINICAL FEATURES
• Small strictures may remain asymptomatic however some may obstruct the
esophageal lumen significantly causing progressive dysphagia for solids.

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• Odynophagia may or may not be present.
• Differential diagnosis being esophagitis due to candidiasis especially in HIV
positive patients.
• Features of esophageal corrosive lesion:
➢ Acute/ immediate: lasts for 3 weeks
o Severe pain, shock, laryngeal edema
o Mediastinitis, septicemia, hemorrhage, perforation
➢ Late/chronic
o Dysphagia
o Stricture-50%
o Severe malnutrition
o Recurrent respiratory infection
o Esophageal shortening
o Malignant changes
o Tracheo-esophageal fistula formation
• Corrosive strictures can be multiple. Damage is more in lower 1/3rd of the
esophagus.
• Phases of tissue injury in corrosive ingestion:
➢ Phase 1: Acute necrosis (1-4 days)
➢ Phase 2: Ulceration-Granulation (4-12 days)
➢ Phase 3: Cicatrisation and scarring (3weeks-6 months)
• Degrees of burns after corrosive esophageal and gastric burns:
➢ 1st degree: mucosal hyperemia and edema
➢ 2nd degree: small bleeding, exudates, ulcers, pseudomembrane
➢ 3rd degree: mucosal slough, deep ulcers, massive bleed, complete
obstruction, charring, perforation

DIAGNOSIS
• Initial evaluation via barium swallow may reveal the presence of
stricture. It establishes the length and width of the stricture. It shows a
Cork-screw esophagus (differential diagnosis: esophageal spasm).
• Esophagoscopy is necessary in all cases, since the stricture should be
evaluate for malignancy, also useful to determine the appropriate
treatment. It should be done with caution as the danger of perforation
is high. Figure 72: Cork-
Screw esophagus

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MANAGEMENT
• The esophagus is visualized endoscopically and bougie dilators are carefully
passed through the stricture, each successful dilation is done with progressively
larger dilator.
• Dysphagia is relieved in most cases following adequate dilatation of the
esophageal lumen.
• The principal aim of dilatation is to stretch the stricture gradually to achieve an
esophageal lumen of 10-15mm in diameter.
• The most feared complication of dilatation is esophageal rupture. Other
complications include hemorrhage and bacteremia.
• Management of corrosive esophageal strictures:
➢ Acute phase management:
o Neutralize with vinegar or citrus food if it is alkali ingestion (if pH of
solution <11.5 then damage is less). With acids give antacids, milk, egg
whites. Early endoscopy is needed to assess the severity and extent.
o Emetics and sodium bicarbonate are avoided as they may precipitate
perforation.
o 1st degree burns:
- 48 hours observation
- Oral feeds are started once patients swallows saliva painlessly
- Regular follow-up endoscopy at 1st, 2nd and 8th month. Stricture if
formed can be identified by this time
o 2 and 3rd degree:
nd

- Fluid therapy, Antibiotics, nutrition, resuscitation, PPIs, aerosolized

steroirds
- Fiberoptic guided airway intubation if needed/tracheostomy,
endoscopic esophageal stenting, feeding jejunostomy, laparoscopy or
evaluation
- Unstable patients have high mortality. Laparotomy is done in such
patients. If esophagus and stomach shows full thickness necrosis,
resection of these parts is done and end cervical esophagostomy with
jejunostomy is done. When in doubt re-exploration for second look is
done after 36-58 hours to assess the stomach.
➢ Careful early gentle repeated endoscopy is mandatory
➢ Though advocated often for 2-3 weeks, use of steroids is controversial and
under debate.

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➢ Antibiotics if there are chances of aspiration or perforation
➢ Regular esophageal dilatation is done for strictures. The stricture is dilated
endoscopically using guidewire. Dilators are solid type with gradual increase
in diameters. Often radiologic C-ARM guidance is needed to pass the guide
wire into the stomach. Dilatation should be done up to a minimum 16 mm
diameter. Pneumatic or balloon dilatation is also practiced. Gum elastic
dilators, Savary-Gilliard dilators, balloon dilators are other dilators used.
Earlier, blind dilatation using esophageal bougies of increased diameters was
the practice which is followed even now in many places but changes of
perforation are higher.
➢ Esophageal resection in corrosive strictures is technically difficult and may be
hazardous. Esophageal bypass is better and easier and following later by
regular endoscopic surveillance for malignant transformation (5%). Colon is
used as replacing conduit as stomach itself may be diseased in corrosive
pathology.
➢ In multiple strictures esophageal resection and colonic transposition may be
advocated if risk of malignancy is considered.
• Malignance can develop in corrosive strictures (5%)

BARRETT’S ESOPHAGUS

ESOPHAGEAL HERNIA

ESOPHAGEAL DIVERTICULAE

PLUMMER VINSON

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ACHALASIA CARDIA (CARDIOSPASM)
• Achalasia (From the Greek working meaning failure to relax) is a motility
disorder characterized by failure of the lower portion of the esophagus to relax
during swallowing.
• It is the most common primary esophageal motility disorder caused by
inflammation of the myenteric plexus of Auerbach leading to fibrosis with
decrease or loss of the myenteric ganglion cells and selective destruction of non-
cholinergic, non-adrenergic inhibitory neurons. There is reduce nitric oxide and
VIP (mediators of LES relaxation)
• The resulting dysphagia is due to 3 mechanisms:
➢ Complete absence of peristalsis in the esophageal body
➢ Incomplete/impaired relaxation of the LES after swallowing
➢ Increased resting tone of the LES (>25mmHg)
• There is elevation of intraluminal esophageal pressure, esophageal dilation and
subsequent progressive loss of normal swallowing mechanisms- a functional
holdup of ingested material.
• Achalasia is due to loss of the ganglion cells in the myenteric (Auerbach’s)
plexus, the cause of which is unknown however in South America, chronic
infection with the parasite Trypanosoma cruzi causes Chagas’ disease which has
marked clinical similarities to achalasia.

ETIOLOGY
• There is absence or less numbered ganglions in myenteric plexus
➢ Stress
➢ Vitamin B1 deficiency
➢ Chaga’s disease (T. cruzi)
➢ Diffuse esophageal spasm (corkscrew esophagus)
➢ Most commonly it is idiopathic and there is degermation of Auerbach’s
myenteric plexus along the entire length of the esophagus

PATHOLOGY
• The dilated esophagus contains few ganglion cells (contrast with Hirschsprung’s
disease of the colon where the dilated colon contains normal ganglion cells
proximal to a constricted aganglionic segment).
• Histology of muscle specimens shows a reduction in the number of ganglion cells
(and mainly inhibitory neurons) with a variable degree of chronic inflammation.

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• The mucosa of the esophagus often shows esophagitis with mucosal ulceration
secondary to bacterial proliferation.
• In ‘vigorous achalasia’ which may be an early stage of the disease there is
inflammation and neural fibrosis but normal number of ganglion cells.
• In the early stages the esophagus is of normal caliber and still exhibits contractile
(although non-peristaltic) activity. In some patients these uncoordinated
contractions result in pain as much as a sense of food sticking.
• With time the esophagus dilates and contractions disappear, so that the esophagus
empties mainly by the hydrostatic pressure of its contents. This is nearly always
incomplete, leaving residual food and fluid. The gas bubble in the stomach is
frequently absent as no bolus with its accompanying normal gas passes through
the sphincter.
• The ‘megaesophagus’ becomes tortuous with a persistent retention esophagitis
due to fermentation of food residues and this may account for the increased
incidence of carcinoma of the esophagus.
• ‘Pseudoachalasia’ is an achalasia-like disorder that is usually produced by
adenocarcinoma of the cardia but has also been described in relation to benign
tumors at this level. It has been presumed that the inability of the LES to relax is
linked to the loss of body peristalsis but other cancers outside the esophagus
(bronchus, pancreas) have also been associated with pseudoachalasia.

CLINICAL FEATURES
• Most common in middle life (20-50 years) but can occur at any age.
• Typically presents as generally ill patient with dysphagia, although pain (often
mistaken for reflux) is common in the early stages. Patients often present late and
having had relatively mild symptoms remain untreated for many years.
• Dysphagia for both solids and liquids (there is dysphagia to liquids first). Initially
it is intermittent, of variable severity and may be aggravated by emotional stress
and cold liquids.
• Regurgitation of food is frequent and there may be overspill into the trachea,
especially at night.
• Severe halitosis (due to the decomposition of stagnant food within the esophagus)
• Chest pain occurs in early stage.
• Classic triad of achalasia:
➢ Dysphagia
➢ Regurgitation

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➢ Weight loss
• Leucoplakia is commonly encountered in advanced cases.
• Achalasia with diffuse esophageal spasm is called as ‘vigorous achalasia’.
• GERD produces a sour taste and a gush of saliva due to the
presence of hydrochloride from the gastric acid (water brash)
while achalasia does not. Heartburn is common in 50% of
patient.
• Walking while eating, chin thrusting, neck and shoulder
extension, Valsalva maneuver facilitates emptying of food
from the esophagus.
• Malnutrition, lung abscess formation, odynophagia and
weight loss may also be present.

STAGING Figure 73: Endoscopic view of

• I-proximal dilatation <4 cm achalasia
• II- dilatation between 4-6 cm
• III- dilation >6cm
• IV-sigmoid dilatation

INVESTIGATIONS
• Lateral upright chest X-ray: may reveal a dilated
esophagus and the presence of air-fluid levels in the
posterior mediastinum (double mediastinal strip of dilated
esophagus). PA CXR may show patches of pneumonia.
• Endoscopy may show a tight cardia and food residue in the
esophagus.
• Barium swallow is diagnostic and will show:
➢ Pencil like smooth narrowing of the lower esophagus-
bird’s beak sign (rat tail sign/Steeple sign) due to the
collection of contrast material in the proximal dilated
segment and the passage of a small amount of contrast
through the narrowed LES.
Figure 74: Sigmoid esophagus in achalasia
➢ Grossly distended esophagus proximal to a cardia- Barium X-ray and endoscopic view
tapering stricture at the distal end of the (Image adapted from SRB’s Manual of Surgery
esophagus. 4ed)
➢ Absence of fundic gas bubble
➢ Sigmoid esophagus or megaesophagus

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• The typical features of well-developed achalasia are
often absent and endoscopy and radiology can be
normal
• Esophageal motility study will confirm non-peristaltic
contractions, incomplete LES relaxation and increased
LES tone.
➢ Manometry (Esophageal manometry): there is no
peristalsis. There is raised resting pressure in the
esophagus and the lower end does not relax on
swallowing. This establishes a firm diagnosis.
• Esophagoscopy is indicated to rule out mass Figure 75: Barium study demonstrating a dilated
lesions or strictures and to obtain specimens for esophagus and smooth, tapered gastroesophageal
junction, typical of achalasia (Adapted from First
biopsy. Malignant tumors of the Aid for the surgery Clerkship 2nd Ed)
gastroesophageal junction can mimic the
finding of achalasia (pseudoachalasia)

DIFFERENTIAL DIAGNOSIS
• Carcinoma esophagus
• Stricture esophagus
• Scleroderma

MANAGEMENT
• Achalasia responds well to treatment.
• Medical management:
➢ Drugs that relax the LES- nitrates, calcium
channel blockers (nifedipine, verapamil) and
antispasmodics. Calcium channel blockers
are ineffective for long-term use however, Figure 76: Barium swallow X-ray showing
features of achalasia cardia (image adapted from
sublingual nifedipine may be useful for SRB’s Manual of Surgery 4th Ed)
transient relief of symptoms if definitive
treatment is postponed.
➢ Botulinum toxin (Botox): this is done by endoscopic injection into the LES.
It acts by interfering with cholinergic excitatory neural activity at the LES. It
binds to presynaptic receptors and irreversibly inhibits axonal acetylcholine
release. Symptomatic improvement is obtained in 50% but the effect is not
lasting. The effect is not permanent, and the injection usually has to be

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repeated after a few months. For this reason, its use is restricted to elderly
patients with other comorbidities.
• Surgical management: Esophagomyotomy (Heller’s myotomy) with or without
fundoplication is the treatment of choice for achalasia.
➢ This involves cutting the muscle of the LES and cardia. The major
complication is GERD and most surgeons therefore add a partial anterior
fundoplication (Heller-Dor’s operation). The procedure is ideally suited to
minimal access laparoscopic approach and most surgeons use intraoperative
endoscopy to judge the extent of the myotomy and to ensure that the narrow
segment is abolished. It is successful in more than 90% of cases and may be
used after failed dilatation.
➢ Indications for Heller’s cardiomyotomy:
o Children and young adults
o After failure of pneumatic dilation or botulinum toxin injection therapy
o Patients with co-existent pathology requiring surgical intervention
o Patient’s preference
• Esophagomyotomy: Esopphagus is exposed via a transthoracic (left
thoracotomy), transabdominal, thorascopic or laparoscopic technique. The tunica
muscularis of the esophagus is incised distally with extension to the LES.
Complete division of the LES necessitates the addition of an antireflux procedure
such as Nissen 360o fundoplication or partial fundoplication
• Endoscopic dilatation: has a lower success rate and a higher complication rate. It
involves inserting a balloon or progressively larger sized dilators through the
narrowed lumen which causes tearing of the esophageal smooth muscle and
decreases the competency of the LES.
➢ Note: Esophageal perforation is four times more likely following dilatation
compared to esophagomyotomy.
➢ With a 30-mm balloon, the incidence of perforation should be less than 0.5%.
The risk of perforation increases with bigger balloons and they should be used
cautiously for progressive dilatation over a period of weeks.
➢ Forceful dilation is curative in 75-85% of cases.

COMPLICATIONS
• Risk of squamous cell carcinoma is as high as 10% in patients with long-standing
achalasia (duration 15-25 years).
• Patients may also develop pulmonary complications: Aspiration pneumonia,
Bronchiectasis, Asthma due to reflux and aspiration

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ESOPHAGEAL PERFORATIONS

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ESOPHAGEAL CARCINOMA
• Esophageal neoplasms are almost always malignant.
• Benign tumors account for fewer than 1% of cases and are usually leiomyomas
or congenital cysts.
➢ The only important benign tumor of the esophagus is leiomyoma, which has
a predilection for the lower esophagus.
• The majority of benign tumors are small and asymptomatic but larger ones can
project into the lumen of the esophagus and cause dysphagia. Symptomatic
benign esophageal neoplasms are treated with local resection or enucleation.
• Esophageal carcinoma is the 6th most common cancer in the world accounting for
7% of all GI malignancies.
• Most malignant esophageal neoplasms seen worldwide are of squamous cell
histologic types (90%) whereas adenocarcinoma histology predominates in
industrialized nations.
➢ The increasing prevalence of adenocarcinomas (due to Barrett’s) as compared
to what was mostly squamous cell carcinoma is shifting the epidemiology of
esophageal cancer.
➢ Other tumors of the esophagus are less common (leiomyomas, melanomas,
carcinoids, lymphomas)
• Most cases of adenocarcinoma arise in the distal third or gastroesophageal
junction (80%).
• Esophageal carcinoma is common in
➢ Middle third (50%)
➢ Lower third (33%)
➢ Upper third (17%)
• Metastases are usually to liver, lung, and bones with at least 35% of patients with
distant metastases at the time of diagnosis.
• Early diagnosis is only incidental or discovered on screening studies.
• Prognosis is poor with an overall 5-year survival rate of only 5%.
• In places with high soil nitrosamine content, the prevalence of esophageal cancer
is almost 1% of adults. Esophageal cancer is more common in men (5:1) between
50 and 70 years of age. Whites are affected more.

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RISK FACTORS
• Environmental
➢ Tobacco
➢ Alcohol
➢ Food additives (nitrates in smoked and pickled meats)
➢ Diet deficiency (Vitamin A, C, riboflavin)
➢ Mycotoxin
• Esophageal disorders
➢ Predisposition to squamous cell cancer
o Achalasia
o Plummer-Vinson syndrome
o Esophageal webs
o Strictures associated with lye ingestion and human papilloma virus
infection
o Chronic esophagitis
➢ Predisposition to adenocarcinoma
o GERD/Barrett’s esophagus
• History of radiation therapy to the mediastinum
• Tylosis/Palmoplantar keratoderma (this is an inherited disease with thickening of
the skin of palm and sole)
• Note: Vitamins (A, B12, C, E, folic acid and riboflavin) and trace elements (iron,
zinc, selenium, and molybdenum) are thought to be protective.

PATHOGENESIS
• Mucosal insult seems to be a common pathway toward the genesis of esophageal
cancer.
• Chronic ingestion of extremely hot liquids, esophageal burns from acid or base
ingestions, radiation-induced esophagitis and reflex esophagitis are all implicated
in causing esophageal cancer.
• Alcohol, smoking, nitrosamines, and malnutrition/vitamin deficiency also play a
role in cancer development.
• Barrett esophagus which occurs when the normal squamous epithelium becomes
columnar in response to injury from acid reflux, is considered a premalignant
lesion.

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• About 10% of patients with Barrett esophagus will develop adenocarcinoma. In
patients with achalasia about 5% will develop squamous cell carcinoma of the
esophagus.
• Because there is no serosal layer covering the esophagus, disease is often locally
advanced or metastatic on presentation, leading to poor overall survival rates.

PATHOLOGY
• Squamous cell carcinoma is the common histological type world-wide.
• Adenocarcinoma especially of the lower esophagus and gastro-esophageal
junction is commoner in the West
• Macroscopically the disease presents as:
➢ Stenosing
➢ Polypoid (fungating, protruded)
➢ Ulcerative (excavated)
• Growth of esophageal cancer (squamous cell carcinoma or adenocarcinoma)
occurs by intra-esophageal spread, direct extension and lymphatic or
hematogenous metastases.
• Squamous cell carcinoma more typically invades adjacent structures compared
with adenocarcinoma.
• Distant metastases are present in 25-30% of patients at the time of diagnosis.
• The liver, lungs and bones are the most frequent sites. Early cancer of the
esophagus (confined to mucosa/submucosa) is only detected by screening. Both
types spread to regional lymph nodes once the muscle coat is involved.
• Spread:
➢ Direct:
o Lack of serosal layer in esophagus favors local extension. In upper third
it spreads through muscular layer and get adherent to left main bronchus,
trachea, and left recurrent laryngeal nerve (Causes hoarseness), aorta or
its branches (causes fatal hemorrhage but rare)
o It may perforate and cause mediastinitis
➢ Lymphatic:
o It spreads both by lymphatic permeation and lymphatic embolization
o It can cause satellite nodules elsewhere in the esophagus away from the
main tumor
o Above in the neck, it spreads to supravlavicular lymph nodes
o In thorax, it spreads to paraesophageal, tracheobronchial lymph nodes to
subdiaphragmatic lymph nodes

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o In abdomen it spreads to coeliac lymph nodes
➢ Blood: spreads to liver, lungs, brain and bones

CLINICAL FEATURES
• At time of diagnosis most patients have advanced disease and are not surgical
candidates for curative resection.
• The lack of serosal lining and rich submucosal lymphatic network of the
esophagus allows early extension of tumor into adjacent mediastinal structures
as well as early local lymph node spread.
• About 75% of patients have mediastinal or Extrathoracic lymph node metastases
at the time of diagnosis
• Classic presentation of distal esophageal adenocarcinoma:
➢ Old man with a history of GERD
➢ Progressive dysphagia to solids initially and then to liquids (in 74% of
patients, it is due to invasion of serosal layer). Note: Dysphagia does not
usually develop until 60% of the esophageal lumen is obstructed.
o Progressive dysphagia starts with meat, then other solids, then soft foods,
eventually liquids and finally (in several months) saliva.
o Esophageal obstruction results in malnutrition, weight loss, regurgitation
and occasionally aspiration.
• Typically, patients feel well and have no other symptoms. Some may have
➢ Non-specific GI complaints
➢ Mild weight loss, easy fatigability and weakness (often related to diminished
caloric intake resulting from obstructive symptoms than to cachexia from
metastatic disease).
➢ Chest pain
➢ Odynophagia
➢ Invasion of a recurrent laryngeal nerve causing hoarseness from vocal cord
paralysis
➢ Features of broncho-esophageal fistula in carcinoma of upper third of the
esophagus (30%)
➢ Substernal/abdominal pain
• Patients with esophageal squamous cell carcinoma often have a history of heavy
alcohol and tobacco use and present with more pronounced symptoms owing to
more advanced disease.

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• Physical examination is non-specific and patients appear well unless if significant
metastatic disease is present. Supraclavicular lymphadenopathy at presentation is
rare.
• With advanced disease, the patient will appear cachectic, supraclavicular
lymphadenopathy may be present as may signs of distant metastasis. May
develop symptoms depending on local invasion (stridor, coughing, aspiration
pneumonia, hemoptysis, vocal cord/recurrent laryngeal nerve paralysis).
➢ Hoarseness of voice- recurrent laryngeal nerve palsy
➢ Hiccough- phrenic nerve involvement
➢ Horner’s syndrome- sympathetic fibers involved
➢ Supraclavicular lymph node enlargement
➢ Distant mets e.g. spinal pain

DIAGNOSIS
• Diagnostic investigations:
➢ Barium swallow: detects lesion in 96% of patients.
o Barium swallow must precede the endoscopy to help prevent inadvertent
perforation.
o Findings range from small mucosal defects to “apple core” lesion to
complete obstruction (Shouldering signs and irregular filling defect)
o Irregular stricture with shouldering and moderate proximal dilation
➢ Flexible Endoscopy and biopsy for definitive diagnosis. If Barrett esophagitis
alone is noted, the extent of disease can be determined and biopsies performed
to look for dysplasia or carcinoma in situ.
o ¾ of adenocarcinoma is found in the distal esophagus, most Squamous
cell carcinoma are found in the middle and lower third. The cervical
esophagus is an uncommon site for disease.
➢ Endoscopic ultrasound is used for primary tumor staging and regional lymph
node status. Ultrasound depicts the normal five layers of the esophagus and
can accurately determine the T status in 85% to 90% of patients. Fine needle
aspiration biopsy of abnormal appearance lymph nodes under ultrasound
guidance may be performed.
➢ CT scan and PET scan is best at evaluation of regional and distant disease.
Furthermore, CT scan assess operability but most cases can only get palliative
(rather than curative) surgery.

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Figure 77: A: contrast radiograph showing the typical “Apple core” lesion of carcinoma of the
middle 1/3 of esophagus. B: Ragged edge seen in carcinoma of the distal esophagus (Image from
Blueprints Surgery)

Figure 78: (A) Squamous carcinoma of the middle third of the esophagus. (B) adenocarcinoma
of lower third of the esophagus

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• Supportive: for general fitness and for procedures
➢ Full blood count
➢ Chest X-rays: to check for aspiration pneumonia
➢ Abdominal ultrasound: to look for liver and lymph
nodes status in abdomen
➢ Liver function tests
➢ Urea, electrolytes and creatinine
➢ Blood group and cross match
➢ Bronchoscopy is performed in proximal esophageal
tumors to exclude bronchial Figure 79: Carcinoma esophagus (Endoscopic view)
involvement. This, together with vocal
cord and phrenic nerve paralysis, involvement of mediastinal structures
(especially aorta) and distant metastases, indicate inoperability.

STAGING: TMN STAGING

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MANAGEMENT
• Treatment depends on the stage of the disease and the condition of the patient.
• Some patients with resectable lesions are unfit for surgery by virtue of significant
comorbid disease. The nutritional state of the patient must also be considered and
assessed. In malnourished patients, a period of enteral nutrition is undertaken for
a few weeks before surgery.
• The goals of surgical treatment are removal of the tumor and regional lymph
nodes followed by re-establishment of gastrointestinal tract continuity.
• Treatment of patients who are unfit or have locally advanced disease is by
chemoradiation. This is followed by restaging. Surgery is considered in fit
patients whose disease is downstaged by the treatment.
• Management of localized disease/early stage disease
➢ Surgical resection, especially for symptoms control (right thoracic or
transhiatal approach, gastric pull-up or colonic interposition can be used to
reconstruct the GI tract). Note: essophagectomy provides the possibility of
cure.
o Proximal extent of resection should be 10cm above macroscopic tumor
and distal extent of resection is 5cm from macroscopic distal end of tumor.
Proximal stomach has to be removed commonly especially in lower 1/3 rd
of tumor. Sufficient removal of contiguous structures may be needed in
curative resection.
➢ Radiotherapy for avoidance of perioperative morbidity and mortality (can
shrink tumor but may predispose to local complications and not palliate
dysphagia and odynophagia)
➢ Pre/postoperative chemotherapy to downstage patients with resectable bulky
tumors.
➢ Combination therapy of these three modalities is becoming increasingly
common. Studies have shown that they can improve long term survival
however there remains controversy.
➢ Various operations with varying degrees of invasiveness have been developed
for treating esophageal cancer. In deciding which procedure to perform the
surgeon must take into consideration the location of the tumor, the proposed
esophageal substitute and the physical condition and body habitus of the
patient.

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➢ The most common surgical approaches are transthoracic (thoracotomy) and
transhiatal without thoracotomy. Incisions may be required in the neck, chest
and abdomen.
➢ The most common transthoracic esophagectomy is one called the Ivor Lewis
Esophagectomy (named after Welsh surgeon that developed the procedure)
that involves upper midline laparotomy with mobilization of the stomach and
is followed by right thoracotomy with esophageal resection and anastomosis.
It is useful for patients with tumors in the middle and lower esophagus.
➢ For tumors of the upper esophagus, many surgeons use a modified approach
called McKeown modification which involves additional intrathoracic
esophageal mobilization and anastomosis in the right neck through a separate
cervical incision (three hole technique). The tubularized stomach is used as
the esophageal substitute in most cases. Other possible substitutes are the
colon and small bowel.
➢ Esophagectomy without thoracotomy is termed the transhiatal approach. This
technique uses laparotomy for gastric and esophageal mobilization, followed
by left cervical incision for the anastomosis. The major benefit of this
approach is avoiding the complications that arise from thoracotomy.
➢ With advances in medicine, Esophagectomy can now be performed using
laparoscopic and thoracoscopic techniques. A cervical incision is also used.
This is complex and challenging procedure that has a steep learning curve.
Early results of laparoscopic esophagectomy seem to compare favorably with
open surgery though long-term data isn’t available at the moment.
➢ Post-operative management
o Fluid and electrolyte management
o Antibiotics and proper analgesia
o Respiratory care, ICT care, physiotherapy
o Prevention of DVT-elevation, exercises, heparin
o Monitoring for bleeding, sepsis, leak, oxygen saturation
o Total parenteral nutrition during initial postoperative period and early
jejunostomy feeding for nutrition
• Treatment for advanced stage IV disease
➢ Chemotherapy to promote tumor shrinkage
➢ Palliate care for symptoms as survival rate is poor nonetheless
• Postoperative complications
➢ Fistulae
➢ Abscesses

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➢ Respiratory complications
• Other options include endoscopic laser therapy, endoscopic dilation and stent
placement or placement of a gastrotomy or jejunostomy.
• Non-operative treatment
➢ Radiotherapy:
o This is done by super-voltage external beam radiotherapy may be curative
(radical) or palliative to relieve dysphagia and metastatic bone pain.
o It can also be given as an adjunct to surgical treatment either in the form
of multimodality treatment or after esophagectomy to improve
locoregional control.
o Contraindications to radical radiotherapy:
- Large tumors (>9.0 cm)
- Presence of tracheal broncho-esophageal fistula
o The min disadvantages of radical radiotherapy are the development of a
fibrous stricture in half the patients treated.
o Brachytherapy (intracavity irradiation) with caesium or iridium pellets
loaded into an applicatr and placed in the lumen of the esophagus is
another technique used for palliation of dysphagia.
➢ Chemotherapy:
o Several agents are used in combination treatment regimens for esophageal
cancer.
o These include: 5-fluorouracil (5-FU), Cisplatin, Vindesine, mitomycin C,
paclitaxel and etoposide.
o Paclitaxel achieves a high response rate in metastatic esophageal cancer
and also acts as a radiation sensitizer. Most combination regimens have
5-FU with or without leucovorin. The second most common agent used in
combination regimens is cisplatin.
• Palliation of advanced esophageal cancer:
➢ It is directed to relief dysphagia
➢ Several methods are used:
o Recanalization:
- Photocoagulation using Nd:YAG laser together with dilatation.
- Photodynamic ablation using hematoporphyrin derivative followed
by irradiation with red light (wavelength 630 nm): this combination
causes necrosis of tumor by highly reactive species such as singlet
oxygen.

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- Endoscopic guided fulguration of advanced esophageal neoplasm
with the BICAP probe
- Intratumor injection of absolute alcohol under endoscopic control:
used as adjunct to stenting to deal with tumor overgrowth/ingrowth
o Intubation:
- Most widely used method for palliation of dysphagia in inoperable
esophageal caner.
- Main disadvantage: treatment is performed in a single session, with
dramatic restoration of swallowing.
- Plastic tubes have been replaced by self-expanding metallic stents as
these provide excellent palliation and are relatively easy to insert.
- Several types are available. Some patients develop a malignant
tracheo-esophageal fistula (spontaneously or after radiotherapy) that
can be sealed with covered self-expanding metallic stents.
➢ Surgical bypass is seldom used nowadays.
➢ Gastrotomy should not be done as a palliative procedure.
• Indications for palliative therapy
➢ Patient not fit for major surgery
➢ Metastasis via blood, to adjacent organ or peritoneal/liver
➢ Relieve pain
➢ Relieve dysphagia
➢ Prevent bleeding
➢ Prevent aspiration

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CHAPTER 7: ABDOMINAL SURGICAL CONDITIONS

ABDOMINAL SURGICAL CONDITIONS

ABDOMINAL MASSES
HISTORY
• Most patients with a lump feel it frequently and should be able to tell you about
the history of the clinical features such as:
➢ When the lump was first noticed?
o It is important to be precise with dates and terminology. Do not write “the
lump first appeared 6 months ago”, when in fact you mean “the lump was
first noticed 6 months ago.” Many lumps may exist for months, even years
before being noticed.
➢ What made the patient notice the lump?
o The presence or absence of pain is important particularly if it is the
presenting feature. In general terms, pain is usually associated with
inflammation, not neoplastic change.
➢ What are the symptoms of the lump?
o Describe the history of each symptom carefully.
➢ Has the lump changed since it was first noticed?
➢ Does the lump ever disappear?
o A lump may disappear on lying down or during exercise and yet be
irreducible at the time of your examination.
➢ Has the patient ever had any other lumps?
➢ What does the patient think caused the lump?
o Lumps occasionally follow injuries or systemic illnesses known only to
the patient.
• In a patient presenting with an abdominal mass, the following features should
also be assessed carefully:
➢ Pain: site, nature, aggravating or relieving factors, duration of pain, referred
pain.
➢ Vomiting: type, content, hematemesis, relation to food frequency.
➢ Bowel habits: constipation, diarrhea, bloody diarrhea, furious diarrhea,
tenesmus (straining to defecate without the ability to do so).
➢ Decreased appetite and weight

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➢ Jaundice: it is an important factor in relation to liver, gallbladder or pancreatic
masses.

PHYSICAL EXAMINATION
INSPECTION
• Anatomical location: describe in exact anatomical terms using distance measured
from bony points.
• Size: measure dimensions using tape, asymmetrical lumps will need more
measurements to describe them accurately, sometimes a diagram will clarify your
written description.
• Shape: use descriptive terms such as ‘pear-shaped or kidney shaped’
• Surface and margins: is it smooth, bumpy, regular or irregular
• Movement with respiration
PALPATION
• Extent and borders: the edge of a lump may be clearly defined or indistinct
• Surface: it may be discolored and become smooth and shiny or thick and rough.
• Temperature
• Tenderness: Is the lump tender? Which parts are tender? Always try to feel the
non-tender part before feeling the tender area, and watch the patient’s face for
signs of discomfort as you palpate
• Composition:
➢ Consistency:
o Stony hard (not indentable)- usually bone or calcification
o Firm: hard but not as hard as bone
o Rubbery: slightly squashable similar to a rubber ball.
o Spongy: soft and very squashable but still with some resilience
o Soft: squashable and no resilience
➢ Fluctuation: pressure on one side of a fluid filled cavity makes all the other
surfaces protrude. This is elicited by feeling at least 2 other areas of the lump
whilst pressing on a third.
• Translucence (transillumination):
➢ Transilluminate: contains water, serum, lymph or plasma or highly refractile
fat
➢ Opaque: blood and other fluids
• Mobility
• Pulsatility, compressibility and reducibility

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• Plane of swelling (by leg raising test)
• Presence of other masses
• Often mass needs to be examined for change of position- in sitting, in standing,
in side position, after a brisk walk, in knee elbow position from retroperitoneal
mass and for puddle sign (but difficult to keep patient in this position)
PERCUSSION
• Generally:
➢ Solid and fluid filled lumps sound dull
➢ Gas filled lumps sound hollow and resonant
• Percussion over an abdominal mass however is important in predicting the
anatomical location of the mass.
➢ If mass is dull then it is in the anterior abdominal wall or in front of the bowel
intra-abdominally like liver, spleen, gallbladder.
➢ If the mass is with an impaired resonant note, then the mass is arising from
the bowel like stomach, colon, small bowel.
➢ If the mass is resonant on percussion, then the mass is probably in the
retroperitoneal region.
• Check for fluid thrill over the lump as well as in the abdomen.

AUSCULATATION
• Listen for any bruits and for bowel sounds
VAGINAL AND RECTAL EXAMINATION
• Per vaginal examination is done to assess pelvic masses.

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• Per rectal examination is done to look for any secondaries in rectovesical pouch,
primary tumor or relation of lower abdomen masses (pelvic masses)
• Do not forget to do a general examination and assessment of the lymph nodes
(Especially regional).

ABDOMINAL TRAUMA

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GASTRITIS AND PEPTIC ULCER DISEASE

• The stomach is divided into:
➢ Fundus
➢ Body
➢ Pyloric region (antrum and pyloric canal)
• The stomach acts as a receptacle for ingested food which is partially digested and
hydrolyzed by acid and pepsin into semifluid chyme and then delivered into the
small intestine.
• The stomach possesses the property of adaptive relaxation i.e. increase in
capacity without a significant rise in intraluminal pressure.
➢ Adaptive relaxation is mediated by stretch reflexes and vagal afferents and is
therefore greatly impaired after gastric surgery.
• The mucosa lining the proximal stomach contains the parietal and chief cells
whereas the mucosa lining the more muscular antropyloric segment secretes an
alkaline mucus but contains specialized endocrine (G) cells that release gastrin
under the influence of gastrin releasing peptide.
➢ Parietal cells secrete acid and intrinsic factor
➢ Chief cells produce pepsinogens that are then converted to active pepsin by
HCL.

GASTROINTESTINAL BLEEDING

GASTRIC TUMORS

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ACUTE ABDOMEN

ACUTE ABDOMEN
• Acute abdomen is defined as an abrupt onset of abdominal pain usually
accompanied by 1 or more peritoneal signs:
➢ Rigidity
➢ Tenderness (with or without rebound)
➢ Involuntary guarding
• Most causes are surgical and considered as EMERGENCIES.
• When emergency surgical intervention is required it is also termed surgical
abdomen.
• The pain may be due to inflammation, perforation, obstruction, ischemia,
infarction or rupture of an abdominal organ.
• Recall when assessing pain use SOCRATES: Site, Onset, Character, radiation,
alleviating factors, Timing course, Exacerbating factors and Associated
symptoms

HISTORY
• Should include demographic details, occupation, recent travel, history of recent
abdominal trauma
• Pain is the most common presenting feature.
SITE
• Visceral pain:
➢ Poorly localized, usually dull, achy pain arising from distension or spasm in
hollow organs e.g. crampy pain felt during early intestinal obstruction.
➢ Mid-epigastrium: Stomach, duodenum, hepatobiliary system, pancreas
➢ Mid-abdomen: jejunum, ileum

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➢ Lower abdomen: colon, internal reproductive system
• Parietal pain:
➢ Sharp, well-localized, somatic pain arising from irritation (usually by pus,
bile, urine or gastrointestinal secretions) of the parietal peritoneum. E.g.
inflamed appendix causing sharp right lower quadrant pain due to irritation of
nearby peritoneum.
ONSET
• Is usually abrupt.
CHARACTER
Character of pain Causes
Gradual steady pain • Acute cholecystitis
• Acute cholangitis
• Hepatic abscess
• Diverticulitis
Intermittent colicky pain • Small bowel obstruction
• Inflammatory bowel disease
• Biliary colic
Abrupt excruciating pain • Perforated ulcer
• Ruptured aneurysm
• Ureteral colic
Rapid onset severe constant pain • Acute pancreatitis
• Ectopic pregnancy
• Mesenteric ischemia
• Strangulated bowel
• Acute appendicitis

RADIATION
• Biliary tract pain may radiate to the right shoulder or right scapula (due to right
hemidiaphragmatic irritation).
• Splenic rupture pain may radiate to left shoulder.
➢ Kehr’s sign: pain referred to the left shoulder due to irritation of the left
hemidiaphragm. Often seen with splenic rupture.
• Kidney pain may radiate from flank to groin and genitalia (loin to groin)
• Pancreas pain may radiate to the back.

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ALLEVIATING AND AGGRAVATING FACTORS

• Include:
➢ Change in position
➢ Association with food (better or worse)
➢ Pain that wakes one from sleep (significant)
• If worsened by movement/coughing suspect active peritonitis, pancreatitis is
relieved by sitting forward
ASSOCIATED SYMPTOMS
• Vomiting: pain relieved by vomiting is indicative of small bowel obstruction,
afferent loop syndrome. Vomiting undigested food or bile suggests upper GI
pathology or obstruction while feculent vomiting suggests lower GI obstruction
• Hematemesis or melena
• Bowel habits: constipation or obstipation (no stool or flatus) is suggestive of
bowel obstruction. Stool/urine color
• Mucoid diarrhea with blood (red currant jelly stool) is seen in intussusception.
• Anorexia: very non-specific symptom, however most patients with acute
appendicitis will have anorexia.
• Fever: seen in appendicitis, acute cholecystitis and acute pancreatitis.
MEDICAL AND SURGICAL HISTORY
• History of past abdominal surgery (Small bowel obstruction due to adhesions)
• Atrial fibrillation: increased risk for mesenteric ischemia (embolism) because of
emboli to mesenteric arteries.
• Menstrual and sexual history: Acute salpingitis vs Pelvic inflammatory disease
Vs rupture ectopic
➢ Contraception (including IUCD use)
➢ Last menstrual period
➢ Previous gynecological or tubal surgery
➢ Previous ectopic pregnancy
➢ Vaginal bleeding

PHYSICAL EXAMINATION
• Steps in physical examination of acute abdomen:

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1. Inspection
2. Auscultation
3. Cough tenderness
4. Percussion
5. Guarding or rigidity
6. Palpation:
o One-finger
o Rebound tenderness
o Deep palpation
7. Punch tenderness
o Costal area
o Costovertebral area
8. Special signs e.g. Murphy’s sign in
cholecystitis
9. External hernia and male genitalia
10.Rectal and pelvic examination
• Look out for:
➢ Vital signs: most patients with a surgical abdomen will have vital sign
abnormalities secondary to pain, inflammation, fluid and electrolyte
derangements, and anxiety
➢ General: hydration status, mentation, nutritional status
➢ Chest: auscultation
➢ Abdominal examination (as above)

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Condition Helpful signs

Perforated viscus • Scaphoid tense abdomen
• Diminished bowel sounds (late)
• Loss of liver dullness
• Guarding or rigidity
Peritonitis • Motionless
• Absent bowel sounds (late)
• Cough and rebound tenderness
• Guarding or rigidity
Inflamed mass or abscess • Tender mass (abdominal, rectal or pelvic)
• Punch tenderness
• Special signs (Murphy’s, psoas or obturator)
Intestinal obstruction • Distended abdomen
• Visible peristalsis (late)
• Hyperperistalsis (early) or quiet abdomen (late)
• Diffuse pain without rebound tenderness
• Hernia or rectal mass (some)
Paralytic ileus • Distention
• Minimal bowel sounds
• No localized tenderness

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Ischemic or strangulated bowel • Not distended (until late)
• Bowel sounds variable
• Severe pain but little tenderness
• Rectal bleeding (some)
Bleeding • Pallor
• Shock
• Distention
• Pulsatile (aneurysm)
• Tender (e.g. ectopic pregnancy), mass
• Rectal bleeding (some)

• Note: Serial abdominal exams and observation may be necessary in cases in

which etiology of abdominal pain is initially unclear.

INVESTIGATIONS
• Blood:
➢ Full blood count
➢ Urea, creatinine and Electrolytes
➢ Serum amylase and lipase
➢ Liver function tests for right upper
quadrant pain
➢ Serum glucose
➢ Clotting panel
➢ Blood culture
➢ Malaria slide
➢ Group and save/Cross match
• Imaging
➢ Electrocardiography (ECG): to rule out Figure 80: Erect CXR showing free air under both
myocardial infarction (also do cardiac hemidiaphragms (Arrows)
enzymes if ST-T changes seen) and also
as a pre-operative baseline cardiac assessment
➢ Chest X-ray and Abdominal X-ray to look for free air (can detect as little as
1-2ml): easier to see under right hemidiaphragm. Presence of stomach bubble
obscures it on the left.
➢ Abdominal ultrasound

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➢ Abdominal computed tomography (CT) should be used after the above
assessment is complete and the diagnosis remains elusive (e.g. young male
with clinical signs and symptoms of appendicitis should not undergo CT).
o Contrast for abdominal CT: for the most optimal imaging both oral and
IV contrast is used. In some cases, (such as impaired renal function or
allergy to IV contrast) this is not feasible.
o Non-contrast CT although suboptimal for most cases (Except
nephrolithiasis) still provides a lot of information.
• Urine: Gravindex for all women of childbearing age

MANAGEMENT
• Dependent on the cause.
• Early diagnosis improves outcome.
• Key is deciding whether surgical intervention is needed (Exploratory
laparotomy)
• Indications for urgent surgical interventions:
➢ Physical findings
o Involuntary guarding or rigidity especially if spreading
o Increasing or severe localized tenderness
o Tense or progressive distention
o Tender abdominal or rectal mass with high fever or hypotension
o Rectal bleeding with shock or acidosis
o Equivocal abdominal findings with
- Septicemia (high fever, marked or rising leukocytosis, mental
changes or increasing glucose intolerance in a diabetic patient)
- Bleeding (unexplained shock or acidosis, falling hematocrit)
- Suspected ischemia (acidosis, fever, tachycardia)
- Deteriorating on conservative treatment
➢ Radiological findings
o Pneumoperitoneum
o Gross or progressive bowel distention

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o Free extravasation of contrast material
o Space-occupying lesion on scan with fever
o Mesenteric occlusion on angiography
➢ Endoscopic findings
o Perforated or uncontrollably bleeding lesion
➢ Paracentesis findings
o Blood, bile, pus, bowel contents or urine

SURGICAL CAUSES OF ABDOMINAL PAIN

• Can be divided into infectious, inflammatory, intoxication, ischemic, malignant,
metabolic, obstetric and gynecological, traumatic.
• It may also be classified according to the site.

Site Examples
Right upper quadrant • Perforated duodenal ulcer
• Acute cholecystitis
• Hepatic abscess
• Retrocecal appendicitis
• Appendicitis in a pregnant woman
(commonest surgical emergency in a
pregnant woman)
Right lower quadrant • Appendicitis
• Cecal diverticulitis
• Meckel’s diverticulitis
• Intussusception
Left lower quadrant • Sigmoid diverticulitis
• Volvulus
Left upper quadrant • Splenic rupture
• Splenic abscess
Diffuse • Bowel obstruction
• Leaking aneurysm
• Mesenteric ischemia
Periumbilical • Early appendicitis
• Pain from small bowl obstruction
Suprapubic • Ectopic pregnancy

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• Ovarian torsion
• Tubo-ovarian abscess
• Psoas abscess
• Incarcerated groin hernia

• Some important non-surgical causes of abdominal pain include:

➢ Myocardial infarction
➢ Mittelschmerz (mid-cycle pain due to ovulation)
➢ Poisoning (lead, black widow spider)
➢ Herpes zoster
➢ Lower lobe pneumonia
➢ Endocrine: Addisonian crisis, diabetic ketoacidosis
➢ Sickle cell crisis
➢ Porphyria
➢ Psychological (hysteria)

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INTESTINAL OBSTRUCTION

• The small intestine is divided into:

➢ Duodenum: the first part
➢ Jejunum: the second part
➢ Ileum: the terminal part
• The lining mucosa is folded into villi to increase absorptive surface and these are
covered by tall columnar absorptive cells (enterocytes) that have microvilli at
their luminal surfaces (brush border).
• Goblet cells found interspersed among the enterocytes, synthesize the mucinous
glycoprotein essential for maintaining the surface glycocalyx.
• At their bases, the villi are surrounded by intestinal crypts that contain stem cells
from which the surface epithelium is constantly replaced by a process of mitosis
and migration.
• The primary function of the small intestine is the absorption of nutrients but it is
also involved in digestion by brush-border enzymes that are essential for the final
hydrolysis of peptides and carbohydrates.
• The digestion and absorption of fluid, electrolytes, iron, folate, carbohydrate, fat
and protein is completed in the jejunum.

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• The absorption of bile salts and vitamin B12 only occurs in the terminal ileum
which contains specific transport sites.
• The critical length of small bowel required for maintenance of oral nutrition is
100cm. Below this length some form of parenteral nutritional support is needed.
• Another function of the small intestine is the synthesis of peptide and amine
intestinal hormones. These are located within the enteroendocrine cells and in the
neurons of the myenteric plexus. They influence intestinal secretion and
transport, growth and differentiation, splanchnic hemodynamics and the release
of insulin.
• The small bowl microflora plays an important role in intraluminal metabolism of
various substances. Obstruction and stasis increases bacterial population
substantially. Even in the absence of obstruction this bacterial overgrowth may
produce adverse consequences including malabsorption.
• The normal intestinal mucosa is able to resist invasion by pathogenic bacteria but
this antimicrobial barrier can break down under pathological states with
translocation of pathogens into blood and lymph causing a systemic
inflammatory response syndrome.

INTESTINAL OBSTRUCTION
• Intestinal obstruction happens when there is restriction to the normal passage of
intestinal contents. The obstruction may be complete (total blockage of the
lumen) or incomplete (partial blockage)
• It may be divided into 2 main groups:
➢ Paralytic (adynamic)
➢ Mechanical (dynamic)
• The most common causes of intestinal obstruction are adhesions and hernias.

CLASSIFICATION
• Depends on:
➢ Etiology (Cause):
o Dynamic
o Adynamic

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➢ Speed of onset:
o Acute: common in small bowel. It has a Rapid onset with severe
symptoms
o Chronic: Insidious (gradual, subtle presentation over weeks) E.g. Most
cases of carcinoma of large bowel
o Acute on chronic: common in large bowel. It is a chronic obstruction that
suddenly becomes complete

➢ Site of obstruction
o High- small bowel obstruction
o Low- large bowel obstruction

➢ Nature:
o Simple- bowel is occluded without damage to its blood supply
o Strangulated- blood supply of the involved segment of intestine is cut off
e.g. strangulated hernia, volvulus, intussusception or adhesive band.
Gangrene may occur if untreated.

➢ Whether they are congenital or acquired

o Congenital:
- Anorectal malformation e.g. imperforate anus
- Volvulus neonatorum
- Meconium ileus
- Hirschsprung disease
- Mal-rotation
- Bands and adhesions
- Intestinal atresia
- Duodenal atresia
- Adhesions
- Congenital megacolon
o Acquired:
- Hernia (most common)
- Postoperative
- Intussusception
- Roundworm
- Gallstones
- Tuberculosis

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- Malignancy
- Internal hernias
ETIOLOGIC CLASSIFICATION
• These are either:
➢ Dynamic: due to a mechanical obstruction (peristalsis against a mechanical
obstruction). Can have acute or chronic form. They various causes may be
classified as:
o Extramural
o Intramural
o Intraluminal
➢ Adynamic: peristalsis may be absent e.g. paralytic ileus or it may be present
in a non-propulsive form e.g. mesenteric vascular occlusion or pseudo-
obstruction.

Causes of intestinal obstruction

Dynamic Adynamic
Intraluminal • Paralytic ileus
• Fecal Impaction • Mesenteric vascular occlusion
• Foreign bodies • Pseudo-obstruction
• Food bolus
• Parasites
• Pedunculated tumor
• Bezoars (bolus composed of indigestible
material-orange pith or hair bezoar,
particularly in gastrectomized patients)
• Gallstones ‘ileus’: Large gallstones in a
chronically inflamed gallbladder that has
become adherent to the duodenum erodes
through the 2 organs by a process of pressure
necrosis, thus entering the duodenum and
becoming impacted lower down the small
intestine usually in the small terminal ileum.
Intramural

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• Strictures (TB strictures)
• Tumors: carcinomas, lymphomas etc.
• Congenital atresia
• Diverticulitis
• Inflammatory disease: Crohn’s disease
Extramural
• Bands/ adhesions (commonest cause)
• Hernia: External and internal
• Volvulus
• Intussusception
• Compression by tumors (nodal tumor
deposits)

DYNAMIC OBSTRUCTION
• These are due to mechanical blockage of normal propulsion and passage of
intestinal contents.
• It may occur in an acute or chronic form.
• Causes of dynamic intestinal obstruction are classified:
➢ In the lumen (intraluminal)

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o Fecal impaction
o Foreign bodies
o Food bolus
o Gallstones
o Roundworm (parasites)
o Meconium ileus
o Pedunculated tumors
➢ In the wall (intramural):
o Tuberculous stricture
o Crohn’s disease
o Malignancy
o Congenital atresia
➢ Outside the wall (Extramural): Figure 81: Different causes of intestinal obstruction
o Adhesions-40%
o Hernia-25%
o Volvulus
o Intussusception
• Adhesions commonly cause small bowel obstruction than large bowel
obstruction.
➢ 80% of intestinal obstruction occurs in small bowel.
➢ 20% occur in the colon.
o 70% of colonic obstruction is due to malignancy.
o 30% is due to volvulus, diverticulitis, inflammatory cause like
tuberculosis, etc.
• Mortality is 3% in obstruction without strangulation, 30% in obstruction with
strangulation.
• Recurrent obstruction is more common in adhesions.

PATHOLOGY AND PATHOGENESIS

• There are changes that occur:
➢ Proximal to the bowel obstruction
➢ At the site of obstruction
➢ Distal to the obstruction

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PROXIMAL TO THE BOWEL OBSTRUCTION (BEFORE THE OBSTRUCTION)
• Intestinal obstruction leads to increased peristalsis
(hyperactivity) which may eventually become vigorous in
an attempt to overcome the obstruction and if obstruction
is not relieved peristalsis ceases and there is flaccid
paralysis and dilatation of the bowel.
• The vigorous peristaltic contractions are clusters
contractions that causes severe colicky abdominal pain
experienced by the patient.
• Fluid from saliva (1000ml/day), stomach (2000ml/day),
pancreas (1500ml/day), bile (1000ml/day) and intestine
(3000ml/day) collects just proximal to the obstruction.
• Accumulation of swallowed air and fluids causes the proximal bowl to dilate.
The interface between air and fluid in the dilated loops
accounts for the fluid levels seen in the erect
abdominal film of these patients.
• There is increased transudation across the capillary
membrane as venous drainage of the affected
segments is impaired.
• The wall of the obstructed gut becomes edematous
and because of edema and inflammation, absorption
decreases.
• The fluid and electrolytes that accumulate in the
lumen of the obstructed bowel and within its wall are
effectively lost (sequestrated third-space losses) and
contribute (together with vomiting) to the fluid and
electrolyte deficit in these patients.
➢ In the first 12 hours of obstruction there is only Figure 82: Upright abdominal X-ray
decreased absorption which causes accumulation demonstrating a small bowel obstruction.
of fluid and electrolytes in the lumen. Note multiple air fluid levels. You more
➢ After 12 hours, there is also increased intestinal than 2to make a diagnosis of obstruction
secretion causing further accumulation of the fluid.
• Bacteria overgrowth occurs within the obstructed loops of intestine (E. coli,
Klebsiella, anaerobes, Bacteroides and other organisms). Bacteria multiply and
toxins are released causing toxemia occurs.

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• Unless the distention is relieved, there is progressive occlusion (by stretching) of
intestinal intramural vessels such that, untreated, a mechanical intestinal
obstruction leads to ischemia and eventually necrosis with perforation of the
bowel.
➢ Inflammatory response in the bowel wall (intramural inflammation) causes
accumulation of activated neutrophils and macrophages in the muscle wall
which release reactive enzymes and cytokines which damage secretory and
motor process of muscle leading to dilatation of the bowel.
➢ Increased release of nitric oxide in muscle wall and production of intramural
reactive oxygen metabolites alter gut motility and permeability.
➢ Intestinal hypoxia also causes dilatation.
➢ Dilatation of bowel wall increases intraluminal pressure which exceeds the
bowel wall venous pressure causing ischemia which causes further dilatation
and ischemic injury. This leads into eventual blockage of arterial perfusion
causing bowel necrosis/gangrene.

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AT THE SITE OF OBSTRUCTION
• Initially venous return is impaired, this leads to
congestion, edema of bowel wall which turns
purple.
• Later this jeopardizes the arterial supply and
the bowel loses its shininess & peristalsis and
becomes blackish in color.
• This may lead to gangrene which can cause
perforation leading to bacteria and toxins
migrating into the peritoneum causing
peritonitis.

BOWEL DISTAL TO OBSTRUCTION (AFTER OBSTRUCTION)

• The distal bowel empties to a collapsed state. It becomes Inactive and collapsed

Figure 83: Pathology of Intestinal obstruction

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CLINICAL FEATURES
• Four cardinal symptoms of intestinal obstruction:
➢ Vomiting
➢ Colicky abdominal pain
➢ Abdominal distension
➢ Absolute constipation
• NOTE not all may be present.
HISTORY
• Vomiting: early sign in high obstruction, late or absent in chronic or low
obstruction.
➢ Jejunal obstruction: early and persistent
➢ Ileal obstruction: recurrent occurring at an interval, initially bilious later
feculent. This is caused by bacterial overgrowth in the obstructed small
intestine
o True fecal vomiting only happens in gastrocolic fistula.
➢ Large bowel obstruction: vomiting is a late feature
➢ Note: Vomiting together with sequestration of fluid in the dilated loops,
rapidly leads to dehydration with significant water and electrolyte deficits
particularly sodium and chloride. The dehydration leads to raised PCV and
prerenal azotemia with elevation of blood urea and reduced urine output.
• Abdominal pain:
➢ Pain is first to develop and it is sudden and severe.
➢ Initially it is colicky and intermittent.
➢ Later continuous and severe. Constant severe pain is ominous and indicates
with infarction of the bowel or the onset of peritonitis.
➢ Pain begins usually around umbilicus in small bowel obstruction. In small
bowel obstruction, it is crampy, recurrent paroxysms occurring as short
crescendo/decrescendo episodes (of 30 seconds).
➢ In distal obstruction pain is suprapubic. In large bowel obstruction it is of
longer episodes of minutes (in paralytic/ adynamic ileus pain is diffuse and
mild).
➢ Post op obstruction- may be disguised by general discomfort and by opiates
given to the patient.
• Abdominal distension: becomes progressively more marked the lower the
obstruction is situated and may reach extreme degrees in low colonic obstruction
and paralytic ileus. It is due to accumulation of gas and fluid in obstructed bowel.

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➢ Jejunal obstruction: absent or minimal
➢ Ileal obstruction: obvious visible intestinal
peristalsis (VIP) and borborygmi sounds
(rumbling noise in the abdomen caused by
gas in the intestine)- step ladder peristalsis.
➢ Large bowel obstruction: enormous
distention
• Constipation: it is absolute i.e. neither feces nor
flatus is passed Figure 84: Step ladder peristalsis
➢ It is an early feature of large bowel obstruction
but late feature of small bowel obstruction.
➢ Exceptions: Richter’s hernia obstruction, Gall stone obstruction, mesenteric
vascular occlusion, intestinal obstruction with a pelvic abscess
EXAMINATION
• Dehydration: leads to oliguria and renal failure. There is loss of skin turgor,
hypotension and persistent tachycardia.
• Features of toxemia and septicemia: tachycardia, tachypnea, fever, sunken eyes,
cold periphery.
• In pain, may be rolling about with colic.
• Temperature:
➢ Fever- inflammation in bowel wall/ ischemia/ perforation
➢ Hypothermia can occur when septicemia develops due to lack of pyrogenic
response. It suggests poor prognosis.
• During inspection look for:
➢ Strangulated external hernia- inguinal or femoral (difficult in fat people).
➢ Abdominal scar-previous operation may suggest adhesions or bands.
➢ Abdominal distention, may have visible peristalsis.
• On palpation:
➢ Abdominal tenderness
o It is initially localized but later becomes diffuse- is a feature of intestinal
obstruction.
➢ Rebound tenderness and guarding will not be present in simple obstructions
which are features of strangulation.
➢ A mass may be present (intussusception or carcinoma)
• Features of strangulation:

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➢ Continuous severe pain, shock, tenderness, rebound tenderness (Blumberg’s
sign)
➢ Guarding and rigidity, absence of bowel sounds
➢ In case of strangulated hernia, a swelling which is tense, tender, rigid,
irreducible, no expansible impulse on coughing and history of recent increase
in size is seen.
• On percussion the distended abdomen is resonant to percussion on the anterior
aspect but is dull towards the flanks.
• On auscultation Bowel sounds: they are increased- high pitched metallic (rushes
and groans) sounds followed by metallic tinkling sounds of dilated bowel.
Eventually once fatigue occurs or gangrene develops bowel sounds are not heard-
silent abdomen of peritonitis develops (in paralytic ileus, there are only
continuous metallic sounds of dilated bowel).
• Per-rectum examination: shows empty, dilated rectum, often with tenderness. If
rectal growth is the cause for obstruction, it may be palpable.
➢ May sometimes reveal a mass in the pouch of Douglas, apex of an
intussusception or fecal impaction.
• Digital vagina examination in a female patient is mandatory. This is done before
the rectal examination with the same gloved finger.
INVESTIGATIONS
• Imaging:
➢ Plain Abdominal X-ray
o Supine abdominal X-ray shows distention
of the intestine. It distinguishes small
bowel from large bowel obstruction (see
table below)
o Erect abdominal X-ray is taken if
perforation is suspected.
- Multiple central air-fluid levels in a
step-ladder fashion in small bowel. In
large bowl they are less numerous and
located in the flanks and suprapubic
regions
- Proximal to obstruction: lesser the air
Figure 85: AXR showing air-fluid levels
fluid level

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- Distal to obstruction: more the air fluid level.
o Normally, 3 fluid levels can be seen in plain X-ray film- at fundus of
stomach, at duodenum and often at cecum.
o Jejunum- show valvulae conniventes (Herring bone pattern)/valves of
Kerckring (plica circularis/ valvulae conniventes)
o Ileum is smooth and characterless (by Wangensteen)
o Large bowel shows haustrations of tenia coli.
o Pneumobilia (gas in biliary tree) may be due to gallstone ileus.
➢ Triad of small bowel obstruction in plain X-ray
o Dilated small bowel loops> 3cm
o Multiple air fluid levels in erect X-ray
o Paucity of air in the colon

Figure 87: Small bowel obstruction. Figure 86: Large bowel obstruction. Note
Note the valvulae conniventes, the the haustra which do not traverse the
central position of the bowel and the entire diameter of the bowel. The bowel is
coiled-spring appearance in the periphery

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SMALL BOWEL ON X-RAY LARGE BOWEL ON X-RAY
• Less than 3cm wide • Less than 6cm wide, Cecum and
• Tends to be central sigmoid up to 9cm.
• It is only seen if it contains gas • Tends to be peripheral
• Mucosal folds (valvulae • Ascending and descending colon in
conniventes/valves of fixed positions laterally while
Kerckring) transverse colon and sigmoid have a
• Obstruction on X-ray shows a variable position on the mesentery
“coiled-spring appearance” • Haustral folds do not go all the way
across the lumen
• Contains feces-mottled appearance

➢ Chest X-ray: shows elevation of the diaphragm which is secondary to the

abdominal distention. It may also show free air underneath the right
diaphragm in patients with infective paralytic ileus (secondary to intestinal
perforation).
➢ Abdominal ultrasound:
o Dilated bowel and fluid in the peritoneal cavity.
o Better than X-ray but not as good as CT scan.
o Doppler US is useful in detecting strangulation
➢ Barium enema X-ray

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o Useful in intussusception
o Barium meal is usually contraindicated in acute intestinal obstruction.
o Barium follow through X-ray may be done with caution in
suspected/partial intestinal obstruction under fluoroscopy, otherwise it
may precipitate complete obstruction or may cause perforation and
barium peritonitis which is very dangerous.
➢ CT scan
o Very reliable investigation for intestinal obstruction.
o Gives idea on changes in bowel wall, ischemia, strangulation, mesenteric
edema and thickening. Also shows bowel wall gas, portal venous gas and
mass lesion.
• Blood:
➢ Full blood count: Hemoglobin and Hematocrit (PCV) are raised. The white
cell count is usually normal or slightly elevated unless there is bowel
infarction and/or peritonitis.
➢ Electrolytes, Blood urea and serum creatinine: these are raised as a result of
an element of pre-renal failure due to hypovolemia. Serum sodium and
chloride are low. Hyperkalemia may be observed in patients with infarcted
intestines.
➢ LFTs
➢ Arterial blood gas: acidosis is common

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COMPLCIATIONS OF INTESTINAL OBSTRUCTION
• Hypovolemic and septic shock
• Perforation
• Peritonitis
• Intra-abdominal abscess formation
• ARDS
• Renal failure
DIFFERENTIAL DIAGNOSIS
• Paralytic obstruction
• Pseudo-obstruction
• Ascites
MANAGEMENT
• Resuscitation- ABCs
• Depends on cause.
• Principles of management:
➢ Decompression of obstructed gut
➢ Replacement of fluid and electrical losses
➢ Special conservative measures in certain situations
➢ Surgical intervention
• Acute obstruction of sudden onset, complete and with risk of strangulation is an
urgent problem requiring emergency surgical intervention.
• Chronic large bowel obstruction, slowly progressing obstruction can be
investigated at some leisure with sigmoidoscopy, colonoscopy and barium enema
and treated electively.
DECOMPRESSION
• This is done by insertion of a nasogastric sump suction tube (Salem). This is
aspirated at least every hour and left draining into a bag in the intervening periods.
• The daily aspirate is measured and the amount used in calculating the daily fluid
and electrolyte requirements.
• If the intestinal obstruction responds to conservative management, the daily
amount of aspirate gradually reduces and its nature changes to clear often bile-
stained fluid.
• Nasogastric aspiration: reduce toxic effects, bowel distension and improve
pulmonary ventilation as well as reduce possibility of aspiration pneumonia.

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FLUID AND ELECTROLYTE THERAPY
• Fluids and electrolytes should be given intravenously.
• Fluids used: Hartmann’s solution, normal saline and 5% dextrose.
• Initially large amounts are administered (1L every 3-4 hours) to replace the
losses. Thereafter, maintenance IV fluid therapy is continued until return of
normal bowel function.
• The usual daily requirements of potassium (40-120 mmol) are met by infusing
60-80mmol of KCL in divided doses over 24 hours.
• If hypokalemia is severe, up to 40mmol may be infused over 1h in 400ml of fluid.
It is important to remember that potassium must always be administered slowly
and never given as a bolus injection because of the risk of cardiac arrhythmias
and arrest.
• Catheterize patient and Monitor urine output.
SPECIAL CONSERVATIVE MEASURES
• For certain types of intestinal obstruction, additional specific measures may result
in rapid relief of the obstruction thus avoiding surgical intervention.
• Examples:
➢ Passage of a rectal tube or flexible sigmoidoscope to deflate sigmoid volvulus
➢ Barium contrast enema to reduce an early intussusception in an infant
➢ Manual removal of feces and/or oil retention enema to deal with obstruction
caused by fecal impaction
• It is important to assess the patient frequently to establish progress on
conservative management. This is confirmed by relief of symptoms (vomiting
and pain), improvement of general condition and vital signs (pulse rate,
temperature and blood pressure) and observations such as reduction in amount of
aspirate and abdominal girth and return of normal bowel sounds.
SURGICAL INTERVENTION
• This is undertaken if:
➢ The underlying disease needs surgical treatment (obstructed hernia,
obstructing carcinoma etc.) in this respect, intestinal obstruction due to
adhesions often settles with conservative management and therefore is not
initially treated surgically unless there is clinical evidence of strangulation.
➢ The patient does not improve with conservative treatment
➢ There are signs of strangulation or peritonitis.
• Surgery:

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➢ Immediate laparotomy to relief obstruction.
➢ Warm saline soaked mop is placed over the doubtful area with 100% oxygen
inhalation for 20 minutes if colour becomes normal with peristalsis then bowel
is viable.
➢ If bowel is not viable resection and anastomosis is done. A good peritoneal
wash is given and the abdominal cavity is drained.
➢ Abdomen is closed in layers using non-absorbable sutures. Often tension
sutures are required.
➢ Laparoscopic approach may be useful in partial obstruction, proximal
obstruction due to band. Conversion when needed should be done without
hesitation.
➢ When checking for viability of bowel, look for:
o Peristalsis
o Pulsations
o Colour (black/pink)- dull and lusterless serosa is seen in ischemia
o Serosal shining
o Bleeding in mesentery and bowel wall
o Friability- friable, flabby muscle is seen in ischemia
• A defunctioning loop colostomy or ileostomy may be performed to minimize the
complications of anastomotic leak.
• Post-surgical complications:
➢ Pelvic abscess
➢ Subphrenic abscess
➢ Biliary or fecal fistulas
➢ Burst abdomen
➢ Bands and adhesions
➢ Incisional hernias
ADDITIONAL MEASURES
• ICU critical care.
• Antibiotics: ampicillin, gentamycin, metronidazole, cephalosporins
• Analgesics
• Blood transfusion: FFP or platelet in critical patients.
• CVP for fluid and monitoring- pulmonary capillary wedge pressure monitoring
are often needed in hemodynamically unstable patients.

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INTUSSUSCEPTION

INTUSSUSCEPTION (ISS)
• Intussusception is telescoping or invagination
of 1 portion (Segment) of bowel into the
adjacent segment of bowel.
• Types:
➢ Antegrade: most common
➢ Retrograde: rare (jejunogastric in
gastrojejunostomy stoma)
• It can be single or multiple (Rare)
• It can be ileo-colic (most common type, 75%),
ilieoileal (ileum inside ileum), colocolic
(colon inside colon), ileoileocolic (Ileum
inside cecum or ascending colon). Figure 88: Intussusception
• Intussusception is common in weaning period
of a child (common in males) between 6-9 months.
• It is the commonest cause of intestinal obstruction in
children of 3-18 months age.
• In elderly intussusception:
➢ Colocolic is most common type
➢ Apex is formed usually by growth
➢ No role of hydrostatic reduction
• Causes:
➢ Idiopathic ISS (common in children and occurs in
terminal 50cm of ileum)
➢ During weaning, change in diet causes
inflammation and edema of Peyer’s patches- may
stimulate ISS.
➢ Upper respiratory tract viral infection which
causes edema of Peyer’s patches is also thought as
an etiology for intussusception in children. Figure 89: Ileocolic intussusception

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➢ Other causes in adolescents and adults are submucosa lipoma, leiomyoma,
polys in jejunum (Peutz-Jegher syndrome), other polyps and carcinomas with
papillary projections.
PATHOLOGY
• Apex (leading point): the one which advances
• Intussucipiens: the one which receives (outer
sheath)
• Intussisceptum: tubes which advances (middle
and inner sheath)
➢ Apex and inner tubes will have compromised
blood supply and can become gangrenous.
➢ Because of ischemia, apex sloughs off and Figure 90: Parts of intussusception
bleeds, which mixes with the mucous to
produce the classic red-currant jelly that is passed per anum.
➢ Gangrene which sets in leads to perforation and peritonitis.
➢ Red currant jelly is not commonly observed in ISS in adult but it can occur.
CLINICAL FEATURES
HISTORY
• Common in males (3:2)
• Common in 6-9 months. But can also occur at later age
• Common in spring and winter, coinciding the gastroenteritis and respiratory
infections in respective periods.
• Commonest cause of intestinal obstruction in infancy.
• Initial colicky abdominal pain (75%) which eventually becomes severe and
persistent.
• Sudden onset of pain in a male child with progressive distension of the abdomen,
vomiting, with passage of “red-currant-jelly” stool. It is usually not found in adult
ISS.
• Often ISS is recurrent when it gets reduced, child automatically becomes
asymptomatic (Mother often complains that the child cries during an episode and
sleeps peacefully once it gets reduced).

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EXAMINATION
• A mass is felt either on the left or right of the umbilicus
which is sausage shaped with concavity towards
umbilicus, smooth, firm, resonant, not moving with
respiration, mobile, contracts under the palpating fingers.
• Often mass appears and disappears.
• Right iliac fossa is empty (Sign of Dance).
• After 24-48 hours, abdominal distension appears and
increases progressively with features of intestinal
obstruction.
• Features of intestinal obstruction with step-ladder
peristalsis.
• Blood stained stool is often obvious on digital
examination of the rectum.
• Occasionally ISS can be seen per anally and felt with a
Figure 91: Sausage-Shaped mass
long mesentery. of intussusception
• Eventually, gangrene and perforation occurs with features
of peritonitis.

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COMPLICATIONS
• Intestinal obstruction
• Perforation
• Peritonitis
DIFFERENTIAL DIAGNOSIS
• In children:
➢ Acute gastroenteritis
➢ Purpura with intestinal symptoms
• In adults:
➢ Carcinoma colon
➢ Mesenteric mass
INVESTIGATIONS
• Imaging:
➢ Barium enema shows typical claw sign or coiled spring sign (Pincer end).

➢ Ultrasound shows target sign or pseudokidney sign or bull’s eye sign which
is diagnostic.

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➢ Doppler may show mass with doughnut sign and is useful to check blood
supply of bowel.
➢ Plain X-ray abdomen shows multiple air fluid levels.
MANAGEMENT
INITIAL MANAGEMENT
• Ryle’s tube aspiration (Wide bore nasogastric aspiration)
• IV fluids
• Antibiotics
• Catheterisation
LATER MANAGEMENT: NON-OPERATIVE MANAGEMENT
• Reduction by hydrostatic pressure using either warm saline or micro-barium
sulphate solution or air.
• Barium or saline is infused into the rectum through a catheter (Foley’s catheter).
• Under fluoroscopy, reduction can be observed.
• Child will pass large quantity of air and feces, distension reduces, child shows
recovery and stops crying.
• Air or contrast enters the proximal bowel freely.
• Palpable abdominal mass disappears.
• Rare complication is perforation of colon. It is done in early stage within 24 hours
of presentation.
• 70% cases of ISS will respond to non-operative method. It is contraindicated in
complete obstruction, perforation and peritonitis.
SURGERY
• Cope’s method: if reduction does not occur, laparotomy is done under general
anesthesia. By gently milking out the intussusception with warm packs, it is
reduced. After reduction, viability of the bowel is checked carefully. If manual
reduction is not possible it is likely bowel is gangrenous and so resection and
anastomosis is done. In case of viable bowel, often terminal ileum is anchored to
the ascending colon and Jackson veil band is cut. Patient also require nasogastric
tube aspiration, IV fluids and antibiotics.
• Laparoscopic approach may be used to reduce the intussusception
• If intussusception persists for more than 48 hours or intussusception in adult
requires resection. Ileocolic resection is sufficient.

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VOLVULUS

VOLVULUS
• Volvulus is the twist (rotation) in the axis of the loop of the bowel either
clockwise or anticlockwise.
• 15% of large bowel obstruction is due to volvulus.
• Sigmoid colon is the commonest site (Anticlockwise)-65%.
• The rotation causes early obstruction of the vascular pedicle supplying the
affected portion.
• Unless recognized early, volvulus leads to intestinal infarction which often
involves large segments of the gut.
• Risk factors for small bowel volvulus (which may affect the whole of the mid-
gut):
➢ Adhesions
➢ Bands between the anti-mesenteric aspect of the bowel
➢ Anterior abdominal wall
➢ Congenital mal-rotation of the gut
• Risk factors of sigmoid volvulus:
➢ Chronic constipation
➢ Redundant pelvic mesocolon
CAECAL VOLVULUS
• Caecum is the second common site (clockwise) (C for C)-30%.
• Its common in females, presents as intestinal obstruction.
• Caecal bascule is the presence of constricting band across the ascending colon
(Bascule-French-See-saw and balance).
• Caecum will be markedly distended and found in the center of the abdomen.
• It is due to lack of fixation of the caecum- mobile caecum.
• Occasionally it is associated with mal-rotation.
• Caecal volvulus is the commonest cause of large bowel obstruction in pregnancy.
• X-ray shows round gas shadow in right iliac region. CT scan is very useful.
Barium enema is also helpful.
• Resection and anastomosis (surgery) is the only treatment.
• Volvulus of small intestine (mid-gut) volvulus neonatorum, gastric volvulus are
other volvulus which can occur.

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SIGMOID VOLVULUS • Sigmoid volvulus is common in:
(VOLVULUS OF PELVIC ➢ Ogilvie’s syndrome
COLON) ➢ Mentally retarded individuals
• Common in Asia especially South
India because of high fiber diet.
• Common cause of large bowel
obstruction in Peru and Bolivia due
to high altitude.
• More common in males and old
age.
• It is common in patients with
chronic constipation with laxative
abuse.
• Predisposing factors include:
➢ Adhesions
➢ Peridiverticulitis ➢ Chagas’s disease
➢ Overloaded redundant pelvic ➢ Hypothyroidism
colon ➢ Anticholinergic drugs
➢ Long pelvic mesocolon ➢ Multiple sclerosis
➢ Narrow attachment of sigmoid ➢ Scleroderma
mesocolon. ➢ Parkinson’s disease
• Sigmoid volvulus is always
anticlockwise. TYPES
• It requires one and half turn of • Acute
rotation to cause vascular • Recurrent
obstruction and gangrene which
eventually leads to perforation
either at the root or at the summit of
the sigmoid loop. CLINICAL FEATURES
• Enormous distension of the colon • Pain in the abdomen- initially left
occurs. Sometimes ileum comes to sided, eventually all over.
the root of the sigmoid volvulus and • Absolute constipation
encircles it causing compound (Obstipation- no feces, no flatus)
volvulus in which case knotted • Enormous distension of abdomen,
small bowel also becomes starting from left iliac fossa
gangrenous- ileosigmoid knotting.

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extending to the whole of the • Contrast enema (dilute barium/
abdomen (tympanic abdomen) water soluble contrast media is
• Late vomiting and eventually used)
dehydration ➢ Birds beak sign (Ace of spades
• Features of peritonitis. appearance)- upper end of
• Hiccough and retching can occur. barium column tapers into the
• Tyre like feel of the abdomen is spirally twisted distal sigmoid
diagnostic. colon.
• CT scan (for difficult cases): shows
DIFFERENTIAL DIAGNOSIS
characteristic whirl pattern.
• Ogilvie’s syndrome: it is acute
• Blood- full blood count, renal
colonic pseudo obstruction. It is
function tests, serum electrolyte.
due to malfunctioning sacral
parasympathetic nerves. Splenic TREATMENT
flexure is the junction of collapsed • Ryle tube aspiration
and dilated large bowel. • IV fluids
Descending colon is atonic causing • Catheterisation
acute functional obstruction. It may • Antibiotics
be due to trauma, retroperitoneal • A flatus tube or sigmoidoscope is
irritation, antidepressants, uremia, passed in operation theatre (proper
diabetes, myxedema, hypokalemia care is taken otherwise it leads to
etc. prokinetic drugs, colonoscopic perforation). If it de-rotates, patient
decompression, tube Caecostomy will pass flatus and feces and
are the treatment distention reduces.
• Fecal impaction • If de-rotation does not occur,
• Carcinoma recto-sigmoid region laparotomy through midline
• Idiopathic megacolon incision should done. Dilated
INVESTIGATIONS sigmoid colon is de-rotated
manually and checked for viability.
• Plain X-ray (Diagnostic in 70-80%)
If viable, it can be fixed to the
➢ Omega sign- single, grossly
lateral wall of abdomen or pelvis-
distended loop of colon arising
sigmoidpexy.
out of the pelvis and extending
• If sigmoid colon is gangrenous, it is
towards the diaphragm.
resected and proximal cut end is
➢ Coffee- bean sign or Bent-inner
tube sign. brought out as colostomy and distal
end is brought out as mucous
fistula, from the rectum (Paul-

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Mikulicz operation). Later after 6
weeks, continuity is maintained
after proper preparation. PARALYTIC ILEUS
• Resection of the gangrenous
sigmoid done; proximal cut is PARALYTIC ILEUS
brought out as end colostomy, (ADYNAMIC
distal end closed- Hartmann’s INTESTINAL
operation. Later in 6-12 weeks
OBSTRUCTION)
colorectal anastomosis is
maintained. • Paralytic ileus is a state in which the
intestines fail to transmit peristalsis
• Primary resection and anastomosis
due to failure of neuromuscular
is not advisable because of the
mechanism i.e. Auerbach’s and
contamination and anastomotic
Meissner’s plexus.
leak.
• It may be localized or generalized.
• Mortality in sigmoid volvulus is
due to perforation, peritonitis and • Causes include:
septicemia. ➢ Electrolyte imbalance:
hypokalemia
➢ Postoperative, intestinal
ischemia
➢ Infective- pus, blood (sepsis),
bile, toxins, enteritis
➢ Uremia
➢ Spinal injury and surgery
➢ Retroperitoneal hemorrhage
➢ Plaster jacket
• The small bowel is distended
throughout its length.
• Absorption of fluid, electrolytes
and nutrients is impaired.
• Significant amounts of fluid may be
lost from the extracellular
compartment.
CLINICAL FEATURES
• Usually history of recent operation
or trauma.

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• No passage of flatus and keeping in place for few
• No bowel sounds hours.
• Marked abdominal distention ➢ Most often, patient recovers in
• Vomiting of large volumes of fluid 3-6 days by conservative
• Tachycardia treatment.
• Respiratory distress due to pressure ➢ In prolonged life threatening
over diaphragm paralytic ileus, laparotomy is
done and bowel is
• High pitched tinkling note ‘like
decompressed with Savage’s
bells at evening pealing’
decompressor and closed with
• Dull abdominal pain (not colicky)
tension sutures
• Features of fluid/ protein/
• Catchpole regime: adrenergic
electrolyte imbalance
blocking agent along with
INVESTIGTIONS cholinergic stimulant
• Serum electrolytes: especially (neostigmine) is used rarely only in
potassium. resistant cases as medical therapy.
• ECG
• X-ray abdomen: dilated loops of
ADHESIONS AND BANDS
small bowel. Gas may be present in • This is the most common cause of
the colon. intestinal obstruction in Western
• Ultrasound abdomen to find out the countries.
possible cause of ileus e.g. sepsis • Causes:
➢ Infection due to peritonitis,
TREATMENT appendicitis, post-laparotomy
• Nasogastric aspiration and other acute infective
• Primary cause is treated abdominal conditions.
• IV fluids ➢ Materials used during surgery
• Electrolyte management cause dense inflammatory
• Catheterization and urine output reactions- silk, thread, foreign
measurement body, mop and gauze, talc
• Do not stimulate peristalsis (“Don’t powder, drugs like
flog a tired horse”) sulphonamides and penicillins
➢ Measure abdominal girth to see ➢ Ischemia of bowel due to poor
if patient is recovering or not. blood supply, sepsis.
➢ Decompression of large bowel ➢ Gynae conditions, bowel injury,
can be tried by inserting a flatus radiation induced enteritis,
tube per anally into the rectum

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Crohn’s disease, other o Open surgical adhesiolysis
inflammatory bowel diseases. using fingers gently.
➢ Specific conditions like TB, o Laparoscopic adhesiolysis
malignancy is becoming popular, safer,
• Types of adhesions ideal with less recurrent
➢ Type 1- Fibrinous adhesions (It adhesion rate and gives
is avascular and flimsy) good results.
➢ Type II= Fibrous adhesions (due o Noble’s plication of
to lack/poor blood supply bowel intestines- wherein adjacent
gets attached to part of coils of small bowel are
peritoneum or omentum or other sutured to prevent in going
parts of the bowel with dense for further recurrent
vascular adhesions to maintain adhesions.
blood supply. It will persist and o Childs-Phillips mesenteric
precipitate intestinal plication is similar way of
obstruction, it is often subacute plication of intestinal
and recurrent) mesentery which will
• Clinical features of intestinal prevent crumpling of bowel
obstruction. and adhesion formation.
• Investigations:
➢ Plain X-ray abdomen shows
dilated bowel loops
➢ Oral contrast with CT scan is
very useful
➢ In partial obstruction only
enterocylsis with water-soluble
iodine dyes can be done.
• Treatment:
➢ Initial:
o IV fluids
o Nasogastric aspiration
o Antibiotics
o Often per anal flatus tube
insertion OBSTRUCTION DUE TO BANDS
o Commonly patient responds • Dense fibrous strings attached from
in 4-5 days. one portion of the abdomen to
➢ Later treatment: another area or bowel causing

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entrapment of intestines leading • Diagnosis is usually on table. But
into obstruction and often enterocylsis, contrast CT scan are
dangerous strangulation. useful.
• Common causes are vitelointestinal
TREATMENT
duct, Ladd’s band, omental band,
• Reduction of hernia, release of
postsurgical fibrous band,
adhesion, if bowel is not viable
tuberculous band.
resect and anastomose.
• Clinical features are like of
• Often major vessels may be present
intestinal obstruction.
adjacent to the constriction ring
• Management is release of the band
which may get injured while
either through laparoscopy or
releasing causing torrential
through laparotomy.
hemorrhage.
INTERNAL HERNIA • Decompression is first done prior to
• Is a rare entity. reduction.
• A portion of small bowel gets
entrapped in one of the
retroperitoneal fossae or congenital
internal defect e.g. mesenteric
defect.
SITES
• Mesenteric defect, defect in
transverse mesocolon.
• Foramen Winslow
• Diaphragmatic hernia
• Hernia through duodenal/ Caecal/
appendiceal/ intersigmoid
retroperitoneal fossae
• Hernia through broad ligament
FEATURES
• Herniation occurs in specific site
whenever there are adhesions.
• Features of intestinal obstruction-
acute/ subacute/ recurrent

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APPENDICITIS

APPENDICITIS
• The appendix begins to bud off from the cecum at around the 6th week of
embryological development.
• The vermiform appendix is narrow, of variable length (2-20cm) with its base
attached to the posteromedial surface of the cecum close to the junction of the
ileum and cecum.
➢ Location: terminal end of cecum where 3 taeniae join, about 2cm below the
ileocecal orifice.
➢ Length: 2-20 cm but can be variable.
➢ Diameter of appendix: 3-8 mm
Size of lumen: 1-3 mm (size of a matchstick).
➢ Luminal capacity <1ml
• The mesoappendix an extension of the mesentery contains appendicular artery of
Seshachalam (a branch of ileocolic artery which is derived from the superior
mesenteric artery).
➢ Recall that the appendicular artery is an end-artery (it does not have
collaterals)
➢ Thrombosis of these vessels thus leads to
gangrenous appendicitis.
• The base of the appendix remains in a fixed
position with respect to the cecum, whereas the tip
can end up in various positions. The different
anatomical locations of the appendix include:
1. Retrocecal appendix (most common)
2. Periileal appendix
3. Postileal appendix
4. Pelvic appendix
5. Subcecal appendix
6. Paracecal appendix
• The appendix is composed of the same layers as
the colon wall: Mucosa, submucosa, inner circular Figure 92: Positions of the appendix
muscle, outer longitudinal muscle and serosa (adapted from SRB’s Manual of Surgery)

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• The submucosal layer of the appendix has lymph follicles. When these enlarge
in response to infection, the swollen submucosal layer can block the lumen of the
appendix.
• Although many claim that the appendix is merely a vestigial organ, it is actually
an immunological organ and secretes IgA. However, it is not an essential organ
and can be removed without immunological compromise.
• Acute appendicitis is the inflammation of the appendix.
• It is one of the most common acute surgical diseases.
• It is common in young white males at the peak of lymphoid tissue growth. A
second peak in the incidence of appendicitis occurs in the elderly.
• Fiber rich diet prevents appendicitis while less fiber increases chances of
appendicitis.
• It is common in May and August (seasonal variation) and is often called as
epidemic appendicitis.

ETIOLOGY
• Etiology remains unclear. Diet may be involved (Reduced fiber content) as the
disease is very common in West but rare in Africa.
• Obstruction of lumen (obstructive appendicitis)
➢ Fecalith (small, firm ball of stool most common cause in adults)- it is
associated with gangrene or perforation
➢ Strictures
➢ Tumors
➢ Gallstones
➢ Foreign body
➢ Round/ thread worm/Pinworm (Oxyuris vermicularis)
➢ Adhesions and kinking-carcinoma cecum near the base, ileocecal Crohn’s
disease
• Viral infections: associated with mucosal edema and inflammation (lymphoid
hyperplasia) with a bacterial infection.
➢ E. coli (80%)
➢ Enterococci (30%)
➢ Streptococci and Anaerobic streptococci
➢ Clostridium Welchii
➢ Bacteroides

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• Pseudoappendicitis is appendicitis due to acute ileitis following Yersinia
infection. It is often due to Crohn’s disease.

PATHOGENESIS
• Arise from either:
➢ Obstructive causes
➢ Non-obstructive causes (Catarrhal)
OBSTRUCTIVE
• Luminal obstruction (due to either lymphoid obstruction in young patients or
fecalith commonly seen in older patients) leads to increased mucus production
and inflammation.
➢ Recall: the appendiceal mucosa continues to secrete normally despite being
obstructed
• As inflammatory fluid collects inside the lumen there is distention and increase
in intraluminal pressure leading to blockage of venous & lymphatic drainage. The
resident bacteria also multiply rapidly further increasing intraluminal pressure.
• Intraluminal pressure eventually exceeds capillary and venule pressures, however
Arteriolar blood continues to flow in causing vascular congestion and
engorgement.
• Impaired blood supply results in mucosal ischemia and ulceration with ultimate
bacterial translocation/invasion. Bacterial spread through submucosa and
muscularis propria resulting in acute obstructive appendicitis.
• Inflammation and ischemia progress to involve the serosal surface of the
appendix.
• The appendicular artery can thrombose and cause ischemic necrosis which can
cause gangrene, perforation of the tip/base and peritonitis
• After perforation there is localization by greater omentum and dilated ileum. This
can suppurate forming an appendicular abscess, if pus is not present inside it is
referred to as an appendicular mass.
• Acute appendicitis with blockage at the opening of the lumen results in mucus
collecting inside the lumen of the appendix resulting in its enlargement
(Mucocele of the appendix)
NON-OBSTRUCTIVE
• Acute inflammation of mucus membrane with secondary infection without
obstruction causes acute non-obstructive appendicitis.
• It may lead to:

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➢ Resolution
➢ Fibrosis
➢ Recurrent appendicitis
➢ Obstructive appendicitis
➢ Gangrene (rare)
➢ Peritonitis
➢ Suppuration

TYPES
TYPE COMMENT
ACUTE OBSTRUCTIVE • Pus collects in the blocked lumen of the
APPENDICITS appendix which is blackish, gangrenous,
edematous and rapidly progresses leading to
perforation either at the tip or at the base of the
appendix
• This leads to peritonitis, formation of
appendicular abscess or pelvic abscess
• Most often, there will be thrombosis of the
appendicular artery
ACUTE NON-OBSTRUCTIVE • Inflammation of mucous membrane occurs
APPENDICITIS (CATARRHAL) with redness, edema and hemorrhages which
may result in resolution, ulceration, fibrosis,
suppuration, recurrent appendicitis, gangrene
(rare) and peritonitis
RECURRENT APPENDICITIS • Repeated attacks of non-obstructive
appendicitis leads to fibrosis, adhesion causing
recurrent appendicitis
SUBACUTE APPENDICITIS • Is the milder form of acute appendicitis
STUMP APPENDICITIS • Is retained long stump of appendix after
commonly laparoscopic appendicectomy

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CLINICAL FEATURES
• Rare before age of 2 (common in other age groups & children i.e. 5 to 35 years)
• Murphy’s triad:
➢ Pain
➢ Vomiting
➢ Temperature
SYMPTOMS
• Pain: earliest symptom.
➢ Visceral pain starts around the umbilicus-
T10 distribution (due to obstruction and
distension of appendix and stimulation of
visceral afferent stretch fibers). Pain is a
dull ache or colic (presumably from
obstruction of the appendiceal lumen)
➢ After a few hours somatic pain occurs in
right iliac fossa (due to irritation of parietal
peritoneum because of inflamed appendix)
➢ Pain is severe and diffuse-spread of Figure 93: McBurney's point is the junction of
infection into general peritoneal cavity. lateral 1/3rd and medial 2/3rd of spinoumbilical
➢ Not all patients experience this shift of pain line. McBurney's/Gridiron's/McArthur's incision
is perpendicular to this line in this point. (Image
and the presentation may start with from SRB's Manual of Surgery)
discomfort in the right lower quadrant.
Retrocecal appendicitis may cause pain higher in the right abdomen whereas
appendicitis located in the pelvis may cause vague pelvic discomfort.
➢ Patients often report that movement and coughing induces sharp exacerbation
of the pain.
• Vomiting and nausea: due to reflex pylorospasm
• Anorexia
• Constipation (usual feature)/ diarrhea (20%) (diarrhea common in postileal or
pelvic appendix)
• Fever (low grade)
• Tachycardia
• Urinary frequency: Bladder irritation from contact with inflamed appendix
• Note:
➢ In children it is important to ask about a sore throat or flu-like symptoms as
these often accompany mesenteric adenitis.

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➢ Female patients in particular should be asked about dysuria, frequency and
cloudy/strong smelling urine because UTI can often cause lower abdominal
pain. Likewise, a menstrual history is essential. A missed period may point to
an ectopic pregnancy.
➢ Pain at mid-cycle may indicate that the pain is due to ovulation
(Mittelschmerz) and vaginal discharge may indicate pelvic inflammatory
disease.
SIGNS
• Tachycardia
• Mild pyrexia. A high temperature (>39oC) indicates probable abscess formation
or some other diagnosis such as a viral illness.
• The tongue is also usually furred.
• An appendicular abscess or mass (phlegmon) if present may be palpated in the
right iliac fossa
• Important signs:
➢ Abdominal Tenderness and rebound tenderness in right iliac fossa (Blumberg
sign/Release sign)
o Ask the patient to cough while watching the facial expression. If coughing
produces obvious pain, the patient should be asked to indicate the site of
maximum pain. In acute appendicitis the patient points to the right iliac
fossa.
o Rebound tenderness may be elicited by pressing gently into the right
lower quadrant of the abdomen and then suddenly releasing the hand,
watching the patient’s face for signs of discomfort (Another approach is
to percuss the area, this elicits the same response and is kinder).
➢ Pointing sign- at Mc Burney’s point (a point one third the distance along a
line drawn from the right anterior superior iliac spine to the umbilicus)
➢ Signs of peritoneal irritation
o Rovsing sign- on pressing left iliac fossa, pain occurs in RIF due to shift
of bowel loops which irritate the peritoneum.
o Psoas test (Cope’s)- for Retrocecal appendix, hyperextension of hip
causes pain in the RIF. The patient will get relief by flexing the right thigh
at the hip which relaxes the psoas muscle.
o Obturator test- for pelvic appendix, internal rotation of right hip causes
pain in RIF due to irritation of obturator internus muscle.

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➢ Baldwing test- positive in Retrocecal appendix- when legs are lifted off bed
with knee extended, the patient complains of pain while pressing on abdomen
(Ribs-ilium)
➢ Bastede sign-this is an obsolete sign in chronic appendicitis pain and
tenderness is felt in the right iliac fossa on inflation of the colon with air.
• Hyperesthesia in Sherren’s triangle (this triangle is formed by anterosuperior iliac
spine, umbilicus and pubic symphysis).
• RECTAL EXAMINATION SHOULD ALWAYS BE DONE. It elicits
tenderness on the right.
• Note: in elderly patients presentation tends to be atypical, leading to delayed
diagnosis. The pain is less and it may present as small bowel obstruction. There
is delayed leukocytosis. There is a higher risk of perforation and mortality than
in young patients.
• Perforation at the time of surgery is more often seen in very young children (<5
years) and in older adults (>60 years) as a result of delayed diagnosis.

INVESTIGATIONS
1. Bloods: Full blood count with differential: Leukocytosis (>10, 000 in 90% of
cases), usually with concomitant left shift (polymorphonuclear neutrophil
predominance)
2. Urinalysis: helpful in ruling out genitourinary causes of symptoms. RBCs and
WBCs may be present secondary to extension of appendiceal inflammation to the
ureter. Significant hematuria or pyuria and bacteriuria from a catheterized
specimen should suggest underlying urinary tract pathology.
3. Imaging
➢ Plain X-ray
o Abdominal X-ray: not particularly useful in most cases i.e. in clear-cut
features of acute appendicitis. May reveal appendicolith/fecalith (<15%
of cases). It is indicated if there is some clinical suspicion of intestinal
obstruction or ureteric colic.

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o Chest X-ray: air under the right side of
the diaphragm signifies perforation.
➢ Ultrasound:
o Sensitivity of 85% and specificity of
92% for diagnosing appendicitis
o Positive findings: enlarged (> 6mm),
hyperechoic thickened appendix wall
(>2mm)-target sign i.e. appendiceal
wall thickening, appendicolith,
interruption of submucosal continuity,
periappendicular fluid and non-
compressible appendix (Note: the
appendix will become compressible
after perforation, this is a source of false
negatives)
o Especially useful in ruling out
gynecological pathology. It may rule
out ureteric stones, pancreatitis, ovarian
cysts, ectopic pregnancy and also
confirm appendicular mass or abscess.
➢ Abdominal CT with contrast:
o Very sensitive (95-98%) and Somewhat Figure 94: Ultrasound showing dilated non-
specific (83-90%) compressible appendix in two different patients
o Useful in identifying several other
inflammatory processes that may
present similarly to appendicitis
o Positive findings:
- Dilation of appendix to >6mm in
diameter
- Thickening of appendiceal wall
(representing edema)
- Non-filling of the lumen by contrast
or air.
- Periappendiceal streaking
(densities within perimesenteric
fat) Figure 95: Abdominal CT scan demonstrating
appendicolith and acute appendicitis
- Periappendicular fluid collection

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- Presence of appendicolith
- Presence of mass/abscess
4. Laparoscopy: most useful in female patients in the reproductive age
5. Aspiration cytology: peritoneal fluid is aspirated using a fine catheter introduced
immediately below the umbilicus, the test is positive if more than 50% of the
cells are neutrophils. This indicates the presence of infection.
6. Gravindex: to rule out ectopic pregnancy for female patients.

DIAGNOSIS
• Based on the Alvarado Score (MANTRELS
Score)
➢ M- migration of pain to right iliac fossa-
1
➢ A- anorexia- 1
➢ N-nausea/vomiting-1
➢ T- tenderness in right iliac fossa
(Blumberg sign)-2
➢ R-rebound tenderness-1
➢ E- Elevated temperature (fever 37.3oC)-
1
➢ L-Leukocytosis (>10, 000)-2
➢ S-shift towards neutrophils
(neutrophilia)-1
• Outcomes:
➢ <5: not sure
➢ 5-6: compatible
➢ 6-9: probable
➢ >9: confirmed

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TREATMENT
• Resuscitation (ABCs)
• Preoperative: IV fluids plus antibiotics (Ciprofloxacin + Metronidazole)
• For uncomplicated appendicitis, Appendicectomy can be done
➢ Approaches:
o Gridiron incision: perpendicular to McBurney’s point
o Lanz crease incision: centering at McBurney’s point (cosmetically better)
o Rutherford Morison’s muscle: cutting incision (Muscles are cut upwards
and laterally)
o Right lower paramedian incision/lower midline incision: when in doubt
or when there is diffuse peritonitis Troubles in Appendicectomy
o Laparoscopic approach: becoming
popular and better • During surgery if appendix is found normal,
o Foweler-Weir approach: by other cause for symptoms should always be
cutting muscle medially over the looked for e.g. Meckel’s diverticulum,
rectus Crohn’s disease, ovarian/pelvic causes in
➢ Both open and laparoscopic techniques females, malignancy
are appropriate. Laparoscopic • Appendicular tumor may be found. If it is
appendectomy is associated with less the tip, appendicectomy is sufficient. It
postoperative pain, a shorter hospital could be carcinoid tumor. If it is in the base
course, better cosmesis and faster right hemicolectomy is done.
return to work • Absence of appendix (rare). Caecum and
➢ Postoperative antibiotics are given for taeniae should be traced properly before
5 days (metronidazole and finalizing it.
cefuroxime). IV fluids are also given. • Appendicular abscess/pelvic abscess
Once bowel sounds are heard, oral diet formation
is started. • Malignancy in the cecum is identified on
• Drugs (for 5 days) table- right hemicolectomy should be done.
➢ Ciprofloxacin • If Crohn’s disease is identified during
➢ Benzyl penicillin surgery, appendicectomy can be done with
➢ Metronidazole care if the base of the appendix is normal but
➢ Gentamycin in rare occasions where the appendix is
• Analgesics involve by Crohn’s disease appendicectomy
• Selected advanced cases with appendiceal should not be done but treat only with
abscess may initially be managed antibiotics and steroids otherwise fistula can
nonoperatively with antibiotics and develop

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percutaneous CT-guided abscess drainage. This may be followed by the
development of a fecal fistula but this normally heals spontaneously.
• For perforation: Peritoneal washout and parenteral antibiotics.

DIFFERENTIAL DIAGNOSIS
GASTROINTESTINAL CONDITIONS
• Gastroenteritis
• Mesenteric adenitis
• Meckel’s diverticulum
• Intussusception
• Typhoid fever
• Primary peritonitis
GENITOURINARY CONDITIONS
• Ectopic pregnancy
• Pelvic inflammatory disease
• Ovarian torsion/cyst/tumor
• Urinary tract infection/pyelonephritis
• Ureteral stone
CHILDREN
• Meckel’s diverticulitis
• Acute colitis
• Round worm colic
• Acute iliac lymphadenitis
• Intussuception
• Lobar penumonia
ELDERLY
• Acute diverticulitis
• CA caecum
• Mesenteric ischemia
• Intestinal obstruction
• Aortic aneurysm leak
• Crohn’s disease
FEMALES
• Ruptured ectopic pregnancy

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• Ovarian cyst
• Ovarian abscess
• Oophritis
• Salpingitis
• Mittelschmerz- rupture of ovarian follicle during mid-menstrual period

COMPLICATIONS OF ACUTE APPENDICITIS

1. Relapse and recurrent appendicitis
2. Appendicular mass
➢ Localization of infection occurring 3 to 5 days after an attack of acute
appendicitis. Inflamed appendix, greater omentum, edematous cecum, parietal
peritoneum and dilated ileum (ileus) forms a mass in the right iliac fossa.
➢ The mass is tender, smooth, firm, well localized, not moving with respiration,
not mobile, all borders well made out (well localized) and resonant on
percussion. Patient may have fever and features of toxicity.
➢ Investigation: Ultrasound confirms the mass
➢ Treatment: Conservative as nature has already localized the infection. If
disturbed it will cause a fecal fistula
o Observation (temperature, BP, pulse)
o Marking the mass to identify progression/regression
o Antibiotics (Ampicillin, metronidazole, gentamicin or other drugs given
depending on severity and requirement)
o IV fluids
o Analgesics
o Initial nasogastric aspiration
- Patient usually show response by 48 to 72 hours and mass reduces in
size, temperature and pulse becomes normal. Appetite is regained.
90% of patients respond to conservative treatment
o Patient is discharged and advised to come for interval appendicectomy
after 6 weeks
➢ Contraindication to conservative treatment:
o When diagnosis is in doubt
o Acute appendicitis in children and
elderly
o Burst, gangrenous appendicitis
o In patients in whom diffuse peritonitis
sets in

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3. Appendicular abscess:
➢ Signs and symptoms:
o High fever, features of toxicity, tender smooth, dull (to percuss), soft
welling in right iliac fossa which lies towards right lateral and lower side
with clear upper margin but indistinct lower margin
o Increasing right lower quadrant pain, tender, fluctuant right lower
quadrant mass palpable on rectal examination, anorexia, fever, localizing
peritonitis, leukocytosis
➢ Diagnosis: confirmed by CT scan
➢ Treatment:
o Antibiotics
o Percutaneous or operative drainage, Pelvic abscess is drained per-rectally
or through posterior colpotomy (in females)
➢ Interval appendicectomy is done after 3 months
4. Perforation- 20% mortality
5. Generalized peritonitis, septicemia, Overwhelming sepsis and death
6. Portal pyaemia (Pylephlebitis)
➢ Is rare nowadays. It is septic portal system thrombosis. It is commonly seen
in immunosuppressed individuals. Infection spreads to liver through portal
vein causing rapid multiplication of virulent organisms leading to septicemia
(toxemia with hypotension, tachycardia), jaundice, tender palpable liver.
Patient with be drowsy.
➢ Treatment- antibiotics like cefoperazone, amikacin, metronidazole,
meropenem, fluid management, ventilator support
➢ It carries a poor prognosis.
7. Intestinal obstruction due to obstructive ileus, inflammatory adhesion, formation
of band between appendix and omentum or between appendix and small bowel
8. Intraperitoneal abscess formation, either subphrenic or multiple small intraloop
abscesses

COMPLICATIONS AFTER APPENDICECTOMY

1. Paralytic ileus
2. Reactionary hemorrhage due to slipping of ligature of the appendicular artery.
3. Residual abscess (pelvic, paracolic, local, subdiaphragmatic)
4. Portal pyemia (Pylephlebitis)
5. Recurrent intestinal obstruction due to formation of adhesions and kinking
6. Right inguinal hernia (direct)- due to injury to illoinguinal nerve

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7. Wound infection and sepsis- 10%
8. Fecal fistula usually following drainage of an abscess:
➢ Conservative treatment- antibiotics, IV fluids, dressing, zinc oxide cream over
the skin, observation
➢ Most of the time fistula subsides provided there is no distal obstruction by
adhesion or kinking or specific causes like carcinoma or TB
➢ If persists even after 6 weeks, resection of ileocecal segment and anastomosis
is done
9. Respiratory problems and DVT

DIVERTICULAR
DISEASE

CHRONIC
INFLAMMATORY
BOWEL DISEASE

COLON POLYPS

CARCINOMA OF THE
COLON AND RECTUM

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CARCINOMA OF THE
ANUS

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CHAPTER 8: LIVER AND SPLEEN

LIVER AND SPLEEN

LIVER AND SPLEEN INJURY

LIVER TUMORS
BENIGN TUMORS
• Only 5% of liver tumors are benign, these include:
➢ Hepatocellular adenoma
➢ Focal nodular hyperplasia
➢ Hemangioma (most common)
o Capillary (no clinical consequence)
o Cavernous-7% (capable of attaining large size and rupturing)
➢ Lipoma
• The incidence of adenoma is 1 per million in women with a history of oral
contraceptive use. These medicines increase the risk by a factor of 40. This lesion
most commonly occurs in women between 30 and 50 years.
• Adenoma and focal nodular hyperplasia are 5 times more common in female
patients.
CLINICAL FEATURES
• Symptoms:
➢ Patients with adenomas and hemangiomas can be asymptomatic or present
with dull pain, rupture can produce sudden onset of severe abdominal pain.
These lesions can also become large enough to cause jaundice or symptoms
of gastric outlet obstruction (nausea and vomiting)
➢ Focal nodular hyperplasia is rarely symptomatic.
• Signs:
➢ Large lesions can be palpated
➢ Jaundice may occur in patients if the tumor causes bile obstruction
DIAGNOSIS AND INVESTIGATIONS
• The lesions are most often found incidentally at laparotomy or on imaging studies
requested for other reasons.

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• Lab evaluation is often unremarkable although hemorrhage in an adenoma can
lead to hepatocellular necrosis and a rise in transaminase levels.
• Hemangioma can cause a consumptive coagulopathy.
• Ultrasound differentiates cystic from solid lesions.
• Triple-phase computed tomography (CT) is the best study for distinguishing
between various types of benign and malignant lesions but in certain cases, this
determination is not possible.
➢ Adenomas are low density lesions
➢ Focal nodular hyperplasias may appear with a filling defect or central scar
➢ Hemangiomas have early peripheral enhancement after contrast
administration. Hemangiomas should not be biopsied because of the risk of
bleeding.
MANAGEMENT
• Patients with adenoma who are using oral contraceptive should stop.
• If the lesion does not regress resection should be considered in otherwise healthy
individuals because of the risk of malignant degeneration or hemorrhage.
• Relative contraindications to resection:
➢ Tumor that is technically difficult to resect
➢ Tumor of large size in which a large portion of the liver would need to be
removed
• Symptomatic hemangiomas should be resected, if possible. Because focal
nodular hyperplasia is not malignant and rarely causes symptoms it should not be
resected unless it is found incidentally at laparotomy and is small and peripheral
enough to be wedged out easily.

MALIGNANT TUMORS
• Malignant tumors of the liver may either be primary or secondary.
• The most common hepatic malignancy is as a result of metastases (Secondary
tumor), the primary tumor is usually from colon, breast, lung (especially
bronchogenic carcinoma), pancreas and stomach.
HEPATOCELLULAR CARCINOMA (HEPATOMA)
• This is a malignant tumor derived from hepatocytes frequently found in
association with chronic liver disease particularly cirrhosis.
➢ 80-90% of patients with hepatocellular carcinoma have underlying cirrhosis
with alcoholic cirrhosis being the predominant type in western countries. In
the Far east, post-hepatitis cirrhosis is more common.

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• Hepatocellular carcinoma accounts for 80% of liver cancers and <2% of all cases.
• It is more common in males (3:1) and is usually diagnosed in the fifth or sixth
decade.
ETIOLOGY AND RISK FACTORS
• Infectious:
➢ Hepatitis B
➢ Hepatitis C
➢ Liver flukes
• Non-infectious
➢ Cirrhosis (most commonly due to alcoholism)
➢ Aflatoxins (Produced from fungi found in peanuts)
➢ Hemochromatosis
➢ Alpha-1 antitrypsin deficiency
➢ Anabolic steroid use
➢ Smoking, Vinyl chloride and oral contraceptives
CLINICAL FEATURES
• Symptoms:
➢ Weight loss
➢ Weakness
➢ Dull pain in the right upper quadrant or epigastrium or shoulder
➢ Nausea and vomiting
• Signs:
➢ Signs of portal hypertension including splenomegaly and ascites
o Splenomegaly (33%)
o Ascites (50%)- due to hypoalbuminemia and decreased oncotic pressure
➢ Jaundice
➢ Non-tender hepatomegaly
➢ A bruit can commonly be heard over a hepatocellular carcinoma due to its
abundant vascularity
DIAGNOSIS AND INVESTIGATIONS
• Bloods:
➢ Non-specific: ALP, AST, ALT, Gamma-glutamyl transferase (GGT), and
des-gamma-carboxy prothrombin (DCP) are raised
➢ Specific blood marker: alpha fetoprotein (AFP)

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➢ Hepatitis panel because most cancers occur in the setting of liver disease and
cirrhosis.
• Imaging: differentiate benign and malignant lesions
➢ Contrast CT and Ultrasound can visualize the tumor. Ultrasound can
distinguish cystic from solid lesions, whereas CT or MRI can reveal multiple
lesions and clarify anatomic relationships. They can also demonstrate
nodularity of the liver, hypersplenism, and portal hypertension indicative of
underlying disease.
➢ CT or ultrasound-guided needle biopsy will
give the definitive diagnosis.
MANAGEMENT
• Before resection, assess underlying health of the
liver using Child-Turcotte-Pugh scoring system.
➢ Patients with Child Class B disease may
tolerate a limited resection
➢ Patients with Child class C disease will
generally not tolerate a resection
• A decision to resect the tumor depends on
comorbid disease and the location and size of the
tumor.
• Surgical resection is the only cure, consisting of
Figure 96: Child-Turcotte-Pugh Scoring
either: system for Cirrhosis
➢ Lobectomy
➢ Segmental/wedge resection
• A 1-cm margin is required
• Transplant is also a possibility (Especially for patient with small tumors who are
not candidates for resection because of tumor location or concomitant cirrhosis)
however, there often is a high recurrence ate due to the continued presence of the
underlying risk factors e.g. hepatitis B, C etc.
➢ Milan criteria (tumor <5cm or no more than 3 tumors the largest of which is
<3cm) will receive extra points on the liver transplant list.
• Local chemotherapy infusion into the hepatic artery, hepatic artery embolization
and liposomal chemotherapy are the newer treatment options being explored.
PROGNOSIS
• Most patients die within the first 4 months if the tumor is not resection.

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• After resection or transplant the 5-year survival rate is about 25%.
METASTATIC NEOPLASMS
• Arise most commonly from colon, breast, or lung (especially bronchogenic
carcinoma), pancreas and stomach.
CLINICAL FEATURES
• Patients are usually asymptomatic until the disease is advanced and the liver fails
• Symptoms:
➢ Fatigue
➢ Weight loss
➢ Epigastric fullness
➢ Dull right upper quadrant pain
➢ Ascites
➢ Jaundice
➢ Fever
DIAGNOSIS AND
INVESTIGATIONS
• Bloods:
➢ Increased ALP, GGT, lactic
dehydrogenase (LDH), AST
and ALT (though
nonspecific)
➢ Raised carcinoembryonic
antigen (CEA) is seen in
those with colonic cancer
• Imaging:
➢ Mets will enhance on contrast
CT
➢ Intraoperative ultrasound Figure 97: Abdominal CT in hepatic mets (Note slit like
with liver palpation is the appearance of intrahepatic IVC secondary to compression by
most sensitive diagnostic tool mets. Also note presence of ascites and bilateral pleural effusions,
left greater than right) Image from First Aid for the Surgery
MANAGEMENT Clerkship 2nd Ed..
• Resection, if possible is the
treatment of choice

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➢ When colon cancer metastasizes to the liver, resection of up to 3 lesions has
been shown to improve survival and should be attempted as long as the
operative risk is not prohibitive.
➢ In general, liver metastases from other tumors should not be resected.
• Radiofrequency ablation (RFA) is now extensively done even for multiple
lesions, and the short-term results are promising.

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CHAPTER 9: PANCREAS

PANCREAS
• The pancreas also known as ‘abdominal
tiger’. Previously it was thought to act as a
cushion for the stomach.
• The pancreas is a large central elongated
retroperitoneal gland overlying the vertebral
column (L1-L2) in the supracolic
compartment of the abdomen.
• It lies posterior to the stomach, separated by
the lesser sac.
• The pancreas is divided into:
➢ Head (30% of the gland mass): lies in the
concavity of duodenum, overlying the
body of the L2 vertebra and the vena
cava. Coming off the side of the
pancreatic head and passing to the left
and behind the superior mesenteric vein
is the uncinate process of the pancreas.
➢ Neck: the aorta and superior mesenteric
vessels lie behind the neck of the gland.
Behind the neck of the pancreas near its
upper border the superior mesenteric
vein joins the splenic vein to form the
portal vein.
➢ Body
➢ Tail: reaches the hilum of the spleen
• The pancreas weighs about 80g and is
Figure 98: Posterior relation of the pancreas (Image from
about 15-20cm in length. Bailey and Love Short Practice of Surgery)
• The pancreas is a key regulator of
digestion and metabolism through both endocrine (concerned with the production
of hormones) and exocrine (concerned with the production of enzymes needed
for digestion) function.
• 80-90% of the pancreas is composed of exocrine acinar tissue which are
organized into lobules.

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• The main pancreatic duct branches into interlobular and intralobular ducts,
ductules and finally acini.
➢ The main duct is lined by columnar epithelium which becomes cuboidal in
the ductules.
➢ Acinar cells are clumped around a central lumen which communicates with
the duct system.
➢ The main pancreatic duct (duct of Wirsung) begins in the tail of the pancreas
and runs on the posterior surface of the body and head of the pancreas
receiving numerous tributaries at right angle along its length (Herring bone
pattern).
➢ The main pancreatic duct is joined by the common bile duct (a combination
of the common hepatic duct and the cystic duct) in the wall of the second part
of the duodenum to form hepatopancreatic ampulla of Vater and opens on the
summit of major duodenal papilla (8-10 cm from the pylorus)
• The accessory pancreatic duct (Duct of Santorini) begins in the lower part of the
head and opens into the duodenum at minor duodenal papilla (6-8cm from the
pylorus)
• The endocrine pancreas consists of islets of Langerhans which comprise of 4
recognized cell types:
➢ A cells (-cells)-20% which produce glucagon
➢ B cells (-cells)-75% which produce insulin, islet amyloid-associated
polypeptide and pancreastatin
➢ D cells which secrete somatostatin and probably gastrin
➢ F cells which secrete pancreatic polypeptide
• Within an islet, the B cells form an inner core surrounded by other cells.
Capillaries draining the islets cells drain into the portal vein, forming a pancreatic
portal system.
• The pancreas has a complex vascular supply and venous/lymphatic drainage and
is surrounded by the duodenum and upper jejunum.

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• Arterial blood supply is from:
➢ Pancreatic branches of splenic artery
➢ Superior pancreaticoduodenal artery (a
branch of the gastro-duodenal artery which
arises from the hepatic artery a branch of the
coeliac trunk)
➢ Inferior pancreaticoduodenal artery (a
branch of the superior mesenteric artery)
• Venous drainage follows a similar pattern to the
arteries and is by the superior and inferior
pancreaticoduodenal veins into the portal vein.
• The pancreas receives its parasympathetic
supply from the vagus and sympathetic
innervation from the splanchnic nerves.
• During the embryonic development of the
Figure 99: Arterial and venous blood supply of the
pancreas, there are 9 key processes that pancreas (Images from SRB's Manual of Surgery 2nd
occur. Ed)
➢ Day 26: Dorsal pancreatic duct arises
from the dorsal side of the duodenum.
➢ Day 32: Ventral bud arises from the base of the hepatic diverticulum
➢ Day 37: Contact occurs between the buds. Fusion by the end of week 6
➢ Week 6: Ventral bud produces the head and uncinate process
➢ Week 6: Ducts fuse
➢ Week 6: Ventral duct and distal portion of the dorsal duct form the main duct
(Duct of Wirsung)
➢ Week 6: Proximal dorsal duct forms the duct of Santorini
➢ Month 3: Acini appear
➢ Month 3-4: Islets of Langerhans appear and become biologically active
• Malrotation of the ventral bud in the 5th week results in an annular pancreas while
the mode of ductule fusion in the 17th week produces the various possible ductular
patterns.
• Between 12th and 40th weeks of fetal life, the pancreas differentiates into exocrine
and endocrine elements.
• The primitive ducts and their ductules are responsible for the lobular arrangement
of the pancreas.
• The pancreas is associated with both endocrine and exocrine function.

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• The exocrine secretion contains water and bicarbonate ions and digestive
enzymes secreted as inactive precursors (zymogens) into the duodenum in
response to neural and hormonal influences. Enzyme activation begins after the
zymogens enter the duodenum, where mucosal enterokinase cleaves trypsinogen
into trypsin which activates the other enzymes.
➢ In response to a meal, the pancreas secretes digestive enzymes in an alkaline
(pH 8.4) bicarbonate rich fluid. Spontaneous secretion is minimal
➢ The hormone secretin (produced from the S cell of the duodenal mucosa)
evokes a bicarbonate rich fluid (via cAMP cascade).
➢ Cholecystokinin (CCK) also known as pancreozymin (produced from the I
cells of the duodenal mucosa) is produced in response to food. CCK is
responsible for enzyme release (Through phospholipase C, and calcium
mechanism).
➢ The protein part of the pancreatic juice is secreted by acinar cells, duct cells
secrete fluid and electrolytes.
➢ Vagal stimulation increases the volume of secretion.
➢ About 6-20g of digestive enzymes enter the duodenum each day.
➢ During eating, cephalic phase stimulates 10% of pancreatic secretion through
peripherally mediated acetylcholine, gastric phase stimulates further 15% of
pancreatic secretion through gastrin release and vagal stimulation and finally
in the main intestinal phase 75% of the pancreatic juice is secreted by release
of secretin due to duodenal acidification and by release of bile and CCK
following entry of fat and proteins in the duodenal.
• The main stimulus for insulin secretion is an increase in blood glucose level
(hyperglycemia)
• Other stimuli for insulin release include: amino acids (arginine and lysin) and
other hormones (glucagon, growth hormone, cortisol, placental lactogen,
estrogens). Insulin release is also enhanced by free fatty acids in order to prevent
ketoacidosis which would otherwise occur during fasting in normal individuals.
• Glucagon secretion is stimulated by low blood glucose levels (hypoglycemia). It
has catabolic actions and initiates glycogenolysis, gluconeogenesis and break
down of fat into free fatty acids and glycerol.
• Glucagon inhibits protein synthesis.
• Somatostatin is an inhibitory hormone. It inhibits growth hormone, insulin and
glucagon secretion, gastric acid and pepsin secretion, the release of pancreatic
enzymes and intestinal motility. It reduces splanchnic blood flow.

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• The physiological function of pancreatic polypeptide remains unknown.
• Disorders of surgical importance include:
➢ Acute pancreatitis
➢ Chronic pancreatitis
➢ Pancreatic cancer

PANCREATITIS

PANCREATITIS
• This is inflammation of the gland parenchyma of the pancreas.
• For clinical purposes it is useful to divide Marseilles’ Classification of
pancreatitis into: pancreatitis
➢ Acute Pancreatitis: presents as an emergency
and is usually reversible. 1. Acute pancreatitis
o Acute pancreatitis 2. Acute relapsing pancreatitis
o Acute relapsing pancreatitis 3. Chronic relapsing pancreatitis
➢ Chronic Pancreatitis: prolonged and 4. Chronic pancreatitis
frequently lifelong disorder resulting from the
development of fibrosis within the pancreas. Continuous inflammatory
changes result in irreversible morphological changes.
o Chronic pancreatitis
o Chronic relapsing pancreatitis

ACUTE PANCREATITIS
• Acute pancreatitis is an acute condition Acute pancreatitis should be suspected
presenting with abdominal pain and is usually in the alcoholic who develops an
associated with raised pancreatic enzyme levels “upper” acute abdomen. The classic
in the blood or urine as a result of pancreatic picture has a rapid onset (a couple of
inflammation and hemorrhage. hours). The pain is constant, epigastric,
• Acute pancreatitis may recur but is usually radiating straight through to the back
reversible. with nausea, vomiting and retching.
• The disease may occur at any age, with a peak in Physical findings are relatively modest,
young men and older women. found in the upper abdomen.
• It can be classified as (Atlanta Classification):
➢ Mild acute pancreatitis (edematous): characterized by interstitial edema of the
gland and minimal organ dysfunction. 80% of patients have this. It carries a
mortality of 1%.

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➢ Severe acute pancreatitis (necrotizing): characterized by pancreatic necrosis,
a severe systemic inflammatory response and often multi-organ failure. This
carries a mortality between 20-50% (1/3 of patients die due to multiple organ
failure in the early stages while others die after the first week of onset due to
septic complication).
• Pancreatitis can alternatively also be classified as
➢ Acute edematous pancreatitis: occurs in alcoholics or patients with gallstones.
Presents as epigastric and mid-abdominal pain that starts after a heavy meal
or bout of alcoholic intake. Pain is constant, radiates straight through to the
back and is accompanied by nausea, vomiting and (after the stomach is empty)
continued retching. There is tenderness and mild rebound tenderness in the
upper abdomen. During the early stages serum lipase and amylase are elevated
and after a couple of days their levels increase in urine. A key finding to
establish the edematous nature is an elevated hematocrit. Resolution follows
a few days of pancreatic rest (NPO, NG suction, IV fluids).
➢ Acute hemorrhagic pancreatitis: This is a much deadlier disease. It starts as
the edematous form but an early lab clue is lower hematocrit (the degree of
amylase elevation does not correlate with the severity of the disease). Other
findings have been catalogued by the Ranson’s criteria (See assessment of
severity). Intensive care is needed as a common final pathway for death is the
development of multiple pancreatic abscesses that necessitate daily CT scans
and drainage as well as antibiotics.
➢ Acute suppurative pancreatitis (Pancreatic abscess): may become evident in
someone who was not getting CT scans, because persistent fever and
leukocytosis develop about 10 days after the onset of pancreatitis. Imaging
studies done at that time will reveal collection (or collections) of pus.
Percutaneous drainage and antibiotics will be indicated.
PATHOPHYSIOLOGY
• The underlying mechanism of injury in pancreatitis is thought to be premature
activation of pancreatic enzymes within the pancreas, leading to a process of
auto-digestion.
• Multiple etiologies have been identified with alcoholism and gallstone disease
accounting for 80-90% of cases.
➢ Pancreatic ductal obstruction (by gall stones, duodenal ulcers, duodenal
crohn’s, periampullary diverticulm/tumor, trauma, pancreatitic duct stricture,

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pancreatic divisum, ascaris, or Clonorchis Sinensis) leads to ductal
hypertension.
➢ Alcohol causes direct toxicity, hypersecretion of gastric and pancreatic juices,
reflux, plugging of pancreatic proteins, injury by release of free radicals like
superoxide and hydroxyl, spasms of Oddi and stimulates trypsinogen.
• Anything that injures the acinar cell and impairs the secretion of zymogen
granules or damages the duct epithelium and thus delays enzymatic secretion can
trigger acute pancreatitis.
➢ Trypsinogen is first activated and premature activation of trypsin leads to
activation of other enzymes.
➢ Proelastase is activated to elastase and it causes capillary rupture. Prolipase is
activated to lipase and causes metabolism of triglycerides to glycerol and fatty
acids that combine with calcium forming saponified fat. These effects result
in sequestered fluid, saponified fat, blood, and toxins all together forming a
chicken broth fluid.
• Once cellular injury has been initiated, the inflammatory process can lead to
pancreatic edema, extensive hemorrhage and eventually necrosis.
➢ 2 types of necrosis are seen in acute pancreatitis:
o Liquefactive necrosis: due to denaturation of enzymes
o Fat necrosis: due to saponification of peri-pancreatic fat
• Lecithinase, amylase and factors like lysolecithinase, prostaglandins,
bradykinins, kallikrein, myocardial depressant factor, free radicals, cytokine,
tumor necrosis factor and platelet activation factor are also released to have local
and systemic effects.
• As inflammatory mediators are released into circulation systemic complications
can arise such as hemodynamic instability (hypovolemic shock), bacteremia
(Due to translocation of gut flora), acute respiratory distress syndrome and
pleural effusions, gastrointestinal hemorrhage, renal failure and disseminated
intravascular coagulation (DIC).
➢ Toxins released may lead to acute tubular necrosis and so acute renal failure
➢ Left sided diaphragm gets elevated and left sided pleural effusion occurs
➢ Lecithinase reduces the surfactant in the alveoli of lung and infection leads to
pulmonary insufficiency, ARDS and respiratory failure
➢ Because calcium is utilized for saponification hypocalcemia sets in
➢ Diffuse oozing in pancreatic bed occurs which utilizes platelets and causes
DIC

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➢ In severe cases extensive necrosis with hemorrhage occurs causing acute
hemorrhagic necrotizing pancreatitis (Fulminant pancreatitis) that carries a
high mortality.
ETIOLOGY (TRAPNELL’S ETIOLOGICAL CLASSIFICATION)
• Most common causes:
➢ Alcohol (40--50%): alcohol causes contraction of the Causes of pancreatitis
sphincter of Oddi at the ampulla of vater, this P- posterior perforation of
decreases the drainage of pancreatic enzymes in peptic ulcer
duodenum thus increasing the risk of premature
activation of pancreatic enzymes. It is common in A-Alcohol
men N-neoplasm
o Other implicated mechanisms include: the effect
of alcohol on diet, malnutrition, direct toxicity of C- Cholelithiasis (gall
alcohol and hyperlipidemia. stones)
➢ Gallstones (40%): Passage of gallstones down the R- Renal disease (end stage)
common bile duct causes obstruction of ampulla
leading to premature activation of pancreatic E- ERCP
enzymes. Patients who have small gallstones and a A- Anorexia (malnutrition)
wide cystic duct may be at a higher risk of passing
T- Trauma
stones. Gallstones are common in patients above 60
years. It is common in women. I- Infections
• Other causes include: T-Toxins (Drugs)
➢ Abdominal trauma (e.g. RTA in which a person has
the seatbelt around abdomen and not pelvis) I-incineration (burns)
➢ Hyperparathyroidism and Hypercalcemia (Calcium is S- Surgery/Scorpion bite
required for activation of enzymes)
➢ Hyperlipidemia, Diabetes, Porphyria, Autoimmune diseases (associated with
primary sclerosing cholangitis, Sjogren’s syndrome, biliary cirrhosis)

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➢ Drugs (corticosteroids, valproic acid,
thiazides, estrogens, isoniazid,
cimetidine, salicylic acid, tetracycline)
➢ Scorpion stings, Vascular diseases
➢ Viral infection (mumps, coxsackie B,
cytomegalovirus, EBV-infectious
mononucleosis), Mycoplasma
pneumoniae (usually mild),
➢ Rupture of a posterior duodenal ulcer
➢ Autoimmune pancreatitis
➢ Malnutrition
➢ Post Endoscopic retrograde
cholangiopancreatography (in 1-3% patients): due to disruption of the duct
and enzyme extravasation.
➢ Following biliary, upper gastrointestinal or cardiothoracic surgery
➢ Fulminant liver failure
➢ Hereditary pancreatitis: this is a rare familial condition associated with
mutations of the cationic trypsinogen gene. In normal individuals, small
amount of spontaneous trypsinogen activation into trypsin occurs however
further activation is prevented by trypsin inhibitors. In hereditary pancreatitis
the gene mutation causes defective trypsin inhibitors and trypsin becomes
resistant to its inhibitor leading to accumulation of active trypsin in the
pancreas. Patients often suffer acute pancreatitis in their teens which
progresses to chronic pancreatitis in the next 2 decades. They have a 40% risk
of developing pancreatic by the age of 70 years.
➢ Pancreatic duct obstruction: tumor (Ampullary tumor), pancreatic divisum,
Ascaris infestation
➢ Idiopathic (10-20%): always check for serum calcium level, fasting lipid
profile, autoimmune markers and viral titers in patients with idiopathic acute
pancreatitis.
• Note: it is essential to establish the etiology of pancreatitis before labelling it as
idiopathic as the etiology needs to be addressed as part of the management.

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CLINICAL FEATURES
• Pain is the cardinal symptom
➢ It develops quickly reaching maximum intensity within minutes rather than
hours and persists for hours or even days.
➢ The pain is severe, constant and refractory to usual doses of analgesics.
➢ Pain is usually experienced first in the epigastric region (with radiation to the
back in 50% of patients) but may be localized to either upper quadrant or felt
diffusely throughout the abdomen.
➢ Some patients may gain relief by sitting or leaning forwards.
➢ Acute pancreatitis can mimic most causes of the acute abdomen and should
rarely be discounted in differential diagnosis.
➢ Differential diagnosis:
o Sudden onset: perforated ulcer,
o Right upper quadrant pain: biliary colic and acute cholecystitis
o Radiation to the chest: Myocardial infarction, pneumonia or pleuritic pain
• Nausea, vomiting and retching. Retching may persist despite the stomach being
kept empty by nasogastric aspiration.
• Hiccoughs can be troublesome and may be due to gastric distension or irritation
of the diaphragm.
• Bleeding into the fascial planes can produce bluish discoloration of the flanks
(Grey Turner’s sign) or umbilicus (Cullen’s sign).
➢ Neither sign is pathognomonic of acute pancreatitis.
➢ Cullen’s sign was first described in association with rupture of an ectopic
pregnancy.
• Subcutaneous fat necrosis may produce small, red, tender nodules on the skin of
the legs.
• Occasionally hematesis or melena can occur due to duodenal necrosis, gastric
erosions, decreased coagulability/DIC
• Neurological derangements due to toxemia, fat embolism, hypoxia, respiratory
distress can occur. It may be mild psychosis to coma.
DIAGNOSIS
HISTORY
• Age and sex: incidence peaks between 40-50 years but can occur at any age, equal
incidence in men and women.
• Symptoms:
➢ Sudden epigastric pain which may be relieved by leaning forward

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➢ Pain radiates to the back
➢ Drugs don’t relief pain
➢ Frequent vomiting, nausea and retching
➢ Low grade fever
➢ Many patients have eaten an unusually large meal or drunk some alcohol
before the pain began
• Previous history of biliary tract disease (gallstone) as well as indigestion or illness
with mumps (in children).
• Previous history of pancreatitis.
• History of taking corticosteroids, Isoniazide, cimetidine, thiazide diuretics or
estrogen based therapies.
• Social history:
➢ Alcohol intake
EXAMINATION
• General examination:
➢ Patient may be well or gravely ill with profound shock, toxicity and confusion.
➢ Patients lie still because pain is severe and if they are pale and sweating it
means they may have become hypovolemic. If the patient has become
hypovolemic the JVP and blood pressure may be low.
➢ May become grey, apprehensive, dyspneic and cyanosed if respiration is
impaired.
➢ Tachypnea is common, tachycardia is usual and hypotension may be present
➢ There may be a slight tinge of jaundice if pancreatitis has been caused by a
stone lodged in the lower end of the bile duct. Mild jaundice may also appear
on the second or third day of the illness if edema in the head of the pancreas
is causing compression of the bile duct.
➢ Pyrexia may be present but temperature is rarely greatly elevated (low grade
fever). If acute swinging pyrexia is present suspect cholangitis.
• Abdominal examination:
➢ Inspection
o If pain is severe and the tone of the abdominal muscles is increased the
abdomen will not move with respiration.
o A paralytic ileus may develop causing mild abdominal distention.
o Bruising and discoloration in the left flank (Grey Turner’s sign) and
around the umbilicus (Turner’s sign): these are rare and late signs seen in
patients with very severe hemorrhage.

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o There may be bluish discoloration of the inguinal ligament (Fox’s sign)
➢ Palpation: Tenderness and guarding in the upper abdomen. These signs may
be mild. A mass can develop in the epigastrium due to inflammation.
➢ Percussion: may cause pain if there is peritonitis and may be dull over any
pseudocyts that are developing.
➢ Auscultation: bowel sounds are usually present in first 12 to 24 hours but fade
away if a paralytic ileus develops.
• Note: a pleural effusion is present in 10-20% of patients. Pulmonary edema and
pneumonitis are also described and may give rise to the differential diagnosis of
pneumonia or myocardial infarction.
• Remember:
➢ Bruising and discoloration in the left flank and umbilicus can occur after
a large intraperitoneal or retroperitoneal hemorrhage from another
cause such as a leaking abdominal aortic aneurysm.
➢ A number of patients develop a collection of inflammatory exudates in
the lesser sac. This is initially suggested by fullness in the epigastrium
which may become a more prominent mass if a pseudocyt or abscess
develops
➢ Acute pancreatitis can be extremely difficult to diagnose and as it has no
distinctive features, it is often forgotten and missed thus should always be
considered when dealing with an acute abdomen.
INVESTIGATIONS
DIAGNOSTIC
BLOOD INVESTIGATIONS
• Serum amylase (increases 3 to 4 times normal- >1000 somogyi units) and serum
lipase
➢ Serum lipase is more specific because serum amylase is raised when there is
injury to salivary gland.
o Serum lipase is only found in gastric and intestinal mucosa and liver.
o Serum amylase is found in the salivary glands, small bowel, ovaries, testes
and skeletal muscle
➢ A normal serum amylase does not exclude acute pancreatitis particularly if
the patient has presented a few days later.
➢ Hypocalcemia is a poor prognostic indicator (calcium is used in saponification
in fat necrosis)

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➢ Note Serum amylase or lipase are seen 12 to 48 hours however, amylase and
lipase are present in urine on the 3rd to 6th day.
• Serum calcium, Fasting lipid profile, autoimmune markers and viral titers
especially in idiopathic pancreatitis.
IMAGING
• Abdominal ultrasound- It is thus done to rule out tumors, gall stones etc. It does
not establish the diagnosis of acute pancreatitis, the swollen pancreas may be seen
but ultrasonography should be performed within 24 hours in all patients to detect
gallstones as a potential cause, rule out acute cholecystitis as a differential
diagnosis and determine whether the common bile duct is dilated.
• Plain X-ray- plain erect CXR and AXR are not diagnostic of acute pancreatitis
but are useful in the differential diagnosis.
➢ Suggestive features on AXR:
o Generalized or local ileus (‘Sentinel loop’ of dilated proximal small bowel
i.e. the mid to distal duodenum or proximal jejunum located in the left
upper quadrant. A sentinel loop is characterized as distention and/or air-
fluid level near a site of inflammation, in pancreatitis it is secondary to
pancreatitis associated ileus)
o Distension of transverse colon with collapse of descending colon (colon
cut off sign)
o Air fluid level in the duodenum (signifying perforation)
o Renal halo sign
o Obliteration of psoas shadow
o Calcified gallstones or pancreatic calcification may sometimes be seen
o Localized ground glass appearance (Haziness due to retroperitoneal
accumulation of fluid)
➢ CXR may show pleural effusion and in severe cases a diffuse alveolar
interstitial shadowing suggesting acute respiratory distress.
o Basal atelectasis
o Sub-diaphragmatic fluid collection
o Pleural effusion
• Contrast-enhanced CT: not necessary for all patients, particularly those deemed
to have a mild attack on prognostic criteria. It is done when diagnosis is uncertain,
in severe pancreatitis and in patients with suspected fluid collection, pseudocyst
or a pseudoaneurysm as well as organ failure with signs of sepsis or progressive
clinical deterioration.

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• Cross-sectional MRI may yield similar information as CT.
• Endoscopic retrograde cholangiopancreatography (ERCP) and Endoscopic
ultrasound (EUS) can help in detecting stones in the common bile duct and
directly assessing the pancreatic parenchyma. ERCP allows identification and
removal of stones in the common bile duct in gallstone pancreatitis. In patients
with severe acute gallstone pancreatitis and signs of ongoing biliary obstruction
and cholangitis an urgent ERCP should be done.
• Note: occasionally the diagnosis is only made at
laparotomy (as shown on the image)
• Urinary trypsin and activated peptide (TAP), serum
trypsinogen-2 and C-reactive protein (CRP) are also useful
in differentiation of mild from severe disease. In this
respect CRP is only reliable as an index of severity after the
2nd or 3rd day of the disease. CRP levels in excess of
100mg/dl usually indicates necrotizing pancreatitis
SUPPORTIVE
• FBC, U&E, Creatinine, Liver enzymes
• Chest X-ray- for effusion and ARDS.
DIFFERENTIAL DIAGNOSIS
• Gastritis/Perforated duodenal ulcer Figure 100: Widespread fat necrosis
• Perforated esophagus/peptic ulcer of the omentum. A test tube filled
• Acute cholecystitis and acute cholangitis (both may with blood-stained peritoneal fluid.
This specimen was rich in amylase.
coexist with acute pancreatitis) Fat necroses are dull, opaque,
• Acute appendicitis yellow-white areas suggestive of
• Acute upper small bowel obstruction drops of wax. They are most
abundant in the vicinity of the
• Acute mesenteric ischemia
pancreas but are widespread in the
• Rupture abdominal aortic aneurysm greater omentum and the mesentery.
• Ectopic pregnancy At necropsy, they can sometimes be
demonstrated beneath the pleura
• Salpingitis
and pericardium and even the
• Intestinal obstruction subsynovial fat of the knee joint. Fat
• Diabetic ketoacidosis necroses consist of small islands of
saponification caused by liberation
• Myocardial infarction
of lipase which splits fats into
• Pneumonia glycerol and fatty acid. Free fatty
acids combine with calcium to form
soaps (fatty necrosis)

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ASSESSING SEVERTIY
• The Ranson criteria are well-known prognostic signs used for predicting the
severity of disease on the basis of clinical and laboratory results.
• The ability to predict a patient’s risk of infectious complications and mortality at
the time of admission and during the initial 48 hours allows institution early
therapy during admission.
• In patients with less than 3 of the 11 prognostic factors, the mortality rate is low
(1%), with 3 or 4 factors, 18%, with 5 to 6 factors, 50% and with more than 6
factors, 90%.
• The Glasgow grading is also a similar scoring system

• Both scoring systems have been replaced by the Acute Physiology and Chronic
health evaluation (APACHE II) scoring system which gives better
differentiation and has an added advantage that it can be used at any time in the
course of the disease.
• The APACHE II system allocates 3 sets of points: A, B and C
➢ A: assessment of clinical parameters e.g. Vital signs, electrolytes, arterial
blood gasses etc.
➢ B: points allocated in accordance with age
➢ C: points added for comorbid disease or chronic health of patient.
• The APACHE II score is the sum of A, B and C, if this exceeds 9 the patient
has severe acute pancreatitis. Mortality is very high if the score increases after
admission.

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MANAGEMENT
• Management is dependent on cause but is usually
➢ Conservative (medical 70-90%):
➢ Surgical (10-30%)
• Note:
➢ For mild pancreatitis a brief period of fasting may be sensible in a patient who
is nauseated and in pain, but there is little physiological justification for this.
Antibiotics are not always indicated. Apart from analgesics and anti-emetics,
no drugs or interventions are warranted unless there is evidence of
deterioration.
➢ For severe pancreatitis a more aggressive approach is needed. The patient
should be admitted to a high-dependency or an intensive care unit and
monitored invasively. Aggressive fluid resuscitation guided by frequent
measurement of vital signs, urine output and central venous pressure.
Supplemental oxygen should be given and serial arterial blood gas analysis
should be done. Blood should be sent for hematocrit, clotting profile, blood
glucose, liver enzymes and renal function tests, serum levels of calcium and
magnesium.

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• Conservative management involves the ACUTE PANCREATITIS MANAGEMENT
mnemonic (PANCREAS): BOX
➢ P- pain relief, Protease inhibitors,
plasma • Admit to ICU
o For pain relief use pethidine and • P- Pain management-(Pethidine), Plasma
other analgesics, morphine should products (FFP, Platelets if in DIC or
not be used as it causes spasms of hemorrhage)
the sphincter of Oddi. • A-antibiotics: 3rd generation
o Protease inhibitors: aprotinin, cephalosporins (cefotaxine, cefuroxime,
antisnake venoma, or EACA can be cefoperazone, ceftazidime), Ciprofloxacin
given though they have not been plus metronidazole, and Imipenem
shown to improve outcome. • N- Insert NGT, Cannulate, Catheterize
o Plasma: fresh frozen plasma and and Consider Endotracheal intubation
platelets may be required in when in distress. Give Nasal Oxygen.
anticipation of DIC and Consider nutrition (TPN or NGT feeds).
hemorrhage. • C- Calcium gluconate: 10ml of 10% 8
➢ A- Antibiotics and anticholinergics hourly
o Antibiotics- 3rd generation • R- Rehydrate: 250-400ml/hour ringer
cephalosporins (cefotaxine, lactate, normal saline, dextrose saline,
cefuroxime, cefoperazone, plasma and fresh blood
ceftazidime), Ciprofloxacin plus transfusion/packed cells.
metronidazole, and imipenem. To • E- electrolyte management and
reduce the anticipated sepsis. endotracheal intubation
Should not be given beyond 14 days • A- Antacids: IV ranitidine 50mg 6 hourly
and should be guided by or IV omeprazole 40mg BD
microbiological cultures • S- somatostatin analogue (octreotide
o Anticholinergics to reduce sphincter 50g as loading dose IV, 50 g in 1 hour
pressure in 5% dextrose for maintenance dose)
➢ N- nasogastric aspiration, Nasal Oxygen • Blood should be sent for hematocrit,
and Nutritional support (total parental electrolytes, clotting profile, blood
nutrition though there is no data to glucose, Liver and renal function, serum
support a practice of ‘resting’ the levels of calcium and magnesium
pancreas and feeding only by parenteral • Monitor vitals and urine output
or nasojejunal routes. If nutritional
• Surgery if patient deteriorate
support is felt to be necessary, enteral
• ERCP for gallstones or cholangitis
nutrition via NGT should be used)

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➢ C- calcium gluconate 10ml 10% 8 hourly (for hypocalcemia), Calcitonin,
CVP line (to monitor, for fluid therapy and total parental nutrition),
Catheterization (monitor urine output 0.5-1ml/kg/hr) and cannula
➢ R- rehydration, ranitidine, respiratory support (ventilator), resuscitation when
required
o Rehydration with 250-400ml/hour ringer lactate, normal saline, dextrose
saline, plasma and fresh blood transfusion/packed cells as there is a lot of
fluid sequestration and third spacing.
o IV ranitidine 50mg 6 hourly or IV omeprazole 40mg BD to prevent stress
ulcers
➢ E- endotracheal intubation, Electrolyte management
o Monitor electrolytes and manage in ICU where endotracheal intubation,
ventilatory support, tracheostomy can be done if needed
➢ A- antacids
➢ S-somatostatin and its analogue (Octreotide-50g as loading dose IV, 50 g
in 1 hour in 5% dextrose for maintenance dose) to reduce pancreatic secretions
though their use has not shown any improvement in outcome.
• There should also be management of complications as they arise
• Surgery removes intra and extrapancreatic necrotic materials, pancreatic fluid
and toxins. It permits preservation of viable pancreatic tissue. Open surgery is the
gold standard for infected pancreatic necrosis.
• If gallstones are the cause of an attack of predicted or proven severe pancreatitis,
or if the patient has jaundice, cholangitis or dilated common bile duct, urgent
ERCP should be done within 72 hours of the onset of symmptoms.
Sphincterotomy and clearance of the bile duct can reduce the incidence of
infective complications in these patients.
• In patients with cholangitis, sphincterotomy should be carried out or a biliary
stent placed to drain the duct. ERCP is an invasive produce and carries a small
risk of worsening the pancreatitis.
• Indications for surgery
➢ When diagnosis is in doubt
➢ Severe pancreatitis without improvement with medical treatment
➢ Infected necrosis of pancreas
➢ Correction of associated biliary tract disease
➢ Gallstones pancreatitis (treat with early interval cholecystectomy only after
acute pancreatic inflammation has resolved. Acutely, ERCP with endoscopic
sphincterotomy may be used to relieve biliary obstruction).

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➢ Complications (pseudocysts >6cm, pancreatic abscess)
COMPLICATIONS
SYSTEMIC COMPLICATIONS
• Systemic complications are more common in the first week. They include:
1. Neurological
➢ Visual disturbances
➢ Confusion, irritability and encephalopathy
2. Cardiovascular
➢ Shock
o Hypovolemic shock due to sequestration of fluid as well as extensive
hemorrhage
o Septic shock from perforation and translocation of gut microbiota
➢ Arrhythmias
3. Respiratory
➢ Acute respiratory distress and respiratory failure due to enzymes damaging
the alveolar capillary interface.
➢ Pancreatic pleural effusion (left sided 20%): this is an encapsulated collected
of fluid in the pleural cavity arising from acute pancreatitis. It may coexist
with ascites or there may be a communication with an intra-abdominal
collection. Percutaneous drainage under imaging guidance is necessary
4. Gastrointestinal: Ileus
5. Genitourinary: Renal failure
6. Hematological: DIC (due to activation of coagulation factors by pancreatic
enzymes) and septicemia (common after 7 days)
7. Metabolic
➢ Hypocalcemia- calcium used up in activation of enzymes
➢ Hyperglycemia
➢ Hyperlipidemia
8. Miscellaneous: Subcutaneous fat necrosis and arthralgia
• Note:
➢ Management of systemic complications is multidisciplinary. When there is
organ failure, appropriate supportive therapies including inotropic support for
hemodynamic instability, hemofiltration in the event of renal failure,
ventilator support for respiratory failure and correction of coagulopathies
(including DIC).

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➢ There is no role for surgery during intial period of resuscitation and
stabilization, surgical intervention is contemplated only in the patient who
deteriorate as a result of local complications following successful
stabilization.
LOCAL COMPLICATIONS
• Usually develop after the first week and include:
1. Acute fluid collection:
➢ Fluid is located in or near the pancreas. The wall encompassing the collection
is ill defined.
➢ The fluid is sterile and most such collections resolve.
➢ No intervention is needed unless if there is a large collection causing
symptoms or pressure effects in which percutaneous aspiration under
ultrasound or CT guidance can be done.
➢ Transgastric drainage under endoscopic ultrasound guidance is an alternative
option. If acute fluid collection does not resolve it evolves into a pseudocyst
or an abscess if infected.
2. Sterile and infected pancreatic necrosis:
➢ Sterile necrotic material should not be drained or interfed with however if the
patient shows signs of sepsis it should be determined if the necrotic pancreas
or the peripancreatic fluid is infected.
➢ A CT scan should be performed and a needle passed into the area under CT
guidance, chossing a path that does not traverse hollow viscera.
➢ If the aspirate is purulent, percutaneous drainage of the infected fluid should
be carried out.
➢ The tube drain inserted should have the widest bore possible and the aspirate
should be sent for microbiological assessment and antibiotic sensitivity report.
➢ The fluid may be viscous with particulate matter and the drain may need
regular flushing with full aseptic precautions. If sepsis worsens despite this,
pancreatic necrosectomy should be considered.
3. Pseudocyst of the pancreas:
➢ Fibrous tissue surrounding the liquefactive necrosis and enzymes. There is
persistence of amylase enzyme levels.
➢ Pancreatitic pseudocysts can be a late sequela of acute pancreatitis or of
pancreatic (upper abdominal) trauma. The pseudocyst can rupture and cause
hemorrhage into the abdominal cavity.

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➢ Formation of a pseudocyst requires 4 weeks or more from the onset of acute
pancreatitis.
➢ They can be multiple or single (common). Over 50% communicate with the
main pancreatic duct most commonly in the lesser sac.
➢ They may cause pressure symptoms (early satiety, vague discomfort, a deep
palpable mass).
➢ Endoscopic ultrasound and aspiration of the cyst fluid is useful. The fluid
should be sent for carcinoembryonic antigen (CEA) levels, amylase levels and
cytology.
➢ Fluid in a pseudocyst has low CEA levels and levels above 400ng/ml are
suggestive of mucinous neoplasm. Cytology typically reveals inflammatory
cells in the pseudocyst fluid.
➢ Percutaneous FNA can be done if EUS is not present. Pseudocysts resolve
spontaneously in most cases but can complicate.
➢ Treatment is dependent on the size and age of the pseudocyst. Drainage is
done either percutaneously to the outside, endoscopically into the stomach or
surgcically into the gastrointestinal tract.
➢ Cysts 6cm or smaller, or those that have been present for less than 6 weeks
are most likely to have complications and can be observed for spontaneous
resolution. Bigger (>6cm) or older cysts (>6 week) are more likely to rupture
or bleed and they need to be treated.
4. Pancreatic abscess- due to E. coli (35%), Klebsiella (25%), Enterococcus (25%)
or Other (Staphylococci, Pseudomonas, Proteus, Enterobacter, Anaerobes,
Candida-10%). Patient complains of abdominal pain, high fever, persistently
elevated amylase in the fact of a bout of acute pancreatitis. Percutaneous drainage
with the widest possible drains placed under imaging guidance is the treatment,
along with appropriate antibiotics and supportive care. Repeated scans may be
required depending on the progress of the patient, and drains may need to be
flushed, repositioned or reinserted. Very ocassionally, open drainage of the
abscess may be necessary.
5. Chronic pancreatitis- recurrent pancreatitis leads to fibrosis of pancreatic
6. Hemorrhage: may occur into the gut, retroperitoenum or peritoneal cavity.
Possible causes include bleeding into a pseudocyst cavity, diffuse bleeding from
a large raw surface or pseudoaneurysm. Recurrent bleeding is common, often
culminating in fatal hemorrhage. CT, angiograpy or MR angiography help to
make diagnosis. Treatment involves embolization or surgery.

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7. Pancreatic pseudo aneurysm

8. Pancreatic ascites- This is a chronic, generalized, peritoneal, enzyme-rich
effusion usually associated with pancreatic duct disruption. Paracentesis reveals
turbid fluid with a high amylase level. Adequate drainage with wide-bore drains
placed under imaging guidance is essential. Measures that can be taken to
suppress pancreatic secretion include parenteral or Nasojejunal feeding and
administration of octreotide. An ERCP may allow demonstration of the duct
disruption and placement of a pancreatic stent.
9. Colonic stricture
10.Portal/Splenic vein thrombosis: may develop silently and be identified on CT.
A raised platelet count should raise suspicion. In context of pancreatitis treatment
is conservative. Screen patient for pro-coagulant tendencies. If varices or other
manifestations of portal hypertension develop treat accordingly by endoscopic
injection or banding, beta-blockers etc. Thrombocytosis may mandate use of
aspirin or other antiplatet drug for a period. Systemic anticoagulation if instituted
early in the process may achieve recanalization of the vein but is not routinely
used as it carries a risk of on-going pancreatitis.

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CLINICAL BOX: A case of epigastric pain and vomiting

History
A 50-year-old man presents to the ER with vomiting and epigastric pain which
radiates through to the back. The pain was of gradual onset, coming on over the
last 2 days. He denies any previous episodes. He is not on any regular
medication but admits to drinking in excess of 8 cans of lager a day. He is a
heavy smoker but denies any recreational drug use. He is homeless and relates
his heavy drinking to depression.

Examination
The patient is sweaty and agitated. He says he is unable to lie flat for the
examination and vomits persistently. His blood pressure is 150/80mmHg and
he has a pulse rate of 120/min. Palpitation of his abdomen reveals tenderness in
the epigastrium. The abdomen is not distended and he has normal bowel sounds.
Rectal examination is unremarkable.
MCV shows 102 fL (normal 76-96fL)
Serum amylase shows 4672 IU/dl (Normal 0-100IU/dl)
Gamma-glutamyl transferase (GGT) shows 212 IU/L (normal 11-51 IU/L)
Albumin shows 25g/l (normal= 35-50g/l)

Questions
1. What is the most likely diagnosis?
2. Which important differential diagnosis should be excluded?
3. How will you grade the severity of the condition?
4. What are its causes?
5. What are the other causes of the elevated serum markers of this
condition?
6. How will you manage this condition?
7. Give four potential complications.

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CHRONIC PANCREATITIS
• A percentage of patients with acute pancreatitis development of chronic
pancreatitis.
• The chronic form of disease is characterized by persistent inflammation that
causes destructive fibrosis of the gland.
• Chronic pancreatitis is thus defined as a continuing inflammatory disease of the
pancreas characterized by irreversible morphological change typically causing
pain and/or permanent loss of function.
• Many patients have exacerbations, but the condition may be completely painless.
• The clinical picture is of recurring or persistent:
➢ Upper abdominal pain with evidence of malabsorption
➢ Exocrine pancreatic insufficiency: Steatorrhea
➢ Endocrine pancreatic insufficiency: Diabetes
• The disease occurs more frequently in men (male to female ratio is 4:1) and the
mean age of onset is about 40 years.
• Chronic pancreatitis can be:
➢ Chronic relapsing pancreatitis
➢ Chronic pancreatitis (persistent)
o Chronic non-calcifying pancreatitis
o Calcifying pancreatitis: it can be in the duct (stone in the pancreatic) and
parenchyma
ETIOLOGY AND PATHOLOGY
• 60-70% is caused by high alcohol
consumption but only 5-10% of people
with alcoholism develop chronic
pancreatitis.
➢ The underlying mechanism is unclear
however, some genetic and metabolic
factors have been implicated.
➢ Alcohol reduces pancreatic blood
flow, alter cell viability releases the
free radicals creates pancreatic Figure 101: TIGAR-O Risk Factor Classification 2001
ischemia and activates the pancreatic
stellate cells which produce abundant extracellular matrix and collagen.

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• Other causes:
➢ Pancreatic duct obstruction from stricture formation after trauma, acute
pancreatitis or due to pancreatic cancer
➢ Congenital abnormalities: pancreas divisum and annular pancreas if
associated with papillary stenosis are rare causes of chronic pancreatitis
➢ Hereditary pancreatitis: this is an autosomal dominant disorder with an 80%
penetrance, associated with mutations in the cationic trypsinogen gene on
chromosome 7. Carries an increased risk of pancreatic cancer especially if
present at a young age and if the patient smokes.
➢ Cystic fibrosis
➢ Infantile malnutrition
➢ Idiopathic chronic pancreatitis (30%): can be early or late onset
➢ Hyperparathyroidism, Hyperlipidemia and hypercalcemia
➢ Autoimmune pancreatitis: diffuse enlargement of pancreas, diffuse and
irregular narrowing of the main pancreatic duct and a possible association
with other autoimmune diseases. The changes may be confused with
neoplasia. Autoantibodies may be present and the immunoglobulin (Ig)G4
concentrations are elevated.
• At onset of disease when symptoms develop the pancreas may appear normal,
later the pancreas enlarges and becomes hard as a result of fibrosis.
• The ducts become distorted and dilated with areas of both stricture formation and
ectasia.
• Calcified stones weighing from a few mg to 200mg may form within the ducts.
• The ducts may become occluded with a gelatinous proteinaceous fluid and debris,
and inflammatory cysts may form.
• Histologically, the lesions affect the lobules producing ductular metaplasia and
atrophy of acini, hyperplasia of duct epithelium and interlobular fibrosis.
PATHOGENESIS
• Chronic pancreatitis can be categorized into 2 forms:
➢ Calcific pancreatitis: usually associated with persistent alcohol abuse.
➢ Obstructive pancreatitis: secondary to pancreatic duct obstruction.
• Alcohol induced calcific pancreatitis is the most common form of disease.
➢ Proposed mechanisms of disease include ductal plugging and occlusion by
protein and mineral precipitates.
➢ The resulting inflammation and patchy fibrosis subsequently leads to
parenchymal destruction and eventual atrophy of the gland.

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• Obstructive chronic pancreatitis is due to ductal blockage secondary to scarring
from acute pancreatitis or trauma, papillary stenosis, pseudocyst or tumor which
results in upstream duct dilation and inflammation.
CLINICAL FEATURES
• Abdominal pain is the principal presenting and most frequent indication for
surgery.
• The pain is often dull and gnawing. Severe flare-ups of pain may occur
superimposed on background discomfort.
• The pain is upper abdominal, is either intermittent or persistent and frequently
radiates to the back.
➢ If the disease is mainly in the head of the pancreas the pain is epigastric and
right subcostal
➢ If the disease is limited to the left side of the pancreas, left subcostal and back
pain are seen.
➢ In some patients the pain may be diffuse.
➢ Radiation to the left shoulder usually occurs.
• Patients are often addicted to narcotic pain relievers.
• The pain prevents sleep and time off work is frequent. The number of hospital
admissions for acute exacerbations is a pointer towards the severity of disease.
• Nausea is common during attaching and vomiting may occur.
• Weight loss is common because the patient does not feel like eating.
• Other symptoms result from exocrine insufficiency (malabsorption- foul
smelling steatorrhea in more than 30% of patients) and endocrine insufficiency
(diabetes mellitus)
• All the complications of acute pancreatitis can occur with chronic pancreatitis.
DIAGNOSTIC EVALUATION
• The diagnosis of chronic pancreatitis is best made using imaging techniques that
detect pancreatic morphologic changes rather than test glandular function, given
the functional reserve of the pancreas.
• Only in the early stages of the disease will there be a rise in serum amylase. Tests
of pancreatic function merely confirm the presence of pancreatic insufficiency or
that more than 70% of the gland has been destroyed.
• Pancreatic calcifications may be seen on AXR.
• Ultrasound and CT are useful in the initial imaging process however endoscopic
retrograde cholangiopancreatography (ECRP) is the most accurate means of

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diagnosing chronic pancreatitis because it clearly defines the pathologic changes
of the pancreatic ductal system and the biliary tree.
• ERCP can help determine the type of operation required, if operative intervention
is indicated.
• Radiological signs of chronic pancreatitis:
➢ Heterogeneously inflamed or atrophied gland
➢ Dilated and strictured pancreatic duct
➢ Presence of calculi
TREATMENT
• Medical:
➢ Treat the addition: Stop alcohol intake and involve a psychologist or
counsellor
➢ Alleviate abdominal pain
o Eliminate obstructive factors (duodenum, bile duct, pancreatic duct)
o Escalate analgesia in a stepwise fashion
o Refer to pain management specialist
o For intractable pain consider CT/EUS guided coeliac axis block
➢ Nutritional and digestive measures:
o Diet: low in fat and high in protein and carbohydrates
o Pancreatic exocrine insufficiency is treated with oral pancreatic enzymes
o Correct malabsorption of fat-soluble vitamins (A, D, E and K) and
Vitamin B12
o Medium chain triglycerides in patients with severe fat malabsorption
(they are directly absorbed by the small intestine without need for
digestion)
o Reducing gastric secretions may help
➢ Insulin is used to treat diabetes mellitus.
• Surgical: only undertaken if medical therapy has failed in relieving chronic
intractable pain
➢ Indications for surgery:
o Persistent pain
o GI or biliary obstruction
o Pseudocyst infection, hemorrhage or rupture
o Enlarging pseudocysts
➢ Functional drainage of the pancreatic duct and resection of disease tissue are
the goals of any procedure

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➢ Based on ERCP and CT findings, the correct operation can be planned.
➢ Endoscopic pancreatic sphincterotomy might be beneficial in patients with
papillary stenosis and high sphincter pressure and pancreatic ductal pressure.
➢ Patients with a dominant pancreatic duct stricture and upstream dilation may
benefit by placement of a stent across the stricture. The stent should be left in
for no more than 4-6 weeks as it will block.
➢ Pancreatic duct stones may be extracted at ERCP and this may sometimes be
combined with extracorporal shock wave lithotripsy.
➢ Pseudocysts may be drained internally under EUS guidance. Percutaneous or
transgastric drainage of pseudocysts under US or CT guidance can also be
done.
➢ The role of surgery is to overcome obstruction and remove mass lesion
➢ For patients with a “chain of lakes”- appearing pancreatic duct caused by
sequential ductal scarring and dilation, a longitudinal pancreaticojejunostomy
(Puestow procedure) is indicated to achieve adequate drainage.
➢ A Roux-en-Y segment of proximal jejunum is anastomosed side to side with
the opened pancreatic duct, facilitating drainage.
➢ Distal pancreatic duct obstruction causing localized distal parenchymal
disease is best treated by performing a distal pancreatectomy.
➢ Total pancraetectomy and islet autotransplantation has been reported in
selected patients.

Figure 102: Surgical procedures in Chronic pancreatitis

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PANCREATIC TUMORS
• Pancreatic tumors are classified as follows:
➢ Exocrine tumors
o Benign: benign cystadenoma (Rare)
o Malignant:
- Adenocarcinoma: in ampulla, periampullary or head of pancreas.
Periampullary carcinoma may arise from any component- duodenal
mucosa or CBD or pancreatic duct component or all. Occasionally
squamous cell carcinoma or combination of adenosquamous can
occur.
- Cystadenocarcinoma: commonly found in body and tail of pancreas,
usually attains a large size (5%).
➢ Endocrine tumors
o Insulinoma (beta cells)- Whipple’s triad
o Gastrinoma (G cells)- Peptic ulcer
o Glucagonoma (alpha cells)- Diabetes, necrolytic migratory erythema
o VIPoma (Pancreatic cholera-Verner-Morrison syndrome)- Watery-
diarrhea, hypokalemia, Achlorhydia (WDHA syndrome)
o Somatostatinoma (S/delta cells)- Diabetes, steatorrhea, gallstones
➢ Lymphomas

PANCREATIC ADENOCARCINOMA
• Pancreatic adenocarcinoma is the leading cause of cancer death, trailing other
cancers such as lung and colon.
• Pancreatic adenocarcinoma originates in the exocrine pancreas (ductal cells) and
2/3 occur in the head of the pancreas
• Men are affected more than women by 2:1 ratio.
• The peak incidence is 50-60.
• African-American are affected more (2:1 Black to white ratio)
• Ductal adenocarcinoma accounts for 80% of the cancer types and is usually found
in the head of the gland.
• Local spread to contiguous structures occurs early, and metastases to regional
lymph nodes and liver follows.
• Risk factors:
➢ Increasing age
➢ Race: African-American

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➢ Cigarette smoking (Tobacco use doubles risk)
➢ High energy diet rich in fat
➢ Diabetes mellitus, alcohol abuse, chronic pancreatitis, familial pancreatitis
➢ Hemochromatosis with pancreatic calcification, cirrhosis , obesity
➢ Occupational exposure to carcinogens like DDT, benzidine
➢ Previous cholecystectomy
CLINICAL FEATURES
• Signs and symptoms of carcinoma of the head of the pancreas are intrinsically
related to the regional anatomy of the gland.
• Patients classically complain of:
➢ Obstructive jaundice- dark urine and pale stools (due to obstruction in head),
➢ Weight loss and anorexia
➢ Constant deep abdominal pain (posterior epigastric pain radiating to the back)
due to peripancreatic tumor infiltration.
• Nausea, epigastric bloating, change in bowel habit and vomiting are occasionally
present. In advanced disease, hematemesis and melena may result from direct
invasion of the duodenal mucosa by tumor and duodenal obstruction may
supervene.
• Patients may present with jaundice and a palpable non-tender gallbladder
indicating tumor obstruction of the distal common bile duct (Courvoisier’s sign).
➢ Courvoisier’s law/sign: in the presence of a palpably enlarged gallbladder
which is non-tender and accompanied with mild painless jaundice the cause
is unlikely to be gallstones.
• Pruritus often accompanies the development of jaundice.
• Fever and rigors may accompany the jaundice (bacterial cholangitis) and tend to
occur in long-standing biliary obstruction.
• Migratory thrombophlebitis: Trousseau’s syndrome is seen especially in tumors
of the body or tail though this is not specific for pancreatic cancer.
• On rectal examination a rectal shel may be evident in the rectovesical or
rectovaginal pouch (Blumer’s shelf). There may be evidence of ascites, and
distant metastases may be present in the supraclavicular fossa (Troisier’s sign).
DIFFERENTIAL DIAGNOSIS
• Carcinomas of the ampulla of vater
• Carcinoma head of pancreas
• Carcinoma of Distal common bile duct

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• Carcinoma of duodenum
DIAGNOSTIC EVALUATION
• Most common lab abnormalities are:
➢ Elevated carcinoembryonic antigen (CEA) or CA 19-9 (tumor markers)
➢ Elevated alkaline phosphatase
➢ Direct bilirubin levels indicating obstructive jaundice. The average bilirubin
level in neoplastic obstruction is typically higher than that seen in bile duct
obstruction from gallstone disease.
➢ CT and ERCP are the modalities of choice for the evaluation of pancreatic
cancer.
o CT reveals the location of the mass, extent of tumor invasion or metastasis
and degree of ductal dilation. CT also shows the relationship of the cancer
to the superior mesenteric artery and vein and the coeliac axis, patency of
the portal vein and liver metastasis.
o ERCP defines the ductal anatomy and extent of ductal obstruction and
provides biopsy specimens for tissue diagnosis.
o Drainage stents can be placed into the common bile duct during ERCP for
biliary tree decompression.
o A double duct sign may be seen in periampullary lesions.
TREATMENT
• Tumor head of pancreas: The operation for resectable tumors in the head of
pancreas is pancreaticoduodenectomy (Whipple procedure).
➢ Removal of gallbladder, common bile duct, antrum of stomach, duodenum,
proximal jejunum and head of pancreas (en bloc)
➢ Reconstruction with pancreaticojejunostomy, choledochojejunostomy and
gastrojejunostomy.
➢ An alternative is the modification known as the pylorus-preserving
pancreaticoduodenectomy in which the stomach and duodenum are preserved
to eliminate post-gastrectomy symptoms.
• Tumor of the body/tail: Distal “near-total” pancraetectomy
• Tumors of the pancreatic tail are usually unresectable because they are
asymptomatic during growth and thus present at a late stage. Tumors in the head
of the pancreas however present earlier because they cause biliary obstruction.
• If unresectable (due to liver/peritoneal metastases, nodal metastases beyond the
zone of resection, or tumor invasion of the superior mesenteric artery), palliative
care is considered:

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➢ Relieve biliary obstruction (jaundice and pruritus)
o Endoscopic or transhepatic (radiological) stenting using self-expanding
metallic stents, which have largely replaced plastic stents for this purpose.
o Endoscopic/radiological stenting has replaced surgical biliary bypass,
cholecytojejunostomy or choledochojejunostomy unless duodenal
obstruction is also present when a double bypass (biliary bypass and
gastrojejunostomy) is needed.
➢ Relieve duodenal obstruction (vomiting)
➢ Splanchnic nerve bloc (pain control)
o Percutaneous coeliac plexus block with 50ml of 50% alcohol or 20ml of
6% phenol
o Bilateral thoracoscopic splanchnicectomy
o Opioid analgesia
• Post-operative chemoradiation therapy is controversial but typically includes 5-
fluorouracil (5-FU) and external-beam radiation.

Figure 103: Pancreaticoduodenectomy (Whipple procedure). Preoperative anatomic

relationships (A) and postoperative reconstruction (B)

PROGNOSIS
• Long term survival for pancreatic cancer remains dismal, and most patients die
within 1 year of diagnosis.
• The 5-year survival for all patient with tumors of the head of pancreas is
approximately 3%.
• For individuals with tumors amenable to Whipple resection, the 5-year survival
rate is only 10-20%.
• Tumors of the body and tail are invariably fatal because diagnosis is usually made
at a more advanced stage due to the lack of early obstructive findings.

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OTHER PANCREATIC • Pancreatic endocrine tumors may

be benign or malignant.
TUMORS/NEOPLASMS
➢ Compared with pancreatic
• About 20% of all pancreatic cystic
adenocarcinoma, endocrine
lesions will not be pseudocyst.
tumors, even when malignant
These lesions may be benign or
are slow-growing and many
malignant but even the malignant
metastasize only to regional
ones carry better prognosis than
lymph nodes. Hence curative
adenocarcinoma.
surgical excision is possible in a
• Simple cysts are usually congenital. significant proportion of
When they appear in children, no patients.
treatment is required. ➢ Normal islet cells also
• In patients with polycystic kidney synthesize the protein
disease, 10% will have pancreatic chromogranin along with
cysts, they also do not require specific peptide hormones.
treatment. Elevated plasma levels of
• More complicated cystic disease of chromogranin or neuron-
the pancreas include serous specific enolase are thus useful
cystadenoma and mucinous cystic markers for pancreatic
neoplasms. endocrine tumors.
• Solid and cystic papillary
neoplasms tend to present as large
lesions in young women. Resection
is often curative.
• Intraductal papillary mucinous
neoplasms are distinguished from
other cystic lesions of the pancreas
in that the pancreatic duct is
enlarged because of mucin
deposition. ERCP demonstrates
mucin in the duct. These lesions
have malignant potential and
require resection. Long-term
prognosis is excellent.

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• MEN 1: Inherited autosomal CYSTADENOMA
dominant disorder involving • Common in older and middle-aged
➢ Pancreas: diffuse islet cell disease women.
consisting of micronodular and • Two types are recognized:
macronodular hyperplasia and ➢ Serous: benign
often with multiple tumors o Occurs between 30 and 50
secreting multiple peptide years.
hormones, non-B-cells tumors o They are generally
(especially Gastrinoma) asymptomatic
➢ Parathyroid gland: o Ultrasound reveals a
hyperparathyroidism with complex low-density mass
hyperplasia of the glands with fine septae. The fluid is
➢ Pituitary gland: Pituitary generally clear
adenoma (prolactinoma) o Resection is generally
• MEN 2: inherited autosomal curative.
dominant disorder involving ➢ Mucinous: generally benign but
➢ MEN 2a: Medullary carcinoma of has potential to be malignant.
the thyroid, Pheochormocytoma o Usually require formal
and Parathyroid adenomas partial pancreatectomy.
➢ MEN 2b: Medullary carcinoma of • Treatment: Surgical resection.
the thyroid, Pheochormocytoma ENDOCRINE TUMORS (ISLET
and ganglioneuromas of the oral CELL TUMORS)
mucosa
INSULINOMA
• This is a beta cell neoplasm with
CYSTADENOCARCINOMA
overproduction of insulin.
• Common in females age 40-60
• It is the most common islet cell
years.
tumor.
• Common in the body and tail
• 90% are benign.
• Accounts for less than 2% of all
• It is common in women than men
pancreatic exocrine tumors.
and commonly affects middle-aged
• Prognosis better than patients.
adenocarcinoma
• Most are solitary lesion with even
• Treatment: Surgical resection- distribution in the head, body and
distal/total pancreatectomy. tail of the pancreas.
• It associated with multiple
endocrine neoplasia I (MEN I)

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syndrome (<10% of cases) then indicated to try to locate and
multiple insulinomas may be resect the tumor. Intraoperative
present. ultrasound should be used in this
• Clinical features related to case. Even when metastatic
hypoglycemia triggered disease is present, resection may
catecholamine release. Patients can be indicated for symptomatic
lose consciousness or experience relief.
seizures. ➢ Diazoxide can improve
• Insulinoma is characterized by hypoglycemic symptoms by
Whipple’s triad: inhibiting pancreatic insulin
➢ Symptoms of hypoglycemia release.
with fasting (palpitations, GASTRINOMA (ZOLLINGER-
tachycardia, and shaking) ELLISON SYNDROME)
➢ Fasting glucose <2.8 mmol/l • This is a neoplasm associated with
(50mg/dl) overproduction of gastrin.
➢ Relief of symptoms after eating
• This is the second most frequent
• Differential diagnosis:
islet cell tumor.
Surreptitious (Sneaky) insulin
• The syndrome is slightly more
administration
common in men than in women and
• Diagnosis:
generally affects patients in middle
➢ Fasting serum insulin level >10 age.
uU/ml (Normal: <6uU/ml)
• 25% of gastrinomas are associated
➢ Fasting insulin to glucose ratio>
with MEN-1.
0.3
• The lesions most commonly occur
➢ Proinsulin or C-peptide levels
in the pancreas or duodenum but
should be measured to rule out
can also occur in other areas.
surreptitious exogenous insulin
• 90% are located in the “Gastrinoma
administration
triangle” bordered by
➢ CT or MRI to localize the lesion
➢ Junction of second and third part
and determine whether
of the duodenum
metastases are present.
➢ Cystic duct
• Treatment:
➢ Superior mesenteric artery
➢ Surgical enucleation or
under the neck of the pancreas
resection is usually curative
(90% of patients)
➢ Note: even if the lesion is not
localized, surgical exploration is

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➢ Ulcers in unusual locations (e.g.
third part of duodenum or
jejunum) is highly suggestive.
➢ Octreotide scan to localize
tumor
➢ CT, MRI and U/S have some
utility in localizing the tumor.
• Treatment:
➢ Proton pump inhibitor to
alleviate symptoms
➢ Surgical resection (curative or
Figure 104: Gastrinoma triangle- the debulking)
anatomic triangle in which approximately
90% of gastrinomas are found (Image from
➢ Chemotherapy
First Aid for the Surgery Clerkship 2nd Ed) VIPOMA
• The tumor is small, slow-growing, • This is a tumor associated with the
multiple and 60% of them are overproduction of vasoactive
malignant. intestinal peptide (VIP).
• Clinical features: • It is also known as Verner-
➢ Signs of peptic ulcer disease Morrison syndrome or WDHA
(Especially in patients with syndrome (Watery Diarrhea,
recurrent or unusually located Hypokalemia, Achlorhydia)
ulcers) • Most are malignant, majority have
➢ Epigastric pain most prominent metastasized to lymph nodes and
after eating the liver at the time of diagnosis.
➢ Profuse watery diarrhea • 10% are extrapancraetic.
(Secretory diarrhea) • Clinical features:
• Diagnosis: ➢ Severe watery diarrhea
➢ Fasting serum gastrin level ➢ Signs of hypokalamia:
>500 pg/ml (normal <100pg/ml) palpitations/arrhythmias,
➢ Secretin stimulation test will muscle fasiculations/tetany,
cause paradoxical increase in paresthesias
gastrin in patients with Z-E • Diagnosis: fasting serum VIP level
syndrome (double fasting level >500 pg/ml (normal <200 pg/ml)
or increase of 200 pg/dl over the with exclusion of other causes of
fasting level) diarrhea
• Treatment:

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➢ Surgical resection, • Treated by surgery and
chemotherapy chemotherapy
➢ Octreotide (somatostatin
analogue)- diarrhea control
GLUCAGONOMA
• This is a rare alpha cell neoplasm
resulting in overproduction of
glucagon.
• Most are malignant, large primary
tumors that have usually
metastasized to lymph nodes and
liver at the time of diagnosis.
• Clinical features:
➢ Mild diabetes (hyperglycemia)
➢ Anemia
➢ Mucositis
➢ Weight loss due to low amino
acid level
➢ Severe dermatitis: often a red
psoriatic-like rash with
serpiginous borders over trunk
and lower limbs
• Diagnosis
➢ Fasting serum glucagon level
>1000pg/ml (normal <200
pg/ml)
➢ Skin biopsy to confirm presence
of necrolytic migratory
erythema
• Treatment:
➢ Surgery and chemotherapy
➢ Octreotide to inhibit the release
of glucagon
SOMATOSTATINOMA
• Very rare tumor
• Malignant

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CHAPTER 10: GALL BLADDER

GALLBLADDER
• The gallbladder is a pear-shaped (size=5-12cm) reservoir located in a fossa on
the inferior surface of the liver.
• It consists of:
➢ Fundus
➢ Body
➢ Infundibulum
➢ Neck
• Hartmann’s pouch is a pathological one
located in the infundibular region created
by gallstones.
• The Gallbladder drains through the cystic
duct into the common hepatic duct to form
the common bile duct.
➢ The left hepatic duct is formed by the
ducts draining II, III, IV segments of
the liver.
➢ The right hepatic duct is formed by
the ducts draining V, VI, VII, VIII Figure 105: Anatomy of the gallbladder
segments of the liver.
➢ The right and left hepatic ducts join at the
porta hepatis to form the common
hepatic duct.
➢ The common hepatic duct joints the
cystic duct to form the common bile duct.
➢ The common bile duct is normally 10-
12cm in length and 6-8mm in diameter.
It joins the major pancreatic duct in the
wall of the second part of duodenum to
form the ampulla of Vater.
➢ The intraduodenal part of the common
bile duct is surrounded by smooth muscle
fibers called as sphincter of Oddi. Figure 106: Common bile duct parts

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➢ The extrahepatic biliary tree receives blood from gastroduodenal,
retroduodenal, posterosuperior pancreaticoduodenal arteries.
• The gallbladder is supplied by the cystic artery (A branch of the right hepatic
artery).
• Calot’s triangle is formed by:
➢ Common hepatic duct to the left,
➢ Cystic duct below
➢ Inferior surface of the liver above.
• The cystic artery originating from the right hepatic artery passes behind the
common hepatic artery, and enters the Calot’s triangle to reach the gallbladder.
• Calot’s triangle contains the lymph node of ‘Lund’ (Fred Bates Lund).
• Often the cystic artery, hepatic artery, and cystic duct have anomalous positions
and anomalous origins. Both gallbladder neck and cystic duct contain mucosal
folds called valves of Heister.
• About 1000ml of bile is secreted from the liver which contains water (98%), bile
salts, bile pigments, fatty acids, lecithin, cholesterol and electrolytes (sodium,
potassium, chloride, bicarbonate, calcium, magnesium) with a pH more than 7.0.
• The main function of the gallbladder is to concentrate and store the bile (capacity
of the gallbladder is 40-50ml)
• Bile salts form micelle which make cholesterol soluble.
• Bilirubin conjugated in the liver is secreted into the bile which in the bowel is
converted into urobilinogen by bacteria. Urobilinogen gets absorbed in the
bowel, enters the liver for re-secretion again and part of it is excreted in the urine.
Absence of urobilinogen in urine signifies obstructive jaundice.
• In the absence of gallstones or any other disease, bile is sterile. Symptomatic
gallstone disease shows positive culture for bacteria commonest being E. coli and
Klebsiella.
• Ultrasound is the first line for investigating gallbladder and biliary tree
pathologies.
• Further investigations with computed tomography (CT) or Magnetic resonance
cholangiopancreatography (MRCP)/Endoscopic retrograde
cholangiopancreatography (ERCP) can be done.

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GALLSTONES/ CHOLELITHIASIS
• Cholelithiasis is the presence of gallstones within the gallbladder.
Choledocholithiasis refers to stones in the common bile duct.
• Gallstones are the most common biliary pathology.
• Gallstones are round, oval or faceted concretions found in the biliary tract
containing cholesterol, calcium carbonate, calcium bilirubinate or a mixture of
these elements.
• 80% of stones are composed primarily of cholesterol while the remaining 15%
are pigmented.
• Gallstones are more common in females (2:1) and people above the age of 40
years.
• These are classified based on chemical composition into:
➢ Cholesterol stones: Cholesterol solitaire (Radiating crystalline appearance)
are common and are often solitary. These stones contain 51-99% pure
cholesterol plus an admixture of calcium salts, bile acids, bile pigments and
phospholipids. Cholesterol which is insoluble in water is secreted from the
canalicular membrane in phospholipid vesicles. Whether cholesterol remains
in solution depends on the concentration of phospholipids and bile acids.
Micelles formed by the phospholipid hold cholesterol in a stable
thermodynamic state. When bile is supersaturated with cholesterol or bile acid
concentrations are low, unstable unilamellar phospholipid vesicle form, from
which cholesterol crystals may nucleate and stones may form.
➢ Pigmented stones: are small and often multiple. They contain less than 30%
cholesterol.
o Black or greenish black pigmented stones (20-30%): composed of an
insoluble bilirubin pigment polymer mixed with calcium phosphate and
calcium bicarbonate. Black stones accompany hemolysis, usually
hereditary spherocytosis or sickle cell disease. For unclear reasons,
patients with cirrhosis have a higher instance of pigmented stones.
o Brown pigmented stones: contain calcium bilirubinate, calcium palmitate
and calcium stearate as well as cholesterol. They are rare in the gall
bladder. They form in the bile duct and are related to bile stasis and
infected bile. Stone formation is related to the deconjugation of bilirubin
diglucuronide by bacterial beta-glucoronidase. Insoluble unconjugated
bilirubinate precipitates. Brown pigment stones are associated with the

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presence of foreign bodies within the bile ducts such as endoprosthesis
(stents) or parasites (Clonorchis sinesis and Ascaris lumbricoides)
➢ Mixed stones: 90% common. They contain cholesterol, calcium salts or
phosphate, carbonate, palmitate, proteins and are multiple faceted.
• Gallstones are common in the following populations “5Fs”
➢ Female
➢ Fat
➢ Fertile
➢ Forty
➢ Flatulent

ETIOLOGY/RISK FACTORS FOR GALLSTONE

FORMATION
• Super-saturation of bile
➢ Female
➢ Fertile
➢ Fat, High calorie
➢ Forty
• Altered Gallbladder function
➢ Stasis
➢ Poor emptying
➢ Poor absorption
➢ Infection
• Altered enterohepatic circulation
➢ Ileal resection
➢ Ileal diseases
➢ Altered bowel transit time
➢ Altered bowel flora
➢ Cholestyramine Figure 107: Causes of gallstone
➢ Deoxycholate formation
• Hemolytic diseases
• Pregnancy, oral contraceptives, inflammatory bowel disease, hyperlipidemia, and
total parenteral nutrition (TPN).
• Cholesterol nucleation factors
➢ Mucus and Glycoprotein
➢ Infection

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PATHOGENESIS
CHOLESTEROL STONES
• Cholesterol stones are preceded by the formation of biliary sludge and account
for the vast majority of gallstones encountered in western countries.
• Cholesterol stones have a protein matrix but are composed predominantly of
cholesterol with varying amounts of bile pigments and calcium salts deposited on
the periphery.
• Cholesterol gallstones do not commonly harbor bacteria and are not usually
associated with infected bile.
• They are often radiolucent but cast acoustic shadows on ultrasound.
• They are often multiple and medium-sized but when solitary attain a large size
and have a radiating crystalline cross-sectional appearance.
• The formation of cholesterol stones involves 7 processes:
➢ Super-saturation of bile with cholesterol
➢ Incomplete transfer of cholesterol from biliary vesicles to bile salt micelles
➢ Formation of abnormal high-cholesterol containing biliary vesicles
➢ Aggregation and fusion of unstable vesicles
➢ Cholesterol crystallization (nucleating and antinucleating factors)
➢ Biliary sludge formation
➢ Stone growth

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• Cholesterol which is insoluble in water is secreted from the canalicular
membrane in phospholipid vesicles. Whether cholesterol remains in solution
depends on the concentration of phospholipids and bile acids. Micelles formed
by the phospholipid hold cholesterol in a stable thermodynamic state. When bile
is supersaturated with cholesterol or bile acid concentrations are low, unstable
unilamellar phospholipid vesicle form, from which cholesterol crystals may
nucleate and stones may form.
• There is an imbalance in bile between cholesterol, bile salts and phospholipids
producing lithogenic bile. Cholesterol stones may be associated with
inflammatory bowel disease.
PIGMENTED STONE
BLACK STONES
• Black stones account for 25% of gallstones in the West
though their prevalence is higher in the Far east.
• They are composed of bilirubin polymers without calcium
palmitate, small amounts of cholesterol (<30%) and a
matrix of organic material.
• They are associated with infection in less than 20% of
patients.
• Black pigmented stones are usually multiple, small,
irregular and dark-green to black in color.
• The pathophysiology is largely unknown. Although
hemolytic states predispose to formation of black pigmented Figure 108: Pigmented stones
stone, most occur in patients without detectable chronic showing faceted look
hemolysis.
• They are common in cirrhotic patients who have an
elevated concentration of monoconjugated bilirubin and
lower bile salt concentration than normal.
• Mucins may be involved in the development of pigmented
stones especially those forming in the intrahepatic ducts.

Figure 109: Multiple gallstones collected during

cholecystectomy

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BROWN PIGEMENT STONES
• Brown pigment stones form in the bile ducts (primary ductal calculi) and are
associated with infection of the biliary tract.
• They are brownish yellow, soft and mushy.
• Brown pigment stones contain calcium bilirubinate, calcium stearate, calcium
palmitate and only small amounts of cholesterol bound in a matrix of organic
material.
• Brown pigment stones are caused by infection with gram negative bacteria
(Escherichia coli and Bacteroides fragilis-98%) which elaborate and release -
glucoronidase which causes hydrolysis of soluble conjugated bilirubin to
insoluble calcium bilirubinate.
➢ They form in the bile duct and are related to bile stasis and infected bile. Stone
formation is related to the deconjugation of bilirubin diglucuronide by
bacterial beta-glucoronidase. Insoluble unconjugated bilirubinate precipitates.
Brown pigment stones are associated with the presence of foreign bodies
within the bile ducts such as endoprosthesis (stents) or parasites (Clonorchis
sinesis and Ascaris lumbricoides)
• Brown pigments stones are encountered in biliary tract conditions associated with
stasis and infection and chronic obstructive disease, indwelling biliary
endoprosthesis and around non-absorbable suture material or metal clips used in
biliary tract surgery.
MIXED STONES
• Are associated with anatomical abnormalities, stasis, previous surgery, and
previous infections.

CLINICAL FEATURES
• Most patients are asymptomatic (>80%).
• Symptomatic patients present with
➢ Severe right upper quadrant pain radiating to the back (right shoulder blade),
epigastrium or left upper quadrant that tends to be worse after eating
(especially after fatty foods)
➢ The pain is more often persistent than intermittent. Onset is usually at night.
It is described as colicky but more often is dull and constant
➢ Dyspepsia, flatulence, Nausea and vomiting may also be present
• The symptom complex is called biliary colic and typically resolves over a few
hours (or it may be aborted by anticholinergics). It occurs when a stone

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temporarily occludes the cystic duct. There are no signs of peritoneal irritation or
systemic signs of inflammatory process.
• Jaundice and dark urine may follow an attack of biliary coli and indicate common
bile duct obstruction by a calculus. Jaundice often subsides after a few days but
may persist as a major presenting symptom.
• Mirrizzi’s syndrome is external compression of the common hepatic duct by a
gallstone impacted in the cystic duct.
• Hydrops of the gallbladder occurs when there is complete obstruction of the
cystic duct by a gallstone, causing the gallbladder to fill with fluid from the
gallbladder mucosa. The fluid is often milky white.
• Spectrum of symptomatic gallstone disease includes:
➢ Acute biliary colic/acute cholecystitis and Chronic cholecystitis due to stone
obstruction at the gallbladder neck with superimposed infection
➢ Cholangitis/septicemia: due to obstruction of common bile duct with
superimposed infection
➢ Acute gallstone pancreatitis: due to gallstones passing through biliary system
➢ Biliary fistulous disease
➢ Gallstone ileus: due to migration of a large stone into the gut causing intestinal
obstruction

DIAGNOSIS AND INVESTIGATIONS

• Often incidental, as most patients are asymptomatic
• Blood investigations:
➢ Liver function tests
➢ Full blood count
• Imaging:
➢ Abdominal plain films picks up 15% of
gallstones
➢ Ultrasound: Procedure of choice, classic
findings include an acoustic shadow
(“headlight”) and gravity-dependent
movement of gallstones with patient
repositioning

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Figure 110: Sonogram demonstrating classic "headlight" appearance of cholelithiasis

TREATMENT
• Asymptomatic patients: do not require cholecystectomy unless the patient:
➢ Has a porcelain gallbladder (which has an increased incidence of carcinoma)
➢ Has sickle cell anemia
➢ Has a stone >2-3 cm
➢ Is a pediatric patient
➢ Is immunocompromised or has diabetes
• Symptomatic patients: require cholecystectomy.
➢ A laparoscopic cholecystectomy is ideal and can be performed on 95% of
patients.
➢ Open cholecystectomy is done through right subcostal Kocher’s incision.
Open approach is used if patient is not fit for laparoscopic surgery
(anesthersia), in suspected CBD stones, Mirizzi syndrome, suspected
carcinoma gallbladder.
➢ During laparoscopic cholecystectomy, if there is on table difficulty in
dissection at Calot’s triangle, then conversion into open approach may be
required.

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➢ If an early operation is not indicated one
should wait approximately 6 weeks for
the inflammation to subside before
proceeding to operate.
• An attack of acute pancreatitis, cholangitis
or obstructive jaundice is usually an
indication for prophylactic
cholecystectomy.
• Conservative treatment followed by
cholecystectomy:
➢ Over 90% of cases subside with
conservative measures.
➢ Conservative treatment is based on 4
principles
o Nil per oral (NPO) and intravenous
fluid administration
o Administration of analgesics
o Administration of antibiotics. As the cystic duct is blocked in most cases,
the concentration of antibiotics in the serum is more important than its
concentration in bile. A broad-spectrum antibiotic effective against Gram-
negative aerobes is most appropriate (e.g. cefazolin, cefuroxime or
gentamicin)
o Subsequent management: When temperature, pulse and other signs of
inflammation begin to subside, oral fluids are reinstated followed by
regular diet. Ultrasound is performed to ensure that no local complications
have developed (normal bile duct size without any stone in the bile duct).
Cholecystectomy may be performed on the next available list, or patients
may be allowed home to return when the inflammation has completely
resolved.
• Note: conservative treatment must be abandoned if pain and tenderness increase,
depending on the status of the patient, operative intervention and
cholecystectomy should be performed. If the patient has serious comorbid
conditions a percutaneous cholecystotomy can be performed under ultrasound
control which will rapidly relieve symptoms. A subsequent cholecystectomy is
usually required.
• Medical treatment to dissolve gallstones involves chenodeoxycholic acid or
urosodeoxycholic acid drugs though it is not very successful.

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• Complications of cholecystectomy
➢ Leakage of bile from cystic duct or gallbladder bed
➢ Jaundice due to retained ductal stones. Retained stones can be treated by
ERCP or if a T-tube is in place by extraction with a Dormia basket down the
T-tube track (Burhenne maneuver)
➢ Injury to the common bile duct

EFFECTS AND COMPLICATIONS OF GALLSTONES

• In gallbladder:
➢ Biliary colic
➢ Acute cholecystitis
➢ Chronic cholecystitis
➢ Empyema of the gall bladder: this is pus in the gall bladder. It may be a sequel
of acute cholecystitis or a result of a mucocele becoming infected. Treatment
is drainage and later cholecystectomy
➢ Mucocele
➢ Perforation
• In the bile ducts
➢ Bile obstruction
➢ Acute cholangitis
➢ Acute pancreatitis
• In the intestine
➢ Intestinal obstruction (gallstone ileus)

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CHOLEDOCHOLITHIASIS

CHOLEDOCHOLITHAISIS
• Choledocholithiasis is the presence of stones in the common bile duct.
• Choledocholithiasis can result in transient or complete blockage of the common
bile duct.
• Patients may relate episodes of passing dark urine or light-colored stools caused
by the inability of bile pigments to reach the gastrointestinal tract and form
subsequent renal clearance.
• Choledocholithiasis can also lead to ascending cholangitis, demonstrated by right
upper quadrant abdominal pain, fever and chills.
• Pancreatitis owing to choledocholithiasis (gallstone pancreatitis) typically
manifests with epigastric pain radiating to the back.
• Choledocholithiasis may be associated with jaundice in addition to signs of
biliary colic. It may present as obstructive jaundice, acute cholangitis or acute
pancreatitis.
• Choledocholithiasis is classically associated with increased serum bilirubin and
alkaline phosphatase.
• Choledocholiathisis can be diagnosed by intraoperative cholangiography at the
time of surgery or preoperatively or postoperatively by endoscopic retrograde
cholangiopancreatography (ERCP).
• Management involves cholecystectomy.

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CHOLECYSTITIS

CHOLECYSTITIS
• This is inflammation of the gallbladder wall.
• It can be classified as:
➢ Acute cholecystitis
o Acute calculous cholecystitis
o Acute acalculous cholecystitis
➢ Chronic cholecystitis

ACUTE CALCULOUS CHOLECYSTITIS

• This is inflammation of the gallbladder wall.
• Commonly it occurs in a patient with pre-existing chronic cholecystitis however
it can occur as a first presentation.
• It is usually caused by impacted gallstones in the Hartmann’s pouch obstructing
the cystic duct.
• Causative bacteria include:
➢ E. coli (most common)
➢ Klebsiella, pseudomonas, proteus
➢ Salmonella
➢ Strep. faecalis
➢ Clostridium Welchii
• Infection is through either
➢ Hematogenous spread via the hepatic artery-cystic artery
➢ Portal vein
➢ Through bile after filtering in the liver via portal circulation
PATHOGENESIS AND PATHOLOGY OF CHOLECYSTITIS
• Stones cause obstruction at Hartmann’s pouch or in the cystic duct precipitating
stasis, edema of the wall, bacterial infection, and the various effects seen in acute
cholecystitis.
• Impacted stones may also cause mucosal erosion allowing bile salts to act over
the submucosal tissue as bile is toxic to these tissue. It leads into necrosis further
infection and often perforation of the gallbladder usually at Hartmann’s pouch.

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• Pathology of acute cholecystitis:
➢ Gallbladder is distended with edematous friable wall. The wall contains
dilated vessels
➢ There are areas of necrosis and patchy gangrene in severe cases
➢ Mucosa shows ulceration and necrosis
➢ Lumen contains infection fluid/infected bile or frank pus
➢ Histology shows
o Acute inflammation with neutrophils
o Edema
o Areas of necrosis and cell death
CLINICAL FEATURES
• Sudden onset of pain in the right hypochondrium with tenderness, guarding and
rigidity usually for >3 hour.
➢ The pain may radiate to right scapula area.
• Palpable, tender, smooth, soft gallbladder
• Murphy’s sign: pain on deep inspiration resulting in inspiratory arrest (positive
in 1/3 of patients).
• Sonographic Murphy’s: Pain over RUQ when palpated with ultrasound probe
(87% sensitivity).
• Area of hyperesthesia between 9th and 11th ribs posteriorly on the right (Boas’s
sign)
• Jaundice may be present
• Nonspecific and variable features: Fever, nausea, vomiting, and anorexia
• Palpable tender mass in Gall bladder region (25%)
• Tachycardia, toxic features, ileus and mild abdominal distension may be seen in
severe cases.

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INVESTIGATIONS
DIAGNOSTIC
IMAGING
• Ultrasound of abdomen: very useful,
reveals presence or abscess of
gallstones, pericholecystic fluid, and
thickening of gallbladder wall (>4mm).
Ultrasound will also show a dilation of
the common bile duct if the stone has
passed.
• Plain Abdominal X-ray: 10% of
gallstones are radio-opaque, also rules Figure 111: Ultrasound picture of visualization of multiple
gallstones (Image Courtesy of SRB's Manual of Surgery)
out other causes of acute pain abdomen
(duodenal ulcer perforation,
peritonitis). A gas shadow is
seen in the region of the gall
bladder in emphysematous
gallbladder. Porcelain
gallbladder may be seen as
opacified area in gallbladder
region.
• HIDA scan (Most sensitive):
Non-filling of the gallbladder Figure 112: Ultrasound showing roundworm in gallbladder (Image
even when the small bowel is Courtesy of SRB's Manual of Surgery)
visualized is characteristic of
acute cholecystitis

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Figure 113: Normal HIDA scan on the left demonstrating uptake of contrast in intrahepatic bile
duct and gallbladder at 20 minutes and excretion into small bowel at 30 minutes. On the Right
image note the gallbladder is not visualized even at 4 hours even though the small bowel is, this
is consistent with acute cholecystitis (Images from First Aid for Surgery Clerkship)

SUPPORTIVE
BLOOD
• Full blood count: leukocytosis with predominant
neutrophilia (>10 x 109/L)
• Live enzymes (may increase) to check
functioning of the liver
• Alkaline phosphatase (may be increased)
• Serum amylase (increases but below diagnostic
threshold for acute pancreatitis)
• Total bilirubin (increases)
• Urea, creatinine and electrolytes Figure 114: CT scan showing stone in the neck of the
gallbladder (Image Courtesy of SRB's Manual of
Surgery)

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DIFFERENTIAL DIAGNOSIS
• Duodenal ulcer perforation
• Acute pancreatitis
• Retrocecal Acute appendicitis
• Right sided Acute pyelonephritis
• Lobar pneumonia, myocardial infarction
• Ruptured ectopic pregnancy
• Viral hepatitis
TREATMENT
• Admit patient
• Initial conservative management (non-operative)-95%
➢ Nasogastric aspiration
➢ IV fluids
➢ Analgesics and antispasmodics
➢ Broad spectrum antibiotics (especially Third generation cephalosporins)
o Cefoperazone,
o Ceftazidime,
o Ceftriaxone,
o Cefotaxime + amikacin,
o Tobramycin + Metronidazole
➢ Observation
➢ Follow up ultrasound
• Later after 3-6 weeks, elective
cholecystectomy either by open method
through right subcosatal (Kocher’s incision)
or through laparoscopy is done
• Cholecystotomy is done immediate in patients
with:
➢ Empyema gallbladder Figure 115: A Foley's or Malecot’s catheter is placed in
➢ Persisting symptoms severely ill patients with acute cholecystitis to drain pus
➢ Progressing symptoms initially and later elective cholecystectomy is done. The
procedure is done in elderly, severely ill, empyema GB,
• During Cholecystotomy the gallbladder is Emphysematous GB, perforation of GB (cholecystotomy)
opened and all stones and pus are (Image Courtesy of SRB's Manual of Surgery)

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removed. Either a Foley’s or Malecot’s catheter is placed in the gallbladder and
is exteriorized.
• After 3 weeks, elective cholecystectomy is done
• Indications for cholecystotomy or emergency cholecystectomy (5%)
➢ Empyema gall bladder
➢ Persisting symptoms/failure of medication
➢ Emphysematous cholecystitis
➢ Perforation/peritonitis
➢ Elderly
COMPLICATIONS
• Perforation: this usually occurs in the fundus or in the neck (Hartmann’s). It can
cause cholecystoduodenal, cholecystointestinal or cholecystobiliary fistula.
• Peritonitis
• Pericholecystitic abscess
• Cholangitis and septicemia
• Empyema gallbladder
➢ This is a type of acute cholecystitis carrying high mortality wherein the
gallbladder is filled with pus. In 30% of cases pus may be sterile. It also occurs
in a pre-existing mucocele of the gallbladder where it gets infected.
➢ It is commonly observed in impacted stone, diabetic individuals,
immunosuppressed people like HIV or long time steroid therapy.
➢ It can perforate, form an abscess or causes peritonitis-biliary and bacterial
➢ Clinical features: Fever, toxicity, pain and tenderness in right hypochondrium,
tender, smooth, globular, gallbladder is palpable in right hypochondrium to
the right of the right rectus muscle.
➢ Investigations: Ultrasound of the abdomen, Full blood count (total count is
raised), and radioisotope scan
➢ Treatment:
o Antibiotics: Cefotaxime, Quinolones, Ceftriaxone
o Cholecystectomy- an emergency procedure
o Often initially cholecystotomy is done with either Foley’s or Malecot’s
catheter kept in situ later after 3-6 week cholecystectomy is done.
➢ Complications: septicemia, rupture and peritonitis
• Gangrenous gall bladder.

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ACUTE ACALCULOUS CHOLECYSTITIS
• Acute cholecystitis without evidence of gallstones is thought to be due to biliary
stasis.
• It is not an uncommon entity (5-10%) but can be commonly missed.
• Risk factors: ICU patients (due to bile stasis and stasis) with multi-organ system
failure, trauma (especially after major surgery), burns, sepsis, TPN or any other
stress or in cases of cholecystoses.
• The exact cause is not known. Gallbladder distension, release of activation factor
VII may be the cause
• Pathology is edema and necrosis of the gallbladder wall with features of acute
inflammation
• Presentation is usually acute
• Investigations:
➢ Isotope study (HIDA) to confirm diagnosis,
➢ Ultrasound of the abdomen: biliary sludge and inflammation is seen.
Complications such as gangrene, empyema or perforation of the gallbladder
can be seen
➢ Labs: leukocytosis with increased ALP, LFTs, amylase and total bilirubin
• Treatment:
➢ Urgent Cholecystectomy may be done by open method using Kocher’s
incision (right subcostal) or via laparoscopy by 4-port technique (umbilical
10-mm, Subxiphoid 10-mm and two 5-mm ports)
➢ Percutaneous Ultrasound guided/CT guided or open cholecystostomy
initially, later cholecystectomy is the treatment of choice.
➢ Safe dissection of the Calot’s triangle is key
➢ If the whole GB cannot be safely removed partial cholecystectomy should be
done.

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EMPHYSEMATOUS CHOLECYSTITIS
• This is seen in elderly male patients
• It is common in diabetic and immunosuppressed individuals
• Clostridium Welchii is the causative agent
• Gas is seen in the gallbladder
• It results in life-threatening septicemia
• It causes severe fulminant cholecystitis
• Gangrene, perforation and peritonitis are common
• Emergency cholecystectomy is needed
• Absences of stones is observed in more than 50% of cases

Figure 116: AXR demonstrating rim-like gas within gallbladder (Image from First Aid for the
surgery clerkship)

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CHRONIC CHOLECYSTITIS
• The is chronic inflammation and thickening of the gallbladder.
• The gallbladder is non-functioning and non-distending
ETIOLOGY
• Gallstones
• Chronic acalculous cholecystitis
• Cholecystoses
➢ These are chronic inflammatory conditions of the gallbladder associated with
cholesterol deposits.
➢ They are due to defective transport of absorbed cholesterol which accumulates
in the mucosa. There is also increased absorption of cholesterol by gallbladder
epithelium.
➢ Cholecystoses gallbladder is more prone to infection
➢ It may precipitate stone formation and is a premalignant condition
➢ Types:
o Type 1: Aggregrations of cholesterol crystals in the mucosa or
submucosa- cholesterosis (strawberry gallbladder). Lipoid contents are
present in large foamy cells which has phagocytosed cholesterol. Here
cystic duct is normal. Disease occurs only in gallbladder. It is a
premalignant condition
o Type 2: Cholesterol laden polypoid projections in the mucosa
(Cholesterol polyposis/ Gallbladder polyp)
o Type 3: Granulomatous thickening and hyperplasia of the gall bladder-
cholecystitis glandularis proliferans
o Type 4: Diverticular formation in the wall of the gallbladder
(diverticulosis of gallbladder)
o Type 5: Gallbladder wall fistula
➢ Clinical features:
o Features of acalculus cholecystitis like dyspepsia
o Positive Murphy’s sign
➢ Investigations:
o Ultrasound of the abdomen
o OCG
o Isotope study
➢ Treatment: Cholecystectomy- always should be done whether it is
symptomatic or not as it is potentially malignant.

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• Organisms associated with chronic cholecystitis:
➢ Klebsiella
➢ Streptococci
➢ Salmonella
PATHOLOGY
• Gall bladder is shrunken, contracted, small, non-functioning and fibrotic with a
thickened wall.
• Mucosa proliferates into the lumen creating deep clefts in the wall projecting into
the muscular wall of the gallbladder being lined by epithelium. It is called as
Rokitansky-Ashcoff’s sinuses.
• Muscular wall is atrophied and is often replaced by fibrous tissue.
CLINICAL FEATURES
• Pain in right hypochondrium, may be colicky or persistent
• Positive Murphy’s sign: in the sitting position during deep inspiration, while
palpating in the right hypochondrium the patient winces with pain at the summit
of the inspiration.
• Moynihan’s sign: same as the murphy’s sign however elicited when patient is
lying down.
• Flatulent dyspepsia
• Intolerance to fatty meals
• Biliary dyspepsia
DIFFERENTIAL DIAGNOSIS
• Peptic ulcer
• Pancreatitis
• Hiatus hernia
INVESTIGATIONS
• Ultrasound of the abdomen: may show stone with posterior acoustic shadowing.
Gallbladder wall will be thickened.
• Isotope study may help confirm the infection
• Liver function tests
• Total count may be raised if there is an acute recurrent infection
TREATMENT
• Cholecystectomy (laparoscopic or open method)

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COMPLICATIONS
• Common bile duct stones
• Cholangitis
• Pancreatitis
• Mirizzi’s syndrome

MUCOCELE OF THE GALLBLADDER

• This is due to obstruction of the cystic duct by a stone in the neck (Hartmann’s
pouch) of the gallbladder without any infection or inflammation in the
gallbladder. This causes absorption of all bile and secretion of mucous into the
gall bladder allowing gallbladder to distend causing mucocele of the gallbladder
(Hydrops of the gallbladder)
• Cholangiocarcinoma occluding the cystic duct can rarely also cause mucocele of
the gallbladder.
• The content is usually sterile and milky white.

CLINICAL FEATURES
• Painless swelling in the right hypochondrium
• Non-tender, smooth, soft, globular palpable gallbladder (content is sterile)
• Features of dyspepsia

INVESTIGATIONS
• Ultrasound of the abdomen
• Liver function tests

TREATMENT
• Cholecystectomy, either laparoscopic or open method.

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CHOLANGITIS

TUMORS OF THE BILIARY TRACT

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CHAPTER 11: OBSTRUCTIVE JAUNDICE

OBSTRUCTIVE JAUNDICE
• This is jaundice that develops due to biliary obstruction which may be partial,
complete or intermittent.
• It is also known as surgical or cholestatic jaundice. To convert mg/dl to mol/L
• It causes conjugated hyperbilirubinemia (Serum bilirubin> multiply mg/dl by 17.1 for
2.5mg/dl). bilirubin)
• Normal serum bilirubin level is 0.2-0.8mg/dl.
• Sclera icterus is visible when serum bilirubin levels exceeds 2.5mg/dl (35-40
mol/L)
➢ Jaundice is first seen in the frenulum (underneath the tongue)

METABOLISM OF BILIRUBIN
• Bilirubin is a product of red blood cell breakdown in the spleen. After about 120
days senescent red blood cells are destroyed by the tissue macrophages of the
spleen (in the red pulp of the spleen).
• Hemoglobin is split into heme (iron + porphyrin) and the globin part.
• The globin part is broken into amino acids and is utilized for the re-synthesis of
hemoglobin.
• The iron from heme is reused for hemoglobin synthesis, it is bound to transferrin
and transported to be stored as ferritin in the cells of the liver and bone marrow.
Some iron deposits in tissue as hemosiderin.
• The heme is broken down by heme oxygenase to oxy-heme. Oxy-heme is further
converted by heme reductase to biliverdin a green pigment.
• Biliverdin is converted into unconjugated bilirubin. The enzyme involved is
biliverdin reductase.
• Unconjugated bilirubin is bound to albumin and transported to the liver for
conjugation via the splenic artery that joins the superior mesenteric to form the
portal vein.
• In the liver bilirubin is bound to cytoplastic proteins ligandins and Z- proteins.
Bilirubin is conjugated with 2 glucuronic acid moieties to form conjugated
bilirubin. The enzyme involved is uridine 5’diphosphate (UDP)
glucoronyltransferase.

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• Conjugated bilirubin is then secreted into bile which is stored and concentrated
in the gall bladder. Bile is secreted into the duodenum (in response to CCK from
I cells in the mucosa of the duodenal cells) from the common bile duct at the
major duodenal papilla that is guarded by the sphincter of Oddi at the ampulla of
Vater.
• In the intestines bilirubin is deconjugated by bacterial/intestinal enzyme beta-
glucorinidase to form free bilirubin which can be reabsorbed in the terminal ileum
and taken back to the liver via the portal vein system (the so called enterohepatic
circulation)
• Some bilirubin is converted by bacterial dehydrogenase to urobilinogen (a
colorless substance). Some of the urobilinogen is excreted in the urine and is
converted to urobilin (orange-yellow pigment) by dehydrogenase giving urine its
characteristic color.
• The bulk of urobilinogen, bilirubin and urobilin is excreted in feces by conversion
of stercobilinogen and stercobilin which gives feces their characteristic orange-
yellow color.

CAUSES
• Causes can be classified as:
➢ Intraluminal
o Common bile duct stones
o Biliary strictures
o Pancreatic stricture (due to chronic
pancreatitis)
o Parasitic infestations
o Biliary atresia
o Klatskin tumor (carcinoma at the confluence
of hepatic ducts above the level of the Figure 117: Causes of obstructive jaundice
cystic duct and so will cause (Image adapted from SRB surgery)
hydrohepatosis without GB enlargement)
➢ Mural
o Cholangiocarcinoma
o Ascending cholangitis
o Sclerosing cholangitis: Fibrous obliteration of biliary tract leading to
jaundice cirrhosis and portal Hypertension. Associated with IBD
(especially ulcerative colitis)
o Choledochal cyst

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➢ Extramural
o Carcinoma of head and periampullary region (pancreas, ampulla,
duodenum, distal common bile duct) of the pancreas
o Extrinsic compression of CBD by lymph nodes or tumors

BENJAMIN’S (1983) CLASSIFICATION OF

BILIARY OBSTRUCTION
• Type 1: complete obstruction
➢ Tumors: pancreatic, cholangiocarcinoma
➢ Common bile duct ligation-iatrogenic
➢ Primary/secondary liver tumors
• Type 2: intermittent obstruction
➢ Choledocholithiasis
➢ Periampullary tumor
➢ Choledochal cyst
➢ Bile duct papilloma
➢ Hemobilia
➢ Duodenal diverticula
• Type 3: chronic complete obstruction
➢ Bile duct stricture
➢ Congenital
➢ Traumatic
➢ Post-radiotherapy
➢ Chronic pancreatitis
➢ Cystic fibrosis
• Type 4: Segmental obstruction
➢ Traumatic
➢ Sclerosing cholangitis
➢ Cholangiocarcinoma, intrahepatic biliary stone (hepatolithiasis)

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CLINICAL FEATURES
• Features of Obstructive jaundice:
➢ Severe jaundice
➢ Pruritus (due to deposition of bile salts in the skin), more on the back and
forearms
➢ Dark urine (due to the presence of conjugated bilirubin in urine)
➢ Steatorrhea (fatty stool) due to improper absorption of fats (Recall: bile is
required for absorption of fat, it participates in emulsification of fat).
• Fever, may or may not be present
• Loss of weight and appetite
• Pain in right hypochondrium, palpable gallbladder, hydro-hepatotic palpable,
smooth, soft, non-tender liver are other features.
• Courvoisier’s law suggests inflammatory/neoplastic cause.
➢ Courvoisier’s law: A palpable gallbladder in the presence of jaundice is
unlikely to be due to gallstones.
➢ Usually caused by a neoplastic stricture obstructing the distal common bile
duct.
➢ Rule may not be useful in:
o Absence of gallbladder
o Intrahepatic gallbladder
o Previous cholecystectomy
o Large stone in Hartmann’s pouch
o Empyema gallbladder with CBD stone
o Double impacted stone-one in CBD and one in cystic duct
• Complications of vitamin deficiency:
➢ Vitamin A: night blindness
➢ Vitamin D: Osteomalacia and pathological fractures (poor absorption of
calcium)
➢ Vitamin E: Poor wound healing, recall vitamin E is an antioxidant
➢ Vitamin K: bleeding disorders (Recall factors II, VII, IX and X are vitamin K
dependent clotting factors)
• Charcot’s triad/Reynold’s pentad as presentation in cholangitis.

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INVESTIGATIONS
• Blood investigations:
➢ Serum bilirubin: normal value <1.0 mg/dl (17.1mol/l).
o Both direct (conjugated) and indirect (unconjugated) bilirubin are
assessed
o Direct is increased in obstructive jaundice i.e. conjugated
hyperbilirubinemia
o Van den Bergh’s test is done
➢ Serum albumin, globulin and A:G ratio
o Normal Serum albumin is more than 3.5 g/L
➢ Prothrombin time: normal value is 12-16 seconds. It is significant if it is more
than 4 from the control or more than 1 and half times the control. It is corrected
by injection of Vitamin K, 10mg IM OD for 5 days or by FFP-5-10 units.
➢ Serum alkaline phosphatase, gamma glutamyltransferase (GGT), AST, ALT,
5’ nucleotidase (this is the most reliable since its level is not influenced by
bone disease and the enzyme is not induced by alcohol)
o ALP, 5’ nucleotidase and gamma glutamyltransferase are elevated
o ALT and AST are minimal or sometimes not elevated
➢ Full blood count: Shows neutrophilia in inflammatory conditions.
➢ Tumor markers:
o CA 19/9 is useful for carcinoma pancreas (more than 70 units/L) with
70% sensitivity and 90% specificity. But it may also increase in other
causes of biliary obstruction and cystadenoma.
o Alpha-fetoprotein is raised in hepatocellular carcinoma.

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• Imaging:
➢ Abdominal ultrasound: may show gallstone.
➢ Endoscopic retrograde cholangiopancreatography (ERCP): to visualize the
site of obstruction, brush biopsy, bile sample for analysis.
➢ Percutaneous transhepatic cholangiography (PTC): to decompress, assess
proximal dilated obstructed biliary system if ERCP fails, dine polythene
catheter can be kept in situ to have biliary drainage. PTC-stenting across the
obstruction can be done under image (C arm) guidance
➢ Magnetic resonance cholangiopancreatography (MRCP): Non-invasive
diagnostic tool. It shows 96% sensitivity and 99% specificity.
➢ CT scan in case of tumors to assess operability.
➢ Endoscopic ultrasound (EUS): it is done through endoscope. It is more
accurate in assessing pancreatic mass, staging disease, to identify involvement
of portal venous system, common bile duct stones. It is also useful in
endoscopic ultrasound guided Fine needle aspiration and cytology, celiac axis
neurolysis and EUS guided immunotherapy.
➢ Intraductal ultrasound (IDUS): it is very useful in assessing tumor stage,
tumor margin in bile duct cancer. It is also used in assessing pancreatic duct
to differentiate pancreatic cancer and chronic pancreatitis.
➢ CT/MR angiogram or venogram: in assess vascularity and portal venous
system in malignancy.
• Urine tests: Fouchet’s test for bile pigments, Hay’s test for bile salts and test for
urobilinogen in urine. Conjugated bilirubin is water soluble and is therefore
filtered in the glomerulus and present in urine.
➢ Fouchet’s test: 10ml of urine + 5ml of BaCl2 + Pinch of MgSO4 causes
formation of BaSO4 which is filtered over a filter paper and few drops of
Fouchet’s reagent is added. Green or blue color signifies presence of bile
pigments in the urine.
➢ Hay’s test for bile salts: Sprinkle Sulphur to 2ml of urine. In presence of bile
salts Sulphur sinks to the bottom.
➢ Ehrlich’s test: 5 ml of freshly voided urine + 1ml of Ehrlich reagent (p-
dimethyl amino benzaldehyde) and wait for 5 minutes. Formation of red color
signifies presence of urobilinogen in urine. Normally it is present in traces, in
obstructive jaundice it is absent and in hemolytic jaundice it is in excess.

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MANAGEMENT
• Treat underlying cause
• Management involves:
➢ Establishing the cause of the jaundice
➢ Assessment of the general condition of the patient
➢ Staging in patients with tumors
➢ Appropriate treatment (which may be surgical, endoscopic or radiological)

PREOPERATIVE
• Proper diagnosis and assessment (history and physical examination)
• Correction of metabolic abnormalities, improvement of the general condition and
institution of specific measures designed to minimize the incidence of
complications associated with prolonged or severe cholestasis such as:
➢ Infections (cholangitis, septicemia, wound infection)
➢ Disorder of clotting mechanism
➢ Renal failure
➢ Liver failure
➢ Fluid and electrolyte abnormalities
• Hypokalemia is frequently present and should be corrected.
• Perform a viral hepatitis panel.
• Vitamin K IM 10mg-20mg for 3-5 days.
• Fresh frozen plasma- often requires 6 bottles or more
• Adequate hydration is most important 5/10% dextrose for 12-24 hours before
surgery followed by an osmotic diuretic (mannitol 100-200ml BD IV) or a loop
diuretic administered intravenously at the time of induction.
• Catheterize and monitor urine output hourly
• Blood transfusion in case of anemia
• Oral neomycin, lactulose for hepatic encephalopathy. As well as correction of
hypokalemia, restriction of sedative, hypnotics and potent analgesics with prompt
treatment of infection.
• Repeat monitoring by doing prothrombin time, electrolytes
• Prophylactic antibiotics like third generation cephalosporins especially for:
➢ All jaundiced patients
➢ Patients with rigors and pyrexia
➢ Patients undergoing emergency biliary procedures/operations
➢ Elderly patients

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➢ Patients with common duct stones even if not jaundiced
➢ Patients undergoing secondary biliary intervention
• Calcium supplements e.g. calcium chloride IV
• Preoperative decompression: indicated if bilirubin is >12mg/dl (>150 mol/L),
impending liver failure, sepsis, Hepatorenal syndrome, severe malnutrition or
cardiopulmonary disease
➢ Preoperative decompression is achieved by insertion of a plastic
endoprosthesis or by endoscopic sphincterotomy in patients with
periampullary cancer.
• Correction of coagulopathy, prevention of renal failure, infection, hepatic
encephalopathy, and electrolyte imbalance (correction of hypoglycemia and
dilutional hyponatremia due to water retention, avoiding isotonic saline infusion)

OPERATIVE
• Depends on the cause
• Common bile duct stones- ERCP stone removal, choledocholithotomy,
transduodenal sphincteroplast, choledochojejunostomy or
choledochoduodenostomy.
• Carcinoma periampullary or head of pancreas- Whipple’s operation or triple
bypass or ERCP stenting.
• Biliary stricture- Stenting, choledochojejunostomy, Roux-en-Y
hepaticojejunostomy
• Klatskin tumor- radical resection or palliative stenting
• Biliary atresia- Kasai’s operation or liver transplantation
• Choledochal cyst- excision, hepaticojejunostomy, mucosal resection
• Management of pruritus: pruritus may be due to retention of bile salts which
activates the release of histamine in skin, central mechanism or by release of
endogenous opioids. It is often difficult to treat. Once cause is treated and
obstruction is relieved pruritus will regress.
➢ Drugs and therapies used: Cholestyramine (ion exchange resin binds bile salts
in intestine inhibiting their absorption), rifampin, ondansetron, gabapentin,
sertratine, urosodeoxycholic acid, antioxidants, phototherapy, plasmaphereis.

POST OPERATIVE
• Monitoring with prothrombin time, bilirubin, albumin, creatinine, electrolyte
estimation
• FFP or blood transfusion

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• Antibiotics
• Observation for septicemia, hemorrhage, pneumonia, pleural effusion, bile leak
• Care of T-tubes and drains
• T-tube cholangiogram in 10-14 days.
• Total parenteral nutrition, Central venous pressure line, nasogastric tube, urinary
catheter.

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CLINICAL BOX: A case of fever, pain and jaundice

History:
As the junior doctor on call, you are asked to review the
blood results of an 87-year-old man, who was admitted
that morning with possible appendicitis. He is confused
and unable to give an accurate history. He had been
spiking temperature during the afternoon and had
increasing right-sided abdominal pain.
Examination:
The observation chart shows he has a temperature of 38oC
and tachycardia of 120/min. You notice he has a yellow
discoloration of the skin and sclera and abdominal
examination reveals that the maximal tenderness is in the
right upper quadrant. There are no palpable masses or
abdominal herniae. Rectal examination demonstrates
normal stool stool with no palpable rectal mass. A plain
abdominal radiograph, done that morning, was normal.
Investigations done: FBC, Serum amylase, Urea &
Electrolytes, Creatinine, AST, ALT, GGT, Bilirubin,
Albumin, Blood glucose, C-reactive protein (CRP)

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Questions:
1. What is the likely diagnosis?
2. What are the classical characteristics to indicate this?
3. What are the most common causes?
4. Which are the most common organisms?
5. What investigations should be performed?

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CHAPTER 11: ABDOMINAL MASSES

DIVSIONS OF THE ABDOMEN

• Recall that the abdomen is divided by 4 lines into 9 regions.
➢ Transpyloric line: a line midway between the umbilicus and xiphisternum
➢ Transtubercular line: as the levels of two tubercles on the iliac crest
➢ Right vertical line: through the midpoint of right anterosuperior iliac spine
and pubic symphysis
➢ Left vertical line: through the midpoint of left anterosuperior iliac spine and
pubic symphysis

• The 9 regions are thus:

1. Right hypochondrium
2. Epigastic region
3. Left hypochondrium
4. Right lumbar region
5. Umbilical region
6. Left lumbar region
7. Right iliac fossa
8. Hypogastrium
9. Left iliac fossa

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• The abdomen can also be divided into 4 quadrants by two perpendicular lines
through the umbilicus.

• The 4 quadrants are thus:

➢ Right upper quadrant
➢ Left upper quadrant
➢ Right lower quadrant
➢ Left lower quadrant

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CHAPTER 12: PAINFUL ANAL CONDITIONS

PAINFUL ANAL CONDITIONS

• The rectum is 15cm long and extends from the rectosigmoid to the anorectal line.
It curves with the sacrum and contains 3 folds.
• The rectal wall consists of the mucosa, submucosa and 2 complete muscle layers:
the inner circular and the outer longitudinal.
• The anal canal is 3.5cm long and it extends from the anorectal line to the anus.
• The dentate line (pectineal line) divides the anal canal to an upper part that
contains columnar epithelium and autonomic innervation, from an endoderm
origin as well as a lower part that contains squamous epithelium (continuous with
perianal skin) and pudendal somatic innervation with ectoderm origin.
• The columns of Morgagni begin at this line and extend cephalad.
• Pain from above the dentate line is visceral, diffuse and poorly localized while
pain from below the dentate line is somatic and well localized.
• Within the anal canal lie anal sphincters
➢ The internal sphincter is a circular muscle continuous with the inner circular
smooth muscle layer and is under parasympathetic control
➢ The External sphincter blends with the outer longitudinal skeletal muscle
layer with 3 parts subcutaneous,
superficial and deep muscle and is under
voluntary control via the pudendal nerve
(S4). The superior border of the external
sphincter fuses with the puborecalis
muscle which forms a sling originating
at the pubis and joining behind the
rectum.
• The space between the internal and external
sphincter (intersphincteric plane) is a
fibrous continuation of the longitudinal
smooth muscle of the rectum. Normally 6 to
10 anal glands lie in this space. Each gland Figure 118: Cross-section through the anal canal and
lower rectum showing the important anatomical
has a duct and discharges into the anal crypt relations of the regions
of the dentate line. Infection originating in
these glands is the primary cause of perirectal abscess and fistula in ano.

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HEMORRHOIDS

HEMORRHOIDS/PILES
• The word ‘Hemorrhoid’ is derived from Greek words Haima (bleed) + Rhoos
(flowing), mean bleeding.
• The pile is derived from the Latin word ‘Pila’
means ball.
• Piles- a ball or mass, Hemorrhoids= blood to
ooze.
• The anal canal is lined by the anal cushions,
which consist of 3 thick vascular submucosal
bundles that always lie in the left lateral (3
O’clock), right posterior lateral (7 O’clock) and
right anterior lateral positions (11 O’clock) in Figure 119: Anal cushions
lithotomy position.
• The functions of these cushions is not entirely clear but they aid continence (anal
tone) and engorge during defecation to protect the anal canal from abrasions.
• Hemorrhoids are the downward sliding of the anal cushions abnormally due to
straining or other causes.
➢ Anal cushions are aggregations of blood vessels (Arterioles, venules), smooth
muscles and elastic connective tissue in the submucosa that normally reside
in left lateral, right posterolateral and right anterolateral anal canal.
➢ These positions can be found at 3, 7 and 11 o’clock.
• Hemorrhoids consist of dilated venous plexus, a small artery and areolar tissue.
• Piles can be mucosal or vascular.
➢ Vascular type is seen in young.
➢ Mucosal is seen in old.
• Present concept is weakening of Park’s ligament which is the lower end of the
external sphincter.

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TYPES
• Hemorrhoids can either be:
➢ Internal- above the dentate (pectineal) line,
covered with mucous membrane
➢ External- below the dentate (pectineal)
line, covered with skin
➢ Interno-external- together occur.

CLASSIFICATION Figure 120: Types of hemorrhoids

• Hemorrhoids can be classified according:
➢ Location
➢ Severity
ACCORDING TO LOCATION
• Primary hemorrhoids: Located at 3, 7, 11 o’clock positions related to the branches
of the superior hemorrhoidal vessels which divides on the right side into 2, and
on the left side it continues as 1.

Figure 121: Hemorrhoids

• Secondary hemorrhoids: One which occur between the primary sites.

ACCORDING TO SEVERTIY
• First degree: piles within that may bleed but does not come out
• Second degree: piles that prolapse during defecation but returns back
spontaneously
• Third degree: piles prolapsed during defecation, can be replaced back only by
manual help

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• Fourth degree: pile that are permanently prolapsed.

Figure 122: Classification of piles

• Piles begin as pedicle and it is located at the origin of the internal pile i.e. at the
level of anorectum.

ETIOLOGY
• Hereditary
• Idiopathic
• Morphologic: weight of the blood column without valves causes high pressure.
Veins in the lower rectum are in loose submucosal plane but the veins above enter
the muscular layer, which on contraction increases the venous congestion below
(more prevalent in patients with constipation). Superior rectal veins have no
valves (as they are tributaries of portal vein) and so more congestion.
• Other causes:
➢ Straining, diarrhea, constipation, hard stool, low fiber diet, over-purgation
➢ Carcinoma rectum, portal hypertension (rare cause)
➢ Pregnancy: during pregnancy raised progesterone relaxes the venous wall and
reduces its tone, enlarged uterus compresses the pelvic vein and constipation
is a common problem.

CLINICAL FEATURES
• It occurs at any age but mostly between 30 to 65 years.
• Incidence is equal in both sexes.
• Painless Bleeding- 1st symptom- ‘splash in the pan’- ‘bright red and fresh’- occurs
during defecation
➢ Note: mucus or fecal soiling may occur, though in general changes in bowel
habit are uncommon and should alert to other cause
• Mass per anum
• Discharge- a mucoid discharge

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• Pruritus
• Pain- may be due to prolapse, infection or spasm
• Prolapse of internal hemorrhoids may produce moisture in the anal region or
mucus discharge that causing itching.
• Anemia- secondary

EXAMINATION
• On inspection, prolapsed piles will be visualized
• On P/R examination, only thrombosed piles can be felt.

DIFFERENTIAL DIAGNOSIS
• Carcinoma
• Rectal prolapse
• Perianal warts
• Causes of bleeding per anum
➢ Piles
➢ Fissure in ano
➢ Fistula in ano
➢ Polyps
➢ Ulcerative colitis
➢ Amoebic colitis
➢ Carcinoma rectum and carcinoma colon
➢ Diverticulitis
➢ Intussusception
➢ Vascular anomaly of the colorectum
➢ Mesenteric ischemia

INVESTIGATIONS
• Proctoscopy: note number, degree, size, surface and appearance of piles as well
as features of chronicity of the prolapse.
• Sigmoidoscopy or colonoscopy: malignancy
• Endoscopy to rule out other sources of rectal bleeding e.g. cancer and
inflammatory bowel disease.
• Barium enema: malignancy
• Full blood count-check for anemia (hematocrit) and platelet count

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COMPLICATIONS
• Profuse hemorrhage which may require blood transfusion
• Strangulation- by anal sphincter
• Thrombosis- piles appear dark purple/black, feels solid and tender
• Ulceration
• Gangrene
• Fibrosis
• Stenosis
• Suppuration leads to perianal or submucosal abscess
• Pylephlebitis (portal pyaemia) is rare but can occur in 3rd degree piles after
surgery.

TREATMENT
• External hemorrhoids are best treated with analgesia and warm soaks. If pain is
severe, the thrombosed hemorrhoids must be excised.
• Mild bleeding and protrusion of external hemorrhoids can be controlled with
conservative treatment including avoidance of constipating foods, increasing the
fiber content of the diet and using bulk-forming stool agents.
• The above measures along can resolve all symptoms.
• Rubber-band ligation a simple outpatient procedure can be used to treat 1 st and
2nd degree hemorrhoids. Injection with phenol and almond oil could play a similar
role.
• 3rd and 4th degree hemorrhoids and mixed internal/external hemorrhoids require
hemorrhoidectomy.

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Preventive Therapeutic/curative
Diet- more fiber/ Medical
liquid, laxatives ➢ Sitz bath- immersing anal region for 15-20 minutes, 2-3 times a
day. To reduce edema, pain and promote healing
➢ Analgesics, local anesthetic cream
➢ Antihistamines
➢ Antibiotics
➢ Laxatives
➢ Local anesthetics and anti-inflammatory drugs e.g. annomax
Parasurgical
➢ Sclerotherapy
➢ Banding
➢ Cryotherapy
➢ Infrared coagulation (IRC)
➢ Laser therapy
➢ Doppler guided haemorrhoidal artery ligation (DGHAL): good for
pregnant and diabetic patients
Surgical
➢ Open haemorrhoidectomy (Milligan-Morgan)-Britain
➢ Closed haemorrhoidectomy (Hill-Fergusson)- USA
➢ Stapled haemorrhoidopexy (Antonio Longo)
➢ Anal stretching- Recamier, Lord’s

Severity Medical Parasurgical Surgical

1st degree • Medical • Sclerotherapy can be
interventions done
are usually • DGHAL can be done
enough
2nd degree • Medical • Sclerotherapy can be
interventions done
are usually • Barron’s banding is
enough done
• DGHAL can be done
3rd degree • Medical • Laser therapy can be • Hemorrhoidectomy
interventions done is gold standard
can help • DGHAL can be done
4th degree patients • DGHAL can be done • Hemorrhoidectomy
especially is gold standard
before surgery

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ANAL FISTULA

ANAL FISTULA (FISTULA IN ANO)

• A fistula is an abnormal communication between two epithelial/endothelial lined
surfaces surrounded by granulation tissue.
• A fistula in ano has its external opening in the peri-rectal skin and its internal
opening in the anal canal at the
dentate line.
• Pain is rare with anal fistula.
Patients often complain of peri-
rectal itching, irritation and
discharge.
• It is believed that fistula in ano
can be:
➢ Crytoglandular (90%) and
associated with infection of
the intersphincteric glands
➢ Non-cryptoglandular (other
causes)-10%
Figure 123: Anatomy of anal glands (Cryptoglands of Morgagni)
ETIOLOGY
• Drainage (40%) or rupture of an anorectal abscess (i.e. anal gland infection)
(most common cause)
➢ Anal fistula forms during the chronic stage of an acute inflammatory process
that begins in the intersphincteric anal glands.
➢ Extension of the acute inflammation can result in a supralevator, ischiorectal
or perianal abscess.
➢ With chronic inflammation the abscess communicates with the external
surface forming supralevator trans-sphincteric or intersphincteric fistulae.
• Crohn’s disease
• Diverticulitis with perforation and fistula to the perineum
• Infection: HIV, TB, actinomycosis, lymphogranuloma venereum
• Malignancies of the distal rectum, anal canal or perianal skin
• Trauma: foreign body, iatrogenic, anal fissure
• Hydradenitits suppurative

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CLASSIFICATION
• Fistulae can be either:
➢ Low level fistulas: these open into the anal canal below the internal ring
➢ High level fistulas: these open into the anal canal at or above the internal ring
• Standard classification
(Milligan Morgan-1934
and Goligher-1975)
➢ Pelvi-rectal fistula
➢ Submucosal fistula
➢ Subcutaneous fistula
(most common)
➢ High anal fistula
➢ Low anal fistula
(common)
• Park’s classification (1976)
➢ Intersphincteric fistula (70%-
commonest)
➢ Transsphincteric fistula (25%)
➢ Supralevator/Suprasphincteric
fistula (4%)
➢ Extrasphincteric fistula (1%)

CLINICAL FEATURES
• Persistent sympt /

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o Relates to the location of the internal
and external openings of a fistula in ano.
o Fistulas with an external opening in
relation to the anterior half of the anus
is of a direct type.
o If the anus is bisected by a line in the
frontal plane, an external opening
inferior to that line connects the internal
opening via a short direct tract.
o If the external opening is posterior to the Figure 126: Goodsall's rule
imaginary line, the fistula tract follows a
curved route to the internal opening in the
posterior midline, it may present with
multiple external openings all connected to
a single internal opening.
o An exception is an external opening that is
anterior to this imaginary line and more than
3cm from the anus, in which case the tract
may be curve posterior and end in the
posterior midline.
➢ Examination under anesthesia if there is
significant discomfort
➢ P/R examination shows indurated internal
opening usually in the midline posteriorly.
➢ Most of the fistulae are on posterior half of the
anus.
Figure 127: Goodsall's rule. Anterior
fistulae are having straight track.
INVESTIGATIONS Posterior fistulae are having curved
• Simple fistulas are diagnosed clinically tracks with internal opening in the
• Chest X-ray, ESR and barium enema X-ray. posterior midline
• If required fistulogram is done only under
anesthesia
• MRI/MRI fistulogram is ideal
• Endorectal U/S (US perineum) is useful to assess deeper plane.
• Dscharge study, methylene blue dye study, biopsy
• Colonoscopy often when ulcerative colitis/Crohn’s is suspected

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• Specific blood test

MANAGEMENT
• The mainstay of treatment is to lay the
fistula tract open. Procedure depends on
the type of fistula
• Low fistula tract (superficial,
intersphincteric, low transphincteric)
options:
➢ Fistulotomy in which the fistula is
opened and allowed to heal by
secondary intention
➢ Injection of fibrin glue/sealant
➢ Internal sphincterotomy is the Figure 128: Fistulogram X-ray showing track
treatment for an intersphincteric
fistula
• High fistula tract options:
➢ Fistulotomy and placement of seton cord which is left in fistula to allow
drainage during healing.
o In the first stage, a seton suture is placed around the sphincter to stimulate
fibrosis adjacent to the sphincter muscle
o In the second stage performed 6-8 weeks later, the intersphincteric portion
of the fistula tract is laid open
o This is done to prevent incontinence.
➢ Advancement flaps: adjacent mucosa used to seal internal opening.
➢ Fistula plug
➢ Ligation of intersphincteric fistula tract (LIFT)

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ANAL FISSURE

ANAL FISSURE
• An anal fissure is a tear in the anal canal, frequently associated with sudden pain
or bleeding during defecation.
• The longitudinal tear (ulcer) in the anal canal can occur anywhere from below
the dentate line to the anal margin.
• 90% of anal fissures are in the 6 O’clock position. It may be associated with skin
tags or a sentinel pile.
• Causes:
➢ Straining in constipation
➢ Childbirth
➢ Trauma
➢ IBD
• Management:
➢ Initial advice:
o Avoid staining
o Minimize constipation: increase fiber and fluid intake, consider laxative
o Immerse anus in warm water with shallow bath or Sitz bath kit, 2-3 times
daily.
➢ Topical medical treatment:
o 0.4% Glyceryl trinitrate ointment is first line
o Other options: diltiazem 2%, Botox
➢ Surgical:
o Lateral anal sphincterectomy in which internal sphincter fibers are divided
over the length of the fissure. This may be required for chronic anal
fissures.
o Further option is excision and anal advancement of flap.

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PILONIDAL SINUS

PILONIDAL SINUS
• A pilonidal sinus is a hair-
containing sinus or abscess that
usually involves the skin and
adjacent tissue in the intergluteal
region.
• Most patients have pain, swelling
and drainage when these sinuses
become infected.
• Most investigators believe that this
condition is caused by ingrowth of Figure 129: Pilonidal sinus and abscess
hair, although whether it is acquired
or congenital is not known.
• Pilonidal disease can occur at any age but is most prevalent between adolescence
and the third decade of life.
• Recurrent infections are common.
• The treatment depends on the phase of the disease at presentation.
• Pilonidal abscess is best treated by incision and drainage. However, for a
pilonidal cyst, results of treatment remain imperfect although numerous methods
have been reported. The simplest methods of treatment are incision and drainage,
and curettage with secondary healing or cyst excision and closure.

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ANORECTAL ABSCESS

• Anorectal abscess is due to obstruction of anal glands/crypts at the dentate line

with subsequent infection by gut
bacteria.
• Locations include:
➢ Perianal (60%): limited to
skin of anal canal. It results
when pus spreads
downwards between the 2
sphincters. It manifests as a
tender swelling of the anal
verge
➢ Ischiorectal (20%): crosses
the external anal sphincter. It
is formed if a growing
intersphincteric abscess Figure 130: Common sites of anorectal suppuration
penetrates the external
sphincter below the puborectalis. Infection can spread into the fat of the
ischiorectal fossa and the abscess can become quite large
➢ Intersphincteric: between the internal and external sphincters. It results from
infection in the anal glands. Fecal coliforms are typically the offending
organisms. As the abscess enlarges within the intersphincteric plane, it can
spread in any several directions.
➢ Supralevator (Rare): superior extension above levator. It develops when an
intersphincteric abscess expands upwards between the internal and external
sphincters
• Abscess rupture, spontaneous or surgical leads to fistula formation in 50% of
patients

RISK FACTORS
• These may cause abscess formation via anal gland infection and/or separate
mechanisms:
➢ Bowel inflammation: IBD (especially Crohn’s), diverticulitis, TB,
Hidradenitis suppurativa
➢ Immunosuppression: diabetes, HIV
➢ Trauma: rectal foreign bodies, receptive anal sex

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➢ Demographic and social: male, aged 20-60

CLINCAL FEATURES
• Perianal pain and pruritus. Pain may be worse on siting and defecation
• Constipation due to painful defecation
• Deeper abscesses may cause systemic symptoms
• On Examination:
➢ Perianal swelling (external or felt by P/R)
➢ Purulent/bloody discharge
➢ Examination under anesthesia if there is significant discomfort

INVESTIGATIONS
• Can often be diagnosed clinically.
• Deeper abscesses may require endoanal US or MRI

DIFFERENTIAL DIAGNOSIS
• Pilonidal abscess
• Hydradenitis suppurativa
• Folliculitis
• Periprostatic abscess
• Bartholin gland abscess
• Inflammatory bowel disease
• Actinomycosis
• Tuberculosis

MANAGEMENT
• Incision and drainage:
➢ Can be done in ward/ED for simple perianal abscesses otherwise will require
theater.
➢ The primary opening of the anal crypt is rarely identified.
➢ Most wounds can be left open, without packing. Intersphincteric abscesses
may require post-op drain.
➢ Intersphincteric abscess is treated by using the proctoscope to observe the
bulging area and then performing an internal sphincterotomy over the abscess.
➢ Supralevator abscesses are drained through the appropriate ischiorectal space
or through the rectum.

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➢ Horsehoe abscess (those that surround the rectum) are drained through the
rectum with corner drains placed in each ischiorectal abscess.
➢ Post-procedure, advise frequent sitz baths (water to hip height) and consider
laxative to reduce pain defecation.
• Antibiotics (in addition to Incision and drainage) only if there is evidence of
sepsis, extensive cellulitis or immunosuppression.

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CHAPTER 13: HERNIA

• Femoral hernias account for 17%,

HERNIA umbilical hernias account for 8.5%
• A hernia is a protrusion of a viscus and others account for about 1.5%
or part of a viscus through the wall (excluding incisional hernia).
of its containing cavity. • In general, incisional hernia is next
• A hernia comprises of a hernial sac to inguinal hernia in occurrence.
and neck.
Common herniae
• The abnormal opening may be
artificial or natural (area of • Inguinal hernia (73%)
weakness or disruption of the • Incisional hernia
fibromuscular tissues of the body • Femoral hernia (17%)
wall). • Umbilical hernia (8.5%)
• Herniae may occur in the brain (e.g. • Epigastric
after head injury), in the muscle • Other herniae (1.5%)
through its fascial covering,
internally in the abdomen (internal • Risk factors:
hernia) or externally through a ➢ “Increased intra-abdominal
weak normal opening (inguinal and pressure”
femoral herniae) or an abnormal o Straining, lifting of heavy
opening (e.g. incisional hernia) in weights
the abdominal wall. o Chronic constipation
• 75-85% of abdominal wall hernias (habitual, rectal stricture),
are groin hernias. o Chronic cough
➢ 15% of males will develop groin (tuberculosis, chronic
hernia. bronchitis, bronchial
➢ 5% of females will develop asthma, emphysema),
groin hernia. o Urinary causes: old age
• Inguinal hernias are the most (BPH, carcinoma prostate),
common types of hernias (73%) Young age (stricture
because the muscular anatomy in urethra), very young age-
the inguinal region is weak and also Phimosis, meatal stenosis
due to the presence of natural o Ascites
weakness like deep ring and cord ➢ Wall weakness
structures.

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o Obesity, pregnancy and SAC
pelvic anatomy (especially • This is a diverticulum of
in femoral hernia in peritoneum with mouth, neck, body
females), and fundus.
o Smoking • The neck is narrow in indirect sac
o Previous surgery: but wide in direct sac.
Appendectomy through
• The body of the sac is thin in
McBurney’s incision may
infants.
injure the ilioinguinal nerve
causes right sided direct CONTENTS
inguinal hernia. • Omentum- Omentocele
o Familial collagen disorder- (epiplocele). Difficult to reduce the
Prune Belly syndrome sac later, initially it can be reduced
o Acquired herniation is also easily.
probably due to collagen • Intestine- Enterocele- commonly
deficiency called as small bowel, but sometimes even
metastatic emphysema of large bowel. Difficult to reduce the
Read. sac initially.
o An indirect inguinal hernia • Richter’s hernia: a portion of
occurs in a congenital, circumference of bowel is the
preformed sac i.e. the content.
remains of processus
• Urinary bladder may be the content
vaginalis. Chances of
or part of the posterior wall of the
presence of bilateral
sac- cystocele.
preformed sac is 60%.
• Ovary, often with fallopian tube.
PARTS OF A HERNIA • Meckel’s diverticulum- Littre’s
• The hernia comprises of: hernia.
➢ Covering • Amyand hernia: this is an inguinal
➢ Sac hernia containing the vermiform
➢ Content appendix. It should not be confused
with a De Garengeot hernia in
COVERING which a femoral hernia contains the
• These are the layers of the appendix.
abdominal wall through which the
sac passes.

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CLASSIFICATION OF obstruction to blood flow.
The swelling is tense,
HERNIA tender, with no impulse on
• Hernias can be classified: coughing and with features
➢ Clinically of intestinal obstruction.
➢ According to etiology Features of intestinal
➢ According to the contents obstruction may be absent in
➢ Anatomical classification case of Omentocele,
Richter’s hernia, Littre’s
CLINICAL hernia.
CLASSIFICATION ➢ Inflamed hernia: it is due to
• Hernias can be classified as: inflammation of the contents of
➢ Reducible hernia: hernia gets the sac e.g. appendicitis,
reduced on its own or by the salpingitis. Here hernia is tender
patient or by the surgeon. but not tense, overlying skin is
o Intestine reduces with red and edematous.
gurgling and it is difficult to
reduce the first portion. ETIOLOGICAL
o Omentum is doughy, and it CLASSIFICATION
is difficult to reduce the last • Hernias can be classified as either
portion. ➢ Congenital- common
o Exanpsile impulse on o Occur in a preformed
coughing present. sac/defect. Clinically may
➢ Irreducible (incarcerated) present at a later period due
hernia: contents cannot be to any of the precipitating
returned to the abdomen due to causes like in indirect
narrow neck, adhesions, inguinal hernia.
overcrowding. Irreducibility ➢ Acquired
predisposes to strangulation. o It is secondary to any causes
o Obstructed hernia: it is an which raise the intra-
irreducible hernia with abdominal pressure leading
bowel inside that is into weakening of the area
obstruction, but blood like in direct inguinal
supply to the bowel is not hernia.
interfered.
o Strangulated hernia: it is an
irreducible hernia with

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CLASSIFICATION ANATOMICAL
ACCORDING TO CLASSIFICATION
CONTENTS • Depend on the site of the hernia
• Omentocele- omentum including:
• Enterocele- intestine ➢ Abdominal wall herniae
• Cystocele- urinary bladder o Inguinal hernia
o Femoral hernia
• Littre’s hernia- Meckel’s
o Epigastric hernia
diverticulum
o Umbilical hernia
➢ Note: Littre described Meckel’s
o Paraumbilical hernia
diverticulum in a hernia sac 81
o Incisional hernia
years before Meckel was born.
o Spigelian hernia: this is an
• Richter’s hernia- part of the bowel
interstitial hernia of
wall. Only part of the lumen
abdominal wall. The defect
protrudes, it can cause
occurs at the lateral border
strangulation without obstruction.
of the rectus abdominis,
• Maydl’s hernia (hernia-en-W)- W-
emerging through a defect
shaped loop (two adjacent loops) in
in the transversus and
hernial sac with tight, strangulated
internal oblique fascia
neck. This is a rare form of inguinal
halfway between the
hernia; 2 loops of intestine are
umbilicus and pubic
incarcerated in the sac. The
symphysis.
intervening loop of small intestine
- The swelling is diffuse
remains in the abdominal cavity
and difficult to palpate
becomes strangulated by
as it is covered by the
compression of its mesenteric
external oblique.
vessels at the neck of the sac.
- It may be identified by
• Sliding hernia- contains partly its position above and
extra-peritoneal structures (e.g. medial to the location of
cecum or sigmoid colon) such that an inguinal hernia.
the hernial sac does not totally ➢ Internal:
surround the contents (or in other o Diaphragmatic (hiatus or
words a viscus forms part of the congenital)
wall) o Mesenteric
o Omental

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➢ Others ➢ Ease of repair (size, location)
o Obturator hernia ➢ Likelihood of success (size,
o Lumbar hernia ‘loss of right of abode’)
• Assess the patient for fitness for
surgery, impact of hernia on
lifestyle (job, hobbies)
• Principles of surgery:
➢ Herniotomy: Excision of the
hernial sac.
➢ Herniorrhaphy: repair of the
defect
➢ Hernioplasty (ideal)

Figure 131: Herniae (Image adapted from

SRB’s Manual of Surgery 2nd Ed)

• Herniography (by Gullmo):

injection of contrast material into
the peritoneal cavity and taking
films in supine and prone
positions to diagnose protrusions
of peritoneal sac is called as
herniography.
• It was earlier also used for
diagnosing undescended testis.

MANAGEMENT OF
HERNIA
• Assess the hernia for:
➢ Severity of symptoms
➢ Risk of complications (type,
size of neck)

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INGUINAL HERNIA

INGUINAL HERNIA
• Inguinal hernia is a common complaint, occurring mostly in men. It is twice as
frequent as femoral hernia and in males more than 90% of herniae are inguinal.
• They may occur at any age.
➢ In children they are generally associated with developmental disorder e.g.
persistent processus vaginalis or testicular maldescent.
➢ In young adult males they are also related to congenital defects such as a
persistent processus, which may be precipitated from potential to actual
existence by physical effort.

SURGICAL ANATOMY OF INGUINAL CANAL

• The inguinal canal is an oblique passage in lower part of abdominal wall, 3.5-
4cm long, situated above the medial half of inguinal ligament, extending from
deep inguinal ring to superficial inguinal ring.
➢ In infants both superficial and deep rings are superimposed without any
obliquity of the inguinal canal.
➢ Inguinal canal in female is called as “Canal of NUCK”
• The Superficial inguinal ring is a triangular opening in the external oblique
aponeurosis and is 1.25cm above the pubic tubercle.
➢ The ring is bounded by a superomedial and inferolateral crus.
➢ Normally the ring does not admit the tip of little finger.
➢ It corresponds to the midpoint of the
inguinal ligament (halfway the point
between the anterior superior iliac spine
and the pubic tubercle)
• The Deep inguinal ring is a U-shaped
condensation of the transversalis fascia that
lies 1.25cm above the inguinal ligament
midway between the symphysis pubis and the
anterosuperior iliac spine (mid-inguinal
point).
• The Inguinal (Poupart’s) ligament is formed
by the lower border of the external oblique Figure 132: Anatomy of the inguinal canal (Image
adapted from SRB’s Manual of Surgery 2 Ed)
nd

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aponeurosis which is thickened and folded backwards on itself, extending from
anterosuperior iliac spine to pubic tubercle.
➢ Contents of the inguinal canal:
o Ilioinguinal nerve (L1)
o Spermatic cord in male or round ligament in females
➢ Contents of the spermatic cord:
o Vas deferens
o Artery to vas
o Testicular and cremasteric artery
o Genital branch of genitofemoral nerve (L1, L2)
o Pampiniform plexus of veins
o Remains of processus vaginalis
o Sympathetic plexus around the artery to vas
➢ Coverings of the spermatic cord:
o Internal spermatic fascia from fascia transversalis
o Cremasteric fascia
o External spermatic fascia from external oblique aponeurosis is seen below
the external ring in the scrotum

Figure 133: Coverings and Contents of the spermatic cord (Image adapted from SRB’s Manual
of Surgery 2nd Ed)

➢ Boundaries of the inguinal ligament:

o Anteriorly: External oblique aponeurosis (medial) and conjoined muscle
(internal oblique and transversus abdominis) laterally.

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o Posteriorly: inferior epigastric artery, transversalis fascia and insertion of
the conjoined tendon medially.
o Superiorly (roof): conjoined tendon (Arched fibers of internal oblique and
transversalis abdominis)
o Inferiorly (floor): inguinal ligament

Figure 134: The inguinal canal (Image adapted from SRB’s Manual of Surgery 2nd Ed)

• Defence mechanism of inguinal:

➢ Obliquity of inguinal canal
➢ Arching of conjoint tendon
➢ “Shutter mechanism” of internal oblique
➢ “Ball value mechanism” due to contraction of cremaster muscle which plugs
to superficial ring
➢ When external oblique muscle contracts, intercrural fibers of superficial ring
appose causing “slit valve mechanism”
➢ Hormones

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CLASSIFICATION OF INGUINAL HERNIA (EARLIER)
• This includes:
➢ Anatomical classification
➢ Classification according to the extent
ANATOMICAL CLASSIFICATION (IN INGUINAL HERNIA)
• These can be classified as either indirect hernia or direct hernia.
• Indirect hernia: it comes out through internal (Deep) ring along with the cord. It
is lateral to the inferior epigastric artery. The inguinal ligament is inferior to the
hernia
• Direct hernia: it occurs through the posterior wall of the inguinal canal through
“Hesselbach’s triangle” (bounded medially by lateral border of rectus muscle,
laterally by inferior epigastric artery, below by inguinal ligament). Sac is medial
to the inferior epigastric artery.

Figure 135: Herniae (Image adapted from SRB’s Manual of Surgery 2nd Ed)

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Figure 136: Herniae (Image adapted from SRB’s Manual of Surgery 2nd Ed)

CLASSIFICATION TO EXTENT
• Types:
➢ Incomplete:
o Bubonocele: sac is confined to the inguinal
canal
o Funicular: here sac crosses the superficial
inguinal ring, but does not reach the bottom of
the scrotum.
➢ Complete: here sac descends to the bottom of the
scrotum.
Figure 137: Bubonocele (Image
➢ Saddle-bag or pantaloons hernia sac has got both adapted from SRB’s Manual of
medial and lateral component. Surgery 2nd Ed)
• Note: inguinal hernia is above and medial to the pubic
tubercle. Femoral hernia is below and lateral to pubic
tubercle.

INDIRECT (OBLIQUE) INGUINAL

HERNIA
• This is the most common type of hernia (65%).
• It is more common in younger age group as compared
to direct inguinal hernia which is more common in
elderly. Figure 138: Funicular (Image
adapted from SRB’s Manual of
Surgery 2nd Ed)

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• It is more common on right side in 1st decade but in 2nd
decade the incidence is equal on both sides.
• Hernia is bilateral in 30% of cases.
• An indirect hernia occurs when a sac develops by
emerging through the deep inguinal ring and passing
through the inguinal canal in the spermatic cord
adjacent to the vas deferens and surrounded by the
coverings of the cord.
• Sac is thin in indirect type. Neck is narrow and lies
Figure 139: Complete inguinal
lateral to inferior epigastric vessels. (Image adapted from SRB’s
• The sac, if sufficiently large, may emerge through the Manual of Surgery 2nd Ed)
external inguinal ring (funicular inguinal hernia) or
descend into the scrotum (complete inguinal scrotal hernia)
• Coverings of indirect hernia (from inside out)
➢ Extra-peritoneal tissue
➢ Internal spermatic fascia
➢ Cremasteric fascia
➢ External spermatic fascia
➢ Skin
• It may contain omentum or small bowel and has the potential to become
irreducible and strangulated.
• Precipitating cause: smoking, obesity, respiratory causes (bronchial asthma, TB,
bronchitis), ascites, previous surgery e.g. appendectomy which can cause direct
inguinal hernia, urinary problems like BPH, urethral stricture, straining, multiple
pregnancies, chronic constipation (due to anorectal strictures), rectal stricture due
to chronic proctitis (amoebic), TB of anorectum, previous anorectal surgery,
rectal carcinoma or stricture due to lymphogranuloma venereum.
• Types:
➢ Incomplete
o Bubonocele: where the hernia is limited to the inguinal canal
o Funicular: Processus vaginalis is closed just above the epididymis.
Contents of the sac can be felt separately from testis which lie below the
hernia.
➢ Complete (Scrotal): Testis appears to lie within the lower part of hernia. It can
occur in any age group. It occurs in a congenital preformed sac (processus

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vaginalis). More commonly contents descend into the pre-existing sac, only
when there are precipitating cause which force the content down.

Figure 140: Types of indirect inguinal herniae (Image adapted from SRB’s Manual of Surgery
2nd Ed)

CLINICAL FEATURES
HISTORY
• Prevalence of inguinal hernia is 25% in males, 2% in females.
• It is more common in males (20:1).
• Patient presents with dragging pain and swelling in the groin which is better seen
while coughing and standing and felt together with an expansile impulse.
• In complete type, the content descends down to the scrotum completely.
• Contents are either small bowel, large bowel, omentum or combination of all
these. In females, sometimes ovary and tubes may be the content. In infants,
swelling appears when the child cries and is often translucent.
• It is usually reducible but can go for irreducibility, inflammation, obstruction,
strangulation.
PHYSICAL EXAMINATION
• Internal ring occlusion test:
➢ Internal ring is located half inch (1.25cm) above the mid-inguinal point
(center point between anteriosuperior iliac spine and pubic symphysis). After
reducing the contents, in lying down position, internal ring is occluded using
the thumb.
➢ Patient is asked to cough.
➢ If a swelling appears medial to the thumb, then it is a direct hernia.

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➢ If swelling does not appear and on releasing the thumb swelling appears
during coughing, then it is an indirect hernia confirmed in standing position.
o It is seen above and medial to the pubic tubercle
• Ring invagination test: After reduction of hernia, the little finger/ index finger of
the examiner is invaginated from the bottom of the scrotum, gradually pushed up
and rotated to enter the superficial inguinal ring. The impulse on coughing is felt
at the tip of the invaginated finger. This test is done only in males.
• Zieman’s test: The examiner places his index finger on the deep inguinal ring and
middle finger on the superficial inguinal ring, ring finger over saphenous
opening. The patient is asked to cough or to hold the nose and blow. It the impulse
is felt on the index finger (covering the deep ring), it is indirect hernia.

Figure 141: Zieman’s test (Image adapted from SRB’s Manual of Surgery 2nd Ed)

• Head or leg rising test: this is done to look for abdominal wall muscle tone and
Malgaigne bulging. Valsalva manoeuver is also used to check the tone of
abdominal wall muscles.

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Figure 142: Head rising test (Image adapted from SRB’s Manual of Surgery
2nd Ed)

• Abdominal, respiratory, urological examination is done to look for any

precipitating factors like chronic bronchitis, ascites, stricture urethra, BPH
• Per rectal examination is a must
• Inguinal hernia in females:
➢ Increased thickness of labium majus on palpation, when compared to
contralateral side.

Figure 143: Left inguinal hernia in females (Image adapted from SRB’s Manual of Surgery 2nd
Ed)

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• Silk glove sign: index finger is invaginated across scrotum towards the external
ring. When patient coughs, inguinal hernia is felt as a slit like sensation.
• Palpation of bulbar urethra for stricture (thickening/crescent like feel/ button like
depression).

USE THE FIVE FINGERS OF THE HAND TO

COMPLETE ALL TESTS FOR HERNIA
Thumb- for deep ring occlusion test
Index, middle and ring finger for Zieman’s test
Little finger for superficial ring invagination test

• Rules of hernia examination

➢ Never forget to examine opposite side
➢ Never forget to do Per rectal examination
➢ Never forget to examine urethra
➢ Never forget to check abdominal muscle tone
• Differential diagnosis:
➢ Hydrocele- infantile/ encysted/large vaginal/ bilocular
➢ Undescended testis
➢ Femoral hernia
➢ Lipoma of the cord
➢ Hydrocele of the canal of neck (in females)
➢ Inguinal lymph node enlargement
➢ Groin abscess

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Figure 144: Differential diagnosis for groin swelling (Image adapted from SRB’s Manual of
Surgery 2nd Ed)

INVESTIGATIONS
• Ultrasound of abdomen
• Chest X-ray to rule out chronic bronchitis
• Tests relevant for precipitating causes

DIRECT HERNIA
• Direct hernia occurs through Hesselbach’s triangle which is bounded by inferior
epigastric artery laterally, lateral border of rectus medially and inguinal ligament
below.
➢ The hernia is medial to the inferior epigastric artery with a wide neck. The sac
is thick and often the medial wall or content may be bladder.
➢ Hesselbach’s triangle is divided into medial and lateral halves by obliterated
umbilical artery (medial umbilical ligament).
➢ Direct hernia is classified as medial or lateral depending on which part of the
Hesselbach’s triangle it is arising from.
• Direct hernia accounts for 10-15% of hernias.

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• 50% of direct hernias occur bilateral.
• 35% of inguinal hernias are direct.
• It is uncommon in females and children.
• It is always acquired due to weakening of posterior wall of inguinal canal.
• Coverings of direct hernia (From inside out):
➢ Extraperitoneal tissue
➢ Transversalis fascia
➢ Conjoined tendon
➢ External spermatic fascia
➢ Skin
• Predisposing factors: chronic cough,
smoking, straining, BPH, constipation,
heavy work, previous appendectomy.
• A direct hernia usually appears as a diffuse
bulge that cannot be controlled by pressure
over the internal ring. It is above and lateral
to the pubic tubercle.
• Malgaigne bulgings are often seen in these
patients on examination more often than in Figure 145: Bilateral direct inguinal hernia
indirect hernia. They are protrusions of (Image adapted from SRB’s Manual of
Surgery 2nd Ed)
abdominal wall muscle during leg raising test
as weak, soft, supple, swellings which
signifies poor abdominal muscle tone.
• Direct hernia rarely descends into the scrotum and strangulation is not common
as in indirect hernia. But in longstanding cases, it can descend down to the
scrotum and strangulation can occur.

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Figure 146: Direct inguinal hernia (Image adapted from SRB’s Manual of Surgery 2nd Ed)

• Investigations same as indirect hernia.

INDIRECT INGUINAL HERNIA DIRECT INGUINAL HERNIA
• Can occur in any age (child to adult) • Common in elderly
• Occurs in a pre-existing sac • Always acquired
• Protrusion through the deep ring, • Herniation through posterior wall of
herniation occurs later the inguinal canal
• Pyriform/oval shape, descends obliquely • Globular/round shape, descends
and downwards directly forward
• Can be complete by descent into scrotum • Descent down into the scrotum is rare
• Neck of sac is narrow and lateral to • Neck of the sac is wide and medial to
inferior epigastric artery inferior epigastric artery
• Sac is anterolateral to the cord • Sac is posterior to the cord
• Ring occlusion test does not show any • Test shows impulse even after
impulse after deep ring occlusion occluding the deep ring
• Invagination test shows impulse on the • Invagination test: Impulse is felt over
tip of the little finger the pulp of the little finger
• Zieman’s test shows impulse on the • Zieman’s test shows impulse on the
index finger middle finger
• Commonly unilateral but can be bilateral • Commonly bilateral
• Obstruction and strangulation are • Obstruction and strangulation are rare
common but can occur
• Sac should be opened during surgery • Sac is not necessarily opened unless
obstruction is present

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STRANGULATION
• Strangulation of an inguinal hernia develops when constriction occurs at the neck
of the sac, cutting off the blood supply of the contents.
• Initially the venous blood supply is obstruction. This causes swelling of the
contents (omentum or bowel) and eventually a combination of edema and
constriction interrupts the arterial blood supply and gangrene supervenes in the
strangulated loop.
• These changes are accompanied by:
➢ Severe local pain
➢ Irreducibility of hernia
➢ Tenderness
• The symptoms of small bowel obstruction are also evident with colicky
abdominal pain, nausea and vomiting.
• When the hernia first becomes obstructed it is possible to reduce it by
manipulation. It is important however, to ensure that the hernia is not reduced en
masse into the abdominal cavity with contents still strangulated by the
constricting neck of the sac.
• An irreducible hernia per se does not indicate strangulation and may be
incarcerated (obstructed) with an adequate blood supply but completely
irreducible.
• Management:
➢ Admit patient
➢ Ryle’s tube aspiration
➢ Intravenous fluids to correct dehydration and electrolyte imbalance
➢ Antibiotics
➢ Catheterisation to maintain adequate urine output
➢ Emergency surgery

MANAGEMENT OF INGUINAL HERNIA

• Ideally all inguinal herniae should be repaired by elective surgical operation.
• Surgery is usually performed under general anesthesia but local or regional
anesthesia is also used.
• Surgical repair classically consists of 2 elements:
➢ Excision of the hernia sac (herniotomy) and repair or buttressing of the
weakness in the posterior inguinal canal (herniorrhaphy)

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➢ Note: in direct hernia the sac is not opened and care should be taken at the
medial aspect due to presence of the bladder (which should be emptied before
surgery
• In infants (always indirect herniae), the internal and external rings are
superimposed and only a herniotomy is required for effective treatment.
• Laparoscopic repair of adult inguinal herniae is also performed by surgeons.
• Sometimes a truss may be used to control an inguinal hernia if the patient is unfit
for or refuses surgery. However, trusses are unsatisfactory, do not treat the hernia
and the patient is still at risk of incarceration (obstruction) and strangulation.
• Hernioplasty is the present choice (ideal) for all inguinal and groin hernias. Mesh
is placed either onlay/underlay (over conjoint tendon to inguinal ligament) or
inlay (in preperitoneal space).
➢ A polypropylene mesh is used to strengthen the posterior wall of the inguinal
canal.
➢ Herniotomy is done prior to mesh placement

COMPLICATIONS OF HERNIA REPAIR

• Hemorrhage
• Hematoma: may be in the wound or scrotum
• Acute urinary retention: this frequently follows bilateral repair
• Wound infection: this should be rare as hernia repair is a clean operation
however, it occurs in 5-8%.
• Hematocele
• Post-herniorrhaphy hydrocele, lymphocele
• Chronic pain: trapping of the Ilioinguinal nerve
• Hyperesthesia over the medial side of inguinal canal due to injury to
iliohypogastrc nerve-neuralgia (15%)
• Testicular pain and swelling followed by atrophy usually means that the repair is
too tight and testicular artery is compromised. Testicular atrophy will occur when
the swelling subsides.
• Recurrence of hernia (5%): if it occurs within 3 years it is called early and late if
it occurs after.
➢ Preoperative predisposing factors: smoking, chronic cough, constipation, old
age, anemia, hypoproteinemia, ascites and straining (BPH, carcinoma
prostate, stricture urethra)
➢ Operative: tension in the sutures and weak anterior abdominal wall.

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➢ Postoperative: infection (50%), hematoma formation during early surgery,
retained sac in pantaloons hernia, straining

FEMORAL HERNIA

FEMORAL HERNIA
SURGICAL ANATOMY OF FEMORAL CANAL
• The femoral canal is a the medial most compartment of the femoral sheath, which
extends from the femoral ring above to saphenous opening below.
• The femoral canal is bounded anteriorly by the inguinal ligament, posteriorly by
the fascia over the pectineus muscle (iliopectineal ligament of Cooper, pubic
bone and fascia of the pectineus are all posterior), medially by the lacunar
ligament (Gimbernat’s ligament) and laterally by the femoral vein.
• The canal is 1.25cm long and 1.25cm wide at the base. Below it is closed by
cribriform fascia.
• The canal contains fat, lymphatics and the lymph node of Cloquet.

Figure 147: The Femoral canal and femoral hernia (Image adapted from SRB’s Manual of
Surgery 2nd Ed)

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• A Femoral hernia emerges through the femoral canal and may be felt as a soft
swelling below and lateral to the pubic tubercle.
• It is a protrusion of peritoneum through the femoral canal, below which it
emerges subcutaneously.
➢ It protrudes through the femoral canal, the hernial sac descends down
vertically up to the saphenous opening and then escapes out into the loose
areolar tissue to expand out like a retort.
➢ Because of its irregular pathway and narrow neck, it is more prone for
obstruction and strangulation. During surgery, precaution should be taken
about the femoral vein and pubic branch of obturator artery (or accessory
obturator artery) which often may get injured leading to torrential
hemorrhage.
• It is usually a small sac and may contain omentum or small bowel. Because of its
position below the inguinal ligament it must be distinguished from a saphena
varix which disappears on pressure or on lying down and has a cough impulse.
• It must also be distinguished from femoral artery aneurysm, enlarged lymph
nodes or on very rare occasions, a psoas abscess.
• Etiology of femoral hernia:
➢ Wide femoral canal
➢ Multiple pregnancies

CLINICAL FEATURES
• It is common in females (2:1), common in multipara.
• Rare before puberty.
• 20% occur bilateral however more common on right side.
• Presents as:
➢ Swelling in the groin that is below and lateral to the pubic tubercle (inguinal
hernia is above and medial to the pubic tubercle)
➢ Swelling, impulse on coughing, reducibility, gurgling sound during reduction,
dragging pain are the usual features.
➢ When obstruction and strangulation occur (40%):
o Painful, tender, inflamed, irreducible swelling without any impulse is
seen.
o Abdominal distension, vomiting and features of toxicity may be present.
• Strangulation and Richter’s hernia are common in femoral hernia.

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• Often on medial side, a portion of bladder forms the wall of the femoral hernial
sac (Sliding-femoral hernia)
• Often femoral hernia can be associated with inguinal hernia also.
• Gaur’s sign: in femoral hernia, distension of superficial epigastric and/or
circumflex iliac veins occurs due to the pressure by the hernial sac.
• Hydrocele of femoral hernia occurs when adherent omentum which is the content
secretes fluid into the sac.
• Herniation through a gap in the lacunar ligament (medial) is always strangulated
and is called as Laugier’s femoral hernia (L for L)
• In congenital dislocation of hip, femoral hernia occurs behind the femoral vessels
(Narath’s femoral hernia)
• If sac lies under the pectineal fascia it is called a Cloquet’s hernia

DIFFERENTIAL DIAGNOSIS
• Inguinal hernia
• Enlarged Cloquet lymph node of any cause
• Psoas abscess- psoas spasms with flexed hip but difficulty in extension
• Lipoma
• Femoral aneurysm
• Distended psoas bursa (disappears on hip flexion)
• Saphena varix- this is an enlarged terminal portion of the long saphenous vein. It
is soft, disappears on lying down, fluid thrill, impulse on coughing and venous
hum on auscultation are present. There is associated varicose veins on leg.
• Hematoma in the region.

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MANAGEMENT
• Because femoral herniae are most likely to lead to strangulation than inguinal
hernia, they should always be
repaired without delay.
• A truss should not be used.
• Surgically the hernia may be
approached from:
➢ Below (femoral approach)
➢ Above via the inguinal canal
(Lotheissen approach)
➢ Rectus abdominis muscle
(McEvedy approach)
• The contents of the sac are emptied,
the sac is excised and the femoral
canal is obliterated with 3
interrupted non-absorbable sutures. Figure 148: Different surgical approaches for femoral hernia
• Polypropylene mesh can be buttressed (Image adapted from SRB’s Manual of Surgery 2nd Ed)
over the femoral canal to close the
defect.

UMBILICAL HERNIA

UMBILICAL HERNIA
• True umbilical hernia is common
in infants (Especially in Africans)
and is due to a persistent defect in
the abdominal wall at the
umbilicus.
• The majority close spontaneously
and surgical closure is rarely
necessary.
• Intervention is required in the
unlikely event of strangulation or
incarceration. Figure 149: Congenital umbilical hernia (Image
from Clinical Surgery 2nd Ed)

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PARAUMBILICAL HERNIA

PARAUMBILICAL HERNIA
• These herniae occur in obese adult women and are prone to strangulate.
• The defect occurs through the midline just above the umbilicus.
• The sac may contain omentum or small intestine or both and because of the
narrow neck, strangulation is relatively common.
• With long-standing herniae, adhesions occur between the contents and the wall
of the sac so that the hernia becomes
irreducible.
• Strangulated herniae are repaired as an
emergency.
• Long-standing herniae should be
repaired electively. The Mayo repair is
commonly used.
➢ With this technique the contents of
the sac are freed from its wall and
reduced.
➢ The sac is excised and the fascial
defect is repaired transversely with
the upper flap overlapping the lower,
thereby doubling the strength of the
repair. Figure 150: Paraumbilical hernia (Image from
Clinical Surgery 2nd Ed)
EPIGASTRIC HERNIA

EPIGASTRIC HERNIA
• These usually small but often quite painful swellings occur in the midline
between xiphisternum and umbilicus.
• The swelling most frequently consists of herniation of Extraperitoneal fat through
a small defect in the linea alba.
• Sometimes it carries a peritoneal sac with it that may contain omentum but this
is rare.
• Pain is localized to the site with tenderness on pressure but it may also simulate
the symptoms of peptic ulcer.

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• Clinical examination reveals a tender swelling in the midline. Sometimes
incarcerated fat becomes devascularized and necrotic.
• Treatment is surgical and may be carried out under local anesthesia, enlarging
the defect, excising the fat and suturing the defect with non-absorbable sutures.

INCISIONAL HERNIA

INCISIONAL HERNIA
• This is a hernia that protrudes through a defect in an old abdominal wound.
• It is common in old age and obese individuals.
• It occurs in 10% of abdominal surgeries, 70% occurs in first 5 years and 30%
occurs in 5-10 years.
• Types of defects in incisional hernia:
➢ Small defect <2cm
➢ Large and wide defect >2cm
➢ Very large defect
➢ Massive/diffuse
➢ Multiple defects- Swiss cheese pattern
• Predisposing factors:
➢ Vertical incision has got high chances of incisional hernia than horizontal
scars.
➢ Layered closure of the abdomen has got higher chance than single layer.
➢ Continuous closure has got higher chances than interrupted closure
➢ Using absorbable suture material has got higher chances of hernia than non-
absorbable sutures
➢ Emergency surgical wound has higher chances than elective surgical wounds.
➢ Laparotomy for peritonitis, acute abdomen and trauma can commonly cause
incisional hernia
➢ Drainage through the main laparotomy wound may precipitate formation of
incisional hernia
➢ Chronic cough, smoking, obstructive uropathy, constipation can precipitate
incisional hernia
➢ Diabetes, old age, malnutrition, malignancy, anemia, hypoproteinemia,
jaundice, ascites, liver disease, uremia, steroid therapy, immunosuppressive
disease are other precipitating factors.

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• The margins of the defect in the abdominal wall under the old incision can be felt
and the hernia is easily demonstrated by asking the supine patient to raise his or
her head off the pillow (thus tensing the abdominal muscles).
• An incisional hernia often contains bowel that is adherent to the peritoneal sac.
• Clinical features:
➢ Swelling in the scar region
➢ Pain
➢ Impulse on coughing
➢ Gurgling sound
➢ Often bowel peristalsis may be visible under the skin
➢ Eventually features of irreducibility, obstruction, strangulation is seen.
➢ Hernia is common in lower abdomen
➢ It may be small or large, huge or massive (diffuse)
➢ Scar, its extent and location whether healed primarily or secondarily, skin over
the scar and swelling is noted. Details of the swelling with expansile impulse
on coughing and examination both in lying down and standing are done.
➢ Gap cannot be assessed in an irreducible hernia.
• Surgical repair requires excision of the sac and identification and apposition of
the margins of the hernia.
• Occasionally, with a very large incisional hernia, it is not possible to bring the
muscle edges together and a polypropylene mash (Marlex) has to be inserted to
close the abdominal wall defect.
• Complications of incisional hernia:
➢ Irreducibility
➢ Obstruction
➢ Strangulation
➢ Incarceration

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CHAPTER 14: ORTHOPEDICS

ORTHOPEDICS
GENERAL PRINCIPLES

GENERAL PRINCIPLES OF FRACTURES

• A fracture (sometimes abbreviated FRX or Fx or Fx or #) is a partial or complete
break in the structural continuity of a bone which may or may not be involved
with soft tissue injury.
• If the overlying skin remains intact it is a closed (or simple) fracture.
• If the skin or one of the body cavities is breached it is an open (or compound)
fracture, liable to contamination and infection.
• Bone is the only tissue in the human body other than liver that heals by
regeneration instead of by scarring.
• For regeneration to occur the bone must be immobilized to allow uninterrupted
formation of new bone.

CLASSIFICATION
• Classification aims to have a standard interpretation of a fracture for research and
clinical management, tell you the severity of a fracture and how it could have
been caused as well as better management.
• Fractures can be classified according to:
➢ Clinical classification
➢ Anatomical site
➢ Etiology (mechanism of injury)
➢ Radiological appearance (Radiological pattern of fracture)
➢ Eponyms

CLINICAL CLASSIFICATION
• Fractures are either classified as:

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➢ Open fractures (Compound fractures)
➢ Closed fractures (simple fractures)
OPEN FRACTURES (COMPOUND FRACTURES)
• There is a wound on the skin surface leading to the site of the fracture i.e. a direct
communication exists between the body surface and the fracture.
• Open fractures are liable to contamination by organisms and are thus true
orthopedic emergencies.
• The amount of communication can vary from a small puncture wound in the skin
to a large avulsion of soft tissue that leaves the bone exposed.
• Prognosis depends on extent of soft tissue injury and by type/level of bacterial
contamination.
• Treatment plan: prevent infection (Broad spectrum antibiotics and Tetanus
prophylaxis), restore soft tissues (Wound cleaning and debridement), achieve
bone union (reduction, immobilization), avoid malunion and institute early joint
motion and muscle rehabilitation.

CLOSED FRACTURES (SIMPLE FRACTURES)

• There is no communication between the site of the fracture and the exterior of the
body.

Figure 151: Open fracture (Left) vs Closed Fracture (Right)

ANATOMICAL SITE
• Fractures are classified by their anatomical location in relation to a specific bone
identifying a fracture by location does not indicate whether the fracture is open
or closed nor does it indicate the type of fracture (transverse, oblique, spiral etc.).
• Fractures may affect the proximal, middle or distal end of a bone.

ETIOLOGY (MECHANISM OF INJURY)

• According to etiology fractures are divided into 3 groups:

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➢ Traumatic fractures
➢ Stress/Fatigue fractures
➢ Pathological fractures
TRAUMATIC FRACTURES
• These are the most common types. They occur in bones previously free of
disease.
• Fracture caused by sudden and excessive force which may be direct or indirect.
• They can either be due to:
➢ Direct force: the bone breaks at the point of impact; the soft tissues also are
damaged. A direct blow usually splits the bone transversely or may bend it
over a fulcrum so as to create a break with a ‘butterfly’ fragment. Damage to
the overlying skin is common, if crushing occurs the fracture pattern will be
comminuted with extensive soft-tissue damage.
➢ Indirect force: bone breaks at a distance from where the force is applied, soft
tissue damage at fracture site is not inevitable. Most fractures due to a
combination of forces (twisting, bending, compressing or tension), the x-ray
patterns reveal:
o Twisting: causes a spiral fracture- (A)
o Compression causes a short oblique fracture- (B)
o Bending results in fracture with a triangular ‘butterfly’ fragment- (C)
o Tension tends to break the bone transversely- (D); in some situations, it
may simply avulse a small fragment of bone at the points of ligament or
tendon insertion.

Figure 152: From left to right, (A) Spiral fracture due to twisting (B) Short Oblique fracture due
to compression (C) Triangular butterfly fragment due to bending (D) Transverse fracture due to
tension

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• NOTE: the above description applies mainly to the long bones. A cancellous
bone, such as a vertebra or the calcaneum when subjected to sufficient force will
split or be crushed into an abnormal shape.
STRESS/FATIGUE FRACTURE
• These occur in normal bone which is subject to repeated heavy loading typically
in athletes, dancer or military personnel who have grueling exercise programs.
• These high loads create minute deformations that initiate the normal process of
remodeling- a combination of bone resorption and new bone formation in
accordance with Wolff’s law.
• When exposure to stress and deformation is repeated and prolonged, resorption
occurs faster than replacement and leaves the area liable to fracture. A similar
problem is seen in people on drugs that alter normal balance of bone resorption
and replacement. Stress fractures are increasingly seen in patient with chronic
inflammatory diseases who are on treatment with steroids or methotrexate.
• These types of fractured are confined to bones of lower limb: metatarsal bone
(>50%), calcaneus (25%), shaft of fibula and tibia (20%), neck of femur.
• Onset of pain in the affected bone is gradual, pain increased by continuous
activity and relieved by rest.
• O/E: marked tenderness over affected bone and swelling.
• Radiographic changes occur only 2-4 weeks and may show only a faint hairline.
Rarely is there displacement of fragments.
• Treatment: decreased physical activity
PATHOLOGICAL FRACTURE
• These fractures occur even with normal stresses because the bone has been
weakened by a change in its structure (e.g. in osteoporosis, osteogenesis
imperfect or Paget’s disease) or through a lytic lesion (e.g. a bone cyst or a
metastasis)

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• Some common tumors which
metastasize to bone are thyroid cancer,
breast cancer, prostate cancer, renal
cancer.
• Primary bone tumors causing fractures:
Giant cell bone tumor, Ewing’s tumor
• Causes: local or generalized
➢ Infections: pyogenic osteomyelitis
➢ Benign tumors: chrondroma, giant
cell tumor Figure 153: Osteolytic bone
➢ Malignant tumors: osteosarcoma,
Ewing’s, metastatic carcinoma especially the above-mentioned tumors that
metastasize to bone, multiple myeloma,
diffuse metastatic carcinoma.
➢ Miscellaneous: simple bone cyst,
eosinophilic granuloma, tabes dorsalis,
osteonecrosis after irradiation, paget’s
disease, gaucher’s disease.
➢ Congenital disorders: osteogenesis
imperfect
➢ Diffuse rarefaction of the bone: senile
osteoporosis, parathyroid
osteodystrophy, infantile rickets,
Cushing’s syndrome, nutritional
osteomalacia.
• Osteoporosis is the most common Figure 154: Osteolytic bone
pathologic condition association with
pathologic fractures.
• When treating the broken bone, the underlying condition must be treated as well.

RADIOLOGICAL PATTERN
• This classification is based on the X-ray view of the fracture.
• It is the description of shape and pattern as seen on radiographs.
• Pattern indicates:
➢ Nature of causative violence

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➢ Clue to easiest method of reduction
➢ The likely stability of the fragments
• Common patterns could be:
➢ Transverse
➢ Oblique
➢ Spiral
➢ Comminuted (more than 2 fragments)
➢ Compression or crush
➢ Impacted
➢ Greenstick (incomplete break occurring in resilient bones in children)
➢ Burst
➢ Avulsion
• These patterns fall into 2 well defined groups:
➢ Complete fractures: Fracture split into two or more fragments. X-ray can help
predict behavior after reduction.
o Transverse fractures: fragments
usually remain in place after
reduction.
o Oblique fractures: tend to shorten
and re-displace even if the bone is
splinted
o Spiral fractures: tend to shorten
and re-displace even if the bone is
splinted
o Impacted fractures: Fragments are
jammed tightly together and the Figure 155: From left to right (A) Transverse
fracture line is indistinct (B) Segmental (C) Spiral
o Comminuted fractures: more than
two fragments are present, because there is poor interlocking of the
fracture surfaces, these are often unstable.

➢ Incomplete fractures: Bone is incompletely divided and the periosteum

remains in continuity

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o Greenstick fracture: bone is
buckled or bent (like snapping a
green twig), this is seen in children,
whose bones are springier than
those of adults. Children can also
sustain injuries where the bone is
plastically deformed (misshapen)
without there being any crack
visible on X-ray.
o Compression fracture: Occur when
cancellous bone is crumpled. This
happens in adults and typically Figure 156: Greenstick fracture, note the
where this type of bone structure is Buckle or torus
present e.g. in the vertebral bodies,
calcaneum and tibial plateau.

Figure 157: Fracture patterns

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Figure 158: Fracture patterns

Figure 159: Fracture patterns

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EPONYMS
• Traditional classifications often bear the originator’s name.
• This type of classification can only be used to specific type of injuries however,
even then the term is often inaccurately applied, famously in the case of Pott’s
fracture, which is often applied to any fracture around the ankle though that is
not what sir Percival Pott implied when he described the injury in 1765.
• These are based on the people that first described the fractures:
➢ Gastilo & Anderson- open tibial fracture
➢ Garden’s classification for fracture neck of femur
➢ Neer classification of proximal humeral fractures
➢ Hansen classification for ankle fracture
➢ Muller AO classification of fractures: this is an alphanumeric classification of
fractures developed by Muller and colleagues

Figure 160: Muller's classification

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DISPLACEMENT
• After a complete fracture the fragments usually become displaced, partly by the
force of the injury, partly by gravity and partly by the pull of muscles attached to
them.
• Displacement is usually described in terms of translation (shift), alignment,
rotation and altered length.
TRANSLATION (SHIFT)
• The fragments may be shifted sideways, backward or forward in relation to each
other such that the fracture surfaces lose contact.
• The fracture will usually unite as long as sufficient contact between surfaces is
achieved, this may occur even if reduction is imperfect or indeed even if the
fracture ends are off-ended but the bone segments come to lie side by side.
ANGULATION (TILT)
• The fragments may be tilted or angulated in relation to each other. Mal-
alignment, if uncorrected may lead to deformity of the limb.
ROTATION (TWIST)
• One of the fragments may be twisted on its longitudinal axis, the bone looks
straight but the limb ends up with a rotational deformity.
LENGTH
• The fragments may be distracted and separated, they may overlap, due to muscle
spasm, causing shortening of the bone.

• Types of displacement include: translation (shift), Angulation (tilt), Rotation,

impaction and overlap.
• NOTE: all types can be corrected with closed manipulation except rotational
displacement (must be surgically corrected as it can lead to malunion and
deformities).

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DESCRIBING FRACTURES
• When describing, the description must include:
➢ Clinical classification: is the fracture open or closed? (only comment on this
when there is a patient)
➢ Anatomical classification:
o Which bone is broken?
o Has it involved a joint surface?
➢ Radiological pattern: Only comment on this if there is an X-ray.
o Transverse: slow to join because the area of contact is small, if the broken
surface is accurately apposed, however the fracture is stable on
compression.
o Spiral: joints more rapidly (because contact area is large) but is not stable
on compression.
o Comminuted: slow to join because (1) they are associated with more
severe soft tissue damage and (2) they are likely to be unstable.
➢ Displacement: assess
o Shift or translation- backwards, forwards, sideways, or longitudinally
with impaction or overlap.
o Tilt or angulation- sideways, backwards or forwards.
o Twist or rotation- in any direction.
• Example: Closed, transverse fracture of the shaft of the radius with no
displacement.
• A problem often arises in the description of angulation. ‘Anterior angulation’
could mean that the apex of the angle points anteriorly or that the distal fragment
is tilted anteriorly: in this text it is always the latter meaning that is intended
(‘anterior tilt of the distal fragment’ is probably clearer).

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CLINICAL ASSESSMENT OF A FRACTURE
• Involves:
➢ History
➢ General examination (general signs)
➢ Local examination
HISTORY
• History of injury, followed by inability to use the injured limb- but beware! The
fracture is not always at the site of the injury e.g. a blow to the knee may fracture
the patella, femoral condyles, shaft of the femur or even acetabulum.
➢ What happened? Was there a lot of violence involved or a simple fall? (get
both direct history from victim and collateral history from witnesses)
➢ How did it happen? Can likely injuries be predicted from the patient’s
description of the incident?
➢ Where and when did it happen? Did it happen recently or has the patient come
late?
➢ What was the patient like before it happened? Does the patient have any other
medical problems?
➢ Also ask about patient’s last meal (in case they may need to go to theater)
• The patient’s age and mechanism of injury are important, if a fracture occurs with
trivial trauma suspect a pathological lesion.
• Pain, bruising, swelling are common symptoms but they do not distinguish a
fracture from a soft-tissue injury.
• Deformity is much more suggestive.
• Always enquire about Symptoms of associated injuries: pain and swelling
elsewhere (it is a common mistake to get distracted by the main injury,
particularly if it is severe), numbness or loss of movement, skin pallor or
cyanosis, blood in urine, abdominal pain, difficulty with breathing or transient
loss of consciousness.
• Previous injuries: once the acute emergency has been dealt with, ask about
previous injuries or any other musculoskeletal abnormality that might cause
confusion when the X-ray is seen.
• General medical history: important in preparation for anesthesia or operation.

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• Note: Due to the medicolegal implications associated with accidents, fractures
and injuries it is important to keep meticulous notes at the time or as soon after
the event as possible.
GENERAL EXAMINATION
• Unless it is obvious from the history that the patient has sustained a localized and
fairly modest injury, priority must be given to dealing with the general effects of
trauma:
➢ Follow the ABCs: Airway obstruction, Breathing problems, Circulatory
problems and Cervical spine injury (neck collar).
➢ Ask a simple question such as ‘What is your name?’ if you get a sensible
answer then the patient is conscious with a good airway. However, for most
patients with a single or few injuries, the examination will concentrate on the
injured part and the fitness of the patient for anesthetics.
• During the secondary survey it will also be necessary to exclude other previously
unsuspected injuries and to be alert to any possible predisposing cause (such as
Paget’s disease or a metastasis).
• General signs (a broken bone is part of a patient). Look for evidence of:
➢ Shock or hemorrhage
➢ Associated damage to brain, spinal cord or viscera
➢ Predisposing causes
• Local signs:
➢ Injured tissues must be handled gently. To elicit crepitus (grating or grinding
of the broken bone ends) or abnormal movement is unnecessarily painful, X-
ray diagnosis is more reliable.
➢ Examine the most obviously injured part.
➢ Test for artery and nerve damage.
➢ Look for associated injuries in the region.
➢ Look for associated injuries in distant parts.
INSPECTION (LOOK)
• Look for the following signs:
➢ Swelling, bruising, deformity
➢ Discoloration and loss of function
➢ Deformity; measure and record any:
o Angulation
o Rotation
o Translation

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o Shortening
o These may be better assessed on X-ray
➢ Any compound wounds (i.e. any wounds that reach to the site of the fracture)
These should be assessed accurately and measured and recorded using the
Gustillo classification (of an open tibial fracture):
o Grade 1:
- Wounds <1cm,
- Simple fracture pattern,
- No skin crushing, clean wounds (mild contamination)
o Grade 2:
- Wounds measuring 1-10cm but without significant soft tissue
crushing, including no flaps, degloving or contusion.
- # pattern may be more complex.
- Moderate contamination
o Grade 3:
- Wounds >10cm, also includes injuries older than 8 hours,
- Severe contamination plus:
- A: no periosteal stripping
- B: Periosteal stripping
- C: neurovascular damage
- Tip: to remember A, B and C the mnemonic “AA”-Apparent
apposition (i.e. no periosteal stripping), “BB”- bone bare (periosteal
stripping), “CC”- Circulatory compromise (i.e. neurovascular
damage)
➢ Note also the posture of the distal extremity and the color of the skin (for tell-
tale signs of nerve or vessel damage).
PALPATION (FEEL)
• Bony tenderness
• Warmth
• Distal pulses
• Move joints for crepitus (a scratching sound made by a broken bone or rough
joint)
• Soft tissue damage, this is often graded as follows:
➢ Grade 0: little or no soft tissue injury
➢ Grade 1: superficial abrasion with moderate swelling and bruising
➢ Grade 2: deep abrasion, tense swelling with bruising and blistering

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➢ Grade 3: extensive contusion, tense swelling, compartment syndrome and/or
vascular damage
MOVEMENT (MOVE)
• Abnormal/painful movement: do not cause the patient extra discomfort just to
confirm abnormal movement. Furthermore, such abnormal movement may cause
further soft tissue damage and further periosteal stripping.
• Simply do an X-ray.
INVESTIGATIONS
IMAGING
X-RAYS
• Follow the “rules of twos”
➢ TWO views: usually an anterior/posterior view (AP) and a lateral view. This
gives a better view of a fracture or dislocation. For some injuries e.g. the hand
oblique views are better.
➢ TWO joints: include the joint above and the joint below the bone under
consideration. In the forearm or leg, one bone may be fracture and angulated.
Angulation however is impossible unless the other bone is also broken or a
joint dislocated.
➢ TWO sides: useful for comparison, particularly in children because it allows
comparison of the epiphyseal lines in immature bones and distinguishes them
from the fracture line.
➢ TWO injuries: Severe force often causes injuries at more than one level. Thus
with fractures of the calcaneum or femur it is also important to also X-ray the
pelvis and spine.
➢ TWO occasions: repeat X-ray 10-14 days (1-2 weeks) later
• All x-rays should be centered on the area of maximal tenderness.
• Radiographic features of a fracture:
➢ Lucencies at the site of the fracture
➢ Discontinuity in the cortex or surface of a bone or joint.
• MRI can be used to view extent of soft tissue injury.
ULTRASOUND
• May help detect joint effusions.

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RADIOISOTOPE BONE SCAN
• When there is doubt, radioisotope bone scanning can help determine whether a
bone is fractured. This is most useful about 2 weeks after the injury. It is a highly
sensitive test but does not provide any information about the fracture except that
it is there.
• A useful example is the scaphoid fracture, which may be seen on a second X-ray
at 2 weeks but there can still be doubt. A negative scan is very positive
reassurance in such a situation and may help to allay lingering clinical doubt.
BLOODS
• Full blood count: For Hemoglobin, hematocrit and detection of infection
• Urea, Electrolytes and creatinine: may point towards dehydration and renal
failure secondary i.e. during hemorrhagic shock
• Liver function tests

HEALING OF FRACTURE
• Healing begins as soon as the bone is broken, provided the conditions are
favorable and proceeds through several stages.
• The repair of tubular bone has been classified into 5 stages for simplicity:
➢ Stage of inflammation and hematoma formation: Tissue damage and bleeding.
(immediate response)
➢ Stage of cellular proliferation (subperiosteal and endosteal cells):
Inflammatory cells appear.
➢ Status of callus formation: Osteoblasts and osteoclasts appear. Takes 2-4
weeks
➢ Stage of consolidation: Woven bone replaced by lamellar bone and fracture
united.
➢ Remodeling: New formed bone remodeled to resemble normal structure.

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Figure 161: Stages of Fracture healing

Figure 162: Stages of wound healing

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MANAGEMENT OF FRACTURE
• Since bones are dynamic living tissues with a very rich blood and nerve supply.
The immediate consequences of fractures therefore are severe pain and blood loss
and the strategy of early management is to minimize pain with splints and
analgesics and to anticipate the effects of blood loss i.e. hypovolemic shock.
• General treatment is the first consideration: treat the patient, not only the fracture.
➢ First Aid- ABCs
➢ Resuscitation of patient and treatment of shock
➢ Pain relief
➢ Treatment of the fracture
• When fractures occur with other injuries save life first (resuscitate! Primary and
secondary survey), Save the limb, save the joint and then restore function.
• All fractures unite: somehow, whenever. Be aware of this difference you create
make use of it rationally (P. Demmer)
• Bone is the only tissue in the human body other than liver that heals by
regeneration instead of by scarring.
• For regeneration to occur the bone must be immobilized to allow uninterrupted
formation of new bone.
IMMEDIATE MANAGEMENT
• Follow the ABCs: Airway obstruction, Breathing problems, Circulatory
problems and Cervical spine injury (neck collar).
• Ask a simple question such as ‘What is your name?’ if you get a sensible answer
then the patient is conscious with a good airway. However, for most patients with
a single or few injuries, the examination will concentrate on the injured part and
the fitness of the patient for anesthetics.
RESUSCITATION AND BLOOD LOSS
• For most upper limb and peripheral lower limb fractures blood loss is small and
is tolerated even by the elderly.
• Blood loss may be significant with major pelvic fractures (6+ units) and long
bone fractures particularly the femur (2-3 units) and the tibia (1 unit).
• In general, all patient with long bone injuries should be cross-matched for blood.
• Gain venous access with 2 large bore cannulae.
• Start running fluids (normal saline) as you wait for blood (See chapter on shock).
• Monitor vital signs.

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PAIN RELIEF
• Systemic pain relief with opiates given in adequate doses in combination with an
antiemetic to offset the adverse effects opiates. In injured patients, intravenous
rather than intramuscular opiates should be used. Clinicians, particularly when
new are often afraid to give adequate doses of opiates in fear of affecting
consciousness and clinical signs. In general, however, when serious head or
visceral injury has been excluded, they may be used generously and early.
• Local anesthetic nerve blocks: are frequently effective. Femoral nerve block for
example can remove the need for systemic drugs following femoral fracture
although the anxiolytic benefits of CNS agents should not be underestimated.
• Splintage: can be applied to most fractures before arrival to hospital. This alone
can relieve most intolerable pain. In general, a splint should encompass the joint
above and below the injury. Simple expedients such as binding the arm to the
chest, with or without a sling, or simply binding the legs together is often
sufficient.
TREATMENT OF THE FRACTURE
• Debridement is required for open fractures as they are surgical emergencies.
Formal surgical wound debridement (removal of all dead tissue) should be
performed as soon as possible and preferably within 6 hours of injury.
• Wounds must be left open and closed either as a secondary procedure after a few
days or left to heal spontaneously. Such patients all need supplementary broad-
spectrum antibiotics and some form of tetanus prophylaxis i.e. tetanus toxoid
booster to those with a previous immunization record or human antitetanus
globulin for those with no previous active immunity.
• Treatment of the fracture consists of: Reduction, immobilization and
rehabilitation.
REDUCTION
• This is restoration of the displaced fragments to their anatomical positions.

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• It aims at restoring the anatomy:
➢ Correct axial alignment
➢ Correct rotational deformity
➢ Restore length
➢ Joint alignment
• Methods include: (1) closed
manipulation (2) open reduction (3)
traction
➢ Closed manipulation: is not necessary
when there is no displacement,
displacement does not matter or
reduction is unlikely to succeed. It
may be done under general anesthesia
(manipulation under anesthesia-
MUA)
➢ Open reduction: often accompanied
by internal fixation (ORIF)
➢ Traction (discussed later)
IMMOBILIZATION Figure 163: Closed reduction
• After reduction (whether closed or open)
next is to hold (immobilize)
• Immobilization (or Stabilization) keeps the bony fragments in their position until
union occurs.
• Fixation can be open or closed
• Methods of immobilization include: (1)
Casting and Splintage (2) functional
bracing (3) Internal fixation (4) External
fixation
CASTING AND SPLINTAGE
• After reduction the fracture can be held in
place be a plaster of Paris cast until union
occur.
• The fracture must be held in a position that
maintains it in 3 dimensions (tilt, twist and Figure 164: Plaster of Paris used to treat a forearm
mid-shaft fracture of the radius and ulnar.

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SURGERY MK
shift) and the cast must be the proper length.
• In order to ensure complete control of all
dimensions of the fracture, it is necessary
to control the joint above and below the
fracture otherwise joint movement may
result in distortion in one or more
dimensions.
• Plaster of Paris is relatively brittle, messy
and very difficult to apply well. It is heavy
and awkward, particularly in the elderly
and takes up to 3 days to dry fully. For
these reasons, strong and light glass fiber
and polyurethane resin material have been
developed.
• These are not as versatile as plaster of
Paris and are better for secondary casts,
which are applied after a week or two Figure 165: Splintage
when the fracture swelling has settled.
• Splintage can also be done to hold them together until they unite until they unite,
meanwhile joint movement and function must be preserved.
FUNCTIONAL BRACING
• Casts have many disadvantages such as:
➢ They are heavy
➢ They immobilize the joint and prevent access to the fracture. The immobility
can result in muscle wasting and joint stiffness.
• Functional bracing overcomes the above disadvantages i.e. there is freeing of the
joints while maintaining alignment at the fracture site.
• Functional bracing is highly dependent on a very accurate fit and can be used
only after a few weeks when the pain and swelling have settled.
• In practice, functional bracing is used in the management of fractures of the tibia
and fibula.
INTERNAL FIXATION
• Internal fixation is technically very demanding and has many complications and
most important of all, prevents natural healing. If fixation is to be used it can be
achieved by a number of ways:

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➢ Apposition: once fractures are realigned,
they may only be held in apposition for
healing to proceed satisfactorily. This is
particularly true in children. Apposition is
done by using semi-flexible wires known
as ‘K’ (for Kirschner) wire. They hold
position within producing immobility and
so healing occurs by natural callus
formation. They can be left standing proud
of the bone and can easily be pulled out Figure 166: Internal fixation
once union is established and before
consolidation.
➢ Interfragmentary compression:
usually achieved by screws or
sometimes by tension band wires.
These achieve great accuracy and
are particularly valuable in cancellous Figure 167: Internal fixation
bone around joints. They are also
useful in long bones, particularly in the upper limb but in these situations extra
support is required from an onlay device.
➢ Onlay device: are metal plates that are used to buttress weak structure around
joints and to fix long bones in the upper limb. These very rigid systems inhibit
natural bone union and although they permit early movement, they ultimately
delay healing and full load-bearing.
➢ Intramedullary or inlay devices: are the most satisfactory method of fixation.
They achieve alignment without unduly disturbing natural bone healing. They
are a relatively inaccurate method of restoring anatomical position and so are
not useful around joints. Their great strength makes them ideal devices for
treating long-bone fractures particularly in the lower limb.
EXTERNAL FIXATION
• When fractures are open and associated with extensive soft-tissue damage and
contamination, neither plaster casting nor internal fixation is appropriate.
• Plaster splints are unsuitable because the wounds become inaccessible for
inspection and dressing while internal fixation is hazardous because of the very
high risk of wound infection.

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• A compromise solution is to apply an external fixation device which consists of
a strong metal rod (or series of rods) that runs parallel to the fractured bone and
is attached to the bone by a series of pins.
• Such a device stabilizes the fracture and gives access to the soft tissues for
dressings and secondary surgery such as skin grafting. A disadvantage of external
fixators is the risk of infection at the pin sites.

Figure 168: External fixation

Figure 169: External and internal fixation of right humeral fracture

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TRACTION
• Done using weights and can either be skin or skeletal. (Details discussed in next
chapter)

REHABILITATION
• Rehabilitation: should start as soon as possible after injury, it aims at maintaining
functions of the uninjured parts, and once fracture is united restoring functions of
the injured parts.
• Physiological loading of the bone, so muscle activity and early weight-bearing
are encouraged.
• Rehabilitation by exercise:
➢ Prevents edema
➢ Prevents joint stiffness
➢ Prevents muscle wasting and atrophy
➢ Prevent DVT
➢ Enhance fracture healing
➢ Prevent contractures

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COMPLICATIONS
• Early complications may be either due to direct consequence of injury or in
association with the treatment.
• Late complications are generally related to the fracture but a few are
unfortunately precipitated by treatment (or lack of it).
EARLY COMPLICATIONS
• Hemorrhage- may lead to shock. Internal or external e.g. # femur-2L, Tibia-1/2L,
Pelvis 3-5L
• Hematoma
• Nerve or vascular injury
• Soft tissue injury e.g. visceral organs, urethra etc.
• Tendon injury
INTERMEDIATE
• Infection
• Fat embolism
• Osteomyelitis
• Septic wound/ septicemia in compound #s
• Avascular necrosis
• Compartment syndrome caused by localized swelling
• Joint stiffness
• Volkmann ischemic contractures
• Thromboembolism
LATE
• Malunion (may lead to late neuropathies e.g. valgus deformity at elbow-an ulcer):
due to poor supervision of healing
• Non-union: usually associated with
➢ Excess movement
➢ Insufficient movement
➢ Poor local blood supply due to either anatomy (e.g. tibia) or a lot of trauma
damage
• Delayed union
• Growth arrest in children due to epiphyseal damage
• Osteoarthrosis- common and particular #s especially displaced
• Joint instability/deformity

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• Post-traumatic atrophy
• Osteochiorosis-harden brittle
• Osteoarthritis
• Shortening of bone
• Intra-articular and peri-articular adhesion
• Hypostatic pneumonia
• DVT
• Pressure sores

CAUSES OF NON-UNION
LOCAL
• Local infection (sepsis)
• Interposition of soft tissue
• Inadequate or poor local blood supply e.g. # neck of femur (ischemia)
• Inadequate immobilization
• Bone loss or crushing
• Over traction- loss of apposition in between
• Iatrogenic- wrong open reduction and internal fixation
• Local malignancy- bone destruction
• Severe communication
• Extensive opening
• Dissolution of # hematoma by synovial fluid bathing the joint
SYSTEMIC
• Anemia
• Poor general health
• Mineral and vitamin deficiency especially calcium and vitamin D
• Metabolic disease e.g. uncontrolled DM
• Hyperparathyroidism acidosis help destroy the bone
• Lack of androgen, estrogen hormones

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TRACTION

TRACTION
• Traction is applied to the limb distal to the fracture so as to exert a continuous
pull in the long axis of the bone, with a counterforce in the opposite direction (to
prevent the patient being merely dragged along the bed).
• Traction is safe enough, provided it is not excessive and care is taken when
inserting the traction pin.
• Traction includes:
➢ Skin traction
➢ Skeletal traction

SKIN TRACTION
• Skin traction will sustain a pull of no more than 4 or 5kg (has a limit).
• Holland strapping or one-way stretch Elastoplast is stuck to the shaved skin and
held on with a bandage.
• The malleoli are protected by Gamgee tissue and cords or tapes are used for
traction.
• It is used for individuals between ages of 3 and 18 years.
• Indications include:
➢ Fractures:
o Shaft of femur (main indication in children)
o Other indications in adults include:
- Intertrochanteric fractures
- Fracture of pelvis
- Unstable Hip dislocation
- Intervertebral disc prolapses
- Upper femoral epiphysis separation
➢ Extremes of age:
o Children between 3 to 18 years (longitudinal bone growth may be
arrested)
o Old people-fragile bones
➢ Those reacting to pin
➢ Fixed flexion deformity

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TYPES OF SKIN TRACTION
• These include:
➢ Gallows
➢ Natural
➢ Boot
➢ Lateral
➢ Dunlop (for supracondylar fractures)
ASSESSING A PATIENT ON SKIN TRACTION
• Make general comments:
➢ A patient lying supine in bed, not in any obvious pain and in skin traction.
• On assessing adequacy of skin traction one has to take into account:
➢ Patient
o Alignment: comment on whether the big toe/web space between the big
toe and other big toe are in line with patella & anterior superior iliac spine.
o Leg length: compare the length of both legs from medial malleolus to
anterior superior iliac spine (Discrepancy< 1.5)
o Compartment syndrome: rule out compartment syndrome which is
characterized by severe progressive pain that responds poorly to
analgesia.
o Assess peripheral pulses and passively flex patients toes and there should
not be any pain
➢ Traction system
o Traction kit: bandage must be below the knee generally and distal to
fracture. Bandage should not be too tight so check for signs of edema in
the feet.
o Protection/ cushioning of malleoli must be present
o Traction strings should pass through the pulley and should not shift
sideways
o The weight must not sit on anything and must be suspended in air.
o The contents of the weight must be 1/10 of the body weight for effective
traction.
o Sand bags should be placed under the femur to maintain the slight flexion
of the knee.
➢ Bed Elevation= 4cm x every kilogram of the weights placed.

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ADVANTAGES AND DISADVANTAGES OF SKIN TRACTION
• Advantages:
➢ Non invasive
➢ Easy to apply
➢ Cheap
• Disadvantages:
➢ Has a weight limit: 4-5 kg
➢ Ischemia if the bandage is too tight
➢ Allergic reactions to strapping
➢ Stiffness and contracture formation
LENGTH OF TRACTION

AGE UNION CONSOLIDATION

Child 3 weeks 6 weeks (3 x 2)
Adult 6 weeks 12 weeks (6 x 2)

CHILD
• At 3th week review patient:
➢ Clinically:
o Absence of pain
o Mobility- child playing around in bed
o Callous formation
➢ X-ray
• At 6th week review patient and check x-ray
ADULT
• At 4-6th week review patient:
➢ Clinically:
o Absence of pain
o Mobility
o Callous formation
➢ X-ray
• At 6th week review patient and check x-ray
• At 12th week review patient and check x-ray

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COMPLICATION OF SKIN TRACTION
EARLY
• Compartment syndrome: Severe progressive pain that responds poorly to
analgesics.
• Skin avulsion
• Allergic reaction
INTERMEDIATE
• Gangrene or ischemia
LATE
• Joint stiffness
• Hypostatic pneumonia
• DVT and embolism
• Mal-union, non-union and delayed union with traction that is not properly
applied.
GALLOWS TRACTION (BRYANT)
• This is a type of skin traction used in fractures of the shaft of femur in children
<3 years and weighing <15kg.
• Indications:
➢ Orthopedic: fracture of the femur (main indication)
➢ Non-orthopedic:
o Perineal or gluteal burn/ abscess
o Rectal prolapse
o Hernias- obturator and umbilical
o Non-thrombosed hemorrhoids
o Spinal bifida
• Complications:
➢ Skin avulsion
➢ Allergic reaction to strapping
➢ Compartment syndrome
➢ Joint stiffness
➢ Gangrene or ischemia of distal limb
➢ Hypostatic pneumonia
• Signs due to incorrect application e.g. Hand can’t sweep under buttocks.

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• Advantages:
➢ Easy to apply
➢ Non invasive
➢ Prevents decubitus ulcers
➢ Children don’t find it distressing
➢ Cheap
• Disadvantages:
➢ Weight limitation
➢ Ischemia if too tight
➢ Stiffness and contractures formation
DUNLOP TRACTION
• The main indication of Dunlop is a supracondylar
fracture of the humerus in children.
• Skin traction is placed on the forearm and a special
frame used on the side of the bed.
• Traction is placed along the axis of the forearm as
well as at right angles to the humerus by means of a
broad sling placed around the upper arm.
• Bed blocks are required on the lateral side (Fracture
side up) of the bed.

SKELETAL TRACTION (PERKINS Figure 170: Dunlop traction

TRACTION)
• This is a type of skeletal traction with a patient on a Perkins bed (from under bed
should have springs half way and hallow on the other half to aid in exercises) and
doing Perkins exercises.
• What can you see?
➢ A patient lying supine in bed with leg abducted/adducted
➢ He/she has a # femur
➢ He/she is on skeletal traction with weights
➢ Bed is raised with hard board
STATE OF LEG DURING PERKIN’S TRACTION
• Abducted= # of proximal 1/3 of femur (to avoid angulation after healing)
• Adducted/ straight= all other femur #s

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APPLICATION OF PERKINS TRACTION
• Insert pin 2cm distal and 2cm lateral to the tibial tuberosity.
• Apply 1/7 of body weight (Adults) and for each kilogram of weight raise foot end
of bed by 4cm.
➢ This prevents over-traction & hence non-unions.
• Measure both patient’s legs from the anterior superior iliac spine to the tip of
medial malleoli to make sure they are the same length.
• If necessary, adjust the traction weight and elevation of the foot end of the end
so as to let the bone fragments overlap by about 1 cm.
• Check leg length every day for the next 2 weeks and adjust the weight
appropriately. Then check length every 2 weeks.
• Note when assessing patient on skeletal traction, follow a similar plan to that
described under skin traction.
ADVANTAGES
• Perkins exercise helps to:
➢ Increases blood supply
➢ Promote healing
➢ Controlled movement and compression of the bone ends encourages union
➢ Prevents muscles atrophy- quadriceps
➢ Prevents knee joint stiffness/ contractures
➢ Prevents DVT, Decubitus ulcers and hypostatic pneumonia
➢ Encourages positive psychological effect on patient
DISADVANTAGES
• Injury to common peroneal nerve (foot drop)
• Fracture of tibia at the site of insertion of the pin
• Pin tract infection (Pain, swelling, tenderness, pus), pin traction infection is
prevented by:
➢ Daily wound cleaning with proper technique (follow the 3 “S”):
o S- spread the skin from the pin
o S- squeeze towards the pin
o S- swab around the pin making rotatory movements (use spirit swabs)
o Edges of pins are then covered with spirit swabs
➢ Types of pins used: Denham pin (has teeth in the middle), Steinmann
(Smooth).

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INDICATIONS
• Indications:
➢ Undisplaced incomplete fracture of neck of the femur
➢ All intertronchanteric fractures
➢ Subtrochanteric fractures in which the contraction of the iliopsoas has not
flexed the upper fragment so much as to bring it seriously out line.
➢ All # of the shaft of the femur in patients over 18, including overlapped,
double, spiral, comminuted and open #s and # with severe STI.
➢ Supracondylar # in which the lower fragment has not been too severely flexed
by the contraction of gastrocnemius.
➢ All condyle # of the femur, except those in which a condyle has rotated
completely
CONTRAINDICATONS
• All complete # of the neck of the femur
• Displacement of the proximal femoral epiphysis
• Subtrochanteric # with severe flexion of the proximal fragment
• Supracondylar # with marked flexion of the distal fragment
• Displacement of the distal femoral epiphysis
• # of the condyles in which a fragment has rotated completely.
• All patients under 18. Their epiphyses will not have united and pin may damage
the epiphyseal plate.
• Arthritis of the knee, or a stiff knee from any cause which will make exercise
impossible without moving the fragments too much
• Non-union in # treated by other methods
COMPLICATIONS
EARLY (DURING INSERTION)
• Damage to common peroneal nerve causing foot drop
• Fat embolism
• # of Tibia at the site of insertion of the pin
• Soft tissue injury
• Hemorrhage
• Hematoma
LATE (DURING TRACTION)
• Decubitus ulcer (bed sores)

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• Pin site infection- osteomyelitis
• Pin may become loose
• Osteoporosis- bone resorption because patient is bed bound
• Over traction- causing non-union
• Malunion
• Delayed union
• Joint stiffness (ankyloses)
• Muscle disuse atrophy
• DVT
• Hypostatic pneumonia
• Contractures
PREVENTION
• Some complications can be prevented by careful pin insertion and Perkins
exercise.
• Carful pin insertion:
➢ Trans-tibial pin should be inserted 2cm distal and 2 cm lateral to the tibial
tuberosity (this avoids injury to the common peroneal nerve)
➢ The pin should be inserted from lateral to medial so as to avoid injury to
common peroneal nerve
➢ Can also be pushed into calcaneum or distal femur
• Types of pins
➢ Denham pin: has some teeth in the middle
➢ Steinmann: pin smooth
• Do daily inspection of pin site for possible infection
MANAGEMENT
• Start periods of 10-30 min of active exercise several times a day from the 3rd day.
• Callus in the first 10 days is what determines the outcome
• Testing the femur for clinical union:
➢ No tenderness at the # site
➢ Bone cannot be angulate at the # site
➢ No tenderness on trying to angulate
➢ Callus can be felt
• X-ray should be done on the 4th, 6th and 12th week.
➢ If no callus on the X-ray by the 4th week suspect that there will be a delay in
the union

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➢ When there are definite signs of clinical union usually in the 6th to 10th week
remove the weights and continue exercise- range of movement improves
progressively
➢ Transverse and oblique #s take longer to heal than spiral #s.
• If during the first 2-3 days after a patient has fractured his femur he becomes
disoriented, drowsy or comatose or he has a cough, shortness of breath and
hemoptysis suspect fat embolism.
➢ This is a result of globules of fat escaping from the injured marrow of the
femur and entering the capillaries of the lungs or brain.
➢ Look for petechia over the chest, mouth or in the conjunctiva.
➢ Fat in urine is usually confirmatory.
➢ Management: Restrict fluids, give oxygen and give him diuretics.

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FRACTURES IN CHILDREN • Joint strains that might cause
ligament injuries in adults are liable
to result in separation of the physis
FRACTURES IN in children.
CHILDREN • Over 10% of fractures in children
affect the physis.
GREENSTICK • Fractures involving the epiphyseal
FRACTURES plate were named after Robert B
• This is an incomplete fracture. Salter and William H Harris who
• Fracture breaks like a greenstick. created and published the
• On X-ray buckle is seen. classification system for these types
of fractures.
• Recall the structure of a bone:

Figure 171: Greenstick fracture- needs only

correction of angulation

EPIPHYSEAL
FRACTURES
Figure 172: Anatomy of a long bone
• A Salter-Harris fracture/Epiphyseal
fracture is a fracture involving the CLASSIFICATION
epiphyseal plate or growth plate • There are 5 main types described by
(also called the physis) Salter and Harris (1963)
• This injury is common in children
TYPE I
especially in long bones, this is
because the physis is relatively a
weak part of the bone.

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• Involves a transverse fracture
through the hypertrophic or
calcified zone of the growth plate.
• Even if the fracture is quite
alarmingly displaced, the growing
zone of the physis is usually not
injured and growth disturbance is
uncommon.
• Incidence is about 5%.

Figure 174: Salter-Harris I fracture of distal

Figure 173: Salter-Harris Type I- "Straight radius “Straight through”
through"
TYPE II
• Entails a fracture through the
growth plate and metaphysis
sparring the epiphysis.
• This fracture is essentially similar
to type I but towards the edge the
fracture deviates away from the
growth plate and metaphysis.
• The fracture splits off a triangular
metaphyseal fragment of bone
(sometimes referred to as Thurston-
Holland fragment)
• It accounts for the commonest type
of epiphyseal fracture (incidence of
75%) and takes approximately 2-3
weeks or more in the spine to heal.

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one or the other side, through the
hypertrophic layers of the physis
(as these layers are closer to the
epiphysis than the metaphysis) and
may result in growth disturbance.
• Incidence= 10%.

Figure 175: Salter-Harris Type II with

Thurston Holland fragment - "Above"

Figure 177: Salter-Harris Type III- "Lower"

Figure 176: Salter-Harris Type II fracture

of ring finger proximal phalanx

TYPE III
• A fracture through growth plate and
epiphysis sparing the metaphysis.
• The fracture splits the epiphysis
and then veers off transversely to

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Figure 179: Salter-Harris Type IV-

"Through Everything"

Figure 178: Salter-Harris Type III fracture

of big toe proximal phalanx

TYPE IV
• Fracture through all 3 elements:
growth plate (physis), metaphysis
and epiphysis.
• These fractures are liable to
displacement and a consequent
misfit between the separated parts
of the physis, resulting in
asymmetrical growth. Figure 180: Salter-Harris IV fracture of big
• Incidence= 10%. toe proximal phalanx

TYPE V

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• A longitudinal compression injury ➢ Type III-L= Lower- fracture is
of the physis. below the physis in the
• There is no visible fracture but the epiphysis.
growth plate is crushed and this ➢ Type IV- TE= Through
may result in growth arrest. Everything- fracture through
• Incidence- 1% metaphysis, physis and
epiphysis.
➢ Type V-R= Rammed (crushed)-
the physis has been crushed.
• Alternatively, “SALTER” can be
used for the first 6 types as above
but adding Type V- “E” for
“Everything” or “Epiphysis” and
Type VI- “R” for “Ring”.
• Injuries to the physis usually run
Figure 181: Salter-Harris Type V- transversely through the
"Rammed" hypertrophic or calcified layers of
• Rang (Rang 1969) had added a type the growth plate, often veering off
VI an injury to the perichondrial into the metaphysis at one of the
ring (the peripheral zone of edges to include a triangular lip of
Ranvier) which carries a significant bone.
risk of growth disturbance. The • This has little effect on longitudinal
diagnosis is made usually in growth, which takes place in the
retrospect after development of germinal proliferating layers of the
deformity. physis.
• The mnemonic “SALTER” can be • If the fracture traverses the cellular
used to help remember the first 5 ‘reproductive’ layers of the physis
types: it may result in premature
➢ Type I- S= Slip/ Separated or ossification of the injured part &
straight across- fracture of serious disturbance of bone growth.
cartilage of physis MECHANISM OF INJURY
➢ Type II-A= Above- the fracture • Physeal fractures usually result
lies above the physis or Away from falls or traction injuries.
from the joint. • They occur mostly in road
accidents and during sporting
activities or playground tumbles.

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CLINICAL FEATURES TREATMENT
• These fractures are more common UNDISPALCED
in boys than girls and are usually
• Splinting the part in a cast or a
seen either in infancy or between
close-fitting plaster slab for 2-4
the ages of 10 and 12.
weeks (depending on the site of
• Deformity is usually minimal but
injury and the age of child).
any injury in a child followed by
• Type 3 and 4 fracture- check X ray
pain and tenderness near the joint
after 4 days and again at about 10
should arouse suspicion and X-ray
days is mandatory in order not to
examination is essential.
miss late displacement.
X-RAYS
DISPLACED
• Recall that the physis is made of
cartilage that is radiolucent and • Reduce as soon as possible.
epiphysis may be incompletely • Type 1 and 2- closed reduction, the
ossified thus making it hard to tell part is then splinted securely for 3-
whether the bone is damaged or 6 weeks.
deformed. • Type 3 and 4 demand perfect
• The younger the child the smaller anatomical reduction
the “visible” part of the epiphysis ➢ This is done by gentle
and thus the more difficult to make manipulation under general
diagnosis, comparison with the anesthesia and if successful the
normal side is a great help. limb is held in a cast for 4-8
• Telltale features: weeks (longer periods for type 4
➢ Widening of the ‘Physeal gap’ injuries).
➢ Incongruity of joint or tilting of ➢ If they cannot be reduced
the epiphyseal axis accurately by closed
• If there is marked displacement the manipulation, immediate open
diagnosis is obvious, but even a reduction and internal fixation
type 4 fracture may at first be so (ORIF) with smooth K-wires is
little displaced that the fracture line essential. The limb is then
is hard to see. splinted for 4-6 weeks but it
• If there is the faintest suspicion of a takes that long again before the
Physeal fracture a repeat X-ray child is ready to resume
after 4 or 5 days is essential. unrestricted activities.
• Type 5 and 6 injuries are usually
diagnosed only in retrospect.

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PROGNOSIS • Type 3 and 4: result in premature
• Fractures in children generally heal fusion of part of the growth plate or
relatively fast but may take several asymmetrical growth of the bone
weeks to heal. end.
• Most growth plate fractures heal • Type 5 and 6: premature fusion and
without any lasting effects. retardation of growth. Can also
• Rarely bridging bone may form result in bridging.
across the fracture, causing stunted
growth and/or curving. In such
cases the bridging bone may need
to be surgically removed. • Establish deformity whether from
• A growth plate fracture may also asymmetrical growth or from
stimulate growth causing a longer malunion of a displaced fracture
bone than the corresponding bone (e.g. a valgus elbow due to
on the other side. proximal displacement of a lateral
COMPLICATIONS condylar fracture) should be treated
• Type 1 and 2- if properly reduced by corrective osteotomy. If further
have an excellent prognosis and growth is abnormal the osteotomy
bone growth is not adversely may have to be reported.
affected.
➢ Exception: injuries around the
knee involving the distal
femoral or proximal tibial
physis, both growth plates are
undulating in shape, so a
transverse fracture plane may
actually pass through more than
just the hypertrophic zone but
also damages the proliferative
zone.
➢ Complications such as malunion
or non-union may occur if
diagnosis is missed and fracture
remains unreduced (e.g. fracture
separation of the medial
humeral epicondyle).

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SUPRACONDYLAR FRACTURE OF THE HUMERUS

• These are among the commonest fractures in children.
• The distal fragment may be displaced either posteriorly or anteriorly.
MECHANISM OF INJURY
• Posterior angulation or displacement (95% of all cases) suggests a
hyperextension injury, usually due to a fall on the outstretched hand.
➢ The humerus breaks just above the condyles. The distal fragment is pushed
backwards and (because the forearm is usually in pronation) twisted inwards.
➢ The jagged end of the proximal fragment pokes into the soft tissue anteriorly,
sometimes injuring the brachial artery or median nerve.
• Anterior displacement is rare; it is thought to be due to direct violence (e.g. a fall
on the point of the elbow with the joint in flexion.)
CLASSIFICATION (GATLAND CLASSIFICATION)
TYPE I
• An undisplaced fracture

Figure 182: Undisplaced supracondylar fracture (Gatland Type I)

• Treatment: collar and cuff or backslab.

TYPE II
• An angulated fracture with the posterior cortex still in continuity (periosteal
hinge).

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Figure 183: Angulated fracture with periosteal hinge (Gatland type II)

➢ Type IIA- a less severe injury with the distal fragment angulated.
➢ Type IIB- a severe injury, the fragment is both angulated and malrotated.
• Treatment: Manipulation under anesthesia (MUA) + collar cuff or backslab.
(convert to type I)
TYPE III
• Completely displaced fracture (Although the posterior periosteum is usually still
preserved, which will assist surgical reduction)
• Treatment:
➢ Manipulation under anesthesia (to convert to type 1)
➢ K-wire (Kirschna wires) fixation
➢ After 3 weeks take the patient to theatre to remove K-wire under general
anesthesia and to put a slab.

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FRACTURES IN ADULTS

FRACTURES IN • Prominence or tenderness over the

lower end of the ulna is the striking
ADULTS fracture.
UPPER LIMB • Swelling and often bruising is also
FRACTURES seen in the area.
• Patients also have wrist pain,
GALEAZZI FRACTURE-
instability or both
DISLOCATION OF THE RADIUS
• It may be possible to demonstrate
MECHANISM OF INJURY
the instability of the radio-ulnar
• This injury was first described in joint by ‘balloting’ the distal end of
1934 by Galeazzi. The usual cause the ulna (the ‘piano-key sign’ or by
is a fall on an outstretched hand, rotating the wrist).
probably with superimposed
• It is important to also test for an
rotation force.
ulnar nerve lesion, which may
• It may also be caused by direct occur.
trauma or blow to the radius.
• X-ray:
• The radius fractures in its lower ➢ A transverse or short oblique
third shaft and the distal radio-ulnar fracture seen in the lower third
joint subluxates or dislocates. of the shaft of radius, with
• Remember “Gale-radius” to help angulation or overlap
recall that the Galeazzi fracture is ➢ The distal radio-ulnar joint is
of the distal shaft of radius. subluxated or dislocated
• To also remember the site of
displacement note the joint usually
displaces where the one the
fractured bone is bigger.
CLINICAL FEATURES
• The Galeazzi fracture is much more
common than the Monteggia.
Always assess for distal radial-
ulnar joint disruption in all patients
with radial shaft fractures.

Figure 184: Galeazzi fracture

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TREATMENT o Open reduction is needed to
• Restore the length of the fractured remove the interposed soft
bone. tissue.
• In children closed reduction is often o Triangular fibrocartilage
successful, in adults open reduction complex (TFCC) and dorsal
and compression plating (ORIF) of capsule are then carefully
the radius is successful. repaired and the forearm
• An X-ray is taken to ensure that the immobilized in the position
distal radio-ulnar joint is reduced, of stability (Again usually
there are 3 possibilities: supination, supported by a
➢ The distal radio-ulnar joint is wire if needed) for 6 weeks.
reduced and stable: • Note: non-anatomic reduction of
o No further action needed the radial shaft fractures will
o Arm rested for few days compromise pronation and
then gentle active supination.
movements are encouraged. MONTEGGIA FRACTURE-
o Radio-ulnar joint checked DISLOCATION OF THE ULNA
clinically and radiologically • Previously this described a fracture
during the next 6 weeks. of the shaft of the ulna associated
➢ The distal radio-ulnar joint is with dislocation of the proximal
reduced and unstable: radio-ulnar joint (radial head). The
o Forearm should be
radiocapitellar joint is inevitably
immobilized in the position dislocated or subluxated as well.
of stability (usually
• Recently it also entails any fracture
supination) supplemented if
of ulna associated with dislocation
required by a transverse K-
of the radio-capitellar joint,
wire.
including trans-olecranon fractures
o Forearm is splinted in an
in which the promixal radio-ulnar
above-elbow cast for 6
joint remains intact.
weeks.
• If the ulnar shaft fracture is
o If there is a large ulnar
angulated with the apex anterior
styloid fragment it should be
(most common) then the radial
reduced and fixed.
head is displaced anterior.
➢ The distal radio-ulnar joint is
• If the fracture apex is posterior, the
irreducible:
radial dislocation is posterior.
o Unusual

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• If the fracture apex is lateral, then the upper third of the ulna with
the radial head will be laterally forward bowing.
displaced. ➢ Backward or lateral bowing of
• In children the ulnar injury may be the ulna (which is much less
an incomplete fracture (greenstick common) is likely to be
or plastic deformation of the shaft). associated with, respectively,
posterior or lateral displacement
MECHANISM OF INJURY
of the radial head. Trans-
• Usually the cause is a fall on the olecranon fractures, also are
hand, it at the moment of impact the often associated with radial head
body is twisting, its momentum dislocation.
may forcibly pronate the forearm.
• The radial head usually dislocates TREATMENT
forwards and the upper third of the • Restore length of fractured ulna,
ulna fractures and bows forwards. only then can the dislocated joint be
Sometime the causal force is fully reduced and remain stable.
hyperextension. • In adults: the ulnar fracture must be
• Remember ‘Monte-ulnar’ to recall accurately reduced, with the bone
that this is a fracture of the shaft of restored to full length and then
ulnar with proximal radio-ulnar fixed with plate and screws, bone
dislocation. grafts may be added for safety
• The radial head usually reduces
CLINICAL FEATURES
once the ulna has been fixed.
• The ulnar deformity is usually Stability must be tested through a
obvious but the dislocated head of full range of flexion and extension.
radius is masked by swelling. If the radial head does not reduce or
• A useful clue is pain and tenderness is not stable, open reduction should
on the lateral side of the elbow. be performed.
• The wrist and hand should be • If the elbow is completely stable,
examined for signs of injury to the then flexion-extension and rotation
radial nerve. can be started after very soon after
• X-ray: surgery. If there is doubt, then the
➢ Usual case: head of the radius arm should be immobilized in
(which normally points directly plaster with the elbow flexed for 6
to the capitulum) is dislocated weeks.
forward and there is a fracture of

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fragment collapses into extension,
dorsal displacement, radial tilt and
shortening.
CLINICAL FEATURES
• ‘Dinner-fork’ deformity with
prominence on the back of the wrist
and a depression in front.
• In patients with less deformity there
may only be local tenderness and
pain on wrist movements.
• X-rays:
➢ Transverse fracture of the radius
at the corticocancellous junction
(2.5cm above the wrist through
the epiphysis) and often the
Figure 185: Monteggia fracture-dislocation
ulnar styloid process is broken
COLLES FRACTURE off.
• This was an injury described by ➢ Displacement:
Abraham Colles (1814) o Dorsal shift
characterized by a transverse o Dorsal tilt (proximal tilt)
fracture of the radius just above the o Supination
wrist, with dorsal displacement of o Impaction
the distal fragment. o Lateral shift (Radial shift)
• It is the most common of all o Lateral tilt
fractures in older people, the high o Rotation
incidence being related to the onset • To remember the displacement in
of postmenopausal osteoporosis. colles’ fracture recall: College
• Thus, the patient is usually an older Rotating Doors Shut I’m late
women who gives a history of ➢ College- colles
falling on her outstretched hand. ➢ Rotating- Rotation
➢ Doors
MECHANISMS OF INJURY o Dorsal shift
• Force is applied in the length of the o Dorsal tilt (proximal tilt)
forearm with the wrist in extension. ➢ Shut
• The bone fractures at the cortico- o Supination
cancellous junction and the distal ➢ I’m

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o Impaction ➢ Correct proximal tilt by
➢ Late dorsiflexing the wrist.
o Lateral tilt ➢ Lock the arm towards the little
o Lateral shift (radial shift) finger using a slab (also appears
• Note: Colle’s fracture is described like a “dinner fork” but it is a
in Elderly in children fractures corrected one)
similar to this are known as Colle’s • Request X-ray of the wrist (AP and
like lateral view)-to check if fracture
has been reduced
• Review after 24 hours for
neurovascular state
• Review after 7 days and repeat X-
ray of the wrist to rule out
displacement
• Review after 7 days and repeat X-
ray.
• Review after 3 weeks
• Review after 8 weekS
• If the fracture is displaced in any of
the reviews the patient goes back to
theatre for reduction and the
procedure is repeated.
SMITH’S FRACTURE
• In this injury the distal fragment is
displaced anterior (which is why it
is sometimes called a ‘reversed
Colles’). It is caused by a fall on the
Figure 186: Colles fracture back of the hand.
TREATMENT CLINICAL FEATURES
• Closed manipulation under general • Presentation:
anesthesia: ➢ Wrist injury
➢ Correct the impaction first ➢ No dinner fork deformity
➢ Center it (correct the radial instead a ‘garden spade’
displacement) deformity
• X-ray:

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➢ Fracture through the distal radial ➢ Intertrochanteric #
metaphysis ➢ Subtrochanteric #
➢ Lateral view: distal fragment is ➢ # of the shaft- proximal, mid or
displaced and tilted anteriorly- distal
the opposite of a Colles’
fracture.
➢ The entire metaphysis can be
fractured, or there can be an
oblique fracture exiting at the
dorsal or volar rim of the radius.
• Treatment:
➢ Reduced by traction, supination
and extension of the wrist and
forearm is immobilized in a cast
for 6 weeks.
➢ X-rays should be taken at 7-10
Figure 187: Anatomical fractures of the
days to ensure the fracture has femur
not slipped.
➢ Unstable fractures should be GARDEN’S CLASSIFICATION OF
fixed with percutaneous wires or FEMORAL NECK FRACTURES
a plate. TYPE I
• Incomplete and minimally
LOWER LIMB displaced
FRACTURES
TYPE II
FRACTURE OF THE FEMUR
• Complete break without
• Fractures of the femur are classified
displacement
according to:
➢ Site of fracture TYPE III
➢ Displacement (Garden’s • Complete break and partially
classification) displaced
SITE OF FRACTURE TYPE IV
• Fractures can be classified as: • Complete break with the
➢ Neck of Femur # displacement
o Subcapital • Carries a risk of avascular necrosis
o Transcervical
o Basal

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Figure 188: Garden classification of femoral

neck fractures
Figure 189: Anatomy of the Ankle Mortise
ANKLE FRACTURES
• Any fracture involving the ankle • Note: the talus is not a component
was termed a Potts’ fracture. of the ankle mortise.
• Classification of ankle fractures are
varied and generally complex.
• To understand these types of
fractures it is important to recall the
ankle mortise which is composed
of:
➢ Medial malleolus
➢ Distal articular surface of tibia
➢ Tibio-fibula syndesmosis
➢ Lateral malleolus

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Figure 190: Anatomy of the mortise

• Ankle fractures often carry a history of a twisting injury, acute pain and inability
to bear partial or full weight.
• Presence of swelling and tenderness at one malleolus or over the entire ankle may
be seen as well as pain with motion.
• Fracture of the ankle are classified according to:
➢ Anatomical site
➢ Mechanism of action
➢ Eponym (Weber’s classification- in relation to the fibula)
ANATOMICAL
• These include:
➢ Unimalleolar (medial or lateral)
➢ Bimalleolar (medial and lateral)
➢ Trimalleolar (medial, lateral and posterior)

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MECHANISM OF INJURY (LAUGE-HENSEN CLASSIFICATION)
• Include:
➢ Supination with external rotation
➢ Supination with adduction
➢ Pronation with abduction
➢ Pronation with external rotation
WEBER’S CLASSIFICATION
• This is relation to the fibula and tibio-fibular syndesmosis
➢ Type A: below tibio-fibula syndesmosis
➢ Type B: At the level of the tibio-fibula syndesmosis
➢ Type C: Above the Tibio-fibula syndesmosis

Figure 191: Ankle fractures

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MANAGEMENT
• Stable fractures (lateral malleolar fractures with stable mortise and no medial
swelling or tenderness) can be treated with Cam walkers or short-leg walking
casts.
• Unstable fractures (lateral malleolar fractures with either mortise widening or
medial swelling or tenderness) are treated with plating of the fibula (for spiral or
oblique fractures) and two screws (for most medial malleolar fractures).
• Syndesmostic disruption requires fixation with screws
• Posterior malleolus fractures should be fixed if the fragments comprise >25% of
the plateau joint surface or if there is displacement after reduction.
• Dislocations should be reduced urgently even if surgery will be performed later
to ensure viable soft tissue over the ankle
• Note: The lateral malleolus should be fixed first, which will bring the ankle out
to length, reduction and fixation of the medial malleolus can then be
accomplished.

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JOINT DISLOCATIONS

JOINT
DISLOCATIONS
• This is an abnormal separation in
the joint.
• It is also known as luxation.
• A partial dislocation is referred to
as subluxation.
• Joint dislocations are caused by
sudden trauma on the joint like an Figure 193: Anterior shoulder dislocation
impact or fall.
• They cause damage to the
surrounding ligaments, tendons,
muscles and nerves.
• Dislocations can occur in any joint
major (shoulder, knees etc.) or
minor (toes, fingers, etc.)
• The most common joint dislocation
is a shoulder dislocation.
➢ Dislocated shoulder- 45% of all Figure 194: Posterior shoulder dislocation
dislocations

Figure 195: Shoulder dislocation

Figure 192: Shoulder dislocation
➢ Knee- patellar dislocation
➢ Elbow: posterior dislocation,
90% of all elbow dislocations

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➢ Wrist: Lunate and Perilunate • Plain radiographs usually a
dislocation most common minimum of 2 views
➢ Finger: interphalangeal (IP) or • A dislocated joint usually can be
metacarpophalangeal (MCP) successfully reduce (i.e.
joint dislocations manipulated) back into its normal
➢ Hip: posterior and anterior position.
dislocation of hip
➢ Foot and ankle
• The following symptoms are
common with any type of
dislocation:
➢ Pain
➢ Joint instability
➢ Deformity, Bruising
➢ Reduced muscle strength
➢ Difficult moving joint and
stiffness

Figure 196: Shoulder dislocation

AMPUTATIONS

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 ➢ Uncontrolled sepsis (diabetic
AMPUTATIONS foot) systemic infection.
• This is removal of a limb or other
• Dying
appendage of the body.
➢ Severe laceration
INDICATIONS ➢ Severe fractures
• Indicated when part of the limb is ➢ Partial amputation due to
Dead, Deadly/Dangerous, Dying trauma or burns
and Damn nuisance. • Damn nuisance (deformed/
• Dead (Vitality of limp is neuropathy)
destroyed): ➢ Polydactyly
➢ The limb may be dead when ➢ Severely impaired gait
arterial occlusion or stenosis TYPES OF
causes tissue infarction.
➢ Dry gangrene due to arterial AMPUTATIONS
occlusion or stenosis. 1. Rays amputation
➢ Arterial occlusion: o Amputation of toe with head
o Major vessels- of metatarsal or
atherosclerotic/ embolic metacarpals.
occlusions 2. Tarsometatarsal (Lisfranc’s)
o Small vessel- DM, Buegers 3. Transmetatarsal (Gillies)
disease, Raynaud’s disease, 4. Midtarsal (Chopart’s)
egotism 5. Syme’s
• Deadly/ Dangerous (life saving) 6. Below-knee (Burgees)
➢ Wet gangrene with putrefaction 7. Transcondylar (through knee)
infection. 8. Above-knee
➢ Gas gangrene due to C. 9. Hip-disarticulation
perfringes
➢ Necrotizing fasciitis
➢ Neoplasm: osteogenic sarcoma,
extensive melanoma, Marjolin’s
ulcer
➢ Arteriovenous fistula: life of the
patient is threatened by spread
of a local condition.
➢ Spreading cellulitis
SURGERY MK
LATE
• Phantom limb- typical awareness
of sensation that as if amputated
part is still present partly or in toto.
It is often painful, disturbing or
hyerasthetic.
➢ Exact cause is not known but
probably due to presence of
severe pain at the amputated
part just prior to amputation
making brain area for that part in
alert situation causing phantom
limb. (Cortical plasticity).
➢ Reassurance, prosthesis,
analgesics help to control the
COMPLICATIONS condition.
EARLY ➢ Telescoping of phantom limb:
• Hemorrhage and hypovolemic feeling of the amputated limb
shock getting “shorter”
• Hematoma: • Ulceration of stump:
➢ Identified by pain, swelling over • Flap necrosis: due to poor blood
the stump underneath the flap. • Stump neuroma:
➢ May delay healing, precipitate ➢ Occurs due to proliferation of
infection or flap necrosis due to the nerve fibrils beyond the
pressure point of nerve division and is
➢ It is aspirated using a wide bore usually due to failure of cutting
needle and after aspiration, of the nerve more proximal to
pressure dressing is needed. If the level of division of the bone.
hematoma reforms after 2-3 ➢ It causes pain and tenderness
aspirations it should be drained over the stump. It is usually
by opening the wound on one relieved by analgesics,
corner and inserting hemostat reassurance and prosthesis.
into the wound. Occasionally it may require
• Infection reexploration of the wound,
excision of end neuroma and
also cutting nerve more
proximally.

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• Painful scar • Sequestrum formation
• Stump pain: due to infection, poor • Contracture of joint proximal to the
blood supply, causalgia, stump amputated stump
neuroma, phamtom limb, DVT, • Deformities
adherent scar, formation of spurs • Keloids and hypertrophic scars
and osteophytes at amputated bone
end.

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OSTEOARTHRITIS

OSTEOARTHRITIS
• This is a degenerative bone and joint condition initially involving thinning of the
hyaline cartilage until the underlying bone is exposed and becomes damaged due
to direct stress.
• It can be:
➢ Primary (idiopathic) which is localized or generalized (rare) or
➢ Secondary which is usually localized.
• Nodal osteoarthritis is a primary osteoarthritis involving the hands.

RISK FACTORS
• Age>50 years
• Nodal OA:
➢ Post-menopausal women
➢ Family history
• Secondary:
➢ Mechanical strain from obesity, trauma (fracture into a joint, cartilage tear)
or employment
➢ Joint disease: inflammatory arthritides
➢ Congenital conditions: congenital dislocation of the hip
➢ Metabolic: gout, crystal arthropathy, Hemochromatosis
➢ Infection: tuberculosis
➢ Chronic inflammation: rheumatoid arthritis
➢ Osteoporosis reduces the risk

CLINICAL FEATURES
Primary nodal OA Secondary OA
• Tender, swollen joints with reduce • Typically affects the knee, hip or
movement spine
• Typically affects the distal • Painful joint exacerbated by
interphalangeal joints (DIP), thumb movement and worse in the evening
carpometacarpal (CMC) joint, and knees • Joint gelling- stiffness after resting
• Muscle wasting and instability
• Squaring of hand due to thumb • Hip OA typically radiates to the groin
adduction and bone swelling at CMC and buttocks.

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• Heberden’s nodes at the DIP and • Spin OA may compress a nerve and
Bouchard’s nodes at the PIP radiate down the leg
INVESTIGATIONS
• Diagnosis can be clinical- especially if patient >45 years old- and does not require
radiological evidence.
• X-ray (anteroposterior and lateral views) can be useful to exclude other
conditions and are needed in younger patients or atypical histories. In
osteoarthritis, may see ‘LOSS’:
➢ L-loss of joint space (asymmetrical), reflecting thinning of the cartilage
➢ O-osteophytes, reflecting proliferation and ossification of cartilage in
unstressed areas
➢ S-subchondral sclerosis (thickening)
➢ S-Subchondral cysts, reflecting fluid-filled microfractures
• Bloods:
➢ CRP/ESR to rule out inflammatory cause.

MANAGEMENT
• Lifestyle and physical therapy:
➢ Exercise to improve strength and joint stability
➢ Reduce weight
➢ Walking aids
➢ Physio
• Pharmacological:
➢ Regular paracetamol +/- topical NSAID gel (knee or hands only), then move
up pain ladder if needed. Paracetamol is traditionally preferred for long-term
use over NSAIDs as it is safer but recent research question its efficacy.
➢ If adding/switching to NSAIDs PO (standard or coxib) stop topical NSAID
and give PPI. Unlike paracetamol, there is good evidence of efficacy.
➢ Further option: intra-articular steroid injections, topical capsaicin for hand or
knee OA.
➢ Glucosamine and chondroitin are not recommended
• Surgical: joint replacement

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RHEUMATOID ARTHRITIS

SEPTIC ARTHRITIS

OSTEOMYELITIS
• This is infection of the bone
• It may be:
➢ Acute osteomyelitis: <2 weeks time duration
➢ Chronic osteomyelitis: >2 weeks (typically presents 6 weeks or more after
infection)

ACUTE OSTEOMYELITIS
RISK FACTORS
• Portal to pathogen entry:
➢ Trauma: open fracture or orthopedic surgery
➢ Surgical prosthesis
➢ Intravenous drug use
• Disease
➢ TB
➢ Diabetes
➢ PVD
➢ Immunosuppression
➢ Alcoholism
➢ Sickle cell disease

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PATHOPHYSIOLOGY
• Route of infection is mainly hematogenous (common in children, patients with
urinary catheters or TB), rarely by direct/contiguous spread (e.g. trauma,
cellulitis, abscess, surgery or prosthesis).
• Most cases of acute hematogenous osteomyelitis are caused by Staphylococcus
aureus. Other less common pathogens include:
➢ Streptococcus pyogenes and Hemophilus influenzae (in children)
➢ Gram negative bacilli (in adults)
➢ Pseudomonas aeruginosa (in IV drug users)
➢ Salmonella (in sickle cell patients)
• Bacteria lodge in end artery of metaphysis and multiply.
➢ Most common site for acute osteomyelitis is the metaphyseal end of a single
long bone (especially around the knee)
• There is local increase in serum and white blood cells leading to decrease in blood
flow and pressure necrosis. WBCs also release enzymes that cause bone lysis and
leave necrotic areas (sequestra) with new bone forming around this (involucrum)
• Pus moves to haversian and medullary canals and eventually beneath the
periosteum.
• Chronic osteomyelitis ensues after 6 months of infection.
CLINICAL FEATURES
• History of infection (e.g. skin or throat) or trauma
• Local inflammation, Significant pain in the affected area,
• Systemic symptoms: anorexia, fever, irritability, nausea, malaise and rapid pulse
• Limited joint motion, slight effusion in neighboring joints, tenderness, swelling
of soft tissue and guarding apparent on physical exam.
• Diabetic patients may be asymptomatic due to neuropathy.
• Vertebral osteomyelitis:
➢ Localized spine inflammation. ‘Cold’ in TB
➢ Chronic back pain which is worse at night and at rest
➢ Associated discitis
DIAGNOSIS
• Full blood count: Increased WBC, +/- anemia
• ESR and C-reactive protein are increased
• Blood culture is the gold standard. Also, culture blood, pus, and local joint
effusion.

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• Perform urine urinalysis, microscopy culture and sensitivity to look for cause.
• X-ray may show dark area in bone, soft-tissue swelling however signs may be
minimal in acute infection. MRI provides clearer picture if diagnosis is uncertain.
• Deep circumferential soft-tissue swelling with obliteration of muscular planes
DIFFERENTIAL DIAGNOSIS
• Septic arthritis: Swelling and tenderness directly on the joint with intense pain on
joint movement, high WBC and positive culture.
• Rheumatic fever: more insidious onset, less local and constitutional symptoms
• Ewing’s sarcoma: Early symptoms are more insidious and less intense and
present with bone destruction
MANAGEMENT
• Medical:
➢ Infection must be diagnosed early
➢ Intravenous antibiotics (usually oxacillin or cloxacillin 8-16g adult) started
soon after obtaining specimen for culture. Antibiotics are given for 6 weeks
initially as IV then oral.
➢ Monitor temperature, swelling, pain, WBC and joint mobility
• Surgical:
➢ Open drainage of abscess if antibiotics fail or signs of abscess appear.
➢ After surgical drainage, wound is left open to heal by secondary intention

CHORNIC OSTEOMYELITIS
• This is often seen in lower extremities of a diabetic patient.
PATHOPHYSIOLOGY
• Usually an end result of untreated or treatment failed acute osteomyelitis.
Occasionally it can occur due to trauma or surgery.
• The cause is usually polymicrobial (hence difficult to eradicate).
• Untreated acute osteomyelitis results in a cavity walled off by an involucrum
(new bone) containing granulation tissue, sequestrum (dead bone) and bacterium.
• Drainage of pus into surrounding soft tissue and skin occurs via sinus tracts.
Persistent drainage can lead to carcinoma.
• Bone fragments and exudates are usually unreachable by antibiotics.
• It results in severely deformed bones and pathological fractures.

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CLINICAL FEATURES
• Persistent drainage following an episode of acute osteomyelitis or onset of
inflammation and cellulitis following an open fracture.
• Fever, pain, mild systemic symptoms, tenderness
• Easy to diagnose when drainage is present and X-ray shows bone destruction and
deformity. In cases with abscess of drainage, radionuclide imaging studies are
very helpful.
• Radiological findings:
➢ Areas of radiolucency within an irregular sclerotic bone
➢ Irregular areas of destruction present. Often, periosteal thickening can be
seen.
DIFFERENTIAL DIAGNOSIS
• Acute suppurative arthritis
• Rheumatic fever: examine synovial fluid
• Cellulitis: absence of soft tissue swelling on radiographs
MANAGEMENT
• Varies from open drainage of abscess or sequestrectomy to amputation
• Most effective: extensive debridement of all necrotic and granulation tissue along
with reconstruction of bone and soft tissue defects with concomitant antibiotics
(usually given for 12 weeks).
• Excellent adjunct: temporary placement of polymethylmethacrylate beads in the
wound for a depot administration of antibiotics.
COMPLICATIONS
• Soft tissue abscess
• Septic arthritis due to extension to adjacent joint
• Metastatic infections to other areas
• Pathologic fractures
• If significant spinal involvement, paraplegia

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BONE TUMORS
• Occur due to uncontrolled cellular proliferation of a single clone of cells whose
regulatory mechanisms are defective.
• Benign tumors are 200 times more likely than malignant ones.
• History and physical examination are crucial in diagnosis as they will reveal the
duration of the mass, onset of pain, other associated symptoms and the
chronological sequence of these symptoms.
• The mass should be noted for size, location, consistency, mobility, tenderness,
local temperature, and change with position. Also note any muscular atrophy.
• Radiography is important, it is important to note that bone tumor should not be
diagnosed without an X-ray.
• Bone reacts to a benign or malignant tumor by bone production or destruction.
An X-ray appearance shows a combination of bone production and bone
destruction.
• 3 patterns of X-ray appearance:
➢ Permeative: rapidly spreading intramedullary tumor, tumor replaces marrow
and fat.
➢ Moth eaten: a poorly circumscribed, slow-growing malignant tumor
➢ Geographic: well circumscribed slow-growing tumor, therefore bone has
time to react and results in sclerotic margins
• Bone tumors may be:
➢ Primary
o Benign: Osteoid osteoma, osteoblastoma, osteochondroma,
enchondroma, and Giant cell tumor
o Malignant: Osteosarcoma, chondrosarcoma, Ewing’s tumor and multiple
myeloma
➢ Secondary: more common, always malignant.

BENIGN BONE TUMORS

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MALIGNANT BONE TUMORS
• These include:
➢ Osteosarcoma
➢ Chondrosarcoma
➢ Ewing’s tumor
➢ Multiple myeloma
OSTEOSARCOMA
• This is a tumor made of a malignant spindle cells in the stroma producing osteoid.
• It is overall the commonest primary bone tumor.
• Peak incidence is between the age of 10-30 years and is more common in males
than females.
• There are many subtypes of osteoid forming sarcomas.
• Most common sites:
➢ Around the knee (distal femur, proximal tibia)
➢ Proximal humerus
➢ Mandible (rare)
• Note: Osteosarcoma can occur secondary to Paget’s disease, this is seen in elderly
patients alongside patient with prior exposure to radiotherapy.
CLINICAL FEATURES
• Pain associated with a tender mass
• Dilated veins may be visible on the skin over the mass
• Pathological fractures
• Constitutional symptoms e.g. fever, weight loss
• Features of metastasis to the lungs
INVESTIGATIONS
• Imaging:
➢ Bone X-ray
o Often seen first on X-ray but diagnosis usually involves CT or MRI
o X-ray shows a poorly defined lesion in the metaphysis with areas of bone
destruction and formation.
o Codman’s triangle: due to new bone formation under the corners of the
raised periosteum
o Sun-ray appearance: occurs when bone spicules are formed
perpendicular to the surface of the bone

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➢ Technitium bone scan
➢ CT or MRI
➢ CXR, CT chest, whole body MRI or FDG-PET scan for staging of cancer
• Blood investigations:
➢ Full blood count: shows cytopenia with bone marrow involvement
➢ ALP: increased in osteosarcoma (this is a good indicator for prognosis)
➢ LDH: increased
• Biopsy for histology: Spindle-shaped tumor cells with odd, hyperchromatic
nuclei showing a high mitotic rate. Giant cells may be present.
TREATMENT
• High dose methotrexate, doxorubicin, cisplastin and ifosfamide along with
surgical intervention (usually amputation)
• Tumors hematogenously metastasize to the lung.
• Surgery plus chemotherapy gives a 5-year survival of about 60%. Prognosis is
better if tumor is in a small bone.

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CHAPTER 15: ENDOCRINE

ENDOCRINE
THYROID GLAND

THYROID
DEVELOPMENT
• The thyroid gland is the first
endocrine gland to develop at the
24th day of gestation.
• It develops from a median down
growth of a column of cells from
the pharyngeal floor between the
Figure 197: The thyroid gland
first and second pharyngeal
pouches (subsequently marked by
the foramen caecum of the tongue).
• The canalized column becomes the
thyroglossal duct which is displaces
forward by the developing hyoid
bone and then below the hyoid
(C3), lies slightly to one side, more
commonly to the left.
• The duct bifurcates to form the
thyroid lobes and a portion of the
duct forms the pyramidal lobe.

Figure 198: Development of the thyroid gland

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ANATOMY o Superior thyroid artery: 1st
• The gland weighs about 15-20g and branch of external carotid
is located in the anterior triangle of artery, enters at the superior
the neck (muscular triangle). pole of the gland and
• It originates in early embryonic life bifurcates into a larger
from the foregut endoderm. anterior superficial branch
and a smaller posterior
• The parafollicular cell or C-cells
branch.
are derived from the neural crest
o Inferior thyroid artery: a
(ectoderm).
branch of thyrocervical
• It consists of a right and left lobe
trunk of subclavian artery. It
that are connected by an isthmus
passes behind the carotid
which extends from the 2nd to the 4th
sheath running medially
tracheal rings.
reaching the posterolateral
• Each lobe is 5 x 3 x 1.5 cm in size
aspect of the gland.
and extends from the middle of the
o Thyroidea ima artery: a
thyroid cartilage to the 6th tracheal
branch of aorta or
ring.
brachiocephalic artery
• The thyroid also has a pyramidal enters the isthmus or lower
lobe which is an upward extension pole of one of the lateral
as fibrous strands or muscular lobes (10%).
strands from the junction of the o Tracheal and esophageal
isthmus and left lateral lobe. branches serve blood supply
• The gland is covered by pretracheal to retained thyroid gland
fascia which is attached to the after thyroidectomy.
larynx thus causing the thyroid to ➢ Venous
move on swallowing. This o Superior thyroid vein:
important clinical finding helps to drains in the internal
discriminate thyroid swellings from jugular.
other swellings in the neck. o Middle thyroid vein: short
• Berry’s ligament is a strong and drains into the internal
condensed vascular connective jugular. It is first to be
tissue between the lateral lobe and ligated in thyroidectomy.
cricoid cartilage on each side. o Inferior thyroid veins are
• Blood supply: many in number. Drain into
➢ Arterial brachiocephalic vein.

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SURGERY MK
o Kocher’s vein may be meaningless jargon
present which drains lower purpose of it was
or middle thyroid. unclear.
o Mediastinal nodes.
➢ Secondary:
o Deep cervical nodes
o Supraclavicular nodes
o Occipital nodes

Figure 199: Venous drainage of the thyroid

Figure 200: Lymphatic drainage of the thyroid
• Lymphatic drainage
➢ Primary: • Important Relations
o Tracheao-esophageal ➢ Recurrent laryngeal nerve lies in
nodes. the tracheooesophageal groove
o Pre-laryngeal nodes in relation to Berry’s ligament.
(Delphian nodes). Formerly It supplies the intrinsic muscles
purpose of these lymph of the larynx and vocal cords
nodes were uncertain hence ➢ Superior laryngeal nerve which
the name. gives a branch, external
- Delphi is a place in laryngeal nerve supplies
Greece where Pythia, cricothyroid muscle (A
snake women after tensor/adductor of vocal cords).
sulphurous fume It accompanies superior thyroid
inhalation uttered artery.

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SURGERY MK
➢ Parathyroid glands- four in ASSESSMENT OF A
number, 2 on each side
embedded in thyroid.
PATIENT WITH A
THYROID SWELLING
PHYSIOLOGY HISTORY OF A PATIENT WITH
• Thyroid gland contains 2 secretory A THYROID SWELLING
cells: • When was the swelling first
➢ Follicular cells: secrete noticed?
thyroxine (T4) and tri- • Has it changed over time? Is it
iodothyronine (T3) growing or the same size?
➢ Parafollicular cells (“C” cells)- • Does it cause pain?
secrete calcitonin • Any of the associated symptoms:
• 90% of body iodide uptake is in the ➢ Dyspnea
thyroid gland, whose uptake into ➢ Dysphagia
the follicular cells is regulated by ➢ Dysphonia and hoarseness of
TSH and follicular iodide content. the voice
• Iodothyronins (MIT, DIT) are • Signs and Symptoms of
formed in follicular cells by hyper/hypothyroidism
coupling of inorganic iodide with
• Medical and surgical history
tyrosine under the control of the
enzyme thyroid peroxidase. EXAMINTION OF THE
• These are biologically inert THYROID GLAND
molecules. T4 is formed by • Greet the patient, explain the
coupling 2 DIT molecules and T3 examination to the patient and gain
by coupling 1 MIT and 1 DIT consent.
molecule. Both are bound to • Position the patient to sit with both
thyroglobin which is the primary hands down on their side.
component of colloid matrix. • The examiner should be standing in
• The hypothalamus-pituitary- front and looking at the whole
thyroid axis regulates thyroid patient.
hormone production and releases in • Do not forget to perform a General
a classic feedback system. examination.
• TRH is a regulatory hormone from
hypothalamus and TSH is a
regulatory hormone from the
anterior pituitary.

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INSPECTION ➢ Palpate the supraclavicular
• Comment on the general condition lymph nodes.
of the patient: distress, restless, AUSCULTATION
sluggish.
• Auscultate for bruits over the gland
• Comment on appearance of hair
• Auscultate for heart rate and sound
and their dressing: scanty, warm
• Auscultate for breath sounds
clothes
• Comment on the eyes-
opthalmoplagia, proptosis (do this
• Thank your patient for cooperation.
behind the patient), chemosis
(edema of the conjunctiva), lid lag/
• Summarize your findings and offer
retraction.
a diagnosis.
• Ask the patient to swallow some
➢ Differentials:
water- check for movement.
o Thyroglossal cyst
• Ask the patient to protrude their o Thymoma
tongue- check for movement. o Lymph node enlargement
• Ask the patient to extend their arms o Lymphoma
and place a paper on their hands to o Lipoma
check for tremors. o Thyroid cyst
• Comment on obvious swelling on o Anterior cervical abscess
the neck- size, site, shape. o Pharyngeal pouch
PALPATION INVESTIGATIONS
• Feel the hands for sweatiness 1. Blood investigations
• Feel the pulse- irregularly irregular, ➢ Serum T3 (Serum tri-
bradycardia iodothyronine), T4 (thyroxine)
• Check blood pressure and palpate and TSH (thyroid stimulating
for axillary and cervical hormone)
lymphadenopathy ➢ Free T3 and T4.
• Go behind the patient 2. Imaging
➢ Palpate the thyroid gland with ➢ Neck X-ray: AP view- tracheal
the fingers using the thumb to deviation, Gland calcification-
slightly flex the neck anteriorly bleed easily
➢ Push on one side and use the ➢ Ultrasound of the thyroid: cyst
other hand to feel. or solid mass.
➢ Comment on the consistency, ➢ Chest X-ray: tracheal deviation,
mobility, extent lung mets, retrosternal shadow

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➢ ECG- arrhythmias and ECHO • The connection to the tongue
➢ Radioisotope I123 scan: shows means that the cyst will move on
either cold, hot or warm nodule. protrusion of the tongue.
➢ CT scan
➢ MRI
3. Fine needle aspiration cytology:
shows benign or malignant cells
4. Indirect laryngoscopy: check for
vocal cords (recurrent laryngeal)
5. Baseline:
➢ Urea and electrolytes
➢ Creatinine
➢ Liver function tests
➢ Full blood count

THYROGLOSSAL CYST Figure 202: Patient with a thyroglossal cyst

• The tract left behind (the • The cyst may become infected
thyroglossal tract) usually closes, occasionally leading to a cutaneous
although a portion of the epithelial fistula (thyroglossal fistula).
lining may persist and form a cyst • The causes of midline swellings in
(thyrogossal cyst) usually in the the neck:
late adolescent. ➢ Thyroid (most common): moves
on swallowing
➢ Thyroglossal cyst: moves on
swallowing and protrusion of
the tongue
➢ Dermoid cyst (embryological
skin cyst) does not move on
swallowing or protrusion of the
tone.
• The causes of midline swellings of
the neck can therefore be
differentiated by first asking the
Figure 201: Thyroglossal tract patient to swallow and then to stick
out the tongue.

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GOITER TOXIC (HYPERTHYROID)
• A goiter is an enlargement of the • Diffuse toxic hyperplasia
thyroid gland. (primary): Grave’s disease
• The normal thyroid gland is • Toxic Multinodular goiter
impalpable. (Secondary)- Plummer’s disease
• Goiters are described by: • Toxic adenoma (solitary toxic
➢ Toxicity: nodule)
o Hyperthyroid (Toxic) • Recurrent toxicosis
o Euthyroid INFLAMMATORY
o Hypothyroid (non-toxic) • Autoimmune: Chronic
➢ Nodularity lymphocytic thyroiditis
o Solitary nodule (Hashimoto’s disease)
o Multinodular • Subacute Granulomatous (De
➢ Neoplastic Quervain’s) thyroiditis
o Benign
• Fibrosing: Riedel’s thyroiditis
o Malignant
• Infective: Acute (bacterial
• Diagnosis must have all 3 entities. thyroiditis, viral thyroiditis, ‘sub-
CLASSIFICATION OF THYROID acute thyroiditis’) and chronic
SWELLINGS (Tuberculous, syphilitic)
• To remember the classification of • Other: Amyloid
thyroid conditions, remember
NEOPLASTIC
“S.T.I.N”
• Benign- adenomas (follicular,
• Goiters are classified under:
Hurthle cell)
➢ Simple (nontoxic)
• Malignant
➢ Toxic
➢ Primary
➢ Inflammatory (thyroiditis)
o Papillary carcinoma
➢ Neoplastic
o Follicular carcinoma
SIMPLE NONTOXIC GOITRE o Medullary carcinoma
(EUTHYROID) o Anaplastic carcinoma
• Simple Diffuse hyperplastic: o Lymphoma
physiological, pubertal, pregnancy ➢ Secondary: metastatic deposits
• Colloid goiter
• Non-toxic Multinodular goiter
• Solitary non-toxic nodule
• Recurrent non-toxic nodule

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SOLITARY THYROID NODULE times through the nodule
• This is a common conditions while suction is maintained
affecting 5% of the female on the syringe.
population but only 5% of solitary o The aspirated cells are then
thyroid nodules are malignant. smeared on the slide and
• Investigations are therefore needed wet and/or dry fixed.
to discriminate between a benign o Results of cytology show
and malignant thyroid nodule, as benign cells, suspicious cell,
usually surgery is not required for malignant cells or the
benign solitary thyroid nodules. specimen is inadequate and
• Causes: consists of red cells only
➢ Thyroid cysts (seen in about 10-20% of
➢ Degenerative thyroid nodule thyroid FNAs).
➢ Benign follicular adenoma o If FNA reports suspicious
(including solitary toxic cells, then the nodule should
adenoma) be removed as 30% are
➢ Differentiated thyroid malignant.
carcinoma ➢ Thyroid ultrasound:
• History: distinguishes solid nodules and
➢ Features suggestive of cysts and whether it is a
malignancy: dominant nodule within a
o Previous history of neck multinodular goiter
irradiation e.g. as a child ➢ Technetium 99m scan gives an
o Hoarseness (potentially idea of the function of the
caused by infiltration of the nodule.
recurrent laryngeal nerve) o If the nodule is hot (and if
o Family history of papillary TSH is suppressed the
thyroid carcinoma) nodule is a solitary toxic
➢ Hyperthyroid symptoms adenoma)
➢ Pressure symptoms o If the nodule is cold
• Investigations: 2 most important (Decreased uptake) there is
investigations are TSH and FNA a slight increased risk of
➢ Blood TSH, T3 and T4 malignancy (10%).
➢ Fine needle aspiration (FNA)
o A 21 G needle attached to a
syringe is flushed with
saline, is passed several

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Figure 203: Treatment algorithm for FNA results

• Treatment: follicular adenoma and

➢ A benign thyroid nodule does carcinoma cannot be assed.
not require treatment unless ➢ Patients with malignant nodules
symptomatic or cosmetically should undergo surgery.
unacceptable
➢ Suppression of TSH by INFLAMMATORY
thyroxine therapy is generally THYROID CONDITIONS
unhelpful in trying to reduce the • Include:
size of a benign nodule. ➢ Hashimoto’s thyroiditis
➢ FNA should be repeated after 1 ➢ Sub-acute De Quervain’s
year and if this remains benign Granulomatous thyroiditis
then no further treatment is ➢ Riedel fibrosing thyroiditis
required.
HASHIMOTO’S THYROIDITIS
➢ Patients with suspicious nodules
• This is a chronic autoimmune
on FNA should undergo thyroid
disease characterized by immune
lobectomy as 30% of these are
destruction of the thyroid and
malignant
hypothyroidism.
➢ Frozen section is of little value
at surgery as the degree of • It most commonly causes painless
capsular invasion required to goiter (firm, rubbery, tender and
differentiate between benign smooth) in premenopausal females
more than in males and has a peak
age of 40 to 65 years.

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➢ Usually bilateral but • Antithyroglobulin, antimicrosomal,
occasionally one lobe is and anticolloid antibodies are
involved. present (however these do not
• It is associated with HLA-DR5. mediate the disease)
• It is associated with other • Investigations
autoimmune disease (SLE, ➢ FNAC
rheumatoid arthritis, Sjogren ➢ Serum T3, T4, TSH
syndrome) ➢ Thyroid antibodies assay
• Clinically it presents with: ➢ ESR is very high (over
➢ Initial inflammation that may 90mm/hour)
cause transient hyperthyroidism • Treatment:
(hashitoxicosis) ➢ L-thyroxine therapy.
➢ Hyperplasia causes ➢ Steroid therapy often is helpful.
hyperthyroid (Hashitoxicosis), ➢ If goiter is large and causing
as destruction progresses the discomfort, then subtotal
patient is Euthyroid at a point thyroidectomy is done.
but eventually Fibrosis leads to
SUBACUTE DE QUERVAIN
hypothyroid.
GRANULOMATOUS
➢ Signs of hypothyroidism due to
THYROIDITIS
autoimmune destruction of
• This is the second most common
thyroid tissue. (decreased T4
form of thyroiditis.
and increased TSH)
• It affects females more than males
➢ Hepatosplenomegaly
and has peak age 30 to 50 years.
• Pathology:
• Granulomatous thyroiditis follows
➢ Gross: the gland appears pale
a viral infection (mumps or
and enlarge.
coxsackie virus).
➢ Microscopic:
o Chronic inflammation: • It presents as a tender, firm,
Lymphocytic inflammation enlarged thyroid gland which may
with germinal centers be associated with transient
(increased risk of Non- hyperthyroidism.
hodgkin B-cell lymphoma) • Microscopically there is
and epithelial “Hurthle cell” granulomatous inflammation.
changes. • The disease typically follows a self-
o Hurthle cell changes: some limited course (does not progress to
cells around follicles hypothyroidism).
become more pink. • FNAC is useful

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SURGERY MK
• Prednisolone 20mg for 7 days ➢ FNAC to rule out carcinoma
helps. (anaplastic)
• Treatment:
RIEDEL FIBROSING
➢ Isthmectomy is done to relived
THYROIDITIS
compression on the airway.
• This is a rare disease of unknown
➢ They require L-thyroxine
etiology.
replacement later as
• It is characterized by destruction of
hypothyroidism is common
the thyroid gland by dense fibrosis
➢ High dose of steroid is often
and fibrosis of surrounding
used.
structures (Trachea and
➢ Thyroidectomy is not necessary
esophagus).
➢ There is chronic inflammation THYROID NEOPLASMS
with extensive fibrosis of the • The thyroid contains both benign
thyroid gland. and malignant tumors.
• Females are affected more • Benign tumors include:
frequently than males, with most ➢ Adenomas (follicular adenoma,
patients being middle-aged. Hurthle cell adenoma)
• It presents as hypothyroidism with • Malignant tumors include:
‘hard wood’, non-tender thyroid ➢ Papillary carcinoma (60%)
gland. ➢ Follicular carcinoma (20%)
• The condition may clinically mimic ➢ Anaplastic carcinoma (10%)
carcinoma and present with stridor, ➢ Medullary carcinoma (5%)
dyspnea or dysphagia the only ➢ Malignant lymphoma (<5%)-
difference is anaplastic carcinoma not a primary thyroid tumor
is seen in the elderly while Riedel
fibrosing thyroiditis is seen in the
middle-aged.
• Riedel thyroiditis is associated with
retroperitoneal and mediastinal
fibrosis.
• Investigations
➢ T3 and T4 may be low due to
hypothyroidism.
➢ Radioisotope scan will not show
any uptake

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SURGERY MK
distinction between a follicular
carcinoma and an adenoma can
only be made by histological
examination.
• Follicular adenoma is characterized
by benign proliferation of follicles
surrounded by a fibrous capsule.
➢ Follicles are usually non-
functional however can secrete
thyroid hormone.
• In adenoma there is no invasion of
Figure 204: Classification of thyroid
neoplasms the capsule or of pericapsular blood
vessels i.e. no capsular or vascular
• Secondaries in thyroid are rare but invasion.
can come from colon, kidney, • They can be functional (releasing
melanoma, breast. hormones-‘Hot nodules’) or
• Thyroid cancers are common in nonfunctional (‘Cold nodule’)
females (3:1) • Treatment is therefore by wide
• Papillary carcinoma spreads excision I.e. lobectomy. The
through lymphatics, follicular remaining thyroid tissue is normal
through blood and anaplastic so that prolonged follow-up is
through both lymphatics and blood. unnecessary.
• Thyroid neoplasms typically • It is doubtful if there is such an
present as distinct solitary nodules. entity as a papillary adenoma and
• Thyroid nodules are more likely to all papillary tumors should be
be benign than malignant. considered as malignant even if
• Iodine radioactive (I123) uptake encapsulated.
studies are of importance:
MALIGNANT TUMORS
➢ Increased uptake: Graves’
• The vast majority of primary
disease or nodular goiter
malignancies are carcinomas
➢ Decreased uptake: adenoma and
derived from follicular cells.
carcinoma (this warrants a
• Dunhill classified then into:
biopsy by FNAC)
➢ Histologically differentiated
BENIGN TUMORS o Papillary
• Follicular adenomas present as o Follicular
clinically solitary nodules and the ➢ Histologically undifferentiated

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o Anaplastic o Recurrent laryngeal nerve
➢ Medullary paralysis (suggestive of
➢ Lymphoma (develop sometimes locally advanced disease)
in autoimmune thyroiditis) o Pressure/infiltrative
➢ Secondaries to the thyroid: symptoms:
secondary disease should be - Dysphagia from
considered when there is a compression or
history of malignancy, infiltration of
particularly kidney and breast esophagus
cancer and when the cytology of - Dyspnea from
a thyroid swelling is atypical. compression of trachea
or mets to the lungs
CLINICAL FEATURES OF THYROID
- Dysphonia and
CANCER
hoarseness from
• Clinical features/ effects may be
external laryngeal
due to
involvement.
➢ Primary tumor:
o Symptoms due to functional
o Thyroid swelling:
tumors (those that produce
- A differentiated
hormones)
carcinoma may be
➢ Secondary metastasis of
suspiciously firm and
tumor: mets to bones Tumors with
irregular but often
(flat bones of the skull, mets to the bone
indistinguishable from a
long bones, vertebrae)- ➢ Thyroid
benign swelling.
Pathological fractures ➢ Breast
- Small papillary tumors
➢ Constitutional ➢ Lung
may be impalpable even
symptoms: malaise, ➢ Kidney
in the presence of
weight loss, anorexia, ➢ Prostate
lymphatic metastases.
fatigue, malaise,
- Anaplastic growths are
anemia
usually hard, irregular
and infiltrating. HISTOLOGICAL ENTITIES
o Enlarged cervical lymph PAPILLARY CARCINOMA OF THYROID
nodes. • This is the most common type of
o Dilated veins over goiter thyroid carcinoma (60%).
o Pain referred to the ear in • It is a differentiated tumor that
infiltrative growths. contains a mixture of papillary
(finger-like structures) and colloid-

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filled follicles and in some
follicular structure predominates.
• Note: Presence of any papillary
structure or characteristic cytology
means that the tumor will behave in
a predictable fashion as a papillary
carcinoma.
• Common in females and younger
age group
• Etiology:
➢ Radiation either external or Figure 205: Papillary carcinoma
radioactive iodine therapy.
➢ TSH levels in the blood of these • Gross morphology: it can be soft,
patients are high and so it is firm, hard, cystic. It can be solitary
called as hormone dependent or multinodular. It contains
tumor. brownish black fluid.
➢ The incidence of follicular • Microscopy:
carcinoma is high in endemic ➢ Shows cystic spaces, papillary
goitrous areas, possibly as a projections with psammoma
result of TSH stimulation. bodies (concentric layers of
• Clinically it presents as: calcification), malignant cells
➢ Soft or hard or firm, solid or with ‘Orphan Annie eye’ nuclei
cystic, solitary or multinodular (intranuclear cytoplasmic
thyroid swelling. inclusions)
➢ Multiple foci may occur in the ➢ Orphan Annie eye nuclei are
same lobe as the primary or less identified in histology (Paraffin
commonly in both lobes. section of formalin tissue). It is
➢ Compression features are not seen in FNAC. Orphan
uncommon in papillary Annie is strip cartoon character
carcinoma of thyroid. with empty circle eyes.
➢ Often discrete lymph nodes in ➢ Tall cell type of papillary
the neck (40%) are palpable. carcinoma (10% of papillary
➢ May present with secondaries in carcinomas) is very aggressive
neck lymph nodes with occult type seen in elderly, 30% show
primary. It metastasizes to the capsular and vascular invasion
regional lymph nodes. with 25-30% 5-year survival
rate.

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➢ Columnar type is seen only in • It is slow-growing and eventually
males with near 100% mortality spreads by the hematogenous route.
in 5 years. • Most present as a solitary thyroid
➢ Papillary carcinomas are rarely nodule. Multiple foci are rarely
encapsulated. seen.
• Papillary tumors are slow • Histology: follicular hyperplasia.
progressive and less aggressive. • The prognosis of the tumor depends
• They generally have an excellent on the degree of capsular and
prognosis (90% 20-year survival vascular invasion.
rate) • Patients with minimal capsular
• They are commonly multicentric invasion can be treated by thyroid
and spread within the gland through lobectomy and TSH suppression
intrathyroid lymphatics to other with thyroxine (differentiated
lobes, cones out of the capsule and thyroid carcinomas are TSH
spreads to cervical lymph nodes. responsive and it is therefore
• Usually there is no blood spread. important to keep TSH suppressed
• Extrthyroidal disease- invasion into by administering thyroxine).
thyroid capsule can cause blood • If there is significant capsular or
born secondaries occasionally. vascular invasion the patient is best
• Diagnosis: served by total thyroidectomy and
➢ TSH level in the blood is higher subsequent radioiodine and
➢ Plain X-ray neck shows fine thyroxine therapy.
calcification whereas nodular
goiter shows coarse- ring/rim
calcification
➢ U/S neck or CT scan neck
(better) to identify non-palpable
nodes in neck.
➢ Radioisotope scan shows cold
nodule
➢ FNAC of thyroid nodule and
lymph node
FOLLICULAR CARCINOMA
• Follicular carcinoma of the thyroid • Hurthle cell tumors are a variant of
occurs in an older age group (40-50 follicular neoplasm in which
years). oxyphil cells predominate

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histology. It carries poorer • Medullary carcinoma may be
prognosis. associated with MEN 2A and MEN
2B
MEDULLARY CARCINOMA
➢ MEN 2A: medullary carcinoma
• It is uncommon (5%) type of
of thyroid + Pheochromocytoma
thyroid malignancy.
+ parathyroid adenoma
• It arises from the parafollicular ‘C’
➢ MEN 2B: medullary carcinoma
cells (that produce calcitonin)
of thyroid + pheochromocytoma
which is derived from the neural
+ ganglioneuroma of oral
crest. C cells are more in upper pole
mucosa
of the thyroid gland.
• Medullary carcinoma is associated
• FNAC shows ‘amyloid stroma’
with mutations in RET oncogene.
(due to deposition of calcitonin).
• Detection of RET mutation
Amyloid can be visualized using
warrants prophylactic
Congo Red pigment.
thyroidectomy.
• In these patients blood levels of
• Clinical features:
calcitonin both basal as well as that
➢ Thyroid swelling often with
following calcium or pentagastrin
enlargement of neck lymph
stimulation is high, a very useful
nodes
tumor marker.
➢ Diarrhea, flushing (30%)
• Tumor also secretes serotonin (5-
➢ Hypertension,
HT), prostaglandin, ACTH and
pheochromocytomas and
vasoactive intestinal polypeptide
mucosal neuromas with MEN
(VIP).
2B syndrome.
• Diarrhea is a feature seen in 30% of ➢ Paraneoplastic syndrome like
cases and may be due to 5- Cushing’s and carcinoids
hydroxytryptamine or ➢ Hypocalcemia (Chovstek sign-
prostaglandins produced by the tapping over facial nerve in
tumor cells. front of tragus causes twitching
• It spreads mainly to lymph nodes of facial muscles and Trousseau
(60%). sign- carpal spasms induced by
• It usually presents as a thyroid inflating a sphygmomanometer
nodule in a sporadic form (70% of cuff above systolic pressure)
cases) or can be familial or in o Paresthesia, muscle cramps,
association with multiple endocrine carpopedal spasms
neoplasia (MEN). • Patients with medullary thyroid
carcinoma are best treated by total

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thyroidectomy with central lymph ➢ Positive Berry’s sign-
node clearance. involvement of carotid sheath
• Post-operatively patients are given leads to absence of carotid
thyroxine replacement (but not pulsation.
TSH suppression), postoperatively • Swelling is hard, with involvement
calcitonin measurement is a useful of isthmus and lateral lobes.
tumor cell marker and can be used • FNAC is diagnostic.
as a method of follow-up. • Tracheostomy and isthmectomy
• The prognosis is approximately has got a role to relieve respiratory
60% 5-year survival. obstruction temporarily.
ANAPLASTIC CARCINOMA • Treatment is external beam
radiotherapy and/or chemotherapy,
• This is an undifferentiated very
as usually thyroidectomy is not
aggressive carcinoma (1%) occurs
possible.
in elderly females.
• Adriamycin as chemotherapy
• It is a very aggressive tumor of
• Prognosis is poor (patients die in 12
short duration, presents with a
swelling in thyroid region which is months). Life span is counted in
few weeks to months only.
rapidly progressive causing:
➢ Stridor and hoarseness of voice
due to tracheal obstruction
➢ Dysphagia
➢ Fixity to the skin
• It spreads by blood and lymphatics.
• It is difficult to differentiate from
Riedel thyroiditis.
THYROID LYMPHOMA
• This is a rare tumor usually present in the elderly female with a background
history of autoimmune (Hashimoto’s thyroiditis) as a rapidly growing thyroid
nodule.
• Presents with a large rubbery goiter.
• It may be diagnosed by FNA or Trucut biopsy.
• As for all lymphomas it should be staged with a bone marrow aspirate and CT
scan of the chest and abdomen.
• If confined to the thyroid alone it may be treated by thyroid lobectomy with
subsequent adjuvant radiotherapy and chemotherapy otherwise it is treated by
chemoradiation alone.

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STAGING: TMN STAGING

MANAGEMENT
• Contemporary guidelines increasingly recommend total thyroidectomy for
virtually all cancer followed by thyroid hormone replacement.
• Conservative approach reserves total thyroidectomy for specific indication
namely those in which there is a preoperative diagnosis of high-risk cancer,
bilateral disease or when there is a clear indication for postoperative radiotherapy.
• “Small cancers” confined to one lobe can be managed by lobectomy and TSH
suppression. Unfortunately, there is no general consensus on the definition of
small cancer with arbitrary limits of between 1 and 4cm in use.
• Indications for thyroidectomy:
➢ Malignant goiter

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SURGERY MK
➢ Enlarged thyroid with pressure symptoms
➢ Thyrotoxic goiter unresponsive to medical treatment
➢ Cosmesis
• Complications of thyroidectomy:
➢ Early
o Recurrent laryngeal nerve damage (may be unilateral or bilateral)- leads
to vocal cord collapse and upper airway obstruction
o Laryngeal edema
o Hemorrhage and Hematoma as a result of poor hemostasis- leads to upper
airway obstruction
o Tracheomalacia as seen with a large goiter that erodes the trachea that
collapses after thyroidectomy resulting in upper airway obstruction
o Upper airway obstruction
o Hypocalcemia (removed parathyroid glands)- low calcium, Chvostek’s
sign and Trousseau sign. Treat with calcium gluconate
o Tracheal perforation
o Thyroid storm
- Increased T3 and T4 levels with symptoms (Ill, Toxic looking,
tachycardia, arrythmias, heart failure, pyrexia, tachypnea, sweating
profusely, convulsions, confusion, coma, diarrhea, vomiting and
acute abdomen)
- Due to operation performed on a patient that is not rendered euthyroid.
- Management
 Admit patient to ICU (quiet room)
 Temperature control (Fan, Cold compress/sponging, antipyretics)
 Suppress T3, T4 and TSH production:
▪ Beta blocker and Thioamide (Propylthiouracil 1st line) plus:
Iodine compounds (e.g. Lugol’s solution) to block T4 and T3
release (Give this 1hour after thioamide as otherwise it may
increase thyroid hormone synthesis), Glucocorticoids
(hydrocortisone or dexamethasone- to reduce conversion of
T4 to T3) and Bile acid sequestrants (e.g. Cholestyramine) to
prevent T4 and T3 reabsorption in the gut
 Intravenous fluid
- Prevention: Render the patient euthyroid prior to surgery
➢ Intermediate
o Infections

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 SURGERY MK
o DVT
o Hypostatic pneumonia
➢ Late
o Hypothyroidism
o Keloid and hypertrophic scars
SUMMARY OF THYROID CANCER
Papillary Follicular Medullary Anaplastic
Frequency Most common Not common in populations Not common Rarest but worst
with adequate iodine prognosis
Risk factors Radiation Dyshormonogenesis MEN II in 30- • Prior diagnosis
40% of well
differentiated
thyroid tumor
• Iodine defieciny
Age group 30-40 40-50 50-60 60-70
Clinical • Painless mass • Painless mass • Painless mass • Rapidly
features • Dysphagia • Rarely: hyperfunctional • Palpable enlarging mass
• Dyspnea lymph node (large mass at
• Hoarseness (15-20%) presentation)
• Euthyroid • Dysphonia • Neck pain
• Dyspnea • Dysphagia
• Hoarseness • Hard, fixed
lymph node
(50%)
Diagnosis • FNAC • FNAC • FNAC • FNAC
• CT or MRI (to • CT or MRI (to assess • Presence of
assess local local invasion) amyloid is
invasion) diagnostic
(Congo red)
• Check for
calcitonin
Metastasis Lymphatics Blood • Lymphatic • Blood and
(local neck lymphatics
and • Aggressive
mediastinal local disease
nodes) • 30-50% have
synchronous

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 SURGERY MK
• Local (into pulmonary mets
trachea and at time of
esophagus) diagnosis
Treatment • Minimal • Minimal cancer (<4cm): • Sporadic • Debulking
cancer lobectomy and (80%): total resection of
(<1.5cm): isthmectomy thyroidectomy thyroid gland
limited • Other: Total or near- • Familial and adjacent
lobectomy and total thyroidectomy for (20%): total structures
isthmectomy cancer >4cm thyroidectomy • External
• Other: Total or • For + LN, modified and central radiation
near-total radical neck dissection neck node therapy
thyroidectomy • I-131 ablation for dissection • Doxorubicin-
for cancer patients with residual • No value for I- based
>1.5cm thyroid tissue or LN 131 ablation chemotherapy
• For +LN, mets • Follow
modified patients with
radical neck calcitonin
dissection levels
• I-131 ablation
or thyroid
suppression
(with thyroid
hormone) for
patients with
residual
thyroid tissue
or LN mets
Prognosis Worse for older Worse for older patients Poor
patients with with distant mets, tumor
distant mets. size >4cm, high tumor
Presence of + LN grade. Presence of + LN not
not strongly strongly correlated with
correlated with overall survival
overall survival
Survival 10-year survival: 10-year survival: 60-80% 10-year survival: Median survival: 4-
74-93% 70-80% 5 months

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HYPERTHYROIDISM
• Thyrotoxicosis is a symptom complex due to raised levels of thyroid hormones.
• It refers to biochemical and physiological manifestations (e.g. hyperthermia) of
excessive thyroid hormone.
➢ Thyrotoxicosis= Excessive thyroid hormone release in blood + Clinical
manifestations
• Hyperthyroidism is the term used to refer to overproduction of the thyroid
hormones.
• Hyperthyroidism is divided into:
➢ Primary thyrotoxicosis (pathology is in the thyroid gland)
o Puberty, pregnancy, emotion and infection are the precipitating factors for
primary thyrotoxicosis.
➢ Secondary thyrotoxicosis (pathology not in thyroid gland)

Figure 206: Primary thyrotoxicosis vs Secondary thyrotoxicosis

TYPES
• Diffuse toxic goiter (Primary thyrotoxicosis)
➢ Graves’ disease
➢ Basedow’s disease
• Toxic multinodular goiter (Secondary thyrotoxicosis): Plummer disease
• Toxic nodule (Goetsch’s disease)
• Other causes of thyrotoxicosis without hyperthyroidism include:
➢ Ectopic function thyroid

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➢ Struma ovarii
➢ Functioning metastatic follicular carcinoma
➢ Trophoblastic tumors
➢ Thyrotoxicosis factitia- drug induced due to intake of L-thyroxine more than
normal
GRAVES DISEASE
• This is an autoimmune thyrotoxicosis that is caused by an antibody against the
TSH receptor (TSH receptor antibody).
• Graves’ disease has genetic predisposition and it affects most females (8:1).
• Due to the stimulating TSH receptor antibodies, the acinar of the thyroid undergo
hypertrophy and hyperplasia with absence of normal colloid in the tall columnar
epithelium (normal is flat epithelium
with colloid). As the cells are empty
they look vacuolated. Tissues are
highly vascular.
• Clinical features are those of
thyrotoxicosis. It is also associated with
vitiligo. Exophthalmos producing
substance causes Graves
ophthalmopathy (manifested by lower
eyelid retraction, lid lag, periorbital
Figure 207: Patient with exophthalmos
edema, chemosis or if severe proptosis
and exophthalmos).
• Diffuse goiter, thyrotoxicosis and autoimmune manifestations (infiltrative
ophthalmopathy, dermopathy, myopathy) are essential components of Graves’
disease. Thyroid stimulating antibodies produced against thyroid antigen in
Graves’ disease which is directed to TSH receptor acting as TSH receptor
antibody. TSH receptor antibody is observed only in Graves’ disease.
• Examination reveals a moderate firm goiter which in severe thyrotoxicosis may
have a vascular thrill and bruit.
• Investigations:
➢ Suppressed TSH with raised free T4 and/or T3
➢ 90% of patients have raised TSH antibodies
➢ 70% of patients will have raised thyroid peroxidase antibodies.
• Treatment:
➢ Medical

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o Thyroid uptake blocking drugs to render the patient euthyroid
- Carbimazole
▪ Important side-effects: neutropenia (which presents as sore throat),
profuse diarrhea or hepatocellular failure (which initially presents
as jaundice), skin rash, nausea and joint pain
- Propylthiouracil
o Beta-blockers (Propranolol) can be used if the patient is symptomatic with
sweating, tremor or tachycardia
o Control of thyrotoxicosis usually takes about 6 weeks but maintenance is
required for at least 18 months before cessation of carbimazole.
Alternatively, higher doses of carbimazole can be taken in conjunction
with thyroxine for about 12 months (block and replace).
o If the patient relapses after this then definitive long term treatment is
required either radioactive iodine or if inappropriate (e.g. young children
at home) surgery can be performed.
➢ Surgical
o Patient has to be rendered euthyroid before surgery.
o If surgery is the preferred option, then previously a subtotal
thyroidectomy was performed to render the patient ‘euthyroid’ however
10% of these patients developed recurrent thyrotoxicosis and 70%
develop hypothyroidism in the long run.
o Total thyroidectomy and long term thyroxine postoperative can be done.
TOXIC MULTINODULAR GOITER
• While the majority of multinodular goiters are non-toxic, over a period the
presence of large functioning nodules may render the patient hyperthyroid
leading to toxic multinodular goiter (Plummer’s disease).
• The large goiter may extend retrosternally and cause tracheal deviation and
compression occasionally leading to stridor (a low-pitched crowding noise on
inspiration caused by narrowing of the trachea).
• Examination will reveal multiple nodules either bilaterally or unilaterally.
• If there is a dominant nodule within the gland then this should be investigated as
for solitary thyroid nodule as the risk of malignancy in this nodule is about 10%.
• Elevation of the patient’s arms may lead to venous congestion and stridor if there
is retrosternal extension of the goiter (Pemberton’s sign). The position of the
trachea should be checked for possible tracheal deviation.
• Thyroid ophthalmopathy is not associated with multinodular goiter.

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• Investigations:
➢ TSH: reduced if toxic multinodular goiter.
➢ Fine-needle aspiration of dominant nodule, if present
➢ Ultrasound may confirm multiple nodules
➢ X-ray of thoracic inlet and CT will delineate the extent of retrosternal
extension and the degree of tracheal deviation and compression
• Treatment:
➢ Total thyroidectomy should be performed for non-toxic multinodular goiter if
there is retrosternal extension of the goiter, tracheal compression or if the
patient finds the goiter cosmetically unacceptable.
➢ Toxic multinodular goiter: treat with carbimazole initially and then either total
thyroidectomy or radioiodine depending on the suitability of the patient.
SOLITARY TOXIC ADENOMA
• Occasionally, a single thyroid adenoma may be active
enough to render the patient hyperthyroid.
• The patient normally presents with a solitary thyroid
nodule and should be investigated as such in order to
exclude malignancy.
• In patients with solitary toxic adenoma, TSH is
suppressed and a 99mTcO4 thyroid isotope scan will
show a solitary ‘hot’ nodule.
• Treatment is initially with carbimazole followed by
either thyroid lobectomy or radioactive iodine
depending on preference. Figure 208: 'Hot' nodule on thyroid
isotope scan

CLINICAL FEATURES OF THYROTOXICOSIS

• It is 8 times more common in females.
• Occurs in any age group.
➢ Primary type is seen in younger group.
➢ Secondary type is common in older age group.
• Note: Graves’ disease often presents without any obvious thyroid swelling in the
neck. Whenever there are unexplained behavioral problems, insomnia,
myopathy, unexplained diarrhea or loss of weight, tachycardia, Graves’ disease
should be suspected and evaluated

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SYMPTOMS
SYSTEM SYMPTOMS
CENTRAL NERVOUS • Irritability
SYSTEM • Nervousness
• Insomnia
• Fine tremor (Due to diffuse irritability of grey
matter)
• Heightened emotions
CARDIOVASCULAR • Palpitations (thyroid hormones increase
SYSTEM expression of Beta 1 adrenergic receptors)
• Shortness of breath at rest or on minimal exertion
• Angina
• Irregularity of heart rate (Arrhythmias)
• Cardiac failure in the elderly
• Undue fatigue and muscle weakness
GASTROINTESTINAL • Weight loss in spite of increased appetite
SYSTEM • Diarrhea (due to increased activity at ganglionic
level) and malabsorption
GENITOURINARY • Oligo or amenorrhea
SYSTEM • Occasional urinary frequency
SKELETAL SYSTEM • Increase in linear growth in children
• Bone resorption and hypercalcemia
• Decreased muscle mass with weakness
INTEGUMENTARY • Hair loss, gynecomastia
SYSTEM • Pruritus
• Palmar erythema
METABOLIC • Increase in basal metabolic rate (increase in the
SYSTEM synthesis of sodium-potassium ATPase)
• Hypocholesterolemia

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• Hyperglycemia (due gluconeogenesis and
glycogenolysis)
• Sympathetic over activity causes dyspnea, palpation, heat intolerance, sweating,
nervousness, increased appetite and decrease in weight.
• Because of the increased catabolism they have increased appetite, decreased
weight and so also increased creatinine level which signifies myopathy (Due to
more muscle catabolism).
• Fine tremor is due to diffuse irritability of grey matter.
SIGNS OF HYPERTHYROIDISM/ TOXICOSIS
EYE SIGNS IN TOXIC GOITRE
• Common in primary thyrotoxicosis.
• Lid lag, lid spasm can occur in secondary thyrotoxicosis also.
• Eye signs include:
➢ Lid retraction: the upper eyelid is higher than normal and lower eyelid is in
normal position with visible sclera adjacent to upper eyelid. It is due to
sympathetic over activity causing spasm of involuntary smooth muscle of the
levator palpebrae superioris. It is a sign of thyrotoxicosis not a sign of
exophthalmos.
➢ Lid Lag sign: it is inability of the upper eyelid to keep pace with the eyeball
when it looks downwards to follow the examiners finger.
➢ Staring gaze (absence of normal
blinking)
➢ Exophthalmos: this is proptosis of
the eye, it is caused by infiltration
of retrobulbar tissue with fluids and
round cells with lid spasm of upper
eyelid.
o It is seen with Grave’s disease
and is believed that fibroblast
have TSH receptors and in
response to TSH like antibodies
e.g. Grave’s disease fibroblast
Figure 209: Eye signs in
produce mxyoid substances e.g. hyperthyroidism/Thyrotoxicosis
glycosaminoglycans (GAGs)
which deposit in the retro-orbital tissues.

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o Remember: antithyroid drugs may worsen exophthalmos and the patient
should be observed once antithyroid drugs are started as steroid
supplementation may be required.
CARDIAC MANIFESTATIONS
• Tachycardia (common), take sleeping pulse rate for 3 consecutive nights and
average is taken as the value
➢ Grade 1 <90b/m
➢ Grade 2: 90-110b/min
➢ Grade 3: >110 b/min
• Ectopic heart beats
• Multiple extrasystoles
• Paroxysmal atrial tachycardia & fibrillation
• Persistent atrial fibrillation (not responsive to digoxin)
• Pulsus paradoxus
• Wide pulse pressure
MYOPATHY
• Weakness of proximal muscles occurs i.e. front thigh muscle, arm muscles.
• Weakness is more when muscle contracts isometrically either while getting down
steps or lifting a full bucket.
• Often when it is severe it resembles myasthenia gravis. Once hyperthyroidism is
controlled recovery occurs.
PRETIBIAL MYXEDEMA
• This is a misnomer.
• It is often a feature of primary thyrotoxicosis.
• It is due to deposition of myxomatous tissue (mucin like deposits) in skin and
subcutaneous plane. Glycosaminoglycans (hyaluronic acid) deposition occurs-
same as exophthalmos.
• It is usually bilateral, symmetrical, shiny, red thickened dry skin with coarse hair
in the feet and ankles.
• In severe cases skin of entire leg below the knee with involvement of foot and
ankle can occur.
• It might or might not regress completely after treatment for toxicity.

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• Skin becomes cyanotic when cold. Skin changes in toxicosis are called as thyroid
dermopathy. They include- pretibial myxoedema, pruritus, palmar erythema, hair
thinning, Dupuytren’s contracture.
THYROID ACROPACHY
• Thyroid acropachy is clubbing of fingers and toes in primary thyrotoxicosis.
• Hypertrophic pulmonary osteoathropathy can develop.

OTHERS
• Thrill is felt in the upper pole of thyroid and also bruit on auscultation. It is
because in upper pole, superior thyroid artery enters the gland superficially and
so thrill and bruit can easily be felt. In lower pole inferior thyroid artery enters
the gland from deeper plane and so thrill cannot be felt.
• Hepatosplenomegaly.
INVESTIGATIONS
• Thyroid function tests: Increased T3, T4 and low TSH. Sometimes T3 is the only
thing elevated (T3 toxicosis)
➢ Normal Free T3= 3-9 pmol/L
➢ Normal Free T4= 8-26pmol/L
• Thyroglobulin antibodies
➢ Raised in pregnancy, cirrhosis, hyperestrogenism
➢ Decreased in high androgen levels, hypoproteinemia, acromegaly
• Thyroid antibody estimation- antithyroglobulin and TSH receptor antibody
• Radioisotope study (I-123 or 99mTc-technetium 99m) for hot nodules
➢ I-131 is used for radioactive iodine therapy (beta rays are used)
➢ I-123 is used for diagnostic studies (gamma rays are used)
• ECG- to look for cardiac involvement
• FBC- total count and neutrophil count are very essential base line investigations
before starting antithyroid drugs (as it may cause agranulocytosis)

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MANAGEMENT
• Medical (anti-thyroid drugs)
➢ Indications:
o Toxicity in pregnant women (propylthiouracil is preferred)
o Toxicity in children and young adults
o Before subtotal thyroidectomy to make the patient euthyroid. Note:
antithyroid drugs should be continued during and after surgery for 7-10
days.
o Soon after starting radioactive I-131 therapy for 6 to 12 weeks (effects of
radiotherapy start only in 6 to 12 weeks)
➢ Carbimazole:
o Blocks thyroid hormone synthesis. It also suppresses the autoimmune
process in Graves’ disease
o Dose: 5-10mg exactly 8 hourly/TID (as half-life of carbimazole is 8
hours). Each table is 5mg. It is usually given for 12-18 months.
o Often Tri-iodothyronine 20micrograms QID or thyroxine 0.1 mg daily are
given in combination with antithyroid drugs to prevent iatrogenic thyroid
insufficiency or to prevent increase in size of goiter.
o Side effects: fever, rashes, arthralgia, myalgia, neuritis, lymph node
enlargement, liver cell dysfunction, psychosis, agranulocytosis
➢ Methimazole: like carbimazole. Dose is 5 to 20 mg daily long acting, once a
day dose.
➢ Propylthiouracil:
o Blocks thyroid hormone synthesis and peripheral conversion of T4 to T3
o It also decreases the thyroid autoanibody levels.
o Can be given for hyperthyroidism in children, pregnancy and lactation.
o Dose: 200mg 8 hourly (TID)

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o Side effects: dose unrelated hepatotoxicity, agranulocytosis,
antineutrophilic cytoplasmic antibody (20% of patients on long term use)
➢ Propranolol
o Dose: 40mg TID
o It reduces the cardiac problems as well as blocks peripheral conversion of
T4 to T3.
o Contraindications: bronchial asthma, heart block, cardiac failure.
o Long acting nadolol
➢ Lugol’s iodine (5% iodine + 10% potassium iodide): decreases the vascularity
of the gland and makes it more firm and easier to handle during surgery. Dose
is 10-30 drops/day (minims) for 10 days prior to surgery. Potassium iodide
tablets 60mg TID also can be given instead of Lugol’s iodine. But its use at
present is disqualified. (1 minim =1 drop. 1ml= 16 drops)
o Note: Lugo’s iodine prevents the release of hormone from the gland
(thyroid constipation). After 2 weeks, effects of Lugol’s iodine is lost
causing thyroid escape from iodine control.
• Surgical
➢ Indications:
o Failed medical treatment in primary thyrotoxicosis in young patients
o Autonomous toxic nodule
o Nodular toxic goiter
o When malignancy cannot be ruled out
o Graves’ disease in children, Graves with nodules
o Need for antithyroid drugs for more than 2 years
o Large goiter, substernal/intrathoracic goiter
o Pressure symptoms, Graves ophthalmopathy
o Amiodarone induced thyrotoxicity
➢ Procedures done:
o Subtotal thyroidectomy: both lobes with isthmus are remove and a tissue
equivalent to pulp of finger is retained at the lower pole of the gland on
both side (5-8g)
o Hemithyroidectomy: this is done in an autonomous nodule. The entire
lateral lobe with the whole of isthmus is removed.
o Total thyroidectomy: this is the better option in Graves disease to achieve
the lowest relapse rate and successful stabilization of thyroid
ophthalmopathy as it clears the antigenic focus in thyroid completely.
➢ Complications of thyroid surgery:

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o Damage to the recurrent laryngeal nerve leading to palsy (2% of
thyroidectomies) and causes hoarseness.
o Damage to the external branch of the superior laryngeal nerve, leading to
palsy and causing hoarseness.
o Hypocalcemia due to damaged parathyroid (5% of thyroidectomies)
o Hemorrhage, potentially causing laryngeal edema and respiratory
compromise.
• Radioiodine therapy
➢ Indications:
o Primary thyrotoxicosis after 45 years of age
o Autonomous toxic nodule
o Recurrent thyrotoxicosis
➢ Radioiodine destroys the cells and causes the complete ablation of thyroid
gland. It is given only after the age of 45 years as the chances of genetic
mutation (Damage), leukemia, carcinomas are high in younger individuals.
➢ Usual dose is 5 to 10 millicurie or 160 microcurie/g of thyroid.
➢ The patient is made euthyroid using antihyroid drugs, drug is discontinued for
5 days, I-131 300-600 MBq is given orally, antithyroid drugs are started after
7 days and are continued for 8 weeks. In 30% of patients additional 2 or 3
doses may be required.
➢ It takes 3 months to get full responses and so until then, the patient has to take
antithyroid drugs. Often additional 1 or 2 doses of radioiodine are required to
have complete ablation. Eventually they go for hypothyroidism and so require
maintenance dose of L-thyroxine 0.1 mg daily.
➢ To give therapeutic dose, patient should be admitted and isolated for 7 days
(half-life) to prevent irradiation. It is given orally soon after getting from the
manufacturer without much delay to have optimal efficacy.

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Figure 210: Choice of therapies

HYPOTHYROIDISM
• This is characterized by low thyroid hormones.
• It is common among females (10:1).
CLASSIFICATION
• It may be classified as:
➢ Primary- due to thyroid disease or removal of the thyroid.
➢ Secondary- due to hypopituitarism
➢ Tertiary- due to hypothalamic disease
ETIOLOGY
• Classified as:
➢ Congenital:
o Agenesis or dysgenesis of the thyroid
o Enzyme deficiency (Dyshormonogenetic goiter: peroxidase enzyme
deficiency)
➢ Acquired:
o Iodine deficiency (commonest cause in developing countries)

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o Hashimoto’s thyroiditis (commonest cause in developed countries):
antibodies raised against the enzyme thyroid peroxidase and
thyroglobulin (anti-thyroglobulin antibodies)
o Radioiodine
o Drugs: lithium, amiodarone
o After thyroidectomy (common cause)

CRETINISM MYXEDEMA
• This is hypothyroidism in younger • This is hypothyroidism in adults
children. • Causes:
• It is due to inadequate thyroid ➢ Iodine deficiency
hormone production during fetal and ➢ Hashimoto thyroiditis
neonatal period. (commonest cause of
• Cause: hypothyroidism where iodine is
➢ Thyroid agenesis sufficient)
➢ Inborn error of thyroid ➢ Drug e.g. lithium
metabolism ➢ Surgical removal or radioablation
➢ Dyshormonogenetic goiter: of thyroid
peroxidase enzyme deficiency • Clinical features:
➢ Maternal hypothyroidism during ➢ General: Tiredness, weight gain,
early pregnancy cold intolerance, goiter,
➢ Iodine deficiency (endemic) hyperlipidemia,
• Clinical features: hypercholesterolemia
➢ Mental disability (thyroid ➢ Cardiovascular: bradycardia with
hormones required for normal decreased cardiac output

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brain development- formation of (Shortness of breath and fatigue),
neuronal synapses) angina, cardiac failure,
➢ Short stature with skeletal pericardial effusion
abnormalities ➢ Hematological: anemia
➢ Delayed puberty ➢ Gastrointestinal: constipation,
➢ Coarse facial features ileus
➢ Enlarged tongue ➢ Reproductive: infertility,
➢ Typical hoarse cry menorrhagia, galactorrhea
➢ Thickened skin ➢ Dermatological: dry skin,
➢ Umbilical hernia vitiligo, alopecia, erythema
• It is treated with L-thyroxine OD in ➢ Others: Carpal tunnel syndrome,
the morning myalgia, hoarseness, deafness,
ataxia, depression, psychosis
(myxedema madness)
• Treatment is with L-
thyroxine/Levothyronine,
Glucocorticoids, and antibiotics
• Examination will usually reveal a small firm goiter. If a nodule is present, then
this should be investigated as for a solitary thyroid nodule in order to exclude
malignancy.
• Thyroid lymphoma usually develops on a background of autoimmune
hypothyroidism.
• Extreme hypothyroidism can present as myxedema madness with confusion
leading to coma.
• Note: myxedema is severe thyroid failure
INVESTIGATIONS
• TSH: elevated in hypothyroidism with decreased free T4 and/or T3
• Antibodies: Thyroid peroxidase and antithyroglobulin
TREATMENT
• Patients are rendered euthyroid by treatment with Levothyroxine (L-thyroxine).
• In the elderly patients with ischemic heart disease, L-thyroxine should be
introduced cautiously starting at 25-50 g and increasing the dose every fortnight
in order to avoid precipitating tachyarrhythmias and cardiac failure.
• Normal thyroxine dose= 75-150 g.
• Patients should have their TSH checked every 12-18 months thereafter to ensure
correct thyroxine dosage.

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• For some patients, liothyronine (T3) is an alternative. Initial rapid response can
be achieved by giving L- iodothyronine 20 g TID.
• Myxedema coma is characterized by:
➢ Hypothermia (precipitated by cold)- Drug of choice- T3 (levothyroinin) 10 g
IV QID
➢ Hypotension (precipitated by infection or trauma)- Levothyroxine 300 g IV/
1000 g orally (large dose)
➢ Hyponatremia- give glucocorticoids
➢ Hypoventilation- give antibiotics
➢ Hypoglycemia- slow warming
➢ Bradycardia- electrolyte management
➢ Skin that is cold like a todd
➢ Coma

PARATHYROID GLAND

HYPERPARATHYROIDISM

HYPOPARATHYROIDISM

ADRENAL GLANDS

CUSHING’S SYNDROME

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HYPERALDOSTERONISM

ADRENAL TUMORS
PHAEOCHROMOCYTOMA

ADRENAL INCIDENTALOMA

MULTIPLE ENDOCRINE NEOPLASIA

PITUITARY GLAND
TUMORS OF ANTERIOR PITUITARY

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CHAPTER 16: BREAST

BREAST
• All patients presenting with a breast lump should have a triple assessment
including:
➢ Clinical assessment:
o History
o Physical examination
➢ Radiological assessment:
o Ultrasound (patients below the age of 35)
o Mammogram (patients above 35 years) or
o Ultrasound is particularly useful in assessing whether a lump is solid or
cystic.
o Mammography is good at determining whether benign lumps are very
well defined or have a surrounding halo. Breast cancers are commonly
associated with speculation, architectural distortion or malignant
microcalcification
➢ Pathological assessment:
o Fine needle aspiration: a fine needle
attached to a syringe is inserted into the Classification of cell from FNAC
lump and cells are withdrawn by making C1- inadequate
several passes through the lump with
negative pressure (6ml). Once cells are C2- normal/benign
withdrawn from the breast lump, they can C3- atypia (probably benign)
either be fixed or air-dried on a slide
C4- atypia probably malignant
immediately or drawn into a transport
medium and sent to the lab for them to be C5- malignant
centrifuged and plated on a glass slide,
fixed and stained with either hematoxylin
and eosin or Papanicolaou stain. C5 diagnosis on cytology that is
- Advantage: it allows drainage of a cyst congruous with the clinical and
(if fluid is present, then diagnosis is radiological features allows the
invariably benign). If the fluid surgeon to carry out a definitive
withdrawn is bloody then further surgical procedure for breast cancer
investigation is needed.

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- Disadvantage: a breast cyst can be
associated with presence of an
intracystic papilloma (rarely carcinoma)
and in these cases excision of the cyst is
necessary. Clinically these cysts recur
and an intracystic abnormality is visible
on ultrasound.
o Trucut biopsy: when cytology is inadequate
or unhelpful the next step in diagnosis is core
biopsy.
- This is a minimally invasive procedure
where under local anesthesia a section of
breast tissue is obtained from the lump.
- This carries some advantages over fine-
needle aspiration cytology in that a
histological assessment of tumor grade
(when a lump is malignant) can be made
and estrogen receptor status can also be
assessed.
Figure 211: Breast cytology- Benign
cytology (Up) and Malignant cytology
(below)

Figure 212: Breast histology from biopsy

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APPROACH TO A ➢ Back pain (bone metastasis
especially to lumbar spine)
BREAST LUMP ➢ Hard nodules on skin (skin
HISTORY metastasis)
• Demographic history: Age (young- ➢ Swelling of arms (Axillary
benign conditions, old- malignant) lymphadenopathy)
• Presenting complaint: breast lump • Past Medical and surgical history
• History of presenting complaint: ➢ History of any operation
➢ When was the lump first (lumpectomy, excisions,
noticed? (duration) biopsy).
➢ What brought it to the patients’ ➢ History of breast cancer, ovarian
notice? cancer
➢ What symptoms does it cause? ➢ History of radiation exposure
o Skin changes (ulceration, ➢ Use of Estrogen based oral
dimpling) contraceptives/ hormonal
o Nipple changes (retraction) replacement.
o Nipple discharge • Gynae history:
➢ Has it changed? How much has ➢ Last menstrual period
it changed since it was first ➢ Menstrual regularity and
noticed? Has it increased or volume
decreased in size? ➢ Age of menarche/menopause
➢ Has it ever disappeared or ➢ Age of 1st pregnancy or 1st child
healed? ➢ Number of children (if any)
➢ Does the patient have any other ➢ Breast feeding or not + last time
lumps? of breast feed
➢ What does the patient think • Family history: History and number
caused it? of breast cancer in 1st degree
• Review of systems: Associated relative (mother, sister, daughter)
symptoms: • Social history
➢ Dyspnea, chest pain, cough, ➢ Diet and obesity
hemoptysis (lung mets) ➢ History of alcohol/smoking
➢ Jaundice or abdominal
distension (liver metastasis)

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EXAMINATION OF THE BREAST
• Before the examination always:
➢ Wash hands. Self-breast examination
➢ Greet the patient and introduce Adult women of all ages are encouraged to perform
yourself. a monthly self-breast examination as follows:
➢ Explain the examination to the
patient and gain consent. • In the shower:
• Explain the need for a chaperone: ➢ With the pads of the middle 3 fingers, check
“One of the female ward staff the entire breast and armpit area pressing
members will be present throughout down with light, medium and firm pressure
the examination, acting as a ➢ Check both breasts each month feeling for
chaperone, is it ok?” any lump, thickening, hardened knot, or any
other breast changes
• When explaining the examination this
may be a good time to ask if she has • In front of a mirror:
noticed any lumps or other problems ➢ Visually inspect the breast with the arms on
(discharge, tenderness) and if she the side, next raise them high overhead.
performs a monthly breast self- Look for any changes in the contour, any
examination. swelling, or dimpling of the skin or changes
➢ If she does not, teach her good in the nipples
technique and watch as she repeats ➢ Next rest the palms on the hips and press
the steps of examination after you, firmly to flex the chest muscle. Left and
giving helpful correction as right breasts will not exactly match (this is
needed. normal for some women), look for dimpling,
puckering or changes particularly on one
• Patients sometimes say that their lump
side.
can only be felt when they adopt a
certain posture e.g. standing or lying • Lying down:
on one side, and they should therefore ➢ When lying down the breast tissue evenly
be examined in this position as well. spreads on the chest wall. By placing a
pillow under the right shoulder and the right
• An adequate inspection requires full
arm behind the head use the pads of the left
exposure of the chest but later as you
fingers to palpate the entire right breast
examine one breast you may find it
covering the entire areas and armpits. Use
helpful to cover the other. Expose all
light, medium and firm pressure noting any
of the top half of the trunk.
masses or lumps
➢ Repeat the process on the other breast
➢ Squeeze the nipples and check for discharge

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• Because breasts tend to swell and become more nodular before menses as a result
of increasing estrogen stimulation, the best time for examination is 5 to 7 days
after the onset of menstruation.
• Nodules appearing during the premenstrual phase should be reevaluated at this
later time.
INSPECTION
GENERAL INSPECTION
• Inspection is done with the patient seated. Ask the patient to sit upright, ideally
on the side of the bed.
• Note any obvious masses, swelling, skin changes, scars, asymmetry or nipple
discharge.
CLOSE INSPECTION
• Inspect the breast and nipples with the patient in the following positions:
➢ With the arms on the side laying on the thighs
relaxed
➢ Arms pressed against the hips and push inwards
(to tense pectoralis major): this creates tension on
the suspensory ligaments.
• Check for:
➢ Scars- small scars (lumpectomy)/ Large diagonal
scars (mastectomy)
➢ Size: varies enormously in different individuals.
➢ Symmetry: it is quite normal for there to be a
difference between the side. However, any
marked size difference of recent onset is likely to
be caused by significant pathology.
➢ Masses: note the size and position- look for
overlying skin changes.
➢ Skin changes: color, thickening of the skin and
unusually prominent pores which may accompany
lymphatic obstruction. The skin may be pulled in or puckered by an
underlying cancer.
o Redness (erythema) indicates local infection or superficial malignancy
o Thickening and prominent pores suggest a breast cancer.
o Puckering- underlying malignant mass

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SURGERY MK
o There may be edema caused by obstruction of skin lymphatics by cancer
cells, which is commonly referred to as peau d’orange.
- The skin has ridges or appears pitted like the skin of an orange (peau
d’orange) caused by a buildup of fluid and edema in the breast.
- Indicates inflammatory breast cancer
➢ Characteristics of the nipple
o Contours: look for changes such as masses, dimpling or flattening
- Flattening of the normally convex breast suggests cancer.
o Nipple retraction- congenital/ underlying tumor/ ductal ectasia
o Direction in which the nipples point
- Asymmetry of directions in which nipples point suggests an
underlying cancer
o Any rash, ulceration or any discharge
- Rash or ulceration (Scale) in Paget’s
disease of the breast.
➢ Nipple inversion
o Fixed or Recent flattening or depression of
the nipple suggests nipple retraction. A
retracted nipple may also be broadened and
thickened suggesting an underlying cancer.
➢ Arms over the head
➢ Arms over the head while leaning forward
• Placing the arms over the hips, head and leaning
forward helps to bring out dimpling or retraction
that may otherwise be invisible.
➢ Ask the patient to press her hands against her
hips to contract the pectoral muscles as well as
to place the hands over the head and lean
forward.
➢ Inspect the breast contours carefully in each
position. If the breasts are large or pendulous, it
may be useful to have the patient stand and lean
forward, supported by the back of the chair or
the examiner’s hands.
➢ Dimpling or retraction of the breast in these
positions suggests an underlying cancer. When
a cancer or its associated fibrous strands are

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SURGERY MK
attached to both the skin and the fascia overlying the pectoral muscles,
pectoral contraction can draw the skin inwards, causing dimpling.
➢ Occasionally, these signs may be associated with benign lesions such as
posttraumatic fat necrosis or mammy duct ectasia but they must always be
evaluated with great care.
PALPATION
• Palpation is best performed when the breast tissue is flattened, the patient should
thus be supine.
• Before examining the breast ask the patient if they have any nodes they can feel
or pain in any breast, if present this breast should be examined last.
➢ Always Examine the asymptomatic side first.
• A thorough examination will take 3 minutes for
each breast.
• Palpate all the four quadrants of the breast
including the axillary tail.
➢ Use the finger-pads of the second, third and
fourth fingers, keeping the fingers slightly
flexed.
➢ It is important to be systematic:
o Clock face method- examine each “hour”
of the breast
o Spiral method- start at the nipple and work outwards in a concentric
circular motion
➢ Palpate in small, concentric circles at each examining point, if possible
applying light, medium and deep pressure. You need to press more firmly to
reach the deeper tissues of a large breast. When pressing deeply on the breast
do not mistake a normal rib for a hard breast mass.
• Examine the breast tissue carefully for:
➢ Consistency of the tissue: normal consistency varies widely, depending in part
on the relative proportions of firmer glandular tissue and soft fat. Physiologic
nodularity may be present, increasing before menses. There may be a firm
transverse ridge of compressed tissue along the lower margin of the breast,
especially in large breasts. This is the normal inframammary ridge, not a
tumor.
➢ Tenderness, as in premenstrual fullness

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SURGERY MK
• If a mass is detected, ensure you complete a thorough examination of the
remaining breast tissue before examining the mass further.
• Palpate the axillary tail of the breast:
➢ Breast tissue often extends into the axilla and
is known as the axillary tail.
➢ The majority of breast cancers develop in the
upper outer quadrant so it’s essential this area
is examined thoroughly
• If the patient reports having nipple discharge, ask
them to squeeze the nipple to demonstrate this:
➢ Yellow/ green discharge- infection
➢ Greenish discharge-duct ectasia
➢ Bloody discharge- more suspicious of
malignancy e.g. papilloma.
• Repeat palpation on the other breast, asking the
patient to place their alternate hand behind their
head.
• For every lump the following should be mentioned
➢ Position/Location:
o which quadrant of the breast? (e.g. upper
outer quadrant)
o Using the clock face metaphor, what
“hour” on the clock is the mass located at?
E.g. 2 o’clock
o How far away from the nipple is the mass
located? E.g. 4cm.
➢ Size and shape:
o What are the approximate dimensions of
the mass? E.g. 2cm X 3cm
o What shape is the mass? E.g.
spherical/elongated/ irregular
➢ Consistency: smooth, firm, stony, rubbery
➢ Overlying skin changes: erythema/puckering

522
SURGERY MK
➢ Mobility:
o Does if move freely
o Does it move with overlying skin
o Does it move with pectoral contraction
➢ Fluctuance: hold the mass by its side then apply
pressure with another finger to the center of the
mass. If the mass is fluid filled e.g. cyst then
you should feel the sides bulging outwards
• Palpate each nipple, noting its elasticity.
AXILLA
• The axillary lymph nodes can now be palpated for
lymphadenopathy (malignancy/ infection):
➢ Have the patient sit on the edge of the bed
facing you.
➢ Support the patient’s arm on the side being
examined with your forearm.
➢ If you’re examining the right axilla, use your
right arm to support the patient’s (vice versa for
left).
➢ Palpate the axilla with your free hand covering
the lateral, anterior, posterior walls, central and
apex of the axilla.
• Other lymph nodes to palpate include: submental,
submandibular, pre-auricular, subauricular, post-
auricular, sub-occipital, cervical, supraclavicular,
infraclavicular and parasternal.
• To complete the examination
➢ Thank the patient and cover them up.
➢ Summarize finding.
➢ Suggest further assessments and investigations:
o Biopsy (FNA/ core biopsy)- to determine
histology.
o Ultrasound or Mammography depending on
the age
o Chest X-ray (if necessary)

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SURGERY MK
BREAST ANATOMY • The breast located vertically
between the 2nd and 6th rib in the
• The breast is a modified apocrine
mid-clavicular line and lies over the
sweat gland derived from ectoderm
pectoralis major, serratus anterior
as branching epithelial cords which
and external oblique muscles.
form lactiferous ducts.
• Horizontally it lies from side of
• About 15-20 lobes develop during
sternum to the mid-axillary line
puberty, each of which drains into a
two-thirds of the breast rests upon
single lactiferous duct.
pectoralis major and a third on the
• True secretory alveoli develop
serratus anterior.
during pregnancy and lactation
• At its lower medial quadrant, it
under the influence of estrogen,
rests on the external oblique
progesterone and prolactin.
aponeurosis, which separates it
• The mammary gland develops
from the rectus abdominis
embryologically as invaginations
• The breast lies in superficial fascia.
of surface ectoderm along two
The superficial fascia is divided
ventral lines (milk line/ intrauterine
into a superficial layer and a deep
milk ridge/anterior mammary
layer.
ridge)- which run from the axillae
to the vulva. • Below the superficial fascia lies the
retromammary space (within the
• Breast tissue (and pathology) can
loose areolar tissue), deep pectoral
develop anywhere along this milk
fascia and muscles (pectoralis
line- e.g. Supernumerary nipples.
major, serratus anterior, external
oblique) and the chest wall.
• Retromammary bursa/space:
located between deep layer of
superficial fascia and pectoral
(Deep) fascia allowing free
mobility of breast.
• The breast varies in size and shape
among different individuals but it is
characterized by fullness in the
lower area and ptosis or drooping,
which becomes pronounced with
increasing age.
Figure 213: Accessory nipple (Image
adapted from SRB’s Manual of Surgery)

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SURGERY MK
GROSS ANATOMY o When the axillary tail
• Grossly the breast consists of: enlarges it is often mistaken
➢ Nipple: located at 4th intercostal for a lipoma
space just below the
center/summit of the breast.
o It Contains circular and
longitudinal muscles to
make nipple stiff or flat.
o It is pierced by 15-20
lactiferous ducts.
o Each duct independently
opens into the nipple.
o It has rich sensory nerve
endings and contains
modified sweat and
sebaceous glands.
➢ Areola: Circular pigmented area
Figure 214: Axillary tail of Spence (Image
around the nipple. adapted from SRB’s Manual of Surgery)
o Rich in modified sebaceous
glands which enlarge during
pregnancy and lactation as
Montgomery tubercles.
They secrete oily lubricant
to nipple and areola.
o Areola and nipple do not
contain hair and fat beneath.
➢ Axillary tail of spence:
o This is a prolongation from
the outer part of the gland
which passes up to the level
of the third rib in the axilla
through a defect in the deep
fascia (Foramen of Langer)
where it is in direct contact Figure 215: Hypertrophy of axillary tail (Image
with the main lymph nodes adapted from SRB’s Manual of Surgery)
of the breast (Anterior
axillary nodes).

525
SURGERY MK
• The breast is anchored to the HISTOLOGY
overlying skin and to the • Breast tissue consists of stromal
underlying pectoral fascia by bands tissue and parenchyma.
of connective tissue called ligament • The breast is
of cooper. composed of acini
➢ Contraction of these strands in which make up
cancer due to malignant cell lobules, aggregation
invasion may cause dimpling of of which form the
the skin or attachment of the lobes of the gland.
growth to skin, which in turn • Approximately 10-
cannot be pinched off from the 100 alveoli (Acini)
lump. form lobules.
➢ If cancer grows along the
• Lobules make milk that drains via
ligament of cooper binding the
ducts to the nipple.
breast to the pectoral fascia, the
• The lobes are arranged in a
breast gets fixed to the
radiating fashion like the spokes of
pectoralis major. It then cannot
a wheel and converge on the nipple,
be moved along the long axis of
each lobe is drained by a lactiferous
the muscles.
duct.
• The functional unit of the breast
parenchyma is the terminal duct-
lobular unit.
• About 15-20 lobes develop during
puberty, each which drains into a
single lactiferous duct.
• True secretory alveoli develop
during pregnancy and lactation
under the influenced of:
➢ Estrogen-ductal proliferation
➢ Progesterone- glandular
proliferation
➢ Prolactin- milk production
Figure 216: Structure of the breast ➢ Oxytocin- milk secretion

526
SURGERY MK
the 2nd, 3rd and 4th intercostal
space-60%
➢ Lateral thoracic (from 2nd part of
axillary artery)-30%
➢ Lateral branch of the 2nd, 3rd and
4th intercostal arteries.
➢ Pectoral branches of
thoracoacromion artery
➢ Superior thoracic artery
• Venous drainage
➢ Superficial veins from the breast
characterized by their proximity
to the skin drain to axillary,
Figure 217: Histology of the breast at different internal mammary and
stages intercostal vessels.
• All the ducts and lobules are lined • Nerve innervation: anterior and
by 2 layers of epithelium: lateral cutaneous branches of 4th to
➢ Luminal cell layer: 6th intercostal nerves. (note: milk
o Alveolus- cuboidal (in rest) secretion under control of oxytocin
and columnar (in lactation) not by nerves). The nipple is
o Smaller duct- single layer of innervated by T4.
columnar epithelium • Lymphatics:
o Larger ducts- many layered ➢ Lymphatics drain
columnar predominantly into the axillary,
o Lactiferous duct- stratified internal mammary and central
squamous lymph nodes
➢ Myoepithelial cell layer ➢ Axillary lymph nodes drain
about 80% of the breast whilst
BLOOD SUPPLY, NERVE supraclavicular lymph nodes
INNERVATION AND drain 20%
LYMPHATICS ➢ Axillary lymph nodes include:
o Anterior group (Main
• Arterial supply:
drainage node)- along
➢ Perforating cutaneous branches
lateral thoracic
of internal mammary/thoracic
o Central/medial group (next
artery (from the subclavian) to
common)
o Lateral group

527
SURGERY MK
o Posterior group BREAST IMAGING:
o Apical group
➢ These can be divided into MAMMOGRAPHY
surgical (Berg’s) levels by the • This is a plain X-ray of soft tissue
pectoralis minor muscles of the breast using low voltage and
o Level 1: below and lateral to high ampearage X-rays.
the pectoralis minor • Two films are taken:
(anterior, lateral and ➢ Craniocaudal: from above
posterior) downward
o Level 2: behind/beneath the ➢ Mediolateral: from side to side
pectoralis minor muscle • Mammography is done in patients
(central) above 35 years old. In those below
o Level 3: above and medial 35 years an ultrasound is done
to the pectoralis minor • Findings:
(Apical) ➢ Microcalcifications: signify
malignancy. They are <0.5mm
pleomorphic/heterogenous,
grouped, fine, linear and
branching
➢ Soft tissue shadow may be
smooth, round/oval and regular
in benign conditions or irregular
carcinomas. Lobulated mass is
Figure 218: Levels of lymphatic drainage of the
also suggestive of carcinoma
breast (Image adapted from SRB’s Manual of ➢ Size and location of mass lesion
Surgery) ➢ Spiculations, duct distortion
➢ Spread restricted to level 1 (features of malignancy)
nodes carries better prognosis. ➢ Margin may be circumscribed
➢ Spread to level 2 has poor (benign lesion), microlobulated,
prognosis whilst spread to level obscure, ill-defined, spiculated
3 carries the worst prognosis. or stellate.

528
SURGERY MK
CONGENITAL
ANOMALIES
• Complete absence of breast
development (amazia) can occur
and is usually found in association
with lack of development of the
pectoralis major muscle (Poland’s
syndrome).
➢ Poland syndrome: Amazia,
Absence of sternal portion of
pectoralis major, male
predominance
• Other causes for absence of a breast
Figure 219: Mammography showing include:
calcified lactiferous duct with a benign lesion
(Image from SRB’s Manual of Surgery 2nd
➢ Inadvertent excision of the
Ed) breast bud (breast lumps should
not be excised in children)
BREAST PATHOLOGY ➢ Radiotherapy to the chest wall
• These include: in children
➢ Congenital anomalies • Accessory nipples (as discussed
➢ Inflammatory conditions earlier). Besides being curiosities,
➢ Benign tumors (fibroadenomas, these are also subject to the same
papillomas) and fibrocystic diseases that affect the normal
changes (nodular lesions, cysts breast.
and epithelial hyperplasia)
➢ Breast cancer INFLMMATORY
• Note: CONDITIONS
➢ Breast lump diagnosis varies MASTALGIA
with age • This is pain in the breast.
➢ Fibroadenomas are common in • Incidence: 45% (21% is severe)
young women • Mostly etiology is unknown and
➢ Cysts are common in women poorly understood.
aged 30-50 years • It is not usually associated with
➢ All new lumps in women over breast cancer.
50 years old are cancer until • Mastalgia is seen in patients on
proven otherwise antiretroviral therapy, caffeine,

529
SURGERY MK
tobacco, large pendulous breasts metabolism and improve
etc. transport across
• Breast pain can be divided into: intracellular membranes.
➢ Cyclical- 65% o In refractory cases drugs can
➢ Noncyclical- 30% be used:
➢ Chest pain-5% - Bromocriptine (2.5 mg
• Cyclical BD), Vitamin B6 & B12
➢ It is extremely common and analgesics
➢ Pain related to menstrual cycles. - Tamoxifen usually
When this discomfort is severe 20mg TID for 3 months
or prolonged beyond the usual (not supported by trials
3-5 days it requires intervention. yet)
➢ It is due to an increase in fluid • Non-cyclical
retention however diuretics ➢ Other causes of breast pain are
have no role in its management. peri-ductal mastitis,
➢ Cyclical mastalgia is usually malignancy, cervical root pain,
seen in ANDI (Aberration in musculoskeletal pain, previous
normal development and surgery, Tietze’s syndrome
involution) pathologies like (costochondritis)
fibrocystadenosis. ➢ It is unilateral, chronic, burning
➢ It Present in women of or dragging in nature, occurs
menstruating age group. bother in pre- and
➢ It is bilateral diffuse with postmenopausal age group.
“heavy feeling”. ➢ 5% of breast cancers present as
➢ Treatment: pain during first presentation.
o Reassurance that it is a ➢ Treatment:
physiological condition and o Identify cause
not associated with o Malignancy should be ruled
increased risk of breast out
cancer. o Avoid coffee and stress
o Evening primrose oil o Proper support to breast
1000mg for 3 months o NSAIDs can be given.
(containing free fatty acids • Tietze’s syndrome: costochondritis
particularly gamma-linoleic of 2nd costal cartilage, commonly
acid) have been shown to seen in females, mimics mastalgia.
improve cyclic mastalgia. It
is thought to influence lipid

530
SURGERY MK
MASTITIS ➢ Differential: paget’s disease of
• Inflammation of the breast tissue. the nipple
• Consists of ➢ Treatment: under cover of
➢ Subareolar mastitis antibiotics (Flucloxacillin) pus
➢ Intramammary mastitis is drained by making a
➢ Retromammary mastitis subareolar incision.
(submammary) • Intramammary mastitis
➢ Types:
o Lactational abscess of the
breast
o Non-lactational abscess of
the breast
➢ Lactational abscess
o Seen in lactating women.
o Occurs in 3% of
breastfeeding mother
usually up to 6 months of
lactation.
o Mode of infection:
- Bacteria (Staph aureus-
most common) enters
• Subareolar mastitis during sucking through
➢ Due to infection under areola cracked nipples
caused by cracks in the nipple or occasionally it can
areola. Results from an spread by
infection. hematogenous spread.
➢ Associated with duct ectasia-
causing formation of abscess,
sinus and fistula
➢ Common in non-lactating
women
➢ Clinical features:
o Red, inflamed, edematous
areola with a tender o Staph aureus causes clotting
swelling underneath. of milk in the blocked duct
o Nipple retraction may and multiply.
develop

531
SURGERY MK
o Duct initially gets blocked o Differential: inflammatory
by epithelial debris or by carcinoma of breast.
retracted nipple. Initially it o Treatment:
begins in one quadrant but - Antibiotics-
later involves entire breast. cephalosporins,
o Clinical features flucloxacillin, and
- Continuous throbbing amoxicillin,
breast pain and high - Repeated US guided
grade fever aspirations (avoids
- Diffuse redness, surgery and scars)
tenderness, warmness - Drainage under general
and brawny induration anesthesia, a counter
of breast. incision may be needed
- Purulent nipple - It is not advisable to
discharge wait till the formation of
- Entire breast may get abscess. Often takes
involved eventually very long time to heal
- Occasionally tender after surgery causing
fluctuant swelling distress to patient and
(10%) may be felt, surgeon.
ulceration and
discharge can occur at a
later period.
- Difficult to differential
initial stage of mastitis
(stage of cellulitis) from
stage of breast abscess
formation.
- When it is treated by
antibiotics without
incision and drainage
eventually it may get
organized to form a
non-tender, hard breast
lump with sterile pus
inside- stage of
antibioma formation.

532
SURGERY MK
o Complications: ➢ Investigations:
- Antibioma formation o CXR, FNAC, ESR
- Sinus formation, skin o Peripheral smear
necrosis, fistula o U/S of breast and chest wall
formation o Often CT scan chest may be
- Recurrent infection, needed
bacteremia, septicemia. ➢ Treatment:
o Suppression of lactation if o Treat cause
often required by giving o Drainage through
Bromocyptine 2.5 mg BD submammary/retromammar
for 2 weeks y incision.
➢ Non-lactational abscess
ANTIBIOMA
o Common in duct ectasia and
• If intramammary mastitis is not
periareolar infection
drained but only treated by
o Common organisms:
antibiotics, pus localizes and
bacteroides, anaerobic
becomes sterile (flaques) with a
streptococci, enterococci
thick fibrous tissue cover and it is
and gram negative
called as antibioma.
organisms.
• Clinical features:
o Commonly recurrent with
➢ Previous history of mastitis
tender swelling under the
treated with antibiotics
areola
➢ Swelling which is painless,
o Treatment:
smooth, nontender, hard, fixed
- Antibiotics
to breast tissue without
- Repeated aspirations
involving the pectorals and
- Drainage and later cone
chest wall.
excision of the duct is
done • Investigations
➢ FNAC
• Retromammary mastitis
➢ Mammography
➢ Due to tuberculosis of the
➢ U/S breast
intercostal lymph nodes.
o Other causes: TB of ribs, • Treatment: excision (submammary
suppuration of intercostal incision). Later antibiotics are
lymph nodes, empyema given. It should be sent for
necessitans, infected histology.
hematoma.
➢ Breast is normal.

533
SURGERY MK
TUBERCULOSIS OF THE • Investigations:
BREAST ➢ FNAC
• Rare, infection reaches through ➢ Frozen section biopsy is useful
blood or retrograde lymphatic to differentiate from carcinoma
spread from lymph nodes of axilla. ➢ Excision biopsy
• Associated with active pulmonary • Treatment:
tuberculosis ➢ Antituberculous drugs (INH,
• Common in lactation rifampicin, ethambutol,
• Nipple and areola are not pyrazinamide)
commonly involved. ➢ Drainage of cold abscess
• Presents as a swelling in the breast • Note: mastectomy is not done
with cold abscess, sinuses and a MAMMARY DUCT ECTASIA
typical bluish appearance of (PLASMA CELL MASTITIS)
surrounding skin with matted • This is dilatation of lactiferous
lymph nodes in the ipsilateral ducts due to myoepithelial
axilla. relaxation of duct wall with
• Lump- irregular ill-defined, peau periductal mastitis.
d’orange, discharge, sinus, matted • Also known as ‘plasma cell
axillary nodes often with sinus are mastitis’ as periductal
the features. inflammation contains plasma
cells.
• Commonly many ducts are
involved.
• Hormonally induced myoepithelial
relaxation with poor ductal
absorption of secretions and
desquamated cells causing
obstruction are the probable other
causes and features.
• It is an uncommon condition
usually encountered in parous
women between 40 and 60 years of
Figure 220: Tuberculosis of breast showing
age.
undermined lesion • Clinical features
➢ Greenish discharge or creamy
• Differential: Carcinoma breast paste like nipple discharge

534
SURGERY MK
➢ Indurate mass under the areolar ➢ Capillary ooze causes
which is often tender triglyceride in the fat to
• Differential: carcinoma of breast dissociate into fatty acids.
• Investigations: ➢ It combines with calcium from
➢ Discharge study: FNAC the blood resulting in
➢ Mammography saponification which causes
inflammatory reaction and later
presents as a non-progressive
swelling in the breast.
• Clinical features:
➢ Painless swelling in the breast
which is smooth, hard,
nontender and adherent to breast
tissue
➢ Bilateral and multifocal
Figure 221: Duct ectasia ➢ It is nonprogressive,
nonregressive.
• Treatment:
➢ Nipple retraction at a later stage.
➢ Stop smoking
Slit like retraction of nipple due
➢ Cone excision of involved
to fibrosis occurs
major duct (Adair-Hadfield
➢ Abscess and fistula formation
operation)
➢ Common in smokers- in relation
➢ Antibiotics
of arterial pathology
➢ Melhem Novel modified breast
➢ Common also in multiple
ductal system excision
pregnancies, perimenopausal
TRAUMATIC FAT NECROSIS age, hyperprolactin status
• This is a fibrous scar in the breast ➢ May present with mastalgia
tissue caused by injury, hematoma ➢ Axillary nodes may be palpable
and necrosis of breast fat with as nonspecific
subsequent scarring. ➢ Secondary bacterial infection
• There is history of breast trauma in (anaerobic) is common.
50% of cases. • Investigations
• True is due to either direct or ➢ FNAC: chalky fluid with fat
indirect. globules
• There may be associated superficial ➢ Histology: periductal cellular
ecchymoses. infiltrates and fibrosis
• Pathogenesis:

535
SURGERY MK
➢ Mammography to rule out ➢ Use of spironolactone
malignancy • Treatment involves addressing the
• Differential diagnosis: carcinoma underlying cause however in severe
breast cases is by excision of breast tissue.
• Treatment: surgical excision to
BREAST CYST
exclude malignancy.
• These are fluid filled cavities lined
BENIGN TUMORS AND by epithelium.
• Incidence: 1 in 14 females, above
FIBROCYSTIC
the age of 35 up to menopause (30-
CHANGES 40s).
• These are due to ➢ Uncommon after menopause.
Aberrations/abnormalities of ➢ Hormone replacement can cause
normal development and involution cyst formation in old women.
of the breast (ANDI) pathologies. • They arise from destruction and
• The term ANDI is broad and covers dilatation of breast lobules and
benign conditions of the breast, terminal ductules. It is due to
many of which have overlapping nonintegrated stromal and
features. epithelial involution.
• ANDI are common in younger • Cysts may be microscopic or
premenopausal women and often macroscopic.
cause considerable anxiety. • They contain straw colored, green
• Any breast lump should be colored or opaque fluid.
evaluated by triple assessment for • Cyst size varies with menstruation
risk of malignancy whatever the due to influence of ovarian
likely diagnosis. hormones.
GYNECOMASTIA • They can present as:
• This is the presence of breasts in the ➢ Multiple (50%) and often
male resembling those of the bilateral.
sexually mature female. ➢ Tender
• It is usually physiological but often • Cysts can be recurrent (50%).
needs to be investigated for • On examination they are smooth,
hormonal causes: soft, fluctuant often
➢ Estrogen or steroid therapy transilluminating well-localised
➢ Liver disease swellings.
➢ Pituitary gland tumor • Investigations:
➢ Testicular tumor ➢ U/S of breast

536
SURGERY MK

FIBROCYSTIC CHANGE
• Due to Aberration of Normal
Development and Involution
(ANDI) of normal breast tissue.
Figure 222: Ultrasound showing a breast
cyst
• Presently called cyclical mastalgia
with nodularity.
➢ FNAC • The term fibroadneosis refers to a
➢ Mammography to rule out spectrum of conditions that
associated carcinoma commonly present as lumpiness or
• Differential diagnosis: discomfort on a background of
➢ Bloodgood cyst generally lumpy breasts.
➢ Hematoma cystic necrosis in a • It is an estrogen dependent
carcinoma condition however, Estrogenic
➢ Brodie’s disease (phyllodes) therapy and oral contraceptives do
➢ Galactocele not seem to increase the incidence
➢ Lymph cyst of these alterations and oral
➢ Hydatid cyst contraceptives may in, fact
• Treatment: decrease the risk.
➢ Reassurance • It is due to development of fibrosis
➢ Aspiration for 2 times and cysts in the breast.
➢ Surgical excision is done if cyst • It is the most common breast
recurs after two aspirations or if disease (pre-menopausal) and
there is bloody discharge or occurs in the upper outer quadrant.
residual mass if felt after The changes tend to arise during
aspiration. reproductive age and are most
likely a consequence of the cyclic
breast changes that occur normally
in the menstrual cycle.

537
SURGERY MK
• It is an exaggerated response of overlying myoepithelial
breast stroma and epithelium to cells). Epithelial
hormones and growth factors. hyperplasia is recognized by
• It is rare in the presence of more than 2
nulliparous/ovulating/oral cell layers. It ranges from
contraceptive pill taking women. mild and orderly to atypical
• Breast involution causes changes at hyperplasia (resembling
the microscopic level including carcinoma in situ)
fibrosis (increase in fibrous tissue), o Sclerosing Adenosis:
adenosis (increase in glandular mimics carcinoma. Lesions
elements) and apocrine changes contain marked intralobular
(the normal epithelium lining the fibrosis and proliferation of
ducts becomes sweat gland-type small ductules and acini
epithelium). o Papillomatosis-within the
• In addition, minimal hyperplasia of duct, often with apocrine
the epithelial cells lining the ducts metaplasia
occurs and small breast cysts may • Clinical presentation:
develop ➢ Presents during menstruating
• Stages: age group (35-50 years) as a
➢ Stage I-Stromal proliferation or bilateral, painful, diffuse,
hyperplasia granular, tender, swelling which
➢ Stage II- Adenosis (increased is better felt with palpating
glands) fingers (lumpy breast).
➢ Stage III- cyst formation. Cysts ➢ Common in upper outer
have a blue-dome appearance on quadrant.
gross exam. ➢ Pain and tenderness are more
• Microscopic changes include: just prior to menstruation
➢ Non-proliferative changes (cyclical mastalgia).
(Common) ➢ It subsides during pregnancy,
o Stromal fibrosis with lactation and after menopause.
dilation of ducts ➢ Discharge from the nipple when
o Microcyst formation present will be serous or
➢ Proliferative changes occasionally greenish.
o Epitheliosis (in ducts and • Investigation
acini): normal ducts and ➢ FNAC (Epitheliosis, when
lobules are lined by 2 layers florid is undoubtedly
of cells (luminal cells premalignant)

538
SURGERY MK
➢ Ultrasound hyperplasia and apocrine
➢ Mammography metaplasia
• Treatment: ➢ Slightly increased risk (1.5-2
➢ Conservative (preferred) times)- moderate to florid
o Reassurance, avoid hyperplasia (without atypia),
caffeine, chocolate, salt Ductal papillomatosis and
o Medical drugs: indicated Sclerosing adenosis
when fibroadenosis is not ➢ Significant risk (5 times risk):
increasing in size, no nipple Atypical hyperplasia whether
discharge especially blood, ductular or lobular
no psychological effect • Fibrocystic change can only be
➢ Surgery distinguished from cancer through
o Subcutaneous mastectomy biopsy and histologic examination.
(preserves nipple, areola • Proliferative fibrocystic changes
and skin) with prosthesis usually are bilateral and multifocal
placement – only in severe, and are associated with increased
persistent disease risk of subsequent carcinoma in
o Excision of the cyst or both breasts.
localized excision of the
FIBROADENOMA
diseased tissue
• This is a benign encapsulated tumor
o Indications:
commonly occurring in young
- Intractable pain
females aged 20-30.
- Florid epitheliosis on
FNAC • Presently it is considered as
- Blood good cyst hyperplasia of a single lobule of the
- Persistent bloody beast (classified under ANDI)
discharge • It is the most common benign
- Psychological reason tumor of the breast below the age of
• Note: this condition is benign but 30 years in females.
some fibrocystic-related changes ➢ Incidence: 15% of palpable
are associated with an increased breast lumps
risk for invasive carcinoma ➢ It is common in blacks.
(increased risk applies to both ➢ It is bilateral in 20% of cases
breast) and multiple in 20% of cases.
➢ Minimal or no increased risk: • It is due to an aberration in normal
Fibrosis, cystic changes, mild development (AND) of a lobule,
although it shows similar hormonal

539
SURGERY MK
activities of normal breast like o Pericanalicular- small and
lactation, perimenopausal hard- mainly fibrous.
involution. Stroma with normal duct.
• Fibroadenoma does not turn into • Juvenile fibroadenoma:
malignancy. ➢ Occurs in adolescent girls.
➢ 30% of fibroadenomas may ➢ Rapid growth with stromal and
disappear or reduce in size in 2- epithelial hyperplasia
4 years. ➢ Does not show any alteration in
➢ 10-15% will increase in size stromal epithelial balance or
progressively. They do not cellular atypia or periductal
occur after menopause unless cellular concentration.
women are on hormones. ➢ Clinically mimics phyllodes
• Presentation: tumor but does not turn into a
➢ Painless swelling in one of the phyllodes tumor or a carcinoma.
quadrants
➢ Smooth, firm, nontender
➢ Well-localized and moves freely
within the breast tissue (mouse
in the breast)
➢ Axillary lymph nodes are not
enlarged
• Types:
➢ Gross
o Soft-common after 30 Figure 223: Large fibroadenoma left breast
years, more cellular, often in a 14-year-old female
bilateral
o Hard- common below 30 • Complex fibroadenoma:
years, more fibrous ➢ Occurs in older age group
o Giant (>5cm in size) ➢ Typical fibroadenoma with
common in Africa fibrocystic changes (apocrine
➢ Microscopic: metaplasia, cyst formation,
o Intracanalicular- large and sclerosing adenosis)
soft- mainly cellular. ➢ 15% of proven fibroadenomas
Stroma with distorted duct. are complex
It carries the potential to ➢ Occasionally it may turn into
undergo malignant malignancy unlike usual
transformation. fibroadenomas.

540
SURGERY MK
➢ Core biopsy is needed to
confirm the condition.
• Investigations:
➢ Mammography (well localized
smooth regular shadow)
➢ FNAC
➢ Ultrasound (to confirm solid
nature)

Figure 225: Incisions for excision of

complex fibroadenoma

➢ Fibroadenoma which is small

(<3cm)/ single/ age<30 years
can be left alone with regular
Figure 224: Fibroadenoma on ultrasound follow-up with U/S at 6 monthly
intervals. But anxiousness of
• Treatment:
patient and parents find difficult
➢ Excision through a for this conservative approach.
circumareolar incision
➢ Indications for surgery
(Webster’s) or Submammary
o Size> 3cm
incision (Galliard Thomas
o Multiple
incision) under general o Giant type (usually >5cm)
anesthesia.
o Recurrence
o Cosmesis
o Complex type

541
SURGERY MK
HYPERPLASIA OF THE BREAST ➢ Vascular stalk is present
• Asymptomatic and is usually usually.
discovered by chance. • They often project out like a
• There is an increased in the number pedunculated mass.
of epithelial cells of the lobules and • Rarely a cystic soft swelling may be
ducts. present underneath which is
• Types: probably due to obstruction of the
a. Ductal hyperplasia duct by papilloma.
b. Lobular hyperplasia • Duct papilloma is the most
• Grading based on microscopy is as: common cause of bloody discharge
(1) Mild from nipple.
(2) Moderate • It is usually single, from a single
(3) Florid (more extensive) lactiferous duct.
• This is associated with natural • It blocks the duct causing ductal
changes especially in women >35 dilatation.
years. • Presentation:
ATYPICAL HYPERPLASIA ➢ Papilliferous swelling
(projection) usually seen near
• Abnormal-appearing cells (pattern
the nipple orifice.
or shape)
• Types:
a. Atypical ductal hyperplasia
b. Atypical ductal lobular
hyperplasia
• Sometimes discovered by a breast
biopsy.
• There is increased risk of
developing cancer in atypical
ductal hyperplasia.
DUCT PAPILLOMA
Figure 226: Ductal papilloma
• Duct papilloma are epithelium-
lined-true-polyps of breast ➢ Blood stained discharge from
lactiferous ducts. the nipple. Serosanguinous
➢ They are usually <1cm in size discharge can also occur.
often with a small lump under ➢ Single papilloma is not
areola. But can attain large size. premalignant but multiple

542
SURGERY MK
papillomas in many ducts can be excised with part of the
premalignant. areolar skin.
• Peripheral papilloma should be • Note:
differentiated from invasive ➢ Intraductal papillary carcinoma
papillary carcinoma arises usually not from a
preexisting duct papilloma but
as de novo
➢ Papillomatosis is hyperplasia of
the duct lining, filling the duct
like a polyp without a
pedicle/stalk (not a true polyp),
it is not duct papilloma but part
of fibrocystadenosis.
➢ Axillary nodes are not involved.
Figure 227: Papilloma breast which is large.
Usually it is small intraductal ADENOSIS OF THE BREAST
• Noncancerous enlargement of the
• Types: breast lobules.
➢ Subareolar- common • Adenosis can look like breast
➢ Peripheral- occasional cancer on mammograms, so biopsy
➢ Solitary- common may be needed to rule out breast
➢ Multiple cancer.
➢ Unilateral- common
➢ Bilateral PHYLLODES TUMOR
• Investigation: • Also known as cystosarcoma
➢ Discharge study (FNAC) phyllodes/ serocystic disease of
➢ Injection of contrast into the Brodie.
duct (Ductogram) • They are not simply giant
➢ Mammography may show dense fibroadenoma.
lesion under the areola • Show wide spectrum of activity
• Treatment: ranging from almost benign (85%)
➢ Microdochectomy: probed to locally aggressive and
lactiferous duct is opened and sometimes metastatic tumor (15%).
the papilloma is excised using • They occur in premenopausal
tennis racquet incision. women (30-50 years).
o Probing of lactiferous duct • Presentation:
is done up to 5cm deep and ➢ Unilateral

543
SURGERY MK
➢ Grow rapidly to attain a large • Treatment:
size with bosselated surface. ➢ Excision or subcutaneous
➢ Swelling is smooth, non-tender, mastectomy
soft, fluctuant with necrosis of ➢ If malignant (Sarcoma) total
skin over the summit due to mastectomy is indicated.
pressure.
GALACTORRHOEA
➢ Differs from carcinoma
• It is a secretion of milk not related
because:
to pregnancy or lactation.
o Skin over breast is
stretched, red and with • It is not a symptom of breast cancer.
dilated veins. • It is always bilateral.
o Tumor is warmer, not fixed ➢ Primary galactorrhoea: Stress
to skin or deeper muscles or and other factor. It is
chest wall. physiological in puberty or
o Nipple retraction is absent. menopause. Reassurance is the
o Lymph nodes are usually treatment
not involved ➢ Secondary galactorrhoea:
o Dopamine receptor
antagonists: haloperidol,
methyldopa,
chlorpromazine,
metoclopramide or by
hyperprolactinaemia due to
pituitary tumors. It
enhances the prolactin
activity.
o Hypothyroidism
o Drugs like oral
contraceptives, atenolol,
Figure 228: Phyllodes tumor clonidine, ranitidine
o Ectopic prolactin secreting
• Recurrence is common. tumors usually from lungs
• Investigations: (bronchogenic carcinoma)
➢ U/S o Chronic renal failure
➢ FNAC, core biopsy • Management
➢ Mammography ➢ Estimation of serum prolactin,
➢ Chest X-ray CT chest in T3, T4, TSH, CT/MRI head.
malignancy to seen secondaries

544
SURGERY MK
➢ Bromocriptine therapy • Early menarche/ late menopause:
➢ Treatment of cause. Causative increased duration of estrogen
drug should be stopped and exposure.
different drugs should be used • Genetics: Presence of a 1st degree
for needed condition relative (mother, sister, daughter)-
• Note: Witch’s milk is secretion of incidence is 2-5%.
milk in both male and infants due to ➢ BRCA1, BRCA2, P53, HNPCC
maternal hormonal effects in fetus. and AT genes are associated
It lasts up to 3 weeks after child • Atypical hyperplasia (5 times
birth. increased risk).
GALACTOCELE MODIFIABLE
• Arises during lactation from cystic • Obesity: adipose tissue can convert
dilation of an obstructed duct. Androgen to estrone (a type of
estrogen) so this increases the risk
BREAST CANCER of breast cancer.
• Breast cancer is the most common • Diet low with phytoestrogens and
carcinoma in women by incidence high alcohol intake have high risk
(excluding skin). of breast cancer. Vitamin C reduces
• Breast cancer is the second most the risk.
common cause of cancer mortality. • Null-parity and multiparity both
(Most common being lung cancer). increase risk
RISK FACTORS • Use of estrogen-based
• These can be classified as contraceptive increases the risk
➢ Modifiable
➢ Non-modifiable
NON-MODIFIABLE
• Gender: it is more common in
females (99%) than in males (1%)
• Age: Breast cancer presents most
commonly in a postmenopausal
female but it can also present in
younger females (this is suggestive
of hereditary causes).

545
SURGERY MK

Figure 229: Risk factor classification for breast cancer

• Early child-bearing and o p53 gene is also found on

breastfeeding reduces the chances Chromosome 17
of malignancy. ➢ BRCA 2 is found on the long
➢ Early first child birth reduces arm of chromosome 13.
the risk. Associated with breast cancer in
➢ Late first child birth after 35 males.
years increases the risk. o Retinoblastoma gene is also
• Carcinoma in one breast increases found on chromosome 13.
the risk of developing carcinoma on • Occasionally mutation of BRCA 3
opposite breast by 3-4 times. and p53 suppressor gene is also
Incidence of bilateral carcinoma is involve/d.
2%.
CLASSIFICATION OF BREAST
• Mutation of tumor suppressor CARCINOMA
genes BRCA1/ BRCA 2 is thought • Recall the functional unit of the
to be involved with high risk of breast is the terminal duct-lobular
breast carcinoma. unit.
➢ BRCA 1 mutation is having
• Breast carcinoma arising from
more risk (35-45%) than BRCA
lactiferous ducts is called as ductal
2 mutation.
carcinoma.
➢ BRCA 1 is found on the long
• Breast carcinoma arising from
arm of chromosome 17. It is
lobules is called as lobular
seen in breast (medullary
carcinoma.
carcinoma) and ovarian
• In-situ-carcinoma is pre-invasive
carcinoma (serous carcinoma)
carcinoma which has not breached

546
SURGERY MK
the epithelial basement membrane. • The carcinoma can also arise from
It may either be: mixed connective tissue and
➢ Ductal Carcinoma In Situ epithelial tissue:
(DCIS)- 90% ➢ Phyllodes, angiosarcoma,
➢ Lobular carcinoma in Situ carcinosarcoma
(LCIS)-10% • The degree of differentiation of the
• Invasive carcinoma can occur tumor is usually described using 3
eventually; this can either be: grades:
➢ Invasive ductal carcinoma (most ➢ Well-differentiated (grade 1)
common type-80%)- has many ➢ Moderately-differentiated
subtypes (grade 2)
➢ Invasive lobular carcinoma ➢ Poorly-differentiated (grade 3)
(multifocal and often bilateral)

Figure 230: Classification of breast cancer

DUCTAL CARCINOMA IN-SITU mass- does not produce a mass

(DCIS) because it is limited to the ducts).
• Malignant proliferation of cells in • Comedo type has high grade cells
ducts. with necrosis and dystrophic
• No invasion of basement calcification in center of ducts.
membrane. ➢ Note: calcification is not always
• Detected as calcification on indicative of breast cancer.
mammography (not detected as a Calcification can also be seen
in:

547
SURGERY MK
o Sclerosing adenosis
(fibrocystic change)
o Traumatic fat necrosis- due
to saponification of fats

Figure 232: Paget's disease of Nipple

• It is Almost always associated with
an underlying carcinoma.
• Recall: In extra-mammary Paget’s
disease (malignant cells within
Figure 231: Ductal carcinoma in-situ, epidermis of Vulva) there is no
comedo type
underlying carcinoma.
• Biopsy of calcification is often • Microscopic appearance:
necessary to distinguish between ➢ Large, ovoid cells with
benign and malignant conditions. abundant clear pale staining
cytoplasm in the malphighian
PAGET DISEASE OF NIPPLE
layer of the epidermis.
• This is DCIS that has extended up
the ducts to the skin of the nipple.
• It presents as nipple ulceration and
erythema.
• It presents as an eczema-like
condition of the nipple and areola
which persists despite local
treatment. The nipple is eroded
slowly and eventually disappears.
• If left, the underlying carcinoma
will sooner or later become more
clinically evident. Figure 233: Paget's disease of the
• Nipple eczema should be biopsied nipple, Microscopic appearance
if there is any doubt about its
causes.

548
SURGERY MK
INVASIVE DUCTAL CARCINOMA distinguishes them from normal
• Classically forms duct-like breast tissue which has 2 types of
structures. epithelia)
• Most common type of invasive • Good Prognosis.
carcinoma in the breast, accounting
for more than 80% of cases.
• Presents as a mass detected by
physical examination or by
mammography
➢ Clinically detected masses are
usually 2cm or greater.
➢ Mammographically detected
masses are usually 1cm or
greater.
➢ Advanced tumors may result in Figure 234: Tumor cells in a
dimpling of skin or retraction of desmoplastic stroma (invasive ductal
nipple. carcinoma-tubular subtype)
o Recall that retraction of
• Features that help to determine
nipple can also be due to
malignancy:
inflammatory conditions
➢ Desmoplastic stroma
• Biopsy usually shows duct like
➢ Absence of 2 lining cell types:
structures in a desmoplastic stroma.
epithelial cells and
➢ Desmoplastic stroma:
myoepithelial cells
connective tissue growing with
the tumor. Connective tissue is MUCINOUS CARCINOMA
there to support the tumor • Characterized by carcinoma with
• Important subtypes of invasive abundant extracellular mucin
ductal carcinoma include: (‘tumor cells floating in a mucus
➢ Tubular carcinoma pool’)
➢ Mucinous carcinoma
➢ Medullary carcinoma
➢ Inflammatory carcinoma
TUBULAR CARCINOMA
• Characterized by well
differentiated tubules that lack
myoepithelial cells (which

549
SURGERY MK

Figure 235: Mucinous breast cancer Figure 236: Inflammatory carcinoma

(invasive ductal carcinoma)
• Presents classically as:
• Tends to occur in older women ➢ Inflamed
(average age is 70 years) ➢ Swollen breast (tumor cells
• Relatively good prognosis block drainage of lymphatics)
MEDULLARY CARCINOMA with no discrete mass, can be
mistake for acute mastitis (rule
• Characterized by large, high grade
out mastitis- give antibiotics and
cells growing in sheets with
review in 5-10 days)
associated lymphocytes and plasma
cells.
• Grows as a well-circumscribed
mass that can mimic fibroadenoma
on mammography.
• Relatively good prognosis.
• Increased incidence in BRCA 1
carriers.
INFLAMMATORY CARCINOMA
• Characterized by carcinoma in
dermal lymphatics.
Figure 237: Peau d'orange,
characteristic of inflammatory
carcinoma
• Poor prognosis

550
SURGERY MK
LOBULAR CARCINOMA INSITU CLINICAL PRESENTATION
• Malignant proliferation of cells in • Although any portion of the breast
lobules with no invasion of the including the axillary tail may be
basement membrane. involved, breast cancer is found
• LCIS does not produce a mass or most frequently in the upper outer
calcification and is usually quadrant because this is where most
discovered incidentally on biopsy. breast tissue is found.
• Characterized by dyscohesive cells • Cutaneous manifestations:
lacking E-cadherin protein. ➢ Peau d’orange: due to
• Often multifocal and bilateral obstruction of dermal
• Treatment is tamoxifen (to reduce lymphatics, openings of the
the risk of subsequent carcinoma) sebaceous glands and hair
and close follow up, low risk of follicles get buried in edema
progression to invasive carcinoma. giving rise to orange peel
appearance.
INVASIVE LOBULAR CARCINOMA ➢ Dimpling of skin: due to
• Characterized by cells growing in a infiltration of ligament of
single-file. Cooper
• Cells may exhibit signet-ring ➢ Retraction of nipple: due to
morphology. infiltration of lactiferous duct
➢ Ulceration, discharge from the
nipple and areola
➢ Skin ulceration and fungation
➢ Cancer-en-cuirasse: skin over
the chest wall and breast is
studded with cancer nodules.
appearing like an armour coat.
➢ Tethering to skin
• Most breast cancers will present as
a hard lump which may be
associated with in-drawing of the
Figure 238: Invasive lobular nipple.
carcinoma • Spread to deeper plane
➢ Into pectoralis major muscle (is
confirmed by observing the
restricted mobility of the

551
SURGERY MK
swelling while contracting the ➢ Histology/ Cytology:
pectoralis muscle) o FNAC (Fine Needle
➢ Into latissimus dorsi muscle Aspiration and Cytology)
(extending the shoulder against - Advantages: least
resistance) painful, can be done on
➢ Into serratus anterior (by outpatient basis, reliable
pushing the wall with hands and cheaper
without flexing the elbow)
➢ Into chest wall (breast will not
fall forward when leaning
forward and while raising the
arms above the shoulder, breast
will not move upwards as it is
fixed to the chest wall)
DIAGNOSIS
• This is done by triple assessment:
➢ History and physical
examination
➢ Diagnostic imaging
o Mammogram (for females Figure 239: FNAC vs Mammography
above 35 years): shows o Core needle biopsy for
irregular, speculated, histology
radiopaque mass with
micro-calcification SENTINEL LYMPH NODE
o Ultrasound (for females BIOSPY
below 35)- solid mass or • This procedure consists of injecting
cyst a vital blue dye or radioactive sulfur
o Reasons for using US in colloid of both around the tumor.
patients below 35: • The surgeon often waits 5 minutes
- Breast density in the case of the dye and a few
difference hours in the case of colloid and
- Technical problems dissects the axilla removing only a
(small breast) few nodes that either stained blue or
o X-ray: metastasis radioactive.

552
SURGERY MK
• The principle behind this is that the ➢ M- metastasis
first nodes that drain the dye are the o M0- no distant metastasis
most likely to first drain the tumor. o M1- Metastasis present
• Morbidity is significantly (including ipsilateral
decreased as compared to a full supraclavicular lymph
axillary node dissection and in nodes)
experienced hands, the procedure is ➢ N- metastasis to local lymph
close to 100% accurate in correctly nodes
describing the presence or absence o N0- no palpable axillary
of tumor in the axilla. lymphadenopathy
o N1- mobile palpable
PROGNOSIS OF BREAST
axillary lymphadenopathy
CANCER
o N2- fixed palpable axillary
• Based on the TMN staging lymphadenopathy
➢ T-tumor size o N3- palpable
o T0- no palpable tumor supraclavicular
o Tis- tumor in situ lymphadenopathy
o T1- tumor 2cm or less in its
• Metastasis is most important factor
greatest dimensions, not
(mets out of axilla= poor prognosis)
fixed/tethering
but because most patients do not
o T2- tumor 2-5cm in its
present with this, spread to axillary
greatest dimensions, nipple
lymph nodes becomes the most
retraction or tethering
useful factor.
o T3- tumor more than 5cm
• Sentinel node biopsy is used to
(5-10cm) in its greatest
assess axillary lymph nodes (based
dimensions, infiltration or
on the principle that axillary lymph
ulceration
nodes drain in levels- 1, 2 and 3)
o T4- any size invading skin
➢ If level 1 lymph nodes are
or chest wall- not including
affected there is a chance that
pectoral muscles (10cm),
the tumor has spread to other
ulceration greater than the
lymph nodes so these other
distance of the lump, skin
nodes can also be removed
edema or skin ulceration or
➢ If level 1 lymph nodes are not
satellite skin nodules
affected then the tumor has
confined to the same breast
likely not spread and no need to
or inflammatory carcinoma
remove the axillary lymph
nodes.

553
SURGERY MK
STAGING OF BREAST CACNER • When cell is negative for all it is
STAGE TUMOR NODES METS termed ‘Triple negative’ and carries
0 Tis N0 M0 a poor prognosis.
I T1 N0 M0 • African American women have
IIA T0, 1 N1 MO increased propensity to develop
T2 N0 MO triple negative carcinoma.
IIB T2 N1 MO
T3 N0 MO HEREDITARY BREAST
IIIA T0,1, 2 N2 MO CANCER
T3 N1, N2 MO • 10% of all breast cancer.
IIIB T4 N1, 2 MO • Features suggestive of hereditary
Any T N3 M1 breast cancer:
IV Any T Any N M1 ➢ Multiple 1st degree relative with
cancer
PROGNOSTIC AND ➢ Tumor at premenopausal age
PREDICTIVE FACTORS ➢ Multiple tumors.
• Most important factors are: NOTTINGHAM PROGNOSTIC
➢ ER: estrogen receptor INDEX
➢ PR: progesterone receptor • This is used to determine prognosis
➢ HER2/neu gene amplification following surgery for breast cancer.
• ER and PR associated with • It is calculated using 3 pathological
response to anti-estrogenic agents criteria:
(tamoxifen) ➢ Size of the lesion (S)
• HER2/neu gene amplification is ➢ Number of involved lymph
associated with response to nodes (N)
trastuzumab o 0 Nodes= 1
• Recall HER2/neu is a cell surface o 1-3 Nodes= 2
growth factor receptor, if a cell has o >3 Nodes=3
excess HER2/neu receptor through ➢ Grade of the tumor (G)
gene amplification there is growth o Grade 1= 1
and proliferation cells predisposing o Grade 2= 2
an individual to malignancy. o Grade 3=3
• An individual can thus be positive • The index is calculated using this
or negative for ER, PR and/or formula:
HER2/neu gene amplification. ➢ NPI= [0.2 x S] + N + G
• Prognosis:

554
SURGERY MK
➢ 93% 5-year survival • Lymphatic metastasis
o >/=2.0 to </=2.4 ➢ Occurs primarily to axillary and
➢ 85% 5-year survival internal mammary lymph nodes.
o >2.4 to </=3.4 ➢ Tumors in the posterior 1/3 of
➢ 70% 5-year survival the beast are more likely to drain
o >3.4 to </=5.4 to the internal mammary nodes.
➢ 50% 5-year survival ➢ Involvement of supraclavicular
o >5.4 nodes and any contralateral
MALE BREAST CANCER lymph nodes represents
advanced disease.
• Rare (1%)
• Presents as a subareolar mass under
• Spread by bloodstream
the nipple in older males (majority
(hematogenous)
of breast tissue in males is in the
➢ Often metastasizes to bone.
subareolar region), may produce
➢ Frequent sites include lumbar
nipple discharge (tumor developing
vertebrae, femur, thoracic
underneath nipple).
vertebrae, ribs and skull.
• Usually invasive ductal carcinoma
➢ Deposits are generally
because in the male breast there is
osteolytic.
development of terminal duct but
➢ Metastasis may also commonly
there is no proper development of
occur to the liver, lungs and
lobules.
brain and occasionally the
• Association with BRCA 2 mutation
adrenals and ovaries.
and Klinefelter syndrome.
TREATMENT OF BREAST
SPREAD OF BREAST CANCER
CANCER
• Local spread:
• Treatment is stage dependent.
➢ Tumor increases in size and
• Primary aim is to remove tumor.
invades other portions of the
• Management is usually a combined
breast.
approach:
➢ It tends to involve the skin and
➢ Medical therapy:
to penetrate the pectoral muscles
o Radiotherapy
and even the chest wall if
o Hormone therapy
diagnosed late.
o Chemotherapy
➢ Surgical therapy
SURGICAL THERAPY
• Indications for mastectomy:

555
SURGERY MK
➢ Large tumor/breast size all motor nerves and muscles of
➢ Multifocal tumor (tumor tissues the chest.
within the same quadrant at o Patey’s operation
multiple foci) o Scanlon’s operation
➢ Extensive premalignant change o Auchincloss modified
➢ Tumors in pregnancy radical mastectomy
(particularly first trimester) o Halsted radical
➢ Recurrence of breast cancer mastectomy
following previous breast
MEDICAL THERAPY
conservation
RADIOTHERAPY
• Surgical procedures:
➢ Lumpectomy: resection of the • This is done by external
mass radiotherapy over the breast area,
➢ Quadrantectomy axilla (in some patients if axillary
➢ Semi-mastectomy dissection is not done or more than
➢ Total (Simple) mastectomy 4 positive axillary nodes), internal
o Structures removed: tumor, mammary and supraclavicular area.
entire breast + axillary tail, ➢ Total dosage: 5000 cGY units
areola, nipple, skin over the ➢ 200-cGY units daily- 5 days a
breast. week for 6 weeks
o Often the patient is • Indications for radiotherapy:
subjected to radiotherapy ➢ Patients who undergo
later (external) to axilla conservative breast surgery,
➢ Total mastectomy with axillary breast is irradiated after surgery
clearance (Commonly used ➢ After total mastectomy, external
procedure) irradiation is given to the axilla
o Structures removed: tumor, ➢ Patients with high risk of local
entire breast + axillary tail, relapse after surgery:
areola, nipple, skin over the o Invasive carcinoma
breast, axillary fat, fascia o Extensive in situ carcinoma
and lymph nodes (Level I o Patient under 35 years
and II) o Multifocal disease
➢ Radical mastectomy ➢ Bone secondaries to palliate
➢ Modified radical mastectomy: pain and swelling. If there is a
removal of all breast tissue and pathological fracture in the
axillary node dissection, sparing bone, internal fixation along
with external irradiation is done

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SURGERY MK
➢ Inflammatory breast cancer • Modalities used for hormone
➢ Preoperative to shrink tumor therapy:
size and downstage the tumor ➢ Estrogen receptor antagonist
for operation e.g. tamoxifen
➢ Atrophic scirrhous carcinoma of ➢ Ovarian ablation by surgery
the breast (curative (bilateral oophorectomy) or by
radiotherapy) radiation
➢ >4 positive lymph nodes in the ➢ LHRH agonist (medical
axilla, pectoral fascia oophorectomy)
involvement, positive surgical ➢ Oral aromatase inhibitors for
margins, extranodal spread or in postmenopausal women
patients with axillary status not ➢ Adrenalectomy or pituitary
known/not assessed. ablation
➢ Progesterone receptor
HORMONE THERAPY
antagonist
• Hormone therapy is used in ER/PR
➢ Androgens- injection of
positive patients in all age groups
testosterone propionate 100mg
(it was previously only used in
IM 3 times a week
perimenopausal aged women).
➢ Aminoglutethimide- blocks the
• Hormone therapy is easy to
synthesis of steroids by
administer and safe. It additional
inhibiting conversion of
provides prophylaxis against
cholesterol to pregnenolone-
carcinoma of the opposite breast.
medical adrenalectomy
• Hormone therapy is also used in ➢ Progestogens e.g.
metastatic breast cancer. medroxyprogesterone acetate
• Hormone therapy with tamoxifen is
useful in breast cancer in elderly • Conservative breast surgery
(positive ER) after wide local consists of wide local excision of
excision or occasionally as the tumor.
tamoxifen alone.
• Early breast cancer
• Hormone therapy is not used in ER
negative patients
• The drugs used are shown in the
table below.

557
Presentation Pathology
Painless lump • Fibroadenoma
• Fibrocystic change
• Carcinoma
• Cyst
• Fat necrosis
• Area of fibroadenosis
• Lipoma of breast
• Phyllodes tumor (Brodie tumor)
Painful lump • Menstrual change
• Area of Fibroadenosis
• Cyst
• Periductal mastitis
SURGERY MK
• Abscess (postpartum or lactational)
• Carcinoma (sometimes)
Pain and tenderness but no lump • Cyclic breast pain
• Non-cyclical breast pain
• Carcinoma (very rare)
Nipple discharge • Duct ectasia- Green-brownish
discharge
• Intraductal papilloma- Bloody
discharge
• Associated cysts
• Galactocele
Changes in nipple and/or areolar • Duct ectasia
• Carcinoma
• Paget’s disease
• Eczema
Changes in breast size and shape • Pregnancy
• Carcinoma
• Benign hypertrophy
• Rare large tumors

CHAPTER 17: UROLOGY

• In a healthy individual <1L of

UROLOGY blood per day in urine i.e. 1 million
HEMATURIA RBCs (approximately 1 RBC
passed per glomerulus).
➢ Normal urine should contain <3
HEMATURIA red blood cells per high power
• Hematuria is the presence of blood field of spun urine.
in urine.

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SURGERY MK
• Hematuria can usually be detected o Tuberculosis
1-5 RBC/ L on dipstick or >3-5 o Trauma
RBC/high power field (HPF) on o Polycystic kidney disease
microscopy. o Simple renal cyst
• Types of hematuria include: ➢ Malignant causes
➢ Gross (macroscopic, frank): o Renal tumor
blood is visible to unaided eye o Papillary carcinoma
➢ Microscopic: >5RBCs per high • Ureteric causes
power field ➢ Benign causes
• Hematuria may be: o Ureteric stone
➢ Early (initial): more likely to be o Bleeding disorders
urethral in origin, distal to ➢ Malignant causes: ureteric
external sphincter. tumor
➢ Terminal hematuria: more likely • Bladder causes
to be bladder neck or prostate in ➢ Benign causes:
origin o Cystitis
➢ Diffuse (total) hematuria: o Tuberculosis
source is in the bladder or upper o Bladder stones
urinary tract (ureteric or kidney) o Endemic hematuria
• Discoloration of urine from (Schistosomiasis)
pigments such as food coloring o Benign prostatic
(e.g. beetroots), Drugs (rifampicin, hyperplasia
sulfasalazine) and myoglobin is o Prostatitis
known as false hematuria. Brown ➢ Malignant causes
urine, blood + on dipstick but no o Bladder tumors jo
RBCs on microscopy. o Carcinoma prostate
• Silent hematuria is due to tumors of • Urethral causes
kidney or bladder unless proven ➢ Benign causes:
otherwise. o Urethritis
o Urethral injury
ETIOLOGY ➢ Malignant causes: uretheral
• Kidney causes: tumors
➢ Benign causes
o Pyelonephritis
o Glomerulonephritis
o Infarct
o Renal stones

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SURGERY MK
➢ Urine microscopy, culture and
sensitivity (urine test for
hematuria Benzidine test)
o In working up
microhematuria, assess for
the presence of red cell
casts, which are present in
glomerular bleeding
➢ Urinary cytology for diagnosing
urothelial malignancy
➢ Urinalysis for urinary tract
infections. False positive on
dipstick occurs when myoglobin
Figure 240: Causes of hematuria (Image is present.
adapted from SRB's manual of Surgery) • Blood:
• Note: mild hematuria is a normal ➢ Bleeding time, clotting time,
finding in a patient with recent prothrombin time, platelet count
urologic instrumentation (including for blood dyscrasias
catheterization) ➢ Renal function tests- blood urea,
serum creatinine
CLINICAL ASSESSMENT • Imaging
• On history focus on whether ➢ Kidney, urinary bladder and
hematuria is: ureter (KUB) X-ray
➢ Painful or painless ➢ Ultrasound to look for the stone,
➢ Gross (visible to the naked eye) tumor in the urinary tract.
or microscopic ➢ Cystourethroscopy to look for
➢ Initial (only at the start of the bladder or uretheral pathology
stream) ➢ IVU look for function of the
➢ Terminal (only at the end of kidneys
stream) ➢ CT abdomen
➢ Clots present
➢ Hemospermia (blood also in MANAGEMENT
semen) • Identify and treat cause
• Blood transfusion
INVESTIGATIONS • Antibiotics
• Urine:

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SURGERY MK
• Nephroureterectomy for renal cell
carcinoma, removal of stone for
kidney, ureter, urinary bladder. CYSTIC DISEASES OF
• Treatment of bladder tumor by KIDNEY
cystoscopic resection, intravesical
chemotherapy using BCG,
TYPES
radiotherapy, systemic 1. Genetic
chemotherapy ➢ Adult polycystic kidney disease
(Autosomal dominant)
• Treatment of medical cause like
➢ Infantile polycystic kidney
glomerulonephritis
disease (autosomal recessive)-
• Correction of BPH
fatal
• Correction of bleeding diathesis
o Presents in infants
o Worsening renal failure and
HTN
o Newborns may present with
INFECTIONS OF THE Potter sequence
o Associated with congenital
UROGENITAL hepatic fibrosis and hepatic
SYSTEM cysts
• 2. Non-genetic:
➢ Simple cyst,
➢ Multicystic kidney,
➢ Medullary sponge kidney
3. Acquired renal cystic disease may
develop in patient on long-term
dialysis.

INCONTINENCE AND POLYCYSTIC KIDNEY

NEUROPATHIC DISEASE (PCKD)
• Adult PCKD is inherited as
BLADDER autosomal dominant disease.
DISORDERS ➢ Mutation is in Adult polycystic
• kidney disease 1 (APKD 1) or
APKD 2.
➢ The mutation is present at birth
but cysts develop over time.

562
SURGERY MK
• It is common in females. ➢ Hydronephrosis
• It is bilateral and presents in third ➢ Solitary renal cyst
decade. INVESTIGATIONS
➢ One side presents little earlier • U/S confirms the presence of cysts
than other side
• Intravenous urogram- spider leg
• Cyst formation occurs at the pattern with an elongated
junction of the distal tubule and the compressed renal pelvis, narrowed
collecting duct. (both in renal and stretched calyces.
cortex and medulla)
• Blood urea and serum creatinine
• PCKD is usually associated with:
• Urine shows low specific gravity
➢ Polycystic disease of liver
(18%), pancreas and lungs
➢ Berry aneurysm in the circle of
Willis.
➢ Mitral valve prolapse
• Gross: multiple cysts with a clear or
brownish fluid (due to hemorrhage)
• Clinical features:
➢ Renal mass which is lobular,
firm, mobile, moves with
respiration, ballotable with dull
renal angle and resonant band in (CT showing bilateral, multiple kidney
front. cysts)
➢ Pain, which is due to stretch of
TREATMENT
renal capsule or haemorrhage
• Wait and watch policy
into a cyst.
• If one of the cyst overdistends
➢ Hematuria (25%)- due to
causing pain, hemorrhage,
overdistended cyst rupturing
infection then surgical intervention
into the renal pelvis.
is required.
➢ Infection is due to statsis
➢ Hypertension (75%) • Rovsing operation: The kidney is
➢ Worsening renal failure exposed. The cyst is opening. The
➢ Uremia occurs in later stage due fluid is evacuated. The cut edge is
to renal failure marsupialised.
• Differential diagnosis: • Presently U/S guided aspiration is
➢ Renal cell carcinoma done as a simpler approach.

563
SURGERY MK
• Laparoscopic/retropertoneoscopic • Occasionally, if the cyst is in one of
aspiration/ de-roofing of renal cyst. the pole, partial nephrectomy is
• Once renal failure sets in then done.
initial hemodialysis followed by • Laparoscopic approach.
bilateral nephrectomy is done and
later renal transplantation should be
planned for.

SOLITARY RENAL CYST

• Solitary renal cyst is never
congenital.
• It is due to an earlier trauma or
infection resulting in blockage of
tubule, leading to cyst formation.
• It usually:
➢ Unilateral
➢ Presents as a renal mass which
is smooth, often tender if
infected or haemorrhagic.
• Differential:
➢ Renal neoplasm
➢ Hydronephrosis
➢ Polycystic disease
➢ Hydatid cyst
INVESTIGATIONS
• U/S and Intravenous urogram
confirms diagnosis
• CT scan
TREATMENT
• Kidney is exposed. The cyst is
aspirated and a portion of the cyst
wall us removed (Kirwin’s
operation) and cavity is filled with
perinephric fat.

564
SURGERY MK

URINARY STONES

URINARY STONES
•

URINARY RETENTION

URINARY RETENTION
• This is incomplete voiding of the bladder.
➢ As the bladder fills with urine, the bladder muscle (detrusor) is stretched.
There is an awareness of filling at a volume of 150-250ml and a desire to void
when normal bladder capacity (400-500ml) is reached.
➢ Micturition is achieved by relaxation of the pelvic floor musculature including
the voluntary sphincter. The trigone contracts, opening the bladder neck and
closing the ureteric orifices thus preventing urine reflux during voiding.
➢ The detrusor then contracts, expelling the stored urine.
➢ The pelvic nerves supplying the bladder and urethra with motor and sensory
fibers synapse in the micturition center located in the S2-4 segments of the
spinal cord which corresponds with the T2-L1 vertebral level.

565
SURGERY MK
➢ This center is connected to centers in the pons and cerebrum (especially
frontal lobes) which exert an inhibitory effect that is central to voluntary
control.
• Urinary retention can be classified as:
➢ Acute urinary retention: complete inability to urinate
➢ Chronic urinary retention

ACUTE URINARY RETENTION

• Patients want to void but cannot resulting in a huge distended palpable bladder.
ETIOLOGY
• Male:
➢ Obstruction: Bladder outlet obstruction (commonest cause), Prostate
enlargement (can be precipitated by cold, drugs, abundant fluid intake) and
Urethral stricture
➢ Inflammation: Acute urethritis or prostatitis, Balanitis
➢ Anatomical: Phimosis
• Female:
➢ Obstruction: bladder neck obstruction (rare)
➢ Inflammation: Vulvovaginitis and Vaginal lichen planus
➢ Anatomical: retroverted gravid uterus
• Both:
➢ Urinary obstruction: Blood clot, Urinary tract stones, fecal impaction and
Genitourinary prolapse.
➢ Neurogenic (injury or disease of the spinal cord)
➢ Drugs: anticholinergics, opioids, epidural, tricyclic antidepressants,
sympathomimetic, spinal anesthesia
➢ Others: Rupture of the urethra, Smooth muscle cell dysfunction associated
with ageing, anal pain (hemorrhoidectomy), intensive postoperative analgesic
treatment
➢ Postoperative urinary retention: it is very common, and sometimes
masquerades as incontinence. The patient may not feel the need to void
because of post-op pain medication etc. but will report that every few minutes
there is involuntary release of small amounts of urine. A huge distended
bladder will be palpable confirming overflow incontinence from retention.
Indwelling bladder catheter is needed.

566
SURGERY MK
CLINICAL FEATURES
• No urine is passed for several hours.
• Pain is present
• Bladder is visible, palpable, tender and dull to percussion
• Potential neurological causes should be excluded by checking reflexes in the
lower limbs and perianal sensation.
• It can lead to hydronephrosis
INVESTIGATION
• Urinalysis
• Bloods: FBC, Urea and electrolytes, Glucose
• Ultrasound of bladder to check for post void residual, and kidney scan for
hydronephrosis
• Other imaging: KUB X-ray/ CT (mass, stone), MRI (neurological)
MANAGEMENT
• Treatment is to pass a fine urethral catheter (14F-Frech gauge is defined as the
circumference in millimeters) and arrange urological management to treat
underling cause.
➢ Wash hands thoroughly and don sterile gloves.
➢ Clean genitalia using soapy antiseptic
➢ Lignocaine gel is inserted into the urethra, warning the patient that it may
sting. The jelly should be massaged posteriorly in an attempt to anesthetize
the sphincter region and it is of advantage to place a penile clamp for several
minutes.
➢ A small Foley catheter should be passed while the penis is held taut.
➢ In female patients the labia should be parted using the middle and index
fingers of the left hand which should not be moved once cleaning has been
performed.
➢ Once urine begins to drain it is wise to pass a few more centimeters of catheter
into the bladder before the balloon is inflated to avoid inflation in the prostate.
FORCE MUST NOT BE USED.
• In postoperative retention a warm bath can help.
• After catheterization:
➢ Record the volume of urine drained
➢ Examine the abdomen to exclude other pathology (rupture of an aortic
aneurysm, ureteric colic or diverticulitis can cause confusion)

567
SURGERY MK
• If the catheter will not pass, it is usually due to poor technique, lack of anesthesia,
traumatization of the urethra or a urethral stricture.
• Catheter should be placed for at least 3 days.
• Suprapubic puncture:
➢ Suprapubic puncture with commercially available catheters such as Cystofix
or Lawrence Add-a-Cath catheter is straightforward provided that the bladder
is palpable.
➢ The skin, fascia and retropubic space are anesthetized with 0.5% lignocaine.
Correct placement is confirmed by aspiration.
➢ A large-bore needle is placed into the bladder, down which a fine catheter is
passed (Cystofix) and then secured in position. The other option is to place a
plastic suprapubic trocar and cannula which has a removable plastic strip on
the side.
➢ A standard 12F Foley catheter can be passed down the cannula, the balloon is
inflated, the cannula is extracted and the strip is pulled away from the catheter
(Add-a-Cath)
➢ If urine cannot be aspirated through the fine-bore needle, passing a suprapubic
trocar should not be attempted.
➢ If these devices are not available a catheter can be placed in the bladder under
direct vision through a small incision under local anesthetic.
• Urethral instrumentation in a patient with a known stricture should be done by an
experienced urologist that may elect to dilate the stricture or take the patient to
theatre to carry out an optical urethrotomy.

CHRONIC URINARY RETENTION

• In chronic retention there is no pain.
• These patients are at risk of upper tract dilation because of high intravesical
tension- they require urgent urological referral.
• Men with impaired renal function may develop post-obstructive diuresis
following catheterization. Such men need careful monitoring with replacement
of inappropriate urinary losses by intravenous saline, they are also at risk of
hematuria as the distended urinary tract empties.
• Often it is several days before full renal recovery occurs.

568
SURGERY MK

URINARY TRACT OBSTRUCTION

URINARY TRACT OBSTRUCTION

• Obstruction of the urinary tract may occur at any level from the external urinary
meatus to the ureteropelvic junction (junction between the renal pelvis and the
ureter).
• Obstruction may be classified according to site as:
➢ Upper urinary tract obstruction: bladder and uppers
➢ Lower urinary tract obstruction: distal to the bladder

569
SURGERY MK
• Within each type of obstruction further sub-classification can be done including:
➢ Etiology: congenital vs acquired
➢ Duration: Acute vs Chronic
➢ Degree of obstruction: Partial vs complete

UPPER URINARY TRACT OBSTRUCTION

• Upper urinary tract obstruction may result in renal impairment especially if the
obstruction is prolonged.
• The kidney responds to distal obstruction by a decrease in ipsilateral renal blood
flow with a concomitant increase in contralateral renal blood flow.
• Other protective mechanisms:
➢ Ureteric dilation: this dissipates the increased pressure to some extent
➢ Urine reabsorption: through renal lymphatic and collecting ducts
(pyelointerstitial back-flow)
➢ Papillary shutdown
• Continued unrelieved obstruction produces renal impairment due to a
combination of pressure and ischemic atrophy.
• Upper urinary tract obstruction can be:
➢ Acute: symptomatic with loin pain
➢ Chronic: asymptomatic or produce vague symptoms
• Diagnosis depends mainly on IVU with judicious application of specialized
radiographic techniques such as isotopic renography, ascending ureterography
and perfusion studies (Whitaker test).
• On basis of clinical and radiological findings obstruction may be found to be
➢ Unilateral or bilateral
➢ Complete or partial
➢ Acute or chronic

570
SURGERY MK
UNILATERAL UPPER TRACT OBSTRUCTION
• Lesions can be
➢ Intraluminal: within the ureteric
lumen
➢ Intramural: within the ureteric wall
➢ Extramural: outside the wall of the
ureter compressing it

INTRALUMINAL
• Causes:
➢ Calculi (most common): presents with
acute ureteric colic associated with
hematuria. A plain abdominal film
demonstrates the calculus in 90% of
patients and IVU will confirm the
diagnosis and degree of obstruction.
(Management covered earlier)
➢ Clots from bleeding in the renal pelvis
or kidney (transitional cell carcinoma,
renal cell carcinoma): may mimic
ureteric colic but findings of X-ray of
a filling defect in the renal pelvis or
Figure 241: Causes of unilateral ureteric
distorted calyces gives a clue to the obstruction
correct diagnosis.
➢ Renal papillary necrosis: is uncommon but the sloughed papilla may obstruct
the ureter mimicking the clinical picture of ureteric stone. Causes include
sickle cell disease, diabetes mellitus, and chronic use of NSAIDs. Symptoms
are pain associated with hematuria and sterile pyuria. A typical IVU shows
defects in the medulla where the papillae were and a non-calcified obstructing
ureteric lesion. Sloughed papillae are managed like ureteric calculi.

571
SURGERY MK
INTRAMURAL OBSTRUCTION
• Congenital obstruction of the pelviureteric junction:
➢ This is a common ureteric abnormality caused by a failure of transmission of
peristalsis from the pelvis to the ureter.
➢ This results in a rise in intrapelvic pressure as the renal pelvis and calyces
dilate.
➢ Gradual deterioration of renal function on the affected side is the rule.
➢ The condition may be asymptomatic or it may cause loin pain especially after
an increased fluid load (Dietl’s crises).
➢ IVU will show dilated calyces and pelvis with obstruction at the level of the
pelvic-ureteric junction (PUJ). The ureter is not visible, if it can be seen on
IVU then the diagnosis of PUJ obstruction is incorrect.
➢ A renogram with diuretic will confirm the obstructive nature of the lesion and
give rough estimate of renal function on the obstructed side.
➢ Treatment is surgical. If renal function is poor, nephrectomy is the most
appropriate treatment provided the condition is not bilateral. If renal function
is good then a reconstructive operation (pyeloplasty) is done.
• Obstruction of the ureterovesical junction: Obstruction may also occur at the
ureterovesical junction (obstructed megaureter) and failure of transmission of
peristalsis at the junction is believed to be the mechanism. Pain, hematuria and
infection are usual presenting symptoms. IVU shows a dilated ureter with less
dilated proximally and blunting of the calyces. A diuretic renogram to confirm
obstruction is indicated. Treatment consists of reimplantation of the ureter after
excision of the diseased distal portion.
• Ureteric strictures: may occur after ureteroscopy and stone manipulation, pelvic
surgery, irradiation (for carcinoma of the prostate, cervix or bladder) or chronic
inflammatory conditions (tuberculosis or schistosomiasis)
• Ureteric tumors: account for 1% of all urothelial tumors and may present as
ureteric pain with hematuria mimicking a stone. Diagnosis depends on urine for
cytology and IVU. Treatment consists of nephrouretectomy and regular follow-
up cystoscopy as recurrences in the bladder are common.
EXTRAMURAL OBSTRUCTION
• Extramural obstruction of the ureter is rare.
• Can be caused by:
➢ Retroperitoneal fibrosis
➢ Pregnancy

572
SURGERY MK
➢ Pelvic tumors
BILATERAL UPPER TRACT OBSTRUCTION
• Causes include:
➢ Retroperitoneal and pelvic tumors:
may obstruct both ureters, most
tumors in the retroperitoneum are
malignant, invasion arising from the
cervix, prostate, bladder, breast,
colon, ovary or uterus. The
remainder are primary
retroperitoneal tumors such as
lymphoma or sarcoma. When
treatment of the underlying tumor is
feasible the ureters may be
reimplanted or urinary diversion may
be considered.
➢ Retroperitoneal fibrosis:
Figure 242: Bilateral causes of upper
o This is usually idiopathic though in tract obstruction
some cases is secondary to
malignant disease of the retroperitoneum, irradiation-induced fibrosis, or
drugs such as methysergide or beta blockers.
o As the fibrotic plaque develops the ureters are pulled towards the midline
and progressively obstructed. This may present as backache and gradual
renal impairment. Hypertension and signs of distal venous occlusion are
frequently associated.
o Renal failure occurs in some cases.
o Men are affected more than women and the disease usually presents in
middle age.
o Lab investigations may reveal renal function impairment, anemia and a
raised ESR.
o An IVU will show deviation of the ureters towards the midline and
hydronephrosis.
o CT guided biopsy of the plaque is necessary to rule out underlying
malignancy.
o Initial treatment consists of relieving the ureteric obstruction, although
freeing the ureters from the fibrous plaque (ureterolysis) and wrapping the

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SURGERY MK
ureters in omental tubes to prevent recurrence may occasionally be
undertaken.
➢ Extensive bladder tumors
➢ Bladder outflow obstruction

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SURGERY MK
LOWER URINARY TRACT OBSTRUCTION

LOWER URINARY TRACT OBSTRUCTION

• Outflow obstruction of the lower urinary tract remains one of the most prevalent
and clinically significant diseases in urology.
• Symptoms referable to the lower urinary tract are categorized into:
➢ Obstructive:
o Weak stream
o Hesitancy
o Intermittency
o Dribbling
o Straining to void
➢ Irritative:
o Urinary Frequency
o Urgency
o Nocturia
o Dysuria
o Urge incontinence
• The term ‘prostatism’ refers to a combination of these symptoms including
frequency, urgency, hesitancy and weak stream.
• While the name implies that prostatic obstruction is the cause, this is not always
the case as bladder instability in patients with no evidence of obstruction can
present in an identical fashion.
• The differential diagnosis of lower urinary tract obstruction can be classified as:
➢ Structural causes
o Congenital
- Meatal stricture
- Posterior urethral valves
o Acquired
- Urethral stricture
- Phimosis
- BPH
- CA prostate
- Bladder neck contracture
Figure 243: Differential diagnosis of lower urinary tract
- CA bladder obstruction

575
SURGERY MK
➢ Functional causes
o Neurogenic bladder dysfunction
o Psychogenic voiding dysfunction
o Cystitis
o Prostatitis
o Prostatic abscess
o Balanitis

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SURGERY MK
CONDITION FEATURE
STRUCTURAL CAUSES
Meatal stricture • Obstruction of the distal urethra
• Typically seen in newborn or infant males
• There is usually a congenital web of epithelial tissue
permitting only a pinpoint opening the meatus.
Phimosis • In uncircumcised males, chronic inflammation and
scarring of the prepuce (Phimosis) can cause obstruction
of urine
Urethral stenosis and • Urethral stenosis in females is rare and may be related to
strictures trauma or inflammation
• Urethral stricture is a frequent problem seen in adult
males. Although a common sequel to gonococcal
urethritis in the past, the majority of strictures now seen
are the result of trauma to the urethra from instrumentation
or catheterization
Posterior urethral valves • These are congenital mucosal folds in the area of the
membranous urethra
• They are the most common cause of proximal urethra
obstruction in male infants.
• In adults, obstruction in this region can be both functional
and anatomical. Failure of the external urethral sphincter
to relax secondary to spasm during micturition will
impede flow.
• Several neurological diseases including spinal cord injury
and multiple sclerosis as well as psychogenic causes will
result in this type of obstruction.
Ca prostate • This is a less common cause of obstruction as most
cancers occur in the peripheral regions of the prostate
BPH • This is the most common cause of obstruction in adult
males
• It tends to occur in the periurethral transition zone.

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SURGERY MK
Bladder neck contracture • Contracture of the bladder neck is a common cause of
obstruction and typically seen secondary to surgery or
trauma
• Neurological and idiopathic dysfunctions are less
common and are characterized by failure of the vesical
neck to open completely during micturition without
anatomical cause. This may mimic BPH but usually
occurs in a younger age group.
• In female patients who have had vaginal deliveries or
pelvic surgery, cystocele may develop causing a range of
symptoms from obstruction and retention to urinary
incontinence
CA bladder • Physical obstruction
FUNCTIONAL CAUSES
Neurogenic bladder • Peripheral neuropathies may adversely affect the detrusor
dysfunction muscle contraction by involving the autonomic nerve
supply.
• Causes: diabetes mellitus, chronic alcoholism, uremia,
Guillain-Barre syndrome and trauma
• Certain drugs may exacerbate obstructive symptoms and
precipitate retention. These include anticholinergics
(phenothiazine and some antianxiety medication) inhibit
detrusor contractility, alpha adrenergic agonist
(pseudoephedrine, ephedrine and phenylpropanolamine)
increase sympathetic tone of the bladder neck and
prostatic urethra.
• Both temporary and permanent detrusor dysfunction can
be seen from prolonged over-distension or ischemia of the
bladder (myogenic failure)
Psychogenic voiding • Inability of the bladder to void due to psychological issues
dysfunction
Cystitis • Infection and inflammation of the bladder
Prostatitis • Infectious processes of the prostate can also lead to
Prostatic abscess obstructive symptoms owing to surrounding inflammation
and edema and include acute prostatitis and prostatic
abscesses
Balanitis • Obstruction of the distal urethra due to inflammation of
the glans penis

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SURGERY MK
BENIGN PROSTATIC HYPERPLASIA

BENIGN PROSTATIC HYPERPLASIA

• Benign prostatic hyperplasia (BPH) is a common benign conditions of the
prostate seen in older men.
• It is clinically important because it is the most common cause of bladder outlet
obstruction in men over 50 year of age.
• Incidence in men between 60 and 90 years is slightly over 50%. Early changes
probably occur between the ages of 30 and 40 years.
• If left untreated, bladder outlet obstruction can lead to urinary tract infection and
bladder stones secondary to stasis from incomplete bladder emptying, bladder
decompensation resulting in chronic urinary retention with overflow and most
serious of all renal failure secondary to high-pressure urinary retention.
• The initial change in BPH is the development of microscopic stromal nodules
around the periurethral glands. Around these nodules glandular hyperplasia
originates.

SURGICAL ANATOMY
• The prostate is an accessory gland of male
reproductive system. It is composed of
glandular tissue embedded in fibromuscular
stroma. It surrounds the first 3cm of urethra.
• The prostate consist of 3 structures:
➢ 5 anatomical lobes
o 1 Medial/middle lobe
o 2 lateral lobes
o 1 anterior and 1 posterior lobe
➢ 3 types Secreting glands: secrete into the
urethra
o Urethral glands
o Submucous glands Figure 244: The prostate
o Prostatic glands (Carcinoma prostate
normally arises from these glands)
➢ Capsule

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SURGERY MK
o True capsule (encloses all lobes): formed
by the condensation of the peripheral parts
of the gland, continues with the stroma of
the gland
o Prostatic sheath /False capsule (blends with
pelvic fascia)
o False capsule only present and formed by
compression of the posterior lobe e.g. in
BPH
• The prostate according to McNeal divides the
prostate into 3 zones:
➢ Peripheral zone- prone for carcinoma
➢ Periurethral transition zone where BPH arises Figure 245: Prostate anatomy
➢ Central zone
• Note:
➢ Prostate carcinoma develops in prostatic gland proper
➢ BPH develops in submucosal glands
• Acid phosphatase:
➢ This is an enzyme that splits organic phosphates.
➢ It is found in many human tissue, but more concentrated in prostate.
➢ It is active at pH5
➢ Acid phosphatase secreted by prostate drains into the urethra through prostatic
ducts and so blood levels of this enzyme remain low.
➢ Serum acid phosphatase estimation should be done on empty stomach because
heavy meals alter the level of the acid phosphatase
➢ Normal value= 0-5 King Armstrong units per 100ml of serum
➢ It is raised significantly in carcinoma prostate with metastases
➢ It does not increase in BPH.
➢ Slight increase in acid phosphatase level occurs in acute phosphatase level
occurs in acute prostatitis, Paget’s disease of bone and hepatic cirrhosis.
➢ Prostatic fraction of acid phosphatase is more relevant in carcinoma prostate.
• Prostate specific antigen
➢ It is a protease produced from the prostatic epithelium secreted in the semen
to cleave and liquefy the seminal coagulum formed after ejaculation
➢ PSA is organ specific.
➢ Normal value=4ng/ml of plasma (more than 10ng/ml is significant)

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SURGERY MK
➢ PSA elevation is seen in carcinoma, prostatic hyperplasia and prostatitis.
Increase is much more in carcinoma than in benign conditions.
➢ PSA is in 2 forms:
o Major (bound form): increases in carcinoma
o Minor (free form): increases in benign conditions
➢ PSA density i.e. PSA level per gram of prostate tissue is more relevant
➢ Serial estimation of PSA is very useful to suspect spread and recurrence after
treatment
➢ 25% of men with PSA 4-10 ng/ml show prostate carcinoma
➢ 20% of men with normal PSA (1-4ng/ml) will show prostate carcinoma

Figure 246: BPH

PATHOGENESIS multifactorial with a hormonal

• The etiology of BPH is uncertain, element present.
although it is probably • The gland is influenced by steroid
hormones.

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SURGERY MK
• Recall that the hypothalamus • The periurethral glandular elements
produces luteinizing hormone undergo hyperplasia causing an
releasing hormone which increase in glandular mass that
stimulates the anterior pituitary results in compression of the
lobe to produce luteinizing prostatic urethra and the onset of
hormone. obstructive symptoms.
• Luteinizing hormone in turn causes
the testes (Leydig cells) to produce RISK FACTORS
testosterone. • Age >50 years
• Testosterone is convert to • Hormonal: increase in estrogen and
dihydrotestosterone (DHT) and this decrease in androgens.
stimulates prostatic hyperplasia. • Neoplastic: fibrosis, adenosis,
• Additionally, estrogen has a myosis (fibromyoadenoma)
negative feedback on the
PATHOLOGY
hypothalamic-pituitary axis.
• Prostate grows into the bladder
• The exact mechanism of BPH
• Prostate grows outside bladder
remains unclear.
• Effects: BPH induces gradual
• Interestingly, BPH does not occur
changes in the urinary tract which
in castrated men or
result from interactions between
pseudohermaphrodites both whom
prostatic urethral resistance and
lack the active metabolite of
intravesical pressure.
testosterone, dihydrotestosterone
➢ Urethral:
(DHT).
o Compressed laterally
➢ The enzyme that catalyze the
o Enlongated (from 1.5” to
conversion of testosterone to
4”)
dihydrotestosterone is 5-alpha
o Increased curvature
reductase.
➢ Bladder
• Estrogens have also been
o Hypertrophy of bladder
implicated in prostatic hyperplasia,
(trabeculations)
because in aging men, the levels of
o Sacculation (diverticulum)
estrogen rise and those of
➢ Ureter and Kidney
androgens fall.
o Hydroureter
• The specific area of cellular
o Hydronephrosis
hyperplasia is the transitional zone
o Renal failure
or periurethral area of the prostate.

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SURGERY MK

CLINICAL MANIFESTATIONS
HISTORY
• Variable symptoms. Symptoms are both obstructive and Irritative.
• Any older man presenting with obstructive urinary symptoms must be suspected
of having BPH.
• Symptoms include:
➢ Obstructive symptoms:
o Urinary hesitancy: due to prolonged time required for the detrusor
muscles to overcome the increased urethral resistance
o Decreased force of urinary stream- poor urinary stream due to
compression of the urethra.
o Intermittency, terminal dribbling and sensation of incomplete bladder
voiding: when detrusor muscle can no longer maintain the increased
pressure required to empty the bladder.
➢ Irritative symptoms:
o Frequency- earliest and commonest due to irritation of the bladder trigone,
residual urine in post prostatic pouch and cystitis.
o Nocturia: when patients are asleep, cortical inhibition is decreased as is
urethral tone, leading to nocturia.
o Urgency- due to stretching of internal sphincter by enlarged gland, urine
trickle and irritate the prostatic urethra.
o Dysuria- pain on urination
o Incontinence is a late finding in BPH. When large volumes of residual
urine accumulate in the bladder and overcome urethral resistance this is
called overflow incontinence.
• Acute urinary retention may develop as a result of a precipitation factor
aggravating existing BPH e.g. drugs (alpha adrenergic drugs, anticholinergics,
and psychotropic agents), alcohol, cold and infection
• Secondary symptoms:
➢ High postvoid residual volumes promote bacterial growth, leading to urinary
tract infection.
➢ Stasis can also promote the formation of bladder calculi.
➢ Most seriously, high pressure chronic retention can cause bilateral
hydroureteronephrosis and subsequent renal failure.

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SURGERY MK
• Other symptoms include hematuria from vesical piles, increased libido which is
followed by impotence.
PHYSICAL EXAMINATION
• Physical signs attributable to BPH tend to occur late in the disease.
• Rectal examination reveals and enlarged symmetric rubbery gland (smooth
surface).
➢ Right and left lobes are often not discernible although asymmetry is common
while consistency of the gland may either be soft or firm depending on
whether there are more glandular or fibromuscular elements.
➢ Seminal vesicles are usually not palpable with enlarged glands.
➢ If irregularities of the prostate are felt on digital rectal examination including
firm nodules, induration or generally hard, prostate carcinoma is more likely
and it requires further investigations
➢ The size of the gland has no relationship to symptomatology. A small gland
may produce a high degree of outflow obstruction whereas a large gland may
produce no symptoms at all.
• The suprapubic region should be palpated to rule out a grossly distended bladder.
• Examination of the abdomen may reveal a distended bladder or occasionally a
palpable kidney and flank tenderness from hydronephrosis or pyelonephritis.
• In advanced cases signs of uremia secondary to renal failure may be present:
Hypertension, tachycardia and tachypnea from metabolic acidosis and anemia as
well as neurological changes and uremic fetor.
• Urinalysis should be done to look out for evidence of infection and hematuria. If
hematuria exists other causes referable to the urinary tract should be excluded.

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SURGERY MK

DIAGNOSIS
• Urine microscopy, culture and sensitivity- infections
• Serum urea, electrolytes and creatinine levels should be checked for evidence of
renal insufficiency.
• Full blood count- anemia
• Prostate specific antigen (PSA) to rule out CA prostate.
• Kidney ureter and bladder (KUB) X ray- stones (stasis)
• Intravenous urogram and KUB ultrasound- hydronephrosis, hydroureter, residual
urine, diverticulae.
• Residual volume measurement- the patient empties bladder then catheterize them
(normal residual ~ 30mls), residual volume greater than 100ml would signify
failure of the bladder to empty completely.
• Cystoscopy- it can be done to evaluate BPH prior to transurethral resection of the
prostate. It includes evaluation of the ureteric orifices, presence of bladder tumors
or stones, size and length of the prostate and condition of the urethra.
• Urodynamic studies: Urinary flow rate
➢ A flow rate of less than 10ml/sec is evidence of bladder outlet obstruction,
BPH, detrusor instability, neuropathic bladder (diabetes, parkinsonism,
Alzheimer, CVA or neurosyphilis)

TREATMENT
MEDICAL TREATMENT
• Goal of drug therapy is to relax smooth muscle in the prostate and bladder neck
or to induce regression of cellular hyperplasia thereby enhancing urinary outflow
from the bladder to the urethra.
• Alpha blockade of adrenergic receptors produces smooth muscle relaxation of
both prostate and bladder neck.
➢ An infrequent side effect to alpha-antagonist (e.g. terazosin, tamsulosin) is
postural hypotension (2-8%).
➢ Tamsulosin 400 micrograms PO OD
➢ Useful in small prostates causing obstructive uropathy due to BPH
• Prostatic hyperplasia can also be treated with 5-alpha reductase inhibitor (e.g.
finasteride) that block the conversion of testosterone to DHT without lowering
the serum levels of circulation testosterone.

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SURGERY MK
➢ Effectiveness of 5-alpha reductase inhibitors is less than half that seen with
alpha blockers.
➢ Useful in big prostates causing obstructive uropathy
• Both drugs are usually taken for 6 moths- 1 year to see effects
• There is need to follow up the patient.
• Finasteride 5mg daily, review treatment at 3-6 months and then every 6-12
months (may require several months treatment before benefit is obtained)
• Other medical interventions:
➢ Intermittent self-catheterization
➢ Transurethral balloon dilatation of the prostate
➢ Microwave hyperthermic prostatic therapy
➢ Prostatic urethral stents
➢ Transurethral needle ablation
➢ High-intensity focused ultrasound.
SURGICAL
• Surgical relief of obstruction is necessary when medical therapy fails.
• Indications:
➢ Failed medical treatment
➢ Complications (bleeding hydronephrosis, uremia, bladder calculi, urinary
sepsis, acute or chronic urinary retention)
➢ Post-void residual volume >100mL
➢ Acute urinary retention
➢ Chronic urinary retention with overflow dribbling
➢ Gross hematuria on more than one occasion
➢ Recurrent urinary tract infection
➢ Patient request for restoration of normal voiding pattern because of excessive
nocturia or dribbling.
• Procedures include:
➢ Open method- prostatectomy
o Hospital stay around 10 days
o Limited for patients with extremely large glands that are not suitable for
TURP because of gland size and time required for resection.
o Greater blood loss and higher morbidity and mortality risk
o Majority have a good quality of life after prostatectomy.
➢ Closed method: Transurethral resection of prostate (TURP)- preferred
o Hospital stay around 5 days

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SURGERY MK
o The adenomatous portion of the prostate is removed via a resectoscope
using electrocautery from within the prostatic urethra.
• Open method can be done through
➢ Transversical prostatectomy (Wilson Hey procedure)
➢ Retropubic prostalectomy (Millin procedure)
➢ Perineal prostalectomy (Young procedure)- not practiced.
• The procedure of choice is transurethral resection of the prostate.
➢ With the patient in the lithotomy position, the resectoscope is introduced via
the urethra into the bladder.
➢ The occlusive prostate tissue is identified and under direct vision, the tissue is
shaved away using an electrified wire loop.
➢ As the bladder is constantly irrigated with non-electrolytic isotonic solution
containing sorbitol or glycine, extravasated blood and tissue fragments are
evacuated.
➢ An indwelling catheter is left in place for 1-7 days.

Figure 247: Transurethral resection of the prostate

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SURGERY MK
POST OPERATIVE CARE
• Establish continuous drainage with normal saline.
• High urine output (essential)- oral fluids and IV fluids.
• Early ambulation to avoid DVT and hypostatic pneumonia.
COMPLICATIONS OF PROSTATECTOMY
• Early
➢ Hemorrhage (lavage, clot retention)
➢ Bladder tamponade-this is an emergence insert 22-24G catheter to
decompress
➢ Hyponatremic hypochloremic metabolis acidosis (TURP syndrome) due to
absorption of irrigation fluid containing sorbitol or glycine via venous sinuses
causing hyponatremia and metabolic acidosis in 2% of patients
• Intermediate:
➢ Infection (UTI)- broad spectrum antibiotics
➢ Incontinence of urine- physio, investigate for damage to internal urethral
sphincter
• Late:
➢ Urethral stricture
➢ Renal failure
➢ Sterility- retrograde ejaculation
➢ Impotence
➢ Bladder neck contractures

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SURGERY MK
CARCINOMA PROSTATE

CARCINOMA PROSTATE
• This is the most common malignant tumor in men over 65 years.
• It is the second most frequent cause of cancer deaths.
• It occurs in the peripheral zone in prostatic gland proper i.e. commonly in
posterior lobe. So prostatectomy from BPH does not provide protection against
the development of carcinoma prostate.
• Incidence is 70% in men over 80.

ETIOLOGY
• The following have been suggested as possible etiological factors in the
development of prostatic carcinoma:
➢ Age
➢ Race
➢ Environmental factors
➢ Diet
➢ Nationality
➢ Endocrine environment
➢ Viral infection

PATHOLOGY
• The most common type of prostate tumor is the adenocarcinoma which arises
from the glandular epithelium. It comprises 95% of tumors.
➢ It arises in the outer part of the prostate gland or peripheral zone. As the tumor
enlarges it spreads medially into the remainder of the gland and outwardly to
the surrounding tissue particularly the seminal vesicles.
➢ Invasion of the rectum is uncommon as it is protected by the fascia of
Denonvilliers. The tethering of the rectal mucosa that may occur does not
indicate invasion of the rectum but rather of the fascia beneath it.
• Grading of carcinoma is based on de-differentiation as proposed by Gleason
(Gleason grading system):
➢ A tumor is assigned a single grade on a scale of 2-10
➢ 8-10 indicates a poorly differentiated tumor
➢ 2-4 indicates a well-differentiated tumor
• A Gleason score more than 7 carries poor prognosis.
• Types of carcinoma prostate:

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SURGERY MK
➢ Microscopically latent
➢ Tumors incidentally found either by TURP or by PSA estimation
➢ Early localized carcinoma
➢ Advanced local prostatic carcinoma
➢ Metastatic carcinoma either into the bone commonly or other organs

CLINICAL FEATURES
• Commonly asymptomatic
• Most patients will present with symptoms of bladder outflow obstruction:
➢ Poor stream
➢ Hesitancy
➢ Nocturia
➢ Incomplete bladder emptying
• Sometimes the tumor may present as acute urinary retention
• 40% of patients may present with symptoms of advanced prostatic carcinoma
caused by either
➢ Ureteric obstruction
➢ Bony metastasis: the pain occurs classically at night, waking the patient from
sleep. The pain may be relieved by getting out of bed and walking for a while
• On examination
➢ Prostate may feel normal
➢ On per rectal examination, prostate feels hard, nodular, irregular often with
loss of median groove.
➢ In localized prostatic carcinoma there may be a hard nodule in one of the lobes
or a hard area which has spread into the opposite lobe but with no evidence of
spread outside the gland
➢ If digital rectal examination of prostate reveals the presence of locally
invasive prostate cancer, there may be as hard mass spreading outside the
boundaries of the prostate and involving the seminal vesicles or the side wall
of the pelvis. In this instance, the examining finger may feel a hard prostate
that may be irregular and associated with a fixed gland and sometimes
tethering of the rectal mucosa.

DIFFERENTIAL DIAGNOSIS
• Other causes of retention urine
• Other cause of back pain

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SURGERY MK
SPREAD
• It spreads via 2 ways:
➢ Local spread:
o Upward into seminal vesicles, bladder neck, trigone, later into both ureters
causing anuria.
o Downward into distal sphincter.
➢ Blood spread:
o Into bones commonly the pelvic bone, lumbar vertebrae, femoral head,
ribs, skull- in that order.
o Pathological fractures can occur in
long bones and vertebrae.
Paraplegia may occur if spine is
involved.
o Rarely spread to the liver and
lungs can occur.
➢ Lymphatic spread:
o Into the obturator lymph nodes,
then to internal iliac lymph nodes.
o Through seminal vesicles into
external iliac and retroperitoneal
lymph nodes.
o Eventually mediastinal, left
supraclavicular lymph nodes get Figure 248: A plain X-ray AP view of lumbar spine in a
involved. patient with prostate carcinoma. Note the typical
osteoslcerotic secondaries

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SURGERY MK
INVESTIGATIONS
• These include:
➢ Full blood count and peripheral smear:
in metastatic disease there may be
leucoerythroblastic reaction with bone
marrow invasion causing anemia,
thrombocytopenia, DIC and increased
fibrinogen degradation products.
Anemia may also be due to renal
failure
➢ Kidney function tests (Blood urea,
serum creatinine and electrolytes)
➢ Liver function test
➢ Prostate specific antigen (PSA): more
than 10nmol/ml is suggestive
➢ Prostatic fraction of acid phosphatase
is increased
➢ Chest X-ray
➢ Imaging:
o Plain X-ray, KUB: may show
dense coarse sclerotic
secondaries. Osteolytic or
combination of lytic and sclerotic
lesions are also often seen.
o Transrectal ultrasound-TRUS
(including guided needle biopsy
Figure 249: Osteoblastic secondaries in pelvic boens
of the prostate) and lumbar spine
o Isotope bone scan for the presence
of bony metastases
o MRI to evaluate local invasion and regional lymphadenopathy
o U/S abdomen to see tumor extension into the bladder and to see kidneys
for hydronephrosis
o Technetium radioisotope bone scan to see secondaries
➢ Transrectal prostatic biopsy. 10 biopsy cores are taken.

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SURGERY MK
MANAGEMENT
• Management is dependent on staging (TMN staging)
➢ T1- incidentally confirmed carcinoma after prostatectomy
o T1a- tumor occupying less than 5% of specimen
o T1b- tumor occupying more than 5% of specimen
o T1c- tumor impalpable but suspected by high PSA
➢ T2- tumor nodule palpable on rectal examination
o T2a- single nodule palpable on digital examination within prostate
capsule
o T2b- nodule involving both lobes
➢ T3- Tumor extends through the capsule
o T3a- extension through capsule one or both
o T3b- extension to seminal vesicles
o T4- tumor which is fixed or spread to adjacent structures like pelvic wall
and rectum other than seminal vesicles

• Staging of carcinoma prostate

➢ Occult- diagnosed after
investigation due to suspicion
➢ Stage I (T1)- tumor confined to
prostate/local nodule
➢ Stage II (T2)- tumor involving
capsule or diffuse type
➢ Stage III (T3)- Tumor involving
seminal vesicle
➢ Stage IV (T4)- extension into
adjacent tissue

Figure 250: Staging of prostate carcinoma

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SURGERY MK
• If a carcinoma of the prostate is • The long term survival of patients
suspected, tissue must be removed treated by irradiation or radical
for histological examination and surgery is comparable.
confirmation of diagnosis by:
LOCAL SPREAD (STAGES T3
➢ TURP (especially with outflow
AND T4)
tract obstruction present)
• External-beam radiotherapy is the
➢ TRUS-guided needle biopsy
treatment of choice.
UNSUSPECTED CARCINOMA • In some cases, particularly those
OF PROSTATE (STAGE T0) with incipient ureteric obstruction,
• If the prostate feels normal on endocrine therapy may be required
examination but the specimen from in addition to irradiation. Methods
TURP has revealed well- of therapy include:
differentiated tumor in some of the ➢ Luteinizing hormone- releasing
removed tissue, the recommended hormone agonists (leuprolide,
method is: Goserelin)
➢ Observe patient ➢ Antiandrogens (cyproterone or
➢ Regular digital rectal flutamide)
examination (or ultrasound) ➢ Diethylstibestrol
➢ Regular assessment of serum ➢ Progestational agents
PSA
MESTASTIC DISEASE (STAGES
LOCALIZED PROSTATIC T1-T4, M1)
CARCINOMA (STAGES T1 AND • The treatment centers on androgen
T2) deprivation because the prostate
• There are 3 treatment options: gland is very androgen sensitive.
➢ Radical prostatectomy: the • Methods of therapy:
prostate, seminal vesicle, distal ➢ Luteinizing hormone- releasing
sphincter are removed along hormone agonists (leuprolide,
with reconstruction of the Goserelin)
urethra. It associated with very ➢ Antiandrogens (cyproterone or
low incidence of urinary flutamide)
incontinence and impotence ➢ Bilateral orchidectomy
➢ Radical radiotherapy: may be ➢ Diethylstibestrol-
associated with cystitis and o Initially given intravenously
proctitis and later orally. It is very
➢ Interstitial irradiation with 125I effective.
and 198Au

594
SURGERY MK
o Initially IV 100mg/ daily TESTICULAR
later orally 100mg/daily
o Response starts appearing in CANCER
48 hours
o Complications: cardiac
congestion, DVT,
gynecomastia.
➢ Progestational agents
CANCER OF THE
RENAL CARCINOMA PENIS

TESTICULAR
TORSION
NEPHROBLASTOMA • This is twist of the spermatic cord
causing testicular ischemia.
(WILMS TUMOR) • Peak incidence during the first year
of life and at puberty around the age
of 13 (When growth rates are the
fastest)
TUMORS OF THE • Undescended testis carries a higher
RENAL PELVIS AND risk of ipsilateral torsion.
• Salvage rate is 80-100% if surgical
URETER intervention is <6 hours from onset
of pain.
• Testicular torsion is frequently
preceded by strenuous activity or
CARCINOMA OF THE athletic event.
BLADDER • Testicular torsion can be
intermittent in which pain passes.
However, surgery is still advisable
especially if testicle(s) have a
transverse lie.

595
SURGERY MK
PATHOPHYSIOLOGY muscle elevating the scrotum and
• The testicle twists on its spermatic ipsilateral testis).
cord, causing obstruction of venous • Prehn’s sign: decrease in scrotal
return leading to swelling. pain with elevation of the testicle.
• If obstruction persists venous This action relieves pain in
thrombosis occurs followed by epididymitis but exacerbates it in
arterial occlusion. testicular torsion.
• Infarction ensues quickly in the DIAGNOSIS
absence of blood supply. • Since epididymitis is most
• “Bell-clapper deformity” seen: commonly confused with testicular
insufficient attachment of the torsion, several tests may aid in
testicle to the tunica vaginalis distinguishing the two:
allowing for a pathologically large ➢ Urinalysis and FBC are usually
degree of rotational freedom. This unremarkable in testicular
increases risk of torsion. torsion. Most patients will be
CLINICAL FEATURES afebrile.
• Acute onset of severe pain in • Since the ability to salvage the
testicle (making walking affected testis is dependent on how
uncomfortable), lower abdomen or quickly the testis becomes
the inguinal canal. destorsed, time is of the testis! If the
diagnosis is thought to be torsion,
• Scrotum is elevated, swollen and
surgical exploration is indicated.
tender
• Color Doppler ultrasound (US) or
• May be accompanied by nausea or
nuclear scintigraphy have become
vomiting.
the test of choice, showing the
• Classic signs: high-riding testis
presence or absence of blood flow
with a horizontal lie. However, this
to the suspected testis.
is often difficult to distinguish
• ALWAYS suspect torsion in a
because of degree of swelling in the
patient with inguinal/abdominal
scrotum
pain and an empty scrotum.
• Presence of a reactive hydrocele.
• Loss of cremasteric reflex (The MANAGEMENT
cremasteric reflex is elicited by • Surgical repair is the definitive
stroking the medial aspect of the treatment.
patient’s thigh, resulting in a • If the testis is viable, bilateral
contraction of the cremasteric orchiopexy/orchidopexy (detorsion

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SURGERY MK
and fixation with suture) is
performed.
• If the tissue is necrotic, the testicle
is removed to prevent gangrene.
The contralateral testis undergoes
orchiopexy as a prophylactic
measure.
• Note: the higher the undescended
testicle, the higher the lifelong risk
of cancer (irrespective of whether
the testicle is brought into the
scrotum surgically).

TESTICULAR/SCROT
AL MASSES AND
SWELLINGS

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SURGERY MK

NEUROSURGERY

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SURGERY MK

HEAD INJURY
• Head injury defined as traumatic damage that affects either the skull or brain.

599
SURGERY MK
• Every effort must be made to discover its underlying cause, paying particular
attention to: Cerebral perfusion pressure (CPP)
➢ The likely speed of impact
➢ Any events that may have led to the injury (e.g. • CPP= MAP-ICP
epilepsy, subarachnoid hemorrhage, alcohol • MAP= mean arterial blood
consumption) pressure (avoid systolic blood
➢ Any events after its occurrence (e.g. vomiting, pressure <90mmHg)
2 1
epilepsy, talking) • MAP= (𝐷𝑃) + (𝑆𝑃)
3 3
• Recall that the components of the cranial cavity • Normal MAP= 70-100 mmHg
include: (65-110 mmHg)
➢ Brain tissue: makes up 80% of intracranial • ICP= intracranial pressure,
volume. It is partially compartmentalized by the Normal ICP= 5-10 mmHg
reflections of dura (falx cerebri and tentorium
• ICP>20 mmHg should be treated
cerebelli). Cranial nerve III rungs along the edge
• Normal CPP= 60-80 mmHg
of the tentorium cerebelli. The brain weighs about
• Maintaining CPP between 50
1400g.
and 70mmHg in non-operative
➢ Blood: the brain receives about 15% of the cardiac
brain injury is the fundamental
output (75ml of blood). The brain is responsible
treatment
for 20% of total body oxygen consumption.
• Concept of CPP is important in
➢ CSF: this is formed primarily by the choroid
hypertensive patients. Lowering
plexus at a rate of about 500ml/day with 150ml of
the BP too fast will also decrease
CSF circulating at a given moment. It cushions the
the CPP, creating a new problem
brain. It is drained by the arachnoid villi.
• The Monro-kellie hypothesis entails the pressure-
volume relationship between intracranial pressure,
volume of CSF, blood and cerebral perfusion pressure
(CPP).
➢ The sum of the volume of the brain, blood and CSF
within the skull must remain constant, therefore, an
increase in one of the above must be offset by
decreased volume of others.
➢ It states that the cranial compartment is incompressible
and that the volume inside the cranium is fixed such
that any increase in one of the components (blood, CSF
or brain tissue) is at the expense of the others.
• Recall also the 5 layers of SCALP:
➢ S-skin

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➢ C-dense connective tissue (bleeds the most)
➢ A-aponeurotica Galia
➢ L-loose connective tissue
➢ P-periosteum
• The scalp is highly vascular and may be the source of major blood loss.
• Most head injuries are caused by blows to the head from numerous causes
including motor vehicle accidents, assaults and falls from heights.
• The brain within the skull is liable to injury when deceleration occurs i.e. when
the neck flexes, extends or rotates. As the brain moves within the cranial cavity,
it may strike sharp objects such as the sphenoid wing and the frontal and occipital
poles.
• Points where the brain is tethered such as the foramen magnum and the cranial
nerves are also potential sites of injury. Shaking of the brain when the skull
moves at high speed therefore results in hemorrhage in the subarachnoid space
and at the frontal, temporal and occipital poles and in tearing of nerves and
vessels. The damage can occur with the head without being struck, for example
in a high-speed car crash or in a fall from a height in which the body decelerates
rapidly. It may also be associated with direct damage from a blow or a penetrating
wound.
• Head injury is one of the most common cause of death and disability.

CLASSIFICATION
• Head injury is classified in the following ways:
1. General classification
2. According to Mode of injury (Etiological classification)
3. Pathological classification
4. Clinical classification (according to severity-GCS)
GENERAL CLASSIFICATION
• Injury is classified as:
➢ Open/ Penetrating
➢ Closed/ Blunt
MODE OF INJURY (ETIOLOGICAL CLASSIFICATION)
• These include
➢ Missile injury

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o High velocity: Gunshot wound
- Produce focal and diffuse widespread distraction.
o Low velocity: Catapult, golf ball, skull fractures and epidural hematoma
(injury to middle meningeal artery)
- May cause focal injury
➢ Non-missile injuries
o High velocity
- Typically motor accidents
- Acceleration/deceleration, rotational & direct impact injuries
associated with extensive brain contusion, subdural or intracerebral
hematoma with significant morbidity and mortality.
o Low velocity
- Striking the head against an object (Coup-Contra Coup injury)
- During a fall or in assault
- Injury localized at the site of impact (Coup)
- Injury at opposite site of impact (Contra-coup)
- Consciousness may not be altered.
DIFFUSE INTRACRANIAL LESIONS
CONCUSSION
• Altered mental state that may or may not include loss of consciousness
(momentous loss of consciousness). It is caused by impairment of the reticular
activating system.
• Also known as mild traumatic brain injury.
• Diagnosis is clinical with no CT signs.
• Recovery is often complete, however, residual effects such as headache may last
for some time.
DIFFUSE AXONAL INJURY
• This is caused by microscopic shearing of nerve fibers, scattered microscopic
abnormalities.
• It frequently requires intubation, hyperventilation, CPP monitoring and
admission to a neurosurgical intensive care unit (ICU).
• No mass lesion is seen on CT in Diffuse axonal injury.
• Patients are often comatose for prolonged periods of time (mortality= 33%).

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FOCAL INTRACRANIAL LESIONS
CONTUSSION
• Injury results from focal trauma to the parenchymal blood vessels leading to
petechial hemorrhages and edema (hemorrhagic brain contusion with edema)
• It may occur directly under the site of impact (coup) or on the contralateral side
(contrecoup).
• May result in an expanding mass effect
• Insult is to the gray matter which gradually infiltrates the white matter.
• Most common locations are sub-frontal cortex and frontal lobe.
• Presents with focal neurologic deficits, prolonged confusion or coma.
• They require close observation.
• They progress to herniation, rapidly deteriorate and die.
INTRECEREBRAL HEMORRHAGE
• Caused by traumatic tearing of intracranial blood vessels. It is difficult to
differentiate from a contusion.
• Include: Epidural and subdural hematoma (discussed later)
PATHOLOGICAL
• Includes:
➢ Primary injury
➢ Secondary injury
PRIMARY INJURY
• This arise from the initial injury at the time of impact.
• Results of mechanical forces producing tissue deformation.
• Injury thresholds for different tissues differ. Survival depends on the energy
reaching the brain which in turn depends on the velocity of impact for example
hitting a brick wall at 110km/h will be fatal but a kick to the head playing rugby
will probably not. Similarly, a shot from a high velocity rifle will prove fatal but
a shot from an air rifle will probably not.
• The mechanism is similar however the degree is different.
• Severe primary damage is characterized by coma from impact. The ability to talk,
even a few simple words, after injury indicates that whatever else may happen,
the primary injury was not severe and the injury is theoretically survivable.
• Range:
➢ Scalp laceration

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➢ Skull fractures
➢ Vascular- epidural, subdural, intracerebral/intraventricular and subarachnoid
hemorrhage
➢ Meninges
➢ Cerebral lacerations
➢ Neuronal + axonal injury (without sign on head or face)
SECONDARY INJURY
• These are further insults to the damaged brain. They may further exacerbate
primary injury.
• They are important to understand as they can often be prevented and occasionally
reversed, whereas nothing can be done about primary damage (except avoiding
the accident in the first place).
• The main secondary effects are respiratory complications, perfusion failure,
intracranial hematoma, cerebral swelling, epilepsy, infection and hydrocephalus.
• Secondary injury is often due to secondary insults that include:
➢ Poor oxygenation (hypo-ventilation)
➢ Poor perfusion (hypo-perfusion)
➢ Hypoglycemia of traumatized brain tissue.
• Secondary brain injury:
➢ Hypoxic hypoxia, hypercapnia and obstruction to breathing: head injury
patients are especially prone to respiratory problems because of lack of central
drive, airway obstruction, hemothorax or pneumothorax and/or aspiration
pneumonia. The most important aspect of care in the head-injured patient is
care of the chest.
➢ Ischemic hypoxia and infarction: perfusion failure will lead to cerebral
ischemia and worsening of the clinical state. Head injury itself is rarely a cause
of hypotension and other causes need to be investigated (e.g. rupture spleen).
Resuscitation must be rapid. Patients with head injury accompanied by a
systolic blood pressure of less than 60mmHg for more than a few minutes
rarely survive.
➢ Hypoglycemia
➢ Cerebral edema: there is increased ICP which leads to cerebral perfusion
failure which in turn causes ischemia leading to more brain swelling and a
further increase in ICP. This vicious cycle tends to be worse in those with
severe primary damage.
➢ Cerebral herniation

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➢ Infection: development of meningitis or an abscess after injury can reverse a
good recovery and must be watched for and treated vigorously.
➢ Hypotension
➢ Hypo and hyperthermia
➢ Hematoma (>150ml the brain cannot compensate): intracerebral, subdural and
epidural hematomata occur and can lead to deterioration following head
injury.
o Intracerebral and acute subdural hematomata are usually associated with
severe primary injury and carry a bad prognosis.
o In contrast subacute subdural and epidural hematomata are often
associated with little or no primary injury and bleed slowly over a few
hours or days, removal before intracranial pressure is excessive can lead
to complete recovery.
➢ Seizures: fits are common in head injury and cause ischemia while they are
occurring. They must be stopped rapidly using IV diazepam in small doses
followed by phenytoin or valproate to prevent recurrence.
SEVERITY OF BRAIN INJURY (CLINICAL CLASSIFICATION)
• Most used in assessment and management.
• Can be easily done by most health workers and is easily interpreted.
• It is very useful in assessing progress of the injury
• It is assessed using the Glasgow Coma Scale (GCS)

Value Eye (Out of 4) Verbal response (out of 5) Motor response (out of 6)

6 Obeys commands
5 Oriented & converses (gives Localizes to pain (brings hand above
name, place and date) clavicle to stimulus on head/neck)
4 Opens eyes Disoriented but Converses Withdraws from pain (bends arm at elbow
spontaneously (communicates coherently) rapidly but features not predominantly
abnormal)
3 Opens to verbal Inappropriate response Decorticate/ Abnormal flexion (Bends
command (intelligible single words) arms at elbow rapidly but features clearly
(sound) predominantly abnormal)-“Mummy
pose”

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2 Opens to pain Inappropriate sounds (only Decerebrate/ Extension (Extends arms at
moans/groans) elbow)
1 No response No response No response
• Note:
➢ Decorticate= flexion (upper limbs) and extension of lower limbs
➢ Decerebrate= mid brain injury, all limbs are in extension
• Note:
➢ GCS of 13-15 indicates mild head injury
➢ GCS 9-12 indicates moderate head injury
➢ GCS of 3-8 indicates severe brain injury
o GCS< 8: comatose
PEDIATRIC MODIFICATION
Age Eye Verbal Motor Total
0-6M 4 Cries-2 Flexion-3 9
6 -12M 4 Vocalises-3 Localizes-4 11
1-2Y 4 Words-4 Localizes-4 12
2-5Y 4 Words-4 Obeys-5 13
5 Y+ 4 Orienteted-5 Obeys-5 14

CLINICAL ASSESSMENT
• Primary survey- ABCs (with cervical collar until fracture ruled out by imaging)
• Secondary survey
➢ Full history and possible also collateral history
➢ Complete Examination
➢ Investigations
HISTORY
• Mechanism of injury: direct trauma to the head or deceleration
• Time of injury
• History of loss of consciousness & did the patient regain it (Lucid interval).
• History of convulsions
• History of bleeding from ears/nose or any discharge
• Headache, nausea, vomiting, a falling pulse rate and rising blood pressure
indicate cerebral edema
• Last meal

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• Co-morbidities
• Drugs- aspirin
EXAMINATION
• Complete neurological examination including:
➢ GCS
➢ Pupil light responses and reflexes: pupillary inequalities or abnormal light
reflex indicate intracranial hemorrhage
➢ Tone
➢ Power
➢ Reflexes
➢ Sensation
➢ Co-ordination
• Examine other systems also fully
➢ Pulse
➢ Temperature
➢ Blood pressure
➢ Respiratory rate
INVESTIGATIONS
DIAGNOSTIC
1. Imaging
➢ CT scan (because this is an emergency CT is used for diagnosis, it is cheaper
and faster than MRI): it shows contusions, hematomata, midline shift,
fractures, ventricle & brainstem injury, hydrocephalus and cerebral edema
➢ MRI
➢ X-ray- skull fractures, relative position of the calcified pineal gland, presence
of intracranial air.
o Skull X-ray: AP, lateral and Towne’s views-Cervical
fractures/displacement
o Serial X-rays (Cervical spine, chest, abdomen and pelvic)
➢ Carotid arteriography
SUPPORTIVE
1. Full blood count and Cross match/ Group & save
2. Abdominal ultrasound: for any abdominal injuries
3. Urea and Electrolytes
4. Creatinine

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5. Liver function tests
6. Blood sugar
7. Arterial blood gases

INDICATIONS
INDICATIONS FOR ADMISSION TO A GENERAL HOSPITAL
• Oriented patients with:
➢ Skull fracture or suture diastasis
➢ Persisting neurological symptoms or signs
➢ Confusion or any other depression of the level of consciousness at the time of
examination
➢ Difficulty in assessing the patient (e.g. due to alcohol, young age, epilepsy,
attempted suicide)
➢ Inadequate social conditions or lack of responsible adult or relative
➢ Co-existence of other medical conditions (e.g. coagulation disorders)
• All patients with impaired consciousness
INDICATATION FOR SKULL RADIOGRAPHY AFTER RECENT HEAD INJURY
• Oriented patient with:
➢ History of loss of consciousness or amnesia
➢ Suspected penetrating injury
➢ CSF or blood loss from the nose or ear
➢ Scalp laceration (to bone or >5cm long), bruise or swelling
➢ Violent mechanism of injury
➢ Persistent headache or vomiting
➢ Fall from a significant height in a child (depends in part on the age of a child)
and/or on to a hard surface, tense fontanelle, suspected non-accidental injury
• Patient with impaired consciousness or neurological signs all patients, unless
urgent CT is performed.
INDICATIONS FOR URGENT CT SCANNING AND/OR NEUROSURGICAL
CONSULTATION
• Coma, confusion or neurological signs persisting after resuscitation
• Deteriorating consciousness or progressive neurological signs
• Fractured skull in combination with
➢ Confusion or other impairment of consciousness
➢ Epileptic seizures
➢ Neurological symptoms or signs

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• Open injury with
➢ Depressed compound fracture of skull vault
➢ Fractured base of skull
➢ Penetrating injury
• Unstable systemic state precluding transfer to neurosurgery
• Diagnosis uncertain
• Tense fontanelle or suture diastasis in a child
INDICATIONS FOR NEUROSURGICAL CONSULTATION AFTER CT
SCANNING
• Abnormal CT scan
• High or mixed density intracranial lesion
• Midline shift
• Obliteration of third ventricles
• Relative dilatation of lateral ventricle(s)
• Obliteration of basal cisterns
• Intracranial air
• Subarachnoid or intraventricular hemorrhage

MANAGEMENT
GENERAL MANGEMENT
• Primary survey- ABCs
➢ Head must be positioned at 30 degrees in neutral position.
➢ Fluids- Crystalloid (NS), DO NOT GIVE DEXTROSE!
o If they are hypoglycemic give a bolus of 50% dextrose
➢ Oxygen saturation should be maintained at 90%
➢ BP systolic >90mmHg
➢ Mean arterial pressure should not go below 70 (keep at 80)
• Protection of airway using mouth gag, endotracheal intubation or tracheostomy
whenever required.

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• Throat suction, bladder and bowel care and good nursing (hourly turning to
prevent decubitus ulcers).
• Nasal oxygen or often ventilator support
• IV fluids initially later NG tube feeding
➢ Feeding within first 24 hours and assess if they can swallow (assess if NG
tube is required). Aim to attain normal diet by day 7
• Electrolyte maintenance
• Prevent hyper- or hypothermia
• Patients susceptible to seizure should start on prophylactic medication
(Carbamazepine, phenytoin and phenobarbital) If patient starts to seize treat for
seizures.
• SEDATION SHOULD BE AVOIDED!
• Antibiotics especially in patients with fractures: traditionally prophylactic
antibiotics have been given to head injury patients but are less commonly used
nowadays. Persistent rhinorrhea or otorrhea requires surgical treatment to repair
the skull base defect
➢ Antibiotics like penicillins, ampicillins are given.
• Give analgesia for pain (non-sedating) and Anti-acids (to prevent Cushing’s
ulcers).
• Corticosteroids either dexamethasone or betamethasone are used commonly but
their beneficial effect is not confirmed.
• Dealing with any scalp wound:
➢ Shave hair for at least 2cm around the wound
➢ Remove foreign bodies
➢ Debride the skin edges
➢ Suture the scalp in a single layer, leaving stitches in for at least 7 days
➢ Use lidocaine with adrenaline to reduce bleeding.
• Indications for surgery (craniotomy):
➢ Acute extradural/epidural hematoma
➢ Acute subdural hematoma
➢ Depressed skull fracture
• Procedure: Craniotomy is done and cranial flap is raised. Clot is evacuated
followed by applying hitch stitches between dural layer and scalp. Post-Op
antibiotics, analgesic and anticonvulsants are given.

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MANAGEMENT OF RAISED INTRACRANIAL PRESSURE
• Elevate head at 30 degrees
Measures to lower ICP:
• Diuretics “HIVED”
➢ Mannitol 20% (0.5-1g/kg- slow infusion in 30 minutes)-
200ml IV TDS or • Hyperventilation
➢ Furosemide 40mg IV TDS. It should not be given in case • Intubation with
of intracranial hematoma pretreatment and
• Hypertonic saline (3% saline) sedation
• Hyperventilation (decrease carbon dioxide partial pressure • Ventriculostomy (burr
and increase oxygenation- causes vasoconstriction) hole)
➢ Only done in 30 minutes when other measures have • Elevate the head of the
failed bed
• Decompressive craniotomy (ventriculostomy with burr • Diuretics (mannitol)
holes)

COMPLI CATIONS OF HEAD INJURIES Cushing’s triad for ICP

EARLY • Bradycardia
• Brainstem injury- due to coning • Hypertension and a
• Compression over cerebellum and medulla widening pulse pressure
• CSF rhinorrhea: indicate a tear in the dura following fracture • Decreased
involving the sinuses-frontal, ethmoid, sphenoid sinuses. respiration/apnea
Meningitis is the common complication of CSF rhinorrhea.
Treatment is initially conservative (10-day IV antibiotics and observations).
Surgeries include: reduction of fracture of middle third face and exploration of
anterior cranial fossa.
• CSF otorrhea
• Meningitis
• Pituitary damage and endocrine failure- requires high dose of hydrocortisone
200mg QID.
• Aerocele
• Depressed fractures: often causes injury to dural venous sinuses and may lead to
torrential hemorrhage which may be life threatening. So such depressed fractures
should never be elevated.
LATE
• Chronic subdural hematoma
• Early post-traumatic epilepsy- they need anticonvulsants for 3 years

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• Late post-traumatic epilepsy due to scarring and gliosis of cerebrum
• Post-traumatic amnesia
• Post traumatic hydrocephalus
• Post-traumatic headache

INTRACRANIAL HEMORRHAGE
EPIDURAL/EXTRADURAL HEMATOMA
• This is collection of blood in the extradural space between the dura and the skull.
• The most common site is temporoparietal region. They are usually associated
with fractures of the temporoparietal region.
• It can be unilateral or bilateral.
• Commonly affected vessels:
➢ Middle meningeal veins
➢ Anterior branch of middle meningeal artery
➢ Posterior branch of middle meningeal artery
• It may also result from a torn dural venous sinus

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PATHOLOGY
• Direct blow, like from cricket ball or road traffic accidents or fall and impact or
coup and contre-coup injuries lead to fracture of thin temporal bone and tear of
vessels.
• Bleeding initially outward towards the scalp and under temporalis leading to
formation of a hematoma.
• Gradual stripping of dura from skull and collection of blood occurs.
• In 6-12 hours epidural hematoma occurs which raises the intracranial pressure
leading to coning of supratentorial content (uncus of temporal lobe) through
tentorial hiatus.
• Shift of midbrain towards opposite side which gets injured by sharp edge of the
tentorial cerebelli.
• Corticospinal tract before decussation on opposite side gets injured so
hemiparesis and pupillary changes occur on the same side of hematoma. This
effect is called as Kernohan’s notch effect.
CLINICAL FEATURES
• History of transient loss of consciousness following a blow or a fall.
• Patient soon regains consciousness and again after 6-12 hours starts deteriorating
(Lucid interval).
• Later the patient presents with: confusion, irritability, drowsiness, hemiparesis
on same side of the injury.
• Initially pupillary constriction and later pupillary dilation occurs on the same
side, finally becomes totally unconscious- Hutchinsonian pupils.
• Death can occur if immediate surgical intervention is not done.

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• Features of raised intracranial pressure may be seen:
➢ Hypertension
➢ Bradycardia
➢ Vomiting
➢ Seizures (occasionally)
• Wound and hematoma in the temporal region of the scalp
may be seen
INVESTIGATIONS
• X-ray skull may show fracture of temporal bone
• Electrolyte estimation
• CT scan head is diagnostic. Epidural hematoma shows
biconvex lesion.
TREATMENT
• Immediate surgical intervention is a must to save the life
of the patient.
• Craniotomy is done and cranial flaps are raised. The dura
is opened and the clot is evacuated. The dura is fixed to
galea using interrupted sutures- Hitch stitches.
➢ 5cm vertical incision in parietal region above the
zygoma.
➢ Galea is incised. Skull is opened using perforator and
burr
➢ Meninges are kept aside
➢ Black currant jelly clot is evacuated
➢ Bleeding vessels are cauterized-bipolar cautery
➢ Dural hitch stitches are placed Figure 251: Epidural hematoma
➢ Opposite side if needed should be evacuated
• Antibiotics, analgesia and anticonvulsants are given postoperatively.
• Recovery is good after surgery.
COMPLICATIONS
• Meningitis
• Post-traumatic epilepsy
• Post-traumatic amnesia

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SUBDURAL HEMATOMA
• These are divided into:
➢ Acute subdural hematoma (<24 hours)
➢ Subacute (24hrs-2 weeks)
➢ Chronic subdural hematoma (>2 weeks)
ACUTE SUBDURAL HEMATOMA
• This is a collection of blood between the dura and
the brain. It is due to injury to the cortical veins and
often due to laceration of cortex of brain which
bleeds and blood gets collected in the subdural
space forming a hematoma.
• The hematoma is extensive and diffuse.
• There is no lucid interval. There is severe primary
brain damage.
• Hematoma may be of coup and contra-coupe type.
• Loss of consciousness occurs immediately after
trauma and is progressive
• Convulsion is common
• Features of raised ICP are obvious: high blood
pressure, bradycardia and vomiting
• Focal neurological deficits or hemiparesis can occur
• CT scan shows concavo-convex lesion.
• Treatment:
➢ Antibiotics Figure 252: Subdural hematoma
➢ Anticonvulsants
➢ Surgical decompression is done by craniotomy.
CHRONIC SUBDURAL HEMATOMA
• This is due to rupture of veins between dura and brain (cerebral hemispheres),
causing gradual collection of blood in subdural space.
• It is commonly seen in elderly people following minor trauma e.g. fall, slipping
(which might have gone unnoticed)
• In elderly people, the brain atrophies and even minor injuries can cause shearing
and bleeding from these veins,

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• Blood gradually collects over 2-6 weeks. Plasma and cellular components get
separated. Eventually cellular part gets absorbed leaving only fluid component
called chronic subdural hygroma.
• Usual hematoma collection is 60-120ml and often in 50% of cases is bilateral.
• Patients present with confusion, disorientation, gradually with altered level of
consciousness and drowsiness.
• Later convulsions, features of intracranial hypertension and features of coning
develop.
• Extensor plantar response and pupillary changes develop eventually.
• CT shows concavo-convex lesion.
• Treatment:
➢ Craniotomy and evacuation of clot is done when required on both sides.
➢ Antibiotics
➢ Anticonvulsants for 3 years.
• Complications:
➢ Epilepsy
➢ Meningitis
➢ Coning
➢ Neurological deficits
CHRONIC SUBDURAL EMPYEMA
• This may be a primary infection of the subdural space from sinusitis focus
causing suppuration and pus formation.
• It can be a complication of chronic subdural hematoma
• It is due to secondary bacterial infection of collected clot/fluid.
• Infection is from sinusitis scalp (common)/through earlier trauma
wound/hematogenous
• Commonly gram positive organisms like Streptococci (viridans/milleri) cause
empyema however other virulent organisms like gram negative bacteria
occasionally can cause it.
• There is cortical venous thrombophlebitis and cortical infarction
• Headache, fever, meningism and convulsions are the features.
• MRI is ideal than CT to diagnose
• Treatment: antibiotics, craniotomy and drainage, anticonvulsants, ICU care,
proper monitoring, regular follow up.
• It carries 10% mortality.

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SUBARACHNOID HEMORRHAGE
• This is a type of intracranial hemorrhage into the subarachnoid space usually
from basal cisterns.
• It may be spontaneous or following trauma.
• Causes:
➢ Intracranial aneurysm (50%)
➢ Hypertension
➢ A-V malformations
➢ Blood dyscrasias
➢ Anticoagulant drugs
➢ Brain tumors (malignant)
• Clinical features:
➢ Sudden onset of severe headache (thunderclap headache) with vomiting.
➢ Features of raised intracranial pressure: hypertension, bradycardia and
vomiting
➢ Photophobia
➢ Neck stiffness
➢ Focal neurological deficits: hemiplegia, dysphasia
➢ Eye changes: ptosis, dilated pupil, changes in the eyeball movement
➢ Sudden loss of consciousness
➢ Features of brain edema and cerebral ischemia
➢ In 40% of recovered patients, rebleeding occurs in 6-8 weeks which is
commonly fatal.
• Hunt and Hess grading for SAH:
➢ Grade 1: asymptomatic
➢ Grade 2: severe headache and neck stiffness
➢ Grade 3: drowsy, confused or mild focal deficit
➢ Grade 4: stupor, hemiparesis
➢ Grade 5: decerebrate rigidity, coma
• Fischer grading of SAH:
➢ I- minimal <8mm size
➢ II- moderate 8-15mm size
➢ III-severe >15mm size
• Differential diagnosis:
➢ Meningitis
➢ Coning due to any cause

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• Investigations:
➢ Lumbar puncture should be done to differentiate from meningitis. It has to be
done carefully as it may precipitate coning. In subarachnoid hemorrhage,
blood strained CSF is collected (Xanthochromic)
➢ CT scan
➢ Carotid and vertebral angiogram
• Treatment:
➢ Clipping or wrapping the aneurysm
➢ Craniotomy and proceed.
➢ Ligation of common carotid artery-there is risk of hemiplegia
➢ Therapeutic embolization
➢ Excision of vascular malformations
➢ Coiling of aneurysms with instruments

DEPRESSED SKULL
FRACTURE
• This means fracture depression is more than
the depth of inner table of the skull.
• It may result in:
➢ Tear in the dura beneath
➢ Hematoma in the deeper plane
➢ Injury to the cerebrum
➢ Injury to the venous sinuses-may cause
life-threatening hemorrhage. Fracture
Figure 253: Depressed skull fracture
should not be elevated in such occasion as
it itself can precipitate bleeding.
➢ Convulsions
➢ Meningitis
• Investigations:
➢ CT scan
• Treatment:
➢ Antibiotics, anticonvulsants
➢ Elevation of the depressed fracture: burr holes are made in the adjacent normal
skull. Fracture is elevated. Bony fragments and necrotic material are removed.
Dural tear is closed with interrupted sutures.

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BASILAR FRACTURE
• Signs include periorbital ecchymoses (raccoon’s eyes), retroauricular
ecchymoses (Battle’s sign), otorrhea, Rhinorrhea, hemotympanum and cranial
nerve palsies.
• A ring test for CSF rhinorrhea (in the presence of epistaxis): Sample of blood
from nose placed on filter paper to test for the presence of CSF. If present, a large
transparent ring will be seen encircling a clot of blood.

SPINAL TRAUMA
• Spinal trauma may involve injury to the spinal column, spinal cord or both.
• Recall: the vertebral column is composed of a series of motion segments. A
motion segment consists of two adjacent vertebrae, intervertebral disc and
ligamentous restraints. The neural elements are contained within the spinal canal.
• Spinal injury is 1/10 as common as head injury but the basic pathology is the
same.
➢ Primary injury occurs when the skeletal structures fail to dissipate the energy
of the primary mechanical insult, resulting in direct energy transfer to the
neural elements. The injury may occur directly by flexion, extension, axial
loading, rotation or traction or by compression of the cord by a fragment of
bone and/or disc.
➢ Secondary injury: hemorrhage, edema and ischemia result in a biochemical
cascade that causes the secondary injury. This may result in further loss of
neurological function. Prolonged hypotension and poor oxygenation
compound the situation so it is important that the patient is adequately
resuscitated. The spinal column should be realigned as soon as possible in
cases of cord injury in which dislocation or subluxation is present. Ongoing
spinal cord compression from disc material and/or bony fragments may
require surgical intervention. Secondary effects including hypoxia and
perfusion failure can also occur.
• Compression of the cord is less common than compression of the brain following
head injury.

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• The causes of cord compression are bone fragments, hematomata and acute disc
prolapses.
• Over 50% of spinal injuries occur in the cervical spine with the remainder being
divided between the thoracic spine, the thoracolumbar junction and the
lumbosacral region.
➢ Upper cervical spinal injury is uncommon as the canal is capacious. The
cervicothoracic junction is a transitional zone going from mobile to fixed and
is thus prone to injury. It may be difficult to visualize this area on radiography.
➢ The thoracic spine is relatively rigid because of the stabilizing influence of
the thorax. Significant disruption of the thoracic spine requires major energy
transfer and associated visceral and vascular injuries are common.
➢ The thoracolumbar junction is another transitional zone that is prone to injury,
this is the second most common area of injury.
• Recall:
➢ There are 7 cervical, 12 thoracic, 5
lumbar, 5 sacral and 4 coccygeal
vertebrae.
➢ The spinal cord extends from the
foramen magnum to the T12/L1
junction where it ends as the conus
Medullaris below of which the cauda
equine lies.
➢ The spinal cord consists of central grey
matter (neuronal cell bodies)
surrounded by white matter (axons).
➢ The lateral spinothalamic tracts transmit
pain and temperature sensation, the Figure 254: Cross-section of the spinal cord
lateral corticospinal tracts are
responsible for motor function and the posterior columns transmit position,
vibration and deep pressure sensation.
➢ A spinal nerve root exits on both sides of the spinal cord at each level. There
are 8 cervical nerve roots. The C1 root exits above the C1 body, the C2 root
between C1 and C2 and the C8 root exits below C7. All thoracic (12) and
lumbar nerve roots (5) exit below the pedicle of the same number.
• The cervical spine is the region more vulnerable to injury.
• The thoracic spine is relatively protected due to limited mobility from support of
the rib cage (T1-T10) however the spinal canal through which the spinal cord

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traverses is relatively narrow in this region. Therefore, when injuries to this
region do occur they usually have devastating results.
• The thoracolumbar junction (T11-L1) is a fairly vulnerable region as it is the area
between the relatively inflexible thoracic region and the flexible lumbar region.
• The lumbosacral region (L2 and below) contains the region of the spinal canal
below which the spinal cord proper ends and the cauda equine begins.
• Recall the spinal column can be divided into 3 columns: anterior, middle and
posterior. When all 3 columns are injured the spine is unstable. Instability may
also exist in some two-column injuries.

Figure 255: The three-column model of spinal stability

• There should be a high index of suspicion of spinal injury if any of the following
are evident:
➢ Neurological deficit
➢ Multiple injuries
➢ Head injuries
➢ Facial injury
➢ High energy injury e.g. fall from a height
➢ Abdominal bruising from a seatbelt, suggestive of a possible lumbar spine
injury
• In a conscious patient spinal injury can be excluded if:
➢ There is no pain
➢ Palpation of the spine is non-tender
➢ Neurological examination is normal
➢ There is a pain-free range of movement

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CLASSIFICATION OF SPINAL TRAUMA
• Spinal injuries are classified based on:
➢ Severity:
o Complete: rendering the patient functionless below the level of the lesion
o Incomplete: some sensorimotor function is preserved
➢ Level of neurological (sensory and motor) and bony involvement
➢ Fracture/dislocation type (mechanism, stable vs unstable)

PATHOPHYSIOLOGY
• Spinal cord injury leads to either temporary or permanent dysfunction.
• Spinal injury occurs due to
➢ Direct injury due to bullet firing or accidents (on road, in working place,
during communal violence etc.)
➢ Compression by bone fragments, hematoma or disk material
➢ Ischemia due to rupture of spinal arteries.
• Complete transection of the spinal cord causes immediate loss of sensation and
voluntary movement below the level of the lesion. In quick transection of the
spinal cord the patient feels themselves cut into 2.
• For a while, the patient’s mind remains clear but they feel as if the lower part of
the body below the injury does not exist. This is because the higher centers
remain unaffected but the spinal centers below the level of the injury loose the
function.
• The effects of complete transection of the spinal cord occur in 3 stages:
➢ Stage of spinal shock
➢ Stage of reflex activity
➢ Stage of reflex failure
• If the spinal cord is gravely injured but does not suffer complete division, the
condition is called incomplete transection.
• The stages above are seen also in incomplete transection of the spinal cord though
the features in the second stage differ.
STAGE OF SPINAL SHOCK
• This occurs immediately after the injury. It also known as the stage of flaccidity.
• It may last from seconds to weeks (3 weeks) and does not signify permanent
spinal cord damage therefore long-term prognosis cannot be postulated until
spinal shock has resolved.

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• Flaccid Paralysis (loss of muscle tone) occurs in 2 times or in all 4 limbs.
Paralysis depends upon the level of the injury.
➢ Injury in the cervical region leads to paralysis of all 4 limbs
(quadriplegia/tetraplegia)
➢ Injury to the thoracic, lumbar or sacral segments including cauda equine and
conus Medullaris causes paralysis of the lower limbs (paraplegia)
• All reflexes are lost due to injury to the anterior and posterior nerve roots.
• All sensations are lost due to injury to the posterior nerve roots and sensory
neurons in the posterior gray horn.
• Some visceral organs are also affected especially the urinary bladder and rectum
which become paralyzed. The heart rate is decreased and the pulse becomes weak
and thready.
• Venous return is also reduced. In complete transection of the spinal cord muscle
tone is lost and there is flaccid paralysis so skeletal muscles cannot contract to
push blood back to the heart (muscle pump) in addition, the limbs are immobile
and smooth muscles of blood vessels also loss their tone. Blood accumulates in
the blood vessels of the limbs so they become cold and blue.
• The effect on blood pressure depends upon the level of Neurogenic shock: is a state of
the injury: vasomotor instability resulting
➢ Lesions anywhere below L2 will not affect blood from impairment of the
pressure as much because the sympathetic descending sympathetic
vasoconstrictor fibers leave the spinal cord between pathways in the spinal cord or
T1 and L2 segments. simply a loss of sympathetic
➢ Lesions at or above T2 segment will cause blood tone.
pressure to fall drastically. Mean arterial pressure
falls below 40mmHg. Clinical features:
• Complete transection at the cervical region above C3 • Flaccid paralysis
can be very fatal because the diaphragm and other • Hypotension
respiratory muscles are cut off from respiratory • Bradycardia
centers. It can cause paralysis of respiratory muscles • Cutaneous vasodilation
leading to sudden arrest of breathing. • Normal to wide pulse
• Crush injuries at sacral segments of the spinal cord pressure
results in atonic bladder and loss of micturition reflex.

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STAGE OF REFLEX ACTIVITY
• This is also caused the stage of recovery. After 3 weeks period, depending largely
upon the general health of the patient, the reflex activity begins to return to the
isolated segments of spinal cord below the lesion.
• In complete spinal injury:
➢ Functional activities return to smooth muscle first.
➢ Sympathetic tone to blood vessels returns next as the neurons in gray horn act
independently of vasomotor center. When tone in blood vessels is restored the
blood pressure returns back to normal.
➢ After 3 months tone in skeletal muscle returns. First to the flexors. Though
the tonicity is returned, it is not complete even in flexor muscles. The muscles
remain hypotonic. Limbs in this condition tend to adopt a position of slight
flexion and the paralysis is therefor called paraplegia in flexion. Limbs cannot
support the weight of the body.
➢ After a few weeks reflex movements occur. First flexor reflexes (which can
be elicited by painful stimulus). The first reflex to appear is the Babinski
reflex.
➢ After 1 to 5 weeks extensor reflexes return, initially the knee jerk and then the
ankle jerk.
➢ In some cases, a widespread reaction can be elicited by scratching the skin
over the lower limbs or the anterior abdominal wall, depending on the level
of the lesion. This reaction constitutes the spasm in flexor muscles of both the
lower limbs, evacuation of urinary bladder and profuse sweating. It is called
the mass reflex.
• In incomplete spinal injury
➢ Tone returns to extensors first and not flexor. This is because in incomplete
transection, some of the descending fibers in the lateral column of the cord
especially vestibulospinal and reticulospinal tract may escape injury so some
connections persist between the brainstem and the spinal cord. Fibers of these
tracts mainly reinforce the activity of extensor motor neurons.
➢ Because of the extensor hypertonia, the lower limbs are extended at the hip
and knee with toes pointing slightly downwards, this condition is known as
paraplegia in extension.
➢ The stretch reflex reappears first. Flexor reflexes return later. Philipson reflex
(clasp knife reflex can be elicited)
o Philipson reflex (Clasp knife reflex): In the upper limb, some resistance
is offered when the arm is flexed at the elbow joint passively i.e. the arm

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cannot be flexed, this resistance is offered because of the stretch reflex
developed in the triceps muscles however if the forearm is flexed
forcefully the resistance to flexion is abolished suddenly leading to quick
flexion of arm (just like how a clasp-knife works)
➢ Mass reflex as seen in complete transection is not seen here.
STAGE OF REFLEX FAILURE
• Though the reflex movements return, muscles below the level of injury have less
power and less resistance.
• Usually general condition of the patient starts to deteriorate.
• General infections become common.
• Due to this, the failure of reflex function develops. The reflexes become more
difficult to elicit. The threshold for stimulus increases.
• Mass reflex is abolished and the muscles become extremely flaccid and undergo
wasting.

CLINICAL FEATURES
• Flaccid paraplegia with no preservation of sensation usually indicates a complete
lesion.
• If any sensorimotor function below the level of the injury is seen this constitutes
incomplete injury.
➢ Sacral sparing is a sign of incomplete spinal injury.
➢ The sacral dermatomes are the most resistant to injury and sacral sparing is a
cause for slight optimism (better prognosis)
➢ In sacral sparing there is perianal sensation,
voluntary anal sphincter contraction or voluntary
toe flexion.
PHYSICAL EXAMINATION
• Classification of spinal injuries as complete or
incomplete requires a proper neurologic examination
➢ The entire spine must be palpated and the
overlying skin inspected. A formal spinal log roll
must be performed to achieve this. Significant
swelling, tenderness or palpable steps or gaps
suggest a spinal injury. Note the presence of any
wounds that might suggest penetrating trauma and
Figure 256: Spinal log roll

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document the condition of the skin, particularly over the pressure areas.
• The exam should include testing the 3 readily assessable long spinal tracts:
➢ Corticospinal tract: located in the posterolateral of the spinal cord and
responsible for ipsilateral motor function. It is tested by voluntary muscle
contraction (Grade the power).
➢ Spinothalamic tract: located in the anterolateral aspect of the spinal cord. It is
responsible for contralateral pain (pin prick) and temperature sensation and
tested as such.
➢ Posterior columns: located in the posterior aspect of the spinal cord. It is
responsible for ipsilateral position and vibratory sense and some light touch
sensation. Tested using a tuning fork and position sense of the fingers and
toes.
• Deep tendon reflexes and sacral reflexes may be preserved in complete injuries.

Figure 257: Cross-section of the spinal cord and tracts

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SPINAL CORD SYNDROME
ANTERIOR CORD SYNDROME
• Pattern seen with injury to the anterior potion of the spinal cord or with
compression of the anterior spinal arteries (artery of Adamkiewicz).
• It involves full or partial loss of bilateral pain and temperature sensation
(spinothalamic tract) and paraplegia (corticospinal tract) with preservation of
posterior column function
• It is often seen with flexion injuries and carries a poor prognosis.
BROWN-SEQUARD SYNDROME
• This is seen with hemi-section of the spinal cord usually secondary to a
penetrating injury, but may also be seen with disk protrusion, herniation or tumor.
• It consists of ipsilateral loss of motor function (Corticospinal tract) and posterior
column function with contralateral loss of pain and temperature sensation.
CENTRAL CORD SYNDROME
• Pattern is seen with injury to the central area of the spinal cord often in patients
with a preexisting narrowing of the spinal canal.
• Usually seen with hyperextension injuries, its cause is usually attributed to
buckling of the ligamentum flavum into the cord and/or an ischemic etiology in
the distribution of branches of the anterior spinal artery.
• It is characterized by weakness greater in the upper extremities than the lower
extremities and distal worse than proximal.
• It has a better prognosis than the other partial cord syndromes with a
characteristic pattern of recovery (lower extremity recovery progressing upward
to upper extremity recovery, then the hands recover strength).

ASSESSMENT
• Assessment should answer the following questions:
➢ Is there any neurological injury?
➢ What level is the injury? (the lowest neurological level with normal
neurological function)
➢ Is the cord lesion complete or incomplete?
➢ Is the bony architecture stable or unstable?
• Mechanisms suspicious for spinal injury:
➢ Diving
➢ Fall from >10feet

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➢ Injury above level of shoulders (cervical spine)
➢ Electrocution
➢ High speed motor vehicle crash
➢ Rugby or football injury (tackling)
• If the lesion is incomplete, every effort must be made to prevent deterioration.
Thus the spine must be held in a stable position, hypoxia prevented and
hypotension corrected.
• Early investigation with MRI will exclude cord compression.
➢ Cervical spine films are indicated for: tenderness along cervical spine,
neurologic deficit, good mechanism of injury, presence of distracting injury
and patients with altered sensorium.
• If the bony architecture is displaced or thought to be unstable, it should be
reduced and stabilized.
• When the cervical spine is injured this can be done with traction only but if the
thoracic and lumbar spines are involved open reduction may be required.
• It is now common to perform an early operative fixation with bone grafts and
metal for both incomplete and complete lesions. This allows early mobilization
which in turn reduces the risk of chest complications and deep vein thrombosis.
• At the earliest opportunity the patient should be transferred to a spinal injuries
unit.

MANAGEMENT
• Always start with the ABCs of trauma resuscitation.
• Maintain spinal immobilization throughout the resuscitation.
• Estimate level of neurologic dysfunction during the secondary survey
• Obtain appropriate diagnostic studies
• Establish early neurosurgical consultation
• If blunt spinal cord injury is diagnosed, begin high-dose methylprednisolone
(must be given within 8 hours of injury and not for penetrating injury).
➢ Loading dose of 30mg/kg over 15 minutes during hour 1 followed by a
continuous infusion of 5.4mg/kg/hr, the infusion is continued for 23 hours if
the bolus is given within 3 hours of injury or for 47 hours if the bolus is given
within 8 hours of injury.

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CERVICAL SPINAL INJURY
• Injury to the cervical spine may accompany a head injury and
fractures and dislocations in this area are common after road
traffic accidents (most common cause) and falls.
• These injuries are usually classified based on:
➢ Mechanism: Flexion, extension, compression, rotation or a
combination of these
➢ Location
➢ Stability
• If a patient complains of neck pain or weakness and/or
numbness in the limbs or if there is loss of sphincter control,
an injury to the cervical spine should be suspected.
• Precautions should be taken to prevent further damage.
• Extension and rotation of the neck should be prevented Figure 258: Radiography of
preferably by halter tractions. cervical spine showing fracture
• Skull calipers may be applied later. dislocation of the spine at
C2/C3 level, so called
• Sandbands may help movement in the emergency situation. hangman's fracture
• Collars should be maintained in position until radiography has
been completed.
• 4 vies of the cervical spine should be obtained (lateral, anteroposterior, oblique
and odontoid)
• Lateral radiographs of the cervical spine, including all 7 cervical vertebrae are
done soon as possible. A lateral view alone will miss 10% of cervical spine
injuries.
• Movement of the patient is especially hazardous. 5 individuals are needed to
move the patient, keep the head and neck immobile.
• Patients unconscious following a head injury should be assumed to have a
cervical injury until proved otherwise by normal radiographs of the cervical
spine.

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CERVICAL SPINE FRACTURES AND
DISLOCATION
JEFFERSON FRACTURE
• A Jefferson fracture is a bone fracture of
the anterior and posterior arches of the
C1 (Atlas) vertebra, though it may also
appear as a 3 or 2-part fracture.
• It is a burst fracture.
• It is the most common C1 fracture.
• Results from axial loading on the back of
the head or hyperextension of the neck
such as when the patient falls directly on
his or her head or something falls on the
patient’s head
• Consider all C1 fractures unstable even
though most are not associated with
spinal cord injury
• Clinical features: Figure 259: Jefferson fracture
➢ Pain in the upper neck but no
neurological signs.
➢ There may be damage to arteries in the neck resulting in lateral medullary
syndrome, Horner’s syndrome, ataxia and inability to sense pain or
temperature.
• The use of surgery to treat a Jefferson fracture is somewhat controversial.
• Non-surgical treatment varies depending if the fracture is stable or unstable,
defined by an intact or broken transverse ligament and degree of fracture of the
anterior arch.
• An intact ligament requires use of soft or hard collar.
• A rupture ligament may require traction, a halo or surgery.
➢ Note: the use of rigid halos can lead to intracranial infections and are often
uncomfortable for individuals wearing them, and may be replaced with a more
flexible alternative depending on the stability of the injured bones but
treatment of a stable injury with a halo collar can result in a full recovery.
➢ Surgical treatment involves fusion or fixation of the first 3 cervical vertebrae

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➢ Fusion may occur immediately or later during treatment in cases where non-
surgical interventions are unsuccessful.
➢ A primary factor in deciding between surgical and non-surgical intervention
is the degree of stability as the presence of damage to other cervical vertebrae.
• Though a serious injury, the long term consequences of this fracture are uncertain
and may not impact longevity or abilities even if untreated. Conservative
management with an immobilization device can produce excellent long-term
recovery.
Steels Rule of thirds in regarding
ODONTOID FRACTURES to cervical injury
• Type 1: involves only the tip of the dens (stable) Recall: the anteroposterior
• Type 2: involves only the base of the dense (unstable) diameter of the ring of the atlas
• Type 3: fracture through the base and body of C2 is approximately 3cm.
(generally unstable
• Note: some type 1 fractures may be stable when the The odontoid process and the
transverse ligament remains intact. spinal cord are each
approximately 1cm in diameter
According to steels rule of thirds,
the remaining centimeter of free
space available for cord allows
for some degree of pathologic
displacement

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Figure 260: Normal odontoid (open mouth) view of cervical spine

HANGMAN’S FRACTURE
• This involves fracture of both C2 (Axis) pedicles
(“posterior elements”)
• Usually due to a hyperextension mechanism such
as falls (especially in adults), and motor accidents
due to impacts of high force causing extension of
the neck and great axial load onto the C2 vertebra.
• This type of fracture is often also seen in judiciary
hanging.
• Unstable fracture, however, often not associated
with spinal cord injury because the spinal canal is
at its widest through C2.
• Management is both non-surgical and surgical.
Figure 261: Hangman fracture
CLAY SHOVELER’S FRACTURE
• Usually a flexion injury resulting in an avulsion of the tip of the spinous process
(C7>C6>T1)
• It may also result from a direct blow.
• In Australia in the 1930s men digging deep ditches tossed clay 10 to 15 feet above
their heads using long handled shovels. Instead of separating, the sticky clay

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would sometimes stick to the shovel, the
worker would hear a pop and feel a
sudden pain between the shoulder blades
unable to continue working.
• The mechanism of injury is believed to be
secondary to muscle pull and reflex with
force transmission through the
supraspinous ligaments. The tremendous
forces pulls on the spinous process
producing an avulsion fracture.
• The fracture is diagnosed by plain film
examination.

THORACIC SPINE
FRACTURES
• Most injuries occur at the junction
between the relatively fixed upper Figure 262: Clay Shoveler's fracture
thoracic spine and the mobile
thoracolumbar region (T10-L5). Frequency L1> L2>T1
• When thoracic fractures do take place the results are particularly more
devastating.
• This occurs because the spinal canal through this region is relatively narrow and
the blood supply to this region is in a watershed area (the greater radicular artery
of Adamkiewicz enters the spinal canal at L1 but provides blood flow as high as
T4).
• Most thoracic spine fractures are caused by hyperflexion leading to a wedge or
compression fracture of the vertebral body.
• Most fractures/dislocations in this area are considered stable because of the
surrounding normal bony thorax however neurological impairment resulting
from injuries in this area is often complete.

THORACOLUMBAR JUNCTION AND LUMBAR

SPINE FRACTURES AND DISLOCATIONS
• Results from axial loading and flexion
• Potentially unstable
• Neurologic injury is uncommon but may result in spinal cord compression.

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DISTRACTION OR SEAT-BELT INJURY
• Frequently referred to as a chance fracture.
• Horizontal fracture through the vertebral body, spinous processes, laminae,
pedicles and tearing of the posterior spinous ligament.
• It is caused by an acceleration-deceleration injury of a mobile person moving
forward into a fixed seat belt.
• Abdominal injuries frequently coexist with this fracture/dislocation

THORACIC OUTLET SYNDROME

• Subclavian artery/vein and brachial plexus pass through a space defined by the
clavicle and first rib (thoracic outlet).
• Vascular compromise is more common than neurologic:
➢ Unilateral Raynaud’s phenomenon
➢ Adson’s sign- loss of radial pulse on abduction and external rotation of the
arm
• It can present with T1 sensory loss, wasting of thenar muscles.
• It is caused by:
➢ Fibrous band compressing C8/T1 roots (inferior trunk)
➢ Elongated C7 transverse process- “Cervical rib”
• Treatment: surgical lysis of fibrosis band or removal of C7 transverse process by
either transaxillary or supraclavicular approach to thoracic outlet.

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CNS TUMORS

HYDROCEPHALUS

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CHAPTER 19: MISCELLANEOUS

MISCELLANEOUS
CELLULITIS AND ERYSIPELAS
• Cellulitis is inflammation of the dermis and subcutaneous tissue. It most
commonly Group A Streptococci and Staphylococcus aureus.
• Erysipelas is a superficial cellulitis affecting the dermis and upper subcutaneous
tissue. It is commonly due to Group A Streptococci.
• Cellulitis results from pathogen entry through broken skin. Precipitating lesions:
trauma, ulcer, bite, skin damage from chronic condition.

RISK FACTORS
• Previous cellulitis
• Chronic disease: Diabetes, chronic kidney or liver disease, cancer
• Immunodeficiency
• Venous insufficiency
• Age
• Skin disease e.g. tinea pedis

CLINICAL FEATURES
• Skin:
➢ Inflammation: painful, hot, red, swollen
➢ Cellulitis is typically poorly demarcated, while erysipelas is raised and well-
defined
➢ May be associated with a skin abscess
• Commonest sites:
➢ Lower legs. Bilateral lower leg cellulitis rare and is often misdiagnosis of
venous eczema
➢ Erysipelas may also occur on the face where it can have an (Asymmetrical)
butterfly distribution on the cheeks and bridge of nose.
➢ Cannula site, possibly with phlebitis
• Non-dermal features:
➢ Lymphadenopathy
➢ Systemic symptoms: fever. Commoner with erysipelas, where it may precede
skin signs by hours.

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INVESTIGATIONS AND DIAGNOSIS
• Diagnosis is usually clinical
• Affected area:
➢ Look for portal of entry and ask about trauma
➢ Draw around edge of area to monitor progress
➢ Swab for culture only needed for severe/resistant infection or unusual
exposures (penetrating injury, water-borne, acquired abroad)
• Blood investigations:
➢ Full blood count: increased WBC
➢ C-reactive protein: increased
➢ Blood cultures
➢ D-dimers (to rule out DVT)
• Imaging:
➢ Foot X-ray for osteomyelitis
➢ Ultrasound and Well’s score to rule out DVT

MANAGEMENT
• Antibiotics
➢ Flucloxacillin PO for 5-7 days 1st line for most (for patient allergic to
penicillin use doxycycline or clarithromycin PO)
➢ If near eyes or nose or for human/animal bite wounds use Co-amoxiclav PO
➢ If severe, cefuroxime, ceftriaxone, flucloxacillin, co-amoxiclav, or
clindamycin IV
➢ If MRSA, vancomycin, teicoplanin or linezolid IV
• Analgesia:
➢ Simple analgesia PO
➢ Leg elevation can ease pain
• If at cannula site: remove cannula, re-site, and culture needle tip.

COMPLICATIONS
• Thrombophlebitis
• Sepsis
• Toxic shock syndrome
• Lymphangitis and secondary lymphedema
• Cavernous sinus thrombosis if facial

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NECROTIZING FASCIITIS
• This is a rare but life-threatening infection of soft tissue with high mortality rate

PATHOPHYSIOLOGY
• Bacteria enters through break in the skin. May follow surgery, trauma, IV
injection or insect bite.
• Infection spreads rapidly across fascial layer, leading to tissue death of fascia and
subcutaneous tissue.
• Can be:
➢ Polymicrobial (type 1)
➢ Monomicrobial (type 2): Group A streptococcus is a the most common cause
with tissue destruction driven by exotoxins A, B and C
• Fournier’s gangrene is a polymicrobial necrotizing fasciitis of the male perineum
usually following breach in GI or urethral mucosal. It is commonest in older men.

RISK FACTORS
• IV drug use
• Obesity
• Diabetes

CLINICAL FEATURES
• Rapidly expanding, inflamed area of skin. May progress to bullae and dusky
purplish discoloration
• Sever pain out of proportion to skin signs
• Skin crepitus: crackly on palpation
• Sepsis and systemic symptoms

INVESTIGATIONS
• Bloods:
➢ FBC: increased WBC
➢ Increased CK
➢ Increased lactate
• X-ray, CT or MRI may aid diagnosis, showing gas in soft tissue but should not
delay referral and surgery if clinical suspicion is high

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MANAGEMENT
• Urgent surgical debridement
• IV antibiotics: carbapenem + Clindamycin +/- MRSA cover (e.g. vancomycin)
• Consider IVIG though evidence is limited

GANGRENE
GAS GANGRENE
PATHOPHYSIOLOGY
• Myonecrosis due to alpha-toxin from Clostridium perfrigens. Occasionally
caused by other clostridia species.
• Clostridia usually inhabits soil or normal gut flora. They enter muscle in major
trauma or GI surgery. Rarely it is non-traumatic (spontaneous) due to colorectal
carcinoma or immunosuppression.
CLINICAL FEATURES
• Pain which may have sudden onset and be out of proportion to signs
• Skin crepitus: crackly on palpation
• Skin becomes swollen, dark purple and bullae form
• Septic shock
MANAGEMENT
• Surgical debridement
• IV antibiotics

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HAND INFECTIONS

ISCHEMIA AND SWELLING OF THE LOWER

LIMBS

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SKIN
• The skin is the largest organ in the body (by mass i.e. 4kg).
• Functions of the skin include:
➢ Protection:
o It acts as a physical barrier against thermal and mechanism insults e.g.
friction, shearing force and other material
o It provides protection against infection (innate immunity), chemicals,
ultraviolet irradiation (this is a function of melanin) and desiccation from
trans-epidermal water loss. The skin participates in antigen
presentation/immunological reactions/wound healing.
➢ Sensation: pain, touch and temperature
➢ Synthetic function:
o Ultraviolet induced synthesis of vitamin D: cells of the skin synthesize
vitamin D3 needed for calcium metabolism and proper bone formation.
o Hormonal e.g. testosterone
➢ Homeostatic function: Temperature and water regulation
o Constant body temperature is maintained by the skin’s insulating
components e.g. fatty layer and hair on the head and its mechanism for
accelerating heat loss (Sweat production and a dense superficial
microvasculature.
➢ Sexual signaling: production of sex pheromones by apocrine sweat glands that
are important in attraction.
• The skin consists of 3 distinct layers:
➢ Epidermis (ectodermal origin): consists of stratified squamous epithelium
mainly of keratinocytes which rest on a basement membrane separated from
the underlying layers. The epidermis adheres to the dermis by interlocking of
its downward projections (epidermal ridges or rete pegs) with upward
projections of the dermis (dermal papillae). The epidermis is divided into the
following layers depending on whether it is thick skin or thin skin:
o Stratum basale (basal layer): contains stem cells that divide to produce
keratinocytes which constitute 90% of the epidermis and melanocytes
which produce melanin that gives the skin its pigmentation (Recall:
different color skins are due to the amount of melanin produced and not
the necessarily the number)
o Stratum spinosum: contains cells in layers held tightly by desmosomes
which are visualized as bridges/spikes /spines crossing the cells

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o Stratum granulosum: contains keratohyalin granules that produce
profilaggrin (pro-filament aggregation protein)
o Stratum lucidum: Only seen in thick skin
o Stratum corneum: Upper cells lose their nuclei and become surrounded
by a tough impermeable envelope of various proteins
o Remember the mnemonic: “Black Shoes Go Looking Clean” for
histological layers of the epidermis
➢ Dermis (mesodermal origin): less cellular and contains blood vessels, nerves,
glands (Sweat and sebaceous) and epidermal derived appendages (hair
follicles and sweat glands)
o Papillary dermis: The upper layer of the dermis. It is a thin layer and
contains dermal papillae, loose connective tissue, type I and II collagen,
fibroblast, mast cells, macrophages and other leukocytes.
o Reticular dermis: The deeper layer of the dermis. It is thick and consists
of dense irregular connective tissues (type I collagen) and a network of
elastic fibers to provide elasticity.
➢ Subcutaneous layer/hypodermis: contains adipose tissue
• The cells of the epidermis include:
➢ Keratinocytes: account for 90% of the epidermal cells. They are derived from
the basal cells. It takes 14 days for keratinocytes to reach the stratum corneum
and another 14 days for the cells to desquamate (a total of 28 days).
➢ Melanocytes: found in the basal layer and secrete the pigment melanin which
is synthesized from tyrosine and packaged into melanosomes transferring it to
the keratinocytes via dendritic processes. These are derived from neural crest
cells
➢ Merkel cells: play a role in sensation (fine touch). They are found in the basal
layer and originate either from neural crest or epidermal keratinocytes
➢ Langerhan’s cells: these are dendritic bone marrow derived antigen presenting
cells found in the basal layer.

SKIN TUMORS
• Skin tumors of clinical importance include:
➢ Malignant melanoma
➢ Basal cell carcinoma
➢ Squamous cell carcinoma

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• Basal cell and squamous cell carcinoma are less aggressive forms and common
types of skin cancer whilst malignant melanoma is uncommon but the most
aggressive skin cancer of the three.
• It is generally accepted that these cancers are due to sun exposure.
• Skin cancer seems to be more prevalent in people with light skin or numerus
moles.
MALIGNANT MELANOMA
• Melanoma is the most frequent cause of death of all skin cancer types.
• It results from malignant transformation of the normal melanocytes usually
located in the basal layer of the epidermis.
• Many melanomas are curable by surgical excision.
RISK FACTORS
• Mole showing persistent changes in shape, size, or color. A mole that shows rapid
growth or heterogenous pigmentation should be evaluated and possibly biopsied
to rule out melanoma.
• Giant naevi or persons having more than 100 nevi, atypical/dysplastic naevi
• Personal history or family history of melanoma
• Excess sun exposure (especially in childhood) and sunburn: UV light is suspected
to play a role in the development of all types of skin cancer including melanoma.
Although the precise etiologic role of UV light in the malignant transformation
of skin cells remain unresolved, both UV-A and UV-B are thought to have
carcinogenic potential. UV-A penetrate deep into the dermis, damaging
connective tissue and intrinsic skin elasticity. Excessive UVB exposure results in
sunburn. (A simple mnemonic is that UVA Age and tans hence its use in sunbeds
while UVB Burns and causes cancer)
• Fair complexion
• Tendency to freckle
CLINICAL FEATURES
• Remember the ABCDE’s of melanoma (5 signs of melanoma):
➢ A- asymmetric shape
➢ B- boarders are irregular
➢ C- color is mottled or hyperpigmented
➢ D-diameter is large (>6mm)
➢ E- Enlargement or Evolving lesion
• Common sites:

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➢ Back (males)
➢ Legs (females)
TYPES OF MELANOMA
• They include:
➢ Superficial spreading melanoma
o Commonest type worldwide
o Can occur anywhere on both sun-exposed and non-exposed areas.
o Average age of diagnosis: 40 to 50 years
o Lesions are commonly on the upper back and lower legs
o Lesions show heterogenous pigmentation with irregular margins.
o Growth phase is radial with horizontal spread
➢ Lentigo maligna melanoma
o Usually seen in older individuals (70 years)
o Lesions appear on sun-exposed surfaces, particularly the malar region of
the cheek and temple
o Lesion exhibit horizontal spread
o Carries the best prognosis
➢ Acral lentiginous menaloma
o Unusual distribution. Lesions appear on palms, soles, nail beds r mucous
membranes (most commonly the vulva, other sites include anus,
nasopharynx, sinuses and oral cavity).
o It is common in Africa
o Average age of diagnosis=60 years.
o Spread is in a horizontal pattern
➢ Nodular melanoma
o Can occur at any site and has an a very early malignant potential
secondary to a predominantly vertical growth phase. (in contrast to the
other 3 variants that show radial growth phases with horizontal spread).
o Nodular lesions have well-circumscribed borders and uniform black or
brown coloring.
o It is the most aggressive and carries the worst prognosis.
➢ Amelanotic
STAGING
• Stage 1: local disease <1.5mm
• Stage II: local disease >1.5mm
• Stage III: regional disease

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• Stage IV: metastatic disease
CLARK LEVELS
• This provides an anatomic description of tumor invasion.
➢ Level 1: Tumor confined the epidermis
➢ Level 2: Tumor extends beyond epidermis into the papillary dermis
➢ Level 3: Tumor extends to papillary dermis
➢ Level 4: Tumor extends to reticular dermis
➢ Level 5: Tumor extends subcutaneous layer (Full thickness)
BRESLOW SCALE
• The Breslow scale defines primary melanomas that are <0.76mm thick as local
tumors

Figure 263: The Clark and Breslow classification for melanoma (Image from Blueprints
Surgery)

TNM STAGING
• Stage 1: T1 lesion (≤0.76 mm thick) or T2 lesion (0.76 to 1.50mm) with negative
nodes and no mets.
• Stage 2: T3 (1.51-4.00 mm thick) or T4 lesions (>4. 00 mm thick) with negative
nodes and no mets
• Stage 3: fewer than 3 regional mets (N1) and no distant mets
• Stage 4: Mets in the skin or subcutaneous, distant lymph node mets or visceral
mets

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DIAGNOSIS
• Biopsy of the lesion for histology.
MANAGEMENT
• Management depends on the thickness of the primary lesion, location and stage
of the cancer.
• Primary choice of management: Wide local excision
➢ Most tissue defects are primarily closed without skin graft.
➢ If primary biopsy specimen are found to have tumor-negative margins, no
further surgical treatment is required.
➢ Primary mucosal melanomas have poor outcomes because disease is usually
extensive
➢ Nail bed lesions require amputation at the distal interphalangeal joint for
finger primaries and the interphalangeal joint for thumb primaries
➢ Margins for surgical excision:
o In situ: 5mm margin
o <1 mm thick: 1 cm margin
o >1mm thick: 2 cm margin
• Regarding regional disease, the performance of elective regional lymph node
dissection for nonpalpable nodes is not routine. The thickness of the primary
melanoma is used to predict the chance of regional lymph node metastases.
➢ Thin lesions limited to the epidermis have a low likelihood of lymph node
metastasis whereas thick lesions invading the subcutaneous fat have higher
chance of spread
➢ Regional lymphadenectomy is usually only performed for thick lesions with
a likelihood of nodal spread
➢ Sentinel lymph node biopsy can be done. Using lymphoscintigraphym the
sentinel node of the first order lymph node basin into which tumor initially
drains is identified. Technetium and a sulfur colloid are circumferentially
injected around the primary lesion. Technetium drain via lymphatics to the
sentinel node which is identified using a handheld Geiger counter. The
sentinel node is excised and evaluated microscopically for evidence of
metastasis. Sentinel lymph node biopsy is usually considered for lesions
>1mm in thickness.
• In metastatic disease, individuals with a single in identifiable metastatic lesion
may benefit from surgical resection.

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• Resection is not generally recommended for patients with multiple metastatic
lesions.
➢ Sites of metastasis: Skin, lung, brain, bone, liver, and the gastrointestinal tract
➢ Treatment options: surgery, radiation, chemotherapy and isolated limb
perfusion
BASAL CELL CARCINOMA
• This is the most common form of skin cancer in Caucasians. It is rare in Asians
and exceedingly rare in darkly pigmented individuals.
• The predominant cause is long-term excess exposure to UV-B radiation.
• BCC is a disease of adults and tumors arise from sun-exposed skin, namely the
head and neck.
• The cell of origin of BCC has been thought to be the basal cell of the epidermis
however an alternative theory suggests that the originating cell type is a
pluripotent epithelial cell.
• BCC is the commonest but least dangerous skin cancer. It is also known as
‘Rodent ulcer’ as they burrow through tissue causing local damage but almost
never metastasize.
• BCC is categorized into 3 types:
➢ Noduloulcerative (most common)
➢ Superficial
➢ Sclerosing
CLINICAL FEATURES
• Shiny nodule ‘pearly’ with rolled, red telangiectatic edge and eroded center.
• Slowly increases in size
• Usually on sun-exposed sites especially upper 2/3 of face.
TYPES OF BASAL CELL CARCINOMA
NODULOULCERATIVE
• This is the most common type of BCC.
• Lesions have a pearly, dome-shaped, nodular appearance with associated
telangiectasia and an ulcerated center.
• Telangiectasia is secondary to tumor-induced angiogenesis and ulceration results
from outgrowth of the local blood supply.
• Tumors <1cm in diameter are rarely invasive and can be treated with cautery and
curettage or cryosurgery.

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• Tumors >1cm are treated with surgical excision. High risk sites of tumor growth
are areas with underlying bone and cartilage (i.e. nose, ear), because the growing
tumor tends to track along these structures. High risk tumors and recurrent tumors
should be treated with Moh micrographic surgery to ensure complete excision.
SUPERFICIAL
• This is the second most common BCC.
• Lesions usually appear on the trunk and proximal extremities and clinically
resemble thin, scaly, pink plaques with irregular margins.
• These horizontally expanding tumors are often dismissed as dermatitis,
subsequently tumors may reach diameters of several centimeters by the time of
diagnosis. By this late stage, ulceration and deep dermal invasion are present.
• Standard treatment has been wide-margin excision with skin graft if necessary.
However, this approach may be unacceptably morbid leaving a large skin defect.
• Topical chemotherapy with fluorouracil, cryosurgery and cautery/curettage has
shown cure rates similar to those of traditional wide excision
SCLEROSING
• This is the least common type. The anatomic distribution is similar to that of
noduloulcerative but histologically the lesions appear as narrow cords of tumor
cells encased in a proliferation of connective tissue.
• Macroscopically lesions are smooth atrophic and indurated and easily mimic scar
tissue. This deceptive appearance is unfortunate because sclerosing tumors are
more aggressive than other basal cell tumors.
• The growth pattern follows tissue planes and neurovascular bundles, resulting in
deep soft tissue invasion. Moh micrographic surgery is preferred management
technique.
MANAGEMENT
• Wide local excision biopsy with 4mm margin is the gold standard.
• Alternatives:
➢ Mohs’ micrographic surgery: segments are excised in stages and examined
histologically. Consider for difficult sites where tissue preservation is
important e.g. eyelid.
➢ Curettage: Removal of tumor soft tissue and cautery of the base. Consider for
small BCCs (<1 cm) but downside is that margins are difficult to assess.

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➢ Topical cryotherapy or medication (5-fluorouracil, imiquimod). Incisional
biopsy is still needed to confirm the diagnosis. Higher recurrence rates than
surgery.
➢ Radiotherapy: an alternative or adjunct to surgery. Good cure rate but may
have poor cosmetic outcome.
SQUAMOUS CELL CARCINOMA
• This is second most common form of skin cancer after BCC.
• Tumors arise from the skin and the oral and anogenital mucosa. Multiple
predisposing factors for development of SCC include:
➢ Sunlight exposure
➢ Human papilloma virus infection
➢ Immunosuppression: Transplant recipients, HIV infection
➢ Chronic ulcers
➢ Ionizing radiation (X-rays, gamma rays)
➢ Tobacco use
➢ Scars (burn injury)
➢ Xeroderma pigmentosum
• Squamous cell carcinoma is a malignant proliferation of keratinocytes (squamous
cells).
• Most remain localized, but 5% metastasize usually to lymph nodes.
• Marjolin’s ulcer is a rare SCC sub-type which arises within existing ulcers or
chronically damage skin.
CLINICAL FEATURES
• SCC appears as an indurated nodule or plaque often with ulceration which has
slowly evolved over time. Most lesions are on sun-exposed areas, such as the
face, ears and upper extremities.
➢ Ulcerated, irregular lesion with hard raised edge. May be painful. Increases in
size over months.
• Caucasians exhibit pinkish lesions, whereas darker-skinned individuals have
hypo- or hyperpigmented lesions.
• Regional lymphadenopathy occurs in 35% of SCCs arising in the lip and mouth.
• Aberrant keratinization is often seen in SCC occasionally causing the growth of
cutaneous horns. The base of a cutaneous horn should always be examined for
the presence of squamous cell cancer.

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MANAGEMENT
• Treatment is tumor removal by wide local surgical excision with 4mm margin.
• Consider topical imiquimod or 5FU if superficial
• The remaining defect is closed either primarily for smaller lesion or by skin
grafting or flap reconstruction for larger lesions. Cryosurgery or
cautery/curettage can also be used for small tumors.
• Prognosis is excellent.

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PROCEDURES

SCRUBBING UP AND GOWNING

DONNING GLOVES

SUTURE AND SUTURING TECHNIQUES

LOCAL ANESTHETICS

TYPES OF SUTURES

SUTURING TECHNIQUES

AIRWAY DEVICE INSERTION

LARYNGEAL MASK

ENDOTRACHEAL INTUBATION

CRICOTHYROIDOTOMY

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TUBE THORACOSTOMY

NEEDLE THORACOCENTESIS

URINARY CATHETERIZATION

SUPRAPUBIC CATHETERIZATION

DIGITAL RECTAL EXAMINATION

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DRAWING BLOOD AND INTRAVENOUS

CANNULATION
DRAWING BLOOD
• Before drawing blood ensure you:
➢ Know the patient
➢ Know the tests to be ordered for i.e. you must know the correct bottle with the
correct additive to use
➢ Gain consent from the patient
➢ Complete the blood forms (lab request forms) for the tests required.
➢ Label bottles fully with name, hospital number, date of birth and date of
sample
• Equipment:
➢ Blood taking device (vacutainers, syringe, butterfly)
➢ Tourniquet
➢ Alcohol swab
➢ Cottonwool ball
➢ Plaster
➢ Blood forms
• Procedure:
➢ Gather your equipment as listed above
➢ Ensure the prerequisites are met as stated above
➢ Introduce yourself to the patient and explain what you are going to do and
why

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➢ Attach the tourniquet to the upper arm of the patient and ask them to open and
close their hand (making a fist)
➢ Select a vein, usually the antecubital fossa is the best. Also make sure you are
not taking blood from an arm that has an intravenous drip running into it.
➢ Swab the selected vein with the alcohol
➢ Warn the patient you are about to start and insert the needle at 30 o to the skin
➢ Insert a bottle into the vacutainer barrel, if the needle in the vein, the bottle
will fill with blood, if not adjust the needle
➢ Fill all the bottle required
➢ Remove tourniquet
➢ Place cottonwool ball over needle and withdraw it from the skin, the patient
should apply pressure for 5min.
➢ Dispose of the sharps.
➢ Placed labeled bottle with the completed forms in a bag for transfer to the
laboratory.
➢ Apply a small plaster to the patient’s arm.

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Figure 264: Blood collection bottles

PERFORMING A FEMORAL TAP

• Equipment:
➢ Alcohol swab
➢ Syringe

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➢ Cottonwool ball
➢ Plaster
➢ Blood forms
• Procedure:
➢ Introduce yourself to the patient and explain what you are going to do and
why
➢ The patient should be supine with the groin and leg extended and slightly
abducted
➢ Locate the femoral artery, halfway between the anterior superior iliac spine
and pubic symphysis, 2cm below the inguinal ligament. You should be able
to feel the pulsating of the femoral artery. The femoral vein lies medial to the
femoral artery, mark out the femoral vein.
➢ Clean the skin directly over the vein with an alcohol swab
➢ Fix the vein between two fingers while inserting the syringe and needle at 90o
➢ Slowly advance the needle until there is free flow into the synrine
➢ Withdraw the needle and apply the cottonwool ball pressure for 5 minutes
➢ Place the blood in the appropriate blood bottle and send to the lab.

INSERTION OF AN INTRAVENOUS CANNULA

• Equipment:
➢ Intravenous cannula:
o Blue 22G (very small)
o Pink 20G (small)
o Green 18G (average)
o Grey 16G (large)
o Brown 14G (very large)
➢ Tourniquet
➢ Saline flush or intravenous fluid with giving set
➢ Securing dressing
➢ Sharps bin

• Procedure:
➢ Gather your equipment, introduce yourself to the patient and explain what you
are about to do.

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➢ Apply a tourniquet to upper arm and ask the patient to open and close their
hand
➢ Select a vein that is palpable and straight, if the cannula is for long-term use,
it is best situated away from joints e.g. lower forearm cephalic vein. In an
emergency, select a large-bore cannula in an antecubital fossa vein.
➢ Take the cannula, remove the sheath, open the wings and introduce the needle
into the vein at 30o to the skin. Once the needle is in the vein there will be a
visible flash-back in the barrel of the needle.
➢ Slide the cannula into the vein over the needle while removing the needle
➢ Remove the tourniquet, remove the needle and put white cap on the end of the
cannula
➢ Dispose of sharps
➢ Apply a dressing to the cannula
➢ Flush the cannula with saline
➢ Eliminate any air bubbles from the giving set of the intravenous fluid and then
attach it to the cannula
➢ Set infusion rate and note time infusion started

VENOUS CUT-DOWN
• If emergency intravenous access is required and no other sites are available, then
a venous cut-down can be performed. The most consistent and easily accessible
large vein is the long saphenous vein, alternative sites include the antecubital
fossa and the wrist. Aseptic technique should be used.
• Procedure:
➢ Infiltrate the skin with local anesthetic
➢ A transverse incision is made 1cm above and anterior to the medial malleolus
➢ The vein is gently dissected out, to control the vein two ligatures are passed
under it
➢ The digital ligature is tied, the other is left untied until a cannula is inserted
➢ A large bore cannula is inserted through the skin and into the vein, the
proximal ligature is then tied to keep the cannula in place
➢ The skin is closed and the cannula secured with a further suture and a dressing.
CENTRAL VENOUS CANNULATION
• Access to the central veins is a common requirement in modern practice and is
important for:
➢ Measurement of central venous pressure

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➢ Infusion of irritant drugs e.g. amiodarone, dopamine, streptokinase
➢ Infusion of parenteral nutrition
➢ Measurement of pulmonary artery wedge pressure
➢ Infusion of chemotherapeutic agents
➢ Placement of pacing wires
• It is important to note that although fluids can obviously be given through a
central line, it is not the method of choice if fluid needs to be infused quickly as
central lines tend to be long and thin.
• 2 different approaches can be used:
➢ Supraclavicular approach: preferred vein to cannulate is the right internal
jugular vein because it is easily accessible, has a straight path to the right
atrium and possible injury to the thoracic duct is eliminated. There is also less
risk of damaging the pleural cap and causing a pneumothorax hence it should
be the method of choice for the less experienced practitioner.
➢ Infraclavicular approach: used by more experienced practitioner, there is an
increased risk of pneumothorax and should not be used in patients with
clotting abnormalities as it is difficult to stem bleeding from the subclavian
vein if hemorrhage occurs. This approach makes nursing care of the central
line easier and is more comfortable for the patient.
• Equipment:
➢ Central line set:
o Central venous catheter
o Syringes
o Introducing wire
o Cannulation needles
o Scalpel blade
o Track dilator
➢ Saline
➢ Local anesthetic
➢ Suture material
➢ Antiseptic
➢ Transparent dressing
➢ Giving set
➢ Sterile pack
➢ Sterile glove
• Supraclavicular Procedure (internal jugular approach):

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➢ You need an assistant to pass the items
while you are sterile. Maintain the
uttermost sterility during the procedure
➢ Explain the procedure to the patient.
➢ Remove the pillows from under the head
and tilt the patient 30o head down. Some
patients may not tolerate this especially
those in heart failure.
➢ Place a bag of fluids under the right
shoulder to bring the vessels forward
➢ Expose the area and turn the patient’s Figure 265: Insertion of a central venous cannula:
head to the left internal jugular approach
➢ Scrub and don sterile gloves. With
patient in position paint the area where you are going to inset the central line
with antiseptic
➢ Inject local anesthetic into the skin and deeper tissues at the site of cannulation
➢ The right internal jugular vein runs from the base of the skull anterolaterally
in the carotid sheath below the sternocleidomastoid muscle to meet the
innominate vein and thence into the superior vena cava.
➢ The vein can be approached either high or low.
➢ In the high approach the landmark for cannulation is half distance along a line
between the sternal head of the clavicle and the mastoid and lateral to the
sternocleidomastoid muscle.
➢ Enter the skin with a needle connected to a syringe with saline. Advance the
needle deep to the sternocleidomastoid and point towards the suprasternal
notch until you freely aspirate blood.
➢ In the low approach to the vein, the landmark is the triangle formed by the
sternal and clavicular heads of the sternocleidomastoid, the vein lies between
them.

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• Infrasternal procedure (subclavian approach)
➢ In this approach, the entry point of the needle
should be 3cm below the midpoint of the
clavicle, with the needle angled towards the
jugular notch.
➢ Occasionally, the needle may abut against the
clavicular periosteum, this will be painful, so
it is important to anesthetize down the
clavicle. If the clavicle is encountered, then
gentle downward pressure should be applied
to the needle to help it enter the vein.
Figure 266: Insertion of a central venous
• Seldinger technique: cannula: Subclavian approach
➢ This is common to whichever method of
insertion is used.
➢ After the vein has been cannulated, a flexible wire with a leading J end is
inserted into the needle and fed through the vein towards the right atrium.
➢ ECG monitoring helps gauge whether the wire has been inserted too far and
is impinging on the myocardium.
➢ When the wire has been placed, the needle is removed over the top of it. The
track formed by the wire and placing a dilating device over it. The central
venous catheter is then fed into the vein over the wire, the wire is removed
through the cannula.
➢ The cannula is aspirated and flushed with saline to check it is working, is
sutured in place and a transparent dressing applied and a giving set attached
to the line. Once the patient has received a CXR to check position and exclude
a pneumothorax, the line can then be used.
• Complications of central line insertion
➢ Early
o Hemorrhage
o Misplacement
o Pneumothorax
➢ Intermediate
o Infection
o Blockage
➢ Late
o Scarring
o Myocardial damage

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NASOGASTRIC TUBE INSERTION
• This is a tube inserted into the stomach via the nose and is used for either drainage
or feeding.
• The most commonly used nasogastric tubes (NGT) are of the drainage type, are
made of plastic and are called Ryle’s tubes (16F).
• Tubes used for feeding are likely to be placed for a longer period of time, are
thinner and made of silicon (Fine bore nasogastric tubes) which is softer and
hence more comfortable for the patient and blocks less readily.
• Passage of an NGT is contraindicated in patient with a head injury because of the
risk of passing the tube through a fractured cribriform plate into the brain. If
drainage of the stomach is required, an orogastric tube can be passed.
• This is a skill that is important to know. Most medical schools now have
mannequins to practice this on, although it’s not frequently examined upon.
However, it is very useful to know how to do- you don’t want your first time to
be the middle of the night as a junior doctor when the nurses who normally do it,
call you as they cannot!
• Equipment:
➢ NGT made stiffer by storing in refrigerator
➢ Lubricating jelly
➢ Bladder syringe
➢ Drainage bag
➢ Securing tape
➢ Cup of water
➢ Litmus paper
• Procedure
➢ Wash your hands, don glove, introduce
yourself and explain to the patient that
the procedure is not particularly
pleasant and insertion of the tube may
cause them to retch.
➢ Position the patient upright and facing
forward
➢ Inspect the nose for any obvious
deformities Figure 267: Insertion of a nasogastric tube

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➢ Estimate the length of the tube to be inserted. Do this by measuring the NG
tube from the tip of the nose, to the earlobe and then the xiphisternum (5cm
below it).
➢ Lubricate the tube
➢ Insert the tube into nostril pointing towards the occiput. If you encounter any
resistance change to the other nostril.
➢ Ask the patient to swallow a mouthful of water, and as they do advance the
tube
➢ To check the tube is in stomach aspirate contents and test for acidity (pH 1-
5.5) with litmus. Alternatively instill 30ml of air with the bladder syringe and
auscultate the epigastrium for bubbling
➢ Secure the tube to the nose and attach a drainage bag
➢ Document the result in the patient’s notes.
• Insertion of a feeding tube is similar to that described above, except that feeding
tubes have a wire within them as they have insufficient rigidity for insertion into
the stomach. An X-ray is taken of the epigastrium to check the position of the
wire. When in the correct position the wire is removed leaving the feeding tube
in place.

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ANSWERS TO CLINICAL BOX
A CASE OF EPIGASTRIC PAIN AND VOMITING
1. Likely diagnosis: Acute pancreatitis because:
➢ History: age, positive alcohol drinking, vomiting and epigastric pain radiating
to the back
➢ Raise serum amylase (although serum lipase would have been more specific,
serum amylase can be elevated in a patient with gastric perforation due to
systemic absorption of pancreatic enzymes from the abdominal cavity, an
amylase rise of over 1000IU/dl is usually diagnostic of acute pancreatitis)
➢ Macrocytosis which suggests the alcoholic etiology
➢ Note: an ultrasound may be needed to rule out gallstones
2. Differential diagnosis to exclude:
➢ Gallstones (ultrasound)
➢ Perforated peptic ulcer (Erect chest X-ray which would show free subphrenic
air in 90% of cases)
3. Ranson’s criteria is used to grade the severity of alcoholic pancreatitis but it
takes 48 hours before the score can be used. Each fulfilled criterion scores a
point and the total indicates the severity.
➢ On admission
o Age>55 years
o WBC >16 x 109L
o LDH >600 IU/L
o AST> 120IU/L
o Glucose >10 mmol/L
o Fluid sequestration >6L
➢ Within 48 hours
o Hematocrit fall >10%
o Urea rise >0.9 mmol/L
o Calcium <2 mmol/L
o Partial pressure of oxygen <60mmHg
o Base deficit >4
➢ Points
o 0-2= 2% mortality
o 3-4= 15% mortality
o 5-6= 40% mortality
o >7= 100% mortality

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4. Causes of acute pancreatitis
➢ Alcohol and gallstones (common=80%)
➢ Trauma (RTA)
➢ Hypercalcemia, hyperlipidemia, scorpion stings, rupture of posterior
duodenal ulcer
➢ Rare= infections (mumps, coxsackie B virus), drugs (thiazide, corticosteroids,
salicylates, cimetidine), pancreatic structural anomalies (pancreatic divisum),
ampullary or pancreatic tumors
5. Causes of elevated serum amylase
➢ Perforated peptic ulcer
➢ Mesenteric infarction
➢ Cholecystitis
➢ Generalized peritonitis
➢ Intestinal obstruction
➢ Rupture ectopic pregnancy
➢ Diabetic ketoacidosis
➢ Liver failure
➢ Bowel perforation
➢ Renal failure
➢ Rupture abdominal aortic aneurysm
6. Management
➢ Medical:
o Admit to ICU
o ABCs- prompt fluid resuscitation, a urinary catheter and central venous
pressure monitoring, fresh frozen plasma and blood transfusion
o Total parenteral feeding
o Antibiotics: 3rd Gen cephalosporins (cefotaxime), imipenem
o Anticholinergics
o Calcium gluconate 10ml 10% 8 hourly
o IV omeprazole 40mg BD
o Analgesics- pethidine (Avoid morphine)
➢ Surgical: open surgery is the gold standard
7. Complications
➢ Local: pancreatic pseudocyst, abscess formation, biliary obstruction, fistula
formation, thrombosis
➢ Systemic: renal failure, septic shock, hypovolemic shock, electrolyte
imbalance, ARDS, respiratory failure, multi-organ failure

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CHAPTER 20: END OF BOOK REVISION

END OF BOOK REVISION

TRUE/FALSE
1. Long term sequelae of head injury:
A. Brain atrophy is a feature
B. Focal neurological deficits are not a feature
C. Memory deficits are not a feature
D. Epilepsy is a feature

2. Clinical classification of head injury is based on:

A. Mode of injury
B. Whether it is open or closed
C. Glasgow coma scale
D. Pathological lesion

3. Subdural hematoma follows:

A. Tearing of superior sagittal sinus
B. Tearing of cerebral veins
C. Middle meningeal artery laceration
D. Vertebral artery laceration

4. Head injury patient with subdural hematoma

A. Is likely to deteriorate faster if blood pressure is reducing
B. Is likely to deteriorate if blood pressure is increasing
C. Is likely to deteriorate faster if pupils are starting to become unequal
D. Is likely to deteriorate faster if hemiparesis is starting to present

5. The main source of bleeding in a deep scalp laceration is

A. Periosteum
B. Loose connective tissue
C. Aponeurotica galea
D. Dense connective tissue

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SURGERY MK
6. Epidural hematoma in head injury patient follows:
A. Tearing of cerebral veins
B. Brain laceration
C. Middle meningeal artery laceration
D. Superior sagittal sinus tear

7. Head injury patient who presents with skull fracture crossing the midline
A. Is likely to have epidural hematoma from superior sagittal sinus laceration
B. Is likely to have epidural hematoma from middle meningeal artery laceration
C. Is likely to have cerebral spinal fluid leaking from both ears and nose
D. Is likely to have fracture dislocation of C5/C6 cervical spine

8. Burns are classified in terms of depth as

A. Superficial partial thickness
B. Deep partial thickness
C. Full thickness
D. Full thickness is also known as second degree burns

9. The rule of 9 for estimating extent of burns is as follows:

A. Head and neck 9%
B. Front of trunk 18%
C. Perineum 11%
D. Upper limbs 18%

10.Cerebrospinal otorrhea:
A. Fracture of the patients’ temporal bone is always present
B. Fracture of the base of the skull is the cause
C. Immediate surgical repair is indicated
D. Infection is common
E. Indicates injury to the 6th cranial nerve

11. The comatose patient with a head injury:

A. Is nursed on his side to prevent aspiration of stomach content
B. Must have endotracheal intubation if pharyngeal reflexes are absent
C. Must have a nasogastric tube inserted
D. A urinary catheter is useful for monitoring fluid balance
E. A suction machine is essential

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SURGERY MK
12.Urine output in a burnt patient:
A. In children an output of 1ml/kg/hr must be maintained
B. In adult ensure an output of 70ml/hour
C. Catheterize all patients with extensive burns
D. In a 3-year-old female child size 24 Foley is used
E. Antibiotics are routinely given to catheterized patient

13.Cerebrospinal otorrhea complicating head injury requires:

A. Antibiotic ear drops
B. Plugging the external auditory meatus
C. Syringing with saline
D. Early dural repair
E. Parenteral antibiotics

14.Systemic effects of burns

A. Hyper-metabolism
B. Immunosuppression
C. SIRS
D. Keloids
E. Contractures

15.Complications of burns
A. Marjolin’s ulcer
B. Keloids
C. Systemic inflammatory response syndrome
D. Renal failure
E. Airway obstruction

16.Triage refers to:

A. Surgical wound debridement
B. Categorizing and sorting patients according to priority
C. Casualty evacuation
D. Only B and C are correct

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SURGERY MK
17.In mass casualty injuries, the following injuries require immediate treatment
A. Sucking wounds of chest
B. Flail chest
C. Tension pneumothorax
D. Penetrating wound of the abdomen

18.Complications of intercostal drain insertion:

A. Pneumothorax
B. Injury to intercostal neurovascular bundle
C. Lung and liver trauma
D. Surgical emphysema

19.The edge of a tuberculous ulcer is

A. Shelving
B. Rolled up
C. Undermined
D. Punched out

20.The edge of a malignant ulcer is

A. Shelving
B. Rolled up
C. Undermined
D. Punched out

21.Debridement is
A. The process of making an incision
B. The removal of foreign material or dead tissue
C. The process of obtaining hemostasis
D. None of the above

22.About ulcers:
A. Diabetic ulcer is an example of a specific ulcer
B. Malignant melanoma ulcer is always pigmented
C. Arterial ulcers are located on the medial aspect of the leg
D. Trophic ulcers are painful

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SURGERY MK
23.Acute raised intracranial pressure is treated by:
A. Mannitol
B. Furosemide
C. Hyperventilation
D. Steroids
E. Raising the foot end of the bed

24.Decubitus ulcers
A. Only occur in comatose patients
B. Are a form of ischemic necrosis
C. Cause septicemia
D. Antibiotics cure the condition
E. Surgery is of value in selected cases

25.History taking from a patient

A. Accounts for 10% of the diagnostic process
B. Open ended questions direct the interview
C. Referral letter may reveal important information
D. Occupation of the patient is not important
E. Smoking is associated with pancreatitis

26.Skin grafting
A. Auto graft refers to the use of pig skin
B. Xenograft usually takes and becomes part of the body skin
C. Allograft fails to provide any normal function
D. Split thickness skin grafting needs pedicles to survive
E. Split thickness graft heals with excellent appearance

27.Early signs of a rising intracranial pressure include:

A. Bradycardia
B. Deteriorating conscious level
C. Hypothermia
D. Hypertension
E. Tachypnea

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SURGERY MK
28.The Glasgow coma chart includes details on the following
A. Pupillary size
B. Motor response
C. Urine output
D. Hemoglobin level
E. Injury severity score

29.Pneumothorax
A. Occurs spontaneously sometimes
B. Bullae are a cause
C. Is a complication of flail chest
D. Thoracotomy is frequently indicated
E. A chest tube is always necessary

30.Spontaneous pneumothorax is caused by

A. Tuberculosis
B. Emphysematous bullae
C. Solitary lung cyst
D. Chronic bronchitis
E. Idiopathic

31.Decerebrate rigidity
A. Is commonly seen in patients with Glasgow coma scale of 8 or less
B. Is commonly seen in patients with Glasgow coma scale of 12 or more
C. Is commonly seen in a patient with stiff extension of limbs
D. Is commonly seen in a patient who is well oriented in person, space and time.

32.Brainstem injury is mostly likely to have occurred in patient who presents with:
A. Glasgow coma scale 15/15
B. Glasgow coma scale 15/15 and unequal pupils
C. Cerebral spinal fluid leak from both ears
D. Occipital scalp laceration

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SURGERY MK
33.All end colostomies are:
A. Permanent colostomies
B. Defunctioning colostomies
C. Not suitable for ano-rectal malformation
D. Hartmann’s colostomies

34.Complications of colostomy include

A. Bleeding
B. Diarrhea
C. Prolapse
D. Retraction
E. Parastomal hernia

35.Types of colostomy
A. Spectacle colostomy
B. Double barrel colostomy
C. Ileostomy
D. Gastrostomy
E. Pharyngostomy

36.Indications for permanent end-colostomy

A. Stage 1 carcinoma of the sigmoid
B. Carcinoma of the caecum
C. High fistula-in-ano
D. Inoperable vesicle-vaginal fistula
E. Duke-B squamous cell carcinoma of the anus

37.A patient with flail chest

A. Does not require a chest drain
B. Rarely requires ventilation
C. Should be nursed in a dark room
D. The flail segment moves in on inspiration
E. Should be treated in the intensive care unit

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SURGERY MK
38.Complications of defunctioning loop colostomy of the sigmoid colon include
A. Electrolyte imbalance
B. Excoriation of skin
C. Retraction
D. Prolapse
E. Internal hernia

39.Snake bite results in the following:

A. Visible puncture wounds
B. Swelling of the bitten limb
C. Occasionally gangrene
D. Disseminated intravascular coagulation frequently
E. Fat embolism

40.In a jaundiced patient with palpable gallbladder, the cause of jaundice is most
likely to be:
A. Gall stones in the gall bladder
B. Gall stone in the common bile duct
C. Cancer of head of pancreas
D. Cancer left kidney

41.Generalized peritonitis is likely to follow

A. Delayed diagnosis of perforated duodenal ulcer
B. Acute pancreatitis
C. Ruptured appendicitis
D. Torsion of the testis

42.Bilateral lower abdominal pain in a female patient is most likely caused by

A. Ectopic pregnancy
B. Appendicitis
C. Salpingitis
D. Ureteric stone

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SURGERY MK
43.Small intestinal obstruction is likely to present with
A. Radiating pain to the left shoulder
B. Spreading pain to the right iliac fossa
C. Colic pain in the umbilical region
D. Early vomiting

44.During wound healing fibroblasts migrates across the following protein:

A. Fibrillin
B. Fibronectin
C. Elastin
D. Laminin

45.Regarding collagen
A. It is composed to tropocollagen
B. It is synthesized mostly by mast cells
C. Type II collagen is most common in connective tissue proper
D. None above are correct

46.Basement membrane consists of:

A. Type I collagen
B. Type II collagen
C. Type III collagen
D. Type IV collagen

47.The following factors do not contribute to wound disruption

A. Massive blood transfusion
B. Anemia
C. Abdominal distention
D. Vitamin C deficiency

48.7 days after suturing, tensile strength of a wound will be:

A. 5% of the uninjured tissue
B. 20% of the uninjured tissue
C. 30% of the uninjured tissue
D. 50% of the uninjured tissue

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SURGERY MK
49.Acute appendicitis
A. Pain can be referred to the right subcostal region
B. Pain can shift to right iliac fossa
C. Can be associated with vomiting
D. Can be associated with left hip joint flexion

50.Large bowel intestinal obstruction

A. Early vomiting is a feature
B. Gross abdominal distension is a feature
C. Sigmoid volvulus is a possible cause
D. Rectal carcinoma cannot be the cause

51.Wound healing
A. Is impaired in anemic patients
B. Impaired in hematoma formation
C. Impaired in hypoproteinemia
D. Stimulated by steroids

52.Intestinal obstruction
A. Can be classified depending on the age of the patient
B. Can be made on erect clinical examination
C. Can be due to electrolyte imbalance
D. Pyloric stenosis is caused by lower intestinal obstruction

53.Obstructive jaundice
A. Is associated with biliary atresia
B. Is associated with itching of the skin
C. A patient with obstructive jaundice passes pale stool
D. Obstructive jaundice can be diagnosed by supine X-ray

54.Complications of intercostal drain insertion

A. Pneumothorax
B. Injury to intercostal neurovascular bundle
C. Lung and liver trauma
D. Surgical emphysema

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SURGERY MK
55.In acute appendicitis
A. Central or epigastric pain radiates to right iliac fossa
B. Central or epigastric pain shifts to right iliac fossa
C. Pain precedes nausea and vomiting
D. Nausea and vomiting precedes pain

56.In acute appendicitis

A. Mantrel (Alvarado) scores of 7 out of 10 is highly suggestive of appendicitis
B. Right iliac fossa (McBurney’s point) tenderness and leukocytosis are allotted
2 points each on mantrel scale
C. Rovsing’s sign and obturator test are contributory to diagnosis
D. Digital rectal examination has no value

57.In wound healing

A. Cytokines are solely produced by hemopoeitic cells
B. Cytokines optimize cellular response in inflammation
C. Interleukins are not classified as cytokines
D. Macrophages actively synthesize cytokine growth factors for angiogenesis

58.In a completely healed wound, the tensile strength will be

A. 20% of uninjured tissue
B. 40% of uninjured tissue
C. 60% of uninjured tissue
D. 80% of uninjured tissue

59.Wound closure using suture is termed

A. Closure by primary intention
B. Closure by secondary intention
C. Hemostasis
D. Only (C) is correct

60.Factors which affect wound healing include:

A. Chronic illness
B. Radiation therapy
C. Nutrition
D. All above are correct

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SURGERY MK
61.The following conditions are associated with intestinal obstruction
A. Imperforate anus
B. Hirschprung’s disease
C. Peritonitis
D. Massive potassium loss

62.Common causes of intestinal obstruction in the pediatric age group include:

A. Diaphragm of the duodenum
B. Ileal duplication
C. Intussusception
D. Imperforate anus
E. Peritonitis following a ruptured appendix

63.In the University Teaching Hospital colostomies are commonly performed for
the following conditions
A. Volvulus of the sigmoid colon
B. Vesicovaginal fistula
C. An obstructed umbilical hernia
D. Imperforate anus
E. Meckel’s diverticulum

64.Paralytic intestinal obstruction occurs in

A. Hypokalemia
B. Hyponatremia
C. Peritonitis
D. Hemoperitoneum
E. Retroperitoneal hematoma

65.Mechanical intestinal obstruction occurs in

A. Internal hernia
B. Intussusception
C. Gastric polyps
D. Gall stone ileus
E. Volvulus of the cecum

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SURGERY MK
66.Common causes of peritonitis in Lusaka are
A. Tuberculosis
B. Perforated appendix
C. Typhoid perforation
D. Biliary leak
E. Perforated diverticulum of the sigmoid colon

67.Shift of the falx cerebri occurs in

A. Hydrocephalus
B. Astrocytoma
C. Meningitis
D. Barry aneurysm of the Circle of Willis
E. Extradural hematoma

68.Gall stones cause

A. Acute cholecystitis
B. Acalculous cholecystitis
C. Obstructive jaundice
D. Carcinoma of the gall bladder
E. Torsion of the gall bladder

69.Factors which are known to cause perforation of the ileum include

A. Trauma
B. Typhoid
C. Gall stones
D. Foreign body
E. Diverticulum of the ileum

70.Mechanical ileus is a complication of

A. Hypokalemia
B. Pelvic peritonitis
C. Adhesions
D. Internal hernia
E. Paraplegia of acute onset

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SURGERY MK
71.Paralytic ileus is a complication of
A. Retroperitoneal hematoma
B. Paraplegia of slow onset
C. Hyperkalemia
D. Hypercalcemia
E. Peritonitis

72. Medical conditions which are known to present as acute abdomen include:
A. Sickle cell disease
B. Pneumonia
C. Hypocalcemia
D. Addison’s disease
E. Hemophilia

73.Early signs and symptoms of compartment syndrome include:

A. Absent pulse
B. Paresthesia
C. Inability to move toes or fingers
D. A compartment pressure of less than 10mmHg
E. Decrease in limb pain

74.Pre-operative care before laparotomy for intestinal obstruction

A. Nasogastric tube is mandatory
B. Urethral catheterization may be avoided to prevent infection
C. Antibiotic use should only be instituted after knowing the cause of obstruction
D. X-match should be done for all patients
E. Raised serum urea could be treated by furosemide to flash it through the
kidneys

75.Factors that increase wound infection postoperatively include

A. Wound irrigation
B. Tissue damage
C. Hematoma formation
D. Bacteria load <100 000/g tissue
E. Keeping clean incised wounds dressed for 48 hours

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SURGERY MK
76.Regarding incisions
A. Keloids form more readily on sternal area than abdomen
B. Langers lines are not used for placing incisions
C. Avoid old scars when re-operating
D. Incised wounds heal with minimal scarring
E. Traumatised skin edges can be sites of wound breakdown later

77.The signs of uncomplicated volvulus are:

A. Gross abdominal distention
B. Ballooning of the rectum
C. Dyspnea
D. Severe tenderness on abdominal palpation

78.The usual symptoms of appendicitis are

A. Central abdominal pain with severe vomiting
B. Fever over 40oC
C. Central abdominal pain moving to right iliac fossa
D. Nausea and anorexia
E. Painful micturition

79.The symptoms of acute uncomplicated small gut obstruction are:

A. Continuous severe abdominal pain
B. Absolute constipation
C. Abdominal distension
D. Bilious vomiting
E. Colicky suprapubic pain

80.The signs of acute uncomplicated small gut obstruction are:

A. Oliguria
B. Abdominal distension
C. Tinkling bowel sounds
D. Absence of guarding and rebound tenderness
E. Multiple fluid levels on erect film of abdomen

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SURGERY MK
81.Wound healing by secondary intention occurs:
A. When the wound edges are not approximated
B. When there is excessive skin loss
C. When the wound is infected
D. In anemia patients
E. In jaundiced patients

82.Sigmoid volvulus
A. Is initially treated with a rectal tube
B. Is common in African female
C. Rectal bleeding is common
D. Is an emergency best treated by barium enema
E. Resection and primary anastomosis is an acceptable form of treatment

83.Paralytic ileus (adynamic obstruction) occurs in

A. Patients following laparotomy
B. Peritonitis
C. Uremia
D. Hypokalemia
E. Hypocalcemia

84.Clinical features of acute intestinal obstruction include:

A. Abdominal pains
B. Melena
C. Vomiting
D. Distention of abdomen
E. Constipation

85.Acute intussusception in adults occurs due to

A. Gall stones
B. Change of diet
C. Maximum aggregation of Peyer’s patches
D. Intestinal polyps
E. Head injury

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SURGERY MK
86.The following are predisposing causes of sigmoid volvulus
A. Chronic constipation
B. Redundant pelvic mesocolon
C. Refined dietary intake
D. Hypokalemia
E. Uremia

87.The differential diagnosis of acute appendicitis includes:

A. Tonsillitis
B. Acute cholecystitis
C. Carcinoma of the cecum
D. Ectopic gestation
E. Infection in urinary tract

88.Burst abdomen is caused by:

A. Wound infection
B. Leak of pancreatic enzymes
C. Anemia
D. Jaundice
E. Persistent cough

89.In fracture of the base of the skull the following nerves are commonly injured
A. Olfactory
B. Facial
C. Vestibulocochlear
D. Accessory
E. Hypoglossal

90.Keloid characteristics include

A. Onset is often delayed for months
B. Is cured by cytotoxics
C. Regresses spontaneously
D. Pressure garments are useful following surgery
E. Radiotherapy is contraindicated

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SURGERY MK
91.The epidermis of the skin consists of the following:
A. Stratum corneum
B. Stratum Lucidum
C. Stratum granulosum
D. Stratum Malpighi
E. Stratum basalis

92.Complications of blood transfusion include:

A. Congestive cardiac failure
B. Antibody reaction
C. Infection
D. Disseminated intravascular coagulation
E. Fat embolism

93.Inguinal hernia
A. Indirect hernia is more common than direct hernia
B. Strangulation is more common with direct hernia than with indirect hernia
C. Obstruction is more common with indirect inguinal hernia than direct hernia
D. Direct hernia is likely to protrude through Hesselbach’s triangle

94.Differential diagnosis of inguino-scrotal mass includes:

A. Hernia
B. Hydrocele
C. Meningocele
D. Lipoma

95.The following conditions are associated with abdominal hernias:

A. Chronic cough
B. Multiple pregnancies in women
C. Poor surgical abdominal wound management
D. Ascites

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SURGERY MK
96.An indirect inguinal hernia
A. Is the commonest hernia in young adults
B. Exits through the femoral ring
C. Has its neck medial to the inferior epigastric vessels
D. Does not occur in female patients
E. Is treated with a truss

97.Umbilical hernias:
A. Are common in Zambian children
B. All need herniorrhaphy before 2 years of age
C. Does not give rise to complications
D. All are Paraumbilical
E. Adults do not have umbilical hernias

98.Features associated with incompatible blood transfusion include:

A. Loin pain
B. Tachycardia
C. Bradycardia
D. Cyanosis
E. Jaundice

99.Congenital diaphragmatic hernia

A. Are common
B. Always occur in anterior mediastinum
C. Is invariably fatal
D. Diagnosis is often missed initially in small hernias
E. Are best operated upon at 10 years

100. Concerning hernias

A. Inguinal hernias are more common on the right
B. Femoral hernias are more common in females than in males
C. Inguinal hernias are more common than femoral hernias in females
D. Paraumbilical hernias are acquired
E. Umbilical hernias are always congenital

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SURGERY MK
101. Risk factors for developing inguinal hernias include
A. Male factor
B. Enlarged prostate
C. Chronic cough
D. Ascites
E. Chronic constipation

102. Differential diagnosis of inguinal hernia in a female are:

A. A hydrocele of the canal of Nuck
B. Femoral hernia
C. An encysted hydrocele of the cord
D. Lipoma of the cord
E. Spermatocele

103. An inguinal hernia in a 3-month old baby boy should be treated

A. Because small gut strangulation is a risk
B. By a truss
C. By early operation
D. Left alone because it resolves spontaneously
E. By surgery only if the hernia becomes irreducible

104. Quadriplegia
A. Can be caused by fracture dislocation at C5/C6 cervical spine
B. Can be caused by fracture dislocation at T5/T6 thoracic spine
C. Can be caused by Hangman fracture
D. Hypoventilation is not a feature

105. Second cervical vertebra and odontoid fracture

A. Basal odontoid fracture extending into body of C2 is type III fracture and is
unstable
B. Basal odontoid fracture is type I and is stable
C. Apical fracture of odontoid process is type II
D. Jefferson’s fracture is C3 fracture

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SURGERY MK
106. Patient who presents with goiter, asphyxia and hoarseness of voice:
A. Is likely to have malignant goiter
B. Is likely to have retrosternal goiter
C. Is likely to have unequal pupils
D. Is likely to have dilated pupils

107. Preoperative treatment of toxic goiter

A. Iodine can be given in combination with carbimazole or propranolol
B. Iodine can be given and reduces vascularity of goiter
C. Nadolol is not a beta-blocker to be used in treating toxic goiter
D. It is not necessary to reduce toxic goiter to euthyroid status before operations

108. Secondary thyrotoxicosis

A. Occurs in older patients than those with primary thyrotoxicosis
B. Eye signs including lid lag and exophthalmos are absent
C. Early signs of cardiac decompensation like ankle edema and dyspnea are a
feature
D. Orthopnea is not a feature

109. Malignant thyroid

A. Papillary carcinoma is most uncommon
B. Anaplastic carcinoma is seen in old patients
C. Follicular carcinoma is seen in 20% of patients of middle age
D. Medullary carcinoma is the commonest malignancy

110. Hashimoto’s disease

A. Is common in post-menopausal women
B. On inspection one lobe of the thyroid is larger than the other
C. Symptoms of hypothyroidism are absent
D. Blood test may show antibodies to the thyroid gland

111. Thyroglossal cyst

A. It is anterior cervical midline mass
B. Subhyoid is rare site for thyroglossal cyst
C. Thyroglossal fistula is a rare post-operative complication
D. Moves upwards when the tongue is protruded

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112. The following vessels supply thyroid gland
A. Superior thyroid from external carotid artery
B. Inferior thyroid from thyrocervical trunk of subclavian artery
C. Thyroidea ima artery from arch of aorta
D. All above except “B” and “C”

113. Malignant goiter

A. Medullary carcinoma is the commonest
B. Papillary carcinoma is the commonest
C. Bone metastasis may occur
D. Is slow growing

114. Toxic goiter

A. Patient has good appetite
B. Patient gains weight rapidly
C. Lid lag is not a feature
D. Proximal myopathy is a feature

115. Goiter
A. Is more common in males
B. Compression signs include hoarseness of voice
C. Moves with protrusion of the tongue
D. Moves with swallowing

116. Toxic goiter

A. Lid lag is a feature
B. Lid retraction is a feature
C. Exophthalmos is a feature in secondary thyrotoxicosis
D. Anxiety state is a feature

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117. In thyroid function
A. Coupling stage in thyroid hormone synthesis is catalyzed by deiodinase
enzyme
B. T4 is metabolically more active than T3
C. Thyroid hormone lack in children affects physical growth and mental
development
D. TSH, T3, T4 and radioisotope thyroid scan are useful indices for thyroid gland
activity

118. Examination of non-toxic goiter:

A. Includes asking the patient to swallow on inspection
B. Palpation is best done from the front
C. Palpation is best done behind
D. Determining lower edges helps to check for retrosternal goiter

119. Patient who presents with goiter causing tracheal obstruction

A. Stridor is a presenting feature
B. Dyspnea is a presenting feature
C. Kocher’s test is usually negative
D. Kocher’s test is usually positive

120. Toxic goiter

A. Exophthalmos is not a feature
B. Lid lag is a feature
C. Hot and moist skin and palms is a feature
D. Rapid pulse rate is not present during sleep

121. Secondary thyrotoxicosis

A. Patients are younger than those with primary thyrotoxicosis
B. Eye signs (exophthalmos, lid lag) are absent
C. Atrial fibrillation is a feature
D. Dyspnea is not a clinical feature

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122. Paraplegia can be caused by
A. Stab cervical injury
B. Fracture dislocation of thoracolumbar spine
C. Spinal tuberculosis
D. Schistosomiasis

123. Odontoid fracture

A. Is likely to involve C1
B. Is likely to involve C2
C. Type I fracture is stable
D. Type III fracture is stable

124. Cervical spinal fracture

A. Fracture at C4/C5 level spares phrenic nerve
B. Hangman’s fracture refers to the fractures at C5/C6
C. During hanging there is spinal hyperextension and distribution by body
weight
D. Open mouth X-ray is called town view

125. Regarding iodine metabolism

A. Uptake is solely by thyroid gland
B. Daily iodine requirement is 100micrograms
C. Iodine is trapped as iodide
D. Iodine is organified by carboxylase enzyme

126. Regarding thyroid hormone synthesis

A. Coupling precedes organification
B. T3 and T4 are stored in the follicle bound to thyroglobulin molecule
C. T4 is physiologically more active than T3
D. Serum T3 is 100-160ng/100ml and T4 60-140m/L

127. Carcinoma of the thyroid

A. Vascular and capsular invasion is diagnostic of follicular carcinoma
B. Psammoma bodies and orphan Annie eyed nuclei are diagnostic of medullary
carcinoma
C. Follicular carcinoma metastases is mainly by blood stream
D. Anaplastic carcinoma has the worst prognosis

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128. Medullary carcinoma
A. Arises from parafollicular “P” cells
B. Tumor may be sporadic or familial
C. Pituitary adenoma, parathyroid adenoma and pancreatic adenoma associated
with medullary carcinoma constitutes MEN type I syndrome
D. Tumors in (C) above constitutes MEN type II syndrome

129. Parathyroid adenoma, pheochromocytoma, medullary carcinoma and

mucocutaneous vacuromas constitutes:
A. Sipple syndrome
B. Marfan syndrome
C. Hashimoto thyroiditis
D. None of the above

130. Tumors of the thyroid gland include

A. Lymphoma
B. Follicular carcinoma
C. Anaplastic carcinoma
D. Warthin’s tumor
E. Giant cell tumor

131. Cervical injuries

A. Are commonly associated with head injuries
B. X-ray of the cervical spine down to C6 is adequate
C. An anteroposterior X-ray is more informative than a lateral view
D. Injuries at cord level C5 will cause respiratory arrest
E. During radiological evaluation the shoulders are pulled down caudally

132. Cervical spinal injury

A. Is common in young children
B. Odontoid peg is the commonest site of injury
C. CT scan is required in all cases for diagnosis
D. The phrenic nerve is involved if the injury is below C5
E. Is common in the head injured comatose patient

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133. Carcinoma of the thyroid
A. A common type is papillary carcinoma
B. Medullary carcinoma is associated with pheochromocytoma
C. Follicular carcinoma secretes calcitonin
D. Cold nodules on thyroid scan are associated with malignancy
E. Is seen following irradiation in childhood

134. Patients with spinal cord injury develop

A. Bronchopneumonia
B. Pressure sores
C. Pyelonephritis
D. Amyloidosis
E. Priapism

135. Post thyroidectomy complications include

A. Airway obstruction due to tracheomalacia
B. Recurrent laryngeal nerve palsy
C. External laryngeal nerve palsy
D. Hypercalcemia
E. Voice change

136. The differential diagnosis of mid-line tumors in the neck includes:

A. Dermoid cysts
B. Thyroglossal cyst
C. Goiter
D. Bronchial cyst
E. Pharyngeal pouch

137. Pathological fractures may be associated with

A. Scurvy
B. Hyperparathyroidism
C. Bone cysts
D. All of the above

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SURGERY MK
138. The most frequent offending agent in osteomyelitis of the spine is:
A. Streptococcus
B. Salmonella
C. Tubercle bacillus
D. Staphylococcus

139. The following sites are associated with non-union

A. Colle’s fracture
B. Carpal navicular fracture
C. Patella fracture
D. Clavicle fracture

140. A 3-year-old child with a femoral fracture should be immobilized by:

A. Skeletal traction
B. POP splint
C. Intramedullary nailing
D. Bryant’s traction

141. The following factors favor non-unions after fracture:

A. Muscle interposition
B. Hematoma at fracture site
C. Poor blood supply
D. Infection

142. The following statements are true of Perkins traction

A. It is a form of fixed skeletal traction
B. It can be used both in children and adults
C. It was invented by Prof Sir George Perkins
D. All above correct except “C”

143. Perkins’s exercises:

A. Are commenced 2 weeks after application of traction kit
B. Are commenced within a week after application of traction kit
C. Are commenced after 3 weeks when pain at fracture site has subsided
D. All above correct except “B”

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SURGERY MK
144. Perkins exercises:
A. Ensure accelerated femoral fracture union
B. Delay femoral fracture union due to mobility while performing exercise
C. Are designed to accelerate femoral fracture union and forestall knee stiffness
D. All above correct except “A”

145. Regarding fracture classification

A. Garden classification refers to fracture neck of femur
B. Salter-Harris classification refers to epiphyseal growth plate fractures
C. Le forte classification refers to tarsal fractures
D. All above correct

146. Ankle joint mortice

A. Mortice formed by medial and lateral malleolus only
B. Mortice formed by medial and lateral malleolus and tibio-fibular syndesmosis
C. Mortice formed by (b) above and articular surface of tibia
D. Only (b) above correct

147. Weber “C” ankle fracture:

A. Is fracture below tibio-fibular syndesmosis
B. Is fracture at level of tibio-fibular syndesmosis
C. Is fracture above tibio-fibular syndesmosis
D. Any fracture at ankle joint

148. Torn anterior cruciate ligament diagnosis, the following test are positive:
A. Anterior drawer test
B. Mc-Murray test
C. Lachman test
D. Pivot shift

149. Torn posterior cruciate ligament diagnosis, the following tests are positive:
A. Lachman test
B. Apley’s grinding test
C. Posterior drawer test
D. All of the above correct

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SURGERY MK
150. In classical degenerative osteoarthritis, the following are noted:
A. Osteophytes (lipping)
B. Narrowing joint space
C. Subchondral bone sclerosis
D. Subchondral bone cysts

151. Total hip replacement involves

A. Replacement of femoral head and acetabular cup
B. Replacement of femoral shaft with artificial implant
C. Both hips replacement with custom made implants
D. Replacement of only acetabular cup

152. Anterior shoulder dislocation may be reduced by

A. Kocher’s maneuver
B. Hippocratic method
C. Stimson’s technique
D. Socrate’s method

153. The following factors favor non-union of a fracture

A. Soft tissue inter-position
B. Hematoma at fracture site
C. Poor blood supply
D. When there are two bones if the other bone is intact

154. Salter-Harris type II epiphyseal fractures involves

A. It is a “T” shaped fracture extending into the proximal joint and metaphysis
B. It extends into metaphysis with a triangular component
C. It extends into proximal joint with partially crushed epiphysis
D. None of the above

155. In posterior hip dislocation

A. Dislocation puts sciatic nerve at risk of injury
B. Reduction is achieved under general anesthesia with patient on the floor
C. Skin or skeletal traction should be applied after successful reduction
D. All above correct except “C”

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SURGERY MK
156. In shoulder dislocation
A. Posterior dislocation is commoner than anterior dislocation
B. Axillary nerve is at risk of injury
C. Kocher’s manoeuver may be employed to reduce dislocation
D. All above are correct except “C”

157. In elbow dislocation

A. Anterior dislocation describes humerus lying anterior to radius.
B. Posterior dislocation describes humerus lying posterior to radius
C. The forearm bones provide key to description of the type of dislocation
D. None of above correct

158. In lower limb deformities

A. Genu valgus refers to bow legs
B. Genu varus refers to knock knees
C. Foot drop refers to injury of common fibular nerve
D. All above are correct

159. Secondary metastases to the spine can originate from cancer of

A. Thyroid
B. Breast
C. Lung
D. Prostate

160. Collar and Cuff sling

A. Is an example of external splint
B. Is suitable for displaced humeral fracture
C. Can be used to immobilize femoral fractures in children
D. The flexion angle at the elbow is less than 90 degrees

161. Intramedullary nail is

A. External fixation
B. Internal fixation
C. Suitable for fracture of the femoral shaft
D. Also known as Kuntscher nail

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SURGERY MK
162. The following tumors readily metastasize to bone
A. Rectal adenocarcinoma
B. Basal cell carcinoma of skin
C. Follicular carcinoma of the thyroid
D. Prostatic adenocarcinoma
E. Renal adenocarcinoma

163. Dislocations
A. Do not require urgent management
B. Post-reduction immobilization is required for 3 months
C. The medial nerve is damaged in shoulder dislocations
D. The ulnar nerve is damaged in lunate dislocations
E. All open dislocations require operative reduction

164. Osteoarthritis of the knee joint is a complication of

A. Hemophilia
B. A malunited femoral fracture
C. Total menisectomy
D. Valgus deformity of the knee
E. Gross obesity

165. Supracondylar fractures of the humerus

A. Always check the radial artery pulse
B. Always check nail bed capillary filling in absence of the radial pulse
C. Extension improves limb circulation
D. Nerve damage is uncommon
E. Non-union is uncommon

166. The following fractures commonly lead to ischemic necrosis of a part of the
bone
A. Femoral neck
B. Humeral neck
C. Scaphoid
D. Talus neck
E. Femoral condyle

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167. The following fractures lead to nerve damage in some patients:
A. Femoral neck
B. Neck of fibula
C. Medial epicondyle of humerus
D. Radial shaft
E. Humeral shaft

168. Fracture of the pelvis:

A. A stable fracture requires 3 months bed rest
B. A displaced sacroiliac joint requires skeletal traction
C. Blood transfusion is essential in extensive pelvic fractures
D. Isolated undisplaced iliac bone fractures do not require immobilization
E. Fractures of the pubic rami are relatively common

169. The following are flexors of the wrist joint:

A. Brachioradialis
B. Flexor carpi ulnaris
C. Pronator teres
D. Flexor digitorum profundus
E. Flexor pollicis brevis

170. Osteosarcoma is treated by

A. Radiotherapy
B. Chemotherapy and surgery
C. Immunotherapy
D. Antibiotics
E. Vitamin D

171. The following laboratory tests are useful in evaluating diseases related to
bones
A. Serum parathyroid hormone
B. C-reactive protein
C. Urinalysis for specific proteins
D. Fasting blood glucose
E. Serum uric acid levels

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172. Osteoporosis
A. Is common in premenopausal women
B. Is treated with estrogens
C. Causes pathological fractures
D. Erythrocyte sedimentation rate is elevated
E. Once established cannot be reversed

173. Primary osteoarthritis

A. Starts as a disorder of articular cartilage
B. Results in periarticular osteoporosis
C. Is associated with peripheral vascular disease
D. Occurs more commonly in females
E. Is common in Zambia

174. Dupuytren’s contractures:

A. Causes extension deformity of the wrist
B. Is familial
C. The foot can be involved occasionally
D. Is treated by steroids
E. Trauma is an etiologic factor

175. Carpal Tunnel syndrome

A. Occurs in middle aged men only
B. Symptoms are related to thumb only
C. Does not cause muscle wasting
D. Surgery is indicated
E. Symptoms are worse at night

176. Septic arthritis is best managed by

A. Aspiration of the joint
B. Antibiotics
C. Rest and elevation
D. Gypsona immobilization
E. Arthrotomy, antibiotics and rest for the joint

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177. Acute osteomyelitis
A. Brodie’s abscess is a variety of acute osteomyelitis
B. A common causative organism is Staphylococcus aureus
C. Bone drilling must be done early to prevent further damage
D. X-rays do not show changes in the first week
E. Is common in Zambian children

178. Tuberculosis of the spine

A. Is common in Zambia
B. Usually affects the vertebral bodies
C. Can be adequately treated by anti-tuberculous drugs alone
D. Never produces sequestra
E. Is not diagnosed unless a paraplegia is present

179. A 3-year-old child develops pain in the hip joint, is pyrexial and has a high
erythrocyte sedimentation rate:
A. Treat by traction alone
B. Treat by antibiotics alone
C. Blood culture are to be done
D. Explore the hip joint surgically
E. Take a careful history from the mother and do a full physical examination at
admission

180. Poliomyelitis
A. Anterior horn cells are affected
B. Flaccid paralysis develops
C. Joint contracture may follow muscle imbalance
D. Tendon division may improve function
E. Spread is by nasopharyngeal droplets

181. The following statements are true or false

A. The radial nerve is injured in humeral fractures
B. The ulnar nerve is injured in dislocated shoulder
C. A Colles fractures commonly injures the median nerve
D. Wrist drop occurs with median nerve palsy
E. Circumflex nerve injury causes inability to adduct the shoulder

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182. Acute osteomyelitis of the tibia
A. Not to be drained unless bone changes are present on X-ray
B. Staphylococcus aureus is the causative organism in all cases
C. Requires immediate drainage
D. X-Ray changes are visible within a few days of onset of infection
E. Antibiotics are not indicated

183. Ulnar nerve palsy

A. Occurs in fracture of the lateral epicondyle of the humerus
B. Results in wasting of thenar muscles
C. The little finger cannot be abducted against resistance
D. The ulnar side of the hand becomes dry (no sweating)
E. Dermatome involved is C5

184. Osteoporosis
A. Is a hereditary disease
B. Is same as Osteomalacia
C. Is curable
D. Is common in young premenopausal women
E. Responds to vitamin A

185. The following nerves are injured in a dislocation shoulder

A. Medial
B. Circumflex
C. Axillary
D. Suprascapular
E. The nerve which supplies the deltoid muscle

186. Concerning the menisci of the knee:

A. Injuries are common in elderly people
B. A tear is associated with osteoarthritis of the knee
C. Twists at the knee is the usual cause of meniscal tears
D. Injuries to the lateral one is commoner
E. One function is to improve lubrication

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187. A 39-year-old male with a suspected intervertebral disc prolapse suddenly
develops urinary retention. The following measures should be taken
A. Urgent radiculogram
B. Catheterisation
C. Urgent exploration of spine
D. Bed rest and skeletal traction
E. Send to the next urology clinic

188. A 4-year-old child develops pain in the hip joint with restriction of all
movements, pyrexia, high erythrocyte sedimentation rate and a high white blood
cell count
A. Treat with skin traction alone
B. Give aspirin and bed rest
C. Take blood cultures
D. Explore the hip surgically
E. Is commonly associated with trauma

189. Osteoarthritis has the following features:

A. Occurs in the hand bones
B. Is age related commonly
C. Often follows joint injury
D. Is commoner in males
E. Results in periarticular osteoporosis

190. Sickle cell disease

A. Is hereditary
B. Is due to an abnormal hemoglobin
C. Femoral epiphyseal infarction is a complication
D. Steroids are indicated in all cases
E. Is associated with osteomyelitis

191. Following a nerve injury

A. Neuropraxia has the best prognosis for recovery
B. Neurotmesis has the worst prognosis for recovery
C. Axonotemesis describes complete transection of the nerve
D. Axons regenerate at the rate of 1 mm per day
E. Axons regenerate at the rate of 1cm per day

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192. The following fractures occur at the wrist
A. Colles
B. Barton’s
C. Smiths
D. Pott’s
E. De Quervain’s

193. The following fractures usually require open reduction and internal fixation
A. Oblique shaft fractures of the humerus
B. Colles fracture
C. Greenstick forearm fractures in children
D. A displaced fracture of the lateral condyle of the elbow in a 10-year-old
E. A subcapital femoral fracture in an elderly female

194. A fracture of the carpal scaphoid

A. Is frequently caused by a fall on the outstretched hand
B. Usually occurs through the waist of the scaphoid
C. Avascular necrosis of the distal fragment is a possibility
D. Is commoner in the younger patient than the old
E. Non-union is possible

195. In spinal Tuberculosis

A. Infection starts in bone adjacent to a disc
B. New bone formation is minimal in active infection
C. Radiographs usually show destruction of the body of a vertebra without
involvement of the disc
D. Psoas abscess is a complication
E. Paraplegia is a complication

196. Poliomyelitis
A. Is caused by damage to anterior horn cells
B. Leg length inequality is a possibility
C. Short rigid scoliosis is usually associated with it
D. Foot neuropathic ulcers are common
E. Osteoarthritis is a common feature of the affected limb joints

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197. The following muscles in the hand are supplied by the median nerve
A. Abductor pollicis brevis
B. The first dorsal interosseous muscle
C. Adductor pollicis
D. Abductor digiti minimi
E. Opponens pollicis

198. In chronic osteomyelitis of the femur

A. New bone outside the cortex is the involucrum
B. Sequestrum is more radiopaque than normal bone
C. A loose dead bone is called sequela
D. Cloacae drain pus through the cortex
E. Long standing sinuses heal with antibiotics

199. The early clinical signs and symptoms of ischemia in the forearm and hand
following closed reduction of a supracondylar fracture are
A. Paralysis of median nerve
B. Gangrene of tips of fingers
C. Fixed contracture of the flexor muscles
D. Pain, especially on extension of the fingers
E. Absent radial pulse and poor capillary return

200. The following are complications of a Colles fracture at the wrist

A. Rupute of the extensor pollicis longus
B. Frequent non-union
C. Median nerve compression
D. Malunion
E. Inferior radioulnar subluxation

201. Classification of fractures

A. Radiologically as open or closed fractures
B. Clinically as compound fracture or closed fracture
C. Comminuted fracture when more than 2 fragments are present
D. Pathological fractures when fracture is due to tumor deposit
E. Supracondylar fracture refers to anatomical classification

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202. Concerning fractures of the neck of femur
A. They are more common in elderly men
B. They are usually caused by high energy trauma in the elderly
C. Avascular necrosis of the head of the femur is common complication
D. If treated conservatively they have a higher incidence on non-union
E. They are best managed by skeletal traction

203. Femoral shaft fractures

A. Are associated with an average blood loss of 1000-1500ml
B. In the young patient are usually associated with other life-threatening injuries
C. Are usually adequately treated with traction
D. Are commonly complicated by compartment syndrome
E. Are commonly associated with shortening of the affected limb

204. Regarding Perkin’s traction

A. The usual weight applied is 1/10 of the patient’s body weight
B. Leg lengths are measured once weekly for the first 2 weeks after application
C. Exercises are best commenced within the first 4 days of applying traction
D. The foot end of the bed is normally elevated by 4cm for every Kg of weight
E. A Denham pin may be used for applying the traction

205. Concerning open fractures

A. They are more common in the tibia than in any other long bone
B. They cannot be complicated by compartment syndrome
C. They are commonly associated with delayed union and non-union in the tibia
D. X-rays are not necessary
E. Are best treated with an external fixator

206. The following displacements are characteristic of Colles’ fracture

A. Volar (anterior) displacement of the distal fragment
B. Apex volar angulation
C. Ulnar deviation of the distal fragment
D. Impaction
E. ‘Dinner fork’ deformity

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207. Supracondylar fractures of the humerus in children
A. Are usually of the flexion type
B. Commonly occur after a fall on an outstretched hand
C. Are partly caused by the olecranon being forced into the olecranon fossa
D. Can be complicated by myositis ossificans
E. If presenting with extensive swelling should be manipulated and immobilized
in a collar and cuff

208. Concerning fracture healing

A. Hematoma formation at the fracture site does not influence the rate of fracture
healing
B. It is affected by the nutritional status
C. Upper limb fractures in children take about 3 weeks to heal
D. It is influenced by the type of bone involved
E. It is affected by the hemoglobin level of the patient

209. Concerning acute hematogenous osteomyelitis

A. It is commonly caused by Salmonella Spp
B. Organism normally settle in the metaphysis of long bones
C. In infants it may lead to septic arthritis
D. Radiological signs are present within 24 hours of the infection
E. It is best managed conservatively

210. Differential diagnoses of acute osteomyelitis include:

A. Fracture
B. Sickle cell crisis
C. Rheumatic fever
D. Cellulitis
E. Septic arthritis

211. The criteria for diagnosis of septic arthritis in patients with negative cultures
(according to Morrey and Associates) include:
A. Pain in suspected joint worsened by movement
B. Systemic symptoms
C. Poor response to antibiotic therapy
D. Swelling of suspected joint
E. Fever of more than 38.3 degrees Celsius

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212. Fracture of clavicle
A. Is usually compound
B. Is best treated by open internal fixation
C. Is usually associated with blood vessel injury
D. Is treated by POP immobilization
E. Can be treated by long arm sling alone

213. In Tuberculosis of bone

A. The local reaction is characterized by extensive new bone formation
B. The metaphysis of a bone is the commonest site of involvement
C. The infection is usually secondary to primary focus elsewhere in the body
D. Extension of the bone abscess into a joint is common
E. Associated abscesses show few signs of inflammation

214. Features occurring in children differ from those in adults in the following
respects
A. Fractures unite readily
B. Malunion can be corrected by growth
C. Joint stiffness is rare after immobilization
D. Fractures involve the epiphyseal plate on occasion
E. Fractures usually occur with minimal trauma

215. In fracture of the shaft of the adult femur

A. The estimated blood loss is at least 1 liter
B. Skeletal traction and Perkin’s exercises are effective treatment
C. Healing is faster in Zambians than in Europeans
D. Internal fixation allows earlier mobilization
E. Internal fixation is the treatment of choice in Zambia

216. Carpal tunnel syndrome

A. Is most frequent in middle aged men
B. Symptoms are related to all fingers and the thumb
C. Does not cause muscle wasting
D. Surgical treatment is usually curative
E. The symptoms are worse at night

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217. Dislocation of the hip
A. Common variety is a posterior dislocation
B. Delay in reduction does not increase the risk of late complications
C. Is overlooked if there is an associated fracture of the shaft of femur
D. Leads to dorsiflexion of the foot and great toes
E. Sciatic nerve injury occurs in 50% of patients

218. The following fractures are rarely adequately treated by closed manipulation:
A. Bennet’s fracture
B. Colles fracture
C. Phalages of digits
D. Monteggia
E. Tibial condyle

219. Internal hemorrhoids are arranged in the following manner with the patient in
lithotomy:
A. 3, 7 and 11 O’clock
B. 3, 7 and 9 O’clock
C. 7, 9 and 11 O’clock
D. 3, 9 and 11 O’clock

220. GoodSall’s rule is related to

A. Anal fissure
B. Anal fistula
C. Hemorrhoids
D. Anal abscesses

221. Common causes for rectal bleeding

A. Internal hemorrhoids
B. Anal fissure
C. Carcinoma rectum
D. All correct except (B)

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222. Concerning piles
A. First degree piles bleed but do not prolapse
B. Second degree piles prolapse with defecation and reduce spontaneously
C. Third degree piles are thrombosed piles whether internal or external
D. None above are correct

223. Treatment for first degree piles

A. Hemorrhoidectomy
B. High fiber diet
C. Suppositories
D. All above correct

224. Hemorrhoids
A. Always cause pain and bleeding
B. Sometimes cause pain and bleeding
C. Are always treated by operation
D. Can be due to increased intra-abdominal pressure
E. Are noted in pregnancy

225. The adult anus

A. Is 1cm long
B. Is covered by serosal lining
C. Blood supply is from 3 rectal arteries
D. Has 2 main parts meeting at perineal line
E. Inferior half lymphatics drainage is to the superficial inguinal nodes

226. Thrombosed hemorrhoids

A. Are treated by hemorrhoidectomy
B. Can be commonly seen at three sites: 4, 7 and 11 O’clock
C. Are due to arterial anastomosis
D. Usually have a sentinel pile
E. Common in diabetic patients

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227. Digital rectal examination is diagnostic in
A. First degree hemorrhoids
B. Low carcinoma of the rectum
C. Fissure in ano
D. Acute cystitis
E. Hirschprung’s disease

228. Axillary tail of the breast lies in

A. Upper outer quadrant
B. Upper inner quadrant
C. Lower outer quadrant
D. Lower inner quadrant

229. The breast tissue is located

A. Within subcutaneous layer
B. Within superficial fascia between upper and lower layers
C. Rests directly on pectoral fascia
D. Only “A” above is correct

230. Fibroadenoma of breast

A. Commonest benign tumor
B. It may be peri or intra canalicular
C. It lacks a definite capsule
D. Recurrence after excision is rare

231. Blood stained discharged from nipple may represent

A. Duct papilloma
B. Pagets disease of nipple
C. Galactocele
D. Only “B” and “C” correct

232. The following breast tumors may undergo malignant transformation

A. Phylloides tumor
B. Multiple duct papillomatosis
C. Intracanalicular fibroadenoma
D. All above

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233. Change of breast may also be named as

A. ANDI
B. Benign mammary dysplasia
C. Fibroadenosis
D. Chronic mastitis

234. Reference to ANDI of breast, histological features include:

A. Adenosis
B. Epitheliosis
C. Duct ectasia
D. Fibrosis

235. In Lactational mastitis

A. Cracked nipple permits entry of bacteria
B. Staphylococcus aureus is the main pathogen
C. There is good response to broad spectrum antibiotics
D. May be complicated by breast abscess

236. The following cannot affect breast tissue

A. TB
B. Syphilis
C. Fungal infection
D. All above

237. Triple assessment of breast pathology

A.Is only relevant to malignant conditions
B.Involves taking history and performing clinical examinations only
C.Involves as well U/S scan for females above 35 years old and mammogram
for females below 35 years of age
D. Fine needle aspiration cytology (FNAC) is preferred to incisional or
excisional biopsy snice it is specific and easy to interpret

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238. Pagets disease of the nipple
A. Usually presents as bilateral nipple eczema
B. Unilateral nipple eczema
C. Related to underlying duct carcinoma
D. All above true except (B)

239. Fibroadenoma of breast

A. It may present as mobile, painless mass
B. Has ill-defined edges
C. It may be intra or peri-canalicular
D. Recurrence common after excision

240. Fibrocystic breast disease presents as:

A. Fibroadenosis
B. Cystic formation
C. Epitheliosis
D. Fibrosis and lymphocytosis

241. The following drugs are used in breast cancer

A. Cyclophosphamide
B. 5-fluoro-uracil
C. Methotrexate
D. Adriamycin

242. The following features present advanved breast cancer

A. Peau d’orange
B. Nipple retraction/ulceration/bleeding
C. Fixity to underlying pectoral musclce
D. Hepatomegaly

243. Phyllodes tumor on histology

A. Might be benign
B. Might be borderline
C. Might be frankly malignant
D. Cellular stroma is characteristic

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244. Breast tissue lies
A. Within retromandibular space
B. Deep to pectoral fascia
C. Within superficial fascia
D. May extend to the axilla

245. Breast cancer

A. Carcinoma in-situ tumor has not yet breached basement membrane
B. Lobular carcinoma tends to be multicentric in origin more than ductal
carcinoma
C. Ductal carcinoma tends to be multicentric in origin more than lobular
carcinoma
D. None of the above

246. Breast cancer markers/receptors include:

A. ER/PR
B. HER-2/NEU
C. Tamoxifen is useful in ER positive receptors
D. Trastuzumab (Herceptin) is useful in advanced breast cancer that are HER-
2/NEU receptor negative

247. Supraradical mastectomy involves

A. Mastectomy, axillary node clearance and excision of pectoral muscles
B. The clavicle and sternum were spared
C. Procedure abandoned due to post op arm edema and weak upper limb
D. Operation is now obsolete

248. Radical mastectomy

A. Improves on supraradical mastectomy
B. It spared clavicle and sternum
C. Pectoralis major was spared
D. Also referred to as complete Halsted

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249. Patey’s mastectomy
A. Improved on radical mastectomy
B. It spares pectoral major muscles
C. Axillary and pectoral nodes clearance done
D. Power limb was an advantage

250. Lymph node involvement in breast cancer includes the following

A. Axillary lymph nodes
B. Supraclavicular lymph nodes
C. Cervical lymph nodes
D. Inguinal lymph nodes

251. Triple assessment is used in making a diagnosis of breast disease and consists
of the following:
A. Clinical examination, imaging, and fine needle aspiration cytology
B. Triple imaging-ultrasound, chest X-ray, mammography
C. Triple diagnosis- mammography, radioisotope studies and CAT-scan
D. Nipple cytology, thermography and MRI

252. A breast lump in an adolescent can be one of the following

A. Fibroadenoma
B. Giant fibroadenoma
C. Galactocele
D. Dysgerminoma
E. Hurtle cell tumor

253. An enlarged prostate

A. Can be determined by digital rectal examination
B. Can be identified by ultrasound evaluation
C. Doses not cause acute urinary retention
D. Prostatic specific antigen is an indicator of malignant disease in the prostate
E. Acid phosphatase is a specific test for prostatic cancer

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SURGERY MK
254. Prostatectomy is performed using one of the following approaches
A. Suprapubic transvesical
B. Retropubic (Millin’s)
C. Transurethral
D. Perineal
E. Pfannenstial incision

255. Complication of prostatectomy include

A. Excessive bleeding
B. Inflammation of the vas deferens
C. Bladder neck stricture
D. Gastric atony
E. Subphrenic abscess

256. Cancer of the prostate

A. Is common in the elderly
B. Is often asymptomatic
C. Treatment of choice is prostatectomy
D. Prostate specific antigen is a reliable guide to prognosis
E. Metastases are always osteolytic

257. Fibroadenoma of the breast

A. Occurs in early adult life
B. May be multiple
C. Adheres to the pectoralis major
D. Is painful
E. Disappears spontaneously

258. In hypernatremia
A. Fever and edema are absent
B. Restlessness and raised BP are present
C. There is increased urine output
D. Only C is correct

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SURGERY MK
259. In hyperkalemia patient will present with:
A. Increased reflexes and ECG changes
B. ECG shows inverted “T” waves
C. ECG shows peaked “T” waves
D. Oliguria, muscle weakness and respiratory distress are a feature

260. Treatment of hyperkalemia include:

A. Kayexalate
B. IV insulin and glucose
C. Lasix and stop potassium containing fluid
D. Dialysis if severe

261. In respiratory alkalosis

A. PCO2 rises
B. PCO2 falls
C. PCO2 remains the same
D. None above are correct

262. In metabolic acidosis

A. CO2 combining power rises
B. CO2 combining power falls
C. CO2 combining power remains the same
D. Only C is correct

263. Under normal conditions the colloid osmotic pressure of blood is about
A. 75mmHg
B. 50mmHg
C. 25mmHg
D. 10mmHg

264. Signs and symptoms of hyperkalemia include

A. Peaked “T” waves on ECG
B. Increased cardiac contractility
C. Muscle weakness
D. Respiratory distress

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SURGERY MK
265. Treatment of hypernatremia include:
A. Stop IV normal saline
B. Glucose and insulin intravenously
C. Lasix
D. Dialysis if severe

266. Administration of potassium to correct hypokalemia

A. Give potassium as intravenous bolus
B. Not more than 20mEq with 40mEq as maximum
C. Ensure good urine output
D. Cardiac monitor not essential

267. The following intravenous solutions are commonly used to treat hemorrhagic
shock in the University Teaching Hospital
A. 0.9% saline
B. 5% dextrose
C. Ringer’s lactate
D. Hypertonic saline
E. Darrow’s solution

268. Septic shock

A. Is particularly associated with Celestin tube insertion
B. Is often due to gram negative organisms
C. Is particularly seen in patients with indwelling intravenous catheters
D. Surgery for acute cholecystitis is a cause
E. Does not occur in gram positive septicemia

269. The following intravenous fluids contain potassium

A. Darrow’s
B. Ringer’s
C. Blood
D. Dextrose 5%
E. Dextran solution

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SURGERY MK
270. Patients needing supplementary feeds include those with
A. Recent weight gain
B. Serum albumin >30g/dl
C. Serum albumin <30g/dl
D. Negative nitrogen balance
E. Positive nitrogen balance

271. Parenteral feeds

A. Best feeding method
B. Has least side effects
C. Requires feeding nasogastric tube
D. Very expensive
E. May be the only alternative in conditions like acute pancreatitis

272. Body fluids

A. A 70kg man has 42L as total body water
B. Interstitial fluids in a 70kg man is 11 Liters
C. 3 L of plasma in a 60kg man
D. 15L in a 60kg man is extracellular fluid
E. Potassium is an extracellular ion

273. Pancreatitis
A. Can be the cause of chemical peritonitis
B. Absence of bowel sounds is a feature
C. Serum amylase is not raised
D. Laparotomy is indicated in all cases

274. Complications of acute pancreatitis are

A. Pseudocyst formation
B. Disseminated intravascular coagulation
C. Left basal effusion (pleural)
D. Renal failure
E. Ascites

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SURGERY MK
275. Gall stones cause
A. Acute cholecystitis
B. Acalculous cholecystitis
C. Obstructive jaundice
D. Carcinoma of the gall bladder
E. Torsion of the gall bladder

276. Acute cholecystitis

A. Does not occur in sicklers
B. Is usually treated by cholecystostomy
C. Is usually associated with urinary bladder stones
D. Can cause pain in the right shoulder
E. Causes pain and tenderness in the left hypochondrium

277. Acute pancreatitis

A. Often results in hypoxemia
B. Usually gives rise to Cullen’s sign
C. Causes hypercalcemia
D. Can be caused by mumps
E. Occurs after biliary surgery sometimes

278. Esophagus
A. Below the pulmonary roots the vagus nerves are in contact with esophagus
B. The left trunk of the vagus nerve is on the anterior side of the esophagus
C. The right trunk of the vagus nerve is on the posterior side of the esophagus
D. The longest part of esophagus is intra-abdominal

279. Cancer of the esophagus

A. Dysphagia is initially for solids
B. Dysphagia is initially for liquids
C. Barium swallow X-ray shows a smooth constriction giving a rat-tail
appearance
D. Barium swallow X-ray shows irregular and sharp edge constriction giving
shouldering appearance

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SURGERY MK
280. Signs of advanced cancer of the esophagus include:
A. Hoarseness of voice as a sign of involvement of recurrent laryngeal nerve
B. Weight loss of more than 20%
C. Absence of palpable supraclavicular lymph nodes
D. Presence of palpable lymph nodes

281. Esophageal stricture

A. Can be caused by achalasia of the cardia
B. Inflammation of esophagus does not cause strictures
C. Can be caused by cancer of esophagus
D. Can be caused by ingestion of corrosive chemicals

282. Cancer esophagus presents with

A. Weight gain
B. Dysphagia of solids
C. Odynophagia
D. Regurgitation is not a feature

283. Carcinoma of the esophagus is commonly treated by

A. Surgery
B. Radiotherapy
C. Immunotherapy
D. Chemotherapy
E. Gastrostomy

284. Carcinoma of the esophagus

A. Lower third is a common site
B. Is adenocarcicnoma in 90% of cases
C. Is radiosensitive
D. Metastases the scalene node
E. Presents early in Zambia

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SURGERY MK
285. Hepatocellular carcinoma
A. Is the commonest tumor of men in Zambia
B. Is not associated with post-necrotic cirrhosis
C. Is related to ingestion of aflatoxins
D. Presents with intermittent abdominal pain
E. Rarely causes early weight loss

286. Incisional hernias are related to

A. Wound infections
B. Anemia and malnutrition
C. Obesity
D. The use of absorbable suture materials

287. The differential diagnosis of an inguinal hernia in a female include:

A. Vaginal hydrocele
B. Encysted hydrocele of the cord
C. A femoral hernia
D. None of the above

288. A strangulated hernia

A. Is tense
B. Is tender
C. Has a transmitted cough impulse
D. Requires elective surgery

289. A partial thickness burn

A. May heal without grafting
B. May deteriorate into full thickness skin loss
C. Rarely causes severe physiological derangement of the patient
D. Heals within 7 days in the absence of infection

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SURGERY MK
290. Burns
A. History taking should always include- Time of burn, cause, smoke inhalation,
trauma
B. On examination the severity is determined by burn depth, burn size, areas of
circumferential full thickness
C. Full thickness burns will produce very painful charred skin
D. Escharotomy may help in reducing respiratory embarrassment

291. In burns
A. A man with 30% superficial burns does not require fluid therapy
B. A female with 20% superficial burns does not require ATT on admission
C. Parkland’s formula considers fluids therapy in the first 36 hours
D. Browder and Lund charts are used to estimate percentage surface area burnt

292. The skin

A. Is a multilayered organ
B. Good approximation of layers is not vital
C. Crush injury heals better than an incision
D. Langer’s lines run perpendicular to muscle axis
E. Langer lines run mainly longitudinal to muscle axis

293. Upper gastrointestinal hemorrhage can be caused by:

A. Mallory-Weis tear
B. Sigmoid volvulus
C. Periportal fibrosis due to Bilharzia
D. Perforated anterior duodenal ulcer

294. Zollinger-Ellison syndrome

A. Multiple ulcerations are a feature
B. Increased vagal activity is the main cause
C. Fresh red blood rectal bleeding is a common feature
D. Gastrin producing endocrine tumor is a common feature

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SURGERY MK
295. Pyloric stenosis in adult patient:
A. Annulus pancreas can be the cause
B. Chronic duodenal ulcer can be the cause
C. Meckel’s diverticulum can be the cause
D. Cancer of pancreas can be the cause

296. In a patient with peptic ulcer disease

A. Histamine production is increased by stimuli from both vagus nerves and
gastrin
B. The process of exporting hydrogen ions from parietal cells via protein pump
is not a feature
C. Histamine acts on parietal cells via H2-receptors
D. Melena stools is not a feature

297. Investigating a patient who presents with hematemesis includes:

A. Esophagoscopy
B. Gastroduodenoscopy
C. Lower midline laparotomy is advisable
D. Right subcostal mini-laparatomy is advisable

298. Brain abscess in the frontal lobe

A. Is most likely a complication of chronic otitis media
B. Is not likely a complication of paranasal sinusitis
C. Is most likely a complication of infected occipital laceration
D. Is most likely a complication of infected wound on the temporal area of the
head

299. Large supratentotrial space occupying lesions is likely to present with

A. Full consciousness
B. Unequal pupils
C. Contralateral hemiplegia
D. Paraplegia

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SURGERY MK
300. Common causes of congenital hydrocephalus include:
A. Brain abscess
B. Dandy-walker cyst
C. Arterial venous malformation
D. Anold-Chiari malformation

301. Submandibular gland tumors

A. 50% are malignant
B. Facial nerve weakness is a feature
C. Ulceration of overlying skin is not a feature
D. Cervical lymph nodes enlargement is a feature

302. Parotid gland tumors

A. Most common are benign pleomorphic adenomas
B. 10% are malignant
C. Rapid growth with infiltrating of overlying skin is a sign of high-grade
malignancy
D. Enlarged palpable cervical lymph nodes are not a feature

303. Bilateral paralysis of genioglossus leads to

A. Atrophy of the tongue
B. Tongue falls back
C. Obstruction of respiratory passage
D. All above true except “B”

304. Structures embedded in the parotid gland include

A. Facial nerve
B. Retromandibular vein
C. External carotid artery
D. Parotid lymph nodes

305. The following are examples of non-absorbable suture materials

A. Silk
B. Vicryl
C. Nylon
D. Stainless steel

724
SURGERY MK
306. The following suture are
A. Silk is natural material
B. Nylon is synthetic material
C. Vicryl is natural material
D. Stainless steel is synthetic material

307. Knot security after wound suturing

A. Best with vicryl
B. Good with nylon
C. Worst with silk
D. All above correct

308. Clostridium Welchii is

A. Causative agent of wet gangrene
B. Causative agent of gas gangrene
C. Aerobe, sporulating, gram negative bacillus
D. Proliferates in dirty wounds

309. In acute limb ischemia

A. Thrombo-embolism may be a causative factor
B. In-situ blockage of artery by thrombus is factor
C. Buerger’s test is positive
D. Ankle brachial pressure index is useful indicator of severity of ischemia

310. Parotid benign tumors

A. Make up 80 to 90% of parotid tumors
B. Are pleomorphic adenomas
C. Are soft on palpation
D. Mostly arise in the superficial lobe

311. HIV-associated sialadenitis of parotid gland

A. Chronic parotitis in children is pathognomonic of HIV infection
B. Facial disfigurement is a feature
C. CT scan shows characteristics swiss cheese appearance of multiple cystic
lesions
D. Cosmetic surgery is not advisable

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SURGERY MK
312. Causes of leucopenia
A. Lymphoma
B. Sever infections
C. Disease of the spleen
D. Autoimmune disorders

313. Causes of leukocytosis

A. Inflammatory conditions like arthritis
B. Stress
C. Allergic conditions like asthma
D. Pregnancy

314. A rise in monocytes may indicate the following:

A. Chronic inflammatory disease
B. Parasitic infestation
C. Tuberculosis
D. Oral infection

315. Post-op fever after abdominal surgery

A. Is caused by release of pyrogens
B. Intra-abdominal collections
C. Blood and platelet infusions
D. Pulmonary complications like pneumonia or empyema

316. Unilateral ureteric obstruction may be caused by

A. Ureteropelvic stenosis
B. Ureteric stone
C. Posterior urethral valves
D. Neurogenic bladder

317. Unilateral renal artery obstruction may be associated with

A. Increased renin release by the obstructed kidney
B. Angiotensin release and increased aldosterone production by adrenal cortex
C. Increased sodium and water retention
D. Hypotension

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SURGERY MK
318. Chronic bilharzia can cause
A. Bilateral ureteric obstruction
B. Transitional cell carcinoma
C. Bilateral hydronephrosis
D. Squamous cell carcinoma of the bladder

319. Management of obstructive uropathy may include

A. Catheterization
B. Bilateral orchidectomy
C. Endoscopic ureterotomy
D. Urethroplasty

320. Parotid inflammatory swelling

A. Can be caused by mumps
B. Is rare in children
C. Can be HIV associated
D. Does not cause facial disfigurement

321. Superficial parotidectomy

A. Is indicated for benign and low grade malignant tumors
B. Incision is lazy-“S”
C. Facial nerve injury is rare
D. Skin flap is developed to reach anterior border of the gland

322. Parotidectomy complications

A. Frey’s syndrome
B. Facial nerve palsy
C. Hemorrhage
D. Raised T3 and T4

323. Lung cancer

A. Small cell lung cancer makes up 20%
B. Metastasis by lymphatics is rare
C. Metastasis by blood borne spread is common
D. Surgery greatly improves survival

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SURGERY MK
324. When considering fluid spacing
A. First spacing is normal exchanging between intravascular and extravascular
space
B. Second spacing is accumulation fluid into tissues as edema
C. Third spacing is accumulation of fluid in body cavities e.g. Ascites, pleural
effusion
D. All above correct except “C”

325. If vagus nerves are severed the respiratory rate

A. Is increased
B. Is decreased
C. Remains constant
D. Ceases

326. Destruction of pneumotaxic center located in the pons causes

A. Apneustic respiration
B. Forceful expiration
C. Accelerated respiration
D. Apnea

327. Median nerve

A. Is formed from medial and lateral cods
B. Innervates all flexor compartment muscles except flexor carpi ulnaris
C. Is also known as the labourer’s nerve
D. Only (a) is correct

328. Radial nerve

A. Is formed from posterior cord
B. Innervates all extensor compartment muscles except anconeus
C. Is prone to injury in fractures of the shaft of humerus
D. Injury results in wrist drop

329. Ulnar nerve

A. Is a branch of the posterior cord
B. Is known as the musician’s nerve
C. Is the major innervation of muscles of the hand
D. Lesion of the nerve results in ape thumb

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SURGERY MK
330. A 3/0 suture is
A. Larger in diameter than 4/0
B. Smaller in diameter than 4/0
C. Is too small for skin closure
D. Can be used in an adult patient to close the abdominal sheath

331. Boil (furuncle)

A. Can occur on any part of the body except the face
B. Is infection of hair follicle
C. Can cause signs of inflammation
D. Surgical drainage is not indicated

332. Carbuncle
A. Can occur on any part of the body except the neck
B. Is necrotic infection of contiguous hair follicles
C. Patients present with fever and malaise
D. Both surgical drainage and antibiotics are not required for treatment

333. Lymphangitis
A. Common causative organism include streptococci
B. Blood cultures are usually positive
C. Lymph nodes draining the infected area are usually swollen and painful
D. Presents with systemic inflammatory response syndrome (SIRS)

334. Regulations of fluids and electrolytes movement across all membranes is by

A. Diffusion/filtration
B. Active transport
C. Osmosis
D. Characteristics of the membrane itself

335. Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are
hormones involved in regulation of
A. pH of the body fluids
B. Water and electrolyte balance
C. ANP is produced in atrium
D. BNP is produced in ventricles

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SURGERY MK
336. A white leg is due to
A. Femoral deep vein thrombosis
B. Lymphatic obstruction
C. Femoral vein thrombosis and lymphatic obstruction
D. None of the above

337. The following are irritative symptoms of bladder outlet obstruction secondary
to BPH:
A. Weak stream
B. Nocturia
C. Frequency
D. Intermittence

338. Ilio-Psoas muscle for hip flexion is innervated by

A. L1, 2 segments
B. L4, 5 segments
C. L5, S1 segments
D. S1, S2 segments

339. Secondary metastasis to the spine can originate from

A. Thyroid cancer
B. Breast cancer
C. Lung cancer
D. Prostate cancer

340. A seroma is also known as

A. A hematoma
B. A chyloma
C. A collection of serum in the tissue
D. All above correct

341. Choice of suture material

A. Is irrelevant
B. Depends upon the tissue and area of the body
C. Is usually left up to the scrub nurse
D. Is whatever the hospital gives you

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SURGERY MK
342. About swellings
A. A punctum is diagnostic of a lipoma
B. A cyst is lined by some form of epithelium and is fluid-filled
C. A sebaceous cyst exhibits pseudo-fluctuation
D. Carotid body tumor moves only in one plane vertically

343. The following are the reasons why investigations are done
A. Medico-legal purpose
B. To make a diagnosis
C. To establish fitness before surgery
D. For monitoring of a disease process

344. Hypertrophic pyloric stenosis

A. Is never seen in adults
B. Projectile vomiting occurs
C. A mass is never palpable
D. Diarrhea is common
E. Is associated with other congenital abnormalities

345. Indications for surgery in peptic ulcer disease include:

A. Intractable pain
B. Pyloric stenosis
C. Absence of healing after 3 weeks of medical treatment
D. Acute gastric erosion due to analgesic abuse
E. Single episode of hematesis

346. Treatment of peptic ulcer disease includes:

A. Antacids
B. Antibiotics
C. Prostaglandin analogues e.g. misoprostol
D. Omeprazole
E. Cimetidine

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SURGERY MK
347. Operations performed for peptic ulcer disease includes
A. Gastrostomy
B. Gastropexy
C. Vagotomy and gastrojejunostomy
D. Billroth gastrectomy
E. Polya gastrectomy

348. Which of the following conditions give rise to hemoperitoneum?

A. A ruptured ectopic pregnancy
B. Rupture of the bladder neck
C. An injured spleen
D. Spinal injuries
E. An extraperitoneal isolated injury to the kidney

349. Post-operative pulmonary complications commonly occur:

A. In patients with chronic bronchitis
B. In smokers
C. In patients with severe pain
D. Following herniorrhaphy
E. Following splenectomy

350. Open cardiac operations require one or more of the following

A. Extracorporeal circulation
B. Hypothermia
C. Cardioplegia
D. Right second intercostal posterolateral thoracotomy
E. Sternotomy

351. Cardiac arrest is caused by

A. Anoxia
B. Excessive intravenous potassium
C. Exsanguinating bleeding
D. Frusemide
E. Intravenous glucose

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SURGERY MK
352. Cardiac tamponade following trauma:
A. Heart sounds are usually muffled
B. There is venous hypertension
C. There is arterial hypotension
D. Urgent surgical treatment is indicated
E. Urgent artificial ventilation is required preoperatively in all cases

353. Spinal (Lumbar) puncture:

A. Is usually performed at L1-L2 level
B. The cerebrospinal fluid is located in the subdural space
C. The cord ends at a higher level in an infant
D. Must not be performed in the presence of a raised intracranial pressure
E. A complication is venous bleeding

354. The following tumors readily metastasize to bone

A. Rectal adenocarcinoma
B. Basal cell carcinoma of skin
C. Follicular carcinoma of the thyroid
D. Prostatic adenocarcinoma
E. Renal adenocarcinoma

355. A lipoma has the following features

A. A slipping edge
B. Transillumination
C. Is tender to touch
D. Has a central punctum
E. Is only found in subcutaneous tissue

356. Tumors of the parotid include

A. Pleomorphic adenoma
B. Adenolymphoma
C. Papillary carcinoma
D. An enlarged intraparotid lymph node

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SURGERY MK
357. Which investigations demonstrate occlusion of one common iliac artery
A. Inferior venacavogram
B. Translumbar aortogram
C. Doppler ultrasound
D. Intravenous pyelogram
E. Retrograde femoral catheterization of the other side

358. Varicose veins

A. Are tortuous elongated veins
B. Pain is a late feature
C. It is also known as venous hypertensive disease
D. Elastic support stocking are useful
E. Injection sclerotherapy is indicated in some patients

359. Hemorrhage
A. Primary hemorrhage occurs within 24 hours
B. Secondary hemorrhage occurs after a week to 10 days
C. Bleeding time is a measure of fibrinogen activity
D. The normal clotting time is up to 20 minutes
E. Bleeding in cirrhotics is immediately controlled by administering oral vitamin
K

360. Common cause of pyrexia within 2 days of surgery include:

A. Chest infection
B. Blood transfusion
C. Wound infection
D. Venous thrombosis
E. Allergy to the anesthetic agent

361. Bacteroides species

A. Are common in the mouth
B. Are the commonest large bowel commensal
C. Are sensitive to metronidazole
D. Causes necrotizing fasciitis
E. Cause Crohn’s disease

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SURGERY MK
362. An anteroposterior chest X-ray (done to demonstrate a left subphrenic
abscess) will show:
A. Obliteration of the costophrenic angle on the same side
B. Collapse of the left upper lobe
C. Lack of movement on the right cupula of the hemidiaphragm on screening
D. A fluid level below the left hemidiaphragm
E. Shift of the gastric fundus

363. Fournier’s gangrene of the scrotum

A. Is secondary to tuberculosis
B. Is very uncommon in Zambians
C. Minor trauma to the scrotal skin is an etiological factor
D. Metronidazole is indicated
E. Surgery is contraindication

364. The following antibiotics are effective against anaerobic organisms

A. Chloramphenicol
B. Erythromycin
C. Cloxacillin
D. Clindamycin
E. Actinomycin

365. Hand infections

A. The hand is rested with extension of all joints
B. Osteomyelitis is common in untreated pulp space infection
C. Paronychia refers to infection in the palm
D. Commonly follow minor neglected injuries
E. A common infecting organism is E. coli

366. Complications of nasogastric tubes include

A. Gastric perforation
B. Otitis media
C. Chest infection
D. Ulceration of nares
E. Esophageal stricture following prolonged intubation

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SURGERY MK
367. Tetanus
A. Is caused by an anerobic bacillus
B. Is associated with a hypercatabolic state
C. Occurs only after major trauma
D. Tetanus toxoid gives artificial immunity
E. Common cause of death is respiratory failure

368. Streptomycin
A. Is an aminoglycoside
B. It is bactericidal in high dose
C. Causes pseudomembranous colitis
D. Causes jaundice
E. Causes ototoxicity

369. A venous cut down can be done on the following veins

A. Cubital
B. Cephalic
C. Subclavian
D. Umbilical
E. Posterior tibial

370. Torsion of the testis

A. If in doubt of the diagnosis explore
B. In unilateral torsion bilateral fixation is necessary
C. Does not occur in children
D. Is confused with a hydrocele
E. A horizontally placed low testis is diagnostic

371. Congenital hydrocele

A. Can be repaired by Lord’s procedure
B. Is due to closure of the processus vaginalis
C. Phenol may be used to treat the hydrocele
D. May be due to epididymorchitis
E. Presents as inguinal hernia

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SURGERY MK
372. Anesthetic drugs
A. Diazepam may be used for premedication
B. Mist magnesium trisilicate for premedication for cesarian section
C. Thiopentone for induction
D. Etomidate for reversal of muscle relaxation
E. Morphine for post-operative analgesia

373. Post-operative wound breakdown may be due to

A. Use of tight suturing technique
B. Prolonged steroid use before surgery
C. Reduced serum protein
D. Protein energy malnutrition
E. Diabetes mellitus

374. Metabolic response to trauma

A. May be caused by fracture of a distal phalanx
B. Good recovery follows steroid treatment
C. Head injury may be the cause
D. Patient may gain weight in the flow phase
E. May lead to systemic inflammatory response syndrome

375. Peptic ulcer disease

A. With hematemsis may be due to malignant transformation
B. Can be duodenal if pain wakes patient after midnight
C. Can be duodenal if pain is experienced immediately after meals
D. Can be gastric if experienced immediately after food
E. Can be a cause of acute abdomen

376. Cranial nerve that supplies superior oblique which elevates and adducts the
eye is:
A. 7th cranial nerve
B. 6th cranial nerve
C. 5th cranial nerve
D. 4th cranial nerve

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SURGERY MK
377. Sensory component of 5th cranial nerve is tested by
A. Wrinkle formation on the forehead
B. Touch sensation on the face
C. Lifting the shoulder
D. Corneal reflex

378. When a patient has unilateral vagus nerve lesion and is asked to open the
mouth and say AAAG.. The uvula moves and points
A. Away from the lesion
B. Towards the lesion
C. Stays in the midline
D. Elongates within the midline

379. When a patient has unilateral hypoglossal lesion and is asked to protrude the
tongue
A. The tongue points away from the lesion
B. The tongue points to the side of the lesion
C. The tongue will show wasting
D. The tongue will show fasciculations

380. When a patient sustains cranial nerve XI lesion

A. Patient is unable to elevate (shrug) the affected shoulder
B. Patient is able to elevate the shoulder against examiners resistance
C. Sternomastoid muscle power is spared
D. When patient is asked to rotate the chin against examiners resistance he/she
fails to do so

381. When a patient has unilateral cranial nerve V motor component lesion
A. Masseter muscle will feel weak on palpation as patient clenches the teeth
B. Temporal muscle will feel well contracted as patient clenches the teeth
C. The jaw will deviate to the paralyzed pterygoid muscle when patient opens
the mouth
D. The jaw will deviate away from the paralyzed pterygoid muscle when patient
is asked to open the mouth

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SURGERY MK
382. Bilateral 6th cranial nerve palsy is a sign of
A. Cingulate gyrus herniation
B. Uncal herniation
C. Raised intracranial pressure
D. Tonsillar herniation

383. Hyper-resonant chest is likely to be caused by

A. Hemothorax
B. Pleural effusion
C. Pneumothorax
D. Tension pneumothorax

384. Secondary brain injury

A. Can result from hypoxia
B. Can result from hypoperfusion
C. Can result from hypoglycemia
D. Can result from any of the above

385. Breast cancer is common in women with

A. Positive family history
B. History of having breast fed their children
C. History of previous radiation exposure
D. Having the first child at early age

386. Causes of surgical jaundice include:

A. Gall stones
B. Massive hemolysis
C. Ascaris lumbricoides
D. Malignancy of the head of pancreas

387. The most frequent anatomic site for squamous cell carcinoma of the
esophagus is
A. Upper third
B. Middle third
C. Lower third
D. Gastro-esophageal junction

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SURGERY MK
388. Pathological fractures may be associated with
A. Scurvy
B. Hyperparathyroidism
C. Bone cyst
D. All of the above

389. Perkin’s exercises:

A. Are commenced 2 weeks after application of traction kit
B. Are commenced within a week after application of traction kit
C. Are commenced after 3 weeks when pain at fracture site has subsided
D. All above correct except “B”

390. Tachypnea
A. Is respiratory rate of less than 10 per minute in adult patients
B. Can be caused by tension pneumothorax
C. Can be caused by hemothorax
D. Is never associated with tachycardia

391. About investigations

A. Gastroscopy is an example of an imaging technique
B. For biliary pathology, ultrasound is superior to computerized tomography
C. Plain X-rays are sufficient in order to make a diagnosis of fractures
D. There are other methods apart from histology and cytology that are used to
confirm cancer

392. Patients with central nervous system lesion on observation may have
A. Epigastric peristalsis
B. Ptosis
C. Tremors
D. Diaphragmatic respirations

393. These are major symptoms associated with intestinal obstruction

A. Diarrhea
B. Change in skin coloration
C. Hematuria
D. Melena stool

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SURGERY MK
394. Oculomotor nerve lesion presents with
A. Pupil dilation
B. Ophthalmoplegia
C. Lateral rectus palsy
D. Loss of corneal reflex

395. Origin of oculomotor nerve (CN III) is

A. Medulla-oblongata
B. Pons
C. Mid-brain
D. Cerebellum

396. Open skull fracture has occurred when there is

A. Cerebral spinal fluid leak from the ear
B. Depressed skull fracture under the scalp wound
C. Subdural hematoma with superficial bruise on the forehead
D. Subarachnoid hemorrhage regardless of the cause

397. Patients who present with acute abdominal pain starting in the umbilical
region and shifts to the right iliac fossa is most likely caused by
A. Perforated duodenal ulcer
B. Diverticulitis
C. Appendicitis
D. Salpingitis

398. Murphy’s sign

A. Helps to diagnose ureteric stones
B. Helps to diagnose ectopic pregnancy
C. Helps to diagnose appendicitis
D. Helps to diagnose cholecystitis

399. Small intestinal obstruction is likely to present with

A. Radiating pain to the left shoulder
B. Spreading pain to the right iliac fossa
C. Colic pain in the umbilical region
D. Shifting pain to the right iliac fossa

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SURGERY MK
400. Imperforate anus
A. Maybe related to urogenital fistulae
B. X-rays (invertogram) is not helpful
C. Colostomy may be useful initially
D. Cannot be a cause of intestinal obstruction
E. May present with constipation

401. Drugs used for maintenance in anesthesia

A. Nitrous oxide
B. Halothane
C. Isoflurane
D. Oxygen
E. Enflurane

402. Hirschprung’s disease

A. Lacks nerve tissue in the sub-mucosa layer
B. A concentration of nerve tissue in the submucosa layer
C. History of constipation is characteristic
D. History of anal bleeding is characteristic
E. Definitive diagnosis is made on X-rays

403. The gastrointestinal system has

A. 4 basilica layers
B. Mucosa lined by epithelium
C. Muscularis mucosa to produce local movement of mucosa
D. 5 basic layers
E. Serosal lining covering mucosa

404. Normal blood values

A. Total white cell count- 14 x 109/L
B. Serum creatinine- 200umol/L
C. Urea- 10mmol/L
D. Sodium 155mmol/L
E. Potassium 6.5 mmol/L

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SURGERY MK
405. During surgical procedures
A. Doors to operating theaters must always be left open
B. Ventilators can reduce the atmospheric bacterial load
C. The patient is not the most important source of wound infection
D. Shaving must be done ideally the day before operation
E. Commonest organism to cause infection is streptococcus

406. Concerning antisepsis

A. Antisepsis has to do with reducing the bacterial load
B. Sterilization completely destroys all viable organisms
C. Disinfection reduces the bacterial load
D. Disinfection has to do with reducing the tissue bacterial load
E. Ultraviolet light is one way of sterilization

407. Fatty acids

A. Are 75% stored as glycogen in the liver
B. Glycogen stores used up in the stressful situations within 48 hours
C. Digestion is mainly by pancreatitic lipase
D. Liver stores maintain blood levels
E. Insulin is not important in cell uptake of carbohydrate

408. Most of protein digestion and absorption occurs

A. Terminal ileum
B. Stomach and duodenum
C. Stomach and colon
D. In the liver and gall bladder
E. Stomach

409. Concerning suturing of incision

A. Subcuticular sutures are not good for cosmesis
B. Mattress suture is good for hemostasis
C. Continuous sutures are ideal if infection is anticipated
D. Continuous sutures are ideal for long incisions
E. Head and neck sutures must be removed only after the 5th days

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SURGERY MK
410. Monofilament sutures
A. Cause least tissue reaction
B. Causes least wound infection
C. Causes most tissue reaction and scarring
D. Can be braised
E. Can be absorbable

411. Nylon suture

A. Absorbable suture and gives little tissue reaction
B. Non-absorbable and gives a lot of tissue reaction
C. Non-absorbable and gives little tissue reaction
D. Synthetic
E. Naturally occurring

412. On examination of the abdomen

A. Spleen is examined starting from the right iliac fossa
B. There are 9 surface division
C. Inspection is done after palpation
D. Percussion is done after palpation
E. Normal bowel sounds heard every 2 seconds

413. Peptic ulcer disease

A. With hematesis may be due to malignant transformation
B. Can be duodenal if pain wakes patient after midnight
C. Can be duodenal if pain is experienced immediately after meals
D. Can be gastric if experienced immediately after food
E. Can be cause of acute abdomen

414. Congenital hydrocele

A. Can be repaired by Lord’s procedure
B. Is due to closure of the processus vaginalis
C. Phenol may be used to treat the hydrocele
D. May be due to epididymorchitis
E. Presents as inguinal hernia

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SURGERY MK
415. Patients burns major burns
A. Are in negative nitrogen balance
B. Have normal calorie requirement
C. Do not generally become anemic
D. Are resistant to septicemia

416. Patients with raised intracranial pressure

A. Cerebral perfusion pressure is maintained by reduction of arterial pressure
B. Cerebral spinal fluid shifting
C. Uncal herniation is not a feature
D. Coma scale remains unaltered

417. The parafollicular cells of thyroid secrete

A. Calcitonin
B. Amyloid
C. Parathormone
D. Follicle stimulating hormone

418. An indirect inguinal hernia would lie in relation to the inferior epigastric
artery:
A. Medial
B. Lateral
C. Anterior
D. Posterior

419. Fissure-in-Ano is located characteristically:

A. Midline anteriorly
B. Midline posteriorly
C. Right lateral quadrant
D. Left lateral quadrant

420. Post-traumatic intracranial space occupying lesion is likely to present with:

A. Decreased pulse rate
B. Increased blood pressure
C. Irregular pulse
D. Glasgow coma scale of 2/15

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SURGERY MK
421. Paradoxical (Diaphragmatic) respiration can be caused by
A. Odontoid fracture dislocation
B. C2/3 hangman’s fracture
C. C5/6 fracture dislocation
D. T112/L1 fracture dislocation

422. Concerning blood groups

A. Blood group A is associated with increased risk of gastric cancer
B. The risk of gastric cancer is associated with blood group B
C. The risk of gastric cancer is associated with blood group O
D. Only (b) and (c) correct

423. Acute abdomen can be caused by:

A. Perforated duodenal ulcer
B. Sigmoid volvulus
C. Pancreatitis
D. Subcutaneous lipoma

424. The following are true of breast cancer

A. Lobular carcinoma is characterized by ‘Indian File’ pattern of tumors cells
B. Lobular carcinoma tends to be familial, multifocal and bilateral
C. Carcinoma-in-situ implies non-invasive cancer that has not breached
basement membrane
D. Macroscopically schirrhous carcinoma is hard, grey and grates on cutting

425. Symptoms of obstructive uropathy include the following:

A. Weak stream, hesitancy
B. Dribbling, straining to void
C. Polyuria, oliguria
D. Frequency, urgency, urge incontinence

426. Which are the causes of dysphagia

A. Carcinoma, goiter, thymoma, mediastinal lymphadenopathy, aortic aneurysm
B. Motor neuron disease, rabies, tetanus, pseudobulbar paralysis
C. Achalasia
D. Pneumonia, TB of spine

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SURGERY MK
427. Concerning tumors, the term ‘well differentiated’ means
A. The cells are so aggressive, wild and uncontrolled and keep reproducing to no
good end
B. Cells and tissue that have mature (specialized) structures and functions
C. Cancer cells look more like normal cells under a microscope
D. The cells tend to grow and spread more quickly than poorly differentiated
cancer cells

428. About 85-90% radio-opaque urinary stones include the following

A. Calcium oxalate stones
B. Pure uric acid stones
C. Sodium urate and ammonium stones
D. Sulphur containing cysteine

429. Diabetic foot

A. Presence of pathologies such as infection, ulcer and neuropathic
osteoarthropathy
B. Is always present in chronic diabetes mellitus
C. Any chronic foot ulcer that eventually causes diabetes mellitus
D. Patients have associated reduced ability to feel pain

430. Chest injuries

A. Tension pneumothorax causes so-called ‘paradoxical breathing’
B. May cause a rupture of the diaphragm
C. A flail chest result from a wound in the chest wall which acts as a valve that
permits air to enter the pleural cavity but prevents its escape
D. May cause pulmonary contusion

431. Glasgow coma sale

A. Is a neurological scale which aims to give an objective way of recording the
conscious state of a person
B. Is composed of eye, verbal and motor response
C. Glasgow coma scale as high as ≥13 signifies minor head injury
D. The light response and size of the pupil are part of the Glasgow coma scale
assessment

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SURGERY MK
432. Fournier’s gangrene of the scrotum is associated with
A. Infection
B. Minor injuries
C. No obvious cause
D. Filariasis

433. Fibroadenoma
A. Benign tumor with a mixture of stroma and epithelial tissue of breast
B. Painless, firm, solitary, mobile, slowly growing lump in the breast of women
of child-bearing years
C. Leiomyoma in the breast tissue
D. Benign tumor of the fibrous tissue in the sweat glands of the breast tissue

434. Cervical sympathectomy is procedure which is indicated for the treatment of

A. Causalgia
B. Raynaud’s disease
C. PUD
D. Cervical rib

435. The following are causes of secondary varicose veins

A. Klippel Trenuaney syndrome
B. Oral contraceptive pills
C. Pelvic tumors
D. Exercises

436. Varicose veins are one of the causes of thrombophlebitis other causes include
A. Blood transfusion
B. Enteral feeding
C. Chemotherapy
D. Trauma

437. High risk group in the development of DVT would include the following
features:
A. Operation <30 minutes
B. Obesity
C. >40 years age
D. Stroke patient

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SURGERY MK
438. The development of skin malignancy pre-malignant lesions would include:
A. Solar keratosis
B. Keloids
C. Radio-dermatitis
D. Rodent ulcer

439. In hyperthyroidism
A. Serum creatinine is increased
B. Serum cholesterol is increased
C. Serum calcitonin is increased
D. Serum iodine is reduced

440. Causes of pulsatile thyroid swelling

A. Follicular carcinoma
B. Primary thyrotoxicosis
C. Secondary thyrotoxicosis
D. Papillary carcinoma

441. Medullary carcinoma of the thyroid (MCT):

A. Arises from parafollicular ‘c’ cells
B. Associated with MEN I syndrome
C. Associated with MEN IIa syndrome
D. Sporadic is the commonest

442. Tetany is a condition where there is hyper-excitability of peripheral nerves.

The causes include
A. Hypoparathyroidism
B. Respiratory alkalosis
C. Pyloric stenosis
D. Chronic renal failure

443. In etiopathogenesis of carcinoma of the esophagus, precancerous conditions

include:
A. Plummer vinson syndrome
B. Achalasia cardia
C. Corrosive stricture
D. Keratosis palmaris

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SURGERY MK
444. In gastric outlet obstruction electrolyte changes
A. Hypernatremia
B. Hyperkalemia
C. Hypochloremic alkalosis
D. Hypocalcemia

445. In hepatocellular carcinoma alpha-fetoprotein levels are increased. What other

conditions would increase the alpha-fetoprotein levels:
A. Carcinoma stomach
B. Carcinoma pancreas
C. Hepatoma
D. Embryonal cell carcinoma of testis

446. An increase in the level of alkaline phosphatase would be caused by

A. Biliary cirrhosis
B. Metastasis in the liver
C. Hepatocellular carcinoma
D. Hepatitis

447. Acute pancreatitis can be caused by drugs which include

A. Estrogen
B. Diuretics
C. Antifungals
D. None of the above

448. Complications of acute pancreatitis include the following except:

A. Shock
B. Hypocalcemia
C. Pleural effusion
D. Respiratory insufficiency

449. The following are components of wound healing except:

A. Wound contraction
B. Healing by primary intention
C. Epithelization
D. Scar formation

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SURGERY MK
450. Factors affecting wound healing include:
A. Jaundice
B. Debilitation
C. Gender
D. Parity

451. Ludwig’s angina precipitating factors:

A. Cachexia
B. Chemotherapy
C. Dental caries
D. Immobility

452. In a patient with established Tetanus, the possible causes of death would
include
A. Aspiration
B. Cardiac arrhythmias
C. DVT
D. Laryngeal spasm

453. Tropical ulcers occur in Tropical countries. The precipitating factors are:
A. Malnutrition
B. Trauma
C. Insect bite
D. HIV infection

454. The following are causative factors in acute empyema thoracis:

A. Lung infection
B. Subdiaphragmatic abscess
C. Ruptured esophagus
D. Gunshot bullet lodging in pleural cavity

455. The following may complicate chronic empyema thoracis

A. Amyloidosis
B. Brain abscess
C. Bronchopleural fistula
D. Chronic anemia

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456.

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ESSAYS
1. Write short notes on:
a. Salter-Harris classification of epiphyseal fractures
b. Gatland classification of supracondylar fractures
c. Draw and label patterns of fracture of neck of femur

2. Questions:
a. Define excised and incised wound
b. Describe briefly physiology of healing of excised wound
c. List complications of wound healing

3. Questions
a. Briefly trace iodine in food to iodine in thyroid hormone
b. Draw homeostatic loop for T3 and T4
c. List signs/ symptoms of thyrotoxicosis

4. Write short notes on

a. Colles’s fracture
b. Colostomy
c. Shoulder dislocation

5. Question
a. List complications of thyroidectomy
b. Discuss management of thyroid storm (Crisis)
c. Discuss briefly clinical presentation of hypoparathyroidism

6. Write short notes on metabolic body response to acute blood loss.

7. Write short notes on value of sentinel node in investigating breast cancer

8. Discuss briefly common patterns and presentation of hand infection.

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SURGERY MK
9. An 8-year-old child weighing 25kg has 20% burns which occurred at 04:00 hours
and arrives in hospital at 08:00hrs. Calculate fluid requirement using Parkland
formula:
a. Resuscitation fluid
b. Maintenance fluid
10. Write short notes on the complications of blood transfusion

11. What are signs and symptoms of acute appendicitis. Explain the anatomical basis
for these features, where applicable.

12. You are called to a surgical ward, 2 hours after thyroidectomy of a patient with
thyrotoxicosis. Write short notes on what complications your patient might have
now and in the near future.

13. How would you investigate the cause of fever in a patient who develops a fever 3
or 4 days after abdominal surgery?

14. A 70-year-old man presents with acute retention in a male surgical ward. Take a
brief relevant and focused history in order to arrive at a diagnosis

15. Persistent generalized lymphadenopathy is a common presentation of patients to

a surgical clinical in Zambia. How would you evaluate such patients to come up
with a diagnosis? Include in your answer the possible histological diagnostic
description of the common causes.

16. Graves disease is fairly common condition in young women in Zambia. Write
short notes on eye signs and give reasons why these signs do occur.

17. List the possible causes of PUD. Clearly explain how helicobacter pylori causes
this disease

18.What is gangrene? What are the etiological factors of the different types of
gangrene? Your short notes should include pathophysiology of each type of
gangrene.

19.A 26-year-old man has been hit by a moving vehicle. He is brought to casualty in a
coma. How would you evaluate this patient?

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SURGERY MK

20. Write shore notes on presentation and diagnosis of cervical injury

21. Write the hemodynamic changes caused by space occupying lesions in head injury
patients.
22. How much fluid are you going to give a 3-year old child weighing 15Kg with 20%
burns in the first 48 hours?

23. There has been a plane crash in Ngwerere area with a few survivors. How would
you handle the 13 survivors who have been brought to casualty?

24. A 65-year-old male patient presents to the casualty with a very painful ulcer on the
right foot. He is a known hypertension and has been on treatment for several years.
On examination has a moderate sized ulcer on the dorsum of the foot which is
very painful. The ulcer has punched out edge and the base is pale. The SHO
makes a diagnosis of a venous ulcer.
A. What other history would you want to get from this patient?
B. What further clinical examination would you do?
C. Was the diagnosis correct? Give your reasons?
D. What investigation is indicated
E. What is the diagnosis and state your reasons?

25. Discuss the immediate management of a 5-year-old child with 15% burns.

26. Write short notes on flail chest.

27. The signs of intracranial bleeding after a head injury are

A. Conscious level ……………………………………….
B. Pupil on side of lesion ……………………………..
C. Pulse rate …………………………………………………
D. Blood pressure …………………………………………
E. Respiration ……………………………………………....

28. A 65-year-old patient presents with a painful ulcer on the dorsum of his foot. He
complains that he is unable to sleep at night and the pain is not relieved by
moderate pain killer

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SURGERY MK
A. List 2 differential diagnosis for this ulcer
B. What is the most likely diagnosis?
C. What 4 important things would you ask in the history to determine the etiologic
factors?
D. What 2 blood investigations are indicated?
E. What radiological investigation is indicated?
F. Describe the following terms: a. Ankle Brachial pulse index and b. critical
ischemia?

29. A 35-year-old patient is seen in casualty following a road traffic accident (RTA).
The patient smells of alcohol and has a laceration on the occipital area. Answer
the questions below briefly.
A. What two things would you ask in the history?
B. Explain how you would examine the occipital laceration
C. List 4 localizing signs you would look for
D. List 4 reasons you might ask for a CT scan in this patient

30. List the various indications for doing a colostomy

31. Discuss in brief the causes of surgical jaundice

32. Write short notes about Steel’s rule application in a patient with cervical spine
injury

33.A 34 year old woman presents with mild yellowness of eyes, pain in the right
hypochondrium and fever. She gives history of previous episodes which resolve
on antibiotic treatment. Answer the questions below:
A. What is the most likely diagnosis?
B. What is the most likely cause?
C. What other 2 things would you ask for in the history?
D. What 2 blood investigations would you ask for?
E. What 2 signs would be present on abdominal examination?
F. What radiological investigation is indicated?

34.Answer the following questions:

A. Outline briefly the operative blood transfusion check list
B. Discuss measures that you would take to treat an adverse blood reaction

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SURGERY MK

35.Answer the following questions

A. Define goiter
B. Discuss briefly pre-operative investigations for goiter
C. List possible post-operative complications of thyroidectomy
D. How would you recognize and abort a thyroid storm

36.Give an account of thyroid swellings

37.A 46-year-old Zambian female presents to clinic 4 with a thyroid swelling which
is painless and slow growing.
A. What 4 things would you ask in the history to determine the cause?
B. What 4 examinations would you do to determine whether the patient is
euthyroid or toxic?
C. What specific blood tests are indicated?
D. What 3 radiological investigations would you do?
E. List 4 indications for surgery in this patient

38.Answer the following questions

A. Define osteoarthritis
B. Discuss briefly etiological factors in general and clinical presentation of
osteoarthritis of lumbar spine
C. List the four classical radiological findings in osteoarthritis
D. List the treatment modalities available for osteoarthritis.

39.Define the following

A. Fistula
B. Fissure
C. Ulcer
D. Granulation tissue
E. Paralytic ileus

40.Write short notes on the following

A. Define sentinel lymph node
B. Discuss briefly value of sentinel axillary lymph node biopsy in management
of breast cancer

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SURGERY MK
41.A 37-year-old female patient is seen in clinic 4 with a lump in the breast and an
axillary swelling. She gives history of weight loss and back ache. Answer the
questions below.
A. List 2 differential diagnosis
B. What is the most likely diagnosis?
C. What 4 important questions would you ask to determine the possible
etiological factors?
D. List 2 investigations you would do to confirm your diagnosis
E. What 2 radiological investigations would you do to determine whether
metastasis is present?
F. What is the value of the sentinel node in this condition?

42.A 56-year-old patient is seen in casualty with history of failing to pass urine. He
has severe pain and abdominal distention.
A. What is the diagnosis?
B. List 2 possible conditions that can lead to this complication
C. List 4 questions you would ask to differentiate the 2 conditions
D. What single physical examination is necessary in this patient?
E. What one endoscopy and one radiological investigation should be done?

43. A 40-year-old man comes to the emergency ward with acute urinary retention.
What are the possible etiologies, briefly outline how you would investigate.

44.A 34-year-old woman presents with mild yellowness of eyes, pain in the right
hypochondrium and fever. She gives history of previous episodes which resolve
on antibiotic treatment. Answer the questions below
A. What is the most likely diagnosis?
B. What is the most likely causes?
C. What other 2 things would you ask for in the history?
D. What 2 blood investigations would you ask for?
E. What 2 signs would be present on abdominal examination?
F. What radiological investigation is indicated?

45.A beautiful 40-year-old female patient is seen in casualty with right upper
quadrant pain which radiates to the scapula. She gives history of intermittent
attacks associated with fatty foods. On examination Murphy’s sign and

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SURGERY MK
Moynihan’s sign are both positive. The SHO on call makes a diagnosis of Acute
pancreatitis and requests some blood tests. The result shows serum amylase 100
u/L, Alkaline Phosphates 300 u/L, SGPT 30u/L, SGOT 31u/L and bilirubin 25
micronmols/L. The SHO is uncertain of the interpretation of the results and calls
the medical Registrar on call. The Registrar takes the history on the phone. The
medical Registrar is extremely upset with the young SHO, but nonetheless
recommends IV antibiotics, analgesia and an urgent U/S. By the morning round
the SHO has altered his diagnosis and takes the credit for an astute diagnosis from
the newly appointed Prof of Surgery.
A. What other important history should be taken?
B. What diagnosis do both the history and examination point to?
C. What do the investigations show?
D. Is a plain X-ray indicated in this patient?
E. Why was the medical registrar so upset?
F. What were the surgical principles on which the medical registrar gave his
advise?

46.Answer the following questions:

A. Define compartment syndrome and list major etiological factors
B. Discuss briefly the pathophysiology of compartment syndrome
C. With aid of labelled diagram, explain Whitesides saline/needle technique for
measuring intracompartment pressure in a limb

47.Write short notes on assessment of a patient with burns

48.Write short notes on usefulness of intravenous urogram (IVU) in a patient with

bilateral hydronephrosis

49.Describe the steps involved in the synthesis of Tri-iodothyronine (T3) and

thyroxine (T3). Comment on homeostatic (regulatory) feed-back loop

50.Answer the following

A. Define osteoarthritis
B. Discuss briefly pathogenesis of degenerative osteoarthritis
C. List the four cardinal radiological features of osteoarthritis

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SURGERY MK
51.List baseline investigations and their significance in preparation of a patient due
for thyroidectomy

52.Answer the following questions

A. Describe phases of fracture healing in a long tubular bone
B. List in tabular form complications associated with fractures
C. List the methods available for reduction of fractures

53.Write short notes on:

A. Autologous blood transfusion, types, uses and limitations
B. Pre-operative blood transfusion check list
C. Steps to be taken in aborting hemolytic blood transfusion reaction

54.Write short notes on how you would manage a patient you found to have a
ruptured liver during an operation in a district hospital.

55.Discuss the various hormones that are involved following the ruptured spleen in
a 25-year-old man.

56.A 47-year-old female patient is admitted to casualty with swelling of her left leg
of spontaneous onset. She has a fever and the leg feels warm
A. List 2 differentials diagnosis
B. What bacteria is likely to be the cause?
C. What 2 important questions would you ask for in the history to help determine
the etiological factors?
D. What 4 signs would you look for in the examination?
E. What 2 blood investigations would you do?
F. What antibiotic is indicated and what route of administration is
recommended?

57.A 15-year-old boy presents to the casualty department with scrotal pain. He gives
a history of sudden onset with no history of trauma. Answer the questions below.
A. What are the 2 main differentials?
B. What 4 things would you ask for in the history to differentiate the two?
C. What is the most likely diagnosis?
D. What is Prehn’s test? Describe how it is done.
E. What radiological investigation is indicated?

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SURGERY MK

58.A 12 year old boy presents to clinic 3 with a swelling on the upper leg which is
fast growing. The child is ill and give history of weight loss
A. List 2 differential diagnosis
B. What radiological investigation might distinguish the two?
C. What other radiological investigation can be done?
D. List 2 X-ray findings in osteosarcoma

59.A game ranger is brought to the casualty with a gunshot wound to the right leg.
The wound is dirty and 5cm in length. The patient has palpable pulses and nerve
function is normal.
A. What type of fracture has the patient had?
B. What is the classification of open tibia fractures?
C. How would you classify this patient’s fracture?
D. What blood investigations would you do?
E. What 2 organisms would be present on pus swab of this wound?

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SURGERY MK

ANSWERS TO TRUE/FALSE
1. Long term sequelae of head injury:
A. Brain atrophy is a Feature-True
B. Focal neurological deficits are not a Feature-False
C. Memory deficits are not a Feature-False
D. Epilepsy is a Feature-True

2. Clinical classification of head injury is based on:

A. Mode of Injury-False
B. Whether it is open or Closed-False
C. Glasgow coma Scale-True
D. Pathological Lesion-False

3. Subdural hematoma follows:

A. Tearing of superior sagittal Sinus-False
B. Tearing of cerebral Veins-True
C. Middle meningeal artery Laceration-False
D. Vertebral artery Laceration-False

4. Head injury patient with subdural hematoma

A. Is likely to deteriorate faster if blood pressure is Reducing-False
B. Is likely to deteriorate if blood pressure is Increasing-True
C. Is likely to deteriorate faster if pupils are starting to become Unequal-True
D. Is likely to deteriorate faster if hemiparesis is starting to Present-True

5. The main source of bleeding in a deep scalp laceration is

A. Periosteum-False
B. Loose connective Tissue-False
C. Aponeurotica galea-False
D. Dense connective Tissue-True

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SURGERY MK
6. Epidural hematoma in head injury patient follows:
A. Tearing of cerebral Veins-False
B. Brain Laceration-False
C. Middle meningeal artery Laceration-True
D. Superior sagittal sinus Tear-True

7. Head injury patient who presents with skull fracture crossing the midline
A. Is likely to have epidural hematoma from superior sagittal sinus Laceration-
True
B. Is likely to have epidural hematoma from middle meningeal artery Laceration-
True
C. Is likely to have cerebral spinal fluid leaking from both ears and Nose-False
D. Is likely to have fracture dislocation of C5/C6 cervical Spine-False

8. Burns are classified in terms of depth as

A. Superficial partial Thickness-True
B. Deep partial Thickness-True
C. Full Thickness-True
D. Full thickness is also known as second degree Burns-False

9. The rule of 9 for estimating extent of burns is as follows:

A. Head and neck 9%-True
B. Front of trunk 18%-True
C. Perineum 11%-False
D. Upper limbs 18%-True

10.Cerebrospinal otorrhea:
A. Fracture of the patients’ temporal bone is always Present-False
B. Fracture of the base of the skull is the Cause-True
C. Immediate surgical repair is Indicated-False
D. Infection is Common-True
E. Indicates injury to the 6th cranial Nerve-True

11. The comatose patient with a head injury:

A. Is nursed on his side to prevent aspiration of stomach Content-True
B. Must have endotracheal intubation if pharyngeal reflexes are Absent-True
C. Must have a nasogastric tube Inserted-True

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SURGERY MK
D. A urinary catheter is useful for monitoring fluid Balance-True
E. A suction machine is Essential-True

12.Urine output in a burnt patient:

A. In children an output of 1ml/kg/hr must be Maintained-True
B. In adult ensure an output of 70ml/Hour-True
C. Catheterize all patients with extensive Burns-True
D. In a 3-year-old female child size 24 Foley is Used-False
E. Antibiotics are routinely given to catheterized Patient-False

13.Cerebrospinal otorrhea complicating head injury requires:

A. Antibiotic ear Drops-True
B. Plugging the external auditory Meatus-False
C. Syringing with Saline-False
D. Early dural Repair-True
E. Parenteral Antibiotics-True

14.Systemic effects of burns

A. Hyper-Metabolism-True
B. Immunosuppression-True
C. SIRS-True
D. Keloids-False
E. Contractures-False

15.Complications of burns
A. Marjolin’s Ulcer-True
B. Keloids-True
C. Systemic inflammatory response Syndrome-True
D. Renal Failure-True
E. Airway Obstruction-True

16.Triage refers to:

A. Surgical wound Debridement-False
B. Categorizing and sorting patients according to Priority-True
C. Casualty Evacuation-False

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SURGERY MK
D. Only B and C Are Correct-False

17.In mass casualty injuries, the following injuries require immediate treatment
A. Sucking wounds of Chest-True
B. Flail Chest-True
C. Tension Pneumothorax-True
D. Penetrating wound of the Abdomen-True

18.Complications of intercostal drain insertion:

A. Pneumothorax-True
B. Injury to intercostal neurovascular Bundle-True
C. Lung and liver Trauma-True
D. Surgical Emphysema-True

19.The edge of a tuberculous ulcer is

A. Shelving-False
B. Rolled up-False
C. Undermined-True
D. Punched out-False

20.The edge of a malignant ulcer is

A. Shelving-False
B. Rolled up-True
C. Undermined-False
D. Punched out-False

21.Debridement is
A. The process of making an Incision-False
B. The removal of foreign material or dead Tissue-True
C. The process of obtaining Hemostasis-False
D. None of the Above-False

22.About ulcers:
A. Diabetic ulcer is an example of a specific Ulcer-False

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SURGERY MK
B. Malignant melanoma ulcer is always Pigmented-True
C. Arterial ulcers are located on the medial aspect of the Leg-False
D. Trophic ulcers are Painful-True

23.Acute raised intracranial pressure is treated by:

A. Mannitol-True
B. Furosemide-True
C. Hyperventilation-True
D. Steroids-True
E. Raising the foot end of the Bed-False

24.Decubitus ulcers
A. Only occur in comatose Patients-False
B. Are a form of ischemic Necrosis- True
C. Cause Septicemia-True
D. Antibiotics cure the Condition-False
E. Surgery is of value in selected Cases-True

25.History taking from a patient

A. Accounts for 10% of the diagnostic Process-False
B. Open ended questions direct the Interview-False
C. Referral letter may reveal important Information-True
D. Occupation of the patient is not Important-False
E. Smoking is associated with Pancreatitis-True

26.Skin grafting
A. Auto graft refers to the use of pig Skin-False
B. Xenograft usually takes and becomes part of the body Skin-False
C. Allograft fails to provide any normal Function-False
D. Split thickness skin grafting needs pedicles to Survive-True
E. Split thickness graft heals with excellent Appearance-True

27.Early signs of a rising intracranial pressure include:

A. Bradycardia-True
B. Deteriorating conscious Level-False

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SURGERY MK
C. Hypothermia-False
D. Hypertension-True
E. Tachypnea-False

28.The Glasgow coma chart includes details on the following

A. Pupillary Size-True
B. Motor Response-True
C. Urine Output-False
D. Hemoglobin Level-False
E. Injury severity Score-True

29.Pneumothorax
A. Occurs spontaneously Sometimes-True
B. Bullae are a Cause-True
C. Is a complication of flail Chest-True
D. Thoracotomy is frequently Indicated-True
E. A chest tube is always Necessary-False

30.Spontaneous pneumothorax is caused by

A. Tuberculosis-True
B. Emphysematous Bullae-True
C. Solitary lung Cyst-True
D. Chronic Bronchitis-True
E. Idiopathic-True

31.Decerebrate rigidity
A. Is commonly seen in patients with Glasgow coma scale of 8 or Less-True
B. Is commonly seen in patients with Glasgow coma scale of 12 or more-False
C. Is commonly seen in a patient with stiff extension of Limbs-True
D. Is commonly seen in a patient who is well oriented in person, space and Time-
False

32.Brainstem injury is mostly likely to have occurred in patient who presents with:
A. Glasgow coma scale 15/15-False
B. Glasgow coma scale 15/15 and unequal Pupils-False
C. Cerebral spinal fluid leak from both Ears-True

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D. Occipital scalp Laceration-True

33.All end colostomies are:

A. Permanent Colostomies-True
B. Defunctioning colostomies- True
C. Not suitable for ano-rectal Malformation-False
D. Hartmann’s Colostomies-False

34.Complications of colostomy include

A. Bleeding-True
B. Diarrhea-True
C. Prolapse-True
D. Retraction-True
E. Parastomal Hernia-True

35.Types of colostomy
A. Spectacle Colostomy-True
B. Double barrel Colostomy-True
C. Ileostomy-False
D. Gastrostomy-False
E. Pharyngostomy-False

36.Indications for permanent end-colostomy

A. Stage 1 carcinoma of the Sigmoid-False
B. Carcinoma of the Caecum-True
C. High fistula-in-ano-True
D. Inoperable vesicle-vaginal Fistula-False
E. Duke-B squamous cell carcinoma of the Anus-False

37.A patient with flail chest

A. Does not require a chest Drain-True
B. Rarely requires Ventilation-True
C. Should be nursed in a dark Room-False
D. The flail segment moves in on Inspiration-True

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E. Should be treated in the intensive care Unit-True

38.Complications of defunctioning loop colostomy of the sigmoid colon include

A. Electrolyte Imbalance-True
B. Excoriation of Skin-False
C. Retraction-True
D. Prolapse-True
E. Internal Hernia-True

39.Snake bite results in the following:

A. Visible puncture Wounds-True
B. Swelling of the bitten Limb-True
C. Occasionally Gangrene-True
D. Disseminated intravascular coagulation Frequently-True
E. Fat Embolism-False

40.In a jaundiced patient with palpable gallbladder, the cause of jaundice is most
likely to be:
A. Gall stones in the gall Bladder-False
B. Gall stone in the common bile Duct-False
C. Cancer of head of Pancreas-True
D. Cancer left Kidney-False

41.Generalized peritonitis is likely to follow

A. Delayed diagnosis of perforated duodenal Ulcer-True
B. Acute Pancreatitis-True
C. Ruptured Appendicitis-True
D. Torsion of the Testis-False

42.Bilateral lower abdominal pain in a female patient is most likely caused by

A. Ectopic Pregnancy-True
B. Appendicitis-True
C. Salpingitis-True
D. Ureteric Stone-True

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43.Small intestinal obstruction is likely to present with

A. Radiating pain to the left Shoulder-False
B. Spreading pain to the right iliac Fossa-False
C. Colic pain in the umbilical region -True
D. Early Vomiting-True

44.During wound healing fibroblasts migrates across the following protein:

A. Fibrillin-True
B. Fibronectin-True
C. Elastin-True
D. Laminin-False

45.Regarding collagen
A. It is composed to tropocollagen-True
B. It is synthesized mostly by mast Cells-False
C. Type II collagen is most common in connective tissue Proper-False
D. None above are Correct-False

46.Basement membrane consists of:

A. Type I Collagen-False
B. Type II Collagen-False
C. Type III Collagen-False
D. Type IV Collagen-True

47.The following factors do not contribute to wound disruption

A. Massive blood Transfusion-False
B. Anemia-False
C. Abdominal Distention-False
D. Vitamin C Deficiency-False

48.7 days after suturing, tensile strength of a wound will be:

A. 5% of the uninjured Tissue-True
B. 20% of the uninjured Tissue-False

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C. 30% of the uninjured Tissue-False
D. 50% of the uninjured Tissue-False

49.Acute appendicitis
A. Pain can be referred to the right subcostal Region-False
B. Pain can shift to right iliac Fossa-True
C. Can be associated with Vomiting-True
D. Can be associated with left hip joint Flexion-False

50.Large bowel intestinal obstruction

A. Early vomiting is a Feature-False
B. Gross abdominal distension is a Feature-True
C. Sigmoid volvulus is a possible Cause-True
D. Rectal carcinoma cannot be the Cause-False

51.Wound healing
A. Is impaired in anemic Patients-True
B. Impaired in hematoma Formation-True
C. Impaired in hypoproteinemia-True
D. Stimulated by Steroids-False

52.Intestinal obstruction
A. Can be classified depending on the age of the Patient-True
B. Can be made on erect clinical Examination-True
C. Can be due to electrolyte Imbalance-True
D. Pyloric stenosis is caused by lower intestinal Obstruction-False

53.Obstructive jaundice
A. Is associated with biliary Atresia-True
B. Is associated with itching of the Skin-True
C. A patient with obstructive jaundice passes pale Stool-True
D. Obstructive jaundice can be diagnosed by supine X-Ray-False

54.Complications of intercostal drain insertion

A. Pneumothorax-True
B. Injury to intercostal neurovascular Bundle-True

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C. Lung and liver Trauma-True
D. Surgical Emphysema-True

55.In acute appendicitis

A. Central or epigastric pain radiates to right iliac Fossa-False
B. Central or epigastric pain shifts to right iliac Fossa-True
C. Pain precedes nausea and Vomiting-True
D. Nausea and vomiting precedes Pain-False

56.In acute appendicitis

A. Mantrel (Alvarado) scores of 7 out of 10 is highly suggestive of Appendicitis-
True
B. Right iliac fossa (McBurney’s point) tenderness and leukocytosis are allotted
2 points each on Mantrel Scale-True
C. Rovsing’s sign and obturator test are contributory to Diagnosis-True
D. Digital rectal examination has no Value-False

57.In wound healing

A. Cytokines are solely produced by hemopoeitic Cells-False
B. Cytokines optimize cellular response in Inflammation-True
C. Interleukins are not classified as Cytokines-False
D. Macrophages actively synthesize cytokine growth factors for Angiogenesis-
True

58.In a completely healed wound, the tensile strength will be

A. 20% of uninjured Tissue-False
B. 40% of uninjured Tissue-False
C. 60% of uninjured Tissue-False
D. 80% of uninjured Tissue-True

59.Wound closure using suture is termed

A. Closure by primary Intention-True
B. Closure by secondary Intention-False
C. Hemostasis-False
D. Only (C) is Correct-False

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60.Factors which affect wound healing include:

A. Chronic Illness-True
B. Radiation Therapy-True
C. Nutrition-True
D. All above are Correct-True

61.The following conditions are associated with intestinal obstruction

A. Imperforate Anus-True
B. Hirschprung’s Disease-True
C. Peritonitis-False
D. Massive potassium Loss-True

62.Common causes of intestinal obstruction in the pediatric age group include:

A. Diaphragm of the Duodenum-True
B. Ileal Duplication-False
C. Intussusception-True
D. Imperforate Anus-True
E. Peritonitis following a ruptured Appendix-False

63.In the University Teaching Hospital colostomies are commonly performed for
the following conditions
A. Volvulus of the sigmoid Colon-True
B. Vesicovaginal Fistula-False
C. An obstructed umbilical Hernia-False
D. Imperforate Anus-False
E. Meckel’s Diverticulum-False

64.Paralytic intestinal obstruction occurs in

A. Hypokalemia-True
B. Hyponatremia-True
C. Peritonitis-True
D. Hemoperitoneum-True
E. Retroperitoneal Hematoma-True

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65.Mechanical intestinal obstruction occurs in

A. Internal Hernia-True
B. Intussusception-True
C. Gastric Polyps-True
D. Gall stone Ileus-True
E. Volvulus of the Cecum-True

66.Common causes of peritonitis in Lusaka are

A. Tuberculosis-True
B. Perforated Appendix-True
C. Typhoid Perforation-True
D. Biliary Leak-False
E. Perforated diverticulum of the sigmoid Colon-False

67.Shift of the falx cerebri occurs in

A. Hydrocephalus-False
B. Astrocytoma-True
C. Meningitis-False
D. Barry aneurysm of the Circle of Willis-True
E. Extradural Hematoma-True

68.Gall stones cause

A. Acute cholecystitis-True
B. Acalculous cholecystitis-False
C. Obstructive Jaundice-True
D. Carcinoma of the gall Bladder-True
E. Torsion of the gall Bladder-True

69.Factors which are known to cause perforation of the ileum include

A. Trauma-True
B. Typhoid-True
C. Gall Stones-False
D. Foreign Body-True

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E. Diverticulum of the Ileum-False

70.Mechanical ileus is a complication of

A. Hypokalemia-False
B. Pelvic Peritonitis-False
C. Adhesions-True
D. Internal Hernia-True
E. Paraplegia of acute Onset-False

71.Paralytic ileus is a complication of

A. Retroperitoneal Hematoma-True
B. Paraplegia of slow Onset-True
C. Hyperkalemia-False
D. Hypercalcemia-True
E. Peritonitis-True

72. Medical conditions which are known to present as acute abdomen include:
A. Sickle cell Disease-True
B. Pneumonia-True
C. Hypocalcemia-True
D. Addison’s disease-False
E. Hemophilia-True

73.Early signs and symptoms of compartment syndrome include:

A. Absent Pulse-True
B. Paresthesia-True
C. Inability to move toes or Fingers-False
D. A compartment pressure of less than 10mmHg-False
E. Decrease in limb Pain-False

74.Pre-operative care before laparotomy for intestinal obstruction

A. Nasogastric tube is Mandatory-True
B. Urethral catheterization may be avoided to prevent Infection-False

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C. Antibiotic use should only be instituted after knowing the cause of
Obstruction-False
D. X-match should be done for all Patients-True
E. Raised serum urea could be treated by furosemide to flash it through the
Kidneys-True

75.Factors that increase wound infection postoperatively include

A. Wound Irrigation-False
B. Tissue Damage-True
C. Hematoma formation- True
D. Bacteria load <100 000/g Tissue-False
E. Keeping clean incised wounds dressed for 48 Hours-False

76.Regarding incisions
A. Keloids form more readily on sternal area than Abdomen-True
B. Langers lines are not used for placing Incisions-False
C. Avoid old scars when re-Operating-True
D. Incised wounds heal with minimal Scarring-True
E. Traumatized skin edges can be sites of wound breakdown Later-True

77.The signs of uncomplicated volvulus are:

A. Gross abdominal distention- True
B. Ballooning of the Rectum-False
C. Dyspnea-False
D. Severe tenderness on abdominal Palpation-True

78.The usual symptoms of appendicitis are

A. Central abdominal pain with severe Vomiting-True
B. Fever over 40oC-True
C. Central abdominal pain moving to right iliac Fossa-True
D. Nausea and Anorexia-True
E. Painful Micturition-False

79.The symptoms of acute uncomplicated small gut obstruction are:

A. Continuous severe abdominal Pain-False
B. Absolute Constipation-False
C. Abdominal Distension-False

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D. Bilious Vomiting-True
E. Colicky suprapubic Pain-False

80.The signs of acute uncomplicated small gut obstruction are:

A. Oliguria-False
B. Abdominal Distension-False
C. Tinkling bowel Sounds-False
D. Absence of guarding and rebound Tenderness-True
E. Multiple fluid levels on erect film of Abdomen-True

81.Wound healing by secondary intention occurs:

A. When the wound edges are not Approximated-True
B. When there is excessive skin Loss-True
C. When the wound is Infected-True
D. In anemia Patients-False
E. In jaundiced patients-False

82.Sigmoid volvulus
A. Is initially treated with a rectal Tube-True
B. Is common in African Female-False
C. Rectal bleeding is Common-False
D. Is an emergency best treated by barium Enema-False
E. Resection and primary anastomosis is an acceptable form of Treatment-True

83.Paralytic ileus (adynamic obstruction) occurs in

A. Patients following Laparotomy-True
B. Peritonitis- True
C. Uremia- True
D. Hypokalemia-True
E. Hypocalcemia-False

84.Clinical features of acute intestinal obstruction include:

A. Abdominal Pains-True
B. Melena-False
C. Vomiting-True

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D. Distention of Abdomen-True
E. Constipation-True

85.Acute intussusception in adults occurs due to

A. Gall Stones-False
B. Change of Diet-True
C. Maximum aggregation of Peyer’s Patches-True
D. Intestinal Polyps-True
E. Head Injury-False

86.The following are predisposing causes of sigmoid volvulus

A. Chronic Constipation-False
B. Redundant pelvic mesocolon-True
C. Refined dietary Intake-False
D. Hypokalemia-False
E. Uremia-False

87.The differential diagnosis of acute appendicitis includes:

A. Tonsillitis-False
B. Acute cholecystitis-False
C. Carcinoma of the Cecum-True
D. Ectopic Gestation-True
E. Infection in urinary Tract-True

88.Burst abdomen is caused by:

A. Wound infection- True
B. Leak of pancreatic Enzymes-True
C. Anemia-True
D. Jaundice- True
E. Persistent Cough-True

89.In fracture of the base of the skull the following nerves are commonly injured
A. Olfactory-True
A. Facial-True
B. Vestibulocochlear-True

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C. Accessory- True
D. Hypoglossal-True

90.Keloid characteristics include

A. Onset is often delayed for months- True
B. Is cured by cytotoxics- False
C. Regresses Spontaneously-False
D. Pressure garments are useful following surgery- True
E. Radiotherapy is contraindicated- True

91.The epidermis of the skin consists of the following:

A. Stratum corneum-True
B. Stratum Lucidum-True
C. Stratum Granulosum-True
D. Stratum Malpighi-True
E. Stratum Basalis-True

92.Complications of blood transfusion include:

A. Congestive cardiac Failure-True
B. Antibody Reaction- True
C. Infection- True
D. Disseminated intravascular Coagulation-True
E. Fat embolism- False

93.Inguinal hernia
A. Indirect hernia is more common than direct Hernia-True
B. Strangulation is more common with direct hernia than with indirect Hernia-
False
C. Obstruction is more common with indirect inguinal hernia than direct hernia-
True
D. Direct hernia is likely to protrude through Hesselbach’s triangle- True

94.Differential diagnosis of inguino-scrotal mass includes:

A. Hernia-True
B. Hydrocele-True

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C. Meningocele-False
D. Lipoma-True

95.The following conditions are associated with abdominal hernias:

A. Chronic Cough-True
B. Multiple pregnancies in Women-True
C. Poor surgical abdominal wound Management-True
D. Ascites-True

96.An indirect inguinal hernia

A. Is the commonest hernia in young Adults-True
B. Exits through the femoral Ring-False
C. Has its neck medial to the inferior epigastric Vessels-False
D. Does not occur in female Patients-False
E. Is treated with a Truss-True

97.Umbilical hernias:
A. Are common in Zambian Children-True
B. All need herniorrhaphy before 2 years of Age-False
C. Does not give rise to Complications-False
D. All are Paraumbilical-False
E. Adults do not have umbilical Hernias-False

98.Features associated with incompatible blood transfusion include:

A. Loin pain- True
B. Tachycardia- False
C. Bradycardia- True
D. Cyanosis- True
E. Jaundice- True

99.Congenital diaphragmatic hernia

A. Are Common-True
B. Always occur in anterior mediastinum- False
C. Is invariably Fatal-False
D. Diagnosis is often missed initially in small hernias- True

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SURGERY MK
E. Are best operated upon at 10 Years-False

100. Concerning hernias

A. Inguinal hernias are more common on the Right-True
B. Femoral hernias are more common in females than in Males-True
C. Inguinal hernias are more common than femoral hernias in Females-False
D. Paraumbilical hernias are Acquired-True
E. Umbilical hernias are always Congenital-True

101. Risk factors for developing inguinal hernias include

A. Male factor-True
B. Enlarged prostate-True
C. Chronic cough-True
D. Ascites-True
E. Chronic constipation-True

102. Differential diagnosis of inguinal hernia in a female are:

A. A hydrocele of the canal of Nuck-True
B. Femoral hernia-True
C. An encysted hydrocele of the cord-False
D. Lipoma of the cord-False
E. Spermatocele-False

103. An inguinal hernia in a 3-month old baby boy should be treated

A. Because small gut strangulation is a risk-True
B. By a truss-False
C. By early operation-True
D. Left alone because it resolves spontaneously-False
E. By surgery only if the hernia becomes irreducible-False

104. Quadriplegia
A. Can be caused by fracture dislocation at C5/C6 cervical spine-True
B. Can be caused by fracture dislocation at T5/T6 thoracic spine-False
C. Can be caused by Hangman fracture-True

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D. Hypoventilation is not a feature-False

105. Second cervical vertebra and odontoid fracture

A. Basal odontoid fracture extending into body of C2 is type III fracture and is
unstable-True
B. Basal odontoid fracture is type I and is stable-False
C. Apical fracture of odontoid process is type II-False
D. Jefferson’s fracture is C3 fracture-False

106. Patient who presents with goiter, asphyxia and hoarseness of voice:
A. Is likely to have malignant goiter-True
B. Is likely to have retrosternal goiter-True
C. Is likely to have unequal pupils-False
D. Is likely to have dilated pupils-False

107. Preoperative treatment of toxic goiter

A. Iodine can be given in combination with carbimazole or propranolol-True
B. Iodine can be given and reduces vascularity of goiter-True
C. Nadolol is not a beta-blocker to be used in treating toxic goiter-False
D. It is not necessary to reduce toxic goiter to euthyroid status before operations-
False

108. Secondary thyrotoxicosis

A. Occurs in older patients than those with primary thyrotoxicosis-True
B. Eye signs including lid lag and exophthalmos are absent-True
C. Early signs of cardiac decompensation like ankle edema and dyspnea are a
feature-True
D. Orthopnea is not a feature-False

109. Malignant thyroid

A. Papillary carcinoma is most uncommon-False
B. Anaplastic carcinoma is seen in old patients-True
C. Follicular carcinoma is seen in 20% of patients of middle age-True
D. Medullary carcinoma is the commonest malignancy-False

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110. Hashimoto’s disease

A. Is common in post-menopausal women-False
B. On inspection one lobe of the thyroid is larger than the other-False
C. Symptoms of hypothyroidism are absent-False
D. Blood test may show antibodies to the thyroid gland-True

111. Thyroglossal cyst

A. It is anterior cervical midline mass-True
B. Subhyoid is rare site for thyroglossal cyst-False
C. Thyroglossal fistula is a rare post-operative complication-False
D. Moves upwards when the tongue is protruded-True

112. The following vessels supply thyroid gland

A. Superior thyroid from external carotid artery-True
B. Inferior thyroid from thyrocervical trunk of subclavian artery-True
C. Thyroidea ima artery from arch of aorta-True
D. All above except “B” and “C”-False

113. Malignant goiter

A. Medullary carcinoma is the commonest-False
B. Papillary carcinoma is the commonest-True
C. Bone metastasis may occur-True
D. Is slow growing-False

114. Toxic goiter

A. Patient has good appetite-True
B. Patient gains weight rapidly-False
C. Lid lag is not a feature-False
D. Proximal myopathy is a feature-True

115. Goiter
A. Is more common in males-False

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B. Compression signs include hoarseness of voice-True
C. Moves with protrusion of the tongue-False
D. Moves with swallowing-True

116. Toxic goiter

A. Lid lag is a feature-True
B. Lid retraction is a feature- True
C. Exophthalmos is a feature in secondary thyrotoxicosis-False
D. Anxiety state is a feature-True

117. In thyroid function

A. Coupling stage in thyroid hormone synthesis is catalyzed by deiodinase
enzyme-False
B. T4 is metabolically more active than T3-False
C. Thyroid hormone lack in children affects physical growth and mental
development-True
D. TSH, T3, T4 and radioisotope thyroid scan are useful indices for thyroid gland
activity-True

118. Examination of non-toxic goiter:

A. Includes asking the patient to swallow on inspection-True
B. Palpation is best done from the front-False
C. Palpation is best done behind-True
D. Determining lower edges helps to check for retrosternal goiter-True

119. Patient who presents with goiter causing tracheal obstruction

A. Stridor is a presenting feature-True
B. Dyspnea is a presenting feature-True
C. Kocher’s test is usually negative- False
D. Kocher’s test is usually positive-True

120. Toxic goiter

A. Exophthalmos is not a feature-False
B. Lid lag is a feature-True
C. Hot and moist skin and palms is a feature-True
D. Rapid pulse rate is not present during sleep- False

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121. Secondary thyrotoxicosis

A. Patients are younger than those with primary thyrotoxicosis-False
B. Eye signs (exophthalmos, lid lag) are absent-True
C. Atrial fibrillation is a feature-True
D. Dyspnea is not a clinical feature-False

122. Paraplegia can be caused by

A. Stab cervical injury-True
B. Fracture dislocation of thoracolumbar spine-True
C. Spinal tuberculosis-True
D. Schistosomiasis-True

123. Odontoid fracture

A. Is likely to involve C1-False
B. Is likely to involve C2-True
C. Type I fracture is stable-True
D. Type III fracture is stable-False

124. Cervical spinal fracture

A.Fracture at C4/C5 level spares phrenic nerve-False
B.Hangman’s fracture refers to the fractures at C5/C6-False
C.During hanging there is spinal hyperextension and distribution by body
weight-True
D. Open mouth X-ray is called town view-False

125. Regarding iodine metabolism

A. Uptake is solely by thyroid gland-True
B. Daily iodine requirement is 100micrograms-True
C. Iodine is trapped as iodide-True
D. Iodine is organified by carboxylase enzyme-False

126. Regarding thyroid hormone synthesis

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SURGERY MK
A. Coupling precedes organification-False
B. T3 and T4 are stored in the follicle bound to thyroglobulin molecule-True
C. T4 is physiologically more active than T3-False
D. Serum T3 is 100-160ng/100ml and T4 60-140m/L-False

127. Carcinoma of the thyroid

A. Vascular and capsular invasion is diagnostic of follicular carcinoma-True
B. Psammoma bodies and orphan Annie eyed nuclei are diagnostic of medullary
carcinoma-False
C. Follicular carcinoma metastases is mainly by blood stream-True
D. Anaplastic carcinoma has the worst prognosis-True

128. Medullary carcinoma

A. Arises from parafollicular “P” cells-False
B. Tumor may be sporadic or familial-True
C. Pituitary adenoma, parathyroid adenoma and pancreatic adenoma associated
with medullary carcinoma constitutes MEN type I syndrome-False
D. Tumors in (C) above constitutes MEN type II syndrome-False

129. Parathyroid adenoma, pheochromocytoma, medullary carcinoma and

mucocutaneous vacuromas constitutes:
A. Sipple syndrome-True
B. Marfan syndrome-False
C. Hashimoto thyroiditis-False
D. None of the above-False

130. Tumors of the thyroid gland include

A. Lymphoma-True
B. Follicular carcinoma-True
C. Anaplastic carcinoma-True
D. Warthin’s tumor-False
E. Giant cell tumor-False

131. Cervical injuries

A. Are commonly associated with head injuries-True
B. X-ray of the cervical spine down to C6 is adequate-False
C. An anteroposterior X-ray is more informative than a lateral view-True

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SURGERY MK
D. Injuries at cord level C5 will cause respiratory arrest-False
E. During radiological evaluation the shoulders are pulled down caudally-False

132. Cervical spinal injury

A. Is common in young children-False
B. Odontoid peg is the commonest site of injury-False
C. CT scan is required in all cases for diagnosis-False
D. The phrenic nerve is involved if the injury is below C5-False
E. Is common in the head injured comatose patient-True

133. Carcinoma of the thyroid

A. A common type is papillary carcinoma-True
B. Medullary carcinoma is associated with pheochromocytoma-True
C. Follicular carcinoma secretes calcitonin-False
D. Cold nodules on thyroid scan are associated with malignancy-True
E. Is seen following irradiation in childhood-True

134. Patients with spinal cord injury develop

A. Bronchopneumonia-True
B. Pressure sores-True
C. Pyelonephritis-True
D. Amyloidosis-False
E. Priapism-True

135. Post thyroidectomy complications include

A. Airway obstruction due to tracheomalacia-True
B. Recurrent laryngeal nerve palsy-True
C. External laryngeal nerve palsy-False
D. Hypercalcemia-False
E. Voice change-True

136. The differential diagnosis of mid-line tumors in the neck includes:

A. Dermoid cysts-True
B. Thyroglossal cyst-True
C. Goiter-True

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SURGERY MK
D. Bronchial cyst-True
E. Pharyngeal pouch-True

137. Pathological fractures may be associated with

A. Scurvy-True
B. Hyperparathyroidism-True
C. Bone cysts-True
D. All of the above-True

138. The most frequent offending agent in osteomyelitis of the spine is:
A. Streptococcus
B. Salmonella
C. Tubercle bacillus
D. Staphylococcus-True

139. The following sites are associated with non-union

E. Colle’s fracture
F. Carpal navicular fracture
G. Patella fracture
H. Clavicle fracture

140. A 3-year-old child with a femoral fracture should be immobilized by:

E. Skeletal traction
F. POP splint
G. Intramedullary nailing
H. Bryant’s traction

141. The following factors favor non-unions after fracture:

E. Muscle interposition
F. Hematoma at fracture site
G. Poor blood supply
H. Infection

142. The following statements are true of Perkins traction

E. It is a form of fixed skeletal traction

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SURGERY MK
F. It can be used both in children and adults
G. It was invented by Prof Sir George Perkins
H. All above correct except “C”

143. Perkins’s exercises:

E. Are commenced 2 weeks after application of traction kit
F. Are commenced within a week after application of traction kit
G. Are commenced after 3 weeks when pain at fracture site has subsided
H. All above correct except “B”

144. Perkins exercises:

E. Ensure accelerated femoral fracture union
F. Delay femoral fracture union due to mobility while performing exercise
G. Are designed to accelerate femoral fracture union and forestall knee stiffness
H. All above correct except “A”

145. Regarding fracture classification

E. Garden classification refers to fracture neck of femur
F. Salter-Harris classification refers to epiphyseal growth plate fractures
G. Le forte classification refers to tarsal fractures
H. All above correct

146. Ankle joint mortice

E. Mortice formed by medial and lateral malleolus only
F. Mortice formed by medial and lateral malleolus and tibio-fibular syndesmosis
G. Mortice formed by (b) above and articular surface of tibia
H. Only (b) above correct

147. Weber “C” ankle fracture:

E. Is fracture below tibio-fibular syndesmosis
F. Is fracture at level of tibio-fibular syndesmosis
G. Is fracture above tibio-fibular syndesmosis
H. Any fracture at ankle joint

148. Torn anterior cruciate ligament diagnosis, the following test are positive:
E. Anterior drawer test

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SURGERY MK
F. Mc-Murray test
G. Lachman test
H. Pivot shift

149. Torn posterior cruciate ligament diagnosis, the following tests are positive:
E. Lachman test
F. Apley’s grinding test
G. Posterior drawer test
H. All of the above correct

150. In classical degenerative osteoarthritis, the following are noted:

E. Osteophytes (lipping)
F. Narrowing joint space
G. Subchondral bone sclerosis
H. Subchondral bone cysts

151. Total hip replacement involves

E. Replacement of femoral head and acetabular cup
F. Replacement of femoral shaft with artificial implant
G. Both hips replacement with custom made implants
H. Replacement of only acetabular cup

152. Anterior shoulder dislocation may be reduced by

E. Kocher’s maneuver
F. Hippocratic method
G. Stimson’s technique
H. Socrate’s method

153. The following factors favor non-union of a fracture

E. Soft tissue inter-position
F. Hematoma at fracture site
G. Poor blood supply
H. When there are two bones if the other bone is intact

154. Salter-Harris type II epiphyseal fractures involves

E. It is a “T” shaped fracture extending into the proximal joint and metaphysis

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SURGERY MK
F. It extends into metaphysis with a triangular component
G. It extends into proximal joint with partially crushed epiphysis
H. None of the above

155. In posterior hip dislocation

E. Dislocation puts sciatic nerve at risk of injury
F. Reduction is achieved under general anesthesia with patient on the floor
G. Skin or skeletal traction should be applied after successful reduction
H. All above correct except “C”

156. In shoulder dislocation

E. Posterior dislocation is commoner than anterior dislocation
F. Axillary nerve is at risk of injury
G. Kocher’s manoeuver may be employed to reduce dislocation
H. All above are correct except “C”

157. In elbow dislocation

E. Anterior dislocation describes humerus lying anterior to radius.
F. Posterior dislocation describes humerus lying posterior to radius
G. The forearm bones provide key to description of the type of dislocation
H. None of above correct

158. In lower limb deformities

E. Genu valgus refers to bow legs
F. Genu varus refers to knock knees
G. Foot drop refers to injury of common fibular nerve
H. All above are correct

159. Secondary metastases to the spine can originate from cancer of

E. Thyroid
F. Breast
G. Lung
H. Prostate

160. Collar and Cuff sling

E. Is an example of external splint

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SURGERY MK
F. Is suitable for displaced humeral fracture
G. Can be used to immobilize femoral fractures in children
H. The flexion angle at the elbow is less than 90 degrees

161. Intramedullary nail is

E. External fixation
F. Internal fixation
G. Suitable for fracture of the femoral shaft
H. Also known as Kuntscher nail

162. The following tumors readily metastasize to bone

F. Rectal adenocarcinoma
G. Basal cell carcinoma of skin
H. Follicular carcinoma of the thyroid
I. Prostatic adenocarcinoma
J. Renal adenocarcinoma

163. Dislocations
F. Do not require urgent management
G. Post-reduction immobilization is required for 3 months
H. The medial nerve is damaged in shoulder dislocations
I. The ulnar nerve is damaged in lunate dislocations
J. All open dislocations require operative reduction

164. Osteoarthritis of the knee joint is a complication of

F. Hemophilia
G. A malunited femoral fracture
H. Total menisectomy
I. Valgus deformity of the knee
J. Gross obesity

165. Supracondylar fractures of the humerus

F. Always check the radial artery pulse
G. Always check nail bed capillary filling in absence of the radial pulse
H. Extension improves limb circulation
I. Nerve damage is uncommon

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SURGERY MK
J. Non-union is uncommon

166. The following fractures commonly lead to ischemic necrosis of a part of the
bone
F. Femoral neck
G. Humeral neck
H. Scaphoid
I. Talus neck
J. Femoral condyle

167. The following fractures lead to nerve damage in some patients:

F. Femoral neck
G. Neck of fibula
H. Medial epicondyle of humerus
I. Radial shaft
J. Humeral shaft

168. Fracture of the pelvis:

F. A stable fracture requires 3 months bed rest
G. A displaced sacroiliac joint requires skeletal traction
H. Blood transfusion is essential in extensive pelvic fractures
I. Isolated undisplaced iliac bone fractures do not require immobilization
J. Fractures of the pubic rami are relatively common

169. The following are flexors of the wrist joint:

F. Brachioradialis
G. Flexor carpi ulnaris
H. Pronator teres
I. Flexor digitorum profundus
J. Flexor pollicis brevis

170. Osteosarcoma is treated by

F. Radiotherapy
G. Chemotherapy and surgery
H. Immunotherapy

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SURGERY MK
I. Antibiotics
J. Vitamin D

171. The following laboratory tests are useful in evaluating diseases related to
bones
F. Serum parathyroid hormone
G. C-reactive protein
H. Urinalysis for specific proteins
I. Fasting blood glucose
J. Serum uric acid levels

172. Osteoporosis
F. Is common in premenopausal women
G. Is treated with estrogens
H. Causes pathological fractures
I. Erythrocyte sedimentation rate is elevated
J. Once established cannot be reversed

173. Primary osteoarthritis

F. Starts as a disorder of articular cartilage
G. Results in periarticular osteoporosis
H. Is associated with peripheral vascular disease
I. Occurs more commonly in females
J. Is common in Zambia

174. Dupuytren’s contractures:

F. Causes extension deformity of the wrist
G. Is familial
H. The foot can be involved occasionally
I. Is treated by steroids
J. Trauma is an etiologic factor

175. Carpal Tunnel syndrome

F. Occurs in middle aged men only
G. Symptoms are related to thumb only
H. Does not cause muscle wasting
I. Surgery is indicated

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SURGERY MK
J. Symptoms are worse at night

176. Septic arthritis is best managed by

F. Aspiration of the joint
G. Antibiotics
H. Rest and elevation
I. Gypsona immobilization
J. Arthrotomy, antibiotics and rest for the joint

177. Acute osteomyelitis

F. Brodie’s abscess is a variety of acute osteomyelitis
G. A common causative organism is Staphylococcus aureus
H. Bone drilling must be done early to prevent further damage
I. X-rays do not show changes in the first week
J. Is common in Zambian children

178. Tuberculosis of the spine

F. Is common in Zambia
G. Usually affects the vertebral bodies
H. Can be adequately treated by anti-tuberculous drugs alone
I. Never produces sequestra
J. Is not diagnosed unless a paraplegia is present

179. A 3-year-old child develops pain in the hip joint, is pyrexial and has a high
erythrocyte sedimentation rate:
F. Treat by traction alone
G. Treat by antibiotics alone
H. Blood culture are to be done
I. Explore the hip joint surgically
J. Take a careful history from the mother and do a full physical examination at
admission

180. Poliomyelitis
F. Anterior horn cells are affected
G. Flaccid paralysis develops
H. Joint contracture may follow muscle imbalance

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SURGERY MK
I. Tendon division may improve function
J. Spread is by nasopharyngeal droplets

181. The following statements are true or false

F. The radial nerve is injured in humeral fractures
G. The ulnar nerve is injured in dislocated shoulder
H. A Colles fractures commonly injures the median nerve
I. Wrist drop occurs with median nerve palsy
J. Circumflex nerve injury causes inability to adduct the shoulder

182. Acute osteomyelitis of the tibia

F. Not to be drained unless bone changes are present on X-ray
G. Staphylococcus aureus is the causative organism in all cases
H. Requires immediate drainage
I. X-Ray changes are visible within a few days of onset of infection
J. Antibiotics are not indicated

183. Ulnar nerve palsy

F. Occurs in fracture of the lateral epicondyle of the humerus
G. Results in wasting of thenar muscles
H. The little finger cannot be abducted against resistance
I. The ulnar side of the hand becomes dry (no sweating)
J. Dermatome involved is C5

184. Osteoporosis
F. Is a hereditary disease
G. Is same as Osteomalacia
H. Is curable
I. Is common in young premenopausal women
J. Responds to vitamin A

185. The following nerves are injured in a dislocation shoulder

F. Medial
G. Circumflex
H. Axillary
I. Suprascapular
J. The nerve which supplies the deltoid muscle

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186. Concerning the menisci of the knee:

F. Injuries are common in elderly people
G. A tear is associated with osteoarthritis of the knee
H. Twists at the knee is the usual cause of meniscal tears
I. Injuries to the lateral one is commoner
J. One function is to improve lubrication

187. A 39-year-old male with a suspected intervertebral disc prolapse suddenly

develops urinary retention. The following measures should be taken
F. Urgent radiculogram
G. Catheterisation
H. Urgent exploration of spine
I. Bed rest and skeletal traction
J. Send to the next urology clinic

188. A 4-year-old child develops pain in the hip joint with restriction of all
movements, pyrexia, high erythrocyte sedimentation rate and a high white blood
cell count
F. Treat with skin traction alone
G. Give aspirin and bed rest
H. Take blood cultures
I. Explore the hip surgically
J. Is commonly associated with trauma

189. Osteoarthritis has the following features:

F. Occurs in the hand bones
G. Is age related commonly
H. Often follows joint injury
I. Is commoner in males
J. Results in periarticular osteoporosis

190. Sickle cell disease

F. Is hereditary
G. Is due to an abnormal hemoglobin

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SURGERY MK
H. Femoral epiphyseal infarction is a complication
I. Steroids are indicated in all cases
J. Is associated with osteomyelitis

191. Following a nerve injury

F. Neuropraxia has the best prognosis for recovery
G. Neurotmesis has the worst prognosis for recovery
H. Axonotemesis describes complete transection of the nerve
I. Axons regenerate at the rate of 1 mm per day
J. Axons regenerate at the rate of 1cm per day

192. The following fractures occur at the wrist

F. Colles
G. Barton’s
H. Smiths
I. Pott’s
J. De Quervain’s

193. The following fractures usually require open reduction and internal fixation
F. Oblique shaft fractures of the humerus
G. Colles fracture
H. Greenstick forearm fractures in children
I. A displaced fracture of the lateral condyle of the elbow in a 10-year-old
J. A subcapital femoral fracture in an elderly female

194. A fracture of the carpal scaphoid

F. Is frequently caused by a fall on the outstretched hand
G. Usually occurs through the waist of the scaphoid
H. Avascular necrosis of the distal fragment is a possibility
I. Is commoner in the younger patient than the old
J. Non-union is possible

195. In spinal Tuberculosis

F. Infection starts in bone adjacent to a disc
G. New bone formation is minimal in active infection
H. Radiographs usually show destruction of the body of a vertebra without
involvement of the disc

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SURGERY MK
I. Psoas abscess is a complication
J. Paraplegia is a complication

196. Poliomyelitis
F. Is caused by damage to anterior horn cells
G. Leg length inequality is a possibility
H. Short rigid scoliosis is usually associated with it
I. Foot neuropathic ulcers are common
J. Osteoarthritis is a common feature of the affected limb joints

197. The following muscles in the hand are supplied by the median nerve
F. Abductor pollicis brevis
G. The first dorsal interosseous muscle
H. Adductor pollicis
I. Abductor digiti minimi
J. Opponens pollicis

198. In chronic osteomyelitis of the femur

F. New bone outside the cortex is the involucrum
G. Sequestrum is more radiopaque than normal bone
H. A loose dead bone is called sequela
I. Cloacae drain pus through the cortex
J. Long standing sinuses heal with antibiotics

199. The early clinical signs and symptoms of ischemia in the forearm and hand
following closed reduction of a supracondylar fracture are
F. Paralysis of median nerve
G. Gangrene of tips of fingers
H. Fixed contracture of the flexor muscles
I. Pain, especially on extension of the fingers
J. Absent radial pulse and poor capillary return

200. The following are complications of a Colles fracture at the wrist

F. Rupute of the extensor pollicis longus
G. Frequent non-union
H. Median nerve compression
I. Malunion

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J. Inferior radioulnar subluxation

201. Classification of fractures

F. Radiologically as open or closed fractures
G. Clinically as compound fracture or closed fracture
H. Comminuted fracture when more than 2 fragments are present
I. Pathological fractures when fracture is due to tumor deposit
J. Supracondylar fracture refers to anatomical classification

202. Concerning fractures of the neck of femur

F. They are more common in elderly men
G. They are usually caused by high energy trauma in the elderly
H. Avascular necrosis of the head of the femur is common complication
I. If treated conservatively they have a higher incidence on non-union
J. They are best managed by skeletal traction

203. Femoral shaft fractures

F. Are associated with an average blood loss of 1000-1500ml
G. In the young patient are usually associated with other life-threatening injuries
H. Are usually adequately treated with traction
I. Are commonly complicated by compartment syndrome
J. Are commonly associated with shortening of the affected limb

204. Regarding Perkin’s traction

F. The usual weight applied is 1/10 of the patient’s body weight
G. Leg lengths are measured once weekly for the first 2 weeks after application
H. Exercises are best commenced within the first 4 days of applying traction
I. The foot end of the bed is normally elevated by 4cm for every Kg of weight
J. A Denham pin may be used for applying the traction

205. Concerning open fractures

F. They are more common in the tibia than in any other long bone
G. They cannot be complicated by compartment syndrome
H. They are commonly associated with delayed union and non-union in the tibia
I. X-rays are not necessary
J. Are best treated with an external fixator

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SURGERY MK

206. The following displacements are characteristic of Colles’ fracture

F. Volar (anterior) displacement of the distal fragment
G. Apex volar angulation
H. Ulnar deviation of the distal fragment
I. Impaction
J. ‘Dinner fork’ deformity

207. Supracondylar fractures of the humerus in children

F. Are usually of the flexion type
G. Commonly occur after a fall on an outstretched hand
H. Are partly caused by the olecranon being forced into the olecranon fossa
I. Can be complicated by myositis ossificans
J. If presenting with extensive swelling should be manipulated and immobilized
in a collar and cuff

208. Concerning fracture healing

F. Hematoma formation at the fracture site does not influence the rate of fracture
healing
G. It is affected by the nutritional status
H. Upper limb fractures in children take about 3 weeks to heal
I. It is influenced by the type of bone involved
J. It is affected by the hemoglobin level of the patient

209. Concerning acute hematogenous osteomyelitis

F. It is commonly caused by Salmonella Spp
G. Organism normally settle in the metaphysis of long bones
H. In infants it may lead to septic arthritis
I. Radiological signs are present within 24 hours of the infection
J. It is best managed conservatively

210. Differential diagnoses of acute osteomyelitis include:

F. Fracture
G. Sickle cell crisis
H. Rheumatic fever

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SURGERY MK
I. Cellulitis
J. Septic arthritis

211. The criteria for diagnosis of septic arthritis in patients with negative cultures
(according to Morrey and Associates) include:
F. Pain in suspected joint worsened by movement
G. Systemic symptoms
H. Poor response to antibiotic therapy
I. Swelling of suspected joint
J. Fever of more than 38.3 degrees Celsius

212. Fracture of clavicle

F. Is usually compound
G. Is best treated by open internal fixation
H. Is usually associated with blood vessel injury
I. Is treated by POP immobilization
J. Can be treated by long arm sling alone

213. In Tuberculosis of bone

F. The local reaction is characterized by extensive new bone formation
G. The metaphysis of a bone is the commonest site of involvement
H. The infection is usually secondary to primary focus elsewhere in the body
I. Extension of the bone abscess into a joint is common
J. Associated abscesses show few signs of inflammation

214. Features occurring in children differ from those in adults in the following
respects
F. Fractures unite readily
G. Malunion can be corrected by growth
H. Joint stiffness is rare after immobilization
I. Fractures involve the epiphyseal plate on occasion
J. Fractures usually occur with minimal trauma

215. In fracture of the shaft of the adult femur

F. The estimated blood loss is at least 1 liter
G. Skeletal traction and Perkin’s exercises are effective treatment
H. Healing is faster in Zambians than in Europeans

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SURGERY MK
I. Internal fixation allows earlier mobilization
J. Internal fixation is the treatment of choice in Zambia

216. Carpal tunnel syndrome

F. Is most frequent in middle aged men
G. Symptoms are related to all fingers and the thumb
H. Does not cause muscle wasting
I. Surgical treatment is usually curative
J. The symptoms are worse at night

217. Dislocation of the hip

F. Common variety is a posterior dislocation
G. Delay in reduction does not increase the risk of late complications
H. Is overlooked if there is an associated fracture of the shaft of femur
I. Leads to dorsiflexion of the foot and great toes
J. Sciatic nerve injury occurs in 50% of patients

218. The following fractures are rarely adequately treated by closed manipulation:
F. Bennet’s fracture
G. Colles fracture
H. Phalages of digits
I. Monteggia
J. Tibial condyle

219. Internal hemorrhoids are arranged in the following manner with the patient in
lithotomy:
A. 3, 7 and 11 O’clock-True
B. 3, 7 and 9 O’clock-False
C. 7, 9 and 11 O’clock- False
D. 3, 9 and 11 O’clock-False

220. GoodSall’s rule is related to

A. Anal fissure-False
B. Anal fistula-True
C. Hemorrhoids-False
D. Anal abscesses-False

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SURGERY MK

221. Common causes for rectal bleeding

A. Internal hemorrhoids-True
B. Anal fissure-True
C. Carcinoma rectum-True
D. All correct except (B)-False

222. Concerning piles

A. First degree piles bleed but do not prolapse-True
B. Second degree piles prolapse with defecation and reduce spontaneously-True
C. Third degree piles are thrombosed piles whether internal or external-False
D. None above are correct-False

223. Treatment for first degree piles

A. Hemorrhoidectomy-False
B. High fiber diet-True
C. Suppositories-True
D. All above correct-False

224. Hemorrhoids
A. Always cause pain and bleeding-False
B. Sometimes cause pain and bleeding-True
C. Are always treated by operation-False
D. Can be due to increased intra-abdominal pressure-True
E. Are noted in pregnancy-True

225. The adult anus

A. Is 1cm long-False
B. Is covered by serosal lining-False
C. Blood supply is from 3 rectal arteries-True
D. Has 2 main parts meeting at perineal line-False
E. Inferior half lymphatics drainage is to the superficial inguinal nodes-False

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226. Thrombosed hemorrhoids

A. Are treated by hemorrhoidectomy-True
B. Can be commonly seen at three sites: 4, 7 and 11 O’clock-False
C. Are due to arterial anastomosis-True
D. Usually have a sentinel pile-True
E. Common in diabetic patients-True

227. Digital rectal examination is diagnostic in

A. First degree hemorrhoids-True
B. Low carcinoma of the rectum-True
C. Fissure in ano-True
D. Acute cystitis-False
E. Hirschprung’s disease-True

228. Axillary tail of the breast lies in

A. Upper outer quadrant-True
B. Upper inner quadrant-False
C. Lower outer quadrant-False
D. Lower inner quadrant-False

229. The breast tissue is located

A. Within subcutaneous layer-False
B. Within superficial fascia between upper and lower layers-True
C. Rests directly on pectoral fascia-False
D. Only “A” above is correct-False

230. Fibroadenoma of breast

A. Commonest benign tumor-True
B. It may be peri or intra canalicular-True
C. It lacks a definite capsule-True
D. Recurrence after excision is rare-True

231. Blood stained discharged from nipple may represent

A. Duct papilloma-True

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SURGERY MK
B. Pagets disease of nipple-True
C. Galactocele-False
D. Only “B” and “C” correct-False
232. The following breast tumors may undergo malignant transformation
A. Phylloides tumor-True
B. Multiple duct papillomatosis-True
C. Intracanalicular fibroadenoma-True
D. All above-True

233. Change of breast may also be named as

A. ANDI-True
B. Benign mammary dysplasia-True
C. Fibroadenosis-True
D. Chronic mastitis-True

234. Reference to ANDI of breast, histological features include:

A. Adenosis-True
B. Epitheliosis-True
C. Duct ectasia-False
D. Fibrosis-True

235. In Lactational mastitis

A. Cracked nipple permits entry of bacteria-True
B. Staphylococcus aureus is the main pathogen-True
C. There is good response to broad spectrum antibiotics-True
D. May be complicated by breast abscess-True

236. The following cannot affect breast tissue

A. TB-False
B. Syphilis-False
C. Fungal infection-False
D. All above-False

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SURGERY MK

237. Triple assessment of breast pathology

A. Is only relevant to malignant conditions-False
B. Involves taking history and performing clinical examinations only-False
C. Involves as well U/S scan for females above 35 years old and mammogram
for females below 35 years of age-False
D. Fine needle aspiration cytology (FNAC) is preferred to incisional or
excisional biopsy snice it is specific and easy to interpret- True

238. Pagets disease of the nipple

A. Usually presents as bilateral nipple eczema-False
B. Unilateral nipple eczema-True
C. Related to underlying duct carcinoma-True
D. All above true except (B)-False

239. Fibroadenoma of breast

A. It may present as mobile, painless mass-True
B. Has ill-defined edges-False
C. It may be intra or peri-canalicular-True
D. Recurrence common after excision-False

240. Fibrocystic breast disease presents as:

A. Fibroadenosis-True
B. Cystic formation-True
C. Epitheliosis- True
D. Fibrosis and lymphocytosis-True

241. The following drugs are used in breast cancer

A. Cyclophosphamide-True
B. 5-fluoro-uracil-True
C. Methotrexate-True
D. Adriamycin-True

242. The following features present advanced breast cancer

A. Peau d’orange-True

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SURGERY MK
B. Nipple retraction/ulceration/bleeding-True
C. Fixity to underlying pectoral muscle-True
D. Hepatomegaly-True

243. Phyllodes tumor on histology

A. Might be benign-True
B. Might be borderline-True
C. Might be frankly malignant-True
D. Cellular stroma is characteristic-True

244. Breast tissue lies

A. Within retromandibular space-False
B. Deep to pectoral fascia-False
C. Within superficial fascia-True
D. May extend to the axilla-True

245. Breast cancer

A. Carcinoma in-situ tumor has not yet breached basement membrane-True
B. Lobular carcinoma tends to be multicentric in origin more than ductal
carcinoma-True
C. Ductal carcinoma tends to be multicentric in origin more than lobular
carcinoma-False
D. None of the above-False

246. Breast cancer markers/receptors include:

A. ER/PR-True
B. HER-2/NEU-True
C. Tamoxifen is useful in ER positive receptors-True
D. Trastuzumab (Herceptin) is useful in advanced breast cancer that are HER-
2/NEU receptor negative-False

247. Supraradical mastectomy involves

A. Mastectomy, axillary node clearance and excision of pectoral muscles-True
B. The clavicle and sternum were spared-True
C. Procedure abandoned due to post op arm edema and weak upper limb-True
D. Operation is now obsolete-True

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SURGERY MK

248. Radical mastectomy

A. Improves on supraradical mastectomy-False
B. It spared clavicle and sternum-True
C. Pectoralis major was spared-False
D. Also referred to as complete Halsted-True

249. Patey’s mastectomy

A. Improved on radical mastectomy-True
B. It spares pectoral major muscles-True
C. Axillary and pectoral nodes clearance done-True
D. Power limb was an advantage-True

250. Lymph node involvement in breast cancer includes the following

A. Axillary lymph nodes-True
B. Supraclavicular lymph nodes-True
C. Cervical lymph nodes-True
D. Inguinal lymph nodes-False

251. Triple assessment is used in making a diagnosis of breast disease and consists
of the following:
A. Clinical examination, imaging, and fine needle aspiration cytology-True
B. Triple imaging-ultrasound, chest X-ray, mammography-False
C. Triple diagnosis- mammography, radioisotope studies and CAT-scan-False
D. Nipple cytology, thermography and MRI-False

252. A breast lump in an adolescent can be one of the following

A. Fibroadenoma-True
B. Giant fibroadenoma-True
C. Galactocele-False
D. Dysgerminoma-False
E. Hurtle cell tumor-False

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253. An enlarged prostate

A.Can be determined by digital rectal examination-True
B.Can be identified by ultrasound evaluation-True
C.Doses not cause acute urinary retention-False
D.Prostatic specific antigen is an indicator of malignant disease in the prostate-
True
E. Acid phosphatase is a specific test for prostatic cancer-True

254. Prostatectomy is performed using one of the following approaches

A. Suprapubic transvesical-True
B. Retropubic (Millin’s)-True
C. Transurethral-True
D. Perineal-True
E. Pfannenstial incision-False

255. Complication of prostatectomy include

A. Excessive bleeding-True
B. Inflammation of the vas deferens-True
C. Bladder neck stricture-True
D. Gastric atony-False
E. Subphrenic abscess-False

256. Cancer of the prostate

A. Is common in the elderly-True
B. Is often asymptomatic-True
C. Treatment of choice is prostatectomy-True
D. Prostate specific antigen is a reliable guide to prognosis-True
E. Metastases are always osteolytic-False

257. Fibroadenoma of the breast

A. Occurs in early adult life-True
B. May be multiple-True
C. Adheres to the pectoralis major-False
D. Is painful-False

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SURGERY MK
E. Disappears spontaneously-False

258. In hypernatremia
A. Fever and edema are absent-True
B. Restlessness and raised BP are present-True
C. There is increased urine output-True
D. Only C is correct-False

259. In hyperkalemia patient will present with:

A. Increased reflexes and ECG changes-False
B. ECG shows inverted “T” waves-False
C. ECG shows peaked “T” waves-True
D. Oliguria, muscle weakness and respiratory distress are a feature-True

260. Treatment of hyperkalemia include:

A. Kayexalate-True
B. IV insulin and glucose-True
C. Lasix and stop potassium containing fluid-True
D. Dialysis if severe-True

261. In respiratory alkalosis

A. PCO2 rises-False
B. PCO2 falls-True
C. PCO2 remains the same-False
D. None above are correct-False

262. In metabolic acidosis

A. CO2 combining power rises-False
B. CO2 combining power falls-True
C. CO2 combining power remains the same-False
D. Only C is correct-False

263. Under normal conditions the colloid osmotic pressure of blood is about
A. 75mmHg-False
B. 50mmHg-False
C. 25mmHg-True

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SURGERY MK
D. 10mmHg-False

264. Signs and symptoms of hyperkalemia include

A. Peaked “T” waves on ECG-True
B. Increased cardiac contractility-False
C. Muscle weakness-True
D. Respiratory distress-True

265. Treatment of hypernatremia include:

A. Stop IV normal saline-True
B. Glucose and insulin intravenously-False
C. Lasix-True
D. Dialysis if severe-True

266. Administration of potassium to correct hypokalemia

A. Give potassium as intravenous bolus-False
B. Not more than 20mEq with 40mEq as maximum-True
C. Ensure good urine output-True
D. Cardiac monitor not essential-False

267. The following intravenous solutions are commonly used to treat hemorrhagic
shock in the University Teaching Hospital
A. 0.9% saline-True
B. 5% dextrose-False
C. Ringer’s lactate-True
D. Hypertonic saline-False
E. Darrow’s solution-False

268. Septic shock

A. Is particularly associated with Celestin tube insertion-False
B. Is often due to gram negative organisms-True
C. Is particularly seen in patients with indwelling intravenous catheters-True
D. Surgery for acute cholecystitis is a cause-False
E. Does not occur in gram positive septicemia-False

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269. The following intravenous fluids contain potassium

A. Darrow’s-True
B. Ringer’s-True
C. Blood-True
D. Dextrose 5%-False
E. Dextran solution-False

270. Patients needing supplementary feeds include those with

A. Recent weight gain-False
B. Serum albumin >30g/dl-False
C. Serum albumin <30g/dl-True
D. Negative nitrogen balance-True
E. Positive nitrogen balance-False

271. Parenteral feeds

A. Best feeding method-False
B. Has least side effects-False
C. Requires feeding nasogastric tube-False
D. Very expensive-True
E. May be the only alternative in conditions like acute pancreatitis-True

272. Body fluids

A. A 70kg man has 42L as total body water-True
B. Interstitial fluids in a 70kg man is 11 Liters-True
C. 3 L of plasma in a 60kg man-False
D. 15L in a 60kg man is extracellular fluid-False
E. Potassium is an extracellular ion-False

273. Pancreatitis
A. Can be the cause of chemical peritonitis-True
B. Absence of bowel sounds is a feature-True
C. Serum amylase is not raised-False
D. Laparotomy is indicated in all cases-False

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274. Complications of acute pancreatitis are

A. Pseudocyst formation-True
B. Disseminated intravascular coagulation-True
C. Left basal effusion (pleural)-True
D. Renal failure-True
E. Ascites-True

275. Gall stones cause

A. Acute cholecystitis-True
B. Acalculous cholecystitis-False
C. Obstructive jaundice-True
D. Carcinoma of the gall bladder-True
E. Torsion of the gall bladder-True

276. Acute cholecystitis

A. Does not occur in sicklers-False
B. Is usually treated by cholecystostomy-True
C. Is usually associated with urinary bladder stones-False
D. Can cause pain in the right shoulder-True
E. Causes pain and tenderness in the left hypochondrium-False

277. Acute pancreatitis

A. Often results in hypoxemia-True
B. Usually gives rise to Cullen’s sign-True
C. Causes hypercalcemia-False
D. Can be caused by mumps-True
E. Occurs after biliary surgery sometimes-True

278. Esophagus
A. Below the pulmonary roots the vagus nerves are in contact with esophagus-
True
B. The left trunk of the vagus nerve is on the anterior side of the esophagus -True
C. The right trunk of the vagus nerve is on the posterior side of the esophagus-
True

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SURGERY MK
D. The longest part of esophagus is intra-abdominal-False

279. Cancer of the esophagus

A. Dysphagia is initially for solids-True
B. Dysphagia is initially for liquids-False
C. Barium swallow X-ray shows a smooth constriction giving a rat-tail
appearance-False
D. Barium swallow X-ray shows irregular and sharp edge constriction giving
shouldering appearance-True

280. Signs of advanced cancer of the esophagus include:

A. Hoarseness of voice as a sign of involvement of recurrent laryngeal nerve-
True
B. Weight loss of more than 20%-True
C. Absence of palpable supraclavicular lymph nodes-False
D. Presence of palpable lymph nodes-True

281. Esophageal stricture

A. Can be caused by achalasia of the cardia-False
B. Inflammation of esophagus does not cause strictures-False
C. Can be caused by cancer of esophagus-True
D. Can be caused by ingestion of corrosive chemicals-True

282. Cancer esophagus presents with

A. Weight gain-False
B. Dysphagia of solids-True
C. Odynophagia- True
D. Regurgitation is not a feature-False

283. Carcinoma of the esophagus is commonly treated by

A. Surgery-True
B. Radiotherapy-True
C. Immunotherapy-False
D. Chemotherapy-True
E. Gastrostomy-False

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284. Carcinoma of the esophagus

A. Lower third is a common site-True
B. Is adenocarcicnoma in 90% of cases-False
C. Is radiosensitive-True
D. Metastases the scalene node-True
E. Presents early in Zambia-False-False

285. Hepatocellular carcinoma

A. Is the commonest tumor of men in Zambia-False
B. Is not associated with post-necrotic cirrhosis-False
C. Is related to ingestion of aflatoxins-True
D. Presents with intermittent abdominal pain-True
E. Rarely causes early weight loss-False

286. Incisional hernias are related to

A. Wound infections-True
B. Anemia and malnutrition-True
C. Obesity-True
D. The use of absorbable suture materials-True

287. The differential diagnosis of an inguinal hernia in a female include:

A. Vaginal hydrocele-True
B. Encysted hydrocele of the cord-False
C. A femoral hernia-True
D. None of the above-False

288. A strangulated hernia

A. Is tense-True
B. Is tender-True
C. Has a transmitted cough impulse-False
D. Requires elective surgery-False

289. A partial thickness burn

A. May heal without grafting-True

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SURGERY MK
B. May deteriorate into full thickness skin loss-True
C. Rarely causes severe physiological derangement of the patient-True
D. Heals within 7 days in the absence of infection-False
290. Burns
A. History taking should always include- Time of burn, cause, smoke inhalation,
trauma- True
B. On examination the severity is determined by burn depth, burn size, areas of
circumferential full thickness-True
C. Full thickness burns will produce very painful charred skin-False
D. Escharotomy may help in reducing respiratory embarrassment-True

291. In burns
A. A man with 30% superficial burns does not require fluid therapy-False
B. A female with 20% superficial burns does not require ATT on admission-
False
C. Parkland’s formula considers fluids therapy in the first 36 hours-False
D. Browder and Lund charts are used to estimate percentage surface area burnt-
True

292. The skin

A. Is a multilayered organ-True
B. Good approximation of layers is not vital-False
C. Crush injury heals better than an incision-False
D. Langer’s lines run perpendicular to muscle axis-True
E. Langer lines run mainly longitudinal to muscle axis-False

293. Upper gastrointestinal hemorrhage can be caused by:

E. Mallory-Weis tear
F. Sigmoid volvulus
G. Periportal fibrosis due to Bilharzia
H. Perforated anterior duodenal ulcer

294. Zollinger-Ellison syndrome

E. Multiple ulcerations are a feature
F. Increased vagal activity is the main cause
G. Fresh red blood rectal bleeding is a common feature

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SURGERY MK
H. Gastrin producing endocrine tumor is a common feature

295. Pyloric stenosis in adult patient:

E. Annulus pancreas can be the cause
F. Chronic duodenal ulcer can be the cause
G. Meckel’s diverticulum can be the cause
H. Cancer of pancreas can be the cause

296. In a patient with peptic ulcer disease

E. Histamine production is increased by stimuli from both vagus nerves and
gastrin
F. The process of exporting hydrogen ions from parietal cells via protein pump
is not a feature
G. Histamine acts on parietal cells via H2-receptors
H. Melena stools is not a feature

297. Investigating a patient who presents with hematemesis includes:

E. Esophagoscopy
F. Gastroduodenoscopy
G. Lower midline laparotomy is advisable
H. Right subcostal mini-laparatomy is advisable

298. Brain abscess in the frontal lobe

E. Is most likely a complication of chronic otitis media
F. Is not likely a complication of paranasal sinusitis
G. Is most likely a complication of infected occipital laceration
H. Is most likely a complication of infected wound on the temporal area of the
head

299. Large supratentotrial space occupying lesions is likely to present with

E. Full consciousness
F. Unequal pupils
G. Contralateral hemiplegia

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SURGERY MK
H. Paraplegia

300. Common causes of congenital hydrocephalus include:

E. Brain abscess
F. Dandy-walker cyst
G. Arterial venous malformation
H. Anold-Chiari malformation

301. Submandibular gland tumors

E. 50% are malignant
F. Facial nerve weakness is a feature
G. Ulceration of overlying skin is not a feature
H. Cervical lymph nodes enlargement is a feature

302. Parotid gland tumors

E.Most common are benign pleomorphic adenomas
F.10% are malignant
G.Rapid growth with infiltrating of overlying skin is a sign of high-grade
malignancy
H. Enlarged palpable cervical lymph nodes are not a feature

303. Bilateral paralysis of genioglossus leads to

E. Atrophy of the tongue
F. Tongue falls back
G. Obstruction of respiratory passage
H. All above true except “B”

304. Structures embedded in the parotid gland include

E. Facial nerve
F. Retromandibular vein
G. External carotid artery
H. Parotid lymph nodes

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305. The following are examples of non-absorbable suture materials

E. Silk
F. Vicryl
G. Nylon
H. Stainless steel
306. The following suture are
E. Silk is natural material
F. Nylon is synthetic material
G. Vicryl is natural material
H. Stainless steel is synthetic material

307. Knot security after wound suturing

E. Best with vicryl
F. Good with nylon
G. Worst with silk
H. All above correct

308. Clostridium Welchii is

E. Causative agent of wet gangrene
F. Causative agent of gas gangrene
G. Aerobe, sporulating, gram negative bacillus
H. Proliferates in dirty wounds

309. In acute limb ischemia

E. Thrombo-embolism may be a causative factor
F. In-situ blockage of artery by thrombus is factor
G. Buerger’s test is positive
H. Ankle brachial pressure index is useful indicator of severity of ischemia

310. Parotid benign tumors

E. Make up 80 to 90% of parotid tumors
F. Are pleomorphic adenomas
G. Are soft on palpation
H. Mostly arise in the superficial lobe

311. HIV-associated sialadenitis of parotid gland

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SURGERY MK
E. Chronic parotitis in children is pathognomonic of HIV infection
F. Facial disfigurement is a feature
G. CT scan shows characteristics swiss cheese appearance of multiple cystic
lesions
H. Cosmetic surgery is not advisable

312. Causes of leucopenia

E. Lymphoma
F. Sever infections
G. Disease of the spleen
H. Autoimmune disorders

313. Causes of leukocytosis

E. Inflammatory conditions like arthritis
F. Stress
G. Allergic conditions like asthma
H. Pregnancy

314. A rise in monocytes may indicate the following:

E. Chronic inflammatory disease
F. Parasitic infestation
G. Tuberculosis
H. Oral infection

315. Post-op fever after abdominal surgery

E. Is caused by release of pyrogens
F. Intra-abdominal collections
G. Blood and platelet infusions
H. Pulmonary complications like pneumonia or empyema

316. Unilateral ureteric obstruction may be caused by

E. Ureteropelvic stenosis
F. Ureteric stone
G. Posterior urethral valves
H. Neurogenic bladder

317. Unilateral renal artery obstruction may be associated with

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E. Increased renin release by the obstructed kidney
F. Angiotensin release and increased aldosterone production by adrenal cortex
G. Increased sodium and water retention
H. Hypotension

318. Chronic bilharzia can cause

E. Bilateral ureteric obstruction
F. Transitional cell carcinoma
G. Bilateral hydronephrosis
H. Squamous cell carcinoma of the bladder

319. Management of obstructive uropathy may include

E. Catheterization
F. Bilateral orchidectomy
G. Endoscopic ureterotomy
H. Urethroplasty

320. Parotid inflammatory swelling

E. Can be caused by mumps
F. Is rare in children
G. Can be HIV associated
H. Does not cause facial disfigurement

321. Superficial parotidectomy

E. Is indicated for benign and low grade malignant tumors
F. Incision is lazy-“S”
G. Facial nerve injury is rare
H. Skin flap is developed to reach anterior border of the gland

322. Parotidectomy complications

E. Frey’s syndrome
F. Facial nerve palsy
G. Hemorrhage
H. Raised T3 and T4

323. Lung cancer

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SURGERY MK
E. Small cell lung cancer makes up 20%
F. Metastasis by lymphatics is rare
G. Metastasis by blood borne spread is common
H. Surgery greatly improves survival

324. When considering fluid spacing

E. First spacing is normal exchanging between intravascular and extravascular
space
F. Second spacing is accumulation fluid into tissues as edema
G. Third spacing is accumulation of fluid in body cavities e.g. Ascites, pleural
effusion
H. All above correct except “C”

325. If vagus nerves are severed the respiratory rate

E. Is increased
F. Is decreased
G. Remains constant
H. Ceases

326. Destruction of pneumotaxic center located in the pons causes

E. Apneustic respiration
F. Forceful expiration
G. Accelerated respiration
H. Apnea

327. Median nerve

E. Is formed from medial and lateral cods
F. Innervates all flexor compartment muscles except flexor carpi ulnaris
G. Is also known as the labourer’s nerve
H. Only (a) is correct

328. Radial nerve

E. Is formed from posterior cord
F. Innervates all extensor compartment muscles except anconeus
G. Is prone to injury in fractures of the shaft of humerus
H. Injury results in wrist drop

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329. Ulnar nerve

E. Is a branch of the posterior cord
F. Is known as the musician’s nerve
G. Is the major innervation of muscles of the hand
H. Lesion of the nerve results in ape thumb
330. A 3/0 suture is
E. Larger in diameter than 4/0
F. Smaller in diameter than 4/0
G. Is too small for skin closure
H. Can be used in an adult patient to close the abdominal sheath

331. Boil (furuncle)

E. Can occur on any part of the body except the face
F. Is infection of hair follicle
G. Can cause signs of inflammation
H. Surgical drainage is not indicated

332. Carbuncle
E. Can occur on any part of the body except the neck
F. Is necrotic infection of contiguous hair follicles
G. Patients present with fever and malaise
H. Both surgical drainage and antibiotics are not required for treatment

333. Lymphangitis
E. Common causative organism include streptococci
F. Blood cultures are usually positive
G. Lymph nodes draining the infected area are usually swollen and painful
H. Presents with systemic inflammatory response syndrome (SIRS)

334. Regulations of fluids and electrolytes movement across all membranes is by

E. Diffusion/filtration
F. Active transport
G. Osmosis
H. Characteristics of the membrane itself

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335. Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are
hormones involved in regulation of
E. pH of the body fluids
F. Water and electrolyte balance
G. ANP is produced in atrium
H. BNP is produced in ventricles

336. A white leg is due to

E. Femoral deep vein thrombosis
F. Lymphatic obstruction
G. Femoral vein thrombosis and lymphatic obstruction
H. None of the above

337. The following are irritative symptoms of bladder outlet obstruction secondary
to BPH:
E. Weak stream
F. Nocturia
G. Frequency
H. Intermittence

338. Ilio-Psoas muscle for hip flexion is innervated by

E. L1, 2 segments
F. L4, 5 segments
G. L5, S1 segments
H. S1, S2 segments

339. Secondary metastasis to the spine can originate from

E. Thyroid cancer
F. Breast cancer
G. Lung cancer
H. Prostate cancer

340. A seroma is also known as

E. A hematoma
F. A chyloma
G. A collection of serum in the tissue
H. All above correct

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SURGERY MK

341. Choice of suture material

E. Is irrelevant
F. Depends upon the tissue and area of the body
G. Is usually left up to the scrub nurse
H. Is whatever the hospital gives you

342. About swellings

E. A punctum is diagnostic of a lipoma
F. A cyst is lined by some form of epithelium and is fluid-filled
G. A sebaceous cyst exhibits pseudo-fluctuation
H. Carotid body tumor moves only in one plane vertically

343. The following are the reasons why investigations are done
E. Medico-legal purpose
F. To make a diagnosis
G. To establish fitness before surgery
H. For monitoring of a disease process

344. Hypertrophic pyloric stenosis

F. Is never seen in adults
G. Projectile vomiting occurs
H. A mass is never palpable
I. Diarrhea is common
J. Is associated with other congenital abnormalities

345. Indications for surgery in peptic ulcer disease include:

F. Intractable pain
G. Pyloric stenosis
H. Absence of healing after 3 weeks of medical treatment
I. Acute gastric erosion due to analgesic abuse
J. Single episode of hematesis

346. Treatment of peptic ulcer disease includes:

F. Antacids
G. Antibiotics
H. Prostaglandin analogues e.g. misoprostol

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SURGERY MK
I. Omeprazole
J. Cimetidine

347. Operations performed for peptic ulcer disease includes

F. Gastrostomy
G. Gastropexy
H. Vagotomy and gastrojejunostomy
I. Billroth gastrectomy
J. Polya gastrectomy

348. Which of the following conditions give rise to hemoperitoneum?

F. A ruptured ectopic pregnancy
G. Rupture of the bladder neck
H. An injured spleen
I. Spinal injuries
J. An extraperitoneal isolated injury to the kidney

349. Post-operative pulmonary complications commonly occur:

F. In patients with chronic bronchitis
G. In smokers
H. In patients with severe pain
I. Following herniorrhaphy
J. Following splenectomy

350. Open cardiac operations require one or more of the following

F. Extracorporeal circulation
G. Hypothermia
H. Cardioplegia
I. Right second intercostal posterolateral thoracotomy
J. Sternotomy

351. Cardiac arrest is caused by

F. Anoxia

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SURGERY MK
G. Excessive intravenous potassium
H. Exsanguinating bleeding
I. Frusemide
J. Intravenous glucose

352. Cardiac tamponade following trauma:

F. Heart sounds are usually muffled
G. There is venous hypertension
H. There is arterial hypotension
I. Urgent surgical treatment is indicated
J. Urgent artificial ventilation is required preoperatively in all cases

353. Spinal (Lumbar) puncture:

F. Is usually performed at L1-L2 level
G. The cerebrospinal fluid is located in the subdural space
H. The cord ends at a higher level in an infant
I. Must not be performed in the presence of a raised intracranial pressure
J. A complication is venous bleeding

354. The following tumors readily metastasize to bone

F. Rectal adenocarcinoma
G. Basal cell carcinoma of skin
H. Follicular carcinoma of the thyroid
I. Prostatic adenocarcinoma
J. Renal adenocarcinoma

355. A lipoma has the following features

F. A slipping edge
G. Transillumination
H. Is tender to touch
I. Has a central punctum
J. Is only found in subcutaneous tissue

356. Tumors of the parotid include

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SURGERY MK
E. Pleomorphic adenoma
F. Adenolymphoma
G. Papillary carcinoma
H. An enlarged intraparotid lymph node

357. Which investigations demonstrate occlusion of one common iliac artery

F. Inferior venacavogram
G. Translumbar aortogram
H. Doppler ultrasound
I. Intravenous pyelogram
J. Retrograde femoral catheterization of the other side

358. Varicose veins

F. Are tortuous elongated veins
G. Pain is a late feature
H. It is also known as venous hypertensive disease
I. Elastic support stocking are useful
J. Injection sclerotherapy is indicated in some patients

359. Hemorrhage
F. Primary hemorrhage occurs within 24 hours
G. Secondary hemorrhage occurs after a week to 10 days
H. Bleeding time is a measure of fibrinogen activity
I. The normal clotting time is up to 20 minutes
J. Bleeding in cirrhotics is immediately controlled by administering oral vitamin
K

360. Common cause of pyrexia within 2 days of surgery include:

F. Chest infection
G. Blood transfusion
H. Wound infection
I. Venous thrombosis
J. Allergy to the anesthetic agent

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SURGERY MK
361. Bacteroides species
F. Are common in the mouth
G. Are the commonest large bowel commensal
H. Are sensitive to metronidazole
I. Causes necrotizing fasciitis
J. Cause Crohn’s disease

362. An anteroposterior chest X-ray (done to demonstrate a left subphrenic

abscess) will show:
F. Obliteration of the costophrenic angle on the same side
G. Collapse of the left upper lobe
H. Lack of movement on the right cupula of the hemidiaphragm on screening
I. A fluid level below the left hemidiaphragm
J. Shift of the gastric fundus

363. Fournier’s gangrene of the scrotum

F. Is secondary to tuberculosis
G. Is very uncommon in Zambians
H. Minor trauma to the scrotal skin is an etiological factor
I. Metronidazole is indicated
J. Surgery is contraindication

364. The following antibiotics are effective against anaerobic organisms

F. Chloramphenicol
G. Erythromycin
H. Cloxacillin
I. Clindamycin
J. Actinomycin

365. Hand infections

F. The hand is rested with extension of all joints
G. Osteomyelitis is common in untreated pulp space infection
H. Paronychia refers to infection in the palm
I. Commonly follow minor neglected injuries
J. A common infecting organism is E. coli

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SURGERY MK
366. Complications of nasogastric tubes include
F. Gastric perforation
G. Otitis media
H. Chest infection
I. Ulceration of nares
J. Esophageal stricture following prolonged intubation

367. Tetanus
F. Is caused by an anerobic bacillus
G. Is associated with a hypercatabolic state
H. Occurs only after major trauma
I. Tetanus toxoid gives artificial immunity
J. Common cause of death is respiratory failure

368. Streptomycin
F. Is an aminoglycoside
G. It is bactericidal in high dose
H. Causes pseudomembranous colitis
I. Causes jaundice
J. Causes ototoxicity

369. A venous cut down can be done on the following veins

F. Cubital
G. Cephalic
H. Subclavian
I. Umbilical
J. Posterior tibial

370. Torsion of the testis

F. If in doubt of the diagnosis explore
G. In unilateral torsion bilateral fixation is necessary
H. Does not occur in children
I. Is confused with a hydrocele
J. A horizontally placed low testis is diagnostic

371. Congenital hydrocele

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SURGERY MK
F. Can be repaired by Lord’s procedure
G. Is due to closure of the processus vaginalis
H. Phenol may be used to treat the hydrocele
I. May be due to epididymorchitis
J. Presents as inguinal hernia

372. Anesthetic drugs

F. Diazepam may be used for premedication
G. Mist magnesium trisilicate for premedication for cesarian section
H. Thiopentone for induction
I. Etomidate for reversal of muscle relaxation
J. Morphine for post-operative analgesia

373. Post-operative wound breakdown may be due to

F. Use of tight suturing technique
G. Prolonged steroid use before surgery
H. Reduced serum protein
I. Protein energy malnutrition
J. Diabetes mellitus

374. Metabolic response to trauma

F. May be caused by fracture of a distal phalanx
G. Good recovery follows steroid treatment
H. Head injury may be the cause
I. Patient may gain weight in the flow phase
J. May lead to systemic inflammatory response syndrome

375. Peptic ulcer disease

F. With hematemsis may be due to malignant transformation
G. Can be duodenal if pain wakes patient after midnight
H. Can be duodenal if pain is experienced immediately after meals
I. Can be gastric if experienced immediately after food
J. Can be a cause of acute abdomen

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SURGERY MK
376. Cranial nerve that supplies superior oblique which elevates and adducts the
eye is:
E. 7th cranial nerve
F. 6th cranial nerve
G. 5th cranial nerve
H. 4th cranial nerve

377. Sensory component of 5th cranial nerve is tested by

E. Wrinkle formation on the forehead
F. Touch sensation on the face
G. Lifting the shoulder
H. Corneal reflex

378. When a patient has unilateral vagus nerve lesion and is asked to open the
mouth and say AAAG.. The uvula moves and points
E. Away from the lesion
F. Towards the lesion
G. Stays in the midline
H. Elongates within the midline

379. When a patient has unilateral hypoglossal lesion and is asked to protrude the
tongue
E. The tongue points away from the lesion
F. The tongue points to the side of the lesion
G. The tongue will show wasting
H. The tongue will show fasciculations

380. When a patient sustains cranial nerve XI lesion

E. Patient is unable to elevate (shrug) the affected shoulder
F. Patient is able to elevate the shoulder against examiners resistance
G. Sternomastoid muscle power is spared
H. When patient is asked to rotate the chin against examiners resistance he/she
fails to do so

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SURGERY MK
381. When a patient has unilateral cranial nerve V motor component lesion
E. Masseter muscle will feel weak on palpation as patient clenches the teeth
F. Temporal muscle will feel well contracted as patient clenches the teeth
G. The jaw will deviate to the paralyzed pterygoid muscle when patient opens
the mouth
H. The jaw will deviate away from the paralyzed pterygoid muscle when patient
is asked to open the mouth

382. Bilateral 6th cranial nerve palsy is a sign of

E. Cingulate gyrus herniation
F. Uncal herniation
G. Raised intracranial pressure
H. Tonsillar herniation

383. Hyper-resonant chest is likely to be caused by

E. Hemothorax
F. Pleural effusion
G. Pneumothorax
H. Tension pneumothorax

384. Secondary brain injury

E. Can result from hypoxia
F. Can result from hypoperfusion
G. Can result from hypoglycemia
H. Can result from any of the above

385. Breast cancer is common in women with

E. Positive family history
F. History of having breast fed their children
G. History of previous radiation exposure
H. Having the first child at early age

386. Causes of surgical jaundice include:

E. Gall stones

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SURGERY MK
F. Massive hemolysis
G. Ascaris lumbricoides
H. Malignancy of the head of pancreas

387. The most frequent anatomic site for squamous cell carcinoma of the
esophagus is
E. Upper third
F. Middle third
G. Lower third
H. Gastro-esophageal junction

388. Pathological fractures may be associated with

E. Scurvy
F. Hyperparathyroidism
G. Bone cyst
H. All of the above

389. Perkin’s exercises:

E. Are commenced 2 weeks after application of traction kit
F. Are commenced within a week after application of traction kit
G. Are commenced after 3 weeks when pain at fracture site has subsided
H. All above correct except “B”

390. Tachypnea
E. Is respiratory rate of less than 10 per minute in adult patients
F. Can be caused by tension pneumothorax
G. Can be caused by hemothorax
H. Is never associated with tachycardia

391. About investigations

E. Gastroscopy is an example of an imaging technique
F. For biliary pathology, ultrasound is superior to computerized tomography
G. Plain X-rays are sufficient in order to make a diagnosis of fractures
H. There are other methods apart from histology and cytology that are used to
confirm cancer

392. Patients with central nervous system lesion on observation may have

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SURGERY MK
E. Epigastric peristalsis
F. Ptosis
G. Tremors
H. Diaphragmatic respirations

393. These are major symptoms associated with intestinal obstruction

E. Diarrhea
F. Change in skin coloration
G. Hematuria
H. Melena stool
394. Oculomotor nerve lesion presents with
E. Pupil dilation
F. Ophthalmoplegia
G. Lateral rectus palsy
H. Loss of corneal reflex

395. Origin of oculomotor nerve (CN III) is

E. Medulla-oblongata
F. Pons
G. Mid-brain
H. Cerebellum

396. Open skull fracture has occurred when there is

E. Cerebral spinal fluid leak from the ear
F. Depressed skull fracture under the scalp wound
G. Subdural hematoma with superficial bruise on the forehead
H. Subarachnoid hemorrhage regardless of the cause

397. Patients who present with acute abdominal pain starting in the umbilical
region and shifts to the right iliac fossa is most likely caused by
E. Perforated duodenal ulcer
F. Diverticulitis
G. Appendicitis
H. Salpingitis

398. Murphy’s sign

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SURGERY MK
E. Helps to diagnose ureteric stones
F. Helps to diagnose ectopic pregnancy
G. Helps to diagnose appendicitis
H. Helps to diagnose cholecystitis

399. Small intestinal obstruction is likely to present with

E. Radiating pain to the left shoulder
F. Spreading pain to the right iliac fossa
G. Colic pain in the umbilical region
H. Shifting pain to the right iliac fossa

400. Imperforate anus

F. Maybe related to urogenital fistulae
G. X-rays (invertogram) is not helpful
H. Colostomy may be useful initially
I. Cannot be a cause of intestinal obstruction
J. May present with constipation

401. Drugs used for maintenance in anesthesia

F. Nitrous oxide
G. Halothane
H. Isoflurane
I. Oxygen
J. Enflurane

402. Hirschprung’s disease

F. Lacks nerve tissue in the sub-mucosa layer
G. A concentration of nerve tissue in the submucosa layer
H. History of constipation is characteristic
I. History of anal bleeding is characteristic
J. Definitive diagnosis is made on X-rays

403. The gastrointestinal system has

F. 4 basilica layers
G. Mucosa lined by epithelium
H. Muscularis mucosa to produce local movement of mucosa
I. 5 basic layers

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SURGERY MK
J. Serosal lining covering mucosa

404. Normal blood values

F. Total white cell count- 14 x 109/L
G. Serum creatinine- 200umol/L
H. Urea- 10mmol/L
I. Sodium 155mmol/L
J. Potassium 6.5 mmol/L

405. During surgical procedures

F. Doors to operating theaters must always be left open
G. Ventilators can reduce the atmospheric bacterial load
H. The patient is not the most important source of wound infection
I. Shaving must be done ideally the day before operation
J. Commonest organism to cause infection is streptococcus

406. Concerning antisepsis

F. Antisepsis has to do with reducing the bacterial load
G. Sterilization completely destroys all viable organisms
H. Disinfection reduces the bacterial load
I. Disinfection has to do with reducing the tissue bacterial load
J. Ultraviolet light is one way of sterilization

407. Fatty acids

F. Are 75% stored as glycogen in the liver
G. Glycogen stores used up in the stressful situations within 48 hours
H. Digestion is mainly by pancreatitic lipase
I. Liver stores maintain blood levels
J. Insulin is not important in cell uptake of carbohydrate

408. Most of protein digestion and absorption occurs

F. Terminal ileum
G. Stomach and duodenum
H. Stomach and colon

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SURGERY MK
I. In the liver and gall bladder
J. Stomach

409. Concerning suturing of incision

F. Subcuticular sutures are not good for cosmesis
G. Mattress suture is good for hemostasis
H. Continuous sutures are ideal if infection is anticipated
I. Continuous sutures are ideal for long incisions
J. Head and neck sutures must be removed only after the 5th days

410. Monofilament sutures

F. Cause least tissue reaction
G. Causes least wound infection
H. Causes most tissue reaction and scarring
I. Can be braised
J. Can be absorbable

411. Nylon suture

F. Absorbable suture and gives little tissue reaction
G. Non-absorbable and gives a lot of tissue reaction
H. Non-absorbable and gives little tissue reaction
I. Synthetic
J. Naturally occurring

412. On examination of the abdomen

F. Spleen is examined starting from the right iliac fossa
G. There are 9 surface division
H. Inspection is done after palpation
I. Percussion is done after palpation
J. Normal bowel sounds heard every 2 seconds

413. Peptic ulcer disease

F. With hematesis may be due to malignant transformation
G. Can be duodenal if pain wakes patient after midnight

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SURGERY MK
H. Can be duodenal if pain is experienced immediately after meals
I. Can be gastric if experienced immediately after food
J. Can be cause of acute abdomen

414. Congenital hydrocele

F. Can be repaired by Lord’s procedure
G. Is due to closure of the processus vaginalis
H. Phenol may be used to treat the hydrocele
I. May be due to epididymorchitis
J. Presents as inguinal hernia

415. Patients burns major burns

A. Are in negative nitrogen balance-True
B. Have normal calorie requirement-False
C. Do not generally become anemic-False
D. Are resistant to septicemia-False

416. Patients with raised intracranial pressure

A. Cerebral perfusion pressure is maintained by reduction of arterial pressure-
False
B. Cerebral spinal fluid shifting-True
C. Uncal herniation is not a feature-False
D. Coma scale remains unaltered-False

417. The parafollicular cells of thyroid secrete

A. Calcitonin-True
B. Amyloid-False
C. Parathormone-False
D. Follicle stimulating hormone-False

418. An indirect inguinal hernia would lie in relation to the inferior epigastric
artery:
A. Medial-False
B. Lateral-True
C. Anterior-False
D. Posterior-False

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SURGERY MK

419. Fissure-in-Ano is located characteristically:

A. Midline anteriorly-False
B. Midline posteriorly-True
C. Right lateral quadrant-False
D. Left lateral quadrant-False

420. Post-traumatic intracranial space occupying lesion is likely to present with:

A. Decreased pulse rate-True
B. Increased blood pressure-True
C. Irregular pulse-False
D. Glasgow coma scale of 2/15-False

421. Paradoxical (Diaphragmatic) respiration can be caused by

A. Odontoid fracture dislocation-False
B. C2/3 hangman’s fracture-False
C. C5/6 fracture dislocation-True
D. T112/L1 fracture dislocation-False

422. Concerning blood groups

A. Blood group A is associated with increased risk of gastric cancer-True
B. The risk of gastric cancer is associated with blood group B-False
C. The risk of gastric cancer is associated with blood group O-False
D. Only (b) and (c) are correct-False

423. Acute abdomen can be caused by:

A. Perforated duodenal ulcer-True
B. Sigmoid volvulus-True
C. Pancreatitis-True
D. Subcutaneous lipoma-False

424. The following are true of breast cancer

A. Lobular carcinoma is characterized by ‘Indian File’ pattern of tumors cells-
True
B. Lobular carcinoma tends to be familial, multifocal and bilateral-True
C. Carcinoma-in-situ implies non-invasive cancer that has not breached
basement membrane-True

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SURGERY MK
D. Macroscopically schirrhous carcinoma is hard, grey and grates on cutting-
True

425. Symptoms of obstructive uropathy include the following:

A. Weak stream, hesitancy-True
B. Dribbling, straining to void-True
C. Polyuria, oliguria-False
D. Frequency, urgency, urge incontinence-True

426. Which are the causes of dysphagia

A. Carcinoma, goiter, thymoma, mediastinal lymphadenopathy, aortic
aneurysm-True
B. Motor neuron disease, rabies, tetanus, pseudobulbar paralysis-True
C. Achalasia-True
D. Pneumonia, TB of spine-False

427. Concerning tumors, the term ‘well differentiated’ means

A. The cells are so aggressive, wild and uncontrolled and keep reproducing to no
good end-False
B. Cells and tissue that have mature (specialized) structures and functions-False
C. Cancer cells look more like normal cells under a microscope-True
D. The cells tend to grow and spread more quickly than poorly differentiated
cancer cells-False

428. About 85-90% radio-opaque urinary stones include the following

A. Calcium oxalate stones-True
B. Pure uric acid stones-False
C. Sodium urate and ammonium stones-True
D. Sulphur containing cysteine-True

429. Diabetic foot

A. Presence of pathologies such as infection, ulcer and neuropathic
osteoarthropathy-True
B. Is always present in chronic diabetes mellitus-False
C. Any chronic foot ulcer that eventually causes diabetes mellitus-False
D. Patients have associated reduced ability to feel pain-True

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SURGERY MK
430. Chest injuries
A. Tension pneumothorax causes so-called ‘paradoxical breathing’-False
B. May cause a rupture of the diaphragm-True
C. A flail chest result from a wound in the chest wall which acts as a valve that
permits air to enter the pleural cavity but prevents its escape-False
D. May cause pulmonary contusion-True

431. Glasgow coma scale

A. Is a neurological scale which aims to give an objective way of recording the
conscious state of a person-True
B. Is composed of eye, verbal and motor response-True
C. Glasgow coma scale as high as ≥13 signifies minor head injury-True
D. The light response and size of the pupil are part of the Glasgow coma scale
assessment-True

432. Fournier’s gangrene of the scrotum is associated with

A. Infection-True
B. Minor injuries-False
C. No obvious cause-False
D. Filariasis-False

433. Fibroadenoma
A. Benign tumor with a mixture of stroma and epithelial tissue of breast-True
B. Painless, firm, solitary, mobile, slowly growing lump in the breast of women
of child-bearing years-True
C. Leiomyoma in the breast tissue-False
D. Benign tumor of the fibrous tissue in the sweat glands of the breast tissue-
False

434. Cervical sympathectomy is procedure which is indicated for the treatment of

A. Causalgia-True
B. Raynaud’s disease-True
C. PUD-False
D. Cervical rib-False

435. The following are causes of secondary varicose veins

A. Klippel Trenuaney syndrome-True

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SURGERY MK
B. Oral contraceptive pills-True
C. Pelvic tumors-True
D. Exercises-False

436. Varicose veins are one of the causes of thrombophlebitis other causes include
A. Blood transfusion-True
B. Enteral feeding-False
C. Chemotherapy-True
D. Trauma-True

437. High risk group in the development of DVT would include the following
features:
A. Operation <30 minutes-False
B. Obesity-True
C. >40 years age -True
D. Stroke patient -True

438. The development of skin malignancy, pre-malignant lesions would include:

A. Solar keratosis-True
B. Keloids- False
C. Radio-dermatitis-True
D. Rodent ulcer-False

439. In hyperthyroidism
A. Serum creatinine is increased-True
B. Serum cholesterol is increased-False
C. Serum calcitonin is increased-False
D. Serum iodine is reduced-True

440. Causes of pulsatile thyroid swelling

A. Follicular carcinoma-False
B. Primary thyrotoxicosis-True
C. Secondary thyrotoxicosis-False
D. Papillary carcinoma-False

441. Medullary carcinoma of the thyroid (MCT):

A. Arises from parafollicular ‘c’ cells-True

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B. Associated with MEN I syndrome-False
C. Associated with MEN IIa syndrome-True
D. Sporadic is the commonest-True

442. Tetany is a condition where there is hyper-excitability of peripheral nerves.

The causes include
A. Hypoparathyroidism-True
B. Respiratory alkalosis-True
C. Pyloric stenosis-True
D. Chronic renal failure-True

443. In etiopathogenesis of carcinoma of the esophagus, precancerous conditions

include:
A. Plummer vinson syndrome-True
B. Achalasia cardia-True
C. Corrosive stricture-True
D. Keratosis palmaris-False

444. In gastric outlet obstruction electrolyte changes

A. Hypernatremia- False
B. Hyperkalemia- False
C. Hypochloremic alkalosis-True
D. Hypocalcemia- False

445. In hepatocellular carcinoma alpha-fetoprotein levels are increased. What other

conditions would increase the alpha-fetoprotein levels:
A. Carcinoma stomach- False
B. Carcinoma pancreas- False
C. Hepatoma-True
D. Embryonal cell carcinoma of testis-True

446. An increase in the level of alkaline phosphatase would be caused by

A. Biliary cirrhosis-True
B. Metastasis in the liver-True
C. Hepatocellular carcinoma- True
D. Hepatitis-True

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SURGERY MK
447. Acute pancreatitis can be caused by drugs which include
A. Estrogen-True
B. Diuretics-True
C. Antifungals-True
D. None of the above-False

448. Complications of acute pancreatitis include the following except:

A. Shock-False
B. Hypocalcemia-False
C. Pleural effusion-False
D. Respiratory insufficiency-False

449. The following are components of wound healing except:

A. Wound contraction-False
B. Healing by primary intention-True
C. Epithelization-False
D. Scar formation-False

450. Factors affecting wound healing include:

A. Jaundice-True
B. Debilitation-True
C. Gender-True
D. Parity-False

451. Ludwig’s angina precipitating factors:

A. Cachexia-False
B. Chemotherapy-False
C. Dental caries-True
D. Immobility-False

452. In a patient with established Tetanus, the possible causes of death would
include
A. Aspiration-True
B. Cardiac arrhythmias-True
C. DVT-True
D. Laryngeal spasm-True

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SURGERY MK
453. Tropical ulcers occur in Tropical countries. The precipitating factors are:
A. Malnutrition-True
B. Trauma-True
C. Insect bite-True
D. HIV infection-True

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ANSWERS TO ESSAYS
1. Write short notes on:
a. Salter-Harris classification of epiphyseal
fractures
Answer:
Salter and Harris (1963) described 5 different
types of epiphyseal fractures.
➢ Type 1 (“Straight through”)-5%
o Fracture involves a transverse fracture
through the hypertrophic or calcified
zone of the epiphyseal plate
➢ Type 2 (“Above”)-75% (commonest)
o Fracture involves growth plate; it
extends into metaphysis above/ away
from the joint but spares the epiphysis
o Fracture often splits off a triangular
metaphyseal fragment of bone
(sometimes referred to as a Thurston-
Holland fragment)
➢ Type 3 (“Lower”)-10%
o The fracture involves the growth plate
and epiphysis below the joint but spares
the metaphysis
➢ Type 4 (“Through everything”)-10%

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SURGERY MK
o Fracture involves the growth plate, metaphysis and epiphysis (Fracture
forms a T)
➢ Type 5 (“Rammed/Crushed”)-1%
o Due to longitudinal compression injury
of the epiphyseal plate.
o There is no visible fracture but growth
plate is crushed and this may arrest
growth

b. Gatland classification of supracondylar fractures

Answer:
The Gatland classification is divided into 3 types (based on displacement)
➢ Type 1:
o This is an undisplaced supracondylar fracture
o Treatment: collar-cuff or backslab
➢ Type 2:
o Angulated fracture with posterior cortex still intact (periosteal hinge)
o Subdivided into:
▪ Type IIA- less severe injury with distal fragment angulated
▪ Type IIB- severe injury, distal fragments angulated and
malrotated
o Treatment: manipulation under anesthesia and collar cuff or backslab
(convert Type II to type I)
➢ Type 3:
o Completely displaced fracture (although the posterior periosteum is
usually still preserved, which is usually still preserved, which will assist
surgical reduction)

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SURGERY MK
o Treatment: manipulation under anesthesia, K-wire (Kirschna wire)
fixation, after 3 weeks take the patient to theater to remove the K-wires
under general anesthesia and put a slab

c. Draw and label patterns of fracture of neck of femur

Answer:
Fractures can be viewed based on
➢ Site of fracture (Anatomical classification)
➢ Displacement (Garden’s classification)
Site of fracture, include: Subcapital, Transcervical and Basal

Garden’s classification:

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2. Questions:
a. Define excised and incised wound
Answer:
➢ Excised wounds are wounds created by the act of cutting out/ severing/
removing undesired tissue from the body.
➢ Incised wounds are wounds created by the act of cutting into tissue in order
to enter or gain access to an internal part of the body. Edges are usually
linear.

b. Describe briefly physiology of healing of excised wound

Answer:
Excised wounds heal by fibrosis and results in a wide scar often hypertrophied
and contracted. Re-epithelialisation occurs from remaining dermal elements or
wound margins.

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SURGERY MK
The stages of wound healing include:
➢ Stage of coagulation/hemostasis
o Happens almost immediately following injury the clotting cascade is
initiated
o Local vasoconstriction occurs and a platelet clot forms
o Platelet derived growth factor is released
➢ Stage of inflammation
o Begins after vasodilation (0 to 4 days)
o Inflammatory cells reach site of injury. Initially neutrophils and then
macrophages which secrete fibroblast growth factor for angiogenesis and
skeletal development as well as remove tissue debris.
o Lymphocytes secrete inflammatory mediates and oxygen radicals
➢ Stage of proliferation/fibroplasia
o There is formation of granulation tissue
o Lasts 4 to 21 days
o Fibroblast deposits type III collagen, capillaries provide nutrients.
➢ Stage of remodeling
o Takes 3weeks to 18 months
o There is maturation of collagen by cross-linking which is responsible for
tensile strength of the scar.
o There is differentiation of fibroblast into Myofibroblast which contracts
wound.
o Type III collagen is replaced with type I collagen and blood vessels
atrophy.
o Collagenase removes type III collagen and requires zinc as a co-factor

c. List complications of wound healing

Answer:
Early
➢ Wound infection
➢ Septicemia
➢ Septic arthritis
Late
➢ Wound Dehiscence
➢ Contractures
➢ Hypertrophic scars

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SURGERY MK
➢ Keloids
➢ Marjolins ulcer

3. Questions
a. Briefly trace iodine in food to iodine in thyroid hormone
Answer:
➢ Around 50mg of iodine in the form of iodide is required per year (1mg per
week). Source of the iodine is iodated salt. Iodine can also be found bound
to protein as iodine this has to be converted to iodide (by glutathione) as this
is the easiest form to absorbed
➢ Iodides ingested orally are absorbed from the intestine into the blood in
about the same manner as chlorides.
o Absorption of sodium ions through the epithelium creates
electronegativity in the chime and electropositivity in the paracellular
spaces between the epithelial cells.
o Iodide ions then move along this electrical gradient to “follow” the
sodium ions.
➢ Iodide in the blood stream is transported to the thyroid glandular cells and
follicles.
➢ On the basolateral side of the cells sodium-iodide symporter co-transports
one iodide ion along with 2 sodium ions across the basolateral membrane
into the cells. (energy to transport these ions against a concentration gradient
comes from the sodium potassium ATPase pump).
➢ In the follicular cells peroxidase converts iodide ions to an oxidized form of
iodine. Iodine is transported to the colloid through pendrin (an antiporter
for chloride and iodine), in the colloid iodine is then organified (also
catalyzed by the enzyme peroxidase) to thyroglobulin where it binds tyrosine
residues to form monoiodothyronine and diiodothyronine which can
couple to form the hormones thyroxine (T4) and triiodothyronine (T3)- also
in the presence of peroxidase enzyme
➢ The thyroid hormones can then be released in blood via pinocytosis and
secretion.

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SURGERY MK

b. Draw homeostatic loop for T3 and T4

Answer:

c. List signs/ symptoms of thyrotoxicosis

854
SURGERY MK
Answer:
➢ Symptoms
o Nervousness
o Anxiety and hyperactivity
o Increased sweating especially palms
o Hyperthermia and Heat intolerance
o Palpitations
o Hyper-defecation
➢ Signs
o Fine hand tremors
o Warm moist hands
o Tachycardia and atrial arrhythmias
o Systolic hypertension with wide pulse pressure
o Lig lag
o Wide eyed stare gaze
o Muscle weakness

4. Write short notes on

a. Colles’s fracture
Answer:
➢ This is a transverse fracture of the radius about 2.5cm above the wrist joint
with the following displacement (Remember mnemonic “College Rotating
Doors Shut I’m Late”):
o Rotation
o Dorsal tilt (proximal tilt)
o Dorsal shift
o Supination
o Impaction
o Lateral shift (radial shift)
o Lateral tilt
➢ It is found in elderly due to falling on an outstretched hand.
➢ Clinical features: dinner fork deformity with prominence on the back of the
wrist and depression in front, local tenderness and pain on wrist movement
➢ Treatment:
o Closed manipulation under anesthesia

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SURGERY MK
▪ Correct the impaction first
▪ Center the fragments (correct the radial displacement)
▪ Correct the proximal tilt by dorsiflexing the wrist
▪ Lock the arm towards the little finger using a slab (“corrected
dinner fork appearance”)
o X-ray: after reduction (to check of fracture is reduced-post-reduction X-
ray), after 24 hours (for neurovascular state), after 7 (to rule out any
displacement, reduce in theatre if displaced), after 14 days and at 8
weeks
b. Colostomy
Answer:
➢ Definition: this is hollow iatrogenic mucocutaneous fistula between the
colon and the skin.
➢ Types:
o Temporary: done in conditions where diversion is required to facilitate
healing distally in the rectum or distal colon. This type is closed once
purpose is over. Sites of temporary colostomy include the right
hypochondrium and left iliac fossa.
▪ Examples: Loop colostomy, Devine’s double barrel, spectacle,
Hartmann
o Permanent: this is always and end colostomy. It is placed in left iliac
fossa, 6cm above and medial to the anterior superior iliac spine.
➢ Colostomy indications:
o Congenital (congenital megacolon, anorectal malformations,
imperforate anus, Hirschsprung disease, anal atresia, anorectal agenesis,
anal stenosis) and
o Acquired (Intestinal obstruction i.e. sigmoid volvulus, ischemic bowel
disease, tumors i.e. anal and rectal carcinoma, perforation of left sided
colon, high anal fistula, after Hartmann’s operation)
➢ Complications:
o Ischemic gangrene
o Hemorrhage
o Retraction
o Prolapse
o Parastomal hernia

c. Shoulder dislocation:

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SURGERY MK
Answer:
➢ This is displacement of the head of the humerus from the glenoid cavity.
➢ It can be caused by
o High speed trauma (traumatic shoulder dislocation)
o Ligament overstrain (repetitive shoulder ligament overstrain e.g. with
swimming, tennis, throwing sports e.g. baseball)
➢ Dislocation can either be partial (sublaxation) where the head of the
humerus is partially dislodged from the glenoid cavity or complete (luxation)
where the head of the humerus is completely dislodged from the glenoid
cavity.
➢ Dislocation can either be in the anterior (common) or posterior direction.
➢ Signs and symptoms:
o Deformity
o Swelling
o Numbness
o Weakness
o Bruising
o Muscle spasms
o History of trauma or sporting activity before injury
➢ Treatment: closed reduction
➢ Rehabilitation: immobilize in a sling for a few weeks, apply ice to shoulder
3 to 4 times.

5. Question
a. List complications of thyroidectomy
Answer:
➢ Early
- Bleeding
- Hemorrhage and Hematoma
- Injury to recurrent nerve
- Tracheomalacia
- Upper airway obstruction
- Hypocalcemia
- Tracheal perforation
- Thyroid storm- atrial fibrillation
➢ Intermediate
- Infections

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SURGERY MK
➢ Late
- Hypothyroidism
- Hypocalcemia with pathological fractures
- Keloids and hypertrophic scars

b. Discuss management of thyroid storm (Crisis)

Answer:
➢ Admit to ICU/High dependency unit
➢ Perform ABCs
➢ Rehydration: IV fluids and oral fluids
➢ Control hyperthermia (ice pack/Cold compress/sponging/fan, antipyretic-
IV paracetamol)
➢ Administer beta blockers: Propranolol (avoid in asthmatic patients use
calcium channel blockers instead such as verapamil and diltiazem)
➢ Administer antithyroid drugs e.g. propylthiouracil to block T4 and T3
synthesis and release
➢ Administer potassium iodide (Lugol’s solution)
➢ Administer glucocorticoids e.g. hydrocortisone or dexamethasone (to
reduce conversion of T4 to T3)
➢ Administer bile acid sequestrant e.g. cholestyramine to prevent T4 and T3
reabsorption from the gut
➢ When patient is stabilized (euthyroid) thyroidectomy can be performed with
appropriate hormone replacement after

c. Discuss briefly clinical presentation of hypoparathyroidism

Answer:
Presents with hypocalcemia. Clinical features include:
➢ Neuromuscular excitability
o Carpopedal spasm: tetany (involuntary contraction) of feet or hands
o Chvostek’s sign: facial twitch on parotid tap
o Trousseau’s sign: carpal tetany in response to a tightened Blood
pressure cuff that is pumped above systolic blood pressure
o Paresthesia of peripheries, tongue and mouth
o Cramps and aches
o Airway: laryngospasm and bronchospasms
➢ CNS

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SURGERY MK
o Seizures
o Papilledema
o Dementia
o Parkinsonism
o Anxiety, Depression, fatigue
➢ Other signs (in chronic disease)
o Cataracts
o Dry, coarse, puffy skin
o Reduced tooth growth (if patient is young)

6. Write short notes on metabolic body response to acute blood loss.

Answer:
➢ There are 2 phases of the response
- Initial phase (EBB phase)
o Occurs within the first 48hours to 2 days
o Physiological role of the ERB phase is to conserve circulating
volume and energy stores.
o It is characterized by hypovolemia, decreased cardiac output,
decreased metabolic rate, hypothermia and lactic acidosis.
o Blood loss triggers the hypothalamus, pituitary glands, adrenals,
thyroid gland, pancreas and renin angiotensin aldosterone axis.
This results in release stress hormones (catecholamines, cortisol,
glucagon, growth hormone) and other hormones such as
aldosterone, angiotensin and thyroid hormones.
o Catecholamines produce the following changes: increase in heart
rate, respiratory rate, and temperature
▪ Accentuated clinical signs e.g. tachycardia (more than
90b/m), tachypnea (more than 20b/min), hyperthermia (38
degrees or more), hypothermia (36 degrees or less) are
indicative of systemic inflammatory response (SIRS)
▪ Any 2 of the 4 parameters above= SIRS
o Cortisol increases the blood sugar (through gluconeogenesis,
glycogenolysis)
o Aldosterone increases sodium and water reabsorption (under the
control of ADH)

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SURGERY MK
o WBC count also increases and there is also increase in the
production of pro-inflammatory cytokine such as IL-1 and TNF-
alpha
- Flow phase
o Occurs from day 3 to about day 10.
o Associated with chronic neuroendocrine response.
o It is divided into:
▪ Catabolic phase day 3 to 10
▪ Anabolic phase: can last weeks depending on severity
o It is associated with the mobilization of body energy stores for
repair and replacement of damage tissue

7. Write short notes on value of sentinel node in investigating breast cancer

Answer:
The sentinel node is used during a sentinel lymph node biopsy. The procedure
consists of injecting a vital blue dye or radioactive sulfur colloid or both around the
tumor. The surgeon often waits 5 minutes in the case of the dyes and a few hours
in the case of colloid and then dissects the axilla removing only a few nodes that
either stained blue or radioactive. The principle behind this is that the first node
that drains the dye are most likely to first drain the tumor as it metastasizes. In
doing so the nodes are examined and if found to have signs of malignancy it
indicates that the breast cancer may have metastasized from the local area however
if the nodes show no signs of malignancy it is assumed that the tumor has not
metastasize. This has helped reduce morbidity as compared to a full axillary node
dissection and in experienced hands the procedure is close to 100% accurate in
correctly describing the presence or absence of tumor in the axilla.

8. Discuss briefly common patterns and presentation of hand infection.

Answer:
➢ General features:
o Infection spreads faster in all areas.
o Infection causes edema over the dorsum of the hand due to lax skin and
more lymphatic network even though infection per se is more over the
volar aspect. Hand looks like a frog hand.
o There is restricted movement of fingers and hands.
o The hand functions like hook, pinch, grip, grasp are lost.
o There is severe pain and tenderness with fever.

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SURGERY MK
o Tender palpable axillary lymph nodes are often present
o They can be superficial or deep and can be localized or spreading
➢ Different types of hands infection include:
o Acute paronychia (most common hand infection, occurs in subcuticular
area under the eponychium) presents as severe throbbing pain and
tenderness with visible pus under the nail root. Nail on touch is very
tender. Caused by minor injury, implicated organisms Staphylococcus
aureus and Streptococcus pyogenes
o Chronic paronychia- commonly due to fungal infection (Candida), nail
is diseased with ridges and pigmentation, itching in the nail bed,
recurrent pain, and discharge. Secondary bacterial infection may
supervene
o Terminal pulp space infection (felon)- second most common hand
infection. Affect index and thumb mostly, usually caused by minor
injury like finger prick. Presents with pain, tenderness, swelling in the
terminal phalanx, fever and tender axillary lymph nodes. Implicated
organisms include staphylococcus, streptococcus and gram-negative
organisms
o Subungual infection
o Web space infection
o Mid-palmar space infection
o Thenar space infection
o Deep palmar abscess
o Acute suppurative tenosynovitis
o Chronic tenosynovitis of flexor tendon sheath of palm and forearm-
compound palmar ganglion
o Lymphangitis of the hand
o Arthritis of hand joint
o Subcuticular abscess

9. An 8-year-old child weighing 25kg has 20% burns which occurred at 04:00 hours
and arrives in hospital at 08:00hrs. Calculate fluid requirement using Parkland
formula:
a. Resuscitation fluid
b. Maintenance fluid
Answer:

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SURGERY MK
a. Resuscitation fluid:
➢ Volume of fluid in 24 hours= 4ml x Mass (kg) x % burns
➢ Volume of fluid in 24 hours= 4 x 25 x 20
➢ Volume of fluid in 24 hours= 2000ml
➢ Give:
o 1000ml of Ringer’s Lactate Intravenously in 4hours (from 08:00 to
12:00hours) since child was burnt at 04:00 hours so 4hours from 8hours of
first fluid has elapsed.
o 1000ml of Ringer’s Lactate intravenously in remaining 16hours (from
12:00hours to 04:00 next day).
b. Maintenance fluid:
➢ 100ml/kg for first 10kg
➢ 50ml/kg for next 10kg
➢ 20ml/kg for the remaining 5kg
➢ Total fluids in 24 hours= (100 x 10) + (50 x 10) + (20 x 5)
➢ Total fluids in 24 hours= 1600ml
➢ Give 1600ml in 24 hours dextrose-saline (5% dextrose)

10. Write short notes on the complications of blood transfusion

Answer:
➢ Acute hemolytic reactions due to ABO incompatibility (results from
antibodies in recipient’s plasma direct against antigens on donor’s
erythrocytes). It can be either
o Intravascular hemolysis (RBCs are hemolyzed in the blood steam) it causes
hemoglobinemia, hemoglobinuria, acute renal failure, DIC and
complement-mediated cardiovascular collapse. Dyspnea, chest pain,
sweating, fever with chills, tachycardia, hypotension and cardiac arrest occur
in fatal type. Jaundice may also be seen.
o Extravascular hemolysis: Due to Rh or non-ABO antigens. It is seen in
patients usually exposed to antigen through prior pregnancies,
transplantation or transfusion. Antibody titers are too low often to be
detected during screening however production increases with re-exposure to
the initial antigen. Antibodies do not activate complement (no intravascular
hemolysis) instead they coat RBCs which are removed by splenic
macrophages.

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SURGERY MK
➢ Non-hemolytic Febrile reactions: due to formation of cytokines during storage
of blood. Most common complication due to impurities like pyrogens in
blood or in infusion set. Presents as headaches, fever, chills and rigors,
tachycardia, nausea are other features. Transfusion is temporarily stopped or
slowed down with administration of antipyretic.
➢ Allergic/anaphylactic reaction: urticaria and allergy to specific proteins in
donor’s plasma can occur.
➢ Congestive cardiac failure: occurs especially if large quantities of whole blood
are transfused in chronic severe anemia, pregnancy, elderly patients, in
patients who have cardiac problems.
➢ Infections: serum hepatitis, HIV infection, malaria infection, CMV infection,
EBV infection, Syphilis infection, Trypanosoma cruzi infection
➢ Air embolism
➢ Thrombophlebitis
➢ Hemochormatosis/iron overload in patients with chronic renal failure
receiving repeated blood transfusion
➢ Citrate intoxication causing bradycardia and hypocalcemia. (for every 4 units
of blood 10ml of 10% calcium chloride or gluconate should be infused
intravenously)
➢ Transfusion related acute lung injury
➢ Graft vs Host disease: occurs when donor lymphocytes mount immune
response against the recipient lymphoid tissue.

11. What are signs and symptoms of acute appendicitis. Explain the anatomical basis
for these features, where applicable.
Answer:
➢ Symptoms:
o Pain: visceral pain starts around the umbilicus due to distension of the
appendix, after a few hours somatic pain occurs in right iliac fossa (Blumberg
sign) due to irritation of the parietal peritoneal because of inflamed
appendix. The pain is severe and diffuse. Pain migrates to right iliac fossa
with maximum tenderness at McBurney’s point.
o Vomiting and nausea due to reflex pylorospasm
o Constipation (in postileal appendix)/diarrhea (pelvic appendix)
o Anorexia and Low-grade fever
o Urinary frequency: bladder irritation from inflamed appendix

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SURGERY MK
➢ Signs
o Tachycardia
o Tenderness and rebound tenderness in right iliac fossa (Blumberg
sign/release sign)
o Pointing sign- Pain at Mc Burney’s point
o Signs indicative of peritoneal irritation
▪ Rovsing sign- on pressing left iliac fossa, pain occurs in right iliac fossa
due to shift of bowel loops which irritate the peritoneum
▪ Psoas test- for retrocecal appendix, hyperextension of hip causes pain
in the right iliac fossa.
▪ Obturator test- For pelvic appendix internal rotation of right hip causes
pain in right iliac fossa due to irritation of obturator internus muscle
▪ Baldwing test- positive in retrocecal appendix- when legs are lifted off
the bed with knees extended the patient complains of pain while
pressing on abdomen (Ribs-ilium)

12. You are called to a surgical ward, 2 hours after thyroidectomy of a patient with
thyrotoxicosis. Write short notes on what complications your patient might have
now and in the near future.
Answer:
➢ Early
- Bleeding and hematoma as a result of poor hemostasis (can lead to upper
airway obstruction
- Injury to recurrent laryngeal nerve (unilateral or bilateral)- leads to vocal
cord collapse and upper airway obstruction
- Laryngeal edema
- Tracheomalacia with large goiter that erodes the trachea that collapses
after thyroidectomy
- Upper airways obstruction
- Thyroid storm- atrial fibrillation
- Tracheal perforation
- Hypocalcemia with removal of all parathyroid glands
➢ Intermediate
- Infections
- DVT

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SURGERY MK
- Hypostatic pneumonia
➢ Late
- Hypothyroidism
- Hypocalcemia with pathological fractures
- Keloids and hypertrophic scars

13. How would you investigate the cause of fever in a patient who develops a fever 3
or 4 days after abdominal surgery?
Answer:
➢ Blood investigations
o Full blood count with differential- increase in WBC
o ESR and C-reactive protein: increase
o Blood culture: for sepsis
o Urea and electrolytes, creatinine: to check renal function
o Liver enzymes
➢ Pus swab- microscopy, culture and sensitivity (for any pus)
➢ Urine microscopy, culture and sensitivity
➢ Imaging
o Chest X-ray (to rule out pulmonary sources of infection)
o Abdominal ultrasound
o CT scan

14. A 70-year-old man presents with acute retention in a male surgical ward. Take a
brief relevant and focused history in order to arrive at a diagnosis.
Answer:
➢ Onset of the urinary retention
➢ Duration of urinary retention
➢ Number of times urine has been passed compared to normal
➢ Any associated symptoms:
o Weight loss
o Hematuria-initial, terminal or diffuse
o Poor urinary stream
o Terminal dribbling
o Dysuria
o Urgency
o Intermittency
o Back pain

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SURGERY MK
➢ Any history of urinary tract infection?
➢ Any history of urinary stones?
➢ Any history of TB?
➢ Any history of acute renal failure?
➢ Last performed Digital rectal scan, any significant findings?
➢ History of prostate cancer screening?
➢ History of any urogenital surgeries or trauma

15. Persistent generalized lymphadenopathy is a common presentation of patients to

a surgical clinical in Zambia. How would you evaluate such patients to come up
with a diagnosis? Include in your answer the possible histological diagnostic
description of the common causes.
Answer:
➢ History:
o Cough? Productive or non-productive? If production, color and amount
and is blood present?
o Night sweats
o Fatigue
o Weight loss
o Anorexia
o Fever
o Tested for HIV
➢ Physical examination
o Generalized lymphadenopathy
o High temperature, tonsils erythematous with a creamy grey exudate and
appear almost confluent usually symmetrical, hepatosplenomegaly
(infectious mononucleosis)
o Oral thrush oral hairy leucoplakia on tongue, purple lesions on hard palate
(HIV infection)
➢ Investigations
o Lymph node biopsy
o HIV Test, CD4 count and Viral load
o Full blood count with differential count
o Peripheral smear
➢ Differential diagnosis with histological findings
o HIV infection: shows follicular hyperplasia
o Tuberculosis adenitis: show caseaous necrosis

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SURGERY MK
o Lymphoma: Reed-Sternberg cells seen (giant cells with large mirror image
nuclei)
o Infectious mononucleosis: giant cells with 2 large mirror image nuclei (Reed-
sternburg cells)
o Leukemia
o Hyperthyroidism
o Systemic lupus erythematosus

16. Graves disease is fairly common condition in young women in Zambia. Write
short notes on eye signs and give reasons why these signs do occur.
Answer:
➢ Exophthalmos: this is proptosis of the eye, it is caused by infiltration of
retrobulbar tissue with fluids and round cells with lid spasm of upper eyelid.
In Grave’s disease it is believed that the fibroblast have TSH receptors to TSH
like antibodies, in Grave’s disease fibroblast produces mxyoid substances such
as glycosaminoglycans which deposit in the retro-orbital tissues.
➢ Lid retraction: the upper eyelid is higher than normal and lower eyelid is in
normal position with visible sclera adjacent to upper eyelid. It is due to
sympathetic over activity causing involuntary spasms of the smooth muscles
of the levator palpebrae superioris.
➢ Staring gaze: this is due to the absence of normal blinking. First sign to appear.
It is due to widening of palpebral fissure due to lid retraction and also due to
contraction of voluntary part of the levator palpebrae superiors muscle.
➢ Lid lag (Von Graefe’s sign): this is inability of the upper eyelid to keep pace
with the eyeball when it looks downwards to follow the examiners finger

17. List the possible causes of PUD. Clearly explain how helicobacter pylori causes
this disease
Answer:
➢ Causes of PUD
o Infectious causes:
- Helicobacter pylori
o Non-infectious causes:

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SURGERY MK
- Long term use of drugs e.g. Non-steroid anti-inflammatory drugs,
steroids
- Alcohol and smoking
- Stress
- Burns (Curling’s ulcer)
- Cerebral trauma (Cushing’s ulcer)
➢ Helicobacter pylori and peptic ulcer disease
o The organism has the enzyme urease which has the ability to hydrolyze urea
to form ammonia, a strong alkali. Ammonia through negative feedback
causes the release of gastrin on the antral G cells which results in gastric acid
hypersecretion.
o The bacterium produces enzymes e.g. dehydrogenase (converts alcohol to
aldehyde which is toxic to mucosa), and endopeptidase which disrupts the
gastric mucous barrier and the inflammation induce in the gastric epithelium
is associated with the ultimate ulceration.
o Some strains produce cytotoxins such as cagA and vacA gene products
which directly damage the cells of the gastrointestinal tract. The effect of the
organism on the gastric epithelium is to incite a classic inflammatory
response that involves the migration and degranulation of acute
inflammatory cells such as neutrophils and also the accumulation of chronic
inflammatory cells such as macrophages and lymphocytes.

18. What is gangrene? What are the etiological factors of the different types of
gangrene? Your short notes should include pathophysiology of each type of
gangrene.
Answer:
➢ Gangrene is macroscopic death of tissue in situ (in continuity with adjacent
viable tissue) with or without putrefaction. The term necrosis may be used
synonymously. It often affects the distal part of a limb because of arterial
obstruction (from thrombosis, embolus or arteritis).
o A gangrenous part lacks arterial pulsation, venous return, capillary response
to pressure, sensation, warmth and function. The color of the part changes
through a variety of shades according to circumstances (pallor, dusky grey,
mottled, purple) until finally taking on a the characteristic dark-brown,
greenish-black or black appearance, which is caused by the disintegration of
hemoglobin and the formation of iron sulphide.
➢ Causes

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SURGERY MK
o Arterial occlusion e.g. atherosclerosis, emboli, diabetes, Raynaud’s disease,
ergots, arteritis, peripheral artery disease
o Infective: Boil, carbuncle, gas gangrene, Fournier’s gangrene, Cancrum oris
o Traumatic: direct, indirect
o Physical: burns, scalds, frostbit, chemicals, irradiation, electrical
o Venous gangrene
o Smoking, obesity
➢ Types of gangrene
o Dry gangrene: occurs when the tissues are desiccated by gradual slowing of
the bloodstream, it is typically the result of atheromatous occlusion of
arteries. The affected part becomes dry and wrinkle, discolored from
disintegration of hemoglobin and greasy to the touch.
o Wet gangrene: occurs when infection and putrefaction are present, the
affected part becomes swollen and discolored and the epidermis may be
raised in blebs.
o Gas gangrene: It is due to infection with Clostridium species. Myonecrsis is
due to alpha-toxin from Clostridium perfringens.
o Internal gangrene: This affects one or more of the internal organs such as
the intestines, gallbladder or appendix. It occurs when blood flow to an
internal organ is blocked e.g. in appendicitis
o Fournier’s gangrene (necrotizing fasciitis) this is a rare and fulminant form
of necrotizing fasciitis of the male perineum and genital region frequently
due to a synergistic polymicrobial infection Bacteria enters through break in
the skin or it may follow surgery, trauma, IV injection or insect bite.
Infection spreads rapidly across fascial layer, leading to tissue death of fascia
and subcutaneous tissue.
o Progressive bacterial synergistic gangrene (Meleney’s gangrene): this is a rare
type of gangrene typically occurring after an operation with painful skin
lesions developing one or two weeks after surgery. It is a spreading infectious
type of gangrene and is often associated with Streptococcus (which produces
tissue damage mediated by Exotoxins A, B and C) as well as other microbes.

19. A 26-year-old man has been hit by a moving vehicle. He is brought to casualty in a
coma. How would you evaluate this patient?
Answer:
➢ Shout for help as this requires a team effort
➢ Perform primary survey (Perform ABCs)

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SURGERY MK
o A- ensure airway is patent with cervical spine protection
- Check for any signs of airway obstruction, foreign bodies, facial,
mandibular or laryngeal fractures?
- Suction any secretion
- Maneuvers such as chin lift or jaw thrust can be done to establish a clear
airway but protect the cervical spine at all times
- If airway not secure assess for the need of intubation or performing a
cricothyroidotomy or emergency tracheostomy
- If patient can talk, the airway is likely to be safe.
o B- breathing
- Evaluate breathing: perform a chest examination with adequate
exposure. Watch for chest movements (note for any paradoxical
movements in the case of flail chest that may need mechanical
ventilation) check respiratory rate, palpate for any fractures or
subcutaneous emphysema (which may require draining by needle
thoracostomy with subsequent intercostal drainage until defect is
repaired), percuss for any fluids in pleural cavity such as hemothorax
that may require intercostal drainage. Auscultate to ensure there is air
entry in the lungs.
- Provide high flow oxygen through a rebreather mask if not intubated
and ventilated.
o C- Circulation with hemorrhage control
- Assess blood loss rapidly: observe level of consciousness, skin color,
pulse, capillary refill time, bleeding
- Gain venous access with 2 large bore cannulae, obtain blood for
crossmatch and baseline investigations.
- Start running fluids, Ringer’s lactate/ normal saline rapidly as you await
blood
- Arrest any bleeding (Direct manual pressure should be used to stem
visible bleeding), perform chest, abdominal and pelvic compression to
rule out any fractures that may cause internal hemorrhage especially
when not responding to fluid resuscitation.
- Check for blood sugar
- Catheterize the patient and monitor urine output
o D- disability (neurological status)
- Assess level of consciousness, using Glasgow coma scale
- Pupil size symmetry and reaction to light

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SURGERY MK
- Assess level of any spinal cord injury (limb movements, spontaneous
respiratory effort)
- Any lateralising signs
o E-exposure/environmental control
- Undress the patient but prevent hypothermia
- Check for any other injuries, factures, lacerations
- Monitor vitals for signs of deterioration
➢ Secondary survey
o After patient is stabilized, Take a complete history and full physical
examination
- Ask about events that lead to injury,
- AMPLE: any allergies, medication taken, past/present medical illnesses,
last meal, Events surrounding injury
o Document all measures done during primary survey
o Perform X-rays (Head& neck, Chest and pelvic-traumatic series X-rays),
ultrasounds (FAST scan) and other laboratory tests
o If at any point patient deteriorate revert back to primary survey
➢ Definitive care: depends on underlying injuries present.

20. Write shore notes on presentation and diagnosis of cervical injury

21. Write the hemodynamic changes caused by space occupying lesions in head injury
patients.

22. How much fluid are you going to give a 3-year old child weighing 15Kg with 20%
burns in the first 48 hours?
Answer:

Volume of fluid in the first 24 hours= 4ml x Weight x % burns

Volume of fluid in the first 24 hours= 4 x 20 x 15
Volume of fluid in the first 24 hours= 1200ml

In first 24 hours give 600ml of Ringer’s lactate to run intravenously over 8 hours
and 600ml of Ringer’s lactate to run in the remaining 16 hours

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SURGERY MK
Maintenance= (100x10) + (50 x 5)
Maintenance= 1250ml of dextrose-saline in 24 hours on day 2.

23. There has been a plane crash in Ngwerere area with a few survivors. How would
you handle the 13 survivors who have been brought to casualty?

24. A 65-year-old male patient presents to the casualty with a very painful ulcer on the
right foot. He is a known hypertension and has been on treatment for several years.
On examination has a moderate sized ulcer on the dorsum of the foot which is
very painful. The ulcer has punched out edge and the base is pale. The SHO
makes a diagnosis of a venous ulcer.
A. What other history would you want to get from this patient?
B. What further clinical examination would you do?
C. Was the diagnosis correct? Give your reasons?
D. What investigation is indicated
E. What is the diagnosis and state your reasons?

25. Discuss the immediate management of a 5-year-old child with 15% burns.
Answer:
Admit patient to burns ward
ABCs
➢ Secure airway- suction any secretions, assess for need for intubation or
tracheostomy
➢ Ensure child is breath and give child oxygen
➢ Gain venous access (cannulate child)- send blood for group and save, Full
blood count, Urea, Electrolytes and Creatinine, and Liver enzymes.
Catheterize patient, monitor urine output (input/output chart) and Start fluids
➢ Resuscitation fluid
o Volume in first 24 hours= 4ml x 15 x (estimated weight of child
approximately=20kg)
o Volume in first 24 hours= 1200ml
o Give 600ml in first 8 hours from time of burn injury and 600ml in next
16hours
o Fluid of choice= Ringer’s lactate

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SURGERY MK
➢ Maintenance fluid
o Volume= (100 x 10) + (50 x 10)
o Volume in next 24 hours= 1500ml
o Fluid of choice Dextrose 5%
Drugs given
➢ Analgesia
➢ Tetanus toxoid 0.5ml
➢ Broad spectrum antibiotics
Monitor vitals hourly
Daily wound cleaning with application of silver sulphadiazine

26. Write short notes on flail chest.

27. The signs of intracranial bleeding after a head injury are

F. Conscious level ……………………………………….
G. Pupil on side of lesion ……………………………..
H. Pulse rate …………………………………………………
I. Blood pressure …………………………………………
J. Respiration ……………………………………………....

28. A 65-year-old patient presents with a painful ulcer on the dorsum of his foot. He
complains that he is unable to sleep at night and the pain is not relieved by
moderate pain killer
A. List 2 differential diagnosis for this ulcer
Answer:
➢ Ischemic ulcers (arterial ulcer)
➢ Venous ulcer

B. What is the most likely diagnosis?

Answer: Ischemic ulcer

C. What 4 important things would you ask in the history to determine the etiologic
factors?

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SURGERY MK
Answer:
➢ Medical history of diabetes and hypertension
➢ History of stroke, myocardial infarction
➢ Intermittent claudication
➢ Diet/Cholesterol levels

D. What 2 blood investigations are indicated?

Answer:
➢ Random blood sugar
➢ Cholesterol levels

E. What radiological investigation is indicated?

Answer: Doppler ultrasound

F. Describe the following terms: a. Ankle Brachial pulse index and b. critical
ischemia?
Answer
➢ Ankle brachial pulse index is the ratio of brachial pressure over that of the
ankle pressure. It is usually 1
➢ Critical ischemia is present when this ratio is less than 0.6

29. A 35-year-old patient is seen in casualty following a road traffic accident (RTA).
The patient smells of alcohol and has a laceration on the occipital area. Answer
the questions below briefly.
E. What two things would you ask in the history?
F. Explain how you would examine the occipital laceration
G. List 4 localizing signs you would look for
H. List 4 reasons you might ask for a CT scan in this patient

31. List the various indications for doing a colostomy

32. Discuss in brief the causes of surgical jaundice

33. Write short notes about Steel’s rule application in a patient with cervical spine
injury

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SURGERY MK
34.A 34 year old woman presents with mild yellowness of eyes, pain in the right
hypochondrium and fever. She gives history of previous episodes which resolve
on antibiotic treatment. Answer the questions below:
G. What is the most likely diagnosis?
H. What is the most likely cause?
I. What other 2 things would you ask for in the history?
J. What 2 blood investigations would you ask for?
K. What 2 signs would be present on abdominal examination?
L. What radiological investigation is indicated?

35.Answer the following questions:

C. Outline briefly the operative blood transfusion check list
D. Discuss measures that you would take to treat an adverse blood reaction

36.Answer the following questions

E. Define goiter
F. Discuss briefly pre-operative investigations for goiter
G. List possible post-operative complications of thyroidectomy
H. How would you recognize and abort a thyroid storm

37.Give an account of thyroid swellings

38.A 46-year-old Zambian female presents to clinic 4 with a thyroid swelling which
is painless and slow growing.
F. What 4 things would you ask in the history to determine the cause?
G. What 4 examinations would you do to determine whether the patient is
euthyroid or toxic?
H. What specific blood tests are indicated?
I. What 3 radiological investigations would you do?
J. List 4 indications for surgery in this patient

39.Answer the following questions

E. Define osteoarthritis
F. Discuss briefly etiological factors in general and clinical presentation of
osteoarthritis of lumbar spine
G. List the four classical radiological findings in osteoarthritis

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SURGERY MK
H. List the treatment modalities available for osteoarthritis.

40.Define the following

F. Fistula
G. Fissure
H. Ulcer
I. Granulation tissue
J. Paralytic ileus

41.Write short notes on the following

C. Define sentinel lymph node
D. Discuss briefly value of sentinel axillary lymph node biopsy in management
of breast cancer

42.A 37-year-old female patient is seen in clinic 4 with a lump in the breast and an
axillary swelling. She gives history of weight loss and back ache. Answer the
questions below.
G. List 2 differential diagnosis
H. What is the most likely diagnosis?
I. What 4 important questions would you ask to determine the possible
etiological factors?
J. List 2 investigations you would do to confirm your diagnosis
K. What 2 radiological investigations would you do to determine whether
metastasis is present?
L. What is the value of the sentinel node in this condition?

43.A 56-year-old patient is seen in casualty with history of failing to pass urine. He
has severe pain and abdominal distention.
F. What is the diagnosis?
G. List 2 possible conditions that can lead to this complication
H. List 4 questions you would ask to differentiate the 2 conditions
I. What single physical examination is necessary in this patient?
J. What one endoscopy and one radiological investigation should be done?

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44. A 40-year-old man comes to the emergency ward with acute urinary retention.
What are the possible etiologies, briefly outline how you would investigate.

45.A 34-year-old woman presents with mild yellowness of eyes, pain in the right
hypochondrium and fever. She gives history of previous episodes which resolve
on antibiotic treatment. Answer the questions below
G. What is the most likely diagnosis?
H. What is the most likely causes?
I. What other 2 things would you ask for in the history?
J. What 2 blood investigations would you ask for?
K. What 2 signs would be present on abdominal examination?
L. What radiological investigation is indicated?

46.A beautiful 40-year-old female patient is seen in casualty with right upper
quadrant pain which radiates to the scapula. She gives history of intermittent
attacks associated with fatty foods. On examination Murphy’s sign and
Moynihan’s sign are both positive. The SHO on call makes a diagnosis of Acute
pancreatitis and requests some blood tests. The result shows serum amylase 100
u/L, Alkaline Phosphates 300 u/L, SGPT 30u/L, SGOT 31u/L and bilirubin 25
micronmols/L. The SHO is uncertain of the interpretation of the results and calls
the medical Registrar on call. The Registrar takes the history on the phone. The
medical Registrar is extremely upset with the young SHO, but nonetheless
recommends IV antibiotics, analgesia and an urgent U/S. By the morning round
the SHO has altered his diagnosis and takes the credit for an astute diagnosis from
the newly appointed Prof of Surgery.
G. What other important history should be taken?
H. What diagnosis do both the history and examination point to?
I. What do the investigations show?
J. Is a plain X-ray indicated in this patient?
K. Why was the medical registrar so upset?
L. What were the surgical principles on which the medical registrar gave his
advise?

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47.Answer the following questions:
A. Define compartment syndrome and list major etiological factors
Answer:
Compartment syndrome is an entity that results from increased intra-
compartmental pressure within a limited space compromising the circulation
and function of tissues within that closed space. It is characterized by severe,
progressive and persistent pain that poorly responds to analgesics and is
aggravated by passive muscle stretch as well as paresthesia, paralysis,
pulselessness, pallor and poikilothermia.

Major etiological factors include:

o Trauma:
Fractures of the lower limb or upper limbs,
Soft tissue crush injuries
Vascular injuries
Circumferential burns affecting a compartment,
High velocity injuries: gun injuries
Snake bikes
o Iatrogenic: application of tight dressings/plasters
o Lying on one limb in comatous patients

B. Discuss briefly the pathophysiology of compartment syndrome

Answer:
Edema that is often a sequela of trauma occurring in a limited anatomical
space raises the tissue intra-compartmental hydrostatic pressure. As tissue
pressure rises, the pressure on and within the local venous system also rises.
Arterial resistance subsequently increases and inflow is reduced. If untreated
there is vascular compromise and the enclosed muscle becomes ischemic.
Prolonged ischemia results in necrosis and ultimately, fibrosis of the muscle
and surrounding soft-tissue structures. As pressure increases there is loss of
sensation in the distribution of the involved nerves and ultimately the local
pulses are lost (though sometimes the pulse may be present).

C. With aid of labelled diagram, explain Whitesides saline/needle technique for

measuring intracompartment pressure in a limb
Answer:

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SURGERY MK
Intracompartment pressure measured using the Whitesides saline/needle
technique uses an 18G needle connected via a 3 way stop cock to an air filled
20ml syringe. Air filled tubing is connected to a mercury manometer and a
small amount of saline sits in the tube connected to the needle. Compression
of the syringe raises the pressure till saline flows into the compartment (this
is indicated by meniscus moving). Below is a diagram illustrating this

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SURGERY MK
48.Write short notes on assessment of a patient with burns
Answer:
➢ History:
o Time and mechanism of the injury
 Time the person was burnt
 Type of burn i.e. scald (what was the liquid, if tea/coffee was there
milk in it), flame, electrical (what voltage, was there a flash/arching,
what was the contact time) or chemical (Acid or alkaline, how much
exposure?)
o Circumstances around the burn
 How was the person put out?
 How long were they alight for?
 What first aid was carried out? If cooling was performed, what with
and for how long?
 Concomitant injuries (i.e. fall from height, road traffic accident,
explosions)
 Likelihood of inhalational injury (did the event occur in an enclosed
space?)
 Any comorbidities present
 Any suspicion of non-accidental injury?
➢ Physical assessment:
o Assess burn percentage and severity using:
 Lund and Browder chart (most accurate)
 Wallace Rule of nines (in adults): Head and neck (9%), Upper limbs
(9% each), Lower limbs (18% each) Trunk-36% (18% in front and
18% at the back) and Perineum-1%
 Rule of sevens (in children): Head and neck (28%), Upper limbs (7%
each), Lower limbs (14% each) Trunk-28% (14% in front and 14%
at the back) and Perineum-2%
 Rule of palms (the palms represents 1% of total body surface area
o Examine systems:
 Neurological examination: look for alteration of mental status
(confusion)
 Respiratory examination: look out for signs of inhalational burns
(soot in mouth or nostrils, burnt nasal hair, stridor, respiratory
distress, circumferential burns on chest)

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SURGERY MK
 Cardiovascular system: look for signs of shock (tachycardia,
hypotension)
 GIT examination
 Musculoskeletal and skin: look for fractures and assess skin for burn
percentage area
➢ Investigations:
o Full blood count to pick up any cytopenias
o Group and save/ Cross match
o Urea, electrolytes and creatinine to assess renal function and electrolyte
imbalance
o Liver enzymes and function tests
o Pus swab
o For electrical burns: 12 lead ECG monitoring and cardiac enzymes
o For inhalation burns: chest X-ray and Arterial blood gases

49.Write short notes on usefulness of intravenous urogram (IVU) in a patient with

bilateral hydronephrosis

50.Describe the steps involved in the synthesis of Tri-iodothyronine (T3) and

thyroxine (T3). Comment on homeostatic (regulatory) feed-back loop

51.Answer the following

D. Define osteoarthritis
E. Discuss briefly pathogenesis of degenerative osteoarthritis
F. List the four cardinal radiological features of osteoarthritis

52.List baseline investigations and their significance in preparation of a patient due

for thyroidectomy

53.Answer the following questions

D. Describe phases of fracture healing in a long tubular bone
E. List in tabular form complications associated with fractures
F. List the methods available for reduction of fractures

54.Write short notes on:

D. Autologous blood transfusion, types, uses and limitations
E. Pre-operative blood transfusion check list

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SURGERY MK
F. Steps to be taken in aborting hemolytic blood transfusion reaction

55.Write short notes on how you would manage a patient you found to have a
ruptured liver during an operation in a district hospital.

56.Discuss the various hormones that are involved following the ruptured spleen in
a 25-year-old man.
57.A 47-year-old female patient is admitted to casualty with swelling of her left leg
of spontaneous onset. She has a fever and the leg feels warm
A. List 2 differentials diagnosis
Answer:
Cellulitis
Deep vein thrombosis

B. What bacteria is likely to be the cause?

Answer: Streptococcus pyogenes

C. What 2 important questions would you ask for in the history to help determine
the etiological factors?
Answer:
➢ Past medical history of diabetes/immunosuppression
➢ History of trauma/injury

D. What 4 signs would you look for in the examination?

Answer:
➢ Swelling
➢ Hotness
➢ Redness
➢ Pain

E. What 2 blood investigations would you do?

Answer:
➢ Full blood count with differential count
➢ Blood culture/C-reactive protein

F. What antibiotic is indicated and what route of administration is

recommended?

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SURGERY MK
Answer: Penicillins intravenous

58.A 15-year-old boy presents to the casualty department with scrotal pain. He gives
a history of sudden onset with no history of trauma. Answer the questions below.
A. What are the 2 main differentials?
Answer:
Testicular torsion
Epididymorchitis

B. What 4 things would you ask for in the history to differentiate the two?
Answer:
➢ History of nausea and vomiting
➢ Previous episode
➢ Precipitating factors e.g. sex, masturbation, pornographic materials
➢ History of urethritis

C. What is the most likely diagnosis?

Answer: Testicular torsion

D. What is Prehn’s test? Describe how it is done.

Answer: Prehn’s test is done by elevation of the testis. In testicular torsion the
pain increase whilst in epididymitis it reliefs the pain

E. What radiological investigation is indicated?

Answer: Color doppler ultrasound

59.A 12-year-old boy presents to clinic 3 with a swelling on the upper leg which is
fast growing. The child is ill and give history of weight loss
A. List 2 differential diagnosis
Answer:
Osteosarcoma
Osteomyelitis

B. What radiological investigation might distinguish the two?

Answer: Plain X-ray

C. What other radiological investigation can be done?

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SURGERY MK
Answer: Technetium bone scan

D. List 2 X-ray findings in osteosarcoma

Answer:
Codman triangle
Sunray appearance/spicules

60.A game ranger is brought to the casualty with a gunshot wound to the right leg.
The wound is dirty and 5cm in length. The patient has palpable pulses and nerve
function is normal.
A. What type of fracture has the patient had?
Answer: Open tibia fracture

B. What is the classification of open tibia fractures?

Answer:
This is the Gustillo-Anderson classification. It consists of 3 types
Type 1: Wounds are <1cm and clean (mild contamination), simple fracture
pattern and there is no skin crushing
Type 2: Wounds measuring 1-10 cm but without significant soft tissue
crushing, flaps, degloving or contusion. Fracture pattern is more complex and
there is moderate contamination
Type 3: Wounds >10cm, also includes injuries older than 8 hours. There is
severe contamination. It has 3 subtypes
o Type 3A: no periosteal stripping
o Type 3B: periosteal stripping
o Type 3C: neurovascular damage

C. How would you classify this patient’s fracture?

Answer: Type 3B

D. What blood investigations would you do?

Answer:
➢ Full blood count with differential white cell count
➢ Blood cultures

E. What 2 organisms would be present on pus swab of this wound?

Answer:

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➢ Anaerobic Clostridium tetani
➢ Bacteroides

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INDEX

Anal fissure ..................................................................... 375

A Anal Fistula ..................................................................... 371
Acid-base balance .............................................................51 Anaplastic carcinoma of the thyroid .............................. 486
Acute abdomen ..............................................................230 Anorectal abscess ........................................................... 377
Acute Acalculous Cholecystitis ........................................346 Aortic disruption ............................................................ 187
Acute Calculous Cholecystitis .........................................340 Appendicitis .................................................................... 269
Acute Cholecystitis ..........................................................340 ATLS ................................ See Advanced trauma life support
Acute pancreatitis ...........................................................294
Acute subdural hematoma .............................................601
Advanced Trauma Life Support.........................................31

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B Flail segment .................................................................. 182
Fluid balance .................................................................... 51
Bee sting .........................................................................176 Follicular adenoma of the thyroid .................................. 481
Benign prostatic hyperplasia ..........................................567 Follicular carcinoma of the thyroid ................................ 484
Blood collection bottles .....................................................19 Fracture .......................................................................... 407
Blood products..................................................................70 Fractured sternum ......................................................... 183
Blood transfusion ..............................................................70 Fresh frozen plasma ......................................................... 77
Blood transfusion reactions ..............................................78 Frozen red cells ................................................................ 75
BPH ................................... See Benign prostatic hyperplasia
Burns ...............................................................................128
G
C Galeazzi Fracture ............................................................ 452
Gastrostomy ................................................................... 154
Caecostomy ....................................................................155 Goiter ............................................................................. 476
Cardiac tamponade .........................................................186
Chest drain ......................................................................178
H
Chest trauma ..................................................................181
Cholecystitis ....................................................................340 Hashimoto’s thyroiditis .................................................. 478
Cholestatic jaundice ......................................... See Jaundice Head injury ..................................................................... 586
Chronic pancreatitis ................................................ 313, 314 Hemorrhoids .................................................................. 365
Chronic subdural empyema ............................................602 Hemothorax ................................................................... 185
Chronic subdural hematoma ..........................................601 Hernia ............................................................................. 380
Colles' Fracture ...............................................................455 History taking ................................................................... 13
Colostomy .......................................................................155 Human bite ..................................................................... 175
Compartment syndrome ................................................112 Hydrops of the gallbladderSee Mucocele of the Gallbladder
Cryoprecipitate .................................................................77 Hypercalcemia .................................................................. 65
Hyperkalemia ................................................................... 61
D Hypermagnesemia ........................................................... 67
Hypernatremia ................................................................. 59
Depressed skull fracture .................................................604 Hyperthyroidism............................................................. 491
Diabetic foot ...................................................................126 Hypertrophic scar ........................................................... 115
Diaphragmatic injuries ....................................................187 Hypocalcemia ................................................................... 66
Direct hernia ...................................................................395 Hypokalemia..................................................................... 63
Dog bite ..........................................................................172 Hypomagnesemia ............................................................. 67
Dynamic intestinal obstruction .......................................243 Hyponatremia .................................................................. 57
Dysphagia .......................................................................197 Hypothyroidism .............................................................. 502

E I
Electrolyte balance ...........................................................51 ICD See Chest drain
Emphysematous Cholecystitis ........................................347 Ileostomy........................................................................ 155
Enteral nutrition ...............................................................75 Incisional hernia ............................................................. 405
Epidural hematoma ........................................................598 Indirect hernia ................................................................ 390
Epigastric hernia .............................................................404 Inguinal hernia ............................................................... 385
Epiphyseal fracture ...................... See Salter-Harris fracture Intercostal chest drainage ........................... See Chest drain
Esophageal disruption ....................................................188 Intestinal obstruction ..................................................... 240
Esophagostomy...............................................................155 Intussusception .............................................................. 257
Extradural hematoma .....................See Epidural hematoma
J
F
Jaundice.......................................................................... 352
Femoral hernia ................................................................401 Jejunostomy ................................................................... 154
FFP See Fresh frozen plasma
Flail Chest .................................................. See Flail segment

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K S
Keloid ..............................................................................114 SAH ...................................... See Subarachnoid hemorrhage
Salter-Harris fracture ...................................................... 442
L Scorpion sting ................................................................. 176
Simple pneumothorax .................................................... 184
Lower urinary tract obstruction ......................................563 SIRS ........... See Systemic inflamamtory response syndrome
Luxation ............................................... See Joint dislocation Skeletal traction ............................................................. 437
Skin traction ................................................................... 433
M Snake bite ....................................................................... 164
Spider bite ...................................................................... 175
Mammalian bite..............................................................175 Stoma ............................................................................. 154
Medullary carcinoma of the thyroid ...............................485 Sub-acute De Quervain’s Granulomatous thyroiditis ..... 478
Metabolic acidosis ............................................................70 Subarachnoid hemorrhage ............................................. 603
Metabolic alkalosis ...........................................................68 Subdural hematoma ....................................................... 601
MODS ................. See Multiple organ dysfunction syndrome Subluxation .................................................................... 462
Monteggia fracture.........................................................453 Surgical jaundice .............................................. See Jaundice
Mucocele of the Gallbladder ..........................................350 Systemic inflammatory response syndrome .................... 28
Multiple organ dysfunction syndrome..............................28
T
N
Tension pneumothorax .................................................. 183
Nutrition ...........................................................................73 Thyroglossal tract ........................................................... 475
Thyrogossal cyst ............................................................. 475
P Thyroid gland.................................................................. 470
Thyrotoxicosis ..................................... See Hyperthyroidism
Packed red cells ................................................................75 Total parenteral nutrition................................................. 78
Pancreas .........................................................................290 TPN ........................................ See Total parenteral nutrition
Pancreatic cancer............................................................319 Tracheobronchial disruption .......................................... 187
Pancreatitis .....................................................................294 Traction .......................................................................... 433
Papillary carcinoma of the thyroid..................................482 Traumatology ................................................................... 31
Paralytic ileus ..................................................................265
Paraumbilical hernia .......................................................404
U
Pharyngostomy ...............................................................155
Piles........................................................... See Hemorrhoids Ulcer ............................................................................... 117
Pilonidal sinus .................................................................376 Umbilical hernia ............................................................. 403
Platelet concentrate .........................................................76 Upper urinary tract obstruction ..................................... 558
Pneumothorax ................................................................183 Urinary retention............................................................ 553
Prostate carcinoma .........................................................577 Urinary tract obstruction................................................ 557
Pulmonary contusion ......................................................186
V
R
Volvulus .......................................................................... 262
Red cell concentrates............................See Packed red cells
Refeeding syndrome .........................................................69
W
Respiratory acidosis ..........................................................71
Respiratory alkalosis .........................................................69 Wound............................................................................ 105
Rib Fracture ....................................................................182
Riedel fibrosing thyroiditis ..............................................478

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890