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HOW TO TAKE HISTORY IN SURGERY?

+++ QUICK REVISION
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How to take Hx in surgery+++QUICK REVISION Page 1
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GCMHS
Edition 2009/2017
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EDITION
GCMHS
PREFACE
What is new in the second edition?
In this
edition ;
1.
Volume-II ,
2.
Pictures of basic surgical instruments &
3.
Youtube links to basic physical
examination videos are included .(online)
In addition there are some modifications made
on the contents of Volume-1. Which include ;
1. additional notes on long & short cases
with special emphasis on the management
part &
2. modified and enhanced sample histories .
Since this book contains long & short cases ,we hope you will
find it very important when you are preparing for bedsides &
oral examinations in short period of time.(+++QUICK REVISION)
Finally we want to emphasize that the quality of this book will
be kept up to date by the continual comments made by users.
If you have any comment or suggestion on this edition , please
inbox us @ [email protected] or [email protected].
The Authors
DANIEL FENTANEH
&
BIRUK BIRHANU
Gondar collage of medicine & health science
Medical students
Janhoy batch
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Cover Design by Daniel F.

<<>> ACKNOWLEDGEMENT <<>>
First we would like to thank our friends: Cheru Lilay, Ekram Abdu, Daniel
Belhu, Fkadu Alemye, Daniel Kassie & Natnael Alemu, for their
contribution in the first edition by sharing their bedside histories to be used as a
sample history, during their C#1 attachment.
Our sincere thanks & gratitude goes to the following friends for their
unrelenting dedicaton and contribution to this edition by preparing notes on
incomplete parts of the first edition (which were left to be included in VOL-
II):Eyasu Feleke(sms), Elshaday Amare (sms),Cheru Lilay(sms),
Bruh Alem(sms), Daniel Belhu(sms), Endalkachew Belayneh(sms),
Eshetie Endalew(sms) & Dawit Berhanu(sms).
Last but not least we would like to thank Janhoy batch students & Mekdi batch
students (our juniors) for their encouraging comments.
Chief coordinator
DAN ALEMAYEHU
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Message for users
Whenever you go through the long cases of this book...
HPI
We have tried to write the possible clinical presentations of a patient in each
case before we proceed to the sample hx. So, you are expected to characterize
each Clinical Presentation based on your patient to write your HPI.
Positive-negative statements (HPI)
Throughout the long cases of this text book we have tried to focus on this part
because we find it challenging for a beginner. Whenever you go through the
cases, please give attention for the first part of each case that contains the
causes, risk factors, differential diagnosis & complications which are essential
for construction of your positive & negative statements.
Investigations
In bedsides & oral examination, If you are asked to list investigations you want
to do for your patient…try to mention from diagnostic investigation modalities
that are available in your setting & those that are cost-effective then you can list
the others. ወደገደለዉ!!!
Also be ready for the next question of the investigation you
mentioned…”What information do you want to get from this investigation?”
DD x
Notice since almost all epidemiological data are from abroad…for some cases,
the orders of the DDx listed in books (commonleast common) often may
mismatch with our country…
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Acronyms used
 Ass’t = Assessment  LAP = Lymphadenopathy
 ATLS = Advanced trauma life  LOC = Loss of consciousness
support  MOI = Mechanism of injury
 Abd. = Abdominal  MOA = Mechanism of action
 ANDI = Aberration of normal  MVA = Motor vehicle accident
development & involution  Mov’t = Movement
 Ca = Cancer  Mgt = management
 CPs = Clinical presentations  N&V = Nausea & vomiting
 Cmn = Common  NR = Non-reactive
 Cpds = Compounds  No# = Number
 Dx = Diagnosis  P/E = Physical examination
 Dxtic= Dignostic  Pts = Patients
 DRE = Digital rectal examination  +ve = positive
 DOC = Drug of choice  RFs = Risk factors
 G/A = General appearance  R/o = rule out
 Hx = History  Rx = treatment
 INVx = Investigations  Rt = Right
 Lt = Left  U/S = ultrasound
 LNs = Lymphnodes  Ur = your
 # = fracture
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Copyright © 2009/2017
All rights reserved!
This book is dedicated to…

JANHOY BATCH /05
…itt rained while we arrived & named after this event … ጃንሆይ !!!
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Contents
Preface---------------------------------------------------------------------------------------page#02
Acknowledgement------------------------------------------------------------------------------#03
Message for users-------------------------------------------------------------------------------#04
Acronyms------------------------------------------------------------------------------------------#05
Contents-------------------------------------------------------------------------------------------#08
Long cases-----------------------------------------------------------------------------------------#10
Sample case for report (Hx & P/E)---------------------------------------------------------#161
Short cases---------------------------------------------------------------------------------------#170
Basic surgical instruments in picture-----------------------------------------------------#295
References---------------------------------------------------------------------------------------#315
ለትዝታ ---------------------------------------------------------------------------------------------#316
LONG CASES PAGE
1. Thyroid enlargement____________________________11
2. Breast ca__________________________________________34
3. GOO________________________________________________47
4. SBO_________________________________________________61
LBO_________________________________________________69
5. COLORECTAL CARCINOMA________________________74
6. BOO________________________________________________83
7. UROLITHIASIS_____________________________________95
8. CHOLELITHIASIS_________________________________102
9. OBSTRUCTIVE JAUNDICE________________________110
10. LIVER ABSCESS_________________________________122
11. FRACTURE______________________________________132
12. HEAD INJURY__________________________________139
13. ESOPHAGEAL CA________________________________151
14. APPENDICEAL MASS____________________________157
15. PELVIC MASS____________________________3rd edition
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SHORT CASES PAGE
Respiratory related 171
1. Chest injury_____________________________________________________________172
2. Chest tube_______________________________________________________________175
3. Tracheostomy__________________________________________________________177
4. Intubation_____________________________________________________________180
Gastro-intestinal related 182

1. Abdominal injury_____________________________________________________183
2. NGT______________________________________________________________________189
3. Ostomy (Colostomy , ileostomy)_______ _______________________________191
4. Bowel preparation_____________________________________________________194
5. Hernia__________________________________________________________________195
6. Hemorrhoids, anal fissure & fistula in ano__________________________200
Genito-urinary related 205

1. Catheterization________________________________________________________206
2. Suprapubic cystostomy _______________________________________________208
3. Scrotal swelling________________________________________________________210
4. hypospadia,Epispadia & bladder extrophy__________________________216
Musculo-skeletal related 218

1. Amputation____________________________________________________________219
2. Mgt of fracture________________________________________________________221
3. Bone infection & tumor ______________________________________________226
4. Foot deformity__________________________________________________________231
HEENT+Lymphoglandular related 232

1. Salivary gland tumors ,infections & calculi_________________________233
2. Cleft lip & palate_______________________________________________________235
Miscellaneous 238
1. Examination of mass, ulcer, & MSS___________________________________239
2. Wound infection & classification_____________________________________245
3. Ulcer____________________________________________________________________249
4. Burn____________________________________________________________________256
5. Shock____________________________________________________________________264
6. Blood transfusion______________________________________________________273
7. Fluid & electrolyte imbalance________________________________________277
8. soft tissue tumor________________________________________________________288
9. Skin graft_______________________________________________________________289
10. Spinal anesthesia______________________________________________________292
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SAMPLE HISTORY ON THYROID ENLARGEMENT
DDx for anterior neck swelling
 Goiter
o May be
 Diffuse, uni-nodular or multi-nodular
 Non toxic(simple) or toxic goiter
 Lipoma
 Thyroglossal cyst
 Brachial cleft anomalies
 Lymphadenopathy
 Cystic hygroma
 Subhyoid bursitis…
DDx for goiter (enlargement of thyroid gland)

1) Causes of non-toxic goiter
 Endemic goiter
 Iodine deficiency
 Dietary goitrogens
 Cabbage, Cassava…
 Drug induced goiter
 Iodide, amiodarone, lithium
 Thyroiditis (inflammatory goiter)
 Sub-acute, chronic thyroiditis
 Familial goiter
 Dyshormogenesis--inborn errors of metabolism
 Neoplastic goiter
2) Causes of toxic goiter
A. By increasing hormone synthesisthey have increased Radio-Active Iodine Uptake (RAIU)
 Graves’ disease
 TMNG
 Toxic adenoma
 Drug induced goiter
 Thyroid ca.
 Struma ovarii
 GTD (gestational trophoblastic disease)The α-subunit of HCG mimic TSH
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 TSH-secreting pituitary adenoma
B. By releasing pre-formed hormonethey have decreased RAIU
 Thyroiditis
 Acute phase of hashimoto’s thyroiditis
 Subacute thyroiditis
Clinical Presentations (CPs)

1) History (Hx)
*In order to write a good hx on thyroid enlargement follow the orders listed below
A. About the swelling
 When it began?
 How the pt noticed the swelling?
 Painful /painless
 Site & progression
B. Pressure symptoms
 Dyspnea /Stridor
 Dysphagia
C. Abnormal function manifestations
 Hyperthyroidism: symptoms like…
 Heat intolerance
 Palpitation
 Irritability, emotional lability
 Sleep disturbance
 Weight loss despite increased appetite
 Diarrhea
 Tremor (the pt may complain as symptom)
 N & V (nausea & vomiting)
 Oligomenorrhea or amenorrhea…
 Hypothyroidism: symptoms like…
 Cold intolerance
 Weight gain
 Anorexia
 Constipation
 Menorrhagia
 Fatigue
 Slowed intellectual & motor activity …
D. Mention any medication hx (attempted Rx)
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E. Compose ur +ve & -ve statements
 If you are trying to r/o or rule in simple goiter…

 Is the pt from Iodine deficient area/not--endemic goiter
=Ask if there are peoples in the vicinity with similar illness
=Identifying the geographical location from where the pt come fromID
 Is it mountainous /not?
 Because in highland areaslow iodine content of the water
 Goitrogen intake
=Drug hx
 Iodide, amiodarone, lithium
=Dietary hx
 Because diets containing heavy metals compete with iodine to be
taken by thyroid tissue
 Cabbage, Cassava
 Family hx of thyroid disease (similar illness)
 Dyshormogenesis
 If you are trying to r/o or rule in Grave’s disease Vs TMNG…

 Ask the pt about the timing between the goiter & thyrotoxic symptoms
a. The anterior neck swelling first then thyrotoxic symptoms or
b. Did both appear simultaneously?
 If you are trying to r/o or rule in malignancy…

 Rapidly/ slowly growing mass?(duration)
 Constitutional symptoms of malignancy?
 Anorexia
 Easily fatigability
 Wt. loss
 Family hx of thyroid ca.
 Previous head & neck radiation therapy
 If you suspect metastasis…Ask

 Hx of hoarseness of voice (RLN involvement)
 Hx of swelling in the neck (LAP--LN metastasis)
 Hx of hemoptysis, bone pain…(Distal metastasis)
 If you want to r/o or rule in inflammatory causes …Ask

 Pain in the neck
 Fever, chills
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2) Physical Examination (P/E)
 General Appearance (G/A)
 Thyrotoxic ptshot intoleranceSee carefully their dressing…
 Vital Signs (VS)
 BP
 Thyrotoxic ptswide pulse pressure due to systolic hypertension
 PR
 Tachycardia (in thyrotoxic pt(>85bpm))
 Bradycadia (in hypothyroidism)
 BMI
 LGS examination
 Thyroid examination
 On inspection, notice…
 Size (estimate)
 Shape
 Site
 Overlying skin color change
 Visible Pulsation
 Movement with deglutition & protrusion of tongue
o Because thyroid gland is enclosed by pretracheal
fasciait moves with deglutition
o In case of solitary thyroid swelling looks for upward
movement of the swelling on protrusion of the tongue to
differentiate a thyroid nodule from thyroglossal cyst.
 Pemberton’s sign
o Ask the patient to raise both upper limbs above the head
and keep it for @least 1 minute. If retrosternal
prolongation is there, patient will have congestion and
puffiness in the face with respiratory distress.
o Done…when? In pts with…
 Compliant of aero-digestive tract obstruction
 Vascular congestion
 If the lower border of the gland is not visible during
deglutition/ lower tracheal ring isn’t palpable
 On palpation of the swelling, appreciate…
 Temperature
 Tenderness
 Size (measure)
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 Surface (smooth Vs nodular)
 Border (regular Vs irregular)
 Consistency (soft Vs Firm Vs hard)
 Retrosternal extension
=try to palpate the lowest tracheal ring above the sternal notch
 Fixity to overlying structure
 Thrill (on upper pole)
 Position of trachea (central Vs deviated)
 kocher’s testtest for tracheal compression
=The swelling is pressed slightly on either side of trachea. If
trachea is already compressed patient will have stridor
 Berry’s signcarotid pulse palpation
o Berry’s sign positive meanCarotid pulse is not palpable
on the side of the swelling
Methods of palpation
 Standing in front of the pt &
 Standing behind the pt
Percussif you suspect retrosternal extension
=Resonant Vs dull
Auscultation
 Bruit over the swellingupper poles
 Venous humin supraclavicular space
Reporting format
Inspection
There is about 15X10cms butterfly shaped anterior neck swelling which
moves with deglutition. The lower border is visible on swallowing. It’s
slightly deviated to the right side. There is no visible pulsation or
overlying skin color change. Pemberton’s sign is –ve.
Palpation
There is 20X14cms non-tender, nodular, firm anterior neck mass with
regular border & no fixity to the overlying skin. Its temperature is
comparable to other parts of the body. The lower tracheal ring is palpable
above sternal notch. There is no thrill. Kocher’s test is –ve. Carotid
arteries are palpable bilaterally (Berry sign is negative). The trachea is
central.
Percussion
---------------
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Auscultation
No bruit over the swelling
NB*****
Pertinent positive or negative physical examination findings on other systems…
 Signs of thyrotoxicosis
 Tachycardia (on VS)
 Eye signs (on HEENT)
 Exophthalmos= abnormal protrusion of the eye ball
o Top view (see from top)
 Exophthalmos is said to be present when the eyeball is
seen beyond the superior orbital margin
o Visibility of both the upper & lower scleraexophtalamos
 Lid lag (von graefe’s sign)
o Steady the patient’s head with one hand
o ask the patient to look at your finger
o Ask the patient to look up and down following your finger
o In case of thyrotoxicosis, the lid may lag while the eyeball move
downward and the upper sclera become visible.
 Lid retraction (Dalrymple’s sign)
 Visibility of upper sclera due to spasm of upper eyelid.(@rest)
 Absence of wrinkling (Jofroy’s sign)
o Steady the patient’s head with one hand
o Ask the patient to look up at the ceiling.
o In case of thyrotoxicosis, there may be loss of wrinkling of
forehead.
 Failure of convergence
o Ask the pt to look at your finger at distance then bring it
suddenly in front of the pt eye
o In thyrotoxicosis, there is failure of convergence
 Warm moist skin (on IGS)
 Pretibial myxedema (on IGS)
 Tremor (on CNS)
 Finger
o Ask the patient to stretch out both the upper limbs and spread
out the fingers
 Tongue
o Ask the pt to protrude the tongue resting on the lower lip
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 Signs of hypothyroidism
 Bradycardia (on VS)
 Edema of face & legs (HEENT + MSS)
 Delayed relaxation of deep reflexes (on CNS)
 Pendred’s sign (on CNS)
 Goiter + severe sensory neural hearing impairment
 Signs of retrosternal extension
 Increased JVP (on CVS)
 Horner syndrome
 ptosis
 Anhidrosis
 Miosis…
 Signs of metastasis
 Hard cervical LNs (on LGS)
 Never forget to check LNs
 Nodules on skull (on HEENT)
 Rapidly growing, pulsatile & warm swelling
 erosion of the skull may be present
 Long bone metastasis (on MSS)
 Chest effusion & consolidation (on RS)
 Nodular liver & ascites (abd. Examination)
Watch video on how to examine thyroid enlargement @

https://www.youtube.com/watch?v=ta-s-ZWRk6g
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Discussion of the DDx (goiter)
1) Simple goiter
Causes
See causes listed for nontoxic goiter above…
CPs
Mostasymptomatic
If symptomaticoften complain of
+Pressure sensation in the neck
+Compressive symptoms
>Dyspnea
>Dysphagia
>Catarrh--A need for frequent throat clearing
+ Acute pain
>In case of hemorrhage
+ In substernal goiterson P/EPositive Pemberton’s sign
o If Diffuse typeon P/E Soft, diffusely enlarged thyroid gland
Types +diffusedue to persistent stimulation by TSH
o If Multinodular typeon P/ENodules of various size & consistency
+nodules due to fluctuation in stimulation by TSH
Complications
 Tracheal obstruction
 20 thyrotoxicosis
o In 30% of pts
 calcification
 Premalignancy
o Cmn for follicular thyroid ca
NB*
Cmn in females because of estrogen receptors in the thyroid tissue
INVx
 normal TSH
euthyroid
 normal free T4 level
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Mgt
o Large goiters
 Give exogenous thyroid hormone
 to reduce TSH stimulation of the gland growth (-ve feedback
mechanism)
o Endemic goiters
 administer iodine
o Surgical resection
 indications
 toxic feature
 goiters causing obstructive symptoms
 goiters suspected for being malignant or proven by FNA
 goiters cosmetically unacceptable
 Preferred methods of resection Near-total or total
thyroidectomy with lifelong T4 therapy.
2) Toxic goiter (thyrotoxicosis)
A. Diffuse toxic goiter (graves’ disease)
 An autoimmune disease with a strong familial predisposition
 Cmn in females (5:1)
 Thyroidal manifestations
 Thyrotoxicosis
 Diffuse goiter
 Extra-thyroidal manifestations
 Eye signs + CNS symptomscmn
Triggering agents
 Postpartum state
 Iodine excess
 Lithium therapy
 Bacterial & viral infections
CPs
 Related to hyperthyroidism…
 See lists of hyperthyroidism symptoms above…
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 Specific to graves’ disease
 Opthalmopathy
o Lid lag (von graefe’s sign)
o Spasm of upper eye lid (Dalrymple’s sign)
o Prominent staring
o Exophthalmos, conjunctival swelling & congestion,
proptosis…in true infiltrating eye disease
 Dermopathy
o Pretibial myxedema
o Due to deposition of glycosaminoglycans
 Thyroid gland on P/E
 the thyroid is usually diffusely & symmetrically enlarged
 there may be overlying bruit or thrill on thyroid gland
 there may be loud venous hum in supraclavicular space
INVx
 TSH level
o FindingSuppressed
 Free T3 or T4 level
o FindingMay or may not be elevated
 Radioactive iodine uptake (RAIU) & scan
o Findingsincreased uptake + diffusely enlarged gland
Mgt
1) Medical Rx
 Anti-thyroid drugs
 Usually administered for preparing the pt for thyroid ablation with
radioactive iodine or thyroidectomy.
o To render the pt euthyroid
o If notthyroid storm will happen during the procedure
 Dose=titrated as needed in accordance to TSH & T4 level
 Duration= Until the pt is euthyroid (Clinical & Lab. Evidences)
 Anti-thyroid drugs…
o PTU (propylthiouracil)
o 100-300 mg three times daily
o DOC
o Methimazole
MOA:
o both reduce thyroid hormone production by inhibiting the organic
binding of iodine & the coupling of iodotyrosines
o In addition PTU inhibits peripheral conversion of T4 to T3
o Making it DOC for Rx of thyroid storm
o PTUless risk of transplacental transfer compared to
methimazolePreferred in pregnant & breast feeding women
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 β-blocking agents
o To alleviate catecholamine response of thyrotoxicosis;
=…Palpitation, nervousness, emotional lability, hyperkinesis & tremors
o Should be considered in all symptomatic (thyrotoxic) pts &
elderly with cardiac disease
o β-blockers…
o Propranolol
 20-40 mg four times daily
o Atenolol
 Long acting
2) Thyroid ablation with Radio-Active Iodine (RAI)
 indications
 elderly pts with small or moderate sized goiters
 those who relapsed after medical or surgical therapy
 when anti-thyroid drugs or surgery is contraindicated in the pt
 Absolute contraindications for this Rx

 Pregnant or planning to conceive soon (< 6 month ) after the Rx
 Breast feeding mother
 Relative contraindications
 Young pts
 Those with thyroid nodules
 Those with opthalmopathy
3) Surgical Rx
 Indications
 Confirmed ca. or suspicious thyroid nodules
 Enlarged goiters (>80gm) causing compressive symptoms
 Desire to conceive soon (<6 month) after the Rx
 Pts with moderate to severe Grave’s opthalmopathy
 Pre-op preparation
 Pt should be rendered euthyroid with anti-thyroid drugs
 7-10 days prior to surgery give #3drops bid of…
o lugol’s iodine solution or
o Saturated potassium iodide
o MOA: they reduce vascularity of the gland & decrease the risk of
precipitating thyroid storm
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 Procedurethyroidectomy
 Types
Recommended for Graves’
o Total thyroidectomy
disease o Near total thyroidectomy
o Subtotal thyroidectomy
o Lobectomy
o Hartley–Dunhill procedure
o Subtotal thyroidectomy + Total lobectomy
NB*****
In Graves’ disease Appear @ the same
time unlike TMNG
 enlargement of thyroid gland
&
 thyrotoxic signs & symptoms
B.Toxic Multinodular Goiter (TMNG)

CPs
 This pts will have prior hx of non-toxic multi-nodular goiter
o this pts will tell you that “I had anterior neck swelling first”
(non-toxic)
o “Then…after some period of time I started to experience……”
(the thyrotoxic symptoms)
 CVS symptomscmn
 Eye signsinfrequent unlike graves’ disease
INVx
 TSH levelSuppressed TSH
 Free T3 & T4both elevated
 If RAI scan is doneit will show you multiple nodules with increased
uptake
Mgt
1) Control hyperthyroidism
a. Anti-thyroid drugs
b. Β-blockers
2) RAI—thyroid ablation
 Reserved for elderly pts
3) Surgical Rx
 Near total or total thyroidectomy is recommended
o To avoid recurrence & risk of repeating the surgery
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C) Toxic adenoma (Plummer disease)
=Autonomous, solitary overactive nodule with inactive surrounding tissue
=Typically occur in young pts
>>…recent growth of long standing nodule along with symptoms of hyperthyroidism
=Thyroid gland on P/E
>>usually reveals a solitary nodule without palpable thyroid tissue on the contra lateral side
=RAI scan (INVx)
>>Hot nodule with suppression of the rest of the gland
=Mgt
=Smaller nodules
>>Anti-thyroid drugs
>>RAI-- thyroid ablation
=Larger nodules
=Higher dose
>>Anti-thyroid drugs
>>RAI
=Surgery
>>Lobectomy & isthmusectomy
3) Inflammatory goiter
Inflammatory goiter may be toxic or non-toxic
A) Acute (suppurative) thyroiditis
 More cmn in children
 Often preceded by URTI or otitis media
CPs
 Severe neck pain radiating to the jaws/ear
 Fever, chills
 Odynophagia
 Dysphonia
Complications
 Systemic sepsis
 Tracheal /esophageal rupture
 Jugular vein thrombosis
 Laryngeal chondritis & perichondritis
 Sympathetic trunk paralysis
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INVx
 CBC=leukocytosis
 FNA for gram stain, culture & cytology
Mgt
 Parenteral antibiotics
 Drainage of abscesses
 Thyroidectomy
 For persistent abscess
 Failure of open drainage
B) Sub acute thyroiditis (granulomatous thyroiditis)
CPs
May be painful or painless
 Painful
 Thought to be viral in origin or post-viral inflammatory response
 Four stages
 Hyperthyroidismeuthyroidhypothyroidism resolution & return to euthyroid
state
 On Hx
 sudden or gradual onset neck pain
 which may radiate to the mandible or ear
 Hx of preceeding URTI (often)
 On P/E
 Enlarged, tender, firm gland
 INVx.
 Early stage
 TSH dereased, T4 &T3 elevated
 ESR >100mm/h
 RAI uptake=decreased
 MgtSelf limiting disease
 So Rx is primarily symptomatic relief
 pain relief
o Asprin & NSAIDS
o Steroidsin severe cases
 Short-term thyroid replacement may be necessary
o To shorten duration of symptoms
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 Painless
 Considered to be autoimmune
 On P/E
 normal sized or minimally enlarged, firm, non-tender gland
 INVx.
 Similar to the painful one except
o Normal ESR
 Mgt
 Ptswith symptoms
o B-blockers
o Thyroid hormone replacement
C) Chronic lymphocytic thyroiditis /Hashimoto’s/
 A transformation of thyroid tissue to lymphoid tissue
 Leading cause of hypothyroidism
 Cmn in females (10-20:1)
CPs
 Minimally or moderately enlarged firm & nodular gland
 20% present with hypothyroidism while 5% present with
hyperthyroidism
INVx.
 Elevated TSH
 Thyroid auto-antibodies
o Present
Mgt
 Overtly hypothyroid pts
o Thyroid hormone replacement therapy
 Levothyroxine
D)Reide’s thyroiditis
 Replacement of all or part of the thyroid parenchyma by fibrous tissue
CPs
 The pt may present with symptoms of hypothyroidism &
hypoparathyroidismsince the gland is replaced by fibrous tissue
 Typically presents as painless, hard (“woody”) anterior neck mass,
with fixation to the surrounding tissue
Dx
 Open thyroid biopsy
DEBOL
ND
2 EDITION
Mgt
 Surgery
 Hypothyroid ptsthyroid hormone replacement therapy
NB***
Thyroid gland is inherently resistant to infection due to
 Its extensive blood & lymphatic supply
 High iodide content &
 Fibrous capsule
4) Neoplastic goiter
 Benign
o Follicular adenoma
 Malignant
 May be primary or secondary (metastasis to thyroid gland)
i) Primary
 From follicular epithelium well differentiatedslow growth
a. Papillary thyroid ca.(PTC)
 80% of all thyroid malignancies
 Predominant in children & individuals exposed to
radiation
 LN metastasiscmn
 Distant metastasis
 Lungs, bone, liver & brain
 DxFNAC
 Mgt
o Surgical Rx
 Total /near total thyroidectomy
o Post-op
 Radioiodine therapy
 Radiotherapy & chemotherapy
 Thyroid hormone
DEBOL
ND
2 EDITION
b. Follicular thyroid ca.(FTC)
 10% of thyroid ca.
 Occur more commonly in iodine deficient areas
 Often present as solitary thyroid nodule
 Hematogenous metastasiscmn
 Unlike PTC cervical LAP isn’t cmn
 Dx
o FNAC is unable to distinguish benign from malignant
disease
o Difficult to DX pre-op unless distal metastasis
 Mgt
o Surgical Rx
 Lobectomy
 Total thyroidectomy
o Post-op
 Radioiodine therapy
 Radiotherapy & chemotherapy
 Thyroid hormone
c. Hurthle cell ca. (subtype of follicular ca)
o 3% of thyroid ca
o Can’t be DXed with FNAB
 Since it’s characterized by vascular & capsular
invasion
Follicular epithelium de-differentiated
a. Anaplastic ca.
o early local infiltrationaggressive
o Typically pts present with long standing neck mass,
which rapidly enlarges & may be painful+…
1. Dysphagia
2. Dyspnea
3. dysphonia
o pts may experience…
1. bone pain
2. weakness
3. cough
o poor prognosis
DEBOL
ND
2 EDITION
Others
==Medullary ca.
o arise from Para-follicular or C cells
 Lump @ supero-lateral neck
o may occur in combination with adrenal phaeochromocytoma
and hyperparathyroidism
o Mgt
 total thyroidectomy
 External beam radiation
==Thyroid Lymphoma
o Non Hodgkin’s B-cell type
ii) Secondary (Metastasis)

o Thyroid is rare site of metastasis
o Siteskidney, breast, lung & melanoma
NB*
Prognosisparameters;
 Age
 Metastasis
 Size
 Extrathyroidal extension
 Histologic type
 Resectability
DEBOL
ND
2 EDITION
SAMPLE Hx
C/C
Anterior neck swelling of 2yrs duration
HPI
This pt was LRH 2yrs back @ which time her families suddenly noticed a
swelling on her left lower neck. The swelling was painless & it was initially pea
sized but it started to grow slowly upwards & to the right to attain its current
size & location. Associated with this she started to experience stridor which
worsen during sleeping but no difficulty of swallowing or change in voice
quality.
07 months prior to admission she started to experience palpitation, heat
intolerance, profuse sweating & un-quantified weight loss to the extent her
skirts become loose despite good appetite. In addition she started to experience
irregular menstrual cycle for the past 07months which come every 2 or
3months.
03 months prior to admission she visited our hospital where blood sample &
sample from the swelling was taken. Then she was given whitish scored oval
tablet to be taken three times daily & reddish scored circular tablet to be taken
twice daily. She is taking her medications adherently & currently she has no
palpitation, heat intolerance or excessive sweating.
 Many peoples in her vicinity have similar illness. (endemic goiter)
 Her regular dietary habit is ‘injera’ made of ‘teff’ & ‘shirowot’ made of
‘atter.’ She occasionally eats cabbage.(Dietary goitrogens)
 No hx of drug intake except the medication explained above.(Drug induced
goiter)
 No hx of fever, chills or rigor.(inflammatory goiter)
 No family hx of similar illness.(familial goiter or thyroid ca.)
 No hx of head & neck radiation therapy. (RF--if ca)
 No hx of swelling in the neck or axilla. (LN metastasis-if malignant)
 No hx of bone pain, hemoptysis or yellowish discoloration of the eyes.
(distant metastasis-if ca)
 No hx of dyspnea, orthopnea, PND or lower leg swelling. (thyrocardiac disease)
 No hx of chronic cough, contact with a chronic cougher or previous TB Rx
 No self/family hx of DM, HTN or asthma
 She was screened for RVI 7months back & found to be NR (non-reactive)
Finally she was admitted to our hospital walking by herself.
DEBOL
ND
2 EDITION
Investigations (INVx .)
Lab. studies
 TFT (thyroid function test)
 TSH
 Normal=0.5-5µu/mL
 T3 & T4
 Total (reference range)
 T3=1.5-3.5nmol/L
 T4=55-150nmol/L
 Free(reference range)
 T3=3-9pmol/L
 T4=12-28pmol/L
Pathology
 FNAC
 Reliable in…
 Papillary, medullary, anaplastic thyroid ca.
 Not reliable in…
o follicular adenoma vs follicular carcinoma
o hurthle cell ca.
o hashimoto’s thyroiditis Vs thyroid lymphoma
Imaging
 Chest & thoracic inlet radiograph
 What to look?
 Retrosternal goiter
 Tracheal deviation & compression
 Pulmonary metastasis
 U/S
 In evaluation of thyroid nodules
 solid Vs cystic
 size
 multicentericity
 risk of malignancy…by looking @ its echotexture, shape, border,
calcifications, vascularity…
 Targeted aspiration-(USG-FNAC)
 For assessing cervical lymphadenopathy
 CT, MRI & PET
DEBOL
ND
2 EDITION
Thyroid (isotope) scanning
 Size & shape of the gland
 Activity of the gland
 hot
 Warm
 Cold
Anti-thyroid antibody assessment
 Do not indicate thyroid function rather indicate the underlying disorder
 Usually an autoimmune thyroiditis
Management
 See the mgt in each section on the discussion of DDx
Complications of thyroid surgery
 Hemorrhage
 Airway obstruction
 causes
Laryngeal edema
 Mgt
o Intubate then
o Give Steroidsto reduce the edema
RLN injury
 Bilateral
o CPs—respiratory distress
o Mgt
 tracheostomy
 chordoctomy
 unilateral
o CPs--hoarseness of voice
o Mgt
 re-innervation
 medializationinjection therapy (edema)
Haematoma
 CPs—respiratory symptoms due to the compression
 Mgt
o remove all the stitches
o Urgent decompression  release the blood collection
Hypocalcemic tetany
 Laryngeal spasmcause airway obstruction
 Mgt
o Intubate first & then Calcium supplementation
Tracheomalacia
DEBOL
ND
2 EDITION
 Wound infection
 Thyroid storm
 Is a condition of hyperthyroidism accompanied by
fever, CNS agitation or depression,
Cardio-vascular dysfunction (hypotension + tachycardia) &
GI dysfunction, including hepatic failure
 Due to Poor pre-op preparation
 Mgt of thyroid storm
 B-blockers
o propranalol
 Oxygen supplementation
 Hemodynamic support
 Pyrexiagive non-aspirin cpds
 Lugol’s iodine or sodium ipodate (IV route)
 PTU
 Corticosteroids
o To prevent adrenal exhaustion & block hepatic thyroid hormone
conversion
 Hypothyroidism
 Mgt
levothyroxine
 Hypoparathyroidism
 May be
Transient
 Due to ischemia/manipulation
Permanent
 Due to removal of the gland
 May be
Subclinical--asymptomatic
 Elicit signs of hypocalcemia
o Chovestik sign
o Trousseau sign
symptomatic--overt
 CPs
o perioral parasthesia, carpopedal spasm, laryngospasm,
seizure, tetany…
 Mgt
o symptomatic--calcium supplementation
 Superior laryngeal nerve injury
 Cps
can’t produce high pitch sound
 Mgtspeech therapy
DEBOL
ND
2 EDITION
 Other complications
 Keloids
 Stitch granuloma
NB**
β-blocker Rx should be continued 1wk after surgery. Because, the half life of T4
reaches up to 7days.
DEBOL
ND
2 EDITION
SAMPLE HISTORY ON BREAST CANCER
How to approach Breast disorders
Benign Breast disorders Malignant Breast disorders
Infiltrating ca Inflammatory ca.

 Ductal ca.(cmn) Most aggressive
Congenital
anomalies  Lobular ca.
Injury
Inflammation/
Infection
=Inverted nipple
ANDI
=Supernumerary
breast/nipple =Hematoma
=Fat necrosis =Bacterial

=…
mastitis
=Chronic =Cyst
0 inflammatory
abscess =Fibroadenoma
=Duct ectasia / = cyclical

periductal nodularity &
mastalgia
mastitis
=TB of breast
DEBOL
ND
2 EDITION
BREAST CA
Risk Factors
Female sex
Increasing age (65+)
Hormonal
 Increased (unopposed) estrogen exposure due to
 Early menarche
 age <12
 Late menopause
 age >55
 Nulliparity
 Never breastfed
 Breast feeding protective
 First full term pregnancy >30yrs of age
 First child @ early ageprotective
 Exogenous hormones
 Hormone Replacement therapy (HRT) within the last 5yrs
o Increased risk among those taking combined HRT
than single estrogen formulation
 ? OCP use within the last 10yrs
o Up to 25% of ptsincreased risk
o >10 yrs of cessationrisk returns to that of average
population
 Obesity
 In postmenopausal womenthe adipose tissue acts as
major source of estrogen
Non hormonal
 Hx of radiation therapy/high dose/
 E.g. mantle radiotherapy for Hodgkin’s lymphoma
 Alcohol abuse (femalesnot cmn in our country)
 known to increase serum level of estradiol
Genetics
 Familial breast ca
 Ask Hx of first degree relatives with breast ca.
 Hx of endometrial, ovarian or colonic ca
DEBOL
ND
2 EDITION
Clinical presentations
1) History
o Common presentations
 Lump (swelling)
 When the pt noticed the swelling?
 How?
 Site & progression?
 Nipple discharge or retraction
 Color of discharge?
 Ulceration or erythema of the skin
 Axillary mass
 Painusually associated with benign diseases
Pain
Cyclical On History
Non-cyclical
o In advanced caseswhen you suspect metastatic spread, u

can ask…
 Bone pain, fracture hx (pathological one)bone metastasis
 Breathing difficulties (breathlessness)malignant pleural
effusion
 Yellowish discoloration of the eyes & the skinliver
metastasis
 Headache, nausea, vomiting (features of raised
ICP)cerebral metastasis
Spread of breast ca
1. Local spread
o Skin, muscles, chest wall
2. Lymphatic metastasis
o Axillary LNs, internal mammary LNs, supraclavicular LNs
3. Hematogenous metastasis
o Skeletal metastasis (lumbar vertebrae, femur, thoracic vertebrae, rib & skull)
DEBOLo Liver, lungs & brain
ND
2 EDITION
2) Physical Examination
LGS Examination
 Breast examination
Inspection
 First position the pt
1. Arms by side
2. Arms straight up in the air
3. Hands on hips
 Comment on….
 Symmetry with other breast
 Use nipple line for comparison
 breast size & shapecompare both sides
 Edema or peau d’orange appearance
 due to cutaneous lymphatic obstruction
 peau d’orange appearance become more prominent on
elevation of the hands
 Skin or nipple retraction
 skin retraction accentuated by positioning the pt with
arms extended forward, sitting position & leaning
forward
 Nipple discharge
 Ulceration
Palpation
Technique
 Examine all the 04 quadrants with palmar aspect of your
fingers
 Avoid a grasping or pinching motion
o Comment on the swelling…
 Site
 Upper outer quadrant(UOQ)cmn
 Tender / non-tender
 Consistency
 Hard Vs firm Vs soft
DEBOL
ND
2 EDITION
 Border
 irregular Vs regular
 Surface
 Nodular Vs smooth
 Fixation
 fixed to overlying or underlying structures vs not fixed
Watch video on how to examine breast swelling @

https://www.youtube.com/watch?v=_p8PobUp2Yo
On Physical Examiation
Lump-DDX
Based on Surface+ border & consistency
Smooth & well defined Nodular & irregular
Hard in consistency
Hard Rubbery
Cyst Fibroadenoma Carcinoma

#Common35-55 yrs #“Breast mouse”=coz of its free mov’t
#Common  15-25 yrs
DEBOL
ND
2 EDITION
On physical examination
Nipple -areola complex findings—DDx
Discharge Change in appearance
Recent nipple retraction Surface

Single duct Multiple ducts appearance
change
Circumferential
Slit like =carcinoma
Nipple Retraction
 duct ectasia
 chronic periductal
mastitis
Eczema Paget’s disease

1. blood stained
Bilateral Unilateral
a. intraductal ca. Commonly occurs @ lactation Occurs at menopause
b. intraductal Itches Does not itch
papilloma Vesicles No vesicles
c. duct ectasia Nipple intact Nipple may be destroyed
2. serous No lumps there may be an underlying lump
a. fibrocystic
disease 1. blood stained
b. duct ectasia a. ca.
c. ca. b. ectasia
c. fibrocystic disease
2. black/green
a. duct ectasia
3. purulent
a. infection
4. serous
a. fibrocystic disease
b. duct ectasia
c. ca.
5. milk
***important things to check after breast examination in breast ca.

 Axillary + supraclavicular lymphadenopathy (LAP)
 Upper extremity neurologic motor & sensory examination
o In case of infiltration of brachial plexus
DEBOL
ND
2 EDITION
DDX
Approach
TO THE LIKELY
DX
Lump Nipple
Yes No lump Discharge Change in appearance

But painful & tender (including areola)
 Duct ectasia
 Cyclical breast pain  Intraductal papilloma  Duct ectasia
 Non-cyclical breast  DCIS  Carcinoma
pain  Associated with a cyst  Paget’s disease
 Very rarely, carcinoma  eczema
Painless
 Carcinoma
 Cyst
 Fibroadenoma
Painful
Change in breast size/ shape
 An area of fibroadenosis
 Cyst
 Periductal mastitis
 Abscess
usually postpartum or lactational
 Sometimes carcinoma  Pregnancy
 Carcinoma
 Benign hypertrophy
 Rare large tumors
DEBOL
ND
2 EDITION
NB*Bacterial mastitis
Can be
1. Lactational
 Ask hx of crackled nipple or skin abrasion
2. Non-lactational
 periareolar
 periductal mastitis
 peripheral-rare
ask Hx of DM , RA, steroid Rx, trauma
CPs
 cardinal signs of inflammation
o severe pain
o swollen breast cellulitic stage
o Erythema
o warm to touch
 When breast abscess develop there will be…
o high grade fever &
o Fluctuant swellingcan be felt unless deep seated
Mgt
 Cellulitic stage
o Proper antibiotics
 Penicillins or Cephalosporins
o Appropriately fitting supportive bra
o Warm compress
o Analgesia
o Emptying the breast with breast suction pump
o If not resolved within 48hrs or tense indurations after being
emptied/underlying abscess repeated aspirations
 Stage of abscess
o Repeated aspiration with antibiotic coverage with or without u/s
guidance
o Incision & drainage ( I&D)
 For large abscesses with purulent discharge
o Antibioma=large, sterile, brawny edematous swelling that form if

antibiotic is used in the presence of undrained pus
 antibiotic induced swelling=antibioma
NB* Duct ectasia=dilatation of the breast ducts
DEBOL
ND
2 EDITION
SAMPLE Hx
C/C
Breast swelling of 6 months duration
HPI
This is a 38 years old nulligravida lady who was LRH 6months back @ which
time she noticed a small swelling on her left upper lateral breast while she was
taking shower. Initially the swelling was pea sized, and then it started to grow
downwards & medially to attain its current size & shape.01 month prior to
admission she started to experience bright red colored discharge from her
left nipple but no hx of breast pain. Associated with this she started to notice
change in nipple position & orange cover like skin appearance change
over the left breast.
For the above complaints she visited a private clinic in Gondar where aspiration
was taken from her left breast & told to have breast cancer. Then they referred
her to our hospital for better management.
 Her menses started @ the age of 12, It was regular, comes every 28
days, stays for 3-4 days, moderate in amount & associated with mild
abdominal discomfort
 The pt doesn’t notice any cyclical changes of the swelling with her
menses.(ANDI)
 No family hx of similar illnesses. (RF)
 No hx of HRT or OCP use. (RF)
 No hx of radiation therapy. (RF)
 No hx chronic alcohol consumption. (RF)
 No hx of breast trauma
 No hx of breast or abdominal surgery. (Recurrence + surgery for ovarian/ endometrial ca resp.)
 No hx of swelling in the neck or axilla. (lymph node metastasis)

 No hx of bone pain, breathing difficulty or yellowish discoloration of the
eyes.(metastasis)
 No hx of cough, contact with chronic cougher or previous TB Rx. (breast TB)
 No self or family hx of DM, HTN or asthma
 Has been screened for RVI 01 month back & found to be NR.
Finally she was admitted to our hospital walking by her
self.
DEBOL
ND
2 EDITION
Investigations
Imaging studies
1. Mammography
 Mammography=imaging breast either in medio-lateral or cranio-caudal view
by a selenium coated x-ray plate which become in direct contact with the
breast.
 sensitivity of this investigation increases with age as the breast becomes
less dense
 What to look for ca. in mammography?
o a solid mass with or without stellate features
o asymmetric thickening of breast tissue &
o clustered micro-calcifications
2. U/S
 can be used in young women with dense breasts in whom mammograms
are difficult to interpret
 can distinguish cysts from solid lesions
 Can localize impalpable areas of breast pathology
 It can guide
o FNAC, core biopsy…
 Drawback=not ideal for lesions < or =1cm in diameter
 What to look for a cyst on u/s?
o Well circumscribed wall
o Smooth margins
o Echo-free center
 What to look for breast ca. on u/s?
o Irregular walls
o But may have smooth margins
o Acoustic enhancement
 What to look generally for benign breast masses?
o Well defined margins
o Round or oval shape
o Smooth contour
o Weak internal echoes
3. Ductography
 Ductography = Radio-opaque contrast media (injected) +
mammography
 Primarily indicated forblood stained nipple discharge
 What to look in ductography?
If intraductal papilloma
=Small filling defects surrounded by contrast media
If ca.
=May appear as irregular masses or as multiple intra-luminal filling defects
DEBOL
ND
2 EDITION
4. MRI
Pathology
5. FNAC
 The least invasive technique for obtaining a cytological Dx.

Drawbackcan’t distinguish invasive cancer from in-situ disease
6. Core biopsy
 Differentiates invasive ca from in-situ ca
 Pre-op ass’t of hormone receptors can be done
Routine workups
 CBC
o May show Anemia
Metastatic workups
 Lab. studies
o ALP Level
 If increasedBone or liver metastasis
 Radiological
o CXR
o Abdominal U/S
 If there is hepatomegally
o Bone scan
 If the pt is symptomatic or increased ALP level
NB***
Triple ass’t for pts suspicious of carcinoma
 Positive predictive value (PPV)=99.9%
1) Clinical ass’t
Triple
Ass’t
2) Radiological imaging 3) FNAC
 If >40 u/s ,<40 mammography
DEBOL
ND
2 EDITION
Management
*Early breast ca (Stage I & IIA)
 Surgical mgt
 Mastectomy
• Indicated for
 Large tumors
 Central tumors beneath or involving the nipple
 Multifocal
 Local recurrence
 Pt’s preference
• May be
 Simple mastectomy
• Removal of the entire breast tissue
 Modified radical mastectomy (patey)
• Simple mastectomy + removal of pectoralis
minor + axillary block dissection
 Radical mastectomy
• Obsolete nowadays
 Breast conservative surgery
• Lumpectomy+ axillary block dissection
 Lumpectomy
• Removal of the tumor with a rim of at least 1cm of normal
breast tissue
• Indicated for <4cms tumors with well-differentiated histology
 Sentinel node biopsy

• Sentinel LN=The first LN to get enlarged in malignancieshas
metastatic potential
• Considered as standard care for mgt of axilla in early breast
ca with no clinically apparent LNs & non-multicenteric
disease
• Node localized preoperatively by injection of blue dye or
using radio-isotope
• But, if node +ve disease detectedaxillary block dissection
DEBOL
ND
2 EDITION
 Adjuvant treatment
 Radiotherapy
• Indications
 +ve tumor margin
 Breast conservative surgery
 Pectoralis major involved
 Inner quadrant tumor
 High grade tumors
 Axillary clearance not satisfactory
 Chemotherapy
 Hormonal Therapy
NB*
*In case of advanced breast ca, mgt should be aimed at palliation of the
symptoms & Rx of breast ca by hormonal therapy (usually) with or without
radiation therapy.
DEBOL
ND
2 EDITION
SAMPLE HISTORY ON GOO
GOO 20 TO??? DDx
Approach
Benign causes Malignant causes
 PUD Gastric ca.

o Decreasing in incidence due to
triple therapy Pancreatic ca.
 Less frequent
 Infantile Hypertrophic Pyloric o Gastric lymphoma
stenosis/IHPS o Duodenal ca.
o Pediatric groups o Ampullary ca.
 Gastric polyp o cholangiocarcinoma
 Caustic ingestion
 Gastric TB
 Pancreatic pseudocyst
 Bezoars
o Child
o Adults 20 to bariatic surgery
 From vagotomy induced
hypomotility
 Post surgical complication
Mechanism of obstruction & clinical presentation of GOO depend up on the underlying cause.
The following cases are selected for discussion here…
1. PUD
2. Gastric ca
3. IHPS
DEBOL
ND
2 EDITION
I) PUD
Risk Factors
 H. pylori infection
 Predispose to ulcer by increasing acid secretion & compromising the
mucosal defense mechanism.
 Drugs
 Chronic use of NSAIDS… E.g. Aspirin
 Cause ulcer predominantly by compromising the mucosal
defense mechanism.
 Age
 Gastric ulcer—cmn in >40yrs of age
 Lifestyle
 Cigarette Smoking
 2X increased risk than non-smokers
 Smoking cause ulcer by increasing gastric acid secretion &
duodeno-gastric reflex
o It also interferes with the blood flowimpairing healing
process
 Chronic alcohol consumption
 Severe stress like…
 Burn (curling’s ulcer)
 Head trauma (Cushing’s ulcer)
 ZES (gastrinoma)
 Neurological causes
 Genetic factors
Clinical Presentations
1. History
 Abdominal pain
 Site = Epigastrium
 Character = gnawing, burning
 Pattern= may be episodic, seasonal or may become
constant (deeper penetration)
 Radiation= no radiation in typical pts
o referral of pain to the back is usually a sign of
penetration into the pancreas
DEBOL
ND
2 EDITION
 Timing of the pain
o Immediately after a meal
 Gastric Ulcer (GU)
o After 2-3hrs
 Duodenal Ulcer (DU)
 Food is usually emptied in 2-3 hrs. And
food stimulated acid secretion persist 3-
5hrs.
o DU--often awakens the pt @night(nocturnal)
 because
 Hunger aggravates it &
 circadian stimulation of acid secretion is
maximal from 5PM-2AM
 Aggravating & relieving factors
o DU –aggravated by hunger & relieved by eating food
o GU—aggravated during eating & relieved by vomiting
 Associated symptoms
o Nausea, bloating
o wt loss, anemia…
NB*
If the symptoms are severe, sudden onset & with sharp abdominal pain (generalized/
epigastric) suspect the complicated one i.e. perforated PUD
2. Physical Examination
 G/A
o Acutely sick looking Vs chronically sick looking Vs acutely sick looking on
chronic base
o Nutritional status
 V/S
o Hypotension
 Think of complications (like Shock 20 to Upper GI bleeding…)
o Tachycardia
 Complications (like perforation…)
 The pain by itself
o Febrile
 Think of complications (like perforation…)
o BMI
 Clinical findings are few & non-specific for uncomplicated PUD
 For complicated PUD
o See the findings below on complications of PUD…
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Investigations
 Diagnostic studies
 Upper GI endoscopy
 What to look?
 we look for ulcers, protruding mass or any active bleeding
 Benign Vs Malignant Ulcers. How to differentiate on visualization?
 Benign ulcers …
o Have smoother, more regular, rounded edges with a flat, smooth
ulcer base.
 Malignancy is more often associated with…
o A mass that may protrude into the lumen or
o have folds surrounding the ulcer crater (cavity) that are …
 nodular, clubbed, fused, or stop short of the ulcer margin.
o Multiple biopsy specimens are necessary for any of these ulcers to
r/o malignancy.(see the nxt section for gastric ca)
Imaging
o Double contrast barium swallow (meal)
 It demonstrates barium within the ulcer crater
 useful to determine the location and the depth of penetration of the ulcer
as well as the extent of deformation from chronic fibrosis
 larger size, irregular filling defects…suggestive of malignancy
o sitelittle predictive value ,since malignancy can occur in any site.
(see the nxt section for gastric ca)
Laboratory
o H. pylori testing
 Non-invasive tests
 Serology (fecal Ag testing…) and urea breathe test.
 Invasive tests (need sample from gastric mucosa)
 Rapid urease test, histology and culture
 Imaging studies
o An upright chest radiograph
 When ruling out perforationwhat to look for perforated PUD?...air under the
diaphragm
o Abdominal/pelvic CT with IV & oral contrast
 for staging gastric ca.(see the nxt section for gastric ca)
 Lab studies
o CBC o Serum electrolytes
o LFT o Serum Cr level
o serum gastrin level (for ZES)…in patients with ulcers that are refractory to medical therapy or require surgery
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Mgt of PUD
1. Aim
 Symptoms need to be relieved
 The ulcer needs to be healed
 Recurrence must be prevented
2. Non pharmacologic
 Stop smoking
 Avoid alcohol & NSAIDS
3. Pharmacologic Rx
 Antacids
 MOA: by reacting with hydrochloric acid, forming a salt and water to inhibit
peptic activity by raising pH.
 Magnesium antacids tend to be the best buffers
 H2-receptor antagonists
 structurally similar to histamine
 cimetidine ,Famotidine…
 Protein pump inhibitors (PPIs)
 most potent antisecretory agents
 omeprazole…
 sucralfate
 it disassociates under the acidic conditions in the stomach & produce a kind of
protective coating that can last for up to 6 hours
In case of H.pylori infection
 Triple (eradication) therapy
 PPIs + 2 antibiotics
o Antibiotics such as metronidazole, clarithromycin or
amoxicillin
 For 2wks—bid
 For failures or in patients with high metronidazole resistance
quadruple therapy with bismuth added to the triple regimen is
recommended.
4. Surgical Rx
 Indication for surgery;
 perforation
 Hemorrhage
 Intractability (Non healing)
 Obstruction
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 Surgical methods
 Vagotomy
 3 levels…
o Truncal
o Highly Selective Vagotomy (Parietal Cell Vagotomy)
o Truncal Vagotomy +antrectomy
 Subtotal gastrectomy
 Usually reserved for patients with underlying malignancies or patients
who have developed recurrent ulcerations after truncal vagotomy and
antrectomy.
Complications of PUD
1. Bleeding---(most frequent complication)
 CPs
 Melena & or hematemesis
 Shock
 Abd. pain is quite uncmn
 Mgt
 ABC of life & resuscitation
 Hx & P/E
 Localize bleeding
o NGT aspirate
o Endoscopy
 Diagnostic & therapeutic importance
 Initiate therapy
o If the bleeding is controlled…
 Initiate long-term medical therapy. This includes;
 Anti-secretory agents, usually in the form of a
PPI or
 H. pylori treatment (eradication therapy) for
positive test results.
o Eradication of H.pylori should be
documented after therapy.
o If the bleeding continues or recurs, surgery may be
indicated.
2. Perforation---(fatal complication)
 CPs
 Present as acute abdomen
 The patient can typically recall the exact time of onset of abdominal
pain
 frequently accompanied by fever, tachycardia, dehydration, and ileus
 Peritoneal signs +ve
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 INVx
 Upright CXR
o Free Air under the diaphragm—in 80%
 Mgt
 It’s surgical emergency…
o After the diagnosis is made, operation is performed in an
expeditious fashion following appropriate fluid resuscitation.
3. Obstruction---GOO
Clinical presentations of GOO

1) History
 cardinal symptoms
o Nausea & Vomiting
 Non-bilious
 Undigested food
 Others symptoms
o If the obstruction is incompleteGastric retention symptoms like…
 Early satiety
 Bloating/ epigastric fullness
 Indigestion
 Anorexia
 Epigastric pain
o It is not frequent in GOO. Usually related to the underlying
cause…E.g. like this PUD case
o Wt. loss depending on the duration
 Dehydration signs Dehydration
 Distended stomach and succession splash may o
be audible with Stethoscope placed o *Dry skin & tongue
in epigastrium. o *Sunken eye ball
o *Poor venous filling
o *oliguria
NB**
GOO 20 to PUD can occur both in
1. acute setting---due to inflammation & edema
2. chronic setting---due to scarring & fibrosispart of the healing process
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Mgt of GOO
 NGT suction
 for relief of the obstructed stomach
 Dealing with metabolic abnormalities
 Rehydration with IV fluid
o isotonic saline
 Electrolyte repletion
o with potassium & chloride supplementation
NB***
Because of the prolonged vomiting this pts are @ risk of Hypokalemic
hypochloremia
 secondary to loss of gastric juice rich in hydrogen, chloride, and
potassium ions
NB**
Metabolic abnormalities (acid-base disturbance) will be less
pronounced if it’s due to malignancy
 Acid suppression
 Dealing with mechanical obstruction based on the underlying etiology
 Benign obstruction
 As this case we are discussing if it’s GOO 20 to PUD
o Vagotomy & antrectomystandard
o Alternative vagotomy + gastrojejunostomy…
 Malignant obstruction
 see the next section on Gastric ca.mgt
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II) GASTRIC CA.
Risk Factors
 Environmental & host factors
 Age
 elderly
 Diet
 Salted & smoked foods (used as preservative)
 Nitrate rich foods
 Chronic H.pylori infection
 3X increased risk than non-infected individuals
 Causes atrophic gastritis, intestinal metaplasia, dysplasiaprecursors
for Gastric ca
 H.pylori affects about 50% of the population but only 5% of the pop n.
develop cancer, why?
o Genetic susceptibility
o Different strain of H.pylori
 Previous gastric surgery (>10 yrs ago)
 Why? Surgery may alter the normal PH production…
 Pernicious anemia
 IF deficiency
 Radiation exposure
 Smoking
 Write it in #pack years
 Genetic factors
 Family hx of gastric ca
 Blood group A
 Others that’ll predispose to gastric ca
 HNPCC
 FAP…
NB*
Adenocarcinoma 95% cmn
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Clinical Presentations of Gastric ca
1. History
 Earlyasymptomatic
 In advanced cases…
o Constitutional symptoms of malignancy
 Wt. loss, Anorexia & Easily fatigability
o Early satietyMay be due to…
 The tumor mass & or
 Poor stomach distensibility.
o N&V
o Bloating
o Tinnitus, blurring of vision & light headedness
 Due to iron deficiency anemia 20 to Chronic occult blood loss—cmn
o DysphagiaCmn if the tumor arises from GE junction
o Overt bleeding ( <20% of the cases)
 Melena
 Hematemesis
 Paraneoplastic syndromes—rarely present
2. Physical examinationlate events

*P/E is typically normal. If present…usually indicate incurability.
 G/A
 V/S
 Focused examination…
 HEENT
 Look for signs of anemiaPale conjunctiva, Pale buccal mucosa
 Look for liver involvementIcteric sclera
 LGS
 Look for LAP in the neck, axilla…
 Especially …Virchow’s node (left supraclavicular LN)
 Chest examination
 Metastatic pleural effusion
 Inspection
 Chest lag on the affected site
 Palpation
 Tracheal deviation away from the affected site
 Asymmetrical chest expansion
 Decreased tactile fremitus on the affected site
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 Percussion
 Stony dullness on the affected site
 Auscultation
 Absent/decreased air entry on the affected site
 BBS sound above the effusion
 Abd. examination
 Palpable massIf 10 tumor is large
 Palpable mass 20 to metastasis
 HepatomegallyLiver metastasis
 Sister Mary Joseph nodules Periumblical metastasis
 pathognomoic of advanced disease
 Carcinomatosis (metastasis to the peritoneum) including
krukenberg’s tumor of ovary
 Evidence of malignant ascites
 Dull abdomen with fluid shift & or +ve fluid thrill
 In case of GOO 20 to gastric ca
 Distended stomach with succession splash &
 Visible peristalsis may be present
 DRE
 Hard, nodularity mass may be palpable anteriorly & extraluminally
 Drop metastasis on blumer shelf
(in the pouch of Douglas)
 Heme +ve stool on examining finger
 IGS
 Look for signs of anemia
 Palmar pallor
INVx
 See the investigations listed under PUD
Mgt
 Surgical resection (Gastrectomy)
 Radical subtotal gastrectomystandard
 Chemotherapy & radiation…
Complications
GOO
 See GOO above…under PUD complications
Obstruction of gastoesophageal (GE) junction
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III)IHPS
 Cmn3-6wks of age
RFs
 Male sex
o 5Xmore common in males
 Family hx
 Drugs
o erythromycin in early infancy
 B & O blood group
CPS
HX
 Non-bilious vomiting
o Progressively become projectile
o Occurs immediately after feeding
 After vomitingBecome hungrywants to feed again
 Become increasingly dehydrated (see symptoms of DHN in the table below)
o Wet dippers become less frequent
 Yellowish discoloration of the body
o Jaundiceindirect hyperbilirubinemia
P/E
 Palpation of “olive” shaped, firm, movable mass in the RUQpyloric mass
o Best palpated after vomiting
 Presence of visible gastric peristalisis from left to right
o Best seen after eating
 Look for signs of DHN(see signs of DHN in the table below)
 In PediatricsThe 4 important DHN signs in well-nourished child are:
No Dehydration Some Dehydration Severe Dehydration
Alert Restless,irritable Lethargic or unconscious

(mental status)
No sunken eyes sunken eyes sunken eyes

(eye ball)
Drinking normally Eager to drink Unable to drink

(Drinking)
Normal skin turgor Skin pinch returns slowly Skin pinch returns very
(Skin turgor) slowly
DEBOL Ass’ts be like = some/ severe DHN 20 to intractable vomiting 20to ?IHPS
ND
? (Curie)=IREVISION
How to take Hx in surgery+++QUICK have high suspicion of the Dx & I will Rx the pt
GCMHS Page 58
2 EDITION
R/o= I want to rule out this top DDx by investigating the pt
INVx
 U/S
 What to look for IHPS?
 Channel length
 In IHPS>16mm
 Pyloric thickness
 In IHPS >4mm
 Pyloric diameter
 In IHPS<12mm
 Contrast studieswhat to look?

 String sign
 Due to elongated pyloric channel
 Shoulder sign
 Due to bulging of pyloric muscle in to the antrum
 Double tract sign
 Parallel streaks of barium in the narrowed channel
Rx
 Medical emergency not surgical
o Firstfluid resuscitation with correction of electrolyte abnormalities
 NB***Hypochloric, hypokalemic metabolic alkalosis
 Surgical Rxpyloromyotomy
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SAMPLE HX GOO 20 to? Chronic PUD
C/C
Vomiting of 1month duration
HPI
This patient was LRH #1month back @which time he started to experience non-
projectile, non-blood tingled, non-bilious, non-foul smelling vomiting of
ingested matter 2-3X/day about 2hrs after taking a meal. Associated with this
he started to experience loss of appetite, feeling of early satiety &
abdominal bloating. In addition he has significant wt. loss of 4kg for the past
06months (from 70 to 66kg>5% in 06 month). #04 days prior to admission he
started to experience projectile, blood tingled, non-bilious vomiting of
ingested matter 5-6X per day. Concomitantly he started to experience lip
crackling & dryness of the mouth, His families also noticed recent sunkening of
the eyeballs. In addition he has tinnitus, blurring of vision & light headedness.
#From 02years prior to admission till now he was experiencing intermittent
burning type epigastric pain with no radiation which was aggravated by taking
spicy foods like “key wot” but without relieving factor noticed by the pt. The
pain usually awakens the pt @ the night. For the above compliant he visited a
nearby health center where he was given Omeprazole to be taken 2X/day for
10days. For the past #2yrs he was taking this medication repeatedly when his
symptoms reappear.
 No hx drug use except the medication explained above.(NSAIDS--RF)
 No hx of cigarette smoking or chronic alcohol consumption. (RFs)
 His regular dietary habit is ‘injera’ made of ‘teff’ & ‘shiro’ made of ‘atter.’ (Dietary RFs—
smoked food…)
 He has no hx of previous abdominal surgery. (RF)
 No hx of burn or trauma to the head. (stress ulcer)
 No hx of similar illness in the family. (RF-- PUD +Gastric ca)
 No hx of difficulty or pain during swallowing.(Gastric ca @ GE junction)
 No hx of radiation therapy.(RF-gastric ca)
 No hx of swelling in the neck or axilla. (LAP in gastric ca)
 No hx of yellowish discoloration of the eye or itching sensation (hepatobiliary disease with
vomiting-DDx)
 No hx of chronic cough, contact with chronic cougher or previous TB Rx.(gastric TB)
 No self/family hx of DM, HTN or asthma
 Has been screened for RVI 08 months back & found to be NR
Finally he was admitted to our hospital supported by his families
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SAMPLE HISTORY ON SBO & LBO
o
SBO (Small Bowel Obstruction)

SBO 20 to??? DDX
 Volvulus
 Volvulus is a twisting of a portion of bowel about its mesentry.
o Common (cmn) in rural parts of Ethiopia.
* Why?
1. Redundant small bowel (vegeterians)
2. Heavy meal (1-2X/day)
3. Strong abdominal muscle
 Previous abdominal or pelvic surgery
o Post-op adhesion
*Cmn in developed countries & major cities of Ethiopia
 Incarcerated hernia
o Incarcerated=permanent trapping
o Strangulation=arterial + venous occlusion
 Malignancy
o E.g. lymphoma…
 Inflammatory Bowel Disease
o Crohn Disease
 Infection
o Intestinal TB
 Pediatric group
o Intussusception
*peak incidence between 5 & 10months of age
*90% idiopathic, but URTI & AGE may precede the condition
*ileo-colic cmn in most children (77%)
 Clinical presentations (intussusception)
Hx
 bloody diarrhea(currant jelly stool)
 intermittent crying with the laps towards the abdomen
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P/E
o Dance’s sign-elongated mass in RUQ with absence of bowel in
the RLQ
o DREblood stained mucus on examining finger (use little finger)
 Investigations for intussusception
o Barium enema-ileocolic
 Claw sign
o Abdominal u/s = high diagnostic sensitivity
 Dougnut sign
 Appearance of concentric rings transverse section
 Target sign
 Treatment of intussusception
 Resuscitation
 IV antibiotics
 Radiographic (pneumatic or hydrostatic) or surgical reduction
Intra-
luminal Extra-mural
APPROACH TO SBO
Extramural Intra-mural Intra-luminal
 Adhesion  volvulus  Fecal impaction

 Hernias  Malignancy  Worms
 Carcinomatosis  Stricture (A.lumboricoides)
o Mass effect o IBD  Gallstones
 Intussusception
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Clinical Presentations (SBO)
1) History
A. Nausea & Vomiting
i. If frequent
 It tells us the level of obstruction
 More frequent in proximal obstruction
ii. Timing (between the onset of the pain & the vomiting)
 Earlysuspect proximal obstruction
NB*Becarefulrapid dehydrationelectrolyte derangement
B. Crampy Periumblical pain
i. Simple obstructionintermittent pain
ii. Strangulatedsteady pain
*In distal SBO pain is predominant
C. Constipation
i. Absolute constipation/ obstipation
 absence of feces + flatus complete
ii. Relative
 Can pass flatuspartial
d. Distension
 In distal SBO =central distension
 In proximal SBO=minimal distension
 In LBO =pronounced distension
SBO LBO
Proximal Distal
Vomiting Early & profuse delayed Mayn’t have vomiting
Abd. Pain Predominant
(periumblical) lower abdominal
Constipation It may take 1 or 2 days to empty the bowel distal
to the obstruction.coz it was already there!!!
Early
Distension Minimal Central Pronounced distension
distension
Radiograph Little evidence of Multiple dilated The colon proximal to the
dilated loops small bowel obstruction is dilated
loops *Small bowel will be dilated only
if incompetent ileocaecal valve
Cardinal Clinical features of acute obstruction
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Intestinal Obstruction
Based on lumen caliber Based on complication
Partial Complete Simple Strangulated

No complication
 General Appearance
o Quietly lying down/not
 Vital signs Dehydration
o PR,T0 o *Dry skin & tongue
 Signs of dehydration o *Sunken eye ball
 On Abdominal examination # notice… o *Poor venous filling
o Inspection o *oliguria
 Abdominal distension
o Proximal vs distal
 more pronounced in distal obstruction
 visible peristalsis
 Look for surgical scars
 look hernial sites carefully
o Palpation
 tenderness
 mass
o Percussion
 tympanicity
 signs of fluid collection
o Auscultation
 Bowel sounds
o Early
 Hyperactive
o Late
 Hypoactive
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o On DRE...
 If gross blood on examining finger (malignancy or strangulation)
 Presence or absence of fecal matter
 Complete vs partial
***Check the following evidences for<<>> intestinal strangulationsurgical emergency
Physical Examination
1/General appearance
On History  Quietly lying down Investigation
1/ abdominal painbecome steady 2/ 2/Vital signs 1/CBC=leukoctosis
2/Fever  Febrile
 Tachycardic
3/Abdominal exmination
 Peritoneal signs +ve
+ Tenderness
+ Rigidity
NB
**when u try to Dx… approach
1. Is it mechanical obstruction or ileus?
*Colicky pain is not its feature paralytic ileus & it become significant if 72 hrs lapsed after
laparatomy but still…
 No bowel sound
 No passage of flatus
2. What is the underlying cause?
3. Is it partial or complete obstruction?
4. Is it simple or strangulated?
NB
# ureteral colic= G/Appearancerestless patient…busy finding comfortable position
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SAMPLE Hx
C/C
Periumblical abdominal pain of 3day duration
HPI
This pt was LRH 3day back @ which time he started to experience
sudden onset severe intermittent crampy periumblical pain without
known aggravating or relieving factor. About 3-4hrs after the onset of
the pain he started to experience bilious, non-projectile, non-blood
tingled, non-foul smelling vomiting about 5-7X/day. Associated with
this he started to experience failure to pass feces & flatus (write the duration)
with central distension of the abdomen.
For the above compliant…………………………………………………………..
 No hx of previous abdominal surgery.(post-op adhesion)
 No hx of fever, wt loss or swelling in the neck, axilla or
groin.(lymphoma)
 No hx of chronic cough, contact with known TB pt or
previous TB Rx (intestinal TB)
 No hx of yellowish discoloration of the eyes or itching
sensation.(hepatobiliary disease…)
 No hx of smoking, NSAIDS use or chronic alcohol
consumption (RFs for GOO)
 His regular diet is “shiro” made of “atter” & “injera”
made of “teff”, 2-3x/day.
 No self/ family hx of DM,HTN or asthma
 Not screened for RVI but he has no hx of MSP, chronic
diarrhea or HZV attack
Finally he was admitted to our hospital………………………………………..
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Investigations
Diagnostic
 Abdominal radiograph (Erect or supine)
 What to look on x-ray for obstruction? The triad
1) Air-fluid level
2) Width of the bowel
3) Paucity of Colonic air
Dilated if > 03cms
Triad (SBO)
No colonic air
Multiple air fluid level
SBO vs LBO on plain abd. x-ray

* In SBO
1) Site=The obstructed bowel is central & lie transversely
2) Anatomical landmarks
o Valvulae conniventes of small bowel completely pass across the
width of the bowel & are regularly spaced unlike haustral folds in
large bowel
*in LBO haustral folds are spaced irregularly & don’t cross the whole
diameter of the bowel (only 1/3)
3) No or minimal gas is seen in the colon incase SBO
*incase of LBO air may be absent or minimally present only in the rectum
 Enteroclysis
gold standard…partial vs complete
 barium as a contrast is contraindicated if perforation exists peritonitis
 CT-scan & MRI
 U/S
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Lab. Studies
 CBC----in case of strangulation<<>> leukocytosis
 Degree of dehydration
 RFT, Hct
 BUN & Hct rise, giving a secondary polycythemia
 Sr. electrolyte
<<>>dehydration<>electrolyte imbalance
*NB** Dehydration & electrolyte loss are due to
1) Reduced oral intake

2) Defective intestinal absorption
3) Losses as a result of vomiting
4) Sequestration in the bowel lumen
5) Transudation of fluid in to the peritoneal cavity
Management
1. Conservative( supportive) Rx
 Secure NGT
 For bowel decompressionsee page 90 for NGT
 Secure IV line
 Fluid & electrolyte replacement
*Water & sodium lossGive Hartmann’s soln. or Normal Saline
 Analgesics & antiemetic
 Antibiotics (broad spectrum)
 Mandatory for all pts undergoing surgery
2. Surgical Rx

Indication for early intervention
 Signs & symptoms of intestinal strangulation
 Obstructed external hernia
 Obstruction in a ’virgin’ abdomen
Operative decompression
 The type of surgical procedure required will depend upon the cause of
obstruction
 Division of adhesions (enterolysis/adhesiolysis)
 Excision
 Bypass or proximal decompression
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LBO (Large Bowel Obstruction)
Risk Factors
 Age
- Elderly
 Anatomical RFs
 Diet
o High residue diet
 Chronic constipation
LBO 20 to??? DDx
 Volvulus
 Sigmoid volvulus
 Risk factors(RFs)
 Anatomic RF
o Long mesentry
o Narrow base
o Elongated colon (redundant)
 Cecal
 Colonic
 Malignancy
 Colorectal ca.
 Fecal Impaction
 Stricture
 IBD
 Diverticular disease
 Pediatric group
 Imperforate anus
Clinical Presentation
1) History
o Abdominal distension
Ask hx of obstipation
o Nausea & Vomiting
-LBO may not cause vomiting despite markedly distended abdomen
o Crampy abdominal pain
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Ask about…
#The onset
1. Abruptacute obstructive events
Cecal or sigmoid volvulus
2. Chronic constipation, straining @stool
Diverticular disease
Cancer
#stool caliber changeCancer
NB
**Sigmoid colon & rectal tumors cause colonic obstruction earlier than right sided colon.
**Attempt to distinguish
 Complete vs partial
 Simple Vs strangulated
1) General appearance
2) Vital signs
3) Signs of dehydration
4) Abdominal examination
i)Hyper-tympanic on percussion
ii)Hypoactive bowel sound
iii) May be tender
o Inguinal & femoral hernial examination
5) DRE
i) Hard stool impaction
ii) Soft stool obstipation
iii)Empty vaultobstruction proximal to the level that our finger can reach
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SAMPLE Hx
C/C
Failure to pass feces of 2days & flatus of 1day duration
HPI
This patient was last relatively healthy #03 days back @ which time he
started to experience severe intermittent crampy lower left abdominal
pain without known aggravating or relieving factor.#02 days prior to
admission he started to experience failure to pass feces associated
with distension of the lower abdomen which was relieved by passing
flatus.
One day prior to admission he totally failed to pass both feces &
flatus. In addition the abdominal pain & the distension progresses to
become generalized. He has experienced nausea but no vomiting.
He had history of similar episode #03months back for which he was
deflated with rectal tube in our hospital.
 No hx of rectal bleeding, tenesmus or wt loss
 No hx of tinnitus, vertigo or blurring of vision
 No hx of similar illness in the family
 No hx of previous abdominal surgery
 No hx of chronic cough, contact with chronic cougher or
previous TB Rx
 No self/family hx of DM, HTN or asthma
 Screened for RVI 2yrs back & found to NR
Finally he was admitted to our hospital supported

by his families
DEBOL
ND
2 EDITION
Investigations
Diagnostic
 Radiograph (erect /flat)
 Plain abdominal x-ray
*What to look for?
 Dialated bowel loop
 >05 cms for large bowel
 If for small bowel >03 cms is dialated
 Paucity of air
 Absent or reduced air in the rectum
 Important to differentiate complete from
partial obstruction
 Air fluid level
*How to differentiate LBO from SBO?

<<+>>Anatomic markers
 Haustral markingsLBO
 Valvulaie conventiSBO
o Regular spacing & go the whole length
<<+>>Colonic air absent in case of SBO
 Lower GI Endoscope
 E.g. sigmoidosopy
o Has diagnostic & therapeutic importance
 Contrast studies with enema
 Contraindicated in case of perforation or gangrenous change
 CT-scan
Lab. studies
 CBCin case of strangulation<<>>leukocytosis
 Serum electrolyteCoz dehydration can lead to electrolyte imbalance
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Management
 Depends on the underlying cause
LBO 20 to sigmoid volvulus

Is it…
Simple obstruction (viable) Strangulated
 Deflation StrangulatedContraindicated for deflation

o With sigmoidoscopy & a flatus tube  Secure Iv line
o Repeat x-ray to ensure that decompression
has occurred
o Resuscitate
 The tube should be secured for 24hrs  Catheterize
o There is 50% risk of recurrencethe o Follow urine output for
definitive mgt is surgery
adequacy of resuscitation
 Surgery should be done 01-02 weeks
 Antibiotics-broad spectrum
after the deflation
 Anti-pain
*Why?
To buy time for the inflammation & edema to  Laparatomy &
subside. o Gangrenous sigmoid resected
 Pre-op preparation o Hartman’s procedure
o Bowel preparation  Sigmoidectomy
(*See page 113*)  Proximal colostomy
 Surgical options  See colostomy @page 91
o Resection & anastomosis  Closed distal end

o Paul-mikulicz procedure
o Sigmoid colectomy
NB***
Evidences for intestinal strangulation
On History 1/General appearance
1/ abdominal painbecome steady  Quietly lying down
Investigation
2/Fever 2 2/Vital signs
1/CBC=leukoctosis
 Febrile
 Tachycardic
3/Abdominal exmination
 Peritoneal signs +ve
+ Tenderness
+ Rigidity
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SAMPLE HISTORY ON COLORECTAL CANCER
Risk Factors
1) Aging
 >50yrs increased risk
 Median age @ Dx of colorectal ca is 62.
2) Genetic factors
 Progression from premalignant to invasive Ca.
o FAP (Familial adenomatous polyposis)
 Mutation in APC gene
 More than 100 colonic adenomas are diagnostic
 Rare but in known FAP pts life time risk of developing
colorectal ca is 100% by age of 50
 Prophylactic surgery is indicated to prevent colorectal ca.
o HNPCC (hereditary non-polyposis colon ca.) or lynch syndrome
 Error in mismatch repair
 More cmn than FAP & in known HNPCC pts there is 70-
80% life time risk of developing colorectal ca.
 Pts with HNPCC  subjected to regular colonoscopic
surveillance
 Familial colorectal ca.(Hereditary RF)
o Accounts 10-15% of colorectal ca.
o Risk rises with no# of first degree relatives affected
 Hx of breast ca.
o BRCA 2
 Hx prostate or lung ca in men
3) Environmental factors
 “SAD” factors
o Smoking
o Alcohol abuse
o Dietary factors
 High intake of red meat
o Red meat components (haem & N-nitroso cpds) have
shown effect on the DNA in colorectal mucosa
 High intake of animal fat
 Direct toxic effect to the colonic mucosaearly malignant
change
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 Low fiber diet
 Because of increased exposure to dietary
carcinogens
o increased roughage is associated with reduced bowel
transit timereduced exposure
 obesity & sedentary life style
3) Inflammatory
 IBD
o Particularly chronic UC
 Because chronic inflammation predisposes the mucosa to
malignant changes
4) Others
 Previous hx of surgery for colorectal ca.
o Recurrence risk 20-40%
 Pelvic irradiation
 ?Cholecystectomy
o Possibly as a consequence of increased bile acid exposure
 ureterosigmoidostomy
Approach to RFs of colonic ca.

Agingdominant RF
Genetic factors Environmental Inflammatory
 FAP  SAD factors  UC

 HNPCC  Obesity  CD
 Familial colonic ca
DEBOL
ND
2 EDITION
• CPs of colorectal ca depend on tumor size, type & location
1) History
 Rectal bleeding
 Gross
 For suspected occult bleedingFOBT (INVx)
 Change in bowel habit
 Chronic constipation or diarrhea
 May complain of abdominal pain
 Feeling of incomplete voiding
 symptoms of Intestinal obstructionleft sided ca
 Tenesmuscmn in rectal ca
 Anemia symptoms (tinnitus, blurring of vision & light headedness)
 Unexplained iron deficiency anemia
 Cmn as initial presentation in Rt. sided tumors
 Unexplained wt loss
 easy fatigability constitutional symptoms of malignancy
 anorexia
 G/A
o Chronically sick looking/not
o Nutritional status (looks malnourished or not)
 V/S
 HEENT
o Signs of anemia (eye=pale conjunctiva + mouth &throat=pale
buccal mucosa)
o Signs of liver involvement-metastasis…= icteric sclera (eye)
 LGSLAP
 Chest examination
o If metastasis…signs of pleural effusion
 Abd. examination
o In advanced cases there may be…
 Palpable abdominal mass
 Hepatomegally
 Ascites
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o DRE
 In case of rectal ca.
 Characterize tumor size, location, surface,
consistency, fixation to the underlying or
overlying structure
 Blood on examining finger
Modes of spread (colorectal ca)
1) Local NB*
Cmn sites of distal metastasis
2) Lymphatic  Livermost cmn
3) Hematogenous  Lung
4) Transcoelomic  Carcinomatosis
=Diffuse peritoneal metastasis
NB*
 Tumors that arise from distal rectum may metastasis initially to the lung.
 75-80% pts present with localized disease
 Adenocarconoma >95%
 When u write ur ass’t be specificDon’t say colorectal ca…
o Say colonic or rectal ca.
DDx
 Inflammatory bowel disease (IBD)
o CD
o UC
 Diverticulosis
 Hemorrhoids (bright red bleeding +/- pain)
o See page 200 for hemorrhoids
 Anal fissure (bright red bleeding + pain)
o See page 203 for anal fissure
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SAMPLE Hx
C/C
Bleeding per rectum of 06 months duration
HPI
This pt was LRH 06 months back @ which time she started to experience
bleeding per rectum which was tingled with mucoid, foul smelling diarrhea
4-5x/day. Associated with this she started to experience dull aching left lower
abdominal pain without known aggravating or relieving factor noticed by the
pt. #02 month prior to admission she started to experience tinnitus, light
headedness & blurring of vision. In addition she started to experience loss
of appetite, easy fatigability & significant weight loss of 5kg for the past 06
months (from 59 to 54kg. >5% in 06 months).But she didn’t experience
abdominal distension, failure to pass feces or feeling of incomplete defecation.
For the above complaints she visited a local health center @ Dabat 02 months
prior to admission where stool examination was done & treated for amebiasis.
But there was no improvement & finally they referred her to our hospital for
better investigation & management.
 Her father died 20yrs back @ the age of 73 by similar illness.(Genetic
Rfs)
 No hx of breast,endometrial or ovarian cancer.(RFs)
 She has no hx previous abdominal surgery.( for colorectal ca—recurrence)
 Her regular dietary habit is “injera” made of “teff” & shirowot made
of “atter.” (SAD…Rfs)
 She has no hx chronic alcohol cosumption or cigarette
smoking.(SAD…Rfs)
 She has no hx of radiation therapy.(RFs—radiation to the pelvic)
 No hx of yellowish discoloration of the eyes, bone pain or
hemoptysis.(metastasis)
 No hx of chronic cough, contact with chronic cougher or Previous TB
Rx
 She has no self or family hx of DM, HTN or asthma
 She was screened for RVI 4 months back & found to be NR
Finally she was admitted to our hospital walking

by herself.
DEBOL
ND
2 EDITION
Investigations
Diagnostic
 Colonoscopy
Advantages
 You can see the entire colon
 Has advantage on detecting synchronous ca.
 Synchronous colorectal carcinoma refers to more than one primary
colorectal carcinoma detected in a single patient at initial presentation. Or
pt presented with colorectal ca within #06 month after surgery was done
for colorectal ca.
 NB*Metachronous defined as a secondary colorectal cancer occurring
more than 6 months after the index cancer.
 You can take biopsy
Disadvantages
 Most invasive
 Needs bowel preparation & IV sedation
 Risk of perforation or bleeding
 costly
 Sigmoidoscopy
Advantages
 Enemal bowel preparation only but sedation isn’t necessary
 Slight risk of perforation or bleeding
 You can take biopsy
Disadvantages
 you can see only up to splenic flexure (60cms)
 You may miss detecting synchronous polyps
(I.e. you may miss proximal lesions)
 Colonoscopy is required if polyp is found
 Imaging
 Double contrast barium enema (DCBE)
 A double-contrast barium enema is a form of contrast
radiography in which x-rays of the colon and rectum are
taken using two forms of contrast to make the structures
easier to see.
o (1) Liquid containing barium (that is, a radio-
contrast agent) is put into the rectum.
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o (2) Air is also put into the rectum and colon to
further enhance the x-ray.
 What to see?
o Constant irregular filling defects (‘Apple core’ sign)
Advantages of DCBE
 Examines entire colon
 Good sensitivity for polyps >1cm
Disadvantages
 Require bowel preparation
 Less sensitivity for polyps <1cm
 May miss lesions in sigmoid colon
 Colonoscopy required if +ve result
 Abdomino-pelvic CT-Scan
 For diagnosis & staging
* Metastatic workup
 U/S of liver
 CXR
 Abdominal/ pelvic/chest CT-Scan
 Abdominal/ pelvic MRI
Lab studies
 FOBT(fecal occult blood test)
 Blood studies
 CBC
 OFT
 Serum chemistries
 Tumor markers
 Serum CEA levelMore sensitive indicator of recurrence
(important for post-op follow-up) but no role in screening
or Dx.
DEBOL
ND
2 EDITION
Management
Pre-op preparation
 Correct Anemia
o Hct should be >30 for operating
 if emergent surgery is neededconsider blood transfusion
 See page 273 for blood transfusion
 Bowel preparation
o For elective pts
o See page 194 for bowel prep.
Principle of colorectal ca. mgt
o Surgical Rx
o Medical care
 Chemotherapy
 Radiation therapy
1) Surgical Rx
Depend on presentation
Emergency
 Acute on chronic base

presentationobstructive symptoms
 Because the bowel isn’t prepared
o We will not consider anastomosis
of the bowel or definitive Rx
 Defunctioning colostomy
o Loop colostomy proximal to the
tumor
o See page 191 for
colostomy Elective
 Then definitive Rx  Definitive Rx after
preparation
 Principle of resection in colorectal ca/ Definitive Rx/

Complete removal of
1. The tumor 4. Involved adjacent
2. The major vascular pedicles structures (difficult in case of rectal ca.)
3. The lymphatic drainage &
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 Types of resection (colectomy) in colonic ca.
 Right hemicolectomy  Left hemicolectomy  Sigmoid colectomy
 Extended rt.  Extended left  Total colectomy with
hemicolectomy hemicolectomy ileorectal anastomosis
 Types of resection in rectal ca.
= it is based on the distance from the sphincter Rigid proctosigmoidoscopy should
be done to accurately measure the exact distance of the tumor from the anal sphincter.
 Anterior resection
 Lower anterior resection
 Abdominal perineal resection/APRIf below 7cms
o complete excision of the rectum and anus &
o End permanent colostomy
2) Medical care
 Chemotherapy
 Systemic chemotherapy
 Adjuvant
 Radiation therapy
Post-op complications
 Bleeding
 Anastomosis leak
 Colostomy related complications
o See page 192 for the complications
 Intra- op injury to the adjacent structures
 DVT & embolism
 Wound related complications
 Anesthesia related complications
 Recurrence
NB*
Adverse prognosis if
Post-op follow-up
 Nutritional rehabilitation • Younger age < 40 yr
• Longer duration of symptoms
 Serum CEA level
• Obstruction/ perforation
 Metastatic work up • Ulcerative lesion
 Psychological support
DEBOL
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2 EDITION
SAMPLE HISTORY ON BOO
BOO 20 TO??? DDX
1. BPH
2. Prostatic ca
3. Bladder ca
4. Urethral stricture
5. Bladder neck contracture
 E.g. following aggressive resection of a small prostate
6. Bladder stone
7. Bladder trauma
8. Neurogenic bladder—functional obstruction
Discussion of the DDX
I) BPH
*Common cause of BOO in elderly > 70yrs
*LUTS (Lower Urinary Tract Symptoms)
=The voiding dysfunction that results from prostatic enlargement & Bladder Outflow
Obstruction (BOO)
*Not all men with BPH have LUTS & the vice versa
*hyperplasia of the gland  on periurethral & transition zone
1) History
 How to approach symptoms of BPH--LUTS
Voiding (obstructive) symptoms Storage (irritative) symptoms

– Hesitancy – Frequency
– Poor flow Put it in Day:Night ratio
Ask if Improved/ not by straining – Urgency
– Intermittent stream – Nocturia
Stops and starts – Urge incontinence
– dribbling
Including Post-micturition
– Sensation of poor bladder emptying
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Special attention to….
o Onset & duration of symptoms
o Precipitating factors
o General health issues including sexual history
 …Erectile & ejaculatory dysfunction
o Severity of symptoms & how they are affecting the patients quality
of life
o Medication intake
 E.g.--- anti-histamines, anti-hypertensives, anti-cholinergics,
tricyclic antidepressantsthese drugs can induce retention
o Previously attempted Rx
 Focus on
 Signs of anemia
 Kidney erythropoietin production…
 Suprapubic area
 For bladder distension
 DRE
 Prostate
1. Size
*Measure (by finger) & approximate if reachable
2. surface DRE reporting format
3. Consistency
 Inspection
4. Contour o No ulceration or no visible protruding
5. Fixity mass
6. Medial sulcus  Palpation
o Normotonic anal sphincter
o There is palpable mass which is non-
tender with smooth surface, regular
border, firm in consistency, not fixed to
the rectal mucosa & palpable medial
sulcus but the upper border isn’t
reachable.
DEBOL
How to take Hx in surgery+++QUICK REVISION GCMHS o No blood on the examining finger
Page 84
ND
2 EDITION
Possible findings during DRE
BPH Prostatic ca
Size=Enlarged Size=Enlarged
(Measure) Urethral stricture (Measure)
Surface=Smooth  Palpable beadings Surface=May be
Consistency=Firm on urethral
examination nodular
Contour=well Consistency=hard
 Normal prostate
defined findings on DRE
examination
Contour=ill
 you can’t advance a defined/irregular
Fixity=Not fixed to
rectal mucosa catheter Fixity= fixed to
rectal mucosa
Medial sulcus= Medial sulcus
palpable =obliterated
 Also assess…
1. Absence or presence of fluctuation
o Prostatic abscess
2. Tenderness
o Prostitis
 Anal sphincter tone & bulbocavernous muscle reflex
o ...neurological disorder
INVx
 Urine analysis
 Urine culture
 Sr electrolytes
 Sr creatinine
International prostate symptom score (IPSS)
 Hct
*scored out of 35 & has 7 components
*it tells us how severe the patients’ symptoms are
0-7=Mild
8-19=Moderate
20-35=Severe
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Management of BPH
1) Watchful waiting
o For mild symptoms, follow-up1 to 2 times yearly
o Offer suggestions that help to reduce symptoms
 Avoid caffeine and alcohol
 Avoid decongestants and antihistamines
2) Medical mgt
3) Surgical mgt
Medical Surgical
1) α-adnergic blockers
MOA: act on α-receptors in the smooth muscles of prostate & decrease its tone
E.g. tamsolusin
2) 5α reductase inhibitors
MOA: inhibit conversion of testosterone to its potent form (DHT) & shrink the
prostate over several months
NB*this drugs can be given in combination or as a single agent
Indications
1) AUR
2) Chronic urinary retention & renal
impairment
 Hydroureter or hydronephrosis Surgical methods
 Residual urine> or =200ml Minimally invasive procedure
 Raised BUN
1) Trans-urethral resection/TURP
 Uraemic manifestations
*Gold standard Specific complications of the Surgery
3) Complications of BOO
*infection, stone, diverticulum formation… Open surgery 1) Bleeding
4) Symptoms are severe enough to 2)Retropubic 2) retro-grade ejaculation
bother the patient and affect his quality *commonly done in our setup 3) Incontinence
of life (Gondar university hospital) 4) Impotence
5) Failed medical Rx 3)Transvesical 5) Urethral stricture
4)Perineal 6) Bladder neck contracture
DEBOL
*Obsolete nowadays
ND
2 EDITION
NB*
If the pt present with AURthe mgt initially is…
 Urethral catheterization then arrange urological mgt…
o See page 206 for urethral catheterization
When compared to prostatic ca

BPH causes LUTS earlier. WHY?
II) Prostatic ca.

Risk Factors
 Genetics
o Ask similar illness in the family… Prostatic ca.
 Diet  70% arise from peripheral zone
o Dietary hx?  95% are adenocarcinoma
 Fat intake
 Obesity
 Hormonal
o High levels of LH , testosterone : DHT ratio
 Urinary complaints or retention
 Back pain
 Hematuria
 Advanced disease
o Wt loss & anorexia
o Anemia
o Bone pain with /without pathologic fracture
o Neurologic deficit from spinal cord compression
o Lower extremity pain & edema due to obstruction of venous &
lymphatic tributaries by nodal metastasis
Prostatic ca on DRE
Size=Enlarged (Measure) Surface=May be nodular
Consistency=hard Contour=ill defined/irregular
Fixity= fixed to rectal mucosa Medial sulcus =obliterated
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Investigations
• PSA level
– PSA velocity
– PSA density [percentage of free PSA]
• The lower the percentage of free PSA , the higher the likelihood of ca .
• Prostate biopsy
– Done when PSA level is elevated or abnormal DRE
• Ultrasonography
What to look on u/s for prostatic ca.?
• Enlarged prostate
• Nodular surface
• calcification
• Capsular invasion
• CT , MRI for staging

• Bone scan
Mgt of prostatic ca.
Localized disease
 Radical prostatectomy
 Radiation therapy
 Active surveillance
 Androgen deprivation therapy
[ADT]
Metastatic disease
 Palliation of pain
 Attempt to slow further
progression of disease
 LHRH agonists
 Antiandrogens
 Orchidectomy
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III) Bladder ca.
Risk Factors
 Environmental factors (80%)
o Cigarette smoking
o Occupational exposures
 Medical RFs
o Radiation therapy to the pelvis
o Chemotherapy with cyclophospamide
o Prolonged indwelling catheter due to spinal cord injury RF
for Squamous Cell Ca.(SCC)
 S.hematobium SCC
NB**transitional/urothelial/ cell carcinoma is the most cmn-90%

**common in males & elderly
 Irritative bladder symptoms(20-30%)appear before the
hematuria
 Dysuria
 Urgency
 Frequency…
 Painless gross hematuria (80-90% of cases) terminal reddish
discoloration of urine (the discoloration come at the end of
urination)
 In advanced cases
 Pelvic/ bone pain
 Lower extremity edema
1. Due to compression of iliac vessels
 Flank pain
1. Due to ureteral obstruction
NB**
Source of hematuriabased on the timing during
micturation
 @ the beginningurethra
 @ the endbladder neck + prostate
 Throughouthigh up in the kidneys & ureter
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Investigations
• Urinalysis
• urine culture
• before any endoscopic procedure
• Urine cytology
• Cystoscopy
• u/s
• LFT (liver metastasis) , ALP (bone metastasis)
Mgt of Bladder ca.

 Non muscle invasive
o Immunotherapy & chemotherapy

 Intravesical BCG
o TURBT
 Electrocautery
o Radical cystectomy
 High risk
 Muscle invasive
o Radical cystectomy
o Pelvic lymphadenectomy
o Urinary diversion
o Neoadjuvant chemotherapy
 Metastatic
o Chemotherapy
o Radiation therapy
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IV) Urethral Stricture
Causes
 Inflammatory/infectious/ stricture
 Gonoccocal infection
CPsPenile discharge, dysuria…
NB*Bulbar urethra—cmn site
 TB
NB*prostate—cmn site
*multiple strictures @ the site
 Traumatic stricture
--Instrumentation (for therapeutic or diagnostic)
E.g. prolonged catheterization…
--pelvic injury
 The voiding symptoms of urethral stricture are very similar to BPH
 Suspect the Dx in a young man with poor urinary stream
Urethral stricture on P/E

 Palpable beadings/scaring on urethral examination
 Normal prostate findings on PR examination
 you can’t advance a catheter
INVx
 Urethroscopy
o The stricture will be viewed as circumferential scar
 Urethrography
o Show the extent & severity of the stricture
Mgt
 Urethral dilation
 Endoscopic (internal) urethrotomy
 Urethroplasty
NB*
In case of AUR (even though rare)suprapubic catheterization
 See page 208 for suprapubic catheterization
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++ Bladder+prostatic+urethral stone
 Common in male children
 Is the difficulty of urination position dependent or not? bladder stone
 Pain on the tip of the penis + hx of stone passageurethral
++ Bladder trauma
 Triad of symptoms
Gross hematuria
, Difficulty of voiding Suprapubic pain/tenderness
Complications of BOO
 Urinary retention
o Acute Urinary Retention (AUR)
Precipitated by
 postponement of micturation
o Cmn after heavy drinking of alcohol in social gathering
 Medications
 Perianal pain
 UTI
o Chronic urinary retention
 Due to Vesiculoureteral junction incompetence
Bilateral hydronephrosis…
 Renal insufficiency
 Recurrent UTI
 Gross hematuria
 Bladder caliculi
 Dierticulum formation
 Renal Failure-rare
DEBOL
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SAMPLE Hx
ID
Age= 68yrs old
C/C
Difficulty of urination of 06 months duration
HPI
This pt was LRH 06 months back @ which time he started to experience
difficulty of urination associated with straining to initiate & maintain his
urination. In addition he started to experience urgency & frequency of
urination with D:N ratio of 10 to 6 which made his bed time difficult. He has also
a feeling of incomplete voiding & post micturation dribbling but no reddish
discoloration of urine.1 month back he was totally unable to pass urine after
drinking about 1 & ½ Liters of local tella on a social gathering. On the next day
he visited our hospital & he was catheterized which enable him to urinate.
10days prior to admission he returned on the appointed date for catheter
replacement & his catheter was changed. Currently he presented with total
failure to pass urine of 01 day duration after he removed the second catheter
because he felt discomfort.
 No hx of anorexia, easily fatigability or significant wt loss. (malignancy constitutional
symptoms)
 No hx of similar illness in the family. (genetic RF--prostatic ca)
 No hx penile discharge, geital ulcer or MSP (urethral stricture—RFsymptoms)
 No hx chronic cough, contact with a chronic cougher or previous TB R x .
(uretheral stricture—TB)
 No hx trauma to the pelvis. (traumatic stricture)
 No hx of cigarette smoking or radiation therapy to the pelvis. (RF-bladder ca)
 Has hx of river water contact but can’t recall post RWC itching .( RF bladder ca)
 No hx medication intake. (retensionAnti-histamines, anti-cholinergics…)
 No hx of position dependent sudden cessation of urine (bladder stone)
 No hx of fever, chills or rigor. (complication--UTI)
 No hx of tinnitus, blurring of vision or light headedess .(complication—renal
insufficiencyanemia)
 No hx of bone pain, hemoptysis or yellowish discoloration of the eyes . (metastasis)
 No self /family hx of DM, HTN or Asthma
 Screened for RVI & found to be NR 06 months back.
Finally he was admitted to our hospital supported by his families.
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2 EDITION
General list of investigations in BOO
 CBC
o Information we may getAnemia, leukocytosis
 Urine analysis
o Midstream urine
o Information we may getBlood, leukocytes, bacteria, protein or glucose
 Urine cultureTo r/o infectious causes of irritative voiding
o Done if the Urinanalysis shows abnormality
 Sr. electrolytes & RFTchronic renal insufficiency…
 Ultrasound (abdominal ,renal ,trans-rectal)
o Prostate,what to look?
 Size
 Surface
 Smooth/nodular
 Capsular invasion
 calcification
o Bladder ,what to look?
 Size
 stone
o Degree of hydronephrosis
 IVP
 cystoscopy
 Urine cytologyBladder ca.
 PSA
o Screening for prostate ca.
 PSA velocity
 PSA density
o 4ng/ml
 Prostate biopsy
o In pts with elevated PSA
o Abnormal DRE
 CT/MRI
o For staging
 Urodynamic flow studies
o Done in best setups
Mgt
See the mgt in each part of the DDx discussion.
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SAMPLE HISTORY ON UROLITHIASIS
Risk Factors
 Infection…
 E.g. Due to chronic catheterization
o So, ask hx of catheterization
 Dietary + environmental factors…
 Low fluid intake(dehydration)low urine output
o increased concentration of urinary solutes@ risk of stone formation
o So, ask about fluid intake habit & the type of the fluid…
 Vitamin A deficiency
o Cause desquamation of renal epitheliumwhich act as a nidus for
stone deposition
 Diet rich in red meat, fish, eggs (rich in proteins (purines))
o Leads to hyperuricemia
o So, ask dietary hx…
 Living in hot climate area
 Medical conditions…
 Hyperparathyroidism
o Result in a great increase in the elimination of calcium in the urine
 these pts “pass their skeleton in their urine”
 Gout
o Increases uric acid level & causes multiple uric acid stones
o Ask hx of joint pain, swelling, disability
 Especially at the base of big toe
 Crohn’s diseasehyperoxaluria & malabsorption of magnesium
 Obesity
 HTN
 Medication hx
o e.g.
 acyclovir,sulfadiazine
 loop diureticsincrease calcium renal excretion
 glucocorticosteroids increase bone resorption
 Prolonged immobilization
o E.g. paraplegic pt
 Surgical hx
o Gastric bypass procedures, bariatric surgery, short bowel syndrome
 Enhanced enteric oxalate absorptionincreased risk of stone
formation
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 Anatomical…
 Inadequate urinary drainage
E.g. Horse shoe kidney, un-ascended kidney
 Others…
 Prior hx of nephrolithiasisrecurrence
 Family hx of nephrolithiasis
NB*
Renal stone=Nephrolithiasis
Ureteral stone=ureterolithiasis Urolithiasis
Bladder calculi
 May be clinically silent (asymptomatic)
 Symptomatic stones are commonly associated with pain in the flank area
 Site of obstruction determine the location of the pain
 Upper ureteral or renal pelvic obstructions lead to flank pain
o which is dull aching to pricking type
 Lower ureteral obstructions lead to colicky type of flank pain with
radiation from the loin to the groin area
o The radiation is due to irritation of genitofemoral nerve
o Patients are usually quite agitated and have difficulty in getting a
comfortable position unlike peritonitis pts.(writhe)
o The severity of the pain isn’t associated with the size of the stone
 In majority of symptomatic pts there is microscopic or gross hematuria
 Nausea and vomiting commonly accompany ureteral colic…
 as a result of pressure on the renal capsule
o Due to common innervation pathway of the renal pelvis,
stomach & intestine
 Through the celiac axis and vagal nerve afferents
 Due to recurrent UTI the pt may present with
 Fever with chills & rigor
 Burning micturation, increased frequency of micturation & or
 pyuria
 Urinary urgency or frequency may also be present if the obstruction is in
the distal ureter
 On P/E
 there may be guarding & rigidity on the back & abdominal muscles during
severe attacks of the pain
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Complications
 Calculus hydronephrosis
o due to back pressurerenal enlargementpain
 Calculus pyonephrosis
o Calculus hydronephrosisinfected
 Renal failure
o staghorn calculi can lead to renal failure over years if it’s bilateral
 because they don’t typically produce symptoms unless the stone
results in urinary tract obstruction or infection
 Squamous cell ca----long standing stonesincreased risk
DDX
1. Pyelonephritis
CPs
 fever,chills
 N &V
 CVAT
2. Renal Cell Carcinoma (RCC)
RFs
 Cigarette smoking
 Obesity
 HTN
 Long term dialysis
CPs
 Flank pain
 Hematuria
 Palpable abdominal/flank mass
 Firm, homogenous, non-tender & moves with respiration
Mgt principles
 surgery , radiation therapy , chemotherapy , hormonal therapy ,
immunotherapy...combinations
3. Peri-renal abscess
4. Bladder ca
5. Renal trauma
6. Polycystic kidney disease
 Hematuria
 Hypertension
 Bilateral renal mass
 Nodular, firm to hard sometimes cystic
7. Renal TB
 Frequencyearliest
 Sterile pyuria
 Hematuria…
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SAMPLE Hx
C/C
Right flank pain of 2days duration
HPI
This pt was LRH 2 days back @ which time he started to experience sudden
onset severe intermittent colicky right flank pain with radiation to the right
groin area & the right medial thigh which was aggravated by going up stairs but
no relieving factor noticed by the pt. The pain started while he was trying to
urinate after drinking about 2 liters of beer from local beer house. Associated
with this he started to experience nausea & non-bilious, non-blood tingled, non-
foul smelling vomiting of ingested matter about 3-4X/day. One day prior to
admission he started to experience urgency, dysuria with D:N frequency of 5:3
but no fever, chills or rigor. In addition he noticed decreased amount of his urine
when compared to the previous times but no reddish discoloration of the urine.
This pt had hx of deep dull aching right flank pain 01 year prior to admission for
which he visited a private clinic in Gondar town where abdominal x-ray was
done. He was told to have small renal stones and he was given antipain &
advised to drinking plenty of water.
 He usually drinks up to #02 glass of water/day. (dietary RF)
 His regular dietary habit is “shiro” made of “atter” & “enjera” made of “teff.” (dietary RF)
 No hx of catheterization.(UTI--RF)
 No self/family hx of similar illness.( recurrence + RF)
 No hx of prolonged immobilization. (RF)
 No hx of abdominal surgery. (RF--bariatic surgery…)
 No hx of medication intake except the antipain.(medication hx-RF)
 No self/family hx of DM, HTN or gout.(medical conditions-RF)
 No hx of penile discharge, genital ulcer or MSP. (RF-ascending infection)
 No hx of tinnitus, blurring of vision or light headedness. (anemiamay have
microscopic hematuria in this pt)
 No hx trauma to the abdomen or pelvic area. (renal trauma)
 No hx of chronic cough, contact with chronic cougher or previous TB Rx . (renal TB)
 No hx of anorexia, easily fatigability or significant wt loss
 No hx of bone pain or hemoptysis
 He has been screened for RVI 1yr back & found to be NR
Finally he was admitted to our hospital supported by his
families.
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2 EDITION
Investigations
Lab. studies
1. U/A
 Information we get…
o Hematuria
o Bacteria, Leukocytes
o PH
 PH > 7...urea-splitting micro-organisms
a. proteus , pseudomonas , klebsiella , struvite
stone
 PH < 5 = uric acid stones
o crystals
 ca oxalate , uric acid , cystine
2. CBC
 Anemia, leukocytosis
3. Serum electrolytes
4. RFT (BUN & creatinine)
 To r/o renal failure
Radiological studies
5. Plain x-ray (KUB)
 KUB=Kidney+ureter+bladder
 Will identify sufficiently large radio-opaque stones
6. IVU (intra-venous urography)
 It tells us the presence & anatomical position of a calculus
 Also gives us information on the function of the kidneys
 Hydronephrosis, Hydrouretronephrosis can also be seen
o >6mm of ureter – hydroureter
7. Non-contrast enhanced helical CT scan
 Gold standard
8. u/s scanning
 valuable in locating stones for Rx by ESWL
9. Retrograde pyelography
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Mgt
1. Conservative Rx
a. Pain mgt
 NSAIDS
 Diclofenac, indomethacin
b. Hydration
 Small stones <5mm can pass with intake of plenty amount of fluid
 Advice them to drink > 2L of water/day=around #08 glass
c. alpha-adrenergic blockers
 tamsulosin…
 ureteral smooth muscle relaxing effect
2. Medical Rx
a. alkalization of urineto dissolute the calculi
Using NaHCO3 or K+citrate (urinary PH should be between 6.5-7)
 Which stones dissolute?
 uric acid stones
 cystine stones
b. Chemoprophylaxisto prevent recurrence
 Limitation of dietary components
 Addition of stone formation inhibitors (Magnesium & citrate) or
intestinal Calcium binders
 Avoid excess salt / protein intake
 Augmentation of fluid intake(>2L/day)
 Allopurinol
3. Surgical Rx
a. Non-invasive procedures
 PLS (percutaneous nephrolithotomy)
 ECSWL (extracorporeal shock wave lithotripsy)
b. Open surgery
 Pyelolithotomy
 Indicated for stones in the renal pelvis
 Nephrolithotomy
Emergency management of renal colic
a. Secure IV line & give
 analgesics
 NSAIDs , PO
 Parentral narcotics
 Fluid
 IV hydration
 antiemetic
DEBOL b. obstruction / infection
How to take Hx in surgery+++QUICK
 REVISION
needs emergentGCMHS
decompression Page 100
ND
2 EDITION
Indications for surgical removal of a ureteric calculus
■ Repeated attacks of pain and the stone is not moving
■ Stone is enlarging
■ Complete obstruction of the kidney
■ Urine is infected
■ Stone is too large to pass
■ Stone is obstructing solitary kidney or there is bilateral obstruction
Surgical Rx of ureteric calculus

Endoscopic stone removal
 Dormia basket
 Ureteric meatotomy
Ureteroscopic stone removal
 Push bang
 Lithotripsy in-situ
Open surgery
 ureterolithotomy
NB*
If UTI is present, appropriate antibiotic is given & continued during & after surgery
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2 EDITION
SAMPLE HISTORY ON CHOLELITHIASIS
CholelithiasisStone in the gallbladder
Risk factors
 GenderFemale sex
o #03 times increased risk
 Increasing age
 Obesity
 Factors that predispose to gallbladder stasis. E.g. …
o Pregnancy
 Mechanism=Because of increased progesterone exposurereduce gallbladder
contractilitybile stasis
o prolonged NPO with parenteral nutrition(PTN)
 Previous abdominal surgery. e.g.
 vagotomy Mechanism=denervation of gallbladderaffects its motility
 Surgery. E.g. …
o Truncal vagotomy in case of GOO(Rx)
o Post surgical biliary tract stricture
o Terminal ileum resection
 Mechanism=It affects enterohepatic circulation
 Drugs
o Estrogen formulations E.g. OCP, medications for Prostatic ca.
 Mechanism=by increasing biliary cholesterol secretion
o Colfibrate (hypolipidemic drug) Mechanism=by increasing hepatic elimination of
cholesterol via biliary secretion
o Somatostatine analogues Mechanism=CCK inhibition…decrease gallbladder
emptying
 Hereditary 25%
 Disorders of hemolysis
 Sickle cell anemia, Heriditary spherocytosis,Beta-thalassemia…
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2 EDITION
1. Lithogenic stage
2. Asymptomatic stage
3. Symptomatic stage
4. Complicated stage
1) History
*About 2/3 of pts with gallstone present with chronic cholecystits characterized
by recurrent attacks of pain.
 Pain
 characterization of the pain
 Sitelocalized to the RUQ/epigastrium
 Qualitycolicky
 Patternepisodic in chronic one & Persistent in acute cholecystitis
 RadiationMay radiate to the right upper back or between the
scapulae
 Aggravating & relieving factors
o Usually begins postprandially after fatty meal
 Associated symptoms
 Nausea & vomiting
 fever
*Acute cholecystitis is seconday to gallstones in 90-95% of the cases
 about 80% of pts have compatible hx with chronic cholecystitis

 but the pain is unremitting type & may persist for several days
 & the pt is often febrile ,complains of anorexia, N & V + reluctant to move
Pain characterization
2 2
(OPQR S )
 Onset(1)
 Pattern(3)
 Quality(4)
 Radiation(6)
 Relieving & Aggravate factors(7)
 Severity(2)
 Site(5)
E.g…. sudden onset severe intermittent colicky RUQ pain with radiation to the right upper back
which
DEBOLwas aggravated by taking fatty meals & relieved by….
ND
2 EDITION
2) Physical examination
 G/A
 vital signs
 HEENT
 Abdominal examination…
 In chronic cholecystitis P/E may reveal
o Mild RUQ tenderness during episodes of pain
 In acute cholecystitis
o Focal tenderness & guarding are usually present in
RUQ
 Guarding=contraction of abdominal muscles on palpation
o Murphy’s sign +ve

 Inspiratory arrest with deep palpation in the
right subcoastal area
Complications of gallstone
1. Cholecystitis
 Well localized steady pain with rebound tenderness & guarding
 Murphy sign +ve
 No peritoneal signs present unless perforated
 Differentiate calculus vs acalculus cholecystitis
 Calculus Have high suspicion

 Hx of biliary pain index for complication
when there is
 Acalculus
 Persistent steady pain for > 6-8hrs
*Fever
 No previous hx of biliary pain
 In severely ill pts…e.g.elderly with DM *Tachycardia
2. Cholidocolilithiasis + or - Ascending cholangitis *Hypotension

 Charcot triad Reynolds’pentad (see page 69)
3. Acute pancreatitis *Jaundice
 Pain=severe steady sharp epigastric/mid-abdominal
 Radiation to the back
 Relieving factor=leaning 4wrd
 Associated smxanorexia, N & V ,diarrhea may be present
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ND
2 EDITION
4. Gallbladder empyema
5. Gallstone ileus
6. Mirizzi syndrome
 Distended gallbladder causing common bile duct obstruction
 Cause elevated LFT
DDX
 PUD(Perforated/without perforation)
 Acute pancreatitis
 Appendicitis
o Before it shifts to RLQ
 GERD
 Hepatitis
 Liver abscess
 Acute pyelonephritis
 Renal calculi
 Diverticulitis
 Gallbladder ca
o Pain is late manifestation in malignancies
 pneumonia
 Pleuritis
 Myocardial ischemia
 HZA involving IC nerves
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2 EDITION
SAMPLE Hx
C/C
Right upper abdominal pain of 03 days duration
HPI
This patient was LRH 03 days back at which time she started to experience
abrupt onset severe intermittent colicky RU abdominal pain with radiation to
the right upper back which was aggravated by taking fatty meal but no relieving
factor noticed by the pt. Associated with this she started to experience nausea
& bilious,non-projectile,non-blood tingled,non-foul smelling vomiting for about
4-5X/day immediately after taking a meal. Inaddition she started to experience
low grade intermittent fever but no chills or rigor.For the above compliant she
visited a LHC @ Dabat town where she was given #01 bag of IV fluid & they
referred her to our hospital for better investigation & management.
 She was on oral contraceptive pill for the last 3 years but no hx of other
medication intake
 She is a grand mutipara mother
 She has no history of abdominal surgery
 She has no hx of similar illness in the family
 She has history of burning epigastric pain for the past 02 years but no hx
NSAID use or chronic alcohol consumption.(PUD)
 She has no history of yellowish discoloration of eye, itching sensation or
color change in the urine & stool (choledocolithiasis)
 No hx of MSP, contact with jaundiced person or blood transfusion
(hepatitis)
 She has no history flank pain or pain on passing urine(renal colic)
 She has loss of appetite but no significant wt loss or easily fatigability
 She has no history of chronic cough but has history of contact with known
TB patient who was on Anti-TB medication after diagnosed by sputum &
CXR examination.
 She has no self or family history of DM, HTN or asthma.
 She was screened for RVI 9 month back and found to be NR.
Finally she was admitted to our hospital by…
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ND
2 EDITION
Investigations
Imaging modalities
 Abd. Ultrasonography
 Standard Dxtic test
What to look on U/S for Acute cholecystitis?
1. Acoustic shadow ((stone)

2. Gall bladder wall thickening
o Acute cholecystitis if >3mms
3. Pericholecystic fluid
4. Sonographic murphy’s sign
 HIDA Scan+ve if there is lack of filling of the gallbladder in 4 hours
 Computed tomography (CT) scanless sensitive than U/S
Lab. studies
 CBC with differential

 Degree of leukocytosis +++ neutrophil predominance
 LFT
 Sr bilirubin, Albumin, PT & PTT
 In case of Mirrizi syndromeelevated
 Read on components of LFT
 RBS
 DM
 Amylase /Lipase
 Urinalysis
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2 EDITION
Management
Acute cholecystitis
 Conservative Rx
o NPO
o IV fluid
o Antibiotic
 Criteria
o Broad spectrum
o Single
o Effective
o Fast acting
 Drug Of Choice (DOC)
 3rd generation cephalosporin or
 2nd generation with metronidazole
*If allergic to cephalosporinsAminoglycosides with metronidazole
 In our setting(GUH), Ceftriaxone (3rd generation
cephalosporin) with metronidazole is being used
o Analgesics
 Definitive Rxsurgery
o Cholecystectomy
o Timing with in 2-3 days of the illness (preferred)(Source--Schwartz 10th
edition)
 Preparation for operation for Cholecystectomy
 CBC
 OFT
 Prothrombin time
 Chest X-ray and electrocardiogram (if over 45 years or
medically indicated)
 Antibiotic prophylaxis
 Deep vein thrombosis prophylaxis
 Informed consent
 Methods
 Laparascopic cholecystectomy
 Open cholecystectomy
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Chronic cholecystitis
 While waiting for surgery
o Avoid dietary fats and large meals
o Control comorbities
 Cholecystectomy
Indications for surgery
 Symptomatic/complicated cholecystitis
 Rare indications in asymptomatic cholecystitis for prophylaxis
 Elderly with DM
 In individuals to be isolated from medical care for long period of time
 In population with increased risk of gallbladder ca
 Porcelain gallbladder
> Because this pts may develop complications without biliary symptoms
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ND
2 EDITION
Before we proceed to nxt case… Let’s Recall
Jaundice
Unconjugated hyperbilirubinemia conjugated hyperbilirubinemia
Over production
 E.g.Hemolysis…
Reduced uptake
 E.g.Gilbert’s syndrome…
Conjugation defect
Acquired
 E.g. neonatal…
Inherited
o E.g. crigler-najjar I & II
Extra-hepatic cholestasis Intra-hepatic cholestasis

Surgical hepatitis
o viral
Jaundice o alcohol
o drugs
 NASH
 Primary biliary cirrhosis
 TPN…
DEBOL
ND
2 EDITION
SAMPLE HX ON OBSTRUCTIVE (SURGICAL) JAUNDICE
OBSTRUCTIVE JAUNDICE 20 TO ??? DDX
APPROACH
Extra-ductal causes
Intra-ductal causes
 Stone disease  Pancreatitis

 Neoplasms  20 to neoplasms
o Cholangiocarcinoma o Periampullary ca.
o Gall bladder ca.  Portal adenopathy
 Biliary stricture o Metastasis
o Surgical trauma  GIT
o Erosion by gallstone  breast
 Parasitic infection o TB
o A.lumbricoides  Cystic duct stones
 Primary scleorising o Mirizzi syndrome
cholangitis/PSC/
o UnderlyingUC
 AIDS cholangitis
 Choledocal cyst
 Biliary TB--rare
NB
Periampullary ca. includes
1. Pancreatic head ca.
2. Cholangiocarcinoma
3. Duodenal ca.
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ND
2 EDITION
Clinical Presentation Obstructive jaundice
1) History
 Pale stool
 Dark urine
 Pruritus
o May be related to the circulating bile acids or our body response…
 Jaundice
NB*
Urine darkening, stool changes & pruritus are often noticed by the pt
before clinical jaundice. Usually clinical jaundice is noticed by the pt & the
family when it reaches 6-8mg/dl. Physicians can usually detect it @ 2.5-
3mg/dl…
On HxAlso consider
o Pt’s age & associated conditions
o Presence/absence of pain
 Location & character
 Stone in CBDsevere colicky pain
 Periampullary ca. mild discomfort
o Acuteness of symptoms
 Stone in CBDlong duration
 Periampullary cashort duration (1-3months)
o Presence of systemic symptoms
 Fever
 Wt loss--Significant in periampullary ca.
o Symptoms of gastric stasis/GOO/
 Early satiety
 Vomiting
 Belching
o Anemia symptoms--Usually present in periampullary ca.
o Previous malignancy
o GI bleeding
o Hepatitis
o Known gallstone disease
o Previous biliary surgery
o Diabetes or diarrhea of recent onset
o alcohol, drugs & medications
DEBOL
ND
2 EDITION
 G/A
 V/S
 Signs of jaundice
o sclera
o skin
 Gall bladder may be palpable
 Courvoisier sign
 Suspect underlying pancreatic malignancy…
 Neoplasticsuggestive
o Look sign’s of wt loss, adenopathies & occult blood in the stool
o Malignancy is more cmnly associated with the absence of pain &
tenderness
 Signs of cirrhosis
 Ascites
 Collateral circulationGI bleeding
 Xanthomas
o PBC=primary biliary cirrhosis
 Excoriations
o Prolonged cholestasis /high grade biliary obstruction
DEBOL
ND
2 EDITION
DDx +Discussion
1st try to differentiate between obstructive jaundice & medical jaundice
Obstructive jaundice 20 to???
1) Choledocholithiasis(stone disease)
 Gall stone in CBD /cmn bile duct
 cmn20 to passage of stone from gall bladder to CBD
 10less cmn
 Asymptomatic/ 85%
 Symptomatic 
Pain is similar to billiary colic
 Usually with nausea and vomiting
 Usually intermittent
Complications of choledocholithiasis
Acute cholangitis
Charcot triad
1. RUQ pain
2. fever
3. jaundice Severe
Reynolds’
pentad
4. hypotension
5. altered mental status
Acute pancreatitis
painsevere steady sharp epigastric/mid-abdominal pain
Radiation to the back
Relieving factorleaning 4ward
N&V
Anorexia, diarrhea may be present
DEBOL
ND
2 EDITION
2) Periampullary carcinoma
I) Pancreatic ca.
 95% -exocrine portion
 75%-@ the pancreatic head & neck
Etiology+Risk Factors
 Sporadic40%
 Smoking30%
 Dietary factors5-10%
o Esp. red meat –processed kind
 Hereditary5-10%
 DM2X increased risk
 Underlying chronic pancreatitis<5%
 Alcoholnot independent RFs
 Industrial carcinogen exposure
i) History
 Significant wt loss
o Carcinoma associated, or
o Malabsorption from exocrine pancreas insufficiency
 Mid epigastric pain
o Radiation to mid/lower back may be present
o Unrelenting in nature—night time
 Onset of DM within the previous yrs
 Painless obstructive jaundice+ Pruritus
 Migratory thrombophlebitis (Trousseau sign) + venous thrombosis
ii) Physical Examination
 Palpable, non tender gall bladder
 Skin excoriations
 Developing, advanced intra-abdominal disease
o Ascites
o Palpable abd.mass
 Hepatomegally
 metastasis
 splenommegally
 portal venous obstruction
 …advanced
o sister mary joseph nodule
o virchow’s node
o blumer’s shelf also possiblepalpable rectal mass in rectal pouch
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2 EDITION
II) Cholangiocarcinoma
i) History
 jaundice
 clay-colored stools
 dark urinebilirubinemia
 pruritus
 wt loss…(variable)
 abdominal pain…dull ache in RUQ
 palpable gall bladder may be present
o Courvoisier sign
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2 EDITION
SAMPLE Hx 1 OJ 20 to ?periampullary ca.
C/C
Loss of consciousness of 1hr duration
HPI
This is a known DM pt for the past 10yrs on insulin injection, who claimed to be
adherent to his medication.
This pt was LRH 04 wks back @ which time he started to experience dark
colored urine & pale stool. 3 wks prior to admission he started to experience
itching sensation which began from his hands & progresses to include all the
body parts which especially worsens @ night. 2wks prior to admission his
families began to notice persistent light lemon to deep yellow discoloration
of his eyes. Associated with this he started to experience steady epigastric
pain without radiation or known aggravating/relieving factor. In addition he
started to experience low grade intermittent fever but no chills or rigor. 03 days
prior to admission he started to experience nausea & non blood tingled, non
bilious vomiting of ingested matter about 6X/day. For the above complaints he
visited a traditional healer where he was cauterized on his back. One hour prior
to admission he experienced LOC.
 Has hx of anorexia, easily fatigability & unquantified wt loss for the
past 1 month
 Has hx of tinnitus, blurring of vision & light headedness
 No hx of cigarette smoking or chronic alcohol consumption
 His regular dietary habit is “shiro” made of “atter” & “siga wot” by
“injera” made of “teff”
 No hx of similar illness in the family
 No hx of previous abdominal surgery
 No hx of MSP, contact with jaundiced pt or blood transfusion
 No hx of river water contact itching
 No hx of malarial attack for the past 1yr
 No hx of medication except the insulin injection explained above
 No hx of chronic cough, contact with chronic cougher or previous TB Rx
 No self/family hx of HTN or asthma. No family hx of DM
 He has been screened for RVI 1yrs back & found to be sero-negative
Finally, he was admitted to our hospital by ambulance.
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SAMPLE Hx 2 OJ 20 to cholidocholithiasis
C/C
Abdominal pain of 01yr duration
HPI
This pt was LRH 01yr back @ which time he began to experience severe
intermittent colicky right upper abdominal pain with radiation to the right
shoulder. The pain was aggravated while taking fatty meal but no relieving
factor noticed by the pt. 03 months prior to admission he started to experience
low grade intermittent fever but no chills & rigor. 01 month prior to admission
his families started to notice intermittent deep yellowish discoloration of the
eye. In addition he started to experience mild itching sensation all over the body
but no change in urine or stool color. For the above complaints he visited a
traditional healer repeatedly, where he was given herbal medication & got
cauterized. But he didn’t get any relief from his symptoms for which he came to
our hospital.
 He has hx of nausea but no vomiting
 No hx of LOC
 No hx of anorexia, easily fatigability or significant wt loss
 No hx of smoking or alcohol abuse
 No hx of MSP, contact with jaundice person or blood transfusion
 No hx of abdominal surgery
 No family hx of similar illness
 No hx of chronic cough or previous TB Rx but he has hx of contact with
known TB patient which was on medication.
 No self/family history of DM, HTN or asthma.
 He was screened for RVI 9 month back and found to be sero-negative
Finally he was admitted to our hospital…………
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Investigations
Lab.studies
o Serum bilirubin,ALP,transaminaes(AST,ALT), GGT
o PT
 Vit. K administration
 Hepatic failure/cholestasis?
o Hepatitis serology
o Anti-microbial Ab
o Urine bilirubin
o CBC—acute cholangitis
Imaging
o U/S
 Important for documenting stones in the gallbladder (if still
present) & determines size of CBD.
 Dilated CBD when >8mm in diameter
o Contrast CT-scan
o MRI
Cholangiography
o ERCP/endoscopic retrograde cholagiopancreatography
 Endoscopic cholangiographygold standard for Dxing CBD stones +
advantage of therapeutic options @ the time of Dx.
o PTC/ percutaneous transhepatic cholangiography
 Examination of liver and bile ducts by x-rays. This is accomplished by the
insertion of a thin needle into the liver carrying a contrast medium to
help to see blockage in liver and bile ducts.
*In both cases fluorescent fluids are used to create contrasts that make the diagnosis
possible
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2 EDITION
Mgt
1) cholidocolithiasis
 sphincterectomy & ductal clearance, followed by laparascopic clearance
or
 open CBD explorationcholedochotomyT-tube left in place
Complications If cholangitis…
 Stabilize patient with
 IV fluid resuscitation
 IV Antibiotics
 IV analgesia
 15% will not stabilize with conservative Mgt requiring
emergency decompression
If acute pancreatitis…
 Billiary pancreatitis
 Mgt
 Stabilize patients
 ERCP
 Cholecystectomy +/- CBD exploration
2) periampullary ca.
I) Pancreatic ca.
Palliative
 PainNarcotics, Celiac plexuse block
 Jaundice and pruritis
 Stenting
 Cholidochoduodenostomy
 Cholidochojejunostomy
 Cholecystojejunostomy
 Duodenal obstruction (20%)Prophylactic bypass in unresectable
disease is controversial
 Adjuvant theraphy Chemotheraphy (Gemcitabine), Radiotheraphy
Curative
 Surgical resection-whipple’s (with or without pylorus
sparing)
 Adjuvant theraphy
 Chemotheraphy
 Radiotheraphy
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II) cholangiocarcinoma
 Surgery is the only curative treatment
o > half patients have unresectable tumor on intraoperative finding
 billary decompression + cholecystectomy (to prevent cholecystitis)
o Unresectable perihilar tumorRoux-en-Y cholangiojejunostomy
 Distal bile duct tumors often resectable Pylorus preserving pancreatico-
duodenostomy
 No proven benefit of adjuvant chemotheraphy
 intraoperative radiation and external beam radiation for unresectable
tumor
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SAMPLE HISTORY ON LIVER ABSCESS
Liver abscess may be due to……Etiologic wise
1) Pyogenic liver abscess

Risk Factors
 Impaired bile drainage
o Biliary tract diseasecausing ascending cholangitis
 systemic bacteremiaHematogenous dissemination
o Subacute Endocarditis
o Infected indwelling catheter
o Pyelonephritis
 Local spread of infection
o like gangrenous cholecystitis, perforated ulcers and subphrenic
abscesses
o diverticulitis, Crohn’s diseasedirect extension to liver
 hepatic trauma
o penetratingDirect inoculation of microrganisms
o Bluntby causing localized hepatic necrosis + hemorrhage+bile leakage…
 May be b/ce of Complication of…
o Cholangiography, percutaneous transhepatic stents, endoscopic stent
placement, and biliary-enteric anastomosis
NB*
 EtiologyE.coli in 2/3 of cases
Clinical presentation
i) History
Usually sub-acute and nonspecific, leading to delay in presentation, Dx & Rx.
 RUQ painReferred pain to the right shoulder may be present
 Fever, chills
 Anorexia, malaise
 Yellowish discoloration of eyes & skin may present in 1/3rd
of pts
 Anemia of chronic disease
 Cough may be present due to diaphragmatic irritation
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NB**When abscesses are seen in children & adolescents, underlying immune
deficiency, severe malnutrition or trauma frequently exists.
 Tender hepatomegally
o Intercostal tenderness differentiate it from acute cholecystitis
o Palpable mass need not be present
 Decreased breath sounds in the rt. basilal lung zone may be present
 Pleural or hepatic friction rub may be present due to…
o Diaphragmatic irritation
o Inflammation of glisson capsule
 Jaundice may be present(1/3rd of pts) usually when associated with biliary
tract disease
Complications
 generalized sepsis
 Pleural effusions, Empyema, pneumonia.
 intraperitoneal rupture which is frequently fatal.
 Usually the abscess does not rupture, but develops a
controlled leak resulting in a perihepatic abscess.
 hemobilia /Hemorrhage in bile
 Hepatic vein thrombosis
Investigations
Lab. studies
o CBC=Leukocytosis
o Raised ESR
o Elevated ALP level
 Significant abnormality in the remaining LFTs are unusual
o Blood cultureonly in 50% of pts show the causative organism
Imaging
o Liver u/s
 What to look for abscess?
1. Round/ oval hypoechoic lesions
2. Well defined border
3. Variable no# of internal echoes
o CT-scan
 Hypodense with peripheral enhancement
 May contain air fluid level
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Mgt
Antibiotics
 Aminoglycoside + clindamycin + ampicillin/vancomycin.
 Fluoroquinolones can replace aminoglycosides, and
metronidazole can be used instead of clindamycin
 Duration=#02 weeks
Aspiration and Percutaneous Catheter Drainage
 Aspirationuseful in guiding subsequent antibiotic therapy
 Percutaneous catheter drainage is only beneficial for a minority
of pts
 Because most pyogenic abscesses are quite viscous
 Patients in whom percutaneous drainage is not appropriate
include…
 multiple large abscesses
 known intra-abdominal source that requires
surgery
 an abscess of unknown etiology
 Ascites
 abscesses that would require transpleural drainage
Surgical Drainage
 indications
 pts that have failed non-operative therapy
 those who need surgical Rx of the underlying source
 those with multiple macroscopic abscesses
 those on steroids
 those patients with concomitant ascites
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2) Amebic liver abscess
Risk Factors
 Low socioeconomic status and unsanitary conditions are significant
independent risk factors
 Contaminated food & water
 living or visiting an endemic area
 Presence of immunosuppression
NB*
 E. histolyticacausative organism
CPs
 May be acute with
o fever and right upper quadrant (RUQ) pain or
 sub-acute with
o Weight loss and less frequent fever and abdominal pain.
 The usual case of amebic liver abscess does not present with concurrent
colitis, but patients may have had dysentery within the last year.
Complications
 Peritonitis
 due to rupture in the majority and secondary to necrotizing
or perforated amebic colitis
 Thoracic amebiasis
 empyema, bronchohepatic fistulas, and pleuropulmonary
abscess
 If the abscess ruptures into the pleural cavity, it usually
occurs suddenly, collapsing the lung, filling up the pleural
space.
 If the abscess ruptures into the bronchi, this complication
causes sudden onset of coughing with expectoration of
copious brown sputum.
 Pericardial amebiasis
 acute pericarditis with tamponade
 Hematogenous spread to lung, brain, skin and genitourinary tract
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INVx
Lab. studies
 CBC=leukocytosis
 Mildly elevated ALP
 Serologic tests (fluorescent antibody test)can remain +ve after
clinical cure
Imaging
 Ultrasound, CT, and Magnetic resonance imaging (MRI) are all
excellent methods of detecting but are nonspecific.
Diagnostic Aspiration
 Usually done when amebic serologies are negative and a pyogenic
cause needs to be ruled out.
 The fluid of an amebic abscess is odorless, and Gram's stain and
cultures are negative.
 Aspiration should not be done if an echinococcal cyst or a cancer is
suspected.
Mgt
Antibiotics
o Metronidazole DOC750mg, tid #7-10days
Drainage
 Indications
 patients that have no clinical response to drug therapy within 5–7 days
 those with a high risk of abscess rupture (cavity >5 cm in diameter)
 The presence of lesions in the left lobebecause @ risk of rupture into
the pericardium
o Drainage may be by…
 PercutaneousImage-guided
 Procedure of choice for decreasing the size of an abscess.
 SurgicalIndications
1. abscesses that have failed to respond to more
conservative therapy
2. life-threatening hemorrhage
3. when the amebic abscess erodes into a neighboring
viscus
4. Sepsis due to a secondarily infected amebic abscess if
percutaneous treatment fails
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DDX
1) Biliary diseases
o Refer the topic on obstructive jaundice @ page110
2) Hepatocellular ca. (HCC)
Risk factors
 Hep. B & C infection
 Alcoholic cirrhosis
 Hemochromatosis….
CPs
Hx
 Dull, vague, right upper quadrant pain, sometimes referred to the
shoulder
 Constitutional symptoms of malignancy
 Yellow discolaration (50%)
 GI bleeding (10%)
o esophageal varices (50%)
 have an extraordinarily poor prognosis, with a median survival
measurable in weeks.
o intraportal thrombus
 which further increases the portal pressure and makes bleeding
varices more difficult to control
Nb*slow growing tumor but majority of patients present at an
advanced stage and most are beyond curative treatments
P/E
 G/Achronically sick looking, looks severely malnourished
 HEENTpale conjuctive, icteric sclera
 LGSLAP….check Virchow’s node
 Abdominal exam.
 Hepatomegaly nodular, irregular, hard
 Vascular bruit (25%)
 Signs of fluid collection
NB*
…Signs of decompensated liver disease
o Typical symptoms include ascites, jaundice (50%), or encephalopathy.
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INVx
o Imaging
 Abdominal u/s
 CT/MRI
o LabAFP>500ng/dl
o Metastatic work-up
Mgt
 Surgical resection but the majority of patients are not eligible because of
tumor extent or underlying liver dysfunction
 Other treatment modalities available…
o Liver transplantation
o Radiation therapy and stereotactic radiotherapy
o Systemic chemotherapy and molecularly targeted therapies
3) Hydatid cyst
 Parasitic infestationE.granulosus
RFs
 Hx of living or visiting an endemic area
 Ingestion of food or water contaminated by the definitive host
CPs
 CPs depend on
 the site, size, stage of development,
o SiteLiver(63%) & lung (25%)
 whether the cyst is alive or dead, and
 whether the cyst is infected or not.
 Initiallynon-specific…RUQ/ epigastric pain, cough, low-grade
fever & sensation of abd. fullness
 Mass/pressure effectlong time
 liver
o Symptoms of obstructive jaundice & abd. pain
o Biliary ruptureBiliary colic, jaundice & uticaria
 Lung involvementChronic cough, dyspnea, pleuritic
chest pain & hemoptysis
 Cerebral involvementHeadache, dizziness & decreased
level of consciousness
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INVx
 Serology
o Determination of specific antigens and immune complexes of the cyst
with ELISA
 Imaging
o Ultrasound and CTClassic findings include calcified thick walls, often
with daughter cysts.
 Ultrasound defines the internal structure, number, and location of the cysts
and the presence of complications.
 Computed tomography gives more specific information about the location
and depth of the cyst within the liver.
 ERCP
o show communication between the cysts and bile ducts
o Can be used to drain the billiary tree before surgery.
Mgt
 Most are asymptomatic on presentation, but complications such as
o pulmonary infection, cholangitis, rupture, and anaphylaxis give good
reason to consider treatment for all.
 Basic principles of treatment are…
 eradication of the parasite within the cyst
 protection of the host against spillage of scoleces
 management of complications
 The Rx may be…
 Medical
 Anthelmintics
 percutaneous aspiration & drainage
 surgical
Other DDx
Pneumonia, bacterial
Empyema ( pleuropulmonary)
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SAMPLE Hx
C/C
Right upper abdominal pain of 04 months duration
HPI
This pt was LRH 04 months back @ which time he started to experience gradual
onset constant dull aching type right upper abdominal pain with radiation to the
lower back & inter scapular region without known aggravating or relieving
factor noticed by the pt. Associated with this he has low grade intermittent
fever, loss of appetite & nausea but no vomiting, diarrhea or constipation. In
addition he has easily fatigability & significant wt loss abt 8kg for the past
04months. 03 months prior to the re-admission he started to experience tinnitus
& light headedness but no blurring of vision. 01 month prior to the re-admission
his wife noticed yellowish discoloration of his eyes but no itching sensation,
urine or stool color change. For the above complaints he visited a nearby health
center in ‘Chilga’ where he was given #04 drugs; red & yellow circular, white
oval & omeprazole, each to be taken 2X/day for 10days. He kept visiting the
health center repeatedly but he didn’t get relief from his pain. Finally, # 01
month prior to the re-admission he was referred from the LHC to our hospital for
better investigation & mgt. After admission to our hospital, aspiration was
taken from his right upper abdomen. Then he was discharged with
metronidazole to be taken 3X/day, 3@ once for 10 days & he was given
appointment for follow-up. But 20 days prior to admission the pt discontinues
the medication complaining of no improvement by medical Rx & he went to was
a traditional healer & cautherized on both arms & @ the back of his neck.
 He has no hx contact with jaundiced person, blood transfusion or MSP
(hepatitis)
 He used to drink local ‘areke’ up to 50gm/day for > 20 yrs (HCC-RF)
 He has no hx of cough, hemoptysis or bone pain (HCC-metastasis)
 He has hx of palpitation but no dyspnea , orthopnea, PND or lower leg
swelling
 He has no hx of abdominal trauma or surgery (inoculation or blunt)
 He has no hx of contact with chronic cougher or previous TB Rx
 No self or family hx of DM, HTN, asthma
 He has been Screened for RVI 3yrs back & found to be non reactive
Finally he was admitted to our hospital supported by his
families.
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INVx
See the INVx on the discussion under etiologic wise classification & the
DDx.
Mgt
See the mgt on the discussion under etiologic wise classification & the
DDx.
NB*the above pt in the sample hx was finally Dxed to have HCC.
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SAMPLE HISTORY ON FRACTURE
Causes
 Traumatic fracture
o Motor vehicle accidents (MVA)
o Gunshot injuries
o Blast & bomb injuries
o Assaults
 stone, knife, sickle, axe, stick
o Fall down injuries
o Burn
 Stress fractures
 Pathologic fracture
i) History
Write…
 Mechanism of injury (MOI)
 MVA
 Gunshot injury
 Blast & bomb injury
 Stone, knife, sickle, axe or stick assault
 Fall down injury…
 Time of injury (duration)
 Injury Site
 Write the site…
 In case of gunshot injurywrite the entry & exit point of the
bullet
 If there is bleeding or pooling of blood @ the scene (estimated)…
 Degree of violence
 MVA
 Speed of the vehicle
 Crush/not
 Was there external damage to the vehicle, such as deformation
to the front from Head-on collision?
 It raises suspicion of hip dislocation…
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 Pedestrian/passenger
 If passenger
o Pre-crash
 What was the pre-crash location of the pt?
 It can tell us the type of #
o E.g. lateral compression # of the
pelvis from a side impact in vehicle
collision
 Was the pt wearing seat belt/not?
o Post-crash
 What was the post-crash location?
 Inside or ejected?
o If ejecteddistance thrown & landing
condition…
 Was the pt crushed by an object?
 If so, site+weight+duration…
 Gun shot
 Distance of shooting
 Type of gun
 Fall down
 Height or depth of fall
 Landing condition
 Blast & bomb injury
 What was the pts distance from the blast?
 Primary blast injury Vs secondary (from the blast
effectaccelerated debris or objects)
 Change in limb function
 Is the pt able to use the injured limb/not?
 Concomitant injury
 Head injury
 Hx of Loss of consciousness
 Abnormal body mov’t
 Spinal cord injury
 Urine or fecal incontinence or unable to void
 Bladder injury
 Hematuria, suprapubic pain & difficulty of voiding
 As with all trauma patients, documenting any available history regarding pre-existing
medical conditions, medication and drug allergies will be useful…
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 Before taking Hx & doing P/E in traumatic patientyou should first apply
ATLS primary survey (“ABCDE”)
Check the “ABCDE” & act accordingly…
o A=airway
o B=breathing
o C=circulation
o D=neurological examination
o E=exposure
 Hx, P/E ,INVx & Definitive mgt are part of ATLS secondary survey
*See page 242…MSS examination
Signs of fracture (P/E)
Definitive Unspecific
- Deformity - swelling
- Abnormal movement - tenderness
- Crepitus
- Visible fractured bone
Complications of fracture
1. Delayed union(if > 4month)
2. Non-union (if > 6month)
- Tests of union
i. Clinical
1. Absence of mobility between fragments
2. Absence of tenderness on firm palpation
3. Absence of pain when angulation stress is applied
ii. Radiological
1. Visible callus bridging the fracture & blending with both
fragmentsearlyreliable
2. Continuity of the bone trabeculae across the fracture
*Causes of delayed union & non-union
- Inappropriate immobilization
- Infection
- Bone loss
- Soft tissue interposition
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3. Mal-union
- Overlapped or
- Angulated
4. Shortening
- Significant when >2cms
- Causes
i. Malunion
ii. Actual bone loss or crushing
iii. Interference with growth plate (in children)
5. Avascular necrosis
- Death of bone due to deficient blood supply
- Cmn sites
i. Head of the femur after femoral neck fracture/hip dislocation
ii. Proximal half of Scaphoid bone
iii. Body of talus
6. Infection
- Virtually confined to open fractures
- (*See page 226 on bone infection)
7. Neuro-vascular injuries
- Nerves—e.g.
i. Humerus--Radial nervewrist drop
ii. Knee--Common peroneal nervefoot drop
iii. …
- Vascular—e.g.
i. Shoulder dislocation—axillary artery
ii. Supracondylar fracture of humerus/elbow dislocation--Brachial artery
iii. Knee dislocation/proximal tibial fracture --Popliteal artery
8. Compartment syndrome
- Signs(the 6 Ps)
1. Pain 5. Paralysis
2. Pallor 6. Perishingly
3. Pulselessness (extremely)
4. Paresthesia cold
- Cmn sites
i. Lower leg iv. Hand
ii. Forearm v. Gluteal region
iii. Foot vi. Thigh…
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9. Pulmonary complications…
 E.g. Fat embolism
NB*Normal repair of tubular bone has five stages

a. Stage of hematoma
b. Stage of cellular perforation
c. Stage of callus
d. Stage of consolidation
e. Remodeling
NB*generally fracture is classified as Closed or Open based on its
communication to its external environment.
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SAMPLE Hx
C/C
Bullet injury of 02 hours duration
HPI
This patient was apparently healthy 02hours back @ which time he sustained a
bullet injury to his left leg from about 2 meters distance by a known
offender (his neighbour) on land dispute. The bullet entered around his left
knee anteriorly & exited on lateral side of his left thigh. Since then he
completely failed to use his left leg. He has bleeding, swelling & persistent
severe pain from the site of injury.
 No hx of loss of consiousness
 No hx of trauma to other sites
 No hx of tinnitus, vertigo or blurring of vision
 No hx of headache, vomiting or abnormal body movement(ask u
suspect head injury)
 No hx of urine or fecal incontinence (ask if u suspect spinal injury)
 No hx of lower abdominal pain or reddish discoloration of
urine(ask if u suspect bladder trauma)
 No hx of breathlessness or confussion (if u suspect chest injury)
 No self/family hx of DM ,HTN or Asthma
 Not screened for RVI but has no chronic diarrhea, HZA or MSP.
Finally he was admitted to our hospital carried by

his families
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Investigations
1. Imaging
A.X-ray
i. Antero-posterior (AP)
ii. Lateral
Should Answer….
 Traumatic Vs Fatigue Vs pathologic fracture
 Displaced or not
 If displaced, in which direction
 Alignment of the fragments, satisfactory or not
 Recent fracture or not
o If notevidences of union may be there
 Associated injury
 To adjacent joints or bones
NB* Patterns of fracture

1. Transverse
2. Oblique
3. Spiral
4. Comminuted(>2 fragments)
5. Compression (crush)
6. Green stick (peculiar to children)incomplete fracture
…This patterns may indicate
 Nature of causative violence
o Important for choosing easiest method of reduction
 The likely stability of fragments after reduction
B. CT-scan
C. Angiography
D.Arthroscopy
2. Lab.
A. Hct…
Management
*See mgt of fracture on page…221
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SAMPLE HISTORY ON HEAD INJURY
 Normal intracranial contents are…
 Brain tissue
 CSF &
 Arterial and venous blood
 Monro-kellie doctrine
o States that the total volume of the intracranial contents must remain constant.
 Why?
 Because the cranium is a rigid, non-expansible container.
 Total volume=Brain tissue +CSF fluid + intravascular blood
 Venous blood & CSF fluid may be displaced out of the container to
provide pressure buffering by keeping the total volume constant.
 So early after injury the pt may have normal ICP, but once the limit
of displacement reachedICP rapidly increases.
 Classification of head injury
 Based on GCS
• Mild head injury
 GCS=13-15
• Moderate head injury
 GCS=9–12
• Severe head injury
 GCS=3–8
 Based on type of injury
 Blunt
 Penetrating
o High velocitylike gunshot injury
o Low velocitylike stab injury
Scalp injury
 Highly vascularizedsignificant blood loss can occur
 Mgt
o Direct pressure initially controls the bleeding, allowing close inspection to the
injury
o Simple lacerationcopiously irrigate & close primarily
o Lacerationshort, a single layerpercutaneous suture
o Lacerationlong or has multiple arms debridement & closure in OR
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Skull fracture
 Based on site
 Skull vault fracture
 Open Vs Closed
 Closed # do not normally require specific Rx
 Open # require repair of the scalp & operative debridement
 Linear Vs comminuted
 Depressed Vs non-depressed
Indications for craniotomy
 Depression if greater than cranial thickness
o To elevate the #, repair dural disruption & hemostasis
 Intracranial hematoma
 Frontal sinus involvement
 Skull base fracture
 May or may not be associated with CSF rhinorrhoea, otorrhoea or cranial
nerve palsy.
 CSF leakelevation of head off the bed for several days may
heal it. Inaddition lumbar drain can augment this method.
 Lumbar drain=allow the defect to heal by eliminating
normal hydrostatic pressure.
 Traumatic cranial neuropathy
 Facial nerve palsysteroids
 If no response after 48-72hrssurgical
decompression of the petrous portion of CN-VII
may be considered
 Anosmia (CN-I damageloss of smell)
 Battle’s sign (bruising over the mastoid process)
 Raccoon eyes (bilateral periorbital bruising)
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Traumatic brain injury (TBI)—closed head injury
 Primary brain injuryoccurs @ the time of impact and includes
injuries such as …
 brainstem and hemispheric contusions
 diffuse axonal injury &
 Cortical lacerations
 Secondary brain injury occurs @ some time after the moment
of impact and is often preventable. The causes of secondary brain injury
include…
 hypoxia
 hypotensionSBP <90mmHg
 raised ICPICP >20mmHg
 reduced cerebral perfusion pressure
 cerebral perfusion pressure (CPP)= mean arterial pressure (MAP) – ICP
o So, CPP will be reduced if low MAP or high ICP
o In order to maintain the CPP we have to control not only rise
in ICP but also decline in MAP (i.e. hypotension)
 metabolic disturbances
 pyrexia
 Types of closed head injury
o Concussion
 A temporary neuronal dysfunction following non-penetrating head
trauma
 CT-Scan=normal
 Deficit resolve over minutes to hrs
o Contusion
 A bruise in the brain
 Mechanism
 either coup (at the point of impact) or
 countre-coup (on the other side of the head) or
 as the brain slides forwards and backwards over the ridged cranial
fossa floor
 cmnly affected sites
 frontal, occipital and temporal poles
 Edema may developmass effect
 CT-scan= contused areas appear bright
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o Traumatic intracranial hematomas
 May be…
 Extradural hematoma
o Cmn sitetemporal bone--the pterion
 the thinnest part of the skull + overlies the largest
meningeal artery
 Subdural hematoma
 Acute Vs Chronic
o Acute SDH--Due to disruption of a cortical vessel
(venous)accumulation
o Chronic SDH—collection of blood break down products
that is @least 2-3wks old
 Intraparenchymal hemorrhage
 Most often associated with
o HTNsive hemorrhage
o AV malformation
 In traumatic one--bleeding may occur from the contused
areamass effect…
Initial steps in head injuryas in all trauma ptsATLS

o Primary survey & resuscitation
 “ABCDE” of life
 D=Disability…
 pupillary size & reactivity
 GCS
 Presence of focal neurological deficit
…Consider cervical spine injury before 20 survey…
o Then…Secondary survey
 Hx, P/E, INVx & Definitive mgt
 see below for secondary survey components
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1) History
 MOI
 MVA
o Collisions between vehicles
o Pedestrians stuck by motor vehicle
o Bicycle accidents…
 Fall down injury
 gunshot
 Assaults
 Sport related injuries…
 Hx of LOC
o Was the patient responding, moving and talking appropriately after
the incident? …GCS @ the scene
NB*
A head injury with LOC but no clear accidental mechanism of injury…you
should think of non-accidental causes of collapse, such as…
 Syncope, Aneurysmal subarachnoid haemorrhage, medical conditions
(such as hypoglycaemia)
 Hx seizure activity at the scene
 Hx of forgetfulness for events after the injury or preceding the injury
 Amnesia (may be antegrade or retrograde)
 As with all trauma patients, the following should be asked…
 Medical hx
 Medication and drug allergies
o In particular, the use of medications such as anti-coagulants or
anti-platelet drugs will be relevant to a patient with an
intracranial haematoma.
 Hx of prior head injuries
 Is there history of alcohol or illicit drug use?
 remote/active
 carefully consider past psychiatric disease & pre-morbid hx of headaches
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2) Physical examination
 G/A
 V/S
 HEENT
 Head
 Inspect
 There may be evidence of external head injury such as
subgaleal haematoma or scalp laceration…
o Which may be a cause of significant external blood loss
 Palpation of a scalp laceration
 May reveal an underlying skull fracture with or without
a CSF leak
 On HEENTLook for clinical evidence of skull base fracture
 Head= Battle’s sign
 Ear= CSF otorrhea
 Eye= Raccoon eyes
 Nose=CSF rhinorrhea, haemotympanum or active bleeding
 Nervous system examination
 GCS
 Eyes opening (E)
 Spontaneously 4
 To verbal command 3
 To painful stimulus 2
 Do not open 1
 Verbal (V)
 Normal oriented conversation5
 Confused 4
 Inappropriate/words only 3
 Sounds only 2
 No sounds 1
 Intubated patient T
 Motor (M)
 Obeys commands 6
 Localises to pain 5
 Withdrawal/flexion 4
 Abnormal flexion (decorticate)3
 Extension (decerebrate) 2
 No motor response 1
DEBOL *Write it like…GCS=15/15 (E4, V5, M6)

How to take Hx in surgery+++QUICK REVISIONNB*theGCMHS
lowest score is 3/15 Page 144
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 MMSE…
 Cranial nerve examination—focus on…
 Pupillary size & reactivity
 Asymmetrical sluggish responsemay suggest partial third
nerve dysfunction on that side
o implying uncal herniation as a result of a mass on the
ipsilateral side of sluggish pupil
 As the third nerve becomes increasingly compromised the
ipsilateral pupil will become fixed and dilated.
 Anosmia (CN-I)
 Associated with rhinorrheathis pts are @ risk of ascending
meningitis
 CN VI palsy
 Raised ICP
 CN VII & VIII palsy
 Basal skull fracture
 A peripheral nerve examination should record…
o Muscle tone
o Muscle strength
o reflexes &
o sensory loss
Clinical presentation based on the underlying mechanism….

Extradural hematoma pts
 CPs
 Typical presentation
 Initially unconscious
 Then awaken & has lucid interval when the patient
complains of a headache but is fully alert and
orientated with no focal deficit
 After minutes or hrsa rapid deterioration occurs, with
o contralateral hemiparesis,
o reduced conscious level and
o ipsilateral pupillary dilatation as a result of brain
compression and herniation.
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Subdural hematoma pts
 Acute SDH
 Due to brain atrophy, elderly & alcoholics are @ high risk
 CPs
 present with an impaired conscious level from the time of
injury, but further deterioration can occur as the hematoma
expands
 Chronic SDH
 usually occur in alcoholics, the elderly and in those pts on
anti-coagulant/anti-platelet agents
 usually but not always a history of minor head injury in the
weeks or months prior to presentation
 CPs
 Headache, seizures, cognitive decline, focal neurological
deficits, or coma.
 It is important to exclude hypoxic, metabolic and endocrine
disorders in this group of patients
Long term complications of head injury
 neuropsychology
o Post-concussional symptoms include
 headache, dizziness
 impaired short-term memory and concentration
 easy fatigability, emotional disinhibition and depression
 Seizures
 Delayed CSF leak
NB***
1) Symptoms of raised ICP
a. Projectile Vomiting
b. Headache
Classically…a morning headache which may wake the pt from sleep…worsen by coughing /
sneezing, bending & progressively worsens over time…
c. Seizure
d. Decreased consciousness…
2) Signs of raised ICP
a. Papilledema (swelling of optic disc)
b. CN VI palsy
c. Lateralizing signs
d. Cushing’s triad
i. BP=increased systolic blood pressure
ii. PR=widened pulse pressure, bradycardia, and
iii. RR=an abnormal respiratory pattern
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SAMPLE Hx
C/C
Axe injury of #10 hrs duration
HPI
This Patient was last relatively healthy #10 hrs back at that time she sustained
an axe attack to the head & distal forearm by a known offender, her
psychiatric brother in law. She was attacked 02 times; one left side of the head
and the other on the right distal part of her forearm. After the injury she
immediately lost her consciousness. She was found falling on cement floor
by her mother immediately after the attack. They took her to local health center
where they try to stop the bleeding by wound dressing and referred her to our
hospital for better mgt & INVx. 01 hrs prior to admission she gained her
consciousness, while she was on the way to our hospital. She was totally
unable to use her right upper extremity. In addition she experienced 02
episodes of projectile, bilious vomiting on her arrival to our hospital &
throbbing type of generalized headache which worsen during bending. The
only thing she remembered about accident was running & trying to escape from
the attacker but no hx of forgetfulness for events that happened before the
accident or those events after she re-gained her consciousness. She has
tinnitus, blurring of vision & light headedness.
 No hx of failure to use the extremities except the injured one (localizing sign--
ICP)
 No hx of watery or bloody discharge from the ear or nose.(oto/rhinorrhea +
bleeding from earbasal skull fracture)
 She has no hx of urine or fecal incontinence (spinal injury)
 She has no hx of breathlessness, confusion or chest pain (chest injury+peural.
effusion)
 No hx of abnormal body mov’t
 No hx previous headache of head trauma
 No hx of illicit drug use or alcohol abuse
 No self and family hx of DM, HTN or asthma
 Not screened for RVI but has no hx of chronic diarrhea, MSP or HZA.
Finally she was admitted to our hospital carried by an

ambulance.
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Investigations
Imaging studies
a. Skull x-ray
o AP & lateral
b. CT-scan
What to look on CT-scan?
Extradural hematoma
1. hyperdense (bright) lesion
2. lentiform (lens-shaped or biconvex)
3. well defined border (between the skull and brain)
4. may or may not cross the midline
Subdural hematoma
o Acute SDH
1. Hyperdense (acute blood)
2. crescent shaped (lunate)
3. may have less distinct border
4. doesn’t cross midline
o Chronic SDH
1. Variable appearance
a. Acute blood (up to 3dys)--hyperdense
b. Subacute blood—isodense relative to brain
c. Chronic (>2wks)—hypodense
d. Acute-on-chronic SDH
c. MRI
Lab. studies
o Na, Mg level
o PT, PTT, platelet count
o RFT
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Mgt
Mild head injury
 Criteria for discharge
 Pt must have GCS=15/15 with no focal neurological deficit
 verbal and written head injury advice must be given to the pt and pt’s
attendant
 advice to return when the pt experiences persistent or worsening headache
despite analgesia, persistent vomiting, drowsiness, visual disturbance such
as double or blurred vision, and development of weakness or numbness in
the limbs.
Moderate to severe head injury
 Aim of the mgt
 To prevent secondary brain injury
 The cervical spine must be immobilized
 Cerebral contusions mgt
 admit for observation
 because these lesions will tend to mature and expand
48–72 hours following injury
 rarely requires emergent evacuation
 some pts may require delayed evacuation to reduce mass
effect
 Extradural (epidural) haematoma mgt
 neurosurgical emergency
 immediate surgical evacuation via craniotomy & hemostasis
 Subdural haematoma mgt
 Acute SDH
 Evacuation via craniotomy
o Indication
 Thickness >1cm
 Midline shift >5mm
 GCS drop > or =2 from the time of injury to
hospitalization
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 Chronic SDH
 Indication for drainage
o Chronic SDH >1cm or
o Symptomatic pt
 Evacuation via burr hole(s)
 Intraparenchymal hemorrhage
 Pts with contusion on the initial CT-scan should be reimaged 24
hrs after the trauma
 Indication for craniotomy
 Any clot volume >50cm3
 clot volume >20cm3 with
o neurologic deterioration (GCS=6-8) &
o midline shift >5mm or basal cistern compression
Medical mgt of raised ICP

 Position head up 300
 Avoid obstruction of venous drainage from headcheck the collar
 Sedation +/– muscle relaxant
 Normocapnia
 Diuretics:furosemide,mannitol
 Seizure control
 Normothermia
 Sodium balance
 Barbiturates
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SAMPLE HISTORY ON ESOPHAGEAL CA.
By-Eyasu Feleke (sms)
Risk factors
 Hereditary factors
 Cigarette smoking
 Chronic alcohol exposure
o >30 gm/day  for non-smokers and >15 gm/day for smokers
 High BMI especially those with central obesity(> 25 kg/m2 )
 GERD and associated Barrett esophagus
 Diet
o Drinking scalding hot liquids
o Vitamin deficiency (e.g. Riboflavin )
o Certain food staff e.g. betel quid and areca nuts
o Zink deficiency & low selenium level
 Underlying esophageal diseases like achalasia, caustic stricture
 Infectious conditions
o HPV infection(serotype 16 & 18)
o H. pylori infection
 Prior gastrectomy
 Atrophic gastritis
 Tylosis
NB*
 SCC accounts for the majority of esophageal ca. followed by
adenocarcinoma.
 SCC is cmn in middle 1/3 & adenocarcinoma is cmn in the lower 1/3
 More common in men than women (men: women  3-4: 1)
 Occurs at the age of 6th and 7th decade
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1. History
 Dysphagia
o most common presentation
o Initially for solid foods eventually progressing to include liquid food
 Weight loss (2nd most common)
 Bleeding (from the tumor)
 Epigastric or retrosternal pain
 Bone pain(with metastasis)
 Hoarseness of voice(with RLN infiltration)
 Respiratory symptoms(due to invasion or aspiration)
 Persistent cough
2. Physical Examination
 Typically, normal examination results unless the cancer has metastasized
 G/A
o may look chronically sick (with cachexia)
 HEENT
o signs of anemia and metastasis
o look for signs of aero-digestive neoplasia (malignancy of the mouth
& throat)
 LAP in the lateral cervical or supraclavicular areas (esp. Virchow’s nodes)
 Chest finding (in case of metastasis)
 CVS
o Ejection systolic murmur, gallophigh output failure
 Abd. Examination
o Hepatomegaly (if liver metastasis),
o signs of fluid collection
DDx
1. Esophageal Stricture
 majority of the strictures result from long-standing
gastroesophageal reflux
 Rx usually involves dilation combined with acid-suppressive
therapy
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2. Benign esophageal tumors
 Esophageal leiomyoma (accounts for > 50%)
3. Achalasia
 Is characterized by
o Aperistalsis
o Partial or incomplete relaxation of the LES
o Increased resting tone of the LES
 Pathogenesis
o 10  poorly understood
o 20 chagas disease  trypanosome cruzi  distraction of
myoenteric plexuses
o Other causes  DM, polio, sarcoidosis, amyloidosis,
malignancy and caustic stricture.
 Clinical feature
o Similar to that of SCC of the esophagus
o Sensation of food sticking in the lower esophagus
o Nocturnal cough
o Retrosternal Chest pain induced by eating
4. Gastric cancer
 Most pts with gastric ca are symptomatic and already have
advanced incurable disease at the time of presentation
 Clinical features
o Wt. loss and persistent abdominal pain are the most common
symptoms at initial diagnosis.
o Read more on gastric ca @ page 55
5. Esophageal perforation
 Most esophageal perforations are iatrogenic (59 %)
 Causes of non-iatrogenic esophageal perforation is
1. spontaneous rupture 15 % (Most common cause)
2. foreign body ingestion 12 %
3. trauma 9% and
4. malignancy
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SAMPLE Hx
C/C
Difficulty of swallowing of 6 months duration
HPI
This patient was LRH six months back @ which time he began to experience
difficulty of swallowing initially for solid foods like ‘injera’ and bread but latter it
progressed to liquid foods like juice with non-radiating aching type of
retrosternal pain with no known aggravating or relieving factor. Associated with
this he also have unquantified weight loss to the extent his trousers became
loose but no cough, night sweating, fever, chills or rigors. He also has history of
easily fatigability at minimal exertion, tinnitus and light headedness for the past
3 months.
Since 6 years back he had been having retrosternal pain and also epigastric pain
for which compliant he visited our hospital and told to have peptic ulcer disease
and was given 3 unspecified but different tablets to be taken twice a day for 14
days; but no history of hematemesis.
 He has hx of chronic alcohol intake of 20gm/day for the past 25 years but
no hx of smoking.
 He has usually eats “Ingera” made of “Teff” with “Shiro wot” and “Key
wot”, sometimes row meat and occasionally packed refined foods.
 He has no hx of radiation therapy of the neck or chest.
 He has no hx of multiple sexual partners (RFHPV).
 He has no hx of drug use other than mentioned above.
 He has no hx of previous surgery.
 He has no hx of similar illness in the family.
 He has no hx of bone pain, swelling over chest or the neck, axillae or
groin.
 He has no hx of change in voice or voice fatigue.
 He has no hx of cough, dyspnea or hemoptysis.
 He has no hx of vomiting, diarrhea or hematochesia.
 He has no self or family hx of DM, HTN or Asthma.
 He was screened for RVI and found to be non-reactive.
Finally he was admitted to this hospital walking by
himself.
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Investigations
 Esophagoscopy
o to visualize growth and take biopsy.
 Ultrasound
o Endoscopic ultrasound is the most sensitive for determining
 Depth of penetration (T  staging)
 Presence of enlarged periesophageal lymph nodes (N 
staging)
 Barium swallow
o Very sensitive for detecting strictures and intraluminal mass
o Detect mucosal irregularities and filling defects
o Helps to study the distal anatomy in obstructing tumors that are
not accessible for endoscopy
o Does not allow staging or biopsy
 Bronchoscopy
o To exclude invasion of the trachea or bronchus (for ca. of the upper
& middle 1/3 esophagus)
 PET scan
o Detect occult distant lymph node metastasis & bone spread
 Esophageal Monometry
o Measures the motility and function of the esophagus and
esophageal sphincter.
o The pressure of the sphincter and contraction waves is recorded.
 Chest x-ray to
o Rule out aspiration pneumonia
o Mediastinal widening or posterior tracheal indentation
 Baseline investigations
o CBC, Urinalysis, Serum electrolyte, FBS
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Mgt
Rx plan depends on the following
 Staging : nearby structures involvement,  Surgery:

lymph nodes involvement , other o Transhiatal
organs o Rt. Thoracotomy (Ivor –
 Cancer location within the esophagus Lewis)
 General health of the patient o Lt. thoracotomy
o Radical – En – Block
Treatment options  Chemotherapy
 Endoscopic Mucosal Resection o Cisplatin, 5-FU, Paclitaxel,
(EMR) and Anthracyclines
  Radiotherapy (relieving dysphagia )
 Combined-modality therapy
 Palliative Therapy
 Laser
 Phototherapy
 Stent
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APPENDICEAL MASS
By-Elshaday Amare(sms)
Right iliac fossa mass DDx
1. Parietal swellingsbecome more prominent on head or leg raising test
a. Parietal wall abscess
 Pyogenic that occurs in hematoma or pyaemic
abscess in DM pts
 Tender(very), warm surface with fever, chills &
rigor
b. Desmoids tumor
 Unencapsulated fibroma
 In multiparous(repeated stretching of abd. Wall),
abd.wall injury (e.g. laparatomy)
 Firm to hard in consistency
 Rxno capsule..so, wide excision followed by
reconstruction by using mesh
2. Intra-abdominal swellings
a. From normal structures
i. From intestine
1. Appendicular mass
 Tender, soft to firm
 48-72hrs after appendicitis (see below for
appendicitis)
 Consists of omentum, terminal ileum, caecum,
with pericaecal fat & inflammatory edema
 Rxconseratively by oshner-sherren’s regime.
Because attempt to remove the appendix may
result in fecal fistula
 6-8wks lateappendicectomy
2. Appendicular abscess
 Very tender, firm, fixed
 Fever chills & rigor
3. Ileocaecal TB
 Chronic, non-tender, firm, nodular, may have
mobility & slightly higher side (lumbar area)
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 Features of TB are present
 Rxlimited resection followed by ileocolic
anastomosis
4. Carcinoma caecum
 More in females, 40-50yrs
 Bleeding per rectum, severe anemia
 Hard, irregular,fixity/restricted mobility
 Psoas spasmindicate infiltration
 RxRt.radical hemicolectomy
5. Ameboma
 Tender, soft to firm
6. Intussusceptions
 Tender soft to firm
 For detailed info read @ page 61
7. Actinomycosis
 Rare, 2-3months after appendicectomy
 Hard, indurated, tender mass with multiple
sinuses
 Unlike TBno narrowing of gut lumen & LN
enargement
ii. From LNs
1. Acute lymphadenitis
2. Lymphoma
3. Secondaries
iii. Retroperitoneal structures
1. Sarcoma
 Cmn in young
 Huge, nodular, fixed(to the posterior abd. Wall),
edema of legs (IVC obstruction), hydronephrosis
(pressure on ureter)
 Rxwide excision then radio/chemotherapy
2. Aneurysm
 Ileac arteryrare, in older age pts
 Soft pulsatile, bruit & thrill
3. Iliopsoas abscess
 TB of thoracolumbar spine
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 Young…back pain referred to abd. Wall
 Spine mov’t limited, Gibbus
 Dxcross fluctuation test
 Fluctuation present on both sides of
inguinal ligament
4. Chondrosarchoma of ileac crest
 Hard, fixed…can’t be separated from the bone
iv. In females
1. Ovarian cyst
 Smooth surface, round border, cystic, freely
mobile & can be pushed back to pelvis
2. Fibroid of uterus
 Firm to hard, nodular
3. Tobo-ovarian mass
 Tender, soft to firm, can be bilateral,pelvic
infection present
b. From abnormal structures
i. Undescended kidney
 Lobular mass
ii. Normal mobile kidney
 Can be pushed into the loin
iii. Undescended testis (seminoma)
 Hard, irregular, fixed, abscent testis in scrotum
 Para-aortic & supraclavicular LAP
Note on Acute appendicitis
 Peak in teens & early 20’s
Etiology +RFs
o Extremes of age
o Diet
 Reduced dietary fiber & increase refined CHO intake
o Obstruction by faecalith (calcium +PO4+bacteria+epithelial
derbis) or strictures
o Obstruction by carcinoma of caecum (middle age & elderly)
o DM
o Pelvic appendix
o Previous abd. Surgery
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CPs
HX
o Poorly localized colicky abdominal pain
o Pain 1st noticed in the peri-umblical area associated with
anorexia, nausea & vomiting
o Then the pain shift to the right iliac fossa
o Cough & sudden mov’t exacerbate the pain
o Atypical
 Predominantly somatic or visceral & poorly localized
(elderly)
 Inflamed appendix in the pelvis never produce pain in
abdominal wall instead supra-pubic discomfort &
tenesmus with tenderness on DRE.
P/E
o Low grade pyrexia
o Localized abdominal tenderness
o Muscle guarding, rebound tenderness
o Limitation of respiratory mov’t in lower abdomen
o Mc Burney’s pt=point of maximum tenderness
 1/3 from ASIS & 2/3 from umblicus
 Point sign
o pt is asked to point where pain began & where it
moved
 Rovsing’s sign
o deep palpation of Lt iliac fossapain in Rt iliac fossa
 Psoas sign
o pt lie with right hip flexed for pain relief
 Obturator sign
o hip is flexed & internally rotated pain in
hypogastrium
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Sample case for report (Hx & P/E)
History
ID
Here is Ato Mamo Lakew a 55 years old male married orthodox xtn farmer from koladba
admitted to GUH department of surgery ,surgical ward, bed no# 20 on Miazia 20/2009 e.c
Previous Admission
None
C/C
Difficulty of urination of 06 months duration
HPI
This patient was last relatively healthy 06 months back at which time he started to
experience difficulty of urination associated with straining to initiate & maintain his
urination. In addition he started to experience urgency & frequency of urination with D:N
ratio of 10 to 6 which made his bed time difficult. He has also a feeling of incomplete voiding
& post micturation dribbling.
1 month back he was totally unable to pass urine after drinking about 1 & ½ Liters of local
tella on a social gathering. On the next day he visited our hospital & he was catheterized
which enable him to urinate.
10days prior to admission he returned on the appointed date for catheter replacement & his
catheter was changed. Currently he presented with total failure to pass urine of 01 day
duration after he removed the second catheter because he felt discomfort.
 No hx reddish discoloration of urine, bone pain
 No hx of anorexia, easily fatigability or significant wt loss
 No hx of cigarette smoking, radiation therapy, previous medical Rx
 Has hx of river water contact but can’t recall post RWC itching
 No family hx of similar illness
 No hx of fever, chills or rigor
 No hx penile discharge, geital ulcer , or MSP
 No hx of position dependent sudden cessation of urine
 No hx trauma to the pelvis
 No hx chronic cough, contact with a chronic cougher or previous TB Rx
 No self /family hx of DM, HTN or Asthma
 Screened for RVI & found to be NR 06 months back.
Finally he was admitted to our hospital supported by his families.
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Past illnesses
 No hx of childhood illnesses like chicken pox, mumps or small pox. Not vaccinated.
 No hx of previous surgery, trauma, psychiatry problems or drug allergy.
Review of system (ROS)
H.E.E.N.T
 Head: No hx of headache or head injury
 Eyes: No hx of blurring of vision, pain in the eyes, eye itching, or sontaneous
lacrimation
 Ears:
o No hx of Earache, deafness, ear discharge, vertigo or tinnitus
 Nose:
o No hx of nasal bleeding or discharge
 Mouth and throat:
o No hx gum bleeding, tooth extraction
Lymphoglandular system (LGS):

 No hx of swelling in the neck, axilla or groin.
 No hx of heat or cold intolerance.
Respiratory System (RS):

 No hx of cough, chest pain or fast breathing
Cardiovascular system (cvs):

 No hx dyspnea, orthonea or PND
Gastrointestinal system (GIS):

 No hx of diarrhea or constipation
Genitourinary system (GUS):

 No hx of flank pain, see HPI
Integumentary system (IGS):

 No hx of skin rash or ulcers
Muskuloskeletal system (MSS):

 No hx of loss of limb function or joint pain.
Central nervous system (CNS):

 No forgetfulness,abnormal body mov’t or insomnia.
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Personal History
 He was born and raised in koladba, where he lived all his life. He had a healthy childhood and
was an active boy who liked helping his father around the farm. There is no school near his
village and like his parents, he never went to school. But he is able to read and write numbers.
 He is a farmer and also raises cattle, sheep and goat.
 He usually eats ‘injera’ made of ‘teff & ‘shiro’ made of ’atter’
 He is currently married and has ten children. All are alive & healthy.
 He occasionally drinks alcohol but no smoking
Family History
Father and mother:
 Both his father and mother are dead. His father died around 30 years ago at unknown age by
unknown cause while his mother died two years ago at age 86 by natural cause.
Siblings:
 He has two sisters and four brothers. All are alive & well.
Family Diseases:
 No family history of DM, hypertension, Asthma, tuberculosis, allergy or sudden deaths.
General Appearance
Acutely sick looking, not in cardiopulmonary stress, looks well nourished, conscious & alert
Vital signs
BP: 110/70mmHg, right arm, sitting position
PR: 95bpm, Rt radial artery, regular & full volume
RR: 18 breath/min, shallow & regular
T0: 36.20c, axillary, @10 AM
Weight: 65kg
Height: 160cms
BMI: 25.4
H.E.E.N.T
Head: Normal size, shape and hair distribution.No scar or tenderness
Ears: Normal contour of pinna.Clear external ear canal.
Eyes: No periorbital edema, ptosis, exophthalmoses or strabismus.
 Pink conjunctivae, Non icteric sclera
Nose: The nasal septum is central. There is no polyp or active discharge

Mouse and throat: The lips show no fissure or ulceration
 The gums are intact with no ulceration. There are no carious teeth, extraction, dentures or
filling.
 Tongue – no atrophied papillae, The buccal mucosa is pink & wet.
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Lymphoglandular system
 There is no significantly enlarged lymph node over the neck ,axilla or groin
 The thyroid gland is not enlarged
 Descended testicles bilaterally
Respiratory System
Inspection:
 No peripheral or central cyanosis or clubbing or the finger nails
 Breathing is shallow and regular
 No SC or IC retraction
 No chest wall deformity or surgical scar
 No chest lag
Palpation:
 Trachea is central
 No subcutaneous emphysema
 No chest wall tenderness
 Tactile fremitus is comparable on both sides
 Chest expansion is symmetrical
Percussion:
 Resonant all over lung fields
Auscultation:
 Vesicular breath sound all over the lung field
 No added breath sound (wheezing, crepitations, stridor or pleural friction rub)
Cardiovascular system
Arterial:
 All peripherally accessible arteries are palpable
 No thickening of vessels wall
 No radio-femoral delay
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Venous:
 JVP is not raised
 No distended neck vein
 Negative Hepato-jugular reflex
Precordial examination
Inspection:
 No precordial bulging
 Quite precordium
 The apical impulse is not visible
Palpation:
 No palpable heart sound
 The PMI is at the 5th ICS lateral to MCL, localized & tapping.
 There is no parasternal or apical heave. There is no thrill.
Auscultation:
 S1 & S2 well heard
 No murmur or gallop
Abdominal examination
Inspection:
 The abdomen is flat & symmetrical
 It moves with respiration.
 The flanks are not full
 No distended abdominal vein
 No surgical scar
 The umbilicus is inverted with circular slit
 Hernia sites are free
 No visible pulsation or peristalsis
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Auscultation:
 Normo-active bowel sound (8/min)
 No bruit over renal artery, abdominal aorta or liver area
Palpation:
 Superficial palpation:
o There is no tenderness
o No superficially palpable mass
 Deep palpation:
o No organomegally
Percussion:
 No sign of fluid collection(shifting dullness/fluid thrill)

 Total vertical liver span (TVLS) along the right mid-clavicular line =6cms
DRE
 Inspection
o No ulceration or visible mass
 Palpation
o Normal anal sphincter tone
o There is a mass which has smooth surface, regular border, firm consistency, not fixed
to rectal mucosa & palpable medial sulcus but the upper border isn’t reachable
o No blood on the examining finger
Genitourinary System
 No costo-vertebral angle tenderness (CVAT)

 Kidneys are not bimanually palpable
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Integumentary System
 No palmar or plantar pallor

 No rash, scar or ulcer
Musculoskeletal System
 No muscle tenderness or spasm.
 No bone deformity or tenderness.
 No stiffness of joints
 No edema.
Nervous system
Mental Status:
 GCS
o 15/15E4V5M6
 conscious & alert
 MMSE
o He knows what day it is, where he is and what his name is.Orientation
o He remembers what he ate for breakfast. He also remembers where he used to
liveMemory
o He speaks in moderate voice with no hesitancy or gaps in the flow and rhythm of his
words. Speech
Cranial Nerve examination:

CN-I:
o can smells soap via each nostril.
CN-II:
o He can differentiate 2 fingers at about 6 meters. (Visual Acuity)
o He sees waggling of finger approximately 1000 from axis of eye. (Visual Fields)
o He differentiates green and red colors. (Color Appreciation)
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CN-III, IV & VI:
o The eyes can move in all directions. There is no nystagmus or diplopia. The pupils are round,
regular in outline and equal in size. They react to light directly and consensually.
CN-V:
o He identifies light touch and pin prick over the mandibular, maxillary and ophthalmic areas of
the face. He closes his eyes at the touch of the cornea with a cotton swab. Contraction of the
temporal and masseter muscles is symmetrical and strong.
CN-VII:
o The face is symmetrical at rest and during voluntary movements (smiling,frowning). He can
close both eyes equally and forcefully.
CN-VIII:
o He can hears rubbing of the fingers on both ears.
CN-IX & X:
o The soft palate rises in the midline when saying ‘ah!’
o He can swallow his saliva
CN-XI:
o The Sternocleidomastoid and trapezius muscles contract on turning the head and on shrugging
the shoulder against resistance, respectively.
CN-XII:
o The tongue protrudes in the midline and shows no fasciculation or atrophy.
Motor examination:
 Muscle bulk:
o There is no muscle bulk difference between the left and the right side. There is also no
spontaneous as well as induced fasciculation.
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 Muscle tone and power;
TONE POWER
Upper Lower Upper Lower
Right Normo-tonic Normo-tonic 5 5
Left Normo-tonic Normo-tonic 5 5
Reflexes:
 Superficial reflexes:
o Abdominal reflex is absent both in upper and lower quadrants.
o Corneal reflex is intact in both eyes .
o Plantar reflex is down going on both sides.
 Deep tendon reflexes:
Biceps Triceps Supinator Patellar Ankle

Right ++ ++ + ++ +
Left ++ ++ + ++ +
 Clonus: No clonus
Coordination:
Finger to nose, heal to shin and rapid alternating movement of the arm were done without any
abnormalities.
Sensory:
 He identifies light touch and pin prick over the extremities and trunk.
 He appreciates the form of a key by means of only touch (Stereognosis)
 He recognizes writings of different numbers on his palm (Graphesthesia)
 He is able to differentiate 2 pin pricks up to 4 mm apart over the finger tips (2 pt
discrimination).
 He is able to recognize different movements of the toes with his eyes closed.(Position sense)
 Vibration sense was not assessed due to lack of Tuning Fork.
Meningeal Sign:
 No neck stiffness.
 Kernig's Sign is negative.
 Brudzinski's Sign is negative
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RESPIRATORY RELATED
SHORT CASES
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CHEST INJURY
By-Elshaday Amare(sms)
 25% of all injuries
 Investigations
o Radiography is thr first choise after resuscitation
o Ultarasound
o Chest tube (Dx & Rx)
o CT with contrastrib & vertebral #, hematomas, pneuothorax,
pulmonary contusion & thoracic aorta.
Immediate life threatening
1. Airway obstruction
o Dentures, teeth, secretion & blood
o Bilateral mandibular #, expanding neck hematomas, laryngeal
trauma(thyroid & cricoid#) or tracheal injury
o Mgt intubation with cervical spine protection
2. Tension pneumothorax
o 01 way valve air leak from lung or chest wallair forced to into thoracic
cavity without any means to escapecollapse of lungmediastinal
displacementdecreased venous returncompromising opposite lung
o CPs
 Tachypnea, dyspnea, distended neck veins, tracheal deviation,
hyper-resonance & absent breath sound
o Mgt
 Immediate decompression
 Large bore needle in to the 2nd ICS in MCL
 Chest tube in 5th ICS in anterior axillary line
3. Pericardial Tamponade
o Similar CPs as tension pneumothorax
o All pts with penetrating chest injury near the heart + shockcardiac
injury unless proven otherwise
o Classicallyincreased venous pressure, decreased arterial pressure,
tachycardia & muffled heart sounds
o DxCXR of enlarged heart shadow
 Echo—fluid in pericardial sac
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o Mgtneedle pericardiocentesisstabilization until definitive mgt
 But high risk of iatrogenic injury to the heart
 Definitive mgt operative (sternetomy or left thoracotomy &
repair of the heart)
4. Open pneumothorax (sucking chest wound)
o Large open defect in the chest (>3cm)equilibrium between intrathoracic
& atmospheric pressureair in hemothorax not lunghypoventilation
o Mgtclosing defect with sterile occlusive plastic dressing taped on #3
sides to form a #1 way valve (prevents tension pneumothorax) &
chesttube inserted in a site remote from injury site.
 Definitive mgtformal debridement & closure
5. Massive hemothorax
o Usually from IC vessels or internal mammary artery
o CPs
 Hemorrhagic shock (flat neck veins), absent breath sounds & dull on
percussion
o Mgtcorrect the shock (see page 264 on shock)
 Insert IC drain
 Intubation (in some cases)
 Thoracotomyindications
 Drainage of 1500ml of blood or ongoing hemorrhage of
>200ml/hr over 3-4hrs
6. Flail chest
 3 or more contiguous ribs are #ed in @least 02 locations
 Paradoxical mov’t of free floating segment of chest wall
 Mgtmechanical ventilation until fibrous union of broken ribs occur
o 02 administration, adequate analgesia & physiotherapy
Potentially life threatening injuries
1. Thoracic aortic disruption
 CPs
o Asymmetry of upper or upper & lower extremity BP
o Widened pulse pressure
o Chest wall contusion
 CXRwidened mediastinum
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2. Tracheobronchial injuries
 Subcutaneous emphysema with respiratory distress
 Dxbronchoscopy

Mgtintubation of unaffected bronchus followed by operative repair
3. Blunt myocardial injury
 Suspected when in pts with blunt trauma + EEG abnormality
 Echowall motion abnormalities

@ risk of developing sudden onset dysarrythmia
4. Diaphramatic injuries
 Any injuries to or below 5th ICS
 Herniation of abdominal contents to chest & strangulations
 Most are silent
 DxCXR after NGT insertion—herination of stomach
o Contrast studies of the upper & lower GI tract
o CT-scan
5. Esophageal injury
 Usually from penetrating trauma
 CPs
o Odynophagia/ pain on swallowing foods & fluids
o Subcutaneous/mediastinal emphysema
o Pl. effusion
o Unexplained fever with in 24hr of injury
 Mgt operative repair & drainage
6. Pulmonary contusion
 Major cause of hypoxemia after blunt trauma
 CPs
o Natural progression of worsening of hypoxemia for 1st 24-48 hrs
 Dxcontrast CT-scan—confirmatory
o Hemoptysis or blood in endotracheal tube
 Mgt 
o Mild—O2 administration ,aggressive pulmonary toilet & adequate
analgesia
o Severe—mechanical ventilation
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CHEST TUBE INSERTION (THORACOSTOMY)
Indications
1. Pnemothorax
2. Hemothorax
3. Chylothorax
4. Empyema
5. For pleurodesis…
Relative Contraindications
1. Bleeding diathesis
2. Skin infection over the chest tube insertion site
3. Transudative pleural effusion…
 20 to liver failure or CHF
o Because it can resolve with diuretics only
Site of insertion
Generally
o @ 5th Intercostal Space (ICS) in mid axillary line
o @2nd ICS in mid clavicular line for small pneumothorax
Safe triangle
o Anterior border of the latissimus dorsi,
o The posterior border of the pectoralis major and
o The superior border of the fifth rib
When to remove?
To minimize the risk of infectious complications, the tube should be removed as
soon as it is safe to do so.
o Removal Criteria: Pneumothorax
 When the lung is fully expanded
 No visible air leak is present and air does not accumulate when
suction is removed.
o Removal Criteria: Effusion
 When the lung is fully expanded
 Fluid output is less than ~ 200 mL/day.
Complications
1. Hemorrhage
2. Organ injury (lung, mediastinum…)
3. Damage to intercostals nerves & vessels
4. Introduction of pleural infection
5. Subcutaneous emphysema (usually @ the site of insertion)
6. Pulmonary edema
Why?...Due to rapid pulmonary expansion (RPE) because of rapid drainage of
large volumes of pleural fluid. To minimize the risk it’s better to limit initial
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Procedural note on Chest tube insertion
Materials
o Sterile sheets, gloves and gown
o Antiseptic solution, swabs
o Local anesthesia(lidocaine)
o Syringe, scalpel blade and suture
o Needle holder, dissecting forceps, scissors
o Chest drainage tube and
o underwater seal drainage bag containing about 200 mL sterile water
o one straight clamp, one curved clamp,
o Dressing and adhesive tape
Procedure
 Patient lies comfortably in bed with the backrest lifted to about 45 degrees.
 Wash hands and put on sterile gloves and gown.
 Clean the area with an antiseptic solution (savolon, iodine, alcohol) and drape.
 The skin, subcutaneous tissue and the parietal pleura are infiltrated with 3-5mg/kg
injection lidocaine without epinephrine.
 A short skin incision is made with a scalpel blade at the level of the upper border of the
rib at the selected site.
 Using the curved clamp the intercostal muscles are separated and reached up to the
parietal pleura.
 The blunt dissection is completed with the index finger down up to the pleura.
 The chest tube held by a haemostatic forceps is thrashed through the pleura, puncturing
it and the tube is inserted into the pleural cavity.
o Alternatively the tube may be inserted by using a stilette or a trocar to puncture
the pleura.
 The tube is clamped with a haemostatic forceps and the closed end is cutoff…the tube is
connected to a water seal drainage bag so that the tube inside the bag remains under
the level of the water.
 The drain is fixed to the skin by inserting a stitch through the skin but not piercing the
drain.
o Insert a stitch in circular fashion through the skin around the tube and kept
untied (Which will be tied after removal of the tube).
 A sterile dressing is applied at the exit of the tube.
 Control chest x-ray should be done after 08hrs of the procedure to check proper
insertion
NB*
To check functionality of chest tube, see
o Continuous bubbling in the bottle
o oscillations
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TRACHEOSTOMY
Indications
 For mgt of pts who require prolonged artificial ventilation
 Acute upper airway obstruction
o E.g. an inhaled foreign body, a large pharyngo-laryngeal tumor,
or acute pharyngo-laryngeal infections in children
 Bilateral vocal cord paralysis
o E.g.if RLN is injured during thyroidectomy
 Laryngeal fracture or laryngo-tracheal separation in whom
cricothyroidoctomy may cause further damage
 To get access for frequent pulmonary suctioning
 After major surgery involving the oral cavity, pharynx, larynx or neck
o Since there is a potential risk for upper airway obstruction…because of the
likely of edema of upper aero-digestive tract.
 For pts with neurologic deficits that impair protective airway reflex
o to protect them from aspiration
Strong relative contraindication
 anticipation that the blockage is due to laryngeal carcinoma
Site
 2nd & 3rd tracheal rings
Complications
 Intra-op
 hemorrhage
 injury to paratracheal structures
 carotid artery, recurrent laryngeal nerve (RLN)…
 Early
 Hemorrhage
 Pnemothorax
 Pneumo-mediastinum
 Tube blockage
 Late
 Local infection
 Tracheal stenosis
 Difficulty in decannulation
 Persistent tracheo-cutaneous fistula
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Procedural note on tracheostomy
1)Open tracheostomy
2) Percutaneous tracheostomy
Open Tracheostomy
 Position the unconscious or anesthetized patient supine with the neck extended and the
shoulders elevated on a small roll. The awake patient does not tolerate this; therefore, the
procedure is performed with the patient in a sitting or semirecumbent position.
 Palpate the landmarks (eg, thyroid notch, sternal notch, cricoid cartilage) and mark them. Plan a
3-cm vertical incision that extends inferiorly from the cricoid cartilage and infiltrate lidocaine
with epinephrine.
 Make the vertical incision.
o Many advocate the horizontal skin incision, which is made along relaxed skin tension
lines and gives better cosmetics.
 Subcutaneous fat may be removed with electrocautery to aid in exposure and to prevent later
fat necrosis. Dissection proceeds through the platysma until the midline raphe between the
strap muscles is identified.
 Palpate the inferior limit of the field to assess the proximity of the innominate artery. Cauterize
or ligate aberrant anterior jugular veins and smaller vessels. Midline dissection is essential for
hemostasis and avoidance of paratracheal structures.
 The strap muscles are separated and retracted laterally, exposing the pretracheal fascia and the
thyroid isthmus. The lateral retraction also serves to stabilize the trachea in the midline.
 Although the thyroid isthmus, which typically lies anteriorly over the first 2-3 tracheal rings, may
be retracted out of the field, it must often be divided in some cases.
 When preparations for transfer of circuitry tubes are complete, deflate the endotracheal tube
balloon and enter it to the trachea.
 Securing the cricoid with a hook and elevating it superiorly facilitates control of the tracheal
entry.
 For a T-shaped tracheal opening, make a 2-cm incision horizontally through the membrane
between the second and third or third and fourth tracheal rings.
 For a U- or H-shaped tracheal opening, reflect tracheal flaps inferiorly or both inferiorly and
superiorly.
 A permanent stoma can be created with skin flaps developed and sutured to a rectangular
tracheal opening. Removal of small anterior portions of the tracheal rings is required.
 After the trachea is entered, suction secretions and blood out of the lumen.Insert previously
tested tracheostomy tube.
 After the airway is confirmed intact based on carbon dioxide return and bilateral breath sounds,
secure the tracheostomy tube to the skin with 4-0 permanent sutures.
 Attach a tracheostomy collar with the head flexed.
 To avoid the risk of subcutaneous emphysema and subsequent pneumomediastinum, the skin is
not closed. Place a sponge soaked with iodine or petrolatum gauze between the skin and the
flange for 24 hours.
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…ctd
Percutaneous Tracheostomy
Percutaneous tracheostomy is generally carried out in the intensive care unit on a patient who is
intubated and ventilated with continuous monitoring under deep intravenous sedation/analgesia.
 The patient is preoxygenated with 100% oxygen, which is continued during the procedure. A
shoulder roll is placed to extend the patient's neck.
 A 1.5- to 2-cm incision is made through the skin of the neck approximately 2 cm below the
palpable cricoid cartilage.
o Blunt horizontal and vertical dissection with a hemostat is used to carry the dissection
down to a pretracheal plane, attempting to sweep the thyroid isthmus inferiorly. Finger
dissection is used to palpate the cricoid cartilage and tracheal rings.
 A small-caliber, flexible bronchoscope attached to a video camera and monitor is passed via a
swivel adaptor down the endotracheal tube, allowing for ventilation around the scope. The
bronchoscopist withdraws the endotracheal tube and bronchoscope, after deflating the
endotracheal tube cuff, to a subglottic level. Care should be taken not to completely withdraw
the tube from the larynx.
 The surgeon can use the light from the bronchoscope and digital palpation to guide passage of
the needle from the percutaneous tracheotomy kit through the anterior tracheal wall under
direct bronchoscopic visualization.
 Ideally the puncture should be made between the second and third tracheal rings. High
placement of the tracheotomy in the immediate subcricoid position is associated with fracture
of the cricoid cartilage and subglottic stenosis and should be avoided.
 The wire guide is then inserted, the tract is dilated per the kit instructions, and the
tracheostomy tube is inserted over a special introducer that is then withdrawn. The
endotracheal tube and bronchoscope are withdrawn from the mouth, and the tracheostomy
tube is sutured into position and secured with a tracheostomy tube tie.
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ENDOTRACHEAL INTUBATION
Indications
 Airway problemsinability to maintain a patent airway with potential
airway compromise due to…
o inhalational injury
o Retropharyngeal hematoma
o facial fractures
 Breathing problemsinability to maintain adequate oxygenation...
o by face-mask O2 supplementation
o presence of apnea
 Disability problems
o Inability to protect airway due to altered mental status(GCS< or =8)
o Risk of aspiration of blood or vomitus
o Sustained seizure activity
Contraindication (relative)
 Unstable cervical spine injuryneeds care to insert
How to know the correct placement of the tube?
by…
1. Audible breath sound (bilaterally)
2. Hearing no borborygimi in the epigastrium
 If u hear it during inspirationsuggests esophageal intubation
3. CO2 detector (capnograph or calorimetric CO 2 monitoring device
4. CXR
Complications
o Malpositionesophagus
o Vomiting
o Bronchospasm
o Exacerbation of spinal cord injury
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Procedural note on endotracheal tube insertion
Materials
 Laryngoscope (check size – the blade should reach between the lips and larynx – size 3
for most patients), turn on light
 Cuffed endotracheal tube
 Syringe for cuff inflation
 Monitoring: end-tidal CO2 monitor, pulse oximeter, cardiac monitor, blood pressure
 Tape
 Suction
 Ventilation bag
 Face mask
 Oxygen supply
 Medications in awake patient: hypnotic, analgesia, short-acting muscle relaxant (to aid
intubation)
Laryngoscope insertion techique
 Give medications if required

 Pre-oxygenate patient with high concentration oxygen for 3-5mins
 Position patient
o Neck flexed to 15˚, head extended on neck (i.e. chin anteriorly), no lateral deviation
 Stand behind the head of the patient
 Open mouth and inspect: remove any dentures/debris, suction any secretions
 Holding laryngoscope in left hand, insert it looking down its length
 Passing the tongue
o Slide down right side of mouth until the tonsils are seen
o Now move it to the left to push the tongue centrally until the uvula is seen
 Advance over the base of the tongue until the epiglottis is seen
Tube insertion technique
 Apply traction to the long axis of the laryngoscope handle (this lifts the epiglottis so that
the V-shaped glottis can be seen)
 Insert the tube in the groove of the laryngoscope so that the cuff passes the vocal cords
 e ove laryn o co e and in ate the c of the t e ith 15ml air from a 20ml syringe
 Attach ventilation bag/machine and ventilate (~10 breaths/min) with high concentration
oxygen and observe chest expansion and auscultate to confirm correct positioning
 Consider applying CO2 detector or end-tidal CO2 monitor to confirm placement
 Secure the endotracheal tube with tape
o if it takes more than 30 seconds, remove all equipment and ventilate patient
with a bag and mask until ready to retry intubation
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GASTRO-INTESTINAL RELATED
SHORT CASES
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ABDOMINAL INJURY
By -Eshetie Endalew(sms)
 One of the commonest surgical emergency
 Based on post resuscitation physiologic condition Patient with Abdominal injury can be;
a. Hemodynamically normal
b. Hemodynamically stable
c. Hemodynamically unstable
Types
I. Blunt abdominal injury(BAT)
II. Penetrating abdominal injury
BAT
 BAT with poly trauma is the commonest cause of death in young population.
 Etiology of BAT;
I. Road traffic accident(commonest)
II. Fall down injury
III. Seat belt syndrome
IV. Assault
 Mechanism of BAT injury;
1. Rapid deceleration
2. Crushing(compression)effect
 Approach for BAT patient
 Primary survey(ABCDE)and act accordingly
 Resuscitation by crystalloid solution if hypovolemic or shock
 Secondary survey
 HX; pain, abdominal distention, fever
 P/E; Abdominal tenderness, tachycardia, tachypnea
 Abrasion, contusion, ecchymosis over the abdomen
 Decrease bowel sound, guarding, febrile (peritonitis)
 INVESTIGATION
Baseline;
 CBC
 Cross match
 Organ fun test
 Pancreatic enzyme; poor ppv & Npv
Urinalysis; show renal injury (micro hematuria)
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Imaging
 Plain x-ray; give limited information
Use metal marker for penetrating injury on external wound
 Contrast CT; gold standard for intra-abdominal diagnosis.
 Give more accurate information than pain x-ray
 Demonstrate vascular &visceral perfusion of solid organ& severity
grading.
 Sensitive for blood so very important in dx of retroperitoneal injury.
 Difficult in dx of hollow viscous injury (sensitive only 29%-35%)
 Used for stable patient.
 Focused abdominal sonar for trauma (FAST); U/S evaluation of abdomen to look for
intrabdominal blood.
 Bedside investigation of choice to detect intrabdominal fluid.
 Accurate to detect >10ml of free blood (+ve) but operator &experience
dependent.
 Diagnostic laparoscopy
 Diagnostic peritoneal lavage (DPL);used to assess presence of intrabdominal blood.
Steps;
I. Empty stomach and bladder by gastric tube &catheter respectively.
II. Insert cannula below the umbilicus &push posterior caudally
III. Aspirate blood, if >10ml ,insert 1000ml RL solution to the abdomen&
aspirate again
 Interpretation; If RBC >100000/ul & WBC>500/ul it is +ve w/c is equivalent to 20ml of
blood. i,e laparotomy is needed.
Management
 ABC of life
 Resuscitation &look for hemodynamic stability
 For stable patient CT for assessment of injury
 For unstable patient laparotomy.
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LIVER INJURY
 Is the Second common after blunt abdominal trauma.
 The most common after penetrating abdominal injury.
 Occurred in 2.9% of all patients and 39.8% of those with blunt abdominal trauma.
 The mortality associated with these blunt hepatic injuries is 14.9%.
Mechanisms of blunt hepatic injury
1. Rapid deceleration
 Tear hepatic tissue, vascular and ligament attachment.
2. Crushing effect
 Compress b/n force of rib cage and vertebral column.
On Hx
 Trauma to the right upper quadrant, right rib cage, or right flank
 Complain of pain in the right upper abdomen, right chest wall, or the right shoulder due to
diaphragmatic irritation.
On P/E
 Due to hemorrhage
 Hypotension up to shock
 Abdominal distention
 Tachycardia
 Metabolic acidosis
 Symptom of Peritonitis
 right upper quadrant or generalized abdominal tenderness
 abdominal wall contusion or hematoma (e.g, seat belt sign)
 Right lower chest wall tenderness, contusion, or instability due to rib fracture.
Grade hematoma(s.a) laceration(cm) vascular injury
1 Subcapsular tear <1cm parenchymal _

(<10%of surface area) depth
2 Sub capsular tear 1_3cm depth _
10_50% <10cm length
3 Sub capsular tear >3cmdepth
>50%
4 Parenchymal
disruption(25_75% of
H.lob)
5 Parenchymal Juxtahepatic vein
disruption(>75% of injury (Vena cava
H.lobe) Major hepatic vein)
6 - Hepatic avulsion
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Management; depends upon
 The hemodynamic status of the patient,
 Grade of liver injury, and
 Presence of other injuries and medical comorbidities.
 The unstable patient with a positive (fast) scan or (dpa/dpl) requires emergent abdominal
exploration and control of bleeding may be through a damage-control approach or by using
specific techniques for liver hemostasis.
 stable patient who do not have other indications for abdominal exploration can be observed.
 stable patients with right-sided penetrating thoracoabdominal injuries that lacerate the liver
can also be observed, provided there are no associated intraabdominal injuries.
Splenic injury
 Splenic injuries appear as disruptions in the normal splenic parenchyma, frequently with
surrounding hematoma and free intra-abdominal blood.
 The spleen is the most commonly injured abdominal organ in the NTDB, with 3.2% of all
injured patients and 50.7% of patients with blunt abdominal trauma.
 A significant mortality of 10.8% is associated with blunt splenic injury, Mainly by associated
injuries and pre hospital delays.
 Penetrating splenic trauma is less common but is still present in 14.5% of all penetrating
abdominal injuries in the NTDB.
 Spleen is commonly the bleeding intra-abdominal organ in unstable patient undergoing
laparotomy.
Mechanism of blunt splenic injury can include;
 direct compression of the organ in the left upper quadrant of the abdomen

deceleration mechanism that tears the splenic capsule or parenchyma, mainly at areas
fixed or tethered to the retro peritoneum.
SPLENIC INJURY GRADING
 Grade I — Hematoma: 10% of surface area.
Laceration: <1 cm in depth into the parenchyma
 Grade II — Hematoma: 10 to 50% of surface area.
Laceration: 1 to 3 cm in depth.
 Grade III — Hematoma: >50% of surface area.
Laceration: >3 cm in depth or involving a trabecular vessel.
 Grade IV —segmental or hilar vessels laceration & >25 % of spleen is
devascularizes.
 Grade V — Hematoma: shattered spleen.
Laceration: hilar vascular injury which devascularizes spleen.
EVALUATION;
 initial resuscitation,
 diagnostic evaluation and
 management of the patient based on (ATLS) program
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History
 trauma to the left-upper quadrant, left rib cage, or left flank
 left shoulder pain (ie, Behr’s sign) due to irritation of the phrenic nerve.
 medical comorbidities and medical conditions, like coagulopathy
 Associated injuries — to adjacent organs, rib fractures, pelvic fracture, and spinal cord
injury.
On P/E
 left-upper quadrant or generalized abdominal tenderness,
 abdominal wall contusion or hematoma (eg, seat belt sign)
 sign of intrabdominal hemorrhage
INVX
 FAST — hypo echoic (ie, black) rim of sub capsular or intraperitoneal fluid
 On Contrast CT
 Hemi peritoneum
 Hypo density
 Contrast blush-hyper dense areas within the splenic parenchyma
 Active extravasation of contrast -ongoing bleeding
 Plain films,
 organ-based ultrasound imaging and
 MRI
MANAGEMENT
 Unstable & positive FAST scan or DPA/DPL requires emergent abdominal exploration
 Stable $ low-grade (I to III) blunt or penetrating splenic injuries, observed safely by contrast
CT.
 Splenectomy may be a safer option, especially in the unstable patient with multiple potential
sites of bleeding
Small Bowel Injuries
The small intestine is one of the most frequently injured organs after penetrating abdominal trauma,
due to large percentage of the abdomen it occupies.
 Incidence of small bowel injury involves 60% of penetrating abdominal trauma.
 Blunt, small intestinal injuries are less common, present in 2.7% of all blunt abdominal injuries
in the NTDB, but the small bowel is frequently injured as a result of blunt trauma.
 Mortality rates range from 10% to 25%, with most caused by associated vascular injuries.
Penetrating injuries can vary from tiny perforations to large destructive injuries that destroy
circumferential segments of small bowel.
Mechanisms of blunt small bowel injury include;
 crushing between the steering wheel or seatbelt and a rigid structure such as the vertebral
column,,
 Rupture during which the intraluminal pressure rapidly increases, causing a blowout along the
ant mesenteric border.
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Deceleration result in a shearing of the serosa or muscularis throughout a segment of small bowel.
Mesenteric injuries can cause devascularization of sections of small bowel
 Small intestinal injuries are often identified at the time of laparotomy.

The repair of small bowel injuries depends on the extent of intestinal wall destruction in
relation to the luminal circumference.
 Small perforations that can be closed without compromising the intestinal lumen can be
debrided and repaired with one or two layers..
 Injuries occupying over 50% of the intestinal wall circumference should be addressed with
resection and anastomosis either by stapled or hand sewn anastomoses for intestinal
resections. Hand-sewn anastomoses are frequently constructed in two layers
The damage control approach is important for rapid closure of perforations to control
contamination and to control bleeding.
Damage control surgery
Is operation done until the physiological derangement can be corrected.
It has two goals:
 stopping any active surgical bleeding;
 Controlling any contamination.
The initial surgical focus is hemorrhage control, which is followed by control and limitation of
contamination. This is achieved by;
 Simple ligation of bleeding vessels,
 Shunting of major arteries and veins, drainage,
 Temporary stapling off of bowel, and
 Therapeutic packing.
The key philosophy of damage control is:
 to keep the patient alive at any cost
 Be part of the resuscitation process, in which there is initial surgical control of hemorrhage
and contamination followed by rapid closure.
The stages of damage control surgery
I. Patient selection
II. Control of hemorrhage and control of contamination
III. Resuscitation continued in the intensive care unit
IV. Definitive surgery
V. Abdominal closure
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NGT (Naso-Gastric Tube)
Indications
1. Gastric decompression
 Removal of accumulated gastrointestinal air & fluid to relieve its pressure
effect
2. Bowel irrigation
 To lavage (wash) the stomach in case of poisoning or overdose of medications
3. For feeding
 To clients unable to eat by mouth or swallow a sufficient diet without
aspirating food or fluids into the lungs
4. For administration of medication
 To clients unable to swallow medications without aspirating it to the lungs
5. To obtain specimen from gastric contents
 For lab. analysis
6. After bowel surgery
 To promote healing
7. To administer radiographic contrast media to GIT for imaging
Contraindications
 Absolute
1. severe mid-face trauma
2. Recent nasal surgery
 Relative
3. coagulation abnormality
4. Esophageal stricturefear of perforation
5. Esophageal varicesfear of bleeding
How to confirm that the tube is in stomach?
 Aspirate the tube with a syringe if the aspiration is greenish gray colored fluidthe
tube is in the stomach
 Inject about 50mL of air through the tube then listen with a stethoscope over the
epigastriumaudible gurgling sound in the epigastriumthe tube is in the stomach
 Listen to the end of the tube @ the nosethe sound of moving air will indicate that the
tube is in trachea, not in the stomach.
 X-ray
Complications
o Some degree of pt discomfort
 Placement of the tube can induce gagging or vomiting
o GERD
o Esophageal perforation
o Epistaxis
o Respiratory tree intubation /malposition/
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Procedural note on NGT insertion
Materials
o Nasogastric tube
 Adult16-18F
o Glass of water with a straw
o Water-based lubricant
o drainage bag
o adhesive tape
o gloves
o Syringe
o stethoscope
Procedure
o Explain the patient that a tube is going to be inserted through his nose &
that…
 He/she has to swallow the tube
 There may be some cough during insertion of the tube
o Measure distance from the nostril to the tip of ear lobe then from the
earlobe to the tip of xiphoid processmark
o Lubricate the NG tube (Usually no#16Fr or 14Fr) & choose the nostril
which has the wider channel
o Pass the NG tube horizontally through the nose. As the tube touches the
posterior pharyngeal wall the patient will gag
 Patient may be given a little water to sip. The tube is then slowly
advanced as the patient is asked to swallow the tube. During
swallowing the cricopharyngeus muscle will relax and the tube will
enter into the esophagus.
 when the pt breathesStop inserting the tube for a moment
 don’t e force
o The tube is further advanced till the second ring in the tube lies at the level
of nostril when the tip will lie in the stomach
o The tube is secured to the nose with an adhesive tape.
o The tube is then connected to a plastic drainage bag to siphon out the
stomach contents.
o If required the stomach content may be sucked out hourly.
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OSTOMY
General indication
 When restoration of intestinal continuity is contraindicated or not
feasible
OSTOMY
Type
Location Desired role
Colon=colostomy Permanent  Loop
 Double barrel
Ileum =ileostomy Temporary  End
 spectacular
Indication for temporal “ostomy”

1. Gangrenous LBO
2. Penetrating injuries
 Penetrating colon injuries
3. High risk of anastomosis leak
 In…
 Immunocompromised pts
 Severely malnourished pts
4. Hemodynamic instability
 In Pts with…
 Trauma
 Sepsis
5. Complex perianal fistulas
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Indication for permanent “ostomy”
1. After excision of the rectum for carcinoma
2. Total abdominal proctocolectomy for severe IBD
 CD
 UC
“Stoma” complications
 Early (<3months)
 Leakage
 Skin irritation
 Cmn in ileostomy
 Stomal necrosis
 Stomal retraction
 Late
o Parastomal hernia
o Stomal prolapse
o Stomal stenosis
 Psychosocial problem
Colostomy
 Colostomy refers to a surgical procedure where a portion of the large
intestine is brought through the abdominal wall to carry stool out of
the body.
 Colostomy bypasses distal colon, rectum or anus.
 May be
o Temporary
 To decompress an obstructed or perforated distal colon
 To permit healing of fistulous tract or acute inflammatory
process distally
 For protection of distal anastomosis when delayed healing
is anticipated
o Permanent
 In case if distal rectum & anorectal sphincter mechanisms
are removed
NB*
colostomy diarrhea may be present
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Ileostomy
 Ileostomy refers to a surgical procedure where a portion of the small
intestine (the ileum) is brought through the abdominal wall to carry stool out
of the body.
 Ileostomy bypasses the entire colon & rectum.
 May be temporary or permanent
NB*
Ileostomy patients are more likely to develop fluid and electrolyte problems ++
skin irritation
How to differentiate stomas?

1. The content that comes out…
 Mucus dischrge
 in colostomy
 watery discharge
 in ileostomy
2. Skin around the stoma…
 More skin irritation in ileostomy
 Pink in colostomy
3. Odor
 Foul smelling in colostomy
4. Size of stoma
 Wider in colostomy than ileostomy
5. If u insert ur hand in stomas…
 U will be able to differentiate
 Loop Vs end ostomy
6. ?Site?
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BOWEL PREPARATION
By-Daniel Belhu(sms)
 AimTo decrease the bacterial load…
o Which in turn decreases risk of infection & anastomosis leak
 DurationFor #03 days
 Methods used for bowel preparation
1) Prepare the bowel using…
 Using cleansing enema
i) Mechanical bowel preparation o water & soap
Or
ii) Pharmacological bowel preparation  Laxatives
o Castor oil (15ml)
o Polyglycol solution/PEG
2) Keep on fluid dietFor #03 days
4) Antibiotics
o Which drug to choose? Criteria;
 CoverageBroad spectrum
 RoutePO
 Poorly absorbable from GI system
o Drug of choice (DOC)
 Metronidazole & Neomycin
 If neomycin isn’t available we can use others like
Ampicillin, Amoxicillin, erythromycin…
o When?
 If the surgery is scheduled tomorrow morning , the antibiotic
should be given today @ 1:00 PM then @ 2:00PM &
11:00PM.(i.e. 7, 8 in the afternoon & 5 O’clock in the night)
 Antibiotics also should be given 30 minutes prior to surgery
 Gentamycin was DOC but nowadays Ceftriaxone is
being used.
4) NPO (nothing per os)#06 hrs prior to surgery
NB*
Contraindications for bowel prep.
o Complete bowel obstruction
o perforation
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HERNIA
 Abnormal protrusion of viscus through its containing wall.
Etiologies
 Any condition that raise intra-abdominal pressure
 Chronic cough
 Straining on micturation and defecation
 ascites
 Abdominal surgery
 Anatomical weaknesses…
 Where structures pass through the abdominal wall
 Where muscles fail to overlap
 Where there is no muscleonly scar tissue
 Congenitalpersistent processes vaginalis sac
o indirect hernia
 Collagen fiber disorder
o Acquired smoking
Composition of hernia
Consist of 3 parts
1. The sac
 Has mouth, neck, body and fundus
2. Covering of the sac
3. Content of hernia
A. Omentumomentocele
B. Intestineenterocele
C. Portion of intestinerichter’s hernia
D. Bladder
E. Ovaries
F. fluid
G. Meckel’s diverticulumlittre’s hernia
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Classification
<<>>Irrespective of the site
 Reducible
 content can be returned to the abdomen
 Irreducible
 content cannot be reduced but no complication
 obstructed
 bowel in the hernia has good blood supply but bowel is obstructed
 Incarcerated
 The lumen of that portion of the colon occupying a hernial sac is
blocked with feces. But the hernia has good blood supply
 Strangulated
 irreducible + impaired blood supply
Characteristics of asymptomatic/reducible hernias are
 Swelling or fullness at the hernia site

 Aching sensation
 No true pain or tenderness upon examination
 Enlarges with increasing intra-abdominal pressure and/or standing
Characteristics of incarcerated hernias are
 Painful enlargement of a previous hernia or defect

 Irreducible either spontaneously or manually
 Nausea, vomiting, and symptoms of bowel obstruction(possible)
Characteristics of strangulated hernias are
 Patients have symptoms of an incarcerated hernia

 pain and tenderness
 Systemic toxicity secondary to ischemic bowel is possible
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<<>>Depending on the sitein order of decreasing frequency
1. Inguinal
2. Incisional
3. Umbilical and epigastric
4. Femoral
INGUINAL HERNIA
Boundary of inguinal canal
 Anteriorlyexternal oblique aponeurosis
 Posteriorlyfascia transversalis
 Superiorlyconjoined muscle of internal oblique and transversalis
 Inferiorlyinguinal ligament
NB*
Inferior epigastric vessels lie posteriorly and medially to deep inguinal ring.
Contents of inguinal canal
 Spermatic cord
 Ilioinguinal nerve and
 Genital branch of genitofemoral nerve
 Round ligament replace the spermatic cord in females
Hesselbach’s triangle
 Lateral boarder of rectus sheath
 Inguinal ligament
 inferior epigastric vessels
Indirect/oblique inguinal hernia

 most common form of hernia
 mostly due to Congenital causespersistent processes vaginalis sac
 young male
Direct/acquired inguinal hernia

 older male
 due to poor lower abdominal musculature (Hesselbach’s triangle)
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DDx
In males
 Vaginal hydrocele
 Encycted hydrocele of the cord
 Spermatocele
 Undescendeded or ectopic testis
 empty scortum on affected side
 Lipoma of cord
 Femoral hernia
In females
 Hydrocele of the canal of nuck (females)

 Femoral hernia
FEMORAL HERNIA
 common in multiparous women
DDx
 Inguinal herniamedial & above to inguinal ligament
 femoral hernialateral & below to inguinal ligament
 Saphenavarix
 fluid thrill may present
 An enlarged femoral lymph node
 Lipoma
 Femoral aneurysm
 Psoas abscess
 Distended psoas bursa
 Rupture of the adductor longus with hematoma formation
INCISIONAL HERNIA
Risk factor
-Obesity -DM -Ascites
-Steroid -Smoking - Wound infection
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Physical examination of hernia
Inspectionon standing position
 Shape of the swelling
 location of the swelling
 unilateral or bilateral
 overlying skin
 see for expansile cough impulse
Hernia with no expansile impulse
 omentocele with adhesion
 obstructed hernia
 strangulated hernia
 see position of penis
Palpation
 temperature
 Tenderness
 Consistency
 Soft and elasticenterocele
 Firm and doughyomentocele
 Tense and tenderstrangulation
 Bag of warmvaricocele
 Reducibility
 Direct inguinal hernia reduce by itself on lie down
 Indirect inguinal hernia manually reduce
 Enterocele the first part difficult to reduce but the last reduce easily
 Omentocele the first part reduce easily but the last reduce with difficulty
due to adhesion
 Not reducestrangulated
 Invagination of scrotal skin by index finger to examine
 Size of superficial inguinal ring
 Direction of the hernia sac
 Direction of expansile impulse
 Not performed in children
Do Internal ring occlusion test
 Examine normal side
 Examine abdomenfor any surgical scar
Watch video on how to examine hernia @

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https://www.youtube.com/watch?v=JR27rKrhvkE
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Hemorrhoids, anal fissure & fistula in ano
Hemorrhoids
Hemorrhoids are pathologically swollen blood vessels in the lower rectum.
Classification
I. Internal hemorrhoids______________
By dentate line
II. External hemorrhoids
Risk Factors
 Constipation & Straining
 Pregnancy
o Postpartum hemorrhoids from straining during labor
 Low fiber diet
 Age (elderly)
 Family hx
 Chronic diarrhea
 prolonged toilet sitting
 Colon malignancy
 IBD
 Heavy weight lifting
i) Hx
 Rectal…
o Bleeding
 Usually bright red
 If it’s darker or blood mixed with stoolbetter to suspect
a more proximal cause of bleeding
o Pain
 External Vs internal
 External painfullbecause of somatic innervation
o Pruritis
o Prolapse
 Ask if reducable (by itself or manually) or not
 Change in bowel habit
 Ask pt’s immune status…
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ii) P/E
 Inspection of the rectum
o Skin tagsRedundant tissue from old thrombosed external hemorrhoids
o Fissure
o Fistula
o Signs of infection or abscess formation
o Rectal /hemorrhoidal prolapse
 DRE
o Indurated/ulcerated area
o Masses, tenderness, mucoid discharge or blood
o Rectal tone
o Palpate the prostate in all men
Grading of internal hemorrhoids
I. Projection into the anal canal + often bleed + no prolapse
II. Protrusion beyond anal verge with defecation + spontaneous reduction
III. Protrusion + manual reduction
IV. Chronic protrusion + not reducible
 This pts are @ risk of strangulation
DDx
 Condyloma acuminata
 Anal fissure
 Anal fistula
 Anal abscess
 Proctitis
 Rectal prolapse
 Colorectal ca
HPI
 This pt was LRH 02 weeks back @ which time he started to experience
bright red bleeding per rectum at the end of defecation. In addition he
has manually reducible, painless per rectal swelling…
Investigations
 Lab
o CBC
 Infection, anemia
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 Anoscopy & flexible sigmoidoscopy
Mgt
1. Conservative Rx
a. Give stool softener
b. Advice on
i. high fiber diet
ii. increasing fluid intake
iii. Avoidance of straining
iv. Good hygiene
2. Non-surgical
a. Rubber band ligation
b. Infrared photo-coagulation
c. Sclerotherapy
3. Surgical
a. Excision of thrombosed external hemorrhoids
b. Operative hemorrhoidectomy
Complications of hemorrhoidectomy
o Post-op pain
o bleeding
o Urinary retention
o Infection
o Transient incontinence
o Anal stenosis
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Anal fissure
 Anal fissure is a tear in the anoderm distal to the dentate line.
 Acute if <6wks
 Tend to occur in younger & middle aged persons
Risk Factors
 Trauma
o From passage of hard stool or
o Chronic diarrhea
 Low fiber diet
 Prior anal surgery
 Severe pain during bowel mov’t…
o Afraid of bowel mov’tsconstipation(hard stool)more anal pain
o Burning, tearing or cutting type of pain
 Bright red blood (hematochezia) on the toilet or stool (few drops)
 Spasm of the anus
 Fissures can often be seen in the anoderm
 Cmn siteposterior mid line
o Off the midline …raise the possibility of
 CD(IBDs), AIDs, Syphilis, TB, leukemia
 Pts are always too tender to tolerate DRE
Mgt
1) Conservative Rxto minimize anal trauma
 Bulk agents
 Stool softeners
 Warm sitz baths
 Analgesic creams
2) Surgical Rxfor chronic fissures that failed medical therapy
 Lateral sphincterotomy
o To decrease spasm of internal sphincter by dividing a portion of the
muscle
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Fistula in ano
Fistula in ano is an abnormal tract or cavity with an external opening in the perianal area by
identifiable internal opening.
Risk Factors
 Previous anorectal abscess
 Cryptoglandular infection
o Infectionabscessfistula
 Trauma
 CD ( Crohn’s disease)
 Anal fissures
 Anal carcinoma
 Radiation therapy for prostatic ca.
 Actinomycosis
 TB
 LGV
Parks classification
I. Inter-sphincteric
 70%
II. Trans-
III. Sub- sphincteric
IV. Extra-
i) Hx
 Perianal discharge
 Pain
 Swelling
 Bleeding
 Diarrhea
 Skin excoriation
ii) P/E
Look for
 an external opening
 Spontaneous discharge
DRE/digital rectal examination/
 Fibrous/chord like tract beneath the skin
 Abscess if not yet drained
 Indurations
Mgt
 Drainage
 Eradicating the fistulous tract
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GENITO-URINARY RELATED
SHORT CASES
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URETHRAL CATHETERIZATION
Indications
 Therapeutic
 Acute Urinary Retention(AUR)
 Due to BPH or
 Blood clots
 For initiation of continuous bladder irrigation
 Chronic urinary retention that causes hydronephrosis
 Hygienic care for bedridden pts with incontinence
 To Instill medication
 Diagnostic
 For collection of uncontaminated urine specimen
 To monitor urine output
 Imaging of the urinary tract
Contraindications
 In presence of traumatic injury to lower urinary tract
o E.g. Urethral tear
 This condition must be suspected in patients with a pelvic or straddle-
type injury.
 Relative contraindication
o Urethral stricture
o Recent urethral or bladder surgery
Complications
 UTI
 Urethral stricture
 Urethral perforation
 bleeding
 Paraphimosis
 Non deflating retention balloon
 Chronic catheterization may lead to…
o Bladder calculi formation
o Bladder ca.
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Procedural notes on urethral catheterization Types of catheter
1) condom catheter
Materials 2) straight catheter(1 way)
 Sterile gloves, sterile dressing, sterile draping sheet 3) Indwelling catheter(2 way)
 Foley’ catheter, urobag E.g. Foley catheter
 lubricant,antiseptic soln. 4) suprapubic catheter
 syringe, distilled water 5) #3 way catheter
 lidocaine *for continuous bladder irrigation
Procedure
 Explain to the patient that a catheter is going to be introduced through his urethral orifice.
o Reassure that it will be a painless procedure.
 Scrub and put-on sterile gloves
 Position supine with legs apart (frog leg position with knees flexed)
 clean the genitalia with antiseptic solution and drape the area
 The uncircumcised foreskin is retracted, and the glans penis and the corona exposed
o The glans penis is cleaned with antiseptic solution
 Using a syringe with no needle, instill 5-10 mL of lidocaine gel 2% into the urethra. Place a finger
on the meatus to help prevent spillage of the anesthetic lubricant. Allow 2-3 minutes before
proceeding with the urethral catheterization
 The penis is held vertically upwards to straighten the penile urethra
o by encircling a sterile gauge around the penis
 The lubricated Foley's catheter is then pushed gently through the external urethral meatus and
gradually advanced till it reaches the bladder
o urine will be seen coming through the catheter
 The catheter is advanced a little further
 About 15–20 mL of water is introduced through the side channel of the catheter to inflate the
balloon
 After the balloon is inflated the catheter is gently pulled outward to confirm that the balloon is
properly inflated
 The catheter is then connected to urobag.
 The preputial skin is brought back over the glans penis to prevent development of paraphimosis
 In case of chronic retention the bladder should be emptied slowly.
What may be the cause of failure to insert a catheter?
 catheter may be too large
 Stricture of urethra
 Prostatic enlargement
 Bladder neck stricture
 tight phimosis
 Meatal stenosis.
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Suprapubic cystostomy
Indications
1. AUR
 When urethral catheter cannot be passed 20 to
 Urethral stricture
 Bladder neck contractures…
2. Urethral trauma
 Have high index of Suspicion in
 Pelvic fracture
 Saddle-type injuries
Triad (CFs)
1. Blood @ urethral meatus
2. Inability to urinate &
3. Palpably distended bladder
3. Mgt of complicated lower genito-urinary tract infection
 E.g. acute bacterial prostatitis
4. Requirement for long term urinary diversion
 E.g. neurogenic bladder<<>>unable to void
Contraindications
1. Absolute
a. If the bladder is not distended
b. Hx of bladder ca.
2. Relative
a. Coagulopathy
b. Previous lower abdominal or pelvic surgery
c. Pelvic cancer
Complications
 Inadvertent urethral catheterization
 Intraperitoneal & or extraperitoneal extravasation
 Obstruction of tubing (by blood, mucous, or kinking)
 Immediate complications include gross hematuria (which is usually transient)
 Serious complications of the procedure include bowel perforation and other intra-
abdominal visceral organ injuries
 Possible complications from long-term catheter use include; recurrent symptomatic
UTI, bladder and renal calculi formation, deterioration of renal function, and increased
risk of bladder cancer.
o Suprapubic catheter use may be additionally complicated by exit site infections or
leakage.
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Procedural note on suprapubic cystostomy
Percutaneous Suprapubic Cystostomy

Initial steps
 Clean the abdominal wall. Shave the suprapubic operative field with clippers. Prepare the site
with an antiseptic
 Create a surgical field with 4 sterile towels, ensuring that the pubic symphysis can be visualized
and palpated.
 Remove the introducer and catheter from the packaging, using aseptic technique, and place in
the sterile field.
 Ensure that the patient has a full and palpable bladder to confirm urine return. Palpate the
distended bladder, and use a marking pen to note the site of percutaneous catheter placement,
2 finger breadth above the pubic symphysis in the midline
avoid placing the catheter in natural skin creases
 Fill a 10-mL Luer-Lok syringe with 5 mL of 1% lidocaine and 5 mL of 0.25% bupivacaine.
o Attach the syringe to a 22-gauge, 7.75-cm spinal needle.
 Raise a skin wheal at the marked site, and infiltrate the anesthetic into the subcutaneous tissue
and rectus abdominis muscle fascia, aiming the needle at a 10-20° angle toward the pelvis.
 Advance the needle in this direction, while aspirating the syringe; urine should be easily
aspirated when the bladder is entered.
 After this point, placement techniques de end on the ty e of the catheter et…
 1) Cystostomy with Peel-Away Sheath suprapubic catheter set
 2)Cystostomy With Rutner Suprapubic Catheter Set……………………………..
1) Cystostomy with Peel-Away Sheath suprapubic catheter set
 Once needle entry into the bladder has been confirmed by aspiration of urine
 Remove the Luer-Lok syringe from the spinal needle, and advance a guide wire through the
needle into the bladder.
 While holding the wire securely (this is now the route of access to the bladder), carefully remove
the needle over the wire, leaving the wire in place.
 Directly posterior to the wire, use a scalpel with a No#11 blade to make a stab incision through
the skin and subcutaneous tissue.
 Pass the Peel-Away Sheath and the indwelling fascial dilator together over the wire and into the
bladder.
 Remove the guide wire and the fascial dilator, leaving only the Peel-Away Sheath inside the
bladder.
 Pass a Foley catheter (of appropriate size) through the indwelling intravesical sheath and into
the bladder.
 Aspirate urine to confirm proper placement.
 Inflate the Foley balloon with 10 mL of sterile water, using a Luer-Lok syringe.
 Gently withdraw the Peel-Away Sheath from the bladder and anterior abdominal wall; using
each side of the Peel-Away Sheath, split the sheath into 2 parts, leaving the catheter in place.
 Connect the indwelling suprapubic Foley catheter to a drainage bag.
 secure the catheter to the skin of the anterior abdominal wall. & Place 2 drain gauze pads (4 × 4
in) at the cystostomy site.
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Scrotal swelling
DDX for scrotal swelling
1. Hernia (see hernia @ page195)
2. Hydrocele
 Fluid collection in the tunica vaginalis of the scrotum or along the spermatic
cord.
 May be vaginal or infantile hydrocele
3. Hematoma
4. Epididymal cyst
 Cystic degeneration of the epididymis filled with crystal clear fluid.
5. Testicular torsion (see below…)
6. Epididymo-orchitis (see below…)
7. Testicular tumor
 Seminoma=carcinoma of the seminiferous tubules
 Non-seminoma=malignant germ cell tumor
8. Varicocele
 is a result of dilation of veins that drain into the internal
spermatic veins
 the left sidemost commonly affected
 Examination of a man with varicocele when he is upright reveals
a mass of dilated, tortuous veins lying posterior to and above
the testis. It may extend up to the external inguinal ring, and the
Valsalva maneuver can increase the degree of dilation
9. Syphilitic gumma
How to differentiate?
Answer the following during your Physical Examination…
1. Can you get above the swelling?
2. Can you identify the testis & epididymis?
3. Is the swelling translucent?
4. Is the swelling tender?
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https://www.youtube.com/watch?v=CCpxEePuc24
Then use the algorithm below…
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Scrotal swelling
Not confined to the scrotum Confined to the scrotum
Hernia Infantile Testis & epididymis not definable Definable testis & epididymis
Cough impulse hydrocele
(+ve) No cough impulse
Reducible Not reducible Opaque Translucent Opaque Translucent

Testis palpable Testes not palpable
Opaque Translucent
Epididymal cyst
Vaginal hydrocele
Tender Non tender Tender

 Acute epididymo-orchitis
 Torsion  Chronic
 Severe epididymo- hematocele
Non tender
orchitis  Gumma
 Tumor
 Acute hematocele  Tumor
 Tuberculous epididymitis
Possible investigations to rule out the DDx

Lab.studies
 CBCleukocytosis--Incase of epididymo-orchitis/strangulated hernia…
 Serum a-fp , HCGTesticular tumor
 Urinalysis & cultureEpididymo-orchitis…
Imaging
 UltrasoundTesticular tumor…
 Doppler u/sTorsion/ epididymo-orchitis…
 Plain abdominal X-ray
 Acute hydrocele Vs incarcerated herniaGas overlying the groin
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Testicular torsion
 Testicular torsion refers to the twisting of the spermatic cord structures
resulting in subsequent loss of blood supply to the epididymis & the
testis.
 a urologic emergency that requires rapid diagnosis and intervention in
order to maintain viability of the testicle
 RFs for torsion
o Undescended testis
o Testicular tumor
o “bell clapper deformity”
 High investement of the tunica vaginalis causes the testis to
hang within the tunica vaginalis like a clapper in a bell
 Precipitants
o Straining on stool
o Lifting of a heavy wt
o coitus
 CPs
o History
 Sudden onset of testicular pain
o at a distinct point in time
 Subsequent swelling
 The patient feels nauseated & may vomit
o Physical examination
 Inspection
 Swollen, asymmetric scrotum
 Palpation
 Tender, firm testicle
 high riding testicle
 may have horizontal lie of testicle
 The posteriorly positioned epididymis may be
positioned differently
 No pain relief with elevation of the testiclemakes it
worse
 The spermatic cord may appear thickened
 cremasteric reflexlost
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 Investigation
o Doppler ultrasound
 What to look?
 Decreased intra-testicular blood flow relative to the
contra-lateral testis
 Other advantages
 Can rule out an associated testicular tumor
o NB*Diagnostic testing should not delay treatment
 Mgt
o Immediate surgical exploration
 Early diagnosis and treatment are vital to saving the testicle and
preserving future fertility.
 The rate of testicular viability decreases significantly after 6 hours from
onset of symptoms
 Immediate surgical exploration (<6hrs after the onset of
symptoms) can salvage an ischemic testis in >80% of pts
 if 12 hrs lapsed the rate decreases to 20%
o During surgical exploration
 Detorsion
 the testicle is rotated to its normal position to restore blood
flow to the testicle.
 Assess for viability after being given time for normal blood flow
to resume
o Intra-op blood flow ass’t
 Doppler u/s or
 Incising the tunica vaginalis & examining for blood
 If viable
 orchiopexy of the affected and the contralateral testicle is
completed.
 If the affected testicle is nonviable
 orchiectomy of the affected testicle
o To avoid later risk of abscess formation if the testis is
clearly necrotic
 orchiopexy of the contralateral side
o Fixed to dartos fascia
 Why the contralateral normal testis also explored?
 because of the possibility that the same anatomic defect
allowing torsion exists on the contra-lateral side
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Epididymo-orchitis
 Inflammation confined to the epididymis is epididymitis…
 Infection spreading to the testis is epididymo-orchitis.
Causes
 Is typically result of bacterial infection originating in the urinary
tract
 Generally epididymitis arises
 In sexually active young men from a genital infection
 Common causative agent of epidydimitis chlamydia
trachomatis
 Older male from urinary infection (as in case of BOO) or
May be secondary to urethral catheterization
CPs
 History
 Unilateral scrotal pain
 The onset is fairly rapid, but not as sudden as testicular
torsion
 swelling of the epididymis & or testis
 Often with fever
 May have initial symptoms of urinary or genital infection
 Physical examination
 The scrotum wall become red, edematous & shiny
 May become adherent to the epididymis
 Elevation of the testis reduces the pain
Investigations
 CBC
 WBC count is often raised
 Ultrasound
 May provide supporting evidence
 Such as increased blood flow to the epididymis
 A reactive hydrocele may be present
 Reduced testicular blood flowIn case of
ischemic orchitis 20 to intratesticular infection
 U/A pyuria
 Will usually show leukocytosis
 In young pts urethral swabschlamydial testing
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Mgt
 Antibiotics
 Route-PO
 If the pt is not markedly febrile & is otherwise stable
 Route-Parenteralhospitalization
 If high fever or significantly elevated WBC or if
hemodynamically unstable
 Initial DOC in young pts
 Doxycycline (100-200mg daily) or
 Quinolone
 Contact tracing Rx if necessary
 Initial DOC in older pts
 Quinolone
 If evidence of systemic sepsis
 IV antibiotics directed @ urinary pathogens
 Duration
 It should continue for at least 02 wks or until the
inflammation has subsided
 Other measures
 All pts should drink plenty of fluid
 Local measures include;
 Scrotal support
 Analgesia
 Surgery
 Drainage
 If suppuration occurs
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Hypospadia, epispadia & bladder etrophy
By-Bruh Alem(sms)
Hypospadias
is the most common congenital abnormality of the urethra in males in which
it opens abnormally on the ventral surface of the penis (one in 200–300 male
live births).
There are 3 characteristic features
 external meatus opens on the underside of the penis or the perineum,
 ventral aspect of the prepuce is poorly developed (‘hooded prepuce’) and
 ventral deformity of the erect penis (chordae).
Classification
 Glandular hypospadias
o placed on the glans penis, but proximal to the normal site of the external
meatus(blind pit).
 Coronal hypospadias
o placed at the junction of the underside of the glans and the body of the penis.
 Penile and penoscrotal hypospadias
o on the underside of the penile shaft.
 Perineal hypospadias
o bifid scrotum, urethra opens between its two halves with testicular maldescent,
rarest and most severe
Features
 Absence of urethra and corpus spongiosum distal to abnormal urethral
orifice.
 Bowing or bending of penis distal to abnormal urethral opening
(chordee), with poorly developed prepuce over inferior aspect.
 Urine soakage over the scrotum with dermatitis and infection.
 Associated congenital anomalies are known to exist.
Treatment
 Does not cause either obstruction or urinary tract infection. Surgery is
indicated to improve sexual function, to correct problems with the urinary
stream and for cosmetic reasons.
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Epispadias
Urethral opening is on the dorsum of the penis and is associated with an
upward curvature of the penis. Epispadias are very rare but often coexists with
bladder exstrophy and other severe developmental defects. Most common site
is at the abdominopenile junction.
Treatment
 Correction of incontinence of urethra
 Urinary diversion.
Bladder exstrophy
Incomplete development of the infraumbilical part of the anterior abdominal
wall and anterior wall of the bladder. Associated with the spina bifida and other
anomalies. 1:50 000 births (m:f-4:1)
Features
 penis is broad and short ± bilateral inguinal hernia.
 Red mucus membrane of posterior bladder wall protrudes out
 with visible urine efflux from ureteric orifice.
 Umbilicus absent with separation of the pubic bones.
 females, defective external genitalia
Problems
 Repeated soakage,
 Ulceration,
 Pain,
 Recurrent pyelonephritis,
 Renal failure (50% of pt die)
Long-term complications
 stricture at the site of anastomosis,
 hyperchloremic acidosis,
 adenoma and adenocarcinoma at the site of a ureterocolic
anastomosis(20-fold)
Treatment
 bladder is closed in the 1st yr of life, osteotomy of both iliac bones,
reconstruction of the bladder neck and sphincters.
 urinary diversion ( ureterosigmoid anastomosis, ileal or colonic conduit,
continent urinary diversion)
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MUSCULO-SKELETAL RELATED
SHORT CASES
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AMPUTATION
Indications
1. PVD/peripheral vascular disease/
 DM accounts around 50%
2. Trauma
 High grade open fractures with associated nerve injury, soft tissue loss &
ischemia + un-reconstructable neurovascular injury
3. Tumor
 Malignant bone & soft tissue tumors
4. Infections
 fulminating gas gangrene
 acute/ chronic bone infection that is unresponsive to antibiotic/ surgical
debridement
5. Congenital anomalies/ deformities
6. Burns & frostbite
Contraindications
 Poor health that impairs the patient’s ability to tolerate anesthesia & surgery
Types of limb amputations
 Leg amputations can be divided into 2 broad categories:
Major amputations:
 Below-knee amputation/BKA.
 Knee disarticulation Minor amputations:
 Above-knee amputation (transfemoral)  Amputation of digits
 Rotationplasty
 Partial foot
Foot being turned around and reattached to allow the ankle joint to be used as a
knee amputation
 Hip disarticulation  Ankle disarticulation
 hemi-pelvectomy
 Arm amputations
o Amputation of digits
o Metacarpal amputation
o Wrist disarticulation
o Forearm amputation (transradial)
o Elbow disarticulation
o Above-elbow amputation (transhumeral)
o Shoulder disarticulation and forequarter amputation
o Krukenberg procedure
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Complications of Amputation
1. Phantom pain
2. Hematoma
3. Infection
4. Failure of wound to heal
5. edema
6. Contracture
7. Neuroma
8. Psychological distress
9. Complications due to immobility & pressure
Amputation procedure
 General principle of amputation
o Appropriate mgt of…
 Skin
 Bone
 Nerves
 Vessels
 Procedure
o Remove the diseased tissue and any crushed bone
o Smooth uneven areas of bone
o Seal off blood vessels and nerves
o Cut and shape muscles so that the stump, or end of the limb, will be
able to have an artificial limb (prosthesis) attached to it
Types of prosthesis
1. Endoprosthesisimplants used in orthopedics surgery
2. Exoprosthesis external replacement for lost limb
 May be temporary or permanent
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FRACTURE MANAGEMENT
ATLS
1. Primary survey & resuscitation
 ATLS assess “ABCDE”& act accordingly…
 Air way
 Breathing
 Circulation
 Neurological exam
 Exposure
2. Secondary survey
 Take Hx
 Do P/E
 Work up the pt
 Definitive mgt
 Reduction
 Immobilization
 Rehabilitation
Definitive mgt of fracture
A.Reduction
1. Closed manipulation
 Using general anesthesiasometimes local/regional--may be
possible
 Grasp the fragments through the soft tissue then adjust them as
nearly as possible to their correct position
2. Mechanical traction (With or without manipulation)
 Used when the contraction of large muscles exert a strong
displacing force
 Traction
o Weight or
o Screw device
3. Operative reduction
 Reduction under direct vision
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B. Immobilization
…Why we immobilize them?
 To prevent angulation/displacement
 To prevent mov’t that may interfere with union
 To relieve pain
 Immobilization must include the joint above & below the #
...How???
1) POP (plaster of Paris)
Indications
1. Undisplaced fractures
2. Tolerable displacement
3. Closed reduction of displacement possible
4. Fracture in children ( Upper and lower extremities)
Types
 Padded
 Un padded
 Circular
 Slab
 Hip spica
Application of POP
 Long arm POP
 Short arm
 Long leg
 Short leg
Advantages;
- Easy
- No risk of infection
Disadvantages;
- Damage to vessels & nerves by compression
Compartment syndrome
Mgt =
 All constrictive dressings must be released
 If no significant change after 30-60 min
monitoringfascioctomy is required
-Difficult for wound care

- Needs strict control
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2) Splinting==continual traction
<<>> Traction
A. Skin traction
 In children
B. Skeletal traction
 Pin insertion sites
i. condyle of the femur (distal femur)
ii. proximal tibia
 Pin, insert fromlateral to medial
 Where?1 finger below then 1 finger lateral to
tibial tuberosity
 Why?...to prevent neurovascular damage
 If cmn peroneal nerve is affected foot drop
**Weight applied=1/6th up to 1/10th of pts weight
iii. Calcaneus
 Pin, insert frommedial to lateral
 Weight appliedusually up to 3kg
 Cmnly used for femoral neck fracture
Disadvantages
i. Long immobilization time (usually up to 06 wks)
ii. bed sore
o on bony prominences
iii. Infections (pin site infection…)
o Pin site infection grading
 Grade Ipain(tenderness)
 G II all cardinal signs of inflammation present
 G III Serous discharge
 G IV Purulent discharge
 G V Bone involvement (osteomyelitis)
o When to act
 G Vremove
 G IV + loose pinremove
 G IIIAntibiotics
 …
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iv. Joint and muscle contracture
v. Deep vein thrombosis, pulmonary embolism
o Should be given heparin prophylaxis
*Follow-up after traction
=Follow by measuring the true length
=Shortening up to 2cms may be acceptable
=For a significant shortening add weight & for lengthening the vice versa.
3) External & internal fixation

I) Internal fixation
Methods
 Metal Plate & held by screws
 Intramedullary nailing with or without cross screw fixation
o Site=femur, Tibia, Humerus
 Tension band wiring
o Site=patella , olecranon , Ankle
 wire tied over 2 kirschner wires or pins
II) External fixation

 For grade III open fractures (see the Gustilo and Anderson grading below)
 External fixator should be applied 1.5-2cms away from the
wound site
 Advantage
o wound accessible for treatment<<>>wound care
o skin graft or flap rotations possible after wound
healing
 Disadvantage
o pin tract infection
Operative treatmentAdvantages;
*Anatomical reduction
*Early mobilization & return of function
Disadvantages;
 Expensive
 Risk of infection
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C. Rehabilitation
 Purpose
 to preserve & restore functions to normal as far as possible
 Should begin as soon as fracture comes under definitive
treatment
 By Physiotherapist
*Gustilo and Anderson Open Fractures classification

Criterias for the classification
o Wound size
o Level of contamination
o Soft tissue injury (STI)
o Bone injury
Level of
Type Wound Contamination Soft Tissue Injury Bone Injury
I <1 cm Clean Minimal Simple, minimal

long comminution
II >1 cm Moderate Moderate, some muscle damage Moderate comminution
long
III
A Usually High Severe with crushing Usually comminuted; soft
>10 cm tissue coverage of bone
long possible
B Usually High Very severe loss of coverage; Bone coverage poor;
>10 cm usually requires soft tissue variable, may be moderate to
long reconstructive surgery severe comminution
C Usually High Very severe loss of coverage plus Bone coverage poor;
>10 cm vascular injury requiring repair; variable, may be moderate to
long may require soft tissue severe comminution
reconstructive surgery
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Bone Infection & Tumor
I) OSTEOMYELITIS
Osteomyelitis
Acute Chronic
 Following sequestra formation
 Prior to formation of sequestra
 Other hallmarks
o Involucrum
o Local bone loss
o Sinus tracts
NB*
Sequestrum=necrotic bone
Involucrum=new bone formation around the dead bone
NB*
 Although the time limits delineating one category from the other are
somewhat arbitrary, as a rule
 infections up to 3 months' duration are termed acute,
 While those enduring longer than 3 months are termed chronic.
 Some include a third category, "subacute," for patients who exhibit
symptoms that endure longer than 3 months but who have not
developed extensive necrotic bone
Etiology
 Pyogenic osteomyelitis /Staph.aureus/cmn
o Cmn Sites
 In children
 long bones--metaphysis
 in adults
 Vertebrae
 tuberculous osteomyelitis
o the spine is the most cmn sitepott’s disease
Routes of organism entry
Hematogenousmost cmn Direct implantation after compound

fracture or orthopedic surgical procedures
Direct extension from infected joint or soft tissue

e.g. diabetic foot ulcer
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Risk factors
 Immunodeficiency disorders
 Sepsis
 Minor trauma coincident with bacteremia
 Indwelling vascular catheters
 Chronic hemodialysis vascular access
 Sickle cell disease
Clinical features
 Classic signs of inflammation
o local pain/bone pain
o swelling
o Redness…
 Fever
 Draining sinus
Investigations
 CBC
o Leukocytosis may be observed in the setting of acute osteomyelitis but is unlikely
in the setting of chronic osteomyelitis
 Increased ESR & CRP
 Blood culture
o may be positive in about half of cases of acute osteomyelitis
 Discharge analysis Culture and Gram staining
 Radiograph may be normal up to 10dys
o Within 72 hr deep-soft tissue edema (swelling) with displacement of the deep
muscle planes
o In 5-7 daysPeriosteal reaction
o After 7-14 daysLytic bone changes, which are not visible until 30-50% of the
bony matrix is destroyed.
o Infection in flat and irregular bones can take longer to appear.
 Radionuclide scanning
 MRI
o MRI is very sensitive for the detection of acute osteomyelitis and demonstrates
abnormal marrow edema as early as three to five days following onset of infection
Complications of chronic osteomyelitis
o Pathologic fracture
o Sepsis, endocarditis
o Squamous cell carcinoma (Marjolin’s ulcer) of sinus tract
o Osteosarcoma
o Growth plate involvement in children may result in impaired bone growth
o Septic arthritis
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Mgt
Acute recent infection
1. Establish free drainage
2. Antibacterial medication
 Antibiotics choice depends on
 Age
 Underlying medical condition
 Suspected pathogens and their susceptibility pattern
 Antibiotic safety and efficacy and availability
 DOC
 Cloxacillin /Naficillin /clinidamycin plus
 Ceftriaxone /cefotaxime /cefuroxime or chloramphenicol
 Duration of treatment 3-6 weeks
 Changing antibiotics from the intravenous route to oral administration
 When patient condition has stabilized, usually 5 -10day of IV antibiotics
 The patient has been afebrile for 48 to 72 hours
 Local signs and symptoms of infection are reduced considerably
 Peripheral leukocyte count has normalized
 ESR has decreased by at least 20 percent or there has been a 50 percent
decrease in the concentration of CRP
Indicators of quiescence are…
o Discharge of pus ceases
o Wound becomes lined by healthy granulations
NB*@ this stage wound closure may be attempted either by 20 suture, if
practicable or alternatively by grafting with split skin or covering with a local flap
3. Indication & Principles of surgical Rx
 Indications
 When unresponsive to specific antimicrobial Rx
o Prolonged fever
o Persistent pain and swelling
 When there is evidence of persistent soft tissue abscess or
subperiosteal collection
 If concomitant joint infection is suspected
 Chronic osteomyelitis
 Principle of surgical mgt
 Adequate drainage
 Extensive debridement of necrotic tissue
 Mgt of dead space
 Adequate soft tissue coverage
 Restoration of blood supply
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II) Bone Tumors
Risk Factors
 Paget’s disease
 Radiation
 Fibrous dysplasia
 hereditary
Classification of bone tumors
Primary Secondary/metastasis cmn

1. Breast
2. Prostate
osteogenic tumors 3. Lung
1. Benign 4. Renal
a. Osteoid osteoma 5. Thyroid
b. osteoblastoma
2. malignant
a. osteosarcoma Chondrogenic tumors
1. Benign
Osteochondroma
2. Malignant
chondrosarcoma
Marrow derived
Malignant
o Myeloma
o lymphoma
Others
 Ewing’s sarcoma
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Primary
Bone forming/ osteogenic tumors
 Benign
 Malignant/ Osteosarcoma
 Most common primary bone malignancy
 Most cmn in distal femur, followed by proximal tibia
 aggressive lesions that metastasize through the blood stream early in their
course
 The lungs are common sites of metastases
Cartilage tumors
o Osteochondroma
 benign cartilaginous capped bony projectiongrowing away from the joint
towards the diaphyseal region
 can be pedunculated or sessile
o chondrosarcoma
 2nd most common malignant bone tumor
 They arise in central portions of the skeleton
 Patients present with painful progressively enlarging masses
 Metastases show predilection for lungs and skeleton
Others
 Ewing’s sarcoma
o Tends to arise in the diaphyses of long bones/pelvis
o CPspainful mass +general symptoms with fever, anemia
o Increased ESR
o X-ray’moth-eaten’ bone + ‘onion skin’ periosteal rxn
Metastatic (20) tumor
 Can be Cmn sites of metastasis
 LyticKidney, Lung…  Spine
 ScleroticProstatic ca.  Proximal femur
 Mixed…  Proximal humerus
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FOOT DEFORMITY
By- Endalkachew Belayneh(sms)
 It is a disorder of the foot and can be congenital or acquired
 Examples of acquired causes
 bunion/Hallux valgus
 Hallux virus
 hammer toe
 foot drop
 flat feet
 Examples of congenital causes
o pigeon toe
o club foot
o pes caves
o rocker bottom foot….etc
Club foot (congenital talipes equinovarus)
It is a congenital deformity involving one foot or both. The affected foot appears
to have been rotated internally at the ankle. Without treatment, people with
club feet often appear to walk on their ankles or on the sides of their feet.
However, with treatment, the vast majority of patients recover completely
during early childhood and are able to walk and participate in athletics just as
well as patients born without the deformity.
 It is a relatively common birth defect, occurring in about one in every
1,000 live births. Approximately half of people with clubfoot have it affect
both feet, which is called bilateral club foot. In most cases it is an isolated
disorder of the limbs. It occurs in males twice as frequently as in females.
Diagnosis
o By looking after birthinspection
o Foot x-rayDr’s interest
o In-utero ultrasound
Treatment
o French method
o ponseti method
o surgery
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HEENT + LYMPHO-GLANDULAR RELATED
SHORT CASES
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SALIVARY GLANDS
Major Minor
1. Parotid Dispersed throughout the
2. Submandibular aerodigestive tract
3. sublingual
I) Salivary gland tumors (SGTs)

 Clinical Presentation of benign SGTs
o Painless, slow growing mass
o Well circumscribed
o Almost always freely mobile
 Faceparotid gland
 unaffected facial nerve function(benign)
 Angle of jawDDx
 Submandibular gland
 Tail of parotid gland
 Floor of mouthSublingual gland
 Parotid80% of the SGTs
 80% benign
 pleomorphic adenomasmst cmn-60%
 warthin tumor5-15%--2nd cmn
 Clinical signs of malignancy
o Rapid growth
o pain
o Bleeding
o Airway compromise
o Nerve dysfunction
 E.g. paresthesia, facial palsy…
o Skin fixation
 See how to examine mass on page… 239
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II) Salivary gland infection & calculi
 80% in Submandibular gland
Submandibular calculi/ sialolithiasis/
 factors which encourage stasis in the submandibular duct
1. Anatomy of the duct  gravity
2. Quality of mucus
CPs
 The main symptoms are
1. swelling
 start to worsen just before eating
2. Pain
 dull aching
 worsen during eating
 goes away before the swelling
***purulent saliva may be present
Submandibular sialadinitis
o 20 to the presence of a stone in its duct or
 the damage done by a stone which has passed through the
duct.
o Staphylococcuscmn
CPs
o Pain, which is
 severe, throbbing, continuous
 Exacerbated by eating.
o Heat & tenderness
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CLEFT LIP & PALATE
By-Bruh Alem(sms)
 Clefting of the lip and/or palate is felt to occur around the eighth
week of embryogenesis, either by failure of fusion of the medial nasal
process and the maxillary prominence or by failure of mesodermal
migration and penetration between the epithelial bilayer of the face.
Etiology----Multifactorial
 Familial—more common in cleft lip or combined cleft lip and palate (Risk
increased by 4%).
 increased parental age, drug use (steroids /diazepam) and infections
during pregnancy
 Protein and vitamin deficiency.
 Rubella infection.
 Radiation.
 Chromosomal abnormalities.
 smoking during pregnancy
Classification
I. Cleft lip alone
 Central
o RareIn upper lip. Between two median nasal processes. (Hare lip)
 Lateral
o maxillary and median nasal process, commonest; can be unilateral or bilateral
 Incomplete cleft lip does not extend into nose
 Complete  cleft lip extends into nasal floor
 Simple  cleft lip is only cleft in the lip
 Compound cleft lip is cleft lip with cleft of alveolus
II. Cleft of primary palate (in front of incisive foramen) only
a. Complete—means absence of pre-maxilla (anterior hard palate)
b. Incomplete—means rudimentary pre-maxilla
i. Unilateral.
ii. Bilateral.
iii. Median.
III. Cleft of secondary palate (behind the incisive foramen) only
a. Complete—nasal septum and vomer are separated from palatine process.
b. Incomplete
c. Sub mucous
It can be - Cleft with soft palate involvement.
- Cleft without soft palate involvement.
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IV. Cleft of both primary and secondary palates
V. Cleft lip and cleft palate together

 Defect is often associated with other congenital anomalies of cardiac, gastrointestinal,
neurological system e.g., Pierre-Robin syndrome, Klippel-Feil syndrome, Stickler’s syndrome,
Shprintzen’s syndrome, Down’s syndrome, Treacher-Collin’s syndrome, Apert’s syndrome and
trisomy.
Problems in Cleft Disorders
 Difficulty in sucking and swallowing. This is commonly observed in cleft
palate than in cleft lip.
 Speech is defective especially in cleft palate, mainly to phonate B, D, K, P,
T and G.
 Altered dentition or supernumerary teeth.
 Recurrent upper respiratory tract infection.
 Respiratory obstruction (in Pierre Robin syndrome)
 Chronic otitis media, middle ear problems.
 Cosmetic problems.
 Hypoplasia of the maxilla.
 Problems due to other associated disorders.
Treatment for Cleft Lip
 Principles of cleft lip repair
 “Rule of 10’ should be fulfilled
o 10 pound in weight
o 10 weeks old
o 10 gm % hemoglobin
 Before 6 months it should be operated
 Proper postoperative management like control of infection, training for
sucking, swallowing and speech.
 Millard advancement flap is commonly used for unilateral cleft lip repair
 Bilateral cleft lip repair can be done either in single or two stages (with 6
months gap between each stage)
 Management of associated primary or secondary cleft palate deformity.
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Cleft Palate
 It is due to failure of fusion of the two palatine processes.
 Defect in fusion of lines between premaxilla (developed from median nasal
process) and palatine processes of maxilla one on each side.
 When premaxilla and both palatine processes do not fuse, it leads into
complete cleft palate (Type I cleft palate)
 Incomplete fusion of these three components can cause incomplete cleft
palate beginning from uvula towards posteriorly at various lengths. So it
could be Type II a–bifid uvula, Type II b–bifid soft palate (entire length) or
Type II c –bifid soft palate and posterior part of hard palate (but anterior
part of hard palate is normal).
Feature
 Small maxilla with crowded teeth, absent/poorly developed upper lateral
incisors.
 Bacterial contamination of upper respiratory tract with recurrent
infection is common.
 Chronic otitis media with deafness may occur.
 Swallowing difficulties to certain extent and speech problems can occur.
 Cosmetic problems can occur.
Treatment for Cleft Palate
 cleft palate is usually repaired in 12-18 months. Early repair causes
retarded maxillary growth (probably due to trauma to growth center and
periosteum of the maxilla during surgery if done early). Late repair causes
speech defect.
 Both soft and hard palates are repaired called palatoplasty.
 Regular examination of ear, nose and throat during follow up period
 Postoperative speech therapy.
 Secondary management:
o Hearing support is given using hearing aids if defect is present;
control of otitis media.
o Speech problems – speech therapy is given.
o Dental problems corrected by proper dentist opinion, and
reconstructive surgery.
o Orthodontic management with alveolar bone graft, maxillary
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MISCELLANEOUS
SHORT CASES
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Examination of mass, ulcer & MSS
Examination of swelling/mass
Inspection
 Site/location
 Overlying skin color change
 Any ulceration
Palpation
 Warmness  compare
 Tenderness
 Size
o Measure or estimate
 Number
 Surface
o Smooth
o Nodular
 Border
o Regular
o irregular
 Fixity
o To the overlying or underlying tissue
 Consistency
o Soft
o firm
o hard
For soft swelling
 Fluctuation
Indicate fluid within the swelling
 Transillumunation
 Reducibility
 Compressibility
Characteristic of vascular hemangioma
 Pulsatility
Watch video on how to examine swelling @
https://www.youtube.com/watch?v=GUX6UpRiU9c
NB*
When you are asked to list DDx for a swelling…think of the structures that are found
under/overlying the swelling like fibrous connective tissue, adipose tissue, vessels,
skeletal muscles, nerves & bones…then list the benign & malignant disease forms of
each structure.E.g. fibroma, fibrosarcoma (for fibrous CT)
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Examination of ulcer
Inspection
 Location of ulcer
e.g.
 Varicose ulcerlower leg
 Rodent ulcerface-nose
 Tuberculosis ulcerover the neck
 Size
 Number
 Single or multiple
 Is there any similar ulcer in other part of body?
 Margin
Type of margin
1. Healing ulcer
 Have 3 line
 white-outer
 blue-center
 red-inner
2. Inflamed margin
 Red, irregular with inflamed surrounding skin
3. Fibrosed margin
 Thicken white skin margin without the blue line of
growing epithelium
 Floor of the ulcer (surface of ulcer)
 Granulation
 slough
 discharge
 Surrounding skin
 Redness
 Pigmentation
 Dark pigmentation of skin typical for varicose ulcer
 Hypopigmentation of surrounding skinin non-healing ulcer
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Palpation
 Surrounding skin for hotness and tenderness
 UlcerEdge confirm size
 Floor
 see if it bleeds on touch
 check the involvement of underlying structures
Related examination
 Related lymph node
 Related arteries, veins and nerves
 Movement in neighboring joints
 Restriction to movement indicates muscle involvement or
painful inflammation…
Watch video on how to examine ulcer @

https://www.youtube.com/watch?v=S1FpVuyUJ6Q
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Examination of musculoskeletal system(MSS)
General approach
 Inspection [look]
 Palpation [feel]
 Range of Motion (ROM) [move]
 Measurement [measure]
i)Look
 Expose both sides , adequate light
Specific to the site of interest

 Look for asymmetry between sides
 Deformity
 Visible fractured bone
 Swelling
 Laceration
 Bruising /discoloration
 Abnormal movement
 Atrophy
ii)Feel
 Temperature
o Compare both sides of extremities for warmness with ur back of hand
 Tenderness
 Never forget to check pulses
 If lower extremity
Dorsalis pedis artery
Posterior tibialis artery
Popliteal artery…
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 If upper extremity
Radial artery
Brachial artery
 Compare muscle bulk
o By measuring with tape meter
 Asses capillary refill
o If >2secabnormal
 Swelling characterize…
iii)Move
Range of motion (Active )

 Ask the patient to move the affected site
 Watch for decreased or increased movement of the joint compared to

the other side as well as the normal
 Watch for pain with movement
 Listen for crepitus or “popping”
 Watch for abnormal movements
ROM (passive)
 Move the joints passively, comparing the end points to the active
 Again note any decreased or increased movement
 Pain with the movement
 Crepitus or “popping”
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iv)Measure
Apparent length
 From xiphisternum or umbilicus to medial malleolus
Real length
 From greater trochanter of the femur up to the medial malleolus
True length
 Between two bony prominences
NB
During short examination on fracture mgt, first u will be asked “What do u see on this
patient?”So, start by commenting if there is anything visible…like
External fixation
POP
Traction
Surgical dressing….
*For fracture mgt see page 221
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WOUNDS
By –Bruh Alem(sms)
DefinitionA wound is a break in the integrity of the skin or tissues, associated with
disruption of the structure and function.
CLASSIFICATION OF WOUNDS
I. Rank and Wakefield Classification
a. Tidy wounds
• Incised (sharp objects), clean, healthy wound without any tissue loss. Healing by
primary intention. Primary suturing is done.
b. Untidy wounds
•
crushed, devitalized, unclean. Wound dehiscence, infection, delayed healing is
common. Liberal excision of devitalized tissue and heal by secondary intention is the
management. Secondary suturing, skin graft or flap may be needed. E.g--crushing,
tearing, avulsion, devitalized, vascular injury, multiple irregular wounds and Burns
II. Classification based on Type of Wound
a. Clean incised woundclean-cut wound with linear edge.
b. Lacerated woundsragged edges with devitalization.
c. Bruising and contusion
•
soft tissue injury with discoloration and haematoma formation without skin break.
d. Hematomablood collection in subcutaneous/intramuscular/ subfascial/intra-articular.
• Small hematoma get absorbed. Large hematoma once get infected should be drained
under general/regional anesthesia adequately.
e. Closed blunt injury
f. Puncture wounds and bites.
g. Abrasionsuperficial shearing of skin (only epidermal injury). heals by epithelialization.
h. Traction and avulsion injury.
i. Crush injurycaused by war wounds, road traffic accidents, tourniquet.
--leads to Compartment syndrome, Muscle ischemia Gangrene and loss of tissue.
j. War wounds and gunshot injuries.
k. Injuries to bones and joints, may be open or closed
l. Injuries to nerves, either clean cut or crush.
m. Injuries to arteries and veins (major vessels).
n. Injury to internal organs, may be of penetrating or nonpenetrating (blunt) types.
o. Penetrating wounds
• Commonly due to stab injuries. Common example is stab injury abdomen.
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III. Classification based on Thickness of the Wound
• Superficial woundonly epidermis and dermal papillae.
• Partial thickness  deep dermis with only deepest part of the dermis, hair follicle
shafts and sweat glands are left behind.
• Full thickness entire skin and subcutaneous tissue causing spacing out of the skin
edges.
• Deep wounds across deep fascia into muscles or deeper structures.
• Complicated wounds  associated with injury to vessels or nerves
• Penetrating wound penetrates into either natural cavities or organs.
IV. Classification based on Involvement of Structures
• Simple wounds  only one organ or tissue.
• Combined wounds  mixed tissues.
V. Classification based on the Time Elapsed
• Acute wound up to 8 hours of trauma.
• Chronic wound after 8 hours of trauma. e.g. pressure ulcer
VI. Classification of Surgical Wounds
a. Clean wound
• Herniorrhaphy, Excisions, Surgeries of the brain, joints, heart, transplant.
Infective rate is less than 2%.
b. Clean contaminated wound
• Appendicectomy, Bowel surgeries, Gallbladder, biliary and pancreatic
surgeries. Infective rate is 10%.
c. Contaminated wound
• Acute abdominal condition,Open fresh accidental wounds.Infective rate is 15-
30%
d. Dirty infected wound
• Abscess drainage, Pyocele, Empyema gallbladder, Fecal peritonitis. Infective
rate is 40-70%
WOUND HEALING
Wound healing is complex method to achieve anatomical and functional integrity of
disrupted tissue
Types of Wound Healing
Primary Healing (First Intention) 
• clean incised wound or surgical wound. Wound edges are approximated with
sutures. more epithelial regeneration than fibrosis. heals rapidly with
complete closure. Scar will be linear, smooth, and supple.
Secondary Healing (Second Intention) 
• extensive soft tissue loss like in major trauma, burns and wound with sepsis.
heals slowly with fibrosis. a wide scar, often hypertrophied and contracted.
may lead into disability.
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Healing by Third Intention (Tertiary Wound Healing or Delayed Primary Closure) 
• After wound debridement and control of local infection, wound is closed with
sutures or covered using skin graft. Primary contaminated or mixed tissue
wounds heal by tertiary intention.
Stages of Wound Healing
• Stage of inflammation.
• Stage of granulation tissue formation and organization. fibroblastic activity
synthesisation of collagen and ground substance occurs.
• Stage of epithelialization.
• Stage of scar formation and resorption.
• Stage of maturation.
Phases of Wound Healing
Inflammatory Phase (Lag or Substrate or Exudative Phase)
• It begins immediately after wound healing. It lasts for 4-6 days.
• Features of inflammation are rubor, calor, tumour, dolor and loss of function.
• Macrophages secrete fibroblastic growth factor which enhances angiogenesis.
• Polymorphonuclear leukocytes (PMN leukocytes) appear after 48 hours which secrete
inflammatory mediators and bactericidal oxygen derived free radicals.
• These cells also remove clots, foreign bodies and bacteria.
• Chemical factors involved in wound healing are: Growth factor—platelet derived,
epidermal, transforming. Interleukin. Tumour necrosis factor. Prostaglandins.
Collagenase. Elastase.
These actions are reduced in diabetes mellitus, Cushing’s syndrome and immunosuppression
increasing the rate of sepsis.
Proliferative Phase (Collagen/Fibroblastic Phase)
• Collagen and glycosamines are produced by fibroblasts.
• It begins in 7 days and lasts for 6 weeks.
• Hydroxyproline and hydroxylysine are synthesized by specific enzymes using iron,
alpha ketoglutarate and vitamin C.
• Tropocollagen is produced which aggregates to form collagen fibrils.
• 80–90% of their final strength (in postoperative wounds) is achieved in 30 days.
Remodeling Phase (Maturation Phase)
• It begins at 6 weeks and lasts for 2 years.
• There is maturation of collagen by cross-linking which is responsible for tensile
strength of the scar.
• Collagen production is not present after 42 days of wound healing.
Scar strength is 3% in 1 week; 20% in 3 weeks; 80% in 12 weeks. But it will never get its
original strength.
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Management of Wounds
 ABCD of life
 Incised wound------primary suturing after thorough cleaning.
 lacerated wound -------wound is excised and primary suturing
 Crushed or devitalized wound ------- there will be edema and tension in the wound.
So, after wound debridement or wound excision edema is allowed to subside for 2-6
days. Then delayed primary suturing is done.
 Deep devitalized wound -------- after wound debridement it is allowed to granulate
completely. Later, if the wound is small secondary suturing is done. If the wound is
large a split skin graft is used to cover the defect.
 Wound with tension ---------- fasciotomy is done so as to prevent the development of
compartment syndrome.
 Vascular or nerve injuries are dealt with accordingly
 Internal injuries (intracranial by craniotomy, intrathoracic by intercostal tube
drainage, intra-abdominal by laparotomy) has to be dealt with accordingly. Fractured
bone is also identified and properly dealt with.
 Antibiotics, fluid and electrolyte balance, blood transfusion, tetanus toxoid (0.5 ml
intramuscular to deltoid muscle), or antitetanus globulin (ATG) injection.
 Wound debridement (wound toilet, or wound excision) 

 is liberal excision of all devitalized tissue at regular intervals (of 48-72 hours)
until healthy, bleeding, vascular tidy wound is created.
 Primary suturing 
 means suturing the wound immediately within 6 hours. It is done in clean
incised wounds.
 Delayed primary suturing 
 means suturing the wound in 48 hours to 10 days. It is done in lacerated
wounds. This time is allowed for the edema to subside
 Secondary suturing
 means suturing the wound in 10-14 days or later. It is done in infected wounds.
After the control of infection, once healthy granulation tissue appears,
secondary suturing is done.
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ULCER
By –Bruh Alem(sms)
DefinitionAn ulcer is a break in the continuity of the covering epithelium,
either skin or mucous membrane.
Parts of an Ulcer
 Margin: It may be regular or irregular. It may be rounded or oval.
 Edge: Edge is the one which connects floor of the ulcer to the margin.
Different edges are:
 Sloping edge It is seen in a healing ulcer. Its inner part is red because of red, healthy
granulation tissue. Its outer part is white due to scar/fibrous tissue. Its middle part is
blue due to epithelial proliferation.
 Undermined edge is seen in a tuberculous ulcer. Disease process advances in deeper
plane (in subcutaneous tissue)
whereas (skin) epidermis proliferates inwards.
 Punched out edge is seen in a gummatous (syphilitic) ulcer and trophic ulcer. It is due
to endarteritis.
 Raised and beaded edge (pearly white) is seen in a rodent ulcer (BCC). Beads are due
to proliferating active cells.
 Everted edge (rolled out edge)It is seen in a carcinomatous ulcer(SCC) due to spill of
the proliferating malignant tissues over the normal skin.
 Floor: It is the one which is seen. Floor may contain discharge, granulation
tissue or slough
 Base: Base is the one on which ulcer rests. It may be bone or soft tissue.
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Classification
 Clinical
a. Spreading ulcer:
 Here edge is inflamed and edematous
b. Healing ulcer:
 Edge is sloping with healthy pink/red granulation tissue with serous discharge.
c. Callous ulcer:
 Floor contains pale unhealthy granulation tissue with indurated edge/base. It lasts
for many months to
years. Ulcer does not show any tendency to heal. It is due to callous attitude of
the patient.
 Pathological
 Specific ulcers:
Tuberculous ulcer
Syphilitic ulcerIt is punched out, deep, with “wash-leather” slough in the
floor and with indurated base
Actinomycosis
 Malignant ulcers:
Carcinomatous ulcer
Rodent ulcer
Melanotic ulcer
 Nonspecific ulcers:
1. Traumatic – (Footballers ulcer)
• Physical  Electrical
• Chemical Caustics
• Mechanical Dental ulcer, pressure from splint, etc…
2. Arterial--Atherosclerosis, TAO, Raynaud’s disease
3. Venous--Venous ulcer, Postthrombotic ulcer, gravitational ulcer
4. Neuropathic
 (Neurotrophic or Perforating) Diabetes, leprosy, tabes dorsalis, spina
bifida, paraplegia, syringomyelia
5. Tropical ulcers--Tropical countries
6. Metabolic Diabetes – Gout
7. Secondary to diseases like
– Rheumatoid arthritis
– Erythrocyanosis frigida
– Osteitis Deformans (Paget’s disease of the bone)
– Avitaminosis
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8. Ulcers complicating blood diseases
– Sickle cell anemia
– Mediterranean anemia
– Felty’s syndrome (look for spleen)
9. Ulcer occurring on paralysed leg
 usually seen in anterior poliomyelitis
10. Factitious ulcer (Artefact ulcer)
11. Diphtheritic desert sore
12. Yaws
13. Decubitus ulcer
14. Iatrogenic ulcer extravasation of IV fluid
15. Ulcers in congenital arteriovenous fistula
16. Miscellaneous Martorell’s ulcer
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GRANULATION TISSUE
It is proliferation of new capillaries and fibroblasts intermingled with red blood cells and
white blood cells with thin fibrin coverover it. Granulation tissue signifies healing. It is usually
pink with red dots. The red dots are seen at the sites of capillary loops.
Types
Healthy granulation tissue
• It occurs in a healing ulcer. It has got sloping edge. It bleeds on touch. It has got serous
discharge. 5 Ps of granulation tissuePink, Punctate hemorrhages, Pulseful, Painless, Pin
head granulation. Skin grafting takes up well with healthy granulation tissue.
Unhealthy granulation tissue

• Pale with purulent discharge. Its floor is covered with slough. Its edge is inflamed and
edematous. It is a spreading ulcer
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INVESTIGATIONS FOR AN ULCER
• Study of dischargeCulture and sensitivity, AFB study, cytology.
• Edge biopsyBiopsy is taken from the edge because edge contains multiplying cells. Usually
two biopsies are taken. Biopsy taken from the centre may be inadequate because of central
necrosis.
• X-ray of the part to look for periostitis/osteomyelitis.
• FNAC of the lymph node.
• Chest X-ray, Mantoux test in suspected case of tuberculous ulcer
Assessment of an Ulcer
• Cause of an ulcer should be found—diabetes/venous/arterial/infective
• Clinical type should be assessed.
• Assessment of wound is important—anatomical site; size and depth of the wound; edge of the
wound; mobility; fixity; induration; surrounding area; local blood supply. Wound perimeter
may be useful in assessing this. see page 240 for ulcer examination
• Wound imaging is done by tracing it on a transparent acetate sheet at regular intervals.
• Presence of systemic features; regional nodal status; function of the limb/part; joint
movements; distal pulses; sensations should be assessed
• Severity of infection should be assessed—culture of discharge.
• Specific investigations like edge biopsy; X-ray of part; blood sugar; arterial/venous Doppler;
angiogram.
Debridement of an ulcer
• It is removal of devitalized tissue. Small ulcers are debrided in ward. Large ulcers are debrided
in operation theatre under general anaesthesia. All dead, devitalised, necrotic tissues are
removed. Slough should be separated adequately before debridement. Often devitalised
tissue separates on its own by autolysis if nt enzymes like collagenase are used for
debridement. Hydrotherapy and dressings are mechanical nonselective method of
debridement.
• Ulcer cleaning
o is done using dilute povidone iodine and normal saline (better and
ideal). It should be done daily or two times a day depending on the
severity.
• Dressing of an ulcer
o is done to keep ulcer moist, keep surrounding skin dry, reduce pain,
soothen the tissue, protect the wound and as an absorbent for the
discharge
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Some common ulcer types
TRAUMATIC ULCER
♦ Such ulcer occurs after trauma. It may be mechanical— dental ulcer along the margin of the tongue
due to tooth injury; physical like by electrical burn; chemical like by alkali injury.
♦ Such ulcer is acute, superficial, painful and tender. Secondary infection or poor blood supply of the
area make it chronic and deep.
♦ Footballer’s ulcer is a traumatic ulcer occurring over the shin of males due to direct knocks on the
shin. It is staphylococcal infection with a chronic and deep ulcer.
♦ Traumatic ulcers can occur anywhere in the body due to trauma.
♦ Trauma causes infection, necrosis, fasciitis, crush injury, endarteritis of the skin leading into
formation of large/deep nonhealing ulcer.
♦ Treatment depends on size and extent of ulcer. Regular dressing, later skin grafting is done.
TROPHIC ULCER (PRESSURE (BED) SORE/ DECUBITUS ULCER)
Pressure sore is tissue necrosis and ulceration due to prolonged pressure. Blood flow to the skin stops
once external pressure becomes more than 30 mmHg (more than capillary occlusive pressure) and this
causes tissue hypoxia, necrosis and ulceration. It is more prominent between bony prominence and
an external surface.
Clinical Features
♦ Occurs in 5% of all hospitalised patients.
♦ Painless ulcer which is punched out.
♦ Ulcer is nonmobile with base formed by bone.
Investigations
• Study of discharge, blood sugar, biopsy from the edge, X-ray of the part, X-ray of spine.
Treatment
♦ Cause should be treated.
♦ Nutritional supplementation.
♦ Rest, antibiotics, slough excision, regular dressings.
♦ Vacuum assisted closure (VAC):
• It is the creation of intermittent negative pressure of minus 125 mmHg to promote formation
of healthy granulation tissue. Negative pressure reduces tissue oedema, clears the interstitial
fluid and improves the perfusion, increases the cell proliferation and so promotes the healing.
A perforated drain is kept over the foam dressing covered over the pressure sore. It is sealed
with a transparent adhesive sheet. Drain is connected to required vacuum apparatus.
♦ Once ulcer granulates well, flap cover or skin grafting is done.
♦ Excision of the ulcer and skin grafting.
♦ Flaps—local rotation or other flaps (transposition flaps).
♦ Cultured muscle interposition
PREVENTION
♦ Proper care: Change in position once in 2 hours; lifting the limb upwards for 10 seconds once in 10
minutes; nutrition; use of water bed/air bed/air-fluid floatation bed and pressure dispersion cushions to the
affected area; urinary and faecal care; hygiene; psychological counselling. Regular skin observation; keeping skin
clean and dry (using regular use of talcum powder); oil massaging of the skin and soft tissues using clean,
absorbent porous clothing; control and prevention of sepsis helps in the management .
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DIABETIC ULCER
Causes
♦ Increased glucose in the tissue precipitates infection.
Sites
♦ Foot-plantar aspect—is the most common site.
♦ Leg.
♦ Upper limb, back, scrotum, perineum.
♦ Diabetic ulcer may be associated with ischaemia.
♦ Ulcer is usually spreading and deep.
Investigations
♦ Blood sugar both random and fasting.
♦ Urine ketone bodies.
♦ Discharge for culture and sensitivity.
♦ X-ray of the part to see osteomyelitis.
♦ Arterial Doppler of the limb; glycosylated haemoglobin estimation.
Treatment
♦ Control of diabetes using insulin.
♦ Antibiotics.
♦ Nutritional supplements.
♦ Regular cleaning, debridement, dressing.
♦ Once granulates, the ulcer is covered with skin graft or flap.
♦ Toe/foot/leg amputation.
♦ Microcellular rubber (MCR) shoes to prevent injuries; care of foot
TUBERCULOUS ULCER
It is due to Mycobacterium tuberculosis. It is usually due to cold abscess later forming ulcer in the
neck, chest wall, axilla and groin.
• It can also be primary tuberculosis of the skin (commonly in face).
• Ulcer can be single or multiple; oval or rounded; with undermined edge (due to progression of
disease outwards underneath and healing inwards by skin), painful and tender with caseating
material on the floor.
• Ulcer is usually not deep. Regional lymph nodes may be enlarged matted, firm, and
nontender.
Management:
Discharge study for epithelioid cells (modified histiocytes), AFB; edge biopsy, antituberculous drugs
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BURN
By –Dan Alemayehu(sms)
Definition: Burn is a type of coagulative necrosis caused by heat(usually > 44°C)
transferred from the source to the body.
Causes/types of burns
Thermal
Radiation
Electrical (Ac/Dc)
Chemical
 Flame
 Scald By production
 Frost bite Conversion of of cellular
electrical toxins
energy into  Acid
heat  Alkali
Pathophysiology
 In burn by far the most common organ affected is the skin. However,
burns can also damage airway and lungs. As in all trauma related deaths
burn deaths occur immediately after the injury or weeks later as a result
of multisystem organ failure.
 The following mechanisms have been proposed in the pathophysiology of
burns shock
•Increased capillary permeability • intracellular fluid accumulation
•Decreased plasma oncotic pressure • increased osmotic pressure in burned tissue
•Increased capillary hydrostatic pressure •increased Evaporative water loss
•Reduced clearance of fluid and protein •depressed myocardial function
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Burn wound assessment
Classified according to depth of injury or extent of BSA involved
Degree Extent Characteristics Remark
First degree or Localized to the Erythema,blanch to touch,painful Eg.Sunburns

superficial Epidermis Doesn’t result in
scars
Second Superficial Epidermis + portion of Erythema,blanch,painful,often There may be
degree dermis(papillary) blister and weeping slight skin
discoloration
after healing
Deep Epidermis + dermis( up More pale,mottled,do not blanch Heals with sever
to reticular dermis) to touch,not sensitive to touch but scarring
sensitive to pin prick
Third degree Full Hard,leathery,eschar,painless and Require excision
thickness(epidermis nonblanching with skin
+dermis), no grafting
epidermal or dermal
appendages remain
Fourth degree Involving organs Common in
beneath the skin such electrical burn
as muscle or bones
Local changes in burn

The area of cutaneous or superficial injury has been divided in to 3 zones
Zones Damage Blood flow Remark
Zone of coagulation Irreversible None

(center of the
wound)
Zone of stasis Can be reversible or Decreased perfusion Vascular damage
become irreversible and vessel leakage
based on the wound
environment
Zone of hyperemia Reversible (contains Vasodilation Healing process
clearly viable tissue) begins here
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Burn size estimation
Rule of nine is a quick and easy method that divides the body adequate for
initial assessment for adult burns.
NB*palm methodsmall or patchy burns can be approximated by using the surface area of the
patients palm.The entire(including fingers) is approximately 1% and is used in pediatric burn patients.
INJURY TO THE AIRWAY AND LUNGS

 Physical burn injury to the airway above the larynx:
o The hot gases can physically burn the nose, mouth, tongue,palate and larynx.
Once burned, the linings of these structures will 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 an airway
 Physical burn injury to the airway below the larynx(rare):
o steam has a large latent heat of evaporation and 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
 Metabolic poisoning:
o There are many poisonous gases that can be given off in a fire, the most
common being carbon monoxide. This is the usual cause of a person being
found with altered consciousness at the scene of a fire. Carbon monoxide binds
to haemoglobin with an affinity 240 times greater than that of oxygen and
therefore blocks the transport of oxygen. Levels of carboxyhaemoglobin in the
bloodstream can be measured.
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o Concentrations above 10% are dangerous and need treatment. Other gases
such ashydrogen cyanide causes a metabolic acidosis.
 Inhalational injury
o Inhalational injury is caused by the minute particles within thick smoke, which,
because of their small size, are not filtered by the upper airway, but are carried
down to the lung parenchyma and can cause chemical pneumonitis which
causes alveolar edema with in24hrs.
OTHER LIFE-THREATENING EVENTS WITH MAJOR BURNS
 The immune system and infection:
o Cell-mediated immunity is significantly reduced in large burns leaving them
more susceptible to bacterial and fungal infections.
 Changes to the intestine:
o The inflammatory stimulus and shock can cause microvascular damage and
ischaemia to the gut mucosa. This reduces gut motility and can prevent the
absorption of food.
NBcurling ulcer: occurs within 24 hrs after burn due to decreased GI blood flow and
mucosal damage,this can be treated with H2 blockers,mucoprotectants and early
enteral nutrition.
 Danger to peripheral circulation:
o In full-thickness burns, the collagen fibres are coagulated. The normal
elasticity of the skin is lost. A circumferential full-thickness burn to a
limb acts as a tourniquet as the limb swells. If untreated, this will
progress to limb-threatening ischemia.
IMMEDIATE CARE OF THE BURN PATIENT
Pre-hospital care
o ensure rescuers safety
o Stop the burning process
o Check for other injuries
o Cool the burn wound
o Give oxygen
o ElevateSitting a patient up with a burned airway may prove life-
saving in the event of a delay in transfer to hospital care
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Criteria for admission
o Suspected airway or inhalational injury
o Any burn likely to require fluid resuscitation
o Any burn likely to require surgery
o Pts with burns of any significance to the hands, face, feet or perineum
o Pts whose psychiatric or social background makes it inadvisable to
send them home
o Any suspicion of non-accidental injury
o Any burn in pts @ extremes of age
o Any burn with associated potentially serious sequelae including high-
tension electrical burns & concentrated hydrofluoric acid burns
Hospital care
o The principles of managing an acute burn injury are the same as in any acute
trauma case:
o “ABCD” of life plus E and F (exposure and fluid resuscitation)
Airway/Breathing
 3 components
 Upper airway swellingEdema occurs within 12-24 hours
 Early intubation indicated
 Look for stridor, wheezing, grunting
 Acute respiratory failure
 Carbon monoxide intoxication
 100% O2
 Decreases CO half life
Fluid resuscitation
Types of fluids
 There are three types of fluid used. The most common is Ringer’s lactate
or Hartmann’s solution;
 Some centers use human albumin solution or fresh-frozen plasma,
and some centers use hypertonic saline.
 It…
 Restores plasma volume
 Avoids microvascular ischemia
 Maintains vital organ function
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 Use parkland formula to calculate the required fluid…
 Parkland formula4 x Wt(kg) x %TBSA = mL to be given in 1 day
 Half over 1st 8hrs (subtract what was given)
 Give other Half over next 16 hours
o TBSAFigure it out by
 “rule of nines” or
 entire palmar surface of pt’s hand = 1%
o Do not give colloid in first 24 hrs
Monitoring of resuscitation
 The key to monitoring of resuscitation is urine output.
o Titrate to UOP of 0.5mL/kg/hr in adults and 1mL/kg/hr in children
 If the urine output is below this, the infusion rate should be increased by
50%. If the urine output is inadequate and the patient is showing signs of
hypo-perfusion (restlessness with tachycardia, cool peripheries and a high
haematocrit)then a bolus of 10 ml/kg body weight should be given.
Other managements
 pain management
 Avoid hyperthermia
 Topical antibiotics
o silver sulfadiazine, silver nitrate solution, and silver-impregnated
dressing
 Energy balance and nutrition
 Physiotherapy
 Psychological support
 Escharotomy
o Circumferential full-thickness burns to the limbs require emergency
surgery. The tourniquet effect of this injury is easily treated by
incising the whole length of full-thickness burns.
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Electrical burns
 Coagulation necrosis
 Frequently only entry (yellow-white) and exit (blow out) wounds are visible
masking extensive tissue damage.
 Types of Electrical Current
 Direct current
 Lightning, car batteries, and defibrillators
 Alternating current
 Household appliances
 More dangerous than direct current at low voltage
 High voltage, high frequency AC is equally damaging as DC
 Currents >15mA result in tetany preventing voluntary
release:
 NO LET GO PHENOMENON
 1000 volts is the minimum value for extensive tissue
necrosis and loss of limbs
NB*
 AC injuries have 3 times higher mortality/morbidity than DC.
 Electrical burns are more severe at the point of exit.
Severity of Electrical Shock
 Voltage and amperage of the current
 Alternating or Direct current
 Amount of time the patient is exposed
 Amount of body surface in contact with water
 Area of the body through which the current passes
 Amount of moisture on the patient
Pathophysiology
 Current Follows path of least resistance towards ground Nerve, blood
vessels, muscle, skin, tendon, fat and then bone(in order of increasing
resistance). Electrical energy is converted to heat in direct proportion to
the resistance of the tissue.
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Specific organs affected
Neurological system
 Most commonly affected
 May experience
 Numbness/tingling
 Loss of consciousness
 Amnesia
 Coma
 Spinal cord involvement
Cardiac Injuries
 cardiac dysrhythmia’s
 Sudden death (Ventricular Fibrillation)
Vascular Injuries
 Result of vascular spasm
 Coagulation
 Vascular occlusion
 Compartment Syndrome
 Acute ischemic insult
 Rhabdomyolysis
Renal Injuries
 Occur due to:
 Rhabdomyolysis
 Myoglobinuria
 Acute Renal Failure (ARF)
 Myoglobin crystallization
Musculoskeletal
 Spasms, tetany, contractures, compartment syndromes
 Fractures due to powerful muscular spasm
Gastrointestinal
 Ileus
Pulmonary
 Muscular paralysis
Management
Peculiarities
 High voltage burns require large amounts of fluid.
 Maintain adequate ventilationrisk of Central apnea in Lightning strike
 TBSA may be difficult to assess
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SHOCK
By –Cheru Lilay(sms)
Approach to the Patient with Shock
 Shock is defined as a failure to meet the metabolic demands of cells and tissues and
the consequences that ensue.
 A central component of shock is decreased tissue perfusion. This may be a direct
consequence of the etiology of shock, such as in hypovolemic/hemorrhagic,
cardiogenic, or neurogenic etiologies, or may be secondary to elaborated or released
molecules or cellular products that result in endothelial/cellular activation, such as in
septic shock or traumatic shock.
FORMS OF SHOCK
 Strict adherence to a classification scheme may be difficult from a clinical standpoint
because of the frequent combination of two or more causes of shock in any individual
patient can be happened.
HYPOVOLEMIC SHOCK
 most commonly encountered in surgical practice
 results either from the loss of red blood cell mass and plasma from hemorrhage or
from the loss of plasma volume alone due to extravascular fluid sequesteration or GI,
urinary, and insensible losses
 The signs and symptoms of non hemorrhagic hypovolemic shock are the same as
those of hemorrhagic shock, although they may have a more insidious onset.
 According to ATLS classified into four…
1. Class I
 Mild hemorrhage( up to 750 ml )
 Up to 15% Blood Volume Loss of total blood volume
 This condition is exemplified by voluntary blood donation
 There is no change in vital signs & Capillary refill is normal
 no treatment, and blood volume is restored within 24 hours by
transcapillary refill and the other compensatory methods.
2. Class II
 15% to 30% Blood Volume (750 to 1500 mL)
 tachycardia and tachypnea
 The SBP may be only slightly decreased, especially in the supine
position,
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 pulse pressure is narrowed (because increased DBP due to an
increase in peripheral vascular tone and resistance by
catecholamines ).
 Urine output is reduced only slightly
 Mental status changes e.g., anxiety
 Capillary refill is usually delayed
 Patients usually can be resuscitated with crystalloid solutions,
but some may require blood transfusion
3. Class III
 30% to 40% ( 1500-2000ml)Blood Volume Loss
 almost always present with the classic signs of inadequate
perfusion
 marked tachycardia and tachypnea, significant changes in
mental status,
 and a measurable fall in systolic pressure
 cool, clammy extremities with significantly delayed
capillary refill
 this is the least amount of blood loss that consistently causes a
drop in systolic pressure (Class III represents the smallest volume
of blood loss that consistently produces a decrease in systolic
blood pressure)
 The resuscitation of these patients frequently requires blood
transfusion in addition to administration of crystalloids
 The decision to transfuse blood is based on the patient’s
response to initial fluid resuscitation
4. Class IV
 More than 40% (>2,000 mL)Blood Volume Loss
 representing life-threatening hemorrhage
 marked tachycardia, a significantly depressed SBP,
 narrowed pulse pressure or unobtainable diastolic
pressure.
 The mental status is depressed and the skin is cold and
pale.
 Urine output is negligible.
 These patients require immediate transfusion for
resuscitation and frequently require immediate surgical
or intervention
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 What is the difference between hypovolemic Shock secondary to plasma or free fluid
loss & hemorrhagic shock?
 Hemoconcentration, elevated blood urea nitrogen (BUN) and creatinine, and
hypernatremia are typical of acute plasma and/or free water losses and are not
necessarily present in other forms of shock
MANAGEMENT OF HEMORRHAGIC SHOCK

 The basic management principle is to stop the bleeding and replace the volume loss.
 Mostly this is associated with trauma so first apply ATLS why?
 Ensuring a patent airway & breathing are the first priority in the primary
survey. This is essential, because efforts to restore cardiovascular integrity will
be futile unless the oxygen content of the blood is adequate, means the oxygen
status should corrected first, i.e giving blood or fluid before secured oxygen
source is meaningless…!
 How tension pneumothorax shock….?
 Air is trapped in intra-thorax this compress the heart causes decreased venous
return then finally hypotension….
INITIAL FLUID THERAPY FOR HEMORRHAGIC SHOCK
An initial, warmed fluid bolus is given. The usual dose is 2 L RL

or NS for adults and 20 mL/kg for pediatric patients.
Follow BP, PR ,UOP & mental status
An initial, warmed fluid bolus is given.

If not responsive repeat 1x in adult(total 2x)
The usual dose is 2 L RL or NS for adults
& 2x in pediatrics(total 3x)
and 20 mL/kg for pediatric patients.
If not responsive with the above fluid give blood
Failure to respond to crystalloid and blood administration

in the ED dictates the need for damage control surgery
N.B…..And assess other causes of shock E.g septic, Cardiogenic… but in trauma
the most cause of nonresponsive shock is unidentified ongoing bleeding
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 Generally based the response to initial fluid can be divided into 3
 rapid response,
 transient response, and
 minimal or no response.
 RAPID RESPONSE
 rapidly to the initial fluid bolus and remain hemodynamically normal after the
initial fluid bolus
 usually have lost minimal (less than 20%) blood volume
 No further fluid bolus or immediate blood administration
 Typed and crossmatched blood
 should be kept available. Surgical consultation and evaluation are
necessary during initial assessment and treatment, as operative
intervention may still be necessary
 TRANSIENT RESPONSE
 respond to the initial fluid bolus. However, they begin to show deterioration of
perfusion indices as the initial fluids are slowed to maintenance levels,
indicating either
 an ongoing blood loss or inadequate resuscitation.
 Most of these patients initially have lost an estimated 20% to 40% of their
blood volume
 Transfusion of blood and blood products is indicated, but more important is
the recognition that this patient requires operative or angiographic control of
hemorrhage.
 patients who are still bleeding and require rapid surgical intervention.
 MINIMAL OR NO RESPONSE
 Failure to respond to crystalloid and blood in the ED dictates the need for
immediate, definitive intervention (e.g., operation or Angioembolization) to
control exsanguinating hemorrhage.
 So the possible DDX are
 blunt cardiac injury
 cardiac tamponade
 tension pneumothorax
 Non hemorrhagic shock
 Cardiogenic
 Septic
 CVP monitoring and cardiac ultrasonography help to differentiate between the
various causes of shock.
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Summary
INITIAL ASSESSMENT AND SURGICAL SHOCK MANAGEMENT
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Condition How cause shock
Tension pneumothorax  Compress hearted RV pressure finally decreased venous return
Massive hemothorax  Due to lost

 Compression effect, like that of T.pneumothorax
Cardiac temponade  Decreases the cardiac filling

 like that of T.pneumothorax
CARDIOGENIC SHOCK
 The clinical definition is decreased cardiac output with tissue hypoperfusion, despite
presence of adequate intravascular volume.
 Hemodynamic criteria include
 sustained hypotension (i.e., SBP <90 mmHg for at least 30 minutes),
 reduced cardiac index (<2.2 L/min per square meter), and
 elevated pulmonary artery wedge pressure (>15 mmHg)
 Acute, extensive MI is the most common cause of cardiogenic shock
 CVP is increased
 urgent echocardiography confirm the diagnosis
Treatment of Cardiogenic Shock
 maintenance of adequate oxygenation to ensure adequate myocardial O2 delivery
and
 judicious fluid administration to avoid fluid overload and development of cardiogenic
pulmonary edema
 Correct Electrolyte abnormalities, commonly hypokalemia and hypomagnesemia
 Pain is treated with IV morphine sulfate or fentanyl
 Significant dysrhythmias and heart block must be treated with antiarrhythmic drugs
 When profound cardiac dysfunction exists, inotropic support
 consult medical side! For detail
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SEPTIC SHOCK
 defined as a SIRS response to infection in conjunction with arterial hypotension,
despite adequate fluid resuscitation
 Hemodynamic changes are …
 Early septic shock (warm or hyperdynamic) characterized
 peripheral vasodilation,
 flushed and warm extremities, and
 a compensatory elevation in cardiac output
 Although an increase in venous capacitance diminishes venous return
to the heart, cardiac output is maintained via tachycardia and the
decrease in afterload due to systemic vasodilation
 Late septic shock (cold or hypodynamic) characterized by
 impaired myocardial contractility due to local and systemic release of
cardiac depressants,
 worsening peripheral perfusion, vasoconstriction, extremity mottling,
oliguria, and hypotension
 The terms sepsis, severe sepsis, and septic shock are used to quantify the magnitude
of the systemic inflammatory reaction.
 sepsis
 evidence of an infection, as well as systemic signs of inflammation (e.g.,
fever, leukocytosis, and tachycardia).
 Severe sepsis
 Hypo perfusion with signs of organ dysfunction
 Septic shock
 requires the presence of the above, associated with more significant
evidence of tissue hyp operfusion and systemic hypotension.
Treatment of septic shock
 Start with secure of airway and ventilation
 Severely obtunded & those with work of breathing is require intubation and
ventilation
 Empiric antibiotics must be stared
 vasopressors may be necessary to treat patients with septic shock
 For detail refer medical side
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Assessment of Endpoints in Resuscitation
 What are the best indicators of resuscitation?
 Generally those are classified as the following
 Systemic/global
 Lactate
 Base deficit
 Cardiac output
 Oxygen delivery and consumption
 VS(BP, PR)
 Tissue specific
 Gastric tonometry
 Tissue pH, oxygen, carbon dioxide levels
 Near infrared spectroscopy
 Cellular
 Membrane potential
 Adenosine triphosphate
 BP & PR are not definite indicators of resuscitation b.c those are normal in
Compensated shock
 What is compensated shock?
 When inadequate tissue perfusion persists despite normalization of blood
pressure and heart rate.
 Even with normalization of blood pressure, heart rate, and urine output, 80%
to 85% of trauma patients have inadequate tissue perfusion, as evidenced by
increased lactate or decreased mixed venous O2 saturation
 Patients failing to reverse their lactic acidosis within 12 hours of admission
(acidosis that was persistent despite normal heart rate, blood pressure, and
urine output) developed an infection three times as often as those who
normalized their lactate levels within 12 hours of admission
 In addition, mortality was fourfold higher in patients who developed infections
 Both injury severity score and occult hypotension (lactic acidosis) longer than 12 hours
were independent predictors of infection.
 Thus, recognition of subclinical hypo perfusion requires information beyond vital
signs and urinary output.
 Therefore, surrogate parameters have been sought to estimate the O2 debt( adequacy
of resuscitation); serum lactate and base deficit have been shown to correlate with O2
debt.
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 Serum Lactate
 Lactate is generated by conversion of pyruvate to lactate by lactate
dehydrogenase in the setting of insufficient oxygen
 Normally removed 50% by liver & 30% by kidney
 Elevated serum lactate is an indirect measure of the O2 debt,
 When it is corrected is determine the prognosis…e.g
 If it corrected with 24hr 100% survival
 “ “ ‘’ 24-48hr 78% “
 “ “ “ >48hr only 15% “
 But the individual variability of lactate may be affect its accuracy
 So, Base deficit and volume of blood transfusion required in the first 24 hours
of resuscitation may be better predictors of mortality than the plasma lactate
alone
 Base Deficit
 Base deficit is the amount of base or acid in millimoles that is required to
titrate 1 L of whole blood to a pH of 7.40 with the sample fully saturated with
O2 at 37°C (98.6°F) and a partial pressure of CO2 of 40 mmHg.
 Measured by arterial blood gas analysis in clinical practice as it is readily and
quickly available
 Base deficit can
 be stratified into mild (3–5 mmol/L), moderate (6–14 mmol/L), and severe (15
mmol/L)
 Both the magnitude of the perfusion deficit as indicated by the base deficit and
the time required to correct it are major factors determining outcome in shock.
 Indeed, when elevated base deficit persists (or lactic acidosis) in the trauma patient,
ongoing bleeding is often the etiology.
 Trauma patients admitted with a base deficit greater than 15 mmol/L required twice
the volume of fluid infusion and six times more blood transfusion in the first 24 hours
compared to patients with mild acidosis.
 Generally as the base deficit increased @ admission
 The resuscitation should intensive
 Higher rate morbidity and mortality
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BLOOD TRANSFUSION
By –Dawit Birhanu(sms)
Blood components
Banked Whole Blood-
 Now rarely indicated and rarely available. With the new preservatives, the
shelf life has been extended to 40 ± 5 days. At least 70% of the transfused
erythrocytes remain in the circulation for 24 hours after transfusion and are
viable. The hemolysis that occurs during storage is insignificant.
Fresh Whole Blood –
 Refers to blood that is administered within 24 hours of its donation and is
rarely indicated. Because of the time required for testing for infectious
disease, it must be administered untested. One unit of platelet concentrate
has more viable platelets than 1 unit of fresh blood. Fresh whole blood is a
poor source of platelets and factor VIII.
Packed red cells-
 Cells are spun down and concentrated.
 Each unit = 330 ml(hct=50–70%)
 PRCs are stored in a SAG-M solution (saline–adenine–glucose–mannitol) to
increase shelf-life to 5 weeks at 2–6 0C.
Fresh-frozen plasma-
 is rich in coagulation factors & removed from fresh blood and stored at
–40 to –50 0C with a 2 years shelf-life. It is the first-line therapy in the
treatment of coagulopathic haemorrhage .
Platelet -
 pooled platelet concentrate containing about 250 × 109 cells per litre.
Platelets are stored on a special agitator at 20–24 0C and have a shelf-life
of only 5 days.
Cryoprecipitate-
 is precipitate of FFP
 rich in factor VIII and fibrinogen
 stored at –300C with a 2-year shelf-life
 given in low-fibrinogen states or in factor VIII deficiency
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Prothrombin complex concentrate –
 contain factors II, IX and X(factor VII may be included)
 indicated for the emergency reversal of anti-coagulant (warfarin) therapy
in uncontrolled haemorrhage
Indications for blood transfusion
• acute blood loss, to replace circulating volume and maintain oxygen
delivery;
o in case of hemorrhagic shock,major surgery,extensive burns.
• Perioperative anaemia, to ensure adequate oxygen delivery during the
perioperative phase( here GUH cut off for major surgery is HCT 30%)
• symptomatic chronic anaemia without haemorrhage or impending
surgery.
Complications from a single transfusion
ABO incompatibility
• CPs=hematuria,bilateral loin pain,fever,chills,rigor,oliguria(ATN)
• RX=stop blood .send it to blood bank & recheck.
o Repeat coagulation profile
o Iv fluids,monitor UOP,U/A for Hgb
o Diuretic- furosemide
Minor incompatibility reaction
• Due to extra vascular hemolysis(mild ,occura 2-21days)
• CPs-fever,malaise & jaundice
• RX-supportive
Febrile reaction
• Due to sensitization to WBCs or platelets
• ↑ temperature but no hemolysis
• Use of 20-40mm filter or leukocyte depleted blood avoids it.
Allergic reaction
• Due to allergy to plasma products CF-chills,rigor & rashs
• RX- antihistamins
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Embolism
• Although air embolism has been reported as a complication, healthy
individuals can tolerate large amounts of air injected intravenously at a
rapid rate. The normal adult can tolerate an embolism of 200 mL of air.
Smaller amounts, however, can cause alarming signs. Manifestations of
venous air embolism include a rise in venous pressure, cyanosis, a "mill
wheel murmur" over the precordium, tachycardia, hypotension, and
syncope.
• Treatment - consist of placing the patient on the left side in a head down
position with the feet up. Arterial air embolism may be visible in the
retinal vessels or as blood flows from transected vessels. Plastic tubes
used for transfusion can break off within a vein and embolize into the
right atrium or pulmonary artery. Embolized catheters have been
successfully removed.
Thrombophlebitis
• Prolonged infusions into a peripheral vein are associated with venous thrombosis.
Intravenous infusions that last more than 8 hours are more likely to be followed by
thrombophlebitis, with an increased incidence in the lower limbs.
• Treatment consists of discontinuation of the infusion and the application
locally of warm moist compresses. Embolization from superficial
thrombophlebitis or venous thrombosis is extremely rare.
Overtransfusion and Pulmonary Edema
• Overloading the circulation is an avoidable complication. It can occur with
rapid infusion of blood, plasma expanders, and other fluids, particularly in
patients with heart disease. To prevent the complication, the central
venous pressure should be measured whenever large amounts of fluid are
administered. Circulatory overload is manifest by a rise in venous
pressure, dyspnea, and cough. Rales can generally be heard at the lung
bases.
• Treatment consists of diuresis, placing the patient in a sitting position,
and, occasionally, venesection.
Syndrome of transfusion-related acute lung injury (TRALI)
• is sometimes seen after transfusion and is characterized as mild to life-
threatening. Noncardiogenic pulmonary edema is often accompanied
by fever, rigors, and a "white out" chest x-ray.
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• Treatment is discontinuation of any transfusion, notification of the
transfusion service, and intensive pulmonary support, sometimes
including intubation. This type of pulmonary edema does not respond
to diuretics and is thought to be caused by infused donor
antigranulocyte or anticlass I or II MHC antibodies.
Infection:
• Bacterial infection - contamination of infused blood is rare and can be
acquired from contaminated collection bags or poor cleaning of the
donor's skin. Gram-negative organisms, especially coliform and
Pseudomonas species, which are capable of growth at 4oC (39.2oF), are
the most common cause. Clinical manifestations include fever, chills,
abdominal cramps, vomiting, and diarrhea. There may be hemorrhagic
manifestations and increased bleeding. If the diagnosis is suspected, the
transfusion should be discontinued and the blood cultured. Emergency
treatment includes oxygen, adrenergic blocking agents, and antibiotics.
• Hepatitis,HIV,malaria ,syphilis.
 it is mandatory to screen the blood for these diseases before
transfusion.
Complications from massive transfusion
• The term massive transfusion implies a single transfusion greater than
2500 mL or 5000 mL transfused over a period of 24 hours
 Coagulopathy
 Hypocalcaemia
 Hyperkalaemia
 Hypokalaemia
 Hypothermia
 iron overload due to repeated transfusions over long periods
of time (eg. Thalassaemia )
 (Each transfused unit of RBCs contains 250 mg of
elemental iron.)
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Fluid & electrolyte imbalance
By –Cheru Lilay(sms)
BODY FLUIDS
 Total Body Water(TBW)
 Is relatively constant for an individual and is primarily a reflection of body fat.
 Lean tissues such as muscle and solid organs have higher water content than
fat and bone. In an average young adult male 60% vs. young adult female it
is 50%
 The highest percentage of TBW is found in newborns, with approximately 80%
of their total body weight comprised of water.
Classification of Body Fluid Changes
 Disorders in fluid balance may be classified into three general categories:
• disturbances in
a) volume,
b) concentration, and
c) Composition.
 Although each of these may occur simultaneously, each is a separate entity with
unique mechanisms demanding individual correction
Disturbances in Fluid Balance
 Extracellular volume deficit is the most common fluid disorder in surgical patients and
can be either acute or chronic.
• Acute volume deficit is associated with cardiovascular and central nervous system
signs(shock), whereas chronic deficits display tissue signs, such as a decrease in
skin turgor and sunken eyes( dehydration) , in addition to cardiovascular and
central nervous system signs.
• Shock vs. DHN???
FLUID AND ELECTROLYTE THERAPY

 Parenteral Solutions
 The type of fluid administered depends on the patient's volume status and the
type of concentration or compositional abnormality present.
 Both lactated Ringer's solution and normal saline are considered isotonic and
are useful in replacing GI losses and correcting extracellular volume deficits.
 Causes of correcting extracellular volume deficits are any GI loss, burn,
dehydration….
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 Crystalloids
 Solutions of electrolytes and water are collectively referred to as crystalloids
 the most widely used fluids for parenteral administration
 Inexpensive , highly effective for fluid maintenance and replacement, and have
outstanding safety profiles
Types of crystalloids
 Lactated Ringer's
 slightly hypotonic in that it contains 130 mEq of lactate.
 It is ideal for the replacement of existing fluid deficits when serum electrolyte
concentrations are normal why?
 Because Lactate is used rather than bicarbonate because it is more
stable in IV fluids during storage. It is converted into bicarbonate( used
to buffer acid base imbalance) by the liver after infusion, even in the
face of hemorrhagic shock.
 Sodium chloride(0.9%) (NS)
 is mildly hypertonic, containing 154 mEq of sodium that is balanced by 154
mEq of chloride.
 The high chloride concentration imposes a significant chloride load on the
kidneys and may lead to a hyperchloremic metabolic acidosis.
 So, it is an ideal solution, for correcting volume deficits associated with
hyponatremia, hypochloremia, and metabolic alkaloids
 D5( 5% dextrose) mean ..
 50 g of dextrose per liter
 supplies 200 kcal/L
 dextrose is always added to solutions containing <0.45% sodium
chloride(hypotenic) to maintain osmolality and thus prevent the lysis of
red blood cells that may occur with rapid infusion of hypotonic fluids.
The addition of potassium is useful once adequate renal function and
urine output are established.
 0.45% sodium chloride
 useful for replacement of ongoing GI losses as well as for maintenance fluid
therapy in the postoperative period.
 This solution provides sufficient free water for insensible losses and enough
sodium to aid the kidneys in adjustment of serum sodium levels.
 Because this is hypotonic causes RBC lysis to prevent this …
 add 5% dextrose (50 g of dextrose per liter)
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Alternative Resuscitative Fluids
 Hypertonic saline
 Hypertonic saline solutions (3.5% and 5%)
 used for correction of severe sodium deficits
 Hypertonic saline (7.5%)
 has been used as a treatment modality in patients with closed head
injuries.
 It has been shown to increase cerebral perfusion and decrease
intracranial pressure, thus decreasing brain edema.
 appears to increase intravascular volume in patients more quickly than
isotonic solutions, and the total resuscitation volume requirement may
be decreased
 reduces the systemic inflammatory response syndrome (SIRS) and may
attenuate multiple organ dysfunction syndrome
 These cardiovascular and hemodynamic effects are short-lived, in
general lasting from 60 to 120 minutes. The addition of colloids such as
dextran or hetastarch can prolong the effect.
 Adverse effect
 increased bleeding, because hypertonic saline is an arteriolar
vasodilator
 electrolyte abnormalities such as hypernatremia
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 Colloids
 also are used in surgical patients
 Due to their molecular weight, they are confined to the intravascular space,
and their infusion results in more efficient transient plasma volume expansion.
 However, under conditions of severe hemorrhagic shock, capillary membrane
permeability increases; this permits colloids to enter the interstitial space,
which can worsen edema and impair tissue oxygenation
 Colloid solutions with smaller particles and lower molecular weights exert a
greater oncotic effect but are retained within the circulation for a shorter
period of time than larger and higher molecular weight colloids.
 Are limited in use because of their doubtful effectiveness, cost, and potential
complication.
 Four major types of colloids are available
 Albumin
 Dextrans
 hetastarch, and
 Gelatin
 Albumin (molecular weight 70,000)
 is prepared from heat-sterilized pooled human plasma.
 It is typically available as either a 5% solution (osmolality of 300 mOsm/L) or
25% solution (osmolality of 1500 mOsm/L).
 Because it is a derivative of blood, it can be associated with allergic reactions.
 Albumin has been shown to induce renal failure and impair pulmonary
function when used for resuscitation in hemorrhagic shock.
 Dextrans
 are glucose polymers produced by bacteria grown on sucrose media and are
available as either 40,000 or 70,000 molecular weight solutions.
 They lead to initial volume expansion due to their osmotic effect but are
associated with alterations in blood viscosity.
 Thus dextrans are used primarily to lower blood viscosity rather than as
volume expanders.
 Dextrans have been used, in association with hypertonic saline, to help
maintain intravascular volume.
 Hetastarches
 Administration of hetastarch can cause hemostatic derangements related to
decreases in von Willebrand's factor and factor VIII
 and its use has been associated with postoperative bleeding in cardiac and
neurosurgery patients.
 Hetastarch also can induce renal dysfunction in patients with septic shock and
in recipients of kidneys procured from brain-dead donors.
 Currently, hetastarch has a limited role in massive resuscitation because of the
associated coagulopathy and hyperchloremic acidosis (due to its high chloride
content).
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General classification of IV fluids
Correction of Volume Abnormalities

 Maintenance Fluid Therapy
 It is the usual daily requirement
 Calculation of maintenance fluid replacement does not include replacement of
either preexisting deficits or ongoing additional losses
 It to replace basal fluid requirement i.e the sensible and insensible losses
 how it is calculated
 In patients who may be intolerant of hypervolemia (i.e., cardiac disease, elderly

patients), the requirement per kilogram over 20 kg is decreased to 15 mL/kg per day.
 E.g for 70kg the MF is 2500ml per day
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 For maintenance therapy, 1 to 2 mEq/kg per day of sodium is required,& Potassium
requirements are approximately 0.5 to 1 mEq/kg per day .
 e.g. If sodium is replaced at 2 mEq/kg per day and potassium is replaced at 1 mEq/kg
per day, a 70-kg patient requires 2,500 mL of water containing 140 mEq of sodium and
70 mEq of potassium. Each liter of parenteral solution would contain 56 mEq of
sodium and 28 mEq of potassium
 Short-term maintenance therapy generally does not require addition of calcium,
phosphate, or magnesium
 Replacement of Ongoing Fluid Losses

 Once volume deficits have been replaced and maintenance fluids have been
calculated and given, the overall fluid balance of the patient can be maintained
by replacement of fluid losses beyond those considered to be maintenance
 Ongoing losses from nasogastric tubes, stomas, fistulas, and other measurable
sources are recorded during the course of care and can be replaced in fairly
straightforward fashion
 Intraoperative Fluid
 Intraoperative replacement with isotonic solutions is usually accomplished at
rates of 500 to 1,000 mL/h.
 Postoperative Fluid Therapy and Monitoring
 is adjusted to the patient's volume status at the completion of the operative
procedure, as well as to anticipated ongoing fluid losses
 Isotonic solutions should be used for volume resuscitation during the early
postoperative period.
 It is best not to give potassium supplements during this period without
indication why…. Surgery by itself causes Hyperkalemia due cell damage &
stress
 Routine monitoring of postoperative fluid status consists
 serial vital signs and urine output measurements
 intake and output data are recorded
 Weight should also be recorded daily b.c
 postsurgical , rapid fluctuations in weight are generally related
to changes in TBW
 Urine specific gravity
 greater than 1.010 to 1.012 indicates that the urine is being
concentrated (relative to plasma)
 less than 1.010 indicates that dilute urine is being produced
 Both volume depletion and cardiac failure are accompanied by
increased urine concentration and low urine outputs.
 Urine specific gravity in the range of plasma (1.010 to 1.012)
may indicate either adequate hydration or the inability of the
kidneys either to dilute or concentrate the urine
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Correction of Life-Threatening Electrolyte Abnormalities
Hypernatremia
 Hypernatremia is a less common problem in surgical patients than
hyponatremia
 Mainly this is due to a Concentration Changes in Body Fluids i.e …
 sodium abnormality are mainly affected by body fluid status (Volume
excess or deficits) than intakes….
 It can happen in low , normal or high volume status…
 Clinical Features
 Symptomatic hypernatremia usually occurs only in patients with impaired
thirst or restricted access to fluid, because thirst will result in increased water
intake.
 Symptoms are rare until the serum sodium concentration exceeds 160 mEq/L
but, once present, are associated with significant morbidity and mortality.
 symptoms are related to hyperosmolarity , central nervous system effects
predominate
 Water shifts from the intracellular to the extracellular space which results in
cellular dehydration
 range from restlessness and irritability to seizures, coma, ataxia, spasm and
death
 Treatment
 Treatment of hypernatremia usually consists of treatment of the associated
water deficit.
 In hypovolemic patients, volume should be restored with normal saline before
the concentration abnormality is addressed.
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 The formula used to estimate the amount of water required to correct
hypernatremia is as follows:
 In other way
 E.g a 70-kg patient with a TBW of 42 L (TBW 60&percnt; of body weight) has a
serum sodium of 170 mEq/L. so what is required water
 Giving is ,current serum sodium =170,TBW=43, tents take normal
sodium is 154
 = ((170-154)x43)/154=4.3L
 How much the rate ? slow for chronic hyponatremia why?
 In chronic hypernatremia, the cells in the brain gradually adapt by
increasing intracellular osmotic solute content, thereby regaining
cellular volume. These cellular changes are not readily reversed. A
sudden decrease in extracellular sodium concentration, and therefore
osmolality, results in cell , brain edema
 The rate of fluid administration should be titrated to achieve a decrease in serum
sodium concentration of no more than 1 mEq/h and 12 mEq/day for the treatment of
acute symptomatic hypernatremia.
 Even slower correction should be undertaken for chronic hypernatremia (0.7 mEq/h),
 Oral or enteral replacement is acceptable in most cases, or IV replacement with half-
or quarter-normal saline can be used
 Frequent neurologic evaluation as well as frequent evaluation of serum sodium levels
also should be performed.
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HYPONATREMIA
 frequently seen in the postoperative or postinjury period when ADH is elevated
as a component of the normal stress response to injury
 as a consequence of either sodium depletion or dilution
 Because volume expansion and hyponatremia diminish the effects of ADH on
the collecting tubules, hyponatremia is usually self-limited under these
circumstances, with serum sodium concentration rarely falling below 130
mEq/L unless exacerbated by exogenous free water administration.
 Clinical Features….when is symptomatic ?
 Chronic hyponatremia is often asymptomatic until serum [Na+] falls below 110
to 120 mEq/L
 in acute drop serum [Na+] to the 120 to 130 mEq/L range may symptomatic
 Symptoms related to the CNS result largely from cellular water intoxication,
and permanent CNS injury can occur if it is left untreated.
 Central nervous system
 Headaches
 Confusion
 Delirium
 Coma
 Seizures
 Gastrointestinal Anorexia
 Nausea
 Vomiting
 Musculoskeletal Weakness
 Fatigue
 Muscle cramps
 Treatment
 Most cases of hyponatremia can be treated by free water restriction and, if
severe, the administration of sodium.
 If neurologic symptoms are present, 3% normal saline should be used to
increase the sodium by no more than 1 mEq/L per hour until the serum sodium
level reaches 130 mEq/L or neurologic symptoms are improved.
 Correction of asymptomatic hyponatremia should increase the sodium level by
no more than 0.5 mEq/L per hour to a maximum increase of 12 mEq/L per day,
and even more slowly in chronic hyponatremia.
 The rapid correction of hypomania not recommended
 Is a compositional changes in body fluids , mainly due to intake & exertion related
other than body fluid imbalance
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Hyperkalemia
 defined as a serum potassium concentration above the normal range of 3.5 to
5.0 mEq/L.
 It is caused by
 excessive potassium intake
 can be either from oral or IV supplementation, or from red cell
lysis after transfusion
 increased release of potassium from cells
 Acidosis and a rapid rise in extracellular osmolality from
hyperglycemia or IV mannitol can raise serum potassium levels
by causing a shift of potassium ions to the extracellular
compartment.
 impaired potassium excretion by the kidneys
 Potassium-sparing diuretics
 Renal insufficiency/failure
 Because 98% of total body potassium is in the intracellular fluid compartment,
even small shifts of intracellular potassium out of the intracellular fluid
compartment can lead to a significant rise in extracellular potassium.
 Clinical feature
 clinical manifestations of hyperkalemia are primarily related to membrane
depolarization related to intra & extracellular imbalance
 The most life-threatening manifestations are related to the cardiac effects
 Arrhythmia, arrest
 peaked T waves (early), widened QRS complex, flattened P wave,
prolonged PR interval, sine wave formation, and ventricular fibrillation.
 Neuromuscular manifestations of severe hyperkalemia include weakness
progressing to flaccid paralysis
 GI… Nausea/vomiting, colic, diarrhea
 Treatment…. The goals of therapy include
 protecting the cells from the effects of increased potassium( neutralization)
 reducing the total body potassium
 shifting potassium from the extracellular to the intracellular space
 For all patients, exogenous sources of potassium should be removed, including
potassium supplementation in IV fluids and enteral and parenteral solution.
 Potassium removal
 Is a definitive therapy
 removed from the body using a cation-exchange resin such as
Kayexalate that binds potassium in exchange for sodium
 Kayexalate it can given
 usual oral dose is 40 g dissolved in 20 to 100 mL of sorbitol
 Each gram removes approximately 1 mEq of potassium
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 Shift potassium
 regular insulin 5–10 units IV & Glucose 1 ampule of D50
 Why D50 added…?...To avoid insulin-induced hypoglycemia
 Bicarbonate 1 ampule IV …MOA
 the increase in extracellular pH shifts potassium into the cells
 Counteract cardiac
 urgent & first Rx in severe cases
 Calcium gluconate 5–10 mL of 10% solution
 to counteract the myocardial effects of hyperkalemia
 The effects are transient and usually last approximately 30 minutes
Hypokalemia
 Hypokalemia is much more common than hyperkalemia in the surgical patient.
 caused by
 inadequate potassium intake
 excessive renal potassium excretion
 potassium loss in pathologic GI secretions, such as with diarrhea,
fistulas, vomiting, or high nasogastric output
 intracellular shifts from metabolic alkalosis or insulin therapy
…increment in PH vs Hypokalemia is expressed by…
 Symptom
 Ileus, constipation
 Decreased reflexes, fatigue, weakness, paralysis
 Cardiovascular Arrest
 Treatment
 consists of potassium repletion, the rate of which is determined by the
symptoms
 Oral repletion is adequate for mild, asymptomatic
 If IV repletion is required, usually no more than 10 mEq/h is advisable in
an unmonitored setting but in monitored setting can be increased to 40
mEq/h
 Caution should be exercised when oliguria or impaired renal function is
coexistent
Pls read the rest…..!

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SOFT TISSUE TUMORS
 Soft tissue = supportive tissue of various organs & the non-epithelial, extra-skeletal
structures exclusive of lymphohematopoietic tissues
NB***
 When you are asked to list DDx for a swelling…think of the structures that are found
under/overlying the swelling like fibrous connective tissue, adipose tissue, vessels,
skeletal muscles, nerves & bones…then list the benign & malignant disease forms of
each structure.E.g. fibroma, fibrosarcoma (for fibrous CT)
Soft tissues & soft tissue tumors
Fibrous connective tissue Adipose tissue Blood / lymph vessels Skeletal mms. PNS
Fibroma Schwannomma
Fibrosarcoma neurofibroma
Lipoma Rhabdomyoma
Liposarcoma Rhabdomyosarcoma
Hemangioma
Angiosarcoma
Lymphangioma
Lymphangiosarcoma
Risk factors
 Genetic factors
 Radiation
 Chronic lymphedema
 Environmental carcinogens
 Infections
 Mass –cmn sign of soft tissue tumor
 Usuallypainless
 If it has hx of rapid growth…suspect malignancy
 See mass examination (P/E)…page 239
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SKIN GRAFT AND FLAP
BY-EYASU FELEKE (SMS)
Graft
 A tissue of epidermis and varying amounts of dermis that is detached
from its own blood supply and placed in a new area with a new blood
supply.
Flap
 Any tissue used for reconstruction or wound closure that retains all or
part of its original blood supply after the tissue has been moved to the
recipient location.
Classification of graft
1. Auto-grafta tissue transferred from one part of the body to the other
body part.
2. Homograft(allograft)a tissue transferred from a genetically different
individual of the same species
3. Xeno-grafta tissue transferred from an individual of one species to
other species.
Indications
 Generally to achieve temporary cover(open wound & to prevent
infection) or permanent cover for
- Skin loss 20 to
o post traumatic (avulsion and degloving injuries)
o post-surgical (excision of burn wound)
o infection
- Mucosal loss (excision lesion of oral cavity or tongue)
- Cosmetic reasons
Contraindication
 Beta hemolytic streptococcal Infection
 Infected wound with copious discharge
 Avascular wound
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Types of skin grafts
Definition
Split- • superficial and some deep layers of skin(contain 100% of the epidermis & some part of
thickness dermis)
grafts • Split-thickness grafts are used for non-weight-bearing parts of the body
• Donor sites: - thigh, buttock $ abdomen
• Can be of two type:- thin split thickness and thick split thickness
Full- • Contains all of the layers of the skin including blood vessels
thickness • For weight-bearing portions of the body and friction prone areas such as, feet and joints.
grafts • Resistant to trauma with minimal secondary contractions
• Donor sites: - groin and medial aspect of the arm
Pinch • quarter inch pieces of skin
grafts • will then grow to cover injured sites (grow even in areas of poor blood supply and resist
infection)
Pedicle • skin used from the donor site will remain attached to the donor area (remainder is
grafts attached to the recipient site)
• Blood supply remains intact at the donor location until the new blood supply has
completely developed.
• Mostly used for hands, face or neck areas of the body
Comparison between grafts
Type of Graft Advantages Disadvantages

- Best Survival - Least resembles original skin.
Thin Split
- Heals Rapidly - Least resistance to trauma.
Thickness
- Poor Sensation
- Maximal Secondary Contraction
- More qualities of normal skin. - Lower graft survival
Thick Split
- Less Contraction - Slower healing
Thickness
- Looks better
- Fair Sensation
- Most resembles normal skin. - Poorest survival.
Full Thickness
- Minimal Secondary contraction - Donor site must be closed
- Resistant to trauma surgically.
- Good Sensation - Donor sites are limited.
- Aesthetically pleasing
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Requirement for graft survival
 Bed must be well vascularized
 Contact between graft and recipient should
be immobile
 Low bacterial count at the site
Factors that contribute for graft failure

 Malnutrition
 Sepsis
 DM, HIV, immune status, malignancy, CRF, liver failure
 Drugs: - steroids, chemotherapy, vasoconstrictors
 Recipient site of the graft like bone, tendon, infected wound &
highly irradiated areas
Donor site
Ideal donor site would provide: -
 Skin that is identical to the skin surrounding the recipient area in terms of
o Color, thickness, hair & texture.
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ANESTHESIA
By-Endalkachew Belayneh(sms)
Anesthesia temporary induced loss of sensation or awareness.
 It may include
o analgesia (relief from or prevention of pain)
o paralysis (muscle relaxation),
o amnesia (loss of memory), or
o Unconsciousness.
TYPES OF ANESTHESIA
1) General anesthesia
o To do most complex surgical procedures.
o It can be divided into three distinct phases: induction, maintenance,
and emergence.
o Induction — for adults is usually achieved with the injection of
intravenous medications.
 propofol is commonly used because of its favorable recovery
profile and short elimination half-life.but bradycardia,
hypotension…
o Other less commonly used :-etomidate & ketamine
-Etomidate : used when vasodilation and cardiac depression are undesirable
-Ketamine: analgesia, preserve respiratory drive, bronchodilator and CVS stimulant.
o Maintenance — achieved with volatile or intravenous (IV)
anesthetics.
 Volatile agents are popular because of their ease of delivery,
reliable recovery,excellent safety profile, and mode of onset.
 But causesfulminant hepatic necrosis
o Emergence ("waking up")- patient backs to a restored state of
consciousness.
 Autonomic hyper-responsiveness short period
of time in which patient’s body is aware of
emergence without full return to consciousness.
o Manifest as hypertension, tachycardia,
bronchospasm, or laryngospasm.
- Short acting narcotics, beta blockers,
or lidocaine can blunt these responses
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2) Peripheral nerve block
o For procedures involving the extremities.
o Common blocked nerve groups
 brachial plexus(interscalene block, infraclavicular block)
 the sciatic nerve (posterior or lateral approach), and
 The femoral nerve group (3 in 1 block).
- Also used for operative anesthesia or post-operative pain control.
- major relaxation and analgesia of the selected area without the
hemodynamic instability
3) Intravenous regional block(Bier block)
- is alternative to peripheral nerve block for extremity surgery, usually the
hand or forearm.
-can be applied in pain therapy (eg, chronic regional pain syndrome)
4) Neuraxial anesthesia
o for patients undergoing surgery of the lower extremities or
abdomen
A) Spinal anesthesia
B) Epidural Anesthesia
A) Spinal anaesthesia
- also called spinal b ,subarachnoid b ,intradural b and intrathecal block
- Involves the injection of a local anaesthetic into the subarachnoid
space.
Indications
 Orthopedic surgery on the pelvis, hip, femur, knee, tibia, and
ankle,
 Vascular surgery on the legs
 Endovascular aortic aneurysm repair
 Hernia (inguinal or epigastric)
 Hemorrhoidectomy
 Nephrectomy and cystectomy in combination with general
anaesthesia
 Transurethral resection of the prostate and transurethral
resection of bladder tumors
 Hysterectomy in different techniques used
 Caesarean sections
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 severe respiratory disease such as COPD as it avoids
intubation and ventilation
Contraindications
 Non-availability of patient's consent
 Local infection or sepsis at the site
 Bleeding disorders, thrombocytopaenia, or systemic
anticoagulation
 Space occupying lesions of the brain
 Anatomical disorders of the spine
 Hypovolemia
 stenosis valvular diseases
 allergy to anesthetics
 multiple sclerosis-controversial…
Complications
o Hypotension (Neurogenic shock) - Due to sympathetic nervous
system blockade.
 treated with iv fluid and sympathomimetic drugs
o post spinal head ache -associated with size and type of spinal
needle used
o Cauda equina injury--very rare, due to the insertion site being
too high
o Cardiac arrest--very rare, usually related to the underlying
medical condition of the patient
o Spinal canal hematoma--Urgent CT/MRI to confirm the dx
followed by
o urgent surgical decompression to avoid permanent
neurological damage
o Epidural abscess--May present as meningitis or and abscess.
 Urgent CT/MRI confirms the dx followed by
antibiotics and urgent surgical drainage
Limitations
 limited to procedures involving most structures below the upper abdomen.
 To administer a spinal anaesthetic to higher levels may affect the ability to breathe by
paralysing the intercostal respiratory muscles, or even the diaphragm in extreme cases
(called a "high spinal", or a "total spinal", with which consciousness is lost), as well as
the body's ability to control the heart rate via the cardiac accelerator fibres.
 Also, injection of spinal anaesthesia higher than the level of L1 can cause damage to
the spinal cord, and is therefore usually not.
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Surgical instruments in picture
Artery forceps
Artery forceps
Abdominal wall retractor
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Abdominal spatula
Alli’s forceps
Alli’s forceps
Ambu bag
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Angel
Angled forceps
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Artery forceps
Artery forceps
Babcock
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Bladder retractor
Blade holder
Cervical thongs traction
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curette
Deaver retractor
Needle holder
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Needle holder
Dissector
Dissector
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Doines retractor
Doines retractor
Filliform & followers
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Tissue forceps
Gally pot
GB forceps
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Intestinal clamp
Intestinal clamp
Intestinal clamp
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Jiggle saw holder
Knife/scalpal
kocher
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kocher
Laryngeal mask
Langenbeck retractor
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Lungenbek retractor
Maggille’s forceps
Maggille’s forceps
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Mastoid retractor
Mastoid retractor
Mosquito forceps
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Speculum
Speculum
Sponge forceps
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Straight scissor
Straight scissor
Stitch scissor
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Suction nozzle-metalic suction tip
Suction
Suspensor
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Tissue forceps, non toothed
Towel clip
Trocar
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Towel clip
Vascular clamps
Vascular clamps
Kkkkkkk…..ha ha ha……….
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ND
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Miscellaneous—watch examination of Varicose Vein
አነሳስቶ ላስጀመረን፣ አስጀምሮ ላስጨረሰን ለአምላካችን ኃይል፣ ክብር፣ ምስጋና ይሁን፡፡
https://www.youtube.com/channel/UCZ0lBTvCctutXxL462pe-RQ
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Visit & subscribe
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References
1. Schwartz principle of surgery 10th edition
2. Bailey & loves 26th edition
3. Up to date 21.2
4. Medscape
5. Sabiston surgery 18th edition
6. Outline of fracture (ADAMS) 11th edition
7. ATLS 9th edition (student course manual)
8. Manipal manual of surgery 4th edition
9. Browse 4th edition
10. Bedside clinics in surgery 2nd edition
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ለትዝታ
T
THHEE A
AUUT
THHO
ORRSS
DANIEL FENTANEH
BIRUK BIRHANU
&
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CHIEF C O O R DI N A T O R
DAN ALEMAYEHU
2ND EDITION EDITORIAL BOARD
Eshetie
Cheru L. Elshaday Dawit B E
Bruh A.
Endalkachew
Daniel B. Eyasu F.
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HOW TO TAKE HISTORY IN SURGERY?

Cover Design by Daniel F.

This book is dedicated to…

Gastro-intestinal related 182

Genito-urinary related 205

Musculo-skeletal related 218

HEENT+Lymphoglandular related 232

DDx for goiter (enlargement of thyroid gland)

Clinical Presentations (CPs)

D. Mention any medication hx (attempted Rx)

 If you are trying to r/o or rule in simple goiter…

 If you are trying to r/o or rule in Grave’s disease Vs TMNG…

 If you are trying to r/o or rule in malignancy…

 If you suspect metastasis…Ask

 If you want to r/o or rule in inflammatory causes …Ask

Watch video on how to examine thyroid enlargement @

 Absolute contraindications for this Rx

B.Toxic Multinodular Goiter (TMNG)

ii) Secondary (Metastasis)

How to approach Breast disorders

Benign Breast disorders Malignant Breast disorders

Infiltrating ca Inflammatory ca.

=Fat necrosis =Bacterial

=Duct ectasia / = cyclical

 Painusually associated with benign diseases

o In advanced caseswhen you suspect metastatic spread, u

Watch video on how to examine breast swelling @

Smooth & well defined Nodular & irregular

Cyst Fibroadenoma Carcinoma

Discharge Change in appearance

Recent nipple retraction Surface

Eczema Paget’s disease

***important things to check after breast examination in breast ca.

Yes No lump Discharge Change in appearance

o Antibioma=large, sterile, brawny edematous swelling that form if

NB* Duct ectasia=dilatation of the breast ducts

 No hx of swelling in the neck or axilla. (lymph node metastasis)

 Sentinel node biopsy

Benign causes Malignant causes

 PUD Gastric ca.

Clinical presentations of GOO

2. Physical examinationlate events

 In PediatricsThe 4 important DHN signs in well-nourished child are:

No Dehydration Some Dehydration Severe Dehydration

Alert Restless,irritable Lethargic or unconscious

No sunken eyes sunken eyes sunken eyes

Drinking normally Eager to drink Unable to drink

 Contrast studieswhat to look?

SBO (Small Bowel Obstruction)

Extramural Intra-mural Intra-luminal

 Adhesion  volvulus  Fecal impaction

Cardinal Clinical features of acute obstruction

Based on lumen caliber Based on complication

Partial Complete Simple Strangulated

***Check the following evidences for<<>> intestinal strangulationsurgical emergency

Finally he was admitted to our hospital………………………………………..

Dilated if > 03cms