Standard Treatment Protocols

Sr.
Contents Page No.

No.
1 Medicine 1-153
2 Pediatrics 154-246
3 Obstetrics and Gynaecology 247-309
4 Dermatology 310-338
5 Psychiatry 339-361
6 ENT 362-397
7 Ophthalmology 392-450
8 Surgery 451-511
9 Orthopaedics 512-556
10 ANAESTHESIOLOGY 557-581
11 Pathology 582-609
12 DENTRISTRY 610-646
Index
1. Medicine
Sr. No. Contents Page No.
1 Fever 2
2 CAP 6
3 Bronchial Asthama 8
4 Pleural Effusion 11
5 COPD 13
6 Bronchiectasis 15
7 Lung abcess 17
8 Pneumothorax 19
9 Lung Cancer 21
10 Pulmonary Embolism 23
11 Hypertension 25
12 Heart Failure 30
13 Ischaemic Heart Disease 32
14 Acute Rheumatic Fever 35
15 Infective Endocarditis 36
16 Diabetes mellitus 40
17 Thyroid 52
18 Cerebrovascular Accident 55
19 Sub-archnoidHaemorrhage 57
20 Pyogenic Meningitis 58
21 Tubercular Mengitis 60
22 Viral Meningitis 61
23 Viral Encephalitis 63
24 Epilepsy 65
25 GBS (Guillainbarre syndrome) 68
26 Apthous ulcer 69
27 Oesophageal candidiasis 70
28 Dyspepsia 71
29 Gastro-oesophageal Reflux 72
30 Peptic ulcer disease 73
31 Vomiting 76
32 Constipation 77
33 Irritable Bowel Syndrome 78
34 Ulcerative Colitis 79
35 Amoebic liver abscess 81
36 Pyogenic Liver Abscess 83
37 IntesitinalProtozoal Infection 85
38 Ascitis 89
39 Hepatitis 90
40 Hepatic Coma 92
41 Nephrotic Syndrome 93
42 Acute Nephritic Syndrome 94
43 Acute Renal failure 95
44 Chronic kidney disease 97
45 Malaria 99
46 Dengue 107
47 Leptospirosis 111
48 Influenza A- H1N1 113
49 Diarrhoeal Diseases 116
50 Rheumatoid Arthritis 121
51 Snake bite 123
52 Scorpion Sting 127
53 Dog Bite 129
54 Poisoning 132
55 Alcohol Intoxication 135
56 Anaemia 136
57 Heat Stroke 138
58 Tuberculosis (RNTCP) 142
59 Leprosy (NLEP) 151
2. Pediatrics
1 Emergency Management in Pediatrics 155
2 Neonatal Resuscitation Guidelines 167
3 Guidelines For Management Of Normal Newborn 169
4 Care of at Risk Neonates 175
5 Care of Sick Neonates 177
6 Management of Low Birth Weight Babies 181
7 Neonatal Sepsis 185
8 Treatment Of Respiratory Distress In Newborn 189
9 Meconium Aspiration Syndrome 191
10 Bleeding Neonate 193
11 Jaundice in the Newborn 196
12 Management of Surgical Neonate 201
13 Vitamin A Deficiency 202
14 Rickets 203
15 Management of Children with SAM 204
16 Mumps 207
17 Case Management of Children with Sever Acute Malnutrition (SAM) 209
18 Fever with Rash 214
19 Enteric fever / Typhoid 216
20 Acute Meningoencephalities 217
20 Tuberculous Meniingities 219
21 Acute Respiratory Infection 221
22 Bronchial Asthama 226
23 Breath holding spell 228
24 Bronchiolitis 229
25 Empyema 230
26 Approach to Fever 231
27 Acute Flaccid Paralysis (AFP) 232
28 Febrile seizures 235
29 Acute Nephritis 237
30 Nepharotic Syndrome 238
30 Congestive Heart Failure (CHF) 240
31 PICA 242
32 Nocturnal Enuresis 243
33 Thrush / Candiasis 244
34 Congenital Hypothyroidism 245
35 Urinary Tract Infection (UTI) (UTI) 246
3. Obstetrics and Gynaecology
1 Normal Pregnancy 248
2 Normal Labour 253
3 Clinical Care for high risk pregnancy 257
4 Obstetric complications 265
5 Medical disorders complicating pregnancy 285
6 Comprehensive Abortion Care 295
7 Common gynecological problems 298
4. Dermatology
Contents Page No.
Sr. No.
1 Infections of Skin 311
Bacterial
Viral
Fungal
Parasitic
2 Non infectious Skin Conditions 319

Urticaria
Psoriasis
Lichen Planus
PityriasisRosea
Pityriasis Alba
Acne
Miliaria
Eczema / Dermatitis
Atopic Dermatitis
3 Sexually Transmitted infections (STI) 324

Syphilis
Chancroid
LymphoGranuloma Venereum (LGV)
Gonorrhoea
Chlamydial infection
Bacterial Vaginosis
Trichomoniasis
Candidiasis
Wart
Herpes Genitalis
4 Syndromic management of STDS 329
5 HIV AIDS 331

5. Psychiatry
Sr. No. Contents Page
No.
1 Mental illness- Introduction 340
2 Evaluation: History and MSE 341
3 Schizophrenia 342
4 Bipolar Mood Disorder 344
5 Major Depressive Disorder 347
6 Anxiety Disorder 349
7 Somatization Disorder 351
8 Organic Brain Syndrome 352
9 Drug Abuse And Substance use disorder 354
10 Intellectual Subnormality 356
11 Child and Adolescent Psychiatry 358
12 Psychiartric Emergencies 360
13 Procedure For Admission to A Mental Hospitel 361
6. Ent
1 Acute Otitis Media 363
2 Chronic suppurative Otitis Media 366
3 Acute Parotis 367
4 Furuncle 368
5 Otomycosis 369
6 Neck Swellings 370
7 Atrophic Rhinities 371
8 NasalMyasis 372
9 Forign body in the Nose 373
10 Deviated nasal septum 374
11 Nasal obstruction 375
12 Tonsillitis 376
13 Adenoiditis 377
14 Peritonsillar abscess 378
15 Acute Pharyngitis 379
16 Hoarsness of voice 380
17 Stridor 381
18 Facial Palsy 382
19 Sensory Neural Hearing Loss 384
20 Vertigo 386
21 Fracture Involving Nasal Bone 388
22 Fracture Involving Maxilla 389
23 Penetrating neck injury 391
24 Blunt External Laryngeal Trauma 393
25 Epistaxis 394
26 Premalignant lesion of oral cavity 395
27 Acute upper airway obstruction 396
28 Deaf mutism 397
7. Ophthalmology
Sr. Contents Page
No. No.
1 Lid 399
2 Dacryocystitis 402
3 Conjunctiva 405
4 Cornea / Ulcer 409
5 Sclera 412
6 Uveitis 414
7 Glaucoma 416
8 Cataract 421
9 Ophthalmitis 425
10 Retinal Detachment 428
11 Refractive Error 429
12 Diabetic Retinopathy 434
13 Ocular injuries 437
14 Ocular Emergencies 441
15 Pediatric Ocular Problems 443
16 Low Vision 448
17 Eye Banking 449
8. Surgery
1 452
Abdominal Pain
2 456
Wounds & Abscess Management
3 458
Head Injury
4 460
Chest Injury
5 465
Abdominal Injury
6 466
Gangrene
7 468
Burn
8 470
Dressings
9 472
Breast
10 477
Congenital Anomalies
11 488
Venous Thromboembolism
12 490
Varicose Veins
13 492
Genito Urinary Disorder
14 493
Ano-rectal diseases
15 497
Tracheostomy
499
16 Urinary Catheterization
17 506
Triage
9. Orthopaedics
1 Infections in Orthopaedics 513
2 Arthritis 516
3 Congenital Disroderrs 518
4 Metabolic Disorders of Bone 520
5 Regional Conditions 521
6 Common Spine Disorders 524
7 General fracture management 526
8 Poly Trauma 530
9 Pelvic Injury 531
10 Fractures of upper limb 533
11 Fractures of lower limb 539
12 Dislocatons 544
13 Ligamentous injuries 547
14 Spinal trauma 548
15 Mangled Extremeties ( amputation) 552
16 Common Fractures in children 553
17 Bone Tumors 554
10. Anaesthesiology
Sr. Contents Page
No. No.
1 Introduction: General Protocol of Anaesthesia 558
2 Protocol of Difficult Air way 567
3 Pre AnaesthesiaCheck up Protocol 568

4 Conduct of Anaesthesia 569
5 Complications of Anaesthesia 570
6 Regional Anaesthesia Clinical Protocol 571
7 Cardio Pulmonary Resuscitation 573
8 Anaesthesia Obstetric Protocol 577
9 Spinal Anaesthesia 580
11. Pathology
1 Introduction 583
2 Haematology 584
3 Serology 595
4 Biochemistry 598
5 Histopathology 599
6 Cytology study 600
7 Blood Bank 601
8 Normal Lab Values 603
9 Laboratory tests performed at PHC/RH/SDH/DH 609
12. Dentistry
1 Dental Caries 611
2 Diseases of Dental Pulp &Periapical Tissues 614
3 Periodontal Diseases 619
4 Spread of Oral Infection 625
5 Oral Mucosal Diseases 627
6 Premalignant lesions and conditions 630
7 Orofacial Pain 635
8 Traumatic injuries to teeth 636
9 Discoiouration of Teeth 638
10 Maxillofacial Injuries 639
11 Temporomandibular Joint disorders 642
12 Dental Impactions 645
Abbrevations Used
Sr.No. Abbreviation Forms
1 ASHA Accredited Social Health Activist
2 AFB Acid Fast Bacillus
3 AIDS Acquired Immuno Deficiency Syndrome
4 AMTSL Active Management of Third Stage of Labor
5 AFP Acute Flaccid Paralysis
6 ARF Acute Renal Failure
7 ARDS Acute Respiratory disease syndrome
8 ARDS Acute Respiratory Distress Syndrome
9 ANC Ante Natal Care
10 APH Ante Partum Hemorrhage
11 ARV Anti Rabies Vaccine
12 ART Anti Retroviral Treatment
13 ASV Anti Snake Venom
14 ATT/AKT Anti Tuberculosis Treatment
15 ARM Artificial Rupture of Membranes
16 BSL Blood Sugar Level
17 BUN Blood Urea Nitrogon
18 BMI Body Mass Index
19 CRP C Reactive Protein
20 CRT Capillary Refill Time
21 CPD Cephalo Pelvic Disproportion
22 CPK ceratinizephospho kinase
23 CVA CerebvoVasculan Accident
24 CIN Cervical Intra epithelial Neoplasia
25 CS Cesarean Section
26 COPD Chronic Obstructive Pulmonary Disease
27 CRF Chronic Renal Failure
28 CAP Community Acquired Pneumonia
29 CQS Complete Blood Count
30 CT Scan Computerized Tomography
31 CTEV Congenital TalipesEquinoVarus
32 CCF Congestive Cardiac Failure
33 CPAP Continuous Positive Ambulatory Pressure
34 CMV CytoMegalo Virus
35 DHF Dengue Hemorrhagic fever
36 DNS Dextrose Normal Saline
37 D&C Dilatation and Curettage
38 DOT Directly Observed Treatment
39 DMARDS Disease Modifying Anti Rheumatic Drugs
40 DIC Disseminated Intra vascular Coagulation
41 DIC Disseminated Intravascular Coagulation
42 DUB Dysfunctional Uterine Bleeding
43 ECG Electro Cardiograph
44 EEG Electro Encephalon Graph
45 ELISA Enzyme Linked Immuno Assay
46 EBV Epstein Barr Virus
47 ESR Erythrocyte Sedimentation Rate
48 ESR Erythrocyte Sedimentation Role
49 EDD Expected Date Of Delivery
50 FBM Expressed Breast Milk
51 XDRTB Extensive Drug Resistant Tuberculosis
52 F-IMNCI Faculty based Integrated Management of Newborn Child and
Infant
53 FHR Fetal Heart Rate
54 FHS Fetal Heart Sound
55 FNAC Fine Needle Aspiration cytology
56 FRU First Referral Unit
57 FRU First Referral Unit
58 FFP Fresh Frozen Plasma
59 GERD Gastro Esophageal Reflux Disease
60 GIT Gastro Intestinal Tract
61 GDM Gestational Diabetes Mellitus
62 GFR Glomerular Filteration Rate
63 HA Health Assistant
64 HCC
65 HDN Hemolytic Disease of Newborn
66 HE Hepatic Encephalopathy
67 HSV Herpes Simplex Virus
68 HDL High Density Lipids
69 HCG Human Chorionic Gonadotropins
70 ADCV Human Diploid Cell Vaccine
71 HIV Human Immune Deficiency Virus
72 HPV Human Papilloma Virus
73 HTN Hypertension
74 HSG HystroSalpingoGraphy
75 IG Immunoglobulin
76 IVF In Vitro Fertilization
77 IVC Inferior Vena Cava
78 IDDM Insulin Dependent Diabetes Mellitus
79 ICTC Integrated Counseling and Testing Centre
80 IMNCI Integrated Management of Newborn Child and Infant
81 ICU Intensive Care Unit
82 ICCU Intensive Coronary Care Unit
83 IPPR Intermittent Positive Pressure Respiration
84 IHBD Intra Hepahic Biliary Duct
85 IUD Intra Uterine Death
86 IUGR Intra Uterine Growth Retardation
87 IUI Intra Uterine Insemination
88 IDA Iran Deficiency Anemia
89 IFA Iran Folic Acid
90 IBS Irritable Bowel syndrome
91 IHD Ischemic Heart Disease
92 JVP Jugular Venus Pressure
93 KMC Kangaroo Mother Care
94 KFT Kidney Function Test
95 LMP Last Menstrual Period
96 LVH Left Ventricular Hypertrophy
97 LFT Liver Function Test
98 LBW Low Birth Weight
99 LDL Low Density Lipids
100 LRTI Lower Respiratory Tract Infections
101 LSCS Lower Segment Cesarean Section
102 MRI Magnetic Resonance Imaging
103 MVA Manual Vacume Aspiration
104 MCV Mean Cell Volume
105 MCHC Mean Corpuscular Hemoglobin Concentration
106 MMR Vaccine Measles, Mumps, Rubella Vaccine
107 MTP Medical Termination of Pregnancy
108 MAM Medium Acute Malnutrition
109 MOHFW Ministry of Health and Family Welfare
110 MDRTB Multi Drug Resistant Tuberculosis
111 MPW Multi Purpose Worker
112 MI Myocardial Infration
113 NACP National Aids Control Programme
114 NICU Neonatal Intensive Care Unit
115 NBSU New Born Stabilization Unit
116 NGO Non Government Organization
117 NSAID Non Steroidal Anti Inflammatory Drug
118 OC Oral Contraceptive
119 ORS Oral Rehydration Salt
120 PCV Pack Cell Volume
121 PEF Peak Expiratory Flow
122 PEFR Peak Expiratory Flow Rate
123 PID Pelvic Inflammatory disease
124 PUD Peptic Ulcer Disease
125 PMN Poly Morpho Nuclear
126 PCR Polymerase Chain Reaction
127 PEEP Positive End Expiratory Pressure
128 PEP Post Exposure Prophylaxis
129 PET Scan
130 PPH Post Partum Hemorrhage
131 PROM Premature Rupture of Membranes
132 PID Prolapse Intervertebral disc
133 PT Prothrmbin Time
134 PPD Purified Prohine Derivative
135 RDT Radical Drug Treatment
136 RF Renal Failure
137 RNTCP Revised National Tuberculosis Control Programme
138 RVH Right Ventricular Hypertrophy
139 RL Ringer Lactate
140 SAM Sever Acute Malnutrition
141 STD Sexually Transmitted Disease
142 STI Sexually Transmitted Infections
143 SGA Small for Gestational Age
144 SNCU Special New Born Care Unit
145 SLR Test Straight Leg Raising Test
146 SAH Sub Arachnoid Hemorrhage
147 SVC Superior Vena Cava
148 TSH Thyroid Stimulating Hormone
149 TIA Transient Ischemic Attack
150 UC Ulcerative Colitis
151 USG Ultra Sonography
152 URTI Upper Respiratory Tract Infections
153 VLBW Very Low Birth Weight
154 VIA Visual Inspection of Cervix with Acetic Acid
155 WHO World Health Organization
MEDICINE
Page 1
1. FEVER
Body temperature is controlled by the hypothalamus.
The normal core body temperature is 36.5-37.5C
2. Causes
(97.7-99.5F).The morning temperature of >98.9F
Malaria
and the evening temperature of >99.9F defines
Sepsis
fever. Abscess
Brucellosis
1. Definition Lymphoma
Since an oral temperature is 0.5F (0.3C) to 1F Night sweats Characteristic of Tuberculosis, but
(0.6C) lower than a rectal or tympanic temperature: sweating from any cause is usually worse at
Rectal temperature 100.4F - Core temperature night.
Recurrent fever Cholecystitis, Cholangitis and
Tympanic temperature 100.4F - Core Temperature Urinary tract infection with obstruction or
Oral temperature 99.5F-99.9F calculi.
Headache Fever due to any cause can produce
Axillary temperature 99.0F-99.5F headache. If severe and with photophobia
Note: suspect- Meningitis.
Delirium Common in elderly and young ones.
This is not absolute, remember that fever is a
relative condition. Muscle pain Myalgia classical of viral fever,
Have a lower threshold for fever at 6am or 6pm. Influenza, Malaria, Leptospirosis and
Keep antipyretics and recent intake in mind Brucellosis.
when considering fever.
Feeling hot-does not necessarily imply fever. 3. Evaluation of Febrile Patient
Rigors profound chills accompanied by Although fever is a normal response, prolonged
chattering of teeth &severe shivering implies a episodes can cause damage so always evaluate for
rapid rise in body temperature. stability of patient (regardless of what you think is
the cause).
Table 1: Evaluation of fever patient

1.Temperature Axillary temperature >990F
2.White Blood Cell Count >12,000 or <4,000 or
>10% bands
3.Heart Rate >90 bpm*
4.Respiratory Rate >24 bpm^ or PaCO2<32mm Hg
Sepsis = SIRS** + infection
Severe sepsis = SIRS** + infection + end organ damage
Septic shock = Severe sepsis + refractory hypotension
(<90 mm Hg or 40% below baseline)
* beats per minute
^ breaths per minute
**SIRS- systemic inflammatory response syndrome
3.1. Fever Pattern 3.2. Relation to Pulse
It is important to note that the cycle of fever pattern is Liebermeisers rule: For everyone degree rise of
often not very helpful in determining the cause of the temperature above normal, the pulse will increase by
disease. 8-10 beats per minute.
Possible exceptions are: Tertian and quartan Malaria, Fagets Sign: The exception to Liebermeisers Rule.
Abscesses, Pel-Ebstein fever and drug fever.
Page 2
This Relative bradycardia may be useful when
present, although it is associated with a substantial
6. Common associated
differential diagnosis, including Typhoid fever, symptoms
Rickettsial diseases, Yellow fever, Legionnaire's
disease, Psittacosis, Leptospirosis, Drug fever, i.Fever only
Brucellosis, Mycoplasma infections, Neoplasm and ii.Neurologic
Factitious fever. iii. Abdominal
iv. Pulmonary
4. Types of fever v. Rash
vi. Haemorrhage
Continuous fever - Does not fluctuate more than vii. Bone and joint
1C in 24 hr. e.g. Lobar Pneumonia, Typhoid viii. Gynaecologic
fever, Brucellosis, Urinary tract infection.
Intermittent fever- Temperature elevation for a
certain period then returning back to normal. eg. 6.1 Fever only
Malaria, Pyaemia, Septicemia. Malaria
Quotidian- Periodicity of 24 hr- Plasmodium Typhoid fever
Falciparum Malaria. Dengue
Tertian fever- 48 hr periodicity- Plasmodium Leptospirosis
Vivax and Ovale. Rickettsia
Quartan fever - 72 hr periodicity-Plasmodium Relapsing fever
Malaria Other viral illnesses
Remittent fever- Temprature remains above HIV
normal throughout the day with fluctuations
more than 1C in 24 hr eg. Infective
Endocarditis. 6.2 Neurologic symptoms
Fever, headache, altered mental status, convulsions,
5. Hints to be obtained from coma
Cerebral malaria
history Meningitis
Encephalitis
(Since Presentation can be nonspecific) Chronic Meningitis: TB, Cryptococcal
Meningitis
Detailed fever history Rabies
Medication review Japanese Encephalitis
Family illnesses West Nile Encephalitis
Ethnicity HIV
Detailed history of past surgeries Toxoplasmosis
Recent sick contacts and TB contacts/risks HIV dementia
Host factors (Immunocompromised) Trypanosomiasis (Sleeping Sickness)
Recent travel
Environmental exposures associated with jobs
or hobbies 6.3 Abdominal symptoms
Animal exposure Fever, abdominal pain
Unusual dietary habits Typhoid
High risk behavior Infectious colitis: Shigella, E. coli, salmonella,
Sexual history including Contraceptives Campylobacter, Ameba
Gynecologic history Amebic liver abscess
Hypersensitivities to environmental Abdominal TB
agents/medicines or family history of such Appendicitis, Pyelonephritis
diseases HIV
Page 3
6.4 Fever and rash i. Urinary tract infection
Fever and skin rash ii. Pelvic inflammatory disease
iii. Sexually transmitted disease
Chicken pox
Measles
Dengue 7.3. Abdominal symptoms
Other viruses Diarrhoea with or without blood, weight loss
and abdominal pain
i. Gastroenteritis
6.5 Haemorrhagic symptoms ii. Intra-abdominal sepsis
Hematemesis, melena, epistaxis, petechiae, purpura, iii. Inflammatory bowel disease
puncture site bleeding iv. Malignancy
Dengue
Relapsing fever
Ebola, Lassa, Marburg 7.4. Skin rash-appearance &
Yellow fever distribution will give a clue
i. Macular - Measles, Rubella, Toxoplasmosis
ii. Haemorrhagic - Meningococcal, Viral
6.6 Bone and Joint haemorrhagic fever
Fever with joint or bone pain
iii. Vesicular - Chicken Pox, Shingles, Herpes
Sickle cell disease
Simplex
Septic arthritis iv. Nodular - Erythema nodosum- TB & Leprosy
Osteomyelitis v. Erythematous - Drug rash and Dengue fever.
Pyomyositis
Rheumatic fever 7.5 Joint symptoms-
Chickungunya Joint pain, swelling or limitation of movement is
Brucellosis suggestive of active arthritis
i. Distribution-mono, oligo, polyarticular
ii. Appearance-fleeting-Rheumatic fever
6.7 Gynaecological symptoms iii. Oligoarthritis-infective, Kochs
Fever, pelvic pain, vaginal discharge
iv. Polyarticular-Rheumatoid arthritis, Osteoarthritis
PID v. Axial skeleton involvement
Tubo-ovarian abscess Spondyloarthropathy, Psoratic
Postpartum endometritis
Septic abortion
8. Hints to obtain from
7. Symptom Analysis of Fever examination
i. Verify presence of fever- true/factitious Vital Signs: Monitor all of the vital signs for
ii. Duration-acute/chronic stability
iii. Mode of onset- abrupt/gradual General appearance: Do they look sick?
iv. Progression- continuous/intermittent Anxious? Do they have altered sensorium?, look
v. Severity- how it affects the daily work /physical for pallor, icterus, cyanosis, clubbing and
activities? lymphadenopathy.
vi. Relieving and aggravating factors Oral examination: Oral cavity infections, dental
vii. Treatment received and outcome examination, gum examination, sinuses
viii. Associated symptoms- localising features. Cardio vascular examination: Any murmurs
Respiratory examination: Bronchial sounds,
7.1. Respiratory tract symptoms Decreased breath sounds, Adventitious sounds
i. Sore throat, nasal discharge, sneezing-URTI Central nervous system examination: Fundus
ii. Sinus pain & headache- Sinusitis examination, Mental Status, Encephalopathy,
iii. Cough, sputum, wheeze or breathlessness-LRTI
look for any neurological deficit.
Per abdomen: Tenderness, Organomegaly,
7.2. Genitourinary Symptoms Ascites
Frequency of micturition, loin pain, vaginal or Skin: Rashes, Nail Exam, Wounds/Decubitus
urethral discharge suggesting Ulcers
Page 4
Musculoskeletal examination: Joint examination, Sputum Cultures
Muscle tenderness. Skin biopsy
Genital/pelvic examination and rectal
examination. 10.3. ESR
Look for indwelling devices. Normal: Men = Age/2, Women = Age+10/2
Elevated in:
9. Differential diagnosis Acute or Chronic Inflammation
Infection (TB, UTI/Prostatitis, Endocarditis, Infection
Abscess, Line Infection, Sinusitis, Meningitis, Tissue Injury
Arthritis, Osteomyelitis, Wound infectious, Thyroid Disease
Diarrhea) Azotemia
Inflammatory (Rheumatic Disorders, An elevated ESR does not rule in or out disease
Vasculitis) As opposed to the ESR, the CRP increases more
Drug Fever (Beta-Lactam antibiotics, quickly with an acute process, and decreases for
Amphotrecin B, Chemotherapy, Drug quickly when the underlying state resolves.
Interactions)
Thrombotic (DVT/PE/MI) ESR > 100
Neurologic (Hypothalamic disorder, Spinal Cord T - TB
Injuries, ICH) O - Osteoarthritis
Endocrine (Thyrotoxicosis, Adrenal E - Endocarditis
Insufficiency, Subacute Thyroiditis) V - Vasculitis (Temporal Arteritis)
Gastrointestinal (IBD, Pancreatitis, A - Abscess
Cholecystitis) N - Neoplasm (especially Lymphoma, Plasma
Malignancy Cell dyscariasis)
10. Fever Workup 10.4. Blood cultures

The bacteriologic burden is highest in the blood
10.1 Minimum in all patients stream approximately 1 hour before fever spikes.
So collect blood cultures 1 hour before fever
CBC with differential and micro review spike.
Blood smear- for malarial parasites If you are suspecting Endocarditis, tell the lab to
CXR PA and Lateral. Add Decubitus if needed. continue following the cultures for at least 4
Infiltrates negative if dry weeks.
Urine analysis (with Microscopy) and Urine
Culture 11. Treatment of Fever Itself
2 sets of blood cultures + Cultures from any
central catheter Give empiric Antibiotics when there is high
Electrolytes and Metabolic Panel, LFTs, suspicion of the source of infection or if the
Hepatitis Panel, HIV Test source is unknown and the patient is unstable.
Tab Paracetamol 500mg orally 4 times a day for
10.2 Other Specific procedures/labs most fevers with discomfort.
to obtain data Dont always lower the temperature so readily.
Autoimmune Workup (RF, ANA, etc as history
This decreases your ability to know when to draw
guide, ESR, CRP)
cultures and may lower the patients defense
Specific Viral Serologies
mechanism. Once workup has been performed (and
Lumbar Puncture, Thoracentesis, Arthrocentesis, possibly repeated) then temperature can be lowered.
Paracentesis However, have low threshold for lowering the
CT Scan of Head temperature when there is a hypermetabolic state that
CT PE Protocol/Dopplers of extremities would be damaging (i.e concurrent MI, CVA) or if
Echocardiogram the patient is very symptomatic.
Stool Cultures - Gram Stain, Clostridium difficle
toxin etc

Page 5
2. COMMUNITY ACQUIRED PNEUMONIA
[CAP]
Other presentations may include headache and
1. Introduction myalgia
Pneumonia is an infection of pulmonary
Certain etiologies, such as legionella, also may
parenchyma that causes them to function
produce gastrointestinal symptoms
abnormally
Signs -
Classified as typical or atypical, although the
clinical presentations are often similar. Tachycardia
Approximately 20-33% of episodes result in
hospitalization Tachypnoea
Typical: Up to 70% usually caused by Streptococcus Dullness to percussion of chest, crackles or rales
pneumoniae on auscultation, bronchial breath sounds, tactile
fremitus, and egophony (E to A changes)
Atypical: 30-40%(My Lungs Contain Viruses)
Patients with typical pneumonia are more likely
Mycoplasma pneumoniae to present with dyspnea and bronchial breath
sounds on auscultation
Legionella pneumophila
Chlamydia pneumoniae 3. Radiological imaging
Viruses: Influenza, Adenovirus 1) Chest x ray (PA and Lateral)
2. Clinical features Lobar consolidation more common in typical
pneumonia
Symptoms:
Bilateral, diffuse infiltrates commonly seen in
Cough, fever, chills, fatigue, dyspnea, rigors, and atypical pneumonia
pleuritic chest pain
If performed early in the course of the disease,
cough may be persistent and dry, or it may may be negative
produce sputum
Figure 1 - Chest X-Ray PA VIEW - CAP

2) CT scan- Could be performed in patients 4. Laboratory Diagnosis
with a negative chest radiograph when there is a high
clinical suspicion for pneumonia and to rule out other Complete blood count, sputum, gram stain and
pathologies. cultures, blood sugars, blood urea, serum creatinine.
Page 6
Cap Amoxicillin 1gm thrice a day x 5 days plus
5. Treatment TabAzithromycin/Clarithromycin as above
Initial treatment of CAP is based on physical doses
examination findings, laboratory results and patient OR
characteristics. After examination you must decide Cap Amoxicillin and Clavulunate 2gm twice a
whether to treat patient on OPD basis or to admit the day x 5 days plus a tab
patient. Azithromycin/Clarithromycin as above doses
OR
Patients with any one of following features must be
Tab Levofloxacin 750mg OD, OR
admitted
Moxifloxacilline 400mg OD, OR Gemifloxacin
Respiratory rate >30/min 320mg OD x 5-7 days
Systolic BP<90mmHg or diastolic <60mmHg OR
New onset confusion or impaired level of Tab Cefpodoxime 200mg BD or Tab
consciousness Cefuroxime 500mg BD Plus macrolide
Comorbid illness- Diabetes, Ischaemic Heart antibiotics
Disease, Alcoholics, Immunocompromised,
Multilobar pneumonia 5.4. Inpatients
Therapy for pneumonia is empiric because specific - I.V. Cefotaxime 1-2 gm 8 hrly or
pathogens usually are not identified at the time
treatment is initiated. - I.V. Ceftriaxone 1-2 gm OD or
- I.V. Ampicilin 1-2 gm 4-6 hrly or
5.1. Duration of therapy
- I.V. Ampicillin Sulbactum 2 gm 8 hrly x 4 days
S. pneumoniae: 7-10 days or until afebrile 3 days
Mycoplasma/Chlamydia pneumoniae: 10-14 plus
days, up to 21 days Tab Azithromycin or in severe cases I.V.
Legionella: 10-21 days Azithromycin 1gm on day one and then 500mg
OD next 4 days orTab levofloxacin,
5.2. CAP, not hospitalized moxifloxacinas above.
No comorbidities After clinically stable (T<100.00F, HR<100
beats/min, RR<24/min, SBP>90mmsg, O2
Cap Amoxycillin 500mg three times a day x 5 sat>90%) and able to tolerate oral intake, may be
days switched to oral antibiotics for remainder of
Tab Azithromycin 500mg PO x 1, then 250mg therapy
once a day -5 days OR
Tab Clarithromycin 500mg twice a day -5 -7 PPV23 is recommended for all adults65 years
days OR of age and in younger patients with a number of
Cap Doxycycline 100mg twice a day -10 days conditions that increase the risk of invasive
pneumococcal disease.
5.3. CAP, not hospitalized
With comorbidities 6. Complications
Lung abscess, pleural effusion, empyema. These
patients need to be referred to district hospital.
Page 7
3. BRONCHIAL ASTHMA
Peak expiratory flow- by using peak expiratory
1. Introduction flow meter >20% of diurnal variation on 3 days
Asthma is defined as a chronic inflammatory disease in a week for 2 week.
of airway that is characterized by increased
Diagnosis of asthma is established by
responsiveness of tracheobronchial tree to a
demonstrating reversible airway obstruction.
multiplicity of stimuli.
Reversibility is defined as 12%
a increase in
FEV1 15 minutes after two puffs of a
2. Precipitating factors adrenergic agonist (salbutamol) on spirometry.
Childhood infections Respiratory syncytial
virus 6. Treatment
Allergen exposure Allergy to feathers, animal Drug treatment: Classified in to:
danders, dustmites, molds
6.1. Controller: To be taken on longterm basis
NSAID, aspirin, beta blocker, sulfite containing to control asthma through their anti-inflammtory
topical ophthalmic solution, food preserving effects
agent
(a) Inhaled corticosteroids(ICS)
Wood and vegetable dust, industrial chemicals
and plastic Beclomethasone 200mcg/metered dose twice a day
OR
Exercise, emotional stress.
Budesonide 200-400 mcg/metered dose twice a day
3. Symptoms OR
Fluticasone- 100-250mcg/metered dose twice a day
Dysponea, cough and wheezing
Sense of constriction in the chest (b) Systemic corticosteroids
Cough that produces thick, stringy mucus. Oral Prednisone or Prednisolone once daily for 5 to
Increase mucus production, typically tenacious 10 days
mucus.
(c) Leukotriene modifier
4. Signs Tab Montelukast 10mg once a day X 5 days.
Tachyponea, tachycardia, mild systolic hypertension (d) Long acting inhaled 2 agonist-
Respiration become audibly harsh, rhonchi heard on -Salmeterol (MDI 21ug/puff, 2 puff 12 hourly OR
auscultation.
- Formeterol (1 to 2 puffs 12 hourly)
In severe cases - Accessory muscle become visibly
active, Paradoxical pulse, Cyanosis, Silent chest. In (e) Theophylline-Tab Deryphylline 150 mg twice a
some severe cases patients may land in to respiratory day X 5 days.
failure.
5. Investigation 6.2. Reliever: Used on or as needed basis to

Sputum and blood examination for eosinophilia quickly relieve symptoms by their bronchodilator
properties. These are:
Chest X-ray showing hyperinflated lungs
Simple spirometry shows air flow limitation with
deceased FEV1, FEV1 / FVC and PEF.
Short acting inhaled 2 agonist (SABA) Salbutamol 100mcg/metered dose 1-2 puffs, Levosalbutamol
50mcg/metered dose 1-2 puffs as needed, Terbutaline
Page 8
Systemic glucocorticoid - Tab Prednisolone 40-60mg/day
Short acting oral 2 agonist - Tab Salbutamol 2-4mg/day
Anti cholinergic - Ipratropium inhaler
Theophylline - 100-300mg three times a day
6.3. Combinations available as Formoterol/Budesonide 1-2 puffs twice daily

Salbutamol/Beclomethasone.
inhaler and rotacaps Inhaled drugs are preferred over oral due to less dose,
Salmeterol/Fluticasone 1-2 puffs twice daily less side effects, quick onset of action.
OCS
LABA LABA LABA
ICS ICS ICS ICS
Low dose Low dose High dose High dose
Short acting 2 agonist as required for symptom relief
Mild persistent Moderate Severe persistent Very severe
Mild intermittent
persistent persistent
Figure-1: Step wise approach to asthma therapy according to the severity of asthma and ability to control
symptoms.
ICS = Inhaled corticosteroid; Bradycardia or arrhythmia

LABA = Long acting 2 agonist Confusion, coma.
OCS = Oral corticosteroid
7. Acute severe asthma: (Status 7.3. Treatment
asthamaticus) Oxygen 40-60 % nasally to achieve oxygen
Can be fatal and must be treated promptly. saturation >90%
Inj Hydrocortisone-200mg I.V. stat and then
7.1. It is characterized by 100mg 8 hrly
Severe dyspnoea Salbutamol (2.5-5mg) and Ipratropium Bromide
Respiratory rate 25/min (0.5mg) alternately inhaled through the
Heart rate 110/min. nebulizer.
Inability to complete sentence in single breath. Inj. Aminophylline 500mg in 500 ml of 5%
PEF (peak expiratory flow)35-50% predicted Dextrose over 12 hours if patient is not receiving
theophylline previously.
7.2. Life threatening features Inj. Ampicillin 500 mg 6 hrly till patient is stable
PEF<33% predicted and then oral Ampicillin 500 mg TDS X 5 days.
SpO2<92% silent chest In very severe cases patient may require
ventilatory support.
Cyanosis
Normal or raised PaCO2 (suggests impending
respiratory failure) Refer to higher center with above life threatening
signs.
Feeble respiratory effort
Page 9
Rotahaler Spacer Metered dose inhaler
Figure 2 Types of Devices used in Bronchial Asthma
Page 10
4. PLEURAL EFFUSION
A pleural effusion is an abnormal excess amount of Cancer
fluid in the pleural space Liver disease (Cirrhosis)
End-stage renal disease
1. Symptoms Nephrotic syndrome
Breathlessness Congestive heart failure
Cough Pulmonary embolism
Fever Constrictive pericarditis
Pleuritic chest pain Lupus and other autoimmune conditions
2. Signs 4. Investigations
Decreased breath sounds 4.1. Chest X-ray film
Stony dullness on percussion P-A view, lateral decubitus, lateral view
Decreased vocal resonance
Blunting of CP angle, Ellis S shaped in large
3. Common Causes effusions
Tuberculosis
Pneumonia
Figure 1: Chest radiograph showing left-sided pleural effusion
Figure 2: Massive right pleural effusion with shift of mediastinum towards left
4.2. Ultrasound 4.3. Blood tests

Useful in small amounts of fluid, loculated, CBC, ESR, Renal and liver function blood tests:
septations
Page 11
4.4. Thoraco centesis 5. Treatment
Once a pleural effusion is identified on imaging, a Management of common pleural effusions
fluid sample is usually taken to determine the pleural
effusion's character and seriousness, a procedure 5.1. Tuberculosis
called thoraco centesis.
Is the commonest cause of pleural effusion?
A sample of fluid is removed with a needle inserted
between the ribs Straw coloured effusion
Cell count - lymphocyte predominance
Pleural fluid tests: routine, microscopy cytology and Pleural fluid protein > 3g/dl
ADA (Adenosine diaminase) levels
Cob web formation
There are two different types fluid ADA level is high.
Transudative OR Exudative Tubercular pleural effusion is treated as per RNTCP
guidelines
i. Transudative: clear fluid
Clear fluid, low protein content, cell count is low. 5.2. Para pneumonic effusion
eg. Congestive cardiac failure, liver cirrhosis,
Nephrotic syndrome. Chest X-ray consolidation features along with
effusion
ii. Exudative: Cell count predominantly neutrophilic
Straw coloured, high protein content, cell count Appropriate antibiotics
is high. Thoracocentesis toensure that empyema has not
By the gross characteristics of the fluid. developed
Frankly purulent fluid indicates an empyema.
A putrid odor suggests an anaerobic empyema. 5.3. Malignant effusion
A milky, opalescent fluid suggests a chylothorax,
Cytology positive
resulting most often from lymphatic obstruction
Refer to higher centre
by malignancy or thoracic duct injury by trauma
Treatment of underlying cause in heart failure,
Grossly bloody fluid result from trauma, malignancy,
nephroticsyndrome, liver cirrhosis
Page 12
5. CHRONIC OBSTRUCTIVE PULMONARY
DISEASE (COPD)
cause cough with expectoration on most days for at
1. Introduction least 3 months a year for more than 2 consecutive
COPD is a chronic lung disease characterized by years.
airflow limitation that is not fully reversible.
ii. Emphysema
It includes chronic bronchitis and emphysema.
It is defined as distension of air spaces distal to the
i. Chronic Bronchitis terminal bronchiole with destruction of alveolar
This is a condition associated with excessive septa.
tracheobronchial mucus production sufficient to
Table-1: Differentiating features between Emphysema and Bronchitis

Features Predominant emphysema (Pink Predominant bronchitis (Blue
puffer) bloater)
1. Age of onset 6th decade 5th decade
2. Cough After dyspnea Before dyspnea
3. Dyspnea Severe Mild
4. Sputum Scanty, mucoid Copious, purulent
5. Infections Less common Common
6. Respiratory insufficiency Often terminal Repeated attacks
7. Chest x-ray Hyperinflation +/- bullous changes; Increased bronchovascular marking;
small heart large heart
8. PaCO2 (mm Hg) 35-40 50-60
PaO2 (mm Hg) 65-75 45-60
9. Pulmonary hypertension Mild Moderate to severe
10. Cor pulmonale Preterminal stage Common
11. Diffusing capacity Decreased Normal to slight reduction
Table-2: Differences between Pink puffer and Blue bloater
Pink puffer Blue bloater

1. Course Progressive dyspnea Intermittent dyspnea
2. Sputum Scanty Profuse
3. Polycythaemia Uncommon Common
4. X-ray Attenuated peripheral vessels Normal peripheral vessels
5. pCO2 Normal Increased
6. Alveolar gas transfer Reduced Normal
2. Etiology 3. Signs
Smoking (active and passive), Smoke from biomass Sitting and bending forward with hands on
fuel (firewoods, burnt plastics) knees(tripod position).
Page 13
Pursed lip breathing Inhaled bronchodilators include -
Cyanosis Ominous sign Short acting beta agonists -Salbutamol, 1-2 puffs
three times a day, terbutaline 1.5mg three times a day
Forced expiratory time Normal - 4 secs, COPD - 6
secs and above Long acting beta agonis (Salmeterol, Formoterol), 1-
2 puffs twice a day
Barrel chest
Short acting anticholinergics (Ipratropium) 1-2 puffs,
Hyper resonant chest 2-3 times a day
Diminished breath sound and bilateral wheeze Long acting anticholinergic (Tiotropium) 1-2 puffs
Spirometry showing obstruction (Fev1 / Fvc < 70%) once a day.
even after bronchodilator confirms the diagnosis of (d) Theophylline
COPD.
Inj Aminophylline 250mg in 500 ml of 5 % Dextrose
4. Treatment slowly over 8-10 hrs in acute attacks.
Tab Theophylline 100-300mg three times a day
4.1. Non pharmacological
Side effects: tachycardia, nausea, arrhythmias and
Rehabilitation convulsions
Exercise
Nutrition (e) Glucocorticoids
Education Inhaled corticosteroids should be given in severe
Avoid smoking COPD or in those with repeated exacerbation.
4.2. Pharmacological Fluticasone 1-2 puffs twice a day
(a) Oxygen therapy Budesonide 1-2 puffs twice a day
(b) Antibiotics Systemic corticosteroids should be given only in

patients with acute exacerbationof COPD.
Antibiotics are required as infection often precipitates
acute attacks. Inj benzyl penicillin 10 lakhs units 6 Tab Prednisolone 30-40 mg /day for 8-10 days in
hrly 5-7 days or Inj ampicillin 500mg 6 hrly 5-7 days tapering doses
(c) Bronchodilators 5. Complications

Inhaled bronchodilators are preferred to oral i. Pneumothorax
formulations in view of better efficacy and lesser side ii. Respiratory failure
effects. iii. Cor pulmonale
Page 14
6. BRONCHIECTASIS
1. Defination 3. Symptoms
Bronchiectasis is chronic, irreversible dilation and Cough with production of large quantities of purulent
distortion of the bronchi caused by inflammatory and often foul-smelling sputum.
destruction of the muscular and elastic components of Fever, generalized malaise, weight loss, Hemoptysis
the bronchial walls. It may be focal or diffuse. It is Dry bronchiectasis; usually involve the upper lobes
categorized as cylindrical, tubular, varicose or cystic.
Recurrent pneumonia
2. Etiology 4. Signs
Conditions associated with the development of
bronchiectasis Early phases or dry variety: normal
Severe or secondary infection: persisting
2.1. Post infection crackling rales in the same part of lung
Later stage: Emphysema and cor pulmonale.
Bacterial pneumonia Moist crackles at lung bases
Tuberculosis Halitosis, skin pallor
Pertussis
Measles 5. Laboratory tests
Influenza
Fungus Sputum for Gram stain, C&S, and acid-fast
bacteria (AFB)
2.2. Proximal airway obstruction CBC with differential (leukocytosis with left
shift, anemia).
Foreign body aspiration Serum protein electrophoresis to evaluate for
Benign airway tumors hypogammaglobulinemia.
Antibody test for aspergillosis.
2.3. Abnormal host defense Sweat test in patients with suspected cystic
Ciliary dyskinesia (Kartageners syndrome) fibrosis.
Alpha 1 antitrypsin deficiency
6. Evaluation
2.4 Immuno deficiency
6.1. Chest x-ray:
HIV, Hypogamaglobulenimia
Increased in size and numberof ronchovascular
2.5 Genetic disorders markings (quiet nonspecific). Presence of Tram-
track indicates dilated airways suggestive of
Cystic fibrosis bronchiectasis.
6.2. CT or HRCT:
High sensitivity and specificity
Page 15
Figure 1- HRCT showing Bronchiectasis
Tram track sign: The bronchial wall is thicken and 8.2. Acute General Treatment
visible; the bronchi lose the trend of narrowing from
proximal end to distal end. Supplemental oxygen for hypoxemia.
The choice of antibiotics should be accurate by
Signet ring sign: Dilated bronchi appear as ring
the results of sputum culture and drug sensitivity
structures with internal diameters greater than those
test.
of their accompany pulmonary artery branches.
Empirical therapy - Antipseudomonal
antibiotics. Cipofloxacin and Gentamicin or
7. Differential diagnosis Antibiotic therapy is based on the results of
Differentiate from: sputum, Gram stain, and C&S
Chronic bronchitis, Lung abscess, Tuberculosis Bronchodilators are useful in patients with
Congenital pulmonary cyst. demonstrable airflow obstruction.
8. Treatment 8.3. Chronic Treatment

Avoidance of tobacco.
8.1.Non-Pharmacologic Therapy Maintenance of proper nutrition and hydration
Chest physiotherapy helps the Postural drainage Prompt identification and treatment of infections.
and enhances removal of respiratory secretions. Pneumococcal vaccination and annual influenza
Adequate hydration, mucolytic administration vaccination
Page 16
7. LUNG ABSCESS
Symptoms are generally insidious and

1. Introduction prolonged, occurring for weeks to months
A lung abscess is an infection of the lung Fever, chills, and sweats
parenchyma resulting in a necrosis and cavitation Cough
of lung. Sputum production (purulent with foul odor)
Commonest site is right lung and involves the Pleuritic chest pain
posterior segment of the right upper lobe, the Hemoptysis
superior segment of the lower lobe, or both Dyspnea
The bacterial infection may reach the lungs in Malaise, fatigue, and weakness
several ways that most common is aspiration of Tachycardia and tachypnea
oro-pharyngeal contents.
Dullness to percussion, whispered pectoriloquy, and
2. Microbiology bronchophony
The most common anaerobes are 4. Lab.Studies

Peptostreptococcus, Bacteroids, Fusobacterium
species & Microaerophilic streptococcus. CBC- leukocytosis
Other organisms that may infrequently cause Sputum for gram stain, culture & sensitivity.
lung abscess include Staphylococcus aureus, If T.B. is suspected, acid fast bacilli stain &
Streptococcus pyogens, Streptococcus mycobacterial culture is requested.
pneumoniae (rarely), Hemophilus influenza, Blood culture may be helpful in establishing the
Actinomyces species, Nocardia species, & Gram etiology.
negative bacilli (Pseudomonas) Obtain sputum for ova & parasite whenever a
Mycobacterial tuberculosis is a common cause. parasitic cause for lung abscess is suspected.
Non-bacterial pathogens may also cause lung
abscesses. Parasites [Paragonimus, Entamoeba] 5. Radiological imaging
Fungi [Aspergillus, Cryptococcus, Histoplasma,
Blastomyces, Coccidioides] seen in 5.1. CXR
immunocompromised patients. Lung abscesses are most commonly found in the
posterior segment of the right upper lobe. They
3. Clinical presentation appear as irregularly sharp cavity with an air-fluid
level inside.
Figure 1- X-Ray Showing Lung Abscess
Page 17
5.2. CT Scan
- An abscess is rounded radio-lucent lesion with a
thick wall & ill-defined irregular margins.
Figure 2 CT-SCAN Showing Lung Abscess
Cephalosporins that have gram-positive, gram-

6. Medical care negative, and anaerobic coverage, may be used
Antibiotic therapy: when a polymicrobial infection is suspected as
cause of lung abscess.
IV Clindamycin 600mg 3 times a day, till Duration of therapy is generally for 4-6 weeks to
afebrile then oral 300mg four times a day for 7 as long as 14 weeks.
days.
Alternative is IV Amoxycillin/Clavulanate Antibiotic treatment should be continued until the
1.2gm thrice a day or I.V. Ampicillin chest radiograph has shown either the resolution of
/sulbactum 1.5gm thrice a day then to oral lung abscess or the presence of a small stable lesion.
Amoxicillin/Clavulanate for 7 days, with I.V. Patients with poor response to antibiotic therapy
Metronidazole 500mg 8 hrly is an effective drug include bronchial obstruction with a foreign body or
against anaerobic bacteria for 7 days. neoplasm or infection with a resistant bacteria,
In hospitalized patients who have aspirated and Mycobacteria, or fungi.
developed a lung abscess, antibiotic therapy
should include coverage against staph aureus and 7. Complication
Enterobacter and Pseudomonas species and as
per the identified pathogen. Rupture into pleural space causing empyema, Pleural
fibrosis, bronchopleural fistula.
Page 18
8. PNEUMOTHORAX
Stature.
1. Definition
3.2 Secondary spontaneous - less
The presence of air within the pleural cavity.
common
2.Classification Chronic bronchitis &emphysema, (35%).
Asthma,(0.8).
2.1.Spontaneous Suppurative pneumonia like staphylococci,
klebsiella, HIV (2-4%).
Primary. TB of lungs.
Secondary.
3.3 Traumatic Iatrogenic
2.2.Traumatic Paracentesisthoracis, (28%).
Central venous cannulation, (22%).
Non-iatrogenic. Barotrauma (mechanical ventilation).
Iatrogenic. Tracheostomy.
3.4 Traumatic non iatrogenic

2.1 Spontaneous pneumothorax
Pneumothorax occuring in the absence of trauma may
be described as spontaneous. Open & closed chest injury, (road traffic
Presents in 3 ways: accident).
Open Pneumothorax- air moves freely in & out Stab or gun shot wounds.
of pleural space during breathing. Rib fractures.
Closed pneumothorax- no movement of air from
the pleural space due to closure of the 4. Symptoms
communication, air slowly gets absorbed & the
lung re-expands. Small pneumothorax is asymptomatic.
Tension pneumothorax- a check valve Chest pain - Sharp unilateral associated with
mechanism is produced; this allows air to enter shortness of breath is commonest presentation.
pleura & accumulate to raise the intrapleural Sharp & stabbing Chest pain exacerbated by
pressure above the atmospheric pressure and deep inspiration & postural change.
leads to compression on lung & shifting of Anxious, restless, tachypnoeic, struggling for
mediastinum to opposite side. breath, rapid low volume pulse & hypotension.
May large pneumothorax produce respiratory
a. Primary spontaneous distress, signs of shock.
pneumothorax Closed pneumothorax usually does not produce
severe symptoms.
Commonly occurs in healthy subjects with no Tension pneumothorax medical emergency.
h/o of pre-existing lung disease.
Disease of young adult. 5. Physical signs
b. Secondary spontaneous Small pneumothorax difficult to detect on
pneumothorax physical examination.
Absence or diminished breath sounds on affected
Coexisting structural or functional abnormality side.
in the lung. Chest movement diminished on affected side
Decreased vocal fremitus.
3. Causes of Pneumothorax Hyper resonant percussion note.
Ipsilateral enlargement of chest due to decrease
3.1 . Primary spontaneous elastic recoil of the collapsed lung.
Apical blebs (90%). Shift of mediastinum on opposite side.
Page 19
Increased JVP. ECG- Diminished anterior QRS amplitude.
Respiratory distress. Radiographic appearances.
Diaphoresis.s
Cyanosis. X-ray chest-sharply defined lung edge convex
Hypotension. outwards separated from chest wall by translucency
Crepitus is seen if there is associated with no lung markings &mediastinal displacement
subcutaneous emphysema. depending upon the extent of pneumothorax.
6. Diagnosis
Plain X-ray film of the chest showing

hyperleucency without any lung
markings on right side of the chest
(Pneumothorax)
Figure 1 X-Ray Showing Pneumothorax
If pneumothorax small but patient mild

7. Differential diagnosis symptomatic, admit the pt& administer high.
Transmural myocardial infarction-ECG changes flow oxygen, resulting nitrogen gradient will
& left sided pneumothorax changes resolve once speed resorption.
re-expansions. If pneumothorax larger than 15% to 20% or
Emphysema confused with pneumothorax but x- more than mildly symptomatic, insert a
ray main diagnostic tool. thoracostomy tube.
Massive emphysematous bulla or congenital Secondary pneumothorax- pts are symptomatic
cyst, when ruptures may confused with & require lung re-expansion.
pneumothorax but previous x-ray, lateral Often bronchopleural fistula persists & larger
decubitus view helpful in differentiating upper thoracostomy tube & suction are required.
lobe bulla/cyst. Iatrogenic pneumothorax--due to barotrauma
from mechanical ventilation always persistent air
8. Complications leak & should be managed with a chest tube &
suction.
Recurrence, Haemopneumothorax, Pyopneumothorax Tension pneumothorax--decompress the affected
and Respiratory failure when tension pneumothorax hemithorax immediately with a14 gauge needle
present. attached to a fluid filled syringe, release of air
with clinical improvement confirms the
9. Treatment diagnosis. Seal chest wound with an occlusive
T/T depends on cause, size, degree of physiological dressing & arrange the placement of a
derangement Primary pneumothorax-smaller without thoracostomy tube.
pleural air leak may resolve spontaneously.
Page 20
9. LUNG CANCER
1. Definition 3. Risk factors

Uncontrolled growth of malignant cells in one or Smoking: Smokers have 10 fold or greater
both lungs and tracheo-bronchial tree. increase in risk.
Radiation Exposure.
2. Epidemiology Family history: 1st degree relatives 2 to 3 fold
increase risk.
Lung cancer was initially thought to be
Environmental/ Occupational Exposure:
infrequent in India.
Asbestos, arsenic, chromium, mustard gas,
Rare below age 40.
nickel, Radon, polycyclic & hydrocarbons.
Increasing until age 80 after which rate tapers
Scarring.
off.
Probability developing lung cancer
approximately 8% & 6% in males & females.
4. Signs and Symptoms
Table No. 1
Signs & symptoms Range of frequency
Cough (persistent for > than 2 weeks) 8-75%
Weight loss 0-68%
Dyspnoea 3-60%
Chest pain (poorly localized deep chest discomfort) 20-49%
Hemoptysis (seen more in central tumours) 6-35%
Bone pain 6-25%
Clubbing 0-20%
Fever 0-20%
Weakness 0-10%
SVC syndrome 0-4%
Dysphagia 0-2%
Wheezing & stridor 0-2%
Large cell Carcinoma 10-15%,
undifferentiated, giant or clear ce
5. Types of Lung Cancer
5.2. Small cell Carcinoma (20-25%,
5.1. Non small cell carcinoma oat, intermediate cell)
Squamous Cell Carcinoma (25-40%, epidermoid
derived). 6. Diagnosis
Adenocarcinoma (25-40%, bronchial, acinar, History and Physical exam: Physical signs like
papillary, solid, broncioalveolar). clubbing, lymphadenopathy, hoarseness of voice
(vocal cord palsy on indirect larygoscopy) along with
chest x ray signs of mass lesion and. collapse which
are pointers towards the diagnosis of malignancy.
Page 21
Non resolving pneumonia in an elderly individual or Chest X-ray identifies nodules usually >1cm
in smoker, lung malignancy needs to be excluded. HRCT Chest- mass lesion along with its
morphology and vascularity can be better
6.1. Diagnostic tests visualised
Figure 1: Chest X ray showing Left parahilar lung mass
Bronchoscopy - It is the most useful Focal neurologic signs, papilledema.

investigation. Soft tissue mass.
Pleural tapping - cytological examination of the Hematocrit < 40%in men, <35%in women.
pleural fluid is necessary to establish the Elevated alkaline phosphatase, GGT, SGOT,
diagnosis. calcium levels.
Esophageal compression dysphagia.
6.2. Staging tests Laryngeal nerve paralysis hoarseness.
CT chest/abdomen. Symptomatic nerve paralysis - Horners
Bone scan. syndrome.
Bone marrow aspiration. Cervical/thoracic nerve invasion - Pancoast
PET scan helpful in staging to determine tumour.
degree of metastases Lymphatic obstruction _- pleural effusion.
MRI/CT brain useful in looking at CNS Vascular obstruction - SVC syndrome.
involvement. Pericardial/cardiac extension - effusion,
tamponade.
7. Clinical findings suggestive of
metastatic disease 8. Treatment
Medical, surgical and radiation therapy modalities
Lymphadenopathy [>1 cm]. considered according to the type and stage of the
Bone tenderness. cancer.
Hepatomegaly [>13cm span].
Page 22
10. PULMONARY EMBOLISM
Sometimes patients are asymptomatic.

1. Introduction
Differential Diagnosis - Myocardial ischemia-angina,
Thrombosis that originates in the venous system and myocardial infarct, pneumonia, pericarditis,
embolizes to the pulmonary arterial circulation .DVT congestive heart failure etc.
in veins of leg above the knee (>90%), DVT
elsewhere (pelvic, arm, calf veins, etc.), Cardiac
thrombi.
3. Investigations
Risk factors-obesity, smoking, OC pills, surgery, Chest xray- atelectasis, westermark sign
trauma, malignancy, thrombophilia. increased lucency in area of embolism,
Hamptons hump-peripheral wedge shaped
density above diaphragm, pleural effusion.
2. Signs and symptoms ECG- Sinus tachycardia, Classic S1Q3T3
Massive PE Severe dyspnoea, hypotension, pattern, signs of RV strain-Rin V1 V2 with t
cyanosis, tachycardia. inversion.
ABG - hypoxia, hypocapnia, respiratory
Moderate PE- cough, pleuritic pain,hemoptysis
alkalosis Normal does not rule out PE.
fever.Other signs are anxiety agitation, raised JVP,
loud P2, right ventricular heave.
ECG Findings
Figure-1: ECG changes seen in Pulmonary Embolism
Page 23
D-dimer is raised (high sensitivity but poor
specificity).
4.Treatment
CT Pulmonary Angiography is gold standard. Thrombolysis in massive PE. Inj streptokinase
V/Q Lung scan identifies areas of lung that are 2.5 lakhs bolus then 1.0 lakh per hour.
ventilated but not perfused. Unfractionated heparin 80u/kg bolus then
US Venous Doppler to detect deep venous 18u/kg/hr with goal of PTT 46-70 secs.
thrombosis. LMWH-inj enoxaparin 1 mg/kg 12 hrly. To
overlap with warfarin and to continue it for 3-6
months.
Page 24
11. HYPERTENSION
Blood pressure is lateral pressure exerted by column

of blood on the walls of artery when it flows through 4.2. Basic investigations for initial
it. evaluation: Always includes
Hematocrit / Hb.
1. Definition
Serum BUN, Creatinine.
Hypertension - Defined as any one of the
following: Serum potassium.
Systolic blood pressure > 140 mmHg and / or Fasting blood sugar.
Diastolic blood pressure >90 mmHg, Total cholesterol, S Triglycerides.
Patient taking antihypertensive medications. Urine analysis for albumin, blood, glucose.
Essential HT: When the cause is not known (90 ECG for left ventricular hypertrophy and ST-T
to 95 % cases).
changes.
Secondary HT: Specific organ dysfunction is Fundoscopy for HT retinopathy.
detected (5 to 10 % cases).
4.3. Investigations usually included
2. Symptoms depending on cost & other
Often asymptomatic (silent killer). factors
Due to Elevated pressure: Headache (Occipital), i. TSH
vomiting, giddiness, breathlessness, palpitations. ii. Complete blood count.
Due to Vascular disease: Cerebrovascular iii. HDL, LDL cholesterol.
accident, Acute Myocardial Infarction.
iv. Serum calcium, phosphorus.-
Due to Underlying disease: symptoms of
underlying organ affected. v. Serum Uric Acid.
vi. Chest X-ray - Cardiomegaly.
3. Signs
vii. USG renal system - cortical scarring, shrunken
Blood vessels Bruits over carotid. size, obstructive uropathy.
Abdominal Bruit To rule out reno-vascular viii. Echocardiography LVH, Diastolic
hypertension. dysfunction, Ejection Fraction.
Spells of sweating, tachycardia 4.4. Special tests to screen for
Pheochromocytoma.
secondary HT(only in indicated
Tremors, neck swelling Thyroid Disorder.
cases)
Snoring, Daytime somnolence Obstructive Renovascular disease: renal doppler, MR
sleeps Apnoea. angiography, DTPA scan.
Asymmetry of pulses, Radiofemoral delay Renal parenchymal: kidney biopsy.
Takayasu Disease, Coarctation of Aorta.
Pheochromocytoma: 24 hr urine metanephrine
4. How to investigate? & catecholamines.
Cushings syndrome: Sr cortisol,
4.1. Accurate BP measurement dexamethasone suppression test.
The average of two or more seated blood pressure Aldosteronism: plasma aldosterone:renin ratio.
during each of two or more outpatient visits.
Page 25
4.5. Annual tests in hypertensive Fundoscopy.
subjects 5. How to treat?
Hemogram.
Renal profile. 5.1. Goal BP 150/90 mm Hg in elderly and
140/90 mmHg in all others (including DM, CKD).
Lipid profile.
5.2. Life style changes
Urinalysis.
ECG.
Table 1: Lifestyle changes to manage hypertension
Modification Aim
Weight reduction Attain and maintain BMI < 25 kg/m2
Adopt DASH eating plan Diet rich in fruits, vegetables & low-fat dairy products with
reduced content of saturated and total fat
Dietary sodium reduction < 4.8-7.4 g NaCl/d
Physical activity Regular aerobic activity- brisk walking for 30 min/d
5.3. Guidelines for management

Table 2: Hypertension management guidelines
Lifestyle
BP Classification SBP mmHg DBP mmHg Drug Therapy
Modification
Normal <120 and <80 Encourage No
Prehypertension 120-139 or 80-89 Yes No
Stage 1 Hypertension 140-159 or 90-99 Yes Single Agent
Stage 2 Hypertension 160 or 100 Yes Combo
Page 26
5.4. Treatment protocol
Figure 1: Treatment Protocol for HT Age > 30 Yr.
History & Physical examination
Confirmation of diagnosis by
BP > 140/90 mm of Hg.
Educate Patient on nutrition, saltrestrictions, physical activity

de-addiction and regular follow up. ( Refer to Health Workers Manual )
Start the Treatment
Age 60 Yr. Age < 60 Yr.

Goal of Treatment Goal of Treatment
BP < 150/90 mm Hg. BP < 140/90 mm Hg.
1) IF BP is 140-160 1) IF BP is 140-100
Start CCB Start ACE inhib.*( Not recommended in Renal Failure)
T. Amlodipine 5mg OD T. Enalpril 5 mg OD
Goal achieved Goal achieved

Cont. Rx Cont. Rx
Goal Not Achieved Goal Not Achieved
T. Enalpril 10 mg OD
T. Amlodipine 10 mg OD
Goal achieved Goal achieved

Cont. Rx Cont. Rx
Goal Not Achieved

Goal Not Achieved
Goalachieved
Goalachieved Cont. Rx
Cont. Rx
T. Enalpril + T. Hydrochlorthizide
T. Amlodipine + T. Hydrochlorthizide 5 mg OD + 12.5 mg OD
5 mg OD + 12.5 mg OD
Goal not achieved

Goal Not Achieved
Page 27
Goalachieved
Cont. Rx
Age 60 Yr.
Goal of Treatment
BP < 150/90 mm Hg.
Age < 60 Yr.
Goal of Treatment
BP < 140/90 mm Hg.
2) If BP is>160 mm of Hg
2) If BP is>160 mm of Hg
Start
T. Amlodipine + T. Hydrochlorthizide
Start
5 mg (OD) + 12.5 mg (OD)
Goal achieved 5 mg (OD) + 12.5 mg (OD)
Cont. Rx
Goal achieved
Goal not achieved Cont. Rx
Goal not achieved

T. Amlodipine + T. Hydrochlorthizide
10 mg (OD) + 25 mg (OD)
10 mg (OD) + 25 mg (OD)
Goal achieved
Cont. Rx
Goal achieved
T. Amlodipine + T. Hydrochlorthizide + T. Enalpril cont. Rx
10 mg OD + 25 mg OD + 5mg OD
Goal not Achieved
Goal not Achieved

T. Enalpril + T. Hydrochlorthizide + T. Amlodipine
Goal achieved
Cont. Rx
Goal achieved
Goal not Achieved Cont. Rx
Goal not Achieved

T. Amlodipine + T. Hydrochlorthizide + T. Enalpril
T. Enalpril + T. Hydrochlorthizide + T. Amlodipine
Refer to DH
Goal Achieved Refer to DH

Cont. Rx
Goal Achieved
Cont. Rx
Goal not achieved
Goal not achieved
Page 28
If age < 30 yr & BP> 140/90 - immediately refer
to DH (District hospital).
6. Vigilance for End Organ
When patient is on drug if systolic BP is < 100 Damage in hypertensive
mm of Hg withhold the drugs (anti-hypertensive
drugs) and refer to DH. patients
BP >160/100, Start min 2 anti-hypertension Congestive heart failure.
If initial BP is > 200/100 refer to DH after a shot IHD.
of Inj. Frusemide 60 mg stat. Chronic kidney Disease.
If Sr. Creatinine > 1.5mg% refer to DH. Stroke.
Hypertensive Retinopathy.
5.5. Hypertension in Pregnancy
Tablet Methyl Dopa -500mg-1000mg/Day in 7. When to refer?
three divided dose.
Tablet Nifedepine Extended Release Preparation Annual Work-up of known Hypertensive
30- 60 mg OD/BD. subjects.
Other drugs that can be given-Labetalol, Young Hypertensive/ secondary HT.
Hydralizine, Beta Blocker. Resistant Hypertension (Target BP not achieved
ACE inhibitors and ARBS avoided. with 3 drugs including diuretics).
Pregnant subjects.
Hypertensive emergencies (BP > 180/ 110 mm
Hg with e/o end organ damage).
Page 29
12. HEART FAILURE
ii. Also, once the features can be demonstrated on
1. Introduction clinical examination, the underlying causes of
It and congestion in the veins that drains into it. right heart failure should be looked for; e.g.
History of smoking and signs of COPD, or signs
2. Types of heart failure of Mitral Valve Disease.
The heart consists of two distinct parts; right and left Investigations for Right Heart Failure:
receiving blood from different venous system and The diagnosis of Right Heart failure is a clinical one.
perfusing distinct parts of the body; the right heart Investigations are basically to diagnose the
perfusing Heart Failure is a condition where the heart underlying cause of right heart failure.
is unable to perform its functions optimally; leading
to decreased perfusion of the tissues supplied by the Treatment of Right Heart Failure:
lungs for gaseous exchange and the left heart Right heart failure is not a medical emergency and
perfusing the systemic circulation. doesnot cause immediate fatality. There is no direct
Hence there are two types of heart failure. treatment of Right Heart failure. This condition is
alleviated by effective treatment of the cause of
Right heart failure. failure.
Left heart failure. Hence attempts should be made to manage COPD
effectively, like:
2.1 Right Heart Failure
Antibiotics in acute exacerbation.
The right receives blood from the systemic veins and Effective bronchodilation using inhalers and oral
pumps blood into the pulmonary artery through the long acting Xanthines (Deriphyllin).
pulmonary valve. Low flow oxygen inhalation which is the
Hence the cause of Right heart failure would be; treatment of choice for Cor Pulmonale.
increased pressure in the pulmonary artery Effective treatment of Mitral stenosis including
(Pulmonary Hypertension) or pulmonary valve Low salt diet, Diuretics, and Digoxin.
stenosis. When to Refer a Case of Right Heart Failure to
Causes of Pulmonary Hypertension: Higher Centre:
i. Chronic obstructive Pulmonary disease (COPD)
A case of right heart failure needs to be referred for
seen commonly in smokers. Cor Pulmonale.
specialized treatment only for management of non
ii. Mitral valve stenosis seen in Rheumatic heart
responsive chronic obstructive airway disease. Incase
diseases.
the cause of right heart failure is Mitral valve disease
Clinical features of Right heart failure: which is not amenable to medical management, such
cases should be referred to a cardiac centre for
As the right heart receives blood from the systemic definitive management of the condition.
veins, the main clinical features involves features of
congestion in the systemic venous system. 2.2. Left Heart Failure:
i. Raised Jugular Venous Pressure with engorged [Pulmonary Oedema]
superficial neck veins.
ii. Tender Hepatomegaly: Painful, soft liver The left heart receives blood from the pulmonary
palpable in the right hypochondrium. vein and pumps blood in the systemic circulation.
iii. Dependent Oedema: Pitting oedema Causes of left heart failure:
demonstrable on the shin of the tibia and ankles.
i. Systemic Hypertension is the commonest
When to Suspect Right Heart Failure: cause for left ventricular failure
i. Right heart failure should be suspected if the ii. Valvular heart diseases: Aortic stenosis, Aortic
clinical features are present like swelling in the regurgitation and Mitral regurgitation are all
legs and engorged neck vein. causes or acute left heart failure.
iii. Myocardial infarction involving significant
part of left ventricle can cause L.V.failure.
Page 30
Clinical features: i. The patient should be treated in the propped up
position using a backrest or raised head end of
i. Sudden onset breathlessness is the main
the bed.
symptom.
ii. There may be continuous cough with pink ii. High flow Oxygen inhalation should be given.
frothy sputum.
iii. Sedation preferably with Morphine 10mg I.V or
iii. The patient will be very anxious and restless.
Pentazocin 30 mg is the management of choice.
iv. The patient will choose to be in the sitting
position and unable to lie down. If these powerful narcotics are not available, any
v. On auscultation of the chest, crepitations will form of sedation will be of help.
be heard most prominently in the bases.
vi. General examination will reveal high blood iv. Intravenous Frusemide (Lasix) 60mg I.V should
be administered.
pressure which is the commonest cause.
vii. Such patients are likely to present with v. Acute reduction of blood pressure must be done
cyanosis. (Bluish discoloration of tonque, lip, if the cause of left heart failure is Hypertension:
oral mucosa and fingers and toes. I.V. infusion of Nitroglycerine (5 microg/kg) by
BP monitoring, should be tried for the purpose.
Investigations:
Left ventricular failure is a medical emergency and vi. Anti platelets, statins to be continued.
time should not be wasted in any investigation. When to Refer the Patient:
However after stabilizing the patient investigations Treatment of left heart failure must be attempted at
may be carried out to find the underlying cause. the peripheral level. Once stabilized the patient may
be referred to higher centre for management of the
Treatment:
underlying cause.
Left heart failure or Pulmonary oedema is a medical
emergency and speed of administration of treatment Failure of the patients breathlessness to resolve, may
require, endotracheal intubation or non invasive
is of paramount significance.
positive pressure ventilation and patient should be
referred to such a centre if facilities for the same is
not available.
Page 31
13. ISCHAEMIC HEART DISEASE AND
ACUTE CORONARY SYNDROME
ECG taken at that time may show ST elevation or

1. Introduction depression or T inversion. In between anginal
episodes, the ECG may be normal.
1.1. Ischemic heart disease (IHD) A treadmill stress test would confirm angina in over
It is a condition in which there is an inadequate 95% of these cases in referral hospital.
supply of blood and oxygen to a portion of the Echocardiography to measure left ventricular
myocardium. It typically occurs when there is an function and rule out segmental dyskinesia
imbalance between myocardial oxygen supply and suggestive of earlier myocardial infarction.
demand.
1.2. Patients with ischemic heart 2.3. Treatment

disease fall into two large Daily exercise, Stop smoking,Dietary modification
groups. low cholesterol, low fat diet with high roughage.
i. Patients with chronic coronary artery disease Control of hypertension, Diabetes Mellitus and
(CAD) who most commonly present with Dyslipidemia.
stable angina.
ii. Patients with acute coronary syndromes
(ACSs). Drug Treatment
a. Patients with acute myocardial infarction (MI) Tab Aspirin 75 mg once daily.
with ST-segment elevation on their Tab Clopidogrel 75 mg per day.
presenting electrocardiogram (ECG).
Tab Atorvastatin 40 mg per day.
b. With unstable angina (UA) and non-ST-
segment elevation MI. Nitrates -Sublingual glyceryl trinitrate300-500
microgram tds or Isosorbide dinitrate 10 mg
2. Stable Angina thrice a day. If there is headache lower dose of 5
mg twice or thrice daily can be tried.
2.1. Clinical Presentation
Chest pain Retrosternal, dull aching, constricting or Betablockers - Tab Metoprolol 50 200 mg /
burning, radiating to neck, jaw, shoulders or arms day (PO in divided dose).
usually precipitated by exertion or stress and relieved
by rest or nitrates. Angina is crescendo and Potassium channel activators- Nicorandril 10mg
decrescendo in nature and typically last for 2-5 BD.
minutes. Calcium channel blockers like Tab Amlodepine
The physical examination is often normal in patients 5-10 mg OD.
when asymptomatic. Examination during an anginal Refer for coronary angiogram and revascularisation
attack and transient left ventricular failure, there can therapy.
be a third, fourthheart sound, and systolic murmur of
mitral regurgitation.
2.2. Investigations 3. Unstable Angina and Non-

CBC, Urine, Blood sugar, Lipidprofile, and Xray
ST-Segment Elevation
chest PA view may be helpful. Myocardial Infarction
Page 32
UA is defined as angina pectoris or equivalent
ischemic discomfort with at least one of three
4. ST segment elevated
features: Myocardial Infarction
(1) It occurs at rest (or with minimal exertion), 4.1. Clinical Presentation
usually lasting >10 minutes. Chest Pain- commonly occurs at rest, severe, and
lasts longer. Typically, the pain involves the central
(2) It is severe and of new onset (i.e., within the prior
portion of the chest and/or the epigastrium, and, on
46 weeks); and/or
occasion, it radiates to the arms, abdomen, back,
(3) It occurs with a crescendo pattern (i.e., distinctly lower jaw, and neck.
more severe, prolonged, or frequent than previously).
Sudden-onset breathlessness, Sweating, loss of
consciousness, a confusional state.
3.1. Clinical Presentation Sensation of profound weakness, the appearance of
Chest pain, typically located in the substernal region an arrhythmia, an unexplained drop in arterial
or sometimes in the epigastrium that radiates to the pressure.
neck, left shoulder, and/or the left arm.
4.2. Laboratory Findings
3.2. Electrocardiogram CBC, Blood sugar, lipid profile, Xray chest.
ST-segment depression, transient ST-segment
elevation, and/or T-wave inversion. Cardiac markers-CPK-MB elevated.
TrpT,I released within 4-6 hours and elevated for
3.3. Cardiac Biomarkers 2 weeks.
CPK-MB and troponin raised in Non ST segment
elevated MI. Electrocardiogram Convex ST segment
elevation with either peaked upright or inverted
T waves. Q waves if necrosis occurs.
3.4. Treatment
Bed rest. Echocardiogram - regional wall motion
abnormality.
Sublingually Nitroglycerin .3-.6 mg stat can
repeat after 5 min - 3 Doses.
If symptoms persist, intravenous Nitroglycerin 4.3. Complications
infusion at dose of 5-10. microgm/min. once Arrhythmias.
pain has resolved Oral isosorbitrate dinitrate 10
Acute Heart failure.
mg BD can be given.
Rupture of papillary muscle.
Asprin initial dose of325 mg followed by
150mg/day lifelong. Embolism leading to stroke.
Clopidogrel -Loading dose of 300mg followed Ventricular remodelling.
by 75 mg/.day for 2 years.
Ventricular aneurysm.
Tab Atorvastatin 40mg / day lifelong.
Intravenous beta blocker metoprolol 5-15 mg 4.4. Treatment
over 5 mins followed by tab metoprolol 50-
Bed rest.
100mg/day in divided doses with BP check.
Oxygen therapy-2-4L/min.
Unfractionated Heparin (UFH) bolus 6070
U/kg (maximum 5000 U) IV followed by Sublingually Nitroglycerin .3-.6 mg stat can
infusion of 1215 U/kg per h (initial maximum repeat after 5 min - 3 Doses if symptoms persist,
1000 U/h) titrated to A PTT 5070 s. intravenous Nitroglycerin infusion at dose of 5-
10 microgm/min. once pain has resolved Oral
or
isosorbitratedinitrate 10 mg BD can be given.
Enoxaparin 1 mg/kg SC every 12 hr.
Aspirin 325mg and then 150mg OD.
Clopidogrel 300mg and then 75mg BD.
Page 33
Atorvastatin 80mg and then 40mg HS. Stool softeners Bisacodyl (Dulcolax) 10 mg at
night.
Reperfusion therapy: If presenting within 12
hours of chest pain with ECG showing ST Message
elevation > 1 mm then give Inj. Streptokinase 1.5
Acute myocardial infarction is an emergency
million units over 1 hour (contraindications- a
whatever treatment possible should be started at the
history of cerebrovascular hemorrhage at any
center and patient should be transferred to District
time, a nonhemorrhagic stroke or other
Hospital or any hospital where ICU facility is
cerebrovascular event within the past year,
available in a cardiac ambulance. Patient should not
marked hypertension at any time during the acute
be allowed to walk for even short distances and
presentation, suspicion of aortic dissection, and
absolute Bed Rest is important. Treatment of
active internal bleeding).
complications like Heart failure, Arrythmias may
Beta blockers: ), Metoprolol 25 to 50 mg BD, need expert opinion.
Atenolol 25 to 100 mg OD(if pulse rate > Coronary Angiography and revascularisation therapy
60/mm, BP > 90/60 mm Hg ,lung fields clear). should be advised.
ACE inhibitors Enalapril 2.5 20 mg / day in
divided doses twice a day.
Page 34
14. ACUTE RHEUMATIC FEVER (ARF)
Acute rheumatic fever (ARF) is a multisystem

1. Introduction disease resulting from an autoimmune reaction to
infection with group A streptococcus.
2. Criteria for diagnosis of ARF

Major manifestations Carditis (Pancarditis)
Polyarthritis (Migratory)
Chorea
Erythema marginatum
Subcutaneous nodules
Minor manifestations Clinical: fever, polyarthralgia
Laboratory: elevated erythrocyte sedimentation rate or leukocyte
count
Electrocardiogram: prolonged P-R interval
Supporting evidence of a preceding Elevated or rising anti-streptolysin O or
streptococcal infection within the last 45 days
other streptococcal antibody, or
A positive throat culture, or
Rapid antigen test for group A streptococcus, or
Recent scarlet fever
Two major or one major and two minor precipitating group A streptococcal infection.
manifestations plus evidence of preceding group A Penicillin is the drug of choice and can be given
streptococcal infection. orally [as phenoxymethyl penicillin, 500 mg (250 mg
for children 27 kg) PO twice daily, or Amoxicillin 50
3. Investigations mg/kg (max 1 g) daily, for 10 days] or as a single
White blood cell count, Erythrocyte sedimentation dose of 1.2 million units (600,000 units for children
rate, C-reactive protein, Blood cultures if 27 kg) IM Benzathine Penicillin G.
febrile, Electrocardiogram, Chest x-ray if clinical or 4.2 Aspirin in initial dose of 80100 mg/kg per
echocardiographic evidence of carditis, day in children (48 g/d in adults) in 45 divided
Echocardiogram (consider repeating after 1 month if doses is used for the treatment of arthritis, arthralgia,
negative). Throat swab (preferably before giving and fever for 4 weeks.
antibiotics)culture for group A streptococcus.
4.3 Inj. Benzathine Penicillin G 1.2 IU (6 lakhs
Anti-streptococcal serology: both anti-streptolysin O units for children 27 kg) IM every 3 weeks as
and anti-DNase B titres, if available. prophylactic dose up to the age of 25 years.
4. Treatment 5. When to refer
4.1 Antibiotics Evidence of Congestive cardiac failure, Arrhythmia.
All patients with Acute rheumatic Fever (ARF)
should receive antibiotics sufficient to treat the

Page 35
15. INFECTIVE ENDOCARDITIS
1. Definition Streptococci, Pneumococci Enterococci,

Staphylococcus aureus, Coagulase-negative
Infective endocarditis is a form of endocarditis, or staphylococci. Fastidious gram-negative coccobacilli
inflammation, of the inner tissue of the heart (such as (HACEK group i.e. Haemophilus species,
its valves) caused by infectious agents. The agents Aggregatibacter Aphrophilus, Cardiobacterium,
are usually bacterial, but other organisms can also be Eikenella, Kingella), Gram-negative bacilli,Candida
responsible. spp.
Infection most commonly involves heart valves either
native or prosthetic.
3. Clinical Manifestations
2. Organisms Causing Major (Symtoms and signs)
Symptoms- Fever, chills, arthralgia, Fatigue.
Clinical Forms of
Endocarditis
Figure 1: Signs of Infective EndcarditisSigns
Page 36
haemorrhages,conjuctival
4. Diagnosis haemorrhages,Janeway lesion
iv. Immunological
Modified Dukes Criteria phenomenon;(glomerulonephritis;Oslernodes;
Roths spots;rheumatoid factor)
4.1 Major Criteria v. Microbiological evidence positive blood
cultures but not meeting major criteria or
i. Positive blood culture serological evidence of active infection with
Two separate positive blood cultures with organism consistent with infective
microorganism(s) typical for infective endocarditis.
endocarditis:viridians.
streptococci,streptococcus bovis HACEK Documentation of 2 major / one major and 3 minor/5
group, staphylococcus aureus, community minor criteria allow a diagnosis Infective
acquired enterococci endocarditis.
or
Persistently positive blood culture defined as
5. Investigations
presence of micro organism consistent with
infective endocarditis from blood cultures
drawn >12 hrs apart. CBC-Anaemia,Leucocytosis.
or Urine-Microscopic haematuria.
Single positive blood culture for coxiella Elevated ESR, Elevated CRP.
burnetti or phase one IgG antibody titer of >1 : Blood culture 3 sets of two bottle blood. culture
800. from different venipuncture site separated from
one another by atleast one hour over 24 hours.
ii. Echocardiographic evidence of endocardial Echocardiography.
involvementTypicalvalvular
lesions;vegetations,abscess,or new partial 6. Complications
dehiscence of a prosthetic valveNew Valvular
regurgitation. Blood clots or emboli that travel to brain,
kidneys, lungs, or abdomen.
4.2 Minor Criteria Brain abscess.
Congestive heart failure.
i. Predisposition;predisposingheart condition or Glomerulonephritis.
intravenous drug use. Jaundice.
ii. Temperature greater than 38.0 C. Neurological changes.
iii. Vascular phenomenon;major arterial Rapid or irregular heartbeats, including atrial
emboli,septic pulmonary infarcts,mycotic fibrillation.
aneurisms,intracranial Severe valve damage.
Stroke.
Page 37
7. Treatment
Table 1: Antimicrobial Therapy
Organism Drug (Dose, Duration

Penicillin-susceptible streptococci Inj. Penicillin G (23 mU IV q4h for 4 weeks) or
Inj. Ceftriaxone (2 g/d IV as a single dose for 4 weeks) plus
Inj. Vancomycin (15 mg/kg IV q12h for 4 weeks)
Moderately penicillin-resistant streptococci Inj. Penicillin G (45 mU IV q4h) or ceftriaxone (2 g IV qd)
for 6 weeks plus
Inj. Gentamicin (3 mg/kg qd IV or IM as a single dosee or
divided into equal doses q8h for 6 weeks) Plus
Inj. Vancomycin (15 mg/kg 12 hourly) as noted above for 4
weeks
Enterococci Inj. Penicillin G (45 mU IV q4h) plus
Inj. Gentamicin (1 mg/kg IV q8h), both for 46 weeks
Staphylococci (native valve) Inj. Vancomycin (15 mg/kg IV q12h for 46 weeks)
Staphylococci (prosthetic valves) Inj. Vancomycin (15 mg/kg IV q12h for 68 weeks) plus
Inj. Gentamicin (1 mg/kg IM or IV q8h for 2 weeks) plus
Rifampin (300 mg PO q8h for 68 weeks)
8. Prevention
High Risk cardiac lesions where antibiotic
prophylaxis is needed.
1. Prosthetic heart valve.

2. Prior endocarditis.
3. Unrepaired cyanotic congenital heart disease.
4. Completely repaired cyanotic heart disease
within 6 months.
5. Incompletely repaired cyanotic heart disease
with residual defects.
Page 38
Table: 2: Antibiotic Regimens for Prophylaxis of Endocarditis in Adults with High-Risk Cardiac
Lesion
A. Standard oral regimen
1. Amoxicillin: 2 g PO 1 h before procedure
B. Inability to take oral medication
1. Ampicillin: 2 g IV or IM within 1 h before procedure
C. Penicillin allergy
1. Clarithromycin or azithromycin: 500 mg PO 1 h before procedure
2. Cephalexin: 2 g PO 1 h before procedure
3. Clindamycin: 600 mg PO 1 h before procedure
D. Penicillin allergy, inability to take oral medication
1. Cefazolin or ceftriaxone: 1 g IV or IM 30 min before procedure
2. Clindamycin: 600 mg IV or IM 1 h before procedure
Message- If any valvular heart disease or prosthetic valve patient develops fever, infective
endocarditis should be thought of apart from other normal causes of fever.
Page 39
16. DIABETES MELLITUS
Genetic defects of insulin action.
1. Introduction
Diseases of exocrine pancreas Trauma,
Diabetes mellitus is a clinical syndrome characterized
Pancreatitis, Pancreatectomy, Cystic fibrosis,
by hyperglycemia due to absolute or relative
Fibrocalculous Pancreatic diabetes,
deficiency of insulin.
Haemochromatosis.
Gestational Diabetes Mellitus (GDM) Onset /
2.Classification of Diabetes Recognition of glucose intolerance in pregnancy.
Mellitus
2.1. Type 1 Diabetes Mellitus 3. Diagnosis of DiabetesMellitus
Autoimmune pancreatic B cell destruction; absolute Symptoms of Diabetes Mellitus and Random
insulin deficiency. Blood Sugar > 200 mg% (mg / dl)
Fasting blood sugar > 126 mg % on more than
2.2. Type 2 Diabetes Mellitus one occasion.
Characterized by peripheral tissue Insulin Resistance
/ Relative Insulin deficiency. 2 hours Plasma glucose > 200 mg% during oral
glucose tolerance test with glucose 75g
2.3. Other Specific Types glucose.
Genetic defects of B cell function Maturity

Onset Diabetes in Young (MODY).
Table 1: Criterion for Diagnosis based on blood glucose levels
Normal Glucose Prediabetic Diabetes mellitus

Impairedglucose
tolerance
FPG <100mg/dl 100-125 mg/dl >126 mg/dl
2hr PG <140mg/dl 141-199 mg/dl >200 mg/dl
A1C (Glycosulated <5.6% 5.7-6.4% >6.5 mg/dl

Hemoglobin)
4. Clinical symptoms
Common symptomsare
Other symptoms are tiredness, fatigue, pruritis vulvae
1. Polyuria {increased frequency of micturition), giddiness, burning over feet, and can present with
2. Polydipsia (increased thirst), complications of diabetes.
3. Polyphagia (increased appetite),
4. Weight loss. Table -2: Major differentiating features of Type 1 and
Type 2 diabetes are as follows-
Page 40
5. Management
Type 1 Diabetes Mellitus:
5.1 Type 1 Diabetes Mellitus e) glucosidase inhibitors - acarbose, voglibose,

miglitol
Strict meal plan * Carbohydrate: 50 - 60% * f) DPP4 inhibitors- sitagliptin, vidagliptin
Protein: 10 20% * Fat: 30% (If patient is
dyslipidemic, fat should be 15%) * Caloric Parenteral agents
intake: 30Kcal / kg 1. Insulin
Physical exercise 2. GLP-1 receptor agonist- Liraglutide,Exenatide
Only Insulin (a) Bi-guanides

Dose- 500mg-2000mg/day.
5.2 Type 2 Diabetes Mellitus:
Contra-indications to Bi-guanide therapy: 1. Renal
Strict meal plan failure when creatine clearance < 40 ml / min 2.
Physical exercise Arteriography or intravenous urography as
Oral hypoglycemic agents intravenous iodinated products may precipitate lactic
acidosis on patients with bi-guanides 3. Advanced
Insulin
liver cell failure 4.Alcoholism 5.Cardiac diseases
Oral Hypoglycemic Agents: 6.Diabetes with significant acute and late
complications 7.Pregnancy 8. Old age > 70 years.
a) Biguanides - Metformin
b) Sulphonylureas - Glibenclamide, Glipizide,
Glimeperide,, Gliclazide
(b) Sulphonylureas
c) Glinides (nonsulphonylurea secretogouge) - Mechanism of action- Increases insulin secretion
repaglinide from the beta cells through the ATP sensitive K
channels.
d) Thiazolidinediones pioglitazone
Page 41
Table-3: Sulphonylurea drugs with dosage and side effects
Drug Dose Side effets

Glibenclamide 1.25-20 mg Hypoglycaemia, weight gain
Glimeperide 1-8 mg Hypoglycaemia
Glipizide 2.5 -25 mg Hypoglycaemia
Gliclazide 30-240 mg Hypoglycaemia
Contraindications for sulphonylurea therapy thereby increasing insulin secretion only with the
intake of food. They do not cause hypoglycaemia.
1. Insulin dependent diabetes mellitus (IDDM)
Dose- vidagliptin 50 mg BD, Sitagliptin 100mg OD.
2. Pregnancy
Insulin
3. Patients with severe infections
Consider insulin as initial therapy in patients
4. Allergic reactions
with:
5. Significant liver and kidney disease
Fasting plasma glucose > 250 - 300 mg/dl since
6. Patients undergoing surgery more rapid glycemic control will reduce glucose
toxicity to islet cells, improve insulin secretion
(c) Glinides-(Nonsulphonylureas) secretogoue-
and possibly make oral hypoglycemic agents
Increase insulin secretion
more effective.
Dose-Repaglinide 0.5-3 mg/day.
Lean patients or those with severe weight loss.
(d) Thiazolidinediones-These are insulin sensitisers
Pioglitazone is commonly used. Underlying renal or hepatic disease.
Dose- 15- 45 mg/day. Hospitalized or acutely ill patients.
Side effects- Weight gain, congestive cardiac failure, If response to oral hypoglycemics is not
fractures, adequate. Consider insulin as initial therapy
(e) Glcosidase inhibitors Decreases intestinal Pregnancy

glucose absorbtion and reduce postprandial Types of Insulin
hyperglycemia.
1. Rapid-acting insulin: aspart insulin and lispro
Dose- Acarbose -25 -100 mg/day to be taken with insulin
food. 2. Regular or Short-acting insulin
Voglibose-. 0.2- 0.3 thrice a day 3. Intermediate-acting insulin: lente insulin and
NPH insulin
(f) DPP 4 Inhibitors 4. Long-acting insulin: Insulin detemir and insulin
Mechanism of action They inhibit the enzyme glargine
DPP 4 and increase endogenous GLP-1 action
Figure-1: Treatment Protocol for DM Type II
History & Physical examination

RBS>140 mg/dlSuspect
Page 42
Confirmation of diagnosis by
Fasting bllood sugar - >126 mg/dl OR
Post Prandial B.S->200 mgCC/dl OR
Random Blood Sugar -> 200 mg/dl
Educate Patient on Diet, Physical activity,

De-addiction Foot care and regular follow up.
(Refer to Health Workers Manual)
Take blood for Sr. Creatinine & Other investigation Urine

Start the albumin &Sugar treatment
Fasting B.S:> 126-200 or/and Fasting B.S:>200-300and/orPost Prandial B.S:

>300-350
Post Prandial B.S:> 200-300
Start with combination therapy
Start with monotherary Metformin + Sulphonyl Urea
Tab. Metformin 500mg BD 500mg BD (Glimiprideor Glipizide)
(1 mg OD) (2.5mg OD)
Evaluate after
15 days with Sr. Creat Report
> 1.5 mg%
If Sr. Creat is
< 1.5 mg% Urgent Referral to DH
Target to be achieved with therapy

Fasting 100 126 mg/dl
Target to be achieved with therapy

Fasting 100 126 mg/dl
Target achieved with given Target not achieved with giventherapy

therapy
Continue the Rx and regular follow up Step wise increase the dose of medicine
after 15-30 days.
Page 43
Target achieved Target not achieved
Follow up after 15-30 days. Refer to DH
Steps to increase dose in: 3) 1 gm BD + 2 mg BD Or 5 mg BD (If target

not achieved)
A) Monotherapy: Refer the patients to DH.
I. Start with T. Metformin 500mg BD
( If target not achieved ) * The main aim of this protocol to control raised
II. T. Metformin 750 mg BD ( If Blood sugar however not to complicate by
target not achieved ) Hypoglycemia.
III. T. Metformin 1 gm BD ( If
target not achieved )
Refer the patients to DH. Instruction: - Dont allow patients to fast while
on medication.
B) Combination therapy: -Strict De-addiction state should be
Metformin + Glimepride OrGlipizide. maintained.
1) 500mg BD + 1mg OD Or 2.5mg BD - If sudden rise in blood sugar
(If target not achieved) observed then urgent referral to District Hospital.
2) 750mg BD + 1mg OD Or 2.5mg BD
(If target not achieved)
6. Check list
Page 44
Microvascular complications
7. Complications of Diabetes
Mellitus Eye disease- Retinopathy, Macular edema.
7.1 Acute complications Neuropathy- Sensory and motor neuropathy (mono
and poly),
Hypoglycemia
Diabetic Ketoacidosis (DKA) Autonomic neuropathy
Diabetes and infections
Hyperosmolar Hyperglycemic coma (HHNKC). Nephropathy
7.2 Chronic complications Macrovascular complications
Coronary heart disease

8. Hypoglycemia
Cerebrovascular disease Hypoglycemia is a clinical emergency occurring in
Peripheral arterial disease diabetes characterized by either autonomic or
neuroglycopenic symptoms (or) biochemically
Other gastroparesis, sexual dysfunction, random blood sugar < 60mg, due to antidiabetic
dermatologic agent, food and activity mismatch.
Table-4: Clinical presentation of Hypoglycemia
8.1 Management Dextrose supplementation - Conscious: Oral

Glucose, Sugar, Fruit Juice, Unconscious: 50%
Draw blood sample immediately Dextrose 100ml IV Stat. Followed by 10%
Page 45
Dextrose then by 5% DNS maintenance (or) Inj. Important Note Patient Education:
Glucagon 1mg im if not accessible to Educate patient and his family members about
intravenous route low blood sugars and symptoms
Patient still remains unconscious - To rule out Never miss a meal after insulin / Oral
cerebral edema, If present IV mannitol + Inj. hypoglycemic agents
Dexamethasone 8mg IV Be cautious of unaccustomed physical activity
Stop the antidiabetic agents for 3 days in Type 2 To carry diabetic identity card
Diabetic mellitus patients and recheck blood Always carry simple sugar (biscuits and toffee)
sugars. In Type 1 Diabetic mellitus patients, to avoid low sugar.
recheck blood sugars after 6 hrs and adjust
insulin dose accordingly. 9. Diabetic Ketoacidosis (DKA)
Identify the cause of hypoglycemia Ketoacidosis is a major medical emergency and
If recurrent hypoglycemia, rule out - Renal remains a serious cause of morbidity, principally in
function disorder, Liver function disorder people with type 1 diabetes, which should be treated
Repeat blood sugar value after hypoglycemia in hospital.Patient should be referred to tertiary
correction and monitor blood sugars health centre after the primary management.
Referral: If the patient remains unconscious
even after dextrose administration refer the
9.1 Manifestation of DKA
patient immediately to higher centre for further
evaluation.
Table 5
Page 46
9.2 Investigations ABG for pH and bicarbonate
Urine sugar [positive]
Blood glucose [usually > 250 mg %] Urine acetone [positive]
Blood urea [may or may not be ] Chest X-ray
Serum creatinine [may or may not be ] ECG
Serum electrolyte [Na or , K or decreased] Ultrasonogram abdomen / KUB.
Serum bicarbonate < 10 mmol / l
9.3 Management of DKA
9.4 Referral Anuric

Elevated renal parameters
Refer the patient to a higher centre if:
Evidence of septicaemia
Patient is comatose
Hypotension requiring ionotropic support
Page 47
9.5 Complications of Diabetic Ketoacidosis
10. Hyperglycemic
Hyperosmolar Non-Ketotic
Coma (HHNKC)
10.2 Symptoms
It is an acute metabolic complication in middle aged
and elderly diabetics with high morbidity and Polyuria
mortality. Polydipsia
Severe hyperglycemia (Blood sugar > 600
10.1 Causes mg%)
Profound dehydration
Precipated by Elevated osmolality
Hemianopia, muscle fasciculation, seizures
Infection
Altered sensorium, coma
Trauma
Burns 10.3 Treatment
Infarction
Hyper-alimentation 1. Fluid replacement: normal saline at the rate of
Drugs like - Thiazide, Cimetidine, Phenytoin 2 litre in 1st 2 hours and 1 litre in another 2
and Parentral diuretics hours
2. Low dose insulin.
3. Correction of electrolytes and hyperosmolality.
4. Low-dose heparin to prevent vascular
thrombosis intravascular coagulation.
Page 48
10.4 Distinguishing features
Table-6: Distinguishing features between DKA and HHNKC
Moderate worker 40 kcal/kg Ideal body weight

11. Medical Nutrition Therapy For heavy worker
A non-pharmacological mode of management of In obese people - Reduce 500 kcal from the
diabetes. Medical Nutrition therapy is individualized calculated energy requirement
and should be a tailor made regimen. It is used as a
compliment for an oral glucose lowering agent / For under weight- Add 500 kcal to the calculated
insulin therapy. energy requirement of the total kcal, 45 - 65 %
kcal from carbohydrate and 10-25 % kcal from
Energy Recommendations: proteins
This depends on body weight and physical Fat recommendation - 500ml / month of a blend
activity. 20 kcal/kg Ideal body weight of oils / individual Gingelly oil and any refined
Sedentary worker 30 kcal/kg Ideal body weight
Page 49
vegetable oil could be used (or) Rice brand oil and any refined vegetable oil
Fibre recommendation - 14gm/1000kcal
12. Gestational Diabetes
provided.
Mellitus
Fluid recommendation - 8 to 10 glasses / day of
water except in LVF, CKD, Cirrhosis etc. Gestational Diabetes mellitus is defined as
carbohydrate intolerance of variable severity with
11.1 MNT in Gestational Diabetes onset or first recognition during the present
pregnancy.
Mellitus
12.1 Risk for gestational diabetes
30 kcal / kg Instant Body weight in first trimester
mellitus
30 kcal / kg Instant Body weight + 300 kcal/day
in II and III trimester Age more than 25 years
Protein - 1gm/kg Instant Body weight + 10gm Family history of diabetes mellitus
daily throughout pregnancy
History of unexplained fetal loss
Avoid hypocaloric diets in obese GDM
History of baby being large for gestational age
Provide compulsory bed time and evening snack
to avoid accelerated starvation and nocturnal History of congenitally malformed infant
hypoglycemia Maternal obesity
Gestational Diabetes mellitus:
History of Polycystic ovarian disease
Strict meal plan
Polyhydramnios
Physical exercise
Pre-eclampsia
Insulin
Unexplained intrauterine death
Other specific types
12.2 Methods of screening
Strict meal plan
Physical exercise Spot test: Fasting < 90 mg% [normal 2 hr post-
prandial < 120 mg%, random < 105 mg% values]
Insulin with or without oral hypoglycemic agents
ADA recommendation
Figure-2: Methods of Screening
Page 50
12.3 Diagnostic Criteria Target Glycemic Level
WHO criteria (with 75 gm of glucose ) F - 95 mg % Fasting glucose 90 mg %
1 hr - 180 mg % 2 hr - 155 mg % If any two values 2 hr postprandial 120 mg %
equals or crosses normal value, it is termed as Monitoring Glycemic Control

Gestational Diabetes mellitus. Blood glucose fasting and postprandial every
Important Note OGTT value should never be treated. three days till glycemia is achieved; then every
fortnightly, throughout first and second trimester.
12.4 Treatment Every week in third trimester.
1. Medical Nutrition Therapy [refer MNT] 2. Insulin Glycemic profile monitoring once in 1st and 2nd
is essential if MNT fails to achieve euglycemia trimester and then every month.
Page 51
17. THYROID DISORDERS
* When full replacement is achieved then follow up
1. Hypothyroidism measurement at annual intervals and later by a 2 - 3
yearly interval
Hypothyroidism may be
* Ensure ongoing compliance.
1 Primary 1.4. Special treatment considerations
Common causes of which are autoimmune, iatrogenic
due to Iodine131, antithyroid or lithium treatment A hypothyroid woman should be euthyroid prior
and thyroidectomy to conception and during early pregnancy (effect
on fetal neuronal development). Thyroid profile
2 Secondary should be immediately done after confirmation
of pregnancy and in second and third trimester.
1. Pituitary disease
2. Hypothalamic disease. Dose of Thyroxine should be increased by 50%
during pregnancy and return to previous level
1.1. Symptoms after delivery
Elderly require less Thyroxine (less by upto
Coarse dry skin
20%) especially those with coronary artery
Hoarseness of voice disease, starting dose 12.5 mcg/day with similar
increments every 2 - 3 months until TSH level is
Facial puffiness, weight gain normalized.
Cardiac enlargement and/or pericardial effusion, In hypothyroidism due to low TSH (supra-
thyroid cause is suspected) detailed
Goiter with or without prolonged relaxation investigations are required and patient should be
phase of deep tendon reflexes. referred to a tertiary care level
Myxedema coma is a rare complication of severe Asses the response clinically and by serum TSH
hypothyroidism with hypothermia, hy- (serum T3 in suprathyroid type) at 8 weekly
poventilation, hyponatremia, hypoxia, intervals
hypercapnoea and hypotension. Once euthyroid state is restored, follow-up at 6 -
12 monthly intervals.
1.2. Diagnosis is confirmed by
1.5. Treatment of Myxedema coma
Low serum free T3 and T4
Warm blankets, mechanical ventilation for
Serum TSH raised respiratory failure.
Other investigation blood sugar level and lipid Correction of metabolic disturbances and treat
profile precipitating factors.
Drugs * L-Thyroxine 500 mcg IV bolus, then
1.3. Treatment 50-100mcg IV daily * If intravenous preparation
not available, the same dose is administered
Pharmacological through Ryles tube.
* Tab. L -Thyroxine- 1.6 mcg per kg body weight or * Once acute phase is over, maintain L-Thyroxine
Start with 50 100mcg/day as above.
* Dose to be adjusted based on TSH levels * Inj.Hydrocortisone 100 mg IV stat, 25-50 mg 8
* Goal is normal TSH (lower half of reference range hourly.
* Measure TSH levels after about 6 wks of instituting Caution: Avoid sedatives
therapy
* Adjust by 12.5 or 25 mcg increments if TSH is
high; decrement of the same if TSH is
suppressed.
Page 52
1.6. Patient Education Explain to the patient that the treatment is life
long. Do not modify dose or stop treatment with-
L-Thyroxine should be taken as a single daily out consultation.
dose, ideally on awakening, at least 30 minutes
before breakfast. Over treatment may lead to decreased bone
mineral density and adverse cardiac
Fibre and bran products (e.g., Isapghola husk) complications.
may impair absorption, as also cholestyramine,
cholestipol, iron sulphate, sucralfate, aluminium 2. Hyperthyroidism
hydroxide
Thyrotoxicosis is defined as the state of thyroid
Metabolism of L-Thyroxine is increased by
hormone excess and is not synonymous with
Phenytoin, Rifampicin and carbamazepine.
hyperthyroidism, which is the result of excessive
thyroid function. However, the major etiologies of
thyrotoxicosis are hyperthyroidism caused by Graves'
disease, toxic MNG, and toxic adenomas
2.1. Symptoms
Graves disease is characterized by diffuse goiter, Adjunctive treatment * For adrenergic symptoms
Ophthalmopathy and Dermopathy in varying such as sweating, tremor and tachycardia. Tab.
combinations. Propranalol 40 120 mg a day. Or atenolol 25
mg to 50 mg
Ophthalmopathy in Graves' disease; lid retraction,
periorbital edema, conjunctival injection, and Anti thyroid drug-
proptosis are marked Tab. Propylthiouracil 100 150 mg every 6
8 hours or Tab. Carbimazole 10 20 mg every
2.2. Diagnosis 8 12 hours; After euthyroid state is achieved
in 6 8 weeks once daily dosage. Review with
Diagnosis is confirmed by low to undetectable serum serum TSH and FT3 after 3 4 weeks treatment
TSH and increased Serum free (FT3) and free (FT4) has been initiated.
Once controlled reduce to the smallest effective
Ultra sonography of neck dose or continue initial dose combined with L-
Thyroid scan (if available) Thyroxine
Drugs are given for an average of 2 years.
2.3. Treatment Definitive treatment is surgery/ablation of
thyroid tissue
Pharmacological Subtotal thyroidectomy in younger patients (<30
years) in whom antithyroid therapy has been
unsuccessful and in very large goiters.
Page 53
Radioactive iodine (I131): Method of choice in Treatment with antithyroid drugs given till
* Elderly * Younger patients who have patient is euthyroid.
completed family with recurrent thyrotoxicosis Propranalol may be useful before and after
following surgery or when surgery is refused or radioactive iodine administration.
contraindicated. Caution Radioactive iodine
should never be given in pregnancy. In woman 2.6. Thyrotoxic crisis or thyroid
of childbearing age if radioactive iodine is
planned, a pregnancy test should always be
storm
carried out.
Refer to a tertiary care centre.
2.4. Pregnancy Life threatening hyperthyroidism with fever,
vomiting, diarrhoea, jaundice, delirium and
In pregnant woman surgery should not be coma.
performed in 1st or 3rd trimesters Usually precipitated by acute illness such as
Antithyroid drugs are less risky but may induce stroke, infection, diabetic ketoacidosis, trauma,
hypothyroidism in the foetus and should be used patients undergoing surgery or radioactive iodine
in the smallest necessary dose to keep serum treatment in a poorly prepared patient:
TSH and FT4 in normal range. Tab. Propylthiourcil 600 mg loading dose, then
Propylthiouracil is preferred usual maintenance 200 300 mg every 6 hours orally or through
is 200 mg/day. If > 300 mg/day required during Ryles tube. (or) Tab. Carbimazole 15 25 mg 6
1st trimester, Subtotal thyroidectomy is indicated hourly.
in 2nd trimester 1 hour after the 1st dose of antithyroid drug,
Propranolol should be avoided as it can cause saturated solution of Potassium iodide (SSKI) 5
foetal growth retardation and neonatal drops every 5 hours. (or) Lugols iodine 10 drops
respiratory depression. 3 times a day. (or) Sodium iodide 1 g IV slowly.
Tab. Propranalol 40 60 mg 4 hourly or 0.5 2
Ophthalmopathy: Refer to ophthalmologist. Initiate mg IV every 4 hours.
therapy in mild cases with elevation of head at night, Inj. Dexamethasone 2 mg IV 6 hourly
diuretics to decrease edema, use of tinted sunglasses Continue iodides and dexamethasone until
and 1 % methyl cellulose eye drops to prevent drying normal metabolic stage is achieved and give sup-
and refer patients with severe and progressive portive treatment such as cooling, antipyretics,
exophthalmos to an ophthalmologist. antibiotics for infection, intravenous fluids, etc.
2.5. Toxic multinodular goiter Once euthyroid status is achieved, manage as
already outlined.
Radioactive iodine is the treatment of choice.
Large doses are usually required.
Page 54
18.Cerebrovascular Accidents
sensory aphasia (inability to comprehend) if
1. Definition there is cortical involvement of dominant
A stroke, or cerebrovascular accident, is defined by hemisphere(right side in left handed people, left
this abrupt onset of a neurologic deficit that is side in 90% of right handed people).
attributable to a focal vascular cause. Transient or permanent loss of central vision
due to involvement of ophthalmic artery a
Thus, the definition of stroke is clinical, and branch of internal carotid artery.
laboratory studies including brain imaging are used to
Difficulty in swallowing, speaking due to bulbar
support the diagnosis.
involvement could be a presentation. In cases
The clinical manifestations of stroke are highly where patient has previously had
variable because of the complex anatomy of the brain cerebrovascular accident, fresh infarct now
and its vasculature. TIA (Transient Ischemic Attack) causing bilateral cortical involvement may lead
is a brief episode of neurological dysfunction lasting to dysphagia and dysarthria causing what is
1 hr to 24 hrs without residual deficit. Stroke in known as peudobulbar palsy. On examination in
evaluation means when deficit worsens after patient these patients jaw jerk is brisk.
first presents. Midbrain lesions have ocular involvement.
Cerebral ischemia is caused by a reduction in blood Sensory involvement occurs in stroke involving
thalamus or medulla.
flow that lasts longer than several seconds. If the
cessation of flow lasts for more than a few minutes, The neurological deficit may be preceeded by
infarction or death of brain tissue results. When tingling numbness.
blood flow is quickly restored, brain tissue can TIA - Transient Ischaemic Attack is a
recover fully and the patient's symptoms are only neurological deficit that recovers completely
transient. within 24 hours.
A focal deficit progressing over a period of
Focal ischemia or infarction, conversely, is usually hours and is characteristic of thrombotic. stroke.
caused by thrombosis of the cerebral vessels Any focal deficit preceded by a prolonged
themselves or by emboli from a proximal arterial headache could be due to infarct with
source or the heart. haemorrhagic conversion secondary to cerebral
Intracranial hemorrhage is caused by bleeding venous sinuous thrombosis.
directly into or around the brain; it produces Focal deficit could be accompanied by
neurologic symptoms by producing a mass effect on convulsions.
neural structures, from the toxic effects of blood
itself, or by increasing intracranial pressure. 3. Examination
Patient may have bradycardia if he is on beta
2. Clinical features blockers or due to raised intractanial pressure
Most of the patients are elderly. secondary to cerebral oedema.
There could be a history of hypertension, Blood pressure should be recorded and
diabetes, ischaemic heart disease monitored.
Past history of cerebrovascular accident may be The power of all 4 limbs should be graded and
present. any improvement or deterioration in the power
Hemiplegia or hemiparesis: Paralysis or should be recorded.
weakness of right or left half of the body with Reflexes on the involved side are brisk and
deviation of one side of the face seen. plantar reflex is extensor on the involved side.
Lower limb monoparesis or monoplegia. History of headache, altered sensorium, fever,
Faciobrachial stroke : involving right or left vomiting.
upper limb along with ipsilateral facial
weakness. 4. Investigations
Rarely bilateral lower limb weakness in Non contrast CT scan brain to differentiate
unpaired anterior cerebral artery thrombosis. between infarct and haemorrhage and site of
Hemiplegia or hemiparesis may be accompanied lesion.
by motor aphasia(patient unable to speak) or Routine investigations like HB,CBC,ESR, liver
Page 55
function test , renal function test, serum started in cases of cerebral infarction. As
electrolytes, fasting and post prandial glucose, intracranial bleed is ruled out.
complete lipid profile. Tab atorvastatin 40mg OD H.S.
ECG, X- ray chest, 2D echo especially in young Antiepileptics (inj Eptoin 100mg tds) if
patients to rule out cardiac source of embolism. convulsions are present. But in case the bleed is
Ideally MR angiography in cases of infarction to large and if the patient is going to be shifted to a
look for the stenosis in intracranial vessels. higher centre it may be advisable to give anti-
SOS MR venography if any doubt of cerebral epileptics as the patients general condition might
venous thrombosis. worsen if he gets a convulsion.
Half an hour before ryles tube feeding
5. Complications Domperidom should be administered. Ryles
tube feeding in strict propped up position.
Aspiration pneumonia Inj. Heparin (5000 IU IV bolus and then once a
Deep vein thrombosis in lower limb day to keep PT (INR) 2 to 3 times of normal
complicating further as pulmonary embolism. value) for prophylaxis of deep vein thrombosis
Bed sore in cases of cerebral infarction (not in intracranial
bleed) in patient of hemiplegia.
6. Treatment Physiotherapy.
Blood pressure, blood glucose and temperature Early detection and treatment of complications.
of patients of acute cerebral infarction should be
controlled. 7. When to refer
Anti - hypertensive medication. A blood All young patients of stroke, intracranial bleed
pressure of 150/90 mmhg can be maintained or infarction.
initially to prevent cerebral ischaemia due to Patients diagnosed with cerebral venous
hypoperfusion. thrombosis.
IV Mannitol 100cc 8 hourly in cases of Subarachnoid haemorrhage if seen on the CT.
intracerebral bleed, in large infarcts, brainstem Patient suspected to have AV malformation.
infarction, cerebellar lesions and all patient
Large intracerebral bleeds who might require
having altered sensorium. Serum electrolytes
evacuation to be transferred after stabilizing
and urine output should be monitored (on
blood pressure.
mannitol.)
Tab Aspirin 75-150 mg od after lunch should be
Page 56
19. SUBARACHNOID HEMORRHAGE (SAH)
Excluding head trauma, the most common cause of A detailed history should be sought for use of oral
SAH is rupture of a saccular aneurysm. Other causes contraceptive pills in young females to rule out SAH
include bleeding from a vascular malformation secondary to cerebral venous thrombosis as could
(arteriovenous malformation or dural arterial-venous occur in any procoagulant state.
fistula) and extension into the subarachnoid space
from a primary intracerebral hemorrhage. 2. Investigations
1. Clinical features CT brain, MRI angiography and MRI venography to
rule out cerebral venous thrombosis which could
Most unruptured intracranial aneurysms are present as subarachnoid haemorrhage.
completely asymptomatic. Symptoms are usually due
to rupture and resultant SAH, although some 3. Treatment: Subarachnoid
unruptured aneurysms present with mass effect on
cranial nerves or brain parenchyma. At the moment
Hemorrhage
of aneurysmal rupture with major SAH, the ICP 1. Protecting the airway.
suddenly rises. This may account for the sudden
transient loss of consciousness that occurs in nearly 2. Managing blood pressure before and after
half of patients. Sudden loss of consciousness may be aneurysm treatment, with antihypertensive agent.
preceded by a brief moment of excruciating Preventing rebleeding prior to treatment.
headache. 3. Managing vasospasm, treating hydrocephalus.
The most important characteristic is sudden onset or 4. Maintaining electrolyte balance and hydration
as a change in the patient's usual headache pattern.
The headache is usually generalized, often with neck 5. IV mannitol 100cc 8 Hourly to treat raised Intra
stiffness and vomiting is common. cranial pressure.
Although sudden headache in the absence of focal 6. Treatment with the calcium channel
neurologic symptoms is the hallmark of aneurysmal antagonist nimodipine (60 mg PO every 4 h)
rupture, focal neurologic deficits may occur. The improves outcome, perhaps by preventing
deficits that result can include hemiparesis, aphasia, ischemic injury rather than reducing the risk of
and abulia. vasospasm.
Occasionally, prodromal symptoms suggest the 7. Volume expansion helps prevent hypotension,
location of a progressively enlarging unruptured augments cardiac output, and reduces blood
aneurysm. viscosity by reducing the hematocrit. This
method is called "triple-H" (hypertension,
A third cranial nerve palsy, particularly when haemodilution, and hypervolemic) therapy.
associated with pupillary dilation, loss of ipsilateral
(but retained contralateral) light reflex, and focal pain 8. Acute hydrocephalus can cause stupor or coma.
above or behind the eye, may occur with an It may clear spontaneously or require temporary
expanding aneurysm at the junction of the posterior ventricular drainage. When chronic
communicating artery and the internal carotid artery. hydrocephalus develops, ventricular shunting
Visual field defects can occur with an expanding is the treatment of choice.
supraclinoid carotid or anterior cerebral artery
aneurysm. 4. When to refer
Aneurysms can undergo small ruptures and leaks of A patient diagnosed to be having SAH should be
blood into the subarachnoid space, so-called sentinel transferred to a higher centre at the earliest after
bleeds. Sudden unexplained severe headache at any stabilizing blood pressure for further management.
location should raise suspicion of SAH and be
investigated, because a major hemorrhage may be
imminent.

Page 57
20. PYOGENIC MENINGITIS
Meningitis is a serious disease in which there is On examination meningial signs are positive.
inflammation of the meninges that cover the brain
and spinal cord. Meningeal signs (Can be found in any type of
meningitis)
Bacterial meningitis can be deadly and contagious
among people in close contact. i. Neck stiffness: Stiffness of neck & resistance to
passive movements, with pain & spasm on attempted
Viral meningitis tends to be less severe and most motion. The chin cannot be placed upon the chest.
people recover completely.
ii. Kernigs sign:
Fungal meningitis is a rare form of meningitis and
generally occurs only in people with weakened With the hip flexed, the knee is extended.
immune system. Normally it can be done up to 135 degree. In
meningitis it is restricted due to spasm of
hamstrings.
1. Clinical Presentation
iii. Brudzinskis sign:
Meningitis can present as either an acute
fulminant illness that progresses rapidly in a Neck sign- on flexing the neck, there is flexion
few hours or as a subacute infection that of hips & knees.
progressively worsens over several days.
Leg sign- on flexing one leg, other leg also
The classic clinical triad of meningitis is fever, flexes.
headache, and nuchal rigidity. Nausea, iv. Straight leg raising test (SLR):
vomiting, and photophobia are also common
complaints. With the patient supine & both legs extended, one leg
is passively flexed at the hip keeping the knee
Seizures occur as part of the initial presentation extended. Normally it can be lifted up to 90 degree. It
of bacterial meningitis or during the course of is restricted in meningitis.
the illness in 2040% of patients. Generalized
seizure activity and status epilepticus may be due
to hyponatremia, cerebral anoxia.
2. Diagnosis
CSF Studies
Raised Intracranial Pressure (ICP) is an
expected complication of bacterial meningitis The classic CSF abnormalities in bacterial meningitis
and the major cause of obtundation and coma in are (1) polymorphonuclear (PMN) leukocytosis
this disease. (>100 cells/L in 90%), (2) decreased glucose
concentration [<2.2 mmol/L (<40 mg/dL) and/or
Signs of increased ICP include a deteriorating CSF/serum glucose ratio of <0.4 in 60%,hence it is
or reduced level of consciousness, mandatory that a blood glucose levels be estimated
papilledema, dilated poorly reactive pupils, simultaneously with the CSF study], (3) increased
sixth nerve palsy, decerebrate posturing. protein concentration [>0.45 g/L (>45 mg/dL) in
Cushing reflex (bradycardia, hypertension, 90%], and (4) increased opening pressure (>180
and irregular respirations). mmH2O in 90%). CSF bacterial cultures are positive
in >80% of patients, and CSF Gram's stain
The rash of meningococcemia for demonstrates organisms in >60%
meningococcal meningitis, which begins as a
diffuse erythematous maculopapular rash 3. Treatment
resembling a viral exanthem; however, the skin
lesions of meningococcemia rapidly become i. Intravenous fluids.
petechial. Petechiae are found on the trunk and ii. Inj Mannitol 100mg 8 hourly to 6 hourly.
lower extremities, in the mucous membranes and iii. Inj Dexamethasone 4mg 8 hourly but first
conjunctiva, and occasionally on the palms and dose to be given 20 minutes before first dose
soles. of antibiotics.
Page 58
iv. Antimicrobial therapy of For gram-negative bacillary meningitis, the
third-generation cephalosporins - cefotaxime
(Ceftriaxone 2g twice a day intravenously,
(2gm 4 hourly i.e. total 12 gm per day),
cefotaxime, or cefepime) A 2-week course of
intravenous antimicrobial therapy is ceftriaxone (2gms 12 hourly), and ceftazidime
recommended for pneumococcal meningitis. (2gms 8 hourly) - are efficacious for the
treatment of, with the exception of meningitis
Or ampicillin IV 2 gm 4 hourly (total 12 gm per due to P. aeruginosa, which should be treated
day) for at least 3 weeks. Gentamicin is added in with ceftazidime, cefepime, or meropenem.
critically ill patients (2 mg/kg loading dose, then (2gms 8 hourly). A 3-week course of
7.5 mg/kg per day given every 8 hrs. and intravenous antibiotic therapy is recommended
adjusted for serum levels and renal function). for meningitis due to gram-negative bacilli.
The combination of Trimethoprim (1020
mg/kg per day) and Sulfamethoxazole (50100 4. When to refer
mg/kg per day) given every 6 h may provide an
alternative in penicillin-allergic patients. i. Lumbar puncture requires to be done and facility
not available.
Vancomycin 2g 12 hourly is the drug of choice
ii. Presence of any focal deficit.
for methicillin-resistant staphylococci and for
patients allergic to penicillin. (3 weeks). Note: If meningitis is suspected empirical antibiotic
treatment has to be started immediately.
Page 59
21. TUBERCULOUS MENINGITIS
1. Clinical Manifestations 3. Treatment

The disease often presents subtly as headache IV fluids
and slight mental changes after a prodrome of Inj. Mannitol 100cc thrice a day to four times a
weeks of low-grade fever, malaise, anorexia, and day, should be tapered and stopped to be
irritability. overlapped with oral glycerol 1oz three times a
If not recognized, tuberculous meningitis may day. Patient may have worsening of headache or
evolve acutely with severe headache, confusion, get signs of raised ICT, mannitol should be
lethargy, altered sensorium, and neck rigidity. reinstituted and tapered again.
Typically, the disease evolves over 12 weeks, a For treatment of tubercular meningitis, first-line
course longer than that of bacterial meningitis. drugs are Isoniazid (5mg/kg) along with
Since meningeal involvement is pronounced at pyridoxine 50mg, Rifampin(10mg/kg) given
the base of the brain, paresis of cranial nerves before breakfast, Pyrizinamide (25 mg/kg), and
(ocular nerves in particular) is a frequent finding, Ethambutol (15 mg/kg).
and the involvement of cerebral arteries may Duration of treatment is upto 9 months to 1 year.
produce focal ischemia. Steroids are given as Inj. Dexamethasone 4mg
The ultimate evolution is toward coma, with three times a day for 3 weeks to be continued as
hydrocephalus and intracranial hypertension. Tab Prednisolone 1mg/kg and tapered and
omitted over 1 and a half months duration.
2. Diagnosis
CSF Studies
4. Complications
Hydrocephalous.
In adults, the mean white blood cell (WBC) count
(range, 0-4000 cells/L) with lymphocytic Vasculitis induced stroke.
predominance. The mean protein level in adults Drug induced hepatitis.
averages 224 mg/dL (range, 20-1000 mg/dl). The
proportion with depressed glucose levels (< 45
mg/dL or 40% of serum glucose). 5. When to refer
Patient having any focal deficit.
Diminution of vision.
Patient not improving on treatment.
Page 60
22. VIRAL MENINGITIS
Constitutional signs can include malaise,
1. Clinical features myalgia, anorexia, nausea and vomiting,
Immuno compromised adult patients with viral abdominal pain and/or diarrhea.
meningitis usually present with. Patients often have mild lethargy or drowsiness;
however, profound alterations in consciousness,
Headache, fever, and signs of meningeal such as stupor, coma, or marked confusion do
irritation coupled with an inflammatory CSF not occur in viral meningitis and suggest the
profile. presence of encephalitis or other alternative
Headache is almost invariably present and often diagnoses.
characterized as frontal or retroorbital and
frequently associated with photophobia and pain
on moving the eyes.
2. Etiology
Acute Meningitis
Common Less Common
Enteroviruses (coxsackieviruses, echoviruses, and human Lymphocytic choriomeningitis virus

enteroviruses 6871)
Varicella zoster virus Cytomegalovirus
Epstein-Barr virus
Herpes simplex virus 2
Arthropod-borne viruses
HIV
Acute Encephalitis
Common Less Common
Herpesviruses Rabies
Herpes simplex virus 1 Powassan virus
Varicella zoster virus (VZV) Enteroviruses
Epstein-Barr virus (EBV) Mumps
Arthropod-borne viruses
Cytomegalovirus
Table No.1- Etiology
Page 61
Fluid and electrolyte status should be monitored.
3. Diagnosis IV fluids should be administered.
The most important laboratory test in the diagnosis of Oral or intravenous acyclovir may be of benefit
viral meningitis is examination of the CSF. The in patients with meningitis caused by Herpes
typical profile is a lymphocytic pleocytosis (25500 simplex virus -1 or -2 and in cases of severe
cells/L), a normal or slightly elevated protein Epstein-Barr virus or Varicella zoster virus
concentration [0.20.8 g/L (2080 mg/dL)], a normal infection. Seriously ill patients should receive
glucose concentration, and a normal or mildly intravenous acyclovir (1530 mg/kg per day in
elevated opening pressure (100350 mmH2O). three divided doses for 7-10 days i.e. which can
be followed by an oral drug such as acyclovir
4. Treatment: Acute Viral (800 mg, five times daily. Patients with HIV
meningitis should receive highly active
Meningitis antiretroviral therapy).
Treatment of almost all cases of viral meningitis
is primarily symptomatic and includes use of
analgesics, antipyretics, and antiemetics.
Page 62
23. VIRAL ENCEPHALITIS
In rare cases, a pleocytosis may be absent on the
1. Definition initial LP but present on subsequent LPs.
In contrast to viral meningitis, where the infectious
Patients who are severely immunocompromised
process and associated inflammatory response are
by HIV infection, glucocorticoid or other
limited largely to the meninges, in encephalitis the
immunosuppressant drugs, chemotherapy, or
brain parenchyma is also involved. Many patients
lymphoreticular malignancies may fail to mount
with encephalitis also have evidence of associated
a CSF inflammatory response.
meningitis (meningoencephalitis) and, in some cases,
involvement of the spinal cord or nerve roots CSF cell counts exceed 500/L in only about 10%
(encephalomyelitis, encephalomyeloradiculitis). of patients with encephalitis. Infections with
certain arboviruses (e.g., EEE virus or California
2. Clinical Manifestations encephalitis virus), mumps, and LCMV may
In addition to the acute febrile illness with evidence occasionally result in cell counts >1000/L, but
of meningeal involvement characteristic of this degree of pleocytosis should suggest the
meningitis, the patient with encephalitis commonly possibility of nonviral infections or other
has an altered level of consciousness (confusion, inflammatory processes.
behavioral abnormalities), or a depressed level of
Atypical lymphocytes in the CSF may be seen in
consciousness ranging from mild lethargy to coma,
EBV infection and less commonly with other
and evidence of either focal or diffuse neurologic
viruses, including CMV, HSV, and
signs and symptoms.
enteroviruses.
Patients with encephalitis may have hallucinations,
agitation, personality change, behavioral disorders, However, persisting CSF neutrophilia should
and, at times, a frankly psychotic state. Focal or prompt consideration of bacterial infection,
generalized seizures occur in many patients with leptospirosis, amoebic infection, and
encephalitis. noninfectious processes such as acute
hemorrhagic leukoencephalitis. About 20% of
Virtually every possible type of focal neurologic patients with encephalitis will have a significant
disturbance has been reported in viral encephalitis; number of red blood cells (>500/L) in the CSF in
the signs and symptoms reflect the sites of infection a nontraumatic tap. The pathologic correlate of
and inflammation. this finding may be a hemorrhagic encephalitis
of the type seen with HSV; however, CSF red
The most commonly encountered focal findings are
blood cells occur with similar frequency and in
aphasia, ataxia, upper or lower motor neuron patterns
similar numbers in patients with nonherpetic
of weakness, involuntary movements (e.g.,
focal encephalitis.
myoclonic jerks, tremor), and cranial nerve deficits
(e.g., ocular palsies, facial weakness). A decreased CSF glucose concentration is
distinctly unusual in viral encephalitis and
3. Laboratory Diagnosis should suggest the possibility of bacterial,
3.1. CSF Examination fungal, tuberculous, parasitic, leptospiral,
CSF examination should be performed in all syphilitic, sarcoid, or neoplastic meningitis.
patients with suspected viral encephalitis unless
contraindicated by the presence of severely
3.2. MRI, CT, EEG
increased intracranial pressure (ICP). Patients with suspected encephalitis almost
invariably undergo neuroimaging studies and
The characteristic CSF profile is often EEG. These tests help identify or exclude
indistinguishable from that of viral meningitis alternative diagnoses and assist in the
and typically consists of a lymphocytic differentiation between a focal, as opposed to a
pleocytosis, a mildly elevated protein diffuse, encephalitic process.
concentration, and a normal glucose
concentration. A CSF pleocytosis (>5 cells/L) Focal findings on MRI in a patient with
occurs in >95% of immunocompetent patients encephalitis should always raise the possibility
with documented viral encephalitis. of HSV encephalitis. Approximately 10% of
patients with PCR-documented HSV encephalitis
Page 63
will have a normal MRI, although nearly 80% Prior to intravenous administration, acyclovir should
will have abnormalities in the temporal lobe, and be diluted to a concentration 7 mg/mL. (A 70-kg
an additional 10% in extratemporal regions. person would receive a dose of 700 mg. which would
be diluted in a volume of 100 mL.) Each dose should
4. Treatment be infused slowly over 1 h, rather than by rapid or
Vital functions, including respiration and blood bolus infusion, to minimize the risk of renal
pressure, should be monitored continuously and dysfunction. Care should be taken to avoid
supported as required. In the initial stages of extravasation or intramuscular or subcutaneous
encephalitis, many patients will require care in an administration. The alkaline pH of acyclovir can
intensive care unit. cause local inflammation and phlebitis (9%). Dose
adjustment is required in patients with impaired renal
i. Intravenous fluids. glomerular filtration. Penetration into CSF is
ii. IV mannitol 100cc 12 hourly for 3 days excellent, with average drug levels 50% of serum
levels. Complications of therapy include elevations in
Seizures should be treated with standard blood urea nitrogen and creatinine levels (5%),
anticonvulsant regimens (Inj. Diazepam 10 mg, thrombocytopenia (6%), gastrointestinal toxicity
IV or Inj. Midazolam 2mg), and prophylactic (nausea, vomiting, diarrhea) (7%), and neurotoxicity
therapy should be considered in view of the high (lethargy or obtundation, disorientation, confusion,
frequency of seizures in severe cases of agitation, hallucinations, tremors, seizures) (1%).
encephalitis.
iv. Antipyretics for fever
iii. Acyclovir is of benefit in the treatment of HSV
and should be started empirically in patients with
suspected viral encephalitis, especially if focal
5. Complications
Aspiration pneumonia, stasis ulcers and decubitus
features are present, while awaiting viral
ulcer, contractures, deep venous thrombosis and its
diagnostic studies. complications, and infections of indwelling lines and
Adults should receive a dose of 10 mg/kg of catheters.
acyclovir intravenously every 8 h (30 mg/kg per
day total dose) for 1421 days. 6. When to refer
Ideally all suspected patients of viral encephalitis
CSF PCR can be repeated at the completion of this
after starting therapy as mentioned above and patients
course, with PCR-positive patients receiving
of viral meningitis not improving over or worsening
additional treatment, followed by a repeat CSF PCR
over 48 hours should be referred to a higher centre.
test.
Page 64
24. EPILEPSY
1. Definition 3. Investigations
This is a condition characterized by recurrent
Apart patients of epilepsy can be further
episodes of seizures which are paroxysmal abnormal
investigated with an EEG and MRI. from routine
discharges at high frequency from an aggregate of
laboratory investigations.
neurons in cerebral cortex.
4. Treatment
2. Types of epilepsy 1. Correct any metabolic cause (hypo or
2.1 Grand mal epilepsy or Tonic-Clonic Seizures-
hyperglycaemia, hypo or hypernatremia).
Aura, epileptic cry, sudden fall due to tonic
2. Stop drugs like theophylline (CNS Stimulant)
convulsions followed by clonic convulsions
which may cause seizures.
and then prolonged sleep and depression. The
3. Look for any structural CNS lesions like Brain
attack lasts for 1-2 min. Tongue bite, urinary
tumour, vascular lesions, meningitis, CVST or
incontinence may occur.
abscess and treat them.
2.2 Petit mal epilepsy or Absence seizures - No
4. Avoid precipitating factors like sleep
aura, no loss of consciousness. Prevalent in
deprivation, Fasting, video games.
children and episode lasts for few seconds.
There is momentary loss of consciousness 4.1 Antiepileptic should be started
hardly for 5 sec without loss of postural
control. Presence of freezing or staring in one when
direction. 1. A history suggestive of recurrent epileptic
2.3 Partial seizures- Most common seizure types seizure is established.
occurring in 80% of epileptic patients. Seizure 2. An abnormal neurological examination.
activity is restricted to a discrete area 3. Presenting as status Epilepticus.
belonging to one cerebral hemisphere only. 4. Abnormal EEG suggestive of general seizure.
2.4 Other types of seizures: Myoclonic seizures, 5. Family history of epilepsy.
Atonic seizures, tonic seizures.
To start anti epileptics in single isolated seizure is not
2.5 Febrile seizures- Young children develop yet established. Monotherapy should be the mantra of
seizures during high fever. treatment.
4.2 Anti epileptic drugs

Table No.1: Antiepileptic Drugs & their Doses with type of seizure
Seizure Drug Dose

Generalized onset tonic clonic Valproic acid 750-2000mg/day
convulsions
(20-60mg/kg/day)
In divided doses
Phenytoin 300-400mg/day
(3-6mg/kg/day for adult, 4-8mg/kg/day for
Children) BD doses
1 gm 3gm per day
Levetiracetam
1000-3000mg/day BD doses
Lamotrigine
150-500mg/day, BD doses
Topiramate
Page 65
Focal onset tonic clonic Carbamezapine 600-1800mg/day (15-35mg/kg, child) in BD
convulsions doses
Lamotrigine
Same as Above
Levetiracetam
Same as Above
Oxcarbazepine
900-2400mg/day (30-45mg/kg, child) BD
doses
Typical Absence Valproic acid Same as Above
Ethosuximide 750-1250mg/day in BD doses, 20 40 mg
per kg divided in BD doses
Atypical Absence, myoclonic, Valproic Acid, Same as Above
Atonic Seizures Lamotrigine, Topiramite
Same as Above
Phenytoin 15-20 mg/kg, at a rate not to exceed 50

5. Status Epilepticus mg/min (Never mix Phenytoin with a 5% dextrose
Status Epilepticus refers to continuous seizures or solution) put it in a normal saline solution to
repetitive discrete seizures with impaired minimize the risk of crystal precipitation or
consciousness in the interictal period for duration of fosphenytoin 20mg/kg iv to maximum
15-30 minutes traditionally but practically for 150mg/minute.
generalized convulsive status Epilepticus the duration Correct any metabolic imbalances. Control
is 5 minutes. hyperthermia.
It is a medical emergency and must be treated If seizures continue after 20 minutes, give maximum
immediately. rate 50mg/minute or Fosphenytoin 7 to 10 mg/kg to
Monitor vital signs. Maintain airway, breathing, and maximum rate of 150mg/minute.
circulation. Administer supplemental oxygen by If seizures continue after 20 minutes, give
mask. Phenobarbital (20 mg/kg IV at 60 mg/min)
Laboratory analysis-glucose, electrolytes, calcium, Other Antiepileptic Drugs which can be given IV are
magnesium, creatinine, CBC and urine analysis. - Valproate sodium 30mg/kg IV bolus or IV
Establish intravenous access. Levetiracetam 10-50mg/kg
Lorazepam (0.1 mg/kg) IV over 1-2 min, Repeat if no If seizures continue, consider administering general
response after 5 minutes. anesthesia with medications such as propofol,
midazolam, or pentobarbital.
Figure-1: Management of Status Epilepticus algorithm
Page 66
Figure 2: Pharmacological treatment algorithm of non-convulsive status epileptics
Lorazepam (0.1, 0.15 mg/IV) (repeat once if no Admit to ICU and EEG monitoring
seizure supprenssion
Seizures continuing
Phenytoin (7-10 mg/kg Iv) or Fosphenytoin Consider valproate in absence SE (30

(Phenytoin equivalent dose) mg/kg IV)
Seizures continuing
Phenytoin (7-10 mg/kg Iv) or Fosphenytoin (Phenytoin equivalent Consider valproate in absence SE (30
dose) mg/kg IV)
Refractory NCSE
Intravenous anesthetic agents

Midazolam/propofol/pentobarbital
Seizures continuing
Newer AEDs - Topiramate/Ievetiracetam
or
Inhalational anesthestics - Isoflurance/desflurance
All the Patients after initial IV Antiepileptic Drug should be followed by maintenance doses with the oral
antiepileptic drugs regularly.
Page 67
25. GUILLAIN-BARRE SYNDROME (GBS)
1. Definition 4. Investigations
Guillain-Barre syndrome (GBS) is an acute, CSF analysis by lumbar puncture by the end of first
frequently severe, and fulminant polyradiculopathy week Elevated CSF protein 100-1000mg/dl without
that is autoimmune in nature. pleocytosis called as albumino cytological
dissociation.
2. Clinical Features Can refer for electrodiagnosis- Demyelination or
GBS manifests as rapidly evolving areflexic motor axonal involvement seen according to the variant
paralysis with or without sensory disturbance. Usual type
pattern is an ascending paralysis. Weakness typically
evolves over hours to a few days and frequently 5. Treatment
accompany by tingling dysesthesias in extremities.
Treatment should be initiated at the earliest. Each day
Legs are usually more affected than arms. Facial
counts. >2 weeks after the first motor symptoms,
diparesis is present in 50% of affected individuals.
immunotherapy is no longer effective. Either high
The lower cranial nerves are also frequently
dose intra-venous immune globulin (IVIg) or
involved, causing bulbar weakness with difficulty
plasmapheresis can be initiated, as they are equally
handling secretions and maintaining airway. Pain in
effective.
the neck, shoulder or back is also common in the
early stages. 1. Intra-venous immune globulin (IVIg): Total dose
of 2g/kg body weight divided into 5 doses given
Fever and constitutional symptoms are absent at the
over 5 consecutive days.
onset, and if present cast a doubt on the diagnosis.
2. Plasmapheresis: 40-50ml/kg plasma exchange
Deep tendon reflexes disappear within the first few
four times over a week.
days of onset. Bladder dysfunction may occur in
In the worsening phase of GBS, most patients require
severe cases but is usually transient. Autonomic
monitoring in a critical care setting, with particular
involvement is common, usually presenting as wide
attention to vital capacity, heart rhythm, blood
fluctuation in blood pressure, postural hypotension &
pressure, nutrition, DVT prophylaxis and chest
cardiac dysrhythmias.
physiotherapy. Nearly 30% of patients with GBS
Approximately 70% of cases of GBS occur 1-3 require ventilator assistance.
weeks after an acute infectious process, usually
respiratory or gastro-intestinal. 6. When to refer: Any of the
3. Differential diagnosis following
The diagnosis is made by recognizing the pattern of Single breath count 12/min

rapidly evolving paralysis with areflexia, absence of
fever or other systemic symptoms, and characteristic Respiratory failure.
antecedent events. Other disorders that may enter into
the differential diagnosis include:
Fulminant quadriparesis.
Acute myelopathies prolonged back pain and

Poor Gag reflex with risk of aspiration.
sphincter disturbances. Autonomic dysfunction
Botulism pupillary reactivity lost early. Recurrent GBS.
Poliomyelitisfever and meningismus is common.
Page 68
26. APTHOUS ULCERS
Important note Repeated ulcers at the same site or
1. Introduction slow healing ulcers with systemic symptoms eg,
Recurrent aphthous stomatitis (RAS) is a common uveitis, arthritis, fever adenopathy are
condition, restricted to the mouth, that typically starts worrisome.Malignancy should be excluded.
in childhood or adolescence as recurrent small,
round, or ovoid ulcers with circumscribed margins, 4. Treatment
erythematous haloes, and yellow or gray floors. A
positive family history of similar ulcers is common, 4.1 Topical and systemic
and the natural history is typically of resolution in the antibiotics
third decade of life.
Tetracycline 250 mg dissolved in 180 ml of water
and used as swish andspit 4 times a day for several
2. Causes days.Avoid in children and pregnancy.
2.1. Some RAS cases involve a familial and genetic 4.2Probiotics in powder form
basis; approximately 40% of patients with RAS
have a familial history, but inheritance may be placed in oral cavity and
polygenic with penetrance dependent on other swallowed 3 -4 times a day
factors.
2.2. Most relevant studies have found hematinic 4.3 Antiinflammatory
(e.g. iron, folic acid, vitamin B-12) deficiencies
in as many as 20% of patients with recurrent Hydrocortisone pellets 5 mg kept at ulcer base and
ulcers. In addition, deficiencies of vitamins B-1, swallowed every 4 hrs for 3-4 days.Triamcinolone
B-2, and B-6 have been noted in some patient 0.1 % applied to ulcers 2-4 times a day.
cohorts. Betamethasone (Betnesol) mouthwash -0.5 mg tab
dissolved in 5-10 ml of water for mouth wash 6 hrly
during attack.
3. Symptoms
4.4 Immune modulators
Significant pain while chewing food. Minor
apthae are recurrent, painful, single or multiple,
Levamisole 50 mg twice a day
shallow surrounded by erythematous mucosa for three consecutive days for 4
anywhere in the oral cavity. Small ulcers heal weeks, no medication for 2
without scar, while larger and deep ulcers leave a
scar. weeks; then levamisole 150 mg
Fever, adenopathy, gastrointestinal sympyoms
tab, half tab twice daily for 3
are typically absent. days for 2 weeks.
Page 69
27. OESOPHAGEAL CANDIDIASIS
1. Introduction
Oesophageal candidasis is an oppurtunistic infection AIDS, postchemotherapy, uncontrolled diabetes
of the oesophagus by Candida albicans. Occurs in mellitus, chronic steroid therapy.
immune compromised patients like
Figure 1: Endoscopic view of Oesophageal Candidiasis
2.Signs and symptoms 4. Treatment

Oral lesions are painless but oesophageal lesions Nysyatin suspension local application in mouth.
produce painful dysphagia.Discrete or confluent
curdy plaques on the oesophageal mucosa. Clotrimazole oral lozenges 10 mg dissolve 1
lozenge 5 times a day.
3. Investigations Tab flucanozole 100 mg/day for 10-14 days.
Demonstration of pseudohyphae on wet smears and

culture.
Page 70
28. DYSPEPSIA
1. Introduction 5. Treatment
Non specific group of symptoms related to upper Cap Omeperazole 20 mg once a day taken 45
GITract. Also reffered to as non-ulcer dyspepsia, min before breakfast for 4 weeks. or Tab
functional dyspepsia, GERD. Ranitidine 150mg twice a day before food 45
mins for 4-6 weeks.
2. Symptoms For those with dysmotility symptoms-tab
Domperidone 10 mg three times a day 30 mins
Upper abdominal symptoms simulating an ulcer
before food.
disease or heart burn with or without regurgitation,
heaviness, post-prandial fullness or early Antacids 2-3 teaspoon when symptomatic.
satiety.Symptoms of gas in abdomen is common.
Anti H.Pylori treatment is recommended for
those on long term NSAIDS, those with
3. Red flag signs duodenal/gastric ulcers.
Anorexia, weight loss, anemia, dysphagia and mass Treatment of H Pylori- Combination of
in abdomen.
Cap. Omeperazole 20 mg twice a day plus
4. Investigations Cap. Amoxicillin 1gm bd or Tab. Metronidazole
500mg bd for 14 days plus
History and upper GI scopy.
Tab clarithromycin 500mg bd for 14 days
Page 71
29. GASTROOESOPHAGEAL REFLUX
GERD is a common disorder caused by retrograde Antacid with or without alginate acid liquid or
flow of gastric contents through an incompetentent tab 2-3 chewed- 4-6 times a day1/2-1 hr after a
gastroesophageal junction.There are two groups- meal.
erosive GERD and non erosive GERD. Untreated
may result in to oesophagitis, ulceration, stricture, Cap. Omeperazole 20 mg OD/BD OR
and rarely adenocarcinoma. Rabeprazole 20mg OD or Pantoprazole 40mg
OD.
2. Symptoms Esomeprazole 40mg OD, OR
Retrosternal pain, heart burn, regurgitation mostly Lansoprazole 30mg OD.

after meals. Rarely present with chronic cough, All taken 45 mins before meals for 4-6 weeks.
laryngitis, bronchospasm, recurrent
pulmonaryinfections, otitis media etc. Add prokinetic Domperidone10 mg thrice a day
30 mins before meals if regurgitation is
significant.
Page 72
30. PEPTIC ULCER DISEASE
a posterior penetrating gastric ulcer

1. Introduction complicated by pancreatitis.
Peptic ulcer is an important organic gastrointestinal
disease.
4. Alarm features that warrant
prompt gastroenterology
2. Etiology
referral include the
Peptic ulcer disease (PUD) may be due to any of the
following: following
H pylori infection Bleeding or anemia
Drugs Early satiety
Lifestyle factors Unexplained weight loss
Severe physiologic stress Progressive dysphagia or odynophagia
Hypersecretory states (uncommon) Recurrent vomiting
Genetic factors Family history of GI cancer
There is ulceration of the gastric and duodenal
mucosa due to acid and pepsin. 5. Physical Examination
In uncomplicated PUD, the clinical findings are few
3. Clinical features and nonspecific and include the following:
3.1 Obtaining a medical history, especially for

Epigastric tenderness (usually mild)
peptic ulcer disease, H pylori infection,
ingestion of NSAIDs, or smoking, is essential Right upper quadrant tenderness may suggest a
in making the correct diagnosis. Gastric and biliary etiology or, less frequently, PUD.
duodenal ulcers usually cannot be
Guaiac-positive stool resulting from occult blood
differentiated based on history alone, although
loss
some findings may be suggestive.
Malena resulting from acute or subacute
3.2 Epigastric pain is the most common symptom gastrointestinal bleeding
of both gastric and duodenal ulcers. It is
characterized by a gnawing or burning 6. Differential Diagnosis
sensation and occurs after mealsclassically,
shortly after meals with gastric ulcer and 2-3
hours afterward with duodenal ulcer. Food or Acute Coronary Syndrome
antacids relieve the pain of duodenal ulcers but
Aneurysm, Abdominal
provide minimal relief of gastric ulcer pain.
Cholangitis
3.3 Duodenal ulcer pain often awakens the patient
at night. About 50-80% of patients with Cholecystitis
duodenal ulcers experience nightly pain, as Cholecystitis and Biliary Colic in Emergency
opposed to only 30-40% of patients with Medicine
gastric ulcers and 20-40% of patients with
nonulcer dyspepsia (NUD). Pain typically Cholelithiasis
follows a daily pattern specific to the patient.
Diverticular Disease
Pain with radiation to the back is suggestive of
Page 73
Esophageal Perforation, Rupture and Tears 7.1 H pylori Testing
Esophagitis
Gastritis, Acute Testing for H pylori infection is essential in all
patients with peptic ulcers.
Gastritis, Chronic
Endoscopic or invasive tests for H pylori include
Gastroenteritis a rapid urease test, histopathology, and culture.
Rapid urease tests are considered the endoscopic
Gastroesophageal Reflux Disease
diagnostic test of choice. The presence of H
Inflammatory Bowel Disease pylori in gastric mucosal biopsy specimens is
detected by testing for the bacterial product
Viral Hepatitis urease
7. Approach Considerations 7.2 Endoscopy
Testing for H pylori infection is essential in all Upper GI endoscopy is the preferred diagnostic test
patients with peptic ulcers. In most patients with in the evaluation of patients with suspected PUD. It is
uncomplicated peptic ulcer disease (PUD), highly sensitive for the diagnosis of gastric and
routine laboratory tests usually are not helpful. duodenal ulcers, allows for biopsies and cytologic
Documentation of PUD depends on radiographic brushings in the setting of a gastric ulcer to
and endoscopic confirmation. differentiate a benign ulcer from a malignant lesion,
and allows for the detection of H pylori infection
If the diagnosis of PUD is suspected, obtaining with antral biopsies for a rapid urease test and/or
CBC count, liver function tests (LFTs), amylase, histopathology in patients with PUD. (See the images
and lipase may be useful. CBC count and iron below.)
studies can help detect anemia, which is an alarm
signal that mandates early endoscopy to rule out
other sources of chronic GI blood loss.
Figure-1: Endoscopic view of Peptic Ulcer
Hpylori treatment
8. Treatment
Anti H pylori treatment is recommended for patients
on long term NSAIDS, bleeding peptic ulcer.
Drugs Dose(mg) Frequency Duration
PPI Clarithromycin 20mg BD 14 days

Metronidazole 500 400 BD BD
Page 74
PPI Amoxycillin Metronidazole 20mg BD 14 days
1gm bd TDS
400
PPI Amoxycillin Clarithrmycin 20mg BD 14 days
1gm 500 BD BD
Tab ranitidine (150mg)BD, 9. Dos and donts

Famotidine (40mg) OD equally efficacious, but
Avoid alcohol
takes longer time.
Stop smoking
Maintenance dose of PPI for patients on
NSAIDS, IHD patients. Avoid NSAIDs
Prefer paracetamol, avoid foods that aggravate
symptoms
No role of bland diet
Excess milkMeals at regular intervals.
Page 75
31. VOMITING
Vomiting is the forceful expulsion of the gastric Intravenous fluids if dehydrated. Start oral fluids
contents due to contraction of abdominal musculature as soon as patient tolerates.
and simultaneous relaxation of gastric fundus and
lower oesophageal sphincter. Rule out gastric outlet obstruction then
Inj Metoclopramide 10 mg IM repeat after 6 hrs

2. Causes if needed or
1. Central (stimulation of vomiting centre)
neurological disease raised intracranial pressure. Tab Mozapride 5 mg thrice a day, or
2. Vestibular system disorders
Tab Domperidone 10 mg thrice a day or
3. Drugs and toxins
4. Toxic and metabolic disorderssuch as
Tab Metoclopramide 10 mg thrice a day or
ketoacidosis
5. Systemic infections Tab Prochlorperazine 5 mg thrice a day repeat
6. Pregnancy after 4- 6 hrs if needed,or
7. Psychogenic vomitting
8. Obstructive diseases of GIT Tab /inj Ondensetron 8 mg stat dose and
9. Acute gastritis, gastroenteritis repeated 8 hrly.
10. Radiation exposure.
In Pregnancy Tab /Inj Promethazine 25 mg is
3. Investigations safe in the first trimester.
Evaluation should exclude CNS causes and upper GI For motion sickness Tab Cyclizine 50 mg thrice
endoscopy to rule out upper GI pathology. Barium a day.
meal is recommended if upper GI scopy is normal.
Psychogenic vomiting is considered after excluding If vomiting is part of suspected acute abdomen,
organic cause. acute MI, refer for further evaluation.
Page 76
32. CONSTIPATION
Bisacodyl, oral, Adults10-20 mg at night
Common causes of constipation are Diet deficient in
roughage Ignoring the urge to defaecate e.g. due to Or
immobility, lack of exercise. Psyllium (ispaghula husk), oral, Adults5-10 ml once
Other causes are neurological, myxoedema, drugs or twice a day
like Atropine, Codeine, and Malignancy Or
2. Symptoms Liquid paraffin, oral,10-30 ml at night Or Glycerol
suppositories Adults 4mg at night ; 1 mg at night Or
Constipation itself is a symptom. When associated Lactulose liquid, oral, Adults 15-30 ml orally daily
with inability to pass flatus, severe abdominal pain, until response then 10-20 ml daily
or vomiting there may be the need for urgent referral
to a surgeon.
Alternative treatment - Magnesium sulphate,
oral, Adults5-10 g in a glass of water, once or
3. Signs twice daily
Constipation, if associated with frequent high pitched
bowel sounds or absent bowel sounds 6. Dos and Donts
Advice patients to take plenty of fluids, high
4. Investigations fiber diet green leafy vegetables, fruits, avoid
caffeinated drinks.
Stool routine examination
Regular walk and exercise to 1 hr daily,
Stool for occult blood abdominal exercise.
Sigmoidoscopy/Colonoscopy To use Indian closet as far as possible (this will
straighten the anorectal angle).
A rectal examination with a short length colonoscopy
is a must for all patients with recent onset of Avoiding suppression of urge to defecate,
constipation irrespective of bleeding per (making a regular habit).
rectum.When acute, the constipation may be a part of
Avoid purgative frequently to treat constipation,
a serious illness such as acute bowel obstruction.
as it may be habit forming.
These patients present with abdominal pain, vomiting
and distension and non-passage of flatus. These Suppository or simple enema is preferred in IHD
patients should be referred immediately to a higher
center after rectal examination, passage of rectal tube
(for passage of flatus) and a plain X-ray abdomen.
Page 77
33. IRRITABLE BOWEL SYNDROME
Antispasmodics Anticholinergic drugs
1. Definition (dicyclomine)
A constellation of gastrointestinal symptoms Antidiarrhoels Tab Loperamide 2 to 4 mg daily
associated with lower bowel symptoms that occur in for several days
absence of an organic disease.
Anti depressants IBD Diarrhoeal type TCA (
Imipramine)
2. Symptoms IBD constipation type SSRI (paroxetine)
Clinically the diagnosis is made when continuous or Calcium channel activators Lubiprostone
recurrent symptoms of abdominal pain are associated 8microgm x 3 months
with any of the three features viz. Relief by
defecation and / or onset with change in stool Any IBS patient with change in presentation e.g.
frequency or consistency for at least 3 months. change in bowel habit requires re-evaluation.
Supportive symptoms of IBS include passage of
mucous, abnormal stool passage (straining, urgency,
and feeling of incomplete evacuation) and feeling of 4. Dos and Donts
abdominal fullness. Exclude IBS if individual has
alarm symptoms such as fever, weight loss, bleeding Diet should contain high fibre and supplemented
per rectum or anaemia with bulk forming agents such as isaphghul husk
Avoid caffeine and alcohol
3. Treatment Avoid milk and other dietary constituents, which

worsens the symptoms
Stool bulking agents High fibre diet Psychotherapy may be helpful in selected cases
Page 78
34. ULCERATIVE COLITIS
Sulpha-salazine has a higher incidence of side
1. Introduction
effects compared with newer 5-ASA drugs.
Ulcerative colitis is a chronic inflammatory bowel
Selected patients, such as those with a reactive
disease of unknown aetiology.
arthropathy, may benefit.
2. Symptoms Prednisolone 40 mg daily is appropriate for
During the first attack the patient often presents with patients in whom a prompt response is required,
bloody diarrhoea, with systemic symptoms of low to or those with mild to moderate active disease, in
moderate fever, backache, arthralgia.The first attack whom Mesalazine in appropriate dose has been
is a close mimicker of acute infective diarrhoea. A unsuccessful. It should be reduced gradually
stool examination followed by sigmoidoscopy is according to severity of the patient.
mandatory, especially if the bloody diarrhoea persists
Long-term treatment with steroids is undesirable.
for more than a month. It is important to exclude
Patients with chronic active steroid dependent
amoebic infection prior to institution of steroids.
disease should be treated with Azathioprine 1.5
Rectum is uniformly involved in these patients.
2.5 mg/kg/day
Frequency of stool can provide information on
severity of the disease: mild (2 - 4 stools/day), Topical agents (either steroids or Mesalazine)
moderate (4 6 stools/day) or severe (> 6 may be added to the above agents. Although they
stools/day). During remission, patient may be are unlikely to be effective alone, they may
asymptomatic or may have extra-intestinal benefit some patients with troublesome rectal
symptoms. symptoms.
Severe UC: close monitoring at a tertiary centre.

3. Treatment
These patients require a referral to a tertiary unit. 3.2 Maintenance of remission
Aim is induction of remission in acute stage and then Lifelong maintenance therapy is generally
maintenance of remission. recommended for all patients, especially those
Therapeutic decisions depend on disease activity and with leftsided or extensive disease, and those
extent. Patients with severe disease require hospital with distal disease who relapse more than once a
admission, whereas those with mild/moderate disease year.
can generally be managed as outpatients. Discontinuation of medication may be
Disease extent can broadly be divided into reasonable for those with distal disease who have
distal and more extensive disease. been in remission for 2 years and are averse to
such medication. However, there is some
Distal disease (proctitis/procto-sigmoiditis): Topical evidence that maintenance therapy reduces the
management is appropriate.
risk of colo-rectal cancer.
Extensive disease: Oral or parenteral therapy is the
For the maintenance of remission in UC:
mainstay of treatment.
Most patients require lifelong therapy, although
3.1 Choice of drugs some patients with very infrequent relapses
Mesalamine preparations and Steroid preparations (especially if with limited extent of disease) may
remain in remission without maintenance
Treatment of active left sided, or extensive UC:
therapy.
Mesalazine 2 4 g daily or Balsalazide 6.75 g
Oral Mesalazine 1 2 g daily or Balsalazide 2.5
daily are effective first line therapy for mild to
g daily should be considered as first line therapy.
moderate active disease.
Page 79
Sulpha-salazine 24 g daily has a higher Important Note
incidence of side effects compared with newer 5-
Regular surveillance is necessary for UC lasting
ASA drugs.
for more than 10 years.
Topical Mesalazine 1 g daily may be used
Explain to the patient the chronic nature of the
Steroids are ineffective at maintaining remission. disease and continuation of maintenance
Azathioprine 1.5 2.5 mg/kg/day or Treatment for life with regular follow-up. Risk
mercaptopurine 0.75 1.5 mg/kg/day are of colonic cancer after 10 years of disease onset
effective at maintaining remission in UC. must be explained
However, in view of toxicity they should be
reserved for patients who frequently relapse 3.3 Dos and Donts
despite adequate doses of amino-salicylates, or Milk is preferably avoided during the acute phase of
are intolerant of 5-ASA therapy. It is a common illness.
practice to continue amino-salicylates with
azathioprine, but limited evidences that this is
necessary.
Page 80
35. AMOEBIC LIVER ABSCESS
1. Introduction 3.2. Imaging Studies
Liver abscess is the commonest extra-intestinal form Ultrasonography is the preferable initial
of amoebiasis, caused by E. histolytica infection but diagnostic test. It is rapid, inexpensive, and is
occurs in only less than 1% of E. histolytica only slightly less sensitive than CT scan (75-
infections. The disease usually affects young males, 80% sensitivity vs 88-95% for CT scan).
particularly chronic alcoholics, in endemic areas.
Patients commonly affected are between 20 to 40 4. Treatment
years of age with residence in or recent travel to or
emigration from an endemic region. 4.1 Medical Management
1. Tab. Metronidazole 800 mg three times orally
2. Clinical Manifestations (or IV, if necessary) daily for 5-10 days or Tab.
Tinidazole 600 mg 2 times a day for 7-10 days
2.1. History 2. If the patient is very toxic, Inj. Metronidazole
500 mg given 8 hourly until patient improves.
The signs and symptoms of amebic liver abscess Switch over to oral therapy whenever
often are nonspecific, resembling those of pyogenic possible.Followed by Diloxanidefuroate (luminal
liver abscess or other febrile diseases. agent for cysts) 500 mg three times a day for 10
days
Abdominal pain
3. Chloroquine 600 mg orally daily 2 days,
Weight loss
followed by 300 mg daily for 2 weeks; dose is
Fever with rigors
calculated as chloroquine base. Drug is active
Diarrhoea/Dysentry against E.histolyticatrophozoites
2.2. Physical
Fever is the most common sign and is found in
4.2 Indications for drainage of an
as many as 99% of cases. abscess
Hepatomegaly is present in some cases.
1. If pyogenic abscess cannot be excluded
2. No improvement with medical therapy in 72
Signs of complications hours
Signs of peritoneal irritation, such as rebound 3. Impending rupture of abscess (severe pain,
tenderness, guarding, and absence of bowel pleuritic pain, hiccups) - one very close to the
sounds, are present when the abscess ruptures in surface of the liver
the peritoneal cavity. Peritonitis occurs in 2-7% 4. Large left lobe abscess, to prevent rupture in to
of cases. the pericardium
Pericardial friction rub can be audible when the 4.3 Follow-up

abscess extends into the pericardium. This sign is
1. Monitor the patient for resolution of symptoms
associated with very high mortality.
with medical treatment and aspirate if there is
Signs of pleural effusion are present when the any indication.
abscess ruptures in the pleural cavity 2. Abscess cavity may persist for several weeks
even after cure of infection. Frequent US scan is
3. Investigations unnecessary unless patient develops fever etc.
Scan may be repeated after 4 - 6 weeks, after
3.1. Laboratory Studies thepatient becomes asymptomatic.
Examination of the stool for hematophagous
trophozoites of E histolytica must be made on at least
3 fresh specimens because the trophozoites are very
sensitive and may be excreted intermittently
Page 81
4. Maintain good hygiene during food intake to
5. Dos and Donts prevent enteric infections
1. Avoid taking alcohol, specifically if on treatment
with Metronidazole 6. Refer
2. Avoid contaminated food and drinking water.
Vegetables should be cooked or washed well. Patients with abscesses that are large or not
3. Use boiled water (kills the cyst) or bottled water responding to treatment will need to be referred to a
from a known source. physician or surgical specialist.
Page 82
36. PYOGENIC LIVER ABSCESS
Ampicillin: 2 g I/V 6 hourly
1. Introduction
Liver abscess constitutes about 48% of all visceral Gentamicin: 2 mg/kg load, then adjust for renal
abscesses. Pyogenic liver abscess is usually caused function
by spread of infection from peritoneum, abdominal Ciprofloxacin: 400 mg I/V 12 hourly for 10 days
viscera such as appendicitis/ diverticulitis/portal
pyemia or diseases of biliary tract. It is most or
commonly caused by coliform organisms. Inj. Ceftriaxone 1-2 g IV every 12 hours 2 times a
day
2. Clinical Manifestation
or
Fever, abdominal pain, toxaemia, features of
associated problems such as appendicular pain/ Inj. Cefotaxmine 2 g 8-hrly for 10 days
massetc. Mostly abscesses are small and multiple.
Combination of Amoxycillin +Ciprofloxacin
+Metronidazole is also a recommended schedule
3. Investigations
Diagnostic investigations include total counts, USG In the elderly or those with renal impairment: a
scan of the abdomen, blood culture, and pus culture. Penicillin (such as amoxicillin) plus an injectable
CECT and MRI is seldom indicated. Cephalosporin (such as cefotaxime or
cefuroxime) plus metronidazole is recommended
4. Treatment Inj penicillin allergic patients: ciprofloxacin
plus clindamycin
4.1. Drainage
Once the sensitivity is known, antibiotic therapy
Percutaneous catheter or open surgical- remains the is amended accordingly. Duration of therapy is
mainstay of treatment for a large abscess usually from 24 weeks or longer depending on
Patient should be kept nil by mouth and given IV number of abscesses and the clinical response.
fluids if toxic and sick.
5. Follow-up
4.2 Recommended antibiotics 1. Monitor for clinical improvement and modify the
therapy based on culture sensitivity report.
Metronidazole plus ampicillin and gentamicin,
2. Abscess should always be drained.
ciprofloxacin, or a third-generation cephalosporin
3. Surgery is considered if no improvement with
Standard dosage medical treatment and percutaneous drainage
in4-7 days.
Ceftriaxone 2 g intravenously every 24 hours, or
cefotaxime 2 g intravenously every 8 hours. Important Note
Initial empirical treatment should include broad 1. Avoid taking alcohol, specifically if on treatment
spectrum antibiotics. with Metronidazole.
2. Maintain good hygiene regarding food intake to
Various combinations recommended are: prevent enteric infections.
Metronidazole: 500 mg I/V three times daily
Page 83
Figure-1: Approch to Pyogenic Liver Abscess
Page 84
37. INTESTINAL PROTOZOAL INFECTION
giardiasis may contribute to protein-energy
1. Amoebiasis malnutrition in children.
Entamoeba Histolytica is the most prevalent Protein-losing enteropathy has also been described.
intestinal protozoa in India.
1.1 Clinical Features 2.2. Investigations

Diagnosis is made by stool examination and looking
Intestinal Amoebiasis / Amoebic Dysentery: for cysts and trophozoites.
Patient with acute amoebic dysentry present with a 1-
2 weeks history of abdominal pain, tenesmus, and Parasites are best seen in fresh watery stools.
frequent loose stools containing blood and mucus.
Duodenal aspirate is better for isolation but invasive.
Fever may or may not be present.
1.2 Investigations 2.3. Treatment

Treatment is Metronidazole 400mg TID for 5 days
Despite thepresence of ulcerations and occult blood
orally or Tinidazole 2gm PO once is equally
in stools, leucocytes may not be present in stools.
effective.
A definite diagnosis is made by the demonstration of
E. Histolytica cysts/ trophozoites in stools by a WET Furazolidone 6 mg/kg q.i.d for 7-10 days is effective
MOUNT PREPARATION. and well tolerated in children.
1.3 Treatment 3. Spore forming protozoa

The drug of choice for amebic colitis is These include:
tinidazole/metronidazole Doses are:
Tinidazole: 2g/day with food for 3 days or Cryptosporidium parvum
Metronidazole: 750 mg tid orally /iv for 5-10 days. Isospora belli
Cyclospora cyatenensis
Treatment of intraluminal amoebiasis is Diloxanide Microsporidia
Furoate 500mg PO-TID for 20 days or paromomycin The spectrum of diseases caused by these is as
30 mg/kg qd in 3 divided doses for 5-10 days. follows:
2. Giardiasis 3.1 Asymptomatic infection

It is a parasitic infection caused by Giardia Lamblia a This can be seen in immunocompetant as well as
single celled organism. immunocompromised patients.
3.2 Acute infectious diarrhea in
2.1 Clinical Features immunocompetent hosts
Acute symptoms include: Acute watery diarrhea with abdominal pain, with
malaise with or without fever can be seen in all
Crampy abdominal pain
except microsporidia. (generally pathogenic only for
Watery diarrhoea, vomiting and fever which last for immunocompromised patients)
few days.
In the chronic stage: 3.3 Infections in immune
Patients have bloating, nausea, abdominal fullness, compromised hosts
epigastric or substernal burning, malaise and fatigue. All spore-forming protozoa have a predisposition for
more frequent and prolonged infections in patients
Although severe forms of chronic giardiasis may who are immunodeficient.
occur in otherwise healthy individuals, they are Patients with HIV especially with low CD4 count
common in patients with hypoglobulinemia, (<50-100) are more prone.
particularly IgA deficiency in association with
lymphoid hyperplasia of the bowel. Chronic
Page 85
Severe life-threatening watery diarrhea, dehydration Stool examination with a wet mount preparation is
and chronic malabsorption leading to lethargy, failure required for isolation of the parasites.
to thrive, and malnutrition may occur. Modified acid fast staining is used to identify
3.4. Investigations cryptosporidium, isospora and cyclospora as these are
acid fast.
3.5. Treatment
PATHOGEN TREATMENT
Cryptosporidim Nitazoxanide 500 mg b.d for 3 days
Paromomycin 30 mg/kg per day divided
Isospora Septran (TMP/SMX,160/800 MG) four times a day for 10 days and
then 3 times a day for 21 days
Microsporidia No definite drug but albendazole 400- 800 mg/day divided in b.d
can be given
Cyclospora Septran ( TMP/SMX , 160/800 MG)twice daily for 7 days
Supportive treatment with ORS or iv fluids for fluid Pulmonary consolidations

and electrolyte supplementation is necessary.
Eosinophilia
4. Intestinal helminthic Urticaria
(nematodes) infections Asthma

Nematodes are round worms infesting the intestines. Angioneurotic edema
The infective forms are the eggs/larvae transmitted
by the feco oral route. Intestinal invasion:
Generally seen in low socio economic states with
poor sanitation and hygiene. May be asymptomatic (small number).
Their life cycle is complex with stage of passage
through lungs in some worms (ascaris, hookworm, Abdominal pain (usually vague).
strongyloids) leading to various manifestations like Abdominal cramps/colic.
LOEFFLERS SYNDROME.
Diarrhea.
Several clinical signs and symptoms can occur as
Vomiting (rarely).
follows:
Constipation (occasionally).
Lung invasion - Leffler or Leffler like Intestinal obstruction due to worm mass.
syndrome (ascariasis, hookworm infections, The common nematode infections are described
strongyloidiasis) below:
Fever 4.1 Ascariasis

Ascaris Lumbricoides is the largest of the intestinal
Cough nematodes. Symptoms can be divided into 2
Blood-tinged sputum categories: early larvae migration and late
mechanical effects.
Wheezing
In the early phase (4-16 hours after eggs ingestion),
Rales respiratory symptoms occur because of migration of
larvae through the lungs with symptoms of
Dyspnea eosinophilic pneumonia (Loffler Syndrome). Patient
Substernal pain may have fever, non-productive cough, dyspnoea or
wheezing.
Page 86
In the late phase (6-8 weeks after egg ingestion) Inflammatory diarrhea, with eosinophilia.
gastrointestinal symptoms may occur. Patient may
Chronic hookworm infection:
vomit out worms from mouth, nose.
Generally presents with Iron deficiency anemia,
Diffuse abdominal pain, nausea, vomiting, billiary
Hypoproteinemia.
and intestinal obstruction, appendicitis and
pancreatitis. Diagnosis:
Ascarisworms invade the biliary duct and cause Demonstration of eggs in stool examination.
pancreatic-biliary ascariasis. The most common Sensitivity improved with stool concentration.
presenting feature is abdominal pain, observed in
98% of patients. Less common features include Microcytic hypochromic anemia with proteinemia
ascending cholangitis, acute pancreatitis, and, rarely, may be seen in chronic cases. Eosinophilia may be
present.
obstructive jaundice.
Treatment:
Diagnosis
i. In early infection (larval migration): Albendazole 400 mg once/ Mebendazole 500 mg
CBC may show peripheral eosinophilia once/ pyrantel pamoate 11 mg/kg for 3 days.
Sputum may show charcot layden crystals.
Chest X Ray may show patchy infiltrates of Treat anemia with iron supplements.
eosinophilic pneumonia.
4.3 Enterobiosis
ii. In the late stage(adult worm): Enterobius vermicularis / pinworm is prevalent in
most tropical countries.
Stool microscopic examination shows eggs.
The adult worms migrate to perianal area at night and
USG may be used for ascariasis related biliary
release upto 10,000 eggs which after hatching are
disease.
transmitted by hand to mouth passage.
CT abdomen may show adult worms or
Clinical features-
obstruction due to worm mass.
The infection is generally asymptomatic.
Treatment:
The primary symptoms of pinworm infestation occur
Albendazole 400mg one dose orally is the drug of at night which include pruritus in the perianal region.
choice OR Mebendazole 100 mg twice daily for 3
Heavy infection can cause abdominal pain and
days. It is contraindicated in pregnancy.
weight loss.
4.2 Anclostoma Duodenale: Diagnosis:
(Hookworm) Since pinworm eggs are not released in feces stool
Many patients may be asymptomatic carriers. examination is not informative.
Clinical features - Detection of worms/ eggs in perianal cellophone

swab/ cellophane tape applied in the early morning
The symptoms are classified into 2 phases: establishes diagnosis.
Treatment:
In the migratory phase: Single dose Mebendazole 100 mg once /Albendazole
Pruritus and erythema and vesiculation will occur 400 mg once.
once the falciform larvae have penetrated the skin of
the feet and hands. This is called as ground/dermal
4.4 Strongyloidosis
itch in people who goes barefeet.
S. stercoralis is the only intestinal nematode with the
The pulmonary symptoms may develop with A. ability to replicate inside humans, thus leading to
Duodenale during the phase of lung migration like repeated auto infection.
mild transient pneumonitis.
In immunocompramised hosts it can lead to invasive
In the intestinal phase: and disseminated infection which can be fatal.
Patients may present with abdominal pain (often Clinical features:
epigastric).
Page 87
Many patients are asymptomatic. Treatment:
Cutaneous manifestations include recurrent Ivermectin (200 mcg/kg daily for 2 days) is most
urticaria involving buttocks and wrists. effective. In cases with disseminated infection extend
Larva currens: cutaneous migration of larvae the duration for 5 to 7 days or upto clearance of
results in serpiginous eruption which is pruritic, parasites. Albendazole (400 mg daily for 3 days.) is
erythematous. also effective.
Burning or colicky abdominal pain, often
epigastric, occurs and is associated with 4.5 Trichuris Trichura
diarrhea and the passage of mucus. Pain is
aggravated by food. Also called as whip worm.
Some patients with strongyloidosis report Most infections are asymptomatic. Heavy infections
nausea, vomiting, and weight loss, with evidence can cause gastro intestinal symptoms.
of malabsorption or of protein-losing
Common in low socio economic status with children
enteropathy. especially affected.
Massive larval invasion of the lungs and other
tissues may occur with hyperinfection, usually in
immunocompromised hosts. Clinical features:
Disseminated infection in immunocompramised
hosts severe generalized abdominal pain, diffuse Usually mild symptoms with abdominal pain,
pulmonary infiltrates, ileus, shock, and anorexia, diarrhea which can be bloody/mucoid.
meningitis or sepsis due to gram-negative bacilli Rectal prolapse may occur in massive infections in
may occur. children.
Diagnosis:
Stool examination for rhabditiform larvae is Diagnosis:
diagnostic.
Stool examination for eggs.
Doudenal aspirate may reveal the larvae if stool is Proctoscopy for adult worms.
persistently negative.
In disseminated infections filariform larvae should be Treatment:
sought in stool, sputum, broncho alveolar lavage etc. Mebendazole 500 mg once/ albendazole 400 mg
daily for 3 days.
Page 88
38. ASCITES
1. Causes
Cirrhosis is the common cause of ascites. Other Lab tests
causes are malignancy, cardiac failure, tuberculous
ascites, pancreatitis, nephrotic syndrome, alcoholic In general, start with cell count and differential,
hepatitis, acute liver cell failure etc. TP and albumin when uncomplicated ascites due
to cirrhosis is suspected. Culture is also usually
2. Physical Exam sent.
In patients with PMN >250, only 50% of cultures
grow bacteria if sent down to lab in a syringe or
Almost all patients with cirrhosis severe enough plain tube. 80% grow bacteria if inoculated into
to cause ascites will have stigmata of cirrhosis blood culture vials at bedside (prior to
spider angiomata, palmar erythema, and caput antibiotics).
medusiae.
Glucose < 50, LDH > upper limit of normal for
Elevated JVP should raise suspicion of heart serum, TP >1, and culture results can help
failure or constrictive pericarditis as a cause, differentiate secondary from spontaneous
although cirrhosis with tense ascites or peritonitis.
pulmonary HTN may cause this.
SAAG (serum albumin and ascitic albumin
Sister Mary Joseph nodule with ascites may be gradient) > or = 1.1 has ~97% accuracy for
caused by gastric or colon CA, HCC, or portal hypertension.
lymphoma. If found, FNAC can provide a rapid
TP > or = 2.5 can help differentiate cardiac from
tissue diagnosis.
cirrhosis ascites.
When PMN > or = 250, but less than 50% of
3. Investigations WBC, consider peritoneal carcinomatosis and
tuberculous ascites.
Ultra sonography of abdomen is useful to
confirm/refute presence of ascites, cirrhosis,
splenomegaly, biliary obstruction, vessel patency,
4. Management
Goal is to minimize ascitic fluid volume and
signs of portal hypertension, and cancer.
peripheral edema without intravascular volume
CT-abdomen, tumour markers, HBsAg Anti HCV, depletion.
serum amylase are other investigations. First line treatment includes 2 gram per day
sodium restricted diet and oral diuretics
Abdominal paracentesis (spironolactone / lasix).
Along with history and physical exam, ascitic The usual diuretic regimen is single morning
fluid analysis helps in the diagnosis of etiology. doses of 100mg spironolactone and 40mg
It is a safe procedure Ascitic fluid analysis. frusemide (lasix).
The 100:40 ratio generally maintains
Appearance.
normokalemia. Usual max dose is 400mg and
Turbid/cloudy 98% sensitive but only 23% 160mg per day.
specific for SBP.
Other specific management as per the cause of
Milky chylous ascites, TG level usually greater ascites.
than serum TG level and >200mg/dl.
Bloody/pink usually a traumatic tap, but seen 5. When to Refer
in 50% of patients with HCC and 22% with
Acute ascites, bleeding tendency, refractory ascites,
malignancy overall.
hepatic encephalopathy.
Dark brown if bilirubin level is higher than in
serum, worry about ruptured gallbladder or
perforated duodenal ulcer.
Page 89
39. HEPATITIS
hypertension and end stage liver disease
1. Introduction develops.
Onset is gradual or sometimes rapid.
There is fever, fatigue and nausea for a few days 4. Obstructive jaundice
followed by jaundice accompanied by dark urine
Sometimes jaundice is due to obstruction to flow
and sometimes clay- coloured stools.
of bile and not due to a virus.
The severity of jaundice varies.
On such cases the yellowing of eyes is very
On examination liver may be mildly enlarged marked and may even be greenish.
with mild tenderness.
There is much itching and the stools are always
This being the most common cause one must whitish in colour.
always make this clinical diagnosis after the
Usually the liver is enlarged.
exclusion of obstructive or haemolytic jaundice.
In most cases this can be done on clinical Ultrasound of the liver confirms obstruction best
grounds alone. and the patients should be referred to a centre
with ultrasonography facilities.
There are five viruses that are commonly
associated with hepatitis called Hepatitis A, B, Refer to higher centre as these cases need
C, D and E virus. Of these two, hepatitis A and E surgery.
spread through faecal contamination of water.
When there is an outbreak of jaundice in a 5. Haemolytic jaundice
village it is probably this virus. Almost always
this jaundice becomes alright on its own. Except Sometimes jaundice is due to increased
in pregnant women where it can be life breakdown of haemoglobin secondary to
threatening. Three other types of viruses spread destruction of RBCs in a haemolytic anaemia.
through the blood and through unprotected Jaundice is invariable light coloured, and urine is
sexual contact (hepatitis B, C, D). These types also normal in colour.
are more severe, tend to worsen and have more
long term complications. Diagnosis needs to be established by blood
smear examination, by ruling out hepatitis by
2. Acute fulminant hepatitis liver function tests and by specific tests for
Sometimes, especially with hepatitis B and D haemolytic anaemia.
hepatitis turns severe due to cell necrosis.
Patient develops confusion, stupor and then 6. Alcoholic hepatitis
coma and it is difficult to save the life.
Excessive alcohol consumption is a significant cause
Pregnant women are prone to develop this of hepatitis and liver damage (cirrhosis). Alcoholic
picture with all viruses but commonly with hepatitis usually develops over years-long exposure
hepatitis E. to alcohol. Alcohol intake in excess of 80 grams of
alcohol a day in men and 40 grams a day in women is
3. Chronic hepatitis associated with development of alcoholic hepatitis.
Sometimes the liver disease goes on for years Alcoholic hepatitis can vary from mild asymptomatic
without becoming well. disease to severe liver inflammation and liver failure.
Symptoms and physical exam findings are similar to
Such patients have frequent intermittent episodes other causes of hepatitis. Laboratory findings are
of jaundice. significant for elevated transaminases, usually with
elevation of aspartate transaminase (AST) in a 2:1
Elevated liver enzymes over 6 months is enough
ratio to alanine transaminase (ALT).
to make this diagnosis.
Alcoholic hepatitis may lead to cirrhosis and is more
Eventually it can become well but more often common in patients with long-term alcohol
leads to cirrhosis of the liver and portal consumption and those infected with hepatitis C.
Page 90
Patients who drink alcohol to excess are also more 8.1. Treatment for Acute fulminant
often than others found to have hepatitis C. The
combination of hepatitis C and alcohol consumption hepatitis
accelerates the development of cirrhosis. Patient needs hospitalization.
Treatment is supportive & consists of
maintaining parenteral fluids.
7. Investigations for jaundice
Care is taken to treat infections or other
These tests are needed to establish diagnosis & precipitating factors like haematemesis.
monitor improvement.
Urine examination for bile salts & pigments. Gut sterilization with capsule amoxicillin and/or
metronidazole may help.
Serum bilirubin & Serum liver enzymes level.
8.2. Treatment for obstructive

8. Treatment for hepatitis jaundice
Only supportive: rest, hydration, correct but not Refer for Surgery.
specific diet.
Avoid oily spicy foods that are ill tolerated. 8.3. Treatment for Haemolytic
Avoid corticotherapy. NEVER give steroids. anaemia
There are no specific drugs to cure jaundice. Referral for further work up in higher centre with
Fortunately most persons become well on their tests for type of haemolysis.
own.
Remember many drugs commonly used are harmful
when given to a person with jaundice.
9. Vaccine
Vaccine against hepatitis B is available.
Hepatitis-B Vaccine is included in National
Immunization Schedule.
Page 91
40. HEPATIC COMA
coma. Asterixis / flapping tremors is also commonly
1. Introduction seen.
Hepatic Encephalopathy is a term used to describe a Search for precipitating factors every advanced
spectrum of neuropsychiatric abnormalities occurring cirrhotic patient displaying a change in mental status
in patients with significant liver disease and/or porto is septic until proven otherwise. Common
systemic shunting of blood. precipitating are GI bleeding, sepsis, hypokalemia,
high protein load, constipation, hyponatriemia, Other
2. Diagnosis causes include sedative
drugs, superimposed liver injury.
There are 2 major components of HE, altered mental
status and generalized motor disturbance. 3.Grade / Stage the severity of
Disturbunces in awareness and mentation from
forgetfulness and confusion to stupor and finally disease
Table-1: West-Haven Criteria for Hepatic Encephalopathy (HE)
Stage Consciousness Intellect and Behavior Neurologic Findings

0 Normal Normal Normal examination; if impaired psychomotor
testing, consider MHE*
1 Mild lack of awareness Shortened attention span Impaired addition or subtraction; mild asterixis or
tremor
2 Lethargic Disoriented; Inappropriate Obvious asterixis; Slurred speech

behavior
3 Somnolent but arousable Gross disorientation; Muscular rigidity and clonus;
Bizarre behavior Hyperreflexia
4 Coma Coma Decerebrate posturing
*MHE, minimal hepatic encephalopathy.
ii. Rifaximin 400mg PO tid marginally better

4. Treatment than lower doses(400mg-550mg bid) or
A. 4-pronged approach to treatment Neomycin 1gm PO q6 hourly for up to 6 days
Supportive care. (if used chronically, 1-2gm/day).
Search for and correct precipitating factors iii. Dietary protein restriction no longer
Exclude and treat other causes of altered mental recommended.
status. iv. L-ornithine-aspartate promotes waste nitrogen
Start empiric therapy for HE excretion.
i. Lactulose : 30cc bid-qid titrated to goal 2-4 v. Antibioics if sepsis suspected.
soft BMs/day or retention enema 300cc
lactulose + 700cc tap water retained for 1 hour
reduces the ammonia production and 5. When to refer
absorption. Deteriorating sensorium, hematemesis, malena,
bleeding tendencies.
Page 92
41. NEPHROTIC SYNDROME
6. Renal Function Test: Blood Urea Level and
1. Definition Serum Creatinine Level
Nephrotic Syndrome is a clinical complex 7. Renal Biopsy: In Adult patients for a)
characterized by a number of renal and extrarenal Establishing a Definitive Diagnosis b) Guiding
features, the most prominent of which are Therapy & c) Assessing Prognosis.
Proteinuria of 3-3.5gm / 24 hour,
Hypoalbuminemia,
Edema, 5. Treatment
Hyperlipidemia, Lipiduria i. Steroid: Minimal change disease accounts for
about 80% of Nephrotic Syndrome in children
younger than 16 year and 20% of adult.
2. Symptoms and Signs Adult: Tab Prednisolone 1-1.5 mg/kg body
Puffiness of face, increase in morning weight per day for 4 week followed by
Ankle pitting edema with increasing severity to 1mg/kg/day on alternate day for 4 week.
generalised anasarca Ascites, Pleural Effusion Check for urine protein after four weeks if nil
no treatment needed and if present start with
Prednisolone 1.5 mg for 2 weeks
3. Complications ii. HMG Co A Reductase Inhibitor: Tab
Recurrent Infections, hypocalcemia, Anemia,
Atorvastatin 10 Mg Od
Thrombotic Tendencies
iii. Loop Diuretic
iv. Salt Restriction 1-2 Gram per Day.
4. Investigation v. High Protein Diet
1. Urine Analysis for Proteinuria, Protein / vi. Vitamin D Supplementation.
Creatinine ratio
2. Urine Microscopy for Deposit 6. When to Refer
3. 24 Hour Urinary Protein
i. For Renal Biopsy
4. Serum albumin
ii. When Dialysis is required.
5. Ultra sonography abdomen and pelvis
Page 93
42. ACUTE NEPHRITIC SYNDROME
It is Clinical Correlate of Acute Glomerular Blood Urea and Serum Creatinine elevations.
Inflammation Which May Be a Primary Disease OR
Decrease C3 Level, Normal C4 Level
Secondary to Systemic Process.
ASO Titer
1. Definition Ultra sonography renal
It is characterized by sudden onset (over days to
Renal Biospy
weeks) of acute renal failure and Oliguria (400ml/day
of urine) and renal blood flow and GFR fall as a
result of obstruction of the glomerular capillary
4. Treatment
lumen. 4.1 General Management
2. Clinical Features Bed Rest
Tetrad of
Adequate Fluid Intake to ensure 400 ml Urine per
Edema Day
Hypertension mild Salt restriction especially if edema present
Hematuria [macroscopic]
4.2 Managementof Renal Failure
Proteinuria (Subnephrotic Range < 3g/24 Hr)
Tab Frusemide if volume overload hypertension
Symptom:
Not to be given if no evidence of fluid excess
Puffiness of Face
Rarely require Dialysis
Edema of Feet
Cola Coloured Urine
4.3 Antihypertensive Drug
Dyspnea If Pulmonary Edema 4.4 Controlof Infection
Hypertension
Generalized Symptoms- Anorexia, Nausea, 4.5 Renal Biopsy
Vomiting, Malaise, Flank OR Back Pain. If features not suggestive of Post Streptococcal
Glomerulonephritis.
3. Investigation
Urine Microscopy: Dysmorphic RBCs and RBC 5. When to Refer
Cast, Leucocytes
i. For Renal Biopsy
Urine- Gross Hematuria (Red or Smoky Urine) ii. When Dialysis is required.
Subnephrotic range Proteinuria
Page 94
43. ACUTE RENAL FAILURE / ACUTE KIDNEY
INJURY
1. Definition 3. Acute tubular necrosis

AKI is a syndrome characterized by rapid decline in Ischemia, Exogenous toxins: radiocontrast,
glomerular filtration rate (hours to days), retention of chemotherapy, acetaminophen, Endogenous toxins:
nitrogenous waste products and perturbation of rhabdomyolysis, hemolysis, myeloma.
extracellular fluid volume and electrolyte and acid
base homeostasis. 4. Interstitial nephritis
AKI is defined as any of the following (Not Graded): Antibiotic, NSAID, Sulfonamide, eta lactam
Increase in Sr.Creatinine by X0.3 mg/dl (X26.5
Post renal:
lmol/l) within 48 hours; or
Increase in Sr.Creatinine to X1.5 times baseline, Ureter: calculi, blood clot, carcinoma
which is known or presumed to have occurred
Bladder neck: prostatic hypertrophy, calculi,
within the prior 7 days; or
carcinoma
Urine volume 0.5 ml/kg/h for 6 hours
Urethra: stricture, phimosis.
2. Classification
3. Symptoms
Prerenal:
a. Hypovolemia: 3.1. Prerenal
Haemorrhage, burns, dehydration, vomiting, diarrhea, Evidence of true volume depletion- thirst,
pancreatitis, peritonitis. postural or absolute hypotension and
b. Low cardiac output: tachycardia, dry mucous membrane.
Urine- low volume, low sodium and high
CCF, Disease of myocardium, valves and osmolality.
pericardium,
Pulmonary hypertension, pulmonary emboli. 3.2. Renal
c. Altered renal systemic vascular resistence ratio; Symptom and sign of underlying disease affecting
glomeruli or tubule.
Systemic vasodilatation- sepsis, antihypertensive
drug 3.3. Postrenal
Renal vasoconstriction: hypercalcemia
Abdominal or flank pain, palpable bladder.
Cirrhosis with ascitis- hepatorenal syndrome.
Intrinsic renal: 3.4. Symptoms of uremia
1. Renovascular obstruction: Anorexia, nausea, vomiting, Mental status changes,
Pruritus, shortness of breath
Renal artery obstruction: atherosclerosis, thrombi,
emboli, Renal vein obstruction: thrombi, compression
4. Signs
2. Disease of glomeruli: Asterixis, Pericardial rub, Pedal edema, pulmonary
Glomerulonephritis and vasculitis, Hemolytic uremic edema, Raised JVP
syndrome, DIC, toxemia of pregnancy, Accelerated
hypertension. 5. Investigation
Urine analysis: routine microscopy
Page 95
Routine blood chemistry: BUN, creatinine, Serology: ANA, ANCA, anti GBM, complement,
electrolyte, ca, po4 ASO
Complete hemogram Imaging: Renal ultrasound, Plain radiograph of
abdomen.
Special test: bence jones protein
Renal biopsy.
6. Staging of aki
STAGE Serum creatinin criteria Urine output criteria

I 1.5 to 2 fold increase <0.5 ml/kg/hr for > 6 hr
II 2 to 3 fold increase <0.5 ml/kg/hr for >12 hr
III >3 fold increase , absolute value > 4 mg/dl < 0.3 ml/kg/hr for 24 hr or anuria
for 24 hr.
IV.Calcium gluconate (10ml 10% solution)

7. Treatment Inhaled 2 agonist- Salbutamol
IV glucose insulin infusion (100ml 25% dextrose
7.1. Prerenal with 10 unit of human actrapid in 1 hour)
Restore blood volume (with isotonic saline 0.9%, or Dialysis.
blood, plasma)
Treat underlying cause.
7.5. Treatment of metabolic
7.2 Renal acidosis
Inj Na bicarbonate iv
Eliminate toxins, Nephrology consultation
7.3. Postrenal 7.6. Dialysis: indication

Metabolic acidosis, Hyperkalemia, Encephalopathy,
Relieve obstruction, Urology consultation Volume overload, Pericarditis
7.4. Hyperkalemia
8. Complication
COMPLICATION MANIFESTATION
1.Metabolic Hyperkalemia, hypocalcemia, hyperphosphatemia, hypermagnesaemia,
hyperuricemia, metabolic acidosis.
2.Cardiovascular Cardiac arrhythmia, pulmonary edema, pericardial effusion, pericarditis
3.Gastrointestinal Gastrointestinal hemorrhage
4.Neurological Altered sensorium, seizures
5.Hematological Anaemia, bleeding.
9. Prevention
Nephrotoxic drug should be stopped if patient is at
Apropriate and adequate fluid management
Optimization of hemodynamic risk of developing AKI.
Management and prevention of sepsis
Page 96
44. CHRONIC KIDNEY DISEASE
3. Nondiabetic glomerular disease- Nephritic and
1. Definition nephrotic presentation
4. Cystic kidney disease
A. Presence of marker of kidney damage more than 5. Tubulo interstitial disease.
3 month as defined by structural or functional
abnormality of the kidney with or without decrease 3. Staging
GFR manifested by either pathological abnormality According to GFR (glomerular filtration rate)
or other marker of kidney damage. Cockcroft-Gault equation for calculation of
B. GFR < 60 ml/min/1.73m2 for more than 3 month creatinine clearance:
with or without sign of kidney damage.
(140- Age) Body weight (kg)
2. Causes 72 plasma creatinine (mg/dl)
1. Diabetes Multiply by 0.85 for women.
2. Hypertension
Table-1: Staging of CKD
STAGE DESCRIPTION GFR(ml/min/1.73m2

1 At increased risk of kidney damage with normal or raised 90
GFR
2 Kidney damage with mildly Decreased GFR 60-89
3 Moderately decreased GFR 30-59
4 Severelydecreased GFR 15-29
5 Renal failure <15
4. Symptoms and signs 6. Evaluation and

Hypertension, proteinuria, anemia, deep
respiration(Kussmauls respiration), tiredness,
management of patient of
breathlessness, pruritus, anorexia, nausea, vomiting. ckd
5. Risk factors 6.1. History and physical
Age> 65yr examination
Diabetes
H/O HTN, DM, use of analgesic Measure blood
Family h/o renal disease pressure
Autoimmune disease 6.2. Laboratory investigation

Systemic infection
Haemoglobin level.
Urine for proteinuria and hematuria

UTI, stone, urinary tract obstruction,
Blood urea,serum creatinine
HTN
Page 97
Blood sugar level 6.3. Imaging study
Serum electrolyte
USG abdomen for the renal size and
Serum calcium,phosphorus level Corticomedullary differentiation.
Table-2: To Delay Progression to Next Stage:
MEASURES GOAL
1.ACE inhibitors/ARB Proteinuria <0.5 g/day and GFR decline<2ml/min/yr.
2.Additinoal antihypertensive drug as needed BP<130/80 if proteinuria<1 gm/day
BP<125/75 if proteinuria>1gm/day
3.Dietary protein restriction 0.6 to 0.8 gm/kg/day
4.Glycaemic control HbA1C <7 %
5.Anaemia correction Target Hb 10 to 12 gm/dl
6. Cholesterol lowering agent LDL <100 mg/dl
7. Dietary salt restriction 3 to 5 gm/day
6.4. Treatment diseases, Anaemia: target Hb 11 gm/dl, Use of iron

and erythropoietin injection, Renal osteodystrophy:
1. Slowing the progression of CRF:
target Ca 8.8 9.7, phosphorus 3.5 5.5, Use of
Protein restriction 0.6gm/kg/day calcium carbonate, phosphorus restriction avoid
2. Slowing diabetic renal disease: dairy product,meat,colas Oral calcitriol.
Glucose control target HbA1c <7.2 4. Renal replacement therapy:
3. Managing complications of CRF:Cardiovascular Dialysis: refer to higher center, A-V fistula; if GFR
complication-yearly screening of cardiovascular <25ml/min Serum creatinine> 4 mEq/L.
Page 98
45. MALARIA
Fever comes down with profuse sweating. The
1. Introduction temperature drops rapidly to normal and skin is cool
Malaria is a protozoal disease caused by infection and moist. The pulse rate becomes slower; patient
with parasites of the genus plasmodium and feels relieved and often falls asleep. This stage lasts
transmitted to man by female anopheles mosquito. It for 2-4 hours.
is a very important public health problem in India The febrile paroxysms occur with definite
particularly due to Plasmodium falciparum which is intermittent periodicity repeating every third or
prone to various complications. fourth day depending upon the species of the parasite
involved. The classical 3 stages (cold, hot and
2. Agent sweating) may not always be observed due to
Malaria in man is caused by Plasmodium vivax, maturation of generations of parasite at different
Plasmodium falciparum, Plasmodium ovale and times. The disease has a tendency to relapse and is
Plasmodium malaria. Out of these, Plasmodium characterized by enlargement of the spleen and
vivax and Plasmodium falciparum are very common secondary anaemia.
in India including Maharashtra. In patients with P.falciparum infection the primary
fever in its first few days is usually irregular or even
3. Mode of transmission continuous and then the classical 48 hour periodicity
Direct through blood or plasma. becomes established or the fever may continue to be
irregular and the hot and cold stages, so typical of
Vectors bite of female anopheles mosquito. other malarial infections are less clearly separated
from one another, in persons with poor immunity.
4. Incubation Period The paroxysms are associated with marked
prostration. Headache, nausea and vomiting are
The duration varies with species of parasite.
usually more severe, and there is greater tendency
12(9-14) days for falciparum malaria. towards the development of delirium, haemolytic
14(8-17) days for vivax malaria. jaundice and anaemia. The mortality is much greater
than in other forms of malaria.
5. When to suspect With P. vivax infection, symptoms are same but are
usually milder and more regularly divided into hot
The typical attack comprises three distinct stages viz.
and cold stages than in P.falciparum infections.
cold stage, hot stage and sweating stage.
Cold Stage:
6. Complications
The onset is with lassitude, headache, nausea and
chilly sensation followed in an hour or so by rigors. The complications of P. falciparum malaria are
The temperature rises rapidly to 39-41C. Headache cerebral malaria, acute renal failure, liver damage,
is often severe and commonly there is vomiting. In gastro-intestinal symptoms, dehydration, collapse,
early part of this stage, skin feels cold; later it anaemia, black water fever etc. The complications of
becomes hot. Parasites are usually demonstrable in P. vivax, infection are anaemia, splenomegaly,
the blood. The pulse is rapid and may be weak. This enlargement of liver, herpes, renal complications,
stage lasts for -1 hour. ARDS etc.
Hot Stage:
7. Investigations
The patient feels burning hot and casts off his
clothes. The skin is hot and dry to touch. Headache is
intense but nausea commonly diminishes. The pulse Diagnosis of Malaria: One of the above clinical
is full and respiration rapid. This stage lasts for 2 to 6 features, supported by blood smear examination
hours. for malarial parasites.
Fever with splenomegaly in a patient with the
Sweating Stage: above mentioned clinical features make
diagnosis of malaria more likely.
Page 99
Confirmation of diagnosis always depends on ensure treatment with full therapeutic dose with
seeing the parasite in the blood. In all cases, appropriate drug to all confirmed cases. Presumptive
thick and thin smears should be examined. treatment of malaria with a single dose of
Blood smears may be negative in severe and chloroquine has been stopped.
chronic forms and this would need repeated All fever cases diagnosed as malaria by either RDT
smears. or microscopy should be promptly given effective
treatment. The medicine chosen will depend upon
8. Diagnosis of Malaria whether the patient has vivax malaria or falciparum
It is stressed that all fever cases should be suspected malaria as diagnosed by the blood test. The flow
of malaria after ruling out other common causes and charts in different settings for diagnosis and drug
should be investigated for confirmation of malaria by selection for the treatment of malaria are mentioned
Microscopy or Rapid Diagnostic Kit (RDK) so as to below.
Where microscopy result available within 24 hours
Suspected malaria case
Take slide and send for microscopic examination
Result?
Positive for Positive for Positive for Negative

P. vivax P. falciparum Mixed infection No anti-malarial
Treat with: Treat with: SP-ACT 3 days Treatment.
CQ 3 days + ACT-SP + Treat as per
PQ 0.25 mg for 3 days + PQ 0.75mg Primaquine clinical
per kg body per kg body 0.25 mg per kg diagnosis
weight daily for weight body weight
14 days Single dose on daily for
second day 14 days.
Figure-1: Management chart for suspected Malaria case
Page 100
ACT-SP- Artemisinin-based Combination Where microscopy result is not available within 24
Therapy(Artesunate+Sulfadoxine-Pyrimethamine)CQ hours and Monovalent RDT is used
Chloroquine PQ Primaquine
TfR= Test falciparum rate
Where TfR>=1%, and In other areas, if

Pf %> 30% in any of Patient not
last at high risk of Pf*
3 years
Do RDT for detection Wait for slide result. Give

of CQ 25mg/kg over 3 days
Malaria & only if high suspicion of
Prepare slide malaria
Positive for Positive for

Positive for RDT Negative:
P. vivax P. falciparum
P. falciparum Wait
CQ if not In other states:
Treat with: ACTSP for slide result.
already Treat with: ACTSP
for 3 days + Give CQ 25mg/kg
given + for 3 days
PQ Single dose over 3 days, if
PQ 0.25 + PQ Single
on second day high suspicion of
mg/kg single dose onPQ 0.75mg
dose for 14 per kg body
If confirmed as days over weight
Pv 3days, if high Single dose on
CQ if not already suspicion of second day
Given PQ 0.25 malaria
mg/kg/day over
14 days
Figure-2: Management of suspected Malaria
Note: if a patient has severe symptoms at any ACT-SP- Artemisinin-based Combination

stage, then immediately refer to a facility with Therapy (Artesunate+Sulfadoxine-
indoor patient management. Pyrimethamine) CQ Chloroquine PQ
Primaquine.
Note: PQ is contra-indicated in pregnancy
and in children under 1 year (Infant). Where microscopy result is not available
within 24 hours and Bivalent RDT is used
Page 101
Do blood test with RDT
Positive for Positive for Positive for Negative

P. falciparum P. vivax Mixed infecion No anti-
Treat with: ACTSP Treat with: SP-ACT 3 days + malarial
for 3 days + CQ 3 days Primaquine 0.25 mg per Treatment
PQ Single dose on second + PQ 14 days kg body weight daily for
day malaria case 14 days.
Figure-3: Suspected Malaria management based on RDT results
ACT-SP- Artemisinin-based Combination Therapy Drug schedule for treatment of P vivax malaria:
(Artesunate+Sulfadoxine-Pyrimethamine).
i. Chloroquine:
CQ Chloroquine PQ - Primaquine
25 mg/kg body weight divided over three days i.e.
Differential Diagnosis:
10 mg/kg on day 1,
Other causes of fever like Dengue, UTI, URTI. All
10 mg/kg on day 2 and
D/D can be excluded by using lab investigation
(microscopy/RDT). 5 mg/kg on day 3.
ii. Primaquine:
0.25 mg/kg body weight daily for 14 days.
9. Treatment
Primaquine is contraindicated in infants, pregnant
9.1. Treatment of Vivax Malaria women and individuals with G6PD deficiency.
Diagnosis of vivax malaria may be made by the use
of RDT (Bivalent) or microscopic examination of the 14 day regimen of Primaquine should be given under
blood smear. On confirmation following treatment is supervision.
to be given:
Table-1: Dosage Chart for Treatment of Vivax Malaria

Day 4 to 14
Day 1 Day 2 Day 3
Age
CQ (150 PQ CQ (150mg PQ (2.5 CQ (150mg PQ (2.5mg) PQ (0.25
mg base) (2.5mg) base) mg) base) mg)
Less than
0 0 0 0
1 yr
1-4 years 1 1 1 1 1 1
5-8 years 2 2 2 2 1 2 2
9-14 years 3 4 3 4 1 4 4
Page 102
15 yrs or
4 6 4 6 2 6 6
more*
Pregnancy 4 0 4 0 2 0 0
Note: Chloroquine250mg tablet is having 150 mg base
9.2. Treatment of Falciparum Treatment of uncomplicated P.falciparum cases in

pregnancy:
Malaria 1st Trimester: Quinine salt 10mg/kg 3 times
Diagnosis of falciparum malaria may be made by the daily for 7 days.Quinine may induce
use of RDT (Monovalent or Bivalent) or microscopic hypoglycemia; pregnant women should not start
examination of the blood smear. It is imperative to taking quinine on empty stomach and should eat
start the treatment forfalciparum malaria immediately regularly, while on quinine treatment.
on diagnosis. The treatment for falciparum malaria is 2nd and 3rd trimester: ACT as per dosage
as follows: schedule given above.
Dose schedule for Treatment of uncomplicated
P.falciparum cases:
i. Artemisinin based Combination Therapy (ACT- 9.3. Treatment of mixed infections
SP)* (P.vivax + P.falciparum) cases
Artesunate 4 mg/kg body weight daily for 3 days Plus All mixed infections should be treated with full
Sulfadoxine (25 mg/kg body weight) course of ACT and Primaquine 0.25 mg per kgbody
Pyrimethamine (1.25 mg/kg body weight) on first weight daily for 14 days.
day. SP-ACT 3 days + Primaquine 0.25 mg per kg body
* ACT is not to be given in 1st trimester of wt. daily for 14 days.
pregnancy.
ii. Primaquine: 0.75 mg/kg body weight on day 2.
Table-2: Treatment of mixed infections
Day 4to
Day 1 Day 2 Day 3
14
Age As tablet SP tablet PQ (2.5 As tablet PQ (2.5 As tablet PQ PQ (0.25
(50 mg) mg) (50mg) mg) (50 mg) (2.5mg) mg)
Less than
1 yr 0 0 0 0
1-4 years 1 1 1 1 1 1 1 1
5-8 years 2 1 2 2 2 2 2 2
9-14 years 3 2 4 3 4 3 4 4
15 yrs or
more 4 3 6 4 6 4 6 6
All cases of mixed infection are to be treated as Pf treatment and is still having symptoms after 72 hours,
plus primaquine for 14 days. treatment failure may be suspected.
When a patient fails to respond to treatment The course of action when a patient has persistent
(symptoms fail to disappear, or they reappear), one symptoms is:
should think of the possibility of drug resistance in Ask the patient and the family a series of
such case refer patient to FRU. In the absence of any questions to help rule out some of the causes
of these conditions, if a patient has completed full (Did the patient get the drug from an authentic,
designated provider? Did the patient get the right
Page 103
amount of the drug? Was all of it swallowed as Macroscopic haemoglobinuria.
prescribed? Was the drug vomited out? How Hyperthermia.
many days has it been since drug treatment was Hyperparasitaemia.
begun (if it is not yet72 hours, one can wait)? Foetal and maternal complications are more common
Can you see the packing to check the expiry in pregnancy with severe malaria; therefore, they
date? Are there symptoms of other obvious need prompt attention.
causes of fever? If the symptoms had
disappeared and then reappeared, how long was 10.2 In children, febrile convulsions, repeated
the interval (if more than 15 days, it could be a vomiting and dehydration are common if the
fresh infection)?) temperature is high due to any cause.
If it appears that the drug was not adequately Therefore, these symptoms are not
taken or retained, a fresh course may be given necessarily indicative of severe malaria.
unless the patient has symptoms of severe However, children with such symptoms
malaria. Take a fresh blood11smear (take two, should be managed as severe malariain
for checking in different laboratories, if need be), routine program situations, and a diagnosis
and ask the nearest health care provider to keep of malaria should be confirmed at the
an eye on the patient. earliest.
Refer any patient who has symptoms despite
taking and retaining a full course of treatment, or 10.3 In pregnancy, malaria, especially
who has developed symptoms of severe malaria. P.falciparum is a serious disease because
with each bout of malaria, there is a
reduction in haemoglobin and profound
10. Severe and complicated anaemia may develop rapidly. They are also
malaria at high risk of abortions or intrauterine
growth retardation because sequestration of
10.1. Clinical Features parasites in placenta restricts oxygen and
Severe manifestations can develop in P. falciparum nutrients flow to the fetus. The management
infection over a span of time as short as 12-24 hours of severe malaria is possible in health
and may lead to death, if not treated promptly and facilities which are equipped with the
adequately. Severe malaria is clinically characterized following:
by confusion or
Parenteral Antimalarials, antibiotics,
Drowsiness with extreme weakness (prostration) anticonvulsants, antipyretics.
along with one or more of the following features: Intravenous infusion equipment and fluids.
Impaired consciousness/coma Special nursing for patients in coma.
Repeated generalized convulsions Facilities for blood transfusion.
Renal failure (Serum Creatinine>3 mg/dl) Well-equipped laboratory.
Jaundice (Serum Bilirubin >3 mg/dl) Oxygen respirator.
Severe anaemia (Hb<5 mg/dl) Often these items are not available at the PHC level.
Pulmonary oedema/acute respiratory distress Under such circumstances, the MedicalOfficer, PHC
syndrome and paramedical staff should be able to administer
Hypoglycaemia (Plasma glucose <40 mg/dl) emergency treatment and refer the case without delay
to other institutions where such facilities are
Metabolic acidosis
available.
Circulatory collapse/shock (Systolic BP<80 mm
Hg, <50 mm Hg in children). 10.4. Treatment of severe malaria
Abnormal bleeding and disseminated
intravascular coagulation. cases
Haemogolobinuria. Severe malaria is an emergency and treatment should
Hyperthermia (Temperature >106F or 42C). be given as per severity and associated complications
which can be best decided by the treating physicians.
Hyperparasitaemia (<5% parasitized RBCs in
low endemic and >10% in hyperendemic areas). The guidelines for specific antimalarial therapy is as
follows:
Metabolic acidosis.
Circulatory collapse/shock. Parenteral artemisinin derivatives or quinine should
Spontaneous bleeding and laboratory evidence of be used irrespective of chloroquine resistance status
DIC. of the area with one of the following options:
Page 104
Table 3: Chemotherapy of severe and complicated malaria
Initial parenteral treatment for at least48hours:CHOOSE Follow-up treatment, when patient can takeoral
ONE of following four options medication following parenteral treatment
Artesunate: 2.4 mg/kg i.v. or i.m. given on admission Full oral course of Area-specific ACT:
(time=0), then at 12 h and24 h, then once a day.
In other states: Treat with: ACT-SP for 3days + PQ
Single dose on second day
Quinine: 20mg quinine salt/kg body weight on Quinine 10 mg/kg three times a day
admission (IV infusion or
with:
divided IM injection) followed by maintenance dose
doxycycline 100 mg once a day or
of10 mg/kg 8 hourly;
Clindamycin in pregnant women and children under 8
Infusion rate should not exceed 5 mg/kg per hourin
years of age,- to
normal saline. Loading dose of 20mg/kg should not be
given, if the patient has already received quinine. Complete 7 days of treatment.
Note: The parenteral treatment in severe malaria cases should be given for minimum of 24 hours once started
(irrespective of the patients ability to tolerate oral medication earlier than24 hours).
Note:
The parenteral treatment should be given for minimum of 48 hours.
Once the patient can take oral therapy, give:
Quinine 10 mg/kg three times a day with doxycycline 100 mg once a day orclindamycin in pregnant women and
children under 8 years of age, to complete 7days of treatment, in patients started on parenteral quinine.
Full course of ACT to patients started on artemisinin derivatives.
Use of mefloquine should be avoided in cerebral malaria due to neuro psychiatric complications associated with
it.
Supplementary treatment
In unconscious patient, monitor blood glucose level every 4 to 6 hours and treat hypoglycemia with IV dextrose. If
blood sugar estimation is not available one can presume hypoglycemia in all cases of severe and complicated
malaria especially cerebral malaria and treat with intravenous glucose 100 ml of 25% glucose before giving
quinine.
All unconscious patients on quinine should receive a continuous infusion of 5 to10%dextrose.
Parasite count and hematocrit level should be measured every 6 to 12 hourly.
Transfuse whole blood or packed cell concentrate when hematocrit drops to <20%.
Renal function should be checked daily, institute early hemodialysis if necessary.
Fluid management should be carefully done.
Treat convulsions with IV diazepam and shift the patient to an Intensive Care Unit with facilities for ventilator
support.
10.5. Some donts in severe malaria case management

Do not use corticosteroids, give intravenous mannitol, use heparin as anticoagulant, administer adrenaline or
overhydrate.
In recent years, increased attention has been drawn to severe malaria caused by P.vivax, especially in Indonesia and
Papua New Guinea, where this parasite has become chloroquine resistant. Some cases have been found in India, and
there is reason to fear that this problem will become more common in the coming years. Historically, P.vivax has
been an important cause of death in India and in Europe, and this parasite can no longer be considered as benign.
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10.6. When to refer: Any of the following
i. Platelet count 20,000/cmm.
ii. Pregnancy with malaria.
iii. Any feature of complicated malaria.
iv. Renal failure.
v. ARDS.
vi. Malaria with sepsis.
vii. Malaria with shock.
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46. DENGUE
DF/DHF is caused by a group B arbovirus
1. Introduction (Flavivirus) and includes serotypes 1, 2, 3 and 4
(Den-1, Den-2, Den-3 and Den-4). Infectionwith any
In Maharashtra State, cases of Dengue Fever / one serotype confers lifelong immunity to thevirus
Dengue Hemorrhagic Fever occur eitherin post- serotype, but no cross protection for other serotypes.
monsoon period when breeding of mosquitoes is It is caused due to bite of an infected female Aedes
highest due to accumulation of rainwater in discarded aegypti mosquito.
materials or during scarcity season due to Aedes
breeding in stored waterin cement tanks and earthen Mode of Transmission It is transmitted through
pots which are not emptied regularly. bite of Ades aegypti mosquito.
Incubation period: Varies from 5-10 days.
2. Etiologic agent
3. Diagnosis
Table-1: Recommended diagnostic tool according to laboratory service level
Primary health District health Reference

care centres centres centres
Genome Detection Yes
NS1 Ag detection Rapid tests Yes Yes Yes
ELISA Yes Yes
IgM detection Rapid tests Yes Yes Yes
ELISA Yes Yes
IgG detection ELISA Yes
IHA Yes
Neutralization assay Yes
ELISA = enzyme-linked immunosorbent assay; IgG = immunoglobulin G; IgM = immunoglobulin M; IHA = indirct
haemagglutination; NS1 Ag =non- structural protein 1 antigen.
4. Clinical spectrum
Following is the spectrum of dengue viral
infection.
Figure-1: Dengue Clinical Spectrum
Dengue Viral infection
Asymptomatic Symptomatic
MILD MODERATE SEVERE
Undifferentiated fever Dengue fever Dengue Hemorrhagic fever
Without Bleeding With bleeding DHF DSS
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precedes rise in hematocrit. A rise of more than
5. Clinical management 20% indicates need for intravenous fluid
Depending upon severity of infection, management therapy.
of the cases differs. Early diagnosis & admission of If hematocrit determination is not possible,
DHF patients is important in order to reduce case hemoglobin estimation may be carried out as an
fatality rates. alternative.
Hematocrit should be determined daily from
5.1. Dengue fever the third day until the temperature remains
normal for one or two days.
Management of Dengue fever is symptomatic and
supportive. Paracetamol is recommended to keep
temperature below 400c. Dosages of
Bed rest is advisable during acute febrile phase.
paracetamol recommended are: 1 - 2 years: 60-
Antipyretics and sponging is essential to keep
120 mg/dose, 3 - 6 years: 120 mg/dose & 7 - 12
body temperature of patient below 370C. Do
years: 240 mg/dose.
not prescribe Salicylates (Aspirin) to suspected
Plenty of fluids like ORS & or fruit juices
DF patient. Paracetamol is preferred.
should be given orally, to the extent patient
Analgesic or a mild sedative may be prescribed
tolerates.
for severe pain.
Management of Grade II DF/DHF
ORS solution is recommended for patients with
excessive sweating, nausea, vomiting or Any person who has DF with
diarrhoea to prevent dehydration. thrombocytopenia & hemoconcentration &
Patients should be monitored in DHF area until presents with abdominal pain, black tarry
they become afebrile & after platelet & stools, epistaxis, bleeding from gums etc. needs
hematocrit determinations are normal. to be hospitalized. Such patient should be
observed for signs of shock.
5.2 Dengue Hemorrhagic Fever The critical period for development of shock is
transition from febrile to afebrile. phase of
Management of Grade I DF/DHF
illness, which usually occurs after third day of
Management during febrile phase is similar to
illness.
that of DF.
A rise of hematocrit of 20% or more reflects
Patient should be monitored closely. Critical
need for IV fluid therapy.
period for monitoring is transition from febrile
to afebrile stage, which usually occurs after If despite of treatment, patient develops features
third day of illeness. of shock, management of grade III & IV should
be started.
Platelet count & hematocrit estimation is
essential. Blood transfusion may be indicated in patients
with severe shock, massive bleeding and DIC.
Drop in platelet count to <1,00,000/cumm i.e.
1-2 platelets per oil immersion field usually
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5.3. Figure-2: Management of grade I & II DHF - Volume replacement flow chart
Hemorrhagic tendencies, Thrombocytopenia, hematocrit rise, pulse

pressure low
Initiate IV therapy 6ml/kg/hr with crystalloid solution for 1 - 2 hours
Improvement No Improvement
Reduce IV 3ml/kg/hr Increase IV 10ml/kg/hr

crystalloid solution, 6-12 hrs crystalloid solution, 2 hrs
Further Improvement
No Improvement
Improvement
Unstable vital signs
Discontinue IV after
24 hrs
Hematocrit rises Hematocrit falls

Reduce IV 6ml/kg/hr
cry. solution, with
further reduction to IV colloid Dextran Blood transfusion
3ml/kg/hr, discontinue (40) 10ml/kg/hr, 10ml/kg/hr,
after 24-48 hrs duration 1 hr duration 1 hr
Improvement
IV therapy by crystalloid. Successively reduce the flow from 10 to 6 & 6

to 3ml/kg/hr. Discontinue after 24 - 48 hours
Improvement: Hematocrit falls, pulse rate & BP stable, urine output rises
No improvement: Hematocrit, pulse rate rises, pulse pressure falls below 20 mm Hg, urine
output falls
Unstable vital signs: Urine output falls, signs of shock
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Figure-3: Management of grade III & IV DHF - Volume replacement flow chart
Unstable vital signs

Urine output falls, signs of shock
Immediate, rapid volume replacement: Initiate IV

therapy 10-20 ml/kg/hr crystalloid solution for 1 hr
Improvement No improvement
IV therapy by crystalloid. Oxygen
Successively reduce the flow from 20

to 10, 10 to 6 & 6 to 3ml/kg/hr.
Hematocrit Hematocrit falls

Further RISESRISESNBN
Improvement
IV colloid (Dextran 40) or plasma Blood transfusion 10

Discontinue IV 10 ml/kg/hr as IV bolus (repeat if ml/kg/hr if, hematocrit is
after 24 hrs necessary) still more than 35%
Improvement
IV therapy by crystalloid.
Successively reduce the flow from 10 to 6 & 6 to

3ml/kg/hr. Discontinue after 24 - 48 hours
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47. LEPTOSPIROSIS
Hypotension & circulatory collapse.
1. Introduction
Jaundice Important clinical feature.
Leptospira is an infectious disease caused by
spirochetes leptospire interrogans Mild to severe.
Leptospires enter the host through abrasions in the Starts after 4 to 7 days of illness.
skin or through intact mucosa, especially the Hepatomegaly liver tenderness usually present.
conjunctiva and the lining of oro- and nasopharynx
when they come in contact with water contaminated Almost invariably present is renal involvement.
with leptospira. ATN and interstitial nephritis are pathologic
features.
2. High risk group
Hematuria and cola coloured urine with RBC
Agricultural workers. casts.
Fisherman,sewer workers. Oliguria and anuria.
Lorry drivers and masons. Edema, facial puffiness, breathlessness,
Usually starts at the onset of rainy season and convulsions.
declines as the rains recede. Renal impairment worsens in 1st to 2nd week,
recovers by the end of 4th week with treatment.
3. Anicteric leptospirosis
Lung-Hemorrhagic pneumonitis with interstitial
Acconts for 90% cases, usually recover completely and alveolar hemorrhages.
with proper treatment.
High mortality.
Fever - with chills. Moderate to severe.
Death occurs within few hrs to 2 days.
Myalgia very characteristic finding. Calf,
abdominal& lumbosacral muscles are very Mild cases- cough, chest pain and hemoptysis.
painful & severely tender. Increase in serum
Severe cases- breathlessness increases and
Creatinine Phosphokinase.
patient goes into respiratory failure.
Conjunctival Suffusion reddish colouration.
Pancreatitis and acalculous cholecystitis can
Headache commonly in frontal region.
occur.
Renal involvement is invariable.Asymptomatic
Cardiac involvement
in the form of mild proteinuria with few casts in
urine. Hypotension shock- cold clammy skin,
tachycardia and hypotension due to dehydration
Cough chest pain & few cases hemoptysis.
and peripheral vasodilation.
Bleeding tendency in few cases.
Arrhythmias- palpitations, syncope and irregular
All cases of fever with myalgia & conjunctival pulse, AV blocks and ST and T wave changes.
suffusion should be considered as a suspect case
CNS Meningitis usually present. Headache,
of leptospirosis.
irritability, restlessness, seizures and late stage is
coma.
4. Icteric leptospirosis
Maculopapular erythematous skin lesions over
Weils disease. face, trunk and extrimities.
Fever, Myalgia, Headache, Conjunctival Bleeding in leptospira not directly related to the
suffusion. level of thrombocytopenia.
Oliguria, anuria, proteinuria.
Nausea, vomitting,diarrhoea, abominal pain.
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Rise in enzyme level is not very high as
5. Investigations compared to that in viral or alcohalic hepetitis.
CBC Thrombocytopenia is characteristic. Raised CPK helps to differentiate from viral and
LFT direct hyperbilirubinemia., raised alcoholic hepatitis.
Alk.PO4 ,rise in bilirubin is very fast & reaches Raised serum creatinine levels.
high level. Urine albuminuria.
Table 1: Lab Investigations for Leptospirosis
CULTURE MICROSCOPY IMMUNOLOGICAL MOLECULAR
Blood (10 days) Dark Field MAT PCR

Urine (10-30 days) Silver impregnation ELISA
CSF (5-10 days) Latex agglutination tests
Labotratory diagnosis for current leptospirosis AVOID NEPHROTOXIC DRUGS in cases with
renal involvement
Culture positive
Severe cases- meticulous correction of
MAT- seroconversion/four fold rise in the titre
hypovolumia and electrolyte imbalance, fluid
High titre management as per CVP.
ELISA/Latex agglutination positive. Patient with renal failure may require
hemodialysis.
6. Treatment
6.1 Mild Case 7. Complications
Tab. Doxy 100 mg BD for 7 days Fluid overload, hyperkalemia, acidosis
Cap. Ampi and Cap. Amox 30-50 mg/kg 5-7
LUNG INVOLVEMENT-Continue O2 therapy
days.
Inj. CP 20 lac units 6 hrly AST for 5-7 days or In patients with alveolar hemorrhages with
Inj ampicillin 500mg-1 gm 6 hrly 5-7 days ARDS, they require mechanical ventilation with
low tidal volume and high PEEP.
Mortality is very high.
6.2 Severe case Supportive treatment with Platelet conc, FFP, Vit
K.
Inj. Ceftriaxone/ Cefotaxime or Erythromycin
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48. INFLUENZA A- H1N1 (SWINE FLU)
We have faced pandemic of this Communicable air

borne disease in 2009. This is commonly known as
5. Mode of transmission
swine flu. Influenza spreads form person to person by droplet
infection created by sneezing, coughing or talking.
1. Epidemiological factors The portal of entry is the respiratory tract.
Pandemic Influenza A (H1N1) 2009, currently the

most common circulating strain of influenza virus
6. Incubation period
globally, first caused illness in Mexico and the It could range from one to seven days, and most
United States in March and April, 2009. likely from one to four days.
2. Agent factors 7. Signs and symptoms

The causative agent is Influenza virus. It is an An acute Respiratory Tract Infection (RTI), caused
enveloped RNA virus and belongs to the family by Influenza virus, characterised by sudden onset of:
Fever/chills, Headache, myalgia, Sore throat, Cough,
orthomyxoviridae. The size of the virus is 80-200 nm
Coryza, and Prostration.
/.08 -0.12 micron in diameter. There are three types Range of symptoms differs by age. Vomiting &
of influenza viruses, namely A, B & C which are diarrhea in children/elderly. Fever alone in infants
characteristically distinct and bear no cross may be atypical in elderly. Serious complications can
immunity. The virus contains two surface antigens H occur among high risk groups.
(hemagluttinin) and N (neuraminidase).
8. Diagnosis
3. Host factors The recommended test to confirm the diagnosis of
H1N1 influenza A virus is real-time Polymerase
The disease can occur in all ages and both sexes. Chain Reaction (RT-PCR) in designated laboratories.
Also viral culture and four-fold rise in new influenza
4. High Risk Groups A (H1N1) virus-specific eutralizing antibodies can be
done.
These risk groups include:
8.1. What sample to be collected?
Children younger than 5 years old;
Nasopharyngeal/oropharyngeal swabs.
Adults 65 years of age and older;
Brochoalveolar lavage.
Chronic pulmonary condition (including
Tracheal aspirates.
asthma), cardiovascular (except hypertension),
renal, hepatic, hematological (including sickle
Nasopharyngeal/oropharyngeal aspirates as
washes.
cell disease), neurologic, neuromuscular, or
metabolic disorders (including diabetes Samples should be collected in VTM.
mellitus);
8.2. Transportation of samples:
Immunosuppression, including that caused by
medications or by HIV; All samples should be kept at 2-8 degree Celsius
Pregnant women; until they can be placed at -70 C.
Residents of nursing homes and other chronic- Samples transported on dry ice in triple
care facilities; packaging.
Obesity. Clear labels with patients complete information.
Samples should be sent to within 24 hrs.
Page 113
9. Treatment Patients on long term cortisone therapy.
Obese persons.
Treatment with oseltamivir or zanamivir is
No tests for H1N1 is required for Category-B
recommended for all people with suspected or
confirmed influenza who require hospitalization. It is (1) and (2).
given in a dose of 75 mg Bid in adults.
All individuals seeking consultations for flu like All patients of Category-B (1) & (2) should
symptoms should be screened at healthcare facilities confine themselves at home and avoid mixing
both Government and private or examined by a with public and high risk members in the family.
doctor and these will be categorized as under: Broad Spectrum antibiotics as per the Guideline
for Community-acquired pneumonia (CAP) may
9.1. Category- A be prescribed.
Patients with mild fever plus cough / sore

throat with or without bodyache, headache,
9.3. Category-C
diarrhoea and vomiting will be categorized as In addition to the above signs and symptoms of
Category-A. They do not require Oseltamivir Category-A and B, if the patient has one or more of
and should be treated for the symptoms the following:
mentioned above. The patients should be
Breathlessness, chest pain, drowsiness, fall in
monitored for their progress and reassessed at 24
blood pressure, sputum mixed with blood, bluish
to 48 hours by the doctor.
discolouration of nails;
No testing of the patient for H1N1 is required.
Children with influenza like illness who had a
Patients should confine themselves at home and
severe disease as manifested by the red flag signs
avoid mixing up with public and high risk
(Somnolence, high and persistent fever, inability
members in the family.
to feed well, convulsions, shortness of breath,
difficulty in breathing, etc).
9.2. Category-B Worsening of underlying chronic conditions.
1. In addition to all the signs and symptoms

All these patients mentioned above in Category-C
mentioned under Category-A, if the patient has
require testing, immediate hospitalization and
high grade fever and severe sore throat, may
treatment.
require home isolation and Oseltamivir;
2. In addition to all the signs and symptoms
mentioned under Category-A, individuals having 9.4. Oseltamivir Medication -Doses
one or more of the following high risk conditions Details
shall be treated with Oseltamivir:
Children with mild illness but with predisposing Oseltamivir is the recommended drug for treatment.
risk factors.
In the current phase, if a person confirms to the case
Pregnant women;
definition of suspect case, should be provided
Persons aged 65 years or older;
Patients with lung diseases, heart disease, liver Oseltamivir.
disease,kidney disease, blood disorders, diabetes,
neurological disorders, cancer and HIV/AIDS;
Page 114
Dose for treatment is as follows:
By Weight:
For weight <15kg 30 mg BD for 5 days
15 -23kg 45 mg BD for 5 days
24 -<40kg 60 mg BD for 5 days
>40 kg 75 mg BD for 5 days
risk persons (DM, HT, Obese, Respiratory diseases,

10. Vaccine Immuno comproised).
A Vaccine is available for swine flu. It gives imunity
for one year. It is given to pregnant mothers, high
Page 115
49. DIARRHOEAL DISEASES
Diarrhoeal diseases include acute diarrhoea, Acute diarrhoea Cholera, Rota virus, Food
persistent diarrhoea (diarrhoea duration two weeks poisoning, gastrointestinal disorders and
or more) and dysentery (blood stained stools with medications (rare).
fever). Diarrhoeal diseases are one of the most
common causes of epidemic in our State. Most of Persistent diarrhoea Chronic bacterial
the deaths in diarrhoeal diseases are due to infections, inflammatory bowel disorders,
dehydration which is preventable by timely and malabsorption syndrome.
adequate replacement of fluids. Dysentery Amoebiasis, Giardiasis,
Shigellosis.
1. Following are important
causes of diarrhoeal
diseases in rural areas
Table-1: Diagnosis of diarrhoea

Sign/symptom Acute diarrhoea Persistent diarrhoea Dysentery
Frequency of stools/day Three or more Three or more Three or more
Consistency of stools Watery Variable Variable
Duration of diarrhea Less than 2 weeks Two or more weeks Less than 2 weeks
H/o fever No Variable Yes
H/o blood stained mucus No Variable Yes
Effect on appetite No Loss of appetite Loss of appetite
Dehydration Important, may lead to Patient may have Patient may have
severe dehydration if not some dehydration. some dehydration
treated in time.
Treatment principle Management of Start management of Start management of
dehydration is priority dehydration. dehydration.
Simultaneously find Simultaneously start
cause of persistent appropriate
diarrhoea and treat antibiotics.
accordingly.
Long term effects No long term effect for If not treated Repeated attacks may
occasional episodes. correctly, child may lead to Protein
Repeated attacks may get severe Protein Energy Malnutrition
lead to PEM. Energy Malnutrition
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Table-2: Dehydration Diagnosis Chart
Severity of symptoms and signs (Encircle the finding)
Sign/Symptom
No dehydration Some dehydration Severe dehydration
General condition of Patient well alert Restless and irritable Lethargic, unconscious,
Patient floppy
Presence of thirst Normal/not thirsty Thirsty, drinks water Not able to drink
immediately when
offered
Dryness of mouth and Moist mouth and tongue Mouth and tongue dry Mouth and tongue very
tongue dry
Condition of eyes Normal Sunken Very sunken, patients
face looks like old
man's face.
Condition of tears Tears appear while Tears appear while No tears, dry eyes even
crying crying in crying child
Skin turgor Normal. Pinch to skin Pinch slowly goes back Pinch remains as it is
immediately goes back and takes some time to for 2-3 seconds and then
to normal. become flat. slowly goes back.
Classification of No dehydration Some dehydration Severe dehydration
dehydration
Treatment of Plan A Plan B Plan C
dehydration
Symptoms and signs of cholera are entirely due to

2. Important diseases causing loss of large volume of isotonic fluid and resultant
diarrhoea or dysentery in depletion of intravascular and extra vascular fluid
leading to severe dehydration, metabolic acidosis
adults and hypokalemia. Patient develops thirst, cramps,
Cholera and anxiety due to depleting isotonic fluid.
Cholera is the most important diarrhoeal disease Diagnosis

which leads to rapid dehydration. Suspect cholera when patient has severe watery
Etiologic agent diarrhoea and vomiting. Collect stool sample of
suspected cases in Cary Blair media and transport to
Cholera is caused by bacteria Vibrio cholerae which District Public Health Laboratory. However,
exists in two biotypes, Classical and El tor. Each treatment and control measures should be started
biotype is further divided into two subgroups Inaba immediately on the basis of clinical
and Ogawa. symptomatology without waiting for laboratory
Clinical manifestations confirmation.
Cholera is an acute infection of small intestine Treatment

manifested as watery diarrhoea and vomiting. Carefully examine patient for signs of dehydration
Clinical spectrum of cholera is broad, ranging from and treat as per dehydration status. Most important
in-apparent infection to cholera gravis, which may treatment of cholera is rehydration of patient with
be fatal in few hours. Incubation period of 24 to 48 ORS and Ringers Lactate. In addition to this, start
hours is followed by abrupt onset of painless, one of the following antibiotics to patient -
profuse and watery diarrhoea associated with
vomiting. Cap. Doxycycline 6 mg/kg/ day as a single
dose for 3 days OR
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Cap. Tetracycline 50mg/kg/day in 4 divided Principle of treatment
doses for 3 days OR
As diarrhoea is continuing, there is continuous loss
Tab. Erythromycin 30mg/kg/day in 3 divided of water and electrolytes from body of patient
doses for 3 days. which may lead to dehydration. Therefore principle
of Plan-A schedule is correction of whatever loss of
3. Diagnosis of dehydration water and electrolytes before the patient develops
signs of dehydration. Plan-A can be advised at
Although number of organisms are responsible for home to caretaker of patient. However make sure
causing diarrhoea, clinical presentation is same i.e. that care taker has understood danger signs of
passage of watery stools leading to dehydration in dehydration (like thirst). Following steps are
all these cases. Therefore assessment of recommended in Plan-A.
dehydration status and correct management of
dehydration by ORT is mainstay of diarrhoeal a. Home available fluids
disease control programme. Advise to give Home Available Fluids (HAF)
e.g. sarbat, lassi, vegetable soup, khir,
4. Management of buttermilk, tea, coconut water, etc. i.e. any
dehydration liquid available at home to patient as much
he/she can drink.
Most important aspect in management of diarrhoeal
diseases is correction of dehydration. Continue breast feeding and feeding If child
is being breastfed, then breast-feeding should
Treatment of dehydration is divided into three plans be continued. Regular feeding of non-breast fed
as follows - child should also be continued.
Plan-A: For patients with no dehydration b. ORS to prevent dehydration
principle is to prevent dehydration.
If frequency and amount of diarrhoea is not
Plan-B: For patients with some dehydration declining or amount of stool is large, then start
principle is treatment of some dehydration and ORS.
preventing patient from going into severe
dehydration. Contents of WHO ORS are as follows (New
low osmolarity ORS).
Plan-C: For patients with severe dehydration -
This is life saving plan. Rehydrate patient as Sodium chloride - 2.6 grams
early as possible and prevent from going again Potassium Chloride - 1.5 grams
into severe dehydration.
Trisodium Citrate - 2.9 grams
Description of treatment plans in details is as
follows. Glucose - 13.5 grams
4.1. Plan-A
Plan-A is for patients who are having diarrhoea but
no signs of dehydration.
Dissolve the packet in one litre of water to prepare Add whole packet of ORS into one-litre of
ORS. water and stir till all powder is dissolved. Now
ORS is ready for use.
Show caretaker how to prepare ORS.
Following steps should be carried out for Give ORS by cup or spoon to small children
preparation of ORS - and by glass to bigger children and to adults as
per indicated dose.
Take clean pot of one and half litre capacity
and one clean spoon. If patient has vomiting, wait for 5 minutes and
start again.
Pour 1 litre of clean drinking water in the pot.
(No need to boil water). Keep ORS covered. Once prepared ORS should
be used within 24 hours. Do not use ORS
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beyond 24 hours, as there are chances of Less than 6 months - 50ml
contamination.
6 months to 2 years - 50 - 100 ml
If child develops swelling on eyelids, stop ORS
2 to 5 years - 100 - 200 ml
as it indicates overdose.
Ask her to give ORS in following doses after
passage of each liquid stool.
4.2. Plan -B Principle of treatment
Start Plan-B treatment to patients showing signs and Patient with some dehydration should be given ORS
symptoms of some dehydration as per dehydration for correction of dehydration.
diagnosis chart. Aim of this plan is to correct Dose of ORS: Dose of ORS is calculated preferably
dehydration and prevent patient from going into according to weight of patient. Give ORS in a dose
severe dehydration. of 100ml/kg in 4 hrs. If weighing is not possible,
calculate age wise ORS requirement for four hours
as follows
Table -3: Age wise ORS requirement for four hours
Age < 4 months 411 months 1223 months 2 4 years 5 14 years 15 + years
Dose 200-400 ml 400 600 ml 600 800 ml 800 1200 ml 1200 2200 ml 2200-4000 ml
Continue breast feeding and feeding If child is Re-examination of patient

being breastfed, then breast-feeding should be Re-examine patient after every four hours for status
continued. Regular feeding of non-breast fed child of dehydration with the help of Dehydration.
should also be continued.
Table-4: Management advice based on re-examination findings

Condition of patient on re-examination Management advise
Patient improves, no signs of dehydration on Keep patient under observation for 24 hours. Continue
examination and diarrhoea stops HAF. Observe if diarrhoea and/or vomiting start again.
Patient improves, no signs of dehydration on Continue giving ORS in doses suggested in Plan-A, re-
examination but diarrhoea continues examine after four hours.
Dehydration status same Continue with Plan-B. Check whether ORS is being
given in correct dose. Re-examine after four hours.
Signs of severe dehydration appear Switch on to Plan - C (start IV fluids). Continue to give
ORS as much as possible.
4.3. Plan C
If signs and symptoms of patient are suggestive of Principles of management
severe dehydration, start Plan C. This is Principle of management of severe dehydration is
emergency plan. Incorrect or incomplete replacing fluid loss by giving rapid IV infusion.
management of severely dehydrated patient may Only Ringer's lactate should be used as IV fluid and
lead to death of patient. Medical Officer must the dose is 100ml/kg body weight.
personally examine patient and treat for severe
dehydration.
Page 119
Table -4: Details of Ringers Lactate administration
Duration of
Age group Intensive phase Maintenance phase Remarks
treatment
Infants (0-1 30-ml/kg body wt. 70ml/kg body wt in Assess patient after
6 hrs
year) during first 1 hour. next 5 hours. every 6 hours
Older children 30-ml/kg body wt. 70ml/kg body wt in Assess patient after
3 hrs
and adults in first half hour. next 21/2 hrs. every 3 hours
Re-examination of patient dehydration with the help of dehydration diagnosis
chart and decide management plan as follows -
Re-examine patient after every six hours in infants
and three hours in adults for status of
Table-5: Treatment advice based on condition of patient
Condition of patient Treatment advise
Patient improves, no signs of dehydration on Keep patient under observation for 24 hours as patient
examination and diarrhoea stops may start diarrhoea/vomiting again
Patient improves, no signs of dehydration on Continue giving ORS (Plan-A)
examination but diarrhoea continues
Patient improves, signs of some dehydration Stop IV fluids after required dose is administered.
on examination. Continue giving ORS (Plan-B)
Dehydration status same Continue with Plan-C. Check for any complications
like anuria. If yes carefully examine the patient and
decide for referral. Continue giving IV during
transportation of patient.
ORS or Oral rehydration therapy (in case ORS is

5. Use of antibiotics and not available), irrespective of type of dehydration.
other drugs Zinc administration as per age of child:
Antibiotics are recommended only to suspected a) Children from 2-6 months:

patients of cholera and dysentery. Other drugs like Children aged between 2-6 months should be given
anti motility drugs, binding agents, anti secretary 10 mg of elemental zinc per day for a total period of
agents and steroids are not of any use in 14 days from the day of onset of diarrhoea. A tablet
management of diarrhea. They are harmful to of zinc contains 20 mg of elemental zinc. Therefore
patients and therefore not at all recommended for half tablet should be given to the children in this age
treatment. Judicious use of antibiotics is appropriate group. Zinc when supplied in the form of
in selected patients. Severely ill patients with febrile dispersible tablets, easily dissolves in breast milk or
dysentery can be treated with ciprofloxacin 500mg water. Therefore, in infants below 6 months of age,
bd for 3-5 days. the tablet should be given by dissolving in breast
Use of Zinc Tablets milk and in infants above 6 months of age, it should
be given by dissolving in breast milk or water.
Zinc Dosage Recommendation:
b) Children above 6 months:
Zinc is very safe drug and has a very large window
of safety. Zinc dispersible tablets are to be given in One full tablet (20mg) should be given to all
each diarrhoeal episode along with low osmolality children with diarrhoea above 6 months of age. It
should start from the day of onset of diarrhoea and
continued for a total period of 14 days.

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50. RHEUMATOID ARTHRITIS
Early morning joint stiffness lasting more than 1
1.Introduction hour and easing with physical activity.
Rheumatoid arthritis (RA) is a chronic inflammatory Earliest involved joints typically the small joints
disease of unknown etiology marked by a symmetric, of the hands and feet.
peripheral polyarthritis. It is the most common form The wrists, metacarpophalangeal (MCP), and
of chronic inflammatory arthritis and often results in proximal interphalangeal (PIP) joints stand out
joint damage and physical disability. as the most frequently involved joints.
Flexor tendon tenosynovitis is a frequent
hallmark of RA.
2. When to suspect Deformities are swan-neck deformity,
boutonnire deformity, Z-line deformity.
The incidence of RA peaks between 25 and 55
years of age.
Figure-1: Hand changes in RA
Extra-articular features
i. Neurologic-atlanto-axial dislocation, cervical
3. Investigations
myelopathy. The clinical diagnosis of RA is largely based on signs
ii. Hematological-anemia of chronic disease, and symptoms of a chronic inflammatory arthritis,
neutropenia, splenomegaly, feltys syndrome. with laboratory and radiographic results providing
iii. GI-vasculitis. important supplemental information.
iv. Skeletal- osteoporosis.
v. Ocular-episcleritis, scleritis, 3.1 Rheumatoid factor
keratoconjunctivitis sicca.
Serum IgM RF found in 75-80% of RA patients;
vi. Oral -xerostomia, periodontitis.
therefore the negative result does not exclude RA.
vii. Pulmonary pleural effusion, pulmonary
nodules, interstitial lung disese, pulmonary Found in other connective diseases as well.
vasculitis, organizing pneumonia.
viii. Cardiac- pericarditis, IHD, myocarditis, 3.2 Anti CCP antibodies
cardiomyopathy, mitral regurgitation.
Highly specific 95%
ix. Renal membranous nephropathy.
x. Skin rheumatoid nodules, pyoderma So, useful for distinguishing RA from other forms of
gangrenosum. arthritis.
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3.3 Synovial fluid analysis- Other findings include soft tissue swelling,
symmetric joint space loss, subcondral erosions.
Inflammatory state.
Synovial fluid WBC count ranges from 5000 to
3.5 MRI
50000 WBC/u3. Offers greatest sensitivity for detecting synovitis,
joint effusions as well as early bone and bone marrow
Useful for confirming inflammatory arthritis,
changes.
excluding infection or crystal induced arthritis.
3.4 X ray hands

Juxta articular osteopenia, 4. Treatment
Table-1: Treatment of RA
Non pharmacologic treatment Pharmacologic treatment

Counselling, physical therapy, diet NSAIDS
Stress reduction, exercise Glucocorticoids
DMARDS
4.1 NSAIDs 4.3 DMARDS

Tab. Ibuprofen (200 mg BD or TDS) / Tab. Hydroxycloroquine, Methotrexate, Leflunomide,
Diclofenac (50 mg BD) - Now considered to be Sulfasalazine, Biologicals, anti TNF agents,
adjunctive therapy for management of symptoms Rituximab.
uncontrolled by other measures.
5. When to refer
4.2 Glucocorticoids Severe case of rheumatoid arthritis not responding to
first line therapy (Hydroxycloroquine, Methotrexate,
May be administered in low-to-moderate doses to NSAIDS), with extra articular manifestations should
achieve rapid disease Control before the onset of be referred to Higher institute for further work up.
fully effective DMARD therapy, which often takes
several weeks or even months.
Page 122
51. SNAKE BITE
Immobilisation of the part, Getting to Hospital
1. Introduction without delay and Telling the doctor of any
Envenoming by poisonous animals (Snakes, symptoms that develops.
Scorpions, Wasps, Ants and Spiders) is an
occupational hazard often faced by farmers, farm
laborers. Poisoning by venomous snakebite is a 2. Common Poisonous snakes
common acute life-threatening time-limiting medical
emergency.The majority of current first aid methods in India
adopted by the victims such as tourniquet, cutting and
suction and herbal remedies are completely (1) Cobra (2) Krait (3) Russells Viper (4) Saw
ineffective and dangerous. It is now recommended to Scaled Viper (5) Indian Pit Viper
adopt what has been called the Do it R.I.G.H.T. (6) Sea snake
approach, stressing the need for Reassurance,
HISTORY OF SNAKE BITE
ABSENT LOCAL EDEMA PRESENT
Floor bed BLEED

Neuroparalysis DIC Bleeding
SHOCK
Abdominal colic l RF
Pain Pain
Neuro-paralysis
RUSSELLS ECHIS
KRAIT COBRA VIPER CARINATUS
ASV, Ventilator ASV, N + A, ASV, Dialysis, ASV, Dialysis,

N+A Ventilator Blood transfusion Blood transfusion
Snake Bite: Diagnostic Algorithm and Treatment

(ASV- Antisnake venom, N- Neostigmine, A- Atropine, RF- renal failure, DIC- Disseminated intravascular
coagulation)
(Bungarus Caeruleus)
3. Clinical manifestations
Local Names- Kala gandait, Kala taro, Kandar,
3.1. Common Indian Krait Manyar chitti, kattu viriyan and valla pamboo.The
Page 123
common krait is regarded as the most dangerous AChEI or not can be confirmed by putting ice-filled
species of venomous snakes in the Indian glove finger over eyelid. Hypothermia sensitizes the
subcontinent. Majority of krait bite cases are reported Ach receptors of acetyl choline. If there is slight
between 11pm 5 am. improvement in ptosis, you can try AChEI.
Neostigmine 50ug/kg over first hr. & then 25 ug/kg
Symptoms
in the next hour preceded by Atropine
Mild pain at the site
Parasthesia or numbness 3.2. Cobra Bite
Abdominal pain/vomiting/chest pain Cobra bite tends to occur during day time.
Difficulty in bringing tongue beyond teeth
margin Symptoms
Slurred speech Pain at site
Difficulty in breathing Progressive swelling /ecchhymosis
Signs Blurred vision
Bradycardia, hypotension Signs

Bilateral ptosis, external ophthalmoplagia, Sinus bradycardia, hypotension
dysphagia Ptosis, bulbar palsy
Paralysis, coma Respiratory depression
Management Management
(a) First aid at home or place where bite happens: Victim should not be allowed to walk or run and the
If one succeeds in locating the bite site on the bitten part should be kept below heart level.
victims body, clean the surface where venom is On arrival 100ml (10 vial) ASV to be added to 200
deposited by clean cloth or cotton. Keep the bitten c.c. of normal saline run over 30-50 minutes.
part below heart level.
Maximum dose 200-250ml (20-25 vials).
Neostigmine 50ug/kg over first hr. & then 25 ug/kg
(b) At hospital: in the next hr preceded by Atropine
Thorough clinical examination including If patient develop respiratory paralysis intubate the
neurological exam patient and refer to higher centre
Haemogram, urine exam, ECG, serum electrolytes, Local wound care is done by intravenous antibiotic,
renal profile sterile dressing and skin grafting of all victims with
Anti-snake venom (ASV): non-healing wound.
- On arrival 100ml (10 vials) ASV to be added to 3.3. Sea snakes

200 cc of normal saline run over 30-50 minutes. Sea snake bite cases are reported from coastal region.
- Repeat dose of 100ml (10 vials) after 30 min if Fishermen accidentally handle sea snake resulting in
no improvement in neurological manifestation. envenoming. Its venom is neurotoxin, myotoxic and
haematotoxic.
- Maximum dose 200ml (20vials).
Symptoms
Ventilation
Indicated if victim has pooling of saliva, unable to lift Headache
the neck from pillow, reduction in oxygen saturation, Nausea
respiratory failure, abdominal-thoracic respiration, Vomiting
suffocation and signs of cerebral hypoxia. Tinglingnumbness
Refer the patient to higher centre with intubation and Foreign body sensation in throat
Ambu bag ventilation Swelling of tongue
Severe muscle pain
Anticholine esterase inhibitor (AChEI): Brown coloured urine
Indian common krait venom contains both pre and Signs
post synaptic blocker. Whether victim responds to
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Trismus Management
Muscular paralysis - No tourniquet
Respiratory arrest
Myoglobinuria - Bitten part should be kept below heart level
Management - No intramuscular injection unless 20MWBCT is

done and blood clots within 20 minutes.
On arrival 100ml (10 vial) ASV to be added to 200 cc
of normal saline run over 30-50 minutes. 20 minutes whole blood clotting test (20 MWBCT)
Ventilator for respiratory failure. Refer to higher Before injection of ASV take 2-3 ml of blood in a
centre with intubation. new dry glass test tube which is not irrigated by any
detergents. Keep the tube undisturbed for 20 minutes
Correction of hyperkalemia- Calcium gluconate, and then tip it off. If blood does not clot, it confirms
insulin glucose drip (10% dextrose 100ml add 12 hypofibrinogemia. ASV 100 ml (10 Vials) ASV
units insulin for 6hrs), salbutamol nebulization or diluted in 200 ml of 5% dextrose run over 30 minute
dialysis. by intravenous route. If external bleeding does not
stop within 20-30 minutes one can repeat 50 ml of
3.4. Russells viper ASV. Thrombocytopenic, abnormal fragmented
RBCs are a diagnosis of DIC. In addition, if victim
It is found in South Asian Countries. In Pakistan,
is too late in such situation in addition to ASV one
India, Sri Lanka, Bangladesh, Burma and Thailand it
has to try plasma products and whole blood
ranks amongst the most important causes of snakebite
transfusion which is rarely required if ASV is
mortality. With protecting the paddy, wheat by
administered in time with adequate dose.
containing rodents (rats), the Russells viper kills
Hypotension is to be managed with fluid and
many farmers unlucky enough to treat on it during
inotropic agents. Severe hypotension due to bleed in
harvesting.
adrenal and pituitary glands and abdominal bleed and
Symptoms endothelial dysfunction with capillary leak needs
heavy doses of intravenous methyl-prednisolone and
Severe local pain at the site of bite. correction of electrolytes.
Rapid swelling progresses to whole limb
within six to eight hours. Renal failure
Signs One should keep in mind and look for renal failure
from the time of admission. Risk factors such as
Regional lymphagntis with ecchymosed hypotension, hypovolumia can be corrected.
skin. Intravenous frusemide 80-100 mg and oral acetyl
Development of compartment syndrome cysteine 600mg three times a day may help to arrest
characterized by swelling, hypotension and the renal damage.
shock.
Refer to higher centres for haemo-dialysis, if needed.
Renal dysfunction 3.5. Saw scaled viper or Carpet

20-40% cases subsequently develop anuria, oliguria, viper or Echis-cariniatus
acute renal failure. Renal angle tenderness is most Farmers, hunters, labourers and persons walking bare
important clinical sign for early diagnosis of renal foot or in jungle and rocky areas are often bitten by
failure. There is serial rise in blood urea and serum this snake.
creatinine with acidosis and hyperkalaemia.
Generalized anasarca, renal failure is due to tubular Clinical manifestations
damage by venom itself.
Soon after the bite within one hour there is
Hemoglobinuria, hypotension and micro thrombi in development of swelling over the bitten part.
the kidney contribute to the acute tubular necrosis Swelling progresses in more than one segment. The
which is the most common cause of death. Ptosis, victim experiences a painful lymphadenopathy at the
bulbar palsy, internuclear opthlamoplegia and drainage area of the bitten part.
respiratory paralysis due to presynaptic
neuromuscular block in a Russells viper bite At times if the patient remains untreated, bleeding
poisoning are often seen and reported from kerala persists for 1-2 weeks in the form of blood stain
(South India) and Sri Lanka. sputum, haematuria and disappears on its own. Such
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patients are markedly anemic and report to hospital The approximate serum half life of antivenom in
for weakness or non-healing cellulites with envenomed victims ranges from 26 to 95 hours.
uncontrolled bleeding from cellulites. Before discharge envenomed victims should be
closely observed daily for minimum 3 to 4 days.
Management
ASV doses and repeat doses
Local wound care
The recommended initial dose of ASV is 8 to 10 vials
ASV required is 30-50 ml administered over 1 hr.
3.6. Green pit viper and bamboo Repeat doses for neurotoxic species is based on 1-2
hr rule.
pit (Trimeresurus)
Repeat doses for haematotoxic species is based on
Pit viper victims report during the monsoon season. the 6 hr rule.
Clinical manifestation The maximum recommended dose for neurotoxic bite
is 20 vials of ASV.
It shows up in sudden rapid development of massive
edema without regional involvement. Rarely the The maximum recommended dose for haematotoxic
victim manifests external bleeding or renal failure. bite is 30 vials of ASV.
Management
ASV Reactions
Antivenom should be administered as soon as signs
of systemic or severe local swelling are noted. No ASV test doses are to be administered.
At the first sign of an adverse reaction the ASV is
The mean times between envenoming and death are
halted
8 hours (12 minutes to 120 hours) in cobras, Adrenaline 0.5 ml is given SC
18 minutes (3-63 hours) in bungarus caeruleus, Steroid and antihistamine perform a secondary
supportive function to Adrenaline.
3 days (15 minutes to 264 hours in Russells viper (National Snakebite Management Protocol 2008)
5 days (25 to 41 days) for echis carinatus.
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52. SCORPION STING
1. Introduction Grade 1: Severe excruciating local pain at the

sting site radiating along with corresponding
Scorpion envenomation is an occupational dermatomes, mild local oedema with sweating at the
hazard for farmers, farm labourers, migrating sting site, without systemic involvement.
population and hunters.
Grade 2: Pain, paresthesias remote from the site
The endemic areas are western Maharashtra, of sting, in addition to local findings.
Karnataka and Konkan Region.
Severe Scorpion stings are due to Grade 3: Either cranial nerve / autonomic
MesobuthusTamulus species of scorpion. dysfunction.
Cold extremities, tachycardia, hypotension
2. Clinical features (Respiratory rate > 24 perminute, basal rales or
crackles in lungs).
2.1. The venoms of genera Hadrurus,Vejovis and
Uroctonus has local effects only including sharp Grade 4: Combined cranial nerve / autonomic
burning, swelling and discoloration at the bite site. dysfunction and somatic nerve dysfunction.
2.2. The second type of venom produced by the 4. Investigations

genera of the poisonous varieties of Centruroides and ECG- Tall T waves is a common finding. Others are
Mesobuthus contain neurotoxins which block sodium atrial arrhythmias, non sustained ventricular
channels. This leads to spontaneous depolarization of tachycardia, and various conduction defects seen.
parasympathetic and sympathetic nerves which Chest Xray- shows pulmonary edema.
results in stimulation.
In adults, the first time is rarely dangerous. But if the 5. Management
second time, the person may die if not treated soon. If it is for the first time in adult, do the following:
The body becomes allergic after the first sting. So it
Give Paracetamol if possible, put ice on sting.
is important to find out if he had an earlier scorpion
Infiltration of site with local anaesthetic may
sting. relieve pain and anxiety.
Anti histaminic tablets can be given
2.3. Severe pain, redness and swelling at the site of If the sting is for the second time in adult, or is
the sting. in children under 5, do the following
- IV Fluid management
2.4. Clinically autonomic storm evoked due to - Inj. Scorpion antivenom 30ml in 200ml of
venomous envenoming is characterized by transient normal saline neutralises circulating venom.
parasympathetic stimulation- vomiting, profuse - If evidence of myocarditis and pulmonary
sweating, ropy salivation bradycardia, ventricular pre oedema, strict bed rest and management of
heart failure is indicated.
mature contraction, priapism in male, hypotension
- Prazosin 0.5mg 3hrly orally for first 2 days
and prolonged sympathetic stimulation - cold (or 0.25mg in children and for adults) is
extremities, hypertension, tachycardia, pulmonary acceptable therapy
edema and shock. - Injection Frusemide 20 to 60mg I.V. to
control Pulmonary edema
3. Gradation - Inj.Dobutamine 5-20 microgram/kg/min I.V.
given in heart failure, tachycardia ,
On basis of clinical manifestations at the time of pulmonary edema with warm extremities
arrival to hospital and according to severity they are - Patients in Pulmonary edema may need inj
graded in 4 grades. NTG drip 5 microgram/kg
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- At times with severe respiratory distresss mechanical ventilation.
may need non invasive ventilation or
Stage- 1 - Stage- 2 Stage-3 - Stage-4 - Stage-5 -

(0-4hrs) (4-6hrs) (6-10hrs) (10-12hrs) (>12hrs)
- - - - - - - - - -
Sweating Hypertension - Tachycardia - Massive - Warm -
Salivation Tachycardia Hypotension pulmonary extremities
Mydriasis Cold extremiries Pulmonary edema edema Tachycardia
Priapism Cold extremities Hypotension
Hypertension Pulmonary
Hypotension edema
Cold Gray
extremities pallor(warm
shock)
- - - - - - - - - -
ASV + Prazosin ASV + - ASV +Prazosin - ASV - Dobutamine -
Prazosin + +
Dobutamine SNP or NTG
+
NIV/MV
Scorpion sting: stages, clinical presentation and treatment.ASV Anti Scorpion Venom, SNP- Sodium Nitro
Prusside, NTG- Nitroglycerine, NIV-Non inavasive ventilation, MV Mechanical Ventilatioin
Page 128
53. DOG BITE (RABIES)
Rabies can be transmitted by dog bites or licks of Treatment (post-exposure prophylaxis)
rabid animals on abraded skin and intact mucosa.
Other animals which can transmit rabies are cat, 2. Categories of dog bite
monkey, horse, sheep, goat, mongoose, jackal, fox,
Category I Touching or feeding animals, licks
hyena and bat. Exposure to rodents, rabbits and hares
on the intact skin
seldom, if requires specific anti-rabies treatment.
Category II Nibbling of uncovered skin, minor
1. Clinical features scratches or abrasions without bleeding, licks on
Prodromal symptoms- such as headache, malaise, broken skin
sore throat and fever last about 3-4 days. Pain and Category III Single or multiple transdermal
tingling at the bitten site. bites or scratches, contamination of mucous
Stage of excitation- Patient is intolerant to noise; membrane with saliva from licks; exposure to
bright light or a cold draught. Aerophobia may be bat bites or scratches
present. Hydrophobia is a characteristic symptom of The WHO recommended classification of animal bite
rabies. Examination shows increased reflexes, for post-exposure treatment should be followed.
dilatation of pupils, increased sweating, lacrimation Every instance of human exposure to a suspected
and salivation. Mental changes include fear of death, rabid or wild animal must be treated as a category III.
anger, irritability and depression. Convulsions may The post-exposure treatment is a three-pronged
occur resulting in death.The last stage is that of approach. All three carry equal importance and
paralysis and coma. The total duration of illness lasts should be done simultaneously:
for 2-3 days.
Table-1: WHO Guide for post-exposure treatment against rabies
Category
Type of contact with a suspect or confirmed rabid Recommended treatment.
domestic or wild animal or animal unavailable for
observation
I. Touching or feeding of animals Licks on None, if reliable case history is available
intact skin
Administer vaccine immediately. Stop treatment if
II. Nibbling of uncovered skin Minor scratches animal remains healthy throughout an observation
or abrasions without bleeding Licks on period of 10 days or if animal is killed humanely and
broken skin found to be negative for rabies by appropriate
laboratory techniques
III. Single or multiple transdermal bites or
scratches Contamination of mucous Administer rabies immunoglobulin and vaccine
membrane with saliva (i.e. licks) immediately. Stop treatment if animal remains healthy
throughout an observation period of 10 days or if
animal is killed humanely and found to be negative
for rabies by appropriate laboratory techniques.
A. Exposure to rodents, rabbits and hares seldom, if ever, requires specific anti-rabies treatment
B. If an apparently healthy dog or cat in or from a low-risk area is placed under observation, The situation
may warrant delaying initiation of treatment.
Page 129
C. This observation period applies only to dogs and cats. Except in the case of threatened or endangered
species, other domestic and wild animals suspected as rabid should be killed humanely and their tissues
examined using appropriate laboratory techniques.
Equine antirabies serum (ERIG) 40 IU/kg (max 3000

3. Treatment of dog bite IU), available in concentration of 300 IU/ml, given
3.1. Management of wound after prior skin sensitivity testing, single dose on day
0. Half the dose is infi ltrated around the bitten
Immediate washing of the wound is a priority. wound and the rest is given I.M.
Wound toilet must be done even if several hours or (Caution: A negative skin test must never reassure
days have elapsed. The wound is immediately the physician that no anaphylactic reaction will
flushed and washed with plenty of soap and water occur. Avoid alcohol, glucocorticoids and
(avoid direct touching of wounds with bare hands). chloroquine during vaccination; avoid multiple
Punctured wounds should be irrigated with the help needle injections into the wound. Must not exceed the
of catheters followed by 70% alcohol or povidone total recommended dose of IG as it may reduce the
iodine application.The application of irritants (like efficacy of the vaccine).
chillies, oil, turmeric, lime, salt etc.) is unnecessary
If the calculated dose of IG is insufficient to cover
and damaging.
infiltration in all wounds, sterile saline can be used to
Do not suture bite wounds immediately. If suturing is dilute 2 or 3 fold to permit thorough infiltration.
required, hold it for 24-48 hours, applying minimum
RIG is notindicated beyond the seventh day after
number of stitches under the cover of antirabies
administration of the first dose of vaccine.
Immunoglobulin locally. Anti tetanus treatment can
be given after local wound treatment.
3.2. Passive immunization with 3.3. Active immunization with

rabies immunoglobulin RIG) antirabies vaccine:
Local infiltration of RIG in category III rabies-RIG Antirabies vaccine (ARV)
should be infiltered in the depth and around the Intramuscular schedule.
wound even if the lesion has begun to heal followed
The course for post-exposure prophylaxis consists of
by administration of antirabies vaccine.
five injections (days 0, 3, 7, 14 and 28) irrespective
(Caution: RIG should never be administered in the of severity of exposure. The 6th injection (day 90) is
same syringe or at the same anatomical site as optional for immunologically deficient and extremes
vaccine). of age and on steroid therapy. The dose of vaccine
Doses of rabies immunoglobulin (IG) per injection is 2.5 IU/dose/ml for HDCV. Preferable
site is deltoid; anterolateral thigh in children
Human rabies immunoglobulin (HRIG) 20 IU/kg (Caution: Must NOT be given into gluteal muscle).
(max 1500 IU), available in concentration of 150
IU/ml, it does not require any prior sensitivity testing. Intradermal (ID) schedule.
SHOULD NEVER BE INJECTED (i) The 2 site ID TRC schedule (2-2-2-0-1-1) to be
INTRAVENOUSLY. The antirabies sera should administered: One ID injection of 0.1 ml per ID site
always be brought to room temperature (20-25C) over each right and left deltoid on days 0, 3, 7 and 0.1
before use. ml at a single site on days 28 and 90 or as per
Or updated TRC schedule (2-2-2-0-2) on days 0, 3, 7
and 28.
Page 130
Note: Correct ID injection should result in a raised at 1 site) on days 0 and 3, but no rabies
papule with an orange peel appearance. If a papule is immunoglobulin. Proper wound toilet should be
not observed, the needle should be withdrawn and done.
vaccine re-administered correctly nearby.
(ii) The 8-site ID method (8-0-4-0-1-1) for use with
4. Pre-exposure prophylaxis
HDC/PCECV in emergency, when no RIG is Indications: Laboratory staff working with rabies
available. virus, veterinarians, animal handlers and wildlife
officers. Three full IM or ID doses of tissue culture
The intradermal route is preferred as it reduces cost
vaccine given on days 0, 7, and 28. Laboratory staff
but must not be used in case of immunocompromised
and others at high continuing risk of exposure should
patients, individuals receiving long-term
have their neutralizing antibody titer checked every 6
corticosteroids or other immunosuppressive therapy
months. If it is less than 0.5 IU/ml, a booster dose of
or chloroquine.
vaccine should be given. Such individuals on getting
Antirabies vaccine should be kept and transported at exposed to rabies virus after successful pre-exposure
a temperature range of +2C to 8C. The immunization require only two booster injections of
reconstituted vaccine should be used immediately or vaccine given on days 0 and 3 without any antirabies
within 6-8 hours of reconstitution. serum/RIGs.
3.4. Post-exposure treatment of 5. Patient education

persons previously vaccinated Dog bite (category II and III) is an emergency and as
Managing re-exposure following post-exposure a general rule rabies postexposure treatment should
treatment with tissue culture vaccine (TCV) not be delayed or deferred.
If re-exposed, persons who have previously received Immediate washing with plenty of water and
full post-exposure treatment with a potent cell-culture disinfecting with alcohol/iodine.
vaccine should be given only two booster doses,
intramuscularly (0.5 ml/1 ml)/intradermally (0.1 ml
Page 131
54. POISONING
Anilides
1. Introduction
Poisoning due to the pesticides is increased due to the 3. Stepwise Case Approach
accessibility to the pesticides used in agriculture. Of
the total burden of acute pesticide poisoning the Diagnosis - Suspect and identify poison, if
majority of deaths are from self-poisoning with possible.
organophosphorus pesticides, aluminium phosphides Management includes basic principles,
and paraquat. antidotes, symptomatic and supportive
treatment.
2. Classification of Pesticides Anticipate complications, preserve evidence and
prevent sequelae as well as recurrence
2.1. Insecticides
Acetylcholinesterase inhibitors 4. Organophosphorus
Organophosphates
Carbamates
Compounds
Organochlorines Broadly OP compounds can be divided in to
Pyrethrins 1] Dimethyl compounds - Dichlorvos, Fenthion,
Pyrethroids Malathion, Methamidophos, Dimethoate
2.2. Herbicides 2] Diethyl compounds Chlorpyrifos, Diazinon,
Parathion-ethyl, quinalph
Dipyridyl pesticides
Paraquat and diquat 4.1. Mechanism of toxicity
Chlorphenoxyacetate weed killers
Bromoxynil, 2,4-D 1] Organophosphosphorus compounds inactivate
acetylcholinesterase by phosphorylation leading to
2.3. Fungicides accumulation of acetylcholine at cholinergic
synapses.
Substituted benzene
Chloroneb The rate of spontaneous reactivation of AChE is very
Chlorothalonil slow with diethyl OPs while it is relatively fast with
Thiocarbamates dimethyl OPs. Further, there is ageing of the
Organomercurials phosphorylated enzyme after which the enzyme
Methylmercury cannot be reactivated by oximes. The half-life of
Phenylmercuric acetate ageing of dimethlyphosphorylated and
diethylphosphorylated AChE in vitro is 3.7 hours and
Molluscicides Metaldehyde
33 hours, respectively, and the therapeutic windows
2.4. Rodenticides therefore are 13 and 132 hours, respectively (4 times
the half-life).
Aluminium phosphide
Zinc phosphide 4.2. Organophosphorus intoxication
Warfarin and superwarfarin compounds
Yellow phosphorus results in triphasic illness
Heavy metal : Thallium containing pesticides including
2.5. Insect repellants (a) Acute cholinergic syndrome
Diethyl toluamide (DEET) (b) Intermediate syndrome
2.6. Miscellaneous (c) Organophophate-induced delayed polyneuropath
Page 132
(a) Acute cholinergic syndrome 2. Further contamination is prevented by removal
from the site of exposure and of contaminated
Acute cholinergic syndrome may occur within clothing. Skin should be cleaned thoroughly with
minutes water.
Pathognomonic features via muscarinic and
nicotinic receptors- 3. The airway is cleared and high-flow oxygen is
administered.
Muscuranic effects Include miosis, bronchorrhoea,
salivation, lacrimation, pain in abdomen, bradycardia, 4. Direct mouth to mouth and nose resuscitation
urination, defecation must be avoided.
Nicotinic effects Muscle fasciculation, muscle 5. Following ingestion, gastric lavage must be done
cramps, flaccid muscle weakness with reduced within an hour of intake, followed by activated
tendon reflexes, tachycardia, hypertension charcoal via nasogastric tube after establishing
intravenous and airway protection.
Central nervous systemeffects Headache, dizziness,
confusion, convulsions, central respiratory Sample should be collected from the gastric lavage,
depression, coma sealed and handed over to the police registering the
medicolegal case.
(b) Intermediate syndrome
6. Convulsions are treated with intravenous
This begins 48 hours after poisoning in diazepam 10mg or midazolam 2mg.
approximately 20% of patients but may be
delayed for 72-96 hours. 7. Monitoring of ECG, blood gases, temperature,
The onset is often rapid with progression of muscular blood urea and serum electrolytes, amylase and
weakness from ocular muscles to neck and proximal glucose is mandatory.
limbs to respiratory muscles over 24 hours.
For muscuranic effects
Endotracheal intubation and ventilation are to be
Injection Atropine 1.8-3mg bolus immediately
done, if not instituted early, cyanosis, coma and
double the dose every 5minutes until atropinized.
death may follow rapidly.
Once patient is atropinized give 20%- 30% dose
(c) Organophosphate induced delayed required for atropinization as infusion/hour
polyneuropathy [5mg/hour]. The best guide to adequate atropinisation
is to monitor features of cholinergic poisoning
This occurs 1-3 weeks after acute exposure and (Bradycardia, Sweating, miosis, bronchorroea and
uncertain period following chronic exposure due hypotension). A confused, agitated, febrile patient
to degeneration of long myelinated nerve fibres. with no bowel sounds and a full bladder with urinary
Cramping muscle pain in the legs are followed retention certainly has atropine toxicity, indicating
by numbness and parasthesia in distal upper and the need to reduce or stop atropine temporarily.
lower limbs.
Symmetrical flaccid paralysis in distal muscles
especially in the legs. The dominant hand may For nicotinic effects
be more affected.
Pralidoxime chloride- Cholinesterase reactivator
4.3. Investigations which reverses the nicotinic effects and some CNS
effects. It is given 1gm bolus in 30minutes then
Plasma cholinesterase (pseudocholinesterase) is less infusion at 0.5gm/hour. (Loading dose of 30mg/kg
reliable. Red cell cholinesterase level falls to 20% of and 10mg/kg/hour infusion).
normal when symptoms appear.
4.4. Treatment of Treatment of the intermediate syndrome

Organophosphorus Poisoning
Early institution of ventilatory support, which may be
1. Airway, breathing and circulation should be required for a prolonged duration, is essential for
ensured and monitored. management. Close monitoring of respiratory
function such as chest expansion, arterial blood gas
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monitoring and oxygen saturation is essential to related to OCs, associated solvents may produce
identify the onset and monitor the progress of the aspiration pneumonitis.
intermediate syndrome. Some patients develop an
offensive and profuse diarrhoea and it is important to
maintain a close watch and a positive fluid balance. 5.5. Management
Recovery usually occurs without residual deficit.
Nasogastric aspirate may be useful if liquid
preparation has been taken and should be kept and
5. Organochloride handed over to medical official for medicolegal
purposes.
Compounds (OC)
Activated charcoal is given within 1hour of
5.1. The commonly used OC insecticides are Endrin, ingestion.
Aldrin, Benzene Hexachloride (BHC), Endosulphan, Seizures should be treated with Benzodizapenes.
Dieldrin, Toxaphene, DDT, Heptachlor, Kepone, (Diazepam 10mg or Midazolam 2mg I.V.)
Dicofol, Methoxychlor, etc. DDT, the most toxic OC, Patients should be kept on cardiac monitor. Use
is available in dry powder form or as a mixture with Dopamine instead of Epinephrine if patient has
other pesticides in powder or liquid form. hypotension, as OC compounds sensitise the
myocardium.
5.2. Mechanism of toxicity
OC compounds impair nervous system function by 6. Carbamate Poisoning
depolarization of the nerve membranes they also
Carbamate insecticides- Aldicarb,
cause sensitization of the myocardium to both
Carbofuranmethomyl inhibit a number of tissue
endogenous as well as exogenous catecholamines and
esterases-AchE. Aldicarb, Benomyl, Carbaryl,
predispose to arrhythmias.
Carbendazim, Carbofuran, Propuxur, Triallate, etc.
5.3. Clinical effects within minutes are the commonly used carbamates.
to hours
Nausea
6.1. Clinical features
Vomiting Clinical featuresare similar and less severe compared
Agitation to organophosphorus poisoning.
Fasciculations
Parasthesia of face and extremities 6.2.Complications
Seizures dizziness
Tremors Pancreatitis and death.
Myoclonus
Coma 6.3. Treatment
Respiratory depression and death
Nasogastric aspirate may be useful if liquid
5.4. Complications preparation has been taken and should be kept and
handed over to medical official for medico-legal
Hyperthermia, Rhabdomyolysis, Pulmonary oedema purposes.
and Disseminated intravascular coagulation. Lindane
is particularly toxic to the central nervous system. It Injection Atropine 0.5-1mg I.V. in small doses for an
can also produce alterations in the ECG including adult till atropinization occurs.
rhythm abnormalities and changes in STT waves
suggesting hyperkalaemia. Besides the features Role of PAM is unclear.
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55. ALCOHOL INTOXICATION /ALCOHOL
WITHDRAWL
7.1. When to Suspect iii. CBC, LFT, obtaining toxicology screens for
opioids or other CNS depressants
Alcohol has CNS depressant effect; hence person
intoxicated with alcohol will present with depressed iv. Neuroimaging
level of consciousness, sometimes with respiratory
depression, cardiac arrhythmia, or blood pressure
7.3. Treatment
i. Adequate nutrition and oral or I.V. Vitamin B
instability.
complex, including 50100 mg of Thiamine daily for
If the patient agrees to stop drinking, sudden a week
decreases in alcohol intake can produce withdrawal
ii. Inj Dextrose 25% in patients of altered sensorium
symptoms, many of which are the opposite of those
(dose 100 cc 25% dextrose)
produced by intoxication. Features include tremor of
the hands (shakes); agitation and anxiety; autonomic iii. Administering any depressant in doses that
nervous system overactivity including an increase in decrease the agitation- 2550mg of Chlordiazepoxide
pulse, respiratory rate, and body temperature; and or 10mg of Diazepam given PO every 46 hr on the
insomnia. These symptoms usually begin within 510 first day, with doses then decreased to zero over the
hrs of decreasing ethanol intake, peak on day 2 or 3, next 5 days.
and improve by day 4 or 5. About 25% of alcoholics
experience a withdrawal seizure. iv. Rehabilitation
7.2. Investigation 7.4. When to Refer

i. History of Alcoholism i. Those with poor Glasgow coma scale, Recurrent
Seizure, Focal neurological deficits or with delirium
ii. Blood ethanol level (Avoid cleaning with spirit tremens / korsakoff psychosis.
while collecting Sample)
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56. ANAEMIA
vii. H/O chronic diarrhea, malabsorption
1. Introduction viii. H/O chronic illness e.g. chronic renal failure,
Anemia is one of the most common disease a TB or any other causing anemia of chronic
physician can come across in the community. It can disease
be defined as HB < 13 g/dLfor male and < 12 g/dL ix. H/O blood transfusion in the past
for females as per WHO. x. H/O similar complaints in the past
xi. H/O pure vegetarian diet causing Vit. B12
Anemia can be due to nutritional deficiency, blood
deficiency causing Megaloblastic Anemia
loss, and increase in destruction of RBCs or due to
disturbance in formation of RBCs in bone marrow.
Detailed history and clinical examination is must to
4. Signs
reach the diagnosis. Patients especially females dont i. Pallor Conjunctiva, mucous membranes, skin
report to clinics until they have severe anemia. ii. Nails platynychia (flat) or koilonychias
Chronic anemia patients are usually well adjusted to (spoon shaped) nails in iron deficiency anemia
HB as low as 5 g/dL. (IDA)
iii. Severe anemia signs of hyper dynamic
2. When to suspect circulation eg. tachycardia, flow murmurs
(ejection systolic loudest at apex),
Symptoms cardiomegaly
i. Easy fatigability iv. Congestive Heart failure with edema feet,
ii. Breathlessness right hypochondriac tenderness, raised JVP
iii. Swelling of feet and basal crepitation
iv. Hypomenorrhea, amenorrhea v. Other signs of etiology may be found eg.
v. Stunted growth in adolescent icterus, Lymphadenopathy, stigmata of TB
3. History to be inquired for

etiology of anemia 5. How to Investigate
3.1. Acute 5.1. Complete blood count
The most important investigation gives maximum
i. H/O blood loss hematemesis, hemoptysis or information regarding diagnosis.
any other Mean Cell Volume (MCV) -Normal 76 -96
ii. H/O Fever or jaundice acute blood loss due
to either hemolysis or blood loss due to Low MCV (microcytic anemia)
coagulopathy
Iron deficiency anemia (IDA) most common
iii. H/O petaeche, ecchymosis or
Hereditary hemolytic anemia eg Thalassemia
lymphadenopathy with fever Acute
Leukemia Normal MCV (normocytic anemia)
iv. Recovering from recent surgery
Acute blood loss
Hemolysis
3.2. Chronic Anemia of chronic disease
i. Antenatal or postnatal female Chronic renal failure
ii. H/O passage of worms in stool causing Pregnancy
chronic blood loss
Bone marrow failure e.g Aplastic anemia
iii. H/O Chronic blood loss Hemorrhoids,
Hypothyroidism
Malena, Menorrhagia
iv. H/O Chronic Alcoholism leading to Vit. B12 High MCV (Macrocytic anemia)
deficiency
v. H/O Anorexia or any GI complaints leading Vit. B12 or folate deficiency (strict vegetarian
to malnutrition diet, Pernicious anemia)
vi. Poor socioeconomic status leading to Alcoholism
malnutrition Mylodysplastic syndromes(MDS)
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Drug induced e.g Phenytoin - Elemental Iron 100mg once daily can be
5.2. Stool examination increase up to 300mg OD
Parasites, occult blood, malabsorption Repeat HB at the end of 1 month to confirm
response to treatment, if HB is increasing then
5.3. Other Baseline investigations repeat after 3months.
FBS, Creatinine, Liver enzymes, reticuolyte count, ii. Megaloblastic anemia-
LDH Oral supplementsVit. B12 (7.5mcg) +Folate
(0.75mg) BD for 1 month.
5.4. Iron studies, serum folic / Vit. iii. Deworming - All patients Tab Albendazole
(400mg) 1 stat, can be repeated after 2 weeks
B 12 levels iv. Treat etiology if possible
v. Packed cell transfusion if hemoglobin is less
5.5. Bone marrow biopsy if than 7
malignancy suspected 7. When to refer
Severe anemia (HB < 4g /dL) requiring blood
transfusion
6. Treatment Signs of Heart failure
i. IDA No response to oral supplements of Iron or B12
and folate at the end of 2 months
Oral iron Ferrous Sulphate (200mg) thrice a
Any suspicion of leukemia, lymphoma, MDS or
day for 3 months.
Aplastic anemia
Or (300mg) BD No apparent cause found
- Ferrous fumarate, Ferrous ascorbate can also
be used
Page 137
57. HEAT STROKE
central nervous system (CNS) depression, core
1. Definition temperatures usually above 40C (1050F), and typical
Heat Stroke is a syndrome of acute thermoregulatory biochemical and physiologic abnormalities.
failure in warm environments characterized by
Figure 1: Effects of Heat Exhaustion and Stroke
Hyperthermia: Hypothalamic set point is Heat Exhaustion

unchanged; does not respond to antipyretics.
Distinct from fever (pyrogens change Heat Stroke
Hypothalamic temperature set point).
Uncontrolled increase in body temperature

3. When to Suspect Heat
that exceeds the body's ability to lose heat Stroke
due to failed thermoregulation. i. In any patient exercising in hot weather or in
susceptible individuals; mainly elderly
Life-threatening medical emergency. population.
ii. Coma or profound stupor is nearly always
Core temperature >40 C (105 F) & CNS present.
disturbances in patients with a history of iii. Diagnostic criteria for Heat Stroke should
heat exposure. include
a. A core temperature above 40C
2. Clinical spectrum of heat b. Severely depressed mental status or
Coma on Central Nervous System examination
illness
c. Elevated Serum Creatinine and Serum
Heat Edema Electrolyte levels (Hyperkalemia)
d. Compatible historical setting.
Heat Rash (miliaria)
Heat Cramps 4. Causes

1) Increased Heat production- Exercise,
Heat Tetany Fever, Thyrotoxicosis, Amphetamines, Atropine
toxicity.
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2) Impaired Heat loss- High ambient temperature or Exertional: Typically seen in healthy young
humidity, Ineffective voluntary control, Lack of adults who over exert themselves in high
acclimatization, Dehydration, Cardiovascular ambient (Surrounding) temperatures or in a hot
diseases. environment to which they are not acclimatized
(To adapt). Sudden inability to dissipate / Lose
3) Drugs- Anticholinergics, Phenothiazines,
body heat through perspiration (evaporation) or
Butyrophenones, Thiothixenes, Barbiturates,
cutaneous vasodilatation (convection),
Anti-Parkinson's agent, Alcohol.
especially after strenuous physical activity in hot
4) Debilitating conditions- Skin diseases, Cystic weather. (Increased heat production).
fibrosis, Central nervous system lesion, older
age. Non-exertional (classic): Usually affects elderly
and debilitated patients with chronic underlying
5. Clinical examination of disease. Result of impaired thermoregulation
combined with high ambient temperatures. Often
patient with Heat Stroke due to impaired sweating.
Anhidrosis often present (but is no longer a 7. Management

criteria for diagnosis)
Primary therapy includes cooling and decreasing
(hot, dry skin) thermogenesis.
Altered mental State. i. Evaporative cooling methods involve placing a
Often missed in physically inactive patients. nude patient in a cool room, wetting the skin
with water and encouraging evaporation by the
Baseline body temperature increased (core use of fans.
temperature).
ii. Direct external cooling involves immersing the
Non-glass medical thermometer. patient in water. Close monitoring of
Rectum preferred site haemodynamics i.e Pulse, Blood pressure,
respiration and urine output is mandatory.
Axillary and inguinal sites are unreliable
6. Types
Figure: Primary therapy of hyperthermia
Seek medical attention immediately-continue It is not advisable to give the victim anything by
first aid to lower temprature until medical help mouth (even water) until the condition has been
takes over. stabilized.
Do NOT give any medication to lower fever- It Body cooling methods
will not be effective and may cause further harm.
Body immersion in iced water
Do NOT use an alcohol rub
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Evaporative cooling: Spraying water and the use - Avoid alcohol and caffeine, which dehydrate the
of fans over the patient facilitates evaporation body.
and convection
- Avoid foods that are high in protein, which
Gastric lavage with cold water / ice, bladder, or increase metabolic heat.
peritoneal lavage - Stay indoors when possible.
Immersion method of body cooling - Take regular breaks when engaged in physical
Aggressive ice water immersion is gold standard activity on warm days.
for life threatening heat stroke - Take time out to find a cool place.
Advantages: Cools patients faster; cooling rate of
0.20C/min for iced water 9. Complications
Disadvantages Acute renal failure
Rhabdomyolysis
- May cause peripheral vasoconstriction (not Liver failure
clinically relevant in RCT) Disseminated intravascular coagulation(DIC)
Acute respiratory distress syndrome (ARDS)

- Difficult in patients with reduced level of

CNS: Altered Mental state, confusion, delirium
Seizure, decorticate posture
consciousness
Coma and Death
Dehydration
- For alert - It is uncomfortable and often Caution - Overhydration
intolerable
Electrolyte Imbalance
Hypernatremia
- Shivering leads to worsening Hyperkalemia
Other cooling methods Hypokalemia
Localized muscle pain on active/passive flexion
(a) Placement of ice packs in the axillae, groin, of limbs
and neck Urine- Hemoglobinuria, Myoglobinuria
- Easy method, slower cooling
(b) Gastric, peritoneal, and bladder lavage with 10. Management of
cold water
complications
- Used in resistant cases i. Benzodiazepines- Lorazepam (2 to 4mg I.V.
(c) Cooling gloves slowly) or Midazolam (2 to 5mg I.V. slowly)
Indicated in patients with agitation & shivering to
Supportive treatment prevent heat production. Also given in patients with
convulsions.
- Treated in ICU settings
- IV Fluids, treat electrolyte disturbance ii. Rhabdomyolysis- Common in Exertional heat
stroke & in patients with hypotension.
- Mechanical Ventilation
Signs& symptom
8. Preventing heat- related - Dark urine
illness - Acute renal failure
- Treatment
- Wear loose, lightweight, light-coloured clothing. - I.V. fluids
Light colours will reflect away some of the suns - Alkalinisation of urine sodium Bicarbonate
energy.
iii. Metabolic support- Correcting the electrolyte
- Wear hats or to use an umbrella. disturbances like hyponatremia, hypercalcemia,
- Drink water- Carry water or juice with you and hypocalcemia, hyperphosphatemia
drink continuously even if you do not feel iv. Hepatic injury- Monitor liver function tests
thirsty. - Avoid hypoglycemia
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- Early recognisation & treatment of DIC
- Respiratory support
11. When to Refer
v. Pulmonary injury- Pulmonary edema is ii. Evaporative and direct external cooling
common complication. methods fail to reduce the temperature.
ARDS- Patient should be referred for iii. Arrhythmias, metabolic acidosis and
mechanical Ventilation. cardiogenic failure complicate the early
management of hyperthermic crises.
iv. Those with evidence of renal failure,
vi. Renal injury- ARF may develop due to many disseminated intravascular coagulation or
reasons. These patients may need hemodialysis superadded infections.
& so referred to higher centre.
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58. TUBERCULOSIS (RNTCP)
evening rise, night sweats, chest pain, shortness of
1. Introduction breath, anorexia and haemoptysis.
Tuberculosis is an infectious disease caused a. Pulmonary TB Suspects
predominantly by Mycobacterium tuberculosis.
Pulmonary tuberculosis is the most common form of A pulmonary TB suspect is defined as:
TB (more than 85% of all TB cases), while extra
pulmonary tuberculosis can affect almost any organ An individual having cough of 2 weeks or more.
in the body. Transmission occurs by the airborne Contacts of smear-positive TB patients having
spread of infectious droplets and droplet nuclei cough of any duration.
containing the tubercle bacilli. The source of Suspected/confirmed extra-pulmonary TB
infection is a person with sputum smear-positive having cough of any duration.
pulmonary TB. Transmission often occurs indoors, HIV positive client having cough of any
where droplets and droplet nuclei can stay in the air duration.
for a long time.
b. Extra-Pulmonary TB Suspects
2. Epidemiology of A patient with extra-pulmonary TB (EP TB) may
Tuberculosis have general symptoms like weight loss, fever with
evening rise and night sweats. Other symptoms
TB is a bacterial disease caused by depend on the organ affected.
Mycobacterium tuberculosis. These organisms
are also known as tubercle bacilli or as acid-fast Examples of these symptoms are, swelling of a
bacilli. lymph node in TB lymphadenitis, pain and swelling
of a joint in TB arthritis, neck stiffness and
Transmission of tuberculosis occurs by airborne disorientation in a case of TB meningitis. Patients
spread of infectious droplets and droplet nuclei. with EP TB, who also have cough of any duration,
Source of infection is patient of tuberculosis who should have sputum samples examined. If the smear
spreads tuberculosis bacilli during coughing, result is positive, the patient is classified as
sneezing, etc. pulmonary TB and his/her treatment regimen will be
that of a case of smear-positive pulmonary TB.
Most common symptom of pulmonary TB is
persistent cough for two weeks or more, usually
with expectoration. Persistent cough for 2 weeks
4. Screening for TB among
or more may be accompanied by one or more high risk groups
symptoms such as weight loss, loss of appetite,
tiredness, evening rise fever, chest pain, a) Contact investigation among the diagnosed
shortness of breath and hemoptysis. smear-positive cases is to be systematically
implemented and monitored, and it offers a
Incidence of tuberculosis is usually similar in major opportunity for early case detection.
both sexes below 15 years of age, thereafter b) HIV care centres: Intensified TB case finding
incidence is higher in males than females and should be implemented in all facilities providing
difference is greatest in old people. HIV care, like ICTCs, ART Centres, Care and
support centres etc.Involve NGOs working with
Early detection of sputum positive tuberculosis
HIV programmes in TB case finding activities.
case and conversion into sputum negative by
c) Diabetic patient: regularly screening for TB in all
effective treatment are most important measures
diabetic patients at each visit.
for tuberculosis control.
d) Elderly patients.
e) Smokers.
3. Diagnosis of TB f) Other High risk groups: Malnutrition, patients
Identification of Tuberculosis Suspects with silicosis, patients on corticosteroids and
other chronic diseases need to be screened for
The most common symptom of pulmonary TB is TB regularly.
persistent cough, usually with expectoration.
Persistent cough may be accompanied by other
symptoms such as weight loss, tiredness, fever with
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5. Tools for diagnosis of TB 7. Management of Patient
Following are RNTCP recommended diagnostics after receiving the sputum
tests for TB results
Sputum smear microscopy.
Histopathology/cytology/radiology. 7.1 Smear positive pulmonary TB.
Solid/liquid culture and DST for diagnosis TB
and Drug Resistant TB. Patients with at least one sputum positive smear
PCR based newer rapid diagnostic tools for resultout of two samples are diagnosed by the
diagnosis of TB/drug resistant TB eg. physician as having smear-positive pulmonary TB.
Line probe assay (LPA), CBNAAT. They are further classified as a new or re-treatment
case based on their previous treatment history and
6. Guidelines for collecting appropriate regimen is prescribed.
sputum 7.2 Follow up of the sputum

negative symptomatic
The patient is given the sputum container with
Laboratory Serial Number written onits side. The Patients, who are negative for AFB in both the
patient is instructed to inhale deeply 23times samples, will be prescribed a course of antibiotics for
with mouth open, cough out deeply from the duration of 10-14 days. In such cases antibiotics such
chest, open the container and spitout the sputum as fluoroquinolones (Ciprofloxacin, Ofloxacin,
into it. Sample should be at least 2 ml. If the Levofloxacin, and Moxifloxacin etc.),
quantity is less, then the procedure can be clavulunatemacrolides, rifampicin or streptomycin,
repeated. Once adequate quantity of sample is which are active against tuberculosis, are not to be
collected, the container should be closed. This is used. Antibiotics of choice include Cotrimoxazole,
the first spot specimen (A). Amoxycillin, & doxycycline. Most patients are likely
The patient is given a labelled container with to improve with antibiotics if they are not suffering
instructions to cough out sputum intothe from TB. If the symptoms persist after a course of
container early in the morning after rinsing the broad spectrum antibiotics, repeat sputum smear
mouth, before breakfast. This is the early examination (2 samples) must be done for such
morning specimen (B). patients.
The person collecting the sputum specimens should However, if repeat sputum examination turns to be
follow the guidelines specified below: negative, they are subjected for chest x-ray
If the sputum specimens are to be sent examination. If chest x-ray is suggestive of
immediately to the laboratory, the person should pulmonary TB, they will be diagnosed as smear
put the container into a special box meant for negative pulmonary TB and treated accordingly. If
transport. chest x-ray is not suggestive of TB, then they should
be evaluated for other respiratory diseases.
If the sputum specimens are not being sent
For patients infected with HIV, antibiotic trial is not
immediately to the laboratory, these should be
indicated and Chest X-ray needs to be taken to avoid
stored in a cool and shady place in the referring
delay in diagnosis of smear negative TB.
health facility.
Patients with suspected EP TB should be referred to a
The person should wash hands thoroughly with
competent medical practitioner / doctor / specialist
soap and water every time when the material is
for expert opinion. Diagnosis of such patients may be
handled.
made using appropriate diagnostic procedures (such
Patients should be told to come back to receive as FNAC/Biopsy/Radiology) as well as clinical
the results of sputum examination. methods.
Alternatively, sputum results may be sent to the Diagnosis of TB by chest X-ray alone is unreliable
referring health facility by hand. Laboratory because no radiological pattern is pathognomic of
serial number (and/or specimen identification pulmonary TB. Unless the prescribed algorithm is
number) should be clearly written on the side of followed, a large number of patients who do not have
the sputum container. TB will be falsely diagnosed and treated.
Page 143
its duration, and the need for prompt evaluation of
8. Diagnostic Algorithm children under six years or contacts with cough of
any duration living in the household. The patient
When the referring doctor receives the results of
should also be informed that his address would be
sputum examination, and it is decided to put the
verified by a competent person prior to the start of
patient on chemotherapy, health education must be
treatment.
imparted to the patient. The patient is told about TB,
how it spreads, precautions to be taken to prevent the
spread, importance of directly observed treatment and
Figure-1: Diagnostic Algorithms for Pulmonary Tb
9. Treatment of TB
MO must undertake detailed clinical examination and V. Culture / Drug Susceptibility Test (DST)
history before starting the TB treatment. report from RNTCP certified laboratory (if
available).
The following is required before starting treatment:
I. History of patient, including history of any 9.1. Directly Observed
previous treatment for TB.
II. Sputum smear examination results from an Treatment (DOT)
approved DMC.
RNTCP Definitions: Case Definitions, Types of
III. Chest X-ray report if the case warrants
Cases and Treatment outcomes
radiographic examination.
IV. Other supporting investigation reports, if any.
Page 144
Table-1: Definitions under RNTCP
alternate days and lasts for 2 months (8 weeks, 24

9.2.Treatment Regimens doses).
For the purpose of treatment regimen to be used, TB This is followed by the continuation phase, which
patients are classified into two groups, namely, consists of 4 months (18 weeks; 54 doses) of
New or Previously Treated, based on the history isoniazid and rifampicin given thrice a week on
of previous treatment. alternate days with at least the first dose of every
week being directly observed. If the sputum smear is
i. Regimen for New cases positive after 2 months of treatment, the intensive
This regimen is prescribed to all new pulmonary phase of four drugs (H, R, Z and E) are continued for
(smear-positive and negative), new extra pulmonary another one month (12 doses), and sputa sent for
and new others TB patients. culture and drug susceptibility testing (C&DST) to an
The regimen is 2H3R3Z3 E3 / 4 H3R3. accredited RNTCP C&DST laboratory. Treatment
remains continued as per regimen if C&DST report is
Treatment is given in two phases. For New Rifampicin-sensitive. Sputum is examined after the
patients, the intensive phase consists of isoniazid (H), completion of the extension of intensive phase.
rifampicin (R), pyrazinamide (Z) and ethambutol (E) Irrespective of the sputum results after this extension
given under direct observation thrice a week on of the intensive phase, the 4 months (18 weeks) of the
continuation phase is started.
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If the sputum smear is positive after 5 or more duration of treatment is 8 months. Relapses,
months of treatment, the patient is declared as a Treatment after Default, Failures and Others are
Failure and is placed on the Previously Treated treated with this regimen.
treatment regimen afresh. If patient remains smear
The regimen is IP: 2S3H3R3Z3 E3+ 1H3R3Z3 E3
positive in any follow-up sputum examination, then
CP: 5 H3R3 E3.
sputum samples are sent for culture and drug
susceptibility testing (C&DST) to an certified Treatment is given in two phases. For Previously
RNTCP C&DST laboratory. If the report indicates Treated cases, the intensive phaseconsists of two
Rifampicin resistant, then the Cat I regimen is months (24 doses, 8 weeks) of isoniazid (H),
stopped and patient is counselled and referred to rifampicin (R), pyrazinamide(Z), ethambutol (E) and
District / Drug Resistance TB centre for pre- streptomycin (S), followed by one month (12 doses, 4
treatment evaluation and treatment initiation.While weeks) ofisoniazid, rifampicin, pyrazinamide and
treating TB meningitis(TBM) in New patients, ethambutol, all given under direct observation thricea
streptomycin is to be used in place of ethambutol week on alternate days. Patient is subjected for
during the intensive phase (H3R3Z3S3 instead of follow-up sputum examination at theend of three
H3R3Z3E3). The continuation phase of treatment for months. If the sputum smear is positive at the end of
patients with TBM or spinal TB is for 7 months. 3 months of treatment, the intensive phase drugs (H,
Hence, the total duration of treatment will be for 9 R, Z and E) are extended for another one month (12
months. doses,4 weeks). Irrespective of the sputum results at
the end extended intensive phase, 5 months(22
ii. Regimen for Previously Treated weeks) of continuation phase is started. If the sputum
cases remains positive at the end ofthe extended intensive
This regimen is prescribed for TB patients who have phase, sputum is sent to an accredited RNTCP
had more than one month anti-tuberculosis treatment C&DST laboratory for culture and drug susceptibility
previously. These patients are at a higher risk of testing. The continuation phase consists of 5 months
having drug resistance. Hence all such patients are (22 weeks; 66 doses) of isoniazid, rifampicin and
also subjected to C&DST for identification of ethambutol given thrice a week on alternatedays,
MDRTB. If C&DST report is expected beyond 7 with at least the first dose of every week being
days, then patients are initiated on Cat II regimen directly observed.
with 5 drugs in the intensive phase, and the total
Table-2: Treatment regimine under RNTCP
Regimen1
Treatment groups
Type of patient Intensive phase (IP) Continuation phase
(category)
(CP)
New Sputum smear-positive 2H3R3Z3E3 4H3R3
(Cat I: Red Box) Sputum smear-negative
Extra-pulmonary
Others
Previously Smear-positive relapse 2H3R3Z3E3S3 5H3R3E3
Treated** Smear-positive failure / 1H3R3Z3E3
/Retreatment case Smear-positive treatment after
(Cat II: Blue Box) default
Others2
1. The number before the letters refers to the number 1500 mg, Ethambutol (E) 1200 mg, Streptomycin (S)
of months of treatment. The subscript after the letters 750 mg.
refers to the number of dosesper week.
Patients who weigh 60 kg or more receive
The dosage strengths are as follows: Isoniazid (H) additional rifampicin 150 mg.
600 mg, Rifampicin (R) 450 mg, Pyrazinamide (Z) Patients who are more than 50 years old receive
streptomycin 500 mg. Patients who weigh less
Page 146
than 30 kg, receive drugs as perPaediatric weight
band boxes according to body weight.
9.3. Pediatric TB
Pediatric cases are to be treated under RNTCP with
2.In rare and exceptional cases, patients who are the same thrice weekly short course chemotherapy
sputum smear-negative or who have extra-pulmonary regimens (New or Previously Treated) given
disease can have recurrence or nonresponse.This under DOT as for adult patients. They are to be
diagnosis in all such cases should always be made by registered in the respective RNTCP TB Register.
an MO and should be supported by culture or Pediatric patient-wise boxes are available with
histological evidence ofcurrent, active TB. In these different dosages as two product codes to be used
cases, the patient should be typed as Others and under four weight bands for children weighing 6 to
given treatment regimen for previously treated. 10 kgs, 11 to 17 kgs, 18 to 25 kgs and 26 to 30 kgs.
Note: - All doses in Intensive phase and at least first
dose in Continuation phase should be directly
observed by DOT provider.
Table-3: Pediatric patient wise boxes for new cases according to weight band
INH Chemoprophylaxis
9.4. Monitoring of Treatment
All children aged < 6 years in contact with smear- Follow up of patient
positive pulmonary TB case are screened by MO to
rule out TB. If suffering from TB, should be treated
appropriately. Children not having TB are to be
administered preventive chemotherapy with INH,
10mg/kg body weight for 6 months.
Table-4: Follow up of DOTS patients

CAT Follow up sputum If smear + at the end of IP Remarks
Action Follow up
sputum
CAT-I At 2,4,6 months of Extend IP for another one 3,5,7 months If sputum +ve at 5 months,
treatment month of treatment declare patient as failure and
put on CAT-II
CAT-II At 3,5,8 months of If +ve at 3 months then 4,6,9 months -
treatment extend IP, 4 drugs for one of treatment
more month
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Default retrieval action Definitions
In spite of counseling and health education at the MDR-TB case: A TB patient whose sputum is
time of diagnosis and follow up by health workers, culture positive for Mycobacteriumtuberculosis and
some patients remain irregular for treatment. is resistant in-vitro to isoniazid and rifampicin with
Defaulter retrieval action is action taken to bring or without otheranti-tubercular drugs based on DST
back patients for treatments who do not take results from an RNTCP-certified Culture &
medicines regularly. DOT provider should take DSTLaboratory.
defaulter action. Following actions are suggested
under RNTCP for defaulter patients- XDR TB case: An MDR TB case whose recovered
M. tuberculosis isolate is resistant toat least isoniazid,
If patient does not come as scheduled during rifampicin, a fluoroquinolones (Ofloxacin,
Intensive Phase (IP) then health worker / DOT Levofloxacin, orMoxifloxacin) and a second-line
provider makes home visit immediately same injectable anti-TB drug (Kanamycin, Amikacin,
day or next day and brings patient for regular orCapreomycin) at a RNTCP-certified Culture &
treatment. DST Laboratory.
If patient is in Continuation Phase (CP) home Diagnosis of MDR-TB
visit should be made and patient should be
retrieved within a period of a week after missed Presently, 3 technologies are available for diagnosis
dose. of MDR TB viz. the conventional solidEgg-based
In case of community DOT provider / ASHA/ Lowenstein-Jensen (LJ) media, the liquid culture
Anganwadi, the respective ANM/MPW of that areas (MGIT), and the rapid molecular assays such as Line
should supervise the DOT provider fortnightly for Probe Assay (LPA) and similar Nucleic Acid
ensuring DOT implementation and assist in ensuring Amplification Tests likeXpert MTB/Rif (CBNAAT).
patient adherence, timely follow-up. Molecular/genotypic tests are much faster than
phenotypic tests, as molecular tests dont require
growth of the organism, and M. tuberculosis is
9.5. Programmatic notoriously slow growing. The turnaround time for
Management of Drug C-DST results by Solid LJ media is around 84 days,
by Liquid Culture (MGIT) is around 42 days, by LPA
Resistant TB (PMDT) is around 72 hours and by CBNAAT is around 2
MDR-TB Suspects hours. Currently LPA does the DST of INH and
Rifampicin and CBNAAT gives the DST of
The following are the criteria to label a patient as Rifampicin. Liquid culture DST is used to do the
MDR-TB suspect. DST of second line drugs Oflox/Kanamycin.
All previously treated pulmonary TB cases at RNTCP MDR/XDR-TB Treatment

diagnosis.
Any smear positive follow up result in new or As per PMDT guidelines, a specializedcenters named
previously TB cases. Drug Resistant TB Centres are been established at
tertiary care hospitals like medical college/ TB
HIV TB co-infected cases at diagnosis.
hospitals/civil hospital for admission of MDR TB
All pulmonary TB caseswho are contacts of
patients for pre-treatment evaluation and to initiate
known MDR TB case
treatment.Patients should receive counselling at every
Once the districts will have adequate laboratory
level on 1) the nature and duration of treatment, 2)
capacity for DST, all TB patients will be
need forregular treatment, 3) possible side effects of
provided DST at the time of diagnosis.Two fresh
these drugs and 4) the consequences of irregular
sputum samples (Spot and early morning) are to
treatment or pre-mature cessation of treatment.
be collected from MDR TB suspects and
transported from DMC/PHIto the RNTCP Regimen for MDR-TB
certified C & DST laboratory in cold chain by
using transport mechanism (courier/post/human This regimen comprises of 6 drugs - Kanamycin,
carrier) within 72 hrs. Levofloxacin, Ethionamide, Pyrazinamide,
Ethambutol and Cycloserine during 6-9 months of the

Intensive Phase and 4 drugs-Levofloxacin,
Page 148
Ethionamide, Ethambutol and Cycloserine during the Follow-up monitoring in XDR TB
18 months of theContinuation Phase.
XDR TB requires more intensive monitoring during
All drugs should be given in a single daily dosage follow-up.
under directly observed treatment (DOT) by a DOT
Provider. All patients will receive drugs under direct Complete Blood Count with Platelets Count:
observation on 6 days of the week. On Sunday, the weekly in first month, then monthly torule out
oral drugs will be administered unsupervised whereas bone marrow suppression and anaemia as a side
injection Kanamycin will be omitted. If intolerance effect of Linezolid.
occurs to the drugs, Ethionamide, Cycloserine and, Kidney Function Test- monthly creatinine and
addition of monthly serum electrolytesto the
PAS may be split into two dosages and the morning monthly creatinine during the period that Inj
dose administered under DOT. The evening dose will Capreomycin is being administered.
be self-administered. The empty blister packs of the Liver Function Tests: monthly in IP and 3
self-administered doses will be checked the next monthly during CP.
morning during DOT. Pyridoxine should be CXR every 6 months.
administered toall patients on Regimen for MDR TB. No difference to follow-up Culture for patients on
Drugs are provided to the DOT provider in monthly regimen for MDR TB and XDR TB.
patient wise boxes (PWB). PWBs are prepared at
State Drug store as per the five weight bands- <16kg, M/XDR TB Treatment Outcome definitions
16-25Kg, 26-45kg, 46 -70kg and > 70kg.
Standardised treatment outcome definitions are to be
If patient gains or loses >5 kg weight during used following treatment of an MDRTBcase. These
treatment and crosses the weight band range, definitions apply to patients with rifampicin
Committee may consider moving the patient in higher resistance (who are taken to beMDR TB for
or lower weight band in next supply of drugs. management purposes), and XDR TB cases as well:
Follow-up investigations during MDR TB Cure: A patient who has completed treatment
treatment and has been consistently culture negative (with
at least 5 consecutive negative results in the last
One specimen for follow up culture at the end of 12 to 15 months). If one follow-up positive
3,4,5,6,7,9,12,15,18,21,24 months of treatment. culture is reported during the last three quarters,
Monthly weight. patient will still be considered cured provided
Chest X-ray during pretreatment evaluation, end this positive culture is followed by at least 3
of IP, end of treatment and whenever indicated. consecutive negative cultures, taken at least 30
Physician evaluation every month for 6 months days apart, provided that there is clinical
and then every 3months for 2 years. evidence ofimprovement.
Serum Creatinine monthly for first 3 months and Treatment completed: A patient who has
then every 3 months till inj. Kanamycin is given. completed treatment according to guidelinesbut
TSH during pretreatment evaluation and when does not meet the definition for cure or treatment
indicated. failure due to lack of bacteriological results.
Patients will be considered culture converted Treatment failure: Treatment will be
after having two consecutive negative cultures considered to have failed if two or more of the
taken at least one month apart. Based on culture fivecultures recorded in the final 12-15 months
conversion patient is shifted from IP to CP. are positive, or if any of the final threecultures
are positive.
Regimen for XDR TB Death: A patient who dies for any reason during
the course of M/XDR-TB treatment.
The Intensive Phase will consist of 7 drugs Treatment default: A patient whose treatment
Capreomycin (Cm), PAS, Moxifloxacin (Mfx), High was interrupted for two or more
dose-INH, Clofazimine, Linezolid, and Amoxyclav. Consecutive months for any reasons.
Transfer out: A patient who has been
The Continuation Phase will consist of 6 drugs
transferred to another reporting unit (DR-TB
PAS, Moxifloxacin (Mfx), High dose-INH,
Centre in this case) and for whom the treatment
Clofazimine, Linezolid, and Amoxyclav.
outcome is not known.
Page 149
Switched to Regimen for XDR TB: A By an RNTCP certified C-DST laboratory,
MDR-TB patient who is found to have who subsequently switched to a regimen
XDR-TB. forXDR TB treatment initiated.
Page 150
59. LEPROSY (NLEP)
2) Thick and/or Tender nerve
1. Cardinal signs of leprosy Selection of Leprosy case on clinical sign &
1) Hypopigmented / Erythematousanesthetic symptoms.
patch/s.
Figure-1: Algorithm for Confirmation
Treatment for 6
PB case month (6 BCP in
Confirmation of
9 Month)
Suspect Case cases at
PHC/RH
MB case Treatment for 12
month (12 BCP
in 18 Month)
Table-1: Cardinal signs for classification of Leprosy Case
Clinical aspects PB (Paucibacillary) MB (Multibacillary)

Skin lesions 1 to 5 skin Patches with definite sensory 6 & 6 + skin Patches with
deficit definite sensory deficit
Nerve involvement And/or one definite thicken or tender And/or More than one definite
peripheral nerve involvement thicken or tender peripheral nerve
If any one or both signs present in suspected case then it is diagnosed as leprosy.
2. Management
Table-2: Management of Leprosy case as per classification2
Multi Drug Treatment for PB leprosy
Drug Adult Children 10- Children below 10 years Frequency
14 yrs
Rifampicin 600 mg 450 mg 300 mg
Once a month
Dapsone 100 mg 50 mg 25 mg
25 mg daily or 50 mg alternate day Daily/ alternate
Dapsone 100 mg 50 mg
day
Page 151
Multi Drug Treatment for MB leprosy.
Drug Adult Children 10-14 yrs Children below 10 years Frequency

Rifampicin 600 mg 450 mg 300 mg
Dapsone 100 mg 50 mg 25 mg Once a month
Clofazimine 300 mg 150 mg 100 mg
Dapsone 100 mg 50 mg 25 mg Daily
50 mg 50 mg 50 mg
Clofazimine weekly twice
(Daily) (Alternate day)
The appropriate dose for children under 10 Dapsone: 2 mg per kilogram body weight daily.
years of age can be decided on the basis of
MDT Multi drug Treatment is safe and well tolerated
body weight. by most of the patients.
Rifampicin: 10 mg per kilogram. 3. Management of Reaction
Clofazimine:6mgperkilogrammonthlyand1mgper
kilogramperbody weight daily.
Table-3: Features of Lepra Reaction

Features Type I Type-II
Skin Existing lesions suddenly become red, Red, painful, tender, subcutaneous (deep)
swollen, warn and tender. New lesions nodules (ENL) appear commonly on face,
may appear arms and legs. They appear in groups and
subside within a few days.
Lesions when subsiding, may show scales
on surface
Nerves Nerves close to skin become enlarged, Nerves may be affected but not as common as
tender and painful with loss of nerve in Type-I reaction
function.
Other organs Not common Fever, joint pains fatigue
Treatment of Lepra Reaction (Type-I and Type 15 mg OD for first7-8 weeks.

II) 10 mg OD for first 9-10 weeks.
5 mg OD for first 11-12 weeks.
Assurance to the patient & family (The total duration should not exceed 12 weeks even
in type 2).
Early diagnosis & prompt treatment to prevent
Cap Clofazimine 100mg T.D.S. in type 2 reaction for
deformity.
12 weeks,followed by 100 mg od for 12 weeks &
Removal of precipitating factor wherever 100 mg od for 12-24 weeks.
possible. Rest: Adequate rest to the affected nerve until
symptoms clear, by applying a padded splint or
Tab.Prednisolone
any other suitable material to immobilize the
40 mg OD for first 2 weeks.
joints near the affected nerve.
Page 152
Continuation of Anti Leprosy Treatment only if the appearance of reactions with new
not completed. development of the disease.
It has been observed that many medical officers
become panicky and start MDT again equating
Figure-2: MDT Blister Packs
Page 153
PEDIATRICS
Page 154
1. Emergency Management in Paeditrics
In children under five years of age Pneumonia, Keepthebabyunderaradiantwarmerandre-

diarrhoea, Birth asphyxia, Low birth weight and warmsoastobringthechildstemperatureto36.5
neonatal infections were the most important causes C.Payspecialattentiontoavoidchillingtheinfantdur
of death. Many children suffer from more than one ingexaminationorinvestigation.
illness at a time and also many different diseases
presents with similar symptoms. It describes a Monitortemperature everyhalfhourly
sequential process for managing sick young infants forfirst2hrsandthenevery2hourly.
and children as soon as they arrive in the facility.
Only the key protocols from Integrated Management 4. How to Treat Hypoglycemia
of Childhood Illness (IMNCI) and Facility Based
Check for blood glucose in all children presenting
IMNCI (F IMNCI) are re-emphasized.
with emergency sign, those with severe acute
malnutrition and all sick young infants (0-2
1. Emergency Management months):
process of the sick child (0- i. Ifhypoglycemiadetecteddefinedas
5 years) ii. a) <45mg/dlforyounginfants andb)
<54mg/dlinoldersickchildrenbeyond2 months.
The firststep in assessing children referred to a iii. GiveI.V.
hospital should be triage The process of rapid bolusdoseof10%dextrose,inthedoseof2ml/kgfory
screening to decide to which of the following ounginfants,and5ml/kgforolderchildren.
group(s) a sick child belongs: iv. Ifyoucannotmeasurebloodglucose,givebolusdose
Firstassesseverychildforemergencysigns.Thos asabove. Refer the case to higher center.
ewithemergency signs require immediate 5. Airway and Breathing :
emergency treatment.
Ifemergencysignsarenotpresent,lookforpriorit
ysigns.Thosewithpriority signs should alert
you to a patient who is seriously ill and needs
immediate assessment and treatment.
Childrenwithnoemergencyorprioritysig
nsaretreatedasnon-urgent cases.
2. Triage
All sick children are assessed for Airway,
Breathing, Circulation, Coma, Convulsions and
Severe Dehydration (ABCD). Table 1
Efforts should be made to maintain euglycemia and
euthermia while managing ABCD. Thus Blood
sugars should be done for every sick
Newborn,Infant and older children.
3. How to keep baby warm

Keeptheinfantdryandwellwrapped.
Cap,glovesandstockingsarehelpfultoreduceheatl
oss.
Keeptheroomwarm(atleast25C)makingsurethatt
hereisnoheatsourcedirectedstraightatthenewbor
n.
Page 155
Table-1: Assessment of Airway and Breathing
Table-1: Assessment of Airway andBreathing

No Manageairway
ASSESS AIRWAY
breathingorgaspingor Providebasiclifesupport
AND BREATHING
Centralcyanosis (No breathing/gasping)
ANY SIGN POSITIVE
Or Giveoxygen
Severerespiratorydistre Makesurechildiswarm
ss
Severe lower chest in-drawing

5.1. Signs of severe respiratory Head nodding
distress Grunting
Apnoeic spells
Respiratory rate Unable to feed due to respiratory distress
0 -2 months > 60,
Stridor in a calm child
2 months 1 year > 50 &
>1 year 5 years > 40.
5.2. Management of airway in a child with gasping or who has just stopped
breathing.
Table-2: Positioning to Improve the Airway when no neck trauma suspected.
Child Conscious Child Unconscious

Inspectmouthandremoveforeignbody,ifpresent. Opentheairwayby Head tilt andChinliftmethod.
Clearsecretionsfromthroatusingsuctioncatheter. Inspectmouthandremoveforeignbody,ifpresent.
Letchildassumepositionofmaximalcomfort. Clearsecretionsfromthroat.
GiveOxygen. Checktheairwaybylookingforchestmovements,
Continuewith furtherassessment. listening for breath sounds and feeling for breath.
5.2.1. Head tilt-chin lift maneuver (Fig 1)

Theneckisslightlyextendedandtheheadistiltedbyplacin Figure-1: Position for opening airway
gonehandontothechildsforehead.Liftthemandibleup
and outward by placing the fingertips of other hand Children of all age.
under the chin.
a) Positioning to improve the Airway when
neck trauma suspected b) Neck trauma suspected (possible cervical
To limit the risk of aggravating a potential cervical spine injury)
spine injury, open the airway with a jaw thrust while Stabilizetheneck,asshowninfigure2.
you immobilize the cervical spine. It is safe to use in
cases of trauma for Inspectmouthandremoveforeignbody,
ifpresent.
Clearsecretionsfromthroatbysuctioncatheter.
Checktheairwaybylookingforchestmovements,li
steningforbreathsoundsandfeelingforbreath.
5.2.2 Jaw thrust maneuver
The jaw thrust is achieved by placing two or
three fingersunder the angle of the jaw on
both sides, and lifting the jaw upwards and
outward. The jaw thrust maneuver is
alsoused to open the airway when bag-mask
ventilation is performed.
Page 156
Figure-2: Using Jaw thrust without head tilt
If after any of these maneuvers the child starts
breathing, an oropharyngeal airway should be put
and start oxygen.
If the child is not breathing even after the above Figure-3: Difference in padding for an infant and
maneuvers or spontaneous ventilation is older child
inadequate (as judged by insufficient chest Bags and masks should be available in sizes for
movements and inadequate breath sounds), the entire pediatric range (size 0, 1 and 2).
ventilate with a self-inflating bag and mask
It is important for the mask to be the correct
5.3. Ventilation with Bag and mask size for the child;it must completely cover
the
Positioning (Fig 3)
Mouth and nose without covering the eyes
A sniffing position (padding under
or overlapping the chin.
theshouldertopreventexcessiveflexionofthenec
kthatoccurswhentheirprominentocciputrestsont
hesurface onwhich the child lies without
hyper-extension of the neck) is usually
appropriate for children less then 2 years old. .
In correct sniffingposition, the opening of the
external ear canal should be in line with or in
front of (anterior to) the anterior aspect of the
shoulder. Extreme hyperextension of the infant
neck can produce airway obstruction.
In children older than 2 years you may need to Figure-4: Bag and mask ventilation
give padding under the occiput to
The correct size and position are shown in
Obtain optimal airway position. the figure4 & 5
Figure 5: Choosing the correct mask size
Page 157
Self-inflating bags of minimum volume 450- the chest by completely releasing the pressure
500ml should be used. Use force and tidal but maintaining contact with the compression
volume just enough to cause the chest to rise site.
Minimize interruptions in chest compressions.
visibly.
During cardiopulmonary resuscitation, chest
Reservoir and oxygen (5-6 L/min) compressions must always be accompanied by
should be connected to the self inflating positive-pressure ventilation.
bag during resuscitation. Avoid giving a compression and ventilation
After two effective ventilations, check simultaneously, because one will decrease the
the pulse (femoral, brachial or carotid) efficacy of the other.
for no more than ten seconds. If pulse is Therefore, the 2 activities must be coordinated,
with one ventilation interposed after every third
absent, the second person should start
compression (3 compressions followed by one
chest compression. ventilation), for a total of 30 breaths and 90
compressions per minute
5.3. Chest compressions:
The techniques for chest compression vary
for a child under 1 year and those between
1-8 years and are detailed below: 5.3.2 Chest compressions for the child (1 to 8
years of age)
Place the heel of one hand over the lower half of the
5.3.1 Chest compression in the infant (less sternum. Lift your fingers to avoid pressing on the
than 1 year of age) ribs.
There are two techniques for performing chest
compression. These techniques are:
Thumb technique, where the 2 thumbs are
used to depress the sternum, while the
hands encircle the torso and the
fingerssupport the spine
Figure-7: Chest compression for the child (1 to 8

years of age)
Figure-6: Thumb technique
Depress the sternum 1/3 to 1/2 of the depth of
2-fingertechnique, where the tips of the middle the chest. This corresponds to a 1 to 1- inches.
fingerand either the index fingeror ring
fingerof one hand are Compress at the rate of approximately 100
times per minute.
usedtocompressthesternum,whiletheotherhandi
susedtosupportthebabysback(unlessthebabyiso Theratioofchestcompressionsandventilationshou
naveryfirmsurface). ldbe 15:2(Fifteen compressions followed by
two ventilation).
Using either method to give chest
compressions, compress the lower half of the Bag and mask ventilation is a very effective
sternum but do not compress over the xiphoid. way of ventilation if done correctly.
After each compression allows the chest to
recoil fully because complete chest re- Setup an intravenous or an intraosseous line for
expansion improves blood flow into the heart. use of any drugs, whereneeded.
Push hard: push with sufficient force to
depress the chest approximately one third to
one half the anterior- posterior diameterof the 6. Use of Adrenaline
chest. Adrenaline 0.1 ml /kg (1:10,000) intravenous can be
Push fast: push at a rate of approximately 100 used in a child who does not respond toinitial
compressions per minute. ventilation and chest compressions and his pulses
Release completely to allow complete recoil of are absent. Two such doses can be used 3-5 minutes
apart.
Page 158
7. Giving Oxygen to a child
with respiratory distress
With a Head box (8-10 L/min) or a Face mask
(5-6 L/min).
Should be allowed to take a comfortable
position of his choice and should be given
oxygen.
Continue giving oxygen continuously until the
child is able to maintain a SaO2 > 92% in
room air. When the child is stable and
improving, take the child off oxygen for a few
minutes. If the SaO2 remains above 92%,
discontinue oxygen, but check again hour
later, and 3 hourly thereafter on the first day
off oxygen to ensure the child is stable. Where
pulse oximetry is not available, the duration of
oxygen therapy is guided by clinical signs,
which are less reliable. Figure-8: Capillary refill time
Any child who has been successfully

resuscitated or any unconscious child who is 8.1.1 Checking capillary refill
breathing and keeping the airway open should Weak & Fast Pulse: Evaluation of pulses is critical
be placed in the recovery position. This to the assessment of systemic perfusion. The radial
position helps to reduce the risk of vomit pulse should be felt. If it is strong and not obviously
entering the childs lungs. It should only be fast the pulse is adequate; no further assessment is
used in children who have not been subjected needed.
to trauma. A child with cyanosis or severe Weak and fast pulse is defined:
respiratory distress should be allowed to take a
comfortable position of his choice. In Infants : >160 per min.
Organize Urgent Transfer to higher centers in In children - > 140 per min.
Ambulance and ensure doctor accompanies the Thus if the child has cold extremities, a capillary
sick child. refill time more than 3 seconds, and a fast weak
pulse, then he or she is in shock.
8. Circulation: 9. Treatment of Shock:

After the Airway has opened, assess if a child has a If the child has any bleeding, apply pressure
circulation problem you need to know: to stop the bleeding. Do not use a tourniquet.
The letter Cin ABCD stands for Circulation, Give oxygen.
Coma and Convulsions.
Give fluids and other treatment for shock.
Assess the circulation for signs of shock
Themostcommoncauseofshockinchildrenisduetoloss 9.1 Young Infants:
offluidfromcirculation,eitherthroughlossfromthebody Fluid bolus of 20ml/kg of normal saline over
as in severe diarrhoea or when the child is bleeding, 20-30 minutes.e.g. in a baby weighing 3 kg,
or through capillary leak in a disease such as severe 60 ml of normal saline should be infused over
Dengue fever. 20-30 minutes. If no or partial improvement
Inallcases,itisimportanttoreplacethisfluidquickly.Anin (i.e. tachycardia and CRT still prolonged),
travenouslinemustbeinsertedandfluidsgivenrapidlyins repeat a bolus of 20 ml/kg of normal saline.
hocked children without severe malnutrition.
If the signs of poor perfusion persist despite 2
Capillary Refill Time: To assess the fluid boluses, start vasopressor support,
circulation, take the childs hand and feet in your except in infants with severe dehydration
own. If it feels warm, the child has no circulation who should be treated as per Plan C of
problem and you do not need to assess capillary diarrhea management.
refill or pulse. If the childs hands and feet feel cold,
you need to assess the capillary refill.
9.2 Children above 2 months of
Page 159
age:The recommended volumes of fluids to Managethe Airway
treat shock depending on the age/weight of a) Coma
child.If the child has severe malnutrition, you
must use of different fluid and a different rate Managing the airway is done in the same way
of administration and monitor the child very as treating any child with an airway or
closely. Therefore a different regime is used breathing problem. This has been discussed
for these children. earlier. Give oxygen for the emergency
setting.
b) Convulsion
10. Coma and Convulsion
Calso represents Coma and Convulsion. To manage the airway of a convulsing child
gentle suction of oropharyngeal secretions
Assess the child for coma and convulsion should be done & child put in recovery
10.1 Coma position and oxygen started.
Table-3: For assessment of the conscious level of a Do not try to insert anything in the mouth to
child is, a simple scale (AVPU) is used. keep it open.
A isthechildAlert?Ifnot,
V isthechildrespondingtoVoice? Ifnot, 10.3.2 Put the child in Recovery Position
P isthechildrespondingtoPain? Any unconscious child who is breathing and
keeping the airway open should be placed in
U the child who is Unresponsive to voice (or being the recovery position.
shaken) AND to pain is Unconscious.
T hispositionhelpstoreducetherisk
A child who is not alert, but responds to voice, is
ofvomitenteringthechildslungs.
lethargic.
An unconscious child may or may not respond to Ifneck trauma is not suspected
pain. Turnthechildonthesidetoreducerisk
A child with a coma scale of P or U will ofaspiration
receive emergency treatment for coma as described Keeptheneckslightlyextendedandstabilizebypl
below. acingthecheekononehand
10.2 Convulsions Bendonelegtostabilizethebodyposition
The child must be seen to have a Position of unconscious child (trauma
convulsion during the triage process for
emergency treatment for convulsion.
Convulsion ARE RECOGNIZED by the
sudden loss of consciousness associated
withuncontrolledjerkymovementsoftheli
mbsand
ortheface.Thereisstiffeningofthechildsarm
sandlegsanduncontrolled movements of
the limbs. The child may lose control of
the bladder, and is unconscious during Position of unconscious child (no trauma)
and after the convulsion.
Sometimes, in infants, the jerky Figure-9: Position of Unconsious child
movements may be absent, but there may
be twitching (abnormal facial If trauma is suspected
movements) and abnormal movements of - Stabilize the child while lying on the back.
the eyes, hands or feet.
- When the patient is not being moved, a
sandbag placed on each side or a cervical
collar can splint the neck.
10.3 Treatment of Coma - Use bottles or rolled towels in case
&Convulsions is similar and is sandbag
LogareRoll
not available as shown in the
as follows: figure10 belo
Page 160
Figure 12
10.3.4 Inserting an oropharyngeal airway in
an infant: convex side up
Selectanappropriatesizedairway
Positionthechildtoopentheairwayasdescribeda
bove, taking
carenottomovetheneckiftraumasuspected.
Figure 10 Usingatonguedepressor,inserttheoropharyngea
lairwaytheconvexsideup.
Use the log roll technique to turn the child
on the side if the child is Re-checkairwayopening.
Vomiting. Useadifferentsizedairwayorrepositionifnecess
ary.
Giveoxygen.
Management of Convulsions in
infantup to 2 weeks of age :
SecureIVaccess.
Ifbloodsugar<45mg/dl,give2ml/kg10%dextros
e.
Ifseizurescontinue:IV10%Calciumgluconate2ml
/kg to be diluted in distilled water in proportion
1:1over10minutes to be diluted in
whilemonitoringheartrate(in younginfants).
Ifseizurescontinue:IVphenobarbitone20mg/kg
Figure 11 in 20ml of 5% dextrose or saline
Insertionof an oropharyngeal (Guedel) over20min(Table1).
airway Ifnocontrol:Repeatphenobarbitone10mg/kgtill
atotalof40mg/kg.
The oropharyngeal or Guedel airway can be
used in an unconscious patient to improve Ifseizurescontinue:Givephenytoin20mg/kg in
airway opening. 20 ml of normal saline over20min.
It may not be tolerated in a patient who is Inj. Phenobarbitone intravenous dose
awake and may induce choking or vomiting. (200mg/ml)
Guedel airways come in different sizes

(Guedel size 000 to 4). An appropriate sized Weight Initial Repeat dose
airway goes from the centre of the teeth of Infant dose
(incisors) to the angle of the jaw when laid
on the face with the convex side up.
2 kg or 0.2 0.1 ml
less ml
2 to 4 kg 0.3 0.15 ml
ml
Page 161
Dose of Phenobarbitone for young convulsing in front of you. No drug should
infants (Table 4) be given if the convulsion has stopped.
Caution: Diazepam can be given by the rectal or
DonotuseDiazepamforcontrolofconvulsionsin intravenous route.
Neonates<2weeks. Rectal diazepam dose is 0.5mg/kg (0.1ml/kg)
Managingconvulsions more than 2 by tuberculin syringe or a catheter acts within
weeks of age: 2 to 4 minutes. Hold the buttocks together for
Diazepam is the firstdrug used to stop a few minutes
convulsions (anticonvulsant), if the child is
Intravenous dose is 0.25mg/kg (0.05 ml/kg)
over 1 minute.Diazepamcan
affectthechildsbreathing,soitisimportanttore
assesstheairwayandbreathingregularly.
Per rectal dose of Diazepam (Table 5)

Diazepam given rectally 10 mg / Diazepam given IV
2 ml solution 10 mg / 2 ml solution
Age / weight
Dose 0.1 ml/kg Dose 0.05 ml/kg
2weeksto2months(<4kg) 0.3 ml 0.15 ml
2-<4months(4-<6kg) 0.5 ml 0.25 ml
4-<12months(6-<10kg) 1.0 ml 0.5 ml
1-<3years(10-<14kg) 1.25 ml 0.6ml
3-<5years(1419kg) 1.5 ml 0.7ml
12. Dehydration
If convulsions do not stop after 10 minutes The letter D in the ABCD formula stands for
of second dose of diazepam. Dehydration. Assess for severe
Inj Phenytoin can be given intravenously if Dehydration:To assess if the child is severely
access has been achieved. 15 - 20 mg/kg dehydrated ask for:
Phenytoin is diluted in about 20 ml of saline Lethargic
and given slowly (not more than 1 mg/kg
Phenytoin per minute). Childhavesunkeneyes
Alternatively phenobarbitone can be used in Skinpinchtakelongerthan2secondstogo back

a dose of 15- 20mg/kg IV (in 20 ml 5%
dextrose or saline) or IM.
At this stage, seek help of a senior or more
experienced person, if available If child has diarrhea with any two of the above signs
he is classified to have severe dehydration.
11. If there is high fever: 12.1 Treatment of severe
Spongethechildwithroom- dehydration in an emergency
temperaturewatertoreducethefever.
setting
Donotgiveoralmedicationuntiltheconvulsionhas
beencontrolled(dangerofaspiration).
Page 162
12.1.1 Severe dehydration (without severe IV fluidsfor severe dehydration (Table 6)
acute malnutrition)
StartIVfluidimmediately.Ifthechildcan AGE First give 30 Then give 70
drink,giveORSbymouthwhilethedripissetup.Gi ml/kg in ml/kg in
ve100ml/kgRingerslactatesolution (or
ifnotavailable,normalsaline)dividedasfollows:
*Repeatonceifradialpulseisstillveryweakornot
detectable.
Reassessthechildevery15-
30minutes.Ifhydrationstatusisnotimproving,giv Infants (Under 12 1hour* 5 hours
etheIVdripmorerapidly. months)
AlsogiveORS(about5ml/kg/hour)assoonasthechi
ldcandrink:usuallyafter3-4hours(infants)or1-
2hours(children).
Volume of ORS (Table 7) Children (12 months 30minutes* 2 hours

up to 5 years)
Weight Volume of ORS solution per hour
<4kg 15 ml
4-<6kg 25 ml
6-<10kg 40 ml
10-<14kg 60 ml
14 19 kg 85 ml
Themothercanmaintainhydration by giving the

If IV treatment not possible, give ORS 20 child ORS solution by mouth.
ml/kg/hour for 6 hours (120 ml/kg/day) by NG tube 12.1.2 Severe dehydration with severe acute
Reassessaninfantafter6hoursandachildafter3h malnutrition
ours.Classifydehydration.Thenchoosetheappr It is difficult to determine dehydration status in a
opriateplan(A,B, or C) to continue treatment severely malnourished child, as the usual signs
as you have learned in IMNCI / F-IMNCI. of dehydration (Such as lethargy, Sunken eyes)
may be present in these children all of the time
Giveoralantibioticforcholeraifchild2is whether or not they are dehydrated.
yearsorolder.
Signs of Dehydration
Lethargy
Restless, irritable:
Ifpossible,observethechildforatleast6hoursaft
errehydrationtobesurethat Sunken eyes
Thirsty
Page 163
Skin pinch goes back slowly RECORD the respiration rate.
Treatment of dehydration in the children In addition the following should be recorded:
with SAM without shock Pulse rate.
If the child has had watery diarrhea or vomiting, The capillary refill time
assume dehydration and give ORS. WHO The malnourished child is managed preferably by:
recommends use of ReSoMal, which is not available
commercially. Use either WHO-low Osmolarity Clinical signs of improvement and
ORS with potassium supplements (15 ml Clinical signs of over-hydration.
ofpotassium chloride syrup added to one litre ORS)
as mentioned in step 4 or ReSoMal prepared from 13. MANAGEMENT OF
WHO-low Osmolarity ORS
SHOCK IN CHILDREN
Calculate amount of ORS to give WITH SAM
Table-8: Give ORS as follows in amounts based on Give this treatment only if the child has signs of
the childs weight shock and is lethargic or has lost consciousness
How often to give ORS Amount to give 13.1 Weigh the child Estimate the
Every 30 minutes for the 5 ml/kg body weight weight if child cannot be
first 2 hours
Alternate hours for up to 5-10 ml/kg weighed or weight not
10 hours known
The amount offered in this range should be based on
the childs willingness to drink and the amount of
13.2 Give oxygen
ongoing losses in the stool. Starter (diet is given in 13.3 Make sure child is warm
alternate hours during this period until the child is 13.4 Insert an IV line and draw
rehydrated.
blood for emergency
BEFORE starting any rehydration treatment:
laboratory
WEIGH the child (The weight should be taken on
admission)
MARK the edge of the liver and the costal margin
on the skin
Page 164
Investigations
Give IV 10% Glucose (5ml/kg)
Give IV fluid 15 ml/kg over 1 hour of either ringers lactate in 5%
Dextrose or half-normal saline with 5% glucose
Measure the pulse and breathing rate at the start and every 5-10 minutes
If the child fails to

Improve after the first If the child deteriorates
15ml/kg IV During the IV
(RR increases by 5/min or
PR by 15 beats per min)
Repeat same fluid IV
15ml/kg over 1 hour
more; then Stop the infusion and reassess
Give maintenance IV
fluid (4 ml/kg/hr) Assume
The child has septic shock
Start dopamine
Sign of improvement
(PR and RR fall)
Rehydration
Review antibiotic treatment
Switch to oral or nasogastric rehydration

With ORS 10ml/kg/hr up to 10hours Initiate re-feeding as soon as
Initiate feeding with starter formula Possible
Figure-13:Treatment of shock
Page 165
The management of shock in child with severe acute 13.6 How to give Dopamine (By
malnutrition is given is char3
infusion pump)
13.5 Broad spectrum antibiotic Amount of dopamine (mcg) to be added =
should be administered weight in kgX6
Immediately to all SAM with septic shock (table2) To convert this dose into amount to ml of
packed RBCs 10ml/kg should be given over dopamine dived by 40 (1 ml of dopamine=
40mg of doplamine
4-6 Hours if HB is less than 4 gm/dl or active Add this amount of dopamine (ml) to make 10
bleeding. If there is no improvement with fluid ml of total fluid.
Bolus start dopamine at 10pg/kg/min if there is no 0.1 ml/hour of this fluid gives 1 mcg/kg/minute
improvement in next 24-48 hours upgradesan To give 10 mcg/kg/minute gives infusion at the
ntibiotics. rate on 1ml /hr
Amount of dopamine to be added = 5X6=
30mcg
Page 166
2. NEONATAL RESUSCITATION GUIDELINES
Stabilization (warm, position, clear airway, dry,
1. What is Neonatal stimulation, reposition )
Resuscitation? Ventilation
Neonatal resuscitation means to revive orrestore life Chest compression
to a baby from the state of asphyxia. Intubation
The following guidelines are intended to neonates Drug administration
undergoing transition from intrauterine to extra (The decision to progress from one category to
uterine life. another should be assessed by vital signs;
respiration, heart rate, colour. Approximately 30
seconds is allotted to complete each step)
2. A rapid assessment of the
following 4 characteristics: 3. Preparing for Birth
Was the infant born full-term gestation? Essential:
Is the amniotic fluid clear of meconium and i. A draught free, warm room with
evidence of infection? temperature >25 degree Centigrade
Is the infant crying or breathing, colour of ii. A clean, dry and warm delivery surface
baby? iii. A radiant warmer / overhead lamp with
Does the infant have good muscle tone? 200 watt bulb if available
iv. A newborn size self inflating bag
If the answer is to all 4 of these question is yes, the v. Infant masks in two sizes: size 1 for
infant does not need resuscitation and should not be normal weight baby and 0 for small baby.
separated from mother. vi. A suction device, feeding tube 6F/8F/9F
Observation of breathing, activity, and colour vii. Oxygen (if available)
should be ongoing. viii. Endotracheal Tube size 2.5/3/3.5
If answer is no then the infant should receive 1 or

more of the following 4 categories in sequence.
ix. Laryngoscope 0/1
Page 167
Table-1: Immediate Newborne Care
Immediate Newborn Care
Assess by checking
Is the baby term gestation?
Is the amniotic fluid clear?
Is the baby Breathing or crying?
Does the baby have Good muscle tone?
If yes, provide Routine careRoutine If no
Place the baby on the mother's abdomen. Dry the baby

with a warm clean sheet. Do not wipe off vernix. Proceed for
Wipe the, mouth and nose with a clean cloth. resuscitation
Clamp the cord after 1-3 min and cut with a sterile instrument. Tie the cord with a sterile tie.
Examine the baby quickly for malformations/birth injury.
Leave the baby between the mother's breasts to start skin-to skin care.
Support initiation of breastfeeding.
Cover the baby's head with a cloth. Cover the mother and baby with a warm cloth.
Place an identity label on the baby.
Give Inj Vit K 1 mg IM (0.5mg for preterm).
Record the baby's weight
Refer if birth weight <1500g. has major congenital malformations or has severe respiratory
distress
Page 168
3. GUIDELINES FOR MANAGEMENT OF
NORMAL NEWBORN
- Endotracheal tubes (3, 3.5 mm)

1. Care at Birth:
The four basic needs of ALL newborns at the time - IV cannula (24G)
of birth and for the firstfew weeks of life are:
- Drugs (Inj. Epinephrine , Normal saline,
1. To be warm Inj.Vitamin K)
2. To breathe normally
3. Immediate Newborn Care
3. To be protected (prevent infection)
of a NormalNewborn at
4. To be fed
the time ofBirth:
Most babies would require routine care; 5-10%
Module I : Care ofthe normal baby atbirth
2. Newborn Care Corner may need assistance to establish adequate

breathing and therefore will need resuscitation.
2.1 This is a space within the Deliverthebabyontoawarm,cleananddrytowell
delivery room for facilitating orclothandkeeponmother's
immediate care of the abdomenorchest(betweenthebreasts).
Dry the Baby with a warm clean sheet. Do not
newborn. This area is wipe off vernix
mandatory for all health Wipeboththeeyesseparatelywithsterileswab.
facilities where deliveries take Clampandcuttheumbilicalcordafter1to
place. 3minute,ifbabyisbeathing.
2.2 Equipment and supplies that Well.

should be available in the Assessthebaby'sbreathingwhiledrying.
corner: Examine the baby quickly for Malformation and
birth injury.
2.2.1 Equipment: - Radiant warmer with
bassinet Leavethebabybetweenthemother'sbreaststostartskin
- Suction equipment -to-skincareforatleastan hour.
- Weighing machine Coverthebaby'sheadwithacap.Coverthemotherandb

abywithawarmcloth.
- Self inflatingresuscitation bag (500 ml) with masks
(size 0, 1) Placeanidentitylabel/band/tag onthebaby and mother
- Oxygen source Encouragemothertoinitiatebreastfeeding(withinhalf

anhourofbirth).
- Laryngoscope (straight blade, size 0,1)
- Wall Clock
- Room thermometer
4. Ensuring WARM
CHAIN'
2.2.2 Supplies: - Clean baby sheets
4.1. At delivery
- Sterile cord ties Ensurethedeliveryroomiswarm(25-
- Sterile Gloves 28C),withnodraughtsofair
Drythebabyimmediately; removethewetcloth.
- Sterile blade/scissors Put the baby on the mothers abdomen.
- Mucus extractors Coverthebaby and mother withcleandrycloth
Keep the baby in skin to skin contact with mother
- Suction catheters (10F, 12F) on chest or abdomen
- Feeding tube (6F, 8F) Postpone bathing/sponging for at least 12 hours or
next day
Page 169
4.2. After delivery stump.
Keep the baby clothed and wrapped with the head Leave stump uncovered and dry.
covered.
Avoid bathing especially in cool weather or for 5.4. Care of the eyes
small babies. No routine eye care is required
Keep the baby close to the mother
Use kangaroo care for stable LBW babies and Do not instill any medicine in the eyes
for re-warming stable bigger babies
Show the mother how to avoid hypothermia, 6. Weighing the baby
how to recognize it, and how to re-warm a cold Weigh all babies before transfer from the delivery
baby. room
The mother should aim to ensure that the
baby's feet are warm to touch Initiate breastfeeding within 1 hour
Support mother to initiate breast feeding within
4.3 If mother and babys the first hour.
separation is necessary, do the The babys first feed of colostrum is very
following. important because it helps to protect against
Wrap the baby in a clean dry warm cloth and place infections.
under a radiant warmer. If warmer is not available
ensure warmth by wrapping the baby in a clean dry The baby can feed from its mother whether she is
warm cloth and cover with a blanket. Ensure babys lying down or sitting; baby and mother must be
head, hands and feet are covered. comfortable
Re-start Skin-to-skin contact as soon as mother and Do not give artificial teats or pre-lacteal feeds to the
baby can be roomed-in newborn e.g. sugar water or local foods or even
water.
5. Prevention of infections: 7. Examine the baby
CLEAN CHAIN' 7.1 A complete examination should
5.1. Clean delivery (WHOs six be performed within about 60
cleans) minutes after birth
Clean attendant's hands (washed with soap)
Clean delivery surface Count the number of breaths during one minute.
Clean cord- cutting instrument (i.e. razor, blade) Observe the movement of the limbs when
Clean string to tie cord awake, their position when not moving and
Clean cloth to cover the baby their tone.
Clean cloth to cover the mother Observe the skin color.
Inspect the following body areas for
abnormalities: head, face, mouth and palate,
5.2. After delivery chest, abdomen, genitalia, anus, limbs and skin
All caregivers should wash hands before handling
the baby 7.2 A well baby should have
Feed only breast milk
Keep the cord clean and dry; do not apply anything Normal temperature , warm to touch, pink with
Use a clean absorbent cloth as a diaper/napkin Weight > 2.5 kg
Wash your hands after changing diaper/napkin. Breathe easily at 40-60 breathes/minute
Keep the baby clothed and wrapped with the head Move arms and legs equally when active and
covered rest with limbs flexed
Explain to mother the examination findings to
allay her concern.
5.3. Immediate Cord Care Document in case record and ask her to inform
Clamp the cord after 1-3 min of delivery and cut you , in case any other concerns develop
with a sterile instrument subsequently.
Tie the cord between 2 to 3 cms from the base and 8. Give Vitamin K
cut the remaining cord. Vitamin K will protect babies from serious
bleeding.
Observe for oozing blood. If blood oozes, place a
second tie between the skin and first tie. Give Vitamin K by intramuscular (IM)
injection 1.0 mg for every newborn (0.5 mg
Do not apply any medication/substance on the for <1000 gms).
Page 170
Encourage mothers to breastfeed their baby skincontactasanyothermotherandbaby.
during the injection for comfort.
Exclusivebreastfeedingistherecommendedfeedingch
oiceintheir first6
9. Monitoring the Baby months,irrespectiveofthefactthatthemotherisonARTe
Table-1: Monitoring the baby in the first hour after arly(or)infantis
birth providedwithprophylaxisfor6weeks.(preferably)*
Parameter Whattolookfor? If mother chooses replacement feeding,

prepare formula for the first few
feeds.Ensureitissafe,affordableandsustaina
bleforfamily.
Allothercare(includingcordcareandeyecare)remainst
Breathing Listenforgrunting;Lookforchestin- hesame.
drawingandfastbreathing
Giveoralnevarapineforsixweekstotheneonateaspernat
ionalpolicy.
Mothershouldbecounseledregardingthemodeoff
Warmth Check to see if baby's feet are eedingbeforedelivery
cold to touch (by using dorsum of anddangersofmixedfeeding.
your hands)
11. Postnatal Care of
Normal Baby
Ideally, allpregnant women should be counseled
regarding the care of the baby during the
Color Evaluatethecolorofthetrunkandextremitie antenatalperioditself.Thiswouldhelpthemtobementa
s llypreparedtotakecareoftheirbabies afterbirth.
11.1. Postnatal environment

Ensure that the room is warm without air currents.
Keep mother and baby close together in same room
10. Special Situations and same bed.
10.1 Caesareansection,instrumentaldelivery:
Provide bed nets to sleep.
Skin-to-skin contact and breastfeeding in
difficult deliveries (caesarean section, 11.2 The key areas of every day
instrumentalandbreechdelivery):
Breastfeedingcanbegivnassoonasthemotherisco
care of a newborn baby
mfortableandabletorespondto include:
herbaby.Itdoesnothavetobedelayed
11.2.1. Breastfeeding
Amotherwhowasgivenageneralanaestheticagent
Supportexclusivebreastfeedingondemanddayan
shouldbegivenskin-to-skincontact
dnight.
assoonassheisabletorespondtoherbaby.Thismayb
Askthemothertogethelpifthereisabreastfeedingdi
einitiatedwithinonehourof birth.
fficulty.
Amotherwhohashadanepidural
Assessbreastfeedingineverybabybeforeplanning
(spinal)anaesthetiamaybeabletostartskin-to-
fordischarge.
skincontactverysoonaftersurgery
If
Thesemotherswill
themotherreportsabreastfeedingdifficulty,assess
needadditionalassistanceinpositioningandattachi
breastfeeding
ngthebaby
andhelpherwithattachmentandpositioning.
comfortably.Breastfeedinginlyingdownposition
DONOTdischargethebabyifbreastfeedingisnotes
maybemorecomfortableinthefirst days
tablished.
10.2 HIV and newborn care at birthCare of a baby
born to HIV+ve mother 11.2.2Keeping the cord healthy
Care of the baby at delivery should be no different Washhandsbeforeandaftercordcare.
PutNOTHINGonthestump.
from the care already described.
Foldnappy(diaper)belowthelevelofthestump.
Standardsafetyprecautionsmustbefollowedaswithany Keepcordstumplooselycoveredwithcleanclothes.
otherdelivery. If stump is soiled, wash it with clean water and
soap.
Babycanhaveimmediateskin-to-
Page 171
Dry it thoroughly with clean cloth.
Lookforsignsof infection (daily).
12. Ensure immunization
Allbabiesshouldreceivethefollowingvaccinesim
- Pusdischargefromthecordstump. mediately after birth
beforedischargefromthehealthfacility:
-
- BCG,
Rednessaroundthecordespeciallyifthereissw
elling. - OPV-0,
- High temperature (more than 37.5C) or other - Hepatitis B(HB-0)
signs of infection 13. Criteria for discharge
Explain to the mother that she should seek care
if the umbilicus is red or draining pus or blood.
from a health facility
Feeding well (suckling effectively) at least 8
It is important to teach the mothers that the times in 24 hours
umbilical stump should be left dry; they SHOULD No danger signs
NOT APPLY ANYTHING on the stump. Mother is confident to take care of baby
11.2.3 Ensuring hygiene Understands the need for follow up and danger
Wash the face, neck, and underarms of the baby signs when to report early
daily. For small baby below 2500gms: feeding well
Do not bathe the baby before 24 hours of age or and gaining weight adequately
if the baby is cold.
In case of small babies, bathe only 14. Advise on essential care
after the baby reaches a weight of
2000g.
for neonate at discharge
If bath is given 14.1. Feed breast milk
Ensureroom is warm and there is no draught Breast milk is the best and is the only food
while changing clothes, washing and bathing baby needs for first six months Mother needs
Use warm water for bathing to breastfeed day and night, at least eight
Thoroughly dry the baby, dress and cover after times in 24 hours Mothers need to take
bath nutritious meals and should drink lots of
Take extra precautions if the baby is small clean water.
Wash the buttocks when soiled. Dry thoroughly. For a smallbaby who finds difficult to
Use cloth diaper on baby's bottom suckle,express breast milk and collect in a
to collect stool. Dispose off the clean cup to feed the baby with a paladai, cup
stool as for woman's pads. Wash or spoon.
hands after disposing.
Do not apply Kajal on eyes 14.2. Keep clean
Wash your hands with clean water and soap
11.2.4 Looking for danger signs and giving before every feed and after visiting toilet and
treatment handling baby's faeces / urine.
Itisimportantthatmothers,caregiversandhealthwork Keep the surroundings clean
ersareableto recognize thesigns Keep the cord stump clean; do not apply
andsymptomswhichindicatethatthebabyisnot well anything on cord
('DANGERSIGNS').
Earlyrecognition of the danger signs will help in 14.3. Keep warm
identifying those babies who need urgent care and Keep the baby well wrapped in a clean dry
treatment. cloth or blanket (in cold season) Cover baby's
head with part of cloth / blanket or put a cap
Danger Signs are - on the head Keep the room warm avoid direct
Not feeding well draught of air
No movement Keep next to mother for warmth; it promotes
Fast breathing (more than 60 breaths per lactation and mother-baby bonding
minute) Encourage KMC for Low birth weight babies
Moderate or severe chest in-drawing
Jaundice on day 1 or palms or sole stained 14.4 Counsel and educate the
yellow any age abnormal movements. mother and family
Fever (temperature >37.5C) Build confidence of the family intaking care
Temperature <35.5C or not rising after re- of baby at home
warming Ensure that the family understands
Normal neonate: Preparing for discharge importance of administering prescribed
Page 172
medicines for the whole duration. term neonates which begins on the face and
Educate mother when to reportfor follow up spreads down to the trunk and extremities in
after discharge about 24 hours. This should be differentiated
Educate mother when to reportearly if from pustules which need treatment.
thereisworsening of condition at any time It disappears spontaneously after two to three
after discharge days without any specific treatment. The
Educate mother for signs of well babyfeeds exact cause is not known.
on breast, active behavior,pink extremities
and trunk &extremities are warm to touch. Weight loss of 6-8% (10-12% in preterm
Ensure baby is infants) in the first few days of life is normal
gaining weight on and most infants regain their birth weight by
follow up. 10-14 days.
Advicefor timely immunization
15.5. Bowel disorders.
No medication should be prescribed for passage of
15. Management of Common stools after each feed (exaggerated gastrocolic
Clinical Conditions in reflex) as this is normal in some babies. From 3rd to
14 days many exclusively breasfed babies pass
New Borns loose stools (10-15 times/day) without
There are several phenomena after birth that are illness/dehydration. These are transitional stools and
normal and mothers only need reassurance. These require no medication.
include:
Developmental variations & Physiological
15.6. Delayed passage of urine.
conditions
Non-passage of urine by 48 hours after birth may
Knowledge of developmental variations, suggest urinary tract anomalies. Such babies need to
physiological conditions and their evolution be investigated. Crying before passing urine is
innewborns is important for advising and assuring normal.
the mother. Mothers observe their babies very
Jitteriness is abnormal only when it is excessive or
carefully and are often worried by minor physical
persists even during feeding and then it may suggest
peculiarities, which may be of noconsequence and
hypoglycaemia or hypocalcaemia.
do not warrant any therapy.
15.7. Dehydration fever.
15.1. Mastitis neonatorum
Engorgement of breasts occurs in term babies Transitory moderate fever (up to 38.50C) usually
of both sexes on the third or fourth day and during the second or third day of life in summer
may last for days or even weeks which is due months in an active baby, who sucks well, is normal
to persistence of maternal hormones for some and responds to lowering the environmental
time. temperature.
Local massage, fomentation and expression
of milk should not be done as it may lead to 15.8. Excessive crying.
infection. Mother should be reassured that
this regresses on its own. Most baby cry when either they are hungry or are
having discomfort such as due to full bladder before
15.2. Vaginal bleeding passing urine, wet napkin, nose block, etc.
Vaginal bleeding may occur in female babies Excessive inconsolable crying or high-pitched
about three to five days after birth which is crying is indicative of meningitis or any other
because of withdrawal of maternal hormones. painful inflammatory conditions.
The bleeding is mild and lasts for two to four
days. 15.9. Umbilical granuloma.
Additional vitamin K is unnecessary.
A red flesh-like nodule at the base of umbilical cord
15.3. Mucoid vaginal secretions can be managed by cautery with Silver Nitrate or
Most female babies have a thin, grayish, application of common salt for 3 to 4 days.
mucoid, vaginal secretion, which should not
be mistaken for purulent discharge. 16. Normal phenomena in
15.4. Toxic erythema or Erythema new born
Peeling skin: Dry skin with peeling and
neonatorum exaggerated transverse sole creases is seen in
This is an erythematous rash with a central all postterm and some term babies.
pallor appearing on the second or third day in
Page 173
Milia: Yellow white spots on the nose or face hard palate. Similar lesions may be seen on the
due to retention of sebum, are present in prepuce. They are of no significance.
practically all babies and disappear Sucking callosities: The presence of these
spontaneously. buttons like, cornified plaques over the centre
Storkbites (Salmon patches or nevus simplex): of upper lip has no significance.
These are discrete, pinkish- gray, sparse, Tongue Tie: It may be in the form of a fibrous
capillary hemangiomata commonly seen at the frenulum with a notch at the tip of the tongue.
nape of neck, upper eyelids, forehead and root This does not interfere with sucking or later
of the nose.. They invariably disappear after a speech development.
few months. Non retractable prepuce: The prepuce is
Mongolian blue spots: In babies of Asiatic normally nonretractable in all male newborn
origin irregular blue areas of skin pigmentation babies and should not be diagnosed as
are often present over the sacral area and phimosis. The urethral opening is often pinpoint
buttocks, though extremities and rest of the and is visualized with difficulty. The mother
trunk may also be affected. These spots should be advised against forcibly retracting the
disappear by the age of six months. foreskin.
Subconjunctival hemorrhage: A semilunar arc Hymenaltags: Mucosal tags at the margin of
of sub-conjuctival hemorrhage is a common hymen are seen in two-third of female infants.
finding in normal babies. The blood gets
reabsorbed after a few days without leaving any Umbilical hernia: Umbilical hernia may
pigmentation. manifest after the age of two weeks or later.
Epstein Pearls: These are white spots, usually Most of these disappear spontaneously by one
one on either side of the median raphe of the or two years of age.
Page 174
4. CARE OF AT-RISK NEONATES
The care of 'at-risk' neonate should be initiated at

1. An 'at-risk' neonate has the health facility itself under direct supervision.
one or more of the After initial improvement, further care can be
provided at home
following features:
Weight 1500-2499g 2. The care of at-risk babies
Temperature (axillary) 36.0C-36.4C
Babies with moderate or severe hypothermia
is outlined below:
who respond to warming 2.1. Warmth:
Cried late (>1min) but within 5 minutes of Grading of hypothermia
birth
Sucking poor, but not absent sucking reflex Normal temperature: 35.5-36.5C
Depressed sensorium, but is arousable Cold stress : 36.4-36.0C
Respiratory rate of over 60 per minute, but no Moderate hypothermia : 35.5-
chest retractions 32C
Jaundice present, but no staining of Severe hypothermia : <32C
Module 8:Care ofAt-risk and Sick Neonates
palms/soles
Presence of any one of the following:
- Diarrhea or vomiting or abdominal distension
- Umbilicus draining pus or pustules on skin
- Fever
The steps are dependent up on the current temperature of the baby (see below). (Table 1)
Temperature Management
Normal -Prevent hypothermia
temperature - Wrap the baby in layers of clothing
- Cover the head and limbs
- Place the baby in direct contact with mother
- In winter months, the room may have to be warmed with heater,
etc
Cold stress -Treat hypothermia

(temperature - Wrap the baby with extra layers of clothing
36.0C and 36.4C) - Cover the head and limbs
-Place the baby in close contact with the mother, preferably skin-to skin
In winter months, heat the room with a heater , etc.
Hypothermia - Requires immediate exposure to a radiant

(Temperature heat source (such as radiant warmer) or heater
2.2. Stabilization Most of these babies do not require stabilization
Page 175
other than prevention for hypothermia as above. If sucking well, she is provided expressed breast milk
there is occasional apnea, physical stimulation may by spoon or paladai. Occasionally, expressed
be provide breast milk may have to be given by gavage
feeding.
2.3. Feeds
The baby is started on direct breast feeding. If not 2.4. Specific therapy
Some simple conditions can be readily treated at the health facility and later at home. (Table 2)
Condition Treatment
Umbilical redness - Local application of 1% gentian violet
And Discharge -Syrup Amoxycillin 1.25ml TDSx7days
Skin pustules Local application of 1% gentian violet.
Syrup Amoxycillin 1.25ml TDSx7days
Module 8:Care ofAt-risk and Sick Neonates

Pneumonia (Respiratory
rate >60/min, no chest syrup Amoxycillin 1.25ml TDSx7days) retractions)
2.5. Monitoring 2.7. Communication

The following signs should be monitored everytwo Communication with the family, especially the
hours: mother is very important during the management of
at-risk and sick neonates.
Signs to be monitored
Communication with the family
Temperature
1. Reassure the mother and family.
Convulsion
Sucking
2. Prepare a note regarding baby's condition and
care.
Bleeding
3. If baby improves and is to be sent home,
Sensorium explain care of the baby at home.
Diarrhea 4. If baby does not improve or worsens,
explain the need for referral and care
Respiration
during transport.
Vomiting
Apnea
3. FOLLOW - UP
Advice about follow-up visits
Abdominal distension
Keep the baby warm
Cyanosis
Provide exclusive breast milk feeding
2.6. Re-evaluation Continue the prescribed treatment
Observe progress of baby
After stabilization and/or specific therapy, the baby
Counsel and educate the mother and family
has to be re-evaluated for improvement.The two
Follow-up:
cardinal signs of improvement are:
A home visit by the health worker one day after
i. The temperature will become normal evaluation at hospital is desirable. Thereafter
(36.5C -37.5C) and the baby should be seen again after 2 and 7
ii. The baby will accept feeds well. days by health worker.
Page 176
5. CARE OF SICK NEONATES
Infuse IV 10% Dextrose @ 60ml/kg/day
1. A sick neonate is the one Inject Vitamin K 1.0 mg intramuscular
who has any of the Provide oxygen
Consider and assess for sepsis
following features:
Weight <1500 g 3. Prevent hypothermia: warm
Temperature <36C despite warming for one
hour chain
Cried after 5 minutes of birth Baby must be kept warm at all times right from
Absent sucking birth. The "warm chain" is a set of 10 interlinked
Not arousable procedures carried out at birth and later
Respiratory rate more than 60/min with chest
retractions Warm delivery room (>25C)
Apnea or gasping respiration Warm resuscitation
Central cyanosis Immediate drying
Jaundice staining palms/soles
Skin-to-skin contact between baby and the
Convulsions
Bleeding mother
Major malformation Breast feeding
Presence of two of the following Bathing and weighing postponed
- Diarrhea or vomiting or abdominal distension Appropriate clothing and bedding
- Umbilicus draining pus Mother and baby together
- Multiple skin pustules Warm transportation
- Fever
Training/awareness-raising of healthcare
Alsorememberthatifan'at- provider
risk'neonatedoesnotimprovewhilebeing
observedunderyourcare,heisalsoconsideredasickneo 4. Expression of breast milk
nate. Breast milk expression is required for optimal
feeding of newborns for preterm, low birth weight
2. Grading and management and sick newborns that cannot breastfeed but can
of hypothermia tolerate assisted feeding.
Baby who is cold to touch both centrally and Expressing breast milk
peripherally or temperature is less than 35.5C
4.1. Teach the mother to:
2.1. Management of hypothermia Wash hands with soap and water before
expression. Hold, handle or cuddle the baby
Record the actual body temperature Sit comfortably and hold the clean container
Re-warm a hypothermic baby as quickly as near the breast
possible: Put thumb and index finger on the breast at the
Severe hypothermia Radiant warmer rim of the areola opposite each other. Support
Mild to moderate hypothermia- Kangaroo the breast with other three fingers.
Press thumb and index finger slightly inward
mother care or Radiant warmer
towards the chest wall
If hypothermia still persists despite taking above Press the breast between the fore-finger and
measures, infection should be suspected thumb. Press and release, press and release.
This should not hurt
Press the areola in the same way from the sides,
this ensures that milk is expressed from all
2.2. Management of severe segments of the breast
Avoid rubbing or sliding fingers along the skin
hypothermia Express one breast for at least 3-5 minutes until
Keep under radiant warmer the flow slows; then expresses the other side;
Reduce further heat loss and then repeats on both sides
Page 177
To express breast milk adequately it may take Feed with cup or spoon or paladai, never feed
20-30 minutes with bottle
4.2. Storing expressed breast milk 5. Assisted feeding of low

(EBM) birth weight neonates
Cover the container of EBM with a clean cloth
or a lid 5.1. Newborns that require
EBM can be kept at room temperature for 8 assisted feeding:
hours and in the refrigerator for 24 hours Preterm <34 weeks or birth <1800 g
EBM stays in good condition longer than Babies having mild respiratory distress
animal milk. Do not boil the EBM. For Babies with inability to feed at breast or by
warming place the container in a bowl of warm katorispoon/paladai
water Oro-facial defects/malformation (Cleft lip or
Before feeding gently shake the container or palate)
use a stirrer to recombine the separated fat
globules with the rest of the milk
Table 1
Guidelines for the modes of providing fluids and feeding
Birth weight (grams) < 1200 1200-1800 >1800

Gestation (weeks) < 30 30-34 >34
Initial feeding Intravenous fluids try Gavage, try katori- Breastfeeding, if
gavage feeds, if not spoon if not sick unsactisfactory, give
sick katori-spoon feeds
After 1-3 days Gavage Katori-spoon Breastfeeding
Later (1-3 weeks) Katori-spoon Breastfeeding Breastfeeding
After some more time Breastfeeding Breastfeeding Breastfeeding
(4-6 weeks)
5.2. Mode for providing fluids and Leave oro-gastric tube in situ
Pinch the oro-gastric tube during withdrawal
feeds Measure pre-feed abdominal girth just above
Breast milk is the ideal feed for low birth weight
the umbilical stump. Do not attempt pre-feed
babies.
aspirates
Those unable to feed directly on the breast can be Evaluate baby for ileus, if abdominal girth
fed expressed breast milk (EBM) by gavage OR increases by >2cm from baswline
katori-spoon or paladai.
5.3. Techiques of assisted feeding: 5.4. ROUTINE RE-FEED

Gavage feeds GASTRIC ASPIRATES ARE
Place an oro-gastric feeding catheter of size 5-6 NOT RECOMMENDED
Fr after measuring the correct insertion length Katori-spoon/paladai feeds
from ala of nose to tragus and from tragus to Place the baby in a semi-upright posture
midway between xiphisternum and umbilicus Place the milk filled spoon at the corner of
Check correct placement by pushing in air with mouth
10 ml syringe and listening with stethoscope Allow milk flow into baby's mouth slowly,
over upper abdomen allowing him to actively swallow, avoiding
Attach 10 ml syringe (without plunger) at the the spill
outer end of the tube, pour measured amountof Reapeat process till required amount has been
fed
milk and allow milk to trickle by gravity. Close
Try gently stimulation if baby does not
outer end of tube after feeding actively accept and swallow the feed
Place baby in left lateral position for 15 to 20 If unsuccessful, switch back to gavage feeds.
minutes to avoid regurgitation
Page 178
Change the IV infusion set and fluid bag
6. Intravenous fluid therapy every 24 hours
for newborn: Before infusing IV fluid, carefully check:
Expiry date of the fluid
6.1. Criteria for starting Seal of the infusion bottler or bag
intravenous fluids Fluid is clear and free from any visible
Among newborns particles
Neonates with lethargy and refusal to feed
Moderate to severe breathing difficulty 6.4. Monitoring of babies receiving
Babies with shock
Babies with severe asphyxia
IV fluid:
Inspect infusion site every hour for redness
Abdominal distension with bilious or blood
and swelling
stained vomiting
If redness and/or swelling is present, stop
6.2. Choice of intravenous fluids infusion, remove cannula, and establish a
Determine required volume of fluid as per new IV line in a different vein
birth weight and age (Table 2) Check the volume of fluid infused, compare
Use 10% Dextrose for initial 48 hours of life to the prescribed volume and record all
After 48 hours, if baby is passing urine, use findings
commercially available IV fluids such as Measure blood glucose every nursing shift,
lsolyte P i.e. 6-8 hours
If the premixed solution is not available or If the blood glucose is less than 45 mg/dl,
baby requires higher GIR (Glucose infusion treat for low blood glucose
rates) If the blood glucose is more than 150 mg/dl
Take normal saline (NS) 20 ml/kg body on two consecutive reading: Change to 5%
weight Dextrose solution-measure blood glucose
Add remaining fluide volume as 10% again in three hours
Dextrose Weigh the baby daily. If the daily weight loss
Add 1 ml KCL/100 ml of prepared fluide is more than 5% increase the total volume of
fluid by 10 ml/kg body weight for one day
6.3. Administration of IV fluid If there is no weight loss in the initial 3 days
Use micro-drip infusion set (where 1 ml=60 of life, do not give the daily increment
microdrops) If there is excessive weight gain (3-5%)
In this device, ml of fluid per hour is equal to decrease t he fluid intake by 15-20 ml/kg/day
number of micro-drops per minute Check urine output: Normally a baby passes
e.g. 6ml/hr = 6 micro-drops/minute urine 5-6 ml/kg/day
Calculate rate of administration, monitor to Check urine output: Normally a baby passes
ensure that micro-dropper deliver requires urine 5-6 times everyday
rate Fluid requirements of newborns
Establish an IV line. Infuse a bolus of 2 ml/kg
Table 2 body weight of 10% dextrose slowly over 5 min
If baby had convulsions, give bolus of 4-5 ml/kg of
Day of life Amount of fluids required 10% dextrose
(ml/kg/day)
Birth weight > Birth weight
7. Management of
1500 g <1500 g hypoglycaemi
1 60 80 Hypoglycemia in newborns is defined as blood
2 75 95 glucose levels less than 45 mg/dl
3 90 110 Management of hypoglycaemia
4 105 125 Establish an IV line. Infuse a bolus of 2 ml/kg
5 120 140 body weight of 10% dextrose slowly over 5 min
6 135 150 If baby had convulsions, give bolus of 4-5
ml/kg of 10% dextrose
Day 7 150 150
If an IV line is not available, administer 2 ml/kg
onwards body weight of 10% dextrose by gastric tube
Hypoglycemia in newborns is defined as blood Start infusion of dextrose at the daily
glucose levels less than 45 mg/dl maintenance volume to provide at the rate of 6
Management of hypoglycaemia mg/kg/min
Page 179
Measure blood glucose after 30 min and then Repeat bolus of dextrose as above
every four to 6 hrs Increase to infusion rate of 8 mg/kg/min
If blood glucose < 25 mg/dl:
Page 180
6. Management of Low Birth Weight Babies
Nearly 75 percent neonatal deaths and 50 percent Low birth, weight may result from either
infant deaths occur among the low birth weight prematurity (gestational age <37 weeks) or
neonates. Even after recovering from neonatal intrauterine growth retardation (IUGR), which is
complications, some LBW babies may remain more also called small for date baby (SFD).
prone to malnutrition, recurrent infections, and
Preterm babies have distinct physical features
neurodevelopment handicaps. Low birth weight,
that help in their recognition These are:
therefore, is a key risk factor of adverse outcome in
early life. 1.2.1 Skin:The skin of preterm neonate is thin,
transparent and gelatinous whereas that of aterm
1. Low birth weight neonate is thick gelatinous and keratinized.
Low birth weight (LBW) baby is the one who Hair: The back of the preterm babies has abundant
weighs less than 2500 g at birth. growth of fine hair called lanugo.
1.2.2 Ear Cartilage:The external ear or the pinna is soft and devoid of
cartilage in preterm neonates and hence, it does not recoil back promptly
on being folded. In a term baby there is instant recoil.
Figure 1
1.2.3 Breast Nodule:Breast nodule measures less than 5mm in

preterm neonates and 5 mm or more in term babies.
Figure 2
1.2.4 Sole Creases:Anterior one third of the sole reveals a deep

transverse skin crease in preterm neonates and in term neonates they are
present over the anterior two-thirds.
Figure 3
1.2.5 External Genitalia:In males, the scrotum does not have rugae
and testes are not descended into the scrotum. In female infants, the labia
are widely separated, not covering the labia minora, resulting in the
prominent appearance of the clitoris.
Page 181
Figure 4
1.3 Pre-Term Full-Term spells. In an apneic spell the baby stops

Small-for-dates neonates have an emaciated look breathing; develops slow heart rate and turns
and loose folds of skin because of lack of blue.
subcutaneous tissue. These are particularly Intra-ventricular hemorrhage (IVH): Preterm
prominent over the buttocks and the thighs. They infants also have immature vascular bed around
look alert and often plethoric. the brain ventricles. These delicate vessels may
rupture and cause intra-ventricular hemorrhage.
2. Problems of preterm Hypoglycemia - Immature metabolic pathways
of preterm infants predispose them to develop
neonates hypoglycemia.
The basic underlying feature of the preterm LBW Hyperblirubinemia
infant is immaturity of its organ system. They are Infection is another major problem among
prone to develop preterm babies and indeed an important killer
because they are immuno-compromised hosts.
Asphyxia necessitating resuscitation.
Retinopathy of Prematurity (ROP):Preterm
Hypothermia
infants given excess oxygen may develop
Feeding problems - Preterm neonates less than
blindness because of damage to the immature
34 weeks of gestation cannot coordinate
retina.
sucking and swallowing. Therefore, they are
unable to feed from the breast.
Respiratory distress syndrome (RDS): Preterm 3. Problem of SGA neonates
babies especially those less than 34 weeks have
immature lungs, hence they develop RDS The basic underlying problem amongst them is in-
characterized by rapid and labored respiration, utero undernutrition and hypoxia. They are prone to:
indrawing of the chest, grunting and cyanosis. Fetal distress,meconium passage in utero and
Apneic spells: Because of the immature birth asphyxia.
respiratory control mechanisms these babies Hypothermia.
also have a tendency for apneic Hypoglycemia
Congenital malformations.
provided by the father or any other adult.
Request the mother to sit or recline comfortably.
Undress the baby gently, except for cap, nappy
4. Treatment: and socks.
Indication for hospitalization are : Place the baby prone on mother's chest in an
upright and extended posture, between her
Birth weight of less than 1800g; Gestational age breasts, in Skin to Skin contact; turn baby's head
of less than 34 weeks; to one side to keep airways clear.
Neonate who is not able to take feeds from the Cover the baby with mother's blouse, 'pallu' or
breast or by cup (Katori) and gown; wrap the baby-mother duo with an added
A sick neonate (irrespective of birth weight and blanket or shawl.
gestation). Breastfeed the baby frequently.
If possible, warm the room (>250C) with a
4.1. Keeping LBW Babies warm: heating device.
Room temperature should be kept between Skin to Skin contact is the most practical,
28to300C. preferred method of warming a hypothermic
Baby should be provided skin to skin contact infant in a primary health care facility. If not
care (KMC) in the following ways : possible:
Provide privacy to the mother. If mother is not Cloth the baby in 3-4 layers, cover head with a
available, skin to skin contact may be cap and body with a blanket or a shawl; hold
Page 182
baby close to caregiver's body, OR katori-spoon feds should be put on the breasts
Place the baby under overhead radiant warmer, before each feed for 5 to 10 minutes. This will
if available. promote lactational and enable the baby to learn
Keep the young infant warm on the way to the how to suck.
hospital When shifting a baby from one mode of feeding
By Skin to Skin contact OR to another, be very careful. Introduce in new
Clothe the baby in 3-4 layers, cover head with a mode for only some of the feeds to begin with.
cap and body with a blanket or a shawl; hold The feeding of every baby should be
baby close to caregiver's body. individualized. The above recommendations
4.2. Nutrition & Fluids should only serve as broad guidelines.
Neonates weighing less than 1200 g. or those Ensure use of expressed breast milk & start with
having sickness should receive intravenous fluid small volume, and gradually build up.
initially. Most LBW babies weighing more than 1800 g
Enteral feeds should be introduced gradually by are able to feed directly from the breast. In a
gavage as the baby's acute problem begins to stable, growing LBW baby daily intake of feeds
settle. should be gradually built upto 180-200ml/kg.
Infants weighing 1200-1800 g and not having LBW babies should be fed every 2-3 hours
significant illness should be put on gavage feeds starting at 2 hours of age.
initially.
In order to promote lactation and enable the
baby to learn sucking, all babies on gavage or
Table 1
Guidelines for the modes of providing fluids and feeding

Age Categories of neonates
Birth weight (gm) < 1200 1200-1800 > 1800
Gestation (weeks) < 30 30-34 > 34
Initial - IV fluids Gavage feeds - Breast feeds
- Triage - If unsatisfactory, give
- Gavage feeds if not cup-spoon feeds
sick
After 1-3 days Gavage feeds Cup-spoon feeds Breast feeds
Later (1-3 wks) Cup-spoon feeds Breast feeds Breast feeds
After some time Breast feeds Breast feeds Breast feeds
(4-6 wks)
Note: 4 weeks (to ascertain a weight gain of at least

i. On the first day the fluid requirements range 200-300g) and then every month. Hospitalized
from 60 to 80 ml/kg. LBW babies should be weighed every day on
ii. The daily increment in all the groups is the same weighing machine.
around 15 ml per kg till 150 ml/kg is reached. Excessive weight loss, or inadequate weight gain
iii. Adequacy of therapy is indicated by weight indicates inadequate feeding, cold stress, excessive
pattern in the expected range. insensible water loss or systemic illness (like
4.2.1 Judging adequacy of nutrition anemia, sepsis, late metabolic acidosis etc).
The key measure of optimal feeding is the
weight pattern of the baby. A pretermLBW
baby loses upto 1 to 2 percent weight every day 4.3 LBW babies require dose
amounting to 10 percentcumulative weight loss
during the first week of life. Birth weight is
monitoring and follow up of
regained bythe14th day. Growth monitoring- head circumference and
SGA-LBW babies who are otherwise healthy weight
should not have any appreciable weight loss at Developmental assessment and early
all and they should start gaining weight early. stimulation
It is desirable to weigh all LBW babies at 2
weeks (to check regaining of the birth weight),
Page 183
Intraventricularhaemorrhage screening by receive Injection Vitamin K 1 mg and 0.5 mg,
ultrasound cranium on day 1, 3,7& at 4-6 Intramuscular, as per the birth weight > = 1000
weeks. gm and < 1000 gm respectively.
Screening tests for hearing at discharge
All pre-terms < 2000gms should receive oral
Retinopathy of pre maturityscreening at 1
Vitamin and mineral supplement in doses shown
month of age
below:
Screening for osteopenia of prematurity
Multivitamin preparation 0.3-0.6 ml (5-10
4.4. Vitamin Supplements: drops) / day (which usually provides vitamin A
All LBW Babies should receive intramuscular of 1000 IU/day and vitamin D 400 IU/day)
Vitamin K at birth. Every new born should
Calcium 80-100 mg/kg/day.
Phosphorous 40-50 mg/kg/day
4.4.3 All these supplements to be given till at 5.3 Children awaiting splenectomy
least 6 months of age.
Iron should be started at a dose of age. Immunization with pneumococcal, Hib, and
1mg/kg/day at 4 weeks of age and provided till meningococcal vaccine should be initiated a
12 months of few weeks prior to splenectomy.
Vaccination in LBW Babies
5.4Vaccination in children with
If the LBW baby is not sick, the vaccination
schedule is the same for as the normal babies. A
HIV infection:
sick LBW babies however, should receive these Immune response may be suboptimal as it
vaccines only on recovery. depends on the degree of immunodeficiency at
that point of time. Re-administration of
Vitamin A 1000 IU orally daily from 1 week
childhood immunization may be considered
age onwards
when their immune status has improved
following anti-retroviral therapy.
5.. Immunization in special
circumstances 5.5Lapsed immunization:
There is no need to restart a vaccine series
5.1Immunization in preterm regardless of the time that has elapsed between
infants: individuals doses. In case of unknown or
uncertain immunization status, however, it is
In general, all vaccines may be administered as appropriate to start the schedule as for an
per schedule according to the chronological age unimmunized child.
irrespective of birth weight or period of
gestation. Very low birth weight / preterm 5.6Minor illnesses,
babies can be given or period of gestation. Very
low birth weight / preterm babies can be given e.g. fever, diarrhea, respiratory infections and
immunization, if they are stable otherwise. malnutrition should not be construed as
contraindications to immunization.
5.2Children receiving
corticosteroids: 6. Prognosis
Mortality of LBW babies is inversely
Children receiving oral conticosteroids in high
related to gestation and birth weight and directly
doses (Prednisolone 1-2 mg/kg/day) for more
tothe severity of complication.
than 14 days should not receive live virus
vaccines until the steroid has been discontinued In general, over 90% Low birth weight
for at least one month. Killed vaccines are safe babies who survivethe newborn period have no
but may not be completely effective in such neurodevelopment handicaps.
situations. Patients on topical or inhaled
steroids should not be denied their age Therefore, essential care of theLBW
appropriate vaccine. neonates is a highly rewarding exper
Page 184
7.Assessment of Neonatal Sepsis
Neonatal sepsis is one of the three major causes of 1.5 CNS:
neonatal mortality. Sepsis is largely preventable.
Fever, seizures, blank look, high pitched cry,
1. Clinical manifestations of excessive crying/irritability, neck retraction, bulging
fontanel
neonatal sepsis
2. Laboratory diagnosis of a
1.1 Non-specific:
newborn with sepsis
Lethargy, refusal to suckle, poor cry, not arousable,
comatose Sepsis Screening: Any of two tests that come
positive out of the following five tests strongly
1.2 Gastrointestianal: indicate presence of sepsis:
Abdominal distension, diarrhea, vomiting, poor 1. Leukopenia (TLC/ Total leucocyte count
weight gain <5000/cmm)
1.3 Cardiovascular: 2. Neutropenia (ANC/ Absolute neutrophil count

<1800/cmm)
Hypothermia, poor perfusion, shock, bleeding and
sclerema 3. Immature neutrophil to total neutrophil (I/T) ratio
(>0.2)
1.4 Respiratory: 4. Micro ESR/Erythrocyte sedimentation rate
Cyanosis, tachypnea, chest retractions, grunt, (>15mm 1st hour)
apnea/gasping 5. Positive CRP/ C-reactive protein
Page 185
3. Figure-1: Approach to newborns at- risk of sepsis
Neonate at risk of sepsis
Symptomatic Asymptomatic
High suspicion Low suspicion Do sepsis screen

Blood culture
Blood culture Sepsis Screen Negative Positive

Blood Culture Take blood
culture
And start antibiotics
Start antibiotic Negative screen Repeat sepsis screen

After 12 hr after 12 hr
Positive screen
Negative screen Duration - acc

to
Clinical
Course& culture*
Duration according Monitor clinically Monitor clinically

To clinical course
Culture sterile - 7-10 days Culture Positive - 10-14 days
Escherichia coli, Staphylococcus aureus and

4. Antibiotic therapy for a Klebsiella pneunoniae
newborn with sepsis A combination of Ampicillin and Gentamicin is
recommended for treatment of sepsis and
4.1 Choice of antibiotics pneumonia
Antibiotic therapy should cover the In suspected or confirmed meningitis, add
Cefotaxime with an aminoglycoside
common causative bacteria, namely
Page 186
Following table provides the antibiotics and
dosages of antibiotics for newborn sepsis
4.2 Antibiotic therapy of

neonatal sepsis
4.2.1 Septicemia of Pneumonia
Table-1: Antibiotic Management for Septicemia of Pneumonia
Antibiotic Each dose Frequency Route Duration

<7 days age >7 days age
Inj Ampicillin or 50 mg/kg/kg/dose 12 hourly 8 hourly IV 7-10 days
Inj Cloxacillin 50 mg/kg/kg/dose 12 hourly 8 hourly IV 7-10 days
and
Inj Gentamicin or 5 mg/kg/kg/dose 24 hourly 24 hourly IV 7-10 days
Inj Amikacin 15 mg/kg/kg/dose 24 hourly 24 hourly IV 7-10 days
4.2.2 Meningitis
Table-2: Antibiotic management of Meningitis
Antibiotic Each dose Frequency Route Duration

<7 days age >7 days age
Inj Ampicillin or 100 mg/kg/kg/dose 12 hourly 8 hourly IV 3 weeks
and
Inj Gentamicin 2.5 mg/kg/kg/dose 12 hourly 8 hourly IV 3 weeks
OR
Inj Gentamicin or 50 mg/kg/kg/dose 12 hourly 8 hourly IV 3 weeks
and
Inj Amikacin 2.5 mg/kg/kg/dose 12 hourly 8 hourly IV 3 weeks
Infuse 10% dextrose 2 ml/kg stat
Inject Vitamin K1 mg intramuscularlyStart
5. Supportive care of a oxygen by hood or mask, if cyanosed or
grunting
newborn with sepsis Provide gentle physical stimulation, if apneic.
Provide warmth, ensure consistently normal Provide bag and mask ventilation with oxygen
if breathing inadequate
temperature
Avoid enteral feed if hemodynamically
compromised, give maintenance IV fluids
Consider use of dopamine if perfusion is
Start intravenous line persistently poor
If CFT >3 seconds, infuse normal saline 10

ml/kg over 20-30 minutes, repeat the same 1-2
times, if perfusion continues to be poor
6. Summery of commonly used doszge in neonates

Page 187
Table-3: Administration of commonly used drugs
Drug Dose Route

Ampicillin Age <7 days: 50 mg/kg/dose, q 12 hour IV
Age <7 days: 50 mg/kg/dose, q 8 hour

Gentamycin Sepsis/ pneumonia IV
5 mg/kg/dose, q 24 hour
Meningitis
Age <7 days: 2.5 mg/kg/dose, q 12 hour
Age <7 days: 2.5 mg/kg/dose, q 8 hour

Amikacin <7 days: 15 mg/kg/dose, q 24 hour IV
Cefotaxime <7 days: 50 mg/kg/dose, q 12 hour IV
<7 days: 50 mg/kg/dose, q 8 hour

Chloramphenicol 12 mg/kg/dose, q 12 hour IV
Aminophylline 5 mg/kg loading, IV
then 2 mg/kg/dose q 8-12 hour

Vitamin K 1 mg IM
Phenobarbitone 20 mg/kg loading over 10-15 minutes Loading IV Then
IV, IM or oral
then 3-4 mg/kg q 24 hour
Phenytoin 15-20 mg/kg loading over 10-15 minutes IV
then 5 mg/kg q 24 hour

Dopamine/ Dobutamine 5-20 micro g/kg/minute IV continuous
Page 188
8. Treatment of Respiratory Distress
In Newborn
im od for
1. Incidence:Increases as 2 days
Gestation age decreases OR
28 weeks => 60 %
Dexamethasone => 6mg im bd 2 Days
28-34 weeks => 30%
(NOTE: validity of this injection is for one week
34 weeks => 5-10%
And have to repeat after that if more delay in
delivery
2. Prevention: Can be
prevented by giving steroid 3. Assessment after delivery:
gestational age
to mother
Temperature
Antenatally
Indicated for those who are at risk for Heart rate
preterm
Sao2
delivery in next 8 days
Treatment for Prevention Capillary refill time
Betamethas
one 12 mg

Silverman anderson score

Figure 1
4. Scoring Chart
Table 1: Scoring Chart
Page 189
Interpretation: Start CPAP
SA score=> 3 Oxygen by hood CPAP Begin With 4-6 cm of waterpressure
3 -7 => CPAP ventilation And use Fio2 10
% more than required
>7Mechanical ventilation
Monitor ABG
4.2 Investigation : W/F Apnea
X ray chest: PA view Increase CPAP BY 1-2cm up to 8cm water pressure
Septic screening And Fio2 up to 100%
Blood culture Start Mechanical ventilator: if with Fio2 of 100% and

CPAP of 8cm
Serum electrolyte
ABG
Blood glucose
SA score is > 7
5. Management:
In general: OR
Maintain temperature = Baby with persistent Apnea
36.5 -37.5 c
Other
Restrict fluid to 2/3 maintenance Watch for diuresis
Maintain Sao2 88-95% Watch for clinical improvement
Give maintenance of fluid
Antibiotics if septic screen +ve
Main management 5.4 Fluid management
If fio2 requirement is < 30% & SA score <3 If CRT is more than 3
Oxygen by hood
Watch for diuresis Give 10ml/kg NS bolus
If improvement noticed give maintenance Monitor liver size
Fluid and start feed
If require give Dopamine 5-10 microgr/kg/min
If fio2 Requirement is > 30% & SA score >3
OR Dobutamine 10 microgr/kg/min
Page 190
9. MECONIUM ASPIRATION SYNDROME
1. Management in delivery
Vertex or breech presentation
room
1.1 If MAS watch for Colour Birth Asphyxia
/consistency of meconium Perineal suction With Dee Lee mucus Aspirator at

delivery of Head of baby
Figure-1: Indication of Endotracheal intubation
MAS -----------------> IF babys cry is vigorous
If cry is not vigorous No Intubation
ROUTINE CARE
Intubation ------------------ Meconium not retrieved
Under cord suction No suction
Meconium retrieved
Continue suction HR < 100/min
HR > 100 /min IPPR
Continue suction
Page 191
2. Management in NICU
2.1 Assessment of baby: 2.2 Interpretation
Gestational age score
r/o IUGR 1 -3 => mild respiratory distress => Oxygen by
r/oU.cord /nail/skin hood
staining
4-6 => moderate respiratory distress=> CPAP
Downe ventilation
score >6 => severe respiratory distress => Ventilator
0 1 2 3. Investigation: CBC, ABG, x
Respiratory rate <60 ray chest, blood culture
60-80 >80
Grunting NO Audible with
4. Supportive management
Audible without Pass infant feeding tube=> gastric lavage
Stethoscope Stethoscope Iv fluid initially if require
Antibiotic if respiratory distress OR
Cyanosis NO In room air If septic screen is positive
with 40% oxygen Treat complication
Ventilator if required along with surfactant
Air entry good decrease
markedly decrease
5. Complication
Retraction NO mild
severe Atelectasis
Hypoxic Ischaemic encephalopathy
Pneumothorax
PPHN (Persistant primary pulmonary hyper
tension) requiring nitrousoxide and sildenafil
Page 192
10. BLEEDING NEONATE
Slipped ligature
1. Common causes Vit k deficiency
G I BLEEDING Skin: petechiae
Swallowed maternal blood Sepsis
Hemorrhagic disease of New Born Platelet disorder
Sepsis Ecchymosis
Stress ulcer
Platelet defect Sepsis
Clotting factor deficiency Clotting factor deficiency
Umblical cord
1.4 Occult blood Cephalehematoma Preterm

Intra VentricularHaemorrhage Vit.k deficiency
Subdural Heaemrrahe sick neonate
2. APPROCH
Maternal History INCREASE RISK OF
2.1.1 Antenatal infection
eg. TORCH Thrombocytopenia
2.1.2 Drugs given to mother

Phenytoin
Phenobarbitone Heamorrhagic disease of NB
Aspirin/Anticoagulant
2.1.3 Bleeding in mother = Thrombocytopenia
eg.ITP /SLE
Birth Asphyxia
Trauma DIC
Time of Bleeding
2.2.1< 24hrs = Swallowed maternal blood
Hemorrhagic disease of NB
2.2.2> 24 hrs = Classical hemorrhagic disease
of NB
Sepsis /DIC
Platelet abnormality
Trauma
Liver dysfunction
2.1.3 Other clinical features
Petechiae Jaundice
Echymosis Hepatosplenomegaly
Pallor Bulging Ant .fontannel
3. Investigation
Page 193
Figutre-1: Apt .test:
1 ml gastric aspirate + 5ml distilled water
Centrifuge to formSupernatant
4 ml of Supernatant + 1ml NAOH 1%
Change of colour to colour remains to pink

Yellow /brown
Maternal blood fetal blood
Figure-2: Differential Diagnosis
Platelet PT PTT
Thromobocytopenia N N
Haemohagic disease N
Of newborn
Clotting factor N N
Deficiany
Dic
Page 194
4. Management
A) If APT test showns Maternal =>parental counseling
B) If APT test shows fetal blood
a) Injvit k 1 mg IV stat
b) if PT/PTT increases OR in sick neonate
10-15ml /kg FFP (IF required repeat after 12hrs)

c) If Hb<10 gm% = Give fresh blood transfusion
d) If platelet <50000 in sick Neonate
OR <25000 in Healthy Neonate
Platelet transfusion 10-20ml/kg
C) Treat for sepsis / DIC / primary disease

Antibiotics: Ampicilline 50 to 100 mg/kg in divided doses IV.
Gentamycin 7.5 mg/kg in divided doses IV. If not responding to these then start higher antibiotics such
as ceftriaxone, merupenum etc.
Treatment of DIC.
Treatment of primary disease.
Page 195
11. JAUNDICE IN THE NEWBORN
1. Introduction: 3. Pathological jaundice:
Hyperbilirubinemia is the commonest morbidity in A TSB concentration exceeds 5 mg/dl on first
the neonatal period and 5-10% of all newborns day of life in term neonate, 10 mg/dl on second
require intervention for pathological day, or 12-13 thereafter.
jaundice.Nearly 60% of term newborn becomes Any TSB elevation exceeding 17 mg/dl.
visibly jaundiced in the firstweek of life. In most Appearance of jaundice within 24 hours, peak
cases, it is benign and no intervention is required. TSB levels above the expected normal range,
Presence of clinical jaundice beyond 3 weeks
2. Physiological jaundice: and conjugated bilirubin (dark urine staining
the clothes and light colored stool)
Jaundice attribute to physiological immaturity of
neonates to handle increased bilirubin production. 4. Signs &Symptons:
Visible jaundice usually appears between 24-72
hours of age. Total serum bilirubin (TSB) level 4.1 Clinical examination of
usually rises in full-term infants to a peak of 6 to 8
mg/dL by 3 days of age and then falls. A rise to jaundice:
12mg/dL is in the physiologic range. In premature The newborn should be examined in good
infants, the peak may be 10 to 12 mg/dL on the fifth daylight.
day of life, possibly rising over 15 mg/dL without
any specific abnormality of bilirubin metabolism. The skin should be blanched with digital
pressure and the underlying color of skin and
subcutaneous tissue should be noted.
Dermal staining in newborn progress in a
cephalo-caudal direction. Newborns detected to
have yellow discoloration of the skin beyond the
legs should have an urgent laboratory confirmation
for levels of TSB.
Fig. 1: Levels of Jaundice

4.2 Clinical determination of jaundice by Kramers criteria
Area of body Range of serum bilirubin (mg%)

Head and neck 4-8
Upper trunk 5-12
Lower trunk and thigh 8-16
Arms and lower limbs 11-18
Palms and soles >15
5.
Page 196
This is suspected by increasing lethargy with
Investigations: risingbilirubin levels but recovery following or
Following investigations must be done in a prompt exchange transfusion.
case of neonatal jaundice
6.2 Kernicterus.:
Serum bilirubin direct and indirect.
This term has been traditionally used to describe the
Blood grouping of mother and child ABO and
pathological findings of bilirubin toxcity within the
Rh.
brain. This includes staining and necrosis of neurons
Direct coombs test in infant. in the basal ganglia, hippocampal cortex,
Haematocrit and peripheral smear for RBC subthalamic nuclei and cerebellum followed by
morphology and reticulocyte count. gliosis of these areas, should the baby survive. The
Indirect coombs test in mother if she is Rh cerebral cortex is generally spared, but 50 % of
negative babies have extraneuronal lesions with necrosis of
renal tubular cells, intestinal mucosa and pancreatic
6. Complication: cells. They may manifest as gastrointestinal
Transient encephagopathic: Early bilirubin induced hemorrhage or hematuria
neurologic dysfunction is transient and reversible.
Clinically, kernicterus is described in phases, which
may progress over 24 hour to 7 days:
FIGURE-1: DIAGNOSTIC WORKUP FOR HYPERBILIRUBINEMIA

Page 197
IN NEWBORN
Clinical jaundice
Measure bilirubin( total serum bilirubin-TSB)
Bilirubin >12mg/dl bilirubin <12mg/dl

Age <24hrs old age >24hrs old
(pathological) (physiological)
Coombs test observe
POSITIVE NEGATIVE Follow

bilirubin
Rh
ABO Direct bilirubin
Kell
Less than 2mg%
Hct
NORMAL OR LOW HIGH POYCYTHEMIA
RBC morphology
Reticulocyte count
ABNORMAL NORMAL
Spherocytosis Enclosed hemorrhage
ABO incompatibility Brestmilk jaundice
Red cell enzyme defect Hypothyroidism
Alpha thalassemia Crigler-najjar syndrome
Gilbert syndrome
7.
Page 198
TREATMENT HYPERBILIRUBINEMIA
MODALITIES OF
Hydration 7.2. Phototherapy (table 1 and 2)
Phototherapy (Do not keep in sunlight).
Exchange transfusion Special blue lights to be used
Drugs to increase conjugation. 45cm distance between baby and phototherapy

unit
7.1. HYDRATION Eys and genitelia shuld be covered
Double surface phototherapy is preferred
Countinued and frequent breast feeding 8-10
Watch for side effects(diarrhoea, skin rash,
times/day
hyper/hypothermia)
TABLE 1- Guidelines for Phototherapy according to APP
Healthy, term newborn (>37 weeks)
Age (hours) ConsiderPhototherapy TBS (mg/dl) Phototherapy

TSB (mg/dl)
< 24
25-48 >12 >15
49-72 >15 >18
>72 >17 >20
NOTE: TSB-Total serum bilirubin

TABLE 2- Phototherapy indications
7.2.2 Based on birth weight and health of the newborn
Borth weight(grms) Healthy; TSB Sick ; TSB

(mg/dl) (mg/dl)
<1000 5-7 4-6
1001-1500 7-10 6-8
1501-2000 10-12 8-10
2001-2500 12-15 10-12
TERM
>2500 15-18 12-15
Page 199
Fig. 2 : Namogram for age & serum bilirubin level
7.3 Points to remember 7.4 Exchange transfusion.

Try to establish diagnosis before instituting Choice of blood
phototherapy by carrying out necessary
7.4.1 Choice of blood
investigations.
If baby and mother is Rhve use only Rh-ve
Check blue light functioning; life of these light
blood.
is 1500-2000hrs(appox 3 months). Keep lights
Always cross match donors blood with both
at distance of 18 from the baby.
mothers and babys blood.
When blue lights are not available four pairs of
white tube light may be usedinstead. 7.4.2Criteria for Exchange Transfusion
Change the position of baby after every 2 hrs. Cord bilirubin more than or equal to 4.5mg%
Babies can be taken out of phototherapy for and Hb < 11g%
breast feeding Rate of rise of bilirubin >1mg/dl despite
Monitor babys temperature 2 hourly. phototherapy
Monitor fluid balance daily weight and urine In LBW babies indirect bilirubin> (weight in
output. Increase fluid as necessary. g)/100
Shield the eyes in both sexes to prevent the Exchange earlier at level of 2 mg% less for
retinal damage and genitals in male to prevent following criteria-
mutation defect in adulthood. Sepsis
Monitor rise or fall of bilirubin every 12 hourly. RDS
Do not give phototherapy for direct Asphyxia
hyperbilirubinemia. Acidosis
Hypoglycemia.
Page 200
12. MANAGEMENT OF SURGICAL NEONATE
Neonatal surgical problems 1.2.2 Gastrointestinal
1.1 Major: Esophageal Atresia

Cong. Hyperpyloric stenosis (CHPS)
Tracheoesophagial fistula Gastrochiasis
Diaphragmatic hernia Abdominal wall defect
Intestinal Obstruction
Neural tube defect Omphalocele
Omphalitis
Other:
Chest Deformities
1.2.1 Orofacial
Congenital Lobar emphysema
Cleft lip Vascular Ring
Cleft palate Orthopedic
ChoanalArtesia CTEV (Cong Talipus Equine Varus)
Pierre robin sequel Developmental dysplasia of hip
Laryngeal web Other
Clavicle fracture
Humerus fracture
Femur fracture
Page 201
13. VITAMIN A DEFICIENCY
1. Introductions 3.2 Importatant aspects of Vit A

Vit A deficiency Symptons If the child more than 1 year of age and weighing
Delayed dark adaptation less than 8 kg., then Vit A dose is 1,00,000 IU to
More prone for intestinal , respiratory and avoid hypervitaminosis A
urogenital infections Give oil based preparation
Bottles have solution strength of 100000IU Vitamin
2. Classification A/ml
XN------Night Blindness Cold chain is not required.
X1A----ConjunctivalXerosis Shelf life of unopened opaque container is 2 years.
X1B-----Bitot Spots Opened liquid is to be used in 6to 8 weeks.
X2-----Corneal Xerosis Capsules are partially protected against loss of
X3A---Corneal Ulceration <1/3 potency.
X3B---Corneal Ulceration >1/3 3.3 Treat Night blindness
XS----Corneal Scarring Conjunctivalxerosis, Bitotspots, Cornealxerosis,
XF---Xeropthalmic Fundus Cornealulceration, Keratomalacia in all except
3 Treatment immediately women of reproductive age group.
In acute corneal lesion, patient should be referred to
after diagnosis hospital on emergency basis.
3.1 Age wise doses of Vit A High dosages of Vit A can causes pseudotumar
<6 months-----------50,000IU VitaminA orally cerebri which will manifest as vomiting headache
6 to 12 months------100000IU Vitamin A orally and bulging anterior fontenelle
>12 months----------200000IU Vitamin A orally
Next day-------------------------Same age specific 3.4 Corneal Xeropthalmia
dose i. Topical Antibiotic ointment (Tetracycllin 1%, eye
At least 2 weeks later-------Same age specific dose oitment, Tobramycin eye ointment 3% bd)
ii. Eye protection
Page 202
14. RICKETS
1. Metabolic disease of childhood in which the Malabsorption
osteoid, the organic matrix of bone fails to Renal disease
mineralise, due to interference with calcium Celiac disease
metabolism. Hepatic osteodystrophy
Anti - epileptic drugs
Vitamin D deficiency
Fig. 1 : Clinical features in Rickets
Investigations Loss of transverse trabeculae
3.1 Seriology No sub-periosteal resorption of bone
Serum calcium - normal or decreased, 4. Treatment:

Serum phosphorus - decreased, Single oral dose of 6 lakh IU of vitamin D
Alkaline phosphotase - increased 2nd dose after 3 to 4 weeks (if no sclerotic
change is seen in x-ray)
3.2Urine Exam If the child responds to above treatment
maintenance dose of 400 IU of vitamin D is
Urinary calcium - decreased given once Serum alkaline phosphotase is
nomal, consider corrective surgery, If any.
3. X- ray: Calcium - 0.5 to 3 gm/day for 3 months
Generalized demineralization Vitamin D - 10,000 IU/day once a month
High protein diet
Page 203
15. MANAGEMENT OF CHILDREN WITH
ANAEMIA
Mild to moderate anaemia is a common co- mayhavehyperpigmentationofknucklesandocca

morbidity in children attending health facility sionally bleeding manifestations due to
for various conditions. Hence, anaemia/pallor thrombocytopenia.
should be looked for in each patient attending The onset of anaemia in young children is
the health facility. generally after 6 months of age. Before this,
Severe anemia in a child is suggested by the iron in breast milk is sufficient to meet the
presence needs of a breastfed child.
ofseverepalmarpallorandmaybeassociatedwitha In India, diets for children in the age group 6
fastpulserate,difficultyinbreathing,orconfusionor 23 months are predominantly plant-based and
restlessness. provide insufficient amounts of micronutrients
Nutritionalanaemiaisthemostcommoncauseofan to meet the recommended nutrient intakes.
aemiainchildren.
Nutritionalanaemiaresultsfromdeficiency
ofiron,folicacidandvitaminB12.
Childrenhavinganaemiaduetofolicacidand/orB1
2deficiency (megaloblasticanaemia)
Table 1
Clinicalassessmentofanaemiainchildrenlessthan5years
Findings on anaemia in children

History Examination
Durationofsymptoms Severepalmarpallor
Usualdiet(beforethecurrentillness) Skinbleeds(petechialand/orpurpuricspots)
Familycircumstances(tounderstandthechildssocialbackgr Lymphadenopathy
ound)
Hepato-Splenomegaly
Prolongedfever
Signsofheartfailure(galloprhythm,raisedJVP,
Worminfestation
respiratory distress, basal crepitations)
Bleedingfromanysite
Lymphnodeenlargement
Previousbloodtransfusions
Similarillnessinthefamily(siblings)
Facility level management All children referred from field to health

Any child reporting to any facility (PHC level facility due to palmar pallor will undergo Hb
and above) with any illness will be assessed level estimation before initiating treatment
clinically by the attending Medical Officer for Children will be categorised as having mild,
anaemia routinely and should undergo Hb moderate and severe anaemia on the basis of
estimation if found to be anaemic clinically Hb levels and will be managed as per Table
below.
Page 204
Table 2
Treatment of Anaemia
Level of HB Treatment Follow-up Referral

No Anaemia (>11 20 mg of elemental iron and 100 mcg of folic acid in biweekly regimen
gm/dl)
Mild Anaemia (10 3 mg of iron/ Kg/ day for Follow-up every 14 In case the child has not
10.9 gm/dl) 2 months days by ANM responded to the treatment of
anaemia with daily dose of
And Hb estimation after
iron
completing 2 months
Moderate Anaemia
of treatment to for 2 months, refer the child to
(79.9 gm/dl) document Hb>11 the FRU/DH with F-IMNCI
gm/dl trained MO/ Paediatrician /
Physician for further
investigation
Severe Anaemia Refer urgently to DH/FRU

(<7 gm/dl)
Note: malnutrition and in a known case of

After completion of treatment of anaemia and haemoglobinopathy and anaemia in these cases
attaining Hb level >11.5 gm/dl, the should be treated as per the standard treatment
IFAsupplementation to be resumed guidelines, by the attending physician, as per
Treatment of anaemia with iron should be the merit of the individual case.
withheld in case of acute illness, severe acute
3.1 Dose of IFA surup

Table 3
Dose of IFA syrup for anaemic children 6 months5 years
Age of Child Dose and Frequency
6 months12 months (610 kg) 1 ml of IFA syrup Once a day
1 year3 years (1014 kg) 1.5 ml of IFA syrup Once a day

3 years5 years (1419 kg) 2 ml of IFA syrup Once a day
Page 205
Table 4
Management of severe anaemia at FRU/DH (as per F-IMNCI) in children 6 months5 years and 5-10 years
3.2.1 History of Examination
History to be taken for Examination for

Duration of symptoms Severe palmar pallor
Usual diet (before the current illness) Skin bleeds (petechial and/or purpuric spots)
Family circumstances (to understand the Lymphadenopathy
childssocial background) Hepato-splenomegaly
Prolonged fever Signs of heart failure (gallop rhythm, raised
Worm infestation JVP, respiratory distress, basal crepitations)
Bleeding from any site
Any lumps in the body
Previous blood transfusions
Similar illness in the family (siblings)
3.2.1 Investigation & blood transfusion indication
Table 5: Investigation & Management
Investigations Indication for Blood Transfusion Blood Transfusion

Full blood count and All children with Hb 4 gm/dl If packed cells are available, give
examination of a thin film Children with Hb 46 gm/dl with any 10 ml/kg over 34 hours
forcell morphology of the following: preferably. If not, give whole
Blood films for Dehydration blood 20 ml/kg over 34 hours.
malariaparasites Shock
Stool examination for ova, Impaired consciousness
cystand occult blood Heart failure
Deep and laboured breathing
Very high parasitaemia
(>10% of RBC)
Page 206
16. MUMPS
1. Introduction:
Mumps is swelling of parotid glands due to
infection of the parotids by mumps virus. Apart
from parotids, it affects some other vital organs and Un-immunized host gets infected from a case.
systems in the body and can have serious Patient is infective l-2 days before appearance
complications with risk of morbidity and mortality. to 2-3 days after disappearance of parotid
Therefore it is important to know the course of swelling. Incubation period ranges between 2-3
illness, various complications, early detection for weeks. 30-40% infections are sub clinical. After
prompt management, and preventive measures. entry through air, the virus multiplies in
respiratory tract and reaches all organs via
blood. Prodromal symptoms are in the form of
2. Signs &Symptons: fever, muscle pains, neck pain, and malaise.
Fig. 1: Mumps : Paritid Swelling
are presenting symptoms in a patient with

3. Investigation: mumps
Diagnosis: is mainly clinical more suggestive with Deafness - transient or permanent unilateral or
the history of contact. Typical painful tender bilateral nerve deafness may follow mumps.
bilateral parotid swelling with systemic symptoms is Arthritis - Migratory ploy arthralgia or even
diagnostic. arthritis may be seen. These complications
should be treated symptomatically.
4. Complication:
4.1 CNS-Aseptic meningitis-meningoencepnalitis 5. Management:
along with parotitis or 10 days later. Meningitis
indistinguishable from other meningitis. Treatment:
Orchitis,Epididymitis - Occurs in older pts. Mainly symptomatic with paracetamol and
Occurs one week following parotitis with frequent gargling with warm saline.
painful swelling of testes. Illness lasts for about Watch for evidence of complications. If orchitis
4 days. Testicular atrophy may follow in l/3 or arthritis occurs, prednisolone can be used to
patients with rare affection of fertility. reduce pain.
Oopharitis in females may rarely occur.
Pancreatitis -Epigastric pain, tenderness, 6. Prevention:
vomiting, fever are suggestive. Laboratory MMR vaccine - combination of mumps,
evidence of raised amylase confirms the measles, and rubella offers above 95%
diagnosis. protection. Primary immunization at the age of
Thyroiditis - May follow after one week in 15 months, followed by revaccination at l0
adults with development of antithyroid anti years,
bodies. Since it is a live viral vaccine, immuno-
Myocarditis - Mild- moderate myocarditis with compromised hosts should not be vaccinated.
ST changes on ECG is found in some older Isolation of the affected child is not useful to
patients. Chest pain, bradycardia and fatigue prevent spread to other children in usual
contact. However, fresh contacts like guest
Page 207
children can be protected if the affected child is always gives lifelong protection against
isolated from them. another, therefore, such children do not benefit
Children usually recover from mumps in about from any immunization later.
10-12 days- First arrack of mumps almost
Page 208
17. SEVER ACUTEMALNUTRITION (SAM)
Standardsor
1. Introduction Bipedaledema.
Malnutritionremainsoneofthemostcommoncauses If weight-for-height or weight-for-length cannot be

ofmorbidityandmortalityamongchildren.Thehighc measured, use the clinical signs for visible severe
asefatalityratesamongseverelymalnourishedchildr wasting
encan
bereducedbyusingstandardizedandeasilyimplemen 3. Assessment of severely
tableprotocols. malnourished child
2. Criteria for hospital A good history and physical examination is
required for deciding the treatment but always start
admission the emergency
Weightforheight/length<-3z Treatment
scoreofmedianofWHOchildgrowth first.Thedetailsofhistoryandexaminationcan
berecorded later.
Table 1:
History Examination
Recentintakeoffoodandfluids Anthropometry-weight,height/length,midarm
Usualdiet(beforethecurrentillness) circumference
Breastfeeding Oedema
Durationandfrequencyofdiarrhoeaandvomiting Pulse,respiratoryrate
Typeofdiarrhoea(watery/bloody) Signsofdehydration
Lossofappetite Shock(coldhands,slowcapillaryrefill,weakandrapid
Familycircumstances(tounderstandthechildssocial pulse)
backgronnd) Severepalmarpallor
Chroniccough EyesignsofvitaminAdeficiency:
Contactwithtuberculosis - dry conjunctiva or cornea,
Recentcontactwithmeasles -Bitotsspots
Known orsuspectedHIVinfection. -Cornealulceration
Immunizations -Keratomalacia
Localizingsignsofinfection,includingearandthroatinfection
s, skin infection or pneumonia
Fever(temperature37.5Cor99.5F)or
hypothermia(axillarytemperature <35.0 Cor<95.0 F)
Mouthulcers
Skinchangesofkwashiorkor:
- Hypo or hyperpigmentation
-Desquamation
-Ulceration(spreadingoverlimbs,thighs,genitalia,groin,and
behind the ears)
-Exudativelesions(resemblingsevereburns)oftenwith
secondaryinfection(includingCandida)
Serum electrolytes (sodium, potassium)

3. Laboratory Tests
Screeningforinfections:
Haemoglobinorpackedcellvolumeinchildrenwit - Total and differential leukocyte count,

hseverepalmarpallor. blood culture (If possible)
Bloodsugar. - Urineroutineexamination
Page 209
- Urineculture preparationofappropriatefeeds,andtocarryoutreg
ular feeding during the day and night. Accurate
- Chestx-ray
weighing machines are needed, and records
should be kept of the
4. Organization of care feedsgivenandthechildsweightsothatprogresscan
On admission, the child with severe malnutrition bemonitored.
should be separated from infectious children and
kept in a warm area (2530C, withnodraughts), 5. Providing general
and
constantlymonitored.Washingshouldbekepttoamini
treatment for malnutrition
mum, after whichthechildshould be dried Thereare10essentialstepsintwophases: an
immediately. initialstabilizationphaseandalongerrehabilitationphase
.
Facilitiesandsufficientstaffshouldbeavailabletoensu
recorrect
Table-2: Treatment for Malnutrition
Stabilization Rehabilitation
Days1-2 Days3-7 Weeks2-6
1. Hypoglycaemia
2.
3.
4. Electrolytes
5. Infection
6.Micronutrient Noiron withiron
7. Initiate
8. Catch-
9. Sensory stimulation
10. Prepareforfollow-up
rferewiththebodysimmunemechanismsagainstprolife
5.1 Important things not to do and ratingbacteria.
why?
5.1.1Do not give I/V fluids
routinely.I/Vfluidscaneasilycausefluidoverloadandhea 5.2 Treat hypoglycaemia
rtfailure.OnlygiveI/Vfluidstochildren with signs of
shock. Ifthechildislethargic,unconscious,orconvulsing,
giveIV10%glucose5ml/kgfollowedby50mlof10%gluc
5.1.2Do not gives diuretics to treat oedema. The oseorsucrosebyNGtube.IfIVdosecannotbegivenimme
oedema will go away withproper feeding. Giving diately, givetheNGdosefirst.Give appropriate
diuretics will antibioticsandstart feeding as soon as possible.
worsenchildselectrolyteimbalanceandmaycausedeat
h. Ifnotlethargic,unconscious,orconvulsing,givethefirstf
eedofstarterformula(75cals/100ml),ifitisquicklyavaila
5.1.3Do not gives high protein formula. Almost all
severely malnourished children have infections, bleandthencontinuewith2hourly feeds.
impaired liver and intestinal function. Because of Ifthefirstfeedisnotquicklyavailablegive50mlof10%gluc
these problems, they are unable to tolerate the usual oseorsugarsolution(4roundedteaspoonofsugarin200
amount of dietary protein.
mloronecupofwater)orallyorbynasogastrictube,follo
5.1.4 Do not give iron during the initial feeding wedbythefirstfeedassoonaspossible.
phase.
Give2-
Add iron only after the child has been on catch-up hourlyfeeds,dayandnight,atleastforthefirstday.
formula for2days Giveappropriateantibiotics.
(usuallyduringweek2).Givingironearlyintreatmenthas
beenassociatedwithfreeradicalgenerationandmayinte Keepthebabywarmandchecktemperature.
Page 210
Prevent hypoglycaemia/Begin Starter Formula antibiotics.Ifaspecificinfectionisidentified(suchasShige
Feed2hrly,startingimmediatelyor,ifnecessary,rehydra lla),givespecificappropriateantibioticsaccordingtocond
tefirst.Continuefeedingthroughoutthenight. ition
5.3 Infection identified.Hypoglycaemiaandhypothermiaareoftensign
sofsevereinfection.
5.3.1 Presume and treat infection
5.3.2 Select antibiotics and prescribe regimen
Assume all children with severe malnutrition Select antibiotics as shown in the chart below.
admitted in a hospital have an infection and give
broad spectrum
Table 3: Antibiotic Treatment
Status Antibiotic
All Inj.Ampicillin50mg/kg/dose6hrlyandInj.Gentamicin7.5mg/kgoncea
admitte day for 7 days
d cases AddInj.Cloxacillin50mg/kg/dose6hrlyif staphylococcalinfectionis
suspected
Revisetherapybasedonsensitivityreport
For septic IVCefotaxime50mg/kg/dose6hrlyorInj.Cerftriaxone50mg/kg/dose12hrlyplusInj.A
shock or mikacin15mg/kg/onceaday
worsening/ no
improve
ment in
initial
ho urs
Meningi IVCefotaxime50mg/kg/dose6hrlyorInj.Ceftriaxone50mg/kg/dose12
tis hrlyplusInj.Amikacin15mg/kg/onceaday
Dysente Inj.Ceftriaxone100mg/kgonceadayfor5days
ry
5.3.3 Duration of antibiotic therapy depends on the InvestigateandfollowHIVguidelines.

diagnosis i.e.: 5.4.5
Suspicion of clinical sepsis: at least 7 days Severeanaemia:Givewholebloodorpackedcelltransfus
Culturepositivesepsis: 10-14days Meningitis: ionifHbis<4g/dlorHbis4-
atleast14-21days 6g/dlandchildhasrespiratorydistress.Give10ml/kgslo
Deepseatedinfectionslikearthritisandosteomyelitis: wlyover4-
atleast4weeks 6hoursandgiveInj.Frusemide1mg/kgatthestartofthetra
nsfusion.Donotrepeatbloodtransfusionwithin4days.
5.4.5 Ifeyeproblems(keratomalacia) due
tovitaminAdeficiency,inadditiontovitaminAdosesinsti
5.4 Treat Associated Conditions llciprofloxacineyedrops2-3hourly
5.4.1 Giveantimalarials andatropineeyedrops3timesadayfor7-
ifbloodsmearpositiveformalariaparasites. 10days.Alsocovertheeyeswithpadandbandage.
5.4.2 5.4.6Skinlesions:Batheorsoaktheaffectedareasfor10
StartATTiftuberculosisisdiagnosedorstronglysuspect minin1%potassium
ed(Mountaux TestandXraychest). permanganatesolutionandapplygentianvioletornystati
ncreamifavailable
5.4.3 toskinsoresandanybarriercream(zinccream)totheraw
SuspectHIVifhehasalsootherproblemslikepersistentd areas.
iarrhoea,oral
5.4.7
Thrush, Persistentdiarrhoea:Diarrhoeaiscommoninseveremal
pneumonia,parotidswellingorgeneralizedlymphaden nutritionbutwithcautiousrefeeding,itshouldsubsidedu
opathys. ringthefirstweek.Intherehabilitationphase,
Page 211
thepoorlyformedloosestoolsarenotacauseforconcern, severeoedema),80-
providedthechildsweightgainissatisfactory.Ifthechild
100Kcal/kg/dayand1-1.5g/kg/dayofproteins.
has persistentdiarrhoea,screenfornon-
intestinalinfectionsandtreatappropriately.Continuebr
eastfeedingandtrytogivefeedswithlowlactoseinitiallya Usenasogastricfeedingtillchildtakesorally75%ofallfee
ndsubsequently change to lactose free options if ds.
diarrhoea persists.

Ifchildbreastfed,continuebreastfeedingbutgivethefeed
first.
5.4 Micronutrients
5.4.1 Give oral vitamin A in a single dose. Ensurenightfeeds.
Vitamin A orally in single dose as given below:

5.6.1 Starter Formula
<6months :50000IU (if
clinicalsignsofdeficiencyarepresent). Starterformulaistobeusedduringinitialmanagement.Iti
sstartedassoonaspossibleandcontinuedfor2-7days
6-12months:1lakhIU.
untilthechildisstabilized.Severelymalnourishedchildr
Olderchildren: 2lakhIU. encannottolerateusualamountsofproteinsandsodium
atthisstage, or high amounts of fat. They may die if
Children<8kgirrespectiveofageshouldreceive1la given too much protein or sodium. Starter formula is
khIUorally. specially made to
meetthechildsneedswithoutoverwhelmingthebodys
Givehalfoftheabovedoseifinjectable systemsintheinitialstageoftreatmentwhichprovides75
(intramuscular)vitaminAneedstobegiven. calories/100mland0.9gmofprotein/100ml.
GivesamedoseonDay0, 1and14 5.6.2 Feed the child Starter formula orally, or by NG
ifthereisclinicalevidenceofvitaminAdeficiency. tube if
Necessary: Oral feeding
5.5.2 Other micronutrients should be given Itisbesttofeedthechildwithacupandspoon.Encourag
daily for at least 2 weeks: ethechildtofinishthefeed.Ittakesskilltofeedaverywea
kchild,sonursingstaffshoulddothistaskfirstandmothe
Multivitaminsupplement(shouldcontainvitaminA, rmayhelpwithfeedinglaterwhenchildbecomesstrong
C,D,EandB12&
er.Encouragebreastfeedingondemandbetweenstarte
NotjustvitaminB-complex): r formulafeeds.
2RecommendedDailyAllowance.
Nasogastric feeding
Folicacid:5mgonday1,then1mg/day.
ItmaybenecessarytouseaNGtubeifchildisveryweak.U
Zinc: 2mg/kg/day. seanNGtubeifthechilddoesnottake75%ofthefeedfor2
Copper:0.3mg/kg/day -3consecutivefeeds.
(ifseparatepreparationnotavailableuse Remove the NG tube when the child takes:
Commercialpreparationcontainingcopper). 75%ofthedaysamountorally;or
Whenweightgaincommencesandthereisno Twoconsecutivefeedsfullybymouth.
diarrhea add3mgofiron/kg/day.
5.6Initiate feeding
Essentialfeaturesofinitial feedingare:
Startfeedingasearlyaspossible.
5.6.3 Record intake and output on a 24-Hour
Feedthechildifalertanddrinkingevenduringrehydratio food intake chart.
n.
Criteriaforincreasingvolume/decreasingfrequencyoff
eeds
Givefrequentandsmallnutrientrichfeedsoflowosmolar
ityandlowlactose. 1. Ifthereisvomiting,significant
diarrhoea,orpoorapetite,continue2-hrlyfeeds.
Offer130ml/kg/dayofliquids(100ml/kg/dayifchildhas
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2.
Ifthereislittleornovomiting,diarrhoeaislessthanbefore,and 5.6.4 Monitoring
mostfeedsareconsumed,changeto3-hrlyfeeds. Monitorandrecord(seeAppendixformonitoringcharts
3. Afteradayon3- )
hrlyfeeds:Ifthereisnovomiting,occasionaldiarrhoea,andm Amountsoffeedofferedandleftover
ostfeedsareconsumed,changeto4-hrly.
Stoolfrequencyandconsistency
Recommended schedule with gradual increase in Vomiting
feed volume is as follows
Canreplacefreshmilk30mlwith3.5gmwholedriedmilk Dailybodyweight
Page 213
18. FEVER WITH RASHES
Varicella, herpesvirus, coxackievirus, enterovirus,
1. Introduction : meningococcal, group A streptococcal and
Fevers associated with generalized skin eruptions/
rashes (exanthematous fevers) are common in Pseudomonas infections.
childhood. These are often seen as epidemics in the
periods of 'season change' like March-April and 4. Petechial/purpuric
October-November when adenoviruses become
active.
Epstein barr virus, echovirus 9, cytomegalovirus,
Differential Diagnosis of Exanthema
Macular and/or papular rash rickettsial, malaria, pneumococcal, meningococcal
and Listeria infections.
a) Measles, rubella, erythema infectiosum, roseola,
coxackievirus, echovirus, CMV, hepatitis B 1. Measles
infections. Measles is a communicable disease manifesting
with fever, cough, coryza, lacrimation and Koplik
b) Erythema multiforme due to herpesvirus, Epstein spots in the pre-eruptive phase and a maculopapular
barr rash starting on 4th or 5th day of illness. The rash
virus,adenovirus,chlamydiae,Salmonella,Mycobacte heals leaving brawny pigmentation.It is caused by a
ria,histoplasma or coccidioses. RNA virus classified as Morbillivirus, belonging to
paramyxovirus family.Clinical Features: Incubation
2. Nodular period is 8-12 days.
a)Fungal diseases, atypical mycobacterial and
pseudomonas infections. Prodromal Phase: The onset is acute with moderate
elevation of temperature, dry hacking cough,
b) Erythema nodosum. Due toStreptococcus, running of nose, sneezing, redness of the eyes and
Mycobacterium tuberculosisand leprae, Yersinia, excessive lacrimation.
hepatitis C, sarcoidosis, drugs and inflammatory
bowel diseases. 1.1. Signs &Symptons:
Diffuse erythematous with peeling or desquamation Typical measly look in young babies is due to
conjunctivitis, stomatitis and rhinitis due to viral
Scarlet fever, toxic shock syndrome, Kawasaki rash. The first place for the rash to be seen is around
opening of parotid ducts in the mouth/inner cheeks
disease, staphylococcal scalded skin syndrome,
(Koplik's spots). Rash appears on face and
Stevens Johnson syndrome. progresses to appear on trunk and limbs over the
following three to four days. Drying of rash and
3. Vesiculobullous peeling of skin appears in the same sequence in
next4- 5 days.
1.3. Complication:
Acute precipitation of Vitamin A deficiency in a
child with measles can occur and hence corneal
ulceration is a complication to watch out for and to
prevent. All children with measles should routinely
receive vitamin A orally 2 lakh units each on day
l, 2 and 14 (for infants the dose is half)
Due to depressed immunity due to measles, child
can catch infections like diarrhoea, otitis media,
pneumonia and TB. If the child continues to get
fever even after the rash is dry, bacterial pneumonia
Figure 1 : Various types of Rashes
should be suspected. Continued low fever and lack
of appetite should make one suspect TB infection.
1.2. Investigation: Extra-feeding during convalescence and when
HB,TLC, DLC, X-RAY Chest, measle the child gets well is important to prevent
antibody test. malnutrition after measles.
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1.4. Management: Measles immunization as routine immunization
Symptomatic treatment should be given should be promoted.
Paracetamol 10 to 15 mg per kg for fever and Immunization given early to contact of measles
Antihistaminics (Cetrizine) 0.5 to 1mg per kg for case can prevent severe disease in the contact.
itching and rhinitis. Advice continued feeding. Keep 2. Chicken-pox:
baby clean by sponging or quick clean bath.
Treatment with antibiotics (Amoxycilline 30 2.1. Signs &Symptons:
mg per kg per day in 2 to 3 divided doses for 5 Symptom of chicken-pox is characteristic rash.
days) for superadded bacterial infections when The rash is often more severe in older children and
detected. adolescents. The rash appears in several "crops" of
macules (red spots) quickly turning into watery
1.5. Prevention: vesicles and pustules over the next 2 to 3 days and
then drying after scab formation over next 5 days.
Figure 2: Chicken Pox Rash

Due to multiple 'trops" appearing over a week or so, symptoms. Chicken-pox patient is infective till all
one can observe all types of lesions simultaneously scabs are formed. Itching is prominent and
on a patient's body. The rash is more on covered scratching can lead to super added staphylococcal
areas like trunk of body, and can appear inside infection.
mouth. conjunctivae. Vagina leading to irritation
o
Figure 3: Vescicles & umbilication in chicken pox
2.2. Investigation: available; as this is a very serious condition with

Clinically Diagnosed high mortality rate.
2.3. Complication: 2.4. Management:

Aspirin given to a child with chicken-pox infection Sympromatic treatment with Paracetamol 10
may precipitate acute fatty infiltration of liver. Liver to 15 mg per kg per day for 5 days and anti-
failure and encephalopathy (Reye's syndrome). histaminics (Cetrizine) 0.5 to 1mg per kg per day for
Reyes' syndrome is to be suspected if there is 5 days is advised. Daily bath is also advised.
disproportionate vomiting, rapid breathing (in the Acyclovir in the dose of 20mg/kglday in 4 divided
absence of chest signs suggestive of pneumonia) doses for 5 days can be given to immuno-
and altered sensorium. The patient should be compromized patients and patients with
referred for specialist care, where respirator is encephalopathy.

Page 215
19 ENTERIC FEVER / TYPHOID
1. Introduction: 2. Clinical Manifestations :

Although Enteric fever is still a common infection Classical presentations are becoming rare. Common
its presentation has changed partly due to specific manifestations are -
vaccination and partly due to institution of Relative bradycardia compared to fever.
antibiotics early in the course of illness. Tumid tender abdomen (abdomen feels like balloon
filled with water)
Diagnosis is problematic since blood
Cloudy sensorium.
cultures may not reveal much and Widal test is
Maculopapular erythematous rash on abdomen
positive only after 1 week and has many false
blanching on pressure (Rose. spots)
positive and false negative results. Bone marrow
Centrally coated tongue.
culture is more informative, but not practical.
Soft spleen - 1-2 cm tender.
Hence possibility of enteric fever must be Continuous fever, not touching the baseline. (If
borne in mind while treating any pyrexia, which antipyretics are not given)
shows toxicity, and signs suggestive of enteric like Pea soup diarrhea, nausea, vomiting.
confused sensorium, (no meningeal focal Headache, myalgia, anorexia, malaise.
neurological signs). Enteric fever in children.is more severe as compared
to adults.

Fig. 1: Rose spot in typhoid
Chloramplenicol -75 mg/kg/dayOr
3. Investigation: Amoxiycillin 100mg/kg/day (with clavulinic acid)
HB, TLC, DLC, WIDAL TEST (RISING
Or
TITERS),BLOOD CULTURE.
Trimethoprim Sulphamethaxazole 10& 50
Complication: Shock, enteric perforation, mg/kg/day are also used with some success.
haemorrhagemeningits, myocarditis. can complicate
the illness. 4.3 Early institution of steroids
Management: Dexamethasone 3 mg / Kg
stat dose followed by:
4.2 Drug Treatment 1 mg/kg 6 hourly for 48 hours improves the survival
Multi-drug resistant typhoid fever has emerged and of patients in shock, myocarditis' CNS
is difficult to treat. Following drugs are found to be complication.
useful:
Third generation cephalosporins
Cefixime 20 mg /kg 1 day in 2 divided doses 4.4 Intestinal perforation
Or Ceftriaxone 50 mg/Kg per day requires broader spectrum
OrCiprofloxacin 20 mgl Kg per day,
Or Ofloxacin15 mg/Kg 1 day. antibiotics,
Platelet transfusions for severe thrombocytopenia
with haemorrhages' This treatment demands
referral to higher level'
The antibiotics should be continued at least 5-7
days after effervescence.
Page 216
20.ACUTE MENINGOENCEPHALITIS
1. Introduction 2. Clinical Manestations

Acute meningoencephalitis is an acute infl Fever, headache, vomiting, irritability altered state
ammatory process involving meninges andbrain of consciousness signs of meningeal irritation and
tissue, due to infectious causes. The common seizures.
aetiological agents are viruses and bacteria.
Children of any age may be affected.
3. Investigations
CSF examination differentiates the viral from
bacterial cause of acute meningoencephalitis
CSF findings in meningoencephalitis
Table 1: CSF Findings
Pressure Glucose
(mmH2O) Leucocytosis Protein (mg/dl)
(mg/dl)
(mm3)
Normal 50-80 <5, >75% 20-45 >50 or
lymphocytes
75% serum
glucose
Acute bacterial Meningitis Usually 100-10,000 100-500 Decreased

Elevated PMNs*
(<40)
(100-300) predominate
Acute viral Normal or r Rarely 50-200 Normal

Meningoencepha litis elevated >1000 PMNs early
rarely decreased
but
lymphocytes
predominate in
the most of the
course
Tubercular Usually elevated 100-500 PMNs 100-3000 <50
Meningoencephalitis early but later
lymphocytes
predominate
*PMNs = Polymorphonuclear leucocytes
Treatment
Supportive treatment is the mainstay of therapy and is started immediately.
a. Maintain airway, breathing and circulation.
b. Control of seizures with IV injection of Diazepam 0.2 to 0.4 mg/kg stat followed by Inj. Phenytoin 10-20
mg/kg stat followed by 5 mg/kg/day in divided doses.
c. Increased intracranial tension is treated by proper positioning of patient with headelevated at 15-30 position,
fluid restriction to 2/3rd of maintenance, 20% Mannitol5 ml/kg over 10-15 min followed by 3 ml/kg every 6
hourly for 48 hours and thenSOS. Or Acetazolamide 50-75 mg/kg/day in 3 divided doses through feeding tube Or
Glycerine 1 ml/kg/day through feeding tube may be added, if increased intracranial tension persists.
d. Fever is controlled as given in section on fever.
(Caution: Never give aspirin).
e. The intravenous fluid at two-thirds of the maintenance requirement initially. The electrolyte concentration of
the blood is monitored very closely. Any imbalance is treated promptly. Fluid restriction is not done, if patient is
dehydrated or is inshock.
Page 217
f. Feeding: Initially the patient is kept nil orally for first 24-48 hours. Later on the feeding is guided by the level of
sensorium. A tube feeding is helpful for feeding as well as for giving medicines.
4.2 Specific treatment

Until a bacterial cause is excluded, parenteral antibiotic therapy should be administered.The choice of antibiotics
depends upon age of the patient and prevalence of organismin the area.
4.2.1 Age 0-3 months

1. Inj Cefotaxime 200 mg/kg/day IV in 4 divided doses for 14 days.
2. Inj Ampicillin 300 mg/kg/day IV in 4 divided doses for 14 days.
4.2.2 Age 3 months-12 years

1. Inj Ceftriaxone 100 mg/kg/day IV over 30-60 minutes in 2 divided doses for 10 days Or Inj Cefotaxime 200
mg/kg/day IV in 3 divided doses for 10 days
Or Inj Ampicillin 300 mg/kg/day IV in 4 divided doses for 10 days
2. Inj Chloramphenicol 100 mg/kg/day in 4 divided doses for 10 days
If Meningococci is suspected/isolated, Inj Penicillin G 300,000-400,000 IU/kg/day in 4 divided doses for 7-10
days.
4.2.3 Treatment of Viral meningoencephalitis

Herpes simplex virus (generally diagnosed by focal encephalitis or CT scan):
Inj Acyclovir 30 mg/kg/day in 3 divided doses for 14-21 days. Non-HSV viral
Encephalitis is treated by supportive therapy only.
Lumbar puncture is repeated at 48 hours to see the response. However, if the patient is improving well, a repeat
lumbar puncture may not be necessary.
5. Advice at discharge
Regular follow-up for neurological assessment including deafness is advised.
Anticonvulsant therapy to be continued, if seizures are recurrent during course of meningitis. Children with
sequalae would require assessment of handicap and multidisciplinary management.
Occupational/physiotherapy may be taught during hospital stay itself.
Page 218
21. TUBERCULOUS MENINGITIS
1. Introduction
Tuberculous meningitis is the inflammation of MRI of brain maybe normal during early stages
meninges due to lymphohaematogenous spread of of the disease. Later, it can show exudates in
the primary infection of tuberculosis to the thebasal cisterns of brain, periventricular ooze
meninges, found in about 0.3% of untreated primary and hydrocephalus. Some may
infection in children. It is the most dangerous form showtuberculomas even.
of extrapulmonary tuberculosis. 70% of the cases
are found in children less than 5 years of age.
6 Treatment
Treatment consists of proper supportive care,
2. Clinical Manifestations including nonpharmacological treatment, specific
The clinical progression of tubercular antitubercular therapy, treatment of increased
meningitis (TBM) may be rapid or gradual.The intracranial tension and, if required, surgical
signs and symptoms progress slowly over treatment.
several weeks and can be divided into three
stages. 6.1 Nonpharmacological
Nutrition: After initial stabilization, nutritional
2.1 Stages rehabilitation should be done as given in section on
protein energy malnutrition.
2.1.1 The 1st stage, which typically lasts 1-2 Skin care and prevention of bedsores.
weeks, is characterized by non-specific symptoms, Care of bowel and bladder.
such as fever, headache, irritability, drowsiness and Physiotherapy and occupational therapy should be
malaise. Focalneurologic signs are absent. instituted early to preventdeformities and
3.1.1 The 2nd stage usually begins more contractures.
abruptly. The most common featuresare lethargy,
neck-rigidity, seizures, positive Kernig or 6.2 Pharmacological
Brudzinski signs, Hypertonia, vomiting, cranial 1. Appropriate fluid therapy to correct dehydration
nerve palsies and other focal neurologic signs. due to frequent vomiting anddecreased oral intake.
3.1.2 The 3rd stage is marked by coma, 2. Treatment of SIADH. Fluid restriction to three
hemiplegia or paraplegia, hypertension, fouth or two third of maintenance. Treatment of
Decerebrate posturing, deterioration of vital signs, raised intracranial tension
and eventually, death. 3. Inj. Dexamethasone: 0.15 mg/kg IV 6 hourly for
2 weeks followed by Tab.Prednisolone 1.5
4 Complications: mg/kg/day orally through feeding tube for 4 week
Survivors may have motor deficits, cranial this should be tapered over another 2 weeks. A total
nerve deficits, mental retardation, learning of 6-8 weeks therapy with steroid is recommended.
disabilities, seizures, hydrocephalus, blindness, 4. Mannitol (20% solution) 1.5 to 2 g/kg or 8-10
deafness and diabetes insipidus. ml/kg over 30-60 minutes. Repeat every 6-8 hours
for 7 days. Lower doses (0.25 g/kg/dose) can also be
tried. Or Glycerol 1 ml/kg/dose every 6-8 hours,
5 Investigations diluted in orange juice or water, given through
The diagnosis is made by analysis of CSF on feeding tube. Or Tab. Acetazolamide 50 mg/kg/day
lumbar puncture, which shows lymphocytic in 3 divided doses for 2-3 weeks.
leucocytosis with elevated protein and a low 5. Presence of seizures necessitates treatment with
sugar (for details see Table 19.21 in section on phenytoin or carbamazepine in appropriate doses
Meningoencephalitis). (for details see section on Epilepsy in Chapter).
Demonstration of AFB in CSF confirms the 6. Specific antitubercular therapyas given in
diagnosis, but the yield is very poor. management of tuberculosis (seeSection on
Culture of CSF shows growth of M. Tuberculosis).
tuberculosis, takes too much time. 7. Surgical treatmentventriculoperitoneal shunt
Positivetuberculin skin test corroborates the (VP shunt): TBM shows somedegree of
diagnosis but may be negative in hydrocephalus by 4 weeks. Obstructive
severelymalnourished/disseminated disease. 20- hydrocephalus should be shunted immediately. Non-
50% of children have a normal chestradiograph obstructive hydrocephalus with increased
others may show primary disease. CT scan or intracranial pressure as shown by ventricular tap or
Page 219
CT scan will also be benefi ted by VP shunt. An causes of increased ICP is untreated hydrocephalus
early shunt is preferable. or blocked shunt.
2. Check compliance to drugs and ensure that
occupational therapy/physiotherapy isbeing
continued.
3. Assess physical, mental, visual and auditory
handicap and take expert opinion for rehabilitation
from other specialists. Patient/parent education
Seriousness of disease must be explained.
Contact survey should be done and any other
member in the family found to have active TB
should be counselled to attend TB clinic for therapy.
6.3 Follow-up Need for compliance should be emphasized.
1. Patient should be kept under follow-up after Drug toxicity and side effects must be explained.
discharge from the hospital andassessed for Neurological defi cits may appear even in a patient
neurological deficit and features of increased on therapy.
intracranial pressure(ICP). One of the common
Page 220
22. ACUTE RESPIRATORY INFECTION
disease and can be managed in the community with
1. Introduction oral co-trimaxazole. Severe ARI cases require
Acute Respiratory Infection (ARI) is an important urgent referral to a facility where injectable
cause of infant and child mortality and also the antibiotic therapy and supportive care are available.
commonest cause of morbidity among children
below five years. ARI is the infection of any part of 2. Diagnosis & management
respiratory tract, which includes cough, common
cold, pharyngitis, pneumonia, laryngitis and ear
of ARI
infection. Classification and management of ARI is based
Acute respiratory infections in children can involve upon three important factors. These are age of the
upper respiratory tract (nose, throat) or lower child, respiratory rate and danger sign like chest in-
respiratory tract (bronchi, lung). Lower respiratory drawing.
tract infections (broadly termed as pneumonias) are
a major cause of death of infants and children in
2.1Age of the child and respiratory
India, accounting for about 30% under-five deaths. rate
Timely treatment, based on well-researched
Children are classified into three age groups for ARI
algorithms can save most children with ARI.
management. These age groups and criteria for fast
Majority of the cases of ARI have non-severe
breathing are given in table below
Table 1 : Cut of points for fast breathing

Sr. Age group Criteria for fast breathing
1 0 - 2 months Respiratory rate more than 60 / minute
2 2 months to 1 year Respiratory rate more than 50 / minute
3 1 year to 5 years Respiratory rate more than 40 / minute
No pneumonia
Chest in-drawing Severe pneumonia/Very severe illness
In normal child, during respiration, chest expands
when the child breathes in and compresses when the 2.3.1 No pneumonia
child breathes out. In children with severe
pneumonia, chest moves in when the child breathes
If respiratory rate of child is less than 60/minute
in. This is called chest in-drawing.
then the child is classified as 'No Pneumonia'.
2.3 Pneumonia in 0-2 months age
Give Paracetamol tablet if there is fever and
group demonstrate to the mother how to clean nose
Important aspects about pneumonia in age group 0-2 with normal saline drops.
months are as below: Advise mother to continue breast-feeding.
In these children, there are no usual features of Inform mother about danger signs of
pneumonia like fever, cough, etc. pneumonia, e.g. breathlessness (rapid
Child may have only fast breathing and/or chest movement of abdomen), inability to drink,
in-drawing. excessive drowsiness, hypothermia, high fever
etc. Ask mother to immediately bring the child
Pneumonia in child less than 2 months age is back to health facility, if she observes any of
always severe & mortality is high the signs mentioned above.
Severe pneumonia/Very severe illness
If child below 2 months presents with fast breathing
Such cases should be treated in the facility where (RR > 60/minute) and/or chest in-drawing
specialist & ICU are available. Plus
Classification
Page 221
One or more of the following signs - - Cyanosis
- Inability to drink - Hypothermia
- Excessive drowsiness - Convulsions
- Stridor, wheeze Such child shouldbe referred to specialist.
In case referral can not be executed treat the child as below

Table 2: Treatment of Pneumonia
Antibiotic Dosage Frequency Route

Age < 7 days Age > 7 days - 2
months
Inj Benzyl penicillin 50,000 12 hrly 6 hrly IV/IM
OR IU/kg/dose
12 hrly 8 hrly IV/IM
Inj Ampicillin AND 50 mg/kg/dose
12 hrly 8 hrly IV/IM
Inj Gentamycin 2.5 mg/kg/dose
tohealth facility if she observes any of the
danger sign.
2.4 Pneumonia in 2 months to 5
years age group 2.4.2 Pneumonia
Children with ARI of 2 months to 5 years age are If child has fast breathing (RR: 2-12 mts > 50/ min.
classified into four groups as follows - & 1-5 yrs. > 40/ min.) and no chest in-drawing,
diagnose child as Pneumonia
- No pneumonia
a. Treatment of pneumonia
- Pneumonia
Give child Cotrimaxazole for 48 hrs. Treatment
- Severe pneumonia schedule for pediatric cotrimaxazole is -
- Very severe illness 2-12 months:
2.4.1 No pneumonia 2 tablets twice daily or syrup 5 ml. twice daily
When respiratory rate is normal and no sign of chest 1-5 yrs: 3 tablets twice daily or syrup 7.5 ml. twice
in-drawing is seen child is disgnosed as no daily.
pneumonia. These children should be treated at
home & observed for appearance of danger signs Pediatric tablet contains Sulphamethaxazole 100 mg
(increase in RR and chest in-drawing) by mother. & Trimethoprim 20 mg.
Following points should be advised to mother - Syrup 5 ml. contains Sulfamethaxazole 200 mg
Continue breast-feeding if child is breast-fed. and Trimethoprim 40 mg.
Give plenty of oral fluids including water or If fever is present, give Tab. Paracetamol. (5 to
ORS to child. 10 mg./kg)
If fever is present, give Tab. Paracetamol. Teach mother how to clean nose with normal
saline. This will clear airway of child and
Teach mother how to clean nose with saline improve breast-feeding.
water. This will clear airway of child and
improve breast-feeding. Keep baby warm by covering with warm
clothes and keeping in lap.
Assess child after 48 hrs:
In community, many home remedies are used
If improvement - Continue CTZ for 3 Days
for ARI. One of the best among them
Child has: - Chest in-drawing
is honey & ginger. Advise mother to give honey
and ginger to child. And
Inform mother about danger signs of RR may be fast complete 5 days course
pneumonia, e.g. breathlessness, inability to
If no improvement or child gets deteriorated
drink, excessive drowsiness, hypothermia, high
refer child to specialist.
fever etc. Advise her to bring child back
Page 222
Severe pneumonia: - Child with chest in- Treatment
drawing & having RR normal or fast is
a. Treat for first 48 hrs by
diagnosed as severe pneumonia should be
treated by specialist. Give oxygen if child has
cyanosis till the child is referred.
Table 3
Treatment of severe Pneumonia
Antibiotic Dosage Interval Route
Inj Benzyl penicillin OR 50,000 IU/kg/dose 6 hrly IM
Inj Ampicillin OR 50 mg/kg/dose 6 hrly IM
Inj Chloramphenicol 25 mg/kg/dose 6 hrly IM
b. Assess after 48 hrs

i. If improvement, continue for next 3 days as below
Table 4
Treatment of severe Pneumonia
Antibiotic Dosage Interval Route
Inj Procaine penicillin OR 50,000 IU/kg (Max 4 lac units) Once IM
Tab Ampicillin OR 50 mg/kg/dose 6 hrly Oral
Tab Chloramphenicol 25 mg/kg/dose 6 hrly Oral
ii. If no improvement, change antibiotic as below

If Ampicillin was given earlier then change 2.4.4 Very severe illness
to Inj Chloramphenicol a) Child has:
If Chloramphenicol was given earlier change Chest in-drawing and RR may be fast or normal
to Inj Cloxacillin 25 mg/kg/dose 6 hrly IM + plus
Gentamycin 2.5 mg/kg/dose 8 hrly IM.
One or more of following signs -
iii. Important aspects of antibiotic treatment
Inability to drink
Treatment with antibiotics should be
continued for at least five days. Excessive drowsiness
Stridor, wheeze
Cyanosis
Hypothermia
Convulsions
Continue treatment for at least 3 days after child
recovers. Diagnose the child as suffering from very severe
illness & refer the child to specialist having facility
If cloxacillin & gentamycin are started continue for of intensive care unit.
three weeks.
In addition to this give following 3. Treatment of childhood
Administer Oxygen if required community-acquired
Continue breast feeding during illness pneumonia
If fever, give tablet or syrup Paracetamol Themanagementofpneumoniaisguidedbytheseverity
ofthediseaseaslistedinTable below:
Table 5: Signs & symptems
Page 223
Sign or symptom Classification Treatment
Centralcyanosis Very severe pneumonia Admittohospital

Severerespiratorydistress Managetheairway
Not abletodrinkduetorespiratory Giveoxygen
Distress. Giverecommendedantibiotic
Treathighfeverifpresent
Chestindrawing Severe pneumonia Admittohospital

Giverecommendedantibiotic
Fastbreathing Pneumonia Giveappropriateantibioticfor5

days
2monthsupto12months:50breaths/
Soothethethroatandrelievecough
min
with a safe remedy
(a) There is a rapid progression of the disease, or

3.2 Treatment of very severe
illness (b) There is pneumatocoele, or pneumothorax, or
effusion on chest X-ray, or
3.2.1 Admit the child in hospital
3.2.2 Obtain a radiograph (c) Child has large skin boils or abscess or infected
scabies, or
ofthechestiffacilities
areavailableforthesame.Radiographyinverysever (d) post-
epneumoniaisrequired at admission to assess measlespneumoniawhichisnotrespondingwithin48ho
the extent of disease and to rule out presence of urstotheinitialtherapy.Ifstaphylococcalpneumoniaissu
puemothorax or effusion In case spected,addInjCloxacilin(50mg/kg/dose,every6hourl
ofseveredistress,stabilizeandoxygenatethechildb y)toanyoftheabovechoice of antibiotics.
eforesendingforradiograph. Whenthechildimproves,continueCloxacillinorally4ti
3.2.3 Give antibiotics mesadayforatotalcourseof3weeksatleast.Childrenwit
hcomplicatedpneumonia(Empyema)needlongerthera
- pyfor4-6weeks.
GiveInjectableAmpicillin(50mg/kgIM/IVevery6hours
)andGentamicin(7.5mg/kgIM/IVonceaday).Ifthechild 3.2.4 Give Oxygen
respondswell,dischargeafter5daystocontinuetreatm -
ent Wherepulseoxymeterisavailable,useoxygensaturatio
athomewithoralAmoxicillin(15mg/kgperdosethreeti noftheblood(SaO2)toguideoxygentherapy.Maintain
mesaday)plusIMGentamicinoncedailyforafurther5da SaO292%.Continuewithoxygenuntilthesignsofhyp
ys. oxia(suchasseverelowerchestwallin-drawing or
breathing rate of 70/min)arenolongerpresent.
-Alternatively,
giveInjectableChloramphenicol(25mg/kgIMorIVever 3.2.5 Give supportive care
y8hours)untilthechildhas -
improved.Thencontinuethesamedrugorallyinthesa Ensurethatthechildreceivesdailymaintenancefluidsap
medosefor3timesadayforatotalcourseof10days. propriatetochildsage.Encouragebreastfeedingandora
- lfluidsoncethedistresssettlesandthechildisabletofeed.
Ifthechilddoesnotimproveby48hourstoanyoneofthe
- If the child has fever
setreatments,reassessforcomplicationsandswitchto
(38.5C)whichappearstobecausingdistress,gi
InjectionCeftriaxone(80mg/kgIMorI/Voncedaily )
veoralParacetamol(15mg/kg/dose).
for10days.
-Ifwheezeispresent,givearapid-
- Staphylococcal pneumonia is suspected if:
Page 224
actingbronchodilator(asdescribedinthenextsection). - Improved ability to eat and drink.
- 3.2.7 Watch for complications
Removeanythicksecretionsinthenose/throat,whichth -
echildcannotclear,bygentlesuction. Ifthechildhasnotimprovedaftertwodays,orifthechild
3.2.6 Monitor the child sconditionhasworsened,lookforcomplicationsoroth
erdiagnoses.Ifpossible,obtainarepeatchestX-
- ray.Considertransfertoahigherfacilityincaseofpoor
Thechildshouldbecheckedbynursesatleastevery3hou response or deterioration despite second-line
rsandbyadoctoratleasttwiceaday.Monitorfor signs of therapy.
improvement. A patient who is improving on
treatment should have: 3.2.8 Monitoring
Thechildshouldbecheckedbynursesatleastevery6ho
- An improvement in the respiratory rate.
ursandbyadoctoratleastonceaday.Monitorforsignso
- Less indrawing of the lower chest wall. f improvement as discussed above.
- Less fever, and /or Table 5
Table 6 : summary of management of ARI cases.

No. Type Who can manage Where can be managed
Age group 2 months to five years
1 No pneumonia ASHA Anganwadi Worker, MPW Home management
2 Pneumonia MPW/HA, MO Management at home or PHC
3 Severe pneumonia PHC MO / specialist PHC/ referral center
4 Very severe illness Specialist Specialist with ICU facility
Age group below 2 months
Child should be referred immediately after giving one dose of CTZ
Page 225
23. BRONCHIAL ASTHAMA
Less Preferred treatment: Monteleukast

1. Introduction: Theophylline Chromoglycate and treatment of mild
Bronchial asthma is a disease characterized by an intermittent asthama
increased responsiveness of the trachea and bronchi
to various stimuli. It manifests by widespread 3.2 Moderate persistent
narrowing of the airways causing paroxysmal Symptoms > 2 times/ week
dyspnea, wheezing or cough. The diffuse
obstruction to the airflow is reversible in a large Nocturnal symptoms >1/week
majority of cases, either spontaneously or in PEFR 60-80%
response to treatment. Bronchial reactivity is a
necessary component of asthma. Asthma is a result 3.2.1 Treatment
of multifactorial inheritance. Inhaled steroid med dose
2. Signs &Symptons: If response not satisfactory

Recurrent cough Add inhaled LABA
Breathlessness Salmederol/ Formeterol/Monteleukast/ long acting
Wheezing theophylline
3. Clinical classification
1) Mild Intermittent 3.3 Severe Persistent
2) Persistant Daily symptoms often severe
a) Mild Activity limited
b) Moderate Growth affected
c) Severe Frequent Nocturnal symptoms
3.1 Mild Intermittent Frequent hospitalization

Symptoms < 2times a week and asymptomatic in PEFR<60%
between
3.3.1 Treatment
Nocturnal symptoms < 2 times /month
Inhaled steroids high dose
3.1.1 Treatment
Salbutamol inhaled (100 MCG/puff) Inhaled LABA / Monteleukast / long acting
theophylline
1-2 puffs as per requirement
If response not satisfactory
For children less than 2 years use face mask with
spacer Oral Prednisolone2mg/kg/day in three divided doses
& inhaled salbutamol as required
OR
1) Pulmonary function test
Salbutamolsyrup/tablet
0.1-0.2 mg/kg/dose three times a day till symptoms 2) Absolute Eosinophili count
subside 3) Chest X-ray
Mild Persistent 4) Skin test & Allergy test
Symptoms > 2times/week but, 1time/day
Nocturnal symptoms > 2 times / month
Asymptomatic in between exacerbations peak flow
3.4 Treatment Guidelines for acute
rate( PEFR) > 80% exacerbation of Asthama
3.1.2 Preferrence of Treatment O2 by mask (4-6 liters /min)
Preferred treatment: Inhaled steroids (low dose) 2 Salbutamol MDI (100MCG/puff)with spacer and
puffs twice / day mask for < 2 years 4-8 puffs every 20 min x 3 OR
Salbutamol nebulization 0.15mg/kg(min 2-5mg)
Page 226
diluted in 3 ml saline can be repeated 3 times every Good response
20 min
Send home: salbutamol MDI+ Tab Pednisolone
InjAdrenaline (1:1000) or Terbutaline (0.01mg/kg) 2mg/kg/Day x 5-7 days
s/c may be repeated thrice every20 min if both
above are not available
AND Inj Hydrocortisone hemisuccinate 4. Investigation:
10mg/kg/dose 4 times a day OR Inj
1) Pulmonary function test
Dexamethasone0.2 mg /kg/dose
This must be converted to oral prednisolone once 2) Absolute Eosinophili count
patient is stable 3) Chest X-ray
If response not satisfactoryRefer to higher center
4) Skin test & Allergy test
statIMP: Evaluate after 1 hour
Medication Dosage form Dosage
Formoterol DPI: 12 ug per single-use capsule 1. Capsule every 12

years
Salmeterol MDI: 25 ug per puff 1-2 puff every 12 hours
Fluticasone/salmeterol DPI:100, 250, or 500 ug of fluticasone 1 inhalation twice daily;
with 50 ug of salmeterol dosage depends on
severity of asthma
Cromolyn MDI: 1 mg per puff 1-2 puffs 3 to 4 times

daily
Nebulizer solution :
1 ampule 3 to 4 times
20 mg per ampule
daily
Nedocromil MDI: 1.75 mg per puff 1-2 puffs 2 to 4 times

daily
Montetelukast 4 or 5 mg chewable tablets, Age 12-23 months: 4 mg
oral
4 mg packet of oral granules,
granules at bedtime
10 mg tablets
Age 2-5 years: 4 mg at
bedtime
Zafirlukast 10 & 20 mg tablets Age 7-11 years: 20

mg daily in
Theophylline Liquids, sustained- release Starting dosage is 10 mg /kg

per day
Tablets and capsules.
< 1 years : ( 0.2 [age in
weeks] ) + 5
= mg per kg day 1 years :
16 mg
per kg per day
Table1. Drugs used in the long-term control of asthma in children
Page 227
24. BREATH HOLDING SPEL
1. Introduction: 3. Complication:Local trauma,

Aspiration pneumonia.
A baby with crying followed by loss of
consciousness, tonic posturing (features of cerebral
anoxia). Cyanotic Breath holding spell more
4. Management:
common form: Usual age of onset is 6 months, peak Examination to rule out other seizure mimicking
by 2 years, abate by 5 years. After a shrill cry, conditions.
forced expiration followed by apnea and cyanosis
leading to loss of consciousness associated with i. Reassurance of parent that these are not
clinical jerks or posturing. seizures, EEG not required, inter-ictal EEG is
normal.
2. Signs &Symptons: ii. Should not reinforce this behavior, put the
child in safe place and avoid cuddling.
Baby may be cyanosed (blue)\ Baby may be pale iii. Iron supplements if anemia, delayed weaning
etc.(3 mg/kg for 3 months.)
History of a predictable stubborn behavior,
iv. Syrup Piracetam( 40-100 mg /kg in BD) may
precipitating event like upsetting the infant
be used for few months if the breath holding
History of painful stimulus or hit on head cyanosis spells are very frequent,
leading to loss of consciousness associated with v. Parental counseling to prevent reinforcement
clinical jerks or posturing Less common, Apnoea of this behavior.
followed by pallor, hypotonia and tonic seizure.
Page 228
25. BRONCHIOLITIS
Supportive measures such as oxygen by hood (10

1. Introduction: litres / mt) or by mask (5 lits / mt); IV fluids if child
is not able to feed orally.
Viral in aetiology (Respiratory syncitial virus) most
frequently in children < 12 months of age
IV fluids if child is not able to feed orally.
2. Signs &Symptoms:
An antibiotic has no role.
Initial URI symptoms followed by Increasing
cough, Respiratory distress, Wheeze and feeding
difficulty
4.2 Monitoring
(RR, Respiratory distress, pulse oximetry) - A trial
3. Investigations: dose of Nebulised salbutamol / epinephrine if
wheezing is marked as child improves wean off
CXR: Hyperinflated lungs with patchy infiltrates oxygen and increase oral feeds if child develops
severe respiratory distress, increasing hypoxemia,
4. Management: cyanosis or fatigue ventilatory support may be
4.1 Treament of bronchiolitis is essentially required.
symptomatic.Child should be treated in a humid
atmosphere preferably in sitting position with head
and neck elevated.
Page 229
26. EMPYEMA
USG chest: size, site of effusion, adhesions or
1. Introduction: loculations can be made out.
Characterised by presence of pus or microorganisms Diagnostic thoracocentesis: usually in fifth
in the pleural fluid occurs as a complication of intercostal space over mid-axillary line using a
Pneumonia, Influenza. Streptococcus Pyogenes, large bore needle Pleural fluid for Gram stain,
Staph aureus, Streptococcus Pneumoniae, culture and sensitivity, Pleural fluid pH, sugar
Hemophilus are the common organisms. are reduced and protein is elevated.
2. Signs &Symptoms: 5. Management:

Common symptoms are 5.1 Treatment comprises of chest drain and
Fever antibiotics.
Chills Chest drainage using an intercostal drainage tube

inserted in the region of maximal dullness (usually
Toxaemia V or VI intercostal space in axillary region) and
connecting to a sterile under water drainage bottle
Respiratory distress
Chest drainage is kept till the drainage decreases to
Grunt and < 25 ml/day and there is good lung expansion. If
there is no chest expansion by clinical or
Chest pain (pleuritic pain)
radiological methods, surgical opinion is sought
3. on examination 5.2 Antibiotics
Decreased chest expansion Cloxacillin with cefotaxime or ceftrioxone is the
Diminished breath sounds first line antibiotic; switch over to oral antibiotics
after child becomes afebrile and chest tube is
Dullness on percussion on affected side and removed. Total duration of 4 - 6 weeks of antibiotic
Mediastinal shift to opposite side therapy or
Cloxacillin: 100 - 200 mg/kg/day in 4 div. doses
4. Investigations:
Cefotaxime: 150 - 200 mg/kg/day in 3 or 4 div.
Chest X-Ray: obliteration of costophrenic doses
angle; diffuse homogenous opacity.
Supportive care: oxygen, good nutrition
Page 230
27. APPROACH TO FEVER
1. History: 3. Basic investigations

Type of fever
Associated symptoms chills / rigor, cough, sore
In high risk group and
throat, ear pain, urinary symptoms, bleeds etc. fever beyond 5 days in low
Previous illness and treatment. if any Feeding
difficulty, respiratory distress. risk:
Total count, differential count, peripheral smear,
2. Clinical Examination Platelet count
Check Temperature, Blood pressure, Pulse,
Perfusion Urine analysis, urine c/s
Skin: Rashes, Bleed, Cyanosis Blood culture and sensitivity
Eyes: Pallor, Icterus Chest x-ray
Mouth: Ulcer, Thrush C-reactive protein
Ear: Discharge, Redness, Tenderness Mantoux test
Throat: Congestion, Tonsillitis CSF analysis if required
CNS: Meningeal irritation, altered sensorium Other investigations
Abdominal examination: Hepatomegaly, Liver function test

Splenomegaly Renal function test
Respiratory System: Tachypnoea, Retraction, Creps, USG abdomen
Wheeze
Blood for leptospirosis
Serology for dengue
Widal
Bone marrow
4. Refer if,
Fever with unconsciousness
Fever with shock
Severe respiratory diseases
Bleeding diathesis
Refractory seizures
Page 231
28. ACUTE FLACCID PARALYSIS (AFP)
1. Defination :
A case of AFP is defined as any child aged <15
1. SALIENT FEATURES
years, with acute onset of Flaccid paralysis without The paralysis is of acute onset (<4 weeks) and the
any obvious cause (e.g. severe trauma or electrolyte affected limb(s) are flaccid (floppy or limp). If the
imbalance like (hypokalaemia). AFP is a notifiable AFP is due to polio, then sensation is never affected.
disease and all cases must be reported immediately Other important differentials to be considered in
to Nodal Officer and District Surveillance Officer, cases with AFP are detailed in Table-1. This
NPSP Unit, Directorate of Family Welfare. India includes possible illness due to Guillian-Barre
has shifted to the virological system of case syndrome, transversemyelitis, traumatic neuritis;
classification, i.e. within 90 days of paralysis onset; viral infections caused by other enteroviruses,
all cases should undergo final classification as toxinsand tumours. Isolated facial paralysis is also
confirmed polio, non-polio AFP or compatible with included.Pseudoparalysis due to pain in congenital
poliomyelitis. India has been declared polio free syphilis, osteomyelitis, abscess, scurvy,
since 3 years. unrecognized trauma leading to contusions, slipped
epiphysis or fractures, etc. can also mimicAFP.
2. Differential Diagnosis:
Table 1- Important differential diagnosis of AFP (adapted from Field Guide, MOHFW, GOI)
Signs and Polio GBS Transverse Traumatic

symptoms myelitis or injection
neuritis
Age Most cases occur Usually above 2 Mostly above 4 No age limit
under 3 years of years of age years of age
age
Progression of 24-48 h onset to Hours to days Hours to 4 days Hours to 4 days

paralysis full paralysis
Fever onset High always Not common Rare Commonly

present at onset of present before,
flaccid paralysis during and after
disappears the paralysis
following day
Flaccidity Acute, Acute, Acute Acute,

asymmetrical, symmetrical, lower limbs asymmetrical
Proximal Distal symmetrical Limb
Muscle tone Diminished Diminished Diminished in Diminished in

lower limbs affected limb
Deep Decreased or Absent Absent in lower Decreased or

tendon absent extremities, later absent
refl exes hyper-refl exia
Sensation Severe myalgia but Cramps, tingling Pain in gluteal

no sensory defi cit hypoanaesthesia of Anaesthesia of region
palms and soles the lower limbs
with sensory loss
Cranial nerve Only in bulbar or Often present Absent Absent

bulbospinal cases. affecting VII, IX,
Page 232
Loss of gag reflex X, XI, XII
most common Only
in bulbar or
bulbospinal cases.
Loss of gag reflex
most common
Respiratory Only when bulbar In severe cases Sometimes Absent
insufficiency and bulbospinal
involving
respiratory muscles
CSF WBCs High WBCs. <10 Normal Normal
proteins Normal or slightly High Normal or Normal
increased slightly elevated
Bladder Absent Transient Present Never
dysfunction
Nerve Abnormal, anterior Abnormal, Normal of Abnormal in
conduction horn cell disease demyelination abnormal has no sciatic nerve
velocity in 3rd diagnostic value
EMG 3rd week Abnormal Normal Normal Normal

Sequelae at 3 Severe Symmetrical Flaccid Moderate
months and up asymmetrical atrophy of distal atrophy only in
to a year atrophy, skeletal muscles, diplegia, affected lower
deformities may atrophy after years limb
develop later
laboratory in good condition (i.e., no desiccation, no

3. Confirmation leakage, with adequate documentation and evidence
An AFP case is confirmed as Polio only by the that the cold chain was maintained.)
isolation of wild poliovirus from any stool
specimen.An AFP case is classified as non-polio 4. Treatment for acute POLIO
AFP if wild poliovirus is not isolated from
adequate stool specimens.If stool specimens are
like illness
inadequate, final classification of the AFP case as All cases should be treated as below except patients
either nonpolio AFP or compatible with Polio will with isolated single lowerlimb involvement and
depend on the results of 60 days follow-up reporting after 4 days of onset of paralysis and
examination. If the 60 days follow-up examination currently not progressing for more than 48 hours.
shows no residual weakness, the case is classified as
non-polio AFP. The final classification of the case
4.1 Nonpharmacological
as compatibleor discarded as non-polio AFP is Complete bed rest and correct positioning of the
determined by the National Expert Review affected limbs in the optimal
Committee (ERC) which meets every month in New Position as follows:
Delhi to review all such cases.
Hipslight flexion, knee5 flexion, foot90
3.1 Adequate stool: Two specimens collected within with support against the soles. Both legs should be
14 days of paralysis onset and at least 24 hours supported from the lateral sides with pillows or
apart;each specimen must be of adequate volume (8- rolled towels
10 grams) and arrive at a WHO-accredited
or salt/sand packs to prevent rotation. relieving painthe jointsfor about 10 minutes, 2-3
If transient urinary retention occurs times a day.
When pain subsides passive movements of
alternate hot and cold compresses over the
suprapubic region.
4.2 Pharmacological
(Caution: No massage or intramuscular injections as There is no specific drug therapy for polio. For fever
it may further precipitateparalysis. Watch for and pain, use paracetamol or ibuprofen (see section
progression, particularly for the involvement of the on Fever in Chapter 1). Referral to a tertiary care
respiratorymuscles.) centre witha ventilatory support facility, if there is
progression of paralysis, respiratory distress,bulbar
Warm water fomentation using hot packs with
involvement, paralysis of upper limbs which is <3
soaked towels wrapped around the affected partsfor
days old (there is higherrisk of diaphragmatic
about 10 minutes, 2-3 times a day help in
Page 233
involvement in such cases), marked drowsiness or Note: Post-polio residual paralysis should be
any other complication. referred for rehabilitative services to an appropriate
centre.
Patient/parent education No dietary restrictions,
however, continue breastfeeding or other
regular feeding.
5 Action expected on
Paralysis progresses usually for about 4-7 days admission of suspected
after onset. Recovery may startthereafter over AFP case:
days to weeks with little recovery of strength - Report to higher authority immediately
after 6 months ofillness. A regular
physiotherapy facilitates recovery of muscles. - Take adequate stool sample
- Send the stool sample maintaining cold chain to
district headquarte
Page 234
29. FEBRILE SEIZURES
aprolonged or atypicalfebrile seizure, delayed

1. Introduction developmental milestones and an abnormal
neurologicalexamination.
Febrile seizures are brief (2-5 min), generalized
tonic-clonic and self-limited seizures followed by a 5. Treatment
brief post-ictal period of drowsiness, in an otherwise Most febrile seizures are brief and would be over by
healthy, febrilechild of 6 months to 5 years of age, the time a child is brought to the doctor or health
without any evidence of underlying facility. Management includes definitive diagnosis,
neurologicaldisease. They are the most common restraint in investigations, treatment of an acute
seizure disorder during childhood, with a episode, prophylaxis for future episodes and family
uniformlyexcellent prognosis. They occur rarely counselling. Role of defervescence in preventing
before 6 months and after 5 years of age. The peak febrile seizures is questionable.
age of onset is approximately 14-18 months of age, 5.1. Nonpharmacological
found in 3-4% of young children. There is a strong Clear the airway, semi-prone lateral position and
family history of febrile convulsions in siblings and oxygen therapy.
parents, suggesting a genetic predisposition. Except
for the cases at high risk, simple febrile seizures 5.2. Pharmacological
rarely develop into epilepsy. 5.2.1 In cases presenting with seizures, the mainstay
of management is prompt administration of
2. SALIENT FEATURES anticonvulsants.
5.2.2 Thebest drug
Febrile seizures usually occur when the temperature
isDiazepam/Midazolam/Lorazepam in a dose of 0.3
is rising rapidly, to generally 39C (102F) or more
of core temperature. They are of two types: mg/kg by slow intravenous or rectal route. It can be
repeated, if seizures do not subside (per rectal dose
(i) Typical (simple) febrile seizure occurs on day 1 may be given up to 0.5 mg/kg/dose).
of fever, does not last formore than 10 minutes; 5.2.3 Intermittent prophylaxis (during febrile
generalized tonic-clonic; generally not more than illness)
oneepisode within 24 hours. 5.2.4 It is a safe and effective method of prophylaxis
but does not reduce the risk of future epilepsy.
(ii) Atypical or complex febrile seizure may persist
Tab Clobazam 0.75 mg/kg for 2-3 days in 2 divided
for more than 15 minutes;it could be focal in nature;
doses during fever or Tab/Syr. Diazepam 0.3
more than one episode of seizure in 24
mg/kg/dose every 8 hours (1 mg/kg/day) for 2-3
hours;associated with abnormal neurological
days of febrile illness,started on the day of onset of
findings or deficits. An organiccause such as an
fever. Dose can be adjusted, if over sedation or
infectious or toxic process should be considered
ataxia noted.
andinvestigated.Late onset febrile seizures,
persistent febrile seizures, generalized epilepsy 5.3 Continuous prophylaxis
andfebrile seizure plus (GEFS+) and febrile status
epilepticus (FSE) are part of thespectrum of febrile Febrile status, complex and recurrent febrile
seizures seizures (>6/year in spite of intermittent
prophylaxis) may need EEG, neuroimaging and
continuous prophylaxis with AED.Phenobarbitone
3. Investigations and valproate may be used in infants and older
3.1 Lumbar puncture: A lumbar puncture with
children, respectively, for 1-2 years. Carbamazepine
examination of CSF is essential to rule out
and phenytoin are not useful.
possibility of meningitis in cases with first episode
of febrile seizures.
3.2 EEG has no role in case of simple febrile 6. Patient/parent education

seizures. However, in cases withatypical febrile The parents and caretaker should be assured of
seizure or in a child with high risk for developing the benign nature of the disease andshould be
epilepsy, itmay be helpful. told that no neurological deficit or mental
4. High risk for developing retardation occurs as a result ofsimple febrile
seizure. They should be taught about control of
epilepsy, fever at home. They can be taught to give
It include a positive family history of epilepsy,initial diazepam per rectally at home.
febrile convulsion prior to 9 months of age,
Page 235
Routine immunization as per schedule should 4th day from the day of vaccination and given
be followed. After DPT vaccination, oral for 3 to 4 days to avoid precipitation of febrile
paracetamol 15 mg/kg/dose every 6 h for 2 or 3 seizures.
days and similarly, after measles vaccination,
oral paracetamol in the same dose started on the
Page 236
30. ACUTE NEPHRITIS
1. Introduction:
It follows streptococcal infection of throat or skin by 1-2 weeks. Glomerular injury will clinically present as acute
nephritis In majority of pediatric patients it is PSGN Age group 3-12 years. Disease is self-limiting and generally
resolves in one moth; however, microscopic urinary changes may perists up to one year.
2. Signs &Symptons:
Hematuria, Oedema, Hypertension, Varying degree of oliguria or anuria May present with CCF Many primary or
secondary Glomerular diseases will present as acute Nephritis.
3. Lab Investigations:
3.1 Urine exam: RBCs, RBC casts, significant proteinuria2+/3+
3.2 ASO titre increases
3.3 Chest X-ray:
Cardiomegaly, Pulmonary vascular congestion, Effusion
3.4 Hemogram: Normocytic normochromic anaemia
3.5 BUL, SerCreatinine raised
4. Complication:
Congestive heart failure, encephalopathy may occur in a few patients.
5. Treatment
5.1 Diet-Proteins,
Sodium, potassium should be restricted. Urine output should be measured accurately.
5.2 Daily monitoring of weight.

Protein restriction up to 0.6mg/kg/day
5.3 Drugs:
Oral Penicilline 25000-50000u/kg/Day OR
Inj Penicliilne 25000-50000 u/kg/Day im/iv in 4 divided doses x 7 days
OR
5.4 Erythromycin 40mg/kg/dayin 4 divided doses X 7 days
5.5 Diuretics: Frusemide1-2mg/kg/day in 1-2 divided doses
5.6 Antihypertensives: Nifidepine 1 to 2 mg per kg/ Atenolol 0.08 mg per kg/Enalapril 50 mg per day
5.7 Rest
6. Refer patient to higher center

CCF
Uncontrolled HTN or its complications
Page 237
31. NEPHROTIC SYNDROME
Serum cholesterol raised
1. Introduction: 4. Management
Nephrotic syndrome ischaracterized by massive 4.1 1st Episode
proteinuria, hypoalbuminemia and edema.
Hyperlipidemia is usually associated; hematuria, The child should receive a high protein diet no extra
hypertension and impaired renal function are salt is given.
occasionally seen.
Prednisolone (2mg/kg/Day)in 2-3 divided doses
More than 90% of childhood nephrotic syndrome is along with antacid Given till patient goes into
primary (idiopathic). Other causes are amyloidosis, remission(Urine Albumin 1+/absent for 5 days)
vasculitis, SLE; post-infectious GN and hepatitis B
OR up to 8 weeks and then tapered to
nephropathy.Nephrotic syndrome in children can be
2mg/kg/alternate day x3-6 months and then stopped
divided into two groups based on renal histological
characteristics: Ideal calculation 60mg/m2 BSA
i)Minimal change nephritic syndrome(MCNS).
4.2 Relapse:
This is usually sensitive to steroids with a
satisfactory long-term outcome. Urine Albumin 2+ >5 days / oedema
ii) Nephrotic syndrome with significant lesions. Sometimes resolves in a week if precipitated by
infection, then infection is treated. If not resolved
It is usually associated with less satisfactory continue Prednisolone 2mg/kg/day in 2-3 doses till
course, tends to be steroid resistant and a significant urine is protein free for 5 days then taper alternate
proportion progress to chronic renal failure. day x 4 week and then stop
General care
2. Clinical Features:
Ca++ & K+ supplement if on frusemide
The onset is insidious with edema first noticed
around the eyes and subsequently around the Frusemide1-2mg/kg/day for edema with expert
legs.Gradually edema may become generalized, advise
with ascites, hydrothorax and hydrocele. A severe
muscle wasting is seen. It is a triad of 4.3 Treatment of frequent
hypoproteinemia, hypercholesterolemia and
proteinuria.
relapses:
i) Long term alternate day prednisolone. Following
3. Investigations: completion of treatment for relapse, alternate day
prednisolone is slowly taoered to minimum
Urine >3+ proteinuria maintenance dose (0.3 0.7mg/kg). The dose is
maintained for 9-12 months.
No RBCs/ Casts
ii) Levamisole: After inducing a remission,
Azotemia not significant
levamisole is administered at a dose of 2-2.5 mg/kg
on alternate days. Alternate day prednisolone is
given in decreasing doses, until a dose of 0.3-
0.5mg/kg is reached, for 2-3 months.
Serum proteins< 3.2gm/dL Cyclophosphamide and cyclosporine A are used in

some cases.
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Persistence of Hypertension /azotemia/ Hematuria
5. Refer to higher center
Steroid dependent or resistant or frequent relapse
For confirmation of diagnosis
Systemic features: arthritis/ Rash /

Hepatospleenomegaly
Page 239
32. CONGESTIVE HEART FAILURE (CHF)
1. Rheumatic fever and RHD

Introduction:
Every Cardiac patient has potential to develop CHF. 2. CHD complicated by anemia infection
It is not a diagnosis; it is a clinical syndrome due to
an underlying anatomical or pathological cause 3. Hypertension
which is the primary diagnosis.
4. Mycarditis
Definition:
5. Upper respiratory obstruction.
Congestive cardiac failure is defined as inability of
the heart to maintain an output, at rest or during Symptoms:
stress , necessary for the metabolic needs of the
body(systolic failure) and inability to receive blood Slow weight gain, easy fatiguiability, persistant
into the ventricular cavities at low pressure during horse crying, wheezing, excessive perspiration,
diastolic(diastolic failure) . puffiness of face, edema.
Signs:
Etiology
The causes of diastolic failure are given below: Left sided failure is indicated by tachypnea and
i) Mitral or tricuspid stenosis. tachycardia, Persistant cough, wheezing, crepts in
the chest.Right sided failure signs are hepatomegaly,
ii)Constrictive pericarditis
facial edema, edema on feet.
iii)Restrictive cardiomyopathy
Treatment:
iv)Acute volume over load (acute aortic or mitral
regurgitation) It is based on following principles:
v)Myocardial ischemia i)Reducing cardiac work.
vi)Marked ventricular hypertrophy
ii)Augmenting myocardial contractility.
vii)Dilated cardiomyopathy
iii)Improving cardiac performance by reducing the
The causes of systolic failure or mixed systolic
heart size.
diastolic failure can be divided into two groups
according to age (refer to causes of CCF below). iv)Correcting the underlying cause.
The commonest cause of CCF in infants is
congenital heart disease, whereas in the older Control of excessive salt and water retention with
children it is rheumatic fever and rheumatic heart diuretics. Improve cardiac contractility with
disease. digoxin. Prevent and reverse neurohormonal
changes that lead to progressive worsening of
Causes of Congestive Cardiac Failure cardiac status with beta blockers, ACE inhibitors.
Infants: Digoxin
Drug of choice in chronic CHF with atrial
1. Congenital heart disease fibrillation
2. Myocarditis and primary myocardial disease In CHF with sinus rhythm it gives
symptomaticbenefit
3. Paroxysmal tachycardia Dose
Total digitalizing dose in children 30 - 40 mcg/kg
4. Anemia the total dose stat: after 8 hrs; after 16 hrs Daily
maintenance dose of total digitalizing dose. Once
Children in day or two divided doses.
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Note: Enalapril: 0.1 mg/kg/dose oral every 12 - 24 hourly
Hypokalemia may aggravate digitalis toxicity upto 0.5 mg/kg/day or
especially with concomitant diuretic administration.
-blockers is an integral part of congestive heart
Use oral Kcl supplement or use potassium sparing
failure therapy nowadays.
diuretics such as spironolactone.
Metaprolol or carvedilol is also used
Oral Diuretics Diet Calories
Frusemide: 1 - 2 mg/kg/day or Recommended daily dietary allowance plus 20 -
30% in shunt lesions Avoid salty foods and
Hydrochlorothiazide: 1 - 1.5 mg/kg/dose every 12 -
additional salt in cooking Iron supplementation
24 hours or
When to refer
Spironolactone: 1 - 2 mg/kg/day
Severe respiratory distress
ACE inhibitors
Acute pulmonary oedema
Indicate for all patients with congestive heart
failure. Refractory CCF
Captopril: 0.1 to 0.5 mg/kg/dose oral every 8 to 12 Cardiogenic shock
hourly upto 4 mg/kg/day or
Page 241
33. PICA
1. Introduction: 3. Treatment
Pica involves repeated and chronic ingestion of non- - Pica below two years does not need any
nutrient substances including mud, plaster, paint, intervention.
earth, clay, etc. Children with PICA usually have
- Children with pica are at increased risk of lead
history of neonatal insults. Most of the time, it is
poisoning, iron deficiency, and parasitic
self-limiting and represents manifestations of family
infections. They should be investigated for
disorganization, poor supervision, and affectional
these problems and if present, treated suitably.
neglect. Testing or mouthing of strange objects is
normal in infant and children up to age of 2 years. - Education, guidance and counselling of the
Common in children from lower socieoeconomic family.
strata and at times in the malnourished and mentally
- The child has to be kept occupied in other tasks
subnormal children.
and provided with the environmental
stimulation.
2. Signs &Symptoms:
Pallor and chronic abdominal pain are main
complaints.
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34. NOCTURNAL ENURESIS
1. Introduction: Rule out organic causes. Restrict fluid intake in

Enuresis is defined as normal nearly complete the evening.
evacuation of the bladder at a wrong place and time Bladder exercises:
at least twice a month after the fifth year of life.
Bedwetting at night is known as nocturnal (i) Hold urine as long as possible during the day.
enuresis.Enuresis may be primary or secondary: (ii) Practice repeated starting and stopping the
stream at the toilet bowl.
2. Primary enuresis: (iii) Emotional supportto child.
Repeated passage of urine into clothes/bed during
night in a child more than 5 years of age. Most (iv) Behaviour modification- Child should not be
common cause in primary enuresis is inappropriate given liquids after meal in the evening. Practice
toilet training. Other causes could be genetic, sleep getting up from bed and going to the bathroom at
disorder, reduced ADH at night. In some cases there bedtime before sleep.
may be organic etiology such as obstructive
uropathy or UT. There may be associated with (v) Alarm device- alarm device is used to elicit a
mental retardation or spinal cord abnormalities. conditioned response of awakening to the sensation
of a full bladder.
3. Secondary enuresis: 6.2. Pharmacological
The child has been dry for several months and again Indicated only in children > 6 years where sufficient
starts bedwetting. Too enthusiastic and immature trial of non pharmacological management has failed
toilet training, emotional stress, parent child with following:
maladjustment, urinary tract infections, diabetes
mellitus or diabetes insipidus. can cause secondary Tab. Imipramine: (0.9-1.5 mg/kg/day/PO) 6-8 year
enuresis. (25 mg), 9-12 year (50 mg), >12 year (75 mg) once
a day at bedtime. Success rate 30-60%, relapse rate
4. Signs &Symptoms: 90%. or
SALIENT FEATURES Tab. Desmopressin: 0.1-0.5 mg at bedtime.
Involuntary discharge of urine after the age at Or
which bladder control should have been
established (5 years). Desmopressin acetate (nasal spray, 10 mcg per
spray): Start with 10 mcg given at bedtime daily and
In primary nocturnal enuresis, child has never increase gradually by 10 mcg/per week to a
been dry at night while in secondary, child has maximum of 40 mcg per day. If effective, it should
been continent for at least 6 months before the be used for 3-6 months. Success rate is 40-60%,
child begins to wet again. relapse rate is 90%.
5. Investigations: (Caution: Not effectively absorbed in rhinorrhoea. If
Full medical history not used properly may cause hyponatraemia)
Genital and neurological examination 7. Referral
Urine for albumin, sugar, microscopy, specific
Refer the patient to a higher centre, if organic cause
gravity and culture.
is suspected or when
USG voiding cystourethrogram and Diagnosis is in doubt.
urodynamic studies.
8. Parent education
Reassure the parents that condition is self-limiting.
Ask the parents to maintain a diary record of dry
6. Treatment nights; reward the child for such nights. Avoid
6.1. Nonpharmacological punitive measures.
(Effective in 30% cases)

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35. THRUSH / CANDIDIASIS
1. Introduction:- 2. Salient Diagnostic Features:

Candida fungal infection in the oral cavity is Thick white patches on an angry red base in the
common and may be seen as early as 7_10 days mouth may spread to involve the lips, buccal
of age (peak 4th week of life). mucosa, tongue and palate.
After infancy it is usually secondary to Asymptornatic or may cause pain in the mouth,
treatment with broad-spectrum antibiotic. discomfort, anorexia and feeding difficulty.
Chronic or recurrent oral candidiasis is seen in Diagnosis is confirmed by the fact that on
children having immuno-deficiency. HIV removing the plaques, spots of bleeding are
AIDS, undergoing cancer therapy and in severe seen on the mucosal surface.
malnutrition. Avoid bottle feeding. Faulty sterilization of
Hypoparathyrodism, Addison's disease, bottle and nipple causes persistent or recurrent
autoimmune disorders are other rare causes. infections / thrush.
Fig. 1: Candidiasis / oral thrush.
In resistant/ chronic cases (patients with major

3. Treatment: underlying disease)
Drugs Tab. Fluconazole 3-6 mg/kg once daily for 5-7

days.
In case of breast fed baby, the medicine has to be
applied to mothers nipples also to prevent cross / Prevention:
re-infection. Emphasize on avoiding bottle feeding
3.1 clotrimazole 1% cream, gel or lotion, oral /bottle hygiene, care/ hygiene of the nipple and
application 3-4 times/day after feeding for 5-7 treatment of vaginal candidiasis in expectant
days (or 1-2 days beyond recovery). mother.
Or
Gentian violet 1% aqueous solution, 1-2 times a
day, for 5-7 days (can stain tissues and clothes).
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36. CONGENITAL HYPOTHYROIDIM
Aim: to normalize serum T4, avoid

1. Introduction: hyperthyroidism,promote normal growth and
It may be familial or sporadic, goitrous or development
nongoitrious. In about 85% cases the etiology is
dysgenesis. All new born babies should be screened.
4.3 Repeat T4 and TSH at 2 and 4
2. Signs &Symptons: weeks after initiation of
At birth hypothermia/bradycardia, shock therapy.
Develop with passage of time
Large tongue After one year tests to be done 1-2 monthly
Hoarse cry
Facial Puffiness Between 1 and 3 years do tests 2 to 3 monthly
Umbilical Hernia
Hypotonia Over 3 years do tests yearly till growth is complete
Mottling
Cold hands and feet
Lethargy
ProlongedUnconjugated Hyperbilirubinemia
Constipation
Hypothermia
Large Anterior fontanelle
Posterior fontanellemore than 0.5 cm
3. Investigation:
TSH level should be estimated after 72 hours of life
if TSH is more than 20 mu / L then
Hypothyroidism is considered and Eltroxin should
be started.
Second screening at 2 to 6 weeks (routinely in
VLBW and NICU graduates)
4 Treatment of Congenital
Hypothyroidism
As soon as possible diagnosis.
4.1 Counseling of Parents
4.2 Eltroxin 10-15 microgram/kg---

start higher dose
Do NOT use liquid preparation
On above dose, T4 Normalises in 1 weekand TSH in

one month
Page 245
37. URINARY TRACT INFECTION (UTI)
indicate significant bacteriuria. Presence of any

1. Introduction : bacteriuria in suprapubic specimenis significant. For
the purpose of management UTI is divided into
Approximately 8% of girls and 1 - 2% of boys are complicated and uncomplicated UTI.
likely to get UTI during childhood. A significant
proportion of children less than 2 years developing
UTI have underlying urinarytract anomalies, most
5. Complicated UTI
Temperature > 39C, persistent vomiting, renal
often vesico ureteric reflux (VUR). UTI in a setting of
angle tenderness and systemic toxicity are featuresof
VUR may lead to renal scarring, an important cause of
complicated UTI Infants below 3 months of age and
chronic renal disease. Early recognition and treatment
those with complicated UTI should receive parenteral
of UTI and urinary anomalies is essential to
antibiotics initially.
preventsuch complications.
2. Signs & Symptoms 6. Treatment

2.1 Neonates 6.1 In young infants (< 3 months) entire treatment is
Sepsis like features with fever or hypothermia, parenteral
lethargy, poor feeding, poor weight gain, aundice and
shock; urinary symptoms may be absent.Infants and 1. Cefotaxime 100 - 150 mg/kg/day in 3 div doses, or
children below 2 yearsUnexplained fever; urinary 2. Ceftriaxone 75 mg/kg/day in 1-2 doses, or
symptoms minimal or absent.
3. Gentamycin 5 - 7.5 mg/kg/day single dose, or
2.2 Adolescents 4. Amikacin 15 - 20 mg/kg/day single dose, or
Mostly related to lower urinary tract such as dysuria,
frequency, urgency and suprapubicpain. Renal In young infants (< 3 months) entire treatment is
parenchymal involvement is indicated by high fever, parenteral
chills, rigors and flankpain.
6.2 For older children, after first 2 - 3 days, oral
antibiotics may be started based on
3. Investigations: antimicrobialsensitivity Total duration of treatment is
3.1 Urine analysis 10 - 14 days.
May suggest UTI in the form of increased leukocytes
in urine. Gram stain of centrifugedurine specimen may Oral antibiotics
show bacteria.Dipstick for nitrite reduction and Amoxicillin 20 - 40 mg/kg/day in 2 - 3 doses, or
leukocyte esterasemay help in rapid diagnosis.
Cefadroxil 30 mg/kg/day in 2 doses, or
3.2 Urine culture Cephalexin 50 mg/kg/day in 3 doses, or
This is the only confirmatory test for UTI. Every
effort must be made to properly collect and senda Cefixime 8 mg/kg/day in 2 doses, or
urine sample before antibiotic is started. In infants and
young children UTI should be suspected if there is Ciprofloxacin 10 - 20 mg/kg/day in 2 doses
unexplained fever.A midstream clean catch specimen
is ideal. Soap or antiseptic solution should not be used 7. Uncomplicated UTI
beforecollection. In infants urine can be obtained by Children > 3 months of age and those who do not have
suprapubic aspiration. features of complicated UTI can be treated withoral
amoxicillin (10 to 15 mg per kg) or cefadroxil (5 to
4. Common organisms 10 mg per kg) for 7 to 10 days (based on sensitivity).
Though fluoroquinolones are effective and safe for
responsible for UTI are UTI, they are not the first-line antibiotics
E. coli, Occasionally Klebsiella, Staph epidermidis or
Strep fecalis may be responsible.
A colony count of > 105 colony forming units (CFU)
/ ml of single species in a clean catchspecimen
Page 246
OBSTETRICS
AND
GYNAECOLOGY
Page 247
1.NORMAL PREGNANCY
Antenatal period is the most crucial period as the complications during after delivery (PPH,
services provided during this period can have positive Retained Placenta, Infection)
impact on health of both the mother and her child. Past history: Hypertension, Diabetes Mellitus,
Tuberculosis, Asthma, Heart disease, any other,
1. Essential obstetric care to surgical procedures undergone, medications
taken during pre conceptional period, history of
every pregnant woman bleeding.
Registration of all pregnant women before 12 H/O current symptoms, perception of fetal
weeks. movements if pregnancy> 16 weeks.
2. Detailed history at first visit 3. Schedule of Examination

Menstrual histor y: Regularity of cycles, date of Ideally all the ANCs should be examined monthly
LMP, calculate EDD and record on Mother after registration. If it is not possible to attend ANC
Child Protection (MCP) card clinic monthly, then checkup should be carried out at
Obstetric history:Number of prior pregnancies least five times during the pregnancy. First 8-12
and outcome of each pregnancy (full term birth, weeks, second between 14-20 weeks, third at 22-26
preterm birth, abortion), place and mode of weeks, fourth at 28-32 weeks and fifth at 36-40
delivery, weight of baby, Live birth/stillbirth, weeks.
Table 1: Examination at antenatal clinic

*Height *Breast examination
*Weight : Compare with previous visit (calculate *Systemic examination : Auscultate chest
BMI in first trimester)
*Pallor, icterus *P/A: Fundal height & its correlation with period of
amenorrhoea (POA)
*Edema over feet, hands, face *Fetal presentation and position after 32 weeks
*Blood pressure *Fetal heart rate
* During first check up

The last two visits are important as many of the Medical officer should perform at least one
pregnancy complications are detected during last checkup during the third trimester and auscultate
trimester. For 'high risk' mothers more frequent her chest to r ule out any systemic abnor mality.
examinations will be required.
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4. Investigations
Table 2:
Hemoglobin estimation VDRL
Urine Analysis: Protein and s ugar Voluntary HIV testing
Test for sickling in selected tribal area Blood sugar testing
Blood grouping, Rh typing Hepatitis B surface antigen (HBsAg)
Ultrasonography (16 to 18 weeks) Malarial parasite in Ende mic area.
5. Examination and action to be taken during ANC check up

Table 3:
Examination Action
Ede ma Examine whether ede ma is on one leg or both legs and is it pitting. Look for
edema over face, hands, and abdomen. Check for proteinuria and
hypertension.
High blood pressure and albuminuria, refer to specialist as she has pre-
eclampsia.
History of kidney disease, if yes refer to specialist.
If edema is on one leg, refer to specialist.
If bilateral pedal edema without albuminuria and normal BP: Reassure
mother, c heck for anemia and give IFA tablets as required
Weight gain Record monthly weight on MCP card of mother, calculate weight gain since
the previous visit
Weight gain more than 3 kg. in a month: Suspect pre-eclampsia
Weight gain less than 1 kg. in a month: Suspect fetal growth retardation.
Blood Pressure If 140 / 90 mm Hg or more, advise mother to rest for half hour and then
repeat the BP recording. Check for proteinuria
If systolic between 140-160 and /or diastolic 90 or above: advise extra rest
and refer to MO PHC
If systolic 160 or more or diastolic > 100 : refer to specialist
Fundal Height Examine fundal height in weeks and compare with calculated duration of
pregnancy as per LMP. If it is greater or lesser refer to specialist. Causes of fundal
height less or more than expected are given in table below.
Fetal Presentation Noncephalic (correction can be attempted at 36 weeks in suitable cases)

byObs/Gyn specialist.
Fetal Heart Rate FHR < 120 or > 160 /minute : Refer to specialist.
Hemoglobi n % Hb 11 gm% or more: IFA 100 tablets

Hb between 7-11 gram%: Start IFA double dose* and re-examine after one month
- If improvement of Hb by more than 1gm%, continue IFA. Give tab
Page 249
Examination Action
Albendazole(during second trimester)
Hb< 7 gm % - Refer anemia treatment guidelines
Proteinuria If proteinuria present suspect pre-eclampsia and refer to specialist.
Risk factors All high-risk pregnancies should be checked by MO and then referred to specialist
if necessary for further checkup or during delivery depending upon the risk factor.
* For better absorption, IFA tablets should be taken 1.30 hours before meals
Table 4:
Fundal height < Period of Amenorrhea Fundal height > Period of Amenorrhea
Wrong dates Wrong dates
Infrequent periods prior to conception Poly hydramnios
Intrauterine Growth retardation(IUGR) Twins
Oligohydramnios Big baby
Intrauterine fetal death. Hydatidiform mole
Uterine fibroids
discharge per vaginum, blurred vision, excessive

6. Education and counseling vomiting, reduced fetal movements.
regarding care during Consumption of iron folic acid 100 tablets for
anemia prophylaxis.
pregnancy Tetanus Toxoid 2 doses/booster dose.
Calcium through diet and Calcium carbonate
6.1. First and second trimester: tablets 1.2 Gm daily.
Diet: More than one meal a day and evening
snacks (mos t impor tant), inclusion of sprouted 6.2. Third trimester:
legumes, pulses, green leafy and other Avoid heavy work and jerky travel on bad roads.
vegetables, seasonal fruits.
Importance of institutional delivery, safe
Rest: 2 Hours in afternoon and 8 hours at night delivery, inform TOLL free No.102 and 108 for
in lateral position. free ambulance service, JSY, JSSK and other
Exercise: Walking for 30 minutes daily. benefits, Plan for place of delivery, preparation
Habits: Avoid tobacco in any form, avoid for delivery.
alcohol. Importance of early initiation of colostrum
Practicing safe sex. feeding within Half an hour of birth & exclusive
Self-reporting of danger signals, e.g.Abdominal breast-feeding for 6 months, child immunization
pain, severe headache, giddiness, palpitations, and contraception especially PPIUCD.
easy fatigability, breathlessness, fever, Ask about birth companion.
generalized edema, vaginal bleeding, watery
Page 250
1. Identify high-risk mothers:
Table 5:
Risk factors detectable during Abnormalities developing during

first check up Current pregnancy
Age : Teenage/ elderly primi, Anemia

Para 4 and above Hypertension, proteinuria
Short stature, limping gait, vertebral spine Vaginal bleeding during pregnancy
abnormalities
Premature rupture of membranes (PROM)
Bad obstetric history: H/O stillbirth, neonatal
death, LBW baby, recurrent abortions Gestational diabetes mellitus (GDM)
Fundal height < POA or > POA
Previous Caesarean delivery
H/O PE/eclampsia, PPH, retained placenta Uterus over distension: Twins,
Polyhydramnios
during previous pregnancies
Fetal malpresentation persisting near term
Preexisting medical conditions : Heart
disease, diabetes mellitus, renal disease Pregnancy > 41 w eeks
HIV /VDRL positive gravida Reduced fetal movements
Rh negative gravida
2. Actions sugge sted for some high risk indicators:
Table 6:
RISKS ACTION
1. Elderly Primi
Hypertension during pregnancy Refer to specialist soon after registration for evaluations to
exclude fetal anomalies (biochemical markers and
Gestational diabetes ultrasonography)
Difficult labour - Chances of Regular ANC: B.P, urine analysis every month
caesarean section are higher
Pelvic assessment at or after 36 weeks.
Fetal abnormalities.
Institutional delivery under care of specialist.
2. Teenage primi
Hypertension during pregnancy Regular antenatal care

Anemia Hb%, BP, urine analysis more frequently
Pre-term labour Adequate rest
Fetal growth retardation. IFA tablets, nutrition guidance
Difficult labour Pelvic assessment at 36 weeks
Hospital delivery.
3. Primi : Height less than 145 cms Regular ANC check. Assessment of place of delivery by
Page 251
RISKS ACTION
specialist. Observe progress of labourpartographically.
4.Primi having vertebral /limb deformity Regular check up at PHC, Assessment by specialist for place of
delivery.
5. Grand multipara (para 4 and more)
Anemia Supplement IFA, nutrition guidance
Malpresentation At 34 and 36 weeks look for fetal malpresentation
Atonic PPH Hospital delivery - Avoid Injudicious use of oxytocics for
augmenting labour
Uterine rupture
Active management of 3rd stage of labour - Keep IV line
ready
Page 252
2.NORMAL LABOUR
1. Pelvic Assessment
Table 1:
Parameter Adequate Suggestive of abnormality

Sacral promontory Not felt Felt easily
Diagonal Conjugate* >11.5 cms < 11.5 cms
Sacral curvature Well curved Flat
Lateral Pelvic walls Parallel Converging
Ischial spines Both cannot be palpated simultaneously Both spines can be palpated
simultaneously
Subpubic Angle Accommodates two fingers (850) Acute
Inter tuberous diameter Accommodates closed fist (4 Knuckles) Cannot accommodate 4 knuckles
* If sacral promontory is felt, the distance between the sacral promontory and the lower border of pubic symphysis
is measured.
Push the head into the pelvic inlet and note

2. Clinical Examination for whether it descends into the pelvis (felt by
CPD fingers in vagina) or overhangs on the public
symphysis.
Place the woman in dorsal position. If head descends with no overlap at public
Hold the fetal head by left hand. symphysis: No inlet CPD.
Place two fingers of gloved right hand into the If the head is engaged it indicates that the pelvic
vagina at the level of ischial spines. inlet is adequate.
Place the thumb of right hand on the pubic Get urine sample tested for protein, sugar and note
symphysis. volume.
3. Monitoring during active phase
Table 2:
Examination / Observation Periodicity
Maternal pulse and FHR Every 30 minutes
Uterine contractions Every 30 minutes
Maternal temperature, BP, urine volume Every four hours
Vaginal Examination Every four hours
Note the time of rupture of membranes and To assess cervical dilatation, station and position
perform va ginal examination immediately of vertex.
To rule out cord prolapse and see the color of Assess and monitor the progress of LABOUR by
liquor. using Simplified Partograph adopted by GOI to
Page 253
record FHR, liquor, cervical dilatation, uterine a) First stage of labour showing satisfactory
contractions, medications administered during labour, progress: Continue observation till second stage
maternal pulse, blood pressure and temperature. starts.
b) Second stage of Labour:
Points to Reme mber
Cervix is fully dilated.
This graph is used only during active phase of Signs of imminent delivery: Mother starts
labour. pushing (bearing down). Fetal scalp seen at
The complications requiring immediate vulva, perineum bulges, anus gapes. Mother gets
interve ntion need to be excluded first. sensation of defecation.
Encourage the mother to push only during
3.1. Partograph contraction.
On this graph, one square represents one hour on Monitor progress and fetal wellbeing during
horizontal axis. On vertical axis, one square second stage.
represents cervical dilation of one centimeter. Note FHR every 15 minutes.
Assess descent of presenting part (fetal station)
3.1.1 Phases of first stage and alert and action every 15 min.
line: Look for caput, molding, meconium staining of
Latent phase: Cervix dilates very slowly up to 4 liquor.
centimeters. It may take up to eight hours for Suppor t the perineum and de liver the head gently
this. Deliver the shoulders
Active phase: 4 cm onwards; cervix dilates Keep the baby on mothers abdomen on a pre-
rapidly at the rate of about 1 centimeter per hour. warmed towel and give immediate care.
Alert Line: An obl ique line on the graph from 4 Conduct delivery. Follow universal bio safety
to 10 centimeters progressing at the rate of 1 precautions.
centimeter per hour.
Delivery of baby takes place usually within 30
Action Line: Parallel line Four hours to the right minutes in a multi and 60 minutes in a primi
of alert line para.
Give mediolateral episiotomy under local
3.1.2 Recording o n partog raph: infiltration anesthesia by Injecting 1%
Initiate recording when cervix is 4 cm dilated lignocaine, if mother is unable to push or if there
and immediately if the cevix is > 4 cm dilated on is undue delay.
admission to the Labo ur ward.
Record the dilatation in cm (symbol x) on the
alert line and record the time at which c) Third stage of Labour: Deliver the placenta by
observation has been made on the horizontal axis active management of third stage of LABOUR
below this point.
Perfor m vaginal examination every 4 hours and 4. Active Management of Third
note the cervical dilatation and mark it on the Stage of labour (AMTSL)
graph.
Join the points and interpret the observations. Active management of 3 rd stage of LABOUR reduces
the amount of blood loss due to uterine atony,
3.1.3 Interpretation: reduces the chances of having atonic PPH and
Satisfactory progress: Cervical dilatation lies requirement of blood transfusion significantly
on left side of alert line, active phase progression thereby helping to reduce maternal mortality due to
> 1 cm/ hour, Fetal and maternal health severe PPH.
parameters are normal. It is an integral part of skilled attenda nce at birth and
Slow progress: Alert line crossed, careful is mandatory for all deliveries (vaginal and
monitoring to note the progress. At subcentre abdominal). The steps are as follows:
and PHC the arrangements for referral to FRU.
Action line reached or crossed: Careful review After the childbirth, exclude presence of another
to find the cause for delay followed by baby by abdominal palpation
appropriate interventions. Give Inj. oxytocin 10 IU IM. immediately after
birth (Oxytocin should be kept in refrigerator).
When oxytocin is unavailable, tabletmisoprostol
600 mcg (3 tablets) may be given orally.
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Check for uterine contraction. traction by other hand pushing the uterus
Clamp and cut the cord. upwards towards umbilicus. Repeat this during
Deliver the placenta by controlled cord traction. contraction as required.
When the uterus is well contracted , give gentle After delivery of placenta, give uterine massage
downward traction on cord while giving counter to keep the uterus contracted.
Figure 1: Controlled Cord Traction
If vertex is engaged and cervix is well applied to

5. After delivery the vertex then controlled ARM can be
performed to hasten the progress.
Examine the perineum, vulva, lower vagina for
tears. After ARM review progress after two hours. If
progress is still slow, assess uterine contractions.
Examine the placenta and membranes carefully
If uterine contractions are infrequent and weak
for completeness and any abnormality.
then consider oxytocin augmentationafter
Observe the mother every 15 minutes for two excludi ng contraindications.
hours for general condition, pulse, vaginal
If there is no progress after augmentation or if
bleeding, pallor, uterine contraction.
signs of fetal distress develop, an emergency
Repeat uterine massage every 15 minutes for 2 caesarean section might be required. Hence such
hours. a woman should be referred to a well-equipped
Encourage mother to take the baby to breast maternity unit.
within hour of delivery.
6.2.Oxytocin Augmentation: (only

6. Augmentation of Labour where specialist is available)
6.1. Care of woman showing slow Exclude contraindications before starting oxytocin
/unsatisfactory progress of
Labour CPD, Fetal distress
Grandmultiparity, Malpresentations, Scar on the
Alert line crossed or the action line reached uterus
Causes: Hypotonic uterine action, occipito
posterior position, deflexed head, CPD etc. Refer 6.2.1 Dose and Administration
the case to higher level of care.
Add 2.5 IU to 500 ml of normal saline or
Labo uraugmentation by amniotomy (artificial Ringers lactate. Start infusion at the rate of 8-10
rupture of membranes) and oxytocin infusion are drops/min. Observe uterine contractions.
offered as per the clinical situation. If contractions are mild increase the drip rate by
Labo uraugmentation should be done in places 8-10 drops /min every 30 min until she gets 3
where clinical expertise and facilities for contractions in 10 minutes, each contraction lasts
operative delivery are available.
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for 40-45 seconds and there is good relaxation of Discontinue the drip
uterus in between the contractions (optimum Maternal repositioning (left lateral position),
response). Oxygen therapy
Drip rate can be increased maximum up to 60 Terbutaline 250 mcg can be given IV slowly for
drops/minutes. If the contractions are inadequate tocolysis if required
at this rate, prepare another drip with 5 IU /500
ml and start it at the rate of 30 drops/min, Caution:
increase by 5 drops every 30 minutes and
observe the response
For augmentation of Labour oxytocin should
never be give n intramuscularly.
6.2.2 Monitoring:Monitorfollowing parameters
Cautious use in multiparous women as the uterus
every 15 minutes,
tends to rupture.
Drip rate, Uterine contractions frequency and 6.2.5 When to discontinue the drip:
intensity
FHR and Maternal pulse
If six hours of strong stimulated uterine activity
Progress of labour
is unable to bring progress of labour, discontinue
the drip and review the case.
6.2.3 Complications: If there are signs suggestive of fetal distress.
If after initial satisfactory progress, cervical
Hyperstimulation : > 5 uterine contractions / 10 dilatation does not progress for two hours or
minutes, each lasting for > 60 sec more in established active phase of Labo ur then
Uterus failing to relax between the contractions review her. This could be due to cephelo-pelvic
Fetal bradycardia (distress) disproportion or large head with deflexion. Such
Uterine rupture if drip is not supervised patient may need operative intervention.
vigilantly.
Water intoxication if too much of electrolyte free Prolonged second stage
infusion is administered. If second stage is prolonged for more than 2 hours in
Neonatal hyperbilirubinaemia primi and for > 1 hour in multi, then
Assess size of baby and pelvis again.
6.2.4 Treatment of Hyperstimulation: See whether fetal head is still palpable in
suprapubic region.
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3. CLINICAL CARE OF HIGH RISK
PREGNANCY
Common Risk Indicators: 1.1.3 Risk Factors:
Bad obstetric history: Previous history of pre- Risk is highest among couples where the age of
term Labo ur, stillbirth, early neonatal death, woman is 35 years.
recurrent pregnancy loss. The risk increases after each successive
Post caesarean pregnancy. pregnancy loss, reaching approximately 40%
Vaginal bleeding during pregnancy. after three consecutive pregnancy losses.
Rh negative pregnant woman , husband Rh +ve
Fetal malpresentation (Breech/transverse lie) 1.1.4 History:
persisting at 36 weeks.
Diagnosed twins, polyhydramnios. Detailed obstetric history about each pregnancy.
Pregnancy be yond 41 w eeks. Duration of pregnancy at mishap. Whether USG
documented cardiac activity was seen, fetus was
Medical diseases: Anemia, diabetes mellitus,
live born/stillborn ( fresh/macerated stillbirth),
cardiac disease, chronic hypertension, kidney
baby normal/abnormal.
disease, tuberculosis.
H/O Consanguinity, history of infertility,
Refer to other high risk indicators mentioned in
menstrual abnormality, infections, STD.
earlier chapter.
Personal history: Tobacco, alcohol, caffeine,
1. Bad Obstetric History medications.
Personal/familial H/O thrombosis, autoimmune
Bad obstetric history is a term used in day to day disorder.
practice for describing unsuccessful pregnancy
outcome in previous pregnancies. A variety of 1.1.5 Physical examination:
unsuccessful outcomes are included in this such as a) Look for obesity, hirsutism, acanthosis, thyroid
previous H/O stillbirth, preterm delivery, recurrent enlargement, galactorrhoea
midtrimester/early abortions. b) P/S & P/V examination: Look for uterine
fibroids, double uterus, bicornuate uterus, genital
1.1. Recurrent Pregnancy Loss infection, torn or short cervix
(RPL) c) Investigations: Carry out the relevant
investigations as indicated and available
1.1.1 Definition:Three or more consecutive depending on whether the woman has presented
pregnancy losses during pregnancy or after the mishap.
d) During pregnancy:
1.1.2 Causes: Hematology, blood group and Rh typing, VDRL
Urine analysis
Genetic Rule out diabetes
Environmental and occupational exposure to Antiphospholipid antibody testing
organic solvents, ionizing radiation, toxins, USG: For uterine abnormalities, Monitoring
tobacco, alcohol early pregnancy
Uterine anomalies, Cervical incompetence, Thyroid function, Prolactin
Uterine synechiae (adhesions), Uterine fibroids
Infections e) Non pregnant state:
Endoc rine Dysfunction: Polycystic ovary Pelvic USG for polycystic ovaries (PCOS),
syndrome (PCOS), Luteal phase inadequacy Hysterosalpingography(HSG), Hysteroscopy for
(LPI), Diabetes mellitus, Thyroid dysfunction, uterine abnormalities
Prolactin disorders. Parental karyotype
Antiphospholipid antibody syndrome (APLAS) Mid luteal serum progesterone and
Unexplained: In some cases no cause can be thrombophilia profile if available
detected. f) Soon after miscarriage:Chromosomal studies of
conceptus
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1.1.6 General Measures:
3. Infections
Quitting cigarette smoking, tobacco, alcohol and Generally cause sporadic pregnancy loss.
caffeine consumption Toxoplasmosis, rubella, cytomegalovirus, herpes and
Weight reduction in PCOS cases listeria infections do not cause recurrent pregnancy
Therapies depending upon cause. loss and routine TORCH screening is not indicated.
Psychological counseling & support is extremely Active syphilis during pregnancy can lead to
helpful. recurrent pregnancy loss.
50% Success even if no treatment is given.
3.1. Syphilis during pregnancy
Some common conditions are as follows:
3.1.1 Effects: Late abortions, stillbirths, neonatal
deaths, infant having active congenital
2. Cervical incompetence syphilis.
Premature softening and dilatation of internal 3.1.2 Diagnosis is serological: VDRL at booking.
cervical os during pregnancy can lead to Note titers, titers 1:8 or more are significant.
protrusion of membranes, rupture of membranes Treponemal test (TPHA) is confirmatory.
and fetal expulsion during second trimester or 3.1.3 Treatment: Treatment of maternal disease
early third trimester can prevent fetal infection and also treat
Typical obstetric history is diagnostic: Repeated established fetal disease
midtrimester or early third trimester pregnancy Benzathine penicillin single Injection 2.4 Mega
terminations, relatively painless, rapid, often units deep IM after sensitivity test as Penicillin is
preceded by rupture of membranes followed by the only antibiotic that can cross the placenta in
expulsion of fresh or live fetus adequate amounts to treat the fetus.
Symptoms : Low backache, mucoid vaginal For latent disease > 1 year duration, 3 Injections
discharge at weekly interval.
P/S: Bag of membranes may be seen through the Penicillin sensitive individuals require
cervical os desensitization.
Vaginal examination: Internal cervical os dilated Erythromycin 2 gms daily in divided doses for
in absence of uterine contractions, cervix may be 14 days can be considered however Penicillin is
short. more effective.
Infant of a VDRL positive mother needs care by
specialist.
2.1 Investigation: Safe sex counseling.
USG may show short cervix, funneling of
cervix, membranes dipping into the cervical 4. Hypothyroidism
canal.
USG assessment of cervical length (25mm or Hypothyroidism can be due to iodine deficiency
less) bytransvaginal scan before 24 weeks in or thyroid autoantibodies.
women having previous history of preterm Infertility, menstrual problems due to Ovulation
LABOUR is considered significant for disturbances.
prediction of preterm LABOUR. Increased risk of miscarriage due to luteal phase
insufficiency.
2.2 Treatment: PHC: Anemia, gestational hypertension, placental
Refer the case to specialist soon after abruption and postpartum hemorrhage are
registration. common.
At RH/DH:Prophylactic cervicalos tightening at Fetal/neonatal problems: Preterm birth, low birth
16 weeks by McDonald method under short weight, congenital malfor mations, neonatal
general anesthesia. respiratory distress, perinatal death. Cretinism.
Follow up: Extra rest, avoid exertion. TSH. If elevated thyroid function tests and
Stitch removal at 37 weeks or at the onset of antibod y testing.
LABOUR whichever is earlier. Anticipate rapid Treatment by thyroxine can correct ovulatory
delivery. dysfunction and help achieving pregnancy and
successful outcome.
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Counsel pregnant women for consumption of should be followed by administration of anti D
iodized salt. immunoglobulin.
Targeted case finding approach is followed. It is recommended to give 300 mcg anti D
Universal TSH screening is currently not immuno globulin during pregnancy at 28 weeks
recommended. for reducing the risk of antepartum sensitization.
At delivery, cord blood sample to be tested for:
Infants Rh, ABO grouping, hemoglobi n and
5. Rh Negative Pregnant hematocrit.
Woman Direct Coombs test, Direct and indirect bilirubin
estimation.
A major cause of hemolytic disease of newborn Administration of 300 mcg of anti D Ig IM to
(HDN) is Rh blood group incompatibility between mother within 72 hours of delivery (earlier
the mother and her fetus. When Rh negative mother within 24 hours is still better). 300 mcg
bears Rh positive fetus, the Rh antigen from fetal red neutralizes 15 ml of fetoplacental hemorrhage
cells enters the maternal circulation and results in (FMH). If it has not been given within 72 hours,
antibody formation in mother. These antibodies cross should be given up to one week with some
the placenta and cause destruction of fetal red cells benefit.
resulting in fetal Anemia. Prevention of such The baby is referred to neonatology specialist
sensitization is pos sible by antenatal screening and and is observed for icterus, anemia.
appropriate care.
5.2.2 Sensitized woman:
5.1. Pregnancy outcome
If ICT is positive, it indicates that the woman is
First child usually escapes. Subsequent babies suffer sensitized and has got antibodies against Rh
from mild hemolytic anemia, rapidly increasing antigen in her blood. Note the titres reported.
hyperbilirubinemia within 24 hours of birth or There is no use of giving Anti D Ig to sensitized
hydrops fetalis resulting in intrauterine fetal death. mother.
The adverse perinatal outcome occurs earlier during Sensitized woman must be referred to a tertiary
pregnancy with each subsequent pregnancy. care centre having equipment and expertise for
cordocentesis and intravascular fetal transfusion.
5.2. Management
Every pregnant woman should be tested for Rh 6. Post Caesarean Pregnancy
typing at registration.
Those testing negative should have their Pregnancy with h/o previous caesarean section (CS)
husba nds Rh typi ng done. is a high risk condition as there is increased risk of
Take detailed histor y about every pregnancy and complications during childbirth after each caesarean
its outcome. H/O neonatal jaundice, hydrops, section (Scar rupture, placenta previa, adherent
stillbirths etc. placenta, PPH)
Note history of receiving anti D
immunoglobulin, time, dose during/following
every pregnancy.
Perform indirect Coombs test (ICT) on blood
sample to detect maternal sensitization.
5.2.1Nonsensitized woman:
Negative ICT indicates that the woman does not

have detectable antibodies against Rh antigens.
Refer her to gynecologist at FRU. ICT is
repeated monthly.
Do not perform external cephalic version for
malpresentations. Any episode of bleeding or
manipulation, procedure such as amniocentesis
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6.1 Risks
Table 1: Risk Factors
Maternal Fetal/neonatal
Scar dehiscence during Labour Fetal distress
Scar rupture leading to severe Fetal death due to scar

haemorrhage& shoc k rupture
Chances of repeat CS are high Neonatal asphyxia
All cases having CS in previous delivery should be Perform clinical pelvic assessment at or after 36
referred to specialist at FRU/district hospital during weeks.
third trimester. At 36 weeks she should have a
review by specialist regarding plan for delivery
either by repeat elective CS or trial for vaginal birth 6.4 Investigations
USG assessment of fetal weight, localization of
after CS which depends on indication of prior CS
placenta. Look for morbidly adherent placenta if
and assessment of scar integrity.
placenta previa.
6.2 History 6.5 Selection for Trial of Labour
Indication for CS, elective or emergency, when after caesarean section
in labour it was done.
Place and person operating , performed at term Indication for previous CS non recurrent (fetal
or preterm. distress, breech, placenta previa.)
Type of CS :Lower segment transverse incision Only one prior low transverse CS delivery. No
or classical . other uterine scars or previous rupture.
(Vertical scar is very weak having high chances Vertex presentation, Clinically adequate pelvis.
of scar rupture which is likely to happen during No other obstetric complication ( APH, breech
late pregnancy and during labour with increased presentation)
risk to the mother and fetus hence elective Surgeon, anesthetist immediately available for
caesarean section should be performed at term in emergency CS.
such cases)
Review operation notes regarding Repeat CS: Women not eligible for vaginal trial will
complications, inverted T extension of incision, need an elective repeat CS. which should be
lateral extension of tears, post-operative performed at 39 weeks for the best neonatal
infection, blood transfusion, prolonged hospital outcome, if there is no maternal or fetal indication to
stay. perform it earlier.
Inter pregnancy interval < 24 months increases
the risk.
All post caesarean pregnancies should only be
6.3 Examination managed in equipped hospitals with personnel
Anemia:Correction before term is important as readily available for emergency caesarean section
the chances of requiring repeat CS are high. when needed carefully selected women can be
Note the size of baby, presentation, presence of
any other risk factor or complication in current allowed to have trial of vaginal birth under expert
pregnancy. supervision.
Pregnancy complication: Twins,
polyhydramnios, APH.
Look for scar tenderness.
Page 260
6.5.1 Manage ment of labour following caesarean
section:
7. Twin Pregnancy
Refer post caesarean delivery to higher centers. 7.1 Antenatal Diagnosis and
Counseling and informed consent for trial of Management
Labo ur.
Keep operation theatre ready for CS, arrange The incidence of twin gestation is increasing as a
blood. result of infertility treatment. With modern assisted
Monitor progress of labour. reproduction techniques higher order of multifetal
Watch for early signs of fetal distress, scar gestation is common.
dehiscence and perform immediate caesarean
7.1.1 History:
section if these signs appear.
If satisfactory progress, cut short the second Ovulation induction by clomiphene or
stage of labour and deliver. gonadotropin Injections for infertility.
After vaginal delivery, watch for PPH/intra Maternal family histor y of twins, adva nced age,
peritoneal hemorrhage. high parity.
6.5.2 Symptoms & Signs of impe nding rupture 7.1.2 Signs:
during labour:
Suprapubicpain persisting in between uterine Suspect twins when the fundal height is greater
contractions. than the period of amenorrhoea and multiple
Slight fresh vaginal bleeding. fetal parts are felt.
Unexplained tachycardia, tenderness over Palpation of 2 heads, 3 major poles
uterine scar. May have associated polyhydramnios
Alteration in fetal heart rate, sudden signs of Two pe rsons simultaneously hearing FHS at two
fetal distress. different locations with a difference of > 10
Hematuria. beats/min.
Falling BP with increasing pallor is a late sign
of uterine rupture.
7.1.3 Investigation:
6.5.3 Contraception:
Ultrasonography. Early sonographyin second
Counseling for contraception for increasing inter trimester helps in assessing chorionicity
pregnancy interval.
Postpartum IUCD insertion at operation before
closure of uterine incision is safe.
7.2Risks
Table 2: Risk to baby according to type of complication
Pregnant Woman Baby
Hyperemesis gravidarum Prematurity

Anemia IUGR
Pre-eclampsia Malpresentations
Antepartum haemorrhage due to Placenta previa and Fetal asphyxia
also abruptio placentae is likely
Preterm LABOUR Twin-to-twin transfusion
Hypotonic uterine action, prolonged LABOUR Fetal malformations
Postpartum haemorrhage Fetal death
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Difficult delivery Perinatal mortality is high
7.3 Management during pregnancy 8.2. Causes

Detection and correction of anemia. Fetal anomalies: Anencephaly, esophageal
Nutrition counseling, extra nutrients to meet the atresia.
need of two fetuses.
Maternal diabetes, Multiple pregnancy.
Avoiding exertion, extra rest in left lateral
position. Idiopathic, Placental chorioangioma.
Early diagnosis of preeclampsia.
Can be mild, moderate or severe. Development can
Refer to specialist for antenatal care and delivery be acute or chronic
at FRU.
Explaining warning signals for preterm Labo ur.
8. Polyhydramnios
8.1. Definition 8.3 Risks
Excessive volume of amniotic fluid
Table 3: Risk according to complication type
Pregnant Woman Baby

Hypertension Prematurity
Risks due to associated diabetes mellitus Malpresentations
Risks due to associated twins Fetal asphyxia due to cord prolapse or placental
abruption
APH : Placental abruption Fetal malformations
Preterm labour, PROM, cord prolapse Problems due to associated complications :
twins/preeclampsia/APH
Hypotonic uterine action, prolonged labour
Postpartum haemorrhage
Difficult delivery
8.4. Diagnosis Hydramnios should be differentiated from ascites

and large ovarian cyst.
Fundal height is > POA. Abdomen is over
distended.
Fluid thrill can be demonstrated.
8.5 Management
Fetal parts are not well felt if the abdomen is
tense. FHS may not be clearly heard. Mild cases: No intervention required. Extra rest in
USG confirms the diagnosis by demonstrating comfortable position.
large amount of amniotic fluid. Amniotic fluid
Symptomatic women need to be hospitalized.
index (AFI) 24-25 cm
Association with twins and fetal malformations Specialist can offer following interventions
need to be looked for. depending upon the case.
Severe hydramnios can lead to edema, severe
Tablet Indomethacin: 50-100 mg stat followed
breathlessness, inability to sleep and may require
by maximum 200 mg in 24 hrs for 24-48 hrs. at
immediate attention by specialist.
< 30-32 weeks of pregnancy (As there is risk of
Maternal diabetes mellitus needs to be excluded. premature closure of fetal ductusarteriosus)
Page 262
Amniocentesis to relieve the maternal distress. 9.3 . Risk Factors
The success is transient and repeated fluid Primiparity, pervious history of post term
removal is required. Complications such as pregnancy, sedentary life style, anencephalic
preterm Labo ur, rupture of membranes, fetus. Genetic predisposition
chorioamnionitis, and placental abruption are
likely.
Delivery in a well-equipped institution under
9.4 Prevention
care of a specialist.
Accurate calculation of EDD. Ask whether
Oxytocin augmentation if contractions are weak. menstrual cycles before conception had been
Risk of placental abruption is high when the regular.
membranes rupture and a large volume of Instruct ASHA, ANM to refer a woman who has
amniotic fluid is drained sudde nly. Preserving crossed her EDD to the medical officer.
membranes is important. When required,
At 40 weeks: Check for any complications. In
controlled ARM is done.
pregnancies complicated by hypertension,
Active management of third stage as there is a preeclampsia, IUGR the fetus is at greater risk of
risk of atonic PPH. asphyxia. Hence these women should not be
Examine the baby for congenital malformations allowed to cross their EDD. They should be
(Esophageal atresia or trachea- esophageal referred to specialist as they need to be delivered
fistula) early.
Uncomplicated pregnancy: Wait until 41 weeks.
Instruct the woman to report if fetal movements
9. Prolonged Pregnancy are reduced.
Vaginal examination: Assess whether the cervix
9.1. Definitions is ripe or unripe (Bishop Score).
Sweeping of membranes should be done during
Post term pregnancy: Pregnancy that has crossed 42
this examination as it decreases the chances of
weeks.
post term pregnancy.
At 41 weeks: At PHC, once pregnancy has
9.2. Risks reached 41 weeks, refer her to FRU for further
Post maturity syndrome: In about 20 % cases evaluation and i nterve ntions.
of prolonged pregnancy there is placental
insufficiency which results in a pathologic 9.5 Management of post term
syndrome in which there is fetal growth
retardation associated with meconium stained pregnancy at FRU
amniotic fluid, oligohydramnios and fetal There are two options of managing 41 weeks
distress. The newborn is at risk of meconium pregnancy: Immediate induction of labouror
aspiration syndrome. The baby shows loss of expectant management until 42 weeks, while
subc utaneous fat, wrinkled, dry, cracked skin monitoring the fetal wellbeing.
(old man look). It has long thin body and long 9.5.1In low-risk pregnancies routine induction of
nails. Associated oligohydramnios increases the labour at 41 weeks is associated with reduction in
likelihood of postmaturity. perinatal mortality. The risk of fetal distress is
In other cases not complicated by placental reduced by induction of labour.
insufficiency, there is continued growth of the
fetus leading to macrosomia, with increased risk 9.5.2 Follow up:If expectant management option is
of abnormal labour, shoulder dystocia, and chosen, the mothers should be advised to come for
Injuries to baby. fetal surveillance test at 41 weeks and twice between
41 and 42 weeks.
Increased perinatal mortality in pregnancies
continuing > 42 weeks. History:
Mother: Difficulties in labour due to fetal a) Accurate assessment of gestational age to
macrosomia, Shoulder dystocia. avoid delivery of a preterm baby. Errors likely if
Increased chance of caesarean delivery. prior irregular menstrual cycles or if she has
conceived soon after cessation of oral contraceptive
pills.
Page 263
Review the early USG reports and the date of 9.6 Induction of labour
detection of positive UPT.
Cervix unfavorable (Bishops score < 6):
Ask about history of di minished fetal movements. Vaginal misoprostol 25 mcg 6 hourly for
induction of Labo ur. Oral misoprostol 25 mcg 2
b) On examination: hourly can be used.
Less amount of liquor on abdominal palpation, Pre induction cervical ripening can also be
achieved by intra cervical PGE2 gel or by Foley
Baby may be of large size. catheter. Cervix is reassessed for improvement in
c) USG: bishop score. Induction can then be carried out
with oxytocin infusion.
Look for oligohydramnios: Amniotic fluid index Favorable cervix: Induction with oxytocin
(AFI) 5 cm or less or there is no vertical pocket > 2 infusion and ARM.
cm. This is a marker for fetal compromise. Note:
estimated fetal weight and check for macrosomia. 9.7 During labour (Induced or
d) Nonstress test: spontaneous)
Reactive or nonreactive. [FHR increased by > 15
Partographic monitoring of Labo ur. Monitor
beats lasting for 15 seconds in response to fetal
FHS and color of liquor, (electronic monitoring
movement is assuring]
if available). watch for signs of fetal distress.
Fetal compromise is indicated by reduced AFI, CS is indicated for intra partum fetal distress and
nonreactive NST, reduced fetal movements when for large baby.
immediate delivery is indicated. Second stage : Risk of shoulder dystocia.
e) At 42 weeks:Labour is induced. If the baby is too Episiotomy, assisted delivery may be performed
large or severely compromised, caesarean section is as required.
performed.
Table 4: Bischop score
Parameters 0 1 2 3
Cervical dilatation in cm Closed 1-2 3-4 5+
Cervical effacement in % 0-30 40-50 60-70 80+
Fetal station -3 -2 0 +1 +2, +3
Cervical consistency Firm Medium Soft
Cervical position Posterior Middle Anterior
Page 264
4. OBSTETRIC COMPLICATIONS
1. Preeclampsia and Eclampsia Proteinuria: One plus or more.
Pre-eclampsia is a condition specific to pregnancy,
Oedema of hands, face, abdominal wall (generalized
arising after the 20th week of gestation, characterized
by hypertension and proteinuria. edema) may be present but it is not a diagnostic
Eclampsia is pre-eclampsia with convulsions. feature. Excessive weight gain. 1 kg or more in a
week or 3 kg in a month could be a warning signal.
1.1. Signs of preeclampsia
1.2 Classification of pre-eclampsia
Hypertension: BP 140/90 mmHg or more on at
least 2 occasions 4 hours apart after 20 weeks of Mild and severe.
gestation.
Table-1: Classification of PIH
Finding Mild Pre-eclampsia Severe Pre-eclampsia

Blood Pressure (BP) BP > 140/90 but <160/110 BP 160/110 mm Hg or
mmHg more
Proteinuria Present, 2+ or less *3+ or greater

GeneralisedOedema (including in the face & hand) May or may not be Present
present
Headache Absent Present
Visual Disturbances Absent Present

Upper abdominal pain Absent Present
Oliguria Absent Present

Fetal growth restriction (IUGR) Absent Present
Pulmonary Oede ma Absent Present
Decreased foetal Movement Absent Present

Platelet count Nor mal Less than 1 lac
It is not necessary that all these signs are present in all cases
1.3. Diagnosis At each prenatal visit, check the woman's BP, urine
for presence of protein; look for oedema and record
There are no symptoms in mild preeclampsia. Look her weight. If there is a rise in BP, monitor the
for signs woman's BP weekly.
Page 265
Table-2: Dangers
Maternal Fetal/Neonatal
Eclampsia IUGR
Cerebral haemorrhage, thrombosis, oedema Stillbirth
Acute renal failure Neonatal asphyxia

Aspiration bronchopneumonia, Pulmonary oedema,
HELLP syndrome (haemolysis, elevated liver enzymes, low platelet count)

Disseminated intravascular coagulopathy (DIC) leading to hemorrhage
1.4 Management of mild pre- Biweekly LFT, KFT, Platelet count, NST,
umbilical artery doppler weekly if available.
eclampsia
Antihypertensive drugs are not beneficial in mild
1.4.1 Gestation more than 37 weeks: hypertension.
Admit the woman to a hospital. Check BP. Test Diuretics are not recommended.
for proteinuria. Monitor FHR. During observat ion if BP starts rising,
Assess cervix. Induce labour if cervix is ripe. Do (diastolic BP 100 mm Hg or more) start
not allow her to cross her EDD. antihypertensive .
In mild cases when maternal and fetal condition Tab Alpha methyl dopa 250-500 mg 6-8 hourly
is well, can await spontaneous onset of labour orally (maximum up to 2 gm in 24 hours) OR
until 37-38 weeks. Tab Nifedipine sustained release preparation 10
mg orally twice a day (maximum up to 80 mg in
1.4.2 Gestation less than 37 weeks
24 hrs) OR
Advise her to avoid exersion. Encourage her to rest in
Tab Labetalol 100 mg orally twice a day
left lateral position. Counseled her about diet. She is
Terminate pregnancy if there are signs of fetal
allowed to take normal salt in food but no extra salt
compromise, BP is persistently rising or if there
should be added to the food.
is worsening protienuria.
Hospitalization. Mode of delivery: Vaginal or caesarean section
Check BP, urine protein, urine output, weight depending on gestational age, cervical status,
daily. maternal and fetal condition.
Check for generalized body oedema. During observation anytime if systolic BP is 160
Exclude symptoms of severe pre-eclampsia mm Hg &/or diastolic BP 110 mm Hg: Manage as
Monitor foetal growth, ask the woman about severe preeclampsia. She should be referred to a
foetal movements, check daily fetal movement district hospital/ medical college for further care.
count (DFMC), FHR.
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1.5. Management of Severe pre- 1.7. Obstetric management
eclampsia Gestation < 24 wks: Fetal salvage is difficult so
proceed with termination of pregnancy.
Hospitalize patient.
If gestation > 24 wks - < 34 wks : Treatment
Control hypertension: Give anti-hypertensive should be individualized.
drugs. Maintain diastolic blood pressure between Give Inj Dexamethasone 6 mg 12 hourly 4
90-100 mmHg. doses.
If BP controlled keep woman under regular
Nifedipine 10 mg orally. After 30 minutes, if BP maternal & fetal surveillance.
is not brought under control, another 10 mg of
Deliver the woman at 37 wks. Induce LABOUR
the drug can be repeated. Caution needed while before 37 weeks if BP uncontrolled or worsening
of clinical/ biochemical parameters or
using Nifedipine as there may be a sudde n and
appearance of signs of fetal compromise.
massive fall in B P.
Assess cervical status. If cervix is unripe
induction by oral or vaginal misoprostol. 25 mcg
Labetalol can be given.
or intra cervical dinoprostone gel can be used for
preinduction ripening of the cervix.
Monitor vital signs, reflexes & fetal heart rate.
If cervix is ripe induce with oxytocin infusion
Auscultate lung bases frequently and look for
and amniotomy.
signs of pulmonary edema. If rales are heard give
LSCS may be done for deteriorating maternal
Frusemide 40 mg IV. condition, adverse fetal condition, failed
induction or other obstetric indications.
Perform bedside clotting test.
Watch for warning symptoms and signs which 2. Eclampsia
may appear before getting fits. Sharp rise of BP,
Eclampsia is characterized by hypertension and
increased proteinuria, exaggerated knee jerk.
proteinuria. (Preeclampsia) and convulsions/fits
Severe headache, drowsiness, mental confusion,
followed by coma.
visual disturbances (e.g. blurred vision, flashes
of light, double vision) epigastric pain, nausea, Convulsions may occur in the antepartum, intra
vomiting, decreased urinary output. partum or the postpartum period.
Prevent fits: Give prophylactic Magnesium Status eclampticus: Convulsions continue one after
Sulphate( full loading & maintenance dos e as in the other.
Eclampsia )
Encourage the woman for delivery at the FRU 2.1. Differential diagnosis of
convulsions during pregnancy
1.6. Investigations Eclampsia: Hypertension, proteinuria.
Urine- Albumin, sugar, culture & sensitivity, 24 hrs Epilepsy: Past H/O fits, normal BP.
urine protein.Hb%, PCV, Platelets, bleeding time, Cerebral malaria: Fever, Anemia, jaundice,
clotting time, serum fibrinogen, Blood urea, serum Malaria tests positive.
creatinine, serum uric acid, serum bilirubin, serum Meningitis/encephalitis, Tetanus.
proteins, SGOT, SGPTFundoscopy.
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2.2. Management of Eclampsia 2.2.2 Controlling fits
Principles: Magnesium sulfate is the drug of choice.
i. General care Loading Dose: Give Inj. Magnesium sulphate 4 g

(20 ml of 20% solution) slow IV in 5 min. (not to
ii. Control fits
be give n as a bol us rapidly). Then administer Inj.
iii. Control blood pressure Magnesium sulphate 10 gm deep IM, 5 g in each
iv. Expedite delivery gluteus muscle ( 10 ml of 50% solution, in each
buttock) with 1 ml of 2% Lignocaine in the same
v. Maintain fluid balance
syringe.
vi. Postpartum care If convulsions recur after 15 minutes, give
2.2.1 General care additional 2 g of Magnesium sulphate (10 ml of
20 % solution) IV over 5 minutes.
Keep the patient in a quiet room in a bed with
Maintenance Dose: Give 5 g of 50% Magnesium
padded rails on sides. Place the woman on her
sulphate solution IM with 1 ml of 2 %
left side.
Lignocaine every 4 hours alternately in each
Evaluate vital signs.
buttock.
Clean the mouth & nos trils by appl ying gentle
Magnesium sulphate to be continued till 24 hours
suction.
after delivery or the last convulsion whichever
Give oxygen.
occurs later.
Prevent Injury to tongue by putting airway or by
Before giving the next dose of Magnesium
placing padded tongue blades.
sulphate, e nsure:
Start IV line with Ringer lactate/ normal saline :
The Urine output is at least 100 ml in previous 4
60 ml/hour.
hours.
Catheterize patient. Monitor hourly urine output.
Knee jerk reflexes are present
Send investigations as for severe pre-eclampsia
The respiratory rate (RR) is at least 16
If not breathing check airway and give ba g and
breaths/min.
mask ventilation.
Postpone the next dose if the above criteria are
not met.
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Table-3: Magnesium sulphate solution for loading dose
Preparation of 20 % Magnesium sulphate solution for loading dose
Inj. Magsulf is supplied as a 50 % solution in 2 ml vial. 1 amp of 2 ml = 1 g Magsulf

4 amp of 2 ml 50% solution = 4 g Magsulf in 8 ml solution

Add 12 ml distilled water or saline to make 20 ml 20 % Magsulf solution and
Give slowly IV in 5 min
For initial intramuscular dose:
5 amp of 2 ml 50% solution =5 g MgSO4. Give 10 ml deep IM in each buttock
Table-4: Magnesium sulphate for maintenance dose
Preparation of 50 % Mag nesium sulphate for maintenance dose
1 amp 2 ml 50% solution = 1g. 5 amp = 5 g Magsulf.

Give deep IM in alternate buttock every 4 hourly
Table-5: Precautions
Precautions:
Do NOT give 50 % Magnesium sulphate solution IV without diluting it to 20 %
Do NOT give rapid IV infusion of MgSO4 as it can cause respiratory failure or death.
If respiratory depression occurs (RR < 16 breaths/minute) do not give the next dose.
Give antidote Calcium gluconate 1 g IV (10 ml of 10 %) over a period of 10 minutes.
2.2.3 Controlling bloo d pressure 2.2.4 Delive ring t he baby
Nifedipineis the drug of choice for controlling BP. The mode of delivery should be decided depending
Tab. Nifedipine 10 mg orally, followed by 6 hrly on whether or not the woman has gone into labour
after taking BP. and the stage and progress of labour. In eclampsia,
delivery should occur within 12 hours of the onset of
Labetalol: Intravenous Labetalol (1 blocker) is
convulsions.
another commonly used dr ug for severe hypertension.
It is given in a dose of 20 mg IV initially. If BP has If woman is in active labour: Monitor the
not decreased to the desirable level in 10 min then 40 progress of labour and deliver. Watch for signs
mg is given. If the BP has still not decreased in the of fetal distress. Augment labour by amniotomy
next 10 minutes, an incremental dose of 80 mg may and oxytocin infusion as required.
be given. This may be followed by another 80 mg Cut short the second stage of labour.
every 10 min if needed till a maximum of 220 mg has
Do not give Inj Methyl ergometrine.
been administered. Cardiac monitoring is required.
Avoid in bronchial asthma and in cardiac disease.
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If woman is not in labour: Assess condition of 3. Vaginal Bleeding During
cervix and induce labour with va ginal or oral
misoprostol 25 mcg or ARM & Oxytocin Early Pregnancy
infusion.
1.1. A woman may present with history of a short
Mode of delivery depending on fetal condition period of amenorrhea followed by
and condition of cervix.
Perform LSCS if: Cervix unfavorable, Fetal Vaginal bleeding.Abortion, vesicular mole and
distress, Fits are not controlled, labour is not ectopic pregnancy are the common underlying
progressing well despite induction/ augmentation conditions, while an occasional woman may simply
or for any other obstetric indication. have a delayed menstruation.
2.2.5 Maintaining the fluid balance
3.1 Ask patient following
Monitor urine output. It should be at least 30
ml/hour. Period of amenorrhea, LMP, symptoms
Record the fluid intake. Give all the necessary suggestive of pregnancy.
fluids slow IV @ 60 ml per hour. (Urine output + Amount and duration of bleeding, it may be
500ml) fluid DNS. scanty in threatened and missed abor tion and
Maintenance of proper fluid balance is essential profuse in incomplete / inevitable abortion. Prior
to prevent water intoxication, dehydration, H/O abortion, ectopic pregnancy.
hyponatraemia, or pulmonary oedema. Nature and severity of pain (severe in ruptured
Diuretics should not be used unless there are ectopi c pregnancy)
signs of pulmonary e de ma. Clinical presentation may be asThreatened
abortion, Inevitable abortion, Incomplete
abortion, Complete abortion, Missed abortion or
2.2.6Post Partum Care Septic abortion.
Fits can also occur for the first time in the immediate Arrange for ultrasonography and pr egnancy test.
postpartum period. Monitor BP and the urine output Arrive at the diagnosis with the help of following
after delivery. Continue antihypertensives to maintain chart.
diastolic BP between 90 100 mm Hg. Advise the Refer to specialist for further management.
woman to have her BP checked regularly until BP
returns to nor mal. If BP remains high at 12 weeks
diagnose her as chronic hypertension and refer her to 3.2 Different diagnosis
physician for evaluation.
Table 6: Differentiating features according to condition
Particulars Threatened Incomplete Missed abortion Vesicular/H Ectopic

abortion abortion Mole pregnancy
Uterine Size Equal Smaller Smaller Bigger Smaller

to POA Intos open
Internal os closed
Vaginal Slight Profuse Absent or Recurrent Slight

bleeding brownish small
discharge
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Pain Mild or Absent Cramping pain Absent Absent Severe,
significant continuous
G.C. pallor Fair Proportional to Fair Fair Out of

/tachycardia blood loss proportion to
visible blood
loss.
Tenderness Absent Absent (Unless Absent Absent Marked

Abd/vag infected)
USG Intrauterine viable Some products in Nonviable Snowstorm Empty uterus

pregnancy uterine cavity pregnancy appearance pelvic / adnexal
mass
Risks Preterm Hemorrhage Blood Hemorrhage Shoc k

coagulation
/IUGR Sepsis
failure
Manage ment Expectant Surgical evacuation Termination of Suction Laparoscopy or

pregnancy evacuation
Antibiotics Laporotomy,
Blood
Blood
transfusion if
transfusion
required
3.3. Management of Threatened Uterus is < 12 weeks: Manual/electrical vacuum

aspiration.
abortion
Uterus > 12 weeks: Pregnancy termination by
Avoiding exertion, sexual abstinence and regular misoprostol.
follow up to monitor the growth of the fetus are
recommended. The role of progesterone therapy or 3.5. Septic abortion
human chorionic gonadotropin is unproven.
Unsafe abor tion. Anemia, delay in emptying the
Follow up: Regular ANC check up every 15 days. uterus in cases of incomplete abortion, failure to
The pregnancy has higher risk of having recurrent follow adequate aseptic precautions.
episodes of bleeding, bleeding in late pregnancy due
to APH, fetal growth retardation and preterm Symptoms and signs: Fever, tachycardia, lower
delivery. abdominal pain, offensive vaginal discharge and
pelvic tenderness.
3.4. Management of Missed Investigations - Bleeding time, clotting time,
Abortion prothrombin time, platelet count are done as there is
risk of coagulation failure.
Investigation: Ultrasonography. Bleeding time,
clotting time, prothrombin time, platelet count (risk Treatment: Antibiotics. Inj.Ampicllin 1gm stat IV
of coagulation failure with prolonged retention of followed by Inj. ampicllin 500 mg.6 hourly,
dead fetus). Inj.Gentamicin 80 mg 12 hourly, Inj.Metronidazole
100 ml IV 8 hourly slowly.
Treatment: The pregnancy needs to be terminated
for maternal anxiety and for risk of blood coagulation Surgical evacuation of uterus if there are retained
failure leading to excessive bleeding. products.
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Cases having severe sepsis with complications need Treatment: Management of shoc k. Urgent surgical
to be referred to district hospital. exploration to stop the bleeding. Blood transfusion as
required.
3.6. Ectopic pregnancy
The commonest site of ectopic pregnancy is the
3.7 Hydatidiform Mole
fallopian tube. An abnor mal pregnancy where there is no fetus, no
Clinical presentation: Unruptured tubal pregnancy; amniotic sac and the uterus is full of proliferated
tubal abortion or tubal rupture with severe trophoblastic tissue.
intraperitoneal bleeding leading to shock. Symptoms: The pregnancy vomiting is often
3.6.1 Unruptured ectopic pregnancy: Diagnosis exaggerated and there is recurrent vaginal bleeding
requires a high inde x of suspicion. The woman can rarely with passage of grape like vesicles.
reveal some of the risk factors for ectopic pregnancy, Signs: Uterus is larger than the POA and soft /
will present with signs and symptoms of pregnancy, doughy in consistency Tachycardia, pallor.
may have a unilateral adnexal mass.
Investigation: Ultrasonography reveals snow storm
UPT positive; ultrasonography reveals an empty appearance, absence of fetus, amniotic fluid. The
uterus. ovaries may be enlarged with multiple cysts.
Refer to specialist for laparoscopic surgery. Pregnancy hormone Beta HCG is markedly elevated.
Medical management for selected cases: Inj Treatment: The pregnancy is terminated by suction
Methotrexate under careful monitoring. evacuation under general anesthesia. Blood is
3.6.2 Tubal abortion: Symptoms: arranged.
Complications:
Significant pain in lower abdomen, vaginal bleeding
could be slight or even absent.
Severe hemorrhage and uterine perforation
Signs: Tenderness in lower abdomen. during evacuation.
P/V: Cervical movements extremely painful and Infection.
tenderness in fornices. Development of gestational trophoblastic
neoplasia.
Pallor and tachycardia depending on the amount of
internal bleeding. Follow up: Baseline X ray chest and beta HCG
Clinical condition usually stable. levels tested before discharge. Regular beta HCG
monitoring till it falls to normal level and for 6
Investigations: Ultrasonography reveals free fluid in months thereafter as there is risk of development of
abdomen. gestational trophoblastic neoplasia.
Treatment: Referral to gynecologist for surgical It is important to avoid pregnancy by using reliable
management. contraception during this follow up period. Oral pills
3.6.3 Ruptured ectopic pregnancy: can be give n. Intrauterine contraception is not
recomme nded.
Severe and acute pain in abdomen with severe During follow up: Look for abnormal vaginal
intraperitoneal bleeding which is continuing. bleeding, enlarged soft uterus, evidence of any
Signs: The patient presents with tachycardia, severe metastasis (lungs, brain, anterior vaginal wall)
pallor and hypotension. The abdomen is tender and Pregnancy is allowed when beta HCG remains
distended. Signs of free fluid in abdomen (shifting normal for 6 months. Referral to tertiary care centre
dullness). Vaginal examination is extremely painful is indicated for chemotherapy if Beta HCG levels
and an ill defined mass may be felt in posterior and show initial decline followed by a rise or it remains
lateral fornix. static (plateau).
USG: Free fluid in abdomen and vague ill defined
mass may be seen.
Culdocentesis: Blood is aspirated which fails to clot
on observation.
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4.Antepartum Haemorrhage Passage of urine.
Prior USG reports if available.
(APH) H/O trauma, internal examination/ coitus
aggravating the bleeding.
4.1. Definition:
2.4. Examination:
Bleeding from vagina after 20 weeks of pregnancy
and before the birth of child. Two major causes: Note pallor, tachycardia, general condition,
Abruptio placentae: Bleeding from premature record blood pressure.
separation of normally located placenta in the In concealed accidental hemorrhage, although
upper uterine segment. the woman is in shock, her BP may be nor mal as
Placenta Previa: Bleeding from premature she could be having hypertension. Therefore
separation of low lying placenta located in lower degree of pallor and tachycardia are more
uterine segment. important for assessment of amount of bleeding
and general condition.
4.2. Dangers: P/A :
Maternal mortality is high due to hemorrhagic shoc k Uterus is relaxed, contracting and relaxing or
hard.
and its complications like acute renal failure (ARF),
coagulation failure due to DIC. There is increased Uterine tenderness present/absent (localized or
risk of atonic PPH after delivery. Lacerations of generalized)
friable cervix also cause bleeding. Operative delivery Presentation, FHS
rates are high. No vaginal examination to be done until placenta
Fetal and neonatal mortality is high due to previa is ruled out
prematurity (Spontaneous & iatrogenic), LBW and 4.3.3 Investigations:
asphyxia.
Urgent USG to locate placenta and assess the
4.3.Case Management of APH fetal condition and its gestational age.
Blood tests: Hb, PCV, Coagulation profile
4.3.1 History: (Bleeding & clotting time, clot observation test,
Ask the period of amenorrhoea, fetal platelet count, prothrombin time.
movements, Time of onset of bleeding, amount, Liver function and renal function tests.
prior H/O warning hemorrhages.
Abdominal pain present or absent and its
severity.
4.4 PlacentaPrevia
Figure 1: Placenta previa
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4.4.1 Differentiate between Placenta Previa a nd Abruptio placentae
Table-7: Differentiation between placenta previa and mixed abruotio placentae
Particular Placenta previa Concealed or mixe d abruptio placentae
Pain Painless recurrent vaginal bleeding Painful bleeding
General Pallor, tachycardia, restlessness proportional Pallor, tachycardia disproportionately more

condition to visible amount of blood lost than the visible amount of vaginal bleeding
Uterus Relaxed, non-tender, fetal parts felt well Tense, tender, woody hard, fetal parts
cannot be felt
Presentation May be abnormal or head may be high floating Presentation cannot be made out
Fetus Fetal condition usually well if mother not in Fetus often distressed or dead. FHS may not
shoc k be heard
Maternal Hypovolemic shock Shoc k, acute renal failure, DIC
Dange rs
Action No P/V examination. IV fluids, referral IV fluids, referral, monitor
4.4.2 Complications: If pregnancy duration is > 36 weeks or if there is

life threatening bleeding then pregnancy is
Maternal:Hypovolemic shock, malpresentations,
terminated.
operative delivery, PPH
Expectant management For clinically stable
Baby: Prematurity, low birth weight, fetal/neonatal patient with moderate blood loss having fetus
asphyxia alive and preterm until 36 weeks.
4.4.3. Manage ment: P/S : Exclude local genital causes (cervical
growth, polyps, vascular ectropion)
Even if bleeding is only a very small amount,
Pregnancy is terminated in maternal interest at
hospitalization is required.
any time during the observation period if there is
Assess the blood loss.
furious uncontrolled bleeding or when pregnancy
Full blood count and clotting studies. > 36 weeks.
Arrange cross matched blood
4.4.4 Mode of delivery:
Perform gentle palpation of abdomen to assess the
gestational age of fetus, presentation and position. Caesarean section for major degree placenta
previa and for cases having type II posterior
Assess fetal condi tion. Arrange urgent
placenta previa with a salvageable fetus.
ultrasound.
Previous CS & anterior placenta previa: There is
Rh negative woman: With every episode of
risk of morbidly adherent placenta leading to
bleeding, give prophylactic anti-D
furious hemorrhage. Refer such case to tertiary
immunoglobulin.
care centre. Such case needs to have 4 units of
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blood to be kept ready and preparations for CS amniotomy followed by oxytocin infusion.
hysterectomy if required. Arranging blood and the delivery at well
Cases having low lying placenta, (type II equipped institution is necessary.
anterior) can be delivered vaginally by
4.5 Abruptio Placentae
Figure 2: Abruptio placentae
4.5.1 Diagnosis:
May present with va ginal bleeding and USG shows placenta in upper uterine segment
abdominal pain. and may show retroplacental hematoma.
Ask H/O trauma, prior hypertension. Errors in diag nos is
Assess blood loss: Look for pallor, tachycardia,
The case could be misdiagnosed as preterm
general condition, urine output, record BP. Labo ur.
Hypertension and pr oteinuria may be present. A patient of concealed accidental hemorrhage
can be misdiagnosed as patient in labour with
P/A uterus hard, tender, not relaxing severe anemia with fetal death.
(Hypertonus) In Labo ur, uterine rupture can be misdiagnosed
as concealed accidental hemorrhage.
In cases of severe abruption, fetal parts may not
be felt well, fetus may be distressed/dead. When 4.5.2 Manage ment:
the fetus is dead at least 1,500 ml of blood is lost,
hence shoc k is usual, uterus is firm-to-hard and If fetus is alive and salvageable an urgent CS is
performed, hence referral to nearest facility is
very tender. Blood pressure may be normal in indicated.
spite of being in shoc k as the initial BP may be If fetus is dead, it indicates massive
retroplacental hemorrhage. Hemodynamic
high. Coagulation failure leading to severe stability is assessed (pulse, BP, pallor). Foley
bleeding is common.
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catheter is introduced and hourly urine output is Previous H/O preterm birth, mid trimester
monitored. Coagulation profile is checked. abortion. Risk increases with each additional
Correction of hypovolemia: Ringer lactate preterm birth.
infusion and by blood transfusion. Incompetent cervix, uterine malformations.
Refer the woman to tertiary level of care having Vaginal infections : Bacterial vaginosis.
facility of providing blood and blood products Overdistended uterus (Twins, polyhydramnios),
for treatment of DIC. Vaginal bleeding during pregnancy,
Induce labour by ARM and oxytocin infusion. Chorioamnionitis.
Diabetes, hypothyroidism, heart disease, chronic
4.5.3 DuringLabour: hypertension, HIV illness, urinary tract
infection(UTI), periodontal infections.
First stage of Labo ur is augmented by ARM and Fall, psychological stress, abdominal surgery
oxytocin infusion. during pregnancy.
If fetus is alive, watch for signs of fetal distress .
Second stage of Labo ur is cut short.
5.2. Prevention
Active management of third stage of labour. Treatment for UTI, correction of anemia,
Placenta is examined and the retro placental clot improving oral hygiene.
is weighed. Nutritious diet and consumption of IFA tablets.
Hemoglobin and hematocrit estimation following Counseling: Avoid strenuous work, take extra
delivery. rest, quitting tobacco, alcohol.
Women with previous history of preterm birth:
Refer to specialist.
5. Preterm labour Vaginal sonography to see the length of cervix.
Prematurity and low birth weight is the important Weekly Injections of 17 hydroxy progesterone.
causes of neonatal deaths in India. Cervical os tightening in selected cases are some
of the preventive interventions.
Preterm labour is onset of labour from 24 weeks to
37 completed weeks of gestation. 5.3. Prediction by warning
From survival point of view, the gestational age of 34
symptoms
weeks is important as after this period the fetal lungs
are mature enough for independent survival outside Cramping discomfort/pain in lower abdomen,
low backache.
the uterus.
Increased mucoid vaginal discharge.
A single course of antenatal corticosteroids Intermittent uterine contractions felt during
administered between 24 to 34 weeks of pregnancy discomfort.
has been shown to reduce the neonatal mortality Heaviness in pelvis (something descending
significantly in preterm bor n babies. down).
5.1. Risk Factors for preterm

Labour 5.4. Diagnosis
Assess pregnancy duration accurately
Maternal weight < 40 Kg in first trimester. (BMI
< 19.8 kg/m2), Obesity ( BMI> 30 kg/m2). Confirm onset of Labo ur: Intermittent painful uterine
Teenage pregnant women, Short inter pregnancy contractions (4 in 20 min or 8 in 60 mins) along with
interval. progressive change in the cervical dilatation and
effacement assessed over 2 hours
Short stature, maternal under nutrition ,anemia.
Inadequate weight gain during pregnancy 5.5. Management principles
Strenuous working, long hours of work, inability
to take adequate rest. 5.5.1 If pregnancy is < 34 weeks
Tobacco, smoking, heavy alcohol use, illicit drug
use. Antenatal Dexamethasone therapy
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Inhibition of preterm labour by administering Nifedipine 20 mg oral stat followed by 10 mg 4
tocolytic medicine. hourly till contractions stop or maternal pulse
In Utero transfer. exceeds 120 beats/min. Continue drug till steroid
Safe conduct of preterm labour. cover is complete or for 8 hours after last
contraction. Then taper the dose slowly.
Special care of preterm neonate.
Alternatively, beta adrenergic receptor agonists
(Ritodrine, Turbutaline, Isoxusprine) can be
a) Antenatal corticosteroid therapy given. Turbutaline is a selective beta agonist
Inj Dexamethasone administered between 24- 34 having lesser cardiovascular side effects that can
weeks of pregnancy in cases of threatened be administered subcutaneously. However their
preterm labour is effective in lowering the risk of value is not proven.
respiratory distress syndrome (RDS) & neonatal Cardiac disease needs to be excluded before
mortality if birth was delayed by at least 24 giving these drugs. While administering tocolytic
hours after initiation of therapy. The effect drugs careful monitoring is required for side
persists for 7 days after completion of course of effects. Monitor pulse, BP, signs of respiratory
steroid therapy. distress, uterine contractions, loss of amniotic
Injection Dexamethasone 6 mg IM 12 hourly for fluid or blood, FHR, fluid balance, blood
48 hours, total 4 doses. Repeated courses should glucose. Watch for maternal acute pulmonary
not be give n. oedema when combination of steroids and
tocolysis is used.
Who can receive the therapy?
All women having spontaneous onset of preterm

labour and those having complicated pregnancies Do NOT give tocolytic drugs for more than 48
(Severe preeclampsia, antepartum hemorrhage hours.
etc).
c) In Utero transfer: If the period of gestation is <
Preterm rupture of membranes before the onset
34 weeks, and Labo ur continues despite tocolysis, or
of labour pains (PROM)
if the woman is already having cervical dilatation >3
cm, refer to district hospital/medical college with
Which women should not receive corticosteroid NICU/ SNCU facility for delivery. Before referral
therapy? always give at least the initial shot of steroid
mentioning the time on the referral note. Record BP,
If there is chorioamnionitis, (infection of fetal urine test result on referral note.
membranes) delivery is not to be postponed.
d) Safe conduct of preterm labour
Early delivery is safer for both mother and her
baby. Signs are. Do not inhibit preterm labour and allow it to
Fever, lower abdominal pain, Tenderness over progress if
the uterus The cervix is >3 cm dilated.
Fetal tachycardia (FHR > 160/minute), Foul There is active bleeding, severe pre-eclampsia,
smelling liquor amnionitis
Fetus is distressed, dead or has an anomaly
b) Inhibition of uterine contractions by tocolytic incompatible with survival.
drugs: If a woman presents with preterm labour which
Tocolyticdrugs stop contractions temporarily but is progressing rapidly, there may not be adequate
rarely prevent preterm birth. However the time available for referral. Still give the first dose
delivery is delayed long enough for getting the of Inj. Dexamethasone as even 1 dose few hours
benefits of administration of Dexamethasone. before delivery has some beneficial effects.
Indication for Tocolysis Check fetal presentation as possibility of
If Labo ur starts between 24 weeks to 34 weeks. abnormal presentations is higher in preterm
labour needing skilled attendance.
The cervix is <3 cm dilated.
There is no foetal distress. Monitor the progress of Labo ur.
Tocolysis is not indicated in Amnionitis, pre Prevent birth trauma and birth asphyxia while
conducting breech delivery.
eclampsia, active bleeding &foetal distress.
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Avoid delay in second stage by giving 7. Breech delivery
episiotomy to prevent trauma to the babys head.
Do not use vaccum extractor as the risk of If the full term breech presentation is diagnosed in
intracranial bleeding is high. early labour the case should be referred to higher
If Labo ur continues and the gestation period is < centre. Decision to deliver by caesarean section or
37 weeks; although evidence is not in favour of allowing va ginal delivery needs to be taken after
prophylactic antibiotics but as woman is coming careful evaluation by specialist. Maternal age, parity,
from hygienically poor area, antibiotics can be pelvic capacity, status of membranes, type of breech,
given to reduce the chances of infection in the estimated weight of baby, other complicating medical
neonate. (Cap. Ampicillin, Tab Metronidazole /obstetrical conditions, scar on uterus are some of the
and Inj Gentamicin) important considerations for this decision.
However sometimes woman arrives in advanced
e) Special care of preterm neonate labour when you are required to conduct her delivery
by performing the following steps:
If needed, refer neonate to the nearest NICU/
SNCU after appropriately stabilizing new born Check the delivery tray, episiotomy tray, baby
Intrapartum Complications tray and newbor n resuscitation equipment
Start IV infusion
Abnormal Presentations:
Tell the woman to bear down with contractions
Diagnosis of fetal malpresentation during Labour: only when the cervix is fully dilated and the
Vaginal examination buttoc ks are in the va gina
Wash hands with soap and water and put on
6.1 Breech Presentation sterile gloves.
Take the woman to the edge of the table
In complete breech presentation the presenting part is Clean the vulva with antiseptic solution and
buttocks with feet, in frank breech buttocks only and drape the mother.
in footling presentation only feet are felt. Catheterize the bladder, if necessary.
The chance of cord prolapse is highest in footling Give pudendal block or local perineal infiltration
breech while it is lowest in frank breech. It is for episiotomy.
necessary to avoid rupturing membranes during Give episiotomy when the buttocks distend the
vaginal examination. perineum.
Do not pull the baby or interfere in any way
6.2 Transverse lie When the baby is bor n up to umbilicus, pull a
Fetal shoulder felt. After rupture of membranes hand loop of cord and keep it aside. Cover the baby
prolapse occurs, cord prolapse may occur. These with a clean sheet and gently hold the buttoc ks of
cases need to be referred to FRU urgently for the baby but do not pull.
caesarean delivery. If the legs do not deliver spontaneously, deliver
one leg at a time.
6.3 Face presentation: Ask the mother to continue pushing with
Chin and face felt. If the chin is anterior (left or right contractions.
mentoanterior position) vaginal face delivery is Check whetherr arms are on the chest. Allow the
possible specially in a multipara having average sized arms to get rotated and disengage spontaneously.
baby. However in mentoposteriorposition caesarean If the arms are stretched above the head or folded
delivery is often required. Refer these women to around the neck (Winging of the scapulae
FRU, however a midwife should accompany with a indicates extension of arms) use
delivery tray during referral. Lovsetsmanoeuvre to deliver arms.
Deliver the head by Burns Marshal manoe uvre or
6.4 Brow presentation: Mauriceau-Smellie-Veitmanoeuvre (jaw flexion
`Babys forehead and part of the face is felt and chin and s houlder traction).
is not easily felt. A good sized babys head is unable Observe babys breathing and initiate
to get engaged in the pelvis and the LABOUR is resuscitation as required (Breech born baby takes
likely to get obs tructed. Such woman should be longer time to start normal breathing)
referred to FRU for caesarean section.
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Perfor m active management of the third stage of Determine the lie and the presenting part
Labo ur. Note the fetal heart rate
Check the birth canal for tears and repair P/V to determine the stage of Labo ur and the
episiotomy. presenting part
Gently feel for the cord pulsations. Push the cord
8. Twins delivery in the va gina
If first stage; push the head upwards to relieve
A case of diagnosed twin pregnancy arriving in early pressure by presenting part on cord and give
labour should be referred immediately as the babies head low position to mother. Alternatively, insert
are often LBW and require special care. However, if a Foleys catheter in urinary bladder and rapidly
the mother is admitted in advanced labour the fill the bladder with 300-500 ml Normal Saline
following steps should be taken to deliver her. to elevate the fetal presenting part. Clamp the
Check presentation of first baby , check FHS catheter. The clamp must be released and the
Start IV Ringer lactate bladder drained before any delivery attempt.
If first baby is presenting by vertex allow Refer immediately to FRU for Caesarean
LABOUR to progress and deliver the first baby. Section.
Leave a clamp on the maternal end of the cord of If in second stage; expedite delivery with
the first twin and do not give Oxytocin. episiotomy and vacuum/forceps delivery.
Palpate abdomen to determine the lie of second Perform breech extraction, if the baby is
fetus. If it is breech or transverse attempt to presenting by breech.
perform external cephalic version. Check for breathing and resuscitate the newborn.
Check the presentation of second baby by If the baby is very premature or dead
vaginal examination. If vertex, allow labour to spontaneous delivery can be awaited.
progress and deliver the baby.
If the uterine contractions become weak and
delivery of second baby is getting delayed start 10. Shoulder Dystocia
oxytocin drip slowly.
If the baby is big the chances of shoulders getting
If the presenting part is breech conduct breech stuck after delivery of head are high. Many babies die
delivery. If delivery is getting delayed or if fetus within few minutes of the head being delivered. It is
shows signs of distress, perform breech important, therefore, to manage the problem
extraction carefully. efficiently and carefully so as to avoid Injuries to the
If second baby is transverse refer to FRU for CS. baby or mother.
(If the baby is small and very preterm sometimes
it may deliver spont aneously, hence it is Call for help
necessary to accompany her with preparations to Discourage maternal bearing down effort
conduct delivery during transfer) Apply Mc Roberts maneuver, bring knees as far
Give Oxytocin soon after delivery of second as possible up to the chest and abduct and rotate
baby and conduct active management of third legs outwards
stage of labour. Appl y firm suprapubic pressure using the heel of
Anticipate risk of PPH and check for hardness of the hands
uterus and massage the uterus. Start IV Oxytocin Make adequate episiotomy
infusion ( 20 I U in 500 ml of Ringer lactate) Rotate the babys body so that the posterior
Weigh both babies and take steps for special care shoulder moves anteriorly.
needs if the babies are LBW. If these measures fail to deliver shoulders,
attempt internal rotation maneuvers to deliver
anterior or posterior shoulder. ( Application of
9. Cord Prolapse pressure to the anterior/posterior shoulder in the
direction of the babys chest)
Cord prolapse is more common if the presentation is Check babys breathing and initiate resuscitation
breech or transverse. In vertex presentation cord gets
severely compressed as head descends and baby gets Complications: PPH, vaginal/perineal tears and
Injuries to baby.
severely asphyxiated and needs urgent delivery and
prompt resuscitation
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11. Obstructed Labour 12.2 Diagnosis
11.1 Causes Cessation of uterine contractions after prolonged
obstructed Labo ur.
Cephalopelvic disproportion due to contracted Continuous pain in abdomen.
pelvis or large head. Maternal tachycardia, restlessness, increasing
Transverse lie, Brow presentation, mento pallor, hypotension, fresh va ginal bleeding,
posterior face presentation, Deep transverse haematuria.
arrest of fetal head. Fetus dead.
Abdomen distended, tender all over, fetal parts
11.2 Diagnosis may be felt easily.
Non progressive Labo ur, prolonged Labo ur. Signs of free fluid in abdomen.
Maternal exhaustion: Tachycardia, restlessness, In LABOUR, presenting part may recede
sweating, mild fever, signs of dehydration. upwards.
Signs of fetal distress or death.
12.4 Dangers:
11.3 Signs of obstruction Maternal shock and death due to severe internal
hemorrhage.
Lower uterine segment over stretched
Bandles ring seen which is rising progressively 12.4 Action
towards umbilicus.
Suprapubic bulge Edematous bladder. Urgent referral to tertiary care centre where
Presenting part High, abnormal or showing blood transfusion facility is available.
excessive moulding. IV infusion of 1 liter of fluids, start antibiotics,
On catheterization, scanty high colored/ blood monitor vitals.
stained urine. Exploratory laparotomy, blood transfusion.
Early signs include edematous cervical lip, At laparotomy: Hysterectomy or repair of tear.
increasing moulding of fetal head. If only repair of the rent is done, there is risk of
uterine rupture in subsequent pregnancy and an
11.4 Action elective caesarean section is required.
Urgent referral. IV infusion during referral will help
in correcting dehydration. Delay in referral can result 13. Third Stage Complications
is uterine rupture, infection due to prolonged labour
and foetal death. 13.1 Postpartum Hemorrhage
Vesico-vaginal fistula may develop if presenting part 13.1.1Definition:
is deep in the pelvis for prolonged period as in deep Excessive vaginal bleeding > 500 ml after delivery.
transverse arrest.
Even moderate amount of bleeding could lead to
At the institution the patient will be delivered mostly shoc k in women who are anemic or have
by caesarean section. preeclampsia.
13.1.2 Types: Within first 24 hours after childbirth.
(Immediate PPH)
12. Uterine Rupture
After 24 hours up to 42 days after childbirth (Delayed
12.1 Causes PPH).
Scarred uterus (previous caesarean section, Although PPH is more common in cases of twin
uterine perforation etc.) pregnancy, APH, over distended uterus, grand
Obstructed Labo ur multiparas, it is an unpredictable complication and
can occur in any low risk woman.
Incorrect use of oxytocic agents like Oxytocin,
prostaglandi ns 13.1.3 Probable cause of Excessive Bleeding and
Internal podalic version, manual removal of Shock after childbirth.
placenta.
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Table 8: Causes of excessive bleeding and shock after Childbirth.
Clinical Presentation Probable diagnosis

Uterus is flabby, not contracted, fundus is rising. Atonic PPH
Uterus is well contracted. Speculum examination of cervix and va gina Traumatic PPH
reveals cervical/vaginal lacerations/tears.
Placenta not delivered within 30 minutes after delivery. Retained placenta
Placenta incomplete, torn vessels in the membranes. Retained lobe of placenta
Bleeding continues even after treatment. Blood does not clot for > 15 Coagulation failure
minutes.
Uterine fundus not felt per abdo minally. Inverted uterus seen in va gina or Acute Uterine Inversion
outside vulva.
Delayed PPH. Uterus is larger for the postnatal day, soft, may be tender, Uterine infection, retained
bleeding may have foul smell. lobe/fragments of placenta
Monitor womans GC, pulse, blood pressure,

13.1.4 Initial Manage ment of Atonic PPH: respiratory rate, temperature every 15 minutes.
Note pallor. Assess whether the woman has
The management includes, uterine massage, heavy bleeding and s he is in shoc k.
bimanual compression of uterus, administering
uterotonic drugs along with blood volume Uterine temponade with condom catheter may be
tried.
replacement and evaluation to look for other causes.
If bleeding is controlled by drugs, repeat uterine
Check for flabby uterus, retained placenta, tears massage every 15 minutes for 2 hours.
and lacerations in vagina and cervix. Monitor vitals closely every 10 minutes for 30
If the uterus is flabby/soft, give continuous minutes, every 15 min for next 30 mins, and
uterine massage and bimanual compression of every 30 min for next 3-6 hours or until.stable.
uterus immediately. Continue oxytocin infusion. (max 100 IU in 24
Secure intravenous access and collect blood hours)
samples Two 16 or 18 gauge cannulae are If the bleeding does not stop, explore uterine
inserted in two veins for correcting hypovolemia cavity for retained placental bits/lobe.
by rapid infusion of IV Ringer lactate/Normal If the uterus is hard, explore the lower genital
Saline. tract in good light to look for genital trauma and
Start Oxytocin infusion 20 IU in 500 ml of repair any tears followed by firm packing of
Ringer lactate@ 40-60 drops/minute. Other vagina to stop the oozing from lacerations.
Oxytocic agents (Inj Methyl ergometrine 0.2 mg, If the blood sample fails to clot, reversal of
Inj 15 methyl PGF 2 , tablets Misoprostol) can be coagulation defects needs to be achieved by
given in dos age give n in table if uterus remains administering blood and blood products. Execute
flabby. urgent referral to higher facility.
Send blood sample for cross matching of 3-4 Arrange urgent referral to FRU, with
units of blood accompanying HCW and relatives. Continue
Send blood sample to laboratory for full blood oxyt ocin infusion & oxygen during transit.
count, coagulation profile, baseline urea and If the woman is in shoc k manage shoc k. The first
electrolytes testing. drip should be fast and timed for approximately
Inspect placenta if she is recently delivered. 1 litre in 20 min. Estimated replacement is
Auscultate lung bases frequently to rule out usually 3times the blood loss. Attempt
pulmonary ede ma. compressing the abdominal aorta by firm
Oxygen is given by face mask: 8 L/min pressure with a closed fist just above the
umbilicus during transit.
Keep the woman warm. Elevate the legs.
Wash hands and wear surgical glove s. If it is delayed PPH, look for signs of infection
and administer the first dose of antibiotic.
Insert Foleys catheter and monitor hourly urine
output. Urine output less than 20 ml /hour
indicates poor perfusion of tissues.
a) Oxytocics for Management of Atonic PPH
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Table-9: Manage ment of Atonic PPH
Oxytocin Methyl Ergo metrine Misoprostol 15 Methyl

PGF2alfa
Dose & Route IV infusion 20 I U in 0.2 mg IM or IV slowly. 800 micrograms 0.25 mg IM Can
500 ml of RL/NS @ Can be repeated after 15 (4 tablets of 200 be repeated
40-60 drops/min mins, thereafter 4 mcg each) per every 15 minutes
hourly if required rectally
Maximum dose 100 IU in 24 hours 5 Injections (Total 1.0 800 micrograms 8 doses (Total 2
mg) mg)
Precautions & Do not give as IV Preeclampsia, Safe drug Rule out Asthma
contraindication bolus Inj hypertension, heart
s disease
Side effects Hypotension if Vomiting Nausea, vomiting, Nausea,
given IV bol us chills vomiting,
diarrhea
Remarks Safe and effective Causes sustained Stable at room Refrigeration is
retraction of uterus temperature, cheap required
Refrigeration is
required Refrigeration is required
First Oxytocin,if not responded Methyl Ergometrine, 13.2.2 Manage ment (Manual re moval of placenta)
if not responded Misoprostol, if not responded 15
Methyl PGF 2alfa. Check womans pulse, blood pressure,
respiration. Assess the amount of blood loss.
b) Uterine Temponade with a sterile condom is a Check whether she is in shoc k.
simple procedure which can be carried out by any Wash hands, Wear plastic apron, gown, mask
SBA as a life saving measure before referral. After and long surgical glove s.
putting the patient in the lithotomy position, under
Start IV Ringer lactate, start Oxytocin infusion.
aseptic precautions a sterile rubber catheter is
inserted within the condom and tied near the mouth Catheterize the bladder and monitor urine output.
of the condom by a silk thread and introduced in the Give premedicationClean the perineum and the
uterine cavity. The condom is inflated with 250-500 vagina with antiseptic solution.
mL normal saline. The uterine condom kept tight in Hold the cord with left hand and introduce the
position by ribbon gauze pack placed in the vagina. whole right hand in the vagina, pass it through
The condom catheter is kept for 24-48 hours, the cervical canal into the uterine cavity. Suppor t
depending upon the initial intensity of blood loss. It the fundus with left hand. Locate the edge of the
is gradually deflated when bleeding is controlled. placenta, separate it completely by slicing
Uterine contraction is maintained by oxytocin drip movement, remove the separated placenta and
for at least 6 hours after the procedure. Antibiotic explore the uterine cavity to check that it is
cover is given. empty Continue oxytocin drip, massage the
uterus.
For uncontrolled PPH surgical procedures may be
required. Inspect the birth canal for any Injury.
Give antibiotics. Monitor the vital signs.
13.2 Retained Placenta If the placenta cannot be removed completely, if the
13.2.1 Definition:When the placenta fails to deliver woman is in shock or needs blood transfusion refer
for 30 minutes after the birth of baby in spite of her to tertiary care centre immediately. Morbidly
routine measures including administration of adherent placenta causes furious bleeding requiring
oxytocin Injection and controlled cord traction, it is urgent lifesaving hysterectomy.
necessary to perform manual removal of placenta
(MRP)
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13.2 Acute Inversion of Uterus Urinary tract infection, Mastitis, breast abscess.
Thrombophlebitis, deep vein thrombosis
13.3.1 Definition:
Malaria, pneumonia, typhoid, HIV related
Uterus turns inside out and may protrude outside infections.
vulva.
13.4.2 Symptoms:
The woman gets very severe hemorrhage and goes in
profound shock. Fever with chills and rigors, Foul smelling
lochia.
Usually occurs due to mismanaged third stage, giving
traction on cord when placenta is yet not separated Malaise, headache, nausea, anorexia, vomiting.
and the uterus is relaxed.
13.3.2 Manage ment: 13.4.3 Signs:
O/E: Pulse feeble and fast. Hypotension. Depending upon severity of infection
P/A: Cupping of fundus, fundus may not be felt at all. Tachycardia, fever, hypotension in septic shock,
Inverted uterine fundus may be seen at vulva or in swelling in one leg, calf tenderness. (DVT)
vagina. P/A: Subinvol uted tender uterus, tenderness in
iliac fossae, distension, guarding, absent
Check whether placenta is separated and delivered or peristalsis in peritonitis.
is still attached. Local examination: Episiotomy oedematous, pus
No oxytocics to be given until the fundus is discharge, foul smelling lochia.
manually reposed. Vaginal examination: Uterus subinvol uted,
tender, fornices tender, Bogginess in posterior
Start IV infusion preferably in two veins, give Ringer
fornix if pelvic abscess.
lactate infusion, arrange Blood transfusion and treat
Shoc k.
13.4.4 Risk Factors:
The freshly inverted uterus can be often replaced in
pos ition by pushing up on the fundus with the hand Prolonged labour, PROM, Unclean delivery.
immediately after inversion. In case of delayed Anemia, under nutrition, Diabetes Mellitus, HIV
diagnosis short uterine relaxant inhalation anesthesia infection.
helps successful reposition.
After reposition, inhalation anesthesia is discontinued 13.4.5 Investigations:
and Oxytocin 20 IU in 500 ml of Ringer lactate is
given along with bi manual compression of the uterus CBC with WBC total and differential count.
to maintain the uterine retraction and the reposition. Smear for malarial parasite.
Correct management of third stage of LABOUR is Urine routine, microscopy, culture & sensitivity
important for preventing this dangerous in suspected cases of UTI.
complication. Do not give any traction on cord until USG for retained products, collection in pelvis.
the uterus is firmly contracted and retracted which Chest X-ray.
indicates the onset of placental separation. High vaginal and cervical swab smear, culture
sensitivity.
13.4 Puerperal Sepsis Blood culture in seriously ill cases.
About 8% of maternal deaths are attributed to post 13.4.6. Manage ment:
abortal or postpartum sepsis. It is a preventable a) Genital sepsis
complication. Early detection and prompt treatment On examination patient has pallor, tachycardia,
can save a lot of morbidity associated with it. uterus is soft, tender, sub involuted (i.e. large for the
13.4.1 Causes of Fever in Puerperium: day of puerperium), abdomen soft, non-tender.
Mild sepsis can be treated at PHC level by giving
Wound infection: Episiotomy, Caesarean oral antibiotics for 7 days.
section.
Puerperal sepsis due to postpartum
endomyometritis, pelvic cellulitis, septicemia,
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Cap Ampicillin/Amoxicillin orally 500 mg 6 hourly If a patient of puerperal sepsis is looking very ill,
for 7 days, Tab Metronidazole 400 mg orally 3 times febrile, restless, has marked tachycardia and has
a day. distention of abdomen, guarding, tenderness over
abdomen, peristalsis is sluggish or absent then such
Give Hematinics. Review after 48 hours.
patient is having generalized peritonitis. She may
If response is seen, continue treatment for 7 days. In have septicemia. Refer her to tertiary care center, as
case of deterioration, refer the patient. Antibiotics she requires special care in critical care unit, higher
includi ng Inj Gentamicin 80 mg IM should be antibiotics and may need surgical interventions.
initiated by ANM/MO at the first suspicion of sepsis There is risk of death due to endotoxic shoc k, acute
before referral. renal failure, DIC.
b) Pelvic peritonitis Any degree of puerperal sepsis when associated
with severe anemia, there is risk of rapid
If P/A examination reveals tenderness in lower deterioration. Hence refer such patient to a
abdomen (iliac fosse) with or without distention and specialist at district hospital.
guarding, suspect pelvic peritonitis and refer to FRU
after giving loading dose of antibiotics. Inj. d) Surgical treatment:
Ampicillin 1 gm IV, Inj. Gentamicin 80 mg, IV
Metronidazole 500 mg. Retained products in uterine cavity: Evacuation
of uterine cavity.
This patient needs hospitalization and parenteral Pelvic abscess is drained by colpotomy.
antibiotics for 7-10 days. Inj. Ampicillin 1 gm IV General peritonitis may require laparotomy.
followed by 500 mg 6 hourly. Inj. Gentamicin 80 mg
twice a day I.M. IV Metronidazole 500 mg 8 hourly. Breast abscess: Incision and drainage.
IV fluids are given. After 48 hours if patient 13.4.7 Preve ntion of sepsis:
improves and resumes oral intake, Cap Ampicillin
and Tab Metronidozole can be given orally. During pregnancy: Nutrition, IFA prophylaxis,
Change in antibiotics as per results of antibiotic anemia correction, Diabetes control.
sensitivity testing is required if there is no response to Intranatal and postnatal: Strict aseptic measures,
treatment within 48 hours. minimum number of vaginal examinations, early
delivery in PROM cases & antibiotic
c) Generalized peritonitis or septicemia: prophylaxis.
Page 284
5. MEDICAL DISORDERS COMPLICATING
PREGNANCY
1. Anemia in Pregnancy 1.1. Definition:
Anemia during pregnancy is a major contributory Anemia in pregnant women is haemoglobi n level of
cause for maternal deaths. Nutritional deficiency is less than 11 g/dL.
the commonest cause.
Table-1: Anemia Classification
Degree Hb(gm/dl)
No Anemia 11
Mild 9 -10.9
Moderate 7- 8.9
Severe Less than 7
1.2. Causes of Anemia During Precordial soft systolic murmur.
Pregnancy Signs of cardiac failure, crepitations at the base of

lungs.
i. Nutritional (Iron, folic acid, proteins)-
deficiency anemia commonest cause. 1.5. Investigations
ii. Wor m infestations.
iii. Twin/ multifetal pregnancy. Hb estimation, Haematocrit, Blood counts.
iv. Malaria. Peripheral blood smear (PBS) to know whether
v. Urinary tract infection, tuberculosis. Iron deficiency or B 12/ Folate deficiency.
vi. Blood loss. Haematological indices- MCV, MCH, MCHC.
vii. Acquired hemolytic anemia.
viii. Hemoglobinopathies: Sickle cell disease, To find out the cause of anemia.
Thalassemias. Examination of stool for worms and occult
ix. Rare causes : Aplastic anemia, leukemia. blood.
Urine examination routine, microscopic, culture
if required.
1.3. Symptoms PBS (thick and thin smear) for malarial parasite.
Weakness,Lassitude and fatigue,Anorexia and Sickling test: Solubility test.
indigestion,pa lpitation,dyspnoea,giddi ness and Serum bilirubin: Hemolysis, megaloblastic
swelling of legs. anemia.
Hemoglobin electrophoresis in suspected
1.4. Signs hemoglobinopathy.
Pallor,glossitis and stomatitis, edema, signs of 1.6. Complications
nutritional deficiencies, Koilonychias, platynychia.
Anemia contributes to 20 % of maternal death
Table 2: Complications
Maternal Baby
Increased risk of cardiac failure. Fetal growth retardation. (IUGR)
Page 285
Inability to withstand third stage hemorrhage, can go in Prematurity
shock with moderate blood loss.
During Puerperium: Risk of puerperal sepsis, Poor Poor stores of iron at birth, risk of
establishment of lactation. anemia during infancy.
Puerperal venous thrombos is , Pulmonary embol ism.
1.7 Treatment 200 mg iron sucrose in at least 200 ml of normal

saline is given over a period of 30 minutes on
Treatment depends upon: alternate days. Keepi ng emergency dr ugs is a must at
every clinic.
Severity of anemia, cause of anemia and gestational
period at which anemia is detected. e) Severe anemia:
1.7.1 Nutritional deficiency ane mia Patients with Hb level <7gm% or moderately anemic
patients with associated obstetrical or medical
a) Prophylaxis (Hb =/> 11 G/dl):
complications should be referred to specialist for
Oral IFA tablets (Elemental iron 100mg with Folic evaluation and management. Hospitalization helps in
acid 0.5mg/day) one tablet daily for 6 months during complete evaluation for cause of anemia.
pregnancy and 6 months during lactation. Bloo d transfusion is indicated if
b) Mild/Moderate anemia: (Hb< 11 G/dl): Hb< 5 gm/dl any time during pregnancy
Therapeutic double dose: Oral IFA one tablet twice a Severe anemia seen after 36wks of pregnancy
day. For better absorption it should be taken before Refractory anemias
meals. Check response after 4 weeks. The treatment Patients needing operative delivery
should be continued till the Hb becomes normal, then
Continued bleeding
one tablet daily is to be continued to replenish the
iron stores. Packed red cells are transfused slowly and under
supervision, diuretics are given to avoid circulatory
Nutritional guidance is given. Protein is overload.
supplemented.
Tab Albendazole (400mg) single dose after first 17.2 Treatment of other causes for
trimester. anemia
c) Response of therapy is evidenced by Should be given as indicated: Antimalarial treatment,
Sense of well-being, increased appetite within 3- appropriate care for bleeding piles etc.
4 days.
After a lapse of 2 weeks hemoglobin starts rising 17.3Management during Labour
at the rate of 1gm % per week.
a)1st stage:
If no significant improvement is evident
clinically and haematologically after 4 weeks The patient should be in bed, propped up
refer the woman to FRU as diagnostic reposition, Oxygen inhalation.
evaluation is needed. Strict asepsis. Monitor vitals, auscultate lung
d) Parenteral iron therapy is indicated if: bases.
Intolerance to oral iron. c) 2nd stage:
Patient not co-operative to take oral iron. Avoid exersion and delay: Episiotomy,
Poor responders to oral iron. prophylactic low forceps or vacuum delivery.
Severely anemic mothers. d) 3rd stage:
Iron sucrose is safe. It helps in replenishing iron Active management of 3 stage of labour with
stores faster than oral iron. prophylactic oxytocin.
Blood t ransfusion if required
Calculated dose: (2.4 W D +500mg for storage Precaution against post partum overloading of
iron) where W= weight in kg (Prepregancy), D = heart.
(target Hb in gm% - actual Hb in gm %), rounded up
to the nearest 100 mg. Total iron is given in divided d) Puerperium
doses. Oral iron is to be stopped before 24 hours.
Page 286
Prophylactic antibiotics 2. Diabetes Mellitus (DM) in
Pre delivery Anemia therapy continued till 3
months after nor malization of Hb. Pregnancy
Baby: Due to lifestyle factors and dietary habits, incidence
of type 2 DM is increasing. Gestational Diabetes
Prone to sepsis in neonatal period. Mellitus (GDM) results in higher maternal and
Special care if low birth weight. Iron suppl ements as perinatal morbidity and requires meticulous control
stores are poor. and special care. Of all GDM patients, > 50%
develop type 2 DM in later life.
17.4 Patient education and 2.1. Two types of cases

counseling Pregestational DM: DM diagnosed before
pregnancy.
Proteins, Iron and vi tamin rich diet Gestational DM: Glucose intolerance detected
Correct cooking habits for the first time during pregnancy.
Precaution against malaria
Spacing between pregnancies
2.2.Effects of GDM on the mother & on the fetus

Table-3: Effects of GDM
Mot her Baby

Pre-eclampsia Unexplained s udde n fetal death during third trimester.
Polyhydramnios Congenital abnormalities.
Caesarian section more common due to fetal Macrosomia (big baby > 4 Kg ) , Birth trauma. (due to
macrosomia and CPD. shoulder dystocia)
Shoulder dystocia, maternal Injuries due to Neonatal hypoglycemia
macrosomia.
Chorioamnionitis and postpartum endometritis. Hyaline membrane disease. (RDS)
Miscarriages in uncontrolled diabetes. Hypocalcemia, hypomagnesemia.
Recurrent UTI, fugal vaginitis, skin infections. Prematurity, Jaundice, Apnea and bradycardia.
Long term risk of type-2 diabetes mellitus. Polycythemia/hyperviscosity syndrome.
The risk of fetal anomalies is high in pregestational 28th weeks of pregnancy or earlier if any of the risk
DM. It is not increased in GDM patients. However, factors are present.
the risks of unexplained still births (during the last 4-
One step screening and diagnostic test is very
8 weeks of gestation) is similar to pre-gestational
convenient for pregnant women in Indian scenario.
diabetes.
As advised by DIPSI (Diabetes in Pregnancy study
2.3. Screening and diagnosis of Group India) and WHO 75 gm Glucose load is given
to women attending ANC irrespective of meal status
Diabetes in pregnancy and blood sugar is estimated after 2 hours.
All Indian women should be screened for gestational A value of 140 mg and above is considered
Diabetes Mellitus as they belong to a high risk diagnostic of GDM. A value of < 120 mg/dl is
ethnicity.Screening is initiated between the 24th and normal. Value between 120 139 mg/dl is
considered as gestational glucose intolerance.
Page 287
Elective induction is done at 38 completed weeks or
earlier if indicated by fetal monitoring tests.
Caesarean section: Large baby and other obstetric
2.4. Management of Diabetes in indications.
Pregnancy
The woman should be referred to gynecologist at
2.5. Care of Pregestational diabetes
district hospital. A team of specialists including mellitus
diabetologist, sonologist and neonatologist should
manage the case in consultation. 2.5.1 Before pregnancy:To reduce the risk of fetal
malformations and fetal macrosomia, counsel for
2.4.1 Medical nutrition therapy: planning pregnancy when glycated hemoglobi n levels
Calories calculation for 24 hours according to weight are normal. Advise pre conceptional Folic acid.
and occupation. 2.5.2 During pregnancy: Special investigations for
30-35 kcal/ kg body weight and for obese women 25- detecting fetal malformations, as
30 kcl/kg/day. practicableBiochemical screening (10 weeks) PAPP
Composition of diet It should include carbohydrates A, -hCG, USG (11-12 weeks) for nuchal
(50-55%), proteins (20-30%) and fats 20-30%) with translucency.
saturated fat <10%. Triple screen (16-18 weeks), level II scan (18-22
Three major meals and 3 snacksare advised. weeks) foetal echocardiography (20-22 weeks)
2.5.3 Third trimester: Assess fetal growth and
2.4.2 Exercise:Walking 3- 4 times weekly for 20-30
liquor volume by USG. NST and umbilical artery
min/session.
doppler studies to decide time and mode of delivery.
Blood sugar monitoring should be done after 1-2 2.5.4 Delivery:For uncomplicated pregnancy with
weeks of starting diabetic diet. well controlled diabetes one can wait until 40 weeks.
Recomme nded glycemic goals:Fasting blood However, in view of adverse perinatal outcomes
glucose < 90 mg/dl; associated with poor control, induction of labour at
38 -39 weeks is a safe practice unless indicated
2 hour postprandial blood glucose < 120 mg/dl earlier.
BSL monitoring 2 weekly from 28 weeks onwards, Elective LSCS if foetal weight 4 kg.
weekly from 32 weeks. More frequently as required.
a) Management during Labo ur:
2.4.3 Insulin Therapy:IfMNT fails to achieve
glycemic goals within two weeks of therapy. Regular glucose monitoring Urine testing for
Insulin requirements increase as pregnancy advances. sugar and ketones.
Consult a physician or endoc rinologist for insulin Regular insulin: Low-dose infusion depending
administration. The starting insulin dos e can be upon blood sugar levels.
calculated on the basis of the patient's weight. For Prophylactic antibiotics.
non obese patients usual doses are 0.8 U/kg and for Baby needs monitoring and special care.
obese 0.9-1.0 U/kg. Calculate total dose. Give 2/3 in
morning and 1/3 in evening. Adjust dose with blood 2.5.5 Postpartum management:
sugar levels.
2.4.4 Obstetrical Management: After delivery insulin requirement decreases hence
dose needs to be adjusted. Fasting and postprandial
Antepartum foetal monitoring: Nonstress test and blood sugar should be checked before discharge.
Amniotic fluid index are performed periodically Patients who are diagnosed to have GDM during
during third trimester to prevent IUD and plan pregnancy are subjected to oral glucose tolerance test
delivery. Umbilical artery doppler studies help in with 75g glucose at 6 -12 weeks.
timing the delivery. More frequent monitoring is
done if there is history of stillbirth, hypertension, and
uncontrolled blood sugars.
2.5.6 Contraception:
For well controlled uncomplicated cases can waitupto
40 weeks. Do not allow to cross EDD in any case. Condoms. Intrauterine device safe
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Rheumatic valvular disease (Mitral stenosis,
3. Pregnancy with Cardiac regurgitation) is common for m in India. Currently
Disease congenital heart disease cases are being diagnosed
early and surgically corrected. Such women are also
Cardiac disease complicates around 1% of presenting during pregnancy.
pregnancies. The disease worsens during pregnancy,
delivery and postpartum period. It is one of the
important indirect cause of maternal mortality.
3.1. Risks
Table-4: Maternal and foetal Risks in Cardiac Disease
Maternal Fetal/Neonatal
Cardiac failure, Acute pulmonary ede ma Prematurity
Subacute bacterial endocarditis IUGR leading to LBW

Thromboembolic complications
Atrial fibrillation & other arrhythmias
Twins, polyhydramnios
3.2. Risk of failure Tachycardia due to any cause: Physical exertion,
emotional upset
The cardiac patient faces greater risk of cardiac
failure at each of the time points when there is 3.3.Diagnosis
significant rise in cardiac output.(at around 12-16
weeks, 28-32 weeks, during labour with each Normal pregnancy is associated with fatigue,
successive stage of labour, soon after delivery and dyspnea, decreased exercise capacity, peripheral
first 24 hours after delivery). edema, and jugular venous distention. Most pregnant
women have audible physiologic systolic murmurs
Obstetric and medical complications increase the risk
and a physiologic third heart sound (S3).This makes
of cardiac failure.
diagnosis of heart disease during pregnancy di fficult.
Infection: Urinary, respiratory, dental.
Anemia, hypertension, preeclampsia,
hyperthyroidism.
Table-5: New York Heart Association (NYHA) Functional Classification
NYHA Class Symptoms
I No symptoms on ordinary physical activity such as walking or climbing stairs.
II Mild symptoms and slight limitation during ordinary activity.
III Marked limitation in activity due to symptoms, even during less-than-ordinary

activity such as walking short distances (20-100 m). Comfortable only at rest.
IV Severe limitations. Experiences symptoms even while at rest.
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3.4. Symptoms Around 28-32 weeks depending on social
circumstances.
In grade 1 and 2 the woman may not have any 3.7.4 Care during labour:Await spontaneous
symptoms. LABOUR. Induction only for obs tetric indications
Grade 3: Breathlessness on accustomed exertion,
fatigue, syncope, chest pain. a) First stage:
Grade 4: Breathlessness even at rest, nocturnal Rest in propped up position; Avoid fluid
cough, hemoptysis. overload.
Prophylactic antibiotics depending upon risk of
3.5. Signs complications: Ampicillin, Gentamicin.
Pain relief.
Cardiac murmurs: Systolic grade 3 or more , any
diastolic murmur. Monitor pulse, respiratory rate, BP, temperature,
lung bases.
Abnormal heart sounds , Arrhythmias.
Monitor oxygen saturation; Oxygen as required.
Signs of cardiac failure : Progressive dyspnoea,
Neck veins engorged, Palpable tender liver, HJR Keep cardiac drug tray ready.
positive. Monitor Labo ur progress, fetal condition.
Pitting oedema over feet. b) Second stage:
Crepitations at the lung bases.
Do not allow the woman to have strenuous
3.6. Investigations bearing down effort.
Cut short the 2nd stage by prophylactic
ECG, 2D Echo cardiography vacuum/forceps delivery.
3.7. Management: c) Third stage:
3.7.1 Before conception-Women with preexisting Do not give Inj Methyl ergometrine. Provide
cardiac lesions should receive preconception physiologic management.
counseling regarding maternal and fetal risks during Give Inj Oxytocin IM 10 IU if there is excessive
pregnancy and long-term maternal morbidity and bleeding.
mortality. Women with NYHA class III and IV face a
high mortality and morbidity. These women should d) During Postpartum period:
be strongly cautioned against pregnancy. Monitor vitals. Watch for signs of failure.
3.7.2Care during pregnancy: Encourage ambulation to preve nt
thromboembolism.
Every pregnant woman should be completely Watch for signs of puerperal sepsis and give
examined between 4-6th month by the medical antibiotics.
officer. Chest auscultation is a must during this
examination. Suspected cases must be referred to Breast feeding is advisable.
physician. 3.7.5 Contraception:
Complete evaluation by physician/ cardiologist.
Risk determination, counseling Combined oral contraceptive pills are
Watch for signs of cardiac failure. contraindicated.
Care of teeth, treatment of urinary tract infection. Condom is safe.
Prevention or early correction of anemia.
After completing family tubal ligation can be
Monitoring blood pressure. performed at district hospital or in tertiary care
Early detection and prompt treatment of centre. Male partner may be encouraged to
pregnancy complications. undergo vasectomy.
3.7.3 Hospitalization: MTP ( if requested) can be performed at district
Grade 3 & 4 dyspnoea kept in hospital hospital after stabilizing cardiac condition.
throughout pregnancy.
Women with obstetric or medical complications.
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4. Peripartum cardiomyopathy There is risk of profuse bleeding hence delivery
should always take place in tertiary care
This is an idiopathic dilated cardiomyopathy that institution. Protamin sulfate is antidote.
develops in the last month of pregnancy or within 5 These cases need regular Laboratory monitoring
months of delivery and is characterized by left to adjust the dose of medications. Also they
ventricular systolic dysfunction with ejection fraction might need fresh frozen plasma for bleeding
(LVEF) <45%. hence they should be under care of specialists at
the tertiary care centre during pregnancy and
4.1 Risk factors: delivery.
Advanced maternal age, multiparity, multiple Breast feeding is allowed.
gestation, obe sity, malnutrition, gestational Combined oral contraceptives are
hypertension, preeclampsia, cesarean section, family contraindicated.
history, abuse of tobacco, alcohol, or cocaine.
The mortality rate is 25% to 50%, half of those die 6. Malaria during Pregnancy
within the first month of presentation and the
majority die within three months postpartum. Death Malaria during pregnancy is more common, more
results from progressive cardiac failure, atypical, can be more serious and can be fatal.
thromboembolic events, and arrhythmias. Of the
patients who survive, approximately 50% recover
normal left heart function. Prognosis is related to left 6.1. Effects on Pregnancy Outcome
ventricular dysfunction at presentation.
The chances of spontaneous abortion, preterm
4.2Management birth, fetal growth retardation,foetal distress and
still birth are increased.
Medical management includes fluid and salt Rarely transplacental spread to the foetus
restriction, Digoxin, Diuretics, Vasodilators, and resulting in congenital malaria.
Anticoagulants. These women need to be in a tertiary
care centre having cardiac ICU facility under care of 6.2. Complications
cardiologist.
Profound Anemia may develop rapidly as there is a
reduction in haemoglobi n. Anemia can have serious
5. Women receiving consequences during Labo ur. In the last two decades
anticoagulation for in India, an increasing proportion of P. falciparum
infections is proving to be resistant to Chloroquine.
surgically corrected heart
disease and Pregnancy 6.3. Clinical presentation
Women with prosthetic valves are receiving warfarin, Fever, Spleenomegaly
a vitamin K antagonist orally for anticoagulation. Anemia may be the presenting feature of
Warfarin freely crosses the placenta and causes malaria, therefore all cases of anemia should be
adverse fetal effects. The risk of warfarin tested for M.P.
embr yopa thy is highest when warfarin is Fetal growth retardation.
administered during 6 to 12 weeks gestation.
Heparine does not cross the placenta and is safe for 6.4. Diagnosis
the fetus.
Microscopy of stained thick & thin smear is the
Anticoag ulat ion: Warfarin must be discontinued gold standard.
and heparin should be administered during this Rapid diagnostic tests. All fevers particularly in
period. After 12 weeks heparin is stopped and malaria endemic areas should be tested for
warfarin is restarted and continued until 36 malaria.
weeks. After 36 weeks again LMWH or
unfractionated heparin is started which is In endemic areas the pregnant woman should be
routinely tested for malaria at all antenatal visits
stopped 4-6 hours before delivery and restarted 6
by RDT even if she does not manifest any
hours after delivery if there are no bleeding
symptoms of malaria.
complications (24 hours after caesarean section).
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Table-6: Treatment of Uncomplicated Malaria during Pregnancy
Day 1 Day 2 Day3
P. Vivax CQ 250 mg CQ 250 mg CQ 250 mg

(150 mg base) 4 tablets 4 tablets 2 tablets
P. Falciparum
First trimester Quinine Quinine Quinine 10mg/kg 3

times daily Continue
10mg/kg 3 times daily for 7 days. 10mg/kg 3 times
upto 7 days.
daily.
2nd, 3rd AS 200 mg 1 tablet SP 2 tablets ( 750 + AS 200 mg 1 tablet AS 200 mg 1 tablet
trimester 37.5mg each)
P. Vivax + P. AS 4 tablets of 50 mg 3 SP tablets AS 4 tablets of 50 AS 4 tablets of 50 mg

Falciparum mg
(500mg + 25 mg each)
(Mixe d)
CQ: Chloroquine 250 mg tablet containing 150 mg

base; 25 mg/kg body weight divided over three days
i.e.10 mg/kg on day 1, 10 mg/kg on day 2 and 5
mg/kg on da y 3.
AS: ArtesunateSP:Sulfadoxine+ Pyrimethamine 6.5.3 Mixe d infections(P .vivax + P.

falciparum)treated as falciparum malaria
6.5. Treatment 6.6 Prevention:
6.5.1 Vivax Malaria:Chloroquine for 3 Use of personal protection measures includi ng
days.Primaquine is contraindicated in pregnant insecticide treated bed nets (ITN) / Long lasting
women. To prevent the relapse, suppressive insecticidal nets (LLIN) should be encouraged.
chemoprophylaxis with Chloroquine 300mg base,
once a week until delivery. 7. HIV Infected Pregnant
6.5.2 P.falciparum Malaria:As pregnant women Woman
having falciparum malaria are more prone to develop
complications, they should be referred to nearest Every pregnant woman during her first visit should
FRU immediately. be counseled for voluntary HIV testing at an ICTC to
know her HIV status.
Treatment during first trimester: Quinine. It may
induce hypoglycemia; do not give quinine on 7.1. Care of HIV positive pregnant
empty stomach and tell the woman to eat
regularly, while on quinine treatment. woman during pregnancy
ACT is not to be given in first trimester of 7.1.1 Points to be noted in history:
pregnancy
High risk be havior in her and her spouse
During 2nd & 3rd trimester: ACT-SP
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Pregnancy duration, number of previous pregnancies, Give ARV medicines as per protocol.
live children, receipt of any antiretroviral medicines Immediate clamping of umbilical cord.
earlier.
Clean the baby of the maternal blood and body
If pregnancy is unwanted and is < 20 weeks refer her fluids before handing over to the relatives.
to MTP centre.
7.3 Care of mother after delivery
If she wishes to continue current pregnancy, refer her
to PPTCT centre soon after confirmation of Refer to PPTCT centre for care of mother and
pregnancy to start the antiretroviral medicines for baby.
reducing the risk of vertical transmission. ART centre
Watch for signs of sepsis.
will be initiating HIV medicines from 14 weeks and
will be doing CD4 testing and other evaluations. Nutritious diet, nutrient supplements.
Encourage to use reliable contraception; safe sex
Screen for TB and STI at every visit. practices.
7.1.2 Specific education & counseling
regarding:
7.4 Treatment at PPTCT/ART
Nutritious diet, consumption of micronutrient centre
suppl ements. The new protocol consists of triple ART to
Safe sex practices for preventing new STIs and pregnant woman and extended nevirapine
other strains of HIV which could harm the baby. therapy for the exposed infant.
Adherence to HIV medicines. Baseline investigations: Hb, urine, VDRL,
Follow up at ART & PPTCT centers as screening for hepatitis B and C, ALT, CD4,
instructed. urea/creatinine, blood sugar, lipid profile.
Institutional delivery. Triple antiretroviral therapy (ART) initiated
Safe infant feeding practices, infant care. irrespective of CD4 count and continued
lifelong.
7.2 Care during delivery If CD4 is < 250 Cotrimoxazole (CPT) 1 ds tab
Insist on institutional delivery at a PPTCT centre as daily.
she requires ARV medicines during labour which ART drugs at ART centre: Given in table below.
need to be continued postpartum. If she is in If there is no prior exposure to EFV/NVP, triple
advanced labour, conduct her delivery by following ARV regime consisting of Tenofovir,
principles: Lamivudine and Efavirenze is started from 14
weeks onwards to be continued throughout
Do not rupture membranes. pregnancy and Labo ur.
Follow universal safety precautions during If there is H/O prior exposure to NVP/EFV then
conduct of delivery. EFV is not given and a protease inhibitor is
Avoid: Episiotomy, perinealInjuries, vacuum given (Lopinavir/Ritonavir).
delivery.
Table-7:Dosage Schedule and Associated Side Effects of ARV Medicines
Name of ARV Dose Major Side Effects

Tenofovir (TDF) 300 mg OD Nephrotoxicity, hypop hosphatemia
Lamivudi ne (3 TC) 300mg OD Very few
Hypersensitivity, rarely pancreatitis
Efavirenz (EFV) 600 mg OD Neuropsychiatric symptoms (hallucinations, suicidal
ideation, nightmare
*Lopinavir/Ritonavir 400/100 mg BD GI disturbance, glucose intolerance, lipo-dystrophy &
(LPV/r) hyperlipidemia
* For prior exposure to EFV or NVP; LPV/r FDC tablet of LPV 200 mg/r 50 mg: 2 tablets BD
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Laboratory tests: EID +ve babies are started on ART irrespective
After 2 weeks of initiating ARV Hb, ALT. of CD4
At 4 ,8,12 weeksHb testing. 7.5.4 After 6 months, if breast feeding option has
Every 6 months BUN, S Creat, ALT, CD4, been chosen, breast feeding is continued as
Urine analysis (imp in TDF based regimes). per EID stat us:
If on PI based treatment: BSL & Lipid profile EID ve babies: Continue BF upto 1 year +
every 6 months. Complementory feeding; No abrupt stopping
of breast feeding
EID +ve baby on ART: Breast feeding
7.5 Care of HIV exposed infant: continued upto 2 years
7.5.1 Infant is give n Nevirapine (NVP) syrup 7.5.5 Growth & nutrition monitoring,
for 6 weeks. immunization as per schedule.
7.5.2 Appropriate infant feeding is initiated 7.5.6 Repeat HIV testing at 6, 12 months and 6
asper informe d choice (following AFASS weeks after stoppage of breast feeding; (If
counseling): Upto 6 months: Exclusive rapid test + ve DBS followed by WBS).
breast feeding. No mixed feeding. At 18 months: Confirmation of HIV status
7.5.3 At 6 weeks : by 3 rapid antibody tests.
Start cotrimoxazole (CPT) prophylaxis,
Early infant diagnosis (EID) by dry blood spot 7.5.7 Counseling: Counsel for adherence to ARV
test (DBS); if DBS +ve Whole blood spot (WBS) and AKT if co-infected with tuberculosis.
confirmatory testing. Encourage safe infant feeding practices.
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6. COMPREHENSIVE ABORTION CARE:
MEDICAL TERMINATION OF PREGNANCY
Unsafe abortion still accounts for nearly 9 %

maternal deaths. Provision of easily accessible, free
6.6 Methods for first trimester
safe abortion service can reduce the burden of MTP
maternal morbidity and mortality.
6.6.1 Surgical methods:
6.1. Legal limit Manual vacuum aspiration (MVA) is the safe
Is 20 weeks of pregnancy. A trained medical officer
recommended technique for pregnancy up to 12
at Primary Health Center is authorized to perform
weeks.
MTPs up to 12 weeks.
Electrical vacuum aspiration is also safe and
6.2. Indications effective.
Pregnancy likely to enda nger womans life or D&C should not be used as a method for MTP.
likely to cause grave Injury to her physical or Give antibiotics prophylaxis: Cap. Doxycycline
mental health. 100 mg orally twice a day for seven days may be
Child is likely to suffer from serious physical or given.
mental disability. Follow adequate infection control practices.
Pregnancy caused by rape.
Pregnancy following contraceptive failure. a) Before MVA:
6.3. Consent for MTP: Check the eligibility and consent

An adult woman who is not mentally ill can undergo
MTP with only her ow n consent. Consent of legal Give pain relief
guardian is required for minors and mentally ill Start prophylactic antibiotics
women.
If uterus is > 9 weeks size, cervical softening can
6.4. Record and register be achieved by administering 400 mcg (2 tablets)
Consent in for m C of the MTP Act. of misoprostol orally/vaginally 3-4 hours before
MVA.
Certify MTP within 3 hours on for m I specifying
the indication. Keep the charged syringe ready, perfor m the
Admission register (Form III). This register is a MVA procedure.
secret document. b) Complications:
6.5. Clinical evaluation: Incomplete abortion, hemorrhage, infection,
Medical history, date of LMP, complete physical Uterine perforation
examination. Determine size of uterus on va ginal Anesthesia related complications.
examination. Failed termination with continuation of
pregnancy. Woman should be counseled to
6.6. Investigations: report if she continues to be amenorrhoic after
Hemoglobin, blood group, Rh typing, urine testing MTP. Repeat termination of pregnancy can be
for sugar and protein. undertaken.
Ultrasonography is not manda tor y. It may be helpful 6.6.2 Mifepristone-misoprostol abortion
for knowing the pregnancy duration in women having (MMA):
irregular cycles, lactationalamenorrhoea, when on In India, MMA is permitted up to 49 days. However
examination the uterine size is uncertain or discrepant by using combi pack it can be performed up to 63
with the period of amenorrhoea and to exclude an days by protocols given below:
ectopic gestation.
a) Information to Women:
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MMA is safe and effective. Efficacy up to 95% If treatment fails, surgical termination is
Three visits are necessary, day 1 Mifepristone, necessary; pregnancy cannot be continued, as
day 3 Misoprostol tablets and day 14 for post there is risk of fetal malformation.
treatment evaluation Vaginal bleeding and uterine cramping may
occur for 7-14 days.
b) Protocol
Table-1:Protocols for Mifepristone-Misoprostol Abortion
Mifepristone Misoprostol
Day 1 Day 3
Gest Age Dose Route Dose Route
Upto 49 days 200 mg (1 tab) oral 400 mcg (200 mcg, 2 tablets) Oral/vaginal
49-63 days* 200 mg (1 tab) Oral 800 mcg (200 mcg, 4 tablets) Vaginal
* The Central Drugs Standard Control Organization, Uncontrolled hypertension, BP > 160/100
Director general of health services, Govt of India has
Uncontrolled seizure disorder.
approved a combi pack of one 200 mg tablet of
mifepristone and four 200 mcg tablets of misoprostol d) Contraception after MMA:
for MTP for gestation between 49-63 days.
OC pills or Inj DMPA can be started on day 3 or day
WHO recommends MMA upto 63 days 15 when abortion process appears to be complete.
In the event that vomiting ensues within 30 minutes of IUCD insertion after one normal menstrual period.
oral misoprostol the medication should be repeated. Tubal ligation after next cycle.
There is no need to keep a woman in the facility till
she aborts. e) Counseling:
Misoprostol given by vaginal route has lesser side Early abortion is safer. MTPs should not be
effects, is absorbed slowly and is effective for a performed repeatedly. Using contraception is
longer time whereas by oral route it is absorbed important. Concomitant female sterilization or IUCD
quickly, is effective for a shorter time and leads to insertion at the time of surgical abortion is safe.
more gastrointestinal side effects. Inform the woman to report early for symptoms
suggestive of complications.
c) Contraindications:
6.7 Methods for Second Trimester
Ectopic pregnancy, either confirmed or
suspected, or undiagnosed adnexal mass MTPs
6.7.1
Hemorrhagic disorder.
Allergy to mifepristone, misoprostol or a) Mifepristone Misoprostol:
another prostaglandi n.
These drugs are recommended by WHO for second
Current anticoa gulant therapy, Current use of trimester MTPs. Combination improves the efficacy.
long-term systemic corticosteroids.
The suggested protocol is 200 mg mifepristone
Intrauterine device in place (remove before followed after 36 48 hours by 400 micrograms of
giving Mifepristone). vaginal, sublingual or oral, misoprostol every 3 6
hours up to 5 doses. Before 18 weeks 3-4 hourly
Chronic adrenal failure. Inherited porphyria. interval is preferred. At or after 18 weeks consider 6
Caution: Haemoglobin<8 gm %. hourly dosing interval.
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Vaginal misoprostol is more effective than oral Safe method, however the drug is not currently
available.
Cautious use in cases having scarred uterusCheck and
record vital signs 4 hourly until onset of strong d) Abdo minal Hysterotomy:
contractions, thereafter 2 hourly. Major surgery done only in selected cases. Eg.
Cancer cervixSecond trimesters MTP procedures
b) Use of Misoprostol alone
require hospitalization for few days. They are likely
Is less effective as compared to combination
to be associated with more bleeding, more chances of
400 mcg 3-6 hourly upto 5 doses. incomplete abortion and other complications.
Provi der needs to make sure that the woman is not
If fetal expulsion does not occur after 24 hours from seeking a sex selective abortion.
initial dose perform abdominal examination and USG
to rule out uterine rupture. Additional legal requirements: MTP centre approved
for 2nd trimester MTP, experienced RMP as stated in
c) Extraamniotic Instillation of Ethacridine Lactate, MTP Act, and the requirement of opi nions of two
0.1 %, 150 ml registered medical practitioners are necessary.

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7. COMMON GYNECOLOGICAL PROBLEMS
1.2.2 Congestive Dysmenorrhoea:
1. Dysmenorrhoea
a) Common causes: Chronic pelvic inflammatory
2. Abnormal Uterine Bleeding: disease (PID), endometriosis, Genital tuberculosis,
pelvic adhesions.
a. Menorrhagia
b) Symptoms: Chronic pelvic pain. Pain is
b. DUB experienced few days before period and is usually
relieved with the onset of menstrual bleeding. It is
3. Post-Menopausal Bleeding continuous dull aching pain in lower abdomen and
low backache. Often associated with dysparunia,
a. Endometrial Cancer vaginal discharge, menorrhagia and i nfertility.
b. Cervical Cancer c) Signs of chronic PID:
P/A: Tenderness in lower abdomen

4. Infertility
P/S: Discharge from cervical canal in STIs
5. Pelvic Organ Prolaps
P/V: Retroverted fixed uterus, cervical movements
painful.
1. Dysmenorrhoea
1.1 Definition: Tenderness in fornices and tender adnexal mass
Nodularity in posterior fornix in endometriosis.
Dysmenorrhoea is painful menstruation.
d) Investigations:
1.2 Types:
Ultrasonography to detect pelvic pathology
Spasmodic (Primary) and Congestive (Secondary). (adnexal mass, ovarian cyst).
Diagnostic laparoscopy helps in diagnosis of
1.2.1 Spasmodic Dysmenorrhoea genital TB, endometriosis, adhesions.
a) Symptoms:Colicky pain in lower abdomen starts e) Treatment:

on first da y of menstruation and usually lasts for a
day. Nausea, vomiting may occur. Assurance and treatment of cause.
b) Treatment: NSAIDs for pain relief: Mefenamic acid,
Ibuprofen.
Usually reassurance is adequate. Antibiotics for treatment of PID.
Majority get relief with antispasmodics Progestins for endometriosis.
(Dicyclomin) or antiprostaglandi ns Specialist referral for treatment of
likeMefenimic acid 500 mg tds as needed. endometriosis, genital TB.
If no response: Combined oral contraceptive pills Laparoscopy for diagnosis of cause for chronic
for 3 cycles. pelvic pain and treatment of adhesions,
Rarely pain may be very severe not responding endometriosis.
to medicines and may need further evaluation
and management by specialist.
c) Investigations: If pain is persistent, USG to rule

2. Abnormal Uterine Bleeding
out endometriosis and uterine anomalies. Abnormal uterine bleeding (AUB) accounts for 20%
of all gynecologic visits.
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2.1 . Definitions H/O Drugs, IUCD.
Menorrhagia:Excessive uterine bleeding Antipsychotic medications (Dopamine
occurring at regular intervals or prolonged antagonists), Phenothiazines and antidepressants
uterine bleeding lasting > 7 days. can cause hyperprolactinemia and AUB.
Dysfunctional uterine bleeding (DUB):
Abnor mal uterine bleeding occurring in the Combination OC pills can cause breakthrough
absence of identifiable pathology. It can be bleeding.
ovulatory or anovulatory DUB.
Prolonged use of high doses of progestational
Metrorrhagia: Acyclical menstrual bleeding agents.
occurring at irregular intervals.
Breakthrough bleeding: Unpredictable Anticoagulant medications.
bleeding that occurs while on exogenous
Digitalis, Phenytoin, and Corticosteroids.
hor mones (eg hor monal contraception).
Oligo menorrhea: A menstrual cycle interval of Copper- intrauterine devices.
more than 35 days.
Polymenorrhea: A menstrual cycle interval of
less than 21 da ys. 2.4. Physical Exam
Postmenopausal bleeding: Vaginal bleeding
occurring more than 12 months after the last Note pallor, thyroid examination.
menstrual period.
Breast examination: Galactorrhoea.
Amenorrhea: Absence of menstrual bleeding.
P/A examination: Pelvic mass (fibroids),
2.2. Differential diagnosis of AUB tenderness in lower abdomen. (PID)
Abnormal uterine bleeding can occur in all age Speculum examination: Cervical pathology.
groups. The diagnostic testing and treatment (growth, ulcer, polyp)
approach should take into consideration the age
group a nd fertility choices of the woman. P/V: Cervical motion tenderness, size and
contour of uterus, and presence of any palpable
Adolescent girls: Anovular DUB is common. adnexal masses or tenderness.
Pregnancy related conditions should be kept in
mind. Bleeding disorders can be present in some
cases. 2.5. Investigations
Women between 20-40 years: Pregnancy related
conditions, ovular DUB, pelvic infection and Complete blood count
benign neoplasia like fibroids are common. Ultrasonography abdomen and pelvis and
Perimenopa usal AUB is commonly due to transva ginal ultrasonography (TVUS) for
anovulation and fibroids. However it is necessary diagnosing fibroids, polyps, adnexal mass.
to exclude polyps, endometrial hyperplasia and Thickness of endometrium can be measured.
malignancies. Intrauterine pregnancy and ectopi c pregnancy
can be excluded.
Postmenopa usal bleeding: Malignancy needs to
be excluded. Endometrial biopsy in women over age 35 and
women having risk factors for endometrial
2.3. History cancer. It helps in diagnosing ovular or anovular
bleeding, endometrial hyperplasia, endometrial
Detailed menstrual history, sexual histor y, past precancerous lesions and endometrial carcinoma.
medical history, gynecologic and obstetric
Endometrial sampling is a rapid, safe, and cost-
histor y. Note any change in the patient's weight,
effective procedure that can be performed in the
and exercise pattern.
office to evaluate AUB. A potential drawback is
History of bleeding disorders, possible that the biopsy does not sample the entire
pregnancy. endometrium and a localized lesion may be
missed.
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Dilation and Curettage (D&C) can be both b) Hormones:
diagnostic and therapeutic.
Oral Progestins: Useful in anovulatory bleeding.
Hysteroscopy is the gold standard for evaluating
the endometrial cavity. It provides direct For acute heavy bleeding: Medroxy progesterone
visualization of the endometrial cavity and can acetate 10 mg tablet 2-3 times a day till bleeding
be performed in the office setting or operating stops. It is tapered and continued 1 tab daily for a
room. It can be both diagnostic and therapeutic, total duration of 21 days. Withdrawal bleeding
allowing for directed biopsies and excision of starts in few days. Further cyclical therapy (10
polyps and small sub mucus myomas. mg daily) is given from day 5 to 25th day for 2
more cycles. Response is awaited.
Saline infusion sonohysterography for detecting Norethisterone tablet 5 mg can be used similarly
endometrial polyps or uterine leiomyoma. for a period of 21 days, initially 1 tab 3 times a
day until bleeding stops, then 1 tab twice a day
Thyroid stimulating hor mone (TSH) and for few days and then tapered to 1 tab daily
Prolactin estimation: Hypothyroidism and thereafter. Side effects of progestins include
hyperprolactinemia can lead to anovulation and breast tenderness, weight gain, and headaches.
DUB.
Combined oral contraceptive pills can be given
Bleeding disorders should be evaluated if from day 5 to 25 for 3-6 cycles in women
historical or clinical features suggest specific between 20-40 years of age not having
conditions. contraindications for estrogens and who also
wish to have contraception.
2.6. Dysfunctional Uterine Bleeding
c) Antifibrinolytic medications(e.g. Tranexamic acid)
Dysfunctional uterine bleeding (DUB) is a decrease menstrual blood flow by 50%, and need to
diagnosis by exclusion of other causes of AUB be taken during menses only. However, there are
without a demonstrable pathologic cause. The concerns about their pro-thrombotic potential.
predominant causes of DUB are anovulation or
2.6.2 Surgical Treat ment for DUB:
oligo ovulation.
Diagnostic D&C may have some therapeautic
Long-term anovulation, polycystic ovary effect. However it does not have a sustained
syndrome: Resulting unopposed estrogen state
therapeutic effect.
increases the risk of endometrial hyperplasia.
Morbid obesity with associated elevated estrogen Endometrial ablation: Endometrial ablation is not
levels. Can also cause DUB. recommended in women who desire future
fertility.
In some cases DUB may be associated with Hysterectomy provides definitive treatment for
ovulator y cycles. menorrhagia and may be a reasonable option in
women with severe menorrhagia, who have
completed their childbearing and are refractory
2.6.1 Medical therapy: Treatment of Anemia should to medical and less invasive surgical therapy.
be initiated. Women who are severely anemic or not
The women not responding to medical line of
responding to medical treatment should be referred to
treatment should be referred to specialist at
specialist.
FRU/DH for surgical treatment.
a) Nonsteroidal anti-inflammator y dr ugs (NSAIDs)
may reduce menstrual blood loss by about 30% in 2.7 Menorrhagia
women with menorrhagia and can be given as the 2.7.1 Causes of Menorrhagia
first line therapy. They need to be taken during
menses only. The options are: 1. General medical causes associated with
me norrhagia: Hypertension, cardiac failure, hepatic
Mefenamic acid 500 mg three times a day for 5 dysfunction can be associated with AUB.
days during menstruation.
2. Genital Infection: Chronic PID and genital
Ibuprofen 600-1200 mg /day. tuberculosis.
Naproxen sodium 500 mg 1, then 250 mg 3. Endometrial Pathology & Genital Neoplasia:
every 6-8 hourly.
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a. Endometrial Polyps can present as menorrhagia USG. Symptomatic fibroids need surgical
ormetrorrhagia. Diagnosis is by saline infusion treatment by a specialist.
sonogram and hysteroscopy. Endometrial polyps can
be removed by operative hysteroscopy. d) Endometrial Cancer: It is mostly seen in
postmenopausal women and is rare in patients
Cervical polyps can be removed by grasping with younger than 40. Postmenopausal bleeding is the
forceps, twisting them off, and cauterizing the base. presenting symptom which should be assumed to
b. Endometrial Hyperplasia: A precursor to represent endometrial cancer until proven
endometrial carcinoma. It is classified into simple or otherwise. The women should be referred to
complex, based on architectural features, and typical specialist for further evaluation and treatment.
or atypical, based on cytologic features. Endometrial
hyperplasia tends to occur during periods of long- e) Cervical Cancer: Bleeding patterns associated
term unopposed estrogen exposure, either secondary with cervical carcinoma are intermenstrual and
to anovulatory cycles or exogenous use. AUB is the postcoital bleeding. Cervical biopsy is
most common presenting symptom. diagnostic. The woman should be referred early
to district hospital or a cancer treatment centre.
Diagnosis by endometrial biopsy
Treatment depends upon age, desire for future f) Ovarian Cancer: Estrogen-producing ovarian
fertility and presence of atypia in the pathology tumors, can produce endometrial hyperplasia and
specimen. AUB. USG will reveal the tumor. The woman
should be referred to district hospital or a cancer
Simple hyperplasia can be treated with
progestogens. treatment centre for surgical treatment.
Cyclic Medroxyprogesterone Acetate (MPA 10
mg/day for 12 to 14 days/cycle for 3 to 6 3. Postmenopausal Bleeding
months) in young anovulator y women to i nduce
monthly withdrawal bleeding. 3.1 Definition:
Local Progesterone administration:
Vaginal bleeding occurring one year after cessation
Levonorgestrel-releasing intrauterine system.
of menses.
(Mirena)
Uterine bleeding is often due to endometrial cancer,
polyps or endometrial hyperplasia. Genital tract
Atypical endometrial hyperplasia is more likely malignancy and precancerous.conditions need to be
to progress to carcinoma or may coexist with excluded in these cases. Hence immediate referral to
endometrial carcinoma. Hence hysterectomy is gynecologist is necessary for further evaluation and
advised. treatment.
c) Uterine Fibroids: Menorrhagia is the most 3.2 Differential diagnosis:

common presenting symptom. Diagnosis is by
Table-1: Differential diag nosis of postmenopausal vag inal bleeding.
Endometrial causes Ovarian causes

Endometrial Hyperplasia Benign tumors of ovary
Endometrial carcinoma Malignant tumors of ovary
DUB Hormone secreting tumors of Ovary
Endometrial polyp (Granulosa- theca cell tumor)
Senile endometritis
TB endometritis
Cervical causes : Exogenous Estrogens

Cancer cervix, Polyp, HRT for menopa usal symptoms can cause
Decubitus ulcer on prolapse irregular bleeding
Cervicitis
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Vulvo-Vag inal causes: Non ge nital causes:
Senile atrophic vaginitis Hypertension
Foreign bod y in va gina like pessary Bleeding diathesis
Malignant lesions on vulva Urethral and rectal bleeding can sometimes
be misreported as vaginal bleeding
3.2.1 Endometrial Cancer vaginal discharge. Suspect uterine myoma or

malignancy if firm irregularly enlarged uterus
a) Risk Factors for Endometrial Cancer: Refer the woman to the gynecologist for further
evaluation.
Conditions associated with excessive estrogens Refer for USG includi ng transva ginalsonography
unopposed by cyclical progesterone are for assessment of endometrial thickness and
commonly responsible for postmenopausal other uterine and ovarian pathology.
bleeding. Estrogens could have been produced in
the bod y (endogenous) or given in medicinal c. Management
for m ( exogenous)
At RH/DH:
Age at menopa use > 52 years
Nulliparity, infertility. If gross cervical pathology seen cervical biopsy,
Obesity, hypertension, diabetes mellitus polypectomy
Family history of uterine, breast, colorectal Pap smear if no gross lesion seen
cancer Colposcopy for unhealthy cervix, abnormal Pap
Drugs: Estrogen therapy, Tamoxifen smear, vulval lesions
b) Management: Ultrasonography : TVS or Saline infusion
sonography
At PHC: Hysteroscopy and directed biopsy is the gold
standard for evaluation: It permits direct visual
History: inspection of uterine cavity with greater accuracy
of diagnosis as focal lesions are not missed. It is
Ask symptoms: Irregular bleeding, spotting, superior to blind dilatation and curettage in
brown discharge, post-coital bleeding, number of which neoplasia may be missed.
bleeding episodes Fractional curettage under GA if hysteroscope
Age of woman, late menopause (> 52 years), unavailable
nulliparity, Treatment is planned according to pathology
H/O receiving hor mones found.
(estrogen/progestogen), dr ugs (tamoxifen) Endometrial hyperplasia: Abdominal total
Family history of endometrial cancer hysterectomy with bilateral salpingo
Diabetes mellitus, hypertension oophorectomy
Cervical/Endometrial malignancy: Treatment as
Examination: per stage
Ovarian tumors: Staging laparotomy (Total
Look for obesity, hypertension hysterectomy + bilteralsalpingo oophorectomy
Examination of vulva for any lesion, ulcers, for benign tumors. Tretment as per stage for
growth, atrophy, polyp. malignant tumors)
P/S examination of va gina and cervix to look for Senile vaginitis: Vaginal estrogen therapy
any growth, polyp, ulcer, estrogenization,
infection. If cervical pathology is seen refer to d. Screening for endometrial cancer:
gynecologist for cervical biopsy, polypectomy as
necessary TVS for endometrial thickness is a simple, non-
Vaginal examination: Look for uterine invasive, reliable screening technique for the
enlargement, Suspect pyometra if soft uniformly diagnosis of Ca endometrium. All postmenopausal
enlarged tender uterus with intermittent offensive women should have annual trans vaginal sonographic
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assessment for endometrial thickness. Women having Pap smear (cytology screening)
endometrial thickness > 4 mm need further Visual inspection of cervix with acetic acid
evaluation to rule out endometrial cancer. (VIA)
3.2.2 Cervical Cancer HPV testing for high risk types (it is expensive
Cervical cancer is the second most common cancer and available only in some centres. Useful in
among women in India, the first being breast cancer. increasing the screening interval in women
In 2012, about 1,23,000 new cases of cancer cervix above 30 years age)
were detected in India and 67,000 women died due
to cervical cancer, but this cancer can be prevented. i) Pap s mear (cytology screening):
Human papillomavirus (HPV) is the causal agent for Pap smear requires LABOURator y infrastructure,
cervical cancer and about 15 high-risk types of HPV quality control, a system for informing the results to
are known. HPV infection is a very common the women and further referral for colposcopy.
infection. Those women who cannot clear this Material:Cuscos bivalve speculum, Ayres spatula,
infection by their natural immunity are at risk of endo-brush, fixative spray or jar containing fixative
cervical cancer. solution, 95% ethanol or ether-alcohol mixture, glass
a. Screening for Cervical Cancer: slides.
Cervical cancer is preceded by a long phase of Procedure:
premalignant lesion called as cervical intraepithelial Schedule the procedure following abstinence for
neoplasia (CIN). This stage may last for about 10-20 24 hours and when there is no vaginal bleeding.
years before developing into a frank malignancy. Confirm that no va ginal examination has been
When the abnormal cells are limited to the lower done in previous 24 hours. No vaginal antiseptics
third of the epithelium it is labeled as CIN 1, when should be used
lower two thirds of the epithelium is involved, it is Use speculum to inspect the cervix
termed as CIN II and when the entire thickness of the Do not take smear if there is vaginal bleeding or
epithelium is involved, it is termed as CIN III. CIN active infection
can be diagnosed by a pathologist on
histopathological examination of cervical biopsy Place the Ayres spatula against the cervix and
rotate it firmly against the cervix through 360
specimen. CIN lesions can be treated by simple
degrees to scrape the transformation zone.
treatment modalities and cervical cancer can be
Spread the sample on the spatula evenly on a
prevented.
glass slide. Endocervical cells are obtained by
The World Health Organization (WHO) has
endo-brush or cotton tipped applicator rolled in
recommended that at a minimum, as a priority,
cervical canal. Place the sample on another glass
screening is recomme nded for every woman 3049
slide
years of age at least once in a life time. Screening
should be initiated at 30 years of age. For HIV- Fix the smears by putting in fixative jar or by a
infected women screening should be initiated as soon fixative spray. Send the smears to an expert
as the infection is diagnosed. cytopathologist
Cervical cancer screening can be done by following Currently Bethesda system (2001) is used for
different tests: repor ting of smears.
Figure 1 Scraping from ectocervixFigure 2 Endocervical sampling
ii) Visual inspection of cervix with acetic acid VIA involves application of 5% acetic acid on the
(VIA): cervix for one minute and visual inspection of
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colour change s in the cervi x. VIA is simple, cheap, Apply acetic acid to the cervix for one minute
it can be performed by trained health care workers and simultaneously obs erve if any color change
and provides an opportunity to treat screen positive develops
women during the same sitting thus reducing the Observe any changes in the color/ appearance of
challenges of lost to follow up. the cervix after one minute. Give special
Materials and equipme nt needed for screening: attention to abnormalities close to the SCJ
Look for any raised and thickened white plaques
Sterile gloves and Cuscos speculum or acetowhite epithelium.
Autoclaved cotton balls and sponge holding Use a fresh swab to remove any remaining acetic
forceps/ autoclaved cotton-tipped swabs acid solution from the cervix and vagina. Gently
Freshly prepared acetic acid solution (5%) remove the speculum.
The test results are reported as follows:
Procedure: VIA positive - when there is a dense white,

opa que lesion touching the squamo-columnar
Insert a bivalve speculum, get the view of the junction (SCJ)
cervix VIA negative when such lesion is not seen
Remove any discharge, blood or mucus from the VIA positive-invasive cancer when there is a
cervix by a saline moistened cotton swab clinically visible growth which turns dense
Ide ntify the squamo-columnar junction (SCJ) aceto-white and bleeds on touch.
and the area around it
Figure 3 VIA positive cervix
After screening WHO guidelines (2013):
If the test is negative, repeat test in 3-5 years. Screen and Treat approach, using a screening test
For HIV infected woman repeat testing within 3 giving immediate results (like VIA) followed by on
years. the spot treatment (cryotherapy) of detected lesions
to eligible women, without any further tests, when
there is no suspicion of cancer. This has been shown
b) Treatment strategy for screen positive cases: to be an effective strategy. This is a single visit
appr oach which is conve nient for rural women.
GOI-WHO (2006): Screening women between age
30 -59, by VIA by trained HCW at PHC. Referral of
VIA positive to DH.
A comprehensive approach to cervical cancer
At DH repeat VIA followed by pap smear, prevention and control invol ves health education and
colposcopy, directed biopsy from abnormalareas screening of all women and treatment before
followed by cryotherapy /LEEP as required at the progression to invasive disease. Awareness among
same sitting. women and doctors that cervical cancer can be
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prevented by early detection and treatment of CIN is 4.1.1 Infertility Male Factor
critical for the success of cervical screening.
a) History in Male Partner: Age, occupation,
Primary prevention of cervical cancer is now previous marriage if any, substance abuse, coital
possible by HPV vaccination of girls between 9 to 13 histor y (Frequency of intercourse / Knowledge of
years of age before initiation of sexual activity. But fertile period / Coital difficulties related to erection /
HPV vaccines are currently expensive and not yet penetration / ejaculation).
available in the government programs. Past history:
4. Infertility Mumps/Genital trauma/STIs/Surgery/Tuberculosis),

Current histor y: Any illness, dr ug treatment.
4.1 Definition: b) Physical Examination - Rule out hernia,
hydrocele, undescended testis, absence of testis. Note
Infertility is defined as failure to conceive after one
the size of testis. Look for varicocele in upright
year of regular, unprotected sexual intercourse. It can
position.
be primary or secondary:
c) Investigations:
i. Primary: The woman has never conceived in
past. Bloo d and urine routine testing
ii. Secondary: The woman has previously
conceived but is subsequently unable to Semen Analysis: Sample collected after 2-3 days of
conceive for 12 months. abstinence and examined within 2 hours of
collection.
Infertility affects 10 15% of the general population. Male partner should be evaluated first by
It is the problem of the couple. Male factor is performing semen analysisIn humans ittakes
responsible in 30%, Female factor responsible in about 75 days for spermatogonia.
50%, and the combined factors are responsible in
10%. Unexplained infertility in observed in 10%.
To develop into mature If semen report is abnormal, the test should be

repeated twice at least at 2-4 weeks interval before
Table 2: Minimum normal criteria for semen
considering it as abnormal. Ideally a
analysis: WHO revised criteria.
Parameter WHO 2010

period of 3 months should be considered for
evaluation of any improvement as a result of therapy.
Volume 1.5 ml
Persistently abnormal semen parameters require
further evaluation at speciality infertility clinic.
Sperm
15 million/ml
concentration e) Male Partner- Treatment
Progressive i. Medical therapy: Antioxidants, clomifene

32% citrate, gonadotropins.
motility
ii. Intra-uterine Inse mination (IUI): Mild male
factor infertility.
Nor mal for ms 4% iii. Donor inse mination: For azoospermia
d) Counselling for male: (Primary testicular failure)
iv. Adoption: For cases with recurrent
Regular intercourse 2-3 times/week, stop smoking, unexplained failed IVF cycles.
alcohol & any addictive drugs, wear loose fitting v. Surgical restoration of duct patency: For
underwear and trousers, and avoid Occupational or obstructive azoospermia (previous vasectomy).
social situations that might cause testicular heating. vi. Intra-cytoplas mic Sperm Injection (ICSI):
Treat any ps ycho-sexual problem if present. For severe male factor or for recurrent
unexplained failed IVF cycles.
4.1.2 Infertility Female Factors
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a. Causes of fertility in females d) Investigation in Female Partner
Anovulatory infertility-
Pelvic USG:Diagnosis of PCOS, uterine fibroids,
i. Anorexia nervosa / Stress related / Exercise adnexal mass, uterine malfor mations,
induced. endo metrioma.
ii. Hyperprolactinemia , Thyroid disorders. Serial trans-vaginal sonography for confirmation
iii. Polycystic ovarian disease. of ovulation and timing of ovulation.
iv. Decreased ovarian reserve, Premature ovarian Hormonal assay: Mid luteal serum progesterone..
failure. TSH, Prolactin, FSH & LHin selected patients
with anovulation
Tubal infertility:
Endometrial sample collected by premenstrual
Genital tuberculosis, PID, Tubectomy curettage is sent for histopathological and
Uterine factors: microbiological evaluation to exclude
endometrial tuberculosis in suspected cases.
Submucous fibroids, Tubercular endometritis, Laparoscopy helps in diagnosis.
Endometrial polyps, Intrauterine adhesions. Hysterosalpingography (HSG)-Performed
Peritoneal factors: Endometriosis, Chronic PID between Day 6 Day 11 of the menstrual cycle,
at the Radio- diagnosis department.
Cervical factors:
Immunologic, infections, surgical trauma Contraindicat ions:
(amputation, conization, deep cauterization of
cervix). Current PID, suspected Genital TB, cervicitis.
b) History in female Partner: HSG also helps in detecting intra uterine pathology.
Age, years since marriage, occupation, substance Laparoscopy with chromot ubat ion
abuse. History suggestive of reproductive tract
infections (Vaginal discharge/Pruritus This is an invasive surgical procedure indicated
vulvae/Chronic pelvic pain), Tuberculosis, when HSG is abnormal, there is failure to
Endoc rinopa thy (Weight & Hair changes/Discharge conceive within 6 months in spite of a nor mal
from nipples/cold intolerance/dryness of skin), HSG, and for suspicion of endometriosis.
Premature ovarian failure (H/O Mumps, hot Usually done in the pre ovulatory period.
flushes/oligomenorrhoea/amenorrhoea), Abdo minal Diagnostic laparoscopy helps in diagnosing
Surgery. Coital frequency & knowledge of fertile tubal, uterine pathology and also helps in
period, dyspareunia detecting endometriosis, pelvic adhesions, pelvic
tuberculosis. Surgical treatment for adhesions,
H/Oprevious pregnancies, pregnancy outcome, post endometriosis can be done laparoscopically.
partum infection.
Hysteroscopy:
Family history: egTuberculosis Endoscopic direct visualization of the uterine
Menstrual history: cavity.Submucous fibroids, endometrial polyps,
Menarche, regularity of cycles, dysmenorrhoea, flow, adhesions, malformations and foreign bodies can
LMP.:Regular cycles, dysmenorrhoea, be visualized.Hysteroscopic, resection of uterine
mittelschmertz (mid cycle pain), premenstrual breast septum, submucusmyoma and adhesiolysis for
heaviness and mastalgia are suggestive of ovulatory intrauterine adhesions can be offered.
cycles. Laparoscopy can be combined with
hysteroscopy.
c) Examination of female partner:
Look for obesity or gross underweight (BMI), e) Counselling for Fe male Partner:
lymphadenopathy, thyroid enlargement, hirsutism, Regular intercourse 2-3 times/week. stop smoking,
galactorrhoea, acanthosisnigricans. alcoholand addictive drugs, and follow a supervised
Systemic exam weight loss programme if obese. Treat psycho-sexual
problem if present.
Speculum & per va ginal exam: Look for anatomic
abnormalities. f) Treatment of Fe male Partner:
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Induction of Ovulation:
For women with ovulator y dysfunction.
Clomiphene citrate is the first line drug for Surgical Treat ment
ovulation induction.
50 mg orally daily for 5 days from day 2 to day 6 i. Laparoscopic adhesiolysis
of menstrual cycle. Ovulation is monitored by ii. Hysteroscopic tubal cannulation, resection of
USG follicle monitoring. If ovulation doe s not intrauterine adhesions, pol yp or
occur, the dose can be increased by 50 mg daily submucusmyoma.
in successive cycles up to 150 mg daily. Risk of iii. Laparotomy for tubal reconstructive surgery.
multiple pregnancies should be explained.
Failure of ovulation or conception after treatment
for 3 cycles requires careful review and
evaluation. 5. Pelvic Organ Prolapse
Women with polycystic ovary syndrome who
have not responded to clomifene citrate should Pelvic organ prolapse (POP) is a common
be offered laparoscopic ovarian drilling gynaecological problem in women above the age of
Gonadotropins for ovulation induction requires 40 years. POP includes anterior vaginal prolapse
special expertise and careful monitoring. There is (cystocele), uterine prolapse, and posterior vaginal
risk of multiple pregnancy prolapse (rectocele, enterocele).
Hyperprolactinaemia: Treatment with
bromocriptine.
Hypothyroidism: Thyroxine therapy restores
ovulator y cycles
5.1 Symptoms
Intra-uterine Insemination (IUI): Unexplained
infertility and cases with minimal endometriosis.
Table-3: Symptoms
Lower urinary t ract symptoms Bowel symptoms Sexual symptoms Other symptoms
Incomplete emptying, Constipation Interference with Pelvic pressure,

sexual activity heaviness, pain
recurrent UTI, frequency, urgency
nocturia
Stress urinary incontinence Straining Dyspareunia Presence of vaginal

bulge/mass
Voiding difficulty: may require to Incomplete Decreased sexual Low back pain
reduce prolapse before passing evacuation desire
urine
5.2. Signs
P/A:Look for any lump, ascites, obesity
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Local exam: Inspection of the vulva with in healing. In older women having severe vaginal
coughing and straining demonstrate severe atrophy, vaginal application of estrogen cream
prolapse and may demonstrate stress helps in rapid healing. The ulcer will usually
incontinence ( provided the bladder is full) heal within 7 da ys.
Examination using Sims speculum: Note type of 5.4.2 At FRU/DH: The women should be evaluated
prolapse, degree of uterine descent, anterior and completely for planning the treatment modality. Most
posterior vaginal wall prolapse. Look for women will be candidates for surgical treatment. In a
decubitus ulcer on cervix, elongation of cervix young woman following childbi rth conservative
Vaginal examination: Note uterine size, pos ition, measures should be advised for 3 to 4 months.
adnexal mass a) The nonsurgical treatment is useful in following

Rectal examination, to differentiate rectocele women Women having mild degree of prolapse
from enterocele
Pregnancy and Postpartum
Assess anal sphincter tone, assess levator tone,
Unfit or unwilling to undergo surgery.
perineal body
Kegel exercises to strengthen the pelvic supports.
Ring pessary: Woman unfit for surgery, can provide

5.3. Predisposing factors temporary relief.
Injuries to supports of pelvic organs during b) Surgical treatment:

childbirth Surgery can be of two types. Vaginal hysterectomy
Obesity, chronic cough, chronic constipation, with vaginal wall prolapse repair and uterus
Atrophy and loss of tone due to aging, estrogen conserving surgical repair. Choice of surgical
deficiency procedure depends on age, parity and wish for further
Congenital weakness of tissues can lead to pregnancy and medical fitness. In younger women
nulliparous prolapsed desirous of retaining fertility, conservative surgical
repair operations are indicated, whereas in the
5.4. Management
perimenopausal and menopausal women, vaginal
hysterectomy with repair of the pelvic floor is
5.4.1 At PHC:Preoperative care given at PHC can
performed.
help in shortening the hospital stay and reduce the
number of visits to the district hospital. 5.5. Prevention
Treat urinary tract infection. Correct Anemia,
Antenatal physiotherapy, relaxation exercises
control diabetes
and due attention to weight gain and Anemia are
Treat the decubitus ulcer before surgery:
important.
Reposition of prolapse and maintaining it in
Proper management of second stage of Labo ur.
reposed position helps in healing of ulcer.
Avoiding undue prolongation of second stage by
Glycerine-acriflavin vaginal packing daily helps
timely assisted delivery.
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Immediate and accurate suturing of perineal tear Provision of adequate rest for the first 6 months
after delivery. after delivery
Postnatal exercises and physiotherapy are Contraception: Too many births at too short
beneficial. intervals are avoided.
Early postnatal ambulation.
Page 309
DERMATOLOGY
Page 310
1. INFECTIONS OF SKIN
1. Bacterial infections of Skin

d. Furuncle
It is infection of skin caused by bacteria. Persons
Erythematous, painful, tender
with poor personal hygiene, old age, Diabetes and
Immunocompromised patients are prone to bacterial Form discrete follicular nodules with
infection of skin. Perifollicular edema.
1.1. Pyoderma
1.1.1 Types
a. Impetigo
Starts as an erythematous Macule
Develops into a vesicle with erythematous halo
Vesicle breaks down with oozing
Dries to form golden yellow crust Spreads by
auto i noc ulation
b. Ecthyma
Deeper infection
An ulcer covered with adherent crust e. Carbuncle
Heals with scarring Infection of multiple adjoining hair follicles
Rule out Diabetes Mellitus in case of recurrent Presents with painful, tender plaque with
furunculosis and carbuncle. ulceration.
Rule out Diabetes Mellitus in case of recurrent
c. Folliculitis furunculosis and carbuncle
Follicular oriented pustules without peri-
follicular oedema.
1.1.2 Investigation: - CBC, BSL (R) Systemic antibiotics Erythromycin (250 or

500 mg QID) / Cefadroxil (250 or 500mg BD)
1.1.3 Treatment guidelines: for 7 days
Good personal hygiene Azithromycin 250 mg bd for 7 days
Wash with soap and water For recurrent pyo derma:
Topical antibacterial cream Neomycin 0.5 % Topical application of mupirocin 2 % to carrier
/ Framycetin1 % / Mupirocin / Fusidicacid - sites especially anterior nares and natal clefts
Local application two times in a day for 7 for 2 weeks.
days.
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1.1.4 Erysipelas H/o minor injury may be present
Erysipelas is a superficial form of bacterial Present as sharply defined erythematous tender
cellulitis Swelling.
Usually seen over the face
Treatment:
Systemic antibiotics- Azithromycin 250 bd for 1.1.5 Cellulitis
5-7 days / Cloxacillin / Amoxicillin-
Clavulanicacid - 625 mg bd for 7 days. Cellulitis is a deep subcutaneous infection with
IV antibiotics for severe cases -Inj.Cefotaxime lymphangitis and adenopathy
1 gmIvbd for 7 days. Borders of the lesion are poorly demarcated
Non steroidal anti-inflammatory drugs - Tab. Vesicles and bullae may be seen over the
Brufen 1 bd for 7 days. surface in both conditions.
Treatment:
2.1.1 Tineacapitis
Non steroidal anti-inflammator y drugs - Tab. Presents with different clinical types and is
Brufen 1 BD for 7 days. more common in children.
Amoxycillin + Clavulinic acid 625mg BD / a. Gray patch
Cloxacillin for7-10 days Well defined scaly circular patches
IV antibiotics for severe cases - With partial alopecia showing broken off hair.
Inj.Cefotaxime 1 gm IV BD for 7 days.
2. Fungal infections of skin

2.1 Dermatophyte infections
Superficial fungal infections of keratinized tissue
caused by dermatophyte fungi. Persons with
diabetes, Obesity and Immunocomprised patients
are prone to infections.
Dermatophytosis is classified according to the body
part involved.
Page 312
b. Black dot
Broken off hair near the surface give
appearance of black dot.
Diffuse and poorly circumscribed lesions with
low grade folliculitis.
c. Kerion
Boggy purulent inflammator y nodules and
plaques with sinus for mation and pus discharge
which leads to thick crusting & matting of
adjacent hairs.
d. Fav us Systemic antibiotics in case of secondary

infection - Azithromycin 250 BD for 5-7 days
Perifollicular erythema and matting of hair / Cloxacillin / Amoxicillin-Clavulanic acid -
with fetid odour
625 mg BD for 7 days.
Heals with scarring alopecia. Tab. Fluconazole 150 mg / week for 4 to
e. Investigation: - CBC, BSL (R) 6weeks.
f. Treatment 2.1.2 TineaCorporis
g. Topical anti-fungals (lotions / creams) Dermatophytosis of the skin with the exclusion
of palms, soles and groin is called
Clotrimazole - 1% Local application BD for 15 TineaCorporis
days 1 month.
Miconozole - 2% Local application BD for 15 Well defined scaly annular patches
days 1 month. With or without vesicles, pustules at margin
h. Systemic anti-fungals Single or multiple scattered lesions
Tab. Griseofulvin 10mg/kg/da y for 4 to 6
Itching Present
weeks
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2.1.3 TineaCruris
Infectionof groin area and includes infection of
genitalia, pubic area, perianal and perineal skin.
Treatment:
Topical cream
Clotrimazole - 1% Local application BD for 4-
6 weeks.
Miconozole - 1% Local application BDfor 4-6
weeks.
Systemic
Tab.Griseofulvin 250 to 500 mg BD for 3
weeks
Tab.Fluconczole 150mg one per week X 4 -6
weeks
2.1.4 TineaPedis
Dermatophyte infection of the feet.
Treatment:
Topical cream
Clotrimazole 1% Local application BD for 4-
6 weeks.
Miconozole - 2% Local application BD for 4-6
weeks.
Systemic
Tab. Griseofulvin 250 to 500 mg BD for 3-6
weeks
Tab.Fluconczole 150mg one per week for 4 -6
weeks
2.1.5 TineaManum 2.1.6 TineaUnguium
Dermatophyte infection of palms and inter-digital Dermatophyte infection of nail plate whitish or
areas of hand. brownish yellow discoloration of nail.Separation of
nail bed and nail plate
Page 314
Nails becomes friable and discolored a. Chronic paronychia
Treatment: Infection of nail fold
Erythema and swelling of finger tips
Griseofulvin 1 gm per Day for 4-6 months for
finger nails and 12-18 months for toe nails
b. Intertrigo
Tab.Fluconczole 150mg one per week for 6
Seen over intertrigenous areas,groin,inbetween
months for finger nails & 12 months for toe
toes, be low the neck in children
nails.
Sharply demarcated pol ycyclic erythematous
2.1.7 Candidiasis: eroded patches with satellite pustules
Rule out underlying Diabetes Mellitus.
Caused by yeast like fungi candida albicans
c. Diagnosis
KOH mountDirect examination of scrapings
under microscope from lesions with KOH
mount will reveal budding yeasts with hyphae
or pseudo hyphae.
d. Treatment
Keep intertrigenous areas dry
Treat underlying Diabetes mellitus
Clotrimazole 1% Local application BD for 4-
6 weeks. 2.1.8 Tineaversicolor
Miconozole 2% Local application BD for 4-6
Chronic superficial fungal infection caused by
weeks.
malassezia furfur. Lesion vary color from white,
Tab. Fluconazole 150 mg per week for 4 weeks. pink to brow n usually consisting of coalescing
macules, pa tches with fine scales on trunk and neck.
a. Treatment:
Oral Fluconazole given as single dose of 400 Selenium Sulphide suspe nsion - Local
mg application half an hour before bath for 4
weeks.
b. Locally apply: Clotrimazole 2% solution local application for
Ketoconazole 2% shampoo Local application 4 to 6 weeks
half an hour before bath for 4 weeks.
Page 315
Disseminated herpes zoster occurs in
3. Viral infections immunocompromised individuals
3.1 Herpes Zoster 3.2 Herpes simplex
3.2.1 Infection occurs in two types
a. HSV1 usually responsible for cutaneous,
oropharygeal and ocular infections.
b. HSV2 invol ved in genital infections and
infections of new bor n.
Oral Infections shows vesicle, erosions are
seen on buccal mucosa or perioral skin with
severe pain and high fever.
Vulvovaginitis in female and painful penile
lesions in men with appearance of vesicles and
erosions seen.
3.1.1 Prodromal Symptoms

Pain at the site
Closely grouped reddish papules, vesicles
and pustules in continuous or interrupted
band in one or adjacent dermatomes
Usually unilateral and does not cross the
midline
Thoracic segments most commonly
involved.
3.2.2 Treatment:
Orally Acyclovir 200 mg 5 times daily for 7 days
(1-1-1-2)
3.3 MolluscumContagiosum
3.3.1 Clinical manifestations:
Molluscumcontagiosum A viral infection of the
skin caused by a poxvirus. It is a contagious disease
particularly common in young children. After
approximately two to three months of the virus
incubating, small, round growths begin to emerge.
These are light pink or tan colour and can look
similar to warts. They can sometimes become red
and irritated or have a tiny white depressed spot in
the centre.
3.3.2 Treatment:
Needling
3.1.2 Treatment Curette most commonCryotherapy with
liquid Nitrogen
Tab Acyclovir 800mg 1-1-1-2 x5-7 days. Electrocautery
3.1.3 Herpes Eye:In herpes zoster Topical 50% trichloroacetic acid Twice a
week till resolution
opthalmicus, refer to ophthalmologist for
further management.
3.4 Warts
Fillform or digitate warts
Plantar warts
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a. Common warts:
Firm keratotic papules with rough hor ny
surface
b. Plane warts
Multiple smooth, flat or slightly elevated round
or polygonal papules (1 to 5 mm)
c. Filiform or Digitate
Composed of one or more finger like
projections 2 to 10 mm in length.
d. Planter Warts e. Treatment:
Sharply defined rough keratotic lesion. Spontaneous resolution possible

Topical keratolytics
Surrounded by a smooth collar of thickened 16.7 % salicylic acid and 16.7% lactic acid in
hor n. collodion baselocal application daily till
resolution or
50% Trichloroacetic acid applied weekly
tillresolution or
Topical 5% flurouracil ointment local
application daily till resolution.
Electrocautery or liquid nitrogen therapy
Podophyllin 25 % for genital wart twice
weekly tillresolution.
Cryotherapy with liquid nitrogen for genital
wart
Page 317
Scrofuloderma
4. Cutaneous Tuberculosis
It is infection of skin caused by mycobacterium
tuberculosis. Persons with malnutrition and 4.1.1 Lupus vulgaris:
Immunocompromised patients are prone to Reddish brown plaque which spreads with foci
tuberculosis. of scarring
4.1 Clinical types Has an active advancing edge and areas of
Lupus vulgaris Scarring.
Tuberculosis verrucosa cutis
4.1.2 TuberculosisVerrucosa Cutis: 4.2 Investigations

Indurated warty papule or nodule or a plaque,
with surrounding erythema. TT (Tuberculin Test )
There may be fissuring and di scharge from the Xray chest PA view Screen for pulmonary
surface. tuberculosis.
Irregular extention leads to serpigenous Skin biopsy to confirm diagnosis.
margin.
Treatment after confirmation.
4.1.3 Scrofuloderma:
It occurs over the underlying focus of 4.3 Treatment
tuberculosis like caseating lymph Antituberculous treat ment 6 months
gland,bone,joint etc. 4 Drugs 2 months
Present as painless bluish red swelling which 2 Drugs 4 months
breaks down to from sinus orundermined Refer RNTCP guidelines.
ulcer.
Page 318
2.Non Infectious Skin conditions
1. Urticaria 1.1. Provoking factors
Elevated erythematous itchy swelling i. Drugs
Transient in nature ii. Food

iii. Infection
Worsened by scratching
iv. Stress
Acute < 6 weeks
v. Systemic Diseases
Chronic >6 weeks
Angio-oedema involves the deeper structures
Figure 1 Urticaria
1.2. Treatment 2. Psoriasis

Eradication of the etiological factor
2.1 Clinical features
In acute urticaria with laryngopharyngeal
edema 0.5 to 1 ml of subcutaneous i. Erythematous well defined scaly plaques
epinephrine.
ii. Predominantly extensor aspect of the bod y
iii. Scales are silvery and loosely attached to the
Antihistamines lesion
Cetrizine 10 mg /day for 2 to 4 weeks or iv. Koebner phenomenon (it is isomorphic reaction
to trauma or injury) in which positive new
T. Levocetrizine 5 mg per day for 2 to 4 weeks
lesion occurs at the site of trauma
or
Loratidine 10 mg /day for 2 to 4 weeks.
Severe extensive cases or unresponsive cases

Predinisolone 0.5 to 1 mg /kg per day and
gradually tapered
T.Albendazole 400 mg single dose
Ref to higher centre if no response
Figure 2 Psoriasis
Page 319
Scalp: 3.2 Treatment
Scaling that extends be yond the hair line Topical steroids - Clobetasol Propionate. 0.05
% local application twice daily for 2 weeks.
Nails:
Tab. Cetrizine 10 mg daily for 2 weeks.
Collection of keratotic material under the nail lifting Generalized forms - Systemic steroids like
the distal part of the nail from the nail bed and Nail Tab. Prednisolone 0.5 mg/kg per day.
pitting Gradually tapered over the next 4-6 weeks
Refer to higher centre for extensive lesions.
Joints may be involved
4. PityriasisRosea
2.2 Treatment
i. Potent topical steroids for localized lesion 4.1 Clinical features
Clobetasol Propionate 0.05 % local application Initial lesion 2 to 6 cm circular asymptomatic
twice daily for 2 weeks. erythematous scaly plaque called herald patch
Within days crops of papules and oval patches
ii. Topical keratolytics Salicylic acid 3% or 6% with wrinkling surface and a bor der of fine
twice daily for 2 weeks. scales
iii. Liquid paraffin for external use or use of any Trunk and proximal extremities are commonly
other emollients local application twice daily involved {covered part}
for 2 weeks. Lesion heal with hyper or hypo pigmentation
iv. Tab.Cetrizine 10 mg per day if itching persists

v. 5% Coal tar ointment local application twice
5. Acne
daily for 2 weeks. 5.1 Clinical features
vi. Calcipotriol cream local application twice daily Common in adolescents
for 2 weeks. Present as comedones, papules, pustules, nodules,
Patients with extensive involvement, abscess, cysts, scars
arthropathy, pustular psoriasis, erythrodermic Sites Face, chest, back, shoulder
psoriasis refer to higher centre.
Note: avoid use of systemic steroids.
3. Lichen Planus
Welldefined,violaceous,polygonal flat topped
papules
Itching present
Common Sites : legs and forearm
Koebner Phenomenon + ve
Involvement of hair leads to alopecia Figure 4 Acne
Oral mucosa : lacy network of whitish patche
Differential diagnosis:
Psoriasis
Secondary syphilis
Tineacorporis
Note - Systemic Steroids should be avoided
Treatment:
Mostly do not require treatment
Symptomatic treatment like topical
moisturizers local application BD for 7 days.
Tab. Cetrizine 10 mg per day if itching is
Figure 3 Lichen Planus present
Daily Sun exposure of covered part if possible.
Page 320
Sequelae: Hyper pigmentation and scarring. 5.2.2 Grade II
5.2 Treatment Papules, comedones, pustules:
5.2.1 Grade I Washing of Face with soap and water when it
Comedones / Occasional papules. becomes oily.
Washing of Face with soap and water when it Topical antibiotics Clindamycin local
becomes oily. application BD for 2 weeks.
Removal of comedones by Comedone extractor. Erythromycin 2 to 4% local application BD for
Topical Retinoic acid (0.025%) local 2 weeks.
application HS for half hour for 2 to 4 weeks. Benzoyl peroxide local application HS for half
Benzoyl Peroxide(2.5%) local application HS hour for 2 to 4 weeks.
for half hour for 2 to 4 weeks Retinoic acid local application HS for half hour
for 2 to 4 weeks.
5.2.3 Grade III 6.2 Differential diagnosis
Predominant,pustules,nodules,abscesses;
Early vitiligo
Washing of Face with soap and water when it
becomes oily.
Pityriasisversicolor
Topical benzoyl peroxide local application HS Leprosy
for half hour for 2 to 4 weeks. Post inflammatory hypo pigmentation
Retinoic acid local application HS for half hour
for 2 to 4 weeks.
Azithromycin 500 mg OD 3 days per week, 6.3 Treatment
may be repeated; maximum duration 3 months, Reassurance
or Bland emollients for external application like
Doxycycline 100 mg OD for 2 to 6 weeks, or liquid paraffin local application BD.
Isotretinoin 0.5mg/kg/day for 16 to 24 weeks Multivitamins like SypCalcivit 1 tsf HS for 1
(only after expert opi nion) month.
Treatment of worm infestation if any Tab
Albendazole 400 mg HS single dose.
5.2.4 Grade IV Cap Vit A 50,000 IU OD for 4-6 wks.
Mainly cysts,abscess,widespread scarring
Washing of Face with soap and water when it
becomes oily. 6. Miliaria
Systemic antibiotics and Isotretion as in grade
III
Small discrete itchy non follicular erythematous
Aspiration of cysts
confluent macules or papules forming sheets
Intra-lesional steroids for cysts Inj.
Pricking sensation
Triamcinolone acetonide 10 mg / ml weekly.
Occurs more in summer and heat condition.
5. Pityriasis Alba
6.1 Clinical features 7.2 Treatment
Asymptomatic round or oval hypo- Avoidance of excessive exposure to heat
pigmented scaly patches usually on the Calamine lotion local application BD for 5
face. days.
Single or multiple Antihistamines Tab. Cetrizine 10 mg HS for 5
Spontaneous resolution may recur. days.
Age group 3 years to puberty Tab. Vitamin C 500 mg OD for 5 days.
Loose cotton dresses
Plenty of oral fluids etc.
Page 321
8. Eczema
8.1 Stages
These are synonymous terms signifying
inflammator y response of skin to different
factors
Figure 5 ECZEMA / DERMATITIS
Caused by exogenous or endogenous factors

Generally, 3 stages acute, subacute and
chronic
8.1.1 Acute Stage-Characterised by erythema, oedema, vesicles Azithromycin 250 bd for 5-7 days /
and oozing Cloxacillin 500mg three times a day 5 to 7
days / Amoxicillin-Clavulanic acid - 625 mg
8.1.2 Subac ute stage Erythema, oedema,
bd for 7 days.
vesicles decrease and are replaced by
moderate oozing, crusting & Scaling iii. Emollients like liquid paraffin applied daily.
8.1.3 Chronic Stage Mainly consists of hyper iv. Mild cases Hydrococortisone 1% ointment
pigmentation and lichenfication. Highly daily
pruritic in all stages.
v. Moderate cases Betamethasone 0.1% cream
8.2 Treatment or ointment twice daily
Treatment is according to stage of dermatitis. 8.2.5 Symptomatic relief by anitihistamines
8.2.1Acute eczema
Tab Chlorpheneramine (4 mg) TID as needed or
Wet soaks / compresses of Potassium
permanganate (4-5crystals in 500ml water) Tab Promethazine (10-25 mg) 6-8 hourly as needed
local application 3 times in a day. in severe cases.
Refer to higher centre to confirm diagnosis and for
Antihistaminics Tab cetrizine 10 mg BD for 5
management of complicated cases.
days.
Topical corticosteroids- Clobetasone 0.05 % 8.2.6 Management as per severity
local application 3 times in a day. Mild or moderate infectedEczema
Systemic Antibiotics if secondary infections. Soaks or compresses of plain tepid water or
normal saline
8.2.2Subacute eczema
Severe
Wet compresses for crust removal like acute
Eczema local application 3 times in a day. Tab Prednisolone (5 or 10 mg) 0.5 to 1mg/kg
with gradual tapering, if infection present Tab
Betamethasone or mometasone topical Erythromycin (250 to 500 mg) one tablet QID
application in cream form local application 3 for 5 to 10 days
times in a da y. Tab.Chloropheniramine Maleate (4 mg) one
tablet TID for 5 to 10 days.
Systemic Antibiotics if secondary infections.
8.2.3Chronic eczema
Corticosteroid ointments - Clobetasone
9. Dermatitis
0.05 % local application 3 times in a day. 9.1 Atopic Dermatitis Diagnostic
Feature
Tab Cetrizine 10mg BD for 5 to 10 days. Chronic pruritic dermatitis over face, neck and
8.2.4Acute infected Eczema flexures. Seen mainly in infants &children
i. Wet dressing with light weak pink potassium
permanganate soaks for 5 days where 9.2 Treatment Guidelines
indicated Tab Chlorpheniramine (4 mg) one tablet TID for
ii. Whenever infection is present. It has tobe 3 Days Topical steroid (Clobetasone Butyrate
treated with appropriate antibiotics like cream (0.05%)) local application BD for 3
Page 322
weeks.
Tacrolimus 0.03 % BD X 3 months topically
9.3 General Guidelines Figure 6 Atopic Dermatitis

Use soft non irritating cotton clothing
Use emollients such as oils applied over wet skin.
Avoid foods which tend to aggravate lesions e.g.
nuts, eggs, wheat, cows milk, fish.
Accentuation under Woods lamp
Skin as well as mucous membranes can get
involved.
9.4 Treatment
Moderately potent corticosteroids - fluticasone
/ mometasone cream topically for 6 weeks
Tacrolimus 0.03% for face ; 0.1% for trunk and
extremities for 3 months
Extensive/ resistant cases refer to higher
centre
10. Alopecia areata 10.2 Treatment

10.1 Diagnostic features Moderately potent corticosteroids
Loss of hair in patches (Mometasonefuroate, Fluocinloneacetonide,
Patches of non-scarring alopecia especially over the Fluticasone) for 6 to 12 weeks
scalp and the beard area. Usually round or oval in
shape with a normal appearing superficial skin. 11. Androgenetic alopecia
Asymptomatic, Exclamation mark appearance of the
Underlying susceptibility of hair follicles to
hair
androgenic miniaturization.
Avoid irritating strong soap chemicals
Affects up to 70% of men and 40% of women
Exclusive breast feeding in infants
Treatment:
Review patient after 2 weeks. Topical Minoxidil solution (2 to 5%)BD application
for 4 to 6 months.
9. Vitiligo
9.1 Diagnostic feature
Depigmented macules and patches which can
occur anywhere on the body
Figure 7 Vitilligo
Page 323
3. Sexually Transmitted Infection (STI)
1. Syphilis Tab Erythromycin 500 mg orally QID x 2 weeks
1.1 Early Syphilis c. Follow Up:

1.1.1 Primary Syphilis After treatment the patient should be examined
clinically and serologically once a month for first 3
Causative agent Treponemapallidum months and quarterly till the end of second year
Incubation period -9 to 90 days
Genital ulcer (primary chancre) classical lesion 1.2 Late Syphilis
Regional lymphadenopathy in 50 % of cases In untreated early syphilitic patients will have the late
Primary chancre resolves in 3 to 6 weeks syphilitic manifestations after 5-15 years from the
After 3 weeks of appearance of chancre,VDRL onset of infection.
becomes reactive 1.2.1 Late latent syphilis
Treponemapallidum can be demonstated from the After 2 years from the onset of infection No signs and
chancre symptoms
In the case of untreated primary syphilis, patient may Non-infectious
develop secondary syphilitic lesions in 3-6 months 1.2.2 Late benign syphilis(Gumma)
interval. After 5-7 years from the onset of
infection,Visceralgumma
1.1.2 Secondary Syphilis: 1.2.3 Cardiovascular syphilis
Skin Rash After 10-15 years from the onset of infection
Maculopapular Uncomplicated aortitis
PapulosquamousPsoriatiform Aortic regurgitation, Coronary ostial stenosis Aortic
Annular Pustular Follicular aneurysm
Rash is generalized, bilaterally symmetrical non 1.2.4 Neuro-syphilis
itchy After 10-15 years from the onset of infection
meningitis, meningo-vascular General Paresis of
Mucosal lesion
Insane (GPI),Tabesdorsalis
Snail track ulcers
CNS gumma
Condylomatalata
Painless discrete, rubbery lymphnodes, systemic 1.2.5 Treatment:
manifestations a. Late latent Syphilis and Late Benign Syphilis
Highly reactive VDRL (Gumma)
Inj. BenzathinePenicilin 2.4 mega units IM
Treponemapallidum can be demonstrated from the Weekly for 4 consecutive weeks or
skin lesions, Cutaneousgumma
Inj. Procaine Penicilin 1.2 mega units IM daily
1.1.3 Early latent Syphilis: for 21 days
No Signs and symptoms b. Cardiovascular syphilis and neuro syphilis
2years period is demarcation between early and Inj. Procaine Penicilin 1.2 mega units IM /day for
late latent syphilis 21 days under the cover of steroids.
1.1.4 Treatment:
a. Penicillin treatments c. In Penicilin allergic patients
For all the above 3 conditions Cap.Doxycycline 100 mg orally BD x 4weeks
Injection: Benzathine penicillin 2.4 mega units deep Cap.Tetracycline 500 mg orally QID x 4 weeks
IM after test dose (or)
Tab.Erythromycin 500 mg orally QID (4 Weeks)
b. In Penicillin allergic patients: d. Follow-up
The patient should be monitored at 6 months interval
Cap Doxycycline 100 mg orally BD x 2 weeks clinically and serologically along with repeat cerebro
(or) spinal examination.
Cap Tetracycline 500 mg orally QID x 2 weeks
(or)
Page 324
1.3 Congenital syphilis 2. Chancroid
Untreated early syphilitic mother may deliver a
congenital syphilitic child. 2.1 Clinical features
Causative agent Haemophilusducreyi
1.3.1 Early: Incubation period Usually 3 to 5 days but it can
Skin lesions, Rash,Bullae,Condylomatalata extend upto 14 days.
Lymphadenitis,Hepatosplenomegaly,Osteochond Multiple, painful, non indurated ulcers with
ritis ragged and undermined edges. Floor is covered
CNS, Kidneys, Lungs, Testes involvement. by a yellowish grey necrotic exuda tes ove rlying
1.3.2 Late: granulation tissue that bleeds on manipulation.
Interstitial keratitis In 50% of the patients, a tender inguinal adenitis
Neuros yphilis (usually unilateral) occurs (Inflammatory Bubo)
Bone and joint involvement School of fish appearance in smears
Sensori-neural deafness
Gummatous lesions
Cardiovascular syphilis involvement.
1.3.3 Stigmata:
Bulldog facies
Hutchinsons teeth
Rhagades Salt and pepper Fundus Gummatous
scars.
1.3.4 Treatment:
a. Early:
Inj. Benzathine penicillin 5000 units /kg/day
divided in 6 hourly doses for 7 days.
b. Pat ient Education:
To seek early and appropriate treatment
To avoid sexual contact until the treatment is Figure 1 Chancroid
completed
Insisting epidemiological treatment of sex
partners with regular follow-up
c. Preve ntion: 2.2 Treatment
Sexual abstinence Cap. Doxycycline 100mg oral BD for 14 days or
Avoid high risk behavior Tab. Erythromycin 500 mg orally QID for 14
Consistent and correct usage of condoms days or
Safer sex practices Tab. Azithromycin 1 gm oral stat or
Tab. Ciprofloxacin 500 mg oral BD for 3 days
Page 325
3. LymphogranulomaVenereum 5. Gonorrhoea
(LGV) 5.1 Clinical features
Causative agent Neisseria gonorrhoeae
3.1 Clinical features Incubation period 1 to 14 days
Caused by Chlamydia trachomatis serovars
Presents as urethritis in male and cervicitis in
L1,L2, L3
female
Incubation period 3 to 12 days
Primary Transient genital ulcer Lymphnode s
(bubo)
Figure 3 Gonorrhoea
5.2 Complications
5.2.1 Male:
Posterior urethritis
Figure 2 LymphogranulomaVenereun Infection of cowpers and tysons gland Epididymitis
Prostatitis
Tertiary complications include:
Seminal Vesiculitis
Elephantiasis of genitalia
Fistulae Strictures Peri-urethral abscesses
5.2.2 Fe male:
3.2 Treatment Salpingitis, Peritonitis, PID
Cap. Doxycycline 100mg oral BD for 3 weeks (
or) Bartholinitis,Proctitis
Tab. Erythromycin 500mg oral QID for 3 weeks Chronic urethritis
4. Venereal granuloma 5.2.3 Other forms:
(Donovanosis) Disseminated gonococcal infection
Gonococcal arthritis
4.1 Clinical features Meningitis
Causative agent- Anorectal and
Calymmatobacteriumgranulomatis Pharyngeal gonorrhea
Incubation period 1 to 3 months
Granulomatous ulcer 5.3 Treatment
Calymmatobacteriumgranulomatis (Donovan Tab.Azithromycin 2 g oral stat (or)
bodies)seen inside large mononuclear cells in InjCeftriaxone 250 mg IM stat
tissue smears.
6. Non gonococcal urethritis
4.2 Treatment
6.1 Clinical manifestation
C. Doxycycline (100mg)BD or T.Cotrimoxazole
(800mg + 160 mg) BD or Causative agent
InjCeftrioxone 250 mg single dose IM Chalmiydia trachomatis ureapalsmaurealyticum,
14 to 21days or Mycopa smagenitalium
T. Erythromycin (500mg) 4 times a day in Urethritis
pregnant women for14 Days or Increased polymorphononuclear leucocytes in
Inj. Ceftriaxone (1gm) daily IM injection for 7 uretheral smear or sediment of first voided urine.
days 7. Chlamydial infections
Page 326
Agent Chlamydia trachomatis 9.3 Treatment
Incubation period -1 to 3 weeks
Tab. Metronidazole 400 mg bd for 14 days (or)
7.2.1 Male: Tab. Secnidazole 2g stat dose
Urethritis
Littritis 10. Candidiasis
Epididymitis
Prostatitis 10.1 Clinical features
Proctitis Predominantly caused by candida albicans
Reiters syndrome
Predisposed by pregnancy, diabetes, HIV and
immunosuppression
7.2.2Female:
Cervicitis, Urethritis,Bartholinitis
Endometritis,Salpingitis
Fitz HughcurtisSyndrome (It is fever with lower
abdoman pain after cervical movement. There are
adhesions in pelvic cavity, may lead to infertility.)
7.3 Treatment
Tab.Azithromycin 1 gm oral stat (or)
Cap Doxycycline 100 mg oral BD for 14 days
(or) Tab Erythromycin 500 mg QID for 14 days.
8. Bacterial Vaginosis
8.1 Clinical aspects Figure 4 Warts (CondylomataAcuminata)
Polymicrobial Syndrome
GardnellaVaginalis
Causes Balanoposthitis in males
Mycoplasma hominisBacteroids
Clinically erythema and swelling with a macular
Excessive,homogenous,unifor mlyadherent /papular rash over glans penis.
vaginal discharge, elevated Vaginal pH > 4.5
A white Subpreputial discharge ,increased skin
Positive Amine test (Whiff test) Marking, Fissuring of the glans and Fore skin
Presence of Clue Cells (Epithelial cells occasionally regional lymphadenopathy may be
studde d with organisms) present
Causes vulvo vaginal candidiasis in females -
8.2 Treatment oedema, fissures, erosions, curdy white
Tab Metronidazole 400 mg BD for 14 days (or) discharge.
Tab Secnidazole 2g stat dose Demonstration of candidiasis by 10 % KOH
Yeast cells, mycelia seen.
9. Trichomoniasis
10.2 Treatment
9.1 Epidemiology Commonly used antifungals include oral fluconazole
Caused by trichomonasva ginalis and topical clotrimazole.
Incubation period 4 to 28 days Vaginal candidiasis a single dose of oral fluconazole
(150mg)
9.2 Clinical features diagnosis
Clotrimazolepessary for 7 days daily
Copious, homogenous, malodorous, yellowish
green va ginal discharge Clotrimazole cream (1%) or miconazole cream (2%)
Punctuate hemorrhages over cervix Strawberry daily bd
cervix Application for 7 to 14 days
Demonstration of motile trichomonads in wet
film smears under direct microscopy 11. Warts(CondylomataAcuminata)
Culture gold standard for diagnosis
Page 327
Caused by Human papilloma Virus Predominantly By HSV -2 also by HSV 1
Incubation period 1 to 8 month Incubation period 5 to 14 days
Skin coloured multiple verrucous lesions
Ballooning degeneration and giant cells seen in
11.2 Treatment HPE
Topical podophyllin 25 % local application twice Primary Severe associated with systemic
weekly. symptoms starts as grouped vesicles ulcerate -
pol ycyclic margin
Cryotherapy
Cautery Recurrence less severe
Surgery
12. Herpes Genitalis

12.2 Complications
CNS involvement dissemination Secondary infection
Recurrence
Transmissible during pregnancy and de livery
11.3 Treatment
11.3.1 For Primary
Tab Acyclovir 200 mg 5 times a day for 7 days
Figure 5 Herpes Genitalis 11.3.2 For Recurrence

Tab Acyclovir 400 mg 3 tims a day for 5 days
Page 328
4.SYNDROMIC MANAGEMENT OF STD
1. Syndromic Approach 2. Why Syndromic

Provision of STI/RTI care services is a very Management
important strategy to prevent HIV transmission
and promote sexual and reproductive health STI signs and symptoms are rarely specific to a
particular causative agent.
under the National AIDS Control Programme
(NACP III) and Respective and Child Health Laboratory services may not be available.
(RCH II) Dual infections are quite common and both
Syndromic case management (SCM) with clinician and labor atory may miss one of them.
appropriate laboratory tests is the cornerstone of Waiting time for lab. Results may discourage
STI/RTI management under NACP III. some patients.
SCM is a comprehensive approach for STI/RTI Failure of cure at first contact.
control endorsed by the WHO.
Diagnosis is based on the identification of 3. The common STD
syndromes, which are combi nations of the
symptoms the client repor ts and the signs the Syndromes
health care provider observes. Genital ulcer diseases
The provision of the most effective therapy at Urethral discharge
patient's first contact with a health or medical Vaginal discharge
facility. Bubo ( inguinal Swelling)
The recommended treatment is effective for all Lower abdominal pain in female
the diseases that could cause the identified Scrotal swelling
syndrome. Ophthalmianeonatorum
Provides single does treatment as far as
possible. Syndromic approach for STI s is useful and practical
Comprehensive to include patient education on strategy for offering , high quality, effective and
risk reduction, counseling, condom promotion acceptable care for prevention and treatment of
and provision, partner notification, follow up. sexually transmitted infections (Guidelines from
National Aids control Organization (NACO) has
been used)
Table 1:NACO Guidelines
Kit Color Compostionof kit Syndrome / disease
1) Gray Tab.Azithromycin 1 g stat + Tab. Urethral discharge (UD), Cervical, discharge (CD),
Cefixime 400 mg. anorectal discharge (ARD), Presumptice treatment
(PT), Painful scrotal swelling.
2) Green Tab.Secnidazole 2 g stat + cap. VD {Vaginal discharge.}

Fluconazole 150 stat
3) White Inj.BenzathinePenicilin 2.4 MU IM Genital ulcerative disease (GUD); non herpetic)

stat + Tab Azitromycin 1 g stat
4) Blue Cap Doxycycline 100 mg BD for15 (GUD); non herpetic)

days + Tab Azitromycin 1 g stat
5) Red Tab Acylovir 400 mg TDS for 7 (GUD); herpetic)

days
Page 329
6) Yellow Tab Cefixime 400 mg stat + Tab. Lower abdominal pain (LAP)
Metronidazole 400 mg BD for 14
days + Cap. Doxycycline 100 mg
BD for 14 days.
7) Black Cap doxycycline 100 mg BD for 21 IB { Inguinal Bubo}

days + Tab Azitromycin 1 g stat
Page 330
5. HIV AIDS
1. HIV
Invades the helper T cells (CD4 cells) in the body of 2. AIDS
the hos t (defense mechanism of a person)
Acquired Immunodeficiency Syndrome HIV is the
Human Immunode ficiency Virus A unique type of virus that causes AIDS
virus (a retrovirus)
Disease limits the bodys ability to fight infection
Preventable, managable but not curable. due to markedly reduced helper T cells.
Patients predisposed to multiple opportunistic
infections leading to death.
Figure 1 The Viral genome
Lasts for an average of ten years

3. Modes of HIV/AIDS This stage is free from symptoms
Transmission There may be swollen glands
The level of HIV in the blood drops to low
Through Bodily Fluids levels
Blood products Semen and Vaginal fluids HIV antibodies are detectable in the blood
Sharing Needles without sterilization Increases

the chances of contracting HIV 4.3 Stage 3 Symptomatic
Unsterilized blades The immune system deteriorates
Through Sex Unprotected Intercourse Oral, Opportunistic infections and cancers start to
sexual, Anal appear.
Mother-to-Baby - Before Birth, During Birth,
After Birth 4.4 Stage 4 - HIV AIDS
The immune system weakens too much as CD4
4. Stages cells decrease in number.
4.1 Stage 1 Primary
Short, flu-like illness - occurs one to six weeks
after infection 5. Opportunistic Infections
Mild symptoms associated with AIDS
Infected person can infect other people
CD4<200
4.2 Stage 2 Asymptomatic Bacterial infections, Tuberculosis (TB), Herpes
Page 331
Simplex, Herpes Zoster, Vaginal candidiasis, Hairy 1% in HIV)
leukoplakia, Kaposis sarcoma
5.1 Tb & HIV Co-Infection 6. Testing Options for HIV

TB is the most common opportunistic infection in 6.1 Anonymous Testing
HIV and the first cause of mortality in HIV infected No name is used
patients (10-30%) Unique identifying number
10 million patients co-infected in the world. Results issued only to test recipient
Immuno-suppr ession induced by HIV modi fies the
clinical presentation of TB: Subnormal clinical and 6.2 Blood Test
roentgen presentation
High rate of MDR/XDR
High rate of treatment failure and relapse (5% vs<
Blood Detection Tests :Table No: 1
HIV enzyme-linked immunosorbent assay (ELISA) Screening test for HIVSensitivity> 99.9%
Western Blot
Confirmatory test
Specificity> 99.9% (when combined with ELIZA)

HIV rapid antibody test
Screening test for HIV
Simple to perform
Absolute CD4 lymphocyte count Predictor of HIV progression
Risk of oppor tunistic infections and AIDS when

<200
HIV viral load tests Best test for diagnosis of acute HIV
infection correlates with disease
progression and response to HAART
7. Treatment Options
7.1 Treatment of opportunistic infection
Table 1 : Managing Ols before starting ART

Drug reaction Do not start ART during an acute reaction
Acute diarrhea which may reduce absorption of ART Diagnose and treat first, start ART when diarrhea is
stabilized or controlled
Non-severe anemia ( Hb<8g/ liters) Start ART if no other causes for anemia are found (
HIV is often the case of anemia ): avoid AZT
Skin conditions such as PPE and sebor rhoeic Start ART (ART may resolve these problems)
dermatitis, psoriasis, HIV-related exfoliative
dermatitis.
Suspected MAC , cryptosporidiosis and Start ART (ART may resolve these problems)
microsporidiosis
Cytomegalovirus infection Treat if drugs available; if not, start ART
Page 332
Table 1 : Managing Ols before starting ART
Toxoplasmosis Treat; start ART after 6 weeks of treatment and when
patient is stabilized.
Figure 2 HAART = highly active anti retroviral treatment
7.2 Antiretroviral Therapy Regimens adva ntages (procurement and stoc k management),
improve adherence to treatment and thus reduce
Currently, the national programme provi des the the chances of development of drug resistance.
following drugs/ combinations for first-line The current national experience show that bid
regimen. (twice a day) regimens of FDCs are well tolerated
Fixed- dose combinations (FDCs) are preferred and complied with.
because they are easy to use, have distribution
Page 333
Table 2 : Revised NACO ART Regimen 2012
Regimen I Zidovudine + First line Regimen for patients with Hb 9 gm/dl and not on
concomitant ATT
Lamivudi ne +
Nevirapine
Regimen I (a) Tenofovir + First line Regimen for patients with Hb< 9 gm/dl and not on
concomitant ATT
Lamivudi ne +
Nevirapine
Regimen II Zidovudine + First line Regimen for patients with Hb 9 gm/dl and not on
concomitant ATT
Lamivudi ne +
Efavirenz
Regimen II (a) Tenofovir + First line Regimen for patients with Hb< 9 gm/dl and not on
concomitant ATT. First line for all patients with Hepatitis B and /
Lamivudi ne +
or Hepatitis C co-infection First line Regimen for pregnant
Efavirenz women,with no exposure to sd-NVP in the past.
Regimen III Zidovudine + Regimen for patients on AZT containing first line regimen, who
develop toxicity to both NVP and EFV Also second line regimen
Lamivudi ne +
for those who are on TDF containing first line regimen if Hb 9
+ Atazanavir/ gm/dl
Ritonavir
Regimen III (a) Tenofovir + For patients of regimen III who develop severe Atazanavir
toxicity First line regimen for patients with HIV-2 infection with
Lamivudi ne +
Hb 9 gm/dl
+ Lopinavir /
Ritonavir
Regimen IV Tenofovir + Second line regimen for those who are on AZT / d4T containing
regimen in the first line. Also for patients on TDF containing first
Lamivudi ne +
line regimen who develop toxicity to both NVP and EFV.
Atazanavir / Ritonavir
Regimen IV (a) Tenofovir + For patients on regimen IV who develop severe Atazanavir
toxicity First line Regimen for patient with HIV 2 infection with
Lamivudi ne +
Hb 9 gm/dl First line Regimen for all women exposed to sd-
Lopinavir /
NVP in the past.
Ritonavir
Regimen V Stavudine + Second line for those who are on TDF containing regmen in the
Lamivudi ne + first line if Hb 9 gm/dl
Atazanavir / Ritonavir
Regimen V (a) Stavudine + For patients on Regimen V who develop severe Atazanavir
Lamivudi ne + toxicity.
Lopinavir /
Ritonavir
Page 334
Antiretrovi ral Drugs Higgly active anti 9. Post Exposure Prophylaxis
retrovovival treatments
(PEP)
Nucleoside Reverse Transcriptase inhibitors
(NRTI) Steps to be taken on exposure to HIV
AZT (Zidovudine), Lamividine, Ditanosine, infected blood, body fluids and contaminated
Abacavir, Empricitadine, Tinofavir (Nt RTI) sharps etc
Non-Nucleoside Transcriptase inhibitors 1. Actions to be taken
(NNRTI) Immediately following on expos ure:
Viramune (Nevirapine), Effvirenz
Protease inhibitors (PI) i. Needles pricks and cuts should be washed
Ritonavir, Lopinavir with soap and water
ii. Splashes to the nose, mouth or skin should be
8. Primary Prevention flushed with water
Five ways to protect yourself: iii. Eyes should be irrigated with clear water,
saline or sterile irrigant
Abstinence
iv. Do not pa nic
Monogamous Relationship
Protected Sex v. Pricked finger should not be put in to mouth
Sterile needles by reflex
New shaving/cutting blades vi. Do not squeeze the pricked finger to expel
the contaminated blood
vii. PEP should be started within 72 hours of
expos ure, within 2hrs is ideal.
2. Post Exposure Prophylaxis (PEP)
The decision to start PEP is made on the basis of

degree of expos ure to HIV and the HIV status of
the source from where the expos ure infection has
occurred.
2.1 Exposure Code Determination
Page 335
Figure 3 Exposure Code Determination
Is the source of material blood, body fluid, other potentially

infectious material (OPIM) or an instrument contaminated with one
of these substances
YES No No PEP Needed
OPIM Blood or Body Fluid
What Type of Exposure has occured
Mucous membrane or Skin Intact Skin only Percutaneous

integrity contaminated Exposure
Volume No PEP needed Severity
Small i.e. Few drops, Large e.g. several Less severe e.g. solid More severe e.g.
short duration drops major blood needle superficial large base hollow
splash and / or scratch needle, deep
longer duration punctures, visible
(i.e. several blood or device,
minutes or more) or needle used in
source patients
EC1 EC2 EC2 EC3
Page 336
2.2 Determination of HIV status of source :
Figure 4 Exposure Source
THE HIV STATUS OF THE EXPOSURE SOURCE
HIV NEGATIVE HIV STATUS SOURCE

POSITIVE UNKNOWN UNKNOWN
NO PEP
NEEDED
LOWER TITRE HIGHER TITRE EXPOSURE

EXPOSURE (e.g. (e.g. ADVANCED AIDS
ASYMPTOMATIC AND PRIMARY HIV INFECTION &
HIGH CD4 COUNT ) HIGHER INCREASING VIRAL
LOAD OR LOW CD4 COUNT )
HIV SCI
HIV SC2
HIV SC
UNKNOWN
Page 337
2.3 Pep recommendation based on exposure code & source code
Figure 5 PEP
EC HIVSC PEP Recommendation
1 1 PEP may not be warranted
1 2 Considered basic regimen
2 1 Recommend basic regime
(mos t expos ures are in this category)
2 2 Recommend expanded regimen
3 1 or 2 Recommend e xpa nded regimen
2/3 Unknown If the source (in the case of an unknown source) the settings were the exposure
occurred suggested a possible risk for HIV
exposure and ec 2 or 3 consider PEP basic regimen
*- Details of Exposure code at Annexure 1

** - Details of HIV Source Code at Annexure 2
a. In case of intolerance to Efavirenz, regimen a. containing Tenofovi r + Lamivudine + Pl

b. (ATV/r or LPV/r) can be used after expert dose should be given at bed time with clear
consultaion by an experienced physician. instruction to take it 2-3 hours after dinner & to
avoid fatty food in dinner.
2.4 PEP regimen
c. Wherever PEP is indicated and source is ART 2.5 In case of Sexual Assault :
nave or unknown: recommended regimen is
3 PEP should be provided to exposed person in case
Tenofovir 300 mg + Lamivudine 300 mg +
of sexual assault as a part of overall package of
Efavirenz 600 mg once daily for 28 days.
post sexual assault care.
Wherever available, single pill containing these
formulations should be used. Dual drug regimen
should not be used any longer in any situation for
PEP.The first dose of PEP regular should be
administered as soon as possible, preferably
within 2 hours of expos ure and the subsequently
Page 338
PSYCHIATRY
Page 339
1.MENTAL ILLNESS
tosevere impairment in Social and
1. Introduction Occupa tionalfunctioning).
15 to 20 % of general population suffers from Schizophrenia.
major or minor type of psychiatric illness Bipolar Mood Disorder.
causing significant degree of morbidity &
Major Depressive Disorder.
mortality in society.
It is therefore necessary to know about 2.1.2 Other disorders
commonly occurring mental illnesses & their
primary management. a) Anxiety disorders -
General Anxiety disorders.
Phobias.
2. Classification of Psychiatric Obsessive & Compulsive Disorders.
Disorders Somatoform Disorder and Conversion Disorder.
b) Special Group Disorders -

2.1 Psychiatric illnesses can be
Dementia/ Alzheimers Disorder.
broadly divided into two Substance use disorder.
categories: Children and Adolescent Disorder.
2.1.1 Major psychiatric illnesses (Abnormality in Intelligence Disability Disorder.
thinking,e motions, and behavior leading Psychiatric Emergencies ex. Suicide, violence.
Page 340
2. EVALUATION: HISTORY& MENTAL
STATUS EXAMINATION (MSE)
History: Data from patient (subjective) / from procedures, head injury, Epilepsy and Medico-
reliable informant (objective) Legal issues.
Demographic details:- Family h /o of ps ychiatric illness, addictions,
o Name suicide.
o Sex/Age Developmental history.
o Address Level of education.
Presenting complaints:-Onset/duration/progress. Occupational history.
Past h /o of psychiatric illness/treatment. Marital history.
Past h/o of medical illnesses (Hypertension, Personal history - anyaddiction.
Diabetes, TB, Enteric Fever etc) / surgical Premorbid personality.
Table No 2.1: Mental Status Examination For mat
1. Appearance Tidy untidy

Appropriately dressed Over dressed
2. Attitude Cooperative Uncooperative
3. Behavior (psychomotor DullNor malIncreased
activity)
4. Eye to eye contact PresentAbsent
5. Rapport Established Difficult to Establish
Not Established
6. Speech NormalMute Speaking very few wordsOver talkative
CoherentIncoherent
RelevantIrrelevant
Flight of ideas Thought block
7. Mood Euthymic AnxiousIrritable
Elevated SadDepressed
8. Affect NormalCheerfulHappy Tearful
Depressed Blunt
9. Hallucinations (Abnormal AuditoryVisual OlfactoryTactile
perception without external Gustatory
stimulus)
10. Delusions (Firm & false Persecution Grandiosity Reference Infidelity
belief)
11. Obsessive Cleaning WashingArranging
thoughts/compulsive RitualsVerbal
behaviors
12. Suicidal/Homicidal ideation PresentAbsent
13. Level of consciousness Alert DrowsyStuporous
14. Orientation TimePlace Person
15. Attention & concentration SustainedNot sustained
16. Memor y IntactImpaired
17. Intelligence Average Below average
18. Judgment IntactImpaired
19. Insight PresentAbsent
**Delusions and Hallucinations are the cardinal features of Schizophrenia / Psychosis

Page 341
3. SCHIZOPHRENIA
Anxious and fearful affect.
1. Introduction Poverty of speech.
Delusion of Persecution and/or Reference.
Schizophrenia is a mental disorder of chronic nature
in which there is primary impairment of thought s, Audi tory Hallucinations.
emotions and behavior which leads to sever socio- Lack of Insight.
occupational impairment and personality Impaired Judgment.
deterioration.
4. Investigations
2. Symptoms No diagnostic investigations available.
Suspiciousness. Complete Haemogram, Blood Sugar, Renal
Fearfulness. Function Test, Liver Function Test, Serum
Social withdrawal. Electrolytes, Urine Routine, Chest X-Ray (If
Muttering / smiling to self. necessary).
Poor self care.
Disturbed sleep.
5. Complications
Work impairment. Severe agitative behavior,
Homicidal tendencies,
3. Signs Self harm / Suicidal behavior.
Unkempt appearance. Catatonic Stupor/Excitement.
Increased or decreased Psychomotor activity.
6. Treatmentand Management:
6.1 Antipsychotics:Primary care phys ician can start single drug a nd titrate it up to o ptimum level
Table No3.1 Antipsychotics
Name Strength Recommended doses** Duration/ Remark

Trifluoperazine 5mg 10-40 mg/day Drugs to be started in low
Trihexyphenidyl 2mg 2-6 mg/day dos es and gradually
Haloperidol 5mg 10-30mg/day increase till 80 %
Risperidone 2mg 4-8mg/day improvement.
Olanzepine 5mg 5-20mg/day
Quetiapine 50/100mg 50-300mg/day Maintenance doses to be
Clozapine 50mg 50-200mg/day continued long term
Chlorpromazine 50mg 50-200mg/day
To be given in divided doses:- It is to be monitored by ps ychiatrist.
6.2 Sedatives:
Table No3.2 Sedatives
Name Strength Recommended doses Duration/ Remark

Lorazepam 2mg 1-4mg HS Drugs to be started in low
Diazepam 5mg 5-10mg HS doses preferably at night
Clonazepam 0.5mg 0.5-1mgHS and to be tapered off
Nitrazepam 5mg 5-10mg HS within 2 weeks
Page 342
6.3 Modified Electro-Convulsive 6.5 Maintenance Therapy:
Therapy: All patients with Schizophrenia have to be
Minimum of 8-15 sessions of modified ECT are maintained on long term antips ychotics oral or
required. injectable treatment.
Depot Inj:
6.4 Treatment and Management of Inj Haloperidol Decanoate 50mg once a month deep
Complications: IM
Inj. Haloperidol 10mg BD/ SOS for 2/3 days. OR
Inj. Promethazine* 50 mg BD/ SOS for 2/3
days Inj Fluphenazine 25mg once a month deep IM.
(*Not to exceed 100mg/da y.) OR
Elecro-convulsive Therapy. Inj Flupe nthixol 40mg once a month deep IM.
Inj. Diazepam 10mg or Lorazepam 4mg if
required.
6.6 Side effect & management:

Table No3.3 Common Side Effects and Management
Side Effect Manage ment Durat ion/ Remark

Tremors at extremities/ Salivation Trihexyphenidyl 2-6mg along with antipsychotic
drugs.
Dystonic Reaction/ Rigidity Inj. Promethazine 50mg Stat / SOS SOS
Dry Mouth/Constipation Reduce dos e of Trihexyphenidyl 1 week
Neuroleptic Malignant Syndrome Stop Antipsyc hotics Till patient recovers and CPK level
(Rigidity, Fever, Disorientation, comes to normal.
Inj Lorazepam, Tab.
Reduced urine output)
Bromocriptine, Supportive
Management
6.7 Counseling and Psychotherapy

Refer to higher centre if needed.
Page 343
4. BIPOLARMOOD DISORDER
1. Introduction 5. Signs of Depression
Distinctive episodes of abnormally and Dull, withdrawn.
persistently elevated, expansive, irritable or Poor eye contact.
depressive mood. Decreased productivity of speech.
Patient may be in Mania or Depression or Crying spells.
present with mixed features. Feelings of guilt.
Suicidal thoughts, ideas & plans.
2. Symptoms of Mania Decreased appetite.
Over talkative. Sleep disturbances.
Hyperactive.
Over familiar/ Over religious/
Overspending/Over grooming. 6. Investigations
Big talks. No diagnostic investigations available.
Decreased need for sleep. Complete Haemogram, Blood Sugar, Renal
Work Impairment. Funtion Test, Liver Function Test, Serum
Electrolytes, Urine Routine, Chest X-Ray (If
necessary).
3. Signs of Mania
Increased psychomotor activity.
Pressured speech/ flight of ideas.
7. Complications
Grandiosity. 7.1 Mania:
Easily distractible/ irritable. Severe agitative behavior,
Hypersexual behavior. Homicidal tendencies.
Audi tory hallucinations of God/ Actors talking to
him. 7.2 Depression:
Self harm / Suicidal behavior.
4. Symptoms of Depression
Persistent and pervasive low/ sad mood.
Lack of energy/interest/initiative.
8. Treatment and Management
Hopelessness/ worthlessness/ helplessness. of Mania
Feeling of guilt, agitation. 8.1 Antipsychotics:
Suicidal ideas/ attempts. Primary care physician can start single drug a nd
Decreased sleep, appetite and libido. titrate it up to optimum level
Sometimes hearing of voices.
Work impairment.
Table No 4.1 Antipsychotics
Name Strength Recomme nded doses** Durat ion/ Remark

Trifluoperazine 5mg 10-40mg/da y Drugs to be started in low
Trihexyphenidyl 2mg 2-6 mg/day dos es and gradually
Risperidon 2mg 4-8mg/day increase till 80 %
Olanzepine 5mg 5-20mg/day improvement.
Quetiapine 50/100mg 50-300mg/day
Chlorpromazine 50mg 50-200mg/day Maintenance doses to be
continued long term
**To be given in divided doses
Page 344
8.2 Sedatives:
Table No 4.2 Sedatives

Lorazepam 2mg 1-4mg HS Drugs to be started in low
Diazepam 5mg 5-10mg HS doses preferably at night
Clonazepam 0.5mg 0.5-1mg HS and to be tapered off
Nitrazepam 5mg 5-10mg HS within 2 weeks.
8.3 Mood Stabilizers

Table No 4.3 Mood Stabilizers

Carbamazipine 100/200mg 100 to 600mg/ da y Drugs to be started in low
Lithium 300mg 300 to 900mg/da y dos es and gradually
Divalproex 250/500mg 500 to 1500mg/da y increase till 80 %
improvement.
Maintenance doses to be
continued long term .
8.4 Side effects of mood Modified Electro-Convulsive

stabilizer: Therapy: Minimum of 8-15 sessions of modified
Carbamaz epine- Giddiness, blurred ECT are required.
vision, rash, hypotension.
Lithium- Tremors, muscle twitching, 9. Treatment and Management
disorientation.
Divalproex Sodium-Gastric irritation, of Depression
weight gain, lethargy, confusion, 9.1 Antidepresent:
tremors. Primary care physician can start single drug a nd
titrate it up to optimum level.
Table No 4.4 Treatment and Management of Depression

Imipramine 25mg 50 to 150mg/da y To be started in low doses
Amitriptyline 25mg 50 to 150mg/da y & gradually increase till
Sertraline 25/50mg 25 to 100mg/da y 80 % improvement. To
Escitalopram 5/10mg 5 to 20mg/da y continue at least 6 months
Mirtazapine 7.5/15mg 15 to 30mg/da y & more if necessary
Desvenlafaxin 50mg 50 to 100mg/da y
9.2 Sedatives
Table No 4.5 Sedatives

Lorazepam 2mg 1-4mg/HS Drugs to be started in low
Diazepam 5mg 5-10mg/HS doses preferably at night
Clonazepam 0.5mg 0.5-1mg/HS and to be tapered off
Nitrazepam 5mg 5-10mg/HS within 2 weeks
Page 345
9.3 Modified Electro-Convulsive 9.5 Precautions for Suicidal patients
Therapy:8-15 sessions if needed. 24 hrs continuous supervision.
Do not isolate the patient.
9.4Treatment and Management of Do not keep any sharp objects, ropes,
blades near patient.
Complications during Mania: Do not allow patient to lock room/
Inj. Haloperidol 10mg BD/ SOS for 2/3 bathroom from inside.
days.
Inj. Promethazine* 50 mg BD/ SOS for 2/3 Note - Reduce doses of mood stabilizers if above
days ( *Not to exceed 100mg/day) side effects are seen.
Elecro-convulsive Therapy.
Inj. Diazepam or Lorazepam 1 amp stat if 9.6 Counseling and Psychotherapy
needed. Refer to higher centre if needed.
In case of Depression,Elecro-convulsive
Therapy 8-12 sessions if patient shows
suicidal tendencies.
Page 346
5.MAJOR DEPRESSIVE DISORDER (MDD)
Sometimes psychotic symptoms like
1. Introduction hallucination and reference ideas.
Depression is major public health problem.
Atypical symptoms,
By 2020, it will be the major cause of worldwide o Overeating
morbidity and mortality. o Oversleeping
MDD is a disabling condition that severely o Agitation
affects a persons family work, sleeping, eating o Decreased libido
habits and general health
It is the leading cause of suicide.
4. Investigations
2. Types: Mild, Moderate, No diagnostic investigations available.
Severe. Complete Haemogram, Blood Sugar, Renal
Funtion Test, Liver Function Test, Serum
Electrolytes, Urine Routine, Chest X-Ray (If
3. Signs and Symptoms of necessary).
MDD
Pervasive and persistent low mood.
Low self esteem.
5. Complications:
Self harm / Suicidal behavior.
Loss of interest or pleasure in normally enjoyed
activities.
Lack of energy and e nthusiasm, easy fatigue.
Loss of appetite, weight loss
6. Treatment and Management
Disturbed sleep. of Depression
Hopelessness, Helplessness, worthlessness.
Suicidal thoughts, ideas or attempts. 6.1 Antidepressants:
Table No6.1 Treatment and Management of Depression
Name Strength Recomme nded doses Durat ion/ Remark

Imipramine 25mg 50 to 150mg/da y To be started in low doses &
gradually increase till 80 %
Amitriptyline 25mg 50 to 150mg/da y improvement. To continue at least
Sertraline 25/50mg 25 to 100mg/da y 6 months & more if necessary.
Escitalopram 5/10mg 5 to 20mg/da y
Mirtazapine 7.5/15mg 15 to 30mg/da y
Desvenlafaxin 50mg 50 to 100mg/da y
6.2 Sedatives:
Table No6.2 Sedatives

Lorazepam 2mg 1-4mg/HS Drugs to be started in low doses
preferably at night and to be
Diazepam 5mg 5-10mg/HS
Page 347
Clonazepam 0.5mg 0.5-1mg/HS tapered off within 2 weeks
Nitrazepam 5mg 5-10mg/HS
**To be given in divided dosesIf Psychotic features are present, add low dose antipsychotics.
6.3 Modified Electro-Convulsive

Therapy:8-15 sessions are required.
6.4 Treatment and Management of Precautions for Suicidal patients
24 hrs continuous supervision.
Complications Do not isolate the patient.
Elecro-Convulsive Therapy Do not allow patient to lock room/ bathroom
Daily ECTs(if needed), minimum for three from inside.
days.
Counseling and Psychotherapy play a major role.
Refer to higher centre if needed.
Page 348
6. ANXIETY DISORDER
of public places, closed spaces, heights, animals,
1. Introduction water etc.
Anxiety is a nor mal emotion experienced by
everyone at times of stress.
Symptoms of anxiety are psychological, physical 2.4 Post Traumatic Stress Disorder
or mixture of bot h. (PTSD):
Anxiety becomes a disorder when symptoms Disabling fear, intrusive flashbacks or vivid
become severe, disabling and reduce quality of dreams and emotional disturbances after
life. traumatic life event causing avoidance of similar
Anxiety spectrum disorders tend to be chronic. situations.
2. Presentation 2.5 Obsessive Compulsive Disorder:

Frequent intrusive thoughts producing
apprehension and fear or worry and leading to
2.1 Generalized Anxiety Disorder compulsive, repetitive behavior aimed to reduce
(GAD): the anxiety.
This involves excessive, unrealistic worry and
E.g. Frequent thoughts of contamination leading
tension without any definite reason.
to compulsive washing. Frequent checking of
Signs and Symptoms
locks, gas knobs, counting money etc.
Palpitation, dry mouth, tremors, sweating,
difficulty in breathing, frequency of urination,
abnormal feeling in the gut, muscle tension,
dizziness. 2. Investigations
No diagnostic investigations available.
2.2 Panic Attacks: Complete Haemogram, Blood Sugar, Renal
Can occur in pa tients with GAD Funtion Test, Liver Function Test, Serum
Signs and Symptoms include all of the above Electrolytes, Urine Routine, Chest X-Ray (If
with severe choking sensation and s hortness of necessary).
breath with impending feeling of death or going
crazy. The attack lasts for few minutes and
subsides on its own. 3. Complications
If panic attacks occur frequently, then it is called
as Panic Disorder. Any of the anxiety spectrum disorder can lead to
Major Depressive Disorder making person vulnerable
to suicide.
2.3 Phobia:
Intense and irrational fear of a specific object or 4. Treatment and Management
situation leading to phobic avoidance. E.g. Fear IncludesDrug and Non Drug Treatment.
Page 349
4.1 Drug Treatment
Table No 6.1 Drug Treatment
Drug Treatment Durat ion/ Remarks

SSRIs (Any O ne) As anxiety disorders tend to be chronic, treatments
1. Escitalopram 10-20mg/day should be give n for long duration.
2. Paroxetine 12.5-25mg/day
3. Mirtazepine 7.5-15mg/day
4. Fluvoxamine 50-150mg/day (Preferred in OCD)
5. Sertraline 25-50mg/day
TCA
Clomipramine 25-75mg/day
Anxiolytic Drugs(Any O ne)

6. Clonazepam 0.5-1mg/da y
7. Lorazepam 1-2mg/da y
8. Diazepam 5-10mg/day
-Blocker
Propranolol 10-40mg only in panic disorder
4.2 Non Drug Treatments

Table No 6.2 Non drug Treatment
Reassurance
Supportive Therapy
Relaxation Therapy
Expos ure and Response Preve ntion Therapy
Cognitive Behavior Therapy
Yoga and Exercises
Self help techniques
*Comprehensive treatment including drugs and psychotherapies are most effective .
Page 350
7. SOMATIZATION DISORDER
1. Introduction 3. Conversion Reaction
Excessive thoughts, feelings or behavior related Altered voluntary motor or sensory function with
to the somatic symptoms or associated health incompatibility between the symptom and
concern. recognized medical/neurological condition.
Persistently high level of anxiety about health Causes significant distress in social, occupational
symptoms. and other important areas of functioning.
Excessive time and energy spent over these Possession Attack is an example of Conversion
symptoms and their investigations and Reaction.
treatments.
4. Investigations
2. Signs and Symptoms Psychiatric assessment
Pain in different areas- Laboratory Investigation
Head/Back/Stomach/Joint etc o No diagnostic investigations available.
GI symptoms like nausea, vomiting o Complete Haemogram, Blood Sugar, Renal
One pseudo-neurological condition (Paresis, Funtion Test, Liver Function Test, Serum
Loss of Voice, Loss of Vision). Electrolytes, Urine Routine, Chest X-Ray (If
Symptoms cannot be explained by a medical necessary).
condition.
5. Management
5.1 Antidepressants (Any One)
a) Tab Sertraline 25-200mg/day in divided doses For 10
b) Tab Amitriptyline 25-100mg/day in divided days.Review
doses
after 10 days
c) Tab Escitalopram 5-20mg/day in divided doses
& then taper
5.2 Anxiolytics (Any One)
a) Tab Lorazepam 2mg HS/SOS Gradually.
b) Tab Clonazepam 0.5-1mg HS/SOS
c) Tab Diazepam 5-10mg HS/SOS
5.3 Counseling and Psychotherapy- Supportive, Cognitive Behavioral, REBT
5.4 Stress Management andLifestyle changes.
Page 351
8. ORGANIC BRAIN SYNDROME
1. Introduction 2.1.3Risk factors are:

Primary biochemical or structural disturbances Old age, preexisting dementia, very young,
(damage) to the brain resulting in impairment of postoperative, burns victim, alcoholic and
mental functions affecting memory, orientation Benzodiazepine dependence.
and cognition.
2. Types of organic brain 2.1.4 Signs and Symptoms:
syndrome Confusion.
Acute organic brain syndrome- Delirium Clouding of Consciousness.
Chronic organic brain syndrome- Dementia Visual illusion and hallucination.
Other/ Sub-Acute Organic Brain Syndrome- Labile affect.
Amnestic syndrome. Disorientation to time, place, person.
Hyperactivity or hypoactivity.
2.1 Delirium: 2.1.5 Investigations:
2.1.1 Definition: Complete Haemogram, Blood Sugar, Renal Function
It is a clinical syndrome of fluctuating global Test, Liver Function Test, Serum Electrolytes, Urine
cognitive impairment of consciousness, attention Routine, Chest X-Ray (If necessary).
and orientation. 2.1.6 Manage ment:
Additional disturbances in memor y, language Ide ntify and treat the precipitating cause.
and perception may occur.
Provide environmental & supportive care.
Commonly occurs in hospitalized patient with
Avoid sedation. But for severely agitated
history of major preexisting medical,
patients it may be necessary to induce sedation in
neurological or surgical illnesses.
order to facilitate investigations and treatment.
2.1.2 Causative Factors: Regular clinical review, close vigilance.
Substance intoxication (alcohol, cannabis, opioid
2.1.7 Medication:
etc).
Important:
Substance withdrawal. Watch for level of consciousness before giving
Medicine induced. injectables.
Delirium due to preexisting medical conditions
e.g. Hepatic Encephalopathy. Use single medication - Start low, go slow.
Haloperidol - 1-4mg /da y

Lorazepam - 0.5-1mg daily Initially for 3 days,
Risperidone - 1mg daily review & titrate
Quetiapine - 25mg 100mg daily the dose.
(To be given in divided doses)
Page 352
All anti psychotics and sedatives to be tapered CT brain, MRI.
gradually, once symptoms are relieved. EEG abnor mal dependi ng upon the cause.
2.1.8 Refer to higher center. 2.2.5 Treatment and Manage ment

For Counseling and Psychotherapy.
a. Cog nitive Enhancers
2.2. Dementia: (ACE inhibiter)
2.2.1Definition: Oral Donepezil 2.5-10mg / day lifetime.
Itis a syndrome characterized by progressive, usually
irreversible, global cognitive deficits primarily b. NMDA antagonist
characterized by me moryi mpairme nt and Oral Memantine 5mg.
dysfunction in Activity of Daily Living (ADL). Associated Psychosis/agitation
2.2.2 Common Causes of Dementia Tab. Quetiapin 25mg - - 1
OR
Vascular dementia (20%). Tab. Risperidone 1mg /day Titrate the dose, regular
Substance Use Disorders (10%). follow up and then stabilize the dose for two years.
Subdural hematoma. Taper the dose after two years.
Vitamin B12 deficiency. c. Associated Depression/Insomnia
Metabolic causes,Hypothyroidism. Tab Sertraline 25mg/day, for 2 months & then
titrate the dose.
All Anti psychotics and Sedatives to be tapered
Tab Escitalopram 10mg/day, Lorazepam 0.5
gradually once symptoms are relieved.
mg/da y.
Refer to higher centre for Counseling and
Psychot herapy. Anti-psychot ics and Anti-depressants to be
discontinued once symptoms relieve d.
2.2.3 Signs and Symptoms:
Memory impai rme nt. 2.2.6 Treatment of co-morbid medical illnesses:
DysphasiaDeficiency of words, name
generation. a.Supportive
Agnosia Inability to recognize parts of body. High doses of Multi Vitamins.
Aprax ia Inability to perform purposeful action
and draw objects. b. Assistance
Impaired exe cutive function Inability to plan For routineactivitieslike bath, food etc.
and take action accordingly.
Personality disintegrationResulting in Keep surroundings of patient safe and calm and
maladaptive behavior. well lit.
2.2.4 Investigations:
Complete Haemogram, Blood Sugar, Renal c. Psychological support
Funtion Test, Liver Function Test, Serum To both patient and caregiver.
Electrolytes. d. Functional manage ment
Urine Routine. Maximize mobility & independence, assist
Chest x Ray. communication.
Thyroid Function Test.
e. Social management
HIV. Shelter homes, recreational activities, assistance
Vit B12,Folate levels. in financial and legal matters.
ECG.
Page 353
9. DRUG ABUSE&SUBSTANCEUSEDISORDER
consequences in physical, social, legal aspects of
1. Introduction life.
When substances like alcohol, caffeine,
cannabis, inhalants, opioids, sedatives and Patients of addictions, especially of alcohol, are
hypnotics etc are taken in excess quantities, they the most commonly treated cases in rural set up.
produce intense activation of the brain and
disinhibition.
2. Common Substance
Addiction- Repeated, compulsive use of a Disorder
substance that continues in spite of negative
Table No 9.1 Common Substance Disorders
Condition Sign & Symptoms Manage ment Durat ion

Alcohol intoxication Aggressive behavior, mood No active treatment Till symptoms
Caused by excessive lability, slurred speech, needs to be given. recover.
consumption of Alcohol incoor dination, unsteady gait, Manage
nystagmus, impaired symptomatically.
judgment.
If excited-
Inj.Haloperidol 5mg +
Inj.Phenergan 50mg
IM.
IV fluids SOS.
Alcohol withdrawal Autonomic hyperactivity, Inj.Thiamine 100 mg 5-7 doses on alternate
tremulousness, insomnia, and Multivitamin days
Caused by Cessation or
psychomotor agitation, infusion.
reduction of alcohol use that
nausea/ vomiting, transient
has been heavy and Inj. Lorazepam 1 2-3 days
visual, tactile, auditory
prolonged earlier. ampule BD/ HS.
illusion or hallucinations.
4-5 days and taper
Shift to Tab.
gradually.
Loazepam 1mg TDS
/SOS.
IV Fluids As necessary.
Delirium Tremens Tremors, disorientation, 1. IV Inj.Thiamine 10 days

It is a severe form of confusion, hyperactivity, 100mg /day in 100
Withdrawal insomnia, illusions, ml NS.
severe anxiety, seizures 2. IV 5% Dextrose As needed.
Close monitoring of vital hallucinations. and DNS.
functions like pulse, BP, 3. Inj.Diazepam 5mg 5 days.
temperature, input and IM TDSor Inj
output is very essential. lorazepam 2 mg
IM/IV TDS.
4. Tab.Diazepam 5mg As needed.
TDS or Tab.
Lorazepam 6-12
mg/day in divided
doses.
Page 354
5. Inj. 6 days.
MVI(MultiVitmin
Injection) + 5%
Dextrose drip.
6. If severe agitation Till psychotic symptoms
or perceptual recover.
abnormality present
Tab.Olanzapine
2.5-10mg or
Tab. Risperidone
2-4mg per da y in
divided doses.
Cannabis intoxication Dryness of mouth, 1. Supportive As needed.
tachycardia, reduced motor treatment and IV
skills, euphoria, sleepiness, Fluids.
apathy, laughter, paranoia, 2. Benzodiazepines
hallucinations. eg. Clonazepam
0.5mg / Lorazepam
1mgTDS.
3. Tab Olanzapine 5 days.
5mg HS.
Cannabis withdrawal Anxiety, irritability, 1. Supportive 3-5 days.
depressed mood, restlessness, treatment and IV
insomnia, loose motions, Fluids
2. Benzodiazepines
eg. Clonazepam
0.5mg / Lorazepam
1mgTDS.
Opioid withdrawl Dysphoric mood, 1. Lorazepam 1-2 mg 2-3 times a day for 1 st
Heroin, Gard, Afeem, MD, insomnia, muscle aches, oral/I.M./I.V. for Week.
Brown Sugar, Inj. Fortwin nausea or vomitting, anxiety and
diarrhea, lacrimation or decreased sleep.
rhinorrhea, yawning.
2. Tab. Brufen 400mg As needed.
or Tab. Naproxen
250 500mg Or
Paracetamol TDS.
3. Tab. Clonidine As needed.

0.1mg can be give n
2-3 times a day
during
detoxification.
4. IV fluids and As needed.
Supportive Care.
Remark:
All patients with substance addiction should be motivated to enroll in de-addiction centres and to attend support
groups like Alcohol Anonymous(AA) and Narcotic Anonymous(NA).
All other Substance Use Disorder patients should be treated symptomatically and referred to higher centre.
Page 355
10. INTELLECTUAL SUBNORMALITY
A state of mind with intellectual and functional iii. Postnatal - CNS infections, trauma,
deficits commonly known as Mental Retardation. uncontrolled epilepsy.
1.Incidence 3. Types of Mental Retardation

3 to 4 cases per 1000 population.
1. Borderline
2. Etiology: 2. Mild
3. Moderate
i. Prenatal (1 in 1000 live birth) due to genetic,
4. Severe
intrauterine viral infections, injuries, maternal
5. Profound
metabolic disorders
Refer to the table for details and management.
ii. Perinatal - All causes leading to hypoxia
during birth.
Table No 10.1 Mental Retardation Classifications
Types Borderline Mild Moderate Severe Profound

Dull Slow
Nor mal Learner
I Q range 80 to 90 70 to 80 50 to 70 35 to 50 35 to 15 up to 15
Salient - Scholastic - Can tell rightleft - May not be - May not be able - Cannot feed self.
backwardness in laterality able to tell to name or gans
Clinical - Cannot protect
some subjects but laterality
- Can recognize - May notable to self.
features may complete
coins. - May not recognize
- 10th Standard with recognize all
extra years
- Can use money.
coins Colors
- Can do simple Coins
- And additional
calculation .
- May not tell Count
coaching. all colors
- Can tell relations. - May not
- May not count recognize own
- Can pass 10th beyond 10. family members
std. in selected
- May not be but recognize
subjects.
able to
recognize familiar faces.
relations like
cousins,
uncles.
ADL - Independent - Independent - May need -Needs assistance -Needs to be fed,
help for for bath, bathed,
(Activities of - Can travel on own. - Can use
grooming, protected.
telephone. cleanliness but
Daily bath.
- Good social Can feed self.
Living) - May be able
skills.
to move in
e.g. bath, village but
food, not faraway.
Page 356
grooming etc.
Trainability - Trainable. - Trainable. - Trainable for - Non trainable - Non trainable

- Can earn. - Can earn. - Repetitive - Soremains - So remains
work dependent for life dependent for
long. life long.
- Under
supervision.
-May be able to
earn as
shepherd,
helper
% Disability <50 but eligible for > 40 % > 50 % > 75 % 100%
subject selection.
4. Management
Anti-Psychotics in low doses for behavioral 5. Special Guidance
disturbances. Get IQ assessment certificate and Disability
Anti-Epileptics if the patient has co-morbid certificate from concerned Civil Hospital.
Epilepsy.
ADL training. Enrollment in government employment facility for
Vocational training. gainful employment.
Caregiver education.
Page 357
11. CHILD& ALDOLESCENT PSYCHIATRY
Certified patients can avail the provision of a writer
1. Introduction and extended time to write a paper in 10th std. and
Child & adolescent form a major percentage of 12th std. board examinations. Remedial teaching by
population specially trained teachers either one to one or in
Many psychiatric problems are present in this groups of a few children is very effective.
age group.
Early detection and treatment of these conditions
will prevent complications and significantly B. Pervasive Developmental Disorder of
reduce the morbidity. Childhoo d or Autism
Commonly seen disorders are behavior Such children do not mix or communicate verbally or
disorders, anxiety disorders and depressive emotionally even with their parents. They are self-
disorders. engrossed in non goal directed activities. Usually non
complaining & self-sufficient. Odd motor
2. The child Usually presents as poor movements, peculiar speech pattern,attracted by
music. Those with normalIQ may excel in some arts
scholastic performance, disobedience, somatic
like music, dr awing.
pain.
Some such patients may need small dose
antipsychotic if self-destructive. Tab. Haloperidol
2.1 Assessment: 1.5 mg half tablet HS.They need special training in
History to be taken from parents, school teacher one to one setup.
and care taker as well as other colleague
children.
2.2.2 Psycho e motional disorders :
Child to be taken into confidence by talking to
him alone.
A. Attention Deficit Hyper Activity Disorder -
A large number of these age group patients belong to ADHD/ADD. not uncommon.
the intellectual sub normality disorder.
Clinical symptoms
InattentionI.e. not able to mentally focus at a
2.2 Important childhood given task adequate enough to understand it or
disorders: perform it. Easily distractible & so, forgetful.
2.2.1 Psycho-developmental disorders : Hyper activity Always driven by some
move ments; cannot sit still; runs around; climbs
A. Learning Disorders or Dyslexias windows; cupboards.
IQ of the child is normal but still he lags in scholastic Impulsivity Acts before thinking; shifts from
performance due to specific learning disability i. e. one activity to another; disruptive.
Writing dyslexia - wrong spellings and Plenty of complaints from the school, neighbors.Most
grammatical mistakes. of the children show good response to psycho
Reading dyslexia - unable to read sentences stimulant medicine.
and words with proper pronunciations. Tab. Methylphenidate 5 to 10mg OD
Arithmetical dyslexia - conf usion in or
mathematical symbols e. g. +, -, x, 3, 6, Cap Atomoxetine 10 to 25mgOD.
i. e. geometrically reverse symbols, resulting
into poor performance in solving and B. Childhoo d Depression common.
understanding mathematics. C. Nocturnal Enuresis due to environme ntal
Global dyslexia - all of above. stress.
Detection of dyslexia is usually done by the school
Common.
teacher and confirmation has to be done by
Shows good response to Tab. Imipramine
government approved agency such as special units in
25mgHS.
teaching hospitals / medical colleges.
Page 358
2.2.3 Performance Anxiety, Phobia, Oppositional disobedient, negativistic, temper
Childhoo dDepression, Tension headac he, tantrums, argumentative, stubborn, not yielding to
Somatization disorderare also commonly rules.
seen among children facing stress at home or
Manage ment:
at Aashramshala or in the school . They need to
Small doses of antidepressant e.g.Tab. Imipramine
be managed with medication (discussed
25mg 0-0-1 or Tab. Sertraline 25 mg - 0 0 to 1-
already) and along with counseling.
0-0 for a short period. Benzodiazepines should be
Clinical symptoms:
avoided.
Headache, pain in abdomen, migraine, loose
motions, vomiting, exacerbations of asthma, Behavioral modification using positive/negative
fever, skin rash. reinforcers,
Irrational fear and phobia of animals, ghosts,
Childhood psychoemotional disorders are
darkness, school which ultimately resulting
usually secondary to environmental stress. So,
into avoidance to school.
modification of the stressful environment and
Sleep disturbances, nightmares, enuresis. improving childs coping capacity must be
Child remains withdrawn and introvert, not taken care to relieve symptoms. Medication is
playing, crying spells, excessively shy, as mentioned, to be given only till symptoms
Temper Tantrums. active, and in dosages appropriate to weight.
Small doses of antidepressant e.g.Tab.
Imipramine 25 mg HS or Tab. Sertraline 25
mg - 0 0 to 1-0-0 for a short period. Note:All suspected cases need exhaustive evaluation
Benzodiazepines should be avoided. by psychiatrist, so must be referred if not
responding to above medication.
2.2.4 Conduct disorder
In adolescents Antisocial behaviors like violating
rules, showing aggression, running away from home,
lying, stealing, lack of guilt feeling.
Page 359
12.PSYCHIATRICEMERGENCIES
1.Suicidal Attempt
4. Catatonic Stupor
1.1 Causes: Patient develops complete mental and physical
Severe depression - associated with financial inactivity, becomes statue like and non
burden, crop failure, love affair failure. communicative. Does not eat for many days and
Schizophrenia. develops dehydration.
Drug induced ps ychoses like alcoholic
hallucinations. 4.1 Causes:
Impulsive act. Depression.
Psychotic illness.
1.2 Management: Organic brain disorder.
Immediate physical resuscitation.
Treatment for psychiatric illness ECT and 4.2 Management:
medicines. I.V. fluids.
24 hrs continuous supervision. Inj. Lorazepam 1mg slowly BD till
Do not isolate the patient. symptoms reduce.
Do not keep any sharp objects, ropes, blades Ryles tube feeding.
near patient. ECTs.
Do not allow patient to lock room/ bathroom Low doses of antipsychotic.
from inside.
Counseling and ps ychotherapy.
6. Dystonic Reaction
Sustained muscles contractions causing twisting
2. Psychotic excitement and repetitive movements or abnormal postures.
2.1 Causes: e.g. neck dystonia, tongue protrusion.
Schizophrenia.
Mania. 5.1 Causes:-Use of antipsychotics like
Psychoactive drug abuse like charas, ganja, Haloperidol,Trifluoperazine,Risperidon,
alcohol. Olanzapine.
2.2 Management: 5.2 Management:

Injection Haloperidol 10mg IM twice a day Taper off the anti psychotic.
Injection Promethazine 50mgIM twice a day Injection Phenergan 50mg IM twice a day
till excitement controlled. to be tapered off over next 4-5 days
Restrain the patient to avoid injuries to self depending upon symptom relief.
or others or destruction of property. Tab. Benzhexol 2mg 1-1-1 till symptoms
I.V. fluids if patient not eating / R. T. subside.
feeding to maintain hydration and nutrition. I.V. fluids till patient able to eat orally.
Oral antipsychotics. Change of antips ychotic by Psychiatrist.
ECTs.
Note: all patients of psychiatric emergencies need to
be referred to psychiatrist as early as possible, once
3. Delirium they are fit to travel.
Management as given under topi c of same name.
Page 360
13. PROCEDUREFOR ADMISSIONTOA
MENTAL HOSPITAL
the Reception Order from the concerned (i.e
1. Introduction: the district of the patients residence) court.
All admissions to any government or private mental
hospital are governed by the Mental Health Act- 2.4 Reception Order - By the concerned
1987. District Civil Court is issued only on
The act provides guidance for - admission confirmation of the mental illness and then, the
and discharge procedures of civil & criminal patient can stay beyond 90 days till recovery.
patients. such a patient eve n on discharge can extend his
Management of prope rty of the patients. order with the leave of absence facility for 60
Safeguarding human rights of the patients. days forever (i.e. he can be readmitted with the
original R.O. any time in future without further
legal procedures).
2. Admissions
2.1 Voluntary Boarder -Patient himself 3. Documents required
signs the application requesting the Documents required for above legal procedures:
superintende nt of a mental hospital to allow him 3.1 Address proof of the patient or his caretaker.
to stay in the hospital for treatment of his mental 3.2 Photographs of the patient and his caretaker.
illness. Maximum stay 90 days. 3.3 Undertaking to pa y hospital charges by the
2.2 U/s. 19 (Mental health Act)-When caretaker unless exempted by court order or by
patient not capable of signing above application provisions under the GR ---
due to his mental illness then, he is examined by 3.4 Medical Certificates by 2 Psychiatrist for U/s.
2 Psychiatrist indepe nde ntly and if found to need 19 and for obtaining R. O. if patient admitted as
admission, can be admitted for maximum 90 D.O.
days. 3.5 Medical Certificates in prescribed format by
one Medical Officer in government service and
2.3Detention Order - A suspected mentally by any Registered Medical Practitioner for
ill person can be admitted to a mental hospital
application for R.O.
for 10 days of observation period by the
Detention Order of the Hon. District Civil Judge
Note:
or the CP of the area.
i. All court procedures to be done during court
This section usually used for admission of
timing i.e between 10 am to 5.45 pm.
wandering mentally ill people suffering of
ii. Patient and all documents to be presented to the
schizophrenia, mental sub normality, delirium,
court.
dementia etc. Also for criminal people behaving
iii. No legal procedures needed for admission at a
abnor mally.
Civil Hospital or a General Hospital, as the
On certification after observation period,the stay
patient is not isolated from society. Hence, such
in the hospital for treatment can be extended by
admissions to be encouraged.

Page 361
ENT
Page 362
1.ACUTE OTITIS MEDIA (AOM)
An acute inflammatory condition of the middle ear
1. Definition - space. Common in children usually associated with
fevers.
Fig 1. Congestion of eardrum

Level 1 (PHC)& Level 2 (Rural Hospital): Diagnosis
& above mentioned treatment with regular checkup.
1.2 Symptoms& Signs - Non improvement or detoriation,then refer to higher
1. Pain, Fever center.
2. Congestion of the eardrum (Tympanic membrane) At Level 3-Distrtict Hospital Referral Hospital
& loss of normal light reflex
1.Diagnosis, Investigations and Treatment of the
3. Hearing Impairment case.
4. Bulging Tympa nic Membrane & tinnitus 2. Referred case from Level 1 & Level 2,
Reassessment & further treatment.
In Children - Fever, Vomiting, Loose motion, 3.2. Treatment:-

Irritability. 1. If the tympanic membrane is bulging Or if
Common childhood disease by age of 5 yr, complication are suspected myringotomy should be
done by ENT specialist under microscope with a
- (80 % of children. will get at least one episode of coverage of antibiotics (Ampicillin/Amoxycillin 5 to
AOM) 10 mg/kg in child for 5 days. Adult dose 500mg TID
- If not diagnosed & treated may lead to ASOM/ for 5 days/Amoxycillin + ClavunicAcid 625 mg BD
CSOM for 5 days.
Decongestants - Oxymetazoline nasal drops, 0.1%
1.3 Treatment - Nasal drops, 2-3 in each Nostril thrice daily/
1. Counselling- advice to mother about correct Xylometazoline Nasal Drop 0.05% in children.
feeding techniques 2. Mastoid exploration may be required in cases
2. No ear drops, ear mopping to be done only with of coalescent mastoiditis or other
good illumination facility, not to blow nose complication.
3. Symptomatic - Analgesic (Tab.Diclofenac -50 mg 3. Neurological/Pediatric Physician
t.i.d x5days)or Ibuprofen 200mg t.i.d, Antipyretic Opht halmologists Consultation may be
(Paracetamol-325 mg t.i.d x5days) required in unresolved cases & management in
accordance with them.
1.4 Treatment levels -

Page 363
1. Dry moppi ng/ Suction Clearence
2. Acute Suppurative Otitis
2. Antibiotic (ampicillin/amoxycillin 500 mg thrice
Media (ASOM) daily or , Amoxycillin + Clavunic Acid 625 mg
bd x 5 days). If needed parenteral antibiotics IV
2.1. Definition - cefotaxime 1 gm 12 hourly in adult for 5 days.
An Acute inflammatory condition of middle ear cleft 3. Anti inflammatory drugs( TabIbuprofen 200 mg
which includes Eustachian tubes, middle ear, Antrum + Paracetamol 325 mg b.i.d)
(opening of mastoid air cells in middle ear) with pus
discharge from external auditory canal due to 4. Decongestant - Oxymetazoline nasal drops,
bacterial infection or following exanthematous 0.1% nasal drops, 2-3 in each nostril thrice daily/
fevers. It is also called safe ear if infection limited to Xylomatazoline Nasal Drop 0.05% in children.
lower part of Eardrum.
2.3.3Stages
2.2. Symptoms- a) Inactive stage -
1. Severe Pain, Fever Antibiotic not required and ear toileting may be done
regularly Antibiotic ear drops (Ciprofloxacin ear drop
2. General malaise
2 drops BID) may be needed.
3. Vomiting/Loose Motions
b) Quiescent stage may not require any active
4. Irritability treatment as the ear is dry
5. Discharge from ears: c) In active case of the disease Symptoms and Signs:-
Mucopurulant discharge after dry mopping or 1. Ear Discharge - Non foul,
suction Tympanic membrane may show smelling/intermittent/profuse and associated
congestion, perforation and pulsatile discharge with uppe r respiratory tract infection.
6. Signs of upper respiratory tract infection like 2. Hearing Loss - conductive in nature and
sinus, nasal & throat involvement. gradually progressive
2.3. Treatment- 3. May be associated with tinnitus,Autophony

4. Otoscopic examination - shows central
2.3.1 Level 1 (at PHC level) & Level 2 (Rural perforation in the tympanic membrane with
Hospital):- pulsatile dishcharge coming out to external
1. Dry mopping, suction, clearance of ear discharge canal.
2. Treatment of other septic focus - Eg. Acute 4.5. Active stage:

Adeno Tonsillitis, Rhinosinusitis with
antibiotics, anti inflammatory drugs and Diagnosis is generally clinical. History with
decongestant (mentioned earlier) otological findings of central perforation is
characteristic. Patient is advised to avoid risk factors
a. Systematic antibiotics - antibiotics - in the form of avoiding excessive cold. Treatment is
(Ampicillin/Amoxycillin) 5 to 10 mg/kg in child as mentioned above. Patient advised to keep ear dry
for 5 days. Adult dose 500mg TID for 5 days. and avoid water going into the ear.
b. Anti inflammatory/Anti pyretic TREATMENT:
Ibuprofen(200mg) with Paracetamol ( 325 mg)
in divided doses for 5 days. 1. Antibiotic treatment as per the culture and
sensitivity reports.
c. Decongestant - Oxymetazoline nasal drops,
0.1% nasal drops, 2-3 in each nostril thrice 2. Regular ear cleaning and antibiotics ear drops
daily/ Xylometazoline Nasal Drop 0.05% in in addition to oral/parental drugs.(Ampicillin
children. /Amocycillin 500mg TDS x 5 days or
Amoxycillin + Clavunic Acid 625 mg BD x 5
days. Parental drugs. Inj.Cefotaxime 1gm IV
Level 3 (Referral Hospital/Dist. Hospital):- 12 hourly x 5da ys.
2.3.2 Treatment -
Page 364
3. Treatment of the foc us of infection - Indications of Tympanoplasty - There should be
Chronicadeno Tonsillitis, Deviated nasal
(i) Well sensorineural hearing preserved
septum and any sinus pathology.
(ii) Eustachian tube should be patent
4. The corrective surgery:- The myringoplasty /
Tympanoplasty can be performed once the ear (iii) Stapes mobile
is dry with perforation with no disease activity.
iv) Repeated attacks with no healing of disease.
Page 365
2. CHRONIC SUPPURATIVE OTITIS MEDIA
(CSOM)
2.1. Definition: 2.4. Investigations and

It is a chronic inflammatory disease characterized by Treatment:
foul smelling ear discharge with cholesteatoma 2.4.1 -At Level 1:
formation in atticoantal region. If attic involved, it is
Ear toileting if unresolved refer to higher centers.
called as unsafe ear (infection may get routed to
nearby structures leading to complications. The 2.4.2 At Level 2:
cholesteatoma is aggressive in nature and has got
tendency of bone erosion leading to intracranial and Essentially aggressive treatment in the form of ear
intratemporal complications. It is also called as Atti toileting, antibiotics (Ampicillin/Amoxycillin 500 mg
co antral disease or unsafe type of CSOM. thrice daily or Amoxyclav 625mg b.i.d x
5 days) to avoid complications.
2.2. Symptoms and signs: 2.4.3 At Level 3:
1. Scanty, foul smelling, continuous ear
a) Investigations
discharge,occasionally blood stained.
1. Oto microscopy
2. Hearing loss- conductive or sensorineural in
nature 2. Aural swab for culture and anti bacterial
sensitivity test
3. Vertigo- if inner ear is involved eg-labyrinthitis
3. X-ray mastoids/CT-scan/MRI to confirm the
4. Patient may have:
destructive pathology and spread of disease
a. Fever- Due to acute mastoiditis, meningitis,
4. Pure tone audiometry
lateral sinus thrombosis (fever chill and rigors)
b. Headache- Due to meningitis, extradural abscess 5. Investigations to assess the co-morbid
c. Vertigo,tinnitus, vomiting - Due to labyriynthitis, conditions.(Biochemical & other Lab
brain abscess, increased intracranial tension, investigations)
meningitis
d. Facial weakness or paralysis b) Treatment
e. Post aural swelling due to mastoiditis. Cholesteatoma being aggressive and destructive in
nature-definitive management is surgery- in the for m
2.3. Complications: of Tympanoplasty OR Modified Radical
Mastoidectomy
1. Facial Nerve palsy
Aim: Removal of disease.
2. Labyrinthitis
Aims of modified radical surgery are
3. Meningitis
1. To make ear safe to patient by removing the
4. Brain abscess - Extradural, subdural abscess
cholesteatoma by surgery.
5. Lateral sinus thrombosis
2. To make ear dry and prepare a self cleansing
6. Mastoiditis mastoid cavity
7. Petrositis 3. To prevent complications of CSOM.
4. Establishing hearing mechanism of the ear
(Reconstruction).
Page 366
3. ACUTE PAROTITIS -VIRAL/BACTERIAL
secondary infections), results in bacterial parotitis . It
1. Viral Mumps(Viral is prevalent in debilitated patients.
Parotitis)
2.2. Symptoms & signs
Caused by Paramyxovi rus. Disease is contracted by
droplet infection and fomites. Children were Severe Pain
commonly affected. Incubation period 2 -3 weeks. Swelling over parotid
Tenderness
1.1. Symptoms & Sign- Indurations of gland
1. Parotid swelling - Unilateral or Bilateral Erythema of skin and or al mucosa
Fever.
2. Pain over gland, ear pain
3. Low-grade fever Arthralgia Malaise
2.3. Management
Headache Appropriate antibiotics - ampicillin/amoxycillin
500 mg thrice daily (5 to 10 mg/kg of body
1.2. Complication - weight for paediatric patients for 5 days).
Orchitis with painful and tender testis Adequate hydration

AspticMenigitis or meningoencephalitis may Oral antiseptic gargles.
occur with or without the salivary gland
invol ment Good Oral hygiene
Unilateral sensorineural hearing loss Warm compression over gland
Other complications-
Thyroiditis,myocartitis,nephritis and arthirits. Bimanual massage to milky purulent discharge /
calculi from the gland
1.3. Investigation - Stone in the distal duct - can be manully
expressed & remove d by pushing in mouth
Haemagglutination inhibition test ope ning of gland
Complement fixation test
Abscess drained out with a small incision.
1.4. Treatment - organised Abscess, to be confirmed by
Sialography,CT scan Or USG. Needs open
Supportive Measures - Bed rest, adequate surgical interve ntion.
hydration, Antipyretics
Prevention MMR(Mumps,Measles,Rubella) Surgical drainage: Elevation of anteriorly - based
vaccine at 10 months of age flap over super facial parotid fascia, Parallel to
branches of facial nerve with placement of
2. Bacterial Parotitis external drain.
Rule out tumor mass by CT/MRI before surgical
2.1. Definition excision.
Infection leading to Mechanical blockage of salivary
duct (stasis of salivary secretions coupled with
Page 367
4. FURUNCLE
1. Definition: 4. Investigation:
Infection of root of hair follicle usually caused by
Hb, CBC, Blood sugar & culture & sensitivity test of
staph aureus. This infection occurs in cartilaginous
discharge/pus.
ear canal.
2. Symptoms: 5. Treatment:
Severe earache 5.1 Local-packing the ear with
Movement of pinna painful antibiotic ointment
Blocking sensation
5.2 Systemic:
Antibiotics (Ampicillin/Amoxycillin 500 mg thrice
3. Signs: daily (5 to 10mg/kg of body weight for pediatric
Tragal cartilage area tenderness patients for 5 days)or amoxyclav 625 mg bid in adult
Otoscopy- swelling in ear canal for 5 days) Analgesics (Diclofenac 50mg BD for 5
Post auricular lymphadenitis (swelling) Days)Recurrent furunculosis: rule out diabetes
Page 368
5. OTO-MYCOSIS
1. Definition: 3. Treatment:
Fungal infection of ear canal caused by fungus like Removal of fungal debris by ear toileting (mopping
Candida albicans or Aspergillusniger or suctioning)Antifungal ear drops
(Clotrimazole/Flucanozole 2 drops TID for 5
2. Symptoms & signs: Days)Analgesics Tab Diclofenac 50 mg bid for 5
days.Application of gentian violetTreatment of
Severe irritation and itching in the earSevere diabetes (If associated)
earacheWhitish wet paper like discharge
(candida)Black spores (aspergilous) or combination 4. Preventive:
of both fungus.
Keep ear dry,Avoid swimming in polluted water,Care
in rainy season.
Page 369
6. NECK SWELLING
Differential diagnosis depends on swelling occupying Pain: Present-acute inflammation
particular (Anterior& Posterior) triangle of neck.
Absent-granulomatous disease or malignancy
1. Classification: Size: rapid increase malignancy
Cervical lymph nodes:classified as 7 groups
Level la: submental
3. Diagnosis:
Blood investigations:CBC, ESR, HIV
Level lb: submandibular Cytology: FNAC (Fine Needle Aspiration
Cytology)Chest X-ray, Ultrasound
Level ll :upper jugular
CT/MRI
Level lll: middle jugular Lymph node diagnostic excision biopsy
Level lV: lower jugular
Level V: posterior triangle 4. Treatment:
Level Vl: pretracheal, prelaryngeal
4.1 7 to 14 days course of
Level Vll: mediastinal
antibiotics
Ampicillin/Amoxycillin 500mg thrice daily (5 to 10
mg/kg for paediatric patients for 5 days)/Amoxyclav
625 BD 5 to 7 days and follow up evaluation
2. Symptoms and signs:
Neck swelling-lymph node consistency: 4.2 Surgical excision of neck
1. Stony hard: malignancy/metastatic swelling
2. Firm to rubbery: lymphoma
3. Soft: infection /inflammation 4.3 Malignancy
Search for primary and treat accordingly, as neck
4. Matted: tuberculosis nodes appears secondary (Metastatic)to primary
malignant focus.
Page 370
7. A TROPIC RHINITIS
Nasal irrigation and removal of crusts -

1. Definition: byretracted Nasal douching with saline,
glucose, glycerine solution.
Chronic inflammation of nose characterized by
atrophy of nasal mucosa and turbinate bones. The Nasal douching - The patient must be asked to
nasal cavities becomes roomy and full of foul- douche the nose at least daily with
smelling crusts. Saline solution:
Sodium Bicarbonate - 28.4 gm and
SodiumChloride - 56.7 gmmixed in 280 ml of
2. Clinical Symptoms and luke warm water thrice a day till crust
signs: disappears.
25 % glucose in glycerin: - After crusts
Commonly seen in females and s tarts around removal nose painted with 25% glucose in
puberty. glycerin twice a day for 1 month.
Foul smelling form nose Potassium iodide can be prescribed orally to the
Feeling of Nasal Obstruction patient in an attempt to increase the nasal
secretion.
Formation of crusts in the nose
Epistaxis may occure after crusts removal Placental extract injected submucosally in the
nose has been attempted with varying degrees
Roomy nasal cavitiy
of success.
Anos mia
Atrophy of Nasal turbinates,nasal mucosa looks
pale and atrophied 3.2. Surgical management:
Saddle nose deformity( destruction of cartilage) 1. Sub mucous injections of paraffin
Sometimes nasal septal perforation ( erosion of 2. Teflon strips, and autogenously cartilages
cartilage) grafting
3. Wilson's operation - Sub mucosal injection of
50% Teflon in glycerin paste.
3. Management: 4. Young's operation - This surgery aims at
closure of one or both nasal cavities by plastic
3.1. Conservative: surgery in rare cases.
Aims at maintainaing nasal hygiene by removal

of crusts and lessening.putrified smell due to
erocian& destruction.
Page 371
8. NASAL MYASIS
Nasal Myasis commonly known as maggots in the iii. Cellulites of the nose and face may develop.
nose. It is an infestation of the nose by maggots iv. Fever and toxaemia may be present.
which are larvae of fly. Maggots are living foreign
bodies in the nose.
3. Treatment:
1. Causes: i. Remova l of maggots by installing Liquid
paraffin may be used to stifle the worm. Liquid
Poor hygiene, Leprosy, atrophic rhinitis & other nasal
diseases which forms crust with foul purulent paraffin bloc ks or chokes the lung of the
discharge and loss of nasal sensation attracts flies to maggots, thereby killing them. The killed worms
the nose. can easily be removed.
ii. Turpe ntine packs can be kept in the nose which
irritate the maggots. Nasal saline douching is
2. Clinical Features: done for removal.
i. Maggots are seen crawling in the nose. They iii. Surgical procedure: nasal endoscopic complete
come out of the nose. removal of the worms & infected parts of nose.
ii. Foul nasal discharge is present.
Page 372
9. FOREIGN BODIES IN NOSE
1. There are two types of 3. Investigation:

foreign bodies in nose (i) Anterior Rhinos copy gives site of foreign body
in the nose.
(i) Non-living: Organic like seeds and grams.
Inorganic like beads, paper or buttons. (ii) Nasal endoscopy will locate exact site of the
body.
(ii) Living: Maggots.
(iii) Xray will detects only radio-opaque foreign
(iii) Iatrogenic: Cotton wool, pledgets or swabs may body.
be left behind accidentally.
(iv) Commonestoccurrence by mishaps in children, 4. Treatment:
age group 0-5 years (self insertion)
(i) Generally Blowing the nose or induction
sneezing may expel the foreign bod y.
2. Clinical Features:
(ii) Removal of foreign body by Eustachian tube
History of insertion of the foreign bod y may be catheter, which is inserted behind the foreign
available from patient/pain in the nose bleeding. body.(without destructing nasal mucosa &
Blocking of the nose. touching F.B. Otherwise bleeding may obs cure
visibility. It is performed under local
Sneezing may be present. anaesthesia.
Unilateral Foul Smelling Bloo d stained (iii) Endoscopy:underGeneral Anaesthesia
Discharge - oneshould suspected old foreign
body in the nose.
Page 373
10. DEVIATED NASAL SEPTUM
1. Introduction: 3. Investigation:
The septal deformities are of the following History, examination of the nose by anterior
types:- rhinoscopy& posterior rhinoscopy. X Ray PNS
waters view/CT scan PNS.
(i) Deviations are smooth deflections which are
upper or lower, anterior or posterior. I.e. C- 4. Treatment:
shaped deviation
Required only if the patient has persistent or
(ii) Spurs are isolated thickenings at the junction of recurrent symptoms due to the deviated septum or
the bone and the cartilage. blockage of nose. Permanent relief is obtained by the
(iii) Thickening may result from trauma leading to Submucous Resection of the Nasal Septum or
ove rriding of the cartilaginous fragments, which Septoplastysugery.
grow later in double layers.
(iv) Dislocation:The anterior edge of the septal
4.1. Sub mucous resection of
cartilage may be displaced to one side causing nasal septum:
the widening of the coluella of the nose.
Indications for sub mucous resection of nasal septum:
v) S Shaped Deformity
1. Marked septal deviation occurring behind the
vi) Bony posterior deformity of vomarine/ethemoid vertical line passing between the nasal processes
bone. of the frontal and maxillary bones. This deviation
must be the cause for the patient's symptoms.
2. Clinical features: 2. Closure of septal perforations
Unilateral or bilateral blocking of the nose. 3. Source of grafting material
Headache due to sinusitis. 4. To obtain surgical access in hypophysectomy, and
Recurrent Colds. vidianneurectomy
Epistaxis. 4.2. Septoplasty:

Anos mia. Indicated as tailor-made operation without disturbing
External deformity associated with deviation of nasal mucosa of other nasal fossa,where only
the septum. obstructing part is removed.It can be associated with
Rhinopl asty surgery.
Page 374
11. NASAL OBSTRUCTION
1. Introduction: 4. Management:
The common causes of nasal obstruction are DNS,
nasal polyps, hypertrophied turbinates& old nasal
4.1. Medical:
foreign bod y like rhinolith. Local nasal decongestants Xylometazoline 0.1 %
2drops BID for 3 days,
2. Clinical feature is nasal Local nasal steroid spray like Fluticasone once daily,
Antibiotics (Ampicillin/Amoxycillin 500 mg thrice
obstruction daily / Amoxycillin + ClavunicAcid 625 mg BD (5
to 10 mg/kg of body weight for paediatric patients for
5 days), Antihistaminic (Cetrizine 5mg BD for 7
3. Investigations: days)
History, examination of the nose by anterior
rhinoscopy& posterior rhinoscopy& functional nasal
endoscopy (FESS). 4.2. Surgical:
Cottles test used to check the nasal obstruction is Nasanpolypectomy
due to abnormal nasal valve.
Radiological : XRay PNS/ CT PNS region Turbinopl asty, turbinectomy
Septoplasty
Endoscopic sinus surgery
Page 375
12. TONSILLITIS
1. Acute tonsillitis 2. Chronic tonsillitis

2.1 Definition:
Definition:
It is chronic inflammation/ infection of palatine
1.1. It is acute infection/ tonsils.
inflammation of palatine tonsils. It is characterized by recurrent episodes of acute
tonsillitis. A history of 3-4 episodes of acute
tonsillitis in a year should be labelled as Chronic
1.2 Pathological types: tonsillitis
a. Acute parenchymatous tonsillitis
b. Acute follicular tonsillitis
c. Acute membranous tonsillitis 2.1. Clinical features:
. 2.2.1 Symptoms:
Recurrent history of sore throat, Odynophagia
1.3. Clinical features: and fever with symptom free interval between
1.3.1 Symptoms- the two attacks
Sore throat Halitosis
Odynophagia. Change of taste
Fever, malaise, headache may be present. Dry cough: Hawking due to irritation in throat.
Pain may be referred to the ears Failure to thrive: Seen in children
1.3.2 Signs-
Patient may look toxic and febrile. 2.2.2 Signs:
Tonsils are enlarged and congested; may be Tonsils may be enlarged ( Parenchymatous type )
studded with follicles or membrane.( Scanty pus or Fibrotic and small (Fibrotic type)
may come out) Yellowish cheesy material is seen in tonsillar
Anterior pillars are congested crypts which oozes out when the tonsils are
Tongue is coated pressed by tongue depressor.
Jugulodiagastric lymph nodes are enlarged and Enlarged jugulodiagastric lymph nodes.
tender. Occasionally, yellowish cystic swelling
(retention cyst ) may be seen on the surface of
1.4 Treatment: tonsil.
Bed rest. Redness of the ante pillar
Soft bland warm diet
Avoid cold, oily, spicy food 2.3 Investigation:
Antibiotics for 5-7 days.: Amoxycillin500mg- Hematological:Hb%, CBC,ESR,BT,CT, PT, XRAY
3times/day, Amoxycillin with clavulenic acid neck lateral view for adenoiditis &Xray chest for
625 mg twice/day x 5 days preoperative evolution.
Anti-inflammatory analgesics to reduce pain,
fever and i nflammation: Ibuprofen with
Paracetamol ( 200+325)mg 2 times/day x 5 days 2.4 Treatment:
Tonsillectomy by dissection method under
Antiseptic gargles
general anesthesia.
Multivitamins orally BD x 5da ys.
Page 376

13. ADENOIDITIS
1. Introduction: 2.3 General symptoms: (Adenoid

Inflammation of adenoids is called adenoiditis. Facies)
Failure to thrive.
Adenoids are also called as nasopharyngeal tonsils. It High arched palate
is group of lymphoid tissue situated at the junction of Crowded and protruding teeth
the roof and posterior wall of nasopharynx.Adenoids Halitosis
usually atrophy by the age of 13-14
Pinched and narrow nose
(puberty).However in some patients it may be
Mask like face
hypertrophied and produce symptoms, then treatment
is required.
3. Investigations:
2. Symptoms: X ray soft tissue nasopharynx: It shows enlarged
Symptoms and signs occur due to the following: adenoids and compression of airway.
2.1 Due to nasal obstruction- 4. Treatment:

Mouth breathing 4.1 Medical Treatment
Snoring
Drooling of saliva Acute infection is treated with:
Difficulty in breathing Antibiotics: Antibiotics of choice are-
Change of voice Amoxycillin 500mg TID, Amoxycillin with
Rhinitis and sinusitis Clavulenic acid 625mg BD for 5 days.
2.2 Due to Eustachian tube Anti-inflammator y agents like Ibuprofen 200 mg
BD for 5 days
obstruction: Nasal decongestants: Xylomethazoline 0.05%
Ear pain (adult : 0.1%)
Ear blockage due to secretory otitis media. Antihistaminic: Levocetrizine 5 mg OD for 5
Decreased hearing. days
4.2 Surgical treatment:
Adenoidectomy under G.A.
Page 377
14. PERITONSILLAR ABSCESS (QUINSY)
the tonsillar region. CervialIymphadenopathy is
1. Introduction: commonly seen.
It is collection of pus in the peritonsillar space which
is in between the capsule of tonsil and the superior
constrictor muscle. 4. Investigation:
It usually follows acute tonsillitis. As mentioned in chronic tonsillectomy section.
2. Clinical Features: 5. Treatment:

These are generally due to septicaemia and resemble
any acute infection. Symptoms like fever, chills &
5.1 Medical management:
rigors, general malaise,bodyaches,headache, nausea IV antibiotics Inj.Ampicilin 500mg 12 hourly for 5
and constipation are present. Local symptoms like days, IV fluids, and analgesics like Paracetamol 500
unilateral severe throat pain, odynophagia, muffled mg bid for 5 days, good oral hygiene
thick speech like hot patato voice. Foul breath,
Ipsilateral earache, trismus. 5.2 Surgical Management:
Incision and drainage of abscess (I & D)
3. Examination findings: Interval tonsillectomy
On examination tonsil, pillars & soft palate on the
involved side are congested and swollen, uvula is
swollen and oedematous, bulging of the soft palate
and anterior pillers. Mucopus may be seen covering
Page 378
15. ACUTE PHARYNGITIS
Oede ma, congestion and i nflammation of
1. Definition: posterior pharyngeal wall and soft palate
It is acute infection / inflammation of pharynx.
Ulcerative pharyngitis:Ulceration and sloughing
of the posterior pharyngeal wall. It is rare and
2. Etiology: may occur in immune compromised patients.
Granular pharyngitis:Red granulations over the
a. Infective posterior pharyngeal wall. (due to hypertrophied
b. Associated with Tonsillitis, Rhinitis, Sinusitis. lymphoid tissue)
c. Associated with Gastro-oesophageal reflux. 4. Treatment:

3. Clinical features: Bed rest and improvement of oral hygiene.
Soft bland diet with plenty of fluids
3.1. Symptoms- Antibiotics: Antibiotics of choice are.
Amoxycillin500mg 3 times/day x 5, Amoxycillin
Sore throat or raw sensation in throa t with with clavulenic acid 625 BD x 5days.
halitosis
Antacids : Tab. Ranitidine 150 mg/Cap.
Fever, malaise
Omperazole 20 mg daily in case of reflux.
Odynophagia ( Pain during swallowing )
Anti-inflammator y agents like Diclofenac and
Dry, irritating cough Paracetamol (50+325mg) BD x 5days.
Antiseptic gargles like Betadine or
3.2. Signs- Chlorehexidine.
Catarrhal pharyngitis:
Page 379
16. HOARSENESS OF VOICE
1. Introduction: 4. Treatment:
Hoarseness is term used to describe changes in voice 4.1. For habitual dysphonia
quality. It result from changes in vocal cords. Main stay of treatment is prevention by easing vocal
A hoarse voice is rough and unpleasant, and it results abuse
from lesions of the vocal cords. The causes of
hoarsense may range from innocent acute laryngitis 4.1.1 Things to do
to larynegal diphtheria and malignancy. Rest to the voice
Drink plenty of water
2. Evaluation of hoarseness:
In the absence of upper respiratory tract infection any 4.1.2Things to avoid
patient with hoarseness persisting for more than two Tobacco
weeks needs evaluation. Shouting
Drinking alcohol
3. Physical examination: Trying to talk excess when there is cold or laryngitis
Whispering loudly or for very long
1. Thorough head and neck examination. Trying to c hange naturally speaking voi ce
2. Assessment of hearing acuity
3. Upper airway mucosa, tongue mobility. 4.1.3 Voice therapy-
Cranial nerve examination. Maladaptive vocal habit and techniques are replaced
4. Laryngeal examination. with appropriate use of vocal mechanism.
If not responded to this then surgery may be advi sed
a. indirect laryngoscopy
b. Flexible nasolaryngoscopy 4.2. For organic causes
Treatment of the cause, mostly surgical interventions,
c. Strobolarygoscopy followed by speech therapy
5. Examination for signs of systemic disease
such as hypothyroidism or neurologic 4.3. For psychogenic
dysfunction such as Tremors or Parkinson's Suppor t and i nstructions on how to cope with
disease. emotional and stressful conditions. Speech therapy to
patient.
Page 380
17. STRIDOR
3. Cough
1. Definition: 4. Hoarseness
It is an auditory manifestation of disordered 5. May have difficulty in de glutition
respiratory functions due to airflow changes within 6. Dysphonia
larynx, trachea or bronchi.
It may be-
4. Investigation:
Xray neck lateral view, x-ray chest, direct
1. Inspiratory- When obs truction is at the level of
laryngoscopy, bronchoscopy & C.T.scan to find out
supraglottis and above.
cause & level of stridor.
2. Expiratory- When obs truction is at the level
bronchioles.
3. Biphasic- i. e. Both during inspiration and
5. Treatment:
expiration and obstruction is at the level of
trachea or sub glottis.
5.1. General measures:
1. Humidified oxygen
2. Types: 2. Steroids (Prednisolone up to 40mg/day x 7 days.
3. Antibiotics- Ampicillin 500mg TDS x 5days
1. Congenital 4. Intubation or tracheostomy is indicated if stridor
2. Acquired is severe to relieve airways obstructions
3. General features of stridor: 5.2. Surgical
1. Stridor is not a disease but a symptom or sign. With the help of investigation, cause & level to be
2. Noisy breathing which may be wheezing, find out & depends upon that cause, surgical
crowing, whistling, croaking, sighing,rattling or interve ntion is needed.
snoring.
Page 381
18. FACIAL PALSY (BELL'S PALSY)
1. Introduction: 3. Clinical Features:

It is an Idiopathic condition leading to peripheral Sudde n onset
facial paralysis or paresis which is of acute onset. Patient is unable to close his eyes completely
High Risk cases ofBells palsy are diabetics and Dribbling of saliva from angle of mouth
pregnant women. (weakness of angular oris muscle)
Face become asymmetrical
2. Causes: Epiphora - Tears flow down from the eye
Pain in the ear
Viral infection due to herpes simplex,herpes zoster or Noise intolerance due to stapedial paralysis
E.B.virus& other condition leading to external Loss of taste due to involvement of chorda
pressure on facial canal. tympani.
Fig 1. Facial palsy
Reassurance,pain relief by analgesics

4. Investigation &Diagnosis:- (Tab.Diclofenac 50mg BID for 7 days), eye care,
It requires careful history, completeotological physiotherapy, massage of facial muscles, use of
and head a nd neck examination eye pads.
X-ray studies, blood test- CBC, ESR,blood sugar Acyclovir - 200 - 400 mg 5 times a day for 5-7
and serology days
Nerve conduction & excitability tests to monitor Medical
nerve degeneration
Topodiagnosis - localize site of lesion
5.2 Steroid therapy -
Prednisolone 1 mg/kg per day in a divided doses
for 5 da ys, if paralysis recovers with the dose of
prednisolone, then it is tapered for next 5 days,if
5. Treatment:- paralysis remains the same dose continued for
5.1 General
Page 382
next 10 days and thereafter tapered in next 5
days
Contraindications for Steroid therapy - Pregenancy,
Diabetes, Hypertension, Peptic ulcer, Pulmonary 5.3 Surgical Treatment-
tuberculosis and glaucoma. If there are no signs of recove ry within 7 da ys then
opt for surgical interve ntion.
5.2.2 Ascorbic acid 500Mg OD for 7 days Facial nerve decompression exploring fallopian canal
where facial nerve is encased to release pressure.
5.2.3 Multivitamins
vit B1, B6, B12 1BD for 7 days
Page 383
19. SENSORINEURAL HEARING
LOSS AND ITS MANAGEMENT
1. Sensorineural hearing loss
(SNHL) 4. Management:
Result from lesions of the cochlea, VIII thnerve &
Early detection of SNHL is important as measures
central auditory pathways. It may be present at birth
can be taken to stop its progress, reverse it or to start
(congenital) or start later in life (acquired).
an early rehabilitation & interventions.
2. The characteristics of 5. SPECIFIC FORMS OF
sensorineural hearing loss HEARING LOSS
are:
5.1 Inflammations of labyrinth
1. A positive Rene test i.e. air AC>BC. (Bone
conduction impaired) 1. Viral labyrinthitis
2. Bacterial
2. Weber test lateralized to better ear (better 3. Syphilitic
hearing ear).
3. ABC test: Bone conduction reduced on absol ute 5.2 Ototoxicity
bone conduction tests. 1. Amino glycoside antibiotics - Neomycin,
4. More often involving high frequencies. Kanamycin, Amikacin,Streptomycin and
Dihydrostreptomycin are cochleotoxic drugs
5. No gap between air and bone conduction curve with Selective destruction of outer hair
an audiometry. cellsPatients particularly at risk those are having
6. Loss may exceed 60 dB. impaired renal function.
2. Diuretics- Frusemide and Ethacrinic acid
7. Speech discrimination is poor.
3. Salicylates - Symptoms of salicylate ototoxicity
8. There is difficulty in hearing in the presence of are tinnitus and bilaterial sensory neural loss.
noise. (Hearing loss particularly affecting higher
frequencies.)
3. Diagnosis: 4. Quinine - Ototoxic symptoms due to quinine are
1. History tinnitus and sensorineural hearing loss
2. Duration of illness - sudden or slowly 5. Chloroquin - Effect is similar to that of quinine
impairment or since birth. and permanent deafness can result.
3. Severity of deafness 6. Cytotoxic drugs - Nitrogen mustard, cisplatin
and carboplatin can cause cochlear damage.
4. Type of audiogram, whether loss is high
frequency, low frequency, mild 7. Miscellaneous -Erythromycin, Ampicillin, and
Chloramphenicol,indomethacin,
Frequency or flat type.
Phenylbutazone,Ibuprofen, Tetanus antitoxin,
5. Site of lesion i.e. cochlear, retrocochlear or Propranolol PropylthiouracilAlchohol, Tobacco
central by BERA test. & Marijuana also cause damage to the inner ear
6. Brainstem Evoked Response Audiometry 8. Topical Ear drops -Chlorhexidine drop
(BERA) helpful in profound sensorineural loss. containing aminoglycoside antibiotics. E.g.
Neomycin, Framycitin& Gentamycin.
Page 384
1. Infection - Mumps, Herpes zoster, Meningitis,
Encephalitis, Syphilis, Otitis media.
2. Trauma - Head injury, Ear operations, Noise
trauma, Barotraumas, Spontaneous rupture of
5.3 Noise Trauma cochlear membrane.
3. Vascular Haemorrhage, Embolism or
Hearing loss associated with exposure to noise has Thrombos is of labyrinthine or Cochlear artery or
been well-known in boiler operators, iron & their vasospasm.
coppersmiths & artillery men. Lately, noise trauma 4. Ear (otologic) - Meniere's disease, Cogan's
has assumed greater significance because its being an syndrome
occupational hazard, the compensation asked for & 5. Toxic - Ototoxic drugs.
the responsibilities thrust upon the employer & the 6. Neoplastic - Acoustic neuroma. Metastases in
employee to conserve hearing. High level of sound cerebellopontine angle, carcinomatous
pollution, use of speaker walls leads to Noise truama. neuropathy.
TYPES 5.4.3 Manage ment -
1) Acoustic trauma-Very high sound decibel level for 1. Bed rest.
short duration 2. Steroid therapy- Prednisolone 40-60 mg in a
2) Noise Induced Hearing Loss- Over period of time single mor ning dos e for one week & then tailed
off in a period of 3 weeks.
5.4 Sudden Hearing Loss 3. Inhalation of carbogen- (combination of CO2 &
O2) It increases cochlear blood flow & improve
5.4.1 Definition: oxygenation.
It is defined as Sensory neural hearing loss that has 4. Low molecular weight de xtran
developed over a period of hours or a few days. Loss 5. Hyperbaric oxygen therapy
may be partial or complete. Mostly it is unilateral. it 5.4.3 Preve ntion as pects-
may be accompanied by tinnitus or temporary spell
of vertigo. 1. Immunisation of child & ANC mothers.
2. Avoidance of ototoxic drugs.
5.4.2 Etiology - Most often the cause of sudden 3. Use of driving saftygazets.
deafness remain obscure, in which case it is called 4. Ear infection prevention & treatment in time
the idiopathic variety. 5. Avoiding sound pollution areas
Page 385
20. VERTIGO
1. Definition: 2.2.2 Central Vestibular Disorder
Revolving around or spinning around. 1. Vertebrobasilar insufficiency
2. Posterior inferior cerebellar artery syndrome
2. Disorder of vestibular 3. Basilar migraine
system cause vertigo & is 4. Cerebellar disease- Cerebellum may be affected
divided into: by haemorrhage infraction, infection or
tumours.
2.1 Peripheral 5. Multiple sclerosis - It is a demyelinating disease
Which involve vestibular end or gans& their first affecting young adults. Vertigo & dizziness are
order neurons. The cause lies in the internal ear or the common complaints.
8thnerve. They are responsible for 85% of all cases of 6. Tumours of brainstem & floor of IVth ventricle
vertigo. - Gliomas, astrocytomas may
2.2 Central arise from pons & midbrain, epidermoid cysts
or teratomas may arise from floor of IVth
Which involve central nervous system after the ventricle.
entrance of vestibular nerve in the brainstem and
involve vestibulo-ocular, vestibulo-spinal and other 7. Epilepsy
central nerves system pathways. 8. Cervical vertigo - Vertigo may follow injuries
2.2.1 Peripheral Vestibular Disorders of neck 7-10 days after the accident
1. Meniere's disease (endolymphatichydrops) -It is 3. Investigations:

characterized by trio of vertigo, fluctuating
hearing loss, tinnitus with sense of pressure in 3.1Examination:-
the involved ear. Vertigo is of sudden onset,
lasts for a few minutes to 24 hours 3.1.1History:
2. Benign paroxysmal positional vertigo (BPPV) History of diagnosis,
giddiness,deafness,tinnitus,othorrhoea,cvs&
It is related to positional changes. Certain neurological symptoms. Past history of
provoked position leads to attack of vertigo. giddiness,injury,diabetes,hypertension, medication
3. Vestibular neuronitis and surgery should be noted. Histor y of Tabacco and
alcohol consumption should be noted.
4. Labyrinthitis
3.1.2 Otoscopy:
5. Vestibulotoxic drugs - Drugs like
Gentamicine&Amikacin cause ototoxicity by 3.1.3 For attic perforation with cholesteatoma to be
damaging the hair cells of the inner ear. rule out.
6. Head Trauma - Head injury may cause 3.1.4Blood pressure measurement, CVS & CNS
concussion of labyrinth, completely disrupt the exam includes tests for co-ordination, gait,
bony labyrinth or VIII th nerve or cause a past-pointing test, Romberg's test and corneal
perilymph fistula. reflexes.
7. Perilymph fistula 3.2 Ear Function Test:-
8. Syphilis (i) Hearing test tunning's forks test,Audiometry
etc.
9. Acoustic neuroma - It has been classified in (ii) Labyrinthine tests: Caloric test, ENG
peripheral vestibular disorders as it arises from
CN VIII within internal acoustic meatus
Page 386
4.2.1 The manoeuvre consists of five positions.
3.3 X-Ray mastoid cervical spine Position 1 - With the head turned 45 degrees, the
patient is made to lie down in head hanging position.
and skull: (Dix Hallpikemanoe uvre). It will cause vertigo and
3.4 Lab investigations nystagmus. Wait till vertigo and nystagmus subside.
3.4.1 CBC with Hb%
Position 2 - Head is now turned so that affected ear is
3.4.2 Glucose tolerance test for diabetes
up.
3.4.3 Serum cholesterol
3.4.4 V.D.R.L Position 3 - The whole bod y and head are now
3.4.5 Thyroid Function tests. rotated away from the affected ear to a lateral
3.5 Electrocardiogram. recumbent position in a face-down position.
3.6 CT Scan & M.R.I. of the head. Position 4 - Patient is now brought in a sitting
position with head still turned to the unaffected side
by 45 degrees.
4. Management: Position 5- The head is now turned forward and chin
brought down 20 degrees.
4.1 Medical: There should be a pause at each position till here is
4.1.1 Reassurance regarding the nature of the no nystagmus or there is showing of nystagmus,
disease,no jerks,avoidance of provocative before changing to the next position. After
posture manoeuvre is complete, patient should maintain an
4.1.2 Labyrinthine sedatives like prochlorperazine upright for 48 hours. Eighty percent of the patients
5mg BD for 7 days will be cured by a single manoe uvre. If the patients
4.1.3 Vasodilators like Cinnarizine 25/75 mg BD for remains symptomatic, the manoeuvre can be
7 days or vestibular sedatives like betahistidine repeated. A bone vibrator placed on the mastoid bone
8/16 mg BID for 7 days or for a long time. helps to loosen the debris.
4.1.4 Vitamins like B1,B6 and B12 can be used in
supplementary doses 4.3 General:
4.1.5 Diuretics (Frusemide 20/40Mg for 3 to 5 days)
Smoking and alcohol should be avoided.
and low salt diet for reducing the tension of
endolymph. 4.4 Surgical:
(i) Operations which reduce the tension of
4.2. Labyrinthine Exercises are endolymph
helpful in regaining the (ii) Vestibular nerve section.
confidence of the patient: (iii) Labyrinthectomy
Page 387
21. FRACTURE INVOLVING NASAL BONE
1. Introduction: 4. Investigation:
Two all pieces of nasal bone present on nasal bridge 1. Imaging study like X-ray nose lateral view, X-
which usually get fractured in Head andsm Facial ray PNS, CT scan.
trauma, assault, RTA, sport or industrial accident. 2. Anterior & Posterior rhinoscopy
3. Routine Biochemical & Serological Laboratory
2. Symptoms and Signs: Test.
4. Preinjury photographs if available.
1. History of Trauma
2. Nasal deformity with swelling. 5. Management:
3. Pain
4. Bleeding nose 5.1. Medical:
5. Nasal blockage
6. Discoloration of nasal skin Head up position, cold compression to reduce
oedema.
3. Signs: Suturing of open wound
1. Epistaxis (active or clots in nasal cavity) Anti inflammatory drug (Tab. Diclofenac 50 mg BD
2. Crepitus on palpation over nasal bone area. x 7 da ys.
3. Deformity
4. Oedema on and around nose Antibiotics (Amoxy 500mg TID x 5 days or
5. Nasal obstruction. Parenteral Amoxyclav 1.2gm I.V. 12 Hourly
6. Associated traumatic injury
7. Black eye 5.2. Surgical:
5.2.1. Closed reduction under General Anesthesia
with septal elevation.
5.2.2. Open reduction with wiring in case of multiple
fractures.
Page 388
22. FRACTURE INVOLVINGMAXILLA
1. Introduction: Laboratory Test.
Maxillary bones are present on either side of nose & 5. Types of Maxillary fracture:
are part of skull bone. Fracture maxillary bone occurs
in Head and Facial trauma, assault, RTA, sport or Le fort type I - Floating fracture
industrial accident. Le fort II - Midlevel/ sub zygomatic fracture
2. Symptoms: Le fort III - Craniofacial fracture at supra
zygomatic, zygomaticomaxillary complex
1. History of Truama
2. Nasal deformity with swelling. fracture or Tripod fracture.
3. Pain
4. Bleeding nose 6. Management:
5. Nasal blockage
6. Discoloration of nasal skin 6.1 Emergency care -
Airway maintenance, control of oral & nasal
3. Signs: bleeding.
1. Epistaxis (active or clots in nasal cavity) 6.2 Medical Management -
2. Crepitus on palpation over nasal bone area.
3. Deformity Includes emergency care &stabilisation of general
condition.
4. Oedema on and around nose
5. Nasal obstruction. Anti inflamatory drug (Tab. Diclofenac 500mg BD x
6. Associated traumatic injury 7 days.
7. Black eye Antibiotics (Amoxy 500mg TID x 5 days or
Parenteral Amoxyclav 1.2gm IV 12 Hry
4. Investigation:
6.3 Surgical-
1. Imaging study like X-ray nose lateral view,
X-ray PNS, CT scan PNS. Multi displinary approach with involvment of ENT
2. Anterior & Posterior rhinoscopy surgeon, Maxillofacials& Neurosurgeon may needed
3. Routine Biochemical & Serological depending upoun types & severity of fracture.
Page 389
Figure 1Flowchart of fracture involving Maxilla
History of Trauma to Face: 1. Vitals

Assault 2. Check for ventilation/Circulation
RTA Le fort I/ Floating fracture
Gunshot wounds
Sports 3. Mobility of maxillary alveolar segment (floating
fracture)
Falls 4. Pain and tenderness while speaking or
Industrial accidents clenching
Any Other 5. Ecchymosis or laceration in labial or buccal
vestibule
6. Swelling and oedema of upper lip
7. Mal occlus ion
8. Bilateral epistaxis
Suspect Fracture Involving Maxilla 9. Brusing o f palatal tissues (15-20% of cases)
10. On palpation tenderness over buttress area
11. Percussion of teeth cracked pot sound
Le fort II/ Pyramidal fracture/ Mid level
i. Zygomaticomaxillary fracture/ Subzygomatic fracture
complex # (tripod fracture)
LeFort I, II, III # 1. Oedema mid third of face (Moon face) (Panda faces)
2. Paresthesia of cheek
ii. Zygomatic arch # 3. Bilateral circumorbital ecchymosis
4. Bilateral subconjunctivalhaemorrhage
iii. Alveolar process of maxilla # 5. Dish face deformity
6. Depressed nose
iv. Smash fractures # 7. Epistaxis
8. CSF rhinorrhea
9. Limited ocular movement (Diplopia)
10. Mal occlus ion
11. Inability to ope n mouth
Percussion of teeth cracked pot sound
Le fort III/ Craniofacial dysfunction/

High level fracture/ Suprazygomatic
fracture
1. Oedema of face (Panda faces)

2. Bilateral periorbital edema
Emergency Care: 3. Bilateral circumorbital ecchymosis (Racoon eyes)
1. Airway imme diately evaluated for obstruction 4. Bilateral subconjunctivalhaemorrhage
5. Dish face deformity
6. Depressed nose, flattening of nose
If not maintaining SPO2 - ETT / Tracheostomy 7. Epistaxis
8. CSF rhinorrhea
9. Limited ocular movement (Diplopia, Enophthalmos)
If Cervical Spine fracture - No endotrac heal intubation
10. CSF otorrhoea
Tracheostomy Rather than ETT
11. Mal occlus ion posterior gagging of occlusion
Cervical collar 12. Inability to ope n mouth
Control of oral or nasal bleeding by- 13. Mobility of fractured fragment at NF, FZ sutures
If active Anterior/ Posterior nasal bleeding -AN / PN 14. Tenderness over zygomatic bo ne, arch and FZ suture
Packing Ecchymosis at mastoid process (Battles sign
1. Start Secured IV line for Fluids Replace ment
Page 390
23. PENETRATING NECK INJURY
1. Causes: 4. Immediate Treatment:
Gunshot
Airway
Stab
Breathing
Penetrating shrapnel with or without speed.
Circulation maintenance
2. Levels: These requires immediate intervention.
Includes skin and pl atysma.
5. Investigations:
Includes importunt structures like major vessels
CT neck/Angiography/ Laryngoscopy/
(carotid & jugular vein), trachea, oesophagus,
Bronchoscopy/GI scopy.
cranial & other nerves.
Involvement of spine &vertibrae. 6. Treatment:
3. Look for 6.1 Emergency medical interve ntion to maintain BP
through IV fluid, airwaymaintenance throgh
Dysphasia, Hoarseness of voice, oropharyngial plastic airway in mouth or intubation.
bleeding, neurological deficit, Hypotension, sub 6.2 Surgical intervention includes Haemostasis of
cutaneous emphysema & air bubbles through wound major bleeding vessels & operative management
& tracheal area. for respective truamatised organ & treatment of
head injury component (If associated with).
Page 391
Figure.1 Flowchart of Penetrating Neck injury
Investigations and s urgical referrals
History of: Stab wound

i. Gunshot wounds PenetratingPlatysma
ii. stab wounds
iii. penetrating debris e.g. glass or
shrapnel
Primary
survey:
Assess ABC
No airway Potential for

Airway compromise
compromise- airway interve ntion required:
continue with compromise: Call help and Prepare - for
primary survey Call help from surgical airway -
tracheostomy or
cricothyroidotomy
ENT/Anaesthesia
Look For: Consider OT for
i. Dysphagia Tracheal and/or airway
esophageal injury Any of the following
ii. Hoarseness Tracheal and/or 1. Vascular &/or spinal cord injury
esophageal injury (especially 2. Hypotension
recurrent laryngeal nerve) 3. Subc utaneous emphysema
iii. Oronasopharyngeal bleeding 4. Strider/resp distress
5. Haematome (explanding)
Vascular, tracheal, or
6. Active external hemorrhage from the wound site
esophageal injury 7. Bruit/thrill
iv. Neurologic deficit Vascular 8. Pulselessness/pulse deficit
v. Hypotension Nonspecific; 9. Multitrauma
may be related to the neck
injury or may indicate trauma
elsewhere Soft sign
vi. Subc utaneous emphysema Dnysphagia CT angiography
Tracheal, esophageal, or Hoarseness neck/angiography
pulmonary injury Oronasopharyngeal
bleeding
vii. Air bubbling through the
Laryngeal and/or
Supicion of airway injury
esophageal injury
Suspicion for csophageal consider
Hematoma (expa ndi ng) injury consider UGI bronchofibrescopy/DL
Vascular injury scopyor barium study or scopy
Active external hemorrhage booth
Page 392
24. BLUNT EXTERNAL LARYNGEAL TRAUMA
(FLOW CHART)
Page 393
25.EPISTAXIS
Duration & frequency

1. Definition:
Site, Side, Type, Any medical disorder
It is defined as bleeding from inside the nose.
Drug intake
2. Types: 4.2. First aid -
2.1 Anterior Littles area compression- Pinch the nose with thumb
More common, site of bleeding is littles area, in and index finger for 2 min. & ask the pt. breath
children and young adults. orally.
4.3.1 In Anterior Epistaxisanaesthesize the bleeding
2.2 Posterior point and cauterize with bead of silver nitrate
Less common, site of bleeding is posterior superior or coagulate with electro cautery.
area, seen in adults. Anterior Nasal packing
3. Causes: 4.3.2 Posterior. Nasal Packing
4.3.3 Endoscopic cauterization
4.3.4 If above measures fails then ligation of
3.1 Local vessels.
Injuries to nose, Vascular malformation, fracture of 4.3.5 External carotid- after the origin of superior
maxilla, fracture nasal bone, nasal surgery, acute thyroid artery
sinusitis, rhinitis, nasal diphtheria, atrophic rhinitis, 4.3.6 Maxillary artery - approached through
rhinitis sicca, tuberculosis, syphilis, Rhinosporidiosis, caldwell- luc operation.
foreign body in nose like maggots, deviated nasal 4.3.7 Ethmoid artery ligation
septum.
4.4 General Measures:-
3.2 Nasopharyngeal - Sit up with back rest
Adenoids, Juvenile angiofibroma,Malingnant tumors
Record blood loss in spitting & vomiting
3.3 General causes - Reassure
hypertension, leukemia, hemophilia, aplastic anemia, Mild sedation
cirrhosis of liver, nephritis, patient with anti
coagulant therapy, influenza, chickenpox, malaria. Check vital signs
Maintain haemodynamics-blood transfusion if
4. Management: required
Intermittent oxygenation
4.1. Enquire about
Investigate & treat
Mode of onset
Page 394
26. PREMALIGNANT LESIONS OF THE ORAL
CAVITY
Lip: Inspect and palpate inner and outer surfaces
1. Introduction: of the upper and lower lip.
Oral cavity cancer accounts for approximately 3% of Buccal mucosa
all malignancies and is a significant worldwide health Inspect and palpate buccal mucosa and cheek.
problem. Most oral malignancies occur as squamous Inspect and palpate parotid duct to express
cell carcinomas (SCCs); Most of the oral SCCs saliva.
develop from premalignant conditions of the oral Gingival and alveolar ridge: Inspect and palpate
cavity. The early detection of cancer is of critical gingival and alveolar ridge on facial and lingual
importance because survival rates markedly improve aspects.
when the oral lesion is identified at an early stage Tongue
(early intervention) Inspect and palpate dorsal and ventral surfaces
with accompanying retraction of the tongue with
2. Types gauze.
2.1 Leukoplakia Inspect and palpate lateral borders from anterior
White patch or plaque to posterior with manual retraction.
2.2 Erythroplakia Floor of the mouth
A fiery red patch with a soft, velvety texture Inspect and palpate floor of the mouth.
2.3 Proliferative verrucous leukoplakia Inspect and palpate submandibular ducts to
Proliferative verrucous leukoplakia (PVL) is a unique express saliva.
form of aggressive disease. Hard palate: Inspect and palpate.
2.4 Palatal lesion of reverse smokers Soft palate and oropharynx: Depress the dorsal
The palatal lesion of reverse smokers is unique to surface of the tongue and inspect soft palate and
individuals who place the lit end of a cigarette inside anterior oropharynx.
the mouth. Salivary glands: Palpate the parotid,
2.5 Oral submucousfibrosis (SMF) submandibular, sublingual, and minor salivary
It is a chronic progressive condition.In which nor mal glands. Ensure clear salivary flow.
mucosa with blood supply is replaced by fibrous
tissue leading to narrow mouth ope ning. 4. Investigations:
2.6 Other forms: Biopsy of the lesion and histopathological
Lichen planus, discoid lupus erythematous, and diagnosis is the gold standard investigation.
epidermolysisbullosa. Oral cytology
3. Work-up and the Early Oral cytology describes a diagnostic technique used
to sample oral tissue for histopathogical analysis. To
Detection of Oral Cancer: obtain a tissue sample, the clinician applies a stiff
The standard criteria for diagnosis and identification brush to the oral mucosa with enough pressure to
of oral lesions is histopa thology analysis via the induce pinpoi nt bleeding, which ensures a full-
procurement of a tissue sample by surgical biops y. thickness or trans-epithelial tissue sample. These
cellular samples can then be analyzed by a variety of
3.1 Oral cavity examination: unique diagnostic measures, including
cytomorphometry, DNA cytometry, and
Extra oral immunoc ytoc hemical analysis.
Inspect the head a nd neck.
Palpate cervical lymph nodes and salivary glands
Page 395
27. ACUTE UPPER AIRWAY OBSTRUCTION
gagging,4 Signs of hypoxaemia
1. Introduction: andhypercarbias.a. Anxiety,confusion,lethargy
Upper airway consist of nose, nasopharynx, pharynx, and cynosis may be present as the obstruction
larynx and trachea upto carina. Different pathologies worsen.4 Powerful inspiratory efforts against an
in this area can lead to acute airway obstruction. obstruction may produce ecchymosis and
subc utaneous emphysema.
Obstruction here may be partial or complete. This is
also called as extra thoracic airway. The airway 3. Management:
collapses during inspiration and dilates during
expiration. 3.1. General measures:
1. Reverse hypoxia-100% Oxygen or as close as
2. Clinical presentation possible.
2. Iv access as soon as possible.
May be partial or complete 3. Continuous monitoring and observation.
2.1. Complete upper air way
3.2 Airway management techniques
obstruction: 3.2.1 Airway manoeuvres
1. Universal chocking sign: patient is unable to
a. Jaw thrust.
breath, speak or cough and may hold the throat
b. Oropharyngeal or nasopharyngeal airway may be
between the thumb and finger.
useful in the unconscious patient.
2. Vigorous attempts at respiration with
d. If the patient is not immediately intuba ted, t hen
intercostals and supraclavicular retraction.
give coma position i. e. Semi prone,slightly head
3. Heart rate and blood pressure raised. Patient
down.
becomes rapidly cyanosed.
4. This is followed by diminished respiratory
efforts, loss of consciousness,bradycardia,and 3.2.2 Endotracheal intubation.
hypotension.
5. Cardiac arrest Surgical airway:
6. Death is inevitable if obstruction is not relieved 1. Indicated when endotracheal intubation not
within 3-5 minutes. possible.
2. Percutaneous transtracheal jet ventilation.
2.2. Partial airway obstruction 3. Cricothyroidectomy.
1. May be stable or their may be progressive 4. Formal tracheostomy under local anaesthesia
deterioration may be tried before emergency treacheostomy.
2. Signs and symptoms may be mild but as they 5. Emergency tracheostomy rarely required.
worsen patient develops inspiratory
stridor,dysphonia,aphonia, chocking, drooling
Page 396
28. DEAF MUTISM
1. Definition: 4. Investigation:
Deaf Mutism is the inability to acquire speech due to Brainstem Evoked Response Audiometry
profound or high degree hearing loss (congenital or (BERA) - It is of value to find out the threshold
early acquired childhood) of sensor y neural type in of hearing in infants, pa rticularly the high risk
both ear. group & in the diagnosis of retrocochlear
pathology.
Oto acoustic emission (OAE)
2. Causes: Audiometric examination
Free field audiometry
2.1 Prenatal- Visual reinforce audiometry
i. Genetic Defect Play audiometry
ii. Maternal Infection Electro- cochleography -
iii. Drugs During Pregnancy Impedance audiometry
1. Amino glycosides
High- resolution CT scan
2. Quinine
3. Chloroquine
iv. Radiation to Mother in first trimester 5. Treatment:
v. Other factors: Nutritional deficiency, diabetes,
toxaemia& thyroid deficiency Bilateral hearing aid
Surgical interventions includi ng Coc hlear
2.2Perinatal - implant
1. Anoxia Audi tory training
2. Prematurity Language communication
3. Birth injuries
4. Neonatal Jaundice 6. Referral:
5. Ototoxic drugs
If deaf mutism is suspected after investigation, the
2.3 Post natal - child should be referred to a higher centre for
1. Genetic Cochlear implant.
2. Non-Genetic
7. Prevention:
3. Identification of Deafness:
Vaccination to child, avoidance of ototoxic drugs,
History regular antenatal checkup & care.
Responses of hearing in child by investigations
Page 397
OPHTHALMOLOGY
Page 398
1. LID SWELLING
1. Stye (HordeolumExternum)
1.1 Definition
It is an acute suppurative inflammation of the Zeis
/Moll glands.
Figure 1.1 Stye
1.2 Etiology At night time Ciprofloxacin eye ointment for 7

days.
Bacterial- Staphylococcus Tablet Ciprofloxacin 500mg (systemic
antibiotics) twice daily and Tab. Diclofenac
1.3 Symptoms Sodium 50mg bid (anti-inflammator y) for three
Pain or four days.
Lid swelling When pus poi nts out it should be let out by
Watering pulling the affected eye lash Epilation.
1.4 Sign
A painful swelling at the lid margin.
2. HordeolumInternum
2.1 Definition
1.5 Treatment It is an acute suppurative inflammation of the
Hot fomentation 2-3 times per day. Meibomian glands.
Ciprofloxacin 0.3 % (Antibiotic) eye drops. 1-2
drops six times per day for 5 days.
Page 399
Figure 1.2 HordeolumInternum
2.2 Symptoms The pus should be drained by incising it.

Pain, lid swelling and watering.
2.3 Sign 3. Chalazion

A painful swelling at the lid margin.
3.1 Definition
2.4 Treatment It is a chronic granulomatous inflammation of
Ciprofloxacin 0.3 % eye drops six times per day the Meibomian gland.
for 5 days
Tablet Ciprofloxacin 500mg (Systemic
antibiotics) twice daily and Tab. Diclofenac
sodium 50mg BD (anti-inflammatory) for three
days.
Figure 1.3 Chalazion
3.2 Etiology
Uncontrolled Diabetes Mellitus in adults.
Refractive errors.
Page 400
Very rarely a malignant change may occur
(Meibomian carcinoma) especially in old age
3.3 Symptoms with a history of recurrence.
Swelling of the lid and Watering.
3.4 Sign 3.6 Treatment

Painless nodular swelling away from the lid margin. Incision and curettage under Proparacaine 0.5 %
eyedrop (local anesthesia.
3.5 Course In Marginal chalazionintralesional injection of
Spontaneous resolution. Triamcinolone 40mg/ml (Depot steroids) : 0.1 to
If secondarily infected, then it is called as 0.2 ml once may be helpful.
Internal Hordeolum. Correction of refractive errors, if any.
It may burst through the conjunctiva.
4. Blepharitis 4.1 Definition

Inflammation of the lid margin is called as
Blepharitis.
Figure 1.4 Blepharitis
4.2 Causes 4.4 Signs

SeborrhoeicBlepharitis due to dandruff at the Edema of lid margin, dandruff /ulcer at the root of
base of eye lashes. eye lashes.
Ulcerative Blepharitis because of infection by
Staph.Epidermidis / Streptococci. 4.5 Treatment
Clean the lid margin with warm water 2-3 times
4.3 Symptoms a day.
Itching / rubbi ng of eyelids. Chloramphenicol- Polymixin B combination
(Ocupol) eye oi nt. 3 times a day for 3weeks.
If a Chalazion recurs soon after removal or is rapidly growing in size or ulcerates, a biopsy must be done to rule
out any malignancy.
Page 401
2. DACRYOCYSTITIS
1. Acute Dacryocystitis 1.1 Definition:

Acute Dacryocystitis is a suppurative infection in the
lacrimal sac caused by ablocked nasolacrimal duct.
(NLD)
Figure 2.1 Acute Dacryoc ystitis
1.2 Pathogenesis: There is also Tear Lake, fullness,

When the ope ning of NLD is blocked, tears and conjunctivalcongestion (i.e. watering and redness of
mucous will remain within sac, forming a deposit that eyes.)
gets easily infected.
1.6 Associated symptoms:
Fever, malaise.
1.3 Microorganism:
Most commonly Staphylococcal infection and
Streptococcal infection. 1.7 Treatment:
i. Tab.Ciprofloxacin 500mg twice daily initially
for 5 days.
1.4 Stages: ii. Tab. Ibuprofen 3 times a day (Non Steroidal
i. Stage of cellulitis. Anti Inflammatory Drug).
ii. Stage of lacrimal abscess. iii. Hot fomentation 3 times a day.
iii. Stage of fistula formation. iv. Ciprofloxacin 0.3% eye drop one drop four
times a da y and Ciprofloxacin eye oi ntment at
night time for 5 days.
1.5 Clinical features: v. If there is a pus point, drainage of pus is
Acute onset, painful, red, hot, firm swelling over
required.
lacrimal sac area.
In severe cases there may be a pus point, which may
NO SYRINING IS DONE IN ACUTE CASES OF
burst
DACRYOCYSTITIS
Page 402
1.8 Complications : 1.9 Referral:
Acute conjunctivitis, corneal ulcers, lid abscess, When acute attack of Dacryocystitis is subsided,
orbital cellulitis, cavernous sinus thrombosis. patient is referred to higher centre for sac surgery
(DCR) and Fistulectomy, if required.
2.2. Chronic Dacryocystitis: 2.1 Definition:

Chronic low grade inflammation of lacrimal sac is
called as Chronic Dacryoc ystitis.
Figure 2.2 ChronicDacryocystitis
2.2 Pathogenesis: 2.4 Treatment:

Stricture formed due to chronic inflammation. Topical Ciprofloxacin 0.3% eye drops four times a
day. Syringing with Ciprofloxacin 0.3% daily once
Obstruction of lower end of nasal nasolacimal duct
caused by polyp or hypertrophied inferior turbinate. for 5 days.
2.3 Clinical Picture:

Essential symptom is watering of eyes. 2.5 Complications:
Chronic intractable conjunctivitis, corneal ulcer,
There may be swelling at lacrimal sac area ectropion.
(Mucocele).
Regurgitation test (on pressure over medial
canthus of eye i.e. over sac region) is positive
2.6 Referral:
For sac surgery (Dacryoc ystor hinos tomy or
(Mucopus, pus).
Dacryocystectomy).
3. Congenital Dacryocystitis
3.1 Definition:
Non canalization of nasolacrimal duct leading to
blockage of drainagepassage may lead to congenital
Dacryoc ystitis.
Page 403
Figure 2.3 Congenital Dacryoc ystitis
3.2 Symptoms:
Baby is brought with complaints of watering from 3.4 Treatment:
Moxifloxacin 0.5 % eye drops 4 times a day.
one/bot h eyes.
Crigglers Massage over sac region.
3.3 Signs: If the block persists for more than 6 months
Swelling at sac region,discharge on pressure over probing of nasolcrimal duct is done by
swelling. ophthalmologist under general anaesthesia.
Page 404
3. CONJUNCTIVITIS
Infectious conjunctivitis can be bacterial or viral.
1. Defination :
Inflammation of conjunctiva is called as 2.1. Mucopurulent/purulent
conjunctivitis. (Bacterial) conjunctivitis
2.1.1 Definition:
2. Types
Acute purulent inflammation of conjunctiva.
It can be Infectious or Allergic.
Figure 3 Conjunctivitis
2.1.2 Causes:
Staphylococci ,Streptococci,Pneumococci, 2.1.5 Treatment:
Gonococci etc.
Moxifloxacin 0.5 % eye drops two hourly for 7
2.1.3 Symptoms: days.
Acute redness of eyes, grittiness of eyes with Chloramphenicol 1% eye oint. At bed time for 7
mucopurulent/ purulent discharge.
days.
2.1.4 Signs: Dark goggles.
Conjunctival congestion, mucopurulent / purulent
discharge (no diminution of vision, photophobia), 2.1.6 To prevent spread of infection:
matting of eye lashes due to discharge. Frequent hand washing.
Avoid crowded places.
Avoid sharing of handkerchief, towels, napkins,
pillows etc.
Page 405
2.2 Viral conjunctivitis 2.2.1 Definition:
Acute conjunctival inflammation caused by viruses.
Figure 3.2 Viral Conjunctivitis
2.2.2 Causative organisms :

To prevent the spread of infection
Herpes simplex, Herpes zoster, adenovirus etc.
2.2.3 Symptoms: Frequent hand washing to be done.
Avoid crowded places.
Acute redness of eyes, grittiness of eyes, watering
Avoid sharing of handkerchief, towels, napkins,
from eyes, photophobia.
pillows etc.
2.2.4 Signs: AVOID USE OF STEROIDS (BOTH TOPICAL
AND SYSTEMIC).
Local:Conjunctival congestion, follicular
hypertrophy withpreauricular
lymphadenopathy.
Systemic: Patient may have fever, Upper respiratory

tract infection.
2.2.5 Treatment:
Usually self limiting course.
Acyclovir 3% eye oint. 5 times a day for 14 days
with,
Prophylactic Moxifloxacin 0.5% eye drops four
times aday for 7 days with,
Fluromethonolone 0.02% eye drops four times a
day for 7 days.
In case of H.ZosterOphthalmicus refer to

Ophthalmologist immediately.
2.3. Allergic conjunctivitis 2.3.1 Definition:Conjunctivitis caused as allergic
reaction to pollens, dust,etc.
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Figure 3.3 Allergic Conjunctivitis
2.3.2 Symptoms:
Recurrent attacks of redness, ropy discharge,

irritation, itching.
2.3.3 Signs:
Conjunctival congestion,mucoid discharge, papillary
hypertrophy.
2.3.4 Treatment:
If there is secondary infection, use combination Carboxymethylcellulose 1% eye
ofTobramycin 0.3%&Flurometholone 0.02% eye drops(Lubricating eye drops) one drop 4 times a
drops,One drop 4 times a day for 15 days, along day for 15 days.
with OR
Olopatidine 0.1% eye drops, One drop twice a
day for 1 week.
Prevention of spread of infection is equally important as that of treatment
Page 407
PTERYGIUM
Figure 3.4 Pterygium
Pterygium
A Pterygium is a triangular sheet of fibro vascular

tissue which invades the cornea. Pterygia typically
develop in patients who have been living in hot
climates and may represent a response to chronic
dryness and exposure to the sun.
Signs .
The conjunctiva then overgrows the opacities

and progressively encroaches onto the cornea
in a triangular fashion.
Early cases show small, grey, corneal

opacities near the nasal limbus.
Treatment
Surgical excision is indicated either for cosmetic
reasons or in cases of progression towards the visual
axis. The excision of theconjunctival component
followed by auto grafting or amniotic membrane grafting.
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4. CORNEALULCER
Corneal ulcer is defined as breech or discontinuation
1. Definition: of corneal epithelium with necrosis of surrounding
corneal tissue.
Figure 4.1 Hypopyon Corneal ulcer
2. Etiology Of Corneal Ulcer:

Etiology Of Corneal Ulcer
________________________________________________________________
NONINFECTIVEE
INFECTIVE
________________________________________________________
FUNGI VIRUSES
BACTERIA PROTOZOAS
Pathoge ns can inva de intact corneal epithelium & can cause ulceration.
Infective agents:
N. Gonorrhoea, C. Diptherium, N. Meningitidis.
Page 409
NONINFECTIVE
Traumatic PostSurgical Lacrimal Lids& Lashes
Neurological Immunological Dermatologic Nutritional
Others
Figure 4.2: Etiology of Corneal ulcer
Iritis
3. Clinical features
Post. Synechia
3.1 Symptoms: Lens nor mal
Redness
IOP Normal/ Raised
Pain
Sac (Dacryocystitis)
Watering / discharge
Photophobia
Diminution of vision 4. Investigations:
Fluorescein Staining
Corneal Scrapings
3.2 Signs:
Lid Ede ma Gram Staining
Conjunctival Congestion Giemsa Staining
Ciliary Congestion KOH Mount
Corneal Ulcer Culture & Sensitivity
Hypop yon Sac syringing
Anterior Chamber Depth Shallow (Indicates Routing Investigation

Perforation)
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Blood Pressure DiclofenacSodium 50mg BD (anti-
inflammator y) for three or four da ys.
Blood sugar
Refer the patient to Opthalmologist.
5. Treatment:
Cleanliness 6. Complications after
Fortified topical antibiotic eye drops like perforation:
Amikacin 80mg/2ml.
Adherent leucoma
Tobr amycin with a syringe, Inj 2ml of
Ant. Staphyloma
Tobramycin (40mg/ml) directly into a 5 ml
bottle of tobramycin (0.3%) eye drop. Use Corneal fistula
within 14 da ys. keep in refrigerator.
Pseudocornea
Antibiotics :Topical Moxifloxacin 0.5% eye
drops 2hrly. Spread of infection to other ocular tissues
Cycloplegics -Atropi ne sulphate 1% eye oi nt Expulsion of the lens / vitreous

twice a day. Expulsive choroidal hemorrhage
Hot fomentation. Spontaneous evisceration
Rest. Endophthalmitis / Panophthalmitis.
Systemic antibiotic Tab.Ciprofloxacin 500mg
BD for 5 days.
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5. SCLERA
Figure 5.1 Episcleritis
1. Episclerities
Unilateral mild discomfort
It is a common, benign, self-limiting and frequently Tenderness to touch
recurrent disorder which typically affects young
adults. It is seldom associated with a systemic Watering
disorder and never progresses to a true scleritis.
4. Treatment
2. Types of Episcleritis
Mild cases
2.1 Simple Episcleritis Topical steroids, Ciprofloxacin 0.3% +
It is characterized by sectoral or rarely, diffuse dexamethasone 0.1% eye drops,one drop three
redness. It usually resolves spontaneously with times a day or topical NSAIDs, Ketorolac
1-2 weeks. Promethymene eye drops 0.5% one drop three
times a day for one week.
2.2 NodularEpiscleritis
It is localized to one area of the globe, Unresponsive recurrent cases Systemic
for ming a nodule with surroundi ng congestion. Flurbiprofen 100mg three times a day.
1. Symptoms
2. Scleritis 2.1 Defination
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Scleritis is a granulomatous inflammation of the
sclera.
Figure 5.2 Scleritis
2.3 Types Rheumatoid Arthritis
2.2.1 Anterior scleritis Connective tissue disorders
a. Non-necrotizing diffuse or nodular. Miscellaneous conditions like relapsing

Polychondritis, Herpes Zoster.
b. Necrotizing with or without inflammation.
2.5 Treatment
2.2.2 Posterior scleritis
Oral NSAIDs Flurbiprofen 100mg three times
2.4 Symptoms a day for 5 days.
Unilateral mild discomfort Oral Prednisolone 40-80mg a day tapered
according to response.
Tenderness to touch
Combined therapy with a NSAID and low dose
Watering steroid.
2.5 Associated systemic diseases If it does not respondrefer to Opthalmologist.
About 45% of patients with scleritis have associated
systemic diseases like,
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6.UVEITIS
1. Definition: Inflammation of Uveal tract is known as

Uveitis.
Figure 6.1 Uveitis
Keratic precipitates and aqueous cells/flare can be

2. Causes: seen on slit-lamp e xamination.
Auto immune
Infective 3.2 Intermediate uveitis
3.2.1 Symptoms:
3. Classification:
Depending on the anatomical part of Uvea involved it Decrease in vision (usually slight blurring)
is classified as Black spots in front of eyes (floaters)
1) Anterior (Irido-cyclitis)
2) Intermediate (Pars-planitis)
3) Posterior (Choroiditis) 3.2.2 Signs:
4) Panuveitis (all parts are involved) Ciliary Congestion.
Tenderness OverCiliary Body.
3.1 Acute Anterior Uveitis
3.1.1 Symptoms: Snow Banking and Vitreous haze seen on
Ophthalmoscopy.
Redness
Pain dull-aching pain , more during night
3.3 Posterior uveitis
3.3.1 Symptoms:
Watering No pain , Decrease in vision
Photophobia (intolerance to light) Black spots in front of eyes (floaters)
Decrease in vision (usually slight blurring)
3.1.2 Signs: 3.3.2 Signs:
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Vitreous haze, focal inflammatory lesions and Visual acuity.
macular ede ma detected on ophthalmoscopy. Pupillary reaction.
Slit-lamp examination for keraticprecipitates,
3.4 Panuveitis: aqueous cells and flare.
Symptoms and signs of both anterior and posterior Dilated fundus examination for vitreous haze,
uveitis are present. snow banking, chorioretinitis lesions, cystoid
macular ede ma.
4. Complications:
Complicated cataract 5.2 Investigations:
Secondary Glaucoma Depending on most likely cause in a particular case
following investigations may be required,
Cystoid macular edema
Complete Blood Count
Retinal Detachment Blood sugar levels
X-ray chest , ESR and Monteux test to rule out
Phthisis Bulbi (shrunken eye)
Tuberculosis.
VDRL / TPHA to rule out Syphilis.
5. Evaluation of a Case of ELISA for HIV.
Uveitis:
5.3 Treatment:
History
Detailed history of previous episodes, treatment Topical steroids Prednisolone Acetate 1% eye
and response to treatment. drops (1hrly initially then tapered according to
History of associated systemic conditions like response to treatment).
Tuberculosis, Syphilis, HIV infection, Cycloplegic Atropine Sulphate 1% eye drops
Rheumatoid Arthritis, AnkylosingSpondylitis, TDS.
malignancies, Diabetes Mellitus etc. Antibiotics and systemic steroids are usually not
required.
5.1 Ocular examination:
Uveitis is a vision threatening condition. Refer the patient immediately on

suspicion of Uveitis .
Long term use of steroids can cause Cataract and Glaucoma.
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7. GLAUCOMA
1. Introduction :- 3. Classification
Second major cause of blindness. 3.1 According to aetiology
Often asymptomatic in early stage. Primary
Damage is irreversible. Secondary
Effective treatment is available. Congenital- Present at birth.
IOP Depends on the balance between production Infantile,present in first year of
and removal of aqueous hunour. life.Juvenile,pr esent in the late childhood.
2. Definition: 3.2 According To ApperanceOfThe

Chronic progressive optic neuropathy caused by Angle
a group of oc ular conditions which lead to
damage of the optic nerve with loss of visual Open angle Glaucoma
function. Closed angle Glaucoma
Combined mechanism Glaucoma
Pathogenesis
Raised IOP ( Intra Ocular pressure)-

4. Investigations :-
mechanical changes - decreased axoplasmic flow
IOP with Applanation/Schiotz Tonometer
- ganglion cell death apoptosis.
SLE (Slit Lamp Examination)
Reduced optic nerve head perfusion Ischemia.
Fundus Examintion
Gonioscopy
Visual field testing
OCT ( Optical Coherence Tomography)
Open-Angle Glaucoma
Figure 7.1 Open-Angle Glaucoma
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3.2.1 Open-angle Glaucomathe most common Defects in nerve fiber layer.
form of Glaucoma, accounting for at
least 90% of all Glaucoma cases: d. Manage ment:
Start TimololMaleate 0.5% twice daily if patient
It is caused by the slow clogging of the drainage is not Asthmatic or not Hypertensive, according
canals, resulting in increased intra ocular to response.
pressure Start Latanoprost 0.005 % /Travoprost 0.004 %
(Prostaglandi n analogues ) one Drop Once Daily
Has a wide and open angle between the iris and in the Eve ning if patient is Asthmatic or
cornea. Hypertensive , according to response.
Develops slowly and is a lifelong condition. Systemic Tab. Acetazolamide 250-1000 mg /day
orally.
Has symptoms and damage that are not noticed. Surgical Treatment Trabeculectomy
Refer the patient to a higher centre for evaluation
It causes SLOW damage to the optic nerve
and management .
causing gradual and irreversible loss of vision.
Open-angle means that the angle where the iris 3.2.2 Primary Angle Closure Glaucoma
meets the cornea is as wide and open as it should
be. Open-angle Glaucoma is also called primary a. Introduction :-
or chronic glaucoma. It is the most common type
of Glaucoma, Angle-closure glaucoma, a less common form of
a. Risk Factor : glaucoma:
Age - 6th decade. Is caused by blocked drainage canals, resulting
Sex Common in Female . in a sudde n rise in intraocular pressure.
Race Common and more severe in Black.
Family Histor y and Inheritance First degree Has a closed or narrow angle between the iris
relative of patients with POAG( Primary Ope n and cornea.
angle Glaucoma ) are at increased risk of Develops very quickly.
developing the disease.
Refractive error- POAG is common in Myopia Has symptoms and da mage that are usually very
noticeable.
b. Clinical features: Demands immediate medical attention.
Generally asymptomatic headache.
It is also called acute glaucoma or narrow-angle
Frequent changes in Presbyopic correction.
glaucoma. Unlike ope n-angle glaucoma, angle-
Difficulty in dark adaptation.
closure glaucoma is a result of the closure of angle
Scotoma (especially in inferior field).{Blindness between the iris and cornea.
in particular sector}
b. Definition:
c. Signs:
Spectrum of conditions in which the peripheral iris
Intraocular pressure > 21 mmHg moves forward to block the openings of the
(SchiotzTonometer). trabecular meshwork at the angle, causing a rise of
Optic nerve head changes - C:D ratio > 0.5. intraocular pressure.
Asymmetry between two nerve heads > 0.2.
Narrowing/notching/pallor of NRR.
Disc hemorrhages.
Visual field defects.
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Figure 7.2 Angle-Closure Glaucoma
c. Predisposing factors: Stony hard eyeball ( very high Intra Ocular

Short eye, Hypermetropia.
pressure).
Smaller corneal diameter. e. Treatment:
Shallow anterior chamber.
Relative forward positioning of lens-iris diaphr agm. Systemic - Intravenous Mannitol 20% 1-2 gm
per Kg over an hr.
d. Clinical features:
Tab. Acetazolamide , 250-1000mg per day in
Unilateral headache or brow ache. divided doses should be given if the patient is
Blurring of vision on the same side. not nauseated or vomiting and can tolerate oral
Unbroken colored halos around lights during the medication.
episode. One drop of 2% Pilocarpine placed in the eye
Gross diminution of vision. every 5 min till pupil constricts,then One drop
Red eye. QID.
Nausea, vomiting.
One drop of TimololMaleate 0.5 % twice daily.
Ciliary and conjunctival congestion, hazy cornea.
Vertically oval, mid dilated pupil.
3.2.3 Congenital Glaucoma

(Buphthalmos)
a. Definition:
Glaucoma appearing between birth and the
ages of 3-4 years.
Page 418
Figure 7.3 Congenital Glaucoma
b. Pathogenesis: Intolerance to light.
Corneal edema.
Failure / abnormal development of the trabecular
meshwork. Watering.
Angle remains closed by persistent embryonic Blue sclera.
tissue. Iridodonesis.
c. Clinical features: d. Manage ment:

Urgent referral to higher center for Goniotomy /
Enlarged e ye. Trabeculotomy.
Hazy cornea - frosted glass appearance.
3.2.4. Lens Induced Glaucoma

Definition:
It is a type of Optic Neuropathy secondary to raised
IOP due to Cataractous lens (hypermatureCataract).
Figure 7.4Lens Induced Glaucoma
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Complete Blood Count.
a. Classification: Blood Sugar Level estimation.
Phacolytic glaucoma. Kidney Function Test .
Phacomorphic glaucoma. Serum Electrolytes.
Phacoanaphylacticglaucoma . Serology.
b. Symptoms: B-Scan.
Diminution of vision.
Pain .
e. Aims of Manage ment:
Redness of eyes.
Headache. To relieve pain.
c. Signs: To minimize optic nerve insult secondary to

raised IOP.
Decreased visual acuity .
To remove the cause.
Conjunctival congestion.
Corneal edema. To reduce the IOP
IV Mannitol (20%) 1-2 gm/kg over 30 min.
Anterior Chamber shallow ( phacomorphic
glaucoma). IV or systemic Acetazolamide 250-1000
mg/day till IOP reduces.
Flare, cells, sterile hypop yon.
f. Surgery:
Pupil sluggishly reacting to light.
After controlling IOP.
Lens mature or hypermatureCataract.
ExtracapsularCataract Extraction with PCIOL
IOP raised. implantation.
Fundus Absent Glow. Post Operative IOP monitoring.
d. Investigations:
Visual damage in Glaucoma is irreversible hence early detection by regular screening is important.
Once diagnosed, Glaucoma is lifelong, which needs continuous lifelong treatment and follow up.
Treatment is aimed at preserving the vision.
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8. CATARACT
A cataract is clouding of the lens of the eye, which Risk factors for age-related cataract include Diabetes,
impedes the passage of light. Most cataracts are prolonged exposure to sunlight, tobacco use and
related to ageing, although occasionally children may alcohol consumption. Vision Can be restored by
bor n with this condition, or cataract may develop surgically removing the affected lens, and replacing it
after an injury, i nflammation or disease. by an artificial one.
Figure 8.1 Cataract
1. Definition:
Any opacity of lens or its capsule whether
congenital or acquired is known as cataract.
2. Types of cataract : 2.3 Complicated cataract

2.1 Senile cataract 2.4 Metabolic cataract
2.2 Traumatic cataract
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Figure 8.2 SenileCataract
Figure 8.3 Traumatic Cataract
Figure 8.4 Complicated Cataract
Page 422
Figure 8.5 Metabolic Cataract
eyedrops one drop six times a day for one week

3. Stages of Cataract: tapered every week up to six weeks & topical
Immature cataract NSAIDs, Ketorolac Promethymene eye drops
Intumescent 0.5% one drop three times a day for two week.
Mature cataract Tropicamide 1% eye drops one drop at night
Hypermature- Mor gagnian time for two weeks.
Sclerotic First follow up at end of the first week & final
follow up after 40 days for spectacle correction.
4. Clinical features:
Painless progressive diminution of vision, glare, 6.2 Complications of cataract
black spots before the eyes, distortion of objects, surgery:
polyopia.
Complications of hypermaturity like Uveitis and
Lens dislocation, Glaucoma. Early- Striate Keratitis, corneal ede ma, prolapse
of iris, Hyphema, Anterior Uveitis, delayed
formation of anterior chamber, early
5. Investigation :- Endophthalmitis, Toxic Anterior Segment
Syndrome(TASS).
V/A, IOP, Syringing. Late- Bullous Keratopathy, Cystoid Macular
Blood Pressure, Blood sugur, ECG, Urine edema, posterior capsular opacification,
routine. secondary Glaucoma, Retinal Detachment, late
A-scan. Endophthalmitis.
Xylocain sensitivity test.
Physician fitness. It is imperative for a Medical officer to recognize
late complications of cataract surgery.
6. Treatment:Surgery- 6.2.1 Bullous keratopathy

Conventional Extra Capsular Cataract Extraction Corneal oedema due to corneal decompensation.
with Posterior Chamber Intra Ocular Lens Managed in initial stage, by local hypertonic saline
Implant (PCIOL). eye drops (four times a day and eye ointment at
Manual Small Incision Cataract Surgery (SICS) night) & oral tablet Acetazolamide 250mg three
with PCIOL. times a day. If unresponsive, Keratoplasty is the
Phacoemulsification with PCIOL treatment of choice.
6.2.2 Posterior Capsular Opacification

It is the thick capsular opacification of posterior
6.1 Post Operative Management capsule after extra capsular cataract surgery .It can be
managed by Nd:YAGcapsulotomy.
Topical Steroid + antibiotic eye drop
Ciprofloxacin 0.3% + Dexamethasone 0.1% 6.2.3 Cystoid Macular Edema.
Page 423
Relatively uncommon in uncomplicated ConjectivalChemosis.
phacoemulsification, occurs more often after the A/C Reaction, Irits, Corneal Haze, Hypop yon,
complicated surgery. Peak incidence 6-10 weeks. Circumcorneal congestion.
6.2.4 Post OperativeEndophthalmitis d. Risk factors:

a. Definition:- Post operativeEndopthalmitis.
Refers to intraocular inflammation predominantly Environmental factors : Improper OT
involving the vitreous cavity and anterior chamber as fumigation, Improperly cleaned OT.
a result ofpost operative intraocular colonization by Improper sterilization techniques.
microor ganisms. URTI in Surgeon / staff/ patient.
Instrumentation with improperly autoclaved
b. Symptoms instruments.
Infection of Sac Blepharits.
Pain, Diminution of vision, redness and watering Open wound leak.
of eye. Poor patient hygiene .
c. Signs:- Poor compliance in putting post operative
Decrease visual acuity. medicine.
Lid swelling. Post operative rubbing of eyes/ Trauma.
Discharge.
Corneal edema.
e. Types (onset)
Immediate Delayed
Within 24-48 hrs. 48-72 Hrs.
Confection : Complete loss of eye sight if no timely - Fortifide Gentamycin eye drop every 15min.for 2
interve ntion done. hrs. then one hourly three days.
- Moxifloxicilin 0.5% eye drops hourly.
f. Treatment: - Cycloplegics Atropine Sulphate 1% eye
It is an acute ophthalmic emergency ointment, eye drops.
- Start intrusive systemic and topical antibiotics. - Urgent referral to Ophthalmologist is required.
Page 424
9. OPHTHALMITIS
1. Endophthalmitis:
1.1 Definition : Endophthalmitis is the clinical term used to describe
the inflammator y response of the eye to oc ular
infection.
Figure-9.1: Endopthalmitis
Acc to aetiological agents

Based on aetiological agents
Endophthalmitis
Bacterial Fungal
Fungal Viral
Parasitic
Page 425
1.2Types :
1.3 Risk Factors Contaminated IOLs, viscoelastics, poor OT

Hygiene, hospital construction activities.
1.3.1 Bacterial
Defects in sterilization of instruments.
1.4 Symptoms
Contamination of tap water. Patient presents with symptoms most commonly on
Multiple dose fluids and drugs. the second day after surgery.
1.3.2 Fungal Pain
Contaminated irrigating solutions. Red
Decreased vision. Hence, intravitreal injections are treatment of

Hazy cornea. choice.
Hypop yon. Intravitreal injections bypass the blood retinal
Post-operative endophthalmitis is the most barrier and rapidly achieve therapeutic levels at
common form. the sites of infection.
It comprises 70% of infective endophthalmitis. Large majority follow cataract surgery, most
common surgical procedure (approx prevalence
0.082%-0.1%)
1.5 Management Post-operative endophthalmitis is one of the
In established endophthalmitis, antibiotics when most dreaded complications of cataract surgery
given orally or I.V., have poor penetration into and constitutes a true emergency.
the vitreous cavity.
Page 426
Late onset Endophthalmitis
May be due to i nfection by or ganism of low virulence
or fungi. Toxic reaction to Intra Ocular Lens (IOL)
may also present as late Endopthalmitis. An urgent
referral to ophthalmologist is required.
2. Panophthalmitis
2.1 Definitions :-
Refer to the inflammation of all coats of the eye
includi ng intraocular structures. It can also extend
with the tissue surrounding the eyeball.
2.2 Symptoms of Panophthalmitis

Eye pain.
Burst opening of the eye ball.
Protruding eyeball.
Loss of Vision.
Page 427
10. RETINAL DETACHMENT(RD)
It is one of the major ocular disease conditions Trauma

causing visual loss.
Post-cataract vitreous incarceration
Predisposing factors
Pars Planitis
High myopia.
Exudative RD
Trauma.
Family history of retinal detachment.

4. Prophylaxis
Intraoc ular Surgery-Aphakia,Pseudop hakia Indicated in retinal breaks
Inflammation. In Aphakic eyes.
Peripheral Retinal degenerations ( Lattice/ More than 1 clock hour of break.
Snailtrack).
Family history of RD.
1. Definition: Any symptomatic tear.
It is a separation of neurosensory retina from retinal Asymptomatic tears and holes can be observed.
pigment epithelium due to accumulation of fluid in 3 Modalities of prophylaxis.
the sub-retinal space through a retinal break, hole or a
tear. Laser Photocoagulation on slit lamp or IDO (
IndirectOphthalmoscope) with indentation.
2. Symptoms: Cryotherapy at the break to seal it.
Occurrence of flashes of light (Phsotopsia) more
serious in nasal field. Scleral buckling surgery for large tears(rarely).
Floaters in the vision.

5. Treatment:
Curtain/ Veil in front of eye in any portion, more
appreciated in lower field than upper. RD surgery can be done only by tertiary eye care
centres with infrastructure and trained pe rsonnel.
Sudden significant loss of vision, If macula is
involved.
A large bullous detachment. 6. Complications of long
standing RD
3. Types: Uveitis.
Rhegmatogenous RD. Complicated cataract.
Tractional RD. Glaucoma.
Diabetic Retinopathy Pthisisbulbi.
In cases of high suspicion of Retinal Detachment, patient should be refered to tertiary eye care centre
because timely treatment has better chances of saving vision.
Page 428
11. REFRACTIVE ERRORS
a focus is not achieved, a refractive error results and

1.Introduction vision is not clear.
Nor mally, the rays of light entering the eye are When parallel rays of light from a distant object are
brought to a precise focus on the retina the light
brought to focus on the retina with the eye at rest,is
sensitive layer lining the back of the eye. When such
called as Emmetropia(that is not accommodating).
Figure 11.1 Emmetropia
2.Causes of Refractive Errors 3.Types of Refractive Error

The eyes ability to refract or focus light- sharpl y on Myopia.
the retina-is primarily based on three features.
Hypermetropia.
1) The overall length of the eye. Astigmatism.
2) The curvature of the cornea. Presbyopia.
3) The curvature of the lens inside the eye.
4. Myopia
Page 429
A Diopteric condition of eye in which parallel rays of
light from infinity come to focus in front of retina
4.1. Definition: when eye is at rest.
Figure 11.2 Myopia
4.2Etiology: Best corrected vision is 6/6.

Fundus exam. Shows Myopic crescent,
Axial lengthening of eyeball (1mm=3D). Tigroidfundus and optic nerve degeneration
Curvature- abnormal curvature of cornea . with or without retinal break.
eg.Keratoconus (0.1=3D). 4.3.3Pathological Myopia:

Inde x myopi a eg. Old age, Nuclear Sclerosis. Essentially degenerative and progressive
condition , manifests in early childhood.
Acquired Myopia due to trauma.
The defect can reach up to 30D to 40D.
4.3Types: The defect has strong heredity more common in
female than male.
Developmental.
Simple. Rapid increase in Myopia during puberty.
Pathological.
Retinal evaluation is mandator y /compulsory.
4.3.1Developmental Myopia :
4.4Clinical feature:
Abnormally long eyeball Myopia 10D. Inability to see the distant object and holding the
Fundus - marked choroidal sclerosis, book close to the eye in simple Myopia.
hyperpigmantation and myopic crescent. Eye strain and headache.
Black spot in front of eye.
In pathological myopia-eye unusually prominent
Usually stationary image. with slightly dilated pupil.
4.3.2.Simple Myopia: Ophthalmoscopy reveals vitreous degeneration

and opacity.
Commonest , progressive from childhood to
adult, seldom exceeds 5-6D. Chorio-retinal degeneration patches at posterior
Pole,choroidal sclerosis and Foster Fuchs spot at
Generally stop progression by 21 year of age. macula, Posterior Staphyloma.
Page 430
4.5Complications : Refractive surgery like RK, PRK, ICR, LASIK
Retinal hemorrhage due to pos t vitreous 4.7 Other important aspects

detachment. Avoid contact sports where chances of blunt trauma
Lattice degeneration with retinal tear. is more
Complicated Cataract. Low vision aid- in pathological Myopia LVA is

helpful. Glasses or contact lens does not
4.5Treatment: improve the vision.
Genetic counseling.
Optical lens- concave lenses with slight under
General health-nutritional diet.
correction.
Outdoor activity.
Contact lens.
Near work in good illumination.
4.6Surgery:-
5.Hypermetropia
5.1Definition:
It is an error of refraction wherein parallel rays of
light coming from infinity are foc used be hind the
retina with accommodation at rest.
Figure 11.3 Hypermetropia
5.2Etiology: Latent .
Axial Manifest- Facultative.
-Absolute.
Curvature
Inde x
5.4Clinical feature:
Posterior dislocation of lens Low degree- no symptoms.
Aphakia High de gree-eye strain,headache.
5.3Types: Latent convergent squint in young.
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Presbyopia develops at an early age. Optical lens- convex lens.
Predisposed to angle closure glaucoma. Contact lens.
Fundus may show features of pseudopapillitis. 5.6 Surgery -
Increased chances of acute angle closure.(Risk of Laser, Thermal Keratoplasty, LASIK, Phakic
Angle Closure Glaucoma). intraocular lenses
5.5Treatment:
6. Astigmatism
6.1. Definition:
Astigmatism is condition wherein refraction varies in
different meridian of the eye hence the point of foc us
cannot be formed on retina.
Figure 11.4 Astigmatism
ii. Irregular
6.4Clinical features :
Small Astigmatism Often asymptomatic.
Severe symptom in hyperopic astigmatism
6.2. Etiology: where accommodation brought in play to
overcome hyperopia.
Curvature Astigmatism- most common with
corneal curvature. Irregular astigmatism is caused by corneal scar,
Inde x Astigmatism- inadequacies of refractive penetrating injury to e ye, Keratoconus.
index of lens in different sector.
6.5Treatment:
6.3. Types: Cylindrical glasses.
With the rule.
Contact lens.
Against the rule.
i. Regular
6.6 Surgery :
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LASIK, PhotoastigmaticKeratectomy, Incisional Corneal transplantation.
correction (LRI), IOL, Conductive Keratoplasty,
7. Presbyopia:
Normal aging process, when near images cant be
focused on the retina due to reduced accommodative
ability.
Figure 11.5 Presbyopia
The foc us is behind the retina as in hyperopia. If initially hyperopic :Presbyopia occurs earlier.
If initially Emmetropic: Person begins to hold Corrected with a convex lens for reading (bifocal).
reading material farther away and distance vision is
unaffected.
All refractive errors should be detected and treated in childhood by regular school health
checkups and should be fully corrected.
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12. DIABETIC RETINOPATHY
Mellitus for more than 15-20 years duration. Early
1. Introduction : diagnosis and intervention is crucial in dealing with
India has become the Diabetic capital of the world. this malady. Incidence and severity is more in type I
There is a high incidence of Diabetic Retinopathy, (IDDM) than type II (NIDDM).
among patients who are suffering from Diabetes
2.Classificaion :
Figure 12.1NPDR (Non Proliferative)
Figure 12.2 PDR (Proliferative)
2.Vitreous hemorrhage.
1. Risk Factors:
3.Traction RD.
1.Advanced Diabetic Eye disease.
4.Neovascular Glaucoma.
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Maculopathy (Clinically Significant)
Figure 12.3 CSME
4. History
Duration of Diabetes. 6. Diagnosis
Symptoms: decreased vision, floaters .
Control of Diabetes.
On examination.
Other systemic illness.
Visual acuity.
F/H/O severe vision loss due to DR.
IOP.
Neovascularisation of iris.
5. Systemic Evaluation
Control of systemic risk factors is the Gonioscopy: Neovascularisation of the angle.
cornerstone in management of DR. Dilated fundus examination.
Glycemic control: Besides Blood Sugar Level,
HbA1c levels more than 7.0 % is a known risk 7. Fundus:
factor. Veins dilated and tortuous.
Hypertension more than 130/90mmHg. Dot and Blot hemorrhages.
Increased Triglycerides, cholesterol Decreased Hard exudates.

HDL. Cottonwool spots.
Smoking, Sedentary life style. Micro-aneurysms.
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NPDR stage. Antioxidants.
New vessels and traction bands seen. Control of Diabetes.
PDR stage. 8.2 CSME:
Vitreous hemorrhage and traction RD
Focal/ Grid photocoagulation
complicates the picture.
Maculopathy runs as a distinct disease entity 8.3 PDR:
with maximum visual defect.
Pan Retinal photocoa gulation.
Fundus Fluorescein Examination (FFE).
Intra vitreal injection of VEGF inhibitors
Iodine based dye is injected into the i. Bevazizumab
antecubital vein and fundus pictures taken
and di gitally analysed. ii. Ranibizumab
Leaks and ischemic areas can be picked up. Vitrectomy may be needed for Vitreous
hemorrhage, Tractional RD.
Optical Coherence Tomography:
Non-invasive retinal tissue pictures 9. Prevention:
Intensive glycaemic control immediately after
diagnosis of DM leads to lessenthe
8. Treatment: complications.
8.1 NPDR : Today Telemedicine has taken sophisticated
technology to the rural masses yet the cornerstone is
Periodic observation. increasing awareness in public.
Fundus examination with dilated pupil must be done for all newly diagnosed Diabetic patients and
thereafter atleast once a year.
A tight glucose control from the beginning has more long term benefits as compared to a tight control
many years after diagnosis or after an end organ damage.
Page 436
13. OCULAR INJURIES
Chemical.
1. Introduction :
Mechanical injuries.
Eye can get injured by chemicals, heat, radiation and
mechanical trauma. Ocular injuries are emergencies 2.1. Chemical injuries :-
and treatment in first few hours can affect the visual
prognosis. Common chemicals causing injuries are,
Alkalis lime, ammonia, sodium hydroxide, cement,
2. Type of Injuries :- detergent soaps.
Figure 13.1 Alkali burn
Acids Hydrochloric, Sulphuric, Acetic acids Distressing pain.

(vinegar), Toilet cleaners.
Watering from eyes.
2.1.1 Alkali burn:Alkalis can penetrate through
cornea causing severe inflammation. They cause Decrease /Loss of vision.
occlusion of limbal vessels causing ischemia and Inability to ope n the eye.
necrosis of ocular surface. Necrosed tissue is
sloughed off causing ulceration and healing by Signs:
granulation tissue giving rise to abnormal adhesions Severe Blepharospasm (forceful closure of
between lid and ocular surface (symblepharon), lids).
severe dry eye, vascularised opaque cornea and even
Conjunctival congestion.
phthisis bulbi.
2.1.2 Acid burn: Coagulates the ocular surface tissue Raised IOP.
but usually does not penetrate inside the eye. Acids 2.1.4Diagnosis:
can cause limbal ischemia, severe dry eye, History of the chemical causing injury should be
vascularised corneal opacities. elicited.
Examination is difficult because of severe
2.1.3 Clinical features:
a. Symptoms: Blepharospasm.
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Ocular examination should be done under surface
anaesthesia and if required sedation (especially in 2.1.6 Medical management at higher centre
children). includes
Assessment of limbal ischemia.
Topical steroids - Ciprofloxacin 0.3% +
Dexamethasone 0.1% eye drops-one drop 4
2.1.5 Immediate treatment:
times a day first 7 days.
Removal of any particulate matter.(with special
attention to lime pest/powder). Topical lubricating eye drops -
Carboxymethylcellulose 1% eye drops one
Simple treatment is WASH-WASH-WASH the drop 4 times a day for 15 days.
eye with water.
Prevention of symblepharon formation by
Continuous irrigation with one bottle of normal
symblepharon ring.
saline over a period of 30 minutes.
Surgical treatment in the form of amniotic
Topical , Ciprofloxacin 0.3% + Dexamethasone
membrane transplant, limbal stem cell
0.1% eye drops-one drop 4 times a day.
grafting or Keratoplasty.
Topical Atropine sulphate 1% eye drops one
drop twice daily. 2.1.7 Complications:
Dry eye
Tab Ibuprofen 400mg twice daily for pain relief. Corneal ulcer
Lid scarring
Tablet Acetazolamide 250mg. ( carbonic
Symblepharon
anhydrase inhibitor) one tablet four times a day.
Phthisis bulbi (shrunken eye)
After primary care patient should be referred to
ophthalmologist for further management.
Note :- Keep Limestone /Chuna And Other Sourses

Of Chemical Ocular Injuries Away from The Reach
Of Children.
Figure 13.3 Symblepharon and corneal opacity
Immediate Copious irrigation with normal saline minimizes the damage.

Use protective glasses at work place (Prevention better than cure! )
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2.2 Mechanical Injuries :
Ocular trauma classification
Mechanical eye injury
Closed globe injuies Open globe injuries
Contusion
Laceration Rupture
Superficial foreign body Perforating injry
Intraocular foreign body

Lamellar laceration
Penetrating injury
2.2.1 Superficial foreign bodies husk of seeds, wing/ mouth part of insects, caterpillar
Common extra ocular foreign bodies are particles of hair, thorns etc.
dust, coal, emery, steel, lime particle, grain of corn,
Patient gives history of foreign bod y in the eye.
Figure 13.4 foreign bodies
Forceful closure of lids.

2.2.2Symptoms:
Redness. Anaesthetize the eye with 4% xylocaine eye drops
Pain (pricking). /proparacaine eye drops (0.5%).
Watering.
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Examine the conjunctiva by everting/double everting tangent to cornea to avoid perforation)
the upper lid. under surface anaesthesia of eye with 4%
Examine the cornea (stain with sterile fluorescein xylocaine or paracaine eye drop.
strip if necessary) to locate the foreign body. Ciprofloxacin eye drop0.3 (Antibiotic) four
times a day for 5 days.
2.2.3Treatment:
Removal of foreign body. Homatropine 2% eye drops three times a day for
Conjunctival foreign body can be removed by 4 days in case of corneal foreign body.
cotton bud or irrigation. Eye pad for 24 hrs.
Corneal foreign bod y should be removed by Follow up to rule out infection.
cotton bud or 26 G needle (hold the needle
If patient gives history of foreign body but it is not found on examination,

suspect intraocular foreign body and carefully examine for wound of entry.
Immediate Copious irrigation with normal saline minimizes the damage.

Take precaution by using protective glasses at work places. (Prevention
is always better than cure).
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14. OCULAR EMERGENCIES
1. Ocular conditions requiring

emergency ophthalmological
consultation.
Trauma -Ruptured Globe
Endophthalmitis.
Lid Lacerations.
Angle Closure Glaucoma.
Chemical injuries. Severe Uveitis.
Corneal Ulceration.
Acute Vision Loss.
Optic Neuritis.
Orbital cellulitis.
Lens induced Glaucoma.
2. Common causes of sudden

diminution of vision :
Table-14.1:Common causes of sudden diminution of vision
Painful diminution of vision Painless diminution of vision
Acute congestive Glaucoma Vitreous hemorrhage

Chemical injuries Retinal Detachment
Mechanical injuries Central retinal artery occlusion
Endophthalmitis Ischemic central retinal vein occlusion
Panophthalmitis Optic Neuritis
Malingering
3. Common Causes Of Acute

Red Eye
Page 441
Figure 14.1 Conjunctivitis
Conjunctivitis (with mucopurulent /purulent Endophthalmitis (severe pain with Diminution of

discharge)Subconjunctival hemorrhage vision).
(painless). Panophthalmitis (severe pain, proptosis,with
Corneal ulcer. painful ocular movements).
Acuteiridocylitis (dull aching pain and slight Orbital cellulitis (severe pain, proptosis,with
blurring of vision). painful ocular movements).
Page 442
15. PAEDIATRICOCULAR PROBLEMS
Eliminating childhood blindness will lead to a

1. Introduction :-
greater reduction in the number of blind ye ars
Out of 45 million people worldwide who are blind, experienced by adults.
around 1.4 million are children under 16years of age.
The vast majority of childhood blindness happens 3. Causes of childhood
before the age of five a period when 75 per cent of
learning is through sight.
blindness :-
Refractive errors.
2. Why is childhood blindness
(For details please refer to refractive error topic).
a priority?
Corneal scarring (scarring of the outer eye
There are several reasons why stakeholders believe
because of vitamin A deficiency & trauma).
that eliminationg childhood blindness is a
priority. Cataract for ms 39 per cent of all childhood
blindness.
There are an estimated 500,000 new cases each
year of childhood blindness roughly one per Infections -
minute. Ophthalmianeonatorum.
Blindness in children is often preventable if Congenital Dacryocystitis.
communities and parents become aware of the
Blepharitis.
causes.
Squint.
Without early intervention for cataract blindness,
Ocular Trauma.
children may go bl ind pe rmanently.
Blinding conditions increase child mortality up Congenital and Developmental Cataracts .
to 50% of children who become blind die within Leukocoria.

two years.
Congenital anomalies
90% of children who are blind dont go to
school.
3.1 Ophthalmianeonatorum 3.1.1 Definition:

Conjunctivitis occurring during 1st month after birth.
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Figure 15.1 Ophthalmianeonatorum
3.1.2 Mode of presentation, differential

diagnosis &treatment :
Table-15.1: Ophthalmianeonator um - mode of presentation, differential diagnosis and treatment
Time of onset Differential diagnosis Treatment
Within the first 48 hrs. NeisseriaGonorrhoeae Inj. Ceftriaxone IM,
Gentamycin / Moxifloxacin eye drops 1hrly

(till discharge decreases), followed by 4 times a
day for 7 days.
Bacitracin eye oint. 4 times a day for 7 days.
Chemical Wash the eyes, Erythromycin eye oint 4 times a

day for 3 days
48 hrs to 72 hrs. Other bacteria Gentamycin /Tobramycin eye dops two hourly
for 7 days.Neomycin-Bacitracin eye oint 4
times a day for 7 days.
5-7 days Herpes Simplex Virus(HSV II) Acyclovir eye oint 5 times a day for maximum
14 days.
>1 week Chlamydia Trachomatis(D-K) Erythromycin eye oint./Chloramphenicol eye

oint. 4 times a day for two weeks.
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3.2. Squint :
It is a condition where the eyes do not look in the to force the use of the affected eye. Sometimes
same direction. Whilst one eye looks forwards to surgery is needed to correct the appearance of a
foc us on an obj ect, the other eye turns either inwards, squint. Squints are common and affect about 1 in 20
outwards or downwards. A child with a squint may children. Most squints develop before preschool age,
stop using the affected eye to see with. This can lead usually by the time a child is three years old.
to visual loss called Amblyopia, which can become Sometimes squints develop in older children, or in
permanent unless treated early in adults.
childhood.Treatment involves patching the good eye,
Figure 15.2 Esotropia Figure 15.3 Exotropia
3.2.1 Definition: Latent squint The eye turns only when it is

covered or shut, but looks fine when the eye are
Malalignment of visual axes is called as squint. open.
It can be Esotropi/Exotropia or vertical malalignment Concomitant squint The angle (degree) of the
i.e. hypertropia or hypotropia. squint is always the same in every direction that
you look.
Incomitant squint The angle of squint can vary
according to direction
3.2.2 Types of Squint :-
3.2.3 Symptoms:
Esotropia An eye that turns inwards. Squint(deviation of eye), diminution of vision
Exotropia - An eye that turns outwards
Hypertropia - An eye that turns upwards. 3.2.4 Signs:
Hypotropia - An eye that turns dow nwards. Squint, diminution of vision, Amblyopia (lazy eye).
Constant The squint present all the time. 3.2.5 The aims of treatment of squint are :-
Intermittent The squint comes & goes. Preserve or restore vision.
Manifest squint The affected eye turns when Straighten the eyes.
the eyes are open and being used.
Restore binocular vision.
3.2.6 Treatment:
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Refractive correction. Exercises and if necessary surgical correction is
done.(before 10 yrs.of age to have binocular
Amblyopia treatment. vision).
Evaluation of the squint by ophthalmologist at the earliest is must.
3.3. Leukocorea : 3.3.1 Definition:

White pupillary reflex is called as Leukocorea.
Figure 15.4 Leukocorea
3.3.2Common Causes:
It is the cancer of the eye in children. It originates
Congenital Cataract. from the retina, the light sensitive layer, in eye. It is
Retinoblastoma. the commonest tumor of the eye in childhood. As the
Retinopathy of Prematurity. child does not complain of any poor vision, the tumor
Toxoplasma /ToxocaraEndophthalmitis. may remain undetected. The most common way of
presentation is a white reflex (leukocorea) behind the
Persistent Hyperplastic Primary Vitreous.
pupil. It may also present as squint (crossed eye),
3.4Congenital Cataract :- poor vision, painful red eye, inflammation of
It is clouding or opacity of the normally transparent thetissue surroundi ng eye, protrusion of the eye ball
lens inside the eye. Babies are sometimes born with (proptosis) etc.
cataracts as a result of an infection, injury, or poor The aim of treatment in retinoblastoma, ina order of
development before they were born, or they may priority, is to save the life, eye sight and cosmesis of
develop during childhood. the child. There are many treatment modalities for
this tumor.
It is very important to treat this condition as soon as
possible to get the best results. The treatment
optionsand the timing of surgery will be decided by
the ophthalmologist, based on the following factors : 3.6 Retinopathy of Prematurity :
Age of the child. The most important determinant of any ROP
management program is an effective screening
Density of cataract.
strategy.
Whether cataract involves one eye or both eyes.
3.5 Retinoblastoma : 3.6.1 Whom to screen for ROP :
Page 446
All infants born below 1750 grams birth weight
must undergo screening and all infants between Laser Photocoagulation.
1750 grams and 2000 grams must be screened in
case of any risk factor. For advanced stages like retinal detachment
surgical treatment is required.
All infants born below 34 weeks of gestation
must undergo screening and all infants between
34-36 weeks must be screened in case of any risk 3.7 Congenital anomalies -
factor.
3.7.1 Ptosis :
Ptosis refers to drooping of an upper eyelid of one or
3.6.2 When to start screening :-
both eyes. The droop may be barely noticeable, or the
All babies must be screened not later than 30
lid can descend over the entire pupil. Surgery usually
days of life or 4 weeks after birth.
is the best treatment for drooping eyelids. Children
Babies born < 1200 grams or < 28 weeks must born with moderate or severe ptosis require treatment
be screened by the 2nd 3rd week of life. in order to get proper vision for subsequent
development of child. Failure to treat ptosis can result
in Amblyopia.
3.6.3 Treatment :-
All these are potentially vision threatening conditions which need immediate referral to ophthalmologist.
Every time the when the baby is brought for immunization look for pupillary reflex.
Page 447
16. LOW VISION
Low vision is a reduced level of vision that cannot be
fully corrected with conventional glasses. It is not the 2. Causes
same as blindness. Unlike a person who is blind, a
person with low vision has some useful sight. Although low vision can occur at any stage in
However, low vision usually interferes with the life, most of people develop low vision because
performance of daily activities, such as reading or of eye diseases.
driving. A person with low vision may not recognize
Common causes of low vision, particularly with
images at a distance nor able to differentiate colors of
similar tones. older adults, include Macular Degeneration,
Glaucoma, and Diabetic Retinopathy.
You are legally blind when your best corrected
central acuity is less than 20/200 (perfect visual
acuity is 20/20) in your better eye, or your side vision 3. Tests and Diagnosis :
is narrowed to 20 degrees or less in your better eye.
Refraction (to assess your vision and determine
People who are legally blind may still have some
the prescription for your glasses, if glasses may
useful vision. If you are legally blind, you may
qualify for certain government benefits. It is be of any use).
estimated that approximately 17 percent of people Visual field (to assess your peripheral vision).
over the age of 65 are either blind or have low vision.
4. Treatment and Drugs

1. Symptoms
Optical devices to help you adapt, such as
Difficulty in recognizing objects at a distance magnifiers, telephones, or closed-circuit
(street signs or bus signs). televisions.
Difficulty in differentiating colors (particularly Adaptive non-optical devices, such as large-
in the green-bl ue-violet range).
print cookboo ks and talking watches.
Difficulty in seeing well up close (reading or
Occupational Therapy.
cooking).
Page 448
17. EYE BANKING
Eye bank collects, evaluates and distributes the eyes 7. Eye removal does not leads to any disfigurement
donated by the donors. All eyes donated are in eye.
evaluated using strict medical standards.
8. Only the transparent section of the eyes called
cornea is taken out and not the complete eye
1. Functions of eye bank: ball.
Those donated eyes which are found unsuitable for 9. A small quantity of blood will be drawn to rule
transplantation are used for valuable research and out communicable diseases.
medical education purpos ein the eye ba nk.
10. Anyone can pledge eyes.
1. Availability of trained staff round the clock at Eye
donation center in all District hospitals & all Eye
11. The eyes can be pledged to any eye bank
bank to attend the calls.
preferably the nearest one.
2. Evaluate and provide quality corneas to corneal

12. The identities of both the donor and the recipient
surgeons.
remain confidential.
3. Enable corneal research using eyes unsuitable for

13. One pair of eyes gives vision to TWO corneal
grafts to find newer techniques, improve preservation
blind people.
methods and train cor neal surgeons.
14. Eyes donated to the Eye-Bank that are not
4. Increase public awareness about eye donation and medically suitable for transplant may be used for
eye ba nking. medical research and education purposes.
2. Eye donation : 2.2 Process of Eye donation

Pledging for eye donation procedure:
2.1 Important aspects of eye
donation : 2.2.1 Eye donation can be done in either of
these two ways.
1. Eyes are to be donated only after death.
1. She/He can walk in to a nearest Eye Bank and
2. Eyes must be remove d within 4-6 hours after PLEDGE their eyes for donation. For this, a
death. pledge form needs to be filled, signed by a
witness (can be your relative/friend) and given
3. In case of death,nearest eye bank should be back to the eye bank. At the time of donors
informed immediately. death, his/her relative/friend, who was a witness
for the pledge form or any other family
4. Eyes must be removed only by a trained doctor. member/friend who had the knowledge that the
person who passed away intended to donate the
eyes, should call the nearest eye bank. One
5. The eye bank team may remove eyes at home of important aspect to be noted here that it is not
the deceased or at a hospital. sufficient if a person pledges for donating his/her
eyes after the death, his/her relatives and friends
6. Eye removal process is simple and takes only 10 should be well informed and be well aware to
to 15 minutes. call the nearest eye bank, for donating the eyes
after their death.
Page 449
2. After death, a relative or a friend of the deceased 2.2.4 What happens after eye donation?
person can infor m the eye ba nk and tell them that
they wish to donate the eyes of their bereaved The donor's family receives a certificate of
folk. appreciation from the eye bank.
2.2.2 Donation procedure: The eyes are taken to the eye bank and evaluated
by trained staff.
If there is an unfortunate death occurs of one of Eyes are preserved in a solution of Optisol GS
your family member/close relative/close friend, pick and refrigerated. This solution contains
up the phone and dial to the nearest eye bank. Please chemicals and drugs that are needed to keep the
note that this should be done WITHIN 6 hours of the living cells of cornea healthy and functional.
death.
Give the eye bank officials the location of the house Tests are carried out and the report is sent to the
along with a landmark so that they can come and corneal surgeon
collect the eyes as quick as possible. These eyes will The eyes are used for a corneal transplant
give a new vision to two blind people. operation within 72 hours, but with present day
availability of special storage media the eyes can
2.2.3 Important points to be taken care after be stored for a longer time before being
a person's death, before eye donation: transplanted.
The recipient is chosen from the eye ba nk's
waiting list and called for corneal transplant.
After the death of a person, call the nearest eye bank within
SIX HOURS of the death of the person. Neither the patient knows whose cornea is used
for him, nor the relatives of the donor know who
has received the cornea. This information is
Switch off fans & keep AC on, if you have one. strictly confidential.
Close the eye lids gently and keep a moist cloth
over the eyes. Periodic follow-up of the recipient is done over
the time to ensure that the graft is successful.
Raise head with a pillow.

Page 450
SURGERY
Page 451
1. Abdominal Pain
Acute Abdomen is a term used synonymously for a

condition that needs immediate intervention
1. Causes of acute abdomen:
Figure 1: Acute abdomen causes
Abdominal Pain can be due to various orga ns Ranitidine 150 mg.bd or Omeprazole 40 mg od
involve d with underlying causes & patient will and alike drugs on empty stomach for 15 to 30 days
present accordingly. Intestinal motility regulators Domperidon 5 to 10 mg
bd after meals for 15 to 30 days
2. Gastric & Duodenal ulcer: Liquid antacids
2.3.2 If perforation is diagnosed
2.1. Presentation: NBM, RT aspiration
Burning pain epigastric region ref. to ba ck
I.V. fluids RL, DNS, D 5% 1000-1500 cc in 24
worsened (gastric ulcer) or relieved by intake of hrs to stabilize the patient
food (duodenal ulcer)
Antibiotics Cefotaxime 1 gm I.V.bd , iv Genta -
Dyspepsia, nausea/vomiting, occasionally 80 mg/ bd,
haematemesis/malena.
IV Metronidazol - 400 mg / bd
Complication with aggravation/progression of
Stabilize the patient & shift the patient for
illness may cause perforation
surgical interve ntion within 4-6hrs
2.2. Investigation:
Routine investigation (Hb, CBC, Urine ) 3. Biliary Tract & Pancreas:
X-ray abdo men standi ng - shows gas under
diaphragm in perforation 3.1. Presentation:
Gastroscopy Colicky pain in right upper abdomen ,
Dyspepsia, nausea/vomiting
2.3. Treatment: Occasional jaundice
2.3.1 Drugs-
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3.2. Investigation: 4.1.2 Investigation:
Routine investigation Routine investigation
USG abdomen X-ray abdo men standi ng - Shows multiple
Serum amylase estimation. gas-fluid levels.
4.1.3 Treatment:
3.3. Treatment: e) NBM, RT aspiration
Analgesics Aceclofenac 50 mg / bd, f) I.V. fluids - RL DNS, D 5% 1000-1500 cc in 4 to
Dicyclomine 20 mg / bd 6 hrs to stabilize patient
Antibiotics - Cefotaxime 1 gm IV bd , IV g) Antibiotics Cefotaxime 1 gm IV bd , IV
Gentamycin 80 mg/ bd Gentamycin 80 mg/ bd,
IV Metronidazol - 400 mg / bd h) IV Metronidazole 400 mg / bd
Stabilise the patient & as diagnosed- biliary i) Stabilize the patient & shift patient for surgical
stone/ Pancreatitis patient may be referred for interve ntion within 4-6 hrs.
expert management to higher center within 12-24
hrs.
4.2. PERFORATION
4.2.1 Presentation:
3.4. Acute epididymo-orchitis / Severe pain in abdomen , vomiting
Pyocele Distension of abdo men
Acute epididymo- architis is an infection in
epididymis, testes & spermatic cord & manifests as 4.2.2 Investigation:
Acute Pain in Scrotum may be associated with fever. Routine investigation
When infection involves tunica vaginal sac at X-ray abdo men standi ng - Shows gas under
manifeds as pyocele. diaphragm
3.4.1 Symptoms - 4.2.3 Treatment:

- Pain is scrotal area. j) NBM, RT aspiration
- Erythema in local area. k) IV. fluids - RL DNS, D 5% 1000-1500 cc in 4-6
- Difficulty is walking due to pain. hrs to stabilize patient
- Fever l) Antibiotics Cefotaxime 1 gm I.V.bd , IV
Gentamycin 80 mg/ bd,
3.4.2 Investigation m) IV Metronidazole 400 mg / bd
- USG Abdomen. n) Stabilize the patient & shift patient for surgical
- CBC interve ntion within 4-6 hrs.
3.4.3 Treatment: 5. RENAL & URETERIC

a) Antibiotics
b) Inj. Cefotaxim 1 gm iv / hrly. COLIC
Inj. Metronidazole400mg iv / 8 hrly. It's type of pain caused due to irritation or obstruction
Inj. Diclofenac 50 mg /im 8hrly. by stone, in kidney or ureter itself. It is repeated
c) Magsulf dressing : It reduces inflammation & spasmodic pain of longer or shorter duration till
pain. cause is removed i.e stone removal or expulsion.
d) Surgical intervention Surgical intravention is
required if conservative treatment does not give Renal pain most of the time is located in lumbar or
relief. Pyocele has to be drained for relief. back region. Ureteric pain is typical colic,
mild or severe in nature radiates from lumbar to

4. Small & Large Intestine: scrotal region.
4.1. OBSTRUCTION 5.1. Sign & symptoms

4.1.1 Presentation:
Severe pain in abdomen, vomitings Abdo minal pain from loin to groin on one side or
Distension of abdomen both sides in flank & back. Pain is associated with
burning micturation, nausea , vomiting, fever &
chills. Patient complains haematuria.
Page 453
5.2. Investigations Renal profile
X-ray abdomen (KUB)
Haemogram USG - abdomen & Pelvis
Urine- m/e, c/s
5.3. Treatment
Analgesics- Inj. Diclofenac 50 mg/im.
Antibiotics- Inj. Ampicilline 500 mg.IV./6 hrly .
Inj. Gentamycin 80 mg. IV./12 hrly. 3 to 4 days
Inj. Metronidazole 400 mg. IV./8 hrly.
IV Fluids -Ringer lactate, DNS, Dextrose 5%
Catheterization SOS
Give the treatment to stabilize the patient and / or refer the patient to higher center.
Inj. Gentamycin 80 mg.i.v./12 hrly.

6. Acute Appendicitis Inj. Metronidazole 400 mg.i.v./8 hrly.
The acute appendicitis is essentially a surgical IV Fluids -Ringer lactate, DNS, Dextrose 5%
condition & can be defined as pain of sudden onset in If patient is responding/improving, give above
right lower abdomen. treatment for 5 to 6 days
6.1. Presentation:
Pain at first starts around the umbilius or 6.3.2 Surgical Treat ment
epigastrium and later it shifts to the right iliac If during the conservative treatment there is evidence
fossa. of gangrene, perforation, generalized peritonitis or
Sudden disappearance of pain without abscess formation, operation is indicated. If patient
improvement of general condition means starts deteriorating with conservative line of
gangrene and perforation. But, pain invariably treatment then patient may be posted for emergency
returns later. appendectomy.
Nausea and Vomiting Emergency appe ndectomy is contra indicated when
Fever diagnosis is appendiculer mass.
Mucus diarrhoea
Pulse-rapid and it is proportionate to temperature 7. Obstructed Inguinal Hernia
except in cases of Gangrene, Perforation and It is due to obs truction/ retention of abdo minal
Generalized peritonitis. visceral organs in hernial sac.
Tenderness in right iliac fossa /guarding and
rigidity Patient presents with- non-reducible inguinoscrotal
swelling, pain in abdomen, distension of abdomen
6.2. Investigation: repeated vomiting . In late stages fever, septicemia.
Routine haemogram
RFT
Urine examination
X-ray abdomen, KUB 7.1. Investigations:
Abdominal Sonography
Routine heamogram
X-ray abdomen standing position -shows
6.3. Treatment: multiple gas fluid level
6.3.1 Conservative Treatment USG abdomen & pelvis
Appendicitis with signs of localization No cough impulse.
Rest in a hospital
Nothing by mouth 7.2. Treatment:
Analgesics- Inj. Diclofenac 50 mg/im 8 hourly NBM, Ryle's tube aspiration, head low position
/sos. IV Fluids - Ringer lactate, DNS, dextrose 5%
Antibiotics- Inj. Ampicilline 500 mg.i.v./6 hrly . Analgesics- Inj. Diclofenac 50 mg/im.
Page 454
Antibiotics- Inj. Ampicilline 500 mg.i.v./6 hrly . Try to reduce the hernia if not pos sible, then
Inj. Gentamycin 80 mg.i.v./12 hrly. after stabilization of patient within 4 to 6 hours
Inj. Metronidazole 400 mg.i.v./8 hrly. shift the patient for further needful surgical
interve ntion at higher center.
Page 455
2. WOUNDS AND ABSCESS MANAGEMENT
From the earliest times the healing of wounds has infection, to be done by secondary suturing, skin
been the central problem in surgical practice. This grafting.
applies equally to the wounds of warfare and human
assault, to the wounds of accidents, and to the 3.3.1 Suture Material:
wounds which the surgeon makes deliberately in the Non-absorbable -linen, silk, nylon, proline,
course of surgical operations. ethilone
The breach in the surface of the bod y, the skin, Absorbable- cat gut, vicryl
exposes the deeper tissues to the danger of bacterial
infection (sepsis), and this danger persists until the 3.3.2 Suture Types:
healing process has restored an intact surface. Simple - single or continues
Mattress - single or continues
1. Commonly occurring Tension sutures - when there is requirement of
forced alignment of wound edges
injuries can be open or
3.4 Supportive treatment to the
closed.
associated injury/illness as
Abrasions, bruises required- fracture site
Contusions
Lacerated wounds
stabilization etc.
Penetrating wounds
Incised 4. Abscess
Crush wounds
De-glovi ng injury- wounds with skin loss 4.1 Clinical features :
Vascular injuries An abscess is a tender mass generally surrounded by
a colored area from pink to deep red. Abscesses are
2. Observe for often easy to feel by touching. The middle of an
abscess is full of pus and debris.
2.1 Three 'B'
Painful and warm to touch, abscesses can show up
Bleeding any place on your body. The most common sites are
Breathing in your armpits (axillae), areas around your anus and
Breaks (fracture) vagina (Bartholin gland abscess), the base of your
spine (pilonidal abscess) around a tooth (Dental
2.2 Wound Contamination abscess) and in your groin. Inflammation around a
hair follicle can also lead to the formation of an
2.3 Concealed bleeding (internal) abscess, wich is called a boil (furuncle).
3. Management:
3.1 Cleaning of wounds
3.2 Debridement of dead or
devitalised tissue 4.2 Treatment
3.3 Suturing of wounds Unlike other infections, antibiotics alone will not
Wound healing may be usually cure an abscess. In general an abscess must
First intention- this is brought about by joining open and drain in order for it to improve. Sometimes
together the edges of the wounds by sutures, draining occurs on its ow n, but generally it must be
clips, adhesive materials opened by a doctor in a procedure called incision and
drainage (I&D)
Second intention- when the wound edges are not
brought together as there is- skin loss, wound
Page 456
Other risk factors for abscess include exposure to Supplementary/supportive Vit.C 500 od 3 to 4
dirty environments, exposure to persons with certain days
types of skin infections, poor hygiene, and poor
circulation. 4.4. Prevention
4.3 Self-Care at Home Maintain good personal hygiene by washing your
skin with soap and water regularly
If the abscess is small (less than 1 cm or less
than a half-inch across), applying warm Take care to avoid nicking yourself when shaving
compresses to the area for about 30 minutes 4 your underarms or pubic area
times daily can help. Seek immediate medical attention for any puncture
Do not attempt to drain the abscess by pressing wounds, especially if associated with some debris in
on it. This can push the infected material into the the wound, associated medical conditions, patient
deeper tissues. on steroids or chemotherapy
Do not stick a needle or other sharp instrument
into the abscess center because you may injure 4.5. Important points
an underlying blood vessel or cause the infection
to spread. Once treated, the abscess should heal
How long the abscess has been present Many people do not require antibiotics
Any injury to that area
Medicines being taken The pain often improves immediately and subsides
more each day
Any allergies
Fever at home Wound care include wound repacking, soaking,
washing, or bandaging for about 7 to 10 days. This
4.2. Examination and test usually depe nds on the size and severity of the
abscess
4.3.2 Drugs: After the first two days, drainage from the abscess
Antibiotics - Cap. Ampicillin 500mg qid 4 to 5 should be minimal to none. All sores should heal in
days or 10-14 days.
Tab. Ciproflox 500mg bd 4 to 5 days or Synonyms and Keywords
Tab. Cefadroxil 200mg bd 4 to 5 days Abscess, abscesses, boils carbuncles, furuncles,
hileradenitis, suppurative, pilonidal abscess, pustules,
Symptomatic treatment by analgesic, anti and whiteheads.
inflammator y dr ugs
Page 457
3. HEAD INJURY
Head injuries comprises of injuries to skin, skull, 2.1 Intracerebral haemorrhage - in

intracranial organs with vessels, in combination or
singly. the brain substance it is usually
Skull is the protective bony cage/vault for brain associated with lacerations in
though it is not a perfect fit considering weight & brain.
vol ume of brain which may turn in to injury to the
brain by inclusive of skin & vault or singly by mere
2.2 Subarachnoid- in the pre
inertia to brain & its membrane. As the brain is arachnoids mesh.
suspended by superior cerebral veins from above
antero - posteriorly to the membranes and laterally by 2.3 Extradural Haemorrhage:
attachments of dural process causing direct impact
injuries to site - coupi injuries or indirectly to the Extradural - outside the dura between dura and the
opposite side of skull called counter coupe injuries. periosteum of inner table of skull.
It is a injury causing blood accumulation between
1. Injuries can be classfied skull & dural membrane. This causes pressure effects
grossly as on brain & its functioning. It causes phase of
Concussion unconsciousness with period of apparent recovery
between two periods of unconsciousness is known as
Contusion
lucid interval.
Laceration
2.4 Subdural Haemorrhage:
1.1 Cerebral Concussion: Subdural -under the dura but outside the arachnoids
matter.
It is distortion and displacement of brain substance
minimally. Producing sudde n loss of consciousness, It is usually from the veins causing blood
motor & sensory paralysis of variable duration from accumulation beneath the dural membrane.
seconds to minutes. There is a complete recovery in
this injury. 3. Signs & Symptoms &
1.2 Cerebral Contusion: findings:
Vomiting
In this injury distortion, displacement is of severe Headache
nature along with injury to brain matter- neural Bleeding - ENT
fibers, this additional sliding movement between gray Convulsions
& white matter in toto producing damage to nerves & Irritability, loss of consciousness, disorientation
axons
4. Clinical Examination
Examine level of consciousness, reaction and
1.3 Cerebral Laceration: size of pupils
In this injury internal changes are same but the brain Blood pressure, pulse, respiratory rate
surface is actually torn. Clinically causing prolonged
unconsciousness
5. Investigations:
Routine investigations
2. Intracranial Haemorrhages: Skull X-ray
There are four anatomical types of intracranial CT-Scan
haemorrhages MRI
Page 458
6. Management:
6.4 Maintenance of air way, throat
Depends upon site, severity of injury, general
condition of patient & relevant complications. & nasal suction
6.1 Nil by mouth 6.5 Control of bleeding
6.6 Care of associated injuries
6.2 IV fluids,RL, D-10% 500-1000 6.7 Oxygen inhalation with mask,
cc SOS intubation / tracheostomy
6.3 Drugs 6.8 Management of shock
6.9 After stabilization,patient to be
IV Mannitol 100 cc/bd shifted to higher center for
IV Dexamethasone 4-8 mg/bd expert neurosurgical
Inj. Phenytoin 200-600 mg/ day or Inj.Sodium management 8-10hrs.
Valproate 400-2000 mg/ day
Inj. Cefotaxime 1gm/ bd
Inj.Gentamycin 80 mg/ bd
Inj. Aceclofenac/Dicyclomine 2 cc/im/bd
Page 459
4. CHEST INJURY
Chest injury is common in road accident, fall from After stabilization,patient to be shifted to higher
height, stab injury center for expert management within 4-8hrs
1. Chest wall 7. Common injuries we come

Fracture ribs
Flail chest
across which need primary
Fractured sternum treatment to stabilize the
patient are:
2. Pleura:
Penumothorax 7.1. Fracture Ribs:
Tension penumothorax 7.1.1 Clinical presentation
Traumatic haemothorax May be single or multiple, simple or compound. with
or without Pneumothorax
3. Lung: Patient may present with- pain, di fficulty in breathing
Pulmonary contusion in a latter stage some times inability to take breath
Pulmonary laceration secondary to Pneumothorax,
7.1.2 Diagnosis & management
4. Mediastinal structures: patient needs to be investigated by X-ray chest
Ruptured thoracic aorta
Ruptured br onchus Analgesia
Ruptured diaphragm Breathing
Blunt injury to the heart Strapping
Haematopericardium
7.2. Flail Chest
5. Penetrationg injuries: 7.2.1 Clinical presentation
Bullet This type of injury is commonly seen in accidents
Stab wounds to the chest due to multiple rib fractures causing paradoxical
movement of chest wall. Resulting in to respiratory
6. Early Treatment: insufficiency & retention of pulmonary secretion.
Relief of pain - analgesics Inj. 7.2.1 Diagnosis & management
Aceclofenac/Dicyclomine 2 cc/im/bd
To be diagnosed by X-ray Chest
Stabilisation of the chest wall- strappi ng
Removal of pleural blood or air -Simple Patient needs following treatment.
aspiration, air tapping by needle,ICD
Propped up position
Removal of tracheo-bronchial secretions
Oxygenation by mask
Tracheostomy
Chest wall stabilization by strapping
Oxygen administration by mask
NBM Tracheostomy-SOS
IV Fluids - Ringer lactate, DNS, dextrose 5%
Antibiotics-
Inj. Ampicilline 500 mg. IV/6 hrly .
7.3. Traumatic Pneumothorax:
Inj. Gentamycin 80 mg. IV/12 hrly. 7.3.1 Clinical presentation
Inj. metronidazole 400 mg.IV/8 hrly. It is a trapped air in plural cavity due to penitrating
wounds to chest wall, pleura and or lungs. It may be
Blood t ransfusion SOS associated with hemothorax.
Page 460
7.3.1 Diagnosis & management After stabilization of the patient as and where
required as per condition of injury & patient to be
a) To be diagnosed by X-ray Chest-evidence of shifted to higher center in ALS transport vehicle.
fracture ribs, lung collapse black radiolucent chest
cavity area on injured sides. Sometimes air fluid level
in Hemo/Pneumothorax.
8. INTERCOSTAL
b) Patient needs with ICD as above
DRAINAGE
7.4. Tension pneumothorax: 1. Indications for Chest Tube
7.4.1 Clinical presentation Insertion:
Pneumothorax
A tension pneumothorax develops when there is a
one-way valvular leak of air into the pleural cavity. Hydropneumothorax
Air rapidly accumulates, compressing the lung, and
urgent treatment is required, as it is a life threatening Haemothorax
emergency. Empyema
7.4.1 Diagnosis & management
To be diagnosed and treated as above in addition 2. PREPARATION
patient needs.
a) Simple needle aspiration to release tension 2.1 Requirements for Chest Tube Insertion
b) ICD with under water seal procedure:
Chlorhexidine or povidone-iodine solution
7.5. Haemothorax: Sterile towels and drapes
7.4.1 Clinical presentation Sterile sponges
1% lidocaine without epinephrine (40 ml)
An accumulation of blood i n the pleural cavity can 10-ml syringe
occur from injury to the muscles in the chest wall, 18-, 21-, and 25-gauge needles
lung, heart or great vessels. There may also be a Mayo scissors
pneumothorax in association. Standard tissue forceps
Patient may be presented with pain, breathlessness, Towel forceps
shoc k. On examination there are signs of pleural Needle holder
collection with lack of breath sounds & dull 0-Silk suture with cutting needle
percussion note. Scalpel handle and no. 10 blade
Chest tubes (24, 28, 32, and 36 French)
7.5.2 Diagnosis & management Chest tube drainage system (filled appropriately)
2-in. adhesive tape
a) To be diagnosed by X-ray Chest
Sterile gowns and gloves, masks, caps
b) Patient needs following treatment with ICD
Blood t ransfusion SOS
Page 461
Figure 1: Intercoastal Drainage tube
3. Pneumothorax / Haemothorax artery forceps in thrust into the pleura along the
same direction.
ICD insertion procedure: 3.4 Position the ICD tube:
3.1 Part Preparation
all the holes of the tube should be in the pleural
Parts shaved and prepared
cavity
Consent taken
3.5 Fix t he ICD tube with a skin stitch:
Parts painted and draped Air bubbles are seen coming out and a column of
Position: Semi recumbent (45%) on a backrest fluid moving with respiration. /Blood is seen
coming out and a column of fluid moving with
Turn the patient's head on the opposite side respiration in Haemothorax.
3.2 Anaesthesia: LA
Clinically, the patient improves:The
3.3 Site: tachypnoea settle. Respiratory sounds are heard.
2nd inter costal space, mid-clavicular line for chest X-ray shows lung expa nsion.
pneumothorax. 3.6 Inter costal drain is re move d when the
7th inter costal space, in the mid-axillary line for indication is ove r:
Haemothorax. X-ray Chest shows full expansion, Column of fluid
Cut skin, Subc utanous tissue Split the muscles in the IC drain stops moving.
with an artery forceps, till the pleura is reached.
Keep the inter costal tube ready - Malecot's 3.6.1 Romoval:
catheter or Portex ICD tube. Keep the Cut the skin stitch, pull the IC drainage tube out
underwater drain and drainage tube ready. and give immediate strapping ( vaseline gugze
Plunge the artery forceps into the pleura. The airtight)
ICD tube mounted on another long & blunt
Page 462
Figure-2: Site for Lidocaine Infiltration
Figure-3: Intercostal Tube insertion
Page 463
Figure-4: Intercostal Tube fixation
4. POST INSERTION: Volume capacity of this tube should exceed of

patients maximum inspiratory volume (otherwise
water may enter chest)
4.1 X-ray chest zatch for complications:
Volume of water in bottle should exceed of
patients maximum inspiratory volume to prevent
Not draining (check for kinking) in drawing of air during inspiration
Organ injury (lung, liver, spleen, heart, Drain should always stay at least 45cm below
vessel) careful insertion patient (prevention of removed fluid or water
Blood loss careful observation refluxing into patient)
Surgical emphysema (small hole and good Clamp drain when moving
suturing) Waterlevel above tube in another bottle
Infection (sterile technique) determines the amount of suction applied before
air drain through tube (safety suction limiting
5. Safety features: device).
First tube connecting drain to drainage bottles

must be wide to decrease resistance
Page 464
5. ABDOMINAL INJURIES
The abdomen has only muscle layers protecting the Cold clammy extremities
internal organs anteriorly and laterally. Restlessness
Breathlessness
1. Blunt Trauma Sweating
Occurs when the offending agent is blunt and wide Altered level of consciousness
area of contract occurs at the time of impact. Severity External injuries
of the injury depe nds on the force of the offending 3.3 Stabilize the hemodynamically
agent.
unstable patient first,
2. Penetrating trauma investigate later.
Occurs when injured by sharp instruments and the 3.4 Cardiothoracic, head and
depth and direction of the wound is more important spinal injuries get priority over
than the size of the wound.
abdominal and other skeletal
2.1. Cause:- and surface injuries.
Accidents (Traffic, industrial and disasters) Refer patient immediately for
Falls
Assaults emergency surgery & expert
In children (child abuse, bicycling, swimming, managements.
etc) 3.5 Blood transfusion SOS.
2.2. Investigation 3.6 Treatment
The history of the traumatic event is important in NBM, RT aspiration
determining the nature and severity of the intra- IV Fluids - Ringer lactate, DNS, Dextrose 5%
abdominal organ injury. Analgesics - Inj. Diclofenac 50 mg/im.
Antibiotics- Inj. Ampicilline 500 mg IV./6 hrly
3. Presentation & Management OR
3.3 Life saving measures such as Inj. Cefotaxime 1 gm/bd.
ABCDE Inj. Gentamycin 80 mg.IV /12 hrly.

Airway patency Inj. Metronidazole 400 mg. IV/8 hrly.
Bleeding control
Circulation maintenance 4. Proceed in the following
Breathlessness
Deformity (cervical stabilisation and fracture
order for haemodynamically
immobilisation) should be done first before stable patient:
transport to the hospital. Complete clinical examination
3.1 Examine head to toe thoroughly on Plain X-ray abdo men - Erect or left lateral
arrival of the trauama patient to identify position
all the injuries Categorise patient Diagnostic peritoneal tapping
immediately into hemodynamically Ultra sound abdomen (FAST)
stable or unstable. Abdominal CT
3.2 Haemodynamically unstable patient will If there is progression in illness/detected internal
have the injury, patient to be shifted for further expert
Following features treatment to higher center.

Page 465
6. Gangrene
ulcers. Dry gangrene usually results in patients with
1. Definition: chronic critical limb ischemia without infection or
without any other complicating factors like diabetes,
Macroscopic death of the tissues with superadded osteomyelitis etc. It is characterized by dry shriveled
putrefaction. appearance, with clear line of demarcation and no
Rest pain is an ominous symptom and usually foul smell.
requires revascularization because this form of Wet gangrene is characterized by no clear line of
advanced ischemia generally progresses to tissue demarcation, foul smell, purulent discharge, evidence
loss. of proximal spread in form of skip areas
Patients with diabetes or renal failure are more
susceptible to the development of ischemic pedal
Figure 1: Dry Gangrene Figure 2: Wet Gangrene
2. Treatment:
Analgesics- Inj. Diclofenac 50 mg/im.
Antibiotics- Inj. Ampicilline 500 mg. IV/6 hrly . OR
Inj.Cefotaxim 1gm. IV/12 hrly
Inj. Gentamycin 80 mg. IV/12 hrly. 3 to 4 days
Inj. Metronidazole 400 mg. IV/8 hrly.
IV fluids -Ringer lactate, DNS,dextrose 5% 1000-1500 cc
Dry gangrene: Treat the cause Requires urgent assessment and s hift the patient as
required for further surgical treatment.
Wet gangrene: Exclude Diabetes by repeated Blood Sugar
estimation.
Stabilize the patient hemodynamically.
Page 466
Within one/two da ys, extensive gangrene of the
3. Fournier's Gangrene scrotal skin occurs resulting in sloughing of the
Idiopathic Gangrene of scrotal skin scrotal skin exposing the testicles. In few, the
gangrene can invol ve skin of the penis, anterior
Clinical features abdominal wall, medial side of thigh, perianal
Common in young apparently healthy region. In such situations, it is described as
individuals. perianeal phlegmon
Sudden appcarance of scrotal inflammation - Luckily, the testis does not get involved in
red swollen, very painful. Paitent is toxic with fourniers gangrene because of thick tunica
fever, prostration albuginea.
Treatment
Antibiotics- -Inj. Ampicilline 500 mg. IV./6 hrly OR
-Inj. Cefotaxime 1 gm/bd.
-Inj. Gentamycin 80 mg. IV/12 hrly 12-24 hrs.
-Inj. Metronidazole 400 mg. IV/8 hrly.
IV Fluids - RL , DNS 500-1000 cc
If there is no regression in ischaemic changes shift patient to higher center.
* Exclude Diabetes by blood sugar levels. When graranulations occur, skin

grafting is needed.
Page 467
7. Burns
1. Definition/ Introduction: 2. Clinical features:

A common surgical emergency. Children and females Clinically burns can be classified as follows:
are more vulnerable in India. Commonest are Burns >10% in children and >25% in adults require
accidental scalds due to hot water or oil in children Intravenous fluid therapy. In addition certain specific
and stove burst or suicidal/ homicidal burns in cases as shown in figure1, preferably need to be
females. managed i n Burn Centres.
Figure:1: Calculation of Burns percentage
according to Parkland Formula and administer.

3. Treatment: Monitor strictly pa tients intake and urine
3.1 Medical : output after catheterization. If the burn surface
Reassure the patient. All patients having more area exceeds 35%, consider keeping the
than 10% burns in children and >25% burns in patient NBM and put ryles tube anticipating
adults should receive intra venous fluid therapy. paralytic ileus.
Burn surface calculation using Wallace rule
of '9' and Calculate fluid requirement
(BSA = Burn percentage)
Page 468
Figure 2 Figure 3
3.2 Dressing : 3.4 Other

3.2.1 Open
wounds to be cleaned with distilled water 3.4.1 Venesection may be required in case if
and antiseptic lotion (Povidon Iodine) apply peripheral lines are all collapsed. Preferably
antiseptic ointment/creams Furacin, venesection is done at the ante cubital fossa.
Silversulfadaizine+Chlorhexidine, etc. But if not possible due to extensive burns,
3.2.2 Close then long saphenous ve in can be canulated
Deep burns need close dressing by for administering f luids.
autoclaved bandage after completion of
procedure mentioned above or use 3.4.2 Endotrac heal intubation SOS
Tullegras(nonadhesive dressing) of Tracheostomy in patients with airway and
Silversulfadaizine+Chlorhexidine, Povidon- breathing difficulty.
Iodine etc. 3.4.3 Ischarotomy incisions may be required for
circumferential deep burns involving the
3.3 Proper antibiotics coverage extremities or the chest. The ischarotomy
Burn patients should be give n antibiotics incisions are as shown in the figure.
like Inj. Cefotaxin 1gm bd, I nj. Gentamycin 3.4.4 daily needful dressing under aseptic
80 mg bd, IV Metronidazole 400 mg 8 precaution
hourly etc. for 7 to 8 days keeping in view 3.4.5 Adequate oral hydration
the condition of the pa tient.
4. When to refer:
All patients requiring special burn centre care
as listed earlier.
Patients in septicaemic shock
Page 469
8. Dressings
1. Aim of wound dressing: 4.1 Antiseptics and wound

cleaning solutions
In an open wound which is being allowed to heal by Povidine iodine
secondary intention, or is being prepared for a Cetrimide
delayed reconstructive procedure, the requirements Glacial Acetic acid 10% - infected greenish
are prevention of desiccation of the surface, removal wounds (pseudomonas)
of excess wound exudates, protection from physical Normal saline
damage and reduction of risk of infection Hydrogen peroxide
EUSOL
2. Types of wound dressing: 4.2 Dressing material
2.1 Occlusive (covered) Cotton gauze / pads / bandage
Hydrocolloid dressings
2.2 Non occlusive (open) Paraffin / non adhesive gauze ( BACTIGRAS
)
2.1 In most cases, occlusive wound dressings are
Collagen granules
preferable since they prevent bacterial contamination,
keep the wound moist and provide a cover over the Adhesive strips
wound allowing normal activities.
5. Types of wounds and
2.2 Non occlusive wound dressing may be used in
special cases of clean granulating wounds, burns, dry dressings:
Eschertic where the patient is well informed and
educated regardi ng keepi ng the wound clean and 5.1 Clean open wounds: Such wounds
local hygiene. require simple cleaning with normal saline
followed by a light dressing with non adherent
3. Indications for wound gauze such as Bactigras / plain paraffin gauze.
Adherent dressings such as plaincotton gauze
dressing: should be avoided as they tend to damage the
granulation tissue on dressing change.
The primary determinant of the need for a 5.2 Clean sutured wounds: Electively
dressing is the depth and degree of bacterial sutured clean wounds require only a light
contamination of the wound. dressing of cotton gauze. The treating doctor
Superficial clean wounds are best managed by may or may not place a layer of antiseptic
infrequent dressing. ointment over the wound (eg: povodine iodine,
Deep clean wounds are best managed by soframycin). Repeat dressings are not
immediate suturing and light dressing ( for required.
physical protection only )
Contaminated / Dirty wounds are best managed
5.3 Contaminated sutured wounds:
Contaminated wounds require thorough
by surgical debridement / wash followed by
cleaning with copi ous amounts of nor mal
regular wound dressing
saline. If the de gree of contamination is high,
All electively sutured surgical wounds DO NOT this should be followed by hydrogen peroxide.
require regular wound dressing. At most they
The wound should then be irrigated with an
require a light dressing for physical wound
antiseptic solution and covered with cotton
protection.
gauze. Dressing change may be performed at
24 hrs and is primarily to assess the presence
4. Dressing components: of a collection or infection in the wound. The
presence of either should prompt removal of
some or all the sutures converting the wound
into an open contaminated wound. Such
Page 470
wounds may also require systemic cover of removal of gross necrotic tissue and debris.
antibiotics depending on the degree of Debridement may have to be repeated.
contamination. Depending on the degree of slough, this may
5.3 Contaminated open wounds: be performed bedside or may require an OT
Such wounds require regular (daily) dressing. and anesthesia. The dressing should be
Irrigation with hydrogen peroxide should be performed with hydrogen peroxide, followed
performed followed by normal saline to by nor mal saline and antiseptic solution. The
decrease the physical contamination of the covering cotton gauze should be soaked in
wound. Antiseptic solution irrigation should normal saline or EUSOL. Dressing changes
then be performed. Such wounds tend to need to be frequent and may have to be
discharge, so a bulkier dressing with more repeated thrice daily. The covering material
absorbent gauze may be required. should ideally be kept moist with saline /
EUSOL. The wounds with surrounding
5.5 Dirty wounds: Such wounds are cellulitis, oedema should be covered with
characterized by presence of slough, necrotic Magsulf. Dressings. It absorbs the fluids,
tissue, eschar or frank gangrene. These reduce oedema and pain. Large granulating
wounds require initial surgical debridement for wounds should be sent for Skin grafting.
Page 471
9. BREAST
If associated with a lump (mass)

1. Common presentations Unilateral persisting pain in postmenopausal
1.1. Lump: women
Any new discrete lump (Mass) in breast or
axillae
1.3. Nipple Discharge:
Blood stained discharge
New lump (Mass) in pre-existing modularity
Persistent single duct discharge
Asymmetrical modularity that persist after one
or two menstrual cycle 1.4. Nipple retraction or distortion /
Abscess or breast inflammation which does not nipple eczema
settle after treatment
Recurrent mass/swelling
1.5. Skin retraction of long
1.2. Pain: duration
Figure 1: signs of Breast Cancer.
With patient sitting note change contour, skin

2. Examination of breast: tethering, nipple tethering, arms above her head
some key Steps Tethering of lesion to the chest wall
Examination of axially tail with flat of hand
The patient (naked to the waist) is examined in Lump should be assessed for size (measured by
the presence of a female attendant calipers) shapes, consistency, tenderness,
mobility and fixity to the overlying skin/
Page 472
underlying chest wall , skin changes in the for m
of oedema ( pain-d-orange)
5. Other conditions (Non
Both axillae should be examined for palpable malignant)
lymph node s ensuring the anterior, medical
posterior and apical nodes. The size, numbers 5.1. Fat necrosis
and fixity should be recorded Fat necrosis following trauma can occur. Small
Note that clinical assessment of axillary nodes cancer may clinically and radiologically mimic fat
may not reflect their pathology status. For TNM necrosis. Treatment is by reassurance or excisional
staging it is impor tant. biopsy.
The supraclavicular and infraclavicular fossae
and cervical region should also be examined for 5.2. Mastalgia : breast pain :
palpable lymph nodes Can be symptom in malignancy of Breast in less
Any other symptomatic regions should be than 10%
examined as required for signs for metastatic Chest wall disease should be excluded
diseases Intraabdominal (gall stones) intrathorac`ic
All examination findings must be recorded in (cardiac, pleural) pain may all present as breast
sketch or written form, as part of good clinical pain.
practice and for medico legal reasons Exclusion of significant breast pathology,
Initial assessment, investigations and staging of reassurance and non-steroidal drugs can provide
breast symptoms should be notified. symptomatic relief.
3. Benign Breast Conditions 5.3. Gynaecomastia:

Pubertal gynecomastia
Fibroadenoma
Gynecomastia secondary to drugs therapy liver
Cyst
disease testicular tumours hyperthyroidism renal
Duct papilloma disease should be excluded.
Fibroadenosis or Fibrocystic disease of Breast.
4. Inflammatory conditions 6. Malignant lump (cancer) :

6.1. Definition:
Abscess the risk of developing distant metastasis increase with
Fistula tumour size. Early breast cancer is defined as the
condition in which tumour is confined to the breast,
size 2cm with obvious no metastasis.
Page 473
Figure 2
T.N.M.: classification
6.2 T.N.M.: classification N3- Homolateral supraclavicular and infraclavicular

nodes and/or oedema of arm.
T-primary tumor N-nodes M-metastasis
6.2.3 M Metastasis
6.2.1 T Primary tumor mass
This classification is internationally accepted and Mo - No distant metastasis
widely used to describe the extent of the tumor, M1 - Distant metastasis
regional nodes and metastasis.
To - no demonstrable tumor
6.3. Screening for breast cancer:
Tis - carcinoma in situ Beneficial in women over 40 + years age
T1-tumour diameter 2cm or less without fixation Can detect smaller tumour with lower mass of
lymph node, metastasis
T2-2cm to 5cm without fixation Early detection of breast cancer. By examination
T3-tumour greater than 5c m and mammography reduces morbidity in
screened patients.
T4 - Extension of a tumor of any size to skin or chest
wall.
(Pu.d.orange, skin tethering and nipple retraction 6.4. High Risk factors:
doesnt affect T classification) Strong family history of Breast or Endometrial
cancer
Carcinoma of Contralateral Breast
6.2.2 N-regional lymph nodes. A history of intraductal papilloma
No-No palpable homolateral axillary nodes Childless women and those conceiving after 30
yrs of age
N1 Mobile homolateral axillary nodes Breasts with dense parenchyma with prominent
N2- fixed homolateral axillary nodes. duct patterns (fatty breasts with minimal
connective tissue elements are at risk)
Page 474
6.4. Diagnosis of breast cancer:
6.4.1 Physical examination of breast (self-

examination of breast fortnightly)
Figure 3
6.4.2 FNAC: fine needle aspiration cytology
Figure 4: FNAC
Page 475
6.4.3 Imaging methods/ mammography
Figure 5: Mammography
Routine mammography screening should be Chemotherapy

avoided under 50 yrs.of age to avoid radiation Hormonal therapy
hazards.
7. Surgical management:
6.5. Investigation: a) Surgical manage ment includes
Biopsy, trucut biopsy of the lesion for Modified radical mastectomy (pateys)
histopathological evidence Radical mastectomy (halted ) not done
Estrogen, Progestron Hor monal receptor status commonly
MRI spine for Metastasis in the vertebras. Breast conservative procedure (quadrantectomy,
USG Liver for secondaries. lumpectomy, wide local excision )
Simple mastectomy for ulcerated, foul smelling
lesion of breast (toilet mastectomy)
6.6. Treatment: Breast reconstruction cosmetic surgeries-after
6.6.1 Aim: complete removal
To reduce morbidity and extends 5 yrs to 10 yrs
survival rate. b) Radiot herapy:
To conserve the breast, if possible Pre-operative for tumor mass depletion/regression
To achieve the control of disease. Post operative as advi sed by Surgeon
6.6.2 Treatment options: c) Hormonal therapy : eg Tomoxifen tabs.

Surgical management
Radiotherapy d) Chemot herapy
Page 476
10. Congenital Anomalies of G.I.T
CL and CP are facial malformations that occur during
1. The most common embryonic development and they are the most
anomalies are: common congenital deformities of the head and neck.
i. Cleft Lip or Cleft Palate They may appear separately or more often together.
ii. Hernias
iii. Esophageal Atresia 1.1.1 Definitions:
iv. Anorectal malformations a) CL : is a congenital fissure in the upper lip.
b) CP: is a midline fissure of the palate that results
from failure of the two sides to fuse.
1.1 Cleft Lip (CL) or Cleft Palate
(CP)
Figure 1 Figure 2
CL and palate
Figure 3
Page 477
1.1.2 Important feature of CL/CP One or both sides.
Small notch Unilateral clefts are nine times more
Extending into the base of the nose. common than bilateral clefts.
Unilateral or bilateral. 60% to 80% of children born with cleft
CL/CP may involve the soft and hard lip and palate are male.
palate.
Figure 4
1.1.3. Diagnostic evaluations: Prenatal diagnosis after 13-14 w eeks when

Apparent at birth. the soft tissue of the fetal face can be
Examining the palate. visualized.
Figure 5
Page 478
1.1.4. Why CP more serious thanCL? Inefficient functioning of the muscles of the soft
palate and nasopharynx.
It interferes more with feeding and breathing, more
difficult to repair. Improper tooth alignment.
Therapeutic Management Varying degree of hear loss.
The management of CL involves the cooperative Improper drainage of the middle ear.
efforts of a multidisciplinary health care team.
Recurrent Otitis media with scarring of the
7 Pediatrics tympa nic membrane.
8 Plastic surgery 1.1.7. Nursing consideration
9 Speech/ language pathology
It is important for nurse to emphasis not only the
10 Audiology infants physical needs but also on the parents
11 Nursing and social work emotional needs.
CL or CP reduces the infants ability to suck,
1.1.5. Management is directed toward:
interferes with compression of the areola.
Closure of the clefts, Surgery can be done after 6 Feeding is best with the infants head in upright
months of age with Hb more than 10 gms and position.
baby weight more than 10 kg..
Large, soft nipple with large holes have been
Prevention of complications. advised and used.
Facilitation of normal growth and development Large syringe with soft rubbe r tubi ng can be
in the child. used.
1.1.6. Prognosis: With some infant spoon feeding works best
Even with good anatomic closure most children Breast pump may be useful to stimulate the let
have: dow n reflex.
Some degree of speech impairment .
Page 479
Figure 6
1.1.8. Postoperative care for CL: 1.1.9. Postoperative care for CP:
Elbow restrains are used to prevent the infant Lie on the abdo men.
from rubbing or disturbing the suture line.
Feeding by bottle, breast or cup.
Older infants who roll over will require a jacket
restraint to prevent rolling on the abdo men and Oral packing, it is usually removed after 2 to 3
days.
rubbing the face on the sheet.
Elbow restrains.
Adequate analgesia is required to relieve pain.
Clear liquids are offered when the infant has Instruct the parents to keep the restrains at home
until palate is healed (2 to 6 weeks).
fully recovered from anesthesia.
Mild sedatives may be prescribed.
The suture site is carefully cleansed.
Soft food after discharging the patient as per
A thin layer of antibiotic ointment may be
applied. advice of surgeon.
Gentle aspiration of mouth and nasopharyngeal

secretions.
An upright infant position.
Page 480
1.2. Hernias The abdominal wall, or
Is a protrusion of a portion of an visceral organ The inguinal canal.

through an abnormal or normal opening. Commonly 1.2.1. Diaphragmatic Hernias
seen hernias are :
Protrusion of abdo minal organs through ope ning in
The diaphragm, diaphragm.
Figure 7 : Congenital Diaphragmatic Hernia
Figure 8 : Congenital Diaphragmatic Hernia
Page 481
a) Symptoms Resuscitation, maintain suction, oxygen.
IV fluids
Mild to severe respiratory distress Positioning head up.
Tachypnea , c yanosis, dyspnea Administer medication
Absent breath sound. Post operative:
Shoc k Carry out routine postoperative care and
observation.
b) Diagnosis:
1.2.2 Hiatus Hernia:
Symptomatic Protrusion of stomach through esophageal hiatus.
Radiographic study
a) Symptoms:
c) Treatment Dysphagia, vo miting,
Supportive treatment of respiratory distress (Use Bleeding (haematemesis)
of endo tracheal intubation, oxygenation).
Prophylactic antibiotics (Ampicillin 50 mg/kg) b) Manage ment:
Surgical reduction of hernia and repair of defect. Conservative management maintaining
posture. Surgical repair
d) Nursing care:
Preoperative:
Page 482
Figure 9 & 10 : Hiatal Hernia
Page 483
Figure 11
1.2.3 Umbilical Hernia a) Symptoms:

Weakness in abdominal wall around umbilicus,
Noted by inspection and palpation of the
incomplete closure of abdominal wall allowing
abdomen.
intestinal contents to protrude through opening.
High incidence in premature.
b) Manage ment
Surgical repair
Page 484
Umbilical Hernia
Figure 12
1.3 Esophageal Atresia 1.3.1. Clinical manifestation:
Excessive salivation.
The esophagus instead of being an open tube from
the throat to the stomach is closed at some point. A Coughing, choking, cyanosis,
fistula is common between the trachea and Apnea
esophagus.
Abdominal distention.
Site of attac
Figure 13 : Types of Tracheoesophagial Fistula (TEF)
Page 485
1.3.2. Nursing alert: The gastrostomy tube is connected to gravity
drainage until the infant can tolerate feeding.
Any infant who has an excessive amount of frothy
saliva in the mouth or difficulty with secretions and Tracheal suction with extreme caution to avoid
unexplained episodes of cyanosis should be injury to the suture line.
suspected of having an EA / TEF and referred The initial attempt at oral feeding to make sure
immediately for medical evaluation. that the infant can swallow without choking.
Oral feedings are begun with sterile water,
1.3.3.Therapeutic Management:
followed by frequent small feeding of formula.
Maintenance of patent airway. Infants are usually not discharged until they are
taking oral fluids well and the gastrostomy tube
Prevention of pneumonia. is removed.
Surgical repair of the anomaly.
1.2.4. Anorectal malformations
Avoid oral intake, start IV fluids. Abnormal development of genitourinary and
Remova l of mouth secretion by suction. pelvic organs.
The rectum and urinary tract separate completely
Broad spectrum antibiotic therapy. by the seventh week of gestation.
Gastrostomy and repair of the TEF. a) Imperforate anus
1.3.4. Nursing role: Is the mos t common congenital anomaly of

GIT in newbor n.
Nursing responsibility for detection of this Investigation :Invertogram- X ray.
malformation immediately after birth.
Invertogram will tell type of anomaly Low or High.
After feeding the infant and swallows, but
sudde nly coughs and the fluid return through t he Diagnosis:
nose or mouth, report immediately.
There is no a nal ope ning.
The infant placed in incuba tor oxygen is The nurse is unable to insert the thermometer.
administered. No passage of meconium.
Later on abdominal distention and pain occur.
Intermittent or continuous suction of nose.
Oral fluids are withheld, the fluid intake met by Treatment :
IV fluids or gastrostomy. High anomaly will require immediate colostomy
while for low anomaly Local incision and Dilatation
1.3.5. Postoperative care: will be required.
The infant is returned to radiant warmer or
incuba tor.
Page 486
Figure 14: Imperforate anus
Postoperative care: The excoriations of skin occurs around

Colostomy area due to digestive enzymes from
The anal area should be kept dry and clean. intestinal juices leaking from the side of bag. To
prevent this aluminium paint should be painted
If a colostomy has been done the skin around the on the skin around the Colostomy site.
wound must be clean and apply colostomy clean
dressing.
Figure 15
Page 487
11. Venous Thromboembolism
1. Introduction : The more common acquired risk factors

include advanced age, hospitalization and
Despite increased awareness and use of prophylactic immobilization, hormone replacement and oral
modalities, DVT and pulmonary embolism (PE) contraceptive therapy, pregnancy and the recently
remain important preventable sources of morbidity postpartum state, prior VTE, malignancy, major
and mortality. The incidence of DVT ranges between surgery, obe sity, nephrotic syndrome, trauma and
5 and 9 per 10,000 person-years in the general spinal cord injury, long-haul travel (>6 hours),
population, and the incidence of VTE (DVT and PE varicose veins, antiphospholipid syndrome,
combined) is approximately 14 per 10,000 person- myeloproliferative disorders, and polycythemia.
years. Heritable risk factors include factor V Leiden;
prothrombin 20210A gene variant; antithrombin,
protein C, and protein S deficiencies; and
dysfibrinogenemias.. 9
Figure 1
2. Clinical Evaluation 3. Investigations:

Early in the course of DVT development, venous Color Doppler will confirm the diagnosis.
thrombosis is thought to begin in an area of relative
stasis, such as a soleal sinus vein or immediately
downstream of the cusps of a venous valve in the 4. Treatment:
axial calf veins. Isolated proximal DVT without tibial
vein thrombos is is unusual. Early in the course of a 4.1 Antithrombotic Therapy :
DVT, there may be no or few clinical findings such
as pain or swelling. Even extensive DVT may Antithrombotic therapy may be initiated with IV or
sometimes be present without signs or symptoms. SC unfractionated heparin, SC low molecular weight
History and physical examination are therefore heparin, or SC fondaparinux (a synthetic
unreliable in the diagnosis of DVT. In addition, pentasaccharide). This initial therapy usually is
symptoms and signs generally associated with DVT, continued for at least 5 days, while oral vitamin K
such as extremity pain and/or swelling, are antagonists are being simultaneously administered.
nonspecific The initial therapy typically is discontinued when the
international normalized ratio (INR) is 2.0 for 24
hours
Page 488
Hemorrhage is the primary complication of UFH monitoring include those with significant renal
therapy. The rate of major hemorrhage (fatal, insufficiency or failure, pediatric patients, obese
intracranial, retroperitoneal, or requiring transfusion patients of >120 kg, and patients who are pregnant.
of >2 units of packed red blood cells) is
approximately 5% in hospitalized patients
undergoing UFH therapy (1% in medical patients and 4.2 Vitamin K antagonists :
8% in surgical patients). For patients with UFH-
related bleeding complications, cessation of UFH is which include warfarin and other coumarin
required, and anticoagulation may be reversed with derivatives, are the mainstay of long-term
protamine sulfate. Protamine sulfate binds to UFH antithrombotic therapy in patients with VTE.
and forms an inactive salt compound. Each milligram Warfarin therapy usually is monitored by measuring
of protamine neutralizes 90 to 115 units of heparin, the INR, Vitamin K antagonist may be started on the
and the dosage should not exceed 50 mg IV over any same day as the initial parenteral anticoagulant,
10-minute period. Side effects of protamine sulfate usually at doses ranging from 5 to 10 mg. Smaller
include hypotension, pulmonary ede ma, and initial doses may be needed in older and
anaphylaxis. malnourished pa tients, in those with liver disease or
congestive heart failure, and in those who have
Most patients who receive therapeutic LMWH do not recently undergone major surgery and depends on
require monitoring. Patients who do require liver function, diet, age, and concomitant medications
Page 489
12.VaricoseVeins
Figure 1: Varicose veins
1. Definition/ Introduction: 3. Etiology and Risk Factors

Varicose veins are dilated, tortuous and elongated Heredity, Age over 40 , Prolonged standing
superficial ve ins of the lower limbs ,Pregnancy , Obesity , Sede ntary lifestyle ,
Surgery or trauma , Use of hor monal
Age old disease known since Hippocrates, medications.
Mentioned in Ebers Papyrus in 1550.
Incidence - F>M , Prevalence 1023% in men
3040% in women 4. Complications
Skin changes 5% , Active ulcers 0.5%. 4.1 Ankle edema, Ankle flare,
Pigmentation , Venous eczema,
2. Clinical features: Venous ulcer, Profuse
Patient usually has Cosmetic concerns Hemorrhage, Superficial
Symptoms of tiredness & heaviness in legs and Thrombophlebitis, Equinous
itching and eve n leg ulcer
deformity, Calcification.
Page 490
4.2 Deep vein thrombosis: 6.2 Surgical treatment
One of the important etiology as well as 6.2.1 Flush ligation at sapheno femoral
complication of varicose veins. It presents junction with stripping of Long
clinically as swollen woody calf, pain, ankle saphenous Vein.
edema and redness. Patient may have fever. 6.2.2 Perforator ligation
Subfacial.
5. Investigations: Sclerotherapy - Ultrasound-guided
foamsclerotherapy for short segments or
Doppler ultrasound is most ideal for complete recurrent varicosity.
evaluation. Radiofrequency ablation (Closure),
EndoVenous Laser Ablation.
Ambulator y phlebectomy, or a .
6. Treatment: combination of these treatments.
Management options at glance
Bisguards exercise Heel raises atleast 7. Instructions to patient:
3 4 timesevery day. Life style changes, Follow Bisguards exercises
Compression stockings For early daily, Use of compression stocking through the day
varicosities without complications. Types of can be removed at night. While sleeping raise the
stocking are foot end of the bed to aid venous return.
Below/Above knee
Mid thigh 8. Dos and Donts:
In case the varicosity starts bleeding do not panic,
immediately lie down flat on the ground a nd raise the
bleeding limb above the heart level and apply
compression.
Page 491
13. GENITO URINARY DISORDERS
1. PARAPHIMOSIS
Reduction of the paraphimosis is followed by a
1.1 Clinical features : course of antibiotics and after 8-10 days perform
Circumcision (at surgical center).
This condi tion occurs when a tight foreskin
(phimosis) is forcibly retracted back off the glans and .
cannot be pulled forwards again. The tight band
causes obs truction of ve nous returns followed by 2. TORSION TESTIS:
swelling of the distal foreskin and glans. It can occur
at any age. Condition is very painful & if not taken It is a condition caused by the twist of suspended
care may cause Ischemic/Pregangrenous changes. testis.
2.1. Patient presents with

1.2 Treatment:
Technique of Reduction- Parts shaved & prepared Sever scrotal pain of sudden onset referred to lumbar
Patient in OT Parts painted & draped. Local region Vomiting, fever, Scrotal swelling with gross
anaesthesia 2% Xylocaine infiltrated at the root of the tenderness up to the cord
Penis.
Manual compression and reduction 2.2. Investigation:
By giving multiple needle punctures over Routine investigation
swollen & oede matous fore skin of pe nis and
squeezing it to drive out the oedema fluid USG Scrotum - Doppler study - shows decreased
followed by mechanical reduction by pulling it blood flow & also viability of the testis.
to normal position.
Dorsal slitting at 12' O clock position and 2.3 Diagnosis-
reduction. Colour Doppler study of Scrotum.
2.3. Treatment:
2.3.1 I.V. fluids - Ringer lactate, DNS, dextrose 5%
2.3.2 Analgesics- Inj. Diclofenac 50 mg/I.M.
2.3.3 Antibiot ics-Inj. Ampicillin 500 mg. I.V/6 hrly . 12 to 24 hrs.
Inj. Gentamycine 80 mg.I.V./12 hrly.
Inj. Metronidazole 400 mg. I.V./8 hrly
If not relived after stabilization of patient to be referred to surgical center.
3. EPIDIDYMO-ORCHITIS
It is a inflammatory & infective condition affecting 3.3. Treatment:
epididymis and testis 3.3.1 Analgesics tablet aceclofeanac 10-20 mg/ BD
OR Dicyclomine 50 mg/ BD
3.3.2 Antibiotics Ofloxacine 400 mg/ BD for 5 to 7
3.1. Patient present with: days OR Cefadroxine 200 mg/ BD 5 to 7
Scrotal pain days.
Testicular swelling 3.3.3 Anti inflammatory Seratiopeptidase -5 to 10
Low grade fever with chills mg/ TDS 5 to 7 days
3.3.4 Ibuprofen 200-400 mg/ TDS 5 to 7 days
3.2. Investigation: 2.3.4 Scrotal support for 2-3 weeks
Routine investigation
USG Scrotum - Doppler study

Page 492
14. ANO-RECTAL DISORDERS
1. Hemorrhoids 1.4 Complications:-

Profuse hemorrhage
Hemorrhoids are clumps dilated veins occurring in
Fibrosis
relation to the ano-rectal junction (commonly known
as piles) Thrombosis
Infection
1.1. Classification: Pyelophlebitis
Ulceration
1.1.1. By descent Gangrene
Suppuration
Grade 1- Bleeding Portal pyemia
Grade 2- Protrusions with spontaneous reduction
Grade3- Protrusions regressing with manual 1.5 Treatment:-
reduction 1.5.1 Conservative management:
Grade4- Irreducible protrusions Dietary improvement high fiber diet
Avoid straining at defecation
1.1.2. By Location
External:-arise from inferior hemorrhoidal plexus, 1.5.2 Active Surgical Treatment
and are covered by modified squamous epithelium. Sclerotherapy
Occurs below pectinate line. Banding
Internal- arise from superior hemorrhoidal plexus, Photo coagulation
also above pectinate line.
Hemorrhoidectomy
Iterno e xternal- when both are persent.
1.2. Clinical Features

1.2.1 Symptoms:- 1.6 Postoperative care
Bleeding, bright red and painless, frequent
bleeding may led to a nemia
Prolapse
Pain on prolapse
Mucus discharge
Pruritus / itching
1.3 Investigations:-
Direct Visualisation
Digital Rectal Examination
Proctoscopy
Basic investigation (Hb, CBC, Urine )
Blood grouping and RH typing
USG Abdomen (Associated portal hypertension)
Colonoscopy
Page 493
Table 1: Post Operative Care and Complication
Post Operative care Post Operative Complication

Watch for bleeding Early
Sitz bath twice daily in the postoperative period Pain acute retention of urine
Analgesics Reactionary Hemorrhage (24 hrs)
Stool softners and laxatives Constipation
Avoids digital rectal examination in the early Late
postoperative periods Secondary hemorrhage (24 hrs)
Anal stricture
Anal fissure
Fecal incontinence
1.7 Important note:- 2.3. Examination:-
Surgery is for failure in conservative Acute fissure Pain during per rectal examination
management or in severe cases with or without palpatory mucosal abrasion
Colonic carcinoma to be ruled out (colonoscopy)
Chronic fissure Skin tag fibrosed ano-rectal mucosa
Anemia to be corrected pre-operatively (Blood
transfusion if required) 2.4. Investigations:-
Muco-cutaneous bridges should be preserved
Basic investigation Hb, CBC, Urine
during surgery to pr event anal stenosis
Conservation treatment preferred in pregnant Colonoscopy
ladies and elder.
2.5. Treatment:-
2. Anal Fissure
2.5.1 Conservative Manage ment
2.1. Defination: Laxatives Cremaffine 30ml at bed time / stool
Anal fissure is an ulcer or a crack in the canal or anal bulking agents -
verge that may extend from mucoc utaneous junction
Ointment to relax anal sphincter and improve blood
to dentate line. Anal fissure is of particular concern if
flow like Diltiazem / Nifedipine cream / glyceryl
it is acute because the degree of patient discomfort,
trinitrate ointment
pain and disability are extremely high.
Sitz bath
The type of fissure is acute and c hronic.
High fiber diet
Acute anal fissure is a deep tear through the skin of 2.5.2 Surgery:-
the anal margin extending into the anal canal. There
is little inflammatory induration or edema of its Anal dialation under GA
edges. There is accompanying spasm of the anal
Fissurectomy
sphincter muscles.
Chronic anal fissure is characterized by inflamed 3. Pilonidal Sinus

indurated margins, and a base consisting of either
scar tissue or the lower border of the internal 3.1Clinical features :
A pilonidal sinus is a depression in the skin or small
sphincter muscle. Chronic anal fissure doe s not heal
pit that occurs at the bottom of the tailbone (coccyx)
with conservative measures.
and can become infected and filled with pus. Once
infected, the technical term is pilonidal abscess.
2.2. Symptoms:- pilonidal abscesses look like a boil at the bottom of
the tailbone, just above the crack of the buttocks. It is
Pain during the defecation and / or after defecation more common in men than in women. It usually
happens in young people up into the fourth decade of
Slight bleeding / streaking
life.
Page 494
3.2 Treatment : Discharge of pus from the rectum
3.2.1 Medical treatment Fatigue and general malaise
Antibiotics (Cap. Ampicillin 500 mg TDS x
Fever night sweats, and chills
5 days)
Analgesics (Tab. Diclofenac 50 mg BD x 5 Lump or nodule, swelling, redness, tenderness at
days) edge of anus
3.2.2 Surgery Painful, hardened tissue
Anal dilatation under GA.
In infants, the abscess often appears as a swollen, red,
Fissurectomy tender lump at the edge of the anus. The infant may
be fussy and irritable from discomfort, but there are
4. Anorectal abscess usually no ot her symptoms.
4.5 Investigations
4.1 Defination :
A rectal examination may confirm an anorectal
Anorectal abscess is a collection of pus in the area of abscess.
the anus and rectum.
A proctosigmoidoscopy may be done to rule out
other diseases.
4.2 Causes
Rarely, you may need a CT scan, MRI or ultrasound
Common causes of anorectal abscess include: to determine where the pus collection is located
Blocked glands in the anal area
4.6. Treatment:-
Infection of an anal fissure
4.6.1 Analgesics-
Sexually transmitted infection Inj. Diclofenac 50 mg/IM BD/sos
Deep rectal abscess may be caused by intestinal 4.6.2 Antibiot ics-
disorders such as crohn's disease or diverticulitis. Inj. Ampicillin 500 mg. I.V./6 hrly . 5 days
Inj. Gentamycine 80 mg. I.V./12 hrly.
4.3. Risk factors
Inj. Metronidazole 400 mg. I.V./8 hrly.
Anal sex
4.6.3 Treatment involves surgery, open and drain
Chemotherapy drugs used to treat cancer the abscess, patient may be shifted at surgical
Diabetes center.
Inflammatory bowel disease (crohn's disease and 4.6.4 Post operative care
ulcerative colitis) After surgery patient needs warm sitz baths ( sitting
Use of medications such as prednisolone. in a tub of warm water) this may help to relieve
pain, reduce swelling and make the abscess easier to
Weakened immune system (such as from drain.
HIV/AIDS)
Drained abscesses are usually left open and have no
The condition may occur in infants and toddlers who stitches.
are still in diapers and who have a history of anal
fissures. Patient should be advised to take stool softeners,
practice good hygiene and eat a soft or liquid diet
4.4. Symptoms until the abscess has healed.
4.4.1 Swelling around anus and constant 4.7. Possible complications

throbbing pain, fever are the most common
Anal fistula
symptoms. Pain with bowel move ments may be
severe. Body-wide infection (sepsis)
4.4.2 Other symptoms may include:- Continuing pain
Constipation Problem keeps coming back (recurrence)
Page 495
Scars intercourse, including anal sex, to preve nt such
infections.
4.8. Prevention:- 4.8.2 Frequent diaper change s and proper
4.8.1 Prevention or prompt treat ment of sexually cleaning during diaper changing will help to
transmitted diseases may prevent this cause of preve nt both fissures and perianal abscesses in
anorectal abscesses. Use condoms during infants and toddlers.
Page 496
15. Tracheostomy
1. Introduction 5. Inner Cannulas

Tracheostomy is one of the most common surgical The inner cannulas should be used at all times in the
procedures performed in the ICU and is the airway of ICU. They serve to extend the life of the
choice for patients requiring mechanical ventilation tracheostomy tubes by preventing the buildup
for more than 2 weeks. secretions within the tracheostomy. The inner
cannulas can be easily removed and either cleaned or
2. Procedure replaced with a sterile, disposable one. Disposable
Patients neck is extended and the surgical field is inner cannulas have the advantage of quick and
exposed from the chin to several inches below the efficient changing, a decrease in nursing time,
clavicle. This area is prepered and draped and decrease risk of cross-contamination, and guaranteed
prophylactic antibiotics are administered at the sterility. The obturator should be kept at the bedside
discretion of the surgeon. A vertical or horizontal at all times in the event that reinsertion of the
incision may be used; however, a horizontal incision tracheostomy is necessary.
will provide a better cosmetic result. The platysma
muscle is divided in line with the incision and the 6. Humidification
strap muscles are separated in the midline. The One of the functions of the uppe r airway is to
thyroid isthmus is then mobilized superiorly or is moisten and humidify inspired air. Since
divided as needed to access the trachea. In the event tracheostomies bypass the upper airway, it is vital to
of a low-lying cricoid cartilage, dissection on the provide patients who have tracheostomies with warm,
anterior wall of the trachea helps to mobilize the humidified air. Humidification of inspired gases will
trachea out of the mediastinum, and also the use of a prevent complications in patients with
cricoid hook will elevate the trachea to expose the tracheostomies. Failure to humidify the inspired
second or third tracheal ring. Following identification gases can obstruct the tube by inspissated secretions,
of the second or third tracheal ring, a vertical impair mucociliary clearance, and decrease cough.
tracheostomy is created or a tracheal flap (Bjork flap)
is fashioned to create a fistulous tract by suturing the 7. Suctioning
tracheal mucosal flap to the skin in the incision Patients with tracheostomies frequently have
increased amounts of airway secretions coupled with
3. Postoperative Care decreased ability to clear them effectively. Keeping
The care of a tracheostomy tube after surgery is the airways clear of excess secretions is important in
important. Highlighted below are some specific decreasing the risk of lung infection and airway
issues that all intensivists need to know when caring plugging. Suctioning is frequently required in
for patients with tracheostomies. patients with poor or ineffective cough. Suction
techniques should remove the maximal amount of
4. Wound and Dressing Care secretions while causing the least amount of airway
Daily examinations of the stoma are important in trauma. Routine suctioning, however, is not
identifying infections or excoriations of the skin at recommended.
the tracheostomy site. In addition, keeping the wound
clean and free of blood and secretions is very 8. Tracheostomy Tube
important, especially in the immediate post
tracheostomy period. Dressing changes should be
Changes
performed at least twice a day and when the dressings Tracheostomy tubes do not require routine changing.
are soiled. Some authors recommend cleaning the In general, the tube only needs to be changed under
stoma with 1:1 mixture of hydrogen peroxide and the following conditions: (a) there is a functional
sterile saline. When changing dressings and tapes, problem with it, such as an air leak in the balloon; (b)
special care is needed to avoid accidental dislodging when the lumen is narrowed due to the buildup of
of the tracheostomy tube. dried secretions; (c) when switching to a new type of
tube; or (d) when downsizing the tube prior to
decannulation. Ideally, a tracheos tomy tube should
not be changed until 7 to 10 days after its initial
Page 497
placement. The reason for this is to allow the tracheal Cardiorespiratory arrest (uncommon)
stoma and the tract to mature. Patients who have their Tracheo-laryngeal injury (uncommon)
tracheostomy tube changed before the tract is fully Crushed airway from dilational tracheostomy-
mature risk having the tube misplaced into the soft uncommon
tissue of the neck. If the tracheostomy tube needs to
be replaced before the tract has had time to mature,
the tube should be changed over a guide, such as a
9.2. Intermediate Complications
suction catheter or tube changer. (from day 1 to day 7)
Persistent bleeding
9. Complications of Tube displacement
Tube obs truction (mucus, blood)
Tracheostomies Major atelectasis
Wound infection/cellulitis
9.1. Immediate Complications (
24 hours) 9.3. Late Complications (>day 7)
Tube displacement Tracheoinnominate artery fistula
Arrhythmia Tracheomalacia
Hypotension Hypoxia/hypercapnia Tracheal stenosis
Loss of airway control Necrosis and loss of anterior tracheal cartilage
Pneumothorax Tracheoesophageal fistula
Pneumomediastinum Major aspiration
Acute surgical emphysema Chronic speech and swallowing deficits
Major hemorrhage Tracheocutaneous fistula
Bacteremia
Esophageal injury (uncommon)
Page 498
16. URINERY CATHETERZATION
bedside commode or when accurate urinary output is

1. Indication: required.
Urinary catheterization is done when a person is
unable to urinate using a toilet, bedpan, urinal,
Figure 1: Diagrammatic presentation of Urinary Catheter assembly
2. Types of catheters: 2.2 A straight catheter:

3 is used when the catheter is to be inserted and
2.1 A condom catheter: removed immediately.
consists of a soft plastic or rubber sheath, tubing,
and a collection bag for the urine. The sheath is
placed over the penis and the collection bag is 2.3 An indwelling catheter:
attached to the leg. Collects urine when there is also known as Foley catheter, is left inside the
no need for catheter insertion. bladder to provide continuous urine drainage.
Page 499
2.4 A suprapubic catheter: 2.5 A 3-way catheter:
is a type of indwelling catheter. The suprapubic for continuous bladder irrigation (CBI) is a type of
catheter is inserted into the bladder through a surgical indwelling catheter. Irrigate the bladder to prevent
incision made in the abdominal wall, right above the obstruction (i.e bleeding)
pubic bone.
Red rubber Latex Silicon
Figure -2
Catheters
Straight Condom
Suprapubic Indwelling
Page 500
3. Sizes & Subtypes:
Figure 4
3.1 Most common sizes are 8 F to 28 6. Emptying Urine Drainage

F. Bags:
3.2 1 F is equivalent to 0.33 mm =
Urine measured at the end of each shift or every
.013" = 1/77" of diameter. 4 hourly in ward, e very hourly in ICU.
3.3 Coud" (French for elbowed) Urine drainage bags should also be emptied if
catheters have a 45 bend at the they are full.
tip to allow easier passage Leg bags need to be emptied frequently because
through an enlarged prostate they are smaller, and hold less urine.
3.4 "Councill tip" catheters have a 7. Quantity:
small hole at the tip which allows
Be sure to monitor urine output
them to be passed over a wire
Amount
5. Caring for a Person with an Characteristics (color, clarity, sediment,
Indwelling Urinary hematuria, odor)
Catheter: Less than 30 ml/hr of urine indicates a

problem
The catheter tubing is secured loosely to the
persons body near the insertion site using a
catheter strap or adhesive tape
4. Catheter Insertion:
Securing the tubing to the persons body 4.1. Equipment:
prevents the catheter from being accidentally (check packages and expiry dates)
pulled out during repositioning
Catheter tray (with drapes, fenestrated drape,
The drainage bag is then secured to the bed cotton balls, swab holder, bowl)
frame at a level lower than the persons
bladder. Catheter 14-16 Fr (for wome n) 12 Fr for young
girls
16-18 Fr (for me n)
Sterile drainage tubing with collection bag
Correct size syringe (check catheter balloon)
Sterile water
Page 501
Cleansing solution: Chlorhexidine 4%, Povidone Ide ntify meatus and assess skin integrity
Iodine 10%
Lubricant anaesthetic jelly Identify potential difficulties (i.e enlarged
Sterile gloves prostate)
Specimen container
Tape to anchor tubing 4.3. Important aspects
Arrange equipment
4.2. Assess Wash hands
Review physicians order and understand Provide privacy
purpose of inserting catheter
Raise bed, stand on left side of bed if right
Assess client (last urination, level of awareness, handed (right side if left handed)
understanding)
Water proof pad under client
Palpate bladder
Position & drape client
Figure 5 Figure 6
4.4 Position
4.4.1 Fe male: dorsal recumbent (supine with knees
flexed) or Sims position (side-lying with uppe r leg
flexed at knee and hip)
Figure 7
4.4.2 Male: supine position

With disposable gloves, wash perineal areas
Page 502
Anatomy:
Figure 8
Figure 9
Page 503
4.5 Procedure: men: over thighs and fenestrated over penis
4.5.1 Anaesthetic Lubricant jelly
4.4.2 Place sterile tray and contents between legs
4.5.2 Apply sterile drapes keep gloves sterile
4.4.3 Cleanse meatus:
women: under buttocks and fenestrated over
perineum
Cleaning of part Male Urethra Catheter in situ

Figure 10 Figure 11 Figure 12
a) Men: retract foreskin, hold penis below clean in a circular motion from meatus down to
glans, maintain position of hand, with forceps base of glans, repeat three more times
Cleaning of part Draping Catheter in situ
Figure 13 Figure 14 Figure 15
b) Women: 4.3 Insertion :

With nondominant hand, expos e meatus, maintain a) Hold end of catheter loosely coiled in
Position of hand, clean with forceps, wipe from front dominant hand, place end of catheter in tray
to back, each time take new cotton ball for each b) Insert catheter:
swipe, far labial fold, near and directly over meatus
Page 504
Wome n: Ask client to bear down as if to void, 4.6. Evaluate:
insert 5 to 7.5 cm or until urine flows, then
advance another 2.5 to 5 cm Palpate bladder
Men: Hold penis perpendicular, ask client to Assess comfort
bear down, insert 17 to 22.5 cm or until urine
flows, then advance to bifurcation Characteristics and amount of urine
c) Collect specimen if indicated 4.7. Document:
d) Allow bladder to empty unless policy
restricts (800 to 1000 ml) Pelvic floor blood Report and record type and size of catheter
vessels may become engorged from the
sudden release of pressure, leading to Amount of fluid used to inflate balloon
possible hypotensive episode. This may also
Characteristics of urine, amount, reason for
cause painful bladder spasms.
catheter, specimens, clients response
e) Inflate balloon with amount indicated (10
ml)
8. Procedure for removal:
If client complains of pain, aspirate solution and
advance catheter further and inflate Deflate the bulb completely with syringe
Gently pull to feel resistance If bulb cannot be deflated then
Attach catheter to collection bag and attach to Cut the one way valve
bed frame below bladder Puncture the channel with needle
Anchor catheter (thigh if appropriate and coil Go on puncturing from distal most end to most
tubing on bed and attach to mattress) proximal end
USG guided suprapubic needle puncturing of the
bulb
Inflate further till it gets bursted.
Page 505
17. TRIAGE
Triage process should be completed within five
1. Introdution : minutes.
Method of quickly identifying victims who have 4.1 Important steps
immediately life threatening injuries & have the best
chance of surviving. 4.1.1 Start System:
Classification is based on
Process which place the right patient in right place at
right time to receive he right level of care. Respiration
Perfusion
Triage involve a dynamic equilibrium between needs
Mental Status
and resources
Needs= Number of wounded and types of wounds 4.1.2 Shift
Identify and remove
Resource =Infrastructure and equipment at hand &
competent personnel present Select those severely injured
The dead
2. The Triage Team The slightly injured
The uninjured
Triage team leader coordinator
4.1.3 Sort:
Clinical triage officer
Categorize the most severely injured based on:
Head nurse, matron ; chief organizer
Life-threatening conditions (ABC)
Nursing groups
Anatomic site of injury
Red Cross Wound Score
3. Triage Documentation: Treatment available in terms
3.1 General information Serious wounds: resuscitation and immediate
surgery
Name, Age, Gender, chief complaints, history of past Second priority: need surgery but can wait
illness, mechanism of injuries, past medical and Superficial wounds: ambulator y management
surgical history, allergy to food or drug and current Severe wounds: supportive treatment
medication. Date of last tetanus immunization, last
menstrual period for female age 11 to 60 years
5. Categorization:
3.2 Vital sign- temperature, Pulse,
B.P & respiration etc. 5.1Category
3.3 Level of consciousness i: Resuscitation and immediate
surgery
3.4 Visual inspection for
Patients who need urgent surgery life saving
deformities, laceration, and have a good chance of recovery. (e.g. Airway,
bruising, rashes etc. Breathing, Circulation: tracheostomy, haemothorax,
haemorrhaging abdominal injuries, peripheral blood
4. Triage Process vessels)
Gathering information at point of triage.

Perform initial assessments at point of triage.
Page 506
Figure 1 Figure 2
5.2 Category ii: Need surgery but A large number of patients will fall into this
can wait group.( e.g. non-haemorrhaging abdo minal injuries,
wounds of limbs with fractures and/or major soft
Patients who require surgery but not on an urgent tissue wounds, penetrating head wounds GCS > 8.)
basis.
Figure 3
Page 507
Figure 4
Figure 5
Page 508
5.3 Category iii: Superficial Patients with wounds requiring little or no surgery. In
practice, this is a large group, including superficial
wounds (no surgery, wounds managed under local anaesthesia in the
ambulatory treatment) emergency room or with simple first aid measures.
Figure 6
5.4 Category iv: Very severe Patients with such severe injuries that they are
unlikely to survive or would have a poor quality of
wounds (no surgery, survival.
supportive treatment)
The moribund or those with multiple major injuries
whose management could be considered wasteful of
scarce resources in a mass casualty situation.
Page 509
Figure 7
Seizures
6. Hospital Triage Setting: Asthma
Doctor performs daily triage on a routine basis every Acute Bleeding or Acute Pain
day in emergency department. Depressed Level of Consciousness
6.1 Aim: 6.2.3 Urgent : Category 2 Colour Code

It is to identify those patients who have the highest YELLOW
degree of compromise for the purpose of providing Those conditions that are serious and if not treated in
rapid care to sickest patient first. timely manner are likely to become critical.Time
needed, s erious illness or injury that must be attended
to, b ut wait upto two hrs.
6.2 Hospital Triage System Example:
i. Emergent Complex long bone fractures

ii. Urgent Bleeding Controlled with a pressure dressing
iii. Non Urgent Acute psychiatry problems
iv. Deceased High fever with other vital signs stable
6.2.1 Emergent : Category 1 Colour Code 6.2.4 Not Urgent : Category 3 colour code
RED GREEN
Those patients that are life threatening but likely to
be amenable to rapid intervention. Condition that can wait without likelihood of
deterioration. Time needed, condition can wait for
Time required treatment immediately or within 15 to more than 2 hrs.
30 minutes.
Example:
Example:
Minor lacerations which requires sutures
Cardiac Arrest
Minor joint trauma requires x-ray for diagnosis
Airway Obstruction Chronic conditions that are stable such as pre
Haemorrhage with shoc k existing skin rashes.
Complicated Delivery
Page 510
iv. Category 4 colour code Black 7. Conclusions:
Dead to be honoured and to be taken care as marked Triage is method of quickly identifying victims
in end session, if not possible by assigned agency who have immediately life threatening injuries
earlier. AND who have the best chance of surviving.
Key elements of the START Triage Systems are:
Respiration, Perfusion and medication.
Reverse Triage is used for mass casualty
incidents.
Page 511
ORTHOPAEDICS
Page 512
1. INFECTIONS IN ORTHOPEDICS
Infections of bone are difficult to treat due to 1.3. Most Common Organism:
precarious blood supply. Most common is Staphylococcusaureus
Hematogenous spread.
1. Osteomyelitis 1.4. Type:

Acute, Sub-Acute&Chronic
1.1. Classification:
Based on duration and mechanism of Infection 1.5. Most Common Site:
Durat ion: Around Knee and Hip (in Paediatric cases)
1. Acute
2. Sub-Acute Diagnosis:
3. Chronic
Mechanism: 1.6. Clinical Features:
1. Exogenous Open fracture, Surgery or Pain and swelling
contagious Constitutional symptoms
2. Hematogenous
Warm to touch
Restricted movements
1.2. Factors increasing
susceptibility to Infection: 1.7. Laboratory studies:
Patient dependant factors are nutritional and
immunological status. HB, TLC, DLC&ESR
Surgeon dependant factors are skin preparation, Aspiration of fluid(>50000wbc/cu.mm.)
operation room, environment and prophylactic Gram Stain sensitivity (30%)
antibiotic therapy Culture sensitivity (90%)
Blood Culture
Fig 1.2 Xray showing Osteomylitis of tibia Fig 1.2.1 Inflammation of Skin
1.8. Imaging studies:

X-Ray
Computed Tomography (CT)
Radionuclide scanning
MRI
Page 513
1.9. Treatment: NSAIDs such as Tab.Diclofenac sodium 50mg thrice
a day along with Antacids until Inflammation
subsides and supportive treatment such as
1.9.1. Medical Therapy(Conservative)
multivitamins.
Immobilize the joint with splint for pain relief
Antibiotic therapy of Osteomylitis. 1.9.2. Surgical therapy
Treat with intravenous Antibiotics for 3 to 6 weeks Debridement

Cephalosporins and Aminoglycosides. Sequestrectomy
Saucerisation
Paediatric dosage Sinus tract excision
Inj.Cefotaxime 750mg twice a day for 3 to 6 2. Tuberculosisof Bone:

weeks.
Inj.Amikacin 250 mg/ Inj.Gentamycine 20mg IV
Bone is most common extra pulmonary site of
twice a day for 3 to 6 weeks.
Infection of Mycobacterium Tuberculosis.
Adult Dosage
2.1. Source:
Inj.Cefotaxime 1500mg IV twice a day for 3 to 6 Always secondary.
weeks.
Inj.Amikacin 500mg/Inj.Gentamycine 40mg IV 2.2. Site:
twice a day for 3 to 6 weeks. Most common site is spine followed by hip and
Knee. Commonly occurs in first three decades
Treat for atleast 3 weeks with IV Antibiotics initially of life.
and then shift to or al for another 3 weeks.
Antibiotics should be used in accordance with
Antibiotic protocol of Institute. 2.3. Agent:
Mycobacterium Tuberculosis.
Fig 2.1 Picture of Destruction of Spi ne Fig 2.2 Cross Section of Koc h Spi ne
2.4. Clinical features:

a. Mono articular.
b. History of Night cries, loss of weight,
anorexia.
c. Decreased joint movement.
d. Wasting of muscles.
Page 514
e. Pain and Tenderness. Bed rest and Traction in acute and early stages,
f. Cold abscess. Splints and braces.
2.6.2 Operative
2.5. Investigations:
a. Capsulotomy.
b. Synovectomy.
a. HB,TLC, DLC & ESR.
c. Curettage.
b. X-rayearly De-calcification & Late Joint
d. Excision.
destruction.
c. Confirm diagnosis by biopsy or culture and
2.6.3 Abscess
start treatment.
d. MRI. Incision and dr ainage.
2.6. Principles of Treatment: 2.7Complication of Bone Infections:

a. General Support Protein rich diet.Haematinics. 1) Pathological fracture.
b. Chemotherapy-Anti-tuberculous treatment as 2) Non-union / Mal union.
per RNTCP CAT-II 3) Para-paresis in spinal tuberculosis.
2.6.1 Local Treatment
Page 515
2. ARTHRITIS (JOINT DISEASES)
1.Osteoarthritis 1.1. Clinical Features

It is degenerative disease of joint which commonly Pain.
involves Knee, Hip and Ankle joint. Swelling.
Restricted range of movements.
Primary Osteoarthritis is degenerative process
without any precipitating factors.
Secondary Osteoarthritis is mostly due to
1.2. Investigations
X-ray ofinvolvedjoint.
Trauma,Infection and avascular necrosis.
Fig .1 X-ray Showing Severe Osteoarthritis Changes
1.3 Treatment 1.3.2 Physiotherapy
1.3.1 NSAIDS 1.3.3 Local Hydrocortisone acetate Injection 40mg

Intra articular once. Dosage can be repeated
1. Tab.Diclofenac sodium 50mg Thrice a day for 1
after 2-3 months as and when needed (under
week and SOS later Or
aseptic precautions.)
2. Tab.Indomethacin 25mg thrice a day for 1 week
and SOS later Or
3. Tab.Ibubrufen 400mg Thrice a day for 1 week 1.3.4 Surgery ( joint replacement )
and SOS Later
NSAIDs cause hyperacidity hence antacids such
as Cap. Omeprazole 20mg or Tab.Pantoprazole 2. AnkylosingSpondylitis
40mg once a day should be give n.
Local application of Diclofenac sodium Gel 4-5 Chronic progressive inflammatory disease of
times per day. sacroiliac joints and the axial skeleton, having
insidious onset affecting young patients age less than
40 years.
Page 516
2.1. Clinical Features 2.5. Treatment:
Backache. 2.5.1. Conservative Manage ment
Restricted movements of spine and hip.
Rest.
Morning stiffness, improvement with exercise,
NSAIDS.
persistence for more than 3 months. 1. Tab.Diclofenac sodium 50mg Thrice a day for 1
2. Tab.Indomethacin 25mg thrice a day for 1 week
2.2. Extra Articular Manifestations and SOS later Or
3. Tab.Ibubrufen 400mg Thrice a day for 1 week
Acute iritis.
and SOS Later
Pericarditis. NSAIDs cause hyperacidity hence antacids such as
Aortic incompetance. Cap. Omeprazole 20mg or Tab.Pantoprazole 40mg
Subluxation of atlanto-axial joints. once a da y should be given.
Physiotherapy / back exercise.
2.3. Investigations Occupational therapy.
General preventive measures like genetic
Haemogram. counseling.
HLA B27.
2.5.2 Surgical Treatment:
X-ray, Pelvis and Spine.
Spinal Osteotomy.
Total Hip replacement.
2.4. Diagnostic Criteria Total Knee replacement.
HLA B27 positive and X-ray picture showing
bamboo spine and ankylosed SI and hip joints. Recent trends:
Tumor necrosis factor antagonist (Etanercept) is
being us
Fig 1: X- ray Showing Bamboo Spine InAnkylosing Spondylitis

Page 517

3. CONGENITAL DISORDERS
1. Congenital Torticollis
(Wryneck): 2.2. Various splints include
Von Rosen splint.
Usually due to contracted sternocleidomastoid
muscle. Pavlik harness.
Head tilted towards and chin rotated away from Triple diapers.
affected side. Craig splint.
A firm swelling at junction of mid and distal 3rd
of the muscle may be felt.
Associated with congenital anomalies in cervical
2.3. Treatment
spine. 2.3.1 Age 1 - 3 Years
Treatment includes stretching exercises, if
Initially closed reduction is tried. If it doesnt give
deformity persists for 2 yrs surgical correction
the needed result then surgical correction is opted for.
lengthening of sternocleidomastoid muscle.
Surgery is planned after a period of traction. If the
Early identification and immediate child is more than 18 months only surgical
implementation of treatment gives good results.
procedures can help.
Earlier the treatment, better are the results.
The methods are

2. CDH: Removal of the interposed soft tissue from the
Congenital Dislocation of Hip. If displacement of joint.
femoral head from its normal position within the Innominate osteotomy.
aceTab.ulum is found at birth. It is regarded as CDH Femoral osteotomy.
or Developmental Dysplasia of the Hip (DDH).
2.3.2 More than 3 Years
Preliminary traction followed by open reduction.
2.1. Clinical Features: The methods are
More common in females. Removal of limbus.
Asymmetric groin folds. Salter innominate osteotomy.
Shortening of limb. Pemberton pericapsular osteotomy of ilium.
Ortoloni and Barlow tests - Performed to test the Rotation osteotomy of femur.
vulnerability of the Hip to dislocate and relocate
within the aceTab.ulum. 2.4. Complications:
Telescopy test - Performed with Hip and Knee Avascular necrosis of femoral head.
flexed in 90 degree and axial force applied to the
Neglected cases develop painful insTab.ility of
thigh and the greater trochanter movements in
hip and degenerative arthritis in later life.
relation to the ASIS (Anterior Superior Iliac
Persistent dislocations presenting in adulthood
Spine) are seen.
with OA can be treated with total hip
X-ray shows broken shentons line.
replacement arthroplasty.
Head lying outside the aceTab.ulum.
Dysplastic aceTab.ulum / femur. Congenital Clubfoot
Early identification and immediate
implementation of treatment gives good results
3. Congenital
good p hysical examination. TalipesEquinoVarus
- Plane Radiography.
- Ultrasonography. (CTEV)
Page 518
3.1. Etiology: Foot is twisted and turned inwards so that it
Unknown but mostly attributed to mechanical causes. faces posteromedially.
Germ plasm defect and primary soft tissue Foot is plantarflexed, inverted and adducted at
abnormalities. forefoot. The leg muscles are smaller and heel
cord is tight and associated internal tibial torsion
Features are usually obvious at birth.
may be present.
Fig 1 Clinical Appearance of Bilateral Idiopathic CTEV before Treatment
3.2. Treatment: Talonavicular reduction and maintenance.

3.2.1 Conservative
Aim of treatment is to produce and maintain a Methods
painless supple plantigrade foot. Preferably should be Turco.
started within a day or two after birth. Manipulative Carroll.
correction and maintenance in cast. External fixator correction.
JESS: Less than 7 years.
Methods Ilizarov: More than 7 years upto 12 years.
French b) Bone procedures
Ponseti method produces best results which Done in case of deformity that has persisted for
comprises correction of deformity in order of more than 3 yrs.
CAVE (Cavus,Adduction,Varus&Equinus) with In addition to posteromedial release lateral
serial castings followed by column shortening and / or medial column
tendoa chillestenotomy and retention of lengthening procedures can be done.
correction in steinbeik shoes till walking age. Late / relapsed cases.
3.2.2 Surgical correction Options

Should be opted for in cases that have failed Soft tissue and bone procedures with tendon
conservative line of management. transfers, gradual correction using Ilizarov
method.
a) Soft tissue procedure Neglected cases can be treated by triple
Closed Tendo Achilles Tenotomy. arthrodesis.
Lengthening of medial and posterior structures.
Page 519

4. METABOLIC DISORDERS
1. Osteoporosis Complaints of back pain.
Increased thoracic kyphosis.
Osteoporosis is defined as abnormally porous bone
Treatment:
and its strength is less than normal for a person of
that age and sex. Physiotherapy.
Bisphosphonate
1.1. Clinical features: Alendronate 70mg once weekly give n with full
Bone pain. glass of water before breakfast (in severe cases)
for 3 months.
Fractures. Vitamin D 1000IU/ day for 3 months.
Kyphosis. Calcium - both diet and drug
Tab. Calcium carbonate 500mg twice a day for
Weakness. 2-3 months. Can be extended later
Hormone replacement therapy in selected cases.
Fatigue.
Calcitonin Nasal spray (200IU/day) once a week for
1.2. Investigations: 3 months minimum, Inj.ecTab.le calcitonin, limited
use.
X-rays.
Special investigations (if needed) includes. If and when combination of Calcium and
DEXA Scan. Vitamin D is available it should be used.
1.3. Diagnosis: 1.5. Secondary osteoporosis

SD > 2.5 below the average for premenopausal Nutritional.
women for that pop ulation group. Endoc rine.
Drug induced.
X-ray features:
Malignant disease.
Loss of trabecular definitions. Ide ntify the cause and treat it accordingly.
Thinning of cortices. Correct the nutritional deficiency.
Correction of hormonal imbalance.
1.4. Primary osteoporosis:
Physiological bone depletion that normally 1.6. Surgerys
accompanies ageing and loss of gonadal activity.
Vertebroplasty&Kyphoplasty in presence of
neurode ficit.
Post menopausal osteoporosis
Ions
Page 520
5. REGIONAL CONDITIONS
Destruction of lateral condyle due to sepsis.
1. PeriArthritis Shoulder Tardy-ulnar nerve palsy may be present - treated
with anterior transpos ition of ulnar nerve.
(Frozen Shoulder) Gross deformity supracondylar osteotomy.
Significant restriction of both active and passive
shoulder motion. 3. CubitusVarus
1.1. Clinical Features: Inward deviation of forearm at elbow.
Most common cause is malunion of
Night pain, inability to reach overhead and reach supracondylar fracture.
away from the body. Change in arc of motion with hyper extension
and restricted flexion.
1.2. Investigations: Deformity needs supracondylar osteotomy.
X-ray.
Blood - rule out meTab.olic causes. 4. Dequervain's Disease
Ultrasound (Dynamic ultra sound).
Chronic constrictive tenosynovitis of abductor
MRI (Thickness of the capsule and pollicislongus and extensor pollicisbrevis.
synovium>4mm) to rule out other pathology.
1.3. Treatment: 4.1. Clinical features:

Diffuse pain at distal end of radius laterally,
Supportive - Diathermy, Ultrasound, TENS. tenderness and painful movements of thumb.
Medications
1) Tab..Diclofenac sodium 50mg thrice a day for 1 Finkelstein's test positive.
2) Tab.. Indomethacin 25mg thrice a day for 1 week 4.2. Treatment:
and SOS later Or Early - splint wrist and thumb in full extension.
3) Tab..Ibubrufen 400mg thrice a day for 1 week
Anti inflammatory drugs.
and SOS Later 1) Tab..Diclofenac sodium 50mg thrice a day for 1
NSAIDs cause hyperacidity hence antacids such week and SOS later Or
as Cap. Omeprazole 20mg or Tab.. Pantoprazole 2) Tab. Indomethacin 25mg thrice a day for 1 week
40mg once a day should be give n. and SOS later Or
Intra- articular steroids. Inj.Hydrocortisone 3) Tab.Ibubrufen 400mg thrice a day for 1 week
acetate 40mg once every 3 months. and SOS Later .
Physiotherapy -Streching exercises. NSAIDs cause hyperacidity hence antacids such as
Manipulation under general anaesthesia (if Cap Omeprazole 20 mg or Tab. Pantoprazole 40 mg
symptomatic > 6 months). once a da y should be given.
Surgical Release (If not response to above
treatment). Local administration of Inj.. Hydrocortisone
Open or Arthroscopic release at specialized 40mg once every 3 months.
centres. Later soft - tissue release can be done.
2. CubitusValgus 5. Carpel Tunnel Syndrome

Outward deviation of forearm at elbow.
Normal carrying angle is 100 in male and 150 in Most commonly found in IT professionals and
females. students.Median nerve is involved.
Causes.
Nonunion fracture of lateral condyle of humerus. 5.1 Clinical features:
Page 521
It is caused by entrapment of medial nerve in carpel
tunnel. Also seen in malunited lower end radius
fractures and in pregnant women. 7.2 Treatment:
Tinels sign It is reproduction of tingling sensation 7.2.1 Medical treatment
in palm and wrist by tapping over the course of 1) Tab..Diclofenac sodium 50mg thrice a day for 1
nerve. week and SOS later Or
2) Tab.. Indomethacin 25mg thrice a day for 1 week
and SOS later Or
5.2Treatment: 3) Tab.. Ibuprofen 400mg thrice a day for 1 week
5.2.1 Conservative and SOS Later
NSAIDs NSAIDs cause hyperacidity hence antacids such
1) Tab..Diclofenac sodium 50mg thrice a day for 1 as Cap. Omeprazole 20mg or Tab. Pantoprazole
week and SOS later Or 40mg once a day should be give n.
2) Tab.. Indomethacin 25mg thrice a day for 1 week
Local Steroids. Inj. Hydrocortisone acetate
and SOS later Or 40mg once every 3 months.
3) Tab..Ibubrufen 400mg thrice a day for 1 week 7.2.2Surgical release
and SOS Later.
NSAIDs cause hyperacidity hence antacids such as 8
Cap. Omeprazole 20mg or Tab. Pantoprazole 40mg 8. Avascular Necrosis of
once a da y should be given.
Or Femoral Head
5.2.2SurgicalRelease Death of bone due to gradual vascular impairment or
sudden infarction. Clinically there is pain in groin,
6. Tennis Elbow radiates to thigh and knee, local tenderness, limitation
of movements, loss of abduction and internal
6.1 Lateral epicondylitis due to repetitive stress rotation, preserved flexion.
Injury Commonly seen in housewifes and
players:
8.1. Radiological Features(X-rays):
6.2 Treatment: Stage1- Pre radiologic stage no radiologic
6.2.1 Medical treatment findi ngs.
1) Tab..Diclofenac sodium 50mg thrice a day for 1 Stage 2- Osteoporosis, sclerotic cystic areas.
week and SOS later Or Stage 3- Partial collapse, Flattening of femur
2) Tab.. Indomethacin 25mg thrice a day for 1 week head,Increased density and deformity of head.
and SOS later Or Stage 4 -Secondary deterioration of the articular
3) Tab..Ibubrufen 400mg thrice a day for 1 week cartilage.
and SOS Later.
NSAIDs cause hyperacidity hence antacids such as 8.2. Other Investigations
Cap. Omeprazole 20mg or Tab.. Pantoprazole 40mg
Radio-isotope scanning.
once a da y should be given .
MRI most sensitive to detect ischemic
necrosis.
Local Steroids. Inj.. Hydrocortisone acetate
Bone-marrow pressure measurements.
40mg once every 3 months.
Supportive splints . Intramedullary ve nography.
6.2.2 Surgical release Core biopsy of femur head.
8.3. Treatment
7. Golfers Elbow Early - Bedrest, traction, weight reduction,
withdrawal of steroid and alcohol.
7.1 Medial epicondylitis which is due to repetitive Stage 2 - Core decompression of head, muscle
stress Inj.ury commonly seen in housewifes pedicle bone grafting.
and players : Stages 3, 4 - Osteotomy and replacement
arthroplasty.
Page 522
Knee
Plantar Fasciitis
Figure 1 Bilateral Grade 4 Avascular Necrosis Of Femur Head
Tab.Diclofenac sodium 50mg thrice a day

9. Plantar Fasciitis / Calcaneal for 1 week and SOS later Or
Spur Tab. Indomethacin 25mg thrice a day for 1
Tab. Ibuprofen 400mg thrice a day for 1
9.1. Clinical Features: week and SOS Later.
Pain bot h heels. NSAIDs cause hyperacidity hence antacids
Unable to bear weight. such as Cap. Omeprazole 20mg or Tab.
Tenderness over medial tuberosity of calcaneum Pantoprazole 40mg once a da y should be
X-ray - lateral view of calcaneum may show given.
spur.
9.2.3 Local Steroids
Investigation X-ray calcaneum lateral view to rule
Inj. Hydrocortisone acetate 40mg once
out spurBlood sugar to rule out diabetes. every 3 months.
Surgical release.
9.2. Treatment:
9.2.1 Soft sole pad in the heel 9.2.4 Ultrasound therapy
9.2.2 Medical
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6.DISORDERS OF SPINE
s
If you see any of the red flags refer urgently to higher
1. Lumbar Spondylosis center with surgical facility.
1.1 Clinical Features: 2. Cervical Spondylosis
Low back ache is a very common problem faced in
day to day life. Not all of them, are caused by disc 2.1 It is a degenerative condition of the cervical
pathology. Clinical features suggestive of disc spine occurring over 50 yrs of age. Involves
pathology include backache associated with para the intervertebral discs, posterior intervertebral
spinal spasm, stretch pain and leg pain. joints. Commonest at C5 - C6.
1.2 Investigation: 2.2. Clinical Features:

X-rays lumbosacral spine AP. Pain and s tiffness.
Radiating pain to shoulder or downwards on the
1.3 Treatment: outer aspect of the forearm and hand.
Rest. Giddiness on and off.
Medical management. On examination there is loss of normal cervical
1) Tab.Diclofenac sodium 50mg thrice a day lordosis and limitation in neck movements.
for 1 week and SOS later Or Tenderness over the lower cervical spine or in
2) Tab. Indomethacin 25mg thrice a day for 1 the muscles of the paravertebral region.
3) Tab. Ibuprofen 400mg thrice a day for 1 2.3. Investigations:
week and SOS Later. X-ray cervical spine AP and Lateral.
as Cap. Omeprazole 20mg or Tab. Pantoprazole 2.4. Treatment:
40mg once a day should be give n. Rest.
Local Application of Muscle relaxant gel such as Medical management.
diclofenac sodium gel. 1)Tab.Diclofenac sodium 50mg thrice a day for
Education about proper back posture 1 week and SOS later Or
maintenance of lumbar lardosis with erect 2) Tab. Indomethacin 25mg thrice a day for 1
posture or lumbar pillow. week and SOS later Or
Physiotherapy interferential therapy, traction 3) Tab. Ibuprofen 400mg thrice a day for 1 week
Epidural steroid Injections. and SOS Later.
1.4. Operative Indications: as Cap. Omeprazole 20mg or Tab. Pantoprazole
40mg once a day should be given Local
CaudaEquina syndrome - especially with bowel Application of Muscle relaxant gel such as
and bladder involvement.
diclofenac sodium gel.
Patients with persistent pain not relieved by
Education about proper Neck Posture.
conservative measures for 6 - 8 weeks.
Physiotherapy,interferentialtherapy,Cervical
Unilateral leg pain extending below knee that has traction.
lasted atleast 6 weeks.
Discectomy is performed usually by posterior
approach and patients will have good
3. Kyphosis
postOperative pain relief. Is a posterior curvature of the spine.
1.5. Watch For Red Flags Signs: Types

Bowel-bladder involvement. a. Smooth rounded kyphosis.
Hypos thesia around a nus. Scheuermanns disease.
b. Angular kyphosis.
Tuberculosis spine.
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Traumatic.
4. Scoliosis 4.3. Investigations:

4.1. Definition: Radiography of the whole spine.
Degree of the curve is measured by the Cobbs
Scoliosis is defined as lateral curvature of the spine. angle.
Scoliosis is named according to the level and side to Skeletal maturity by the fusion of the iliac
which the main conve xity of the curve is directed. apophysis (Rissers sign) is an indicator of end
The common patterns are. of growth of spine.
a. Thoracic scoliosis.
b. Thoraco-lumbar.
4.4. Treatment:
c. Cervico-thoracic scoliosis (depending upon the Mild cases Conservative with serial custom
site of primary curve). made braces.
Moderate cases - Spinal and breathing exercise
4.2. Clinical Features: with correction by Milwaukee Brace.
Rib hump, prominence of posterior chest wall. Test Severe cases - Cobbs angle > 40 deg. Surgical
done to decide whether deformity is mobile or rigid. correction with instrumentation and Fusion
Make the patient lie in the lateral position on the carried out with cancellous bone graft.
concave side. Curvature is diminished in mobile
cases.
Fig.1 Scoliosis OfDorso - Lumbar Spine
Page 525
7.GENERAL FRACTURE MANAGEMENT
Routine X-ray AP and Lateral view.
1. Definition Special views if necessary.
Disruptions of bone tissue are called fracture, visible
disruption of articular cartilage is also called
fracture(Chondral fracture). 6. Management includes
2. Types of fractures Conservative management for closed fracture
and Type I - open fracture for which closed
Closed fracture and open fracture. manual reduction tried and patient put on
Incomplete fracture or greenstick fracture and appropriate plaster of paris splint for 3 - 4 weeks.
complete fracture. Surgical management.
Linear fractures - transverse, Oblique.
Spiral, Comminuted (more than two fragments).
Segmental fracture, fracture with bone loss and 6.1. Initial management of open
Impacted fracture. Injuries:
Stress fracture.
Pathological fracture. Record vitals, start lifeline, I.V. fluids, I.V.
antibiotics, analgesics.
3. Gustilo-Anderson Immediately debride the wound of contaminated
wound, devitalized tissue look for4 Cs,
classification of open Consistency, Colour, Contractility, Circulation.
fracture Irrigate copiously with saline Type I 3 L
saline, Type II 6 L saline, Type III 9 L saline.
Type I Open fracture with wound < 1c m Bone is Enlarge the wound if necessary for adequate
not exposed. debridement.
Type II Wound > 1cm without extensive soft Remove contamination in the medullary canal.
tissue da mage / skin flaps avulsion. If wound can be closed, suture the surgically
Type III A Ope n fracture with extensive soft created wound, put loose stitch for other wounds
tissue damage, but with adequate soft tissue over a drain if necessary. If closure is not
coverage of bone. It also includes segmental possible, leave the wound open.
fracture, comminuted fracture with laceration <
1cm. 7. Complications
Type III B Extensive soft tissue loss with
periosteal stripping with bony exposure. 7.1 Acute:
Type III C Open fracture with an arterial Injury Shoc k.
that require immediate repair regardless of size ARDS.
of the wound. Thrombo-embolism.
Neuro-vascular Injuries.
4. Clinical features Crush syndrome.
Pain. DVT.
Swelling. 7.2 Chronic:
Inability to use the affected limb. Delayed union, Non-union, Malunion.
Deformity. Growth disturba nces.
Crepitus. Joint stiffness.
Abnormal mobility. Volkmanns ischemic contracture.
Loss of transmitted movement. Myositis ossificans.
Post-traumatic arthritis.
5. Investigations Avascular necrosis.
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7.3 Peculiar to open fractures are: osteotomy with internal or external fixation with or
without bone grafting.
Infection.
Tetanus.
Gas gangrene.
Osteomyelitis. 13. Joint stiffness
Hypovolemic shock.
Due to inappropriate fracture immobilization,
intraarticular fractures, periarticular adhesion of soft
8. Crush Syndrome tissues, capsules and muscle contractures.
Severe crush Injury of limbs and muscles results in
release of myoglobin leading to renal failure. 13.1 Treatment:
Treatment is managing acute renal failure and Physiotherapy.
Maintain hydration.
Exercises.
Manipulation under anesthesia.
9. Compartment Syndrome Surgical excision and lengthening of
It is due to ischaemic necrosis of structures of contractures.
anterior compartment of fore-arm / legs.
It is defined by the following signs (6 Ps).
a. Pain. 14. Myositis Ossificans
b. Pallor. It is a reactive lesion (ossification) occurring in
c. Paraesthesia. soft tissues and in stripped periosteum followed
d. Paralysis. by trauma and ill advised massage.
e. Pulselessness.
f. Positive Passive stretch. 14.1 Treatment:
Treatment.
a. Emergency surgical decompression by Drugs:
fasciotomy. Low dose Indomethacin (25mg TDS) for 1
month.
Mobilization and ROM excision till painfree
10. Delayed union joint range.
Union is considered delayed, when healing has not
advanced at the average rate for the location and the 15. Fractures of Necessity
type of fracture, usually 3 - 6 months. Conservative For these fracture, surgery is always necessary.
management with functional cast for addi tional 4 - 12
weeks or ORIF with appropriate implant with or Lateral humeral condyle fracture.
without bone grafting. Femoral neck fracture.
Distal tibial epiphysisfracture.
11. Non-union
16. PhysealInjuries
A diagnosis of Non-union is justified either by
clinical or X-ray findings which show healing has Salter and Harris classification of PhysealInjuries.
ceased, minimum of 9 months elapsed since Injury
Type I Epiphyseal separation through
and the fracture shows no vi sible progressive signs of
physis only with or without displacement.
union for 3 months.
TypeII Triangular metaphyseal spike
Time period attached to separated epiphysis. (Thurston
Holland sign.)
Fracture of long bone - 6 to 9 months.
TypeIII Physeal separation with fracture
Fracture of neck of femur 3 months. through the epiphysis into the joint. If there is
displacement joint incongruity occurs.
12. Malunion TypeIV Fracture through the metaphysis,
A malunited fracture is one that has healed with the physis,epiphysis.
fragments in a non - anatomical position. Corrective TypeVCompression fracture of the physis
producing growth arrest, diagnosed
retrospectively.
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TypeVIBruise or contusion to the periphery of
the physis producing growth disturbances.
I II III IV V
Epiphyseal Fracture through Fracture through Fracture of Epiphyseal damage to the
slip on ly Epiphyseal plate with theEpiphyseal and shaft, crossing Epiphyseal plate
triangle of sheft extending into theEpiphyseal
attached Epiphyseal plate plate
Fig 1: Epiphyseal Injuries
16.1 Management: Details of splinting and transport of trauma patient

are mentioned in treatment of individual fractures.
Majority of childrens fracture are treated
conservatively. Few fractures require open reduction 2. PreparationOf Cast/Slab
and internal fixation or closed pinning. Application:
17. Open fractures In Children It is essential to prepare the patient and all necessary
material and equipment before beginning the
Frequent and vigorous debridement with irrigation processes of fracture reduction and cast application.
and adequate stabilization of fracture will reduce the
rate of non-union and secondary infection. Rarely Required materials.
after closed reduction hematogenous osteomyelitis Examination couch or Table
occurs at the fracture site.
2-4 rolls 150 mm padding.
18. SplintageAnd Transport of 8-9 plaster of Paris (POP) rolls, 150 mm wide.
Trauma Patient Bucket with cool water.
1. Guidelines: Pillows to support casted leg.
1) Immobilize one joint above and below. Aprons to protect team members and patient.
2) Usage of readily available materials such as
umbrella, plaster of paris, folded paper, wooden Paper to cover the floor.
stick.
3) Splintage should neither be too tight or too loose. Everything must be assembled and ready before
4) Do Not transfer patient unless his vitals are beginning the procedure.
stabilized.
Page 528
Fig 2: Materials ForApplying Slab/Cast
3. Method: applied over dorsal or ventral surface with cotton

padding and bandage.
Slab is prepared by overlaying of plaster of parisrolls
of adequate length and layers to splint the fracture Cast is cylindrical application of plaster of paris rolls
along with adjacent joints in anatomical position and over adequate cotton padding over the fractured limb
in anatomical position.
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8.POLYTRAUMA
1. PolytraumaIs Defined As 2.4 Golden Hour:

Injury severity score (ISS) 16 or above. First one hour after Injury, with threefold increase in
Systolic blood pressure below 80 mm Hg. mortality for every 30 minutes.
Glasgow coma score less than 15.
Higher fluid resuscitation requirements. 3. Follows ABCDE
Chest, head, abdominal organ Injuries. Airway.
Fractures of more than one long bone. Breathing.
Circulation.
2. Stage of Care Disability.
Expos ure.
2.1 Acute Resuscitation Period:
(1-3 hrs) 4. Initial Management of
From the first point of contact with medical
service to the control of acute life threatening
patient In Shock
conditions. Direct control of obvious bleeding by direct
Rapid systemic assessment to identify life pressure - (preferable), tourniquet clamping of
threatening conditions. blood vessels.
Then Airway, Breathing, Circulatory (ABC) Large-bore intravenous access.
support should be made. This involves airway a. Ringer lactate infusion.
control, thoraco-centesis, rapid control of b. Blood replacement as indicated, by serial
external bleedings, vigorous fluid and blood haematocrit estimation and blood pressure.
replacement therapy. Traction with Thomas Splints or extremity
Then complete diagnostic check up if there is no splints to limit hemorrhage from unstable
acute life threatening situation. fractures
2.2 Primary Stabilization Period: Consideration of angiography or immediate
operative intervention for Hemorrhage control.
(upto 48 hrs)
From the control of acute life threatening 4.1HaemorrhagicShock:
situation and complete Stability of respiratory,
haemodynamic and neurologic symptoms. Diagnosed by hypotension, tachycardia, seen in
Here acute management of fractures associated patients with large open wounds, active bleeding,
with arterial Injuries and acute compartment pelvic and / femoral fractures and abdominal or
syndrome are managed. thoracic trauma.
Fractures are temporarily Stabilized with In the absence of open hemorrhage bleeding into
external fixators and compartments. voluminous space (chest, abdomen, pelvis, thigh)
must be ruled out.
2.3 Secondary Regeneration Period: This may require peritoneal lavage, angiography,
(2 - 10 days) CT, MRI.
In this, general condition of the patient is Managed by aggressive fluid replacement, blood
Stabilized and monitored. transfusion, Angiographic embol isation,
Systemic inflammation and multiple organ operative intervention, fracture Stabilization, etc.
dysfunction syndrome are managed.
Tertiary reconstruction and rehabilitation period 4.2 Blood Replacement:
(weeks to months) after trauma. Fully cross matched blood is preferable.
Necessary surgical procedures. In case of life threatening situations O-
Definitive treatment of complete mid-phase negative blood can be used.
fractures. Warming of blood prior to administrations
Specialized procedures to achieve fracture prevents hypothermia.
correction or joint reconstruction.
Page 530
Monitor coagulation factors, platelets and d. Rectal tone and sensation.
calcium levels. GCS = Eye opening score + Verbal (intubated or
non-intubated) score + Motor score.
GCS if < 13, systolic BP < 90, RR< 10 / min or
5. Indications For Immediate > 30 / min warrants Emergency trauma care.
Surgery
Hemorrhages secondary to liver, splenic renal 6. Radiographic Evalution
parenchymal Injury Laporatomy.
X-rays of Skull, pelvis, spine and Extremities.
Aortic, caval or pulmonary vessel tears Ultra sound abdomen.
Thoracotomy.
CT, MRI.
Depressed skull fracture or acute intracranial
hemorrhage Craniotomy. Assess the concomitantInjuries such as head Injuries,
Disablity (Neurologic Assessment). thoracic Injuries, genitourinaryInjuries and refer the
a. Assess level of consciousness by GCS. patient to higher centers for tertiary care
b. Pupillary response sensation. management.
c. Motor response in all extremities.
Pelvic Fracture
Page 531
9.PELVIC INJURIES
If it is < 2.5 cm treat conservatively.
1. Introduction If it is > 2.5 cm external fixation or open
It is an emergency in orthopa edics which reduction and internal fixation.
involves multispeciality intervention. If there is unstable Fracture with vertical
Mode of Injury. displacement then treat with ORIF.
a. High energy Injuries. If haemodynamicallyunstable, then stabilize the
b. Crush Injuries. pelvis with external fixator at the casualty itself
c. Impact Injuries. without shifting the patient and follow the above
Associated with complications and other steps.
fractures.
4. Associated Complications
2. Clinical Features AndTreatment
Shoc k-blood transfusion and fluid replacement.
Pain and tenderness at affected site.
Embolisation of bleeding pelvic vessels.
Range of movements painful. (intervention radiology)
Shoc k. Urethral ruputure - diagnosed by blood in
Intra-abdominal / Urethral / Vascular Injuries. urethra, perineal hematoma, distended bladder,
managed by Urologist.
Bladder rupture-extravastation of urine-Urologist
3. Management and Surgeon.
Evaluate ABCDE and stabilize the patient. Bowel and intra-abdominal Injuries are managed
Evaluate for other associated Injuries head, by General surgeon.
chest, abdomen and spine. Thrombosis - DVT prophylaxis, vascular opinion
If haemodynamicallystable, assess radiologically must be obtained.
with X-ray pelvis AP view, inlet and outlet view. Post operatative-
If there is no or minimal displacement, treat a. Infection rate (0-25%) managed accordingly.
conservatively with strict bed rest and analgesics. b. Thrombo-embolism.
If there is displacement with anterior opening c. Pin tract infection.
type (unstable Fracture) then assess the d. Death inevitable in certain situations.
displacement.

Page 532
10. FRACTURES OF UPPER LIMB
Bennetts Fracture.
1. Mode of Injury
Intra-articular fracture through base of first
a. Fall on Outstretch hand.
metacarpal bone in which the fractured shaft is
b. Road Traffic Accident.
displaced laterally due to unapposed pull of APL.
c. Associated Poly Trauma.
(Abductor PollicisLongus)
2. Type of Fracture a) Investigation
X- ray of hand antero posterior and oblique
2.1. Fracture of Hand: views.
a. Fracture of the base of the first metacarpal.
b) Treatment
b. Fractures of the other metacarpal bones.
c. Fractures of the phalanges. Primary Stabilization in anatomical position with
the help of available splinting material.
Closed or open reduction and internal Fixation
2.2. Fractures Around Wrist: with 'K' wire.
a. Fracture of the scaphoid bone.
b. Fractures of other carpal bones. c) Rolando Fracture
c. Dislocations of the carpal bones. It is a common extra articular fracture of base of first
d. Fracture of the lower end of the radius .(Colles' metacarpal bone.
and Smith's) d) Investigation- X-ray of hand antero posterior,
e. Galeazzi fracture dislocation. lateral and oblique views.
f. Fracture separation of the lower radial e) Treatment
epiphysis. Primary stabilization in anatomical position with
g. Fracture of the shafts of the forearm bones. the help of available splinting material.
Closed or open reduction and internal Fixation
with 'K' wire ORIF by K wire.
2.3. Fractures Around Elbow: External fixation.
a. Fracture of the head and neck of the radius.
Mini fragment T plate fixation.
b. Fracture of the uppe r end of the ulna with
dislocation of the head of the radius.(Monteggia 2.5.2 Fracture of The Other Metacarpal Bones
fracture dislocation)
a) Investigation -X-ray of hand antero posterior and
c. Fracture of the coronoid process.
oblique views .
d. Fracture of the olecranon process.
e. Fractures of the epicondyles and condyles. b) Treatment
f. Supracondylar fracture. Primary stabilization in anatomical position with
Conservative - cock up splint.
2.4. Fracture OfThe Humerus:
a. Fracture of the shaft. Surgical Close or open reduction and internal
fixation with K wire or mini plate.
b. Fracture of the greater tuberosity.
c. Common Fracture of Proximal Humerus/ External fixation for compound (open) fracture.
Fracture of greater tuberosity.
2.1.3Fracturesof the phalange s
2.5. Fractures OfThe Shoulder a) Symptoms - Pain & Swelling and bo ny

Girdle deformity with loss of active movements.
a. Fractures of the clavicle. b) Signs - Tenderness at Fracture sitealong
b. Fractures of the Scapula. with Crepitus and Abnor mal Mobility.
c) Investigation - X- ray of hand AP and
2.5.1 Fractures of Hand Oblique views.
Fractures of base of the first metacarpal.
Page 533
d) Treatment- Conservative - Buddy strapping, POP slab,
Primary stabilization in anatomical position with finger splints.
Fig 1: Finger Splint
e) Surgical K (Kirschner) wire or JESS 2.2.3 Dislocations of the carpal bones

(Joshi's External stabilization System) Complete dislocation of the wrist is very uncommon
fixator. and incomplete carpal dislocation involve one or
more of the carpal bones and are as follows:
1) Dislocation of lunate bone .
2.2. Fractures Around Wrist: 2) Perilunar dislocation of the carpus.
2.2.1 Fracture of the scaphoid bone A. Symptoms Pain, swelling, defor mity and
restriction of move ment of the wrist joint.
It is common in young adults usually caused due to
fall on outstretch hand, often overlooked. B. Signs Tenderness and loss of anatomical
a) Symptoms Pain, swelling and restriction of position of wrist and hand.
wrist move ment.
b) Signs Tenderness in anatomical snuff box and C. Investigations
impairment of wrist move ment. X-ray of the wrist in AP, lateral and oblique
c) Investigations - X-ray of wrist in AP, lateral and views.
two oblique projections. CT Scan.
d) Treatment - Primary stabilization in anatomical
(glass holding) position with the help of D. Treatment
available splinting material. Primary stabilization in anatomical (glass
Conservative - Plaster immobilization usually holding) position with the help of available
till 2 to 3 months. splinting material.
Surgical Closed or open reduction and internal Conservative Manipulative reduction under
fixation with a special compression screw. anaesthesia and plaster immobilization.
e) Complications: Surgical operative replacement of carpal bones.
The incidence of complications is high.
Delayed or non-union. E. Complications
Avascular necrosis. Avascular necrosis.
Osteoarthritis. Osteoarthritis.
Injury to median nerve.
2.2.2 Fractures of other carpal bones
These are less common serious fractures. The 2.2.4 Fracture of the lower end of the radius:
treatment is conservative management with plaster
immobilization. A.Colles' fracture - It is a fracture of the lower end
Page 534
of radius at metaphyseal region which manifests in C.Investigation - X- ray forearm with elbow and
bent fork deformity due to dorsal and radial wrist in AP and lateral projection.
displacement of the distal fragment. D.Treatment
Primary stabilization in anatomical position by
B. Smith's fracture It is reverse of the Colles' appl ying gentle axial traction and splinting with
fracture with ventral displacement. the help of available material. (moulded splints,
folded newspaper, card board or wooden plank)
C. Symptoms - Pain, swelling and bo ny de for mity of Surgical - Mostly needed for prevention of
the wrist with loss of active movements malunion.
- Open reduction and i nternal fixation with plate
D.Signs - Tenderness at fracture site along with or and screws.
without crepitus and abnormal mobility
2.2.6 Fracture separation of the lower radial
E.Investigation - epiphysis:
X-ray of forearm with wrist AP and Oblique It is seen in children before physeal fusion in which
views. the epiphysis is fractured and separated from the
X-ray Wrist in Ulnar deviation. metaphysis and results into gross defor mity, if not
treated adequately.The clinical features and
F.Treatment management are same as that of fracture of lower end
Primary stabilization in anatomical (glass of radius in adults except surgical intervention which
holding) position with the help of available is rarely needed.
splinting material.
Close reduction and plaster immobilization. 2.2.7 Fracture of the shafts of the forearm bones:
Close reduction with K wire fixation. The forearm bones, radius and ulna get fractured
Close reduction with K. wire fixation and either single or both and are very common Injuries
external distractor application. which result into gross defor mity and functional
Open reduction and internal fixation with restriction, if not treated.
multiple K wires, plate and screws.
A. Symptoms Pain, swelling over forearm and
2.2.5 Galeazzi fracture dislocation bony deformity.
B. Signs - Tenderness, crepitus, abnormal mobility
It is the fracture of radial diaphysis at the junction of with or without signs of compartment syndrome.
middle and distal third of the shaft with associated C. Investigation - X-ray of the forearm with wrist
disruption of distal radio ulnar joint. and elbow in AP and lateral projections.
A.Symptoms - Pain, swelling, de for mity and D. Treatment:
shortening of the forearm. 1. Primary stabilization in anatomical position by
appl ying gentle axial traction and splinting with
B.Signs - Bony deformity & tenderness, crepitus & the help of available material. (moulded splints,
pain aggravated by passive stretching of wrist. folded newspaper, card board or wooden plank)
2. Splintage.
Page 535
Fig 2:SplintageForFracture Radius /Ulna And Lower End OfHumerus
3. Conservative - Closed reduction and plaster Excision of radial head in severely damaged and
application under anaesthesia, mostly in children. displaced fractures.
4.Surgical 2.3.2Fracture of the uppe r end of the ulna with
dislocation of the head of the radius
Closed reduction and internal fixation with (Monteggia fracture dislocation)
elastic (in children) or rigid intramedullary nails.
This is uncommon Injury with characteristic
Open reduction and internal fixation with plates displacement the ulna is angled forwards and the
and screws. head of radius is dislocated forwards which is
obvi ously seen on clinical and X-ray examinations.
External fixator application in case of open Clinical features are same as the forearm fractures.
fractures.
Treatment
2.3. Fractures Around Elbow: Accurate fracture reduction is essential. It is
seldom possible to reduce both the dislocation
2.3.1Fracture of the head and neck and fracture by closed method.
of the radius: Open reduction and internal fixation with plate
One of the commonest fractures of the upper limb in and screws is essential.
young adults.
Symptoms : Pain and swelling on lateral aspect of 2.3.3 Fracture of the coronoid process:
elbow and restriction of movement.
Signs : Sharp local tenderness and impaired The coronoid process is seldom fractured unless in
move ments. ( Flexion of elbow and pronation and association with posterior dislocation of the elbow.
supination)
Investigations: X-ray of elbow joint with forearm 2.3.4 Fracture of the olecranon process:
in AP and lateral projections.
The olecranon process is fractured by a fall on the
Treatment: poi nt of the elbow usually in adults.
Clinical feature same as fractures above with distinct
1. Primary stabilization in anatomical position disruption of three point bony relation of the elbow.
(flexion at elbow and midprone position of (It is a triangle formed by the tip of olecranon and the
forearm). two epicondyles)
2. Conservative in case of slight damage to the The treatment depends upon the type of fracture i.e.
radial head and neck with plaster immobilization. plaster immobilization in case of crack fracture,
3. Surgical. internal fixation for fracture separation and excision
Open reduction and internal fixation in case of in case of comminuted fracture.
severe damage to the radial head and neck.
Page 536
2.3.5 Fractures of the condyles and epicondyles: three point bony relation maintained. The brachial
Condylar fractures are relatively uncommon, but and radial artery pulsations should be confirmed all
often troublesome and oc cur main in children. the time during the treatment.
A. Symptoms Pain, swelling and restriction of B. Treatment:

movement of the elbow. Conservative Closed reduction and plaster
immobilization.
B. Signs Surgical Open reduction and internal fixation,
Marked tenderness and widening of the elbow. if closed manipulation fails.
Disruption of the three point bony relation.
C. Complications:
C. Investigations - X-ray and CT Scan. Injury to the brachial artery leading to Volkmann's
D. Treatment ischaemic contracture in delayed or neglected cases.
Conservative - In case of simple crack fracture, Injury to median nerve.
with plaster immobilization and followed by a Malunion.
course of mobilizing exercises.
Surgical Displaced fractures must be treated 2.3.7 Inter Condylar Fracture Humerus
with closed or open reduction and internal A. Clinical features Pain, swelling and deformity.
fixation to prevent disability.
B. Investigation X-ray elbow, AP and lateral
E. Complications: views.
Non-union. C. Treatment
Deformity-Cubitus valgus with instability. Conservative plaster immobilization.
Osteoarthritis. Surgical - Closed or open reduction and internal
fixation with K wires or cancelloussrews.
Epicondylar fractures occur in children and mostly
treated conservatively.
2.4. Fracture of Humerus:
2.4.1 Fracture of the shaft
2.3.6 Supracondylar fracture:
A. Clinical Finding Pain and Swelling ove r arm
It is one of the commonest and most important
abnormal mobility, crepitus.
fractures of the childhood and potentially dangerous
B. Investigation X-ray of arm with shoulder &
because of the risk of Injury to the brachial artery
elbow AP and Lat.
near the metaphyseal region of the humerus.
C. Treatment
A. Clinical features-Are characteristic with lower
Splintage.
fragment displaced and tilted backwards, but the
Fig3: SplintageOfFracture OfHumerus
Page 537
Surgical Closed nailing by 2.4.3 Common Fracture of Proxi mal Hume rus/ Fracture
- Rush nail of greater tuberosity
- Enders nail Children A.Clinical Finding
- Flexible nail Pain and Swelling ove r Shoulder.
- Humerus Inter locking Nail. Painful Move ments of Shoulder.
- Open reduction and internal fixation with plate & Crepitus, Tenderness.
screws.
- External fixator. B. Investigation X-ray Shoulder AP &CT Scan.
Watch for wrist drop. (radial nerve Injury pre C. Treatment
and pos t reduction) Conservative Arm to chest strapping.
Surgical Cancellous screws or plate fixation.
2.4.2 Fracture of Surgical Neck Hume rus Primary shoulder replacement.
A. Clinical Finding
Pain and Swelling ove r Shoulder.
2.5. Fractures Of The Shoulder
Painful Move ments of Shoulder. Girdle:
Crepitus, Tenderness. 2.5.1 Fracture of Clavicle
A. Clinical Finding Pain and Swelling ove r
B. InvestigationX-ray s houlder AP and shoulder.
Lateral view (special views if needed) Bony Deformity.
C. Treatment Conservative Immobilization. Crepitus, tenderness.
Surgical K wire fixation. B. Investigation X-ray Shoulder AP
Buttress plating. C. Treatment
Conservative Figure of 8 bandage. (Clavicle
brace)
Fig 4: Figure Of 8 Banda ge
Surgical - Closed reduction and K wire fixation 2.5.2 Fracture of Scapula

for fracture of lateral end and open reduction and A. Clinical Pain and Swelling ove r shoulder
internal fixation with plate and screws for painfull Movements of shoulder.
midshaft fractures.
B. Investigation X-ray Shoulder AP.
C. Treatment - Shoulder immobalization.
Page 538
11. FRACTURE OF LOWER LIMB
Mode of Injury Fracture shaft femur.
1) Road Traffic Accident. Fracture Lower end femur.
2) Associated Poly Trauma. i) Intra articular.
ii) Extra articular.
Type of Fracture Fracture Patella.
Fracture Upper end tibia.
Fracture upper end femur . Fracture shaft tibia.
i) Intra capsular. Fracture around ankle joint.
ii) Extra capsular . Fracture of bones of foot.
iii) Femur head fracture . Splinting of Lower limb Injuries.
Fig 1 Step 1 Traction
Page 539
Fig2Step 2 Limb Splinting
Fig3 Step 3 Buddy Strapping
Page 540
Fig 4 Alternate Method Of Splinting
1.2. The aim of treatment is to achieve union of the

1. Fracture Neck of Femur fracture and a durable hip joint afterwards.
(Intra-capsular)
Introduction- Principles of management include:
Fracture neck of femur more common in old age due
to Slip and fall.
1.2.1Osteosynthesis
1.1. Classification According to the i. Screws, Moores Pins etc.
site of fracture
ii. DHS, Blade Plate.
Subcapital.
iii. Internal Fixation + Fibular Grafting.
Transcervical.
iv. Muscle pedicle Graft + Internal Fixation.
Basicervical.
1.2Osteotomy
Usually caused by trivial fall in the elderly due to
presence of osteoporosis, however metastasis from i) Pauwels valgus osteotomy.
malignancies can also lead to the pathologic
fractures. ii) Mcmurrays osteotomy.
Page 541
1.3Arthroplasty ii) Surgical
Closed reduction and internal fixation with
Hemiarthroplasty. Dynamic Hip Screw and plate (DHS).
Proximal Femoral Nail (PFN).
Total Hip Replacement. Intramedullary Hip Screw.
Dynamic Condylar Screw (DCS).
Excision Arthroplasty. For subtrochanteric fractures a DCS is the implant of
choice after closed or open reduction. Other
modalities like PFN, Angled blade plate,
2. Trochanteric Fractures Reconstruction nail or Modi fied Kuntschers nail
(Extra-Capsular Fracture may also be used as per the preference of the
surgeon.
Neck Femur)
2.1 Fracture of Greater Trochanter: 3. Fracture ShaftOfFemur
This is isolated fracture of greater trochanter due to
fall on the side of pelvis, usually minimally displaced
Fractures of the shaft of the femur are mostly due to
and managed with pelvic strippi ng and non-weight
high-energy trauma.
bearing.
2.2 Fracture of Intertrochanteric
3.1 TypesOf Femoral Shaft
Region:
Intertrochanteric hip fractures are more common in Fractures Are As Follows:
road traffic accidents in young adults and domestic
fall in elderly. Type I - Spiral or transverse. (most common)
Type II Comminuted.
2.3 Fracture of Type III Open.
Subtrochanteric:Region:
Occur between lesser trochanter and a point 5 cm
distally and are seen as independent entities or as an 3.2 Investigations:
extension of ntertrochanteric fractures. X-ray shaft femur with X-ray of pelvis and knee for
associated Injuries.
3. Classification 3.3 Treatment:

3.1 Trochanteric fractures are classified according 3.3.1 Conservative manage ment
to Boyd and Griffin classification: Conservative management of fractures in children in
spica cast or with skeletal traction.
3.2 Subtrochantericfractures are classified
according to Seinsheimers classification: 3.3.2 Surgical management
A. Clinical features:
Symptoms - Pain, swelling, br uising, shor tening
of the limb and inability to stand or walk. Kuntschers nail for isthmic fractures.
Interlocking Nailing in comminuted fractures.
Signs -
i) Severe tenderness and swelling around hip Plating for lower third fractures.
region. Plating of shaft femur fracture in children.
ii) Shortened a nd e xternally rotated lower limb.
iii) Inability to do straight leg raising. Blood transfusion if needed and correct hypovolumic
shoc k.
Investigations:
i) X-ray of pelvis with both hips in AP view and
affected hip in axial view. 4. Fracture Of Tibia/Fibula
ii) CT Scan.
4.1 Introduction:
Treatment: Mostly due to road traffic accident.
i) Conservative initial traction and
immobilization in NRB (Non Rotatory Boot) in 4.2 Signs /ymptoms:
undisplaced fracture Pain, swelling, tenderness
Page 542
4.3 Investigation: 5. Fracture Calcaneum
X-ray of Tibia along with X-ray of knee and ankle
joint. 5.1 Mode:
Fall from height.
4.4 Treatment: 5.2 Sign /Symptoms:
Swelling, oedma, pain, tenderness.
4.4.1 Conservative - In Undisplaced fracture, closed
reduction and above knee cast for 12 weeks. 5.3 Investigation:
4.4.2 Surgical Displaced fracture, Interlock nail or X-ray of heel
plating depending on fracture anatomy. CT scan for intra articular fractures.
5.4 Treatment:
Conservative (Boot Cast). Strict non-weight bearing
till fracture heals.
Intra-articular fractures of calcaneum involving sub-
talar joint should prefebaly treated with restoration of
anatomical fracture geometry is must.
Page 543
12.DISLOCATIONS
Loss of alignment of joint surfaces which should be 1.1. Types
treated as emergency.
Anterior.
Posterior.
1. Shoulder Dislocation Inferior. (luxatioerecta)
Most common dislocation.
Fig1 - X-ray Picture Of Shoulder Dislocation
1.2. Mechanism: 1.4. Investigation:

Most commonly indirect / direct violence X-ray - AP, Scapular view, Axillary view, CT
Posterior dislocation is common in electric shock scan.
and convulsions.
1.5. Treatment:
1.3. Clinical Features: Reduction Traction Counter Traction,
1.3.1 Anterior Abduction, extension, external rotation
Patient comes with Injured s houlder in abduction reduction.
and external rotation. Stimson sedation and prone position with 5 lb
1.3.2Posterior weight.
No striking de for mity, shoulder in abduction and Surgery.
internal rotation. Irreducible dislocation.
1.3.3Luxatio erecta Displaced fracture dislocation with ORIF.
Salute position abduction forward elevation.
Severe pain, neuro vascular deficit, more with
latter two.
1.6. Complications:
Recurrent dislocation.
Axillary nerve and artery Injury.
Brachial plexus Injury.
Stiffness.
Page 544
Occurs because of blow to the back in
2. Elbow Dislocation squatting position.
Most common: Central
Posterior Dislocationof elbow
3.1.3 Central dislocation: Occurs due to direct blow
over the trochanter
2.1 . Mechanism:
Posterior - elbow hyperextension, valgus stress, 3.2. Clinical Features:
arm abduction, fore-arm supination.
Anterior-direct force over posterior fore-arm 3.2.1 Posterior
with elbow in flexed position. Limb in flexion, adduction, internal rotation,
limb shortening
2.2. Clinical Features: Sciatic nerve Injury.
Gross instability. 3.2.2 Anterior
Swelling. Limb in flexion, abduction, external rotation,
Three point bony relation altered. limb lengthened
Associated Injuries - radial head and coronoid Injury to femoral nerve.
Fracture.
2.3. Investigation: 3.3 Investigation:

X-ray.
X-ray elbow AP and lateral. Hip AP and lateral.
Closed manual reduction under GA, followed CT, MRI.
with above elbow posterior slab 90 degree
flexion.
3.4 Management:
2.4. Operative Indications: Resuscitate, CPR attempted with in-line traction
with patient lying supine, under general
Redislocation. anesthesia.
Non-concentric reduction. Methods used are the classical Watson-jones,
Surgery: Open reduction and repair of soft Bigelow and reverse bigelow, Allis, Stimson
tissues, hinged external fixation, pinning of the gravity method.
joint. Maintain it with skeletal traction.
If irreducible, non concentric, ipsilateral neck
2.5. Complications: Fracture or acetabular Fracture then ope n
Loss of motion. reduction is done.
Neurologic compromise.
Vascular Injury. 3.5. Complications:
Compartment syndrome. Osteonecrosis.
Redislocation. Post-traumatic osteoarthritis.
Myositis ossificans. Recurrent dislocation.
Neurovascular Injury.
3. Hip dislocation Femoral head fractures.
Heterotopic ossification.
3.1. Types of dislocation: Thrombo-emblism.
3.1.1 Posterior: Posterior dislocation
Is the most common type of dislocation. Occurs 4. Knee dislocation
mainly due to dash board Injury.
Mode of Injury: high energy / low energy.
3.1.2 Anterior: Anterior dislocation Hyperextension with or without varus / valgus.
Page 545
Fig2 - X-ray Picture Of Knee Dislocation
4.1. Clinical features: 4.3. Treatment:

Gross knee distortion is present. Immediate closed reduction, avoid direct
A neurovas cular examination must be done. pressure over the popliteal fossa after reduction,
splint at 20 - 30 degrees of flexion.
Operative indications:
4.2. Investigations: Unreduced, residual soft tissue interposition
First reduce the dislocation. Open Injuries, ORIF with ex-fix.
Then take X-rays AP and lateral, 45 degree Reconstrucion of ligaments at later setting.
oblique, patellar sunrise views.
MRI. 4.4. Complications:
Arthroscopy.
Assess the ligament Injuries. Limited range of movements.
Ligamentous laxity and instability.
Vascular compromise.
Nerve traction Injury.
Page 546
13.LIGAMENTOUS INJURIES
1. Mode of Injury 4. Treatment

Indirect, Twisting Or Bending Forces On The Knee. 4.1 Initial management with brace/splint and
NSAIDs
2.Clinical Features Conservative management with bracing and
Pain, swelling, tenderness, loss of range of motion physiotherapy
and positive patellar tap. Bracing for 2 weeks followed by MRI
3. Investigations 4.2 Operative: arthroscopic ligament repair.
X-ray of associated joint and MRI.
Page 547
14. SPINAL TRAUMA
Nor mal Motor, Sensor y, Or Autonomic Function.
1. Spinal Cord Injury (SCI)
Is An Insult To The Spinal Cord Resulting In
AChange, Either Temporary Or Permanent, In Its
Figure 1 Head to Toe Stabilization In Case Of Spinal Injury OnSpi ne Board
2.1.1 Clinical Diagnosis:

2. Optimal Diagnostic
After the ABC have been taken care of, the patient is
Criteria, Investigations, gently log rolled and whole of the spine is palpated
Treatment & Referral for tenderness or a palpable step-off deformity.
Neurogenic shock, incontinence of bowel, bladder
Criteria and penile erection indicate severe spine Injury. A
careful and detailed neurological examination is then
2.1 Rural Hospital / SDH: performed and meticulously documented.
OptimalStandards of Treatment in Situations where
technology and resources are limited.
Table 1: Assessment of motor function
Diaphragm C3-5
Shrug shoulders C4
Deltoids/elbow flexion C5
Extend wrist C6
Extension of elbow/ flexion of wrist C7
Abduct fingers C8
Page 548
Active chest expansion T1-T12
Hip flexion L2
Knee extension L3-4
Ankle dorsiflexion L5-S1
Ankle plantar flexion S1-2
Table2: Assessment of sensory function
Deltoid area C5
Thumb C6
Middle finger C7
Little finger C8
Nipple T4
Xiphoid T8
Umblicus T10
Symphysis T12
Anterior thigh L2
Anterior knee L3
Antero-lateral ankle L4
Dorsum of great and 2nd toe L5
Lateral side of foot S1
Posterior calf S2
Perianal sensation S2-5
2.1.2 Frankels grades: 2.1.3 Investigations:

Spinal Cord Inj.ury is mos t commonly graded using All patients with suspected spinal Inj.ury should have
Frankels grades (A to E). radiographic evaluation.
A: Complete motor and sensory loss
a) Initial screening can be done by conventional
B: Sensation only present below lesion
antero-posterior and lateral x-rays. The cervical spine
C: Sensations present and motor function is
radiographs must include the C7-T1 junction to be
present but useless
considered adequate
D: Motor useful but not nor mal
E: No neurological deficit. Additional Open-mouth views should be done to
evaluate odontoid Inj.ury.
After the motor and sensor y examination, presence
Whole spine should be evaluated with a patient of
of sacral sparing may be noted by voluntary rectal
spinal Inj.ury.
sphincter tone and toe flexor contractions. Presence
of sacral sparing indicates a better neurological b) The patient should be referred for advanced
prognosis. diagnostic modalities only when the patient is
sTab.le:
Although spinal shock is ove r by 24 hours, rarely
it may be prolonged. A positive bulbocavernous i. CT
reflex or a positive anal wink indicates the end of ii. MRI
spinal shock. If no motor or sensory function can be
documented at this stage, a complete spinal cord 2.1.4 Out Patient care
Inj.ury is present. A secondary hospital is expected to provide
outpatient care to the spinal cord Inj.ury patients who
may be referred back from specialized centers after
Page 549
definitive treatment. This may be in for m of 2.2 At District Hospital
i. physiotherapy for passive mobilisation of all joints 2.2.1 Clinical Diagnosis:
and active exercises for muscles iv. As described above (in situation 1)
ii. Teaching of clean intermittent cathetrisation Investigations:
iii. Counselling of the patient and attendants
iv. Care of bed sores 2.2.2 Radiographic evaluation of patients with
spinal Inj.ury.
2.1.5 Day Care i. Initial screening can be done by conventional
antero-posterior and lateral x-rays.
Day care might be needed for situations like ii. Additional Open-mouth views should be done to
debridement of bed sores. evaluate odontoid Inj.ury.
iii. Special views like swimmers view and oblique
views can be done to see junctional areas
2.1.6 Referral criteria:
iv. CT scan of the whole spine should be done if in
i. The pa tient should be hemodynamicallysTab.le presence of clinical suspicion but fractures
and fully resuscitated at the time of referral cannot be demonstrated on x rays or if junctional
ii. All the patients who need surgery (indications areas are not visualised.
discussed in the next section) need to be referred v. MRI should be done to evaluate ligamentous
to a specialized tertiary care centre. Inj.ury, spinal cord Inj.ury.
iii. The decision of need for surgery can only be vi. In patients with pre-Inj.ury morbidities such as
made by an experienced spinal surgeon either Ankylosing
orthope dic or neuros urgeon. In absence of these vii. stiff spi ne CT and MRI should be done to rule
all patients with proven or suspected spine out occult instability eve n if x-rays arenormal.
Inj.ury should be referred to a higher center. viii. Whole spine should be evaluated with a patient
of spinal Inj.ury
Fig 2 Xray view of cervical spine trauma Fig 3 MRI of spine trauma
Treatment: Standard Operating procedure Inj.uryreaches the emergency, thepatient should be

(a) On arrival in emergency room: transferred off the backboard onto a firm padded
surface while maintaining spinal alignment. A
Once the patient with a potential spinal
baseline skin assessment can be performed at the
Page 550
time of shifting the patient from spine board to be employed for logrolling during patient
hospital bed. Adequate number of personnel should repos itioning, turning and transfers.
Fig4 Log Rolling while examining and shifting of spi nal Inj.ury patient
No clinical evidence exists to definitively Screen for thoracic and intra-abdominal Inj.ury in all
recommend the use of any neuroprotective patients with spinal cord Inj.ury.
pharmacologic agent, including steroids, in the
treatment of acute spinal cord Inj.ury to improve Perform early sTab.ilization of extraspinal fractures.
functional recovery. However high dose methyl- Perform this surgery as early as possible to facilitate
prednisolone may be used as per NASCIS III early rehabilitation and concomitantly with any
recommendations (Methylprednisolone: Bolus dose required spinal stabilization if the patient is
of 30 mg/kg of body weight over 15 minutes, medically stable.
followed by a 45-minute pa use, and then a 23-hour Surgical treatment.
continuous infusion of mg/kg/hr,(If patient presents
between 3 and 8 hrs, give the above steroid infusion (b) Out Patient
for total of 48 hrs) if the patient presents within 8
hours of Inj.ury. The risk of complications as Out patient care is needed for non surgically treated
infection, sepsis, respiratory complications and patients on ambulatory care and Surgically treated
gastrointestinal hemorrhage should be kept in mind patients. This will entail:
while administering steroids, It is basically a
Prescription of appropriate orthoseshysiotherapy
treatment option,not standard care.
servicesCounselling: social,
Once initial resuscitation is done, complete a
psychological,vocational
comprehensive tertiary trauma surve y in the patient
with potential or confirmed spinal cord Inj.ury.
(c) Day Care
In the patient with acute spinal cord Inj.ury,
particularly higher cervical Inj.ury, assess
Referral criteria:
frequently and early document any evidence of
Surgically treated patients may be referred back to
traumatic brain Inj.ury (TBI) in the form of loss of
secondary hospitals for physiotherapy, and care of
consciousness and posttraumatic amnesia .
back, bladder and bowel.

Page 551
15. MANGLED EXTREMITIES (AMPUTATION)
1. Introduction 4. Standard treatment protocol
for management of mangled
Traffic is increasing day by day and so are road
traffic accidents.
extremities at RH/SDH/DH
Most of RTA involve trauma to extremities to
varying level. No Delay in receiving the patient and starting
treatment
Multi-systemic approach
2. At PHC/Sub Center level Patient should be examined according to ATLS
protocol of ABCDE
Follow ATLS guidelines of A B C D E
Look for signs of poly trauma, involvement of
After STab.ilization of patient, examine for other
head Inj.ury, spine or abdominal and pelvic
associated Injuries such as pelvis and spine
Injuries.
which are common in poly trauma
If such Injuries are present then refer the case to 4.1. Informed consent
higher center without any delay.
If absent then grade the Inj.ury according to Two surgeons should certify that the limb needs
MESS (Mangled Extremity Severity Score) amputation
which is useful for decision making regarding
Consent of the patient ( if conscious and co-
definitive surgical treatment (Salvage or
operative ) should be taken
Amputation of the limb) and refer the patient to
Consent of Relative should be taken if patient is
the higher centre.
non responsive
Detailed informed consent in their local language
3. Before referring should be taken
Wash the wound primarily with nor mal saline, 4.2. Pre operative care
iodine solution and Hydrogen Peroxide till all
visible contamination in remove d. Pain management
Stop any active bleed with help of compression Clinical assessment
banda ge or tourniquet
Decision making
Avoid Excessive handling of Inj.ured limb to
Discharge planning
avoid neurovascular complications
Record keeping
Infuse IV fluids and Blood
Inj.ect first dose of higher antibiotics 4.3. Peri operative care
Give Inj. TT. O.5 ml intra muscular
Things to be done Before Referral The scheduling of ope rations
Operation undertaken
Inform the concern center about MESS score and Antibiotic prophylaxis
expected time of arrival of patient Thromboprophylaxis
Arrange for proper transport
Make sure that patient will be 4.4. Post operative care
hemodynamicallysTab.le during entire duration
of transport. Pain management
Wound care
Rehabilitation
Page 552
16. COMMON FRACTURES IN CHILDREN
Mode Fall on out-stretched hand Fractures of lower limb

1.6 EpiphisealInj.ury around hip and kneeClosed
1. Common fractures reduction and immobilization in splints
1.1 Lower end radius 1.7 Surgical treatment ope n reduction and
Treated by closed reduction internal fixation with multiple cancellous
1.2 Greenstick fracture both bone forearmClosed screws or mini DHS plateFractures around hip
reduction under General anesthesia Surgical treatment
1.3 Supracondylar fracture humerus Depe nding on
classification , either closed reduction or 1.8 Shaft femur
closed reduction with cross k-wire or open
Undisplaced Conservative
reduction
Displaced Shaft tibia
1.4 Fracture lateral condyle humerus
Undisplaced Conservative
Requires open reduction
Displaced Surgical in the form of closed or
1.5 Fracture clavicle ope n reduction a nd i nternal fixation with either
elastic nails or plate and screws.
Figure of 8 bandage
Page 553
17. BONE TUMORS
Primary neoplasms of the skeleton are rare, Complications - bursitis, neuropathy, limitations
amounting to only 0.2% of the overall human tumour of movement, malignant transformation
burden. However, children are frequently affected (chondrosarcoma) occur rarely
and the etiology is largely unknown. Significant X-ray - bony growth made up of mature cortical
progress has been made in the histological and bone and marrow. Cartilaginous gap not visible
genetic typing of bone tumours. Furthermore, Treatment- excision including periosteum.
advances in combined surgical and chemotherapy
have lead to a significant increase in survival rates 1.1.3 Fibrous Dysplasia
even for highly malignant neoplasms, including Normal bone is replaced by fibrous tissue.
Osteosarcoma and Ewing sarcoma. Erodes the cortices of bone from within.
Thin layer of sub - periosteal bone forms around
1.Primary bone tumors: the mass, so bone appears expanded. Site- upper
end of femur, tibia, ribs.
1.1 Benign Tumors Mono-ostotic one bone is affected. Poly-ostotic
1.1.1 Osteoid Osteoma many bones are affected.
True benign tumor of bone Clinical features - pain, deformity, pathologic
Age group: 5 - 25yrs fractures.
Commonest site: Diaphysis of long bone. eg X-ray - ground glass appearance.
tibia. Treatment - curettage and bo ne grafting.
Clinical features Night pain, relieved by 1.1.4 Osteoclastoma (Giant Cell Tumor)
salicylates.
Pathology - Consists of a nidus surrounded by Common bone tumor with variable growth
dense sclerotic bone potential
X-ray - Zone of sclerosis surroundi ng a nidus Age group - 20 - 40 yrs
Treatment - Complete excision of nidus with Site - starts in epiphysis and extends into
sclerotic bone. metaphysis
Prognosis - Good Commonly lower end of femur, upper end of
tibia
1.1.2 Osteochondroma
Pathology
Commonest benign tumor of bone, arises from Cell of origin is uncertain
adjoining epiphysis to metaphysis Tumor consists of undifferentiated spindle
Age group - adolescents cells with multinucleated giant cells
Clinical features - painless swelling around a Clinical feature - swelling, vague pain
joint, sessile or pedunculated X-ray
Multiple site involvement is called Lytic expansile lesion
Diaphysealaclasia Eccentric location
Soap bubble appearance pathognomonic.
Page 554
Figure 1: Soap bubble appearance of giant cell tumor
Excision with reconstruction Occurs most often in distal femur, may also be in
Curettage with or without suppl ementary the humerus, tibia, and ulna.
procedures like chemical ablation, cryotherapy, Develops on surface of bone and progresses
PMMA implantation slowly.
Amputation: aggressive tumors, recurrence
Radiation: tumor involving vertebrae. Treatment
Surgery
1.2 Primary malignant bone Tumor resection, possible amputation
tumors: Inter-scapulothoracic surgery
Hemi-pelvectomy
1.2.1Osteogenic Sarcoma Chemotherapy.
Usually in males aged 10 to 20
Occurs most often in femur, but also in tibia and
1.2.3Chondrosarcoma:
humerus
Usually in males ages 30 to 50
Occasionally, in fibula, ileum, vertebra, or
mandible Occurs most often in pelvis, proximal femur,
ribs, and shoulder girdle
Tumor arises from bone-forming osteoblast and
bone-digesting osteoclast. Develops from cartilage, and grows slowly
Usually painless, locally recurrent and invasive
Hemipelvectomy
Treatment
Surgical resection (ribs)
Surgery
Radiation, and / or Chemotherapy.
Radical Tumor resection
Mega Voltage Radiotherapy and / or
chemotherapy or combi nation of bot h. 1.2.4 Multiple Myeloma
It is the mos t common primary malignancy of bone
1.2.2 ParostealOsteogenic Sarcoma: having short duration onset and aggressive in nature.
Usually in females ages 30 to 40.
Page 555
Age of occurance commonly around 60yrs. 2% less
than forty.
2. Metastatic bone tumors:
The most common bony malignancies are
Clinical features: metastatic carcinomas.
Bone pain Metastatic lesions represent the most common
cause of pathology fractures due to a neoplasm.
Weakness
Usually are multiple, but can be solitary.
Weight loss
The most common primaries are breast, prostate,
Anemia
lung, kidney and thyroid, in that order.
Thrombocytopenia
Renal metastasis are quite vascular and have cold
Peripheral neuropathy
bone scans.
Hypercalcaemia
Renal failure Clinical features:
It manifests in pathological fractures commonly in Patients with known primary malignancy
spine followed by ribs and pelvis. presents with symptoms suggestive of
secondaries in bone.
Laboratory studies:
Bony pain, commonest site is spine.
Urine - Bence Jones Protein present in 30% of Pathological fractures most common in spine.
cases
Blood - Very high ESR, A/G ratio reversal Investigation:
Serum electrophoresis - Abnormal spike in X-ray - Majority are osteolytic, few are
gamma globulin region in 90% cases. osteoblastic. eg., male- prostatic secondaries,
Treatment: female breast secondaries
Blood - High ESR, elevated serum calcium,
Chemotherapy - Melphalan is the drug of choice. elevated serum acid phosphatase in prostatic
Given in combination with Vincristine, secondaries.
Prednisolone and sometimes Cyclophosphamide.
Cycles are repeated 3 - 4 weeks for 6 - 12 cycles. Treatment:
Splintage of diseased part. Symptomatic relief of pain, and prevention of
Radiotherapy- Useful in case of neurological pathologic fractures
compression. Chemotherapy
Surgical intervention in advanced tumors Radiotherapy
Page 556
ANESTHESIOLOGY
Page 557
1. INTRODUCTION
noxious stimuli with different inhalational and
1. Definition: intrave nous drugs.
Anesthesia is the reversible state of unconsciousness
with amnesia, analgesia and unresponsive ness to
2. Types of Anesthesia
GENERAL
Types of Anaesthesia
General (GA) Regional Total Intra Monitor

Intravenous Venous Anaesthesia
Anaesthsia Regional Care
(Short GA)
Anaesthesia (MAC)
with mask (G1 A)
Stand By
or without mask
Central Nerve Block Local Localized or

Neuroaxial selective
block nerve block
With
With PNS/USG Without PNS/USG PNS/USG
Sub Arachnoid Epidural Caudal Epidural Combined Spinal

Spinal Block Blocks Block Epidural Block
Figure 1: Anesthesia General Protocol
Page 558
3. Pre-Anaesthetic Checklist
Check function of high vacuum suction Check gas supplies, both cylinder, pipeline &
machine. circuit
Check reserve oxygen suppl y. Check oxygen suppl y failure alarm & oxygen
Check function of breathing system. flush.
Check vaporizer. Check oxygen nitrous oxide ratio.
Check absorber if in use. Mechanical ventilator.
Inspect equipment for Waste gas scavenging system.
a) Endo tracheal intubation Check reserved gas supply
b) Intrave nous infusion Appl y and c heck monitoring system &
c) Resuscitation cautery, circuit and tourniquet.
Set appropriate alarm level.
Magills forceps (Adult & Pediatric), Scissors,

4. Recommended minimum Ampoule cutter, Torch, Thermometer.
essentials in operation IV sets, Micro Sets, Blood sets, three way IV
extension tube & central line.
theatre IV fluids crystalloids RL, DNS, D5, and Colloids
plasma expanders.
4.1 Minimum essentials required: For Difficult Airways fiber optic boogie,
Continuous supply of oxygen via central pipeline LMA(Classic & Pro seal), Igel, tracheostomy,
or jumbo cylinders. tube , percutaneous tracheostomy set, combi tube
Anesthesia machine with to oxygen and a nitrous and all size stylate(flexible & Rigid).
oxide input connections. Disposable spinal needles 23, 24, 25, 26, 27,
One small oxygen cylinder mounted on Boyles Epidural set 16, 18.
other than jumbo or central line and nitrous Radiant warmer/blanket, heating mattress, fluid
oxide cylinder along with cylinder valve opener warmer.
should be there. Postoperative recovery room with oxygen supply
Boyles machine should have Hypoxic and alarm and monitors.
safety system. Working BP apparatus & Stethoscope.
Wor king suction machine (Foot driven and Vaporizers-(Goldman) Halothane & Isoflurane.
Electric) with all connectors, tunings, and Capnography To monitor End Tidal
suction round tip and e xhaust fans. Carbondioxide (ETCO2) Where laparoscopic
Multi-parameter (Pulse Oxymeter, NIBP, ECG, surgeries are done.
ETCo2). New Born resuscitation kit weighing scale.
Defibrillator (adult & pediatric). Paediatric resuscitation kit with all masks &
OT table with tilting facility. LMA & stylate.
Adult (Bain) & Pediatric (JR) Circuit. Flexible smooth rubber cord for tourniquet to
Set of oral and nasal Airways sizes 00, 1, 2, 3, secure IV line.
4. Central line (cava fix, double & triple Lumen).
Silicon bag with all sizes of masks & cuffed and Glucometer, peak flow meter, height scale &
plain Endo tracheal Tubes. Working refrigerator (for blood sample).
laryngoscope with 5 sizes of blades
Page 559
4.2 Emergency medicine kit:
Chart No. 1. EMERGENCY MEDICINE KIT
Injections Metapranolol Nebulizer
Hydrocortisone Hemolock
Atropine
Dexamethaxone Butroclot
Glycopyrolate
Potassium chrolide Neloxone
Adrenaline
Calcium gluconate. ECG Lead.
Noradrenaline
Soda bicarbonate.
Dopamine. Tablets
Magnesium 25% & 50%
Dobutamine.
Mannitol Nifedepin
Mephentermine
Tranaexamic acid. Captopril
Ephedrine hydrochloride.
Dextrose 25% & 50% Sorbitrate
Phenylephrine.
Insulin. Atenolol
Vasopressin
Deriphylline
Prostaglandi n
Aminophylline
Isopr enalin
Amiodarone.
Digoxin
Xylocard 2%
Esmolol
Furosemide (lasix)
Propranolol
4.2 Doses and indication for emergency drugs:

Chart No 2. E MERGENCY DRUGS & DOSES
Drug Indication Dose

Sodium bicarbonate Acidosis 2-4 m eq/kg
Atropine Bradycardia 0.03 mg/kg
Naloxone Narcotic depression 5-10 micro gm/kg
Calcium gluconate Low perfusion 0.6 ml/kg
Epinephrine Asystole 5 Microgram/kg of 1:1000 solutions.
4.3 Various Types of anesthesia drugs:

Chart No. 3. A NAESTHESIA DRUGS
A. Premedication D. Inhalational Anasthetic Agent

1. Anticholinergics. a) Halotane.
a) Inj Glycopyrrolate b) Isoflurane.
b) Inj Atropi ne c) Sevoflurane.
2. Antacid d) Desflurance.
a) Inj Ranitidine.
b) Inj Pantaprazole
3. Antiemetic E. Reversal Agent
a) Inj Metoclopramide.
b) Inj Onda nstaron. a) Inj Neostigmine.
Page 560
c) Inj Granisatron. F. Obstetric Drugs
4. Opiods
a) Inj Oxytocin.
a) Inj Pentazocine (Fortwin)
b) Inj Methyl ergomtrine.
b) Inj Butophanol
c) Inj Prostaglandin F2 alpha.
c) Inj Fentanyl.
d) Inj Magnesium Sulphate.
5. Benzodiazepines
a) Inj Diazepam. F. Spinal Anaethesia drugs
b) Inj Midazolam.
a) Inj Lignocaine (heavy) 5 %
b) Inj Bupivacaine (heavy) 0.5%
G. Local Anesthetics.
a) Inj Lignocaine 2%.
b) Inj Lignocaine 2% with
B. Induction Agents Adrenaline.
a) Inj Thiopentone Sodium. c) Inj Bupivacaine 0.5%

b) Inj Propofol. d) Inj Bupivacaine 0.25%
c) Inj Ketamine.
preservative free.
e) Inj Rocuronium 0.75%.
H. Other Drugs.
a) Inj Tramadol
b) Inj Diclofenac.
C. Muscles Relaxants.
c) Diclofenac Suppository.
Depolarizing Muscles Relaxants. d) Inj Buprenorphine.
e) Inj Dexmeditomidine.
a)Inj Suxamethonium. f) Inj. Clonidine.
Non- Depolarizing Muscles Relaxants g) Inj Bupivacaine 0.5% heavy.
h) Lignocaine Jelly 2%.
a) Inj Pancuronium.
b) Inj Vecuronium.
c) Inj Rocuronium.
d) Inj Atracurium.
4.6 Doses of intravenous anesthesia agents:
Chart No. 4. INTRAVENOUS AGENTS IN ANAESTHESIA
INTRAVENOUS AGENTS USED IN ANAESTHESIA

DRUG DOSE REPEAT DOSE/ INFUSION RATE
Thiope ntone 5-6 mg/kg 2 mg/kg.
Propofol 1-3 mg/kg 0.2-1 mg/kg
Ketamine 1.5-2 mg/kg 40mcg/kg/min.
Fentanyl 0.025-2 microgm/kg 4-10 mcg/kg/hr. (I)
Alfentanil 5-10 microgm/kg 05-10 mcg/kg/min. (I)
Sufentanil 0.1 microgm/kg 0.01 mcg/kg/min.) (I)
Page 561
Succinyl Choline 2mg/kg 4-10 mg/min. (I)
Pancuronium 0.08 mg/kg 0.02 mg/kg
Atracurium 0.5 mg/kg 4-12 mcg/kg/min (I)
Vecuronium 0.08-0.1 mg/kg 0.12-2 mcg/kg/min. ( I)
Rocuronium 0.6 mg/kg 9-12 mcg/kg/min. ( I)
Diazepam 0.1-0.3 mg/kg
Midazolam 0.5-0.1mg/kg
Flumazenil 0.1-0.5mg
Neostigmine 0.05 mg/kg
Adenosine 0.1 mg/kg
Digoxin 15-20 mcg/kg
Diltazen 0.15-0.35 mg/kg
Benadr yl 1 mg/kg
Furosemid 1-2 mg/kg
Mannitol 0.25-1 mg/kg
Esmolal 100-300mcg/kg/min. (I)
Dopamine 5-15mcg/kg/min. (I)
Dobutamine 7-15mcg/kg/min.(I)
NTG 1-1.5 mcg/kg/min. (I)
Amidaron 15mg/kg (loading) (I)
5mg/kg/hr. ( maint)
KCL 0.5mEq/kg/hr. (I)
Sodium 40-100mcg/min. (I)
Nitroprusside
Atropine 0.01 mg/kg
Glyco pyrolate 4 microgm/kg
Dexamethasone 0.1 mg/kg
Paracetemol 15 mg/kg
Diclofenac sodium 1.5 mg/kg
Neostigmine 0.05 mg/kg
Noradrenaline 4 mcg per mL In titrated dose
Bitartrate
Labetalol Hcl 20 mg IV push over two minute In titrated dose
40-80 over two 10 minute
I = Infusion Do not use Broom inside Operation Theatre.

Do Fogging after infected case and enter in register.
5. Operation Theatre cleaning
In between the two cases, clean O.T.
protocol
Page 562
1) Remove linen, instrument sets and used material. bacteria, viruses, molds and spores. It is non toxic,
eco friendly. It liberates nascent oxygen having
2) Clean surface, wipe with Bacillocide solution.
strong oxidizing effect.
3) Mop the floor (ideally with Lysol 3% or
Bacillocide) 6.3. Procedure:
For 350 sq. ft. OT take 1000 ml (1lt) water in tank
6. Operation Theatre and add solution in that.
fumigation protocol (Power Keep fumigation machine on floor .
Jet and auto mist) Keep machine near to door so after fumigation you
can easily switch off machine.
6.1. Fumigation agents
Daily moppi ng of OT is compulsory with sol ution
For O.T. fumigation 20% aqueous solution of
Hydrogen Peroxide 11 % and Silver Nitrate solution Please cover all electro medicos, digital and water
0.01% should be used. For 1000 cu. ft. Take 400 ml resistance equipment (C arm monitor microscope
clean water and add 80 ml. of fumigant solution etc.) with cloth or plastic sheet.
Hydrogen Peroxide 11 % + Silver Nitrate 0.01 % Empty the machine tank and use balance solution.
solution in a fogging machine. Keep the room / OT
closed for 60 min. Mop the flooring with clean floor Do not run (pow er jet) machine continuously more
soaked in the same solution. than 35 minutes and total one hour in a da y; keep 4 to
6 hours of interval in between two running.
6.2. Advantages: Do not operate machine in presence of patient and do
Solution has broad spectrum of antimicrobial activity, fumigation in vacant room only.
effective against HIV, HBV and other pathogenic
7. Grading of patients & fluid requirements:

Chart No. 5: GRADING
ASA 1 : ASA 2 : ASA 3 :

A Normal Healthy A patient with mild systemic A patient with severe systemic disease that limits
Patient with only surgical Disease (like, HTN, DM etc. activity but is not a incapacitating (Disease is not
Condition under control with treatment ) under control with treatment but not life
threatening)
Weight (kg.) Hourly Fluid Requirement

<10 4 ml/kg
11-20 40ml + 2ml/kg > 10
>20 60ml + 1ml/kg> 20
ASA Ame rican Society of Anesthesiology
Page 563
8. Fluid requirements for children:
Chart No.6: FLUID REQUIREMENT FOR CHILDREN
MONITORING STANDARDS FASTING GUIDELINES
ESSENTIALS: Ingested Minimum Fasting

1) Continuous presence of qualified material Period (h)
Anesthesiologist.
2) Oxygen suppl y failure alarm Clear Liquids 2
3) Observation of reservoir bag & chest Breast Milk 4
expa nsion.
4) Ventilator disconnect alarm. Infant for mula 6
5) Oxygen analyzer of inspired gases. Non-human Milk 6
6) Pulse oximetry.
7) Electrocardiogram. Light Meal 6
8) Non-invasive arterial blood pressure.
These recommendations apply to healthy patients
STRONGLY RECOMMENDED: of all age group who are undergoing elective
procedure.
1) Temperature. Clear liquids: water, fruits without pulp,
2) End tidal Carbon dioxide. carbonated, beverages, tea & black coffee.
3) Monitoring of neuromuscular blockade.
9. Adrenaline doses:
Chart No. 7: ADRENALINE DOSES BY AGE
Adult : Pediatric: Neonatal :

1 mg 0.01 mg/kg (0.1 ml/kg) IV or intra 0.01 mg/kg to 0.03 mg/kg (0.1-0.3
osseous ml/kg)
Repeat Q 3-5 min
Maximum does 1 mg IV/IO or 10 IV, intra osseous, or umbilical
Higher IV doses NOT
mg ET repeat Q 3-5 min
recommended. Repeat Q 3-5 min.
No Higher IV doses. ET does 0.1
ET dose 2 to 2.5 mg Higher IV doses NOT recommended
mg/kg (ten times IV dos e)
Drip 1-10 mcg/min. ET does 0.1 mg/kg (ten times IV
Strong preference for IV/IO!
dose)
Drip 0.05-1 mcg/kg/min
REACTION
Breathing Circuits
Jackson Rees circuit Use for neonate & children less than 25kg
Bain Circuit Most commonly used circuit weight more than 25 kg
Page 564
10. Airway:
Chart No.8 ORAL AIRWAYS
Formula for size of ETT
Neonate 2.5 or 3
Children < 6 years age/3 + 3.5
Children > 6 years age/4 + 4.5
Adult female ET Tube number 7 or 7.5
Adult male ET Tube number 8.5 or 9
11. Biomedical waste:

Chart No. 9: SEGREGATE MEDICAL WASTE
Red Bag Blue Bag Yellow Bag Sharp puncture proof
Container
Plastic Waste General Waste Anatomical Waste Waste Sharps
Infectious waste i.e. Pads, Plastic and rubber Appendix, Uterus, Blade
Spirit swabs, Plaster casts articles such as IV Sets, extracted teeth,
Needle
soiled with secretions catheters, venflow, urine
Placenta
bags Cut Ampoule
All Sharp objects
12. Important aspects of anesthesia:

Chart No. 10: Ten Golden rules of anesthesia
1 Do an adequate preoperative assessment.

2 Nil by mouth for six hours
3 Put patient on a tipping table
4 Check your machine and c ylinders before you start
5 Keep a suction instantly ready
6 Keep patients airway clear
7 Be ready to control patients ventilation
8 Have a vein open
9 Check patients pulse and blood pressure
10 Always have someone who can apply cricoid pressure in emergency
Page 565
13. Universal precaution for health care workers in operation
theatre
Proper hand washing before and after Dispose all sharps in puncture proof container.
CONTACT with each patient and handling Avoid spills of blood & body fluids, If it occurs,
patients specimens. Do not leave sharps on bed cover it with absorbent material like gauze over
or beside of patient which 1 % solution of sodium hypochlorite
Use of gloves, mask, gowns and protective eye- should be poured and left for 10-15 minutes
wear (ideal 30min). Clean the area with a bleach mop.
Prevent needles stick injuries with other sharp Wash and dr y the mop.
instrument Proper segregation and disposal of Bio-Medical
DO NOT BEND OR RECAP NEEDLES waste
In case of needles stick injuries or cuts, wash the Immunization (for Hepatitis B)
area properly with water and soap and Contact
for post exposure prophylaxis treatment
Page 566
2. DIFFICULT AIRWAY ALGORITHM
Assess the likely hood and clinical impact of basic cannot incubate-(CVCI) Emerge ncy sur gical
management problems: In case of Difficult airway (i.e. Crico thyrotomy) ma y be necessary
Intubation and difficult Ventilation awake intubation if the patient is hypoxic.
should be carried out. In case you ca nnot ventilate,
FIGURE-1: INTRODUCING LARYNGEAL MASK AIRWAY Ge
Page 567
3. PRE-ANAESTHESIA CHECK UP PROTOCOL
11. History of smoking, alcohol, addictive drugs,
1. Pre Anaesthesia Checkup BOH.
(PAC) 12. History of Dentures, braces, crown, loose teeth,
Pre anesthetic check up should be carried on prior implanted pacemaker, implanted cardiac
day of surgery to avoid unnecessary postponement of Defibrillator, Prosthetic Heart valve, orthopedic
patients. implant, or gan recipient.
1.1 Following history should be 13. History of STD, Drug resistance.
asked 14. History of anesthesia with histor y of headache
after anesthesia, Awareness during anesthesia,
1. High blood pressure, Diabetes, Asthma, Heart
transfusion reaction, admission to ICU after
Disease, Stroke, Cough and Cold in the past 2
surgery, any complication after anesthesia.
weeks
2. History of Shortness of breath, Difficulty in 2. Following history should be
breathing on lying flat, Difficulty in breathing on
climbing stairs, Chest pain, palpitation, chronic asked
cough. 1.1 Investigations as advice by surgeon and
3. History of cardiac illness such as heart failure, anesthetist.
heart valve problem, high cholesterol level, 2.2 ASA: (American Society of Anaesthiologist)
RHD, CHD or Cardiac arrest. Assessment of patient in terms of
I/II/III/IV/V/VI/E with additional risk factor.
4. History of respiratory problems such as chronic 2.3 Do prope r systemic examination of
bronchitis, Allergic rhinitis, Snoring, cardiovascular system, respiratory system,
Tuberculosis, Lung cancer, Chest infection or central nervous system.
pneumonia. 2.4 Evaluate the patients airway - Thyromental
5. History of neurological probl ems such as distance (If < 3finger anticipated difficult
epilepsy, fainting, coma, paralysis, chronic intubations), dentition, mouth opening.
headache, dizziness, Parkinsonism, brain tumor.
6. History of muscle or bone problems such as 3. Consent
Osteoporosis, Neck pain or neck stiffness,
Difficulty to open mouth, Spine problem, Info med consent of pa tient should be taken before
congenital muscle disease. surgery which means consent given to a proposed
7. History of kidney problem such as dialysis. specific intervention, without any force, undue
Gastric problem such as Heartburn, Reflux, influence, fraud, threat, mistake or misrepresentation,
Jaundice. and obtained after disclosing to the person giving
consent adequate infor mation includi ng risks and
8. History of blood or endocrine problems such as benefits of, and alternatives to, the proposed
Anemia, receipt of blood transfusion, prolonged intervention in a language and manner understood by
bleeding, Thelecemia, sickle cell anemia, thyroid such person with no binding to consent after being
disease. infor med. Consent should be attested by staff nurse
9. History of allergy. of ward. There should be common consent for
surgery and anesthesia unless it is essential to take
10. History of medications such as diabetes, consent for anesthesia separately.
hypertension, asthma, psychotropic drugs,
steroids.
Page 568
4. CONDUCT OF ANAESTHESIA
1. Anesthesia can be conducted Keep glucometer and shor t acting regular insulin
ready for intra-operative use.
taking 5Ps into Assess target organ function and monitor
accordingly
consideration
They are:- 2.3 Obstetric patients
Prepare operation theatre ready for emergency
Pre operative Assessment of Patients. LSCS.
Patients Preparation. Follow anti-eclamptic regimens for patients with
Preparation of Operation Theatre. pregnancy induced hypertension.
Premedication. Verify the availability of blood.
Plan of Anesthesia. Keep the difficult intuba tion kit ready.
Take care of prophylactic measures to treat
2. Anesthesia to different aspiration (Mendelson Sydrome).
Keep the Infant resuscitation bag, smaller
groups of patients endotrachaeal tubes, laryngoscope, suction
apparatus, infant radiant warmer, oxygen hoods
2.1 Hypertensive Patients & emergency dr ugs for resuscitation.
Advise to take all anti-hypertensive drugs early
in the morning of surgery. 2.4 Trauma Patients
Avoid ACE inhibitors on the day of surgery to Stabilize the patients taking into consideration
avoid intra operative fall in BP. ABC (Air, Breathing & Circulation) of
Keep anti-hypertensive drugs like resuscitation.
Nitroglycerine, Nifedipine and Metoprolol ready. Stabilize the cervical spine (with collar for
Keep volume expanders like colloids ready. suspected C-spine injuries).
Place the inter costal drainage for chest injuries.
2.2 Diabetic Patient Splint the fractures.
Advice to skip the morning doses of insulin and Assess the GCS (Glasgow coma score).If<8,
oral hypoglycemic. intubate for airway protection.
Check fasting blood sugar, urine ketones and Transport the patient to referral centre with
serum electrolytes on the mor ning of surgery. portable ventilator, oxygen cylinder, ambu bag
on standby.
Place the diabetic patients first in the list of
surgery.
Inform the patient`s details to referral centre prior to
Specific care of the patients with autonomic or during transport.
disturbances.
Page 569
5. COMPLICATIONS OF ANAESTHESIA
Figure-1: Complications of Anesthesia
During General Anaesthesia
CARDIOVASCULAR RESPIRATORY NEUROLOGICAL THERMAL

PERTURBATIONS
Hypertension Pulmonary Convulsions
aspiration Hypothermia&
Hypotension Delayed Recovery
Arrhythmias Hypoxia Nerve palsies Shivering
Myocardial Ischemia Hypercarbia
Cardiac arrest Bronchospasm
1. Management of common Titrate the doses of opiods. Use appropriate dose

to avoid respiratory depression. Give adequate
complications during sedation to obese and gediatric patient.
Keep Flumazenil (antidote for Benzodiazepine)
General Anaesthesia & Naloxone (antidote for Opiods) ready to
manage complications of over dosage.
1.1 Aspiration: 1.6 Nerve Palsies
Position the patient appropriately to prevent
Follow appropriate fasting guidelines.
pressure on the nerves.
Administer anti-aspiration prophylaxis like H2
blocker, Proton pump inhibitors, In prone position avoid pressure on eyes ball
Metoclopramide. Ondensatron, Granisatron. and avoid over abduction of arms to prevent
Brachial Plexus injury.
Intuba te by rapid sequence technique in full
stomach patients. In lateral decubitus position, keep axillary roll
beneath axilla to pr event Brachial Plexus injury.
1.2 Hypercarbia In lithotomy position, care must be taken to
Ventilate appropriately as hypoventilation is the avoid injury to the lateral popliteal nerve.
commonest cause.
1.7 Hypothermia and Shivering
1.3 Hypertension Increase theatre temperature (210C for adults &
Maintain good plane of anaesthesia. 280C for children).
Use opiods for adequate pain relief Use warm intravenous fluids.
1.4 Hypotension Use warm blankets and forced air warming to
Manage blood loss appropriately. combat hypothermia.
Preload the patient adequately before spinal Use IV Dexamethasone or IV Pentazocine or IV
anaesthesia. Tramadol to treat shivering.
1.5 Post Operative Apnoea:
Commonly due to over dosage or sensitivity of
Barbiturates, Opiods and inhalational agent and
inadequate reversal.
Page 570
6. REGIONAL ANAESTHESIA
1. Indication: 6. Treatment of over dosage:
For the production of local anesthesia Treatment of patient with toxic manifestations
consist of arresting convulsions and assuring
2. Dosage and Administration: adequate ventilation with oxyge n, if necessary
The dose is adjusted according to the response by assisted or controlled ventilation (
of the patient and site of administration. respiration) if convulsions occur they must be
treated rapidly by intravenous injection of
3. Contraindications: Thiopentone 100 to 200mg. Alternatively,
Hypersensitivity knows to anaesthetics of the Diazepam 5 to 10mg may be used and Intralipid
amide type. Solution containing adrenaline is (1.5 mg/kg body weight.)
contraindicated for anesthesia of fingers, toes, Once convulsions have been controlled and
tip of nose, ears and penis. Bupivacaine is adequate ventilation of the lungs e nsured, no
contraindicated for i.v. regional anaesthesia other treatment is generally required. If
hypotension is present. However a vasopressor,
4. Precautions: preferably one with inotropic activity, e.g.
Shock, heart block, known drug sensitivity, Ephedrine 15 to 30 mg. s hould be given
liver disease, kidney disease, epilepsy, impaired intravenously in diluted from titrated dose.
respiratory function.
Anxiety or slight twitchng, a small intravenous
5. Adverse Reaction: dose of Inj Diazepam,ma y be given carefully
Over dosage ma y cause CNS reaction: and slowly; Oxygen s hould also be given. In
Numbness of tongue, light-headedness severe circulatory depression barbiturate such as
dizziness, and blurred vision, tremors, followed Thiopentone is contra-indicated when
by drowsiness, convulsions, unconsciousness convulsion has developed. Cardiovascular
and possibly respiratory arrest. Cardiovascular collapse is treated with vasopressors & plasma
reactions of over dosage include hypotension infusion, Inj intralippid
and myocardial depression.
Concentration dependent adverse reactions for Lignocaine

Plasma con. Mcg/ml Adverse reactions
4 Light-headedness, tinnitus, circumoral numbness
6 Visual disturba nce
8 Muscle twitching
10 Convulsions
12 Unconsciousness
20 Respiratory arrest
24 Circulatory depression
Chart No.1 DRUG TOXICITY OF LIGNOCAINE
Methae moglobinaemia may be treated by the

intravenous administrations of 1% solution of 7. Local Anaesthetics:
Methylene blue in a dose of 1mg/kg. Inj.Li gnocaine 2 % (3 to 4 mg/kg body
weight)
Inj. Lignocaine hydrochloride (2%) with
Page 571
Adrenaline (5 to 7 mg/ kg
body weight)
12. Explanatory Footnotes on
Inj. Ropivacaine ( 0.75%) or Inj. Above Protocol:
Bupivacaine (0.5 %).
12.1 Local Anesthetics:
8. Sedation: For consistency, 0.75% ROPIVACAINE is
Inj. Midazolam 0.05 mg/kg a nd Inj. Ketamine primarily used for blocks, with a dose of 20-
0.5mg/kg and Inj. Propofol infusions in 25- 40ml depending on the type of block
75mcg/kg/min range a nd deep sedation (50 to ropivacaine results in 12-24 hrs block duration.
100 mcg in drip for deep sedation) 2% Lignocaine for 3-4 hour duration. Mixing a
short acting and long acting local anaesthetic
9. Interscalene: together appears to significantly decrease the
Success rate in posterior interscalene (Cervical duration of the block.
PVBs) approach is more than a nterior-lateral
approach 12.2 Adjuncts:
1. De xamethasone 2-4mg and/or Clonidine
10. Spraclavicular 50-100ug for an average of 3-6 hour
increased duration
/Infraclavicular: 2. Epine phrine and Clonidine . Increase
inferior-posterior quadrant of plexus for duration of regional block .
Supraclavicular Block and Infra Clavicular 3. Inj. De xamethasone . 4mg to 8 mg dose
Block near posterior cord. as it may result in very prolonged blocks.
4. Bicarbonate . dose is 1meq/10ml. in Bier
11. Sciatic (Infragluteal): Block.
Infragluteal approach are more comfortable to
patients than classic Labat approaches.
Page 572
7. CARDIO PULMONARY- RESUSCITATION
(CPR)
CPR consists of a series of maneuvers by which perform cardiac massage if HR<60/min with signs of
oxygenated blood supply to brain and vital organs is poor perfusion.
maintained during cardiopulmonary arrest (CPA) i.e.,
3.1.2 Airway
cessation of respiration and circulation. In children,
Clear airway cleaning blood, secretions, foreign
CPA is not sudden but end result of long period of
particles (suction if available).
hypoxemia secondary to inadequate ventilation,
Prevent posterior displacement of tongue due to
oxygenation or circulation. Therefore, prompt
muscle relaxation during CPA, by head tilt and chin
management of these is essential to prevent CPA, the
or jaw thrust (may use an airway if available). Head
outcome of which is poor.
tilt: Put a hand at forehead and tilt head back to
sniffing or neutral pos ition in an infant and little more
1. Diagnosis of Cardiac arrest: in older children and adults. (Caution: In a patient
with suspected cervical spine injury head tilt should
1. Absence of pulse in major arteries (carotid or
be avoided) Chin lift: Put finger of other hand under
femoral in older children and femoral or brachial
bony part.
in infants as carotid is difficult to palpate due to
Jaw thrust: Place 2-3 fingers under each side of lower
short neck).
jaw at its angle and lift jaw upward with the elbow
2. Absence of heart sounds on auscultation.
resting on the surface on which victim is lying.
3. A systole / ventricular fibrillation on ECG.
3.1.3 Breathing
2. Respiratory arrest: Determine the absence of breathing. Give mouth to
mouth / nose / mask / airway breath (may use bag and
Absence of respiration on looking (absent chest mask if available). Inhale and then make a seal
movements), listening (absent air flow on bringing around the mouth and nose together in infant and seal
ears in front of mouth) and feeling (absent air flow on mouth only in older children and adults (nose
keeping hands in front of mouth or nose). pinched with the hand used for head tilt) to exhale
smoothly. Rate of breaths should be 20/min for
3. Levels of CPR: infants, 15/min in older child and 10-12/min in
adults.
There are two levels of CPR:
Rescuer should stand or kneel at the side of the
1. BLS (Basic life support) the elements of CPR patient so that his hips are on a level with the victims
provided without additional equipment, skill and chest.
speed are more essential.
In a newborn 2 thumbs are positioned side by side on
2. ACLS (Advanced cardiac life support) Use of
sternum just below the nipple line, with fingers
equipment and drugs for assisting ventilation or
encircling chest and suppor ting the back and
circulation.
compress sternum by 0.6 1.2 cm (120/min).
3.1 Basic Life Support: In an infant put inde x finger at the intersection of
intermammary line and sternum. Use 2 3 fingers
Call for help; position the victim supine on firm flat (index, middle and ring) to compress sternum by 1.5
surface with head level with the heart. As per New 2.5 cm (100/min) and do not lift the finger when
AHA 2014 Guidelines ABC (Airway Breathing compression is released. Two thumb encircling
Circulation) changed to CAB (Circulation - Airway hands technique can also be used.
Breathing ) and chest compression and rescue breath
ratio is 30:2. In children (1-8 years) use heel of hand on lower half
sternum with long axis of heel same as long axis of
3.1.1 Circulation sternum and compress 2.5 3.5 (100/min) In adults
Determine the absence of pulse after 2 breaths the heel of one hand is placed on the lower sternum
(rescue breaths). External cardiac massage if asystole and the other hand placed on top of the first. The
and unresponsive to rescue breaths. In children, elbows should be locked in position with the arms
straight and the shoulders over the hands. Sternum
Page 573
should depress by 3.5 5.0 cm and the rate of b) Inj. Lignocaine
compression should be 80 to 100/min. (CAUTION:
Do not exert pressure on the ribs, costal cartilages or Indication: Ventricular tachycardia or fibrillation non
xipoid) responsive to recurs after defibrillation. In adults:
Initials bolus dose is 1.5 mg/kg. Additional bolus of
3.1.4 Combination of ve ntilation and Cardiac 0.5-1.5 mg/kg can be given 5-10 minutes during CPR
massage up to a total dose of 3mg/kg. In children: Inj. 1mg/kg
If both cardiac and respiratory arrest Compression: IV stat followed by infusion at 20-50 mcg/kg/min.
ventilation = 30:2 in adults and children > 8; Children
and infants 1-8 years = 5:1; Neonates =3:1. c) Inj.Amiodarone
3.2 Advanced Cardiac Life Indication: Refractory shock with ventricular
Support (ACLS) fibrillation (as an alternative to or after failure of
Lignocaine). In adults : Initially 300 mg rapid
If ACLS facility is available, shift the patient to infusion in 20-30 ml saline followed by 150 ml over
ACLS as soon as possible. If this is not available then 10 minutes followed by 1 mg/min for up to 0.5
continue cardiac massage till spontaneous HR is mg/kg/da y.
more than 60-80/ min and continue Endotrachal
intubation with IPPV till adequate respiratory efforts d) Inj. Atropine
are present (good chest movement, no cynaosis or
shock). For ALCS proceed in the following order: Indication: Vegally mediated bradycardia during
intuba tion, HR<80 or asystole in an infant and
3.2.1 Procedures symptomatic bradycardia with AV block in any child.
I. ECG monitoring (if available) Dose and route : 0.02 mg/kg bolus (not <0.1 mg or>
0.5 mg for a child and 1.0 mg for an adult) This dose
a) If ventricular fibrillation defibrillation. may be repeated after 5 minutes for a maximum total
b) In adults, first shock at 200 Joules; if the first is dose of 1.0 mg for a child and 2.0 mg for an adult.
unsuccessful then a second shoc k at 200 -300 Joules.
If both fail, additional shocks at 300-360 Joules are e) Inj. Naloxone
given.
Indication: Narcotic overdose or poisoning and
In children, 2 Joules / kg and can be repeated a few
newborn resuscitation (if mother has been given
time (if does not revert to normal rhythm). Continue
Morphine or Pethidine during labour). Dose and
cardiac, massage in the mean time.
route 0.1 mg/kg IV.
c) All patients require oxygen (100%) because even
with best CPR, only a fraction of the cardiac output is f) Inj. Sodium Bicarbonate (NaHC03)
provided and also there are other factors causing
ventilation perfusion mismatch. Not required routinely as it can cause alkalosis later
d) Establish IV line as early as possible to give drugs and worsen respiratory acidosis by releasing CO2 in
and fluids and intubation of trachea should be done to inadequate ventilation. Indication : Hyperkalaemia,
continue artificial ventilation. significant metabolic acidosis (pH<7.2) or prolonged
CPR. In adults and in children : Inj. Sodium
bicarbonate 1 mEq/kg stat and 0.5 mEq/kg every
3.2.2 Drugs are used in the 10minutes in protracted resuscitation.
following order if indicated. g) Inj. Calcium
a) Inj. Adrenaline Indication: Not used routinely now a days unless

there is hyperkalemia, hypocalcaemia or calcium
Indication: A systole symptomatic bradycardia channel blocker toxicity. Dose and route : (in
unresponsive to ventilation. In adults: 1 mg IV every children) 0.5 ml/kg of Calcium gluconate IV. In
3 5 minutes. In children : 0.1 ml/kg of 1:10,000 adults 10 ml to be given as a slow infusion under
solution (0.01 mg/kg) IV, intra-osseous or 0.1 ml/kg ECG monitoring.
of 1:1000 solution by endotracheal tube followed by
several positive pressure breaths. Can be repeat every h) Inj. Glucose
5 minutes by either route. IV route is preferred and
Indication Hypoglycaimia Dose and route : - 0.5-1
should be used as soon as IV access is achieved
g/kg IV. Try to get ABG, serum electrolytes and
(Intracardiac route is not desirable).
Page 574
blood suger (dextrose stick /glucometer) post 3.2.3 Monitoring
resuscitation care.
Maintain mechanical ventilation for several Pulse should be palpable and chest expa nsion should
hours to ensure adequate oxygenation and be seen during effective CPR, blood pressure, Sp02,
ventilation. ET CO2 (In intubated patient and if facility
Look for and treat seizures. available), ABG should be monitored during and
soon after CPR.
Inj. Mannitol 0.5 -1 g/kg IV if raised intracranial
tension.
Maintain temperature, fluid and electrolyte 3.2.4 Termination of CPR
balance and ABG.
If asystole persists for >10 minutes after CPR has
Treat shock with fluids, dopamine, dobutamine
been performed, ventricular fibrillation eliminated,
and adrenaline infusion as required.
and confirmed, adequate ventilation provided and
Treat the underlying pa thology causing CPA.
appropriate medications given.
3.2.5 Summery of CPR
Table 1: CPR GUIDELINES FOR HEALTH CARE PROVIDERS
(Method, compression rate, and ventilation to compression ratio)

Adult Child Infant Newborn
(<8 yr) (< 1 yr)
Lone If known asphyxia arrest, 5 5 cycles of CPR Ventilation priority,
Rescuer cycles unless sudde n compressions for HR<60,
Priority CPR witnessed collapse
Compression 1-hand 2-thumbs 2-thumbs
method Or Or 2-fingers or 2-fingers
2-hands 2-Hand If single for access to
Rescuer umbilical vein
Compression Rate 100/min 100/min 100/min 200/min

Ratio of 30:2 until intubated. 30:2 until intubated. 30:1
compressions to 8-10 breaths/min 8-10 breaths/min
ventilations After ET. After ET.
Use of AED Immediate AED Immediate AED Consider No
Consider 5 cycles 5 cycles CPR if >4-5Min Recommendation
CPR if > 4-5 min Unwitnessed Arrest. (for infant &New Born)
Unwitnessed arrest
Page 575
PULMONARY EDEMA
Assist breathing as needed oxygen
Take blood pressure Begin working on IV line Cardiac monitor
Is arrhythmia the cause?
Due to Bradycardia? Due to tachyarrhythmia?

Bradycardia Algorithm Tachycardia Algorithm?
Sublingual Nitroglycerin 0.4 mg

Inj. furosemide 0.5-1 mg/kg IV
Propped position
Consider also:
Albuterol aerosol
positive airway pressure
Not responding?
Nitroprusside 0.1-5 mcg/kg/min
OR
Nitroglycerin 120-20 mcg/min
Consider intropic
support
Still in distress?
Consider intubation
Systolic BP>100? Systolic 70-100 or signs of shock?

Dobutamine 2-20 mcg/kg/min Dopamine 5-15 mcg/kg/min
Page 576
8. ANAESTHESIA OBSTETRIC PROTOCOL
1. Orientation 3. Antacid Prophylaxis
Labour room and the operation theatre should be All patients for elective Caesarean section must
connected with each other. All the anaesthetic receive oral antacid premedication. If the patient
equipments and preparations should be ready 24/7 posted for an emergency Caesarean section then
days apart from it. Laryngoscopes with stubby handle consider IV Metoclopromide 10mg, Inj. Ondensetron
and McCoy blade should be available. NICU and 4mg, IV Ranitidine 50mg, Emptying the stomach
prenatal ICU should be on the same floor. Emergency with a large orogastric tube, keep it until patient
drugs and plasma expanders (e.g. hetastarch & anaesthetised and up to e xtuba tion.
voluven) should be present in the O.T. Blood and
blood products should be available at nearest possible 4. Regional Anaesthesia for
place. Aanaesthesiologist should check for
anaesthesia machines, defibrillator, Oxygen, other Caesarean Section
equipments and the required dr ugs.
4.1. Advantages:
The avoidance of the hazards of aspiration of gastric
2. Labour analgesia with contents and failed intuba tion during general
epidural technique anaesthesia. A reduction in blood loss /
thromboembolism/absence of Neonatal depression.
2.1 General Aspects Postoperative analgesia may be provided using spinal
or epidural opioids.
i. Proper pre-operative evaluation with
counselling of the patient and the relatives. 4.2. Disadvantages:
ii. Explaining the procedure and its adva ntages
and disadvantages. Hypotension can occur due to aorto-caval
iii. Secure broad gauge I.V. cannula with starting compression despite the use of left uterine
I.V. with crystalloid for preloading. displacement and seemingly adequate preload.
iv. Epidural catheter inserted with standard
technique in lateral or sitting position under 4.3. Nausea and vomiting:
aseptic precautions at L3-L4, OR L4-L5 space. The incidence of this is often related to hypotension
No CSE should be performed above L1 level. and hence should be treated immediately. Nausea
v. The catheter should not be more than 2 to 3 following a regional block is an indication of the B.P.
cms inside the epidural space. Check for any fall. Consider giving 100% oxygen and legs up
fluid coming out of the catheter. position before iv Ephedrine. Use Oxytocin for
vi. Can give the analgesic dose of local uterine contraction.
anaesthetic agent, preferably 0.125% of
Bupivacaine about 8 ml with 2mcg / ml of Diclofenac-
fentanyl can be give n. Do not administer Diclofenac to those allergic to
vii. The dose can be repeated as per the patients NSAIDs. Do not give it to unstable asthmatics. Also
demand. The pt. should be haemodynamically avoid in those with renal dysfunction, peptic ulcer
monitored closely till the end of delivery. disease and severe pre-eclampsia especially if
viii. If interve ntion needed then continue the oliguria or thrombocytopoenia.
epidural anaesthesia with higher conc. of
Bupivacaine i.e. 0.5% around 8 to 10ml. can 5. General Anaesthesia for
be given for LSCS.
Caesarean Section
5.1 Pre operative assessment:
2.2 Complications
Thorough pre-operative assessment. 1. Antacid
Epidural-Bloody Tap prophylaxis. 2. NBM status. 3 informed consent
Patchy action or unilateral block from relatives 4. Make arrangement for blood and
blood products 5. Patients should be transferred to
Subdural Block
Page 577
theatre in left lateral position. 6. Administer Sodium epidural catheter intrathecally. Approximately 2cms
citrate prior to pre-oxygenation. 7. IV access 14G or should be threaded into the subarachnoid space. c)
16G cannula. 8. Position of the mother supine on the Remove the Touhy needle and insert at a different
table with 15 degree left lateral tilt with slight head level. Don't perform a CSE. Intrathecal catheter - top
up. 10. Pre-oxygenate the mother using 100% up only by the anaesthetist. You can administer
oxygen for 3 minutes unless there is severe maternal either: 1ml 0.25% Bupivacaine + 15-25g of
and foetal emergency. 10. ECG,NIBP and pulse Fentanyl as regular top up. Or 0.5 - 2ml of standard
oximeter during pre- oxygenation and ETCO2 is LDM as regular top up. After delivery remove
switched on. 11.Perform RSI using Thiopentone 5-6 catheter as usual. If epidural in situ treat as normal
mg/kg and Suxamethonium 1.5mg/kg. Intubate after intrathecal epidural, but each top-up to be given by
adequate action of Suxamethonium anaesthetist under strict aseptic conditions.
Ple a se re me mbe r - patie nts die from
prolonge d atte mpts to intubate le ading to
8. Central Neural Block
hypoxia and from unre cognise d oesophage al
int ubation and not from failure to intubate .
8.1. Indications:
"If in doubt, take it out" Ensure that the ETT is Labour analgesia. Anticipated difficult or operative
correctly placed by observing the capnograph trace delivery (e.g. multiple pregnancy, breech, premature
and by listening to breath sounds. Give Atracurium foetus). Obstetric disease (e.g. pre-eclampsia).
when Suxamethonium action wears off. Maternal disease (e.g. specific cardiac, respiratory or
neuromuscular disease). Surgery during pregnancy
5.2 Intubation Hints:
i. Optimise the patient's position. A smaller ETT is
8.2. Contraindications:
often needed in obstetrics. An unexpected This list contains both absolute contraindications:
invisible larynx is often due to incorrectly Patient Objection. Local Sepsis, Coagulopathy
applied cricoid pressure. And short stubbed Relative contraindicat ions- Haemorrhage
laryngoscope or polio blade. An anterior larynx with hypovolaemia, Raised intracranial pressure,
just out of reach of the ETT can usually be Some forms of anticoagulant therapy, Disease of the
cannulated with a well lubricated gum elastic nervous system, Gross spinal deformity, Systemic
bougie. sepsis, Severe foetal distress.
6. Anticoagulation and 8.3. Central Neural Block - Special

regional anaesthesia Considerations
i. The incidence of epidural haematoma is less Low Platelet Count: A platelet count of <50000
than 1: 100,000 is an absolute C/I to a regional block.
ii. NSAIDS are not a contraindication to CNB. Enoxaparin /L MWH: Many patients at risk of
iii. Enoxaparin 40mg sc post-operatively. venous thrombos is are on daily sub cutaneous
iv. If the woman is on antenatal Enoxaparin.
thromboprophylaxis. a) Enoxaparin should be Unfractionated Heparin (UH): If UH has been
stopped 12 hours prior to performing CNB. b) given, wait 4-6 hours before siting an epidural
Epidural catheters should be removed 2 to 4 block. Remove the epidural catheter at least 4
hours prior to administration of Enoxaparin hours after the last dose of UH.
v. Heparin a) Heparin should be stopped 4 hours Aspirin: Patients on aspirin can have a regional
prior to attempting neuraxial blockade or block. A bleeding time is not required.
removal of epidural catheters. b) Pre-eclampsia (PIH): Patients with mild to
Unfractionated Heparins should not be moderate PIH should have a recent (within 24
administered for 2 to 4 hours after catheter hrs) platelet count before a regional block.
removal. Maternal Pyrexia: Administer antibiotics.
Haematological Disorders: The most common
7. Management of a Dural tap type of patient presenting for regional
blockade are Haemophilia Carriers and
Don't pa nic! Place you thumb against the hub of the
patients with Von Willebrand's Disease.
Touhy needle, relax and think. You have 2 options: a)
HIV: HIV is not a Conba Indications to a
Can give 0.5% Bupivacine 2 2.5 CC intrathecally
regional block nor indeed to a blood patch.
and do LSCS under spinal anaesthesia b) Insert
Page 578
Standard high risk precautions should be b) All patients should be given blood of their
taken when instituting a block. Consider own group as soon as possible. However for
double glove protection / eye protection / do patients with severe haemorrhage,
not resheath needles when performing a uncrossmatched group O, Rh negative can be
block. lifesaving.
Prolapsed Intervertebral Disc (PIVD) c) The principles of intelligent management are:
Epidural or spinal analgesia / anaesthesia are While blood is gushing out it is useless and
not contraindicated. wasteful to give clotting factor or platelet
Harrington Rods / Spinal Instrumentation replacements. Once surgical haemostasis has
Many of these patients have severe scoliosis been more or less achieved, continued oozing
with consequent cardiorespiratory may be due to blood clotting factor
compromise. The surgical site should be deficiencies. Further blood samples should be
avoided. The epidural needle should be sent for coagulation screen and platelet count.
advanced towards the convexity of the curve. d) If there is massive blood loss the MASSIVE
Multiple Sclerosis (MS) MS is a CNS TRANSFUSION PROTOCOL should be
demyelinating disease with an incidence of instigated. This will ensure that FFP is
1:10,000. It is a disease of relapse and available and platelets are ordered. While FFP
remission. can up to a point be issued "blind" as already
mentioned, the possibility of low platelets or
DIC may need different blood components for
9. Placenta Praevia their correction. This can only be identified by
9.1. Anaesthetic management: laboratory testing.
e) A pressure bag system is essential in order to
Ensure adequate IV access (2x 14 or 16G infuse fluids rapidly.
cannulae) f) Use a blood warmer as soon as possible.
Two anaesthetists preferable if Grade 4, g) Blood filters are NOT needed and will slow
previous praevia or previous LSCS; this is dow n transfusion.
mandatory if proceeding under regional (see h) Early use of CVP monitoring and direct
below). arterial pressure monitoring.
Manage major haemorrhage according to i) Think ahead to order blood and blood
guidelines. products in plenty of time.
Anaesthetic technique - considerations: j) Use the Hemocue (available in Theatre) to aid
estimation of transfusion requirements.
9.2.6 Measure the patient's temperature.
9.2. Action: 9.2.7 Additional Calcium is rarely needed and only
9.2.1 Ensure adequate airway / conscious level. if there is evidence of a calcium deficiency.
Give high flow oxygen. 10% calcium chloride is preferable to calcium
9.2.2 At least 2 peripheral lines will be needed of gluconate.
not less than 14- 16G. If the decision is made 9.2.8 Treatment of the cause may involve delivery
to set up invasive monitoring, it must not of baby and placenta, repair of lacerations and
interfere with resuscitation. administration of oxytocics (Oxytocin
9.2.3 Prevent aorto caval compression. Ergometrine; 15- methyl PGF2a [Carboprost -
Hemabate]; PGE2 [Misoprostol].
9.2.4 Take at least 20ml of the patient's blood for: 9.2.9 All patients with more than moderate
Blood grouping / cross matching continuing haemorrhage need proper
Full blood count monitoring of pulse rate, CVP, blood gases,
Coagulation studies (including fibrinogen / and urinary output as well as dedicated care by
FDP's if abruption or other cause of DIC the midwifery and medical staff. Serious
suspected). consideration should be given to the potential
9.2.5 Blood Transfusion adva ntages of transfer to a n HDU.
a) Order a minimum of 4 units of blood.
Page 579
9. SPINAL ANAESTHESIA
incidenc of headache than conve ntional cutting edge
1. Definition: needle.
Spinal anesthesia is produced by introducing a Hyper
local anesthetic into cerebrospinal fluid in the Pre existing neurological deficit has to be
subarachnoid space result in to loss of sympathetic documented i.e. Diabetic neuropathy, Hansons
tone, sensation and motor function. disease, Traumatic neuropathy
Sympathetic block is 2-3 segments higher than the 2.3 Drugs used for spinal anesthesia
sensory and the motor block 2-3 segment lower than
the sensor y block. HEAVY-
Position 1) Sitting 2) lateral 1) Inj.Lignocaine 5% solution 2)Inj.Bupivacaine
0.5% solution 3) Inj. Ropivacaine 0.75% solution
with adjuva nt-1) Inj.Clonidine 2) Inj.Buprigesic
2. Approach - Median and par
median. 2.4 Advantages
2.1 Saddle block given in sitting 1) Economical 2) Minimum equipment required 3)
position by hyperbaric Control hypotension and bradycardia reduces the
bleeding at the site of surgery 4) less respiratory
anesthetic drug. infection 5) Less incidence of thromboembolic and
Spinal cord usually ends at the level of L2 in adult pulmonary complication 6) Useful in sickle disease /
and L3 i n children. trait and in Diabetic patient (Less stress related
hyperglycemia )
Important land mark is that line joining the top of the
iliac creast corresponds to L4-5 2.5 Contraindications
2.2 Practical implication- 2.5.1 Absolute
While administering spinal anesthesia spinal needle Allergy to local anesthetics, Local infection at needle
pierce 1) Skin 2) Subc utaneous fat 3) Supraspinious insertion, Increased intracranial pressure (herniation
& Interspinious ligament 4) Ligamentum flavum 5) of brain stem)
Epidural space 6) Dura 7) sub arachnoid space. 2.5.2 Relative-
Patient is adequately prepared, with the procedure Hypovolaemia, Anticoagulation treatment, Systemic
fully explained, has reliable intravenous access, is in sepsis, Neurological diseases- multiple sclerosis,
a comfortable position and resuscitation equipment is tabes dorsalis, syringomyelia, amyotrophic lateral
immediately available. sclerosis, Tumors of the spine, Airway compromise,
To be done under all aseptic precaution. Read the Low back pain and peripheral neuropathies,
label. haemorrhagic CSF.
Patient should be well hydrated and NRM at list 6 2.6 Complications-
hrs.
2.6.2 Peri-operative
Strict intra operative vital parameters monitoring is
mandatory. Height of analgesia is directly hypotension due to vasodilatation and brady-cardia
proportional to curvature of spinal column and due to increased vagal tone as a result of sympathetic
volume of drug, specific gravity, force and rate of blockaed, Respiratory insufficiency due to intercostal
injection, barbotage technique. blockde, Poor anaesthesia because of loculations of
arachnoid.
Small bore needle make smaller hole in the dura i.e.
separate caudafilum and are associated with a lower 2.6.3 Post- Operative-
Page 580
Headache due lo leakage of CSF or aseptic one Inj. Ephedrine 30 mg (6mg/cc) Inj.
inflammatory reactions, Urinary retention, Backache, Phenylepinephirine. Inj Noradrenaline, Infusion.
Infection,- Meningism, arachnoiditis, transverse (titrated)
myelitis or the cauda equine syndrome with varying
2.7.2 Total Spinal -
patterns of neurological impairment and sphincture
disturbances. Para-paresis and rarely paraplegia due Needs to be quickly recognized and treat patient will
to the anterior spinal artery syndromei.e initially be unable to talk louder that a whisper and
prolonged vasospasm of the anterior spinal artery by will then stop breathing. These patients have to be
the vasoconstrictor adjutants or due to prolonged intubated and ventilated until the local anaesthetic
uncorrected hypotension. effect wears off and also maintain the hemodynamic
stability.
2.7.3 Headac he post dural puncture headac he
2.7 Treatment- (PDPH)-
1 Hypotension Nausea and vomiting may be the Encouraged to drink water, give intrave nous fluids to
first sign of hypotension .Give adequate I.V.Fluid maintain adequate hydration, strict bed rest,
Oxygen by mask, increasing the patients circulating Paracetamol, Aspirin or Codeine tea, coffee, epidural
volume is by raising their legs, Vasopressors drug blood patch, Tab. Samaritan.
Page 581
PATHOLOGY
Page 582
1. INTRODUCTION
The Pathology department basically deals with

diagnosis of disease by means of various types of
3) Section III
tests performed on body fluids, blood and tissues. Biochemistry section:
It is divided into 4 Sections: It deals with different types of biochemical terms
to detect functions of liver, kidneys, Lungs, heart
etc.
1) Section I
Haematology section: 4) Section IV
Inwhich the blood e xamination and Urine and
Stool examination done to detect any Histopathology
abnormality like anemia,leukemia, Renal &Cytopathology:
Infection and bow el infection and infestation
In this section mainly tissue cell morphology is
studied to detect infection/tumor in body.
2) Section II
Serology section:
It deals with the Rapid terms to detect
M.P.,typhoid,V.D.,H.I.V.etc.along with
blood culture to detect typhoid etc.
Page 583
2. HAEMATOLOGY SECTION
Blood is one of the most common specimens studied in
1. Specimen Collection: laboratories. Blood will clot within few minutes after it
is removed from the body unless an anticoagulant is
Every specimen must be accompanied by a request used.
slip, which should indicate date, patients full name,
age and sex, hospital identification number, name of 1.1.1. Whole Blood:Blood with anticoagulant is called
referring doctor, provisional diagnosis, kind of whole blood.
specimen, laboratory services and equipped, exact time 1.1.2. Plasma: Fluid portion of unclotted blood is
the specimen was obtained and the name of the person called plasma and is obtained from anticoagulated
who collected the specimen with signature. It is blood.
necessary that the request slip be complete and clearly
written. Incomplete information may lead to total loss 1.1.3. Serum: Fluid portion of clotted blood and is
of the report. obtained from clotted blood, which is collected without
any added anticoagulant.
Specimens should be processed as early as possible.
Temporary storage in refrigerators is advisable except 1.2. Anticoagulant:
for C.S.F. and specimens submitted for bacteriological
cultures. Urine and other body fluid should be The anticoagulant prevents the blood from clotting.
processed as early as possible (Before 2 hrs.) as delay Most of anticoagulants remove calcium. Which is one
causes disintegration of cells and loss of morphology. of factor required for coagulation.
1.1. Blood:
Table 1: Various types of bulbs & its uses
Sr. Type of bulb Content(Anticoagulant) Used for

No.
1 EDTA Na and K salt of EDTA Routine Haematological work
2 Trisodium Citrate Sodium Citrate ESR
3 Heparin Heparin PCV, Osmotic Fragility test
4 Double Oxalate mixture NH4 and K Oxalate CBC, Blood Group
5 Sodium Fluoride Na Fluoride and K Oxalate Sugar
1.3. Vaccutainers: 1.3.2. GREY Cap: Sodium fluoride + Pot oxalate for
glucose estimation
These are plastic tubes with coloured cap with capacity
of3-5ml blood used in laboratory now a days. These
may be with or without vacuum.(The small glass 1.3.3. PURPLE Cap: Potassium EDTA for CBC, Hb,
bottles can also be used for sample collections after it TLC, DLC, PBS (Peripheral Blood Smear),
is properly prepared). The colour of the cap indicates Reticulocyte count, ESR
the presence of anticoagulant present inside the tubes.
The label is attached with the tube for patients
identification. Following are the types and uses. 1.3.4. LIGHT BLUE Cap: 3.2% sodium citrate for
1.3.1. RED Cap No chemical for serum separation coagulation studies (PT, APTT, TT, FDP, D-Dimer,
(Biochemistry and Serological test) Factors VIII & IX assay)
Page 584
2. Hemoglobin Estimation 2.2. Principle
When blood is added to N/10 HCL, Hb is converted to
2.1. SAHLI`S (Acid Haematin) brown coloured acid Haematin. The resulting colour
Method after dilution is compared with standard brown glass
This method used in small laboratories at PHC level. reference blocks of Sahlishaemoglobinometer.
Table 2: Haemoglobin estimation according to Sahli's method
Sr.
Test Name Methods Normal Value Interpretation
No.
1 Haemoglobin a) Sahlis Method Male 13-18gm/dl Mild Anaemia up to 10gm%
b) Hemocue Method Female 12-16.5gm/dl Mod. Anaemia up to 8 gm%
c) Cellcounter Method Pregancy 11-14gm/dl Severe Anaemia below 7gm%
Raised Hb- Polycythaemia
Table 3: WHO classification for Anaemia
Population Non Anae mia Anaemia(Haemoglobi n in grams per litre)

Mild Moderate Severe
Children 6 - 59 months of age 11 or higher 10 - 10.9 7 - 9.9 Lower than 7
Children 5 - 11 years of age 11.5 or higher 11 11.4 8 - 10.9 Lower than 8
Children 12 - 14 years of age- 12 or higher 11 11.9 8 - 10.9 Lower than 8
Non-pregnant women (15 years of 12 or higher 11 11.9 8 - 10.9 Lower than 8
age and above)
Pregnant women 11 or higher 10 10.9 7 - 9.9 Lower than 7

Men (15 years of age and above) 13 or higher 11 12.9 8 - 10.9 Lower than 8
3. Leucocyte count: 3.2. Automated Differential

3.1. Peripheral blood smear: Leucocyte Counting:
This system is able to replace manual differential
Preparation and staining of peripheral blood film is
leucocyte count to a great extent. When any abnormal
performed for doing total leucocyte count (TLC) and
cell count or abnormal morphology of cells in seen,
differential leucocyte count (DLC).
this system shows a flagging thereby suggesting a
visual count mandator y in such cases.
Page 585
Figure 3: Various types of White blood cells
Sr.
No.
2 Total Leucocyte Manual by counting 4000-11000/cells mm Raised TLC in viral Bacterial -
count TLC Infections, Leukemia's
Cell counter method
Decreased TLC - Septicemia,
Enteric fever, Aplastic Anemia.
3 Differential Cell Counter Polymorphs 40-65% Raised in Acute Bacterial
Leucocyte count Infections.
(DLC) Manual by staining Lymphocytes 20-35% Raised in chronic infection like
Slides tuberculosis, leprosy
Eosinophils - 2-4% Raised in worm infestation,
allergic skin infection, Tropical
Eosinophilia -
Monoc ytes - 2-8% Raised in viral infection
Basophils - 0-1% Raised in Leukemia's
erythroc ytes in a given interval of time is the ESR

4. Estimation of erythrocyte (erythrocyte sedimentation rate).
sedimentation rate (ESR): Stages in the ESR three stages in the ESR can be
observed:-
4.1. Principle: i. In the initial 10 minutes, there is rouleaux
When well mixed anticoagulated blood is allowed to formation.
stand undisturbed in a vertical tube the erythroc ytes ii. For about 40 minutes, sedimentation occurs at a
tend to sink to the bottom. Two layers are formed the constant rate.
upper plasma layer and lower one of red blood cells. iii. Sedimentation slows in the final 10 minutes as
The length of fall of the top of the column of cells pack at the bottom of the tube.
Page 586
Sr.
No.
4 ESR Wintrops Tube Method Male 0-10 mm at 1 hr. Raised in chronic infection like
Westergren tube Method Female 0-20mm at 1 hr. tuberculosis, leprosy, chronic
anemia.
4.2. Interpretation or clinical 6. Clotting time:

significance of ESR:
The whole blood clotting time is one of the simplest,
ESR is markedly elevated in monoclonal blood protein
imprecise, methods to determine the efficiency of the
disorders, such as multiple myeloma or
clotting process. Many conditions can disrupt the
macroglogulinemia, polyclonalhyperglobulinemia, due
pathways that produce a clot, including hereditary
to inflammatory disease and in hyperfibrinogenemia.
disorders, liver disease and drugs that interfere with the
Moderate elevations are seen in active inflammation
normal function of platelets and coagulation factors.
such as rheumatoid arthritis, chronic infections such as
tuberculosis, collagen diseaseand neoplastic disease.
Although ESR is a nonspecific phenomenon, this an METHODS:
indicator of the presence of an active disease. If patient i. Capillary tube method
is improving ESR tends to fall. It provides an index of
ii. Lee and white method
progress of diseases such as TB, rheumatoid arthritis. It
is also a useful screening test in routine examination.
An elevated ESR occurs as an early feature in Normal Range for clotting time 5-10 minutes.
myocardial infarction.
ESR is especially low in (0-1 mm) polycythaemia, 7. Prothrombin Time:
hypofibrinogenemia, CHF, and sickle cell anaemia.
PT test is an indicator of the efficiency of common
5. Bleeding time: pathway and extrinsic coagulation pa thway, in which
This test measures the time taken for blood vessel preformed thromboplastin is added to the test plasma
constriction and platelet plug formation to occur. No in the presence of calcium and the time taken for
clot is allowed to form, so that the arrest of bleeding clotting of plasma is noted. The main factors involved
depends exclusively on blood vessel constriction and in the pathway are V, VII, X, II and I. Deficiency of
platelet action. This is one of the most important any one of them leads to prolongation of PT. The PT
preliminary test for bleeding disorders and test is used to monitor patients taking certain
preoperative investigation in patients going for medications (e.g. Control of anticoagulant therapy) as
surgery. well as sensitive to the presence of heparin in blood
The duration of bleeding from a standard puncture and to low fibrinogen levels.
wound of the skin is a measure of the function of
platelets as well as the integrity of the vessels wall.
Commonly used methods are: Dukes Method &Ivy's
Method.
Bleeding t ime is prolonge d in:

i. Thrombocytopenia (Dengue Fever) - DIC
(Disseminated Intravascular Coagulation)
ii. Acute Leukaemia - Von Willebrands disease
iii. AplasticAnaemia - Aspirin intake
Page 587
Sr.
No.
5 Bleeding Time Duke's Ivy's Method 1-5 min Raised in Coagulation defect,
B.T. vasoculotoxic snake bite, rat
poisoning, Hemophilia's, ITP.
6 Clotting Time Capillary method 4-9 min
C.T.
7 Prothrombin Time Quicks method or 12-16 sec
P.T.
Semi- 12-16 sec Raised P.T. (factor no. II V, VII,&
automatedcoagulometer X)
8. Test for sickle cell anaemia

Sickle cell test is done for all ANC patients, forall Initially the patients are screened by Solubility test. If
population in tribal area & also done for all patients of Solubility test comes positive, then it is confirmed by
severe anaemia. Hb Electrophoresis.
Sr.
No.
8 Sickle cell Solubility test or Sickle (Hbs) Present & less than
Anemia Hemoglobi n 40% is sickle cell trait or
Electrophoresis test or
(Hbs) is carrier
HPLC method nor mally absent
Hbs more than 40% is
sickle cell disease
Laboratory Tests
1. Routine screening tests (in any haematology 8.1. Sickling test
laboratory) Na Metabisulphite is used
2. Definitive or special tests (in reference laboratory)
Cells form sickle shape under low Oxygen tension
Laboratory testing
3. Screening tests Homozygotes 1 hour at 37 C
4. Sickling test
Heterozygotes longer time
5. Solubility test
Figure 2 Sickling Test showing sickle cell
Page 588
8.2. Solubility Test Working solution : 10 ml of stock solution + 0.1g
Na dithionate just be fore use
Reagents : Phosphate Buffer (pH 7.1)
Procedure : 20 ul RBCs (washed) + 2ml working
Stoc k solution : KH2PO4 125 g solution
K2HPO4 217 g Read after 10 minutes
Saponin 2.5 g
DW gsp 1 litre
Figure 3 Solubility Test
8.3. Confirmatory Test by ii. The detection of metabolic or systemic disease

not directly related to the kidneys.
Electrophoresis
Confirmatory test for HbS after Hb electrophoresis iii. Microscopic examination of the sediment may
indicate the kind of lesion present or the state of
Reason: Sensitivity is 93% compared to HPLC activity of a lesion.
Cannot differentiate between Hb AS & HBSS 1. Collection of Urine:-
Preliminary test in remote area but confirmation For routine work 15 ml or more is preferred and it
must be done by HPLC or Hb electrophoresis should be collected in a clean container, after properly
cleaning the external genital area to avoid vaginal
URINE EXAMINATION
secretions and cellular debris of the urethral meatus.
The urine examination is referred to as a liquid tissue
2. Specimen Evaluation:
biops y of the urinary system
This includes proper labelling (name, date and time of
It is useful in - collection), proper specimen, proper receptacle, storage
condition, preservative (Thymol, formaldehyde if
i. Diagnosis and management of renal or urinary
added)
diseases.
Page 589
3. Physical Examination: Green+
Following parameters are looked for:
Greenish Blue++
i. Quantity
Blue+++
ii. Colour.
Deep Blue++++
iii. Appearance
5. Microscopic Examination:
Character. Examination of urinary sediment the specimen
should be examined while fresh since casts begin to
iv. Odour
lyse within 1 to 3 hrs. Mix the specimen well. Take 10
v. Specific gravity ml of urine in centrifuge tube, centrifuge at 2000
rotation /min for 5 minutes. Remove the supernatant.
4. Chemical examination Place a drop of sediment of slide and put a cover slip.
i. Test for Proteins Examine under both low power & high power
ii. Reducing Substances in Urine(Urine for Sugar) Cells RBC, WBC, Epithelial cells.
iii. Ketone Bodies Cast - Hyaline, granular, epithelial, WBC cast, RBC
cast, Fatty, waxy.
iv. Bile Pigments
Crystal and amorphous chemical deposits
v. Bile Salts
Miscellaneous Mucus, spermatozoa, bacteria, yeast,
parasite
4.1 Benzidine Test (for occult blood)
Compare the urine strip results with the colour on
Results: Faint Green-Trace bottle
Table 1:Urine Examination
Finding Interpretation
A ROUTINE EXAMINATION
1 Physical examination
1.1 colour Yellow, redish Yellow in Hyperbilirubinema, red in Hematuria
1.2 appearance - clear / turbid Turbid in UTI, Nephrotic syndrome, Preeclampsia, Eclampsia.
2 Chemical Examination
2.1 Albumin - +/- UTI, Nephrotic syndrome, Preeclampsia, Eclampsia
2.2 Sugar - +/- Diabetes, Hyperglycemia
2.3 Ketone bodies - +/- Present in starvation, Diabetic ketoacidosis.
2.4 bile salts & Bile pigment - +/- Present in Hyperbilirubinema,
B Microscopic Examination
1 No of RBCS / HPF Hematuria, renal calculi, nor mal menses
Page 590
2 No. of Pus cells/ HPF UTI
3 No. of Epithelial cells /HPF Normally present
4 Casts - Present /Absent Nephropathy
5 Crystals - Present / Absent Present in Calciurea (OxalatePhosphate,Ureate crystals)
6 Trichomonas - Present / Absent It is motile parasite
7 Spermatozoa - present /absent Present in contamination with semen
8 Bacilli - present / absent UTI
9. Detection of Malaria Parasite 2. Interpretation:

In case of positive test, band for respective kind of
byMalarial Antigen test (RDK) malaria is visible.
Malaria is serious, sometimes fatal, parasitic disease
characterized by fever, chills and anemia caused by a In case of negative test, band is absent.
parasite that is transmitted from one human to another
by the bite of infected Female Anopheles Mosquitoes. 3. Peripheral blood smear for
There are four kind of malaria that can infect humans: Malarial Parasite
Plasmodium Falciparum, Plasmodium Vivax,
Plasmodium Ovale and Plasmodium Malaria. Specimen collection by using Lancet
1. Principle: Pierce tip of finger with sterile lancet & take one drop
Malaria antigen kit contain a membrane strip which is of blood on clean glass slide & spread it with the help
pre-coated with one monoclonal antibody and one of spreader to make thin blood smear
polyclonal antibody as two separate lines across Fixation- Fix the blood smear by alcohol spray or spirit
attached strip. One monoclonal antibody (test line PF)
are specific to the HRP-II (Histidine Rich Protein- II, Staining of smear-Staining of blood smear by field A
Specific to Plasmodium Falciparum) and other & B stain.
polyclonal antibody (Test Line PAN) are Pan specific Microscopic Examination of peripheral smear:- After
to the Lactate dehydrogenase of plasmodium species applying oil on smear with the help of oil emulsion
(P. Falciparum, P. Vivax, P.Malariaeand P.Ovale). lens screen the morphology of RBC's & any of the
following form of Malarial parasite.
Malaria Thick & thin smear Ring form Ring form - multiple small rings - Falciparum,
Detection under oil emulsion Trophozoit / schizoit single large ring - vivax
form, Gametocyte form Trophozoit / schizoit form
Commonly present Gametocyte form in
Falciparum.
Fig. 4: Different form of Malarial Parasite.
Page 591
Plasmodium falciparum
Maurers Dots
Trophozoites
Gametocytes
Plasmodium vivax
Schuffners Dots
Trophozoites
Gametocytes
Schizonts
10. Rapid test for Leptospirosis

1. Principle:-Qualitative and differential definition
of IgG and /or IgM antibody to Leptospira in
human serum or plasma. It is only a screening
test.
2. Method:-Rapid test is solid phase
immunochromatographic assay.
Page 592
3. Sample:-Serum or plasma. 1. Collection of Sample:-
Take approximately 5-10gm of stool passed by the
4. Procedure:-Remove test device from sealed
patient at the end of de fecation, it is usually semi
pouch and place horizontally. Add 5 micro liter
solid with the half of wooden spatula (Ice cream
of plasma or serum in sample well(s) Added 4
stick) into a plastic container with cap (Urine
drops of diluents in another well provided. Read
collection cup). Morning sample is preferred and
interpretation in 20 minutes.
is transported to laboratory immediately.
5. Interpretation:-
2. Preservation of Faecal Sample:-
1) Negative only one color line at control in When sample cannot be examined immediately or
result window . it has to be transported. The sample of stool is
made into thin paste with tap water. To this an
2) Positive equal part of steaming 10% formalin and left for a
IgM positive- Two color lines at control (c) and few hours. The supernatant is discarded. It should
at Ig M (M) be noted that formalin preserved oval become in a
IgG Positive- Two color lines at control (c) & at ratio of 30:1 to stool sample. Ova can be examined
IgG for about one month.
IgM and Ig G Positive -Three color lines at 3. Examination of Stool for Ova and cyst
control (c), IgM (M) &IgG
Methods
3) Invalid Test No control line in & result
window. i. Direct Smear
- No color line in (c) & also in Ig M (M) and / or Ig G. ii. Concentration by floatation method
result window iii. Direct Centrifugal floatation.
Examination of stool for ova and cysts
Stool Examination:
Finding Interpretation
A Routine Examination
1 Physical Examination
1.1 Colour - Black, White, Red 1. Black in Occult blood in upper G.I. bleed. 2.Redish in lower G.I.
bleed, 3,white in biliary obstruction
1.2 Consistency - soft, loose, hard, Loose in Diarrhea & Dysentery , Hard in chronic constipation
semisolid
1.3 Wor ms Adult worm - AscarisLumbricoides pin worm (small sound worm)
2 Chemical Test
2.1 Reducing subs tance for Lactose intolerance in infants
2.2 Occult blood upper G.I. bleed

B Microscopic exam
1 PUS cells +/- / HPF Diarrhoea&Dysentry
2 RBCS +/- /HPF lower G.I. bleed
3 OVA & Cyst Cyst of 1.Entamoeba histolytica, Giardia Lamblia 2,Entersobins
vermicularis (Pinworm) 3,Ancylostoma duodenale ( Hook worm)
4. Taeniasolium (Tape Worm)
4 mucous +/- AmeboebicDysentery
Page 593
11. Sputum for AFB 3. Direct Examination of Sputum
Work safely with the sputum as it is
infectious.
1. Introduction:
If possible bleach the specimen with 5%
Sputum should be obtained from the lower sodium hypochlorite or bleach (1:1)
respiratory tract(Bronchi of the lung) Saliva
produced by the salivary gland in the month is not 4. Acid fast staining (Ziehl-Nelson
sputum, but is frequently and mistakenly sent to the
laboratory instead of sputum. method)
Note:-Purity of the specimen should be checked Result:
true sputum should contain fewer than 10 All acid fast bacilli are not pathogenic. So the
squamous epithelial cells and more than 25 result should be reported as-
leucocytes/ low power filed.
o AF organism present or positive.
2. Specimen Collection: o AF organism absent or negative.
The patient should be instructed prope rly as to the
type of the specimen required. Specimen is Technician should examine 10 microscopic
collected in the early morning. It must be coughed fields under oil immersion and then repor t as
up from deep down in the chest. Apply the aerosol follows.
technique if the patient is unable to produce the
required specimen.
Page 594
3. SEROLOGY SECTION
Serological tests usually done in laboratory are pneumonia. Any positive result must be confirmed by
broadly classified into following two groups. other serological assay (e.g. TPHA).
Agglutination Tests: This group includes tests like
Widal test, VDRL test, RA factor test, Blood Group
2. HBsAg Test
test, ASO test, CRP test, HbsAg test etc.
Rapid Tests (Also known as Spot/ Line Tests) :
2.1. Principle:
This group includes tests like, HbsAg test, HIV The HBsAg one-step Hepatitis B surface antigen test
test, Dengue test, Malaria test, Hepatitis C test device (serum/plasma) is a qualitative, solid phase,
etc. two-site sandwich immunoassay for the detection of
Serological Tests: HBsAg in serum or plasma.
Various serological tests are done for diagnosis of 2.3. Interpretation:

diseases. Here we are discussing common serological
tests like VDRL, HBsAg, HIV, Widal, RA factor, Double line- Positive
dengue antibody test.
Single line with control - Negative
1. RPR Test for Syphilis 3. Rheumatoid factor test
(VDRL) Principle
The RPR carbon reagent is a stabilized suspension of
The RF reagent is a suspe nsion of pol ystyrene latex
cholesterol crystals coated with cardiolipin. Lecithin is
particle sensitized with specially prepared Human IgG.
added to adjust the sensitivity and charcoal particles to
When serum containing RF is mixed with the latex
improve the reading of the reaction. The reagent act as
reagent visible agglutination occurs. When serum
antigen against antibodi es present in person suffering
containing greater than 0.8mg/dl RF is mixed with the
from syphilis caused by Treponemapallidum. Reagins
latex reagent, visible agglutination occurs.
are a group of antibodies against some components of
the damaged tissue from patient infected by Result: In pos itive case agglutination occurs.
Treponemapallidum.
This test is rapid method for diagnosis of syphilis, 4. ASO titer
macroscopic agglutination indicate positive result.
Principle
1.1. Storage: It is an immunological reaction between streptococcal
exoenzyme bound to biologically inert latex particles
Kit should be stored at 2-8C and protected from light. and streptococcal antibodies in the test specimen.
When serum containing greater than 200 IU/ml of
1.2. Patient Sample: ASO titre is mixed with the latex reagent, visible
Fresh serum (Free of Haemolysis) agglutination occurs.
Result: In pos itive case agglutination occurs.
1.3. Interpretation of Result:
Medium & Large aggregates against white back
5. Widal test
ground Reactive
Principle
Finely dispersed aggregates against white back ground Widal kit contains killed bacterial suspension of
Weak Reactive salmonella which carries specific Oand H antigen.
This react with immunospecific antibodies present in
No aggregates, even grey back ground - Non Reactive
the sample resulting in agglutination.
False positive results can be seen in diseases like
leprosy, SLE, infectious mononucleosis, malaria, viral
Page 595
6. HIV Tridot spot test 3. Requirement: -
Confirmation with Elisa test
Glass slide, covers tip, pipettes, Neubauer counting
chamber, pH paper, semen diluting fluid, wide mouth
7. Dengue container for semen collection.
Spot test Elisa test
4. Specimen-
8. Urine Pregnancy Test (UPT) Freshly Collected Semen
1. Principle: - 5. Physical Examination:

Qualitative detection of human chorionic gonadotropi n Colour, volume, viscosity of semen.
(HCG) in urine in early detection of pregnancy.
6. Chemical Examination-
2. Method: pH, Detection of fructose in semen.
Pregnancy test device (Urine) is rapid chromatography
immunoassay for qualitative detection of HCG. 7. Microscopic Examination:
3. Sample: Under low and high power
Study of sperm motility & its percentage
Early morning sample for early detection of pregnancy Morphology's Abnormal forms & its percentage
Pus cells, RBC or epithelial cells / HPF
4. Interpretation Determination of sperm count with help of
Neuba uer chamber & semen diluting fluid.
Negative:-
Note: It is necessary to note while reporting for routine
One coloured line appears in control line region and no semen examination
any coloured line appears in test region (+)
Abstinence- da ys
Positive:- Method of sample collection
One coloured line in control and other coloured line in Time & place of Sample collection
test. Swine Flu Diagnosis / Sample collection
Invalid test:- Principle - Detection of H1N1 (swine Flu) Virus by
polymerase chain Reaction (PCR) method.
No colour line in control (c).
Sample- Throat & nasal swab
9. Semen Analysis/Examination. Reagent- Sterile swab, Viral Transport media (VTM)
1. Indication: Procedure- One throat swab & nasal swab by sterile
swab should be taken & place in one VTM with
(a) To rule out male infertility universal precaution
(b) Post vasectomy VTM is kept at 2 to- 8C & transported to virology lab
by maintaining temperature with icepack in thermocol
2. To perform routine examination container or vaccine carrier
of semen Detail History sheet should be provided with sample.
Page 596
Common Rapid Test:
1 Leptospirosis RDK card method Positive/Negative IgM indicates recent infection

detected for of Lepto, IgG indicates old
Leptospirosis infection of Lepto
2 Dengue RDK card method Dengue NS1, IgG&IgM Dengue NS1present in 1st 5
can be detected for days of infection,IgM
Dengue indicates recent infection of
Dengue, IgG indicates old
infection of Dengue
3 HIV RDK card method HIV I & II can be HIV I or II & HIV I & II can
detected be detect.
4 HbsAg RDK card method Positive/ Negative Hepatitis B viral infection
detected for Hepatitis B
5 Malaria RDK card method Pl Vivax& PL Pl. Vivax& Pl. Falciparum is
Falciparum can be detected
detected
6 UPT RDK card method Positive / negative Pregnancy can be detected
detected for pregnancy
7 Widal Test Rapid Agglutination Positive /Negative to Enteric /Typhoid Fever can
Method detect Enteric /Typhoid be detected
Fever
8 CRP Test Rapid Agglutination Positive/Negative to detected in infection &
Method detected infection & septicemia
septicemia
9 RA Test Rapid Agglutination Positive/Negative to detected in Rheumatoid
Method detected Rheumatoid Arthritis
Arthritis
10 VDRL Rapid Agglutination Positive/ Negative to Detected in Syphilis infection
Method detected Syphilis
infection
Page 597
4. BIOCHEMISTRY SECTION
Biochemistry tests usually done in labor atory include 6) SGPT
following tests. These tests are done with available 7) Alkaline Phosphatase
standard biochemical kits on semi-automatic / fully 8) Serum Total Proteins
automated auto-analyzer. Procedure, method and 9) Serum Albumin
interpretation varies as per available kit. 10) Serum Na/K/Cl
11) Serum LDH
1) Blood Sugar
12) Serum Cholesterol
2) Blood Urea/ Blood Urea Nitrogen
13) Serum HDL Cholesterol
3) Serum Creatinine
14) Serum Triglycerides
4) Serum Bilirubin
5) SGOT
Page 598
5. HISTOPATHOLOGY
1. Definition: 3. Fixation
It is a branch of pathology which deals with the study 3.1. Definition:
of disease in a tissue section.
The tissue undergoes a series of steps before it reaches It is a complex series of chemical events which brings
the examiners desk to be thoroughly examined about changes in the various chemical constituents of
microscopically to arrive at a particular diagnosis. cell like hardening, however the cell morphology and
structural detail is preserved.
To achieve this it is important that the tissue must be
prepared in such a manner that it is sufficiently thick or Unless a tissue is fixed soon after the removal from the
thin to be examined microscopically and all the body, it will undergo degenerative changes due to
structures in a tissue may be differentiated. autol ysis and putrefaction so that the morphology of
the individual cell will be lost.
The objective of the subsequent discussions will be to
acquaint the staff with their responsibility; the basic 3.2. Principle of fixation:
details of tissue handling, processing and staining.
The fixative brings about crosslinking of proteins
The term histoche mistrymeans study of chemical
which produces denaturation or coagulation of proteins
nature of the tissue components by histological
so that the semifluid state is converted into semisolid
methods.
state; so that it maintains everything in vivo in relation
The cell is the single structural unit of all tissues. The to each other. Thus semisolid state facilitates easy
study of cell is called cytology. manipulation of tissue.
A tissue is a group of cells specialized and 3.3. Tissue Processing
differentiated to perform a specialized function.
Collection of different type of cells forms an organ. The tissue processing is the heart of any tissue section
which will be cut adequately only if the tissue is
2. Type of material obtained in properly preserved and processed. The study of this
laboratory: topic is to understand the coarse and fine details of
tissue processing so that excellent sections are
The human tissue comes from the surgery and the
obtained.
autops y room.
From surgery two types of tissue are obtained. 4. Staining
i. As biopsy- A small piece of lesions or tumor The sections, as they are prepared, are colourless and
which in sent for diagnosis before final removal different components cannot be appreciated. Staining
of the lesion or the tumor (Incisional biopsy). them by different coloured dyes, having affinities of
specific components of tissues, makes identification
ii. If the whole of the tumor or lesion is sent for
and study of their morphology possible.
examination and diagnosis by the pathologist, it
is called excisional biopsy. Tissues from the
autopsy are sent for the study of disease and its
course, for the advancement of medicine.
Page 599
6. CYTOLOGY STUDY
Cytology is divided into four groups fix by bio fixatives and are stained with PAP
stain.
1) Fine needle aspiration Results
cytology (FNAC) Nucleus - blue
Cytoplasm and background pink
It is done for diagnosis of any lump/mass in
body. With the help of 20 bore needle fine
aspiration from any lump or mass in the body is
3) Body fluid cytology
done. And smear is made from aspirated material It is done on CSF / Pleural fluid / Ascitic fluid /
is fixed with bio fixative and stained with Synovial fluid etc. All the body fluids are
Haematoxylin and Eosin staining(H & E). examined for physical / chemical examination.
Cell count is done on neubars chamber. The
Results smear of the deposited material is stained with
Nucleus - blue leishman stain, Gram stain and ZN stain.
Cytoplasm and background pink
4) Bronchial lavage cytology
2) Exfoliative cytology Smears are stained with H&E, Gram stain, a nd
ZN stain.
It is done in the female patients to diagnose
gynecological pathology. The cervical smears
Page 600
7. BLOOD BANK
Blood grouping(ABO & Rh 1.3. Methods for ABO Grouping:
system) The two main methods of ABO grouping for a routine
blood bank are:
There are more than 300 blood group systems but
ABO and rhesus (Rh) systems are of impor tance from i. Slide method: The slide test is not recommended
clinical point of view. These are inherited characters as it is not reliable. It is less sensitive than the
which give rise to antigen-antibody reactions. tube test. The slide is prone to drying effect that
may be wrongly interpreted as agglutination.
1. ABO system: ii. Tube method: The tube method is recommended
It was discovered by Landsteiner in 1900. The red cells
because:
contain different types of antigens (Agglutinogen),
while plasma contains antibodies (Agglutinins). In 1.1. It allows longer incuba tion of antigen-antibody
order to determine the blood group of a subject, the red mixture without dr ying.
cells are allowed to react with a sera containing known
1.2. Tubes can be centrifuged which enhance
antibod y (Agglutinin).
antigen-antibody reactions.
1.1. Practical aspects of ABO 1.3. Both cell and serum grouping can be performed.
grouping: 1.4. Weaker antigens and antibodies can be detected.
Routine ABO grouping must include both cell and 1.5. Less reagents are required.
serum grouping as each test serves as a check on 1.6. Results can be read comfortably as there is no
the other. drying.
ABO groupi ng test should be done at room
temperature. Testing at 37 C weakens the 2. Rh blood group system:
reaction. Rh blood group system was first reported Landsteiner
and Weiner in 1940.
Tubes, slides, reagents and microplates should be
labelled properly. In contrast to ABO system, Rh antigens are present on
red blood cells only and Rh antibodies develop only in
Serum should be added before adding cells and response to a known stimulus. Rh factor is present in
examine each tube after serum has been added. 85-95% of human beings.
Tubes or slides should be clean and dry and
disposable plastic tubes may be used. 2.1. Methods of Rh Grouping:
Microscope should be used to examine reactions The two main methods of Rh groupi ng for a routine
that appe ar negative by naked e ye. blood bank are:
Results should be recorded immediately after i. Slide method: The slide test is not recommended
observation. as it is not reliable. It is less sensitive than the
tube test. The slide is prone to drying effect that
1.2. Blood sample may be wrongly interpreted as agglutination.
ii. Tube method: The tube method is recommended
Clearly labelled samples of blood in plain tubes. because:
No sign of haemolysis should be there.
1.1 It allows longer incuba tion of antigen-antibody
If serum has not completely separated or become mixture without dr ying.
clear, centrifuge the blood sample at 1000-3000
rpm for 3 minutes. 1.2 Tubes can be centrifuged which enhance
antigen-antibody reactions.
Take one to two millilitres of serum in pipette and
place into a prelabeled tube for serum grouping 1.3 Both cell and serum grouping can be performed.
and other tests. 1.4 Weaker antigens and antibodies can be detected.
Page 601
1.5 Less reagents are required
4. Procedure of blood
1.6 Results can be read comfortably as there is no
drying. TRANSFUSSION: Important aspects:
The blood bag received in the ward for transfusion to
2.2. Interpretation: the patient is to be maintained at room temperature for
one hour, so that it will come to the body temperature.
i. Agglutination in the tube test and in the tube Pretransfusion medication to patient is done half hour
positive control and smooth suspension of before blood transfusion.
cells in the tube negative control: This is The blood bag should not be warmed in hot water
interpreted as test cells Rh (D) positive. otherwise hemol ysismay take place.
Do not transfuse the blood bag immediately after
ii. A smooth suspension of red cells in tubes of receiving because at that time the blood bag is at 4 to 6
test and negative controls and agglutination degree centigrade.Transfusion of cold blood may get
in the tube labelled as positive control: This is transfusion reaction.
interpreted as test cells Rh (D) negative. Rate of blood transfusion should be such that it will
iii. Blood Donor red cells found negative should be take 4 hours to transfuse the ba g. In emergency the
further tested by AHG test for weak D. clinician will take decision.
During transfusion the patient is monitored for body
iv. If in any test negative control gives temperature/ pulse/blood pressure/respiratory rate and
agglutination or positive control does not give watch for transfusion reaction.
agglutination, the results are invalid.
4.1. Blood transfusion reaction:
3. Cross Match
1) Febrile
Major crossmatch: Recipients serum is cross 2) Pain
matched with donor red cells for IgM and IgG 3) Jaundice
antibodies compatibility. 4) Allergic
Minor crossmatch: Donor serum is cross 5) Other
matched with recipients red cells for IgM and In case of blood transfusion reaction, BTO should be
IgG antibodies compatibility. If donors serum informed immediately after stopping blood transfusion
is tested negative for unexpected or irregular and blood bag along with blood transfusion reaction
antibodies, minor crossmatch can be avoided. card duly filled should also be returned to blood bank.
If incompatibility is not detected in cross
matching, then it is likely that the donor blood 4.2. Complication of blood
transfused into patient will survive normally. transfusion reactions-
Finding of incompatibility indicates that i. Haemolytic transfusion reactions which could be
transfusion of such blood is potentially immediate or delayed.
dangerous and further steps should be taken to ii. Allergic reactions like 1) Fever 2) Anaphylactic
identify the antibod y. reaction 3) Allergic reactions 4) Graft versus- hos t
Note: It is mandatory to test the blood for the diseases
following transfusion transmissible infections before it iii. Circulatory overload leading to pulmonary
is taken on stoc k and issued to the patient. congestion and acute Heart failure,
thrombocytopenia & dilution of coagulation factors.
i. HIV antibod y screening by ELISA iv. Transmission of infections e.g. Hepatitis B & C,
ii. Hepatitis B surface antigen (HBsAg) by ELISA malaria, HIV Infection, syphilis, infectious
iii. Hepatitis C antibody by ELISA mononucleosis, toxoplasmosis.
iv. Syphilis by RPR test
v. Malaria by thick and thin blood smear or In case of blood transfusion reaction, for carrying out
malaria antigen. investigations pre and post- blood transfusion patients
After the testing is complete, the blood bag is labelled blood and urine sample is needed. Blood bag along
and then taken on stoc k and used for crossmatch and with blood transfusion reaction card duly filled should
issue to the patients. also be returned to blood bank by the medical officer.
Page 602
8. NORMAL LAB VALUES
Hematology
Hemoglobin
: 13.5-17.5 g/dl
:12.0-16.0 g/dl
Hematocrit : 39-49%
:35-45%
Red Blood Corpuscles : 4.3-5.7 (108/ul )
:3.8-5.1 (108/ul )
Platelet 150-450 103/ul
White Blood Cells (differential below) 4.5-11.0 103/ul

Neutrophils 57-67%
Lymphoc ytes 22-33%
Monoc ytes 3-7%
Eosinophils 1-3%
Basophils 0-1%
Erythroc yte Sedimentation Rate (ESR) :<15mm/hr
:<20mm/hr
Ferritin : 20-250 ng/ml
:10-120 ng/ml
Fibrinogen 150-350 mg/dl
Haptoglobin 26-185 mg/dl
Hb A1c 5.0-7.5%
Mean Corpuscular Hemoglobi n 26-34 pg
Mean Corpuscular Hemoglobi n Concentration 33-37%
Mean Corpuscular Volume 80-100fl
Prothrombin Time 10-14 sec
Activated Partial Prothrombin Time 20-40 sec
Reticulocytes 0.5-1.5%
Total Iron Binding Capacity 250-400 ug/dl
Transferrin 200-400 mg/dl
Chemistries
Sodium 135-145 mEq/l
Potassium 3.5-5.3 mEq/l
Page 603
Chloride 95-105 mEq/l
Bicarbonate 22-29 mEq/l
Blood Urea Nitrogen 10-26 mg/dl
Ceratinine 0.6-1.3 mg/dl
Glucose 70-115 mg/dl
Anion Gap 7-16 mEq/l
Osmolality 275-300 mOsm/kg
Calcium Total 8.5-10.5 mg/dl
Calcium Ionised 4.65-5.28 mg/dl
Magnasium 1.3-2.4 mEq/l
Phosphate 2.5-4.5 mg/dl
Alfa Fetoprotein <10 ng/mol
Albumin 3.5-5.5 g/dl
IgA 70-312 mg/dl
AgG 640-1350 mg/dl
IgM 56-350 mg/dl
Lactate 0.5-1.3 mEq/l
Protein (Total) 6.0-8.0 g/dl
Uric Acid : 3.0-7.4 mg/dl
:2.1-6.3 mg/dl
Zinc 55-135 ug/dl
Liver/Pancreas
SGOT/ALT 0-40 IU/l
Alkaline Phosphatase : 38-126 U/l
: 70-230 U/l
Ammonia 10-50 umol/l

AST/SGPT 7-40 IU/l
Bilirubin (Total) 0.2-1.0 mg/dl
Bilirubin (Conjugated) 0-0.2 mg/dl
Lecithin dehydrognax 90-190 U/l
Amylase 25-125 U/l
C Peptide 0.7-1.89 ng/ml
Lipase 10-140
>60yo: 10-180
Lipids
Page 604
Total Cholesterol <200 mg/dl
Low density Lipoproteins <130 mg/dl
High density Lipoproteins : >29 mg/dl
: >35 mg/dl
Triglycerides : 40-160 mg/dl
: 35-135 mg/dl
Other
Phosphokinase : 38-174 U/l
: 26-140 U/l
Phosphokinase MB <5%
Acid Phosphatase <0.8 IU/ml
B12 100-700 pg/ml
CA-125 <35 U/ml
Copper (Cu) : 70-140 ug/dl
: 80-155 ug/dl
Folate 3-15 ng/ml
Lead (Pb) <10 ug/dl
Zinc (Ionized) 70-150 ug/dl

Blood Gases
Arterial Venous
Ph 7.35-7.45 7.32-7.42
pCO2 35-45 41-51
pO2 80-100 25-40
HCO3 21-27 24-28
Oxygen Saturation 95-99%
Urine
Ph 5-9
Minimal Vol ume 0.5-1.0 mg/kg/hr
Specific Gravity 1.015-1.030
Osmolality 600-1400 mOsm/kg
Creatinine : 14-26 mg/kg/day
Page 605
: 11-20 mg/kg/day
Creatinine Clearance : 100-150 ml/min
: 90-140 ml/min
* Rough estimate only varies with BMI
Urea Nitrogen 12-20 g/day
Calcium (Ionized) 100-300 mg/day
Potassium (Ionized) 25-125 mEq/day
Sodium (Ionized) 40-220 mEq/day
Phosphate 0.4-1.3 g/day
Uric Acid 250-750 mg/day
Albumin 10-100 mg/day
Amylase 1-17 U/hr
Glucose <0.5 g/day
Protein 10-100 mg/day
CSF
Pressure 60-180 mmH2O
White Blood Cell 0-5 /ul
Protein 15-45 mg/dl
Glucose 40-80 mg/dl
Synovial Fluid
White Blood Cell <200 /ul
Trauma, OA, SLE <3,000/ul
Gout. RA >4,000/ul
Septic >60,000/ul
Protein <3.0 g/dl
Glucose >50 mg/dl
Uric Acid <8.0 mg/dl
Endocrine
Aldosterone Supi ne: 3-10 ng/dl
Upright: 5-30
Cortisol 0800h: 6-23 g/dl
1600h: 3-15 g/dl
2200h:50% of 0800h value
Gastrin <100 pg/ml
Growth Hor mone (<60yr) : <2 ng/ml
Page 606
: <10 ng/ml
Growth Hor mone (>60yr) : <10 ng/ml
: <14 ng/ml
Estrogen Follicular: 60-200 pg/ml
Luteal: 160-400 pg/ml
Menopa use: 130 pg/ml
Follicle stimulating Hormone Follicular: 1-9 mU/ml
Ovulation: 6-26 mU/ml
Luteal: 1-9 mU/ml
Menopause: 30-118 mU/ml
Luteinizing Hor mone Follicular: 1-12 mU/ml
Mid-Cycle: 16-104 mU/ml
Luteal: 1-12 mU/ml
Menopause: 16-66 mU/ml
Progesterone Follicular: 0.15-0.7 ng/ml
Luteal: 2.0-25 ng/ml
Prolactin <20 ng/ml
Para Thyroid Hormone 10-65 pg/ml
Sperm 20-200 million/ml
Testosterone Free 52-280 pg/ml
Total 300-1000 ng/dl
T3 Uptake 0.82-1.18
Total 100-200 ng/dl
T4 Total 5.0-12.0 g/dl
Free 0.3-2.3 ng/dl
Thyroid stimulating Hormone <10 uU/ml
>60yo : 2-7.3 uU/ml
>60yo : 2-16.8 uU/ml
Toxic Levels
Acetaminophen >200 ug/ml
Ethyl Alcohol (in a non-alcoholic patient) Intoxicated >100 mg/ml
Lethargic >200 mg/ml
Coma >300 mg/ml
Resp. Distress Death >500 mg/ml
Page 607
Ethylene Glycol >20 mg/dl
Lead >100 ug/dl
Salicylate >300 ug/ml
Differential of Cerebral Spinal Fluid
Opening
Glucose Protein
Color Pressure Cells (#mm3)
(mg/100ml) (mg/100ml)
(mmH2O)
Adult (nl) clear 70-180 45-80 0-5 lymphs 15-45
Newborn clear 70-180 2/3 serum 40-60 lymphs 20-120
Page 608
9. LABORATORY TESTS PERFORMED
Clinical Services Rural / Sub-district District Hospitals and all
PHC
Related to: hospital 100 bedded hospitals
Viral infection Blood smear Blood smear Blood smear, serology test
Bacterial Infection Urine exam, blood smear, Urine exam, blood smear, Urine exam, blood smear,
sputum examination, Widaltest,CSF exam, Widal test, CSF exam,
Gram stain, ZN stain Gram stain , ZN stain serology , Gram stain, ZN
stain
Protozoal Urine exam, Stool, Urine exam, Stool, Urine exam, Stool,
Malarial parasite Filaria Malarial parasite, Rapid Filaria,Blood smear
Blood smear malaria test,Filaria, Blood
smear,
STD Urine exam, Blood smear Urine exam, Blood Urine exam, Blood
smear,HIV& VDRL tests smear,HIV& VDRL tests,
serology
Poisoning cases Urine exam, Blood smear Urine exam, Blood Plasma Cholinesterase,
smear, S.creatine in aluminum
phoshpmide poisoning
Animal Bites Urine exam, Blood smear Urine exam, Blood smear Urine exam, Blood smear
Environmental disorders Urine exam Urine exam, Blood Urine exam, Blood smear,
smear,
Sr Creatinine & urea
Sr Creatinine & urea
Gastro-intestinal Tract Stool exam, Blood smear Stool exam, Blood Stool exam, Blood smear
Disorder smear,Total Eosinophilic
Total Eosinophilic count
count
Respiratory disorder Sputum Gram & AFB Sputum Gram & AFB Sputum Gram & AFB stain
stain exam, Blood smear stain exam, Blood smear exam, Blood smear
Cardio-vascular Disorder Urine exam, Blood smear Urine exam, Blood Urine exam, Blood smear,
smear, SGOT Sr CMB, Troponin,
Hematological Disorder Hb %,Blood smear Hb %,Blood smear, Hb %,Blood smear,
sickling tests, BT & CT sickling tests, RBC
indices,BT, PT, APTT
Page 609
DENTISTRY
Page 610
1. DENTAL CARIES
Dental caries is a microbial disease of the Cavity formation and food lodgment.
calcified tissues of the teeth, characterized by Sensitivity if caries reaches to the dentin.
demineralization of the inor ganic por tion and Pain and swelling in vicinity area if pulp is
destruction of the organic substance of the involved due to caries.
tooth Periapical abscess & draining sinus in
advancedstages
1. Signs and Symptoms:
Grayish black discolouration of tooth in pit
and fissure areas.
Dental Caries
Figure 1
2. Diagnosis: 2.2 Tactile Examination:

Includes determining roughness or softness of tooth
2.1 Visual Examination : surface / discontinuity of enamel with a sharp
For visual examination teeth should be cleaned, explorer. Discolouration of pits and fissures may be a
dried with compressed air and illuminated under universal finding in nor mal healthy adult teeth may
adequate light source and observe for cavitation, be mistaken for presence of caries.
surface roughness, opacity of marginal ridge or
occlusal area, discolouration. 2.3 Radiographic investigation:
Figure 2OPA X-Ray Showing Radiolucent Carious lesion
Page 611
Radiograph shows dental caries and its extent as
radiolucent lesion due to demineralization of
tooth structure.
Figure 4: Stages of Dental Caries
3. Treatment: 4. Prevention of Dental Caries

Avoid extreme hot and cold beverages. 4.1 Diet modification / Dietary
Restoration of cavitated lesions if limited to
enamel and de ntin. counseling:
Endodontic therapy for pulp involvement due to
caries.
4.2 Maintenance of oral hygiene:
4.2.1 Daily removal of plaque by tooth-
Abscess drainage followed by endodontic brushing/flossing/rinsing is the best measure for
therapy
preventing caries and periodontal disease.
Tooth extraction may be performed in advanced 4.2.2 Proper brushing technique
cases when conservation of tooth structure is 4.2.3 Flossing should be done in the interdental areas
critical. to maintain the proximal surface clean.
Figure 5
4.2.4 Antimicrobial Agents: USE OF FLUORIDE:
a) Antimicrobial agents like chlorhexidine, a) Systemic use: systemic fluoridation can be
fluoride, antibiotics available to help prevent achieved by community water fluoridation
caries. (1ppm) in the areas of low fluoride content
b) 0.12 0.2% Chlorhexidi ne mouth rinse (below 1ppm).
prescribed for home use at bedtime as a 30- b) Topical use:
second rinse.
Self-application: Daily use of fluoridated toothpastes
4.2.5 Fluorides: and mouthwashes
To reduce caries risk primarily achieved by systemic Professional application: application on tooth
and topical fluoridation. surfaces.
Page 612
a) Use of APF gel 1.23%. Sealants mechanically fills pits and fissures with
an acid resistant resin.
b) Use of 2% sodium fluoride.
Renders pits and fissures easier to clean by tooth
brushing and mastication.
5 Pit & fissure sealants:
KEY MASSAGE:
Avoid sticky and food with rich sugar content.
Brush the teeth twice a day with prope r brushing technique.
Visit your doctor every six months for regular dental check up and get the treatment done at early
stages.
Page 613
2. DISEASES OF DENTAL PULP AND
PERIAPICAL TISSUES
Diseases of the dental pulp initiate dental pain of The pain persists for several minutes to
pulpal origin can be due to pulpitis, apical hours, lingering after removal of the
periodontitis periapical abscess. thermal stimulus.
In early stages the pain is sharp shooting,
piercing while in later stages pain is more
1. Pulpitis is an inflammation severe and is generally described as boring,
of pulp may be acute or gnawing or throbbing and may be more
intense.
chronic. Inspection generally discloses a deep cavity
extendi ng to the pulp or decay under
1.1. Acute reversible pulpitis:- filling. The pulp may be already expos ed.
Mild to moderate inflammatory conditions of pulp 1.2.2 Investigation:
caused by noxious stimuli in which pulp is capable of Radiograph may disclose an interproximal
returning to the uninflamed state following removal cavity, or may suggest involvement or
of the stimuli. expos ure of pulp, c aries under filling.
Vitality Test.
Sharp momentary pain on exposure to sweet 1.2.3 Treatment:
or thermal stimuli (cold). Removal of inflamed pulp tissues with
It does not occur spontaneously and does not endodo ntic therapy.
continue when the cause has been removed. Cap. Amoxicillin 250/500mg 3 times a
Reacts normally to percussion, palpation and day for 3 to 5 days.
mobility and the periapical tissue is normal Tab. Diclofenac 50mg 1BD for 3 days.
on radiograph.
1.1.2 Treatment: 1.3. Chronic pulpitis:
Removal of etiology and restoration of the 1.3.1 Clinical features:
tooth.
It occurs as the chronic type of pulpal
Cap. Amoxicillin 250/500 mg 3 times a day disease from its onset.
for 3 to 5 days.
Dull pain is present which is more often
Tab. Diclofenac 50mg 1BD for 3 days. intermittent and there is a delayed response
in vitality testing.
1.2. Acute Irreversible 1.3.2 Treatment:
pulpitis:- Endodontic treatment
A persistent inflammator y condition of pulp
symptomatic or asymptomatic caused by a noxious 1.4. Chronic hyperplastic
stimulus.
pulpitis (Pulp polyp):
It is a productive pulp inflammation due to an
1.2.1 Clinical features: extensive carious exposure of a young pulp.
Sharp pain usually caused by thermal
stimuli and can occur spontaneously.
Chronic hyperplastic pulpitis
Page 614
Figure 1 Figure 2
1.4.1 Clinical features

Occurs generally in children and young
1.2 Investigation:
adults. Radiographic examination may show a thickened
Involved teeth with large, open carious periodontal ligament or a small area of rarefaction if
lesions. a pulpless tooth is involved and it may show normal
periradicular structures if a vital pulp is present.
1.4.2 Signs & Symptoms:
1.3 Treatment:
Chronic hyperplastic pulpitis is
symptomless, except during mastication, If the inflammation is caused by occlusal trauma it
when pressure of the food bolus may cause should be relieved by selective grinding. If due to
discomfort. spread of pulpal infection RCT is indicated.
Pulp appe ars as a pinkish red globule of Cap. Amoxicillin 250/500 mg 3 times a day for
tissue protruding, from the pulp chamber 3 to 5 days.
1.4.3 Investigation: Tab. Metronidazole 200/400 mg 1BD for 3
days.
Radiograph shows large open cavity with Tab. Diclofenac 50mg 1BD for 3 days.
direct access to the pulp chamber.
2. Acute alveolar abscess:
1.4.4 Treatment: Acute alveolar abscess is a localized collection
of pus in the alveolar bone at the apex of a
Elimination of the polypoid tissue followed tooth following death of pulp with extension of
by RCT, provided the tooth can be restored the infection through the apical foramen into
otherwise extraction is needed. periradicular tissue.
Cap. Amoxicillin 250/500 mg 3 times a day
for 3 to 5 days.
Tab. Diclofenac 50mg 1BD for 3 days.
2.1 Clinical features:
The patient has severe throbbing pain with
2. Diseases of periapical swelling of the ove rlying soft tissue.
tissues: Pus may exude through tiny openings.
1. Apical periodontitis: 2.2 Treatment:
Apical periodontitis is a painful inflammation of the
periodontium as a result of trauma, irritation or Establishing drainage and completion of RCT
infection around the root apex regardless of whether after subsidence of symptom is done.
the pulp is vital or non- vital. Cap. Amoxicillin 250/500 mg 3 times a day
for 3 to 5 days.
1.1 Clinical features: Tab. Metronidazole 200/400 mg 1BD for 3
There is pain on mastication and tooth is tender on days.
percussion. Tab. Diclofenac 50mg 1BD for 3 days.
Page 615
3. Chronic apical periodontitis: It isa serious sequel of periapical infection that often
results in a diffuse spread of infection throughout
(periapical granuloma): medullary space, with subsequent necrosis of variable
Localized mass of chronic granulation tissue formed amount of bone.
in response to infection.
3.1 Clinical features:
Severe pain, trismus and parasthesia of lips
The involved tooth is non- vital and slightly tender to in case of mandibularinvolvement and
percussion. Patient may complaint about mild pain on manifests an elevation of temperature with
biting. The patient feels tooth is slightly elongated in regional lymphadenopathy.
its socket. The teeth in the area of involvement are
3.2 Radiographic examination loose.
Pus exude from gingival margin.
Periapical granuloma appears as a radiolucent area of In the maxilla the disease is well localized to
variable size attached to root apex. the area of initialinfection and in mandible
3.3 Treatment: bone involvement is more diffuse &
widespread.
Root canal treatment with or without subsequent Radiograpically: little evidence of its
apicoectomy. presence until the diseasehas developed for
Cap. Amoxicillin 250/500mg 3 times a day for 3 to 5 at least one to two weeks. At this time
days. diffuse lytic changes in the bone, radiolucent
Tab. Metronidazole 200/400mg 1BD for 3 days. areas begin to appear, ill- defined margins
Tab. Diclofenac 50mg 1BD for 3 days. and have moth- eaten appearance.
4. Radicular cyst: 5.1.2 Treatment:

It is slowly growing epithelial cyst at the apex of the General principles of management include
tooth. Radicular cyst presupposes physical, chemical
or bacterial injury resulting in death of pulp. Debridement
Drainage and
4.1 Clinical features: Cap. Amoxicillin 250/500 mg 3 times a day
The majority of cases are asymptomatic. The for 3 to 5 days.
associated tooth is non- vital or shows deep carious Tab. Metronidazole 200/400 mg 1BD for 3
lesion or a restoration which is seldom painful or days.
even sensitive to percussion. Tab. Diclofenac 50mg 1BD for 3 days.
4.2 Investigation: If sequestrum is small it gradually exfoliates through

the mucosa.If large, surgical removal may be
Roentogenographic features:-Radiolucent area necessary unless proper treatment is instituted. Acute
surrounded by radiopaque border attached to root suppurative osteomyelitis, may proceed to
apex. development of periostitis, soft tissue abscess or
4.3 Treatment: - cellulitis.
Involved tooth is extracted and periapical tissue is
carefully curetted.
5. Osteomyelitis: 5.2 Chronic Suppurative osteomyelitis:

Inflammation of bone and its marrow contents. It may develop in inadequately treated acute
5.1 Acute suppurative osteomyelitis: osteomyelitis or may arise from dental infection
without preceding acute stage.
Page 616
Chronic Suppurative osteomyelitis
Figure 3
Figure 3.5
5.2.1 Clinical features Occur at any age but is most common in

Similar to acute suppurativeosteomyelitis older person especially in edentulous areas.
except all signs and symptoms are milder.The Vague pain, unpleasant taste and mild
suppuration may perforatethe bone and overlying suppuration with the spontaneous for mation
skin or mucosa to form fistulous tract and empty on of fistula when acute exacerbation of
surface . dormant chronic infections.
5.4.2 Investigation:
5.3 Chronic focal sclerosing osteomyelitis: Radiographic feature: - Diffuse patchy,
A reaction to mild bacterial infection entering sclerosis of bone often described as cotton
the bone through a carious tooth in persons who have wool appearance. Radiopaque lesion may be
a high degree of tissue resistance and tissue extensive and is sometimes bilateral. The
reactivity. border between sclerosis and normal bone is
5.3.1 Clinical Features indistinct.
Most commonly in children and young 5.4.3 Treatment:
adults. Conservative treatment of acute episodes by
Commonly invol ve mandibular first molar antibiotic administration.If the tooth is present
Mild pain associated with an infected pulp in one of these sclerotic areas must be
5.3.2 Investigation: extracted.
Cap. Amoxicillin 250/500mg 3 times a day for 3
Radiographic features show well
to 5 days.
circumscribed radiopaque mass of sclerotic
Tab. Metronidazole 200/400mg 1BD for 3 days.
bone surrounding and extending below the
apex of carious tooth involving one or both
roots. Intact lamina dura. Periodontal
ligament space is widened.
5.3.3 Treatment: Extraction of carious tooth. The
sclerotic bone constituting the osteomyelitis is
not attached to the tooth and remains after the 5.5 Chronic osteomyelitis with proliferative
tooth is removed. Surgical removal of sclerotic Periostitis:
lesion is not indicated unless symptomatic. There is focal gross thickening of periosteum
Cap. Amoxicillin 250/500mg 3 times a day for with peripheral reactive bone formation
3 to 5 days. resulting from mild irritation or infection.
Tab. Metronidazole 200/400mg 1BD for 3 5.5.1 Clinical feature:
days. Occurs exclusively in the mandible, in
Tab. Diclofenac 50mg 1BD for 3 days. children and youngadults and most cases
5.4 Chronic Diffuse sclerosing osteomyelitis: occur in the bicuspid and molar region.
It is a proliferative reaction of the bone to low- The patient complains of toothache or pain
grade infection. Portal of entry for the in the jaw and a bony hard swelling on outer
infection is through diffuse periodontal surface of jaw.
disease. 5.5.2 Radiographic features:
5.4.1 Clinical feature:
Page 617
Intra oral periapical X- ray will reveal a 5.5.3 Treatment:
carious tooth. Extraction of carious tooth
Occlusal roentgenogram shows a focal Cap. Amoxicillin 250/500mg 3 times a day for 3
overgrowth of bone on the outer surface of to 5 days.
the cortex which may be described as Tab. Metronidazole 200/400mg 1BD for 3 days.
duplication of cortical layer of bone. This Tab. Diclofenac 50mg 1BD for 3 days.
mass of bone is smooth and well calcified
and may itself show a thin but definite
cortical layer.
Page 618
3. PERIODONTAL DISEASES
Periodontium is the anatomical structure surrounding

tooth which involves gingiva periodontal ligament,
cementum, alveolar bone.
Figure 1
Diffuse puffiness and softening of gingiva.

1. Gingivitis Redness of gingiva.Presence of exudates.
Inflammation of gingiva is called gingivitis.
Plaque usually present and calculus is often
1.1 Clinical features seen.
1.1.1 Acute gingivitis:
Figure 2: Gingivitis
Sloughing with grayish debris adhering to Soggy puffiness that pits on

eroded surface pressure.Marked softness and friability with
Vesicle formation fragmentation on exploration with probe.
1.1.2 Chronic Gingivitis Firm, Leathery consistency
1.2 Treatment: Scaling and pol ishing
Page 619
Figure 3
Rinsing with 3% H202 + Equal quantity of

2. Acute Gingival Infections: water2-3 hourly. And / or 0.12%
Chlorohexidi ne mouth wash BD
2.1 Necrotizing Ulcerative
After 2 days if pseudo membrane is absent
Gingivitis: and erythematous gingiva are present,
It is microbial disease of gingiva characterized by evaluate for scaling, if sensitivity permits.
death and sloughing of gingival tissue. After 5 days discontinue hydrogen peroxide
2.1.1 Clinical Features gargles but continue with chlorhexidine
gargles
Sudden onset sometime with respiratory Vit.B complex 1 OD for ten days.
tract infection
Lesions are punched out crater like 2.2 Pericoronitis:
depressions on crest of interdental papilla
Inflammation of the gingiva in relation to the crown
Ulcers are covered with grey of an incompletely erupted tooth is called
pseudomembranous slough.
pericoronitis.
Spontaneous gingival hemorrhage and also
bleeding on slightest provocation. 2.2.1 Clinical features:
Constant radiating, gnawing pain of gingiva.
Metallic foul taste.
Partially erupted or impacted mandibular
third molar is common site of pericoronitis.
Excessive amount of pasty salivary
secretions. Pericoronitis is exacerbated by trauma, or
foreign body trapped under tissue flap.
Local lymphadenopathy
Trismus may or may not be present
In severe and acute cases high grade fever,
loss of appetite, generalized lassitude, Pericoronitis presents as a red swollen
insomnia, constipation, headache, mental sometimes suppurating lesion with
depression may be seen. tenderness, and pain radiating towards ear,
nose or floor of mouth.
Necrotizing ulcerative gingivitis is caused
Fever and malaise may be present.
by fusiform bacilli and spirochetes
Difficulty in swallowing may be present.
2.1.2 Treatment of Acute Necrotizing Many a times infection may spread to
different tissue spaces leading to tonsillar
Ulcerative Gingivitis (ANUG) abscess formation, cellulitis or Ludwigs
With moist cotton and lignocaine jelly gently remove angina.
pseudo membrane.
2.2.2 Treatment:
Antibiotic and Analgesic Cap.
Amoxycillin 500mg 8 hrly 10 days for Area should be anesthetized.
patient sensitive to amoxicillin. Drainage is established by gently lifting the
soft tissue operculum.
Cap. Erythromycin 500mg x 8 hrly.
Tab.Diclofenac 50mg 1BD for five days
Page 620
Area should be irrigated by normal saline to Gingival abscess, localized, painful, sudden
remove debris. onset, rapidly expanding.
Cap. Amoxicillin 250/500 mg 3 times a day Usually on marginal gingival or interdental
for 3 to 5 days. papilla
Tab. Diclofenac 50mg 1BD for 3 days. Appears as a red swelling with a smooth
shiny surface
Advice warm saline gargles every 2 hours. Purulent exudates may be present
Tooth sensitive to percussion
Once swelling subsides, partially erupted
tooth should be treated by excision of 3.1.2 Chronic inflammatory enlargement
pericoronal flap or by extractions. Clinical Features
Ballooning of marginal gingiva and
3. Gingival Enlargement: interdental papilla or both.
Progresses slowly and painlessly
Increase in size of gingiva is a common feature called Appears like pedunculated mass on gingiva
as gingival enlargement or gingival hyperplasia or Painful ulcerations may occur
gingival hypertrophy. Exposed gingival surface appears red
edematous and s hiny in mouth breathers.
3.1 Inflammatory Enlargements: 3.1.3 Treatment
3.1.1 Acute Inflammatory enlargements
Scaling and root planing
Clinical Features If the shrinkage of fibrotic tissue doe snt
occur then surgical therapy is the treatment
of choice.
Drug Induced Gingival Enlargement

Figure 4
3.2 Drug Induced Gingival Possibility of discontinuing the drug or

changing should be assessed by consulting
Enlargement the physician.
3.2.1 Clinical features Plaque control helps to limit the
Painless bead like enlargement. enlargement and subsequent periodontal
May enlarge to cover crown portions. diseases.
Enlargement is generalized. If required by assessing the periodontal
Enlargement more in anterior teeth. status go for periodontal surgical
Recurs after surgical excision. procedures like gingivectomy or flap as
Patient gives history of taking medicines indicated.
like anticonvulsants, immunosuppressant,
and calcium channel blockers.
3.3 Gingival Enlargement
3.2.2 Treatment Associated with Systemic
Diseases:
Page 621
3.3.1 Pregnancy Gingivitis Scaling and root planning.
Gingival enlargement may be marginal or Required periodontal surgery.
generalized, single or multiple tumors like Systemic antibiotics
masses. Cap. Amoxicillin 250/500 mg 3 times a day
It occurs due to increased progesterone and for 3 to 5 days.
estrogen levels in pregnancy especially in Tab. Metronidazole 200/400 mg 1BD for 3
third trimester. days.
Treatment of Pregnancy Gingivitis:
Removal of local irritants in early stages of Tooth removal if required
pregnancy and emphasis should be give n on
preventing gingival diseases. 3.6.1 Periodontitis
3.6.1 Chronic Periodontitis
3.3.2Gingival Enlargement in Vitamin C An infectious disease resulting in inflammation
Deficiency (SCURVY): within the suppor ting tissues of the teeth, leading to
Acute vitamin C deficiency itself does not progressive attachment loss and bone loss.
cause inflammation. But it does cause
hemorrhage, collagen de generation, oede ma Clinical Features:
of gingival tissue. Supragingival and subgingival accumulation
These changes are in response to plaque. with calculus for mation.
Regular intake of vitamin C and Gingival inflammation and pocket
maintenance of oral hygiene prevents for mation.
scurvy. Loss of periodontal attachment and alveolar
bone.
3.4 Pyogenic Granuloma: Occasional pus discharge and poor oral
3.4.1 Clinical features: hygiene.
It is a tumor like gingival swelling that is Moderate swelling of gingiva with pale red
considered as exaggerated conditioned to magenta colors.
response to minor trauma. Blunt or rolled gingival margins.
It presents as a pedunculated spherical tumor Bleeding on probing may be present.
like mass. Sometimes tooth may be mobile.
It is red or purple. It may be localized or generalized.
It can be firm or friable. Sometimes surface 3.6.2 Necrotizing Ulcerative Periodontitis
may be ulcerated and purulent. Necrotizing ulcerative periodontitis is an extension of
necrotizing ulcerative gingivitis. Historically it is
3.4.2 Treatment described as Vincents infection or trench mouth.
Excision of mass and removal of local irritating
factors. Clinical features
3.5 Periodontal Abscess: Areas of ulceration and necrosis of
3.5.1 Clinical features interdental papilla with yellowishwhite soft
Mild to severe discomfort. layer of pseudomembrane is present.
Localized red, ovoid swelling. Lesions are painful.
Periodontal pocket,Exudation. Bleed without provocation.
Mobility. Punched out lesions present.
Tooth elevation in socket. Associated with malodor, localized
Tenderness to percussion or biting lymphadenopathy, fever and malaise.
Elevated temperature,Regional Destructive progression of disease includes
lymphadenopathy. destruction of periodontalattachment and
Radiograph shows periodontal angular bone bone loss.
loss and furcation radiolucency. Deep interdental osseous craters are very
typical with necrotizing
ulcerativeperiodontisis.
3.5.2 Treatment: Tooth mobility with untimely loss of
Drainage through poc ket retraction or tooth is a common feature.
incision.
Page 622
Rate of bone loss is four fold as compared to
3.6.3 Aggressive Periodontitis chronic periodontitis.
a) Localized aggressive periodontitis: Mobility of teeth increases fast.
(Juve nile periodontitis): Sensitivity to root surfaces.
Usually first molar or incisor are Deep dull, radiating pain during mastication.
affected with interproximal bone loss. Usually disease starts around beginning of
There is lack of inflammation despite loss of puberty.
deep periodontal pocket. Radiological vertical bone loss is seen.
Generalized Aggressive Periodontitis

Figure 5
b) Generalized Aggressive Periodontitis Breath odor is defined as subjective perception after

Affects individuals below the age of 30. smelling someones breath. If unpleasant, the term
Gives very poor response to antibiotics. breath mal odor, halitosis or bad breath can be
Characterized by generalized nterproximal applied.
attachment loss affecting at least 3
permanent teeth other than first molar and 3.7.1 Etiological factors:
incisor. Deep caries with infection, candidial
Periods of advanced destruction is followed infections, pericoronitis, periodontitis, oral
by stages of quiescence of variable length ulcerations, xerostomia, tongue and tongue
(weeks to months to years). coating especially in fissured tongue and
Quantity of amount of plaque seems hairy tongue.
inconsistent with the amount of periodontal Infections like pharyngitis, sinusitis, and
destruction. chronic purulent tonsillitis,chronic
Deep poc kets and s uppuration . bronchitis, bronchiectasis, bronchial
Systemic manifestation may be seen such as carcinoma,gastric hernia, regurgitation,
weightloss, mental depression and general esophagitis, and intestinal gas production,
malaise. chronic glomerular nephritis,diabetes.
Trimethylaminouria hereditary metabolic
c) Treatment: disorder causes typical fishy odor.
Conventional periodontal therapies for
aggressive periodontitis consist of
patient education, oral hygiene 3.7.2 Treatment:
improvement, scaling and root planing The treatment of malodor is cause related.
and recall maintenance. Mechanical reduction of plaque and
Resective periodontal surgery can be microorganisms by cleaning dorsum of
effective to reduce pocket depth. thetongue by tongue scrapper and
Anti microbial therapy consists of Cap interdental spaces by interdental brush and
Tetracycline (500 mg 1BD for 14 days proper cleaning of oral cavity. If required
every 8 weeks). professional periodontal treatment is to be
3.7 Oral Malodor (HALITOSIS) done.
Page 623
Reduction of oral microbial load by mouth Masking the malodor with rinses and mouth
rinsing with Chlorhexidine0.12% sprays.
mouthwash twice a day for 15 days.
KEY MESSAGE
Maintenance of prope r oral hygiene by using correct teeth br ushing technique and rinsing the
mouth to avoid food lodgement.
Local etiological factors like accumulation of dental plaque, calculus must be eliminated in the
dental clinic.
Rule out and manage systemic disorders leading to periodontal diseases.
Page 624
4. SPREAD OF ORAL INFECTION
Many of the fascial spaces of head and neck Dysphagia is present
communicate either directly or indirectly with each Difficulty in breathing
other, thus infection in the oral cavity spread from Midline of palate is displaced to unaffected side
one region to another through these spaces. and uvula is swollen
The spaces that get first infected are called Medial displacement of the lateral wall of the
primary spaces. pharynx.
Spaces which get infected later are called as Redness and edema of the area around the third
secondary spaces. molar.
The fascial spaces in head and neck are the potential Differential diagnosis:
spaces between the various layers of the fascia The Pterygomandibular space abscess must be
normally filled with loose connective tissue and distinguished from Peritonsillar abscess. In
bounded by anatomical barrier usually bone, muscle peritonsilllar abscess there is no dental involvement
and fascial layer. and less trismus.
1. Important space infections 1.5 Submandibular space:

1.1 Canine space:- Clinical features:
Swelling of cheek and uppe r lip
Obliteration of nasolabial fold Firm swelling in submandibular region, below
the inferior border of mandible.
Drooping of angle of the mouth
Edema of lower eyelid it indicates pointing of Redness of ove rlying skin, dysphagia, mode rate
abscess below medial corner. trismus
1.6 Submental space

1.2 Buccal space abscess:- Clinical feature:
Space infection is dome shaped and periorbital
edema develops due to impaired venous, and Distinct, firm swelling in midline beneath the
lymphatic drainage. chin.
Swelling be gins at the lower border of the Dysphagia.
mandible and extends upwards to the level of the
zygomatic arch. 1.7 Sub lingual space
Trismus is not usually present. Clinical features:-
1.3 Submassetric space:- Swelling in the floor of the mouth

Dyspnea
Clinical features: Dysphagia
Swelling over the masseter muscle i.e. the
swelling is seen extending from lower border of 1.8 Treatment:
the mandible to zygomatic arch and anteriorly to
All space infections need antibiotics &analgesics,
anterior border of the masseter and posteriorly to
incision& drainage dependi ng upon severity.Cap.
posterior border of the mandible.
Amoxicillin 250/500mg 3 times a day for 3 to 5 days.
Pain over the region Tab. Metronidazole 200/400mg 1BD for 3 days.Tab.
Severe trismus is present Diclofenac 50mg 1BD for 3 days.
Tenderness over the angle of the mandible
Pyrexia and malaise 2. Cellulitis
1.4 Pterygomandibular space Cellulitis is a diffuse inflammation of soft
tissues, tends to spread through tissue spaces
Clinical features: and along fascial planes.
Severe trismus
Cellulitis of face and neck most commonly
Extreme radiating pain results from dental infection either as sequelaof
No evident extraoral swelling
Page 625
apical abscess or osteomyelitis or following advised not to massage the affected area with
periodontal infection or pericoronitis any medication.
2.1 Clinical features: 3. LudwigsAngina:

Painful swelling of the soft tissues Massive, firm, brawny cellulitis, beginning usually in
involved that are firm and brawny. submaxillary space and secondarily involving the
Patient is moderately ill and has raised sublingual and submental space bilaterally.
temperature and leukocytosis.
If the facial cellulitis persists the infection 3.1 Clinical feature:
frequently tends to become localized and a
facial abscess may form. When this A rapidly developing board like swelling
happens the suppurative material present of the floor of mouth and subsequent
seeks to point or discharge upon a free elevation of the tongue.
surface. If early treatment is instituted a Swelling is firm painful and diffuse.
resolution usually occurs without drainage Trismus, dysphagia
through a break in the skin. Difficulty in breathing
High fever, rapid pulse and fast respiration
2.2 Treatment: Tongue may be raised against palate
As the disease continues, the swelling
Administration of antibiotics and removal of
involves the neck, and edema of the glottis
the cause of infection. Cap. Amoxicillin +
may occur. This carries the serious risk of
Clavalunic acid 375/625 mg 1BD for 5 days.
death by acute respiratory failure or
Tab. Diclofenac 50mg 1BD for 5 days. To
septicemia.
avoid the further spread of infection or
solidification of abscess the patient should be
Figure 1
3.2 Antibiotic therapy: IV) TID for 3 days
Injection Diclofenac sodium 3CC for 3 days
Usually IV antibiotics with proper dosage and Injection Ranitidine 2ml 1 BD for 3 days
frequency are necessary according to age and Magnesium Sulphate dressing till the swelling
severity. subsides
Injection Ampicillin 250/500mg 6 hourly for 3 I.V fluids to maintain the electrolyte balance.
days Refer to higher center for further management
Injection Gentamycin 40/80mg 1BD for 3 days immediately.
Injection Metronidazole 50 mg ( 100ml bottle
KEY MASSAGE:
Avoid hot fomentation or application of any counter irritants locally.
Perform incision and drainage of abscess at earliest to avoid further spread of infection.

Page 626
5. ORAL MUCOSAL LESIONS
Clinically it appear as a linear or diffuse lesion
1. Chronic cheek or lip biting irregular opaque white. In some cases lacerated,and
Superficial lesions produced by frequent and reddened area usually with patch of partly detached
repeated rubbing, sucking or chewing surface epithelium.
movements that abrade the surface of a wide It is rough on palpation as area becomes thickened
area of lip, buccal mucosa, lateral border of and scaled.
tongue without producing discrete ulceration.
1.2. Treatment:
1.1. Clinical feature:
Recommendation to stop the habit, smoothening of
It can occur at any age, common sites are buccal sharp edges of teeth .Acrylic shields can be fabricated
mucosa at the level of occlusion, lip and lateral to cover the facial surface of teeth and there by
border of tongue. restricting access to buccal and labial mucosa.
Traumatic Lesion involving buccal mucosa and lateral border of tongue

Figure 1 Figure 2
wiped out with wet gauze leaving a bright red raw

2. Oral Candidiasis: bleeding surface. In some cases it may present as a
Candidiasis is the disease caused by infection with brightly erythematous mucosa with only scattered
yeast like fungus Candida albicans. It can occur
white patches.
either solely confined to the oral mucosa or as a part
of any of the several mucocutaneous candidiasis
syndromes. 2.1.2 Treatment:
Topical treatment
2.1 Oral Thrush or Clotrimazole: One oral Troche (10 mg
Pseudomembranous oral tablet) dissolve in the mouth 5 times daily.
candidiasis. Nystatin oral pastille, 1 or 2 pastilles
Candidiasis is the disease caused by infection with dissolves slowly in the mouth 5 times a day.
yeast like fungus Candida albicans. Clotrimazole 1 % mouth paint topically1 to
2 times/day till lesion subsides.
2.1.1 Symptom: Nystatin suspension 100,000 units (1 ml of
Burning sensation and rapid onset of bad taste. suspension held in the mouth before
Clinical features- Common sites are roof of the swallowing)
mouth, retromolar area and mucobuccal fold. Systemic treatment:
Clinically pearly white or bluish white plaques are Nystatin -250 mg TID for 2 weeks.
present on oral mucosa. Patches are loosely adherent Suppl imental therapy by Vit B12. Tab Vit B
to oral mucosa. Mucosa adjacent to it appears red Complex 1OD for 10 days.
and moderately swollen. White patches are easily
Page 627
2.2 Denture Stomatitis: - AIDS. Treatment include correction of primary
Denture stomatitis is a common form of oral cause.
candidiasis that manifest as a diffuse inflammation of
the denture bearing areas and often associated with 3. Ulcerative lesions of oral
angular cheilitis.
2.2.2 Treatment:- cavity
Troches containing Clotrimazole and Nystatin 4-5 Ulcerative lesions are a group of common oral
times should be applied on the denture after meals. mucosal lesions. The most common causes of these
Antifungal therapy and cessation of denture wearing lesions are mechanical and reactive factors, infectious
till elimination of mucosal inflammation. Rinsing the diseases and neoplasms as well as autoimmune and
denture and applying antifungal cream before hematological disorders. The main clinical feature in
inserting the denture. all these conditions is an ulcer.Ulcer consist of
margins, edges, floor and base. Site, Size, Shape of
the ulcer should be examined.
2.3 Angular Cheilitis:-
Angular cheilitis is the term used for an infection
involving the lip commissures. The majority of cases 3.1. Recurrent aphthous stomatitis
are candida associated and respond promptly to (RAS)
antifungal therapy. Other possible etiologic cofactors RAS is a disorder characterized by recurring ulcers
include reduced vertical dimension, nutritional confined to the oral mucosa in patients with no other
deficiency (Iron de ficiency anemia and Vit-B or Folic signs of disease.Precipitating factors are trauma,
acid deficiency)and rarely diabetes, neutropenia and endocrine conditions,stress, allergy, immunological
abnormalities and nutritional deficiency.
Figure-3: Aphthous Ulcer
3.1.1 Clinical features: size erosion that gradually enlarge and coalesce.
a) Sites: Occurs most commonly on buccal& labial Lesions are more painful. Patient get relief
mucosa,buccal& lingual sulci,tongue and soft immediately with 2% Tetracycline mouth wash.
palate.It begins with prodromal stage of tingling,
burning or itching for 1 to 2 days before the ulcer 3.1.2 Treatment: -
occur.Lesions are round to oval in shape, Medication prescribe should relate to the severity of
symmetric,single or multiple.Superficial ulcers the disease.
covered by grey membrane.It is surrounded by i. Anaesthetic cream - topical protective
localized area of erythema. emollient base in mild cases with two or three
b) Minor aphthae : Minor apthae are less than 1 cm small lesions. Pain relief can be obtain with
in diameter and heal completely in 7 to 10 days use of topical anaesthetic agent.
c) Major aphthae: Size of the lesion is larger than 1 ii. Topical Corticosteroid - Triamcinolone
cm and may reach up to 5 cm in diameter. They Acitonide 3 to 4 times daily. Nutritional
interfere with speech and eating. The lesions heal suppl ementswithTab. B Complex 1 BD for 10
slowly and leave scars. days.
d)Herpetiform ulcers: Multiple small ulcers iii. Maintenance of oral hygiene: - Chlorhexidine
often upto 100 in number. It is found on any 0.12 % mouth wash twice a day for 10 days to
intra oral mucosal surface. It begins as small pin head maintain oral hygiene.
Page 628
Herpetic gingivostomatitis
Figure 4 Figure 5
trauma, fatigue, menstruation, pregnancy, upper
respiratory tract infection, emotional upset etc.
4. Viral Infection
Herpetic gingivostomatitis: 4.3 Clinical feature:
Herpes simplex, an acute viral infectious disease Recurrent herpes simplex infection may occur at
caused by herpes simplex virus. widely varying intervals, from nearly every month in
some patients to only once a year or even less in
4.1 Clinical features: others. Lesion may either at the site of primary
The disease occurring in children is frequently inoculation or in adjacent area supplied by the
primary attack and is characterized by development involved ganglion. In may develop on lips (recurrent
of fever, irritability, headache, pain upon herpes labialis) or intra-orally. The lesions are
swallowing,regionallymphademopathy. Within few preceded by burning or tingling sensation and a
days mouth becomes painful and the gingiva become feeling of tauntness, swelling or slight soreness at the
intensely inflamed appe ar erythematous and location in which vesicle are small 1mm or less in
edematous. The lips, tongue, buccal mucosa, palate diameter, tend to occur in cluster and coalesce to
may be involved. Shortly yellow fluid filled vesicles for m large ulcer. These gray or gray-white vesicle
develop. These rupture and form shallow, ragged rupture quickly leaving a small red erythematous
extremely painful ulcers cove red by an erythematous halo.
halo. They heal spontaneously with 7 to 14 da ys and
leave no scar.
4.4 Treatment:
i. Acyclovir : Acyclovir cream for lips apply 4 hourly
4.2 Recurrent or secondary herpetic for 5 days.
labialis and stomatitis:- Tab Acyclovir 200 mg 5times /day for 3 to 5 days.
It is usually seen in adult patients and manifest itself ii. Chlorhexidine 0.12% mouthwash twice a day for 10
clinically as an attenuated form of primary disease. days
The recurrent form of disease is often associated with iii. Avoid stress.
Page 629
6. PREMALIGNANT AND MALIGNANT
LESION
1. Oral leukoplakia:- 1.2 Nodular or speckled
It is a whitish patch or plaque that cannot be leukoplakia:
characterized clinically or pathologically as Also called as leukoplakia erosiva. It is a
any other diseases and which is not associated mixed red white lesion in which small
with any other physical or chemical causative keratotic nodules are scattered over an
agent except the use of tobacco. atrophic patch of oral mucosa. Nodules may
be pin head sized or even larger. It has got a
1.1 Homogenous leukoplakia: high malignant potential.
It is also called as leukoplakia simplex,
uniform raised white plaque formation,
varying in size, with regular edges.
Oral leukopl akia
Figure 1
1.3 Ulcerated leukoplakia: In some lesions of leukoplakia red component

is present. This intermixed lesions is called as
It is characterized by red area, which at times erythroleukopl akia.
exhibit yellowish area of fibrin giving the
appearance of ulceration white patches are
present at the periphery of the lesions. 1.6 Treatment:
Patient should be asked to cease tobacco
related habits immediately.
1.4 Verrucous leukoplakia: Removal of chronic irritant like sharp,
It is also called as leukoplakia verrucosa. It is broken teeth dissimilar metal restorations
characterized by verrucous proliferation above and other predispos ing factors like syphilis,
the mucosal surface. These lesions alcohol, etc should be controlled and
demonstrate sharp and blunt projection. eliminated.
1.6.1 Conservative treatment:-
VitaminA: It is given orally, parentally or
1.5 Erythroleukoplakia: topically. Therapeutic dose -75000-300000.
IU for 3months.
Page 630
Antioxidant therapy: --Carotene associated with heavy smoking. Erythropl akia is
supplementation can be beneficial for asymptomatic.
treatment of leukoplakia.
Vitamin B: complex: it is given as 2.2 Diagnosis:
supplement in cases of commissural and Red velvety patch with no sign of infection and
lingual lesions. inflammation
1.6.2 Surgical management:-
Conve ntional surgery, Cryo surgery, Fulguration 2.3 Treatment:
(electro cautary and electro surgery), Laser treatment.
Removal of cause: elimination of suspected irritant
Biopsy may be carried out if there is no change in and observation for one to two weeks. Prompt biopsy
leukoplakia after cessation of stimulus and may if lesions persist.If biopsy shows dysplasia or
require conservative or surgical treatment carcinoma total excision is indicated.
1. Erythroplakia: 3. Oral submucous fibrosis

Erythroplakia is bright red velvety plaque or patch (OSMF):
which cannot be characterized clinically or
pathologically as being due to any other condition. Etiological factors are chilly and spicy food, betel
Erythroplakia is premalignant lesion with nut, tobacco & lime, nutritional deficiency, etc.
frequency less than leukopl akia but more malignant
potential. 3.1 Clinical features:
It affects both sexes, majority of patients are
2.1 Clinical feature: between 20 to 40 years, of age.
Erythroplakia occurs predominantly in older men, in The most frequent location of OSMF is
the sixth and seventh decades of life. Erythroplakia buccal mucosa and retromolar area. It also
are more commonly seen on the floor of the mouth, commonly involves soft palate, palatal
the ventral tongue, soft palate and tonsillarfauces. fauces, uvula, tongue and labial mucosa.
Although the etiology is uncertain, most cases are Oral submucous fibrosis
Figure 3
Some times floor of mouth and gingival. The most common and earliest sign is
The onset of condition is insidious and is blanching of mucosa.
often of 2 to 5 years of duration. As disease progresses the mucosa becomes
Initial symptom commonly seen as burning stiff and vertical fibrous bandappears. This
sensation of oral mucosa aggravated by bands can be palpable easily.
spicy food followed by either hyper The mobility of soft palate is restricted.
salivation or dryness of mouth. Vesiculation, Uvula when invol ved is shrunken.
ulceration, recurrent stomatitis Tongue becomes smooth and its mobility is
Late symptoms are trismus, difficulty in limited.
tongue protrusion, swallowing.
Page 631
3.2Treatment: Local Injection Hydrocortisone 1.5 ml (25
mg/ml) locally in the area of fibrosis
The treatment of patients with OSMF depends on the twiceaweek for four weeks or more as per
degree of clinical involvement. conditions.
Systemic A therapy with Hydrocortisone
3.2.1 Restriction of habit/ behavioural 25mg tablet in doses of 100mg per day for 7
therapy days is useful in relieving burning sensation
The preventive measure should be in the form without untoward effects.
of stoppage of habit, through health education. Placental extract 2 ml biweekly or weekly
Affected patients should be explained about for three to four weeks locally injected
the disease and its malignant potential. around fibrous bands.
Improvement in clinical features like- gradual
increase in interincisal opening has been
observed in most of patient who discontinue 3.2.3 Surgical treatment like Conventional
the habit.
surgery ,Laser ,Cryosurgery
3.2.4 Oral Physiotherapy
This includes mouth opening and ballooning
3.2.2 Medicinal therapy of mouth.
Administration of Vit.B complex and
antioxidants as supportive therapy. 3.2.5 Diathermy
Vitamin rich diet along with iron preparation
is helpful to some extent. 4. Oral Lichen Planus:
B-Complex preparation Intramuscular
injection starts with small doses and It is a chronic immunologic inflammatory
continuing with larger doses (2ml ampule mucocutaneous disorder that varies in appearance
daily). The course of 5 injection is repeated from kerototic (reticular or plaque like) to
after 7days. erythematous and ulcerative lichen planus
Steroids
Oral Lichen Planus

Figure 4 Figure 5
4.1 Clinical feature: papules in a linear, annular or retiform arrangement

It may occurs in adulthood with age range for males forming typical lacy, reticular patterns, rings and
35- 44 years and for females 45-54 years. It has streaks over the buccal mucosa to a lesser extent on
lip, tongue and palate. Tiny white elevated dots are
more predilections for females.
present at the intersection of white lines called as
Wickhams straie.
4.1.1 Sites:Common are buccal mucosa and to Types are reticular, papular, plaque, atrophic,
lesser extent tongue, lips, gingiva, floor of mouth bullous, hypertrophic, annular and erosive.
and palate
4.1.2 Symptoms:Patients may repor t with burning 4.2 Treatment:

sensation of oral mucosa. Small and moderately sized either erosive or
ulcerative painful lesions can be treated with
triamcinolone acitonide cream base. Systemic
4.1.3 Clinical feature:Oral lesion is characterized
steroid tab. Prednisolone (5 mg tab.) in tapering
by radiating white and gray velvety thread like
Page 632
doses of 30 mg per day for the first of the three superadded with infections.
weeks, 15 mg per day for 2nd week and 5 mg per Radiographicallyitmayshow bone erosion.
day for 3rd and final week. 6.1 Clinical features:-
Symptomatic treatment with topical analgesic, 6.1.1 Benign Tumors:-
topical anesthetic and antihistaminic rinse.
Encapulated tumor
Psychotherapy
Base of tumor is of two types sessile and
pedunculated
5. Cyst of Jaws: Not involving the adjacent tissue
It may be epithelial or non-epithelial. Epithelial cyst Painless and slowly growing
may be odontogenic or non odontogenic. Clinically 6.1.2 Malignant Tumors:-
presenting as smooth, hard, painless Ulcero proliferative lesion
prominence.Dentigerous cyst are mainly associated Invading into adjacent structures
with impacted molars and canines. Pain, paraesthesia
Odontogenickeratocyst are seen in the lower third Trismus
molar area extending into ramus. Radiographically Bony erosion
cyst appears as well defined round or oval areas of Mobility of teeth
radiolucency circumscribed by a sharp radiopaque
Not encapsulated
margin.
Palpable Lymphnodes
Pathological Fracture of the bone
5.1 Treatment of Cyst:
Investigation:
1. Marsupialisation Lateral oblique X-ray,OPG.
2. Enucleation of cyst
6.2 Common Cancers
Squamous cell carcinoma
6. Tumors: A malignant epithelial neoplasm exhibiting squamous
Presenting as intra oral swelling may be odontogenic differentiation as characterized by formation of
or non odo ntogenic variety, may be central or keratin and/or presence of intercellular bridges. The
peripheral, epithelial or connective tissue origin. The most important task is to establish an early diagnosis
most common tumor occurring in oral cavity is at the first stages of the disease. Risk factors include
squamous cell carcinoma. Tobacco, alchohol, use of tobacco in its various forms, alcohol,
smoking are the predisposing factors. The patient ultraviolet light, chronic irritation to oral mucosa,
may present with a swelling, ulceroprolifertive
human papilloma virus infection.
growth with involvement of lymphnodes. Pain may
accompany if it involve the adjacent structures or
Figure-6: Carcinoma of buccal mucosa
Page 633
6.2.1 Clinical features:- 6.2.2 Prevention: -
a) Symptoms:- Oral cancers can be prevented by /sensible
attitude towards maintenance of oral care
Ulcerative lesion in the oral cavity that does and regular checkups.
not heal. Proper education regarding the adverse
A persistent red or white patch effect of the dreaded habits
Loosening of the teeth or pain around the successful persuasion to quit the bad habits
teeth or jaw. (smoking, alcohol consumption, gutkha)
Voice changes. The presence of persistent grayish white
patches developing in people who smoke or
b) Site:- Tongue, floor of mouth, lower alveolus, chew tobacco needs to be investigated.
buccal mucosa, upper alveolar / hard palate, Maintenance of good oral hygiene.
retromolar area, lip, floor of mouth. Any faulty restoration or a sharp tooth needs
c) Signs -Clinically almost all oral cancers, to be corrected
except those in earliest stages have two
characterized feature in the form of ulceration 6.2.3 Treatment:
and indurated margin. Treatment includes surgical interve ntion,
radiation therapy and c hemotherapy.
6.2.2 Diagnosis: - 7. Tobacco Cessation Centers
History and detail clinical examination, lymph
node examination. (TCC):
It is important for early detection to decrease Setting upTCC facilities at district hospital level. At
mortality rate. the district hospital Tobacco cessation centers are
combined with dental units.
Key massege:
Any discolouration or grayish white patch in the oral cavity must be properly evaluated and managed at early
stage considering possibility of oral malignancies. Cessation of tobacco consumption and self-examination
by patients should be promoted.
Page 634
7. OROFACIAL PAIN
Carbamazepine: - effective therapy for greater
An unpleasant sensory and emotional experience
than 85% of newly diagnosed
associated with actual or potential tissue damage, or
cases.Tab.Carbamazepine as an initial dose,
described in terms of such damage associated with
100 mg is given twice daily until relief is
oral lesions.
established.
1. Trigeminal Neuralgia Baclofen: - Patient who do not respond to
(TIC DOULOUREUX) Carbamazepine alone may obtain relief from
Baclofen or by combining Carba mazepine
1.1 Clinical Features: with Baclofen
Age Middle and old age group Refer to higher centre for further management
Episodes of intense shooting
,stabbingpainthatlastsfor a few seconds 2. Glossopharyngeal
andthen completely disappears neuralgia
Quality of pain Electric shock like ,
unilateral along the course of the affected (Ninth cranial nerve neuralgia)
nerve
Maxillary branch is most commonly 2.1 Clinical features
affected followed by the mandibular branch Characterized by severe paroxysmal pain in
and (rarely) the ophthalmic branch. the tonsils and ear
Invol ve ment of more than one branch occurs Less intense than trigeminal neuralgia
in some cases. Similar clinical features as trigeminal
Trigger zones precipitated by light touch on neuralgia
a trigger zone present on the skin or Precipitating factors Yawning, talking,
mucosa within distribution of the involved chewing, swallowing.
nerve branch. Common sites for trigger
Trigger zone: pain sensation following the
zones include nasolabial fold and the corner
distribution of glossopharyngeal nerve
of the lip
namely, the pharynx, posterior tongue, ear
Pain aggravated by: - Shaving, showering,
and intraarticularretromandibular area.
eating, speaking or even exposure to wind.
Number of attacks varies from 1-2 per day 2.2 Treatment:
to several per minute
Similar to trigeminal neuralgia.
1.2 Treatment:- Good response to Carbamazepine and
baclofen.
Drug therapy
Page 635
8. TRAUMATIC INJURIES TO TEETH
Class IX Traumatic injuries to primary teeth.
1. Classification :
Traumatic injuries are classified as 2. The various effect of
Class I Simple fracture of the crown, involving trauma to teeth are
little or no dentin. 2.1 Crown Fracture:
Class II Extensive fracture of the crown, If it involves only enamel and dentin
involving considerable dentin but not the (Uncomplicated fracture) aesthetic restoration of the
dental pulp. teeth is sufficient.
Class III Extensive fracture of the crown, 2.1.1 Enamel dentin fracture :
involving considerable dentin and Radiograph is mandatory to determine the full
expos ing the de ntal pulp. extent of the injury.
2.1.2 Fracture Crown without pulp
Class IV Traumatized tooth that become non- exposure:Objective in treating a fractured
vital, with or without a loss of crown crown without pulp e xpos ure is three fold.
structure.
Elimination of discomfort.
Class V Teeth lost as a result of trauma. Preservation of vital pulp.
Class VI Fracture of the root, with or without a Restoration of fracture crown.
loss of the crown structure.
The tooth should be tested with electric pulp tester or
with ice or ethyl chloride spray. If the pulp test is
Class VII Displacement of a tooth, without fracture vital and tooth is comfortable itshould be checked
of the crown or root. again a week, 3 weeks, 3 months, 6 months and 1
year.
Class Fracture of crown en mass and its
VIII replacement.
Figure-1: Crown fracture without pulp e xpos ure

2.1.3 Fracture with pulp involvement:
Figure-2: Crown fracture with pulp expos ure
Page 636
If there is involvement of pulp(Complicated Fracture) remarkably low. It will occur only 25% of the
vital pulp therapy canbe done for which optimal time time and in majority of cases, necrosis will
is first 24 hours. occur only in the coronal segment and only
In traumatic exposure after 72 hours in that is Root Canal treated.
immature teeth, full pulpotomy can be 2.2.1 Root Fracture
considered for apexogenesis. In mature If at the free gingival margin Root Canal
teeth, pulpectomy should be done. Treatment (RCT) & Restore with pos t and
core and crown.
In non-vital teeth with the ope n ape x, If at the apical 1/3 of root: Tooth should be
apexification is indicated to create an apical stabilized by splinting, RCT & may need to
stop. resect fractured root por tion by surgery and
2.1.3 Treatment followed by retrofilling.
Crown with pulp expos ure: Following If in the middle 1/3 of root: If tooth is
treatments are possible : restorable stabilize, RCT, Resect fracture
Pulpotomy (Pulp is vital). portion,restoration. If tooth is not restorable or
unable to stabilize extraction is needed.
Apexification (Pulp is necrotic).
Endodontic treatment. 2.3 Displacement injuries:
Lateral Luxation and avulsion: Lateral
Luxation, extrusion, and avulsion need
2.2 Root fracture: emergency splinting & later RCT if required.
In this coronal segment is reduced quickly and
functional splint is placed for 2 to 4 weeks.
When attended in time, pulp necrosis is
Figure 3: Splinting of traumatically displaced upper anterior teeth
Page 637
9. DISCOLOURATION OF TEETH
1. Introduction:
Discoloration of teeth is a cosmetic problems that is
often the patients primary concern. Although
restorative procedures are available, discoloration can
often be corrected totally or partially by a more
conservative approach.
2. Etiology of Tooth Discolouration:
Extrinsic stains Intrinsic stains

Diet related Dental Fluorosis
Bacterial strains
Tetracycline staining
Medications
Tobacco related Habits Amelogenesisimperfecta
Poor oral hygiene Erythroblastosisfoetalis
Porphyria
Jaundice
Pulpal necrosis
Intrapulpalhaemorrhage due to trauma
Dentin hypercalcification
3. Treatment:
Discolouration can be minimized by oral prophylaxis,
bleaching techniques, composite resine, laminates.
Page 638
10. MAXILLO-FACIAL INJURIES
Any injury to either a soft tissue or hard tissue of face Fractures which communicate to the exterior through
caused by an assault, road traffic accidents, sharp skin or mucous membrane
instruments, fall, sports injuries or violence can
cause loss of soft tissue and hard tissue which has to
be handled by an oral or dental surgeon meticulously
2.3. Greenstick fracture:
It occurs in immature bone where one surface is
at the time of casualty. compressed and opposing surface is stretched leads to
fracture.
1. Soft tissue injuries:
Abrasion,contusion,ecchymosis,haematoma,avulsion 2.4. Dentoalveolar fracture:
or degloving injury
Fracture of dentate alveolus may occur as a
separate clinical entity or in conjugation
2. Hard tissue injuries: with other
Fracture: External force beyond the modulus of Facial bone fractures are usually associated
elasticity of the bone with injury to teeth like fracture, subl uxation
or avulsion.
2.1. Simple fracture: Fractures of maxillary tuberosity and antral
Closed linear fractures of bone. floor are relatively common complications
which occurs during exodo ntia.
LeFort fractures
2.2. Compound fracture:
Figure 1Facial Deformity
3. Mandibular fractures angle, ramus, condylar process,

coronoid process,and alveolar
3.1 Classification: process.
Fractures of mandible are more common.
3.1.2 Mandibular fractures are
3.1.1 Mandibular fractures are classified
by the anatomicareas involved. These
areas are as follows: symphysis,body,
Page 639
Figure 2
also classified into simple, compound, Anesthesia, Paresthesia, or Dysesthesia of the

and comminuted. Lower Lip
3.1.3 An important classification of Abnormal Mandibular MovementsMandibular

mandibular angle and body fractures fracturelimited opening and trismus,deviation on
relates to the direction of the fracture opening toward the side of a mandibular
condylar fracture, Inability to close the jaw.
line and the effect of muscle action on
the fracture fragments. Change in Facial Contour and Mandibular Arch
Form
Angle fractures may be classified as
i. Vertically favorable or unfavorable and Lacerations, Hematoma, and Ecchymosis
ii. Horizontally favorable or unfavorable. The diagnostic sign of ecchymosis in the floor of
the mouth indicates mandibular body or
symphyseal fracture.
3.1. Diagnosis of mandibular
Loose Teeth and Crepitation on Palpation
fractures
Dolor, Tumor, Rubor, and Color
The patients health history may reveal pre-existing
systemic bone disease, Tenderness on palpation
The type and direction of traumatic force can be 3.3. Radiology
extremely helpful in diagnosis. Fractures sustained in
vehicular accidents are usually far different from Panoramic radiograph
those sustained in personal alterations. Lateral oblique radiograph
Posteroanterior radiograph
3.2. Clinical Examination Occlusal view
The signs and symptoms of mandibular fractures are Periapical view
as follows. Reverse Towne's view
Temporomandibular joint, including
Change in Occlusion tomograms
Any change in occlusion is highly Computed tomography (CT) scan, CBCT
suggestive of mandibular fracture.
Page 640
Figure 3: Orthopa ntomogram (OPG) Figure 4: 3D Computed
tomography (CBCT) scan
3.4. Management of mandibular Gunning type splints

fractures 3.4.2 Open reduction with direct skeletal
3.4.1 Closed reduction basic methods fixation
Direct interdental wiring Allows the bones to be directly manipulated through an
Indirect interde ntal wiring incision so that the fractured ends meet, then they can be
Continuous or multiple loop wiring secured together either rigidly (with screws or plates and
Arch bars screws) or non-rigidly (with transosseous wires).
Close Reductionof fracture mandibleOpen Reduction of fracture mandible

Figure 5 Figure 6
3.4.3 Post-operative care: Oral hygiene maintenance by using mouth

Soft diet and liquids rinses
Control of infection
Page 641
10. TEMPOROMANDIBULAR
JOINT DISORDERS
1. Trismus: 1.3. Investigation:

OPG,CTscan,MRI
Restriction of normal oral opening or inability to
ope n the mouth fully. Trismus is also defined as a
condition in which muscle spasm on contracture 1.4. Management:
prevents opening of the mouth (due to infection or i. Before starting treatment reassure the patient.
other condition which alter muscle) ii. Anti-inflammatory dr ugs and a nalgesics.
iii. Antibiotics in case of infection.
1.1. Causes of trismus iv. Space infection:-antibiotics, incision and
1.1.1 Articular:- drainage.
i. Ankylosis: - Fibrous ,Bony v. Muscle relaxants and mouth gags followed by
ii. Arthritis: - Stills disease (children) ,Rheumatoid physiotherapy.
(adults) vi. Tetanus- IM Immunoglobulin followed by
iii. Pyogenic arthritis antibiotics.
iv. Osteoarthritis vii. Tetany- IV Calcium Gluconate 10mg.
v. Psoriatic viii. Splints (soft as well as anterior bite planes)
vi. Reiter Syndrome ix. Fracture: - Reduction and fixation either closed
vii. Gout or open under LA or GA.
viii. HarieStrumpell disease x. Surgical intervention.
ix. Congenital syphilis
x. Fracture Condyle
2. Dislocation, Subluxation,
1.1.2 Extra Articular Hypermobility of
i. Myositis ossificans: - following trauma to the
masticatory muscles especially masseter. Temporomandibular Joint
ii. Infection:-Orofacial infection around the TMJ
area can bring about trismus or limitation of
(TMJ):
oral opening. Odontogenic infection like
pericoronitis, Ludwigs angina, submassetric
2.1 The dislocation can be
space infection, mumps, tuberculosis unilateral or bilateral
osteomyelitis, parotid infection i. Anterior mandibular dislocation
iii. Oral Submucous fibrosis ii. Acute
iv. Systemic causes: -Tetanus,Tetany. iii. Chronic recurrent (habitual) subl uxation
v. Trauma:-Fractures involving zygomatic arch, iv. Long standing
fracture of mandible also causes trismus, pain
and tenderness or muscle spasm. The term luxation is used for complete dislocation.
vi. Malignancies of oral cavity: Either due to Subluxation or hypermobility is a partial or
infiltration or due to pain incomplete dislocation.
vii. Osteomyelitis
viii. Coronoid hyperplasia 2.2. Causes:
ix. Scarring of the temporalis Extrinsic or Iatrogenic causes:-
x. Fibrosis of pterygomandibularraphae due to
cleft palate surgery. i. Blow on the chin while mouth is ope n
ii. Injudicious use of mouth gag during general
1.2. Clinical examination: anaesthesia.
iii. Excessive pressure on mandible during dental
Detailed clinical history. Inspection, Palpation,
extraction.
Auscultation in an around thetemporomandibular
iv. Post traumatic.Intrinsic or Self-induced:
joint and muscles of mastication.
Page 642
i. Excessive yawning, 2.3.2 Bilateral acute dislocation:-
ii. Vomiting,
iii. Opening mouth too wide for eating o Pain, inability to close the mouth, tense
masticatory muscles.
iv. Hysterical fits.
Difficulty in speech.
Profuse drooling of saliva
2.3. Clinical feature: Protrudi ng chin
2.3.1Unilateral acute dislocation. Mandible is protruded and movements are
restricted.
Difficulty in mastication and swallowing Patients complains of pain in temporal region
Difficulty in speaking rather than the joint.
Profuse drooling of saliva Distinct hollowness can be felt in both
Deviation of the chin toward contralateral side preauricular regions.
Deviation produces a lateral cross and open bite
on the contralateral side
The mouth is partly open and the affected
2.4. Treatment:
condyle cannot be palpable. Reassuring the patient.
Tranquilizer or sedative drugs.
Pressure and massage of the area.
Manipulation with or without anesthesia.
Press his gemclar teeth

downwards at the same time
press the undermoach of his
chin upwards and backwards
Figure 1
2.4.1 Manipulation:- below the chin to elevate it by giving upward

pressure. The downward pressure overcome
Remains the same irrespective of type of anesthesia. spasm of muscle, plus it brings the locked
First of all patient should be given assurance condylar head below the level of articular
about procedure and asked to relax completely. eminence and then backward pr essure is given to
Operator has to stand infront of the patient, he push the entire mandible posteriorly.
has to grasp the mandible with both the hand one After this reduction procedure, the mouth is
on each side. closed and patient is asked to keep the mouth
The thumb of operator should be covered opening restricted.
with gauze to prevent injury during Immobilization can be carried out by giving
manipulation. The thumbs are placed on occlusal barrel bandage for 10 to 14 days period. Patient
surfaces of lower molars and finger tips are is kept on semisolid diet. Anti-inflammatory
placed below the chin. Operator has to exert full analgesics prescribed for 3to 5 days.
body pressure on posterior teeth to depress the
jaw and at same time the finger tips are placed
Page 643
Long standing acute dislocation which do not iii. A clicking or popping noise in the
respond to above procedure can be reduced by temporomandibular joint.
administering general anesthesia. If manual reduction iv. Limitation of jaw motion unilaterally or
fails than open surgical procedure as last resort. bilaterally.
3.4. Differential diagnosis:

3. Temporomandibular Cluster headache, migraine headache, post herpetic
disorder (TMD): neuralgia, temporal or giant cell arteritis, trigeminal
neuralgia.
Temporomandibular joint syndrome or
temporomandibular disorder (TMD) is the most 3.5. Treatment:
common cause of facial pain after toothache. TMD
can be classified broadly as TMD secondary to Counselling regarding self-care and reversal of
myofacial pain and dysfunction (MPD) and TMD parafunctional habits.
secondary to true articular disease. Heat application to increase local circulation
MPD form is associated with pain without apparent which act as a sedatives and lowers muscle
destructive changes of the TMJ on x-ray. It is tension to be given for 15 to 20 minutes 4
frequently associated with bruxism and daytime jaw times a day.
clenching in a stressed and anxious person. Cryotherapy with Ice packs application to
the painful area 4 times a day for 20 minutes
for relief of pain followed by an acute injury
superimposed over a chronic TMD.
3.2. Etiology:
Mild analgesic Tab.Diclofenac 50 mg 1 BD.
The etiology of TMD is multifactoral and includes Anti-anxiety agents for short duration in
malocclusion, jaw clenching, bruxism, personality acute pain like.Tab Diazepam 2 to 5 mg a
disorders, increased pain sensitivity and stress and bed time for 10 days.
anxiety. Physiotherapy andActive stretch exercise.
Intraoral appliances: Use of Splints,
3.3. Clinical feature: orthopedic appliances, bite guards, night
i. Pain guards or bruxing guards.
ii. Muscle tenderness Stress management
Page 644
11. DENTAL IMPACTION
An impacted tooth is one that is erupted, partially
1. Introduction: erupted or unerupted and will not eventually assume
Impaction is cessation of eruption of tooth caused by nor mal arch relationship with other teeth and tissue
physical barrier or ectopic positioning of tooth. commonly seen with third molar and sometimes
maxillary canine teeth
Figure 1
Figure 2
2. Types of Impaction: relation to long axis of second

Soft tissue impaction. molar
Bony impaction. Mesioangular
Distoangular
3. Third molar impaction can Horizontal
Vertical
be classified by angulation in Buccoangular
Linguoangular
Page 645
4. Clinical Features: 5. Investigations:
Difficulty in ope ning the mouth and de glutition. IOPA X-Ray, lateral oblique x-ray, OPG,
Localized tenderness and swelling. Complete haemogram
Radiating pain towards ear and sometimes 6. Treatment:
headache.
Advice antibiotics and analgesics.
Purulent discharge may be present from the site Cap.Amoxicillin 500mg 1 BD for 5days.
of infection. Tab.Diclofenac 50mg 1 BD for 5days.
Surgical removal of impacted tooth.
Page 646

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Contents Page No.

3 Obstetrics and Gynaecology 247-309

2 Non infectious Skin Conditions 319

3 Sexually Transmitted infections (STI) 324

4 Syndromic management of STDS 329

5 HIV AIDS 331

3 Pre AnaesthesiaCheck up Protocol 568

Table 1: Evaluation of fever patient

10. Fever Workup 10.4. Blood cultures

Figure 1 - Chest X-Ray PA VIEW - CAP

5. Investigation 6.2. Reliever: Used on or as needed basis to

Short acting oral 2 agonist - Tab Salbutamol 2-4mg/day

Anti cholinergic - Ipratropium inhaler

Theophylline - 100-300mg three times a day

6.3. Combinations available as Formoterol/Budesonide 1-2 puffs twice daily

ICS = Inhaled corticosteroid; Bradycardia or arrhythmia

Figure 2 Types of Devices used in Bronchial Asthma

Figure 1: Chest radiograph showing left-sided pleural effusion

4.2. Ultrasound 4.3. Blood tests

Table-1: Differentiating features between Emphysema and Bronchitis

Table-2: Differences between Pink puffer and Blue bloater

Pink puffer Blue bloater

2. Sputum Scanty Profuse

3. Polycythaemia Uncommon Common

4. X-ray Attenuated peripheral vessels Normal peripheral vessels

5. pCO2 Normal Increased

6. Alveolar gas transfer Reduced Normal

4.2. Pharmacological Fluticasone 1-2 puffs twice a day

(a) Oxygen therapy Budesonide 1-2 puffs twice a day

(b) Antibiotics Systemic corticosteroids should be given only in

(c) Bronchodilators 5. Complications

8. Treatment 8.3. Chronic Treatment

Symptoms are generally insidious and

The most common anaerobes are 4. Lab.Studies

Figure 1- X-Ray Showing Lung Abscess

Figure 2 CT-SCAN Showing Lung Abscess

Cephalosporins that have gram-positive, gram-

3.4 Traumatic non iatrogenic

Plain X-ray film of the chest showing

Figure 1 X-Ray Showing Pneumothorax

If pneumothorax small but patient mild

1. Definition 3. Risk factors

Figure 1: Chest X ray showing Left parahilar lung mass

Bronchoscopy - It is the most useful Focal neurologic signs, papilledema.

Sometimes patients are asymptomatic.

Figure-1: ECG changes seen in Pulmonary Embolism

Blood pressure is lateral pressure exerted by column

Table 1: Lifestyle changes to manage hypertension

5.3. Guidelines for management

History & Physical examination

Educate Patient on nutrition, saltrestrictions, physical activity

Start the Treatment

Age 60 Yr. Age < 60 Yr.

Goal achieved Goal achieved

Goal Not Achieved Goal Not Achieved

Goal achieved Goal achieved

Goal Not Achieved

Goal not achieved

Goal not achieved