CAPSULE

THIRD EDITION

20
GOVT. MEDICAL COLLEGE TRIVANDRUM 21
C A P S U L E
T H I R D E D I T I O N
A COMPLETE FINAL YEAR MANUAL

PUBLISHED BY
SFI MEDICAL COLLEGE UNIT
GOVT. MEDICAL COLLEGE, TRIVANDRUM

EDITOR
Dr. ANJALI U.

COVER PICTURE
DHRUVAN SIVAKUMAR
DISTRIBUTORS
ADARSH ANIL
+91 8921454353

AHAMMAD KABEER
+91 8921837128

ALL RIGHTS RESERVED, NO PART OF THIS PUBLICATION IS

TO BE PRODUCED IN ANY FORM OR BY ANY MEANS FOR
COMMERCIAL PURPOSE WITHOUT WRITTEN PERMISSION.
 CAPSULE COMMITTEE
CONVENOR
DR. ANJALI U.

CO-CONVERNOR
DR. JINAN R.S.

TYPING
DR. KENSON

MEDICINE PAEDIATRICS SURGERY

DR. ANAGHA PREM DR. ASHA AJITH DR. ABHILASH
DR. GOMATHY ARATHY DR. DEEPAK IYPE KOSHY DR. GOURI K.
DR. ANJALI U, DR. ARYA S.L. DR. KALYANI KRISHNAN
DR. ANANDAN DR. JASIM BIN JAFFER DR. NABIEL SALAM
DR. NAMITHA THERASA DR. KUMAR NAMITHA VIMAYA DR. NAMITHA MARIYAM
DR. DEVIKA M. DR. PARVATHY K.S.

OBS & GYNAEC

DR. RAMEESA
DR. ANJANA NAIR
DR. ANN LIZA
DR. ARUNIMA
DR. B. ATHIRA

GOVERNMENT MEDICAL COLLEGE

T H I R U V A N A N T H A P U R A M
 MESSAGE

Students Federation of India is one of the major students’ organisations in India found-
ed in 1970. As of 2015, it has a membership strength of nearly 43 lakhs among Schools,
Universities, Professional Institutes and Research Academies. SFI strongly follows the
principle that everyone deserves to be educated. It ensures that there is no barrier to
education for common people, especially in a country like India, where regressive
forces still prevail. SFI considers the fact that knowledge that is gained throughout the
education period enables each and every individual confident about their life and
opens various doors to the opportunities of achieving better prospects in life. SFI is an
umbrella organisation which brings together all the diverse ideologies of students and
is aware of its role in the society. It is totally committed to the idea of independence,
democracy and socialism. We utilise this occasion to pay our deep respect and love to
great visionaries of the past, like Dr. Ernesto Che Guevara, the doctor-poet-revolution-
ary, who is the legendary epitome of the leftist revolutionary movement.

Devu S Jayan Aslam Sagar

President Secretary
 EDITORS NOTE
The people of TMC takes immense pride in presenting the completely revised edition of
CAPSULE, a final year practical guide which was conceptualized and actualized by our
seniors years back. Given that the final year students are largely dependent on this con-
cise book for their preparation for practical exams, we have realised that an update in
long overdue.

We have done a thorough review of all the subjects and the salient features include
addition of case format for all long and short cases, relevant discussion points included,
more tables and diagrams for easier understanding and quick review. OSCE spotters
commonly asked in all the departments have been introduced along with basic examina-
tion techniques needed for demonstration especially for Surgery Practical exams. In
addition, the Radiology and Drugs section of all departments have been updated.

The main objective of the book is to provide a basic idea towards what to expect and
how to perform in the KUHS Final year practical examinations. We fully understand the
performance pressure and mental dilemma that each and every final year student under-
goes whilst appearing for a practical, as we ourselves have gone through the same. So
we have focused on incorporating sections that are lacking while largely maintaining the
essence of the book.

We thank each and every contributor to this venture, be it batchmate, junior or senior.
We also thank The Principal and various faculty members who have given their whole-
hearted support and encouragement for this book to be a reality.

We genuinely believe that this book will prove to be an indispensable aid for the entire
final year fraternity.

Dr. Anjali U
Convenor
“He who studies medicine without books sails in an uncharted sea, but
who studies medicine without patiens does not go to sea at all”

-William Osler
MEDICINE
CASE FORMAT 10
GENERAL EXAMINATION 23
1.BUILT 23
2.NOURISHMENT 23
3.PHYSICAL ATTITUDE 23
4.PALLOR 24
5.JAUNDICE/ICTERUS 25
6.CYANOSIS 26
7.CLUBBING 27
8.LYMPHADENOPATHY 28
9.OEDEMA 29
10.GENERAL EXAMINATION WITH RELEVANCE TO PARTICULAR SYSTEMS 30
11.VITAL SIGNS 30
PULSE 30
BLOOD PRESSURE 32
RESPIRATION 33
TEMPERATURE 34
JUGULAR VENOUS PRESSURE (JVP) 35
CVS CASE FORMAT 39
MITRAL STENOSIS 47
MITRAL REGURGITATION 50
AORTIC STENOSIS 52
AORTIC REGURGITATION 54
CONGENITAL HEART DISEASE IN ADULT 56
MANAGEMENT OF A/C RHEUMATIC FEVER 56
INFECTIVE ENDOCARDITIS PROPHYLAXIS 57
CNS ANATOMY 59
FUNCTIONAL AREAS OF BRAIN 59
BLOOD SUPPLY OF BRAIN 60
INTERNAL CAPSULE 62
BRAINSTEM 63
CEREBELLUM 64
Spinal Cord 65
CORTICOSPINAL TRACT 66
LATERAL SPINOTHALAMIC TRACT 67
ANTERIOR SPINOTHALAMIC TRACT 68
DORSAL COLOUMN PATHWAY 69
CRANIAL NERVE 70
Horner’s syndrome 72
INTERNUCLEAR OPHALMOPLEGIA 76
ACUTE STROKE SYNDROME 80
APPROACH TO HEMIPLEGIA 96
MANAGEMENT OF STROKE 99
LATERAL MEDULLARY SYNDROME/ 104
SYNDROME OF WALLENBERG 104
MEDIAL MEDULLARY SYNDROME 106
BRAIN STEM SYNDROMES 107
Mid brain syndromes 108
Pontine syndromes 109
LOCKED IN STATE 109
ATAXIC HEMIPARESIS 110
FACIOBRACHIAL MONOPLEGIA 110
PARAPLEGIA 111
SPINAL CORD SYNDROMES 120
LANDRY GUILLAIN BARRE SYNDROME 124
A/C TRANSVERSE MYELITIS 125
HYPOKALEMIC PERIODIC PARALYSIS 125
BELL’S PALSY 126
PARKINSONISM 127
PERIPHERAL NEUROPATHY 128
NEUROGENIC BLADDER 130
RESPIRATORY SYSTEM CASE FORMAT 133
CONSOLIDATION 140
PLEURAL EFFUSION 143
FIBROCAVITY 145
COPD 146
COLLAPSE 150
BRONCHIECTASIS 152
INTERSTITIAL LUNG DISEASE 153
BRONCHOGENIC CARCINOMA 154
LUNG ABSCESS 155
CHRONIC LIVER DISEASE 157
WILSON’S DISEASE 171
HEMOCHROMATOSIS 172
INSTRUMENTS 179
DRUGS 186
RADIOLOGY 191
EMERGENCY MEDICINE 197
 CASE FORMAT
Biodata:
 Name
 Age
 Sex
 Residence
 Occupation

Presenting complaints
 In chronological order

History of presenting complaints

 Remember to write review of other systems

History of past illness

Treatment history

Personal history
 Remember to include menstrual history in case of females

Family history
 Draw pedigree chart

Socioeconomic history

GENERAL EXAMINATION
 General comment
 Height, weight and BMI *write couldn’t assess if not possible]
 Pallor, icterus, cyanosis, clubbing, generalized lymph node enlargement
or edema
 Positive findings in head to foot examination if any
 VITALS
- Pulse
- Blood pressure

10
 - Respiratory rate
- Temperature [better to write values than afebrile]

EXAMINATION OF RESPIRATORY SYSTEM

UPPER RESPIRATORY TRACT

1. Nose: nasal mucosa,DNS,Discharge,polyps
2. Paranasal sinuses: erythema/swelling/tenderness over region of
paranasal sinuses
3. Oral cavity:oral hygiene,teeth,gums,buccal mucosa, tonsils and
fauces,posterior pharyngeal wall,post nasal dripping

EXAMINATION OF CHEST
Inspection
1. Shape of chest
2. drooping of shoulder or hollowing or prominence
3. Position of trachea
4. apex beat
5. Respiratory movements
6. intercostal retraction, crowding of ribs
7. dilated veins,visible pulsations,scars,sinuses or oedema of chest wall

Palpation
1. position of trachea
2. apex beat was felt on – th left intercostals space ---- cm medial/lateral to
or in midclavicular line
3. Respiratory movements
LEFT RIGHT

Anterior chest –

 upper part
 Lower part
Posterior chest –

 upper part
 Lower part
11
4) Chest expansion
-total
-differential

5)anteroposterior diameter:Transverse diameter Ratio

6) vocal fremitus R L
Supraclavicular area
Infraclavicular area
Mammary area
Axillary area
Infraaxillary area
Suprascapular area
Interscapular area
Infrascapular area

PERCUSSION
1)Area
Kronig’s isthmus
Infraclavicular area
Mammary area
Axillary area
Infraaxillary area
Suprascapular area
Interscapular area
Infrascapular area
2)liver dullness
3)traube space
4)tidal percussion- [if lower right areas shows dullness]
5)shifting dullness

AUSCULTATION
1)Intensity of breath sounds
Supraclavicular area

12
 Infraclavicular area
Mammary area
Axillary area
Infraaxillary area
Suprascapular area
Interscapular area
Infrascapular area

2)adventitious sounds
3)vocal resonance R L
Supraclavicular area
Infraclavicular area
Mammary area
Axillary area
Infraaxillary area
Suprascapular area
Interscapular area
Infrascapular area

EXAMINATION OF CARDIOVASCULAR SYSTEM

 Examination of arterial pulse

 Arterial blood pressure :
upper limb
Lower limb
 Jugular venous pressure

INSPECTION
1)Shape of precordium
2)Apical impulse
3)visible pulsations
4) dilated veins or visible scars

PALPATION
1)apex beat palpated at____

13
2)left parasternal heave
3)sub xiphoid pulsation/epigatric impulse
4) pulmonary artery pulsation
5)other palpable pulsations
6)thrills

PERCUSSION
(To be written as)
The left border of the heart corresponds to the apex beat in the ___intercostal
space___ cm medial/lateral to/in midclavicular line ,the right border
corresponds to right sterna edge and the dullness in the 2nd space do not
extend beyond 2.5 cm on either side of sternum.

AUSCULTATION
1)Heart rate
 mitral area:
 Tricuspid area:
 Pulmonary area:
 1st aortic area:
 2nd aortic area:

EXAMINATION OF GASTROINTESTINAL SYSTEM

 Signs of chronic liver disease

 Signs of liver failure

Examination Of Upper Gi Tract

 Lips, gums, teeth, tongue, buccal mucosa, palate,tonsils, fauces,
posterior pharyngeal wall
 bad breath
 Examination of oesophageal function – Comment as normal if the
patient can swallow liquid and solid items without difficulty
 EXAMINATION OF ABDOMEN

Inspection
14
 1) Shape of abdomen
2) Umbilicus – position, inverted/in level with skin/everted
3) Movements of abdominal wall : see whether all quadrants move with
respiration, visible pulsations,visible peristalsis
4) Skin and surface of abdomen
5) Superficial veins: to be commented on after examining in standing
position only
6) Hernial orifices
7) External genitalia

Palpation
1) Local rise of temperature
2) Tenderness
3) Palpation of liver : if palpable comment as how many centimeters below
costal margin in MCL. Border(whether sharp or rounded), consistency,
tender or not
4) Palpation of spleen: if palpale, comment as how many cms in a line
perpendicular to left costal margin, surface,consistency, tenderness,
look for noches
5) Other palpable masses
6) Abdominal girth
Percussion
1) Liver dullness was percussed in ……. Right ICS in midclavicular line, ……
right ICS in midaxillary line,…..right ICS in scapular line
2) Liver span
3) Percussion of traube space
4) Fluid thrill
5) Shifting dullness

AUSCULTATION
1) Bowel sounds
2) Bruit/venous hum/hepatic friction rub/splenic rub

 Examination of groin
 Examination of external genitalia

15
  Per rectal examination- not done

EXAMINATION OF NERVOUS SYSTEM

 Handedness
 Education
 Occupation
 Languages

Higher Mental Functions

1) level of consciousness
2) appearance and behavior
3) orientation in time,place and person
4) attentive or not
5) memory
6) speech – fluency , comprehension,repetition,naming, reading and
writing
7) intelligence
8) mood

EXAMINATION OF CRANIAL NERVES

RIGHT LEFT
I)Olfactory nerve
Smell
h/o anosmia,parosmia
II)Optic nerve
a)visual acuity – near vision
-distant vision
b)field of vision
c)colour vision
d) fundus- not examined

III,IV& VI) Occulomotor, trochlear and abducent nerve

a) eyelids
b) extraocular movements
16
 c) convergence
d) nystagmus
e) pupil
-size and shape
-light reflex –direct
- indirect

V) Trigeminal nerve
a) motor part
- inspection of temporal fossa and angle of
Jaw, look for hollowing /wasting
- muscles of masticaton
b)sensory part
- touch,pain and temperature in all 3 divisions
c)reflexes
- conjunctival reflex
- corneal reflex
- jaw jerk

VII) Facial nerve

a. deviation of angle of mouth
b. motor part
-wrinkling of forehead
-blinking
-Bell’s phenomenon
-forced eye closure
-nasolabial fold
-clenching of teeth
-blowing of cheek
-whistling
-platysma
c. sensory part- taste in anterior 2/3rd of tongue
d. h/o hyperacusis
e. salivation and lacrimation

17
VIII) Vestibulocochlear nerve
- h/o tinnitus,vertigo,nystagmus
- earwax, discharge or perforation
- Rinne’s test
- Weber’s test
- Absolute bone conduction test

IX & X ) Glossopharyngeal and Vagus nerve

- Nasal twang/ hoarseness of voice

- Nasal regurgitation
- Uvula central/not
- Arches of palate
- Reflex – gag reflex
-palatal reflex

XI)accessory nerve
-Turning of head against resistance (sternocleidomastoid)
-shrugging of shoulders (trapezius)

XII) hypoglossal nerve

- Wasting or fasciculations of tongue
- Deviation of tongue
- Power of tongue muscle

EXAMINATION OF MOTOR SYSTEM

1)Bulk of muscle
- Upper arm
- Forearm
- Thigh
- Calf

2)Tone of muscle

18
 - Upper limb
- Lower limb

3)Power of muscle
 neck
- flexion
- extension
 hand grip
 fingers-
- flexion
- extension
 wrist
- flexion
- extension
 elbow
- flexion
- extension
 shoulder joint
- flexion
- extension
- adduction
- abduction
 hip joint
- flexion
- extension
- adduction
- abduction

 knee joint
- flexion
- extension

 ankle joint –
- dorsiflexion
- plantar flexion
19
 - inversion
- eversion
 great toe
- flexion
- extension
-
4)Examination of reflexes
Superficial reflexes
1) Corneal reflex
2) Conjunctival reflex
3) Palatal reflex
4) Gag reflex
5) Abdominal reflex
6) Plantar reflex
7) Cremasteric reflex

Deep tendon reflexes

1) Jaw jerk
2) Biceps jerk
3) Supinator jerk
4) Triceps jerk
5) Ankle jerk
6) Knee jerk

Primitive reflexes
1) Grasp reflex
2) Avoidance reflex
3) Palmomental reflex
4) Sucking relex
5) Snout reflex
6) Rooting reflex
7) Glabellar reflex

20
CO-ORDINATION
-Upperlimb
1) Finger nose test
2) Finger to finger nose test
3) Rebound phenomenon
4) Past pointing
5) Dysdiachokinesia

-Lowerlimb
1) Heel knee test
2) Toe finger test

-Nystagmus
-Rebound phenomenon
-Gait
-Tandem walking
-Involuntary movements

EXAMINATION OF SENSORY SYSTEM

-Superficial sensations
 Pain
 Touch
 Temperature
-Deep sensations
 Position
 Passive movement
 Vibration
 Pressure
-Cortical sensations
 Two point discrimination
 Tactile localization
 Stereognosis
 Graphesthesia
 Double simultaneous stimulation
21
-Romberg sign

SIGNS OF MENINGEAL IRRITATION

 Neck stiffness
 Krenig sign
 Brudzinkis sign
 Straight leg raising test

EXAMINATION OF PERIPHERAL NERVES

EXAMINATION OF SKULL AND SPINE

SUMMARY

PROVISIONAL DIAGNOSIS

22
 GENERAL EXAMINATION
1.BUILT
Assess the skeletal framework of the individual and compare it with the normal
for his/her age. Comment as Poorly/Moderate/Well built.

Tall stature (above 97th percentile) Dwarfism (below 3rd percentile)

▪ Racial or Familial ▪ Constitutional
▪ Idiopathic ▪ PEM ,Rickets
▪ Marfans ▪ Cretinism, Hypopituitarism
▪ Gigantism and Acromegaly ▪ Downs, Turners syndrome
▪ Klinefelters ▪ Achondroplasia
Note: imp in CVS case- marfans , turners(coarctation of aorta)& downs(VSD,
PDA)

2.NOURISHMENT
The nutritional state of a patient may provide an important indicator of
disease, and prompt correction of a deficient nutritional state may improve
recovery.
BMI= WEIGHT(KG)/HEIGHT(m2)

In Asians:
• Normal BMI: 18-23
• Overweight: 23.1-28
• Obese: 28.1-33
• Grossly obese: >33.1
In Europeans:
• Normal BMI: 20-25
• Overweight: 25.1-30
• Obese: 30.1-35
• Grossly obese: >33.1

CAUSES of EMACIATION CAUSES of OBESITY

• Pulmonary tb • Idiopathic
• Diabetes mellitus • Physical inactivity
• Thyrotoxicosis • Cushings syndrome
• Malignancy • Hypothyroidism
• AIDS • Iatrogenic-steroid,estrogen

3.PHYSICAL ATTITUDE
Patient is in the standing/sitting/supine position
Look whether patient is comfortable or in distress

23
4.PALLOR
Pallor is the paleness of skin and mucous membrane. It depends on thickness
and quality of skin, and quality and amount of blood in the capillaries. Thus,
pallor and anemia are not interchangeable terms. There are many causes of
pallor, and anemia is commonest of them. Anemia is a pathological condition
while pallor is a clinical entity.
Anemia: It is defined as the qualitative or quantitative diminution of RBC and /
or hemoglobin concentration in relation to standard age and sex, and is
clinically manifested by pallor.

Sites: Causes:
1. lower palpebral 1. Blood loss
conjunctiva 2. Decreased production-
2. Dorsum of tongue iron deficiency,vit B12 & folic acid def, aplastic
3. Palate anemia, bone marrow infiltration
4. Nail bed 3. Hemolysis-thalassemia, spherocytosis, AIHA
5. palms 4. Chronic malaria, TB, malignancy
6. sole 5. Endocrine- addisons disease,
myxoedema,sheehans syndrome

Systemic features in case of pallor

CVS: tachycardia, water hammer pulse, cervical venous hum(devil’s hum),
cardiomegaly, hyperdynamic apex, mitral systolic murmur, pulmonary haemic
murmur
G.I. tract : Hepatosplenomegaly may be present.
Respiratory system Basal crepitations.
Nervous system Features of polyneuropathy, subacute combined degeneration
Lymphoreticular- sternal tenderness
Others- dyspnoea, ankle edema

CAUSES OF POLYCYTHEMIA Pallor without anemia

• COPD • Peripheral circulatory failure/ shock/
• High altitude vasoconstriction
• Myxoedema
• Cyanotic congenital heart
• Oedematous conditions, e.g., anasarca
disease • Thick skin (e.g., scleroderma).
• Polycythemia vera • Very tight AS or MS
• Severe dehydration • Acute myocardial infarction

24
5.JAUNDICE/ICTERUS
Yellowish discolouration of skin, mucous membrane and other tissue due to
excess of circulating bilirubin (serum level >1mg/dl)
 Hemolytic jaundice: lemon yellow tinge of conjunctiva, acholuric urine,
high coloured stool,anaemia, splenomegaly

Causes (hemolysis)
Causes of non-hemolytic unconjugated
1. Thalassaemia hyperbilirubinemia
2. mismatched blood 1. Hereditary- Gilbert’s, Criggler Najjar
transfusion 2. Acquired transferace deficiency- breast milk
3. snake bite jaundice,drug inhibition as by chloramphenicol
4. malaria 3. Decreased hepatic intake-prolonged fasting,
sepsis

 Hepatocellular Jaundice: orange yellow conjunctiva, anorexia, nausea,

abdominal pain, tender hepatomegaly, purities

Causes
• viral hepatitis • acute fatty liver of pregnancy
• drugs like rifampicin ,INH • cirrhosis
• paracetamol overdose • weil’s disease
• copper sulphate poisoning • Wilson’s disease

 Obstructive jaundice: greenish yellow conjunctiva, deep yellow urine,

pale coloured stools, purities, sinus bradycardia, xanthelesma, bleeding
manifestations due to vit K deficiency

CAUSES
Intrahepatic Extrahepatic
• cholestatic viral hepatitis • Gallstones
• lymphoma or TB • pancreatic carcinoma
• hepatic mets • stricture of CBD
• drugs like chlorpromazine, OCP, erythromycin, • sclerosing cholangitis
methyl testosterone,anabolic steroids

25
6.CYANOSIS
Cyanosis is a blue discoloration of the skin and mucous membranes that occurs
when the absolute concentration of deoxygenated haemoglobin is increased in
the capillary blood.
A minimum of 5gm/100 ml of reduced hemoglobin is necessary before
cyanosis can be detected clinically. So, in patients with severe anaemia,
cyanosis may not develop because the amount of reduced hemoglobin does
not reach 5gm/100 ml.

SITES D/Ds of bluish discoloration of body

Under surface of tongue
Mucous membrane of • Cyanosis
mouth • CO poisoning
Lips • drugs like amiodarone
Finger tips
Nail bed
Ear lobes

Note: Pigmentation may be mistaken for cyanosis. This can be differentiated

by pressing with a glass slide. Cyanosis will disappear while pigmentation will
not.

Central cyanosis is due to reduced Peripheral cyanosis is due to reduced

arterial O2 saturation(hypoxic hypoxia) and slow blood flow to the limbs
Causes because of vasoconstriction of blood
• CCHD (TOF,TGA) vessels
• a/c pulm oedema, • exposure to cold,
• Eisenmenger’s syndrome, • CCF,LVH
• COPD*, cor pulmonale, • shock,
• resp failure, • Raynaud’s phenomenon
• a/c severe asthma* • Reduced cardiac output
• high altitude.

Differential cyanosis-Eisenmenger’s PDA(cyanosis only in lower limbs)

Reverse differential cyanosis-CoA with TGA(cyanosis more in hand than in
feet)
Intermittent cyanosis –Ebstein’s anomaly
26
7.CLUBBING
Clubbing is the bulbous enlargement of the distal segments of fingers and toes
due to proliferation of soft tissues(capillaries & connective tissue) espes\cially
on their dorsal surface.

GRADES OF CLUBBING
Grade 1-increased fluctuation at nail base
Grade 2-obliteration of angle (nail-nail fold)
Grade 3-drun stick/parrot beak appearance
Grade 4- Hypertrophic pulmonary osteoarthropathy(HPOA)

PROCEDURE –Bring the patient’s finger(index finger of the non-dominant

hand) to the examiner’s eye level and look tangentially across the nail bed. For
eliciting fluctuation-Support patient’s index or middle finger on the pulp of
both the thumbs of the examiner.Then,place the examiner’s two index fingers
over the patient’s skin at the base of the nail.Press with one index finger and
feel the fluctuation with the other index finger.

Lovibond’s sign –angle between nail and nailbed becomes more than 160
degree in early clubbing.
Schamroth’s sign-Keep the nails of the two index fingers together by flexing
the interphalangeal joint. Keep at the examiner’s eye level & look between the
nails. Diamond shaped space visible between the two nails and the nail beds
will be obliterated in clubbing.

Causes of Clubbing

 Congenital cyanotic heart disease like TOF

 Subacute bacterial endocarditis (SBE)
Cardiac  Rarely in cardiac tumors ( atrial myxoma)
 Eisenmenger’s syndrome, primary pulmonary
hypertension
 Bronchitis  Pulmonary AV fistula
 Lung abscess  Pleural mesotheiloma
Lung and Pleura  Bronchogenic  Fibrosing alveolitis
carcinoma  Cystic fibrosis
 Empyema thoracis

27
 Endocrine  Hyperthyroidism

GIT  Ulcerative Colitis  Crohn’s disease

 Malabsorption  Polyposis coli
Liver  Biliary cirrhosis
 Sometimes in hepato-cellular failure
Genetic  May be a familial condition

Idiopathic  Found normally in some people

Causes of HPOA
- lung abscess
- empyema
- bronchiectasis
- bronchogencic carcinoma

Painful clubbing- Broncogenic carcinoma,SBE, lung abscess

Unilateral clubbing-Presubclavian CoA, Broncogenic carcinoma,cervical
rib,Pancost’s tumor
Unidigital clubbing-local trauma,sarcoidosis
Differential clubbing-only in the lower limbs-Eisenmenger’s PDA, infected
abdominal aortic aneurysm,infected arterial grafts.
Koilonychia-spoon shaped nails-develops as a result of retarded growth of nail
plates-seen in long standing Fe deficiency anemia, idiopathic, overuse of
solvents and detergents

8.LYMPHADENOPATHY
Lymphadenopathy refers to nodes that are abnormal in either size, consistency
or number(Inflammatory or non inflammatory)
Total number of nodes: 400-450
Nornal size:<0.5cm in diameter
Generalised lymphadenopathy- involvement of 3 or more non-contiguous
extra inguinal lymph node areas.
Note site, number, size, consistency, tenderness, mobility, matted/discrete,
fixity to skin, condition of overlying skin & area of drainage
SITES: submental, submandibular, preauricular, JDN, supraclavicular,
deepcervical, scalene, posterior auricular, occipital, epitrochlear, axillary,
inguinal, popliteal

28
Causes of generalized lymphadenopathy-
 Neoplasms-lymphoma,ALL,CLL;
 Infections-Disseminated or military TB,HIV,IMN,measles
 Others-secondary mets, Collagen vascular disease(SLE), Amyloidosis

Causes of localized lymphadenopathy-

 cellulitis,
 lymphangitis,
 abscess,
 injury

HSM with lymphadenopathy- lymphoma, leukemia, disseminated TB, SLE,

Sarcoidosis

Lymphadenopathy with fever- lymphoma, TB, ALL, SLE, IMN, AIDS

Causes of epitrochlear lymphadenopathy- IMN, non-Hodgkin’s lymphoma,

2°syphilis, local pathology, pyoderma of upper limb

9.OEDEMA
Accumulation of excessive amount of tissue fluid in the subcutaneous tissue
due to increase in extravascular(interstitial) component of the ECF volume
resulting in swelling of tissue.
Mechanisms of edema formation – low plasma oncotic pressure
(hypoproteinemia, cirrhosis);high capillary hydrostatic pressure
(CCF,DVT);increased capillary permeability (acute inflammation);obstructed
lymphatic drainage (filariasis,radiation).
SITES- lower extremities & presacral region
Apply gentle pressure with thumb over the bony area (shin of tibia,medial
malleolus,sacrum) and look for pitting. Comment as pitting/non-pitting
edema.
• PITTING- due to accumulation of fluid in s/c tissue-CCF, liver cirrhosis,
nephrotic syndrome, hypoproteinemia, portal HTN, pericardial effusion,
constrictive pericarditis
• NON-PITTING-due to infiltration of s/c tissue by collagen tissue or lymph-
myxoedema, lymphoedema, angioneurotic oedema, scleroderma .
GENERALIZED EDEMA(ANASARCA)- CCF, liver cirrhosis, nephrotic syndrome,
drugs, hypoalbuminemia,
LOCALIZED EDEMA-SVC syndrome, varicose veins, DVT, filariasis, TB, Ca breast,
Milroy’s diseas, angioneurotic oedema, trauma,cellulitis
29
Unilateral pedal edema – DVT,cellulitis,filariasis,trauma

10.GENERAL EXAMINATION WITH RELEVANCE TO PARTICULAR

SYSTEMS
CLD
AR(PERIPHERAL SIGNS)
Marfan’s
Respiratory failure
Neurocutaneous syndroms
Hypothyroidism


11.VITAL SIGNS

PULSE
Expansile impulse transmitted along vessel wall as a result of LV ejection
against partialy filled aorta and transmitted with more velocity than blood flow
to periphery and palpated in an artery while pressed against bony prominence

Palpation: shoulders abducted, semiflexed elbow, semipronated & semiflexed

wrist, supported by right palm and palpate using left by trisection method.
Middle finger to count and others to know condition of vessel. Count for 1
minute.

1.Rate 60-80/min

Tachycardia >100/min
Physiological Exercise, high altitude, anxiety
CVS causes Non- CVS causes
Tachyarrhythmia Hyperthyroidism
Pathological MI (anterior wall) Fever (10 C rise = 18bpm)
Shock Beri Beri
Myocarditis Drugs (atropine,
salbutamol)

Bradycardia <60/min
Physiological Elderly, sleep, athletes
CVS causes Non- CVS causes

30
 Bradyarrhythmia Hypothyroidism
Pathological MI (inferior wall) Hypothermia
Increased ICT
Drugs (beta blocker,
digoxin)
Obstructive jaundice

2.Rhythm- regularity with which each beat follows the other.

Regularly irregular:
Sinus arrhythmia- increase on inspiration & decrease on expiration ( Bain
Bridge reflex)
With tachycardia- ventricular bigemini
With bradycardia- wenkebachs phenomenon

Irregularly irregular: AF, mulifocal AT, multiple ventricular ectopics

3.Volume- amplitude of expansion of vessel wall produced by a pulse wave

High:
Collapsing- AR,PDA(palpation-feel pulse by base of fingers of right/left hand &
raise abv head level)
Non collapsing- MR, VSD, SYSTEMIC HYPERTENSION
Low:
MI, obstructive valve disease

4.Character -palpate carotid or brachial artery.

Normal pulse has
 Tidal wave:it is due to pressure transmitted by isovolumetric LV
contraction
 Percussion wave: because of blood ejection into carotids
 Dicrotic wave:due to back pressure from small vessels
 Dicrotic notch represents closure of aortic, pulmonary valve(S2)

Abnormalities
• Hyperkinetic pulse – increase in amplitude –high cardiac output states
• Hypokinetic pulse – decrease in amplitude –low cardiac output states

31
• Pulsus parvus et tardus- AS (slow riseing and late peaking)
• Pulsus bisferiens- all beats equal volume with 2 peaks in systole(AR+AS,
severe AR )
• Dicrotic pulse- 2 peaks one in systole & other in diastole (shock)
• Pulsus alternans- normal rhythm with alternate strong & weak beats( acute
LVF)
• Pulsus bigemini – regularly irregular rhythm with alternate strong & weak
beats(digitalis toxicity,3:2 )

5.Palpate all peripheral pulses

6.Condition of vessel wall- atherosclerosis (thickened)

7.Radiofemoral delay
Causes
• Coarctation of aorta –young hypertensive, prominent suprasternal and
carotid
• pulsation, Suzman’s sign(collateral pulsation),bruit over collaterals
• Atherosclerosis of aorta
• Aortoarteritis

BLOOD PRESSURE
Systolic pressure indicates stroke volume - pressure when heart contracts
Diastolic indicates peripheral resistance -when heart relaxes
Do both palpatory & auscultatory method so as not to miss the silent gap...

32
Korotkoff’s sound
Phase 1 Appearance of tap sound, this marks the systolic BP
Phase 2 Sound takes up the murmuring quality, auscultatory gap
may appear in this phase.
Phase 3 Sound become very loud and gauging in quality
Phase 4 Sound suddenly becomes muffled
Phase 5 All sounds disappear, DBP recorded here

In lower limb BP –patient in prone position, put cuff on thigh and palpate
popliteal artery.
Normal values- systolic <130 & diastolic 85mm Hg (classification –davidson
pg.509)
(In cvs case take BP in 3 limbs- right upper limb, left upper & lower limb
In case of AF record 2 diastolic BP and take the average )
Anisosphygmia – difference of>10mm Hg btwn dominant & non dominant
limbs
Unequal BP in supravalvular AS and coarctation of aorta
Normal difference between upper & lower limbs is <40mmHg.due to increased
axial blood flow and muscle mass in lower limb.
If >40 – hill’s sign, seen in AR
Postural hypotension- systolic falls by 10mm Hg in standing

Pulsus paradoxus: exaggerated fall of systolic BP (>10mm)

asthma SVC obstruction

COPD constrictive pericarditis
cardiac tamponade

Pulsus alternans: demonstrated by sphygmomanometer noting the doubling

of Korotkoff’s sound- in acute LVF

RESPIRATION
Rate: normal 16- 20/min
• >20- tachypnoea= fever, exertion, acid poisoining,pneumonia, pul oedema,
ARDS, pneumothorax, pleural effusion
• <16-bradypnoea= raised ICT, narcotic poisoning,hypothyroidism

Rhythm: abnormalties-

33
• Cheyne stoke’s – rhythmic alterations of apnoea & hyperapnoea due to
anoxemia. Seen in infants, high altitude, deep sleep, raised ICT, narcotic
poisoning, uremia,severe LVF
• Kussmal’s breathing- deep & rapid breathing. Seen in diabetic ketoacidosis
• Biot’s breathing- always pathological...irregularly irregular breathing seen in
meningitis.

Type :normally thoracoabdominal in femals & abdominothoracic in males

• Predominantly thoracic- diaphragmatic paralysis, peritonitis,ascitis
• Predominantly abdominal- pleurisy, massive collapse of lung

TEMPERATURE
normal: 36.6-37.20C or 98-990F
Sites-
• oral (0.50C less than rectal)
• Axilla(0.50C less than oral)
• Rectal (most accurate)

Fever: elevation of body temperature above the normal circadian variation

(37.20C or 98.90F in morning and 37.70C or 99.90F in evening)in conjunction
with an increase in hypothalamic set point
• Continuous- fluctuation of temp <10C or 1.50F during 24 hrs, but do not
touch
normal. Occurs in lobar pneumonia, enteric fever, endocarditis

• Remittent – daily fluctuation >20C in TB, viral fever,non infectious cause of

fever
• Intermittent – rises and falls touching normal in between. As in malaria
• Hyperpyrexia: temperature is >41.60C or >1070F.
CAUSES- septicemia, heat stroke, thyroid storm,cerebral malaria
• Hyperthermia: elevation of body temp without rise in hypothalamic set
point.
• PUO- was defined as (1) temperatures of >38.3°C (>101°F) on several
occasions; (2) a duration of fever of >3 weeks; and (3) failure to reach a
diagnosis despite 1 week of inpatient investigation

34
JUGULAR VENOUS PRESSURE (JVP)

JUGULAR VENOUS PULSATIONS- it is the transmitted waves in the right internal

jugular vein due to changes in the right atrial pressure.
JVP is important as it is the indirect measurement of central venous pressure
at bedside. It is of paramount importance, especially in fluid overload and
congestive heart failure.
Right IJV is taken for measurement as it is
• In direct continuity with RA,
• Valveless
• Non- tortuous
• reflects pressure changes in RA as well as CVP.

CLINICAL MEASUREMENT – Ideally, patient is in 45 degree. Use 2 scales.1

vertical at sterna angle,the other horizontal kept at sterna border.Express in
cms of blood column Normal -2-3 cm above sternal angle
It is measured from angle of Louis/sterna angle because :
• easily located,
• visible bony point,
• its relation to centre of RA remains constant irrespective of position of body.
• It is 5 cm from RA always.
• So, CVP- height of blood column above sternal angle + 5 cm

45 degree elevation is preferred as otherwise IJV will collapse and so upper

level will not be visible.

CAUSES OF RAISED JVP

• cardiac failure
• cardiac tamponade
• SVC obstruction
• fluid overload (over transfusion of fluids,acute renal failure)
• increased intra abdominal pressure (ascites,pregnancy)
• tricuspid stenosis

VENOUS PULSATIONS ARTERIAL PULSATIONS

Better seen than felt Better felt than seen
Wavy in nature Jerky abrupt

35
More prominent on expiration No change
More prominent on lying down No change
More prominent on application of No change
abdominal pressure (hepato jugular
reflux)
Can be obliterated with pressure No effect
2 positive waves seen 1 positive wave seen
Has definite upper level No such level seen
Reflects pressure changes in RA No relation

WAVES
‘a’ wave: due to right atrial contractions
absent ‘a’ wave Atrial fibrillation(ineffective
contraction)
Giant ‘a’ wave TR,RVH(due to PAH),RV failure,
Cardiac tamponade
Cannon ‘a’ wave Regular :junctional rhythm
Irregular: complete heart block, AV
dissociation with ventricular
tachycardia

‘C’ wave –closure & bulging of tricuspid valve

X’ descent-atrial relaxation with downward descent of tricuspid valve (ejection

phase)

decreased /absent TR,AF

deep ‘x’ descent cardiac tamponade,
constrictive pericarditis

‘V’wave – passive RA filling during ventricular systole

Giant ‘v’ wave TR

Absent ‘v’wave SVC obstruction

‘Y’descent- RV filling with atrial emptying

Prominent constrictive pericarditis, severe
‘y’desent cardiac failure, severe TR,
36
 restrictive cardiomyopathy
slow ‘y’ TS, RA myxoma
descent

HEPATOJUGULAR REFLUX – apply firm pressure over right hypochondrium for

about 10-30 seconds.note the upper level of JVP.Nly,it rises and immediately
falls.In patients with RVF,upper level rises by 2-3 cm,remains elevated,as long
as pressure over abdomen is applied.

KUSSMAUL’S SIGN –Normally ,upper level of JVP falls during inspiration.

Kussmaul’s sign is present when upper level of JVP increase during inspiration.
Seen in severe Cardiac failure, c/c constrictive pericarditis ,restrictive
cardiomyopathy, RV infarction,rarely in cardiac tamponade.

Features of AF
• Irregularly irregular pulse
• ECG
- Absent p wave
- Fibrillating baseline
- Irregularly irregular R-R interval
• JVP
- Absent ‘a’ wave

37
CARDIOVASULAR SYSTEM

38
 CVS CASE FORMAT
Common Presenting Symptoms:
 Chest pain
Use SOCRATES for history taking.
Exertional Chest pain – heaviness or tightness radiate into arms, neck or
jaw and shortness of breath.
Causes of Angina
Impaired Myocardial oxygen supply Increased Myocardial Oxygen
 Coronary Artery Disease Demand
 Coronary Artery Spasm
 Congenital Coronary Artery  Left Ventricular
Disease Hypertrophy
 Severe Anaemia or Hypoxia  Tachyarrhythmias

Refer – Levine Sign, Types of Angina

- Other causes of Chest Pain –Herpe Zoster, Costochondritis,
Myalgia etc.
 Dyspnoea
Abnormal awareness of breathing occurring either at rest or at an
unexpectedly low level of exertion
Type Definition Pathology Causes

Orthopnoea Dyspnoea on Increased 1.LVF

recumbent venous return 2.a/c Asthma
position. cause steep rise 3.a/c COPD
in Pulmonary 4.MS
Arterial 5.Bilateral
Pressure and Diaphragmatic
increase lung Palsy
Congestion
PND(cardiac Dyspnoea 2-5 Redistribution Asthma
Asthma) hrs after of oedema fluid Sleep Apnoea
sleep,often reduced
39
 associated sympathetic
with nocturnal drive
cough.
Trepopnea Dyspnoea on 1.Heart d/s
Lateral 2.Pleural d/s
Decubitus
Position

Platypnea Dyspnoea on 1.Left Atrial

erect Position Myxoma
2.Hepatopulmonary
Syndrome

.
 Fatigue
Exertional fatigue ->Heart Failure
- more towards the end of the day
 Palpitation
Awareness of Heart Beat and is indicative of abnormal Cardiac
Rhythm.
Regular Sustained: SVT,VT
Irregular Sustained:AF
Positional:Atrial Myxoma
Ask the patient: -to tap the rhythm
Onset at rest or exertion
Duration
Associated Symptoms.

Important causes
Anxiety,AR,MR,Pulmonary Embolism,
Misc.: Tobacco,coffee
 Dizziness and Syncope
Occurs by transient hypotension resulting in abrupt Cerebral
Hypoperfusion.

EXCLUDE A RESPIRATORY CASE -Chest Pain and Dyspnoea can occur in both
40
ARRANGE THE SYMPTOMS IN A CHRONOLOGICAL ORDER
ASD – Angina, Syncope, Dyspnoea for Aortic Stenosis. (AS)
PDS – Palpitation, Dyspnoea, Syncope for Aortic Regurgitation. (AR)
PDF – Palpitation, Dysnea, Fatigue for Mitral Regurgitation (MR)
Exertional Dyspnoea, Early Orthopnoea, PND for Mitral Stenosis.

Past HistoryFamily History

 Stroke, TIA, Renal Impairment,
 Cardiac Disease
 Rheumatic Fever,POVD
 Sudden Death
 r/c Resp infection

Personal History & Drug History

 Diabetes, Hypercholestrelemia
 Statins
 Smoking, Hypertension, Rheumatic Prophylaxis

GENERAL EXAMINATION
 General Appearance – Comfortable,Breathless,Pale
 Inspect for clubbing, Splinter hemorrhages ,Nicotine staining
 Chest wall
- Pectus Excavatum
- Median Sternotomy scar – CABG
- Lateral Sternotomy scar – Mitral Valvotomy
- Visible Pulsations – Large ventricular or Aortic Aneurysm
- Venous Collaterals – SVC obstruction
 Anaemia – exacerbate Angina and Heart Failure
 Cyanosis –
- Peripheral Cyanosis – Cold Exposure, Heart Failure
- Malar Flush – in Mitral Stenosis
- Central Cyanosis – Pulmonary oedema & Congenital Heart Disease
 Clubbing – Infective Endocarditis
 Cutaneous and Ocular Signs – SplinterHemorrhages ,Osler’s nodes.
 Coldness of Extremities – Severe Heart Failure
 Pyrexia – Low Grade /Swinging – Paravalvular abscess

41
  Oedema – Congestive Heart Failure.
 Signs of Marfan’s Syndrome and Peripheral Signs of AR has been dealt
under the section of AR.
 Arterial Pulse( explained in detail in General Examination)
 Rate :Expressed in beats per minute
 Rhythm : Normal sinus rhythm is regular
 Irregular Rhythm – Examine for Pulse Deficit
 Character : Volume and waveform of pulse – Rt. Carotid Artery
 Symmetry: of Radial ,Brachial, Carotid, femoral ,popliteal and pedal
pulses should be confirmed
 Blood Pressure & JVP – Dealt in General Examination

Examination of Chest
Inspection
1. Shape of Precordium – Bulging,retraction
2. Position of Apical Impulse – Position in relation to nipple in male (don’t say
the intercostal space)
3. Visible Pulsations – Looked for at supraclavicular, suprasternal,2nd
intercostals spaces and other areas of precordium and in epigastric region.
4. Visible scars- midline sternotomy, lateral thoracotomy.
Palpation
Carried out in warm room.
Finger Tips – Pulsations
Base of fingers – thrills
Proximal Palm – Heave

1. Palpation of Apex Beat

Lower most and outer most point of definite cardiac impulse. Patient in
Supine Position only.
Character of Apex should be described in Supine position only
Learn Definitions of Normal, Tapping, Forceful, Heaving and Diffuse Apex. (
Consensus– 42)
Examine for Palpable S3 or S4 , EjectionClick, Late Systolic Bulge of HCM or
Apical Thrills in left Lateral Position.

42
2. Left Parasternal Heave
Felt in Right Ventricular Hypertrophy or Left Atrial Impulse (severe MR) which
occurs after Apical Impulse.
Palpate with Ulnar Border of hand with patient in Supine position in Left
parasternal Regions.
Press firmly with Proximal Palm and try to Obliterate Pulsations.
Learn LPH Grading from Consensus- 43
3. Sub Xiphoid Pulsation
Done with extended Index Finger kept at Epigastrium and Patient is asked to
take a Deep Inspiration.
Right Ventricular Hypertrophy – Impulse felt on finger tips
Aortic Pulsations- felt on Pulp of Fingers.
Right Ventricular S3 and S4 – felt at this site.

4. Palpation of Pulmonary Arterial Pulsation

Firm Palpation with Index Finger over the 2nd left ICS is required. Pulsations and
Palpable S2 may be felt.
Palpation over the 3rd left intercostal space may be reveal :
Right Ventricular outflow tract obstruction – Ebstein Anomaly.

5. Other Palpable Events

Palpate over other areas of Precordium.
Prominent Aortic Pulsations in Aortic Aneurysm felt in Upper Sternum ,1st and
2nd Rt ICS and both Sternoclavicular Joints.
Pulsation of Left Ventricular Aneurysm/Dyskinetic Segment – above and medial
to apex

6. Thrills
Palpable Murmurs. Looked for in entire precordium.
Felt using Base of Fingers.
Thrill of Mitral Mid Diastolic Murmur – felt in Left Lateral Position .
Location commented at Exact Anatomical Site and not at the auscultatory
areas
Thrill must be timed with Carotid Pulse or Apex Beat.
Occuring with Carotid Pulse/Apex Beat – Systolic ,Others are Diastolic.

43
Percussion

Contraindicated in patients with past history of Haemoptysis and Myocardial

Infarction.
(So percussion is rarely done, but don’t say percussion not done during case
presentation ,instead comment on the normal borders of heart and that too
only if there are no contraindication)
Done to identify Pericardial Effusion and Right Atrial Enlargement.
Patient lies Supine.
Percussion Started from left Mid axillary line and carried out medially along
4th or 5th ICS to reach the apex.
Upper Border of Liver is percussed out.
Percussion of right border of Heart is then percussed out from right
midclavicular line medially one space above the liver dullness along 3rd or 4th
ICS.
Percussion of Great Arteries carried out medially from midclavicular lineon
either side along the 2nd ICS.

Auscultation
Done in a Sound proof room.
Areas for Auscultation: Five Areas- Mitral Area(M) ,Tricuspid Area(T),
pulmonary Area(P),1st and 2nd Aortic Area(AA1 and AA2). Lets label the areas
in the above manner for making it concise. Please don’t use these
abbreviations during case presentation.
Learn Surface Marking of Auscultatory areas from Consensus – 45
1. Count heart rate and look for Pulse deficit by Simultaneous Auscultation by
Examiner and heart rate is counted by another person.
2. Area Wise Auscultation is done in the order – M – T – P – AA1 – AA2.( Event
wise auscultation may also be done)
First Describe the Heart sounds and then the murmurs are described.
First Heart Sound(S1)
S1 is best heard in the Apex ,
Splitting of S1 ->tricuspid area.
Second Heart Sound(S2)

44
Ideal site is the Pulmonary Area where A2(Aortic Valve component of S2) and
P2(Pulmonary Valve component of S2) are well heard.
 Abnormal P2 :If P2 is as loud or louder than A2,or if P2 is heard well in
other areas ( M,T )
 Splitting of S2
Ask patient to breathe slowly and regularly
Split is well heard in Pulmonary Area normally.
Heard Clearly during Inspiration only.
Abnormal Splitting of S2
Learn Definitions of Single S2,Narrow Split ,Wide Split, Paradoxical Split.
Third and Fourth Heart Sound (S3 and S4)
Low Frequency Sounds best heard with Bell.
Other Low Frequency sounds are – Mid-diastolic Murmur and Tumour Plop.
S3 – Early part of Diastole
S4 – Presystolic sound
Left Ventricular S3 and S4 – Apex in left lateral Position.
Manoeuvres to augment sound – Passive leg Raising, Coughing and Valsalva
release
Right Ventricular S3 and S4 – Tricuspid Area

Have Inspiratory Augmentation and heard in Epigastric area in

emphysematous patients.

Ejection Sounds
High Frequency sounds.
Aortic sounds – heard in AA1/2 or Apex
Pulmonary Sounds – Pulmonary area and It is phasic if of Valvular Origin
Other Sounds
 Opening Snap- Immediately after S2 in early part of Diastole,High
Pitched and widely Conducted
 Mitral Valve Prolapse Click
 Pericardial Rub – Pericardial Effusion
 Tumour Plop – Left Atrial Myxoma
 Prosthetic Valve Sounds

45
Murmurs

This Section of Cardiology may be confusing to at least few of you. But let me
tell you my dear friends this is no rocket science. Please be regular at wards
and spend some time in systematic auscultation and you will be an expert at
Murmurs.

Murmurs are due to turbulence of blood at or near Valve or an abnormal

Connection within or outside the heart.
Bruit – Murmur over an artery – Due to Arterial Stenosis or Turbulent Arterial
Blood Flow.

Timing and Duration

Murmur is classified into :-

SYSTOLIC- Heard Between S1 and S2. Occurs along with Apex Beat or Carotid
Pulse.
 Ejection Systolic
 Pan Systolic
 Early Systolic
 Late Systolic

DIASTOLIC –Heard between S2 and S1.

 Early Diastolic
 Mid Diastolic
 Late Diastolic
CONTINUOUS

Point of Maximum Intensity

Area where Murmur is maximal heard.
Frequency, Shape and Character
Frequency – Low, medium or High pitched.
Shape – Ejection Systolic – Crescendo/decrescendo
 Early Diastolic – Decrescendo

46
Character – High Pitched – Soft and blowing .
Low Pitched – Rough and Rumbling.
Intensity – Levine and Freeman’s Grading .Cons – 48
Conduction – Selective Propagation of murmur heard with same intensity
Transmission – heard with intensity away from the original site.

Dynamic Auscultation
1. Variation with respiration
2. Passive Leg Raising
3. Squatting and Standing
4. Valsalva
5. Isometric Hand Grip.
Examine other systems also

DIAGNOSIS
 Acquired / congenital Valvular heart disease
 Rheumatic in origin / congenital anomaly
 Name of disease
 Normal sinus rhythm/ AF
 No evidence of Infective Endocarditis
 No evidence of acute rheumatic fever
 NYHA I/II/III/IV

CLINICAL APPROACH

MITRAL STENOSIS
History
 Dyspnoea
 Recurrent LRTI in childhood
 Cough + haemoptysis- coughing up of blood
 Palpitation occurs once AF starts

47
 10-20 years after first episode

Right Heart Failure

left Heart Failure

Past history and rest are common for all valvular diseases and has been dealt
earlier.
General Examination
 Face – Mitral Facies
 Pedal Edema
 Pulse – Low volume pulse
 Blood Pressure
- Calculate Pulse Pressure
= SBP – DBP <20 → Hypokinetic /low volume
 JVP - Prominent a wave.
 If AF
- Irregularly Irregular Pulse ,
- Absent ‘a’ wave on JVP
- Absent P on ECG.
CVS Examination
Inspection
 Apex – not shifted
 RV hypertrophy : - Left Parasternal Impulse
 Epigastric Pulsation
Palpation
Apex –

Tapping Apex (loud S1)Tapping Apex (loud S1)

Diastolic thrill+/-
Parasternal Heave
Epigastric Pulsation

48
Auscultation
 S1 S2 heard, Loud S1
 Opening Snap at Apex
 Low pitched ,rough rumbling
 At Apex – MDM of Grade 4/4 with PSA – Pre systolic accentuation
 Best Heard with Bell
 Patient in Left Lateral Position ,breath held in expiration.
 If Atrial Fibrillation –
- Pre -systolic accentuation is
- Irregularly Irregular Pulse
- a wave absent in JVP
- p absent in ECG

DIAGNOSIS (very imp)

Acquired Valvular Heart disease, probably Rheumatic
Severe /mild/moderate Mitral Stenosis
No signs of Infective endocarditis
Atrial Fibrillation
Acute Rheumatic Fever
NYHA Grading I/II/III/IV

Investigation
ECG
- P Mitrale( AF– absent P)
- Rt. Axis Deviation.
CXR
- Double Density Shadow within Shadow
- Straightening of Left heart Border
- Antler Sign
- Kerley B Sign

49
 - Mitralisation of heart
Echocardiography
- Hockey stick appearance in RHD (of Mitral valve leaflet )
Look for
- Mitral valve structure
- Mitral valve area < 1.5 cm2

Complication
LA Thrombus
Thrombus at auricle (LA appendage )
Echo + Doppler

Management of Mitral Stenosis

 RHD -> Secondary Prophylaxis
 Lifestyle – Avoid Strenuous exercise
Sodium < 2g/d & H2O <2 L/day
 Treatment of AF
 Drugs – Vasodilator – Anti- remodelling drugs

Interventions
 PBMV – Percutaneous Mitral Balloon Valvotomy
 Surgical – Mitral Valve Repair / Replacement (chance for clot - so
anticoagulated life long)
Indications – Pulmonary Artery Hypertension/P2 loud
Loud S1,OS,Murmur
Left Atrial Myxoma – mimic like MS
MDM Murmur heard on standing disappears on lying in left lateral position.

MITRAL REGURGITATION
History
 Palpitation
10-15 yrs

Dyspnoea on exertion /orthopnea /PND

50
 Fatigue

General Examination
 Pulse – Hyperkinetic / High volume
 AF – Irregularly Irregular
 BP – SBP – DBP > 60 mm Hg
 JVP – Usually Normal
- If LA enlarged -> Prominent a
- AF - >Absent a

CVS Examination
Inspection
 Apex – Down and out ( LV enlarged )
Palpation
 Apex - Down and out
 Hyperdynamic Apex – Finger elevated < 2/3
 Thrill – Systolic Thrill or 4/6
Auscultation
 S1 Soft
 S2 normal
 S3 is heard ( at apex)
 Murmur - Pansystolic Murmur of Grade 3/6 to 6/6
 Heard best with diaphragm
 Radiating to Axilla or base.
 Best with patient in left lateral
 Breath held in expiration
 +/- MDM of Grade 3/4 at Apex

DIAGNOSIS
Acquired
Valvular heart disease
Rheumatic inorigin/Mitral Valve Prolapse
In Atrial Fibrillation
No signs of Infective Endocarditis
51
 Acute Rheumatic Fever
Heart Failure – currently NYHA I /II/III/IV

Investigation
 ECG
 ECHO – MVP or not
 Chest X ray
- LV hypertrophy – Cardiothoracic Ratio > 0.5
- Left Axis Deviation
 Trans – oesophageal Echo

Management of Mitral Regurgitation

Medical Management
 Avoid strenuous activity
 Reduce salt intake < 2g/day + Diuretics
 Vasodilators with anti -remodelling ( ACE Inhibitors)
 Secondary Prophylaxis for Rheumatic fever
 Manage AF
Interventions
 Surgical ( Repair> Replacement )
 Catheter Based – Mitra clip
 Mitral Valve Prolapse
- Floppy Mitral Valve /Barlow’s d/s / Billowing MV
- 3% of Population
- Association – Marfan syndrome, Ehler Danlos syndrome.
- Midsystolic Click – Best heard in Apex

AORTIC STENOSIS
History
 Angina
 Syncope
 Dyspnea

General Examination
 Pulse – Parvus Et Tardus
 BP – SBP < 160
52
  Raised DBP due to Hypertension

CVS Examination
Inspection
 Apex – not shifted or Down and out.
Palpation
 Apex – Confirm position
- Heaving Apex
- Thrill-AA1-Systolic
↓
- Carotid-Carotid Shudder
Auscultation
 S1 Normal
 S2 Soft /Absent
 S3 and S4 at apex
 At AA1, Harsh, Diamond shaped (Crescendo, Decrescendo), Ejection
systolic murmur, grade 3/6 to 6/6, Radiate to carotids, AA2, AA3.
 Heard with diaphragm
 Patient leaning forward
 Breath held in expiration

DIAGNOSIS
 Acquired
 Valvular heart disease
 Senile degenerative/Rheumatic
 Severe aortic stenosis
 Normal sinus rhythm
 No IE/ARF
 NYHA I/II/III/IV

INVESTIGATION
 ECG- Signs of left ventricular hypertrophy
 CXR-Calcification of aortic arch/Aortic valve
 ECHO-Mobility of valves

MANAGEMENT
53
  Avoid strenuous activity
 Avoid dehydration
 Vasodilators with anti-remodelling action
 Secondary prophylaxis in RHD (young)
 Treat angina

Intervention
 Transcatheter aortic valve repair
 Aortic valve replacement

AORTIC REGURGITATION
History
 Palpitation
 Nocturnal angina
 LVF – dyspnoea on exertion, PND, orthopnoea

General Examination
 Pulse – Collapsing Hyperkinetic Pulse
 BP – PP > 60 mmHg
 JVP – No change
 Peripheral signs of AR
 Forehead- Light house sign
 Head – De Musset’s head nod
 Eye- Ashrafian’s pulsatile pseudo proptosis
 Pupil- landolffi’s pulsatile pupil
 Uvula- Muller’s sign
 Corrigan’s Dancing carotids
 Upper Limb-Locomotor brachialis
 Nail Bed- Quinke’ssigns
 Enlarged Pulsatile Liver- Rosenbach’s sign
 Enlarged Pulsatile spleen- Gerhardt’s sign
 Stethoscope on Femoral Artery-Pistol Shot Femoral’s
 Distal Pressure in Femoral Artery – Diastolic Murmur – Duroziez’s
Diastolic Murmur or sign
 Dorsalis Pedis Pulse palpable after 75yrs – Sherman’s sign

54
CVS Examination
Inspection
 Apex – Down and out
Palpation
 Confirm Apex position
 Hyperdynamic Apex ( <2/3 of Systole)
 Thrill +/- at AA2
Auscultation
 S1 Normal, S2 Soft
 S3 and S4 – Severe
 Murmur – At second Aortic Area – Blowing decrescendo murmur
- Early diastolic murmur – Grade 3/4 to 4/4
- Best heard with diaphragm
- Sitting up /leaning forward
- breath held in expiration.
 +Apex- MDM
 +AA1 – Flow ESM

DIAGNOSIS
 Acquired
 Valvular Heart Disease
 Rheumatic in origin – most likely
 Severe Aortic Regurgitation
 Normal Sinus Rhythm
 No evidence of Infective Endocarditis
 No evidence of acute Rheumatic Fever
 NYHA Class I/II/III/IV

Investigation
 ECG – Left Ventricular Hypertrophy
 CXR – Left Ventricular Enlargement
 ECHO – Anatomy of AoV / Bicuspid AoV
 Doppler – Quantify AR

Management of Chronic AR
55
  Avoid strenuous activity
 Reduce salt intake < 2g/day + diuretic
 Vasodilators with anti – remodelling action
 Secondary Prophylaxis in RHD

Intervention
 Valve Repair
 Valve Replacement
 Two Surgeries
Bentall Procedures- Root and Valve Replaced
David – Only root is replaced – valve sparing surgery

CONGENITAL HEART DISEASE IN ADULT

History
 Asymptomatic – Incidental murmur
 Right heart failure in pregnancy/anaemia

Examination
 Pulse/BP/JVP- Normal
 Inspection- Left parasternal heave/Epigastric pulsation
 Palpation- Apex normal, LPH present
 Auscultation- Ejection systolic murmur at pulmonary area
 Grade 3/6 or S

DIAGNOSIS
 Congenital Heart Disease, ASD
 Pulmonary Hypertension
 No signs of heart failure
 No signs of IE, NSR

MANAGEMENT OF A/C RHEUMATIC FEVER

 Bed Rest
 Inj. Benzathine penicillin 1.2 Million unit I/M stat .
 Salicylates: Aspirin 100mg/kg / day reduced to 75 mg/kg per day as ESR
comes down

56
  Corticosteroids: For severe carditis, and severe arthritis
 Supportive Therapy

SECONDARY PROPHYLAXIS :With T.Pencillin V 250mg PO BD daily or

T.Erythromycin 250mg PO BD twice a day

No Carditis For 5 years or until 18 years

whichever is longer
Resolved Carditis For 10 years or until 25 years
whichever is longer
Severe RHD – Valve d/s Lifelong

INFECTIVE ENDOCARDITIS PROPHYLAXIS

Standard oral regimen: Amoxicillin 2.0g PO 1h before procedure
Inability to take oral medication: Inj. Ampicillin 2.0g IV or IM within 1h before
procedure
Penicillin Allergy: Clindamycin 600mg PO 1h before procedure

57
NERVOUS SYSTEM

58
 CNS ANATOMY

FUNCTIONAL AREAS OF BRAIN

Function Area Number Location

Primary motor area 4 Precentral gyrus

Premotor area 6 ,8 Posterior part of sup ,

middle, and inf frontal
gyri

Supplementary motor MII Medial frontal gyrus

area

Prefrontal area Frontal lobe – ( motor

+ premotor areas )

Motor speech area ( 44 ,45 Inferior frontal gyrus

Broadmann’s area )

Sensory area 3,1,2 Post central gyrus

Sensory speech ( 39,40 Superior temporal

Wernicke;s area) gyrus

59
 Frontal eye field 8 Middle frontal gyrus
anterior to precentral
gyrus

Visual area First area -17 Occipital lobe

Sec area- 18

Third area- 19

Auditory area 41,42 Transverse temporal

gyri

BLOOD SUPPLY OF BRAIN

CIRCLE OF WILLIS

60
5 Branches of vertebral artery
1. Anterior spinal artery
2. Posterior spinal artery
3. Medullary branches
4. Meningeal branches
5. PICA- posterior inferior cerebellar artery

5 Branches of Basilar artery

1. AICA – ant inf cerebellar artery
2. Labrynthine artery
3. Pontine artery
4. Superior cerebellar artery
5. Posterior cerebral artery

5 Branches of internal carotid artery

1. Anterior cerebral artery
2. Middle cerebral artery
3. Anterior choroidal artery
4. Posterior communicating artery
5. Ophthalmic artery
ICA has no extracranial branches

61
INTERNAL CAPSULE

BLOOD SUPPLY
UPPER PART OF ANTERIOR LIMB, GENU , POSTERIOR LIMB - LENTICULOSTRIATE BRANCHES OF
MCA
LOWER PART
1. ANT LIMB- RECURRENT BRANCH OF HEUBNER (ACA) AND PERFORATING BRANCHES OF
ANTERIOR CEREBRAL ARTERY
2. GENU- DIRECT BRANCH OF ICA AND PERFORATING BRANCHES OF ANTERIOR CHOROIDAL
ARETRY

62
 3. POST LIMB –PERFORATING ANTERIOR CHOROIDAL ARTERY
4. RETROLENTIFORM PART AND SUBLENTIFORM PART – DISTAL PERFORATING BRANCHES OF
ANTERIOR CHOROIDAL ARTERY

BRAINSTEM

REFER CUT SECTION OF BRAIN STEM AT DIFFERENT LEVELS FROM NEUROANATOMY TEXTBOOK

63
BLOOD SUPPLY

i. MEDULLA
- ANT SPINAL ARTERY - PYRAMID, MEDIAL LEMNISCUS, HYPOGLOSSAL
NUCLEUS
- POST SPINAL ARTERY – GRACILE AND CUNEATUS NUCLEUS
- POST INF CEREBELLAR ARTERY - RETRO OLIVARY REGION
ii. PONS
- PONTINE BRANCHES OF BASILAR ARTERY , ANT INF CEREBELLAR RTERY, SUP
CEREBELLAR ARTEY

iii. MID BRAIN

- BRANCHES OF BASILAR ARTERY, POSTERIOR CEREBRAL ARTERY, SUPERIOR
CEREBELLAR artery, PICA

CEREBELLUM

I. ARCHICEREBELLUM - FLOCCULONODULAR LOBE - MAINTANCE OF EQUILIBRIUM

II. PALEOCEREBELLUM - ANTERIOR LOBE – MUSCLE TONE
III. NEOCEREBELLUM – POSTERIOR LOBE – COORDINATION AND REGULATION OF FINE
DELICATE VOLUNTARY MOTOR ACTIVITY
BLOOD SUPPLY – SUPERIOR CEREBELLAR ARTERY, ANTErior inferior cerebellar artery,
POSTERIOR INFERIOR CEREBELLAR ARTERY

CEREBELLUM HAS 3 PEDUNCLES

i. SUPERIOR CEREBELLAR PEDUNCLE
ii. MIDDLE CEREBELLAR PEDUNCLE
iii. INFERIOR CEREBELLAR PEDUNCLE
MCP- HAS ONLY AFFERENT FIBERS – FRONTOPONTOCEREBELLA TRACT

64
Spinal Cord

BLOOD SUPPLY
- PAIRED POST SPINAL ARTERY – POST 1/3 RD OF SC
- UNPAIERD ANT SPINAL ARTERY – ANT 2/3 RD OF SC
- ARTERY OF ADAMKIEWICZ T9- T12 (BRANCH OF AORTA)

65
CORTICOSPINAL TRACT

Fibres to bilateral cranial

nerve nuclei except lower
half of facial nerve nucleus &
hypoglossal nerve (for
genioglossus )

66
LATERAL SPINOTHALAMIC TRACT (pain, temp, itching, tickling)

Ascends as spinal
lemniscus

67
ANTERIOR SPINOTHALAMIC TRACT (crude touch, crude pressure )

Ascends as spinal
lemniscus

68
DORSAL COLOUMN PATHWAY (fine touch, deep pressure, vibration sense,
proprioception, stereognosis, tactile localization & discrimination)

Ascends as medial
lemniscus

69
 CRANIAL NERVE
 Majority of cranial nerve have bilateral cortical representation. ( except
XII, part of VII nerve nucleus supplying lower part of face –controlled by
the opposite cerebral cortex only, IV nerve nucleus –controlled by
cerebral cortex on the same side only)
 Strokes above brain stem usually do not affect cranial nerves
 Mostly cranial nerve damage occurs outside the brain stem
 Pure sensory nerves: I, II, VIII
 Pure motor: III, IV, VI, XI, XII
 Mixed :V, VII, IX, X

V, XII --- deviated to same side of lesion

Deviation of part
VII- sevEN
X- tEN
XI- elevEN
Deviated to opposite side

Location of cranial nerve nuclei in the brain stem

- Midbrain:III, IV
- Pons : V, VI, VII
- Medulla: VIII, IX, X, XI, XII

CN – I Olfactory
 Any damage to the olfactory bulb can cause loss of smell in that nostril
 Frontal lobe tumor
 Fracture of cribriform plate
 Degenerative conditions: Alzheimer’s, parkinsonism, multiple sclerosis
 Temporary loss in common cold, atrophic rhinitis
CN II –optic nerve
Visual pathway
 Stimulus: light rays
 Receptors: rods and cones

70
 First order neurons :bipolar cells
 2nd order neurons : ganglion cells of retina
 Axons of ganglion cells form the optic nerve Unites with optic nerve of
opposite side to form optic chiasma ( only nasal fibres cross)Optic tract
rd
 lateral geniculate body (3 order neurons) optic radiation  occipital
cortex.

Light reflex
Light  Retina optic nerve  optic chiasma  optic tract  pretectal
nucleus  Edinger westpal nucleus of both sides ciliary ganglion Short
ciliary nerve pupillary constriction of same eye (direct light reflex),
pupillary constriction of opposite eye ( consensual light reflex)
Lesions of pupillary light reflex pathway
 Lesion of optic nerve of one side –direct light reflex lost and indirect
light reflex in the same eye present since the opposite optic nerve is
intact
 Lesion of optic chiasma and optic tract- when light falls on the sound half
of the retina, both direct and indirect light reflex are present.
71
 If light falls on the blind half of the retina, both direct and indirect light
reflexes will be absent. (Wernicke’s hemianopic pupillary reaction )
 Lesion of pretectal nucleus: Both direct and indirect pupillary reflexes
will be absent.
Accomodation reflex will be present since the visual pathway to the
visual cortex is unaffected. (Argyll robertson pupil)
Seen in tabes dorsalis and neurosyphilis.

Accommodation pathway
Rods and cones visual cortex frontal eye field on frontal cortex
midbrain (accommodation convergence region near oculomotor nucleus
), causes contraction of medial rectus leading to convergence of eye
balledinger westpal nucleus ciliary ganglion short ciliary
nervessphincter pupillae  constriction of pupil

Short ciliary nervesrelaxation of suspensory ligament increase in

anterior curvature of lens.

Horner’s syndrome
Damage to cervical sympathetic fibres
1st order neurons from posterior hypothalamus
Fibres descend uncrossed through brain stem
Intermediolateral horn cells of 1st and 2nd thoracic spinal cord
segments ( 2nd order neurons)
 Through white rami communicantes exit spinal cord
 Enter inferior cervical ganglion( no relay)
 Ascend upto superior cervical ganglion(3rd order neurons)
 Ascend along common carotid, then along ext and int carotid.
 Via internal carotid pupillary fibres join V1 ( opthalmic branch of
trigeminal)nasociliarylong ciliary nerve to ciliary body dilator
pupilae.
Components of horner’s syndrome (code:PREMA)
 Partial ptosis
 Loss of ciliospinal Reflex
 Enophalmos

72
  Miosis
 Anhydrosis
Central and peripheral horner’s syndrome
Central Peripheral
Site :1st and 2nd order 3rd order neurons
neurons
Sweating affected Sweating spared

Ciliospinal refex present Lost

Causes of horner’s syndrome

Level of lesion Causes
Central(1st order 1)Lat. Medullary syndrome
neurons) 2)Brain stem tumors
3)Syringomyelia, syringobulbia
4)Spinal cord tumors
Preganglionic (2nd order 1)Pancoast tumor
neurons) 2)IVDP
3)Neck lesions(neck, trauma, post surgical)
rd
Postganglionic(3 order 1)Cluster headache
neurons) 2)ICA dissection
3)Nasopharyngeal carcinoma
4)Cavernous sinus lesion
5)Carotid and aortic dissection and aneurysm
6)Diabetic autonomic neuropathy

3, 4, 6 –Oculomotor, trochlear, abduscent

III –medial rectus—adduction
Superior rectus--- elevation of abducted eye
Inferior rectus – depression of abducted eye
Inferior oblique –Elevation of adducted eye
IV ---(code SO4)
Superior oblique – Depression of adducted eye
VI—(code LR6)
Lateral rectus –Abduction
73
3rd nerve palsy
 Complete ptosis
 All EOM except LR and SO paralysed, so the resultant eye –down and
out eye
 Damage of parasympathetic fibres in the periphery of 3rd nerve damaged
mydriasis
 Direct light reflex lost
 Consensual in the other eye present
th
6 nerve palsy
 Ipsilateral abduction lost
 Diplopia on lateral gaze
th
4 nerve palsy
Superior oblique is the only depressor of the eye ball during abduction,
therefore in trochlear nerve palsy
 Eye is extorted and elevated due to unopposed action of inferior
oblique.
 Diplopia on reading a book

Q Nerve supply of upper eyelid

Levator palpebare superioris 3rd nerve
Muller’s muscle cervical sympathetics

Q Common causes of ptosis

 3rd nerve palsy(complete )
 Horners syndrome (partial)
 Myasthenia gravis
 Snake bite
 Myotonic dystrophy

Q Difference between 3rd nerve palsy and horner’s syndrome induced

ptosis
rd
3 nerve palsy Horners syndrome

*complete ptosis *partial ptosis

*Dilated pupil *constricted pupil

74
*squint *No squint
*extraocular palsy present *absent

Q Difference between diabetic (ishemic 3rd nerve palsy and compressive

3rd nerve palsy)
In diabetic /ischemic 3rd nerve palsy, pupil will be normal, because pupillary
fibres are passing through the periphery.
Ischemia affects mainly the central fibres.
Ptosis and pupil
 Ptosis with mydriasis--3rd nerve palsy
 Ptosis with miosis—horner’s syndrome
 Ptosis with normal pupil – DM, myasthenia, muscle disease

Q Sudden onset ptosis with headache.. possible etiology

Posterior communicating artery aneurysm compressing 3rd nerve

Q Painful ptosis /opthalmoplegia

 Orbital cellulitis
 Cavernous sinus syndrome
 SOF syndrome
 Opthalmoplegia migraine

Q Causes of miosis
Unilateral –horner ‘s syndrome
Bilateral –
 OP poisoning
 Old age
 Barbiturate /morphine poisoning
 Pontine hemorrhage

Q Structures passing through superior orbital fissure (SOF)

Code – LFT NAD
 Lacrimal nerve
 Frontal nerve
 Trochlear nerve

75
  Nasociliary nerve
 Abduscent
 Division of oculomotor

INTERNUCLEAR OPHALMOPLEGIA
 Occurs due to lesion in MLF (Medial longitudinal fasciculus )
 MLF – white matter tracts responsible for transmitting information
that is vital for coordination of different eye movements.
 It connects 3, 4, 6 CN nuclei
(Here we are concerned about only 3 & 6)
 Saccades are initiated by frontal eye field (FEF) which sends signals
to the contralateral PPRF (paramedian pontine reticular formation)
 PPRF stimulates Ipsilateral 6th nerve nucleus which sends signals to
the lateral rectus muscle on the same side and to the contralateral
medial rectus subnucleus of 3rd nerve nucleus through MLF, thus
resulting in horizontal gaze opposite to the initiated FEF.
 Cardinal sign of INO is impaired adduction of same side on the MLF
lesion.
 Contralateral abducting eye may demonstrate a dissociated
horizontal nystagmus. This is thought to be a compensatory
response to overcome the weakness of adducting eye.

76
 V- TRIGEMINAL NERVE
Lesions of trigeminal nerve presents following clinical features
 Loss of general sensations from the face and mucous membrane
of oral and nasal cavities.
 Loss of corneal reflex
 Flaccid paralysis of muscles of mastication
Jaw deviates to the side of lesion due to unopposed action of
lateral pterygoid muscle.
 Hypoacusis ( partial deafness to low pitched sounds due to
paralysis of tensor tympani muscle)

Trigeminal neuralgia
Paroxysmal severe pain of sudden onset and short duration in the
area of cutaneous distribution of one or more of the divisions of
the trigeminal nerve, usually affecting the 2nd and 3rd divisions.

VII –FACIAL NERVE

Course *very important *
 2 roots—motor root and nervus intermedius (sensory, secretory,
parasympathetic fibres)
 Enters the internal auditory meatus
 Unite to form the trunk of facial nerve
 Runs above the bony labyrinth of internal ear and then bends
posteriorly in the medial wall of middle ear, forming genu of facial
nerve.
 Finally, nerve turns 90° and runs in the posterior wall of middle
ear till it reaches the stylomastoid foramen
 Enters the parotid gland
 Divide into 5 terminal branches
Branches
 Greater petrosal nerve—joined by deep petrosal nerve
pterygopalatine ganglionlacrimal, nasal, palatine glands
 Nerve to stapedius

77
  Chorda tympani joins the lingual nervesubmandibular
ganglion  Ant 2/3rd of tongue, sublingual, submandibular
salivary gland.
 Posterior auricular nervesupply occipitalis and posterior
auricular muscle
 Nerve to posterior belly of digastric and stylohyoid
 Terminal branches—Temporal, zygomatic, buccal, marginal
mandibular, cervical

Clinical correlation
The part of facial nerve supplying the muscles of lower part of face
receives corticonuclear fibres from opposite cerebral hemisphere
but part of motor nucleus which supplies upper part of face
receives corticonuclear fibres from botj hemispheres.
As a result in supranuclear lesions (UMN), the upper part of face is
spared and lower half of the face is affected on the opposite side.
In LMN lesions, whole of the face on the same side is affected.

Vestibulo cochlear Nerve ( VIII)

 Can get affected in lateral medullary syndrome
 I/L Giddiness, hearing loss

IX –Glossopharyngeal nerve
Lesions produce following clinical features
 Loss of gag reflex
 Loss of general sensations in pharynx, tonsils, fauces, posterior
one-third of tingue
 Hypersensitive carotid sinus syndrome (syncope )

X – VAGUS
Lesions produce following clinical features
 I/L paralysis of soft palate leading to sagging of palatal arch. Uvula
deviates towards opposite (healthy side)
 Loss of gag reflex ( due to interruption of efferent limb)
 Hoarseness of voice due to unilateral paralysis of laryngeal
muscles.
78
XI – Accessory nerve
 Unilateral peripheral lesions of spinal root (spinal accessory nerve ) leads
to paralysis of sternocleidomastoid and trapezius muscle
 Paralysis of SCM will result in turning of face towards the same side and
bending of the head to the opposite side due to unopposed action of
opposite healthy muscle.
 Paralysis of trapezius results in drooping of shoulder and inability to
shrug the shoulder towards the side of injury.

XII – Hypoglossal nerve

 UMN lesions
Since hypoglossal nucleus receives corticonuclear fibres only from the
contralateral hemisphere, UMN lesions cause weakness of opposite half
of the tongue, on protrusion, tongue deviates to opposite side of lesion
 LMN lesions
Paralysis of ipsilateral half of tongue and on protrusion the tongue
deviates towards side of lesion due to unopposed action of genioglossus
of the healthy side.

79
 ACUTE STROKE SYNDROME
HISTORY
A) Motor – weakness
 Onset
- abrupt (WITHIN MINUTES )
- Sudden ( within hrs )
- Sub acute ( within days / wks )
- Chronic ( within months / yrs )
 Progress – static, progressing, regressing (embolic)
 Describe time of occurrence, what he was doing, how others came
to know, how he was taken to hospital i.e., carrying / walk with
support, his condition by the time he reached to hospital
 When was weakness completed or maximum
 Any loss of consciousness
 Which limb – upper/ lower
 Site affected first – distal /proximal
- Upper limb- proximal muscle – difficulty to eat , raising arm
to put shirt , drying the hair , taking things from up . If distal
weakness- difficulty in buttoning, holding cup, making food
bolus, writing, turning key.
- Lower limb- proximal weakness- difficulty to get up from
squatting, difficulty in walking. Distal weakness – inability to
wear sandals, inability to grip chappals, slipping of chappals
knowingly or unknowingly.
 Trunk muscle weakness – difficulty in turning in bed or getting up
from bed
 Feeling of log of wood with stiff drag of leg, tipping of toes (
grazing of toes on ground )
 Whether dense ( means equal weakness of upper and lower limbs
) or minim al weakness

B) Sensory – feeling of touch, pain, temperature, any abnormal sensation (

paresthesia, hyperaesthesa, allodynia , hyperalgesia hyperpathia – study
definitions ), numbness – reduced sensory symptoms

C) Cranial nerves
 1- olfaction – abnormal smell , reduced smell

80
  2- sudden loss of vision , blurring of vision, U/L OR B/L field defect
 3, 4, 6 – double vision , drooping of eyelid , difficulty in looking to
sides
 5- loss of sensation over face difficulty in chewing
 7- deviation of angle of mouth , drooling of saliva , collection of
food between cheek and gum margin , difficulty in eye closure
 8- vertigo, abnormal eye movements (nystagmus ) , difficulty in
hearing
 9, 10 nasal regurgitation , nasal twang , difficulty in swallowing,
hoarse voice , slurring of speech, choking while swallowing
 11- difficulty in moving head, shrugging
 12- dysarthria
D) Cortical symptoms – seizure , speech abnormality ( aphasia )
If history of seizure present differentiate it from syncope – aura , tonic
phase, clonic movements , tongue biting, up rolling of eyes , urination,
post ictal confusion, etc present in seizures
E) Features of raised ICT – headache , vomiting, altered sensorium
F) Bowel, bladder symptoms – retention, incontinence , urgency,
precipitancy, hesitancy
G) Cerebella signs – swaying to one side , inability to sit up straight, tremor
esp. intention tremor , abnormal eye movements ( nystagmus )
H) Associated symptoms – chest pain, dyspnea, palpitation ( regular /
irregular ), fever , trauma
I) Present condition – moving limbs , speaking etc
History of past illness
H – hypertension , diabetes mellitus , hyperlipidemia , heart disease
I – injury to head
S – STD , neurosyphilis
T – TIA , similar episodes in past
O- OCP & other drugs ( anticoagulants , aspirin )
R – rheumatic fever history and pencillin prophylaxix
I – infection – fever , wt loss, night sweats, neck pain ( r/o TB, meningitis
, cerebral abcess )

Personal history
 Smolking , alcoholism, obesity, sedentary habit
 Veg / non veg diet
 Sleep and appetite
81
Family history
Similar illness, hypertension, diabetes mellitus, hyperlipidemia, heart
disease, epilepsy, migraine
Examination of CNS - discussion
1. Higher metal functions
 Consciousness - state of awareness of oneself and environment
Study – levels of consciousness from consensus + Glassgow coma scale
 SPEECH
Aphasia or dysphasia is an acquired disorder of language function.
(Hutchison)

Types of aphasia
Type Naming Fluency Comprehension Repetition
Global Impaired
Motor ( Impaired N Impaired
Broca’s )
Sensory N Impaired Impaired
(Wernicke’s IMPAIRED
)
TCMA Impaired N N
TCSA N Impaired N
Conduction N N Impaired
Isolation Impaired Impaired N
Nominal N
Never forget to check repetition it is impaired in conduction aphasia ,
it is a very common type.
While checking comprehension it is better to avoid asking to point at
axial organs. Instead you can ask him to point towards the fan or light
for one step test.

Dysarthria - defective articulation and enunciation of syllables.

Causes of dysarthria – table 25.18 pg 1087 of DAVIDSON.

2. Cranial nerves
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 I. Olfactory - before checking for olfaction inspect the nasal cavity for
any obstruction. Avoid using irritant smells that can stimulate
trigeminal nerve instead. Check each side separately.
Anosmia - commonly seen in neurodegenerative d/s like Lewy body
d/s, Parkinson’s disease.

II. Optic –
 Visual acuity for distant vision ideally Snellen’s chart and
 for near vision Jaeger chart and
 for colour vision – Ishihara chart.
 Visual field – before checking ensure patient has a counting finger vision.

III, IV, VI.

 Eye movements
- Superior rectus – lateral and upwards
- Inferior rectus - lateral and downwards
- Superior oblique – medial and downwards
- Inferior oblique – medial and upwards
 Recti are abductors
 Oblique are adductors
 SO -4, LR -6 all others occulomotor
 Conjugate eye movement

VII ,VIII,IX,X,XI,XII Covered with cranial nerves.

3. Motor system
Read consensus also
UMN lesion LMN lesion
Damage to motor tracts above Damage at or below anterior horn
anterior horn cell or cranial cell or cranial nerve nuclei.
nerve nuclei.

Groups of muscle affected Individual muscles are affected.

Hypertonia Hypotonia
Spastic paralysis Flaccid paralysis

83
 Atrophy slight and due to disuse Atrophy pronounced
Superficial reflexes lost. Deep reflexes Superficial and deep reflexes are
exaggerated. absent
Plantar reflex and Babinski sign +ve Plantar no response
Fasiculations absent Fasiculations present

Hypertonia
Causes
1. UMN lesion (clasp knife rigidity)
2. Extra pyramidal lesion (lead pipe or cog wheel rigidity)
3. Anxiety
4. Hyperthyroidism
5. Tetanus
6. Strychnine poisoning
7. Hypocalcemia
8. Frontal lobe d/s (paratonia / Gegenhalten )

Types of hypertonia

Spasticity
Velocity dependent increase in tone
One group of muscles more affected
than the other eg: in UL – flexors are
more involved than extensors, and in
L.L – extensors more than flexors
Pyramidal l lesion
Exrensor plantar
Clasp knife phenomenon –resistance
increases as stretch increases ,
reaches a maximum and then
releases.
CVA, multiple sclerosis, traumatic
spinal injury, degenerative
spondylotic myopathy.
84
Rigidity
Length dependent increase in
tone
Both group of muscles affected
( agonist and antagonist )
Extra pyramidal lesion
Flexor plantar
Lead pipe rigidity – uniform
resistance to passive movement
Cog wheel rigidity – when
rigidity is associated with
tremor
More coomonly seen in
Parkinson’s d/s
CLONUS – rhtymic series of involuntary muscle contraction evoked by sudden
stretch of muscles. Sustained clonus indicate damage to UMN

Earliest manifestation of hypertonia- pronator spasm in UL and adductor

spasm in LL.

Hypotonia
Causes :
1. LMN lesion
2. UMN lesion neuronal shock
3. Cerebellar lesions
4. Chorea
5. Hypothyroidism
6. Hypokalemic or hyperkalemic periodic paralysis
7. Sleep
8. Sedatives
9. Muscle relaxant drugs

 Winging of scapula can be due to weakness of serratus anterior or

trapezius .
 If serratus anterior winging occurs without rotation of scapula. ( ie;
medial border of scapula is parallel to spine ).
 If due to weakness of trapezius – winging with rotation of scapula ( ie;
upper part of scapula wings more and scapula is rotated downwards and
laterally )best brought on by attempt to over head.
 Fasiculations – subcutaneous twitches overlying muscle bellies when
muscles are at rest.seen in LMN lesions.
 Myoclonus – sudden jerk like muscle contraction which invoves one or
more muscles of whole limb. Focal or diffuse. Normal when falling to
sleep in some people. Other conditions – CJD , SSPE , familial myoclonic
epilepsies and anoxic cerebral damage.
 Chorea – irregular, jerky, semipurposive and ill sustained mvts.
Causes:
- Humtingtons chorea
- levodopa (long term with PD )
- Sydenhams chorea –( post streptococcal)
- Wilson’s d/s

85
 - SLE
- APLA
- metabolic – disorders affecting thyroid , parathyroid, glucose, Na,
Ca, Mg, balance
 Tremor – rhythmic movement resulting from alternating contraction and
relaxation of group of muscles.
Read causes of tremor Table 25.16 Davidson pg 1085.
Power testing
i. Isometric testing – ask the patient to contract a group of muscles
powerfully as possible and then to maintain that position while the
examiner tries to overpower the muscle group being tested.
ii. Isotonic testing – ask the patient to put the joint through a range of
movement while attempting to halt the movement progression.
REFLEXS
1. SUPERFICIAL REFLEXES.
Superficial reflex Afferent Efferent Root value
Corneal 5th 7th
Conjunctival 5th 7th
Gag 9th 10th
Palatal 5th 10th
Abdominal T7-T12 T7-T12 T7-T12
Cremastric Femoral nerve- Genital branch of L1,L2
obturatornerve genitofemoralnerve
Bulbocavernous Pudendal nerve Pudendal nerve S3-S5
ANAL Pudendal nerve Pudendal nerve S3-S5
Plantar Tibial nerve Tibial nerve if L5-S1
flexor, common
peroneal nerve if
extensor.

ABDOMINAL REFLEX
They have a cortical pathway in addition to a spinal reflex (polysynaptic ). The
afferent path travels up in spinal cord upto paretial cortex and efferent fibers
descend to anterior horn cells in the spinal cord through or in close association
with pyramidal tract. A lesion in the pyramidal tract anywhere in its course also
involves these cortical loop fibers. This leads to abolition reflex.

86
NOTE; MND, Hereditary spastic paraplegia – abdominal reflex is preserved in
the presence of CST involvement.

PLANTAR REFELX
Read CONSENSUS every point regarding plantar reflex.
Mechanism of plantar – normally on stimulating plantar surface in IUL or first 5
months of life will get extension of all toes. As age advances, when there is
complete myelination of nerve fibers, this reflex is suppressed as part of
walking. Those nerve fibers which are concerned with suppression of these
reflex comes along with pyramidal tract. So when there is hemiplegia , those
fibers are involved which leads to release reflex.
Normal plantar – flexor - components
1. flexion of big toe
2. flexion and adduction of all the toes
3. dorsiflexion and inversion of ankle
4. flexion of hip and knee

Extensor plantar
1. extension of big toe
2. extension and adduction of all other toes
3. dorsiflexion and eversion of ankle
4. flexion of hip and knee
Study – other methods of eliciting plantar , plantar equivalents in upper limb ,
minimal plantar , steps to do plantar reflex
B/L extensor plantar is a false localising sign in neurology (another eg is U/L or
B/L abducent palsy).

Causes of B/L extensor plantar

1. infants
2. deep sleep
3. coma
4. after an episode of seizure
5. raised ICT
6. metabolic encephalopathy

Reinforcement for plantar response – turn face to opposite side

If big toe absent while eliciting plantar –
87
 1) check for mvt of other toes
2) look for contraction of tensor fasicalata and hamstrings – if contraction
of TFL > Hamstrings then it is flexor response and if TFL < hamstrings
extensor plantar
3) Rossolimo reflex- percussion of the tips of the toes causes an
exaggerated flexion of toes.
NOTE ; if medial aspect of sole is stimulated , it may elicit flexion (even in the
presence of UMN lesion ) of all the toes as part of grasp reflex .
Extensor plantar + absent ankle jerk
1. subacute combined degeneration
2. taboparesis
3. Friedreich’s ataxia
4. Conuscauda lesion

Flexor plantar + brisk ankle reflex

1. Thyrotoxicosis
2. Hepatic precoma

Remember while eliciting plantar see whether the foot of patient is dry
beforehand itself otherwise you may get a wrong response.

Deep reflexes
Reflex Root value Peripheral nerve
Biceps C5,C6 Musculocutaneous
Supinator C5 , C6 Radial
Triceps C6,C7 Radial
Knee L2,3,4 Femoral
Ankle S1,2 Tibial
Pendular knee jerk – cerebellar lesion ( >3 oscillations )
Hung up knee – chorea
Ideal method of eliciting delayed relaxation of ankle jerk in hypothyroidism –
photomotogram .

Components of reflex arc

1. Sensory receptor
2. Afferent – sensory nerve
88
 3. Centre – spinal cord
4. Efferent motor nerve
5. Effector – organ
 Stretch reflex is the basis of deep tendon reflexes. Stretch reflex is
characterised by reciprocal innervation ie; excitation of group of muscles
being stimulated is associated with inhibition of antagonistic group.
 If very stong stretch applied – instead of muscle contraction there is
relaxion of muscle – INVERSE STRETCH REFLEX / lengthening reaction .
 Clasp knife phenomenon is an exaggerated form of inverse stretch reflex
eg; when arm is hypertonic , increased sensitivity of muscle spindles in
extensor muscles cause resistance to flexion of arm . finally tension in the
triceps increases to the point that it stimulates golgi tendon organ
stimulating inverse stretch reflexand causes triceps to relax and arm flex
like a Jack knife
 Clonus is also an eg of inverse stretch reflex.
 Brisk reflex – increased amplitude
 Exaggerated reflex – increased amplitude and duration
Study primitive reflexes from consensus

Abnormal movements
Chorea Caudate lobe
Athetosis Putamen
Hemiballisums Subthalamic nucleus
Study abnormal movements –tremor (table in Davidson ) , causes of chorea ,
and definitons

CEREBELLUM
Findings in cerebellar lesion
1. Head nodding
2. Eye
- gaze evoked nystagmus
- down beating nystagmus
- skew deviation
3. Speech – scanning speech , staccato speech
4. Hypotonia
5. Pendular knee jerk (>3 oscillations )
6. Coordination defect
7. Ataxia – wide based gait

89
 a) Dysmmetria– past pointing ( patient overshoots the examiners
finger )
b) Dyssynergia– generalised incordination and clumsiness of
movement
c) Intention tremor
d) Dysdiadokokinesia – slowness and incordination when performing
rapid alternating movements.

Lesions of vermis – truncal and gait ataxia

Romberg’s sign is not a test for cerebellum …….it tested for posterior
coloumndefect .

Sensory system – read consensus

Pain , temperature , itching, tickling Lateral spinothalamic tract

Crude touch , crude pressure Anterior spinothalamic
tract
Fine touch , deep pressure , vibration sense , Dorsal coloumn pathway
proprioception,tactile localisation, two point
discrimination

DISCUSSION
HEMIPLEGIA Paralysis of one half of the body
(especially of face, arm and leg). The
trunk is exempted due to bilateral
innervation.
Weakness of one half of the body (i.e.
HEMIPARESIS power more than 3).

PARAPLEGIA- Paralysis of both lower limbs.

PARAPARESIS- Weakness of both lower limbs.

DIPLEGIA B/L hemiplegia of cortical origin LL

more affected than UL (CP).

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- QUADRIPLEGIA -Paralysis of all four limbs
BRACHIAL MONOPLEGIA - Paralysis of one upper extremity.

CRURAL MONOPLEGIA Paralysis of one lower extremity.

- -Paralysis of I/P Cr nerve + C/L
CROSSED HEMIPLEGIA hemiplegia

Causes of hemiplegia
1. CVA
2. ICSOL- Tumors, tuberculoma, brain abcess
3. Demyelination
4. Degenerative disease
5. Vasculitis
Based on time of onset
1. Acute ( within 48 hrs) – vascular causes , trauma
2. Sub acute – demylinating disease (multiple sclerosis) ,encphelitis (JE,
Herpes encephalitis )
3. Chronic – ICSOL , Chronic SDH
CVA
Acute Stroke syndrome ( cerebrovascular accident ) – acute onset of focal
neurologic deficit lasting > than 24hrs or resulting in death of the patient.
Transient ischemic attacks – ischemia of brain , spinal cord or retina lasting less
than 24 hrs with no evidence on imaging ( diffusion weighted MRI).

91
 Thrombotic Embolic Hemorrhagic

Onset Acute or sub a/c – Abruot onset – Abrupt onset –

occurs at night and following may follow
often patient wakes exertion exertion
up with deficit .

Progress Gradually increasing Maximum deficit Sometimes max

weakness at onset deficit at onset ,
can worsen with
STROKE IN
time also. Depends
EVOLUTION
on size of bleed .

ALTERED
CONSIOUSNESS is
a feature

History of TIA ++

Risk factors Atherosclerosis- Valvular heart HTN ( drug default

Hypertension, d/s , IHD, DCM, ), amyloid
HOCM, SABE angiopathy,
hypercholesterolemia
coagulopathy,
Alcoholism, smoking ICSOL

Seizure Uncommon Most common common

Headache Uncommon Uncommon Severe

Vomiting Uncommon Uncommon Severe

Most common risk factor for hemorrhagic stroke is hypertension.

Commonest type of stoke in hypertension is thrombotic.

Sites of hypertensive bleed.

1.putamen

2.thalamus

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3, deep white matter

4, deep cerebellum

5, pons

Features of pontine haemorrhage – 3Ps ( pyrexia, pinpoint pupil , paralysis of 4

limbs )

LOCALISATION OF STROKE
CORTICAL I. A) dominant lobe – aphasia
b) non dominant lobe –
neglect

II. Non dense hemiplegia

II. C/L gaze palsy

III. Seizures
IV. Loss of cortical sensation –
(refer consensus)
V. Bladder abnormality
VI. Higher mental function
abnormality
VII. Quadrantanopia
Corona radiate i. non dense hemiplegia
ii. no cortical features
Internal capsule i. dense hemiplegia
ii. hemianesthesia
iii. homonymous hemianopia
Brainstem stroke Crossed hemiplegia + altered
sensorium

Discussed in detail later

Carotid hemiplegia i. I/P visual disturbances

ii. C/l hemiplegia
Dominant hemisphere – lesion can cause
1. Dysphasia / aphasia
2. Dyslexia
3. Dysgraphia
4. Dyscalculia
93
 5. Dyspraxia / apraxia
NB; Gerstmann syndrome – loss of four neurologic functions –
dysgraphia, dyscalculia , finger agnosia and left – right disorientation

Non dominant lobe lesion

1. Neglect of opposite side
2. Spatial disorientation
3. Anosognosia
4. Dressing apraxia
5. Constructional apraxia
6. Asterognosis
7. Impaired musical skill
8. Impaired non verbal memory
9. Impaired emotional aspects of speech

BLOOD SUPPLY OF AREA

ARTERY SUPPLY
ACA a. Legs
b. Paracentral lobule (urination)
c. Frontal lobe – (emotions - loss
of supply causes abulia and
dysinhibition )
d. Faciobrachialmonoplegia ( deep
branch of heubner )
MCAI - lenticulostriate branch dense hemiplegia

MCA – IIA Dominant lobe – motor aphasia +

hemiplegia
Non dominant lobe – neglect +
hemiplegia

MCA –II B Sensory aphasia , memory

( hippocampus)

MCA stem occlusion i. Desnse hemiplegia

ii. Dense hemianesthesia
iii. Aphasia
iv. Seizure
PCA i. homonymous hemianopia
( damage to visual cortex )
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 ii. cerebellar syndrome
iii. cranial nerve syndrome

LACUNAR infarct – is the most common type of ischemic stroke , resulting from
the occlusion of small penetrating arteries.

Lacunar stroke syndromes and the site of lesion

1. pure motor hemiparesis (most Post limb of internal capsule
common )
2. pure sensory stroke Thalamus

3. ataxic hemiparesis Frontopontocerebellar tract

4. dysarthria clumpsy hand Pons

syndrome
5. motor and sensory stroke Both internal capsule and thalamus

DIAGNOSIS
Cerebrovascular disease
Right/left sided hemiplegia ( if hemianesthesia , hemianopia + )
Probably thrombotic/embolic in origin
Site of lesion – left internal capsule
With/without any complications and comorbidities

95
APPROACH TO HEMIPLEGIA

Hemiplegia

Dense

+ -
Cranial nerve assesment Cortex of corona radiata

Ipsilateral Facial Controlateral Cranial

Nerve Nerve Involvement

Internal Capsule Brainstem

Recurrent stroke causes

1. Cardio embolic -
- atrial fibrillation
- Valvular heart disease
- Left atrial myxoma
- Infective endocarditis
- Post M.I
- DCM
2. Atheroembolic
3. Thrombosis- Carotid stroke ( stuttering stroke )
4. Hyperhomocystinemia
5. Diabeties
6. Acute leukemia

96
Young Stroke
1. Prothrombotic states – eg APLA , factor V protein C,S deficiency ,
hyperhomocystinemia
2. Cardioembolic
3. Bleeding disorders
4. Sickle cell anemia
5. Fabri’s disease
6. Acute leukemias

Stroke Mimics
1. TIA
2. Hypoglycemia
3. Todds paralysis- seziure
4. Migraine
5. Hyponatremia
6. Trauma- EDH ,SDH
7. Hypokalemia/ hyperkalemia
8. Tumor

Stages of stroke
i. Stage of neuronal shock
ii. Stage of recovery
iii. Stage of residual paralysis

UMN AND LMN

 UMN- Neuron whose cell body originates in cerebral cortex or
brainstem and terminates within the brainstem or spinal cord
 LMN- tracts which descend from anterior horn cells in spinal cord or
similar congeners from brainstem motor nuclei and descend to muscle .
Peripheral nerve- part of nervous system lying outside the piamater , including
31 pairs of spinal nerves + cranial nerves 3-12.

Complications of stroke
1. UTI
2. Bedsores
3. Aspiration pneumonia
4. Epileptic seziures
97
 5. Depression , anxiety
6. Deep vein thrombosis
7. Pulmonary embolism
8. Painful shoulder

Causes of mortality in stroke

1. Cerebral edema – coning (most common )
2. Aspiration pneumonia
3. Bed sores
4. DVT
5. Coronary events

Cerebral edema –types cytotoxic (ischemic stroke), vasogenic (hemorrhagic

stroke ) , interstial
CF of cerebral edema
1.Altered consciousness
2.Anisocoria
3.Bradycardia
4.Bilateral extensor plantar
5.Cheyn strokes respiration
6.Papilloedema

Bulbar palsy pseudobulbar palsy

Dysarthria + +

Dysphagia + +

Voluntary movements of - -
palate
Gag reflex - +

Respiratory mvt + -

Jaw jerk hypoactive Exaggerated

Emotional liability - +

Intellectual impairement - +

98
 Causes of bladder involvement in hemiplegia
1. Cerebral edema – altered consciousness
2. Sympathetic strike of normal cortex – during stroke it takes some time
for the normal cortex to take over the actions of affected side (diachisis )
3. Thrombosis of unpaired ACA
4. An asymptomatic previous infarction on one side ,now presenting with a
fresh lesion on opposite side- like multiple infarcts or Biswangers disease

MANAGEMENT OF STROKE
a. Supportive
b. Specific
c. Surgical
d. Secondary prevention of stroke (long term prophylaxis)

SUPPORTIVE MANAGEMENT
1. Maintain airway, breathing, circulation
2. Monitor vitals
3. Propped up -30° to relieve cerebral edema
4. Secure IV line and give hydration preferably RL (judiciously)
5. Ryle’s tube – to avoid aspiration pneumonia and maintain nutrition
6. Continuous bladder drainage if necessary
7. Investigations:
 ECG – to rule out AF (source of cardiogenic emboli)
 GRBS – monitor blood sugar levels (maintain at around 140mg/dl),
rule out stroke mimics
 Non contrast CT scan – investigation of choice
Aim: to rule out haemorrhagic stroke as infarct is usually detected only
after 24- 48 hrs
Early signs of ischaemia
 Hypoattenuating brain tissue
 Obscuration of lentiform nucleus
 Insular ribbon sign
 Dense MCA sign
8. Maintain nutrition

99
 9. BP – do not lower BP very drastically unless there is heart failure,
hypertensive encephalopathy, renal failure, aortic dissection
Reason: loss of cerebral autoregulation produces relative ischaemia of
penumbra

In ischaemic stroke if BP>220/130 for >48 hrs , treat it

For thrombolysis <180/110
For intervention reduce further

In haemorrhagic stroke, reduce BP if >160/110

10.Fever -give antipyretics if febrile as it can increase infarct size

11.Frequent change of position – prevent bed sores
12.If any signs of raised ICT, 100ml 20% mannitol over 20 mins max 100ml
TDS
Alternatives: oral glycerine 30-50 ml 6th hrly (CI in IHD, renal failure, HTN,
hyponatremia )

SPECIFIC MANAGEMENT
A. Antithrombotic
B. Reperfusion therapy
C. Neuronal protectives
If the patient comes within the window period of 4.5 hrs and there are no
other contraindications, the treatment of choice is reperfusion
Contraindications :
 Recent bleed: GI bleed within 3 weeks
 Major surgery within 2 weeks
 Sustained BP >185/110 mm Hg
 Prior stroke or head injury within 3 months
 Platelet count <1 lakh, PCV <25%, glucose<110mg% or > 400mg%
Ideal age group : >18 yrs and <80 yrs

REPERFUSION THERAPY
Thrombolytic
 rtPA (recombinant tissue plasminogen activator)
100
  Alteplase dose – 0.9mg/kg IV
 10%IV stat and 90%infusion over 1 hr
 Improving collateral circulation

By decreasing blood viscosity

Agents:
 Dextran 40
- Causes hypervolemic haemodilution
- C/I: abnormal RFT
 Pentoxifylline (phosphodiesterase inhibitor):
- Increases RBC deformability and hence RBC can easily pass through
vessels (rheological agent)

ANTITHROMBOTIC
1. Antiplatelet
- Aspirin 325 mg loading dose followed by aspirin 75 mg OD
- Clopidogrel 75 mg OD given if aspirin is contraindicated
- Other agents: prasugrel, ticagrelor
2. Anticoagulation
 Absolute indication – established embolic stroke
 Other indications:
- Posterior circulation stroke
- Non septic venous thrombosis
- Recovered TIA or h/o TIA
 Drug of choice : heparin
- Dose : 1000U/hr infusion
- While giving heparin monitorAPTT
- After 3-4 days depending on APTT start oral anticoagulant +
heparin
 Warfarin 2-3mg (usually given in the evening)
- While giving warfarin monitor PT/INR (target 2)(done in the
morning)
- After 3 days heparin is stopped
- Dose of warfarin adjusted ae per PT/INR

101
  LMWH (specific Xa inhibitor)
- Eg. Enoxaparin
- Dose : 0.4-0.6ml S/C BD for 5-21 days
- Advantages: close observation not needed, can be given once or
twice daily, lower bleeding tendency

NEURONAL PROTECTIVES
 Nimodipine:
- used as antivasospastic agent, antihypertensive action absent
- absolute indications: SAH
 NMDA receptor antagonist- Memantine
 Citicoline- increases blood flow
 Na channel Blocker- phosphenytoin (especially if the patient has
dysphagia)
 Antioxidants – Vit E, selenium

SURGICAL MANAGEMENT
● Carotid endarterectomy: if .70% stenosis on symptomatic side on carotid
duplex study
● Surgical decompression
● Endovascular intervention

SECONDARY PREVENTION
If the ECG shows normal sinus rhythm, then discharge the patient on
 Antiplatelet drugs : Aspirin 75mg OD or Clopidogrel 75mg OD
 Statins : atorvastatin 40mg
 Antihypertensive
 Lifestyle modification
- Cessation of smoking, alcohol intake
- Low fat, sugar
- More exercise
If ECG shows AF, Do TFT and Echo
If hyperthyroidism present, manage accordingly
Management
 Cardioversion
 Antiarrhythmics
102
  Anticoagulation
If no Contraindication, warfarin with target INR 2-3 (3.5 if mechanical
prosthetic valve)
Direct oral anticoagulant as other alternatives
Other measures as mentioned in normal sinus rhythm
MANAGEMENT OF WALKING STROKE

Antiplatelets + Physiotherapy

MANAGEMENT OF HAEMORRHAGIC STROKE

 SUPPORTIVE MANAGEMENT
As mentioned above
 MEDICAL MANAGEMENT

1. Anti hypertensives
Frusemide/Nifedipine/Labetalol – Donot lower below 180/110 as
mentioned
2. Anti epileptic drugs
Phenytoin 100 mg TDS or Leviteracetam 0.5 -1 gm BD to prevent
seizures

Reason – Blood is a potent irritant of brain tissue hence there are chances of
seizures

3. Antimengitic measures – If indicated

Inj .Ceftriaxone 2g i/v BD × 10- 14 days
Inj . Amikacin 750 mg i/v OD ×10 -14 days
Inj. Metronidazole 500 mg i/v TDS ×10 -14 days
4. Neuronal protective – Citocholine /Donepezil for cognitive
improvement
Nimodipine given for SAH

AVOID ANTIPLATELETS / ANTICOAGULANTS

 SURGICAL MANAGEMENT
Decompressive Hemicraniotomy
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 LATERAL MEDULLARY SYNDROME/
SYNDROME OF WALLENBERG
 Dorsolateral part of medulla is supplied by posterior inferior cerebellar
artery, which is usually a branch of vertebral artery. This artery also
supplies the inferior surface of cerebellum.
 Thrombosis of PICA therefore affects a wedge shaped area on the dorso-
lateral aspect of medulla and inferior surface of cerebellum and produce
following signs & symptoms.

Ipsilateral
 Ataxia – D/t involvement of inferior cerebellar peduncle and cerebellum
 Giddiness, nystagmus, diplopia, nausea, vomiting –D/t involvement of
vestibular nucleus
 Horners s/d –D/t involvement of descending sympathetic pathway in
the reticular formation of medulla
 Loss of pain & temperature sensation over the face –D/t involvement of
spinal nucleus & spinal tract of trigeminal nerve.
 Loss of taste—nucleus tractus solitarius
 Dysphagia, dysarthria, loss of gag reflex—nucleus ambiguous
 Weakness of lower face—genu flexed UMN fibres to ipsilateral facial
Contralateral

 Loss of pain & temperature sensation in the trunk and limbs –D/t
involvement of spinothalamic tract

 5 branches of vertebral artery

1. Anterior spinal artery
2. Posterior spinal artery
3. Medullary branches
4. Meningeal branches
5. PICA

104
 5 branches of basilar artery
1. AICA
2. Labyrinthine artery (80%are branches of ALCA, 20% from
basilar artery)
3. Pontine artery
4. Superior cerebellar artery
5. Posterior cerebral artery

 5 branches of internal carotid artery

1.Middle cerebral
2.Anterior cerebral
3.Anterior choroidal
4.posterior communicating
5. Ophthalmic artery
ICA has no extra cranial branchesbranches..

105
 MEDIAL MEDULLARY SYNDROME
(Dejerine’s anterior bulbar syndrome )
Paramedian region of medulla is supplied by branches of vertebral artery. The
vascular involvement (ischemia ) of this region produces following signs &
symptoms

Contralateral

 Hemiplegia /paralysis of arms and leg –D/t damage of pyramid

 Loss of position & vibration sense –d/t damage of medial lemniscus
Ipsilateral

 Paralysis / atrophy of the half of the tongue –d/t damage of hypoglossal

nerve

106
 BRAIN STEM SYNDROMES
Features of brain stem stroke
 Crossed hemiplegia
 Altered level of sensorium due to involvement of ARAS
 Associated involvement of cranial nerve

Crossed hemiplegia
 Ipsilateral LMN type of cranial nerve palsy
 Contralateral hemiplegia

In all strokes involving mid brain, there is ipsilateral 3rd nerve palsy..

107
Mid brain syndromes

Mid brain s/d Site of lesion C/F

Weber syndrome Anterior cerebral I/L 3rd nerve palsy + C/L

peduncle hemiplegia ( corticospinal
tract)

Benedicts syndrome Red nucleus I/L 3rd nerve palsy+ C/L

tremor, chorea, athetosis

Northnagel syndrome Superior cerebellar I/L 3rd nerve palsy + I/L

peduncle cerebellar ataxia (
cerebellum always same
side)

Claude syndrome ( Red nucleus +sup I/L 3rd nerve+ C/L chorea
Benedicts + north cerebellar peduncle athetosis, tremor+ I/L
nagel) cerebellar ataxia

Perinaud syndrome Dorsal midbrain Vertical gaze palsy,

/tectum convergence retraction
nystagmus, lid retraction,
light near dissociation

108
Pontine syndromes
MiliardGubler Ventral pontine I/L 6th nerve palsy+ I/L LMN
syndrome Syndrome type of facial palsy+C/L
(Lateral inferior hemiplegia
pontine s/d)
Foville syndrome Lower dorsal C/L hemiplegia+INO+ I/L
(Medial inf. Pontine pontine s/d gaze palsy + (6th nerve
s/d) nucleus +PPRF) +I/L LMN
facial palsy + C/L
hemisensory loss (pain,
temperature due to
involvement of Medial
lemniscus and
spinallemniscus)

LOCKED IN STATE
 Involvement of b/l ventral pons
 Damage to b/l corticospinal tract ( Quadriplegia )
 B/l 7th nerve palsy( entire face paralysed)
 B/L 6th nerve palsy ( Lateral gaze palsy)
 3rd nerve nucleus sapred( vertical gaze normal)
 Preserved consciousness ( RAS Intact )
 Unable to speak( involvement of b/l corticobulbar fibres to nucleus
ambiguous and XII)
 Cause—Osmotic demyelination (rapid correction of hyponatremia)

109
 ATAXIC HEMIPARESIS
Cerebellar signs & hemiparesis (grade 4 & above) on ipsilateral side

Sites of Lesion
Frontopontocerebellar tract at..
1. Frontal lobe
2. Corona radiate
3. Thalamocapsular lesion
4. Midbrain at red nucleus
5. Ventral pons/basispontis

Cerebellar signs
 Titubation / head nodding, truncal ataxia
 Speech - dysarthria of staccato / scanning type
 Nystagmus (gaze evoked nystagmus)
 Hypotonia
 Pendular knee jerk
 Intention tremor
 Past pointing on finger- nose & finger - to- finger- nose test
 Dysdiadochokinesia
 Rebound phenomenon
 Overshooting in heel- knee test
 Romberg’s sign negative
 Gait - wide- based drunken gait (truncal ataxia). Sensitive test of early
ataxia is tandem gait.

FACIOBRACHIAL MONOPLEGIA
Diagnosis made when ipsilateral UMN facial palsy & upper limb involvement
present & ipsilateral plantar is flexor (for some examiners, extensor plantar but
with power enough to walk is considered as faciobrachial monoplegia).

Sites of Lesion
A. Cortex -middle cerebral artery territory
B. Genu of internal capsule - Heubner’s artery

110
 PARAPLEGIA
History taking
 Onset
- Acute- within minutes / hours?
- Subacute-within days /weeks?
- Chronic – within months /years?
 Was there a h/o trauma?
 Fall from height /road traffic accident / direct injury?
 Was there a h/o back pain?
 Duration / maximum intensity / history of spinal surgery?
 Is there any girdle pain/sensation?
 Pain around thorax / abdomen?
Is it unilateral / bilateral?
 Does it increase with coughing /sneezing?
 Is there any h/o root pain?
Is it unilateral /bilateral?
 Does it radiate to limbs?
 Does it aggravate with coughing?
 Any pyramidal tract involvement?
 Buckling of knees/slipping of chappals /tripping on objects?
 Symmetry of symptoms??
- Is the motor weakness symmetrical?
- Is the sensory symptoms symmetrical?
- Or they are asymmetrical?
 Any lower motor neuron involvement?
 Loss of tone, wasting and fasciculation
 Any dorsal column involvement?
 Any swaying while walking / inability to sit upright /incordination

History of past illness

 H/o viral infections?
Viral infection /chicken pox/herpes zoster/HSV 1&2/HIV /CMV/HTLV
 H/o vaccination?
Anti rabies vaccination /polio vaccination /Others?
 H/o tuberculosis?
Anywhere in the body-pulmonary/interstitial/lymphnodal/miliary
111
  H/o malignancy

Personal history
 Any bladder involvement?
Retention /overflow incontinence /bladder sensation?
 Any bowel involvement?
Constipation /bowel incontinence /bowel sensation?
 Any sexual dysfunction?
Morning erection/loss of libido/sexual promiscuity?
 Any autonomic dysfunction?
 Excessive sweating /absence of sweating

EXAMINATION
 Higher mental function : normal
 Speech, language :normal
 Cranial nerves : normal

General examination
 Spinal deformities, tenderness
 Decubitus ulcer

Motor examination
 Bulk—reduced below level of lesion bilaterally
 Power—reduced below level of lesion
 Tone—Increased below level of lesion
Normal above the level of lesion
Sensory Examination
 Assess both spinothalamic (pain, temperature )
And posterior column (vibration )
 Look for sensory level

Reflex
 DTR lost at the level of lesion
 DTR exaggerated below the level of lesion
 DTR normal above the level of lesion

112
 Mode of onset of paraplegia
 Acute
Transverse myelitis, traumatic paraplegia, anterior spinal artery
syndrome
 Sub acute
Pott’s paraplegia, spinal epidural abscess, spinal cord tumors
 Chronic
Familial spastic paraplegia, amyotrophic lateral sclerosis, cranio-
vertebral junctional anomalies

What are subjective sensory symptoms?

 Radicular (root pain)/ Girdle pain
Unilateral / bilateral sharp shooting pain of dermatome distribution
Exacerbated by coughing, sneezing /valsalva
 Vertebral pain
Aching pain confined to a point of spine accompanied by point
tenderness
Neoplastic /inflammatory dural lesion likely
 Funicular pain
Deep seated ill defined dull ache distant from the affected cord level
Common with intramedullary lesion

What are the objective sensory deficits?

 Segmental hyper aesthesia
 Hypoesthesia ( decreased touch sensation )
 Hypoalgesia ( decreased pain sensation )
 Loss of all modalities below a level
 Loss of position and vibration sense
Dissociated sensory loss
Suspended segmental loss of pain and temperature
Loss of pain& temperature below a particular level
What are the changes in the superficial reflexes??
 Abdominal reflex of all 4 quadrants are absent
 Cremasteric reflexes absent bilaterally

113
  Plantar extensor bilaterally
D7 lesion
Abdominal reflexes of upper quadrant present
Lower quadrant absent
Beever’s sign positive
Plantar extensor bilaterally
D10 lesion
Abdominal reflexes of all quadrant present
Both cremasteric reflexes are absent
Plantar extensor bilaterally
L1 lesion

What are the changes in the deep tendon reflexes??

Loss of DTR at the segmental level with exaggerated DTR below the level
indicate level of lesion
 Biceps –C5
 Supinator –C5
 Inversion of supinator –C5, C6
 Triceps –C7
 Knee jerk –L2 3
 Ankle jerk –L5, S1

Is there any evidence of LMN / UMN lesions??

 LMN signs alone would indicate the possibility of
 Anterior horn cell lesion
 Nerve root disease ( radiculopathy)
 Peripheral nerve lesion(peripheral neuritis )
 Myoneural junction abnormality( myasthenia )
 Primary muscle disease (myopathies)
 LMN signs of a segmental distribution indicates an appropriate level of
lesion
 Bilateral UMN findings below that level indicates a transection of
corticospinal tract on either sides
 Both UMN &LMN signs at the same level suggest the possibility of motor
neuron disease.

114
Localisation
 Upper cervical cord
Quadriplegia and weakness of diaphragm
 Lesion C5-6
Loss of power & reflex at biceps, inverted biceps, inverted supinator
 Lesion of C7 segment
Triceps, wrist extensors and fingers
Paradoxical triceps jerk
 Lesion of C8- T1 segments
Finger and wrist flexion, Horners
 Lesion of thoracic region
 T10 lesion
Beevor’s sign
 L2-4 segments
Knee jerk lost, brisk ankle jerk
 S1 S2 segments
Ankle jerk lost, intrinsic muscles of foot
 S3-4 segments
Saddle anesthesia, bladder and bowel

Movement and root value

 Hip flexion: L1
 Hip extension :S1
 Hip abduction : L5
 Hip adduction :L2
 Knee flexion: S2
 Knee extension : L3
 Ankle dorsiflexion:L5
 Ankle plantar flexion :S1
 Subtalar eversion: L5
Inversion :L4
 Shoulder abduction :C5
 Elbow flexion in semiprone:C6
 Elbow extension, wrist dorsiflexion:C7
 Small muscles of hand:C8

115
Corresponding vertebral examination
 Inspection : Deformity
Narrowing of disc space
Gibbus
Meningocele
 Palpation :tenderness
 Percussion :tenderness
 Auscultation :bruit

Cord segments Vertebra

Upper cervical Same as cord segment
C1-4
Lower cervical Cord segment -1
C5-8
Upper thoracic T1-6 Cord segment -2
Lower thoracic T7-12 Cord segment -3
Lumbar cord segments Vertebra T10-12
Sacral cord segments Vertebra L1

Causes of UMN type/spastic paraplegia??

 Cortical lesion:
Tumor falxcerebri
Superior sagittal sinus thrombosis
 Spinal cord lesion
Compressive myelopathy
Non compressive myelopathy

Compressive Noncompressive
Short duration Longer

Upper level Not usually present

Asymmetric Symmetric
Root/bone pain Absent

116
Early bladder Late

Compressive myelopathy can be divided into extra medullary and intra

medullary

1)Extramedullary
Extradural—Disc lesions, vertebral lesions, others
Intradural—Meningioma, neurofibroma, arachidonitis

2)Intramedullary
Syringomyelia, hematomyelia, ependimoma, glioma, astrocytoma

Extramedullary Intramedullary
Radicular pain common, Unusual
early
Vertebral pain common Unusual

Funicular pain less common May occur

UMN signs present & early Present but late

Parasthesia ascending Descending dissociated

progression suspended anesthesia

Sphincter involvement late Early bladder involvement

Trophic changes uncommon Common

 Compressive lesions
Non -neoplastic
 Trauma
Vertebral body # /dislocation
Hyperextension injury
Direct puncture, stab/missile
117
  Spondylosis
Cervical stenosis
 Lumbar stenosis
 Intervertebral disc herniation
 Infectious disorder (absecss, TB)
 Inflammatory (rheumatoid arthritis, ankylosing spondylitis, sarcoid)
 Hemorrhage (epidural hematoma)
 Syringomyelia
 Arachinoid cyst
 Pagets disease
Neoplastic
 Meningioma
 Neurofibroma
 Leptomeningeal metastasis
Non compressive myelopathy
 Demyelinating( multiple sclerosis, ADEM)
 viral myelitis ( varicella zoster, AIDS related myelopathy)
 Vit B12 deficiency
 Ischemia and hemorrhage from vascular malformations
 paraneoplastic
 Spirochetal disease(syphilis, lyme disease )

Conus medullaris Cauda equina syndrome

L1-2 vertebra L2 vertebra to sacram(lumbar
(S1-5 spinal cord segments & sacral nerve roots)
Damage to conus Damage the lumbar and sacral
nerve roots
Cause:Trauma> IVDP, vascular Tb, myeloma, tumors

Sudden onset Gradual onset

Usually bilaterally symmetrical Usually asymmetric

Radicular pain less common Common

118
Back pain common Less common

Knee jerk preserved, ankle jerk lost Knee jerk, ankle jerk lost

Babinski + Plantar absent

If above S1(UMN)
Less LMN weakness((UMN)) Severe asymmetric weakness of
lower limb(LMN)

B/L saddle aneathesia Asymmetric saddle area

anesthesia

Early bowel/bladder incontinence No bowel/bladder involvement

Poor outcome Usually improves

DISCUSSION
Q) What are the possible causes?
- Refer DDs

MANAGEMENT
Investigations for confirming diagnosis
 Blood RE
 Urine RE
 RBS, LFT, RFT,
 Calcium, Phosphorus, ALP
 X-ray chest & spine
 MRI spine
 CSF analysis
 S. Electrophoresis
 Workup for primary malignancy
 VDRL/HIV
 VIT B12
 Vasculitic work up
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TREATMENT
General :
1. Good nutritious diet
2. Care of bowel,bladder and trophic ulcer
- Bowel- ISC , antibiotics for UTI
- Bowel- Laxatives (constipation), Manual evacuation
- Bed sores- Keep dry and clean, change position, Special beds
3. Muscle spasm - Diazepam,baclofen
4. Definite - depends on diagnosis
- Anti TB drugs
- Anti cancer drugs
- GB syndrome - I/V immunoglobulins or Plasmapheresis
- Transverse myelitis- Steroids
5. Physiotherapy

SPINAL CORD SYNDROMES

1. Pancord s/d
2. Brown Sequard s/d or Hemisection
3. Central cord s/d
4. Dorsal cord s/d
5. Ventral cord s/d
6. Conus medullaris s/d
7. Cauda equina s/d
8. Dorsolateral cord s/d
9. Anterior horn cell d/d

 Pancord s/d
 Definite motor,sensory and reflex levels
 Causes
- Transection of spinal cord-trauma
- Transverse myelitis
- Compressive myelopathies due to severe compression (eg-due to
TB, spinal epidural abscess, metastasis)

 Brown Sequard s/d or Hemisection

 Ipsilateral weakness
 Ipsilateral loss of dorsal column sensations
 Contralateral loss of spinothalamic sensations-STT sensations will be lost
at a level lower than the lesion(2-3 segments below)
120
  Band of hyperaesthesia on same side
 Cause-Stab injury
 It is a very rare s/d.

 Central cord s/d

 b/l STT sensations lost
 suspended dissociated sensory loss
 early bladder involvement
 If it extends anteriorly,anterior horn cells may be affected leading to
wasting of muscles
 Causes
- Syringomyelia
- Ependymoma
- Cervical cord whiplash
- Hydromyelia
- Intramedullary glioma

 Dorsal cord s/d

 Dorsal column-Fasciculus gracilis & fasciculus cuneatus
 Sensory ataxia
 Romberg’s test +ve—It was first described for Tabes dorsalis
 Causes
- Tabes dorsalis
- Diabetic neuropathy

 Ventral cord s/d

 Causes-Anterior spinal artery occlusion
 Antrior spinal A supplies anterior two third of spinal cord
Infarction of Clinical feature
Coticospinal tract Paraplegia with UMN signs

Anterolateral tracts(STT) Loss of pain and temperature distal to

the lesion

Fibres of sphincter control Loss of bladder control

 Cauda equine s/d

 L2 downwards
121
  Severe root pain
 5 ‘A’s
- Atrophic
- Areflexic
- Atonic limb
- Assymetric involvement
- Assymetric saddle anaesthesia
 Causes
i. IVDP
ii. Lumbar spondylosis
iii. Trauma
iv. Mets
v. Multiple myeloma
vi. Neurofibroma
vii. Meningioma

 Conus Medullaris s/d

 S2,3,4,5
 Symmetrical involvement
 Bladder, bowel, potency- affected early; LMN/ Autonomous bladder
 Symmetric saddle anaesthesia
 BCR, Anal reflex, Anal tone- lost
 Flexor plantar
Q.)Cerebral causes of paraplegia?
i. Cerbral diplegia
ii. Superior sagittal sinus thrombosis
iii. Parasagittal meningioma
iv. Thrombosis of unpaired ACA
Q.)Causes of spinal cord compression?
Intramedullary Extramedullary
1. Glioma 1. Intadural
2. Ependymoma 1. meningioma
3. Syringomyelia 2. neurofibroma
4. Tuberculoma 2. Extradural

122
 5. Mets 1. Caries spine
2. Metastasis to vertebrae
3. Trauma-fracture or dislocation of
Vertebra
4. IVDP
5. Spinal epidural abscess

Q.Difference between compressive and non compressive myelopathy?

Compressive Non compressive
1.Bony deformity + -
2.Bony tenderness + -
3.Root pain + -
4.Girdle like sensn + -
5.zone of hyperaesthesis + -
6.onset and progress gradual May be acute
7.symmetry Asymmetrical Majority- symmetrical
8.Bladder and bowel early Late ( a/c transverse
invlt myelitis)
9.Flexor spasm Common absent
10. eg Caries spine Motor neuron d/s

Q.Difference between extramedullary (intradural) and intramedullary lesions?

Extramedullary Intramedullary
1. Root pain Early and common Rare
2. Sensory deficit No dissociation of Dissociation of
sensation sensations
3. Sacral sensation Lost Sacral sparing
4. LMN invlt Segmental Marked with widespread
atrophy,fasciculations
seen
5.UMN invlt Early and prominent Less pronounced,late
6.Reflexes Markedly increased and Minimal and late
early
7.Bladder and bowel Late Early
invlt
8.Trophic changes Not marked Common
9.Vertebral tenderness May be sensitive to local No bony tenderness
pressure
10. Changes in CSF- frequent Rare
raised protein
123
Q.) Name some demyelinating diseases.
 LMN type
- Guillian Barre S/d
 UMN type
- Multiple Sclerosis
- Neuromyelitis
- Transverse myelitis

LANDRY GUILLAIN BARRE SYNDROME

 A/c polyradiculoneuropathy
 Pathogenesis -molecular mimicry
 Antecedent events-infection(C.jejuni,CMV,EBV etc),immunisation
I. MOTOR
 GBS-predominant motor invlt-paraplegia/quadriplegia
 Proximal muscles more affected. Distal also affected
 Ascending paralysis
 Cranial nerves-most common is b/l LMN facial palsy which is
assymetrical
 Reflexes-areflexia
 Plantar-flexor/no response

II. SENSORY
 No sensory abnormalities on examination but the patient may
complaint of distal paraesthesia. Mild loss of vibration in distal feet

III.BLADDER AND BOWEL

 Not involved- If bladder dysfunction is a prominent feature and comes
early in the course of d/s-possibilities other than GBS should be
considered.

Definite sensory level and bladder is AGAINST GBS

SUBTYPES OF GBS
 AIDP-a/c inflammatory demyelinating polyneuropathy
 AMAN-a/c motor axonal neuropathy
 AMSAN-a/c motor sensory axonal neuropathy
 Miller Fisher s/d

124
Investigation- CSF-ALBUMINOCYTOLOGICAL DISSOCIATION(increased
protein in the absence of cells [<5 cells,>45 protein])

Treatment- IVIG/plasmapheresis; severe cases-ventillatory support

A/C TRANSVERSE MYELITIS

 Non compressive myelopathy which behaves like compressive variety
 Often follows viral illness or post vaccinal
 Onset-a/c or suba/c
 Fever may be present before paralysis
 Most common site-Mid thoracic region
I.MOTOR
 Back pain and progressive paraparesis often presenting symptom
 Plantar-extensor
II.SENSORY
 Sensory-partial or complete sensory losswith definite upper level
 No root pain,spinal tenderness
III.BLADDER
 Bladder involved early

HYPOKALEMIC PERIODIC PARALYSIS

 Onset at adolescence
 Men more affected
 Autosomal dominant
 Episodic weakness
 Proximal muscles more involved than distal
 Ocular and bulbar muscles less likely involved
 Attacks provoked by meals high in carbohydrate or following prolonged
exercise

Note : Episodic weakness with onset after 25 years almost never due to
periodic paralysis

125
 BELL’S PALSY
General examination
 Look for any vesicles on pinna, signs of lateral tarsorraphy, corneal ulcer
/ exposure keratitis on affected side.

Cranial nerve examination

 Facial nerve examination -since it is an LMN lesion, on affected side:
- Loss of taste sensation
- Hyperacuisis (subjective) present
- Corneal reflex lost
- Bells phenomenon present

 If 8th nerve involvement also present, cerebellopontine angle tumor is a

better diagnosis as
 Bell’s palsy is isolated 7th nerve palsy.

Discussion
Q.Difference between bilateral UMN and bilateral LMN facial palsy?
1. Normally CST fibres and emotional fibres comes together and there is an
inhibition over emotional fibres by the CST fibres.When there is b/l UMN
lesion the inhibition is lost and there is emotional burst out by the
patient
2. In b/l UMN lesion above pons, jaw jerk will be exaggerated.
3. Primitive reflexes may be present in b/l pyramidal lesion.

Q.Causes of b/l LMN facial palsy?

 GBS, sarcoidosis, Hansen’s disease, diabetes

Q.Complications of Bell’s palsy

1. Exposure keratitis
2. Facial hemispasm
3. Facial contracture
4. Synkineseis-attempts to move one gp of muscles result in contrn of all
5. Crocodile tears
6. Jaw winking

Q.)Treatment of Bell’s palsy(Ref-Dhingra)

126
 i. Steroids-Prednisolone 1mg/kg/day divided into morning and evening
doses for 5 days. Patient seen on 5th day-If improving-taper over 5
days(total10 days)
ii. If paralysis remains incomplete-give steroids for another 10 days-taper
over 5 days(total 20 days)
iii. Antiviral-Acyclovir 800mg 5 times a day for 7 days
iv. Supportive-eye padding; massage of weakened muscles; anlgesics to
relieve ear pain
v. Artificial tears to moisten the eye.

PARKINSONISM

PARKINSONS DISEASE PARKINSONISM

Idiopathic Secondary
Tremor +++ Tremor+/- but symmetric akinetic type
Eg: Drug induced,
Wilson’s d/s,
Post encephalitic Parkinson,
Vascular Parkinsonism

General examination
 Mask like facies (infrequent blinking & staring look, no facial
expressions)
 Coarse, pill rolling tremor of hands.
 Jaw tremor or head nodding usually seen.
 Stooping posture.

Nervous system examination

 SPEECH
- slow, indistinct, monotonous speech
 MOTOR SYSTEM
- Bulk - no wasting
- Tone - hypertonia - lead pipe rigidity in upper & lower limbs, cog-
wheel rigidity in hands due to tremor
- Power - grade 4 or above
- Involuntary movement - tremor in hands, jaw, tongue,
legsipsilateral to the tremulous hand can have tremor

127
 - Reflexes - deep reflexes normal / hyperreflexia (but never clonus),
glabellar tap positive (Meyerson’s sign)
- Gait - festinant gait (short, shuffling), difficulty in initiating
(freezing/bradykinesia) & stopping movement, paucity of
automatic movement of upper limb (swaying of arms)

Quick Facts About Parkinsonism

• Degeneration of NIGROSTRIAL tract
• TRAP
T- tremor
R- rigidity
A-Akinesia
P- postural imbalance
• Normal deep tendon reflexes
• Plantar flexor
• Festinant gait

PERIPHERAL NEUROPATHY
Common Causes
- Alcoholism
- Diabetes mellitus
- Leprosy
- Deficiency- vitamins B1, B12, B9, B3, B6, E
- GBS
- Diphtheria
- Connective tissue disease
- Lymphoma
- Drugs - INH, nitrofurantoin, vincristine

General Examination
- Look for anemia (megaloblastic)
- Enlarged parotid glands, gynaecomastia, flushed facies (alcoholism)
- White anaesthetic spots (leprosy)
- Foot drop

Nervous System Examination

• Examination of peripheral nerves (refer consensus)
• Cranial nerve examination - palatal palsy in diphtheria & 7th nerve palsy in
GBS(often b/l)

128
• Motor system- look for
- wasting of limbs & small muscles of hand & feet
- tone & power - decreased in affected limbs
- reflexes - diminished / lost (plantar - usually no response)
- coordination - test if power is grade 4 or above
- gait - high stepping gait in foot drop
• Sensory system
- look for glove & stocking distribution
- Pain, temperature, touch decreased / lost
- Vibration sense (1st to be lost in DM), position sense, joint sense lost
- Cortical sensations cannot be tested if primary sensations lost.

Quick Facts About Peripheral Neuropathy

 SENSORY
Symmetric distal sensory loss(glove and stocking type of
anaesthesia)
 MOTOR
Symmetric weakness
Muscles of feet and legs affected earlier
Areflexia/ hyporeflexia
 AUTONOMIC
Orthostatic hypotension & syncope
Erectile dysfunction

129
 NEUROGENIC BLADDER

Afferent arc –
1. By distension of bladder wall, stretch receptors are stimulated
2. reach the intermediolateral horn cells of S2-4 the detrusor center
3. ascends up to the brainstem micturition center

Efferent arc –
1. Parasympathetic – voiding
2. sympathetic – holding

Control of micturition

1. Cortical micturition centre Paracentral lobule – inhibitory to PMC

2. Pontine micturition centre
(Barrington’s nucleusn)
3. Spinal centers
4. Peripheral nerves
Dysfunction – loss of social control of
bladder
a) Lateral region – continence ,
storage
b) Medial region – micturition
a) Sympathetic – T11 – L2 – filling
of urinary bladder.
b) Parasympathetic – S2,3,4 –
emptying of bladder
S2,3,4- voluntary control of
micturuition

130
Types of neurogenic bladder
Type Site of lesion Effect Causes
Social bladder/ Above pons Bladder sensation Frontal lobe
cortical –present infarct ,
disinhibited Bladder parasagittal
bladder evacuation –
meningioma , ACA
sudden
Bladder control aneurysm
(initiation
&inhibition)
lost…..hence
patient urinates
in inappropriate
situation
UMN Bladder / Below PMC and Acute stage – Transverse
automatic/ above S2 atonic bladder. myelitis,
spastic bladder Post spinal shock syringomyelia
– hesitancy,
,spinal cord
urgency,
precipitancy trauma above
S2etc
LMN /automatic Spinal cord lesion Painless Conuscauda d/s ,
bladder at sacral level retention leading trauma
Mixed sensory to overflow
and motor loss incontinence
Motor Efferent pathway Inability to Lumbar canal
denervated initiate/ maintain
stenosis ,
bladder micturition lumbosacral
Painful retention
meningomyelocele
, abdominopelvic
surgeries
Sensory Afferent pathway Overdistension of DM, syringomyelia
denervated bladder
bladder Can initiate
voluntarily
Big painless
distension with
overflow
incontinence
131
RESPIRATORY SYSTEM

132
 RESPIRATORY SYSTEM CASE FORMAT
Common presenting symptoms:
• Breathlessness : Breathlessness (or dyspnoea) denotes the feeling of an
‘uncomfortable need to breathe’.
Causes
Acute Subacute Chronic
Airways obstruction Pneumonia* COPD*
Anaphylaxis Exacerbation of COPD* Pleural effusion*
Asthma Angina Malignancy
Pneumothorax* Cardiac tamponade Chronic pulmonary
emboli
Pulmonary embolus Metabolic acidosis Restrictive lung
disorders,
Myocardial infarction Pain Congestive cardiac
failure
Pulmonary oedema Pontine haemorrhage Valvular dysfunction
Arrhythmias Cardiomyopathy
Anxiety

• Cough : Cough can be defined as acute (lasting less than 3 weeks) or chronic
(lasting more than 8 weeks). A cough may be dry or it may be productive with
sputum.
Cough >2weeks : consider TB
Causes of cough Examples
Respiratory Viral or bacterial infection, bronchospasm, COPD, non-
asthmatic eosinophilic asthma, bronchiolitis,
malignancy, parenchymal disease e.g. ILD,
bronchiectasis, cystic fibrosis, sarcoidosis, pleural
disease, aspiration
Upper airways disease Post nasal drip, sinusitis,inhaled foreign body, tonsillar
enlargement
Cardiovascular disease LVF, mitral stenosis
Gastro-oesophageal GORD
Neurological disease Aspiration
Drugs and irritants ACE inhibitors, cigarette smoke

• Sputum
Purulent→Pneumonia
Purulent +foul smelling →lung abscess

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• Wheezing : Wheeze describes the high-pitched musical or ‘whistling’ sounds
produced by turbulent air flow through small airways narrowed by
bronchospasm and/or airway secretions. It is most commonly heard during
expiration, when airway calibre is reduced.

• Haemoptysis : Haemoptysis means coughing up blood from the respiratory

tract. It can complicate any severe forceful cough but is most commonly
associated with acute or chronic respiratory tract infections.

Causes of haemoptysis
 Malignancy and benign lung  Pulmonary infection
tumours,
 Bronchiectasis  Pulmonary emboli
 AV malformation  Congestive heart failur
 Chest trauma and foreign  Severe pulmonary
bodies hypertension
 Anticoagulation or  Drugs, e.g. cocaine,
coagulopathy thrombolytics

•Stridor
This harsh, grating respiratory sound is caused by vibration of the walls of the
trachea or major bronchi when the airway lumen is critically narrowed by
compression, tumour or inhaled foreign material.

• Chest pain
Chest pain may originate from musculoskeletal, respiratory, cardiovascular and
gastro-oesophageal disease.

• Constitutional features
Consider CA lung or TB

• Complications
Right heart failure

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Past medical history:
TB, reccurent LRTI(bronchictasis) ,
COPD and Exacerbations

Personal history:
Smoking index

Family history:
TB, passive smoking

Treatment history:
ATT(duration,completion), Pleural aspiration

GENERAL EXAMINATION:
 Built- COPD patients may be emaciated
 Attitude—wheather in distress
 Pallor or plethora(smokers, COPD)
 Clubbing(carcinoma, lung abscess, ILD)
 Cyanosis(feature of respiratory failure)
 Lymph nodes (TB, malignancy)
Oral cavity and upper airway:
 DNS , Polyps in asthma , features of infection, PNS
Examination of chest :
Inspection
1.Shape of chest
• Volume loss →Collapse , Fibrosis
• Prominance →Effusion , Pneumothorax
• Kyphoscoliosis and any retraction

2.Position of TRACHEA(upper lobe lesions) Indicate mediastinal shift

3.Position of APEX BEAT(lower lobe lesions)

• Shifted to side of lesion→Fibrosis & Collapse

• Shifted away from lesion→Pleural effusion & Pneumothorax
• Central trachea with lung disease
Unilateral→ (Consolidation , Cavity)
Bilateral → (ILD, emphysema, airway disease)

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4.Respiratory Movements
 Will be reduced at the site of lesion
5.Respiratory rate
 normal 16- 20/min
6.Rhythm
•Cheyne stoke’s – rhythmic alterations of apnoea & hyperapnoea
due to anoxemia. Seen in infants, high altitude,deep sleep,raised ICT,
narcotic poisoning, uremia,severe LVF
•Kussmal’s breathing- deep & rapid breathing. Seen in diabetic
ketoacidosis
•Biot’s breathing- always pathological...irregularly irregular
breathing seen in meningitis.
•Apneustic breathing – pons damage
•Ataxic breathing – random shallow, apnea and deep breathing
7.Type of breathing
 normally thoracoabdominal in femals & abdominothoracic in males
8.Intercostal retraction
 Working of assessory muscles of respiration
9.Any scars or dilated veins

Palpation
1.Confirm position of trachea
2.Apex beat
3.Respiratory movements
• Upper anterior
• Lower anterior
• Upper posterior
• Lower posterior

Surface marking of fissures

• the oblique fissure in either lung can be shown by a line drawn from
the spinous process of the T2 to the sixth rib in the mid-clavicular line
• The horizontal fissure in the right lung is indicated by a line
drawnfrom the point where oblique fissure cuts the midaxillary line, to
the midsternal line at the level of the fourth costal cartilage.
• Corresponding areas
 Upper lobe→Supraclavicular
Infraclavicular(upto 3rd rib)
Suprascapular(above T2) &
136
 Interscapular(upper part)
 Middle lobe→Mammary (3rd to 6th rib)

 Lower lobe →Interscapular(lower & middle)

Infrascapular(T7 spine to 10th rib)
Infraaxillary(4th to 8th rib)

4.Chest expansion
 Total→normal(>5cm)
 Differrential

5.Antero-posterior and Transverse diameters

 Normal ratio→5:7
 Barrel chest→1:1(emphysema)
 Flat chest →decrease in AP diameter (fibrosis)
•Pectus excavatum(depression of sternaum)
•Pectus carinatum(forward protrusion of sternum)

6.Vocal fremitus
• Normally equal on both sides

Emphysema
Pleural effusion
Decreased fremitus
Obesity
Pneumothorax
Collapse
Consolidation
Increased fremitus Upper level of effusion

Impaired fremitus Fibrosis

7.Intercostal narrowing
 If there is volume loss

Percussion
• Resonant → normal lung
• Hyperresonant → emphysema , pneumothorax
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 • Dull → consolidation , collapse
• Stony dullness → pleural effusion
• Impaired → fibrosis
• Tympanic → hollow viscera
• Tidal percussion → to differrentiate b/t right lower lobe
consolidation and subphrenic abscess
• Shifting dullness → hydropneumothorax

Auscultation
1.Intensity of breath sounds
• Normally equal on both sides

Reduced in
 Pleural effusion
 Pneumothorax
 Obesity
 Severe airway disease 

2.Type of breath sound
• Vesicular breath sound →Normal
Full inspiration + no gap in between
Soft & low pitch

 Bronchial breath sound →Early to mid inspiration + gap in

between + full expiration
Loud & high pitched
Types of Bronchial breath sound :
 Tubular(consolidation,upper level of effusion, mass over bronchus)
 Cavernous(superficial cavity)
 Amphoric (large cavity)
Causes of bronchial breath sound
Physiological Pathological
 Over trachea  Consolidation, collapse
 Right upper lobe(bronchus  Cavity
is superficial)
3.Additional sounds
• Crepitations / crackles
Wet (loose secretions in the airway) bronchictasis,abscess,pulm edema
Dry (sudden opening of collapsed Fibrosis of airway(ILD)
airway)
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Types according to timing
Inspiratory Expiratory
Early (large Mid(medium Late(small Lung abscess
airway) sized airway) airway) Bronchiectasis
Tracheitis, Bronchiectasis Alveolar edema, COPD
Resolving Fibrosis,
pneumonia, pneumonia
COPD

Based on character
Fine Coarse
Early pneumonia,Pulmonary edema Resolving pneumonia, Bronchiectasis
ILD COPD

•Ronchi
Monophonic →due to single site narrowing (lymph node/mass compressing)
Polyphonic → due to small airway or due to both small & large airway

Large + small airway narrowing Small airway only

• Ronchi in both inspiration and • Expiratory ronchi

expiration Eg : COPD(predominantly small airway)
Eg: Asthma(paneirway disease)


•Pleural rub
Cracking sound due to rubbing of inflammed pleura
It is late inspiratory and late expiratory(mirror image sound)
With onset of effusion rub will disappear

Summary and Diagnosis

• Anatomical (right/left)& lobe?
• Pathological (effusion/consolidation/fibrocavity)
• Etiological
• Complications and comorbidities
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 Clinical approach
CONSOLIDATION
History
• Presenting complaints → fever, cough, expectoration, breathlessness,
associated chest pain
• Past History →any pre-existing conditions- COPD, TB, bronchiectasis,
immune compromised states. DM, AIDS, GERD, etc
• Personal history →smoking index( imp), occupation, alcohol.

General examination
 toxic/ dyspnoeic / severe distress?
 Look for pallor , clubbing( to identify any underlying cause, in lung
abcess-painful clubbing)& generalised lymphadenopathy
 Cyanosis – assess o2 saturation Cold or warm extremities
 PULSE: tachycardia, high volume (if hypercapnoeic)
 Respiratory rate, type, use of any accessory muscles measure
temperature

Examination of the chest

Inspection
• Shape of chest, chest movements –use of accessory muscles,
intercostals retractions, may be reduced if there is assc. Effusion

Palpation
• Trachea- CENTRAL, NO MEDIASTINAL SHIFT. Mediastinal shift may be
present if associated with synpneumonic effusion (to opp side) or collapse
consolidation(to same side)
• VOCAL FREMITUS INCREASED

Percussion
• WOODY dull note over the areas.(stony dullness in effusion – a hard
resistance felt on fingers while percussing)

Auscultation
• TUBULAR BRONCHIAL BREATHING (learn mechanism of normal vesicular
sound and bronchial breathing)

140
 • VOCAL RESONANCE – increased
• Bronchophony — seems to appear from the earpiece of stethoscope
•Whispering pectoriloquy —Patient whispers. Increased sound is heard
clearly or distinctly, i.e., syllable by syllable (pectoriloquy).It seems to be
spoken right into the auscultator’s ear. Bronchophony and whispering
pectoriloquy are classically heard over consolidation.
• Aegophony — This is a qualitative change in vocal resonance with nasal
intonation .It is classically found over consolidation .
• Crepitations may be heard. No rhonchi.

Diagnosis
 Right/Left
 Upper/Middle/Lower lobe consolidation
 With/ without pleural effusion
 Patient in resp failure/not
 Any predisposing aetiology
 Complications and other comorbidities

Discussion points
• Why is this consolidation?
• DD :Pleural effusion, collapse, TB, Bronchogenic CA. ( prepare and learn
points in favour and against)
• Definition pneumonia, CONSOLIDATION (exudative solidification of lung
parenchyma), stages , classification, ( ref kundu, Davidson), atypical
pneumonia
COMPLICATIONS
(1) Pulmonary :
1. Delayed resolution. 5. Pneumatocele.*
2. Lung abscess or cavitation. 6. Pyopneumothorax.
3. Pleural effusion 7. Fibrosis of lung, rarely
4. Empyema thoracis 8. Respiratory failure
(2) Neurological
1. Mental confusion 3. Meningism
2. Meningitis 4. Cerebral abscess
(3) CVS :
1. Myocarditis 3. Endocarditis
2. Pericarditis 4. Peripheral circulatory failure
(4) Musculo-skeletal :
1. Septic arthritis
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(5) Septicaemia, herpes labialis, thrombophlebitis, uraemia, ARDS, multi-organ
failure.

Investigations :
•BRE , sputum – AFB& GRAM staining (read AFB and gram staining),
culture sensitivity, blood culture,
•Chest X ray : opacities appear within 12 – 18 hrs, complete resolution by
4 weeks

MANAGEMENT :

•General /symptomatic : position, O2 inhalation, bronchodilators,

expectorants, bed rest, diet.
•Specific : ANTIBIOTICS

• CRITERIA for admission : CURB 65 ( Consciousnes, S. Urea >20 mg dl,

Resp rate >30, BP <90/60 , Age >65)
score 1-2 : home, 2 : hospital, >3 treat as severe pneumonia

Antibiotic treatment for community-acquired pneumonia*

Uncomplicated CAP
• Amoxicillin 500 mg 3 times daily orally
If patient is allergic to penicillin
• Clarithromycin 500 mg twice daily orally or Erythromycin 500 mg 4
times daily orally

If Staphylococcus is cultured or suspected

• Flucloxacillin 1–2 g 4 times daily IV plus
• Clarithromycin 500 mg twice daily IV

If Mycoplasma or Legionella is suspected

• Clarithromycin 500 mg twice daily orally or IV or Erythromycin
500 mg 4 times daily orally IV plus
• Rifampicin 600 mg twice daily IV in severe cases

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Severe CAP
• Clarithromycin 500 mg twice daily IV or Erythromycin 500 mg 4
times daily IV plus
• Co-amoxiclav 1.2 g 3 times daily IV or Ceftriaxone 1–2 g daily IV or
Cefuroxime 1.5 g 3 times daily IV or
• Amoxicillin 1 g 4 times daily IV plus fucloxacillin 2 g 4 times
daily IV

PLEURAL EFFUSION
Presenting complaints
• Chest pain- increase on inspiration and coughing ,postural variation
Cough
• Fever
• Gradually progressive breathlessness

Past h/o:
• h/o suggestive of TB, malignancy, lymphoma, trauma, collagen vascular
disease h/o DM, smoking
• h/o cardiac, renal or liver disease, thyroid disease, drug intake( read
drugs causing effusion)

On Examination
• Built and nourishment(malnourished?), PICCLE, RR
Inspection
• TRACHEAL SHIFT away from the side of lesion
•RESPIRATORY MOVEMENTS reduced on the affected side
• Look for fullness of intercostal spaces
Palpation
• TRACHEA to the normal side
• APEX BEAT may not be palpable if effusion on the left side, look for shift
of apex
• RESPIRATORY MOVEMENTS reduced on the affected side
CHEST EXPANSION hemithorax expansion reduced
• VOCAL FREIMITUS reduced on the affected side
Percussion
• Stony dull→The dullness will be at a higher level at the axilla

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 • If it is hydropneumothorax dullnesss will be in a stright line
•Right sided effusion is continuous with liver dullness and left sided
effusion is with cardiac dullness
• Shifting dullness absent in pleural effusion
• Tidal percussion : dullness will be supradiaphragmatic after inspiration
• Traube’s space percussion : dull on left sided effusion
Auscultation
• Breath sounds reduced on the affected side.
• No adventitious sounds
• Vocal resonance reduced
• Succusion splash absent in pleural effision
DIAGNOSIS
• Left sided pleural effusion probably tuberculous in origin / following
pneumonia with /without any features of respiratory failure with /
without any co-morbidities.

INVESTIGATIONS
• RBE
• CXR →Homogenous opacity with higher level at axilla Obliteration of
cardiophrenic and costophrenic angle Displacement of mediastinum to
opposite side
• SPUTUM EXAMINATION→Gram staining & AFB staining
• ASPIRATION OF PLEURAL FLUID (atleast 50 ml) → Transudate/ Exudate
(LIGHT’ s criteria)
• Smear examination
• Culture of aspirated fluid PCR
• Mantaux test
• USS –detects small amount of fluid
• PLEURAL BIOPSY –Confirms TB
TREATMENT
• Rest with good nutritious diet
• NSAID to relieve chest pain
• Aspiration of pleural fluid if suffers from respiratory distress Or if there
is rapid collection
• Chest physiotherapy for expansion
• Management of aetiology(TB ,PNEUMONIA)

144
 Read DD, lights criteria, causes of effusion, encysted effusion, pleural
thickening, malignant effusion, sclerosing agents, DD of right and left sided
effusions, bilateral and recurrent effusion, findings at upper border of
effusion, hemothorax, chylothorax, effusion with no tracheal shift DDs,
phantom tumour, subpulmonic effusion, massive effusion, complications of
effusion .
FIBROCAVITY
Presenting complaints
• Fever
• Cough
• Respiratory distress
Inspection
• FEATURES OF VOLUME LOSS →Drooping, Supraclavicular hollowing,
Infraclavicular flattening, Crowding of ribs, Intercostal retraction
• TRACHEAL SHIFT to side of lesion
• APEX SHIFT to side of lesion(indicates lower lobe fibrosis)
• RESPIRATORY MOVEMENTS & HEMITHORAX EXPANSION reduced on
affected side
Palpation
• Look for shift of trachea and apex beat
• VOCAL FREMITUS increased over cavity and reduced if there is
associated fibrosis
Percussion
• Resonant over a cavity( cracked pot resonance) Impaired if associated
with fibrosis
Auscultation
• Fibrosis : Reduced vesicular breath sounds
• Cavity :Bronchial breathing(cavernous), post tussive crepitations/suction
Fine crepitations and occasionally rhonchi heard in fibrosis
• VR increased if no pleural fibrosis, decreased if pleural fibrosis present
DIAGNOSIS
• Fibrocavity lesion of right upper lobe
• Probably post tuberculous
• with / without features of respiratory failure
• with / without comorbidities
INVESTIGATIONS
• BLOOD INVESTIGATIONS –Hb, TC ,DC,ESR
• CXR
• Sputum examination
145
 • Lung function test
• Bronchoscopy

TREATMENT
•Treat TB
Read
• types of fibrosis, causes of upper and lower lobe fibrosis,types and def
of bronchial breathing, causes of cavity
• Pulmonary tuberculosis – read about primary and post primary
tuberculosis, presentations, complications, investigations, DOTS, AFB
staining, poncets arthritis, steroids in tb, ghons focus, rankes complex
• External manifestations of TB: lupus vulgaris, erythema nodosum,
srofuloderma, phlycten, choroid tubercles, epididymo orchitis.

COPD
Presenting complaint
• Classical picture: c/c Cough & breathlessness in a patient usually above
the age of 40,male smoker +/- symptoms of c/c cor pulmonale like
swelling of legs, abdominal distension,excessive daytime
somnolence,atypical chest pain etc

H/o Present Illness

• Cough-duration(long durn c/c
cough),onset,episodic/not,postural/diurnal /seasonal
variation,aggravating/relieving factors,dry/wet, if sputum present-its
frequency of
production,colour,qty,bloodstained,foulsmelling/not,postural/diurnal
(esp early morning) variation for sputum production
• Breathlessness-onset,before/after cough,rest/exertional,history s/o
PND,orthopnea/positional variation,aggravating/relieving factors.
• Another symptom of advanced d/s is morning headache,s/o
hypercapnia.
• The three most common symptoms in COPD are cough, sputum
production, and exertional dyspnea.
• R/O other DDs by asking symptoms like fever,hemoptysis,pleuritic chest
pain,cardiac symptoms,features of cardiac failure etc.

H/O Past Illnesses

146
 • Similar episodes in past,no.,treatment done,on any medication-
oral/inhalational now..H/O TB,cardiovascular,respiratory disease.

Personal history
• Take the smoking history in detail esp.pack years. It is unusual to
develop COPD with less then 10 pack years.

Family history
• Any family history of bronchial asthma,TB ,or other respiratory disease.
General examination
• Face may be dusky plethoric. Nicotine staining of fingernails.
• Cyanosis may be present in blue bloaters.
• Clubbing is not a feature of COPD,it warrants investigation for other
causes especially lung cancer in a smoker.
• Pedal edema present if patient has c/c cor pulmonale.
• Advanced disease may be accompanied by systemic wasting, with
significant weight loss, bitemporal wasting, and diffuse loss of
subcutaneous adipose tissue.
• Pulse –tachycardia,may be water-hammer in character,regular.

Examination of chest
Inspection
• Barrel shaped chest
• Tachypnea;stooping forward position in bed( characteristic ‘tripod
position’);intercostal retraction;accessory muscles of respiration may be
working .

Palpation
• Apex beat may not be palpable in emphysema/outward apex in RVH.
• AP:Transverse diameter normal is 5:7, in barrel chest it may become
1:1.
• Total Chest expansion may be reduced.
• B/L decreased chest movements.
• Vocal fremitus may be diminished all over the chest uniformly.
• Cor pulmonale- Raised JVP,Palpable P2,LPH,Liver soft,enlarged &
tender.

147
 Percussion
• Increased resonant note all over chest with loss of hepatic & cardiac
dullness in emphysema.

Auscultation
• Decreased vesicular breath sounds with prolonged expiration.
Occasional rhonchi +/- coarse creps(if infn +).
• Vocal resonance-decreased over the chest uniformly. Cor pulm.-Loud
P2,RV gallop,PSM of TR.
DIAGNOSIS
• A/c exacerbation of Chronic obstructive pulmonary disease,
•probably chronic bronchitis/emphysema,
•with/without a/c resp. infection,
•with patient in resp. failure, and
•signs of cor pulmonale with any co-morbidities
DDs
• Bronchial asthma
• Tuberculosis
• Congestive cardiac failure
• Bronchiectasis
• Acute bronchopneumonia
• Tropical eosinophilia, allergic, aspergillosis.

Discussion
• Definition of COPD→ is defined as a disease state characterized by airflow
limitation that is not fully reversible . COPD includes emphysema, an
anatomically defined condition characterized by destruction and enlargement
of the lung alveoli; chronic bronchitis, a clinically defined condition with chronic
cough with sputum prodn for atleast 3 consecutive months for atleast 2
consecutive years; and small airways disease, a condition in which small
bronchioles are narrowed .
Read through
• risk factors: smoking>atmospheric pollution>indoor pollution,
• pathophysiology.
• Pulmonary & systemic features of COPD( Davidson),
• difference with asthma
• Modified MRC scale for dyspnea-imp.
• Complications

148
 • freq. resp infn
• pneumothorax
• Cor pulmonale.*def
• resp. failure – types, Rx.
• Blue bloaters & pink puffers; mechanism of pursed lip breathing-imp.

INVESTIGATIONS
• Complete blood count
• Spirometry-GOLD criteria for COPD severity.
• chest x-ray/ HRCT if required
• Sputum AFB
• ECG,Echo if cor pulmonale suspected.
• S. electrolytes.
• Measurement of lung vol by He diln technique/body plethysmography;
exercise tolerance tests; pulse oximetry for starting domiciliary O2 Rx;
alpha1 antiproteinase assay in a young p/t with predominant basal
emphysema

MANAGEMENT

• Stable COPD - Only three interventions—smoking cessation, oxygen

therapy in chronically hypoxemic patients, and lung volume reduction
surgery in selected patients with emphysema.
• smoking cessation
• bronchodilators
• inhaled corticosteroids
• Pulm. Rehabilitation
• Surgical intervention
• Other measures- N-acetyl cysteine has been used in patients with COPD
for both its mucolytic and antioxidant properties
• palliative care.

Read
• GOLD guidelines for COPD Rx, BODE index. A/C exacerbation
• O2 therapy:1-2 L/min
• bronchodilators-nebulising with salbutamol combined with anti-
cholinergics, •parenteral-Inj.Aminophylline/Deriphylline
• corticosteroids-oral/nebulization

149
 • Antibiotics- broad sprectrum
• Non-invasive ventilation
• additional therapy.
COLLAPSE
Collapse- decrease in lung parenchymal volume secondary to a cause.
Types:
• Active-Complete obstruction from foreign body, mucous plug
• Passive-Pleural effusion,pnuemothorax
• Compressive-Mass lesion, bronchial carcinoma,mediastinal
lymphadenopathy Cicatricial-Fibrosed,shrunken lung
• Adhesive-Surfactant deficiency and parenchymal collapse
History taking:
Symptoms have considerable overlap
•Fever, chills, rigor, rashes, cough, sputum (Pnuemonia).
Chest pain, respiratory distress, decreased movements
(Pnuemothorax,effusion,Acute severe asthma)
• Night sweats, loss of weight/appetite, evening rise of temperature,
malaise, hemoptysis (TB, carcinoma/2°s,lymphoma-leukemia)

Others : effusions common in hypothyroid, lhf, nephroticsyndrome,

hypoproteinemic patients..elicit a complete past history of diseases and
family history.
• Smoking, alcoholism, bowel –bladder habits..
• Diseases causing generalized/mediastinal lymphadenopathy (TB,
sarcoidosis, lymphoma, other malignancies like thyroid, breast),
• mass effect causing dyspnea, dysphagia, hoarseness of voice from huge
retrosternal goiters esophageal tumours,
• Neuorological symptoms like those of horners syndrome,
laryngeal/diaphragmatic palsies. Causes of ARDS. Near drowning,
inhalation of toxic fumes etc..
General examination:
• Any stigmata of TB (for it can cause consolidation, effusion, fibrosis.),
Marfans like arm span, height, UL:LL ratio, thumb/wrist signs
etc.(Spontaneous pneumothorax), Malignancy like cachexia or post
radio/chemotherapy findings
• Superior vena caval syndrome-Puffy face, dilated veins (mediastinal
lymphadenopathy) Anemia, Clubbing, Cyanosis, Lymphadenopathy,
evidence of malnutrition.
• Pulse rate,Blood pressure,Respiratory rate,Temperature..
150
 Examination of chest
• Signs of volume loss like..
 Drooping of shoulder
 Supra/infra clavicular hollowing
 Tracheal shift
 Intercostal narrowing,crowding of ribs
 Pulled up diaphragm
• Mediastinal shift to same side
• Chest movements →reduced
• Percussion note is dull
• Breath sounds reduced, tubular breathing (peripheral obstruction)
• Vocal fremitus /resonance →reduced

DIAGNOSIS
• Collapse lung R/L.of upper/middle/lower lobe
• from consolidation/pneumothorax/effusion/fibrosis
• probable etiology being pneumonic infection
• (bact/viral/fungal)/TB/malignancy/other mass effect
• and patient in respiratory failure/not
• and associated co morbidities

DD:
• all causes of collapse
• can be patchy collapse(ATELECTASIS) as in ARDS

INVESTIGATIONS :
• Blood-TLC,DC,ESR,Hb,
• Peripheral smear
• Chest Xray-PA +/- lateral view- Opacity homogenous (effusion) /
heterogenous (consolidation)
• Tracheal/Mediatinal shift
• Collapsed lung borders and pitch black lung fields with no broncho-
vascular markings in pnuemothorax
• Tenting of diaphragm in basal collapse

• Sputum studies,AFB
• HRCT lung
151
 • Lung function tests
• Bronchoscopy
• Biopsy
TREATMENT:
• Of cause:
• Consolidation from CAP-Antibiotics
• Pnuemothorax-Emergency needle aspiration/Chest tube with under
water seal
• Effusion-Plueral tap/ICD
• Bronchoscopic removal of foreign bodies
• Tumour-Resection/Radio-chemo-laser therapy. Palliative bronchial
stenting
• TB-ATT

BRONCHIECTASIS
History
• Persistent or recurrent cough with purulent sputum, postural variation,
hemoptysis , dyspnoea in widespread disease , chest pain
• Past Illness- history of severe pneumonia, tuberculosis, whooping
cough, measles, recurrent upper respiratory infections,foreign body
inhalation,drowning, alcoholism, epilepsy, any disease like cystic fibrosis,
GERD, inhalation of toxic gases
• Family History- ask about children (for males- infertility?), cystic fibrosis,
immune deficiency

Physical examination-
• Look for clubbing, pallor
• Any combination of crackles, rhonchi and wheezes may be heard over
area of bronchiectasis. Coarse leathery mid inspratory crepitations
characteristic
• Look for signs of right heart failure (Cor Pulmonale)- elevated JVP, soft
hepatomegaly, pedal edema

INVESTIGATIONS
• Chest X ray (not specific) shows honey comb appearance ( DDs- bullous
emphysema, interstitial lung disease) and tram track or ring shadow
appearance(dilated, thickened bronchi)or gloved finger pattern
152
 • HRCT ( standard investigation)
• Sputum analysis
• PFT
• Bronchoscopy for focal disease (obstruction?)
• Tests for cystic fibrosis, semen analysis (for young patients with diffuse
disease)
MANAGEMENT
• Treatment of infection
• Improved clearance of secretions
• Reduction of inflammation
• Treatment of underlying problem
• Surgery may be an option in localised cases

DISCUSSION :
• Definition of bronchiectasis?
Bronchiectasis is an abnormal and permanent dilatation of bronchi
• Which level of bronchi are affected in bronchiectasis?
At the level of segmental or subsegmental bronchi
• Name some infectious causes of bronchiectasis ?
Tuberculosis, pertussis, infection from staphylococcus,
klebsiella,adenovirus, influenza virus
• Name some respiratory causes of hemoptysis?
Tuberculosis, bronchiectasis, pneumonia, bronchogenic carcinoma,
mycetoma, autoimmune causes like lupus pneumonitis, bronchitis

Read : chest physiotherapy, antibiotic therapy

INTERSTITIAL LUNG DISEASE

History :
• gradually progressive breathlessness, non productive cough
• Any h/o suggestive of autoimmune disease, drug intake(busulfan,
methotrexate, amiodarone), radiation, smoking, occupational history
Examination:
• cyanosis, clubbing, tachypnoea
• Auscultation: bilateral basal late inspiratory Velcro crepitations( only
reliable finding)
• Also look for features of pulmonary hypertension and cor pulmonale

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Discussion:
INVESTIGATION
•chest x-ray – linear streaking, reticular pattern, honey combing, irregular
opacities
• Pulmonary function test,
• HRCT chest diagnostic,
• biopsy- gold standard

TREATMENT :
• steroids, immunosuppressant
• Study definition, classification

BRONCHOGENIC CARCINOMA
History :
• cough, chest pain,dyspnoea, hemoptysis, wheeze/stridor, loss of weight
or appetite, shoulder pain or pain in inner aspect of arm, also ask for h/o
suggestive of mediastinal invasion like dysphagia or voice changes,
metastasis like seizures, bone pain, jaundice
• History of smoking (pack years), occupational history, family history of
cancers
Examination :
• cachexic, look for PICCLE, nicotine stains
• Findings : can present as mass lesion, effusion, collapse, pancoast
syndrome, svc obstruction
• Mass lesion overlying a bronchus:
•Tracheal shift to opposite side but no mediastinal shift
•Dull on percussion
•Tubular bronchial breathing
•Increased Vocal Resonance(VR)
• Mass lesion not overlying bronchus:
•Tracheal shift to opp side but no mediastinal shift
•Dull on percussion
•Decreased breath sounds
•Decreased VR
INVESTIGATIONS:
• chest xray, CT chest, sputum cytology, bronchoscopy and biopsy,

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 • Pleural fluid aspirate, LFT, USG abdomen

TREATMENT :
• depends on stage
• Surgery , radiotherapy, chemotherapy esp for small cell CA
Read : extra pulmonary manifestations, management of malignant effusion,
risk factors , classification

LUNG ABSCESS
• What is the definition of lung abscess?
Lung abscess is defined as pulmonary parenchymal necrosis and
cavitation resulting from infection
• Most common cause of lung abscess?
Aspiration
• Most common causative organism?
Anaerobic bacteria
• What are the symptoms?
cough with purulent sputum
pleuritic chest pain
fever
hemoptysis
• What are the physical findings?
Rales or evidence of consolidation may be present. Clubbing may occur in
chronic cases
• What is the X ray finding?
Thick walled cavity in dependant areas with an air fluid level
• What are the differential diagnosis?
Mycobacterial infection, pulmonary sequestration, malignancy,
pulmonary infarction, infected bulla
• What is the treatment?
Antibiotics against anaerobic bacteria like clindamycin for 4 to 6 weeks
• What are the indications for surgery?
 Refractory hemoptysis,
 inadequate response to medical therapy,
 need for a tissue diagnosis

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GIT

156
 Chronic Liver Disease
Presenting complaints

Specific and non specific symptoms

Non specific symptoms

 Initial symptom –usually non specific

 Fatigue—most common and usually the 1st symptom of CLD
 Nausea—especially to fatty food
 Vomiting – chemoreceptor trigger zone in medulla are activated by
toxins like ammonia and urea. So vomiting can occur in CLD. but
persistant vomiting is highly unlikely

Definition –Vomiting is the forceful ejection of upper GI contents

through the mouth as a result of forceful and sustained contraction of
gut, abdominal muscles & diaphragm against a closed glottis
 Weight loss –can occur in acute liver disease & end stage of CLD
 Diarrhoea –ask for steatorrhoea (foul smelling profuse greasy stools)
Definition of diarrhoea—more than 3 stools per day or increase in daily
stool weight > 200 gm

 Constipation—Not a feature of CLD but if present can precipitate

hepatic encephalopathy

Specific symptoms

 Yellowish discoloration of eyes and urine—Ask for colour of urine and

stools to differentiate different types of jaundice
 Abdominal distension - whether progressive or not
 Reduced urine output - hepatorenal syndrome
 Fever abdominal pain- spontaneous bacterial peritonitis
 Itching-bile salts irritate free nerve endings leading to itching
Feature of obstructive jaundice and late stage of hepatocellular jaundice
 Clay colored stools --obstructive jaundice

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  Hematemesis,
 Melena
MALENA—black tarry sticky foul smelling stools indicative of bleeding in the
upper digestive tract proximal to ligament of treitz

A history of upper GI bleed in the form of hematemesis / melena is an

essential clue to the diagnosis of portal hypertension

False positive black stools—Fe tablets, bismuth

 Easy bruiseability – clotting factors synthesized by liver

Vit K malabsorption in obstructive jaundice—vit K required for gamma
carboxylation of factors II, VII, IX, X

 Inversion of sleep rhythm, personality changes—To rule out hepatic

encephalopathy

Finally comment on the course of the disease, condition of the patient at

present.

HEMOPTYSIS HAEMATEMESIS
Bright red colour (oxygen rich Coffee brown colour(acid
blood) hematin)
Associated sputum/froth Associated with food particles
Preceded by cough Preceded by nausea
Melaena absent Present
Other respiratory symptoms Other GIT symptoms may be
may be present present
Causes of recurrent jaundice
Hemolytic anemia
Congenital hyperbilirubinemia
Malaria
Wilsons disease

PAST HISTORY

 Previous h/o jaundice

 Previous h/o haematemesis

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  H/o blood transfusion—transfusion associated hepatitis (B, C)
 H/o risky sexual behaviour
 H/o abdominal surgery
 H/o involuntary movements ( wilson’s disease)

PERSONAL HISTORY
 Appetite – nausea to fatty food
 Sleep- inversion of sleep rhythm in hepatic encephalopathy
 Bowel and bladder habits- constipation can precipitate hepatic
encephalopathy
 Addictions (substance abuse)
Comment as –My patient is a habitual consumer of alcohol for 25 years.
He started consumption from the age of 22 and drinks toddy and rum.
He drinks around 30 gm alcohol per day.
1 unit of alcohol= 10 gm of alcohol =30 ml whisky / brandy=100ml
wine=250 ml beer
(Using this formula, amount in ml can be converted to gm)
One bottle of alcohol =750 ml
Risk for alcoholic liver disease
>20 gm for more than 10 years

FAMILY HISTORY

 Similar illness in the family

 Neuropsychiatric illness in the family (wilson’s disease )
 Malignancy

TREATMENT HISTORY
 Ask for drugs that have worsened the disease status
 NSAID, Aspirin, anticoagulants, Paracetamol, Erythromycin, herbal
medicine

GENERAL EXAMINATION
 Pallor
Causes
 Haematemesis
 Hypersplenism
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  Anemia of chronic disease
 Nutritional – Fe deficiency, beriberi
 Icterus
Ideally to be examined in good sunlight

Lemon yellow hemolytic jaundice

Orange yellow hepatocellular

jaundice

Greenish yellow Obstructive jaundice

 Cyanosis
Hepatopulmonary syndrome

 Clubbing in GIT
 Primary biliary cirrhosis
 Hepatopulmonary syndrome
 IBD
 Hepatocellular carcinoma
 Ameobic liver abscesa

 Lymph node enlargement
Causes of hepatosplenomegaly with lymph node enlargement
 Miliary TB
 IMN
 Lymphoma
 Leukemia
 Hepatoma
 HIV
 Pedal edema
Causes in alcoholics
 CLD (due to hypoalbuminemia)
 Severe malnutrition
 Cardiac failure (alcoholism leading to thiamine deficiency leading
to high output cardiac failure)
 Renal causes—increased incidence of IgA nephropathy
 Hepatorenal syndrome
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  Vitals
Pulse – bradycardia in obstructive jaundice
Bounding pulse may be found in CLD
Blood pressure
Respiratory rate—Ascites may be ass with pleural effusion
Temperature – SBP

HEAD TO FOOT EXAMINATION

1)Stigmata of chronic liver disease

Eyes Icterus
Bitots spots
Xanthelesma
KF ring
Hands Palmar erythema
Clubbing
Asterixis(flap)
Dupytren’s contracture
Nails- koilonychia, leuconychia, white bands
Face Glossitis
Alopecia
Parotid gland enlargement
Hepatic flush
Fetor hepaticus
Trunk Loss of hair
Muscle wasting
Scratch marks
Spider naevi
Gynecomastia

Abdomen Ascites
Umbilical hernia
Caput medusa
Pedal edema
Testicular atrophy
Abdominal striae
Skin Darkening

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 Bruises
Skin bleeding

Stigmata which may point to alcohism as an etiology of cirrhosis :

 Bilateral parotid enlargement
 Dupytrens contracture
 Gynecomastia
 Testicular atrophy
Nail changed in CLD
Terry’s nail -finger nails and/ toe nails appear white with a characteristic
ground glass appearance with no lunula. Due to decrease in vascularity and
an increase in connective tissue within the nailbed.

Gynecomastia
Hypertrophy of glandular tissue of male breast. A breast nodule will be
palpable. Check for gynecomastia with thumb and index fingerheld
horizontally.
Drugs causing gynecomastia (code-ICDS)
 Isoniazid
 Cimmetidine
 Digoxin
 Spironolactone

Testicular atrophy
 Loss of testicular sensation (earliest sign)
 Sparse depigmented hair
(Always palpate testis in a case Of CLD)
Confirmation of testicular atrophy
Prader’s orchidometer

2)Features of hepatic precoma

 Flapping tremor(asterixis)
Asymmetrical arrhythmic lapse in the voluntary sustained posture of
head neck and extremities.Seen in
 CLD

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  CKD
 Respiratory failure
 Constructional apraxia
Ask to copy the figure of a star or clock or by number connection test.
It can also be tested by asking the patient to button and unbutton the
shirt(dressing apraxia)
 Micrographia- ask to write his name. The letters get progresively
smaller.
 Reversal of sleep rhythm
Grades of hepatic encephalopathy
Grade 1- Poor concentration, slurred speech, slow mentation, disordered sleep
rhythm.
Grade 2- Drowsy but easily arousable, occasionally aggressive behaviour,
lethargic
Grade 3-Marked delirium, drowsy, sleepy but responds to sleep and voice,
gross disorientation
Grade 4-Unresponsive to voice, may or may not respond to painful stimuli,
unconcious.
EXAMINATION OF GIT

Upper GIT

 Look for foetor hepaticus

 Features of vitamin deficiency (Glossitis, stomatitis etc.)

Examination of abdomen

 Palpation of liver* very very imp* (Study all methods)

 Checking for splenomegaly . Apart from the methods practiced in ward,
there are 3 other methods. They are:
1. Middleton’s method( hooking method of spleen palpation )
Patient lies supine
Patient’s fist under their left posterior chest
Stand on the left side

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 Hook the fingers over the coastal margin and look for
splenomegaly
2. Nixon’s method of percussion
Patient in right lateral position
Begin percussion midway along left coastal margin
Proceeds in a line perpendicular to the left coastal margin
If upper limit of dullness exceed 8 cm from the left coastal margin,
it indicates splenomegaly
3. Castell’s method
Patient lies supine
Flex hip and knee
Percuss 8th 9th intercoastal space in the anterior axillary line.
Normally the area is resonant during full inspiration. If dull on full
inspiration, it indicates an enlarged spleen.

Spleen
 Mild-- <2cm
 Moderate 2 -7cm (upto umbilicus )
 Severe > 7 cm (crossing the midline)

Kidney
 Ballotable
 Bimanually palpable
 Band of colonic resonance

Palpable kidney
 Polycystic kidney disease
 Renal cell carcinoma
 Hydronephrosis
 Pyonephrosis

Hepatomegaly – Pathological classification

 Infection
- Viral hepatitis

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 - Malaria
- Kala azar
- Ameobic liver abscess
- Pyogenic liver abscess
 Obstruction to outflow tract
- Venous obstruction
- CCF
- Budd chiari syndrome ( hepatic vein tbrombosis )
- Biliary obstruction :
- Gall stones
- Ca head of pancreas
 Infiltration
- Leukemia
- Lymphoma
 Malignancy
- Primary
- Secondary

Massive hepatomegaly
 Hepatocellular carcinoma
 Secondaries
 Pyogenic and amoebic liver abscess
 Infiltrarive disease—leukemia, lymphoma, amylodosis ,storage disease

Hypersplenism
 Disorder in which spleen becomes increasingly active and then rapidly
and prematurely destroys blood cells.
 Causes:
- Splenomegaly due to hematological disorders
- Felty syndrome
- Portal hypertension
- Lymphoma
Palpable tender liver
 Viral hepatitis

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  Rt heart failure
 Hepatic amoebiasis
 Alcoholic liver disease
 Budd chiari syndrome

Pulsatile liver
 Systolic – TR, Severe AR

Mild spleen Moderate spleen

 Cld with portal hypertension  Cirrhosis
 Dengue, malaria lepto  Amyloid
 Brucellosis  ITP
 SLE  Splenic abscess
 Splenic infarct
Massive spleen
 Chronic malaria
 CML
 Chronic hepatitis
 Myelofibrosis
 Tropical splenomegaly
syndrome
 Kala azar
 Hairy cell leukemia
 Storage disorder

Traube’s space boundaries

 Superior -- 6th rib
 Laterally-mid axillary line
 Inferior – Left coastal margin
 Medially – lower boarder of liver
Space is normally resonant

Dull –
 splenomegaly,
 Lt pleural effusion,
 Ca stomach

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 ASCITES
Methods Minimum amount of fluid to elicit
Puddle sign 120 ml
Shifting 1000 ml
Dullness
Fluid Thrill 2000 ml

 While eliciting shifting dullness, why do we wait for 30 seconds after turning
the patient to one side?
Though ascitic fluid takes only few seconds to shift, we wait for 30 s for the
bowel loops to float. It is the bowel loop that float on the ascitic fluid which
gives the resonant note.

At the end of GIT examination in case of CLD don’t forget to examine the
testis and left supraclavicular lymph node(hepatoma).

Importance of examining other systems in CLD

CNS
 Neuropsychiatric manifestations of hepatic encephalopathy
Stage of precoma
 Disorientation in time, place and person
 Dysarthria
 Asterexis + micrographia
 Constructional apraxia
 Rigidity
 Ankle clonus may be present
 Plantar response -flexor
 Gait-ataxic

Stage of hepatic coma

 Patient in deep coma
 Flaccid
 Deep tendon reflex absent
 Plantar -extensor
 Flap – absent
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Respiratory system
 Look for right sided pleural effusion

CVS
Circulatory changes in hepatocellular failure (hyperkinetic circulation)
 Bounding pulse
 Capillary pulsation
 ESM at apex
 Hyperdynamic apex
 Alcoholic cardiomyopathy(DCM)

How to write your diagnosis??

 Chronic liver disease, probably cirrhosis, ethanol related

 Compensated / decompesated
( all our cases are decompensated ie, presence of ascitis, jaundice, upper
GI bleed )
 With /witbout portal hypertension, ascites
 With/without hepatic encephalopathy
 Any complications?? SBP
 Any comorbidities

Definition of cirrhosis
End stage of any chronic liver disease charecterised by
 Parenchymal nodules encircled by fibrosis
 Bridging fibrous septa connecting portal tract with one another and
portal tract with terminal hepatic veins.
 Disruption of hepatic architecture
 Common cause of cirrhosis in Indian children- Indian Childhood
Cirrhosis

Definition of CLD
Documented biochemical or clinical evidance of liver dysfunction >6
months.
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Precipitating factors of hepatic encephalopathy
 GI bleed
 Excess protein in the
diet
 Infection
 Surgery
 Paracentesis abdominis
 Acute alcohol bout
 Uremia
 Constipation
 Anemia
 Hypoglycemia
 Hypotension

169
  Overzealous use of diuretics ( due to hypokalemia ammonia
cannot be converted to NH4 )
Reasons for sudden worsening of stable cirrhosis
 Development of SBP
 Precipitating factors of hepatic encephalopathy
 Transformation into hepatoma
 Portal vein thrombosis
 Formation of chylous ascites due to rupture of dilated abdominal
lymphatics

Complication of cirrhosis
 Portal hypertension -variceal bleeding, hypersplenism
 Spontaneous bacterial peritonitis, ascites
 Coagulopathy
 Hepatorenal syndrome
 Hepatopulmonary syndrome
 Portal vein thrombosis

Sites of portosystemic anastomosis

 Lower end of oesophagus
Lt gastric, short gastric with hemiazygous vein, diaphragmo oesophageal
vein, intercoastal vein
Results in oesophageal varices
 Anterior abdominal wall
Paraumbilical vein with superficial veins of anterior abdominal wall.
Results in caput medusae
 Anorectal junction
Superior rectal with middle and inferior rectal vein
Results in haemorrhoids
 Bare area of liver
Veins of sapey with diaphragmatic veins

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Causes of ascites

Low SAAG ( exudative) High SAAG (transudative)

 Malignant disease –hepatic,  Cardiac failure

peritoneal  Hepatic cirrhosis
 Acute pancreatitis  Hypoproteinemia :
 Lymphatic obstruction Malnutrition, protein losing
 TB enteropathy
 Nephrotic syndrome  Hepatic venous obstruction
 Hypothyroidism Budd chiari syndrome, veno
occlusive disease
 Meigs syndrome
 Constrictive pericarditis

SBP
 Abd pain, rebound tenderness, absent bowel sounds, fever
 Monabacterial
 Ecoli
 Neutrophils > 250

WILSON’S DISEASE
 Autosomal recessive
 ATP7B mutation
 Recurrent acute hepatitis
 Extrapyramidal features—tremor, chorea, athetosis, parkinsonism,
dementua
 KF ring—greenish brown ring –in desemet’s membrane
 Sunflower cataract
 Low serum ceruloplasmin
 24 hr urinary Cu excretion after giving D-penicillamine >25 micromol/24
hrs
 Drug of choice –Penicillamine

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HEMOCHROMATOSIS
 Amount of total Fe increased
 Hepatomegaly
 Leaden grey skin pigmentation
 Bronze diabetes
 Impotence
 Libido, testicular atrophy
 Increased ferritin, raised plasma Fe, saturated plasma Fe binding
capacity
 Transferrin saturation > 45%
 Management : weekly vesection
Congenital non hemolytic hyperbilirubinemia

 Unconjugated
Gilbert’s
Crigler Najjar
 Conjugated
Dubin johnson
Rotor’s

Palmar erythema

 Predominantly in the thenar eminance

 Due to hyperdynamic circulation
 Causes:
 CLD
 Normal individuals
 Pregnancy
 Rheumatoid arthritis

Spider naevi
 In the superior venacava territory
 Central arteriole surrounded by capillaries
 Due to hyperestrogenism
 Seen in CLD
 2% normal people have 1-2 spider naevi
 Pregnancy -3rd trimester
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Cruveilheir Baumgarten Disease

Umbilical or paraumbical veins are distended with an abdominal wall bruit

(cruveilheir baumgarten bruit) and palpable thrill.
Other features
 Portal hypertension with splenomegaly
 Hypersplenism
 Oesophageal varices
 Normal/small liver
BILIRUBIN METABOLISM

Causes of hemetamesis
 Peptic ulcer disease
 Ruptured oesophageal varices
173
  Erosive gastritis
 Oesophagitis
 Ca stomach
 Ca oesophagus
 Mallory weiss syndrome
 Leiomyoma stomach

Causes of abdominal distension (5 F )

 Fat
 Fluid
 Fetus
 Feces
 Flatus

Causes of edema
 CLD ( due to hypalbuminemia) : Abdominal distension , Pedal edema
 CKD : Periorbital puffiness
 Heart failure : Elevated JVP, Pedal edema
 Hypothyroidism
 Angioneurotic edema
Causes of unilateral pedal edema
 DVT
 Cellulitis
 Lymphedema
 Filariasis
 Snake bite
 Insect bite
Features of CLD
 Portal hypertension
 Hepatocellular dysfunction
Jaundice+ Anemia+splenomegaly
Hemolytic anemia
Management of CLD
Investigations

174
 Blood routine
Hb—usually reduced
TC—reduced if there is hypersplenism, increased in SBP
DC
ESR—Increased in TB, hepatoma, SBP, autoimmune hepatitis
Pt count—decresed in hypersplenism, increased in hepatoma
 PT INR
[Prothrombin time of the test ÷prothrombin time of control]^ISR
ISR—international standardisation ratio
Normal value –1.5 to 2.5
If prolonged we give FFP
 Urine routine
Urine sugar-as part of general screening
Deposits – UTI can precipitate hepatic encephalopathy
Bile salt, bile pigment, urobilinogen- Ubg absent in obstructive jaundice
 LFT
 S. Albumin (normal 3.5 – 5 g/dl)
Most imp single indicator of CLD
Reasons-- * exclusively synthesised in liver
Half life of 21 days. So marker of chronic liver injury
 liver enzymes
Normal values AST, ALT ≤ 50 U/L
In ethanol related CLD, SGOT ÷ SGPT >2
In other causes ( viral hepatitis ) SGPT > SGOT
 Bilirubin – increased
Normal : Indirect – 0.3 – 1.2 mg/dl
Direct -- <0.4 mg/dl
Total --- 0.3 -1.2 mg/dl
 Viral markers
 Urea, creatinine, Na, K
Hepatorenal syndrome
Hyponatremia, hypokalemia can precipitate hepatic encephalopathy
S.electrolytes are to be checked if patient with ascites is on diuretics
 RBS
175
 Hypoglycemia can precipitate hepatic encephalopathy
Hemochromatosis – bronze diabetes
 Ultrasound scan
To look for evidence of portal hypertension
 Splenomegaly
 Ascites
 Dilated portal vein >12 mm
Look for hepatoma
 Ascitic fluid tap
To differentiate exudate from transudate
Diagnosis of SBP
To calculate SAAG ( serum albumim ascitic gradient), >1.1 g /dl is
predictive of ascites due to portal hypertension
 Chest Xray
Evidance of pleural effusion
Radiological evidence of TB –in case of tuberculous ascites
 CT
If malignancy is suspected
 Liver biopsy
Final confirmatory investigation

Treatment

1. Treatment of upper GI bleed

 Stabilize the patient
 Circulation, Airway, Breathing
 Monitor vitals
 2 IV lines
 Take blood for investigations, give IV fluids
 Ryles tube aspiration—NPO
 Medications
- PPI 80 mg stat f/b 8 mg/hr infusion ×3 days
40mg TID ×3 days
BD×14 days
176
 - Octreotide 50 microgm bolus f/b 50microgm/ hr× 2-5 days
- Injection vit K
 Upper GI endoscopy, banding, sclerotherapy
 Balloon tamponade

2.Management of portal hypertension

2 options –pharmacological, surgical
 Pharmacological—B blockers
- Propranolol 80-160 mg / day
- Reduce portal venous pressure
 Surgical—shunting
- Nonselective portocaval shunt
- Selective—splenorenal shunt

3.Hepatic precoma regimen

 Ryles tube aspiration
 Bowel wash BD
 Lactulose 15- 30 ml TDS
 L-ornithine L-aspartate (LOLA) - Only if RFT is normal . Converts
ammonia to urea
 Rifaximin 400 mg TDS

4.MANAGEMENT OF ASCITES

a) General measures
- Daily wt monitoring
- Strict intake output recording
- Abdominal girth monitoring
- Estimation of serum &urinary electrolytes&RFT
- Bed rest
b) Fluid restriction
- 1 – 1.5 L / day

c) Salt restriction

177
 d)Diuretics
- Spironolactone –100-400mg /day
- Side effects –gynaecomastia, hyperkalemia
- In such cases, amiloride (5 -10mg /day)

Refractory ascites: Patients who do not respond to doses of 400mg

spironolactone and 160 mg furosemide
e)Paracentesis

f) TIPSS -Transjugular intrahepatic portosystemic stent shunt

5.Management of SBP

 Broad spectrum antibiotics - cefotaxime or piperacillin/tazobactam

 Prophylaxis –norfloxacin 400mg /day

Definitive treatment - LIVER TRANSPLANTATION

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INSTRUMENTS
1. BD NEEDLE
 Bectel and Dickinson needle *for im injection ,iv,s/c,i/d * collection of
blood.
 Size described in gauges ( 21= 1/21th of an inch) as gauge size increases
size of needle decreases.

2. SALAHS BONE MARROW ASPIRATION NEEDLE (* short stout needle)

 Parts: stillete, needle, adjustable guard.
 *guard used to adjust depth of penetration to avoid injury to underlying
structures.
 Diagnostic indications:
- anemia due to any cause
- hematological malignancies { leukemia, lymphoma,multiple
myeloma}
- thrombocytopenia{ differentiate immune from non immune}
- PUO- infections { kala azar- not very common but demonstration
of LD bodies is the diagnostic test}, typhoid , TB
,brucellosis,malaria.
- granulomatous infections
- storage disorders
 Therapeutic uses:
- obtaining bone marrow for transplantation{ given i.v,,,now
replaced by peripheral stem cell transplantation}
 contraindications :-
- local infections
- Bleeding disorders( thrombocytopenia not c/I because bleeding
due to
- thrombocytopenia can be controlled by pressure)
 complications:
- bleeding
- Infections
- Injury to underlying structures
- Dry tap ( faulty technique, aplastic anemia, myelofibrosis}
 site: posterior superior iliac spine { children ;sternum, tibia}
 position:left lateral
 Gaping sensation when periosteum pierced
 Successful aspiration indicated by suction pain
 dry tap= no bone marrow , only blood

179
  absolute indication= aleukemic leukemia

3. JAMSHEDIS BONE MARROW TREPHINE BIOPSY NEEDLE

 only needle with handle
 Parts: stillete, needle, obturator.
 uses: bone marrow trephine biopsy
 Indications: same as aspiration (see salah needle) especially on dry tap
with aspiration.
 Obturator used to remove bone marrow particles.
 absolute indication: aleukemic leukemia{ peripheral smear will be
normal}

4. LUMBAR PUNCTURE NEEDLE

 Long slender needle with a lock at the base
 ( aspiration needle= no lock at base)
 Uses: obtain csf for studies
 csf obtained by
1. Lumbar puncture
2. cysternal puncture
3. ventricular puncture
4. during surgery- open biopsy
 DIAGNOSTIC:
1. Cns infections- meningitis , encephalitis , meningoencephalitis.
2. GBS
3. MU
4. Multiple sclerosis
5. Cns syphilis
6. Carcinomatous meningitis
- pyogenic meningitis- polymorphonuclear pleocytosis, elevated
pressure , reduced sugar
- Tb meningitis- lymphocytic
- Viral meningitis- lymphocytic , normal sugar
- GBS-albuminocyto disassociation
- Multiple sclerosis- oligoclonal bands
- Syphilitic meningitis- csf vdrl +
- Carcinomatous meningitis- abnormal cells
 CONTRAINDICATIONS:
1. Raised intracranial pressure
2. local infections/ sepsis /spinal deformities
 PRINCIPLE of doing LP:
180
 - Spinal cord ends at L1, so potential space below that.
- Usually done at L3-4 ,, If failed- L2-3
- Direction of needle - anteriorly & cranially . bewelled edge should
face upwards.
- Stillete removed, never aspirate
 Normal csf
- pressure= 50-150 mm of csf
- Protein- 30-40 mg%
- Sugar- 40-80 mg% / 2/3rd of blood sugar
 COMPLICATIONS:
- Post LP headache due to continuing csf leak
- Keep patient prone position/ elevate foot end ,, paracetamol
- Infection
- Hemorrhage
- Coning or herniation
- r/o raised raised intracranial pressure by fundal examination / ct
scan
 GUARDED LP- DONE WHEN YOU SUSPECT RAISED ICT: USE smallest size
needle/remove as little fluid as possible
 Difference between traumatic LP and SAH

CSF characteristics Traumatic Tap True SAH

Colour gets lighter with Yes No
subsequent tubes
RBC count in first and Count decreased Stay constant
last tube
Clotting of blood in CSF Yes No
Xanthochromia in Rare with RBC count less Present within 4hrs of
supernatant than 200000 SAH, max at 1wk, persist
for about 3 weeks

5. VIM SILVERMAN LIVER BIOPSY

 ONLY BIFID NEEDLE
 USE:
- Liver biopsy
- pleural biopsy ( only if asked !)
 INDICATIONS:
- Histological diagnosis of cirrhosis of liver ( micro, macro, mixed)
- granulomatous hepatitis—tb , sarcoidosis ,
- Chronic hepatitis—Wilsons disease,, hemochromatosis
181
 - Drug induced hepatitis- methotrexate
- Storage diseases
- Hepatocellular carcinoma - radiological plus elevated alpha feto
protein sufficient ; biopsy done when markers negative or normal
 CONTRAINDICATIONS:
- Suspected hemangioma
- suspected hydatid cyst
- Bleeding disorders:prothrombin time > 6 secs over control
- Platelet count <60000
- HCC
- tense ascitis
- dilated biliary radical - leads to biliary peritonitis
 COMPLICATIONS –
- infection
- Hemorrhage
- Biliary peritonitis
 PREPARATION FOR PROCEDURE:
- check platelet and PT
- VIT. K 1 amp i/v 3days
- arrange blood
- all coagulation studies
 PROCEDURE : clean , local anaesthesia , subcostal in the 10th intercostal
space in mid axillary line, small nick and introduce trocar or canula.
Remove trocar and split needle introduced, liver tissue cut and taken
out.
 FOLLOW UP : look for tachycardia / fall in bp : concealed hemorrhage
 OTHER NEEDLES : menghini, trucut, gunshot needle

6. THREE WAY TAP:

 USES:
- For aspiration of body fluids: blood ,ascetic , pericardial {flow of
fluid can be controlled by the tap}
- administering multiple drugs simultaneously
- in i.c.u for measuring central venous pressure.
 PLEURAL ASPIRATION: in sitting position , 8th intercostal space or at
maximum dullness in mid-axillary line.
 COMPLICATIONS:
- SYNCOPE
- PNEUMOTHORAX
- REEXPANSION PULMONARY EDEMA
182
  aspirate less than 1 litre in <15 minutes

7.STOMACH WASH TUBE/ GASTRIC LAVAGE TUBE

 USE: for doing stomach wash in poisoning.
 PARTS: 1.5 METRE RUBBER TUBE.
- funnel
- rubber tube
- suction bulb in the middle [ create negative pressure]
 IDEAL TIME: within one hour. maximum 4 hours.
 OTHER METHODS OF REMOVING INGESTED POISON:
- Activated charcoal
- induced vomiting/ emesis
- laxative /purgatives
- hemodialysis: methanol, ethanol , ethylene glycol
- forced alkaline dialysis: aspirin , barbiturate , methanol
 CONTRA INDICATIONS :
- CORROSIVE POISONING: perforation
- PETROLEUM PRODUCTS: kerosene ; perforation , chemical
pneumonitis
- A/C Myocardial infarction
- Pregnancy
- COMATOSE [ ASPIRATION RISK HIGH] [ INTUBATE FIRST THEN
LAVAGE]
 PROCEDURE:
- Left lateral position, foot end elevated. Mouth gag;introduce tube
through it, ask patient to swallow, once it reaches stomach;
auscultate over epigastrium and suction pumping, keep funnel
above heart level , 500ml of luke warm water, then bring funnel
below heart into a bucket ; if not coming give suction pumping
- Take sample from 1st wash for toxicological analysis
- Repeat at least 20 times or till clear wash
- After last wash, add absorbent[ activated charcoal]
- Then remove tube
 COMPLICATIONS:
- ASPIRATION
- PERFORATION

8. RYLE’S TUBE :
 For external feeding in unconscious patients /coma patients /intolerant

183
 Aspiration of stomach contents: non corrosive poisoning ; suspected
upper gastro intestinal bleed
 Stomach wash in infants
 Diagnosis of hiatus hernia and trachea oesophageal fistula
 MARKINGS:
- 40- oesophageogastric junction/ cardiac
- 50-fundus
- 60-body
- 70-gastro duodenal junction/pylorus
 IDEAL POSITION: sitting position and ask the patient to swallow
 CONTRA INDICATIONS: corrosive poisoning
 COMPLICATIONS: aspiration ; rupture of oesophagus

9. FOLEY’S CATHETER :
 FOLEYS self retaining urinary catheter
 INDICATIONS:
- Retention of urine
- Incontinence in females[ males:condom catheter]
- Assess renal output to rule out a/c kidney failure
- Urine sample hourly in diabetic keto acidosis
 preferred method: intermittent self catheterization: preserve bladder
tone
 COMPLICATIONS: INFECTION
 Hemorrhage

10.INSULIN SYRINGE
 1 CC
 IDENTIFY: both tuberculin and insulin 1cc:
 look markings:
- insulin= 0- 40or 0- 100
- Tuberculin= only two marking 0.5 and 1
 Piston :
- insulin = red
- tuberculin = blue

11.ENDOTRACHEAL TUBE
 7.5 FG - female
 8.5 FG- Male
 INDICATIONS:
- Respiratory failure due to COPD,
184
 - massive pneumonia ,
- respiratory muscle paralysis
- Artificial respiration
- Clear the airway and prevent aspiration
- Administration of anaesthesia
 CONTRAINDICATIONS: Trauma / carcinoma of upper respiratory tract
Laryngospasm

12.METERED DOSE INHALER

 Drugs administered :
- beta agonists{ salbutamol, terbutaline , salmeterol}
- steroids{ beclomethasone , budesonide }anti cholinergic
{ipratropium bromide }
- mast cell stabilizer { Na chromoglycate}
 ADV:
- rapid onset of action
- Low dose required
- Less side effects
 DISADV:
- technique and skill required { SPACER can be used}
- Steroids can predispose to pharyngeal infection

13. THERMOMETER:
• TYPES: mercury; electronic; skin patch
• Markings: in Centigrade and Farenheit : c/5=f-32/9
• Range: 94-108in Fahrenheit and 35- 42 in centigrade

185
 DRUGS
ADRENALINE :
 DOSE : 0.1-0.5 ml s/c or i/m ( 1 in 1000 in 1 ml )
 INDICATIONS : anaphylaxis , cardiac resuscitation , bronchial asthma .
 CONTRA INDICATIONS : ischemic heart disease , hypertension ,
tachycardia, cardiac, dysrrhytmia
 ADVERSE EFFECTS : angina , pallor , palpitation , tremor , headache ,
sudden elevation of BP , ventricular dysrrhythmia in patients with
infarction

DOPAMINE :
 DOSE :
- 2.5-5 MICROGRAM / KG / MIN = RENAL DOSE ;
- 5-10 MICROGRAM/KG/MIN =CARDIAC STIMULATION
 INDICATION : cardiogenic shock , hypotension , cardiac arrest ,
refractory heart failure
 CONTRAINDICATION : hypertrophic cardiomyopathy
 ADVERSE EFFECTS : nausea , vomiting , chest pain , palpitation ,
arrhythmias

ATROPINE :
 DOSE : 0.6-12 mg /ml
 INDICATIONS : organophosphorus poisoning ,complete heart block , pre
anaesthesia, for mydriasis amd cycloplegia ,.
 CONTRAINDICATIONS : glaucoma , psychosis , pyloric stenosis , paralytic
ileus
 ADVERSE EFFECTS : palpitation , retension of urine , glaucoma , dry
mouth , psychosis .

SALBUTAMOL :
 DOSE : 4mg / 8th hourly , 100-200 micro gram by inhalational
 INDICATIONS : bronchial asthma ,hyperkalemic periodic paralysis.
 CONTRAINDICATIONS : cardiac tachyarrythmia , narrow angle glaucoma .
 ADVERSE EFFECTS : Tremor , Palpitation , Nervousness , Hypokalemia

DISODIUM CROMOGLYCATE / NEDOCROMIL SODIUM :

 DOSE : 20MG 6TH HOURLY INHALATIONAL
 INDICATIONS : bronchial asthma ; allergic rhinitis
 CONTRAINDICATIONS : acute asthmatic attacks , status asthmaticus .
186
  ADVERSE EFFECTS : local irritation , wheezing , breathlessness

NIFEDIPINE
 DOSE : 10-20 mg / 8th hourly
 INDICATIONS: systemic hypertension , hypertensive emergencies ,
ischemic heart disease, raynuad’s phenomenon .
 CONTRAINDICATIONS : hypotension , cardiogenic shock , acute
myocardial infarction, 2nd - 3rd degree heart block .
 ADVERSE EFFECTS : tachycardia , ankle edema , flushing , gum
hyperplasia ,
 hyperkalemia, headache , constipation .

CAPTOPRIL :
 DOSE:12.5-75mg/ 12th hourly .
 INDICATIONS : systemic hypertension , congestive cardiac failure ,
diabetic nephropathy
 CONTRAINDICATIONS : pregnancy , renal failure , aortic stenosis.
 ADVERSE EFFECTS : cough , hyperkalemia , pancytopenia , fever.

FRUSEMIDE :
 DOSE : 20-80mg
 INDICATIONS : congestive cardiac failure , acute pulmonary edema ,
cerebral edema, hypertensive emergencies .
 CONTRAINDICATIONS: hypotension , hypokalemia , hepatic precoma .
 ADVERSE EFFECT : hyponatremia , hypokalemia , pancreatitis ,
hyperglycemia

SPIRONOLACTONE :
 100-400mg
 INDICATIONS : renal edema , congestive cardiac failure , cirrhosis of liver.
 CONTRAINDICATIONS : hyperkalemia , addisons disease.
 ADVERSE EFFECTS : gynaecomastia , hyperkalemia , diarrhea , confusion.

ACETAZOLAMIDE :
 250-500mg / day
 INDICATIONS : as diuretic , glaucoma , resistant epilepsy ,periodic
paralysis.
 CONTRAINDICATIONS : hepatic disorders , hyperchloraemic acidosis
 ADVERSE EFFECTS : hypokalemia , acidosis , bone marrow depression

187
GLYCERYL TRINITRATE :
 DOSE : 0.2-0.6 MG sublingual , 2% skin , 2.5-5 mg oral
 INDICATIONS : angina pectoris , lvf , pulmonary hypertension ,cyanide
poisoning
 CONTRAINDICATIONS : glaucoma , hypertropic cardiomyopathy,
hypotension
 ADVERSE EFFECTS : headache , flushing , dizziness.

ASPIRIN :
 DOSE : 300-500 mg 8th hourly
 INDICATIONS: analgesic , antipyretic ,anti inflammatory , IHD , TIA
,rheumatic fever.
 CONTRA INDICATIONS : g I bleeding , gout , bronchial asthma , bleeding
tendency
 ADVERSE EFFECTS : G I bleed , wheeze , vertigo tinnitus ,reye’s syndrome

PARACETAMOL (Acetaminophen)
 DOSE: 325-650mg (children 10-15mg/kg) 3-5 times daily
 INDICATIONS : analgesic (headache, dysmenorrhea, musculoskeletal
pain), osteoarthritis, antipyretic
 ADVERSE EFFECTS: in isolated antipyretic doses, paracetamol is safe and
well tolerated. Nausea, rashes occurs occasionally, leukopenia is rare
 Study paracetamol poisoning

METOCLOPRAMIDE
 DOSE : 10mg TDS oral
 INDICATIONS: antiemetic, GERD, Dyspepsia, gastrokinetics
 ADVERSE EFFECTS : sedation, dizziness, loose stools, muscle dystonia
 Long term use can cause parkinsonism, galactorrhea, gynecomastia

MORPHINE :
 DOSE : 10-15mg
 INDICATIONS : analgesic , acute LVF , pre anaesthesia .
 CONTRA INDICATIONS : Acute hepatic disorder , respiratory depression ,
paralytic ileus, COPD / Astma .
 ADVERSE EFFECTS : respiratory depression , bronchoconstriction ,
constipation, retention of urine , nausea vomiting

188
LITHIUM :
 DOSE : 900-1500 mg
 INDICATIONS : acute mania , hypomania ,recurrent depression , cluster
headache ,
 CONTRA INDICATIONS : electrolyte disturbance , renal impairment
 ADVERSE EFFECTS : confusion , blurred vision , goiter , diabetes insipidus
SODIUM VALPROATE :
 DOSE : 750-1250mg /day
 INDICATIONS : epilepsy , febrile convulsions
 CONTRA INDICATIONS : hepatic disorder , thrombocytopenia .
 ADVERSE EFFECTS : sedation , alopecia , bone marrow depression .

LEVO DOPA :
 DOSE : 2-8 mg / day
 INDICATION : parkinsonism
 CONTRA INDICATION : closed angle glaucoma , severe psychosis ,
hypertension .
 ADVERSE EFFECTS : dyskinesia , postural hypotension , on off
phenomenon ,hallucinations .

INH :
 DOSE : 300mg /
 INDICATION : tuberculosis .
 CONTRA INDICATIONS : hyper sensitivity , severe jaundice , convulsions .
 ADVERSE EFFECTS : drug fever , peripheral neuropathy , hepatitis ,
psychosis .

PYRIZINAMIDE :
 DOSE : 450mg
 INDICATIONS : tuberculosis .
 CONTRA INDICATIONS : hepatitis , gout .
 ADVERSE EFFECTS : hepatis , hyperuricaemia , fever , skin rash ,
arthralgia .

ARTESUNATE :
 DOSE : day 1 : 100mg bd , day 2-5 : 50 mg bd , taotal :600mg
 INDICATION : multi drug resistant pv / pf malaria
 CONTRA INDICATION : hyper sensitivity

189
  ADVERSE EFFECTS : brady cardia , 1st degree heart block .

ATORVA STATIN :
 Dose : 10-80 mg /day
 INDICATION : hyper cholesterolemia , mixed hyperlipidemia .
 CONTRA INDICATIONS : acute liver disease , hyper sensitivity .
 ADVERSE EFFECTS : myopathy , fatigue , head ache .

190
 RADIOLOGY
X RAY RESPIRATORY:
 PA VIEW : plate on chest anteriorly
- Scapula wide apart
- Clavicle straight
- Beam passes P TO A
- Thoracic spine not prominent
 AP VIEW: ambulatory patients
- Scapula close
 Over exposed film : inter vertebral spaces seen
 Under exposed films : spinous process seen
 Lordotic view : to view apical mass
 LOOK FOR :
- Subcutaneous emphysema [ pneumothorax , ICD TUBE]
- Breast shadow
- Look for all bones , at 6 -7 diaphragm starts : notch in ribs [ co arctation
of aorta ] holes in ribs [ metastasis]
- Shape of diaphragm left side [ lower placed ] air bubble under
diaphragm is normal if not present - achalasia cardia , after food intake
- Lung shadows costophrenic angle - should be acute, check margins
- if 1st and 2nd rib +axilla involved : massive pleural effusion [ in
malignancy]
- Trachea shifted –
opposite - passive collapse
same side - active collapse
- Pushed down diaphragm : emphysema [ tubular heart + horizontal ribs ]
- Reticulonodular shadows : bronchopneumonia ;bronchogenic Ca.
reticulonodular shadows can also be confluent [secondary bronchogenic
Ca ]
- Discrete reticulonodular shadows are seen in milliary tuberculosis [1-2
mm size]
- Fibrosis : lines along lung - TB
- CONSOLIDATION : air bronchogram, way of air movement can be seen
- Vascular markings : normal; if not present suspect pneumothorax
- Diaphragm : pushed up in phrenic nerve palsy
- Cystic : cystic bronchiectasis ;congenital cystic fibrosis ;hydatid cyst ;
wegner’s granulomatosis
- Fluid level seen : abscess ; encysted hydropneumothorax
- Multiple abscess : staph pneumonia

191
- Solitary pulmonary nodule : well demarcated margins; < 5 cm size ,
solitary [ check for calcifications , margins , doubling time : very long [
benign ] very short [infection] in between [malignant]( x ray after 1
month )
- Pleural effusion : slight rise towards axilla .
- Mass lesion : homogenous , eroded , trachea towards same side;
encysted pleural effusion
- Silhouette sign : outline lost
- ICD : more than 20% air in hemi thorax ; any symptomatic patient
- Abnormalities : too black -increase in air; too white -increase in lung
parenchyma/exudates ; in the wrong place ; too big
- Hidden areas : both apices ; the hilum ; under surface of diaphragm
;look for cervical rib
- Too white : consolidation ; pleural effusion ; collapse lung ; mass lesion ;
fibrosis ;pneumonectomy ; pleural thickening .
- Consolidation [solidification of lung parenchyma ] : homogenous opacity
with air bronchogram [ black shadows which are patent bronchus in
areas of consolidation]; no mediastinal shift in uncomplicated
consolidation ; usually confined to a lobe
- Pleural effusion : homogenous opacity with obliteration of angles and
concavity upwards; mediastinum may or may not be shifted ; unless
there is collapse , it is shifted towards opposite side
- Inter lobar effusion : collection of fluid in fissure ,which can appear as
fluid level corresponding to fissures .
- Collapse : will be able to demonstrate collapse margin ; increase in air
- Fibrosis : streaky lines usually with mediastinal shift to same side .
- Multiple opacities :
o >miliary motling : opacity , 2 mm ; involve all of both lungs ;
ideally in low beam
o >reticular shadows
o >nodular shadows
o > solitary pulmonary nodule : single radiological opacity on the
chest x ray less than 5 cm; .5 cm =mass lesion; either benign or
malignant - irregular margins /spiculations= malignant; presence
of calcifications - rules out malignant; peripheral position -
malignant ; doubling time <1 month or > 1 year -benign [ 30%
increase in diameter is doubling ]
- Bronchiectasis [ permanent dilatation / distension of bronchus }]:
1. Ring shadows : diseased bronchi in end on view
2. Honey comb : collection of ring shadows

192
 3. Tramline shadows : diseased bronchi in side on view
4. 4.Tubular shadow : tramline shadows containing exudates
5. Glove finger shadows : collection of tubular shadows .

- TOO WHITE :
- Emphysema (COPD) : 1. Hyper inflated lung ( diaphragm below 8th rib)
2. Tubular heart( since diaphragm is pushed down 3. Horizontal ribs
- Pneumothorax : will be able to demonstrate margins; no lung markings;
collapsed margins ;increased translucency; mediastinum shifted to
opposite side ( look horizontally )
- Sub cutaneous emphysema : black areas even in soft tissue shadows
- Lung abscess : abscess wall and air fluid level .
- Lateral view is required to differentiate right middle lobe from lower
lobe .
- Central mediastinum in pleural effusion : 1. Bilateral effusion 2. Minimal
effusion 3.Associated collapse 4. Encysted effusion
- Lung cavity : thin walled ; not dense opacity ; angle obliterated
- Lung abscess : thick walled ; very dense ; air fluid above ; angle not
obliterated
- MULTIPLE OPACITIES : 1. MILLIARY TB 2. Bronchopneumonia 3. Acute
lung injury
- Upper lobe cavity : think of TB
- Upper lobe fibrosis : look for compensatory emphysema below that .
- Milliary motling : hematogenous spread of TB .
- Reticulonodular : 2-4 mm ; interstitial lung disease ; infiltrating lung
lesions ( milliary <2 mm)
- Honey comb DD : cystic bronchitis ; idiopathic interstial lung disease ,
silicosis, sarcoidosis , rheumatoid lung , berriliosis , extrinsic allergic
alveolitis
- Cannon ball shadows : usually secondaries .

X RAY CVS
• All x rays in i.c.u are portable and AP.
• PA view: posterior ribs prominent; position of scapula .
• Film taken under full inspiration : 10 posterior ribs visible ; 6 anterior ribs =
good quality
• Over penetrated -dark film
• Under penetrated-white film
• For rotation : medial ends of clavicle equally separated .
• Intervertebral space seen through heart : good quality .

193
• Expiratory film : small pneumothorax
• Kerley lines : normally continous flow of fluid from pulmonary veins to inter
tubular lymphatics; longer (>2cm); unbranching lines Also seen in sarcoidosis ,
interstitial spread of pneumonia
3 types: a,b,c
• Alveolar oedema : when pulmonary venous pressure >25 mm of Hg
;inner 2/3rd of lungs (bat wing )
• ARDS: collapsed / distended alveoli ; bilateral

X RAYS
1. Cardiomegaly :
- if massive : combined regurgitant lesion (AR = MR ) ;DILATED
CARDIOMYOPATHY ; pericardial effusion ; congenital anomalies (
ebstein : multiple heart sounds )

2. Trachea deviated to same side :

- non homogenous opacity of upper lobe [right] , ribs crowded:
- diagnosis : fibrosis of right upper lobe
- Compensatory emphysema - left side
- DD : TB ;silicosis ; radiation fibrosis ; ankylosing spondylosis
;sarcoidosis ; rheumatoid arthritis

3. Non homogenous opacity right middle and lower zone with a breaking
down lesion :
- sis: consolidation with lung abscess { read causes of lung abscess }

4. Homogenous opacity :
- encysted effusion (mediastinum not shifted ) ; pleural
mesiothelioma

5. Miliary shadows :
- shadows ,2mm ;bilateral
- DD : TB, tropical eosinophilia [absolute eosinophil >2000]
,carcinomatosis lymphangiectasis , pmeumoconiosis , sarcoidosis.

6. Homogenous opacity right upper zone :

- fissure going up , elderly patient , (pneumonia with breaking down
lesion ) ^sis : klebsiella pneumonia [ look for bulging fissure sign ]

194
7. Lung abscess : air fluid level ; costophrenic angle obliterated ;ICD may
be present

8. Bilateral non homogenous opacity with multiple cavities :

- DD : 1. Bilateral TB 2. If short h/o -staph pneumonia =b/l creps =
rhonchi , aspiration pneumonia ,severe pulmonary oedema ,
COPD + respiratory infection, bronchopneumonia

9. Trachea grossly deviated to left + left dome of diaphragm elevated +

crowding of ribs on left side + homogenous opacity in left side fully.^sis :
fibrothorax ( pathologically : destroyed lung )

10.Homogenous opacity : upper zone +lower zone

- Pneumonia & rule out malignancy if more than one lobe involved

11.Pleural effusion :
- indications for aspiration :
1. Respiratory embarrassment dyspnea
2.Cardiac embarrassment [hypotension , tachycardia ]
3. Empyema
4. Therapeutic

12.Pneumothorax :
- causes : rupture of bullae , iatrogenic , subpleural focus rupture

13. Gross pulmonary artery hypertension : cardiomegaly (moderate)

, vascular markings prominent …; DD : MS +MR
, ASD {not much vascularity }

14.Reticulonodular shadows :
- DD : BRONCHIECTASIS, asbestosis , sarcoidosis , interstitial lung
disease , lofflers .

15. Cardiomegaly {right ventricular type } with gross pulmonary artery

hypertension :
- right ventricle dilated[maximum transverse diameter >16 right or
>18 left =pulmonary artery hypertension ] ;
- if young female -suspect primary pulmonary artery hypertension

16.Cervical rib :

195
 - suspect if apparent normal x ray is provided
- also look for :subcutaneous emphysema retrosternal thyroid , gas
under diaphragm , rib notching ,rib erosions ,
pneumomediastinum .

17.Homogenous opacity + fibrotic mass = pulmonary edema , mass lesion

18.Pulmonary artery grossly dilated = rule out pulmonary artery

hypertension ; old patient , gross pulmonary artery
hypertension +cardiomegaly +non homogenous opacities = cor
pulmonale

19.Cardiology with bulge = ventricular aneurysm treatment required =it can

embolise ppt cardisc failure,rupture; commonly in acute myocardial
infarction

20.Bilateral non homogenous opacity , right upper zone hazy : bilateral TB

;pulmonary TB but x ray normal - endobronchial TB present5s with
massive hemoptysis

21.Bilateral opacity lower zone : interstitial lung disease , if acute:

bronchopneumonia

22.Hydropneumothorax : if no mediastinal shift -encysted

hydropneumothorax; [ also a mass lesion in upper zone and fibrotic
bands in opposite side would suggest TB

23.Cannon Ball secondaries: source of primary- secondary to RCC,

choriocarcinoma, prostate carcinoma, synovial carcinoma, endometrial
carcinoma, head and neck Ca, Ca breast, GIT malignancy (colon,
stomach, and pancreace). Learn solitary pulmonary nodule from
Davidson.

24.ARTIFICIAL VALVE : cupping of post surgery scar seen ; mechanical

valves in young patients, biological valves in old patients [ mechanical
valves require life long anti coagulation ;biological valves got a short life ]

25.Bilateral non homogenous opacity = if acute : bronchopneumonia

; if chronic: pulmonary TB

196
 26. X RAY findings in MS :
- mitral valve calcification, pulmonary hemosiderosis [ after
hemoptysis blood degraded ], kerley b lines
- Kerley’s line : A line : ragged , unbranched lines which run
centripetally towards hilum ;seen near the apex
- Kerley’s B line : fine , dense horizontal lines at the base of the
lungs (near costophrenic angles )
- Kerley’s C line : fine , interlacing lines and are seen in the central
and parahilar region.

27.Milliary shadows : other DD ; but first mention bronchopneumonia

28.Lung abscess cavity : air fluid level at lower zone

29.Encysted pleural effusion : young female , hemoptysis , laterally placed

homogenousopacity = bronchial adenoma

30.Aortic aneurysm : clinical sign = tracheal tug; tracheal descent =

emphysema

EMERGENCY MEDICINE
Following are some of the frequently asked topics for management of
emergency
medical conditions :
1. Diabetic ketoacidosis
2. Dengue : dengue shock syndrome/ dengue hemorrhagic fever : (refer park
or OP ghai for flow chart)
3. Acute severe asthma
4. Bacterial meningitis
5. Organophosphorus poisoning .
6. Acute myocardial infarction
7. Stroke
8. Migraine
9. Snake bite
10.Acute viral hepatitis
11.Status epilepticus
12.Malaria (refer park )

197
SURGERY
BREAST LUMP 200
THYROID SWELLING 217
PERIPHERAL OCCLUSIVE VASCULAR DISEASE 230
(POVD) 230
OBSTRUCTIVE JAUNDICE 249
PAROTID SWELLING 256
VARICOSE VEINS 269
CARCINOMA STOMACH 278
RIGHT HYPOCHODRIAL MASS- ENLARGED LIVER 285
CARCINOMA OF UNKNOWN PRIMARY (CUP) 290
RETROPERITONEAL TUMOR 295
SOFT TISSUE SARCOMA (STS) 299
LEFT ILIAC FOSSA MASS 312
ORAL CAVITY MALIGNANCY 315
EXAMINATION OF AN ULCER 321
EXAMINATION OF A SWELLING 326
LIPOMA 333
HERNIA 335
HYDROCELE 341
OPERATIVE PROCEDURE 344
X RAY 352
SPECIMENS 354
INSTRUMENTS 355
 Breast lump
History-Taking
Presenting Complaints
• Lump
• Pain
• Nipple discharge
• Nipple retraction
• Breathlessness/ Cough/ Hemoptysis/ Abdominal distention/ Bone
pain/ Headache/Focal neurological deficits (features of metastasis from
Ca breast)
Past Medical History
• Loss of weight
• Recurrence of breast complaints
• Previous radiation to breast region
• Trauma to breast(traumatic fat necrosis is an imp. DD of EBC (Early
breast carcinoma)
Drug History
• “ICDS”- Isoniazid, Cimetidine, Digoxin, Spironolactone cause
gynaecomastia
Personal History
• Unmarried/Nulliparity/Late parity ??
• Early menarche (before 12yrs) and late menopause (after 50yrs)??
• Breast feeding duration
• Alcohol and Obesity
• OCP use and HRT(Hormone replacement therapy)
Family History
•1st degree relative(mother/sister) with Ca breast

Local Examination of Breast

• Sitting position is MC adopted
• Inspect for asymmetry of breasts, visible lumps, nipple-areola complex and
peau d’orange appearance
• Palpate the lump for skin fixity, breast tissue fixity, underlying muscle &
fascia fixity and chest wall fixity
• Examine axillary and cervical(especially supraclavicular) LN
• Examine C/L breast
• Examine the abdomen (hepatomegaly), chest (pleural
effusion/consolidation) and bony tenderness (ribs, skull & spine, long bones of
the body)

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DIAGNOSIS
Broadly two entities:
Benign breast disease(Left/Right) probably ______.
OR
Carcinoma Left/Right Breast ,Stage 1/2/3/4
With Co-morbidities like DM,HTN,TB,etc., and Complications like pleural
effusion,bone pain etc.
[Stage 1 and 2 is EBC (EARLY BREAST CARCINOMA)
Stage 3 is LABC (LOCALLY ADVANCED BREAST CARCINOMA)
Stage 4 is MBC (METASTATIC BREAST CARCINOMA]

DISCUSSION
There are 4 common presenting complaints in a breast case:
• Lump
• Pain
• Nipple discharge
• Nipple retraction
1)Lump
 MC presentation
 Elicit the history as that you follow for a ‘swelling’ (onset, duration,
progression ,etc.,)
 Short history and fast growth - suggests carcinoma
 Long history and slow growth - suggests benign condition of breast
Q)Which breast carcinoma is slow-growing?
Ans)Atrophic scirrhous carcinoma (‘Scirrhous’ means ‘woody’)
2)Pain
Pain in a breast case-5 main possibililites:
1)Acute mastitis
2)Fibroadenosis(pain aggravated during menses)
3)Periductal mastitis(after menopause)
4)Referred pain from musculoskeletal diseases
5)Bony mets. pain from metastatic breast carcinoma
Note: all benign and malignant neoplasms of breast are painless to start with.
A notable exception is inflammatory carcinoma of breast which mimics breast
abscess with short history, rapid progression, pain, etc., which carries grave
prognosis. So be very cautious when you want to commit “Pain” is a suspected
Ca breast case..!
3)Nipple discharge
• Fresh/Altered bloody discharge - Duct papilloma /Carcinoma

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 • Serous/Greenish/Black discharge - Duct ectasia, Fibroadenosis
• Pus discharge - Mammary abscess
• Milk - Lactation, Galactocoele, Mammary fistula(due to c/c subareolar
abscess) (Hypothyroidism and pituitary tumour too cause milk discharge
(rare))
Q) MC cause of bloody nipple discharge?
Ans)Duct papilloma
Q) Blood stained nipple discharge with sizeable cystic sweilling is a feature of?
Ans) Disease of Reclus (Intracystic papilliferous carcinoma)
4)Nipple Retraction
•Recent retraction of nipple (usually due to underlying carcinoma)
• Nipple retraction for quite a long time or since puberty may be
developmental!!

Note :Be very clear as to which structures are involved in the following
findings:
• “Nipple retraction” - due to lactiferous duct involvement
• “Dimpling/Puckering” - due to Cooper’s ligaments’ involvement
• “Peau d’ orange appearance” - due to lymphatic obstruction (by tumour
cells) + sparing of hair follicle region (edema)
Other imp. Points to be checked for/ruled-out in history. 4 of them:
1)Loss of weight??
• Ca breast
• TB of breast
• Chest wall TB leading to retromammary abscess
2)Past medical history??
•Recurrence of breast complaints: Fibroadenosis
•Recurrence of abscess(in congenital retraction of nipple)
•Ca of opposite breast
• Previous radiation: Increases the risk if occurred during breast
development. ‘ Mantle Radiotherapy’ given for Hodgkin’s disease is a
culprit; Ca breast develops after a decade
• Trauma to breast : Traumatic fat necrosis is an imp. DD of EBC (Early
breast carcinoma)
3)Personal history??
•Unmarried/Nulliparous women/Late parity : Ca breast / Fibroadenosis
[Breast feeding is protective against Ca breast]
•Dietetic factors : Diet low in phytoestrogens and high intake of alcohol
increases the risk of Ca breast

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Q)What is the role of OCP’s and HRT(Hormone replacement therapy) in the
development of Ca breast?
Ans)Both increases the risk; but benefits will far outweigh the small putative
risk

4)Family history??
• Positive family history (1st degree relatives-mother,sister) is a risk factor
for development of Ca breast
• Genetic factors : BRCA 1 & 2 mutations, Ataxia telangiectasia, Li-
Fraumeni syndrome and Cowden syndrome too are risk factors for Ca
breast

Q) What percent of Ca breast are inherited/familial?

Ans) Less tha 5% (major genes involved are BRCA1,BRCA2 and p53)
Q) Which gene is associated with the development of male breast carcinoma?
Ans) BRCA 2 (on chromosome 13q)
[BRCA 1 gene is located on chromosome 17q]

The following are the 4 common benign breast diseases:

1)Mastitis
2)ANDI(Aberrations of Normal Development and Involution)
3)Duct ectasia/Periductal mastitis
4)Pregnancy-related (galactocoele,puerperal abscess)

Note: Periductal mastitis is a.k.a. Zuska’s Disease; it has very strong

association with smoking and seen in perimenopausal /menopausal age group]

ANDI***
Q) Classification of ANDI? (BAILEY 836; box 50.2)
1)Fibroadenosis (cyclical nodularity and mastalgia)
2)Fibroadenoma (“Breast mouse”)
3)Breast Cysts
Q)Pathology of ANDI?
1)Cyst formation 3)Hyperplasia
2)Fibrosis 4)Papillomatosis
Q)2 drugs given to treat mastalgia in ANDI?
1)Evening primrose oil(500mg OD,orally for 3 months)
2)Danazol (100mg TDS)
Q)Who introduced the term ‘ANDI’?
Cardiff Breast Clinic(London)

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If case of malignancy/carcinoma, following are the possibilities:
1)Invasive ductal carcinoma(MC)
2)Invasive lobular carcinoma(Multifocal and bilateral)
3)Colloid carcinoma
4)Medullary carcinoma
5)Tubular carcinoma
Note: 3, 4 and 5 have better prognosis than 1 and 2
Inflammatory Ca of breast: Presents with painful, swollen breast, mimics
breast abscess, very aggressive and carries poor prognosis; also involves atleast
1/3rd of breast(imp point. for clinical diagnosis)
Paget’s disease of Nipple: It is a superficial manifestation of an underlying
breast carcinoma,mimics eczema which persists after local treatment.
Local Examination of Breast(Essential points)
• Sitting posture is adopted for examining the breast
• Semi-recumbent(45 degree),Recumbent and Bending forward position
are adopted to reveal more information; for eg. Bending forward position
gives information regarding retraction of nipple
Inspection
When you present the breast case,tell the following:
“Inspection of breast was done in 4 positions namely:
a)With the arms by the side of the body
b)With the arms raised straight above her head
c)With the hands on her hips,pressing and relaxing as commanded
d)With the patient bending forwards from the waist”
Q)Why is the inspection done like this??
“a” to look for skin over the breast, engorged veins, dimpling, nodules,
ulceration/ fungation, level of breasts/nipples
“b” causes the lump or dimpling to be more marked. Also, nipple will be
drawn towards the lump in the abnormal breast
“c” elicits abnormal movement of nipple and causes exaggeration of skin
dimples
“d” inorder to make the breast fall forward (failure of 1 nipple to fall
forward means abnormal fibrosis behind the nipple)
Q)How do you compare the level of nipples on both sides?
Ans) Vertical distance from the clavicle
OR
Horizontal distance from the midline
*Inspect arm and thorax, axilla and supraclavicular fossa;

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*“Cancer en cuirasse”- Multiple cancerous nodules and thickened infiltrated
skin like a coat of armour seen in arm and thoracic wall]

Palpation
• Done is Sitting, Semi-recumbent (45 degree) and Recumbent positions
• Done with “hand flat” and not with the “flat of the hand”
• Palpate for 4 quadrants of breast, axillary tail and behind the nipple
serially and without fault (carefully examine for carcinoma behind nipple)
Q)What is the palpatory finding of a normal breast(how do you describe it)?
Ans) Soft and Smooth
OR
Firm Lobulated with Nodularity
Note : If a lump is detected during palpation, describe it like that of a
swelling(Local rise of temp. & tenderness, situation(quadrant), number, size &
shape, surface, margins, consistency, fluctuation and transillumination test)

Imp. Points:
Carcinoma is stony-hard in consistency
Ill defined margins - Fibroadenosis
Fibroadenoma is firm in consistency
Well-defined margins- Fibroadenoma/Ca
Fibroadenosis is firm,sotty OR gives “diffuse India rubber feel”
Q)How to check for fluctuation in a breast lump?
Ans)
1-Examiner stands behind the patient
2-Examiner’s two hands should go above the patient’s shoulders
3-Hold the lump/cyst with one hand; with the index finger of the other
hand,gentle tap is made on the centre of the lump/cyst
[Fluctuation is positive in Breast cyst, Chronic abscess and Lipoma]
Note: In breast, “A true lipoma is very rare” !! (

Fixity of lump to :
1)Skin
2)Breast tissue
3)Underlying muscles(pectoralis major and serratus anterior) and
fascia(pectoral fascia)
4)Chest wall
How to check for the above??
 Fixity to skin:- 3 methods are there:
1)Try to pinch up the skin over the lump

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 2)Try to make the skin slide over the lump
3)Try to move the lump side to side OR up and down:
 If some independent movt. of the lump(with respect to the
overlying skin) is possible and dimpling/puckering of skin occurs
at extremes of movt.,then lump is “TETHERED TO SKIN”
 If independent movt. of the lump is not possible,then lump is
“FIXED TO SKIN”
*“Tethering” is due to involvement of Cooper’s ligaments+
*“Fixity to skin” is due to direct infiltration of the skin by the tumour+

 Fixity to Breast:
Hold the breast tissue in one hand and try to move the lump
• Fibroadenoma: Not fixed to breast tissue(“Breast Mouse”);easily
moved within the breast substance.
• Carcinoma : Fixed to breast tissue; can’t be moved within the breast
tissue
 Fixity to Underlying Muscles/Fascia:
• Pectoralis major/Pectoral fascia : Check for restriction of movt. of the
lump along and at right angle to the direction of muscle fibres when the
patient is asked to press her hip as hard as possible with her hand of the
affected side
• Serratus anterior : Check for restriciton of movt. of the lump when the
patient is asked to push against a wall with the outstretched hand of the
affected side
 Fixity to Chest Wall:
• If the lump Is fixed irrespective of contraction of any muscle,it is fixed
to the chest wall
Note: “4 fixities” should be checked diligently as it alters the staging of Ca
breast!!
Palpation of Lymph Nodes in a Breast Case:
2 groups : Axillary & Cervical
Axillary LN Examination :
There are 6 groups of Axillary LN :
1)Anterior group (PECTORAL GROUP) - along Lateral Thoracic vessels
2)Posterior group (SUBSCAPULAR GROUP) - along Subscapular vessels
3)Lateral group (BRACHIAL GROUP) - along Axillary vein
4)Central group - embeded in fat in the centre of axilla
5)Apical group - above the level of Pectoralis minor tendon; in continuity
with the lateral group of LN

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 6)Rotter’s LN (INTERPECTORAL LN) - located between pectoralis major
and minor muscles; can’t be clinically examined
Note: Posterior grp of LN is examined by standing behind the patient while all
others by standing in front of the patient “1”, “4” and “5” are palpated with
the opposite hand as that of the side to be examined(eg. right hand for left-
sided nodes and vice-versa) WHILE “2” and “3” are palpated with the same
hand as that of the side to be examined(eg. left hand for left-side nodes and
vice-versa)

Cervical LN Examination
• Check for Supraclavicular LN by standing behind the patient
(Supraclavicular LN have connections with Apical group of Axillary
LN).Passive elevation of shoulders would relax the muscle and fascia of
neck,to facilitate palpation.

Q)What is the lymphatic drainage of breast?

Ans) 85% via Axillary grp of LN & 15% via Internal mammary LN(lie deep to the
plane of costal cartilages and drain posterior third of breast)
Systemic Examination in a Breast Case
In a suspected Ca breast case, check the “LLB status”:
• Lung - Pleural effusion in Ca breast mets.
• Liver - Hepatomegaly in Ca breast mets.
• Bone - Bony tenderness in Ca breast mets(over ribs,spine,long bones in
the body) plus pathological fractures
Q) What is the importance of rectal/vaginal examination in a suspected Ca
breast case?
Ans) To detect Krukenberg’s tumour of ovary (Transcoelomic spread of
tumour)
Q) MC cause of death in Ca breast?
Ans) Pleural effusion
Note: In a gynaecomastia case,check for “ICDS” drug history (Isoniazid,
Cimetidine, Digoxin, Spironolactone) and examine for “LLT status”:
• Liver- Cirrhosis causes gynaecomastia
• Leprosy - Leprosy causes gynaecomastia
• Testis - Anorchism, Crytorchidism, Teratoma cause gynaecosmastia

MANAGEMENT OF BREAST CARCINOMA

Management is divided into that for Early Breast Carcinoma (EBC), Locally
Advanced Breast Carcinoma (LABC) & Metastatic Breast Carcinoma (MBC).

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TNM Staging
 Tx – Primary cannot be assessed
 T0 – No evidence of primary
 Tis – Carcinoma in situ
 T1- less than or equal to 2 cm
 T1mi – tumor less than or equal to 1mm in greatest dimension
 T1a – more than 1mm but less than or equal to 5mm
 T1b – more than 5mm but less than or equal to 10mm
 T1c- more than 10mm but less than or equal to 20mm
 T2 – More than 2 but less than or equal to 5cm
 T3 – More than 5cm
 T4a – Extension to chest wall ( Ribs, Intercostal muscles, Serratus
Anterior)
 T4b – Involvement of skin ( Peau d’ orange; satellite nodules; ulceration)
 T4c – a+b
 T4d – Inflammatory carcinoma

 N0 – No regional node metastases

 N1 – I/L mobile axillary LN
 N2a – I/L Matted axillary LN
 N2b – I/L internal mammary LN with no axillary LN involvement
 N3a – I/L infraclavicular LN
 N3b – I/L internal mammary + axillary LN
 N3c – I/L supraclavicular LN

 M0 – No evidence of metastasis
 M1 – Distant metastasis

Staging of Carcinoma Breast

N0 N1 N2 N3 M1
T1 I II III III IV
T2 II II III III IV
T3 III III III III IV
T4 III III III III IV

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EBC Management – Stage 1 and 2
1) Triple Assessment– it includes: Clinical examination, Radiology and
Cytopathology
RADIOLOGY
(a)USS breast, if <35yrs because there is no risk of radiation exposure
and since the breast tissue is denser in the younger age group, USS has
more tissue penetrance and will detect microcalcifications.
Features in USS:
• Hypoechoic with posterior acoustic shadowing,
• irregular margins,taller than wide lesions;
• complex cyst;
• asymmetry;
• architectural distortion.

(b)MAMMOGRAM, if >35yrs ( not preferred for younger women because

they have dense breast tissue and X ray has less tissue penetrance ; there is
also a risk of radiation exposure.)

 Mammogram uses low voltage – high amperage Xrays; radiation dose is

0.1cGy.
 Views: Craniocaudal and Mediolateral Oblique view
- A ‘mass’ is a space occupying lesion that can be detected in both the
projections.
- If a finding is only seen on one projection, it is referred to as a ‘density’.
 Always take bilateral mammogram to
(1) Compare both sides for diagnosis
(2) Detect bilateral ca breast
(3) Check for multicentricity or multifocality

 Features : Architectural distortion; Asymmetry; Clustered linear

branching pleomorphic microcalcifications(<0.5mm) ; Spiculation; Skin
thickening; Taller than wide lesions.

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  BIRADS (Breast Imaging Reporting And Data System) – developed by
American College of Radiology to standardize mammographic
reporting.
 0 - Need additional imaging evaluation (add views or do USS)
 1 - Negative (do annual mammography)
 2 - Benign (do annual mammography)
 3 - Probably benign (check cytology,do U/L mammography after
6 months and B/L examinations 12 and 24 months after initial
examination)
 4 - Suspicious abnormality (consider biopsy)
 5 - Highly suggestive of malignancy ( do biopsy )
 6 - biopsy proven malignancy
(c)MRI :
 In case of breast with implants,
 To distinguish scar from recurrence,
 When the presenting complaint is an axillary lymph node alone and
there is no breast lump.
 For follow up surveillance of high risk patients with a positive family
history or BRCA 1/ BRCA 2 mutation

CYTOPATHOLOGY
(a) FNAC
- Taken with 23G needle; 6 passes are needed.
- If there are 2 lumps, do FNAC from both.
- If negative/inconclusive, it can be done upto 3 times.
- Least invasive; but can have false negatives; Cannot differentiate
between in situ and invasive lesions; Cannot assess ER PR status.
(b) TRU-CUT BIOPSY
- After trial with FNAC.
- Can differentiate between in situ and invasive lesions.
- Can assess ER PR status.
- For assessing Ki-67 index
(c) INCISIONAL BIOPSY
(d) EXCISIONAL BIOPSY
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2) If clinically and radiologically no lymph nodes are found, do sentinel lymph
node biopsy. ( Learn the procedure)
3) Metastatic work-up : Chest X-ray, USS abdomen, and if symptomatic – X
ray bone.
4) TREATMENT
Surgery is the 1st line of treatment +/- Chemotherapy +/- Radiotherapy(RT) +/-
Hormone therapy +/- Targeted therapy.
BREAST CONSERVATION THERAPY is the preferred Rx for EBC. It includes
a) Wide local excision with 2mm clearance (Breast Conservation Surgery or
BCS)
b) RT for 6 weeks
c) Axillary dissection upto level 2 LN.
Follow up after BCS:-
 once in every 3months for 1st 2 yrs
 once in every 6months for next 3yrs
 once in every year for the next 5yrs
Contraindications for BCS:
1. LABC/MBC
2. Multicentricity/ Multifocality
3. Previous history of radiation
4. Any collagen vascular disease
5. Pregnancy
6. Large tumour in a small breast
7. BRCA 1&2 Mutation carriers / Women with a strong family history of
breast cancer.
8. Patient’s wish

2nd option is Modified Radical Mastectomy (MRM) – Types are Patey’s,

Scanlon and Auchincloss. ( Learn the procedure of Auchincloss MRM ) .
Indications:
a) When adequate margins cannot be attained
b) When LNs cannot be cleared properly due to fixity or lymphovascular
invasion
c) High grade DCIS
Indications for CHEMOTHERAPY:

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 a) Node positivity
b) Size >1cm
c) High grade tumour
d) ER PR Status negative
CAF Regimen is given – Cyclophosphamide, Adriamycin, 5-Fluorouracil
Indications for RT:
1) BCS
2) Lymph node positivity
3) Large tumours
4) High grade
5) Positive margins
Indications for axillary RT: extracapsular spread, Extensive nodal mets,
Lymphovascular invasion.
If axillary clearance done, don’t give RT to axilla.
HORMONE THERAPY
If ER/PR status is positive,
 Premenopausal: Tamoxifen (SERM) 20mg OD for 5yrs; after that if still
premenopausal continue for another 5yrs.
 Post menopausal: Aromatase inhibitors (Letrozole, Exemestane)
TARGETED THERAPY
If HER2/neu positive, give Trastuzumab infusion (every 3 weeks for 1yr or every
week for 9weeks).

LABC Management – Stage 3

1) Triple Assessment (Here, instead of FNAC, do tru-cut biopsy to assess
ER/PR and HER2/neu status because chemotherapy can cause
modification in this).
2) Metastatic workup:
CT chest and abdomen ;
Bone scan if symptomatic (bone pain).
3) Treatment
(i) Here treatment starts with chemotherapy - 6 cycles – CAF regimen
(anterior chemo or neoadjuvant chemo). Targeted therapy can be
started along with chemo if HER2/neu is +ve.
(ii) Modified Radical Mastectomy.
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 BCS can be considered, but do axillary clearance.
(iii) Radiotherapy to chest wall and supraclavicular area and NOT axilla.
If axillary clearance not done RT to axilla also given.

Indications:
a) Extensive nodal mets
b) Lymphovascular invasion
c) Extracapsular spread
d) Large tumor
e) High grade
f) +ve margins
(iv)Hormone therapy if ER/PR +ve
Haagensen’s criteria of inoperability:
 Extensive edema of breast
 Satellite nodules
 Inflammatory carcinoma
 Parasternal tumor (spread to internal mammary LN)
 Supraclavicular LN mets
 Edema of arm

MBC Management

Multidisciplinary team approach is needed:

1. Chemotherapy for any visceral involvement - CAF Regimen or CMF

Regimen (M – Methotrexate).
2. Hormone therapy if ER/PR +ve , after chemo.
3. Targeted therapy if HER2/neu +ve.
4. Radiotherapy if there is solitary vertebral involvement.
5. The maximum surgery that can be done is simple mastectomy/ BCS ; it
can improve survival in months.

Q) Inflammatory Breast Carcinoma

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It is a clinicopathological entity characterised by diffuse erythema and edema
of the breast, often without underlying palpable mass and can occur with
tumors of either ductal/ lobular histology. The skin changes are due to
lymphedema caused by tumor emboli within dermal lymphatics.
Rx - similar to LABC.

Q) Rx of Paget’s disease
Wide excision of the nipple and areola + axillary staging + RT
(MRM + Axillary staging can be done after taking into account the lump size
and LN.
After thoroughly ruling out occult multicentric disease, Lumpectomy +
Radiation can also be done)
Q) Risk factors for Ca Breast – Advancing age, prolonged estrogen exposure
states (early menarche, late menopause, late 1st child birth, not
breastfeeding,HRT), radiation exposure, obesity,family history, gene
mutations( BRCA1, BRCA2,pTEN, p53, Ataxia telengiectasia gene, RB gene,
Lynch II..)

Q) Levels of axillary LN?

Level 1 – lateral to Pectoralis minor ( anterior, posterior and lateral LN
groups )
Level 2 – deep to Pectoralis minor ( central LN group)
Level 3 – medial to Pectoralis minor (Apical LN group)
There are about 20 – 25 LN in axilla.

Q) Lymphatic drainage of breast?

The axillary nodes receive approximately 85% of the drainage and are arranged
in the following groups:

 lateral, along the axillary vein

 anterior, along the lateral thoracic vessels;
 posterior, along the subscapular vessels;
 central, embedded in fat in the centre of the axilla;
 interpectoral, a few nodes lying between the pectoralis major and minor
muscles;

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  apical, which lie above the level of the pectoralis minor tendon in
ontinuity with the lateral nodes and which receive the efferents of all
the other groups.
The apical nodes are also in continuity with the supraclavicular nodes and drain
into the subclavian lymph trunk, which enters the great veins directly or via the
thoracic duct or jugular trunk.

The internal mammary nodes are fewer in number. They lie along the internal
mammary vessels deep to the plane of the costal cartilages, drain the posterior
third of the breast

Q) Trace ca breast mets to ovary. (Pathway of Gerota)

Int. mammary LN Sub diaphragmatic plexusTranscoelomic spread or via
liver to ovary.

Q)Natural history of ca breast?

Atypical hyperplasia  Dysplasia  in situ  ca

Q) Halstedian concept of local spread; Fischer’s concept of systemic disease;

Helman spectrum theory.

Q) What is triple negative?

- Negative for ER/PR status and HER2/neu.

Q) Ductal ca in situ (DCIS)

Van Nuys prognostic index helps in deciding which patients are at increased
risk of local recurrence and who may benefit from adjuvant radiotherapy and is
based upon grade, size, presence or absence of comedo necrosis and margin
width.
Management:- DCIS is classified into widespread(more than 4cm size) and
localized type. For widespread type, the treatment of choice is mastectomy
because 2/3rd cases will progress. The options are
 Simple mastectomy
 BCS and Radiotherapy to breast and if ER positive, Tamoxifen for 5yrs
 Lumpectomy without Radiotherapy if the tumor is small (less than
0.5cm), Unicentric and low grade.
Follow up: Physical examination every 6 months for 5 yrs and mammogram
every 12 months.
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Q) Indications for prophylactic mastectomy
 BRCA 1 and 2 mutations
 Lobular Ca in situ (because chance of B/L involvement is 40%)

Q)Halsted Radical mastectomy

Structures removed – those in MRM + Pectoralis major and minor + Axillary
vein.
The muscle preserved is Serratus anterior.

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 THYROID SWELLING

Presenting Complaints
• Ask about the swelling…onset, duration etc…
• H/o pain
• h/o pressure effects- dyspnoea, dysphagia, hoarseness of voice, stridor
• Symptoms of primary thyrotoxicosis … anxiety, insomnia, nervousness,
irritability, loss of appetite, preference for cold, tremor, proximal myopathy,
eye signs(protruding eyes, double vision, swelling of conjunctiva),
amenorrhea, loose stools, excessive sweating
• Symptoms of secondary thyrotoxicosis…palpitation, dyspnoea on
exertion, chestpain, swelling of Leg (Exophthalmos and Tremor are usually
absent)
• Symptoms of hypothyroidism. increase in weight, intolerance to cold, dry
skin, facial oedema, loss of hair, muscle fatigue, lethargy, constipation,
oligomenorrhea/menorrhagia
• Symptoms of malignancy/mets…bony swelling, scalp swelling, bone pain,
loss of appetite and weight, jaundice, abdominal distension, cough,
hemoptysis, dyspnoea

Past Medical History

• Course of treatment
Drug History
• Whether taking a single drug once in the morning (empty stomach) for
thyroid complaints - Probably for Hypothyroidism (Thyroxine/Eltroxine)
• Whether taking a drug three times a day for thyroid complaints -
Probably for Hyperthyroidism (PTU,Carbimazole,etc.,)
Personal History
• Mention about diet..sea food?,”brassica” family vegetables (goitrogens)?
Family History
• Medullary carcinoma & MNG run in families (also in cases of MEN-2
syndrome where Medullary carcinoma is the hallmark entity)

General Examination
• Look for built & nourishment…thin/obese?(hyper/hypo thyroidism)
• Look skin..dry & inelastic(myxodema)/moist & hot(primary
thyrotoxicosis)
• Look for anaemia & cachexia…thyroid carcinoma
• Look for pretibial myxoedema (in primary hyperthyroidism)

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 • Look for arrhythmias in pulse (The stages of development of thyrotoxic
arrhythmias are : Multiple extrasystoles → Paroxysmal atrial tachycardia
→Paroxysmal atrial fibrillation→ Persistent atrial fibrillation, not responsive
to digoxin
LOCAL EXAMINATION…AS PER DAS + MENTION THE FOLLOWING..
• CERVICAL NODES (METS)
• OTHER SYS, RESP (METS)
• CNS. REFLEXES (delayed relaxation phase,especially evident while doing
Ankle jerk in hypothyroidism patients is k/a Woltman’s sign)
• SKULL & SPINE
• LONG BONES
• GAIT
• SIGNS OF HORNER SYNDROME(METS)

SOME IMPORTANT POINTS IN EXAMINATION.

ALWAYS WHEN YOU TELL ABOUT THE SWELLING, TELL ONLY WHAT YOU SEE..
Eg-if you don’t see the margins clearly on inspection, never comment as ‘well
defined margins’..you may say that “margins are well defined on swallowing”.
Also say the number of nodules you see on inspection.
Q) Will a thyroid nodule becomes more prominent/less prominent on neck
extension?
Ans) More prominent !!
Q) How to check for mobility of thyroid gland?
Ans) Normally, we check the mobility of a structure/organ in its relaxed
position .But, the mobility of thyroid is tested for after extending the neck
Q) How will you check for exophthalmos?
Ans) Stand behind the patient. Extend the neck of the patient & ask him to
look straight. Now standing from behind, look through the superciliary ridges
of the patient & see if you can see the upper sclera. Normally this cant be seen.
If you can see the upper sclera , it means there is exophthalmos..this method is
called NAFFZIGER’S METHOD
 The most commonly used instrument to measure exophthalmos is
HERTEL’S Exophthalmometer

GRADING OF EYE SIGNS

 MILD - Stellwag sign +ve
 MODERATE - Joffroy’s sign +ve
 SEVERE - Moebius’ sign +ve

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ALWAYS LOOK FOR BRUIT ON THE SUPERIOR POLE OF THYROID (SUPERIOR
THYROID ARTERY HERE) USING THE BELL OF THE STETHOSCOPE!!
Q) How to distinguish b/w exophthalmos & proptosis?
Ans) You can evert the eyelid in proptosis but you can’t in exophthalmos
because of infiltration of the eyelid.
Q)In any thyroid case never ever forget to examine the abdomen, cvs, reflexes.
Why?
 Hepatosplenomegaly can occur in…->thyroid malignancy, Grave’s
disease, thyroiditis, lymphoma, toxicity(tender hepatomegaly) and very
rarely due to amyloidosis of medullary carcinoma
 CVS→Arrhythmias, CCF
 Reflexes→ exaggerated in hyperthyroidism & vice versa

SLEEPING PULSE RATE is used as an index to measure the degree of

thyrotoxicosis
 <90 -normal
 90-110 -moderate hyperthyroidism
 >110-severe hyperthyroidism.
The NORMAL THYROID REQUIREMENT IS 100-150 microgram/day

DIAGNOSIS
 IF TOXICITY H/S +VE, WAS ON DRUGS & PRESENTLY NO SIGNS…> say
“TOXICITY UNDER CONTROL”
 IF TOXICITY H/S +VE, BUT NOT ON DRUGS & PRESENTLY NO SIGNS..>
say “EUTHYROID”
 IF TOXICITY H/S +VE, PRESENTLY SIGNS +VE…> say “HYPERTHYROID”
EG: “MNG, TOXICITY UNDER CONTROL WITH DIABETES AS COMORBIDITY”

DISCUSSION

Q)Why does thyroid move with deglutition?

Ans) Inferior constrictor muscle is attached to thyroid cartilage, so when this
muscle contracts during swallowing, the gland also moves up. Also the
Suspensory ligament of Berry ( condensation of PRETRACHEAL FASCIA!)
attaches the gland to larynx (cricoid cartilage) which also moves with
deglutition

Q)Other swellings which move with deglutition?

 Thyroglossal cyst
 Subhyoid bursitis

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  Prelaryngeal/pretracheal LN fixed to the larynx or trachea
Q)What is the difference in the plane of swelling of a thyroglossal cyst and a
thyroid swelling?
 Thyroglossal cyst is superficial to deep fascia of neck
 Thyroid swelling is deep to deep fascia of neck
 Blood supply of thyroid…
 Nerves related to thyroid..
 Deep cervical fascia.. parts &attachments

MANAGEMENT OF THYROID SWELLING

TNM classification
 Tx- Primary tumor cannot be assessed
 T0- No evidence of primary tumor
 T1- Less than or equal to 2cm in greatest dimension, limited to thyroid
 T1a - less than or equal to 1cm
 T1b- more than 1cm but less than or equal to 2cm
 T2- More than 2 but less than or equal to 4cm
 T3-
 T3a- More than 4cm but limited to thyroid
 T3b- extrathyroidal extension to strap muscles
 T4- Gross extrathyroidal extension

 Nx- Regional LNs cannot be assessed

 N0- No evidence of LN mets
 N1-
 N1a- level VI or VII LN
 N1b- level I, II, III,IV or V LN

 M0- No distant metastasis

 M1- Distant metastasis

INVESTIGATIONS
 Basic Investigations :
1) Blood Routine - ESR

220
 2) TFT - to know the functional status of the patient (hypo/hyper) and to
prepare for surgery. (1-4% of thyroid malignancies can be hyper)

Normal values (Bailey)

TSH - 0.3 to 3.3 mU/L (most sensitive)

Free T3 - 3.5 to 7.5 micromol/L (half life 6 - 8 hrs)
Free T4 - 10 to 30 nmol/L (half life 6 - 8 days)

Indications for free T3 and T4: autoimmune conditions, subnormal TSH, to

assess response in treatment of toxic goiter.

 Diagnostic Investigations:

1) USS neck

Features to look for:

 Echogenicity - hypoechoic
 No: of nodules, whether they are cystic or solid
 Increased vascularity
 Irregular margins
 Microcalcifications
 Incomplete/Absent perinodular halo
 Taller than wide lesion
 Lymph node- loss of fatty hilum, increased vascularity, irregular
border, central necrosis
 B/L carotid- displaced/not, vascularity
 Trachea assessment

TIRADS ( Thyroid Imaging Reporting and Data System )

Grades
1- Normal thyroid gland
2- Benign condition
3- Probably benign
4- Suspicious of malignancy
4a - 5 to 10%
4b - 10 to 80%
5- Probably malignant
6- Proven malignancy

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 2) USS guided FNAC
23 G needle is used.
Classification of report according to Bethesda System:
Thy 1 - Non diagnostic
Thy 1c - Non diagnostic cystic
Thy 2 - Non neoplastic
Thy 3 - Follicular
Thy 4 - Suspicious of malignancy
Thy 5 - Malignant

FNAC features of:

Papillary ca
Nuclear - Nucelomegaly, Nuclear crowding, Nuclear overlap, clear karyoplasm -
Orphan Annie Eye Nuclei,
Nuclear grooving (coffee bean appearance), Nucleocytoplasmic inclusion,
Psammomma bodies

Medullary ca - Amyloid stroma

Follicular ca - cannot distinguish between adenoma and malignancy by FNAC.

Contraindication for FNAC - Toxic goitre because gland is highly vascular, can
cause bleeding leading to subcutaneous hematoma and cause sudden death.
Therefore control the toxicity 1st.

3) FNAC lymph node - atypical cells from thyroid malignancy

4) X Ray Neck- lateral and AP view
 To look for tracheal deviation/compression (If tracheomalacia is present,
then thyroid is the only structure which maintains the lumen of trachea.
So after removal of thyroid, sudden collapse of trachea can occur leading
to severe respiratory obstruction)
 Retrosternal extension
 Calcification

5) NCCT scan, in case of retrosternal extension reaching upto arch of aorta;

recurrence; malignancy.

If done, also check trachea, carotids, tracheo esophageal groove( r/c laryngeal
nerve).

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 6) Direct laryngoscopy before surgery (to rule out silent unilateral cord
palsy, so that this is not attributed to as caused by the surgery later)

7) Indications for pre operative radio isotope scanning -

 Toxic patient with nodule- to differentiate a toxic
adenoma(hemithyroidectomy can be done) and a toxic nodular
goiter( total thyroidectomy)
 Solitary nodule with suspicion of ca.
 Solitary thyroid nodule with LN FNAC negative for mets.

8) Indications for tru cut biopsy: Anaplastic carcinoma, Thyroid Lymphoma.

9) Metastatic workup - Chest X Ray (cannon ball mets), USS abdomen ( rule
out MEN syndrome).

 Pre operative Ix: CBC, ECG, CXR, LFT, RFT, Coagulation workup.

a) Treatment of MNG

Make the patient euthyroid.

Total Thyroidectomy if there are indications (suspicious of malignancy,

pressure symptoms, cosmesis, patient’s wish) + supplementation of thyroxine.

( LEARN THE PROCEDURE OF THYROIDECTOMY)

Complications of Thyroidectomy :-
 Immediate - Primary hemorrhage, RLN injury, Accidental removal of
parathyroid, Thyrotoxic crisis.
 Early - within 6 to 72 hrs - Reactionary hemorrhage, Transient
hypocalcemia
 Late - after 72 hrs - hypothyroidism, hypoparathyroidism, stitch
granuloma, keloid, wound infection
Management of complications – (Bailey Pg:815).

b) Treatment of solitary nodule thyroid - hemithyroidectomy

c) Treatment of Thyroid carcinoma - Total thyroidectomy.

 For papillary ca diagnosed pre operatively -total thyroidectomy .

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  For papillary ca diagnosed postoperatively:If hemithyroidectomy was
done previously, do completion thyroidectomy and follow up as
mentioned later.

 For papillary ca with Level 3 or 4 LN involvement: Total thyroidectomy

with functional neck dissection.( MRND Type III)
 For follicular ca: Total thyroidectomy + follow up as given later
 For Medullary ca: total thyroidectomy + central neck node dissection +
removal of those nodes that are involved (No role for radioiodine). -->
follow up 6 monthly with calcitonin.

 For Anaplastic ca: Treatment of choice is radiotherapy (Surgery is done

only to relieve tracheal obstruction).

Thyroxine Replacement after Thyroidectomy

 Supplementary - 50 to 100 microgram
 Replacement - 200 mcg
 Suppressive - 300 to 400 mcg

Follow up of differentiated thyroid carcinoma (Papillary and Follicular) (VERY

VERY IMPORTANT)

 Classify the patient as high/low risk according to AMES/AGES criteria

(Age, Mets, Extrathyroid extension, Size, G- Grade).

Give Suppressive dose of thyroxine to suppress TSH as both these ca are TSH
dependent. Maintain TSH at 0.1 to 0.3 for low risk patients and less than 0.1
for high risk patients.
↓
Iodine uptake study to be done within 6 weeks. Withdraw thyroxine 2 weeks
before Iodine uptake to increase TSH level to 30.

↓
Do radioactive iodine uptake study with Iodine-123 (half life 12 to 13 hrs),
dose- 2 to 3mCi.

 No uptake --> Thyroxine supplementation in suppressive dose.

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  Uptake present -->within 1 week do Radioactive iodine Ablation using 30
to 50mCi of Iodine- 131 (half life 12-13 days, so isolate the patient for
these days). If LN involved - 100 to 150mCi, Bone - 200 to 250mCi. Then
give suppressive dose of thyroxine.
↓

Once every 6 months for 1st 3 yrs and yearly for next 5yrs, do thyroglobulin
level(TG).
 If less than 0.01 ng/mL , continue thyroxine.
 If more than 0.01ng/mL, do radioactive iodine uptake scan.
a) Negative scan and TG is only around 0.01  Continue thyroxine
b) Negative scan but highly elevated TG (nearly 100)  do FDG PET If
positive uptake  Radioactive iodine Ablation with secondary dose (
100 to 200mCi ).
c) Positive scan - Ablation with secondary dose.

Thyroxine to be given lifelong.

TREATMENT OF TOXIC GOITRE

3 modalities:
 Antithyroid drugs
 Radioiodine therapy
 Surgery
Treatment is decided based on age and status of the patient.

1) Antithyroid drugs

Carbimazole and Propylthiouracil are commonly used (But antithyroid drugs

will not cure a toxic nodule).

Carbimazole -0.1 to 0.2mg/kg/dose BD, once euthyroid change to 5mg TDS for
6 to 24 months. Another option is to give a very high dose of carbimazole and
inhibit all T3 and T4 production by giving maintenance dose of 0.1 to 0.15mg of
throxine daily ( BLOCK & REPLACEMENT TREATMENT ).

Side effect: Bone marrow suppression causing agranulocytosis, patient

develops sorethroat due to decreased immunity. Stop Carbimazole for 5-7
days, restart if TC is more than 4000.

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Propythiouracil (drug of choice in pregnancy) 100 to 300mg TDS for 4 to 6
weeks followed by 100mg TDS.

Other drugs- beta blockers (Propranolol 10mg BD) to decrease sympathetic

symptoms, Lugol's iodine, Lopanoic acid.

2) Radioiodine therapy
It destroys thyroid cells.
Given for patients more than 45yrs for primary thyrotoxicosis.
After making patient euthyroid with antithyroid drugs, discontinue the drugs
for 5 days.
Dose - Iodine 131 at 5 to 10mCi. May be repeated after 12 weeks. Max 2 to 3
doses can be given.
Contraindicated in extremes of age, pregnancy, lactation, children.

3) Surgery
It is the Rx of choice in both primary and secondary thyrotoxicosis.

Give beta blocker for 7 days after surgery since half life of T4 is 6 to 8 days.

COMMONLY ASKED QUESTIONS

Q) Classify goitre - Simple, Toxic, Neoplastic, Inflammatory (Table 50.3 Pg 805

Bailey).
Q) Natural history of simple goiter (Bailey Pg 806).
Q) DDs of midline neck swellings: Submental LN, Subhyoid bursitis,
Thyroglossal cyst, Nodule in isthmus, Pre and para tracheal LN, Venous
malformation of communicating vein.

Q) Embryology of thyroid.
 Thyroglossal duct develops from the median bud of the pharynx and it
migrates caudally .
 The foramen caecum at the junction of the anterior 2/3rd and posterior
1/3rd of the tongue is the vestigial remnant of the duct.
 Inferior parathyroid - from 3rd pharyngeal pouch
 Superior parathyroid - from 4th pharyngeal pouch
 Parafollicular cells from the neural crest reach via the ultimobranchial
body.

Q) Anatomy of thyroid gland

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  Weight - 20 to 25g
 Arterial supply - Superior thyroid artery, a branch of external carotid;
Inferior thyroid artery, a branch of thyrocervical trunk, and sometimes
the thyroid ima artery.
 Venous drainage : the Superior and Middle thyroid vein drain into the
Internal Jugular Vein, whereas Inferior Thyroid vein drains to
Brachiocephalic Vein.
 Occasionally, 4th Thyroid vein (Kocher’s vein ), emerges between middle
and inferior thyroid veins and drains to Internal Jugular Vein.
 Extent: Oblique line of thyroid cartilage to 5th or 6th tracheal ring.
 Coverings: True capsule(fibrous) and false capsule( pretracheal layer of
cervical fascia).

Q) WHO definition of large goitre:

 Protrusion beyond chin/jaw
 Weighs 80g or more after excision
 Largest neck circumference crossing the goiter 40cm or more
 Large gland evident from a distance

Q) DDs of SNT: Dominant nodule, Toxic adenoma, Malignancy, Hashimotos.

Q) Indications of thyroidectomy - Neoplasia (FNAC positive Thy 3-5 or clinical
suspicion), Toxic adenoma, Pressure symptoms, Cosmesis, Patient’s wish.

Q) Classification of thyroid neoplasms.(Bailey Pg 816 table 50.6)

Q) Preoperative preparations of a toxic patient.(Bailey Pg 813)
Q) Postoperative assessment after thyroidectomy.(Bailey Pg 816)

Q) Retrosternal Goitre.
Types: Substernal (when neck is extended, inferior border is visible),
Plunging (even on extending the neck, inferior border not visible but
palpable on deglutition), Intrathoracic (not visible or palpable)
Management:
 Resection can be carried out from the neck most often; sometimes
median sternotomy is essential.
 1st the cervical part of the goitre is mobilized by ligation and division of
the superior thyroid vessels and the middle thyroid vein.
 Then retrosternal goitre is delivered by traction, which maybe facilitated
by inserting a finger or a series of sutures.
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  The RLN should be identified before delivering the retrosternal goitre.
 If goitre can't be delivered intact, piecemeal delivery is done.
 Avoid fragmentation when malignancy is likely.

Q)Thyroid operations:-
All thyroid operations can be assembled from three basic elements:
 Total lobectomy
 Isthmusectomy
 Subtotal lobectomy

a)Total thyroidectomy = 2 × total lobectomy + isthmusectomy

b)Subtotal thyroidectomy = 2 subtotal lobectomy +
isthmusectomyc)Near-total thyroidectomy = total lobectomy +
isthmusectomy + subtotal lobectomy (Dunhill procedure)
d)Lobectomy = total lobectomy + isthmusectomy

Q) Intraoperative assessment of Recurrent Laryngeal Nerve:-

 Riddle’s triangle
 Tracheo esophageal groove
 Just below the attachment of Berry’s ligament
 Tubercle of Zuckerkandl

Q) Triangles associated with thyroid:

Joll’s triangle: formed laterally by the upper pole of the thyroid gland and the
superior thyroid vessels, superiorly by the attachment of the strap muscles to
the thyroid cartilage and medially by the midline.
Riddle’s triangle: formed laterally by common carotid artery, superiorly by
inferior thyroid artery and medially by tracheo esophageal groove.
Simon’s triangle: anteriorly by recurrent laryngeal nerve, posteriorly lies the
common carotid artery and the base of the triangle is formed by the
cricothyroid muscle

Q) Indications for prophylactic thyroidectomy:

 MEN2A (less than 1yr)
 MEN2B (less than 3yrs)

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Q) Management of subacute thyroiditis:
The specific treatment for the acute case with severe pain is to give
prednisone l0–20 mg daily for 7 days and the dose is then gradually reduced
over the next month. If thyroid failure is prominent, treatment with thyroxine
may be required until function recovers.

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 PERIPHERAL OCCLUSIVE VASCULAR
DISEASE
(POVD)
History-Taking
Presenting Complaints
• Pain (onset,severity-claudication
distance,character,radiation,aggravating & relieving factors and REST
PAIN present or not)
• Paraesthesia
• Swelling/Redness (due to superficial phlebitis as in TAO- Thromboangiitis
obliterans )
• Impotence
• Fainting/Transient black out/Chest pain/Blurred vision/Abdominal pain
(to exclude occlusive arterial disease anywhere in the body)
Past Medical History
• Diabetes mellitus
• Hypertension
• Cardiac illness
• Stroke/TIA
• Dyslipidaemias
• Exposure to cold (Frost Bite)
Drug History
• Diuretics,inhaled LABA’s (Long acting beta-2 agonists) and Statins
produce leg pain/cramps
• Opioid analgesics (Ergot) and intra-arterial Thiopentone sodium(TPS)
cause gangrene
Personal History
• Smoking (causes TAO -Thromboangiitis obliterans and aggravates
atherosclerosis)
• High fatty food (aggravates dyslipidaemia and atherosclerosis)
• Inability/difficulty to obtain erection during coitus (bilateral internal iliac
artery occlusion)
Family History
• Atherosclerosis (often familial)

Local Examination
Inspection
1. Attitude of limb*
2. Change in colour of limb
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3. Signs of Ischaemia ( look at the Skin, Hair, Nails ,Fat and Pressure points)
 Skin - Thinning of skin
 Hair - Loss of hair
 Nails - Brittle and showing transverse ridges
 Fat - Loss of s/c fat
 Pressure points (heel,malleoli, ball of the foot,tips of the toes) -
Ulcers
4. Buerger’s Postural Test and comment on the Vascular angle (roughly)
5. Capillary filling time
6. Venous refilling time
7. In case of established gangrene,comment on the following points too:
 Site,Extent and Colour
 Type of gangrene (Dry/Moist)
 Line of demarcation (well marked/poorly marked)
 Limb above the gangrene (Normal/Dry/Glossy)
8. Wasting/Edema of limb
9. Any ulcers/varicose veins

Palpation
1. Local rise/fall of temperature and tenderness present or not
(corresponding areas of both limbs to be checked in order)
2. Capillary and Venous refilling
3. Crossed leg test (Fuchsig’s test)- Test for patency of popliteal artery
4. Palpate the gangrenous area and comment as dry/wet gangrene
describing the features; ‘Crepitus’ is a feature of GAS GANGRENE
5. Palpate the limb above the gangrene and comment about any
abnormality
6. Palpation of Blood vessels (proceed distal to proximal):
7.
Dorsalis Proximal end of 1st intermetatarsal space,lateral to the
Pedis A. tendon of EHL (over the Navicular bone)
Posterior Just behind the medial malleolus (over the medial
Tibial A. malleolus/medial aspect of calcaneum)
Peroneal A 1cm medial to lateral malleolus
Anterior midway anteriorly b/w the 2 malleoli,lateral to the tendon
Tibial A. of EHL (over the lower end of tibia)
Popliteal A. Lower part of popliteal fossa posteriorly (with the knee
flexed and the heel resting on the bed,over the tibial
condyle)
Femoral A. - At the groin just below the inguinal ligament midway b/w
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 ASIS and pubic symphysis (also k/a MID-INGUINAL POINT)
Radial A. At the wrist in front,lateral to the tendon of FCR (over the
lower end of radius)
Ulnar A. At the wrist in front,lateral to the tendon of FCU (over the
lower end of ulna)
Brachial A. In front of the elbow medial to the tendon of biceps (over
the lower endof the humerus)
Axillary A. Felt in the apex of the axilla (over the head of the humerus)
Subclavian Just above the middle of the clavicle/middle of
A. supraclavicular fossa(over the 1st rib)
Common In the carotid triangle in front of sternomastoid muscle
Carotid against the carotid tubercle of the sixth cervical vertebra
(‘Chassaigne tubercle’)
Superficial Felt just in front of tragus
temporal A.

8. Test for Sensations over the limb ( Neurological examination of the

Sensory System)
9. Measure the Girth of the limbs and compare the values(> 1cm difference
indicates muscle atrophy)
10.In a case of suspected Thoracic Outlet Syndrome,perform the following
tests in the upper limb:
 Allen’s test
 Adson’s test
 Roose Test/Elevated Arms Test
 Costoclavicular compressive manoeuvre test
 Hyperabduction manoeuvre test
11.Examination of the venous system of leg (very imp. if varicosities are
present)
12.Examination of the Regional LN

Auscultation
1. Check for bruit (bruit over an artery indicates turbulent flow beyond
stenosis):
 Coeliac bruit - check at epigastrium
 Iliac bruit - check at hypogastrium
 Renal bruit (in Renal Artery Stenosis)- check at a point just lateral to
umbilicus or at renal angle
 Subclavian bruit (in TOS)- during Costoclavicular compressive
manoeuvre/test
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  Axillary bruit (in TOS) - during Hyperabduction manoeuvre/test
2. Continuous machinery murmur is heard in A-V Fistula

Systemic Examination
1.Cardiovascular System
• Signs of Congestive Cardiac Failure (Raised JVP, Pedal edema,Ascites)
• Cardiac Murmurs (Valvular heart diseases can cause embolic stroke)
• Cardiac Arrhythmias (eg. Atrial fibrillation (AF) can lead on to cause
embolic occlusion of central/peripheral vessels)
2.Respiratory System
• Basal crepitations and Pleural effusion (in congestive cardiac failure)
3.Nervous System
• Sensory or Motor disorders (Thrombotic/Embolic stroke)
• Speech problems (Aphasia)
• Temporary visual loss (Atheromatous fragments in the retinal vessels)
4.GIT
• Look for ascites and tender hepatomegaly (Congestive Cardic Failure)
• Intestinal Angina (pain after meals- due to occlusion of mesenteric
vessels: AMI (Acute mesenteric ischaemia))

DIAGNOSIS
• “Peripheral Occlusive Vascular Disease of Right or Left or Both
Upper/Lower Limb,
• Acute Arterial Occlusion/ Chronic Limb Ischaemia/ Aneurysm ,
• Probably due to Atherosclerosis,
• Causing thrombosis OR embolism occluding ______ (level of lesion),
• With or Without Gangrene (Dry/Wet),
• With/No complications (eg., Ischaemic Ulcers)”
• With or without Co-morbidities like DM,HTN,Heart Disease,etc., •

Thrombosis is usually a chronic process (chronic limb ischaemia) while

Embolism is usually an acute process (Acute arterial occlusion); exceptions
are there (eg.,sudden dislodgement of a thrombus). Therefore a diagnosis
of “Acute on Chronic Limb Ischaemia” is acceptable

 TAO(Thromboangiitis obliterans) also k/a ‘Buerger’s disease’, is a close DD

to atherosclerosis in causing POVD

‘Clinical’ differences between atherosclerosis and TAO are:

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 • TAO usually affects young men < 40yrs, while atherosclerosis affects
male > female above 40yrs
• TAO has a striking association with smoking, while atherosclerosis can
occur without smoking
• TAO affects distal small vessels of limbs earlier than proximal vessels and
therefore the symptoms appear first in the foot region (Foot
Claudication),while atherosclerosis affects proximal large vessels of
limbs earlier than distal vessels and therefore the symptoms appear first
in the thigh or buttock regions (Thigh/Buttock Claudication)
• TAO has associated features of inflammatory reaction especially in the
veins producing the characteristic migratory,recurrent superficial
phlebitis,while atherosclerosis is not associated with superficial phlebitis

 severity of the disease is assessed by ‘Fontaine Classification’ which is as

follows:
• Stage I - Asymptomatic
• Stage II - Intermittent claudication [ IIa is well compensated (>300m) and
IIb is poorly compensated (<150m)]
• Stage III - Rest pain
• Stage IV - Ulceration/Gangrene

DISCUSSION

History-Taking
1. Claudication history (Cramp-like muscle pain occurring while the limb is
exercised, like during walking) should be well elicited while history
taking.
Claudication distance (distance after which pain starts during walking) should
also be conveyed while presenting the case because it marks the severity of
the peripheral vascular disease.
Q) How do you grade claudication?
Ans) Boyd’s Classification
• Grade 1 - Pain after walking some distance.It disappears and the patient
continues to walk
• Grade 2 - Pain persists and still the patient continues to walk
• Grade 3 - Pain compels the patient to take rest
Q) Which substance’s accumulation causes claudication?
Ans) Substance P
Q) What is the cause of paraesthesia (pins and needles’ sensation) when
muscle pain begins in claudication?

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Ans) Due to shunting of blood from the skin to the muscle
Q) Do the arterial occlusion symptoms increase/decrease on application of
warmth?
Ans) Increase
Q) *What is the effect of elevation of limbs on arterial occlusion and venous
occlusion symptoms?
Ans) Arterial occlusion symptoms INCREASE on elevation of the limb
BUT
Venous occlusion symptoms DECREASE on elevation of the limb

2. Impotence
It can occur as part of Leriche’s syndrome, due to aorto-iliac disease,
characterised by
• Thigh,Hip and Buttocks claudication
• Impotence (erection failure) due to internal iliac artery occlusion which
cuts-off the blood suppply to penis
Local Examination
Inspection
1. Change in colour of the limb:
• Marked pallor- feature of sudden arterial occlusion
• Congestion and Cyanosed - features of severe ischaemia and pre-
gangrenous stage
Q) What is Raynaud’s syndrome and give its treatment?
Ans) A series of attacks of local syncope, local asphyxia and local gangrene
secondary to an underlying systemic disease (eg.,SLE, RA) is k/a Raynaud’s
syndrome.
• Local Syncope - Cold and White digits with tingling and numbness (d/t
spasm of the digital arteries)
• Local Asphyxia - Painful and Cyanosed digits (d/t slowing of circulation
and accumulation ofreduced Hb)
• Local Recovery - Digits become normal (d/t release of spasm of digital
arteries)
Treatment: ’PNS’- Treatment of the Primary condition, Nifedipine and Steroids

Q) What is Raynaud’s disease and give its treatment?

Ans) It is an idiopathic condition due to abnormal sensitivity of the arterioles to
cold resulting in the classical triphasic colour response seen in Raynaud’s
syndrome.In simple words, Raynaud’s disease is Idiopathic Raynaud’s
Syndrome
Treatment: ‘CNS’ - Protection from Cold, Nifedipine and Sympathectomy

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 2. ’Signs of Ischaemia’
• Skin - Thinning of skin
• Hair - Loss of hair
• Nails - Brittle and showing transverse ridges
• Fat - Loss of s/c fat
• Pressure points (heel,malleoli, ball of the foot,tips of the toes) - Ulcers

3. Buerger’s Postural Test

• In case of an ischaemic limb,elevation of the limb to a certain degree
(with the knees straight) will cause marked pallor on the limb
• The angle b/w the limb and the horizontal plane at which such pallor
appears is called ‘Vascular angle’ or ‘Buerger’s angle’.
 Normally,there won’t be pallor even when the limb is raised to 90
degree from the bed (horizontal)
 Vascular angle less than 30 degree indicates severe ischaemia
4. Capillary filling time
 Ischaemic limb becomes pale when elevated and pink when the leg is
made to hang down
 The time taken for the above change is k/a ‘capillary filling time’
 Normal limb won’t become pale on elevation of the limb
 Capillary filling time about 20-30 seconds indicates severe ischaemia
5. Venous refilling time
 The time taken for the veins to refill when it is laid flat on the bed
after elevating the limb for a while(’30 seconds’ ) is k/a ‘venous
refilling time’
 Normal venous refilling time - within 5 seconds ; delayed in ischaemic
limb
 In normal limb - gradual collapse/guttering of veins when the limb is
elevated to even 90 degrees from the horizontal
 In ischaemic limb - veins are seen collapsed either in the horizontal
position or when lifted to even 10 degrees from the horizontal

Palpation
1. Local rise/fall of temperature and tenderness
• Test for temperature change with the back of the fingers and always
compare the limbs
• Remember,ischaemic site has cold skin; if there is phlebitis,the site
will be warm
2. Capillary and Venous refilling
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 • Capillary refilling is tested by noting the time for the blanched skin to
turn pink when the tip of the nail or the pulp of the finger/toe is
pressed for a few seconds (‘2 seconds’ PEARLS) and the pressure is
released
• Normally,capillary refilling occurs suddenly as the pressure is
released;
delayed in ischaemia
• Venous refilling is tested in the same manner as we look for the
direction of blood flow in veins!
• Venous refilling is poor in ischaemic limb and increased in A-V Fistula
Q) What is ‘Harvey’s sign’?
Ans) Poor venous refilling in ischaemic limb and increased venous refilling in a-
v fistula is k/a Harvey’ssign
3. Crossed leg test (Fuchsig’s test)-
 Test for patency of popliteal artery
 It is done to check the patency of POPLITEAL ARTERY
 NORMALLY,crossed leg will show oscillatory movts. of the foot which
occur synchronously with the pulse of the popliteal artery
 Oscillatory movts. of the foot are ABSENT if the popliteal artery is
blocked
4. Palpation of the the Gangrenous area + Limb above the Gangrenous area
:
• Comment as dry/wet gangrene describing the features; ‘Crepitus’ is a
feature of GAS GANGRENE
• Limb above the gangrene should be commented without failure ;
‘normal/glossy/dry’
Q) Define gangrene?
Ans) Macroscopic death of tissue with putrefaction
Note: Necrosis is microscopic death of tissue

Q) What are the clinical types of gangrene and how do you differentiate them?
Ans) 2 types: DRY and WET gangrene
• DRY GANGRENE: Affected part becomes
dry,shrivelled,hard,mummified and discoloured (due to
disintegration of hemoglobin)
• WET GANGRENE : Affected part becomes oedematous with blebs
with associated signs of inflammation and putrefaction
Q) What are the signs of gangrene? (VERY VERY IMP)
• Colour change (pale->blue->purple->black)
• Loss of pulsations

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 • Loss of temperature
• Loss of sensation
• Loss of function
NOTE: If not sure about the “loss” finding after clinical examination, you may
use the term ‘Pregangrene’ while you put forward your diagnosis
“The term ‘Pregangrene’ is used to describe the changes in the tissue to
indicate that its blood supply is so precarious that it will soon be inadequate to
keep the tissue alive ”- DAS

Q) Clinical features of Acute Embolism (6P’s)

• Pallor
• Pulselessness
• Poikilothermia (cold limb)
• Pain
• Paralysis
• Paraesthesia
Note: ‘Pain and Pallor’ are features of Acute Embolism (Acute Arterial
Occlusion) while ‘Loss of Sensations and Cyanosis (bluish-black)’ are features of
Gangrene
5. Palpation of Blood vessels (proceed distal to proximal in any limb)
Note: anterior tibial artery is palpated, “against the lower end of tibia” (DAS).
But some senior clinicians say that it is “against the neck of talus” that we
palpate the anterior tibial artery.
Q) Describe the consistency of a thrombosed vessel?
Ans) It feels midway b/w firm and soft and one can feel something within the
artery” (DAS)
6. Test for Sensations over the limb ( Neurological Sensory System)
• This is important especially in cases like long-standing diabetes,
where there is associated sensory neuropathy.
7. In a case of suspected Thoracic Outlet Syndrome(TOS) Neurogenic/
Arterial/ Venous, perform the following tests in the upper limb:
• Allen’s test- To know the patency of Radial and Ulnar arteries
• Adson’s test- In the sitting posture, the patient is asked to take a
deep breath in and to turn the face to the affected side (with the
neck fully extended), while the examiner checks his radial pulse.It
will be obliterated in TOS due to compression on subclavian artery
[ This position tightens anterior and middle scalene muscles,
decreasing interspace and magnifying pre-existing compression of
subclavian artery]

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 • Roose Test/Elevated Arms Test- The patient is asked to abduct his
shoulders to 90 degrees with the upper limbs externally rotated fully.
Now the patient is asked to open and close his hands for a period
of 5 minutes.A patient with TOS will complain of pain, fatigue,
paraesthesia in the forearm and hands
• Costoclavicular compressive manoeuvre test- The patient is asked
to throw his shoulders backwards and downwards (exaggerated
military position) while the examiner checks for his radial pulse.In
TOS,there will be diminishing/disappearance of the pulse (due to
compression of the
subclavian artery b/w the “costa” (1st rib) and the “clavicle”)
• Hyperabduction manoeuvre/ test- The affected arm is passively
hyperabducted while the patient’s radial artery is palpated. In TOS,
there will be diminishing/disappearance of the pulse (due to
compression of the subclavian artery by Pectoralis minor tendon)
Q) What are the dimensions of thoracic outlet?
Ans) AP diameter - 5cm Transverse diameter - 10cm

Q) Give the important aetiologies of TOS?

• Cervical Rib
• Congenital Fibrous Band Between First Rib & C7
• Abnormal Fusion of Scalene Muscles at the Insertion Site
• Clavicular Fracture Callus/ Traumatic
• Exostosis of First Rib/ Neoplastic
• Narrowing of Costo Clavicular Space
• Compression by Pectoralis minor Tendon
• Long Transverse process of C7
Q) What are the 4 types of cervical rib?
• Complete Cervical Rib
• Cervical rib ending in a bony mass
• Cervical rib tapering as a Fibrous band
• Complete Fibrous Band - No Radiological Finding
Q) What is the diagnostic triad of TOS?
Ans) It is k/a ‘SELMONOSKY TRIAD’ and consists of:
• Tenderness in the Supraclavicular Area
• Abduction & Adduction weakness of 4 &5 fingers (C8 - T1)
• Pallor / Paraesthesia on elevation of the Limb
Q) What are the important DD’s of TOS?
• Cervical Spondylosis
• Cervical Disc Prolapse

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 • Cervical Cord Compression
• Carpel Tunnel Syndrome
• Raynaud’s disease / Pancoast Tumour
Q) What are the investigations done in a suspected TOS case?
1. Plain X-ray Neck and Chest (Cervical rib,Fracture callus)
2. MR Angiogram/Venogram (to evaluate arterial/venous TOS)
3. Nerve Conduction Velocity (NCV) studies (to evaluate neurogenic
TOS)
4. MRI Spine (To rule out cervical disc/canal pathologies)
Q) What is the Rx of TOS?
Ans) Conservative and Surgical

Conservative:
• Maintain a Proper posture
• Weight Reduction ( Obesity predisposes to TOS )
• Physiotherapy (Exercise to strengthen the Shoulder girdle to prevent
drooping)
• Stop any repetitive activity or work for prolonged period
Surgical:
• Excision of the Cervical Rib/Scalenotomy Operation -
[Anterior/Posterior/Trans Axillary Approaches]
• Indications for Surgical Rx :
1. Failure of Conservative Management for 6 months
2. Progression of the Neurological Symptoms
3. Occlusion of Subclavian Artery
4. Thrombosis of Subclavian/ Axilliary vein (Venous TOS or otherwise
k/a PAGET- SCHROETTER syndrome)
• Complications of surgery are grave. eg.Phrenic N. injury, Brachial
plexus injury, Subclavian A. & V. injury and Pneumothorax!

8. Examination of Regional LN
•  Inguinal LN will be enlarged in lower limb
inflammation,phlebitis,etc.,
• Auscultation
• ‘Continuous machinery murmur’ - A-V Fistula
• Renal Bruit - Renal artery stenosis
• Subclavian bruit - in TOS during Costoclavicular compressive
manoeuvre/test
• Axillary bruit -in TOS during Hyperabduction manoeuvre/test
Systemic Examination

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 • Cardiovascular system should be diligently examined in a POVD
case,especially in Acute limb ischaemia (arterial), which is MC due to
peripheral emboli.
• Cardiogenic source of peripheral emboli constitutes 80% of all
peripheral emboli,out of which AF (Atrial fibrillation) constitutes 50%
and Myocardial infarction constitutes 25% .

Management of a POVD (Chronic Limb Ischaemia)

Investigations
1. Blood examination (r/o anaemia), RBS (Random blood sugar), Lipid
profile
2. Doppler ultrasound of the limb :
• It tells us whether the blood is ‘moving’ or not in the limb.
• Detects Stenosis,Occlusion,Collaterals,Venous involvement and
Calcification
• Doesn’t indicate the ‘Viability’ of the limb (whether the blood flow
detected is sufficient to prevent limb loss) and the ‘Severity’ of the
pathology of the limb
3. Duplex imaging of the limb :
• It’s a combination of Doppler and B-mode ultrasound. B-mode
ultrasound can image the vessels. Duplex imaging can provide the
anatomical details of the pathology in the limb, along with the
direction of blood flow and turbulence
• Duplex can provide (in extra to doppler) the details of the ‘Severity’
of the stenosis/occlusion + Details of the collaterals + indicates
‘Viability’ of the limb
The above are the essential non-invasive investigations to be done in a POVD
case.
If a surgical intervention is planned,
• other non-invasive techniques like CT angiography (CTA) or MR
angiography(MRA) of the limb needs to be done to delineate the
anatomical details.
The advantages of MRA over CTA is that,MRA doesn’t involve ionizing radiation
and it can be used in patients with compromised renal function (‘Gadolinium
dye’ used in MRA is not nephrotoxic).But MRA is costlier.
• Arteriography is almost outdated, as non-invasive methods like CTA
or MRA are available.There are 2 techniques available for
arteriography namely:
1)The Seldinger technique

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 2)Translumbar method for aortography
Complications of arteriography are ‘Puncture Site/Catheter Related’ and
‘Contrast Agent Related’.In this context,remember ‘BLUE TOE SYNDROME’
which occurs due to lodging of atheroemboli debris in the most distal vessels
of the toes(complication of catheter placement) and may cause loss of the toe.
It occurs in only a small fraction of cases.

Q) What is the importance of Chest X-ray in a POVD case?

Ans) It helps in detecting:
• Calcifications (aortic)
• Aneurysms (aortic)
• Cervical Rib
• Gas gangrene (subcutaneous emphysema)
Q) Name a quick ‘screening test’ and is the cornerstone of diagnosis in arterial
occlusion?
Ans) ABPI (Ankle Brachial Pressure Index): It the ratio of systolic blood
pressures at the Ankle (Dorsalis pedis/Posterior tibial A). and Arm (Brachial A.)
• Normal ABPI is 1.0 - 1.2, i.e., one or slightly more than 1
• If less than 0.9, vascular disease is confirmed
• 0.5 - 0.8 : Claudication
• 0.3 - 0.5 : Rest pain
• < 0.3 : Gangrene
Q) Give 2 conditions where false elevation of ABPI are obtained (>1.4)
Ans) In extensive vascular calcification, as in
 Diabetic patients
 Chronic Renal Failure patients
Q) Doppler and Duplex assess the status of ‘macrocirculation’ (large
vessels).Name one simple, good test to assess the status of
‘microcirculation’(small vessels)?
Ans) Transcutaneous Oximetry (tcPo2): It measures the intracutaneous oxygen
tension (Po2) by placing the probe over the skin surface and assess the tissue
perfusion ; Sites like thigh, calf,etc., can also be assessed. It can be used pre-
and post-operatively
 Normal tcPo2 is 40-70mm of Hg
 “Values greater than 40mm Hg are predictive for healing of foot
lesions or primary forefoot amputations; values less than 10mm Hg
are almost universally associated with failure to heal.Values in the
middle range are not particularly useful as isolated measurements
and must be placed in clinical context”

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TREATMENT
3 modalities of Rx are there in POVD:
1. General measures
Specific treatment, which includes
2. Drug therapy
3. Surgery (Direct arterial surgery, Lumbar sympathectomy and
Amputations)

General Measures: (imp)

1. Stop smoking (Behaviour modification,Counseling,Nicotine analogues)
2. Physical activity (at least 30 minutes of moderate exercise like
walking,jogging,cycling)
3. Diet control & Weight reduction
• Goal : LDL< 100mg/dL; HDL > 35mg/dL; TG < 200mg/dL; <120% of
ideal body weight
[In Diabetes mellitus, Active Coronary artery disease and Metabolic
syndrome patients, LDL should be maintained at levels < 70mg/dL]
• Approach : Diet : <30% fat, <7% saturated fat and <200mg/day
cholesterol plus Physical activity
4. Control of DM and HTN
Fasting Blood Sugar(FBS) should be maintained preferably <100mg/dL
And Blood pressure values <140/90mm of Hg
5. Care of the Foot
Well fitting footwear with 1cm ‘heel raise’
‘Heel raise’ will improve claudication distance

Drug Therapy
1. Analgesics - Ultracet [Tramadol + Acetaminophen ) is given very
commonly in the OP setting to manage pain. 1-2 tablets Q6H is the usual
dose upto a maximum of 8 tablets/day
Composition of Ultracet : Tramadol(37.5mg) + Acetaminophen (325mg)
2. Antiplatelet drugs - Aspirin (75-325mg/day)
Newer drugs likle Ticlopidine and Clopidogrel can also be used
3. Lipid profile maintaining drugs
Statins, Clofibrate, Gemfibrozil, Niacin,etc., are used according to the
lipid profile status
Atorvostatin 40mg/day at night is very commonly used
2 newer drugs are
• Ezetimibe (inhibit cholesterol uptake at the small bowel brush
border)

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 • Torcetrapib (blocks the cholesterol ester transfer protein and thus
increases the proficiency of ”reverse-transport” of lipids)
Note: Statins have the A/E of myopathy,which may cause leg pain/cramps
4. Drugs that improve microcirculation and claudication
• Cilostazol 100mg OD is commonly prescribed in the OP,to improve
microcirculation ;It’s common trade name is ‘PLETOZ’
• Pentoxifylline 400-800mg TDS improves blood viscosity and useful
in intermittent claudication
• Venusmin (newer venotonic agent which is ‘Calcium dobexylate’)
improves claudication
5. Drugs to manage diabetes mellitus (oral hypoglycaemic agents/insulin)
and hypertension

Surgery (in case of absent pulsations!!)

There are 3 broad groups :
• Direct Arterial Surgery (It includes PTA & Stenting, Endarterectomy,
Bypass Grafting)
• Lumbar Sympathectomy
• Amputations

The indications for Direct Arterial Surgery are mainly 3:

• Critical Limb Ischaemia (1-Rest pain[ABPI : 0.3 - 0.5] that persists for
more than 2 weeks,requiring regular analgesics, and, 2-
Ulceration/Gangrene of the foot or toes)
• Severe Intermittent Claudication (Claudication symptoms occur when
ABPI is 0.5 - 0.8)
[Note: Salvage operations should not be performed for intermittent
claudication
alone. Gangrene and loss of limb may occur if the operation fails.So the term
“Severe intermittent claudication” is important!!+
• To lower the level of Amputation

The choice as to which ‘Direct Arterial Surgery’ should be resorted to depends

on
various principles and factors .The following points are helpful in decision-
making:

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PTA & Stenting
• Is better for ‘Stenosis > Occlusion’, short segment (focal stenosis) lesions
(<5-8cm) in large-caliber vessels (preferably > 4mm) and high-flow
arteries
• 2 types of stents are available : Balloon-expandable and Self-expanding
stents
• Stents are used to prevent restenosis by
 minimizing elastic recoil & constrictive remodeling(shrinkage)
 reducing intimal hyperplasia by delivery of antiproliferative agents
(drug-eluting stents) or ionizing radiation (brachytherapy)
• Most suitable sites for PTA & Stentnig : Distal abdominal aorta and iliac
Arteries.

Surgical Endarterectomy
 Is better for ‘Stenosis > Occlusion’, short segment (focal stenosis) lesions
in large-caliber vessels (preferably > 5-6mm) and high-flow arteries
 4 methods are there : Open, Semiclosed, Extraction and Eversion ; All
involve blunt separation of the plaque by developing a cleavage plane
b/w the plaque and the underlying deeper media (Remember :
Atherosclerosis is localized to the intima and inner media of vessels)
 Most suitable sites for Endarterectomy : Carotid bifurcation,Common
femoral and Aortic branch lesions

Surgical Bypass Grafting

 Is preferred in either ‘Stenosis or Occlusion’, any length of segmental
lesions in both long and shorter caliber vessels (> 2mm) and high/low
flow arteries.
 Because of the above advantages over PTA & Stenting and
Endarterectomy, Bypass Grafting has evolved as the most widely
applicable technique for the Rx of arterial occlusive lesions
(Coronary,Abdominal and Peripheral vascular beds)
 “Whenever possible,segments bearing minimal disease are selected for
anastomotic sites because this greatly facilitates both vascular occlusion
as well as suturing”
 Anastomoses are most commonly performed either in :
 End-to-side configuration (broader application and easier ; entry
angle < 45 degrees to minimize turbulence)
OR
 End-to-end configuration (the two ends are slightly beveled [45
degrees]to enlarge the opening)
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  Most suitable sites for Bypass Grafting : Aortic arch through Distal
extremity. Eg.,Femoropopliteal bypass grafting, Aortobifemoral bypass
grafting,etc.,
Q) What are the materials used for Bypass grafting?
 Long Saphenous vein is the most successful graft material ; Short
Saphenous vein, Axillary vein etc., may also be used (diameter of atleast
3mm is essential for the graft vein)
 For large vessels (eg.,Aorta), DACRON is preferred (2 types: ‘Woven’ and
‘Knitted’)
 For smaller vessels (eg.,Femoral,Popliteal), PTFE -
Polytetrafluoroethylene is preferred
Q) Name one novel procedure used to treat Aortic graft rejection?
Ans) NAIS Procedure (creation of NeoAortoIliac System using Femoropopliteal
vein replacement).it is a technically demanding, long operation (nearly 8hrs!!)

The indications for Lumbar Sympathectomy are as follows:

• Non-healing ischaemic ulcers
• Ischaemic rest pain (in Buerger’s disease)
• Hyperhydrosis
• Raynaud’s disease
Note : Lumbar sympathectomy has no role in the management of intermittent
claudication

The indications for Amputations are as follows:

• Dead limb (Gangrene)
• Deadly limb (Wet gangrene,Spreading cellulitis,Malignancy)
• Dead-loss limb (Crush Injury)
Q) What are the major types of Amputations?
• Ray amputation (for digits/toes)
• Transmetatarsal amputation (for forefoot)
• BK (below knee) amputation - Incision put 5.5 inches below the tibial
tubercle
• AK (above knee) amputation - Incision put 11 inches below the
greater trochanter of femur
Q) What is the severity classification/grading of ALI (Acute limb ischaemia)?
Ans) SVS (Society for Vascular Surgery) Grading is followed :
 I - Viable [No sensory or muscle weakness + Audible arterial and
venous doppler signals + Elective intervention required]

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  IIa - Marginally threatened [Minimal NM findings
(numbness/paraesthesia) + Often Inaudible arterial and Audible
venous doppler signals + Urgent intervention required]
 IIb - Immediately threatened [NM findings with Pain + Usually
Inaudible arterial and Audible venous doppler signals + Emergent
intervention required]
 III - Irreversible [Profound deficits + No doppler signals + Emergent
intervention required]
Q) Describe in brief the management of Acute limb ischaemia?
General Measures
 Plenty of IV fluids (Normal saline is used ; no potassium until renal
function is determined)
 Supplemental Oxygen
 Aspirin (per oral OR per rectal)
 IV Heparin bolus 100-150 U/Kg, and then titrated to maintain an aPTT of
2-2.5 INR
 Send the blood for investigations (Hb,TC,DC,ESR,Coagulation
profile,CPKestimation)
 ECG-12 leads (to check for cardiac pathology)
Note: Laboratory markers may help predict major amputation risk in those
with ALI. CPK elevation and Neutrophilia upon presentation confer a tenfold
increased risk of amputation, as compared to those without CPK.

Specific Treatment
The selection is to be made b/w 2 therapies (after considering the factors of
‘Mortality’ and ‘Amputation occurrence’)
 Endovascular Therapy (Angiography and Thrombolysis) and
 Surgical Therapy (embolectomy/Bypass)

In those pateints with embolic etiology (Class IIb and III limb ischaemia),
Surgical embolectomy is preferred (amputation is significantly less than with
failed thrombolysis)
 IV Heparin should be continued through the procedure and until the
patient is fully anitcoagulated with Warfarin, started approximately
24hrs after the procedure and should be continued for at least 6
months
 For Class I and IIa limb ischaemia patients,Endovascular therapy is
done,after considering the contraindications for thrombolysis like
Recent stroke, Recent surgery, H/o GI
hemorrhage,Pregnancy,Uncontrolled hypertension and Allergy to the
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 agent.It takes about 48 hours to lyse the thrombus,so cannot be done in
a limb threatened with gangrene.

Q) How do you assess the success of thrombolytic therapy?

Ans) Clinical examination!!
By assessing the improvement in
 Limb temperature
 Capillary refill
 Pulses
 Patient symptoms

Q) Name some thrombolytic agents?

1. Fibrin-specific agents (eg.,tPA-tissue plasminogen activator)
2. Non-fibrin specific agents (eg.,Streptokinase,Urokinase)
3. Modified tPA -modern bioengineered versions (Alteplase, Reteplase,
Tenecteplase)
Q) Name a few catheters used for surgical embolectomy?
 Fogarty catheter (standard embolectomy catheter)
 ACC (Adherent Clot catheter) - used for removing older clot of
thrombotic origin
 GTC (Graft Thrombectomy catheter) - used in case of synthetic grafts
only
Q) Give the names of two landmark studies/trials which suggested that
thrombolytic therapy had equivalent outcomes to surgical therapy in patients
with ALI?
 STILE (Surgery or Thrombolysis in Lower Extremity Ischaemia)
 TOPAS (Thrombolysis or Peripheral Artery Surgery)

Q) How many compartments are there in the leg ?

Ans) There are 4 compartments in the Leg, namely
 Anterior (innervated by deep peroneal nerve)
 Posterior - superficial (innervated by Sural nerve)
 Posterior - deep (innervated by Tibial nerve)
 Lateral (innervated by Superficial peroneal nerve

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 OBSTRUCTIVE JAUNDICE
Presenting complaints
The sequence of symptoms: Reduced appetite, nausea →yellow discoloration
→ itching→ abdominal pain→ delineate etiology according to rest of
symptoms.
Yellow discoloration appears in urine→ eyes→ oral mucosa→ skin

 First about jaundice

Duration, progression, intermittent/waxing and waning (In intermittent,
patient is completely free of jaundice in intervening period...indicates
gallstones; waxing and waning points to sloughing of tumor, and jaundice only
decreases in the period)
 Now establish as obstructive:
More severe, longer (>2 weeks), itching, clay colored stools. (Medical jaundice
in viral hepatitis has a phase of partial obstruction)
 Now the etiology:
 Gallstones: intermittent jaundice, dull constant or colicky pain in right
hypochondrium, nausea, dyspepsia, flatulence, food intolerance
(especially fats), Charcot’s triad in cholangitis(intermittent fever,
intermittent jaundice and intermittent pain), previous h/o gallstones.
Reynold’s pentad is triad+ hypotension + CNS hypoperfusion
 Periampullary carcinoma: older age(65-75),progressive(Ca head of
pancreas) or waxing and waning over 2 months(periampullary) jaundice,
silvery or whitish stools, loss of appetite, loss of weight, epigastric pain
or pain radiating to the back(Ca head of pancreas), rarely malena
Vomiting can occur due to duodenal infiltration, ascites due to portal
vein & SMA involvement
 Cholangio Ca- Progressive jaundice, cola or amber colored urine, severe
anorexia and weight loss
 Viral hepatitis: Fever, blood transfusions.
 Testicular malignancy (presents with abd lump) : No h/o scrotal swelling
 Now symptoms of mets,
 Liver- ask for liver failure-first symptom is inversion of sleep rhythm.
Altered sensorium, bleeding manifestations.
 Bone- low backache
 Lungs- recurrent cough with hemoptysis
 Brain- visual disturbances, headache, seizures
 Any other swellings in the body, supraclavicular region.

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Past history
 h/o jaundice
 h/o gallstones
 h/o recently detected DM
 h/o smoking, alcoholism
 h/o blood transfusion
 h/o abd surgeries/biliary surgeries (strictures)/cholecystectomy
(gallstones)

Drug history
 ATT, OCP, chlorpromazine, erythromycin, testosterone all predispose to
cholestasis
Personal history
 Alcoholism and smoking-risk factors for Ca pancreas
 Fat, Fertile, Female of Forty are risk factors for gallstone disease

Family history
 Jaundice with anemia (hemolytic anemias)

General examination-Always state that patient was examined in good

sunlight
 Pallor, Icterus (imp) , also bradycardia due to bile salt deposit in SA node,
and scratch marks due to bile salts irritating nerve endings and yellow
discoloration of abdomen if present.
 Look for supraclavicular node
 Thyroid and breast as routine
 Stigmata of chronic liver disease
 Leg ulcers (hemolytic anemia)
Oral cavity examination
 icterus, tobacco staining, pigmentation to be checked in GIT (FAP and
Peutz Jegher syndrome)
Abdomen examination as per Das...ALWAYS mention PR not done
(Cases for exam will usually have palpable gall bladder and discussion inclines
towards CA pancreas... swelling palpable in ____ region, lower, medial and
lateral margins palpable, upper margin deep to costal margin or continuous
with liver dullness, moves with respiration)
DIAGNOSIS
Obstructive jaundice probably due to gall stones/CA head of
pancreas/Periampullary carcinoma with no complications, no comorbidities.

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DISCUSSION
 Periampullary Ca is any Ca within 2 cm of ampulla of Vater.
 Duodenal adeno Ca is commonest type.
 A small proportion of Ca head of pancreas are periampullary

FAQs
1. Define jaundice, clinical, Benjamin classification
2. Anatomy of hepatobiliary system and Bilirubin metabolism
3. Causes of obstructive jaundice
 Intraluminal: Choledocholithiasis (primary-within CBD , secondary- from
GB) , Foreign body (stent), Parasites like ascaris, clonorchis (Do NOT say
liver flukes, and say this cause last)
 Intraductal: Tumors (periampullary, cholangio Ca), stricture, atresia,
choledochal cyst
 Extraluminal: CA head of pancreas, LNE of porta hepatis (CA stomach
commonly metastasizes here), Vascular anomalies like trihepatic artery
4. Courvoisier’s law and its exceptions: (very very important)
In obstruction of the common bile duct due to a stone, distension of the
gallbladder seldom occurs; the organ usually is already shriveled.
Exceptions:
a) Double impaction of stones(one in cystic and other in CBD)
b) Oriental cholangiohepatitis
c) Pancreatic calculus obstructing ampulla of Vater
d) Mucocoele of GB due to stone in cystic duct
e) Nodes in porta hepatis
f) Ca GB with multiple mets to the liver
5. Courvoisier’s sign: Palpable, non tender GB
6. Trace malignancy from Ca pancreas to left supraclavicular LN
Ca→ Porta hepatis→ Pre and para aortic LN→ Cisterna chyli(T12 level) →
Thoracic duct→ Jn of brachiocephalic and IJV→SC LN
7. Causes of abd distension(rare) in obstructive jaundice:
i.Hypoalbuminemia
ii. Peritoneal deposits
iii. Liver secondaries
iv. Portal HTN
v. Gallstone ileus
8. Study types of gallstones and pathophysiology of stone formation:
Cholesterol stone, Pigmented stone (brown, black), Mixed stone

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MANAGEMENT
Investigations
1.Complete blood count
2. LFT:
i. Bilirubin(Nl:0.2-1.2mg/dL;clinical jaundice when> 2.5): Direct/conj fraction
elevated (>20% of total bilirubin)
ii. ALP (40-140IU/L) : >4 times upper limit → check for GGT and
5’nucleotidase elevation.
These 3 enzymes are markers of cholestasis
iii. Serum albumin for nutritional status
3. Urine: Urobilinogen absent
4. USS: Intrahepatic biliary radicle dilatation
Normal CBD: 5-8mm (>8mm is abnormal)
CHD: upto 4 mm
IHBR: normally not visible
Other findings may be: distended gall bladder, ascites, calculi, liver
secondaries
5. CECT: Investigation of choice
All findings in USS + tumor site, vascular invasion and lymph node
involvement can be seen
6. ERCP:
i. Used when there is no mass on CT and you want to confirm, and for
ii. Stenting in unresectable cases to relieve obstruction,
iii. To take biopsy before chemotherapy Look for any lesion, at ampulla also,
if present, biopsy, if not, stenting can help restore albumin as obstruction is
relieved. Then if no secondaries present, surgery can be done.

Preop stenting is done

a. when there is a delay between diagnosis and surgery with the patient
deeply jaundiced(>15) and pruritic,
OR
b. features of cholangitis (here, after stenting, give antibiotics)
OR
c. (c)low albumin
OR
d. coagulation failure not responding to vitamin K.

Look for signs of inoperability(see under surgery) and also CT chest to rule out
distant mets
7. CA 19-9: Follow up

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Staging
T1 <2cm; N1 1-3 Ln M1-distant mets
T2 2-4cm; N2 4or more Ln
T3 >4cm;
T4 invades adjacent structures,coeliac trunk, common hepatic artery,SMA
Stage I- T1, T2 – surgery indicated
II- all between I and III- surgery
III- any T4, any N2- Neoadjuvant chemo, then surgery
IV- Mets- Palliative surgery and chemo

TREATMENT
Pre op preparations
i. Nutrition status: Albumin corrected by nutrition, NOT by infusion; at least
to 3 (NL is 3.5-5 mg/dL)
ii. Hydration by skin pinchability, dry tongue
iii. Prothrombin time: corrected with Vitamin K, FFP
iv. Cardiac status: Ejection fraction
v. Respiratory status: PFT. Incentive spirometry to improve function, ideally
preop
vi. Adequate blood transfusion
vii.Prophylactic antibiotics: 30 min to 1 hr before skin incision
Easier to remember:
A-correct anemia
B-broad spectrum antibiotics
C-cholestyramine (itching)
D-biliary drainage
E-electrolyte correction
F-fluid correction i.e. hydration decreases jaundice
Vitamin K 10mg IM X 5 days
Mannitol to flush kidney. bilirubin is large, difficult to pass mesangium
TPN if needed

PPPD(Pylorus Preserving PancreatoDuodenectomy)

3 steps: Exploration and assessment, Resection, Reconstruction
1. Exploration and assessment
Signs of inoperability:
i. Peritoneal metastases
ii. Liver metastases
iii. Ascites with malignant cells

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 iv. Infiltration to IVC
v. Unreconstructable portal vein
vi. Invasion to coeliac trunk, common hepatic artery, SMA

2. Resection: order is BSJP (Biliary tract, Stomach, Jejunum, Pancreas)

Cholecystectomy + Proximal 10cm jejunum from DJ flexure +
Pancreaticoduodenectomy and a local lymphadenectomy (retroperitoneal
nodes)
In the original Whipple’s surgery,-40% distal stomach, ie gastric antrum also
removed.
Structures removed: Gallbladder, lower end of CBD, C loop of duodenum,
Head and neck of pancreas, distal 40% of stomach, proximal 10cm of jejunum

3. Reconstruction: order is P B Sreenivas (Pancreas, Biliary, Stomach) PJ + CCJ +

GJ
Adjuvant chemotherapy
 With 5FU orgemcitabine for 6 months in resected duodenal adenoCA
Palliation is important: Study Box 68.10,Bailey
i. Relieve jaundice and treat biliary sepsis
ii. Improve gastric emptying
iii. Pain relief
iv. Symptom relief and quality of life
v. Consider chemo

MANAGEMENT in gallstones: Investigations similar.

 Indications of cholecystectomy:
(a)Acute cholecystitis
(b)Chronic cholecystitis
(c)Solitary stone > 10mm size if in Hartmann’s pouch
(d)Multiple stones
(e)Gallbladder polyp > 10mm diameter (prophylactic).

 Prophylactic cholecystectomy in silent gallstones:

(a)Diabetics or immunosuppressed patients
(b)Porcelain GB
(c)Large stones (>2.5cm)
(d)Candidates for renal transplant

 Study steps of cholecystectomy

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 Test Prehepatic Hepatic Post hepatic
Total bilirubin Normal or Increased Increased
increased
Conjugated Normal Increased Increased
Unconjugated Normal or Increased Normal
increased
Urobilinogen Normal or Increased Decreased/-ve
increased
Urine color Normal Dark Dark
Stool color Normal Paler Paler

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 PAROTID SWELLING

Presenting Complaints
 Swelling
 Onset, Duration, Progression, Any sudden enlargement recently
 Whether the swelling increase in size, becomes tense and painful during
meals - characteristic of parotid duct calculi
 Pain
 Throbbing pain - Parotid abscess
 Colicky pain during meals - Parotid duct calculi or stricture
 Ear lobe numbness (“falling of ear rings” or “injury during shaving” may be
a hidden history!!)- due to the involvement of the Great Auricular nerve
 Ear pain (referred pain due to the involvement of Auriculotemporal nerve)
 Watery discharge from the parotid region (Parotid fistula)
 Malaise/Weight loss/Night sweats - Leukemia and Lymphoma can cause
B/L parotid enlargement
 Drying of eyes and mouth along with joint pain - Sjogren’s syndrome

Past Medical History

• Recurrence of parotid swelling (Pleomorphic adenoma, Subacute /Chronic
parotitis, Lymphoma, Leukemia)
• “MCH” history (Mumps,Collagen diseases,HIV)
• Diabetes mellitus (sialadenosis)
•Cirrhosis liver (B/L parotid swelling belongs to stigmata of chronic liver
disease)
•Recent illness, Major surgery

Note : “reduced salivary flow secondary to dehydration results in ascending

infection via the parotid duct into the parotid parenchyma”

Drug History
“PATH” drugs cause sialosis/sialadenosis:
• Anti-Psychotic drugs
• Anti-Asthmatic drugs
• Anti-Thyroid drugs
• Anti-Hypertensive drugs

Personal History
• Alcoholism ( causes sialadenosis,CLD)

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• Bulimia-eating disorder (causes sialadenosis)

Local Examination
Inspection
• Ear lobule raised (“PARA” - around; “OTIC” - ear) - Examiner should stand
behind the patient and compare the level of both ear lobules
• Obliteration of the normal hollow just below the lobule of the ear
• Size,shape and extend of the swelling ; Curtain sign (A parotid swelling
never extends above Zygoma as the strong parotid fascia is attached to it)
• Skin over the swelling (any ulceration)
• Deviation of angle of mouth (due to facial nerve palsy in malignant parotid
tumour)
• Inspection of Oral cavity (look for Oral hygiene, Opening of Stenson’s duct
[blood and pus], Position of Tonsil-whether pushed medially which is a feature
of deep lobe involvement)
• Inspection of the Ear (local pathologies) ; it may be the culprit of facial nerve
palsy and not parotid!!

Palpation
• Consistency,Margins and Surface of the swelling (Cystic Parotid tumour-
Warthin’s tumour)
• Check for masseter fixity of the swelling (after asking the patient to clinch
his teeth, mobility of the swelling is tested)
• Bimanual palpation of deep lobe of parotid
• Bidigital palpation of Stenson’s duct(parotid duct)
• Check for signs of facial nerve palsy
• Check for LN palpability (Pre-auricular, Parotid and Submandibular LN are
mostly involved)
• Check for movements of jaw (it is restricted if growth is malignant and has
involved the periarticular tissue of TMJ; also, trismus is a feature of parotitis)
and fixity of the swelling to the jaw
• Palpate the superficial temporal artery and comment ‘pulsation normal/
absent’
• Examine the ear (Tragus sign positive in otitis externa)

Systemic Examination
• Examine the eyes, lacrimal glands if you suspect Mikulicz’s syndrome or
Sjogren’s syndrome

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• Findings may be elicited in respiratory, cardiovascular, GIT, nervous,
musculoskeletal and urinary systems if the parotid involvement is due to
autoimmune/collagen vascular diseases like SLE, RA, etc.,
• Massive splenomegaly (>8cm/crossing the midline) is seen in CML (Chronic
myeloid leukemia)
• Systemic findings may be elicited in HIV also
DIAGNOSIS
• Broadly, you can put forward your diagnosis in 2 ways :
“Parotid swelling (Right/Left/Bilateral), probably Parotitis
(Acute/Subacute/Chronic) / Parotid Abscess”
OR
“Parotid Tumour,probably Benign/Malignant”
• Co-morbidities like DM, HTN, etc., should be mentioned along with the
diagnosis
Friends,the immediate question after you put forward your diagnosis (in case
of parotid tumour)

DISCUSSION
Presenting complaints
1)Swelling
• Onset
• Duration
• Progression (Growth rate)
• Exact site (Warthin’s tumour almost always arises in the lower part of the
parotid gland, overlying the angle of the mandible)

Note the following points:

 Sudden onset of swelling with or without pain - Acute parotitis
 Brawny oedematous swelling of the parotid region with pain - Parotid
abscess
 A slow growing parotid swelling for years - Pleomorphic adenoma
 A slow growing parotid swelling suddenly starts growing rapidly -
Malignant transformation of
 adenoma
 Generalized enlargement of all major salivary glands including lacrimal
glands - Mikulicz’s syndrome
 Dry eyes+ Dry mouth + Arthritis - Sjogren’s syndrome
 Fever+ Parotid swelling + Anterior uveitis + Facial palsy - Heerfordt’s
syndrome

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  Parotid swelling becomes tense,tender and enlarging during meals -
Parotid duct calculi

Note: “Calculus is rarely formed in the parotid gland as the secretion is watery”

Q) Are parotid duct calculi radioopaque or radiolucent?

Ans) Radiolucent [Submandibular duct calculi (80%) are radioopaque (BAILEY )]

2) Pain
Pain is associated with parotid swelling in the following 4 conditions:
• Acute parotitis
• Parotid abscess - ‘Throbbing pain’
• Parotid duct calculi/strictures - ‘Colicky pain’ during meals
• Malignant transformation of adenoma

3) Watery discharge from the parotid region

• It is significant of a parotid fistula
• It is particularly seen during meals

4) Ear Pain
It occurs due to the involvement of Auriculotemporal nerve, which is related to
the upper pole of the parotid gland. The nerve supplies External auditory canal
too which is the cause of otalgia.

Q) “Features suggestive/indicative of malignancy in parotid swelling”.

 Facial Nerve weakness
 Rapid enlargement of the swelling in short time
 Induration or Ulceration of the overlying skin
 Cervical node enlargement

Note: “Unfortunately, pain is not a reliable indication of malignancy as benign

tumours often present with pain in the affected gland, presumably due to
capsular distension or outflow obstruction” (Bailey). So, comment ‘pain’ as an
indication of malignancy as last but never first!!

Past Medical History

1.Recurrent swelling of parotid gland is a feature of subacute /chronic
parotitis. Other features of them are as follows:
• U/L or B/L

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• Particularly seen during meals
• Gland feels firmer,slightly tender and rubbery
• Purulent/Watery saliva is ejected from the opening of Stenson’s duct while
gentle pressure is exerted over the gland
[Note : Diabetes mellitus,Pleomorphic adenoma,Lymphoma,Leukemia should
also be kept in mind in case of ‘recurrence’+

2.”MCH” history (Mumps,Collagen diseases,HIV)

Q) Does mumps causes suppurative or non-suppurative parotitis?

Ans) Non-suppurative

Q) Is ‘fluctuation’ an early or late feature of suppurative parotitis?

Ans) Late feature!! This is due to the presence of strong parotid fascia
Q) HIV and Parotitis??
Ans) “Chronic parotitis in children is pathognomonic of HIV infection”!!
Q) Name the systemic diseases causing parotid enlargement/infiltration?
Ans) Diabetes mellitus, Lymphoma, Leukemia, Sjogren’s syndrome, Sarcoidosis,
Amyloidosis

Local Examination
Inspection and Palpation
• Describe the swelling with reference to proper anatomical points like ear
lobule, angle of mandible, mastoid, etc.,
• Raising of ear lobule is a very characteristic feature of parotid swelling ; if
present, it should be mentioned without
• “Obliteration of the normal hollow just below the ear lobule” should be there
in presentation because that is the location of ‘parotid fossa’ where the gland
lies.

Great clinicians say this, “A swelling in the region of parotid fossa arises from
the
parotid unless proved otherwise”!!

Never forget to inspect and palpate the oral cavity in a parotid case; Comment
on the oral hygiene (a common predisposing factor of acute parotitis) ,opening
of the Stenson’s duct- opposite the crown of the 2nd upper molartooth and
any medial displacement of the tonsil (due to the deep lobe involvement)

Q)What are the boundaries of parotid fossa/parotid bed/parotid mould?

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Ans)
 Front - Posterior border of ramus of mandible + Medial pterygoid and
Masseter muscles attached to the ramus
 Behind - Mastoid process and Sternocleidomastoid muscle
 Above - External auditory canal and posterior part of TMJ
 Below - Posterior belly of Digastric and Stylohyoid muscles
 Medially - Styloid process and Styloid group of muscles

***There is slight difference b/w boundaries of parotid fossa and the surface
marking of parotid gland.

Surface marking of Parotid gland

• Superiorly - Upper border of the mandibular condyle
• Inferiorly - 2cm Posteroinferior to the angle of mandible
• Anteriorly - Just above the centre point of masseter muscle
• Posteriorly - Upper part of the anterior border of mastoid
Surface marking of Parotid gland duct (Stenson’s duct)
 About 1 fingerbreadth below the inferior border of the Zygomatic bone
OR
 Middle-third of the line joining the midpoint b/w the ala of the nose and
the red margin of the upper lip AND the lower border of the concha of
the ear

Note : Posterior belly of the digastric muscle is an excellent anatomic landmark

because behind it are the carotid arteries, jugular vein, cranial nerves X, XI,
and XII, and the sympathetic chain.
Q) Other than the anatomic location, what are the clinical points to diagnose a
parotid swelling?
1. It is deep to parotid fascia (checked by asking the patient to open the
mouth; fascia becomes taut and the swelling becomes less prominent)
2. It is superficial to masseter (checked by asking the patient to clinch his
teeth; muscle becomes taut and the swelling becomes more prominent)
3. Curtain sign : A parotid swelling never extends above the Zygoma as the
strong parotid fascia is attached to it
Q) How will you differentiate a parotid swelling from pre-auricular LN?
Ans) Pre-auricular LN is outside the capsule of the gland; it is very mobile
unlike parotid swelling which has got restricted mobility. It may extend above
the zygomatic arch.

261
Q) How will you differentiate parotid swelling from parotid lymph node
enlargement?
Ans) Both are located deep to parotid fascia; contraction of
sternocleidomastoid is helpful here.
 Parotid LN is located under sternocleidomastoid; therefore it becomes
less prominent on contraction of the muscle while,
 Parotid swelling is located over sternocleidomastoid; therefore it shows
minimum change in size on contraction of the muscle

Q) Give the origin, insertion, nerve supply and action of Masseter and
Pterygoid muscles?
Ans) Masseter
• Origin : Zygomatic arch and Zygomatic process of maxilla
• Insertion : Lateral surface of Ramus of the mandible and Coronoid
process of the mandible
• Nerve supply : Masseteric nerve (a branch of anterior division of
mandibular nerve)
• Action : Elevates mandible to close the mouth to bite

Medial Pterygoid
• Origin : Maxillary tuberosity, medial surface of Lateral pterygoid plate
and adjoining Process of Palatine bone
• Insertion : Medial surface of Angle and adjoining Ramus of mandible
• Nerve supply : Nerve to Medial Pterygoid (branch of the main trunk of
Mandibular nerve)
• Action : Elevates and Protrudes mandible
Lateral Pterygoid
• Origin : Greater wing of sphenoid and lateral surface of Lateral pterygoid
plate
• Insertion : Neck of mandible (pterygoid fovea) and Capsule of TMJ
• Nerve supply : A branch from anterior division of Mandibular nerve
• Action : Depresses and Protrudes mandible
Q) How do you check for styloid group of muscles clinically?
Ans) Ask the patient to swallow saliva while he pushes his tongue against the
soft palate. The patient is unable to perform this in case of styloid muscle
group involvement by the tumour !!
Q) What are the attachments of the parotid capsule?

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Ans) Parotid capsule is formed by the investing layer of the deep fascia which
splits b/w the angle of the mandible and the mastoid process into ‘superficial’
and ‘deep’ lamina
 The superficial lamina (thick)-k/a Parotid fascia is attached above to the
zygomatic arch
 The deep lamina (thin) is attached to the styloid process,the mandible
and the tympanic plate
 A portion of the deep lamina extending b/w the styloid process and the
mandible,is thickened to form the stylomandibular ligament which
separates the parotid gland from the submandibular salivary gland

Signs of Facial Nerve Palsy (Motor function)

• Unable to move the eyebrows upward
• Unable to close the eyes
• Paralysed side blows out more when asked to puff out the cheeks
• Deviation of angle of mouth to the normal/healthy side when asked to
show his teeth
Facial nerve is k/a “Queen of the Face” !!

Q) How do we check TMJ (Temperomandibular joint)??

Ans) 2 methods (clinician stands behind the patient):
Place the fingers over the joint just below and in front of the tragus to
appreciate the movements of the condyle (ask the patient to open and close
the mouth)
OR
Insert a little finger into the external ear with the pulp directed forwards and
then
appreciate the movements of the condyle (ask the patient to open and close
the mouth)
Q) How do you test for mandibular (lower jaw) involvement in a parotid
tumour?
Ans) ’Bimanual palpation’ is adopted for testing mandible (lower jaw)
 Put one finger inside the mouth and the fingers of the other hand are
applied externally and the swelling is palpated
Note : Organs in the body that are ’Bimanually palpable’ : Deep lobe of Parotid,
Submandibular gland, Mandible, Kidney, Intestine, Uterus

Q) How do you grade ‘trismus’?

Ans) Grading of Trismus is as follows (distance b/w the upper and lower
incisors when the jaw is fully opened is taken into consideration for grading):

263
  Grade 1 : 2.5 - 4cm
 Grade 2 : 1 - 2.5cm
 Grade 3 : < 1cm
Q) How do you differentiate ‘inflammatory trismus’ from ‘tetanic trismus’?
Ans) Tetanic trismus is abolished by general anaesthesia while inflammatory
trismus is not!!
Q) Name 4 common DD’s of mandibular swellings?
 Epulis (Arising from the mucoperiosteum)
 Odontomes (arising from the tooth germs) - eg.,Dental cyst, Dentigerous
cyst, Adamantinoma
 Osseous tumours
 Inflammatory swellings (Alveolar abscess, Osteomyelitis, Actinomycosis)

Note: A long history of a slow growing large tumour with ‘Egg-shell crackling’ is
suggestive of Adamantinoma

Q) Name the common benign tumours of parotid?

1. Pleomorphic adenoma (MC swelling/tumour of parotid)
2. warthin’s tumour /Adenolymphoma/ Papillary cystadenoma
lymphomatosum (2nd MC benign tumour of parotid)
3. Oxyphil adenoma(Oncocytoma) : “When Warthin’s tumour becomes
devoid of lymphoid element and is composed entirely of epithelium it is
called an oxyphil adenoma”

Q)Name the malignant tumours of parotid(in order of frequency)?

1. Mucoepidermoid carcinoma (MC malignant tumour of parotid)
2. MMT (malignant mixed tumour)
3. Acinic cell carcinoma
4. Adenocarcinoma
5. Adenoid cystic carcinoma (It shows PERINEURAL INVASION; It is the
MC salivary gland tumour in children!! It never metastasizes to LN but
via blood to lungs!!!)
6. Squamous cell carcinoma(Epidermoid carcinoma)

Note : ‘3’ and ‘5’ are Low grade tumours , while ‘4’ and ‘6’ are High grade
tumours. ‘1’ has got both low grade and high grade varieties

Q) Name the malignancies that arise from pleomorphic adenoma?

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 1. Carcinoma ex- pleomorphic adenoma (Carcinoma arising from
pleomorphic adenoma) It is the carcinoma parotid with worst prognosis
(5-yr survival rate is <40%)
2. de novo malignant mixed tumour (Benign pleomorphic adenoma that
metastasize)

Q) Which parotid tumour is ‘cystic and fluctuant’?

Ans) Warthin’s tumour ,Though cystic and fluctuant, Warthin’s is not
translucent

features of Warthin’s Tumour**

 Soft and Fluctuant, Non-translucent parotid tumour
 Lower pole location of parotid overlying the angle of the mandible
 Very strong association with ‘Males’ and ’Smoking’
 10% Bilaterality
 ‘Hot Spot’ in Tc99m scan
 No malignant potential
*Note: A female with Warthin’s tumour is very very rare +

Management of Parotid Tumour

Investigation
1. FNAC is the investigation of choice for parotid tumours.It can distinguish
between benign and malignant tumours
2. If you suspect deep lobe involvement or there is trismus, order for CT
3. If facial nerve is involved, order for MRI
4. Tc 99m scan if Warthin’s tumour is suspected (it reveals a ‘hot spot’ due to
high
mitochondrial content within the cell)
Note: Biopsy is contraindicated in parotid tumours for the following reasons :
 Seeding of the tumour will occur
 Chance of parotid fistula
 Chance of facial nerve injury
[BAILEY says, “open surgical biopsy is contraindicated unless malignancy is
suspected,and preoperative histological diagnosis is required as a prelude to
radical parotidectomy”+
Q) Give 2 malignancies where the use of FNAC is contraindicated?
Ans) Testicular cancer
Malignant melanoma
Q) What is the indication of OPG (Orthopantomogram) in Parotid tumour?
Ans) To evaluate mandibular invasion/fixity of a parotid tumour
265
  OPG shows a 2-D view of a half-circle from ear to ear. An OPG relies on
tomography i.e. images of specific radiographic planes are taken to
make up the larger panoramic image
 OPG is also k/a DPR (Dental Panoramic Radiograph)

TREATMENT (Surgery and RT)

1.Surgery
• Superficial parotidectomy ( if only superficial lobe is involved, except in
indications for radical parotidectomy)
• Total conservative parotidectomy (if both superficial and deep lobes are
involved without involvement of facial nerve, or deep lobe alone is involved,
except in indications for radical parotidectomy)
• Radical parotidectomy (in case of high grade malignant tumours and
squamous cell carcinoma).It includes
 Removal of all parotid gland
 Elective sectioning of the facial nerve
 Removal of ipsilateral masseter muscle
Note: however malignant the tumour may be, if the facial nerve
is NOT involved, don’t sacrifice it.

Q) What are the surgical landmarks of facial nerve?

• Conley’s Pointer - The Inferior portion of the Cartilaginous Canal.The facial
nerve lies 1cm deep and inferior to its tip
• Upper border of the Posterior Belly of Digastric muscle.The facial nerve is
located immediately superior to it
• The Stylomastoid artery (branch of Posterior Auricular artery which is a
branch ofExternal carotid artery) lies immediately lateral to the facial nerve

Remember,The Main trunk of the facial nerve is always located in the triangle
formed by the mastoid, the angle of the mandible, and the cartilaginous ear
canal, medial to the mastoid

Q) What is ‘Plane of Patey’?

Ans) It is the plane where the facial nerve is seen superficial to the posterior
facial vein in the substance of the parotid gland. It is also k/a Faciovenous
plane of Patey.
Q) What is the order of relation (from superficial to deep )for the following
structures within in the parotid gland?
ECA (External Carotid Artery) , RMV (Retromandibular Vein), Facial nerve
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Ans) Facial Nerve, RMV, ECA
Q) Which 2 branches of facial nerve are to be preserved to the maximum
during parotid surgery?
Ans) Zygomatic branch (injury causes inability to close the eyes)
Marginal mandibular branch (injury causes deviation of the angle of mouth)

2.Radiotherapy

Dose : 50-70Gy in 5-8 weeks time

Timing : 3-6 weeks after surgery
Indications:
• Size more than 4cm/extraparenchymal extension
• Skin,ear canal,mandible,facial nerve,carotid artery or skull base
involvement
• High grade tumours
• Deep lobe involvement
• Perineural/Vascular invasion
• Multiple LN involvement
• Close margins
Q) Is there any indication for RT in case of pleomorphic adenoma?
Ans) After surgery for recurrence
Q) What are the indications for RT in malignant parotid tumours?
Ans) Though the indications were given above,the most important ones are the
following :
 LN positivity
 Margin of excision not clear
 High grade tumours
 Residual tissue

Q) Is there any role for CT (chemotherapy) in Parotid tumours?

Ans) NO

Q) How do you manage positive LN in parotid malignancy?

Ans) Radical neck dissection

Q) Give the 2 major complications of parotid surgery and the Rx for them?
1. Facial nerve injury
Rx : Repaired using Sural nerve Cable graft
2. Frey’s syndrome (“Gustatory sweating”)
Rx : Antiperspirants (aluminium chloride)

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 Tympanic neurectomy
Injection of BOTOX (Botulinum toxin injection ; it is simple and effective
but costly)
Q) How do you prevent Frey’s syndrome pre-operatively?
Ans) The principle is the placement of a barrier b/w the skin and parotid bed to
prevent inappropriate regeneration of autonomic nerve fibres
(Auriculotemporal nerve) after surgery. This is achieved by
 Temporalis fascial flap
 Sternomastoid muscle flap
 Artificial membrane b/w the skin and parotid bed

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 VARICOSE VEINS
History Taking
Presenting Complaints
• Dilated veins over leg/lower extremities (Cosmetic complaints
especially in women)
• Pain/Heaviness (whole of the leg/part of the leg)
• Ache/Cramps
• Ankle swelling/Ulcer/Bleeding
• Itching/Restless leg/Paraesthesia
• Abdominal/Pelvic complaints (Abdominal and Pelvic tumours may
present as varicose veins!)
Past Medical History
• Any surgery (Pelvic/Lower limb surgeries) underwent
• Any major illness requiring prolonged recumbency - DVT
Drug History
• Use of OCP’s - DVT
Personal History
• Prolonged standing posture (Policemen, Teachers,Surgeons,etc.,)
• Prolonged sitting posture(eg.,Computer professionals) - “E
Thrombosis”
• History of “white leg” during previous pregnancies (due to swollen
limb from excessive oedema or lymphatic obstruction)
• Recent long air travel (Economy class syndrome) - DVT
Family History
• Any family members suffering from varicose veins?? (Often patient’s
mother and sisters might have suffered from this disease); Inherited mutations
of “FOXC2 gene” is responsible for this

Examination of Varicose Veins

1.Inspection
• Examine the patient in standing position
• Expose the patient from umbilicus to toes
• Check for inequality of circumference of lower limb
• Identify the anatomical distribution of the varicose veins(Long
saphenous /Short saphenous /Both are involved)
• Describe any swelling and skin of the limb (colour and texture)
• Morrissey’s test (Ask the patient to cough; look for impulse on
coughing at the saphenous opening; known as SAPHENA-VARIX)
2.Palpation
The essential tests to be performed are:
269
 • Brodie-Trendelenburg Tests 1 & 2 (To identify saphenofemoral and
perforator incompetences respectively)
• Multiple Tourniquet Test (To identify which perforator is incompetent
if Brodie-Trendelenburg test 2 is positive)
• Modified Perthes’ Test (For noting the patency of deep veins and to
rule out DVT)
3.Percussion
• Schwartz Test : If the most prominent parts of the varicose veins are
tapped,an impulse can be felt by the finger at the saphenous opening
4.Auscultation
• Continuous machinery murmur is heard in A-V fistula ,which is an imp.
DD of Varicose veins
5.Examination of Regional LN : Inguinal LN are enlarged in case of venous
ulcer
6.Examination of Arterial system : Check for pulsations
7.Examination of the other limb
8.Systemic Examination : Examine the abdomen (including per rectum)
thoroughly to rule out abdominal/pelvic tumours like fibroids,ovarian
cyst,Ca cervix,Ca rectum and abdominal lymphadenopathy which may cause
pressure on the external iliac vein leading to secondary varicosity

DIAGNOSIS
“Varicose veins, left lower limb/right lower limb/bilateral, probably Primary
OR Secondary, with or without complications” with/without Co-morbidities like
DM,HTN,etc.

Primary Varicose Veins(85%) - Cause is not known after your clinical

examination
•‘Wall theory’-weakness of vessel walls
• ‘Valve theory’ - weakness of valves
Secondary Varicose Veins(15%) - mainly due to 4 entities:
• Obstruction to venous outflow(Abdominal/Pelvic tumours, Pregnancy,
Ascites ,Iliac vein thrombosis, etc.)
• Destruction of valves - from DVT (Post - phlebitic syndrome)
• High pressure flow - from A-V fistula
• Post traumatic
Note: Never forget to examine the abdomen in a varicose vein case..!

Complications of varicose veins

(remembered by the pnemonic “PHD after LP and UP”)
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 • Phlebitis (Varicose veins become extremely tender and firm. The
overlying skin becomes red and oedematous)
• Haemorrhage
• Deformity (like equinus deformity in a case of long-standing ulcer.If the
patient finds that toe-walking relieves pain, he continues to do so and
ultimately the Achilles tendon becomes shorter to cause this defect)
• Lipodermatosclerosis (Skin becomes thickened,fibrosed and pigmented
due to FIBRIN accumulation around the capillary-DUE TO HIGH VENOUS
PRESSURE- and it activates the white blood cells)
• Pigmentaton/Eczema
• Ulceration
• Periostitis (In case of long-standing ulcer over the tibia ; will be felt as
irregularity of bony surface of tibia-shin region)

DISCUSSION
History-Taking
• The symptomatic complaints of varicose veins like aching, swelling,
cramps, heaviness, itching become evident and aggravate towards the
evening ; they are usually absent in the morning!
• Don’t relate the size of the veins with the severity of the symptoms ;
often, symptoms are more severe during the early stages of the
development of varices
• If the patient complains of bursting pain while walking and there is
history of night cramps, it indicates Deep vein thrombosis(DVT); any
other clue towards DVT like prolonged recumbency for any illness, use of
OCP’s should be elicited by the examiner from history because if there
are features of DVT in a varicose vein patient, you should not post the
patient for Varicose vein surgery; the patient will end-up in losing his/her
leg due lack of venous circulation in the limb - causing Edema followed by
Gangrene!! The reason for the above is simple. 90% of venous blood in
lower limb is carried by deep venous system. So, whatever venous
circulation going on in a DVT patient is by the superficial venous system
(which is only 10% of the total).So if we manipulate the superficial venous
system during varicose vein surgery in a DVT patient, the functioning 10%
of venous circulation is destroyed. In result, patient will be devoid of
blood circulation in the lower limb concerned.
“Deep vein thrombosis is mostly an asymptomatic disease. Only one-
fourth of the cases of deep vein thrombosis present with minor
complaints.”

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Examination of Varicose Veins
Inspection
• Identify which vein has been varicosed - Long saphenous/Short
saphenous/Both.
• Localised swelling is a feature of varicose veins or superficial
thrombophlebitis while generalised swelling of the leg is mostly due to
DVT
• Phlegmasia alba dolens (White leg) - due to excessive oedema or
lymphatic obstruction (eg.,pregnancy)
• Phlegmasia cerulea dolens - congested and blue limbs due to DVT
Palpation
Essentially, 3 tests are to be done:
• Brodie-Trendelenburg Tests 1 & 2 (To identify sapheno-femoral and
perforator incompetences respectively)
• In Test 1,pressure at the sapheno-femoral junction is relieved suddenly
(to test for sapheno-femoral incompetence)
• In Test 2,pressure at the sapheno-femoral junction is continued (to test
for perforator incompetence)
• Named perforators (of long saphenous vein) are remembered by the
pnemonic “ Delhi, Bombay, Calcutta to Madras”, that is
 Dodd’s perforator : Mid-thigh perforator
 Boyd’s perforator : Gastrocnemius perforator
 Cockett’s perforators(3) : Leg perforators- 5,10 and 15cms above
the medial malleolus
 May’s/Kuster’s perforator : Ankle perforator
Q)Name one named perforator of short saphenous vein?
Ans) Bassi’s perforator (5cm above the calcaneum)
• Multiple Tourniquet Test (To identify which perforator is incompetent
if Brodie-Trendelenburg test 2 is positive)
4 Tourniquets are required for this test:
 1st tourniquet is tied at the ankle
 2nd tourniquet below the knee
 3rd tourniquet above the knee
 4th tourniquet below the saphenous opening

Note: For the Brodie-Trendelenburg Tests and Multiple Tourniquet Test,veins

are first emptied by elevation of limb and then occlusion by pressure or
tourniquet is done.For the Modified Perthes’ Test described below,there is no
need to empty
the veins prior to applying the tourniquet.
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 • Modified Perthes’ Test (For noting the patency of deep veins and to
rule out DVT)
if the test is positive, it is an absolute contraindication for varicose vein
surgery!!
Q) What is the difference between Perthes’ Test and Modified Perthes’ Test?
Ans) In Perthes’ test,the whole lower limb is wrapped with elastic bandage
WHILE In Modified Perthes’ Test, single tourniquet is tied in the upper part of
the thigh. The objective of elastic bandage/tourniquet is to prevent any reflux
down the the superficial venous system and thus check the patency of deep
venous system. For that, single tight tourniquet to occlude the superficial
system is enough!!

Percussion
Schwartz Test : Tap the most prominent parts of the varicose veins and
check for the impulse at the finger placed at SAPHENOUS OPENING
Note: Saphenous opening is located 4cm inferolateral to pubic tubercle
BUT Sapheno-femoral junction is located 2.5cm inferolateral to pubic tubercle

Auscultation
An important DD of varicose veins is Arterio-Venous Fistula(A-V Fistula)
In a case of A-V fistula,we get a continuous machinery murmur over the
dilated vessels
Q) Give one clinical sign to confirm A-V fistula?
Ans) Nicoladoni-Branham sign
To elicit this sign,press an artery proximal to the fistula.This causes:
• Reduction in the size of dilated vessels
• Disappearance of murmur
• Reduction in heart rate
• Normalisation of pulse pressure

Q) Define ‘Varicose veins’?

Ans) The pathological dilated,tortuous veins in the body are called varicose
veins
Q) Describe briefly the anatomy of venous system of leg?
Ans) It consists of Superficial Trunk (lies above muscle fascia) & Deep Trunk
(lies below muscle fascia).
Superficial trunk consists of Greater Saphenous Vein (GSV) and Lesser
Saphenous Vein (LSV)
• GSV joins the FEMORAL VEIN at a point 2.5cm inferolateral to pubic
tubercle (sapheno-femoral junction)

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 • LSV joins the POPLITEAL VEIN at a variable site in the popliteal fossa
(sapheno-popliteal junction)
• Deep trunk arises from 3 pairs of VENAE COMMITANTES and
accompany the 3 crural arteries, namely Anterior tibial, Posterior tibial
and Peroneal arteries.
• The above 3 pairs of venae commitantes intercommunicate to form
POPLITEAL VEIN(in the popliteal fossa)
• Popliteal vein passes through adductor hiatus before entering the
subsartorial canal to form FEMORAL VEIN
• Femoral vein passes behind the inguinal ligament to form EXTERNAL
ILIAC VEIN(EIV)
• EIV joins with INTERNAL ILIAC VEIN (IIV) in the pelvis to form COMMON
ILIAC VEIN (CIV)
• Left CIV joins with Right CIV to form IVC (INFERIOR VENA CAVA)
Q)What is the clinical grading of varicose veins (CEAP Grading)?
Ans)
 Class 0 - No visible/palpable sign of venous disease
 Class 1 - Telangiectasias or Reticular veins
 Class 2 - Varicose veins
 Class 3 - Edema
 Class 4 - Skin changes (Pigmentation,Eczema or Lipodermatosclerosis)
 Class 5 - Skin changes + Healed ulceration
 Class 6 - Skin changes + Active ulceration
Q) What is the pressure at the foot veins during standing and walking?
Ans) During standing - about 100mm of Hg
During walking - about 200-300mm of Hg
Q) Which single phrase explains the pathophysiology of varicose veins?
Ans) Ambulatory Venous Hypertension
Q) What is ‘Champagne bottle leg’ with reference to varicose veins?
Ans) Contraction of the skin and s/c tissue [due to lipodermatosclerosis in long-
standing varicose veins] occurs in the ankle area causing narrow ankle and
prominent calf. This is referred to as ‘Champagne bottle leg’ (also k/a “inverted
beer bottle appearance”).
Q)What is ‘gaiter area’?
Ans) An area immediately above the medial malleolus and less commonly
above the lateral malleolus where skin changes of long-standing venous
hypertension(lipodermatosclerosis,eczema,ulceration,etc.,) are seen is k/a
‘gaiter area’.

MANAGEMENT OF VARICOSE VEINS

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1.Doppler ultrasonography is the minimum investigation to be carried out in
the evaluation of a varicose vein case
It gives details like
 Presence/absence of blood flow
 Identifies reflux
 ‘Biphasic signals’ imply flow in both direction
[Note : Doppler is not suited for detecting LSV incompetence]
2.Duplex ultrasonography
It is a combination of Doppler + B-mode ultrasound,which gives high-quality
pictures.
Advantages of Duplex over Doppler include the following:
 Duplex imaging gives anatomical (eg.,valve pathology), physiological
(eg.,direction)and functional (eg.,flow) details
 Venous flow,lumen,direction and reflux can be visualized
 Site of perforator incompetence can be determined accurately
 Can be used to find out DVT
Therefore, Duplex is the most important non-invasive investigation for
practically all venous disorders.
3.USS of abdomen is ordered for in case of suspicion of an abdominal
pathology that may cause varicose veins (Tumour ,Lymph node, Cyst, Ascites )
4.If a venous/varicose ulcer is present, pus should be sent for Culture &
Sensitivity; in case of longstanding ulcer, scrapings from the edge of the ulcer
should be sent for Biopsy
5.Plain X-ray of the limb - to r/o periostitis or osteomyelitis

TREATMENT
A) If the venous duplex reveals that it is a case of Primary varicose veins,
Trendelenburg Operation with or without Perforator Ligation is the
treatment. Trendelenburg Operation includes ‘SFJ Flush Ligation’ + Ligation
of 5 proximal tributaries. Perforator ligation is done if the duplex reveals
perforator incompetence. Stripping of vein is not practised widely now and
the vein is reserved for CABG surgery in the future, if any!! If Stripping of
vein is done, it is done upto thigh level to avoid injury to Saphenous nerve.
[Note: Stripping is not included under the ‘components’ of Trendelenburg
surgery]
Note:
‘SFJ Flush ligation’ means ligation done as close to the SFJ
The 5 proximal tributaries that are ligated are
 1.Superficial external pudendal vein
 2.Superficial inferior epigastric vein

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 3.Superficial circumflex iliac vein
 4.Posteromedial vein (medial accessory saphenous vein)
 5.Anterolateral vein (lateral accessory saphenous vein)
B) If there is SPJ (sapheno-popliteal junction) incompetence, perform ‘SPJ
Ligation’
C) If there is no SFJ incompetence, Sclerotherapy (Sodium tetradecyl
sulphate, Polidocanol, Ethanolamine oleate, etc.,) can be carried out (thread
veins, spider veins)
D) If the duplex reveals Secondary varicose veins(Deep venous obstruction),
don’t perform surgery;
Rx options are Elastic compression and Valvuloplasty.
Q) What is the mechanism of action of Sclerosing agents?
Ans) “Aseptic inflammation”
Q) What is the post-operative mgt. in varicose veins?
Ans)• Compression bandaging is applied to the limb at the end of the
operation(to prevent bruising)
• After 2 days, the bandage may be replaced with thigh length high
compression stockings
Q) What are the Endovascular procedures available for treating varicose veins?
Ans) Endovenous thermal Ablation using the following catheters:
 Radiofrequency(RF)
 Laser

RF Method
RF catheter treats 7cm segments of the vein (standard size).The RF
generator, k/a VNUS Medical recognizes the catheter type and is
preprogrammed for the appropriate temperature (120o C) and treats the
vein for a 20-second cycle.
Laser Method
 The goal is to utilize enough energy to perform successful ablation,yet
the
minimum effective energy should be used inorder to reduce the side
effects of pain,phlebitis and bruising
 Optimal energy delivery is usually b/w 60 and 100 Joules per linear
segment of vein (Linear Endovenous Energy Density or LEED),ie.,60-
100J/cm of vein.Larger LEED is recommended for the larger or
aneurysmal vein segments
 Wavelength is not as important as the technique.Various wavelength
lasers are available (810,940,980,1064,1320,1470nm)
Q) What is the special local anaesthesia used for Endovascular procedures?

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Ans) Tumescent anaesthesia
Components are:
500cc normal saline + 30cc 1% lidocaine with epinephrine (1:100,000) + 5cc
Sodium bicarbonate. It is warmed to body temperature just before use
Q) Name 3 surgical options for deep venous insufficiency ?(done only in few
centres!)
Ans)
• Kistner Valvuloplasty (vein valve repair)
• Valve Transposition
• Axillary vein transplantation
Q) Name 2 surgical options for deep venous obstruction?
Ans)
• Palma operation (mobilization of GSV from the opposite leg)
• May-Husni Procedure (GSV is connected to popliteal vein to overcome the
obstruction of superficial femoral vein)

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 CARCINOMA STOMACH
Personal details
Age: middle age and above
Sex: more in males
Occupation: stressful job, carcinogens like certain dyes, rubber or coal
workers
Residence: Japan
Presenting complaints
 May be asymptomatic
Any symptom...explain from onset till now
 Features due to local disease:
 Dysphagia(proximal stomach),
 early satiety(middle),
 vomiting(distal),
 anorexia,
 nausea,
 bloating,
 distension.
 Lump may be present(30%) in right hypochondrium or epigastrium.
 Differentiate post prandial fullness from loss of appetite(liver mets)
 Ballrolling sensation-due to gastric peristalsis;if present look for visible
gastric peristalsis
 Features due to infiltration into surrounding structures:
 Epigastric pain with radiation to back (most common because
infiltration is towards stomach bed on posterior side)
 Clasically post prandial pain
 Features of dissemination:
 Supraclavicular lymph node,
 nodules around umbilicus (Sister Mary Joseph nodule),
 axillary LN (Irish node),
 ascites,
 hepatomegaly (abd distension),
 jaundice,
 bone pain,
 lung mets (chest pain, breathlessness, cough, hemoptysis)
 Loss of weight,often profound
 Bleeding causing hematemesis with coffee color vomitus, malena, iron
deficiency anemia (fatigue, poor concentration etc)

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  Thrombophlebitis(Trousseau’s sign), DVT

 Negative history:
 Subacute peptic ulcer perforation: Pain related to food in the past,
fever
 Trichobezoar: Psychological disturbances
 Hepatoma- chronic alcoholism, weight loss with jaundice and abd
distension, edema, impotence, breast swelling
 Amoebic liver abscess-Fever with chills, blood and mucus in stool,
pain referred to shoulder or pain on coughing
 Hydatid cyst-urticaria
 GB(empyema or hydrops)- flatulence, dyspepsia, biliary colic, high
fever with chills and jaundice,blood disorders in family
 Pancreas- no recent acute attack of epigastric pain radiating to back
relieved by stooping, associated with vomiting, diarrhea with frothy
offensive stools, progressive jaundice with weight loss and malena
 Epigastric hernia : dragging pain, discomfort or pain after food
 Transverse colon Ca- alternating constipation and diarrhea with fresh
blood in stool, colicky pain
 TB-History of pulmonary TB
 Lymphoma- swellings in neck, axilla, groin
 Secondaries- no h/o scrotal swelling

Past medical history

 Medical comorbidities affect management
 Any drainage procedures/surgery in the past- stomach bed recurrence
 Joint diseases/related complaints that require NSAID

Drug history
 Painkillers especially (NSAIDs cause gastritis and ulcers)
Personal history
 Diet-spicy food, smoked foods, salted fish and meat
 Sleep-duodenal ulcer disturbs sleep
 Loss of appetite imp in management
 Substance abuse-Alcoholism
Family history
 May be hereditary; first degree relative

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General examination
 Poorly built and nourished, pallor, icterus, dehydration in GOO,
Virchow’s node
Examination in Das-(always include oral cavity exam and PR and hernial
orifices and external genitalia) + visible gastric peristalsis (give a glass of
water) + auscultopercussion (with steth over area, outline stomach by
percussion) + succussion splash + mets found
 Succussion splash should be checked before giving water (to know
GOO). Never check within 2-2.5 hrs after a meal, it will be positive
anyway. If positive after, then GOO.
 VGP is not at all a classical feature of CA stomach (due to infiltration of
wall, peristalsis may even be absent) but rather of pyloric stenosis (left
to right).
 In transverse colon: VGP is right to left
 In SI obstrn: stepladder pattern
Lump of ca stomach-
 intraabdominal (never forget this point),
 hard,
 irregular,
 mildly tender,
 mobility can vary,
 Upper border cannot be defined since hidden under costal margin,
fingers can be insinuated b/w lump and costal margin,
 May or may not move with respiration,
 Disappears with rising test(used for those more to the midline) and leg
lifting test (lateral swelling).
If a swelling moves up down with respiration, definitely intra abdominal, if it
does not, it proves nothing.

DIAGNOSIS
Gastric outlet obstruction, probably due to Carcinoma stomach with
complications and comorbidities if any

Important topics:
1. Blood supply of stomach
2. Premalignant conditions
3. Bormann and Lauren classification
4. Types of gastrectomy and drainage procedures
5. Vagotomy(truncal, selective and highly selective)
6. Pyloroplasty, GIST
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7. Will Roger’s phenomenon is the seemingly better outcome of treatment in
CA stomach patients with adequate pathological staging
8. 3 MC sites of recurrence? Anastomotic sites, gastric bed, regional lymph
nodes
9. The most important prognostic factor? Depth of invasion
 Based on this,early gastric Ca- mucosa or submucosa with or without LN
 Advanced-muscularis and serosa invaded
10. 60% are seen in lower esophagus, OG junction and cardia
11. AdenoCA is commonest
12. Spread of CA stomach:
 Direct- through wall to pancreas, colon, liver
 Lymphatic(in diffuse type)-does NOT imply systemic dissemination
 Hematogenous (in intestinal type): To liver, lung and bone
 Transperitoneal: Ascites, Krukenberg tumor, Blummer shelf, Sister Mary
nodule
13. WHO classification
I. Epithelial tumors
a. Intraepithelial neoplasia- Adenoma
b. Carcinoma
i. Adeno-intestinal, diffuse
ii. Papillary AC
iii. Tubular AC
iv. Mucinous AC
v. Signet ring cell CA
vi.Adenosquamous CA
vii. SCC
viii. Small cell CA
ix. Undifferentiated CA
x. Others
c. Carcinoid (welldifferentiated endocrine neoplasm)
II. Non epithelial tumors
a Leiomyoma
b. Schwannoma
c. Granular cell tumor
d. Glomus tumor
e. Leiomyosarcoma
f. GIST- benign, uncertain malignant potential, malignancy
g. Kaposi sarcoma
h. Others
i. Malignant lymphoma- Marginal zone B cell lymphoma of MALT type

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 Mantle cell lymphoma ,Diffuse large B cell lymphoma, Others
III. Secondary tumors

14. LN stations:

N1 nodes (1-6) N2 nodes (7-11) N3 and N4 nodes Other nodes

1 Right cardiac 7 Left gastric 12Hepatic pedicle 19 Infradiaphragmatic
2 Left cardiac artery 13 Retropancreatic 20 Oesophageal
3 Lesser 8 Common 14 Mesenteric root hiatus
curvature hepatic artery 15 Middle colic 110 Lower esophagus
4 Greater 9 Coeliac artery artery 111
curvature 10 Splenic hilum 16 Para aortic Supradiaphragmatic
5 Supra pyloric 11 Splenic nodes
6 Infra pyloric artery

15. D1 gastrectomy : gastric resection with 2 cm clear margin and perigastric

node (N1) removal
D2 : gastric resection with clear margin +
Omental bursa, greater and lesser omentum, anterior layer of mesocolon,
anterior pancreatic capsule + Perigastric and periarterial LN (N1 and
N2)dissection
Followed by Roux en Y loop reconstruction
16.T1- a-lamina propria, b-submucosa
T2-muscularis propria
T3- subserosa
T4- a-serosa, b-adjacent organsN1: Mets in 1-6 regional nodes
N2: 3-6
N3a:7-15
N3b: >15 the station

17. Study UICC staging (TNM) Bailey Table 63.5

MANAGEMENT

Investigations:
1. Routine
2. Upper GI endoscopy + biopsy (6-7 samples)
3. USS-------if signs of inoperability (see below): palliation. If none,
4. CECT abdomen ------ if mets present: palliation. If none,

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5. CT chest and pelvis -----if mets present: palliation. If none,
6. Staging laparoscopy (posterior fixity, peritoneal mets assessed) -----if mets
present(peritoneal deposits confirmed by biopsy): palliation.
If none,
7.
 T1b,T2 lesions → Surgery and adjuvant chemo
 T3, T4→ Neoadjuvant chemo, reassess with CECT, do surgery and give
adjuvant chemo
8. Other investigations:
 BRE-anemia
 Stool occult blood
 LFT, CXR-for mets
 Endoscopic and laparoscopic USS are most sensitive for staging, pick up
liver mets not seen on axial imaging
 Tumor markers- CEA, CA 19-9
 Ascites tap, cytology
 Barium meal
 FNAC LN

Signs of inoperablility: By the time they present, 50 % are inoperable

 a.M1, T4b
 b.Distant peritoneal involvement
 c.Para aortic LN, supraclavicular LN
 d.Fixity to fixed structures
 e. Sister Mary Joseph nodule

Uses of USS
Tumor location, LN stations, liver mets, ascites, pelvic deposits

TREATMENT

For GOO:
 Fluid and electrolyte correction
 Gastric stasis correction
 Nutritional improvement
 Obstruction relief(G-Jstomy)

For CA stomach:
Multidisciplinary approach- Surgery, Chemo, Radio, Targeted therapy

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Stage I
 Early gastric Ca confined to mucosa (seen in endoscopic USS) and less
than 3 cm (on endoscopic assessment) →Endoscopic mucosal resection
(mucosectomy)
 Early gastric carcinoma involving submucosa and > 2 cm → D1 dissection
gastrectomy (open or laparoscopic)

Stage II and III :

Radical surgery (if operable), palliative treatment (if not)
Principles of radical surgery:
 Tumor excision with clear margin (2cm in EGC and 5 cm in AGC)
 Clearance of LN with one step ahead
Neo adjuvant/adjuvant chemo → T3, T4, N+
 ECF regimen: Epirubicin + Capecitabine + 5FU
 3 cycles pre and 3 post op
 If not detected pre op, give as adjuvant

Stage IV:
 Palliative chemo: ECF regimen
 Indications for intervention:
 Bleeding- arterial embolization
 Obstruction -Surgery, laser or stent
 c.Pain- celiac block
 Non operative treatment preferred like stenting and laser therapy,
 Operative if no improvement-palliative gastrectomy (preferred), bypass
surgery(gastrojejunostomy)
 Radiotherapy can be used for palliation.

Post Operative complications:

 a.Leak of OJ and duodenal stump
 b.Fistula formation
 c.Nutritional deficiency
 d.Dumping and diarrhoea
Follow up:
40-80% recurs in 3 yrs hence this period important
a. Clinical examination every 3 months
b. CT/CXR every 6 months
c. Endoscopy every year
d. Laparoscopy when required
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 RIGHT HYPOCHODRIAL MASS- ENLARGED
LIVER
Relevant Anatomy
It is the largest organ in the body, weighing 1500g. It is surrounded by fibrous
sheath-Glisson’s capsule
Ligaments Associated With Liver
 Round ligament- Remnant of obliterated umbilical vein
 Falciform ligament
 Ligamentumvenosum- obliterated ductusvenosus
 Triangular ligaments –Right and left
 Coronary ligaments
Segmental Anatomy
Liver separated into right and left lobes by plane from gallbladder fossa to IVC
called Cantlie’s line
Couinard divided liver into eight segments, numbering in clockwise direction,
beginning with caudate lobe as segment 1. Each segment has its own branch
of hepatic artery, portal vein and bile duct.

Introduction
A right hypochondrial mass can be liver, gall bladder, enlarged hepatic flexure
and many more. Most commonly it is the liver. A liver swelling can be primary
or secondary, of which secondary is commoner (Ratio of primary: secondary in
liver is 1:20).

Classification of liver lesions

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Benign
 Cyst
 Hemnagioma
 Focal Nodular Hyperplasia
 Adenoma
 Biliary hamartoma
 Abscess
Malignant
 Hepatocellular carcinoma
 Cholangiocarcinoma( bile duct cancer)
 Gallbladder cancer
 Metastatic colorectal cancer
 Metastatic neuroendocrine cancer(carcinoid)
 Other metastatic cancers
Source of Secondaries
 Colorectal – most common.
 Lung
 Pancreas
 Breast
 Stomach
History Taking
Patient usually presents with vague complaints of abdominal pain, abdominal
distension, jaundice, melena etc.
The most important point once you get a liver swelling is to find out what it is
due to.
The first DD should be a secondary liver, as it is the commonest.
Ask for symptoms from possible primary site:-
Early satiety-abdominal distension-vomiting-loss of appetite-loss of
weight (Ca Stomach), Altered bowel habits(Ca colon), Scrotal heaviness
& swelling (Ca. testes), jaundice- itching-clay coloured stools-short
duration history(obstructive jaundice) etc.
Examination
General examination
 Anaemia (Carcinoma colon, stomach)

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  Jaundice (periampullary carcinoma)
 Bilateral pedal oedema (IVC obstruction by enlarged liver
 Spine tenderness (metastasis)
 Absence of testes in scrotum (seminoma of undescended testes)
Abdominal examination
On examination, a right hypochondrial mass, which is dull on percussion,
dullness continuous with liver dullness and unable to insinuate between
the swelling and the costal margin is obtained.
Criteria for Liver secondaries
 Both lobes enlarged.
 Sharp lower border.
 Nodular surface
 Hard consistency
 Umbilication(central necrosis of a nodule)
Criteria for Liver Primary-HCC
 Both lobes are enlarged.
 Rounded lower border
 Hard consistency
 Irregular surface
Always do a detailed abdominal examination and look for epigastric mass (Ca
Stomach), right iliac fossa mass(Ca Colon).

DIAGNOSIS
Enlarged Liver, possibly due to metastasis from possible Carcinoma Colon (as
according to the case)
INVESTIGATIONS
1) Blood Routine
2) Urine rouine
3) LFT- Raised Alkaline phosphatase is the most consistent abnormality in liver
secondaries.
4) USS abdomen to know the origin of the mass, whether both the lobes
enlarged, gall bladder, CBD size, ascites +/-, other mets. Look for the possible
primary sites.Mosaic pattern of tumour with thin halo and lateral shadows
5) Triple phase Multi slice Spiral CT abdomen is the investigation of Choice in
Liver secondaries
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6) CT portography is the most sensitive investigation in liver secondaries.
7) Tumour markers – Alpha Fetoprotein will be raised
8) Liver Biopsy- done only in unresectable cases/metastatic cases/ when
diagnosis is unclear (using Okuda-Chiba Liver Biopsy Needle)

MANAGEMENT
A) According to primary cause
 First confirm the diagnosis using relevant investigations. If suspecting Ca
colon, do colonoscopy and get a tissue diagnosis and then only start
treatment. Similarly for Ca stomach, pancreas etc. That is Treatment of
Primary + Treatment of Liver secondaries is the method to be followed.
 If Ca colon, Resection of the Liver mets can be done because this will
help in palliation as well as increase the survival of the patient (in
solitary mets. Resection is done, while for unilobar secondaries,
right/left Hemihepatectomy is done)
 In all other cases, you don’t resect the liver generally (exceptions are
there)like in Ca stomach, where the patient has liver mets+vomiting, we
do palliative stenting/feeding jejunostomy.
 In case of Ca colon adenocarcinoma- give chemotherapy. Unresectable
liver secondaries may become resectable after such treatment. Do
colectomy if there is colonic obstruction.
B) Treatment Options for Liver Secondaries.
A) RESECTION
 Mainly palliative(But resection is the best treatment for HCC)
 Up to 3 segments of the liver can be resected.
 Functional Liver remnant (FLR) should be >20% of standard total liver
volume after resection.
B) ABLATION
 Cryotherapy
 Radiofrequency ablation.
 Laser insterstitial Thermal Therapy
 Microwave coagulation therapy
 TransArterial Radio Embolisation(TARE)
 Intratumoral Alcohol infection
C) CHEMOTHERAPY
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  Neoadjuvant
 Intraarterial
 Systemic
 Trans Arterial Chemo embolization(TACE)
Chemotherapy provided is usually Doxorubicin, 5 FU. Sorafenib is the drug of
choice in advanced HCC
More Questions
Q) How will you clinically differentiate between Primary (HCC) and Liver
secondaries on Abdominal Examination?? (Given above)
Q) Which are the metastatic liver swellings where liver resection is indicated?
 Ca Colon metastasis
 Neuroendocrine tumour mets (insulinoma) and Carcinoma tumour mets.
Q) What are the types of liver resections?
Liver has eight functional segments called Couinard segments. Segments
I-IV in the left lobe and segments V-VIII in the right lobe of Liver.
 Right hemi-hepatectomy – Segments V, VI, VII, and VIII removed.
 Right trisegmentectomy (Right Lobectomy) - Right hemi –
Hepatectomy + Segment IV (Quadrate lobe) removed.
 Left hemi-hepatectomy- Segments II, III, and IV removed.
 Left trisegmentectomy –Left hemi-hepatectomy + Segments V and
VIII removed.
 Left lateral segmentectomy (left Lobectomy) - segments II and III
removed.
Q) What precautions taken before Liver Biopsy
 BT, CT, PT should be normal. Otherwise Vitamin K injection 10 mg is
given IV or SC for 3 days
 If there is bleeding tendency, this procedure should not be done.
 Broad Spectrum antibiotics are given before the procedure.

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 CARCINOMA OF UNKNOWN PRIMARY (CUP)
This can be kept as a long/short case.

Presenting Complaints
Usually, patient presents with single /multiple lymph nodes in the neck/vague
abdominal /respiratory symptoms. In all cases where you didn’t get a definite
mass on examination, always look in detail for lymph nodes.
HISTORY TAKING
 Ask in detail about the swelling.
 H/o any other swellings in the body.
 Ask in detail about his other major symptoms if any, which had made
him come to the hospital. (Abd pain, altered bowel habits, coughs
etc.)
When a pt present with a node, we have to start right from the top
of the head…because even a small scalp swelling can cause a
cervical node.
 H/o scalp infection, fever, trauma
 H/o fever sore throat ( tonsillitis )
 H/o ear pain, ear discharge (Infections )
 H/o long standing ulcer in the tongue (Ca tongue)
 H/o dysphagia, odynophagia ( Ca tongue, hypopharynx)
 H/o epistaxis (Ca nasal cavity)
 H/o hoarseness of voice (Ca thyroid, Ca glottis)
 H/o any thyroid symptoms
Papillary carcinoma is notorious to present as a cervical node even
in the absence of a palpable thyroid swelling (lateral aberrant
thyroid )
 H/o testicular sweeling ( Ca testis)
 H/o abdominal symptoms—abd pain, altered bowel habits, jaundice,
abd distension ( to rule out 2° from GIT)
 H/o chest symptoms –cough, breathlessness, chest pain, hemoptysis.
(Rule out 2° from lungs)
 H/o TB –fever, cough, night sweats, evening rise of temperature, h/o
contact with TB
 Always look for any other swellings in the body –may be a case of
lymphoma
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  Look for any malignant change in a previous moles ( malignant
melanoma)
 Ask for smoking, alcoholism.

On examination…
 Which level of nodes are involved
 Any other nodes in the neck
(Level 5 mostly from the chest, abdomen, thyroid,
Level 2 &3 mostly from oral cavity)
 Do abdominal examination as per DAS. Look for liver, spleen, ascites,
any abdominal mass.. never forget to examine the external genitalia
(Testicular swelling)
 Always mention” PR not done”. Important in the case of ca
colon.(Blummer’s shelf)
 Examine scalp ear, oral cavity, tongue, tonsils, posterior pharyngeal
wall, salivary gland including their openings.
 Respiratory system examination according to the complaints of the
patient

How to write the diagnosis??

Cervical lymphadenopathy, probably metastasis from carcinoma oral
cavity, tongue, abdomen (according to the case)

Discussion
 Occult primary
Pathologically proven metastatic lymphadenopathy for which 1°site
remains undetected even after clinical examination and relevant
investigation.
 Features of malignant nodes
Hard in consistency, Immobile
In lymphoma, rubbery consistency
 Levels of cervical lymph nodes
1a-submental

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 1b-submandibular
2- Upper jugular
3- Middle jugular
4-Lower jugular
5- posterior triangle
6-Central compartment (prelaryngeal, pre and para tracheal)
7-Superior mediastinal

 Causes of lymphadenopathy
1) Reactive
D/t proliferation… seen in paediatric age group

2) Inflammatory
 Infective—acute-bacterial :staphylococcus,streptococcus
Acute Viral:Mumps, echo, coxsackie, enterovirus
Chronic -Bacterial :TB, leprosy, syphilis
Fungal:Actinomycosis, cryptococcosis, Histoplasmosis
 Non infective—Sarcoidosis, SLE

3)Neoplasm
 1°_hodgkin’s
 2° _from other malignancies
 Occult 1°
 Most common occult 1° in head and neck region—squamous cell
carcinoma
 Most common occult 1° as a whole – adenocarcinoma
Among scc, >80% --above the clavicle
Among adeno carcinoma, >80% infraclavicular
Grading of trismus
Grade 1: 26-35 mm
Grade 2: 16 - 25mm
Grade 3: <15 mm
Muscles of tongue
Intrinsic muscles: superior longitudinal, inferior longitudinal, transverse,
vertical

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Extrinsic muscles: Genioglossus, hyoglossus, styloglossus, palatoglossus

All are supplied by hypoglossal nerve except palatoglossus. (supplied by

pharyngeal plexus)

How do you proceed in the case of an occult primary??

1)If there is a node, the first investigation is a tissue diagnosis

 If multiple nodes, do FNAC

 If single node, do biopsy. [single node is precious for diagnosis. FNAC
can distort the architecture of the node]
 In case of lymphoma, directly do biopsy

2)If FNAC is inconclusive

Repeat FNAC

If again inconclusive, do excision biopsy

Result may come as scc, adenocarcinoma, melanoma, lymphoma etc..
 Since, scc is the most common in the head and neck region, do a
detailed ENT examination.
 Take CXR, US abdomen,US scrotum. If positive do biopsy. If
negative, do pan endoscopy (laryngoscopy, bronchoscopy,
esophagoscopy, nasopharyngoscopy)
 If positive, take biopsy
 If negative, take blind biopsy from possible 1°sites.(base of
tongue, fossa of rossenmuller, retromolar trigone, pyriform fossa,
vallecula)
 If negative, CT scan of head, chest, abdomen,
 If still negative, we label it as occult 1°
If biopsy shows adenocarcinoma, it can be from thyroid, salivary gland, lungs,
ovary, testis.

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Staging and Management

Staging
Management

N1 Single lymph node <3cm MRND

N2 a Ipsilateral single node 3-6cm MRND + RT
N2b ipsilateral multiple < 6cm MRND + RT
N2 c bilateral / contralateral nodes <6cm Bilateral MRND + RT
N3a >6cm MRND + RT +/- CT
N3b extranodal extension preop RT + MRND+ CT
Neck dissections
 Radical neck dissection (RND)
All lymph nodes in levels I -V including spinal accessory
nerve(SAN), sternocleidomastoid (SCM), internal jugular vein( IJV)
 Modified radical neck dissection (MRND)
Excision of same LN bearing area as RND with preservation of one
/ more non lymphatic structures..(SAN, SCM, IJV)
MRND 1 : SAN alone is preserved
MRND 2 : both IJV & SAN preserved
MRND 3: SAN, IJV, SCM preserved
 Selective neck dissection
Preservation of one/ more LN groups
Subtypes:
 Supraomohyoid : Removal of LN groups 1 -3
Posterior limit is cervical plexus and posterior boarder of
SCM.
Inferior limit- omohyoid muscle overlying IJV
 Lateral: removal of LN grops 2-4
 Posterolateral: LN groups 2 – 4 + Suboccipital+ posterior
auricular
 Anterior : level 6

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 RETROPERITONEAL TUMOR
Relevant anatomy
1. Boundaries of retroperitoneum
Anteriorly Parietal peritoneum
Posteriorly Muscles
Superiorly Diaphragm
Inferiorly Pelvis
Medially Spine divides into two
Laterally Imaginary line from tip of 12th rib to iliac
crest

2. Contents of retroperitoneum (SAD PUCKER)

 Supra-renal glands
 Aorta & IVC
 Duodenum (2nd and 3rd parts)
 Pancreas (except tail)
 Ureters
 Colon (ascending and descending colon)
 Kidneys
 E
 Rectum
 In addition to the above, vessels, nerves, lymph nodes, fat,
muscles and sympathetic trunk are also present
Introduction
 Uncommon tumors with an incidence of 0.3-3%
 Tumors of retroperitoneal organs are not included in retroperitoneal
tumors traditionally
 Most common retroperitoneal malignancy in adults is Liposarcoma
(50%) and in children is rhabdomyosarcoma
 About 1/3rd of liposarcoma originate from perinephric fat
 Usual age group of liposarcoma is 40 to 70 years

History taking
 Commonly asymptomatic , Can present as progressive abdominal
distension or large abdomen without any other symptoms

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  History of therapeutic radiation or exposure to vinyl chloride (present in
plastics, cigarette)
 History related to Paraneoplastic Syndromes
Liposarcoma intermittent hypoglycemia (d/t insulin
production)
Paragangliomas hypertension (d/t catecholamine
production)
Germ cell tumors precocious puberty
Neuroblastoma myoclonus in children
 Back pain and leg pain may occur due to compression and stretching of
lumbar and pelvic nerves
 Ask about pressure effects
 B/l pedal edema due to iliac vein obstruction and Deep Vein
Thrombosis
 Ureteric compression causing hydronephrosis (decreased urine
output)
 General features of malignancy (loss of weight and appetite)
 Family history of malignancies - Gardner’s syndrome (colonic polyps +
osteomas + soft tissue tumors), Retinoblastoma, Neurofibromatosis, Li
Fraumeni syndrome

EXAMINATION
 Take temperature and BP as RP tumors produce fever and hypertension
 Look for ascites and dilated abdominal veins
 The mass is found to be intra-abdominal by Carnet’s head raising test
 Retroperitoneal swellings
 doesn’t cross the midline (except neuroblastoma)
 are usually fixed (except pedicled swellings)
 don’t move with respiration
 does not fall forward in knee elbow position (picker’s position)
 are resonant on percussion due to bowel loops in front
 Look for lower limb edema and varicocele

INVESTIGATIONS
1. CE-CT abdomen
 Investigation of choice
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  Gives details of nature of mass (solid/cystic) and proximity of mass to
great vessels (Cystic swellings are usually benign)
2. MRI abdomen : Greater accuracy than CT (100% vs 80%)
3. Tissue diagnosis (Trucut biopsy) done under CT or Ultrasound guidance
4. Additional investigations
 CT chest to rule out mets (sarcoma metastasizes to periphery of
lung which may be missed in Xray chest)
 IVU in case of urinary complaints
 LFT, RFT needed in late presentations

MANAGEMENT
i. Surgery is the best treatment. If surgery is not possible as in cases of
tumor adherence to great vessels, chemoradiotherapy is done.
Wide en-bloc excision with 1-2 cm margin all around is needed. This is
achievable in only 30% cases. Therefore, adjuvant chemoradiotherapy is
essential.
ii. Chemotherapy is given using MAID regimen – Mesna, Adriamycin,
Ifosfamide, Dacarbazine
iii. Radiotherapy (especially intraoperative radiotherapy) is effective in
lowering the incidence of local recurrence.
iv. Nodal involvement has very poor prognosis
Most important factors deciding prognosis are histological grade and
completeness of surgical excision
Three-tiered grading determined by mitotic activity + extent of necrosis
+ differentiation
v. Follow up in RP tumor
 Physical examination every 2 to 3 months
 If symptoms occur do CT/MRI
 In asymptomatic patients CT/MRI is to be done every 6 months for
the first 3 years

More questions …
1. Sarcoma with lymph node metastasis- SCREAM
 Synovial sarcoma
 Clear cell sarcoma
 Rhabdomyosarcoma

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  Epitheloid sarcoma
 Angiosarcoma
 Malignant fibrous histiocytoma
2. Cystic lesions of retroperitoneum (diagnostic investigation is US
abdomen)
 Retroperitoneal Mesenteric cyst
 Teratomatous cyst
 Dermoid cyst
 Abdominal cystic lymphangioma
 Parasitic cyst

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 SOFT TISSUE SARCOMA (STS)
Introduction
 Soft tissue sarcomas are rare and unusual neoplasms accounting about
1% of adult human cancers and 15% of paediatric malignancies. These
are tumours of mesenchymal origin.
 Most commonly occurs in extremities (more in lower limb-most
common in thigh) followed in order by visceral, retroperitoneal,
trunk/thoracic and other locations.
 Common STS are undifferentiated pleomorphic sarcoma-most common
overall (previously called malignant fibrous histiocytoma), liposarcoma
(most common STS in retroperitoneum)leimyosarcoma, and
Rhabdomyosarcoma(most common in children)
 For predisposing factors and more theory, refer pearls.

History Taking
Presenting Complaints
Patient usually presents with swelling in the lateral aspect of the thigh
gradually increasing in size. Swelling in extremity-60%, trunk-30%, head&
neck-10%.
 Ask in detail about the swelling.
 Ask h/o pain. Pain occurs when the sarcoma presses on the nerve or
when it infiltrates the nerve.
 Ask h/o difficulty in moving the limb, inability to flex/extend the leg
 Ask h/o neurovascular deficit. ischemic pain-ulcers(artery), numbness
paraesthesia(nerve), edema of the limb(vein).
 Ask h/o fever., h/o trauma to r/o infective etiology& hematoma
 Ask h/o any other swelling elsewhere in the body. (Regional lymph
nodes).
sarcomas metastasize to the lungs)
 Ask h/o abdominal symptoms…Jaundice, bowel habits
(retroperitoneal& visceral tumours metastasize to liver parenchynma)
Past Medical History
 h/o swelling I the same site before and in the treatment done
 h/o exposure to radiation.

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Family History
 h/o Neurofibromatosis, Retinoblastoma in the family.

Local Examination
 Examine in detail the swelling.
 Look for dilated veins indicate the vascularity of the tumour
 Most importantly assess the plane of the swelling.Remember that STS is
not always deep todeep fascia..it depends on the variety of STS.STS can
even be subcutaneous. The variety called liposarcoma.where youcannot
pinch the skin over it. STS can be either superficial or deep to
deepfascia,depending on which the staging is done.A recurrent swelling
with variable consistency favours a STS over a lipoma.
 Depending on where the swelling is present, you have to examine the
relevant site. Foreg:- if the swelling is present on the back close to the
spine & the scapula, you have toexamine the spine, scapula..its
movements etc..
Similarly if the swelling is present in the intercostal region,you have to
examine for
impulse on coughing to r/o possible lung aetiology for the swelling.
 Check for the movements of the joints both proximal and distal to the
swelling.
 Always examine the motor system and sensory system inorder to know
the extent of neurovascular deficit.
 Look for wasting of the limb.
 Always examine the chest to r/o lung mets..
 Always examine the abdomen…never forget to do the PR examination.
 Always examine for anyother swelling elsewhere in the body especiolly
for the regionallymph nodes.

MANAGEMENT
INVESTIGATIONS
1. CORE BIOPSY should be the first important investigation…why? a simple
FNAC will just tell about the cell component like a spindle cellneoplasm or so.
300
Inorder to confirm the diagnosis we need the tissue diagnosis. Core biopsy
yields tissue diagnosis by which you can grade the tumour, decide the
staging, & identify theprognostic factors.
Grading is done based on the mitotic activity: <3/hpf, 3-20/hpf, >20/hpf.

2. If core biopsy is negative you do INCISIONAL (>3cm) OR EXCISIONAL

(<3cm). But unlike other incisional biopsies.
 The incision should be longitudinal to the long axis of the
limb..suchthatb the future surgical scar for the excision is included in it.
 No drain should be kept..this is because, malignant cells do not have the
natural adherence like normal cells. Hence if we apply a
negativepressure, thesemalignant cells can easily track down. But
rememberthat after compartmental excision you can keep drain.
 Flaps should not be raised...so that lymphatics are not much exposed.
 Do not undermine the skin margins..
 Achieve adequate haemostasis.

Always better to do the imaging before doing biopsy, because core biopsy
distorts the
architecture.
3. X-Ray of the affected limb... to know the bony enlargement, to know the
pressure effects
4. Metastatic workup.
• CXR- to r/o lungmetastasis. Only if CXR is +VE, we do a CT chest
• Abdominal USS..to r/o liver metastasis in retroperitoneal & visceral tumours
5. MRI is the investigation of choice in extremity tumours. bcoz it can very
well delineate the nerve, artery & the vein.
6. SPIRAL CT is the investigation of choice for truncal tumours. except for GIST
form
7. MR angiogram can be done to know the feeding vessels.
8. PET scan is the latest modality. do not mention it under the routine
investigations.

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TREATMENT
SURGERY
The treatment of choice is LIMB SPARING, FUNCTION PRESERVING WIDE
EXCISION of the tumour with 1cm margin for low gradetumours & 2cm margin
for high grade tumours.
 >10cm - give preop chemo, then do wide excision, then give post op
chemo.
 5-10cm & high grade - do wide excision + post op chemo.
 >5cm & low grade - do wide excision, NO chemo.
 <5cm - do wide excision alone.

CHEMOTHERAPY
 Given when tumour more than 5 cm or high grade tumours.
 Most important chemotherapeutic agents used are IFOSPHOMIDE &
DOXORUBICIN(Adriamycin)
 Commonly MAID regime is followed which consists of methotrexate,
Adriamycin, ifosfamide, and Dacarbazine)

RADIOTHERAPY
 Adjuvant radiotherapy helps in improving local control.
 It can be either Brachytherapy or External beam radiotherapy
 Brachytherapy for high grade lesions.
 External beam radiation therapy for large (>5cm) high or low grade
lesions.

For subcutaneous or intramuscular high grade sarcomas smaller than 5cm

or any size low grade sarcoma, surgery alone is considered if adequate wide
excision with a good 1 to 2cm cuff of surrounding fat and muscle can be
achieved. If the excision margin is close, particularly with extra muscular
involvement, or if local recurrence would result in the sacrifice of a major
neurovascular bundle or amputation, adjuvant radiation therapy is added to
the surgical resection to reduce the possibility of local failure (SABISTON)

More Questions
1. Types of STS.
2. STS with lymph node spread.
Code is MARCES, which includes
 Malignant Fibrous histiocytoma
 Angiosarcoma
 Rhabdomyosarcoma
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  Clear cell sarcoma
 Epithelial sarcoma
 Synovial sarcoma
Hence for these, lymph node clearance is required

3. Types of excisions..intralesional,marginai,compartmental.
4. Types of amputations done for STS.

Staging of soft tissue sarcoma

G, Histologic Grade
GX Grade cannot be assessed
G1 Well differentiated
G2 Moderately differentiated
G3 Poorly differentiated
G4 Undifferentiated
T, Primary Tumor Size
TX Primary size cannot be assessed
T0 No evidence of primary tumor
T2 Tumor less than 5 cm
T1a Superficial tumor
T1b Deep tumor
T2 Tumor 5cm or greater
T2a Superficial tumor
T2b Deep tumor
N, Regional Nodes
NX Regional nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Regional lymph node metastasis
M, Distant Metatasis
MX Presence of distant mets cannot be assessed
M0 No distant mets
M1 Distant mets present
Staging Grouping
Stage 1 G1-2 T1a, 1b, 2a, 2b N0 M0
Stage 2 G3-4 T1a, 1b, 2a N0 M0
Stage 3 G3-4 T2b N0 M0
Stage 4 Any G Any T N1 M0
Any G Any T N0 M1

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RIGHT ILIAC FOSSA MASS
Important Differential Diagnosis
1. Ileocecal TB
2. Appendicular Mass
3. Carcinoma Cecum
4. Right ovarian cyst/ tumour - Females
5. Pelvic Inflammatory Disease (PID) - Females
6. Iliac Lymphadenopathy
7. Psoas abscess
8. Tumour in undescended testis - Males
9. Unascended kidney
10.Retroperitoneal Tumours
11.Chondrosarcoma of ilium
12.Crohn’s disease

Comparison of the clinical features of the most important causes of RIF mass
Appendicular Lump Ileocecal TB Carcinoma
Cecum
Age (most imp Younger age group Middle age Above 50 yrs.
criteria)
Onset A/c-3 days after Suba/c-recurrent attacks Insidious/
initial symptoms asymptomatic
Symptoms Migratory pain + Recurrent attacks of Abdominal lump
Nausea/vomiting + abdominal pain, altered + loss of weight
Fever (Murphy’s bowel habit + evening
triad) rise of temperature/ loss
of weight
Nature of mass Irregular, firm, Irregular, doughy, fixed Hard, fixed
tender, fixed
Response to Becomes smaller No response No response
antibiotic and then disappears
Radiological No specific signs  Pulled up cecum Irregular filling
signs  Fleischner sign defects in cecum
 Sterlin sign which is in
 Obtuseileocecal normal position
angle

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Relevant anatomy

1. Arterial supply of colon (look up diagram)

 Superior mesenteric artery - ileocolic artery, right colic artery, middle
colic artery
 Inferior mesenteric artery - left colic artery, sigmoid artery
 Marginal artery of Drummond - Single arterial trunk, superior rectal
artery along the concave part of large intestine from ileocecal junction
to rectosigmoid junction forming a communicating channel between
superior and inferior mesenteric arteries. It gives off vasa recta which
run perpendicular to the colonic wall.
 Arc of Riolan - Collateral branches connecting proximal middle colic
artery to left colic artery
 Griffith’s point - weak point of anastomosis between middle and left
colic arteries at splenic flexure
 Sudek’s point - weak point of anastomosis between sigmoid and
superior rectal arteries
2. White line of Toldt - The ascending and descending colon has no peritoneal
covering on their posterior aspects but has areolar tissue (fascia of Toldt),
which represent the embryonic fusion of mesentery to posterior
peritoneum. At the lateral parietal wall, it reflects as the white line of Toldt.
This line is used as the plane for avascular mobilisation of colon.
History taking

[Describe each in detail in such a way to reach a diagnosis from the history]

 History of TB in past or contact with TB, any surgeries

 Family history of malignancies of colon, stomach, endometrium and
ovary (FAP, HNPCC)
 Careful gynaecological history with history of vaginal discharge,
dysmenorrhea, last menstrual period
Examination

Rule out other lymph node enlargementin TB and mets in CA cecum:

 Supraclavicular nodes
 Rectal examination to rule out rectal shelf of Blumer
Rule out other Differentials:

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  If the RIF mass is soft look for a swelling below inguinal ligament and
check its cross fluctuation (psoas abscess will track down to thigh
below inguinal ligament)
 Examination of genitalia to rule out undescended testis
 Look for a primary growth in the drainage area of inguinal and iliac
nodes
 Pelvic examination to rule out adnexal and cervical tenderness

INVESTIGATIONS
I. In suspected Ileocecal TB
a) Blood examination
 Anaemia and high ESR and features of TB
b) Mantoux test (highly non-specific)
 Positive Mantoux test indicates latent TB infection
 Positive in BCG vaccinated individuals as well
 Negative in immune-compromised individuals as well
c) Plain Xray Chest may show features of Pulmonary TB
d) Plain Xray Abdomen may show calcified LNs and intestinal dilatation
(due to obstruction) or perforation (gas under diaphragm)
e) Ultrasound abdomen may show features of mass lesion, fluid
collection, LN enlargement. (Necessary investigation in any
abdominal lump)
f) Double contrast Ba enema or Ba meal follow through may show
some specific radiological signs
 Pulled up cecum (normally it is seen close to the ileal bone)
 Fleischner sign (thickening of ileocecal valve and it is wide open)
 Sterlin sign (fibrotic terminal ileum opening into a contracted
cecum)
 Obtuse ileocecal angle
g) Now, investigation of choice in abdominal TB is CE-CT abdomen
Gold standard investigation in abdominal TB is CBNAAT
h) Ascitic fluid study
Estimation of ADA (Adenosine Deaminase): >95% specific for
abdominal TB
SAAG (Serum Ascitic Albumin Gradient): >1.1 is suggestive of
abdominal TB
i) Peritoneal biopsy: ideally laparoscopic biopsy, not needle biopsy
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 II. In suspected Carcinoma Cecum
1) Diagnostic Investigations
a) Sigmoidoscopy - Rigid/Flexible
b) Colonoscopy -can visualise the growth and take biopsy, look for
a second malignancy (present in 5% cases)
c) Double contrast Ba enema – irregular filling defects, apple core
appearance, demonstration of polyps
2) Staging investigations
a) Chest X-ray
b) LFT
c) Ultrasound for liver mets, free fluid, ureteric obstruction
d) CE-CT for local invasion
e) CEA (Carcinoembryonic Antigen)
III. In suspected Appendicular mass
Mostly a clinical diagnosis

MANAGEMENT
I. Ileocecal TB
 ATT (Anti-Tuberculous Therapy)
 2HRZE+ 4HRE
 Fixed Dose Combination of
Isoniazid 75 mg + Rifampicin 50 mg + Pyrazinamide 400 mg
+ Ethambutol 275 mg
 Daily doses as per weight bands
 Surgery is indicated in case of Intestinal obstruction, Bleeding,
perforation
 In case of intestinal obstruction, surgery is needed:
 Stricturoplasty when the lesion is confined to ileum and the
strictures are few in number
 Ileocecal resection when the disease involves ileum and
cecum
 Right hemicolectomy is needed for extensive strictures
(limits of Right Hemicolectomy- proximal: 10cm from
ileocecal junction, Distal: point of entry of right branch of
middle colic artery into transverse colon; in case of

307
 extended hemicolectomy the distal limit is upto splenic
flexure i.e upto ascending branch of left colic artery)
II. Carcinoma Cecum
Right hemicolectomy which includes a radical resection of involved colon
along with its lymphovascular drainage. Suspicious lymph nodes are
taken for biopsy.
III. Appendicular Mass
 Conservative management known as Oschner-Sherren regimen
 Nasogastric tube aspiration, nil per oral
 Fluid and electrolyte maintenance
 Careful monitoring of vitals including temperature and
leucocyte counts
 Broad spectrum antibiotics

Elective
Conservative
Lump reduces appendicectomy
management
after 6 wks

 Criteria to stop conservative management

 Rising pulse rate
 Increasing/ spreading abdominal pain
 Increasing size of mass
 Why appendicectomy is contraindicated in appendicular mass?
 Mass will resolve with conservative management alone in
90% cases
 Immediate appendicectomy is technically more difficult
 Routine interval appendicectomy is unnecessary in majority of
patients
 Patients above 40 years should undergo a colonoscopy after
successful conservative management of appendicular mass to
avoid missing a malignancy
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 More questions …

1. Difference between ulcerative and hypertrophic types of intestinal TB

Ulcerative Hypertrophic
Secondary to pulmonary TB by Due to ingestion of low
swallowing tubercle bacilli virulent organisms by a person
with high resistance
Patient is very ill Not very ill
Absence of filling of ileum, Filling defect in the terminal
cecum and ascending colon ileum, pulled up cecum, obtuse
ileocecal angle
Presence of gross caseation Absence of gross caseation
Obstruction is not usually seen Obstruction is common
2. Why ileocecal region is most commonly affected in intestinal TB?
 More lymphatic follicles are seen in terminal ileum
 Stasis in terminal ileum
 Spread of genital TB from adjacent fallopian tube in females
3. Abdominal Cocoon: The adhesions in abdominal TB completely obliterate the
abdominal cavity forming a cocoon
4. Features of HNPCC

5. Difference between right and left sided colonic malignancy

Right-sided Left-sided

Larger diameter (E.g. cecum – 7.5 Narrow lumen (E.g. rectosigmoid –

cm) and fluid content 2.5 cm) and solid content

Ulceroproliferative growth Stenosing growth

Present with ill-defined pain and Present with alternating constipation

pallor consequent to melena and diarrhoea and early intestinal
obstruction (colicky pain)

Late diagnosis and therefore bad Early diagnosis due to obstruction

prognosis and therefore good prognosis

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 6. Commonest sites of Colorectal carcinoma(reference bailey)
Rectum 38%
Sigmoid 21%
Cecum 12%
Transverse 5.5%
colon
Ascending 5%
colon
Descending 4%
colon
Splenic flexure 3%
Hepatic flexure 2%

7. Predisposing causes of Colorectal cancer

 Diet rich in meat (Fibre diet is protective)
 Inflammatory bowel diseases like Ulcerative colitis and Crohn’s disease
 Exposure to radiation
 Breast carcinoma

8. Appendicular mass
 Complication of acute appendicitis. It follows a small perforation in
appendix where omentum comes & tries to seal the perforation. Therefore,
it is a palpable conglomerate of inflamed appendix, adjacent viscera and
greater omentum
Appendicular abscess
 Develops during the course of conservative treatment of appendicular mass
if there is rising pulse rate/ abdominal pain/ size of mass or patient is
looking ill
 Imaging shows presence of fluid inside
 Managed by sonographically-guided percutaneous catheter drainage

9. Alvarado score in acute appendicitis

Valentino appendix – Duodenal ulcer perforation mimicking acute appendicitis

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10. DDs of RIF pain of acute onset
a) Lobar pneumonia and pleurisy h) Mesenteric infarction
b) Perforated peptic ulcer i) PID
c) Acute pancreatitis j) Ectopic gestation
d) Acute cholecystitis k) Twisted right ovarian cyst
e) Meckel’s diverticulitis l) Right ureteric colic
f) Intussusception
g) Carcinoma cecum

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 LEFT ILIAC FOSSA MASS
 H/o lump as in that of swelling
 Parietal swelling: No specific parietal swelling except an iliac abscess that has
burrowed through.
 Intra abdominal swellings:
1. Sigmoid colon- usually patient above 40 yrs of age
(a) Carcinoma: Lump unlikely,or small. Increasing constipation. Dull aching or
colicky pain. Loaded colon proximal to stenosis pits on pressure. Risk factors
are smoking, smoked food, red meat, low fibre, ulcerative colitis, family
history(FAP,HNPCC)
(b) Diverticulitis: Bleeding PR, Flatulence, abdominal distension. Later, fever,
malaise and pain in left iliac fossa

2. Iliac abscess: h/o trauma to the region and pain restricted there with irregular,
firm, fixed, tender mass.
3. Iliopsoas cold abscess: h/o TB, bone pain in thoracolumbar spine
4. Lymph nodes: any swelling in neck, axilla or groin(lymphoma) h/o scrotal
swelling, filariasis (attacks of fever with chills, tender LN swelling), tuberculosis,
rapid enlargement in young (lymphosarcoma)
5. Unascended kidney or undescended testis
6. Retroperitoneal sarcoma
7. Splenic enlargement: fever and repeated infections, fatigue, weight loss, bone
pain(leukemia), h/o chronic liver disease(portal HTN), family history of jaundice
with anemia(hemolytic anemia), h/o repeated purpuric rashes(ITP)
8. Spigelian hernia: elderly patient, intermittent pain, discomfort on straining,
change in bowel habits.
9. Ovarian mass: Mass from one side, later central, dull on percussion,
menstruation may be affected, ascites may be detected.

MANAGEMENT of CA colon
*Read blood supply of colon

Investigations:
1. Routine: Hb very important
2. Stool for occult blood
3. Colonoscopy and biopsy
4. LFT to look for liver mets
5. CECT abdomen for extent of invasion, intra abdominal mets, staging.
6. CXR: to r/o pulmonary mets
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7. CEA: baseline before surgery essential. Persistent elevation implies a missed
focus or incomplete resection. Recurrence can also be seen.
8.USS: No use regarding malignancy.to look for ascites, liver or pelvic deposits

Signs of inoperability:
(a)Multiple secondaries in liver, Disseminated peritoneal seeding, ascites and
omental deposit: Here, only palliative resection
(b)Fixed metastatic LN
Staging:
→Study Duke’s staging.
T1- invades submucosa
T2- muscularis propria
T3- subserosa
T4a- to surface of visceral peritoneum
T4b- directly invades or is adherent to adjacent organs or structures
N1- Mets in 1-3 regional nodes
N2- 4 or more
→Study TNM staging

Treatment:
Stage I: Only surgery
Stage II and III: Surgery and adjuvant chemo (Neoadjuvant only for rectum)
Stage IV:
 If resectable growth, palliative resection
 Isolated liver or lung mets resected
 5FU based chemo
Pre op:
 Correct anemia
 Gut preparation by liquid diet for 24 hrs and irrigation with
polyethylene glycol
 Antibiotic prophylaxis started 24 hrs before.
 Usually margin of 5 cm from the tumor line for resection.

Left hemicolectomy: if lesion in descending colon. ( rectum involved- anterior

resection; sigmoid involved- sigmoidectomy). Resection of transverse colon left of
middle colic vessels to upper rectum.

Right hemicolectomy: distal 30 cm ileum, caecum, ascending colon, proximal

1/3rd of transverse colon. For cecum and ascending colon.

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Subtotal (rectum remains) or total colectomy in one side pathology is when
multiple colon cancer or associated neoplastic polyps have occurred
→Study Right and left extended hemicolectomy and lymphatic drainage of colon

No touch technique of Turnbull: Before the tumor is handled, blood vessel to it is

ligated to prevent dissemination
LIGATE→RESECT→ANASTOMOSIS

Chemotherapy: 5FU + leucovorin + oxaliplatin for 6 months

Radiotherapy- after surgery; only in case of rectum

→Palliative procedures in unresectable growth:

(a)Right colon- bypass ileotransverse anastomosis
(b)Left colon- transverse colostomy
(c)Sigmoid or rectal growth- sigmoid colostomy proximal to growth.

Follow up:
During first 2 years 3 monthly; for next 3 years. 6monthly; then yearly
(a)Clinical examination (b)LFT (c)CEA assay (d) CXR

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 ORAL CAVITY MALIGNANCY
Relevant Anatomy

1. Boundries of oral cavity

 Anterior – vermillion border of lips
 Posterior – junction of posterior 1/3rd and anterior 2/3rd of tongue
 Lateral- on both side cheeks
 Above- palate
 Below- floor of mouth
2. Lined by squamous epithelium. Thus, the most common malignancy is
Squamous Cell Carcinoma. Other malignancies possible are Adenocarcinoma
of minor salivary glands, BCC and Malignant melanoma of skin
3. Nerve supply of tongue:
 Sensory - Ant 2/3rd Lingual N. (general sensory) and Chorda tympani
N. (special sensory),
 Post 1/3rd Glossopharyngeal N.
 Motor - Hypoglossal N.
Introduction
 Predominantly a disease of elderly
 Arise from mucosal surface after chronic exposure to carcinogenic
substances like tobacco and alcohol (commonly)
 the common risk factors are:
a. Tobacco
b. Alcohol (has a synergistic effect with tobacco)
c. Areca nut in pan masala
d. HPV
e. Plummer Vinson Syndrome (Fe deficiency anemia)
f. Poor nutrition lacking in Vitamin A and fruits and vegetables

six S – Smoking, Spirit, Spices, Sharp tooth, Syphilis and Sepsis

 Premalignant Conditions of Oral Cavity

1) Leukoplakia
 Any white patch or plaque that can’t be characterized clinically
or pathologically as any other disease

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  Rx: Stop tobacco and alcohol, all lesions are biopsied and if
required surgical excision/CO2 laser is done, regular follow up
at 4 monthly intervals
High risk lesions
2) Erythroplakia
3) Speckled erythroplekia
4) Chronic hyperplastic candidiasis
Medium-risk lesions
5) Oral Submucous Fibrosis (strongly associated with areca nut and
characterized by restriction of mouth opening and palpable fibrous
bands over buccal mucosa, retromolar area, etc.)
6) Syphilitic glossitis
7) Sideropenic dysphagia (Plummer Vinson Syndrome)
Low-risk/equivocal-risk lesions
8) Oral lichen planus
9) Discoid lupus erythematosus
10) Dyskeratosis congenita

 Oral cavity malignancy may involve 4 anatomical sites:

A. Lip
95% on upper lip, LN mets to submental or submandibular nodes
B. Tongue
60% as bleeding ulcer on lateral aspect of tongue, may be associated
with ankyloglossia (restriction of tongue mobility)
C. Oral cavity (Floor of mouth, Buccal mucosa, Alveolus)
Very common in India due to tobacco chewing, may be associated
with trismus (if there is pterygoid muscle involvement)
D. Oropharynx
Presents much later than other oral cancers, may be associated with
otalgia (irritation of lingual nerve is referred to the auriculotemporal
nerve)

History taking
 Ask about Risk Factors: Tobacco or alcohol use, ill-fitting dentures,
recurrent oral ulcers consequent to sharp molars

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  Onset and progression of the swelling or ulceration (usually > 3 weeks
duration)
 Associated symptoms:
 Difficulty in mouth opening(can be due to SMF or involvement of
muscles of mastication or TMJ), tongue protrusion or swallowing
 Excessive salivation (d/t difficulty in swallowing + irritation of nerve
fibers of taste)
 Earache
 Slurring of speech (d/t involvement of tongue)
 Unexplained tooth mobility
 Painless neck lump

Examination
 Examination of swelling and ulcer along standard lines; ulcer often bleeds
on touch
 Look for ankyloglossia (inability to protrude the tongue)deviation of tongue
(in case of hypoglossal nerve involvement)
 Examine cheek, gums, floor of mouth, retromolar trigone and tonsils for a
second primary (second primary refers to anoher lesion seen simultaneous
in areas which share common developmental origin as oral cavity –
pharynx, upper airwy, fossa of Rossenmuller, Synchronus lesion refers to a
new lesion which develops within 6 months of diagnosis of primary, often
during the course of it’s treatment )
 Examination of last 4 cranial nerves (as these are closely related to base of
skull)

Investigations
 wedge biopsy of the lesion under local anesthesia from the most suspicious
area (usually at the periphery, avoid areas o f necrosis)along with the
adjacent normal tissue
 MRI is the investigation of choice and helps to evaluate invasion
 Ultrasound-guided FNAC of lymph node
 Orthopantomogram to know about mandibular involvement
 CT has limited value. However, CT chest should be done in all cases where
facilities are there to rule out lung mets

317
 Management
i. Two principle treatment modalities: Surgery and Radiotherapy. Chemotherapy
has a minor role because oral cavity malignancies are characterized by more
local spread.
Surgery is preferred in young, when there is bone involvement or involvement of
multiple sites.
ii. TNM Staging (Remember the numbers 2 and 5 in Breast Carcinoma while 2 and
4 in Head and Neck malignancies)
T1 Tumor<2cm
T2 2-4 cm
T3 >4cm
T4a Invades cortical bone, inf alveolar nerve, floor of mouth, skin of
face
4b Invades masticator space, pterygoid plates, skull base or encase
internal carotid artery
N0 No LN mets
N1 Mets in single ipsilateral LN up to 3cm
N2a Single ipsilateral LN of 3-6 cm
N2b Multiple ipsilateral less than 6 cm
N2c Bilateral or contralateral LN of less than 6 cm
N3 Node of >6cm or ExtraNodal Extension present
M0 No distant mets
M1 Distant mets

iii. Surgery of primary lesion

A. Lip: V or W shaped excision with 1 cm margin or Total excision and defect
repair with forearm flap
B. Tongue: Partial/hemiglossectomywith 2 cm margin or Major resection or
Total glossectomy with flap repair
C. Oral cavity: Resection and flap repair with mandibulectomy if needed
Mandibulectomy is of 3 types: marginal mandibulectomy, segmental
mandibulectomy, hemimandibulectomy
D. Oropharynx: Chemoradiotherapy is preferred to Surgery due to high
morbidity
iv. Management of cervical lymph nodes
 Clinically node negative:
318
 Prophylactic neck dissection is considered best in the treatment of lateral
tongue, floor of mouth and mandibular alveolus cancers as up to 30% of
such patients have micromets to nodes
 Types of neck dissection
Type Lymph nodes Indications
removed
Selective
SupraOmoHyoid (SOHND) I-III CA of lateral tongue,
floor of mouth,
mandibular alveolus
of N0 and N1
Extended SupraOmoHyoid I-IV CA tongue with N1
nodes
Radical
Modified (Bocca) Type I- spinal accessory alone CA tongue with N1,
preserved Neck skin
Type II- spinal accessory and involvement
SCM preserved
Type III- spinal accessory ,
SCM, and IJV preserved.
MRND (Type III is also known
as Functional Neck
Dissection)
Crile I-V levels N2, N3, neck
recurrence

v. Other modalities
 Indications of adjuvant radiotherapy
 Large primary tumor (above T2)
 Extensive nodal mets (above N1)
 Positive surgical margins
 Lymphovascular invasion
 Neo adjuvant chemotherapy only if primary surgery is not possible
Commando operation: old operation where combined excision of primary tumor +
block dissection of cervical lymph nodes + removal of the intervening body of
mandible
319
SHORT CASE

320
 EXAMINATION OF AN ULCER
HISTORY
1. MODE OF ONSET-traumatic/spontaneous/associated varicose veins/arterial
insufficiency
2. DURATION
3. PAIN-painful in c/o inflammation, painless in syphilitic/trophic/malignant
ulcers(malignant painful if nerve infiltration present)
4. DISCHARGE- if present, its nature(serum/pus/blood)
5. ASSOCIATED DISEASE, if present. –TB/diabetes/syphilis/nephritis/tabes
dorsalis/peripheral neuritis/transverse myelitis.

PHYSICAL EXAMINATION-malnutrition/TB/syphilis/general atherosclerosis

LOCAL EXAMINATION

A. INSPECTION
1. SIZE AND SHAPE
2. NUMBER
3. POSITION
4. EDGE
 Undermined edge.(TB)
 Punched out edge.(gummatous/deep trophic ulcer)
 Sloping edge.(healing traumatic/venous ulcer)
 Raised and pearly white edge.(rodent ulcer)
 Rolled (everted) edge.(squamous cell carcinoma/ulcerated
adenocarcinoma)
5. FLOOR(exposed surface within the ulcer) – red healthy granulation
tissue(healing)/pale smooth granulation tissue(slowly healing)
6. DISCAHRGE-its character, amount and smell
7. SURROUNDING AREA- (glossy,red and edematous/eczematous and
pigmented)

B. PALPATION
1. TENDERNESS
2. EDGE AND MARGIN
321
 (EDGE is the area between the margin and the floor of the ulcer and
MARGIN is the junction between normal epithelium and the ulcer.)
3. BASE(on which ulcer rests)
4. DEPTH
5. BLEEDING(whether bleeds on touch)
6. RELATION WITH THE DEEPER STRUCTURES(whether fixed or not)
7. SURROUNDING SKIN
C. EXAMINATION OF REGIONAL LYMPH NODES
D. EXAMINATION FOR VASCULAR INSUFFICIENCY-
 If ulcer situated on the lower part of leg, search for Varicose Veins on
the upper part of leg or thigh.
 Also examine condition of arteries proximal to ulcer(raynauds
disease, atherosclerosis, buerger’s disease)
E. EXAMINATION FOR NERVE LESION
 Trophic ulcers(seen in the sole or weight bearing parts)-indicates
sensory loss(peripheral neuritis,tabesdorsalis,transverse myelitis)

GENERAL EXAMINATION
 Presence of syphilitic stigma/other lymph nodes in the
body/presence of generalized atherosclerosis/any nervous disease.

DISCUSSION
ULCER – is a break in the continuity of the covering epithelium (skin or mucous
membrane) following molecular death of the surface epithelium or its traumatic
removal.

Classification of ulcers
I. Acute or chronic
II. Painful or painless
III. Clinically,
a) Spreading ulcer
322
 b) Healing ulcer
c) Callous or chronic ulcer

IV. Pathologically,
a) Non-specific ulcer
b) Specific ulcer
c) Malignant ulcer

SPREADING ULCER HEALING ULCER CALLOUS ULCER

The surrounding skin The surrounding skin is Induration of the

of the ulcer is not inflamed. edge and
inflamed and surrounding tissue.
edematous.
No evidence of Floor will have reddish Floor will have pale
granulation tissue. granulation tissue. granulation tissue.

The floor is covered The edge shows BLUE No tendency towards

with slough. ZONE(bluish outline of growing healing.
epithelium)and a WHITE
ZONE(fibrosis of the scar).
Discharge of pus will Minimal serous discharge Copious serous discharge.
be there. present.

 Spreading ulcer will be painful and the draining lymph nodes are inflamed,
enlarged and tender.

Examples of:

Non-specific ulcers Specific ulcers Malignant ulcers

 Traumatic  Tuberculous  Epithelioma

 Arterial ulcer  Syphilitic  Marjolins ulcer
323
  Venous ulcer  Soft sores  Rodent ulcer
 Neurogenic(trophic)  Actinomycosis  Malignant
 Associated with  Herpes simplex melanoma
malnutrition-Tropical  Fungal
ulcers.
 Associated with
diseases-diabetes, gout,
anemia, rheumatoid
arthritis.
 Miscellaneous ulcers-
Bazin’s ulcer, Martorell’s
or hypertensive ulcer.

Features of Arterial ulcer

 Due to peripheral arterial disease(commonest-atherosclerosis) and poor

peripheral circulation(more often seen in older people).
 Pain is the main complaint.
 Arterial ulcer tends to occur below the medial malleolus.
 Usually history of intermittent claudication and even rest pain present.
 If leg kept elevated above heart level, ulcer shows no signs of healing and
patient complains of pain.
 O/E, punched out ulcer with destruction of deep fascia .
 Tendons,bone or underlying tissue exposed in the floor of ulcer with
minimal granulation tissue.
 Always feel for peripheral pulses.(dorsalis pedis feeble or absent)
 Look for ischaemic changes(pallor, dry skin, loss of hair)

Features of venous ulcer

 Also called ‘varicose ulcer’/ ‘post-thrombotic ulcer’/’gravitational ulcer’
 Basic Cause- ambulatory venous hypertension
 Usually of age group 40-60.
 women affected more than men.
 Painful in the beginning, but once it becomes chronic, it is PAINLESS.
324
  Associated discomfort and tenderness of the skin, pigmentation and
eczema for months or years before ulcer develops.
 Site-mainly in lower part of leg in the medial aspect above the medial
malleolus, never seen above the junction of middle and upper thirds of leg.
 O/E, any shape and size,edge is sloping and pale purple-blue in colour.
Margin is thin and blue. Floor-pale granulation tissue present
 Ulcer usually shallow and flat(Never penetrates the deep
fascia),seropurulent discharge seen, base fixed to deeper structures.
 Surrounding skin – signs of chronic venous hypertension+
 Most important complication –development of carcinoma (MARJOLINS
ULCER) from the growing edge of ulcer.

MANAGEMENT
1. Identify and correct comorbid factors like DM, Anemia etc.
Investigations – FBS(control DM),PPBS, Peripheral smear, Hb, TLC, X-Ray
chest(to r/o TB).

2. Determine the etiology:

 Biopsy from the edge
 Pus- culture and sensitivity.
 X-Ray of part – to r/o Osteomyelitis
3. Adequate drainage and desloughing.

4. Care of the ulcer.

 Daily dressing
 Avoid antiseptic solutions, use normal saline for cleaning.
 Use non adherent non allergic dressing.
 Use microporous poly urethane film permeable to gases and water &
impermeable to micro organisms.
 “Four-Layer Banding System” for venous ulcer(refer Bailey)
5. Treat the underlying cause.
 ATT/treatment of varicose veins/revascularization (in c/o arterial
ulcer)
6. Excision of the ulcer and skin grafting (if the ulcer is not healing).

325
 EXAMINATION OF A SWELLING
History

 DURATION - first noticed v/s first appeared

 MODE OF ONSET - whether after trauma/spontaneously/from pre-existing
conditions/ noticed casually
 PROGRESS -whether slowly/quickly/sudden increase after remaining
stationary for a period
 EXACT SITE
 OTHER ASSOCIATED SYMPTOMS -like pain/ difficulty in
respiration/difficulty in swallowing/ interference with
movement/disfiguration
 PAIN - the nature of pain/site/time of onset
*Most malignant swellings are painless to start with, pain only appears due to
involvement of nerves, deep infiltration, ulceration, fungation or associated
inflammation and often indicates inoperability.

 FEVER -seen in ℅ inflammatory swelling/abscess/lymphadenitis/ hodgkin's

disease
 SECONDARY CHANGES - like softening, ulceration, fungation, inflammatory
changes etc.
 PRESENCE OF OTHER LUMPS
 RECURRENCE OF SWELLING
 IMPAIRMENT OF FUNCTION - particularly of the limb or spine may be
associated with a swelling near about.
 LOSS OF BODY WEIGHT - associated with malignant growth or cold abscess
with generalized tuberculosis.
 PRESSURE SYMPTOMS

PAST HISTORY - similar swellings in the past, past history of TB/syphilis

PERSONAL HISTORY - any addictions ( history of habit of eating betel leaf,betel

nut,slaked lime or tobacco in ℅ growth in the mouth, tongue, cheek or lip)

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FAMILY HISTORY - of TB, Malignancy

PHYSICAL EXAMINATION

 Any Cachexia /Malnutrition/abnormal attitude

 Raised temperature and pulse rate in ℅ inflammatory swellings

LOCAL EXAMINATION

A. INSPECTION
 SITUATION and also note the extent of the swelling in both horizontal and
vertical directions.
 SHAPE
 SIZE - mention the horizontal and vertical dimensions
 SURFACE
 COLOR
 EDGE - clearly defined or indistinct
 NUMBER
 SKIN OVER THE SWELLING - whether red and edematous/glossy with
venous prominence/any pigmentation/presence of scar/peau d’ orange
 PULSATION
 Visible PERISTALSIS (in ℅ abdominal swellings)
 MOVEMENT WITH RESPIRATION (in ℅ abdominal swellings)
- seen in swellings arising from liver, spleen, stomach,
gallbladder,hepatic and splenic flexures of the transverse colon.
 IMPULSE ON COUGHING
 MOVEMENT WITH DEGLUTITION(in ℅ swelling in front of neck)
- Eg : swellings fixed to larynx or trachea like thyroid
swellings,thyroglossal cysts,subhyoid bursitis and pre- and
paratracheal lymph nodes.
 MOVEMENT WITH PROTRUSION OF TONGUE (in ℅ swelling in front of neck)
- Eg : thyroglossal cyst
 ANY PRESSURE EFFECT
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 - like edema/wasting of limbs/venous engorgement
B. PALPATION
 LOCAL TEMPERATURE
 TENDERNESS
 SIZE, SHAPE AND EXTENT
 SURFACE - smooth(cyst)/lobular with smooth bumps(
lipoma)/nodular(matted lymph nodes)/irregular and rough(carcinoma)
 EDGE - whether well defined or indistinct(merging imperceptibly into
surrounding structures)
 well defined margins -seen in ℅ neoplastic and chronic inflammatory
swellings, where
 benign growths have smooth margins
 malignant growths have irregular margins
 ill-defined or indistinct margins -seen in acute inflammatory swellings
 *Benign tumour and a cyst - both have a smooth margin, what
differentiates them is that the margin of benign tumour like lipoma slips
away from the palpating finger but does not yield to it, while margin of a
cyst yields to the palpating finger and cannot slip away from the finger.(SLIP
SIGN)

1 - LIPOMA 2 - CYST

1. CONSISTENCY - UNIFORM(soft,cystic,firm,bony hard,stony hard)/VARIABLE

consistency
2. FLUCTUATION - seen in swellings which contain liquid or gas
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 ● test always performed at right angles to each other
● the two fingers kept as far apart as size of swelling allows
● in ℅ a freely movable swelling, it should be held fixed with thumb and
forefinger of one hand, while the swelling is compressed by thumb and
forefingers of other hand(as in the ℅ a hydrocoele)
● in ℅ very small swelling(cannot accommodate 2 fingers)
1. Paget's test - press the swelling at its centre(swelling with fluid will be
softer at the centre than the periphery, while a solid swelling will be
firmer at the centre)
2. 1st figure shows how a small swelling may be displaced as a whole by
the displacing finger shifting it towards the watching finger (eliciting a
false sense of fluctuation even though the swelling is solid)

The 2nd method shows the CORRECT method of eliciting fluctuation in case of a
small swelling.

W - Watching fingers, D - Displacing fingers

● for very large swelling, 2 or even 3 fingers used for providing pressure and
palmar aspect of 4 fingers of other hand used to perceive movement of
displaced fluid
● false positive yielded in soft swellings - eg: lipoma,myxoma,soft
fibroma,vascular sarcoma etc.

3. FLUID THRILL - in ℅ a
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 ● Big swelling - tap swelling on one side with 2 fingers while percussion
wave felt on other side with palmar aspect of the hand
● Small swelling - 3 fingers placed on the swelling and middle finger is
percussed with the other hand while percussion wave is felt by the other 2
fingers on each side

4. TRANSLUCENCY - means swelling can transmit light through it.

So the swelling must contain clear fluid eg: water, serum, lymph, plasma or highly
refractile fat.

5. IMPULSE ON COUGHING - seen in those swellings in continuity with

a.) abdominal cavity - eg:hernia, ilio-psoas and lumbar abscesses

b.) pleural cavity - eg: empyema necessitans

c.) spinal or cranial cavity - eg : spinal or cranial meningocele

6. REDUCIBILITY - (when the swelling reduces and completely disappears when it

is pressed upon, as the contents are displaced into the cavity from where they
have come out and may not come back unless an opposite force, such as
coughing or gravity is applied)
eg : Hernia, lymph varix, saphena varix, varicocele, meningocele

7. COMPRESSIBILITY - (when the swelling can be compressed, but would not

disappear completely, as the contents are not actually displaced, so the
swelling immediately reappears as the pressure is taken off)
eg : Swellings which may not have connection with
abdominal/pleural/spinal/cranial cavity, mostly liquid-filled vascular
malformations like arterial, capillary or venous hemangiomas, lymphangiomas.

8. PULSATILITY - whether expansile or transmitted pulsation

9. FIXITY TO OVERLYING SKIN - look for skin pinchability
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10.RELATIONS TO SURROUNDING STRUCTURES
● swellings arising from the subcutaneous tissue are free from overlying skin
and from underlying contracted muscle
(if lipoma is pushed sideways, puckering is seen in some places over the
tumor)

● tumors arising from overlying subcutaneous tissue, but which is fixed to the
muscle, becomes more prominent and cannot be moved along the line of
muscle fibres when muscle is made taut
● in ℅ tumors arising from the muscles or deep fascia, the tumor can be
moved sideways with muscle relaxed, but when the muscle is made taut, its
size will be diminished and tumor becomes fixed
● if tumor lies deep to the muscle, it will virtually disappear as soon as muscle
becomes taut
● swelling in connection with tendon moves along with the tendon and
becomes fixed when muscle is made taut
● swellings in connection with the vessels and nerves do not move along the
line of vessel or nerve but moves a little extent at right angles to it
● swelling in connection with a bone is absolutely fixed even when the
overlying muscle is relaxed and cannot be moved apart from the bone

C. STATE OF REGIONAL LYMPH NODES - Examine the draining lymph nodes.

r/o generalized lymphadenopathy.

D. PERCUSSION - resonant/dull note over hernia,

tenderness over Brodie's abscess,

Hydatid thrill.

E. AUSCULTATION - auscultate pulsatile swellings to r/o bruits or murmurs.

F. MEASUREMENTS - to find out increase in swelling at definite intervals/ to
find out wasting distal to swelling.
G. MOVEMENTS - examine the movements of the nearby joints to r/o any
impairment.
H. EXAMINATION FOR PRESSURE EFFECTS
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 ● Examine arterial pulse distal to the swelling- swelling may press on the
main artery and cause weak pulse distally
● Neurological examination- pressure by swelling can cause
paresis/paralysis of muscles with or without sensory disturbances
● Examine the subjacent bone - erosion seen in aneurysm and dermis cyst
on the skull.

GENERAL EXAMINATION

● In case of a malignant swelling, examine for any evidence of metastasis.

- Respiratory System - enquire about hemoptysis or chest pain,
examine for pleural effusion or consolidation.
- Liver should always be examined
- Abdominal Examination carried out to r/o peritoneal mets
- The Spine, Pelvis, Trochanters of Femurs, Skull should be examined
for bony metastases.
● In case of lymph node enlargement always examine the other groups of
lymph nodes.
● If swelling is suspected to be a gumma, examine for other syphilitic
stigmas.

DISCUSSION
DIAGNOSIS OF A SWELLING

 First find out the origin i.e swelling is originating from the skin, the
subcutaneous tissue, the muscles, the vessel, the nerve, the bone
 And Secondly, the cause of the swelling - i.e whether the swelling is
congenital, traumatic, inflammatory, neoplastic or otherwise
➔ A LUMP is a vague mass of body tissue.
➔ A SWELLING is a vague term which denotes any enlargement or
protuberance in the body due to any cause(like
congenital/inflammatory/traumatic/neoplastic/miscellaneous).
➔ A TUMOR/NEOPLASM is a growth of new cells which proliferate
independent of the need of the body.

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 LIPOMA
• What is lipoma?
It is a benign tumor arising from adult fat cells.
• What are the diagnostic points for lipoma?
1. Lobulation
2. Slip sign
3. Soft swelling with pseudofluctuation
4. Transillumination positive if it is subcuta-neous
5. The overlying skin may show prominentveins when the lesions are large.

• What is the cause for pseudofluctuation?

Intracellular fat is fluid at body temperature.Therefore the swelling will be soft
andfluctuation will be elicited in one plane. For atrue cyst one should elicit
fluctuation in twoplanes at right angles to each other which is notpossible in
the case of lipoma and therefore it iscalled pseudofluctuation.

•Why it is called universal tumor or ubiquitous tumor?

Lipomas can occur anywhere in the body where fat is present and therefore it
is called universal tumor.

• What is the commonest plane of lipoma?

Subcutaneous (between the deep fascia and skin).

• What will be the finding in transillumination test?

Subcutaneous lipomas may be transilluminant. Big lipomas and deep lipomas
may not be transilluminant.

• What are the symptoms of lipoma?

1. Swelling (lump)
2. Cosmetic (unsightly swelling)
3. Interfere with movement
4. Pain (due to trauma and fat necrosis)

• What are the complications of lipoma?

1. Myxomatous degeneration
2. Calcification
3. Pressure effects
4. Fat necrosis (if they are situated over prominent areas and subjected
to trauma)
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 5. Ulceration (repetitive friction cause ulceration)
6. Intussusception in submucous lipoma.
Note: Lipomas never turn malignant. Liposarcomas arise de novo and not in a
benign lesion.

• Which are the areas where liposarcomas are commonly seen?

1. Proximal thigh 2. Retroperitoneum 3. Mediastinum

• What are the investigations required?

1. FNAC from the swelling
2. Radiology of the part
3. If the swelling is big and sarcoma is suspected, core biopsy and MRI are
done.

• What is the surgical treatment recommended in the given case?

Excision of the swelling under general anesthesia (if the swelling is small
excision is done under local anesthesia using 1% lignocaine with or without
adrenaline).

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 HERNIA
History
 Age:
Indirect usually in young
Direct usually in older people.
 Occupation : Strenuous work ( associated weakness of abdominal muscles
Complaints
 Pain: Dragging & aching pain in the beginning, which gets worse as the day
passes.
When the hernia is very painful & tender, it is probably strangulated.
 Lump-
? How did it start? Whether on straining like coughing /weight lifting.
? Where did it first appear?
? What was the size & extend when it was first seen?
? Does it disappear on lying down?
 Systemic symptoms
Intestinal obstruction: colicky abdominal pain, vomiting, abdominal
distension, absolute constipation
 Other complaints
Persistent coughing, constipation, frequency of micturition/urgency of BPH
Read out anatomy of prostate, BPH, management.
Past history
 Previous surgery
 H/o hernia repair

Local examination
Expose from level of umbilicus to mid thigh
Position of the patient: First examined in standing position, then in the
supine position.
Inspection
 Swelling :
Size, shape
Position & extend
Visible peristalsis
 Skin over the swelling

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 Normal/reddness /discoloration & streaks of brown pigmentation d/t
deposition of hemosiderin. Scar of previous repair
 Impulse on coughing
 Position of penis

Palpation
Describe like the examination of a swelling
Only relevant points are given here.
 Position & extend
When it descends into the scrotum, obviously an inguinal hernia
When confined to the groin:
Above the inguinal ligament & medial to the pubic tubercle, inguinal
hernia
Below the inguinal ligament & lateral to the pubic tubercle, femoral
hernia
 To get above the swelling
To differentiate a scrotal swelling from an inguino scrotal swelling.
In inguinal hernia, one cannot get above the swelling.
 Consistency
Doughy & granular –omentum
Elastic –enterocele
Tense & tender—strangulated hernia
 Relation of swelling to the testis & spermatic cord
Inguinal hernia: Infront & sides of spermatic cord
 Impulse on coughing :
Always performed in standing position.
Absent in the case of strangulated hernia, incarcerated hernia & when the
neck is blocked by adhesions.
Zieman’s technique: Index finger over deep inguinal ring ( ½ inch above the
mid inguinal point), middle finger over superficial inguinal ring, ring finger
over saphenous opening (4cm below & lateral to the pubic tubercle)
Can only be applied when no obvious swelling / after the hernia has been
completely reduced.
If impulse is felt on the
Index finger- indirect inguinal hernia
Middle finger -direct
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 Ring finger- femoral hernia

 Is the swelling reducible??

 Invagination test
 Ring occlusion test
Standing position
Confirmatory test to differentiate between direct from indirect inguinal
hernia.
A thumb is pressed on the deep inguinal ring. Patient is asked to cough. A
direct hernia will show a bulge medial to the occluding finger but an
indirect hernia will not find access.

Percussion
Resonant note over a hernia—enterocele
Dull—omentum/ extraperitoneal fatty tissue
Examine the testis, epididymis, spermatic cord
Examine the tone of abdominal muscles:
Malgaigne’s bulge

System examination
Resp : Bronchitis
GIT: intestinal obstruction

Q) How many fingers are needed to examine a case of hernia?

5 fingers
Index, middle, ring fingers for zieman ‘s test
Thumb for ring occlusion
Little finger for invagination
Q) If an examiner has his index finger amputated, how will he perform zieman’s
test?
He can use any other finger.
But, result should be correctly interpreted.
Two classical signs of an uncomplicated hernia are
(1) impulse on coughing
(2)Reducibility

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DISCUSSION
Definition: Abnormal protrusion of whole or part of a viscus through the wall
that contains it.
Classification: Internal and external (90%)
External Hernias: Groin hernias and ventral hernias
Groin hernias: Includes direct and indirect inguinal and femoral hernia. Protrusion
through the osseomyopectineal orifice of Fruchard.
Inguinal Hernia: protrusion is through superficial inguinal ring.
Groin defined as area coming in contact when you flex the hip.
Learn anatomy of inguinal canal: (very very important)
 Boundaries, length, surface marking of SIR and DIR
 Contents of spermatic cord and inguinal canal
 Coverings of indirect and direct inguinal hernia
 Direct Hernia : Learn boundaries of Hesselbachs Triangle.
Parts of a hernia : Sac and contents. Sac consists of mouth, neck, body and
fundus.
Classifiaction of groin hernias
NYHUS Classifaction :

GILBERTS classification :
Gilbert Description
type
1 Indirect inguinal hernia with snug internal inguinal ring
Indirect inguinal hernia with moderately dilated internal
2 ring less than 4cm
Indirect inguinal hernia with a large dilated and
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 3 distorted internal ring more than 4 cm
Direct inguinal hernia with full blow-out of the posterior
4 wall. Internal ring intact; no peritoneal sac
Direct inguinal hernia. Diverticular defect of the
5 posterior wall. Internal ring intact, no peritoneal sac
EUROPEAN HERNIA SOCIETY Classfication : Primary or Recurrent , Lateral ,
medial or femoral, 1 , 2 or 3 finger size defect
Clinically, can be reducible, irreducible, obstructed, inflamed, incarcerated and
strangulated (Natural history of hernia)
(Learn definition of each from new BAILEY )
Q What are the causes of irreducibility in a hernia?
Q What are the symptoms of strangulation ? (hint : pain out of proportion,
redness, fever, tachycardia
Q What is richters hernia ? Why is it more dangerous ?
Q What are the symptoms of obstruction ? ( pain, vomiting, obstipation)
Q 2 causes of acute urinary retention in a hernia case? ( BPH, BOO)
Q What are the DDs of inguinal hernia ?
(FH, LNs, Saphena varix, Psoaas abcess, undescended testis, Femoral A
Aneurysm, rupture of adductor magnus tendon )
Q Significance of past and personal history in a hernia case
Q How to differentiate between omentocele or epiplocele and enterocele ?
Q What is a spigelian hernia?
Q Rare types of hernia : learn Amyand, littles , littres , Maydls,
Q Mechanism of inguinal canal
Q What are the risk factors for a hernia ? ( Hint : Classify as causes of
increased abdominal pressure, such as chronic cough, constipation and
BPH, and weak abdominal muscle tone causes, apart from congenital
causes. )
Q Why is smoking a risk factor ? (hint : Type 3 collagen involvement )
Q Are weight lifters predisposed to hernia ? ( Refer Bailey )
Q What are the two cardinal features of a hernia ? ( Refer DAS – expansile
impulse on coughing, reducibility )
Q What are Malgaigne bulges?
Q What is Taxis? How will you do taxis?
Learn each test of indirect and direct hernia clearly from das, including
position of patient, and side of hand used by examiner for each test. (Find
out why different fingers and different hands are used for different tests)
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 Q What are the investigations you will do in this case? Note; hernia is usually
a clinical disagnosis. Baseline investigations must be done. A pelvic and
abdominal ultrasound may be done to rule out predisposing factors. Rarely
– CT abdomen in case of recurrent hernia and in case of complications.
Herniogram – obsolete. Transrectal ultrasound to find residual urine

TREATMENT OPTIONS:
Herniotomy – congenital hernia / hydrocele
Herniorraphy – Bassinis, Shouldice repair (learn how many layers, material used
in shouldice, problems with bassini – non physiological connection of conjoint
tendon to inguinal canal)
Hernioplasty – Lichensteins repair ( size of mesh used – 15 by 7 cm ), laparascopic
repair : TEPP, TAP
Advantages and disadvantages of TEPP and TAP
Complications of hernia repair (Hint; recurrence, meshoma, mesh infection,
testicular atrophy etc )
Refer : What is a truss? What is a sliding hernia, Gilberts PHS, abdominal
compartment syndrome, bilobed hydrocele, types of indirect hernia –
bubonocele, funicular, scrotal
MUST KNOW : Triangle of doom , Triangle of pain : boundaries, contents.

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 HYDROCELE
History
• History of painful micturition and frequency of urine
• History of trauma
• History of pain and discomfort in the testis
• History of malaise and weight loss (tumor)
• History of filariasis
• History of tuberculosis and family history of tuberculosis
Inspection
• Size
• Shape
• Extent: confined to scrotum
• Surface: smooth; absence of rugosities
• Margin:well defined
• No cough impulse (differentiation between inguinoscrotal hernia)
Palpation
In addition to the usual findings, in case of hydrocele
• Can get above the swelling
• Fluctuation present
• Cystic consistency
• Transilluminant
• Testes cannot be palpated separately
Percussion
• Dull on percussion

DISCUSSION
A hydrocoele is an abnormal collection of serous fluid in a part of the processus
vaginalis, usually the tunica vaginalis.

TYPES:
• Congenital : By connection with the peritoneal cavity via a patent
processus vaginalis
• Acquired :
❖Primary : Idiopathic
❖Secondary : usually as a result of infection, trauma or tumor
MANAGEMENT
• Congenital hydrocoeles are treated by herniotomy if they do not resolve
spontaneously.
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 • Small acquired hydrocoeles do not need treatment. If they are sizeable and
bothersome for the patient, then surgical treatment is indicated.
• Surgery is the mainstay of treatment. There are three main surgical
techniques for hydrocoeles (learn procedures).
 Lord's plication
 Jaboulay's procedure
 Excision
Testicular malignancy is an uncommon cause of hydrocoele that can be
excluded by ultrasound examination.

VIVA QUESTIONS
• What are the conditions in which it is not transilluminant?
Infected hydrocele (Pyocele) b. Hematocele c. Chylocele d. Thickened and
calcified sac.
• What is the color of the hydrocele fluid?
Hydrocele fluid is amber-colored [color of urine].
• How will you rule out a tumor in a case of hydrocele?
a) By palpation of testis
 Testis will be separately palpable in case of tumor
 The testis becomes relatively heavy in neoplasm
 The testicular sensation will be absent
 The testis will be nodular, indurated and irregular.
b) By ultrasound examination – one can rule out a mass lesion in the
testis
c) By tumor markers – β hCG and α fetoprotein.
• Layers of scrotum
“Some Dirty Englishmen Called It Testes”
 Skin
 Dartos
 External spermatic fascia
 Cremasteric fascia
 Internal spermatic fascia

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VIVA STATIONS

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 OPERATIVE PROCEDURE
1. INGUINAL HERNIA
Indication: Indirect inguinal hernia, direct inguinal hernia
Pre-operative preparation: Treatment of chronic cough, BPH, constipation,
stop smoking
Anaesthesia: local, spinal, general
Position: supine
Incision: half inch above and parallel to the medial 2/3rd of inguinal ligament
Procedure:
incision deepened through superficial layers.
External oblique cut, cord structures delivered and sac isolated.
Sac opened and contents reduced back;
transfixation sutures put at region of deep ring, excess sac excised= Herniotomy
Other methods: herniorrhaphy, hernioplasty
Post operative management: early ambulation, Avoid strenuous work for 6
months
Complication: wound infection, injury to inferior epigastric artery, injury to
ilioinguinal nerve, recurrence

2. Lichtenstein Tension Free Mesh Repair( LTFMR )

Initial steps same as inguinal hernia repair till procedure
Procedure:
Mesh- Polypropylene mesh 8x16 cm mesh tailored as required and is cut in the
shape of a sole. A slit is made in the lateral border junction of lower 1/3rd and
upper 2/3rd
Placement: medially sutured to the tissue overlying the pubic tubercle
Laterally the two slit ends encircle the spermatic cord and fish-tailing of ends is
done
Inferiorly to the inguinal and the lacunar ligament
Superiorly to the conjoint tendon
Mechanism of action: fibroblasts and capillaries grow over the mesh,
converting it into a thick fibrous sheath and strengthens the posterior wall
Advantage of PPM: high tensile strength, non-absorbable, ideal porosity for
high visibility and colonization, cheaper, flexible for any anatomic placement

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3.EVERSION TV SAC
Indication: Hydrocele
Anaesthesia: local, spinal, general
Position: supine
Incision: Vertical incision on scrotal wall, parallel to median raphae
Procedure: Incision deepened till tunica vaginalis reached. Sac separated from
rest of the coverings by 2 fingers, sac incised and the fluid emptied. Allow the
testis to come out through the opening. The tunica vaginalis everted and margins
sutured behind the testis. Drain placed insitu. Closure done in layers
Post operative management: Patient should wear suspensory bandage
(scrotal support)
Complication: Oedema, infection, haematoma, injury to vas, testis, testicular
atrophy

4.HEMORRHOIDECTOMY
Indication: Third degree piles, symptomatic piles( I degree / II degree)
Anaesthesia: spinal
Position: lithotomy
Procedure: Anal sphincter is stretched, traction is applied on each pile mass, ‘V’
shaped cut made at the base of piles at the muco-cutaneous junction. Blunt
dissection is done to expose the external sphincter. Pedicle is transfixed, Pile
mass excised distal to the ligature. Haemotasis achieved, T- bandage applied
Post operative management: Laxatives for 3 days, liquid diet for 3 days

5. MODIFIED RADICAL MASTECTOMY

Indication: Carcinoma breast
Anaesthesia: general
Position: Supine , arm abducted and placed over an arm support. Small sand bag
placed beneath the scapula to elevate the breast
Incision: Transversely placed elliptical incision which will include nipple areolar
complex (Stewart)
th
Procedure: Upper flap reflected upto clavicle, lower flap till 6 I/C space. Breast
tissue along with nipple areolar complex and the tumour dissected out from
underlying pectoral fascia and muscles. Lift it towards axilla. Axilla entered by
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 opening the clavipectoral fascia. Identify the axillary vein, axillary lymph
nodes, fatty areolar tissue dissected /cleared inferior to axillary vein after
retracting the pectoralis minor. Axillary vein,long thoracic nerve of Bell,
cephalic vein, thoraco-dorsal trunk are preserved. Removal of breast with
axillary contents. Skin closure with a suction drain
Post operative management: Pressure dressing, Physiotherapy of shoulder
th
joint, Drain removal on 5-7th day, Suture removal on 9 day
Chemotherapy or radiotherapy depending upon indication
Complication: Hematoma, infection, seroma, flap necrosis, Oedema of arm,
frozen shoulder, injury to nerves, recurrence

6. TOTAL THYROIDECTOMY
Indication: Carcinoma thyroid, MNG?, Toxicity?
Anaesthesia: General
Pre-operative preparation: Achieve euthyroid status, Specific investigations,
Consent
Position: Supine, head end up, sand bag between shoulder blades, neck
extended
Incision: Kocher’s curvilinear collar incision put through lower neck crease
Procedure: Incision deepened through s/c fatty layer and platysma, upper flap
reflected up to thyroid cartilage, lower flap reflected down till suprasternal
notch. Joll’s self retaining thyroid retractor placed. Investing layer of deep
fascia opened in mid line, strap muscles retracted.
Thyroid gland with nodule mobilized from tracheo oesophageal groove by blunt
dissection. Middle thyroid vein ligated and divided, superior pedicle ligated
and divided close to the gland, inferior pole ligated and divided away from
the gland. Intra capsular ligation of inferior thyroid artery branches done-
after supplying para thyroids
Total removal of glandular tissue done after preserving the recurrent laryngeal
nerve and parathyroids . Haemostasis achieved,suction tube drain placed
insitu; closure done in layers
st
Post operative management: Drain removed on 1 post op day, suture
th
removed on 5 post op day. Post op period - eltroxine

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Complication: Haemorrhage, respiratory obstruction, recurrent laryngeal nerve
palsy, thyroid insufficiency, parathyroid insufficiency, thyroid storm, wound
infection, Stitch granuloma, keloid

7. TRENDELENBURG OPERATION
Indication: Varicose vein with SFJ incompetence
Pre-operative preparation: Doppler study, Mark sites of perforators, Treat
ulcer - if present
Anaesthesia: spinal , GA, LA
Position: supine
Incision: Oblique incision put 2cms below medial third of inguinal ligament
Procedure: Incision deepened, LSV identified and tributeries (superficial
circumflex iliac, superficial inferior epigastric, superficial external pudendal)
ligated and divided, 2 inches of proximal segment of LSV removed. Stripping
may be done for thigh segment. Perforator ligation done
Post operative management: Compression bandage for 3 days, elastic
th
stockings, mobilization, sutures are removed on 7 post op day
Complication: Bruising, bleeding, haematoma, pain, injury to saphenous
nerve/sural nerve, DVT, recurrence

8. CIRCUMCISION
Indication: Religious, phimosis, paraphimosis, balinitis, balanoposthitis, Ca
prepuce, STD eg Herpes infection
Anaesthesia: children-GA, Adults-LA
Position: supine
Incision: dorsal skin incision
Procedure: Dorsal skin cut upto the corona, then circumferentially and ventrally
(optimum skin is cut ventrally). Frenular artery transfixed and ligated ventrally.
Skin is apposed to cut edge of corona with interrupted chromic catgut sutures
Other method: Hollister Bell cup technique (Plastibel device)
Post operative management: analgesics, antibiotics

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Complication: reactionary hemorrhage, infection, stricture urethra, chordee,
priapism
Contraindication: hypospadias, epispadias, penile torsion

9. APPENDICECTOMY
Indication: a/c appendicitis, recurrent appendicitis
Anaesthesia: GA, spinal, epidural
Position: supine
Incision: McBurney’s gridiron incision, Lanz curved transverse incision
(cosmetically better)
Layers opened: skin-subcutaneous tissue-camper’s fascia-scarpa’s fascia-
external oblique aponeurosis (along fibres)-internal and transervse abdominal
muscles split-peritoneum
Features: inflamed turgid appendix, pus in the RIF, omentum in the RIF,
gangrene, faecolith.
Procedure: trace the taenia coli. Hold the mesoappendix with babcock forceps,
vessels divided and appendix freed. At base purse string suture (silk) placed and
crushed, another suture applied above it and appendix cut in between.
Closure: peritoneum with catgut, muscles with Vicryl, external oblique with silk,
subcutaneous tissue with Vicryl, skin interrupted silk. Place drain if appendix
gangrenous or large amount of pus in RIF.
Post operative management: RTA, IV fluids- 24-48 hrs. oral fluids given after
bowel sounds are heard. Antibiotics, suture removal on the 7th day
Complication: fever- thrombophlebitis, UTI, sepsis, wound infection, intra-
abdominal abscess, faecal fistula
Contraindication: appendicular mass.

10. LAPAROSCOPIC APPENDICECTOMY

Advantages: diagnosis is confirmed, other parts of the abdomen are visualized,
pelvic structures are assessed properly, and trauma of access is less, faster
recovery
Disadvantages: technical difficulties especially in burst appendix, cost factor and
availability.
Anaesthesia: done under GA.
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Position: head down position with right tilt, surgeon and camera man on left side,
scrub nurse on the right side and monitor is kept at the foot end.
Procedure: 10 mm port is placed at the umbilicus. Working ports are two 5 mm,
one on each side of the lower abdomen or one on left and other on the lower
midline. pneumoperitoneum is created with CO2. Continue the rest of the
procedure as above and remove the appendix through the 10 mm port. Umbilical
port closed in two layers, other ports closed by skin sutures.
Post operative management: oral food can be given after 12 hours.
Complication: injury to the bowel, vessels during port placement. Complication of
pneumoperitoneum, bleeding, accidental cautery injury, bowel perforation,
peritonitis, ligature slipping.

11. CHOLECYSTECTOMY
Indication: symptomatic gall stones, acute cholecystitis, empyema GB, mucocele
GB.
Anaesthesia: GA
Position: supine
Incision: right sub costal incision (Kocher’s incision), or right paramedian incision,
or horizontal incision, or Mayo- Robson incision.
Procedure: after the abdomen is opened the bowel is pushed down and stomach
is pushed medially.
Duct- Calot’s triangle is dissected, cystic artery and duct ligated close to the GB.
Gall bladder is separated from the GB fossa and removed.
Fundus- done in case of dense adhesions, fundus is separated from the liver bed,
dissection is done proximally and then cystic duct and artery are ligated. Drain is
placed. On table cholangiogram is a must after cholecystectomy.
Post operative management: drain removed after 72 hours. antibiotics and
analgesics.
Complication: infection and subphrenic abscess, bleeding from cystic artery or
liver bed, injury to CBD, hepatic duct. Bile leak and fistula formation. Biliary
stricture formation. Injury to colon duodenum and mesentery.

12. LAPAROSCOPIC CHOLECYSTECTOMY

Position: supine, head end up and right side up.
Ports: 10 mm port in the umbilicus to pass telescope. 10 mm port in the midline
as a working channel. Two 5 mm ports at the midclavicular line and anterior
axillary line in the subcostal region
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Procedure: pneumoperitoneum- ports- with lateral port GB grasper forceps is
passed and the fundus is held and pushed up to the diaphragm. Through the
other5 mm port grasper is passed and holds the Hartmann’s pouch. Through the
10 mm working channel dissector is passed and Calot’s triangle is dissected, cystic
duct is identified. First posterior dissection is completed and cystic artery and
duct are clipped and ligated. GB is dissected off the liver bed using cautery or
harmonic scalpel. GB is removed through the 10 mm port with reducer. Bleeding
points coagulated. Wash is given to the bed. If needed a tube drain is placed
through the 5 mm port. All ports are closed.
Post operative management: Drain removed in 24hrs, oral foods started after 24
hours. Patient can be discharged in 48 hours.

13. WHIPPLE’S PROCEDURE

Indication: Ca head of pancreas, pancreatic cyst, pancreatitis, periampullary
carcinoma, bile duct cancer.
Anaesthesia: GA
Position: supine
Incision: midline incision.
Procedure: examine the area and assess respectability of the tumour ie. the
tumour has not spread to nearby structures. GB is mobilized and bile duct is
divided. Next the distal 40% of the stomach is divided and the pancreas is visible.
The pancreas is then excised with clear margin from the tumour. Avoid injury to
superior mesenteric artery and veins and portal veins. At last the proximal 10 cm
of the jejunum is also divided and the entire specimen is freed and removed.
reconstruction is done in steps. First the remaining pancreas are connected to
proximal part of jejunum in end to side fashion (pancreaticojejunostomy). Next
bile duct is connected to the jejunum (choledochojejunostomy). Finally stomach
anastomoses to the jejunum is done via Roux en Y procedure
(gastrojejunostomy). Drain is placed in situ.
Postoperative management: RTA for 24 hours, start on oral fluids and by 72
hours start on oral food. Drain can be removed on the 5th post operative day.
Antibiotics, analgesics, dietary changes, promotility agents, pancreatic enzyme
replacement.
Complication: delayed gastric emptying, bile leak, pancreatic leak, cholangitis,
bleeding, biliary sepsis, DVT.

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14. INCISION AND DRAINAGE
Indication: Pyogenic abscess
Anaesthesia: usually general, if abscess superficial and pointing- local
Position: depending on site of abscess
Incision: stab incision using scalpel blade no. 11
Procedure: Stab incision at the most prominent part (skin red, thinned
out and pointed), pus sent for C&S. Sinus forceps used to break the
loculi and pus drained out. Cavity irrigated with iodine solution and
normal saline. Wound not closed, drain kept for 24 hours
Post operative management: Antibiotics, diabetes control.
Complication: hematoma, injury to nerves and vessels
NB: To prevent injury to the neurovascular structures skin incision is
preferred especially in the neck and axilla. Eg in parotid abscess to
prevent facial nerve injury Hilton’s method is used.

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 X RAY
When given an xray comment on
1. VIEW
PA view-anterior structure are better seen
AP view-taken for spinal pathology
2. ANATOMIC PART-chest xray ,abdomen Xray
3. PLAIN/CONTRAST
4. Phase Of Respiration-normally in full expiration
5. Exposure-over/adequate/under
6. Position-look at the trachea and clavicle on either side, comment if its
rotated
7. Soft tissue shadow
8. Bony cage
9. Lung fields
10. Diaphragm

Important points and questions

 D/d air pocket in soft tissue
 surgical emphysema
 multiple rib fracture
 rupture esophagus
 tracheal injury
 penetrating trauma
 emphysematous bullae rupture
 whats the clinical sign in surgical emphysema- Crepitations
 Look for 1st rib- rule out cervical rib (cervical rib x-ray otherwise may be
perfectly normal)
 Flail chest-Definition, treatment
 Intercostal drainage-safety triangle, when to remove
 Cannon Ball secondories in lung-
why are they round shaped ? lung is elastic, equal pressure is exerted from all
sides.
Sites of likely primary-thyroid, breast, soft tissue sarcoma, renal cell
carcinoma
 Pneumothorax ,hemopneumothorax (airfluid level)
 Cardiac tamponade
 Gas under diaphragm-d/d perforation of hollow viscus-only in 60-70% cases
its seen. causes:-
peptic ulcer,
stomach carcinoma,
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 ca colon,
Typhoid ulcer,
IBD
penetrating injury
Chiladiti syndrome-colon loop between liver and diaphragm
infection by gas forming organisms
post operative-after laproscopy
tubal insufflation test
P.S. always confirm the side of the x-ray first. Do not get confused and say gas
under diaphragm for fundic gas bubble!
 X-ray cervical spine -important in thyroid surgery-lateral view-scabbard
trachea, retrosternal extention
 Plain x-ray abdomen -d/d of radio-opaque shadow in lumbar region
Fecolith, phlebolith, renal stone, gall stone, calcified lymph node, costal
Cartilage,calcification
*read about Gall stone-it will be asked in long case-obstructive jaundice,
Cholecystectomy specimen, X-ray
 X ray of pancreatic stones-multiple opacities crossing midline at L1-
causes,treatment
 X Ray Abdomen showing peritonitis(ground glass appearance)
 Intestinal Obstruction- multiple air fluid levels. normally 3 areas of Air-Fluid
levels are seen- fundus, duodenal cap, ileocecal valve
 identification of bowel segments-
jejunum-concertina appearance of mucosa
ileum -characterless
colon-haustrations
learn causes of intestinal obstruction(most common-post op
adhesions),classification volvulus, intususseption
 Contrast X Ray:
Barium swallow-BaSO4 paste (75BaSo4:25%water)
Barium meal-BaSo4 cream(50:50) only upto ileocecal valve is seen
Barium follow through-BaSo4 cream is used
Barium enema-baSo4 solution(25:75)
 X ray of Ca Esophagus(rat tail appearance) ,Achalasia cardia (bird beak
appearance)
 Barium meal picture-Ca stomach, GOO, intususseption,
 Read about IVU-preparation ,procedure , complication
 read about Kidney stones,hydronephrosis
 T tube Cholangiogram- done 10th day post operatively to look for retained
stone-its removed by Burhannes technique, read indication for on table
cholangiogram, management of bile duct stones and gall bladder stones
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  X ray Sigmoid Volvulus
 X ray Diaphragmatic hernia
 X ray Coin in trachea
 X ray Ulcerative colitis
 X ray Mammogram
 X ray Bladder calculi

SPECIMENS
Why does a surgeon need to learn pathology specimens?

To know the morphological differences during surgery and modify the surgery
accordingly.

1. wet mount specimen of lung- showing multiple round lesions-

metastatic Carcinoma
why do they appear round ,sites of primary
2. wet mount Mastectomy specimen - fibroadenoma/ca breast
Classification, investigation, treatment, riskfators, MRM, BCT,
3. wet mount Cholecystectomy specimen with stone-types of stones,
management, investigation
4. wet mount Thyroidectomy specimen
5. Liposarcoma
6. Testicular Carcinoma-Classification, investigation, orchidectomy- high
inguinal is for malignancy and low inguinal is for torsion. Chavasu
manouvre- cut open testis vertically and take frozen section (can preserve
the testis if no malignancy)
7. Renal cell carcinoma
8. Small intestine -ulcer,jejunal polyp-APC,PJS,HNPCC
9. CA colon
10.Mandibulectomy specimen- adamantinoma

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 INSTRUMENTS
1. Sponge holding forceps
Uses
 for draping
 wiping tissues in depth(pelvic surgeries)
 hold fundus of gall bladder
long shaft prevents accidental touching of sterile gloves on patients unsterile
body
2. Towel clips
 Backhaus towel clip- tip closes when we approximate the finger bows
 Cross action towel clip- tip opens when we approximate the finger bows
uses
 fix draping sheets
 fix cautery wire
 hold tongue in oral surgeries
 temporary closure of abdomen-to prevent abdomen compartment
syndrome
3. Surgical Blade, Bard parker handle
 There are 2 sets of blades -smaller of size 10 11 12 13 14 15 & larger ones
>18
 BP handle- No 3 is for smaller blades No 4 is for larger blades
 Use artery forceps to insert blade into handle
uses –
 to put incisions
 raising flaps-in MRM, thyroidectomy
 to divide pedicle
4. Adsons Thumb forceps-
 to hold tissues
 2 forms -toothed-skin fascia
 non toothed-muscle, blood vessels, thyroid gland
5. Spencer wells artery forceps -curved/straight
 mosquito -small artery forceps (why its called mosquito forceps-it can hold
even proboscis of a mosquito!)
6. Needle holder
7 .Listers sinus Forceps-
 it has no catch or lock& there’s no gap btw the blades
 to avoid accidentaly injuring any nerves and vessels
uses
 I&D of abscess-by Hiltons method
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  make sure theres pus inside(aspiration)
 skin incision done with scalpel
 lister forceps is advaned
*another forceps without a catch-desjardins choledocholithotomy forceps
8. Allis tissue holding forceps-
 it is used to hold skin, rectus sheath
 it has a set of teeth at its tip
9. Babcocks forceps-
 it s used in thyroidectomy, appendicectomy, holding intestines,
 its tip is curved & fenestrated
10. Lanes tissue forceps- its used in large tissue as in mastectomy
11. Kochers Forceps-its toothed, its used to hold tough tissues,
12. Volsellum forceps-
13. Cheatles forceps
14. Desjardins choledocholithotomy forceps
15. Cord forceps-to hold spermatic cord in males, round ligament in females.
DONOT call it acord clamp.
16. Mayos scissors-curved is used to cut tissues, straight is used to cut suture
17. langen becks retractor used in Thyroid surgery
18. Kellys retractor used in cholecystectomy, pelvic surgeries
19. Morris retractor used to retract abdominal wall in laprotomy
20. Jolls self retaining retractor-used to retract flaps in thyroidectomy
 open end faces the surgeon,concave surface faces the patient
21.Kochers thyroid dissector-used in ligating the superior pedicle,kept below the
pedicle
 it has long handle, short tip with 3 longitudinal gooves
22. Hernia director –it should not be confused with thyroid dissector .(Hernia
director has only a single groove while Thyroid dissector has Three grooves)
It’s used to safeguard contents in obstructed/strangulated hernia by
keeping it in between ring and the content, to divide the constriction ring
23. Tracheal dilator-used in tracheostomy
24. Peyers Crushing clamp -used in appendicectomy, vascularity of the bowel is
also lost
25. Occlusion clamp-vascularity is retained.only lumen is occluded
26. Foleys catheter-biluminal
 1 F = 0.33mm-outer circumference of the catheter
 connector in foleys is color coded
 length - 40cm
 16F-male(orange)14F -female (green)

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  indication-acute retention,to assess urine output,pelvic surgery,urological
surgery
 other than its use as urinary catheter-used in epistaxis, feeding
jejunostomy , cholecystostomy,suprapubic cystostomy ,amnioinfusion
 it should not be kept beyond 3 weeks
 if foleys catheter is stuck-puncture the balloon under US guidance
, puncture the balloon by over inflation, chemical injection of ether
 capacity of ballon-30 ml, usually we inflate it with 5-10 ml of sterile water,
if saline is used crystallisation can occur
 do not forget to pull back foreskin-to prevent priapism
27. Malecot catheter - flower like tip, not used for urethral catheterisation
28. Bakes dilator -used in serial dilatation of CBD
29. Right angled forceps-hook out veins in varicose vein surgery, pedicle in
thyroidectomy
30. Ryles tube-length 105cm, markings at 50 60 70cm
 absolute contraindication-base of skull fracture
31. Suture materials
 Types
 Natural absorbable-catgut
 non absorbable-silk
 Synthetic absorbable-Polyglactin
 non absorbable-polypropylene,poly amide
 Monofilament(less chance of infection)-Catgut,poltpropylene
 Polyfilament(more tensile strength)-silk ,polyglactin
32. Barrons ring applicator for Hemarroidectomy
33. Laryngoscope

34. Oropharyngeal airway

35. Cuffed endotracheal tube

36.2% Lignocaine

37. Elastic crepe bandage

38. Proctoscope

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ORTHOPAEDICS
System of practical examination in orthopedics
One short case for 25 Marks with viva which can be based on the case, its
management, relevant theory or any related xrays and instruments.
One viva station, usually instruments.

Most important short cases kept for exam:

1. Non-union, malunion
2. Chronic osteomyelitis
3. Cubitus
a. Varus: gunstock deformity (supracondylar # complication)
b. Valgus: ununited #lateral condyle humerus
4. Genu
a. Varum
b. Valgum
5. Swelling (bone tumour) most commonly osteochondroma
6. Knee swelling: Arthritis, Synovitis
7. Popliteal fossa swelling: Baker’s cyst, Semimembranosus bursa
8. Unreduced elbow dislocation
9. Isolated nerve injuries
10.Ganglion

Examination of orthopaedics short case:

Relevant history :
 Age of onset: certain tumors affect particular age groups ( refer
osteosarcoma, Ewings sarcoma, gct, multiple myeloma )
 History of trauma , if present , mechanism and mode of injury : example,
fall on outstretched hand, fall from bike, if it was a high velocity injury or
not, if fracture : open or not.
 History of pain : apart from routine questions also highlight duration,
nature and intensity of pain. ( acute severe pain in osteomyelitis, dull
aching in gct,tb and night cries in tb arthritis. Extra edge point : relief of
pain in osteoid osteoma and reason )
 Any swelling ?
 Is a deformity present, any restriction of movement, discharging sinus,
limp ?
Physical examination :
Inspection :
 Swelling : site – say epiphyseal / diaphyseal/ metaphysical, shape,
size,extent- part or whole of circumference, surface, edge, color, texture of
overlying skin, scars sinuses,
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  Note any deformity or gait abnormality
 Any disparity in length of limbs
 Muscle wasting, pressure effects.

Palpation :
 local rise of temp an tenderness
 Confirm swelling findings. Fluctuation, translucency, fixit, plane of swelling.
 Bony swellings are usually hard and immovable. In addition look for egg
shell cracking in gct and a groove may be rarely felt in case of exostosis.
 Assess distal neurovascular status !!
 Movements at the proximal and distal joints BOTH ACTIVE AND PASSIVE :
if restricted say how many degrees approximately if possible , for example
:flexion possible only upto 10 degrees
 Measurements proximal and distal to the joint

Last minute checklist :

NEVER FORGET
1. to inspect the ATTITUDE of the affected limb, learn to describe the attitude:
position of each joint proximal to distal. Eg the right shoulder is adducted,
internally rotated, elbow semiflexed, forearm pronated
2. inspect for DEFORMITY or swelling. Compare with opp side.
3. palpation, first mention tenderness, local rise in temperature
4. palpate the whole length of bone, compare with opposite side. Look for any
thickening,
5. irregularity, bony defect, crepitus
6. Always check for abnormal mobility and absence of transmitted mobility in
a case of nonunion
7. MEASUREMENT: both length and circumference of BOTH sides
8. MOVEMENTS
a. BOTH ACTIVE AND PASSIVE
b. BOTH JOINTS DISTAL AND PROXIMAL TO THE SITE
9. Atlast, always check distal pulse, sensations to rule out neurovascular
injury.

Relevant theory with respect to particular cases :

1. Non-union and malunion

Definitions:
I. Delayed union: when a fracture takes more than usual time to unite
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 II. Non-union: when a fracture shows no clinical or radiological evidence of
union. ( friends, say this first , if examine does not accept then say fda panel
definition ) Or
when fracture union has come to a complete standstill(serial xrays) OR
A period of 6 months have elapsed totally and the # has not united OR 3
months have elapsed and there is no progress.
FDA panel definition: Non union is said to be established when a minimum
of 9 months have passed since injury and fracture shows no radiological
visible progressive signs of healing continuously for 3 months.

Classifcation of non union :

i. Paleys classification:
 type ‘a’ with less than 1 cm bone loss and
 type ‘b’ more than 1 cm bone loss

ii. Weber and Muller s classification : hypervascular and avascular

 Hypervascular: again divided as elephant foot or hypertrophic, horse hoof
and oligotrophic
 Elephant foot : exuberant callus causes- insecure fixation and
premature weight bearing
 Horse hoof : unstable fixation
 Oligotrophic : major displacements, poor fixation

NOTE : there are two essential requirements for a fracture to heal. One is callus
formation and the other is alignment and fixation, any disparity in either of these
can lead to non union
 Types of avascular non union : torsion wedge, comminuited, atrophic and
gap or defect non union

Causes of non union : refer table in maheswari ( classify as local, fracture related ,
systemic and treatment related causes )
Diagnosis of non union : xray ap and lateral view : look for gap, callus, sclerotic
ends, comminuited fragments, and any decreased density from osteoporosis

X-ray appearance
 Delayed union:
#line visible, inadequate bridging calus
 Nonunion:
- # line visible,
- no bridging callus,
- medullary cavity obliterated,
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 - #ends rounded,
- smooth sclerotic
Serial x rays taken when diagnosis not clear

Management: depends on whether infected or not

 If infected : debridement, split skin graft 1 week later and bone grafting 6
months later is the classical method. Active method and ilizarovs technique
are other options
 Non infected : M/M depends on whether avascular or hypervascular.
For avascular, bone graft is a must: grafting do open reduction and bone
grafting. Bone graft can be cancellous, cortical or phemister ( subperiosteal
) grafts. Learn types of grafts from maheswari : 3 types auto allo and xeno
grafts
 Also electrical stimulation may be tried in non union

Eurist theory: mechanisms by which bone grafts work:

1. osteogenesis: graft itself produces bone
2. osteoinduction: graft induces parent bone to form new bone
3. osteoconduction: structural scaffold over which new bone is laid

Bone graft can be

1. cortical: eg fibula (structural support)
2. cancellous: tibial condyle (better for nonunion)
3. both: iliac crest

Treatment of non union options

1. open reduction + internal fixation + bone graft
2. excision of fragment with or without prosthesis
3. no treatment required: eg scaphoid
4. Ilizarov technique in nonunion:
Indication: lower limb nonunion + infected nonunion: infected bone when
nibbled off produces shortening, which produces disability esp when lower limb is
affected
Eg: infected nonunion tibia
Compression at # site to assist in union and distraction (@0.25mm/6hours) at a
point away from fracture site.
Refer : the O s of bone grafting, ilizarov technique : principle, principle for
application in infections, types, advantages, disadvantages, other uses.

iii. Malunion: when a # does not unite in proper position where the
resulting disability is of clinical significance.
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 1. Brachial Plexus and Peripheral Nerve Injury : Identify the nerve involved,
site of lesion. Learn all the tests for each peripheral nerve

Seddons and Sunderlands Classification

 Nerve Repair : Primary Repair, Delayed primary, Secondary Repair

 Techniques : Nerve Suture, Nerve graft, Neurolysis – internal and external,
Reconstructive Surgery – Tendon transfer, Arthrodesis, Muscle transfer,
Amputation.
 Methods of closing nerve gaps ; Mobilise, cut, dissect, transpose, relaxation
 Tinels Sign
 Tendon transfer - principles ; refer Pg 86 Maheswari
 Named tendon transfers : Jones Transfer – radial nerve palsy

2. Osteoarthritis Knee :
• Degenerative, non inflammatory, joint disease with destruction of
articular cartilage and formation of new bone at joint surfaces and margins
• Misnomer ; non inflammatory, Usually affects synovial joint
• Can be primary or secondary
• Genetic tendancy ( twice as that of OA hip)
• Risk factors : Obesity, Senility, Trauma, Emotional stress, Osteoporosis,
Alcohol, Rigorous lifestyle, Taxing profession, Repetitive injury, Indian
cultural factors, Family tendancy , Smoking
• Pain – type, difficulty, Mild swelling or effusion, Minimal tenderness, Coarse
crepitus, Loose bodies if present, ROM, Late – genu varum, limp , palpable
osteophytes
• ACR criteria fro diagnosis, Radiological : Kellegren and Lawrence Grading
• Treatment options : CONSERVATIVE – NON
PHARMACOLOGICAL,PHARMACOLOGICAL Analgesics- topical, oral , nsaids,
opioids, Food supplement, Inj hyaluronic acid, Inj steroids
• Surgical Indications : Pain refractory to other methods, Ho frequent locking
episodes, Hemarthrosis, Deformity, Joint instability, Progressive Rom

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 • Options : Excision of osteophytes ,loose bodies, mensicectomy,
synovectomy, Arthroscopic debridement , Slocum’s proximal tibial
osteotomy, Distal femoral osteotomy, Chondral resurfacing, TKR, UKA,
Arthrodesis, Patellectomy, Macquets High Tibial Osteotomy

3. Rheumatoid Arthritis : Refer Medicine. Learn deformities, criteria,

complications, orthopedic management
4. Knee Injury / Knee effusion : Unhappy triad of knee, Learn up all the tests
refer Pg 354 Maheswari
5. Tumors : examination described before.
6. TB spine :
Mc type of skeletal tb. MC site : dorsal spine. Reason : more spongy bone,
increased weight bearing, increased verterbral mobility
C/F : insidious onset, non specific symptoms, specific nerve root
compression symptoms, gibbus, paraplegia, kyphosis
Sites of TB spine : anterior, central, posterior,appendiceal, metaphysesal,
true arthritis
Typical attitudes : upper cervical - Wry neck, lower cervical - Military
position, lower thoracic-Aldermans gait
Diagnosis – Xrays- decreased vertebral space,anterior wedging, concertina
collapse
Treatment : Read latest NTEP guidelines, costotransversectomy,
Complications: Paraplegia, Cld Abcess, sinuses, secondary infection,
amyloidosis

Examination findings

NON UNION
History: of trauma.

INSPECTION: Deformity*. Compare with the opposite side

PALPATION: Tenderness may or may not be present.

Defect may or may not be palpable.
Bone thickening may be detected on palpation, compare with opp side.
Most important points for diagnosis are
• Abnormal mobility* in both transverse and AP directions.
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• No transmitted mobility*.
MEASUREMENT: Shortening*
For forearm bone nonunion, measure both Lateral epicondyle-radial styloid and
medial epicondyle-ulnar
styloid distances and compare with opp forearm.
DISTAL NEUROVASCULAR DEFECT: NEVER FORGET to look for distal pulse,
sensation, muscle power and wasting

MALUNION
Examination:
the fracture has already united=>no abnormal mobility. Transmitted mobility will
be present but not united in proper position=>look for deformity*, shortening*
and limitation of movement*
Look for distal neurovascular deficit

Indications for treatment:

1. deformity: supracondylar # gunstock deformity
2. shortening of lower limb: produces disability
3. functional limitation: rotation in forearm

Treatment options:
1. osteoclasis
2. redoing the # surgically
3. corrective osteotomy
4. excision of protruding bone

CHRONIC OSTEOMYELITIS
Most common site lower end of femur
INSPECTION: Sinus. Discharge seropurulent to thick pus. Small bone fragments
may be visible.
PALPATION: Tenderness on deep palpation
Sinus FIXED to underlying bone
Palpate the bone and compare with opp side. Bone thickened and irregular
MEASUREMENT: Look for shortening
MOVEMENTS: joint stiffness
Discussion: read up theory of c/c osteomyelitis
Causes, Xray appearance, DDs, treatment, complications

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 INSTRUMENTS
1. Austin Moore prosthesis:
a. Full name: Self locking intramedullary femoral endoprosthesis devised by
Austin Moore
b. Indication: Hemiarthroplasty: for displaced # neck of femur, physiological age >
60 years,otherwise normal hip
c. Parts:
i. Head: Size = Diameter in mm 35-59 (odd numbers)
ii. Neck/ Collar: hole for the hook of extractor (to remove it later)
iii. Posteromedial corner of neck rests on calcar femorale
iv. Stem: contains fenestrations to increase stability
d. Other devises for same purpose: Thompson prosthesis and bipolar prosthesis

2.K-nail: Kuntscher’s nail

a.Cross section is like a clover leaf (clubs of playing cards)
b.Eye(hole) meant for extraction
c.3 pt fixation-trochanter ,isthumus,condyle
d.Indication: isthumus fracture of femur, when there is no facility of an image
intensifier(for interlocking nail)
e.Best suited for transverse/oblique # at junction
f.Disadvantage: OPEN nailing: fracture site is exposed. Less rotational stability.

3.Interlocking nail for femur

a. Preferred devise for internal fixation of # shaft femur
b. “closed” nailing = # site not opened = # hematoma not disturbed = biological
fixation
c.Requires image intensifier
d.Steps: first, reduction under image intensifier, guidewire introduced through
greater trochanter- pyriform fossa, nail passed along it.
e.“interlocking” two bolts above and below for rotational stability
f.Should be removed within 1.5 years

4. Interlocking nail for tibia:

smaller than that for femur. Bend with apex directed posteriorly

5. V nail:
cross section “V”. for #shaft humerus, tibia

6. Ender’s nail:
a. 6 point fixation. 2 nails used together
b. Uses: #femur of children, #shaft humerus, tibia
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7. Closed gear universal handle:
a. drill used to bore holes, k-wire, Steinmann pin

8. Universal rod, universal clamp AO*

a. External fixation
b. Learn Gustilo Anderson classification of open #
c. Type 3B high chance of wound infection. External fixation necessary for
wound healing

9. Cancellous screw
a. Partially threaded
b. Use:multiple cancellous screw used for fixing #neck of femur

10. Cortical screw

a. Fully threaded

11. Osteotome
a. Both edges beveled
b. Eg: McMurray’s osteotomy for #neck femur, corrective osteotomy

12. Chisel
a. Only one side beveled
b. Use:remove protruding bone, excess callus, osteochondroma

13. Mallet(hammer)

14. Spanner: nut and bolt used for Ilizarov

15. K-wire Kirschner wire

a. Both ends are sharp, cross section is round
b. Use: fixation of #small tubular bones

16. Steinmann pin

a. Only one end pointed
b. Skeletal traction
c. When inserting into upper end of tibia, direction lateral to medial

17. L-plate: shaped like an L

18. T- plate: T and L used for tibial condyle # “Buttress plating”

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19. Cobra plate: #distal femur
20. DCS Dynamic condylar screw, plate

21. DCP Dynamic compression plate

a. Uses: internal fixation of # shaft of
i. Femur: when medullary canal is too wide(can’t use nail) size AO 4.5
heavy duty
ii. Tibia 4.5
iii. Humerus 4.5
iv. Ulna, radius 3.5

22. LCDCP: limited contact DCP: undulated undersurface=> better periosteal

blood supply

23. LCP: Locked compression plate: screw head is threaded. It is “locked” and
won’t come out.
a. Use of LCP: better for osteoporotic bone

24. Ilizarov’s half circle: read about ilizarov’s technique, uses, coticotomy, rate of
distraction

DO NOT confuse between

• the K’s of K nail and K wire
• Osteotome and Chisel: clue: O &C. the letter C is curved only on “one side”. O
curved on “both sides”.
• Cortical and cancellous screws: cancellous partially threaded
• k-wire and Steinmann pin: Kwire both ends sharp

368
PAEDIATRICS
CASE FORMAT 371
ANTHROPOMETRY 375
GROWTH ASSESMENT 379
DEVELOPMENT 380
IMMUNISATION 386
NUTRITION 405
MALNUTRITION 417
ACUTE GLOMERULONEPHRITIS 424
NEPHROTIC SYNDROME 429
JAUNDICE 435
ACUTE DIARRHEAL DISEASE 443
PNEUMONIA/LRI 449
BRONCHIAL ASTHMA 459
ACUTE BRONCHIOLITIS 469
CONGENITAL HEART DISEASE 472
ACUTE RHEUMATIC FEVER 486
PYREXIA OF UNKNOWN ORIGIN 495
URINARY TRACT INFECTIONS 501
KAWASAKI DISEASE 505
IMMUNE THROMBOCYTOPENIC PURPURA 507
HEMOLYTIC ANEMIA 511
HENOCH SCHONLEIN PURPURA 514
DOWN SYNDROME 515
CONGENITAL RUBELLA SYNDROME 517
CEREBRAL PALSY 518
FEBRILE SEIZURE 522
ADVICES 524
CHARTS 531
INSTRUMENT 538
X-RAYS 542
 CASE FORMAT
Personal Data
 Name
 Age
 Sex
 Address
 Informant -whether history reliable or not
 DOA & DOE
 Presenting complaints
 History of present illness
 History of past illness-
- similar illness in the past
- previous hospitalizations
- history of contact with TB
- h/o of other illness,vaccine preventable d/s
- h/o CHD, rheumatic fever
Life History
Antenatal History
 age of mother & father at time of conception
 antenatal care- TT intake, folic acid & calcium intake
 any systemic illness/pregnancy related illness( GDM, GHTN),
 exposure to exanthematous fever, drug/radiation
 USS scans taken- any abnormality

Natal history
 gestational age(term /preterm),mode ( vaginal/ caesarean (indication) )&
place of delivery, any complications

Post natal history

 first cry, birth wt,breastfeeding when initiated
 any resuscitation required ,any h/o jaundice/cyanosis/seizures or feeding
problems,
 when discharged from hospital.

Development history
 gross motor, fine motor , social & language

Immunization history

371
  Adequately immunized for age or / not as per national immunization
schedule
 If not why? Ignorance/lack of facility, misconceptions
 BCG scar +/-( left arm)
 Pulse polio immunization
 Optional vaccines taken or not

Dietary history
 Breast feeding history: when put to breast,exclusively breastfed till what
age.
 In a exclusively breastfed child , ask no of feeds/ day, sleep duration after
feed, urine passed,passage of stools , let down reflex to know the adequacy
of breast feeding
 Complementary feeding &family pot feeding when started
 Any dietary modifications adviced as part of treatment
 Calculate daily calorie & protein intake, comment whether
adequate/inadequate

Item Quantity Kcal Protein

Cooked rice 1 cup 175 4
Dosa 1 70 2
Tea 1 cup 70 2
Vada/bonda 1 50 1
Biscuit 1 20 0.5
Puri 1 35 1
Upumma 1 cup 250 6
Banana 1 100 1
Plantain 1 50 1
Egg 1 80 6
Uncooked ragi 6 tsp 100 2
SAT mix 6 tsp 125 2.5
Cooked dhal 1 tsp 10 0.5
Nestum 6 tsp 100 2
Fish 1oz 80 6
Mutton 1oz 50 6
Beef 1oz 30 6
Pappad 1 20 0.5
Sambar 1cup 50 2.5
Coconut 100g 444 4.5
Sugar 1tsp 20 0
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Ghee/butter/oil 1tsp 40 0
Cow’milk 100ml 70 3
Human milk 100ml 67 1.1

Family history
 Draw pedigree chart, age of parents, consanguinity ,
 similar illness in family
 H/o of TB / allergic d/s,DM/ CHD/genetic disorders.
Socio-Economic History
 Occupation of parents , Education of parents & income
 Housing & surroundings-
- pucca, concrete,ceiling, brick walls, cement flooring
- kutcha- thatched, mud walls
 number of rooms , whether there is overcrowding / not
 source of drinking water- tap / well water; boiled/ not, sanitary well
present/ not
 Sanitary latrine present or not, whether everyone using it
 Source of pollution- air/ water pollution( nearby factories), smokes in
house, firewood for cooking, any pets in house

PHYSICAL EXAMINATION
1. General comment-child looking active & playful or sick
2. Vitals- pulse, BP, respiratory rate, temperature
3. PICCLE
4. HEAD TO FOOT EXAMINATION
5. ANTHROPOMETRY
observed expected % comment
W/A
H/A
W/H
6. Other relevant measurements like MUAC, HC etc to be taken
7. DEVELOPMENT ASSESSMENT
8. SYSTEM EXAMINATION
9. SUMMARY
10.DIAGNOSIS- SPECIFIC DIAGNOSIS WITH COMMENT ON GROWTH &
DEVELOPMENT
NOTE:
Apex beat is normally located ½ - 1 cm medial to left midclavicular line in fifth
space . upto 2 years, apex may be normally in 4 th intercostal space in
midclavicular line.after 4 - 5 yrs it assumes adult location.
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 BP cuff size
Age BP cuff size
Newborn 3 cm
Infant 5 cm
Child 7 cm
Adult 12.5 cm

 BP usually between -SBP 90 +( 2 x age) & DBP 70 ++( 2 x age)

 Resting respiratory rates in children

Age RR
Newborn 40/ min
Infant 30/ min
Toddler 25/ min
School 20/ min

 Normal values of palpable liver

- Upto 4 yrs- 3 cm
- >4 yrs- 1 to 2 cm

 Normal liver span

Age Liver span (cm)
< 1 yr 4-5
1-5 yrs 6-7
5- 12 yrs 8-9

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 ANTHROPOMETRY
Expected measurements in a full term newborn baby
 Weight-3 kg(2.5 to 4)
 Length-50 cm(>45 may be taken as normal)
 Head circumference-34 cm (33 to 36cm)
 Initial weight loss-upto 10% of birth weight in first 10 to 14 days and then
gains 20 to 40 gm/day
 Weight gain at the rate of
- 200gm/week for first 3 months
- 150 gm/week for next 3 months
- 100 gm/week for next 6 months
Weight

Birth Weight (BW) of a newborn 3 kg

5 MONTHS 2 x BW (BW doubles)
1 YEAR 3 x BW (BW triples)
2 YEAR 4 x BW (BW quadruples)

Formula for calculating weight (x= age)

3-12 months 𝑥𝑥 + 9
2
1-6 years 2x+8
7-12 years 7x-5

Height
 Term Height used in children >2 years - measured using stadiometer
 Term length used instead of height in < 2 years - measured using
infantometer
Age Length( Height)
At birth 50 cm
3 months 60 cm
6 months 65 cm
9 months 70 cm
1 year 75 cm
4 year 100 cm

 Height doubles by 4 year

 Height of a child beyond age of 1 year =6x +77 ( Weech’s formula)
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  Short stature: is defined as height below 3rd centile or more than 2
standard deviation below the median height for that age & sex according
to population standard.

Causes of short stature

Physiological Pathological
1. Familial 1. Undernutrition
2. Constitutional 2. c/c systemic illness-c/c renal
failure,congenital heart d/s,cystic
fibrosis,asthma,malabsorption,c/
c liver d/s
3. endocrine causes- GH
deficiency,hypothyroidism,cushin
g s/d
4. psychosocial dwarfism
5. SGA babies
6. Achondroplasia,rickets
7. Genetic s/d-Turner s/d, Down s/d

Feature Constitutional growth delay Familial short stature

Height Short Short
Height Normal Normal
velocity
Family history Of delayed puberty Of short stature
Bone age Less than chronological age Normal
Puberty Delayed Normal

Mid Parental Height (MPH)

 MPH gives an approximate estimate of the child’s genetically determined
potential
- MPH(boys)= (Mother’s Height +Father’s Height +13) ÷2
- MPH(girls)= (Mother’s Height +Father’s Height -13) ÷2

Head circumference(HC)
 Head circumference at birth -34 cm (33 to 36cm)
 Thereafter it increases by 2cm/month for first 3 months
 1cm/month for next 3 months
 0.5cm/month for next 6 months
 (HC increases by 4+3+2+1+1+1 every 2 months in first year (46 cm))
376
  2 cm is gained in the whole of 2nd year (48 cm)
 1 cm is gained in the whole of 3rd year (49 cm)
 By age of 12, Head circumference is 52 cm
 Microcephaly
Microcephaly is HC below 3 standard deviation(SD) below normal
(1SD=1.25 cm)
 D/D of Microcephaly
- Familial Microcephaly
- Craniosynostosis
- Intrauterine infections
- Fetal alcohol s/d, or fetal hydantoin s/d
 D/D of large head
- Hydrocephalus
- Rickets
- Achondroplasia
- Haemolytic anaemia
- Familial macrocephalus
- c/c subdural hematoma

Mid upper arm circumference(MUAC)

 >13.5 cm-normal
 <11.5 cm- Severe acute malnutrition(SAM)

Age Independent Anthropometric Parameters

1. MUAC
2. Kanawati and Mclaren index- MUAC/HC
3. Quaker arm circumference measuring stick(quac stick)
4. Shakir tape method/MUAC tape -has coloured zones
- Red-<12.5 cm(wasted)
- Yellow- 12.5 to 13.5 ( borderline)
- Green >13.5( normal)
5. Bangle test: A bangle with internal diameter 4cm is passed above the
elbow. In severe malnutrition it is passable above elbow, in normal children
it is not.
6. Skin fold thickness: It is an indication of subcutaneous fat which indirectly
indicates the energy reserve of the child.it is measured over the triceps or
subscapular region using Harpenden calliper. It is usually > 10 mm in
normal children whereas in severely malnourished,it is < 6mm.

Upper Segment Lower Segment Ratio ( US:LS)

377
  Upper segment is from vertex to pubic symphysis.
 Lower segment is from pubic symphysis to foot.
 At birth it is 1.7:1 which reduces 0.1 each year and becomes 1:1 at 7 to 10
years. In adult it is 0.9:1

US>LS US<LS
Achondroplasia Disorders of spine( scoliosis)
Rickets Spondoepiphyseal dysplasias
Congenital hypothyroidism

Arm span
 For measuring armspan,child is asked to stand straight with arms extended
outwards parallel to the ground.
 length between the tip of middle fingers is the armspan.
 Arm span is shorter than length by 2.5 cm at birth,equals height at 11 years
and thereafter greater than height by a couple of cms.

Arm span> height Arm span< height

Klinefelter syndrome, achondroplasia
marfan s/d
Scoliosis,homocystinuria

Chest circumference (CC)

 It is measured at the level of nipples in mid respiration.
At birth HC>CC
9 Months to 1 year HC=CC
>1 Year HC<CC

Ponderal Index
Wt (gm ) x 100
 Ponderal index =
Ht (cm )˄3
- Normal : > 2.5
- Borderline PEM: 2 to 2.5
- Severe PEM: < 2
Wt (gm ) x 100
 Ponderal index In newborn=
Length (cm )˄3
 >2 = normal baby or symmetrical IUGR( hypoplastic SGA)
 <2 = assymetrical IUGR (malnourished SGA)

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 GROWTH ASSESMENT
Weight for Age (W/A %)

OBSERVED WEIGHT x 100t(gm ) x 100

W/A=
EXPECTED WEIGHT

The result is interpreted as ____Grade PEM as per IAP classification for W/A

IAP classification for W/A

W/A Grade
71-80% Grade 1PEM
61-70% Grade 2 PEM
51-60% Grade 3 PEM
<50% Grade 4 PEM

Welcome trust classification of W/A

W/A INTERPRETATION
80 -60% without oedema underweight
80 -60% with oedema kwashiorkor
<60% without oedema marasmus
<60% with oedema Marasmic kwashiorkar
Height for age (H/A %)
OBSERVED HEIGHT x 100
 H/A=
EXPECTED HEIGHT
The result is interpreted as___ degree stunting as per Waterlow classification for
H/A

Waterlow classification for stunting (H/A)

H/A DEGREE STUNTING
>95% Normal
90-95% First degree stunting
85-90% Second degree stunting
<85% Third degree stunting

Weight for height (W/H%)

OBSERVED WEIGHT x 100
 W/H =
EXPECTED WEIGHT FOR HEIGHT
The result is interpreted as___degree wasting as per Waterlow classification for
W/ H

379
Waterlow classification for wasting (W/ H)
W/H DEGREE WASTING
>110% Overweight
90-110% Normal
80-90% First degree wasting
70-80% Second degree wasting
<70% Third degree wasting

WHO classification of malnutrition

Moderate malnutrition Severe malnutrition
Symmetrical No Yes
oedema Oedematous malnutrition
(kwashiorkor & Marasmic
kwashiorkor)
W/H(wasting) 70-79% (SD score b/w -2 to -3) <70%% (SD score b/w -2 to -3)
H/A(stunting) 85-89% (SD score < -3) <85%%(SD score < -3

Acute Malnutrition Chronic Malnutrition

W/A is low (underweight present) W/A is low (underweight present)
H/A is normal (no stunting) H/A is low(stunting present)
W/H is low (wasting present) W/H is normal (no wasting)

DEVELOPMENT
Development refers to maturation of functions and acquisition of various skills for
optimal functioning of an individual. It is related to the maturation and
myelination of nervous system.
DOMAINS OF DEVELOPMENT
a) Gross motor development
b) Fine motor skill development
c) Personal and social development and general understanding
d) Language
e) Vision and hearing
Do not forget to mention vision and hearing in the case sheet.
MILESTONES (very important)
GROSS MOTOR
Age Milestone
3 months Neck holding(head control)
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4-6 months Rolls over( at first, from back to side and later, from back to
stomach; prone to supine followed by supine to prone)
6 months Sits in tripod fashion(sitting with own support)
8 months Sits without support; crawling( abdomen, chest on ground)
9 months Stands holding on( with support)
10 months Creping( abdomen, chest off ground)
11 months Cruising (walking sideways while holding onto furniture); pivoting(
turns around to pick up an object)
12 months Creeps well; walks but falls; stands without support
15 months Walks without support; creeps upstairs
18 months Runs;explores drawers
2 years Walks up and downstairs(2 feet/step); walks backward; jumps
3 years Rides tricycle; alternate feet going upstairs
4 years Hops on one foot; alternate feet going downstairs
5 years Skips without falling to either side

Pull to sit Newborn- head lag

6 weeks- head control beginning
12 weeks- slight head lag
20 weeks- complete head control
5 months- flexes head onto chest

Ventral suspension Upto 4 weeks- Head flops down.

6 weeks- momentarily holds head in the horizontal
plane
8 weeks- can maintain this position well
12 weeks- can lift head above the horizontal plane

In prone position 2 weeks- legs high pelvis, knees drawn up

4 weeks- chin up, momentarily in the midline
6 weeks- flat pelvis and extended hips
8 weeks- face lifted up at 45 degree
12 weeks- can bear weight on forearms with chin and
shoulder off the couch and face at 45 degree
6 months- bears weight on extended arm
381
Sitting 8 weeks- back rounded, able to hold head
4 months- back much starighter

FINE MOTOR
4 months Bidextrous reach (reaching out for objects with both hands)
6 months Unidextrous reach( reaching out for objects with one hand);
transfers objects; ulnar( immature) palmar grasp; foot play
8 months Radial( mature) palmar grasp
9 months Immature pincer grasp; probes with forefinger
12 months Mature pincer grasp; releases objects on request; feeds from a cup
with spillage
15 months Imitates scribbling; tower of 2 blocks; inserts pellet in bottle; turns
pages, 2-3 at a time; feeds from a cup without much spillage
18 months Scribbles; tower of 3 blocks; feeds from a cup well using a spoon
2 years Tower of 6 blocks;makes train with blocks; vertical and circular
strokes
2 ½ years Makes train with chimney using blocks
3 years Tower of 9 blocks; copies circle
4 years Copies cross; bridge with blocks
5 years Copies triangle; gate with blocks
6 years Steps with blocks
7 years Diamond
9 years Cylinder
11 years Cube
Refer O P Ghai for drawing skills and block skills at various ages (Fig 3.35 and
3.36).
SOCIAL
2 months Social smile(smiles after being talked to)
3 months Recognizes mother; anticipates feeds
6 months Recognizes strangers; stranger anxiety; smiles at mirror image
9 months Waves bye bye
10 months Plays peek-a-boo
12 months Comes when called; plays simple ball games
15 months Jargon speech; points to objects
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18 months Copies parents in task( domestic mimicry)
2 years Asks for food, drink, toilet; pulls people to show toys; dry by day
with only occasional accidents
2 ½ -3 years Parallel play( plays with kids without interaction)
3 years Shares toys; knows full name and gender; dry by night if lifted out
in the evening
4 years Plays cooperatively in a group( group play- plays with interaction);
able to discriminate right and left; goes to toilet alone
5 years Helps in household tasks; dresses and undresses; able to follow 3-
step command
LANGUAGE
1 month Alerts to sounds
3 months Coos (musical vowel sounds)
4 months Laughs loud
6 months Monosyllables( ba, da, pa); ah-goo sounds
9 months Bisyllables( mama, baba, dada)
12 months 1-2 words with meaning
15 months Jargon speech; follows simple commands; may name a familiar
object( ball)
18 months 8-10 word vocabulary
2 years 2-3 word sentences; uses pronouns- I, Me, You
3 years Asks questions; knows full name, age and gender
4 years Says song or poem; tells stories; can count 4 pennies
5 years Asks the meaning of words; able to identify 4 colours; able to
repeat 4 digits

MISCELLANEOUS MILESTONES
Mouthing- 6 months
Object permanence( able to understand that object continues to exist even when
not visible)- 9 months
Separation anxiety- begins at about 10 months and tapers off by 18 months
Handedness- 3 years
Hand regard
 Child plays with his own hands
 Appears by 3 months( 12 weeks)
383
  Disappears by 5 months( 20 weeks)
VISION
Following objects
Newborn- upto 45 degree
 1 month- upto 90 degree
 3 months- upto 180 degree
 Grasping with eye- 3 months
 Binocular vision- well established by 4 months
HEARING
Murphy’ s sequence of hearing
 Newborn- startling
 4 months- looks horizontal at the source of sound
 6 months- looks downwards at the source of sound
 7 months- looks upwards at the source of sound
 10 months-diagonal localization of source of sound

DEVELOPMENTAL QUOTIENT
 DQ=Average age at attainment/ Observed age at attainment *100
 DQ= Developmental age/ Chronological age* 100
 Developmental delay- DQ<70
 Global developmental delay- Developmntal delay in >/=2 domains
eg: cerebral palsy
In preterm infants, the corrected age rather than the post natal age is used till 2
years of age. For example, a child born at 32 weeks of gestation (gestational age),
seen at 10 weeks of age (postnatal age) should be considered as a 2 week old
child.
DEVELOPMENTAL DELAY
Upper limit of age for attainment of milestone (Red flag signs)
Visual fixation or following 2 months
Vocalization 6 months
Sitting without support 10 monhs
Standing with assistance 12 months
Hands and knees crawling 14 months
Standing alone 17 months
Walking alone 18 months
384
Single words 18 months
Imaginative play 3 years
Loss f comprehension, single words or phrases at any age
The medical evaluation includes history, physical examination and laboratory
testing.
History
 Is there a delay?
 Is it a global developmental delay or confined to certain spheres of
development?
 If it is a global delay, is there a proportionate delay in all spheres or some
affected more than others?
 Is delay due to static or progressive disorder?
 Rule out treatable causes like hypothyroidism, PEM.
 Family history- multigenerational origin of family dysfunction
 Prenatal history- exposure to teratogens including radiation or medications,
infectious illnesses, fever, additive substances, trauma
 Perinatal history- birth weight, gestational age, APGAR score, any medical
complications
 Poatnatal medical factors that are commonly overlooked include chronc
respiratory or allergic illness, recurrent otitis, head trauma, sleep problems
(particularly signs of obstructive sleep apnoea)
Physical Examination
 Growth parameters, HC
 Facial and other dysmorphology
 Eye findings( eg: cataract in inborn errors of metabolism)
 Neurocutaneous markers (cafe-au-lait spots in Neurofibromatosis,
hypopigmented macules in tuberous sclerosis)
Laboratory Tests
 No single set of laboratory tests indicated
 For PKU, hypothyroidism and other metabolic conditions, do screening in
the neonatal period.
 Iron deficiency and lead toxicity are common contributors to
developmental delays and are easily detected.

385
  EEG and neuroimaging are not routinely indicated but should be used if
there is clinical suspicion of seizure or encephalopathy or in cases of
microcephaly or rapidly expanding HC.
 The medical evaluation for intellectual disability and autism should include
chromosomal and molecular biology testing for Fragile X syndrome.

TO READ:
1. Rules of development
2. Developmental surveillance- Screening tests and definitive tests
3. Neonatal reflexes
4. Most common genetic cause of intellctual disability
5. Preventable causes of intellectual disability
6. Causes of global development delay
7. Causes of isolated speech delay

IMMUNISATION
National Immunisation Schedule 2019

Time Vaccine Dose and Route Site

BCG 0.05 mL till 1 Left upper arm at

month. 0.1 mL till 1 insertion of deltoid
year. Intradermal

At Birth
Hepatitis B birth 0.5 mL Anterolateral part
dose intramuscular of left mid thigh

b-OPV zero dose 2 drops oral within

2 weeks

Pentavalent 1 0.5 mL Anterolateral part

6 weeks
intramuscular of left mid thigh

386
 Time Vaccine Dose and Route Site

f-IPV 1 0.1 mL intradermal Upper arm right

b-OPV 1 2 drops oral

PCV 1 0.5 mL Anterolateral part

intramuscular of right mid thigh

Rota 1 5 drops oral

(Rotavac)

Pentavalent 2 0.5 mL Anterolateral part

intramuscular of left mid thigh

10 weeks b-OPV 2 2 drops oral

Rota 2 5 drops oral

(Rotavac)

Pentavalent 3 0.5 mL Anterolateral part

intramuscular of left mid thigh

f-IPV 2 0.1 mL intradermal Upper arm right

14 weeks b-OPV 3 2 drops oral

PCV 2 0.5 mL Anterolateral part

intramuscular of right mid thigh

Rota 3 5 drops oral

(Rotavac)

387
 Time Vaccine Dose and Route Site

MR 1 0.5 mL Upper arm right at

subcutaneous insertion of deltoid

JE 1 0.5 mL Upper arm left

9 completed subcutaneous
months
PCV 3 0.5 mL Anterolateral part
intramuscular of right mid thigh

Vitamin A 1 lakh IU (1 mL)

oral

MR 2 0.5 mL Upper arm right at

subcutaneous insertion of deltoid

JE 2 0.5 mL Upper arm left

subcutaneous
16 to 24 months DPT booster 1 0.5 mL Anterolateral part
intramuscular of left mid thigh

b-OPV booster 1 2 drops oral

Vitamin A 2 lakh IU (2 mL)

oral

3rd to 9th dose Vitamin A 2 lakh IU (2 mL)

Vitamin A at 6 oral
month intervals till
5 years

388
 Time Vaccine Dose and Route Site

DPT booster 2 0.5 mL Anterolateral part

5 to 6 years
intramuscular of left mid thigh

Td 0.5 mL Upper arm

10 years
intramuscular

HPV (2 doses, 6 to 0.5 mL Upper arm

Girls 11 to 13 years 12 months apart) intramuscular

Td 0.5 mL Upper arm

16 years
intramuscular

Cold Chain
• System of storing and transporting vaccines at recommended temperatures
from the point of manufacture to the point of use.
• Test done to determine whether adsorbed vaccines have been frozen at some
point in the cold chain: Shake test

Seroconversion and Seroprotection

• Seroconversion: Change from antibody negative state to antibody positive
state.
• Seroprotection: State of protection from disease due to a certain level of
antibody titre.
• Thus, seroconversion does not necessarily mean seroprotection

General Recommendations of Immunisation

1) There should be a minimum interval of 4 weeks between 2 doses of the same
killed vaccine
Exception: Rabies vaccine
2) Different live vaccines have to be separated by at least 4 weeks
3) Killed vaccines can be given at any time before or after any vaccine
389
4) Oral vaccines can be administered simultaneously or at any time before or after
a vaccine
5) Any number of vaccines may be given on the same day
6) Multiple vaccines may be given on different anatomic sites. If more than one
vaccine is needed to be given on the same limb, they should be given at least 1
inch apart so that their local reactions do not overlap.
7) Vaccines administered upto 4 days before minimum age or interval is
considered valid. If given5 or more days before recommended age or interval, it is
deemed invalid and needs to be repeated.

Vaccine Placement
• Freezer compartment: Ice packs
• Top shelf: Live viral vaccines (OPV, Measles, Varicella) and BCG
• Second shelf: DPT, Td, TT, Typhoid, Hepatitis A
• Third shelf: Hepatitis B, Pentavalent
• Lower: Diluent

Mission Indradhanush (Box 10.2 OP Ghai)

• Launched: Dec 2014
• Objective: Fully immunise more than 90% infants by 2020
• Personnel: AWW, ASHA, ANM

Intensified Mission Indradhanush

• Launched: Oct 2017
• Objective: Fully immunise more than 90% newborns by Dec 2018
• Implementation: Week long immunisation drives from 7th of each month

Individual Vaccines (Learn all vaccines in NIS at least)

BCG Vaccine
• Bacillus Calmette and Guerin
• Danish 1331 strain
390
• Lyophilised powder in vacuum sealed dark multi dose vials
• In freeze dried form because:
1. In liquid phase, organisms tend to be temperature sensitive
2. Potency drop with time
• Heat and light sensitive
• Cell mediated immunity. Therefore, maternal antibodies do not interfere with
immunisation
• Protects against severe forms of TB like military TB, TB meningitis
• Protection against other disorders like leprosy and buruli ulcer
• Reconstituted in NS. Discard after 4 hours (in order to prevent bacterial
contamination as it does not have any antibacterial substance).
• Intradermal injection with 26 G needle
• Produces a 5 to 7 mm wheal which becomes a papule by 1 week that enlarges
to 4 to 8 mm. It will then ulcerate by 5 to 6 weeks and heals by scarring in 6 to
12 weeks
• 1% of population will not get a BCG scar
• Complications:
1. Inadvertent subcutaneous injection causes persistent ulceration and
ipsilateral cervical or axillary lymphadenopathy (BCG adenitis)
2. In severe immunodeficiency, children may develop disseminated BCG
disease 6 to 12 months after vaccination. These people may also develop
osteomyelitis and scrofuloderma
• Contraindications: Cellular immunodeficiency, symptomatic HIV
• Max age of giving BCG vaccine according to NIS: 1 year. According to IAP
schedule: 5 years
• BCG Test: An accelerated response after injection of vaccine is observed in
individuals suffering from TB. An induration of > 5 to 6 mm after 3 days of BCG
vaccine is considered to be a positive reaction

OPV (Sabin Vaccine)

• Live attenuated vaccine
391
• Stabiliser: Magnesium chloride
• Colour: Pink (due to phenolphthalein)
• Dose: 2 drops (0.05 mL each)
• Currently bivalent OPV is used (since April 2016). It has types 1 and 3. Switch
was done as part of the Polio Eradication and Endgame Strategic Plan (2013-
2018)
• Type 2 removed because:
1. Wild polio virus 2 eradicated from India in 1999
2. Inhibits take of types 1 and 3
3. Causes most cases of VDPV (Vaccine Derived Polio Virus)
• Contraindications:
1. Immunodeficiency
2. Pregnancy
3. Household contacts of immunodeficient and pregnant people
• Breastfeeding and mild diarrhoea are not contraindications
• Adverse reactions: VDPV, VAPP (Vaccine associated paralytic polio)
• VAPP has neurovirulence, but not neurotransmissibility. Hence, it is seen in
recipients or close contacts
• Types of VDPV:
• c VDPV (circulating VDPV)
• i VDPV (immune deficiency associated VDPV)
• a VDPV (ambiguous VDPV)
• OPV is preferred vaccine for eradication of poliomyelitis
• Pulse Polio Immunisation:
• Launched in India in 1995
• Sudden simultaneous mass administration of OPV on a single day
• Irrespective of immunisation status, all children 0 to 5 yrs of age are given 2
drops of OPV
• Formerly conducted twice a year. In 2019, government held it only once due
to fear of VDPV
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• Polio eradication: No cases of paralytic polio by wild polio virus in last 3
calendar years along with absence of wild polio virus in the community where
excellent clinical and virological survey exists and coverage of routine OPV is
more than 80%
Objectives of polio eradication and endgame strategic plan 2013 to 2018 are:
- Detect and interrupt all poliovirus transmission
- Strengthen immunisation systems and withdraw OPV
- Contain poliovirus and certify interruption of transmission
- Plan post polio legacy

• Polio elimination: Zero cases of paralytic polio in one calendar year with other
criteria as in eradication
• Last wild polio case in India was from Howrah: Jan 13, 2011.
• WHO South East Asian region declared polio free on 27 March 2014
• Endemic transmission continues in: Pakistan, Afghanistan
• Study AFP Surveillance
• See Fig 10.16 for Vaccine vial monitor

IPV (Salk Vaccine)

• Formaldehyde killed poliovirus grown in monkey kidney, human diploid or vero
cell culture
• Advantage: Does not cause VAPP and VDPV
• IPV introduced in India in 2015-16
• Introduced in NIS as part of Polio Eradication and Endgame Strategic Plan
(2013-2018)

• Advantages of f-IPV:
- Lower dose needed (2 doses of 0.1 mL intradermal instead of 0.5 mL
intramuscular)
- Better immunogenicity than a single IM dose

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 OPV IPV
Live Killed

b OPV has serotypes 1 and 3 Has all 3 serotypes

Can cause VAPP and VDPV No risk of VAPP and VDPV

Gives herd immunity No herd immunity

Better intestinal immunity Poorer intestinal immunity

No local side effects Mild erythema, induration

Contraindicated in Can be used in immunocompromised

immunocompromised

DPT Vaccine
• Triple vaccine: Diphtheria toxoid, whole cell killed pertussis and tetanus toxoid
• 0.5 mL deep IM on left anterolateral thigh (Vaccine has aluminium hydroxide as
an adjuvant. Therefore, if not given deep IM, it can cause local irritation,
granuloma formation and tissue necrosis).
• Schedule: 16 to 24 months, 5 to 6 years
• Adverse effects:
- Local (erythema, pain, swelling)
- Systemic (fever, febrile seizures, persistent cry, hypotensive hyporespontsive
episodes, encephalopathy)
- Paracetamol is usually given after DPT to control fever
- Tetanus vaccine can cause brachial neuritis within 28 days

• Contraindications:
- Progressive neurological diseases
- Immediate anaphylaxis after previous dose
- Development of encephalopathy within 7 days of vaccination
• Precautions: (if it recurs, further doses are contraindicated)
- Persistent inconsolable cry (> 3 hrs) within 48 hrs
394
 - Hypotensive hyporesponsive episode within 48 hrs
- Fever (> 40.5 C) within 48 hrs of DPT administration
- Febrile or afebrile seizures within 72 hrs of DPT administration
• Wherever DPT is contraindicated, use DT which has similar doses of diphtheria
and tetanus toxoids as in DPT. In children > 7 yrs, use Td.
• Quadruple vaccine: DPT + IPV
• DPT is not given in gluteal region because:
- Risk of injury to sciatic nerve
- Vaccine may get deposited in fat pad adjacent to muscle tissue resulting in
inadequate response
• DTaP: Acellular pertussis vaccine. It causes lesser side effects compared to
whole cell pertussis vaccines
• Tdap: Usual dose of tetanus toxoid. Lower doses of diphtheria toxoid and
acellular pertussis components
• Acellular pertussis is a subunit vaccine

Td Vaccine
• Lower dose of diphtheria toxoid in order to decrease reactogenicity against
diphtheria toxoid while providing protection against both diphtheria and
tetanus
• WHO has recommended the use of Td vaccine instead of standalone tetanus
toxoid in all situations including pregnancy and wound management where TT is
indicated
• Pregnancy (NIS recommendations):
- Currently TT is still being given
- 2 doses of TT, 4 wks apart with first dose at first contact. Second dose is
preferably given before 36 weeks of gestation. TT may still be given for
mothers sake if she comes late in her pregnancy or presents when in labour
- If next pregnancy is within 3 years, a single booster dose will suffice

Tetanus prophylaxis following wound

395
 Past doses of Clean minor wound All other wounds
TT
TT Tetanus Ig TT Tetanus Ig
Unknown or
<3 doses or Yes No Yes Yes
immunodeficie
nt
>= 3 doses No No
Taken if more Taken if more
than 10 yrs No than 5 yrs No
since last dose since last dose

Measles Containing Vaccine

• Measles vaccine: Edmonston-Zagreb strain
• Vaccines available are Measles vaccine, MR (measles rubella), MMR (measles,
mumps, rubella) and MMR-V (MMR and varicella)
• Live attenuated vaccine
• Protection by maternal antibodies till 6 to 9 months. Hence given at end of 9
completed months. Even then, there might be 15% chance of vaccine failure
causing a second dose to be necessary at 15 months.
• In outbreaks, vaccines may be given earlier (around 6 months of age) with a
repeat dose at 12 to 15 months
• Measles vaccination is also done in children(>6 months) admitted in health care
facility with SAM
• Measles vaccine loses potency rapidly after reconstitution and should be
discarded after 4 to 6 hrs as contamination can cause staphylococcal sepsis and
toxic shock syndrome
• Following MR campaign in Feb 2017, measles vaccine in NIS is being replaced by
MR vaccine
• Haphazard use of MMR vaccine without ensuring optimal immunisation
coverage (> 80%) may result in an epidemiological shift of disease with more
cases in adulthood and a paradoxical increase in congenital rubella syndrome
• Rubella component: RA 27/3 strain
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• Mumps component: Jeryl Lynn strain
• Contraindications:
- Pregnancy
- Immunosuppression
- Immunodeficiency including symptomatic HIV
- Malignancy
- Recent infusion of immunoglobulin containing blood product
- MMR is contraindicated in anaphylaxis to neomycin
• Egg protein allergy is not a contraindication
• Adverse effects:
- Local pain, tenderness, febrile seizures
- Measles vaccine: Fever, transient macular rash
- MMR vaccine: Arthralgia, aseptic meningitis, lymphadenopathy
- Toxic shock syndrome if contaminated
- Rubella vaccine can cause chronic arthritis within 6 wks
• Post exposure prophylaxis:
- With immunoglobulin for immunocompromised contacts (0.5 mL/kg) and 6
to 12 month old infants (0.25 mL/kg) within 6 days of exposure
- Unimmunised immunocompetent contacts > 12 months should receive
measles or MMR vaccine within 72 hrs of exposure
- IVIG 400 mg/kg can also be used

Hepatitis B Vaccine
• HBsAg produced by recombinant DNA technology in yeast, adsorbed onto
aluminium salt as adjuvant
• Most freeze sensitive vaccine
• 0.5 mL intramuscular in anterolateral thigh or deltoid (avoid gluteal region)
• 1 mL is used in immunosuppressed children, malignancy, hemodialysis and in
adults
• NIS: birth, 6,10,14 weeks
• Catchup: 3 doses at 0,1,6 months
• If mother is known to be HBsAg positive, give HBIG along with vaccine
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• If HBIG is not available, 3 doses at 0,1,2 months with an additional dose at 9 to
12 months

Hemophilus Vaccine
• Conjugated polyribosyl ribitol phosphate (PRP), which is a capsular
polysaccharide
• 0.5 mL intramuscular on left anterolateral thigh
• Diluent: DPT vaccine
• NIS: 3 doses as part of pentavalent vaccine at 6,10,14 weeks
• IAP Schedule and catchup:
- 3 doses at >= 6 weeks given >= 4 weeks apart with a booster at 15 to 18
months
- 6 to 12 months: 2 doses >= 8 weeks apart, one booster at 15 to 18 months
- 12 to 15 months: one dose and one booster at 18 months
- 15 months to 5 years: one dose
- > 5 years: Not recommended, except hypo or asplenia

Pneumococcal Vaccine
• Conjugate vaccines: PCV13, PCV10
• Polysaccharide vaccine: PPV23
• Conjugate vaccines provide herd effect by reducing nasopharyngeal bacterial
carriage
• Polysaccharide vaccines stimulate B cells independent of T cells and is thus
poorly immunogenic in < 2 year olds and immunological memory is low. PCV is
used in children <2 years
• Vaccination is not needed beyond 5 years except high risk categories like:
- sickle cell anaemia
- immunodeficiency (primary or acquired)
- immunosuppressed including organ transplant recipients
- nephrotic syndrome
- hypo or asplenia
- chronic cardiac, liver, renal or pulmonary disease
398
 - diabetes mellitus
- children with cerebrospinal fistula
- cochlear implants
• NIS: 3 doses at 6 weeks, 14 weeks, 9 months
• IAP Schedule and catchup (PCV):
- 3 doses after >= 6 weeks given 4 weeks apart with a booster dose at 15 to 18
months
- 7 to 11 months: 2 doses > 4 weeks apart with a booster dose at 15 to 18
months
- 12 to 23 months: 2 doses > 8 weeks apart
- 24 to 59 months: 1 dose
- > 5 years: 1 dose, only if high risk

Rotavirus Vaccine
 Types:
• Rotashield:
- Live oral tetravalent vaccine
- Withdrawn due to risk of intussusception
• Rotarix
- Monovalent live attenuated vaccine
• Rotateq
- Human bovine reassortant vaccine
• Rotavac
- Indigenous monovalent live attenuated vaccine
- Inexpensive with low risk of intussusception
- used in NIS as 5 drops at 6,10,14 wks
• All 3 rotavirus vaccines are not given during an episode of acute gastroenteritis
• All 3 do not increase risk of intussusception
• Immunisation should be complete by 8 months of age
• 1st dose at a minimum age of 6 wks and not after 14 wks 6 days
• Given with precaution in people at increased risk of intussusception (chronic GI
disease, gut malformations)
399
• OPV and rotavirus can be administered together

HPV Vaccine
• Recombinant vaccine
 Types:
- Gardasil: quadrivalent (strains 6, 11, 16, 18)
- Cervarix: bivalent (strains 16 and 18)
• 0.5 mL intramuscular at upper arm (deltoid)
• Included in NIS of few states. 2 doses, given 6 to 12 months apart in girls 11 to
13 years
• Minimum age for HPV vaccine according to IAP schedule: 9 years
• Catchup can be done upto 45 years

JE Vaccine
 Types:
• Live attenuated vaccine based on SA-14-14-2 strain
- 0.5 mL subcutaneous at 9 months and 16 to 18 months at anterolateral
thigh
- In Kerala, it is given in Trivandrum and Alappuzha
• Inactivated purified vero cell derived vaccine
• Inactivated mouse brain derived vaccine (Nakayama strain) (not available)

Typhoid vaccine
 Types:
• Vi capsular polysaccharide vaccine (S typhi strain Ty2)
- Given in children > 2 yrs as single dose
- Revaccination every 3 yrs
- 0.5 mL subcutaneous or IM in anterolateral thigh or deltoid
• Conjugate vaccines (Vi antigen is coupled with a carrier protein)
- Recommended in IAP schedule: first dose at 9 to 12 months. Booster at 2
yrs
- Catchup: single dose upto 18 yrs
400
 - 0.5 mL IM in anterolateral thigh or deltoid
• Live attenuated oral Ty21a vaccine (mutant strain of S typhi) (not available in
India)
- Ty21a has mutation in gal E gene and hence lacks enzyme UDP gal 4
epimerase
- Enteric coated capsule which has to be swallowed whole. Thus,
unsuitable for young children
- Given as 3 doses
- Avoid antibiotics for 3 days before to 7 days after taking vaccine
- Repeated every 3 yrs
• Whole cell inactivated typhoid vaccine having S typhi, S paratyphi A and B
(not used now)

Varicella Vaccine
• Live attenuated vaccine with sterile water as diluent
 Oka strain
 Not included in NIS because:
• Chicken pox is not a public health priority
• Expensive
• High rates of immunisation coverage is needed to prevent an
epidemiological shift to older individuals causing more severe disease
• IAP schedule: 2 doses, > 3 months apart, preferably at 15 to 18 months and at 4
to 6 yrs
• Catchup: 2 doses > 3 months apart. If > 12 yrs old, 2 doses > 1 month apart
• Given especially in high risk groups:
- Chronic cardiac or lung disease
- Asymptomatic HIV infection with CD4 > 15%
- Leukaemia in remission and off chemotherapy > 3 months
- Anticipated prolonged immunosuppression
- Prolonged aspirin therapy (discontinue aspirin for 6 wks after)
• Adverse events: breakthrough infection (mild afebrile illness with few lesions
and predominance of papule over vesicles)
401
• Post exposure prophylaxis within 72 hrs after contact
• MMR V is associated with a higher risk if adverse events in 12 to 23 month olds
than MMR and Varicella separately. Therefore, IAP cautions against use of
MMR- V in this age group. It can be used safely in older patients

Influenza Vaccine
 Types:
• Inactivated influenza vaccine:
- Tri or quadrivalent vaccine with 2 influenza A and one or two influenza B
strains
- Derived from viruses grown in chick embryo or cell culture
- 0.25 mL (in < 3 yr children) or 0.5 mL (>= 3 yrs) intramuscular
- Anterolateral thigh or upper arm
- Contraindication: use with caution in suspected egg allergy or GBS
• Live attenuated intranasal vaccine:
- 0.25 mL in each nostril
• IAP schedule: 2 doses > 4 wks apart at 0.5 to 9 yrs, 1 dose if > 9 yrs. Annual
revaccination with one dose before rainy season

Rabies Vaccine
 Types:
• Nerve tissue vaccines (not recommended now due to low efficacy and high
incidence of adverse effects)
• Cell culture vaccines (Purified duck embryo vaccine, purified chick embryo
cell vaccine, human diploid cell vaccine and purified vero cell vaccine)
 Post exposure prophylaxis:
• Category 1: Animal touch or lick on intact skin
• Category 2: Minor scratches or abrasions without bleeding, licks on broken
skin, nibbling of uncovered skin
• Category 3: Single or multiple transdermal bites, abrasions which bleed,
contamination or scratches of mucus membrane with saliva or licks
• Category 2 and 3 need wound management and rabies vaccine
402
 • Category 3 and immunocompromised individuals in category 2 need
immunoglobulin also
 Rabies immunoglobulin types:
• Equine RIG:
- 40 U/kg (maximum 3000 IU)
- Given after test dose
• Human RIG
- 20 U/kg (maximum 1500 IU)
• RIG is infiltrated in and around wound as soon as possible, at least within 7
days. For large wounds or multiple wounds, it is diluted in NS to infiltrate entire
wounded region. If there is any RIG left, it is given IM at a site away from
vaccination site, usually deltoid or anterolateral thigh
• Essen regimen: 5 doses on days 0, 3, 7, 14 and 28. Additional dose on day 90 in
immunocompromised and severely malnourished people
• Updated Thai Red Cross schedule: 2 intradermal doses (0.1 mL each) on days 0,
3, 7 and 30
• Pre exposure prophylaxis: 3 intramuscular doses (0.5 mL) on days 0, 7, 21 or
28. Booster after 1 year and every 5 years thereafter

Hepatitis A Vaccine
• Given > 1 year of age
 Types:
- Formalin inactivated vaccine with aluminium hydroxide as adjuvant
- Live attenuated vaccine
• Effective as post exposure prophylaxis if given within 10 days of exposure
• 0.5 mL intramuscular in deltoid
• IAP schedule and catchup:
- 1 to 18 years: 2 doses, 6 months apart, 0.5 mL
- > 18 years: 2 doses, 6 months apart, 1 mL

Meningococcal Vaccine
• Polysaccharide vaccines and conjugate vaccines are available
403
• Conjugate vaccines preferred because:
- Higher immunogenicity
- Prolonged efficacy
- Potential for herd effect
• Both can be given as 0.5 mL intramuscular in anterolateral thigh or upper arm
as a single dose. A second dose may be given after 3 to 5 years

Yellow Fever Vaccine

• Live attenuated vaccine (17D 204 strain)
• Contraindicated in severe egg allergy
• Single dose of 0.5 mL subcutaneous at least 10 days before travel
• IAP and WHO recommends revaccination after 10 yrs

Adverse Events Following Immunisation (AEFI)

1) Vaccine induced: Event caused or precipitated by active component of
vaccine (eg VAPP, BCG adenitis, pertussis encephalopathy)
2) Vaccine potentiated: Event precipitated by vaccination, but may have
occurred without vaccination (eg first febrile seizure)
3) Injection reaction: Event from anxiety or pain due to injection (eg syncope)
4) Program error: Event due to error in vaccine preparation, handling or
administration (eg toxic shock syndrome due to contaminated measles
vaccine, abscess at injection site)
5) Coincidental: Temporally linked by chance or due to unrelated illness (eg
gastroenteritis after MMR injection)

404
 NUTRITION
Recommended Daily Allowance (RDA) (Pg 88)
• Nutrient specific and technical
• Formulated based on current knowledge of nutritional requirement of different
age and sex groups depending on anthropometry (weight and height), body
composition, climate and environment, physical activity, physiological status
and body demands
• RDA covers the needs of people within mean + 2 SD (97.5%)

Holliday and Segar formula

• Upto 10 kg: 100 Cal/kg/day
• 10 to 20 kg: 1000 Cal + 50 Cal/kg/day for each kg above 10 kg
• > 20 kg: 1500 Cal + 20 Cal/kg/day for each kg above 20 kg

ICMR Guidelines for Protein and Calorie Requirement (Table 7.3)

Group Age Energy (Cal/day) Protein (gm/day)

0 to 6 months 90 Cal/kg/day 1.2 gm/kg/day
Infants
6 to 12 months 80 Cal/kg/day 1.7 gm/kg/day

1 to 3 years 1050 17

Children 4 to 6 years 1350 20

7 to 9 years 1700 30

Boys 10 to 12 years 2200 40

Girls 10 to 12 years 2000 40

• Calorie and protein requirement is calculated based on the expected weight

for age and not according to the childs weight

405
• Working formula for calories: 1000 Cal at 1 year. Add 100 Cal for every year
thereafter

Essential Amino Acids (Pg 86)

• Isoleucine, Leucine, Lysine, Methionine, Phenyl alanine, Threonine, Tryptophan,
Valine
• Semi essential amino acids: Arginine and Histidine. These are essential during
infancy as their rate of synthesis is inadequate to sustain growth
• Arginine, Cysteine and Taurine are essential for LBW babies

Protein quality (Pg 87)

• Biological value (BV) = (Nitrogen retained / Nitrogen absorbed) x 100. It is the
percentage of absorbed protein which is retained. BV is 100 for egg protein. Egg
protein is the reference protein.
• True digestibility (TD) = (Nitrogen absorbed / Nitrogen intake) x 100
• Net Protein Utilisation (NPU) = (TD x BV)/100. NPU can also be expressed as
(Nitrogen retained / Nitrogen intake) x 100. It is the percentage of ingested
protein which is retained.

Cereals
• Poor quality protein which lacks lysine
• Phytates hinder absorption of Fe
• Deficient in Vit A, C, D, Ca
• Rich in Vit B1, B2, folic acid
• Rice: 100 gm has 350 Cal and 7 gm protein. Limiting aa is lysine
• Wheat: 100 gm has 350 Cal and 12 gm protein. Limiting aa are lysine and
threonine
• Maize: 100 gm has 350 Cal and 11 gm protein. Limiting aa is lysine and
tryptophan. It has excess leucine which prevents conversion of tryptophan to
niacin, resulting in pellagra

406
• Ragi: 100 gm has 350 Cal, 7 gm protein, 3.14 mg Ca, 3.9 mg Fe and is also rich in
iodine. It is a good weaning food as it is easily digestible and is rich in Fe and Ca

• Preparation of ragi: Ragi is soaked in water for 8 to 10 hrs. Water is drained and
ragi is dried. It is then grinded. Powder is stored in a dry place. For preparation,
add 2 to 3 teaspoon in water and boil. Jaggery is added to it and made into a
porridge. Consistency should be such that it slides down a plate slowly when
kept tilted or like a string when poured from a spoon.

• Parboiling:
- Hot soaking process
- Rice is put in hot water (65 to 70 degree C for 3 to 4 hrs)
- Drain water and steam for 5 to 10 mins
- Dried and milled
• Advantages:
- Essential aa diffuses into endosperm
- Hardens rice
- Starch is gelatinised
- More insect resistant and storage life

Pulses
• Poor quality protein lacking in methionine
• Phytates hinder absorption of Fe
• Good source of energy, Ca, Fe, P, Vit B1, Vit B2, folic acid
• Lacks Vit A and C
• Germinating pulses are rich in Vit B and C
• Groundnut is rich in carbohydrate, protein, Vit A and B1, B3
• Soyabean: Vegetarian source of omega 3 fatty acids
• Supplementary action of proteins: Protein quality improves when 2 proteins
with different limiting aa are combined in diet (eg cereals and pulses)

407
 Pulse Energy (Cal) Protein (gm)
Green gram 350 24
(cherupayaru)

Red gram (sambar 350 20

parippu)

Black gram (uzhunnu) 350 24

Bengal gram (kadala) 350 17

Soyabean 432 43

Groundnut 540 24

Green Leafy Vegetables

• Rich in Vit A, B, Ca, Fe, Carotene
• Deficient in Vit B12
• 100 gm has 25 to 50 Cal and 4 gm protein
• Drumstick leaves are rich in Fe, Ca, K
• Amaranthus: Carotenoid rich
• Carrot: Rich in carotene
• Tomato: Rich in Vit C, carotene

Fruits
• Mango: Rich in fibre (pectin, carotene). Ripe mango has Vit C. Raw mango has
Vit C and K
• Amla: Richest source of Vit C. Also rich in Ca, Fe, P, fibre
• Sitaphal (custard apple): Rich in Ca
• Banana: Rich in carotene, fibre, Fe. It is a rich source of energy, but a poor
source of K
• Apple: Rich in Vit A, C, antioxidants
• Watermelon: Water, iron, fibre
408
Fish
• Rich in Ca, protein, Vit B12, omega 3 fatty acids
• 100 gm has 100 Cal and 20 gm protein

Egg (very important)

• Reference protein
• High quality protein (BV is 100)
• Rich in Vit B12
• Deficient in carbohydrate, fat, Fe and Vit C
• Contains all essential aa
• 60 gm egg (1 egg) has:
- 80 Cal
- 6 gm protein
- 6 gm fat
- 30 mg Ca
- 1.5 mg Fe
- 250 mg cholesterol
• Avidin: Antinutrient in egg reducing biotin availability
• Egg yolk is introduced by 6 months of age and egg white by 1 year of age as it is
more allergenic

Milk (very important)

• Deficient in Vit C and Fe
• Provide high quality protein, lactose and saturated fats
• Rich in Ca and P
• Skimmed milk: Fat removed. It is a good source of Ca and protein
• Vegetable milk: from soyabean, groundnut
• Source of Vit B12 in vegetarians
• Use of boiled milk in infants may result in Vitamin C deficiency
409
• Benefits of breastmilk (Pg 145):
- Cheap
- Nutritionally and immunologically superior
- High concentration of lacked provides the galactose which is needed for
formation of galactocerebrosides
- Easily digestible protein
- Has cysteine and taurine which are necessary for neurotransmission and
neuromodulation
- Rich in PUFA
- Complete food for infants
- Baby does not need additional water
- Helps uterine involution
- Reduced incidence of PPH
- Lactational amenorrhea
- Reduced risk of ca breast and ovary
- Best method to shed the extra weight gained in pregnancy
• Composition of breast milk (100 mL):
- 65 Cal
- 1.1 gm protein (whey protein). Whey:casein ratio is 70:30
- 7.4 gm carbohydrate
- 3.4 gm fat
- More bioavailability of Fe
- Deficient in Vit D (30 to 40 IU/L) and Vit K. Thus, Vit D supplementation at a
dose of 400 IU/day is done to prevent nutritional rickets in exclusively
breastfed infants. Vit K is produced by gut flora. It may take some time for
the newborn gut to be colonised by bacteria and start producing Vit K. Thus,
all babies receive Vit K at birth to prevent hemorrhagic disease of newborn
(0.5 to 1 mg IM)
• Types of breast milk (Pg 147):
- Colostrum: initial 3 to 4 days. Thick with high amounts of antibodies and
immunocompetent cells
- Transitional milk: till 2 wks. Fat and sugar content increases
- Mature milk: follows transitional milk. Has all nutrient essential for optimum
growth
410
 - Preterm milk: has more proteins
- Fore milk: at start of feed. Rich in protein, sugar, vitamins, minerals and
water to quench thirst
- Hind milk: towards end of feed. Rich in fat giving more energy and feeling of
satiety
• Composition of cow milk:
- 73 Cal
- 3.2 gm protein (casein) (higher)
- 4.9 gm carbohydrate (lower)
- 4.4 gm fat (higher)
- Low bioavailability of iron

Fibre
• Determines the quality of carbohydrates
• Complex unabsorbed carbohydrate in vegetables, fruits, cereals
• Soluble fibres: gums, pectins
• Non soluble: Cellulose
• Wholegrain cereals and vegetables are rich sources of fibre
• Advantages:
- Increases bulk
- Prevents constipation
- Reduces cholesterol absorption
- Reduced risk of ca colon
- Decreases GI transit time
• Disadvantage: Reduced absorption of minerals and fat soluble vitamins

RESOMAL
• Rehydration solution for the malnourished
• 2 L water + 1 sachet WHO low osmolarity ORS + 50 gm sugar + 1 scoop of
commercially available combined minerals and vitamins mix or 40 mL of mineral
mix solution

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SAT Mix
• Roasted, powdered mixture of rice, wheat, black gram, sugar in ratio 1:1:1:2
• 100 gm has 380 Cal and 8 gm protein

• Amylase Rich Foods (ARF) (very important)

• Preparation: Soak in 3 times water for 12 hrs. Drain the water and wrap in
moist muslin cloth and keep for 48 hrs. Germinated grain is dried in sunlight for
8 hrs. Remove the sprouts and roast for 10 mins. Grind into a powder and store
• Advantages:
- Due to amylase, digestibility is increased
- Vitamin and mineral bioavailability is increased
- Less viscosity (Therefore, child can eat more quantities at a time)
- Increased calorie density
• Wheat has shortest germination period and highest amylase content and is thus
preferred for production of ARF

Anti nutrients
• Phytates: in cerals. Binds Fe and Zn
• Tannins: in tea. Binds Fe
• Oxalates: binds Ca
• Avidin: in egg. Reduced bioavailability of biotin
• Goitrogens: Brassicaceae family (cabbage), tapioca

Vitamin A (Pg 110)

• Sources: Cod liver oil (most richest source), carrot, dark green vegetables,
oranges, tomato
• RDA:
- Infants: 300 to 400 microgram
- Children 400 to 600 microgram
- Adolescents: 750 microgram

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• 1 lakh IU Vit A has 30 mg of retinol

WHO Classification of xerophthalmia (Table 8.1)

• Primary signs:
- X1A: Conjunctival xerosis (first sign)
- X1B: Bitot spots
- X2: Corneal xerosis
- X3A: Corneal ulceration < 1/3 of cornea
- X3B: Corneal ulceration > 1/3 of cornea
• Secondary signs:
- XN: Night blindness
- XF: Fundal changes
- XS: Corneal scarring
• Vitamin A prophylaxis program (Pg 110):
- Total 5 doses (Formerly 9 doses)
- At 9 completed months, 1 lakh IU give with measles vaccine
- At 18 months, 2 lakh IU given and repeated every 6 months till 3 yrs of age
(formerly till 5 years of age)
• Treatment of Vit A deficiency:
- Oral Vit A dose of 50000 IU in children < 6 months, 1 lakh IU in 6 months to 1
year, 2 lakh IU in > 1 year children
- Doses taken on days 0, 1 and 28
• Indications for Vit A supplementation:
- Vit A deficiency
- Measles
- SAM
• Vit A is teratogenic if taken in high doses in early gestation

Vitamin C (Pg 120)

• Sources: alma (richest source), citrus fruits, vegetables like cauliflower and
cabbage, human milk
• Osteoid is not formed in Vit C deficiency (Scurvy)
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• Infantile scurvy is called Barlows disease
• Scurvy
- Bleeding gums
- Delayed wound healing
- Skin and mucus membrane bleeds
- Pseudoparalysis: Child in frog leg position with semiflexion at hips and knees
and resents handling due to pain which is a result of subperiosteal
haemorrhage
- Scorbutic rosary (angular swelling at costochondral junction)
• Xray features:
- Pencil thin cortex
- White line of Frankel (white line at metaphsysis)
- Trummerfeld zone (zone of rarefaction proximal to white line)
- Pelken spurs (lateral part of rarefaction appears as triangular defect)
- Wimberger ring sign (epiphsysis surrounded by thin white line)

Vitamin D Deficiency (Nutritional Rickets) (Pg 112)

• Vit D is the sunshine vitamin
• Rickets means “twisted”
• Signs (Pg 113):
- Frontal bossing
- Delayed closure of anterior fontanelle
- Craniotabes (soft skull bones)
- Delayed dentition
- Rachitic rosary (beaded appearance of anterior costochondral junction)
- Harrison sulcus (site of insertion of diaphragm which is visible due to the pull
of diaphragm in the weakened chest wall)
- Swelling of wrist and ankle
- Pectus carinatum
- Bow legs (genu varum)
- Knock knees (genu valgum)
- Visceroptosis (palpable liver and spleen due to ligament laxity)
- Protuberant abdomen
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 - Kyphoscoliosis
- Hypocalcemic seizures
- Muscle weakness
- Hypotonia
- Pathological fractures
- Pelvic deformities which can lead to cephalopelvic disproportion in the
future
• Xray features (Wrist Xray):
- First sign: Loss of normal zone of provisional calcification seen adjacent to
metaphysis seen as a blurring or frayed appearance of metaphyseal margin
(Fraying)
- Cupping: Cartilage hypertrophy causes widening of growth plate
- Splaying: Widening of metaphyseal ends
- Elevated periosteum
- Reduced bone density (Osteopenia)
• Treatment:
- Daily doses of 2000 IU (infants), 3000 to 6000 IU (1 to 12 years), 6000 IU (>12
years) for 12 weeks followed by maintenance dose of 400 to 600 IU/day
- Stoss therapy: 6 lakh IU Vit D as a single oral dose or over 10 days (60000 IU
daily on alternate days). Used in suspected non compliance to daily therapy
- Oral calcium supplements 30 to 75 mg/kg/day given to all patients for 2
months
- Radiological evidence of healing in 4 months
- Joules solution is used for management of hypophosphatemic rickets and
has 30.4 mg of phosphate per mL

Making up for Nutritional Deficiency

• Refer to anganwadi
• Frequent small feeds
• Energy dense foods
• Mix creaks and pulses
• Use germinating pulses

415
• Add sugar to milk
• Use milk with cream
• One egg per day
• Groundnut and jaggery
• Ragi given with jaggery and oil or ghee

Important Terms:
• Weaning: It is the process of gradually introducing an infant to its adult diet
while withdrawing the supply of breast milk. The ideal weaning food is ragi.
• Complementary feeding: It refers to food which complements breast milk and
ensures that the child continues to have enough energy, protein and other
nutrients to grow normally
• Supplementary feeding: It is the provision of meals, drinks or snacks to children
or families additional to their normal diet. e.g. Anganwadi supplementary
nutrition
• Beneficiaries of supplementary nutrition in ICDS:
- Children (6 months to 6 years): 500 Cal, 12 to 15 gm protein
- SAM children (6 months to 6 years): 800 Cal, 20 to 25 gm protein
- Pregnant and lactating mothers: 600 Cal, 18 to 20 gm protein

Few other important points:

• 3 Ds of pellagra: Diarrhea, dermatitis, dementia. 4th D is death
• Zinc deficiency: Acrodermatitis enteropathica
• Zinc is a part of superoxide dismutase
• Selenium is a constituent of glutathione peroxidase
• Selenium deficiency causes Keshan disease
• Learn spectrum of iodine deficiency disorders from Table 8.5 page 124

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 MALNUTRITION
Cardinal determinants of undernutrition:
• LBW
• Infections
• Low food intake

Marasmus (Pg 95)

• Weight for age < 60% without edema
• Grading of marasmus based on fat loss:
- Grade 1: Axilla and groin
- Grade 2: Buttocks and thigh
- Grade 3: Chest, abdomen and back
- Grade 4: Buccal pad of fat
• Features:
- Severe wasting
- Monkey facies: loss of buccal pad of fat
- Baggy pants appearance: loose skin of buttocks hanging down
- Alert children
- No edema

Kwashiorkor (Pg 96)

• Triad: weight for age 60 to 80%, edema, mental changes
• Appearance: Fat sugar baby appearance
• Mild to gross edema which can contribute to 5 to 20% of weight
• Grading based on edema:
- Grade 1: Pedal edema
- Grade 2: Pedal edema and puffy face
- Grade 3: Grade 2 + chest and paraspinal areas
- Grade 4: Grade 3 + ascites
• Muscle wasting and hypotonia

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• Skin changes: increased pigmentation, desquamation, dyspigmentation, flaky
paint dermatosis
• Mucus membrane lesions: smooth tongue, cheilosis, angular stomatitis
• Hair changes: Flag sign, lustreless and easily pluckable hair
• Mental changes: Apathy or irritability with sad intermittent cry
• Neurological changes: tremors during recovery
• GI system: anorexia and vomiting, fatty liver (reversible)
• Nutritional anemia
• CVS: bradycardia, hypotension, diminished cardiac output

Criteria for SAM (Pg 97)

• SAM among children 6 to 59 months of age is defined by WHO and UNICEF as
any of the following 3 criteria:
- Weight for height below 3 SD on WHO growth standard
- Presence of bipedal edema
- MUAC below 11.5 cm (not a criterion for children < 6 months)

Management of SAM (Fig 7.8, Table 7.10)

• 2 methods of management:
- Community based
- Facility based
• Indications for admission:
- Severe edema
- Low appetite (failed appetite test)
- Medical complication
- IMNCI danger signs
• Uncomplicated SAM management in panel 1 on page 99

• 10 steps in 2 phases (Learn fig 7.8)

- Stabilisation phase (2 to 7 days)
- Rehabilitation phase (several weeks)
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1) Hypoglycemia:
• Blood glucose level < 54 mg/dL
• Hypoglycemia, hypothermia and infection generally occur as a triad
• Treatment:
- Asymptomatic hypoglycaemia: 50 mL of 10% glucose or sucrose orally or by
nasogastric tube followed by first feed with starter F75 every 2 hrly at day
and at night
- Symptomatic hypoglycaemia: 10% dextrose IV 5 mL/kg. Follow with 50 mL
of 10% dextrose or sucrose solution by nasogastric tube. Feed with F75
every 2 hrly during day and at night. Start appropriate antibiotics
• Prevention: Feed 2 hrly starting immediately. Prevent hypothermia.

2) Hypothermia:
• Rectal temp < 35.5 degree C or 95.5 degree F or axillary temp < 35 degree C or
95 degree F
• Always screen for infections and measure blood glucose in presence of
hypothermia
• Treatment:
- Clothe the child with warm clothes. Ensure that the head is covered with a
scarf or cap
- Provide heat using overhead warmer, skin contact or heat convector
- Avoid rapid rewarming as it may lead to dysequilibrium
- Feed immediately
- Give appropriate antibiotics
• Prevention:
- Place childs bed in a draught free area
- Keep child well covered with special attention to the head
- Skin to skin contact with mother
- 2 hrly feeding

3) Dehydration:

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• Difficult to assess in SAM child. Signs of dehydration in SAM are thirst,
hypothermia, weak pulse, oliguria
• Assume that all SAM children with watery diarrhoea have some dehydration
• Hypovolemia can coexist with edema
• Treatment:
- Rehydration and maintenance with reduced osmolarity ORS with potassium
supplements
- Amount depending on how much the child wants, whether there is vomiting,
amount of stools
- Initiate feeding within 2 to 3 hrs of starting rehydration
- F75 used on alternate hrs with reduced osmolarity ORS
- ORS is given over 12 hrs
- Be alert for signs of over hydration
• Prevention:
- Reduced osmolarity ORS 5 to 10 mL/kg after each watery stool to replace
stool losses
- Continue breastfeeding
- Initiate refeeding with F75

4) Electrolytes:
• Supplemental potassium 3 to 4 mEq/kg/day for at least 2 wks
• On day 1, 50% magnesium sulphate (equivalent to 4 mEq/mL) IM once (0.3
mL/kg, maximum of 2 mL)
• Extra magnesium is given at 0.8 to 1.2 mEq/kg/day
• Excess body sodium is present even though plasma sodium may be low.
Therefore, restrict salt in diet

5) Infections:
• Assume serious infection and treat
• Usual signs of infection like fever are absent
• Majority of blood stream infections are due to gram negative bacteria

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• Hypoglycaemia and hypothermia are markers of severe infection
• Treatment:
- Parenteral ampicillin 50 mg/kg/dose 6 hrly for at least 2 days followed by
amoxicillin orally 15 mg/kg//dose 8th hrly for 5 days and gentamicin 7.5
mg/kg or amikacin 15 to 20 mg/kg IM or IV once daily for 7 days
- If no improvement after 48 hrs, change to IV cefotaxime (100 to 150
mg/kg/day 6 to 8 hrly) or ceftriaxone (50 to 75 mg/kg/day 12th hrly)
- If other specific infections are identified, give appropriate antibiotics
• Prevention:
- Hand hygiene
- Measles vaccine if child > 6 months and not immunised or if child more than
9 months and vaccinated before 9 completed months
6) Micronutrients:
• Use unto twice the RDA
• On day 1, give Vitamin A orally (50000 IU in children < 6 months, 1 lakh IU in 6
months to 1 year and 2 lakh IU in > 1 year)
• Folic acid 1 mg/day (give 5 mg on day 1)
• Zinc 2 mg/kg/day
• Copper 0.2 to 0.3 mg/kg/day
• Iron 3 mg/kg/day, once child starts gaining weight in stabilisation phase

7) Initiate refeeding:
• Start feeding asap with small frequent feeds
• If unable to take orally, give via NG tube
• Total fluid recommendation is 130 mg/kg/day (reduce to 100 mg/kg/day in
presence of severe edema)
• Continue breastfeeding
• Start with F75 2 hrly 11 mL/kg/feed
• If persistent diarrhea, give a cereal based low lactose F75 diet
• If diarrhoea continues on low lactose diets, use F75 lactose free diet which is
rarely needed
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• 100 mL of F75 has 75 Cal and 0.9 gm protein
• On daily weight monitoring, there will be a tick sign. This is due to initial loss of
weight which occurs due to loss of edema

8) Catchup growth:
• Once appetite returns in 2 to 3 days, encourage higher intake
• Increase volume offered at each feed and decrease frequency of feeds to 6 per
day
• Continue breastfeeding
• Gradual transition from F75 to F100
• Increase calories to 150 to 200 Cal/kg/day and protein to 4 to 6 gm/kg/day
• Once child achieves rapid weight gain, F100 is changed to RUTF and then to
home food
• 100 mL of F100 has 100 Cal and 2.5 to 3 gm protein
• RUTF:
• Ready to Use Therapeutic Food
• Locally produced or commercially available
• Pre prepared and stored in containers
• Taken uncooked
• Little available water
• Calorie and protein dense
• Standard RUTF has 543 Cal and 15 gm protein in 100 gm
• Weight adjusted dose of RUTF is used for appetite test

9) Sensory stimulation:
• Cheerful stimulating environment
• Age appropriate structured play therapy for at least 15 to 30 mins/day
• Age appropriate physical activity as soon as child is well
• Tender loving care
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10) Prepare for followup:
• Primary failure to respond is indicated by:
- Failure to regain appetite by day 4
- Failure to start losing edema by day 4
- Presence of edema on day 10
- Failure to gain at least 5 gm/kg/day by day 10
• Secondary failure to respond is indicated by:
- Failure to gain at least 5 gm/kg/day for consecutive days during
rehabilitation phase

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 ACUTE GLOMERULONEPHRITIS
Presenting complaints
 Cola coloured urine, fever, facial puffiness
History
Haematuria
 Is discolouration present throughout the urine stream?
 Frequency ofurination? amount?(oliguria)
 Causes of haematuria: AGN, HSP, HUS, drugs, SLE, bladder stone(terminal
haematuria!)UTI, NS(atypical presentation),bleeding disorder,renal
malignancy,I.E
 Ask negative history to R/o the above conditions..
 Ask for H/O trauma,intake of foods that can cause coloured urine.
 Whether BP was recorded on admission & whether it was high?

Facial Puffiness
 Increases during early morning,more around the eyes
 how to assess severity of oedema from history?
 Is the child able to open his eyes
 Is there assosciated pedal oedema or abdominal distension or scrotal
oedema

History to R/O Other Causes of Oedema

 Cardiac-h/o of PND,orthopnoea
 Hepatic - jaundice
 Malnutrition
 Hypothyroidism-constipation,lethargy
 Angioneurotic oedema- exposure to allergens

History to R/O Complications

 No H/O headache or blurring of vision(hypertensive encephalopathy)
 No oliguria , anuria or vomiting(ARF)
 No dyspnoea , orthopnoea, PND(CCF)

Past History
 Pyoderma?-1 month back?(TYPE 49)
 Tonsillitis? 2weeks back(TYPE 12)
 No similar illness in the past(IGA NEPHROPATHY)
 NO H/O hepatitis,malaria,lepto
 No H/O of intake of drugs like rifampicin,ibuprofen
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Nutrition History
Don’t forget to mention the dietary restriction!

Family History
 Similar episodes in family?-ALPORTS,SLE,IGA NEPHROPATHY,PCKD
 No h/o Deafness in family(to r/o alports)

EXAMINATION
 Look for pyoderma scars!!
 Examine the oral cavity for signs of tonsillitis!!
 Pallor , icterus(HUS), oedema
 Pulse
 JVP(volume overload)
 Tachycardia- CCF Bradycardia=hypertensive encephalopathy
 BP is very important

Systemic examination
GIT
 Ascites, renal angle tenderness,external genitalia
CVS
 R/O CCF
 Look for JVP!
RESP
 Look for B/L basal creps,signs of pleural effusion
DIAGNOSIS
Acute post infectious glomerulonephritis with hypertension, no malnutrition

DISCUSSION
Causes
1) Post infectious
Streptococci, staphylococci, pneumococci, meningococci, T.pallidum,
salmonella, leptospira
P.malariae, P.falciparum, Toxoplasma, Filaria
Hep B, C, CMV, parvovirus, EBV, varicella, echo virus
2) Systemic vasculitis
HSP, microscopic polyarteritis, Wegener granulomatosis
3) Others

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 Membranoproliferative glomerulo nephritis, IgA nephropathy, Hereditary
nephropathy, SLE

INVESTIGATIONS
1 . URINE
- Albumin 1+,2+
- microscopy-RBC casts(important)
- More than 15% of dysmorphic rbc
- WBC(due to inflammation)
2.BLOOD
- Hb , TC , DC,ESR,
3.RFT
- S:Urea, creatinine(elevated)
4. Serum K+ & Na+
5. Evidence of Streptococcal infection
- ASO titre ,anti DNAse B
6. C3 levels in serum low
7. Ultrasound abdomen
8. Renal biopsy( only if there are indications.. not done as routine investigation)

MANAGEMENT
1. Maintain charts
- Intake output charts
- BP charts
2. Diet
- salt n fluid restriction,
- protein as per RDA . Protein restriction needed only when renal failure sets
in.
- in case of hyperkalemia- restrict intake of vegetables, n fruits
(apple,banana), tender coconut water.
3. Specific Rx
- RX of hypertension- CCB +diuretic (liberal use unlike in NS)
- in case of hypertensive encephalopathy: Na nitroprusside and Labetalol
4. When the pt is going for renal failure
- Restrict fluid intake
- Previous days output+insensible loss(15-30mg/kg)

Hyperkalaemia management(>6.5meq/l)
- Stop intake of K rich food,
- give 10% Ca gluconate,
426
 - NaHCO3,
- glucose+insulin,
- salbutamol
Persistent hyperkalemia, azotemia, pulmonary oedema, cardiac failure despite
medical measures are the indications for doing DIALYSIS!

PROGNOSIS(important)
 Macroscopic haematuria subside by 2-3 weeks.
 Microscopic haematuria by 6mnths-1 yr
 C3 normalises by 6 weeks.
 If not do a renal biopsy to rule out other causes of AGN

Alport Syndrome
 X linked
 Mutation in gene encoding alpha subunit of collagen IV ( COL4A)
 Clinical features
- Microscopic hematuria,
- Moderate proteinuria,
- Progressive kidney failure
- Sensorineural deafness, ocular defects( lenticonus, cataract, macular
changes)
 Treatment
- Supportive,
- ACE inhibitors

Conditions associated with low complement activity

 Bacterial infections esp Neisseria
 Cirrhosis
 Glomerulo nephritis
 Lupus nephritis
 Hereditary angioedema

Causes of hematuria (> 5 RBC / high power field)

 Glomerular causes
- postinfectious GN
- IgA nephropathy
- HSP
427
 - Membranoproliferative GN
- Rapidly progressive GN

 Non glomerular causes

- Hypercalciuria
- Renal calculi
- UTI
- Hemorrhagic cystitis
- Trauma
- Interstitial nephritis

IgA nephropathy
 Predominant deposition of IgA in the glomeruli
 Gross hematuria following URTI
 Each episode lasts for 2-5 days
 Renal histology shows mesangial proliferation.

 Treatment
- Pts with hematuria & non nephrotic proteinuria are treated with
ACEI.
- Those with nephrotic range proteinuria, deranged renal function are
treated with corticosteroid & alkylating agents.

Indication of renal biopsy in acute GN

1) Systemic features :fever, rash, joint pain, heart disease
2) Absence of serological evidence of streptococcal infection
3) Normal level of C3 in the acute stage of illness.
4) Mixed features of glomerulonephritis & NS
5) Delayed resolution :
- Oliguria, hypertension and/or azotemia persisting past 7-10 days
- Gross hematuria persisting past 3-4 weeks
- Nephrotic range proteinuria beyond 2 weeks
- Low C3 level beyond 12 weeks
- Persistent proteinuria beyond 6 months

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 NEPHROTIC SYNDROME

Presenting Complaints
 oedema
 Reduced urine output
History Taking
OEDEMA
 causes
- Renal
- CVS
- Liver disease
- Allergy, anphylaxis
- Malnutrition
Negative history for oedema
 CVS-exertional dyspnoea?,PND?,orthopnoea?
 Liver - jaundice? ,
 Allergy /anaphylaxis- h/o allergy? , drug intake? , insect bite
 To rule out AGN: hematuria present/not
Rule out complications
 No fever , abd pain(bacterial peritonitis),sudden onset of haematuria, flank
 pain(Renal Vein Thrombosis), breathlessness , chest pain (PLEURAL
EFFUSSION),Weakness of any part of the body(stroke), growth retardation
(steroid toxicity)

Past History
 Very important to take the past treatment history in detail.( eg:NS child
who is steroid dependent now in relapse)
First episode? , number of relapses? , duration and dose of drugs?, after
how many days of stopping/reducing d dose did d child get recurrence of
oedema?
 h/o asthma?(we can miss NS in a patient with asthma under steroid Rx)
 h/o jaundice?TB(imp….steroid therapy can lead to reactivation of latent
TB)?vaccine preventable diseases?any major illness?

Dietary history
Don’t forget to mention about the dietary advices given to the patient.

EXAMINATION
 cushingoid features?
429
  distended abdomen? ,
 oedema ,scrotal oedema,
 peripheral pulses
 BP - important…(can have hypertension secondary to steroid Rx)

Anthropometry
 GROWTH retardation can occur as a complication of steroid treatment
GIT
 Look for ascites, external genetalia
 Look for renal mass,renal angle tenderness
 examination of external genetalia is very important
RESP
 look for pleural effusion
CVS
 R/O CCF
CNS
 Stroke

DISCUSSION

Remission - NIL or trace urine albumin for 3 consecutive days

Responder- responds within 4 weeks
Resistant- not responding to steroid Rx within 8 weeks
Dependance - a NS child who has gone into remission goes for relapse when
changed to alternate day regimen or within 2 weeks of stopping the steroids
Relapse - recurrence of proteinuria (3+ or more) for 3 consecutive days
Frequent relapse- 4 or more relapses in one year

Differential Diagnosis
1. AGN
2. CCF
3. PEM
4. Angioneurotic oedema
5. Hepatitis B

MANAGEMENT

INVESTIGATIONS
1. URINE
 24 hr urine protein- >40mg /m2/day
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  Urine protein 3+/4+
 Protein / creatine > 2
 Urine microscopy-hyaline casts++,
 Heat & acetic acid test( grading of proteinuria)
 Culture and sensitivity(to R/o UTI)
2. BLOOD
 Albumin
 Cholesterol
 Calcium(hypocalcaemia-decrease in albumin bound fraction)
 Na - low (dilution due to water retention)
 RENAL FUNCTION TEST is usually normal unlike in AGN
 C3 levels are normal unlike in AGN
3.CHEST X-RAY
 Imp to R/O TB and complications like pleural effusion, pneumonia
4.Mantaux and sputum examination
5.R/o Hepatitis & TB before giving steroids

Note: Rule out TB before steroid therapy!!

6.Ascitic fluid tap (in presence of SBP)
7.US abdomen- ascites,kidney size(usually normal)
8. TO RULE OUT SECONDARY CAUSES-in case of atypical presentations, frequent
relapse, steroid resistance
 Peripheral smear(malaria)
 ANA , anti ds-DNA , (COLLAGEN VASCULAR DISEASES)
 ASO , HBsAg , VDRL
 RENAL BIOPSY( study indications)

TREATMENT
1. Rest- mild to moderate restriction of activity,
2. Admit the child and maintain charts
- Input output chart
- Weight gain chart
- Abdominal girth
- BP chart
- Urine albumin
3. Diet
- Salt and fluid restriction(not as strict as in AGN)
- Protein rich diet(with high bioavailability -egg white)
- Decreased intake of food likely to increase cholesterol levels-beef,egg yolk
4. Antibiotics for infection
431
 - DRUG of choice -crystalline penicillin IV
5. Specific Rx –STEROIDS

PRIMARY NEPHROTIC SYNDROME

- Prednisolone 2mg/kg/day(max 60mg/day) in 3 divided doses for 6 weeks
followed by
- Prednisolone 1.5 mg/kg/day (max 40 mg/day) single morning dose on
alternate days for 6 weeks

Rx OF RELAPSE

1. INFREQUENT RELAPSE
- Prednisolone 2mg/kg/day Till remission
- Then 1.5mg/kg on alternate day for 4 weeks.

2. FREQUENT RELAPSE
- Prednisolone 2mg/kg/day till remission. Then ,
- Prednisolone 1.5mg/kg/day to maintain remission on alternate days. Then
- Taper the dose

- a. Threshold <0.5 mg/kg

Continue for 9-18 months

- b.Threshold > 0.5mg/kg/day or in case of steroidtoxicity

Levamisole, cyclophosphamide, tacrolimus, cyclosporine

 2° causes of NS
- Amyloidosis
- vasculitis
- SLE
- Post infectious GN
- Hep B nephropathy

 Infectious causes of NS
- Malaria
- Hep B
- Syphilis
- Toxoplasmosis

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  Findings that you look for in other systems
- Resp--pleural effusion
- CVS -- CCF
- CNS—stroke

 Complications
- Edema
- Infections
- Thrombotic complications : renal, pulmonary, cerebral veins
- Hypovolemia, Acute renal failure
- Steroid toxicity : Cushingoid features, short stature, hypertension,
osteoporosis, sub capsular cataract

 Features of NS with significant lesions

- Age at onset: older children
- M=F
- Hematuria :usual
- BP : normal / increased
- GFR: normal/ decreased
- Renal biopsy : Changes of varying severity, C3, immunoglobulin
deposits
- Serum C3: Low in MPGN
- low severity of proteinuria
- Response to steroids : unsatisfactory

 Causes of edema
- Massive proteinuria &hypoalbuminemia

 Reason for hyperlipidemia

- Hypoalbuminemia induces hepatic synthesis of beta lipoproteins resulting
in hypercholesterolemia

Therapy for steroid sensitive NS

- Prednisolone: 0.3 -0.7 mg/kg on alternate days for 9-18 months
- A/E: Cushingoid body habitus, hypertension, short stature, cataract,
hirsutism.

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 - Levamisole: 2-2.5 mg/kg on alternate days for 1-2 years.
- A/E: Leukopenia, rash, flu like symptoms

- Mycophenolatemofetil: 20-25 mg/kg /day for 1-3 years

- A/E: Gastrointestinal discomfort, diarrhea, leukopenia

- Cyclosporine: 4-5 mg/kg /day

- Tacrolimus: 0.1-0.2 mg/kg/day
- A/E: Acute & chronic nephrotoxicity, elevated transaminase, hirsutism, gum
hyperplasia, hypertension /hyperlipidemia ( CsA>Tac) Hyperglycemia,
neurotoxicity with headache & seizures ( Tac>CsA)

- Rituximab:375 mg/m2 IV once a week 1-2 doses

- A/E: Infusion reactions ( fever, rash, bronchospasm), neutropenia

Longterm outcome
Children with minimal change NS : excellent prognosis
Frequency of relapses decreases with time & majority of pts outgrow the
condition by adulthood.
Mortality rate - 1-4% is associated with infections & hypovolemia that should be
preventable

Parent education
-Explain about the disease & usual outcome.
-They are taught how to examine the urine for protein, which should be done
periodically to detect a relapse early.
-During the period of remission, no dietary restrictions are impose

Why NS child is prone for infections?

-Edema fluid is a good culture media

-Loss of immunoglobulins in urine
- Loss of properidin factor in urine, which is needed for opsonisation
- Immunodeficiency due to steroids
-Splenic hypoperfusion

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 JAUNDICE
Presenting complaint
 Yellowish discolouration of eyes or urine
H/o present illness
 Jaundice- onset, duration, progression
 Colour of urine- duration and severity of yellowish discolouration
Keeping the etiologies in mind, we can ask the rest of the history.
a. A/c viral hepatitis
 Fever, anorexia, nausea and vomiting, abdominal pain- rt
hypochondrial/ epigastric, fatigue
 H/o blood transfusion, surgery, injections, tattooing, ear piercing
(Hep B), food from outside, similar symptoms in family members
(Hep A)
b. Leptospirosis
 Fever, conjunctival congestion, myalgia
 Contact with contaminated water like bathing in pond, walking
barefoot in water-logged area, wound in legs
c. Malaria
 Fever with chills and rigor
 Travel/ residence in endemic area
 Anaemia- exertional dyspnoea, fatigue, palpitations, abdominal
distension, pain (splenomegaly)
 Bone pain, chest pain, leg ulcers- sickle cell anaemia
 Blood transfusions
 Oliguria, hematuria, dysentery- HUS
d. Obstructive jaundice
 A/c viral hepatitis has a cholestatic phase.
 Fever with chills and rigor, colicky abdominal pain, clay coloured
stools, itching, LOW, LOA
e. Other causes
 Drug intake- Paracetamol, all ATTs except Streptomycin and
Ethambutol, Anti-epileptics- Valproate, Chemotherapeutic agents,
Anti-psychotics (Viva question- Drugs causing jaundice)
 Other diseases like typhoid, dengue, IMN, Wilson’s disease, Gilbert’s
disease, autoimmune diseases, Amanita poisoning
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H/o complications
 Bleeding manifestation- hematemesis, malena (Learn definitions from
Medicine book)
 Edema, ascites
 Reduced urine output- mostly due to vomiting, could be due to
hepatorenal syndrome also
 Altered sleep rhythm, altered sensorium- hepatic encephalopathy
What was done after admission to the hospital?
Medication for fever, dietary changes, bowel wash/ enema done
Past history
 Similar illness in the past, contact with similar cases, contact with
tuberculosis, Ayurvedic treatment
 Most of the points in h/o present illness can be asked in past history.

Antental history
 Rh incompatibility- blood group of parents, costly injections (Anti-D), blood
group of parents, stillbirth
Natal and postnatal history
 H/o difficult labour, instrumental delivery, prematurity (neonatal jaundice)
 Hypothyroidism
 Umbilical sepsis (onset usually in 5-9 days, caused by usual skin flora, i.e.,
Staphylococci- fever, lethargy, apnoea, poor feeding, vomiting,
irritability,jaundice, redness and swelling around the umbilicus, discharge
from the umbilicus)- can lead to portal hypertension
Diet history
 Anorexia, steatorrhoea
 Any food fads- aversion to meat, usually seen in viral hepatitis
 Food from outside
 Vitamin intake- B complex in excess can sometimes cause jaundice.
Immunization history
 Vaccines especially Hep A,B
Family history
 Jaundice, illnesses causing jaundice in family members
 Whether vaccinated against Hep A and B
 Neuropsychiatric illness in family- Wilson’s disease
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  Blood transfusion, splenectomy in family members
Socio-economic history
 Detailed socio-economic history should be taken.
 Source of drinking water, whether boiled or not, presence of sanitary well
and sanitary latrine, whether the child is using sanitary latrine
General examination
 Temperature, pallor, icterus

Head to foot examination

 Head
Hair colour (malnutrition), open AF (hypothyroidism), cephalhematoma,
microcephaly
 Face
Dysmorphism (genetic abnormalities), haemolytic facies
 Eyes
Jaundice, KF ring, cataract, subconjunctival haemorrhage, Bitot spots
(malnourished child)
 Mouth
Angular stomatitis, cheilitis, red/magenta tongue (vitamin deficiency),
tonsillar enlargement, gum hypertrophy, bleeding spots in soft palate
 Stigmata of chronic liver disease

GIT examination
 Inspection- ascites, dilated veins
 Palpation- tenderness, liver, spleen, abdominal circumference
 Percussion- free fluid, liver span

Diagnosis
 According to etiology- eg: acute viral hepatitis, probably due to Hepatitis A
infection, in icteric stage with no signs of hepatic failure
DISCUSSION
Management
Investigation
a) RBE- Hb, TC, DC

437
 b) LFT- Bilirubin (conjugated and unconjugated), SGOT, SGPT, S.Albumin, PT-
INR
c) URE- Urobilinogen, bile salts, bile pigments
d) Viral markers- HBsAg, Anti-HBc, Anti-HAV, Anti-HCV
Yoyo phenomenon- fluctuating levels of transaminases in Hep C infection
Serological markers of Hep B- IMPORTANT- Fig. 11.8, pg 217
In Hep B, first antibody to appear is IgM Anti-HBc
e) USS abdomen
f) Investigation to rule out malaria, Weil’s disease, Wilson’s disease

Read LFT charts and lab findings in pre-hepatic, hepatic and post-hepatic jaundice
from Medicine textbook.

Treatment
Indications for hospital admission in acute viral hepatitis
 Persistent vomiting
 Fever (In uncomplicated hepatitis, fever is expected to come down once
jaundice gets established. Persistence of high fever should prompt
additional investigation for fever.)
 Altered sensorium, sleeplessness (could point towards precoma)
 Bleeding tendency
 Decreased urine output (mostly due to vomiting, could be due to
hepatorenal syndrome also)
 High bilirubin, elevated PT, elevated blood urea

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a) Bed rest till serum bilirubin is normal to aid the natural recovery. Early
activity and intercurrent infections may cause an apparent relapse.
b) Isolation. Universal precautions. Precautions during discarding needles,
disposal of excreta.
c) Diet-high carbohydrate diet, frequent feeding (prolonged fasting-
gluconeogenesis- burden for liver, fat reduced if not tolerated (cholestasis-
bile needed for the absorption of fats not reaching the intestine in
sufficient quantity), normal requirements of good quality proteins when
appetite returns (aids in recovery)
d) When oral intake not tolerated, IV fluids given.
Hepatic drip
Normal saline- 100ml
10% glucose- 400 ml
15% potassium chloride- 5 ml
B- complex vitamins- 2ml
Calcium added sometimes.
e) Observe for early signs of precoma- shrinking of liver, flapping tremor,
altered sleep rhythm, altered handwriting
f) Address the potential precipitants of coma. These include:
 Hypokalemia- Sweet lime juice, coconut water, orange- good source
of potassium. Diuretics must be avoided.
 Fever- High fever shoots up metabolic demands. Infections can
precipitate coma. Sponging is the only safe method to bring down
fever Antipyretics, in general are deleterious.
 Constipation- Ensure regular bowel movements. Lactulose (dose
adjusted to produce 2-3 stools per day), daily bowel wash, bowel
sterilization using antibiotics like Ampicillin. READ PRECOMA
REGIMEN.
 GI bleed- Due to deficiency of coagulation factors. It adds to the
ammonia load. Continuous nasogastric aspiration, Vit K IM. FFP and
blood transfusion may be needed. Ranitidine may be given.
 Hypoglycemia- Glucose in IV fluids (eg: hepatic drip), continuous
monitoring of blood glucose levels
 Avoid hepatotoxic drugs.
g) Cerebral edema- 30 degree head end elevation, Mannitol, hyperventilation

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 h) Seriously ill patients- plasmapheresis, exchange transfusion, hemoperfusion
for short periods of time (eg: pending liver transplantation)
i) Follow up after 6 months with viral marker HBsAg to rule out chronicity.
j) Vaccine advised in a patient with Hep B- Hep A vaccine
Acute liver failure (ALF)
INR>/= 1.5 with hepatic encephalopathy or INR>/=2 without hepatic
encephalopathy along with biochemical evidence of liver injury in the absence of
underlying chronic liver disease.
CLD in children with an acute presentation mimicking ALF-Autoimmune liver
disease and Wilson’s disease

READ (O.P Ghai- pg 311-313, Table 12.26-12.30):

1. Causes of ALF
2. Stages of hepatic encephalopathy
3. Investigation for causes of ALF
4. Monitoring of children with ALF
5. Management
6. Specific treatment
Important questions
1. Vaccines- Hep A and Hep B IMMUNIZATION
2. Passive immunization- Hep A and Hep B immunoglobulin-dose
3. Hepatotropic viruses, other viruses causing hepatitis
4. Incubation period, routes of transmission, prognosis, complications,
chronicity in %, carrier state, treatment
Hep A- 10-50 (avg 25-30) days
Hep B- 50-180 (avg 60-90) days
Hep B is a DNA virus. Read antigens, phases.
Hep C- 40-120 days
Hep D- 2-12 weeks
Hep E- 3-8 weeks
5. Serological markers in Hep B- pg. 217, Fig.11.8
6. Drugs for the treatment of chronic Hep B in children- Interferon (thrice
weekly injections for 6 months), Oral Lamivudine, combinations of IFN
alpha 2a or 2b with Lamivudine
New drugs- Adefovir (>12 years), Entecavir (16 years), Telbivudine (>16
years), Tenofovir (>12years). Chronic Hep C- Interferon, Ribavirin
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 NOT USED IN ACUTE HEPATITIS
7. Gianotti- Crosti syndrome- complication of Hep B- papular acrodermatitis of
infancy
8. Acute, subacute and fulminant hepatic failure. Factors leading to fulminant
hepatic failure, management
9. Paracetamol poisoning – clinical features, management
Toxic dose: >200mg/kg.Toxicity due to formation of NAPQI
Patient either recovers completely in 3 weeks or progress to fulminant
hepatic failure.

Stage Time after Characteristics

ingestion
1 12-24 h Asymptomatic; nausea and vomiting

2 24-48h Resolution of earlier symptoms; evidence of

elevated liver transaminases

3 3-5days Anorexia, nausea, vomiting; multi-organ

dysfunction; peak transaminase elevation

4 4-14 days Recovery phase with resolution of clinical

symptoms and improvement in hepatic
function

MANAGEMENT
 Gastric lavage within 4h

Blood for acetaminophen levels atleast 4 h post ingestion

Plot on Rumack-Matthew normogram.

Acetaminophen levels below the broken line Acetaminophen levels are above the solid line.


Do not give NAC(N-Acetyl cysteine). Stop, if already Thrapy with NAC
started.

441
 Antidote- NAC
- Oral: 140 mg/kg loading dose; then 70 mg/kg q4h (for 17 doses)
- IV: 150mg/kg for 1h; then 50mg/kg over 4h; followed by 100mg/kg
over 16h
 King’s College criteria for liver transplantation
- Acidemia (serum Ph< 7.3) after adequate fluid resuscitation
- Coagulopathy (INR>6)
- Renal dysfunction (Creatinine >3.4mg/dL)
- Grade 3 or 4 hepatic encephalopathy

442
 ACUTE DIARRHEAL DISEASE
History Taking
 Loose stool
- Stool frequency(>1epi/3hr)
- Consistency-Watery/bloody/mucus/frothy(osmotic diarrhea)
 vomiting? (>3epi/1hr)
 Asso symptoms
- Vomiting, abd pain, fever
 Any complications
- Urine output(no/scanty for>6hr)
- Increased thirst ,irritability
- Abdomen distention(hypokalemia)
- Sunken eyes,absence of tears while crying
 Probable etiology
- H/o contact with similar cases?
- H/o food from outside/recent travel outside
- Any h/o ear discharge/UTI/pharygitis/pneumonia
- Any h/o drug intake- to r/o antibiotic assosciated diarrhea
 Condition of child
What is he getting now?
Active/ playful

Past history
 H/O of TB or measles

Dietic history
 Any prelacteals, cow’s milk intake
 whether breast feeding is continued/stopped
 any diet modification
 type of fluids child is given
 bottle fed or not?
 If bottle fed-adequecy,hygiene,improper dilution
 food from outside

Immunization history
 measles , rotavirus vaccination

Socio economic history

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  Detailed SEC history including source of drinking water, whether its boiled
or not, presence of sanitary well & latrine, whether the child is using
sanitary latrine

Examination
 sunken eyes,
 skin pinchability(check on abdomen)
 depressed frontanelle
 dry tongue,oral mucosa
 pulse ,BP
 give a cup of water & assess thirst.
Condition Well alert Restless Lethargic
Eyes Normal Sunken Very sunken
Tears Present Absent Dry
Tongue and Moist Dry Dry
mucosa
Thirst Not Thirsty, but Not able to
increased drinks drink
Skin pinch Goes back Goes back Slow
quick quick
Classify No Some Sever
dehydration dehydration
Loss of 5% 5-10% >10%
water
 Star signs -altered general condition, thirst, skin pinchability
 first sign-increased thirst

MANAGEMENT
Plan A–NO DEHYDRATION

 Treated at home after explanation of feeding and the danger signs to the
mother
Age ORS after each ORS to provide
loose stools use at home
<24 months 50-100 ml 500 ml/day
2-10 years 100-200 ml 1000 ml/day
>10 years Ad lib 2000 ml /day
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  Danger signs requiring medical attention
- Continuing diarrhea beyond 3 days
- Increased volume/frequency of stools
- Repeated vomiting
- Increasing thirst
- Refusal to feed
- Fever
- Blood in stools

Plan B – Some dehydration

All cases with obvious signs of dehydration need to be treated in a health
centre/hospital
Fluid requirement is calculated under the following three headings

 Daily requirements
Upto 10 kg -- 100ml/kg
10-20 kg – 50 ml/kg
>20 kg—20 ml/kg

 Deficit replacement
75 ml/kg of ORS over 4 hrs
If after 4 hrs, the child still has some dehydration, then another treatment
with ORS(as in rehydration ) is to be given.

 Maintenance fluid therapy to replace losses

This phase should begin when signs of dehydration disappear, usually
within 4 hrs ,10 ml/kg /stool.

Plan C –severe dehydration

IV Ringer lactate /normal saline /Ringer lactate with 5% dextrose.

100ml/kg over 6 hrs in children <12 months & over 3 hrs in children > 12
months.

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Age 30 ml/kg 70ml/kg

<12 mon 1 hr 5 hr

>12 mon 30 min 2. 5 hr

Oral rehydration therapy

 Glucose dependent sodium & water absorption is the principle behind
replacing glucose & sodium in 1:1 molar ratio in WHO ORS.
 Low osmolarity ORS – 245 mmol/L

Composition of ORS
Constituent g/L Ion/osmole Mmol/L

NaCl 2.6 Na 75

Glucose 13.5 Cl 65

KCl 1.5 Glucose 75

Trisodium 2.9 Potassium 20

citrate Citrate 10

Total 245
osmolarity

Home available fluids for acute diarrhea

 Fluids that contain salt ( preferable )
oral rehydration solution, salted drinks(eg: salted rice water, salted
yoghurt), vegetable /chicken soup with salt.
 Fluids that do not contain salt( acceptable )
Plain water, water in which cereal has been cooked(eg: unsalted rice water),
unsalted soup, yoghurt drinks without salt, green coconut water, weak
unsweetened tea, unsweetened fresh fruit juice
 Unsuitable home available fluids
Ccommercial carbonated beverages, commercial fruit juices, sweetened tea

When is ORT ineffective?

446
  High purge rate ( > 5 ml/kg/hr)
 Vomiting (> 3 episodes /hr)
 Glucose malabsorption
 Inappropriate method of preparation
 Abdominal distension, ileus

Role of zinc in diarrhea

 Zn losses during diarrhea aggravate pre existing Zn deficiency.
 Zn supplementation decreases the duration &severity of diarrhea.
 Also decreases the risk of persistent diarrhea.
 Zn is supplemented as sulfate, acetate, gluconate.
 Dose : 20 mg of elemental Zn /day for children > 6 months for a period of
14 days.

Dysentery
 Bacillary dysentery is much common in children than amebic dysentery.
 Bacteria : Shigella, Salmonella, entero invasive & entero hemorrhagic E coli.
 Treatment :
Sick child: IV ceftriaxone ( 50-100 mg/kg/day for 3-5 days)
Stable child: Ciprofloxacin/ oral cefixime
Monitored for clinical improvement within 48 hours.

Persistant diarrhea
An episode of diarrhea, of presumed etiology, which starts acutely but lasts for
more than 14 days.

Chronic diarrhea
Insidious onset of diarrhea of > 2 weeks duration in children &> 4 weeks in adults.

Causes of diarrhea with seizures

 Meningitis
 Encephalitis
 Hypokalemia
 Cerebral venous sinus thrombosis
 Febrile seizures
447
  Reyes syndrome

Probiotics
Microorganisms that exert beneficial effects on human health when they
colonize the bowel
- Lactobacillus rhamnosus
- L.plantarum
- Enterococcus faecium
- Saccharomyces boulardii

ReSoMal
Used for preparation of an ORS exclusively for people suffering from severe acute
malnutrition.

Composition

Glu: 125 mmol/L

Na: 45 mmol/L
K : 40 mmol/L
Cl: 70 mmol/L
Mg: 3 mmol/L
Zn: 0.3 mmol/L
Cu: 0.045 mmol/L
Citrate: 7 mmol/L
Total – 290.345 mmol/L

448
 RESPIRATORY SYSTEM
PNEUMONIA/LRI
Common presentation

 fever, cough, breathlessness/ fast breathing

Atypical presentations
 Abdominal pain, fever
History of present illness
a) Fever- onset, duration, grade, pattern, chills and rigor, diurnal variation,
relief with mediation. Refer PUO case.
b) Cough- onset, duration, productive/non-productive (if productive, sputum-
amount, colour, smell, blood staining; if non-productive- dry/wet-
children<5 years not likely to be able to cough up sputum), diurnal
variation, postural variation, seasonal variation (more important for
asthmatic cough)
c) Breathlessness/fast breathing- onset, duration, progression, aggravating
and relieving factors, diurnal, postural and seasonal variation, chest
indrawing, orthopnoea/PND (for older children)
d) H/o ear pain, ear discharge, throat pain, nasal discharge, rhinitis
e) H/o wheeze, stridor, abdominal pain, seizures
f) Danger signs- altered sensorium, cyanosis, inability to feed, seizures,
grunting, severe malnutrition, hypothermia, stridor in a calm child, wheeze
in a calm child
Causes of seizures
 Febrile seizures- previous history, family history, whether occurred
within 24h of onset of fever, features suggestive of complex seizures
(Refer Febrile seizures case.)
 Meningitis/ encephalitis- high fever with chills and rigor, neck pain,
vomiting
 Atypical pneumonia- Legionella
 As a danger sign of pneumonia
 Meningism

449
 g) Symptoms referable to other systems- abdominal pain (due to irritation of
pleura, jaundice, diarrhoea), CVS symptoms (important because congenital
heart disease can present as recurrent respiratory infections)
h) H/o foreign body aspiration (especially in a child with pincer grasp)

Past history- in all respiratory system cases

 Similar illness
 Recurrent respiratory tract infections
 Asthma and allergy
 Contact with tuberculosis
 Previous hospital admission
 Drug allergy
 Surgery
 Vaccine preventable diseases
Causes of recurrent respiratory tract infections- congenital heart disease,
malnutrition, rarely immunodeficiency
Life history
 Antenatal
 Natal- low birth weight, prematurity/preterm delivery
 Postnatal- NICU admission, congenital heart disease
Dietary history
 Should be taken in detail
 Malnutrition- LRI more common, more difficult to diagnose (typical
features msked), more serious
 Duration of exclusive breastfeeding, details of complimentary feeding
(respiratory tract and GIT infections more common during this period)
Development history
Immunization history
 Whether fully immunized for age
 Optional vaccines- if any, ask for details.
 BCG scar. Ask specifically for BCG immunization
 H/o measles and measles immunization.
Measles depresses cell mediated immunity and predisposes to infections. It
also aggravates malnutrition. Read about the complications of measles
from Infectious diseases. Enanthem in measles- KOPLIK SPOTS
450
Family history
 Similar illness
 Tuberculosis in family
Socioeconomic history
 Socioeconomic status- assessed using Kuppuswamy index
 Overcrowding
 Cooking fuel
 Any pets in house
 Any smokers in house
 Ventilation
 Water supply (whether boiled or not)
 Sanitary latrine
General examination
 Build and nourishment (more details to be taken in anthropometry)
 Pallor- malnutrition
 Cyanosis- can be a danger sign or sign of congenital heart disease
 Clubbing- congenital heart disease
 Icterus, lymph node enlargement, edema
 Vital signs- pulse rate usually elevated, respiratory rate increased (very
important- ARI control programme), temperature usually elevated
(hypothermia in small infants and malnourished)
Head to foot examination
 Signs of malnutrition- flag sign of hair, edema, loss of subcutaneous fat
 Signs of allergic rhinitis- overbite, high arched palate, allegic shiners, allergic
salute, allergic crease, Dennie Morgan fold, conjunctival congestion,
periorbital edema
Anthropometry – special attention in a malnourished child

Examination of respiratory system

Upper respiratory tract

 DNS, nasal or ear discharge, pharyngeal congestion, flaring of alae nasi
Lower respiratory tract
Inspction
 Respiratory rate- increased
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  In consolidation- no change in position of trachea or apex (no mediastinal
shift)
 Chest movements decreased on the affected side side especially when
pleurisy is present
 Look for intercostals retraction and lower chest indrawing.
Palpation
 Confirm the findings on inspection.
 Respiratory movements- to localize the side and specific site
 Vocal fremitus increased over the consolidated area
Percussion
Percussion is always done last as the child may become uncooperative. Look for
dullness over lung areas and tidal percussion.
Auscultation
 Breath sounds- diminished over the affected lung fields. Look for bronchial
breathing.
 Adventitious sounds- Crepitations are the hallmark of consolidation.
Describe- fine/coarse, inspiratory/ expiratory, if inspiratory, early/mid/end
inspiratory. Rhonchi may be present during stage of congestion when fluid
is present in alveoli.
 Vocal resonance- increased over affected lung fields
 Miscellaneous sounds- bronchophony, aegophony, whispering pectoriloquy

Examination of CVS, GIT and CNS

In CVS, look for any congenital heart disease as they can cause recurrent
respiratory tract infections
summary

Diagnosis
 Acute lower respiratory tract infection, possibly lobar pneumonia/
bronchopneumonia with
 right/left lobe consolidation (for lobar pneumonia)
 No signs of respiratory failure
 No complications
Comment on growth, development, nutrition and immunization.

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DISCUSSION
Except during neonatal period, ARIs are the most common cause of illness and
mortality in children under five years of age.
Upper respiratory tract- Consists of airways from nostrils to vocal cords in the
larynx including PNS and middle ear. Nasopharyngitis, sinusitis, ear infections,
acute tonsillopharyngitis (sore throat)
Lower respiratory tract- Covers the continuation of airways from trachea and
bronchi to bronchioles and alveoli. Pneumonia, bronchiolitis, croup ( acute
epiglottitis, laryngitis, laryngotracheobronchitis, spasmodic laryngitis)
Pneumonia
Consolidation of alveoli or infiltration of interstitial tissue with inflammatory cells
or both
Classified anatomically as:
 Lobar pneumonia-The organism causes inflammatory exudates involving
many contiguous alveoli. Radiologicallly appears as non-segmental
consolidation.
 Bronchopneumonia- Inflammation involves conducting airways, especially
terminal and respiratory bronchioles and the surrounding alveoli.
 Interstitial pneumonia- Inflammation confined to interalveolar septa.
Reticulr pattern in chest X-Ray
Lobar pneumonia Bronchopneumonia
Cause- 90%- Pneumococci, few Caused by Staphylococci,
cases- Klebsiella pneumonia, Streptococci, H.influenzae, Proteus,
S.aureus Pseudomonas
Occurs usually in adults, but should Occurs in infants, elderly and those
be clinically ruled out in paediatric suffering from chronic debilitating
cases illness or immunosuppression
Sudden onset with high grade Insidious onset with low grade
fever, shaking chills and bloody or fever and productive cough of
rusty sputum purulent sputum
Consolidation of whole lobe Patchy pneumonic consolidation of
whole lung, can be bilateral
Complications- bacteremia, Complications- fibrosis,
meningitis, endocarditis, septic bronchiectasis, lung abscess
arthritis
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Investigation
 Blood- Hb, TC, DC, ESR
 X-Ray chest PA view
 Sputum microscopy and culture
 Sputum AFB to rule out tuberculosis
 Blood culture in suspected sepsis
 ABG in a very sick child
 Ultrasound if effusion is suspected
 Pleural tap and pleural fluid study if effusion is present
Etiology
 Viral- RSV, Influenza, Parainfluenza, Adenovirus
 Bacterial
- Frist 2 months-
Gram -ve -E.coli, Klebsiella
Gram +ve- Pneumococci, Staphylococci
- 3 months-3 years- Pneumococci, H.influenza, Staphylococci
- After 3 years- Pneumococci, Staphylococci
- Community acquired pneumonia- Chlamydia, Mycoplasma
- Immunocompromised- P.jiroveci, Histoplasma
 Aliphatic hydrocarbon associated pneumonia
 Loeffler syndrome- caused by larvae of nematodes
Pneumococcal pneumonia
 Droplet transmission with IP 1-3 days
 Abrupt onset with headache, chills, cough, high fever, chest pain, rapid
respiration, grunting, chest indrawing, difficulty in feeding, cyanosis
 Treatment- Penicillin G 50,000IU/kg/day IV/IM in divided doses X7 days OR
IV Cefotaxime, Ceftriaxone or Co-amoxiclav

Staphylococcal pneumonia
 Primary infection of parenchyma or secondary to staph septicemia or
pyoderma, can be complication of measles, influenza and cystic fibrosis
 Broncho alveolar destruction with multiple microabscesses formation
 Progressive infiltration results in formation of pneumatocele .
 Abscess erode pericardium causing purulent pericarditis .

454
  Pulmonary infection is associated with disseminated disease with abscesses
in liver, joints, bone, muscles, pericardium, mastoid or brain.
 Treatment: Hospitalisation, Antipyretics, IV fluids, Oxygen administration,
antibiotic therapy with Penicillin G, Ceftriaxone, Coamoxiclav .If patient
doesn’t respond, Vancomycin or Teicoplanin is given.

Haemophilus pneumonia
 Occur in age group 3 months to 3 years
 Infection begins in nasopharynx and spreads locally or through blood
 Clinical features: Moderate fever, dyspnoea, grunting, retraction of
lower intercostal spaces
 Complications: Bacteremia, pericarditis, empyema, meningitis,
polyarthritis
 Treatment: Parenteral Ampicillin(100mg/kg/day) and Coamoxiclav OR
Cefotaxime(100mg/kg/day) and Ceftriaxone(50-70mg/kg/day)

Streptococcal pneumonia
 Important cause of respiratory distress in newborns
 Clinical features: Abrupt onset with fever, chills, cough, dyspnoea, rapid
respiration, blood- streaked sputum
 Complication: Thin serosanguinous or purulent empyema
 Diagnosis:
 Radiograph shows interstitial pneumonia with segmental involvement,
diffuse peribronchial densities or effusion
 Blood count shows neutrophilic leukocytosis
 Treatment: Penicillin G 50k to 100k IU/kg daily in divided doses× 7- 10
days OR 2nd or 3rd generation cephalosporins

Primary atypical pneumonia

 Etiology: Mycoplasma pneumoniae, Chlamydia, Legionella
 Droplet transmission
 Incubation period: 12- 14 days
 Clinical features: Malaise, head ache, fever, sore throat, myalgia, cough,
cervical lymphadenopathy
 X-Ray findings: Infiltrate usually involve one lower lobe

455
  Diagnosis: Detection of IgM antibodies by ELISA during acute stage, IgG
antibodies are present after 1 week, confirmed using PCR
 Treatment: Macrolide antibiotics( Erythromycin, Clarithromycin) or
Tetracyclin for 7- 10 days

Viral pneumonia
 RSV is the chief cause
 Other organisms include parainfluenza, influenza and adenovirus.
 Presents with extensive interstitial pneumonia
 Radiological signs include perihilar and peribronchial infiltrates .

Aliphatic hydrocarbon associated pneumonia

 Usually due to kerosene
 Inactivation of Type 2 pneumocytes, causing surfactant deficiency
 Clinical features include cough, dyspnoea, high fever, vomiting, drowsiness
and coma.
 X-Ray chest shows ill defined homogeneous or patchy opacities.
 Management of hydrocarbon poisoning- Supportive- Oxygen, IV fluids, Beta
agonists, Monitoring of respiratory and neurological status, Chest X-Ray, No
Steroids or prophylactic antibiotics. Gastric lavage or induction of emesis
not recommended because of the risk of aspiration. Observe for atleast 6h
irrespective of clinical status. Cautious evacuation of gastric contents (after
endotracheal intubation) in patients with products contaminated by
pesticides, heavy metals or other toxins.

Loeffler syndrome
 Caused by larvae of nematodes
 Clinical features: Cough, low fever, crepitations, eosinophilia
 Radiograph shows pulmonary infiltrates of varying sizes .
 Treatment is symptomatic.
Acute respiratory tract infection (ARI) control program– VERY IMPORTANT
Case management
 Classifying the severity of illness using clinical signs such as:
 Fast breathing:
˃60/mt, below 2 months of age
˃50/mt in 2 months- 1 year
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 ˃40/mt in 1- 5 years
 Chest indrawing
 General danger signs such as lethargy, central cyanosis, poor feeding,
seizures
 Then applying appropriate treatment which includes:
 Home care advise
 Antibiotics
 Referral to a higher level health facility
Revised WHO recommendations for treatment of pneumonia
Recommendation 1
 Children with fast breathing pneumonia with no chest indrawing or
general danger signs should be treated with oral Amoxicillin 40mg/kg
twice daily (80mg/kg/day) for 5 days.
 In areas with low HIV prevalence, give Amoxicillin for 3 days.
 If first line treatment fails, there must be an option of referral to a
facility where there is second line treatment.
Recommendation 2
 Children aged 2- 59 months with chest indrawing pneumonia should be
treated with oral Amoxicillin 40mg/kg twice daily(80mg/kg/day) for 5
days.
 Amoxicillin is more effective when given in higher doses(80mg/kg/day).
 Amoxicillin can be given twice instead of thrice daily for children with
fast breathing and chest indrawing pneumonia.
Recommendation 3
 Children aged 2- 59 months with severe pneumonia should be treated
with parenteral Ampicillin or penicillin and Gentamicin as supportive
care as a first line treatment.
Ampicillin: 50mg/kg or Benzyl Penicillin 50,000 units/kg im/iv every 6
hours for 5 days
Gentamicin: 7.5mg/kg im/iv once a day for 5 days
 Ceftriaxone is used as second line treatment .
Recommendation 4
 Ampicillin or Penicillin plus Gentamicin or Ceftriaxone are recommended
as first line antibiotic regimen for HIV infected and exposed infants and
under 5 children with chest indrawing or severe pneumonia.
457
  If first line treatment fails, Ceftriaxone is recommended for use as a
second line treatment.
Recommendation 5
 Empiric Cotrimoxazole treatment for suspectrd P. jiroveci pneumonia is
recommended as an additional treatment for HIV infected and exposed
infants aged 2 months- 1 year with severe or very severe pneumonia.
 This is not recommended for children over 1 year of age.

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 BRONCHIAL ASTHMA
Presenting complaints (in chronological order)
 Breathlessness, wheezing, cough,
 usually >2 years with previous history of similar episodes is the classical
presentation in asthma.
History of present illness
 Breathlessness- onset, duration, progression, aggravating and relieving
factors, diurnal, postural and seasonal variation, any chest indrawing,
orthopnoea /PND (for children)
 Wheeze- onset, duration, progression, precipitating factors (exposure to
cold, exercise), diurnal and seasonal variation
 Cough- onset, duration, productive/non-productive (if productive, sputum-
amount, colour, smell, blood staining; if non-productive- dry/wet-
children<5 years not likely to be able to cough up sputum), diurnal
variation, postural variation, seasonal variation (more important for
asthmatic cough)
 Clinical course- Case usually present as an acute exacerbation, which
warrants hospital admission. Attack is precipitated by various factors like
house dust, pollen, exposure to cold, exercise, certain food items,
characterized by sudden onset of breathlessness and wheeze which
progresses rapidly. In severe cases, the child is bedridden and gasps for
breath and needs to pause for breath while talking. The hallmark is that
these symptoms are rapidly relieved by nebulisation. Ask for these points in
history.
 Red flag signs in asthma- indicate acute severe asthma- drowsiness,
agitation, cyanosis, inability to vocalize, silent chest, dehydration,
hypotension, poor capillary refill, pulsus paradoxus
In severe obstruction, the airflow decreases markedly and breath sounds
are feeble. Wheezing which was earlier audible may disappear. The child
shows air hunger and fatigue. Hyperresonance due to air trapping.
During clinical recovery, airflow increases and wheezing may reappear.

Past history
 H/o similar illness n the past
 Frequency of attacks
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  Frequency of daytime and night time symptoms
 Number of acute exacerbations requiring hospital admission
 Details of treatment taken- for each episode, regular long term treatment-
drug, dose, duration, step up/step down of treatment, currently on which
drug
 Precipitating factors of attacks- exercise, house dust, pollen, whether
symptoms improved on removal of that factor
Case scenario- 8 year old child experiencing asthmatic attack for the last 1.5 years
and completely symptom free before. One should suspect that some change had
occurred within the last 1.5 years which may be the cause of attacks. On further
enquiry, change of residence 1.5 years before, present residence being in a place
with trees in he vicinity which sheds pollen in large numbers seasonally. Her
attacks coincide with pollen shedding.
 H/o atopy, drug allergy
 Restriction of day to day activities (no. of days absent from school)
 Recurrent respiratory tract infections
 Similar illness before 2 years (bronchiolitis- can predispose to asthma later)
 H/o heart disease, vaccine preventable disease
Life history
 Antenatal
 Natal- low birth weight, premature/ preterm delivery
 Postnatal- NICU admission, congenital heart disease
Dietary history
 Food allergies
 Duration of exclusive breastfeeding and details regarding complimentary
feeding
Development history
Immunization history
 Whether fully immunized for age
 Optional vaccines- if any, ask for details.
 BCG scar. Ask specifically for BCG immunization
Family history
 Similar illness in the family, siblings. Details of illness, if present like age of
onset, drug therapy
 Atopy- atopic dermatitis, allergies, urticaria
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  Tuberculosis in family
Socioeconomic history
 Socioeconomic status- assessed using Kuppuswamy index
 Overcrowding
 Cooking fuel
 Any pets in house
 Trees, plantations, farmhouses in the vicinity
 Whether living close to any industrial centres
 Change of residence
 Any smokers in house
 Ventilation
 Water supply (whether boiled or not)
 Sanitary latrine

General examination
 Build and nourishment (more details to be taken in anthropometry)
 Pallor- malnutrition
 Cyanosis- can be a danger sign or sign of congenital heart disease
 Clubbing- congenital heart disease
 Icterus, lymph node enlargement, edema
 Vital signs- Pulse rate may be elevated. Bradycardia is a danger sign. Pulsus
paradoxus is a red flag sign. Respiratory rate is very important.
Temperature reading is usually normal. Fever can occur in severe exertion
of breathing.
Head to foot examination
 Signs of malnutrition- flag sign of hair, edema, loss of subcutaneous fat
 Signs of allergic rhinitis- overbite, high arched palate, allegic shiners, allergic
salute, allergic crease, Dennie Morgan folds (extra skin folds on the lower
eyelids), conjunctival congestion, periorbital edema

Anthropometry- special attention in a malnourished child

Upper respiratory tract
 DNS, nasal or ear discharge, pharyngeal congestion, flaring of alae nasi
Lower respiratory tract
Inspection
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  Long standing cases may have barrel chest
 Acute exacerbations- increased respiratory rate, intercostal retraction,
lower chest indrawing
Palpation- no findings
Percussion- Percussion is always done last as the child may become
uncooperative.
Hyperresonance may be seen in severe cases.
Auscultation
 Breath sounds- normal
 Adventitious sounds- Bilateral expiratory rhonchi are the hallmark of
asthma. Describe the sounds you hear i.e., monophonic or polyphonic
 Vocal resonance- unaffected
 Miscellaneous sounds- nil
Examination of CVS, GIT and CNS
Summary
DIAGNOSIS
Reactive airway disease, probably bronchial asthma, now presented with acute
mild/moderate/severe exacerbation, no signs of respiratory failure, no
complications

DISCUSSION
Bronchial asthma is a disease characterized by increased responsiveness of
airways to various stimuli. Widespread narrowing of airways causes paroxysmal
dyspnoea, wheezing or cough. Diffuse, reversible airway obstruction in majority
of cases either spontaneously or in response to treatment.
Pathophysiology
a) Edema and inflammation of mucous membranes lining the airways
b) Excessive secretion of mucus, inflammatory cells and cellular debris
c) Spasm of smooth muscle of bronchi
Classification
 Atopic (earlier called extrinsic; IgE mediated; triggered by allergens)
 Non- atopic (earlier called intrinsic; non-IgE mediated; triggered by
infection)
 Mixed
 Exercise induced
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  Aspirin induced

Diagnosis
CLINICAL DIAGNOSIS- Recurrent attacks of wheezing and spasmodic cough.
Sputum is clear and mucoid, but may be yellow due to large number of
eosinophils. Investigation supportive.
 Pulmonary function tests (PFTs)- for diagnosis of doubtful cases and
monitoring response to therapy
Spirometry- Peak expiratory flow rate (PEFR), FEV1, FVC, FEV 25-75- all
decreased
PEFR abnormalities suggestive of asthma:
a) Diurnal variation >20%
b) </= 80% of predicted
c) Improvement of >/=20% after bronchodilator therapy
 Absolute eosinophil counts- eosinophilia
 Chest X-Ray- bilateral and symmetric air trapping
 Sputum study- Charcot Leyden crystals, Curschman’s spirals, Creola bodies
 Allergy tests- skin test, RAST, blood IgE levels
DD- bronchiolitis, congenital malformations with obstruction (vascular rings due
to aberrant right subclavian artery or double aortic arch, bronchogenic cysts,
tracheomalacia), aspiration of foreign body, bronchopneumonia, WALRI,
hypersensitivity pneumonitis, cystic fibrosis, congenital immunodeficiencies

MANAGEMENT
Management of acute exacerbation of asthma

a) Mild exacerbation
A- Alert
B- No increase in the work of Breathing (no significant retractions, but RR may
be slightly increased)
C- Circulatory status (normal capillary refill, no cyanosis)
Child sitting comfortably and talking without frequent breaks for breath. On
auscultation, widespread expiratory rhonchi

Treatment
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  Nebulized Salbutamol 150 mcg/kg/dose (min dose 2.5mg) in 3mL saline
once
 Assess for response
 If the response adequate and child comfortable,discharge on oral
Salbutamol (0.1-0.2mg/kg/dose q6h). If already used to inhaler, Salbutamol
inhaler 2 puffs 4-6 hourly instead of oral Salbutamol).
 After initial nebulisation, if the child is not improving adequately, shift to
the management protocol of moderate exacerbation.
 If the child has had a recent life threatening asthma episode, observe for
atleast 4h before discharge to ensure that the initial relief is lasting.

b) Moderate exacerbation
Alert, normal circulatory status, work of breathing increased (retractions+,
cannot talk without frequent pauses for breath). Wheeze expiratory and partly
inspiratory.
Treatment
 Nebulized Salbutamol 150 mcg/kg/dose (min dose 2.5mg) in 3mL saline
every 20 min, 3 times in 1 hour. Use oxygen driven nebulizer (6L/min).
 Assess for response.
 If the response is adequate, space out nebulisation intervals to 2-4 hourly.
Observe the child for 6-8h. If the relief is sustained, discharge on oral
Salbutamol 0.1-0.2mg/kg/dose q6h or Salbutamol inhaler 2 puffs 4-6
hourly.
 If the response is not adequate, start oral Seroids (Prednisolone 1-
2mg/kg/day). Continue nebulisation. In ase of deterioration, manage as
severe exacerbation.
 If nebulizer is not available (eg: failure of power supply), 2-6 puffs of Beta
agonist by MDI using spacer (and mask for small children0 every 20 min, 3
times or SC inj of Terbutaline.
 Adrenaline not preferred now as it may produce CVS side effects (already
hypoxic myocardium)-eg: arrhythmia

c) Severe exacerbation (Acute severe asthma)

464
 Child drowsy or irritable, work of breathing increased. Sometimes arir entry is
so poor that hardly any wheezing is heard (silent chest with severe
retractions). Circulation not normal, may be cyanosed. Red flag signs present.

Treatment
 Admit in ICU.
 Oxygen inhalation- 1-2L/min or more- to prevent hypoxia
 Nebulized Salbutamol 150 mcg/kg/dose(min dose 2.5mg) in 3mL saline
every 20 min, 3 times in 1 hour. Use oxygen driven nebulizer (6L/min).
Depending on response, continue nebulisation 1-4 hourly.
 Nebulized Ipratropium bromide 12.5 cg/kg/dose every 20 min, 3 times in 1
h. Can be mixed with Salbutamol in he sae nebulizer chamber. After initial 3
doss, Ipratropium is used every 6-8h.
 Inj. Hydrocortisone 10mg/kg initially followed by 4-5mg/kg/dose q6h or
Methylprednisoone 2mg/kg. If oral tolerated, oral Prednisolone
2mg/kg/day
 Inj. Aminophylline 5mg/kg/dose diluted as IV infusion q6h
 IV fluids (paediatric maintenance solution)- 1-1.5 times the maintenance
amount of fluids; should contain potassium (causes of potassium depletion-
Beta2 agonists, Steroids, diuretic effects of Theophylline, vomiting)
 If not improving,
- X-Ray chest to rule out complications (pneumonia, pneumothorax,
pneumomediastinum, subcutaneous emphysema- crepitus on
palpation)
- Continuous nebulisation with Salbutamol0.5 mg/kg over 1h.
- IV Magnesium sulphate infusion
- Terbutaline IV infusion
- Ventilation
 Sedation is not allowed except when the child is being ventilated. Level of
sensorium is an important parameter to assess severity of asthma.

Long term management of chronic asthma

a) Identification and elimination of exacerbating factors
b) Pharmacological therapy

465
 c) Education of the patient and parents about nature of the device and steps
to avoid acute exacerbation- acceptance of the fact that asthma is
controllable, but may not be curable, written protocol for the management
of acute exacerbation and regarding continued medication, asthma diary,
proper use of inhalation devices
Pharmacological therapy
i. Assessment of symptom control
ii. Assessment of risk of exacerbation
iii. Selection of medication
iv. Selection of appropriate inhalation device
v. Monitoring and modification of treatment
Assessment of symptom control- in the past 4 weeks
Feature Controlled: All of Partially Uncontrolled
the following controlled: Any
measure present
in any week
Day time None (twice a More than twice a 3 or more
symptoms week or less) week features of
Limitation of None Any partially
activity controlled asthma
Nocturnal None Any present in any
symptoms, week
awakening
Need for reliever None (less than More than twice a
or rescue drugs twice a week) week
Assessment of risk of exacerbation
 Symptoms of uncontrolled asthma
 One or more severe exacerbation requiring hospitalization in previous year
 Ever intubated or PICU admissions
 Start of the usual ‘flare up’season
 Exposure: tobacco smoke, indoor or outdoor air pollution, indoor allergens
 Major psychological or socioeconomic problems for child or family
 Poor adherence with controller medication or incorrect inhaler technique
 Co-morbidities: obesity, rhinosinusitis, confirmed food allergy
Selection of medication
466
Drugs for quick relief Drugs for prevention
 Short acting beta 2  Inhaled Coricosteroids- Beclomethasone,
agonists- Salbutamol, Budesonide, Fluticasone
Terbutaline-  Mast cell stabilizers- Inhaled sodium
inhalation/oral/injectio cromoglycate, Nedocromil, oral Ketotifen
n  Sustained release preparations of
 Anticholinergics- Theophyllins
Ipratropium bromide-  Long acting beta 2 agonists- Salmeterol,
inhalation Formoterol
 Theophylline- oral/  Leukotriene receptor antagonists-
injection Monteleukast, Zafirleukast
 Adrenaline injection

READ- Omalizumab, Zileuton, Immunotherapy

Refer O P Ghai for more details.
Selection of appropriate inhalation device
 <4 years old: MDI with spacer and face mask
 >4 years old: MDI with spacer
 >12 yeas ld- MDI directly. Use of spacer improves drug deposition
READ- Advantages, disadvantages and correct technique of use of inhalation
devices
Monitoring and modification of treatment
Stepwise treatment
Symptoms Treatment
Severe persistent Continuous High dose ICS+LABA
Limited physical activity Add Monteleukast.
Refer to specialist.
Moderate persistent Daily use of Beta 2 Low dose ICS+LABA
agonist OR
Daily attack affects Medium dose ICS
activity.
Mild persistent Low grade symptoms Low dose ICS
twice a month SABA, whenever
Nighttime awakening symptoms
once a month
Intermitent Infrequent SABA whenever
Asymptomatic and symptoms
467
 normal PEFR between
attacks

 Low dose ICS: Budesonide 200-400 mcg or equivalent daily

 Medium dose ICS: Budesonide 400-800 mcg or equivalent daily
 High dose ICS: >800 mcg or equivalent daily

 The patient should be seen every 4-12 weeks after initiating treatment.
 History, inhlation technique, compliance, asthma diary
 Assessed as contolled/partially controlled/uncontrolled
 In case of partially controlled/uncontrolled, the causes apart from disease
severity could be poor compliance, wrong technique of inhalation,
continued use of empty canister, inappropriate doses, associated infections
or continued exposure to allergens.
 If no cause is found, step up, i.e. increase in dose and frequency required.
 Once control is achieved for a reasonable period of time (3-6 months), step
down with stepwise reduction in treatment.
 Children on high dose ICS or oral Corticosteroids should be monitored
periodically (height, BP, ophthalmological evaluation for cataract)
 For exercise induced asthma- prophylactic SABA before exercise/LABA in
the morning/ Sodium cromoglycate 20 min before exercise/Leukotriene
modifiers as alternative to LABA

468
 ACUTE BRONCHIOLITIS
Essential features
 Affected infants are in the age group of 1-6 months, but can affect children
upto 2 years
 Organisms- RSV (MC), parainfluenza, adenovirus, influenza, rarely
M.pneumoniae
 Spreads by fomites
 Protection against RSV is mediated by antibodies of IgG3 subclass (short t ½
, does not cross the placenta in substantial amount to offer protection to
infant)
 Breastfeeding reduces the risk as colostrums contain high amounts of
secretory IgA.
 Self- limiting illness, subsiding in 3-7 days
 Begins as upper respiratory infection
 Paroxysmal wheezing, cough, dyspnoea, irritability
 After few days, high fever, rapid breathing, respiratory distress
 Death due to respiratory failure in 1% of severely ill patients
 Bronchial asthma in later life in ¼th of the cases
On examination,
 High fever, rapid breathing (RR- 60-80/min)
 Severe disease- retraction of lower intercostal spaces and suprasternal
notch, cyanosis
 Auscultation- expiration prolonged, fine crepitations+, rhonchi+, in severe
cases, breath sounds faint or inaudible
 AP diameter increased (air trapped in lungs- liver and spleen pushed down)
 Percussion- hyperresonance

Diagnosis
Reactive airway disease, probably acute bronchiolitis, no signs of respiratory
failure, no complications

DD- bronchial asthma, heart failure, foreign bodies, bacterial pneumonia

Differentiating from asthma

 Bronchiolitis presents in age< 2 years
469
  Usually first episode of dyspnoea in an infant. Previous history of similar
attacks will be absent.
 Also more common in LBW babies, non-breast fed babies and babies in day
care centres
 A classical case of bronchiolitis will have relatively no chest signs but will
have severe respiratory distress in the aforementioned age group and risk
populations.
 Response to bronchodilators is more consistent in children with asthma,
compared to bronchiolitis.
Investigation
 WBC count- normal or slightly elevated
 X-Ray chest- hyperinflation, infiltrates, diaphragm pushed down, lung fields
abnormally translucent
 A rapid test on nasopharyngeal aspirate can identify the presence of RSV.
Treatment
 Symptomatic
 Nurse in humid atmosphere, preferably30-40 degree head and neck
elevation.
 Mild disease- home; increased respiratory distress or feeding problems-
hospitalization required
 Mainstay- moist oxygen inhalation- continuously even in the absence of
cyanosis
 Maintain fluid and electrolyte balance.
 Very sick infants may need a concentration of 60% oxygen given through a
hood to maintain oxygen saturation >92%.
 No role of antibiotics- given when bronchopneumonia cannot be excluded
or clinical picture suggestive of sepsis
 Ribavirin (antiviral agent) delivered by a nebulizer 16h a day for 3-5 days- in
infants with underling congenital heart disease, chronic lung disease and
immunodeficiency- no role in previously healthy infants
 Bronchodilators (nebulazation salbutamol 2.5 mg for <5 years), inhaled or
systemic steroids, epinephrine ( 0.2 mL/kg-1:1000 solution)- not useful
 If there is improvement with bronchodilator or epinephrine, further doses
every 4-6h

470
  Inhaled hypertonic saline (effective in a subgroup of patients)- routine use
not recommended- nebulisation with 3% saline 4mL 3-4 hourly
 Respiratory failure- CPAP or assisted ventilation
 ECMO (Exracorporeal membrane oxygenation) in severe cases
Indications of CPAP in acute bronchiolitis- apnoea, falling oxygen saturation,
severe distress with evidence of respiratory muscle fatigue
Read pathogenesis from O P Ghai (pg 381).

WALRI (Wheeze associated lower respiratory tract infection)

Read WALRI from Handbook of Pediatrics (pg 195).
Main challenge is differentiating from asthma.
WALRI Asthma
Toddler age group Any age
Preceding viral infection Many triggers including
preceding viral infections
No family history of allergic Family history of allergic rhinitis,
rhinitis, asthma, atopy asthma, atopy
Not IgE mediated Likely to be IgE mediated
No dramatic response to Dramatic response to
bronchodilators bronchodilators
Likely to remit as the child grows Natural history enerally follows
(may be because the airway that of family
calibre increases or the incidence
of viral infections comes down or
both)

471
 Congenital Heart Disease
Classification:
1) Acyanotic heart disease
a) Volume overload: VSD, ASD, PDA
b) Pressure overload: AS, PS, CoA
2) Cyanotic heart disease
a) Reduced pulmonary blood flow: ToF
b) Increased pulmonary blood flow: TGA, TAPVC, Persistent truncus
arteriosus, hypoplastic left heart syndrome (HLHS)

• In reduced PBF, there is oligemic lung fields on CXR

• In increased PBF, there is pulmonary plethora on CXR and recurrent chest
infections

Presenting Complaints
• Recurrent respiratory tract infections
• Bluish discolouration in cyanotic CHD
• Exertional dyspnea
• Cyanotic spell and squatting in ToF

History of Present Illness

• Onset of disease, duration
• History of respiratory tract illness: no of episodes per yr
• h/o suck rest cycle
• h/o breathlessness, precipitating factors, relieving factors (orthopnea relieved
by putting to shoulder)
• Excessive perspiration over forehead on feeding
• h/o decreased food intake
• h/o failure to gain weight (h/o failure to thrive)
• h/o cyanosis: what precipitates cyanosis, duration, relieving factors
• h/o squatting episodes
472
• h/o CNS manifestations: h/o recurrent fever, seizure, recurrent headache, focal
neurological deficit
• h/o edema over legs or body
• h/o decreased urine output
• Rule out IE: h/o protracted fever with chills, bleeding tendencies

History of Past Illness

• h/o similar episodes
• h/o frequent hospitalisation
• h/o respiratory infection precipitating CCF
• h/o danger signs
• h/o hospitalisation, ICU admissions
• Details about drugs given
• Duration of IV medications
• h/o infective endocarditis
• h/o any surgery advised
• Drug prophylaxis
• Condition of child in between each episode

Antenatal, Natal and Postnatal history

Antenatal History
• 1st trimester:
• Age of mother at time of conception
• h/o fever with rash (intrauterine infection)
• Exposure to radiation
• Intake of anticonvulsant, antithyroid drugs
• h/o rubella in mother is associated with PDA (most common), CoA, VSD,
peripheral PS
• 2nd and 3rd trimester:
473
 • h/o GDM (increased chance of TGA) and other congenital heart diseases like
VSD. Asymmetrical septal hypertrophy is the most common cardiac defect
seen in infant of diabetic mother.
• h/o hypertension in pregnancy
• h/o fetal echo

Natal history
• Rule out prematurity (increased incidence of PDA and VSD)
• h/o cyanosis at birth (tricuspid atresia, TGA)

Postnatal history
• h/o cyanosis
• h/o petechiae (symptom of intrauterine infection)
• h/o hospitalisation after birth

Developmental history
• Rule out growth derangement
• Immunisation and diet history taken as usual

Family history
• h/o consanguineous marriage
• h/o heart disease in family members
• Socioeconomic history taken as usual

General Examination
• Look for polycythemia, cyanosis, clubbing (features of cyanotic heart disease)
• Look for pedal edema or sacral edema
• Look for prominent veins
• Look for skeletal abnormalities associated with congenital heart disease (Holt
Oram Syndrome has ASD with absent radius, hypo plastic or triphalangeal
thumb)
474
• Rule out syndromes like Down syndrome, Turner syndrome, William syndrome
• Look for feature of infective endocarditis
• Look for signs of failure to thrive
• Look for dysmorphic features (Congenital rubella syndrome)

Examination Findings
 VSD:
• Look for PEM, increased work of breathing
• No cyanosis and clubbing (Cyanosis in reversal of shunt)
• CVS examination:
• Normal pulse
• JVP elevated in cardiac failure
• BP: normal
• Inspection:
- Precordial bulge
- Hyper dynamic precordium
- Pulmonary area pulsation
• Palpation:
- Apex beat shifted to left. Character is forceful
- Palpable P2 when there is Eisenmenger syndrome (reversal of shunt)
- Systolic thrill may be present on 3rd and 4th intercostal spaces at the
left sternal border
• Percussion: Percuss out the borders for cardiomegaly
• Auscultation:
- Heart sounds: may be normal. S2 may have a wide variable split (early
A2 and late P2)
- In large VSD with PAH, S2 is loud and single
- Harsh PSM best heard in the lower left sternal border radiating widely
(starts early and masks S1 and ends after A2 completely masking it as
even after closure of aortic valve, LV pressures are higher than RV
pressures)
475
 - Very small VSD has ESM
- ESM at pulmonary area (cannot be differentiated from PSM)
- Delayed diastolic murmur at apex due to increased flow across a
normal mitral valve accompanied by loud S1 (loud M1 with normal T1)
- Diastolic murmur of AR is a complication of VSD
• Look for features of PAH and heart failure

 ToF:
• Cyanosis, polycythemia,clubbing
• a wave slightly prominent on JVP
• CCF rarely occurs in ToF
• On palpation, a systolic thrill may be obtained in pulmonary area
• No cardiomegaly on percussion
• Auscultation:
- Normal S1
- Single loud S2 (A2): RV outflow tract (RVOT) obstruction results in a
delayed P2. As pulmonary artery pressure is low, P2 is reduced in
intensity. This soft and late P2 is often not audible. A2 is loud as the aorta
is somewhat anteriorly placed
- Aortic ejection click in severe cases
- ESM in pulmonary area

 PDA:
• No cyanosis or clubbing (Differential cyanosis in PDA with Eisenmenger)
• Pulse: high volume and collapsing (wide pulse pressure). In a newborn,
dorsalis pedis is not palpable. It is however palpable in PDA
• JVP normal in uncomplicated PDA
• Apex beat: shifted to left in a significant shunt. Character of apex is forceful
• Systolic or continuous thrill may be felt in 1st and 2nd left intercostal spaces

476
 • Murmur: Continuous machinery murmur (Gibsons murmur) maximal in the
2nd left intercostal space radiating to below the left clavicle. Multiple clicks
are heard due to eddy currents
• MDM may be heard at apex due to increased flow across the normal mitral
valve with a loud S1
• Delayed closure of aortic valve results in a late A2. In large left to right
shunts, the S2 may be paradoxically split

 ASD:
• No cyanosis and clubbing
• Pulse and JVP normal
• Epigastric pulsations and RV impulse in parasternal area
• Heart sounds:
- S1 may be normal or loud due to tricuspid component
- S2 widely split and fixed. Loud P2
• No shunt murmur
• Soft ESM at pulmonary area and MDM at tricuspid area due to increased
flow through normal pulmonary valve and tricuspid valve

Symptoms of Cardiac Failure in Children (Table 16.4) (very important)

• Poor weight gain
• Difficulty in feeding (Suck rest cycle)
• Breathes too fast
• Breathes better when placed against shoulders
• Persistent cough and wheezing
• Irritability, excessive perspiration and restlessness
• Dependent edema

Signs of Cardiac Failure in Children (Table 16.5) (very important)

• Left sided failure:
477
 - Tachypnea and tachycardia
- Persistent cough, hoarse cry, wheezing
- Basal crepitations may be audible
• Right sided failure:
- Hepatomegaly
- Facial puffiness
- Dependent edema
• Common to left and right sided failure:
- Cardiac enlargement
- S3 gallop
- Poor peripheral pulses
- Failure to thrive

Management of cardiac failure in children (Pg 395):

1) Reducing cardiac work
2) Augmenting myocardial contractility
3) Improving cardiac performance
4) Correcting underlying cause

Syndromes Associated with CHD:

• CATCH 22 (diGeorge syndrome): ToF
• William syndrome: Supravalvular aortic stenosis, Peripheral pulmonary
stenosis, Elfin facies
 Down syndrome: Endocardial cushion defect
 Turner syndrome: Bicuspid aortic valve, CoA
 Noonan syndrome: PS
• Holt Oram Syndrome: ASD
• Congenital Rubella syndrome: PDA, CoA, VSD
 Congenital lupus: Complete heart block

Nadas Criteria (Table 16.11)

• For assessment of presence of heart disease
 Major criteria:
478
 • Systolic murmur grade 3 or more
• Diastolic murmur
• Cyanosis
• CCF
 Minor criteria:
• Grade 1 or 2 systolic murmur
• Abnormal second sound
• Abnormal ECG
• Abnormal CXR
• Abnormal BP
• Presence of heart disease is indicated by presence of one major or 2 minor
criteria

Ross Functional Classification

• Class I: Asymptomatic
• Class II:
- Minimal forehead sweating during feeds
- Mild tachycardia and tachypnea during feeds
- Not severe enough to stop feeds
• Class III:
- Marked tachycardia and diaphoreses during feeds
- Suck rest cycle. Therefore, duration of feed increases, however, inadequate
feeds taken resulting in FTT
• Class IV:
- Symptomatic even at rest with FTT

Management of Cyanotic Spells (Pg 408) (very important):

 Immediate steps:
• Check airway: Deliver oxygen by face mask or nasal cannula
• Knee chest position
• Sedate with morphine 0.2 mg/kg subcutaneous
479
 • Sodium bicarbonate 1 to 2 mL/kg
• Correct hypovolemia (10 mL/kg of DNS)
• Transfuse PRC if Hb < 12 gm/dL
• Metoprolol 0.1 mg/kg IV slowly over 5 mins. Repeat every 5 min for a max of
3 doses
• Monitor saturation, heart rate, BP. Keep heart rate below 100 beats per min

• Persistent desaturation and no significant improvement:

- Consider vasopressor infusion: Methoxamine or phenylephrine
- If spells persist, paralyse, electively intubate and ventilate. Plan for palliative
or corrective surgery
- Seizures are managed with diazepam 0.2 mg/kg IV or midazolam 0.1 to 0.2
mg/kg/dose IV

• Following a spell:
- Conduct careful neurological examination (with CNS imaging if focal
neurological deficit is present)
- Initiate therapy with beta blocker at maximal tolerated dose (propranolol 0.5
to 1 mg/kg q 6 to 8 hr)
- Do echocardiography
- Plan early corrective or palliative surgery
- Administer iron in therapeutic (if anemic) or prophylactic dose

• Prevention:
- Counsel parents about possibility of recurrence and precipitating factors
(dehydration, fever, pain)
- Encourage early surgical repair

ASD (Pg 409):

 Classification of ASD:
• Fossa ovalis ASD (Ostium secundum ASD)
• Sinus venosus ASD
480
 • Ostium primum ASD
• Coronary sinus ASD
• ECG of ostium secundum ASD:
• Right axis deviation
• RVH
• ECG of ostium primum ASD: Left axis deviation beyond -30 degree
 Chamber which is never dilated in ASD: left ventricle
• Assessment of severity:
• Intensity of flow murmurs especially MDM at tricuspid area
• Cardiac size
 Treatment:
• Fossa ovals lesions with good margins can be closed percutaneously in
cardiac catheterisation lab with occlusive devices
• Small defects (< 8 mm) can be observed
• Spontaneous closure is well recognised in small defects that are diagnosed in
infancy or early childhood

VSD (Pg 411)

 M/c CHD identified at birth
 Become symptomatic at 6 to 10 wks of age with CCF
 Types of VSD:
- Membranous and perimembranous
- Muscular
- Inlet
- Outlet
• 70% of all VSDs become smaller in size and a smaller percentage disappear
completely
• In 90% people with spontaneous closure of defect, it occurs by 3 years of age
• Muscular VSD has highest likelihood of spontaneous closure
• Perimembranous VSDs close with the help of septal leaflet of tricuspid valve

481
• Subpulmonic VSD becomes smaller as aortic valve prolapses through it
 Complications:
• CCF
• FTT
• Pulmonic stenosis due to hypertrophy of RV outflow tract
• PAH
• AR due to prolapse of aortic valve leaflets in subpulmonic VSD
• IE (m/c CHD complicated by IE)
 Treatment:
• Medical management:
- Control CCF
- Treat chest infection
- Prevention and treatment of anaemia and IE
• Surgical treatment is indicated in:
- CCF in infancy
- Pulmonary flow is more than twice systemic flow
- Associated pulmonic stenosis, PAH, AR
• Surgical treatment:
- Closure of VSD with a patch
- Device closure for muscular and perimembranous VSD

PDA (Pg 414):

• Ductus arteriosus closes anatomically and functionally after birth
• Flow through PDA occurs both during systole and diastole as a pressure
gradient is present between aorta and pulmonary artery throughout the cardiac
cycle
• Murmur: Starts in systole after S1, reaches a peak at S2, it then diminishes in
intensity and is audible only during a part of diastole. Thus, it is a continuous
murmur
• Assessment of severity:
- Larger the heart size, larger the left to right shunt
482
 - Audible delayed diastolic flow murmur at mitral area indicates a large shunt
- Wide pulse pressure indicates large shunt
 Complications:
• Develop CCF Around 6 to 10 wks of life
• PAH
• Infective endarteritis
 DDs of continuous murmur:
• Ruptured sinus of Valsalva
• Coronary AV fistula
• Aortopulmonary window
• Aortopulmonary collateral murmurs
• VSD with AR can simulate continuous murmur of PDA
 Treatment:
• Indomethacin or ibuprofen in preterm babies < 2 wks
• Newborns not responding to these agents need surgical ligation
• PDA in term infants may close as late as 1 month after birth and is worth
waiting
• Device closure and surgical closure can be done in children and adults

ToF (Pg 417):

 m/c cyanotic CHD encountered after 1 yr of age
• Hemodynamics explained by VSD-PS physiology
 Components:
- VSD
- RV outflow tract obstruction
- Overriding of aorta over septal defect
- RVH
• Pentalogy of Fallot: ToF + ASD
• Concentric RVH without cardiac enlargement

483
• Basic pathology: Conal septum is displaced anteriorly and to the right and does
not join with muscular septum. Thus, there is a narrow RVOT and a VSD is
formed
• VSD is silent as the pressures in LV and RV are identical
• Severity of cyanosis is proportional to severity of pulmonic stenosis as when PS
increases, flow to pulmonary artery decreases and right to left shunt increases
• Intensity of systolic murmur is inversely proportional to severity of PS
• RV is effectively decompressed by the VSD. Hence, chances of CCF are very low.
Exceptions are:
- Anaemia
- IE
- Systemic htn
- RV dysfunction from long standing severe hypoxia
- AR or TR
• m/c CHD where squatting is seen
 Squatting results in:
• Increased systemic vascular resistance
• Increased venous return
• Increased pulmonary blood flow
 ECG:
• Right axis deviation with RVH
• Tall R waves in V1 with sudden transition to rS complex in V2
• Diagnosis: Confirmed by echo
 Complications:
• IE
• Neurological complications:
Hemiplegia due to:
- Anoxic infarction
- Paradoxical embolus
- Polycythemia
Brain abscess
484
 • CCF is a rare complication which occurs especially in presence of anaemia
 Treatment:
• Medical management:
- Prevention and treatment of complications
- Prevention and treatment of anaemia
- Management of cyanotic spells
• Surgical management:
- Definitive management: Intracardiac repair - Closure of VSD and relief of
RVOT obstruction
- Palliative options: Blalock Thomas Taussig shunt (BT shunt): Subclavian
artery anastomosed to homolateral pulmonary artery using a Goretex
graft

485
 Acute Rheumatic Fever
• Rheumatic fever is an immunological disorder initiated by Group A beta
haemolytic Streptococci
• Antibodies formed against selected Streptococcal cell wall proteins and sugars
react with connective tissues of body as well as heart and result in rheumatic
fever
• Rheumatogenic strains of Strep: 1, 3, 5, 6, 14, 18, 19, 24
• Commonly affects 5 to 15 yr old children
• First episodes are rare before 3 yrs and above 30 yrs
• Mitral valve disease and chorea is more common in girls while aortic valve
involvement is more common in boys
• Predisposing factors: Low socioeconomic conditions, unhygienic living
conditions, overcrowding
• History of preceding sore throat in 50% patients
• There is a latent period of 10 days to several weeks before onset of rheumatic
fever after sore throat
• Only heart valves are permanently damaged during an episode of rheumatic
fever

Presenting Complaints
• Fever
• Joint pain
• Fatigue
• Chest pain
• Exertional dyspnea
• Involuntary movements (chorea)
• Palpitation
• Rash or nodules

486
History of Present Illness
• Joint pain:
- Onset
- Joints involved (usually large joints like knees, ankles and elbows)
- Progression:
• Usually a migratory polyarthritis
• Pain and swelling appear rather quickly, lasts for 3 to 7 days and subsides
spontaneously to reappear in some other joint)
• Aggravating and relieving factors, any swelling or limitation of movement
- Rule out other causes of joint pain like juvenile rheumatoid arthritis, septic
arthritis (h/o trauma), leukaemia (h/o bleeding tendencies, loss of weight),
TB, hepatitis
- Arthritis is an early manifestation
• Fever: Onset, duration, h/o chills and rigor, grade, diurnal variation
• Breathlessness: Onset, duration, aggravating and relieving factors, relation to
position and exertion, h/o cough and wheeze
• Chest pain: Site, duration, radiation, aggravating and relieving factors, relation
to exertion, food intake and breathing. Pain of pericarditis is a retrosternal
stabbing type of pain which is relieved on sitting up and leaning forward
• Involuntary movements (Sydenhams chorea):
- Onset, duration, ability to do routine work, present during sleep or rest, any
change in writing, gait, speech
- h/o seizures, emotional disturbance
- Drops things he or she is carrying
- h/o headache or trauma
- Late manifestation (about 3 months after onset of acute rheumatic fever)
• Rash or nodule: site, size, shape, number, whether painful, h/o itching, whether
palpable
• h/o UTI to r/o reactive arthritis

History of Past Illness:

• h/o similar episodes
487
• h/o respiratory infection precipitating CCF
• h/o danger signs
• h/o hospitalisation, ICU admissions
• Details about drugs given
• Duration of IV medications
• h/o infective endocarditis
• h/o any surgery advised
• Drug prophylaxis
• Antenatal, Natal and Postnatal history to rule out congenital heart disease
• Immunisation history, Development history, Nutrition history and Family history
taken as usual
• Socioeconomic history: overcrowding (increased incidence of rheumatic fever)

General Examination
• Look for features of rheumatic fever like subcutaneous nodules, erythema
marginatum
• Look for features of cardiac failure (pedal edema, sacral edema)
• Look for features of infective endocarditis: pallor, splinter haemorrhages,
clubbing, Janeway lesions (painless), Osler nodes (painful), splenomegaly

Examination Findings
 Features of carditis:
• Pericarditis
- Pericardial friction rub
- Diffuse apex
- Muffled heart sounds
• Soft S1
• Protodiastolic (S3) gallop
• Cardiac enlargement on percussion
• Congestive cardiac failure
488
 • Carey Coombs murmur (soft delayed diastolic murmur heard transiently
during course of acute rheumatic fever across inflamed thickened mitral
valve)
• Endocarditis:
- Pan systolic murmur of mitral regurgitation
- Aortic regurgitation murmur may be associated
- Pan systolic murmur of tricuspid regurgitation in 10 to 30% people with
carditis
- Pulmonary valve is very rarely involved

Investigations
• Blood: Hb, TC, DC, ESR
• CRP
• Throat swab
• ASO titre
• Anti DNAase B
• Chest X ray
• ECG
• Echocardiography
• Mantoux test (rule out Poncets arthritis)
• Rheumatoid factor

Revised Jones Criteria for Diagnosis of Rheumatic Fever (Table 16.16)

(very important)
• Low risk populations (incidence < 2 per 1 lakh in school going children,
rheumatic heart disease prevalence < 1 per 1000):
 Major criteria:
• Carditis (clinical or subclinical)
• Arthritis (polyarthritis only)
• Chorea

489
 • Erythema marginatum
• Subcutaneous nodules
 Minor criteria:
• Polyarthralgia
• Fever (>38.5 degree C)
• ESR > 60 mm in first hr
• CRP >= 3 mg/dL
• Prolonged PR interval after accounting for age variability (unless carditis
is a major criterion)

• Moderate and high risk populations:

 Major criteria:
• Carditis (clinical or subclinical)
• Arthritis (polyarthritis, mono arthritis)
• Polyarthralgia
• Chorea
• Erythema marginatum
• Subcutaneous nodules
 Minor criteria:
• Monoarthralgia
• Fever (>38 degree C)
• ESR > 30 mm in first hr
• CRP >= 3 mg/dL
• Prolonged PR interval after accounting for age variability (unless carditis
is a major criterion)

• For all populations:

- Initial episode of rheumatic fever: 2 major or 1 major + 2 minor
- Recurrent episodes of acute rheumatic fever: 2 major or 1 major + 2 minor
or 3 minor
490
 - Essential criteria: Previous evidence of Group A beta haemolytic Streptococci
infection

Differential Diagnoses
• SLE
• PAN
• Seronegative spondyloarthropathies
• HSP
• Reactive arthritis (viral, gonococcal, Reiters disease, Poncet arthritis)
• Lyme disease
• Brucellosis

Carditis
• in 90% people
• Pancarditis
• 80% who develop carditis do so in the first 2 weeks of illness
• Pericarditis can result in non specific ST-T changes on ECG
• Associated with small effusions which do not result in cardiac tamponade or
constrictive pericarditis
• Subclinical carditis is identified by echocardiography which shows MR
• MDM of MS is differentiated from a Carey Coomb murmur by the presence of
opening snap and loud S1 in the former

Arthritis
• Arthritis vs arthralgia: In arthritis, there will be local rise of tempertature,
swelling, tenderness and limitation of movement in addition to pain and
tenderness

Subcutaneous Nodules
• Appear on bony prominences like elbow, shin, occiput, spine
491
• Vary in size from pinhead to almond
• Non tender (Osler nodes seen in pulp of finger in IE are tender)
• Better seen than felt
• Late manifestation which occurs around 6 wks after onset of disease
• People with subcutaneous nodules almost always have carditis

Sydenhams Chorea or St Vitus Dance

• Chorea is a semipurposeful jerky movement resulting in deranged speech,
muscular incoordination, awkward gait and weakness
• Distal > proximal
• Disappears in sleep
• Jack in the box phenomenon
• Milkmaid sign
• Hung up knee jerk
• Hypotonia
• Self limiting in 2 to 6 wks

Erythema Marginatum
• Early manifestation
• Predominantly over trunk
• Evanescent rash
• Starts as red spot with pale centre
• Increases in size and coalesces with adjacent spots to form a serpiginous outline
• Non itching

Evidence of Strep infection

• ASO titre: Normal value in children is below 320 U/dL. However, a rising titre is
a better indicator of recent Strep infection
• Anti DNAase B
492
TREATMENT (very important):
1) Rest

Rest Restricted Activity Schooling At

No carditis 2 wks 4 wks 6 wks

Mild carditis 2 wks 6 wks 8 wks

Severe carditis 4 wks 8 wks 12 wks

Severe carditis, Till CCF is 8 wks 12 wks

CCF controlled

2) Treatment of Streptococcal infection:

• Single IM injection of benzathine penicillin 1.2 million units (in people >= 30 kg)
or 0.6 million units (in people < 30 kg)
• Oral Penicillin V 250 mg QID x 10 days
• Erythromycin 250 mg QID x 10 days in penicillin allergy
3) Suppressive therapy
• Aspirin or Steroid used for a total duration of 12 wks
• Severe carditis: Steroids
Severe carditis is the presence of any one of the folloqing:
- CCF
- Cardiomegaly (clinical or Xray)
- Multivalvular involvement
- Pericardial rub
• Carditis without CCF: Either steroids or aspirin (steroids are preferred)
• No evidence of carditis: Aspirin
• Aspirin is given at a dose of 90 to 120 mg/kg/day in 4 divided doses for 10 wks
and then tapered over next 2 wks

493
• Prednisolone is given at 2mg/kg/day, maximum dose of 60 mg, is given for 3
wks and then tapered over the next 9 wks by 5 mg every 3 days and aspirin is
started at 75 mg/kg/day for 8 to 10 wks

4) Treatment of complications
• CCF: Furosemide, ACE inhibitors, digoxin
• Chorea: Haloperidol, diazepam, carbamazepine

5) Secondary prophylaxis for prevention of further infection

• Benzathine penicillin 1.2 million units (in people >= 30 kg) or 0.6 million units (in
people < 30 kg) once every 3 wks. Injection is painful and administered on
weekends to avoid school absence
• Penicillin V 250 mg BD orally
• Erythromycin 250 mg BD orally
• Duration:
• No carditis: 5 yrs or till 21 yrs of age whichever is longer
• Carditis present: 10 yrs or 25 yrs of age, whichever is longer
• Established rheumatic heart disease: Lifelong or at least till 40 yrs

Complications
• Cardiac failure
• Valvular lesions
• Infective endocarditis

494
 PYREXIA OF UNKNOWN ORIGIN
Presenting complaints
 Fever
 associated symptoms along with fever
 Loss of consciousness,seizures,headache,vomiting( meningitis)
 Resp symp-Nasal dripping/ear discharge/throat pain /Cough/ hemoptysis
 Urinary symp-dysuria/hematuria/oliguria
 GI symp-Vomiting/diarrhea/abd pain
 Chest pain/palpitation/dyspnoea
 Rash/pyoderma
 Bleeding disorders/tendency
 Joint pain
 Yellowish discolouration of eyes & urine
 Any swellings noticed in the body

H/o presenting complaints

 Fever
- Onset
- Duration
- Diurnal variation
- Type
- Asso. chills & rigor
- Any change with medication
 Resp. symp
- Onset & duration
- Ear discharge-type/colour/odour/quantity/blood stained
- Cough-productive or not/periodicity/aggravating,relieving factors
- Hemoptysis-quantity/odour
 Urinary symp
- Urine-quantity/colour/blood in urine
- Frequency of micturition
- Pain /burning sensation during micturition
 GI symp
- Vomiting-onset/frequ/quantity/food particles/blood stained/odour
- Diarrhea-onset/freq/clour/odour/blood stained
- Yellowish discolouration of eyes & urine
 Rash
- Size
- Colour
- Distribution pattern
495
Also ask about
 Loss of wt
 Bleeding disorders/tendencies
 Retro orbital pain
 Myalgia
 Joint pain
 Bone pain
 Yellowish discolouration of eyes & urine
 Any swellings noticed in the body

Examination Findings
 Head -Sparse hair
 Face-hemolytic facies.
 Eyes-conjuctivitis,subconjunctival hemorrhage
 Mouth -Pharyngitis/oral thrush/caries teeth/pale tongue/aphthous ulcer
 Ear discharge
 Palpable lymph node
 Any murmurs
 Signs of respiratory distress
 Hepatosplenomegaly
 Rash/skin infections/wounds
 Arthritis/bony tenderness
 Renal angle tenderness
 Reflexes

DISCUSSION

PUO is defined as fever > 101 degree Celsius lasting for 3 weeks or more for
which no cause is apparent after 1 week of outpatient investigations. So the cases
we get cannot be termed as PUO.

D/D
Common causes

1.IMN
 Fever+sore throat +rash +fatigue
 o/e enlarged tonsils +hsm+ gen. lymphadenopathy

2. Typhoid
496
  Fever(step ladder)+ abdominal pain+ diarrhoea
 o/e coated tongue, relative bradycardia, sometimes HSM, rose spots

3.Dengue
 Fever,headache,retroorbital pain
 Rash,arthralgia,myalgia
 Leucopenia, +ve tourniquet test, h’gic manifestations

4.Weils disease
 Fever,conjuntival congestion, headache
 myalgia + +arthalgia+rashes
 H/O contact with contaminated water like bathing in pond,walking
barefoot in water-logged area.

5.Hepatitis
 Fever, Anorexia,Nausea & Vomiting,
 Abdominal pain-Rt.hypochondrial/epigastric.
 H/O blood transfusion,surgery,injections,food from outside,similar
symptoms in family members.

6. UTI:
 fever + inc. freq +enuresis+dysuria+abd pain
 suprapubic pain - cystitis
 flank pain / renal angle tenderness pyelonephritis

7. RTI

8. TB
 fever +loss of wt + cough
 Decreased growth

9. Malaria--3 stages
 fever chills +rigor headache nausea malaise anorexia..—cold stage
 inc respn/thirst -hot stage
 temp dec by crisis---sweating stage

10.Sepsis

Uncommon
1. Malignancy:
497
  fever prolongd+ bleeding tendencies
 bone pain+loss of wt

2. Connectitve tissue disorders

3. Can also be atypical presentations of

 infective endocarditis,
 rheumatic fever,
 meningitis

MANAGEMENT

Investigations
 Routine blood exm- Hb/TC/DC/ESR
 Peripheral smear- r/o malaria/atypical lymphocytes/blast cells
 Urine routine exm -pus cells/hematuria
 Mantoux test
 Sputum culture
 Chest X ray- l/f hilar+ paratracheal lymphnodes
 Widal test - H> 200, O > 100
 Weil’s antibody +creatine phosphokinase
 RF/ANA/ anti DNA ase
 Bone marrow aspiration
 Lumbar puncture
 Echo
 Lymph node biopsy

TREATMENT

TYPHOID
 Uncomplicated : Oral cefixime 20 mg/kg /day is the drug of choice.
 Second line drugs:
- Azithromycin 10-20 mg /kg/day
- Chloramphenicol 50mg/kg /day
- Amoxicillin
- Cotrimoxazole

 Severe illness:
498
 - IV Ceftriaxone 100mg/kg/day or
- IV Cefotaxime 200mg/kg/day
 In patients with h/o Penicillin /Cephalosporin allergy, Chloramphenicol (in
higher than usual dose) & Cotrimoxazole (in higher than usual doses) are
used as second line agents.
 Parenteral therapy until defervescence, thereafter switched to oral
Cefiximeto complete a total duration of 14 days.

MALARIA
 Vivax malaraia
 Chloroquine
- 10 mg/kg day 1
- 10 mg/kg day 2
- 5 mg/kg day 3
 Primaquine 0.25 mg/kg for 14 days

 Falciparum malaria (uncomplicated )

Artemisinin based combination therapy ( ACT)
 North eastern states: ACT SP
- Artesunate 4 mg/kg OD for 3 days
- Sulfadoxine25 mg/kg single dose on day 1
- Pyrimethamine 1.25 mg/kg single dose on day 1
- Single dose of Primaquine 0.75 mg/kg

 Other states : ACT AL

- Artemether 20 mg, Lumefantrine120 mg

 Cerebral malaria
IV Quinine 20 mg/kg loading dose in 10 mg/kg of glucose in 4 hrs.
After loading dose, Quinine continued at a dose of 10 mg/kg infusion over 2
hrs every 8 hrly.
Parasite count start declining after 24 hrs.It is switched to oral Quinine as
soon as possible.
 Supportive measures
 IV fluids
 Blood transfusion if required
 Fever: Tepid sponging, paracetamol
499
  Seizures: Oxygen inhalation, anticonvulsant
 Transfusion of FFP, Vit K for bleeding tendancy
 Hypoglycemia : IV glucose
LEPTOSPIROSIS
 Severe: Parenteral Penicillin G ( 6-8 million U/m2/24 hr q 4 hr IV for 7 days)
drug of choice
 Alternatives: Ceftriaxone and IV tetracycline
 For oral treatment :
- Amoxicillin
- Doxycycline ( > 8 yrs)
DENGUE
 Undifferentiated fever: (Non -specific symptoms )
- Paracetamol for fever
- Monitor for development of complications
 Dengue w/o warning signs (Fever, rash, body ache, minor bleeding )
- Paracetamol
- Drink plenty of fluids
 Dengue with warning signs
- Abdominal pain/tenderness
- Mucosal bleeding
- Persistent vomiting
- Increase in PCV
- Liver enlargement >2cm
- Clinical fluid accumulation
( code: ABVP Liver fluid )

Study flow chart 11.9, page no. 222 (Ghai 9 th edition )

 Severe dengue
- Severe plasma leakage leading to shock/fluid accumulation with
respiratory distress
- Severe bleeding
- Severe organ involvement :AST, ALT> 1000U/L, impaired
consciousness, involvement of heart and other organs.

Study flow chart 11.10, page no. 222

500
 URINARY TRACT INFECTIONS
History
 Age and gender-
- beyond infancy: more in females,
- infancy: female = male ( higher incidence of UT anomalies in males
and hematogenous spread of infection)
 Symptoms –
- Neonates- sepsis features: fever, vomiting, diarrhea, jaundice, poor
weight gain, lethargy
- Older infant- fever, freq. micturition, convulsions(occasionally)
- GROSS HEMATURIA IS VERY RARE, CONSIDER UNDERLYING RENAL
PATHOLOGY
- Urinary obstruction features -
 Crying/ straining during micturition
 Dribbling/ weak/ abnormal urine stream
 Palpable bladder
- Simple/ Complex UTI
 Simple- low grade fever, dysuria, frequency, urgency
 Complex- high grade fever, systemic toxicity, persistent
vomiting, dehydration, renal angle tenderness, raised
creatinine (laboratory finding)
 Complications – nephrotic or nephritic features
 Rule out other causes of fever, dysuria

Past History
 Similar episodes in past – classically recurs within 3 months of one episode
 Predisposing factors for recurrence
- Female
- Age < 6 months
- Obstructive uropathy
- Severe Vesicoureteric Reflux (VUR)
- Voiding dysfunction
- Constipation
- Repeated catheterization
- Immunosuppressive therapy & malnutrition
 History of surgery for meningomyelocele, anorectal malformation

501
Family History
 History of urinary tract malformations in family
 History of recurrent urinary tract infections

Socioeconomic History
 Personal Hygiene – proper cleaning and disposal of excreta
 Sanitary latrine
 Drinking water

EXAMINATION
 Vitals- tachycardia, raised body temperature
 Head to foot examination- genital area: vulval synaechiae, tight phimosis
 Anthropometry – to assess malnutrition
 Abdominal examination- palpable kidney, renal angle tenderness,
distended bladder
 Neurological deficit in lower limb

DIAGNOSIS
 Significant number of organisms of a single species in urine
 Significant bacteriuria-
- Clean catch sample- >105/ml
- Urethral Catheterization- >50,000/ml
- Suprapubic aspirate- any colonies
 Asymptomatic Bacteriuria – Significant count without symptoms
 Screening –
- >10 leucocytes/mm3 in fresh uncentrifuged sample
- >5 leucocytes/hpf in centrifuged sample
- Dipstick examination (leukocyte esterase + nitrite)

TREATMENT (refer table 17.11 OPG, Pg: 479)

 INFANTS <3MONTHS OF AGE / CHILDREN WITH COMPLICATED UTI : 10-14
days
- Parenteral antibiotics(2-3 days)- Ceftriaxone 75-100 mg/kg/day in 2
divided doses IV or Gentamicin 5-6mg/kg/day, single dose IV or IM
- Oral antibiotics(after 48-72hrs of starting Rx)- Ciprofloxacin 10-
20mg/kg/day 2 div doses, Coamoxiclav 30-50mg/kg/day of amox, in 2
div doses
502
  OLDER INFANTS / SIMPLE UTI: ONLY ORAL Rx. For 7-10 days
 ADOLESCENT WITH CYSTITIS: ANTIBIOTICS FOR 72 HOURS
 ASYMPTOMATIC BACTERIURIA: NO TREATMENT REQUIRED

IMAGING STUDY
 Following treatment of first episode of UTI, imaging is done to evaluate the
urinary tract to
- Identify urologic anomalies predisposing to pyelonephritis:
obstruction, VUR
- Evidence of renal scarring
 Evaluation based of age
- Below 1 year – US, MCU & DMSA
- 1-5 years – US & DMSA, MCU if any 1 out of 2 abnormal
- Above 5 years – US, if abnormal do MCU & DMSA

NAME TIME OF USE

PERFORMING
ULTRASOUND During UTI Rx Detecting Hydronephrosis or
anomalies of urinary bladder
MICTURITING 2-4 WEEKS after 1. Diagnosis and grading of VUR
CYSTOURETHROGRAM UTI Rx 2. Urethral and Bladder anatomy
(MCU)
DIMERCAPTOSUCCINIC 3-4 MONTHS after 1. Cortical scarring ( regions of
ACID SCINTIGRAPHY UTI Rx decreased uptake with loss of
(DMSA) renal contour)
2. Cortical thinning with
decreased volume

PREVENTING RECURRANCE OF UTI(Refer table 17.13 OPG, Pg: 480)

 Prophylactic antibiotics administered to young infants until imaging results
are available
 Medications – effective, nontoxic and not alter the gut flora or induce
bacterial resistance
 Single bedtime dose-
- Cotrimoxazole: 1-2mg/kg/day of trimethoprim
- Nitrofurantoin: 1-2mg/kg/day
 Long term antibiotic prophylaxis:
503
 - VUR
- Frequent febrile UTI( 3 or more episodes/year) with normal Urinary
tract
OTHER PROPHYLACTIC METHODS TO PREVENT UTI
 Circumcision – for boys and pt with high grade VUR
 Appropriate advice to tackle dysfunctional voiding in recurrent UTI and/or
VUR
 Constipation – dietary modification and medications
 Bladder retraining
 Anticholinergic medication
 Clean intermittent catheterization

504
 KAWASAKI DISEASE
Acute Febrile Mucocutaneous Lymph node syndrome, usually affecting infants
and children less the 5 years old.
DIAGNOSTIC CRITERIA:
A FEVER lasting for more than 5 days
B Any 4 out of 5:-
i) Bilateral nonpurulent conjunctival injection (without discharge)
ii) Changes of mucosae of oropharynx (e.g.: injected pharynx, injected
lips, strawberry tongue)
iii) Changes of peripheral extremities (acute stage: edema, erythema of
hands or feet, convalescent stage: periungal desquamation, Beau
lines on nails)
iv) Polymorphous rash (never vesicular)
v) Cervical Lymphadenopathy (atleast 1 node >/= 1.5cm, usually
unilateral)
C Illness not explained by any other known disease process

HISTORY
 Age of child (>80% under 5 years of age)
 Duration of illness – fever lasting more than 5 days, irritable child
 Any features mentioned in diagnostic criteria – evolving sequentially
 Rule out other causes of Fever (refer case sheet on PUO)
 Seasonal clustering of cases reported
 Reactivation of BCG scar
 Arthritis
PAST HISTORY
 History of rheumatic fever
 Any other vasculitides, SLE
 History of congenital heart diseases
FAMILY HISTORY
 Similar illness in family members
 History of heart disease in family
EXAMINATION
 General comment of child
 Lymph node enlargement
 Vitals (esp. Temperature)
505
  Head to foot examination – injected mucus membrane, desquamation,
rash, BCG scar
 Anthropometry – malnutrition?
 CVS examination
INVESTIGATION
 Diagnosis of exclusion – using clinical criteria
 Routine ECHO assessment for any developing coronary aneurysms,
dilatations or stenosis
MANAGEMENT
 IVIG – Rs 8000 to 10,000 per unit. Dosage: 2g/kg single dose
 Aspirin in anti-inflammatory dose: 30-50mg/kg until afebrile and then in
antiplatelet dose: 3-5 mg/kg for 4-6 weeks
PROGNOSIS
 Coronary Artery Abnormalities: With appropriate treatment: 3%
Without treatment: 15-25%

506
 IMMUNE THROMBOCYTOPENIC PURPURA
Presenting Complaints :
 Petechia, Purpura, or eccymotic Patches in an otherwise healthy child.

Differential Diagonosis:
1. HSP (Henoch Schonlein Purpura)
2. Leukemia
3. Aplastic Anemia
4. Dengue hemorrhgic fever
5. Meningococcemia
6. Hemolytic uremic syndrome
7. Platelet function disorder
8. Wiskott Aldrich Syndrome(Immune deficiency, eczema, thrombocytopenia)
9. VWD,Hemophilia

History of Presenting Complaints:

1. Petechiae/Purpura/eccymotic Patches
 Onset; site; palpable or not ,Progress,precipitating factors
 h/o fever prior to the onset
 h/o upper respiratory tract infection/conjuctival congestion
 h/o easy bleeding from minor trauma
 h/o increased bleeding during dental extraction
 h/o hematemesis /malena/epistaxis
2. To rule out HSP
 h/o associated Edema, Pruritus
 h/o Arthralgia
 h/o Abdominal pain
 h/o hematuria
3. To rule out Anemia
 h/o weakness,dizziness
4. To rule out leukemia
 h/o Bone pain,loss of weight,Bleeding tendencies.
5. h/o any drug intake prior to onset of rash
6. To rule out meningococcemia
 h/o vomiting,convulsions,headache.
7. h/o trauma.
Past History
 h/o increased bleeding on I M Vitamin k injection.
 h/o increased bleeding from umbilical cord
507
  h/o any bleeding disorders
 h/o any drug intake/Anticoagultion

Examination
 Look for pallor ;lymphadenopathy; rash
 look for bleeding gums ; Mucosal hmrges
 If there is ecchymotic patches - comment as “multiple ecchymotic
patches through out body of varrying sizes largest being -& smallest
being-(measurements)
 Look for spleen -tip(+/-) primary ITP
 Large spleen - secondary ITP
 Look for Hepatosplenomology (r/o Leukimia)

CNS ---rule out Intracranial hemorrhge(as it is a rare complication of ITP)

CVS---signs of Anemia-flow murmurs
FUNDUS EXAMINATION - L/F retinal bleeds (Warning sign of IC bleed)

L/F Hyperpigmentation (Fanconi syndrome)

Investigation
ITP is diagnosis of exclusion
 platelet Count ( <500000/mm3)
 Complete Blood Count (rule out Aplastic Anemia)
 Peripheral Smear
 Bone marrow examination -Indicatons?
 Pallor, HSM,Lymphaderopathy- to r/o leukemia
 Before starting steroids
 c/c ITP (> 6 months)
 P.T. aptt- to r/o coagulation disorders
 platelet function studies
 for chronic ITP
 ANA; Anti ds DNA, HIV
 Direct coombs test to rule out Evan’s syndrome

Treatment
 Watch & wait ; as it is self limiting
 Avoid IM injections
 Bed rest
 Steroids - Prednisolone 4 mg/kg in divided doses for 4 days followed by 2
mg/kg for ten days and taper over next 7 days
508
  Or IV Ig 0.8- 1 g/kg single dose
 Or Anti Rh (D) 25 micro gram /kg *3 days
 Platelet transfusion only if life threatening bleeds, count <20,000/mm3

 Chronic ITP : splenectomy is a choice (done only after 6 years ;children

should receive H.influenza & pneumococcal vaccine 3 weeks prior to
splenectomy)

Summary
 ITP is commonest bleeding disorder in 1-7 years
 No lymphadenopathy or Hepatosplenomegaly in ITP (If present suspect
Leukaemia / collagen vascular diseases.
 Complete recovery in 90% children
 I C bleed-rare complication
 Read coagulation pathway,

Other questions
Pathogenesis of ITP
Immune pathogenesis
Against platelet gp IIb/IIIa complex
Pt with surface antibodies are trapped in the spleen and removed by
macrophages.

Causes of thrombocytopenia
 Infection: Malaria, kala azar, DIC, dengue hemorrhagic fever, HIV, Hep B, C,
TORCH infections
 Medications: Valproate, penicillin, heparin, quinine, digoxin
 Hypersplenism
 ITP
 Thrombotic microangiopathy: TTP, HUS
 Malignancy: Leukemia, lymphoma, neuroblastoma
 Autoimmune / related disorder : SLE, evan syndrome, APLA
 Bone marrow failure : Thrombocytopenia with absent radii, Fanconi anemia
 Platelet dysfunction

Q) Define petechiae , purpura, ecchymosis

Petechiae:
509
Red/purple dots that represent bleeding from
leaking capillaries. ( <2mm)
• Ecchymosis occur deeper in the dermal layers( >1cm)
Purpura ( 2-4mm)
Petechiae that have coalesced and become bigger

Indications of platelet transfusion in ITP

 Serious hemorrhage
Indications of splenectomy in ITP
 Chronic ITP

Management of chronic ITP

 Alternate day low dose steroid
 Splenectomy
 Drugs: Danazol, Rituximab, Cyclosporine, Azathioprine, Vincristine
( code: DR.CAV)

510
 HEMOLYTIC ANEMIA
(Thalassemia or Herditary spherocytosis)

Presenting complaints
 Child is brought for Blood transfusion (in case of thalassemia)
 If hereditary spherocytosis -Neonatal jaundice or icterus in an asympotamic
child.
Clinical Evaluation
Thalassemia
 Pallor Present (> 4 to 6 months of age )
 History of previous several transfusion
 Jaundice very rare (absent)
 Large head (rarely chipmunk facies)
 O/E Hepatosplenomegaly & Hemic murmus.
 Family history present (as it is autosomal recessive)
Herditary spherocytosis
 Neonatal jaundice/mildicterus in an asymptomatic child.
 Anemia (rarely requires transfusion)
 Splenomegaly ++
 Gall stones (increased biliribin turn over )
 Examine parents for splenomegaly (as it is autosomal dominant )

Differential Diagonosis
Pallor + Hepatosplenomegaly +jaundice
 Hemolytic Anemia
 Leukemia
 Malaria, IMN
 Liver disease
 Storage disorders
Note :- Splenomegaly absent in Sickle cell Anemia.

Fe deficiency Anemia (DD of Thalassemia )

 Commonest cause of anemia (DD of Thlassemia)
 No jaundice
 After 6 months
 No HEPATOSPLENOMEGALY (only 5%)

INVESTIGATIONS
 Hb - degree of pallor
511
  TC,DC,Platelet Count -r/o Aplastic Anemia
 Red cell Indices - to classify Anemia
 MCV,MCH,MCHC,RDW (Red cell distribution width)
 RDW-degree of Anispoikilocytosis.
 Peripheral Smear (Single most important test)
 Reticulocyte count
 Bonemarrow Biopsy -rule out Bone marrow failure syndromes, Leukemia
 Osmotic fragility test (increased in herditaryspherocytosis Decreased in
thalassemia)
 Hb Electrophoresis
 HPLC-For thalassemia
 Direct Coombs test - Auto immune Hemolytic Anemia
 For Fe Deficiency- S.Fe, S.Ferritin, S.TIBC
 Stool culture - Occult blood,Parasites
 X-ray skull - Hair on end appearance (thalassemia)

DD’s of Microcytic hypochromic Anemia

 Fe def Anemia
 Thalassemia
 Sideroblastic
 Pb poisoning
 Macrocytic -Megaloblastic anaemia, hypothyroidism, liver d/s, drug Induced
(phenytoin)
 normocytic- Aplastic,anaemia of c/c d/s,hemolytic anaemia, hemorrhage
 Nutritional Anemia-Dimorphic
 Chronic renal failure –Normocytic

Treatment
Thalassemia
 Ideal is bone marrow transplantation if cross matched donor is available
& affordable cost.
 Regular Blood transfusion every 3 weeks to keep Hb>9 gm/dl
 Hypertransfusion therapy.
 Fe chelation (Desferrioxamine 20-40 mg/kg)
 Vaccination against Hepatitis
 Splenectomy (if transfusion requirements shoot up ) (only after 6 years)
 Avoid food rich in Fe
 Folic acid 1 mg/day
Herditary spherocytosis
 Folic acid 1 mg/day
512
  If Aplastic crisis - transfusion required
 Splenectomy will be curative.
Causes of hemolytic anemia
Acquired
 Mechanical:Macroangiopathic ( artificial heart valve) microangiopathic
(DIC, HUS, TTP)
 Infections : Malaria, kala azar, Clostridium welchii
 Antibody mediated : AIHA
 Transfusion reactions:immediate and delayed
 Hemolytic disease of new born
 Drugs: cefotetan, ceftriaxone
 Hypersplenism
 Chemical injury: Snake bite, lead arsenic toxicity
Inherited
 Hemoglobinopathies : thalassemia, sickle cell disease
 Red cell membrane defects: G6PD deficiency
 Disorders of the cytoskeletal membrane : Hereditary spherocytosis
 Unstable hemoglobins
 Lipid membrane defects
 Porphyria
Cutoffs for Hb and hematocrit proposed by WHO to define anemia
Age group Hb g/dl Hematocrit%
6 m- 5 yrs <11 <33
5-11 yrs <11.5 <34
12-13 yrs <12 <36

513
 HENOCH SCHONLEIN PURPURA
History taking & DD - refer ITP

HSP
 IgA vasculitis of small vessels
 Mainly a clinical diagnosis
Diagnostic criteria
 Palpable purpura(95%) with atleast one of the following
 Diffuse abdominal pain(15%)
 Arthritis(75%) / arthralgia
 Renal involvement (35%)( hematuria, proteinuria)
 Biopsy : leukocytoclastic vasculitis with predominantly IgA deposition

Rash
 Begins as purpuric rash
 More over the extensor aspect of lower extremities and buttock
 Macular /maculopapular/urtricarial

Complication
 Nephritis ,Stroke,Intussusception

Investigations
 Ig A levels raised
 Stool -occult blood
 BRE -Non specific (Pallor & Blood loss)
 Skin biopsy
 Renal biopsy - Mesangial deposition of Ig A
 Urine analysis - RBC
TREATMENT
 Analgesics for pain.
 Avoid activities that may result in trauma
 Steroids are given in active cases
 Prednisolone (1-1.5 mg/kg/day *3 wks)
 Good Prognosis

514
 DOWN SYNDROME
Presenting Complaints
 Abnormal facies
 Mental retardation
 Delayed milestones
 Difficulty in feeding
Prenatal, Natal ,Post natal history
 Age of conception
 Any exposure to radiation or drugs
 Any h/o spontaneous abortion
 Delay in passage of Meconilium
 Prolongation of Physiological jaundice
Development history -Development delay
Head to Foot Examination
General Attitude
 Playful, Co-operative,Fond of music
 Head & Face
 Microcephaly,flat occiput,flat facies,Mongoloid slant of eyes, Epicanthal
folds,Depressed nasal bridge,narrow short high arched palate,small teeth,
furrowed tongue, small & dysplastic low set ears, Facial Grimace, cataract,
Hazy cornea, jaundice.
 Limbs: Clinodactyly,Simian crease,More ulnar loops in finger,Sydney
crease, sandal gap, subhallucidal pad of fat, Single longitudinal & deep
crease on sole (kennedy crease )
Other systems
 CVS - PDA,VSD,ASD,(Endocardial cushion defects)
 GIT - Duodenal Stenosis,Hiroschsprungs disease
 CNS - Hypotonia, Poor moro reflex*
 Blood - Acute leukemia

Management
 No definite treatment
 TENDER LOVING CARE
 Chromosome analysis to confirm
 Prenatal diagonosis (Triple testing ,CVS,Aminocentesis)
 Investigate for associated conditions - and early intervention
Questions
 Cytogenetics
Trisomy 21 (95%)
515
 Mosaic (1%)
Translocation (4%)
 Triple test
Test for chromosomal abnormalities
AFP, estradiol, beta hCG.
 Quadruple test
Triple test + Inhibin A

 Turner syndrome
45 XO
 Lymphedema of dorsum of hand and feet
 Loose skin folds at the nape of neck
 Short stature
 Short neck, webbing
 Low posterior hair line
 Anomalous ear
 Prominent narrow &high arched palate
 Small mandible
 Epicanthic gold
 Widely spaced hypoplastic nipples
 Increased carrying angle
 Sexual maturation fails to occur
 Congenital defects: Horse shoe kidney, double/cleft renal pelvis, CoA,
perceptive hearing defect

 Patau syndrome –Trisomy 13

 Edward syndrome –Trisomy 18
 Klinefelter syndrome –47 XXY

516
 CONGENITAL RUBELLA SYNDROME
Incidence
 1st trimester - 80% risk
Clinical effects
 Sensorineural deafness
 Cataract
 Congenital heart disease -PDA,Pulm-Art,Stenosis
 CNS defects - Microcephaly ,MR,developmental delay
 Thrombocytopenia
 Hepatosplenomegally
 Late → Diabetes
Encephalitis → Extended Rubella syndrome
Hearing loss
 Acute infection at Birth
 Hemolytic Anemia
 Purpura
 Myocarditis with failure
 Hepatitis /Encephalitis

Prevention
 By immunisation (women of child bearing age) (Avoid pregnancy for 8
weeks)
 If Pregnant women gets primary infection in early trimester - MTP
 Vaccine - RA 27/3.

Other Questions
 Forscheimer spots in Rubella (soft palate)
 Clinical features of Rubella infection.

517
 CEREBRAL PALSY
Presenting complaints
 Recurrent LRTI’s, Feeding problem, devlpmental delay, Seizure, Abnormal
movments.
 Complaints in early childhood-Delay mile stone, difficuly in changing
diapers, Scissoring at lower limbs.

H/o Presenting illness

 Detailed H/o Seizures

Developmental h/s
In nervous system ask abt-
 HMF- behavioral,intellectual & speech
 Cranial nerves-Whether child is following light or not(CN 1)
 Abnormal mvments of eyes/Squint(CN 3,4,&6)
 Facial deviation(CN 7)
 Responding to voices/deafness(CN 8)
 Drooling of saliva(CN 9,10,11)
 Swallowing of food(CN 9,10,11)
 Nasal regurgitation/nasal twang in voice(CN 9,10,11)
 ALWAYS ASK FOR & ASSESS VISION ,HARING & SPEECH

Also ask abt h/o complication

 Bedsores
 Aspiration pneumonia
 Feeding difficulty
 Behavioral problems
 Bladder& bowel problems

Past history
 H/o Seizures,jaundice,TB

Antenatal history
 Fever with rash
 Radiation , drugs
 H/o trauma
 H/o UTI
 Delayed quickening
518
  H/o DM/Ht- Macrosomia -> difficult labour
 Maternal sepsis
 H/o chorioamnionitis

Natal history
 Preterm/term
 Vaginal/CS- indication, vertex/breech
 Hosp/home delivery
 Birth wt- decerased in IU infection & Increased in DM
 Any instrumentation/PROM/birth injuries
 H/o meconium stained liquor
 Big head- toxoplasmosis

Post natal history

 CSAB?
 Any h/o Sz,jaundice,bld transfusion/phototherapy
 Any h/o ABO or Rh incompatability
 Any feeding difficulty,fever,convulsions,resp problems
 Umbilical sepsis
 Ask abt breast feeding & passage of meconium & urine

Developmental history
 All 4 spheres should be assessed
 ALWAYS CHECK IF ANY ATTAINED MILESTONE HAS BEEN LOST-THEN NOT
CP
 Neck steadiness attained or not?
 Roll over phenomenon
 Early hand preference(Before 1&1/2 yrs)
 Paucity of mvments on one side
 Commando crawl
 Bottom shuffling
 Specify what all milestone attained & what all things he is able to do now

Diet history
 These children invariably develop PEM.So take a detailed history & assess
deficit
Immunisation history
 Pertussis vaccine can be given in CP
 All vaccine according to NIS
Family history
519
  H/o similar illness
 H/o Seizure,mental retardation,devlpmental delay
 Maternal age.35
 Consanguinity

Examination
 Do general examination, note vitals, head to foot examination,
Anthropometry.
 In nervous system examination
- Assess HMF,CN(esp motor part)
- Motor system- bulk, tone, power ,co-ordination ,reflex, involuntary
mvments & gait
- Sensory system & meningeal signs.

DISCUSSION

Definition
Non progressive disorder of posture & movement often associated with defects
in vision, hearing, intellect & epilepsy caused by a static insult to the developing
brain.(Static encephalopathy)

Etiology
Prenatal Postnatal
Chromosomal/genetic Prematurity
IU infection Neonatal Sz
PIH,IGDM Hypoglycaemia
Prolonged labour, APH Neonatal jaundice
Twins Any h/o exchange transfusion
PROM,cord prolapse

Classification
1. Spastic CP
2. Dyskinetic CP
3. Ataxic CP
4. Mixed CP
5. Atonic CP

D/D
- Spastic- PKU,MSUD
- Dyskinetic-Neurodegenerative d/s,Glutaric aciduria
520
 - Hypotonic CP-LMN d/s, IEM,Musular dystrophy,
- Ataxic- ataxia telengectasia

MANAGEMENT
Investigations
 CT scan
 MRI
 EEG
 TFT-To r/o occult hypothyroidism
 Investigations to r/o D/ds

Treatment
 Physiotherapy
 Tranquilizers-for behavior disturbances
 Muscle relaxants
 Baclofen-to reduce spasticity
 Orthosis & surgical procedures
 Occupational therapy
 Educational &social support
 Orthopedic support.
 Rehabilitation & vocational guidance

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 FEBRILE SEIZURE
Febrile seizure refer to seizures associated with high grade fever(38°C) occurring
in neurologically healthy children between 6 months and 5 years of age , without
underlying intracranial infection and without history of prior unprovoked seizures.

History
 Age of child (6mon to 60 mon )
 Duration of fever to seizures (fever 1-2 days prior to the event)
 Condition at the time of seizures (high/low grade fever)
 Seizures generalized/focal
 Tonic clonic seizures /posturing/absent seizures
 Duration of the seizure activity (<5 min usually,>30 min status)
 Mode of termination of seizures (self terminated/upon administration of
drugs)
 Post termination sensorium (usually very short post ictal state)
 Anything to suggest atypicality (prolonged focal, recurring with in the same
febrile illness)
 Complications
 Rule out other causes of seizures ( raised ICP, h/o vaccination,drugs )

Past history
 Febrile seizure/ seizure disorder
Family history
 Seizure disorder

Examination
 Vitals
 Temperature recording is must
 Growth assessment
 Neurological assessment - look for any neurological deficit
Investigation
 Blood glucose examination
 Blood count, sepsis screen, blood culture
 Serum electrolytes
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  Csf analysis
 EEG done only after 2 weeks ,imaging not recommended if the child is
neurologically normal

Management
 Protect from injury
 Semiprone position to prevent aspiration
 Oxygen inhalation
 Control seizures with diazepam 0.2-0.3mg/kg iv or 0.5 mg/kg rectally ,or
0.2mg/kg midazolam iv or intranasal
 Tepid sponging and antipyretics
 Reassure parents, explain the risk for recurrence
 Iron supplementation in iron deficiency as it is a known trigger

Prophylaxis
 Prophylaxis is advised for children with frequent recurrence that is ≥3 in 6
months or ≥4 in 1 year.
 At the beginning of fever intermittent prophylaxis is adviced
 Tepid sponging
 Paracetamol
 Oral benzodiazepines (diazepam 0.6-0.8mg/kg/day in 3 divided doses or
clobazam 0.8-1mg/kg/day in 2 divided doses) should be started at the first
sign of any febrile illness and continued for first 3 days of febrile illness.
 Continuous prophylaxis - phenobarbitone/sodium valproate

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 ADVICES
General points to remember
 Create Rapport with the mother
 Explain the condition clearly and reassure that proper treatment will
cure/control the disease
 Ask about the vaccination status of the child
 Ask if she has any doubts

1. Advice on prophylaxis of febrile seizures

• Explain the condition to the mother (affected age grp is 6 months to 6 yr.It
occurs in the first two days of fever and never recur in the the same febrile
episode)
• During febrile seizure explain her to decrease temperature by using
o Light clothing
o Ventilated room
o Tepid sponging
o Tab paracetamol
o Tab diazepam (oral/suppo)
• Rush to the doctor if temperature does not subside
• In case of seizure
o Keep the child away from dangers
o Don’t put anything in the mouth
o Keep the head tilted to one side

2. Advice on discharge of child with nephrotic syndrome

• Explain the condition clearly—that the child is losing protein through urine and
there is chance of high BP and blood cholesterol. There are chances of relapses.
• Give dietary advice -avoid egg yolk, fatty foods, butter, ghee and excess salts.
Include egg white, steamed food like idly, puttu, idiappam, fish curry.
• Weekly BP monitoring
• Chance of infections are more and infections itself can precipitate relapses.
Hence all infections should be treated early.
• Explain the side effects of steroids and its side effects like appearance of moon
face.
• Educate mother on heat and acetic acid test, the procedure and interpretation.
Take ¾ th of a test-tube with clean urine, heat it by tilting over a flame, then add
8 drops of vinegar and note the colour.
Keep in front of newspaper and try reading it
Can read small letters clearly Nil
Can read but unclear 1+
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Can read only headlines 2+
Cannot read headlines but can see them as dark areas 3+
Cannot see the paper at all 4+
If the reading comes to 3+ or 4+ for 3 consecutive days then ask her to report to a
doctor
• Mention the importance of immunization,optional vaccines(varicella,
pneumococcus, influenza)

3. Advice on immunization
• Ask the age of the child
• Explain the importance of immunization
• Explain the immunization schedule
• Ask about vaccination like BCG(injection on left arm),OPV(oral drops),DPT(inj
on lat aspect of thigh)
• Tell her about optional vaccines
• Tell her that it is available at her nearest PHC on all Wednesdays
• Even in case of slight fever, get the child for immunization
• It will not cause any harm to the child
• Explain the importance of pulse polio immunization
• Ask if she has any doubts

4. Advice on diarrhea with no dehydration (plan A)

• Explain the disease to the mother
• Explain the importance of ORS in diarrhea and tell her that it is available at free
of cost
• Explain preparation of ORS
Boil and cool 1 litre of water (5 glasses). 1 packet ORS is then dissolved in it.
The solution made should be used only for 1 day
 After every bout of diarrhea, ½ -1 glass for >2yrs (¼- ½ glass for >2yrs) should
be given
 If child vomits wait for 10 minutes restart as sips of 1-2 teaspoons every few
minutes
• Explain about other home available fluids (lemon juice,lassi kanji water etc.
with a pinch of salt added to it)
• Educate mother on signs of dehydrations and to bring back the child when
needed.
• Encourage breast feeding and normal diet
• If ORS is used up return for more
• Avoid food with fibre content during acute phase e.g.-fruits

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• After recovery give the child an extra meal for 2 weeks. This will help to regain
his weight
• Explain the importance of immunization
• Personal hygiene(hand washing before handling food, periodic trimming of
nails)
• Use only boiled water for drinking
• Exclusive breast feeding till 4-6 months followed by proper complementary
feeding practices

5. Advice on diarrhea with some dehydration(PLAN B)

• Explain the condition to the mother, that the child has lost some water and salt
from his body
• Tell her that child will be kept in observation for 4 hrs. Child should get 75ml
/kg within 4 hr
drinking small quantity at regular intervals.
• If child vomits wait for 10 minutes restart as sips of 1-2 teaspoons every few
minutes
• Educate on danger signs
• After 4 hrs if child has no dehydration he sent to home to ORS
• Mention preparation of ORS
• Encourage breast feeding and normal diet
• If ORS is used up return for more
• Explain the importance of immunization
• After recovery give the child an extra meal for 2 weeks. this will help to regain
his weight
• Personal hygiene(hand washing before handling food, periodic trimming of
nails)
• Use only boiled water for drinking
• Exclusive breast feeding till 4-6 months followed by proper complementary
feeding practices

6. Advice on breastfeeding
• Mention the advantages of breastfeeding
o Emotional bond between child and mother
o Exclusive breast milk is adequate for the growth till 6 months
o It has immunological factors which protect against infections
o Breast milk protein is easy to digest than cows milk
o For the mother it gives protection against pregnancy in the initial 2-3
months.

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• Explain about the positioning of the child (tummy to tummy, chest to chest,
signs of good attachment)
• Only after completing from one breast, you should change to the next side.
Feed alternatively from both breast
• How to know breast milk is adequate
o Child sleeps for 2 hrs after every feed
o Frequently passes urine
o Child gains weight adequately
o Let down reflex in mother present
• Exclusive breast feeding till 4-6 months followed by proper complementary
feeding practices

7. Mother of 3 month child complains that child is not feeding adequately.

Weight of the child is 4.2 kg and the child has incessant cry during evenings.
• Ask for birth weight
• Reassure that child has adequate weight gain
• Ask whether child is sucking properly (8-10 feeds per days, sleeps for 2 hrs
after each feed, passes urine frequently, let down reflex present)
• Explain positioning of child
• Ask whether she changes diapers as the child passes urine(a reason for
incessant cry is wet diaper)
• Ask for fever(meningitis)
• Explain on immunization
• Exclusive breast feeding till 4-6 months followed by proper complementary
feeding practices

8. Advice on the care of a preterm/LBW baby

• Explain the problems of preterm (Hypothermia, hypoglycemia, infections,
feeding problems, exaggerated jaundice)
• Measures to tackle hypothermia
o Adequate covering of baby-with head cap, socks
o Kangaroo mother care
o Avoidance of bath
• Frequent feeding to avoid hypoglycemia
• Minimum number of visitors to avoid infections
• If sucking is not proper, feed the child with expressed breast milk using
gokarnam
• Explain the importance of immunization and exclusive breastfeeding

9. Advice on discharge of rheumatic fever child

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• Explain the disease and prognosis.(disease affect joints, heart; usual age grp
affected is 5-15 yr; disease occurs after throat infection; importance of treating
sore throat in children)
• Risk of recurrence
• Explain on administration of steroids for carditis and its side effects
• Explain primary prevention(adequately treating all sore throat)
• Secondary prevention-penicillin oral bd;isolated rheumatic arthritis-Px till 21
yrs or 5 yrs after the initial attack whichever comes later;carditis without residual
valvular lesions-Px till 25 yrs or 10 yrs after the last attack whichever comes
later;valvular lesions-Px lifelong or atleast till 40 yrs

10. Advice on discharge of asthmatic child

• Explain the disease and reassure that proper treatment will control the
disease.
• Explain the trigger factors (dust, cold weather, pollen etc)
• Avoid sweeping instead wet the floor.
• Hanging things should be avoided
• Prevent exposure to firewood, pets, perfumes, flowers
• Make an asthma diary; note the possible triggers of asthma attack, timing of
attacks, timing of drugs etc
• If child is using inhaler, wash mouth properly after use.
• Treat respiratory infections properly

11. Advise the mother of a Down syndrome child

• Explain the disease; that the child has got a genetic disease
• Talk in simple and positive language giving hope
• Tell the mother that the child’s physical and mental growth will be less
compared to children of the same age
• Discuss the known problems and associated disorders
• About 40% will have cong. Hrt disease. Hence they should have a cardiac
evaluation
• They are at increased risk of cataract, squint. They need evaluation in the first
year and then every year thereafter.
• Hearing defects are common. They should have audiological evaluation
• Thyroid function test at the neonatal period and then every year
• Highlight the importance of early stimulation
• If planning another pregnancy, chromosomal analysis of parents is advised
• Mention the risk of recurrence
• Women 35 yrs or less who have a child with Down syndrome have a 1% risk of
having another. Risk is increased if mother is more than 35.For translocations
inherited from mother; risk is 10%, whereas it is 4-5% when father is carrier
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• Mention prenatal diagnosis. If downs syndrome is diagnosed before 20 wks,
they have option for termination.

12. Advice on complementary feeding

• Breast milk alone can satisfy the nutritional requirements till 6months,
afterwards complementary feeding should be started.
• Complementary feed is not a substite for breast milk. It should be given in
addition to breast milk
• Weaning must be started with mono cereal (raggi, banana powder are the
usual weaning foods).
• Proper hygiene should be maintained while preparing food
• Transient vomiting, diarrhea may occur, but it is self limited. If vomiting /
diarrhea persist, intolerance is suspected and consult a doctor

13.Mother of normal baby upon discharge

 Advice on adequate breastfeeding (refer qns 6)
 BFHI and importance of rooming in
 Vaccinations to be taken later and their importance (esp in 6, 10 and 14
weeks)
 Pulse polio and optional vaccines
 Vitamin supplementations
 Advice regarding hygiene of the baby – changing nappies and bathing the
child
 Bring child to hospital on seeing any signs of difficulty in feeding, incessant
crying, head sweating, bluish discolouration of lips and face

13. Kawasaki Disease

 Regarding the disease – acute febrile mucocutaneous lymph node syndrome,
irritable child less than 5 years old
 One of the leading causes of acquired heart disease, affecting coronary
arteries
 Features of identification – high grade fever, irritability, injected eyes, mouth
and lips, desquamation, erythema of palms and soles, rash ( never vesicular),
cervical lymph nodes, arthritis, reactivation of BCG scar
 Importance of appropriate treatment-
IVIG – Rs 8000 to 10,000 per unit. Dosage: 2g/kg single dose
Aspirin in anti-inflammatory dose: 30-50mg/kg until afebrile and then in
antiplatelet dose: 3-5 mg/kg for 4-6 weeks
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 Prognosis – appropriate treatment: 3%, without treatment: 15-25% cardiac
abnormalities
 Signs of recovery – periungal desquamation
 Reassure the parent, yearly echo for assessing prognosis

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 CHARTS
Q1. 5 year old child is admitted with 3 days history of reduced urine output, dark
colored urine, head ache and vomiting.
-What is the most probable diagnosis?
-What clinical parameter is to be examined immediately and to be monitored
further?
- What relevant recent past history you should ask ?
- What diet modification is to be advised for the time being?
 Acute glomerulonephritis
 Blood pressure
 .Pyoderma/acute pharyngitis
 Salt and fluid restriction and no fruits

Q2. 2 year old child is brought with complaints ofpuffiness of face of week,
generalized edema and reduced urine output of 3 days duration.
– What is the most probable diagnosis?
–Name 3 investigations you would order to confirmthe diagnosis?
– What is the drug of choice?
–Name 2 most important complications?
 Nephrotic syndrome
 Urine albumin, serum albumin, serum cholesterol
 Prednisolone
 Spontaneous bacterial peritonitis, venous
thrombosis

Q3. 4 year old girl is brought with high fever with vomiting and rigors of 2 days
duration and left flank pain.
– What is the most likely diagnosis?
–Name two diagnostic investigations.
– What is the drug of choice in this situation?
–Name two most common organisms implicated.
 Urinary tract infection (more specific answer would
be acute pyelonephritis).
• Urine culture, USG abdomen
• IV 3rd generation cephalosporins (IV ceftriaxone)
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 • E coli, Klebsiella

Q4. 7 year old boy is brought with bilateral ankle painand swelling of 4 days,
abdominal pain of 2 days and reddish non pruritic rashes on lower legs
andbuttocks of 1 day duration.
– Give the most probable diagnosis?
–Name 2 acute complications (surgical complications)
– What is the drug of choice in complicated cases?
– What is the chronic complications the child maydevelop?
 Henoch Schonlein purpura
 Acute: intussusception, torsion testis, intestinal perforation
 Corticosteroids
 Renal disease (nephrotic syndrome, nephritis, end stage renal
disease)

Q5. 1 year old boy develops irritability , lethargy andoliguria following an episode
of dysentery.
– What is the most probable diagnosis?
– Which organism is most commonly implicated?
–Name 3 most diagnostic blood investigations.
– What is the long term prognosis?
 Hemolytic Uremic Syndrome
 E coli producing Shiga like toxin(E coli 0157:H7)
 Hb, platelet count, Serum creatinine (low Hb, low platelet , deranged renal
function tests in this clinical setting is diagnostic)
 Long term chronic renal disease and end stage renalfailure may occur
(especially in those havingneurological problems like seizures in the
acutestage).

Q6. 10 year old girl is brought with fever of 5daysduration, migrating joint
swellings affecting, rightknee, right ankle and left elbow one after the other.She is
in severe pain. Her chest is clear, but CVS
examination reveals laterally shifted apex, soft heartsounds, S3 and a grade 3/6
PSM at apex.
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-- What is the complete diagnosis?
– What all laboratory investigations would help inthe diagnosis?
– What specific treatment is to be instituted?

 Acute rheumatic fever with carditis ‐mitralregurgitation.

 Throat swab, ASO, ESR, CRP, ECG, X‐ray chest, Echo
 Inj.Penicillin,
Anti inflammatory: Prednisolone2mg/kg/day for 2 weeks and then slowly
taper while introducing Aspirin 80mg/kg/day for 10 weeks

Q7.NEONATAL JAUNDICE
Causes:
 Hemolytic- ABO or Rh incompatibility, G6PD deficiency, thalassemia,
hereditary spherocytosis
 Non-hemolytic- prematurity, hypothyroidism, breast feeding jaundice,
cephalhematoma, breast milk jaundice
Investigation:
 Serum total bilirubin,
 Blood group
 Direct Coomb’s test
 Hemoglobin and hematocrit
 Peripheral smear- to look for hemolysis
 Other specific tests
Treatment:
 Phototherapy and exchange transfusion
Complications:
 Acute bilirubin encephalopathy, kernicterus , intracranial hemorrhage,
seizures, cerebral palsy, deafness

Q8. ACUTE RESPIRATORY INFECTION PNEUMONIA

Causes:
 <3months- E coli, Klebsiella, RSV, Group B Streptococci, Staphylococcus
 3months to 5 years- RSV, Pneumococcus, H.influenza, Staph aureus
 >5 years- Mycoplasma, Chlamydia, Staphylococcus, Streptococcus
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XRAY findings:
 Lobar pneumonia- lobar consolidation, air bronchogram, effusion

Treatment:
LEARN ARI CONTROL PROGRAM
 Drugs- Oral – Amoxicillin 40mg/kg BD for 5 days
 Parenteral- Ampicillin 50mg/kg or Benzyl Penicillin 50,000 units/kg Q6H for
5 days
 Gentamicin 7.5mg/kg im/iv once a day for 5 days
 2nd line- Ceftriaxone

Complications:
 Pulmonary- pleural effusion, empyema, lung abscess, collapse, respiratory
failure
 Extrapulmonary- pericarditis, endocarditis, meningitis, suppurative arthritis

Q9. NEONATAL SEIZURES

Causes:
 Perinatal complications- birth asphyxia, intracranial injuries, hypoxic-
ischemic encephalopathy
 Metabolic- hypocalcemia, hypoglycemia, sepsis, hypomagnesemia, hypo or
hypernatremia
 CNS infections
 Inborn errors of metabolism
Diagnosis:
 history, blood investigations, EEG monitoring, LP in meningitis
Treatment:
 Treat underlying cause
 Drugs- acute episode- lorazepam 0.1mg/kg
First choice long acting drug is Phenobarbital 20mg/kg
Others- Phenytoin, Fosphenytoin

Q10. KANGAROO MOTHER CARE

Components:
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  Kangaroo position- skin to skin contact (early, continuous and prolonged).
Baby is kept between mother’s breast in vertical position
 Kangaroo nutrition - exclusive breast feeding
 Kangaroo discharge- once baby is stable, proper sucking and swallowing,
gaining weight, mother is practicing KMC at home
When to stop: Once baby attains 2500g and gestation age of 37 weeks

Q11. DIFFERENCE BETWEEN TERM AND PRETERM BABY

Features Preterm Term
Ear Pinna soft , slightly Pinna firm, well
curved, slow recoil curved, instant
recoil
Skin Smooth,pink, visible Cracked, leathery,
veins no veins
Lanugo Abundant Bald
Breast bud Poorly formed Well formed (5-
10mm)
Genitals male Scrotum empty, Scrotum well
light pigmentation, pigmented ,
few rugae pendulous, deep
rugae
Genitals female Clitoris and labia Majora cover
minora prominent clitoris and minora
Plantar surface of Faint lines or Deep creases over
leg anterior transverse entire sole
crease only

Q12. RESPIRATORY DISTRESS IN NEWBORN

Causes:
 Pulmonary- respiratory distress syndrome, pneumonia, meconium
aspiration syndrome, transient tachypnea of newborn, persistent
pulmonary hypertension
 Congenital malformations- trachea-esophageal fistula, diaphragmatic
hernia
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  Cardiac- CHF, congenital heart disease
 Metabolic- hypothermia, hypoglycemia, metabolic acidosis

ARDS
Clinical features:
 occurs within 6 hours of life, tachypnea, retractions, grunting, cyanosis
Investigation:
 chest X-ray will show reticulogranular pattern, ground glass opacity, low
lung volumes, air bronchogram and white out lungs
 Blood gas analysis- hypoxemia, hypercapnia, metabolic acidosis
Management:
 IV fluids and oxygen
 Mild to moderate- CPAP
 Moderate to severe- intra tracheal surfactant followed by CPAP
 InSurE- Intubate, give Surfactant and then Extubate and immediately put
on CPAP
Prevention-
 antenatal steroids should be given to mothers in preterm labour (<35
weeks)
Q13. MENINGITIS
Causes:
 Neonates- Ecoli, Group B Streptococci, Listeria monocytogenes
 Infants and children (2months to 12 years)-Pneumococcus,H.influenzae, N.
meningitidis
CSF findings:
Normal Bacterial Viral TB meningitis
meningitis meningitis
Appearance
Opening Elevated , Normal or Elevated ,
pressure(cm of 100-300 slightly 100-500
H20)<28 elevated
WBC 1000- 100-1000, 10-500,
count(cells/mm3 10,000, mostly predominantl
) <5 PMNs lymphocyte y lymphocytes
predominate s
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Protein (20- Elevated, Slightly Highly
45mg/dL) 100- elevated, elevated ,
500mg/dL 50- 400-
100mg/dL 5000mg/dL
Glucose Decreased, Usually <40mg/dL
(>50mg/dL or <40mg/dL or normal or
75% of serum <50% of slightly
glucose) serum decreased
glucose
Culture and Gram stain Acid fast
microscopy and culture bacilli
Others PCR or latex PCR Elevated ADA,
agglutinatio CBNAAT
n

Sequelae:
cranial nerve palsies, subdural effusion, SIADH,encephalitis(disorientation,
movement disorders), hydrocephalus
Hemi or paraplegia, blindness, deafness, mental retardation
TB meningitis- communicating hydrocephalus due to basal exudates, ischemic
infarcts and tuberculoma

Drugs:
Empirical therapy in >2months - Ceftriaxone 100mg/kg in 2divided doses for 14
days
TB meningitis- Intensive phase (2 months)- HRZE; Continuation phase (10
months)- HR

537
 INSTRUMENT
1) AMBU bag:
 Ambulatory Mobile Breathing Unit
• Parts- self inflating bag, airinlet, oxygen reservoir, oxygen inlet,
inspiratory valve, pop off valve
• Indications- apnoea, bradycardia (HR< 100),persistent central cyanosis
even after oxygenation.
 C/I- congenital diaphgramatic hernia, meconium aspiration
Note: A self inflating bag delivers only room air. To deliver a high oxygen
concentration (60% to 95%), attach an oxygen reservoir to the self-inflating bag.
Maintain an oxygen flow of 10 to 15 L/min into a reservoir attached to a pediatric
bag and a flow of atleast 15L/min into an adult bag.

2) Endotracheal Tube :
Indications
• When bag &mask fails
• When artificial respiration is to be given for a long time
• In meconium aspiration
• Can prevent aspiration of gastric contents
• To administer drugs-lignocaine,atropine,naloxone,epinephrine,surfactant
Size of ET tube
Preterm-2.5 mm
Larger Preterm-3mm
Term-3.5mm
Infant -4 mm
After 1 yr= age/4 +4 mm

Length of ET tube= age/2 + 12; in < 1 yr= birth wt(kg) +6

3) Infant Feeding Tube:

 Has a radio opaque line, blind end, 2 side holes
 No lead balls as in ryle’s tube
 Length required is from nose to tragus & tragus to xiphysternum.
Indications
• For feeding infants
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 • Aspirate gastric contents
• To decompress stomach in intestinal obstruction
• Aspirate GI bleeding
• AFB staining of gastric aaspiration
The length to be inserted is measured from the nostril to the tragus of the ear and
then to the xiphisternum. Once inserted push air through the tube and auscultate
over the epigastrium to check position.

4) Nebulising Chamber:
 Mx of mild ,moderate, severe exacerbation of asthma

5) Spacer:
Age upto which it is used-
Use:
For proper co ordination of inspiration & drug delivery
For prophylaxis in persistent asthma
Correct technique is to be taught to the child and parents
Parts to be explained clearly
6) Metered Dose Inhaler with Face Mask :
Method of using it- O.P.Ghai
Advantages- rapid action very small dose of drug is required to have
desired effect,very little medicine reaches other parts of the body ( so
side effects are minimum)
Disadvantages :
training & skill needed in administration of drug
Candidiasis ( pharyngeal) may occur

7) Bone Marrow Aspiration Needle ( Salas Needle):

Identified by guard which prevents over penetration
Indications:
 Diagnostic- leukemia, aplastic anaemia, Megaloblastic anaemia,
lymphoma
 Therapeutic- bone marrow transplantation, intra osseous infusion
of fluids
Site:
 < 2 yrs- tibial tuberosity,
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  >2 yrs-iliac crest( post superior iliac spine)
C/I- infection at site, bleeding disorders, severe cardiovascular
compromise

8) Trephine Biopsy Needle( JamshediSwain Needle) :

Used when bone marrow aspiration yields a dry tap
Suspected Aplastic anemia and myelofibrosis.

9) Lumbar Puncture Needle :

Site: between L3 & L 4
C/I: raised ICT, unstable cardiorespiratory status, infection at site,
bleeding disorders
Indications
 Diagnostic-meningitis, hydrocephalus, first episode of
convulsions, demyelinating d/s
 Therapeutic-to give drugs, spinal anaesthesia
Complications: infection, head ache, coning, backache

10) Three Way Valve :

Indications
 Pleural &ascitic tap
 To give adenosine in SVT
SAFETY TRIANGLE – bounded by ant: axillary line , post: axillary line, 6th rib
 Site of ICD insertion in pneumothorax: anteriorly in the safety
triangle in the 3 or 4 intercostal space
 Site of ICD insertion in pleural effusion: posteriorly in the safety
triangle in the 5 or 6intercostal space
 Site of ascitic tap: b/w lateral 1/3rd& medial 2/3rdof spinoumbilical
line

11) Thoracocentesis:
Instruments:
Needle (18 – 22G), over the needle catheters (18 –
23G) Specimen collection tubes, 3 way valve assembly, syringe 1
0 ‐ 30ml

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 Indications
• Pleural effusion
• Pneumonia with effusion/ empyema
• Suspected malignancies
Complications:
• Pneumothorax (3‐30%)
 Hemopneumothorax
• Haemorrhage
• Hypotension due to a vasovagal response
 Pulmonary oedema due to lung re- expansion
• Spleen or liver puncture
• Air embolism
• Introduction of infection

12) Umbilical Vein Catheter :

Used in newborns for exchange transfusion and also as venous access
for giving IV fluids drugs etc.
Obtaining samples in preterm when peripheral lines are not available

13) Liver Biopsy :

Indications
 Chronic hepatitis,
 cirrhosis,
 storage disorders
 Malignancies,
 undiagnosed hepatomegaly
 To differentiate between neonatal hepatitis and biliary Atresia.
Pre‐ requisites
 Prothrombin Time
 Blood group & crossmatching
 Vitamin K administration before biopsy

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 X-rays
Systematic approach:
• Bony framework
• Soft tissues
• Lung fields and hila
• Diaphragm and pleural spaces
• Mediastinum and heart
• Abdomen and neck
PA view:
- X rays penetrate through back of patient and on to film placed in front
- Posterior ribs better visible
AP view:
- X ray penetrate through front of patient and on to film placed behind
- Anterior ribs better visible
• Apparent cardiomegaly
• All X-rays in PICU are portable and AP view
• Cardiomegaly:
- From the centre, maximum distance towards the right and maximum
distance towards the left is found and added to find cardiac size
- If cardiothoracic ratio > 55%, there is cardiomegaly in children. (adults: 50%,
infants 60%)
• Right border of heart: SVC, RA, IVC
• Left border of heart: aortic knuckle, main pulmonary artery, LA appendage, LV
• RV enlargement has upturned apex
• LV enlargement has down and out apex
• Pulmonary plethora:
- Divide lung into thirds by 2 vertical lines
- Normally vasculature can be seen upto middle third
- If beyond middle third, plethora
- If only unto medial third, oligemia

542
Important Named Signs:
• Coarctation of aorta: Inferior notching of 3rd to 8th ribs (seen after 10 yrs of
age), Figure of 3 sign
• ToF: boot shaped heart (coeur en sabot)
• Ebsteins anomaly: box shaped heart
• TGA: egg on string appearance
• Supra cardiac or Obstructed TAPVC: snowman appearance or figure of 8 sign
• Pericardial effusion: Water bottle sign
• Thymus: Sail sign
• Hyaline membrane disease: ground glass appearance
• Pneumoperitoneum: Air under diaphragm, Football sign
• VSD: globular heart with biventricular enlargement
• ICSOL: silver beaten skull
• Duodenal atresia: Double bubble sign
• Jejunal atresia: Triple bubble sign
• IHPS (Infantile Hypertrophic Pyloric Stenosis): String sign
• Acute epiglottitis: Thumb sign
• Acute laryngotracheobronchitis (Croup): Steeple sign

Important features:
• Consolidation:
- Opacity with air bronchogram (bronchi appear lucent. It indicates disease of
the lung parenchyma)
- Silhouette sign: in right lower lobe consolidation, loss of cardiac shadow
• Pneumothorax:
- Fully black lung field with collapsed lung margins visible
- Mediastinal shift
- Diaphragm pushed down (in tension pneumothorax)
• Abscess: thick walled cavity with air fluid level
• Pneumatocele (very important)
543
 - Thin walled air filled cavity
- Seen in Staph pneumonia
• Ghons focus:
- Upper part of lower lobe or lower part of upper lobe
- Sub pleural focus with draining lymph node
• Pulmonary edema:
- Cephalisation of pulmonary vasculature
- Kerly A lines
- Kerly B lines
- Batwing appearance (perihilar opacities)
• ToF (very important):
- Boot shaped heart (coeur en sabot)
- Normal heart size
- Pulmonary oligemia
- RV apex
- Concavity in region of main pulmonary artery
- 30% have right aortic arch
• Rickets (very important):
- First sign: Loss of normal zone of provisional calcification seen adjacent to
metaphysis seen as a blurring or frayed appearance of metaphyseal margin
(Fraying)
- Cupping: Cartilage hypertrophy causes widening of growth plate
- Splaying: Widening of metaphyseal ends
- Elevated periosteum
- Reduced bone density (Osteopenia)
• Scurvy:
- Pencil thin cortex
- White line of Frankel (white line at metaphsysis)
- Trummerfeld zone (zone of rarefaction proximal to white line)
- Pelken spurs (lateral part of rarefaction appears as triangular defect)
- Wimberger ring sign (epiphsysis surrounded by thin white line)
• Bone age:

544
 - Conventionally from radiograph of left hand and wrist by Tanner
Whitehouse method or Gruelich-Pyle atlas
• Diaphragmatic hernia:
- Coils of intestine seen in the thorax
• Acute bronchiolitis:
- Hyperinflation of bilateral lungs
- Few infiltrates
• VSD:
- Cardiac enlargement, mainly LV
- Pulmonary plethora
• Thalassemia:
- Hair on end appearance (due to accentuated vertical trabaeculae between
inner and outer tables of skull because of excessive bone marrow
hyperplasia)
- Rodent facies
- Hypopneumatisation of frontal, maxillary and sphenoid sinuses

545
OBSTETRICS
CASE FORMAT 548

NORMAL PREGNANCY 553

MULTIPLE PREGNANCY 557

BREECH 563

TRANSVERSE LIE: 567

MOBILE HEAD AT TERM IN NULLIPARA 569

DIABETES COMPLICATING PREGNANCY 573

HYPERTENSION COMPLICATING PREGNANCY 579

CARDIAC DISEASE IN PREGNANCY 587

ANEMIA IN PREGNANCY 592

PREGNANCY FOLLOWING CAESAREAN SECTION 597

BAD OBSTETRIC HISTORY 602

INTRAUTERINE GROWTH RESTRICTION 607

POLYHYDRAMNIOS 612

OLIGOHYDRAMNIOS 614

FIBROID COMPLICATING PREGNANCY 615

RH ISOIMMUNISATION 616

THIRD STAGE COMPLICATIONS 617

OBSTETRIC INSTRUMENTS 619

DUMMY AND PELVIS 625

O&G SPECIMENS 631

X RAYS 640
 CASE FORMAT
Name:
Age:
Education status:
Name, age and occupation status of husband:
Blood group:

Obstretric score:
Last menstrual period (LMP):
Expected date of confinement (EDC):
Period of amennorhea (POA):
Last child birth (LCB):
Date of admission (DOA):
Date of examination (DOE):

Presenting Complaints:
 No. of weeks of amenorrhea and presently came for safe confinement
 Referred from local hospital and why
 Complaints_BP,DM,CVS complications etc..
 If she had come for any other complaints(eg;fever) then after presenting
illness describe the history of presenting illness
 Current status

History Of Presenting pregnancy

 Planned /not
 LMP,cycles regular or not
 Registered/not, booking visit
 How pregnancy was confirmed
 Whether test was done within 14days of missing periods
 Whether periconceptual folic acid was taken

FIRST TRIMESTER (FIRST 14 WKS)

 Folic acid taken/not
 h/o nausea, vomiting, hyperemesis gravidarum, headache
 increased frequency of micturition
 h/o intake of drugs unknowingly? exposure to radiation?
 h/o infections-fever with rashes, UTI
 h/o spotting, discharge, bleeding P/V
 h/o antenatal checkups
 first trimester ultrasound
548
  whether first dose of TT was taken at 16wks

SECOND TRIMESTER (15-28WKS)

 Regular ANC/not
 Iron and calcium supplementation
 quickening
 second trimester ultrasound
 second dose TT
 h/o bleeding P/V
 h/o anemia, HTN
 vomiting, headache, blurring of vision, epigastric pain(PIH)
 24-28wks-GCT done or not- GDM detected /not.
 If GDM- MNT/insulin
 h/o antenatal checkups

THIRD TRIMESTER (29-40WKS)

 Regular ANC/not
 Good fetal movements appreciated or not
 Iron, folic acid tablets continued
 Headache, oedema
 h/o PIH,GDM
 h/o UTI
 h/o leaking/bleeding P/V
 h/o Frequency of micturition
 Any false labour pains

Menstrual History
 LMP,Age of menarche
 Regularity of cycles,duration of cycles
 Menorrhagia-no. of days,no of pads changed,presence of clots
 h/o dysmennorhea-site,onset and offset,duration
 polymennorhea,oligomennorhea

Marital History
 Age of marriage,duration of married life
 h/o consanguinity,frequency of coitus
 h/o dysparenuria
 h/o contraception,-method used,failure or not
 how many months after marriage she became pregnant
 any period of infertility
549
  infertility treatment, type

Obstetric History
 Any infertility treatment
 h/o previous pregnancies-,fullterm or preterm, type of delivery
 VAGINAL-spontaneous/induced, in hospital/home
 CAESAREAN SECTION- type( elective/emergency), indication,
time(gestation)
 Birth weight, male/ female, condition after birth, NICU admission, if breast
fed as immediately as possible, immunisation status,
 Any postoperative complications, perinatal or postnatal complications
 Time of discharge
 Restoration of menses after each delivery
 ABORTION-period of gestation, spontaneous /induced(if so indication), D&C
done /not, complications if any
 Any ectopic pregnancy ;
 expectant/medical/surgical management

Past History
 h/o TB,DM,HTN,bronchialasthma,jaundice,any cardiac or renal
disease,endocrine or blood diseases
 h/o drug allergy
 h/o epilepsy
 h/o blood transfusion

Treatment History
 any past medical or surgical intervention
 any treatment for infertility

Personal History
 Diet-veg or non/veg(DETAILED DIET H/O TO BE TAKEN FOR
GDM,ANEMIA)
 Sleep and appetite normal/not
 Bowel and bladder habits normal/not
 Any addictions

Family History
 Of any diseases,HTN,DM,mental history
 h/o congenital anomalies
 twinning and infertility,blood dyscrasias
550
  father,mother,siblings,consanguinity

GENERAL EXAMINATION
 Height:
 Weight:
 Weight gain:
 BMI(Calculate using pre pregnant weight):
 Pallor, icterus, clubbing, cyanosis, lymphadenopathy, edema
 Gait:
 Spine:
 Breast:
 Thyroid:

VITAL SIGNS
PULSE:
BLOOD PRESSURE:
RESPIRATORY RATE:
TEMPERATURE

SYSTEMIC EXAMINATION:
- CVS
- RESP
- GIT
- CNS

OBSTRETRIC EXAMINATION

INSPECTION
 Fullness over flanks
 Umbilicus-central?inverted/everted/in level with skin
 Striagravidarum/lineanigra/scars
 Dilated veins or pulsations
 Skin shiny or not
 Hernia orifices and external genitalia
PALPATION
 Symphyseofundal height
 Abdominal girth
 Fundal height corresponds to __ wks

551
Abdominal grips (Leopold’s Maneuvers)

FUNDAL GRIP:
 Soft broad irregular non ballotable mass suggestive of podalic pole-breech
 Smooth,hard and globular balottable mass suggestive of cephalic pole
 No fetal pole can be palpated

UMBILICAL GRIP
 Limb buds are felt in_____,back is felt on______

FIRST PELVIC GRIP: to know presenting part, engagement, bony landmarks

 Head is hard ,round,ballotable,free mobility of head
 Breech is soft,larger,moves with rest of the body,not freely mobile

SECOND PELVIC GRIP

 Vertex:sinciput at higher level than occiput
 Brow:same level(deflexed)
 Face:sinciput lower(extended)

LIQUOR VOLUME: Adequate /not

AUSCULTATION:
 Fetal heart: rate, rhythm, point of maximum intensity(below umbilicus in
cephalic, above in podalic, at level in oblique, in flanks in occipitoposterior)
 Soufflé: funicular/fetal /umbilical: soft blowing murmur synchronous with
FH heard due to rush of blood through umbilical artery
 Uterine: loud,blowing along left side of uterus or all over it due to blood
entering uterine arteries synchronous with maternal pulsation.

SUMMARY:
__yr old GPLA at gestational age of__wks with LMP__and EDC on__admitted
for__with history of__complications with previous FTND/LSCS__years ago.now
regular antenatal check up admitted for___(presenting complaint). On
examination no PICCLE, PR__,BP__ and systems__(WNL). On obstetric
examination__ single live, longitudinal lie, cephalic presentation, with left
occipito anterior with good fetal heart sound and fetal heart rate __

DIAGNOSIS:

552
 NORMAL PREGNANCY
FIRST TRIMESTER
Symptoms:
 Amenorrhea
 Morning sickness at 4-6wks,hyperemesis
 Breast heaviness
 Frequency of micturition
Signs:
 Breast-montgomery’stubercles,increased vascularity
 VAGINA-Jacqeimer’s or chadwick’ssign:bluish hue,8wks
 Osiander’s sign :Pulsations in lateral fornices,8wks
 CERVIX-Goodell’s sign:soft to touch,6wks
 UTERUS-Hegar’s sign:6-10wks
 Piskacek’s sign:12wks,asymmetric growth of uterus
 Palmer’s sign:4-8wks,regular and rhythmic contractions
 Size of uterus
 White discharge per vaginum

SECOND TRIMESTER
 Quickening-18wks(primi),16-18wks(multi)
 Breasts
 Chloasma
 Size of uterus
Signs:
 Skin changes: striae gravidarum, Linea nigra from pubic symphysis to
umbilicus
 Palpate fetal parts by 20wks
 Braxton hicks contractions
 Active fetal movements
 External ballotment by 20 wks
 Fetal heart sounds by 20wks(using steth)

THIRD TRIMESTER
Signs:
 shelving sign(lightening)-36wks

Differential Diagnosis:
 urinary bladder
 fibroid uterus
553
  cystic ovarian tumour
 encysted peritonitis
 pseudocyesis

Investigations:
UPT (read details), hb, PCV, blood grouping and Rh typing, HbsAg, HIV, VDRL,
urine routine examination, GCT

Discussion
 Labour is the process by which products of conception after attaining a period
of viability are separated and expelled from the uterus.
 Mechanism of labour-manner in which fetus adjusts itself to pass through the
partuterine canal with minimal difficulty.
 Cardinal movements of labour:
1.engagement
2.decent
3.flexion
4.internal rotation
5.extension
6.restitution
7.external rotation
 STAGES OF LABOUR
Prelabour:
 lightening
 cervical ripening
 false labour pains
Labour:
First stage - onset of true labour pains to complete cervical dilatation10cm.
Comprises latent phase-cervical effacement and dilatation upto3-4 cm
Active phase-3-4 cm to complete cervical dilatation
Events-
1. uterine contractions
2. cervical changes
3. show
4. formation of lower uterine segment
5. descent of fetus
6. formation of bag of waters and rupture of same
554
 Second stage- Stage of complete dilatation to delivery of baby
Phase 1/passive phase /pelvic phase /phase of descent
Phase 2/active phase /perineal phse /phase of expulsion
Events-
1. descent of head
2. bearing down pains
3. crowning
4. expulsion of fetus

Third stage -stage of placental separation and expulsion.

 Central separation/Schultz method
 Marginal separation/Mathew Duncan method
 ACTIVE MANAGEMENT OF THIRD STAGE OF LABOUR
1. Prophylactic oxytocics after delivery of baby
2. delivery of placenta by controlled cord traction
3. uterine massage

 INDUCTION OF LABOUR
Indications
 Maternal :renal ,liver ds,autoimmuneds,IUFD,lethal malformations
 Fetal: rhesus ds,DM,IUGR,prolonged pregnancy
 Combined:preeclampsia,abruptioplacenta,PROM
1.MEDICAL METHODS
 prostaglandinsPGE2 , PGE1analogue
 antiprogesterones-mifepristone
 Oxytocin
2.SURGICAL METHODS
 Artificial rupture of membranes
3.MECHANICAL METHODS
 Extra amniotic saline instillation
 Stripping of membranes
4.OTHERS
 Relaxin,
 NO donors
 Admissiontest: continuous CTG monitoring for 20min on admission
to labour ward
 CTG:
555
  earlydeceleration-head compression
 variable deceleration-cord Compression
 late deceleration-uteroplacental insufficiency
 EXCELLENT DATES:
 Regular cycles
 3 normal cycles before LMP
 Dating scan corresponds to LMP

 CARDIFF COUNT: women asked to count upto 3 fetal movements in an hour

after 3 meals per day…(.normal-above 10 movements in 12hr period)
 Fetal BIOPHYSICAL PROFILE: (BATMAN)
 B-Breathing movement
 A
 T-tone
 M-movement
 A-amniotic fluid volume
 N-non stress test
 NST and amniotic fluid volume-modified biophysical profile

TO READ:
 antenatal care
 Antepartum surveillance: Cardiffcount, NST, biophysical profile, ultrasound,
CTG
 Partogram
 Pelvis, foetus, foetopelvic relations

556
 MULTIPLE PREGNANCY
H/O Present Pregnancy:
 When was she diagnosed to have twins
 Findings of first and second trimester scans
 Whether the growth of the two foetuses is satisfactory in repeat scans
 Hyperemesis
 Exaggeration of minor symptoms of pregnancy
 Excessive fetal movements
 Pressure symptoms like ankle edema,varicose veins and haemorrhoids
 Pain in polyhydramnios
 h/o threatened preterm labour
 h/o antepartum haemorrhage
 h/o raised blood pressure
Obstretric History:
 Previous h/o twinning
Gynaecological History:
 h/o infertility
 use of ovulation inducing drugs like clomiphene or gonadotrophns
 conception following assisted reproductive technology
Past History:
 h/o pregestational diabetes in polyhydramnios
Personal History:
 increasing age, ethnicity (increased in Africans and least
in orientals)
Family History:
 twinning in family

General examination:
 pallor,
 ankle edema,
 varicoseveins,
 haemorrhoids,
 hypertension due to associated preeclampsia
Obstretric examination:
 Overddistended uterus
 Shiny tense appearance if there is associated polyhydramnios
 Symphyseofundal height more than expected
 Abdominal girth increased
 Palpation of multiple fetal parts(unless there is associated severe
557
 polyhydramnios
 Palpation of more than two fetal poles or two fetal heads
 Malpresentations
 Two fetal hearts with different rates heard by two different examiners
Simultaneously

MANAGEMENT:

FULL TERM FOR TWIN PREGNANCY IS 38WKS

Antepartum management:
 prophylactic iron and folic acid
 Prophylactic steroids as risk of preterm labour or IUGR
 Frequent antenatal visits
 Ultrasound at 9-11wks
 Targeted anomaly scan at 20wks
 3rd trimester-4 weekly scans necessary
Intrapartum management:

 indications for elective caesarean section:

 1st twin presenting as non-vertex
 Monoamniotic twins
 Severe IUGR
 Chronic TTS
 Conjoined Twins At Term
 Previous Caesarean Section
 Obstretric Factors Necessitating Caesarean
VAGINAL DELIVERY:
 IF FIRST TWIN VERTEX
 Done at 38 wks
 After delivery of first twin,IV ERGOMETRINE not given-can cause
entrapment and asphyxia of second twin
MANAGEMENT OF SECOND OF TWIN:
 Vertex:vaginal delivery
 Breech:assisted breech delivery
 Transverse lie:
 do external version
 Then, if vertex-vaginal delivery
 Breech-assisted breech delivery
 If unsuccessful, and ruptured membranes-caesarean section
558
  Intact membranes-internal podalic version and breech extraction

MATERNAL COMPLICATIONS:
ANTEPARTUM: code- (HPA)2
 Hyperemesis
 Hydramnios
 Preecclampsia
 Pressure symptoms
 Anemia
 Antepartum hemorrhage
INTRAPARTUM: code- DR.MOP
 Dysfunctional labour
 Retained placenta
 Malpresentations
 Increased operative delivery
 Postpartum hemorrhage
FETAL COMPLICATIONS:
ANTEPARTUM: code- PrISM TV & AC
 Prematurity
 iugr
 single fetal demise
 monochorionic monoamniotic twins
 twin twin transfusion syndrome
 vanishing twin congenital anomalies
 acardiac twins
 conjoined twins
INTRAPARTUM: code-PAPI
 Prom
 abruption of second twin
 prolapse of cord
 interlocking of twins

SINGLE FETAL DEMISE

 In monochorionic twins, 25% risk of co-twin death & 25% risk of
neurological damage.
 When 1 twin dies, there is sudden acute shift of blood from surviving twin
into dead fetus along the anastomosis. : Acute twin twin transfusion
syndrome.
559
  Management:
 Dichorionic –conservative
 Monochorionic- iffetal maturity: delivery
if premature: not clear. Intensive antepartum fetal surveillance-MCA
dopppler, antiD
MONOCHORIONIC MONOAMNIOTIC TWINS
 Main problem- late IUD due to cord entanglement.
 Best diagnosed in 1st trimester.
 Colour Doppler to detect cord entanglement, serial ultrasounds for TTTS,
antenatal corticosteroids , elective CS @ 34-36 wks
TWIN TWIN TRANSFUSION SYNDROME
 In monochorionic placentation, due to arteriovenous anastomosis with
unidirectional blood flow
 Donor on arterial side—hypovolaemic IUGR, poor renal perfusion,anuria,
severe oligohydramnios
 Recepient twin—hypervolaemic polyuria, polyhydramnios, congestive
cardiac failure,hydrops death
 Prediction:- increased NT, infolding of intertwine membrane at 15-17 weeks
 Ultrasound diagnosis:- discordant fetal size, stuck twin sign, arterial Doppler
abnormality in donor twin, venous Doppler in recipient twin,
 QUINTERO STAGING SYSTEM.
Stage 1 – oligo and polyhydramnios with bladder of donor visible
Stage 2—bladder of donor no longer visible
Stage 3—critically abnormal Doppler in either twin
Stage 4—hydrops in one or both twins
Stage 5—demise of one or both twins
 Management:-after delivery, exchange transfusion
 serial amnioreduction,
 septostomy,
 fetoscopic laser ablation of anastamosis
 selective feticide by ultrasound guided bipolar coagulation of
the cord
VANISHING TWIN
Spontaneous cessation of cardiac activity in a previously viable fetus of multiple
gestation.
560
When fetal death occurs after 1st trimester  thin parchment like body  fetus
papyraceous.
No effect on mother or viable fetus, some cases vaginal bleeding.

ACARDIAC FETUS
Normal twin  pump twin
Artery to artery anastomosis in placenta takes deoxygenated blood of pump twin
in retrograde direction through umbilical arteries of acardiacfetus.-minimal
oxygen extracted by lower part upperpart poorly formed-
Fully deoxygenated blood back to placenta by umbilical vein. Vein to vein
anastomosis to pump twin.
TWIN REVERSED ARTERIAL PERFUSION SEQUENCE (TRAP).
Pump twin---high output cardiac failure, hydrops, polyhydramnios, fetal death.
Varieties Acardiacacephalus, acardiacmyelacephalus, acardiac amorphous.
ULTRASOUND IN MULTIPLE PREGNANCY
 Early diagnosis
 Determination of chorionicity
 Prenatal diagnosis of anomalies
 Assessment of cervical length
 Serial scans for fetal growth
 Presentations at term
 Intrapartum assessment of second twin
 Dx & Mx of TTTS and single fetal demise
 Selective feticide and multifetalpreg reduction

HYPEREMESIS GRAVIDARUM
Causes
 Endocrine:- hCG, oestrogen
 Infection:-h pylori
 Upper GI dysmotility smooth ms relaxation due to high progesterone
 Psychological
 Others: liver dysfunction, altered lipid metabolism, immunological theory
Management
1.Supprtivehospitalisation, iv crystalloids, stop oral feeding- slowly reintroduce
as reponds, vitamins- thiamine 100mg
561
2.ANTIEMETICSdoxylamine 10mg orally OD, Metoclopramide 10 mg orally 4
times. Parenteral promethazine or
metoclopramide.3.Pyridoxine4.Methylprednisolone
5.Lifestyle and diet changes
6.Alternatives-psychotherapy

POINTS TO REMEMBER:
 Incidence of twins: 1% of all pregnancies. Incidence calculated by Hellin’s
rule ( Twins- 1 in 80, triplets- 1 in 802, quadruplets- 1 in 803...)
 Term for MCMA twins is 32-34wks
 TRAP phenomenon occurs in acardiac twins
 Study of twinning-gemellology
 Chorionicity is the type of placentation determined by ultrasound
prenatally, examining the membranes postnatally
 Zygosity-type of conception
 Gonadotropin therapy cause twinning in 20-40%cases while clomiphene
cause twinning in 5-6%
 Most common combination of presentation at term: vertex-vertex (60%)
 Features of Dichorionicity:
2 sacs
2 placenta
Twin peak sign
>2mm thickness of intertwine membrane

562
 MALPRESENATIONS

BREECH
H/O Present Pregnancy
 Overdistension and stretching in polyhydramnios
 Details of anomaly scan (association of anomalies and breech)
 Details of a low lying placenta if known
 Any obstretric or medical complications necessitating caesarean
 External version already performed and failed or breech having reverted
Obstretric History
 Multiparity
 Previous h/o breech presentation
 Previous caesarean
Gynaecological History
 Previous suggestion of uterine anomalies or fibroids on ultrasound or
hysteroscopy
 Previous menorrhagia or pressure symptoms suggesting fibroids
 Periods regular or not

GENERAL EXAMINATION:
 Pallor(due to associated antepartum haemorrhage)

OBSTRETRIC EXAMINATION
 Abdominal wall laxity
 Lie is longitudinal
 Fundal grip reveals a hard ballotable mass
 Head in midline and not freely ballotable in extended breech
 Fetal heart is heard above the umbilicus
 Head slightly to one side and freely ballotable in flexed breech
 First pelvic grip reveals a soft broad non-ballotable mass
 Breech may feel very broad and irregular in flexed breech
 Breech may be slightly compact and ballotable in extended breech
 Liquor(associate poyhydramnios or oligohydramnios)
 Abnormal uterine shape may be made out sometimes

VAGINAL EXAMINATION
 Cervix may be hanging loose and not applied to the presenting part
 Bag of membranes conical in flexed and footling breech
563
  Evaluate for cord prolapse if membranes are absent
 Evaluate for cord presentation if membranes are intact
 Presenting part will be soft
 Flexed breech-both feet,buttocks,ischialtuberosities,anus and sacrum
 Extended breech-feet will not be felt
 Footling breech-only the feet(rest will be high up)
 Evaluate fro cervical fibroid
 Careful assessment of pelvis

MANAGEMENT:

ULTRASOUND IN BREECH DELIVERY:

 Confirms the presentation and type of breech
 Rules out anomalies
 Rules out placenta previa
 Rules out stargazing fetus
 During external cephalic version

TERM BREECH:
ELECTIVE CS, indications
 All complicated breech pregnancies
 Contracted pelvis
 Large babies(>3.5kg)
 Severe IUGR
 Preterm breech(<1.5kg)
 Stargazing fetus
 Footling or knee presentation
 Majority of flexed breech

EMERGENCY CS, indications

 Cord prolapse
 Failure to progress
 Maternal or fetal indication
 Impacted breech

External Cephalic Version:

 Done at 36wks
 Flexed breech preferred
 Performed at term(39wks) and using tocolysis is safe in uncomplicated
Breech
564
METHODS OF VAGINAL DELIVERY:
 Spontaneous breech delivery
 Assisted breech delivery
 Breech extraction

Mechanism of labour
Delivery of breech

1. Engagement in the left oblique diameter

Engaging diameter is bistrochanteric 9.5cm

2. descent with increasing compaction

3. Internal rotation by 1/8th of circle so anterior buttocks lies behind pubic
symphysis
4. Lateral flexion
5. Delivery of trunk and limbs
6. Restitution of buttocks

Delivery of shoulders

1. Engagement in the left oblique diameter

Engaging diameter is bisacromial 12cm

2. Internal rotation of shoulders by 1/8th of circle

3. Birth by lateral flexion
4. Restitution of shoulders

Delivery of head

1. Engagement in Right oblique diameter

Engaging diameter is suboccipitofrontal

2. Descent by increasing flexion

3. Internal rotation so that sagittal suture lies in the anteroposterior diameter
of pelvis
4. Birth by flexion

565
ASSISTED BREECH DELIVERY:
 Indications for vaginal delivery:
 Extended breech
 Average size fetus with no fetopelvic disproportion
 Well flexed head on ultrasound
 No maternal or fetal indication for caesarean section
 Spontaneous onset of labour
 Femoropelvicgrip:baby should be held with forefingers in the groins and
thumbs over the sacrum
 Lovset’smanoeuvre:for delivery of extended arms
 Delivery of after coming head:
 Burns marshall manoeuvre
 Mauriceau smellie veit manoeuvre
 Piper’s forceps for after coming head
 Prague manoeuvre-in chin to pubis rotation

BREECH EXTRACTION:
Done under general anesthesia
 indication:
 Fetal distress
 Maternal distress
 Cord prolapse

566
TOPICS TO READ:
 Assisted breech delivery
 External cephalic version
 Types of breech
 Etiology
 Complications of breech delivery
 Difference between flexed and extended breech
 Problems of breech delivery
FLEXED BREECH EXTENDED BREECH
 Commoner in multipara  Commoner in nullipara
 Head is felt to one side and is  Head is in midline and less
ballotable ballotable(splinting action of legs)
 Breech is broad and bulky  Breech is compact
 Breech is usually mobile  Breech may be engaged
 Fetal heart sounds heard above  May be lower down due to
the umbilicus engagement
 Feet felt along the buttocks  Only buttocks felt on vaginal
on vaginal examination examination
 More chance of cord prolapse  Less chance of cord prolapsed
(6%)
 Limbs may slip out before  Unlikely to occur
full dilatation

POINTS TO REMEMBER:
 Incidence of breech at term-3-4%, at 28wks-25%
 Most common cause is prematurity
 Recurrent breech occur in congenital uterine anomalies
 Main cause of perinatal mortality in breech-
prematurity,congenital anomalies, birth asphyxia due to cord
prolapse,birth trauma
 Extended breech is commonest(65%) because extended legs prevent
spontaneous version

TRANSVERSE LIE:
OBSTETRIC EXAMINATION:
 Abdomen is transversely stretched
 Fundal height is less than the period of gestation
 No fetal pole at the fundus
567
  Ballotable head in one flank and breech in the other
 In dorsoanterior,back is felt as a uniform resistance across the front of
the abdomen
 In dorsoposterior,limbs are felt anteriorly
 Empty pelvic grip

VAGINAL EXAMINATION:
 Conical bag of membranes with very high presenting part
 Hand/shoulder/elbow may be felt
 Identify shoulder by ribs running parallel to each other
 Late in labour,shoulders may be wedged in the pelvis and a hand
frequently prolapses into the vagina
 The thumb of the prolapsed hand,when supinated,points to the head
DIAGNOSIS: by ultrasound
There is no mechanism of labour in transverse lie

NEGLECTED SHOULDER PRESENTATION: bandl’s ring or pathological retraction

ring. managed by CS

MANAGEMENT:
 CS is best option
 External cephalic version may be tried at term or in labour(if membranes
intact and not contrindicated) with stabilising induction

568
 MOBILE HEAD AT TERM IN NULLIPARA
H/O Present Pregnancy
 Is she really term(accuracy of menstrual period, pregnancytest, early
 clinical examination, early scan to confirm dates)
 Ultrasound scans(whether a low lying placenta, fibroid, hydrocephalus)
 h/o ante partum haemorrhage
 h/o gestational diabetes leading to macrosomia and hence CPD
 low backache in late gestation and predominant back pain at the onset
of labour suggests an occipitoposterior position

Previous Obstretric History In Multipara

 H/O CPD in previous delivery
 Birth weights in previous deliveries
 Duration of labour
 Any perineal damage during delivery like 3rd degree perineal tear

Gynaecological History
 Periods regular or not(to double check dates)
 History of infertility(may modify management)
 Previous scans showing fibroid
 Menorrhagia-fibroid

Previous Medical And Surgical History

 Tuberculosis, polio, rickets, osteomalacia-CPD
 Fractures especially involving pelvis or hip joints in the past-CPD
 Corrective surgery such as for congenital dislocation of hip-CPD
 Any endocrine or metabolic cause for short stature such as
hypopituitarism- CPD

Personal History
 Dietary history in case of short stature(associated nutritional deficiency)
 Low socioeconomic status-nutritional deficiency

Family History
 obstetric career of mother and sisters in case of short stature

GENERAL EXAMINATION
569
  Stature
 Weight
 Prepregnant BMI
 Pallor associated with poor nutrition
 Waddling or limping gait
 Spine normal or evidence of kyphosis,scoliosis or compensatory lordosis
 Any lower limb deformity or shortening

OBSTRETRIC EXAMINATION
 Full bladder to be excluded prior to examination
 Pendulous abdomen may suggest CPD
 Subumbilical flattening, shoulders in flanks, limbs readily palpable and
fetal heart in the flanks suggest occipitoposterior position
 Sinciput and occiput palpable at same level suggestive of deflexed head
 Symphseofundal height may be more in macrosomnia, tumours and
polyhydramnios
 Excess liquor in polyhydramnios
 Estimated fetal weight may be increased in macrosomia
 Any palpable fibroids

VAGINAL EXAMINATION
 Evaluate pelvis,presentingpart,cervix
 Munrocker-muller method

DISCUSSION
CAUSES
 Wrong dates
 Full bladder
 Occipitoposterior
 Cephalopelvic disproportion
 Malpresentations
 Tumours in lower segment of uterus
 Placenta praevia
 Cord around the neck
 Tumours of fetal neck
 Polyhydramnios
 Hydrocephalus
 Multiple pregnancy

570
MANAGEMENT OF OCCIPITO POSTERIOR
 WELL FLEXED HEAD: Head rotates through 3/8 circle and baby born
occipitoanterior but prolonged labour
 DEFLEXED HEAD: occurs in ANTHROPOID PELVIS. rotates through 1/8
circle. Baby born face to pubis.
FAILURE TO ROTATION results in :
 Persistent Occipitoposterior
 deep transverse arrest

MECHANISM OF LABOUR IN OCCIPITOPOSTERIOR

Engaging diameters
 Suboccipitofrontal (10.5 cm) in deflexed head
 Occipitofrontal (11.5 cm) in a head, which is further deflexed
Course of labour
1. Anterior rotation
2. Posterior rotation and face to pubis delivery
3. Failure of rotation

Reasons for failure of rotation:

 deflexion of head
 Ineffective uterine contractions
 Weak pelvic floor
 Pendulous abdomen and poor tone
 CPD and android pelvis

DEEP TRANSVERSE ARREST: Occur in androidpelvis. head is arrested with

the sagittal suture in the transverse diameter at the level of the ischial
spines
Management of deep transverse arrest:
 Caesarean section
 Vacuum extraction(posterior cup for occipitoposterior position)
 Forceps:keilland”s forceps
 Manual rotation

CEPHALOPELVIC DISPROPORTION: Disparity in the relationship between the

pelvis and the fetal head

CLASSIFICATION OF PELVIS
1. Gynaecoid pelvis: normal female pelvis
2. Anthropoid pelvis: ape like pelvis
3. Android pelvis: male type
571
 4. Platypelloid pelvis: flat pelvis

TYPES OF CONTRACTED PELVIS

Contraction of: 1) pelvic inlet, 2) midpelvis, 3) pelvic outlet

MUNRO KERR MULLER METHOD

Patient in modified dorsal position. Left hand over abdomen pushes the head into
pelvis. Fingers ot the other hand inserted vaginally, estimate whether vertex
reaches the level of ishial spines.
 Head can be pushed down to the level of the spines: No disproportion
 Head can be pushed down a little, but not upto the level of spines: First
degree CPD
 Head can't be pushed down at all: Second degree CPD
Disadvantages: Only helpful in active labour, not useful to detect midpelvic or
outlet contraction

MANAGEMENT OF CPD
1. Elective caesarian section
2. Trial of labour
In CPD, a trial is said to be successful, if it results in the birth of a healthy
baby vaginally with the mother in good condition. Delivery by caesarian
section or delivery of a dead or deeply compromised baby is considered as
failed trial.
 Selection of patients: Suspected minor or first degree CPD with no other
complications
 Monitoring progress: Partogram, PV every 4 hrs, abdominal palpation,
cardiotocography
 Augmentation of labour: Amniotomy when patient is in active labour,
oxytocin in nullipara
 When to terminate trial by emergency CS
 No progress in cervical dilatation even after oxytocin
augmentation
 Failure of descent of head
 Excessive moulding and caput
 Fetal or maternal distress

572
 DIABETES COMPLICATING PREGNANCY
H/O PRESENT PREGNANCY
 Planned or not
 preconceptional folate taken or not
 preconceptional glycemic control in pregestational diabetes
 infections like vulvovaginits or UTI
 anomaly scan
 third trimester scans, growth
 prepregnancy weight (BMI)
 weight gain
 diet control or insulin
OBSTETRIC HISTORY
 previous history of gestational diabetes
 whether on MNT or insulin in that pregnancy
MENSTRUAL HISTORY
 periods regular or not
 repeated vulvovaginits
 contraceptive use
PAST MEDICAL AND SURGICAL HISTORY
 evidence of retinopathy, nephropathy, vasculopathy in pregestational
diabetes
 whether the diabetes was well controlled before pregnancy
 on insulin or oral hypoglycemic drugs before pregnancy
PERSONAL HISTORY
 diet in detail
 exercise during pregnancy
FAMILY HISTORY
 family history of diabetes

GENERAL EXAMINATION
 obesity ,BMI
 BP and pedal edema ( pre eclampsia is more in diabetes)
 Features of PCOS like hirsuitism, acne and acanthosis nigricans
 Complications of pregestational diabetes like retinopathy, vasculopathy
573
OBSTETRIC EXAMINATION
 Symphyseofundal height is usually increased either due to macrosomia or
polyhydramnios or both
 IUGR may occur in pregestational diabetes with vasculopathy

LOCAL EXAMINATION
 Evidence of vulvovaginits

MANAGEMENT
Investigations

SPOT/ONE STEP ADA TWO STEP

At first visit or 14-16 At 24-28 weeks 75g 50g GCT

weeks OGTT
If 1hr PPBS >140mg/dl,
75g glucose given in After 8 hrs fasting
Do 100g GTT after
300ml water irrespective
fasting
of time o last meal
Diagnosis made if any 1
value
Diagnosis made if any
If 2hr PPBS>140mg/dl
FBS> 92 mg/dl two values:
start MNT
1hr PPBS> 180 FBS> 95
If 2hr PPBS > 200mg/dl
start insulin 2hr PPBS> 153 1hr PPBS >180

2hr PPBS >150

3hr PPBS > 140

MEDICAL MANAGEMENT
● Patient education
● Strict glycemic control
574
  MEDICAL NUTRITIONAL THERAPY (MNT)
MEDICAL NUTRITIONAL THERAPY (MNT)
 30 Cal/kg/day divided into 3 meals and 3 snacks
 40 Cal/kg/day for overweight
 24 Cal/kg/day for underweight
 Food rich in fibre, protein, low in fat
 40-45% carbohydrate
 <35% fat
 15-20% protein
 Add vegetables and avoid refined sugar
 Calorie calculated according to prepregnancy weight
 Exercise 20 mins daily (upper body exercise )
 Trial of MNT given for 1 week, follow up with FBS and PPBS every 3 days
 Monitoring at home by glucometer
 Insulin started if FBS >90 mg/dl ,PPBS >120mg/dl
 Basal bolus regimen : 3 premeal injections of short acting insulin and
intermediate or long acting insulin at bedtime
 Mixture of intermediate acting and long acting insulin 70:30 giving 2/3 at
morning and 1/3 at night
 At home self monitoring with glucometer, signs of hypoglycaemia

OBSTETRIC MANAGEMENT
ANTEPARTUM
 ANC every 2 weeks , check blood sugar
 3rd trimester regular ultrasound monthly to assess fetal well being and
liquor volume
 Antepartum fetal surveillance from 32 weeks
INTRAPARTUM
 Termination of pregnancy
 If on insulin terminate at 38 weeks
 If on MNT can wait upto 40 weeks
 Labour : CS not indicated (unless fetal weight >4kg), continuous CTG
monitoring, anticipate shoulder dystocia if fetal weight by USG >4kg
 Partogram
 CTG ,
575
  RBS, urine ketone body

 Indications for CS
 Macrosomia
 Maternal /fetal complications
 Failure to progress
 Intrapartum glycemic control
 Morning dose of insulin skipped if induction /CS
 Hourly capillary blood sugar taken , if <100mg/dl no insulin required

 Insulin given as infusion in NS or RL using calibrated INSULIN PUMP (1-

1.5 U/hr) ideally
Here if RBS is 100-140 mg/dl, give NS
If >140 give 0.5 units/kg Insulin IV and maintain RBS at < 100 mg/dl

 Neonate
 Early cord clamping
 Monitor for 1st 48 hrs
 Check blood sugar (neonatal hypogylcemia)
 Watch for hypocalcemia

POSTPARTUM
 Prophylactic antibiotics
 75g GTT done at 6 weeks postpartum
 Barrier contraception preferred
MATERANAL COMPLICATIONS
5Ps + ckit
 Preeclampsia
 Preterm labour
 Polyhydramnios
 PROM
 Puerperal sepsis
 Increased chance of CS
 Ketoacidosis
 Infections : vulvovaginits ,UTI
576
  Genital tract trauma
 Worsening of diabetic retinopathy and nephropathy in overt diabetes

FETAL COMPLICATIONS
 Abortion
 Congenital anomalies
 Unexplained inytauterine death
 Prematurity
 Macrosomia
 Shoulder dystocia

NEONATAL COMPLICATIONS
 Respiratory distress syndrome
 Hypoglycaemia
 Hypocalcemia
 Hyperbilirubinemia
 Hyperviscosity
 Polycythemia
 Birth trauma

TOPICS TO READ
 Diabetogenic state of pregnancy
 Definitions
 Gestational diabetes is defined as carbohydrate intolerance of variable
severity with onset or first recognition during the present pregnancy
 Pederson hypothesis
 Risk factors for GDM
 GCT,GTT
 Monitoring of blood glucose
 Contraception in GDM
 Overt diabetes and DKA
 Shoulder dystocia, shoulder dystocia drill
 HELPERR
Points to remember
 In overt diabetes:
577
  Preconceptional counselling
 Tight glycemic control
 Planes pregnancy
 Preconceptional folic acid
 HbA1C< 6 before planning pregnancy
 Turtle sign : failure of restitution due to shoulder dystocia

MAJOR BIRTH DEFECTS

CNS SKELETAL RENAL CVS GIT OTHERS

Anencepha Sacral Renal VSD Duodenal Single

ly agenesis agenesis atresia umbilica
ASD
l artery
microceph /caudal Hydronephro Anorectal
TGA
aly regressio sis atresia
n Coarctation
Double Omphaloco
syndrome of aorta
ureter ele
TOF
Polycystic Tracheo-
(most kidney Hypertrophic eosophagea
specific) disease cardiomyopa l fistula
thy

578
HYPERTENSION COMPLICATING PREGNANCY
Presenting Complaints:
 Ankle edema ,oedema over face,abdominalwall,vulva
 Symptoms of imminent eclampsia -headache,blurring of vision,epigastric
pain,vomiting
 Decreased urine output
 h/o seizures
H/O Present Pregnancy:
 is it multiple pregnancy?
 Whether 3rd trimester scans show IUGR
 Rh status
 Is she on low dose aspirin or heparin?
Previous Obstretric History:
 Previous h/o ecclampsia or preeclampsia
 Previous h/o abruption
 Previous h/o early onset preeclampsia
 Gestational age delivery and mode of delivery
 h/o previous pregnancy loss and early onset preeclampsia(APLA
syndrome)
Gynaecological History:
 Irregular cycles and hirsuitism(PCOD predisposes to preeclampsia)
 New partner
Previous Medical Or Surgical History:
 Chronic renal disease, hypertension antedating pregnancy, previous arterial
or venous thrombosis (thrombophilias) SLE, diabetic nephropathy
Personal History:
 Smoking and use of drugs like cocaine
Family History:
 h/o hypertension or preeclampsia
 h/o coronary heart disease,deep vein thrombosis etc..

General Examination:
 oedema over face, abdomilal wall, vulva
 swelling of fingers
 carpal tunnel syndrome
 pretibial oedema
 obesity
 hirsuitism, acne, acanthosis nigricans-PCOD
 deep tendon reflexes-ecclampsia
579
  blood pressure
 cardiovascular examination-rule out causes of secondary hypertension
Abdominal Examination:
 enlarged and tender liver-HELLP syndrome

Obstretric Examination:
 symphyseofundal height less than expected-IUGR, oligohydramnios
 size more than expected-hydatiform mole
 multiple pregnancy and fetal hydrops -increased chance of preeclampsia

DISCUSSION
Hypertension in pregnancy: systolic BP >140 or diastolic >90 on 2 occasions taken
6hrs apart.
Classification :
1. Gestational HTN: detected after 20wks, returns to normal in 12wks
postpartum.
2. Preeclampsia: GHTN + proteinuria (>300mg/24hrs- dipstick 1+)
3. Eclampsia : preeclampsia + seizure
4. Chronic hypertension: HTN antedating pregnancy / detected before 20
weeks, persisting after 12 weeks postpartum
5. Chronic HTN with superimposed preeclampsia: exacerbation of HTN + new
onset proteinuria

Basic Etiopathogenesis :
 Endothelial dysfunction & vasospasm- defective placentation and abnormal
trophoblastic invasion (read in detail)
 Placenta: acute atherosis
 Kidney: glomerular dysfunction and glomerular endotheliosis

Complications
Maternal Fetal
A ARDS, Abruption Prematurity
B Cortical Blindness IUGR and oligohydramnios
C Cerebral hmrg, sudden postpartum IUD
Collapse
D DIC
E Eclampsia, Pulmonary Edema
F Failures- hepatic, renal
H HELLP, Hemorrhage

580
MANAGEMENT:
INVESTIGATIONS:
Renal Funtion Test (RFT)
 24 HR Urine Protein
 Pus ,Cast
 Serum uric acid
 Blood urea creatinine

Liver Function Test

 SGOT/PT (>70U/L-significant; >150-risk of maternal morbidity)
 Bilirubin (>1.2mg/dl in HELLP)

Hematology
 PCV elevated
 Peripheral Smear: schistocyes, burr cells, fragmented RBCs
(microangiopathic hemolysis)
 Lactate Dehydrogenase(LDH); >600U/L in HELLP
 Thrombocytopenia (<100000/mm3 in HELLP)
 Prolonged Prothrombin Time (PT) & APTT
Fundoscopy

Antepartum monitoring:

Mother
 Daily weight
 Daily BP
 Daily dipstick proteinuria
 PCV, Platelet, RFT, LFT x twice weekly or more frequently in
severe cases
Fetus
 Fetal movement count: just after food lie in left lateral position: 3
kicking movement/hr
 USG
 Doppler: Uterine Artery Doppler at 20-22 weeks- persistent notch
suggest pre-eclampsia
 NST and AFI (biophysical profile) twice weekly

Prophylaxis
581
  Low dose aspirin 75mg for high risk women starting at 12 weeks
and stop at 34-36 weeks
 Calcium supplementation
 FA
TREATMENT

Definitive treatment: Termination of Pregnancy

Anti- Hypertensive Therapy :
 Tab. Labetalol 100mg BD (max upto 200 TDS)
 Tab. Nifedipine 10mg TDS/QID
 Other drugs- alpha methyl dopa (not given due to CNS depression ) and
Hydralazine
ACE, ARBs and Atenololl are CONTRAINDICATED

Mild Pre-Eclampsia:
 Antihypertensives
 Terminate at 37-38 weeks

Severe preeclampsia
BP>160/110 mmHg
Proteinuria >5g/24hr
 Antihypertensives
 Antenatal steroids to accelerate lung maturity and terminate at 34 weeks(
earlier if at risk)
 Expectant management to prolong pregnancy

Indication for immediate termination:

 Uncontrolled hypertension/ increasing organ dysfunction
 Imminent eclampsia/ eclampsia
 Abnormal LFT/RFT/coagulation profile
 HELLP
 Fetal distress
 Abruption
 Severe IUGR
Intraparum
 Maintain diastolic BP at 110mmHg

Acute Management Of Severe Hypertension:

 2mg/min IV Labetalol infusion or S/L Nifedepine
582
  Fluid Management: 80ml/hr or 1ml/kg/hr
 Prophylactic MgSO4 may be given
 Management of HELLP syndrome
 Monitor oxygen saturation
 Central venous line (pulmonary edema)

Obstetrics
Vaginal deliver preferred. Can be induced
Indication for CS:
1. Obstetrics indications
2. Failed induction
3. Worsening maternal and fetal condition

 Continuous CTG monitoring:

uterine hyperactivity, recurrent late/ variable deceleration: suggest
abruption
 Monitor uterine output: catheterise bladder (≥100ml/4hr)
 Epidural anaesthesia (if given inform anesthetist as MgSO4 have synergistic
action with muscle relaxants)
 Cut short 2nd stage of labour

Postpartum
 PPH
Oxytocin/ PGF-2 alpha
Fluids and blood
 Monitoring
Monitor haematological and biochemical parameters
Pulmonary edema
Close monitor for next 48hrs at least
MgSO4 continued for 24 hrs
 Thromboprophylaxis – anticoagulants DVT
 Avoid alpha methyl dopa (cause CNS depression)
 Antihypertensives continue and reduce dose. Subside by 6-8 weeks
postpartum

Long term
Counselling
1. Recurrence risk in next pregnancy
2. Aspirin prophylaxis
583
 3. Scrren for APLA syndrome and thrombophilias
ECLAMPSIA
Phases
1. Prodromal phase:
Aura. Convulsive movements around mouth
2. Tonic
Body gets rigid, face contorted, res[iraion ceases
3. Clonic
Grandmal convulsions: facial muscles to entire body, frothing
4. Recovery
Respiration resumes. Pass into coma(variable duration)
DD’s
 Epilepsy
 CVA
 Meningitis, encephalitis, cerebral malaria
 Metabolic disturbances
 Cerebral venous thrombosis

Indicators of bad prognosis

 Long interval between seizures
 Late referrals
 Coma
 Raised BP
 Impaired RFT/LFT/HELLP syndrome

MANAGEMENT
1. General Management
 Left lateral position; manage ABC
 Open airway, suction
 Oxygen
 IV Line (RL)
 Mouth gag
 Monitor- pulse oximetry and urine output
2. Medical Management
 Antihypertensives:
For eclampsia / impending Eclampsia : IV Labetalol 20mg slow IV in
5ml saline →after 20 mins, BP uncontrolled: 40mg IV → Next 20 min,
BP uncontrolled: repeat 80mg IV (max dose= 220mg/hr)
 Anticonvulsants :
MgSO4
584
MgSO4(magsulph)
MoA : peripheral action at neuromuscular junction by competing wit Ca
for entry to cells.
Dose:
KGOF Regimen
 4g 20% solution IV loading dose over 5 mins
 4g as 2g each buttocks deep IM
 1g/hr infusion x 24 hrs postpartum/24hrs from last seizure
whichever is last
Pritchard’s Regimen:
 IM Regimen
Loading :
 4g 20ml 20% solution slow IV over 10 mins (irrespective of RFT)
 5g 10mL 50% solution each buttock deep IM (persistent
convulsions repeat after 15 mins upto 2 g more 20% solution @
<1g/min)
Maintenance:
 5g 10ml 50% solution alternate buttocks every 4hrs x 24hrs
postpartum/ last seizure whichever is last (alter dose in case of
abnormal RFT)
 IV Regimen
Loading :
 4-6g 20% solution in 100 ml IV fluids over 15-20 mins

Maintenance:
 2g/hr in 100ml IV maintenance solution

Therapeutic level of MgSO4 – 4-8mEq/L. Monitor :

 Patellar reflex
Absent-blood level : 10mEq/L
 Urine output
≥100ml/hr is normal. <30ml/hr be alert
 RR
>16/min is normal. <12 be alert.
585
 Respiratory arrest- blood level : 12mEq/L
Anyone deranged
 Skip next dose
 Monitor SpO2 (<95% significant)
 Stop infusion, give Oxygen
 Antedote : 10ml 10% calcium gluconate / CaCl2 IV
 Respiratory arrest: provide CPR

CTG: small beat to beat variability

Hypomagnesemia at delivery – neonatal depression

Contraindications:
 Myasthenia gravis
 Recent MI

3. Obstetric Management
Terminate after control.
Indication for LSCS:
 Uncontrolled
 Worsening maternal condition
 Delivery not possible in 6-8 hrs

Read :
 features of severe preeclampsia
 Prediction of preeclampsia
Mean arterial pressure (>105 is significant)
Gants roll over test
Uterine artery Doppler
 Angiotensine sensitivity lest
 HELLP syndrome

586
 CARDIAC DISEASE IN PREGNANCY
Presenting Complaints
 Dyspnoea at rest/routine activity/moderate exertion/severe exertion
 Since when did she have dyspnoea at rest?
 Orthopnoea
 Paroxysmal nocturnal dyspnoea
 Cough with haemoptysis
 Palpitations
 syncopal attacks
 Precipitating factor like respiratory infection or rheumatic reactivation
 Was she asymptomatic and detected on routine antenatal check up?
 On drugs like digoxin,beta-blockers,diureticsetc?
 On anticoagulation like heparin or warfarin and details of monitoring
 Any surgical procedure in pregnancy like balloon valvuloplasty?
H/O Present Pregnancy
 Associated hypertension,anemia and other pregnancy complications
 Is it a multiple pregnancy?
 Details of anomaly scan and ECHO(In mothers with congenital heart
disease)
Obstetric History
 Did she have heart disease in previous pregnancies?
 Was she symptomatic and on medication?
 Has she gone into heart failure?
 When was she hospitalised in that pregnancy?
 Was she advised surgery before she embarked on a second pregnancy?
 Was she told it was best to avoid a second pregnancy?
Gynaecological History
 Periods regular or not
 Contraceptive usage?

Previous Medical And Surgical History

 Rheumatic fever in childhood
 On antibiotic prophylaxis or not
 Previous history of cardiac failure prior to pregnancy and precipitating
factors
 Was she on medication prior to pregnancy?
 h/o closed surgery or balloonvalvuloplasty prior to pregnancy
 h/o open heart surgery and valve replacement
 h/o corrected congenital heart disease
587
  on anticoagulant therapy prior to pregnancy

Personal History
 low socioeconomic conditions
Family History
 rheumatic or congenital heart disease

GENERAL EXAMINATION:
 pallor
 cyanosis and clubbing in cyanotic congenital heart disease
 pedal oedema
 raised JVP
 signs of bacterial endocarditis
 evidence of dyspnoea
 pulse(tachycardia,ectopicbeats,irregularly irregular in atrial
fibrillation,collapsing pulse in aortic regurgitation)
 blood pressure in upper and lower limbs
 respiratory rate
CARDIOVASCULAR SYSTEM IN DETAIL
RESPIRATORY SYSTEM

ABDOMINAL EXAMINATION:
 hepatomegaly

OBSTETRIC EXAMINATION
 symphyseofundal height may be less due to IUGR

MANAGEMENT
 Planned pregnancy with preconceptional counselling

INVESTIGATION: ECHO
INTRAPARTUM:
 vaginal delivery is preferred unless obstetric indications
 Adequate analgesia- epidural analgesia or morphine ( contraindicated
in Aortic Stenosis)
 Propped up position and patient kept in left lateral position
 Fluid restriction (upto 75ml/kg/hr). In aortic stenosis & pulmonary
stenosis dehydration should be prevented as there is high risk of
thrombosis
 Monitoring pulse, bloodpressure, pulseoximetry, ECG
588
  Check for basal creps
WATCH FOR PULMONARY EDEMA : Heart rate>100, respiratory rate>24

SECOND STAGE:
 cut short with OUTLET FORCEPS(as it doesn’t require maternal effort)
 I/v frusemide after baby is born. Not given in Aortic stenosis
THIRD STAGE:
 methergin and ergometrine contraindicated
 Use oxytocin I/V
 Keep in labour room for 24 hrs. watch for postpartum
haemorrhage, infection, thromboembolism
 Contraception after pregnancy-barrier is preferred, vasectomy,
progesterone only pills can be given.

MATERNAL COMPLICATIONS FETAL COMPLICATIONS

Congestive cardiac failure Prematurity
Arrythmias Iugr
Subacute bacterial endocarditis Risk of congenital heart disease
Acute pulmonary edema

CARDIAC SURGERY IN PREGNANCY:

 balloon valvuloplasty preferred in second trimester if surgery necessary.
 Pre- requisites: code SIMLA
S- Single valve involvement
I-Isolated mitral valve involvement
M- Mobile, pliable valve
LA- Left Atrium free of thrombus

PREGNANCY FOLLOWING VALVE REPLACEMENT:

ANTICOAGULATION IN PREGNANCY:
 Give warfarin upto 6wks then change to I/V heparin
 At 12wks,change back to warfarin
 At 34-36wks. stop warfarin and restart heparinI/V
 Stop heparin 6 hrs before delivery
 restart heparin 6hrs after vaginal delivery and 12 hrs after CS,
 Start warfarin after 3days
 Infective endocarditis prophylaxis is must

589
DISCUSSION

 Normal cardiac changes in pregnancy that mimic heart disease

 Collapsing pulse (wide pulse pr.)
 HR and ectopic beats increase
 JVP waves more prominent
 Heart size increases
 Apex beat displaced upwards and laterally (pr. from distended abdomen)
 Loud S1
 S3
 ESM (Gr.2 & 3)
 Venous hum in neck and mammary soufflé over breast
 Peripheral edema
 ECG- lt. axis deviation and mild ST changes

 Physiological changes in CVS in pregnancy

 CO increases by 40%
 Stroke vol. increases by 10%
 HR increases by 10% or 15bpm
 Blood vol. increases by 40%
 Decrease in peripheral resistance and diastolic BP

 NYHA classification of dyspnea

 Class I- uncompromised or no limitation of physical activity
 Class II-slight limitation of physical activity; dyspnea on severe exertion
 Class III-marked limitation of physical activity; dyspnea on mild exertion
 Class IV-severely compromised; dyspnea at rest

 IE Prophylaxis
 Prophylaxis is recommended for:
 High risk- prosthetic valves, previous endocarditis, complex
cyanotic heart d/s, surgically constructed shunts/conduits
 Medium risk- most other cong. Cardiac malformations, rheumatic
valvular heart d/s, hypertrophic cardiomyopathy, MVP with
regurgitation or thickened leaflets
 30-60 min before procedure
590
  Ampicillin 2g or cefazoline/ceftriaxone 1g IV (for penicillin sensitive pt.)
OR,
 clindamycin 600mg IV (if there’s h/o anaphylaxis) OR,
 amoxicillin 2g orally OR,
 vancomycin (enterococci)

 Peripartum cardiomyopathy

 Criteria for Dx: (diagnosis of exclusion)

 Cardiac failure in last month of pregnancy or within 5 months of
delivery
 Absence of another identifiable cause for HF
 Absence of another recognizable heart d/s before last month of
pregnancy
 ECHO showing LV systolic dysfunction (ejection fr.<45%, M mode
fractional shortening<30%, LV end diastolic dimension>2.7cm/m2
 Common in older, obese multipara with HTN
 Asso. Pregnancy complications like preeclampsia & multiple pregnancy
 Gross cardiomegaly
 Mx of HF and anticoagulation

POINTS TO REMEMBER:
 Incidence of heart disease in pregnancy: 1%
 Contraindications of pregnancy:
 eisenmenger’s syndrome
 primary pulmonary hypertension
 uncorrected severe coarctation
 marfan’s with aortic involvement
 severe mitral stenosis with complications
 Warfarin monitored by prothrombin time while heparin by APTT
 Complication of warfarin therapy: Warfarin embryopathy.
Features- Microcephaly, Nasal hypoplasis, Optic atrophy,
Chondrodysplasia punctata.( Code: MNOC )

591
 ANEMIA IN PREGNANCY
Presenting Complaint
 Easy fatiguability
 Syncope
 Dyspnoea on exertion or at rest
 Haemoglobin level if known
 Iron therapy taken(oral or parenteral)
 B12 injections taken
 Blood transfusion if any
 Severe pain may suggest a sickling crisis
H/O Present Pregnancy
 On proper antenatal check up or not
 Folic acid taken in first trimester
 Iron tablets taken prophylactically
 Whether iron and calcium were taken together
 Deworming given or not
 Hyperemesis gravidarum
 Preeclampsia and HELLP syndrome more in sickle cell anemia
 h/o antepartum hemorrhagee may be a causative factor
 is it a multiple pregnancy?(more chance of anemia)
Obstetric History
 anemia in prior pregnancies
 antenatal checkups in prior pregnancies
 whether oral iron prophylaxis was taken or not
 postpartum haemorrhage and blood transfusion given
 spacing between pregnancies
Gynaecological History
 h/o menorrhagia or excessive uterine bleeding
 h/o treatment of the same
Previous Medical And Surgical History
 achlorhydria
 hookworm infestation
 malaria
 any chronic disease like renal disease or tuberculosis
 malabsorption syndromes may cause B12 deficiency
 drug intake like phenytoin and phenobarbitone inhibit folate absorption
Personal History
 detailed dietary history
 vegetarian or non-vegetarian
592
  excess alcohol intake can inhibit folate absorption
 ethnic group(sickle cell anemia is more common in certain ethnic
groups)
 low socioeconomic status
 walking barefoot outdoors(hookworm infestation)
Family History
 Sickle cell anemia or thalassemia in the family

GENERAL EXAMINATION
 Weight
 Pallor of skin and mucous membranes
 Jaundice in haemolytic anemia
 Glossitis and stomatitis
 Pedal edema
 Koilonychias
 Tachycardia
 Raised JVP and generalised oedema in cardiac failure
 Hypertension(preeclampsia and HELLP syndrome is more common in
sickle cell anemia)
 Leg ulcers in sickle cell anemia
 Sternal tenderness and lymphadenopathy in leukemias and lymphomas
Cardiovascular System
 Haemic systolic murmurs
Respiratory System
 Basal crepitations
Abdominal Examination
 Hepatomegaly(in cardiac failure)
 Splenomegaly(in haemolytic anemia)

OBSTETRIC EXAMINATION
 Reduced symphyseofundal height and reduced liquor in IUGR
 Multiple pregnancy as chance of anemia is more

MANAGEMENT:
INVESTIGATIONS:
 Hb,PCV
 Peripheral smear-microcytic hypochromic anemia
 Red cell indices-MCV,MCH,MCHC
 Specific tests: s.iron, s.ferritin, total iron binding capacity, transferrin
saturation, protoporphyrin
593
To find cause:
 urine-pyuria,hematuria
 Blood smear-parasite
 Stool examination-occult blood loss,ova,cyst
 Renal function test
 Tests for tuberculosis
Response to iron therapy-reticulocyte count, Hb

PREVENTION:
 100mg iron +500 microgm folicacid
 Single dose albendazole in first trimester
TREATMENT:
 ORAL IRON:
 180mg iron given per day along with meals
 60mg elemental iron TDS. (1 tablet ferrous sulphate TDS till Hb levels
normal then maintenance 1 tab daily for 100 days)
 Side effects: nausea, vomiting, abdominal discomfort, constipation
 PARENTERAL IRON:
 indication-intolerance to oral iron, non-compliance, malabsorption
 iron sucrose preferred now.others available are iron dextrose ,iron
sorbitol
 Iron required=normal Hb-patient’s Hb*weight(kg)*1.21
 BLOOD TRANSFUSION:
 Give frusemide 40 mg (volume overload) and
 Antihistamine (transfusion reaction) prior to transfusion
 Repeat transfusion if necessary only after 24hrs to allow time for
circulatory adjustment
 In severe anemia with cardiac failure-give packed cell transfusion

 IN SEVERE ANEMIA<30WKS- ORAL IRON PREFERRED

 30-36WKS - PARENTERAL IRON PREFERRED
 >36WKS- BLOOD TRANSFUSION PREFERRED

OBSTETRIC MANAGEMENT:

 Keep cross matched blood ready

 Cut short second stage by prophylactic forceps or vacuum
 Active management of third stage-using methergin,ergometrine
 Anticipate postpartum haemorrhage
 Puerperium-deep vein thrombosis,cardiacfailure,sepsis can occur
594
 Maternal complication Fetal complication
Susceptibility to infection IUGR
Preterm labour Prematurity
Inability to withstand PPH Early infantile anemia
Prematurity
Puerperal sepsis
Congestive cardiac failure

DISCUSSION
 Classification of anemia
1. Nutritional anemia
Fe deficiency
Folate deficiency
Combined deficiency
Protein deficiency
2. Anemia due to blood loss
Bleeding during pregnancy
Hookworm infestation
3. Hemolytic anemia
Hemoglobitopaties
Malaria
4. Decreased production of blood
Aplastic anemia

 Etiology of Fe deficiency anemia

1. Deficient intake and absorption
Inadequet diet
Hypermesis
Phosphate and pytates in diet
Achlorhydria and vit. C deficiency
2. Increased demand
Multiple pregnancy
3. Excessive loss
Repeated pregnancies with inadequate spacing
Prolonged lactation
Prior menorrhagia
Hookworm infestation
Malaria
4. Chronic illness

 Iron need in pregnancy

595
  Fetus and placenta - 300 mg
 Red cell expansion – 500 mg
 Loss through sweat, urine, faeces – 200mg
 Blood loss at delivery – 200mg
 Total need – 1200 mg
 Fe saved due to amenorrhoea – 300mg
Net need in pregnancy – 900 mg

 Physiological changes in Fe metabolism in pregnancy

 Plasma volume increase
 Hb and hematocrit decrease
 Serum Fe decreases
 TIBC increase
 % saturation decreases
 Physiological anemia of pregnancy
 Stages of Fe deficiency
1. Depleted Fe stores (reduced serum ferritin)
2. Tissue Fe deficiency w/o clinical anemia (serum transferring receptor
increases, % saturation of transferring and serum Fe decreases, free
reythrocyte protoporphyrin and TIBC increases)
3. Fe deficiency anemia ( low Hb, low red cell indices, hypochromic
microcytic blood smear)

596
 PREGNANCY FOLLOWING CAESAREAN
SECTION
Presenting Complaints
 Pain abdomen/ pain in the region of scar
 Nature of pain (whether continuous or intermittent)
 Blood stained urine
 Vaginal bleeding at anytime
 Leaking per vaginum
 Diminished fetal movements

H/O Present Pregnancy

 Date of first positive urine pregnancy test
 First trimester ultrasound to confirm dates
 Any obstetric or medical complication
 Details of placental localisation (whether anterior placenta)
 Antepartum haemorrhage at anytime (placenta previa)

Obstetric History
 Antenatal complications in previous pregnancies
 Any previous vaginal delivery
 Whether she had an elective or emergency caesarean section
 Indication for the section
 Was it a recurrent indication like contracted pelvis
 Was it done for failure to progress in labour
 Whether done late in labour
 Whether she was told that she should have a repeat section
 Type of CS if known
 What anaesthesia was given and complications if any
 Details of incision whether there was anterior extension
 PPH or adherent placenta
 Postoperative period uneventful or not
 Febrile puerperium
 Wound complications like infection, disruption, burst abdomen
 Any other complications in the puerperium like deep vein thrombosis
 Days of hospital stay after CS
597
  Details of the neonate

Menstrual History
 Regular periods or not
Past Medical And Surgical History
 Any medical complications necessitating a repeat section
 Details of any previous surgery before or after CS (which may cause
adhesions and difficulty in opening the abdomen)
 History suggestive of venous thrombosis (as thromboprophylaxis has to be
considered)

Personal History
 Allergy to any medication
Family History
 History of venous thrombosis

GENERAL EXAMINATION
 Obesity (predisposition to venous thrombosis)
 Pallor
 Thyroid swelling
 Tachycardia
 Blood pressure

SYSTEM EXAMINATION
 Especially cardiovascular and respiratory system as part of assessing fitness
for anaesthesia
OBSTETRIC EXAMINATION
 Symphyseofundal height corresponding or not (if more or less than period
of gestation, trial of scar may not be advisable)
 Lie and presentation
 Singleton or multiple pregnancy
 If vertex whether engaged or not
 Liquor adequate or not
 Estimated fetal weight
 Suprapubic tenderness or bulge

598
  Details of the scar (healing or by primary or secondary intention, keloid or
hypertrophic scar)
 Scar tenderness- palpate just above scar and look for any dimpling ,give
away,pain

VAGINAL EXAMINATION
 Evidence of bleeding or leaking per vaginum
 Bishop’s score to be assessed
 Pelvic assessment in detail
 Assessment of disproportion

MANAGEMENT: either CS or Trial of labour

 VBAC: Vaginal Birth After Caesarean Section

 TOLAC: Trial Of Labour After CS

Successful trial: results in vaginal delivery of a live fetus without scar rupture

Failed trail: when emergency CS is required /scar rupture

SELECTION OF CASES FOR VBAC TRIAL OF LABOUR

 Previous history: prior uterine incision

 Prior indication
 Prior vaginal delivery
 Postoperative infection
 Present pregnancy: no medical or obstetric complication average sized
baby
 No CPD
 Labour: institutional delivery
Continuous CTG monitoring
Facility for emergency CS within 30 minutes of taking decision

CONTRAINDICATIONS FOR VBAC

 Previous classical section
 Previous 2 LSCS
 Previous inverted T or extension of uterine incision
 Malpresentations

599
  Suspicion of CPD
 Medical or obstetric complications
 Multiple pregnancy
 Patient’s refusal

OBSTETRIC MANAGEMENT
 Hospitalisation at 38 weeks in LSCS
 One to one monitoring
 Vitals monitored ½ hourly in the first stage and every 15 minutes in the
second stage
 CTG monitoring
 Awaits spontaneous onset of labour
 Cross matched blood kept ready
 If unsatisfactory progress of labour – do emergency CS
 Second stage cut short with outlet forceps or vacuum
 Look out for signs of scar rupture (if so emergency laporotomy)
 Patient observed for 6 hrs in labour ward

COMPLICATIONS OF PREVIOUS CS
 Scar rupture
 Adherent placenta
 Operative interference
 Peripartum hysterectomy

TOPICS TO READ
 Adherent placenta
 Steps of CS
 Difference between classical and LSCS
 Trial of labour, failed trial definition

POINTS TO REMEMBER
 In cases of anterior placenta with previous CS, anticipate adherent placenta
 Scar dehiscence: separation along the line of previous scar and serosa
intact
 Rupture: when serosa is involved
 Chance of scar rupture in classical CS is 4-8%, in LSCS it is 0.5-2%

600
 LSCS scar Classical scar
Apposition Better apposition Difficult to appose

Healing in peurperium Better as the lower Imperfect due to

segment is quiescent contraction and
retraction of upper
segment
Placental implantation May be over the scar Much more likely over
scar

Rupture 0.5-2% 4-8%

Timing of rupture Usually in labour In pregnancy and labour

STEPS OF CS***

● Pfannenstiel incision
● Retract bladder using doyens retractor
● Incise uterovesical fold
● Incision over lower uterine segment
● Delivery of baby, fundal pressure by assistant, clamp cord
● Oxytocin infusion
● Placenta removed by controlled cord traction
● Closure of uterine incision in 2 layers using vicryl
● Inspect adnexa
● Closure of abdomen

601
 BAD OBSTETRIC HISTORY
Present Pregnancy
 Details of preconceptional counselling
 Folic acid taken or not
 Any chronic diseases controlled preconceptionally (diabetes.SLE ETC…)
 Regular antenatal checkups or not
 Ensure dates by first trimester scan or pregnancy test
 Details of anomaly scan
 h/o preeclampsia, or any other problem in this pregnancy
 whether detected to have diabetes in this pregnancy and if so what
treatment
 suggestion of IUGR on clinical examination or ultrasound
 Rh negative or not

Previous Obstetric History

 Regular antenatal check up or not
 h/o IUGR or preeclampsia in previous pregnancy
 chronic diseases like SLE, chronic renal disease, sickle cell anaemia etc.
 recurrent miscarriage or early onset preeclampsia suggesting APLA.
 Whether she was unsure of her dates and postmaturity could have been
the cause
 Diabetes in the previous pregnancy
 Pain and bleeding suggestive of abruption
 Was there history of trauma?
 Any febrile illness in pregnancy
 Urinary tract infection
 Whether movements stopped prior to labour
 Was she told that the fetus was dead prior to labour?
 Details of any scans and whether there was hydrops, anomalies or IUGR
 Was labour induced and how?
 Duration of labour-whether prolonged
 Delivery spontaneous or assisted or caesarean section
 If assisted whether difficult or not
 Baby born alive or dead
 Whether liquor was meconium stained(IUGR and postmaturity)
 If baby was alive at birth, details of neonatal death and neonatal care
admission
 If dead whether macerated or not
 Cord around the neck
 Evidence of external anomalies
602
  Baby anomalies(low birth weight or macrosomia)
 Baby sent for autopsy or not
 Details of autopsy like anomalies and evidence of birth trauma like
 tentorial tears and karyotyping if available
 Details of other blood tests like TORCH, glycosylated Hb etc..
 APLA testing results
 Details of Rh isoimmunisation if that was the cause
 What she was told by the obstetrician as the cause of death
 Details of counselling at the postnatal check up regarding cause
 Any postpartum depression following delivery

Gynaecological History
 Periods regular or not
Previous Medical Or Surgical History
 h/o diabetes, chronic hypertension, renal disease or any autoimmune
disease
Personal History
 sleep disturbance due to anxiety
 medications
Family History
 Diabetes, hypertension and venous thrombosis
 Congenital malformations or chromosomal anomalies suggesting APLA
 Family history of thrombosis

General Examination:
 Obesity
 Evidence of preeclampsia like oedema and hypertension
 Any stigmata of chronic renal disease like systemic lupus
Obstetric Examination
 Symphyseofundal height(both small and large for gestational age are
significant)
 Malpresentations or a high mobile head will alter management
 Amount of liquor
 Estimated fetal weight
Vaginal Examination
 Examine cervix and assess for disproportion to decide whether vaginal
delivery is an option. This can be postponed to 38wks if there is no
immediate indication for termination of pregnancy
General Examination:
 Obesity
603
  Evidence of preeclampsia like oedema and hypertension
 Any stigmata of chronic renal disease like systemic lupus
Obstetric Examination
 Symphyseofundal height(both small and large for gestational age are
significant)
 Malpresentations or a high mobile head will alter management
 Amount of liquor
 Estimated fetal weight

Vaginal Examination
 Examine cervix and assess for disproportion to decide whether vaginal
delivery is an option. This can be postponed to 38wks if there is no
immediate indication for termination of pregnancy

DISCUSSION
Causes for recurrent miscarriage
1.Chromosomal anomalies-most common cause
2.uterine factors
3.cervical incompetence
4.immunological causes(autoimmune and alloimmune)
5.Inherited thrombophilias
6.endocrine causes
7.infections
8.systemic disorders
Investigations:
 Complete hemogram
 Urine routine
 RFT
 LFT
 TFT,VDRL
 Ultrasound scan-anomalies, IUGR
 Karyotyping for chromosomal defects
 Blood grouping(Rh incompatability)
 Lupus anticoagulant, APTT, anticardiolipin antibodies, ANA, dsDNA, LE cell
 Maternal ultrasound showing polycystic ovarian disease
 Fetal ECHO at 22wks to assess cardiac anomalies
 Transvaginal ultrasound to assess cervical incompetence in pregnant
uterus
 Protein C, protein S, antithrombin ,homocysteine assays
 TORCH screening
604
  GCT,GTT
 Hysteroscopy to assess uterine anomalies

Obstetric management:
 In view of previous unexplained fetal loss, Elective induction at 38wks
 Labour should be monitored one to one, CTG monitoring
 If previous h/o prolonged labour, intrapartum death, CPD,-do CS
 If any other associated complications- do CS
 Management of cervical incompetence-Mcdonald’s cerclage, shirodkar’s
cerclage

ABORTION: Spontaneous termination of a pregnancy before the period of

viability.
CERVICAL INCOMPETENCE: Characterised by painless cervical dilatation in the
second or early third trimester with ballooning of amniotic sac into the vagina,
followed by rupture of membranes and expulsion of a live fetus.
Management: Cerclage
UTERINE ANOMALIES: Bicornuate uterus, septate uterus, Asherman syndrome,
submucous fibroids
Investigations: Transvaginal ultrasound, 3D USG, MRI, hysteroscopy
Treatment: Hysteroscopic septal resection, division of adhesions, myomectomy
APLA SYNDROME
Autoimmune cause for recurrent miscarriage
Investigations: Lupus anticoagulant, anticardiolipin antibodies, beta 2
glycoprotein
Treatment: Low dose aspirin and heparin in pregnancy

POINTS TO REMEMBER:
 CAUSES OF STILL BIRTH: above causes+
 Hyperpyrexia due to any cause
 Rh isoimmunisation
 Diabetes
 Preeclampsia with IUGR
 Unexplained IUGR
 Undetected postmaturity
 Abruptio placenta
 Cord complications-cord prolapse and cord around
 neck)
 Birth asphyxia(prolonged or obstructed labour or
 difficult instrumental delivery)
605
  Nuchal translucency in ultrasound in first trimester-to detect Down
syndrome
 Second trimester tests for detecting downs syndrome:
 TRIPLE TEST- Maternal serum AFP, beta-HCG, unconjugated estriol
 QUADRUPLE TEST- triple test+ inhibin A
 Earliest anomaly to be detected on ultrasound-anencephaly(at 12wks of
pregnancy

Types of abortion: MISTIC

M- Missed
I- Inevitable
S-septic
T- Threatened
I- incomplete
C- complete

Causes of Habitual abortion: I CUTE SIS

I- cervical Incompetence
C- Chromosomal abnormalities
U- Uterine factors
T- Thrombophilias
E- endocrine abnormalities
S- Systemic disorders
I- Immunological disorders ( APLA)
S- syphillis

606
 INTRAUTERINE GROWTH RESTRICTION
Presenting complaint:
 Decreased growth of fetus
History of present pregnancy:
 Check accuracy of dates
 Febrile illness with rash in first trimester
 Exposure to radiation
 Drug exposure in first trimester
 Any first trimester bleeding
 Second trimester scan(anomalies)
 Recurrent urinary tract infection
 Leaking per vaginum
 Antepartum haemorrhage
 Anemia needing blood transfusion
 h/o preeclampsia, on any hypertensive drugs
 h/o pregestational diabetes with vasculopathy
 h/o reduced fetal movements
 third trimester scan and details of fetal growth if known
 weight gain so far in pregnancy
Obstetric history:
 h/o low birth weight babies in previous pregnancies
 previous birth weights if known
 previous miscarriage, still births and neonatal deaths(APLA syndrome)
 previous ecclampsia
 previous LSCS, retained placenta, curettage or postpsrtun haemorrhage
requiring operative interference
Previous medical or surgical history:
 Chronic hypertension,renal disease,autoimmune dieseases like SLE
 Past history of arterial or venous thrombosis(APLA)
 Severe anemia especially sickle cell anemia and thalassemia
 Congenital cyanotic heart disease
Family history:
 Genetic defects in the family
Personal history:
 Low socioeconomic status
 Dietary history
 Severe malnutrition
 Substance abuse like alcohol,smoking or cocaine

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  Passive smoking
 Other environmental pollutants
GENERAL EXAMINATION:
 Maternal height
 Weight(evidence of malnutrition)
 Weight gain
 Pallor
 Cyanosis
 Hypertension and edema

OBSTETRIC EXAMINATION:
 Symphyseofundal height less than expected(deficiency of more than
3cm)
 Decreased liquor
 Breech presentation may be commoner due to decreased liquor
 Fetal parts easily felt
DIFFERENTIAL DIAGNOSIS
 DIFFERENTIAL DIAGNOSIS OF FUNDAL HEIGHT<PERIOD OF GESTATION
 Normal small baby
 Mistaken dates
 Oligohydramnios not associated with IUGR
 Transverse / oblique lie
 IUD

SYMMETRIC IUGR(TYPE I) ASYMMETRIC IUGR (TYPE II)

one-third of IUGR
Intrinsic fetal pathology
Early onset IUGR
Cell number and size affected
All organs equally affected
Symmetrically small
HC/AC and FL/AC normal
Ponderal index normal
Neonatal prognosis poor
Two-third of IUGR
Uteroplacental insufficiency
Late onset IUGR
Cell size affected
Brain sparing effect
Head larger than abdomen
HC/AC and FL/AC Increased
Pondrel index low
Neonatal prognosis better

COMPLICATIONS:

FETAL:
 still births(due to antepartum hypoxia)

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  Fetal distress (intrapartum hypoxia)

NEONATAL:
METABOLIC Due to HYPOXIA Related to cause
Hypoglycemia Meconium aspiration Congenital malformation
syndrome
Hypothermia Hypoxic ischemia Chromosomal
abnormalities
Hypocalcemia Encephalopathy Congenital infections
Polycythemia Necrotising enterocolitis
Pulmonary hemorrhage

LATE SEQUELAE:
 impaired neurodevelopment and cerebral palsy
 Type II diabetes and hypertension in adult life(BARKER’S HYPOTHESIS)
INVESTIGATIONS:
 BIOMETRIC TESTS- USG- TO ASSESS GROWTH SERIALLY(interval of 2wks
between the scans)
 Biparietal diameter(BPD)
 Head circumference(HC)
 Femur length(FL)
 Abdominal circumference(AC)
 Estimated fetal weight(EFW)
 HC/AC and FL/AC ratios(increased in asymmetric IUGR)

 BIOPHYSICAL TESTS: TO ASSESS FETAL WELL BEING

Read biophysical profile, Doppler and NST

 DOPPLER VELOCIMETRY:
 1.umbilical artery Doppler
 3 abnormal flow patterns:
 Decreased end diastolic flow – IUGR
 Absent end diastolic flow- fetus will survive for 1 week
 Reversal of flow- will die in 1-2 days

 2.middle cerebral artery Doppler

 Normally increased resistance flow
 In IUGR, brain sparing effect, hence decreased resistance flow

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  3.venous Doppler
 Absent or decreased flow in ductus venosus-cardiac failure
 Terminal sign-inferior venacaval and umbilical artery pulsations

 OTHERS:
 Karyotyping-In early IUGR-detect chromosomal abnormality
 TORCH screening

MANAGEMENT:
1. Antepartum fetal surveillance
2. Timing of delivery
 If umbilical artery Doppler is normal, with good interval growth-
likely to be a genetically small fetus- can be taken till term
 At 36wks:if Doppler is abnormal, reduced interval growth or severe
oligohydramnios
 32-36wks:when there is reduced end diastolic flow, postpone till 36
wks, provided other tests are normal.
Give antenatal steroids to accelerate maturity
Deliver when NST becomes abnormal & before reversal of EDF
If EDF is absent and gestation >34wks, deliver after steroids
If reversal of flow/ venous pulsation occurs, deliver immediately
 <32 wks: same factors.The fetal survival depends on facilities in
hospital.
3. Antenatal corticosteroids
For gestation <36 wks
Betamethasone 12mg IM, 2 doses 24 hrs apart
Deliver 24 hrs after second dose
4. Intrapartum management:
 Good neonatal facilities required
 CTG monitoring during labour
 Partogram

Indication for CS-

 abnormal venous Doppler
 absent or Reversal of end diastolic flow In umbilical artery
 abnormal CTG

5. Neonatal care
 Neonatal resuscitation at birth
 Early feeding
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TOPICS TO READ:
 Causes of IUGR
Fetal cause Placental Maternal:
 chromosomal  preeclampsia,  poor maternal weight
abnormality,  collagen vascular gain.
 congenital disease, APLA,  Teratogens,
malformation,  inherited  chronic maternal
 congenital infection thrombophilia, disease causing
diabetes with hypoxia (severe
vasculopathy, anemia, congenital
 placental and cord cyanoyic heart disease)
anomalies,
 multiple pregnancy

DEFINITIONS
 LBW – birth weight below 2.5kg
 SGA- fetus with weight below 10th centile for gestational age
 IUGR—fetus has failed to achieve genetic growth potential
 Genetically small fetus- fetus is small but has achieved its own growth
potential

Infections in pregnancy (CHEAP TORCH)

 Chicken Pox
 Hepatitis
 Enterovirus
 AIDS
 Parvovirus
 Toxoplasmosis
 Others
 Rubella
 CMV
 Herpes simplex

POINTS TO REMEMBER:
 Uteroplacental insufficiency is the main pathology in IUGR
 ABDOMINAL CIRCUMFERENCE is the most sensitive parameter to assess
growth

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 POLYHYDRAMNIOS
CAUSES:
FETAL MATERNAL PLACENTAL
Fetal CNS Diabetes mellitus Chorioangioma of
malformations placenta
Multiple pregnancy
Hydrops fetalis(Rh
isoimmunisation)

OBSTETRIC EXAMINATION
 Symphyseofundal height more than period of amenorrhea
 Skin shiny and tense feeling of abdomen,stretched
 Abdominal girth increased
 Fluid thrill may be elicited
 Fetal parts difficult to palpate
 FH may not be heard clearly
DD’s:
 multiple pregnancy
 Maternal or fetal ascites
 Ovarian cyst with pregnancy
 Concealed abruption
 Large baby
 Hydatidiform mole
 Mistaken dates
 Fetal malformations like hydops

DIAGNOSIS: ultrasound AFI>25, SDP>8

COMPLICATIONS
Fetal Maternal
Fetal anomalies incompatable with life Cardiorespiratory embarrassment
Preterm labour Pre-eclampsis
Cord prolapsed Placental abruption
Malpresentation Dysfunctional labour
Abruption (due to rapid Atonic postpartum haemorrhage
decompression)

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MANAGEMENT:
ANTEPARTUM:
Hospitalise if in distress, if preterm ,do amniocentesis and Slow release of liqur
(1000-1500ml at a time)
 Indomethacin can be given(decrease the amount of fetal urine)side
effect- early closure of PDA
 Do GTT,check for maternal diabetes
INTRAPARTUM:
 controlled ARM and slow release of liquor
 Active management of third stage(anticipate PPH)
 Neonatal care-look for fetal anomalies

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 OLIGOHYDRAMNIOS
Obstetric Examination
 Symphyseofundal height less than expected
 Fetal parts may be prominent
 Malpresentations like breech more common
 Reduced liquor
DIAGNOSIS: Ultrasound-AFP<5, SDP<2cm

CAUSES
 IUGR
 Post term pregnancies
 PROM
 Drugs like ACE inhibitors and prostaglandin inhibitors
 Renal anomalies

FETAL COMPLICATIONS
EARLY LATE
Pulmonary hypoplasia Cord compression
Limb deformities like talipes Meconium aspiration syndrome
Deformities like amputation of digits
Potter’s Facies

MANAGEMENT:
 Antepartum:check for anomalies
 If associated IUGR,antepartum fetal surveillance and proper timing of
delivery
 If fetus compromised-CS
 If vaginal delivery,continuous CTG
 If meconium staining of liquor,do amnioinfusion using saline in labour

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 FIBROID COMPLICATING PREGNANCY

 Effect of fibroids in pregnancy

 Increase in size
 Red degeneration
 Torsion of pedunculated fibroid
 Infection

MANAGEMENT:
 Most women-delivery uneventful
 PPH should be anticipated
 In cervical or lower segment fibroids,Prolonged labour-CS
 In CS,if lower segment unapproachable,do classical CS

EFFECT OF FIBROIDS ON PREGNANCY:

ANTEPARTUM INTRAPARTUM POSTPARTUM
Miscarriage Malpresentations Puerperal infection
Preterm labour Non-engagement of head Morbid puerperium
Uterine inertia
Obstructed labour
Postpartum
haemorrhage
Retained placenta
Difficulty at CS

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 Rh ISOIMMUNISATION
Aetiopathogenesis
 Sensitisation
 Immunisation
Factors determining maternal response
 Volume of fetomaternal haemorrhage (0.1 mL - critical sensitising
volume)
 Maternal responsiveness
 Strength of antigenic stimulus
 ABO incompatibility of mother and fetus (protective)
Perinatal complications
 Immune hydrops
 Icterus gravis neonatorum
 Congenital hemolytic anemia
Maternal problems
4. Preeclampsia
5. Polyhydramnios
6. Maternal mirror syndrome

MANAGEMENT

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 THIRD STAGE COMPLICATIONS
 Postpartum haemorrhage
 Retained placenta
 Morbidly adherent placenta
 Inversion of uterus
 Amniotic fluid embolism
Postpartum haemorrhage
Primary postpartum haemorrhage: blood loss more than 500 mL (or >1000 mL
during caesarian section) from the genital tract in the first 24 hrs of childbirth.
Secondary postpartum haemorrhage: Bleeding occuring after 24 hrs and upto
6 weeks postpartum.
Causes
 Atonic PPH
 Traumatic PPH
 Coagulopathy
 Retained placenta and placental fragments
 Morbidly adherent placenta
 Uterine inversion
MANAGEMENT OF PPH
General measures
 Resuscitative measures
 Fluid replacement
 Blood component therapy
 Oxygen therapy
 Other measures
 Investigations
 Lab tests
 Bedside tests
 Monitoring
 Confirmation of diagnosis

Medical methods
1. Oxytocin: 20-40 units in 500 mL NS as infusion; oxytocin 5 units can be given
as slow IV bolus

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2. Ergometrine: Ergometrine 0.25 mg or methergin 0.2 mg IM or IV and
repeated after 15 min. May be repeated every 4 hrs. Can lead to dangerous
hypertension in hypertensive patients
3. Prostaglandin derivatives: Prostodin 250 microgram both IM and
intramurally into the uterine musculature, maximum three doses. PGE1
analogue misoprostol 200 microgram inserted vaginally or rectally upto a
maximum of 800 microgram
Mechanical methods
 Bimanual compression
 Uterine packing
 Balloon tamponade
 Condom tamponade
Surgical methods
1. Undersewing
2. Cho's multiple block sutures
3. B-Lynch or brace sutures
4. Modified B-Lynch (Hayman) sutures
5. Systemic pelvic devascularisation
6. Hysterectomy
Radiological arterial embolization

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 OBSTETRIC INSTRUMENTS
1. Obstetric Forceps
 keilland’s forceps
 piper’s forceps
 Wriglley’s outlet forceps
 simpson’s forceps
Types of forceps:
a. Traction forceps
 Short- Wrigley’s outlet forceps
 Long - Simpson
 Axis traction - not used now.
b. Rotational forceps- Kielland’s in deep transverse arrest
c. Special forceps - Piper’s forceps for after coming head of breech

Parts of forceps : there are 2 halves, each has a blade, shank, lock and handle.
The blades are right & left corresponding to the side of the pelvis they occupy
( except in Kielland’s where they are called anterior & posterior). Each blade
has 2 curves- cephalic curve (conforms to the shape of the fetal head ) & pelvic
curve / curve of Carus( to that of the birth canal) The tip should be pointed
upwards. The lock is usually English lock except in Kielland’s where siding lock
used.

 Indications:
1. Indicated forceps:
 Fetal distress in second stage
 Maternal distress in second stage
 Prolonged second stage
2. Prophylactic forceps (to shorten second stage):
 Medical diseases like cardiac disease, pre- eclampsia
 VBAC
 Preterm head
 After coming head in breech
 Prerequisites for forceps
 Vertex presentation
 Head should be engaged and well rotated
 Position of head should be known precisely
 No CPD
 Cervix should be fully dilated and membranes ruptured
 Bladder should be empty
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Also study: Classification of forceps delivery, complications, application of
forceps (the blades should be equidistant from sagittal suture ).

2. VACUUM EXTRACTOR

 vacuum cups
 vacuum extractor
 Cups are of sizes - 40, 50, 60
 Knob- to know the direction of rotation
 Force- maximum up to 0.8 kg/cm2

Indications & prerequisites : same as forceps

Contraindications:
• Preterm delivery
• Face presentation
• Fetal coagulopathy
Flexion point:
The centre of the cup should be at the flexion point of the fetal head,
Which is a point located on the sagittal suture 3cm in front of the Posterior
fontanelle. Traction here results in maximal flexion. This is also termed
flexing median application.
 Study complications, procedure

Comparison of vacuum & forceps

Vacuum
Advantages
No need of anaesthesia
Less expertise required
Less maternal injuries
Promotes autorotation
Does not occupy space at sides
Does not require full cervical
dilatation
Less traction force needed
Disadvantages
Require maternal effort
Equipment more complex
Takes time in fetal distress
More cephalhematomas
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Forceps
Disadvantages
Requires anaesthesia
More expertise required
More maternal injuries
No autorotataion
occupy space at sides
require full cervical dilatation
More traction force needed
Advantages
No maternal effort needed
Less complex
Quick in case of fetal distress
Less cephalhematomas
 Cannot be used in preterm Can be used in preterm
Cannot be used in other Can be used in face & Breech,
presentations presentation

3. JARDIN’S DECAPITATION KNIFE WITH HOOK

 Indication : decapitation usually in a dead baby in a neglected shoulder
presentation (not done now)
 Study- procedure

4. RAMSBOTHAM’S DECAPITATION HOOK- for decapitation

5. SIMPSON’S PERFORATOR
 for craniotomy
Indications:
• Delivery of a dead fetus in obstructed labour with cephalic
presentation
• Delivery of arrested after coming head in vaginal breech delivery

Perforation sites:
• Vertex- one or the other parietal bone
• Brow- Frontal bone
• Face- orbit or roof of the mouth
• After coming head in breech- occipital bone

Study: procedure

6. WILLET’S SCALP TRACTION FORCEPS

• Used in minor degrees of placenta praevia to catch hold of baby’s scalp
and to bring it down to compress the placental site to stop bleeding

7. KOCHER’S FORCEPS
Indications:
• used for ARM
• for clamping the umbilical cord
c/I - chorioamnionits, IUD
• Mechanism: ARM  PG release  induction & augmentation of labour
Advantages:
• Promotes labour by stimulating release of endogenous PGs
• Encourages application of fetal head to cervix
• Colour of liquor can be observed & MSA can be ruled out

621
 • Permits use of fetal scalp electrode for intrapartum fetal surveillance
Disadvantages:
• Can lead to cord prolapse, if performed before presenting part is
• fixed
• Infection
• Abruption in polyhydramnios
Study ARM-procedure- done during active phase of labour. It is deferred as
long as possible in occipitoposterior position.

8. EPISIOTOMY SCISSORS
Definite Indications for episiotomy:
• Assisted breech delivery
• Face to pubis
• Macrosomia
• Shoulder dystocia
• Forceps & vacuum
• Rigid perineum
Structures cut in mediolateral episiotomy:
• Posterior vaginal wall
• Superficial transverse perineal muscle
• Bulbospongiosus muscle
• Deep transverse perineal muscle
• Part of levator ani
• Fascia overlying muscles
• Subcutaneous tissue
• Skin
Advantages of episiotomy:
• Prevents perineal tears
• A neat surgical incision is easier to repair than a ragged tear

Timing of Episiotomy: During Crowning in Vertex presentation and in Breech

presentation during climbing the perineum.

Study-, differences between midline and mediolateral episiotomy, perineal

tears classification and repair.

9. SPONGE HOLDING FORCEPS

Indications:
• Clean the parts
• To catch hold of pregnant uterus(its non traumatic)

622
 • In traumatic PPH, cervical tear, removal of placental bits, retained
• products of conception ( if perforation occurs with this instrument , do
• immediate laprotomy)
• To hold infudibulopelvic ligament, ovarian ligament during
• Myomectomy
• For the insertion of post partum iucd

10.GREEN ARMYTAGE FORCEPS

Indications:
• In C.S to hold the edges of uterus to decrease bleeding ( not used here)
• To hold the angles

11.DOYENS ABDOMINAL RETRACTOR

Indication:
• to retract the bladder to visualize the lower segment in cs

12.OVUM FORCEPS
• Indication: for evacuation following abortion.

13.SIM’S SPECULUM
Indications:
• To retract posterior vaginal wall after delivery to visualize any vaginal
• or cervical injury
• To inspect the cervix for local causes of bleeding in case of stable APH
• To collect secretions from the cervix in cases of infections & PROM
• Evacuation of any retained placental bits or membranes
• Evacuation of inevitable, incomplete or missed abortion
Disadv: Lesions in posterior wall can be missed.
One lip is longer than the other- used to visualize the longer posterior vaginal
wall

14.CUSCOS’S BIVALVED SELF RETAINING VAGINAL SPECULUM

Indication:
• Intracervical instillation of PGE2 gel for induction of labour
• For colposcopy
• Adv: Self retaining
•
15.MULTIPLE TOOTHED VOLSELLUM FORCEPS
Indications:
• To catch the anterior lip of cervix in evacuation of abortion.

623
 • To catch the posterior lip of cervix for culdocentesis
Disadv: -Can traumatize a vascular cervix of pregnancy
It has got multiple tooth to get a firm hold on the cervix
It has a pelvic curve - upward curve

16. SIM’S DOUBLE EDGED UTERINE CURETTE

Indications:
• To ensure completeness of evacuation after suction evacuation in case
of abortion
• Check curettage in vesicular mole
• Gentle curettage in cases of secondary PPH with retained placental bits
One end is sharp and other end is blunt.

624
 DUMMY AND PELVIS
Pelvis
• In standing position, the plane of pelvic inlet makes an angle of 60degree
with horizontal
• Bones of pelvis - two innominate bones(fused ilium,ischium & pubis),
sacrum & coccyx
• Identification of ischial spine, true pelvis & false pelvis

Planes of pelvis - 4 imaginary planes:

1. plane of pelvic inlet(superior strait) - bounded by sacral
promontory & alae, linea terminalis, horizontal rami of pubic
bones &symphysis
2. plane of greatest pelvic dimensions - at the level of S2,S3 vertebra
3. plane of least pelvic dimensions - at the level of S4,S5 vertebra
and ischial spines
Significance :
 internal rotation begins at this level;
 when engagement occurs, head is at this level;
 landmark of pudendal block;
 external os is at this level;
 ischial spines situated in this plane represent zero station of
head;
 interspinous diameter is the shortest diameter of pelvis
4. plane of pelvic outlet(inferior strait)

DIAMETERS OF PELVIS
PLANE OF INLET PLANE OF LEAST PLANE OF OUTLET
DIMENSIONS OF PELVIC
CAVITY
Obstetric conjugate Anteroposterior Anteroposterior
10.5cm (most imp. AP diameter 11.5cm diameter 12cm
diameter through
which fetus must pass)
Anatomic conjugate
11cm
Diagonal conjugate
12.5cm
Transverse diameter Transverse diameter Transverse diameter

625
13.5cm(widest diameter 10.5cm (extends 10.5cm(extends
of inlet) between ischial spines) between
ischial tuberosities)
Oblique diameter
12.5cm
Posterior sagittal Posterior sagittal Posterior sagittal
diameter 5cm diameter 6cm diameter 7cm
Sacrocotyloid
diameter 9.5cm

Diameters of pelvic inlet

• Subpubic angle in normal females is 85-90degree.when subpubic angle
decreases, transverse diameter of outlet will also be less
• Waste space of Morris : if it is more than 1cm, the available AP diameter
of outlet is reduced
• Axis of birth canal - (curve of carus) is obtained by joining axes of inlet,
cavity & outlet
• Obstetric axis - is the course taken by presenting part as it moves down
through pelvis

MEASUREMENTS OBTAINED FROM PV EXAMINATION – interspinous

diameter, transverse diameter of outlet, transverse diameter of outlet,
diagonal conjugate

Diagonal conjugate - 1.5cm = obstetric conjugate

CALDWELL & MOLOY CLASSIFICATION OF PELVIS

Gynaecoid Anthropoid Android Platypelloid
Inlet Round/transversely Long AP Wedge Transversely
oval oval shaped oval
Transverse > AP AP> Transverse >
transverse >AP
Cavity Sidewalls parallel/ Sidewalls Funnel Sidewalls
divergent parallel shaped & parallel but
side walls reduced
converging capacity
Subpubic 85-90 degree <90degree >>90degree
angle
Diameter of Transverse/ AP Transverse/ Transverse
Engagement oblique oblique

626
 Position of OA/OT Direct OP OP/OT OT
Head
Delivery Normal Face to Deep No difficulty
pubis transverse
arrest
common

Fetal head
• Identification of Bones and suture lines of fetal skull
• Identification of anterior & posterior fontanelle
• Occiput - area occupied by occipital bone & is below & behind
posterior fontanalle
• Vertex - area bounded by 2 fontanalles & parietal eminences
• Sinciput / brow - area bounded superiorly by bregma & coronal
sutures and inferiorly by orbital ridges

DIAMETERS OF FETAL SKULL

Bitemporal diameter 8cm
Biparietal diameter 9.4cm
Submentobregmatic diameter 9.4cm
Suboccipitobregmatic diameter 9.4cm
Occipitofrontal diameter 11cm
Verticomental diameter 13.5cm

During PV examination,
 Sagittal suture palpated gives idea of degree if internal
rotation
 Palpation of posterior fontanalle denotes position of head
 Palpation of anterior fontanalle denotes degree of flexion
of head

MECHANISM & CONDUCT OF LABOUR (read in detail)

No mechanism of labour in transverse lie and brow presentation
1. Normal delivery
2. Breech delivery
3. Occipitoposterior

• ENGAGING DIAMETER is diameter of fetal head &

 DIAMETER OF ENGAGEMENT is pelvic diameter
• REASONS FOR ROP (ABCD)
627
 A. - Android & anthropoid pelvis, anterior insertion of placenta
B. - Big baby
C. - CPD
D. - Deflexion
• Deep transverse arrest

ENGAGING DIAMETERS OF VARIOUS MALPRESENTATIONS

Presentation Engaging diameter
ROP Suboccipitofrontal/Occipitofrontal
Face Submentobregmatic
Brow Verticomental
Flexed breech Bitrochantric diameter(10cm)

• Suboccipitobregmatic (engaging diameter in normal presentation) &

submentobregmatic (engaging diameter in face presentation) diameters are
both 9.4cm, but delivery is difficult in face presentation because moulding is
possible only in cranial bones & not in facial bones.

• Methods of pelvic assessment -

 Inlet : PV examination is done & if sacral promontory can be
reached,diagonal conjugate is measured to find out obstetric
Conjugate (OC=DC-1.5cm). (OC may be short if diagonal conjugate
can be felt)Here, middle finger is on sacral promontory & forefinger of
other hand marks off lower margin of suprapubic ligament.diagonal
conjugate is the distance between tip of middle finger & marked point
 Pelvic cavity :
• sacrum should be well curved
• ishial spines not prominent
• sidewalls parallel or divergent
• sacrosciatic notch admitting 2 fingers
 Outlet : subpubic angle must be atleast 90degree & intertuberous
distance should admit 4 knuckles

Assessment of CPD by Munro Kerr-Muller method(best done at onset

of labour & it assesses disproportion at inlet only)

STEPS
A. Patient is in modified dorsal position with legs flexed & bladder and
bowels empty.
B. Examiners left hand over abdomen pushes head into pelvis while

628
fingers of the other hand inserted vaginally estimate whether the vertex
reaches the level of ischial spines or not.Thumb of right hand palpates
the head over pubic symphysis.

INFERENCE :
A. If head can be pushed to level of spines, there is no CPD
B. Head can be pushed down a little, but not upto the level of spines, &
thumb of right hand is flush with symphysis pubis, there may be first
degree CPD
C. Head cannot be pushed down at all & fetal head(parietal bone) is felt
overriding the symphysis pubis as detected by thumb of right hand,
there may be second degree CPD

CONTRACTION OF PELVIC OUTLET:

Causes:
1. Diseases or injury of pelvic bones-
Rickets, osteomalacia, fractures, new growths
2. developmental anomalies:
• Naegele pelvis: obliquely contracted pelvis due to lack of development
of
one sacral ala
• Robert pelvis:transversely contracted pelvis due to lack of development
of both alae
• Rachitic pelvis:reniform inlet with short anteroposterior diameter
• Osteomalacic pelvis:triradiate pelvis
• Split pelvis:gap between pubic bones.associated with ectopia
vesicae,hypospadiasis
• Assimilation pelvis:pelvis with a variation in the number of vertebra
fused to form sacrum
• Low assimilation-sacrum has 4 vertebra
• High assimilation-sacrum has 6 vertebra
3. vertebral anomalies-kyphosis,scoliosis,spondylolisthesis
4. lower limb deformity-dislocation of femur,loss of a limb,hip joint
Disease

 normal labour : Normal labour is the process by which, the fetus

presenting as vertex is expelled by the natural efforts of the mother,
when the pregnancy has reached term and there are no complications.
 Synclitism & asynclitism(concerned with occipitotransverse position) :

629
 Synclitic engagement is said to occur when the sagittal suture lies in the
transverse diameter of pelvic inlet(midway between pubic symphysis &
sacral promontory).
When sagittal suture is deflected towards pubic symphysis,
posterior parietal bone becomes leading part – posterior
asynclitism/posterior parietal presentation/litzman’s obliquity.It
is common in nullipara.
When sagittal suture is deflected towards sacral promontory,
anterior parietal bone becomes leading part – anterior
asynclitism/anterior parietal presentation/Naegele’s obliquity.It is
commoner in multipara.
Anterior parietal presentation is better than posterior parietal
presentation since fetal head has to negotiate only sacral promontory &
sacrum is well curved.Posterior parietal presentation causes fetus to
negotiate entire pubic symphysis
Advantage of asynclitic engagement : a smaller
diameter,subsuperparietal diameter(8.75cm) presents at pelvic inlet.

 Fixation Vs Engagement : Engagement is when the greatest transverse

diameter of presenting part has passed through pelvic inlet and fixation
denotes passage of presenting part to the pelvic inlet.

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 O&G SPECIMENS
Order of describing the specimens:
1. Type of surgery done
2. Structures removed
3. Abnormality of the tissues involved
4. Indications of surgery
5. Problems during surgery
Terminologies
a. Subtotal hysterectomy: Remove uterus without Cx.
b. Total hysterectomy: Uterus with Cx.
c. Pan hysterectomy: Total hysterectomy + BSO
d. Extended hysterectomy: Total hysterectomy + Upper 1/3rd vagina
e. Radical hysterectomy: TH + Upper 1/3rd vagina + BSO + LNs +
pelvic
Tissues

Classes of HYSTERECTOMY
1. TYPE I : Simple extrafascial hysterectomy
2. TYPE II: (Modified radical hysterectomy) (Wertheim) - medial ½ of
uterosacral and cardinal ligaments removed along with a cuff of vagina
3. TYPE III: (Radical hysterectomy) (Meigs) - Ureter completely freed along
its course, uterosacral and cardinal ligaments divided, upper of 1/3rd of
vagina removed
4. TYPE IV: Periureteral tissue, superior vesical artery, 3/4th of vagina
removed
5. TYPE V: Also distal ureter and bladder are removed..
(TypeIV &V is extended radical hysterectomy)

1) WET MOUNTED TOTAL HYSTERECTOMY SPECIMEN WITH ADNEXA WITH

MULTIPLE SUBSEROUS FIBROID:
• Can be sessile or pedunculated. Can attain huge sizes.
• Usually no menstrual symptoms. Pressure symptoms more common.
• Commonest fibroid is interstitial fibroid
• Types of fibroid?
• Types of degenerations and complications?
• Changes of fibroid in pregnancy?
• Effects of fibroid on pregnancy?
• Management of fibroids?

2) PEDUNCULATED SUBSEROUS FIBROID:

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 • Maximum pressure symptoms and least menstrual symptoms
• Rarely may get detached from pedicle and get nourishment from
omentum - parasitic or wandering fibroid.
3) WET MOUNTED TOTAL HYSTERECTOMY SPECIMEN OF CUT OPEN UTERUS
SHOWING MULTIPLE FIBOIDS AND FETUS INSITU:
• Effect of fibroids in pregnancy?
• Management of fibroids during pregnancy?

4) WET MOUNTED TOTAL HYSTERECTOMY SPECIMEN SHOWING

SUBMUCOUS
FIBROID:
• Produce maximum menstrual symptoms (menorrhagia or
menometrorrhagia), also cause infertility and recurrent miscarriage.
• Contain more smooth muscle tissue. Sarcomatous change is more
common here. Infection is more common in submucous fibroid
• Study types, CFs, Complications and Management?

5)PEDUNCULATED SUBMUCOUS FIBROID:

• CFs: Blood stained foul smelling discharge, mass pv, contact bleeding,
sterility
• DDs: c/c inversion, prolapse, Ca Cx.

6)CERVICAL FIBROID:
• Rare, it may be subserous, intramural or submucous.
• May get impacted in pelvis - urinary retention
• Surgery is extremely difficult, high risk of bladder & ureter injury.
• Cause very difficulty during labour. - obstructed labour
• In such patients, LSCS is difficult, so Classical CS may be necessary.
• Management of cervical fibroid - pre operative GnRH agonists followed
by myomectomy

7) TOTAL HYSTERECTOMY SPECIMEN SHOWING INVERSION OF UTERUS:

• Turning inside out of uterus
• Types: (Acute) = 1st 24 hrs (Subacute) = After 24 hrs but before 4 weeks
(Chronic) = after 4 weeks postpartum
• Causes: Mismanagement of 3rd stage of labour, spontaneous inversion,
placenta accreta
• CFs: Shock & H’ge in 3rd stage, soft globular swelling in vagina or cervical
canal, shabby surface, fundus absent on abd palpation, unexplained
postpartum collapse.

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 • Management: resuscitation, investigations, monitoring, confirm cause
followed by medical, mechanical or surgical methods to arrest PPH.
• Mechanical methods - bimanual compression, uterine packing under
anesthesia, balloon tamponade with sengstaken tube inserted into
uterus, condom tamponade
• Surgical methods - undersewing, block sutures, B lynch suture, uterine &
ovarian artery ligation, internal iliac artery ligation, hysterectomy,
arterial embolisation
• Distinguishing chronic inversion from prolapse -in c/c inversion there is
absence of external os in mass PV and cervical ring can be felt on
examination. On USS fundus of uterus will not be seen in position
• Other important 3rd stage complication is PPH.
• PPH management: code- HAEMOSTASIS
H- Call for Help
A-Assess blood loss( add investigations in this)
E- Establish Cause, Ensure blood & blood products
M- uterine Massage
O- Oxytocin( and rest of medical management)
S- Shift to Operation theatre
T- Tamponade ( add other mechanical mtds also)
A-Apply compression sutures (include other sutures- block
sutures etc)
S- Stepwise devascularisation (Ligation of uterine, ovarian arteries,
internal iliac anterior br) intervention radiography- embolisation
• S- Subtotal Hysterectomy

8) TOTAL HYSTERECTOMY SPECIMEN SHOWING ADENOMYOSIS UTERUS:

• Benign ingrowth of endometrium into myometrium. Diffuse myometrial
hyperplasia. Asymmetrical diffuse enlargement of uterus.
• Cut section: Thickening of uterine wall with a characteristic trabeculated
appearance. No capsule as in fibroid.
• CFs: Asymptomatic, menorrhagia or menometrorrhagia, congestive
dysmenorrhea
• Signs: Uterus enlarged not more than 14 weeks, normal mobility, softer.
• Management: (Young age) - NSAIDs, OCPs (Parous, >40yrs) - Total
hysterectomy.

9) WET MOUNTED TOTAL HYSTERECTOMY SPECIMEN SHOWING UTERINE

DIDELPHYS (DOUBLE UTERUS):
• A mullerian anomaly due to failure of fusion of the 2 mullerian ducts.

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 • There are 2 endometrial cavities each with a cervix. A septus separates 2
Cervix.
• This anomaly has the best reproductive prognosis among all the
mullerian anomalies and live births are usual.
• Classification of mullerian anomalies -
I. Class I Segmental mullerian agenesis/hypoplasia - vaginal, cervical,
fundal, tubal, combined
II. Class II Unicornuate uterus –
A. with rudimentary horn - with communicating endometrial
cavity, with non communicating cavity, with no cavity
B.without any rudimentary horn
III. Class III Uterus didelphys
IV. Class IV Bicornuate uterus - complete up to the internal os,
partial, arcuate
V. Class V Septate uterus - without a complete septum, with an
incomplete septum or uterus subseptus
VI. Class VI uterus with internal luminal changes

10) BICORNUATE UTERUS:

• Mullerian anomaly caused by incomplete lateral fusion of the mullerian
ducts.
• Can be complete or partial. It is complete when the failure of fusion
extends to the cervix or can be partial.
• Problems: Recurrent miscarriage & preterm labour.
• Management - rule out other causes of abortion,strassman
utriculoplasty (transverse fundal incision for reunification of uterine
cavity)

11) SEPTATE UTERUS:

• Mullerian anomaly when there is failure of the medial segments of the
mullerian ducts to separate following fusion. This creates a septum
complete or subseptate.
• Problems: Recurrent miscarriage & preterm labour. (Both 1st and 2nd
trimester loses can occur).
• Management - rule out other causes of abortion,hysterescopic resection
of septum, Tomkins operation

12) RUPTURE UTERUS WITH FETUS:

1. Incomplete rupture: Visceral peritoneum is intact & fetus is inside
uterus

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 2 Complete rupture: all layers including peritoneum torn & fetus
in peritoneal cavity
• Commonest cause of rupture is previous CS scar. Rupture during
pregnancy is very rare.
Causes of rupture during labour:
1. Previous uterine surgery, injury or anomaly
2. Traumatic rupture: Internal podalic version, breech extraction, forceps,
destructive operations, manual removal of placenta.
3. Spontaneous rupture: Overstretching, injudicious use of oxytocin & PGs,
Grand multipara, placenta percreta.
• Why classical scar more likely to rupture??
• CFs:
• Threatened rupture: Signs of obstructed labour (tachycardia, tonic
contraction, and pathological ring), agony, dry tongue, hot dry vagina,
large caput.
• Rupture: FH deceleration (earliest sign), sudden pain followed by
cessation of pains, give away feel, collapse due to H’ge & shock, fetal
parts easily palpable per abd, bleeding through os with hanging loose Cx,
recession of presenting part etc
• Management: Immediate laparotomy and hysterectomy. An attempt to
repair the rent can be done. Sometimes internal iliac artery ligation may
be needed.

13) WET MOUNTED SPECIMEN OF TAH WITH BSO CUT OPEN UTERUS WITH
LIPPES LOOP INSITU:
• Lippes loop is a biologically inert IUCD. Another one is Saf T-coil. Can be
left in situ for many yrs.
• Now these are replaced by Copper and hormone carrying IUCDs.
• Timing of insertion of IUCD:
1) Soon after menstruation (avoid chance of pregnancy)
2) Immediately following evacuation of uterus in abortion.
3) Postpartum period 6 week is advocated in India.
• Uses, Contraindications & complications of IUCDs??
• Mechanism of action??
• Technique of insertion??
• How will u manage misplaced IUCD??
• Advantages of IUCD??
• (read chapter “birth control & MTP” )

14) WET MOUNTED SPECIMEN MODIFIED RADICAL HYSTERECTOMY

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SPECIMEN WITH GROWTH IN CERVCIX - CA CERVIX:
• Aetiology & risk factors?
• Pathology: 1.Squamous cell ca (commonest) 2. Adenocarcinoma
3.Adenosquamous
• Spread?
• Symptoms & signs?
• Investigations?
• Staging & Management?
•
15) WET MOUNTED SPECIMEN TAH WITH CUT OPEN UTERUS SHOWING
VESICULAR MOLE:
• Abnormal pregnancy characterized by hydropic degeneration of
chorionic villi & trophoblastic proliferation. Conceptus appears as grape
like cystic vesicles called moles
• Types: Complete(diploid & exclusively paternal) & partial moles(triploid
or tetraploid)
• Symptoms: Amenorrhoea, grape like vesicles per vaginum, Hyperemesis.
• Signs: Uterus more than POA, no fetal parts or FH, Theca lutein cysts in
ovaries, early onset preeclampsia, thyrotoxicosis.etc.
• Investigations: USG (snow storm appearance), β-hcG levels will be very
high.
• DDs: Threatened abortion, Acute hydramnios, Multiple pregnancy,
• Tumors complicating pregnancy
• Management? Evacuation & follow-up???
• Condition where the lab tests for pregnancy is positive but there
are no breast changes?. ans- Vesicular mole

16) CHORIOCARCINOMA:
• Carcinoma of chorionic epithelium.
• Dark red or purple tumor involving the endometrium & extend outwards
through the myometrium to the serosa.
• Differs from vesicular mole in that it lacks villous pattern.
• CFs: Abnormal uterine bleeding, Symptoms of mets (hemoptysis,
features of ICSOL, vaginal mets, suburethral mets)
• Diagnosis confirmed by HPE of curettage specimen. There is rapidly
increasing levels of β-hcG.
• Management & follow-up???

17) WET MOUNTED SPECIMEN, TAH SPECIMEN WITH B/L TUBOOVARIAN

MASS - HYDROSALPINX:

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 • Cause is PID
• Organisms: Most common are Chlamydia & Gonococci. Others are
streptococcus, staph, ecoli, pseudomonas, etc..
• Risk factors: Young age, multiple sex partners, gonococcal & chlamydia
infection, smoking, IUD insertion.
• Symptoms: B/l lower abd pain, abnormal vaginal discharge,
menometrorrhagia, postcoital bleeding, fever, nausea, right upper
quadrant pain (perihepatitis)
• Signs: Fever, tachycardia, coated tongue, abd tenderness & rigidity, foul
smelling purulent discharge, cervical motion tenderness, tender adnexal
mass, fluctual swelling in POD.
• DDs: Acute appendicitis, ectopic gestation, twisted ovarian cyst, septic
abortion.
• Investigations: Laparoscopy, TVS with power Doppler, MRI,
microbiological investigation using discharge or smear.
• HSG contraindicated in PID
• Management: Give antibiotics (Syndromic approach?), partner
treatment, counseling
• Role of surgery: Non response to drug Rx, Rupture tuboovarian mass,
drainage of pelvic abscess, severe peritonitis, intestinal obstruction,
diagnosis in doubt.
• Long term sequelae: Tubal factor infertility, ectopic gestation, chronic
pelvic pain, increased chance of hysterectomy later.
• Most common site of genital TB is fallopian tube
• Laparoscopic appearance of genital TB - tubercles in intestinal serosa,
omentum, surface of uterus & serous coat of fallopian tubes, multiple
constrictions in fallopian tube,ie: beaded appearance(retort shaped
tubes), thick rigid tubes, violin string adhesions between liver and
diaphragm & tobacco pouch appearance of terminal parts of tube

18) WET MOUNTED OVARIOTOMY SPECIMEN - TERATOMA (DERMOID CYST):

• Commonest germ cell tumor,
• commonest tumor seen in young women,
• commonest tumor in pregnancy,
• commonest tumor to undergo torsion.
• Commonest age grp of teratoma - children and women <21yrs.
• It has high fat content
• <15cm in diameter, capsule is smooth and tense, on cut section:
contents are mainly sebaceous material with hair. Contain derivatives of
ectoderm, endoderm and mesoderm. Wall is lined by epithelium.

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 Contain epidermis, skin, hair, teeth, sebaceous, nervous tissue, thyroid,
intestine, bone, cartilage etc… Rokitansky protuberance is a solid area
containing skin, sweat glands, sebaceous glands, teeth and bones.
• Diagnosis: PV- cystic & mobile mass; USG - cyst with internal echoes,
• Rokitansky protuberance, posterior acoustic shadowing.
• Complications: Torsion , rupture.
• Management of Benign ovarian mass???

19) SIMPLE OVARIAN CYST:

• Types of ovarian tumors?? Benign & malignant??
• Clinical features?? Investigations?
• DDs?
• How will u differentiate b/w benign & m/g tumors??
• Complications ?? Management of both benign & m/g tumors???

20)TORSION OVARIAN CYST:

• Clinical features - severe pain due to ischemia of cyst
• Management of torsion - bimanual pelvic examination to confirm mass
is ovarian, ultrasound abdomen, if ovary can be preserved , surgical
detorsion & cystectomy,if cystecomy is not possible, oophorectomy is
done, TAH + BSO in elderly women who have completed their families
• Commonest cyst to undergo torsion - dermoid cyst (due to high fat
content)

21)CARCINOMA ENDOMETRIUM:
• Types?
• Risk factors?? Prevention??
• Pathology??
• Clinical features??
• Investigations??
• Staging & management??

22)ENDOMETRIAL CARCINOMA + OVARIAN TUMOR:

23)CUT SECTION OF ENLARGED OVARY WITH MULTIPLE FOLLICLES - PCOD :

• Diagnostic criteria:
a. Ovulatory dysfunction such as amenorrhoea, or oligomenorrhoea.
b. Clinical or biochemical evidence of hyperandrogenism
c. Polycystic ovarian morphology on ultrasound scan defined as the
presence of 12 or more follicles in each ovary and an increased

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 • ovarian volume of >10ml.
• Clinical features??
• Investigations??
• Management??

24)PUERPERAL UTERUS WITH ISTHMICAL RUPTURE & AREAS OF

HAEMORRHAGE INSIDE IT :
• Causes: Obstructed labour, scar dehiscence, Iatrogenic (MTP or
abortion)
• Causes of obstructed labour: CPD, Malpresentations, Iatrogenic
(injudicious use of oxytocin,abortion)
• CFs & Management of uterine rupture??

25)DECIDUAL CAST:
• Decidua passed as flat, reddish brown piece of tissue
• Decidual shedding is seen in ectopic pregnancy due to the low level of
hormones and failing pregnancy
• Identification of decidual cast??

26) ANENCEPHALY:
• First anomaly to be detected on USS as ‘frog’s eye
appearance’(diagnosed by 12 weeks of pregnancy)
• Neural tube defects due to failure of fusion of anterior neuropore
• Management - termination of pregnancy
• Other neural tube defects - encephalocele, spina bifida
• USS cranial sign in open spina bifida - lemon sign(scalloping of frontal
bones) & banana sign(abnormal anterior curvature of cerebellum)

27)WERTHEIMS HYSTERECTOMY SPECIMEN:

28) SUBMUCOUS MYOMA:

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 X RAYS
1.Xray singleton pregnancy (see vertebral column & fetal skull)
2.Xray multiple pregnancy(two vertebral columns are seen)
3.HSG showing bicornuate uterus
4. Normal HSG (dye filling uterus and tubes along with spillage into peritoneal
cavity
5. HSG with hydrosalpinx on right side(since there is no spillage of dye from
fallopian tube, there may be distal tubal block)
5. HSG showing Bilateral proximal tubal block
6. Xray pelvis showing calcifications within,most probably a calcified fibroid
7. Ultrasound showing fibroid(fibroid appears as hyperechoic on USS)
8. Xray showing missed IUCD
9. X ray showing lippes loop in situ
10.xray showing breech

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GYNAECOLOGY
DYSFUNCTIONAL UTERINE BLEEDING 643

POST MENOPAUSAL BLEEDING 648

FIBROID/ LEIOMYOMAS 657

OVARIAN MASS 667

PROLAPSE 673

INSTRUMENTS 679
 DYSFUNCTIONAL UTERINE BLEEDING
Presenting complaints
 Menstrual irregularities
 Menorrhagia - 80 ml or >7 days or clots
 Hypomenorrhea—TB, Ashermann syndrome
 Polymenorrhea—endometriosis, PID
Oligomenorrhea—PCOS, hypothyroidism
 Metrorrhagia - polyp, erosion, CIN, CA cervix,submucosal fibroid
 Hormone OCP- (breakthrough bleeding)
 Anemia & Fatigue
 Pain
 Dyspareunia - endometriosis
 Vaginal discharge
 Postcoital bleeding
 PCOS features- Obesity, acne, hirsutism, menstrual irregularity
 Post menopausal bleeding

Causes
Adolescent Reproductive Perimenopausal
DUB Pregnancy DUB ( anovulatory)
Coagulation d/o or Pelvic Pathology CA Endometrium
hematological d/o
PCOS iatrogenic , Coagulation CA cervix
d/o
Endocrine d/o DUB (ovulatory) Fibroid/Polyp

 Pelvic Pathology—Endometriosis, fibroid, polyp, PID ,Carcinoma

 Pregnancy
 Coagulation d/o
 Medical—Cushing d/o, Hypothyroidism, Liver d/o, Renal d/o
 DUB
 Iatrogenic—IUCD, OCP

Complications
Anemia & fatigue

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DUB - heavy and/or irregular bleeding in the absence of organic disease
DUB - ovulatory &anovulatory

General examination:
 pallor, goiter, features of hyper/hypothyroidism, bleeding d/o

System wise examination: CVS, GIT, Resp, CNS

Abdominal examination: to rule out fibroid, mass abdomen etc.

Speculum examination

Bimanual pelvic examination

Per rectal examination (not to be done.. just for completion sake)

Some clues to diagnosis

 Heavy irregular bleeding -- ovulatory DUB or fibroid
 Postcoitalbleeding - polyp, erosions ,CIN, CA cervix
 Dysmenorrheal & dyspareunia --endometriosis ,adenomyosis
 Abdominal pain and vaginal discharge -- PID
Irregular cycles -- PCOS, anovulatory DUB

MANAGEMENT

Investigation
1. Blood routine
2. Coagulation profile
3. Endocrine - TFT,LFT, RFT
4. PAP smear
5. USS - TAS, TVS
6. Endometrial Sampling--- Pipelle, FC, D&C, hysteroscopy with biopsy

644
Treatment
Medical Surgical
1 Correct anemia: Oral/ parenteral/ 1 D&C
blood
2 Hysterectomy
2 Progesterone:
Norethisteroneenanthate-
To stop bleeding 3 Minimally invasive surgery
Medroxy progesterone acetate A Radiofrequency ablation
2nd half of cycle for 3- B HysteroscopicNd-Yag laser
6mnths Ablation
C Microwave endometrial
3 OCP, IUCD, MIRENA Ablation

4 NSAIDs(Mefanemic acid), 4 Uterine tamponade

Ethamsulate, Tranexaemic acid
5 Arterial embolisation
5 GNRH agonist- Danazol
6 Cavaterm balloon therapy
6 Clomephene ( Anovulatory
cycles)

Refer Shiela B page 59, 60, 61 for Treatment Protocol

PALM COEIN CLASSIFICATION

 P—polyps
 A—Adenomyosis
 L—Leiomyoma
 M—Malignancy or hyperplasia
 C—Coagulopathy
 O—Ovulatory dysfunction
 E—Endometrial
 I—Iatrogenic
 N—Not yet classified

ENDOMETRIAL HYPERPLASIA
 Simple hyperplasia—1% risk of ca

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  Complex hyperplasia—3%
 Simple hyperplasia with atypia—8%
 Complex hyperplasia with atypia—29%
If atypishystrectomy
If simple hyperplasia but no atypiaprogestins or LNG-IUS, hysterectomy if
hormonal treatment fails.

ENDOMETRIOSIS
Symptoms
 Dysmenorrhoea
 Dyspareunia
 Deeo seated pelvic pain
 Dysuria
 Dyschezia
 Haematuria
 Infertility
Signs
 Tenderness in cul-de-sac
 Nodularity in cul-de-sac
 Fixed retroverted uterus
 Adnexal tenderness
 Adnexal masses
Investigations:--Transvaginal ultrasound, CA-125,LAPAROSCOPY
Treatment
SURGICAL :-
 Conservative surgerycoagulation, adhesiolysis, fenestration &
drainage(<3 cm), cystectomy( >3cm)
 Preoperative or post operative hormone therapy
 Laparoscopic uterosacral nerve ablation(LUNA)
 Extrapelvic endometriosisexcision
 Radical surgery total hysterectomy+bilateral oophorectomy
Medical treatment
 Non hormonal – prostaglandin synthase inhibitors
 Hormonal—oral contraceptives, oral progestins

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  GnRHAgonistsleuprolide, goserelin
 LNG-IUS
 Newer- Aromatase inhibitors, GnRH antagonists

TREATMENT OF PID
OP Regimen CEFTRIAXONE 250 mg single dose OR cefoxitin 2g im+
probenecid single dose
ADD DOXYCYCLINE 100 mg orally BD * 14 days with or
without metronidazole
IP Regimen ACEFOTETAN 2g every 12 hourly or CEFOXITIN 2g IV every 6 hrly
+DOXYCYCLINE 100 mg orally BD * 14 days
Regimen B Clindamycin 900 mgIV every 8 hrly+ Gentamicin 2mg/kg IV f/b
1.5 mg/kg every 8 hrly
Once improved= oral clindamycin 450 mg 6 thhrly+ Doxycycline
100 mg BD * 14 days.
Surgery drainage of abcess & irrigation.

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 POST MENOPAUSAL BLEEDING

Menopause: Time of last menstrual period followed by 12 months of

amenorrhea.
Differential diagnoses:
 Endometrial atrophy ( most common: 60-80 % )
 Endometrial carcinoma( 10 % )
 Endometrial polyp
 Endometrial hyperplasia
 Atrophic vaginitis
 Estrogen therapy
 Estrogen producing tumors
 Cervical cancer
 Uterine sarcomas
Questions will be focused on endometrial carcinoma and cervical cancer.
Note: Though Cervical cancer is more common in reproductive age group, it
can be a cause of post menopausal bleeding.

HISTORY TAKING

Presenting complaint:
 Bleeding/ spotting PV

History of present illness:

 To assess the severity of bleeding: number of pads used/ day,
completely soaked/not, passage of clots, waking up at night to change
pads.
 Ask for symptoms of anemia: fatigue, breathlessness on exertion,
dizziness, palpitation
 Other symptoms:
 post coital bleeding, (cervical c/a)
 vaginal discharge,( blood stained/ offensive in cervical c/a)
 lower abdominal pain/backache, (mets/ nerve involvement)
 loss of appetite, loss of weight
 fever and constitutional symptoms( PID)

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  bladder and bowel symptoms ( obstructive uropathy, hematuria,
vesicovaginal/rectovaginal fistula)

Past history
 Diabetes, hypertension, dyslipidemia, hypothyroidism, PCOS( all-
predispose to endometrial c/a)
 Drugs: Hormone replacement therapy ,Tamoxifen( both are risk factors
for endometrial c/a)
 OCP( protective against endometrial c/a and risk factor for cervical c/a)
 Aspirin, anti coagulants

Menstrual history
 Early menarche, Late menopause
Marital history
 Age of marriage
Obstetric history
 Nulliparity and infertility (risk factors for Endometrial c/a)
 Increasing parity ( risk factor for cervical c/a)
Personal history
 Smoking( active/passive)- risk factor for cervical c/a
Family history
 Other malignancies (HNPCC-Lynch 2- breast, ovary, endometrial,
colorectal, gastric c/a)
Socioeconomic status
 Cervical c/a more common in low socioeconomic status.

EXAMINATION
 BMI: Obesity- risk factor for endometrial c/a ( Asian classification: 23-
25- overweight, >25-obesity)
 Cachexia in advanced disease

General examination:
 Lymph node enlargement (Supraclavicular LN and inguinal LN)
 Pedal oedema( cervical c/a)
Vitals: BP: Hypertension
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Abdominal examination: Hepatomegaly, ascites

MANAGEMENT
ENDOMETRIAL CARCINOMA
First I would like to complete my examination by doing:
1) Per speculum examination : to look for growths, ulcers in vagina and
cervix
2) Pap Smear (screening)
3) Bimanual pelvic examination:
 direction, size and consistency of uterus
 enlargement of uterus for growth / pyometra
 Adnexal masses(size,consistency,tenderness,mobility)
 nodularity of cul de sac(tenderness)

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Note:
- TVS helps to assess endometrial thickness, polyps, pyometra, fluid
collections. Sonohysterography (saline instillation) is better for
delineating endometrial thickness.
- For premenopausal women: thickness > 8mm is considered significant
- Fc: Fractional curettage- not preferred now. Earlier used to diagnose
cervical extension. But has very high false positive and false negative
rates.

Other Investigations
Aims: To detect local spread, mets, assess fitness for anaesthesia.
- Routine pre op investigations
- Detailed USG to assess myometrial invasion
- CXR for mets
- MRI
- CA-125 (elevated in advanced cases)

Note: MRI is not done routinely.

Uses: To assess local spread to adnexa, cervix, myometrial invasion,
tumor size.
Lymph node involvement not reliably detected by CT/MRI.

TREATMENT

Endometrial hyperplasia(WHO Classification)

Type of hyperplasia Progression to cancer
Simple without atypia 1%
Complex without atypia 3%
Simple with atypia 8%
Complex with atypia 29%

Note: In new classification(2014), theres only hyperplasia with and without

atypia
TREATMENT
1)Simple without atypia: Progesterone
- Dose: cyclical progesterone 10 mg/day for 10 days/month.
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-If severe: Initially high dose continuous progesterone ie, 15-30 mg in divided
doses of any 19-nortestosterone derivatives like norethisterone (primolut-N)
for 1 week. Then taper over 2 weeks. Then put on cyclical medroxy
progesterone acetate 10 mg from day 5- day 25 for 6 months. Repeat biopsy
after 6 months to ensure reversal.
-Note: alternative therapy: LNG-IUS or Mirena

2) Complex or if atypia is present:

Best option: -Hysterectomy
-If fertility needs to be preserved: High dose
contiuousprogestins like Megestrol acetate 40-160 mg/day. Therapy to be
continued for atleast 3 Months. Biopsy done after 3-4 weeks of cessation of
therapy.

ENDOMETRIAL CARCINOMA
-Surgical staging by staging laparotomy (FIGO classification)
Steps: -Ascites/ peritoneal washings for cytology
-Systematic exploration of abdomen and pelvis
-Biopsy of suspicious areas
-Sampling of diaphragm
-Hysterectomy with b/l salpingooophorectomy (TAH+BSO)-
surgical management
Cut open uterus aims: To assess
- tumor size
- depth of myometrial invasion
-cervical involvement
-Remove suspicious pelvic and paraaortic nodes
-Careful documentation of operation findings
Note: * Indications for lymphadenectomy
 Tumor histology- clear cell, papillary, squamous or grade 2-3
endometroid.
 Myometrial invasion more than half
 Extension to cervical glands
 Tumor size> 2cm
 Extrauterine disease

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 *Infracolicomentectomy is done for papillary serous and clear cell tumors.
(They resemble ovarian tumors in intraabdominal spread)
*Depth of myometrial invasion, tumor grade and histology are most
important prognostic indicators

Stage 1:
 TAH +BSO +/- lymphadenectomy +/- infracolicomentectomy +/-
radiation
Stage 2:
 Radical hysterectomy+ BSO + pelvic and paraaortic lymphadenectomy
OR
 Combined radiation and surgery, ie,External pelvic radiation and
brachytherapy with intracavitary radium or Cesium followed in 6 weeks
by TAH + BSO.
Note: Indications for adjuvant radiotherapy in stage 1-2 endometrial cancer
Grade 1 and 2 with no
LOW RISK or minimal myometrial No further treatment
invasion

INTERMEDIATE RISK Grade 3 with no Brachytherapy to vault

invasion
-Grade 3 with any
HIGH RISK invasion Brachytherapy to
-Any patient with vault +
>50%invasion Teletherapy
-Cervical glandular
involvement
-Positive pelvic nodes

Stage 3:
Debulking surgery + chemoradiaition
Stage 4:
Debulking surgery+ palliative treatment
Note:

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 Chemotherapy in stage 3 and 4 :
 cisplatin and paclitaxel.
 Progestins may be useful
 for recurrence:
if tumor is hormone receptor positive
 High dose medroxy progesterone 50-100mg thrice daily or
 Megestrol acetate 80 mg twice daily.
 Continue till disease is static or in remission
 If progestins fail, chemotherapy may be tried
 Agents: doxorubicin, platinum compounds(cisplatin,Carboplatin) and
paclitaxel.

CERVICAL CANCER
First I would like to complete my examination by doing:
1)Per speculum examination
- cauliflower like growth
- barrel shaped cervix
- ulcer
- vaginal involvement
2)Pap smear
3)Bimanual pelvic examination
- classic signs of malignancy: friability, induration, bleeding on
touch, fixity due to parametrial spread.
- Enlarged uterus due to tumor invasion or pyometra
4) Rectovaginal or rectal examination
- induration laterally denoting parametrial spread
- fixed mass due to extension to pelvic side walls
- thick rectovaginal septum
- rectal mucosal involvement

INVESTIGATIONS
- In case of an obvious lesion: Deep punch biopsy
- No obvious lesion: depending on Pap smear report:

Epithelial cell General recommendation

abnormality

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 ASC-US HPV DNA testing
If high risk HPV present,
colposcopy
If absent, cytology at 6 and
12 months
ASC-H Colposcopy and biopsy
LSIL Colposcopy
HSIL and squamous cell Immediate colposcopy and
carcinoma biopsy
AGC, AIS, Immediate
adenocarcinoma colposcopy,endocervical
curettage
Endometrial sampling in
women with risk factors or
if there are atypical
endometrial cells

LSIL- low grade squamous intraepithelial lesion

HSIL- high grade squamous intraepithelial lesion
ASC- atypical squamous cells
-US(undetermined significance),
-H(cant exclude HSIL)
AGC- Atypical glandular cells
AIS- Adenocarcinoma insitu
If a microinvasive carcinoma is suspected on colposcopy, take a cone biopsy

Other Investigations(mainly to assess local spread and mets)

- Barium enema, proctoscopy, sigmoidosopy
- Cystoscopy
- Intravenous pyelogram
- Chest Xray
- Skeletal Xrays
Latest FIGO staging(2018)
Stage Description
I The carcinoma is strictly confined to the cervix (extension to the uterine corpus should be
disregarded)
IA Invasive carcinoma that can be diagnosed only by microscopy, with maximum depth of
invasion< 5mm

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 IA1 Measured stromal invasion <3 mm in depth
IA2 Measured stromal invasion ≥3 mm and <5 mm in depth
IB Invasive carcinoma with measured deepest invasion ≥5 mm (greater than stage IA), lesion
limited to the cervix uteri
IB1 Invasive carcinoma ≥5 mm depth of stromal invasion and <2 cm in greatest dimension
IB2 Invasive carcinoma ≥2 cm and <4 cm in greatest dimension
IB3 Invasive carcinoma ≥4 cm in greatest dimension
II The carcinoma invades beyond the uterus, but has not extended onto the lower third of the
vagina or to the pelvic wall
IIA Involvement limited to the upper two‐thirds of the vagina without parametrial involvement
IIA1 Invasive carcinoma <4 cm in greatest dimension
IIA2 Invasive carcinoma ≥4 cm in greatest dimension
IIB With parametrial involvement but not up to the pelvic wall
III The carcinoma involves the lower third of the vagina and/or extends to the pelvic wall and/or
causes hydronephrosis or non‐functioning kidney and/or involves pelvic and/or paraaortic
lymph nodes
IIIA Carcinoma involves the lower third of the vagina, with no extension to the pelvic wall
IIIB Extension to the pelvic wall and/or hydronephrosis or non‐functioning kidney (unless known
to be due to another cause)
IIIC Involvement of pelvic and/or paraaortic lymph nodes, irrespective of tumor size and extent
(with r and p notations)
IIIC1 Pelvic lymph node metastasis only
IIIC2 Paraaortic lymph node metastasis
IV The carcinoma has extended beyond the true pelvis or has involved (biopsy proven) the
mucosa of the bladder or rectum. A bullous edema, as such, does not permit a case to be
allotted to stage IV
IVA Spread of the growth to adjacent organs
IVB Spread to distant organs

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 Fibroid/ leiomyomas

Presenting complaints: ( mnemonic - MD PAPPI )

 Menstrual disturbances - progressive menorrhagia , polymenorrhagia ,
metrorrhagia ( submucous fibroid) postmenopausal
 Discharge PV
 Pain - congestive , spasmodic ( read difference of both ) Abdominal pain,
A/c pain (torsion,reddeg, Haemorrage)
 Abdominal lump
 Pressure symptoms - bladder & bowel
 Pregnancy loses, Infertility
Types:
A. Intramural
B. Subserous
C. Submucous
D. Cervical
E. Broad ligament
Complications: (mnemonic - DUST BIN)
1. Degeneration
2. Ulceration
3. Sarcomatous change
4. Torsion
5. Bleeding
6. Infection
7. Neoplasm (endometrial CA)

Differential diagnosis: (mnemonic - KAHEE BI POPE)

1. Kidney( pelvic kidney)
2. Adenomyosis*
3. Hematometra ,pyometra*
4. Ectopic pregnancy
5. Endometriosis
6. Bladder ,Bicornuate uterus
7. Inversion uterus
8. Pregnancy , Polyp
9. Ovarian tumour *
10.PID
11.Endometrial CA

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Aetiology
 Estrogen excess
 Early menarche
 Nulliparity
 Increasing body weight
 Exogenous hormones
 Familial association
 Smoking reduces risk

Mechanisms of menorrhagia

Increase in endometrial surface area due to submucous and intramural

fibroids

Increased vascularity

Interference with normal uterine contractility

Endometrial ulceration and haemorrhage over a submucous fibroid

Compression of venous plexuses in myometrium causing venostasis

Associated endometrial hyperplasia and anovulation due to

hyperestrogenism

Increased production of growth factors

Mechanisms for infertility

Mechanical means Defective implantation

Cornual myomas may cause tubal Impaired blood supply causing

atrophy and ulceration of
Occlusion
endometrium overlying a submucous
fibroid

Impaired gamete and embryo Endometrial hyperplasia causing

transport defective implantation

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Altered relation between cervical and Changes in vascular flow altering
vaginal pool of semen delivery of cytokines needed for
implantation

Distortion of cavity Alteration of normal immune

response to the implanting fetus

Causes of acute pain

Red degeneration
Expulsion of submucous fibroid
Hemorrhageinto fibroid
Torsion of pedunculated fibroid
A/c retention of urine in cervical fibroids

Effect of fibroids on pregnancy

Pregnancy Labour After delivery
Early and late Prolonged labour PPH
miscarriage
First trimester bleeding More chance of caesarean Retained placenta due to
submucousmyoma in
lower segment
Preterm labour Difficult delivery of baby Puerperal sepsis
at CS
PROM Classical CS in cervical
fibroids
Abruption Increased bleeding at CS
Placenta praevia
IUGR
Malpresentations

Effect of pregnancy on fibroids

Increase in size
Red degeneration
Torsion of pedunculatedsubserousmyoma

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Infection of submucousmyoma in puerperium

Differences between uterus and adnexal mass on examination

Uterine mass Adnexal mass
Uterus Uterus not felt separate Uterus felt separate
Transmitted mobility Present Absent
Location Likely to be central Likely to be lateral
Groove between mass Absent present
&uterus
MANAGEMENT
 complete clinical examination by doing:
1) Per speculum examination
2) Pap smear
3) Bimanual pelvic examination

 INVESTIGATIONS
To confirm diagnosis:
1. USG- Combined TAS+ TVS
Uses:
 To confirm nature of a pelvic mass (fibroid usually hypoechoic)
 Number and location
 assess ovaries
 Ascites
 assess kidneys and ureters (hydronephrosis)
 myoma mapping in case of multiple fibroids
 Endometrial thickness(cut off in reproductive age group:8mm)
Note:* TVS – high resolution – helps to identify small submucous fibroids and
distortion of cavity
*TAS- to assess kidneys and ureters
* MRI not routinely done. May be done to exclude adenomyosis

2. Sonohysterography
 Instill saline into endometrial cavity during TVS
 To find small submucous fibroids, fibroid polyps when there are
symptoms like menorrhagia, infertility and pain
 Extent of fibroid projecting into cavity can be assessed
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 3. Hysteroscopy
 diagnostic and therapeutic for submucous fibroids
 An endometrial sampling may be taken if h/o irregular bleeding
present
Other investigations:
1. BRE(Hb and PCV for anemia)
2. Thyroid function tests
3. Coagulation profile
4. LFT, RFT
5. Tests for anaesthesia fitness
TREATMENT
1. Surgical
2. Medical
3. Expectant
4. Radiological interventions

Note: Choose which 1 to say 1st according to patients age, completion of family
and wish for future fertility.
A. Surgical
1) Myomectomy
-For those who wish to preserve fertility
Preoperative counselling:
- Risk of recurrence-50% in 5 years
- Conversion to hysterectomy in case of severe intra op
bleeding(take consent)
- Risks and complications of myomectomy
- Arrange plenty of cross matched blood.
- If done for infertility rule out all other possible causes
- Pregnancy rates following procedure

Measures to limit blood loss at myomectomy

Time surgery during immediate postmenstrual period
Controlled hypotensive anaesthesia
Vasopressin instillation into serosa and myometrium
overlying myoma(20 u in 200 ml saline)
Tourniquets at internal os and infundibulopelvic ligament

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 to occlude uterine and ovarian vessels respectively
Bonney myomectomy clamp and ring forceps to occlude
uterine and ovarian vessels respectively
Pretreatment withGnRH agonists to reduce vascularity
Plenty of cross matched blood

Types of myomectomy
a) Open myomectomy
Steps:
1) Incision in uterus :
Anterior (to minimise adhesions) and lower(stronger scar) incision is preferred
Note: Bonney hood incision can be used to remove a single posterior fibroid
where Redundant flap is sutured onto anterior wall to avoid posterior
adhesions.
2) Removal of myomas
 After incising myomasenucleated through cleavage plane of capsule.
 Multiple myomas may be removed through a single incision using
tunnelling incisions
3) Closure
-Mattress sutures for closing myometrial defects with 1-0 to 2-0 vicryl
-Serosa approximated using baseball stitches with 3-0 to4-0 vicryl

b) Hysteroscopic myomectomy
-For pedunculatedand submucous fibroids
- <5 cm in size, >50% projecting into cavity
c) Laparoscopic myomectomy
- For intramural and subserous fibroids
d) Vaginal myomectomy
-For pedunculated submucous myomas

Complications of myomectomy
Intraop
-Primary haemorrhage
-injury to ureters (broad ligament and cervical fibroids)
-Injury to bladder, rectum

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 -Conversion to hysterectomy
Postop
- Myoma fever
- Reactionary and secondary haemorrhage
- Relaparotomy
Sequelae
- Adhesions between uterus and rectosigmoid
- Peritubal adhesions leading to tuboperitonial infertility
-Adhesions render future surgery difficult
-Recurrence
-Persistence of menorrhagia

2) Hysterectomy
In women who have completed their family
- Vaginal hysterectomy preferred (refer prolapse in capsule for steps)
-Abdominal hysterectomy for large fibroids
-Ovaries conserved if normal
Abdominal hysterectomy:
Pre op preparation
Investigations and pre-anaesthetic check up
Intra op antibiotics given
General/ regional anaesthesia
- Pelvic examination done
- Catheterise
- Dorsal supine position
- Clean and drape
Steps:
1) Open abdomen - Pfannensteil incision
2) First pedicle
 Round ligaments clamped cut and ligated
 Ureter should be identified as it crosses the common iliac artery
 If ovaries are to be removed, infundibulopelvic ligament containing
 Ovarian vessels clamped cut and ligated
 If ovaries are to be retained, fallopian tube and ovarian ligaments are
clamped cut and ligated
3) Bladder dissection
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  Dissect bladder from anterior cervix
 Divide peritoneum below attachment to lower uterine segment
 Push it down
4) Second pedicle
 Uterine vessels clamped cut and ligated
5) Third pedicle
 Cardinal ligaments and uterosacrals clamped cut and ligated
6) Vaginal angles and edges
 2 clamps are used to clamp across vagina below cervix
 then divide vagina above these clamps
 Uterus and cervix removed
7) Closure of abdomen
 parietal peritoneum need not be closed
 rectus fascia closed with continuous delayed absorbable sutures like PDS
 s/c fat need not be sutured
 skin closed with absorbable suture

Post op care
 Retain catheter for 24 hrs
 On the day of surgery, only IV fluids
 Next day start oral fluids if bowel sounds heard
 Early ambulation (obese women – heparin thromboprophylaxis)
 Remove dressing on 3rd day
 Discharged on 5th day

Complications
Immediate Late sequalae
Primary hemorrhage Reactionary Incisional hernia
haemorrhage
Ureteral injury Secondary Vault prolapse
hemorrhage
Bladder injury Wound dehiscence
Rectal and bowel Wound infection
injury
Urinary infection

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 Intestinal obstruction

Paralytic ileus
Peritonitis
septicemia
DVT, pulmonary
embolism
Fistula

B. MEDICAL
Uses:
 Reduce tumor size and thus facilitate surgeries
 Relieve symptoms like menorrhagia and correct anemia
 Reduce intraop bleeding
 Women nearing menopause may be managed with medical
management alone
Disadvantages:
 Hypoestrogenism-hot flushes, osteoporosis, vaginal dryness
 a/c degeneration and pain.
 At lap myomectomy, enucleation may be difficult as plane of cleavage
becomes less defined
 Small myomas may be missed which may grow back after surgery
Options:
1) GnRH agonists
-goserelin 3.6mg and leuprolide 3.75 mg as monthly s/c depot injection.
-single dose 11.5 mg 3 monthly may be given
-Optimal duration of treatment prior to surgery -3 months
2) GnRH antagonists
-Certrorelix, ganirelix
3) Antiprogestins
-RU 486/mifepristone, continuously in doses of 25-50mg daily
4) LNG-IUS

C. Expectant management
Criteria :
 Absolute certainty of diagnosis(ovarian mass excluded)
 Asymptomatic

665
  No evidence of ureteral comptression
 Size<12-14 weeks
 willing for follow up

D. Radiological interventions:
1) Uterine artery embolization
Contraindications:
Pregnancy, pelvic infections, malignancy, coagulopathy
Technique:
 Trans femoral approach
 Polyvinylalcohol particles used
 Uterine arteries occluded
 Ischemic necrosis of fibroid
Complications:
Pain, hematoma, fever, infection, vaginal discharge, radiation
exposure

2) Magnetic resonance guided focused ultrasound energy(MRg-FUS)

contraindications:
scars on abdomen, large myomas, desire for future fertility

Important topics:
 Cervical fibroids:
-May compress bladder causing urinary retention
-central cervical fibroid with uterus on top- lantern on dome of St
Pauls
-Surgical challenges: inaccessible, proximity to bladder and ureters
-central ones cause difficulty in pregnancy and labour.
-Obstructed labour, LSCS difficult( Classical CS may be required)
 Broad ligament fibroids:
2 types:
- True: No attachment to uterus. Originate from smooth
muscle fibres In broad ligament. They are lateral to ureter
False: Subserous fibroids arising from lateral uterine wall and
grow between layers of broad ligament. They are medial to
ureter.

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 OVARIAN MASS
Presenting complaint
1. Abdominal swelling
2. Pressure effects- bowel , bladder, cardioresp
3. Hormonal effects - estrogen , androgen
4. A/c pain -torsion , haemorrhage, infection, rupture, malignancy
5. DUB
6. Non specific symptoms mimicking CA stomach (early satiety ,Loss of
appetite &
Weight ) or CA colon ( dyspepsia , bloating)

Etiology :
1. Estrogen excess conditions
2. Family history

Types of ovarian tumours: WHO classification scully 1999

( mnemonic -SMUGGLES )

667
1. Sex cord stromal *
2. Metastatic
3. Unclassified
4. Germ cell *
5. Gonadoblastoma
6. Lipid cell
7. Epithelial (90%)*
8. Soft tissue

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Complications :
1. Torsion ,rupture , hgm ,infection, pseudomyxomaperitoni
2. Malignancy
3. Mets - omentum,liver ,lung

Differential diagnosis - fibroid + dd of fibroid

Clinical features of malignancy:

669
 1.Bilateral ,multilocular
2. >10cm
3. Hard or variable consistency
4. Rapid increase in size
5. Fixity
6. Lymph nodes
7. Loss of appetite or weight
8. Nodularity of pouch of Douglas
9. +ve tumour markers
10.Mets
11.Ascites

Spread:
1. Direct - omentum , paracolic gutter , hemi diaphragm , liver capsule ,
intenstine , mesentry
2. Lymphatic - pelvic , para aortic , supraclavicular
3. Hematogenous - liver parenchyma , lungs

EXAMINATION
Abdominal examination
Mass
Bilateral / unilateral
Consistency (Tense / cystic / variable)
Mobility (fixed/restriced/mobile)
Borders (Well/ ill defined )
Lower border palpable/ not
Surface (smooth/ irregular)
Percussion (dull over mass, resonant flanks)
Ascites (flanks dull), hydrothorax
Other masses (hepatomegaly/ uterus)
PV examination
1. Transmitted mobility (present in uterine mass, absent in ovarian)
2.Fornices (full in ovarian mass)
3.Cul de sac (nodularity)

Investigation:
1. Blood -LFT,RFT
2. For the tumour –
-pap smear and perspeculum examination
- endometrial biopsy

670
 -USS : combined transabdominal and transvaginal
-CT,MRI
-Tumour markers CA 125 and CA 19-9 (read in detail)
-staging laparotomy (read staging laparotomy)
3. Colon - Barium enema , colonoscopy
4. stomach - Barium meal , endoscopy
5. Lung -CXR
6. Bladder - IVU
7. Pre OP work up

USG features suggestive of malignancy

 Solid / echogenic
 Multilocularity
 Thick and fronded septation
 B/L
 Papillary projections
 Doppler: increased vascularity, low resistance flow
 Ascites , hepatomegaly

TREATMENT :

1. Benign
 if young : cystectomy or oophorectomy
 if > 40 yrs :TAH + BSO
2. Malignant
 Staging laparotomy (read in detail)
 Surgery - TAH + BSO + INFRACOLIC OMENTECTOMY
After surgery
 stage 1a or b – no post op chemo
 stage 1c and High risk - adjuvant chemo carboplatin/ paclitaxel for 3-
6 cycles
 advanced cases - maximal cytoreductiove or debulking surgery
 satisfactory – post op chemo 6-8 cycles
 not satisfactory – 3 cycles chemo followed by
interval cytoreductive Surgery and chemo is resumed

STAGING LAPROTOMY
Incison – vertical
1. ascites /peritoneal washing : for cytology

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 2. systemic exploration of abdomen and pelvis – clockwise starting from
caecum
3. biopsy of suspicious areas – send for HPR
4. sampling diaphragm
5. infracolic omentectomy
6. pelvic para aortic node evaluation and lymphadenectomy
7. documentation of intra op findings
cytological and histopathological analysis of samples taken and surgical staging
of tumor.
Read latest FIGO staging !!

Fibroid Ovary
Firm Cystic
Midline Lateral
Hypogastrium Iliac fossa
No fullness of fornices Fullness of fornices
Transmitted mobility No Transmitted mobility
Mobility only if Mobility unless fixed
subserouspedunculated

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 PROLAPSE
Case format
Name , age, place
Occupation (Heavy load workers, Working in squatting position)
__ years postmenopausal
Presenting complaint- Mass per vaginum x 4 months
History of present illness
The patient noticed a mass protruding from the vagina 4 months back. It was
initially small, and gradually increased in size. It is more towards evening and
also on coughing and straining. It decreases in size on lying down.
There is increased frequency of micturition. She experiences difficulty in
initiating micturition, and is able to pass urine only after reducing the mass,
and usually passes urine in standing position. There is also feeling of
incomplete voiding. No h/o dysuria, urgency.
No h/o straining to defecate or feeling of incomplete emptying.
No h/o back pain, pelvic pain.
No h/o discharge pv, bleeding pv.
No h/o chronic cough, constipation.
She consulted a local hospital and was advised to undergo surgery. She was
referred to SATH and is now admitted for surgery.

Menstrual history
*Menopause attained at __ years (Menopause- Most important factor)

Marital history

Obstetric history
 Multiparity
 Vaginal delivery (Pelvic floor trauma)
 Home delivery ( Untrained dais, Premature straining, No episiotomy)
 Prolonged labour
 Instrumental delivery
 Birth weight of baby
 Inter pregnancy interval
 Post natal period
673
Past history
 Chronic cough/COPD
 Constipation
 Abdominal mass
 Previous surgery( Hysterectomy- vault prolapse, Abdominoperineal
resection, radical vulvectomy)
Personal history
Bladder/ bowel complaints

General examination- BMI (Obesity- risk factor)

Systemic examination- Respiratory system- COPD
Abdomen- Mass, ascites, muscle tone
Local examination
 Pubic hair clipped
 Labia majora normal, labia minora atrophic
 A mass of size 3x4 cm, pinkish, is seen protruding through vagina,
leading part is cervix which is hypertrophied. External os seen,
transverse slit like. No bleeding, ulceration, discharge.

Per speculum
 Anterior vaginal wall- pale, decreased rugosity, cystocele present
 Posterior vaginal wall- rectocele present

Palpation
 Not getting above swelling(to differentiate from procidentia)
 Tone of levator ani normal, sphincter tone normal

Diagnosis
3rd degree uterovaginal prolapse, cystocele, rectocele

MANAGEMENT
First, complete the clinical examination.
 Pap smear
 Bimanual pelvic examination

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  Assessment of pelvic floor muscles- Assess pubococcygeus pert of
levator ani at 4 & 8 o’clock position-ask patient to contract the muscle
 Per rectal examination- Assess tone of anal sphincter

Q)How to differentiate between enterocele and rectocele?

5. Retract the posterior vaginal wall with Sims speculum & hold posterior
lip of cervix with Volsellum forceps. The cervix is kept reduced. The
patient is asked to cough & speculum is slowly withdrawn. If bulge
appears from above downwards- enterocele.
6. By per rectal examination
7. By retracting anterior vaginal wall

Q)Decubitus ulcer
 In most dependent part, due to venous stasis
 Should be healed before surgery
 Clean with povidone iodine & keep it reduced
 If non- healing, take biopsy to r/o malignancy

Q)Pessary test
 In case of stress incontinence & to detect occult stress incontinence

Then, investigations.
1. USG abdomen- Assess uterus
- Intraabdominal mass
- Hydronephrosis
2. URE , Urine C&S- To rule out UTI
3. RFT

D/D
Cystocele
1. Gartner’s cyst - Typical location in anterolateral aspect of
vaginal wall. Can be differentiated by catheterization.
2. Urethral diverticulum

UV prolapse

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 1. Chronic uterine inversion- Absence of ext os; feel for the cervical
ring. On USG- uterine fundus not seen.
2. Submucous fibroid polyp- Absence of external os. Confirm by USG.
3. Congenital elongation of cervix- The fornices are deep.

TREATMENT
I. SURGICAL
Vaginal hysterectomy + pelvic floor repair (Ward- Mayo repair)-read in
detail-pg 340,341,410-413
 Anaesthesia- GA/ RA
 Position- Lithotomy
 The part is cleaned and draped
 PV is done and bladder is catheterised with metal catheter
Steps
7. Anterior colporrhaphy & pushing up of bladder
8. Cervical incision is extended posteriorly & pouch of Douglas is opened
9. Uterus is delivered anteriorly & UV fold is incised
10.1st clamp- uterosacral & cardinal ligaments- cut & ligated
11.2nd clamp- uterine vessels
12.3rd clamp- round ligament, fallopian tube & ovarian ligament
13.McCall culdoplasty for enterocele
14.Peritoneum closed by purse string suture
15.Anterior colporrhaphy is completed –bladder buttressing is done &
redundant vagina is removed
16.Posterior colpoperineorrhaphy for rectocele

Vault prolapse
 Sacrospinous colpopexy- Vaginal approach- vaginal vault is attached to
sacrospinous ligament
 Sacrocolpopexy- Abdominal approach- combined with Halban procedure

Nulliparous prolapse
 Abdominal sacrohysteropexy
 Purandare sling operation
 Shirodkar sling operation
 Khanna sling operation

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 Enterocele
 Vaginal procedure- McCall culdoplasty ( Internal/ external)
 Abdominal- Halban and Moscowitz procedures

Other surgeries
 Le Fort operation/ colpocleisis- For elderly women unfit for
surgery.Vaginal epithelium is removed & vagina is obliterated.
 Manchester/ Fothergill operation- Anterior colporrhaphy+ amputation
of cervix+ suturing cardinal ligaments to front of cervix.For women who
completed the family, but wish to retain uterus.
 Shirodkar extended Manchester operation- Cervical amputation is
avoided.

II. CONSERVATIVE
1. Pelvic floor muscle strengthening by Kegel’s exercise
2. Weight loss
3. Treat precipitating factor (cough, constipation)
4. Pessaries
 Used in
- Patient unfit for surgery
- Unwilling for surgery
- Pregnancy
- Lactation
 Types
Support pessary- eg. Ring pessary
Space filling pessary- eg. Gelhorn & cube pessaries
 Read how to fit pessary- pg 339
 Complications- vaginal irritation, discharge, erosion, fistula

*Complications of prolapse- Ulcer, UTI, Hydronephrosis

*BADEN AND WALKER CLASSIFICATION

Grade I- Descent to vaginal midplane
Grade II- Descent to hymenal ring or introitus
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Grade III- Descent to halfway through introitus
Grade IV- Procidentia

SUPPORTS OF PELVIS- VERY IMPORTANT!

DELANCEY CLASSIFICATION
 Level I (Suspensory axis) - Uterosacral and cardinal ligaments- suspends
cervix& upper vagina.
Defects in this level cause apical prolapse (UV prolapse, enterocele, vault
prolapse)

 Level II (Attachment axis) – Supports midvagina by fascial septae to

pelvic sidewall- anteriorly pubocervical fascia & posteriorly rectovaginal
fascia. (fuses to form arcus tendineus fascia pelvis & arcus tendinous
fascia rectovaginalis)
Defect in this level causes paravaginal & pararectal defects.

 Level III (Fusion axis) – Supports lower vagina. Endopelvic fascia fuses
with adjacent structures.
Defects here- rectocele & perineal descent posteriorly, urinary
incontinence anteriorly.

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 INSTRUMENTS
1. Sims’ speculum
• Needs an assistant to hold
• To retract posterior vaginal wall in order to visualize the anterior vaginal
wall and cervix
• Procedures - D&C, polypectomy, cervical biopsy, anterior colporrhaphy,
vaginal
 hysterectomy, etc
• To insert or remove an intrauterine device

2. Cusco’s speculum
• Adv- self retaining
• Disadv- obscures the vaginal walls, hence lesions may be missed
• To visualize the Cervix and take a pap smear
• For cryocauterization and LEEP of the Cervix
• Intrauterine insemination

3. Simpsonsuterine sound
• To confirm the size and direction of uterine cavity prior to any procedure
like D&C
• To measure the length of cervical canal and diagnose supravaginal
elongation of Cervix
• Investigate missing IUD by taking an Xray with sound insitu
• To differentiate b/w polyp and inversion.( sound can pass by the side of
a polyp, but will stop short in inversion)

4. Multiple toothed volsellum forceps

• curve is to occupy the pelvic curve
• To hold the ant. Lip of Cervix in D&C, anterior colporraphy and vaginal
hysterectomy
• To hold the post.lip of Cervix in posterior colpotomy to drain a pelvic
abscess and in
• vaginal hysterectomy while extending the incision posteriorly.
• To hold the post. Lip of Cervix , reduce the prolapse and look for
enterocoele while the patient strains.
• To hold the cervical stump after a subtotal hysterectomy after removing
the rest of the Cervix.

5. Hegars cervical dilators.

• Dilatation of Cervix prior to D&C, evacuation etc
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 • Identify cervical incompetence- no.8 dilator passes easily. (other
methods- USG and HSG)
• Hysteroscopy.
• Amputation of cervix and fothergill’s operation
• Application of intrauterine radium in brachytherapy.
• Pyometra or haematometra.
• Removal of an IUD with missing threads.
• Cervical stenosis.
• For uterine manupilation during hysteroscopy.

6. Uterine curette
• Sharp at one end and blunt at the other.
• Held like a pen.
• To check the completeness of an evacuation of pregnancy-using the
blunt end, to prevent perforation
• For D&C in anovulatory DUB, suspected endometrial cancer. TB
• 7. Cervical punch biopsy forceps.
• To take a biopsy from the Cervix after colposcopy.
• To take a cervical biopsy when there is actual growth.

8. Ovum forceps.
• Does not have a catch.
• Used for evacuation.

9. Allis tissue forceps.

• To hold the peritoneum or rectus fascia while opening and closing the
abdominal wall.
• To hold the margins of vagina in ant. Colporraphy and vaginal
hyserectomy.
• To hold ant. Lip of Cervix in place of a volsellum Forceps.
• To hold the margins of vagina while closing the vagina in an abd
hysterectomy.
• To catch the two torn ends of the external sphincter in repair of a
complete
• perineal tear.

10. Artery forceps.

• To secure bleeding vessels.

11.Kochers clamp.

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 • As a clamp in abdominal and vaginal hysterectomy to clamp the
pedicles.

12.Babcock’s forceps.
• To catch hold of the fallopian tubes in tubal sterilization and tubal
recanalistaion.
• To remove the lymph glands during lymphadenectomy.

13. Dissecting forceps.

• Non-toothed- to hold soft tissues like bowel, bladder etc for suturing in
case of surgery.
• Toothed forceps- to hold rectus fascia.
• Skin suturing.
• Vaginal wall margins in vaginal procedures like ant. Colporraphy, vaginal
• hysterectomy, perineorrhaphy etc.

14.Right - angled forceps.

• To isolate a blood vessel before ligation as in internal iliac artery ligation.

15. Sponge holding forceps.

• To disinfect operating field.
• To inspect Cervix for injuries.
• To catch hold and remove retained membranes.

16. Myoma screw.

• To fix the myoma before applying traction and enucleating it in
myomectomy.
• To give traction to a uterus enlarged with multiple fibroids in abdominal
hysterectomy.

17. Bonney’s myomectomy clamp.

• In myomectomy- to temporarily minimize thre blood supply to uterus
and
thereby reduce bleeding.
• Applied at the level of the internal os, including two round ligaments, to
prevent slipping. Should be released frequently.

18. Mayo scissors.

• For exicising tissues.

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19. Metzenbaum scissors.
• Fine tissue dissection, especially to release adhesions

20. Leech Wilkinson cannula

• To assess tubal patency in infertility- hysterosalphingography,
chromopertubation
21. Rubin’s cannula
• Tubal patency at laparoscopy

22. Colpotome.
• To make an incision in the posterior fornix and drain the cul-de-sac in a
pelvic abscess.

23. Uterus holding forceps

• To hold the uterus atraumatically especially when performing
conservative
surgery on the tubes.

24. sacrospinous colpopexy needles

• Used to anchor the vault of vagina to the sacrospinous ligamnets in
sacrospinous colpopexy.

25. Clamp to remove ovaries at VH.

• A curved clamp which can be used in a vaginal hysterectomy where the
adnexa have to be removed. It can be used to clamp the
infundibulopelvic ligaments without fear of slipping.

26. Suction cannula metallic

• Late first trimester abortion
• Evacuation of vesicular mole

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