Vol

MY FINAL CLINICAL
SEMESTER
RaVi KiRaN – 2K8
Well……this book is collection of Clinical cases taken by me
G.RAVI KIRAN a Student of prestigious GANDHI MEDICAL
COLLEGE Hyderabad, during my final Clinical semester &
I tried to cover all the Exam cases.
After every case a small note on case discussion is given
which are clinical notes given by my teachers during my
case presentation.
Personally I feel that History is important for any case sheet
writing so my teachers emphasized on it which I think
would reflect in this book.
Reasons for Asking particular history,& Relavant theory has
to be studied from your respective Books & Clinical skills
must be & Should be learned in your Clinical wards.
I tried my best to avoid mistakes.
…………..Wish you ALL THE BEST FRIENDS…………..

I would like to Thank my friends Shiva, Bose, prashanthi,

Gouthami for helping me in clinical wards & My teachers
for Sharing their Valuable Knowledge with Us………

Hope this Book Helps you in your Preparation friends 

G.Ravi kran 2k8

Vol 1
 CONTENTS:

1 MEDICINE

2 OBSTETRICS

3 GYNECOLOGY

4 SURGERY

5 PEDIATRICS
2
Page
 1)) Hemiplegia

2)) Ascitis
1
3)) CVS – MS

4)) Pleural effusion

MEDICINE
5)) Manual for short cases
3
Page
 HEMIPLEGIA B/B: regular Sleep: N
Addictions: Non smoker & occasional alchoholic
Vijay/Male/39/Cook/Kudappah/ 17 – 07 – 12
Family H/O:
C/C: No H/O similar complaint in family &
Weakness of R UL & LL & No H/O any chronic illness in family
Deviation of Mouth to L with slurring of speech
Physical examination
from 2 days
(A) general survey –
H/C/C: patient is Consious.
PATIENT WAS APPARENTLY ASYMPTOMATIC 1 Moderately built &
day back then yesterday he went to work, returned adequately nourished
home, had dinner & then he slept & woke up at 11 P (-) I (-) C (-) C (-) K (-) L (-) E (-)
pm went to bathroom , returned to bed then he
No NC markers
suddenly developed weakness of R UL & LL (he
No tendon xanthomas/ xanthalesma
awakened his wife also) simultaneously he
No carotid bruie
developed deviation of Mouth to L with slurring of
Facies: Mouth deviated to Left
speech
on attempted talking
No H/O loss of consciousness
Decubitus:- Normal
NO H/O head trauma
NO H/O headache, projectile vomiting Vitals – a febrile,
NO H/O seizures HR: 84/min N in volume, rhythm
NO H/O pain in neck No RR/RF delay all PP +ve
NO H/O similar complaints in past BP: 120/84 mm hg RUL: supine,
NO H/O hypertension / smoking RR: 20/min regular regular
NO H/O memory loss / behavioural changes
NO H/O symptoms suggestive of other cranial (B) Local examination (CNS)–
nerves
1)) Higher functions
H/O complete weakness of R UL & LL at the time of
Handedness: R
attack but now he is able to move his limbs & eat
Level of consciousness: Fully consciousness
on his own
Orientation: +ve
NO H/O Involuntary movements
Emotional state: Normal
Able to feel ground on walking & Clothes
Memory: preserved
NO H/O tremor of hands while reaching to glass
Speech: Articulation disturbed
H/O passage of urine at the time of attack but now
passage of urine & faces is N (continence 2)) Cranial nerve Examination:
maintained)
I Normal Normal
Past H/O: NO H/O similar complaints in past, HTN, II Normal Normal
DM, TB, epilepsy, chest pain & bleeding disorders Visual acuity
Visual fields
Treatment H/O: No H/O any surgical procedures / Colour vision
Long term treatment III,IV.VI Normal Normal
Light reflex
Personal H/O: Accomodation
4

Diet: mixed Appetite: N Eye movements

Page

Nystagmus
 V Normal Normal Lower Limb K,A: ++ K,A: +
Sensory Visceral reflexes ? ?
Motor Released Absent Absent
VII Forehead & Deviation of reflexes
wrinkling mouth to L on
present showing his
teeth 5)) Sensory system:
VIII
Vestibular Normal Normal Proprioceptive Present & N Present & N
Auditory Exteroceptive Present & N Present & N
IX & X Palatal reflex + & Uvula Cortical Present & N Present & N
gag reflex NOT midline
done
XI Normal Normal GAIT: N tanden walking
XII No deviation / / No wasting & CEREBELLAR: Able to do Knee heel test, finger nose
fasciculations N power test No dysmetria / No dysdiadokokinesia
ANS: No abnormal sweating, constipation
RAISED ICT SIGNS: Absent
3)) Motor System:
MENINGEAL IRRITATION SIGNS: No neck rigidity
A)) Inspection
/ Kernings / Brudzunskie signs
No Gross Muscle wasting / Hypertrophy seen
SKULL & SPINE: Normal
No involuntary Movements
PERIPHERAL NERVES: Normal
B)) Palpation
(C) Systemic examination:
Bulk
UL 26cms 25cms 1)) Abdominal examination:
LL 43cms 43cms
Umbilicus is midline
Tone
NO Lumps palpable / Palpable organomegaly
UL Clasp Knife rigidity Normal
LL Normal (?) Normal NO free fluid
Power 2)) Respiratory system:
UL 3/5 5/5 BLAE: N &
LL N vesicular sounds heard
Involuntary NO adventitious sounds
UL Absent Absent
3)) Cardiovascular system:
LL
Heart sound 1 & 2: Heard & No murmurs heard
Co ordination Able to do Knee heel test, finger
UL nose test No dysmetria / No
LL dysdiadokokinesia Diagnosis: A case of Complete completed Left
hemiplegia due to CVA with Left 7th cranial
nerve UMN type of palsy in the stage of
4)) Reflexes:
recovery (Now hemiparesis) which is probably
Superficial Embolic in origin in MCA territory at the level of
reflexes internal capsule.
Abdominal Lost Lost
Plantar
With alchoholism, Old age, male as risk factors
Deep tendon
reflexes & No complications of recumbancy
5

Jaw jerk ? ?
Page

Upper limb B,T,BR: ++ B,T,BR: +

 ASCITIS Family H/O:
No H/O similar complaint in family &
Ramraju/55/M/warsiguda/Manual labour No H/O any chronic illness in family

C/C: Physical examination

Yellowish Discolouration of eyes – 20 days (A) general survey –
Abdominal distension – 15 days patient is C/C/C . Hepatic facies +ve
blood per stool – 15days P (-) I (-) C (-) C (-) K (-) L (-) E (-)

H/C/C: HR: 88/min N in volume, rhythm

PATIENT WAS APPARENTLY ASYMPTOMATIC 20 No RR/RF delay all PP +ve
days back then he developed yellowish BP: 130/86 mm hg RUL: supine,
discoloration of eyes, insidious In onset, progressive, RR: 22/min regular regular.
associated with itching & yellowish discoloration of
Parotid enlargement +ve (painless)
urine from 15 days
No loss of axillary hair
H/O weight loss & appetite loss – 6m
No hepatic flap
H/O vomiting – 6m 2/3 per day , 30 min after
hands: Normal
food, contained undigested food, yellowish, No
No odor from patient
blood, no odour.
No spider neavi
H/O abdominal distension – 15 days progressive,
No supraclavicular fullness
with H/O 3 tappings (he don’t know the colour)
No allergic signs of Tuberculosis
H/O Abdominal pain – 4 days: sudden, continous,
progressive, twisting type, aggravated after taking (B) Local examination (Abdominal)–
food, partially relieved on medication 1)) Oral cavity:-
H/O back pain, orthopnea – 4 days Tongue, pharynx, faucal pillars, Teeth , tonsils :
H/O passage of black tarry stools – 4 days within normal range
NO H/O hematemesis 2)) Abdomen:
NO H/O facial puffiness a)) Inspection:
NO H/O pedal oedema Abdomen is generally distended,
NO H/O decreased urine output Umbilicus everted & displaced downwards & all
H/O taking local herbal medicine quadrants move equally with respiration , epigastric
H/O alcoholism – 15 yrs – 500ml/day pulsations +ve (probably aortic)
No visible peristalsis,
Past H/O: Jaundice - 1 yr back –treated with local
No engorged veins
medicine & subsided Not associated with fever
No other swellings visible &
NO H/O similar complaints in past, HTN, DM, TB,
Skin over abdomen Normal
epilepsy, chest pain & bleeding disorders
No echymosis over flanks / around umbilicus
Treatment H/O: No H/O any surgical procedures / No skin nodules around Umbillicus
Long term treatment No puncture marks
b)) Palpation:
Personal H/O: No Local rise of temperature/ tenderness/rebound
Diet: mixed appetite: N tenderness/Abdominal wall rigidity present
B/B: bladder regular bowel blood per stool & No lumps palpable
tarry stools passage Liver: Lower border & Left lobe Not palpable
6

Sleep: disturbed Spleen: Not palpable

Page

Addictions: Non smoker & massive alchoholic Fluid thrill –ve

 c)) Percussion: Shifting dullness +ve
Liver upperborder: 5 th ICS in MCL (liver span: 14cm)
Traube’s space:- obliterated (dull)
d)) Auscultation: Bowel sounds heard & Normal
pitch & No venous Hums heard
Blackout episodes – 6months
Where there is brief loss of consciousness, NOT
preceded by any sensation of movement / Aura &
are NOT followed by any confusion / amnesia /
headache

GROIN: Orifices Free H/O easy fatigubility – 1 yr

GENETALIA: N (no loss of pubic hair/ testicular H/O Cough – 5 months , insidious, progressive
atrophy) Productive & is red coloured,
PR: NOT done Aggravated on exertion & on lying down
No H/O penicillin Injections
(C) Systemic examination: No H/O sorethroat with joint pain/swellings
1)) Respiratory system: Past H/O: NO H/O similar complaints in past, HTN,
BLAE: N & DM, TB, epilepsy, chest pain & bleeding disorders
N vesicular sounds heard
NO adventitious sounds Treatment H/O: No H/O any surgical procedures /
2)) Cardiovascular system: Long term treatment / Penicillin prophylaxis
Heart sound 1 & 2: Heard & No murmurs heard
Personal H/O:
Diagnosis: Alcoholic liver disease with liver Diet: mixed & appetite: reduced
cirrhosis in decompensated state. B/B: regular & Sleep: N
Addictions: Non smoker / alchoholic
CVS – MS Family H/O:
No H/O similar complaint in family &
Kumar/17/M/Student/Medak
No H/O any chronic illness in family
C/C:
Physical examination
SOB – 1yr
(A) general survey –
Palpitations – 1yr
patient is C/C/C
Backout episodes – 6m
Moderately built &
L Chest pain – 1 Month
adequately nourished
H/C/C: P (-) I (-) C (-) C (-) K (-) L (-) E (-)
Patient was apparently assymptomatic 1 yr back
N facies
then he developed SOB & Palpitations
NO SC nodules / Erythema marginatum
SOB, Insidious in onset, Exertional. Relieved on NO Splinter haemorrhages
taking rest, gradually progressive, Started as NYHA – NO Osler nodes/janeway lesions
1 now it is NYHA – 3. NO malar flush
H/O PND attacks – 5months: 3episodes/night
Normal statured
H/O Orthopnea – 5months
NO high arched palate
Palpitations - Continous, Regular, Aggravated on NO syn- / Poly- dactyly
exertion & relieved on taking rest.
Vitals –
Not associated with Polyuria / Chest pain /
afebrile,
7

Lightheadedness
HR: 84/min N in volume, regular
Page
 rhythm, No RR/RF delay all PP +ve No other adventitious sounds like Clicks / Tumour
BP: 110/74 mm hg RUL: supine plop / Pericardial rub heard
RR: 16/min regular , TA
(C) Systemic examination:
(B) Local examination (CVS)–
1)) Respiratory system:
1)) Inspection: BLAE: N &
Chest is Normal with No deformities N vesicular sounds heard
Trachea is in midline NO adventitious sounds
Precordium appears Normal 2)) Abdominal examination:
(No buldge / retraction) Umbilicus is midline
No pulsations are seen in M/T/P/A area, NO Lumps palpable / Palpable organomegaly
No pulsations seen in suprasternal, supracavicular, NO free fluid
infraclavicular, epigastric / Back
Apex beat – Not visible Diagnosis: A case of Organic MS Probably of
Back is Normal (No spinal deformities) rheumatic origin with No clinical features of CCF /
2)) Palpation: IE & patient is sinus rhythm at present
Trachea Midline
M:- Apex beat in 5 th ics 1cm lateral to Midclavicular Pleural effusion
line Localized with diastolic thrill & is tapping in
character Rangareddy / 56 / M / Hindu / Nalgonda / Daily
T:- Normal labourer
P:- Pulsations are palpable
C/C:
A:- Normal
Cough from 20 days
prasternal heave :- +ve (grade 3)
L Chest pain from 15 days
No palpable Rub
Difficulty in respiration from 10 days
3)) Percussion:
Right border corresponds to Right sterna border & H/C/C:
left border corresponds to apex & 2 nd ics (pulm Patient is apparently asymptomatic 20 days back
area) is dull then he developed cough which is
4)) Auscultation: Insidious in onset, Progressive, Non productive,
Apex pulse deficient:- 0 No haemoptysis
A mid – diastolic murmur harsh & rumbling is heard No aggravating / relieving factors
best in Mitral area with No radiation & heard best No diurnal variation
in left lateral position with bell & heard best after Chest pain – 15 days, Left sided, Insidous, Stabbing
exercise & end of expiration type, continuous, Aggravated on cough, sneezing
partially relieved on medication, rest & Exertion
M T P A Other
No radiation & is disturbing sleep
S1 Loud S1 N
S1 N S1 N Gibsons
Difficulty in taking respiration – 10 days
S2 N S2 N
P2 Loud A2 N Neoaortic
& S2 N Insidious in onset, present at rest, NON progressive.
split No associated wheeze, Aggravated on exertion &
Murmur Murmur Murmur Murmur Infraclav relieved by lying on his L side
MDM NO ESM NO NO H/O PND attacks
Normal NO H/O Orthopnea
8
Page
 NO H/O fever with evening rise / night sweats
NO H/O Noisy respiration
NO H/O Trauma
NO H/O Inhaler usage
NO H/O Nasal / Ear discharge
NO H/O Recent hospitalization / Ventilation
Past H/O:
NO H/O similar complaints in past, HTN, DM, TB,
epilepsy, chest pain & Bleeding disorders & there is
NO H/O suggestive of Skin rash, Joint pains
(Collagen Vascular Disorders)
NO scrofula / Scrofuloderma
NO small muscles (of hand) wasting
Vitals: HR: 88/min N in volume, rhythm
No RR/RF delay all PP +ve
BP: 130/86 mm hg RUL: supine,
RR: 22/min regular .Abdominothracic
NO use of accessory muscles & there is
NO intercostal / Supraclavicular Suction
JVP: not elevated
(B)Local examination

Treatment H/O: No H/O any surgical procedures / 1)) URT (Favoring Aspiration / not)
Long term treatment Nose (turbinates, congestion , polyps)
& nasal septum: N
Personal H/O: NO nasal discharge
Diet: mixed appetite: N NO Nasal flare
B/B: regular Sleep: N NO lupus pernio
Addictions: Non smoker & occasional alchoholic NO sinus tenderness elicited
No drug allergies Oral hygiene satisfactory
NO halitosis
Occupational H/O: Pharynx (Oro – Teeth, gums, palate, post
No H/O suggestive of Exposure to organic / pharyngeal wall: N, Larynx – NOT examined)
inorganic dusts
2)) LRT
Family H/O:
No H/O similar complaint in family & INSPECTION
No H/O any chronic illness in family from front
Chest is N in shape
General Examination: movements are diminished on left side
(A) Physical examination apical impulse: NOT seen
Patient is C/C/C fullness seen on left side in middle & lower part
P (-) I (-) C (-) C (-) & there is NO wrist tenderness Supraclavicular & Infraclavicular fossa : N
K (-) (NO swellings / Suction / Fullness)
L (-) NO cervical / Scalene LN palpable Both the nipples are at same level
E (-) & There is No Signs of DVT / Erythema NO tracheal deviation
nodosum on legs Skin is Normal (NO scars / Sinuses / Suction marks)
N facies NO crowding of Ribs
Moderately built & Adequately nourished NO chest wall sweelings
Normal decubitus NO venous prominence / arm swelling
N voice & cough NO paradoxical chest Movement
NO Tobacco/nicotine staining.
NO Flapping tremor From back (Standing position)
Eyes : Normal (No ptosis / contracted pupil / Subcj
hemorrhage / Chemosis / ruddy cyanosis / No spinal deformities
9

Phlyctens) Skin is Normal

Page

Both shoulders are at Same level

 Inf border of scapula are at same level Coin percussion & Shifting dullness: Absent
NO winging / Drooping Hepatic dullness is in 5 th ICL R
Spino – Scapular distance: Same on both sides on
inspection AUSCULTATION
NO gibbus R L
Intercostal suction & rib crowding : not seen Ant N vesicular & NO Diminished breath
Adventitious sounds In mammary
PALPATION sounds VR: N & Inframammary
area NO
NO local rise of temperature /
Adventitious sounds
NO local tenderness / Intercostal / punch tenderness VR: decreased in
Slight tracheal deviation to R same areas
NO tracheal Tug Lat N vesicular & NO Diminished breath
Crico Sternal distance is Normal Adventitious sounds In
Apex beat not palpable sounds VR: N infraaxillary
Chest Movements – area NO
Adventitious sounds
Reduced on Left side Lower & middle
VR: decreased in
Chest Expansion – same area
2.5cm on R side & 1cm on L side Post N vesicular & NO Diminished breath
Adventitious sounds In
Vocal fremitus sounds VR: N Infrascapular
NO Adventitious
R L sounds VR:
Ant Diminished in decreased in same
N mammary & area
Inframammary area Apical / N vesicular & NO N vesicular & NO
Lat N Diminished in Kronig’s Adventitious Adventitious sounds
Infraxillary area isthmus sounds VR: N VR: N
Post N Diminished in
Infrascapular area
(C) Systemic examination:
No other Palpable accompaniments (Friction ,
Rhonchila fremitus, pleural / pericardial rub) 1)) Abdominal examination:
Normal palpatory findings on R side Umbilicus is midline
NO Lumps palpable / Palpable organomegaly
PERCUSSION NO free fluid
Free hernia sites
R L
2)) Cardiovascular system:
Ant Resonant Dull in
mammary & Heart sound 1 & 2: Heard & No murmurs heard
Inframammary 3)) CNS: Patient is C/C
area No neck rigidity (TBM)
Lat Resonant Dull in Within N limit
Infraxillary area
Post Resonant Dull in Diagnosis: A case of L sided Pleural effusion
Infrascapular
probably of tuberculous origin
area
10

Apical /
Kronig’s Resonant Resonant
Page

isthmus
 LR Sternal tenderness
Manual – Short cases
1 Ankle oedema (Anemia perse, CCF, Renal disorders
causing Anemia)
Anemia: Qualitative / quantitative decrease in
Hb/RBC in relation to Age / Sex / Altitude clinically 1U packed RBC – raise Hb by 2 gm% (Globally
manifesting as pallor: Chronic Blood loss is the commonest Cause)
•Lower palpebral conjunctiva (polycythemia &
Scleroderma:- tightness during retraction) * Iron deficiency anemia:
•Tongue (tip & dorsum) * •Pica
•Palate •Glossitis / Bald tongue
•Nail beds •Angular stomatitis
•Palms & soles •Platynychia & brittle nails
•Brittle hair & dysphagia (PV Syndrome)*
14.6 – 15.5 gm% - Males &
13.3 - 15.5 gm% - females B2 (Megenta colored) ,
(Clinically 14.5%: 100%) Glossitis / Bald tongue B12 (Raw beefy tongue),
Fe, FA defeciency
Pallor (pathological entity) is waxy appearance of Excessive Alcohol,
skin & mucous membrane (depends on blood flow Tobacco, herpes labialis,
Angular stomatitis B2, B12, Fe, FA
& Qualitaty & quantity of skin) – Anemia (Clinical
deficiency, Candidiasis,
entity) & Low cardiac output states Strp infection
Pale PALM - <7gm %
Pale RETINA - <4gm% Macrocyctic Hypochromic Anemia: Dimorphic
if Hb % is between 81% - 99gm%: it is not evident anemia (Pregnancy & Hook worm infection)
clinically as pallor
Leucoerythroblastic picture: Normoblasts &
H/O Weakness, lassitude, Giddiness, fainting, Myelocytes both are seen in Peripheral Blood in
Palpitations, breathlessness, Tinnitus, Lack of •Myelophthisic anemia
concentration, Dysphagia* (Infiltration by granuloma / umour),
Treatment H/O: NSAID intake •M6 variety AML
Dietary H/O: Dysphagia •Myelofibrosis & Sclerosis
Personal H/O: Alcohol & Walking barefooted
family H/O Polycythemia / Ruddy cyanosis: Mucous membrane
is Dusty Red & Facial Plethora, Suffused Conjuctiva,
Causes: Nutritional, Hook worms, Leukemia, Palmar erythema
Hemolytic disease, Hemetemesis, Chronic Bleeding
hemorrhoids & menorrhagia, Chronic Systemic Anemia & Polycythgemia: Fallots (If hb <18gm%,
diseases (SLE, RA, SBE, Malignancy, Uremia & CLD) PCV <55%: Anemia)

CVS Tachycardia, Functional MI & haemic 2

murmer at pulmonary area, CCF
Hyperdynamic apex, Capillary pulsation, Cyanosis: Bluish discoloration of Skin & MM due to
Ankle oedema, dyspnoea presence of increased amount of Reduced Hb
11

Resp Basal Creps (>5gm%) / Hb derivatives(Sulfa >0.5gm% OR

Nervous Polyneuropathy Methe >1.5gm%:- Enterogenous / pigment
Page

tissue Cyanosis) in capillary blood

 (DD:-CO poisioning, Argyria, Osteogenesis
Imperfecta only sclera, Amiodarone giving bluish
hue to skin – Ceruloderma) Cyanosis + PolyCythemia: CCongenitalHD & COPD

Differential: PDA with Shunt reversal (FEET BLUE) Hypoxia Cyanosis Condition
+ve +ve Rhb >5gm %
Reverse Differential: COA + TGA (FEET RED)
+ve -ve Severe Anemia
Orthocyanosis: Only in upright position (Pulmonary (hb <5gm%)
-ve +ve PCV (red
AV malformations in middle & lower Lobes)
cyanosis)
Peripheral Central
•Nose Tip •Tongue (sides, Under)*
Pigment cyanosis (Spectroscopic Examination): Hb
•Ear lobules • Inner aspect of Lips
•Outer aspect of Lips •Lower palpebral Cnj M, Nitrites & nitrates, Aniline dye poisoning &
•Tip, Nail beds of •Nasal, rectal mucosa & Carboxyhb: Cherry red apppearence – NOT TRUE
fingers & toes Retina cyanosis
Stagnant & Hypoxic Hypoxia
Overutilization Hypoxia 3
•CCF •CCyanoticHD
•Raynauds •Acute Pulm oedma Jaundice: Yellowish discoloration of Skin & MM due
•Shock •Acute severe Asthma / to excess Bilirubin in blood (Clinically >3gm%)
•Arterial diseases: TAO COPD/Embolism/ 1 – 3gm%: Latent jaundice
•Venous diseases: SVC S Laryngeal oedema 0.3gm% - 1gm% : Normal
•Cryoglobulinemia •Pulm AV fistula •Upper bulbar Conjuctiva (Lot of ELASTIN:
•MS (mitral facies) •Eisenmenger Syndrome
Underlying Sclera)
Application of warmth
•Palate
Cyanosis will decrease NO Effect
reverse with Cold •Palms & Soles
Application of Pure O2 Cyanosis may improve •Skin
for 10 min: NO response (DD:- Carotenemia:Only Skin affected,
Clubbing & Atabrine toxicity: Skin & Sun exposed Sclera,
Polycythemia: Usually present Diffuse xanthamatosis)
Absent Usually
Respiratory distress: -ve May be present Unilateral: Hemiplegia & unilateral oedema
Hands: Cold Hands: Warm
Pulse Volume: LOW N / HIGH 4

Pulse: Expansion & Elongation of Arterial wall

Intermittent Cyanosis: Ebstein’s Anomaly imparted by Column of blood & is inturn produced
by Pressure changes in ventricular Systole & diastole)
Cyanosis Clubbing Condition – mentioned in 8 ways
+ve +ve Central
Cyanosis Semi pronated & slightly flexed wrist: lateral to
Peripheral Flexor carpi radialis (For VOLUME & CHARACTER
cyanosis
– Carotid artery)
+ve -ve & Acutely
developing
Pulse deficit: HR – PR (AF >10 / min & Multiple
Central
cyanosis Ectopics <10 / min)
12

-ve +ve SBE , Ulcerative

HR 1min then PR 1min (2 Cardiac cycles)
Page

Colitis
Steth & Palpate for Radial Pulse Count dropped
 Beats (1 Cardiac cycle) Tortuous & Thickened
2 different examiner’s (1 Cardiac cycle) Wall (Atherosclerosis rarely palpable:
Intima)

In ectopic Beat / Premaure beat / Extrasystoles Block Brachial artery & Palpate Radial
(Hypertensive / Thyrotoxis / Cardiomyopathic) OR
: Impulse arises from Ventricular / Atrial wall / AVN Exsanguate with middle fingers & then
– It is small & premature Followed by a palpate with 2 index fingrers
RR delay •Cervical rib
compensatory pause (Dropped / Missed beat)
•Aneurysm of aortic arch
•Takayasu’s arteritis •Iatrogenic:
Absent radial pulse: Anatomical abnormality, Severe
Bllalock taussing’s shunt
Atherosclerosis, Takayasu, Embolism •Pre subclavian
Coaorctation
Mean pressure:- Mean of SBP & DBP + 1/3 Pulse
• Supravalvular aortic stenosis
pressure •Pressure over axillary artery by LN
•Embolism
8 CHARACTERISTICS **Simultaneously Palpate 2 Radial A
Rate 60 – 100 / min
RF delay • Coaorctation of aorta
Tachycardia (>100/min)
•Aortoarteritis
•Sinus tachycardia
•Atherosclerosis of aorta
•Relative tachycardia
** Simultaneously Palpate 2 arteries
•Paroxysmal Tachycardia (SVT / VT)
*** Normally there is difference of
Bradycardia (<60 / min)
0.02 to 0.03 Sec (Femoral 1st) but
•Myxoedema
clinically simultaneous
•Obs jaundice
•Athelets Periph pls Ulnar: Wrist medial side
Brachial: Just medial to biceps tendon
• Increased ICT •Hypothermia
at / just below elbow
•Propanolol / digoxin •Hypoxia
Subclavian: Middle of clavicle
Rhythm Regulary / irregulary irregular
(Shrug Shoulders & palpate from
Regulary irregular:- Extrasystoles, 2
behind)
HB, Pulsus Bigeminus
Carotid: Medial to SCM at / Below
Irregularly Irregular:- AF, Multiple
the level of thyroid cartilage
extrasystoles, Afl
Femoral artery: Midway btw ASIS &
Irregular but N HR:
PT
Digitalised AF, Sinus arrhythmia
Popliteal artery: Semiflexed Knee &
Amplitude / Excursion felt –
Supine with thumbs on Tibial
PULSE PRESSURE (30 – 60mm)
tuberosity & Fingers on middle of PF
•Stroke volume & Arterial compliance
Post tibial artery: Midway Achilles &
High (>60mm)
MM After INVERSION of FOOT
•Hyperkinetic states
N: CATACROTIC pulse
•Complete HB & Bradycardia of any
•Percussion wave
Volume cause
•Tidal wave
•Atherosclerosis
•Dicrotic & Ancrotic Notch
Low (<30mm)
This is Not palpable become it is
•Shock
Obliterated By N vascular tone
•Severe AS & MS
•CCF Anacrotic notch

Wall may be palpable in old age due

13

to Arteriosclerosis / MEDIAL
Page

MONCKEBERG’S SCLEROSIS:

Character
(Volume &
Waveform)
1)) Bounding: Hyperkinetic states
2)) Anacrotic : LOW VOLUME PULSE
WITH UPSTROKE IN ASCENDING
LIMB
•Severe AS
•Actually in AS: PULSUS PARVUS
(low Volume) et TARDUS (slow
rising) – PLATEAU PULSE
3)) Dicrotic: LOW VOLUME PULSE
WITH UPSTROKE IN DESCENDING
LIMB
•Endotoxic shock, hypovolemic shock
& 2 nd week of typhoid fever
• Very low CO + decreased PR
4)) WH pulse: HIGH VOLUME +
SHARP RISE + ILL SUSTAINED +
SHARP FALL pulse
•Also called HIGH VOLUME
COLLAPSING PULSE
•Victorian toy – Half of glass
cylinfder is filled with water & other
with vacuum if turned upside down -
Thud heard by Water strike
• Classically seen in AI
HIGH VOLUME: INCREASED
STROKE VOLUME + DECREASED PR
(due to stimulation of baroreceptors
in aortic arch by large CO resulting in
sympathetic withdrawl)
COLLPASING : DIASTOLIC LEAK
BACK + RAPID DISTAL RUNOFF
14
DUE TO VERY LESS PR
•Other causes of High volume can
Page
also cause this type of pulse wave
** Webs fall on radial artery & rest of
palm on ulnar artery – Examine the
volume (both R & U arteries) Now
elevate the hand (Gravity ¬ fall of
blood column ¬ more amount in
aortic arch ¬ Even more Sympathetic
withdrawal ¬ Even more reduction
of PR ¬ Even more elevation of Pulse
pressure & Also artery will be in line
with aorta SO pressure changes of
rapid rise & rapid fall can be easily
appreciable) & Examine the pulse
(rapidly rises with thud & rapidly
falls)
5)) Pulsus bisferiens:
•HIGH VOLUME & DOUBLE
BEATING (P wave & T wave) :
•AS + AI / Isolated AI & HOCM
•if P > T: AI > AS if T > P: AS > AI
• 1st wave due to Large volume
ejected by LV & 2 nd wave by elastic
recoil & also due to VENTURI &
BERNOULII’S Effect
6)) Pulsus Alternans: ALTERNATE
PULSES ARE WEAK WITH REGULAR
RHYTHM
•Acute LVF
•Compensatory pause absent
• Some Myocardial fibres healthy
some are degenerated (Defective
mechanical coupling)
•Gallop rhythm & Basal creps
7)) Pulsus Bigeminus & Trigeminus:
2/3 BEATS & A PAUSE (because
2 nd/3 rd beat is ectopic so there is
compensatory pause)
•Digitalis toxicity & 3 : 2 HB
8)) Pulsus paradoxus: EXAGGERATED
INSP FALL OF SBP > 10MM HG +
PULSE V DECREASES IN
INSPIRATION & INCREASES IN
EXPIRATION
•Acute severe Asthma , C
tamponade, COPD, Restrictive
Cadiomyopathy, Constrictive
pericarditis
•A)) Intrapericardial pressure raises
more during inspiration
Impedes Diastolic filling thus reducing
the cardiac output
B)) Anti – Bernheim effect: Increased
 intrathoracic pressure ¬ more blood Oral temperature NOT taken if: Bell’s palsy,
is sucked into RV ¬ Reduced Blood inflammatory conditions, Mouth breathers, Trismus,
into LV & Deviation of After Hot tea, Convulsions, Mentally dull people
Interventricular septum to L ¬
Reduction of CO Hyperthermia Hypothermia
• Actual paradox is heart sounds may Malaria Myxoedema coma
be still audible when no pulse is Aseptic fever Enteric fever associated
palpable in radial artery •Heat stroke in Prf / Hmrg
9)) Thready (Low Volume + Rapid •Leukemia & lymphoma Alcohol intoxication
(peripheral c Failure ) / jerky (HIS) •SLE Prolonged Cold
•Pontine haemorrhage exposure
•Porphyria Hypoglycemia
Sphygmomanometer: •Thyroid storm Autonomic dysfunction
1)) Hess capillary fragility test •Acute MI
2)) Latent tetany: TROUSSEAU’S Sign (Raise >SBP Malignant hyperthermia Periodic fever:
for 3min: carpal spasm) •Halothane •Hodgkins
3)) Draw venous blood •Haloperidol •Malaria
Septicemia •brucellosis
4)) Hill’s sign in AI
Encephalitis •Relapsing fever
5)) Assess respiratory reserve Lobar pneumonia
6)) Different types of pulses

Pulsus Paradoxus SBPe > SBPi (>10mm) Hectic temperature: Big swing in temperature
suddenly with chills & rigors & Sudden fall with
Gallavardin’s sign
sweating after few hours
Initially on reducing only
Strong beats are heard •Pent up pus anywhere
Pulsus Alternans SO Heard Beat APPEARS •Septicemia & pyemia
only Half actual value
On further reducing Fall by lysis Fall by crisis
Both strong & weak are Fall of temperature Fall gradually in steps
heard – Original HR suddenly with sweating over several days
heard very fastly in 6 – 12 hrs
•Enteric fever •Uncomplicated EF
WH pulse PP >60mmhg •Acute lobar pneumonia •Rheumatic Fever
•Dengue •Acute
•Adrenal crisis bronchopnemonia
5

Temperature: 98 – 99 F (lowest in morning & For 1F rise of temperature RR increases by 2 – 3/min

highest in evening : diurnal variation of 1.5 F) & PR 10/min (adults) & 12 – 15/min (Childrean)
Hence Oral AM >98.9F & Oral PM >99.9F – Fever
Relative Bradycardia Relative tachycardia
R (1F)> O (0F) > Ax (1F) (Tympanic membrane Rise of PR is Rise of PR is
thermometer fast & Accurate) Proportionatly low Proportionatly high
•Any viral fever •Acute R carditis
Clinical thermometer has a mark at 37C / (98.6F) •1st week of enteric fever •Diphtheric myocarditis
clinically above this is taken as fever •Brucellosis •PAN
•Psittacosis & weil’s
(When kept in axilla)
15
Page
 Thermometer is Triangle in C.S – Magnifies the Drug fever: Sulphonomides, Slaicylates, Iodides,
mercury line & Kink is present to prevent return of Barbiturates, penicillin, quinidine & rifampicin
mercury Line after it is taken from recorded site
6
Intermittent Continued Remittent
Quotidian •RF •Acute Oedema: Excessive fluid in SC space & / OR serous
(daily) •Miliary TB broncho sacs due to increase in Interstitial component of ECF
•Double •2 nd week EF pneumonia
infection with •Amoebic LA 2/3 ICF & 1/3 ECF (3/4 IF & 1/4 Plasma)
Plasmodium Double •UTI & 3 rd
•TB quotidian week EF In ALL patients with oedema SACRUM &
•UTI fever / Camel SCROTUM should be examined…& Never miss
Tertian hump fever PARIETAL oedema (Present particularly over
(Alt days) (Double abdominal wall) :- In upper part of body Sternum,
•Benign (Vivax fever spike in lateral epicondyle, Forehead has to be pressed
& Ovale) single day)
•Tertian •Kala azar Pitting Non pitting
(Falciparum) •Gonococcol CCF, NS, Liver F, Myxoedema
Quartan (2d) Endocarditis Hypoproteinemia, Lymphatic oedema
** Fever **fever DO ** fever DO Constrictive pericarditis, Angioneurotic oedema
present for only NOT FLUCTUATE Pericardial effusion , Sclerederma
few hours & FLUCTUATE more than 3F Wet Beri - Beri
ALWAYS more than 1.5F during 24 hr Generalized Localized
TOUCHES THE during 24 hr period & Anasarca / Dropsy Venous obstruction
BASELINE period & NEVER CCF, NS, Liver F, (Pregnancy, SVC,IVC
SOMETIMES NEVER RETURNS THE Hypoproteinemia, syndrome,DVT)
DURING THE RETURNS THE BASELINE Constrictive pericarditis, lymphatic obstruction
DAY BASELINE Pericardial effusion , Tb, filariasis, Radiation,
Wet Beri - Beri dissection, Infiltration of
LN
Typhoid state: Untreated EF in 3 rd week which is Allergy: AgNO
manifested as neurological manifestations Inflammatory: Insect /
1)) Semi consciousness Snake bite
2)) Coma vegil: Half eyes open but ignorant of
surroundings
Pitting oedema demonstratable if increase In W
3)) Subtulus tendinum: Inv movements of fingers &
>10 – 15 % & Circumference >10%
wrists
4)) Carphology: Plucking of bed sheets CCF : Legs ¬ face ¬ Ascites
Renal: Face ¬ legs ¬ Acsites
Fever with rash Fever with membrane Liver: Ascites ¬ Legs ¬ face
1st day: varicella Follicular tonsillitis Nutritional: Feet + face ¬ Ascites
2 nd day: scarlet fever Faucal diphtheria
3 rd day: Small pox Candidiasis
4rth day: Measles Vincent’s angina •Low oncotic pressure
5 th day: Typhus Infectious MN
•High capillary hydrostatic pressure
6 th day: DEngue
•Increased permeability
•Obstructed Lymphatic Drainage
16

Increased PR ratio: Narcotic poisioning (n: 4:1) •Renal retention (Due to decreased flow, Sec
Decreased PR ratio in Acute lobar pneumonia Hyperaldosteronism, Increased ADH levels)
Page
 Pedal oedema Facial puffiness
CCF, NS, Liver F, CCF, NS, Liver F, •SBE •Lung abscess*
Hypoproteinemia, Hypoproteinemia, •Brochogenic carcinoma •Empyema thoracis*
Constrictive pericarditis, Constrictive pericarditis,
Pericardial effusion , Pericardial effusion , Unilateral Unidigital
Wet Beri – Beri, Wet Beri – Beri
Varicose veins, DVT SVC syndrome, Cushings •Subclavian Coarctation •Hereditary
Syndrome, AngNO / aneurysm •Repeated trauma
•Cervical rib •Sarcoidosis

In renal Causes Swelling of SCROTAL SAC & Upper limb Lower limb
EYELIDS is classical
•Chronic Obs Phlebitis •Infected AAA
7 due to chronic IV drug •PDA with shunt
addiction reversal
Clubbing / Hippocratic fingers / Lovibond’s sign: •Subclavian Coarctation
Bulbous enlargement of Terminal part of Fingers & / / aneurysm ** Acute clubbing
OR toes due to increased pulp tissue mass •Cervical rib (<2W)
(Proliferation of Subungual Soft Tissue + Interstitial
oedema + Capillary Dilation) resulting in increased *** Pseudo clubbing: Subperiosteal Bone resorption
AP diameter & Transverse diameter (NO Pulp tisse enlargement / Increased Curvature)
•Scleroderma
Onychodernal / Lovibond’s Angle: Angle Btw nail & •Acromegaly, Leprosy
nail bed (160) (Adjacent skin fold) – Usually index •Occupational (ViCl2: Acrosteolysis)
finger is 1st to Affected
Koilonychia: Spooning - 3 stages
1 See tangentially for loss of LbAngle* ¬
st
1st: Brittleness 2 nd: Flattening (platynychia)
Fluctuation ¬ Window sign / Schamroths’s sign 3 rd: Spooning

1st degree Fluctuation + loss of Angle Mechanism

2 nd degree 1st + Increase in T & AP diameter Anoxic Opening & Dilation
3 rd degree 2 nd + Increased pulp tissue Toxic SBE
(Parrot beak / Drum stick Appearance) Reflexive / Neurogenic
4 degree 3 rd + wrist / Ankle selling due to HOA
th
Metabolic Thyrotoxicosis
*Most reliable early sign Humoral Acromegaly
Reduced ferritin Dilation & Opening
Causes: (recent view)
Hereditary
1)) Cardiac: Cyanotic HD, ABE, Eisenmenger’s Platelet & Megakaryocytes Release of PDGF &
2)) Lung & pleural: Bronchiectasis, Lung abscess, trapping TNF - α
Empyema thoracis, CF, Pulm AV fistula, CF
3)) Ulcerative Colitis
4)) Biliary Cirrhosis DIGIT RATIO: Calculate diameter at Nail base &
5)) Intestinal: Crohn’s & Coeliac disease distal IPJ – Clubbing (+ve) if Sum of all fingers, >10
6)) Normal / Idiopathic
PHALANGEAL DEPTH RATIO: (Calipers) : Index
7)) Genetic / familial
finger is used & DISTAL PHLANGEAL DEPTH :
INTERPHALANGEAL JOINT ration >1
17

Always Look for swelling & tenderness at wrist

Page

Painful Reversible
 HPOA / Pierre – Marrie – Bamberger Syndrome: If H > 97 th centile
Primary / Hereditary (AD) •Marfan’s syndrome {defective Crosslinking of
Secondary (Any clubbing cause) Mostly collagen due to AD mutation in fibrillin 1 & 2 genes}
•Bronchial Carcinoma (1/2) & Pleural mesothelioma (a)) Skeletal: US < LS, AS > H, Steinberg’s sign /
•Chronic suppurative lung diseases Thumb sign / Hyper extensibility +ve – Thumb
•Chroniv Liver diseases extends beyond ulnar border of Hand, High arched
palate, Straight back syndrome, Wrist sign +ve –
-Pain is aggravated on dependency Little finger & thumb overlap >cm around wrist,
-Pathologically:- Periosteal thickening due to Sub Metacarpal index >8.4 – 4 metacarpals length
periosteal New Bone formation & Digit ends show divided by width at midpoint & values are averaged
Osseous resorption , Pectus carinatum, Pectus Excavatum, Pes planus,
NAIL Condition Cavus, Long & narrow facies / Dolicocephalus
Pitting Psoriasis, Reiter’s disease b)) Ocular: Lens Subluxation (Downwards) & Blue
Onycholysis Psoriasis, Amyloidosis, sclera with myopia
Sarcoidosis c)) Cardiovascular: AI, MVP, A dissection
Onychomadesis Trauma, Kawasaki disease d)) Others: Cystic bronchiectasis, Sp. Pnemothorax)
Beau’s lines Severe systemic illness, •Klinefeltar’s & Hypogonadism:
Pemphigus (US > LS, Tall, +ve barr body, Gynecomastia, MR,
Yellow nails Lymphoedema, pl effusion
Small firm testis, Eunuchoidism)
(Yellow nail syndrome)
Imm dfcny, Bronchiectasis, •Homocystinuria
Terry’s / White nails Liver failure, Cirrhosis (US < LS, Reduced Cystathione reductase, Lens
(Thumb & index) Subluxated downwards, MR,AR, Life threatening
Lindsay’s nails / half Renal failure thrombotic episodes)
& half nail
Mees nails Ars poison & Hodgkins US = LS: Constitutional & familial, Hyperpitutarism
Muehrcke’s nails HypoAlbuminemia (Any)
Horder’s Nails SBE, systemic vasculitis
(linear longt. Hmr)
10
Green nail Psuedomonas infectio
Black nail PEutz – jeghers syndrome
Nutrition:

• Subcutaneous Fat (Triceps – Males: 12.5mm

8
If H <4Feet: dwarfism (below 3 rd Centile)
•Pitutary Dwarf (Juvenile facies, Normal
intelligence, US = LS)
•Thyoid Dwarf / Cretin (Coarse facies, Less
intelligence, US > LS)
•Achondroplasia: AD (Normal intelligence,
US > LS, Short limbs, large head)
•Psedo hyperpara thyroidism (Less intelligence,
Stouty built, Short 4/5 th Mtcrpls)
US = LS: Constitutional & familial
18
(<10mm) & females: 16.5mm (<13mm), biceps,
Infrascapular & Suprailiac region)
•Muscle bulk (Mid arm, Left: 25.5mm males
(<23mm) & 23mm in females (<22mm)
& mid thigh Circumference)
•Signs of vitamin, mineral deficiency
•BMI
•Waist circumference: ASIS & Lower coastal margin
midway :- males >102cm females >88cm – High
risk of metabolic complications
•Hip circumference: 1/3 distance between ASIS &
patella males

•W/H ratio: Truncal obesity :- males >1

9
Page
 females > 0.9 – risks for metabolic complications •definite upper level •NOT seen
•Ponderal Index: H (in) / W in pounds (1/3) seen

Cachexia (Anorexia + Anemia + Emaciation) –

Disseminated Pulm Tb, Advanced malignancy, AIDS,
DM, Anorexia nervosa
> 3 Kg loss in 6 months : Significant weight loss
11
JVP: Jugular venous pulse (CVP / mean RA pressure)
from which we study JV pressure & wave pattern
For Venous pressure measurement Ext jugular vein is
NOT measured
•Prone to kinking due to Superfecial nature
•NOT DRAIN DIRECTLY into SVC
•VALVES, PIERCE FASCIA
• Not a direct reflector of CVP
Right internal jugular preferred because
(Innominate vein may be compressed by aortic
knob which dampens elevates the venous pressure
on Left Jugular vein)
Prerequisite: Trunk angle 45 with relaxed neck
muscles in good light. Btwn 2 heads of
sternocleidomastoid (if in sitting position neck veins
are engorged then it is NOT necessary for TRUANK
ANGLE at 45) – uppermost portion of distension is
taken
Normal value at 45 : 3 – 4cm blood (8 cm Blood =
6mm hg)
HepatoJugular / Abdomino jugular reflex:
(+ve: 10sec of abdominal pressure which shows
elevation of >3cm blood & is sustained throughout
the application of pressure & rapid fall BACK of
venous column more than 4cm of blood on release
of compression)
•Identify Incipient stages of RHF
•Differentiate Arterial / Venous pulsation
• Identify Obstructive (SVC & BC syndrome) &
NON obstructive causes of Engorged Neck veins
•Typical JVP of TR can be elicited even if resting
JVP is Normal
Kussmaul’s sign / Venous pulsus Paradoxus
: C tamponade, Restrictive Cadiomyopathy,
Constrictive pericarditis, Acute RV infarction,
Severe RHF –
Paradoxical Rise of JVP after deep inspiration due to
NON ACCOMODATION of increased venous
return to R heart
Passive RA filling
S2
A. Contraction
S1
S2
• Buldging of TV
& Impact of Adj
carotid in V. Sys
Due to Opening
of Tric. Valve

Venous Arterial In normal people A is visible & X is more prominent

•Wavy •Jerky
•Better seen than felt •Better felt than seen C – X descent: X descent / Systlc collapse: before S2
•On Exp - Promn •NO V – Y descent: Y descent / Diastlc collapse: After S2
• Lying down - Promn •NO
•HJ reflex - +ve •NO X descent is due to: Atrial relaxation & downward
•Prominent movement •Prominent movement movement of Valves during V systole
is INWARD is OUTWARD
•Abolished by gentle •NOT ABOLISHABLE Wave Pattern Condition
19

pressure applied above A Large A waves TS,PS,Pulm Hyptn

Clavicle Regular Cannon waves Junctional Rhythm
Page

•2 +ve waves are seen •1 +ve wave seen Irregular Cannon wave Complete HB
 Absent A waves AF
V Large V waves TR
X Increased Prominence C tamponade & C •Campbell de morgan’s spots / Cherry angiomas –
pericarditis Old age, NOT blanch, Ant abd wall & are Raised
Decreased Prominence TR, AF, RVF •Venous star: high V pressure states, NOT blanch,
Y Rapid Descent TR, C. PeriC Legs & lower part of abd, Fill from Periphery to
(Friedreich’s sign) center
Slow descent TS, C.tamponade
•Rose spots: DO blanch on P, Ant abd wall, EF

13

Palmar erythema / liver palms: Thenar &

Engorged & Pulsatile
• C tamponade & C pericarditis
•TR & TS
•Restrictve Cardiomyopathy
•RHF & Pulm TE
•CHB
Engorged & NON Pulsatile
•SVS syndrome & BC syndrome
•Chronic C pericarditis
• Vasalva manoeuvre
Low JVP
•Dehydration
•After massive Hamerrohage
•After massive diuretic therapy
Pericardial Knock: Sound In EARLY DIASTOLE:
Restrictive effect of adj pericardium on diastolic
expansion of ventricle: C. pericarditis
12
Spider naevi / arterial spider / Spider Angioma /
vascular spider / arterial telangiectasias, centrally
dilated arteriole with numerous vesselss Radiating
from it usually seen in upper part of thorax
(necklace pattern – SVC territory) & Upper back
mainly due to increased O/T ratio
Central arteriole pressed & release:- Immediate
blanching with filling from Centre to periphery
hypothenar eminence & finger pulps – BLANCHES
on pressure
•Alcoholic & long standing RA
• Pregnancy
•Hyperdynamic sirculation , thyrotoxicosis
•Normal people / familial
14
Erythema Nodosum: single / multiple Non
ulcerating bluish red / erythematousnodular lesion
(F > M & Childrean > Adults) generally present on
Extensor surfaces but SHIN is the COMMON site.
Ahich are PAINFUL & TENDER Sometimes
BILATERAL & Symmetrical – Self limiting in 2 – 6 W
– heal without scarring
Causes:
•Tuberculosis (10) & Leprosy
•Sulphonamide therapy
•Sarcoidosis
•UC & Crohn’s
•Rheumatic fever
•Brucellosis, psittacosis
Pathologically: Patchy inflammation of
Subcutaneous tissue (Panniculitis) & small BV
vasculitis – Type 2 Immune complex Deposition .
Shin is common site because Lymphatic supply is
very less & hence bacterial clearance is slow

DD: Erythema induratum, Erythema Chronicum

•2% Normal people
migrans (lyme disease), Erythema multiforme
•Alcoholics
20

•3 rd trimester pregnancy
•RA
Page

•Thyrotoxicosis
 Shin (Erythema Nodosum, Pretibial myxoedema,
Necrobiosis lippoidica diabeticorum, Lichen
amyloidosis)
ENL: Type 2 lepra reaction – Painful crops of
Tender nodules + fever + LN + Arthritis + iritis –
Treatment with THALIDOMIDE / PREDNISOLONE
+ Atropine sulfate
1 7 digits forward / 5 digits Backward &
Telephone number repeat after 30 sec
2 Name of vistors Who came yesterday
Ask morning news
*(index of severity of Organic Brain
disease)
3 Ask imp life events
(Resistant) Ask imp Social events (indpnd day)

15
Intelligence: Calculation (Serial 7 substraction test) +
Subcutaneous Nodules:- NF, Rheumatic nodule, Judgment (Asking what he will he do if car is
Rheumatoid nodule, Tophi, Xanthoma, coming on him)+ Insight (Awarness about illness) +
Cysticercosis, Metastatic deposits Reasoning (tall vs dwarf ??) + Abstract thinking
(meaning of proverbs) + Attention (Tap if number is
Rheumatic nodule, Rheumatoid nodule repeated twice) + Concentration (20 to 1)
Smaller Large
NOT ULCERATE Freq occur Level of consciousness: Conscious > Confused >
TENDER NON TENDER Drowsy > Stupor > Semicoma (respond to only
Skin FREE FIXED to skin Internal stimulus) > Coma OR by using GCS
Assc Active Carditis Associted +ve RFactor Conscious >15 Deeply comatose 3
Sec infection: rare SEC INFECTION: freq
•Extensor surfaces of •Extensor surfaces of Released Reflexes (Dementia, Organic Confusional
elbows elbows states & CONTRALATERAL frontal lobe Lesion)
•Extensor Tendons of •Extensor Tendons of
fingers & Toes fingers & Toes Grasp By distally moving Stimulus on
•Back of head •Back of head radial Aspect of palmar surface
•Margins of patella •Margins of patella of hand – Grasp & Unable to
•Achilles tendon •Achilles tendon relax the Grasp Voluntarily
•Sacrum •Sacrum Forced Groping
** Bony prominences & Pressure points While lying Avoiding* By distally moving stimulus on
on bed Ulnar Aspect of palmar surface
of hand – Hand move away
Xanthomas :- PLANOUS (Around eyes) & Palmo mental** Scrathing THENAR – Chin
TUBEROUS (Wrist, Elbow, Knees, Ankle) ** puckering due to MENTALIS
Prolonged Cholestasis & Familial muscle Contraction
Hypercholesterolemia Sucking Lip / Mouth corner –
Contraction of Tongue, Jaw
Tophi:- Helix antihelix, Olecranon process, Acilles muscles associated with
tendon, & other pressure points Swallowing
Rooting Lips follow Stimulating object
16 when it is touched
Snout Tap with Knuckle on Patient’s
Memory: UPPERLIP – Pouting of lips due
1)) Short term / immediate recall / Rote memory to ORBICULARIS ORIS muscle
2)) Recent memory contraction
3)) Past memory / Long term / Remote memory Myerson’s / Uninterrupted / continuous
Glabellar tap Blinking with tap (N: 3 OR 4)
21

Registration + Retension + Recall + Reproduction * CONTRALATERAL parietal Lobe lesion

** NO LOCALIZING Valu
Page
 17

Speech: Symbolic expression of Thought process

with Words (spoken / written)

Disorder of Production / articulation / Phonation

Speech area L side in 95% R handed & 70% L

handed & also in Ambidextrous

1st Ask name – NO – S/M aphasia – Write Show me

your tongue NO (SENSORY / GLOBAL)

Yes (Action)

MOTOR aphasia

Commonest cause CVA particularly Infarction is

Commonest cause

NOMINAL APHSIA (In BTW ANGULAR GYRUS &

POST part OF SUP TEMPORAL GYRUS): Fails to
name common objects

18

Upper eyelid: LPS – 3 rd N & Muller’s – Sympathetic

Horner’s syndrome: PseudoPtosis + Miosis +

Anhidrosis (Ipsilateral face, neck, Front & back of
upper chest) + Enophthalmosis + Loss of CSp reflex
(Skin poinching of neck - pupil reflex dilation)
22
Page
 1)) Previous LSCS

2)) Diabetes Complicating pregnancy

3)) Heart diseases Complicating
pregnancy
2
4)) Anemia Complicating pregnancy

5)) Bad obstetric History

OBSTERTRICS
6)) Hypertensive disorders Complicating
pregnancy

7)) Breech presentation

23
Page
 Previous LSCS After 2 days baby died, cause Unknown
Stitches are removed on 6 th day &
Tava / 22 / House wife/ ECIL / SE IV. She stayed in hospital for 15 days because of GHTN
W/O Yakub & she stopped anti hypertensive drugs for 6 more
With 6yrs of marital status & is G3P1L1 days & discontinued as per doctor advice
having her puerperal period is uneventful
LMP as 5/2/12 (regular cycles) & present pregnancy:-
EDD: 11/11/12 Came with a Spontaneous Conception
With episodes of vomiting (5 – 6 times/day)1m &
C/C:
No H/O nausea / morning sickness
This lady was admitted for safe institutional delivery
No H/O fever / burning micturition
in view of previous CS
No H/O bleeding PV / White discharge
H/P/I: No H/O radiation exposure
H/O suprapubic pain from 1 week dragging type , No H/O Drug usage
continouswhich is not disturbing sleep, radiating to No H/O leg swelling In 1st 3 months &
back & aggravated on lifting weights & relived on In next 3 Months there was
taking rest. No H/O bleeding / draining Pv
No H/O burning micturition / dysuria / fever with No H/O leg swelling
chills & rigor No H/O fever / burning micturition
No H/O vaginal bleed No H/O dyspnoea / palpitations
No H/O shoulder pain Quickening in 5m &
TT 1st dose in 5m
OBSTETRIC H/O: USG -6m &
Past pregnancies:- In 3 rd trimester
1st – 1 yr after marriage & Spontaneous Conception No H/O bleeding / draining Pv
confirmed by local doctor & booked case of Gandhi No H/O leg swelling
from 5m of gestation. At term she had bleeding PV No H/O blood transfusions
with meconium stained liquor & obstructed labour. TT 2 nd dose in 8m

Then she went emergency LSCS in Gandhi hospital MENSTRUAL H/O :

& she has given birth to male child, cried Attained Menarche at 12 yrs of age. 3/30..
immediately with 2.5 kg weight & breast feeding 4 pads / day
initiated 3 hrs after delivery. No blood tranfusions No H/O white discharge
Stitches are removed on 6 th day & No H/O clot passage
she stayed in hospital for 7 days
puerperal period is uneventful. PAST H/O:
NO H/O HTN
Baby is healthy & No nicu admissions & vaccinated
NO H/O DM, TB, IHD, RHD, epilepsy, chest pain /
breast fed continued for 2 yrs
Jaundice & bleeding disorders
2 nd – pregnancy.
2 yrs after & Spontaneous Conception confirmed by DRUG H/O:
local doctor this time she had GTN & underwent Took IFA Tab.
Elective LSCS in Gandhi hospital because of previous
LSCS. she has given birth to female child, cried FAMILY H/O: Not significant
24

immediately with 1.75 kg weight & breast feeding

PERSONAL H/O:
initiated immediately after delivery. Diet: mixed, appetite: reduced
Page

No blood tranfusions B/B: regular, Sleep: disturbed

 Addictions: Chronic smoker & Non alcoholic & Respiratory Examination: BLAE +ve & N vesicular
NON consangious marriage sounds heard with No adventitious sounds

GCOE: Diagnosis:
Patient is C/C/C. A 22 yr Old G3P1L1D1 with term gestation with
Moderately built & with fundal height corresponding with gestational age
P (+) I (-) C (-) C (-) K (-) L (-) with 2 previous LSCS Done for NON recurrent
Bilateral pedal oedema, Pitting type Indications with No other Obstetric complications
which is upto knee
No thyroid enlargement
Breast Normal Discussion:
Spine & gait Normal
Vitals – afebrile, Whatever is abd inscison : tenderness must be seen
HR: 80/min. N in volume, character, & rhythm No
RR/RF delay No vessel wall thickening on lower segment & From lateral to centre
BP: 120/86 mm hg RUL: Sitting
1 – 14 (1st T)– 28 (2 nd T)- 40 (3 rd T)
RR: 19/min
JVP: NOT raised Cesarean delivery : birth of a fetus through incisions
in the abdominal wall (laparotomy) and the uterine
OBSTETRIC EXAMINATION: wall (hysterotomy). This definition does not include
removal of the fetus from abdominal cavity in case
Abdominal examination of rupture of the uterus or in abdominal pregnancy.
On inspection: 2)) Julis caeser , Lex caesaria, Latin
Abdomen is generally distended
All quadrants move equally with respiration 3)) Incidence rising:
Flanks full -average maternal age is rising,
Umbilicus slit like & inverted -electronic fetal monitoring is widespread.
stria gravidarum & linea nigra present -Most fetuses presenting as breech are now
A curvilinear suprapubic scar is seen which is about delivered by caesarean,
7 cm in length & No puckering which seen healed -The incidence of forceps and vacuum deliveries has
by primary intention -Rates of labor induction continue to rise
No other scars / Sinuses -prevalence of obesity has risen
No engorged Veins
Complete uterine involution and restoration of
Palpation: anatomy may require at least 6 months
Scar tenderness:- absent
Fundal height – 32 weeks (with flanks full) 4)) Steps:
fundal grip – Soft, Non ballotable, Broad mass
probably podalic pole
Lateral grip – Left side hard board like mass felt
probably baby’s back & On right side multiple fetal Different approaches
parts felt
1st pelvic grip – hard ballotable, mass probably 1)) Pfannensteil kerr technique usually
cephalic pole 2)) Joel-Cohen and
3)) Misgav- Ladach methods
Ausultation – Fetal heart sounds – 136/min regular

Per veginal Examination – NOT done Abdominal Incision

25

Infraumbilical midline vertical (quickest) or a

CVS examination- S1 & S2 heard. Murmer in pulm suprapubic transverse incision (modified Pfannenstiel
Page

area (haemic murmer) No other murmers heard incision, the skin and subcutaneous tissue are incised
 using a lower, transverse, slightly curvilinear incision
at upper border of pubic hair line -
Follows Langer lines of skin tension,
and thus,
excellent cosmetic results can be achieved.
decreased rates of postoperative pain
decreased wound dehiscence and incisional hernia.
However: repeat caesarean delivery, reentry
through a Pfannenstiel incision usually is
more time consuming and difficult because of
scarring.)
special circumstances, paramedian
or midtransverse incision (Maylard’s Incision – If
need more space) be employed
Rectus sheath is dissected longitudinally
Recti & pyramidialis is retracted sideways
P.Peritoneum is incised vertically
The reflection of peritoneum above the upper
margin of the bladder and overlying the anterior
lower uterine segment— the bladder flap—is
grasped in the midline with forceps and incised
transversely with scissors. Bladder is separated
Uterine incision: (The uterine incision should be
made large enough to allow delivery of the head
and trunk of the fetus without either tearing into or
having to cut into the uterine vessels)
Incised transversely (Kerr) rarely lower-segment
vertical Incision (Kronig).
Baby delivered (Ant shoulder 1st) & cord clamped
Fundal massage (promote placental delivery)
Manual placental removal if Not extruded
spontaneously
uterine cavity is inspected and either suctioned or
wiped out with a gauze pack to remove avulsed
membranes, vernix, clots, and other debris.
The upper and lower cut edges and each lateral
angle of the uterine incision are examined carefully
for bleeding & vessels are ligated
Uterine Repair:
The uterine incision is then closed with one or two
layers (1st layer 2 nd running lock layer) of continuous
0- or #1 absorbable suture (Chromic catgut) &
serosal edges overlying the uterus and bladder have
been approximated with a continuous 2-0 chromic
catgut suture
Abdominal Closure:
All packs are removed, and the paracolic gutters and
cul-de-sac are emptied of blood and amnionic fluid
26
using gentle suction, rectus muscles are allowed to
fall into place
Page
Peripartum hysterectomy
- Intractable uterine atony
-Lower-segment bleeding associated with
the uterine incision or placental implantation,
-Uterine rupture, or
-Uterine vessel laceration
If there is bladder injury - Cystostomy repair
Increased risk of uterine rupture with multiple
uterine surgeries, uterine tachysystole, attempts at
cervical ripening or Induction with Oxytocin
Some Factors for Consideration
in Selection of Candidates for (VBAC)
• One previous prior low-transverse cesarean
delivery
• Clinically adequate pelvis
• No other uterine scars or previous rupture
• Physician immediately available throughout
active labor capable of monitoring labor and
performing an emergency cesarean delivery
• Availability of anesthesia and personnel for
emergency cesarean delivery
5)) Main risk for labour induction is uterine rupture:
selection of women most likely to have a successful
VBAC, as well as avoiding misoprostol and
sequential use of prostaglandins and oxytocin,
appear to offer the lowest risk of uterine rupture.
(Intravaginal prostaglandins alone, excluding
misoprostol, were not associated
with an increased risk of uterine rupture)
6)) If required epidural analgesia may safely be used
during a trial of labor &surgical Exploration of a scar
dehiscence is necessary
only if significant bleeding is encountered
7)) With multiple C sections there is increased risk of
hysterectomy placenta previa, placenta accreta
particularly
 our hosptl.
Contraindications For VBAC Pain in hypogastric region , sudden in onset, Aching
type, continuous, Not disturbing sleep, radiation to
•Absolute: prior classical cesarean, previous back, No shift of pain & Not associated with fever /
uterine rupture, lack of resources to perform Vomitings / Burning micturition. No aggravating
emergency cesarean delivery during labor.
factors , relieved on medication. Now There is NO
• Relative: two prior uterine surgeries with no
previous vaginal delivery. pain
Dyspnoea – 2 days Sudden in onset, Non
progressive, Aggravated on exertion
(grade 1)
relieved on taking rest,
Associated with palpitations precipitated on
exertion & relieved on rest & are continous
Not associated with cough / chest pain
b No H/O orthopnoea / PND attacks
No H/O syncopal attacks
a No H/O anaemia (thella paskarlu)

a: Lscs b: Lscs / Classical OBSTETRIC H/O:

Spontaneous Conception .
Disadvantages of elective C section:
Pregnancy confirmed by local doctor
1)) Iatrogenic prematurity
With episodes of vomiting (3 – 4/days) for 2m &
2)) Atonic PPH
No H/O nausea / morning sickness
3)) Drainage of lochia difficult (since cervix is not
No H/O fever / burning micturition
dilated)
No H/O bleeding PV / White discharge
4)) Difficulty in suturing (lower segment is not
No H/O radiation exposure
formed)
No H/O Drug usage
TOLAC (Trial of labour after C section) No H/O leg swelling In 1st 3 months &
In next 3 Months there was
C section indications (recurrent / NON recurrent) No H/O bleeding / draining Pv
No H/O leg swelling
Heart disease Complicating pregnancy No H/O fever / burning micturition
No H/O dyspnoea / palpitations
Jyothi / 20 / agricultural labour / Warangal / SE IV.
Quickening in 5m &
With 10months of marital status & is Primi
TT 1st dose in 5m
having her
LMP as 18/2/11 (regular cycles) & USG -6m &
In 3 rd trimester
EDD: 25/11/11 Came with a
No H/O bleeding / draining Pv
C/C: No H/O leg swelling
Difficulty in breathing from 2 days No H/O blood transfusions
TT 2 nd dose in 8m
H/P/I:
Patient was apparently asymptomatic 10 days back MENSTRUAL H/O :
then she developed pain in abdomen, so she went Attained Menarche at 12 yrs of age. 5/30..
27

to local govt hosptl (Siddipet) where she was having 2 pads / day & with Congestive dysmenorrhoea
No H/O white discharge
Page

her regular ANC, from where she was referred to

No H/O clot passage
 PAST H/O: 1st pelvic grip – hard ballotable, mass probably
H/O HTN diagnosed at 3m cephalic pole
NO H/O similar complaints in past,
NO H/O DM, TB, IHD, RHD, epilepsy, chest pain / Ausultation – Fetal heart sounds - ??
Jaundice & bleeding disorders
Perveginal Examination – NOT done
DRUG H/O:
Taking IFA CVS examination
Inspection – NOT done
FAMILY H/O: Not significant Palpation - Apex beat Not shifted (4 th ics 2cm lateral
to MCL) & Parasternal impulse absent
PERSONAL H/O: Auscultation:
Diet: mixed, appetite: reduced
B/B: regular, Sleep: disturbed Area S1 S2 Murmur
Addictions: Chronic smoker & Non alcoholic &
NON consanginous marriage Mitral N + No

GCOE: Tricuspid + + No
Patient is C/C/C.
Pulmonary + N No
Moderately built & with
(Split ?)
P (+) I (-) C (-) C (-) K (-) L (-)
Aortic + + Soft, ESM,
Bilateral pedal oedema, Pitting type which is just
grade 4 & No
above ankle
radiation
No thyroid enlargement
Spine & gait Normal
Vitals – Diagnosis:
afebrile, A 20 yr Old primi with term gestation with fundal
height corresponding with gestational age with
HR: 76/min. N in volume, character, & rhythm No
RR/RF delay No vessel wall thickening Heart Disease probably AS complicating pregnancy
BP: 130/86 mm hg RUL: Sitting
RR: 16/min
JVP: NOT raised Discussion
OBSTETRIC EXAMINATION:
Hemodynamic Changes (%)
Abdominal examination
Cardiac output +43
On inspection: Heart rate +17
Abdomen is generally distended Left ventricular stroke work index +17
Umbilicus slit like & everted Vascular resistance
stria gravidarum & linea nigra present Systemic -21
No scars / Sinuses Pulmonary -34
No engorged Veins Mean arterial pressure +4
Colloid osmotic pressure -14
Palpation:
Fundal height – 32 weeks (with flanks full)
fundal grip – Soft, Non ballotable, Broad mass Parameter Change (Percent)
probably podalic pole 1)) New York Heart Association (NYHA)
Lateral grip – Left side hard board like mass felt • Class I. Uncompromised—no limitation of
28

probably baby’s back & On right side multiple fetal physical activity:
parts felt These women do not have symptoms of cardiac
Page

insufficiency or experience anginal pain.

 • Class II. Slight limitation of physical activity: These
women are comfortable at rest, but if ordinary
physical activity is undertaken, discomfort in the
form of excessive fatigue, palpitation, dyspnea, or
anginal pain results.
• Class III. Marked limitation of physical activity:
These women are comfortable at rest, but less than
ordinary activity causes excessive fatigue,
palpitation, dyspnea, or angina pain.
• Class IV. Severely compromised—inability to
perform any physical activity without discomfort :
Symptoms of cardiac insufficiency or angina may
develop even at rest. If any physical activity is
undertaken, discomfort is increased.
Normal findings in Pregnant woman:
Jugular venous distension
Mammary souffle
S2 P increased; S2 split
S1 M increased and widely split
Occasional S3,
Aortic or pulmonary flow murmurs
2)) Class 3 & 4:
a)) If feasible, women with severe cardiac disease
should consider pregnancy interruption. If
continued, prolonged hospitalization or bed rest is
necessary.
b)) Epidural analgesia for labor and delivery is
usually recommended.Vaginal delivery is preferred
in most cases, and labor induction can usually be
done safely
For pregnant women with mechanical heart
valves, any one of the following anticoagulant
regimens is recommended:
• Adjusted-dose LMWH twice daily throughout
pregnancy.
• Adjusted-dose UFH administered every 12 hours
throughout pregnancy.
• LMWH or UFH as above until 13 weeks’ gestation
with warfarin substitution until close to delivery
29
when LMWH or UFH is resumed.
Page
** In women judged to be at very high risk of
thromboembolism and in whom concerns exist
about the efficacy and safety of LMWH or UFH.
*** Warfarin is suggested throughout pregnancy
with replacement by UFH or LMWH
(as above) close to delivery.
In addition, low-dose aspirin— orally administered.
3)) In MR & AR: Ventricular function
improves with afterload decrease. In MS (heart
failure due to fluid overload) & AS (Moderate
stenosis tolerated; severe is life-threatening with
decreased preload)
4))
MS:
Limited physical activity
dietary sodium is restricted, and diuretic therapy
blocker drug is usually given to blunt the cardiac
response to activity and anxiety
new-onset atrial fibrillation develops,
IV verapamil / electrocardioversion
chronic fibrillation, digoxin,
Therapeutic anticoagulation with heparin is
indicated with persistent fibrillation.
heparinization with severe stenosis even if there is a
sinus rhythm.
Vaginal delivery & elective induction is reasonable
MR:
well tolerated during pregnancy, probably because
decreased systemic vascular resistance results in less
regurgitation. Heart failure
only rarely develops during pregnancy
Intrapartum prophylaxis against
bacterial endocarditis may be indicated
AS:
Narrow margin separating fluid overload
from hypovolemia & During labor and delivery,
such women should be managed on the ―wet‖ side,
maintaining a margin of safety in intravascular
volume in anticipation of possible haemorrhage.
During labor, narcotic epidural analgesia seems
ideal, thus avoiding potentially hazardous
hypotension
AR:
well tolerated during pregnancy. Like MR,
diminished PVR will improve the lesion.
If symptoms of heart failure develop, diuretics are
given and bed rest is encouraged.
 Epidural analgesia is used for labor and delivery, No H/O Swelling of face & limbs
and bacterial endocarditis prophylaxis may be No H/O Oliguria
required. No H/O Bleeding PV / easy bruisability

OBSTETRIC H/O:
present pregnancy:-
IE Prophylaxis with Dental Procedures Spontaneous Conception
Confirmed by local doctor
(1) Prosthetic heart valve With episodes of vomiting (5 – 6 times/day)1m &
(2) Previous infective endocarditis No H/O nausea / morning sickness
(3) Certain forms of congenital heart lesions: No H/O fever / burning micturition
• Unrepaired cardiac lesions causing cyanotic heart No H/O bleeding PV / White discharge
disease, including palliative shunts and conduits
No H/O radiation exposure
• Repaired defect with prosthetic: for 6 months
following repair procedure. No H/O Drug usage
• Repaired defect with residual defects. No H/O leg swelling In 1st 3 months &
In next 3 Months there was
** Prophylaxis is recommended for procedures that No H/O bleeding / draining Pv
involve manipulation of gingival tissue / periapical No H/O leg swelling
tooth region No H/O fever / burning micturition
with any of the following cardiac conditions:
No H/O dyspnoea / palpitations
Quickening in 5m &
TT 1st dose in 5m
USG -6m &
In 3 rd trimester
Hypertensive disorders Complicating No H/O bleeding / draining Pv
pregnancy No H/O leg swelling
No H/O blood transfusions
Rajashri/ 22 / House wife/ Kurnool / SE IV. TT 2 nd dose in 8m
W/O rajashekar
with 3yrs of marital status & is G1P0L0 MENSTRUAL H/O :
having her Attained Menarche at 11 yrs of age.
LMP as 15/2/12 (regular cycles) & 3/28.. 4 pads / day
EDD: 21/11/12 Came with a No H/O white discharge
No H/O clot passage
C/C:
This lady was admitted for safe institutional delivery PAST H/O:
NO H/O HTN
in view of Increased Blood pressure
NO H/O DM, TB, IHD, RHD, epilepsy, chest pain /
H/P/I: Patient is apparently assymptomatic Jaundice & bleeding disorders
2months back & having her regular ANC at Gandhi
DRUG H/O:
hospital & was diagnosied as having high bp in her Took IFA Tab.
7 th month
No H/O Giddiness FAMILY H/O: Not significant
No H/O epigastric distress
30

No H/O Vision blurring & headache PERSONAL H/O:

Diet: mixed, appetite: reduced
No H/O Seizure episodes
Page

B/B: regular, Sleep: disturbed

 Addictions: Non Smoker, alcoholic & NON Respiratory Examination: BLAE +ve & N vesicular
consangious marriage sounds heard with No adventitious sounds

GCOE: Diagnosis: A 22 yr Old Primi with term gestation

Patient is C/C/C. with fundal height corresponding with gestational
Moderately built & with age with Hypertension complicating pregnancy,
P (+) I (-) C (-) C (-) K (-) L (-) With No signs of imminent eclampsia
Bilateral pedal oedema, Pitting type
which is upto ankle
No thyroid enlargement
Breast Normal
Discussion
Spine & gait Normal
Working Group classification
Vitals –
afebrile,
HR: 80/min. N in volume, character, & rhythm No 1. Gestational hypertension—formerly termed PIH If
RR/RF delay No vessel wall thickening preeclampsia syndrome does not develop and
BP: 120/86 mm hg RUL: Sitting hypertension resolves by 12 weeks postpartum ,
RR: 19/min it is redesignated as transient hypertension
JVP: NOT raised 2. Preeclampsia (some have atypical preeclampsia
with all aspects of the syndrome, but without
hypertension or proteinuria, or both) and eclampsia
OBSTETRIC EXAMINATION: syndrome
3. Preeclampsia syndrome superimposed on chronic
Abdominal examination hypertension
4. Chronic hypertension
On inspection:
Abdomen is generally distended ** Proteinuria is defined by 24-hour urinary protein
All quadrants move equally with respiration excretion exceeding 300 mg, a urine P/C ratio of
Flanks full >/=0.3, or persistent 30 mg/dL (1+ dipstick)
Umbilicus slit like & inverted protein in random urine samples
stria gravidarum & linea nigra present
No other scars / Sinuses Risk Factors
No engorged Veins
obesity, multifetal gestation, maternal age older
Palpation: than 35 years, and African-American ethnicity,
Fundal height – 32 weeks (with flanks full)
fundal grip – Soft, Non ballotable, Broad mass *** smoking & Placenta previa
probably podalic pole reduced risk of hypertension during pregnancy
Lateral grip – Left side hard board like mass felt
probably baby’s back & On right side multiple fetal
parts felt
1st pelvic grip – hard ballotable, mass probably 2)) Preeclampsia often affects young and nulliparous
cephalic pole women, whereas older women are at greater risk
for chronic hypertension with superimposed
Ausultation – Fetal heart sounds – ?? preeclampsia,

Per veginal Examination – NOT done 3)) Preeclampsia syndrome is a two-stage disorder.
• Stage 1 (preclinical) is caused by faulty
31

CVS examination- S1 & S2 heard. No murmers heard endovasculartrophoblastic remodeling that

downstream causes the stage 2 clinical syndrome &
Page

• Stage 2 is susceptible to modification by

 preexisting maternal conditions that include cardiac LMP as 2/3/12 (regular cycles) &
or renal disease, diabetes, obesity, or hereditary EDD: 9/12/12 Came with a
influences
C/C:
Hemoconcentration is a hallmark of eclampsia. This lady was admitted for safe institutional delivery
in view of Twin pregnancy
Preeclampsia (culmination of factors that likely
involve a number of maternal, placental, and fetal H/P/I:
factors) No H/O any menstrual abnormalities befor
conception
• Placental implantation with abnormal
trophoblastic invasion of uterine vessels. No H/O similar complaint in past pregnancies
(incomplete invasion of the spiral arteriolar wall by No H/O Cervical discharge
extravillous trophoblasts and results in a smallcaliber
vessels with resistance) OBSTETRIC H/O:
• Immunological maladaptive tolerance between present pregnancy:- 2yr after LCB
maternal, paternal (placental), and fetal tissues Spontaneous Conception
• Maternal maladaptation to cardiovascular or Confirmed by a local doctor.
inflammatory changes of normal pregnancy With episodes of vomiting (5 – 6 times/day)1m &
•Genetic factors including inherited predisposing No H/O nausea / morning sickness
genes as well as epigenetic influences.
No H/O fever / burning micturition
** This finally leads to release unknown factor No H/O bleeding PV / White discharge
(s)—likely placental in origin—are secreted into the No H/O radiation exposure
maternal circulation and provoke widespread No H/O Drug usage
activation and dysfunction of the vascular No H/O leg swelling In 1st 3 months &
endothelium: Increased pressor response,Vasospasm In next 3 Months there was
imbalance between NO & PG levels & between
No H/O bleeding / draining Pv
Angiogenic and Antiangiogenic Proteins
No H/O leg swelling
No H/O fever / burning micturition
No H/O dyspnoea / palpitations
Quickening in 5m &
TT 1st dose in 5m
USG -6m &
Most importantly overproduction of at least two In 3 rd trimester
antiangiogenic peptides from trophoblastic tissue No H/O bleeding / draining Pv
that are released into maternal circulation. No H/O leg swelling
a)) Soluble Fms-like tyrosine kinase 1 (sFlt-1) No H/O blood transfusions
b)) Soluble endoglin (sEng) TT 2 nd dose in 8m
Both these levels are increased before clinical Past pregnancies
syndrome develops
1st pregnancy - 1 yr after marraige
Spontaneous coneption.
Confirmed by a local doctor. Booked case
Breech presentation
Pregnancy was uneventful & delivered at home by
Sneha/ 25 / House wife/ Nalgonda / SE IV. local dai & baby cried immediately - male - 3kg –
W/O Suresh chandra immunized & healthy. Puerpurium also uneventful.
32

With 6yrs of marital status & is G3P2L1 2nd pregnancy - 1 yr after 1st child birth
Spontaneous coneption.
Page

having her
 Confirmed by a local doctor. On inspection:
Had regular ANC Abdomen is generally distended
Pregnancy was uneventful & delivered at home by All quadrants move equally with respiration
Flanks full
local dai & baby cried immediately - female - 2.5kg
Umbilicus slit like & inverted
– immunized & healthy. Puerpurium also uneventful stria gravidarum & linea nigra present
No other scars / Sinuses
MENSTRUAL H/O :
No engorged Veins
Attained Menarche at 12 yrs of age.
4/28.. 3 pads / day Palpation:
No H/O white discharge Fundal height – 32 weeks (with flanks full)
No H/O clot passage fundal grip – hard ballotable, mass probably
cephalic pole
PAST H/O: Lateral grip – Left side hard board like mass felt
NO H/O HTN probably baby’s back & On right side multiple fetal
NO H/O DM, TB, IHD, RHD, epilepsy, chest pain / parts felt
Jaundice & bleeding disorders 1st pelvic grip – Soft, Non ballotable, Broad mass
probably podalic pole
DRUG H/O: Ausultation – Fetal heart sounds – ??
Took IFA Tab.
Per veginal Examination – NOT done
FAMILY H/O: Not significant
CVS examination- S1 & S2 heard. No murmers heard
PERSONAL H/O:
Diet: mixed, appetite: reduced Respiratory Examination: BLAE +ve & N vesicular
B/B: regular, Sleep: disturbed sounds heard with No adventitious sounds
Addictions: Non Smoker, alcoholic & NON
consangious marriage Diagnosis: A 25 yr old Pregnant women with
G3P2L1 came with uncomplicated breech
GCOE: presentation for safe institutional delivery
Patient is C/C/C.
Moderately built & with
P (+) I (-) C (-) C (-) K (-) L (-)
Bilateral pedal oedema, Pitting type
Discussion
which is upto ankle
No thyroid enlargement
Breast Normal COMPLICATIONS
Spine & gait Normal
In the persistent breech presentation, an increased
Vitals – frequency of the following complications can be
afebrile, anticipated:
HR: 80/min. N in volume, character, & rhythm No
RR/RF delay No vessel wall thickening • Prolapsed cord
BP: 120/86 mm hg RUL: Sitting • Placenta previa
RR: 19/min • Congenital anomalies
JVP: NOT raised • Uterine anomalies and tumors
• Difficult delivery
OBSTETRIC EXAMINATION: • Increased maternal and perinatal morbidity
33

Abdominal examination
Page
 Ø Partial breech extraction.
The fetus is delivered spontaneously as far as the
umbilicus, but the remainder of the body is
extracted or delivered with operator traction and
assisted maneuvers, with or without maternal
expulsive efforts.
ØTotal breech extraction.
The entire body of the fetus is extracted by the
obstetrician (Dead baby & 2 nd baby after podalic
version with transverse lie)
Delivery of the Aftercoming Head
1)) Mauriceau Maneuver
2)) Modified Prague Maneuver (necessitated by
failure of the fetal trunk to rotate anteriorly.)
3)) Specialized forceps can be used to deliver the
aftercoming head. Piper forceps or divergent Laufe
forceps may be applied electively or when the
Mauriceau maneuver cannot be accomplished easily
Climbing Up: when buttocks visible at introitus
(similar to crowning in cephalic presentation)
Piper forceps: Also have perineal curve
Cesarean delivery (commonly, but not
exclusively, used in following circumstances)
1. A large fetus
2. Any degree of contraction or unfavorable shape
of the
pelvis determined clinically or with CT pelvimetry
3. A hyperextended head
4. When delivery is indicated in the absence of
spontaneous
labor
5. Uterine dysfunction—some would use oxytocin
augmentation
6. Incomplete or footling breech presentation
7. An apparently healthy and viable preterm fetus
with the
mother in either active labor or in whom delivery is
indicated
8. Severe fetal-growth restriction
9. Previous perinatal death or children suffering
from birth
34
trauma
10. A request for sterilization
Page
11. Lack of an experienced operator.
Factors That May Modify the Success of
External Cephalic Version
Increase Success
Increasing parity
Ample amnionic fluid
Unengaged fetus
Tocolysis
Decrease Success
Engaged fetus
Tense uterus
Inability to palpate head
Obesity
Anterior placenta
Fetal spine anterior or posterior
Duhrssen incision being cut at 2 o’clock, which is
followed by a second incision at 10 o'clock.
Infrequently,
an additional incision is required at 6 o’clock.
The incisions are so placed as to minimize bleeding
from the laterally located cervical branches of the
uterine cavity
External Cephalic Version: A forward roll of the
fetus usually is attempted first. If the forward roll is
unsuccessful, then a backward flip is attempted
(According to whether the head or breech is made
the presenting part, the operation is designated
cephalic or podalic version, respectively.)
Entrapment of the Aftercoming Head:
With gentle traction on the fetal body, the cervix, at
times, may be manually slipped over the occiput.
FAIL
Duhrssen incision / intravenous nitroglycerin / GA
FAIL
Zavanelli maneuver
A cardinal rule in successful breech extraction
is to employ steady, gentle, downward rotational
traction until the lower halves of the scapulas
are delivered, making no attempt at delivery of
 the shoulders and arms until one axilla becomes Quickening in 5m &
visible. TT 1st dose in 5m
USG -6m &
The appearance of one axilla indicates that the In 3 rd trimester
time has arrived for delivery of the shoulders. It No H/O bleeding / draining Pv
makes little difference which shoulder is delivered No H/O leg swelling
first. No H/O blood transfusions
Frank Breech Extraction: TT 2 nd dose in 8m
Frank breech decomposition using the Pinard
MENSTRUAL H/O :
maneuver.
Two fingers are inserted along one extremity to the Attained Menarche at 11 yrs of age.
knee, which is then pushed away from the midline 3/28.. 4 pads / day
after spontaneous flexion. Traction is used to deliver No H/O white discharge
a foot into the vagina No H/O clot passage

PAST H/O:
NO H/O HTN
Diabetes complicating pregnancy NO H/O DM, TB, IHD, RHD, epilepsy, chest pain /
Jaundice & bleeding disorders
Laxmi/ 27 / House wife/ zaheerabad/ SE IV.
DRUG H/O:
W/O nagarjuna Took IFA Tab.
With 6yrs of marital status & is G3P2L1
having her FAMILY H/O: Not significant
LMP as 2/3/12 (regular cycles) &
EDD: 9/12/12 Came with a PERSONAL H/O:
Diet: mixed, appetite: reduced
C/C: B/B: regular, Sleep: disturbed
This lady was admitted for safe institutional delivery Addictions: Non Smoker, alcoholic & NON
in view of Twin pregnancy consangious marriage

H/P/I: GCOE:
Patient is C/C/C.
OBSTETRIC H/O: Moderately built & with
present pregnancy:- P (+) I (-) C (-) C (-) K (-) L (-)
Bilateral pedal oedema, Pitting type
Spontaneous Conception
which is upto ankle
With episodes of vomiting (5 – 6 times/day)1m & No thyroid enlargement
No H/O nausea / morning sickness Breast Normal
No H/O fever / burning micturition Spine & gait Normal
No H/O bleeding PV / White discharge
No H/O radiation exposure Vitals –
No H/O Drug usage afebrile,
HR: 80/min. N in volume, character, & rhythm No
No H/O leg swelling In 1st 3 months & RR/RF delay No vessel wall thickening
In next 3 Months there was BP: 120/86 mm hg RUL: Sitting
No H/O bleeding / draining Pv RR: 19/min
No H/O leg swelling JVP: NOT raised
35

No H/O fever / burning micturition

OBSTETRIC EXAMINATION:
Page

No H/O dyspnoea / palpitations

 Abdominal examination
On inspection:
Abdomen is generally distended
All quadrants move equally with respiration
Flanks full
Umbilicus slit like & inverted
stria gravidarum & linea nigra present
No other scars / Sinuses
No engorged Veins
Palpation:
Fundal height – 32 weeks (with flanks full)
fundal grip – Soft, Non ballotable, Broad mass
probably podalic pole
Lateral grip – Left side hard board like mass felt
probably baby’s back & On right side multiple fetal
parts felt
1st pelvic grip – hard ballotable, mass probably
cephalic pole
Ausultation – Fetal heart sounds – ??
Per veginal Examination – NOT done
CVS examination- S1 & S2 heard. No murmers heard
Respiratory Examination: BLAE +ve & N vesicular
sounds heard with No adventitious sounds
Discussion
There is increasing support for the use of glyburide
as an alternative to insulin in the management of
gestational diabetes
Glyburide Treatment Regimen for Women with
Gestational Diabetes Who Fail Diet Therapy
• Glucometer blood glucose measurements fasting
and 1/2 hours following breakfast, lunch & dinner.
• Glucose level goals (mg/dL): Fasting <100, 1-h
< 155, and 2-h <130.
• Glyburide starting dose 2.5 mg orally with
morning meal.
• If necessary, increase daily glyburide dose by 2.5-
mg/wk increments until 10 mg/d, then switch to
twice-daily dosing until maximum of 20 mg/d
36
reached.
Page
** Switch to insulin if 20 mg/d does not achieve
glucose goals
Diabetes is not associated with increased risk for
fetal chromosomal abnormalities.
Neonatal Problems are:-
•Respiratory Distress Syndrome
•Hypoglycemia
• Hypocalcemia
• Long-Term Cognitive Development
• Inheritance of Diabetes
• Hyperbilirubinemia and Polycythemia
•Cardiomyopathy
Although oral hypoglycemic agents have been used
successfully for gestational diabetes , these agents
are not currently recommended for overt diabetes
except on an investigational basis.
Insulin Management During Labor and Delivery
Recommended by the American College of
Obstetricians and Gynecologists
• Usual dose of itm-acting insulin at bedtime.
• Morning dose of insulin is withheld.
• Intravenous infusion of normal saline is begun.
• Once active labor begins or glucose levels
decrease to < 70 mg/dL, the infusion is changed
from saline to 5-percent dextrose and delivered at a
rate of 100–150 mL/hr (2.5 mg/kg/min) to achieve a
glucose level of approximately 100 mg/dL.
• Glucose levels are checked hourly using a bedside
meter allowing for adjustment in the insulin or
glucose infusion rate.
• Regular (short-acting) insulin is administered by
intravenous infusion at a rate of 1.25 U/hr if glucose
levels exceed 100 mg/dl
GDM risk assessment (Should be
ascertained at the first prenatal visit)
• Low Risk: Blood glucose testing not routinely
required if all the following are present:
— Member of an ethnic group with a low
prevalence of GDM
— No known diabetes in first-degree relatives
— Age _ 25 years
— Weight normal before pregnancy
— Weight normal at birth
— No history of abnormal glucose metabolism
 — No history of poor obstetrical outcome •Fluids
• Average Risk: Perform blood glucose testing at 24 Isotonic sodium chloride
to 28 weeks using either: Total replacement in first 12 hours of 4–6 L
— Two-step procedure: 50-g oral glucose challenge 1 L in first hour
test (GCT), followed by a diagnostic 100-g oral 500–1000 mL/h for 2–4 hours
glucose tolerance test for those meeting the 250 mL/h until 80 percent replaced
threshold value in the GCT. •Glucose
— One–step procedure: Diagnostic 100-g oral 5-percent dextrose in normal saline
glucose tolerance test performed on all subjects. •Potassium
• High Risk: Perform blood glucose testing as soon •Bicarbonate (if pH is <7.1)
as feasible, using the procedures described above if
one or more of these are present:
— Severe obesity
— Strong family history of type 2 diabetes
— Previous history of GDM, impaired glucose
metabolism, or glucosuria.

Diagnosis of Gestational Diabetes by Oral

Glucose Tolerance Testing.
Twin Pregnancy
Time 100-g Glucose 75-g Glucose
Fasting 95 95
In women with a uterus that appears large for
! hr 180 180
gestational age, the following possibilities are
2 hr 155 155 considered:
3 hr 140 - 1. Multiple fetuses
2. Elevation of the uterus by a distended bladder
** The test should be performed in the morning 3. Inaccurate menstrual history
after an overnight fast of at least 8 h 4. Hydramnios
but not more than 14 h and after at least 3 days of 5. Hydatidiform mole
unrestricted diet and physical activity. 6. Uterine leiomyomas
*** Two or more of the venous plasma glucose 7. A closely attached adnexal mass
concentrations indicated below must be 8. Fetal macrosomia (late in pregnancy)
met or exceeded for a positive diagnosis
Pregnancy outcome:
• An ideal dietary composition is 55 percent
carbohydrate, 20 percent protein, and 1)) Spontaneous abortion
25 percent fat with less than 10 percent as saturated
fat. 2)) Malformations (According to Schinzel anomalies
in monochorionic twins generally fall into one of
Management of Db KA in pregnancy three categories )

** Obtain arterial blood gases to document degree

of acidosis present; measure glucose, ketones, and Defects resulting from twinning, acardiac
electrolyte levels at 1- to 2-hour intervals twinning itself anomaly, neural-tube
defects
•Insulin
37

Low-dose, intravenous
Loading dose: 0.2–0.4 U/kg Defects resulting from microcephaly,
Page

Maintenance: 2–10 U/h vascular interchange hydranencephaly,

 between monochorionic intestinal atresia, aplasia
twins cutis,
Defects may develop Talipes equinovarus
from fetal crowding** (clubfoot) or congenital
hip dislocation.
** Dizygotic twins are
also subject to these
3)) Birthweight
Multifetal gestations are more likely to be low
birthweight than singleton pregnancies, due to
restricted fetal growth and preterm
delivery
**The degree of growth restriction in monozygotic
twins is likely to be greater than that in dizygotic
pairs
4)) Duration of Gestation
As the number of fetuses increases, the duration of
gestation decreases (twin gestations have
empirically been considered to be prolonged at
40 weeks.)
Vascular anastomoses between twins are
present only in monochorionic twin placentas
(Most of these vascular communications are
hemodynamically balanced & are little fetal
consequence. In others, however, hemodynamically
significant shunts develop between fetuses.
Two such significant patterns include acardiac
twinning and twin-twin transfusion syndrome.)
Acardiac twinning:
(Twin reversed-arterial-perfusion (TRAP)
serious complication of monochorionic
multifetal gestation).
( In the TRAP sequence, there is usually a
normally formed donor twin who has features
of heart failure as well as a recipient twin who
lacks a heart (acardius) and other structures)
38
TRAP sequence is caused by a large artery-to-
Page
artery
placental shunt, often also accompanied by a
vein-to-vein shunt where ultimatly only the
lower body of rcpt twin is perfused, and
disrupted growth and development of the
upper body results. - Failure of head growth is
called acardius acephalus;
- Partially developed
head with identifiable limbs is
called acardius myelacephalus;
- Failure of any recognizable
structure to form is acardius amorphous
Radiofrequency ablation, which cauterizes
umbilical vessels in the malformed recipient
twin so as to terminate blood flow from the
dono
Twin-Twin Transfusion Syndrome (TTTS):
(In this syndrome, blood is transfused from a
donor twin to its recipient such that the donor
becomes anemic and its growth restricted &
recipient becomes polycythemic and may
develop circulatory overload manifest as
hydrops. The donor twin is pale, and its
recipient sibling is plethoric
Similarly, one portion of the placenta often
appears pale compared with the remainder)
Classically, chronic TTTS results from
unidirectional flow through arteriovenous
anastomoses.
Typically presents in midpregnancy when the
donor fetus becomes oliguric from decreased
renal
perfusion & develops oligohydramnios, and the
recipient fetus develops severe hydramnios
Virtual absence of amnionic fluid in the donor
sac prevents fetal motion, giving rise to the
descriptive term stuck twin or hydramnios-
oligohydramnios–―poly-oli‖–syndrome
Treatment: The prognosis for multifetal
gestations
 complicated by TTTS is extremely guarded.
Therapies currently used:amnioreduction, laser
ablation of vascular anastomoses, selective
feticide, and septostomy (intentional creation
of a communication in the dividing amnionic
membrane
** Once identified, TTTS is typically staged by
the Quintero staging system (I – V) +
cardiovascular
profile score or CVPS
below the 5 th percentile or >24 cm–above the 95th
percentile–was considered abnormal at gestational
ages of 28 to 40 weeks)
4)) Prevention of Preterm Delivery: bed rest–
especially through hospitalization, prophylactic
administration of beta-mimetic drugs or progestins,
and prophylactic cervical cerclage. (How ever none
had valid evidence of improving outcome)
5)) Corticosteroids for Lung Maturation
Anemia Complicating Pregnancy

Discussion
The modest fall in hemoglobin levels during
pregnancy is caused by a relatively greater
expansion of plasma volume compared with the
increase in red cell volume
Monochorionic twins:
The disproportion greatest during the second
trimester. Late in pregnancy, plasma expansion
essentially ceases, while hemoglobin mass continues
to increases

Symmetrical Asymmetrical
Causes of Anemia During Pregnancy
Acquired

Iron-deficiency anemia
Separate Conjoined External Internal Anemia caused by acute blood loss
Ventral Trap Anemia of inflammation or malignancy
Lateral Parasite Megaloblastic anemia
Dorsal TTTS Acquired hemolytic anemia (Cold-agglutinin disease
caudal Fetus in situ may be induced by Mycoplasma pneumoniae or
EBV / Drug induced : penicillin, cephalosporins)
Aplastic or hypoplastic anemia

Antepartum management Hereditary

1)) Diet Thalassemias

2)) Mangaemnt of hypertension
(fetal number and placental mass are involved in the
pathogenesis of preeclampsia. With multifetal
gestation, hypertension not only develops more
39
Sickle-cell hemoglobinopathies
Other hemoglobinopathies
Hereditary hemolytic anemias

often but also tends to develop earlier and to be

more severe.) • Amount of iron diverted to the
Page

3)) Antepartum Surveillance: (An AFI of <8 cm–

 fetus is similar in a normal and in an iron-deficient 2. PCOD
mother, the newborn infant of a severely anemic 3. Other androgen disorders
mother does not suffer from iron-deficiency anemia 4. Diabetes mellitus
& neonatal iron stores are related to maternal iron 5. Thyroid disorders
status and to timing of cord clamping. 6. Prolactin disorders
Infectious factors
Sickle cell anemia: Immunologic factors
Pregnancy complications 1. Cellular mechanisms
Cerebral vein thrombosis 1. Th1 immune responses to reproductive
Pneumonia antigens (embryo or trophoblast)
Pyelonephritis 2. Th2 cytokine or growth factor deficiency
deep-venous thrombosis 2. Humoral mechanisms
Pulmonary embolism a. Antiphospholipid antibodies
Sepsis syndrome b. Antithyroid antibodies
Delivery Complications d. Antitrophoblast antibodies
Gestational hypertension/preeclampsia e. Blocking antibody deficiency
Eclampsia Thrombotic factors
Placental abruption Other factors
Preterm delivery 1. Altered uterine receptivity (integrins, adhesion
Fetal-growth restriction molecules)
2. Environmental (Toxins, Smoking)
3. Placental abnormalities (circumvallate,
marginate)
4. Medical illnesses (cardiac, renal hematologic)
5. Dyssynchronous fertilization
Bad Obstetric History
Traditionally, recurrent abortion has been
defined as the occurrence of three or more For a patient to be diagnosed with APAS, one or
more clinical and one or more laboratory criteria
clinically recognized pregnancy losses before 20
must be present (BARDA’S Criteria) :
weeks from the last menstrual period. Using this
definition, recurrent pregnancy loss (RPL) occurs
in approximately 1 in 300 pregnancies Clinical
● One or more confirmed episode of vascular
Causes of recurrent abortions thrombosis of any type
a)) Venous
1. Chromosomal b)) Arterial
2. Single gene defects c)) Small vessel
3 Multifactorial ● Pregnancy complications
Anatomic factors a)) Three or more consecutive spontaneous
1. Congenital pregnancy losses at less than 10 weeks of gestation
a. Incomplete mullerian fusion or septum resorption b)) One or more fetal deaths at greater than 10
b. Uterine artery anomalies weeks of gestation
c. Cervical incompetence c)) One or more preterm births at less than 34
2. Acquired weeks of gestation secondary to severe preeclampsia
a. Cervical incompetence or placental insufficiency
b. Synechiae
c. Leiomyomas Laboratory
40

d. Adenomyosis ● Positive plasma levels of anticardiolipin antibodies

Endocrine of the IgG or IgM isotype at medium to high levels
Page

1. Luteal phase insufficiency ● Positive plasma levels of lupus anticoagulant


** The presence of antiphospholipid antibodies
(anticardiolipin or lupus anticoagulant) during
pregnancy is a major risk factor for an adverse
pregnancy outcome
Pathogenesis
Antibodies against phospholipids could
increase thromboxane and decrease prostacyclin
synthesis within placental vessels. The
resultant prothrombotic environment could
promote vascular constriction, platelet adhesion,
and placental infarction
1st trimester scan:- Dating scan
2 nd trimester scan:- TIFA (targeted scan for fetal
anomalies) – early 14 – 16w / late >20w
3 rd trimester scan:-
Normal weight gain: starts from 12w (2kg/month)
Investigative Measures Useful in the Evaluation of
Recurrent Early Pregnancy Loss
History
1.Pattern, trimester, and characteristics of prior
pregnancy losses
2.History of subfertility or infertility
3.Menstrual history
4.Prior or current gynecologic or obstetric infections
5.Signs or symptoms of thyroid, prolactin, glucose
tolerance and PCOS
6.Personal or familial thrombotic history
7.Features associated with the antiphospholipid
syndrome (thrombosis, false positive test
for syphilis)
8.Genetic relationship B/W reproductive partners
9.Family history of recurrent spontaneous abortion,
obstetric complications, or any syndrome associated
with embryonic or fetal losses
Physical Examination
41
1.Obesity
2.Hirsutism/acanthosis
Page
3.Thyroid examination
4.Breast examination/galactorrhea
5.Pelvic examination (infection / masculinization)
Laboratory
1.Parental peripheral blood karyotype
2.Thyroid-stimulating hormone level, serum
prolactin level if indicated
3.Anticardiolipin antibody level
4.Lupus anticoagulant (activated partial
thromboplastin time or Russell Viper Venom)
5.Complete blood count with platelets
6.Factor V Leiden, G20210A prothrombin gene
mutation, protein S activity, homocysteine level,
activated protein C resistance
7.Protein C activity, antithrombin level if personal
or family history of VTE
** Postconception Evaluation:
Following conception, patients with histories of RPL
should be monitored closely to provide
psychological support and to confirm intrauterine
pregnancy and its viability.
The incidence of ectopic pregnancy and complete
molar gestation is increased in women with a
history of recurrent spontaneous pregnancy loss.
• There has been increasing support for the Use of
insulin sensitizing agents in the treatment of RPL that
occurs in the presence of PCOS
Therapeutic options that currently exist
1)) Use of donor oocytes or sperm
2)) Use of preimplantation genetic diagnosis
3)) Use of antithrombotic interventions
4)) Repair of anatomic anomalies
5)) Correction of any endocrine abnormalities
6)) Treatment of infections, and a variety of
immunologic interventions and drug treatments.
** Psychological counseling and supportis
recommended for all patients.
 Mechanical
Labour induction
-Transcervical 36F
catheter* *
-Extra-amnionic Saline
Terminology Infusion (EASI)**
-Hygroscopic Cervical
1. Uterine tachysystole is defined as >6 contractions dilators (Laminaria,
in a 10-minute period. magnesium Sulphate)**
2. Uterine hypertonus is described as a single - Membrane Stripping for
contraction lasting longer than 2 minutes. Labor Induction
3. Uterine hyperstimulation is when either condition
leads to a nonreassuring fetal heart rate pattern ** Improve Bishop score (Promote cervical
ripening)
*** Insert has shorter I-D times than gel
LABOR INDUCTION AND AUGMENTATION
As an alternate to the Bishop score, WITH OXYTOCIN
Hatfield’s Score for cervical length was used
Where Cervical length is assessed by In most instances, pre-induction cervical ripening
transvaginal sonography and used to predict and labor induction are simply a continuum. Often,
successful induction. as described above, ―ripening‖ will also stimulate
labor. If not, however, induction or augmentation
may be continued with oxytocin
** However it was found that cervical length
determination by sonography was not superior to
use of the Bishop score

Technique & Agent Route

Regimen Starting Incremental Interval
Pharmacological** dose increase (Min)
0.5–1.5 1 15 - 40
-Prostaglandin E2 Cervical 0.5 mg; Low dose
(dinoprostone) repeat in 6 hr; permit 2 4, 8, 12, 16, 20 15
3 doses total Posterior 25, 30
(GEL – Prepidil / fornix, 10 mg High dose 4 4 15
INSERT - Cervidil) 4.5 4.5 15 - 30
6 6 20 – 40

-Prostaglandin E1 Vaginal, 25 µg; repeat ** With hyperstimulation and after oxytocin

(Misoprostol—Cytotec) 3–6 hr prn Oral, 50– infusion is discontinued, it is restarted at 1/2 the
100 µg; repeat 3–6 hr previous dose and increased at 3 mU/min
prn incremental doses.
(TABLET – 100 / 200 µg) ***Hyperstimulation is more common with shorter
intervals.

-Nitric Oxide Donors

Quickening + 22w = EDD
(isosorbide mononitrate For twins: Gravida 1 para 2
42

and glyceryl Trinitrate)

Page

Grade Level (upto) edema

 1 Ankle
2 Knee •Post position of occiput
3 Ant abd wall •Pelvic contraction
4 anasarca •Pelvic tumours
•High pelvic inclination
•Placenta previa
Physiological Pathological •Conjoined twins
Grade 1 >1 •Deflexed head
During evening times During morning times •Fetal anomalies (Hydrocephalus)
also •Wrong dates
Disappears on early Don’t disappear
morning / 8hrs of bed ** Even at term
rest
> 28 w (usually) Mid trimester also
Venous compression, Anemia, pre eclampsia,
harmones Cardiac

Iminent eclampsia: Confusion, headache, vomiting

+ eigastric pain, visual disturbances, low UO.
H/O decreases fetal movements: in 3 rd trimester

Iron prohylaxis given from 16w: due to increased

demands

Standing L side of patient: Only during lap.

If head is ballotable then don’t do 2 nd pelvic grip.

In HTN: methyl ergometrine & PGF2alpha

contraindicated

For any procedures

before 12w:- 100 Microg anti –D
after 12w:- 300 Microg anti –D
In Rh –ve pregnancy: Clamp is applied immediately
& NO cord milking done

During labour
NO external cephalic version
NO manual removal of placenta
NO artificial rupture of membranes
Trial of vaginal delivery in Platypelloid pelvis:
Engagement takes place for long time , Once it
occurred then delivery is fast (coz Only AP diameter
of inlet is shortened other part is Normal)

Munrokher muller test : NO BRIM cpd

43

Unengaged head reasons (primi) **

Page
 1)) Prolapse Uterus

2)) DUB
3
3)) Fibroid uterus

GYNECOLGY 4)) Ovarian mass

44
Page
 Prolapse yrs – N baby – After 1 yr
Not sterlized
Ananthamma/65/nizamabad/SEIV &
labourer 10 yrs back.
FAMILY H/O: Not significant
C/C:
PERSONAL H/O:
Mass per vaginum – 4 yrs
Diet: mixed, appetite: reduced
H/P/I: B/B: regular, Sleep: disturbed
Addictions: Non smoker & Non alcoholic & NON
Patient was apparently assymptomatic 4 yrs back
consangious marriage
then she noticed mass per veginum which is initially
lemon size gradually progressive to reach present GCOE:
size. Patient is C/C/C.
Reducable manually & increases in size on lifting Moderately built & with BMI ??
weights & coughing P (-) I (-) C (-) C (-) K (-) L (-)
H/O back ache initially for 1st 2 yrs which was Vitals – afebrile,
HR: 83/min. N in volume, character, & rhythm No
localized aggravated on standing & relived on
RR/RF delay No vessel wall thickening
sleeping Now there is No back ache BP: 160/90 mm hg RUL: Supine
H/O difficulty in micturition on straining RR: 18/min regular
H/O lifting weights for 30 yrs JVP: NOT raised
No H/O Chronic cough
No H/O any discharge PV LOCAL EXAMINATION
Perineal examination:
NO H/O wound on mass PV
Scanty pubic hair, gaping introitus,
NO H/O constipation Atrophic labia majora, Labia minora
NO H/O leaking of urine on coughing Not visible, Pink mass per vaginum with
NO H/O irreducibility episodes cervical lips seen
NO H/O fever with chills & rigor with burning On ant vaginal wall - Keratinization (3*3 cm) seen
micturition & vaginal mucosa – atrophic
No H/O frequency of micturition No urine passage with coughing
P/S: Enterocole & No rectocoele
PAST H/O: P/V: Uterus retroverted, Levator ani tone poor.
NO H/O HTN Puborectalis (at 4 & 8 o clock) – poor tone
NO H/O DM, TB, IHD, RHD, epilepsy, chest pain /
Jaundice & bleeding disorders SYSTEMIC EXAMINATION
CVS examination- S1 & S2 heard. No other murmers
MENSTRUAL H/O: heard
Reached menopause 10 yrs back
previous cycles - 4/28.. Respiratory Examination: BLAE +ve & N vesicular
3-4 pads / day sounds heard with No adventitious sounds
No H/O white discharge
No H/O clot passage Diagnosis: A 65 yr old post menopausal women
No H/o dysenorrhoea came with P3L3 with 3 degree uterine prolapse
with cystocoele & Enterocoele & also poor pelvic
OBSTETRIC H/O: P3L3 floor tone.
1st pregnancy – FTNVD – Male - Home – Local Dai –
45 yrs – N baby – After 1 yr
45

2 nd pregnancy– FTNVD – Male - Home – Local Dai

– 43 yrs – N baby – After 2 yr
Page

3 rd pregnancy – FTNVD – female – Local Dai – 45

 symphisis & Highest Point on post vaginal
DISCUSSION: fornix.

Different classifications
1)) Shah’s classification
2)) Malpas Classification:
a)) UV prolapse:
ligament weakening
b)) Nulliparous / general:
Muscle weakening
3)) Jaffcoat’s Classification b)) Surgical: U2/3, L 1/3 with U1/3 (enterocoele)
4)) POP – Q Classification M1/3 (Rectocoele) L1/3 (perineal body prolapse)

POP – Q:The classification uses six points along the
vagina (two points on the anterior, middle &
posterior compartments) measured in relation to the
hymen.
The anatomic position of the six defined points
(Aa,Ba,C,D,Ap,Bp) should be measured in
centimeters proximal to the hymen (negative
number) or distal to the hymen (positive number),
with the plane of the hymen representing zero.
1)) UV prolapse:
Radical / Waldmeyer
[ >40, >35*]
conservative [Shirodkar’s surgery – No stenosis,
patulous & fothergill’s surgery – Stenosis, patulous]
2)) Nulliparous: Abd / Vaginal sling operations &
org (purandeswar’s – Lat sling) / Inorg (shirodkar’s –
Lat. & Khanna – Post)

Three other measurements include genital hiatus, Decubitus ulcer pathology:

perineal body, and the total vaginal length. - arterial kinking
Accordingly divided into stage 0 – stage IV - Venous congestion
- trauma
Treatment
a)) Non surgical (PFMT, pelvic floor muscle tone, Measurement of supravaginal portion of cervix:
Biofeedback in rectocoele & Pessary: Passing sound upto Internal os (resistance felt) –
minus Passing sound into lat fornix (difference gives
the length)

Pessaries Ovarian mass Uterine mass

Support and Space filling Usually cystic Usually firm / hard
1)) Ring pessary (with diaphragm) is
a commonly used support pessary, and R/L Midline
2)) Gelhorn pessary is a commonly used
space–filling pessary. Movable side to side & Movable side to side
also vertcally
** Support pessaries are recommended for
stage I and II prolapse {O,U,R,I pessaries}, Transmitted movements Transmitted movements
*** Space–filling pessaries are used for stage -ve +ve
III and IV prolapse {X,L,M,N,W,G,F}
46

Cystocoele &/or rectocoele {J,I} Can feel all borders Lower border is usually
Page

Pessary measured – Bimanually: pubic

 not felt

Hingorin Sulcus present Absent

between ovarian mass
& uterus

Midline masses: adenomyosis, fibroids, pregnancy,

encysted acsitis, full bladder

Tendercervical movements: Endometriosis & PID

Frozen pelvis: TB, PID, Radiation, retroperitoneal

fibrosis, Invasive mole

Common diseases of reproductive age women:

Fibroids, endometriosis, PID

Dictum any uterus >12w: fibroid

If < 10w: fibroid / adenomyosis

Endometriosis & Adenomyosis: Triple

dysmenorrheal:- pain before, during & after
menstruation
47
Page
 1)) Varicose veins

2)) Thyroid swelling

3)) Breast swelling

4)) Inguinal hernia

5)) Hydrocoele
4 6)) Salivary gland swelling

7)) PVD (Chronic)

SURGERY 8)) Abdominal lump
9)) Ortho Cases
48
Page
 VARICOSE VEINS
Vijay/Male/39/Cook/Kudappah/ 17 – 07 – 12
C/C:
Multiple linear swellings in R Lower limb
From 22 years
wound and pain in R foot from 2 months
H/C/C:
Patient was apparently asymptomatic 22 years back
then he noticed Swellings just below his R knee
which where asymptomatic until 2 months back
when he developed wound on dorsum of R foot
then he went to local Govt hospital (RIMS) where
Some treatment is given and was referred to Gandhi
hospital.
Multiple linear swellings in R lower limb –
22 years.
Insidious in onset & gradually progressive: initially
noticed below knee gradually extended from mid
thigh to mid leg level.
Aggravated during walking & end of day.
Relieved on taking rest & sleeping with elevated leg.
(using a pillow under the foot)
No H/O decrease In size of swelling on walking
No H/O Thickness/tenderness of swellings.
No H/O Rupture & resulting in blood loss.
Not associated with pain
Wound on dorsum of R foot – 2 months.
Insidious in onset & initially progressed for 1 month
with serous discharge then by medication decreased
in size and at present there is no discharge
Associated with pain – insidious in onset , dragging
type , continuous , aggravated on standing &
relieved on sleeping , NO radiation of pain & Not
disturbing the sleep
No H/O intermittent claudication
No H/O Night cramps
No H/O painful swelling / discoloration of Lower
limb
No H/O fever
49
No H/O trauma (orthopedic – knee)
Page
No H/O any swelling in abdomen
No H/O Ankle swelling / Skin Itching
No H/O Constipation
No H/O Hmptysis, chest pain & SOB
No H/O prolonged travel/immobilization
No H/O difficulty In walking.
Past H/O: Jaundice - 1 yr back – hospitalized &
treated with medications.
NO H/O similar complaints in past, HTN, DM, TB,
epilepsy, chest pain & bldng disorders
Treatment H/O: No H/O any Injection treatment &
No H/O any surgical procedures / Long term
medical treatment
Personal H/O:
Diet: mixed Appetite: N
B/B: regular Sleep: N
Addictions: Non smoker & occasional alchoholic
Family H/O:
No H/O similar complaint in family & No H/O any
chronic illness in family
Physical examination
(A) general survey –
patient is C/C/C . Comfortably seated.
Moderately built & adequately nourished with
N gait
P (-) I (-) C (-) C (-) K (-) L (-) E (-)
Vitals – a febrile, HR: 84/min
BP: 120/84 mm hg RUL: supine, RR: 20/min
(B) Local examination –
Patient is undressed upto umbilicus & examined in
standing & supine position
1)) Inspection:
Attitude of limb: N
On inspection multiple linear tortuous, engorged,
dilated, elongated. NON pulsatile swelling are seen
in upper ½ of medial aspect of R leg extending upto
lower ½ of medial aspect of thigh.
Healed ulcer on dorsum of R foot:
Irregular in shape,
extending from 2 cm in front of medial malleolus to
 2 cm behind great toe, (C) Systemic examination:
surrounding skin – healed scars present
discoloration of skin from toe to 2 cm above ankle 1)) Abdominal examination:
is seen & hair loss on foot & brittle nails - present Umbilicus is midline
NO Lumps palpable / Palpable organomegaly
Swellings disappear spontaneously on lying down NO free fluid
NO redness along the swellings 2)) Respiratory system:
NO areas of any Blow outs / NO V.falre are visible BLAE: N &
NO swelling visible at saphaneous opening N vesicular sounds heard
Other limb appear N on inspection NO adventitious sounds
3)) Cardiovascular system:
2)) Palpation: Heart sound 1 & 2: Heard & No murmurs heard
NO local rise of temperature
NO redness along the swellings / ulcer area Diagnosis:
No oedema / Tenderness on lower part leg Primary
Right sided
Brodie trendelenberg test Partial varicosity of Great Saphenous Vein with
Test – 1 : +ve Competent SFJ and Incompetent below knee
Test – 2 : +ve perforators with
Multiple tourniquet test: Below knee perforator in Complicating as venous Ulcer
incompetent
Modified perthes test Discussion:
Schwarz test: - ve If Skin changes : +ve → Chronic venous insufficiency
Fegan’s test: a defect in deep fascia is felt 2cm (CVI) → Treatment Only surgery NO role of
below tibial tuberosity on medial side of leg conservative truss usage.
Morrisay’s cough impulse test: - ve
Homan’s sign: - ve Flush: Close / near to
Mose’s sign: - ve
Short saphenous Vein stripping: NOT done usually
Neuhof’s sign: -ve
1)) Incompetent perforators are hardly found in
All Peripheral pulses: palpable (R & L) association with SSV
Other Limb: N 2)) Causes long standing oedema
3)) May permanently damage Sural Nerve
3)) percussion: Schwartz -ve
Varicose Ulcer management:
4)) Auscultation: Continous Murmur / Bruie absent Bisgard Conservative management →→ surgical
at saphenofemoral junction. correction of varicose veins →→Split skin graft (last)
5)) Regional Lymph nodes examination:

Inguinal (Upper M, Upper L, Vertical: Not palpable)

Popliteal: Not palpable

6)) Measurements – Mid leg circumference

R(31cm)/L( 29cm)
50

7)) Movements – range of movements of lower

Page

limb are with in N range


Pulmonary embolism usually occurs 6 - 11 days after
post - op period
In case of varicosity of Long SV small veins from
sole of foot & ankle which drain into this venous
system through MEDIAL MARGINAL VEINS
becomes dilated, this give rise to swelling of ankle:
ANKLE FLARE.
Perforators:
1)) Indirect (upper part of leg)
2)) Direct in
Thigh: adductor canal
Leg: medial (5cm , 10cm, 15cm above medial
malleolus) 1st 2 enter POST TIBIAL VEIN Where
Soleal venous sinuses also enters it, last perforator
connects long SV with posterior TV.
Central: Short SV to veins of gastrocnemius & soleus
(practically UNIMP).
Lateral (5cm, 12cm,17cm above lateral malleolus)
Short SV & peroneal veins.
51
Page
Drainage of short SV (7 – 13 valves) to Popliteal
fossa: 3 to 7.5cm above the level of knee joint
Forcible contraction of calf muscles → force blood
through perforating veins in reverse direction →
destruction of valves of perforating veins →
varicose veins (rickshaw pullers)
Cramp (sudden change in caliber of communicating
veins which stimulates the muscles through which
they pass) in calf shortly after retiring to bed.
Sclerotherapy: varicose veins confined below knee.
CVI causes (3): HIGH AMBULATORY VENOUS
HYPERTENSION
1)) Varicose veins
2)) DVT (After recanulation gravitational pressure of
blood column transmitted unimpeded to ankles
which alone is not sufficient enough to produce
serious stasis it must occur along with incompetent
perforators)
3)) Perforator incompetence (high ambulatory V
pressure developing within deep veins of calf during
excersie → directly transmitted to superficial venous
system → ↑ capillary pressure in surrounding skin →
oedema, fat necrosis, ulceration
Venous ulcer: Shallow, recurrent, tender,
surrounding bluish discoloration & erythematic. Not
extend beyond deep fascia appear spontaneously
preceded by itching /trivial trauma
.
Surgical management of pulmonary embolism:
1)) Ligation of IVC just distal to R renal vein
2)) venous interruption (lower limb): arterial
sutures/plastic clip : proximal to site of thrombus
(determined by phlebography)
3)) Pulmonary embolectomy
 Above knee stockings are never preferred

Great SV is stripped only up to just below knee. (Avoid damage to saphenous N).

High ambulatory V pressure

defective microcirculation

Extravasation of RBC Fibrin WBC (mast cells,monocytes)

Haemosiderin Fibrin cuff release of ROS & proteolysis E

Eczema & Dermatitis Diffusion block

Hypoxia Poor repair

tissue damage (ulcer)

Loss of SC fat

Std Doppler is NOT AN ACCURATE method of Ulcers due to LSV Varicosity: medial side of calf
establishing Incompetence in SSV coz of its variable Ulcers due to SSV Varicosity: lateral side
termination so Duplex scans is mandatory Post thrombotic: Any part of calf skin

Another cause of ulcer has to be sought is there is Operative Notes:

no surrounding evidence of Lipodermatosclerosis
(Thickening, indurations, inflammation &
pigmentation) / ankle flare.
Venous entrapment: Axillary (1st rib & clavicle) &
Popliteal vein (abnormal insertion of Gastrocnemius
muscle) → Sweeling of limb after exercise
52
1))Incision: femoral pulse is palpated in the groin,
and an oblique longitudinal incision is placed just
medial to this point
2)) The patient is placed in the supine position. The
procedure can be performed under either SA/GA.
The lower abdomen and the affected leg are
prepped, and a stockinette is placed over the leg.
3)) These tributaries are ligated & The junction of 2

Gaiter’s area: area between calf muscles & ankle: veins is dissected and exposed. Next, the greater
COCKETT PERFORATORS JOIN POST TIBIAL VEIN
saphenous vein is divided between clamps
Page

& POST. ARCH VEIN

 approximately 1 cm away from the saphenofemoral
junction.
4)) The saphenofemoral junction is ligated with 0-0
silk sutures, and a 2-0 silk transfixion suture ligature
is placed. Special care is taken not to narrow the
femoral vein during this process.
5)) The next step depends on whether stripping of
the greater saphenous vein is to be performed.
Stripping of the greater saphenous vein can be
avoided because the vein usually collapses and
becomes sclerosed as long as the saphenofemoral
junction and any incompetent perforators have
been ligated. If stripping of the greater saphenous
vein is to be performed, a Goldman vein stripper
with the olive head at the distal end is gently passed
6)) alternative method of addressing the varicosed
venous branches is to ligate the preoperatively
identified perforators in the thigh and the leg
7)) In SSV varicosity: A transverse incision is placed
along the popliteal fossa crease with patient in
prone position varicosed lesser saphenous vein is
identified and followed through the fascia toward
the popliteal vein.
8)) The saphenopopliteal junction is carefully
dissected while avoiding any injury to popliteal
artery and sciatic nerve. The short saphenous vein is
divided between clamps and ligated & finally a
suture ligature is placed at the saphenopopliteal
junction.
HYDROCOELE
Venkatnarayana/55/Khammam/agricultural labour/
31 – 07 - 12
C/C: Swelling of right side of scrotum from 2 years
H/C/C:
The patient was apparently asymptomatic 2 years
back then he developed swelling on R side of
scrotum then went to local Doctor where some
medications are given & used them for 1 month the
swelling did not resolve & started increase in size so
went to local govt hospital from where he was
53
referred to Gandhi hospital
Page
Swelling in R side of scrotum – 2 years Insidious in
onset, gradually progressive, Associated with pain
which is Scrotal in location, dragging type,
Continuous, progressive Rlved by sleeping,
Aggravated by walking, No radiation of pain & pain
Not disturbing the sleep
NO H/O reducibility of swelling
(Spontaneously on sleeping/manually),
NO H/O Increase of swelling with cough / Straining.
NO H/O trauma.
NO H/O fever with chills & Swelling of feet
NO H/O sudden increase / spontaneous decrease of
swelling
NO H/O burning micturition / white discharge
NO H/O of frequency of micturition with
polyura/dysuria & loin pain
NO H/O exposure to venereal diseases
NO H/O evening rise of temperature with cough
& sputum.
NO H/O Significant loss of weight
NO H/O any swellings in abdomen.
NO H/O any surgeries in groin region.
Local examination:
Patient is Undressed from umbilicus to mid thigh
level & examined in standing & supine positions.
1)) Inspection: A 6 (horizontal) x 10 (vertical) x 6
(thickness) swelling is seen on R side of scotum
which is vertically oval extending from root of
scrotum to base of scrotum which is at midthigh
level & Skin over swelling is N except for loss of
rugosity, there is NO scars / sinuses (on POSTERIOR
region of scrotum) / Ulcer (ANTERIOR part of
scrotum) / engorged veins seen.
NO Excoriation of skin.
Surface over swelling is even except there is
constriction in middle at about 4 cm from root of
scrotum.
Penis is deviated to left and buried partially.
2)) Palpation:
NO local rise of temperature.
NO local tenderness.
NO expansile cough impulse.
Getting above swelling: +ve.
Consistency: Firm (cystic)
 Reducibility: -ve hydrocoele),
Compressibility: -ve Infections: treat it (even if then persists – Surgical
Fluctuation: +ve management), Haematocoele → late complication
Transillumination: +ve. testicular atrophy.
Testis: palpable & testicular sensation +ve
3)) Percussion: DULL [In seminoma testis NO BIOPSY/FNAC – scrotum
4)) Local lymph nodes (inguinal): NOT palpable. lymphatic drainage is inguinal, testis lymphatic
drainage is para aortic LN so if done. tumor cells
Abdominal examination: reach tract then skin finally paraoartic LN →
Umbilicus is midline UPSTAGING of cancer.]
NO Lumps palpable / Palpable organomegaly
NO free fluid Operation principle: Evacuation + NO sac + ↑ area
PR: Not done of absorption (Now fluid is exposed to undersurface
of skin → absorption).
Diagnosis:
R sided In Congenital hydrocoele:
primary treatment is HERNIOTOMY
uncomplicated Getting above swelling: -ve
vaginal hydrocoele Cough impulse: -ve (By which Congenital inguinal
hernia is distinguished)
Fluctuation: +ve
Reducability: +ve
Discussion In infantile Hydrocoele: treatment is EVACUATION
+ SAC EVERSION
Hydrocoele: FLUCTUATION +ve (trans
illumination may/may not +ve). In lord’s plication usually drain is NOT kept post
In tense swelling fluctuation is difficult to perform operatively. [ lord’s fibrous band: in midgut
but present. malrotation & Lord’s fundoplication in GERD]
Primary: Moderate to large, comparably tense, testis
NOT palpable, area of constriction may present Usually CORRUGATED rubber drainage tube is kept
(DUMBBELL: NO explanation), (BLUE colour).
Causative history is absent. Testicular sensation: by applying pressure on testis
Vaginal: getting above swelling +ve – Swelling is pain is felt in EPIGASTRIC region.
confined to scrotum.
Scrotal contents: Testis with its coverings +
(To tell hydrocoele never tell coz getting above
epididymis + lower part of spermatic cord.
swelling is +ve – it just tell that the swelling is
During palpation: we feel cord:- Vas + fibres of
confined to scrotum)
cremastric muscle.
Transillumination +ve: Clear fluid + sac is thin
Sometimes Cord may appear thickened: because of
(if any of them / both –ve: Test –ve).
hypertrophied cremastric muscles due to chronically
N vaginal fluid: 3 – 5 ml.
bearing weight of big swelling.
N physiology: visceral layer secretes → Parietal layer
Cord thickened + Appear nodular : Tuberculosis.
absorbs. (Secretion ↑ → secondary & absorption ↓
→ primary hydrocoele) Urogenital TB: always secondary to primary focus
(pulm/renal).
Treatment:
54

Secondary – Small swelling: conservative, Decrease of swelling size spontaneously on lying

Page

Tumour: treat tumour (NO separate treatment for down –

 Inguinal hernia, Varicocoele, lymph varix,
Congenital hydrocoele
Tuberculosis sinus – posteriorly & Chancre –
anteriorly: May be reversed if there is an
ANTEVERTED testis – (7 – 8%) of cases: diagnosed
by examination of opposite testis.
Excoriation of skin in hydrocele:
1)) buried penis – urine pass over the swelling –
excoriation
2)) Rubbing of thigh.
Cystic Swellings of scrotum – hydrocoele,
Chylocoele, Spermatocoele, recent haematocoele,
Cysts of hydatid of morgagni, cysts of epidydims &
Cystic areas of teratoma
Torch never kept posterior in hydrocoele coz testis
obstructs light path making transillumination falsely
–ve: however it is kept posteriorly to see
transillumination of cysts of epidydimis.
Fluctuation: Transmission of impulse at 2 planes
right angles to each other.
Transillumination +ve: Cysts of hydatid of
morgagni, cysts of epidydims, hydrocoele,
Spermatocoele (some cases). Cystic areas of
teratoma.
In transillumination 1st illuminate N side scrotal skin
then interpret diseased side (In some skin is very
thin, with powerful torch is may appear as
transillumination (falsely +ve).
Another use of transillumination is identify position
of testis (N / anteverted)
Nodules on surface of scrotal skin –
1)) sebaceous cysts
2)) herniation of hydrocoele sac – Tunica vaginailis
herniates through fibres of cremastric & spermatic
fascia to lie underneath skin
3)) malignancy of testis.
Inguinal lymph nodes are not enlarged in pyocoele
55
Page
+ve sign of empty – Compressability
(can regain its previous size on its own if pressure is
released).
PR examination – Tubercular epidydimis: enlarged
seminal vesicle sometimes enlarged prostrate also.
Skin rugosity increases in elephantiasis.
In lodd’s operation drain is not kept usually.
Difference between lodd’s & jabouly’s is that in the
later, sac is dissected out of scrotum and then incised
& drained. After opening of sac if testicular atrophy
is present we perform low orchidectomy.
Filariasis of genital areas:
Hydrocoele , chylocoele, Lymph varix, Elephantaisis
THYROID SWELLING
Lakshmi /25 /F /house wife / adilabad / married / -
07 – 12
C/C: Swelling in front of neck
H/C/C:
The patient was apparently asymptomatic 2 years
back then she noticed a swelling in front of neck
which was initially pea sized then she went to local
govt hospital 6 months where she was given some
treatment for 1 month but swelling did not reduce
in size and was finally referred to Gandhi hospital
NO H/O evening rise of temperature & cough
NO H/O any discharge from swelling
NO H/O trauma
NO H/O radiation exposure to neck
NO H/O pain and fever
NO H/O Spontaneous regression/ sudden increase
in size of swelling
NO H/O symptoms suggestive of hypothyroidism
(like loss of hair, memory disturbances, tiredness,
weight gain inspite of decreased appetite,fatigue,
lethargy, Constipation)
NO H/O symptoms suggestive of primary
hyperthyroidism ( weight loss inspite of increased
appetite , Protruding eyes, Double vision, Difficulty
in eye closure)
NO H/O symptoms suggestive of secondary
 hyperthyroidism (chest pain, palpitations,
exertional dyspnoea, Constipation, Ankle swelling)
NO H/O Difficulty in breathing
No H/O preference to Cold/Hot weather
NO H/O difficulty in swallowing
NO H/O recent significant Change in voice
NO H/O noisy respiration
NO H/O similar complaints in neighborhood /
in her village
NO H/O any recent change in menstrual Cycle
NO H/O recent Child delivery
NO H/O Nocturnal dyspnoea
NO H/O scalp / abdominal swelling
NO H/O bone pains
Past H/O: NO H/O similar complaints in past, HTN,
DM, TB, epilepsy, chest pain. Jaundice & bleeding
disorders
Treatment H/O: No H/O any surgical procedures /
Long term treatment
Personal H/O:
Diet: mixed Salt +ve
NO special predilection to cabbage like vegetables,
appetite: N
B/B: regular, Sleep: N
Addictions: Non smoker & Non alcoholic
Menstrual & obstetric history H/O:
Age at menarche – 13 years
5/30 regular , N flow,
No H/O passage of any clots
Marital life: 4 years & 2 children
Family H/O:
No H/O similar complaint in family &
No H/O any chronic illness in family
Physical examination
(A) General survey –
patient is C/C/C. Comfortably seated. N facies
Patient mental status is N (No anxiety/dullness).
Thinly built & adequately nourished with
P (-) I (-) C (-) C (-) K (-) L (-) E (-)
56
Cnj – N & pupils are N & reacting equally.
Eyes & eye lids are N, Eye Movements : N range
Page
No periorbital puffiness & tongue show NO tremors
& there is no enlargement. Legs: Normal
Skin: Normal - Not moist / warm / Inelastic
Vitals – a febrile, HR: 76/min regular
BP: 120/86 mm hg RUL: supine, RR: 16/min
(B) Local examination: Patient is exposed upto
upper chest and examined with neck slightly flexed
in sitting position from behind and from front &
examining at same level as patient. [pizollo’s in
obese & Short necked indivisuals]
(1) Inspection:
A solitary hemispherical swelling of 3 (horizontal) x
3 (vertical) size present infront of neck in midline
with distinct lateral & inferior border.
Extent:- 2 cm above sternal end of clavicle: upper
border. Lateral border is 2cm lateral to midline.
Surface of swelling - smooth & skin over swelling is
N with no engorged veins/ scars/ sinuses.
Surrounding skin is N.
Swelling moves with deglutition.
Trachea is midline
Pemberton’s sign & platysma sign -ve
NO dilated veins over upper part of chest
NO other swellings visible in neck
NO increase in size on coughing (plunging type)
(2) Palpation:
NO local tenderness
NO local rise of temperature
Site size shape extents- confirmatory
Margins well defined & regular (including upper)
Surface: smooth & even
Consistency: uniformly firm
plane of swelling : deep to sternocleidomastoid
Mobility: Horizontal: +ve & vertical –ve
Swelling do not moves on protrusion of toungue.
NO tracheal rings palpated in suprasternal Notch
Fluctuation: -ve
Kocher’s test: NOT done
trachea is NOT deviated
Carotids: palpable & not displaced
Cervical lymph nodes: NOT palpable
Other part of gland is NOT palpable clinically
NO Thrills / pulsations on swelling

(3) Percussion: resonant on sternum.
(4) Auscultation: No Brue heard over swelling.
(C) Systemic examination:
3)) Cardiovascular system:
Heart sound 1 & 2: Heard & No murmurs heard
4)) Musculoskeletal system:
N gait with Spine Normal & No long bone
tenderness

1)) Abdominal examination:

Diagnosis: A case of
Umbilicus is midline
Solitary
NO Lumps palpable / Palpable hepatomegaly
Thyroid nodule (with D/D: adenoma, Tense thyroid
NO free fluid
cyst, Localized hashimoto’s, early differentiated
2)) Respiratory system:
carcinoma, dominant nodule of MNG)
BLAE: N &
involving isthmus &
N vesicular sounds heard
Patient is in Euthyroid state clinically
NO adventitious sounds

Discussion 2)) palpation: trail sign & triple finger test

Trachea in midline:
1)) inspection: chin , laryngeal prominence &
Suprasternal Notch: same line
3)) auscultation:
Auscultated in following 3 areas:-
where breath sounds are heard
more clearly it indicates: Tracheal location
Strap muscles during surgery are cut at upper third
because their N supply comes from below: Ansa
Cervicalis

During surgery:
Recurrent laryngeal nerve is identified because it is
Why thyroid?? the only structure which passes vertically in trachea
NECK, DEEP TO DEEP FASCIA, MOVES ON oesophageal groove.
DEGLUTITION, BUTTERFLY SHAPED SWELLING 1st vein to be ligated in surgery is MTV:
(rarely) 1)) Short vein after cutting mobility of gland is
Thyroid moves on deglutition: increased
1)) enclosed in pretracheal fascia 2)) It is friable & drain directly into IJV if this is cut
2)) berry’s ligament then a direct hole in IJV is created resulting in
3)) post lamina of pretracheal fascia is closely massive hemorrhage.
adherent to trachea Ligation sequence: MTV → superior pedicle →
57

4)) Some times: Levator glandulae thyroidae: Inferior pedicle.

attached to hyoid.
Page
 Pretracheal fascia is cut during surgery vertically to In diagnosis:
enter thyroid, How do we know that we entered 1)) Number
Thyroid: VENOUS PLEXUS IS SEEN OVER. 2)) Thyroid yes/No
We flex neck in standard method of palpation 3)) Location
1)) Relax deep cervical fascia 4)) Physiological status
2)) relax sternocleidomastoid. 5)) benign/malignant
6)) D/D.
Thyroid enlargement occurs posterior mainly
because anterior layer is tough & not yielding & The thyroid swelling may sometimes becomes
posterior layer is thin. prominent on strap muscles contraction
In unilateral swelling dysphagia never occurs – (strapsternohyoid, sternothyroid, and superior belly
Esophagus is a muscular tube & is easily displacable. of the omohyoid):
1)) if present exactly in midline (As in this case)
In Inspection (description) On muscles contraction → fascia relaxes → swelling
1)) Swellling becomes more prominent
2)) Movement 2)) if part of gland is in gap zone (arrow marks) &
3)) Lower margin comment remaining is behind strap muscles then
4)) Trachea On muscles contraction→ pushing Out of the part
5)) Other swelling. behind muscles → swelling becomes more
prominent. IN this case Fascia tense test must be
performed.

In Thyroid swellings see the carotid pulse at (lower part: NOT at classical site):

Classical site (red) Lower site (black)

Benign +ve +ve

malignant +ve -ve

Why isthmus is removed???:

1)) Compensatory hypertrophy compression on trachea.
2)) Adenoma usually occurs at the junction of isthmus & lobe.

Lobe involved is based on trachea position not based on midline

58
Page
 Recurrent laryngeal nerve is usually found in In retrosternal Goitre Duspnoe occur when lying on
Simon’s triangle, which is formed by the inferior 1 side only. Most diagnostic feature is Presence of
thyroid artery superiorly, the common carotid
engorged veins on upper chest.
artery laterally, and the esophagus medially.
Indications for surgery in NON NODULAR goiter
(partial thyroidectomy):
1)) rapid increase in size due to intraglandular
There is NO real dyspnoea, it is rather called hemorrhage
obstructive breathing. 2)) Cosmetic reasons
3)) pressure symptoms +ve
Pre – op measures:
4)) Intrathoracic extension causing respiratory
1)) Routine workup
obstruction.
2)) Serum Ca levels (detect hyperparathyroidism
may coexist.)
3)) Indirect laryngoscopy is performed Crile’s Method: Place thumb on gland ¬ Ask to
preoperatively to evaluate the mobility of the vocal swallow ¬ Nodules are better appreciated
cords and detect unsuspected vocal cord paralysis (if
paralysis is present, it is essential not to damage the Lahey’s method:- Palpation of each Lobe (from
recurrent laryngeal nerve supplying the normal front):- Palpate L lobe by pushing it towards L with
L hand & Plpate it with R hand
vocal cords).
4)) Patients who are thyrotoxic should be rendered
euthyroid. This can be achieved medically by the
use of carbimazole. If the patient has evidence of Age Feature
sympathetic overdrive such as tachycardia, a beta- Malignant 50 – 60 yrs Firm painless
blocker such as propranolol is added. lymphoma mass
indistinguishable
5)) Physiology : Ingested Iodine → iodide → iodine from anaplastic
trapping → PEROXIDASE → iodine → MIT & DIT type
MIT + DIT → TIT [T3] (oxidative condensation) Medullary 50 – 70 yrs Firm smooth
DIT + MIT → R. TIT [R. T3]. carcinoma lump
indistinguishable
Thyroid gland: C5 – T1. from Solitary
Sympathetic: S,M,I cervical ganglia Nodule
Granulomatous 40 yrs Firm irregular
Parasympathetic : External & recurrent lrngl nerves.
Thyroiditis enlargement
Thyroid selling do not moves on deglutition:
50 yrs Soft rubbery
1)) Intrathoracic extension Hashimoto diffuse
2)) Thyroiditis extending to surrounding region Thyroiditis enlargement
3)) Invasion to surrounding structures 20 – 30 yrs Diffuse soft
4)) Very large swelling. Colloid goitre elastic
5)) Redel’s & Granulomatous Thyroid enlargement
59

10 – 20 yrs Diffuse soft

MNG nodules are: colloid, cystic, degenerative, Diffuse elastic
Page

haemorrhagic & calcification hyperplastic enlargement

 type Tremor is demonstrated in Extended & abducted
30 – 40 yrs Diffuse irregular fingers.
MNG enlargement
with Bosellated Relationship of recurrent laryngeal nerve to the
surface inferior thyroid artery
(Nodules with
variable N in TOG (Commenest)
consistency)
N btw branches of Inf thyroid artery
Colloid goiter DD: Lymphadenoid
N lateral to trachea
goiter.(treatment always partial thyroidectomy). N Ant / Post to artery
N far anterior
In Retro Sternal Goitre casuing obstruction NO
place for thyroxin / antithyroid drugs / radioiodine:
RESECTION

** The superior parathyroid is characteristically dorsal to the plane of the nerve, whereas the inferior gland is
ventral to the nerve.

Normal Value Hormone

0.5–5 µU/mL Serum Thyroid-

Stimulating Hormone
55–150 nmol/L Total T4

1.5–3.5 nmol/L Total T3

12–28 pmol/L Free T4

3–9 pmol/L Free T3

H/O radiation exposure: (For what in history): therapeutic radiation has been used to treat conditions such as
tinea capitis (6.5 cGy), thymic enlargement (100 to 400 cGy), enlarged tonsils and adenoids (750 cGy)
60
Page
 MANAGEMENT OF SOLIATRY THYROID NODULE
TSH test

Euthyroid Thyrotoxic

Radio isotope Scan

Cold Warm Hot

Ultrasound neck

Aspirate &
Solid Cystic
analyze

FNAC

Benign malignant Suspicious Benign malignant No cells

Frozen section

Papillary follicular Repeat aspirations

Total throidectomy

Recur even after 3 aspirations

Thyroid Lobectomy
61
Page
 Propyl thiouracil: Prothrombin deficiency – Vit K Multicentricity in papillary carcinoma is not due to
supplementation. direct extection but due to lymphatic spread within
It is given Pre op 100mg thrice daily in the rich intrathyroid lymphatics.
hyperthyroisism to make thyroid euthyroid &
operation performed 2 months later.( if performed Complications Of radioiodine therapy
too early: Thyroid crisis) & propanalol has to be
Acute Long-Term
added in graves disease: to relieve tremor anxiety &
Neck pain, swelling, Hematologic
HR. and tenderness
Thyroiditis Bone marrow
Post op: S.ca – after 6W & Thyroid status – after 6M
Sialadenitis suppression
& then yearly.
Fertility
Cerebral edema infertility
Operative complications:
Vocal cord paralysis Increased spontaneous
Nausea and vomiting abortion rate
Immediate Late
Bone marrow Pulmonary fibrosis
Haemorrhage Thyroid insufficiency
suppression Anaplastic thyroid cancer
Infection Recurrent thyrotoxicosis
Gastric cancer
Recurrent laryngeal N Hypertrophic scar/keloid
Lung cancer
paralysis
Bladder cancer
Thyroid crisis / storm Progressive Hypoparathyroidism
Exophthalmosis Increased risk of cancer
Transient hypocalcemia Wound cellulitis
Respiratory obstruction Parathyroid insufficiency
Horner’s syndrome Operative Points:
Injury to oesophagus
1)) Supine position initially with the neck extended
by placing a ring beneath the head and a sandbag
FNAC
roll beneath the shoulder. The patient is placed in a
reverse Trendelenburg position
1)) 23-gauge needle is inserted into the thyroid
2)) A Kocher transverse collar incision, typically 4 to
mass, and several passes are made while aspirating 5 cm in length, is placed in or parallel to a natural
the syringe. After releasing the suction on the skin crease 1 cm below the cricoid cartilage. The
syringe, the needle is withdrawn and the cells are superior flap extends upward to the thyroid notch
immediately placed on prelabeled dry glass slides and the lower flap extends downward to the sternal
2)) 3 ways notch.
a)) some are immersed in a 70% alcohol solution 3)) The dissection plane is kept as close to the
thyroid as possible and the superior pole vessels are
b)) others are air dried.
individually identified, skeletonized, ligated, and
c)) fewplaced in a 90% alcohol solution for divided low on the thyroid gland to avoid injury to
cytospin or cell pellet. the external branch of the superior laryngeal nerve
3)) The slides are stained by Papanicolaou's or 4)) The inferior thyroid vessels are dissected,
Wright's stains and examined under the microscope. skeletonized, ligated, and divided as close to the
surface of the thyroid gland as possible to minimize
** If a bloody aspirate is obtained, the patient devascularization of the parathyroids (extracapsular
should be repositioned in a more upright position dissection) or injury to the RLN. The RLN is most
and the biopsy repeated with a finer (25- to 30- vulnerable to injury in the vicinity of the ligament of
Berry (Any bleeding in this area should be
gauge) needle.
controlled with gentle pressure before carefully
62

identifying the vessel and ligating it. Use of the

electrocautery should be avoided)
Page
 5)) LN / Parathyroid?? :
a)) Parathyroid glands are small, yellowish brown,
and soft and pliable, in contrast to lymph nodes or
thyroid nodules, which are firm (Parathyroid glands:
been inadvertently removed during the
thyroidectomy should be resected, confirmed as
parathyroid tissue by frozen section, divided into 1-
mm fragments, and reimplanted into individual
pockets in the sternocleidomastoid muscle
b)) single small artery can be seen entering the
gland; the artery radiates out over the capsule in a
fernlike pattern.
6)) Wound closure:
The deep cervical fascia: with 3-0 absb sutures.
The Platysma : reapproximated with interrupted 3-0
absorbable sutures.
The skin : subcuticular 4-0 nonabsorbable
monofilament or absorbable sutures.
7)) Minimally Invasive Approaches
BREAST LUMP
Suguna /30 /F /House wife / Warangal
C/C:
Swelling in the Left breast from 10 years
Pain in the left breast from 3 months
H/C/C:
Patient was apparently asymptomatic 10 years back
when she 1st noticed a swelling in left breast during
feeding her baby, came to Gandhi hospital where
she was assured that is a normal swelling during
lactation & regresses after lactation. But the swelling
did not reduce in size and gradually progressed to
present size and she had developed pain from last 3
months for which she came to Gandhi hospital.
Lump in left breast from 10 years. Insidious in onset,
gradually progressive which was initially pea sized,
noticed in outer & upper part of breast and reached
the present size occupying outer & upper part of
breast.
NO spontaneous regression / sudden increase in
size.
63
Pain in left breast from 3 months, insidious in onset,
Page
pricking type, continuous, aggravated during
Totally endoscopic approaches also have been
described, via the supraclavicular, anterior chest,
axillary, and breast approach. The axillary, anterior
chest, and breast approaches eliminate the skin
incision in the neck but are more invasive
8)) Intrathoracic Goitre
Virtually all intrathoracic goiters can be removed via
a cervical incision. Patients who have
(a) invasive thyroid cancers,
(b) had previous thyroid operations
(c) primary mediastinal goiters with no thyroid
tissue in the neck may require a median sternotomy
** The sternum usually should be divided to the
level of the third intercostal space and then laterally
on one side at the space between the third and
fourth ribs
menstrual cycle & pain relieves partially on
medication, NO radiation of pain & NOT disturbing
the sleep.
Patient is multiparous
NO H/O trauma
NO H/O radiation exposure
NO H/O OCP usage
NO H/O Evening rise of temperature & cough
NO H/O similar complaint in mother/aunt
NO H/O menstrual irregularities & leucorrhea
NO H/O nipple discharge / wetting of breast
garment
NO H/O skin changes
NO H/O axillary swelling
NO H/O swelling of limb
No H/O Significant weight loss
NO H/O of previouis breast disease / biopsies
No H/O of recent nipple retraction
NO H/O fever with or without rigor (inflm carc)
NO H/O pain in back/hip/shoulders
NO H/O chest pain, difficulty in breathing,
Coughing out blood
NO H/O yellowish discoloration of eyes/
abdominal selling/pain/distension
NO H/O convulsions
 Past H/O:.
NO H/O similar complaints in past, HTN, DM, TB,
epilepsy, chest pain & bldng disorders
Treatment H/O: No H/O any surgical procedures /
Long term treatment
Personal H/O:
Diet: mixed appetite: N
B/B: regular Sleep: N
Addictions: Non smoker & non alchoholic.
Married at 18 years
Menstrual and obstetric H/O:
Attained menarche at 14 years.
Cycles: regular 28/4. No clot passage.
No H/O leucorrhoea.
Spontaneous conception
1st child 2 years after marriage
Children ( 2, 6 & 8 yrs). Breast feeding: ( 8 months).
Family H/O:
No H/O similar complaint in mother/ sister/ aunt &
No H/O any chronic illness in family
Physical examination
(A) general survey –
patient is C/C/C. Comfortably seated.
Moderately built & adequately nourished. BMI:
P (-) I (-) C (-) C (-) K (-) L (-) E (-)
Vitals – a febrile, HR: 74/min
BP: 110/80 mm hg RUL: supine, RR: 16/min
(B) Local examination: Patient consent is taken &
undressed to expose both the breasts & axilla up to
abdomen & examination is done in sitting (with
arms by side, on hips, raised) in supine, semi
recumbent & bending forward positions.
(1)Inspection
Breast:
Both the breasts are N in position.
Left breast is enlarged in size showing fullness in
outer & upper quadrant. &
64
Skin over breast shows NO puckering/dimpling/any
ulceration/fungation/engorged veins/scars/peau de
Page
orange/Nodules.
Right side breast appear normal.
NAC:
Left NAC is comparatively bigger than right side.
Nipple is not displaced / elevated / Not prominent /
Flat
NO retraction / active discharge from nipple or
adjacent area (fistula)
Surface appear N with no cracks/fissures/eczema &
Areola appears Normal on both sides
Right side: NAC appear normal.
Arm & Thorax: N on both sides. No browny
oedema of Arm & No nodules / midline swellings
seen.
Axilla & supraclavicular fossa: N on both sides, No
swellings seen.
Submammary folds: N (no nodules/obliteration)
Shoulder movements: No restriction
WITH arms raised: Fullness becomes more
prominent & Both nipples are present at same level
ON bending forward: Both breasts fall freely
(NO fixity to chest wall)
ON supine position: both breasts appear N
(2) Palpation:
(Sitting then Semi recumbent finally in recumbency:
Done with palmar surfaces of fingers with hand flat
NOT with Flat of hand & also between pulp of
fingers & Thumb)
No local rise of temperature.
Tenderness felt in UO quadrant.
A mass is felt in UO quadrant which is about 5 cm
(horizontal) x 4 cm (vertical).
Irregular in shape with ill-defined margin, surface
appear nodular, & uniformly firm in consistency,
fluctuation & transillumination : -ve.
Skin over selling is pinchable, skin can be slide over
it & is not fixed to breast tissue / underlying fascia /
Muscle / chest wall.
On pressing No nipple discharge is seen & on
movement of swelling so puckering / tethering seen.
No mass felt on palpation of sub areolar breast
tissue.
Nipple L 20 cm & 13 cm R 20cm & 12 cm
(clavicle & midline)
 Other part of breast Tissue N including axillary tail PV: NOT done
Other breast N on palpation 2)) Respiratory system:
BLAE: N &
Palpation of LN (both sides): NOT palpable N vesicular sounds heard
1)) Axillary NO adventitious sounds
2)) Cervical 3)) Cardiovascular system:
3)) Supraclavicular Heart sound 1 & 2: Heard & No murmurs heard
(3) Percussion: Resonant: sternum 4)) Musculoskeletal system:
N gait with Spine,pelvis,Sternum Normal & No
long bone tenderness
(C) Systemic examination:
Diagnosis: A case of primary benign neoplasm of
1)) Abdominal examination: left breast probably fibroadenosis involving outer
Umbilicus is midline and upper quadrants.
NO Lumps palpable / Palpable hepatomegaly
NO free fluid
PR : NOT done

Discussion PR examination: for Blummer shelf

PV examination: for Blummer shelf & ovarian
masses.

Anterior chemotherapy – Pre op Chemotherapy FNAC

(down staging)&
Posterior chemotherapy – Post op Chemotherapy Not conclusive
(residual).
True cut biopsy (receptor status, genetic
Liver involvement by: markers, tumour type)
1)) Hematogenous (Parenchymatous)
Not conclusive
2)) Grossman’s pathway (Surface) [breast → rectus
sheath → sub diaphragmatic lymphatics → Excision biopsy
L.falciparum of liver]: basically inferior & medial
quadrants (thus they Not conclusive
have usually associated with free fluid in abdomen)
65

Frozen section biopsy

Page
 Lung metastasis in breast ca.: Cannon ball metastasis
(X ray finding)
Conditions in which carcinoma of breast with lump
But no axillary metastasis
Painful breast: breast abscess, trauma, breast
engorgement, fibroadenosis (No signs of
inflammation), late stages of Ca breast
Nulliparity is risk factor coz
NO breast feed & Continued estrogen exposure.
Fibroadenosis: vary in size, shape, number, latrlty.
5 changes in fibroadenosis (cystosis, epitheliosis,
adenosis, papillosis, Fibrosis).
On table breast fat is differentiated from skin fat
by:- fat lobules size (larger in breast & less vascular)
If excessive SC fat removed: skin flap necrosis (min
of 7 mm SC fat thickness req for survival) if less
amount of breast fat removed: recurrence.
Scar is a place where recurrence occurs usually
Why patient is examined in supine?? – Breast mass
moves towards axilla & MEDIAL breast lumps are
more appreciable. Usually breast enlarges if there is
any lump (Only exception is SCIRRHOUS
ATROPHIC carcinoma)
10 recur
20
If LN are palpable Note: NUMBER, SIZE, FIXITY,
66
CONSISTENCY
Page
1)) Early carcinoma
2)) Medial breast involvement
3)) Rarely may be sarcoma
Bone metastasis:
1)) Breast (osteolytic & osteoblastic)
2)) Thyroid (osteolytic)
3)) prostrate (osteoblastic)
4)) kidney
5)) Lungs
Surgery is always aims at LOCOREGIONAL CURE
Nerve that can be scarified during surgery:
INTERCOSTOBRACHIAL NERVE.
Bone scan pick up bony metastasis earlier than CT
which in turn pick up earlier than X ray. SO x ray
shows pathological fracture/ metastasis – Advanced
stage.
Tumour size if >2cm: Then usually LN:+ve.
1st LN usually involved (central & pectoral) late
(lateral & posterior) last (apical). Puckering +ve:
Tumour extended to Ligaments only
Paeu de orange: Tumour extended to Skin
(Omnious sign of carcinoma)
Breast lump with palpable lymph nodes BUT NOT
carcinoma: BREAST ABSCESS
(Inflammatory signs +ve, LN NOT fixed, Pain
appear 1st later swelling).
 Contra lateral breast is involved through: Internal
mammary LN & by Skin lymphatics. Blood Duct Papilloma & Infiltating / NON
infiltrating duct carcinoma
FNAC must be followed by true cut biopsy.
Green Fibroadenosis, duct ectasia
Carcinomas co exist with breast carcinoma:
breast, uterus, ovary (hyper oestrogen).
Black Duct Papilloma & Infiltating / NON
infiltrating duct carcinoma &
The lymphatics from all groups of axillary LN
Fibroadenosis
ultimately drain into apical & from there efferent
vessels unite to form subclavian trunk which also Pus Acute mastistis
drains suprclavicular LN & opens into R lymph duct
creamy Duct ectasia
on R & Thoracic duct on L.
Family H/O: lobular carcinoma (which is usually co
exists with fibroadenoma).
SPECIAL PREOPERATIVE PREPARATION
Breast is freely mobile over pectoralis muscle: due to
Retromammary space. Review of the following investigations is necessary
before the operation:
Traumatic fat necrosis: haemorrhage → central
liquefactive necrosis surrounded by zone of • Histology of the breast lesion, which may have
inflammation → well defined nodule with firm been obtained by fine-needle aspiration, core
consistency → dense fibrous scar. biopsy, or excisional biopsy.
•Mammogram to evaluate whether the malignancy
Discharge is multifocal or multicentric, because these issues are
important when discussing surgical options.
• Ultrasonography or computed tomography of
Milk Pregnancy, OCP, milk fistula, the liver if metastasis is suspected.
Hyperprolactinemia, galactocoele

Serous Fibroadenosis, duct ectasia/ papilloma,

NON infiltrating duct carcinoma

Management of discharge:

Discharge

1 duct Multifocal

NOT blood stained Blood stained NOT blood stained Blood stained
67

Mammography is performed (> 35 yrs: exclude maliganancy)

Page

Microdochectomy Microdochectomy Cefotaxime/flucloxacillin Hadfield’s operation

 In pericanilicular : enucleation done in
Intracanalicular enucleation not done excision is
done.
Nipple retraction:
1)) Duct ectasia (Slit like).
2)) Carcinoma & periductal mastitis
(circumferential).
3)) Post surgical.
Fibroadenoma (usually seen in lower part of best) is
usually concurrent with Lobular carcinoma in situ
Phylloid tumour: Cut surface is Soft brown & shows
cysts, necrosis, and hemorrhage. Which show
appearance of leaves arranged side by side.
Lymphatic spread is early in scirrhous carcinoma.
Breast lump palpated best with palm of hand is
probably carcinoma coz fibroadenoma & -sis are
better palpated with fingers & thumb.
Lumpectomy / Tylectomy.
Breast cysts:
Mammary dysplasia
Retention cysts
Tumours
Benign
malignant
Misc
The sensitivity of mammography increases with age
as the breast becomes less dense.
US is particularly useful in young women with dense
breasts.
68
Microdochectomy: Tennis racket racquet to
encompass the entire duct / periareolar incision used
Page
Super radical mastectomy (extended radical +
mediastinal & supraclavicular LN removal) Extended
mastectomy (radical + internal mammary LN
removal)
1)) thickened strip of ectoderm, called the
―mammary ridge,‖ develops and extends from the
base of the forelimb to the proximal part of the
hindlimb.
2)) blood supply of the breast is derived from
(a) perforating branches of the internal thoracic
(mammary) artery to the second, third, and fourth
intercostal spaces;
(b) branches of the lateral thoracic artery, which is a
branch originating from the second part of the
axillary artery; and
(c) lateral branches of the intercostal arteries to the
second, third, and fourth intercostal arteries. The
venous drainage corresponds to that of the arteries.
Fibroadenosis
Sclerosing adenosis
Blue domed cyst of blood good
Galactocoele
Papillary cystadenoma
Cystosarcoma phylloides
Intracystic papillary carcinoma
Colloid carcinoma
Medullary carcinoma
Lymph cyst
Blood cyst
and a nipple flap is dissected to reach the duct. The
duct is then excised. A papilloma is nearly always
situated within 4 – 5 cm of nipple orifice.
Cone excision: Bleeding duct is unidentified /
multiple duts +ve peri areolar incision is made &
cone of tissues removed with its apex just deep to
 surface of nipples & its base on pectoral fascia. →
Resulting defect is obliterated by purse string
sutures.
PO: unable to feed & altered nipple sensation.
Paget’s cells are located in malphigian layer of skin.
Peau d’ orange occasionally seen over CHRONIC
ABSCESS.
Lymphangiosarcoma treated with:
Interscapulothorasic (4 quarter) amputation.
BRCA 1: ovarian, colorectal & prostrate carcinoma
Ulceration: Adv carcinoma large Soft fibroadenoma
& Rapidly growing sarcoma (in later 2 it is due to
Pressure atrophy of Skin & Probe test is Useful :
CAN be probed in later 2)
Engorged veins: Huge breast abscess. Phylloid
tumour & Rapidly growing sarcoma
Fluctuation (done from behind +ve): Lipoma, Non
tense cyst & Chronic abscess
Any tumour lying deep to nipple is fixed
(benign & Malignant)
1)) India rubber consistency : fibroadenosis
If axillary LN can’t be palpated in sitting then
performed in lying down position (basically to relax
pectoral fascia)
2)) In supraclavicular LN palpation always Flex the
neck if needed passive elevation of shoulder will
relax muscles & fascia. Breast louse / Floating
tumour
3)) Antibioma is soft in center in contrast to
carcinoma which is hard in center
4)) The deep or posterior surface of the breast rests
on the fascia of the pectoralis major, serratus
anterior, and external oblique abdominal muscles,
and the upper extent of the rectus sheath.
There is Total restriction of mobility along the line
of muscle fibres if it is fixed but slight movement
69
along right angles to fibres is possible
Page
Surgical Notes
1)) Postion: The patient is placed in the supine
position with the ipsilateral arm abducted at 90
degrees. The patient undergoes general anesthesia
and endotracheal intubation. The axilla is shaved.
The skin is prepped & The surgeon stands on the
side of the mastectomy to be performed
2)) Incision: Elliptical usually
3)) The upper limit of the dissection is at the level
of the clavicle & The inferior flap extends down to
the rectus sheath from the fifth rib medially to the
latissimus dorsi laterally. The overall limits of the
dissection include the clavicle superiorly, the lateral
sternal edge medially, the latissimus dorsi muscle
laterally, and the rectus sheath inferiorly
4)) Because the breast tissue is more adherent near
the sternum, this dissection should be started from
the lateral aspect and extended in the medial
direction
5)) Closure: The skin flaps are temporarily aligned
with the aid of staples
** Closure of the incision by 2 closed suction drains
if axillary dissection is laso performed
Gynecomasta: Clinical classification
Grade Mild breast enlargement without skin
I redundancy
Grade Moderate breast enlargement without
IIa skin redundancy
Grade Moderate breast enlargement with skin
IIb redundancy
Grade Marked breast enlargement with skin
III redundancy and ptosis, which simulates a
female breast
Disorder Risk
Nonproliferative lesions of the breast No
No
Sclerosing adenosis
No
Intraductal papilloma
2-fold
Florid hyperplasia
 4-fold angiogenesis index;
Atypical lobular hyperplasia (d) growth factors & growth factor receptors such as
4-fold human epidermal growth factor receptor 2 (HER-2)
Atypical ductal hyperplasia
7-fold Woman leans forward to accentuate any skin
Ductal involvement by cells of atypical retraction .
ductal hyperplasia
Lobular carcinoma in situ 10-
Ductal carcinoma in situ 10-
fold

Biomarkers

(a) indices of proliferation such as proliferating cell

nuclear antigen (PCNA) and Ki-67;
(b) indices of apoptosis and apoptosis modulators
such as bcl-2 and the bax:bcl-2 ratio;
(c) indices of angiogenesis such as vascular
endothelial growth factor (VEGF) and the

Mammography
1)) With screening mammography, two views of the
breast are obtained, the craniocaudal (CC) view
and the mediolateral oblique (MLO) view
2)) The MLO view images the greatest volume of
breast tissue, including the upper outer quadrant
and the axillary tail of Spence.
3)) CC view provides better visualization of the
medial aspect of the breast and permits greater
breast compression.
4)) In addition to the MLO and CC views, a
diagnostic examination may use views that better
define the nature of any abnormalities, such as the
90-degree lateral and spot compression views. The
90-degree lateral view is used along with the CC
view to triangulate the exact location of an
abnormality.
HER-2/ neu Negative HER-2/ neu Positive
(Non–Trastuzumab- (Trastuzumab-
Containing Regimens) Containing Regimens)
70
carboplatin,
trastuzumab)
A¬ CMF Chemotherapy followed
E ¬CMF by trastuzumab
sequentially
CMF
AC x 4
** A= Adriamycin (doxorubicin); C =
cyclophosphamide; E = epirubicin; F = 5-
fluorouracil; M = methotrexate; T = Taxane
(docetaxel or paclitaxel)
Combination of intraoperative gamma probe
detection of radioactive colloid and intraoperative
visualization of isosulfan blue dye (Lymphazurin) is
more accurate for identification of sentinel nodes
** (injected either in the breast parenchyma around
the primary tumor or prior biopsy site or into the
subareolar region or subdermally in proximity to

FAC/CAF the primary tumor site)

Page

TAC (T = docetaxel) TCH (docetaxel,

 1)) Neoadjuant Chemotherapy: Current
recommendations for treatment of operable
advanced local-regional breast cancer are
neoadjuvant chemotherapy with a doxorubicin-
containing or taxane-containing regimen, followed
by mastectomy or lumpectomy with axillary lymph
node dissection if necessary, followed by adjuvant
radiation therapy.

** For inoperable stage IIIA and for stage IIIB breast

cancer, neoadjuvant chemotherapy is used to
decrease the local-regional cancer burden. This may
then permit subsequent modified radical or radical
mastectomy, which is followed by adjuvant
radiation therapy.

2)) Radiotherapy: Current recommendations for

stages IIIA and IIIB breast cancer are
(a) adjuvant radiation therapy to the breast and
supraclavicular lymph nodes after neoadjuvant
chemotherapy and segmental mastectomy with or
without axillary lymph node dissection
(b) adjuvant radiation therapy to the chest wall and
supraclavicular lymph nodes after neoadjuvant
chemotherapy and mastectomy with or without
axillary lymph node dissection
(c) adjuvant radiation therapy to the chest wall and
supraclavicular lymph nodes after segmental
mastectomy or mastectomy with axillary lymph
node dissection and adjuvant chemotherapy.

** For women with stage I, IIA, or IIB breast cancer

in which negative margins are achieved by
segmental mastectomy, adjuvant radiation therapy
is given to reduce the risk of local recurrence

3)) Others: antiestrogen (tamoxifen for

premenopausal women or an aromatase inhibitor
for postmenopausal women & Pamidronate may be
given to women with osteolytic bone metastases
71
Page
 SALIVARY GLAND SWELLING
Raju/60/M/hindu/agricultural labour
C/C: Sweeling below the ear – 6months
H/C/C:
Patient was apparently asymptomatic 6m back then
he developed below the ear, Insidous in onset
slowly progressive – initially pea sized & gradually
reached Present size.
NO change in consisitency/surface of swelling
NO H/O Spontaneous regression/ sudden increase
in size of swelling
NO H/O evening rise of temperature & cough
NO H/O any discharge from swelling
NO H/O trauma
NO H/O pain and fever
NO H/O deviation of mouth while talking
NO H/O any swelling on other side / floor of
mouth/ above the eye NO H/O pain in joints
NO H/O Increase in size / pain during meals
NO H/O Difficulty in mastication
NO H/O Significant weight loss
Past H/O:
NO H/O similar complaints in past, HTN, DM, TB,
epilepsy, chest pain & bldng disorders
Treatment H/O: No H/O any surgical procedures /
Long term treatment
Personal H/O:
Diet: mixed appetite: N
B/B: regular Sleep: N
Addictions: Non smoker & Non alchoholic
Family H/O:
No H/O similar complaint in family &
No H/O any chronic illness in family
Physical examination
(A) general survey –
patient is C/C/C. & Normosthenic
P (-) I (-) C (-) C (-) K (-) L (-) E (-)
72
Vitals – a febrile, HR: 84/min
BP: 124/80 mm hg RUL: supine, RR: 12/min
Page
(B) Local examination:
(1) Inspection: A Hemispherical shaped swelling of
4 X 4 cm is seen just below the earlobe at angle of
jaw, surface over swelling is regular, margins are
well defined. Upper border is 4cm above angle of
mandible. Skin over & surrounding skin is Normal.
Ear lobule is raised.
Retroauricular grove is obliterated
No other swellings are seen (Neck / other side)
Oral cavity: Hygeine is satisfactory.
No pus at opening of parotid duct.
No swelling at floor of mouth.
No uvula deviation
(2) Palpation:
No local rise of temperature
No local tenderness A Hemispherical shaped
swelling of 4 X 4 X 3cm cm is seen just below the
earlobe at angle of jaw, surface over swelling is
regular, margins are well defined. Upper border is
4cm above angle of mandible. Skin over &
surrounding skin is Normal.
No oedema
Curtain sign +ve
Skin over swelling is Pinchable
Swelling is Mobile (In Masseter contarcted & relaxed
positions)
Bimaual palpation: Deep lobe Not enlarged
Bidigital palpation: No Stone in duct
Oral cavity:
No pus / Blood from duct on pressing the swelling
(3) Facial Nerve examination:
No loss of forehead wrinkling,
Eyes are normally closed
No bells phenomenon,
Able to hold air in mouth
No loss of taste Sensation
(4) Lymph node examination:
Cervical & parotid Ln NOT palpable
(5) Jaw movements: Normal
Diagnosis: A case of benign swelling arising from
parptid gland.probably Pleomorphic adenoma &
clinically there is No involvement of deep lobe
 INGUINAL HERNIA
Madhusudhan/55/M/warsiguda/Manual labour/
C/C:
Pain in R groin from 1 year
Swelling in R groin 15 days later the appearance of
pain
H/C/C:
Patient was apparently asymptomatic 1 years back
then he developed pain in R groin which he
neglected & swelling appeared 15 days later during
his occupational work, then he went to local
hospital where he was referred to Gandhi hospital
but he did not admit due to financial reasons, now
he came to Gandhi hospital because of same.
Pain – 1 year
R groin & Insidious in onset
dragging type, continuous & progressive
aggravated by lifting weights & straining
relieving on sleeping & temp on medication
NO shift / radiation of pain
NOT disturbing sleep.
Swelling – 15 days later in R groin
progressive, which was marble size initially &
gradually reached present size. Swelling first
appeared in the outer part of groin & gradually
extending towards scrotum but did not extend into
scrotum
Swelling increases in size by lifting weights &
straining
Do not decrease in size on sleeping but reduces in
size completely by manually.
Swelling do not reach bottom of scrotum
H/O gurgling feeling on reduction
H/O strenuous work with lifting heavy weights
H/O straining at micturition
H/O urinary hesitancy from 1 year
H/O straining at stools from 6 years
NO H/O trauma
NO H/O decrease in swelling by micturition
73
NO H/O chronic cough
NO H/O vomiting / abdominal distension
Page
NO H/O colicky abdominal pain
NO H/O fever
NO H/O any other swelling in other groin
NO H/O truss usage
Past H/O:
NO H/O similar complaints in past, HTN, DM, TB,
epilepsy, chest pain & bldng disorders
Treatment H/O: No H/O any surgical procedures /
Long term treatment
Personal H/O:
Diet: mixed appetite: N
B/B: regular Sleep: N
Addictions: Non smoker & occasional alchoholic
Family H/O:
No H/O similar complaint in family & No H/O any
chronic illness in family
Physical examination
(A) general survey –
patient is C/C/C. & Comfortably seated.
Moderately built & adequately nourished
P (-) I (-) C (-) C (-) K (-) L (-) E (-)
Vitals – a febrile, HR: 74/min
BP: 134/90 mm hg RUL: supine, RR: 14/min
(B) Local examination:
Patient is exposed from umbilicus to midthigh level
& examined in supine & standing positions
(1) Inspection: A Pyriform shaped swelling is
present in R groin. This is about 6cm (horizontal) x
4cm (vertical) in its greatest diameter. With distinct
medial border which is 3cm from midline & lower
border which is 9 cm below umbilicus. Skin over
swelling is N, NO scars/sinuses/ engorged
veins/visible peristalsis.
Expansile cough impulse +ve
Penis is deviated to L side
(2) Palpation:
No local rise of temperature & No local tenderness
 (3) Percussion: Dull (?) 3)) Cardiovascular system:
(4) Auscultation: Bowel sounds heard Heart sound 1 & 2: Heard & No murmurs heard

Diagnosis:
right sided
(C) Systemic examination: indirect
1)) Abdominal examination: incomplete
Umbilicus is midline reducible
NO Lumps palpable / Palpable organomegaly inguinal hernia
NO free fluid probably enterocole
2)) Respiratory system: with straining factor of lifting heavy weights ,
BLAE: N & chronic constipation & BPH
N vesicular sounds heard
NO adventitious sounds

Discussion

Hernia is common on R side: later descent of testis

& more chances of patency of process vaginalis.

Strangulated hernia management:

emergency operation 10)) check viability
1)) Foot end is raised (advantage of gravity for
Intestine Viable NOT viable
reduction)
Circulation Light colour & Persistent dark
2)) ice bag is applied locally (reduce congestion & mesentery colour &
chance of gangrene is delayed) bleeds if mesentery
3)) nasogastric tube, catheterization & IV fluids pricked NOT bleeds if
4)) inj. pethidine & atropine (relax muscles) pricked
5)) an attempt to reduce hernia Peritoneum Shiny Dull & lusture
6)) Anesthesia: G/A or field block by L/A 1inch less
Musculature Peristalsis +ve Peristalsis –ve
Medial to ASIS to anesthesia to ILIO HYPOGASTRIC
& pressure & pressure
& ILIO INGUINAL NERVES rings disappear rings NOT
disappear
7)) incision is extended UPTO FUNDUS & fluids
Mesentery vessel +ve -ve
aspirated (avoid risk of contaminating peritoneal pulsations
cavity & contents will not get an opportunity to slip
back before they are examined) & THEN external
oblique is Cut 11)) If bowel in non viable/ doubtful viable:
Linear patch: invaginating with lambert’s sutures
8)) Constriction ring is cut (deep ring is cut parallel whole loop: end to end anostomosis
to IEA – UPWARDS & INWARDS) & apply hot wet omentum: healthy portion above transfixed & distal
mops for 10 min part excised
Large intestine: PAUL - MIKULICKZ operation
9)) bowel must be drawn out to examine the area
(exterioration & resction )
74

proximal to ring
Page
 12)) Hernioplasty usually NOT performed because
of fear of infection however Biosynthetic meshes
made from collagen and dermis can be used coz
they are more suited for use in contaminated
environment (that too if patient condition permits)
Sites of constriction in order:
deep ring → superficial ring → any where in the sac
→ midway b/w 2 rings.
Contents in constriction in order: Small intestine →
Omentum → large intestine
Gangrene usually occurs : 5 - 6 hrs after Blood
supply obstruction (Bowel)
In Omentum gangrene (usually begins in centre) is
delayed if strangulated coz unlike intestine san
survive even with meager blood supply
Neck of sac is identified during operation by:
1)) Constriction of neck of sac
2)) Preperitoneal pad of fat
3)) Inf epigastric vessels lie medial to it.
Ilioinguinal nerve L1 [(mixed nerve) pierces the IO
muscle fibers & distributing filaments to it & then
enters inguinal canal in its midway & lies below the
spermatic cord].
If sliding hernia is present (suspected in a very large
globular hernia descending well into scrotum & neck
is unduly bulky) No attempt is made to separate it
from perotonium (confused to adhesions) it may
lead to faecal fistula / peritonitis.
Obstructed strangulated
Mild tenderness Severe
Features of inflammation Features of inflammation
(redness, warmth) absent (redness, warmth)
present
Features of septicemia Features of septicemia
(fever, oliguria) absent absent
Damage to it causes in its lateral part which is
predominantly mixed (during appendicectomy):
75
Loss of tone of conjoined tendon (Weakened post
Page
wall & loss of shutter mechanism) → direct inguinal
hernia & in its medial part as during inguinal
surgery, predominantly sensory causes anesthesia in
medial part of thigh.
Besseni’s repair: high recurrence
1)) It is not physiological
2)) It is a tension repair
3)) All groin hernias are due to weakened
Transverse fascialis which is not repaired.
Basically herniotomy will cure indirect hernia
however mesh is used as a preventive measure in
future to prevent recurrence.
Herniotomy: G/A → Skin drape → Inguinal incision
→ EO aponeurosis Incision (along the fibres &
structures beneath are carefully separated from its
deep surface before completing the incision through
superficial inguinal ring & exposure of canal →
securing IIN & incision of spermatic cord →
separating sac from cord structures → incision of sac
→ reduction of contents → twisting → transfixation
→ excision distal to transfixation.
In infants ONLY herniotomy coz: 2 rings overlap →
canal like AP tube→ NO POST wall → NO repair.
In complete /funicular indirect hernia, sac is
intimately related in whole extemnt of cord & its
complete separation from cord causes hematoma of
scrotum and injute testicular vessels hence sac is
transacted in inguinal canal & distal part is left in situ
During reduction watch for 5 points
1)) Gurgling sound (Coz of displacement of
intestinal gases through fluid contents of ileum
through narrow ring)
2)) Speed of reduction (easy in later part for
intestine coz intestines are distended & on initial
reduction → gas is escaped → intestines collapse →
reduce easily)
3)) Consistency
4)) Complete / Partial
5)) present / absent
Varicocoele: Inguinoscrotal swelling where Penis is
not deviated.
Direct hernia herniotomy NOT performed usually
 (No preformed sac, Wide sac, Contents may
sometimes: bladder).
In all cases when there Is NO Straining etiology,
then tell the cause as patent process vaginalis
Strangulation but no obstruction: Omentocoele,
Richter’s & litter’s hernias.
Cough impulse: Lymph varix (lymphangiectasis),
varicocoele [feels like thrill not expansile] ,
Undescended testis with hernia.
Disappear on lying down: Lymph varix
(lymphangiectasis), varicocoele & direct hernia.
Adherent sac is separated from cord →
hydrodisscetion (injecting saline under posterior
wall)
Usually obstructed enterocoele ends as peritonitis
where as obstructed omentum ends as Scrotal
abscess.
In Large inguinoscrotal swelling usual antiseptic
solution is NOT extended to perineal aspect of
scrotum Coz high bacterial contamination.
Obesity → accumplation of fat B/w muscle fibers →
separation of muscle bundles & layers → weakening
of muscle & aponeurosis → direct, hiatus, paraumb.
hernia.
Smoking → Acquired collagen deficiency →
weakening of connective tissues → Hernia. :-
Peritoneal dialysis → enlargement of patent ductus
vaginalis → Hernia when
Polypropele mesh is placed fibroblasts grow through
interstices & lay down collagen making it into a
sheet of dense collagen
Fallacies in deep inguinal ring:
1)) Insufficient force
2)) Double hernia
3)) Ring defect > thumb size
76
Usually diagnosed clinically but investigation is
needed then U/S – 1st choice (particularly obese with
Page
small hernia) coz it gives information about
Prostrate enlargement.
Mesh size usually taken is 16 x 8cm: in lichenstein’s
repair (Tails of mesh are overlapped & crossed
finally single suture is placed to create new internal
ring).
In repair care has to be taken not to pick up
suturing from same tendinous bundle (NO value if
taken from muscle fibres).
If desired the cremastric muscle are reconstituted:
external oblique is directly sutured / overlapped
leaveing a new external ring.
In infants surgery is usually done in child > 3 m age
(earlier if strangulation occurs which is common in
female infants [ovary] & after conservative
management with gallow’s traction fails)
In direct hernia actually the main mass will be
omentum.
DD of inguinoscrotal swellings:
Encysted hydrocoele of cord, Varicocoele, lymph
varix, Diffuse lipoma of cord, Malignant extension
of testis, [funiculitis, Inflammatory thickening of
cord & undescended Testis torsion - strangulated
hernia] retractile testis
DD of groin swellings:
Femoral hernia, saphena varix, enlarged LN, psoas
abscess, enlarged psoas bursae, Undescended &
ectopic testis, Femoral aneurysm, Lipoma,
hyfrocoele of hernia sac
 PERIPHERAL ARTERIAL DISORDER
Venkanna / 40 / M / hindu / manual labour /
adilabad
C/C:
Pain in Left foot – 35 days
Blackish discolouration of left little toe – 15 days
H/C/C:
Patient was apparently asymptomatic 2 months
back then he developed pain in left foot on walking
then he went to local hospital where some
medication is given but pain was not relieved.
Pain In left foot – 35 days, insidious in onset.
initially pain used to appear on walking & then it
used to relieve on continued walking slowly pain
continous with walking & has to stop due to pain &
used to relieve on taking rest for 5-10 min. initailly
used to walk for 400 – 500m then now 10m only,
burning type, aggravated by walking & relived on
taking rest, sleeping on bed, No radiation, disturbs
sleep.
Blackish discolouration of left little toe – 35 days,
initially only tip gradually progressed & involved
entire little toe.
H/O linear red cord like swellings associated with
pain & fever inlegs 15 days back, which subsuded on
its own In 3 days.
H/O smoking – 2 packets/day – 20 years
No H/O other form of tobacco abuse
H/O tingling & numbness sensation on left foot – 10
days
No H/O rest pain
No H/O any ulceration/discharge from toe/foot
No H/O trauma
No H/O severe cold exposure of foot
No H/O black out episodes / paralysis of 1 side of
body
No H/O abd pain/sudden vision loss
No H/O chest pain
No H/O palpitations
No H/O impotency
77
No H/O pain in hands on writing/combing
Page
NO H/O similar complaints in other lower limb
Past H/O: NO H/O similar complaints in past, HTN,
DM, TB, epilepsy, chest pain / Jaundice & bleeding
disorders
Treatment H/O: No H/O any surgical procedures /
Long term treatment
Personal H/O:
Diet: mixed, appetite: reduced
B/B: regular, Sleep: disturbed
Addictions: Chronic smoker & Non alcoholic
Family H/O: No H/O similar complaint in family &
No H/O any chronic illness
Physical examination
(A) General survey – Patient is C/C/C.
Moderatly built & adequately nourished with
P (-) I (-) C (-) C (-) K (-) L (-) E (-)
Vitals – afebrile,
HR: 76/min.N in volume, character, & rhythm No
RR/RF delay No vessel wall thickening
BP: 120/86 mm hg RUL: supine,
RR: 16/min
Gait: Limping with pain
No tendon xanthomas / xanthalesma /
No markers of IE
Facies: Wincing in pain
(B) Local examination:
(1) Inspection:
Attitude: legs hanging by the side of cot
No visible deformity / No wasting of leg muscles
On inspection dry blackish mummified discoluration
of entire Left little toe which is ending as a band of
hypereamia. 2 cm behind little little toe there is
congestion & purple – blue in colour.
No inflammation of superficial veins is seen
No ulcer / skip lesions
No pulsatile swelling in popliteal fossa
Buerger’s postural test: R: N L: 20
Capillary filling time: R: N L: 35 sec
Venous refilling time: R: No venous guttering
L: >5 sec
Skin changes: brittle nails, shiny skin present
(2) Palpation:
Skin temp: Coldness of leg upto 2cm below tibial
 tuberosity. Midline trachea with BLAE: N &
Capillary refilling: 5 sec: L N vesicular sounds heard NO adventitious sounds
Venous refilling: ? 3)) Cardiovascular system:
Fuchsig’s test: +ve on both sides Apex – Normal & Heart sound 1 & 2: Heard &
Cold & warm water test: (not done) normal
NO crepitus No murmurs heard

Peripheral pulses: (No tenderness/vessel wall Diagnosis: A case of dry gangrene of distal half of
tenderness) little toe due to peripheral arterial disorder may be
due to buerger’s disease, with intermittent
Superficial temporal +ve +ve claudication distance of 10 m
C.carotid +ve +ve & cold upto 5 cm below tibial tuberosity.
Subclavian +ve +ve
Discussion
Axillary +ve +ve
Brachial & Ulnar, radial +ve +ve Definitive diagnosis of TAO: Arterial wall biopsy
(excision biopsy)
Femoral +ve +ve
Severe Limb ischemia = Critical (rest pain +/- tissue
popliteal +ve +ve loss like ulceration, gangrene for >2W & ABP
Ant & post tibial +ve -ve <50mm Hg) & Sub critical limb (rest pain only &
D.pedis artery -ve -ve ABP >50mm Hg)

Ischemia Pain is usually at night coz beneficial effects

of gravity on perfusion are lost Patients BP & hence
Movements: 4rth & little toe are limited & ankle perfusion pressure reduces in sleep
movements are normal In diabetes = spuriously high ABPI coz of arterial
Measurements: L: 25cm R: 30 cm calcification.
Neurological examination:
Sensory: all sensations are absent in little toe. ABPI
Remaining foot upto 4cm infront of ankle - >/= 1 Healthy
hyperaesthetic 0.5 – 0.9 IC
sensations in leg – Normal <0.5 CLI
Motor: 0.5 – 0.3 Rest pain
Tone: R: N L: N
<0.3 Gangrene
Power: R: dorsiflexors & plantar flexors: N on both
sides
Reflexes: N on both sides
Regional lymphnodes – Not palpable Left ABI = Higher Of Left ankle Systolic BP (DPA /
PTA) / Higher of Left / Right UL Systolic BP
(C) Systemic examination:

1)) Abdominal examination:

** Limitations of relying on segmental limb
Umbilicus is midline
pressures include:
NO Lumps palpable / Palpable hepatomegaly
78

(a) missing isolated moderate stenoses (usually iliac)

NO free fluid
that produce little or no pressure gradient at rest;
Page

2)) Respiratory system:

(b) falsely elevated pressures in patients with
 diabetes and end-stage renal disease; and
(c) the inability to differentiate between stenosis and
occlusion
Buerger’s
Buerger’s aetiology (Smoking, hormonal, familial,
Autoimmune & rickettsial)
Beurger’s position (head end of bed is raised & at
the same time foot end is gradually lowered about
6inches / day - improve circulation of lowerlimb )
Beurger’s exercise (affected lower limb is elevated
for 2 min & then lowered below the bed side for
another 2min, this is repeated several times in 1
sitting. In a day atleast 3 sittings should be
performed - improve circulation of lowerlimb )
tuberosity anteriorly and the fingers are placed into
the popliteal fossa between the two heads of the
gastrocnemius muscle. The popliteal artery is
palpated by compressing it against the posterior
aspect of the tibia just below the knee.
The posterior tibial pulse is detected by palpation 2
cm posterior to the medial malleolus.
The dorsalis pedis is detected 1 cm lateral to the
hallucis longus extensor tendon, which dorsiflexes
the great toe and is clearly visible on the dorsum of
the foot.
** The foot also should be carefully examined for
pallor on elevation and rubor on dependency, Note
should also be made of nail changes and loss of hair
these findings are indicative of chronic ischemia
Traditional Scale Basic Scale

Beurger’s pathology 4+ Normal 2+ Normal

(Acute lesion – Acute arteritis & phlenitis &
periarteritis & periphlebitis with thrombosis of vessel 3+ Slightly reduced 1+ Diminished
containing microabscess
2+ Markedly reduced 0 Absent
Chronic lesion – Artery, vein & nerve sometimes
bound together by fibrous adhesions & elstic lamina 1+ Barely palpable — —
of artery are thickened)
0 Absent — —
Beurger’s sign (Absence of Post tibial pulse is highly
suggestive of diagnosis)

Abdominal swelling / Lump

Examination of
Joints - Charcot joints of diabetes Ramulu/60/M/Nizamabad/Agricultural
Power - Weakness of flexors & extensors of foot labour/Hindu
may cause Abnormal foot architecture
Reflexes - Hyporeflexia in Ischemic neuritis & In C/C:-
neuropathy of diabetes Lump & Pain in abdomen – 2m

H/C/C:-
Femoral pulse usually is palpable midway between
Patient was apparently asymptomatic 2 months
the anterior superior iliac spine and the pubic
tubercle. back then he developed swelling in upperpart of
abdomen in midline
Popliteal artery is palpated in the popliteal fossa
Sudden in onset
with the knee flexed to 45° and the foot supported
Initially lemon size gradually progressed to reach
79

on the examination table to relax the calf muscles.

Palpation of the popliteal artery is a bimanual present size
Page

technique. Both thumbs are placed on the tibial

 Pain from 2months, Insidous in onset, Progressive,
Continous, Dull aching type, No relation with food
No relieving / aggravating factors, No Shift /
radiation of Pain
No H/O Trauma
No H/O fever with Chills / rigor / evening rise with
cough
No H/O Bloating
No H/O Vomiting / hemetemesis / Indigestion
No H/O excessive beching
No H/O Loss of apetite
No H/O yellowish discolouration of eyes
No H/O Passage of Tarry / Pale / Mucus Containg /
Blood containing Stools
No H/O Oliguria / hemeturia No H/O Change in
bowel habits No H/O Significant loss of weight
No H/O Swellings in neck
No H/O Alchoholism
Past H/O: NO H/O similar complaints in past, HTN,
DM, TB, epilepsy, chest pain / Jaundice & bleeding
disorders
Treatment H/O: No H/O any surgical procedures /
Long term medical treatment
Personal H/O:
Diet: mixed, appetite: reduced
B/B: reducved/regular, Sleep: disturbed
Addictions: Non smoker / alcoholic, No pan/gutka
Family H/O: No H/O similar complaint in family &
No H/O any chronic illness
Physical examination
(A) General survey – Patient is C/C/C.
Lean & adequately nourished with N facies &
P (-) I (-) C (-) C (-) K (-) L (-) E (-)
Attitude: N & Decubitus : N & Supine
Vitals – afebrile,
HR: 82/min.N in volume, character, & rhythm No
RR/RF delay No vessel wall thickening
BP: 116/82 mm hg RUL: supine,
RR: 14/min
Patient is exposed from nipple to midthigh & was
80
examined in supine, lateral, sitting, Knee elbow
postions, by looking from side, tangential & End of
Page
bed views where appropriate
(B) Local examination (Abdominal)–
1)) Oral cavity:-
Tongue, pharynx, faecal pillars, Teeth , tonsils :
Normal
2)) Abdomen:
a)) Inspection:
Contour - Abdomen is Asymmetrically distended,
Umbilicus N (midline & inverted)
& all quadrants move equally with respiration ,
epigastric pulsations +ve (probably aortic)
No visible peristalsis,
No engorged veins
Skin over abdomen Normal expect that brand
marks are seen periumbilically
A sweeling is seen in epigastrium region, extending
into uimbilical, R hypochondrial & Lumbar regions
Irregular in shape,
with indistinct margins
surface of swelling is N.
Exhibit pulsations & doesn’t move with respiration,
with free hernial orifices,
Right iliac fossa: Normal
Spine, paraspinal area: N
Supraclavicular area: No fullness
Renal angle: No fullness
Ext genitalia: Normal
b)) Palpation:
No Local rise of temperature
An IA mass +ve On deep palpation
tenderness +ve (Mild)over sweling with epigastrium
as point of max tenderness
Size & shape : collaborative
Surface: Smooth Margins Well defined (lower: 10cm
above pubic symphysis & lateral margin 6cm to right
of umbilicus)
Uniformly firm consistency
Skin over swelling is N - Not pits on pressure
Not freely mobile
NO rebound tenderness/Abdominal wall rigidity
NO hyperesthesia over swelling
NO fluid thrill
Plane of selling – Intraabdominal (Carnett/s test)
Exhibiting Transmitted Pulsations & do not fall in
 knee elbow position
Liver & Spleen: Not palpable (fingers can be
insuniated below coastal margins)
Renal angle : No fullness / tenderness
No palpable LN in SC area
Hernial orifices: No expansile impulse / free
Genitals N
Supraclavicular fossa: N
Spine & paraspinal Area: N
c)) Percussion:
Swelling in dull on percussion
Not continuous with the liver dullness
Shifting dullness -ve
Liver upper border: 5 th ICS in MCL
(liver span: 14cm)
Traube’s space:- Tympanitic
No IC tenderness / punch tenderness
d)) Auscultation:
Bowel sounds heard & Normal pitch & No venous
Hums heard / Bruie heard
PR: Not done
1)) Respiratory system:
Midline trachea with BLAE: N &
N vesicular sounds heard NO adventitious sounds
2)) Cardiovascular system:
Apex – Normal & Heart sound 1 & 2: Heard &
normal
No murmurs heard
6cm
10 cm
81
Diagnosis:- A 60 Yr old male presented with a
Retroperitoneal swelling probably
a)) Pseudocyst of pancreas
b)) Para aortic LN enlargement
Discussion:
Abdominal pain crisis
• Little’s Crisis
• Ruptured aneurismal pain
• HyperParathyroidism
• Tabes dorsalis spine crisis
• Hepatic neuralgia
• Sickel cell anemia
IDK
Shanker /21 /M /Hindu/ Student /hyderabad
C/C:
Pain in right knee during running & Climbing up
stairs & downstairs – 1 week
H/C/C:
Patient was apparently assymptomatic 1 week back
then one day while he was running there is twisting
of leg after which he developed pain in R knee on
outer aspect.
Pain – continous, aching type, aggravted on running
& Climbing up stairs & downstairs & also on
standing on outer aspect of foot, relived on rest &
medication partially. No radiation of pain & Not
disturbing sleep.
No H/O swelling of knee
No H/O giving away while walking
No H/O locking/unlocking of knee
No H/O Any Click sound from knee during activity
No H/O massage
No H/O fever
Past H/O:
No H/o similar complaint in past. No H/O

suggestive of HTN/DM/TB/Bleeding disorders

Page
 Local examination
(A)Inspection: (Examined in standing from front &
behind (Popliteal fossa) then seated position then
Supine lastly Prone (Popliteal fossa))
Attitude of limb: Normal (Both the ASIS are at
same level, Both patella are facing Upwards &
slightly outwards & toes facing roof)
{In arthritis is assume moderate flexion – Maximum
volm – to Accommodate fluid Late stages TRIPLE
DISPLACEMENT – destruction of CRUCIATE &
COLLATERAL LIGM}
Gait: Normal
NO knee swelling/ swellings around knee –
Parapatellar fossa & Suprapatellar pouch are free
(Usually knee effusion: horseshoe shaped swelling
due to accumulation above patella & sides of patella
& Ligm patellae, Bil effusion – Clutton’s joints &
haemophilia)
{ Swelling around knee: Semimembranous (ABOVE
joint line) / Prepatellar/ Infrapatellar / Suprapatellar
/ bicipital bursa swellings / Morrant bakers cyst
(Herniation through Oblique popliteal ligm below
joint line) Cysts of SL cartilage (lateral side cmn –
lateral to Ligm patellae) popliteal aneurysm -
midline }
NO thigh / calf muscle wasting (usually obvious in
Thigh)
Skin over knee is normal No scars/sinuses
(B)Palpation:
NO local rise of temperature
NO joint line tenderness.
There is tenderness of lateral side between femur &
Fibula head.
There is no tenderness at other Points.
No Joint effusion
No synovial membrane thickening (boggy feel)
{Tenderness Points –
1)) Medialy at femoral attachment – MCL.
2)) In joint line – MSLC & rarely MCL deep fibers.
3)) Midway between Ligm patellae & TCL – Torn
82
ANT. horn of MALC.
Page
(After Knee flexed at 900 if Not Extending from that
position with continued pressure on that point)
4)) Post to TCL - Torn POST. horn of MALC
5)) Either said of LgPtl – Nipped of
INFRAPATELLAR PAD OF FAT}
-Patella: No tenderness / Crepitus (OA &
Chondromalacia patellae)/ irregularity & there are
NO gaps in its Borders & Its articular surfaces are
Normal with No tenderness
Push palpate
Under (for articular surfaces)
(For Demonstrating effusion of knee Joint:
Moderate effusion: Patellar tap in supine &
Fluctuation tests (Thickened synovium +ve On
either sides & above patella)
Smaller amounts: Hollow refilling sign & Patellar tap
in standing position
(Thickened synovium –ve) If bursa is palpable –
Consistency, relation with tendon, mobility &
translucency are determined, Compressable
swellings – Baker’s cyst & Popliteal aneurysm )
-Popliteal fossa Normal (in flexed position – Prone:
VAN, tendons & areolar tissue)
-Lower end of femur – Normal. No Tenderness /
irregularity
-Upper ends of tibia & head of fibula – Normal.
Tibial tubercle , condyles & fibular head has no
tenderness / irregularity (Springing test –ve)
Mcmurray test: M/L SLC (Pain + CLICK in joint
line imp)
Lurchmann test: ACL
Anterior drawer test: ACL
posterior drawer test: PCL
Appley’s grinding test: M/L SLC
Appley’s distraction test: M/L CL
Abduction & adduction stress tests: (performed knee
flex at 200 – 300) M/L CL
 (C)Measurements:
Thigh circumference: ?
Calf circumference: ?
(D) Movements:
Active: Flexion & extension: N range on R & L
Passive: Flexion & extension, rotation (hip & knee
flexed at 900 ), Abduction & adduction (Knee flexed
partially) – N range on Both sides
Abnormal: Absent (Clutton joints)
ANTEROIR DISLOCATION OF
SHOULDER
Yadayya / 40 / M / Hindu / Farmer/ Adilabad
C/C:
Inability to move his left Shoulder from 10 days
Pain in outer aspect of shoulder from 10 days
H/P/I:
Patient was apparently asymptomatic 10 days back
then on 1 day he was travelling in bullock cart & fell
down from it with his left arm outstretched from
which he developed Inability to move his left
Shoulder & Pain in outer aspect of shoulder.
Pain is outer aspect of Shoulder, Continuous, aching
, not disturbing sleep, No radiation aggravated on
attempted Shoulder movement relived partially on
medication, No sleep disturbance
H/O loss of shoulder function
H/O massaging at local bone setter
No H/O fever
No H/O swelling of shoulder
No H/O repeated similar episodes in past
No H/O suggestive of TB
Local examination
(A) Inspection:
Attitude: Supporting his L flexed elbow with R hand
No swelling at shoulder,
No muscle wasting
No scars / sinuses
No Swelling at Clavicle At junction of L1/3 & M2/3
83
No shoulder drooping ( fracture of neck of scapula)
Page
No undue prominence of Acromial/sternal end of
clavicle. (respective displacements)
Flattening of shoulder (Inward displacement of
Humoral head, fracture of neck of scapula, deltoid
wasting due to Tb/Rmt/Osteo arthritis & Chronic
rotator cuff lesions) &
fullness is seen in Deltopectoral groove & there is
lowering of Ant axillary fold,
No irregularity / swelling seen of bony arch (formed
by Clavicle Ant, Acromian process lat & spine of
scapula post.)
(B) Palpation: (from behind the patient & keeping
arm by the side with 1 hand & palpating with other
hand from all aspects)
No local rise of temperature & No Local tenderness
No fullness in Axilla
(inf aspect of joint is lax so fluid accumulation
begins here)
-SC joints (if +ve ANT displ), clavicle & AC joints
(if +ve UP displ.) are Normal.
-Palpation just below acromian process (G
tuberosity) - Loss of resistance (If pain – supra
spinatus tendinitis / GTb fracture) Palpation of Neck
& shaft of humerus is normal, No discontinuity /
Swelling / Local bony tenderness (direction normally
Medial epicondyle – Head & lateral epicondyle – G
tuberosity )
-Transmitted movements to upper part is +ve (No
fracture dislocation)
-Spinous process, vertebral border, axillary border &
inferior angle of scapula – Normal
-Relative position of 3 bony points is altered on L
side
-Drop arm sign: -ve
-Apprehension test
[Three Bony points are important in palpation tip of
coracoids (below is the Ant aspect of shoulder), tip
of Acromian (below is the superior aspect of
shoulder ) & Greater Tuberosity In Codman’s
method of palpation (R hand for left shoulder & left
hand grasp L flexed elbow) Thumb lies below spine
of scapula, tip of index finger just ant to acromian,
other 3 fingers on clavicle ]
 (C) Measurements
Arm length (Angle of acromian {spine of scapula
bends to form acromian} & lateral epicondyle): R:
32 cm L: 26cm (Increased in SUBGLENOID
dislocation & fracture of NECK OF SCAPULA
decreased in SUNCORACOID dislocation & fracture
of NECK &/or SHAFT OF HUMERUS)
Mid arm circumference: R: 15.4cm L: 15cm
Vertical circumference of axilla: ??? (Increased in any
shoulder dislocation & fracture of Neck of scapula /
humerus)
Test to know lowering of A/P axillary folds –
Bryant’s test
Hamilton’s Ruler test: +ve (Any shoulder
dislocation)
(D) Movements: (Exposed upto waist & compared
on both sides, examined from front & Back Scapula
is incline 30 degrees forwards with coronal plane,
Important movements are ER & ABDUCTION {At
shoulder joint – 1000 - 1200 & additional 600 - 800
by forward rotation of scapula but these occur
simultaneously after initial 30 0 where Movement
occur only at Shoulder then every 15 0 movement
there is GH 100 & Scapular movement 5 0. During
start of abduction see for any Shrugging at shoulder
{complete rupture of Supraspinatus whose function
is to start abduction so he bends affected side 30 0 so
that deltoid can take over})
Active: R: Full range (Abduction – 180, Flexion –
90, Extension – 45, rotations, M/L – quarter circle,
circumduction) L: limitation
Passive
Dugas test: Not able to touch his R shoulder with
left hand
(E) Distal NV status – Normal
(F) Elbow & Wrist : Normal ( Which are also
usually effected in this type of injury)
(G) Axillary Lymph nodes – NOT palpable
Diagnosis: Traumatic Anterior Subcoracoid
Dislocation of left shoulder with No Associated
84
fractures of humerus / Scapula with N Distal NV
status
Page
HIP
Rajayya / 50 / M / Hindu / Farmer/ Nizamabad
C/C:
Difficulty in walking – 3months
Pain in left hip – 2months
H/C/C:
Patient was apparently asymptomatic 3months then
he developed difficulty in walking & difficulty is
more when he is climbing steps with
NO H/O morning stiffness
Pain in Hip – 2months insidious in onset , initially
more during night now continuous, Aggravated on
walking & relieved by taking rest & Progressive,
Disturbing sleep, No radiation
H/O fever with evening rise of temperature - 3m
NO H/O trauma
NO H/O any swellings in hip region
Local examination
(A) Inspection: (in standing position from front &
behind)
-Attitude of limb:
Left lower limb is Extended, Externally rotated
Scoliosis of lumbar spine with convexity towards
Left side & ASIS is lower on left side
-Swellings / scars / sinuses: absent (femoral triangle /
gluteal region)
-Length: Apparent lengthening
-NO muscular atrophy seen
(loss of gluteal folds & Adductors)
-Trendelenberg’s test (Normally if entire weight is
bearing by Left leg with right leg flexed then
Adductors on left side contracts & thus Lifting the
pelvis i.e prevent tilting & R side pelvis is Raised –
Evident by buttock on R sided raises)
SO 1st patient is made to stand on normal side then
on abnormal side (SO NORMAL SIDE SINKS –
Gluteal folds & Iliac crest shoes this)
{+ve test – Failure of OSSEO – MUSCULAR
mechanism
•Weak abductors
 •C/P dislocation of hip
•Fracture neck of femur
•Coxa vara
•Perthe’s disease
•Hip arthritis}
+ve in this case
-Any fixed deformaties
(examined with patient lying in bed)
1)) Fixed Adduction / abduction deformity: The leg
is held just above ankle & are abducted & adducted
respectively until the ASIS become Normal & Thus
Angle of deformity is calculated
2)) Fixed Flexion deformity: Compensated by
lordosis of lumbar spine – HUGH OWEN THOMAS
test – Sound thigh is flexed until the Compensation
disappears (Not be forcibly continued) & Then
angle between THIGH & BED is the Angle of flexion
deformity
3)) Fixed M/L rotation deformity: It is always
Revealed L spine cannot compensate this –
Determined by Noting direction of Ant surface of
patella / Tip of great toe with midline
(normally slightly externally rotated – if midline it is
medially rotated)
{Tb hip arthritis: I – Apparent lengthening
( Flxn – concealed by – Lumbar lordosis & tilting
pelvis forwards Abd – Tilting the pelvis downwards
& Scoliosis of lumbar spine with convexity towards
affected side II – Apparent Shortening
Flxn – concealed by – Lumbar lordosis & tilting
pelvis forwards Add – Tilting the pelvis Upwards &
Scoliosis of lumbar spine with convexity towards
Sound side III – Erosion – Real Shortening –
similar to Stage 2 but they are exaggerated – Spasm
of adductors causing erosion of upper part of
acetabulum & thus femoral head get dislocated}
(B)Palpation:
-No local rise of temperature
-Tenderness: below the mid inguinal point
(Any arthritis) & also on pressing greater Trochanter
85
towards each other on L side
Page
–Bony points
1)) Greater Trochanter – NO tenderness {A triangle
is formed by GT , ASIS & Line drawn vertically
downwards from ASIS – BRYANT’S triangle
B
A
A – Shortest side - reduced on Superior migration of
Head of femur: Femur fracture, Post Dislctn of Hip,
separation of upper femoral epiphysis
B – reduced In Ant dislocation & Increases in post
dislocation
If ER +ve but Normal relation is maintained:-
Subtrochantric Fracture – Absence of Normal
Transmitted movement
2)) Head of femur:
(C)Measurements
•Bryant’s triangle:
•Nelton’s line: Most prominent part of ischial
tuberosity to tip of ASIS - Normally this touches the
tip of GT – any upward displacement can thus be
easily demonstratable
•Shoemaker’s Line: Normally line from GT to ASIS
will reach umbilicus – any upward displacement
can thus be easily demonstratable
•Morris bitrochantric Test:
•Chiene’s test: 2 lines are drawn passing ASIS & GT
- normally 2 lines parallel but in Trochanter is raised
it causes convergence on affected side
•Length of lower limb (SOUND LIMB MUST BE
PLACED IN SAME POSITION AS AFFECTED TO
SAME EXTENT – INTERSPINAL LINE MUST BE
HORIZONTAL LEVEL) From ASIS to medial
maleolus (thigh only from ASIS to joint line of knee
on medial side / Adductor tubercle / Upper border
of patella) ONLY OBTURATOR TYPE OF ANT
 DISLC: LENTGHENING
•Limb girth : To identify muscle wasting Not seen
on inspection & a point is made on affected Limb at
a convenient distance from ASIS & this is made on
N side also & Circumferences at that level are
compared
(D)Movements : (Both active & passive) – Pelvis
has to be steadied by clinician
•Flexion: Knee extended (90) knee flexed (120)
•Extension: 15 (tested if there is no flexion
deformity)
•Adduction: 30
•Abduction: 40
•Rotation: ER: 45 & IR 30
(E) Stability tests:
•Telescopic test: (+ve in C/P dislocation & in
Charcots joint) - Hip is flexed at 90 & pelvis is fixed
with 1 hand with other hand knee is grasped &
pushes thigh downwards ALONG THE AXIS OF
THIGH (other hand notes whether GT moves
downwards)
•Ortalani’s test
• Barlow’s test
(F) LN: Not palpable
(G) Distal NV status: Normal

(H) Other Joints: Knee joint, Lumbosacral spine,

sacroiliac joints are Normal
(I) PR: Intrapelvic abscess & Detect Central
dislocation of hip – NOT done
86
Page
 1)) Nutritional value of foods

2)) Milesrones & SE classification

3)) Nephrotic syndrome

4)) Cerebellar ataxia

5 5)) Hydrocephalus

6)) Anemia & Splenomegaly

PEDIATRICS 7)) Fever

8)) Seizures

9)) Traumatic neuritis

10)) Meningitis

11)) DMD

12)) Infantile hemiplegia

** These cases are not exclusive.
any case can be in XM
87
Page
 Food Item Quantity Calories Mile Stones:

Tea One cup 52

Coffee One cup 90 Gross Motor

milk (cow) One cup 67
Supine & pull to sit 6w – 20w
milk (buffalo) One cup 117 Ventral suspension 6w – Head horizontal
12w – above horizontal
Bread One slice 39 plane
Prone position 1m – lifts the chin up
Biscuits (Glucose) One 25 2m – face is lifted 45
3m - face is lifted 90
Egg One 85 6m – head + Chest lift
8m – Crawls**
Samosa one 207 12m - Creeps
Sitting 6m -tripod
Upma 1-1/4 bowl 260
8m – Steady sitting**
10m – Pivot on sitting
Idli Two 130
Standing & walking 9m – Stand (Support)
Sambar 1 bowl 81 12m – Stand (Indpn)**
15m – Walks
Khichadi 1 plate 182 18m – Runs
2y – walk back
Masala Dosa One 192 3y – tricycle
4y – Hop
Paratha Two 297 5y - Skip

Phulka One 85 Fine Motor

Puri 3 240
Hand Eye 3m- hand regard
Rice 1 bowl 111 Coordination 4m – hands (midline)
6m - Ulnar
Dal 1 bowl 100 9m - Radial
12m – Mature & Pincer
Potato Curry 3/4 bowl 131 Hand Mouth 6m – ability to chew
Coordination 12m – tries to feed
Brinjal Potato 1 bowl 134 18m – feed himself well**
Advanced Hand 15m – Scribbles, 2 Blcks
Curd 1 bowl 70 skills 18m – Strokes, 3 Blcks
2y – Circular Stroke, 6
Banana One 116 3y – Copies circle, 9
4y – Copies Cross, Bridge
Mango One 160 5y – Copies triangle
Dressing 1y - Start to pull off
2y – Undress complt
88

3y – Dress & Undress complt

5y – Shoelaces Complt
Page
 Personal & Social Development

Intent regard 1m
Social smile 2m
Recognizes mother** 3m
Stranger anxiety & Vocalizes & Smile at 6m
image
Bye - Bye 9m
Understand simple Q 12m
Point objects (Jargon) 15m
Domestic mimicry 18m
L / R Discrimination, Plays, Toilet alone** 4y
3 steps , 4 colours 5y

Language

Vocalizes with vowels 2m

Laugh loud 4m
Mono syllables 6m
Bi syllables, Imitate sounds 9m
2 words 12m
15 words 18m
100 words, 2 Sentences 2y
Ask questions, Know name & gender** 3y
Says Song / Poem 4y
Ask word meaning** 5y
Score Income (Rs /-)
12 30375
Hearing 10 15188 - 30374
6 11362 - 15187
Turns his head towards Source 4m 4 7594 - 11361
Direct localization 10m 3 4556 - 7593
2 1521 – 4555
Vision 1 1520

Fixate his mother 1m

Grasping with eye 4m
Binocular vision 6w – 4m
Adjust his position to follow obj 6m
Follow rapidly moving obj 1y
89

** To be Asked in History taking – Ideally

Page
 Nephrotic syndrome
Sreenivas / 5 / Hindu/ karimnagar brought by his
mother a reliable informant with a
C/C: of
Swelling of entire body from 15 days
Decreased urine output & frequency From 15 days
H/P/I:
Patient was apparently asymptomatic 15 days back
then he developed swelling of eyes which later
involved entire face within 2 days he developed
swelling of his abdomen, after 1 day he developed
swelling of legs (descending odema) & swelling of
face is more in the morning.
H/O reduced urine output & frequency - 15 days
No H/O passage of red coloured urine
No H/O jaundice, hemetemesis / melena
No H/O SOB before onset of symptoms
No H/O Chronic diarrhoea
No H/O fever with rash / cough with evening rise
of temperature
No H/O Sorethroat / pyoderma before onset of
symptoms
No H/O abdominal pain, Bloody diarrhea, and
vomiting before onset of Symptoms
No H/O Skin rash with joint pains
No H/O Blood transfusion
No H/O fever with chills
No H/O swellings in neck & weight loss
No H/O Abdominal / Flank pain / Abd mass
No H/O Any bleeding manifestations
Past H/O: NO H/O similar complaints in past, No
H/O HTN, DM, TB, bleeding disorders
Treatment H/O:
H/O 1 ascitic tap 2 days back, & patient is on
prednisolone tab. 10 mg
Rantac & paracetmol
patient is on No other treatment
Family history:
90
No H/O of similar complaint in family
Page
No H/O dialysis, or renal transplantation in any
family members
No H/O DM/HTN/Tb/HIV in family
Birth H/O:
Mother is registered case in local hospital & Had
regular ANC & IFA prophylaxis.
Received 2 doses of TT, Pregnancy is uneventful &
had FTNVD at home by local dai.
Baby cried immediately & breast fed for 4m
Immunization H/O:
Immunized as per schedule, OPV & SIP is also taken.
No post immunization hosptalization
Developmental H/O: Gross motor & fine motor
milestones achieved normally
Dietary H/O:
Breast fed 2 yrs (exclusively – 5m)
2 idli & ½ cup milk:
Rice – (4cups):
Dal – (2 cups):
1 banana:
Socioeconomic H/O:
father – Uneducated, barber
PCI – 1000
Socio economic class (K) – V (Lower)
General examination:
Physical examination
(A) General survey –
Patient is C/C/C.
P (-) I (-) C (-) C (-) K (-) L (-)
E (Both legs upto thigh pitting type)
No scrotal edema
Facies: N (Not steroid facies)
Vitals – afebrile,
HR: 83/min.N in volume, regular, character, &
rhythm No RR/RF delay No vessel wall thickening
BP: 100/70 mm hg RUL: supine
RR: 28/min regular, Abdominothoracic
Anthropometry:
Ht:
Wt: 18kg
midarm circumference – 12cm
 C/C: of
Inability to walk properly – 15 days
Discussion: Unsteadiness in reaching out for objects – 15 days
1)) Spontaneous renal vein thrombosis has been H/P/I:
associated with membranous Patient was apparently asymptomatic 15 days back
glomerulonephropathy. then she developed Inability to walk properly &
Nephrotic syndrome may either cause or result from Unsteadiness in reaching out for objects along with
renal vein thrombosis - Renal vein thrombosis in difficulty in sitting
newborns is generally characterized by the sudden H/O fever – 1month back, low grade subsided on
development of an abdominal mass medication not associated with chills/rigor
2)) Hemolytic-uremic syndrome is the most No H/O Cough, abdominal pain, Vomiting or an
common glomerular vascular cause of acute renal exanthem Before onset of symptoms
failure in childhood. Bloody diarrhea is the usual No H/O of Slurring of Speech
presenting complaint, followed by hemolysis and No H/O similar episodes in past
renal failure. No H/O loss of consciousness
Neurologic problems, particularly seizures. use of NO H/O head trauma
antimotility agents and antibiotics is believed to NO H/O headache, projectile vomiting
worsen the disease. NO H/O seizures
Timely dialysis improves the prognosis. NO H/O memory loss / behavioural changes
Some cases, plasma infusion or plasmapheresis NO H/O symptoms suggestive of cranial nerves
involvement
Cause H/O No H/O weakness of UL & LL
Streptococcal grp A H/O Sorethroat / NO H/O Involuntary movements
pyoderma before onset No H/O of Difficulty in feeling ground
of symptoms No H/O of Any bowel / bladder symptoms
Varicella infection H/O fever with rash
No H/O of Slurring of Speech
Hepatitis B Infection H/O Blood transfusion
HIV Infection Family H/O HIV No H/O child in constant motion while awake. &
Malaria H/O fever with chills irregular eye movements
SLE / RA H/O Skin rash with joint No H/O Any discharge from ear / Ear ringing
pains No H/O Any drug intake before onset of symptoms
Sickle cell disease H/O Blood transfusion No H/O of Contact with Tb patient
Lymphoma, leukemia No H/O swellings in No H/O of similar complaint in siblings/family
neck & weight loss No H/O of increasing head circumference
Wilms &
No H/O of Diarrhea / passage of floating foul
PheoChromocytoma
smelling stools
DB
HS purpura No H/O jaundice / abd pain
No H/O Significant weight loss / night blindness

Past H/O: NO H/O similar complaints in past, No

Ataxia H/O HTN, DM, TB, bleeding disorders

Pavithra / 9 yrs / F / Student of 5 th class / Hindu / Treatment H/O:

91

Sainikpuri, hyderbad brought by his mother a Family H/O: No H/O of similar complaint in family
reliable informant with a
Page

No H/O DM/HTN/Tb/HIV in family

 Birth H/O: Wt: 18kg
Mother is registered case in local hospital & had midarm circumference – 12cm
regular ANC & IFA prophylaxis.
Received 2 doses of TT, Pregnancy is uneventful & Local examination (CNS):
had FTNVD in hosp. 1)) Higher functions
No admission of baby in NICU Handedness: R
Baby cried immediately & breast fed for 8m. Level of consciousness: Fully consiousness
Immunization H/O: Orientation: +ve
Immunized as per schedule, OPV & SIP is also taken. Emotional state: Normal
No post immunization hosptalization . BCG mark Memory: preserved
seen Speech: Articulation disturbed

Developmental H/O: Gross motor & fine motor 2)) Cranial nerve Examination:
milestones achieved normally I Normal Normal
II Normal Normal
Dietary H/O:
Visual acuity
Breast fed 2 yrs (exclusively – 5m) Visual fields
2 idli & ½ cup milk: Colour vision
Rice – (4cups): III,IV.VI Normal Normal
Dal – (2 cups): Nystagmus +ve +ve
1 banana: V Normal Normal
Sensory
Socioeconomic H/O: Motor
father – educated - Graduate, Govt emply VII Normal normal
PCI – 3000 VIII
Socio economic class (K) – II Vestibular Normal Normal
Auditory
General examination: IX & X Normal normal
XI Normal Normal
Physical examination XII Normal normal
(A) General survey –
Patient is C/C/C.
3)) Motor System:
P (-) I (-) C (-) C (-) K (-) L (-)
A)) Inspection
No Bulbar/dermal telengectasia
No Gross Muscle wasting / Hypertrophy seen
No NC markers
No involuntary Movements
No Xanthomas / Xanthalesma
B)) Palpation
No Chicken pox scars (Pock marks)
Facies: N Bulk
UL 16cms 16cms
Vitals – afebrile, LL 24cms 24cms
HR: 86/min.N in volume, regular, character, & Tone
rhythm No RR/RF delay No vessel wall thickening UL Normal Normal
BP: 110/80 mm hg RUL: supine LL Normal Normal
RR: 18/min regular, Thoracoabdominal Power
UL 4/5 4/5
92

(B)Anthropometry:
LL
Ht:
Involuntary
Page
 UL Absent Absent NO adventitious sounds
LL 3)) Cardiovascular system:
Co ordination Knee heel & finger nose test –ve Heart sound 1 & 2: Heard & No murmurs heard
UL dysmetria +ve
LL dysdiadokokinesia +ve Diagnosis: A case of acquired ataxia of
cerebellar origin with infective etiology (Acute
cerebellar ataxia)

4)) Reflexes:

Superficial Discussion
reflexes
Abdominal present Present Cause / etiology H/O
Plantar Malignancy (SOL) H/O weight loss ,
Deep tendon headache
reflexes Benign paroxysmal No H/O similar episodes
Jaw jerk ? ? vertigo of children / in past
Upper limb B,T,BR: + B,T,BR: + basilar artery migraine
Lower Limb K,A: + K,A: + Acute cerebellar ataxia No H/O fever, Cough,
Visceral reflexes ? ? (varicella, mumps, abdominal pain,
Released Absent Absent rubella, echovirus Vomiting or an
reflexes poliomyelitis, influenza. exanthem Before onset
Bacterial: scarlet fever ) of symptoms
Drug induced No H/O Any drug
5)) Sensory system: (phenytoin) intake before onset of
symptoms
Proprioceptive Present & N Present & N
Wilsons disease H/O jaundice / abd pain
Exteroceptive Present & N Present & N
Refsum’s disease H/O Night blindness ,
Cortical Present & N Present & N deafness
Chilhood degenerative H/O Memory loss
diseases
GAIT: tandem walking ABSENT
Extrapyramidal Cause H/O Invol movements
CEREBELLAR: +ve H/O similar complaint in
ANS: No abnormal sweating, constipation Spinocerebellar family
RAISED ICT SIGNS: Absent degerative diseases H/O Difficulty in feeling
MENINGEAL IRRITATION SIGNS: -ve 1. Friedreich ataxia (AR) ground
SKULL & SPINE: Normal (Involv of Dorsal , Pyrm,
PERIPHERAL NERVES: Normal Spinocerebellar tracts)

(C) Systemic examination:

2. Dominant ataxia
1)) Abdominal examination: Abetalipoproteinemia H/O of Diarrhea /
Umbilicus is midline passage of floating foul
NO Lumps palpable / Palpable organomegaly smelling stools
Xanthomas
NO free fluid
Dandey walker H/O of increasing head
93

2)) Respiratory system: syndrome circumference

BLAE: N & Cerebellar abscess H/O of Contact with Tb
Page

N vesicular sounds heard patient

 H/O fever with chills & cardiac disease and diabetes
rigors - Death occurs, usually from heart failure or
Polymyoclonus- H/O child in constant dysrhythmias, in the third or fourth decade
Opsoclonus Syndrome motion while awake. &
of Childhood irregular eye movements 4)) Treating underlying conditions
(Infantile Myoclonic
Encephalopathy) Refsums Dietary
Louis-Bar Syndrome / No Bulbar/dermal Wilson’s Cu chelation
ataxia - telengectasia telengectasia Malignancy removal
Drug induced Drug withdrawl / Replcm

Management:

1)) Investigations:
Cerebral palsy
Acute cerebellar ataxia
• CSF: slight lymphocytosis.
Discussion
• CT : normal
• MRI: cerebellar postinfectious demyelinating The term cerebral palsy is a nonspecific term used to
lesions.
describe a chronic, static impairment of muscle tone,
• EEG: normal or may show nonspecific slowing.
• Friedreich ataxia : GAA trinucleotide repeats on strength, coordination, or movements. The term
chromosome 9 can be used for laboratory diagnosis implies that the condition is nonprogressive and
•Mt test & X ray chest: Tb originated from some type of cerebral insult or
injury before birth, during delivery, or in the
2)) Treatment perinatal period.

1)) Acute cerebellar ataxia:

Treatment is supportive. Corticosteroids have not
been shown to be of benefit; IVIG has been used. Seizures (Epilepsy)
** Between 80% and 90% of children with acute
cerebellar ataxia not secondary to drug toxicity
DMD
recover without sequelae within 6–8 weeks. In the Kannaraju / 10 yrs / M / Student of 6th class / Hindu
remainder, neurologic disturbances, including
/ Karimnagar, brought by his mother a reliable
disorders of behavior and of learning , persist for
months or years, and recovery may remain informant with a
incomplete.
C/C: of
2)) Polymyoclonus-Opsoclonus Syndrome :
- Respond variably to ACTH or to IVIG. Meningitis
- Plasmapheresis has been successful.
- Usually the underlying neural crest tumor is benign Vivek/ 7 yrs / M / Student of 3 rd class / Hindu /
(ganglioneuroblastoma); surgical excision may be narayanguda, Hyderbad brought by his mother a
the only oncologic therapy needed. reliable informant with a
94

3)) Friedreich ataxia : C/C: of

Page

- Surgery for scoliosis and intervention as needed for

 H/O of fever - 7days • G/E Findings to rule out Genetic Syndromes
H/O headache – 5 days
H/O hyperirritability – 5 days Genetic Associated
Syndrome Cardiac Defect
H/C/C: Down A & VSD Flat facies
Patient was apparently asymptomatic 15 days back Flat nasal bridge,
Eyes Upward slant,
then the patient developed Headache
Small ears
Clinodactyly
Simian crease
Turner Bicuspid AV, Short stature,
COA, AS Wide Carrying angle,
Webbed neck,
Short 4rth metacarpal

Noonan HCM
Williams- AS, PPS
Beuren
Marfan MVP, MR, Tall stature,
dil. aortic root, High arched palate,
Fetal VSD, ASD
Congenital heart disease alcohol
Suman / 10 yrs / M / Student of 6th class / Hindu / Maternal PDA, PPS
rubella
Malkajgiri, hyderbad brought by his mother a
reliable informant with a

C/C: of

Discussion Stroke
Most congenital defects lead either to decreased Risk Factors for stroke
pulmonary blood flow or increased pulmonary
blood flow with pulmonary congestion. Symptoms
vary accordingly Cardiac disorders
Cyanotic heart disease
Decreased Increased
Valvular disease
Infant/Toddler Vascular occlusive disorders
Arterial trauma (carotid dissections)
Cyanosis Tachypnea with activity/feeds
Squatting Diaphoresis Homocystinuria/homocystinemia
Loss of Poor weight gain Vasculitis
consciousness
Human immunodeficiency virus
Older Child Diabetes
Nephrotic syndrome
Dizziness Exercise intolerance
Syncope Dyspnea on exertion, Systemic hypertension
95

diaphoresis Dural sinus and cerebral venous thrombosis

Page

Hematologic disorders
 Iron deficiency anemia Family H/O: No H/O of similar complaint in family
No H/O DM/HTN/Tb/HIV in family
Polycythemia
Thrombotic thrombocytopenia Birth H/O:
Thrombocytopenic purpura Mother is registered case in local hospital & had
Hemoglobinopathies regular ANC & IFA prophylaxis.
No other drugs taken / infections
Sickle cell disease
Received 2 doses of TT, Pregnancy is uneventful &
Coagulation defects had FTNVD in hosp.
Protein C and S deficiencies No dystocia / Instrumentation
Leukemia No admission of baby in NICU
Baby cried immediately & breast fed.
Intracranial vascular anomalies
Arteriovenous malformation Immunization H/O:
Arterial aneurysm Immunized as per schedule.
No post immunization hosptalization
Carotid-cavernous fistula
BCG mark seen
Transient cerebral arteriopathy
Developmental H/O: recognizes Mother &
Vocalizes Sounds But Not able to loft hos head in
prone position

Dietary H/O:
Breast fed NO supplementary feeds Giving
Hydrocephalus
Socioeconomic H/O:
Raju / 4months/ M / Hindu / Shankarmatt,
Socio economic class (K) – 3
hyderbad brought by his mother a reliable
informant with a General examination:

C/C: of Physical examination

Progressive enlargement of head from birth with (A) General survey –
H/O headache, nausea, Vomiting from 2 months Patient is C.
H/O Poor feeding from birth P (-) I (-) C (-) C (-) K (-) L (-)
Enlargement of head particularly frontal region
H/C/C: Buldging Ant fontanalle (NON pulsatile)
Patient is born with Normal head & has NO
High pitched Cry
difficulty in labour later then he slowly developed
NONC markers
Enlargement of head to reach present size.
NO shunt
H/O poor feeding from birth
NO neck stiffness
H/O Headche , nausea & Vomiting - 2months NO Scalp veins NOT prominent
H/O trauma
Sunsetting sign +ve (Loss of upward conjugate
NO H/O fever
gaze)
NO H/O Swelling at back
Craniotabes +ve
NO H/O Involuntary movements
(Macewen Sign): resonant on percussion /
NO H/O unresponsiveness to loud Sounds
96

Crack – pot sign +ve

NO H/O Convulsions
Facies: N (No dysmorphic features)
Page

NO H/O Altered Sensorium / Weakness of limbs

 Vitals – afebrile, Internal /Obstructive / NON communicating
HR: 96/min.N in volume, regular, character, & (Monro formen / Acqudect of sylvius)
rhythm No RR/RF delay No vessel wall thickening External /NON Obstructive / communicating
BP: 110/80 mm hg RUL: supine (Archanoid villi / Basal cistern)
RR: 25/min regular
Treatment
(B)Anthropometry:
Length: 1)) Mannitol / Furosemide / Acetazolamide
Wt: 4kg 2)) Ventricular tapping
midarm circumference – 9cm 3)) Ventriculo Peritoneal / atrial shunts OR
HC: 40cm Thecoperitoneal Shunts
•Shunt block & infection
Investigations: •Ventricular collapse
•X ray skull (Copper beaten appearance) •Slit ventricle syndrome
– Separation of cranial sutures 4)) Ventriculosty
– Lacunae in cranium 5)) Choroid plexotomy
– Bone thinning 6)) Treating underlying condition if possible
- Erosion of post clenoid process •Steroids for TBM
•USG (V/P ratio: Ventricular dimater at middle •AB for PM
portion of ventricles by Bi parietal diameter >0.33 •Clot / SOL removal
•CT / MRI brain
•Lumbar puncture
•ICF pressure monitoring
•Slit lamp (Chorioretinitis)
•PET & Angiography

Discussion:
DMD
Increase in size of ventricles due to excessive CSF
(Over production / Deficient Absorption / Prem kumar / 8 yrs / M / Hindu / nizamabad
Obstruction) brought by his mother a reliable informant with a

Antenatal C/C of
•Chromosoal Abnormality
•NT defects H/C/C:
•Arnold chiari 2 Malformation
•Dandy walker Malformation Family H/O: No H/O of similar complaint in
•Congenital Craniosynostosis family No H/O DM/HTN/Tb/HIV in family
•Congenital Aqueductal stenosis
Acquired Birth H/O:
•Pyogenic meningitis & TORCH Mother is registered case in local hospital & had
•Post Haemorrhagic (SAH) regular ANC & IFA prophylaxis.
•SOL No other drugs taken / infections
• Arnold chiari 1 Malformation Received 2 doses of TT, Pregnancy is uneventful &
had FTNVD in hosp.
No dystocia / Instrumentation
97

Sunsetting sign +ve because Dilated suprapenial

recess Pressess against tectum producing No admission of baby in NICU
Page

supranuclear palsy Baby cried immediately & breast fed.

 Immunization H/O:
Immunized as per schedule.
No post immunization hosptalization
BCG mark seen

Developmental H/O: recognizes Mother &

Vocalizes Sounds But Not able to loft hos head in
prone position

Dietary H/O:
Breast fed NO supplementary feeds Giving

Socioeconomic H/O:
Socio economic class (K) – 3

General examination:

Physical examination
(A) General survey –
Patient is C.
P (-) I (-) C (-) C (-) K (-) L (-)
98
Page