Case Taking BOOK

Vol
MY FINAL CLINICAL
SEMESTER
RaVi KiRaN 2K8
Wellthis 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
Page
CONTENTS:
MEDICINE
OBSTETRICS
GYNECOLOGY
SURGERY
PEDIATRICS
1)) Hemiplegia
1
MEDICINE
2)) Ascitis
3)) CVS MS
4)) Pleural effusion
Page
5)) Manual for short cases
HEMIPLEGIA
Vijay/Male/39/Cook/Kudappah/ 17 07 12
C/C:
Weakness of R UL & LL &
Deviation of Mouth to L with slurring of speech
from 2 days
H/C/C:
PATIENT WAS APPARENTLY ASYMPTOMATIC 1
day back then yesterday he went to work, returned
home, had dinner & then he slept & woke up at 11
pm went to bathroom , returned to bed then he
suddenly developed weakness of R UL & LL (he
awakened his wife also) simultaneously he
developed deviation of Mouth to L with slurring of
speech
No H/O loss of consciousness
NO H/O head trauma
NO H/O headache, projectile vomiting
NO H/O seizures
NO H/O pain in neck
NO H/O similar complaints in past
NO H/O hypertension / smoking
NO H/O memory loss / behavioural changes
NO H/O symptoms suggestive of other cranial
nerves
H/O complete weakness of R UL & LL at the time of
attack but now he is able to move his limbs & eat
on his own
NO H/O Involuntary movements
Able to feel ground on walking & Clothes
NO H/O tremor of hands while reaching to glass
H/O passage of urine at the time of attack but now
passage of urine & faces is N (continence
maintained)
Past H/O: NO H/O similar complaints in past, HTN,
DM, TB, epilepsy, chest pain & bleeding disorders
Page
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 Consious.
Moderately built &
adequately nourished
P (-) I (-) C (-) C (-) K (-) L (-) E (-)
No NC markers
No tendon xanthomas/ xanthalesma
No carotid bruie
Facies: Mouth deviated to Left
on attempted talking
Decubitus:- Normal
Vitals a febrile,
HR: 84/min N in volume, rhythm
No RR/RF delay all PP +ve
BP: 120/84 mm hg RUL: supine,
RR: 20/min regular regular
(B) Local examination (CNS)
1)) Higher functions
Handedness: R
Level of consciousness: Fully consciousness
Orientation: +ve
Emotional state: Normal
Memory: preserved
Speech: Articulation disturbed
2)) Cranial nerve Examination:
I
II
Visual acuity
Visual fields
Colour vision
III,IV.VI
Light reflex
Accomodation
Eye movements
Nystagmus
Normal
Normal
Normal
Normal
Normal
Normal
V
Sensory
Motor
VII
VIII
Vestibular
Auditory
IX & X
XI
XII
Normal
Normal
Forehead
wrinkling
present
& Deviation of
mouth to L on
showing his
teeth
Normal
Normal
Palatal reflex +
gag reflex NOT
done
Normal
No deviation /
fasciculations
& Uvula
midline
Normal
/ No wasting &
N power
3)) Motor System:

A)) Inspection
No Gross Muscle wasting / Hypertrophy seen
No involuntary Movements
B)) Palpation
Bulk
UL
LL
Tone
UL
LL
Power
UL
LL
Involuntary
UL
LL
Co ordination
UL
LL
5
Page
K,A: ++
?
Absent
K,A: +
?
Absent
5)) Sensory system:

Proprioceptive
Exteroceptive
Cortical
Present & N
Present & N
Present & N
Present & N
Present & N
Present & N
GAIT: N tanden walking

CEREBELLAR: Able to do Knee heel test, finger nose
test No dysmetria / No dysdiadokokinesia
ANS: No abnormal sweating, constipation
RAISED ICT SIGNS: Absent
MENINGEAL IRRITATION SIGNS: No neck rigidity
/ Kernings / Brudzunskie signs
SKULL & SPINE: Normal
PERIPHERAL NERVES: Normal
(C) Systemic examination:
26cms
43cms
25cms
43cms
Clasp Knife rigidity

Normal (?)
Normal
Normal
3/5
5/5
Absent
Absent
Able to do Knee heel test, finger

nose test No dysmetria / No
dysdiadokokinesia
4)) Reflexes:
Superficial
reflexes
Abdominal
Plantar
Deep tendon
reflexes
Jaw jerk
Upper limb
Lower Limb
Visceral reflexes
Released
reflexes
1)) Abdominal examination:

Umbilicus is midline
NO Lumps palpable / Palpable organomegaly
NO free fluid
2)) Respiratory system:
BLAE: N &
N vesicular sounds heard
NO adventitious sounds
3)) Cardiovascular system:
Heart sound 1 & 2: Heard & No murmurs heard
Diagnosis: A case of Complete completed Left

hemiplegia due to CVA with Left 7th cranial
nerve UMN type of palsy in the stage of
recovery (Now hemiparesis) which is probably
Embolic in origin in MCA territory at the level of
Lost
Lost
internal capsule.
With alchoholism, Old age, male as risk factors
& No complications of recumbancy
?
B,T,BR: ++
?
B,T,BR: +
Ramraju/55/M/warsiguda/Manual labour
Family H/O:
C/C:
Yellowish Discolouration of eyes 20 days
Abdominal distension 15 days
blood per stool 15days
(A) general survey
patient is C/C/C . Hepatic facies +ve
P (-) I (-) C (-) C (-) K (-) L (-) E (-)
H/C/C:
PATIENT WAS APPARENTLY ASYMPTOMATIC 20
days back then he developed yellowish
discoloration of eyes, insidious In onset, progressive,
associated with itching & yellowish discoloration of
urine from 15 days
H/O weight loss & appetite loss 6m
H/O vomiting 6m 2/3 per day , 30 min after
food, contained undigested food, yellowish, No
blood, no odour.
H/O abdominal distension 15 days progressive,
with H/O 3 tappings (he dont know the colour)
H/O Abdominal pain 4 days: sudden, continous,
progressive, twisting type, aggravated after taking
food, partially relieved on medication
H/O back pain, orthopnea 4 days
H/O passage of black tarry stools 4 days
NO H/O hematemesis
NO H/O facial puffiness
NO H/O pedal oedema
NO H/O decreased urine output
H/O taking local herbal medicine
H/O alcoholism 15 yrs 500ml/day
HR: 88/min N in volume, rhythm

RR: 22/min regular regular.
ASCITIS
Past H/O: Jaundice - 1 yr back treated with local

medicine & subsided Not associated with fever
NO H/O similar complaints in past, HTN, DM, TB,
epilepsy, chest pain & bleeding disorders
Page

Long term treatment
Personal H/O:
Diet: mixed appetite: N
B/B: bladder regular bowel blood per stool &
tarry stools passage
Sleep: disturbed
Addictions: Non smoker & massive alchoholic
Parotid enlargement +ve (painless)

No loss of axillary hair
No hepatic flap
hands: Normal
No odor from patient
No spider neavi
No supraclavicular fullness
No allergic signs of Tuberculosis
(B) Local examination (Abdominal)
1)) Oral cavity:Tongue, pharynx, faucal pillars, Teeth , tonsils :
within normal range
2)) Abdomen:
a)) Inspection:
Abdomen is generally distended,
Umbilicus everted & displaced downwards & all
quadrants move equally with respiration , epigastric
pulsations +ve (probably aortic)
No visible peristalsis,
No engorged veins
No other swellings visible &
Skin over abdomen Normal
No echymosis over flanks / around umbilicus
No skin nodules around Umbillicus
No puncture marks
b)) Palpation:
No Local rise of temperature/ tenderness/rebound
tenderness/Abdominal wall rigidity present
No lumps palpable
Liver: Lower border & Left lobe Not palpable
Spleen: Not palpable
Fluid thrill ve
c)) Percussion: Shifting dullness +ve

Liver upperborder: 5 th ICS in MCL (liver span: 14cm)
Traubes 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

GENETALIA: N (no loss of pubic hair/ testicular
atrophy)
PR: NOT done
H/O easy fatigubility 1 yr

H/O Cough 5 months , insidious, progressive
Productive & is red coloured,
Aggravated on exertion & on lying down
No H/O penicillin Injections
No H/O sorethroat with joint pain/swellings

BLAE: N &
Diagnosis: Alcoholic liver disease with liver

cirrhosis in decompensated state.
CVS MS
Kumar/17/M/Student/Medak
C/C:
SOB 1yr
Palpitations 1yr
Backout episodes 6m
L Chest pain 1 Month
H/C/C:
Patient was apparently assymptomatic 1 yr back
then he developed SOB & Palpitations
Page
SOB, Insidious in onset, Exertional. Relieved on

taking rest, gradually progressive, Started as NYHA
1 now it is NYHA 3.
H/O PND attacks 5months: 3episodes/night
H/O Orthopnea 5months
Palpitations - Continous, Regular, Aggravated on
exertion & relieved on taking rest.
Not associated with Polyuria / Chest pain /
Lightheadedness

DM, TB, epilepsy, chest pain & bleeding disorders
Long term treatment / Penicillin prophylaxis
Personal H/O:
Diet: mixed & appetite: reduced
B/B: regular & Sleep: N
Addictions: Non smoker / alchoholic
Family H/O:
(A) general survey
patient is C/C/C
Moderately built &
adequately nourished
P (-) I (-) C (-) C (-) K (-) L (-) E (-)
N facies
NO SC nodules / Erythema marginatum
NO Splinter haemorrhages
NO Osler nodes/janeway lesions
NO malar flush
Normal statured
NO high arched palate
NO syn- / Poly- dactyly
Vitals
afebrile,
HR: 84/min N in volume, regular
rhythm, No RR/RF delay all PP +ve

BP: 110/74 mm hg RUL: supine
RR: 16/min regular , TA
No other adventitious sounds like Clicks / Tumour

plop / Pericardial rub heard
(B) Local examination (CVS)

1)) Inspection:
Chest is Normal with No deformities
Trachea is in midline
Precordium appears Normal
(No buldge / retraction)
No pulsations are seen in M/T/P/A area,
No pulsations seen in suprasternal, supracavicular,
infraclavicular, epigastric / Back
Apex beat Not visible
Back is Normal (No spinal deformities)
2)) Palpation:
Trachea Midline
M:- Apex beat in 5 th ics 1cm lateral to Midclavicular
line Localized with diastolic thrill & is tapping in
character
T:- Normal
P:- Pulsations are palpable
A:- Normal
prasternal heave :- +ve (grade 3)
No palpable Rub
3)) Percussion:
Right border corresponds to Right sterna border &
left border corresponds to apex & 2 nd ics (pulm
area) is dull
4)) Auscultation:
Apex pulse deficient:- 0
A mid diastolic murmur harsh & rumbling is heard
best in Mitral area with No radiation & heard best
in left lateral position with bell & heard best after
exercise & end of expiration
P
S1 N
P2 Loud
& S2 N
split
Murmur Murmur Murmur
MDM
NO
ESM
Page
M
S1 Loud
S2 N
T
S1 N
S2 N
A
S1 N
A2 N
Other
Gibsons
Neoaortic
Murmur Infraclav
NO
Normal

BLAE: N &
NO free fluid
Diagnosis: A case of Organic MS Probably of

rheumatic origin with No clinical features of CCF /
IE & patient is sinus rhythm at present
Pleural effusion
Rangareddy / 56 / M / Hindu / Nalgonda / Daily
labourer
C/C:
Cough from 20 days
L Chest pain from 15 days
Difficulty in respiration from 10 days
H/C/C:
Patient is apparently asymptomatic 20 days back
then he developed cough which is
Insidious in onset, Progressive, Non productive,
No haemoptysis
No aggravating / relieving factors
No diurnal variation
Chest pain 15 days, Left sided, Insidous, Stabbing
type, continuous, Aggravated on cough, sneezing
partially relieved on medication, rest & Exertion
No radiation & is disturbing sleep
Difficulty in taking respiration 10 days
Insidious in onset, present at rest, NON progressive.
No associated wheeze, Aggravated on exertion &
relieved by lying on his L side
NO H/O PND attacks
NO H/O Orthopnea
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:
epilepsy, chest pain & Bleeding disorders & there is
NO H/O suggestive of Skin rash, Joint pains
(Collagen Vascular Disorders)
Long term treatment
Personal H/O:
No drug allergies
Occupational H/O:
No H/O suggestive of Exposure to organic /
inorganic dusts
Page
Family H/O:
General Examination:
(A) Physical examination
Patient is C/C/C
P (-) I (-) C (-) C (-) & there is NO wrist tenderness
K (-)
L (-) NO cervical / Scalene LN palpable
E (-) & There is No Signs of DVT / Erythema
nodosum on legs
N facies
Moderately built & Adequately nourished
Normal decubitus
N voice & cough
NO Tobacco/nicotine staining.
NO Flapping tremor
Eyes : Normal (No ptosis / contracted pupil / Subcj
hemorrhage / Chemosis / ruddy cyanosis /
Phlyctens)
NO scrofula / Scrofuloderma
NO small muscles (of hand) wasting
Vitals: HR: 88/min N in volume, rhythm
RR: 22/min regular .Abdominothracic
NO use of accessory muscles & there is
NO intercostal / Supraclavicular Suction
JVP: not elevated
(B)Local examination
1)) URT (Favoring Aspiration / not)
Nose (turbinates, congestion , polyps)
& nasal septum: N
NO nasal discharge
NO Nasal flare
NO lupus pernio
NO sinus tenderness elicited
Oral hygiene satisfactory
NO halitosis
Pharynx (Oro Teeth, gums, palate, post
pharyngeal wall: N, Larynx NOT examined)
2)) LRT
INSPECTION
from front
Chest is N in shape
movements are diminished on left side
apical impulse: NOT seen
fullness seen on left side in middle & lower part
Supraclavicular & Infraclavicular fossa : N
(NO swellings / Suction / Fullness)
Both the nipples are at same level
NO tracheal deviation
Skin is Normal (NO scars / Sinuses / Suction marks)
NO crowding of Ribs
NO chest wall sweelings
NO venous prominence / arm swelling
NO paradoxical chest Movement
From back (Standing position)
No spinal deformities
Skin is Normal
Both shoulders are at Same level
Inf border of scapula are at same level

NO winging / Drooping
Spino Scapular distance: Same on both sides on
inspection
NO gibbus
Intercostal suction & rib crowding : not seen
Coin percussion & Shifting dullness: Absent

Hepatic dullness is in 5 th ICL R
AUSCULTATION
Ant
PALPATION
NO local rise of temperature /
NO local tenderness / Intercostal / punch tenderness
Slight tracheal deviation to R
NO tracheal Tug
Crico Sternal distance is Normal
Apex beat not palpable
Chest Movements
Reduced on Left side Lower & middle
Chest Expansion
2.5cm on R side & 1cm on L side
Vocal fremitus
Ant
L
Diminished in
mammary &
Inframammary area
Diminished in
Infraxillary area
Diminished in
Infrascapular area
Lat
Post
No other Palpable accompaniments (Friction ,

Rhonchila fremitus, pleural / pericardial rub)
Normal palpatory findings on R side
Page
10
PERCUSSION
Ant
R
Resonant
Lat
Resonant
Post
Resonant
Apical /
Kronigs
isthmus
Resonant
L
Dull in
mammary &
Inframammary
area
Dull in
Infraxillary area
Dull in
Infrascapular
area
Resonant
R
N vesicular & NO
Adventitious
sounds VR: N
Lat
N vesicular & NO
Adventitious
sounds VR: N
Post
N vesicular & NO
Adventitious
sounds VR: N
Apical / N vesicular & NO

Kronigs Adventitious
isthmus sounds VR: N
L
Diminished breath
sounds In mammary
& Inframammary
area NO
Adventitious sounds
VR: decreased in
same areas
Diminished breath
sounds In
infraaxillary
area NO
Adventitious sounds
VR: decreased in
same area
Diminished breath
sounds In
Infrascapular
NO Adventitious
sounds VR:
decreased in same
area
N vesicular & NO
Adventitious sounds
VR: N

NO free fluid
Free hernia sites
3)) CNS: Patient is C/C
No neck rigidity (TBM)
Within N limit
Diagnosis: A case of L sided Pleural effusion
probably of tuberculous origin
Manual Short cases

1
Anemia: Qualitative / quantitative decrease in
Hb/RBC in relation to Age / Sex / Altitude clinically
manifesting as pallor:
Lower palpebral conjunctiva (polycythemia &
Scleroderma:- tightness during retraction) *
Tongue (tip & dorsum) *
Palate
Nail beds
Palms & soles
14.6 15.5 gm% - Males &
13.3 - 15.5 gm% - females
(Clinically 14.5%: 100%)
Ankle oedema (Anemia perse, CCF, Renal disorders

causing Anemia)
1U packed RBC raise Hb by 2 gm% (Globally
Chronic Blood loss is the commonest Cause)
Iron deficiency anemia:
Pica
Glossitis / Bald tongue
Angular stomatitis
Platynychia & brittle nails
Brittle hair & dysphagia (PV Syndrome)*
B2 (Megenta colored) ,
B12 (Raw beefy tongue),
Fe, FA defeciency
Excessive Alcohol,
Tobacco, herpes labialis,
B2, B12, Fe, FA
deficiency, Candidiasis,
Strp infection
Glossitis / Bald tongue
Angular stomatitis
Pale PALM - <7gm %

Pale RETINA - <4gm%
if Hb % is between 81% - 99gm%: it is not evident
clinically as pallor
Macrocyctic Hypochromic Anemia: Dimorphic

anemia (Pregnancy & Hook worm infection)
Causes: Nutritional, Hook worms, Leukemia,

Hemolytic disease, Hemetemesis, Chronic Bleeding
hemorrhoids & menorrhagia, Chronic Systemic
diseases (SLE, RA, SBE, Malignancy, Uremia & CLD)
CVS
11
Sternal tenderness
Pallor (pathological entity) is waxy appearance of

skin & mucous membrane (depends on blood flow
& Qualitaty & quantity of skin) Anemia (Clinical
entity) & Low cardiac output states
H/O Weakness, lassitude, Giddiness, fainting,

Palpitations, breathlessness, Tinnitus, Lack of
concentration, Dysphagia*
Treatment H/O: NSAID intake
Dietary H/O: Dysphagia
Personal H/O: Alcohol & Walking barefooted
family H/O
Page
LR
Resp
Nervous
tissue
Tachycardia, Functional MI & haemic

murmer at pulmonary area, CCF
Hyperdynamic apex, Capillary pulsation,
Ankle oedema, dyspnoea
Basal Creps
Polyneuropathy
Leucoerythroblastic picture: Normoblasts &

Myelocytes both are seen in Peripheral Blood in
Myelophthisic anemia
(Infiltration by granuloma / umour),
M6 variety AML
Myelofibrosis & Sclerosis
Polycythemia / Ruddy cyanosis: Mucous membrane
is Dusty Red & Facial Plethora, Suffused Conjuctiva,
Palmar erythema
Anemia & Polycythgemia: Fallots (If hb <18gm%,
PCV <55%: Anemia)
2
Cyanosis: Bluish discoloration of Skin & MM due to
presence of increased amount of Reduced Hb
(>5gm%) / Hb derivatives(Sulfa >0.5gm% OR
Methe >1.5gm%:- Enterogenous / pigment
Cyanosis) in capillary blood
(DD:-CO poisioning, Argyria, Osteogenesis

Imperfecta only sclera, Amiodarone giving bluish
hue to skin Ceruloderma)
Differential: PDA with Shunt reversal (FEET BLUE)

Reverse Differential: COA + TGA (FEET RED)
Hypoxia
+ve
+ve
Cyanosis
+ve
-ve
Orthocyanosis: Only in upright position (Pulmonary

AV malformations in middle & lower Lobes)
-ve
+ve
Peripheral
Nose Tip
Ear lobules
Outer aspect of Lips
Tip, Nail beds of
fingers & toes
Stagnant &
Overutilization Hypoxia
CCF
Raynauds
Shock
Arterial diseases: TAO
Venous diseases: SVC S
Cryoglobulinemia
MS (mitral facies)
Application of warmth
Cyanosis will decrease
reverse with Cold
Application of Pure O2
for 10 min: NO response
Clubbing &
Polycythemia:
Absent Usually
Respiratory distress: -ve
Hands: Cold
Pulse Volume: LOW
Central
Tongue (sides, Under)*
Inner aspect of Lips
Lower palpebral Cnj
Nasal, rectal mucosa &
Retina
Hypoxic Hypoxia
CCyanoticHD
Acute Pulm oedma
Acute severe Asthma /
COPD/Embolism/
Laryngeal oedema
Pulm AV fistula
Eisenmenger Syndrome
NO Effect
Cyanosis may improve
Usually present
May be present
Hands: Warm
N / HIGH
Intermittent Cyanosis: Ebsteins Anomaly

Cyanosis
+ve
12
+ve
Page
Cyanosis + PolyCythemia: CCongenitalHD & COPD
-ve
Clubbing
+ve
-ve
+ve
Condition
Central
Cyanosis
Peripheral
cyanosis
& Acutely
developing
Central
cyanosis
SBE , Ulcerative
Colitis
Condition
Rhb >5gm %
Severe Anemia
(hb <5gm%)
PCV (red
cyanosis)
Pigment cyanosis (Spectroscopic Examination): Hb

M, Nitrites & nitrates, Aniline dye poisoning &
Carboxyhb: Cherry red apppearence NOT TRUE
cyanosis
3
Jaundice: Yellowish discoloration of Skin & MM due
to excess Bilirubin in blood (Clinically >3gm%)
1 3gm%: Latent jaundice
0.3gm% - 1gm% : Normal
Upper bulbar Conjuctiva (Lot of ELASTIN:
Underlying Sclera)
Palate
Palms & Soles
Skin
(DD:- Carotenemia:Only Skin affected,
Atabrine toxicity: Skin & Sun exposed Sclera,
Diffuse xanthamatosis)
Unilateral: Hemiplegia & unilateral oedema
4
Pulse: Expansion & Elongation of Arterial wall
imparted by Column of blood & is inturn produced
by Pressure changes in ventricular Systole & diastole)
mentioned in 8 ways
Semi pronated & slightly flexed wrist: lateral to
Flexor carpi radialis (For VOLUME & CHARACTER
Carotid artery)
Pulse deficit: HR PR (AF >10 / min & Multiple
Ectopics <10 / min)
HR 1min then PR 1min (2 Cardiac cycles)
Steth & Palpate for Radial Pulse Count dropped
Beats (1 Cardiac cycle)

2 different examiners (1 Cardiac cycle)
In ectopic Beat / Premaure beat / Extrasystoles
(Hypertensive / Thyrotoxis / Cardiomyopathic)
: Impulse arises from Ventricular / Atrial wall / AVN
It is small & premature Followed by a
compensatory pause (Dropped / Missed beat)
Tortuous & Thickened

(Atherosclerosis rarely palpable:
Intima)
Wall
RR delay
Absent radial pulse: Anatomical abnormality, Severe

Atherosclerosis, Takayasu, Embolism
Mean pressure:- Mean of SBP & DBP + 1/3 Pulse
pressure
8 CHARACTERISTICS
Rate
Rhythm
Page
13
Volume
60 100 / min
Tachycardia (>100/min)
Sinus tachycardia
Relative tachycardia
Paroxysmal Tachycardia (SVT / VT)
Bradycardia (<60 / min)
Myxoedema
Obs jaundice
Athelets
Increased ICT Hypothermia
Propanolol / digoxin Hypoxia
Regulary / irregulary irregular
Regulary irregular:- Extrasystoles, 2
HB, Pulsus Bigeminus
Irregularly Irregular:- AF, Multiple
extrasystoles, Afl
Irregular but N HR:
Digitalised AF, Sinus arrhythmia
Amplitude / Excursion felt
PULSE PRESSURE (30 60mm)
Stroke volume & Arterial compliance
High (>60mm)
Hyperkinetic states
Complete HB & Bradycardia of any
cause
Atherosclerosis
Low (<30mm)
Shock
Severe AS & MS
CCF
Wall may be palpable in old age due
to Arteriosclerosis / MEDIAL
MONCKEBERGS SCLEROSIS:
RF delay
Periph pls
Block Brachial artery & Palpate Radial

OR
Exsanguate with middle fingers & then
palpate with 2 index fingrers
Cervical rib
Aneurysm of aortic arch
Takayasus arteritis Iatrogenic:
Bllalock taussings shunt
Pre subclavian
Coaorctation
Supravalvular aortic stenosis
Pressure over axillary artery by LN
Embolism
**Simultaneously Palpate 2 Radial A
Coaorctation of aorta
Aortoarteritis
Atherosclerosis of aorta
** Simultaneously Palpate 2 arteries
*** Normally there is difference of
0.02 to 0.03 Sec (Femoral 1st) but
clinically simultaneous
Ulnar: Wrist medial side
Brachial: Just medial to biceps tendon
at / just below elbow
Subclavian: Middle of clavicle
(Shrug Shoulders & palpate from
behind)
Carotid: Medial to SCM at / Below
the level of thyroid cartilage
Femoral artery: Midway btw ASIS &
PT
Popliteal artery: Semiflexed Knee &
Supine with thumbs on Tibial
tuberosity & Fingers on middle of PF
Post tibial artery: Midway Achilles &
MM After INVERSION of FOOT
N: CATACROTIC pulse
Percussion wave
Tidal wave
Dicrotic & Ancrotic Notch
This is Not palpable become it is
Obliterated By N vascular tone
Anacrotic notch
Character
(Volume &
Waveform)
Page
14
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
DUE TO VERY LESS PR
Other causes of High volume can
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 &
BERNOULIIS 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

is sucked into RV Reduced Blood
into LV & Deviation of
Interventricular septum to L
Reduction of CO
Actual paradox is heart sounds may
be still audible when no pulse is
palpable in radial artery
9)) Thready (Low Volume + Rapid
(peripheral c Failure ) / jerky (HIS)
Sphygmomanometer:
1)) Hess capillary fragility test
2)) Latent tetany: TROUSSEAUS Sign (Raise >SBP
for 3min: carpal spasm)
3)) Draw venous blood
4)) Hills sign in AI
5)) Assess respiratory reserve
6)) Different types of pulses
Pulsus Paradoxus
SBPe > SBPi (>10mm)

Gallavardins sign
Initially on reducing only
Strong beats are heard
SO Heard Beat APPEARS
only Half actual value
On further reducing
Both strong & weak are
heard Original HR
heard
Pulsus Alternans
WH pulse
PP >60mmhg
Oral temperature NOT taken if: Bells palsy,

inflammatory conditions, Mouth breathers, Trismus,
After Hot tea, Convulsions, Mentally dull people
Hyperthermia
Malaria
Aseptic fever
Heat stroke
Leukemia & lymphoma
SLE
Pontine haemorrhage
Porphyria
Thyroid storm
Acute MI
Malignant hyperthermia
Halothane
Haloperidol
Septicemia
Encephalitis
Lobar pneumonia
Hypothermia
Myxoedema coma
Enteric fever associated
in Prf / Hmrg
Alcohol intoxication
Prolonged Cold
exposure
Hypoglycemia
Autonomic dysfunction
Periodic fever:
Hodgkins
Malaria
brucellosis
Relapsing fever
Hectic temperature: Big swing in temperature

suddenly with chills & rigors & Sudden fall with
sweating after few hours
Pent up pus anywhere
Septicemia & pyemia
Fall by lysis
Fall of temperature
suddenly with sweating
very fastly in 6 12 hrs
Enteric fever
Acute lobar pneumonia
Dengue
Adrenal crisis
Fall by crisis
Fall gradually in steps
over several days
Uncomplicated EF
Rheumatic Fever
Acute
bronchopnemonia
5
Temperature: 98 99 F (lowest in morning &
highest in evening : diurnal variation of 1.5 F)
Hence Oral AM >98.9F & Oral PM >99.9F Fever
Page
15
R (1F)> O (0F) > Ax (1F) (Tympanic membrane

thermometer fast & Accurate)
Clinical thermometer has a mark at 37C / (98.6F)
clinically above this is taken as fever
(When kept in axilla)
For 1F rise of temperature RR increases by 2 3/min

& PR 10/min (adults) & 12 15/min (Childrean)
Relative Bradycardia
Rise of PR is
Proportionatly low
Any viral fever
1st week of enteric fever
Brucellosis
Psittacosis & weils
Relative tachycardia
Rise of PR is
Proportionatly high
Acute R carditis
Diphtheric myocarditis
PAN
Thermometer is Triangle in C.S Magnifies the

mercury line & Kink is present to prevent return of
mercury Line after it is taken from recorded site
Intermittent
Quotidian
(daily)
Double
infection with
Plasmodium
TB
UTI
Tertian
(Alt days)
Benign (Vivax
& Ovale)
Tertian
(Falciparum)
Quartan (2d)
** Fever
present for only
few hours &
ALWAYS
TOUCHES THE
BASELINE
SOMETIMES
DURING THE
DAY
Continued
RF
Miliary TB
2 nd week EF
Double
quotidian
fever / Camel
hump fever
(Double
fever spike in
single day)
Kala azar
Gonococcol
Endocarditis
**fever DO
NOT
FLUCTUATE
more than 1.5F
during 24 hr
period &
NEVER
RETURNS THE
BASELINE
Remittent
Acute
broncho
pneumonia
Amoebic LA
UTI & 3 rd
week EF
** fever DO
FLUCTUATE
more than 3F
during 24 hr
period &
NEVER
RETURNS THE
BASELINE
Typhoid state: Untreated EF in 3 rd week which is

manifested as neurological manifestations
1)) Semi consciousness
2)) Coma vegil: Half eyes open but ignorant of
surroundings
3)) Subtulus tendinum: Inv movements of fingers &
wrists
4)) Carphology: Plucking of bed sheets
Page
16
Fever with rash

1st day: varicella
2 nd day: scarlet fever
3 rd day: Small pox
4rth day: Measles
5 th day: Typhus
6 th day: DEngue
Fever with membrane

Follicular tonsillitis
Faucal diphtheria
Candidiasis
Vincents angina
Infectious MN
Increased PR ratio: Narcotic poisioning (n: 4:1)

Decreased PR ratio in Acute lobar pneumonia
Drug fever: Sulphonomides, Slaicylates, Iodides,

Barbiturates, penicillin, quinidine & rifampicin
6
Oedema: Excessive fluid in SC space & / OR serous
sacs due to increase in Interstitial component of ECF
2/3 ICF & 1/3 ECF (3/4 IF & 1/4 Plasma)
In ALL patients with oedema SACRUM &
SCROTUM should be examined& Never miss
PARIETAL oedema (Present particularly over
abdominal wall) :- In upper part of body Sternum,
lateral epicondyle, Forehead has to be pressed
Pitting
CCF, NS, Liver F,
Hypoproteinemia,
Constrictive pericarditis,
Pericardial effusion ,
Wet Beri - Beri
Generalized
Anasarca / Dropsy
CCF, NS, Liver F,
Hypoproteinemia,
Wet Beri - Beri
Non pitting
Myxoedema
Lymphatic oedema
Angioneurotic oedema
Sclerederma
Localized
Venous obstruction
(Pregnancy, SVC,IVC
syndrome,DVT)
lymphatic obstruction
Tb, filariasis, Radiation,
dissection, Infiltration of
LN
Allergy: AgNO
Inflammatory: Insect /
Snake bite
Pitting oedema demonstratable if increase In W

>10 15 % & Circumference >10%
CCF : Legs face Ascites
Renal: Face legs Acsites
Liver: Ascites Legs face
Nutritional: Feet + face Ascites
Low oncotic pressure
High capillary hydrostatic pressure
Increased permeability
Obstructed Lymphatic Drainage
Renal retention (Due to decreased flow, Sec
Hyperaldosteronism, Increased ADH levels)
Pedal oedema
CCF, NS, Liver F,
Hypoproteinemia,
Wet Beri Beri,
Varicose veins, DVT
Facial puffiness
CCF, NS, Liver F,
Hypoproteinemia,
Wet Beri Beri
SVC syndrome, Cushings
Syndrome, AngNO
In renal Causes Swelling of SCROTAL SAC &

EYELIDS is classical
7
Clubbing / Hippocratic fingers / Lovibonds sign:
Bulbous enlargement of Terminal part of Fingers & /
OR toes due to increased pulp tissue mass
(Proliferation of Subungual Soft Tissue + Interstitial
oedema + Capillary Dilation) resulting in increased
AP diameter & Transverse diameter
Onychodernal / Lovibonds Angle: Angle Btw nail &
nail bed (160) (Adjacent skin fold) Usually index
finger is 1st to Affected
1 See tangentially for loss of LbAngle*
Fluctuation Window sign / Schamrothss sign
st
1st degree
2 nd degree
3 rd degree
Fluctuation + loss of Angle

1st + Increase in T & AP diameter
2 nd + Increased pulp tissue
(Parrot beak / Drum stick Appearance)
th
4 degree 3 rd + wrist / Ankle selling due to HOA
*Most reliable early sign
Causes:
Page
17
1)) Cardiac: Cyanotic HD, ABE, Eisenmengers

2)) Lung & pleural: Bronchiectasis, Lung abscess,
Empyema thoracis, CF, Pulm AV fistula, CF
3)) Ulcerative Colitis
4)) Biliary Cirrhosis
5)) Intestinal: Crohns & Coeliac disease
6)) Normal / Idiopathic
7)) Genetic / familial
Always Look for swelling & tenderness at wrist
Painful
Reversible
SBE
Brochogenic carcinoma
Lung abscess*
Empyema thoracis*
Unilateral
Unidigital
Subclavian Coarctation
/ aneurysm
Cervical rib
Hereditary
Repeated trauma
Sarcoidosis
Upper limb
Lower limb
Chronic Obs Phlebitis

due to chronic IV drug
addiction
Subclavian Coarctation
/ aneurysm
Cervical rib
Infected AAA
PDA with shunt
reversal
** Acute clubbing
(<2W)
*** Pseudo clubbing: Subperiosteal Bone resorption

(NO Pulp tisse enlargement / Increased Curvature)
Scleroderma
Acromegaly, Leprosy
Occupational (ViCl2: Acrosteolysis)
Koilonychia: Spooning - 3 stages
1st: Brittleness 2 nd: Flattening (platynychia)
3 rd: Spooning
Mechanism
Anoxic
Toxic
Reflexive / Neurogenic
Metabolic
Humoral
Reduced ferritin
Hereditary
Platelet & Megakaryocytes
trapping
Opening & Dilation

SBE
Thyrotoxicosis
Acromegaly
Dilation & Opening
(recent view)
Release of PDGF &
TNF -
DIGIT RATIO: Calculate diameter at Nail base &

distal IPJ Clubbing (+ve) if Sum of all fingers, >10
PHALANGEAL DEPTH RATIO: (Calipers) : Index
finger is used & DISTAL PHLANGEAL DEPTH :
INTERPHALANGEAL JOINT ration >1
HPOA / Pierre Marrie Bamberger Syndrome:

Primary / Hereditary (AD)
Secondary (Any clubbing cause) Mostly
Bronchial Carcinoma (1/2) & Pleural mesothelioma
Chronic suppurative lung diseases
Chroniv Liver diseases
-Pain is aggravated on dependency
-Pathologically:- Periosteal thickening due to Sub
periosteal New Bone formation & Digit ends show
Osseous resorption
NAIL
Pitting
Onycholysis
Onychomadesis
Beaus lines
Yellow nails
Terrys / White nails
(Thumb & index)
Lindsays nails / half
& half nail
Mees nails
Muehrckes nails
Horders Nails
(linear longt. Hmr)
Green nail
Black nail
Condition
Psoriasis, Reiters disease
Psoriasis, Amyloidosis,
Sarcoidosis
Trauma, Kawasaki disease
Severe systemic illness,
Pemphigus
Lymphoedema, pl effusion
(Yellow nail syndrome)
Imm dfcny, Bronchiectasis,
Liver failure, Cirrhosis
Renal failure
Ars poison & Hodgkins
HypoAlbuminemia (Any)
SBE, systemic vasculitis
Psuedomonas infectio
PEutz jeghers syndrome
8
Page
18
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
9
If H > 97 th centile
Marfans syndrome {defective Crosslinking of
collagen due to AD mutation in fibrillin 1 & 2 genes}
(a)) Skeletal: US < LS, AS > H, Steinbergs sign /
Thumb sign / Hyper extensibility +ve Thumb
extends beyond ulnar border of Hand, High arched
palate, Straight back syndrome, Wrist sign +ve
Little finger & thumb overlap >cm around wrist,
Metacarpal index >8.4 4 metacarpals length
divided by width at midpoint & values are averaged
, Pectus carinatum, Pectus Excavatum, Pes planus,
Cavus, Long & narrow facies / Dolicocephalus
b)) Ocular: Lens Subluxation (Downwards) & Blue
sclera with myopia
c)) Cardiovascular: AI, MVP, A dissection
d)) Others: Cystic bronchiectasis, Sp. Pnemothorax)
Klinefeltars & Hypogonadism:
(US > LS, Tall, +ve barr body, Gynecomastia, MR,
Small firm testis, Eunuchoidism)
Homocystinuria
(US < LS, Reduced Cystathione reductase, Lens
Subluxated downwards, MR,AR, Life threatening
thrombotic episodes)
US = LS: Constitutional & familial, Hyperpitutarism
10
Nutrition:
Subcutaneous Fat (Triceps Males: 12.5mm
(<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
females > 0.9 risks for metabolic complications

Ponderal Index: H (in) / W in pounds (1/3)
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
definite upper level

seen
NOT seen
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
Kussmauls 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
of Tric. Valve
Page
19
Normal value at 45 : 3 4cm blood (8 cm Blood =

6mm hg)
Venous
Wavy
Better seen than felt
On Exp - Promn
Lying down - Promn
HJ reflex - +ve
Prominent movement
is INWARD
Abolished by gentle
pressure applied above
Clavicle
2 +ve waves are seen
Arterial
Jerky
Better felt than seen
NO
NO
NO
Prominent movement
is OUTWARD
NOT ABOLISHABLE
1 +ve wave seen
Due to Opening
In normal people A is visible & X is more prominent

C X descent: X descent / Systlc collapse: before S2
V Y descent: Y descent / Diastlc collapse: After S2
X descent is due to: Atrial relaxation & downward
movement of Valves during V systole
Wave Pattern
A
Large A waves
Regular Cannon waves
Irregular Cannon wave
Condition
TS,PS,Pulm Hyptn
Junctional Rhythm
Complete HB
V
X
Y
Absent A waves
Large V waves
Increased Prominence
Decreased Prominence
Rapid Descent
(Friedreichs sign)
Slow descent
AF
TR
C tamponade & C
pericarditis
TR, AF, RVF
TR, C. PeriC
TS, C.tamponade
Campbell de morgans spots / Cherry angiomas

Old age, NOT blanch, Ant abd wall & are Raised
Venous star: high V pressure states, NOT blanch,
Legs & lower part of abd, Fill from Periphery to
center
Rose spots: DO blanch on P, Ant abd wall, EF
13
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
Page
20
Central arteriole pressed & release:- Immediate

blanching with filling from Centre to periphery
2% Normal people
Alcoholics
3 rd trimester pregnancy
RA
Thyrotoxicosis
Palmar erythema / liver palms: Thenar &

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 & Crohns
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
migrans (lyme disease), Erythema multiforme
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
15
Subcutaneous Nodules:- NF, Rheumatic nodule,
Rheumatoid nodule, Tophi, Xanthoma,
Cysticercosis, Metastatic deposits
Rheumatic nodule,
Rheumatoid nodule
Smaller
Large
NOT ULCERATE
Freq occur
TENDER
NON TENDER
Skin FREE
FIXED to skin
Assc Active Carditis
Associted +ve RFactor
Sec infection: rare
SEC INFECTION: freq
Extensor surfaces of
Extensor surfaces of
elbows
elbows
Extensor Tendons of
Extensor Tendons of
fingers & Toes
fingers & Toes
Back of head
Back of head
Margins of patella
Margins of patella
Achilles tendon
Achilles tendon
Sacrum
Sacrum
** Bony prominences & Pressure points While lying
on bed
Xanthomas :- PLANOUS (Around eyes) &
TUBEROUS (Wrist, Elbow, Knees, Ankle) **
Prolonged Cholestasis & Familial
Hypercholesterolemia
Tophi:- Helix antihelix, Olecranon process, Acilles
tendon, & other pressure points
Page
21
16
Memory:
1)) Short term / immediate recall / Rote memory
2)) Recent memory
3)) Past memory / Long term / Remote memory
Registration + Retension + Recall + Reproduction
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)
Intelligence: Calculation (Serial 7 substraction test) +
Judgment (Asking what he will he do if car is
coming on him)+ Insight (Awarness about illness) +
Reasoning (tall vs dwarf ??) + Abstract thinking
(meaning of proverbs) + Attention (Tap if number is
repeated twice) + Concentration (20 to 1)
Level of consciousness: Conscious > Confused >
Drowsy > Stupor > Semicoma (respond to only
Internal stimulus) > Coma OR by using GCS
Conscious >15 Deeply comatose 3
Released Reflexes (Dementia, Organic Confusional
states & CONTRALATERAL frontal lobe Lesion)
Grasp
Forced Groping
Avoiding*
By distally moving Stimulus on

radial Aspect of palmar surface
of hand Grasp & Unable to
relax the Grasp Voluntarily
By distally moving stimulus on

Ulnar Aspect of palmar surface
of hand Hand move away
Palmo mental**
Scrathing THENAR Chin
puckering due to MENTALIS
muscle Contraction
Sucking
Lip / Mouth corner
Contraction of Tongue, Jaw
muscles associated with
Swallowing
Rooting
Lips follow Stimulating object
when it is touched
Snout
Tap with Knuckle on Patients
UPPERLIP Pouting of lips due
to ORBICULARIS ORIS muscle
contraction
Myersons /
Uninterrupted / continuous
Glabellar tap
Blinking with tap (N: 3 OR 4)
* CONTRALATERAL parietal Lobe lesion
** NO LOCALIZING Valu
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 & Mullers Sympathetic
Page
22
Horners syndrome: PseudoPtosis + Miosis +

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

2)) Diabetes Complicating pregnancy
2
OBSTERTRICS
3)) Heart diseases Complicating

pregnancy
4)) Anemia Complicating pregnancy
5)) Bad obstetric History
6)) Hypertensive disorders Complicating
pregnancy
Page
23
7)) Breech presentation
Previous LSCS
Tava / 22 / House wife/ ECIL / SE IV.
W/O Yakub
With 6yrs of marital status & is G3P1L1
having her
LMP as 5/2/12 (regular cycles) &
EDD: 11/11/12 Came with a
C/C:
This lady was admitted for safe institutional delivery
in view of previous CS
H/P/I:
H/O suprapubic pain from 1 week dragging type ,
continouswhich is not disturbing sleep, radiating to
back & aggravated on lifting weights & relived on
taking rest.
No H/O burning micturition / dysuria / fever with
chills & rigor
No H/O vaginal bleed
No H/O shoulder pain
Page
24
OBSTETRIC H/O:
Past pregnancies:1st 1 yr after marriage & Spontaneous Conception
confirmed by local doctor & booked case of Gandhi
from 5m of gestation. At term she had bleeding PV
with meconium stained liquor & obstructed labour.
Then she went emergency LSCS in Gandhi hospital
& she has given birth to male child, cried
immediately with 2.5 kg weight & breast feeding
initiated 3 hrs after delivery. No blood tranfusions
Stitches are removed on 6 th day &
she stayed in hospital for 7 days
puerperal period is uneventful.
Baby is healthy & No nicu admissions & vaccinated
breast fed continued for 2 yrs
2 nd pregnancy.
2 yrs after & Spontaneous Conception confirmed by
local doctor this time she had GTN & underwent
Elective LSCS in Gandhi hospital because of previous
LSCS. she has given birth to female child, cried
immediately with 1.75 kg weight & breast feeding
initiated immediately after delivery.
No blood tranfusions
After 2 days baby died, cause Unknown

Stitches are removed on 6 th day &
She stayed in hospital for 15 days because of GHTN
& she stopped anti hypertensive drugs for 6 more
days & discontinued as per doctor advice
puerperal period is uneventful
present pregnancy:Spontaneous Conception
With episodes of vomiting (5 6 times/day)1m &
No H/O nausea / morning sickness
No H/O fever / burning micturition
No H/O bleeding PV / White discharge
No H/O radiation exposure
No H/O Drug usage
No H/O leg swelling In 1st 3 months &
In next 3 Months there was
No H/O bleeding / draining Pv
No H/O leg swelling
No H/O dyspnoea / palpitations
Quickening in 5m &
TT 1st dose in 5m
USG -6m &
In 3 rd trimester
No H/O leg swelling
No H/O blood transfusions
TT 2 nd dose in 8m
MENSTRUAL H/O :
Attained Menarche at 12 yrs of age. 3/30..
4 pads / day
No H/O white discharge
No H/O clot passage
PAST H/O:
NO H/O HTN
NO H/O DM, TB, IHD, RHD, epilepsy, chest pain /
Jaundice & bleeding disorders
DRUG H/O:
Took IFA Tab.
FAMILY H/O: Not significant
PERSONAL H/O:
Diet: mixed, appetite: reduced
B/B: regular, Sleep: disturbed
Addictions: Chronic smoker & Non alcoholic &

NON consangious marriage
Respiratory Examination: BLAE +ve & N vesicular

sounds heard with No adventitious sounds
GCOE:
Patient is C/C/C.
Moderately built & with
P (+) I (-) C (-) C (-) K (-) L (-)
Bilateral pedal oedema, Pitting type
which is upto knee
No thyroid enlargement
Breast Normal
Spine & gait Normal
Vitals afebrile,
HR: 80/min. N in volume, character, & rhythm No
RR/RF delay No vessel wall thickening
BP: 120/86 mm hg RUL: Sitting
RR: 19/min
JVP: NOT raised
Diagnosis:
A 22 yr Old G3P1L1D1 with term gestation with
fundal height corresponding with gestational age
with 2 previous LSCS Done for NON recurrent
Indications with No other Obstetric complications
OBSTETRIC EXAMINATION:
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
A curvilinear suprapubic scar is seen which is about
7 cm in length & No puckering which seen healed
by primary intention
No other scars / Sinuses
No engorged Veins
Palpation:
Scar tenderness:- absent
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 babys back & On right side multiple fetal
parts felt
1st pelvic grip hard ballotable, mass probably
cephalic pole
Discussion:
Whatever is abd inscison : tenderness must be seen
on lower segment & From lateral to centre
1 14 (1st T) 28 (2 nd T)- 40 (3 rd T)
Cesarean delivery : birth of a fetus through incisions
in the abdominal wall (laparotomy) and the uterine
wall (hysterotomy). This definition does not include
removal of the fetus from abdominal cavity in case
of rupture of the uterus or in abdominal pregnancy.
2)) Julis caeser , Lex caesaria, Latin
3)) Incidence rising:
-average maternal age is rising,
-electronic fetal monitoring is widespread.
-Most fetuses presenting as breech are now
delivered by caesarean,
-The incidence of forceps and vacuum deliveries has
-Rates of labor induction continue to rise
-prevalence of obesity has risen
Complete uterine involution and restoration of
anatomy may require at least 6 months
4)) Steps:
Different approaches
1)) Pfannensteil kerr technique usually
2)) Joel-Cohen and
3)) Misgav- Ladach methods
Page
25
Ausultation Fetal heart sounds 136/min regular

Per veginal Examination NOT done
CVS examination- S1 & S2 heard. Murmer in pulm
area (haemic murmer) No other murmers heard
Abdominal Incision
Infraumbilical midline vertical (quickest) or a
suprapubic transverse incision (modified Pfannenstiel
incision, the skin and subcutaneous tissue are incised
Page
26
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 (Maylards 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 flapis
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
using gentle suction, rectus muscles are allowed to
fall into place
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
Contraindications For VBAC

Absolute: prior classical cesarean, previous
uterine rupture, lack of resources to perform
emergency cesarean delivery during labor.
Relative: two prior uterine surgeries with no
previous vaginal delivery.
b
a
a: Lscs
b: Lscs / Classical
Disadvantages of elective C section:

1)) Iatrogenic prematurity
2)) Atonic PPH
3)) Drainage of lochia difficult (since cervix is not
dilated)
4)) Difficulty in suturing (lower segment is not
formed)
TOLAC (Trial of labour after C section)
C section indications (recurrent / NON recurrent)
Heart disease Complicating pregnancy

Jyothi / 20 / agricultural labour / Warangal / SE IV.
With 10months of marital status & is Primi
having her
Page
27
C/C:
Difficulty in breathing from 2 days
H/P/I:
Patient was apparently asymptomatic 10 days back
then she developed pain in abdomen, so she went
to local govt hosptl (Siddipet) where she was having
her regular ANC, from where she was referred to
our hosptl.
Pain in hypogastric region , sudden in onset, Aching
type, continuous, Not disturbing sleep, radiation to
back, No shift of pain & Not associated with fever /
Vomitings / Burning micturition. No aggravating
factors , relieved on medication. Now There is NO
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
No H/O orthopnoea / PND attacks
No H/O syncopal attacks
No H/O anaemia (thella paskarlu)
OBSTETRIC H/O:
Spontaneous Conception .
Pregnancy confirmed by local doctor
With episodes of vomiting (3 4/days) for 2m &
No H/O Drug usage
No H/O leg swelling
Quickening in 5m &
TT 1st dose in 5m
USG -6m &
In 3 rd trimester
No H/O leg swelling
TT 2 nd dose in 8m
MENSTRUAL H/O :
Attained Menarche at 12 yrs of age. 5/30..
2 pads / day & with Congestive dysmenorrhoea
No H/O clot passage
PAST H/O:
H/O HTN diagnosed at 3m
NO H/O similar complaints in past,
DRUG H/O:
Taking IFA
PERSONAL H/O:
Addictions: Chronic smoker & Non alcoholic &
NON consanginous marriage
GCOE:
Patient is C/C/C.
P (+) I (-) C (-) C (-) K (-) L (-)
Bilateral pedal oedema, Pitting type which is just
above ankle
Spine & gait Normal
Vitals
afebrile,
RR: 16/min
JVP: NOT raised
Page
28
On inspection:
Umbilicus slit like & everted
No scars / Sinuses
No engorged Veins
Palpation:
parts felt

cephalic pole
Ausultation Fetal heart sounds - ??
Perveginal Examination NOT done
CVS examination
Inspection NOT done
Palpation - Apex beat Not shifted (4 th ics 2cm lateral
to MCL) & Parasternal impulse absent
Auscultation:
Area
S1
S2
Murmur
Mitral
No
Tricuspid
No
Pulmonary
No
Aortic
N
(Split ?)
+
Soft, ESM,
grade 4 & No
radiation
Diagnosis:
A 20 yr Old primi with term gestation with fundal
height corresponding with gestational age with
Heart Disease probably AS complicating pregnancy
Discussion
Hemodynamic Changes (%)
Cardiac output +43
Heart rate
+17
Left ventricular stroke work index +17
Vascular resistance
Systemic
-21
Pulmonary
-34
Mean arterial pressure
+4
Colloid osmotic pressure -14
Parameter Change (Percent)
1)) New York Heart Association (NYHA)
Class I. Uncompromisedno limitation of
physical activity:
These women do not have symptoms of cardiac

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 compromisedinability 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
Page
29
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
when LMWH or UFH is resumed.
** 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,

and bacterial endocarditis prophylaxis may be
required.
IE Prophylaxis with Dental Procedures

(1) Prosthetic heart valve
(2) Previous infective endocarditis
(3) Certain forms of congenital heart lesions:
Unrepaired cardiac lesions causing cyanotic heart
disease, including palliative shunts and conduits
Repaired defect with prosthetic: for 6 months
following repair procedure.
Repaired defect with residual defects.
** Prophylaxis is recommended for procedures that
involve manipulation of gingival tissue / periapical
tooth region
with any of the following cardiac conditions:
Hypertensive disorders Complicating

pregnancy
Rajashri/ 22 / House wife/ Kurnool / SE IV.
W/O rajashekar
with 3yrs of marital status & is G1P0L0
having her
Page
30
C/C:
in view of Increased Blood pressure
H/P/I: Patient is apparently assymptomatic
2months back & having her regular ANC at Gandhi
hospital & was diagnosied as having high bp in her
7 th month
No H/O Giddiness
No H/O epigastric distress
No H/O Vision blurring & headache
No H/O Seizure episodes
No H/O Swelling of face & limbs

No H/O Oliguria
No H/O Bleeding PV / easy bruisability
OBSTETRIC H/O:
Confirmed by local doctor
No H/O Drug usage
No H/O leg swelling
Quickening in 5m &
TT 1st dose in 5m
USG -6m &
In 3 rd trimester
No H/O leg swelling
TT 2 nd dose in 8m
MENSTRUAL H/O :
Attained Menarche at 11 yrs of age.
3/28.. 4 pads / day
No H/O clot passage
PAST H/O:
NO H/O HTN
DRUG H/O:
Took IFA Tab.
PERSONAL H/O:
Addictions: Non Smoker, alcoholic & NON

consangious marriage

GCOE:
Patient is C/C/C.
P (+) I (-) C (-) C (-) K (-) L (-)
which is upto ankle
Breast Normal
Spine & gait Normal
Diagnosis: A 22 yr Old Primi with term gestation

with fundal height corresponding with gestational
age with Hypertension complicating pregnancy,
With No signs of imminent eclampsia
Vitals
afebrile,
RR: 19/min
JVP: NOT raised
On inspection:
Flanks full
No engorged Veins
Palpation:
parts felt
cephalic pole
Ausultation Fetal heart sounds ??
Page
31

CVS examination- S1 & S2 heard. No murmers heard
Discussion
Working Group classification
1. Gestational hypertensionformerly termed PIH If
preeclampsia syndrome does not develop and
hypertension resolves by 12 weeks postpartum ,
it is redesignated as transient hypertension
2. Preeclampsia (some have atypical preeclampsia
with all aspects of the syndrome, but without
hypertension or proteinuria, or both) and eclampsia
syndrome
3. Preeclampsia syndrome superimposed on chronic
hypertension
4. Chronic hypertension
** Proteinuria is defined by 24-hour urinary protein
excretion exceeding 300 mg, a urine P/C ratio of
>/=0.3, or persistent 30 mg/dL (1+ dipstick)
protein in random urine samples
Risk Factors
obesity, multifetal gestation, maternal age older
than 35 years, and African-American ethnicity,
*** smoking & Placenta previa
reduced risk of hypertension during pregnancy
2)) Preeclampsia often affects young and nulliparous

women, whereas older women are at greater risk
for chronic hypertension with superimposed
preeclampsia,
3)) Preeclampsia syndrome is a two-stage disorder.
Stage 1 (preclinical) is caused by faulty
endovasculartrophoblastic remodeling that
downstream causes the stage 2 clinical syndrome &
Stage 2 is susceptible to modification by
preexisting maternal conditions that include cardiac

or renal disease, diabetes, obesity, or hereditary
influences
Hemoconcentration is a hallmark of eclampsia.
Preeclampsia (culmination of factors that likely
involve a number of maternal, placental, and fetal

factors)
Placental implantation with abnormal
trophoblastic invasion of uterine vessels.
(incomplete invasion of the spiral arteriolar wall by
extravillous trophoblasts and results in a smallcaliber
vessels with resistance)
Immunological maladaptive tolerance between
maternal, paternal (placental), and fetal tissues
Maternal maladaptation to cardiovascular or
inflammatory changes of normal pregnancy
Genetic factors including inherited predisposing
genes as well as epigenetic influences.
** This finally leads to release unknown factor
(s)likely placental in originare secreted into the
maternal circulation and provoke widespread
activation and dysfunction of the vascular
endothelium: Increased pressor response,Vasospasm
imbalance between NO & PG levels & between
Angiogenic and Antiangiogenic Proteins
Most importantly overproduction of at least two

antiangiogenic peptides from trophoblastic tissue
that are released into maternal circulation.
a)) Soluble Fms-like tyrosine kinase 1 (sFlt-1)
b)) Soluble endoglin (sEng)
Both these levels are increased before clinical
syndrome develops
Page
32
Breech presentation
Sneha/ 25 / House wife/ Nalgonda / SE IV.
W/O Suresh chandra
having her

C/C:
in view of Twin pregnancy
H/P/I:
No H/O any menstrual abnormalities befor
conception
No H/O similar complaint in past pregnancies
No H/O Cervical discharge
OBSTETRIC H/O:
present pregnancy:- 2yr after LCB
Spontaneous Conception
Confirmed by a local doctor.
No H/O Drug usage
No H/O leg swelling
Quickening in 5m &
TT 1st dose in 5m
USG -6m &
In 3 rd trimester
No H/O leg swelling
TT 2 nd dose in 8m
Past pregnancies
1st pregnancy - 1 yr after marraige
Spontaneous coneption.
Confirmed by a local doctor. Booked case
Pregnancy was uneventful & delivered at home by
local dai & baby cried immediately - male - 3kg
immunized & healthy. Puerpurium also uneventful.
2nd pregnancy - 1 yr after 1st child birth
Spontaneous coneption.
Confirmed by a local doctor.

Had regular ANC
Pregnancy was uneventful & delivered at home by
local dai & baby cried immediately - female - 2.5kg
immunized & healthy. Puerpurium also uneventful
MENSTRUAL H/O :
4/28.. 3 pads / day
No H/O clot passage
PAST H/O:
NO H/O HTN
DRUG H/O:
Took IFA Tab.
PERSONAL H/O:
GCOE:
Patient is C/C/C.
P (+) I (-) C (-) C (-) K (-) L (-)
which is upto ankle
Breast Normal
Spine & gait Normal
Vitals
afebrile,
RR: 19/min
JVP: NOT raised
Page
33
On inspection:
Flanks full
No engorged Veins
Palpation:
fundal grip hard ballotable, mass probably
cephalic pole
parts felt
1st pelvic grip Soft, Non ballotable, Broad mass
Diagnosis: A 25 yr old Pregnant women with

G3P2L1 came with uncomplicated breech
presentation for safe institutional delivery
Discussion
COMPLICATIONS
In the persistent breech presentation, an increased
frequency of the following complications can be
anticipated:
Prolapsed cord
Placenta previa
Congenital anomalies
Uterine anomalies and tumors
Difficult delivery
Increased maternal and perinatal morbidity
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.
Total 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
Page
34
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 dysfunctionsome 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
trauma
10. A request for sterilization
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 oclock, which is
followed by a second incision at 10 o'clock.
Infrequently,
an additional incision is required at 6 oclock.
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

visible.
The appearance of one axilla indicates that the
time has arrived for delivery of the shoulders. It
makes little difference which shoulder is delivered
first.
Frank Breech Extraction:
Frank breech decomposition using the Pinard
maneuver.
Two fingers are inserted along one extremity to the
knee, which is then pushed away from the midline
after spontaneous flexion. Traction is used to deliver
a foot into the vagina
Diabetes complicating pregnancy

Laxmi/ 27 / House wife/ zaheerabad/ SE IV.
W/O nagarjuna
having her
C/C:
in view of Twin pregnancy
Page
35
H/P/I:
OBSTETRIC H/O:
No H/O Drug usage
No H/O leg swelling
Quickening in 5m &
TT 1st dose in 5m
USG -6m &
In 3 rd trimester
No H/O leg swelling
TT 2 nd dose in 8m
MENSTRUAL H/O :
3/28.. 4 pads / day
No H/O clot passage
PAST H/O:
NO H/O HTN
DRUG H/O:
Took IFA Tab.
PERSONAL H/O:
GCOE:
Patient is C/C/C.
P (+) I (-) C (-) C (-) K (-) L (-)
which is upto ankle
Breast Normal
Spine & gait Normal
Vitals
afebrile,
RR: 19/min
JVP: NOT raised
On inspection:
Flanks full
No engorged Veins
Palpation:
parts felt
cephalic pole
Discussion
There is increasing support for the use of glyburide
as an alternative to insulin in the management of
gestational diabetes
Page
36
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 2.5mg/wk increments until 10 mg/d, then switch to
twice-daily dosing until maximum of 20 mg/d
reached.
** 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 100150 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

Average Risk: Perform blood glucose testing at 24
to 28 weeks using either:
Two-step procedure: 50-g oral glucose challenge
test (GCT), followed by a diagnostic 100-g oral
glucose tolerance test for those meeting the
threshold value in the GCT.
Onestep procedure: Diagnostic 100-g oral
glucose tolerance test performed on all subjects.
High Risk: Perform blood glucose testing as soon
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.
Time
Fasting
! hr
2 hr
3 hr
100-g Glucose
95
180
155
140
75-g Glucose
95
180
155
-
** The test should be performed in the morning

after an overnight fast of at least 8 h
but not more than 14 h and after at least 3 days of
unrestricted diet and physical activity.
*** Two or more of the venous plasma glucose
concentrations indicated below must be

met or exceeded for a positive diagnosis
Page
37
An ideal dietary composition is 55 percent

carbohydrate, 20 percent protein, and
25 percent fat with less than 10 percent as saturated
fat.
Fluids
Isotonic sodium chloride
Total replacement in first 12 hours of 46 L
1 L in first hour
5001000 mL/h for 24 hours
250 mL/h until 80 percent replaced
Glucose
5-percent dextrose in normal saline
Potassium
Bicarbonate (if pH is <7.1)
Twin Pregnancy
In women with a uterus that appears large for
gestational age, the following possibilities are
considered:
1. Multiple fetuses
2. Elevation of the uterus by a distended bladder
3. Inaccurate menstrual history
4. Hydramnios
5. Hydatidiform mole
6. Uterine leiomyomas
7. A closely attached adnexal mass
8. Fetal macrosomia (late in pregnancy)
Pregnancy outcome:
1)) Spontaneous abortion
Management of Db KA in pregnancy
2)) Malformations (According to Schinzel anomalies

in monochorionic twins generally fall into one of
three categories )
** Obtain arterial blood gases to document degree

of acidosis present; measure glucose, ketones, and
electrolyte levels at 1- to 2-hour intervals
Defects resulting from

twinning itself
twinning, acardiac
anomaly, neural-tube
defects
Insulin
Low-dose, intravenous
Loading dose: 0.20.4 U/kg
Maintenance: 210 U/h
Defects resulting from

vascular interchange
microcephaly,
hydranencephaly,
between monochorionic
twins
intestinal atresia, aplasia

cutis,
Defects may develop

from fetal crowding**
Talipes equinovarus
(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).
Page
38
( 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)
TRAP sequence is caused by a large artery-toartery
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-
oligohydramniospoly-olisyndrome
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 cmabove the 95th

percentilewas 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
Monochorionic twins:
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
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
Separate
Conjoined
Ventral
Lateral
Dorsal
caudal
External Internal
Trap
Parasite
TTTS
Fetus in situ
Page
39
Antepartum management
1)) Diet
2)) Mangaemnt of hypertension
(fetal number and placental mass are involved in the
pathogenesis of preeclampsia. With multifetal
gestation, hypertension not only develops more
often but also tends to develop earlier and to be
more severe.)
3)) Antepartum Surveillance: (An AFI of <8 cm
Iron-deficiency anemia
Anemia caused by acute blood loss
Anemia of inflammation or malignancy
Megaloblastic anemia
Acquired hemolytic anemia (Cold-agglutinin disease
may be induced by Mycoplasma pneumoniae or
EBV / Drug induced : penicillin, cephalosporins)
Aplastic or hypoplastic anemia
Hereditary
Thalassemias
Sickle-cell hemoglobinopathies
Other hemoglobinopathies
Hereditary hemolytic anemias
Amount of iron diverted to the
fetus is similar in a normal and in an iron-deficient

mother, the newborn infant of a severely anemic
mother does not suffer from iron-deficiency anemia
& neonatal iron stores are related to maternal iron
status and to timing of cord clamping.
Sickle cell anemia:
Pregnancy complications
Cerebral vein thrombosis
Pneumonia
Pyelonephritis
deep-venous thrombosis
Pulmonary embolism
Sepsis syndrome
Delivery Complications
Gestational hypertension/preeclampsia
Eclampsia
Placental abruption
Preterm delivery
Fetal-growth restriction
Bad Obstetric History

Traditionally, recurrent abortion has been
defined as the occurrence of three or more
clinically recognized pregnancy losses before 20
weeks from the last menstrual period. Using this
definition, recurrent pregnancy loss (RPL) occurs
in approximately 1 in 300 pregnancies
Causes of recurrent abortions
1. Chromosomal
2. Single gene defects
3 Multifactorial
Page
40
Anatomic factors
1. Congenital
a. Incomplete mullerian fusion or septum resorption
b. Uterine artery anomalies
c. Cervical incompetence
2. Acquired
a. Cervical incompetence
b. Synechiae
c. Leiomyomas
d. Adenomyosis
Endocrine
1. Luteal phase insufficiency
2. PCOD
3. Other androgen disorders
4. Diabetes mellitus
5. Thyroid disorders
6. Prolactin disorders
Infectious factors
Immunologic factors
1. Cellular mechanisms
1. Th1 immune responses to reproductive
antigens (embryo or trophoblast)
2. Th2 cytokine or growth factor deficiency
2. Humoral mechanisms
a. Antiphospholipid antibodies
b. Antithyroid antibodies
d. Antitrophoblast antibodies
e. Blocking antibody deficiency
Thrombotic factors
Other factors
1. Altered uterine receptivity (integrins, adhesion

molecules)
2. Environmental (Toxins, Smoking)
3. Placental abnormalities (circumvallate,
marginate)
4. Medical illnesses (cardiac, renal hematologic)
5. Dyssynchronous fertilization
For a patient to be diagnosed with APAS, one or

more clinical and one or more laboratory criteria
must be present (BARDAS Criteria) :
Clinical
One or more confirmed episode of vascular
thrombosis of any type
a)) Venous
b)) Arterial
c)) Small vessel
Pregnancy complications
a)) Three or more consecutive spontaneous
pregnancy losses at less than 10 weeks of gestation
b)) One or more fetal deaths at greater than 10
weeks of gestation
c)) One or more preterm births at less than 34
weeks of gestation secondary to severe preeclampsia
or placental insufficiency
Laboratory
Positive plasma levels of anticardiolipin antibodies
of the IgG or IgM isotype at medium to high levels
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:-
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:
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
Page
41
Physical Examination
1.Obesity
2.Hirsutism/acanthosis
3.Thyroid examination
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
Terminology
1. Uterine tachysystole is defined as >6 contractions
in a 10-minute period.
2. Uterine hypertonus is described as a single
contraction lasting longer than 2 minutes.
3. Uterine hyperstimulation is when either condition
leads to a nonreassuring fetal heart rate pattern
As an alternate to the Bishop score,

Hatfields Score for cervical length was used
Where Cervical length is assessed by
transvaginal sonography and used to predict
successful induction.
** However it was found that cervical length
determination by sonography was not superior to
use of the Bishop score
Technique & Agent
Route
-Transcervical 36F
catheter* *
-Extra-amnionic Saline
Infusion (EASI)**
-Hygroscopic Cervical
dilators (Laminaria,
magnesium Sulphate)**
- Membrane Stripping for
Labor Induction
** Improve Bishop score (Promote cervical
ripening)
*** Insert has shorter I-D times than gel
LABOR INDUCTION AND AUGMENTATION

WITH OXYTOCIN
In most instances, pre-induction cervical ripening

and labor induction are simply a continuum. Often,
as described above, ripening will also stimulate
labor. If not, however, induction or augmentation
may be continued with oxytocin
Regimen
Pharmacological**
-Prostaglandin E2
(dinoprostone)
(GEL Prepidil /
INSERT - Cervidil)
-Prostaglandin E1
(MisoprostolCytotec)
(TABLET 100 / 200 g)
Page
42
-Nitric Oxide Donors

(isosorbide mononitrate
Starting Incremental
dose
increase
Interval
(Min)
0.51.5
15 - 40
4, 8, 12, 16, 20
25, 30
15
Cervical 0.5 mg;

repeat in 6 hr; permit
3 doses total Posterior
fornix, 10 mg
Low dose
Vaginal, 25 g; repeat
36 hr prn Oral, 50
100 g; repeat 36 hr
prn
** With hyperstimulation and after oxytocin

infusion is discontinued, it is restarted at 1/2 the
previous dose and increased at 3 mU/min
incremental doses.
***Hyperstimulation is more common with shorter
intervals.
High dose
4
4.5
6
4
4.5
6
Quickening + 22w = EDD

For twins: Gravida 1 para 2
and glyceryl Trinitrate)
Grade
Level (upto) edema
15
15 - 30
20 40
1
2
3
4
Ankle
Knee
Ant abd wall
anasarca
Physiological
Grade 1
During evening times
Disappears on early
morning / 8hrs of bed
rest
> 28 w (usually)
Venous compression,
harmones
Pathological
>1
During morning times
also
Dont disappear
Mid trimester also
Anemia, pre eclampsia,
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 dont 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)
Page
43
Munrokher muller test : NO BRIM cpd

Unengaged head reasons (primi) **
Post position of occiput

Pelvic contraction
Pelvic tumours
High pelvic inclination
Placenta previa
Conjoined twins
Deflexed head
Fetal anomalies (Hydrocephalus)
Wrong dates
** Even at term
1)) Prolapse Uterus
Page
44
GYNECOLGY
2)) DUB
3)) Fibroid uterus
4)) Ovarian mass
Prolapse
Ananthamma/65/nizamabad/SEIV &
labourer 10 yrs back.
C/C:
Mass per vaginum 4 yrs
H/P/I:
Patient was apparently assymptomatic 4 yrs back
then she noticed mass per veginum which is initially
lemon size gradually progressive to reach present
size.
Reducable manually & increases in size on lifting
weights & coughing
H/O back ache initially for 1st 2 yrs which was
localized aggravated on standing & relived on
sleeping Now there is No back ache
H/O difficulty in micturition on straining
H/O lifting weights for 30 yrs
No H/O Chronic cough
No H/O any discharge PV
NO H/O wound on mass PV
NO H/O constipation
NO H/O leaking of urine on coughing
NO H/O irreducibility episodes
NO H/O fever with chills & rigor with burning
micturition
No H/O frequency of micturition
PAST H/O:
NO H/O HTN
Page
45
MENSTRUAL H/O:
Reached menopause 10 yrs back
previous cycles - 4/28..
3-4 pads / day
No H/O clot passage
No H/o dysenorrhoea
OBSTETRIC H/O: P3L3
1st pregnancy FTNVD Male - Home Local Dai
45 yrs N baby After 1 yr
2 nd pregnancy FTNVD Male - Home Local Dai
43 yrs N baby After 2 yr
3 rd pregnancy FTNVD female Local Dai 45
yrs N baby After 1 yr

Not sterlized
PERSONAL H/O:
Addictions: Non smoker & Non alcoholic & NON
GCOE:
Patient is C/C/C.
Moderately built & with BMI ??
P (-) I (-) C (-) C (-) K (-) L (-)
Vitals afebrile,
BP: 160/90 mm hg RUL: Supine
RR: 18/min regular
JVP: NOT raised
LOCAL EXAMINATION
Perineal examination:
Scanty pubic hair, gaping introitus,
Atrophic labia majora, Labia minora
Not visible, Pink mass per vaginum with
cervical lips seen
On ant vaginal wall - Keratinization (3*3 cm) seen
& vaginal mucosa atrophic
No urine passage with coughing
P/S: Enterocole & No rectocoele
P/V: Uterus retroverted, Levator ani tone poor.
Puborectalis (at 4 & 8 o clock) poor tone
SYSTEMIC EXAMINATION
CVS examination- S1 & S2 heard. No other murmers
heard
Diagnosis: A 65 yr old post menopausal women

came with P3L3 with 3 degree uterine prolapse
with cystocoele & Enterocoele & also poor pelvic
floor tone.
DISCUSSION:
symphisis & Highest Point on post vaginal

fornix.
Different classifications
1)) Shahs classification
2)) Malpas Classification:
a)) UV prolapse:
ligament weakening
b)) Nulliparous / general:
Muscle weakening
3)) Jaffcoats Classification
4)) POP Q Classification
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.
Three other measurements include genital hiatus,
perineal body, and the total vaginal length.
Accordingly divided into stage 0 stage IV
Treatment
a)) Non surgical (PFMT, pelvic floor muscle tone,
Biofeedback in rectocoele & Pessary:
Pessaries
Page
46
Support and Space filling

1)) Ring pessary (with diaphragm) is
a commonly used support pessary, and
2)) Gelhorn pessary is a commonly used
spacefilling pessary.
** Support pessaries are recommended for
stage I and II prolapse {O,U,R,I pessaries},
*** Spacefilling pessaries are used for stage
III and IV prolapse {X,L,M,N,W,G,F}
Cystocoele &/or rectocoele {J,I}
Pessary measured Bimanually: pubic
b)) Surgical: U2/3, L 1/3 with U1/3 (enterocoele)

M1/3 (Rectocoele) L1/3 (perineal body prolapse)
1)) UV prolapse:
Radical / Waldmeyer
[ >40, >35*]
conservative [Shirodkars surgery No stenosis,
patulous & fothergills surgery Stenosis, patulous]
2)) Nulliparous: Abd / Vaginal sling operations &
org (purandeswars Lat sling) / Inorg (shirodkars
Lat. & Khanna Post)
Decubitus ulcer pathology:
- arterial kinking
- Venous congestion
- trauma
Measurement of supravaginal portion of cervix:
Passing sound upto Internal os (resistance felt)
minus Passing sound into lat fornix (difference gives
the length)
Ovarian mass
Uterine mass
Usually cystic
Usually firm / hard
R/L
Midline
Movable side to side &

also vertcally
Movable side to side
Transmitted movements
-ve
Transmitted movements
+ve
Can feel all borders
Lower border is usually
not felt
Hingorin Sulcus present
between ovarian mass
& uterus
Absent
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
Page
47
Endometriosis & Adenomyosis: Triple

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

2)) Thyroid swelling
3)) Breast swelling
4)) Inguinal hernia
4
SURGERY
5)) Hydrocoele
6)) Salivary gland swelling
7)) PVD (Chronic)
8)) Abdominal lump
Page
48
9)) Ortho Cases
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
Page
49
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
No H/O trauma (orthopedic knee)
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.
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
Family H/O:
No H/O similar complaint in family & No H/O any
chronic illness in family
(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 of medial aspect of R leg extending upto
lower 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,

surrounding skin healed scars present
discoloration of skin from toe to 2 cm above ankle
is seen & hair loss on foot & brittle nails - present
Swellings disappear spontaneously on lying down
NO redness along the swellings
NO areas of any Blow outs / NO V.falre are visible
NO swelling visible at saphaneous opening
Other limb appear N on inspection
2)) Palpation:
NO local rise of temperature
NO redness along the swellings / ulcer area
No oedema / Tenderness on lower part leg
Brodie trendelenberg test
Test 1 : +ve
Test 2 : +ve
Multiple tourniquet test: Below knee perforator in
incompetent
Modified perthes test
Schwarz test: - ve
Fegans test: a defect in deep fascia is felt 2cm
below tibial tuberosity on medial side of leg
Morrisays cough impulse test: - ve
Homans sign: - ve
Moses sign: - ve
Neuhofs sign: -ve
All Peripheral pulses: palpable (R & L)
Other Limb: N
3)) percussion: Schwartz -ve
4)) Auscultation: Continous Murmur / Bruie absent
at saphenofemoral junction.
5)) Regional Lymph nodes examination:
Page
50
Inguinal (Upper M, Upper L, Vertical: Not palpable)

Popliteal: Not palpable
6)) Measurements Mid leg circumference
R(31cm)/L( 29cm)
7)) Movements range of movements of lower
limb are with in N range

NO free fluid
BLAE: N &
Diagnosis:
Primary
Right sided
Partial varicosity of Great Saphenous Vein with
Competent SFJ and Incompetent below knee
perforators with
Complicating as venous Ulcer
Discussion:
If Skin changes : +ve Chronic venous insufficiency
(CVI) Treatment Only surgery NO role of
conservative truss usage.
Flush: Close / near to

Short saphenous Vein stripping: NOT done usually
1)) Incompetent perforators are hardly found in
association with SSV
2)) Causes long standing oedema
3)) May permanently damage Sural Nerve
Varicose Ulcer management:
Bisgard Conservative management surgical
correction of varicose veins Split skin graft (last)
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.
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:
Page
51
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.
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
Haemosiderin
Eczema & Dermatitis
WBC (mast cells,monocytes)
Fibrin cuff
release of ROS & proteolysis E
Diffusion block
Hypoxia
Poor repair
tissue damage (ulcer)
Loss of SC fat
Std Doppler is NOT AN ACCURATE method of

establishing Incompetence in SSV coz of its variable
termination so Duplex scans is mandatory
Another cause of ulcer has to be sought is there is
no surrounding evidence of Lipodermatosclerosis
(Thickening, indurations, inflammation &
pigmentation) / ankle flare.
52
Venous entrapment: Axillary (1st rib & clavicle) &

Popliteal vein (abnormal insertion of Gastrocnemius
muscle) Sweeling of limb after exercise
Page
Gaiters area: area between calf muscles & ankle:

COCKETT PERFORATORS JOIN POST TIBIAL VEIN
& POST. ARCH VEIN
Ulcers due to LSV Varicosity: medial side of calf

Ulcers due to SSV Varicosity: lateral side
Post thrombotic: Any part of calf skin
Operative Notes:
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
veins is dissected and exposed. Next, the greater
saphenous vein is divided between clamps
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
Page
53
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
referred to Gandhi hospital
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
Compressibility: -ve
Fluctuation: +ve
Transillumination: +ve.
Testis: palpable & testicular sensation +ve
3)) Percussion: DULL
4)) Local lymph nodes (inguinal): NOT palpable.
Abdominal examination:
NO free fluid
PR: Not done
Diagnosis:
R sided
primary
uncomplicated
vaginal hydrocoele
Discussion
Page
54
Hydrocoele: FLUCTUATION +ve (trans

illumination may/may not +ve).
In tense swelling fluctuation is difficult to perform
but present.
Primary: Moderate to large, comparably tense, testis
NOT palpable, area of constriction may present
(DUMBBELL: NO explanation),
Causative history is absent.
Vaginal: getting above swelling +ve Swelling is
confined to scrotum.
(To tell hydrocoele never tell coz getting above
swelling is +ve it just tell that the swelling is
confined to scrotum)
Transillumination +ve: Clear fluid + sac is thin
(if any of them / both ve: Test ve).
N vaginal fluid: 3 5 ml.
N physiology: visceral layer secretes Parietal layer
absorbs. (Secretion secondary & absorption
primary hydrocoele)
Treatment:
Secondary Small swelling: conservative,
Tumour: treat tumour (NO separate treatment for
hydrocoele),
Infections: treat it (even if then persists Surgical
management), Haematocoele late complication
testicular atrophy.
[In seminoma testis NO BIOPSY/FNAC scrotum
lymphatic drainage is inguinal, testis lymphatic
drainage is para aortic LN so if done. tumor cells
reach tract then skin finally paraoartic LN
UPSTAGING of cancer.]
Operation principle: Evacuation + NO sac + area

of absorption (Now fluid is exposed to undersurface
of skin absorption).
In Congenital hydrocoele:
treatment is HERNIOTOMY
Getting above swelling: -ve
Cough impulse: -ve (By which Congenital inguinal
hernia is distinguished)
Fluctuation: +ve
Reducability: +ve
In infantile Hydrocoele: treatment is EVACUATION
+ SAC EVERSION
In lords plication usually drain is NOT kept post
operatively. [ lords fibrous band: in midgut
malrotation & Lords fundoplication in GERD]
Usually CORRUGATED rubber drainage tube is kept
(BLUE colour).
Testicular sensation: by applying pressure on testis
pain is felt in EPIGASTRIC region.
Scrotal contents: Testis with its coverings +
epididymis + lower part of spermatic cord.
During palpation: we feel cord:- Vas + fibres of
cremastric muscle.
Sometimes Cord may appear thickened: because of
hypertrophied cremastric muscles due to chronically
bearing weight of big swelling.
Cord thickened + Appear nodular : Tuberculosis.
Urogenital TB: always secondary to primary focus
(pulm/renal).
Decrease of swelling size spontaneously on lying

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)
Page
55
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
+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 lodds operation drain is not kept usually.
Difference between lodds & jaboulys 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
DM, TB, epilepsy, chest pain. Jaundice & bleeding
disorders
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
Page
56
Family H/O:
(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 (-)
Cnj N & pupils are N & reacting equally.
Eyes & eye lids are N, Eye Movements : N range
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
(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. [pizollos 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
Pembertons 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
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
Kochers 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.

4)) Musculoskeletal system:
N gait with Spine Normal & No long bone
tenderness

NO Lumps palpable / Palpable hepatomegaly
NO free fluid
BLAE: N &
Discussion
Trachea in midline:
1)) inspection: chin , laryngeal prominence &
Suprasternal Notch: same line
Diagnosis: A case of
Solitary
Thyroid nodule (with D/D: adenoma, Tense thyroid
cyst, Localized hashimotos, early differentiated
carcinoma, dominant nodule of MNG)
involving isthmus &
Patient is in Euthyroid state clinically
2)) palpation: trail sign & triple finger test

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

Inferior pedicle.
Pretracheal fascia is cut during surgery vertically to

enter thyroid, How do we know that we entered
Thyroid: VENOUS PLEXUS IS SEEN OVER.
We flex neck in standard method of palpation
1)) Relax deep cervical fascia
2)) relax sternocleidomastoid.
In diagnosis:
1)) Number
2)) Thyroid yes/No
3)) Location
4)) Physiological status
5)) benign/malignant
6)) D/D.
Thyroid enlargement occurs posterior mainly

because anterior layer is tough & not yielding &
posterior layer is thin.
In unilateral swelling dysphagia never occurs
Esophagus is a muscular tube & is easily displacable.
The thyroid swelling may sometimes becomes

prominent on strap muscles contraction
(strapsternohyoid, sternothyroid, and superior belly
of the omohyoid):
1)) if present exactly in midline (As in this case)
On muscles contraction fascia relaxes swelling
becomes more prominent
2)) if part of gland is in gap zone (arrow marks) &
remaining is behind strap muscles then
On muscles contraction pushing Out of the part
behind muscles swelling becomes more
prominent. IN this case Fascia tense test must be
In Inspection (description)
1)) Swellling
2)) Movement
3)) Lower margin comment
4)) Trachea
5)) Other swelling.
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.
Page
58
Lobe involved is based on trachea position not based on midline
Recurrent laryngeal nerve is usually found in

Simons triangle, which is formed by the inferior
thyroid artery superiorly, the common carotid
artery laterally, and the esophagus medially.
In retrosternal Goitre Duspnoe occur when lying on

1 side only. Most diagnostic feature is Presence of
engorged veins on upper chest.
There is NO real dyspnoea, it is rather called

obstructive breathing.
Indications for surgery in NON NODULAR goiter

(partial thyroidectomy):
1)) rapid increase in size due to intraglandular
hemorrhage
2)) Cosmetic reasons
3)) pressure symptoms +ve
4)) Intrathoracic extension causing respiratory
obstruction.
Pre op measures:
1)) Routine workup
2)) Serum Ca levels (detect hyperparathyroidism
may coexist.)
3)) Indirect laryngoscopy is performed
preoperatively to evaluate the mobility of the vocal
cords and detect unsuspected vocal cord paralysis (if
paralysis is present, it is essential not to damage the
recurrent laryngeal nerve supplying the normal
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
sympathetic overdrive such as tachycardia, a betablocker such as propranolol is added.
5)) Physiology : Ingested Iodine iodide iodine
trapping PEROXIDASE iodine MIT & DIT
MIT + DIT TIT [T3] (oxidative condensation)
DIT + MIT R. TIT [R. T3].
Page
59
Thyroid gland: C5 T1.

Sympathetic: S,M,I cervical ganglia
Parasympathetic : External & recurrent lrngl nerves.
Thyroid selling do not moves on deglutition:
1)) Intrathoracic extension
2)) Thyroiditis extending to surrounding region
3)) Invasion to surrounding structures
4)) Very large swelling.
5)) Redels & Granulomatous Thyroid
MNG nodules are: colloid, cystic, degenerative,

haemorrhagic & calcification
Criles Method: Place thumb on gland Ask to

swallow Nodules are better appreciated
Laheys method:- Palpation of each Lobe (from
front):- Palpate L lobe by pushing it towards L with
L hand & Plpate it with R hand
Age
Feature
Malignant
lymphoma
50 60 yrs
Medullary
carcinoma
50 70 yrs
Granulomatous
Thyroiditis
40 yrs
Firm painless
mass
indistinguishable
from anaplastic
type
Firm smooth
lump
indistinguishable
from Solitary
Nodule
Firm irregular
enlargement
Hashimoto
Thyroiditis
Colloid goitre
Diffuse
hyperplastic
50 yrs
20 30 yrs
10 20 yrs
Soft rubbery
diffuse
enlargement
Diffuse soft
elastic
enlargement
Diffuse soft
elastic
enlargement
type
Diffuse irregular
enlargement
with Bosellated
surface
(Nodules with
variable
consistency)
Colloid goiter DD: Lymphadenoid
goiter.(treatment always partial thyroidectomy).
MNG
30 40 yrs
In Retro Sternal Goitre casuing obstruction NO

place for thyroxin / antithyroid drugs / radioiodine:
RESECTION
Tremor is demonstrated in Extended & abducted

fingers.
Relationship of recurrent laryngeal nerve to the
inferior thyroid artery
N in TOG (Commenest)
N btw branches of Inf thyroid artery
N lateral to trachea
N Ant / Post to artery
N far anterior
** The superior parathyroid is characteristically dorsal to the plane of the nerve, whereas the inferior gland is
ventral to the nerve.
Normal Value
Hormone
0.55 U/mL
55150 nmol/L
Serum ThyroidStimulating Hormone

Total T4
1.53.5 nmol/L
Total T3
1228 pmol/L
Free T4
39 pmol/L
Free T3
Page
60
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)
MANAGEMENT OF SOLIATRY THYROID NODULE

TSH test
Euthyroid
Thyrotoxic
Radio isotope Scan
Cold
Warm
Hot
Ultrasound neck
Solid
Aspirate &
analyze
Cystic
FNAC
Benign
malignant
Suspicious
Benign
malignant
No cells
Frozen section
Papillary
follicular
Repeat aspirations
Total throidectomy
Recur even after 3 aspirations
Page
61
Thyroid Lobectomy
Propyl thiouracil: Prothrombin deficiency Vit K

supplementation.
It is given Pre op 100mg thrice daily in
hyperthyroisism to make thyroid euthyroid &
operation performed 2 months later.( if performed
too early: Thyroid crisis) & propanalol has to be
added in graves disease: to relieve tremor anxiety &
HR.
Post op: S.ca after 6W & Thyroid status after 6M
& then yearly.
Operative complications:
Immediate
Haemorrhage
Infection
Recurrent laryngeal N
paralysis
Thyroid crisis / storm
Transient hypocalcemia
Respiratory obstruction
Horners syndrome
Injury to oesophagus
Late
Thyroid insufficiency
Recurrent thyrotoxicosis
Hypertrophic scar/keloid
1)) 23-gauge needle is inserted into the thyroid

mass, and several passes are made while aspirating
the syringe. After releasing the suction on the
syringe, the needle is withdrawn and the cells are
immediately placed on prelabeled dry glass slides
2)) 3 ways
a)) some are immersed in a 70% alcohol solution
b)) others are air dried.
c)) fewplaced in a 90% alcohol solution for
cytospin or cell pellet.
3)) The slides are stained by Papanicolaou's or
Wright's stains and examined under the microscope.
62
Complications Of radioiodine therapy
Acute
Long-Term
Neck pain, swelling,

and tenderness
Thyroiditis
Sialadenitis
Hematologic
Cerebral edema
Vocal cord paralysis
Nausea and vomiting
Bone marrow
suppression
Progressive
Exophthalmosis
Wound cellulitis
Parathyroid insufficiency
FNAC
Page
Multicentricity in papillary carcinoma is not due to

direct extection but due to lymphatic spread within
the rich intrathyroid lymphatics.
** If a bloody aspirate is obtained, the patient

should be repositioned in a more upright position
and the biopsy repeated with a finer (25- to 30gauge) needle.
Bone marrow
suppression
Fertility
infertility
Increased spontaneous
abortion rate
Pulmonary fibrosis
Anaplastic thyroid cancer
Gastric cancer
Lung cancer
Bladder cancer
Hypoparathyroidism
Increased risk of cancer
Operative Points:
1)) Supine position initially with the neck extended
by placing a ring beneath the head and a sandbag
roll beneath the shoulder. The patient is placed in a
reverse Trendelenburg position
2)) A Kocher transverse collar incision, typically 4 to
5 cm in length, is placed in or parallel to a natural
skin crease 1 cm below the cricoid cartilage. The
superior flap extends upward to the thyroid notch
and the lower flap extends downward to the sternal
notch.
3)) The dissection plane is kept as close to the
thyroid as possible and the superior pole vessels are
individually identified, skeletonized, ligated, and
divided low on the thyroid gland to avoid injury to
the external branch of the superior laryngeal nerve
4)) The inferior thyroid vessels are dissected,
skeletonized, ligated, and divided as close to the
surface of the thyroid gland as possible to minimize
devascularization of the parathyroids (extracapsular
dissection) or injury to the RLN. The RLN is most
vulnerable to injury in the vicinity of the ligament of
Berry (Any bleeding in this area should be
controlled with gentle pressure before carefully
identifying the vessel and ligating it. Use of the
electrocautery should be avoided)
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 1mm 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.
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
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
Page
63
H/C/C:
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.
Pain in left breast from 3 months, insidious in onset,
pricking type, continuous, aggravated during
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:.
Long term treatment
Personal H/O:
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 &
(A) general survey
patient is C/C/C. Comfortably seated.
Moderately built & adequately nourished. BMI:
P (-) I (-) C (-) C (-) K (-) L (-) E (-)
(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.
Page
64
(1)Inspection
Breast:
Both the breasts are N in position.
Left breast is enlarged in size showing fullness in
outer & upper quadrant. &
Skin over breast shows NO puckering/dimpling/any
ulceration/fungation/engorged veins/scars/peau de
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

Other breast N on palpation
Palpation of LN (both sides): NOT palpable
1)) Axillary
2)) Cervical
3)) Supraclavicular
(3) Percussion: Resonant: sternum
NO free fluid
PR : NOT done
Discussion
Page
65
Anterior chemotherapy Pre op Chemotherapy

(down staging)&
Posterior chemotherapy Post op Chemotherapy
(residual).
Liver involvement by:
1)) Hematogenous (Parenchymatous)
2)) Grossmans pathway (Surface) [breast rectus
sheath sub diaphragmatic lymphatics
L.falciparum of liver]: basically inferior & medial
quadrants
(thus they
have usually associated with free fluid in abdomen)
PV: NOT done

BLAE: N &
4)) Musculoskeletal system:
N gait with Spine,pelvis,Sternum Normal & No
long bone tenderness
Diagnosis: A case of primary benign neoplasm of
left breast probably fibroadenosis involving outer
and upper quadrants.
PR examination: for Blummer shelf

PV examination: for Blummer shelf & ovarian
masses.
FNAC
Not conclusive
True cut biopsy (receptor status, genetic
markers, tumour type)
Not conclusive
Excision biopsy
Not conclusive
Frozen section biopsy
Lung metastasis in breast ca.: Cannon ball metastasis

(X ray finding)
Conditions in which carcinoma of breast with lump
But no axillary metastasis
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
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
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)
recur
Page
66
20
If LN are palpable Note: NUMBER, SIZE, FIXITY,

CONSISTENCY
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
Green
Fibroadenosis, duct ectasia
Black
Duct Papilloma & Infiltating / NON

infiltrating duct carcinoma &
Fibroadenosis
FNAC must be followed by true cut biopsy.

Carcinomas co exist with breast carcinoma:
breast, uterus, ovary (hyper oestrogen).
The lymphatics from all groups of axillary LN
ultimately drain into apical & from there efferent
vessels unite to form subclavian trunk which also
drains suprclavicular LN & opens into R lymph duct
on R & Thoracic duct on L.
Family H/O: lobular carcinoma (which is usually co
exists with fibroadenoma).
Breast is freely mobile over pectoralis muscle: due to
Retromammary space.
Traumatic fat necrosis: haemorrhage central
liquefactive necrosis surrounded by zone of
inflammation well defined nodule with firm
consistency dense fibrous scar.
Discharge
Milk
Serous
Pregnancy, OCP, milk fistula,

Hyperprolactinemia, galactocoele
Pus
Acute mastistis
creamy
Duct ectasia
SPECIAL PREOPERATIVE PREPARATION

Review of the following investigations is necessary
before the operation:
Histology of the breast lesion, which may have
been obtained by fine-needle aspiration, core
biopsy, or excisional biopsy.
Mammogram to evaluate whether the malignancy
is multifocal or multicentric, because these issues are
important when discussing surgical options.
Ultrasonography or computed tomography of
the liver if metastasis is suspected.
Fibroadenosis, duct ectasia/ papilloma,

NON infiltrating duct carcinoma
Management of discharge:
Discharge
1 duct
Page
67
NOT blood stained
Blood stained
Multifocal
NOT blood stained
Blood stained
Mammography is performed (> 35 yrs: exclude maliganancy)

Microdochectomy
Microdochectomy
Cefotaxime/flucloxacillin
Hadfields 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.
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.
Lumpectomy / Tylectomy.
Breast cysts:
Mammary dysplasia
Tumours
Retention cysts
Benign
malignant
Misc
Page
68
The sensitivity of mammography increases with age

as the breast becomes less dense.
US is particularly useful in young women with dense
breasts.
Microdochectomy: Tennis racket racquet to
encompass the entire duct / periareolar incision used
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.
Pagets 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 cant 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
Page
69
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
along right angles to fibres is possible
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
I
Mild breast enlargement without skin

redundancy
Grade
IIa
Moderate breast enlargement without

skin redundancy
Grade
IIb
Moderate breast enlargement with skin

redundancy
Grade
III
Marked breast enlargement with skin

redundancy and ptosis, which simulates a
female breast
Disorder
Risk
Nonproliferative lesions of the breast
No
No
Sclerosing adenosis
Intraductal papilloma
Florid hyperplasia
No
2-fold
Atypical lobular hyperplasia

Atypical ductal hyperplasia
Ductal involvement by cells of atypical
ductal hyperplasia
Lobular carcinoma in situ
Ductal carcinoma in situ
4-fold
4-fold
7-fold
angiogenesis index;
(d) growth factors & growth factor receptors such as
human epidermal growth factor receptor 2 (HER-2)
Woman leans forward to accentuate any skin

retraction .
1010fold
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.
Page
70
HER-2/ neu Negative

(NonTrastuzumabContaining Regimens)
HER-2/ neu Positive

(TrastuzumabContaining Regimens)
FAC/CAF
TAC (T = docetaxel)
TCH (docetaxel,
carboplatin,
trastuzumab)
A CMF
E CMF
Chemotherapy followed
by trastuzumab
sequentially
CMF
AC x 4
** A= Adriamycin (doxorubicin); C =
cyclophosphamide; E = epirubicin; F = 5fluorouracil; 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
the primary tumor site)
1)) Neoadjuant Chemotherapy: Current

recommendations for treatment of operable
advanced local-regional breast cancer are
neoadjuvant chemotherapy with a doxorubicincontaining 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
Page
71
3)) Others: antiestrogen (tamoxifen for

premenopausal women or an aromatase inhibitor
for postmenopausal women & Pamidronate may be
given to women with osteolytic bone metastases
SALIVARY GLAND SWELLING
(B) Local examination:
Raju/60/M/hindu/agricultural labour
(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
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:
Long term treatment
Personal H/O:
Addictions: Non smoker & Non alchoholic
Family H/O:
Page
72
(A) general survey
patient is C/C/C. & Normosthenic
P (-) I (-) C (-) C (-) K (-) L (-) E (-)
(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:
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.
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73
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
NO H/O chronic cough
NO H/O vomiting / abdominal distension
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:
Long term treatment
Personal H/O:
Family H/O:
No H/O similar complaint in family & No H/O any
chronic illness in family
(A) general survey
patient is C/C/C. & Comfortably seated.
Moderately built & adequately nourished
P (-) I (-) C (-) C (-) K (-) L (-) E (-)
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 (?)

(4) Auscultation: Bowel sounds heard

NO free fluid
BLAE: N &

Diagnosis:
right sided
indirect
incomplete
reducible
inguinal hernia
probably enterocole
with straining factor of lifting heavy weights ,
chronic constipation & BPH
Discussion
Hernia is common on R side: later descent of testis
& more chances of patency of process vaginalis.
Strangulated hernia management:
emergency operation
1)) Foot end is raised (advantage of gravity for
reduction)
2)) ice bag is applied locally (reduce congestion &
chance of gangrene is delayed)
3)) nasogastric tube, catheterization & IV fluids
4)) inj. pethidine & atropine (relax muscles)
5)) an attempt to reduce hernia
6)) Anesthesia: G/A or field block by L/A 1inch
Medial to ASIS to anesthesia to ILIO HYPOGASTRIC
& ILIO INGUINAL NERVES
7)) incision is extended UPTO FUNDUS & fluids

aspirated (avoid risk of contaminating peritoneal
cavity & contents will not get an opportunity to slip
back before they are examined) & THEN external
oblique is Cut
Page
74
8)) Constriction ring is cut (deep ring is cut parallel

to IEA UPWARDS & INWARDS) & apply hot wet
mops for 10 min
9)) bowel must be drawn out to examine the area
proximal to ring
10)) check viability
Intestine
Circulation
Viable
NOT viable
Light colour &

mesentery
bleeds if
pricked
Persistent dark
colour &
mesentery
NOT bleeds if
pricked
Dull & lusture
less
Peristalsis ve
& pressure
rings NOT
disappear
-ve
Peritoneum
Shiny
Musculature
Peristalsis +ve
& pressure
rings disappear
Mesentery vessel
pulsations
+ve
11)) If bowel in non viable/ doubtful viable:

Linear patch: invaginating with lamberts sutures
whole loop: end to end anostomosis
omentum: healthy portion above transfixed & distal
part excised
Large intestine: PAUL - MIKULICKZ operation
(exterioration & resction )
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.
Page
75
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):
Loss of tone of conjoined tendon (Weakened post
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.
Bessenis 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,
Richters & litters 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
Page
76
Fallacies in deep inguinal ring:

1)) Insufficient force
2)) Double hernia
3)) Ring defect > thumb size
Usually diagnosed clinically but investigation is
needed then U/S 1st choice (particularly obese with
small hernia) coz it gives information about

Prostrate enlargement.
Mesh size usually taken is 16 x 8cm: in lichensteins
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 gallows 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:
Page
77
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
No H/O pain in hands on writing/combing
NO H/O similar complaints in other lower limb

DM, TB, epilepsy, chest pain / Jaundice & bleeding
disorders
Long term treatment
Personal H/O:
Addictions: Chronic smoker & Non alcoholic
Family H/O: No H/O similar complaint in family &
No H/O any chronic illness
(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: 16/min
Gait: Limping with pain
No tendon xanthomas / xanthalesma /
No markers of IE
Facies: Wincing in pain
(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
Buergers 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.
Capillary refilling: 5 sec: L
Venous refilling: ?
Fuchsigs test: +ve on both sides
Cold & warm water test: (not done)
NO crepitus
Midline trachea with BLAE: N &

N vesicular sounds heard NO adventitious sounds
Apex Normal & Heart sound 1 & 2: Heard &
normal
No murmurs heard
Peripheral pulses: (No tenderness/vessel wall

tenderness)
Diagnosis: A case of dry gangrene of distal half of

little toe due to peripheral arterial disorder may be
due to buergers disease, with intermittent
claudication distance of 10 m
& cold upto 5 cm below tibial tuberosity.
Superficial temporal
+ve
+ve
C.carotid
+ve
+ve
Subclavian
+ve
+ve
Axillary
+ve
+ve
Brachial & Ulnar, radial
+ve
+ve
Femoral
+ve
+ve
popliteal
+ve
+ve
Ant & post tibial
+ve
-ve
D.pedis artery
-ve
-ve
Movements: 4rth & little toe are limited & ankle

movements are normal
Measurements: L: 25cm R: 30 cm
Neurological examination:
Sensory: all sensations are absent in little toe.
Remaining foot upto 4cm infront of ankle hyperaesthetic
sensations in leg Normal
Motor:
Tone: R: N L: N
Power: R: dorsiflexors & plantar flexors: N on both
sides
Reflexes: N on both sides
Regional lymphnodes Not palpable
Page
78

NO free fluid
Discussion
Definitive diagnosis of TAO: Arterial wall biopsy
(excision biopsy)
Severe Limb ischemia = Critical (rest pain +/- tissue
loss like ulceration, gangrene for >2W & ABP
<50mm Hg) & Sub critical limb (rest pain only &
ABP >50mm Hg)
Ischemia Pain is usually at night coz beneficial effects

of gravity on perfusion are lost Patients BP & hence
perfusion pressure reduces in sleep
In diabetes = spuriously high ABPI coz of arterial
calcification.
ABPI
>/= 1
0.5 0.9
<0.5
Healthy
IC
CLI
0.5 0.3
Rest pain
<0.3
Gangrene
Left ABI = Higher Of Left ankle Systolic BP (DPA /

PTA) / Higher of Left / Right UL Systolic BP
** Limitations of relying on segmental limb

pressures include:
(a) missing isolated moderate stenoses (usually iliac)
that produce little or no pressure gradient at rest;
(b) falsely elevated pressures in patients with
diabetes and end-stage renal disease; and

(c) the inability to differentiate between stenosis and
occlusion
Buergers
Buergers aetiology (Smoking, hormonal, familial,
Autoimmune & rickettsial)
Beurgers position (head end of bed is raised & at
the same time foot end is gradually lowered about
6inches / day - improve circulation of lowerlimb )
Beurgers 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 )
Beurgers pathology
(Acute lesion Acute arteritis & phlenitis &
periarteritis & periphlebitis with thrombosis of vessel
containing microabscess
Chronic lesion Artery, vein & nerve sometimes
bound together by fibrous adhesions & elstic lamina
of artery are thickened)
Beurgers sign (Absence of Post tibial pulse is highly
suggestive of diagnosis)
Page
79
Examination of
Joints - Charcot joints of diabetes
Power - Weakness of flexors & extensors of foot
may cause Abnormal foot architecture
Reflexes - Hyporeflexia in Ischemic neuritis & In
neuropathy of diabetes
Femoral pulse usually is palpable midway between
the anterior superior iliac spine and the pubic
tubercle.
Popliteal artery is palpated in the popliteal fossa
with the knee flexed to 45 and the foot supported
on the examination table to relax the calf muscles.
Palpation of the popliteal artery is a bimanual
technique. Both thumbs are placed on the tibial
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
4+
Normal
2+
Normal
3+
Slightly reduced
1+
Diminished
2+
Markedly reduced
Absent
1+
Barely palpable
Absent
Abdominal swelling / Lump

Ramulu/60/M/Nizamabad/Agricultural
labour/Hindu
C/C:Lump & Pain in abdomen 2m
H/C/C:Patient was apparently asymptomatic 2 months
back then he developed swelling in upperpart of
abdomen in midline
Sudden in onset
Initially lemon size gradually progressed to reach
present size
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
DM, TB, epilepsy, chest pain / Jaundice & bleeding
disorders
Long term medical treatment
Personal H/O:
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
Page
80
(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: 14/min
Patient is exposed from nipple to midthigh & was
examined in supine, lateral, sitting, Knee elbow
postions, by looking from side, tangential & End of
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 & doesnt 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)
Traubes space:- Tympanitic
No IC tenderness / punch tenderness
d)) Auscultation:
Bowel sounds heard & Normal pitch & No venous
Hums heard / Bruie heard
PR: Not done
Midline trachea with BLAE: N &
N vesicular sounds heard NO adventitious sounds
Apex Normal & Heart sound 1 & 2: Heard &
normal
No murmurs heard
6cm
Page
81
10 cm
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
Littles 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
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 Cluttons 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:
Page
82

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
ANT. horn of MALC.
(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
Under (for articular surfaces)
palpate
(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 Bakers 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
Appleys grinding test: M/L SLC
Appleys 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:
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
Page
83
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
No shoulder drooping ( fracture of neck of scapula)
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 Codmans
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
Bryants test
Hamiltons 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
Page
84
(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
fractures of humerus / Scapula with N Distal NV
status
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)
-Trendelenbergs 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
Perthes disease
Hip arthritis}
1)) Greater Trochanter NO tenderness {A triangle

is formed by GT , ASIS & Line drawn vertically
downwards from ASIS BRYANTS triangle
+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:
Page
85
-No local rise of temperature

-Tenderness: below the mid inguinal point
(Any arthritis) & also on pressing greater Trochanter
towards each other on L side
Bony points
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
Bryants triangle:
Neltons 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
Shoemakers Line: Normally line from GT to ASIS
will reach umbilicus any upward displacement
can thus be easily demonstratable
Morris bitrochantric Test:
Chienes 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)
Ortalanis test
Barlows test
(F) LN: Not palpable
(G) Distal NV status: Normal
Page
86
(H) Other Joints: Knee joint, Lumbosacral spine,

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

2)) Milesrones & SE classification
3)) Nephrotic syndrome
4)) Cerebellar ataxia
5)) Hydrocephalus
6)) Anemia & Splenomegaly
PEDIATRICS
7)) Fever
8)) Seizures
9)) Traumatic neuritis
10)) Meningitis
11)) DMD
12)) Infantile hemiplegia
Page
87
** These cases are not exclusive.

any case can be in XM
Food Item
Quantity
Calories
Tea
One cup
52
Coffee
One cup
90
milk (cow)
One cup
67
milk (buffalo)
One cup
117
Bread
One slice
39
Biscuits (Glucose) One
25
Egg
One
85
Samosa
one
207
Upma
1-1/4 bowl
260
Idli
Two
130
Sambar
1 bowl
81
Khichadi
1 plate
182
Masala Dosa
One
192
Paratha
Two
297
Phulka
One
85
Puri
240
Rice
1 bowl
111
Dal 1
bowl
100
Potato Curry
3/4 bowl
131
Brinjal Potato
1 bowl
134
Curd
1 bowl
70
Banana
One
116
Mango
One
160
Mile Stones:
Gross Motor
Supine & pull to sit
Ventral suspension
Prone position
Sitting
Standing & walking
Fine Motor
Hand Eye
Coordination
Hand Mouth
Coordination
Advanced Hand
skills
88
Dressing
Page
6w 20w
6w Head horizontal
12w above horizontal
plane
1m lifts the chin up
2m face is lifted 45
3m - face is lifted 90
6m head + Chest lift
8m Crawls**
12m - Creeps
6m -tripod
8m Steady sitting**
10m Pivot on sitting
9m Stand (Support)
12m Stand (Indpn)**
15m Walks
18m Runs
2y walk back
3y tricycle
4y Hop
5y - Skip
3m- hand regard

4m hands (midline)
6m - Ulnar
9m - Radial
12m Mature & Pincer
6m ability to chew
12m tries to feed
18m feed himself well**
15m Scribbles, 2 Blcks
18m Strokes, 3 Blcks
2y Circular Stroke, 6
3y Copies circle, 9
4y Copies Cross, Bridge
5y Copies triangle
1y - Start to pull off
2y Undress complt
3y Dress & Undress complt
5y Shoelaces Complt
Personal & Social Development

Intent regard
Social smile
Recognizes mother**
Stranger anxiety & Vocalizes & Smile at
image
Bye - Bye
Understand simple Q
Point objects (Jargon)
Domestic mimicry
L / R Discrimination, Plays, Toilet alone**
3 steps , 4 colours
1m
2m
3m
6m
9m
12m
15m
18m
4y
5y
Language
Vocalizes with vowels
Laugh loud
Mono syllables
Bi syllables, Imitate sounds
2 words
15 words
100 words, 2 Sentences
Ask questions, Know name & gender**
Says Song / Poem
Ask word meaning**
2m
4m
6m
9m
12m
18m
2y
3y
4y
5y
Hearing
Turns his head towards Source
Direct localization
4m
10m
Vision
Page
89
Fixate his mother

Grasping with eye
Binocular vision
Adjust his position to follow obj
Follow rapidly moving obj
1m
4m
6w 4m
6m
1y
** To be Asked in History taking Ideally
Score
12
10
6
4
3
2
1
Income (Rs /-)

30375
15188 - 30374
11362 - 15187
7594 - 11361
4556 - 7593
1521 4555
1520
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:
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
Page
90
Family history:
No H/O of similar complaint in family

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 & 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:
(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
RR: 28/min regular, Abdominothoracic
Anthropometry:
Ht:
Wt: 18kg
midarm circumference 12cm
Discussion:
1)) Spontaneous renal vein thrombosis has been
associated with membranous
glomerulonephropathy.
Nephrotic syndrome may either cause or result from

renal vein thrombosis - Renal vein thrombosis in
newborns is generally characterized by the sudden
development of an abdominal mass
2)) Hemolytic-uremic syndrome is the most
common glomerular vascular cause of acute renal
failure in childhood. Bloody diarrhea is the usual
presenting complaint, followed by hemolysis and
renal failure.
Neurologic problems, particularly seizures. use of
antimotility agents and antibiotics is believed to
worsen the disease.
Timely dialysis improves the prognosis.
Some cases, plasma infusion or plasmapheresis
Cause
Streptococcal grp A
Varicella infection
Hepatitis B Infection
HIV Infection
Malaria
SLE / RA
Sickle cell disease
Lymphoma, leukemia
Wilms &
PheoChromocytoma
DB
HS purpura
H/O
H/O Sorethroat /
pyoderma before onset
of symptoms
H/O fever with rash
H/O Blood transfusion
Family H/O HIV
H/O fever with chills
H/O Skin rash with joint
pains
H/O Blood transfusion
No H/O swellings in
neck & weight loss
Page
91
Ataxia
Pavithra / 9 yrs / F / Student of 5 th class / Hindu /
Sainikpuri, hyderbad brought by his mother a
reliable informant with a
C/C: of
Inability to walk properly 15 days
Unsteadiness in reaching out for objects 15 days
H/P/I:
then she developed Inability to walk properly &
Unsteadiness in reaching out for objects along with
difficulty in sitting
H/O fever 1month back, low grade subsided on
medication not associated with chills/rigor
No H/O Cough, abdominal pain, Vomiting or an
exanthem Before onset of symptoms
No H/O of Slurring of Speech
No H/O similar episodes in past
No H/O loss of consciousness
NO H/O head trauma
NO H/O headache, projectile vomiting
NO H/O seizures
NO H/O memory loss / behavioural changes
NO H/O symptoms suggestive of cranial nerves
involvement
No H/O weakness of UL & LL
No H/O of Difficulty in feeling ground
No H/O of Any bowel / bladder symptoms
No H/O of Slurring of Speech
No H/O child in constant motion while awake. &
irregular eye movements
No H/O Any discharge from ear / Ear ringing
No H/O Any drug intake before onset of symptoms
No H/O of Contact with Tb patient
No H/O of similar complaint in siblings/family
No H/O of increasing head circumference
No H/O of Diarrhea / passage of floating foul
smelling stools
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
H/O HTN, DM, TB, bleeding disorders
Treatment H/O:
Family H/O: No H/O of similar complaint in family
Birth H/O:
Mother is registered case in local hospital & had
had FTNVD in hosp.
No admission of baby in NICU
Baby cried immediately & breast fed for 8m.
Immunization H/O:
Immunized as per schedule, OPV & SIP is also taken.
No post immunization hosptalization . BCG mark
seen
Developmental H/O: Gross motor & fine motor
milestones achieved normally
Dietary H/O:
Breast fed 2 yrs (exclusively 5m)
2 idli & cup milk:
Rice (4cups):
Dal (2 cups):
1 banana:
Socioeconomic H/O:
father educated - Graduate, Govt emply
PCI 3000
Socio economic class (K) II
Page
92
(A) General survey
Patient is C/C/C.
P (-) I (-) C (-) C (-) K (-) L (-)
No Bulbar/dermal telengectasia
No NC markers
No Xanthomas / Xanthalesma
No Chicken pox scars (Pock marks)
Facies: N
Vitals afebrile,
RR: 18/min regular, Thoracoabdominal
(B)Anthropometry:
Ht:
Wt: 18kg
Local examination (CNS):
1)) Higher functions
Handedness: R
Level of consciousness: Fully consiousness
Orientation: +ve
Emotional state: Normal
Memory: preserved
Speech: Articulation disturbed
2)) Cranial nerve Examination:
I
II
Visual acuity
Visual fields
Colour vision
III,IV.VI
Nystagmus
V
Sensory
Motor
VII
VIII
Vestibular
Auditory
IX & X
XI
XII
Normal
Normal
Normal
Normal
Normal
+ve
Normal
Normal
+ve
Normal
Normal
normal
Normal
Normal
Normal
Normal
Normal
normal
Normal
normal
3)) Motor System:

A)) Inspection
No Gross Muscle wasting / Hypertrophy seen
No involuntary Movements
B)) Palpation
Bulk
UL
LL
Tone
UL
LL
Power
UL
LL
Involuntary
16cms
24cms
16cms
24cms
Normal
Normal
Normal
Normal
4/5
4/5
UL
LL
Co ordination
UL
LL
Absent
Absent
Knee heel & finger nose test ve

dysmetria +ve
dysdiadokokinesia +ve
Diagnosis: A case of acquired ataxia of

cerebellar origin with infective etiology (Acute
cerebellar ataxia)
4)) Reflexes:
Superficial
reflexes
Abdominal
Plantar
Deep tendon
reflexes
Jaw jerk
Upper limb
Lower Limb
Visceral reflexes
Released
reflexes
Discussion
present
Present
?
B,T,BR: +
K,A: +
?
Absent
?
B,T,BR: +
K,A: +
?
Absent
5)) Sensory system:

Proprioceptive
Exteroceptive
Cortical
Present & N
Present & N
Present & N
Present & N
Present & N
Present & N
GAIT: tandem walking ABSENT

CEREBELLAR: +ve
ANS: No abnormal sweating, constipation
RAISED ICT SIGNS: Absent
MENINGEAL IRRITATION SIGNS: -ve
SKULL & SPINE: Normal
PERIPHERAL NERVES: Normal
Page
93

NO free fluid
BLAE: N &
Cause / etiology
Malignancy (SOL)
Benign paroxysmal
vertigo of children /
basilar artery migraine
Acute cerebellar ataxia
(varicella, mumps,
rubella, echovirus
poliomyelitis, influenza.
Bacterial: scarlet fever )
Drug induced
(phenytoin)
Wilsons disease
Refsums disease
Chilhood degenerative
diseases
Extrapyramidal Cause
Spinocerebellar
degerative diseases
1. Friedreich ataxia (AR)
2. Dominant ataxia
Abetalipoproteinemia
Dandey walker
syndrome
Cerebellar abscess
H/O
H/O weight loss ,
headache
No H/O similar episodes
in past
No H/O fever, Cough,
abdominal pain,
Vomiting or an
exanthem Before onset
of symptoms
No H/O Any drug
intake before onset of
symptoms
H/O jaundice / abd pain
H/O Night blindness ,
deafness
H/O Memory loss
H/O Invol movements
H/O similar complaint in
family
H/O Difficulty in feeling
ground
(Involv of Dorsal , Pyrm,
Spinocerebellar tracts)
H/O of Diarrhea /
passage of floating foul
smelling stools
Xanthomas
H/O of increasing head
circumference
H/O of Contact with Tb
patient
PolymyoclonusOpsoclonus Syndrome
of Childhood
(Infantile Myoclonic
Encephalopathy)
Louis-Bar Syndrome /
ataxia - telengectasia
H/O fever with chills &

rigors
H/O child in constant
motion while awake. &
irregular eye movements
No Bulbar/dermal
telengectasia
cardiac disease and diabetes

- Death occurs, usually from heart failure or
dysrhythmias, in the third or fourth decade
4)) Treating underlying conditions
Refsums
Wilsons
Malignancy
Drug induced
Dietary
Cu chelation
removal
Drug withdrawl / Replcm
Management:
1)) Investigations:
Acute cerebellar ataxia
CSF: slight lymphocytosis.
CT : normal
MRI: cerebellar postinfectious demyelinating
lesions.
EEG: normal or may show nonspecific slowing.
Friedreich ataxia : GAA trinucleotide repeats on
chromosome 9 can be used for laboratory diagnosis
Mt test & X ray chest: Tb
2)) Treatment
Cerebral palsy
Discussion
The term cerebral palsy is a nonspecific term used to
describe a chronic, static impairment of muscle tone,
strength, coordination, or movements. The term
implies that the condition is nonprogressive and
originated from some type of cerebral insult or
injury before birth, during delivery, or in the
perinatal period.
1)) Acute cerebellar ataxia:

Treatment is supportive. Corticosteroids have not
been shown to be of benefit; IVIG has been used.
Page
94
** Between 80% and 90% of children with acute

cerebellar ataxia not secondary to drug toxicity
recover without sequelae within 68 weeks. In the
remainder, neurologic disturbances, including
disorders of behavior and of learning , persist for
months or years, and recovery may remain
incomplete.
2)) Polymyoclonus-Opsoclonus Syndrome :
- Respond variably to ACTH or to IVIG.
- Plasmapheresis has been successful.
- Usually the underlying neural crest tumor is benign
(ganglioneuroblastoma); surgical excision may be
the only oncologic therapy needed.
3)) Friedreich ataxia :
- Surgery for scoliosis and intervention as needed for
Seizures (Epilepsy)
DMD
Kannaraju / 10 yrs / M / Student of 6th class / Hindu
/ Karimnagar, brought by his mother a reliable
informant with a
C/C:
of
Meningitis
Vivek/ 7 yrs / M / Student of 3 rd class / Hindu /
narayanguda, Hyderbad brought by his mother a
C/C:
of
H/O of fever - 7days

H/O headache 5 days
H/O hyperirritability 5 days
G/E Findings to rule out Genetic Syndromes
H/C/C:
then the patient developed Headache
Congenital heart disease

Suman / 10 yrs / M / Student of 6th class / Hindu /
Malkajgiri, hyderbad brought by his mother a
C/C:
Genetic
Syndrome
Down
Associated
Cardiac Defect
A & VSD
Turner
Bicuspid AV,
COA, AS
Noonan
WilliamsBeuren
Marfan
HCM
AS, PPS
Fetal
alcohol
Maternal
rubella
MVP, MR,
Tall stature,
dil. aortic root, High arched palate,
VSD, ASD
PDA, PPS
of
Discussion
Stroke
Most congenital defects lead either to decreased

pulmonary blood flow or increased pulmonary
blood flow with pulmonary congestion. Symptoms
vary accordingly
Decreased
Increased
Infant/Toddler
Cyanosis
Squatting
Loss of
consciousness
Tachypnea with activity/feeds

Diaphoresis
Poor weight gain
95
Dizziness
Syncope
Risk Factors for stroke
Cardiac disorders
Cyanotic heart disease
Valvular disease
Vascular occlusive disorders
Arterial trauma (carotid dissections)
Homocystinuria/homocystinemia
Vasculitis
Human immunodeficiency virus
Older Child
Page
Flat facies
Flat nasal bridge,
Eyes Upward slant,
Small ears
Clinodactyly
Simian crease
Short stature,
Wide Carrying angle,
Webbed neck,
Short 4rth metacarpal
Exercise intolerance
Dyspnea on exertion,
diaphoresis
Diabetes
Nephrotic syndrome
Systemic hypertension
Dural sinus and cerebral venous thrombosis
Hematologic disorders
Iron deficiency anemia

Polycythemia
Thrombotic thrombocytopenia
Thrombocytopenic purpura
Hemoglobinopathies
Sickle cell disease
Coagulation defects
Protein C and S deficiencies
Leukemia
Intracranial vascular anomalies
Arteriovenous malformation
Arterial aneurysm
Carotid-cavernous fistula
Transient cerebral arteriopathy
Family H/O: No H/O of similar complaint in family

Birth H/O:
No other drugs taken / infections
had FTNVD in hosp.
No dystocia / Instrumentation
Baby cried immediately & breast fed.
Immunization H/O:
Immunized as per schedule.
BCG mark seen
Developmental H/O: recognizes Mother &
Vocalizes Sounds But Not able to loft hos head in
prone position
Hydrocephalus
Raju / 4months/ M / Hindu / Shankarmatt,
hyderbad brought by his mother a reliable
informant with a
Page
96
C/C: of
Progressive enlargement of head from birth with
H/O headache, nausea, Vomiting from 2 months
H/O Poor feeding from birth
H/C/C:
Patient is born with Normal head & has NO
difficulty in labour later then he slowly developed
Enlargement of head to reach present size.
H/O poor feeding from birth
H/O Headche , nausea & Vomiting - 2months NO
H/O trauma
NO H/O fever
NO H/O Swelling at back
NO H/O unresponsiveness to loud Sounds
NO H/O Convulsions
NO H/O Altered Sensorium / Weakness of limbs
Dietary H/O:
Breast fed NO supplementary feeds Giving
Socioeconomic H/O:
Socio economic class (K) 3
(A) General survey
Patient is C.
P (-) I (-) C (-) C (-) K (-) L (-)
Enlargement of head particularly frontal region
Buldging Ant fontanalle (NON pulsatile)
High pitched Cry
NONC markers
NO shunt
NO neck stiffness
Scalp veins NOT prominent
Sunsetting sign +ve (Loss of upward conjugate
gaze)
Craniotabes +ve
(Macewen Sign): resonant on percussion /
Crack pot sign +ve
Facies: N (No dysmorphic features)
Vitals afebrile,
RR: 25/min regular
(B)Anthropometry:
Length:
Wt: 4kg
HC: 40cm
Investigations:
X ray skull (Copper beaten appearance)
Separation of cranial sutures
Lacunae in cranium
Bone thinning
- Erosion of post clenoid process
USG (V/P ratio: Ventricular dimater at middle
portion of ventricles by Bi parietal diameter >0.33
CT / MRI brain
Lumbar puncture
ICF pressure monitoring
Slit lamp (Chorioretinitis)
PET & Angiography
Internal /Obstructive / NON communicating

(Monro formen / Acqudect of sylvius)
External /NON Obstructive / communicating
(Archanoid villi / Basal cistern)
Treatment
1)) Mannitol / Furosemide / Acetazolamide
2)) Ventricular tapping
3)) Ventriculo Peritoneal / atrial shunts OR
Thecoperitoneal Shunts
Shunt block & infection
Ventricular collapse
Slit ventricle syndrome
4)) Ventriculosty
5)) Choroid plexotomy
6)) Treating underlying condition if possible
Steroids for TBM
AB for PM
Clot / SOL removal
Discussion:
Increase in size of ventricles due to excessive CSF
(Over production / Deficient Absorption /
Obstruction)
Page
97
Antenatal
Chromosoal Abnormality
NT defects
Arnold chiari 2 Malformation
Dandy walker Malformation
Congenital Craniosynostosis
Congenital Aqueductal stenosis
Acquired
Pyogenic meningitis & TORCH
Post Haemorrhagic (SAH)
SOL
Arnold chiari 1 Malformation
Sunsetting sign +ve because Dilated suprapenial
recess Pressess against tectum producing
supranuclear palsy
DMD
Prem kumar / 8 yrs / M / Hindu / nizamabad
brought by his mother a reliable informant with a
C/C of
H/C/C:
Family H/O: No H/O of similar complaint in
family
Birth H/O:
No other drugs taken / infections
had FTNVD in hosp.
No dystocia / Instrumentation
Baby cried immediately & breast fed.
Immunization H/O:
Immunized as per schedule.
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
Page
98
(A) General survey
Patient is C.
P (-) I (-) C (-) C (-) K (-) L (-)

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Vol

Wellthis book is collection of Clinical cases taken by me

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

G.Ravi kran 2k8

5)) Manual for short cases

Treatment H/O: No H/O any surgical procedures /

B/B: regular Sleep: N

3)) Motor System:

5)) Sensory system:

GAIT: N tanden walking

Clasp Knife rigidity

Able to do Knee heel test, finger

1)) Abdominal examination:

Diagnosis: A case of Complete completed Left

HR: 88/min N in volume, rhythm

Past H/O: Jaundice - 1 yr back treated with local

Treatment H/O: No H/O any surgical procedures /

Parotid enlargement +ve (painless)

c)) Percussion: Shifting dullness +ve

Blackout episodes 6months

GROIN: Orifices Free

H/O easy fatigubility 1 yr

(C) Systemic examination:

Diagnosis: Alcoholic liver disease with liver

SOB, Insidious in onset, Exertional. Relieved on

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

rhythm, No RR/RF delay all PP +ve

No other adventitious sounds like Clicks / Tumour

(B) Local examination (CVS)

1)) Respiratory system:

Diagnosis: A case of Organic MS Probably of

NO H/O fever with evening rise / night sweats

Inf border of scapula are at same level

Coin percussion & Shifting dullness: Absent

No other Palpable accompaniments (Friction ,

Apical / N vesicular & NO

(C) Systemic examination:

probably of tuberculous origin

Manual Short cases

Ankle oedema (Anemia perse, CCF, Renal disorders

Glossitis / Bald tongue

Pale PALM - <7gm %

Macrocyctic Hypochromic Anemia: Dimorphic

Causes: Nutritional, Hook worms, Leukemia,

Pallor (pathological entity) is waxy appearance of

H/O Weakness, lassitude, Giddiness, fainting,

Tachycardia, Functional MI & haemic

Leucoerythroblastic picture: Normoblasts &

(DD:-CO poisioning, Argyria, Osteogenesis

Differential: PDA with Shunt reversal (FEET BLUE)

Orthocyanosis: Only in upright position (Pulmonary

Intermittent Cyanosis: Ebsteins Anomaly

Cyanosis + PolyCythemia: CCongenitalHD & COPD

Pigment cyanosis (Spectroscopic Examination): Hb

Beats (1 Cardiac cycle)

Tortuous & Thickened

Absent radial pulse: Anatomical abnormality, Severe

Block Brachial artery & Palpate Radial

1)) Bounding: Hyperkinetic states

3)) Dicrotic: LOW VOLUME PULSE

** Webs fall on radial artery & rest of

intrathoracic pressure more blood

SBPe > SBPi (>10mm)