Case Taking BOOK(1)

7/24/2019 Case Taking BOOK(1)

1/98

MY FINAL CLINICALSEMESTERRaVi KiRaN2K8

Wellthis book is collection of Clinical cases taken by meG.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 givenwhich are clinical notes given by my teachers during mycase presentation.

Personally I feel that History is important for any case sheetwriting so my teachers emphasized on it which I thinkwould reflect in this book.

Reasons for Asking particular history,& Relavant theory has

to be studied from your respective Books & Clinical skillsmust be & Should be learned in your Clinical wards.I tried my best to avoid mistakes...Wish you ALL THE BEST FRIENDS..

Vol

1

G.Ravi kran 2k8Vol 1

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

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

Hope this Book Helps you in your Preparation friends


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Page2

CONTENTS:

1

2

5

4

3

MEDICINE

OBSTETRICS

GYNECOLOGY

SURGERY

PEDIATRICS


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MEDICINE

1)) Hemiplegia

2)) Ascitis

3)) CVS

MS

4)) Pleural effusion

5)) Manual for short cases

1


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HEMIPLEGIA

Vijay/Male/39/Cook/Kudappah/ 170712

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

speechNo 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

nervesH/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

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

Vitalsa 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

Normal NormalII

Visual acuityVisual fieldsColour vision

Normal Normal

III,IV.VI

Light reflexAccomodation

Eye movementsNystagmus

Normal Normal


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V

Sensory

Motor

Normal Normal

VII Foreheadwrinklingpresent

& Deviation ofmouth to L onshowing his

teeth

VIIIVestibularAuditory

Normal Normal

IX & X

Palatal reflex +

gag reflex NOT

done

& Uvula

midline

XI

Normal Normal

XII No deviation /fasciculations

/ No wasting &N power

3)) Motor System:

A)) Inspection

No Gross Muscle wasting / Hypertrophy seen

No involuntary Movements

B)) Palpation

Bulk

UL

LL

26cms

43cms

25cms

43cms

Tone

ULLL

Clasp Knife rigidityNormal (?)

NormalNormal

Power

UL

LL

3/5 5/5

Involuntary

UL

LL

Absent Absent

Co ordination

ULLL

Able to do Knee heel test, fingernose test No dysmetria / Nodysdiadokokinesia

4)) Reflexes:

Superficial

reflexes

AbdominalPlantar

Lost Lost

Deep tendon

reflexes

Jaw jerk

Upper limb

?

B,T,BR: ++

?

B,T,BR: +

Lower Limb K,A: ++ K,A: +

Visceral reflexes ? ?

Released

reflexes

Absent Absent

5)) Sensory system:

Proprioceptive Present & N Present & NExteroceptive Present & N Present & N

Cortical 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:

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 7thcranial

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

internal capsule.

With alchoholism, Old age, male as risk factors

& No complications of recumbancy


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ASCITIS

Ramraju/55/M/warsiguda/Manual labour

C/C:

Yellowish Discolouration of eyes20 days

Abdominal distension15 days

blood per stool15days

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 loss6m

H/O vomiting6m 2/3 per day , 30 min after

food, contained undigested food, yellowish, Noblood, no odour.

H/O abdominal distension15 days progressive,

with H/O 3 tappings (he dont know the colour)

H/O Abdominal pain4 days: sudden, continous,

progressive, twisting type, aggravated after taking

food, partially relieved on medication

H/O back pain, orthopnea4 days

H/O passage of black tarry stools4 days

NO H/O hematemesis

NO H/O facial puffinessNO H/O pedal oedema

NO H/O decreased urine output

H/O taking local herbal medicine

H/O alcoholism15 yrs500ml/day

Past H/O

: Jaundice - 1 yr backtreated with local

medicine & subsided Not associated with fever

NO H/O similar complaints in past, HTN, DM, TB,

epilepsy, chest pain & bleeding disorders

Treatment H/O

: No H/O any surgical procedures /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

Family H/O:




(A) general survey

patient is C/C/C . Hepatic facies +ve

P (-) I (-) C (-) C (-) K (-) L (-) E (-)

HR: 88/min N in volume, rhythm



RR: 22/min regular regular.

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 UmbillicusNo 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 thrillve


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c)) Percussion: Shifting dullness +ve

Liver upperborder: 5thICS in MCL (liver span: 14cm)

Traubes space:- obliterated (dull)

d)) Auscultation

: Bowel sounds heard & Normal

pitch & No venous Hums heard

GROIN

: Orifices Free

GENETALIA

: N (no loss of pubic hair/ testicular

atrophy)

PR: NOT done



BLAE: N &

N vesicular sounds heard

NO adventitious sounds



Diagnosis:Alcoholic liver disease with liver

cirrhosis in decompensated state.

CVS MS

Kumar/17/M/Student/Medak

C/C:

SOB1yrPalpitations1yr

Backout episodes6m

L Chest pain1 Month

H/C/C:

Patient was apparently assymptomatic 1 yr back

then he developed SOB & Palpitations

SOB, Insidious in onset, Exertional. Relieved on

taking rest, gradually progressive, Started as NYHA

1 now it is NYHA3.H/O PND attacks5months: 3episodes/night

H/O Orthopnea5months

Palpitations - Continous, Regular, Aggravated on

exertion & relieved on taking rest.

Not associated with Polyuria / Chest pain /

Lightheadedness

Blackout episodes6months

Where there is brief loss of consciousness, NOT

preceded by any sensation of movement / Aura &

are NOT followed by any confusion / amnesia /

headache

H/O easy fatigubility1 yr

H/O Cough5 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

Past H/O

: NO H/O similar complaints in past, HTN

DM, TB, epilepsy, chest pain & bleeding disorders

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

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


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rhythm, No RR/RF delay all PP +ve

BP: 110/74 mm hg RUL: supine

RR: 16/min regular , TA

(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 beatNot visible

Back is Normal (No spinal deformities)

2)) Palpation:

Trachea MidlineM:- Apex beat in 5 thics 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 & 2ndics (pulm

area) is dull

4)) Auscultation:

Apex pulse deficient:- 0

A middiastolic 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

M T P A Other

S1 Loud S1 N S1 N S1 N Gibsons

S2 N S2 N P2 Loud& S2 N

split

A2 N Neoaortic

MurmurMDM

MurmurNO

MurmurESM

MurmurNO

Infraclav

Normal

No other adventitious sounds like Clicks / Tumour

plop / Pericardial rub heard



BLAE: N &

N vesicular sounds heardNO adventitious sounds




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 pain15 days, Left sided, Insidous, Stabbing

type, continuous, Aggravated on cough, sneezing

partially relieved on medication, rest & Exertion

No radiation & is disturbing sleepDifficulty in taking respiration10 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


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NO H/O fever with evening rise / night sweats

NO H/O Noisy respiration

NO H/O Trauma

NO H/O Inhaler usage

NO H/O Nasal / Ear discharge

NO H/O Recent hospitalization / Ventilation

Past H/O

:

NO H/O similar complaints in past, HTN, DM, TB,

epilepsy, chest pain & Bleeding disorders & there is

NO H/O suggestive of Skin rash, Joint pains

(Collagen Vascular Disorders)

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

No drug allergies

Occupational H/O:

No H/O suggestive of Exposure to organic /

inorganic dusts

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 (OroTeeth, gums, palate, post

pharyngeal wall: N, LarynxNOT 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 RibsNO 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


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Inf border of scapula are at same level

NO winging / Drooping

SpinoScapular distance: Same on both sides on

inspection

NO gibbus

Intercostal suction & rib crowding : not seen

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 Expansion2.5cm on R side & 1cm on L side

Vocal fremitus

R L

AntN

Diminished inmammary &Inframammary area

Lat N Diminished inInfraxillary area

Post N Diminished in

Infrascapular area

No other Palpable accompaniments (Friction ,

Rhonchila fremitus, pleural / pericardial rub)

Normal palpatory findings on R side

PERCUSSION

R L

Ant Resonant Dull inmammary &

Inframammaryarea

Lat Resonant Dull inInfraxillary area

Post Resonant Dull inInfrascapulararea

Apical /Kronigsisthmus

Resonant Resonant

Coin percussion & Shifting dullness: Absent

Hepatic dullness is in 5thICL R

AUSCULTATION

R LAnt N vesicular & NO

Adventitioussounds VR: N

Diminished breath

sounds In mammary& Inframammaryarea NOAdventitious sounds

VR: decreased in

same areasLat N vesicular & NO

Adventitious

sounds VR: N

Diminished breathsounds In

infraaxillaryarea NOAdventitious sounds

VR: decreased in

same areaPost N vesicular & NO

Adventitious

sounds VR: N

Diminished breathsounds In

InfrascapularNO Adventitioussounds VR:

decreased in samearea

Apical /Kronigs

isthmus

N vesicular & NOAdventitious

sounds VR: N

N vesicular & NOAdventitious sounds

VR: N





NO free fluid

Free hernia sites



3)) CNS:

Patient is C/CNo neck rigidity (TBM)

Within N limit

Diagnosis: A case of L sided Pleural effusion

probably of tuberculous origin


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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

14.615.5 gm% - Males &

13.3 - 15.5 gm% - females

(Clinically 14.5%: 100%)

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

Pale PALM -


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(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)

Orthocyanosis: Only in upright position (PulmonaryAV malformations in middle & lower Lobes)

Peripheral Central

Nose Tip

Ear lobules

Outer aspect of LipsTip, Nail beds of

fingers & toes

Tongue (sides, Under)*

Inner aspect of Lips

Lower palpebral CnjNasal, rectal mucosa &

Retina

Stagnant &Overutilization Hypoxia

Hypoxic Hypoxia

CCFRaynauds

ShockArterial diseases: TAO

Venous diseases: SVC S

CryoglobulinemiaMS (mitral facies)

CCyanoticHDAcute Pulm oedma

Acute severe Asthma /COPD/Embolism/Laryngeal oedema

Pulm AV fistulaEisenmenger Syndrome

Application of warmth

Cyanosis will decreasereverse with Cold

NO Effect

Application of Pure O2for 10 min: NO response

Cyanosis may improve

Clubbing &Polycythemia:

Absent Usually

Usually present

Respiratory distress: -ve May be present

Hands: Cold Hands: Warm

Pulse Volume: LOW N / HIGH

Intermittent Cyanosis: Ebsteins Anomaly

Cyanosis Clubbing Condition

+ve +ve CentralCyanosis

+ve -ve

Peripheralcyanosis& Acutelydeveloping

Centralcyanosis

-ve +ve SBE , UlcerativeColitis

Cyanosis + PolyCythemia: CCongenitalHD & COPD

Hypoxia Cyanosis Condition

+ve +ve Rhb >5gm %+ve -ve Severe Anemia

(hb 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


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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 acompensatory pause (Dropped / Missed beat)

Absent radial pulse: Anatomical abnormality, Severe

Atherosclerosis, Takayasu, Embolism

Mean pressure:- Mean of SBP & DBP + 1/3 Pulse

pressure

8 CHARACTERISTICS

Rate 60100 / minTachycardia (>100/min)

Sinus tachycardia

Relative tachycardiaParoxysmal Tachycardia (SVT / VT)

Bradycardia (60mm)

Hyperkinetic states

Complete HB & Bradycardia of anycause

AtherosclerosisLow (


14/98

Page14

Character(Volume &

Waveform)

1)) Bounding: Hyperkinetic states

2)) Anacrotic : LOW VOLUME PULSE

WITH UPSTROKE IN ASCENDING

LIMBSevere ASActually in AS: PULSUS PARVUS

(low Volume) et TARDUS (slowrising)

PLATEAU PULSE

3)) Dicrotic: LOW VOLUME PULSE

WITH UPSTROKE IN DESCENDING

LIMBEndotoxic shock, hypovolemic shock

& 2nd

week of typhoid fever Very low CO + decreased PR4)) WH pulse: HIGH VOLUME +

SHARP RISE + ILL SUSTAINED +

SHARP FALL pulseAlso called HIGH VOLUME

COLLAPSING PULSEVictorian toy Half of glasscylinfder is filled with water & otherwith vacuum if turned upside down -Thud heard by Water strike

Classically seen in AI

HIGH VOLUME: INCREASEDSTROKE VOLUME + DECREASED PR(due to stimulation of baroreceptors

in aortic arch by large CO resulting in

sympathetic withdrawl)COLLPASING : DIASTOLIC LEAKBACK + RAPID DISTAL RUNOFFDUE TO VERY LESS PR

Other causes of High volume canalso cause this type of pulse wave

**

Webs fall on radial artery & rest of

palm on ulnar arteryExamine thevolume (both R & U arteries) Now

elevate the hand (Gravity fall ofblood column more amount inaortic arch Even more Sympathetic

withdrawal Even more reduction

of PR Even more elevation of Pulsepressure & Also artery will be in linewith aorta SO pressure changes of

rapid rise & rapid fall can be easily

appreciable)&Examine the pulse(rapidly rises with thud & rapidlyfalls)

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 1stwave due to Large volume

ejected by LV & 2ndwave by elasticrecoil & 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 (Defectivemechanical coupling)Gallop rhythm & Basal creps

7)) Pulsus Bigeminus & Trigeminus:

2/3 BEATS & A PAUSE (because

2nd/3rdbeat is ectopic so there iscompensatory 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 , Ctamponade, COPD, RestrictiveCadiomyopathy, Constrictivepericarditis

A)) Intrapericardial pressure raises more during inspiration

Impedes Diastolic filling thus reducingthe cardiac outputB)) Anti

Bernheim effect

: Increased


15/98

Page15

intrathoracic pressure more bloodis sucked into RV Reduced Blood

into LV & Deviation ofInterventricular septum to L

Reduction of CO Actual paradox is heart sounds may

be still audible when no pulse is

palpable in radial artery9)) 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 reserve6)) Different types of pulses

Pulsus Paradoxus SBPe > SBPi (>10mm)

Pulsus Alternans

Gallavardins sign

Initially on reducing onlyStrong beats are heard

SO Heard Beat APPEARSonly Half actual valueOn further reducing

Both strong & weak areheardOriginal HRheard

WH pulse PP >60mmhg

5

Temperature: 9899 F (lowest in morning &

highest in evening : diurnal variation of 1.5 F)

Hence Oral AM >98.9F & Oral PM >99.9F

Fever

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)

Oral temperature NOT taken if: Bells palsy,

inflammatory conditions, Mouth breathers, Trismus,

After Hot tea, Convulsions, Mentally dull people

Hyperthermia Hypothermia

MalariaAseptic fever

Heat strokeLeukemia & lymphomaSLE

Pontine haemorrhagePorphyria

Thyroid stormAcute MIMalignant hyperthermia

HalothaneHaloperidol

SepticemiaEncephalitisLobar pneumonia

Myxoedema comaEnteric fever associated

in Prf / HmrgAlcohol intoxicationProlonged ColdexposureHypoglycemia

Autonomic dysfunction

Periodic fever:Hodgkins

Malariabrucellosis

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 by crisis

Fall of temperature

suddenly with sweatingvery fastly in 612 hrs

Fall gradually in steps

over several days

Enteric feverAcute lobar pneumonia

DengueAdrenal crisis

Uncomplicated EFRheumatic Fever

Acutebronchopnemonia

For 1F rise of temperature RR increases by 2 3/m

& PR 10/min (adults) & 12

15/min (Childrean)

Relative Bradycardia Relative tachycardia

Rise of PR isProportionatly low

Rise of PR isProportionatly high

Any viral fever1stweek of enteric feverBrucellosisPsittacosis & weils

Acute R carditisDiphtheric myocarditis

PAN


16/98

Page16

Thermometer is Triangle in C.SMagnifies the

mercury line & Kink is present to prevent return of

mercury Line after it is taken from recorded site

Intermittent Continued Remittent

Quotidian

(daily)

Doubleinfection withPlasmodiumTBUTI

Tertian

(Alt days)

Benign (Vivax

& Ovale)Tertian

(Falciparum)Quartan (2d)

RFMiliary TB

2ndweek EF

Doublequotidian

fever / Camel

hump fever

(Double

fever spike insingle day)

Kala azarGonococcol

Endocarditis

Acutebroncho

pneumoniaAmoebic LAUTI & 3rdweek EF

** Fever

present for onlyfew hours &ALWAYSTOUCHES THEBASELINESOMETIMES

DURING THEDAY

**fever DO

NOTFLUCTUATEmore than 1.5Fduring 24 hrperiod &NEVER

RETURNS THEBASELINE

** fever DO

FLUCTUATEmore than 3Fduring 24 hrperiod &NEVERRETURNS THE

BASELINE

Typhoid state: Untreated EF in 3rd

week which ismanifested 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

Fever with rash Fever with membrane

1stday: varicella

2ndday: scarlet fever3rdday: Small pox4rth day: Measles

5thday: Typhus6thday: DEngue

Follicular tonsillitis

Faucal diphtheriaCandidiasisVincents 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 Non pitting

CCF, NS, Liver F,

Hypoproteinemia,Constrictive pericarditis,

Pericardial effusion ,Wet Beri - Beri

Myxoedema

Lymphatic oedemaAngioneurotic oedema

Sclerederma

Generalized Localized

Anasarca / DropsyCCF, NS, Liver F,Hypoproteinemia,Constrictive pericarditis,

Pericardial effusion ,Wet Beri - Beri

Venous obstruction

(Pregnancy, SVC,IVCsyndrome,DVT)lymphatic obstruction

Tb, filariasis, Radiation,dissection, Infiltration ofLN

Allergy

: AgNOInflammatory

: 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)


17/98

Page17

Pedal oedema Facial puffiness

CCF, NS, Liver F,Hypoproteinemia,

Constrictive pericarditis,Pericardial effusion ,

Wet BeriBeri,

Varicose veins, DVT

CCF, NS, Liver F,Hypoproteinemia,

Constrictive pericarditis,Pericardial effusion ,

Wet BeriBeri

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 1stto Affected

1stSee tangentially for loss of LbAngle*

Fluctuation Window sign / Schamrothss sign

1stdegree Fluctuation + loss of Angle

2nddegree 1st+ Increase in T & AP diameter3rddegree 2nd+ Increased pulp tissue

(Parrot beak / Drum stick Appearance)

4thdegree 3rd+ wrist / Ankle selling due to HOA*Most reliable early sign

Causes:

1)) Cardiac: Cyanotic HD, ABE, Eisenmengers

2))L

ung & pleural: Bronchiectasis, Lung abscess,

Empyema thoracis, CF, Pulm AV fistula, CF

3))U

lcerative Colitis

4)) Biliary Cirrhosis

5)) Intestinal: Crohns & Coeliac disease

6)) Normal / Idiopathic

7))G

enetic / familial

Always Look for swelling & tenderness at wrist

Painful Reversible

SBE

Brochogenic carcinoma

Lung abscess*

Empyema thoracis*

Unilateral Unidigital

Subclavian Coarctation

/ aneurysmCervical rib

Hereditary

Repeated traumaSarcoidosis

Upper limb Lower limb

Chronic Obs Phlebitis

due to chronic IV drugaddiction

Subclavian Coarctation

/ aneurysmCervical rib

Infected AAA

PDA with shuntreversal

** Acute clubbing(10

PHALANGEAL DEPTH RATIO: (Calipers) : Index

finger is used & DISTAL PHLANGEAL DEPTH :

INTERPHALANGEAL JOINT ration >1


18/98

Page18

HPOA / Pierre MarrieBamberger 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 Condition

Pitting Psoriasis, Reiters diseaseOnycholysis Psoriasis, Amyloidosis,

Sarcoidosis

Onychomadesis Trauma, Kawasaki diseaseBeaus lines Severe systemic illness,

PemphigusYellow nails Lymphoedema, pl effusion

(Yellow nail syndrome)

Imm dfcny, Bronchiectasis,

Terrys / White nails(Thumb & index)

Liver failure, Cirrhosis

Lindsays nails / half

& half nailRenal failure

Mees nails Ars poison & HodgkinsMuehrckes nails HypoAlbuminemia (Any)

Horders Nails

(linear longt. Hmr)

SBE, systemic vasculitis

Green nail Psuedomonas infectio

Black nail PEutzjeghers syndrome

8

If H LS)Achondroplasia: AD (Normal intelligence,

US > LS, Short limbs, large head)

Psedo hyperpara thyroidism (Less intelligence,

Stouty built, Short 4/5thMtcrpls)

US = LS: Constitutional & familial

9

If H > 97 thcentile

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 +veThumb

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

(


19/98

Page19

females > 0.9risks 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 lo ss in 6 months : Significant weight loss

11

JVP: Jugular venous pulse (CVP / mean RA pressure)

from which we study JV pressure & wave pattern

For Venous pressure measurement Ext jugular vein is

NOT measured

Prone to kinking due to Superfecial nature

NOT DRAIN DIRECTLY into SVC

VALVES, PIERCE FASCIA

Not a direct reflector of CVP

Right internal jugular preferred because

(Innominate vein may be compressed by aortic

knob which dampens elevates the venous pressure

on Left Jugular vein)

Prerequisite: Trunk angle 45 with relaxed neck

muscles in good light. Btwn 2 heads of

sternocleidomastoid (if in sitting position neck veins

are engorged then it is NOT necessary for TRUANK

ANGLE at 45) uppermost portion of distension is

taken

Normal value at 45 : 3 4cm blood (8 cm Blood =

6mm hg)

Venous Arterial

Wavy

Better seen than feltOn Exp - Promn

Lying down - Promn

HJ reflex - +veProminent movement

is INWARDAbolished by gentle

pressure applied above

Clavicle2 +ve waves are seen

Jerky

Better felt than seenNO

NO

NOProminent movement

is OUTWARDNOT ABOLISHABLE

1 +ve wave seen

definite upper levelseen

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

In normal people A is visible & X is more prominent

CX descent: X descent / Systlc collapse: before S2VY descent: Y descent / Diastlc collapse: After S2

X descent is due to: Atrial relaxation & downward

movement of Valves during V systole

Wave Pattern Condition

A Large A wavesRegular Cannon wavesIrregular Cannon wave

TS,PS,Pulm HyptnJunctional RhythmComplete HB

Passive RA filling

S2

Due to Opening

of Tric. Valve

A. Contraction

S1

Buldging of TV

& Impact of Adj

carotid in V. Sys


20/98

Page20

Absent A waves AF

V Large V waves TR

X Increased Prominence

Decreased Prominence

C tamponade & CpericarditisTR, AF, RVF

Y Rapid Descent(Friedreichs sign)

Slow descent

TR, C. PeriC

TS, C.tamponade

Engorged & Pulsatile

C tamponade & C pericarditisTR & TS

Restrictve Cardiomyopathy

RHF & Pulm TECHB

Engorged & NON Pulsatile

SVS syndrome & BC syndromeChronic C pericarditis

Vasalva manoeuvre

Low JVP

Dehydration

After massive Hamerrohage

After massive diuretic therapy

Pericardial Knock: Sound In EARLY DIASTOLE:

Restrictive effect of adj pericardium on diastolic

expansion of ventricle: C. pericarditis

12

Spider naevi / arterial spider / Spider Angioma /

vascular spider / arterial telangiectasias, centrally

dilated arteriole with numerous vesselss Radiating

from it usually seen in upper part of thorax

(necklace pattern SVC territory) & Upper back

mainly due to increased O/T ratio

Central arteriole pressed & release:- Immediateblanching with filling from Centre to periphery

2 Normal people

Alcoholics

3

rd

trimester pregnancy

RA

Thyrotoxicosis

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

Palmar erythema / liver palms: Thenar &

hypothenar eminence & finger pulpsBLANCHES

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 & SymmetricalSelf limiting in 26 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


21/98

Page21

Shin (Erythema Nodosum, Pretibial myxoedema,

Necrobiosis lippoidica diabeticorum, Lichen

amyloidosis)

ENL:Type 2 lepra reactionPainful 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 LargeNOT ULCERATE Freq occur

TENDER NON TENDERSkin FREE FIXED to skin

Assc Active Carditis Associted +ve RFactorSec infection: rare SEC INFECTION: freq

Extensor surfaces of

elbowsExtensor Tendons of

fingers & ToesBack of head

Margins of patellaAchilles tendonSacrum

Extensor surfaces of

elbowsExtensor Tendons of

fingers & ToesBack of head

Margins of patellaAchilles tendonSacrum

** 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

16

Memory:

1)) Short term / immediate recall / Rote memory

2)) Recent memory

3)) Past memory / Long term / Remote memory

Registration + Retension + Recall + Reproduction

1 7 digits forward / 5 digits Backward &Telephone number repeat after 30 sec

2 Name of vistors Who came yesterday

Ask morning news*(index of severity of Organic Braindisease)

3

(Resistant)

Ask imp life events

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 onlyInternal stimulus) > Coma OR by using GCS

Conscious >15 Deeply comatose 3

Released Reflexes (Dementia, Organic Confusional

states & CONTRALATERAL frontal lobe Lesion)

Grasp By distally moving Stimulus onradial Aspect of palmar surfaceof handGrasp & Unable to

relax the Grasp Voluntarily

Forced GropingAvoiding* By distally moving stimulus on

Ulnar Aspect of palmar surfaceof handHand move away

Palmo mental** Scrathing THENARChinpuckering due to MENTALISmuscle Contraction

Sucking Lip / Mouth cornerContraction of Tongue, Jawmuscles associated withSwallowing

Rooting Lips follow Stimulating object

when it is touchedSnout Tap with Knuckle on Patients

UPPERLIPPouting of lips dueto ORBICULARIS ORIS musclecontraction

Myersons /

Glabellar tapUninterrupted / continuousBlinking with tap (N: 3 OR 4)

* CONTRALATERAL parietal Lobe lesion

** NO LOCALIZING Valu


22/98

Page22

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

1stAsk nameNOS/M aphasiaWrite 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: LPS3rdN & Mullers Sympathetic

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)


23/98

Page23

OBSTERTRICS

1)) Previous LSCS

2)) Diabetes Complicating pregnancy

3)) Heart diseases Complicating

pregnancy

4)) Anemia Complicating pregnancy

5)) Bad obstetric History

6)) Hypertensive disorders Complicating

pregnancy

7)) Breech presentation

2


24/98

Page24

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

OBSTETRIC H/O:

Past pregnancies:-

1st1 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 6thday &

she stayed in hospital for 7 days

puerperal period is uneventful.

Baby is healthy & No nicu admissions & vaccinated

breast fed continued for 2 yrs2ndpregnancy.

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 6thday &

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 (56 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 1st3 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 1stdose in 5m

USG -6m &

In 3rdtrimester


No H/O leg swelling

No H/O blood transfusions

TT 2nddose 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: reducedB/B: regular, Sleep: disturbed


25/98

Page25

Addictions: Chronic smoker & Non alcoholic &NON consangious marriage

GCOE:

Patient is C/C/C.

Moderately built & withP (+) I (-) C (-) C (-) K (-) L (-)

Bilateral pedal oedema, Pitting typewhich is upto kneeNo thyroid enlargementBreast NormalSpine & gait NormalVitalsafebrile,HR: 80/min. N in volume, character, & rhythm No

RR/RF delay No vessel wall thickeningBP: 120/86 mm hg RUL: SittingRR: 19/min

JVP: NOT raised

OBSTETRIC EXAMINATION:

Abdominal examination

On inspection:Abdomen is generally distendedAll quadrants move equally with respiration

Flanks full

Umbilicus slit like & invertedstria gravidarum & linea nigra presentA curvilinear suprapubic scar is seen which is about7 cm in length & No puckering which seen healed

by primary intentionNo other scars / SinusesNo engorged Veins

Palpation:

Scar tenderness:- absent

Fundal height32 weeks (with flanks full)

fundal grip

Soft, Non ballotable, Broad mass

probably podalic poleLateral gripLeft side hard board like mass felt

probably babys back & On right side multiple fetal

parts felt1

st

pelvic grip

hard ballotable, mass probablycephalic pole

Ausultation

Fetal heart sounds136/min regular

Per veginal ExaminationNOT done

CVS examination- S1 & S2 heard. Murmer in pulmarea (haemic murmer) No other murmers heard

Respiratory Examination: BLAE +ve & N vesicularsounds heard with No adventitious sounds

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

Discussion:

Whatever is abd inscison : tenderness must be seen

on lower segment & From lateral to centre

1 14 (1

st

T)28 (2

nd

T)- 40 (3

rd

T)

Cesarean delivery : birth of a fetus through incisionsin the abdominal wall (laparotomy) and the uterinewall (hysterotomy). This definition does not include

removal of the fetus from abdominal cavity in caseof 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 ofanatomy may require at least 6 months

4)) Steps:

Different approaches

1))

Pfannensteil kerr technique usually

2)) Joel-Cohen and

3)) Misgav- Ladach methods

Abdominal Incision

Infraumbilical midline vertical (quickest) or asuprapubic transverse incision (modified Pfannenstieincision, the skin and subcutaneous tissue are incised


26/98

Page26

using a lower, transverse, slightly curvilinear incisionat 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, reentrythrough a Pfannenstiel incision usually ismore time consuming and difficult because ofscarring.)special circumstances, paramedianor 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 anteriorlower uterine segmentthe bladder flapisgrasped in the midline with forceps and incised

transversely with scissors. Bladder is separatedUterine 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-segmentvertical Incision (Kronig).Baby delivered (Ant shoulder 1st) & cord clampedFundal massage (promote placental delivery)

Manual placental removal if Not extrudedspontaneouslyuterine cavity is inspected and either suctioned orwiped out with a gauze pack to remove avulsedmembranes, vernix, clots, and other debris.

The upper and lower cut edges and each lateralangle of the uterine incision are examined carefullyfor bleeding & vessels are ligated

Uterine Repair:The uterine incision is then closed with one or two

layers (1stlayer 2ndrunning lock layer) of continuous

0- or #1 absorbable suture (Chromic catgut) &serosal edges overlying the uterus and bladder havebeen 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 fluidusing 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 cesareandelivery

Clinically adequate pelvis No other uterine scars or previous rupture Physician immediately available throughoutactive labor capable of monitoring labor andperforming an emergency cesarean delivery

Availability of anesthesia and personnel foremergency cesarean delivery

5)) Main risk for labour induction is uterine rupture:

selection of women most likely to have a successfulVBAC, as well as avoiding misoprostol andsequential use of prostaglandins and oxytocin,appear to offer the lowest risk of uterine rupture.

(Intravaginal prostaglandins alone, excludingmisoprostol, 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 scardehiscence is necessaryonly if significant bleeding is encountered

7)) With multiple C sections there is increased risk of

hysterectomy placenta previa, placenta accretaparticularly


27/98

Page27

Contraindications For VBAC

Absolute:prior classical cesarean, previousuterine rupture, lack of resources to performemergency 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



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

Dyspnoea2 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 (34/days) for 2m &





No H/O Drug usage

No H/O leg swelling In 1st3 months &In next 3 Months there was


No H/O leg swelling



Quickening in 5m &

TT 1stdose in 5m

USG -6m &

In 3rdtrimester

No H/O bleeding / draining PvNo H/O leg swelling


TT 2nddose in 8m

MENSTRUAL H/O :

Attained Menarche at 12 yrs of age. 5/30..2 pads / day & with Congestive dysmenorrhoeaNo H/O white discharge

No H/O clot passage


28/98

Page28

PAST H/O:

H/O HTN diagnosed at 3mNO H/O similar complaints in past,


DRUG H/O:

Taking IFA


PERSONAL H/O:Diet: mixed, appetite: reducedB/B: regular, Sleep: disturbed

Addictions: Chronic smoker & Non alcoholic &NON consanginous marriage

GCOE:

Patient is C/C/C.

Moderately built & withP (+) I (-) C (-) C (-) K (-) L (-)Bilateral pedal oedema, Pitting type which is just

above ankleNo thyroid enlargementSpine & gait NormalVitals

afebrile,

HR: 76/min. N in volume, character, & rhythm NoRR/RF delay No vessel wall thickeningBP: 130/86 mm hg RUL: SittingRR: 16/min

JVP: NOT raised



On inspection:Abdomen is generally distended

Umbilicus slit like & evertedstria gravidarum & linea nigra present

No scars / Sinuses

No engorged Veins

Palpation:

Fundal height32 weeks (with flanks full)

fundal grip

Soft, Non ballotable, Broad massprobably podalic pole

Lateral gripLeft side hard board like mass feltprobably babys back & On right side multiple fetal

parts felt

1

st

pelvic griphard ballotable, mass probablycephalic pole

AusultationFetal heart sounds - ??

Perveginal ExaminationNOT done

CVS examination

InspectionNOT donePalpation - Apex beat Not shifted (4thics 2cm laterato MCL) & Parasternal impulse absentAuscultation:

Area S1 S2 Murmur

Mitral N + No

Tricuspid + + No

Pulmonary + N(Split ?) No

Aortic + + Soft, ESM,

grade 4 & Noradiation

Diagnosis:

A 20 yr Old primi with term gestation with fundalheight 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.


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Page29

Class II. Slight limitation of physical activity: Thesewomen are comfortable at rest, but if ordinaryphysical activity is undertaken, discomfort in the

form of excessive fatigue, palpitation, dyspnea, oranginal pain results.

Class III. Marked limitation of physical activity:

These women are comfortable at rest, but less thanordinary activity causes excessive fatigue,palpitation, dyspnea, or angina pain.

Class IV.

Severely compromisedinability toperform any physical activity without discomfort:Symptoms of cardiac insufficiencyor angina maydevelop even at rest. If any physicalactivity is

undertaken, discomfort is increased.

Normal findings in Pregnant woman:

Jugular venous distensionMammary souffleS2 P increased; S2 split

S1 M increased and widely splitOccasional S3,

Aortic or pulmonary flow murmurs

2)) Class 3 & 4:a)) If feasible, women with severe cardiac diseaseshould consider pregnancy interruption. If

continued, prolonged hospitalization or bed rest isnecessary.

b)) Epidural analgesia for labor and delivery isusually recommended.Vaginal delivery is preferredin most cases, and labor induction can usually be

done safely

For pregnant women with mechanical heart

valves, any one of the following anticoagulant

regimens is recommended:

Adjusted-dose LMWH twice daily throughoutpregnancy. Adjusted-dose UFH administered every 12 hoursthroughout pregnancy. LMWH or UFH as above until 13 weeks gestation

with warfarin substitution until close to deliverywhen LMWH or UFH is resumed.

** In women judged to be at very high risk of

thromboembolism and in whom concerns existabout the efficacy and safety of LMWH or UFH.

*** Warfarin is suggested throughout pregnancywith replacement by UFH or LMWH(as above) close to delivery.

In addition, low-dose aspirinorally administered.

3))

In MR & AR: Ventricular function

improves with afterload decrease. In MS (heart

failure due to fluid overload) & AS (Moderatestenosis tolerated; severe is life-threatening withdecreased preload)4))

MS:

Limited physical activity

dietary sodium is restricted, and diuretic therapy

blocker drug is usually given to blunt the cardiacresponse to activity and anxiety

new-onset atrial fibrillation develops,IV verapamil / electrocardioversionchronic fibrillation, digoxin,

Therapeutic anticoagulation with heparin isindicated with persistent fibrillation.

heparinization with severe stenosis even if there is asinus rhythm.

Vaginal delivery & elective induction is reasonableMR:

well tolerated during pregnancy, probably becausedecreased systemic vascular resistance results in lessregurgitation. Heart failure

only rarely develops during pregnancyIntrapartum 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 intravascularvolume in anticipation of possible haemorrhage.

During labor, narcotic epidural analgesia seemsideal, thus avoiding potentially hazardoushypotension

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.


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Page30

Epidural analgesia is used for labor and delivery,and bacterial endocarditis prophylaxis may berequired.

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 heartdisease, 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 / periapicaltooth regionwith 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



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

7thmonth

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:

present pregnancy:-


Confirmed by local doctor






No H/O Drug usage




No H/O leg swelling



Quickening in 5m &

TT 1stdose in 5m

USG -6m &

In 3rdtrimester


No H/O leg swelling


TT 2nddose 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

NO H/O DM, TB, IHD, RHD, epilepsy, chest pain /

Jaundice & bleeding disorders

DRUG H/O:

Took IFA Tab.


PERSONAL H/O:Diet: mixed, appetite: reduced

B/B: regular, Sleep: disturbed


31/98

Page31

Addictions: Non Smoker, alcoholic & NONconsangious marriage

GCOE:

Patient is C/C/C.

Moderately built & withP (+) I (-) C (-) C (-) K (-) L (-)

Bilateral pedal oedema, Pitting typewhich is upto ankleNo thyroid enlargementBreast NormalSpine & gait Normal

Vitals

afebrile,HR: 80/min. N in volume, character, & rhythm NoRR/RF delay No vessel wall thickening

BP: 120/86 mm hg RUL: SittingRR: 19/min

JVP: NOT raised



On inspection:

Abdomen is generally distendedAll quadrants move equally with respirationFlanks fullUmbilicus slit like & inverted

stria gravidarum & linea nigra presentNo other scars / SinusesNo engorged Veins

Palpation:

Fundal height32 weeks (with flanks full)fundal gripSoft, Non ballotable, Broad massprobably podalic pole

Lateral gripLeft side hard board like mass feltprobably babys back &On right side multiple fetal

parts felt

1

st

pelvic grip

hard ballotable, mass probablycephalic pole

AusultationFetal heart sounds??

Per veginal Examination

NOT done

CVS examination- S1 & S2 heard. No murmers heard


Diagnosis:

A 22 yr Old Primi with term gestationwith fundal height corresponding with gestational

age with Hypertension complicating pregnancy,With No signs of imminent eclampsia

Discussion

Working Group classification

1. Gestational hypertensionformerly termed PIH Ifpreeclampsia syndrome does not develop andhypertension resolves by 12 weeks postpartum ,it is redesignated as transient hypertension

2. Preeclampsia (some have atypical preeclampsiawith all aspects of the syndrome, but without

hypertension or proteinuria, or both) and eclampsiasyndrome3. Preeclampsia syndrome superimposed on chronic

hypertension4. Chronic hypertension

** Proteinuria is defined by 24-hour urinary proteinexcretion 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 previareduced risk of hypertension during pregnancy

2))

Preeclampsia often affects young and nulliparouswomen, whereas older women are at greater riskfor chronic hypertension with superimposedpreeclampsia,

3)) Preeclampsia syndromeis a two-stage disorder. Stage 1 (preclinical) is caused by faultyendovasculartrophoblastic remodeling thatdownstream causes the stage 2 clinical syndrome & Stage 2 is susceptible to modification by


32/98

Page32

preexisting maternal conditions that include cardiacor renal disease, diabetes, obesity, or hereditaryinfluences

Hemoconcentration is a hallmark of eclampsia.

Preeclampsia (culmination of factors that likely

involve a number of maternal, placental, and fetalfactors)

Placental implantation with abnormal

trophoblastic invasion of uterine vessels.(incomplete invasion of the spiral arteriolar wall byextravillous trophoblasts and results in a smallcaliber

vessels with resistance) Immunological maladaptive tolerance betweenmaternal, paternal (placental), and fetal tissues

Maternal maladaptation to cardiovascular orinflammatory changes of normal pregnancy

Genetic factors including inherited predisposinggenes as well as epigenetic influences.

** This finally leads to release unknown factor

(s)likely placental in originare secreted into thematernal circulation and provoke widespreadactivation and dysfunction of the vascularendothelium: Increased pressor response,Vasospasmimbalance between NO & PG levels & between

Angiogenic and Antiangiogenic Proteins

Most importantly overproduction of at least two

antiangiogenic peptides from trophoblastic tissuethat 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

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


Confirmed by a local doctor.






No H/O Drug usage




No H/O leg swelling



Quickening in 5m &

TT 1stdose in 5m

USG -6m &

In 3rdtrimester


No H/O leg swelling


TT 2nddose in 8m

Past pregnancies

1

st

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 1stchild birth

Spontaneous coneption.


33/98

Page33

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 HTNNO 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: disturbedAddictions: Non Smoker, alcoholic & NON

consangious marriage

GCOE:

Patient is C/C/C.Moderately built & withP (+) I (-) C (-) C (-) K (-) L (-)Bilateral pedal oedema, Pitting typewhich is upto ankle

No thyroid enlargementBreast NormalSpine & gait Normal

Vitalsafebrile,

HR: 80/min. N in volume, character, & rhythm No

RR/RF delay No vessel wall thickeningBP: 120/86 mm hg RUL: Sitting

RR: 19/minJVP: NOT raised



On inspection:Abdomen is generally distendedAll quadrants move equally with respiration

Flanks fullUmbilicus slit like & inverted

stria gravidarum & linea nigra presentNo other scars / Sinuses

No engorged Veins

Palpation:

Fundal height

32 weeks (with flanks full)

fundal griphard ballotable, mass probablycephalic poleLateral gripLeft side hard board like mass felt

probably babys back & On right side multiple fetal

parts felt1

st

pelvic grip

Soft, Non ballotable, Broad mass

probably podalic poleAusultationFetal heart sounds??


CVS examination- S1 & S2 heard. No murmers heard

Respiratory Examination

: BLAE +ve & N vesicularsounds heard with No adventitious sounds

Diagnosis: A 25 yr old Pregnant women with

G3P2L1 came with uncomplicated breechpresentation for safe institutional delivery

Discussion

COMPLICATIONS

In the persistent breech presentation, an increasedfrequency of the following complications can be

anticipated:

Prolapsed cord Placenta previa

Congenital anomalies Uterine anomalies and tumors Difficultdelivery

Increased maternal and perinatal morbidity


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Partial breech extraction .The fetus is delivered spontaneously as far as theumbilicus, but the remainder of the body is

extracted or delivered with operator traction andassisted maneuvers, with or without maternal

expulsive efforts.

Total breech extraction .The entire body of the fetus is extracted by theobstetrician (Dead baby & 2ndbaby after podalicversion with transverse lie)

Delivery of the Aftercoming Head

1)) Mauriceau Maneuver

2))

Modified Prague Maneuver (necessitated byfailure of the fetal trunk to rotate anteriorly.)

3)) Specialized forceps can be used to deliver theaftercoming head.Piper forceps or divergent Laufe

forceps may be applied electively or when theMauriceau maneuvercannot be accomplished easily

Climbing Up: when buttocks visible at introitus(similar to crowning in cephalic presentation)Piper forceps: Also have perineal curve

Cesarean delivery (commonly, but notexclusively, used in following circumstances)

1.A large fetus2.Any degree of contraction or unfavorable shapeof thepelvis determined clinically or with CT pelvimetry

3.A hyperextended head

4.

When delivery is indicated in the absence ofspontaneouslabor5.Uterine dysfunctionsome would use oxytocin

augmentation

6.

Incomplete or footling breech presentation7.

An apparently healthy and viable preterm fetus

with themother in either active labor or in whom delivery is

indicated8.Severe fetal-growth restriction

9.

Previous perinatal death or children suffering

from birthtrauma

10

. A request for sterilization11.

Lack of an experienced operator.

Factors That May Modify the Success ofExternal Cephalic Version

Increase Success

Increasing parity

Ample amnionic fluidUnengaged fetus

Tocolysis

Decrease Success

Engaged fetus

Tense uterusInability to palpate headObesity

Anterior placentaFetal spine anterior or posterior

Duhrssen incisionbeing cut at 2 oclock, which isfollowed 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 theuterine cavity

External Cephalic Version

:A forward roll of thefetus usually is attempted first. If the forward roll is

unsuccessful, then a backward flip is attempted

(According to whether the head or breech is madethe presenting part, the operation is designatedcephalic 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 rotationaltraction until the lower halves of the scapulas

are delivered, making no attempt at delivery of


35/98

Page35

the shoulders and arms until one axilla becomesvisible.

The appearance of one axilla indicates that the

time has arrived for delivery of the shoulders. Itmakes little difference which shoulder is deliveredfirst.

Frank Breech Extraction:

Frank breech decomposition using the Pinard

maneuver.

Two fingers are inserted along one extremity to theknee, which is then pushed away from the midlineafter 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

H/P/I

:

OBSTETRIC H/O:

present pregnancy:-







No H/O Drug usage




No H/O leg swelling



Quickening in 5m &

TT 1stdose in 5m

USG -6m &

In 3rdtrimester


No H/O leg swelling


TT 2nddose 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:

Diet: mixed, appetite: reducedB/B: regular, Sleep: disturbedAddictions: Non Smoker, alcoholic & NON

consangious marriage

GCOE:

Patient is C/C/C.Moderately built & withP (+) I (-) C (-) C (-) K (-) L (-)

Bilateral pedal oedema, Pitting type

which is upto ankleNo thyroid enlargementBreast NormalSpine & gait Normal

Vitals

afebrile,

HR: 80/min. N in volume, character, & rhythm NoRR/RF delay No vessel wall thickening

BP: 120/86 mm hg RUL: SittingRR: 19/minJVP: NOT raised



36/98

Page36


On inspection

:

Abdomen is generally distendedAll quadrants move equally with respiration

Flanks fullUmbilicus slit like & inverted

stria gravidarum & linea nigra presentNo other scars / SinusesNo engorged Veins

Palpation:

Fundal height32 weeks (with flanks full)fundal gripSoft, Non ballotable, Broad mass

probably podalic pole

Lateral grip

Left side hard board like mass feltprobably babys back & On right side multiple fetal

parts felt1

st

pelvic griphard ballotable, mass probably

cephalic pole

Ausultation

Fetal heart sounds??


CVS examination

- S1 & S2 heard. No murmers heard


Discussion

There is increasing support for the use of glyburideas an alternative to insulin in the management ofgestational diabetes

Glyburide Treatment Regimen for Women withGestational Diabetes Who Fail Diet Therapy

Glucometer blood glucose measurements fasting

and 1/2 hours following breakfast, lunch & dinner.Glucose level goals (mg/dL): Fasting


37/98

Page37

No history of poor obstetrical outcome

Average Risk: Perform blood glucose testing at 24to 28 weeks using either:

Two-step procedure: 50-g oral glucose challengetest (GCT), followed by a diagnostic 100-g oralglucose tolerance test for those meeting the

threshold value in the GCT.

One

step procedure

: Diagnostic 100-g oralglucose 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 obesityStrong family history of type 2 diabetesPrevious history of GDM, impaired glucose

metabolism, or glucosuria.

Diagnosis of Gestational Diabetes by Oral

Glucose Tolerance Testing.

Time 100-g Glucose 75-g Glucose

Fasting 95 95! hr 180 180

2 hr 155 155

3 hr 140 -

** The test should be performed in the morningafter an overnight fast of at least 8 h

but not more than 14 h and after at least 3 days ofunrestricted diet and physical activity.

*** Two or more of the venous plasma glucoseconcentrations indicated below must be

met or exceeded for a positive diagnosis

An ideal dietary composition is 55 percentcarbohydrate, 20 percent protein, and

25 percent fat with less than 10 percent as saturated

fat.

Management of Db KA in pregnancy

** Obtain arterial blood gases to document degreeof acidosis present; measure glucose, ketones, and

electrolyte levels at 1- to 2-hour intervals

Insulin

Low-dose, intravenousLoading dose: 0.20.4 U/kg

Maintenance: 210 U/h

Fluids

Isotonic sodium chloride

Total replacement in first 12 hours of 46 L1 L in first hour

5001000 mL/h for 24 hours250 mL/h until 80 percent replacedGlucose

5-percent dextrose in normal salinePotassium

Bicarbonate (if pH is

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