A good PG case presentation on abdominal case, liver

MEDICINE CLINICS 2012CASE DISCUSSION- ABDOMEN

Dr Yeldho

CASE 1History

Mr S43/ MAgriculturist

Chief complaintsYellowish discolouration of eyes : 4 monthsBilateral swelling of the legs : 2 months

History of presenting IllnessPatient c/o yellowish discolouration of the eys

since last 4 monthsInsidious onsetAssociated with yellowish discolouration of

urinePatient c/o bilateral swelling of the legs since

last 2 monthsIncreases as the day progressesNot painful

H/o Abdominal discomfort since last 1-2 monthsDull aching H/o occasional episodes of passing dark tarry

stools in last 2 monthsNo h/o Bleeding per rectumNo h/o of distension of abdomenNo h/o vomiting, haematemesisNo h/o altered behaviour/ altered sleep pattern

No h/o Dyspnoea, Chest pain, Palpitation, decreased Urine out put

No h/o cough , expectorationNo h/o fever, Weight loss

Past historyNo known comorbidsNo h/o Jaundice in pastNo h/o Blood transfusions

Personal historyConsumes alcohol for >35 years180-240 ml /dayCAGE 4Last binge 2 weeks backNon smokerNo h/o substance abuse

Family historyBorn of Non consanguineous marriageMarried with two kidsNo h/o similar complaints in the family

GENERAL PHYSICAL EXAMINATIONModerately built and nourishedConscious, cooperative, oriented to time place

and personPallor +Icterus+B/L pitting pedal Oedema+NO cyanosis, Clubbing , Lymphadenopathy, JVP- not elevated

PR : 86 bpm, regular, normal volume, no radio-radial or radio femoral delay, Condition of vessel wall is normal, All peripheral pulses well felt

BP : 110/ 70 mm of Hg in Rt arm in supine position, No postural drop

RR : 16 cpm, Abdomino thoracicAfebrile

Bilateral Parotid swelling+Gynaecomastia+, Non tenderTattoo mark present over the Rt forearmLeuconychia+No Bitots spots/ KF ringNo Fetor HepaticusNormal hair distributionNo dilated veins over Chest, Abdomen, backNo spider naeviNo Palmar erythemaNo duputrens contractureNo flaps

Are all these signs of Liver cell failure?

• Jaundice• Bitot’s spots• K-F ring• Sub-conjuctival bleed• Parotid enlargement• Loss of facial/chest hair• Fetor hepaticus• Spider naevi

• Gynacomastia • Palmar erythema• Duputren’s contracture• Asterixis• Splinter haemmorhage• Leukonychia• Koilonychia• Testicular atrophy

Interaction opportunity

Signs which indicate derangement of synthetic or metabolic functions of liver are the signs of

liver cell failure

….rest are just signs of liver disease

Bitots spots

• What is it? • Why it is seen in liver disease?• How common you have seen it in cirrhosis?


Bitot’s spots

• Caused due to Vitamin A deficiency as a consequence of malabsorbtion due to decreased fat content in Bile

• Rare in cirrhosis among adults irrespective of etiology

• It is a sign of liver cell failure

Schiff 7th Edition Diseases of Liver

K-F ring

• Where is it seen ?• What is it?• Where the rings first appear?• Can it occur in non-Wilsonian disorder


Kayser-Fleischer ring

• Named after Bernhard Kayser and Bruno Fleisher

• Copper deposited in descements membrane• First appears at 12 o’clock position then at 6

o’clock position , then encircles completely• A similar ring occurs in cholestasis

Sub-conj bleed and splinter Hge

• Why it occurs?


Bleeding in cirrhosis

• Often thought due to ↓coagulation factors• May occur due to thrombocytopenia• Increase in plasma fibrinolysins in cirrhosis• Dysfibrinogenemia due to ↑sialic acid in

cirrhosis


Parotid enlargement

• Why it occurs?• What happens to the enlargement over a

period of time?


Parotid enlargement

• Occurs in 50% of alcoholic cirrhosis• Painless and soft enlargement• Earlier thought due to hypersecretory parotid• Now appears to be due to edema and fatty

infiltration• Size can fluctuate during heavy alcohol intake


Loss of facial / chest hair

• Why it happens? • Do cirrhotic patients loose scalp hair?


Loss of Facial/Chest hair

• Loss of male pattern of hair• Density of hair over face and chest not

different in cirrhosis compared to controls• Asians by nature have sparse chest hair• Clinical significance is questionable


Fetor hepaticus

• What is it?• Why it occurs?


Fetor hepaticus

• Established reason is mercaptons• Mercaptons are thiols (sulfur containing

compounds) formed due to gut metabolism• Newer evidence point to dimethyl sulphide as

the reason for fetor hepaticus


Velde et al.GC-MS analysis of breath odour compound in liver pts.J Chromat 2008;875:344-348

Spider naevi

• How it looks like?• Where is it seen?• Why it occurs?• Does it give any clue for a impending

complication


Spider angioma

• Often seen in SVC region• Due to shunted steroidal estrogen precursors

causing arteriolar dilatation• Frequency of variceal bleed is 50% if > 20

present• Size more than 15 mm – 80% freq of bleed• DD: venous star, campbell de morgni spots.


Gynacomastia

• Why it occurs?• Any etiological significance?


Gynacomastia

• Occurs due to 2 mechanism• Mech 1: ↑conversion of weak androgenic

steroids to estrogens in peripheral tissues especially adipose tissue causing local fat deposit. Alcohol induces androgenic steroids

• Mech 2: steroidal estrogen precursors escape the entero-hepatic circulation and then undergo peripheral conversion


Palmar erythema

• Which part of the palm is affected?• Why it occurs?


Palmar erythema

• Involves thenar and hypothenar eminence, distal pads of fingers, circumungual areas on dorsum of fingers

• Central part of palm is clear• Represents collection of A-V anastamosis• Steroid estrogen precursors blammed• Can occur in RA,pregnancy and OCP use


Asterexis

• Why it occurs?• Defect in which part of brain produce this• Which non-hepatic conditions produce this?


Asterixis

• Peripheral manifestation of CNS metabolic dysfunction

• Occurs in hypercarbia , uremia, hypoglycemia, barbiturate intoxication

• Descending Reticular activating system is responsible for maintaining posture, muscle tone and reflexes

• Ammonia suppresses descending RAS causing asterixis


Leukonychia

• Why it occurs?


Leukonychia

• Occurs due to severe hypoalbuminemia (<2g)• Widely believed due to ↓ hepatocyte number• Hypoalbuminemia can occur due to alcohol,

malnutrition and altered metabolism of adrenal , testicular,ovarian and thyroid hormones in cirrhosis

• Can occur in hypoalbuminemia due to other causes


Testicular atrophy

• Why it occur• Any etiological significance

Testicular atrophy

• Direct effect of alcohol and not related to estrogen effect.

• Characteristic in alcoholic cirrhosis.• Also occurs in hemochromatosis.


Jaundice in cirrhosis

What are the non-hepatocellular causes?


Jaundice in cirrhosis

• Mostly due to progressive hepato-cellular injury• Can be due to hypersplenism related hemolysis• Can be due to obstruction by gall stones ( increase on

account of hemolysis) or pancreatitis


Are all these signs of Liver cell failure?

• Jaundice• Bitot’s spots• K-F ring• Sub-conjuctival bleed• Parotid enlargement• Loss of facial/chest hair• Fetor hepaticus• Spider naevi

• Gynacomastia • Palmar erythema• Duputren’s contracture• Asterixis• Splinter haemmorhage• Leukonychia• Koilonychia• Testicular atrophy

Examination of AbdomenINSPECTIONAbdomen is uniformly distendedFlanks are fullUmbilicus is normally placedAll quadrants move equally with respirationNo dilated veinsNo visible mass, scars ,sinus, striae or peristalsisExternal genitalia is normalHernial orifices are free

PALPATIONAbdomen is softNo tendernessLiver is palpable• 2cm below the costal margin• Non tender• firm in consistency• Rounded margins• Smooth surfaceNo other palpable massNo testicular atrophyNo renal angle tenderness

Measurements :-Abdominal Girth : 112 cmsXiphi sternum – Umbilicus : 28 cmsUmbilicus to Pubic Symphysis : 26 cmsUmbilicus to ASIS on Right : 27 cms Left : 27 cms

PERCUSSIONLiver dullness is felt in the 5th ICS in the MCLLiver span is 16 cmsNo shifting dullnessTraubes space is resonant on percussion

AUSCULTATIONNormal bowel sounds heardNo hepatic / splenic rubNo Bruit/ Venous Hum

OTHER SYSTEMS

CVS : S1 S2 Heard, No murmersRS : B/L NVBS heard, No added soundsCNS : NFND, No Flaps

Summary43yr / Male / Chronic AlcoholicJaundice and B/L Pedal Oedema -2 monthsNo Bleeding manifestations/ altered behaviorGPE : Pallor/ Icterus/ B/L pitting pedal oedema/ Parotid swelling/ Leuconychia/GynaecomastiaP/A : Non tender hepatomegaly + No splenomegaly/ No Free fluidOther Systems : normal

FINAL DIAGNOSIS

COMPENSATED LIVER DISEASE in the form of Early CIRRHOSIS probably ETHANOL RELATED with no signs of PORTAL HYPERTENSION or ENCEPHALOPATHY

Comments on the case

• Not convinced on gynacomastia and leukonychia • To mention about nodules around umblicus• Mention about divarication of recti• Bedside tests for hepatic encephalopathy• Mention on liver pulsation• Landmark line (MCL,AAL,MAL) for hepatomegaly• Can it be decompensated liver disease in view of

malena

What is decompensated liver disease?

When to suspect?


Compensate: to cover a damage or loss Decompensate: to unmask a damage

DecompensatedLiver

Without cirrhosis eg:FHF , alch hepatitis With cirrhosis

Worsening jaundice along with encephalopathy and or coagulopathy

1.Features of PHT2.Signs of failure to metabolize hormones,eg:spider nevi3.Signs of hepatic encephalopathy4.Signs of coagulopathy

Problem situations

Jaundice > 2mthsNo signs of liver failure

HepatomegalyMalena

No ascitis,splenomegaly,veins

Jaundice > 2 mthsNo signs of liver failure

HepatomegalyAscitis

No splenomegaly , veins

Ascitis

Possible Decompensation Decompensation

Differential diagnosis

What is the natural history of alcoholic hepatitis?

Pattern of onset and circumstances, symptoms ,signs and outcome


Alcoholic hepatitis is a clinical syndrome characterized by rapid development of

jaundice and liver failure most often due to long term alcohol over-consumption

• Nausea and malaise• Fever• Jaundice• Abdominal pain• Altered mentation• Bleeding tendencies• Abdominal and

peripheral edema

• Febrile and tachypneic• Tachycardia• Icterus and edema• Enlarged tender liver• Ascitis• Splenomegaly• Asterixis• Hepatic bruit(<2%)

Symptoms Signs

Presence of spider naevi may indicate co-existent cirrhosis

Outcome of Alcoholic hepatitis27%- histological normalization

18%-progress to cirrhosis55%- persistent AH at 18 months

When to suspect Chronic viral hepatitis?


No clinical symptom or sign is a good predictor

Suspect Chronic HBV / HCV infection in any patient with jaundice

When to suspect autoimmune hepatitis or Wilson’s disease?

Is there a pattern with age?


• Usually female• Usually 15-25 years• Other immune diseases• Recent reports :25 to 50

years increasingly affected

• Can occur even at age>60 years

• Age 3 to 55 years• Case reports suggest a

range of 1 to 60 years

Nature of disease in patients aged > 50 years less clear

CASE 2

Mrs M55 yrs / FemaleHouse wifeChief complaintsEasy fatiguability 2-3 months

PAST HISTORYH/o hospital admission for Haematemisis 40 yrs

backDetails of treatment not knownNo h/o jaundiceNo h/o Blood transfusionsNo known co morbid illness

GENERAL PHYSICAL EXAMINATIONModeratly built and nourishedConscious oriented, cooperative Pallor +No Icterus, Cyanosis, Clubbing, Koilonychia,

Lymphadenopathy, Pedal OedemaPR : 74 bpm regularBP : 120/80 mm of HgRR : 16 cpmAfebrile

Examination of AbdomenINSPECTIONAbdomen is uniformly distendedFlanks are fullUmbilicus is normally placedAll quadrants move equally with respirationDilated and tortuous veins are seen over the

anterior abdominal wall, flanks and BackFlow from below upwardsNo visible mass, scars ,sinus, striae or peristalsisExternal genitalia is normalHernial orifices are free

PALPATIONAbdomen is softNo TendernessNo organomegalyDilated and tortuous veins present over the

anterior abdominal wall, flanks and back with flow from below upwards

Direction of flow in anterior abdominal veins

Cirrhosis Vs IVC obst Vs SVC obstName the anterior abd wall veins


SVC – Femoral vein bypass route!

ITV-Internal thoracic vein

SEV-Superior epigastric vein

IEV-Inferior epigastric vein

SVC-Superior vena cava

FV-Femoral vein

Para-umblical vein

Cirrhosis





FV-Femoral vein

Para-umblical vein

IVC Obstruction





FV-Femoral vein

Para-umblical vein

SVC obstruction





FV-Femoral vein

Para-umblical vein

Dilated back veins

PERCUSSIONLiver dullness is felt in the 5th ICS in the MCLLiver span is 13 cmsNo shifting dullnessTraubes space is resonant on percussion

AUSCULTATIONNormal bowel sounds heardNo hepatic / splenic rubNo Bruit/ Venous Hum

OTHER SYSTEMS

CVS : S1 S2 Heard, No murmersRS : B/L NVBS heard, No added soundsCNS : NFND, No Flaps

SUMMARY55 Yrs/ Female/ Non alcoholicRelatively asymptomatic at presentIncidently found to have dilated veins over the Anterior

abdominal wall and BackPast History of single episode of Heamatemesis 40 Yrs backGPE : Pallor + No External markers of liver cell failureP/A : Dilated and tortuous veins over anterior abdominal wall, flanks and back with direction of flow below upwards. No hepatosplenomegaly No freefluid

FINAL DIAGNOSIS

PRE-HEPATIC OBSTRUCTION OF INFERIOR VENECAVA

Never forget to check for abdomino-jugular reflex when you see dilated abdominal veins

Where is the lesion?


Possible sites of occlusion

Level 1

Level 2

Level 3

Level 1 and Level 2 : Budd-chiari syndrome

Level 1

Level 2

Level 3

Acute :Abdominal painTender hepatomegalyJaundiceRapid onset ascitis No dilated veins

Level 1 and Level 2 : Budd-chiari syndrome

Level 1

Level 2

Level 3

Chronic :HepatomegalyAscitis Tortuous veins in level 1Back veins

Level 3 : Sub-hepatic IVC obstruction

Level 1

Level 2

Level 3

Features :Tortuous veins No ascitis Leg edema

Thank you….. See you as Physicians

A good PG case presentation on abdominal case, liver

Health & Medicine

Transcript of A good PG case presentation on abdominal case, liver