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A nice case presentation by PG SRMC on Liver and abdomen.
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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?
Interaction opportunity
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
Interaction opportunity
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?
Interaction opportunity
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
Schiff 7th Edition Diseases of Liver
Parotid enlargement
• Why it occurs?• What happens to the enlargement over a
period of time?
Interaction opportunity
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
Schiff 7th Edition Diseases of Liver
Loss of facial / chest hair
• Why it happens? • Do cirrhotic patients loose scalp hair?
Interaction opportunity
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
Schiff 7th Edition Diseases of Liver
Fetor hepaticus
• What is it?• Why it occurs?
Interaction opportunity
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
Schiff 7th Edition Diseases of Liver
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
Interaction opportunity
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.
Schiff 7th Edition Diseases of Liver
Gynacomastia
• Why it occurs?• Any etiological significance?
Interaction opportunity
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
Schiff 7th Edition Diseases of Liver
Palmar erythema
• Which part of the palm is affected?• Why it occurs?
Interaction opportunity
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
Schiff 7th Edition Diseases of Liver
Asterexis
• Why it occurs?• Defect in which part of brain produce this• Which non-hepatic conditions produce this?
Interaction opportunity
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
Schiff 7th Edition Diseases of Liver
Leukonychia
• Why it occurs?
Interaction opportunity
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
Schiff 7th Edition Diseases of Liver
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.
Schiff 7th Edition Diseases of Liver
Jaundice in cirrhosis
What are the non-hepatocellular causes?
Interaction opportunity
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
Schiff 7th Edition Diseases of Liver
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?
Interaction opportunity
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
Interaction opportunity
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?
Interaction opportunity
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?
Interaction opportunity
• 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
Interaction opportunity
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
ITV-Internal thoracic vein
SEV-Superior epigastric vein
IEV-Inferior epigastric vein
SVC-Superior vena cava
FV-Femoral vein
Para-umblical vein
IVC Obstruction
ITV-Internal thoracic vein
SEV-Superior epigastric vein
IEV-Inferior epigastric vein
SVC-Superior vena cava
FV-Femoral vein
Para-umblical vein
SVC obstruction
ITV-Internal thoracic vein
SEV-Superior epigastric vein
IEV-Inferior epigastric vein
SVC-Superior vena cava
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?
Interaction opportunity
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