A nice case presentation by PG SRMC on Liver and abdomen.

1. MEDICINE CLINICS 2012
CASE DISCUSSION- ABDOMEN
Dr Yeldho

2. CASE 1
History
Mr S
43/ M
Agriculturist
Chief complaints
Yellowish discolouration of eyes : 4 months
Bilateral swelling of the legs : 2 months

3. History of presenting Illness
Patient c/o yellowish discolouration of the eys
since last 4 months
Insidious onset
Associated with yellowish discolouration of
urine
Patient c/o bilateral swelling of the legs since
last 2 months
Increases as the day progresses
Not painful

4. H/o Abdominal discomfort since last 1-2 months
Dull aching
H/o occasional episodes of passing dark tarry
stools in last 2 months
No h/o Bleeding per rectum
No h/o of distension of abdomen
No h/o vomiting, haematemesis
No h/o altered behaviour/ altered sleep pattern

5. No h/o Dyspnoea, Chest pain, Palpitation,
decreased Urine out put
No h/o cough , expectoration
No h/o fever, Weight loss

6. Past history
No known comorbids
No h/o Jaundice in past
No h/o Blood transfusions

7. Personal history
Consumes alcohol for >35 years
180-240 ml /day
CAGE 4
Last binge 2 weeks back
Non smoker
No h/o substance abuse

8. Family history
Born of Non consanguineous marriage
Married with two kids
No h/o similar complaints in the family

9. GENERAL PHYSICAL EXAMINATION
Moderately built and nourished
Conscious, cooperative, oriented to time place
and person
Pallor +
Icterus+
B/L pitting pedal Oedema+
NO cyanosis, Clubbing , Lymphadenopathy,
JVP- not elevated

10. 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 thoracic
Afebrile

11. Bilateral Parotid swelling+
Gynaecomastia+, Non tender
Tattoo mark present over the Rt forearm
Leuconychia+
No Bitots spots/ KF ring
No Fetor Hepaticus
Normal hair distribution
No dilated veins over Chest, Abdomen, back
No spider naevi
No Palmar erythema
No duputrens contracture
No flaps

18. 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

19. 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

20. Bitots spots
• What is it?
• Why it is seen in liver disease?
• How common you have seen it in cirrhosis?
Interaction opportunity

21. 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

22. K-F ring
• Where is it seen ?
• What is it?
• Where the rings first appear?
• Can it occur in non-Wilsonian disorder
Interaction opportunity

23. 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

24. Sub-conj bleed and splinter Hge
• Why it occurs?
Interaction opportunity

25. 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

26. Parotid enlargement
• Why it occurs?
• What happens to the enlargement over a
period of time?
Interaction opportunity

27. 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

28. Loss of facial / chest hair
• Why it happens?
• Do cirrhotic patients loose scalp hair?
Interaction opportunity

29. 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

30. Fetor hepaticus
• What is it?
• Why it occurs?
Interaction opportunity

31. 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

32. Spider naevi
• How it looks like?
• Where is it seen?
• Why it occurs?
• Does it give any clue for a impending
complication
Interaction opportunity

33. 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

34. Gynacomastia
• Why it occurs?
• Any etiological significance?
Interaction opportunity

35. 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

36. Palmar erythema
• Which part of the palm is affected?
• Why it occurs?
Interaction opportunity

37. 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

38. Asterexis
• Why it occurs?
• Defect in which part of brain produce this
• Which non-hepatic conditions produce this?
Interaction opportunity

39. 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

40. Leukonychia
• Why it occurs?
Interaction opportunity

41. 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

42. Testicular atrophy
• Why it occur
• Any etiological significance

43. 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

44. Jaundice in cirrhosis
What are the non-hepatocellular
causes?
Interaction opportunity

45. 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

46. 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

47. Examination of Abdomen
INSPECTION
Abdomen is uniformly distended
Flanks are full
Umbilicus is normally placed
All quadrants move equally with respiration
No dilated veins
No visible mass, scars ,sinus, striae or peristalsis
External genitalia is normal
Hernial orifices are free

48. PALPATION
Abdomen is soft
No tenderness
Liver is palpable
• 2cm below the costal margin
• Non tender
• firm in consistency
• Rounded margins
• Smooth surface
No other palpable mass
No testicular atrophy
No renal angle tenderness

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

50. PERCUSSION
Liver dullness is felt in the 5th ICS in the MCL
Liver span is 16 cms
No shifting dullness
Traubes space is resonant on percussion

51. AUSCULTATION
Normal bowel sounds heard
No hepatic / splenic rub
No Bruit/ Venous Hum

52. OTHER SYSTEMS
CVS : S1 S2 Heard, No murmers
RS : B/L NVBS heard, No added sounds
CNS : NFND, No Flaps

53. Summary
43yr / Male / Chronic Alcoholic
Jaundice and B/L Pedal Oedema -2 months
No Bleeding manifestations/ altered behavior
GPE : Pallor/ Icterus/ B/L pitting pedal oedema/
Parotid swelling/ Leuconychia/Gynaecomastia
P/A : Non tender hepatomegaly +
No splenomegaly/ No Free fluid
Other Systems : normal

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

55. 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

56. What is decompensated liver
disease?
When to suspect?
Interaction opportunity

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

58. Decompensated
Liver
Without cirrhosis
eg:FHF , alch hepatitis
With cirrhosis
Worsening jaundice along with encephalopathy
and or coagulopathy
1.Features of PHT
2.Signs of failure to metabolize
hormones,eg:spider nevi
3.Signs of hepatic encephalopathy
4.Signs of coagulopathy

59. Problem situations
Jaundice > 2mths
No signs of liver failure
Hepatomegaly
Malena
No ascitis,splenomegaly,veins
Jaundice > 2 mths
No signs of liver failure
Hepatomegaly
Ascitis
No splenomegaly , veins
Ascitis
Possible Decompensation Decompensation
Differential diagnosis

60. What is the natural history of
alcoholic hepatitis?
Pattern of onset and circumstances,
symptoms ,signs and outcome
Interaction opportunity

61. Alcoholic hepatitis is a clinical syndrome
characterized by rapid development of
jaundice and liver failure most often due
to long term alcohol over-consumption

62. • 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

63. Outcome of Alcoholic hepatitis
27%- histological normalization
18%-progress to cirrhosis
55%- persistent AH at 18 months

64. When to suspect Chronic viral
hepatitis?
Interaction opportunity

65. No clinical symptom or sign is a good
predictor
Suspect Chronic HBV / HCV infection in
any patient with jaundice

66. When to suspect autoimmune
hepatitis or Wilson’s disease?
Is there a pattern with age?
Interaction opportunity

67. • 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

68. CASE 2
Mrs M
55 yrs / Female
House wife
Chief complaints
Easy fatiguability 2-3 months

69. PAST HISTORY
H/o hospital admission for Haematemisis 40 yrs
back
Details of treatment not known
No h/o jaundice
No h/o Blood transfusions
No known co morbid illness

70. GENERAL PHYSICAL EXAMINATION
Moderatly built and nourished
Conscious oriented, cooperative
Pallor +
No Icterus, Cyanosis, Clubbing, Koilonychia,
Lymphadenopathy, Pedal Oedema
PR : 74 bpm regular
BP : 120/80 mm of Hg
RR : 16 cpm
Afebrile

74. Examination of Abdomen
INSPECTION
Abdomen is uniformly distended
Flanks are full
Umbilicus is normally placed
All quadrants move equally with respiration
Dilated and tortuous veins are seen over the anterior
abdominal wall, flanks and Back
Flow from below upwards
No visible mass, scars ,sinus, striae or peristalsis
External genitalia is normal
Hernial orifices are free

77. PALPATION
Abdomen is soft
No Tenderness
No organomegaly
Dilated and tortuous veins present over the
anterior abdominal wall, flanks and back with
flow from below upwards

79. Direction of flow in anterior
abdominal veins
Cirrhosis Vs IVC obst Vs SVC obst
Name the anterior abd wall veins
Interaction opportunity

80. 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

81. Cirrhosis
ITV-Internal thoracic vein
SEV-Superior epigastric vein
IEV-Inferior epigastric vein
SVC-Superior vena cava
FV-Femoral vein
Para-umblical
vein

82. IVC Obstruction
ITV-Internal thoracic vein
SEV-Superior epigastric vein
IEV-Inferior epigastric vein
SVC-Superior vena cava
FV-Femoral vein
Para-umblical
vein

83. SVC obstruction
ITV-Internal thoracic vein
SEV-Superior epigastric vein
IEV-Inferior epigastric vein
SVC-Superior vena cava
FV-Femoral vein
Para-umblical
vein

84. Dilated back veins

85. PERCUSSION
Liver dullness is felt in the 5th ICS in the MCL
Liver span is 13 cms
No shifting dullness
Traubes space is resonant on percussion

86. AUSCULTATION
Normal bowel sounds heard
No hepatic / splenic rub
No Bruit/ Venous Hum

87. OTHER SYSTEMS
CVS : S1 S2 Heard, No murmers
RS : B/L NVBS heard, No added sounds
CNS : NFND, No Flaps

88. SUMMARY
55 Yrs/ Female/ Non alcoholic
Relatively asymptomatic at present
Incidently found to have dilated veins over the Anterior
abdominal wall and Back
Past History of single episode of Heamatemesis 40 Yrs
back
GPE : Pallor +
No External markers of liver cell failure
P/A : Dilated and tortuous veins over anterior abdominal
wall, flanks and back with direction of flow below
upwards.
No hepatosplenomegaly
No freefluid

89. FINAL DIAGNOSIS
PRE-HEPATIC OBSTRUCTION OF INFERIOR
VENECAVA

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

91. Where is the lesion?
Interaction opportunity

92. Possible sites of occlusion
Level 1
Level 2
Level 3

93. Level 1 and Level 2 : Budd-chiari syndrome
Level 1
Level 2
Level 3
Acute :
Abdominal pain
Tender hepatomegaly
Jaundice
Rapid onset ascitis
No dilated veins

94. Level 1 and Level 2 : Budd-chiari syndrome
Level 1
Level 2
Level 3
Chronic :
Hepatomegaly
Ascitis
Tortuous veins in level 1
Back veins

95. Level 3 : Sub-hepatic IVC obstruction
Level 1
Level 2
Level 3
Features :
Tortuous veins
No ascitis
Leg edema

96. Thank you….. See you as
Physicians