Abdomen and liver case presentation by PG Chronic decompensated parenchymal liver disease - cirrhosis with portal hypertension probably of alcoholic etiology with no ascites with no features of hepatic encephalopathy and coagulopathy To rule out malignancy

1. ABDOMEN CASE DISCUSSION
Preeti thapar

2. Chief complaints
40 yrs old male patient presented to us with c/o
Jaundice-3months
High coloured urine-2months
 Loss of appetite-2 months
Loss of weight (15kgs)-2 months
Blood stained vomitus -1month
Bleeding gums -1 month
Right sided abdominal pain -1month
h/o fever -1day

3. History
No h/o melena
No h/o abdominal distention
No h/o pedal oedema
No h/o oliguria
No h/o pruritis
No h/o rash
No h/o dyspnea
No h/o loose stools
No h/o cough with expectoration
No h/o altered sleep cycle
no h/o seizures/LOC

4. PAST HISTORY
No h/o blood transfusion
No h/o iv drug abuse
No h/o surgeries in past
No h/o diabetes/TB/hypertension/CADin past
No h/o recent travel

5. Personal history
Married
Chronic alcohol intake present = 180ml of brandy per
day for 10yrs
Occasional smoker
Denied history of exposure

6. Family history
Patient married
Has 2 children
Has 13 siblings
No similar complaints in family members

7. Treatment history
Patient has taken ayurvedic medication as a single
dose for his jaundice 3 months back
No h/o taking siddha,unani medications

8. General examination
Patient is concious ,oriented to time place and person
Vitals ;BP -120/80 HR – 78/MIN
 TEMP -98.4
No pallor,cynosis,pedal oedema,lymphadenopathy
Icterus present
Clubbing +
Alopecia +

9. • Tatoo mark on rt arm
• Scar mark over right shoulder
• Lipoma over forehead
• Hyperpigmented patch over right popliteal
fossa
• No KF ring
• No Bitot spot
• No xanthelasma
• B/l Parotid enlargement present
• Oral cavity –normal

10. General physical exam
Fetor hepaticus absent
Gynaecomastia +
Loss of axillary hair,chest hair +
No scratch marks
No bruises/rash
No spider naevi
No palmar erythema
No dupuytrens contracture
No testicular atrophy

11. Per abdomen
Inspection –normal shape, all quadrants move equally with
respiration ,no visible veins,no scars, all hernial orifices
intact
Palpation
Superficial palpation-normal ,no tenderness
Deep palpation -right hypochondrium tenderness
present,liver enlarged 8 cm below costal margin, rounded
borders,smooth surface ,firm in consistency
Liver span –17.5 cm
Spleen felt 5 cm below costal margin ,splenic notch felt
surface smooth ,firm in consistency
No other mass felt

12. Percussion- liver dulness confirmed by percussion
Traube space is resonant, shifting dulness absent
Auscultation –no bruit heard
No venous hum
No rub

13. Other systems
CVS –S1S2 heard,no murmur heard
Respiratory system – chest b/l symmetrical ,b/l air
entry is equal ,no adventitious sounds heard
CNS –patient is concious ,oriented to time place and
person
Higher functions normal
No flap or tremor seen
Trail making test – 18 sec

14. Provisional diagnosis
Chronic decompensated parenchymal
liver disease - cirrhosis with portal
hypertension probably of alcoholic etiology
with no ascites with no features of hepatic
encephalopathy and coagulopathy
To rule out malignancy

16. Is it a decompensated
cirrhosis?

17. What suggests decompensated
cirrhosis?
• The symptom triad of decompensated
cirrhosis:
1. Abdominal distension (Ascites)
2. Internal / External bleeding
3. Behavioral/Mental changes

18. • What is Reitan Chart?

19. Reitan’s number connection
chart

20. • The number connection chart used to
assess Hepatic encephalopathy
• The maximum score is 24
• The maximum permitted time is 30
seconds

21. • What are the synonyms of asterixis ?
• What is the mechanism of asterixis ?

22. ASTERIXIS
SYNONYM
Hepatic flap, Metabolic tremor
MECHANISM
Negative myoclonus
Impaired inflow of joint position sense to
brainstem RAS resulting in brief lapse of
posture

23. Why etiology is alcoholism?
Other etiology?

24. 11.Why decompensated liver
disease due to alcohol?
• Convincing history
• Parotid enlargement- a sign common in
alcoholism
• Signs of liver cell failure
• Ascites

25. Other etiology
a) Chronic viral hepatitis
b) Wilson’s disease
c) Auto-immune hepatitis
d) Haemochromatosis

26. Pre-hepatic etiology of PHT
Causes…..

27. Pre-hepatic etiology of PHT
1.Non-cirrhotic portal fibrosis [ NCPF]
2.Portal vein thrombosis

28. Non-hepatic intra-abdominal
etiology of ascites
1.Malignancy
2.Tuberculosis peritonitis
3.Protein losing enteropathy, nephrotic
syndrome
4.Pancreatic ascitis
5.Meigs syndrome

29. Acute decompensation of
chronic liver disease
Reasons?

30. Acute decompensation of
chronic liver disease
• Superadded hepatitis
• Sepsis including SBP
• Malignant tranformation

31. What is Non-cirrhotic portal vein
obstruction ?

32. NCPF?
• Common among lower socioeconomic
class
• Mean age of presentation 30 years

33. Symptoms of NCPF?
• Symptoms at diagnosis
GIT Bleed, 50% have multiple episodes
Mass in the abdomen
Pain abdomen
occasionally distension( ascites )
Jaundice rare

34. Signs in NCPF
• Splenomegaly is universal
• Two-thirds have massive spleen
• Mild or no ascites
• No anterior abdominal or back veins
• Liver occasionally enlarged
• No signs of liver cell failure
• Encephalopathy rare

35. What are the different
mechanisms of ascites?

36. Mechanisms of ascitis
1. Underfill theory, S.Sherlock-1963
2. Overflow theory, Libermann-1970
3. Lymph Imbalance theory,Witt-1980
4. Vasodilation theory,Schrier-1988

37. Underfill theory,1963

38. Overflow theory, 1970

39. Lymph imbalance theory,1980

40. Vasodilation theory,1988

41. What is SAAG?

42. Why SAAG is elevated in
PHT?

43. Can SAAG be elevated in
non-PHT causes

44. Serum Ascitic Albumin Gradient
• Serum albumin- Ascitic fluid albumin
• Gives a clue about portal hydrostatic
pressure

45. SAAG
• A gradient >1.1 g/dl indicates PHT as the
probable cause of ascitis
• High gradient due to ↑Portal hydrostatic
pressure pushing the water to peritoneum
leaving albumin in the vasculature

46. Non-PHT causes for ↑SAAG
>1.1g/dL
• Cirrhosis
• Alcoholic hepatitis
• CCF
• Massive hepatic metastases
• Vascular occlusion
• Fatty liver disease of pregnancy
• Myxedema

47. Can you get exudative ascites
in portal hypertension

48. Exudative ascites in portal
hypertension
• Cardiac ascites
• Acute Budd-Chiari syndrome
The concept of exudate and transudate in
the evaluation of ascites is no longer
recommended.

49. Thank you