Decompensated Chronic Liver Disease

Question 1

What are the most common causes of chronic liver disease?

Answer 1

Rule of Three - Common:
ASH (Alcoholic Steatohepatitis)
NASH
Viral Hep

Rule of Three - Metabolic:
Fe (Haemochromatosis) - metabolise formation of free radicals
Cu (Wilsons)
A1AT- deficiency - normally anti-protease

Rule of Three -Autoimmune:
Primary Biliary Cirrhosis
Primary Sclerosing Cholangitis
Autoimmune hepatitis

Other:
NASH
Budd Chiari (hepatic vein thrombosis)
Chronic Biliary Cirrhosis

Question 2

Ix of chronic liver disease

Answer 2

• FBC – anaemia
• U+E – hepatorenal syndrome
• LFT’s – active damage
• Albumin – synthetic function
• Electrolyte - low Na
• Coags – bleeding
• ABG – lactate acidaemia
  alpha-feto protein
• paracentesis: culture and cell count (>250/mm3 = diagnositic for SBP)
• endoscopy – varices
• US: hepatic and portal veins, hepatocellular carcinoma
• CT: hepatocelluar carcinoma
• liver biopsy: staging

Question 3

Why are Na levels usually low in chronic liver disease patients?

Answer 3

CL disease -> increase NO release/decrease clearance -> hyperdynamic state -> peripheral vasodilation -> peripheral vasodilation -> kidney sense decrease IV volume -> Na+ retention and fluid -> dulutional hyponatraemia

Question 4

What are the causes of ascites?

Answer 4

Portal HTN:

• Cirrhosis
• Alcoholic hepatitis
• Cardiac failure or pericarditis
• Budd-Chiari syndrome
• Massive hepatic metastasis

Other:

• Peritoneal carcinomatosis (esp ovarian)
• Pancreatitis
• Nephrotic syndrome
• Peritoneal TB
• Serositis (autoimmune diseases)

Question 5

What are we looking for on a doppler US?

Answer 5

• Confirms ascites presence
• May diagnose cirrhosis (nodular liver)
• May confirm portal HTN: patent ligamentus teres, reversal of flow in portal vein, demonstrate intra-abdo shunts (varices)
• May diagnose portal vein thrombosis
• May diagnose HCC

Question 6

Purpose of ascitic tap?

Answer 6

a. Diagnostic to test for:
- fluid microscopy, culture, sensitivity, ascitic albumin and protein concentration, and rarely cytology if malignancy suspected

b. Therapeutic (drainage of 8+ litres) that is replaced with 200mL 20% concentrated albumin IV for each 2L drained

Question 7

What is the pathogenesis of spontaneous bacterial peritonitis (SBP)?

Answer 7

Leaky membranes, poor opsonisation and suboptimal immune response all predispose to SBP

Question 8

How do we diagnose SBP?

Answer 8

• Diagnosis:
– Polymorphonuclear (pmn) cell count > 250 cells/mm3
– Detectable growth on culture

Question 9

What are the risk factors of SBP?

Answer 9

• Risk factors (in presence of ascites):
– low ascitic protein, high serum bilirubin, Prior SBP
– also variceal bleeding/malnutrition/PPI therapy

Question 10

What is the serum albumin-ascites gradient?

Answer 10

• Calculated
SAAG = [serum albumin]-[ascites albumin]
• Identifies ascites due to portal hypertension
– SAAG > 11 g/L = pHTN (see previous list)
– SAAG 25 g/L)

Question 11

Management of ascites?

Answer 11

• Treat the underlying disease if possible
• Avoid NSAIDs & ACE inhibition (with ACEI or A2RB), can cause Na and H2O retention
• Sodium restriction
– Low salt diet, no added salt to foods
• Fluid restriction
– E.g.,

Question 12

Why restrict the sodium in the presence of hyponatraemia?

Answer 12

• Cirrhosis is associated with vasodilation (decreased systemic
vascular resistance) and a hyperdynamic circulation (increased
cardiac output)
• Compensatory mechanisms lead to salt retention (via reninangiotensis-aldosterone
axis) and water retention (via ADH)
• Patient with ascites have low urinary sodium excretion and
increased total body sodium (hence low salt and diuretic
therapy)
• Hyponatraemia correlates with degree of cirrhosis, progresses
slowly, and is rarely associated with neurological
complications

Question 13

Aetiology of varices?

Answer 13

Aetiology: portal hypertension leads to engorgement of
collaterals (varices) and porto-systemic shunting
– Portal hypertension is most often secondary to cirrhosis, also portal
vein thrombosis or Budd-Chiari syndrome

Question 14

Location of varices

Answer 14

Found in esophagus and fundus of stomach, also rectum and

intrabdominal

Question 15

What determines the risk of variceal haemorrhage?

Answer 15

– Varix size, endoscopic stigmata, previous bleeds
– Hepatic-venous portal pressure gradient (measured at portal
venography) >12 mmHg

Question 16

What is the classification system for decompensated CLD?

Answer 16

Child-Pugh Turcotte Classification that takes into account: ascites, bilirubin, albumin, INR, encephalopathy

Grade A - C

Question 17

List the signs of decompensated CLD.

Answer 17

Albumin (hypoalbuminaemia)
Bilirubin (jaundice)
Coagulopathy (bruising, bleeding)
Distension
Encephalopathy
Foetus Hepaticus 
Variceal bleeding

Question 18

Management of esophageal varices

Answer 18

• Control acute bleeding:
– Endoscopically:
a. Band ligation (banding) of varices
b. Injection of glue or sclerosant (uncommon)
c. Tamponade (Sengstaken or similar orogastric tube)

– Pharmacologically:
a. Splanchnic vasoconstrictor (terlipressin or somatostatin analogue)

– Radiologic decompression (shunt) or occlusion of varices

– Surgical decompression (shunt) (high mortality)

+ treat any ppt for increased portal pressure (esp. sepsis) e.g. octreotide (somatostatin analogue)

Question 19

Primary prophylaxis of variceal bleeding

Answer 19

• Primary prophylaxis (prevent 1st episode of bleeding)
1. Non-selective B-blockade (propranolol) – but hypotension and
bradycardia often tolerated poorly in advanced cirrhosis
2. Endoscopic band ligation if varices large & high risk or advanced
cirrhosis

Question 20

Secondary prophylaxis of variceal bleeding

Answer 20

• Secondary prophylaxis (prevent subsequent bleeding)

* Regular endoscopic band ligation or injection to eradicate varices