Abdominal distension

Question 1

What are the manifestations of portal hypertension which commonly complicates cirrhosis?

Answer 1

Manifests primarily as ascites (+/- SBP) and varices (+/- bleeding)

Question 2

Explain the pathophysiology of ascites accumulation

Answer 2

Peripheral arterial vasodilation theory (most recent): portal hypertension -> increase Nitric Oxide levels -> splachnic & peripheral vasodilation -> decreased effective arterial blood volume. Neurohormonal excitation increases with disease progression -> more renal sodium retention & plasma volume expansion -> overflow of fluid into peritoneal cavity.

Hypoalbuminemia and reduced plasma oncotic pressure also favour the extravasation of fluid

Question 3

What is the appropriate testing of ascites and be able to diagnose spontaneous bacterial peritonitis (SBP)?

Answer 3

Ascitic tap

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

Question 4

Describe the principles of management of ascites (dietary salt restriction and medication)

Answer 4

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

Question 5

Classify cirrhosis using simple scoring systems and understand the relationship between severity and
prognosis (mortality)

Answer 5

Child-Pugh-Turcotte classification

• Points for each of 5 parameters (score 5-15) with max 3 points from each parameter
  1. Ascites
  2. Bilirubin (higher the worse)
  3. Albumin (lower the worse)
  4. INR (higher the worse)
  5. Encephalopathy

Score determines grade A (5-6), B(7-9), C (10-15)

Child-Pugh score predicts mortality risk with major surgery & 1 year survival (without surgery)

•Child-Pugh score mortality risk with major surgery:
Class A: 10%, Class B: 30%, Class C: 82%
•Child-Pugh score 1 year survival (without surgery):
Class A: 100%, Class B: 80%, Class C: 45%

C.f. MELD (Model for End-stage Liver Disease) is more accurate using three lab variables (bilirubin, INR & CREATININE) and used for liver transplant wait lists

Question 6

Explain the pathophysiology of varices formation

Answer 6

Portal hypertension -> encorgement of collaterals (varices) & portosystemic shunting:

• esophagus
• fundus of stomach
• rectum
• intrabdominal

Portal hypertension is due to:

• most commonly cirrhosis
• portal vein thrombosis
• Budd-Chiari syndrome

Question 7

What is the significance of varices and the mortality associated with bleeding?

Answer 7

• Varices should be screened for in cirrhotics
• Bleeding is a life threatening complication or cirrhosis
• Bleeding may be prevented by prophylaxis with propranolol (primary) or band ligation (primary/secondary)

Mortality ~50% with acute variceal haemorrhage

Risk of variceal haemorrhage related to:
–Varix size, endoscopic stigmata, previous bleeds
–Hepatic-venous portal pressure gradient (measured at portal venography) >12 mmHg

Question 8

What are causes of ascites?

Answer 8

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

•Other
–Peritoneal carcinomatosis (esp ovarian)
–Pancreatitis
–Nephrotic syndrome
–Peritoneal tuberculosis
–Serositis

Question 9

What are the top 4 causes of cirrhosis in Australia?

Answer 9

1. Alcohol
2. Hepatitis C
3. NASH
4. Hepatitis B

Question 10

What is the diagnostic test for ascites?

Answer 10

Ascitic tap
–75 polymorphonuclear cells/mm3
–Ascitic albumin concentration 15 g/L

can diagnose SBP (pmn count > 250) and portal hypertension (SAAG > 11 g/L)

–Also may be therapeutic (drainage of 8+ litres)
–Simple outpatient procedure
–Testing:
•Always fluid microscopy/culture/sensitivity
•Generally ascitic albumin & protein concentration
•Rarely cytology (?malignancy)

Not diagnostic but doppler ultrasound can confirm ascites if in doubt (may diagnose cirrhosis, portal hypertension, portal vein thrombosis & hepatocellular cancer as well)

Question 11

Signs of portal hypertension in doppler ultrasound

Answer 11

• Patent ligamentum teres
• Reversal of flow in portal vein
• Demonstrate intra-abdominal shunts (varices)

Question 12

Describe spontaneous bacterial peritonitis (Pathogenesis, Dx, RF)

Answer 12

• a common complication of cirrhosis
• Pathogenesis: leaky membranes, poor opsonisation, suboptimal immune response
• Diagnosis:
–Polymorphonuclear (pmn) cell count > 250 cells/mm3
–Detectable growth on culture
•Risk factors (in presence of ascites):
–low ascitic protein, high serum bilirubin, Prior SBP
–also variceal bleeding/malnutrition/PPI therapy
•If high risk give antibiotic prophylaxis

Question 13

What is serum albumin-ascites gradient?

Answer 13

SAAG = [serum albumin]-[ascites albumin]

•Identifies whether ascites is due to portal hypertension or not
–SAAG > 11 g/L = pHTN (see previous list) i.e. serum albumin&raquo_space; ascites albumin
–SAAG 25 g/L)

Question 14

Describe the relationship between hyponatraemia in cirrhosis & salt restriction

Answer 14

Hyponatremia is a common problem in patients with advanced cirrhosis.

Systemic vasodilation (reduced systemic vascular resistance) & hyperdymaic circulation (high CO) -> salt retention (RAAS) & water retention (ADH) as compensation -> low urinary sodium excretion & increased total body sodium. But due to inability to excrete ingested water -> fall in serum sodium.

Hence low salt & diuretic therapy.

Hyponatraemia correlates with degree of cirrhosis, progresses slowly, and is rarely associated with neurological complications

Question 15

Describe hepatitis C

Answer 15

•Hepatotropic RNA virus & no vaccine
•2nd most common cause of cirrhosis
•Transmitted by blood exposure (rarely sexual)
–IVDU, PHx blood products

Question 16

How do you manage hepatitis C?

Answer 16

•Screen at risk patients with HCV Ab:
–IVDU or those with abnormal LFTs
–Migrants from Asia, Africa, Middle East
–Known other liver disease (? co-factor)
•Confirm diagnosis with HCV PCR
–~20% spontaneous clearance (Ab +ve, PCR –ve)
•Refer for specialist assessment
–Overall >50% (& rising) of HCV can be cured
•Manage cirrhosis if present (supportive care)

Question 17

Describe the hepatic & extra-hepatic effects of alcohol

Answer 17

Alcohol is the most common cause of cirrhosis in Australia & significant if >30g daily for >5 years

Liver: steatosis, steatohepatitis, fibrosis, cirrhosis (+/- hepatoma), liver failure & death

Also extra-hepatic sequelae: neurologic, cardiac, social, trauma, malignancy

Progression ceases with abstinence and improvement continues for > 6 months

Question 18

What does tachycardic & hypotensive mean?

Answer 18

the pt is SHOCKED

Question 19

What are the common causes of upper GI bleeding?

Answer 19

–Peptic ulcer disease
–Varices
–Esophagitis
–Mallor-Weiss tear
–Other: cancer, angiodysplasia/AVM,

In setting of known or suspected cirrhosis assume bleeding is VARICEAL until proven otherwise

Question 20

Rx of esophageal varices

Answer 20

4 ways to control acute bleeding:
1. Endoscopically:
–Band ligation (banding) of varices
–Injection of glue or sclerosant
–Tamponade (Sengstaken or similar orogastric tube)

2. Pharmacologically:
   –Splanchnic vasoconstrictor (terlipressin or somatostatin analogue e.g. octreotide)
3. Radiologic decompression (shunt) or occlusion of varices
4. Surgical decompression (shunt) – high mortality

•Also must treat any precipitant for increased portal pressure (esp. sepsis)

Question 21

How do you prevent variceal bleeding?

Answer 21

•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

• SECONDARY prophylaxis (prevent subsequent bleeding): Regular endoscopic band ligation or injection to eradicate varices
• Rescue therapy (failed/futile prophylaxis or treatment): Decompression (shunt) – radiologic safer than surgical

Question 22

Mx of advanced/decompensated cirrhosis

Answer 22

largely supportive & has a poor prognosis