Liver Cirrhosis and complications

Question 1

What is decompensated liver cirrhosis? (2)

Answer 1

Cirrhosis complicated by encephalopathy, ascites or variceal haemorrhage.

Cirrhosis without any of the above complications if compensated cirrhosis.

Question 2

How can the severity of liver disease be assessed? (2)

Answer 2

• Liver biochemistry: may be normal, most have slight increase in ALP and AST/ALT
• FBC: thrombocytopenia at diagnosis (hypersplenism), leukopenia and anaemia develop later
• Liver function: PT time and albumin levels are best indicators
• U+Es: Low Na indicates severe liver disease secondary to either impaired free water clearance or excess diuretic therapy. Elevated Cr has worse prognosis.
• AFP: raised in liver disease, over 200ng/ml is suggestive of HCC
• Biopsy: grade is level of inflammation; stage is level of architectural distortion

Question 3

Name 3 causes of chronic liver disease and cirrhosis. (3)

Answer 3

Common: alcohol, hepatitis B, C, D

Others:
Autoimmune: AI hepatitis
Drugs: MTX
Inherited: Haemochromatosis, Wilson’s, alpha1-antitrypsin deficiency, CF
Vascular: Budd-Chiari
Chronic biliary disease: PBC, secondary biliary cirrhosis, PSC, biliary atresia
Idiopathic

Question 4

Define cirrhosis. (2)

Answer 4

End stage of chronic liver damage with replacement of normal liver architecture with diffuse fibrosis and nodules of regenerating hepatocytes

Question 5

What is the management of liver cirrhosis? (3)

Answer 5

Treat the cause if possible
Avoid alcohol, sedatives, opiates, NSAIDs and drugs affecting liver
Nutrition is important: involve dietitian and enteral supplements.
Treat complications as they arise.
Consider liver transplant.

Annual flu vaccination
Screen for HCC (AFP and USS 6 monthly)

Question 6

What scoring system can be used to grade severity and prognosis of liver disease? (1)

Name the 5 variables that the score uses. (5)

Answer 6

Child-Pugh score

encephalopathy, ascites, PT time, serum bilirubin and albumin

Question 7

Name 4 complications of liver cirrhosis. (4)

Answer 7

Portal hypertension
Ascites
Porto-systemic encephalopathy
AKI (hepatorenal syndrome)
Hepatopulmonary syndrome
Hepatocellular carcinoma
Bacteraemias, infection
Malnutrition
Osteoporosis

Question 8

Describe the cause of portal hypertension? (4)

Answer 8

• Portal vein is formed by SMV and splenic vein.
• Blood vessels enter the liver via the hilum
• Blood passes through sinusoids and leaves through hepatic vein to join IVC.
• Inflow of portal blood to the liver can be partially or fully obstructed at a number of sites
• This leads to increased pressure proximal to the obstruction
• Blood is diverted into porto-systemic collaterals which are superficial and prone to rupture.

Question 9

The liver has a dual blood supply.

Which is the main supply? (1)

Answer 9

Portal vein (75%)
Hepatic artery (25%)

Question 10

Name the 3 locates of obstruction causing portal hypertension and given an example of each. (6)

Answer 10

Pre-hepatic: portal vein thrombosis
Hepatic: Cirrhosis*, alcoholic hepatitis, schistomiasis
Post-hepatic (rare): Budd-Chiari, RHF, constrictive pericarditis, IVC obstruction

Question 11

Name 2 possible clinical features of portal hypertension. (2)

Answer 11

Splenomegaly
GI bleed from varices
Ascites
Hepatic encephalopathy

Question 12

What pharmacologic options are available to stop oesophageal variceal bleeding? (2)

Answer 12

Terlipressin: vasoconstriction of splanchnic artery, caution in IHD
Somatostatin

Question 13

Reginald has bleeding oesophageal varices.
What is your immediate management? (3)

What are the most common treatments performed during endoscopy? (2)

Answer 13

A-E
2 large bore peripheral cannulae
Haemostasis/stabilise patient
Blood cultures and broad spectrum antibiotics
Check INR, reverse if necessary
Endoscopy once stabilised

Band ligation
Sclerotherapy

Question 14

What is a TIPS procedure? (2)

What is the most serious complication? (1)

Answer 14

Transjugular intrahepatic portosystemic shunting is used when there is a second re-bleed after treatment.
A shunt is placed between portal and hepatic veins, effectively bypassing liver and lowering pressure.
Bypassing liver can lead to complication of encephalopathy as toxins are no longer removed effectively from blood.

Question 15

After an episode of variceal bleeding the recurrence risk is 60-80% over a 2 year period.
What secondary prophylaxis options are there? (2)

Answer 15

Propranolol lowers portal pressure.
Repeated courses of variceal banding at 2 weekly intervals.
TIPS

Question 16

Define ascites. (1)

Answer 16

Presence of fluid in the peritoneal cavity.

Question 17

How does ascites occur? (2)

Answer 17

• In cirrhosis, peripheral arterial vasodilatation leads to reduction in effective blood volume
• This causes activation of sympathetic nervous system and renin-angiotensin system
• This causes water and salt retention
• Oedema is also encouraged by hypoalbuminaemia
• Localised to peritoneal cavity as a result of portal hypertension

Question 18

Ascites can be exudate or transudate.

Name 2 causes of each. (4)

Answer 18

Transudate: portal hypertension (cirrhosis), hepatic outflow obstruction, Budd-Chiari syndrome, HF, Tricuspid regurgitation, constrictive pericarditis

Exudate: Peritoneal TB, Pancreatitis, Nephrotic syndrome,, Peritoneal carcinomatosis, Lymphatic obstruction

Question 19

In all patient with ascites, a diagnostic aspiration should be performed to remove a sample for testing.

What test should be performed on the aspirate? (4)

Answer 19

Albumin - (to determine transudate or exudate)
Neutrophil count - (underlying bacterial peritonitis)
Gram stain and culture - (bacteria and acid-fast bacilli)
Cytology - (malignant cells)
Amylase - (exclude underlying pancreatic ascites

Question 20

Describe the management of ascites due to liver cirrhosis. (4)

Answer 20

1. Diet: sodium restriction
2. Diuretics: spironolactone, furosemide if response is poor. Aim is for loss of 0.5kg body weight daily. (Too fast can cause intravascular depletion)
3. Paracentesis: if tense ascites or resistant to medical treatment. Give albumin immediately after.
4. TIPS occasionally.

Question 21

Name the main complication of ascites. (1)

Answer 21

Spontaneous bacterial peritonitis (e. coli)

Question 22

Which toxin is thought to be the major factor in development of portosystemic encephalopathy? (1)

Answer 22

Ammonia (from protein metabolism)

Question 23

Name 3 clinical features of hepatic encephalopathy? (3)

Answer 23

Increasing drowsiness and comatose
Increased tone and hyperreflexia
Irritable, confused, slurred speech, reversal of sleep pattern in chronic.
Fetor hepaticus, asterixis, constructional apraxia.

Question 24

name 3 factors that may contribute towards portosystemic encephalopathy. (3)

Answer 24

High dietary protein
GI haemorrhage
Constipation
Infection (inc spontaneous bacterial peritonitis)
Fluid and electrolyte disturbance (inc diuretic therapy)
Sedative drugs (opiates, diazepam)
TIPS
Any surgery
Progressive liver damage
Development of HCC

Question 25

What is the management of portosystemic encephalopathy? (2)

Answer 25

• Lactulose is osmotic laxative that reduces colonic pH and absorption of ammonia.
• Antibiotics to reduce number of bowel organisms and hence production of ammonia. Metronidazole 400mg QDS
• Nutrition. Restrict protein to begin with then increase as encephalopathy improves.

Question 26

What is hepatorenal syndrome? (2)

Answer 26

Development of AKI in patient with advanced liver disease.

Usually cirrhosis or alcoholic hepatitis.

Question 27

What is the pathophysiology of hepatorenal syndrome? (2)

Answer 27

Marked peripheral vasodilatation
Leads to fall in systemic vascular resistance (effective hypovolaemia)
Causing vasoconstriction of renal circulation
Causing reduced renal perfusion.

Question 28

How is hepatorenal syndrome diagnosed? (2)

Answer 28

Oligouria
Rising serum Cr over days or weeks
Low urine sodium
Absence of other causes of AKI, lack of response to volume expansion and cessation of diuretics.