113 Cirrhosis of the liver
Salient features
History
Questions
What are the important locations of the portosystemic collaterals?
• Oesophageal submucosal veins: supplied by the left gastric vein and drain into the superior vena cava via the azygous vein
• Paraumbilical veins: supplied by umbilical portion of the left portal vein and drain into abdominal wall veins near the umbilicus. These veins may form a caput medusae at the umbilicus
• Rectal submucosal veins: supplied by the inferior mesenteric vein through the superior rectal vein and drain into the internal iliac veins through the middle and inferior rectal veins
• Short gastric veins: supplied by the oesophageal submucosal veins and drain into the splenic vein
Advanced-level questions
What is the utility of measuring serum ammonia level in patients with altered mental status?
• In patients with established hepatic encephalopathy, monitoring ammonia level during therapy is of limited value
• In patients with acute liver failure, an elevated serum ammonia is a poor prognostic sign: arterial ammonia levels >2.0 mg/l is associated with cerebral herniation in acute liver failure (Hepatology 1999;29:648–53)
• When there is no liver disease, a search for an underlying cause such as total parenteral nutrition, GI bleed, steroid use, portosystemic shunts, inborn errors of metabolism such as urea cycle disorders, drugs such as glycine, salicylates and valporates.
What factors can precipitate hepatic encephalopathy in a patient with previously well-compensated cirrhosis?
What are the laboratory changes seen in cirrhosis?
• Aminotransferases: alanine and aspartate aminotransferases normal or moderately elevated
• Alkaline phosphatase: usually slightly elevated
• Gamma-glutamyltransferase: usually slightly elevated, high in active alcoholics
• Bilirubin: elevates later in cirrhosis; predictor of death
• Albumin: decrease in advanced cirrhosis
• Prothrombin time: increases in advanced cirrhosis since the liver synthesizes clotting factors
• Immunoglobulins: increased, mainly IgG
• Thrombocytopenia: from both congestive splenomegaly and cirrhosis
• Leukopenia and neutropenia: from splenomegaly with splenic margination
What are the diagnostic tests in cirrhosis?
• Serology for hepatitis viruses
• Serology for autoantibodies (anti-nuclear, anti-smooth muscle, anti-mitochondria)
• Ferritin and transferrin saturation: iron overload
• Copper and ceruloplasmin: copper overload
• Immunoglobulin: non-specific but may assist in distinguishing causes
• Cholesterol: primary biliary cirrhosis
How do you manage a patient with cirrhosis?
| Prevention | Treatment | |
|---|---|---|
| Itching | Medication | |
| Constipation | Diet | Laxatives (e.g. lactulose) |
| Variceal bleeding | Non-selective beta-blockers (e.g. propranolol), variceal band ligation | See below |
| Ascites | Salt restriction | See Case 115 |
| Renal failure | Avoid hypovolaemia | Rehydration, stop diuretics, albumin infusion |
| Hepatic encephalopathy | Avoid precipitants | Treat precipitating factors, bleeding, electrolyte inbalance, sedatives |
| Spontaneous bacterial peritonitis | Treat ascites | Antibiotics |
How would you manage variceal bleeding in cirrhosis?
• Blood transfusion to replace falling hematocrit
• Early endoscopy to confirm the bleeding site
• Endoscopic sclerotherapy with octreotide (N Engl J Med 1995;333:555–60)
• Intravenous antidiuretic hormone is less effective than sclerotherapy
• Endoscopic ligatation (N Engl J Med 1999;340:988–93)
• Balloon tamponade is effective in temporarily stopping bleeding while awaiting more definitive therapy
• Combination of vapreotide (a somatostatin analogue) and endoscopic treatment (N Engl J Med 2001;344:23–8)
• Transjugular intrahepatic portosystemic stent shunt (N Engl J Med 1994;330:165–71)
• Combination of nadolol and isosorbide mononitrate (N Engl J Med 1996;334:1624–9).
