Coagulopathy Fresh frozen plasma only if active bleeding, monitor coagulation studies frequently Platelet transfusions as required
Hypoglycemia IV glucose supplied with ≥10% dextrose solution, electrolytes as appropriate
Ascites Restrict fluid intake to 50%-60% maintenance Restrict sodium intake to 0.5-1 mEq/kg/day Monitor central venous pressure to maintain adequate intravascular volume (avoid renal failure)
Renal failure Maintain adequate intravascular volume, give albumin if low Diuretics Vasoconstrictors Dialysis or hemofiltration Exchange transfusion Liver transplantation fibrosis, and biliary obstruction secondary to choledochalcyst are leading causes.
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Chronic liver disease is characterized by the consequences of portal hypertension, impaired hepatocellular function, and cholestasis. Portal hypertension caused by cirrhosis results in risk of gastrointestinal bleeding, ascites, and reduced hepatic blood flow. Blood entering the portal vein from the splenic and mesenteric veins is diverted to collateral circulation that bypasses the liver, enlarging these previously tiny vessels in the esophagus, stomach, and abdomen. Esophageal varices are particularly prone to bleed, but bleeding also can occur from hemorrhoidal veins, engorged gastric mucosa, and gastric var-ices. Ascites develops as a result of weeping of a high-pressure ultrafiltrate from the surfaces of the viscera and is at risk of becoming infected (spontaneous bacterial peritonitis); ascites can often be massive and interfere with patient comfort and respiration. The spleen enlarges secondary to impaired splenic vein outflow, causing excessive scavenging of platelets and white blood cells; this increases the patient’s susceptibility to bleeding and infection.
Impaired hepatocellular function is associated with coagulopathy unresponsive to vitamin K, low serum albumin, elevated ammonia, and hepatic encephalopathy. The diversion
ALT, Alanine aminotransferase; AST, aspartate aminotransferase; CBC, complete blood count; CF, cystic fibrosis; ERCP, endoscopic retrograde cholangiopancreatography; GGT, γ-glutamyltransferase; HBeAg, hepatitis B early antigen; HBsAg, hepatitis B surface antigen.
Serum α1-antitrypsin level α1-Antitrypsin phenotype if low serum level Serum ceruloplasmin Sweat chloride, CF gene tests if CF suspected Testing for other specific conditions as indicated by
HBsAg Hepatitis B viral DNA, HBeAg if HBsAg positive Hepatitis C antibody Hepatitis C antibody confirmatory test if positive Hepatitis C viral RNA, genotype if antibody confirmed
Prothrombin time and partial thromboplastin time Serum ammonia CBC with platelet count *Perform when indicated to obtain specific anatomic information.
of portal blood away from the liver via collateral circulation worsens this process. Malaise develops and contributes to poor nutrition, leading to muscle wasting and other consequences.
Chronic cholestasis causes debilitating pruritus and deepening jaundice. The reduced excretion of bile acids impairs absorption of fat calories and fat-soluble vitamins, which contributes to the poor nutritional state. Deficiency of vitamin K impairs production of clotting factors II, VII, IX, and X and increases the risk of bleeding. Vitamin E deficiency leads to hematologic and neurologic consequences unless corrected.