Liver Failure

Key Points

• Liver failure can be acute (rapid onset, days to weeks) or chronic (progressive cirrhosis leading to end-stage liver disease).
• The liver performs metabolism, protein synthesis, detoxification, and bile production; failure disrupts all these functions.
• Major complications include hepatic encephalopathy, esophageal varices, ascites, coagulopathy, and hepatorenal syndrome.
• Liver transplantation is the definitive treatment for ESLD; the MELD score prioritizes organ allocation.

Pathophysiology

The liver contributes to metabolism, storage of fat-soluble vitamins, protein synthesis (albumin, clotting factors), detoxification of drugs and ammonia, and bile production. When hepatocytes are damaged beyond their regenerative capacity, these functions progressively decline.

Acute Liver Failure

Acute liver failure develops rapidly (within days to weeks) in a previously healthy liver. Common causes include acetaminophen toxicity, viral hepatitis (A, B), drug reactions, and acute fatty liver of pregnancy. The rapid loss of hepatic function leads to coagulopathy, cerebral edema, and multiorgan failure.

Chronic Liver Failure (Cirrhosis)

Cirrhosis represents the end stage of chronic liver injury characterized by irreversible fibrosis and nodular regeneration that distort hepatic architecture. Causes include alcohol-related liver disease, chronic hepatitis B and C, nonalcoholic steatohepatitis, autoimmune hepatitis, and primary biliary cirrhosis. Portal hypertension develops as fibrosis obstructs hepatic blood flow, leading to esophageal varices, splenomegaly, and ascites.

Clinical Manifestations

• Acute: Hypotension, altered mental status, fever, jaundice, right upper quadrant pain, ascites, fluid overload.
• Chronic (cirrhosis): Ascites, jaundice, dark-colored urine, decreased urine output, edema, hepatic encephalopathy, pruritus, light-colored stools, muscle wasting, gynecomastia, esophageal varices, spider angiomata.
• Hepatic encephalopathy: Asterixis (flapping tremor), hyperreflexia, cognitive impairment, anxiety, irritability, balance problems; in severe cases, coma.

Nursing Assessment

NCLEX Focus

Monitor for hepatic encephalopathy: assess mental status changes with rising ammonia levels. Asterixis (liver flap) is a classic finding. Know that lactulose is the first-line treatment to reduce ammonia.

• Assess mental status frequently using a standardized neurological assessment; report any decline.
• Monitor vital signs, particularly for hypotension and tachycardia indicating hemorrhage.
• Measure abdominal girth daily (ascites progression).
• Monitor strict intake and output; assess for oliguria (hepatorenal syndrome).
• Review laboratory values: ALT, AST (elevated), bilirubin (elevated), PT/INR (prolonged), albumin (decreased), ammonia (elevated in encephalopathy).
• Assess for bleeding: oozing from venipuncture sites, melena, hematemesis, petechiae (coagulopathy/DIC).
• Assess skin for jaundice, spider angiomata, and pruritus.

Nursing Interventions

• Elevate the head of bed to reduce intracranial pressure and prevent aspiration.
• Administer lactulose as prescribed to reduce serum ammonia levels (hepatic encephalopathy); monitor for diarrhea and electrolyte imbalances.
• Administer prescribed antibiotics (e.g., rifaximin) to reduce ammonia-producing intestinal bacteria.
• Implement bleeding precautions: use soft toothbrush, avoid rectal temperatures, minimize invasive procedures.
• Manage ascites: administer diuretics (spironolactone, furosemide) as prescribed; assist with paracentesis if indicated.
• Maintain nutrition: high-calorie, moderate-protein diet (protein restriction only in acute encephalopathy); consult dietitian.
• Implement fall precautions for patients with encephalopathy or motor dysfunction.
• Educate about alcohol abstinence and medication safety (avoid hepatotoxic drugs, especially acetaminophen).
• Prepare the patient for liver transplant evaluation when ESLD criteria are met (MELD scoring).

Acetaminophen Toxicity

Acetaminophen is the leading cause of acute liver failure. Administer N-acetylcysteine (NAC) as the antidote within 8-10 hours of ingestion for best outcomes. Educate patients to limit total daily acetaminophen intake.

Related Concepts

• liver-cirrhosis — End-stage chronic liver disease with irreversible fibrosis.
• Hepatic Encephalopathy — Neurological complication of impaired ammonia clearance.
• Portal Hypertension — Consequence of hepatic fibrosis leading to varices and ascites.
• fluid-electrolyte-regulation-by-organs — Ascites management and diuretic therapy.
• hemostasis-coagulation-and-fibrinolysis — Coagulopathy from impaired clotting factor synthesis.

Self-Check

1. What are the key differences between acute and chronic liver failure?
2. How does lactulose reduce serum ammonia levels in hepatic encephalopathy?
3. What laboratory findings are characteristic of liver failure?