Acute Liver Failure Clinical Presentation

The patient history is valuable for suggesting likely causes of acute liver failure and guiding appropriate interventions. If the patient is incapacitated, closely question family members and friends.

In taking the history, collect details on the following:

• Date of onset of jaundice and encephalopathy
• Alcohol use
• Medication use (prescription and illicit or recreational)
• Herbal or traditional medicine use
• Family history of liver disease (Wilson disease)
• Exposure risk factors for viral hepatitis (travel, transfusions, sexual contacts, occupation, body piercing)
• Exposure to hepatic toxins (mushrooms, organic solvents, phosphorus contained in fireworks).
• Evidence of complications (eg, renal failure, seizures, bleeding, infection)

Physical examination includes careful assessment and documentation of mental status and search for stigmata of chronic liver disease. Jaundice is often but not always present. Right upper quadrant tenderness is variably present. The liver span may be small, indicative of significant loss of volume due to hepatic necrosis. An enlarged liver may be seen with heart failure, viral hepatitis, or Budd-Chiari syndrome.

Development of cerebral edema ultimately may give rise to manifestations of increased intracranial pressure (ICP), including papilledema, hypertension, and bradycardia.

The rapid development of ascites, especially if observed in a patient with fulminant hepatic failure accompanied by abdominal pain, suggests the possibility of hepatic vein thrombosis (Budd-Chiari syndrome).

Hematemesis or melena as a result of upper gastrointestinal bleeding may complicate fulminant hepatic failure.

Typically, patients are hypotensive and tachycardic as a result of the reduced systemic vascular resistance that accompanies fulminant hepatic failure, a pattern that is indistinguishable from septic shock. Although this presentation may be intrinsic to hepatic failure, considering the possibility of a superimposed infection (especially spontaneous bacterial peritonitis) is important.

Assess the patient for signs of encephalopathy. See the table below.

Table. Grading of Hepatic Encephalopathy (Open Table in a new window)

Potential complications of acute liver failure include seizures, hemorrhage, infection, renal failure, and metabolic imbalances.

Seizures

Seizures, which may be seen as a manifestation of the process that leads to hepatic coma and ICH, should be controlled with phenytoin. The use of any sedative is discouraged in light of its effects on the evaluation of mental status. Only minimal doses of benzodiazepines should be used, given their delayed clearance by the failing liver. Seizure activity may acutely elevate and may also cause cerebral hypoxia and, thus, contribute to cerebral edema.

Hemorrhage

Hemorrhage develops as a result of the profoundly impaired coagulation that manifests in patients with acute liver failure. Gastrointestinal bleeding may develop from esophageal, gastric, or ectopic varices as a result of portal hypertension. Portal hypertensive gastropathy and stress gastritis may also develop. Any minor trauma may result in extensive percutaneous bleeding or internal hemorrhage.

The first step in management is to correct coagulopathy. The transfusion requirements for coagulation products (FFP, platelets) may be enormous. Multiple transfusions with packed red blood cells may be needed. Consider retroperitoneal hemorrhage if large transfusion requirements are not matched by an obvious blood loss.

Infection

Periodic surveillance cultures should be performed to detect bacterial and fungal infections. Empiric broad-spectrum antibiotics and antifungals should be given in the following circumstances:

• Progressive encephalopathy (all patients listed for transplantation start antibiotics)
• Signs of systemic inflammatory response syndrome (SIRS) (temperature, >38°C or < 36°C; white blood cell [WBC] count, >12,000/μL or < 4,000/μL; pulse rate, >90 bpm)
• Persistent hypotension

Piperacillin/tazobactam (Zosyn) and fluconazole should be the initial choice. In hospital-acquired IV catheter infections, consider vancomycin.

Renal failure

Acute renal failure is a frequent complication in patients with acute liver failure and may be due to dehydration, hepatorenal syndrome, or acute tubular necrosis. To preserve renal function, maintain adequate blood pressure, avoid nephrotoxic medications and NSAIDs, and promptly treat infections.

When dialysis is needed, continuous (ie, continuous venovenous hemodialysis [CVVHD]) rather than intermittent renal replacement therapy is preferred. Hemodialysis may significantly lower the mean arterial pressure such that cerebral perfusion pressure is compromised.

Metabolic imbalances

Alkalosis and acidosis occur in acute liver failure. Identify and treat the underlying cause. Base deficits can be corrected by THAM solution (tromethamine injection), which prevents a rise in carbon dioxide, osmolality, and serum sodium.

Severe hypoglycemia occurs in approximately 40% of patients with fulminant hepatic failure. Although hypoglycemia occurs more frequently in children, blood sugar needs to be monitored in adult patients as well. Blood sugars should be maintained in the range of 60-200 mg/dL, using 10% dextrose solution.

Phosphate, magnesium, and potassium levels tend to be low in acute liver failure. Frequent supplementation is required.