Clinical Assessment Patients may initially complain of fatigue, nausea, vomiting, fever, and diffuse abdominal pain Occasionally, right upper quadrant pain is severe Commonly, a history of a prodromal viral illness can be elicited The presence of jaundice usually initiates the first visit to the physician As liver failure progresses, patients become more jaundiced and lethargic, and may report easy bruising or bleeding History should include any infectious and medication exposures including prescription and nonprescription medications and herbal and other alternative remedies ED physicians should be cognizant of chronic acetaminophen exposure in addition to acute toxicity Family history should be assessed for Wilson disease, α1 antitrypsin deficiency, autoimmune conditions, infant deaths, metabolic or mitochondria disorders, or liver failure of unknown etiology Physical examination findings may include small size, poor nutritional status, jaundice, bruising, or petechiae Hepatomegaly is common and some patients may have splenomegaly Findings associated with chronic liver disease and portal hypertension would suggest an alternative diagnosis Encephalopathy is graded on a scale from I to IV from drowsiness, poor concentration, and irritability to aggressive behavior or unresponsiveness Those with severe encephalopathy can develop cerebral edema and increased intracranial pressure (ICP) Cerebral edema is a major cause of death in patients with liver failure and requires aggressive supportive management Because it may be difficult to diagnose patients clinically, biochemical evidence of liver failure is necessary PT is a helpful measure of synthetic function Other laboratory markers suggestive of severe liver failure include evidence of increasing cholestasis manifested by a rising serum bilirubin level, hypoalbuminemia, and hypoglycemia It is also important to monitor serum transaminase levels Falling transaminase levels usually indicate resolving liver disease, although in the setting of increasing jaundice and coagulopathy, this trend may indicate excessive hepatocyte loss rather than hepatocyte recovery Serum fibrinogen is usually decreased in patients with liver failure In cases in which the patient has splenomegaly, thrombocytopenia and leukocytopenia may be present Hypoglycemia almost always accompanies ALF because the liver is the primary organ for gluconeogenesis and glycogen storage is often depleted This may complicate the signs of encephalopathy Hepatorenal syndrome occurs in approximately 75% of patients who reach severe encephalopathy The cause of hepatorenal syndrome is unclear; however, the result is oliguria