A 24-year-old woman is brought to the emergency department by her roommate because of increasing confusion for the past several hours. Three days ago, she developed nausea, vomiting, and right upper quadrant abdominal discomfort. Her roommate reports that she recently had a viral upper respiratory infection and had been taking “a lot of extra-strength acetaminophen” for symptom relief. Past medical history is otherwise negative. Temperature is 37.2°C (99.0°F), blood pressure is 108/68 mm Hg, pulse is 102/min, and respiratory rate is 18/min. On physical examination, the patient is disoriented and unable to answer questions appropriately. Mild scleral icterus is present. The abdomen is soft with mild right upper quadrant tenderness. Laboratory studies demonstrate the following:
Which of the following best describes this patient’s condition?
The correct answer is:
B) Acute liver failure
This patient has acute liver failure (ALF), a life-threatening syndrome characterized by acute liver injury, coagulopathy, and hepatic encephalopathy in a patient without preexisting cirrhosis. The key clues are the markedly elevated aminotransferases, elevated INR, altered mental status, and absence of a known history of chronic liver disease. The history of excessive acetaminophen use strongly suggests acetaminophen toxicity, the most common cause of acute liver failure in the United States.
The diagnosis of acute liver failure requires three components:
Evidence of acute liver injury
Coagulopathy (typically INR ≥1.5)
Hepatic encephalopathy
The development of hepatic encephalopathy reflects severe loss of hepatic synthetic and detoxification function. These patients are at risk for cerebral edema, intracranial hypertension, sepsis, renal failure, and death. As a result, acute liver failure represents a true medical emergency.
Management includes intensive care monitoring, treatment of the underlying cause, and early consultation with a liver transplant center. In patients with suspected acetaminophen toxicity, N-acetylcysteine should be administered promptly, even when the timing of ingestion is uncertain. Step 2 commonly tests the fact that N-acetylcysteine may improve outcomes even after hepatic injury has developed.
A useful board distinction is that patients with cirrhosis can develop hepatic encephalopathy and coagulopathy, but they have underlying chronic liver disease. Acute liver failure occurs in patients without established cirrhosis.
Answer choice A: Acute alcohol-associated hepatitis, is incorrect.
Alcohol-associated hepatitis may cause jaundice, fever, and elevated liver enzymes. However, AST and ALT are typically below 500 U/L and the AST:ALT ratio is usually greater than 2. The profound transaminase elevations seen here are more characteristic of acetaminophen toxicity.
Answer choice C: Chronic liver disease with decompensation, is incorrect.
Decompensated cirrhosis presents with complications such as ascites, variceal bleeding, and encephalopathy in the setting of longstanding liver disease. This patient has no evidence of chronic liver disease.
Answer choice D: Hepatic encephalopathy due to cirrhosis, is incorrect.
Although hepatic encephalopathy is present, the broader syndrome is acute liver failure. The absence of cirrhosis is the key distinguishing feature.
Answer choice E: Hepatorenal syndrome, is incorrect.
Hepatorenal syndrome occurs in advanced cirrhosis with portal hypertension and severe renal vasoconstriction. This patient has only mild renal dysfunction and does not have established cirrhosis.
Key Learning Point
Acute liver failure is defined by acute liver injury, coagulopathy (INR ≥1.5), and hepatic encephalopathy in a patient without preexisting cirrhosis. Acetaminophen toxicity is the most common cause in the United States and requires prompt treatment with N-acetylcysteine.
