Acute Liver Failure (ALF)

This is an ICU patient who belongs at a transplant center - Care is supportive while the liver recovers or a graft is found, so every ALF patient should be hospitalized at, or referred early to, a center with transplant capability.

Cerebral edema drives the intracranial plan - Head elevation, mannitol, hyperventilation, and other cerebroprotective measures are the mainstay regardless of etiology, and some patients carry an invasive ICP monitor. Grade the encephalopathy before induction and expect sedation to deepen it.

Coagulopathy - An INR of 1.5 or higher is part of the diagnosis, not automatically a transfusion trigger. Correct it for active bleeding or before an invasive procedure, not to normalize a number.

Glucose - Hypoglycemia is common and harmful in ALF and invisible under anesthesia. Check glucose often and run dextrose rather than waiting for a sign.

Electrolytes, counts, and kidneys - Expect hypokalemia, hypophosphatemia, thrombocytopenia, anemia, and a rising creatinine. Once renal failure is established, early renal replacement therapy is indicated.

Drug handling - Hepatic clearance is gone. Titrate everything, plan for prolonged effect and delayed emergence, and scrub the med list for anything that worsens liver injury.

Treat the cause when you know it - N-acetylcysteine for acetaminophen, and it also benefits non-acetaminophen ALF, particularly at early encephalopathy grades. Nucleos(t)ide analogs for hepatitis B. Acyclovir 5 to 10 mg/kg IV every 8 hours for herpes or varicella-zoster hepatitis. IV methylprednisolone 60 mg/day for suspected autoimmune hepatitis. Prompt delivery of the fetus for acute fatty liver of pregnancy or HELLP.

Infection - These patients behave as immunocompromised, and infection and sepsis are the most common cause of graft failure after transplant for ALF. Keep line and airway technique tight.

Prognostic language you will hear on rounds - King's College Criteria are the standard for transplant decision-making, with Clichy criteria, a MELD above 30, and an APACHE II above 15 also in use. ALF and fulminant Wilson disease get Status 1A priority on the US waitlist.

Acute liver failure (ALF) is severe acute liver injury of fewer than 26 weeks' duration with hepatic encephalopathy and impaired synthetic function (INR 1.5 or higher) in a patient with no cirrhosis or preexisting liver disease. It is subdivided by the interval from jaundice to encephalopathy into hyperacute (within 7 days), acute (1 to 4 weeks), and subacute (5 to 12 weeks).

Massive hepatocyte necrosis and apoptosis drive it, with ATP depletion causing cell swelling and membrane rupture. Cerebral edema is what kills: ammonia crosses a blood-brain barrier already altered by inflammatory mediators, accumulates as glutamine, and the resulting oxidative stress and ATP depletion swell the astrocytes. Drug-induced injury, acetaminophen above all, causes nearly half of US cases; viral hepatitis leads worldwide.