Hepatitis A (HAV)

Defer the elective case - Acute hepatitis A is self-limited and resolves in 2 to 4 weeks on supportive care, and normalization of the liver function tests is what defines the episode as over. There is nothing to gain by anesthetizing an acutely inflamed liver for elective surgery — wait for the transaminases to come back down.

Sort inflammation from failure - ALT, AST, ALP, and bilirubin tell you how inflamed the liver is; ALT runs 2- to 100-fold above normal depending on severity, so the absolute number is less useful than the trend. INR/PT, albumin, and ammonia are the ones that tell you whether synthetic function is going, and those are the numbers that change your anesthetic.

Coagulopathy sets the limits - Check INR before any neuraxial technique or invasive line. In acute liver failure, coagulopathy is corrected only for active bleeding or a planned invasive procedure, so ask for product with a reason attached rather than chasing a number.

Encephalopathy means acute liver failure - Encephalopathy plus coagulopathy without pre-existing chronic liver disease is the definition, and the presence of encephalopathy is the key prognostic factor in the King's College Criteria. Do a bedside mental-status check preoperatively; a confused, jaundiced HAV patient belongs in an ICU at a transplant-capable center, not on your elective list.

Protect the brain in fulminant disease - The mainstay of acute liver failure management is preventing cerebral edema: head elevation, mannitol, hyperventilation, and cerebroprotective measures, with ICP monitoring in a few patients. If you are anesthetizing one, run it like an intracranial case — head up, no hypercarbia, no hypotension.

Check the glucose - Hypoglycemia is detrimental in acute liver failure and is prevented with a dextrose infusion. A fasted patient whose hepatic gluconeogenesis is failing will drop, so measure on arrival and recheck intraoperatively rather than assuming.

Add no second insult - Alcohol, hepatotoxic drugs, and over-the-counter supplements are stopped in these patients, acetaminophen above all — acetaminophen-related injury causes 39% to 50% of acute liver failure cases in the UK, US, and Australia. Keep it out of your multimodal plan while the liver is recovering, and pick drugs the liver isn't required to clear.

Renal support - Renal failure is a recognized complication of acute liver failure and early renal replacement therapy is instituted when it develops. Follow creatinine and urine output, and dose accordingly.

Staff and unit precautions - Fecal-oral spread with a household secondary infection rate of about 20%. Hand hygiene and contact precautions during transport and in the OR. Unvaccinated exposed staff get immune globulin as early as possible after exposure — beyond two weeks it is not effective at preventing infection.

No chronic disease to plan around - Once recovered there is no carrier state and no residual hepatic risk. For a patient whose hepatitis persists past six months, work from the Chronic Viral Hepatitis entry and, if portal hypertension is established, Cirrhosis.

Hepatitis A virus (HAV) is a positive-sense, single-stranded RNA picornavirus with a single serotype worldwide. Transmission is fecal-oral through contaminated food and water and close personal contact, with sexual transmission and rare bloodborne spread; concentration is highest in stool and the average incubation period is 30 days. It replicates in hepatocytes and produces an acute hepatitis — fever, malaise, anorexia, nausea, abdominal pain, dark urine, jaundice — that is self-limited and resolves over 2 to 4 weeks with supportive care.

What matters is what it does not do: there are no chronic sequelae and no carrier state, which separates it from hepatitis B and C. The exception is fulminant disease. Fewer than 1% of the 1.5 million annual infections progress to acute liver failure, but hepatitis A, B, and E cause most acute liver failure in the developing world.