Case Presentation:

A 31–year–old man with no past medical history presented with three days of progressively worsening abdominal pain radiating to the epigastrum. The pain was dull in character, and associated with nausea and vomiting. He described chronic headaches for the past two weeks since trying to stop smoking. His vitals were normal. He had anicteric sclera and no jaundice. His abdomen was tender to deep palpation in the right upper quadrant with no hepatoslpenomegaly. His initial AST and ALT were 1844 U/L and 2588 U/L. The LDH was 1618 U/L and the INR 1.5. The viral hepatitis panel, right upper quadrant ultrasound and toxicology screen were normal. His acetaminophen level was 2.2 mcg/mL. He noted he’d taken up to 3 g of acetaminophen a day for relief of his headaches; the last dosage of was 72 h prior to presentation. He described an active binge drinking history in which he would finish 3–4 L of liquor a weekend. He stated he’d been outside working in the 105°F heat. He was treated with N–acetylcysteine and intravenous fluids were initiated. His AST and ALT were recorded as high as 9,453 U/L and 15,553 U/L. His transaminases trended back down to the low 1,000’s and his coagulation studies normalized. We hypothesized his liver injury was related to combination of dehydration with alcohol and ace–tominophen use. Discussion: Elevation in serum aminotransferases is generally a sign of acute hepatocellular damage which can vary from in–creased cellular permeability to fulminant hepatocyte necrosis. Most cases of hepatitis have transaminases in the 100–500 range. The release of extremely high levels of aminotransferases in to the blood signifies a vast hepatocellular injury pattern. Etiologies responsible for this fulminant damage include drug or toxin–induced liver injury, viral hepatitis, ischemic hepatic injury, congestive hepatopathy, Budd–Chiari, and acute common biliary duct obstruction. Alcoholic hepatitis is rarely a cause of transaminases greater than a thousand. The amount of aminotransferase released into the has little prognostic significance; the trend, and not the absolute number, predicts the ultimate prognosis. Complete normalization of the transaminases may reflect a complete liver “burns out,” and subsequent hepatic failure, as much as they predict complete recovery. Biosynthetic function measurements such as the albumen and coagulation studies provide a better sense of recovery. Interestingly, a sudden drop in the patient’s heart rate with normal hemodynamics is a good prognostic sign. As the edematous liver improves, there is a sudden release of bilirubin, which acts as a digoxin congener in stimulating the parasympathetic stimulus to the heart, offsetting the previous tachycardia from the acute hepatitis inflammation.

Conclusions:

An organ such as the liver is ex–tremely complex and undertakes multiple functions to maintain homeostasis. Inherent in this complexity, as portrayed in the case above, is allowance for a multi–factorial cause of failure.