Hypoxic hepatitis and acute liver failure in a patient with newly onset atrial fibrillation and diltiazem infusion

Abstract

Hypoxic hepatitis (HH) most commonly results from haemodynamic instability and disruption of hepatic flow. The vast majority of cases are caused by cardiac failure, respiratory failure and septic shock. We report a case of HH, acute liver failure, acute kidney failure and progressive thrombocytopenia that developed following a hypotensive episode in a patient treated with intravenous diltiazem for a newly developed atrial fibrillation (A-fib). The pre-existing liver diseases, including chronic alcohol use and liver congestion secondary to right heart dysfunction, might have predisposed the patient to the development of HH. The patient was given supportive treatment and experienced full recovery of both liver and kidney function. To our knowledge, this is the first reported case of HH that occurred following ventricular rate control for acute A-fib. For patients with underlying liver diseases, closer blood pressure monitoring is warranted during diltiazem infusion.

Figure 1

Change of aminotrasferase (ALT), alanine aminotransferase (AST), prothrombin time (PT), creatine and platelet count of the patient since admission. (A) Normal serum ALT on admission (admit), abrupt increase on postadmission day 1 (d1) and gradual decrease over 8 days (2–9). (B–E): changes of AST, PT, creatine and platelet.