Case Presentation:

This is a 64–year–old Caucasian male with past medical history significant for non–ischemic cardiomyopathy with recent EF of 19% who presented to the hospital with chief complaint of right upper quadrant pain and admitted with working diagnosis of acute cholecystitis. Upon admission, he was afebrile, hypotensive and examination was significant for right upper quadrant tenderness. His initial labs revealed normal leukocyte count, elevated transaminases (AST–106, ALT–88) with normal Alkaline Phosphatase and elevated INR and bilirubin. CT scan of Abdomen showed gall bladder wall thickening without cholelithiasis. He was started on antibiotics and cholecystectomy was planned. Patient’s respiratory status got worsened. On day 5 of hospitalization, he was found to have markedly elevated transaminases (AST–1039 and ALT–1065) with normal Alkaline Phosphatase and worsening of renal functions. RUQ ultrasound showed gallbladder wall thickening without pericholecystic fluid. Acute Hepatitis panel was negative. A transthoracic echocardiogram revealed EF of close to 8.5%. He was treated with inotropes, bumetamide and digoxin. Repeat Ultrasound did not reveal any evidence of gall bladder wall thickening or edema. Subsequently, it was concluded that his elevated liver enzymes were most likely because of hypoxia secondary to severe congestive heart failure and surgery was deferred. With the medical management, patient’s initial symptoms of nausea, abdominal pain resolved, cardiac status was stabilized; transaminases, and renal functions came back to baseline in three days.


Ischemic hepatitis, also called hypoxic hepatitis or shock liver, may affect up to 10% of patients in an intensive care unit and results from an acute fall in cardiac output due to acute myocardial infarction or arrhythmia, usually in a patient with passive congestion of the liver. It is characterized by centrilobular liver cell necrosis and sharply increasing serum aminotransferase levels. It has been suggested that after systemic hypotension, decreased blood flow to the liver results in anoxic hepatocellular injury. Acute hypoxic hepatitis is still an under diagnosed condition. It is misdiagnosed as fulminant hepatitis or acute cholecystitis in most of the cases. It should be seriously considered in patients with past or present cardiac disease, classical hepatic biochemical abnormalities (marked increase in transaminase activity, contrasting with less severe signs of cholestasis and liver failure), initial renal impairment, which is rare in other causes of hepatitis. Transaminases tend to return very rapidly towards normal when the underlying disorder is treated.


Unnecessary treatment such as surgery and use of antibiotics can be avoided if hypoxic hepatitis is considered in the differential diagnosis with this presentation.