Acute Fulminant Transaminitis Secondary to Ischemic Hepatopathy in New-Onset Severe Biventricular Heart Failure: A Case Report

Marked elevation of aminotransferases, approximately 15 times the upper limit of normal, is typically attributable to ischemic or drug-induced hepatitis.Differentiating ischemic hepatitis from congestive hepatopathy is essential in patients with acute heart failure.This report describes a 45-year-old male with chronic hepatitis C and polysubstance exposure who presented with abdominal pain and dyspnea, and was found to have extreme transaminase elevation, hyperbilirubinemia, coagulopathy, lactic acidosis, and acute kidney injury.Initial evaluation prioritized infectious and primary hepatic etiologies due to leukocytosis (WBC 15.6 ×10³/µL), lactate 2.5 mmol/L, acute kidney injury (BUN 43 mg/dL, creatinine 2.49 mg/dL), and CT findings of bilateral striated nephrograms with perinephric fat stranding.Acetaminophen toxicity and acute viral hepatitis were excluded.Chest radiograph demonstrated cardiomegaly and pulmonary vascular congestion, and transthoracic echocardiography on day 1 revealed newly diagnosed severe biventricular systolic dysfunction (LVEF 20%-25%) with a dilated noncollapsing inferior vena cava, indicating elevated right-sided pressures and impaired forward perfusion.The patient was subsequently diagnosed with severe biventricular systolic dysfunction.Cardiology initiated aggressive intravenous Lasix diuresis and dobutamine infusion for low-output heart failure with evidence of end-organ hypoperfusion.Following initiation of heart failure-specific therapy, renal function progressively improved (creatinine 2.49 → 1.68 mg/dL by day 2), lactate normalized, and aminotransferases declined rapidly within 72 hours.Liver enzymes declined rapidly within 72 hours following hemodynamic stabilization and treatment of acute decompensated heart failure.The clinical course and biochemical pattern were consistent with ischemic hepatopathy secondary to acute-onset heart failure.Hypoxic hepatitis is most commonly associated with cardiac failure and may occur even in the absence of documented hypotension.In this context, reduced forward cardiac output combined with hepatic venous congestion likely resulted in impaired hepatic oxygen delivery.Although this patient exhibited signs of volume overload, including pleural effusions, reduced right ventricular function, and a dilated noncollapsing inferior vena cava, the homogenous echotexture observed on liver ultrasound supports acute cardiogenic liver injury rather than acute decompensation superimposed on established chronic congestive hepatopathy.