AN ATYPICAL CASE OF A DROWNING LIVER

Document Type

Conference Proceeding

Publication Date

6-17-2022

Publication Title

Journal of General Internal Medicine

Abstract

CASE: A 61-year-old man with a medical history of ischemic cardiomyopathy, chronic kidney disease, insulin-dependent type 2 diabetes, and atrial fibrillation presented with confusion, diminished breath sounds at bilateral lung bases, jugular venous distension, and abdominal distension (9 kg over documented dry weight). Laboratory evaluation revealed hypoglycemia (glucose 52 mg/dL), extended prothrombin (115.5 s) and partial thromboplastin times (95 s), very high INR of 16.97, elevated ALT 90 IU/L and AST 80 IU/L, albumin 2.4 g/dL, bilirubin 1.5 mg/dL and BNP 1200 pg/mL. He was treated with IV vitamin K for severely elevated INR and IV diuresis for volume overload. His mental status improved after hypoglycemia correction. Lab results were negative for infectious, autoimmune, hypercoagulable, liver, and biliary etiologies. Ultrasound and abdominal CT imaging were negative for hepatic and biliary pathology. Chest X-ray showed pulmonary vascular congestion with bilateral pleural effusion. Transthoracic echocardiogram showed low ejection fraction of 13%, right atrial pressure of 15 mm Hg, pulmonary artery pressure of 45 mm Hg, and dilated incompressible inferior vena cava. Notably, the patient had 2 previous instances of elevated INR in the setting of congestive heart failure (HF) exacerbation, and warfarin therapy for atrial fibrillation had been stopped 12 days prior to the current presentation, where INR continued to increase. Our patient's INR lowered significantly after supportive treatment for HF exacerbation which allowed us to restart anticoagulation therapy. We concluded that the patient's initial high INR was an unusual manifestation of congestive hepatopathy secondary to end-stage HF. IMPACT/DISCUSSION: Congestive hepatopathy (CH) is a form of liver damage seen in patients with HF. Over time, elevated right-sided heart pressures are transmitted to the liver by passive venous congestion, causing tissue damage and potentially leading to cirrhosis. However, patients are often asymptomatic, highlighting the need for vigilance when treating patients with HF. Liver biochemical abnormalities in CH vary, but elevated bilirubin, aminotransferases, and alkaline phosphatase along with hypoalbuminemia and prolonged prothrombin time are the most common. For our patient, his volume overload, recurring high INR, and hypoglycemia (despite a typical insulin regimen and unchanged oral intake) along with his improvement after aggressive diuresis suggested an atypical presentation of CH. CONCLUSION: Patients with CH may have atypical presentations, which can include hypoglycemia and an unusually high INR. While treatment for underlying HF is standard therapy for CH, managing glucose and water balance may also be critical.

Volume

37

Issue

Suppl 2

First Page

S401

Last Page

S402

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