Presentation of sub-massive pulmonary embolism mimicking acute liver failure.

Document Type

Conference Proceeding

Publication Date

2016

Publication Title

Chest

Abstract

Pulmonary Embolism (PE) remains a challenging diagnosis, requiring a very high index of suspicion. Signs and symptoms of acute right heart failure are often non-specific and vary according to the precipitating cause. We present a case of a middle-aged female, whose initial presentation of evolving liver failure and coagulopathy led to an extensive work up to evaluate the etiology, before the diagnosis of PE was considered as the primary cause of evolving multi-organ failure. CASE PRESENTATION: A 32 year-old female with history of Crohns disease presented to the hospital with worsening nausea, vomiting and lethargy. On admission, she was tachycardic at 110/minute, tachypenic at 25/minute and hypoxic to 87% on room air. Initial lab work revealed markedly elevated transaminases ALT 2350, AST 9616, and new coagulopathy with an INR 1.8. She was admitted for acute liver failure and emergent Hepatology evaluation for transplantation. Initial work-up included a negative toxicology screen for acetaminophen, salicylates and alcohol along with negative autoimmune and viral hepatitis panel. Infectious work-up was negative. She denied use of any new medications or herbal supplements. Given her worsening encephalopathy and liver failure, N-acetyl cysteine protocol was initiated, while awaiting evaluation by multidisciplinary teams for liver transplant. Review of her echocardiographic imaging revealed severe right ventricular (RV) enlargement with systolic dysfunction, along with inter-ventricular septal flattening and elevated pulmonary artery pressure of 53mmHg. Given these findings, there was a shift in the working diagnosis with strong consideration for PE. Diagnosis was confirmed with a high probability V/Q scan and subsequent CT PE which showed multiple large bilateral pulmonary emboli within the main pulmonary arteries with significant clot burden and reflux of contrast into hepatic veins. Treatment with IV heparin was initiated with eventual rapid improvement in liver enzymes. A diagnosis of acute PE resulting in RV decompensation was made which explained the patient's clinical presentation and liver failure. DISCUSSION: RV dysfunction may develop acutely in PE depending on the extent of obstruction. Sudden increase in RV afterload can lead to acute RV failure and decrease in cardiac output which can thereby result in mesenteric hypo-perfusion progressing to multi-organ failure. However, in our case, acute onset of liver failure muddled the classic presentation of PE and led the clinicians to urgently evaluate the various common causes of acute liver injury, thereby delaying the initiation of anticoagulation until day 3 of hospitalization. CONCLUSIONS: This case illustrates the importance for clinicians to maintain a high index of suspicion of PE leading to acute RV failure as another etiology for patients presenting with acute liver injury.

Volume

150

Issue

4

First Page

429A

This document is currently not available here.

Share

COinS