Pulmonary Vascular Disease |

Severe Hypoxic Hepatitis From Pulmonary Hypertension-Associated Right Heart Failure FREE TO VIEW

Suraj Raheja, MD; Kimberly Baker-Genaw, MD
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Henry Ford Hospital, West Bloomfield, MI

Chest. 2015;148(4_MeetingAbstracts):982A. doi:10.1378/chest.2280510
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SESSION TITLE: Pulmonary Vascular Disease Student/Resident Case Report Posters

SESSION TYPE: Student/Resident Case Report Poster

PRESENTED ON: Tuesday, October 27, 2015 at 01:30 PM - 02:30 PM

INTRODUCTION: Pulmonary embolisms (PE) may acutely trigger cardiac, respiratory and circulatory failure, or chronically contribute to pulmonary hypertension. These dynamics draw attention to the heart, lungs and hemodynamics, but not frequently to the liver. With its significant vascularity, our case demonstrates the necessity of routinely assessing the liver in some of the most frequently encountered problems in cardiopulmonary medicine.

CASE PRESENTATION: A 59 year-old female presented with progressive dyspnea of 4 weeks’ duration. She reported a single episode of PE 3 years prior, after which she did not adhere to anticoagulation. Clinical history and exam were now consistent with congestive heart failure (CHF), and an echocardiogram revealed a significantly enlarged right ventricle (Image 1) with poor systolic function, and severely elevated pulmonary artery pressure (average 68 mmHg). CT-angiography found a massive chronic pulmonary artery thrombus (Image 2). Though without stigma of hepatic injury, liver function testing (LFT) was added to her lab work. This showed new severe elevations in transaminase levels, with peak AST 2451 IU/L and ALT 1973 IU/L. Dutiful evaluation of such significant liver injury found no instance of hypotension or systemic shock, no tissue hypo-perfusion elsewhere, and negative viral, toxic, autoimmune, and deposition disease testing. Doppler ultrasound found no hepatic vein thrombosis and no cirrhotic changes. Excluding other potential causes, the significant hepatic dysfunction was attributed entirely to CHF. Further review of imaging revealed reflux into the supra-hepatic IVC and distension of hepatic veins. With pulmonary hypertension-associated progression of right heart failure causing severe hypoxic hepatitis she was diuresed and anticoagulated, improving both her dyspnea and LFTs.

DISCUSSION: Hypoxic hepatitis from decreased blood flow (left heart failure / ischemia), venous congestion (right heart failure), or hypoxemia (respiratory failure) is now the most frequently recognized cause of acute liver injury. Over 10 years, a study reported on 142 cases of hypoxic hepatitis and found AST 732 IU/L and ALT 289 IU/L as the most severe injuries encountered. Other studies reviewing hundreds of cases stated transaminases may rise to 10 times the upper limits of normal; approximately AST 350 IU/L and ALT 400 IU/L. Our patient had levels several multiples higher than any of these.

CONCLUSIONS: This case is presented to expand the awareness of liver injury in cardiopulmonary pathology, not only for its presence but also for the degree of injury that may be encountered.

Reference #1: Naschitz J, et al. Heart Diseases Affecting the Liver and Liver Diseases Affecting the Heart. American Heart. 2000;140:111

Reference #2: Henrion J, et al. Hypoxic Hepatitis: Clinical and Hemodynamic Study in 142 Consecutive Cases. Medicine. 2003; 82: 392

Reference #3: Aslan S, et al. Liver Dysfunction in Patients with Acute Pulmonary Embolism. Hepatology Research. 2007;37:205

DISCLOSURE: The following authors have nothing to disclose: Suraj Raheja, Kimberly Baker-Genaw

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