Acute Right Ventricular Failure in a Patient With Hepatic Cirrhosis

Abstract

Background: Pulmonary embolic disease is mostly commonly due to venous thromboembolism (VTE). However, fat, tumor, and air may all embolize to the pulmonary vasculature. We describe a patient with tumor emboli from a previously undiagnosed hepatocellular carcinoma (HCC) presenting with hypoxemic respiratory failure and shock.: Case A 62-year-old male with COPD, and end stage liver disease (MELD score 15) due to hepatitis C infection, was admitted for dyspnea. Exam was notable for heart rate 95 bpm, respirations 21 bpm, blood pressure 134/78 and oxygen saturation of 85% on RA. Cardiopulmonary exam was remarkable for regular rhythm without murmurs, no right ventricular lift, and diffuse expiratory wheezing without crackles or ronchi. The remainder of the examination was unremarkable, including the absence of peripheral edema, ascites, or cyanosis. Chest x-ray showed no changes of hyperinflation or parenchymal infiltrates, small bilateral pleural effusions and right hemidiaphragm elevation. Arterial blood gas on room air showed a pH of 7.45, PaCO2 of 35.9 and PaO2 of 59. The respiratory alkalosis and increased A-a gradient were concerning for venous thromboembolism (VTE). Lower extremity ultrasound showed no DVT and renal dysfunction (Cr 4.7 mg/dl) precluded CT angiography. A ventilation/perfusion scan showed low probability for VTE. On hospital day two, he developed progressive hypotension, syncope and worsened hypoxemia. A computed tomography of the head was negative for any acute processes. Echocardiography showed a moderately enlarged right ventricle (RV) with decreased systolic function; LVEF was 65%. Over the subsequent 24 hours, the patient developed progressive hypotension refractory to fluid resuscitation and subsequent vasopressor therapy. Repeat echocardiography revealed a small left ventricular cavity (LVEF 50%) with progressive dilation and worsened RV hypokinesis with new, severe tricuspid regurgitation. Supportive measures including mechanical ventilation, vasopressors and renal replacement therapy were instituted but refractory shock persisted. The patient developed asystolic arrest and resuscitation was withheld in conjunction with the family wishes. The patient expired 72 hrs after admission. Post-mortem examination revealed diffuse moderately differentiated HCC throughout the liver with innumerable micro-tumors. No discrete tumor macronoldule was identified. Tumor invaded hepatic and perihepatic vasculature including the portal vein. Microscopically, intravascular HCC tumor emboli were present in both ventricles, and diffusely throughout the pulmonary vasculature. This case illustrates the difficulty of establishing the diagnosis of tumor emboli, especially in the absence of a known primary cancer. It highlights the importance of considering etiologies of embolic disease other than VTE. This abstract is funded by: None Am J Respir Crit Care Med