Pericardial Decompression Syndrome in a Patient With Low Volume Pericardial Fluid Removal

Abstract

SESSION TITLE: Critical Care 3 SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM INTRODUCTION: Pericardial decompression syndrome (PDS), typically presents with hemodynamic and/or pulmonary edema, immediately or up to 1-2 days following surgical pericardiostomy or pericardiocentesis. Many of reported cases noted new onset LV dysfunction, with 70% of those studies demonstrating normalization of LV systolic function. CASE PRESENTATION: A 54-year-old male without prior cardiac or pulmonary history, presented with dyspnea for 1 week and worsening pleuritic chest pain. On presentation suddenly became hypotensive 75/36, tachypneic and diaphoretic. Cardiac enzymes were negative and electrocardiogram showed no acute ST abnormalities. Computed tomography angiography chest was negative for pulmonary embolism. 2-D echocardiogram showed moderate-to-large pericardial effusion with mitral inflow abnormalities suggestive of tamponade. A left anterior thoracotomy with pericardial window & biopsy was performed and approximately 200cc of cloudy watery fluid was removed, with 594 cc removed via chest tubes over the next three days Subsequently, 36 hours later he developed increased dyspnea, requiring Bilevel Positive Airway Pressure (BiPAP) to maintain oxygenation. X-ray (Fig 1) demonstrated diffuse bilateral interstitial and alveolar disease. Treated with lasix and remained on BiPAP for 4 days, and weaned to high flow nasal cannula. Repeat X-ray (Fig 2), decreased bilateral interstitial and alveolar parenchymal. Three weeks later, the echocardiogram revealed ejection fraction, 50-55% with left ventricular diastolic dysfunction. DISCUSSION: Several mechanisms have been proposed for PDS, the hemodynamic hypothesis theorizes that with removal of the pericardial fluid, the rapid restoration of the right ventricular function would result in increased venous return and bowing of the right ventricle into the left, resulting in pulmonary edema and left-sided heart failure. In the case of the ischemic hypothesis the increased pericardial pressure would compress the epicardial arteries, which has shown to reduce coronary blood flow and may incite myocardial stunning and hibernation. Finally, elevated pericardial pressure would also promote activation of sympathetic nervous system, a high catecholamine state, and relief of pressure could unmask a pre-existing compensated LV and/or RV dysfunction. Current understanding has proposed that gradual pericardial fluid removal until the tamponade physiology resolves may reduce the risk of PDS. Interestingly, only 200cc of pericardial fluid was removed initially, with 590cc over 3 days, slowing the hemodynamic change, but still resulting in PDS, but without adverse outcome. CONCLUSIONS: Our case suggests low volume pericardial fluid removal does not negate the occurrence of PDS, but may decrease the severity. Reference #1: Rajesh, Pradhan, et al. Patient characteristics and predictors of mortality associated with pericardial decompression syndrome: a comprehensive analysis of published cases. EHJ-ACVC 2015, Vol. 4(2) 113-120 DISCLOSURE: The following authors have nothing to disclose: Tamer Said Ahmed, Jonathan BarreraCalix, Larry Woods, Daniel Woredekal No Product/Research Disclosure Information