A 28-year-old Filipino male was admitted due to high-grade fevers and dyspnea on a background of chronic cough and weight loss. Due to clinical and echocardiographic signs of cardiac tamponade, emergency pericardiocentesis was performed on his first hospital day. Five days after, chest radiographs showed new pockets of radiolucency within the cardiac shadow, indicative of pneumopericardium. On repeat echo, air microbubbles admixed with loculated effusion were visualized in the anterior pericardial space. Constrictive physiology was also supported by a thickened pericardium, septal bounce, exaggerated respiratory variation in AV valve inflow, and IVC plethora. A chest CT scan confirmed the presence of an air-fluid level within the pericardial sac. The patient was started on a quadruple antituberculosis regimen and IV piperacillin-tazobactam to cover for superimposed acute bacterial pericarditis. Pericardiectomy was performed as definitive management, with stripped pericardium measuring 5–7 mm thick and caseous material extracted from the pericardial sac. Histopathology was consistent with tuberculosis. This report highlights pneumopericardium as a rare complication of pericardiocentesis. We focused on the utility of echocardiography for diagnosing and monitoring this condition on a background of tuberculous constrictive pericarditis, ultimately convincing us that pericardiectomy was necessary, instead of the usual conservative measures for pneumopericardium.

Pericardial decompression syndrome (PDS) is a rare, under-reported and potentially fatal complication of pericardial drainage characterized by paradoxical hemodynamic deterioration. The onset ranges from immediate to as long as 48 h post drainage. We present a case of a 51-year-old woman admitted due to progressive dyspnea. She was hemodynamically stable but with signs of cardiac tamponade. On two-dimensional echocardiography (2D-echo) there was a massive pericardial effusion in tamponade physiology. Immediate surgical drainage was done but intra-operatively there was depressed cardiac contractility necessitating inotropic support. Post-operative 2D-echo showed right ventricular (RV) and left ventricular (LV) systolic dysfunction. She was admitted in the intensive care unit (ICU) for 72 h. Repeat 2D-echo showed marked improvement in RV and LV systolic function. She was then discharged improved on the fifth hospital day. The pathophysiology of PDS is still not very clear. The simplest mechanism is that sudden removal of compressing pericardial fluid causes increased venous return with expansion of the RV at the expense of the LV leading to acute heart failure. There are no published studies to propose preventive measures and treatment remains supportive. There has been only one published case reported here in our country. We report this case of a patient who successfully recovered from PDS.