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.

Infective endocarditis (IE) is the infection of the endocardium or valves of the heart. Morbidity and mortality rates are high if not recognized early and left untreated. Complications such as heart failure, embolism and aneurysmal formation further increase mortality risk. We present a complicated case of IE where these complications coexisted in a single patient. A 27-year-old male diagnosed with rheumatic heart disease (RHD) presented with 3-month history of febrile episodes and 1-week history of left-sided weakness and facial asymmetry. Physical examination revealed subconjunctival hemorrhages, left-sided hemiparesis and left central facial palsy. On auscultation, he had murmurs suggestive of mitral regurgitation and stenosis, and aortic regurgitation. Two-dimensional echocardiography revealed mitral and aortic regurgitation with multiple large-sized vegetations at both valves. Further workup showed a right middle cerebral artery (MCA) infarct, right MCA mycotic aneurysms, and bilateral kidney infarcts with secondary infectious glomerulonephritis and splenic infarct. Blood cultures were negative. He was managed as culture-negative definite IE and was started on ceftriaxone and gentamycin which was later shifted to vancomycin due to lack of clinical improvement. During the course, he also developed severe abdominal pain-CT angiography of the abdomen revealed acute mesenteric ischemia of the superior mesenteric artery, which was managed conservatively. Double valve replacement was contemplated, but acute respiratory failure from hospital-acquired pneumonia posed higher surgical risks. Unfortunately, the patient eventually succumbed to brain herniation from new-onset multiple cerebral infarcts. Literature suggests rarity of multiple complications of IE occurring in a single patient. Because high mortality associated with complications can be averted by early recognition and early intervention, multiple embolisms should be suspected in a patient who already presented embolism in one organsystem.