Introduction Thrombolytic therapy using streptokinase has been widely used for acute myocardial infarction to achieve recanalization in infarct related artery. Bleeding into critical organ and space in a known complication. Inflammation of the pericardium in acute myocardial infarction increases the risk of bleeding after administration of thrombolytic agent.

Case Presentation A 68 year old gentleman with history of inferior myocardial infarction in 2014, dyslipidaemia who defaulted antiplatelet presented with severe central chest pain associated with palpitations, dyspnoea and diaphoresis of sudden onset. He denied having fever, chest trauma, anticoagulant use, or failure symptoms. Clinically, he was alert and hemodynamically stable. He saturated well under room air with clear heart sounds and bibasal crepitations. He had no other signs of heart failure. Initial ECG showed ST segment elevation at lead I, aVL and V2-V6 with pathological Q waves at inferior leads. Bedside echocardiography showed impaired left ventricular ejection fraction ~40% with akinetic anterolateral and inferior wall, no pericardial effusion seen. He was treated as acute anterolateral myocardial infarction KILLIP II and was given IVI Streptokinase 1.5mU. Post thrombolysis, his chest pain improved and ECG post thrombolysis showed >50% reduction of ST segment elevation. 22 hours post thrombolysis, he complained of recurrent chest pain, dyspnoea with desaturation episode. Clinically, he was alert, restless with moderate pulse volume and coolish peripheries. He was tachycardic and hypotensive requiring IVI Noradrenaline 1.2mcg/kg/min. Serial ECG and cardiac biomarkers did not show signs of reinfarction. Bedside echo showed global pericardial effusion with collapsed RV and distended IVC. Pericardial tapping done via apical approach aspirated 250cc blood. Post tapping, his heart rate normalise and inotropic support reduced 0.5mcg/kg/min. He developed left haemothorax which required left intrapleural catheter drainage. CT angiography showed no dissection or arterial bleed. He was hemodynamically stable on day two onwards with well expanded lung on day five. Repeated echo showed residual pericardial effusion of 0.7cm with LV clot. He was started on warfarin therapy and discharged well. Coronary angiography revealed triple vessel disease with LAD being the IRA.

Discussion Pericardial effusion is commonly seen in myocardial infarction and are generally asymptomatic. Expansion of effusion is self-limiting and no specific therapy is needed. Progressive accumulation of fluid within pericardial space will impede diastolic filling of the ventricle which causes tamponade.

Conclusion Hemopericardium in a rare yet major haemorrhagic and potentially fatal complication post thrombolysis. Unexplained hemodynamic instability post thrombolysis following large territory myocardial infarction warrants urgent echocardiography to exclude treatable condition. Timely bedside needle pericardiocentesis followed by drainage will render favourable outcome.