DOI: https://doi.org/10.36347/sjmcr.2026.v14i07.031

Pages: 1747-1751

Severe infection may trigger Takotsubo syndrome (TTS), but recognizing it in the intensive care unit can be challenging because its presentation may resemble both sepsis-induced cardiomyopathy and acute coronary syndrome. We describe a 61-year-old man with diabetes, hyperthyroidism, and severe chronic neurological disability following surgery for craniopharyngioma, who was admitted with bronchopneumonia, hypoxemic respiratory failure, and septic shock. Initial transthoracic echocardiography showed a hyperdynamic left ventricle with preserved systolic function. Less than 24 hours later, repeat echocardiography revealed apical ballooning, akinesia of the apical and mid-ventricular segments, basal hyperkinesia, and a left ventricular ejection fraction of approximately 25%. These changes were associated with a marked rise in troponin and the new onset of a complete bundle-branch block. Despite broad-spectrum antibiotics, invasive mechanical ventilation, vasopressor support, and supportive care, the patient developed refractory shock and died 48 hours after ICU admission. Coronary angiography was considered but could not be performed because his profound hemodynamic instability made transfer and invasive assessment unsafe. Cardiac magnetic resonance imaging was also not feasible, while temporary mechanical circulatory support was unavailable. The abrupt onset of a typical regional pattern of left ventricular dysfunction after a major physical stressor strongly suggested sepsis-triggered TTS. However, acute coronary syndrome and myocarditis could not be definitively excluded, and recovery of ventricular function could not be documented. This case highlights the importance of serial bedside echocardiography and of clearly acknowledging diagnostic uncertainty when confirmatory investigations cannot be safely performed.