Acute urinary retention presenting as inferior pseudo-STEMI: A case report

To describe a case of inferior ST-segment elevation from massive bladder distension resolving with Foley catheterization in the absence of tachycardia, hypertension, or other hemodynamic evidence of sympathetic activation.

A 73-year-old man presented with progressive abdominal distension and markedly decreased urination over several days. Vital signs were notable only for mild hypotension (blood pressure 99/75 mmHg) with heart rate 94 beats per minute and temperature 97.6 °F. Examination revealed a bladder palpable to the xiphoid. An electrocardiogram obtained in response to hyperkalemia (potassium 5.5 mEq/L) unexpectedly demonstrated inferior ST-segment elevation in leads II, III, and aVF with reciprocal depression in leads I and aVL. Computed tomography confirmed massive bladder distension extending to the xiphoid with no obstructing lesion. After discussion with interventional cardiology, Foley catheterization drained approximately 2 L of urine; a repeat electrocardiogram immediately after demonstrated complete resolution of ST-segment changes. Serial high-sensitivity troponin (peak 36 ng/L; reference <22 ng/L) showed no dynamic change. Blood cultures grew Escherichia coli, confirming bacteremic urosepsis.

Unlike prior reports attributing bladder-distension-associated electrocardiographic changes to catecholamine surge with tachycardia and hypertension, this case occurred with entirely normal heart rate and no hypertension. A mechanical diaphragmatic mechanism from a bladder distended to the xiphoid is the more plausible explanation.

Massive bladder distension can produce inferior ST-segment elevation mimicking ST-elevation myocardial infarction, resolving with decompression even without hemodynamic activation. Emergency physicians should consider this entity in the differential for reversible inferior ST-segment elevation.