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05 October 2026 : Case report  Japan

[In Press] Life-Threatening Ventricular Tachycardia and Transient Brugada-Like Electrocardiographic Abnormalities Caused by Severe Hyperkalemia Due to Urinary Retention in a 55-Year-Old Man

Unusual clinical course, Challenging differential diagnosis, Diagnostic / therapeutic accidents, Management of emergency care, Educational Purpose (only if useful for a systematic review or synthesis)

Yoshiyasu Aizawa1ABDE, Tomoko S. Kato ORCID logo2BD, Akio Kawamura3BD

DOI: 10.12659/AJCR.954530

Am J Case Rep In Press; DOI: 10.12659/AJCR.954530  

Available online: 2026-10-05, In Press, Corrected Proof

Publication in the "In-Press" formula aims at speeding up the public availability of the pending manuscript while waiting for the final publication. The assigned DOI number is active and citable. The availability of the article in the Medline, PubMed and PMC databases as well as Web of Science will be obtained after the final publication according to the journal schedule

Abstract

BACKGROUND
Hyperkalemia is a potentially fatal electrolyte disturbance that typically manifests as progressive conduction abnormalities, bradyarrhythmias, and sine-wave electrocardiographic changes. In rare cases, however, severe hyperkalemia also presents with malignant ventricular tachyarrhythmias and transient electrocardiographic abnormalities involving the right precordial leads, potentially leading to diagnostic confusion with primary arrhythmic disorders.
CASE REPORT
A 55-year-old man with no known cardiovascular disease presented with palpitations, dyspnea, and diaphoresis. Electrocardiography demonstrated sustained wide-QRS ventricular tachycardia accompanied by hemodynamic instability. Following electrical cardioversion, recurrent ventricular tachyarrhythmias occurred, requiring repeated defibrillation, cardiopulmonary resuscitation, intravenous amiodarone, and mechanical ventilation. Laboratory testing revealed severe hyperkalemia (7.6 mmol/L), profound metabolic acidosis (pH 7.059, HCO₃⁻ 13.8 mmol/L), and advanced renal dysfunction. Serum potassium was confirmed on repeat testing. Subsequent electrocardiography demonstrated marked QRS widening, terminal conduction delay, and transient right precordial ST-segment abnormalities involving leads V1-V2. Intravenous calcium gluconate and sodium bicarbonate rapidly improved the electrocardiographic abnormalities. Continuous hemodiafiltration and bladder catheterization were performed after postrenal acute kidney injury caused by urinary retention was identified. Correction of hyperkalemia together with treatment of metabolic acidosis resulted in complete resolution of the ventricular arrhythmias and electrocardiographic abnormalities without recurrence. No evidence of structural heart disease or persistent myocardial ischemia was identified during subsequent evaluation.
CONCLUSIONS
This case illustrates that severe hyperkalemia secondary to reversible postrenal acute kidney injury can simultaneously present with malignant ventricular tachyarrhythmia and transient electrocardiographic abnormalities. Recognition of this reversible metabolic condition is essential to avoid diagnostic error and facilitate prompt life-saving treatment.

Keywords: Hyperkalemia; Ventricular Flutter

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American Journal of Case Reports eISSN: 1941-5923
American Journal of Case Reports eISSN: 1941-5923