DOI: https://doi.org/10.36347/sjams.2026.v14i05.033

Pages: 837-839

Ritodrine, a beta-2 adrenergic agonist used for tocolysis, is known to cause hypokalemia during administration, while its discontinuation can occasionally lead to "rebound hyperkalemia" due to the extracellular shift of potassium. Although this rebound effect typically occurs within 2 to 3 hours, the timing and pattern can vary based on the patient's clinical context. We report a case of delayed rebound hyperkalemia in a 34-year-old morbidly obese parturient (BMI 39.1 kg/m²) who presented with placenta accreta and massive hemorrhage following vaginal delivery. Approximately 5.5 hours after ritodrine cessation, during emergency surgery and resuscitation, her serum potassium level was found to be elevated at 6.2 mEq/L, eventually peaking at 7.0 mEq/L at the 7-hour mark. This delayed manifestation may be attributed to several factors, including the reduced extracellular fluid volume and impaired insulin sensitivity associated with morbid obesity, prior potassium supplementation, and the physiological stress of hemorrhagic shock and metabolic acidosis. Despite the severe hyperkalemia, the patient was successfully managed with insulin-glucose therapy and achieved hemodynamic stability after a subtotal hysterectomy. This case underscores the importance of extended electrolyte monitoring for up to 6 to 8 hours after ritodrine discontinuation, especially in high-risk parturients with confounding factors such as obesity or massive hemorrhage, to ensure timely intervention for delayed potassium fluctuations.