SUN-642 - Prolonged Transient Hyperglycemia after Electroconvulsive Therapy in Type 2 Diabetes

Background: Electroconvulsive therapy (ECT) is a widely used treatment for severe psychiatric conditions. Transient hyperglycemia following individual ECT treatments has been described and is attributed to seizure-induced sympathetic and neuroendocrine activation, including cortisol and adrenocorticotropic hormone release. Prior studies show post-ECT hyperglycemia typically peaks within 15–20 minutes and resolves within hours without meaningful impact on long-term glycemic control in diabetic or nondiabetic patients (1). Sustained hyperglycemia extending days beyond ECT is not well characterized. We describe a case of prolonged yet transient severe hyperglycemia following emergency bilateral ECT in a patient with well-controlled type 2 diabetes mellitus (T2DM).

Case: A 66-year-old woman with T2DM (A1c 6.5% on admission) and bipolar I disorder with recurrent hospitalizations for mania, psychosis, and catatonia was involuntarily admitted for a manic episode with psychotic features. Her course was complicated by extrapyramidal symptoms, rhabdomyolysis, acute liver injury, and concern for malignant catatonia. She underwent four sessions of emergency bilateral ECT with marked improvement in catatonia and mania with partial restoration of decision-making capacity.
Following the third ECT session, she developed recurrent severe hyperglycemia with capillary glucose values exceeding 500 mg/dL over six days. Her home regimen consisted of linagliptin 5 mg daily, with no recent steroid exposure and no antipsychotic agents known to worsen insulin resistance. She was started on basal-bolus insulin for presumed stress hyperglycemia; however, despite intermittent refusal of insulin, fasting glucose improved rapidly. Fructosamine was normal (262 µmol/L), indicating preserved glycemic control over the prior 2-3 weeks, arguing against subacute diabetes worsening or falsely low A1c. As her medical and psychiatric status stabilized, insulin was discontinued, oral agents resumed, and glucose normalized.

Conclusion: This case highlights an atypical presentation of prolonged yet transient severe hyperglycemia following ECT, extending beyond the immediate post-ictal period described in existing literature. Normal fructosamine levels and rapid resolution without sustained insulin requirements support ECT-related neuroendocrine stress as the primary driver rather than progression of underlying diabetes. Clinicians should recognize that, although uncommon, ECT-associated hyperglycemia may persist for days in medically complex patients, warranting close monitoring while avoiding premature escalation of long-term diabetes therapy.
Reference: 1. Rasmussen KG, Ryan DA. The effect of electroconvulsive therapy treatments on blood sugar in nondiabetic patients. J ECT. 2005;21(4):232–234.

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