59. SEROTONIN TOXICITY DURING ELECTROCONVULSIVE THERAPY FOR GERIATRIC DEPRESSION: A RETROSPECTIVE CASE SERIES

Abstract

Introduction

Serotonin syndrome is a rare, potentially lethal, adverse effect of serotonergic agents that classically presents as a triad of cognitive-behavioral changes, autonomic nervous system dysfunction, and neuromuscular abnormalities. Since serotonin syndrome was first described, there has been a growing emphasis on the early recognition of serotonin toxicity (a clinical diagnosis with features of but not meeting full criteria for serotonin syndrome) to prevent catastrophic consequences. Although serotonin toxicity is most commonly caused by use of two or more concurrent serotonergic medications, five cases in the literature have documented serotonin toxicity due to concurrent use of electroconvulsive therapy (ECT) and one or more serotonergic medications. To date, our understanding of why ECT may induce serotonin toxicity remains limited and speculative. Here, we report on three cases that meet Hunter’s criteria for serotonin toxicity in the setting of acute ECT treatment. We then provide case commentary, summarize hypotheses regarding ECT and serotonin toxicity, and discuss clinical implications and next steps for research.

Methods

Three cases of serotonin toxicity during acute ECT treatment of geriatric depression were reviewed, summarized, and analyzed retrospectively.

Results

Serotonin toxicity was suspected in case 1 given agitation, hyperreflexia, and tremor, and cases 2 and 3 given spontaneous clonus and hyperreflexia. Serotonin toxicity was treated in case 1 with medication dose reduction and ECT frequency reduction; case 2 with medication dose reduction and stopping ECT; case 3 with medication change and ECT frequency reduction.

Conclusions

At present, serotonin syndrome remains a clinical diagnosis and is often difficult to recognize in the early stages, especially in elderly patients receiving acute ECT treatment. ECT commonly causes cognitive side effects in the elderly in the acute phase including decreased orientation and amnesia, which can confound clinical evaluation. To further complicate matters, serotonin syndrome is wide ranging in its presentation from mild (akathisia, tremor, altered mentation, inducible clonus) to life-threatening (sustained clonus, muscular hypertonicity, and hyperthermia), and not all findings are always present in a single patient. Patients may under report symptoms due to cognitive side effects and severe signs like muscular hypertonicity can mask tremor and hyperreflexia on a clinical exam. Given this, we recommend a high index of suspicion for serotonin toxicity in elderly patients receiving ECT treatment with new-onset tremor, hyperreflexia, or clonus given early detection of serotonin toxicity and prompt removal of offending agents can prevent catastrophic outcomes. Further research is needed to optimize current clinical criteria and improve the tools used to screen and diagnose serotonin syndrome, particularly in specialized settings such as ECT treatment. In the future, improved risk modeling and stratification may lead to better prevention of serotonin toxicity. Timely and accurate diagnosis and prompt and targeted treatment of serotonin syndrome will likely lead to better outcomes.