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4. Serotonin syndrome
Serotonin syndrome is a potentially life-threatening condition associated with increased serotonergic activity in the central nervous system (5). It is seen with therapeutic medication use, inadvertent interactions between drugs, and intentional self-poisoning. Many drugs can contribute to the onset of serotonin syndrome. SSRIs, MAO inhibitors, 5 HT agonists, and amphetamines all lead to increased serotonergic activity and, as in this case, act together to precipitate the syndrome.
The diagnosis of serotonin syndrome is made solely on clinical grounds. Therefore, a detailed history and thorough physical and neurologic examinations are essential. Serotonin syndrome is a clinical triad of mental-state changes, neuromuscular abnormalities, and autonomic hyperactivity caused by excessive serotonergic agonism in the central nervous system.
It encompasses a spectrum of disease where the intensity of clinical findings is thought to reflect the degree of serotonergic activity. Mental status changes can include anxiety, agitated delirium, restlessness, and disorientation. Patients may startle easily. Autonomic manifestations can include diaphoresis, tachycardia, hyperthermia, hypertension, vomiting, and diarrhea. Neuromuscular hyperactivity can manifest as tremor, muscle rigidity, myoclonus, hyperreflexia, and bilateral Babinski sign. Hyperreflexia and clonus are particularly common; these findings, as well as rigidity, are more often pronounced in the lower extremities.
Upon review of the patient’s medications, she was taking a selective serotonin uptake inhibitor (SSRI) escitalopram, as well as other agents that can increase serotonin including ondansetron and other anti-emetics. With the addition of methylene blue, which is a phenothiazine derivative and functions as an inhibitor of monoamine oxidase (MAO-I), she experienced the acute onset of serotonin syndrome (6,7).
What should be done next to treat this patient? (Click on the correct answer to proceed to the fifth and final page)