Case report outlines early indications of serotonin syndrome in a young man, highlighting diagnosis challenges and treatment implications.
Serotonin syndrome can be challenging to diagnose due to its variable clinical presentation and multiple potential drug triggers. This may present from mild to fatal, with symptoms such as autonomic instability, altered mental status, and neuromuscular excitation often manifesting as hyperreflexia and clonus. We present a 20-year-old man with a past medical history of obsessive compulsive disorder (OCD) being treated with clomipramine 25 mg orally (PO) daily and quetiapine 100 mg PO daily, who arrived at the emergency department for agitation. He was found to be in sinus tachycardia with a heart rate (HR) around 140 beats per minute (bpm), with no medical or substance cause identified. He was medically stabilized, continued on his home medications, and transferred to the inpatient psychiatry unit. However, he again became tachycardic at 175 bpm, with muscle rigidity, tremor, agitation, and diaphoresis. The patient's HR stabilized following administration of lorazepam 2 mg intramuscular (IM) and metoprolol 5 mg intravenous (IV), but he remained rigid and diaphoretic for several more hours. The patient reported that he had taken clomipramine in excess prior to admission, so clomipramine was discontinued prior to discharge. In this case, muscle rigidity masked the hyperreflexia and myoclonus often used to diagnose serotonin syndrome, making it even more difficult to recognize. Additionally, collateral information about the patient's excessive use of clomipramine, a potent serotonergic tricyclic antidepressant (TCA), was not obtained early on. Few cases of mild and masked serotonin syndrome have been reported due to the difficulty in recognizing and quickly treating such cases. Cases of serotonin syndrome should continue to be reported in order to familiarize clinicians with the varied presentation.
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Alday et al. (2025) studied this question.
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