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Intensive Care Unit, Hospital Alemám, Buenos Aires, Argentina, josatnik{at}gmail.com
To the Editor:
A 66-yr-old woman was admitted to the intensive care unit after the intentional ingestion of 100 mg tranylcypromine, 20 mg trifluperazin, 10 mg lorazepam, and 60 mg fluoxetine. Her physical examination revealed a comatose nonfebrile patient. Her Glasgow Coma Scale score was 7/15. She had slight generalized rigidity, marked trismus, and conjugated rhythmic ocular movements from side to side without interruption, pause or nystagmus, and an approximate frequency of 20 cycles per minute. Her arterial blood pressure was 230/150 mm Hg, heart rate 130 bpm, respiratory rate 21 bpm, and oxygen saturation was 96%. Mechanical ventilation was initiated after administration of 15 mg midazolam and 4 mg pancuronium bromide. Two hours later, the patient developed agitation, diaphoresis, and oxygen desaturation. A remifentanil infusion was initiated at a rate of 5.7 µg · kg–1 · h–1.
During the following hour, the patient had poorly reactive pupils and the conjugated ocular movements remained unchanged. She did not respond to painful stimuli and had facial myoclonus and generalized hypertonia. Flexion of the extremities was impossible. She had hyperreflexia. Babinski's sign was absent. Because of her worsening clinical condition, the remifentanil infusion was stopped. This was rapidly followed by decreased rigidity, progressive improvement in her level of consciousness, and disappearance of her abnormal ocular movements. An hour later, mechanical ventilation was discontinued. The patient was discharged from the intensive care unit after 48 h and fully recovered.
Typically, the serotonin syndrome is characterized by autonomic instability (hypertension/hypotension, sweating, mydriasis, fever, and diarrhea) mental changes (confusion, agitation, lethargy) and neuromuscular alterations such as hyperreflexia, myoclonus, rigidity, and, rarely, trismus (1). Our patient was exposed to drugs that produce an excess of intrasynaptic serotonin such as monoamine oxidase inhibitors (tranylcypromine) and selective serotonin reuptake inhibitors (fluoxetine). The patient had also taken a neuroleptic drug (trifluoperazine) that could induce neuroleptic malignant syndrome (2). Fink (3) postulated that both syndromes are examples of a generalized neurotoxic syndrome based on the overlapping features. Nevertheless, there are some typical manifestations of serotonergic syndrome, such as mydriasis, hyperreflexia, tremors, myoclonus, and diarrhea, that may help to distinguish them.
Our patient also exhibited a rare neuro-ophthalmologic disturbance named by Selenick (4) as the "ping-pong gaze." Although it was initially described by Fisher (5) in a patient with bilateral brain infarctions, there are four reported cases associated with monoamine oxidase inhibitor intoxication. In this context, the ping-pong gaze should be considered as a functional alteration not always related to severe neurological damage or a poor prognosis.
The ability of opioids to induce rigidity at large doses or in smaller doses in patients receiving fluoxetine or venlafaxine is well known (6,7). The development of serotonergic syndrome resulting from exposure to opioids in a patient taking monoamine oxidase inhibitors in a therapeutic dose has also been reported (8). We think that the remifentanil administrated to our patient probably caused a worsening of the muscular rigidity, based on the impressive improvement in her clinical status associated with the drug withdrawal. We considered this evidence for a potential drug interaction and propose cautious use of opioids in the setting of serotonergic hyperactivity.
References
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