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Case Report Current Practice • Pratique Courante Recognition and Treatment of Serotonin Syndrome

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Case Report Current Practice • Pratique Courante Recognition and Treatment of Serotonin Syndrome Case Report Current Practice • Pratique courante Recognition and treatment of serotonin syndrome Christopher Frank MD FCFP erotonin syndrome is an increasingly common he planned to follow up with his family doctor sev- Sadverse drug reaction, which can be life-threatening.1 eral weeks after hospitalization in order to have his Despite the common use of medications with direct or mood reviewed. indirect serotonergic effects, many physicians are not aware of the presentation and management of serotonin Discussion excess.2 This is particularly true of less severe presen- Cochrane Database of Systematic Reviews, MEDLINE, tations of serotonin syndrome, which still contribute to and Google were searched from January 1990 to patient morbidity.3 December 2006 for articles on serotonin syndrome or Family physicians need to be more aware of sero- serotonin toxicity. Although there are research papers tonin syndrome. This case report explains the syndrome’s related to diagnosis, there are few high-quality data pathogenesis, diagnosis, and management. Physicians on prospective treatment. No guidelines or consensus are encouraged to consider the possibility of serotonin statements have been published for either diagnosis syndrome in patients who use serotonergic medications or management. Recommendations were drawn from and present with autonomic changes, mental status the literature, but there is minimal high-level evi- changes, and neurological hyperexcitability. dence, especially in the realm of treatment. Most of the suggestions in this paper have level II evidence. Case description Serotonin (5-HT) was first identified in the 1940s Mr J.W., an 80-year-old man with a history of and was initially thought to have its primary effect on depression, was admitted to hospital with pneumo- vascular tone. Now serotonin is recognized as hav- nia. His condition deteriorated and he was sent to ing an important role in several central nervous sys- the intensive care unit (ICU) and placed on mechan- tem processes and peripheral physiology, particularly ical ventilation for several days. During his stay in in the gastrointestinal tract. The vast majority of sero- the ICU, his medications were reviewed. His use tonin (90%) is synthesized in the periphery, but brain of fluoxetine, which he’d taken for depression for serotonin levels are the main factor in development of almost 10 years, was discontinued. Following dis- serotonin toxicity.4 charge from the ICU, his mood was noted to be low The main sites of serotonin production in the brain by the medical staff. Approximately 1 week after are the midline raphe nuclei, found in the brainstem from discontinuation of the fluoxetine, he started using the midbrain to the medulla. In presynaptic neurons, the 20 mg of paroxetine daily. amino acid tryptophan is decarboxylated and hydroxyl- Within 24 hours of starting paroxetine, Mr J.W. ated to produce serotonin. Serotonin is released into the was found to be confused and agitated with periods intrasynaptic space after axonal stimulation, and receptors of unresponsiveness. Vital signs revealed a tempera- on the presynaptic neuron play a role in regulating release. ture of 38.5°C and a pulse of 115 beats per minute. A Following reuptake into the presynaptic neuron, intrasyn- neurological examination revealed myoclonus in all aptic serotonin is metabolized by the enzyme monoamine limbs with any stimulation. Assessment by a family oxidase.4 Knowledge of the regulation and metabolism of physician with training in care of the elderly identi- serotonin is relevant to understanding the role of different fied serotonin syndrome as the probable cause of his medications in the development of toxicity. presentation. There are 7 serotonin receptor families (5-HT1 to The paroxetine was discontinued and the patient 5-HT7), which are further subdivided into groups based on was given intravenous fluids to decrease the risk of renal failure. Mr J.W. initially received 2 mg of loraz- Levels of evidence epam intravenously, then received 3, 1-mg doses of lorazepam every 4 hours, resulting in decreased Level I: At least one properly conducted randomized tachycardia, hypertonicity, and clonus. He was dis- controlled trial, systematic review, or meta-analysis charged from hospital without antidepressants, and Level II: Other comparison trials, non-randomized, cohort, case-control, or epidemiologic studies, and This article has been peer reviewed. preferably more than one study Cet article a fait l’objet d’une revision par des pairs. Level III: Expert opinion or consensus statements Can Fam Physician 2008;54:988-92 988 Canadian Family Physician • Le Médecin de famille canadien VOL 54: JULY • JUILLET 2008 Case Report different activities in neural and peripheral organ systems. tends to be more acute than in a condition such as neu- A summary of the effects of serotonin receptor subtypes roleptic malignant syndrome, which shares some other in relation to serotonin toxicity is found in Table 1.4 features with serotonin toxicity. Serotonin syndrome usually manifests with autonomic Clinical presentation changes, mental status changes, and neurological find- The original and revised criteria5,6 for diagnosis of sero- ings. Mild, moderate, and severe signs and symptoms of tonin syndrome emphasize the mental status changes serotonin syndrome are summarized in Table 2.4 There and clinical findings typically observed in more severe are no data on the percentage of cases in the mild, mod- cases. As a result, these criteria have been criticized erate, or severe categories, in part because of the low for not highlighting the wider spectrum of toxic side rates of diagnosis of mild cases. effects that can be seen with this disorder. For this rea- son, some authors prefer to use the term serotonin toxic- Medication factor ity to include findings of earlier or milder cases.7 Various medications are associated with serotonin syn- It is important to note that symptoms of serotonin drome.9-15 Medications that affect any of the steps in syndrome usually present within 6 to 8 hours of initiat- serotonin metabolism or regulation can provoke toxicity. ing or increasing serotonergic medications.7,8 The onset Antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs), are among the most commonly impli- Table 1. Effects of 5-HT receptor subtypes in relation to cated drugs. Drug interactions can cause severe toxicity serotonin toxicity and can involve common over-the-counter medications. Drugs with long half-lives can interact several weeks after 5-HT RECEPTOR MAIN ACTION RELATED TO SEROTONIN TOXICITY discontinuation; fluoxetine interactions have been reported 16 5-HT1A Neuronal inhibition, regulation of sleep, up to 5 weeks after discontinuation. Even single doses of feeding, thermoregulation, hyperactivity SSRIs have been implicated in serotonin syndrome. It is associated with anxiety, hypoactivity relevant to note that serotonin syndrome is not considered associated with depression to be an idiosyncratic drug reaction but is a predictable 11 9,11-15 5-HT1D Locomotion, muscle tone response to elevated levels of serotonin. Table 3 5-HT2A Neuronal excitation, learning, peripheral provides a list of important drugs and drug interactions vasoconstriction, platelet aggregation and the mechanism of increasing serotonin levels. Overdosing with single agents such as SSRIs does not 5-HT2B Stomach contraction often cause severe toxicity. Approximately 15% of SSRI 5-HT3 Nausea and vomiting, anxiety overdoses result in moderate symptoms. Severe cases 5-HT Gastrointestinal motility 4 appear to be more likely after drug interactions, particu- 5-HT—serotonin. larly monoamine oxidase inhibitors (MAOIs) interacting Data from Boyer and Shannon.4 with other antidepressants or with serotonin releasers, Table 2. Signs and symptoms of serotonin syndrome SERIOUSNESS AUTONOMIC SIGNS NEUROLOGICAL SIGNS MENTAL STATUS Other Mild • Afebrile or low-grade • Intermittent tremor • Restlessness fever • Akathisia • Anxiety • Tachycardia • Myoclonus • Mydriasis • Mild hyperreflexia • Diaphoresis or shivering Moderate • Increased tachycardia • Hyperreflexia • Easily startled • Rhabdomyolysis • Fever (up to 41°C) • Inducible clonus • Increased confusion • Metabolic acidosis • Diarrhea with hyperactive • Ocular clonus (slow • Agitation and • Renal failure bowel sounds continuous lateral hypervigilance • Disseminated • Diaphoresis with normal eye movements) intravascular skin colour • Myoclonus coagulopathy (secondary to hyperthermia) Severe • Temperature often more • Increased muscle tone • Delirium • As above than 41°C (Secondary to (lower limb > upper) • Coma increased tone) • Spontaneous clonus • Substantial myoclonus or hyperreflexia Data from Boyer and Shannon.4 VOL 54: JULY • JUILLET 2008 Canadian Family Physician • Le Médecin de famille canadien 989 Case Report such as amphetamines.11 Patient factors associated with cases. To help delineate the spectrum of illness, developing toxicity are not clearly identified in the litera- researchers in Australia reviewed more than 2000 ture but might relate to factors affecting the pharmacoki- cases of self-poisoning with serotonergic drugs and netics of offending agents (eg, renal and hepatic failure). related the clinical findings to a diagnosis of serotonin Patients who are genetically deficient in the cytochrome syndrome made by a clinical toxicologist. From this P450 2D6 enzyme (8% of whites) are more susceptible information, a clinical decision tree was developed. if
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