Case ReportsSerotonin syndrome: a complex but easily avoidable condition
Section snippets
Case report
Ms. A, a 53-year-old Caucasian female with psychiatric history of depression, anxiety and intravenous opiate dependence, presented to the University of Massachusetts Medical Center emergency department with mental status changes. Her medications prior to admission included fluoxetine 40 mg daily, olanzapine 5 mg daily and methadone 50 mg daily. Bupropion 150 mg daily had recently been added due to persistent depressive symptomatology, but Ms. A stopped taking it 4 days prior to presenting to
Discussion
Serotonergic neurons are located in the midline raphe nuclei and play an integral part in the regulation of wakefulness, affective behavior, food behavior, thermoregulation and motor tone. In the periphery, serotonin assists in the regulation of vascular tone and gastrointestinal motility [1], [2]. Serotonin syndrome is not an idiopathic drug reaction but a predictable consequence of excess serotonergic agonism. Overstimulation of serotonin receptors results in a spectrum of clinical
Conclusion
The case described illustrates the complexities of serotonin syndrome and how it can be avoided through continued education of physicians, modifications of prescribing practices and pharmacological research. We believe that this case of serotonin syndrome was precipitated by the combination of venlafaxine, methadone and fluoxetine metabolite, as well as individual vulnerability. With more careful attention to Ms. A's psychopharmacological regime, Ms. A might have benefited from a simpler, less
References (17)
- et al.
Role of selective serotonin reuptake inhibitors in psychiatric disorders: a comprehensive review
Prog Neuropsychopharmacol Biol Psychiatry
(2003) Mechanism of action of serotonin selective reuptake inhibitors: serotonin receptors and pathways mediate therapeutic effects and side effects
J Affect Disord
(1998)- et al.
Receptor mediation of exaggerated responses to serotonin-enhancing drugs in serotonin transporter (SERT)-deficient mice
Neuropharmacology
(2007) - et al.
Venlafaxine: a 2003 update
Clin Ther
(2003) Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity
Br J Anaesth
(2005)- et al.
Serotonin syndrome associated with linezolid treatment after discontinuation of fluoxetine
Psychosomatics
(2005) - et al.
The serotonin syndrome
N Engl J Med
(2005) - et al.
Serotonin syndrome: a brief review
Can Med Assoc J
(2003)
Cited by (67)
Serotonergic syndrome due to coadministration of linezolid and fentanyl: a case report
2023, Acta Colombiana de Cuidado IntensivoHigh risk and low prevalence diseases: Serotonin syndrome
2022, American Journal of Emergency MedicineCitation Excerpt :Cyproheptadine is a reasonable choice for mild cases but has limited utility in moderate to severe cases. Anti-serotonergic medications such as olanzapine and risperidone have been utilized to treat serotonin syndrome, but conflicting reports suggest they may cause serotonin syndrome and are not recommended [33,78]. Chlorpromazine may be used to treat serotonin syndrome due to serotonin antagonist properties, but it may cause hypotension and thus is not a preferred agent [20,30].
Perioperative Pain Management in Hip and Knee Arthroplasty
2017, Orthopedic Clinics of North AmericaAcute effects of amitriptyline on adult zebrafish: Potential relevance to antidepressant drug screening and modeling human toxidromes
2017, Neurotoxicology and TeratologyCitation Excerpt :The rodent SS-like state has also been reported in the literature, presenting as Straub tail, tremor, tics, backward gait, flat/low posture, hypoactivity, fever, forepaw treading, head weaving and hind limb abduction (Haberzettl et al., 2013; Kalueff et al., 2007; Kalueff et al., 2006). Rodent SS-like behavior can be induced experimentally by serotonin-enhancing drugs, including TCAs (Dvir and Smallwood, 2008), further supporting the need to examine the SS-related effects of amitriptyline in various animal experimental models in-vivo. From a conceptual point of view, it is important to consider SS modeling in a broader, ‘cross-species’ context beyond only mimicking human/clinical phenotypes.