Management Of Serotonin Syndrome Research Articles

Management of serotonin syndrome (toxicity)

Serotonin syndrome (toxicity), resulting from an excessive accumulation of serotonin in the central nervous system, it can occur due to various factors such as the initiation of medication, overdose or drug interactions. Diagnosing serotonin toxicity presents challenges as there are no definitive criteria. This review delves into the pathophysiology, incidence, clinical assessment and management of serotonin toxicity, stressing the significance of promptly recognizing and managing severe cases. Diagnosis relies primarily relies on clinical assessment due to the absence of specific laboratory tests. The Hunter Serotonin Toxicity criteria are commonly utilized but have only been validated in the overdose setting. Assessing the severity of toxicity is crucial for guiding management decisions. Supportive care, discontinuation of causative agents and symptomatic treatment are prioritized in management. Mild toxicity often requires withdrawal or reduction of the serotonergic agent, while more severe toxicity requires more aggressive resuscitative and supportive care. Severe serotonin toxicity characterized by hyperthermia and rigidity requires aggressive supportive measures, including benzodiazepines, intubation, paralysis and active cooling. Animal studies suggest potential benefits of 5-HT2A receptor antagonists in preventing hyperthermia and fatalities, but only at high doses. Their clinical effectiveness remains uncertain, and evidence is predominately from case series and case reports. Although commonly used, serotonin antagonists like cyproheptadine lack conclusive evidence of efficacy. Other serotonin antagonists such as chlorpromazine and olanzapine have been explored but evidence is limited to case reports. Hence, the cornerstone of treating severe cases does not lie in 'antidote' administration or even diagnosis but in effective early resuscitative and supportive care.

Serotonin syndrome-A focused review.

Serotonin syndrome is a potentially life-threatening syndrome with manifestations spanning from mild adverse effects to life-threatening toxicity. The syndrome is caused by overstimulation of serotonin receptors by serotonergic drugs. Since the use of serotonergic drugs is increasing, primarily due to the widespread use of selective serotonin reuptake inhibitors, cases of serotonin syndrome have likely seen a parallel increase. The true incidence of serotonin syndrome remains unknown due to its diffuse clinical presentation. This review aims to provide a clinically focused overview of serotonin syndrome, covering its pathophysiology, epidemiology, clinical manifestations, diagnostic criteria, differential diagnosis and treatment, as well as classifying serotonergic drugs and their mechanism of action. The pharmacological context is emphasized, as it is crucial for the detection and management of serotonin syndrome. Focused review based on a literature search using the PubMed database. Serotonin syndrome can occur through therapeutic use or overdose of a single serotonergic drug or as a drug interaction between two or more serotonergic drugs. Central clinical features consist of neuromuscular excitation, autonomic dysfunction and altered mental status, occurring in a patient undergoing new or altered serotonergic therapy. Early clinical recognition and treatment are crucial to prevent significant morbidity.

Assessment and management of serotonin syndrome in a simulated patient study of Australian community pharmacies.

Background:The incidence of serotonin syndrome is increasing due to the widening use of serotonergic drugs. Identification of serotonin syndrome is challenging as the manifestations are diverse. Misdiagnosis can lead to delay in care and inappropriate treatment.Objectives:The objectives of this study were to determine if staff of community pharmacies in Australia could identify the symptoms of serotonin syndrome in simulated patients and recommend an appropriate course of action.Methods:Agents acting on behalf of a simulated patient were trained on a patient scenario that reflected possible serotonin syndrome due to an interaction between duloxetine and recently prescribed tramadol. They entered 148 community pharmacies in Australia to ask for advice about a 60 year old male simulated patient who was ‘not feeling well’. The interaction was audio recorded and analysed for degree of access to the pharmacist, information gathered by pharmacy staff, management advice given and pharmacotherapy recommended.Results:The simulated patient’s agent was consulted by a pharmacist in 94.0% (139/148) of cases. The potential for serotonin syndrome was identified by 35.1% (52/148) of pharmacies. Other suggested causes of the simulated patient’s symptoms were viral (16.9%; 25/148) and cardiac (15.5%; 23/148). A total of 33.8% (50/148) of pharmacies recommended that the simulated patient should cease taking tramadol. This advice always came from the pharmacist. Immediate cessation of tramadol was advised by 94.2% (49/52) of pharmacists correctly identifying serotonin syndrome. The simulated patient was advised to seek urgent medical care in 14.2% (21/148) of cases and follow up with a doctor when possible in 68.2% (101/148) of cases. The majority of pharmacies (87.8%; 130/148) did not recommend non-prescription medicines.Conclusion:While not identifying the cause of the simulated patient’s symptoms in the majority of cases, community pharmacies recommended appropriate action to minimise the health impact of serotonin syndrome by advising to cease tramadol and/or referring to a doctor and not recommending non-prescription medicines to treat symptoms. Raising pharmacists’ awareness of the signs and symptoms of serotonin syndrome, and the importance of taking a comprehensive medication history when assessing a set of symptoms, may help community pharmacies further reduce serotonin syndrome toxicity.

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Introduction: Case Presentation: A 69 year-old woman with a history of depression on paclitaxel and chondrosarcoma underwent left proximal femur resection and replacement in our hospital. Post-operatively, she was noted to have some "shivering" movements and was given fentanyl for pain as well as a dose of meperidine and was admitted to the ward for care. At 4am the following morning, the patient was found to be poorly responsive with a MAP (mean arterial pressure) around 40 mmHg. She then became hypertensive with SBPs in the 200s and MAPs > 100, for which she received 10mg of IV metoprolol and a nicardipine drip was initiated as the patient was transferred to the ICU, where her blood pressure again dropped to MAPs in the 40s and her heart rate slowed to the 50s; nicardipine was stopped, and epinephrine and levophed drips were initiated. Her temperature increased to 38.4°C. The patient had a waxing and waning mental status and bizarre, pressured speech. She also had bilateral myoclonic motions as well as clonus in her lower extremities. The patient was diagnosed with serotonin syndrome by fulfilling Hunter Toxicity Criteria. She received care with withdrawal of paclitaxel, benzodiazepines, and a dose of cyproheptadine with normalization of her blood pressure, mental status, and neurological exam within 24 hours. She has not been restarted on an SSRI (selective serotonin reuptake inhibitor). Discussion: This case provides an opportunity to review the pharmacology, differential diagnosis, clinical spectrum, and management of serotonin syndrome. Our patient met Hunter Toxicity Criteria for the serotonin syndrome by her use of an SSRI as well as one of the following: 1) Spontaneous clonus 2) Inducible clonus plus agitation or diaphoresis, 3) Ocular clonus plus agitation or diaphoresis, 4) tremor plus hyperreflexia, or 5) hypertonism plus temperature > 38 °C (100 °F) plus ocular clonus or inducible clonus. She met multiple criteria. In 2004, there were 48,204 SSRI exposures resulting in an adverse outcome, including over 100 deaths. Several experts argue that "serotonin toxicity" is a more appropriate term than serotonin syndrome, since the clinical spectrum is a predictable consequence of high levels of serotonin rather than an idiosyncratic reaction, such as neuroleptic malignant syndrome. The clinical presentation can run the spectrum from mild tremor to severe autonomic instability, fever and altered mental status. Many medications result in increases in serotonin by a variety of pathways or direct agonism of the serotonin receptor. Common classes that include multiple offending agents include: antidepressants, opiates, anti-emetics, atypical antipsychotics and illicit drugs such as MDMA (Ecstasy). Both fentanyl and meperidine have serotonergic properties, and this patient classically showed symptoms within 24 hours of the additional serotonergic agents. She received supportive care with removal of the agent, which is essential, as well as with short-acting vasoactive medications and benzodiazepines. Antipyretics such as acetaminophen are not advised for serotonin-syndrome related pyrexia. She also received a dose of cyproheptadine, a histamine-1 receptor antagonist with nonspecific 5-HT1A and 5-HT2A antagonism, which can be used in patients who are still having agitation or unstable vital signs despite supportive care. Conclusion: Serotonin syndrome has significant prevalence in the increasing population of patients on chronic SSRI therapy, and its presence is frequently under recognized by physicians as it has a varied clinical presentation. There are many medications that have serotonergic properties and can precipitate serotonin toxicity. It is essential for clinicians to maintain a high suspicion for this disorder to avoid the potentially severe and lethal complication of missing it. It may also be more appropriate to refer to this disease as serotonin toxicity, as it is a predictable consequence of excess serotonin.

Functional Auditory Hallucinations in a Case of Serotonin Syndrome

Functional Auditory Hallucinations in a Case of Serotonin Syndrome

Concurrent Administration of Methylene Blue and a Selective Serotonin Reuptake Inhibitor: A Recipe for Serotonin Syndrome

This case report describes the precipitation of serotonin syndrome in a patient taking a selective serotonin reuptake inhibitor, by infusion of methylene blue dye during a parathyroidectomy procedure. Methylene blue acts as a monamine oxidase inhibitor, thus increasing levels of serotonin in the brain. The authors describe the diagnosis and management of serotonin syndrome and suggest that more caution be exercised in the use of methylene blue.

Serotonin Syndrome: An unusual cause of acute confusion and fever in the elderly

Delirium is a common cause for hospital admission among elderly patients. Although infection is the most common explanation, there is a large number of other potential causes. We present a case of acute delirium due to serotonin syndrome, precipitated by concomitant prescription of clarithromycin and fluoxetine. The symptoms improved following treatment with a benzodiazepine and discontinuation of the fluoxetine. The diagnosis and management of serotonin syndrome is discussed.