Serotonin syndrome is a rare but potentially fatal condition characterized by altered mental status, autonomic hyperactivity, and neuromuscular abnormalities. Although fentanyl is known to be a causative agent of serotonin syndrome, most reports have shown that fentanyl-related serotonin syndrome is caused by multiple drug interactions, and only one case of serotonin syndrome caused by fentanyl alone has been reported in a pediatric patient. In this report, we describe a case of postoperative serotonin syndrome caused by fentanyl alone in an adult patient after cardiac surgery. A 66-year-old male was diagnosed with unstable angina pectoris and underwent off-pump coronary artery bypass grafting. Two hours after the intensive care unit (ICU) admission, he exhibited symptoms of sweating, tremors, and muscle rigidity. Four hours later, the body temperature rose to 40.0 °C, suggesting malignant hyperthermia or a similar condition. Dantrolene was administered to the patient, and all symptoms improved within several minutes. However, the patient experienced a relapse of symptoms every four to six hours, requiring additional dantrolene treatment each time. Although no other serotonergic agents were used, we suspected serotonin syndrome induced by fentanyl alone and discontinued its use on postoperative day three. Following the discontinuation of fentanyl, no further episodes were observed. The patient was discharged from the hospital without any complications on postoperative day 29. During a subsequent check-up, the patient was found to have a sternal dehiscence and underwent one-stage sternal reconstruction. General anesthesia was induced and maintained without the use of fentanyl. The patient was discharged 10 days after surgery without symptoms of serotonin syndrome. In a patient with postoperative hyperthermia and neuromuscular abnormalities, serotonin syndrome should be considered when fentanyl is administered. Dantrolene may be beneficial in managing serotonin syndrome caused by fentanyl alone and/or benzodiazepine resistance.

UNASSIGNED: Serotonin syndrome is characterized by mental status changes, autonomic hyperactivity, and neuromuscular abnormalities. This syndrome results from various medications that engender serotonergic overactivity. Atomoxetine is a norepinephrine reuptake inhibitor used for the treatment of attention-deficit hyperactivity disorder (ADHD). Two case reports have described serotonin syndrome induced by the combination of atomoxetine with venlafaxine or methylphenidate, but no report describes this syndrome induced by atomoxetine alone. This report describes serotonin syndrome induced solely by an overdose of atomoxetine in a patient with ADHD.
UNASSIGNED: The patient in this case was a 21-year-old man who had been treated with atomoxetine for ADHD. He was transported to our hospital 1 h after intentional ingestion of 1200 mg of atomoxetine in a suicide attempt. On admission, he showed profuse diaphoresis, marked agitation, somnolence, slight fever, tachycardia, prolonged QT interval, myoclonus, tremor, and hyperreflexia. He was diagnosed as having serotonin syndrome and was treated with administration of activated charcoal and massive infusion. Three days later, his serotonin syndrome symptoms had disappeared completely.
UNASSIGNED: Findings in this case suggest that atomoxetine alone can cause serotonin syndrome presumably via its effects of serotonin reuptake inhibition. Clinicians should consider this syndrome induced by atomoxetine overdose.

Serotonin syndrome (SS) is a life-threatening condition caused by serotonergic medications. We describe a unique case of SS likely caused by prolonged exposure to propofol and remifentanil alone. A young male presented for vestibular schwannoma resection. Several hours into the case, the patient demonstrated hyperthermia and hemodynamic instability, followed by clonus, rigidity, shivering, and tachycardia after emergence. SS was diagnosed using Hunter\'s criteria and improved with supportive measures. While the patient endorsed a history of methamphetamine use, his urine drug screen was negative. The possibility of SS should be considered when administering propofol and remifentanil, particularly with prolonged infusions.

Serotonin (5-HT) syndrome (SS) consists of changes in mental status as well as autonomic and neuromuscular changes. Though not well understood, serotonergic pathways have been implicated in the mechanism of action of electroconvulsive therapy (ECT). Ketamine has been used as an induction agent in ECT and as therapy for treatment-resistant depression. Utilizing a case report and literature review, we explored the underlying serotonergic mechanisms of ECT and ketamine by which a syndrome of serotonin toxicity may be precipitated. We describe the case of a 72-year-old woman who developed recurrent SS on 2 occasions in similar circumstances involving the administration of ketamine for ECT. In our literature review, we found 5 cases in which SS was associated with ECT and 1 case linking ketamine to SS. There is emerging evidence that the mechanism of ECT involves 5-HT1A and 5-HT2A receptors, the same receptors that are involved in SS. ECT can transiently increase the permeability of the blood-brain barrier, leading to increased levels of antidepressants in the brain. ECT can, therefore, enhance 5-HT transmission and the likelihood of SS in the presence of serotonergic agents. The effect of ketamine on 5-HT transmission is mediated by the glutamate α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor. Ketamine increases α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid activity in the medial prefrontal cortex, which leads to downstream 5-HT release through glutamate. Through this mechanism, ketamine can increase 5-HT transmission, leading to SS. To our knowledge, this is the only case report of recurrent SS with concurrent use of ECT and ketamine. As ketamine is frequently used in ECT and many patients undergoing ECT are on serotonergic medications, it is important to recognize ketamine as a potential risk factor for SS. There is no evidence for added efficacy when combining ECT and ketamine. Thus, one should proceed with caution when combining these treatments. The burgeoning use of ketamine in ambulatory settings makes it necessary to elucidate the risks, which we discuss further. More research is needed into the mechanisms of ketamine and ECT, specifically how the combination of these treatments influence 5-HT levels.

Linezolid is a potent oxazolidinone for the treatment of various gram-positive bacterial infections. However, the drug can cause potential adverse reactions such as thrombocytopenia, hyperlactacidemia and serotonin syndrome, which warrant consideration by the medical team when planning treatment. The existing literature has reported some adverse reactions caused by linezolid, but most of these are based on clinical characteristics and simple treatment measures. Two cases of linezolid overdose resulting in thrombocytopenia, hyperlactacidemia and serotonin syndrome are presented, which were successfully managed with therapeutic drug monitoring. A dose adjustment strategy was adopted to safely and effectively mitigate linezolid-related adverse events.

BACKGROUND: Serotonin syndrome is a potentially life-threatening condition resulting from the use of antidepressants, their interactions with other serotonergic medications, or poisoning. It presents with a triad of psychiatric, dysautonomic, and neurological symptoms and is sometimes fatal. While cyproheptadine is a specific treatment option, the optimal duration of its administration remains unclear. The purpose of this report is to quantitatively assess the endpoints of serotonin syndrome treatment. Based on the hypothesis that neurological pupil index (NPi) on a digital pupil recorder would correlate with the severity of the serotonin syndrome, we administered cyproheptadine using NPi as an indicator.
METHODS: A patient with a history of depression was brought to our hospital after he overdosed on 251 tablets of serotonin and noradrenaline reuptake inhibitors.
METHODS: On day 3, the patient was diagnosed with serotonin syndrome.
METHODS: Cyproheptadine syrup was administered at 4 mg every 4 hours. The NPi of the automated pupillometer was simultaneously measured. On day 5, the NPi exceeded 3.0 cyproheptadine was discontinued.
RESULTS: The patient was discharged on day 7.
CONCLUSIONS: The lack of considerable improvement during the treatment period suggests that the patient may have improved on his own. In this case, the relationship between NPi and the severity of serotonin syndrome could not be determined.

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BACKGROUND: Serotonin toxicity is a well-described phenomenon that is commonly attributed to a variety of drug-drug combinations. Some unregulated herbal supplements have been implicated in the onset of serotonin toxicity, however, there is currently minimal literature available on the potential for black cohosh to contribute to rhabdomyolysis and serotonin toxicity, in spite of its known serotonergic properties.
METHODS: A middle-aged woman presented to the emergency department with serotonin toxicity and rhabdomyolysis shortly after taking black cohosh supplements in the setting of long-term dual antidepressant use. The serotonin toxicity and rhabdomyolysis resolved with IV fluids, benzodiazepines, and discontinuation of the offending drugs. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Patients are sometimes not aware of how over-the-counter supplements might interact with their prescription medications. Female patients taking black cohosh to manage hot flashes and menopausal symptoms could be at risk for developing rhabdomyolysis and serotonin toxicity if they are also taking other serotonergic agents.

UNASSIGNED: Serotonin syndrome and neuroleptic malignant syndrome are caused by 2 distinct pathologies; however, the clinical presentation associated with both syndromes share many features.
UNASSIGNED: We describe a 56-year-old male patient who presented to our facility with seizures, leukocytosis, fevers, extremity hyperreflexia, and signs of autonomic dysfunction as evidenced by cardiovascular instability. The patient was noted to be taking vortioxetine, trazodone, lamotrigine, lurasidone, and carbidopa-levodopa as outpatient medications for his depression, an unspecified mood disorder, and Parkinson disease. Following a robust workup and failure of other therapies, all serotonergic and dopaminergic medications were held, and the patient was tried on cyproheptadine for serotonin syndrome, which led to the cessation of fevers. Bromocriptine was added to the regimen, which led to the resolution of the remainder of the patient\'s symptoms.
UNASSIGNED: The overlapping symptomatology of several key diagnostic criteria for both serotonin syndrome and neuroleptic malignant syndrome as well as their nature as diagnoses of exclusion require an evaluation of the patient\'s aggregate improvement following targeted pharmacologic strategies for both syndromes. The efficacy of both cyproheptadine and bromocriptine when administered concomitantly support the concurrent pathologies.
UNASSIGNED: Clinicians at the bedside must be cognizant of the potential for clinically relevant drug-drug interactions that may present with overlapping pathologies.

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