Drug interaction between a selective serotonin reuptake inhibitor and a triptan leading to serotonin toxicity: a case report and review of the literature

Background Serotonin toxicity is a known side effect of selective serotonin reuptake inhibitors and has previously also been described as a possible side effect of 5-hydroxytryptamine receptor agonist (triptan) medications. However, the literature is conflicted about the risk of developing serotonin toxicity as a result of drug interaction between selective serotonin reuptake inhibitors and triptans. Case presentation A 30-year-old Caucasian woman with a history of depression on regular fluvoxamine presented to the emergency department with right-sided facial and lower limb twitching. The patient had recently been prescribed sumatriptan for migraines and had taken her first ever dose shortly prior to the onset of symptoms. She was tachycardic, diaphoretic, and hypertonic on initial assessment with bilateral lower limb and ocular clonus. Electrocardiogram showed sinus tachycardia with QT interval under the treatment interval, and pathology and imaging findings were unremarkable. Her symptoms improved with supportive management and cyproheptadine. Conclusions This patient’s presentation fulfilled both Sternbach and Hunter criteria for serotonin toxicity, illustrating a potential case of serotonin toxicity as a result of drug interaction between a selective serotonin reuptake inhibitor and a triptan.

Serotonin Toxicity Versus Withdrawal: Clonidine One Size Fits All?

Serotonin discontinuation syndrome (SDS) can result in a constellation of symptoms exhibited by infants exposed to selective serotonin reuptake inhibitors or other psychotropic drugs during pregnancy. Currently, there is no consensus regarding the pharmacologic management of SDS. We report our experience with clonidine for the management of a term infant with poor neonatal adaption. The infant exhibited biphasic symptoms of acute toxicity at birth and a plateauing of symptoms, followed by subsequent withdrawal symptomatology requiring the use of clonidine in doses up to 4 mcg/kg/dose every 3 hours for control of symptoms. The 38-week gestation Caucasian male infant was born to a mother with major depressive disorder, which was managed with sertraline, trazodone, venlafaxine, and buspirone throughout her pregnancy. The infant exhibited severe hypertonia at delivery and continued to have hypertonia, tremors, hypoglycemia, and feeding issues upon admission to the NICU. The initial Modified Finnegan Neonatal Abstinence scores were extremely elevated, and clonidine was started at 1 mcg/kg/dose every 3 hours and then the dose was titrated up to 4 mcg/kg/dose. This is the first report documenting the use of clonidine to manage serotonin toxicity at birth followed by subsequent neonatal withdrawal associated with maternal antidepressant drug use during pregnancy.

An audit on prescribing practice and risk of serotonin syndrome among patients with chronic pain

AimsTo determine the incidence of prescribing practice with associated risk of serotonin toxicity among patients with chronic pain conditions.BackgroundSerotonin syndrome is a potentially life-threatening condition caused by excessive serotonergic activity, usually from drug interactions. Concurrent use of antidepressants is strongly linked to serotonin syndrome, with recent data revealing record numbers of NHS prescribed antidepressants in 2019. Antidepressant medications are also used in chronic pain management for their anti-neuropathic pain properties. However, it is well-recognised that a significant number of chronic pain patients suffer from anxiety and depression. This cohort of patients is therefore vulnerable to being exposed to multiple concurrent antidepressant agents, and thus at relatively higher risk of serotonin syndrome compared to other patient groups. Additionally, these patients are likely to be exposed to the concurrent use of antidepressants and certain analgesic agents particularly phenylpiperidine derivatives which increases serotonin toxicity risk.MethodMedications of patients presenting to a secondary care pain clinic within the last year were looked into. Patients were selected at random by pain management secretaries. Concurrent use of multiple antidepressant agents including Selective Serotonin Reuptake Inhibitors (SSRIs), Serotonin Noradrenaline Reuptake Inhibitors (SNRIs), Tricyclic Antidepressants (TCAs) or Tetracyclic Antidepressant (TeCA) was noted. Additionally, concurrent use of any of these antidepressant agents and phenylpiperidine derivatives such as Fentanyl and Tramadol was noted.ResultData on medications of 97 patients were collected. A total of 28 patients (28.8%) were observed to have at-risk medication combinations. Out of these, five patients were on both SSRI and TCA. Two patients were on both TCA and TeCA. Four other patients were on either a combination of SSRI and SNRI, SNRI and TCA, SSRI and TeCA, or TCA and TCA. Three patients were on both Fentanyl patches and an antidepressant. Fourteen patients were on both an antidepressant and Tramadol. None of these patients were diagnosed with serotonin syndrome; however, it is unclear as to whether these patients experienced milder symptoms of the syndrome.ConclusionA considerable number of patients in this group were on medication combinations putting them at risk of serotonin syndrome. Despite no documented patient harm, there is an urgent need for an increased awareness among prescribers on drug interactions which may lead to this syndrome and a subsequent change in prescribing practice.

Transient musical hallucinations in a young adult male associated with alcohol withdrawal

AimsWe present the case of a 25-year-old male who presented to A&E with isolated musical hallucinations, in the absence of audiological or neurological disease.BackgroundMusical hallucinations (MH) are a form of complex auditory hallucinations whereby an individual experiences an instrumental and/or vocal melody in the absence of auditory stimuli.ResultThe patient had a history of recreational drug use and a family history of psychosis. Hallucinations, which were preceded by discontinuation of alcohol and re-initiation of citalopram for depression, resolved spontaneously after three days.ConclusionAetiological factors are discussed alongside the existing literature. Whilst the underlying mechanisms underpinning musical hallucinations remains elusive, the case illustrates the potential role of alcohol withdrawal, serotonin toxicity, recreational drug use and genetic vulnerability.