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• To enhance your knowledge of serotonin syndrome and its potentially life-threatening symptoms
• To understand the medicine-types that can induce serotonin syndrome
• To familiarise yourself with interventions that can be administered in the emergency department
Serotonin syndrome is a rare but potentially life-threatening condition caused by excess serotonin in the central and peripheral nervous systems. Patients with serotonin syndrome present with a range of mild to severe autonomic, neuromuscular and mental state signs and symptoms. A variety of drugs affect the serotonin pathways by modifying serotonin release and reuptake mechanisms, or reducing metabolism. There are also several genetic polymorphisms and clinical risk factors that affect the development and course of serotonin syndrome. This article describes the pathophysiology of serotonin syndrome and discusses diagnosis and treatment with reference to a case study of a patient who attended an emergency department (ED) with signs and symptoms of the condition following an increase in antidepressant medicines. The article aims to increase clinicians’ awareness of serotonin syndrome to improve identification and treatment of patients who present to EDs with the condition.
Emergency Nurse. doi: 10.7748/en.2021.e2121
Peer reviewThis article has been subject to external double-blind peer review and checked for plagiarism using automated software
Correspondence Conflict of interestNone declared
Loader K (2021) Too much of a good thing? Diagnosis and management of patients with serotonin syndrome. Emergency Nurse. doi: 10.7748/en.2021.e2121
Published online: 14 December 2021
Serotonin syndrome is a potentially fatal iatrogenic condition caused by an excess of the neurotransmitter serotonin in the central and peripheral nervous systems triggered by serotonergic (denoting a nerve ending that releases and is stimulated by serotonin) medicines (Francesangeli et al 2019). The condition can be caused by ‘normal’ dosing in susceptible individuals (Scotton et al 2019), accidental or intentional overdose, or by interaction between prescription and recreational drugs (Simon and Keenaghan 2021). Serotonin syndrome is also termed serotonin toxicity, since patients can present with a range of dose-related signs and symptoms including altered mental state, autonomic dysfunction and neuromuscular abnormalities due to the toxic effects of excess serotonin (Talton 2020).
Serotonin syndrome is regarded as a rare complication, but the actual incidence is unknown (Francesangeli et al 2019), potentially due to clinicians’ lack of knowledge and recognition of the condition (Prakash et al 2020), poor diagnostic criteria (Francesangeli et al 2019), or because mild symptomology is attributed to other conditions (Hudd et al 2019, Isbister 2021). Some authors have suggested that lack of rigorous reporting in case studies has led to confusion about ‘genuine’ cases (Gilman 2006a). Talton (2020), however, argued that serotonin syndrome was becoming more prevalent due to increased prescribing and polypharmacy, resulting in a rise in the use of serotonergic medicines.
The literature includes an abundance of case studies and discussions about serotonin syndrome (Gilman 2006b, Prakash et al 2015), but a lack of information on the processes involved in its development and progression. This information is essential for emergency clinicians, because patients with signs and symptoms of serotonin syndrome are more likely to seek emergency care than to contact their usual care provider (Werneke et al 2016).
This article examines the pathophysiology of serotonin syndrome with the aim of enhancing emergency clinicians’ knowledge of the underlying mechanisms, risk factors, management and treatment in emergency settings. Since patients with mild serotonin syndrome can present with influenza-like signs and symptoms, they might, in the context of the coronavirus disease 2019 (COVID-19) pandemic, be advised erroneously to isolate.
• Awareness of the risks and signs and symptoms of serotonin syndrome can prevent patient deterioration and improve outcomes
• Mild signs and symptoms of serotonin syndrome are challenging to distinguish from influenza, so there is a risk that it may be mistaken for coronavirus disease 2019 (COVID-19) or other viruses
• The COVID-19 pandemic may increase the incidence of serotonin syndrome due to the mental health effects on the public and a rise in antidepressant use
• First-line treatment for serotonin syndrome is to stop any serotonergic medicines even if serotonin syndrome is only suspected. In mild cases, stopping or reducing serotonergic agents is all that is required
Serotonin is a neurotransmitter also known as 5-hydroxytryptamine (5-HT) and is synthesised from the essential amino acid tryptophan in the raphe nuclei situated in the midline brain stem (Francesangeli et al 2019). Serotonin synthesis is limited by the amount of tryptophan that can cross the blood-brain barrier because tryptophan competes with more abundant amino acids (Jenkins et al 2016). Outside of the brain, serotonin is synthesised in the gastrointestinal (GI) system and stored in platelets in the blood (Scotton et al 2019). In the central nervous system (CNS), serotonin is a neurotransmitter, but in the GI system it acts as a hormone (Yadav 2013), and is involved in a number of pathways, such as gut motility (Martin et al 2019), vasoconstriction and platelet aggregation (Scotton et al 2019).
The raphe nuclei have serotonergic projections which extend into almost every area of the brain (Figure 1). Once serotonin has been synthesised from tryptophan, it is moved along these pathways through transporters and stored in vesicles inside presynaptic neurons, where it awaits a signal to be released into the synaptic cleft between the presynaptic and postsynaptic neurons to exert its effects (Francesangeli et al 2019). Serotonin availability is moderated by the serotonin reuptake transporter (SERT) protein and broken down by the enzyme monoamine oxidase (MAO) (Francesangeli et al 2019).
The SERT protein binds to serotonin and returns it from the synaptic cleft to the presynaptic neuron, thereby terminating the action of the serotonin. The class of antidepressants known as selective serotonin reuptake inhibitors (SSRIs) work by binding to sites on the SERT protein and blocking the reuptake of serotonin into the presynaptic neuron after the serotonin has transmitted a signal between neurons; the consequence if this is that there is more serotonin available (Talton 2020). The enzyme MAO metabolises serotonin by converting it into waste products, which are excreted in the urine (Alusik et al 2014). Another type of antidepressant medicine known as monoamine oxidase inhibitors (MAOIs) binds to MAO enzymes, preventing them from breaking down serotonin. This effect increases serotonin availability and its effects (Francesangeli et al 2019). Serotonin syndrome caused by MAOIs results in the most severe signs and symptoms, and these medicines are implicated in more fatalities due to their effect on serotonin metabolism (Francesangeli et al 2019). Figure 2 shows the process of serotonin synapse activity.
The development of serotonin syndrome is complex and multifactorial. There are seven serotonin receptor groups in the CNS (5-HT1 to 5-HT7), and specific serotonin receptor subtypes are thought to produce different signs and symptoms associated with serotonin syndrome (Francesangeli et al 2019). For example, the 5-HT1A receptor is associated with changes in mental state and neuromuscular abnormalities such as hyperactivity and overactive reflexes, which are termed hyperreflexia; overstimulation of the 5-HT2A receptor causes hyperthermia and rigidity; and 5-HT3 receptors mediate GI effects, such as diarrhoea and abdominal pain (Hall and Chapman 2008a).
Serotonin has a higher affinity for the 5-HT1A receptor, which accounts for the increasing severity of signs and symptoms (Hall and Chapman 2008a). As the 5-HT1A receptors become saturated, increasing levels of serotonin lead to overstimulation of 5-HT2A receptors, which produce more severe and life-threatening signs and symptoms (Hall and Chapman 2008a).
Noradrenaline (norepinephrine) is a neurotransmitter known to cause hyperexcitability and high levels can cause agitation. Increased noradrenaline levels can be seen in serotonin syndrome and there are thought to be two mechanisms of action involved. First, high concentrations of 5-HT can increase noradrenaline release; and second, MAO enzymes also breakdown noradrenaline, therefore use of MAOI medicines associated with serotonin syndrome can also act to increase levels of noradrenaline alongside serotonin (Scotton et al 2019).
Various pharmacological interactions, disease pathways and personal risk factors influence development of serotonin syndrome.
The cytochrome (CYP) 450 family of enzymes metabolises many serotonergic medicines (Scotton et al 2019). However, some medicines inhibit groups of CYP enzymes, thereby increasing the risk of serotonin syndrome because the serotonin is not sufficiently cleared (Volpi-Abadie et al 2013). For example, SSRIs and antibiotics such as ciprofloxacin and fluconazole can inhibit CYP enzymes and increase the risk of serotonin syndrome when used in combination (Francesangeli et al 2019). Jurek et al (2019) recommended that clinicians should be aware of the pharmacological interactions of medicines to reduce the risk of adverse effects.
Serotonin syndrome can cause dehydration due to hyperthermia and diaphoresis (excessive sweating). In severe cases, kidney injury results from the breakdown of muscle tissues and the subsequent presence of myoglobin (an oxygen-storing protein found in muscle tissue) in the urine (Boyer et al 2021). Adequate kidney function and hydration are required to ensure the kidneys can excrete excess serotonin metabolites (Hall and Chapman 2008b). People with reduced kidney function can develop elevated serotonin levels and complicated presentations (Alusik et al 2014).
Older people are at a higher risk of developing serotonin syndrome due to their reduced hepatic and renal capacity, alongside a depletion of serotonin receptors as part of the ageing process, which means that less serotonin is required to overstimulate the receptors (Alusik et al 2014). However, Hall and Chapman (2008a) emphasised that reduced serotonin synthesis may balance this risk.
Isbister (2021) reported that there is little evidence that genetic variations affect serotonin syndrome. However, Volpi-Abadie et al (2013) argued that because serotonin syndrome can manifest in a variety of medicine combinations and doses, individual genetic factors have a significant role in this (Alusik et al 2014, Francesangeli et al 2019, Jurek et al 2019, Pandya et al 2020).
Alusik et al (2014) proposed four processes by which serotonin receptors can become overstimulated: serotonin agonists, increased serotonin release, reduced serotonin reuptake and reduced serotonin breakdown. A wide range of serotonergic medicines may trigger serotonin syndrome (Table 1), the most common of which are antidepressant agents, such as SSRIs, serotonin and norepinephrine reuptake inhibitors (SNRIs) and tricyclic antidepressants, which inhibit the reuptake of serotonin (Francesangeli et al 2019).
Serotonin agonists such as triptans and metoclopramide hydrochloride also increase serotonin receptor activity (Simon and Keenaghan 2021), while recreational drugs, such as 3,4-methylenedioxy-methamphetamine (MDMA), cocaine and amphetamines accelerate the release of serotonin and inhibit reuptake (Volpi-Abadie et al 2013). The most severe forms of serotonin syndrome are precipitated by MAOIs, which inhibit the metabolism of serotonin (Simon and Keenaghan 2021).
If there is a suspicion that a patient is experiencing serotonin syndrome, clinicians must take a thorough medicines history, including dose and formulation, recent dose changes and/or additional agents, including over-the-counter medicines, dietary supplements and recreational drugs (Simon and Keenaghan 2021). Polypharmacy, the use of serotonergic agents and pharmacological interactions can accelerate serotonin syndrome. Furthermore, there is significant comorbidity between depression and pain, therefore clinicians must be aware of patients who may be taking antidepressants alongside pain medicines that involve the serotonin pathways (Hall and Chapman 2008a).
Finally, patients who have intentionally overdosed on serotonergic medicines tend to ingest higher quantities and are therefore at greater risk of developing serotonin syndrome than those who have unintentionally overdosed (Boyer et al 2021).
Tina’s signs and symptoms were assumed quickly by her mental health team to be serotonin syndrome, which ensured prompt advice to attend an ED. However, the ED staff were unaware of the condition and instead focused on differentials such as a mental health crisis or recreational drug use. Werneke et al (2016) noted that most patients with signs and symptoms of serotonin syndrome present to EDs for treatment rather than to their usual care team, which emphasises the importance of increasing ED clinicians’ awareness.
The onset of serotonin syndrome is generally sudden and can occur within one hour of increasing the dosage of, or adding another, serotonergic medicine (Francesangeli et al 2019); however, it more typically develops within six to 24 hours (Boyer et al 2021). Onset can be delayed in older people, due to the aged-related reduction in neurotransmitter and receptor activity (Hall and Chapman 2008a), and in those who start taking serotonergic medicines without a sufficient ‘washout’ period – the time required between stopping one medicine and starting another to reduce the risk of adverse interactions (Alusik et al 2014).
Patients with serotonin syndrome typically present with a triad of: mental state changes, autonomic hyperactivity and neuromuscular abnormalities (Alusik et al 2014) (Table 2).
The signs and symptoms of serotonin syndrome range from mild to life-threatening (Jurek et al 2019), and are not necessarily all present or spread equally across the triad categories (Hall and Chapman 2008b). GI issues are not included in the triad, but Skopp (2020) suggested that their presence can support a diagnosis, particularly in the context of differentials such as anticholinergic toxicity (condition precipitated by use of anticholinergic medicines and with similar features to serotonin syndrome). Francesangeli et al (2019) cautioned that mild presentations of serotonin syndrome can be confused with influenza-like signs and symptoms, which is important to note in the context of COVID-19 and seasonal influenza. Other mild signs and symptoms such as restlessness, tremors and sweating can be attributed to the side effects of medicines, deteriorating mental health or a myriad of other conditions; however, if clinicians do not consider or identify serotonin syndrome and patients continue with their medicines regimen, the condition will advance.
Tina (this is a pseudonym) is a 26-year-old woman with cyclothymia, a condition characterised by periods of depression and mild elation. She was receiving treatment from a community mental health team (CMHT) and was established on trazadone hydrochloride 150mg, a tricyclic antidepressant, and duloxetine 60mg, an SNRI. Following a relationship breakdown, Tina presented to the CMHT with low mood characterised by anhedonia (an inability to feel pleasure in normally pleasurable activities), lack of motivation, poor sleep and anxiety with ruminating worries, which were affecting her day-to-day functioning. She reported that these signs and symptoms predated her relationship breakdown and requested a temporary increase of her antidepressants. Tina was referred by her CMHT nurse to the author, a mental health clinical nurse specialist and non-medical prescriber, for a medication review. Following this consultation, the author agreed to increase the duloxetine to 90mg and maintain the dose of trazodone.
Within four days Tina reported to her CMHT that she felt generally unwell with influenza-like signs and symptoms, sweating, restlessness and diarrhoea. Tina’s community nurse discussed this presentation with the author and believed that it could be COVID-19 and that she should isolate. However, Tina’s presentation was also consistent with mild serotonin syndrome in the context of polypharmacy, antidepressant use and recent dose increases. Therefore, she was advised not to take her morning antidepressants and to proceed to an emergency department (ED).
While at the ED Tina’s signs and symptoms progressed and she developed distressing visual disturbances due to ocular clonus (roving eye movements) and dilated pupils. Her observations were: heart rate 130, respiratory rate 40 and temperature 37.8°C. An electrocardiograph confirmed tachycardia, but no other abnormalities. Tina was given diazepam 5mg for agitation and restlessness.
A diagnosis of serotonin syndrome was confirmed by a liaison consultant psychiatrist due to lack of knowledge of the condition among the ED clinicians. Tina was observed in the department for five hours before returning home with advice to maintain hydration, reduce the duloxetine to 60mg and seek an urgent review with her CMHT. Tina’s signs and symptoms resolved fully within five days.
Moderate signs and symptoms of serotonin syndrome include agitation, clonus (muscular spasms), hyperreflexia, tachycardia, hypotension and hyperthermia of 40°C. Patients can be highly unstable and deteriorate quickly, and in severe cases tachycardia can progress to hypotension and shock (Boyer et al 2021). Muscular contractions, spasms and rigidity are believed to be the main drivers of hyperthermia, with temperatures reaching as high as 41°C or more (Talton 2020).
There may also be an increase or decrease in blood pressure and pulse, and episodes of delirium (Jurek et al 2019). The most severe incidences of serotonin syndrome can result in metabolic acidosis, which progresses to rhabdomyolysis, in which patients’ muscle fibres begin to break down, releasing their contents into the blood stream (Jurek et al 2019), in turn leading to kidney damage caused by myoglobin in the urine (Talton 2020). Excess blood clotting secondary to tissue damage can occur throughout the body, which can progress to multiple organ failure, seizures, coma and death (Alusik et al 2014, Jurek et al 2019, Talton 2020).
Diagnosis is based on clinical presentation, medicines history (Volpi-Abadie 2013), and diagnostic criteria (Dunkley et al 2003). A full medicines history is advised, including any illicit drug use.
Physical examination should focus on establishing the presence and extent of autonomic and mental state signs and symptoms (Table 2) and should include a neuromuscular examination (Isbister 2021), to assess the patient’s reflexes and muscle rigidity (Jurek et al 2019). Clonus is one of the most common features of the condition and most easily induced in the ankle. Patients with severe serotonin syndrome will present with spontaneous clonus or abnormally high muscle tone, termed hypertonicity (Isbister 2021). Ocular clonus (roving eye movements) is also a prominent feature and clinicians may also observe dilated pupils and continuous or spasmodic involuntary eye movements during examination (Jurek et al 2019). Tina developed distressing visual disturbances while in the ED and described seeing the floor ‘moving’, which made it challenging for her to walk.
Abdominal examination may reveal hyperactive bowel sounds. Hyperthermia indicates the need for immediate treatment, particularly if combined with neuromuscular signs and symptoms (Isbister 2021).
Additional investigations (Box 1) are not always required but can be used to exclude differential diagnosis (Isbister 2021).
• Urine toxicology in cases of overdose of unknown substances
• Full blood count to discount signs of infection
• Creatine phosphokinase test in patients with clonus (brief involuntary regular muscle spasms) to assess for rhabdomyolysis (breakdown of muscle fibres)
• Electrocardiograph, which may indicate tachycardia associated with serotonin syndrome
The Hunter Serotonin Toxicity Criteria (Dunkely et al 2003) (Box 2) is the most commonly used diagnostic decision tool used for serotonin toxicity, although it has been criticised for relying too heavily on neuromuscular signs and symptoms, which may overlook atypical presentations (Skopp 2020), or more serious cases (Werneke et al 2016). Tina was diagnosed with serotonin syndrome by a liaison consultant psychiatrist using the Hunter Serotonin Toxicity Criteria, which identified her recent use of serotonergic agents, the presence of ocular clonus and psychomotor agitation.
Patients can be said to be experiencing serotonin toxicity if there has been:
OR any of the following combinations:
Serotonin syndrome has several differential diagnoses, which are shown in Box 3, although it is distinguished by neuromuscular stimulation, most commonly clonus, that is absent from the conditions detailed in Box 3 (Isbister 2021). Tina’s signs and symptoms were presumed initially by ED staff unfamiliar with serotonin syndrome to be a mental health crisis, or associated with drug or alcohol misuse. Tina told her CMHT that she felt distressed by being asked repeatedly about her mental health and substance use, and anxious that her insight into her own mental health was being questioned and her physical condition dismissed. Tina’s CMHT nurse had told her that her presentation could be due to excess serotonin, so she was able to ask ED staff assertively for this to be considered and subsequently a liaison consultant psychiatrist was contacted.
• Neuroleptic malignant syndrome (NMS) – NMS has similar presenting features to serotonin syndrome, including tachycardia, hypertension, rhabdomyolysis (breakdown of muscle fibres), excessive sweating and rigidity, and can develop following use of drugs that act on the dopamine pathways. It has slower onset than serotonin syndrome and lack of excitability, noted by slowed movements and reflexes, and classic ‘lead pipe’ rigidity (increased tone in all the muscles surrounding a joint)
• Anticholinergic toxicity – precipitated by anticholinergic use. Similar features to serotonin syndrome include dilated pupils, mental state changes and tachycardia, but patients with this condition develop dry skin and mucosa, and a lack of bowel sounds
• Delirium tremens – potentially fatal complication secondary to alcohol withdrawal. Features include agitation, delusions, hallucinations, tremor, excessive sweating, hypertension and tachycardia
• Malignant hyperthermia – can occur secondary to anaesthesia within 30 minutes to 24 hours of inhalation of the anaesthetic agents sevoflurane, desflurane and suxamethonium chloride. Signs and symptoms include hyperthermia, hyperreflexia and rigidity
(Alusik et al 2014, Francesangeli et al 2019, Jurek et al 2019)
First-line treatment for serotonin syndrome is to stop any serotonergic medicines even if serotonin syndrome is only suspected. In mild cases, stopping or reducing serotonergic agents is all that is required (Isbister 2021). Following this, it is important to identify pharmacological interactions and discuss ongoing medicines options with knowledgeable clinicians such as pharmacists, doctors or non-medical prescribers. Patients with moderate toxicity must be observed in appropriate clinical settings, for example EDs or as inpatients, for a minimum of six hours (Isbister 2021).
Supportive treatment is aimed at stabilising the patient’s signs and symptoms and continued monitoring of their heart rate, blood pressure, temperature and oxygen levels to avoid deterioration. Benzodiazepines can relieve agitation and decrease neuromuscular agitation, heart rate and blood pressure, with the aim of reducing the risk of hyperthermia (Boyer et al 2021). Fluids are recommended to treat dehydration and prevent a cascade of renal complications secondary to hyperthermia and neuromuscular excitation (Alusik et al 2014). Activated charcoal, which reduces the absorption of toxins, can be given to patients who have overdosed on serotonergic agents within one hour of ingestion (Isbister 2021).
Patients with severe serotonin syndrome must be managed in critical care (Isbister 2021), to control neuromuscular excitation and hyperthermia and prevent metabolic acidosis, rhabdomyolysis and organ failure (Talton 2020). Early sedation, intubation and ventilation is advised (Isbister 2021). Muscle paralysis reduces clonus and rigidity, and external cooling can bring down the patient’s core temperature; antipyretics are of little use as the hyperthermia is caused by muscle rigidity (Isbister 2021). Serotonergic antagonists can be used to shorten the progression of serotonin syndrome (Volpi-Abadie et al, 2013). For example, cyproheptadine hydrochloride is a sedative antihistamine with 5-HT-antagonist properties and can be effective in mild-to-moderate serotonin syndrome, although its usefulness in severe cases has not been researched adequately (Scotton et al 2019). Additionally, chlorpromazine hydrochloride, an antipsychotic with less potent 5-HT-antagonist activity, can be administered. Chlorpromazine works by blocking dopamine receptors; however, neuroleptic malignant syndrome is a rare reaction to antipsychotic medicines whereby increased blockade of dopamine receptors causes symptoms such as stiffness and tremor. If clinicians decided to administer chlorpromazine to a patient suspected of having serotonin syndrome, neuroleptic malignant syndrome would first need to be ruled out as a differential diagnosis because administering chlorpromazine could result in deteriorating neuroleptic malignant syndrome symptoms (Jurek et al 2019). Cyproheptadine also exerts some weak anticholinergic properties (Boyer et al 2021), therefore anticholinergic toxicity must be ruled out. As cyproheptadine and chlorpromazine can cause mild hypotension they should be administered with adequate hydration to offset this effect (Hall and Chapman 2008a).
Once Tina’s diagnosis of serotonin syndrome was confirmed, she was monitored for signs of deterioration and given diazepam 5mg for agitation and restlessness, which was effective. On discharge from the ED, Tina was advised to maintain her hydration, reduce her duloxetine to 60mg and seek an urgent review with her CMHT.
Francesangeli et al (2019) reported that 70% of mild-to-moderate cases of serotonin syndrome resolve within 24 hours of treatment initiation, although patients with severe signs and symptoms can take up to two weeks to recover (Hall and Chapman 2008b). Signs and symptoms can persist for longer when medicines have a long half-life, for example norfluoxetine, the metabolite of the SSRI fluoxetine, has a half-life of 16 days (Skopp 2020).
Tina’s signs and symptoms improved significantly within 24 hours and resolved fully within five days. She had an urgent medication review with her CMHT three days after ED discharge, at which it was agreed to maintain the doses of duloxetine at 60mg and trazadone at 150mg, which had been beneficial previously. Tina also had regular contact with the CMHT during her recovery to ensure that she was continuing to improve and there were no further adverse effects.
In the author’s view, serotonin syndrome may become more common. Antidepressant use has increased considerably in the UK (Talton 2020), and the latest data emphasises the effect of the COVID-19 pandemic on the nation’s mental health, with a 6% increase in antidepressant prescribing between October and December 2020 compared to the previous year (NHS Business Services Authority 2021). Volpi-Abadie et al (2013) reported on the increased frequency of polypharmacy prescribing as clinicians become more confident in using two or more serotonergic agents, which also creates the potential for increased incidence of serotonin syndrome. A lack of NHS resources may result in people with common mood and anxiety signs and symptoms being prescribed medicines rather than therapies, which have been stretched further by the mental health effects of the pandemic.
Although suicide rates do not appear to have increased during the pandemic (Appleby 2021), the full extent of the mental health effects on the population may not yet have been seen. People who attempt suicide, or succeed in taking their own lives, are more likely to do so by overdosing their prescribed medicines (Miller et al 2020), which may increase the number of patients who present to EDs with severe serotonin syndrome.
While serotonin syndrome is potentially fatal it is also a predictable outcome of excess serotonin in the CNS. It is vital, therefore, that patients and clinicians are aware of the risks, the range of signs and symptoms, and the need for prompt cessation of serotonergic agents when the condition is suspected or diagnosed. Prevention of complications and deterioration of signs and symptoms is critical to ensure positive outcomes. It is also important to be aware that mild signs and symptoms are challenging to distinguish from influenza and that there is a risk that patients and clinicians might mistake the serotonin syndrome for COVID-19, or other viruses and differential diagnoses.
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