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Potentially severe acute adverse reaction to a serotonin agonist.
Pathophysiology
- excessive stimulation of 5-HT1A and possibly 5-HT2 receptors
- usually result of administration of serotonin agonist to patient who is
already receiving a drug capable of potentiating effects of serotoninergic
pathways
- may also occur as a result of:
- enhanced serotonin release (eg by cocaine or "ecstasy")
- decreased serotonin re-uptake (eg tricyclic antidepressants)
- decreased serotonin metabolism (eg monoamine oxidase inhibitors)
- excessive adminstration of serotonin precursors or agonists (trazodone,
L-tryptophan)
Clinical features
Characterized by cognitive and behavioural changes, autonomic dysfunction and
neuromuscular abnormalities. Usually develops within hours of administration of
precipitating agent.
Cognitive & behavioural changes
Autonomic dysfunction
- hyperthermia
- sweating
- dilated pupils
- tachycardia
- labile BP
- diarrhoea
Neuromuscular abnormalities
- hyper-reflexia
- myoclonus
- shivering
- ataxia
Diagnosis
- clinical diagnosis. There are no specific laboratory findings.
Consider possibility in all agitated patients presenting to emergency
department
- blood serotonin concentrations are not helpful as the syndrome is the
result of increased concentrations at the nerve endings.
- differential diagnosis include neuroleptic
malignant syndrome (NMS)
- NMS characterized by diminished cognition, mental depression and
stupor accompanied by extreme rigidity developing over days-weeks.
Serotonin syndrome is an excitatory syndrome characterized by hyper-reflexia,
tremor, myoclonus and agitation developing over hours
- shivering, dilated pupils, head turning and contractions that are more
intense in the legs than the arms are suggestive of serotonin syndrome
Treatment
- removal of precipitating agent
- supportive therapy
- case reports suggest that non-specific serotonin antagonists (eg
chlorpromazine, methysergide, cyproheptadine or propranolol) may be
beneficial in severe cases
Prognosis
Usually self-limiting and often resolves within 24-36 hours with supportive
therapy alone.
Further reading
Hadad E et al. Drug-induced hyperthermia and muscle rigidity:
a practical approach. Eur J Emerg Med, 2003;10:149-54
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