Serotonin Syndrome

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Serotonin Syndrome

Donald S. Robinson, MD

 

 

 

Primary Psychiatry. 2006;13(8):36-38

 

 

Although serotonin syndrome was described more than 40 years ago,1

most clinicians are unfamiliar with the condition. This potentially

life-threatening adverse drug reaction is a cause of current concern

because of the high utilization of psychopharmacologic therapies with

pro-serotonergic properties. This condition warrants prompt diagnosis

and aggressive intervention to reduce morbidity and prevent

fatalities.2 The majority of physicians are unaware of the

manifestations of severe serotonin (5-HT) toxicity, despite the fact

that serotonin reuptake inhibitors (SRIs), both selective and

unselective, are widely used in clinical practice. These agents

include selective serotonin reuptake inhibitors (SSRIs), dual

reuptake inhibitors, such as venlafaxine and duloxetine, tricyclic

antidepressants (TCAs), and other pro-serotonergic drugs prescribed

for mood and anxiety disorders.3

 

Drug interactions that result in hyperactivity of the serotonin

system are the most frequent cause of serotonin toxicity, due to

additive pharmacologic effects on neuronal pathways modulated by this

monoamine neurotransmitter. Because serotonin syndrome is a

predictable adverse occurrence, not an idiopathic adverse drug

reaction, it is potentially avoidable. An accurate medication history

is critical for recognition and proper diagnosis of the syndrome.

However, even clinicians familiar with the syndrome may initially

miss early and subtle clinical manifestations of serotonin toxicity.

Prompt detection of serotonin toxicity is vital because without

intervention, rapid progression to potentially life-threatening

status can occur.

 

The Hyper-Serotonergic State: Clinical Syndrome

Serotonin toxicity is characterized by the triad of neuromuscular

abnormalities, altered mental status, and hyperactivity of the

autonomic nervous system. All of these manifestations need not be

present, depending on the severity of the reaction. The clinical

picture can range from mild agitation, tremor, and gastrointestinal

(GI) symptoms in less severe cases, to a state of extreme muscle

rigidity with hyperthermia that demands immediate intervention.4

Serotonergic neurons mediate multiple central nervous system (CNS)

functions, including wakefulness, thermal regulation, food and sexual

appetites, affective behavior, and motor tone. In the peripheral

nervous system, serotonin induces GI motility and diaphoresis. This

multiplicity of CNS and peripheral receptors accounts for the highly

variable clinical manifestations of serotonin toxicity.

 

Analysis of an extensive series of cases of serotonin toxicity found

neuromuscular abnormalities to be the most reliable diagnostic

finding. Clonus, hyperreflexia, and muscle rigidity nearly always are

evident, and shivering may be present.2,5 The autonomic hyperactivity

is reflected by diarrhea, increased bowel sounds, dilatation of the

pupils (mydriasis), and sweating. CNS disturbances include akathisia,

agitation, delirium, hyperthermia, and in advanced cases, coma.

Extreme muscular rigidity in severe cases can obscure clonus and

hyperreflexia, exacerbate the hyperthermia, and without aggressive

treatment intervention, be life-threatening.

 

Onset of symptoms in serotonin syndrome is typically acute and

rapidly progressive, following shortly after one or two doses of

offending medication. (snip)

 

http://www.primarypsychiatry.com/aspx/articledetail.aspx?articleid=554