Serotonin syndrome in a child – closed circuit television unmasked the diagnosis

INTRODUCTION

Serotonin syndrome is a clinical condition that occurs due to serotonergic overactivity at synapses in the central and peripheral nervous systems. Excessive synaptic stimulation of 5HT2a receptors results in autonomic and neuromuscular aberrations with potentially life-threatening consequences. Serotonin syndrome is clinically diagnosed by a triad of altered mental status, autonomic hyperactivity and neuromuscular abnormalities. Convulsive ergotism was described between 1085 and 1927 in East of the Rhine in Europe after consumption of grains contaminated with ergot which is produced by the fungus Claviceps purpurea. It causes muscle twitching and spasms, altered mental status, hallucinations and altered autonomic changes due to serotonergic hyperactivity. In this case, we describe a child presenting to us with neurological impairment and behavioural changes acutely after medication.

CASE REPORT

A 2-year 11-month-old male child with normal birth history and development was brought with a sudden onset of swaying with abnormal eye movements (horizontal movements). The mother also noticed slurring of speech, irritability and sleeplessness. At admission, he was sleeping on sedation administered in the referring hospital with no abnormal eye movements on the physician opening the eyes. The deep tendon reflexes were exaggerated with upgoing plantars. Other systems were within normal limits. Initial differential diagnoses included post-infectious cerebellar ataxia, opsoclonus-myoclonus syndrome and acute demyelinating encephalomyelitis. He was irritable and afebrile with no abnormal motor and sensory involvement. Baseline investigations, including complete blood count, electrolytes, septic markers, cerebrospinal fluid analysis and magnetic resonance imaging were normal. At admission, the child was asleep and vital parameters were normal. However, as the child showed drastic improvement, the possibility of accidental consumption of drugs was considered. The parents were unaware of such consumption but the mother could immediately remember the Closed Circuit Television (CCTV) installation at home and when looking through the child was seen consuming his grandmother’s medications which contained paroxetine Selective Serotonin Reuptake Inhibitors (SSRI). Hence, the child was diagnosed with Serotonin syndrome. He was admitted to the paediatric intensive care unit for observation, stayed in the hospital for a couple of days and was discharged home.

DISCUSSION

Serotonin syndrome is a drug-induced life-threatening condition wherein, serotonergic activity is increased in both the peripheral and central nervous system as a result of increased levels of serotonin. There was a widespread epidemic of this condition in the east of the Rhine River between 1085 and 1927 called convulsive ergotism.^[1-4] Decreased serotonin metabolism, increased serotonin synthesis, inhibition of uptake of serotonin and increased release of serotonin activation of receptors are mechanisms of serotonin syndrome associated with drugs. There are many drugs including antidepressants, antihistamines, anxiolytics and prokinetic drugs that can cause serotonin syndrome. In our index case, the child accidentally consumed paroxetine – a selective serotonin reuptake inhibitor and developed symptoms. The clinical features usually range from mild symptoms to life-threatening conditions. The accidentally consumed status – anxiety, confusion, agitation, the overactive autonomic system including increased heart rate, high blood pressure, increased body temperature, vomiting and diarrhoea and neuromuscular hyperactivity including tremors, muscle rigidity and hyperreflexia, forms the triad of clinical features. The syndrome is a diagnosis of exclusion with no single diagnostic test confirming the diagnosis.^[5-7] A detailed history including the drug intake and the family members using medications for various illnesses should be considered. There are many diagnostic classifications available and the most commonly used is the hunter serotonin toxicity criteria focusing on clinical features including generalised or ocular clonus, agitation, tremor and/or hyperreflexia as observed in our index case.

The differential diagnosis includes neuroleptic malignant syndrome, anticholinergic toxicity, malignant hyperthermia, meningitis and encephalitis. Patients need supportive care and ongoing observation and stopping of the offending serotonergic agent. The severe form of serotonin syndrome is a life-threatening emergency wherein hyperthermia, rhabdomyolysis, disseminated intravascular coagulation and acute respiratory distress syndrome require intensive care admission, sedation and ventilation. Usually, the symptoms resolve in 24–72 h as we could see in our index case. The drug paroxetine has a life of 24 h and the symptoms persisted for 24–36 h in our index case. Our index case responded to benzodiazepine indicating a mild form of the disease, the severe form of Serotonin syndrome may need cyproheptadine in addition to all supportive care. This case report highlights the importance of keeping all the drugs out of reach of children and the drug’s utility in all family members.

CONCLUSION

Abnormal accumulation of serotonin leads to acute life-threatening events with overactivity of the autonomic nervous system, neuromuscular overactivity and altered behaviour. It is a preventable condition with a diagnosis of exclusion. The drug history of all the family members is highly required while managing.