Central alpha-2 adrenergic eye drops: case series of 3 pediatric systemic poisonings

Abstract

Three pediatric patients presented with systemic central alpha-2 agonist poisoning-2 cases of bradycardia and apnea resulting from ingestion of ingestion of apraclonidine, with 1 case requiring intubation, and 1 case of bradycardia and altered mental status requiring intensive care monitoring resulting from therapeutic ophthalmic application of brimonidine. Pediatric poisonings involving central alpha-2 adrenergic agonists have been well described, particularly with the prototypical agent clonidine. Characteristic symptoms include sympatholytic effects such as central nervous system depression, respiratory depression, hypotension, bradycardia, miosis, hypothermia, and hyporeflexia. Although structurally similar to clonidine, these compounds are presumed to be safer for pediatric use because they are more polar and less lipophilic than clonidine, thereby limiting their ability to cross the blood-brain barrier and reducing incidence of centrally mediated effects. Systemic toxicities of alpha-2 agonist ophthalmic preparations in pediatric patients are similar to those seen with clonidine poisonings. Symptomatic patients should be treated in the same manner as patients with clonidine poisoning. Treatment of systemic poisoning is primarily supportive. Periodic tactile stimulation seems to be an effective nonpharmacological intervention to improve alpha-2 adrenergic agonist-induced central nervous system depression and respiratory depression. Intubation should be considered when tactile stimulation is not effective.