Clonidine overdose
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Various toxicities following compounding error: case report A 12-year-old boy developed drowsiness, sedation, bradycardia, miosis and hypotension secondary to clonidine toxicity following its overdose due to a compounding error while being treated for autism [time to reaction onsets not stated]. The boy, who had a history of autism, presented to the emergency department (ED) by ambulance due to extreme drowsiness upon waking in the morning. His family member called to emergency medical services when they observed his mental status had not improved since one hour. The emergency medical services noted bradycardia. The boy was treated with atropine and IV fluids. At ED, his BP was 82/48 mmHg (hypotension), HR was 47 beats/min with normal RR, oxygen saturation and temperature. Further examination revealed sedation and decreased interaction with his surroundings, but no focal neurologic deficit was not. His pupils were small (2–3mm) without pinpoint suggestive of miosis. Subsequent cardiovascular examination showed bradycardia with delayed capillary refill at 3–4 seconds. Electrocardiogram revealed sinus bradycardia with normal QRS and QTC intervals. His basic metabolic panel and aminotransferases were within normal limits. Thereafter, his HR and BP stabilised with multiple doses of atropine and IV crystalloid boluses. Over the next 24h, his mental status and BP returned to the baseline. Anamnesis revealed that, he had been receiving compounded liquid formulations of 2.2mL of clonidine 0.09 mg/mL every night along with buspirone as he was unable to take pills. He had been taking these medications for at least a year, and a new bottle of clonidine liquid preparation was started the day prior to presentation. He was then hospitalised with a cardiac monitoring for 36h due to the severity of his symptoms. He was kept under continued inpatient observation for one additional day, after which no recurrence of the symptoms was noted. The symptoms like drowsiness, hypotension, bradycardia and sedation were indicative of clonidine toxicity. After 22h of the last administration of clonidine, a liquid chromatography/tandem mass spectrometry was performed, which showed serum concentration of clonidine at 3.4 ng/mL. At the same time, when he was administered clonidine from the hospital pharmacy, he did not develop significant sedation. His parents reported no extra administration of the medication, and the symptoms were suspected to have developed due to new clonidine liquid preparation that was obtained from the pharmacy. Hence, compounding pharmacy logs were reviewed; however, no significant recipe changes were noted. Due to the concerns of compounding error, his clonidine preparation was sent to a reference laboratory for analysis. Subsequent liquid chromatography analysis revealed that the solution contained clonidine 0.72 mg/mL instead of 0.09 mg/mL, which was approximately eight times higher than that indicated on its label, confirming the compounding error. He had received 1.58mg dose instead of 0.2mg of clonidine. Barbu
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