INTRODUCTION: Reports of acute levodopa-carbidopa overdose are rare and no case of an acute overdose with a controlled-release formulation has been described. We describe such a case in which serial concentrations of catecholamines were measured. CASE REPORT: A 55-year-old man ingested 89 tablets of Sinemet 50/200 (17.8 g of levodopa, 4.45 g of carbidopa). Clinical effects and plasma concentrations of dopamine, noradrenaline and adrenalin were assessed over 66 hours. On admission 2.5 hours after the ingestion, his physical examination was normal except for mydriasis and urine retention. Five hours post-ingestion he had psychomotor agitation, delirium with logorrhea, joviality, visual hallucinations, regular sinus tachycardia and xerostomia. The clinical course included two episodes hypotension and four of transient tachycardia. Treatment was symptomatic and supportive. Clinical toxicity reappeared 48 hours after the intoxication. The patient was discharged at the end of the fourth day with amnesia for the event. DISCUSSION: Dopamine showed an initial plasma concentration peak 14 hours after the toxic ingestion, followed by a second peak 38 hours after the ingestion. The initial peak of noradrenaline occurred 20 hours post-ingestion with a second lower peak at 38 hours. There were no elevations in adrenalin concentrations. CONCLUSION: There appeared to be no correlation between the intensity of the clinical signs and the blood concentrations of dopamine and noradrenaline, although the resolution of the clinical signs did correspond to these catecholamines return to normal values. Patients who ingest controlled-release formulations need to be observed until after the second catecholamine peak.
INTRODUCTION: Reports of acute levodopa-carbidopaoverdose are rare and no case of an acute overdose with a controlled-release formulation has been described. We describe such a case in which serial concentrations of catecholamines were measured. CASE REPORT: A 55-year-old man ingested 89 tablets of Sinemet 50/200 (17.8 g of levodopa, 4.45 g of carbidopa). Clinical effects and plasma concentrations of dopamine, noradrenaline and adrenalin were assessed over 66 hours. On admission 2.5 hours after the ingestion, his physical examination was normal except for mydriasis and urine retention. Five hours post-ingestion he had psychomotor agitation, delirium with logorrhea, joviality, visual hallucinations, regular sinus tachycardia and xerostomia. The clinical course included two episodes hypotension and four of transient tachycardia. Treatment was symptomatic and supportive. Clinical toxicity reappeared 48 hours after the intoxication. The patient was discharged at the end of the fourth day with amnesia for the event. DISCUSSION: Dopamine showed an initial plasma concentration peak 14 hours after the toxic ingestion, followed by a second peak 38 hours after the ingestion. The initial peak of noradrenaline occurred 20 hours post-ingestion with a second lower peak at 38 hours. There were no elevations in adrenalin concentrations. CONCLUSION: There appeared to be no correlation between the intensity of the clinical signs and the blood concentrations of dopamine and noradrenaline, although the resolution of the clinical signs did correspond to these catecholamines return to normal values. Patients who ingest controlled-release formulations need to be observed until after the second catecholamine peak.