The First Use of Pralidoxime in a Child With Rivastigmine Poisoning.

The aim of this report is to describe the successful use of pralidoxime in a pediatric patient who accidentally ingested 12 mg of rivastigmine and presented to the emergency department with weakness, drowsiness, hyporeactivity to environmental stimuli, and full cholinergic syndrome. CASE: The patient presented to the emergency department 2 hours after a suspected ingestion of rivastigmine. He was sleepy but oriented and cooperative, hypotonic, and hyporeflexic and has a Glasgow Coma Scale score of 13 (E3M6V4). Laboratory tests showed a low plasma cholinesterase levels of 2141 U/L (reference range, 5300-12 900 U/L), hyperglycemia (251 mg/dL), and leukocytosis with neutrophilia (21 900/mL, 75.2% neutrophils). CONCLUSIONS: Only 2 pediatric cases of rivastigmine poisoning have been reported in the literature, and there are no previous reports of using pralidoxime in the management of this poisoning. In the present case, intravenous pralidoxime (30 mg/kg) was administered twice at the fifth and sixth hours of ingestion for nicotinic and central effects. There is reasonable theoretical science to suggest pralidoxime in case of acetylcholinesterase inhibitor toxicity. We conclude that observed clinical improvement in weakness temporally associated with pralidoxime administration. Increased plasma cholinesterase activity after pralidoxime administration also makes it useful in this type of poisoning.

Acute cholinergic syndrome in a patient with mild Alzheimer's type dementia who had applied a large number of rivastigmine transdermal patches on her body.

CASE PRESENTATION: A 91-year-old woman was transferred to our Emergency Medical Center and Poison Center with somnolence, hypertension (186/61 mm Hg), and repeated vomiting. Three hours later, 10 transdermal patches, each containing 18 mg of rivastigmine (9.5 mg/24 h), were found on her lower back and both thighs, when miosis, facial and trunk sweating, enhanced bowel sound, hypertension, and sinus tachycardia were noted. She was diagnosed with acute cholinergic syndrome due to rivastigmine poisoning. Her hypertension and sinus tachycardia peaked 8 and 5 h after all the patches were removed, respectively. Her symptoms subsided spontaneously after 17 h. DISCUSSION: In the present case, our patient was presented with acute cholinergic syndrome due to carbamate intoxication after massive transdermal exposure to rivastigmine. Toxicological analysis revealed a remarkably high estimated serum rivastigmine concentration (150.6 ng/ml) and notably low serum butyrylcholinesterase activity (35 IU/l) on admission, with a markedly prolonged calculated elimination half-life of 6.5 h. CONCLUSIONS: Emergency physicians should consider acetylcholinesterase inhibitor exposure (e.g., rivastigmine) when patients are present with acute cholinergic syndrome.