TY - JOUR
T1 - 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
AU - Suzuki, Yoshiki
AU - Kamijo, Yoshito
AU - Yoshizawa, Tomohiro
AU - Fujita, Yuji
AU - Usui, Kiyotaka
AU - Kishino, Tohru
N1 - Publisher Copyright:
© 2017 Informa UK Limited, trading as Taylor & Francis Group.
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2017/10/21
Y1 - 2017/10/21
N2 - 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.
AB - 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.
KW - Alzheimer’s type dementia
KW - Rivastigmine
KW - acute cholinergic syndrome
KW - butyrylcholinesterase
KW - transdermal patch
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U2 - 10.1080/15563650.2017.1329536
DO - 10.1080/15563650.2017.1329536
M3 - Article
C2 - 28594244
AN - SCOPUS:85020416167
SN - 1556-3650
VL - 55
SP - 1008
EP - 1010
JO - Clinical Toxicology
JF - Clinical Toxicology
IS - 9
ER -