2020
DOI: 10.2478/aiht-2020-71-3413
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Cholinergic syndrome: a case report of acute organophosphate and carbamate poisoning

Abstract: AbstractCholinergic syndrome is a common topic at western medical universities yet rarely observed in clinical practice. The treatment involves muscarinic antagonists, acetylcholinesterase reactivation, seizure control, and supportive measures. Here we report a case of a 52-year old Caucasian male who attempted suicide by ingesting a purple crystal powder that turned out to be a mixture of carbofuran and chlormephos. At clinical examination, the patient presented with salivatio… Show more

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Cited by 5 publications
(4 citation statements)
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References 11 publications
(28 reference statements)
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“…The main action mechanism of OP compounds is inhibition of cholinergic enzymes acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), causing accumulation of neurotransmitter acetylcholine in the synaptic cleft and inducing an excessive stimulation of nicotinic and muscarinic receptors in the central and peripheral nervous system, leading to a paralysis of cholinergic synaptic transmission 8 , 9 . Organophosphate poisoning ultimately results in cholinergic crisis and a variety of symptoms such as miosis, bronchoconstriction, bradycardia, excessive salivation, muscle fasciculations, respiratory depression, loss of consciousness and epileptic seizures 6 , 8 10 . Even when exposed individuals receive proper medical care, long-lasting neurological, behavioural and cognitive changes can occur due to excitotoxic damage to the central nervous system 10 12 .…”
Section: Introductionmentioning
confidence: 99%
“…The main action mechanism of OP compounds is inhibition of cholinergic enzymes acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), causing accumulation of neurotransmitter acetylcholine in the synaptic cleft and inducing an excessive stimulation of nicotinic and muscarinic receptors in the central and peripheral nervous system, leading to a paralysis of cholinergic synaptic transmission 8 , 9 . Organophosphate poisoning ultimately results in cholinergic crisis and a variety of symptoms such as miosis, bronchoconstriction, bradycardia, excessive salivation, muscle fasciculations, respiratory depression, loss of consciousness and epileptic seizures 6 , 8 10 . Even when exposed individuals receive proper medical care, long-lasting neurological, behavioural and cognitive changes can occur due to excitotoxic damage to the central nervous system 10 12 .…”
Section: Introductionmentioning
confidence: 99%
“…Cognitive deficiencies associated with AChE inhibition can be explained by the overstimulation and persistent activation of muscarinic and nicotinic receptors due to acetylcholine accumulation in the synaptic cleft. [ 18 ]…”
Section: Discussionmentioning
confidence: 99%
“…[ 17 ] Intoxication by this type of anticholinesterase accumulates the neurotransmitter acetylcholine in the synaptic cleft by inhibiting cholinesterase, inducing excessive stimulation of nicotinic and muscarinic receptors in the central and peripheral nervous system and paralyzing cholinergic synaptic transmission. [ 18 ]…”
Section: Introductionmentioning
confidence: 99%
“…cholinergic symptoms. The clinical picture of OPs intoxication may be differentiated -from cholinergic toxidrome, intermediate syndrome, OP-induced delayed polyneuropathy to chronic OP-induced neuropsychiatric disorder (OPIDN) [7]. Severe cholinergic crisis manifests by salivation, lacrimation, bronchospasm, bradycardia or myosis.…”
Section: Introductionmentioning
confidence: 99%