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emmedonline
Dr. Ajith Kumar J MD
Dept. of Emergency Medicne
KIMS, Kollam
India
editor
Pesticides are classified into
Insecticides
Carbamate
Organochlorines
Pyrethrins/pyrethroids
Neonicotinoids
N,N-diethyl-3-methylbenzamide (DEET)
Herbicides
Chlorophenoxy herbicides
Urea substituted herbicides
Glyphosate
Organophosphate herbicide
Rodenticides
Nonanticoagulants
Anticoagulants
CARBAMATES
N-methyl carbamates are cholinesterase inhibitors that are structurally related to organophosphate compounds.
It includes carbaryl, primicarb, propoxur, trimethacarb.
Carbamates can be toxic after dermal, inhalation and GI exposure.
Carbamates transiently and reversibly bind to and inhibit cholinesterase enzyme through carbamylation. Therefore aging doesn't occur .
Clinical Feature : Similar to cholinergic crisis as in OP poisoning.
Diagnosis : Measurement of cholinesterase is generally not useful. Cholinesterase levels may return spontaneously to normal level by 4-8 hrs after exposure.
Treatment
Atropine is the antidote of choice. The therapy is not usually required for more than 6 -12hrs until the carbamylated cholinesterase enzyme recovers spontaneously
Pralidoxome is not recommended to be used as the binding is reversible spontaneously.
NEONICOTINOIDS
Nicontine was first used as pesticide in 1960. Nicotine poisoning is severe and fatal. It was stopped due to resistance.
Neonicotinoid group includes acetamipid, clothianidin, dinotefuran, imidacloprid. Impidacloprid is now widely used.
Mechanism of action
It acts by binding irreversibly to the acetylcholine receptors leading to spontaneous discharge of nerve impulse and followed by failure of the neuron to propagate any signal.
In insects ach receptors are present only within CNS.
Mammalian nicotinic receptors are of different subtypes and are present at NMJ of CNS as well; but the binding affinity of the imidacloprid at nicotinic receptors in mammals is much less than that of insects. Therefore it is considered less toxic to humans.
Symptoms
Drowsiness,dizziness
Vomiting, disorientation
Fever
Sweating
Tachycardia, tachypnea
Management
There is no specific antitode.
Symptomatic and supportive care
PYRETHRINS & PYRETHROIDS
Pyrethrins are naturally occurring active extract derived form the chrysanthemum plant.
Pyrethroids are synthatetic analog of pyrethrin and are considered safer than organochlorine and organophosphate insecticide.
They are commonly used as aerosol in automated insect spray in public places.
They are rapidly metabolised in liver and therefore are of low toxicity in humans.
Pathophysiology
Pyrethroids block the sodium channel at the neuronal cell membrane, causing repetitive neuronal discharge.
There is additional effect on gamma aminobutyric acid receptors.
It also cause increased nicotininic cholinergic transmission, norepinephrine release and interference with sodium calcium exchange across membranes.
Clinical Feature
These compounds can cause dermal, pulmonary, GI and neurologic illness.
Allergic hypersensitivity reaction is the commonest manifestation.
Contact dermatitis, allergic rhinitis.
Parasthesia, hyperexcitiability, tremors, seizures, incordination, muscle weakness, respiratory failure, dizziness, headache and non specific nausea, vomiting, diarrhea.
Alteration of consciousness, muscle fasciculation, pulmonary edema and seizure can occur.
Treatment
Removal of source
Dermal, ocular or GI decontamination.
Supportive care
Availability
All out : Prallatherin
Good Knight
ORGANOCHLORINES
Dichlorodiphenyltrichloroethane (DDT) is the prototype insecticide of these chlorinated hydrocarbon.
Chlordane, heptachlor, dieldrin and aldrin are compounds used for termite and roach control.
These compounds are banned in US due to its environmental toxicity.
Hexachlorocyclohexane (Lindane) is a general garden organochlorine insecticide . It is well absorbed by ingestion and inhalation. Dermal absorption occurs, particularly if the skin is abraded or repeated application is used.
Pathophysiology
Organochlorines are central neurologic stimulants that can be toxic after dermal, inhalation and GI exposure.
They antagonise GABA mediated inhibition of central neurons, leading to hyperexcitability.
They are also capable of inducing hepatic microsomal enzyme system.
Clinical Feature
Mild poisoning presents with dizziness, ataxia, fatigue, malaise, headache, neurologic stimulation with hyperexcitability, irritability, delirium, apprehension, tremulousness, myoclonus and facial parasthesia.
More severe exposure may result in seizure, coma, respiratory failure and death.
Aspiration pneumonitis.
Cardiac dysarrythmia due to sensitisation of myocardium to endogenous catecholamine .
Treatment
Removal of clothing and skin decontamination with mild detergent and water.
Activated charcoal and gastric lavage are probably useful
Administration of oxygen
Intubation to protect airway from aspiration, seizures and to correct hypoxia.
Seizures are controlled using benzodiazipines.
Epinephrine must be avoided as organochlorines can sensitise the myocardium to endogenous catecholamines.
Exchange resin cholestyramine is potentially useful for symptomatic patients exposed to chlordecone.
N,N Diethyl-3-Methylbenzamide (DEET)
DEET are used as over the counter insect repellent.
DEET is absorbed through skin and is a neurotoxin that causes seizures in large ingestion.
Sytemic toxicity is rare but manifest as restlesness, insomnia, altered behaviour, confusion, neurologic depression, slurred speech, ataxia, tremors, muscle cramps, hypertonia and seizures.
DEET induced hypotension and bradycardia has been reported.
Treatment
Decontamination with mild detergent and water
Activated charcoal.
Benzodiazipines for seizure control.
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emmedonline
Dr. Ajith Kumar J MD
Dept. of Emergency Medicne
KIMS, Kollam
India
editor