Pesticides

ORGANOPHOSPHATE AND
CARBAMATE INSECTICIDES
Principles of Disease
Highly lipid soluble and are readily
absorbed via dermal, gastrointestinal
(GI), and respiratory routes.
Organophosphorus pesticides work
by persistently inhibiting the enzyme
acetylcholinesterase

PESTICIDES IN
DIFFERENT MEDIA
Air
- Respirable particles contaminated with
pesticides
- Respirable aerosols during spraying
- Vapour from volatile residues of pesticides
Soil
- Hand-to-mouth behaviour
- Crawling on the ground
- Dermal contact

 Water
Pesticides in drinking water: tap, well
Food
- Crops routinely sprayed: fruits,
vegetables, grains
- Bioaccumulation in animals and
products fish, meat, eggs, dairy

ROUTES OF EXPOSURE
Ingestion :
Breastfeeding
Accidental ingestion
Residues in food
Mouthing
Inhalation :
Indoor and outdoor spraying
Occupational exposure
Dermal absorption :
Accidental contact
Occupational exposure
Residues on surfaces
Contaminated clothing
Medical use: scabies, head lice

 Because of the global penetration of

organophosphorus compounds, inhibition occurs at
tissue sites:
- true acetylcholinesterase represented by
erythrocyte
- circulating pseudocholinesterase in plasma

Inhibition of cholinesterase results in the accumulation

and subsequent prolonged effect of acetylcholine at a
variety of neurotransmitter receptors :
- sympathetic and parasympathetic ganglionic
nicotinic sites
- postganglionic cholinergic sympathetic
- parasympathetic muscarinic sites
- skeletal muscle nicotinic sites
- CNS sites

Clinical Features

This syndrome represents postganglionic acetylcholine-induced

hollow end-organ general hypersecretion.

Bradycardia is a classic sign of the cholinergic syndrome, but the

increased release of norepinephrine from postganglionic
sympathetic neurons precipitated by excess cholinergic activity at
sympathetic ganglia may result in normal or even tachycardic
heart rates (nicotinic effect).

A combination of sympathetic stimulation, involvement of the Nmethyl-d-aspartate receptor, and enhanced acetylcholine
concentrations seizures

Because the diaphragm is affected, cholinesterase poisoning leads

to respiratory arrest.

Clinical Features

Treatment
Treatment is directed toward four
goals:
(1) decontamination,
(2) supportive care
(3) reversal of acetylcholine excess
at muscarinic sites
(4) reversal of toxin binding at active
sites on the cholinesterase molecule

1. Decontamination
Dermal decontamination : Removal and
destruction of clothing and thorough
flushing of exposed skin
Alternatively, dermal decontamination
can be done with dry agents, such as
military resins flour, sand, or bentonite.
GI decontamination : washed with a 5%
hypochlorite solution to inactivate the
cholinesterase inhibitor.

2. Supportive
Airway and respiratory failure :
suctioning of secretions and vomitus,
oxygenation, and, when necessary,
ventilatory support. Succinylcholine
can be used for intubation but may
have an extremely prolonged
duration.

3. ) reversal of acetylcholine
excess at muscarinic sites
Suggested dosing is 1 or 2 mg of atropine
(0.020.05 mg/kg) intravenously, with doubling
of each subsequent dose every 5 minutes until
there is control of mucous membrane
hypersecretion and the airway clears.
If intravenous access is not immediately
available, atropine may be administered
intramuscularly.
Patients may require 200 to 500 mg of atropine
intravenously during the first hour, followed by
prolonged continuous infusions of 5 to 100
mg/hr to maintain adequate secretion control.

 Oxime, such as pralidoxime (2-PAM, Protopam) or

obidoxime (Toxigonin)
Regimen :
1 or 2 g intravenously (pediatric dose, 2550 mg/kg);
additional doses may be given based on clinical
response and serial cholinesterase levels.
The medication may be given in a bolus of 1 or 2 g
intravenously over 30 to 60 minutes every 4 to 8 hours
or 500 mg/hr (pediatric dose, 1025 mg/kg/hr).
The World Health Organization recommends an initial
dose of 30 mg/kg followed by 8 mg/kg/hr continued for
at least 24 hours or, if an infusion cannot be used, 30
mg/kg every 4 hours.

Carbamates
Carbamates inhibit
acetylcholinesterase for minutes to
48 hours, and the carbamatecholinesterase binding is reversible

Chlorinated hydrocarbon
Insecticides primarily affect axonal membranes,
resulting in neuronal irritability and excitation.
Toxicity occurs in central and peripheral
neurons. Some of the organochlorines can
inhibit the chloride channel of -aminobutyric
acid (GABA) receptors, leading to decreased
inhibition of the central nervous system.
Chlorinated hydrocarbon insecticides & solvents,
may sensitize the myocardium circulate
catecholamines and increase susceptibility
ventricular dysrhythmias (VT & VF)

Primary and secondary

survey

Pre Hospital
Search for clues at scene:

Pills/pill bottles
Drug paraphernalia
Witnesses
Transport all drugs and pill bottles for identification.

Restrain uncooperative patients for patient and

health care giver protection.
Consider co-morbid conditions:
Trauma
Medical illness
Environmental exposure

Pre hospital administration of activated charcoal

may optimize decontamination if prolonged
transport time.

Initial Stabilization
Airway, breathing, and circulation management (ABCs):
Endotracheal intubation as needed for airway protection,
oxygenation, ventilation, and orogastric lavage
Supplemental oxygen for hypoxia
Pulse oximetry
Cardiac monitor
IV access

Hypotension:
Administer 0.9% normal saline (NS) IV fluid bolus.
Trendelenburg
Vasopressors for persistent hypotension

Bradycardia:
Atropine
Cardiac pacing

If altered mental status, administer coma cocktail: thiamine,

D50W (or Accu-Chek), naloxone

Decontamination
Gastric Decontamination.
Prevents systemic absorption of ingested toxin
Orogastric lavage:
Consider in potentially lethal ingestions without known antidote
within 1 hour of ingestion.
Protected airway essential prior to lavage

Activated charcoal:
Most effective within a few hours of most toxic ingestions
Contraindicated if caustic ingestion, unprotected airway, or bowel
obstruction
Drugs not effectively bound to charcoal: metals (borates, bromide,
iron, lithium), alcohols, potassium

Whole-bowel irrigation:
Polyethylene glycol (Colyte, Go-Lytely) evacuates bowel without
causing electrolyte disturbances.
Consider in toxins not well adsorbed by charcoal (e.g., iron and
lithium), body packers/stuffers, sustained release ingestions.
Contraindicated if bowel obstruction, perforation, or hypotension

Enhanced Elimination
Enhances removal of systemically absorbed toxin:
Multiple-dose activated charcoal:
Theophylline
Carbamazepine
Phenobarbital

Urinary alkalinization:
Salicylates
Phenobarbital

Hemodialysis/hemoperfusion:

Lithium
Salicylates
Theophylline
Toxic alcohols

Antidotes

Acetaminophen: N-acetylcysteine
Anticholinergic: physostigmine
Benzodiazepines: flumazenil
Beta-blockers: glucagon
Calcium channel blockers: calcium chloride/gluconate,
insulin
Carbon monoxide: oxygen, hyperbaric oxygen
Coumadin: vitamin K1
Cyanide: cyanide antidote kit
Digoxin: Digibind
Ethylene glycol: ethanol, 4-methylpyrazole
Iron: deferoxamine
Isoniazid (INH): pyridoxine (vitamin B6)
Methanol: ethanol, 4-methylpyrazole
Methemoglobinemia: methylene blue
Opiates: naloxone
Organophosphates: atropine, pralidoxime
Tricyclic antidepressants: NaHCO3

Medication (Drugs)
Activated charcoal slurry: 12 g/kg PO
Dextrose: D50W one amp: 50 mL or 25 g (peds: D25W
24 mL/kg) IV
Diazepam: 510 mg (peds: 0.20.5 mg/kg) IV every
1015 minutes
Lorazepam: 26 mg (peds: 0.050.1 mg/kg) IV every
1015 minutes
Naloxone (Narcan): 0.42 mg (peds: 0.1 mg/kg) IV
or IM initial dose
Thiamine (vitamin B1): 100 mg (peds: 50 mg) IV or
IM

Hydrocarbon

Sign n symptoms
Ccamphor, which can cause seizures and
status epilepticus
Hhalogenated HC, which can cause
dysrhythmias and
hepatotoxicity
Aaromatic HC, which can cause bone marrow
suppression
and cancer
Mmetals (e.g., arsenic, mercury, and lead)
Ppesticides, which can cause cholinergic
crises, seizures,
and respiratory depression

Inhalation poisoning