Organophosphates

and carbamates are potent cholinesterase inhibitors capable of causing severe cholinergic toxicity following cutaneous exposure, inhalation, or ingestion.
Wide:
3,000,000

World

per yr people are exposed. up to 300,000 fatalities.

15

to 18 % of all poisoning in Aleppo. Chemical weapons (nerve gases) are organophosphate agents.

 Organophosphorous

acetylcholinesterase overabundance of acetylcholine in the synapse By time the compound undergoes a conformational change (aging) renders the enzyme irreversibly resistant to reactivation.
Carbamate

compounds bind to

compounds unlike organophosphates, are transient cholinesterase inhibitors.

 Generally

oral or respiratory exposures result in signs or symptoms within three hours.

symptoms of toxicity from dermal absorption may be delayed up to 12 hours.

while

Generally manifests in minutes to hours

Evidence of cholinergic excess

SLUDGE =

Salivation, Lacrimation, Urination, Defecation, Gastric Emptying.

Bradycardia, Bronchorrhea, Bronchospasm.

BBB

Respiratory insufficiency can result from muscle weakness, decreased central drive, increased secretions, and bronchospasm and it is the lead cause of death. Cardiac arrhythmias, including heart block and QTc prolongation may be due to hypoxemia.

ACH: acetylcholine; Epi: epinephrine; NE: norepinephrine; NMJ: neuromuscular junction.

In children

Seizures are more common (22%-25%). Lethargy and coma (54%-96%). Flaccid muscle weakness,

miosis, excessive salivation are common presenting signs.

 10

to 40 % of organophosphorous agent poisoned patients.

24-96 hours after exposure respiratory, and proximal muscle weakness are prominent features.

Occurs Bulbar,

Generally

resolves completely in 1-3 weeks.

 Organophosphate

Induced Delayed Neuropathy (OPIDN). specific organophosphorous agents. Usually occurs several weeks after exposure. Primarily motor involvement (symmetrical
Sensory

motor polyneuropathy) flaccid weakness of lower extremities, ascends to involve upper extremities.

disturbances are usually mild. May resolve spontaneously, but can result in permanent neurologic dysfunction.

88% of parents initially deny any exposure history.

petroleum
If

or garlic-like odor.

doubt exists a trial of Atropine (0.01 to 0.02 mg/kg) may be employed. The absence of signs or symptoms of anticholinergic effects following atropine challenge strongly supports the diagnosis

RBC acetylcholinesterase activity:

provides a measure of the degree of toxicity. determine the effectiveness of antidote therapy.

plasma (or pseudo-) cholinesterase activity:

more easily performed. not correlate well with the severity of poisoning. a depression of 25% or more is strong evidence of excessive organophosphate absorption.

o not delay the treatment until

laboratory confirmation is obtained.

Deliver 100 % oxygen via facemask Strongly consider intubation:

patients who appear mildly poisoned may rapidly

Consider volume resuscitation with normal saline or ringer to treat Bradycardia and hypotension. Use activated charcoal within one hour of an ingestion.

develop respiratory failure.

In cases of dermal exposure aggressive decontamination with complete removal of the patient's clothes and vigorous irrigation of the affected areas should be performed.

 Competes

with acetylcholine at muscarinic receptors.

Initial

dose 0.05 mg/kg IV bolous. Doubled every 3 to 5 min until bronchial secretions and wheezing stop (SaO2). Repeat every 10 to 30 min until all absorbed organophosphate metabolized (few hours to several days; usually 2 to 12 hours).

 Keep

a maintenance dose of atropine for 2-3 days after disappearing of manifestation. and mydriasis are not appropriate markers for therapeutic improvement, as they may indicate continued hypoxia, hypovolemia, or sympathetic stimulation.

Tachycardia

Fever,

muscle fibrillation, and delirium are the main signs of atropine toxicity that indicate that atropine administration should be discontinued, at least temporarily.

Cholinesterase reactivating agent that are effective in treating both muscarinic and nicotinic symptoms.

Use

within 48 hours after poisoning.

Use
Use

with concurrent(bersama) of atropine.

only for moderate to severe Organophosphate poisoning and not carbamate. if neuromuscular dysfunction is present.

Use

 25-50

mg/kg IV in 100 ml NS over 30 min.

Repeated Or

after 1 to 2 hours, then every 10 to 12 hour interval if needed

infusion at 10-20 mg/kg/hour.

Continuous Monitor

Blood pressure during administration

 Prophylactic

Diazepam

diazepam has been shown to decrease neurocognitive dysfunction after poisoning.

0.1-0.2 mg/kg IV, repeat as necessary if seizures occur.

phenytoin

has no effect on organophosphate agent-induced seizures.

hydrocarbon bases; thus, the clinician should consider hydrocarbon pneumonitis and not to do gastric lavage.

Organophosphates are usually dissolved in