organophosphate-and-carbamate-poisoning

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Organophosphate and carbamate poisoning:

Organophosphate and carbamate poisoning Presented by: Dr. Mazen Baroudi supervised by: Dr. Mirella Halabi

Introduction:

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

Mechanism Of Action:

Mechanism Of Action Organophosphorous compounds bind to 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 unlike organophosphates, are transient cholinesterase inhibitors .

Clinical Features:

Clinical Features Generally oral or respiratory exposures result in signs or symptoms within three hours. while symptoms of toxicity from dermal absorption may be delayed up to 12 hours .

Clinical Features (Acute Toxicity):

Clinical Features (Acute Toxicity) Generally manifests in minutes to hours Evidence of cholinergic excess SLUDGE = S alivation, L acrimation, U rination, D efecation, G astric E mptying. BBB = B radycardia, B ronchorrhea, B ronchospasm.

Clinical Features (Acute Toxicity):

Clinical Features (Acute Toxicity) 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.

Clinical Features (Acute Toxicity):

Clinical Features (Acute Toxicity) ACH: acetylcholine; Epi: epinephrine; NE: norepinephrine; NMJ: neuromuscular junction.

Clinical Features (Acute Toxicity):

Clinical Features (Acute Toxicity) In children Seizures are more common (22%-25%). Lethargy and coma (54%-96%). Flaccid muscle weakness , miosis , excessive salivation are common presenting signs.

Clinical Features (Intermediate Syndrome):

Clinical Features (Intermediate Syndrome) 10 to 40 % of organophosphorous agent poisoned patients. Occurs 24-96 hours after exposure Bulbar, respiratory, and proximal muscle weakness are prominent features. Generally resolves completely in 1-3 weeks.

Clinical Features (Delayed Neurotoxicity):

Clinical Features ( Delayed Neurotoxicity ) O rganophosphate I nduced D elayed N europathy ( OPIDN ). specific organophosphorous agents. Usually occurs several weeks after exposure. Primarily motor involvement (symmetrical motor polyneuropathy) flaccid weakness of lower extremities, ascends to involve upper extremities. Sensory disturbances are usually mild. May resolve spontaneously , but can result in permanent neurologic dysfunction .

DIAGNOSIS (Clinical findings):

DIAGNOSIS (Clinical findings) 88% of parents initially deny any exposure history. petroleum or garlic -like odor. If 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

DIAGNOSIS (Laboratory abnormalities):

DIAGNOSIS (Laboratory abnormalities) 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.

DIAGNOSIS (Laboratory abnormalities):

DIAGNOSIS (Laboratory abnormalities) D o not delay the treatment until laboratory confirmation is obtained.

MANAGEMENT (Initial resuscitation) :

MANAGEMENT (Initial resuscitation) Deliver 100 % oxygen via facemask Strongly consider intubation : patients who appear mildly poisoned may rapidly develop respiratory failure. Consider volume resuscitation with normal saline or ringer to treat Bradycardia and hypotension. Use activated charcoal within one hour of an ingestion. 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.

MANAGEMENT (Atropine):

MANAGEMENT (Atropine) 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).

MANAGEMENT (Atropine):

MANAGEMENT (Atropine) Keep a maintenance dose of atropine for 2-3 days after disappearing of manifestation. Tachycardia and mydriasis are not appropriate markers for therapeutic improvement, as they may indicate continued hypoxia , hypovolemia , or sympathetic stimulation. Fever , muscle fibrillation , and delirium are the main signs of atropine toxicity that indicate that atropine administration should be discontinued, at least temporarily.

MANAGEMENT (Pralidoxime) :

MANAGEMENT ( Pralidoxime ) Cholinesterase reactivating agent that are effective in treating both muscarinic and nicotinic symptoms. Use within 48 hours after poisoning. Use with concurrent of atropine . Use only for moderate to severe Organophosphate poisoning and not carbamate. Use if neuromuscular dysfunction is present.

MANAGEMENT (Pralidoxime) :

MANAGEMENT ( Pralidoxime ) 25-50 mg/kg IV in 100 ml NS over 30 min. Repeated after 1 to 2 hours, then every 10 to 12 hour interval if needed Or Continuous infusion at 10-20 mg/kg/hour. Monitor Blood pressure during administration

MANAGEMENT (Benzodiazepines ) :

MANAGEMENT (Benzodiazepines ) Prophylactic diazepam has been shown to decrease neurocognitive dysfunction after poisoning. Diazepam 0.1-0.2 mg/kg IV, repeat as necessary if seizures occur . phenytoin has no effect on organophosphate agent-induced seizures.

Special Considerations:

Special Considerations O rganophosphates are usually dissolved in hydrocarbon bases; thus, the clinician should consider hydrocarbon pneumonitis and not to do gastric lavage .

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