OPC POISOINING

8/8/2019 OPC POISOINING

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Dr.Surendra Khosya

Guided By

Dr. S.R MEENA

Dr. Meenaxi Sharda


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Organophosphates and carbamates are

potent cholinesterase inhibitors capable of

causing severe cholinergic toxicity following

cutaneous exposure, inhalation, oringestion.World Wide: 3,000,000 per yrpeople are exposed.

up to 300,000 fatalities.

Chemical weapons (nerve gases) areorganophosphate agents.


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Organ phosphorous compounds bind to acetyl

cholinesterase

overabundance ofacetylcholine in the synapse

By time the compound undergoes a conformationalchange (aging) renders the enzyme irreversibly

resistant to reactivation.

Carbamate compounds unlike organophosphates,

are transient cholinesterase inhibitors.


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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.


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Niccotinic , Muscarinic & Central

syndrome


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` Cholinergic phase

central

peripheral muscarinic

peripheral nicotinic` Intermediate syndrome

` Delayed neuropathy

` Behavioral effects


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` Generally manifests in minutes to hours

` Evidence of cholinergic excess

SLUDGE Salivation,

Lacrimation,Urination,

Defecation,

Gastric Emptying.

BBB

Bradycardia,

Bronchorrhea,

Bronchospasm.


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` 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 tohypoxemia.


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` In childrenSeizures are more common (22%-25%).

Lethargy and coma (54%-96%).Flaccid muscle weakness,

miosis,

excessive salivation

are common presenting signs.


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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.


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Organophosphate Induced Delayed Neuropathy

(OPIDN).

Usually occurs several weeks after exposure.

Primarily motor involvement (symmetrical motorpolyneuropathy) 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.


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Grading Severity of organophosphate poisoning

Normal serum acetyl cholinesterase/RBC Cholinesterase-8-20 U/I

Level is 8-20U/LMILD MODERATE SEVERE

Walk ,talk Cannot walk Unconscious,no pupillary

Headache,dizzy Soft voice reflex

Nausea,vomiting Musle twitching Muscle twitching,flaccid

Abdominal pain (fasiculation) paralysis

Sweating, salivation Anxity restlessness Increased bronchial secretion

Rhinorrhoea Small pupil(miosis) dyspnoea

Crackles /wheeze

convulsion, respiratory

failure

AChE 1.6-4.0U/I AChE .8-2.0U/I AchE


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88% of parents initially deny any exposure history.

petroleum orgarlic-like odor.

If doubt exists a trial of Atropine (0.01 to 0.02mg/kg) may be employed.

The absence of signs or symptoms of

anticholinergic effects following atropine

challenge strongly supports the diagnosis


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` 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.


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Deliver 100 % oxygen via facemask

Strongly considerintubation: patients who appear mildly poisoned may rapidly develop

respiratory failure.

Considervolume resuscitation with normal saline orringer to treat Bradycardia and hypotension.

Use activated charcoal within one hour of an ingestion.

In cases of dermal exposure aggressivedecontamination with complete removal of the patient's

clothes and vigorous irrigation of the affected areasshould be performed.


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` Forced emesis have no role

` Gastric lavage is indicated once patient is

stabilsed,

` in unconcious, intubated patient repeated after 2-3 hrs. and within 1-2 hrs of ingetion of op/

carbamate or started even after 12 hr of ingestion

and repeated thrice at an interval of 4 hrs

` Repeat stomach wash will remove residul poison


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Competes it et l oli e t muscari icreceptors.

I itial ose . mg/ g IV olous. oubledever to mi until bronchial

secretionsand heezingstop( a 2).

epeat ever to minuntil all absorbed

organophosphatemetabolized(fewhours toseveral days;usually2 to 2hours).


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TARGET END POINT OF ATROPINISATION

Chest clear on auscultation with no wheeze

Heart rate>80 beats/min

Dry axilla

Systolic blood pressure >80 mmhg


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Keep a maintenance dose of atropine for 2-3 days

after disappearing of manifestation.

10-20 % of loading every hrs

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 mainsigns ofatropine toxicity that indicate that atropine

administration should be discontinued, at least

temporarily.


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ATROPINE TOXICITY

Dry Mouth

Dysphagia

Dilated pupils

Drunken gait

Delirium

Drowsiness

Death due to respiratory failure

Dry hot skin

Carphologia

Hallucination and delusion


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GUIDLINE FOR ENTILATOR SUPPORT

1. Respiratory Gas Tension

a. Direct indicesArterial Oxygen Tension50 mmof Hg in the absence of metabolic

alkalosis

b.Derived indices

p ao2/Fio235mm of hg

2. Clinlcal Respiratory Rate>35 beats/ min

3. Mechanical Indices

Tidal olume


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Cholinesterase reactivatingagent that areeffective in treatingbothmuscarinicandnicotinicsymptoms.

Usewithin hoursafterpoisoning.Usewith concurrent ofatropine.

Useonly formoderate tosevererganophosphate poisoningandnot

carbamate.Use ifneuromusculardysfunction ispresent.


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30 mg/kg over 10 -20 min f/b

Continuous infusion at 8-1o mg/kg/hour.

Until clinical recovery or 7 day which haveelapsed whichever is later

Obidoxime 250 mgf/b infusion750 mg/24hrs

Monitor Blood pressure during administration


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Prophylactic diazepam has been shown to

decrease neurocognitive dysfunction after

poisoning.

Diazepam 0.1-0.2 mg/kg I , repeat asnecessary if seizures occur.

phenytoin has no effect on organophosphate

agent-induced seizures.


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OTHER DURG

Magnesium Therapy may inhibit AChE andOP antagonism

Glycopyrolate is equally effective and lessr CNS side effect

With better control of secretion then atropine

Furosemide if pulmonary edema persist after full atropinisation

Antibiotics consider risk of infection

DURG SHOUID BE A OIDED

Morphine

Succinyl choline

Theophylline

Phenothiazine, reserpine

Adrenergic amine only if maked hypotenmsion


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Organophosphates are usually dissolved inhydrocarbon bases; thus, the clinician should

considerhydrocarbon pneumonitis .


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OPC POISOINING