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OP Poisoning

This document summarizes organophosphorous poisoning. It discusses that organophosphates are esters of phosphoric acid that inhibit the enzyme acetylcholinesterase, leading to excessive accumulation of the neurotransmitter acetylcholine. Symptoms include increased salivation, urination, defecation, and others due to stimulation of muscarinic receptors (SLUDGE), as well as muscle weakness and paralysis due to inhibition of nicotinic receptors. Treatment involves decontamination, atropine administration to block muscarinic effects, oxime administration to reactivate acetylcholinesterase, diazepam for seizures, and supportive care.

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Anmol Kudal
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201 views14 pages

OP Poisoning

This document summarizes organophosphorous poisoning. It discusses that organophosphates are esters of phosphoric acid that inhibit the enzyme acetylcholinesterase, leading to excessive accumulation of the neurotransmitter acetylcholine. Symptoms include increased salivation, urination, defecation, and others due to stimulation of muscarinic receptors (SLUDGE), as well as muscle weakness and paralysis due to inhibition of nicotinic receptors. Treatment involves decontamination, atropine administration to block muscarinic effects, oxime administration to reactivate acetylcholinesterase, diazepam for seizures, and supportive care.

Uploaded by

Anmol Kudal
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPTX, PDF, TXT or read online on Scribd
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Organophosphorous

Poisoning
By: Anmol Kudal
Roll No: 59
Organophosphorous Poisons
 They are esters of phosphoric acid and form two series
of compounds .
 Classification
 A)Alkyl phosphates: 1)Tetraethyl pyrophosphate
(TEPP) 2) Hexaethyl tetraphosphate (HETP),
3)Octamethyl pyrophosphoramide (OMPA) 4) Dimefox,
5)Isopestox 6)Sulfotepp 7)Demeton, 8)Malathion (Kill
bug; Bugsoline),9) Trichlorfon
 B)Aryl phosphates: 1) Parathion (Follidol; Kill
phos; Ekato) 2)Paraoxon 3)Methylparathion
(Metacide) 4) Chlorthion 5) Diazinon (Diazion;Tik 20)
 ABSORPTION: They are absorbed by inhalation through the
skin,mucous membranes and the gastrointestinal tract.
 MECHANISM OF ACTION:
 Acetylcholine is a neurotransmitter that affects the
preganglionic and postganglionic parasympathetic synapses
(muscarinic actions), sympathetic preganglionic synapses
including the adrenal medulla (nicotinic actions) and the
neuromuscular junctions (nicotinic actions).
 It is also a transmitter in the central nervous system. At the
synapses, it is hydrolysed by the enzyme, acetylcholinesterase.
The toxic effects of organophosphates are due to the inhibition
of acetylcholinesterase (that is why they are called as
cholinesterase inhibitors), resulting in the excessive
accumulation of acetylcholine at the synapse.
 This initially stimulates and later paralyses the cholinergic
transmission in the CNS, autonomic ganglia, parasympathetic
nerve endings, some of the sympathetic nerve endings and
neuromuscular junctions
CLINICAL FEATURES
 The various signs and symptoms of poisoning may
be classified into the following categories (an acute
garlic odour is a characteristic feature of
poisoning):
 Muscarinic features (parasympathetic): These can
be remembered using the acronym SLUDGE,
denoting salivation, lacrimation, urination,
defecation, gastrointestinal cramping and emesis.
Bronchorrhoea and bronchoconstriction may be
intense and may lead to disturbed respiratory
functions. Miosis is a characteristic feature but is
not present in all cases. The cardiovascular features
include hypotension and bradycardia.
 Nicotinic features (somatic motor and
sympathetic nerve endings): These features
include muscle fasciculations, muscle cramps,
fatigue, loss of deep tendon reflexes, paralysis.
Tachycardia and hypertension may be there

 CNS Manifestations: Various neurological


features include severe headache, restlessness,
tremors, ataxia, generalised weakness, emotional
lability, confusion, coma, seizures and depression
of the cardio-respiratory centre
Fatal Dose (Orally)
 TEPP:100mg
 OMPA:175mg
 Parathion:175mg
 HETP:350mg
 Malathion and diazinon:1g

Fatal Period
Death usually occurs within 24 hrs in untreated
cases, and within 10 days in those treated cases
when treatment is not successful.
CAUSES OF DEATH

 Asphyxia due to paralysis of respiratory muscles


 Respiratory arrest due to failure of respiratory centre
 Pulmonary oedema
 Cerebral oedema
TREATMENT
1.Decontamination:
 Patient is removed from source of exposure,stripped of his
clothes and skin flushed with water.
 Doctor and nurses should be protected with water-
impermeable gowns, masks with eyeshields, and use double
gloves while handling the patient.
 Gastric lavage: It should only be undertaken once the
patient is stable. Gastric emptying should be done with
continuous suction via a nasogastric tube with 1:5000
KMnO4. Activated charcoal should be administrated in doses
of 1 g/kg.
 Patients with ocular exposures should have copious eye
irrigation with normal saline or lactated Ringer's solution. If
these are not available, tap water can be used.
 ii.Atropinization: Atropine blocks the muscarinic
manifestations and has no effect on nicotinic
receptors (on muscle weakness or paralysis) and does
not affect the rate of regeneration of inhibited AChE.
 Dose: 2–4 mg IV (0.05–0.2 mg/kg in children)
repeated after every 5–15 minutes (min) till
atropinization, the dose should be adjusted to
maintain this effect for at least 24 h (maintenance
dose: 0.02–0.05 mg/ kg). Mild to moderate
atropinization includes dryness of tongue, reduced
secretion of oropharyngeal and brochial
tree,tachycardia and flushing.
iii)Cholinesterase reactivators
 Oxime compounds are used , e.g.Diacetyl monoxime
(D.A.M),Pralidoxime chloride,Pralidoxime
iodide,P2S(Pyridine aldoxime methane sulphonate) given
1-2 gm I.V. As 5% solution in isotonic saline slowly in 10-
20min. May be repeated 12-24 hourly.
 Trimodoxime and Obidoxime are better since they better
cross blood brain barrier.
 The therapy should be started early since otherwise
there is maturation of phoshorylated enzyme .After 24
hrs efficacy is less.
 iv. Diazepam: Addition of diazepam for treatment of seizures
and neuropathy improves survival (must not be used with
other CNS depressants). It decreases the cardiac and brain
morphologic damage resulting from OPC seizures. Dose: 0.5–
2 mg IV every 15 min.
 v. Supportive care
Foot-end of the bed is raised to ensure drainage of respiratory
secretions.
 Suction as required, to remove respiratory secretions. Treat
bronchospasm with atropine and not bronchodilators.
Intubate in case of respiratory distress.
 The use of other medication, including opioids for sedation
may worsen CNS manifestations and the degree of
respiratory depression.
 Dextrose: 2–4 ml/kg of 50% dextrose IV.
 Antibiotics to prevent pulmonary infection.
POST MORTEM APPEARANCE
External
 i.Kerosene-like smell from nostrils and mouth.
 iii.Deep postmortem staining.
 iv.Congested face.
 v.Frothy discharge, often bloodstained from the nose and
mouth.
Internal
 i.Mucosa of the stomach and intestine is congested.
 ii.Stomach content may give kerosene-like smell.
 iii. Respiratory passages are congested, contain frothy
hemorrhagic exudates.
 iv. Petechial hemorrhage may be present subpleurally.
 v. Edema and congestion of the lungs and other visceral
organs.
 vi. Edema of brain
MEDICOLEGAL ASPECTS

 Suicidal and Accidental poisoning is common


 Rarely Homicidal due to detectable smell of the
substance used as diluent for the poison and due
to alarming signs and symptoms that appear
rather early. For homicidal purposes, they are
usually mixed with alcohol to mask the smell
THANK
YOU

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