OP Poisoning

INTRODUCTION:
  • Organophosphate compounds are widely used in agricultural sector as PESTICIDES and as chemical war fare.
  • Easily accessible ,associate with self poisoning 200,000 /500,00 Mortality associated self-poisoning with pesticides in rural Asia.
  • 50-70 % in hospital based study.
  • 15-30% in India
  • Suicidal rate with OPC 20.6- 56.3%
MECHANISM OF ACTION OF ORGANOPHOSPATE POISONING:
Irreversibly bind to serine-OH group at the active site of acetylcholinesterase (AChE) à establish covalent bond (phosphorylation)
                   ↓
AGING: loss of alkyl group + strengthening of covalent bond
                   ↓
Phosphorylated AChE is very stable
                   ↓
Inhibition of enzyme activity accumulation of ACh in the synapse and NMJ
                   ↓
Overstimulation of cholinergic receptors


 TYPES:
  • Paralysis due to organophosphate (OP) poisoning can be three types ?
1. Type I (cholinergic phase)
  • It involves acute paralysis secondary to persistent depolarization at the neuromuscular junction caused by persistent stimulation by excessive Ach. Treatment of choice is atropine with or without oximes.
2. Type II
  • It is also called as intermediate syndrome.
  • It develops 1-4 days after resolution of acute cholinergic symptoms.
  • It is manifested as paralysis and respiratory distress.
  • It involves proximal muscles with relative sparing of distal muscle groups.
  • The pathogenesis presumed to be dysfunction of neuromuscular junction caused by downregulation of presynaptic and postsynaptic nicotinic receptors due to release of excessive Ach and Ca' respectively.
  • Atropine is ineffective, symptomatic treatment is given.
3. Type III
  • It involves OP-induced delayed polyneuropathy (OPIDN).
  • It occurs 1-3 weeks after exposure and is associated with demyelination of axons.
  • Delayed onset polyneuropathy after organophosphorous poisoning is seen after a period of 2-4 week
  • It is not caused by cholinesterase inhibition but rather by neuropathy target esterase (NTE) inhibition.
  • It involves distal muscles with relative sparing of neck muscles, cranial nerves, and proximal muscles.
CLINICAL PRESENTATION:
  1. Autonomic Nervous System:
  2. Eye:Miosis, blurred vision, pin point pupil,red tears
  3. Cardiovascular:Bradycardia, hypotension
  4. Glands:Extreme salivation, lacrimation, sweating
  5. Gastrointestinal: Anorexia, nausea, vomiting, diarrhea
  6. Respiratory: Bronchoconstriction, bronchial secretion
  7. Skeletal Muscle: Fasciculations, weakness, paralysis
  8. CNS: Ataxia, confusion, convulsions, coma, paralysis,tremor
  • Death:
  1. Respiratory depression due to bronchoconstriction, 
  2. Increased secretions, 
  3. Paralysis of diaphragm ,Intercostal muscles and central respiratory depression
MANAGEMENT OF OP:
  • Diagnosis is made by Plasma cholinestrase level.
  • Atropine:
  1. Reverses muscarinic but not nicotinic 
  2. 2 mg i.v. repeated every 10 mins till signs of full atropinization i.e dilatation of pupils ,tachycardia.
  • Pralidoxime (2-PAM)
Exam Question
  • Muscarinic signs of OPC poisoning can be remembered as SLUDGE- BBB: Salivation, Lacrimation, Urination, Defecation, Gastric upset, Emesis, Bronchospasm, Blurred vision (Miosis), Bradycardia.
  • Delayed onset polyneuropathy after organophosphorous poisoning is seen after a period of 2-4 weeks
  • Fatality rate of organophosphorous poisoning in India is 15-30%
  • In organophosphorous compound poisoning, organophosphorous compound is a Phosphorylated enzyme Irreversibly inhibit cholinesterase
  • Most specific test for organophosphorous poisoning is Plasma cholinestrase level
  • Organophosphate inhibits Esteratic site ofAchEs
  • Antidote for organophosphorous poisoning is Atropine
Don't Forget to Solve all the previous Year Question asked on OP Poisoning