Poisoning: Organophosphorus Compounds

Introduction:

• Organophosphates  are  esters  of phosphoric  acid.  They  are  used as insecticides.
• OP are a group of insecticides or ‘nerve- agents’ which act at acetyl-cholinesterase.
• Have been used as insecticides, petroleum additives and chemical warfare agents.
• Carbamates are another group of insecticides which act at the same site, with a slight different MOA.

 

	HIGHLY TOXIC	MODERATELY TOXIC
1.	Phosphamidon (Dimecron)	Malathion
2.	Ethyl parathion	Fenthion (Baytex)
3.	Methyl parathion	Temephos (abate
4.	Chloro-thiophos	Fenitrothin (tik-20)
5.	Carbo-phenothion	Diazinon (spectacide)

• Malathione,  HETP  (hexa  ethyl tetra  phosphate),  TEPP  (tetra  ethyl pyrophosphate or tetron),  OMPA (octa  methyl  pyrophosphate),  dimefox,  isopestox,  demeton,  trichlorfon,  dipterex, are  Alkyl Phosphatase.
• Parathiona or nitrostigmine  or killphos  or ekato),  paraoxon , Diazinon  (diazion  or TIK 2O) , methyl-parathion  (metacide),  chlorthion are Aryl phosphatase.
• These compounds  are irrversible  inhibitors  of enzyme  cholinesterase.
• They inhibit  cholinesterase  by  phosphorylating  the catalytic  site  of  enzyme. Less than  50%  of  cholinesterase  activity  is  indicative  of poisoning.

Signs and Symptoms:

• Lacrimation, salvation, Sweating, miosis (pinpoint pupil), bronchospasm  with  asthma like  symptoms,
• pulmonary  edema, bradycardia or  tachycardia, tremor.
• Chromolacryorrhea:  Shedding  of red  colour  tear  due  to  abnormal porphyrin  metabolism.
• Occur when Achestrase levels drop to 30% of its normal activity
• Ocular exposure — persistent miosis
• Onset of systemic symptoms varies with different routes of absorption
• Involuntary Ms + secretory glands are affected first followed by voluntary Ms then brain functions
• Symptoms may begin within 5 min to 2 hrs  And are max in 24 hrsResp. and G.I.T symptoms are more marked depending on the route of entry

 

 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,develops 1-4 days after resolution of acute cholinergic symptoms.
• It is manifested as paralysis and respiratory distress, involves proximal muscles with relative sparing of distal muscle groups.
• Atropine is ineffective, symptomatic treatment is given.

 3. Type III

•  It involves OP-induced delayed polyneuropathy (OPIDN), occurs 1-3 weeks after exposure and is associated with demyelination of axons.
• 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.

Diagnosis:

• Cholinesterase  level  should  be estimated  
• RBC cholinesterase  is  more accrutate than  plasma cholinesterase  as activity  is  markedly  reduced  in  OP poisoning.

Treatment:

• Urgent  resuscitative  managment :  Airway,  breathing,  circulation  etc.
• Atropineis  the  mainstay of  treatment (antidote  of choice), but  does  not  antagonize  nicotinic  effects  i.e.  neuramuscular  blockers.
• Oximes  (Pralidoxime 1-2 g IV)  can also  be  used.  They  antagonize  only  peripheral  effects  but  not  CNS effects.

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