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Organophosphorus Poisoning
Mahesh Mohite
In suspected cases of poisoning if cholinergic toxidromes are noticed then
commonest toxic agents suspected in Indian population are organophosphates
(OPs) and carbamates. Common OP agents observed in poisoning are
malathion, fenitrothion, diclorvos, etc. This poisoning records almost 3–25%
mortality rate.
Pathophysiology
Organophosphate agents are cholinesterase inhibitors, thus increase the
synaptic levels of acetylcholine (Ach). Effects of increased Ach levels are mainly
at three levels:
1. Nicotinic effect: Neuromuscular junctions at skeletal muscles—increased
stimulation at this level cause fasciculations, cramps, and later paralysis,
weakness.
2. Muscarinic effects: Postganglionic parasympathetic stimulation—increased
stimulation leads to increased exocrine secretions in body, e.g. sweat gland,
salivary gland, bronchial secretions and excessive smooth muscle contraction
leading to hyperperistalsis, micturition, etc. The end effect is clinical
presentation of SLUDGE, i.e. Salivation, Lacrimation, Urination, Diarrhea,
gastrointestinal (GI) upset, Emesis. Postganglionic sympathetic stimulation
due to larger doses of intoxication can lead to tachycardia, hypertension and
arrhythmia.
3. Central effects: Direct effect on brain leads to ataxia, disorientation,
drowsiness, seizures, coma, etc.
In pediatric patients, most common presenting complaints are seizures and
coma which may be due to proportionately higher dose of toxin and patients
brought late after consumption.
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Diagnosis
Essentially it is clinical diagnosis but sometimes laboratory support may
be needed for diagnosis as well as for monitoring the patient. Red blood
cell (RBC) cholinesterase levels correlate with central nervous system (CNS)
cholinesterase levels and levels less than 25% of baseline, denote poisoning.
Plasma cholinesterase is liver generated acute phase reactant and is not reliable
parameter for diagnosis.
Serial monitoring of levels are more reliable since baseline levels of individual
patient are not known. This parameter helps more in monitoring recovery of the
patient and levels above 75% denote good recovery.
Rest investigations are done to monitor various system functions while
treatment.
Treatment
The most common cause of death in OP poisoning is hypoxia due to airway
compromise secondary to bronchospasm, bronchorrhea, laryngospasm and
seizures. Equally important cause is hemodynamic failure due to sympathetic
overstimulation in severe intoxication. Aggressive airway, breathing, circulation
(ABC) support and intense respiratory and hemodynamic monitoring is essential
for successful outcome.
Endotracheal (ET) intubation and mechanical ventilation may be needed to
protect the airway and maintain adequate breathing. Invasive hemodynamic
monitoring also may be needed.
Specific treatments are:
Surface decontamination: Organophosphate poisoning can occur through
oral consumption, skin contamination, inhalation and conjunctival
absorption. Patient’s clothing should be removed first and skin should be
cleaned with soap and water. Gastric lavage should be done after protecting
the airway. Conjunctiva can be cleaned with normal saline (NS) or Ringer’s
lactate solution.
Medication:
–– Aggressive treatment with atropine is done. Dose is 0.05 mg/kg IV to
be repeated every 5 minutes. Subsequent doses can be doubled. It is
to be continued till signs of atropinization are achieved, i.e. bronchial
and salivary secretions are dried. Pupillary dilatation is not the sign of
atropinization. Tachycardia is not limiting factor for atropine injections.
Once atropinization is achieved, periodic low dose is needed for next 48
hours while observing for recurrence of signs.
–– 2-Pyridine aldoxime methyl chloride (2-PAM, pralidoxime) should be
used aggressively. OP phosphorylates cholinesterase to deactivate it
temporarily. Subsequently this deactivated enzyme is hydrolyzed in body
to get permanently deactivated. 2-PAM reactivates the phosphorylated
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cholinesterase. 2-PAM is not needed in carbamate poisoning because
cholinesterase is temporarily deactivated in carbamate poisoning. Dose
of 2-PAM is 50 mg/kg in NS infusion over 30 minutes followed by 20 mg/
kg/hour for next 24 hours.
–– Other supplementary medications: Inotropes, cardiac stabilizers like
magnesium sulphate may be needed in acute phase of poisoning.
Suspected case of OP poisoning should be observed for at least 12 hours.
Confirmed case should be observed for at least 48 hours after clinical recovery.
Three types of paralytic syndromes are observed in OP poisoning:
1. Acute paralysis during active poisoning in initial 1–3 days. This will recover
fast with treatment.
2. Intermediate syndrome: Four to eighteen days presentation probably due to
incomplete initial treatment. Mainly proximal and truncal weakness noticed.
3. OP-induced delayed polyneuropathy (OPIDP) due to inhibition of neuropathy
target esterase. It is mainly distal weakness. Starts at 2–3 weeks and may
recover after 12 months.
Algorithm
