Organophosphorus Poisoning

Organophosphorus Poisoning

Organophosphorus Poisoning

1. Initial resuscitation

Patients with a markedly reduced mental condition should immediately undergo 100% oxygen and tracheal intubation. In addition, patients with poisoning may develop respiratory failure rapidly due to central nervous system respiratory central depression, nicotine receptor-mediated diaphragm weakness, bronchospasm, and many secretions. Therefore, even patients with normal mental conditions or normal signs of vitality may require early tracheal intubation.

Doctors should avoid using succinylcholine when performing rapid tracheal intubation (RSI) in patients with organophosphate (OP) poisoning. Succinylcholine is metabolized by acetylcholinesterase (inhibited by OP compounds), which induces exaggerated and prolonged neuromuscular blockage in addicted patients. Nondepolarizing neuromuscular blocking agents like rocuronium may be used, but may be it would be less effective at standard doses because of competitive inhibition on the neuromuscular junction. Therefore, an increased dose of it will be required.

Bradycardia and hypotension are usually present in moderate to moderate poisoning. However, tachycardia or hypertension may occur temporarily due to direct sympathetic stimulation. Proper volume supply with isotonic crystalloids (eg normal saline or lactated Ringer's solution) should be performed in conjunction with other resuscitation and diagnostic efforts.

2. Cholinergic toxicity

Patients who have cholinergic toxicity from organophosphates or carbamate poisoning are usually treated with atropine and oxim therapy (typically pralidoxime) as discussed below.

 Atropine-Atropine competes with acetylcholine at muscarinic receptors to prevent cholinergic activation. For moderate to severe cholinergic toxicity, atropine should be administered starting with a dose of 2-5 mg IV in adults and 0.05 mg/kg IV in children. If this does not work, the dose should be doubled every 3-5 minutes until the muscarinic symptoms and signs of the lungs are alleviated. It is not necessary to supply oxygen before starting treatment with Atropine.

Atropine dosing should be titrated to the end of treatment to eliminate respiratory secretion and stop bronchoconstriction. Tachycardia and mydriasis are not suitable markers for improved treatment. Because it may indicate persistent hypoxia, hypovolemia or sympathetic stimulation. In patients with severe poisoning, hundreds of milligrams of atropine may be needed for several days (IV bolus or continuous infusion).

A personalized approach to treatment is an incremental dose of atropine.
plus infusion) and standard bolus dose plus infusion, supported by an open label randomized trial (n = 156). Mortality was lower in the group of patients administered progressively than in the control group (6 versus 18).

Pralidoxime
Atropine is not effective in treating neuromuscular dysfunction because it does not bind to nicotinic receptors. Pralidoxime (2-PAM) and other oxims like HI-6 and obidoxime are actually cholinesterase reactivating agents which are effective in treating muscarinic and nicotinic symptoms.

Pralidoxime should not be administered without a combination of atropine to prevent worsening of symptoms caused by temporary oxime-induced acetylcholinesterase inhibition.

We suggest oxime treatment in all cholinergic patients, neuromuscular dysfunction patients, or patients exposed to organophosphorous drugs known to cause delayed neurotoxicity. Current World Health Organization recommendations for Pralidoxime IV bolus therapy are at least 30 mg/kg for adults and 25 to 50 mg/kg for children, depending on the severity of the symptoms. Although treatment has not shown to prevent intermediate syndrome or delayed neuropathy (OIDN) by organophosphate drugs, early oxime treatment can help in this situation.

Because rapid administration is sometimes associated with heart failure, pralidoxime should be administered slowly for at least 30 minutes, and slow administration prevents muscle weakness due to temporary inhibition of acetylcholinesterase as the pralidoxime binds to the enzyme. After bolus administration, continuous infusion of pralidoxime at a minimum of 8 mg/kg/hour for adults and 10-20 mg/kg/hour for children seems to show superior antidotal effects.

Serious poisoning can lead to persistent redistribution of toxins. Therefore, continuous IV therapy should be adjusted according to the patient's clinical response and may require several days of therapy. If available quickly, a series of RBC AChE concentrations can be important in determining the efficacy of oxime-induced acetylcholinesterase regeneration.

Evidence of using oxime to treat OP addiction is inconsistent and difficult to interpret. In clinical response to Pralidoxime, there appears to be a great diversity among victims of organotoxicity, which is not well known. We believe that all patients addicted to organophosphorous drugs should be treated with oxime until a better understanding of this diversity and other treatments are available.

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