Organophosphate poisoning

Organophosphate Poisoning

General:

Organophosphates have been used as insecticides. It is a potent cholinesterase inhibitor capable of causing severe cholinergic toxicity following ingestion, inhalation or cutaneous exposure.

Clinical context:

Clinical syndromes

Acute toxicity: Generally manifests in minutes to hours. Evidence of cholinergic excess in the autonomic nervous system, neuromuscular junction, and central nervous system (CNS).

Muscarinic effects: SLUDGE = Salivation, Lacrimation, Urination, Defecation, Gastric Emptying, B88 Bradycardia, Bronchorrhea, Bronchospasm

Nicotinic effects: fasciculations, muscle weakness, and paralysis.

CNS effects: Nicotinic and muscarinic receptors also have been identified in the brain, and may contribute to central respiratory depression, lethargy, seizures, and coma.

Respiratory insufficiency results from muscle weakness, decreased central drive, increased secretions, and bronchospasm.

Intermediate syndrome: Occurs 24-96 hours after exposure and resolution of cholinergic excess. Characteristic neurological findings including neck flexion weakness, decreased deep tendon reflexes, cranial nerve abnormalities, proximal and bulbar muscle weakness and respiratory insufficiency. Generally resolves in 1-3 weeks.

Organophosphorus Agent-Induced Delayed Peripheral Neuropathy (OPIDN): Usually occurs 1-3 weeks after exposure. Presents with transient, painful "stocking-glove" paresthesia, followed by a symmetrical motor polyneuropathy (more in distal muscles group) characterized by flaccid weakness of the lower extremities, which ascends to involve the upper extremities. Sensory disturbances are usually mild. May resolve spontaneously, but can result in permanent neurologic dysfunction.

Investigations:

Check RBS-Hyperglycaemia

RBC acetylcholinesterase activity (<80%)

FBC, Renal & Liver profile

ECG-(Prolong QT, ST-T changes, VT)

Management:

Target end points for Atropine therapy

Clear lung auscultation

Features of Atropine toxicity

Confusion

Absent bowel sounds

Heart rate 80-100 bpm

Pyrexia

SBP >80 mmHg

Dry axilla

Urinary retention

Pupils no longer pinpoint

Flushing

Airway-positioning, Protection and remove secretions

Breathing-supplemental O, via face mask, early intubation is required if associated with respiratory failure; avoid succinylcholine for intubation

Suganthan

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CS CamScanner

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Circulation- Initiate IV crystalloids

Monitor vitals (Continuous ECG monitoring)

Decontamination (if patient is stable)

0 If ingestion is within 1hour give single dose activated charcoal, adult 50g(1g/kg in children)

0 Perform aggressive dermal and ocular irrigation as needed, discard clothing

If ingestion is within 1-2 hours perform gastric lavage

Cholinergic toxicity - Treated with atropine and oxime therapy (typically pralidoxime)

Atropine competes with acetylcholine at muscarinic receptors (does not bind to

nicotinic receptors).

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Beginning at a dose of 2 to 5 mg IV for adults. If no effect is noted, the dose should be doubled every three to five minutes until pulmonary muscarinic signs and symptoms are alleviated.

After desired response is achieved with boluses, administer 10 to 20 percent of the total cumulative bolus dose as an IV continuous infusion per hour. Adjust the infusion rate as needed to maintain adequate response without causing atropine toxicity. (see table)

When atropine toxicity occurs, hold the infusion until toxicity resolves and restart at 70 to 80 percent of the previous infusion rate.

0 Adjust the infusion according to clinical response and taper until recovery.

Pralidoxime (PAM): Cholinesterase reactivating agents, effective in treating both muscarinic and nicotinic symptoms. PAM should not be administered without concurrent atropine in order to prevent worsening symptoms due to transient oxime-induced acetylcholinesterase inhibition.

Slow 2g IV over 30 minutes (30mg/kg), then

Continuous infusion at 8-10 mg/kg/hour or 30mg/kg IV every 6 hours (for 48

hours or longer)

Seizures - Diazepam 10 mg IV, repeat as necessary. Do not give phenytoin

Inhaled ipratropium 0.5 mg may be helpful for bronchospasm; may repeat the dose

Epinephrine - Consider an epinephrine infusion (2-4 mcg/min) for patients whose heart rate remains below 80 bpm or who remains hypotensive with an adequate heart rate (80-100 bpm) despite receiving high doses of atropine. (Either a cumulative atropine dose of 100mg within 6 h following admission or an infusion of 30 mg/h for at least 3h)

Anticipate and treat bronchopneumonia with appropriate antibiotics.

Tachycardia and mydriasis are not contraindications to atropine use

Organophosphate Poisoning Overview:

  • Definition: Organophosphates are a group of chemicals used in insecticides that inhibit cholinesterase, leading to cholinergic toxicity.

  • Symptoms:

    • Acute Toxicity: Symptoms appear within minutes to hours and include SLUDGE (Salivation, Lacrimation, Urination, Defecation, Gastric Emptying), bradycardia, bronchorrhea, and muscle weakness.

    • Intermediate Syndrome: Occurs 24-96 hours post-exposure, characterized by weakness, decreased reflexes, and respiratory insufficiency.

    • Delayed Neuropathy (OPIDN): Can occur 1-3 weeks after exposure, leading to distal muscle weakness and sensory disturbances.

  • Investigations: Evaluate blood sugar, RBC acetylcholinesterase activity, and ECG changes.

  • Management:

    • Atropine: Initiate atropine therapy for symptomatic relief, adjusting doses based on patient response.

    • Pralidoxime (PAM): Administer concurrently with atropine to reactivate cholinesterase.

    • Supportive Care: Manage seizures, respiratory distress, and provide fluid resuscitation.