Maintainance of op poisoning
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Here is a comprehensive overview of the maintenance/management of organophosphate (OP) poisoning, drawn from multiple authoritative sources:
Organophosphate (OP) Poisoning — Management
1. Mechanism of Toxicity
OP compounds inhibit acetylcholinesterase (AChE), causing accumulation of acetylcholine (ACh) at muscarinic, nicotinic, and CNS receptors. The result is a cholinergic toxidrome:
- Muscarinic (SLUDGE/DUMBELS): Salivation, lacrimation, urination, defecation, GI distress, emesis; also bronchospasm, bronchorrhea, bradycardia, miosis
- Nicotinic: Muscle fasciculations, weakness, paralysis (including respiratory muscles), tachycardia, hypertension
- CNS: Anxiety, seizures, coma, central respiratory depression
Death results from bronchorrhea + respiratory muscle paralysis + CNS depression.
2. Immediate Priorities (ABCs)
| Step | Action |
|---|---|
| Decontamination | Remove all clothing, wash skin/hair/nails with soap and water; protect healthcare workers with neoprene/nitrile gloves (not latex) |
| Airway | Suction secretions; intubate if coma, seizures, respiratory failure, severe bronchospasm |
| Breathing | 100% oxygen via non-rebreather mask; mechanical ventilation as needed |
| Circulation | IV/IO access; cardiac monitor; pulse oximetry |
Note on intubation: Prefer a non-depolarizing paralytic (e.g., rocuronium 1 mg/kg). Succinylcholine is metabolized by cholinesterases and may have prolonged effect (4–6 hours) in OP poisoning.
3. Antidote Therapy
A. Atropine — First-Line, Immediate
Atropine competitively blocks ACh at muscarinic receptors (does not reverse nicotinic/skeletal muscle effects).
| Parameter | Details |
|---|---|
| Initial dose (adult) | 1–3 mg IV (double dose every 5 minutes until secretions dry) |
| Initial dose (child) | 0.05 mg/kg IV |
| Endpoint of atropinization | Drying of respiratory secretions, easing of respiratory effort, heart rate >80 bpm, SBP >80 mmHg |
| Maintenance infusion | 10–20% of total cumulative dose required per hour |
| Total dose | May need 200–500 mg in the first hour in severe cases |
Tachycardia and mydriasis are expected side effects — not a reason to stop atropine. Avoid if anticholinergic toxidrome develops (absent bowel sounds, hyperthermia, delirium).
Atropine does not prevent aging of the OP-AChE complex or reverse nicotinic effects.
B. Pralidoxime (2-PAM) — Oxime, Give Early
Pralidoxime binds the OP-AChE complex and reactivates AChE, reversing both muscarinic and nicotinic effects. Must be given before aging of the complex occurs.
| Parameter | Details |
|---|---|
| Adult dose | 1–2 g IV bolus over 5–10 min; may repeat in 1–2 hr if weakness persists; then Q10–12 hr PRN |
| Child dose | 20–50 mg/kg (max 2 g) IV; may repeat in 1–2 hr |
| Continuous infusion | 8–10 mg/kg/hr (adult); 10–20 mg/kg/hr (child) for 24–48 hr |
| Timing | Give as soon as possible; may still benefit up to 24–48 hr after exposure |
Use pralidoxime in moderate-to-severe poisoning: respiratory failure, fasciculations, seizures, dysrhythmias, hemodynamic instability, or when large/repeated doses of atropine are needed.
Five oximes available worldwide: pralidoxime (2-PAM — USA), trimeodoxime (TMB-4), obidoxime (Toxogonin), methoxime, HI-6.
C. Benzodiazepines
For agitation and seizures — give IV benzodiazepines (e.g., diazepam, lorazepam) after airway is secured.
4. Supportive Care — Things to Avoid
| Avoid | Reason |
|---|---|
| Succinylcholine (if possible) | Prolonged paralysis due to cholinesterase inhibition |
| Beta-blockers | Tachycardia is usually from nicotinic stimulation and resolves with antidotes |
| Ester-type anesthetics | Metabolized by cholinesterases |
5. No Role For
- Gastric lavage — no proven benefit
- Activated charcoal — no proven benefit
- Hemodialysis/enhanced elimination — no role in OP poisoning
6. Monitoring & Disposition
- Cholinesterase levels: Plasma butyrylcholinesterase falls first (easier to assay); RBC acetylcholinesterase is more accurate (reduced to <10% in severe poisoning)
- ECG: Monitor for QTc prolongation, ST changes, AV block, VT/VF
- Asymptomatic patients with normal/minimally depressed cholinesterase levels: observe 6 hours, then discharge with close follow-up
- Significant symptoms (seizures, respiratory compromise): ICU admission
7. Delayed Syndromes — Watch For
| Syndrome | Timing | Features |
|---|---|---|
| Intermediate Syndrome (IMS) | 24–96 hr after cholinergic crisis resolves | Proximal limb weakness, neck flexor weakness, respiratory muscle paralysis |
| OP-induced Delayed Neuropathy (OPIDN) | 7–21 days post-exposure | Distal symmetrical sensorimotor axonopathy, leg cramps → weakness/paralysis |
| Chronic toxicity | Long-term low-level exposure | Cognitive dysfunction, mood changes, peripheral neuropathy, extrapyramidal signs |
8. Special Situations
- Nerve agents (sarin, soman, tabun, VX): Extremely potent OP compounds; soman undergoes rapid aging (within minutes) — very little time to administer antidotes
- Carbamate insecticides: Similar toxidrome but do not age (no permanent binding), shorter duration; atropine is the mainstay; oximes are controversial but recommended if severe or cannot differentiate from OP
- Psychiatric follow-up for patients with suicidal intent once medically stabilized
Sources:
- Rosen's Emergency Medicine, 9th ed. — Ch. 152/201
- Tintinalli's Emergency Medicine — Ch. 201
- Adams and Victor's Principles of Neurology, 12th ed.
- Harriet Lane Handbook, 23rd ed. (Pralidoxime dosing)
- Bradley and Daroff's Neurology in Clinical Practice
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