Management of OP Poisoning 2nd year mbbs

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Organophosphate (OP) Poisoning - Management

1. Quick Recap: Mechanism

Organophosphates (e.g., malathion, parathion, chlorpyrifos) irreversibly inhibit acetylcholinesterase (AChE) by phosphorylating its active site. This causes acetylcholine (ACh) to accumulate at all cholinergic synapses - muscarinic, nicotinic (autonomic ganglia + NMJ), and CNS.

Aging: The OP-AChE bond becomes permanently irreversible after a period called "aging" (ranges from minutes to >24 hours depending on agent). Once aging occurs, oximes cannot regenerate AChE; new enzyme must be resynthesized over weeks.

Rosen's Emergency Medicine, p. 3028

2. Clinical Features (Know Your Mnemonics!)

Muscarinic Effects - "SLUDGE" / "DUMBELS" / "Killer Bs"

Mnemonic	Effect
S	Salivation
L	Lacrimation
U	Urinary incontinence
D	Defecation / Diarrhea
G	GI cramping
E	Emesis
"Killer Bs"	Bradycardia, Bronchorrhea, Bronchospasm

Also: Miosis (pinpoint pupils), sweating, increased bowel sounds.

Nicotinic Effects (NMJ + sympathetic ganglia)

Muscle fasciculations, cramps, weakness (including diaphragm)
Tachycardia, hypertension, pallor, diaphoresis
Mydriasis (can oppose miosis)

CNS Effects

Anxiety, restlessness, emotional lability
Tremors, seizures
Coma, respiratory depression

Key point: Death in OP poisoning is usually from respiratory failure (bronchospasm + bronchorrhea + diaphragm paralysis + CNS depression).

Tintinalli's Emergency Medicine, p. 1343

3. Four Clinical Syndromes

Acute poisoning - within 8-24 hrs; full SLUDGE/nicotinic/CNS picture
Intermediate syndrome - 24-96 hrs after acute episode; proximal limb weakness, cranial nerve palsies, neck flexor weakness (not related to AChE inhibition)
Organophosphate-induced delayed neuropathy (OPIDN) - 2-3 weeks later; distal sensorimotor polyneuropathy
Chronic toxicity - subtle CNS complaints, mild visual disturbances, chronic GI symptoms

4. Management

Step 1 - Decontamination (FIRST priority)

Remove all clothing and place in sealed plastic bags (hazardous waste)
Wash skin thoroughly with soap and water (copious amounts) - include scalp, hair, skin folds, nails, conjunctivae
Healthcare workers must wear neoprene/nitrile gloves (NOT latex - latex is permeable to OPs)
Avoid abrasion of skin; contain contaminated runoff

Step 2 - Supportive Care / Stabilization

Oxygen via 100% non-rebreather mask
Cardiac monitor + pulse oximetry
IV access + baseline blood sampling (including cholinesterase levels)
Gentle suctioning of airway secretions
Endotracheal intubation if: coma, seizures, respiratory failure, excessive secretions, severe bronchospasm
AVOID succinylcholine for intubation - it is metabolized by plasma butyrylcholinesterase (inhibited by OPs), causing prolonged paralysis. Use a non-depolarizing agent
Hypotension: IV isotonic crystalloid boluses

Step 3 - Antidote Therapy

A. ATROPINE (Anticholinergic - Muscarinic Blocker)

Competitive antagonist of ACh at muscarinic receptors (does NOT work at nicotinic receptors - will not reverse muscle paralysis)
Indication: Significant poisoning with muscarinic symptoms (excessive secretions, bronchospasm, bradycardia)

Parameter	Adult Dose
Initial dose	1-3 mg IV (0.05 mg/kg in children)
Repeat interval	Double every 5 minutes until atropinized
Maintenance	Infusion at 10-20% of total loading dose per hour
Total required	Can be 200-500 mg in the first hour in severe cases

Endpoints of atropinization (TARGET):

✅ Chest clear on auscultation (dried secretions = most important endpoint)
✅ Heart rate >80 bpm
✅ Systolic BP >80 mmHg
✅ Dry skin and mucous membranes

NOT endpoints: Pupillary dilation is NOT a therapeutic endpoint. Tachycardia is NOT a contraindication.

Key exam point: Absence of anticholinergic effects after an initial large atropine dose is itself diagnostic of OP poisoning (confirms the muscarinic excess).

B. PRALIDOXIME / 2-PAM (Oxime - AChE Reactivator)

Binds to the OP-AChE complex and regenerates the enzyme
Reverses all effects - muscarinic, nicotinic (especially muscle paralysis), and CNS
Must be given EARLY, before aging occurs

Parameter	Dose
WHO recommended dose	30 mg/kg IV bolus over 15-30 min
Maintenance infusion	8 mg/kg/hour IV
Alternative (common)	1-2 g IV over 30 min; repeat hourly as needed
Duration	Continue 24-48 hrs (or up to 7 days); stop when asymptomatic off drug

Indications for pralidoxime:

Respiratory depression or failure
Muscle fasciculations
Seizures
Need for large/repeated atropine doses
Dysrhythmias, hemodynamic instability

Note: Pralidoxime is NOT recommended for carbamate poisoning (carbamates do not age and spontaneously reactivate AChE).

C. BENZODIAZEPINES (for seizures)

Diazepam or lorazepam IV for seizure control
Combined with atropine (which may prevent/abort early cholinergic seizures)

Step 4 - GI Decontamination (Limited Role)

Gastric lavage: Only if within 1 hour of large ingestion AND airway already protected (intubated). No proven outcome benefit.
Activated charcoal: OPs bind in vitro, but no clinical evidence of improved outcome.
Hemodialysis/hemoperfusion: No proven value.

5. Drugs to AVOID

Drug	Why to Avoid
Succinylcholine	Prolonged paralysis (butyrylcholinesterase inhibited)
Ester-type local anesthetics (procaine, cocaine)	Metabolized by pseudocholinesterase
Beta-blockers	May potentiate bradycardia and bronchospasm
Morphine	Respiratory depression
Aminoglycosides	May worsen neuromuscular blockade

6. Monitoring & Disposition

Serum cholinesterase levels (RBC AChE more specific; plasma BuChE quicker to measure)
Minimal exposure: Decontamination + 6-8 hours ED observation
Significant poisoning: ICU admission
Recovery: Most patients recover within 10 days if treated early without hypoxic brain damage
Fat-soluble OPs may cause prolonged symptoms (weeks), requiring continuous pralidoxime

7. Summary Table

Drug	Mechanism	Reverses	Dose
Atropine	Blocks muscarinic receptors	Muscarinic effects only	1-3 mg IV; double every 5 min
Pralidoxime (2-PAM)	Reactivates AChE	Muscarinic + nicotinic + CNS	30 mg/kg IV bolus; 8 mg/kg/hr infusion
Benzodiazepines	GABA-A agonist	Seizures	Diazepam 5-10 mg IV

High-Yield Exam Points

Miosis (pinpoint pupils) is the hallmark - NOT mydriasis
Atropine targets muscarinic effects; pralidoxime also targets nicotinic effects
"Killer Bs" - Bradycardia, Bronchorrhea, Bronchospasm - the life-threatening triad
Endpoint of atropine = drying of secretions (not pupil dilation)
AVOID succinylcholine for intubation
Pralidoxime must be given before aging to be effective
Carbamate poisoning = atropine yes, pralidoxime NOT recommended

Sources: Tintinalli's Emergency Medicine (p. 1343-1344); Rosen's Emergency Medicine (pp. 3027-3030)

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