Organophosphate/Cholinergic Poisoning Management
This clinical presentation—pinpoint pupils (1mm), defecation, and tachycardia—is most consistent with organophosphate or carbamate poisoning, and immediate treatment requires atropine titrated to dry secretions, pralidoxime for organophosphates, benzodiazepines for seizures, and aggressive airway management. 1
Immediate Recognition and Stabilization
The triad of miosis (pinpoint pupils), defecation, and paradoxical tachycardia suggests cholinergic toxicity, though the tachycardia is atypical and may indicate:
- Nicotinic receptor stimulation (causing tachycardia despite muscarinic effects) 1
- Severe hypoxia from respiratory failure (the most common cause of death in organophosphate poisoning) 1
- Mixed toxidrome from co-ingestion
Contact poison control immediately for specialized guidance, as organophosphate poisoning requires toxicological expertise that most clinicians rarely encounter 1, 2
Critical First Steps
Airway and Breathing Priority
- Secure airway immediately if the patient shows signs of respiratory distress, excessive secretions, or altered mental status 1, 3
- Provide bag-mask ventilation or intubation as needed—respiratory failure is the primary cause of death 1
- Suction copious secretions aggressively 1
Antidote Administration
Atropine is the cornerstone of treatment:
- Start with 2-5 mg IV bolus (higher doses than typical ACLS) 1
- Double the dose every 3-5 minutes until secretions dry (bronchorrhea resolves) 1
- Endpoint is drying of secretions, NOT pupil size or heart rate 1
- Massive doses may be required (hundreds of milligrams over hours to days) 1
Pralidoxime (2-PAM) for organophosphates specifically:
- Administer 1-2 grams IV over 15-30 minutes as soon as possible 1
- Most effective when given within 24-48 hours before "aging" of the enzyme occurs 1
- Continue as infusion (500 mg/hour) for severe cases 1
Seizure Management
- Benzodiazepines (diazepam or midazolam) are first-line for seizures 1, 3, 4
- Administer early and aggressively, as seizures worsen outcome 1
Decontamination Considerations
For dermal exposure:
- Remove all clothing immediately and double-bag to prevent secondary contamination of healthcare workers 1
- Irrigate skin with copious soap and water for at least 15 minutes 2
For ingestion:
- Do NOT induce vomiting—this is contraindicated and increases aspiration risk 2, 3, 4, 5
- Activated charcoal may be considered if ingestion occurred within 1 hour and airway is protected, but do not delay definitive treatment 3, 4
Diagnostic Workup
Obtain immediately:
- Arterial blood gas (look for hypoxemia and metabolic acidosis) 2
- Serum cholinesterase levels (red blood cell and plasma)—though treatment should NOT be delayed waiting for results 1
- ECG to assess for QT prolongation and dysrhythmias 6
- Comprehensive metabolic panel including electrolytes, creatinine, and glucose 2, 6
Critical Pitfalls to Avoid
Do not wait for confirmatory testing before initiating atropine and pralidoxime—treat based on clinical presentation 1, 7
Do not under-dose atropine—the required doses are far higher than typical medical use, and inadequate atropinization leads to death from respiratory failure 1
Do not confuse with opioid toxicity—while both cause miosis, opioids cause bradycardia and respiratory depression without the secretory/GI symptoms seen here 1
Tachycardia in this context is a red flag for either severe nicotinic stimulation, hypoxia, or inadequate atropinization—address the underlying cause aggressively 1
Healthcare worker safety is paramount—organophosphates can cause secondary contamination through contact with patient's clothing, skin, or secretions 1