Organophosphate Poisoning Complications
Acute Complications (Within 4 Weeks)
Respiratory failure from bronchorrhea, bronchospasm, and respiratory muscle paralysis is the leading cause of death during the immediate cholinergic crisis and requires early aggressive atropinization and prompt endotracheal intubation. 1
Life-Threatening Respiratory Complications
- Pulmonary edema develops from excessive muscarinic stimulation and requires aggressive atropinization plus early mechanical ventilation to prevent fatal outcomes 1
- Upper airway obstruction may occur from paralysis of tongue and pharyngeal muscles, with delayed asphyxia from bilateral recurrent laryngeal nerve paralysis reported even after initial stabilization 1
- Vigilant airway monitoring is essential throughout the acute phase 1
Neurological Complications
- Seizures occur in approximately 16.66% of patients and result from central nervous system acetylcholine accumulation 2
- Benzodiazepines (diazepam 5–10 mg IV for adults or 0.2 mg/kg IV for children; midazolam 2–5 mg IV for adults or 0.05–0.1 mg/kg IV for children) are first-line therapy 3
- Anxiety, delirium, and altered mental status are common central nervous system manifestations requiring benzodiazepine treatment 1
Cardiovascular Complications
- Bradycardia occurs in approximately 10% of patients from excessive muscarinic stimulation 2
- Dysrhythmias may develop but should not limit atropine dosing; continuous cardiac monitoring is advised 3
- Atropine-induced tachycardia is an expected pharmacologic effect and is not a contraindication to continued dosing 1
Metabolic Complications
- Hyperglycemia develops in approximately 5% of patients during the acute phase 2
Musculoskeletal and Renal Complications
- Severe myonecrosis results from acetylcholine-induced calcium influx into skeletal muscle, leading to myocyte death 1
- Rhabdomyolysis may follow muscle breakdown; serial monitoring of creatine kinase and potassium is essential for early detection 1
- Myoglobinuric renal failure can develop after extensive rhabdomyolysis; treatment requires aggressive intravenous hydration, forced diuresis, and urine alkalinization when urine becomes reddish from myoglobin (not hemoglobin) 3, 1
Atropine-Related Adverse Effects
- Fever and hallucinations are common with high-dose atropine therapy but do not indicate treatment failure and should not prompt discontinuation 1
- These adverse effects are expected with cumulative doses of 10–20 mg in the first 2–3 hours, with some patients requiring up to 50 mg in 24 hours 4
Intermediate Syndrome (24–96 Hours Post-Exposure)
Between 24 and 96 hours after exposure, patients may develop paralysis of respiratory muscles, neck flexors, proximal limb muscles, and motor cranial nerves, even after successful treatment of the acute crisis; this syndrome responds poorly to additional atropine or pralidoxime. 1
Clinical Presentation
- Respiratory muscle weakness is the most critical feature requiring mechanical ventilation 1
- Proximal limb weakness and cranial nerve palsies develop despite resolution of the initial cholinergic crisis 1
- This syndrome can occur even in patients who did not have severe poisoning on admission 5
Management Approach
- The cornerstone of management is supportive respiratory care in an intensive care setting for several days, as antidotal therapy is ineffective 1
- Endotracheal intubation with mechanical ventilation is preferred over CPAP in patients with a full stomach, bowel paralysis, or inability to cooperate 1
- Premature extubation should be avoided; patients must be fully awake, free of secretions, able to protect their airway, and demonstrate adequate spontaneous breathing before tube removal 1
Delayed Complications (After 4 Weeks)
Late neurological complications are less frequent and less life-threatening than acute complications but can cause significant long-term morbidity. 2
Neurological Sequelae
- Monoplegia and mild sensory loss of lower limbs occur in approximately 2.66% of patients 2
- Paraplegia and upper limb weakness develop in approximately 0.66% of patients 2
- Peripheral neuropathies have been associated with organophosphate exposure 6
- Neuropsychiatric abnormalities and extrapyramidal disorders may develop as delayed syndromes 6
- A myasthenic-like syndrome has been reported following organophosphate exposure 6
Critical Management Principles to Prevent Complications
Immediate Interventions
- Administer atropine immediately (adults 1–2 mg IV; children 0.02 mg/kg IV) and double the dose every 5 minutes until full atropinization is achieved 1
- Give pralidoxime loading dose of 1–2 g IV (adults) or 25–50 mg/kg IV (children) followed by continuous infusion as early as possible—ideally within minutes to hours—before the organophosphate-acetylcholinesterase complex "ages" and becomes irreversible 1
- Start benzodiazepines for seizures immediately 1
Monitoring Duration
- Observe all patients for at least 48–72 hours because delayed complications and relapses can occur, especially after ingestion where gastrointestinal absorption may continue 1
- Resolution of the acute cholinergic crisis does not guarantee safety; intermediate syndrome can emerge up to four days later, necessitating continued observation 1
Healthcare Worker Safety
- Healthcare personnel must wear full personal protective equipment (PPE) before patient contact; secondary exposure from contaminated clothing, skin, or gastric contents has caused severe cholinergic crisis in staff requiring atropine, pralidoxime, and intubation for ≥24 hours 1
- Never allow healthcare workers to handle gastric contents without PPE, as organophosphates in emesis and gastric aspirate can cause severe secondary poisoning 3