Poisoning Emergencies in Critical Care: A Comprehensive Review for Post-Graduate Practitioners

Dr Neeraj Manikath , claude.ai

Abstract

Poisoning emergencies represent a significant burden in critical care units worldwide, with mortality rates varying from 2-15% depending on the agent and timing of presentation. This comprehensive review addresses the management of common and high-mortality poisoning cases encountered in intensive care settings, with emphasis on organophosphate and aluminum phosphide poisoning. We present evidence-based management strategies, clinical pearls, and practical approaches that can significantly impact patient outcomes. The review synthesizes current literature while providing actionable insights for critical care practitioners managing these complex cases.

Keywords: Poisoning, Critical Care, Organophosphates, Aluminum Phosphide, Antidotes, Emergency Medicine

Introduction

Acute poisoning accounts for approximately 300,000 deaths globally each year, with developing countries bearing a disproportionate burden. In critical care settings, poisoned patients present unique challenges requiring rapid diagnosis, aggressive supportive care, and specific antidotal therapy. The "golden hour" concept is particularly relevant in toxicology, where early recognition and intervention can dramatically alter outcomes.

Modern critical care management of poisoning has evolved beyond basic supportive care to include sophisticated extracorporeal techniques, targeted antidotal therapy, and precision monitoring. This review focuses on high-impact poisoning scenarios commonly encountered in intensive care units, emphasizing practical management strategies that can be immediately implemented.

General Principles of Critical Care Toxicology

Initial Assessment and Stabilization

The ABCDE approach remains paramount, with toxicology-specific modifications:

Airway Management:

Early intubation considerations for altered mental status (GCS ≤8)
Anticipate difficult airway in caustic ingestions
Consider neuromuscular blockade reversal in organophosphate cases

Breathing:

High-flow oxygen for carbon monoxide, hydrogen sulfide
Mechanical ventilation adjustments for pulmonary edema (cardiogenic vs. non-cardiogenic)

Circulation:

Aggressive fluid resuscitation vs. cautious approach (agent-dependent)
Early vasopressor consideration in distributive shock patterns

Clinical Pearl: The "toxidrome approach" remains valuable but should not delay supportive care. Many severe poisonings present with mixed or atypical features.

Decontamination Strategies

Gastrointestinal Decontamination:

Activated charcoal: 1g/kg (max 50g) within 1 hour for most ingestions
Contraindications: Altered mental status without protected airway, caustic ingestions, hydrocarbons
Whole bowel irrigation: Consider for sustained-release preparations, iron, lithium

Oyster Alert: Gastric lavage is rarely indicated and may increase aspiration risk. Reserve for life-threatening ingestions within 1 hour of presentation.

Enhanced Elimination Techniques

Hemodialysis Indications (SLIME mnemonic):

Salicylates (>100 mg/dL acute, >60 mg/dL chronic)
Lithium (>4.0 mEq/L acute, >2.5 mEq/L chronic with symptoms)
Isopropanol/methanol/ethylene glycol
Metformin (with lactic acidosis)
Ethylene glycol/methanol

High-Priority Poisoning Emergencies

Organophosphate Poisoning

Organophosphate (OP) compounds, including pesticides and chemical warfare agents, cause irreversible acetylcholinesterase inhibition leading to cholinergic crisis. With global pesticide consumption exceeding 4 million tons annually, OP poisoning remains a leading cause of suicide in agricultural regions.

Pathophysiology

OP compounds bind covalently to acetylcholinesterase, preventing acetylcholine breakdown. This leads to:

Muscarinic effects: SLUDGE syndrome (Salivation, Lacrimation, Urination, Defecation, Gastrointestinal distress, Emesis)
Nicotinic effects: Muscle fasciculations, weakness, paralysis
CNS effects: Seizures, coma, respiratory depression

Clinical Presentation

Acute Phase (minutes to hours):

Miosis (pinpoint pupils)
Excessive secretions (bronchial, salivary)
Muscle fasciculations progressing to paralysis
Seizures and altered mental status

Intermediate Syndrome (24-96 hours):

Weakness of neck flexors, proximal limbs, respiratory muscles
No fasciculations or excessive secretions
May require prolonged mechanical ventilation

Management Protocol

1. Immediate Supportive Care:

• Secure airway early - expect rapid deterioration
• High-flow oxygen, prepare for mechanical ventilation
• Large-bore IV access
• Continuous cardiac monitoring
• Seizure precautions

2. Antidotal Therapy:

Atropine Protocol:

Loading dose: 2-5 mg IV bolus (pediatric: 0.02-0.05 mg/kg)
Titration endpoint: Clear lung secretions, NOT pupil size
Maintenance: Double dose every 5-10 minutes until secretions clear
Infusion: Start at 10-20% of total loading dose per hour

Clinical Hack: Monitor heart rate during atropine administration. Paradoxical bradycardia may occur initially due to central cholinergic stimulation.

Pralidoxime (2-PAM) Protocol:

Timing: Most effective within 24 hours (preferably within 8 hours)
Loading dose: 1-2g IV over 15-30 minutes
Maintenance: 200-500 mg/hour continuous infusion
Duration: Continue until muscle strength returns and cholinesterase levels normalize

Pearl: Pralidoxime effectiveness decreases with time due to "aging" of the organophosphate-enzyme complex. Early administration is crucial.

3. Advanced Supportive Care:

Ventilatory support: May require days to weeks
Seizure control: Benzodiazepines first-line, avoid phenytoin
Fluid management: Cautious approach due to increased secretions

Monitoring Parameters

• Cholinesterase levels (RBC and plasma)
• Arterial blood gases
• Electrolytes (hypokalemia common)
• Continuous EKG monitoring
• Daily chest X-rays
• Neurological assessments

Prognosis and Complications

Mortality ranges from 10-30%, primarily due to respiratory failure. Long-term sequelae may include:

Organophosphate-induced delayed neuropathy (OPIDN)
Chronic neuropsychiatric effects
Recurrent paralysis episodes

Aluminum Phosphide (Celphos) Poisoning

Aluminum phosphide (AlP) is a highly toxic fumigant widely used for grain storage. Upon contact with moisture, it releases phosphine gas (PH₃), causing severe cellular toxicity. Case fatality rates exceed 70%, making it one of the most lethal agricultural poisons.

Pathophysiology

Phosphine gas disrupts cellular respiration by:

Inhibiting cytochrome c oxidase
Causing lipid peroxidation
Disrupting cellular membrane integrity
Leading to multiorgan failure

Clinical Presentation

Gastrointestinal Phase (0-6 hours):

Severe nausea, vomiting
Epigastric pain
Garlic-like breath odor
Silver nitrate paper test positive

Cardiovascular Collapse (6-24 hours):

Refractory hypotension
Cardiogenic shock
Arrhythmias (VT/VF common)
Acute coronary syndrome pattern

Multiorgan Failure (>24 hours):

ARDS
Acute kidney injury
Hepatic failure
Metabolic acidosis

Management Strategy

1. Immediate Resuscitation:

• Aggressive fluid resuscitation (crystalloids preferred)
• Early vasopressor support (norepinephrine first-line)
• Avoid sodium bicarbonate (may enhance phosphine release)
• Secure airway for impending respiratory failure

2. Specific Therapeutic Interventions:

Magnesium Sulfate Protocol:

Dose: 3g IV infusion over 3 hours
Mechanism: Stabilizes cellular membranes, antiarrhythmic effects
Monitoring: Serum magnesium levels, deep tendon reflexes
Repeat: Every 6-8 hours based on clinical response

Clinical Pearl: Magnesium sulfate has shown mortality benefit in several case series, though randomized data remains limited.

3. Advanced Life Support Considerations:

ECMO Candidacy Assessment:

Age <60 years with reversible organ dysfunction
Refractory cardiogenic shock despite maximal therapy
No contraindications to anticoagulation
Early presentation (<24 hours)

ECMO Configuration:

Veno-arterial (VA) ECMO for cardiac support
Target flows 60-80 ml/kg/min
Anticoagulation with heparin (ACT 160-180 seconds)

Supportive Care Measures

Cardiovascular:

Continuous hemodynamic monitoring
Echocardiography for cardiac function assessment
Avoid digoxin (increased arrhythmogenicity)

Pulmonary:

Lung-protective ventilation strategies
PEEP optimization for ARDS
Consider prone positioning

Renal:

Early nephrology consultation
Continuous renal replacement therapy if indicated
Maintain euvolemia

Monitoring and Prognostic Indicators

Laboratory Monitoring:

• Serial troponins, BNP
• Comprehensive metabolic panel q6h
• Lactate levels
• Phosphine gas levels (if available)
• Coagulation studies

Poor Prognostic Indicators:

Lactate >4 mmol/L on presentation
Troponin elevation >10x normal
Refractory shock requiring >0.5 mcg/kg/min norepinephrine
Development of ARDS within 12 hours

Other Critical Poisoning Scenarios

Methanol/Ethylene Glycol Poisoning

Oyster: Osmolar gap may normalize as parent compound is metabolized, but anion gap acidosis persists.

Management Pearls:

Fomepizole: 15 mg/kg loading, then 10 mg/kg q12h
Dialysis indications: pH <7.3, vision changes (methanol), renal failure
Continue antidote until methanol/ethylene glycol levels <20 mg/dL

Salicylate Poisoning

Clinical Hack: Mixed acid-base disorder is pathognomonic - respiratory alkalosis with metabolic acidosis.

Critical Management:

Alkaline diuresis: Target urine pH 7.5-8.0
Avoid intubation if possible (loss of compensatory hyperventilation)
Dialysis for levels >100 mg/dL (acute) or CNS symptoms

Carbon Monoxide Poisoning

Pearl: Normal pulse oximetry doesn't exclude CO poisoning - obtain co-oximetry.

Hyperbaric Oxygen Indications:

COHb >25% (>15% if pregnant)
Loss of consciousness
Cardiac ischemia
Neurological symptoms

Special Populations and Considerations

Pediatric Considerations

Dosing Modifications:

Atropine: 0.02-0.05 mg/kg (minimum 0.1 mg)
Pralidoxime: 25-50 mg/kg loading dose
Activated charcoal: 1 g/kg (maximum 25g in children <12 years)

Clinical Pearls:

Children decompensate rapidly - lower threshold for intubation
Weight-based dosing critical for antidotes
Consider non-accidental trauma in recurrent poisonings

Pregnancy Considerations

Management Principles:

Treat mother aggressively - maternal stability ensures fetal viability
Most antidotes safe in pregnancy (atropine, pralidoxime, fomepizole)
Consider perimortem cesarean section if gestational age >24 weeks

Geriatric Considerations

Modified Approach:

Lower threshold for dialysis (decreased clearance)
Careful fluid management (heart failure risk)
Polypharmacy interactions consideration
Increased susceptibility to delirium

Quality Improvement and Systems Approach

Critical Care Team Coordination

Immediate Response Team:

Intensivist
Clinical pharmacist
Respiratory therapist
Nephrology (for dialysis candidates)
Toxicologist (consultation)

Documentation and Communication

Essential Documentation:

• Substance identification and quantity
• Time of exposure/ingestion
• Initial vital signs and mental status
• Antidote administration times and doses
• Response to therapy
• Complications and interventions

Poison Control Center Utilization

24/7 Consultation Available:

United States: 1-800-222-1222
Dose calculations and protocols
Antidote availability and sourcing
Disposition recommendations

Future Directions and Research

Emerging Therapies

Novel Antidotes in Development:

Cobinamide for hydrogen sulfide poisoning
Improved organophosphate scavengers
Targeted cellular protectants for aluminum phosphide

Technological Advances:

Rapid toxicology screening platforms
Artificial intelligence for poisoning pattern recognition
Telemedicine for remote toxicology consultation

Precision Medicine Approaches

Pharmacogenomics:

CYP2D6 polymorphisms affecting drug metabolism
Personalized antidote dosing algorithms
Biomarker-guided therapy selection

Conclusion

Poisoning emergencies in critical care require rapid recognition, aggressive supportive care, and timely antidotal therapy. The management of organophosphate poisoning centers on early atropine administration titrated to clear secretions and pralidoxime within the critical 24-hour window. For aluminum phosphide poisoning, the combination of aggressive supportive care, magnesium sulfate therapy, and consideration for ECMO in appropriate candidates offers the best chance for survival.

Success in critical care toxicology depends on systematic approaches, team coordination, and maintaining high clinical suspicion. The integration of traditional supportive care with targeted therapies, enhanced elimination techniques, and emerging technologies continues to improve outcomes in these challenging cases.

Critical care practitioners must remain vigilant for the evolving landscape of toxicological emergencies while maintaining proficiency in time-tested interventions that save lives. The principles outlined in this review provide a framework for managing these complex cases while emphasizing the importance of early recognition and aggressive intervention.

Key Clinical Pearls Summary

Atropine titration: Endpoint is clearing lung secretions, not pupil size
Pralidoxime timing: Maximum benefit within 8 hours, diminishing returns after 24 hours
Magnesium for AlP: 3g IV over 3 hours may reduce mortality
ECMO consideration: Early evaluation for refractory AlP poisoning in appropriate candidates
Avoid sodium bicarbonate: In AlP poisoning (enhances phosphine release)
Osmolar gap limitation: May normalize while anion gap acidosis persists
CO-oximetry essential: Pulse oximetry unreliable in CO poisoning

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Conflicts of Interest: None declared Funding: None

Sunday, August 17, 2025