Selphos (Aluminium Phosphide) Poisoning

Formulation

• Gray-green tablets, each weighing 3 g, containing 56% active ingredient mixed with urea and ammonium carbonate
• Each tablet liberates 1 g of phosphine gas (PH3)
• Primarily used as a grain fumigant to destroy insects and rodents in stored grain

Mechanism of Toxicity

AlP + 3H2O → Al(OH)3 + PH3 (phosphine gas)

• Mitochondrial dysfunction - inhibits cytochrome c oxidase (complex IV), blocking cellular respiration
• Oxidative stress - generates reactive oxygen species, lipid peroxidation
• Inhibits multiple enzyme systems including catalase and cholinesterase
• Results in multi-organ failure: cardiovascular collapse is the principal cause of death

Fatal Dose and Period

Signs and Symptoms

• Nausea, vomiting, burning epigastric pain
• Intense thirst and diarrhoea
• Garlicky/fishy odour from breath (characteristic)

• Hypotension and shock
• ECG abnormalities: sinus tachycardia, bradycardia, heart block
• Arrhythmias
• Myocardial damage, pericarditis, congestive cardiac failure

• Tightness in chest, dyspnoea
• Severe pulmonary oedema (from inhaled phosphine)
• Respiratory distress in terminal stages

• Excitement and agitation (early)
• Hypocalcaemia, tetany, convulsions, coma
• Oliguria
• Metabolic acidosis
• Cold clammy skin

• P C Dikshit Textbook of Forensic Medicine and Toxicology, p. 573-574
• Parikh's Textbook of Medical Jurisprudence Forensic Medicine and Toxicology, p. 679

Diagnosis

• History of ingestion / exposure
• Characteristic garlicky odour

• Ask the patient to breathe on filter paper impregnated with 0.1 N silver nitrate for 5-10 minutes
• Paper turns black if phosphine is present (silver nitrate is reduced to metallic silver)

• Serial blood phosphine levels
• ABG (metabolic acidosis), serum electrolytes, ECG monitoring
• Serum magnesium, calcium
• Cardiac enzymes (myocardial damage)
• NT-proBNP (predictive biomarker for mortality)

Management

Immediate / Decontamination

• Remove patient from source of exposure
• Wash skin with soap and water (AlP can absorb through skin)
• Healthcare workers must use full-face masks and gloves - do NOT perform mouth-to-mouth; phosphine off-gassing from vomit is hazardous
• Gastric lavage with 3-5% sodium bicarbonate, 1% copper sulphate, 1% potassium permanganate, or mineral/coconut oil - these convert AlP to phosphate within 30 minutes
  • Note: Some recent evidence questions routine gastric lavage since moisture contact during the procedure may accelerate phosphine generation
• Oil-based decontamination (coconut oil) has shown benefit in some studies; a 2024 systematic review and meta-analysis supports oil-based gastric lavage

Supportive Treatment

Emerging/Investigated Therapies

• Intravenous lipid emulsion (ILE) - shown benefit in case reports and a 2024 RCT (acts as lipid sink for lipophilic phosphine)
• Glucose-insulin-potassium (GIK) infusion - pilot RCT showed some benefit for myocardial support
• High-dose insulin therapy - under study (RCT published 2024)
• Hyperbaric oxygen therapy - rare successful cases reported; limited evidence
• Monitoring for 72 hours minimum; continuous cardiac monitoring mandatory

Medicolegal Aspects

• Common method of suicide in rural India, especially in Haryana, Punjab, Uttar Pradesh, and Rajasthan
• Used in dowry deaths (homicidal poisoning) in rural India - only a fragment of a tablet is sufficient
• The resemblance of tablets to medicinal preparations makes accidental ingestion possible
• Autopsy findings include congestion of all organs and frothy fluid in airways

Key Points to Remember

1. Phosphine is the actual toxin, not AlP itself
2. Garlicky/fishy breath odour is the clinical hallmark
3. No antidote exists - all treatment is supportive
4. Cardiac failure (cardiogenic shock) is the primary cause of death
5. Magnesium sulphate is the cornerstone drug for arrhythmias
6. Coconut/mineral oil lavage may reduce phosphine liberation in the stomach
7. High mortality even with aggressive ICU care

Selphos (Aluminium Phosphide) Poisoning - Harrison's 22E Perspective

Important clarification upfront

Harrison's General Framework Applied to Selphos Poisoning

1. Treatment Goals (Harrison's Table 470-3)

2. Supportive Care (Harrison's priority)

• Airway protection - early intubation if respiratory distress or pulmonary oedema develops
• Oxygenation/ventilation - oxygen for hypoxia; positive pressure ventilation for pulmonary oedema
• Treatment of arrhythmias - magnesium sulphate is the agent of choice (IV 3 g bolus, then infusion)
• Haemodynamic support - IV fluids, vasopressors (dopamine/noradrenaline) for refractory shock
• Correction of metabolic derangements - sodium bicarbonate for metabolic acidosis; calcium for hypocalcaemia
• Treatment of seizures - benzodiazepines
• Prevention of secondary complications - ICU monitoring, treat infections

3. GI Decontamination (Harrison's principles)

• Time since ingestion (efficacy drops sharply after 1 hour)
• Severity of expected toxicity
• Risk of complications

• Activated charcoal - Harrison's preferred decontamination method generally, but its efficacy for AlP is uncertain (AlP is an inorganic compound; Harrison's notes that "charged chemicals and inorganic compounds are not well adsorbed by charcoal")
• Gastric lavage - Harrison's reserves this for "life-threatening poisons not treatable by other means" - AlP qualifies. However, a unique concern with AlP is that adding moisture during lavage accelerates phosphine liberation; oil-based lavage (coconut oil/liquid paraffin) is preferred over water to avoid this
• Skin decontamination - wash with soap and water (AlP is dermally absorbed)

4. Enhancement of Elimination

• No extracorporeal method has proven effective for eliminating phosphine
• Hyperbaric oxygen - listed by Harrison's as a modality; isolated case reports suggest benefit in AlP, though evidence remains very limited
• Haemoperfusion/CVVH may assist multi-organ support, not phosphine elimination per se

5. Antidotes

• Magnesium sulphate (physiologic antagonism for arrhythmias)
• N-acetylcysteine, glutathione (antioxidants - metabolic support)
• Intravenous lipid emulsion (ILE) - emerging evidence; acts as a lipid sink
• Glucose-insulin-potassium (GIK) - myocardial support
• Sodium bicarbonate - metabolic antagonism of acidosis

6. Harrison's Global Considerations Note

Bottom Line

• Harrison's Principles of Internal Medicine 22E, Chapter 470: Poisoning and Drug Overdose, pp. 3749-3758

Rat Poison - Classification and Poisoning

1. Aluminium Phosphide / Zinc Phosphide (Phosphide Rodenticides)

Aluminium Phosphide (Celphos, Selphos, Alphos, Quickphos)

AlP + moisture → Al(OH)3 + PH3

• Inhalation of >400-600 ppm phosphine is fatal within 1 hour

• Rapidly absorbed from GI tract by simple diffusion
• Some ALP is absorbed intact and metabolized in the liver (slow phosphine release - prolongs symptoms)
• Phosphine is oxidized to oxyacids and excreted in urine as hypophosphite; also excreted unchanged through lungs

• GIT: Nausea, vomiting, diarrhoea, retrosternal pain
• CVS: Hypotension, shock, arrhythmias, myocarditis, pericarditis, acute CCF - cardiogenic shock is the most common cause of death
• Respiratory: Cough, dyspnoea, cyanosis, pulmonary oedema, respiratory failure
• Hepatic: Jaundice, hepatitis, hepatomegaly
• Renal: Renal failure
• CNS: Headache, dizziness, altered mental state, restlessness, convulsions, hypoxic encephalopathy, coma
• Rare: Muscle wasting, bleeding diathesis (widespread capillary damage), massive GI bleeding

• Garlic-like odour at mouth, nostrils, and gastric contents
• Blood-stained froth in mouth and nostrils
• Congestion of lower oesophagus, stomach, and duodenum mucosa
• Lungs, liver, spleen, kidneys, and brain all congested
• Centrizonal haemorrhagic necrosis of liver

Stomach in aluminium phosphide poisoning - severe haemorrhagic congestion (Courtesy: Dr Manoj Kumar, AIIMS Patna)

• Stomach: Congestion, oedema, leucocytic infiltration, sloughing of gastric mucosa
• Lungs: Congestion, oedema, desquamation of respiratory epithelium, thickened alveoli
• Kidneys: Congestion, necrosis, tubular degeneration
• Adrenals: Congestion, haemorrhage, cortical lipid depletion
• Heart: Congestion, oedema, fibre fragmentation, focal necrosis

1. Mix 5 mL gastric aspirate + 15 mL water in a flask; cover with filter paper impregnated with 0.1 N silver nitrate; heat at 50°C for 15-20 min → paper turns black if PH3 present
2. Patient breathes through silver nitrate-impregnated filter paper mask for 5-10 min → blackening confirms phosphine (positive in breath only if >6 g ALP ingested)

Zinc Phosphide

• Steel-grey crystalline powder with garlicky/fishy odour
• Used as grain preservative and rodenticide
• Same mechanism as ALP - releases phosphine gas on contact with moisture
• Difference: Slower onset (gradual phosphine release); symptoms mimic ALP poisoning
• Death from pulmonary oedema within a few hours, or cardiovascular collapse within 30 hours
• Management same as ALP

2. Long-Acting Anticoagulant Rodenticides (LAARs)

Brodifacoum / Superwarfarins (Bromadiolone, Difenacoum)

• Bleeding diathesis is the hallmark - gross haematuria, oral mucosal bleeding, epistaxis, GI bleeding
• Deaths reported in severe cases
• Notable 2018 US outbreak: >300 patients poisoned by brodifacoum-tainted synthetic cannabinoids

• Markedly prolonged INR (mean INR ~15)
• Selective deficiency of vitamin K-dependent factors (II, V, VII, IX)
• Confirmation: LAAR levels by high-performance liquid chromatography (HPLC)

1. Oral vitamin K1 - all patients; twice-daily dosing, titrate to clinical/lab response
2. IV vitamin K1 - if actively bleeding, for rapid INR correction
3. 4-factor PCC or FFP - for major/life-threatening bleeding
4. Median treatment duration: 140 days (range up to 730 days) - due to fat solubility and high volume of distribution
5. Discontinue vitamin K1 only when INR is consistently normal without it

3. Barium Carbonate

• Profound hypokalaemia
• Prominent U waves on ECG (direct inhibition of cardiac KIR channels)
• Muscle paralysis (inhibition of muscle KIR channels)
• Cardiovascular arrhythmias

• Potassium supplementation (increases plasma K+ and displaces barium from K+ channels)
• Haemodialysis - effective

Summary Comparison

• The Essentials of Forensic Medicine and Toxicology 36th ed. (2026), pp. 499-500
• Brenner and Rector's The Kidney, Chapter on Hypokalaemia
• Henry's Clinical Diagnosis and Management by Laboratory Methods, p. 1510 (Brodifacoum/LAARs)

Organophosphorus (OP) Poisoning

Overview

Mechanism of Toxicity

Clinical Features

Four Clinical Syndromes

Acute Poisoning - The Cholinergic Toxidrome

Muscarinic Effects (mnemonic: SLUDGE / DUMBELS)

• Bradycardia
• Bronchorrhoea
• Bronchospasm

Nicotinic Effects (NMJ and sympathetic ganglia)

• Muscle fasciculations, cramps, weakness
• Paralysis (including diaphragm) → respiratory failure
• Mydriasis, pallor (sympathetic ganglionic stimulation)
• Tachycardia, hypertension (may compete with parasympathetic bradycardia; mixed picture is common)

CNS Effects

• Anxiety, restlessness, emotional lability
• Tremor, headache, dizziness
• Confusion, delirium, hallucinations
• Seizures, coma

Death is most commonly due to respiratory failure - from a combination of bronchorrhoea + bronchospasm + respiratory muscle paralysis.

Other Complications

• Abdominal pain; pancreatitis (rare); peritonitis (rare)
• Myocardial ischaemia in severe toxicity
• Aspiration pneumonia / lipoid pneumonia from hydrocarbon solvents in formulation
• QTc prolongation and arrhythmias

Intermediate Syndrome (IMS)

• Occurs 1-5 days after acute cholinergic phase resolves (reported in up to 40% of ingestions)
• No cholinergic signs - this is key to distinguishing it
• Features: paralysis of neck flexors, cranial nerve-innervated muscles, proximal limb muscles, and respiratory muscles (may need ventilation)
• EMG may assist diagnosis
• Usually resolves within 7 days
• Nerve agents do NOT cause IMS

Diagnosis

• Characteristic hydrocarbon or garlic-like odour
• Pinpoint pupils (miosis) + excessive sweating + hypersecretions + breathing difficulty = classic severe presentation
• Altered mental status

• Plasma BuChE may be depressed 50% in asymptomatic patients - clinical correlation required
• Poor standardisation of normal ranges between labs

Management

1. Decontamination and Stabilisation

• Remove from exposure immediately
• Skin decontamination - remove clothing, wash with soap and water (wear gloves - risk of secondary contamination)
• Eye decontamination - irrigate with water
• Airway first - early intubation if respiratory distress, excessive secretions, or declining consciousness
• IV access and cardiac monitoring
• GI decontamination - activated charcoal (1 g/kg) if ingestion is recent and airway is protected; gastric lavage for large ingestions

2. Atropine (Antidote for Muscarinic Effects)

• Adults: Initial 1.2-3 mg IV (depending on severity)
• Double the dose every 5 minutes until therapeutic endpoint is reached
• Very large amounts (hundreds of milligrams) may be needed in massive ingestions

Pupillary dilatation is NOT a therapeutic endpoint. Tachycardia is NOT a contraindication - tachycardia can be secondary to bronchospasm + hypoxia and may actually improve with atropine.

Important: Atropine dries secretions and reverses muscarinic effects but does NOT reverse muscle weakness - ventilatory support must be provided separately.

3. Pralidoxime / Oximes (Antidote for Nicotinic + Muscarinic + CNS Effects)

• 30 mg/kg IV bolus
• Followed by 8 mg/kg/hour IV infusion
• Continue for 24-48 hours while monitoring AChE levels

• Obtain blood for AChE levels before giving pralidoxime if possible, but do not delay treatment
• Recommended even >24-48 hours after exposure (still give it late)
• Not recommended for asymptomatic patients or isolated carbamate exposures with minimal symptoms
• Current evidence is inadequate to definitively show oximes reduce mortality (controversial), but still standard of care

4. Seizures

• Benzodiazepines (first line)
• Atropine (addresses cholinergic-driven seizures)
• Airway protection + oxygen
• Avoid phenytoin (ineffective for cholinergic seizures)

5. Ventilatory Support

• Endotracheal intubation + mechanical ventilation for:
  • Severe poisoning with respiratory failure
  • Intermediate syndrome with respiratory muscle paralysis
• Avoid succinylcholine (hydrolysed by plasma cholinesterase; prolonged paralysis in OP poisoning)
• Avoid β-blockers (may potentiate poisoning)
• Use non-depolarising neuromuscular blockers if needed

6. Other Measures

• Benzodiazepines for agitation, seizures
• Magnesium sulphate and calcium channel blockers - some evidence of benefit in OP poisoning
• Correct electrolyte disturbances, treat arrhythmias
• Monitor QTc

Summary: Atropine vs Pralidoxime

Carbamates vs Organophosphates

• Tintinalli's Emergency Medicine: A Comprehensive Study Guide, Chapter 201
• The Essentials of Forensic Medicine and Toxicology, 36th ed. (2026)
• Morgan & Mikhail's Clinical Anesthesiology 7e