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Rodenticide Poisoning: Complete Guide

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Overview

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1. ANTICOAGULANT RODENTICIDES (Superwarfarins)

Classification

• Warfarin - biologic half-life ~42 hours
• Diphacinone, chlorophacinone, pindone (indandiones)

• 4-Hydroxycoumarins: Brodifacoum, difenacoum, coumafuryl, bromadiolone
• Half-life of brodifacoum: ~120 days (Tintinalli) / ~150 hours for the compound itself per Rosen's - a single ingestion can cause anticoagulation for weeks to months
• Currently responsible for ~80% of human rodenticide exposures in the US - Tintinalli's EM, p.1349

Mechanism

Clinical Features

• Initial (0-72h): Often completely asymptomatic, even after large ingestions; OR early GI irritation as soon as 8 hours post-exposure
• Delayed (24-72h+): Bleeding anywhere - ecchymosis, epistaxis, hemarthrosis, gingival bleeding, menorrhagia, hematuria
• Life-threatening: Massive GI hemorrhage, intracranial hemorrhage
• Unexplained coagulopathy in a child or depressed adult should raise suspicion - Tintinalli's EM, p.1349

Recent Update (2024): Brodifacoum and difenacoum have been identified as adulterants in synthetic cannabinoids (K2/Spice), causing outbreaks of severe, unexpected coagulopathy and spontaneous intracranial hemorrhage in users who deny ingesting rodenticide. - Rosen's EM; PMID: 38127072

Diagnostic Testing

• Rosen's EM, p.3036

Management

• If presentation within 1 hour of massive ingestion: activated charcoal 100g (or 10:1 AC:poison ratio)
• Do NOT perform gastric lavage - no clinical benefit, and the large OG tube insertion risks inducing GI bleeding - Rosen's EM, p.3036
• For intentional/pediatric cases (Tintinalli): gastric lavage is stated as reasonable for very early presentations before coagulopathy sets in

• Massive blood loss: IV fluid resuscitation + transfusion
• Packed RBCs for blood loss
• Fresh Frozen Plasma (FFP): 10-15 mL/kg for active hemorrhage
• 4-Factor Prothrombin Complex Concentrate (PCC): first-line for urgent reversal
• Recombinant activated Factor VIIa: beneficial as additional option

• Vitamin K1 ONLY (not K3 or K4 - other forms are ineffective and potentially toxic)
• Do NOT give prophylactically - administer only if INR is elevated
• Takes 6 hours to take effect (explains every-6-hour dosing)
• Pediatric: 1-5 mg/day PO in 2-4 divided doses
• Adult (warfarin-type): 20 mg/day PO in 2-4 divided doses
• Massive overdose: doses as high as 800 mg/day may be required
• Treatment may need to be continued for weeks to months with long-acting superwarfarins - Rosen's EM, p.3036; Tintinalli's EM, p.1349

Disposition

• Rosen's EM, p.3037

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2. ALUMINUM PHOSPHIDE (AlP) POISONING

Background

Mechanism

• Inhibits cytochrome oxidase (electron transport chain)
• Has generalized cytotoxic action on all organ systems
• Chemical reaction is accelerated by gastric acid

Fatal Dose & Period

• Fatal dose: 1-3 tablets (1-3g); 1-2g typically lethal
• Inhalation: 400-600 ppm phosphine is fatal within 1 hour
• Fatal period: typically 6-12 hours; majority of deaths within 24 hours

Clinical Features by System

Treatment

1. Gastric lavage with potassium permanganate (oxidizes phosphine to non-toxic phosphate) - after endotracheal intubation; repeat 2-3 times
2. Activated charcoal 100g with sorbitol (adsorbs phosphine)
3. Antacids - reduce GI absorption of phosphine
4. Liquid paraffin - promotes GI excretion
5. No specific antidote available
6. Magnesium sulfate - reduces organ toxicity, corrects hypomagnesemia and arrhythmias; 1g IV, then 1g every 2 hours, then 1-1.5g every 6 hours for 5-7 days continuous IV
7. Fluid resuscitation: 4-6 liters in first 3-6 hours (50% normal saline)
8. Low-dose dopamine: 4-6 mcg/kg/min for shock
9. IV hydrocortisone: 400mg every 4-6 hours (reduces dopamine requirement)
10. Oxygen for hypoxia
11. IV sodium bicarbonate for metabolic acidosis
12. Peritoneal or hemodialysis if needed

Recent Evidence (2024 meta-analysis, PMID: 38496382): Oil-based gastric lavage may improve outcomes in AlP poisoning by slowing phosphine gas release. 2023 RCT (PMID: 38096041): Insulin-euglycemia therapy studied in acute AlP poisoning as adjunctive treatment.

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3. ZINC PHOSPHIDE POISONING

• Steel-grey crystalline powder with garlicky or fishy odor
• Used as grain preservative and rodenticide
• Mechanism: same as AlP (releases phosphine with moisture), but slower onset due to gradual phosphine release
• Deaths: some within hours (pulmonary edema); most within 30 hours from cardiovascular collapse/direct myocardial toxicity
• Treatment: same principles as AlP
• Essentials of Forensic Medicine & Toxicology 36th Ed (2026), p.500

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4. SODIUM FLUOROACETATE (Compound 1080)

Background

• Irreversible inhibitor of the TCA (Krebs) cycle
• Mechanism: fluoroacetate → fluorocitrate ("suicide inhibitor") → blocks aconitase → energy failure in high-demand organs (heart, CNS)
• Banned in the US since 1972 (still used in sheep collars for predator control)
• No antidote

Clinical Features

• GI: Nausea, vomiting, diarrhea
• Respiratory distress, lactic acidosis
• Seizures, coma
• Cardiac dysrhythmias (ST/T changes, PVCs, VT, VF), pulmonary edema
• Hyperkalemia and hypocalcemia common

Treatment (per Tintinalli)

• Activated charcoal
• Seizure and dysrhythmia control
• Supportive chemotherapy regimens include: glycerol monoacetate, calcium gluconate, sodium succinate, ethanol loading
• Toxicology consultation strongly recommended

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5. STRYCHNINE POISONING

Background

• Used to kill moles, gophers, pigeons; also an adulterant in heroin and cocaine
• Mechanism: competitive antagonist of glycine at postsynaptic spinal cord and brainstem motor neurons → uninhibited motor neuron firing

Clinical Features

• "Awake seizure" - patient is fully conscious during violent muscle spasms
• Restlessness, muscle twitching, painful extremity spasms
• Risus sardonicus (sardonic grin), opisthotonus, trismus
• Inability to swallow, facial cramping
• Hyperthermia, rhabdomyolysis
• Respiratory failure and death

Treatment

• Minimize all sensory stimulation (dark, quiet room)
• Activated charcoal
• Avoid gastric lavage (may precipitate seizures)
• Benzodiazepines (first-line for spasms)
• Barbiturates if benzodiazepines fail
• Neuromuscular blockade if necessary for airway
• ICU admission

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6. ELEMENTAL/YELLOW PHOSPHORUS

Mechanism

• Corrosive and mitochondrial toxin; spontaneously combusts at room temperature

Clinical Features

• **"Smoking" or luminescent vomitus and stool (glows in the dark - "smoking stool syndrome")
• Garlic odor; skin burns and fluorescence under Wood's lamp
• Oral/GI burns
• Direct cardiac, renal, and hepatic toxicity
• Cardiovascular collapse, late neurologic depression, hepatorenal dysfunction

Treatment

• PPE mandatory
• Sand or water over solid phosphorus particles
• Cardiac monitoring, electrolyte correction
• Supportive care

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7. THALLIUM POISONING

Background

• Former rodenticide (now banned in most countries); still a rare cause of criminal or suicidal poisoning
• Mimics potassium biologically; interferes with K+-dependent processes

Clinical Features

1. Alopecia (hallmark - delayed by 2-3 weeks after ingestion)
2. Painful peripheral neuropathy
3. Skin rashes + mental confusion/lethargy

Treatment

• Gastric lavage with 1% potassium iodide
• Prussian blue (potassium ferric cyanoferrate): 250mg/kg/day orally - interrupts enterohepatic recirculation
• Activated charcoal
• Forced diuresis; hemodialysis in severe cases

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8. BARIUM CARBONATE POISONING

• Inhibits potassium channels → severe hypokalemia
• Acts as cardioprotective neurotoxicant
• Clinical: within ~8h - severe vomiting, diarrhea, abdominal pain, muscle weakness, paresthesias, paralysis, cardiac dysrhythmias, respiratory failure
• Treatment: Activated charcoal + sodium/magnesium sulfate in lavage solution (converts carbonate to less toxic barium sulfate) + aggressive potassium replacement

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9. ARSENIC (Historical)

• Banned as rodenticide in the mid-19th century; still seen as deliberate poisoning
• Mechanism: binds sulfhydryl groups on proteins
• Acute: cholera-like diarrhea, cardiovascular collapse, seizures, QT prolongation
• Chronic (weeks-months later): peripheral neuropathy, Mees' lines on nails, hyperpigmentation
• Treatment: Activated charcoal + chelation with succimer or dimercaprol

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10. VACOR (PNU - N-3-Pyridylmethyl-N'-p-nitrophenyl Urea)

• Nicotinamide antagonist; banned in the US since 1979
• Damages pancreatic beta cells and autonomic axons
• Features: Orthostatic hypotension, insulin-dependent diabetes mellitus (permanent), neuropathy, coma
• Treatment: IV fluids, activated charcoal, nicotinamide, insulin, steroids

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Comparative Summary Table

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Recent Clinical Updates (2023-2025)

1. Superwarfarin in synthetic cannabinoids (2024): Brodifacoum and related compounds are increasingly used as adulterants in illicit synthetic cannabinoids. Multiple outbreak cases reported with severe coagulopathy and spontaneous intracranial hemorrhage - PMID: 38127072. CT brain is warranted in all cases of unexplained coagulopathy in young adults.
2. AlP treatment innovation (2023 RCT): Insulin-euglycemia therapy trialed as adjunctive treatment for acute AlP poisoning to reduce cardiotoxicity - PMID: 38096041.
3. Oil-based gastric lavage for AlP (2024 meta-analysis): Coconut/vegetable oil as lavage medium may slow phosphine release and improve survival - PMID: 38496382.
4. Anticoagulant rodenticide forensic analysis (2025 retrospective, 88 cases): Long-acting anticoagulant rodenticide (LAAR) poisoning pattern analysis highlighting forensic utility of brodifacoum serum levels and multi-organ pathology - PMID: 40974629.
5. Metallophosphide epidemiology (2025 meta-analysis, Ethiopia): Aluminum/zinc phosphide poisoning is a rising public health problem in sub-Saharan Africa, with high case fatality rates - PMID: 40702417.

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Key Pearls

• INR at 48 hours is the critical monitoring point for anticoagulant rodenticides - normal at 48h excludes significant ingestion
• Vitamin K1 takes 6 hours to take effect and must not be given prophylactically
• Brodifacoum's half-life is ~120 days - outpatient vitamin K may be needed for 4-6 weeks or longer
• Never use K3 or K4 - only K1 (phytonadione) is effective and safe
• AlP poisoning has no specific antidote and mortality ranges 35-100%; cardiogenic shock is the leading cause of death
• Strychnine causes awake seizures (patient conscious throughout) - minimize sensory stimulation and avoid gastric lavage
• Thallium's hallmark late finding is alopecia - consider in any patient with unexplained hair loss + neuropathy
• Synthetic cannabinoid users presenting with unexplained bleeding should be screened for brodifacoum contamination

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Celphos (Aluminum Phosphide) Poisoning: Complete Guide

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What is Celphos?

• Weight: 3 grams (grey-green in color)
• Composition: AlP mixed with urea and ammonium carbonate (to slow phosphine release)
• Each tablet liberates 1 gram of phosphine (PH3) gas
• Known colloquially as "rice tablet," "wheat pill," or "agent of sure death"

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Epidemiology

• Most common cause of pesticide-related death in India, Pakistan, Iran, and parts of Africa
• Predominantly suicidal ingestion (especially in Punjab, Haryana, Uttar Pradesh); occasional accidental
• Homicidal poisoning is rare
• Rising incidence: a 2023 systematic review (350 studies, PMID: 37387512) noted a significant global increase in AlP poisoning reports, especially after 2016
• Mortality: 35-100% in hospitalized cases; no specific antidote exists

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Chemical Reaction

AlP + 3H₂O → Al(OH)₃ + PH₃ (Phosphine)

• PC Dikshit Forensic Medicine, p.574

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Mechanism of Toxicity (Pathophysiology)

Primary Mechanism

• Inhibits cytochrome c oxidase (Complex IV of the electron transport chain)
• Produces generalized cellular energy failure (ATP depletion)
• Disrupts oxidative phosphorylation in all energy-demanding organs (heart, lungs, liver, CNS)

Additional Mechanisms (from recent evidence):

• Reactive oxygen species (ROS) generation - oxidative stress and lipid peroxidation
• Mitochondrial membrane disruption
• Inhibition of catalase and other antioxidant enzymes
• Direct myocardial toxicity - cardiomyocyte necrosis
• Adrenal gland damage - contributing to refractory shock
• Inhibition of acetylcholinesterase at high doses

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Absorption, Distribution, Excretion

• Inhalation: Rapidly absorbed via lungs - most rapid route
• Ingestion: Absorbed by simple diffusion from GI tract → damages internal organs directly; some AlP is metabolized in the liver where phosphine is slowly released (accounts for symptom prolongation)
• Excretion: Phosphine is oxidized to oxyacids → excreted as hypophosphite in urine; also excreted unchanged through the lungs
• Essentials of FM & Tox 36th Ed (2026), p.499

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Toxic Doses

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Clinical Features

Timing

• Onset: Within 30 minutes to 4 hours of ingestion
• Fatal period: Typically 6-12 hours; majority of deaths within 24 hours
• Death has been reported within 1-4 hours after large ingestion

Severity Grading

• Irritation of mucous membranes
• Dizziness, fatigue
• Tightness in chest
• Nausea, vomiting, diarrhea
• Headache

• Ataxia, numbness, paresthesias
• Tremors, diplopia
• Jaundice (early hepatic involvement)
• Muscular weakness, incoordination, paralysis

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Characteristic Features (Clinical Clues)

• Odor: Fishy or garlic-like odor from breath, vomitus, and gastric contents
• Breath odor classification: Fishy/musty = AlP/Zinc phosphide; Garlicky = Organophosphates - Essentials FM & Tox 36th Ed (2026)
• History: Access to grain storage areas, known use in agriculture

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Diagnosis

Bedside/Clinical Test

• Impregnate filter paper with 0.1 N silver nitrate solution
• Apply as a mask - patient breathes through it for 5-10 minutes
• Positive: Paper turns black (silver nitrate → silver metal on exposure to PH3)
• Positive only if >6g AlP ingested
• Can also heat 5mL gastric aspirate + 15mL water in flask at 50°C for 15-20 min with AgNO3 paper over the mouth

Laboratory Investigations

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Management

Critical principle: No specific antidote exists. Treatment is entirely supportive.

Step 1: Immediate Priorities / Resuscitation

• Ensure patent airway; early endotracheal intubation if GCS is depressed, significant respiratory distress, or for gastric lavage
• Oxygen supplementation for all patients

• Use N95 mask or full-face respirator - exhaled phosphine from patient is hazardous to staff
• Avoid mouth-to-mouth resuscitation
• Perform procedures in well-ventilated area

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Step 2: Gastric Decontamination

Key controversy: Traditional teaching supports gastric lavage; recent evidence questions it.

1. Gastric lavage (only after endotracheal intubation):
   • Use potassium permanganate (KMnO4) solution - oxidizes phosphine to non-toxic phosphate
   • Or sodium bicarbonate 3-5% (alkalinizes, slows reaction with HCl)
   • Or 1% copper sulfate (precipitates phosphide)
   • Repeat 2-3 times
   • Perform within 1-2 hours of ingestion
2. Activated charcoal: 100g orally mixed with sorbitol (not water, to minimize phosphine gas generation), using 240mL per 30g charcoal
3. Antacids: Reduce gastric acidity → slow phosphine release, reduce GI absorption
4. Liquid paraffin: Promotes excretion of AlP and phosphine from gut; slows absorption

Recent evidence update (2024 meta-analysis, PMID 38496382): Oil-based gastric lavage (paraffin oil or coconut oil) is an effective adjunct - reduces mortality (RR = 0.62; NNT = 4 for paraffin oil) and reduces need for intubation/mechanical ventilation. Paraffin oil lavage has better evidence than coconut oil lavage (both low-quality evidence from 7 RCTs).

Note: Some recent authorities advise against routine gastric lavage (gastric moisture accelerates phosphine generation), preferring oil-only decontamination.

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Step 3: Hemodynamic Support

• 4-6 liters IV fluids in first 3-6 hours; 50% normal saline, remainder can be D5NS or Ringer's
• Avoid fluid overload (risk of pulmonary edema)

• Norepinephrine is the preferred vasopressor for refractory hypotension
• Low-dose dopamine: 4-6 mcg/kg/min IV infusion (traditional approach)
• IV hydrocortisone: 400mg every 4-6 hours - highly effective; reduces vasopressor requirement (treats possible adrenal insufficiency) - Essentials FM & Tox 36th Ed (2026)

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Step 4: Arrhythmia Management

• Standard dose (Dikshit): 3g IV bolus, then 6g infusion over 24 hours for 5-7 days
• Alternative dosing (Essentials FM & Tox): 1g IV, repeated every 2 hours, then 1-1.5g every 6 hours for 5-7 days as continuous IV infusion
• Reduces organ toxicity, corrects hypomagnesemia, controls arrhythmias
• Caution: Risk of hypermagnesemia in renal failure; avoid if serum Mg >15 mEq/L (risk of cardiac arrest)

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Step 5: Metabolic Correction

• Metabolic acidosis: IV sodium bicarbonate 50 mEq every 15 minutes until arterial HCO3 >15 mmol/L - PC Dikshit
• Hypoxia: Supplemental oxygen → ventilatory support → mechanical ventilation
• Hypoglycemia: IV dextrose
• Antibiotics: For secondary infections (aspiration pneumonia is common)
• Peritoneal dialysis or hemodialysis: If renal failure present and hypermagnesemia develops

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Step 6: Advanced/Experimental Therapies

Insulin-Euglycemia Therapy (GIK/High-Dose Insulin)

• 2023 RCT (PMID: 38096041, n=108): Insulin-euglycemia therapy + norepinephrine vs norepinephrine + placebo:
  • Mortality reduction: 64.8% vs 96.3% in control (p<0.001) - dramatic reduction
  • Fewer vasopressors needed (median 7mg vs 26mg, p=0.006)
  • Less intubation needed (61.1% vs 81.5%, p=0.019)
  • Significantly improved BP, bicarbonate, and lactate
  • Conclusion: Insulin-euglycemia appears safe and effective; vasopressor-only therapy has very poor outcomes
• Protocol: High-dose insulin infusion (1-2 U/kg/hr) + dextrose infusion to maintain euglycemia (4-8 mmol/L) + potassium replacement

N-Acetylcysteine (NAC)

• Rationale: Restores glutathione, reduces oxidative stress from ROS generated by phosphine
• Included in systematic review (PMID: 37387512) as one of treatments that significantly decreased mortality in clinical trials
• Dose: standard toxic ingestion protocol (150mg/kg IV over 1 hour, then 50mg/kg over 4 hours, then 100mg/kg over 16 hours)

Vitamin E

• Antioxidant therapy; included in the 2023 systematic review as mortality-reducing in clinical trials (PMID: 37387512)

ECMO (Extracorporeal Membrane Oxygenation)

• For refractory cardiogenic shock unresponsive to all medical therapies
• VA-ECMO (veno-arterial) is the modality for cardiac support
• 2023 case report (PMID: 37781306): VA-ECMO + intra-aortic balloon pump (IABP) - patient survived 34 days after successful weaning
• 2025 (PMID: 41175537): Impella device used for toxin-induced cardiogenic shock in AlP poisoning - first documented case; highlights need for early transfer to advanced cardiac support centers
• 2026 case (PMID: 42324466): Pediatric inhalation case with VA-ECMO support
• Role: Bridge to recovery while myocardial toxicity resolves; not available in most LMIC settings

Fresh Packed RBCs Infusion

• Mentioned in 2023 systematic review as mortality-reducing in clinical trials
• Theoretical basis: hemoglobin may bind phosphine, reducing free phosphine toxicity

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Summary Treatment Table (Rosen's RATS PANIC vs Textbook Protocols)

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Postmortem Findings

External:

• Garlic-like or fishy odor from mouth, nostrils, and gastric contents
• Blood-stained froth at mouth and nostrils

Internal:

• Congestion of mucous membranes of lower esophagus, stomach, duodenum
• Decreasing GI congestion toward the small intestine
• Congestion of lungs, liver, spleen, kidneys, brain
• Centrizonal hemorrhagic necrosis of liver (characteristic)

Histopathology:

• Essentials of FM & Tox 36th Ed (2026), p.500

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Disposition

• All symptomatic patients: ICU admission
• Even initially asymptomatic intentional ingestions: admit for minimum 24-48 hours monitoring
• Monitor ECG, ABG, electrolytes, cardiac biomarkers, LFTs, RFTs serially
• Early transfer to cardiac surgery center if deteriorating (for ECMO availability)

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Medicolegal Aspects

• Commonly used in suicidal deaths in agricultural communities of North India (Punjab, Haryana, UP)
• Dowry deaths - used as an agent of homicide in some cases
• Poison is widely available without prescription in rural areas
• Forensic chemical test: Silver nitrate paper blackening (bedside), or laboratory detection in gastric contents
• In breath, positive test requires ingestion of >6g AlP
• Essentials FM & Tox 36th Ed (2026); Parikh's Forensic Medicine

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Recent Updates Summary (2022-2026)

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Key Pearls

• Celphos = Aluminum phosphide = "agent of sure death" - fatality is high even with treatment
• No antidote - supportive care is everything
• Cardiogenic shock is the main killer; address hemodynamics aggressively
• Silver nitrate paper test at bedside: blackening = phosphine positive
• Fishy/garlic odor in breath is the clinical clue
• Gastric lavage with paraffin oil (not plain water) - oil slows phosphine release; has meta-analytic mortality benefit
• Insulin-euglycemia is emerging as the most significant treatment advance (2023 RCT: mortality 64.8% vs 96.3% with vasopressors alone)
• MgSO4 for arrhythmias + organ protection; hydrocortisone for adrenal insufficiency/shock
• ECMO should be considered early for refractory cardiogenic shock at capable centers
• Observe minimum 72 hours even if initially asymptomatic (Rosen's)
• PPE for all healthcare workers - exhaled phosphine is toxic to staff

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