Dimethoate Poisoning

Aka: Dimethoate Poisoning, Dimethoate Toxicity, Dimethoate, Cygon, Defend

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II. Mechanism

  1. Insecticide (acaricide) used on crops
  2. Highly toxic organic Phosphorus compound (Organophosphate)
    1. Inhibits Acetylcholinesterase resulting in Cholinergic excess (see Cholinergic Toxicity)
    2. Increased Acetylcholine activity at multiple sites
      1. Autonomic ganglia (associated with vasodilation and Hypotension)
      2. Neuronal receptors (Nicotinic Receptor, Muscarinic Receptor)
      3. Neuromuscular Junction
  3. Dimethoate 40% emulsifiable concentrate is the typical commercial Insecticide formulation
    1. Compounded with surfactants (e.g. alkulbenzenesulfonate salts) and solvents (e.g. xylene, cyclohexanone)
    2. Solvents (esp. cyclohexanone) increase toxicity
  4. Exposures
    1. Ingestion (most common exposure)
      1. Results in severe cardiovascular effects (e.g. refractory Vasoplegia, Acute Respiratory Failure)
    2. Dermal contact
      1. Prolonged exposure may result in severe toxicity (even with unbroken skin)

III. Findings

  1. See Cholinergic Toxicity (mnemonic: SLUDgE + Killer Bs)
  2. Cardiopulmonary
    1. Bradycardia
    2. Bronchospasm
    3. Bronchorrhea
    4. Vasopressor resistant Hypotension
    5. Aspiration Pneumonitis
  3. Neurologic
    1. Miosis
    2. Lethargy or coma
    3. Acute Respiratory Failure (Bellows Failure from loss of respiratory drive)
    4. Muscle Fasciculations
    5. Flaccid Paralysis (including respiratory Muscles)
    6. Seizures (uncommon)
  4. Sludge
    1. Salivation
    2. Lacrimation
    3. Urination
    4. Diarrhea (and Diaphoresis)
    5. Gastrointestinal cramping
    6. Emesis (Nausea and Vomiting)

IV. Labs

  1. See Unknown Ingestion
  2. Complete Blood Count (CBC)
    1. Leukocytosis
  3. Chemistry panel
    1. Hyperglycemia and Ketosis
  4. Creatine Phosphokinase (CPK)
  5. Lipase
    1. Acute Pancreatitis
  6. Toxicology
    1. Plasma butyrylcholinesterase
    2. RBC Acetylcholinesterase level
    3. Plasma Dimethoate concentration

V. Management

  1. See Organophosphate Poisoning Management
  2. ABC Management
  3. Decontamination
    1. Use Personal Protection Equipment (gloves, gown, mask)
    2. Skin Decontamination
      1. Removal all clothing and wash skin with soap and water
    3. Gastrointestinal Decontamination
      1. Indicated in early presentations after massive ingestion (<2 hours)
      2. Orogastric or nasogastric lavage with Activated Charcoal
      3. Requires airway control (Endotracheal Intubation)
  4. Antidotes (Atropine, Pralidoxime)
    1. See Organophosphate Poisoning Management
  5. Hypotension
    1. First-line
      1. Intravenous Fluids
      2. Vasopressors
    2. Advanced measures
      1. Methylene Blue
      2. Hydroxycobalamin
      3. ECMO (in refractory cases)
  6. Disposition
    1. Admit all symptomatic patients to Intensive Care Unit
    2. Minimal or no symptoms at 6 hours after exposure
      1. Patient may be medically cleared

VI. Prognosis: Factors associated with very high mortality

  1. Systolic Blood Pressure <80 mmHg at time of presentation (>80% case fatality rate)
  2. Plasma butyrylcholinesterase <600 mU/ml
  3. Plasma Dimethoate concentration >750 uM

VII. References

  1. Carroll and Yakey (2026) Crit Dec Emerg Med 40(4): 34
  2. Davies (2008) Clin Toxicol 46(9):880-4 +PMID: 19003596 [PubMed]

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