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Opioid Toxicity

Opioid Toxicity

Opioid Toxicity Protocol

Mechanism and Toxicokinetics

Toxic Mechanism: Agonist to the mu receptor creating euphoria, analgesia, dependance, sedation and respiratory depression.

Toxicokinetics:

  • Oral absorption is variable, most are rapid with the exception of controlled-release.
  • Large volumes of distribution 2.6 L/kg to 3.6 L/kg
  • Metabolised in the liver and excreted in the urine
Resuscitation
  • Reduced GCS: Trial of naloxone but some patients may require intubation and ventilation.
  • Ventricular dysrhythmias: Rarely seen with dextropropoxyphene, treatment is with sodium bicarbonate.
Risk Assessment

Life threatening CNS and respiratory depression occur just above the analgesia dose.

Opiate naive or taken with co-ingestants increases the severity of CNS depression

Specific opiates:

  • Dextropropxyphene: 10 mg/kg will cause symptoms, >20 mg/kg will cause CNS depression, seizures and cardiac dysrhythmias (sodium channel blockade).
  • Methadone and oxycodone: QT prolongation (torsades is rare), prolonged toxicity which can last >24 hours.
  • Pethidine: Repeated doses increase the risk of seizures and it can also precipitate serotonin toxicity.
  • Heroin toxicity lasts approximately 6 hours.
  • Controlled release preparations can result in respiratory depression up to 12 hours post ingestion.
Children: Opioid toxicity is the leading cause of death in children. An ingestion of a single table or a mouthful of methadone can cause respiratory depression. >2 mg/kg or codeine in children can start to cause symptoms and >5 mg/kg can cause a respiratory arrest.
Clinical Features
  • CNS and respiratory depression with miosis is the classic toxidrome.
  • Bradycardia is common unless hypoxia or hypercarbia are present.
  • Complications include: Aspiration pneumonia, hypothermia, skin necrosis, rhabdomyolysis, compartment syndrome and hypoxic brain injury.
Summary of Clinical Features:
  • miosis
  • CNS depression
  • respiratory depression
  • complications of hypoxia: seizures, dysrrhythmia, brain injury
Supportive Care & Investigations

Patients need to be observed closely, respiratory rate should be measured while they are asleep or undisturbed and saturations on room air to help detect early signs of toxicity.

If intubated see FASTHUGSINBED for further supportive care.

Investigations

  • Screening: 12 lead ECG, BSL, Paracetamol level
  • Specific: Serum and urine levels are not clinically useful. Specific tests will be indicated only to assess for secondary complications.
Management
  • Decontamination: Activated charcoals not usually clinically indicated due to having a specific antidote, however, those presenting early with a controlled release preparation can be considered.
  • Enhanced Elimination: Not clinically useful.
  • Antidote: Naloxone either as a bolus or sometimes as an infusion for those with CNS or respiratory depression.
Specific Therapy (Naloxone):
  • appropriate use of naloxone can prevent intubation
  • titrated doses until reversal of respiratory depression -> may require an infusion
  • dose: 0.4-2mg IV/IM/SC -> 1-10mcg/kg/hr

Electrolytes and Acid-base: respiratory acidosis

Underlying Cause: addiction counselling/ psychiatric review

Disposition
  • Standard release preparations require 4 hours of observation.
  • Controlled release preparations require 12 hours of observation.
  • Those with mild symptoms from a standard release preparation who did not receive naloxone in the first 4 hours can be observed on a ward.
  • All children who have ingested an opiate require 12 hours of observation unless it is <2 mg/kg of codeine. Discharge should not occur at night.
  • Patients who require a naloxone infusions or intubation will require HDU or ICU respectively.