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Toxicology / Poisoning

Opioid Poisoning

Poisoning resulting from excessive intake (intentional or accidental) of opioid drugs (e.g., morphine, heroin, codeine, tramadol, fentanyl, pethidine). Characterized by a classic triad of CNS depression, respiratory depression, and miosis (pinpoint pupils). Reversible with the antidote naloxone.

Also known as: Opioid Overdose, Narcotic Overdose, Morphine Overdose, Heroin Overdose, Codeine Overdose, Tramadol Overdose

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Referral and warning signs

When to refer

ALL patients with suspected opioid overdose requiring naloxone administration MUST be referred to Hospital (H) for observation due to risk of recurrent respiratory depression. Refer any patient with persistent coma, seizures, pulmonary edema, or requiring ventilatory support or naloxone infusion.

Red flags

  • Respiratory depression (RR < 10/min, shallow breathing, apnea)
  • Cyanosis or low SpO2 (<90%)
  • Altered mental status (stupor, coma)
  • Pinpoint pupils (miosis)
  • Response to naloxone (confirms diagnosis, but requires observation)

Signs and symptoms

  • Classic Triad:
  • 1. CNS Depression: Drowsiness, lethargy, stupor, coma.
  • 2. Respiratory Depression: Slow respiratory rate (bradypnea), shallow breathing, periods of apnea (cessation of breathing). This is the most life-threatening effect.
  • 3. Miosis: Constricted, pinpoint pupils (may be normal or dilated in severe hypoxia, co-ingestions, or with certain opioids like meperidine/pethidine).
  • Other Signs: Hypotension, Bradycardia, Hypothermia, Decreased bowel sounds / Ileus, Nausea/vomiting, Flushing, Pruritus (itching), Non-cardiogenic pulmonary edema (can occur after resuscitation/naloxone), Seizures (especially with tramadol, meperidine/pethidine, propoxyphene, or due to hypoxia).

Risk factors

  • Illicit drug use (heroin, fentanyl).
  • Misuse or abuse of prescription opioids.
  • Intentional overdose (suicide attempt).
  • Accidental overdose (therapeutic error, taking extra doses, confusion, use by children).
  • Switching between different opioids or formulations.
  • Combining opioids with other sedating substances (alcohol, benzodiazepines).
  • Resumption of use after period of abstinence (loss of tolerance).
  • Use in patients with underlying respiratory disease, sleep apnea, renal or hepatic impairment.

Diagnosis

Clinical assessment

Diagnosis is primarily clinical, based on recognition of the opioid toxidrome (CNS depression, respiratory depression, miosis) in a patient with known or suspected opioid exposure. Response to naloxone strongly supports the diagnosis.

Investigations

  • Point-of-care Blood Glucose: Rule out hypoglycemia.
  • Assess respiratory status thoroughly: Rate, depth, effort, oxygen saturation (SpO2 - may be low).
  • Consider: Arterial Blood Gas (ABG) - assess hypoxia, hypercapnia, acidosis. Electrocardiogram (ECG) - check for bradycardia, QTc prolongation (esp. methadone). Chest X-ray - evaluate for pulmonary edema, aspiration. Urine drug screen - may detect opioids but often not rapid enough for acute management and doesn't quantify.
  • Rule out other causes of coma/respiratory depression (head injury, stroke, hypoglycemia, sepsis, other sedative overdoses).

Diagnostic criteria

Clinical triad (CNS depression, respiratory depression, miosis) +/- history of opioid exposure +/- response to naloxone administration.

Management

Non-pharmacological management

  • Stabilization: ABCDE approach.
  • Airway Management: Ensure patent airway (positioning, adjuncts). Prepare for assisted ventilation/intubation if needed.
  • Breathing Support: Provide supplemental oxygen. Assist ventilation with bag-valve-mask (BVM) if spontaneous respirations are inadequate (<8-10 breaths/min) or ineffective. This is critical while preparing/administering naloxone. Intubation and mechanical ventilation may be required for persistent respiratory failure despite naloxone or if naloxone wears off.
  • Circulation Support: Establish IV access. IV fluids for hypotension if present.
  • GI Decontamination: Generally NOT indicated. Activated charcoal is ineffective and risk of aspiration is high due to CNS depression. Gastric lavage only potentially useful for massive recent ingestion of sustained-release products under controlled (intubated) conditions (rarely done).

Pharmacological treatment

  • ANTIDOTE: Naloxone: Pure opioid antagonist. Reverses respiratory depression and CNS depression.
  • Dosing: Adult: Start with 0.4 - 2 mg IV/IM/SC/Intranasal. Repeat dose every 2-3 minutes as needed to restore adequate spontaneous ventilation (aim for RR >10-12/min), NOT necessarily full consciousness (avoid precipitating withdrawal). Titrate to effect. Max dose usually cited as 10 mg, but higher may be needed for potent synthetics (e.g., fentanyl). Child: 0.01 mg/kg initially, may increase to 0.1 mg/kg if no response. Minimum dose often recommended as 0.1mg.
  • Duration: Naloxone has a shorter duration of action (30-90 minutes) than many opioids (esp. methadone, sustained-release preps). Patients require prolonged observation (at least 2-4 hours after last naloxone dose) for recurrence of respiratory depression ('renarcotization'). Continuous Naloxone Infusion may be needed for long-acting opioids or large overdoses (Hospital level): typically infuse at ~2/3 of the initial bolus dose per hour.
  • Route: IV preferred for fastest onset. IM/SC/Intranasal are alternatives if IV access delayed.
  • Withdrawal: Rapid reversal with large naloxone doses in opioid-dependent individuals can precipitate acute withdrawal syndrome (agitation, vomiting, diarrhea, pain, tachycardia, hypertension, piloerection). Use lowest effective dose titrated to adequate ventilation.
  • Treat complications: Benzodiazepines for seizures (esp. tramadol).

Monitoring

Continuous monitoring of: Respiratory status (rate, depth, SpO2) - CRITICAL. Neurological status (GCS, pupil size). Cardiovascular status (HR, BP). Monitor for recurrence of respiratory depression for several hours after naloxone. Monitor for signs of opioid withdrawal if patient is dependent.

Complications

  • Respiratory arrest / failure
  • Hypoxic brain injury
  • Aspiration pneumonia
  • Non-cardiogenic pulmonary edema
  • Rhabdomyolysis (due to immobility/hypoxia)
  • Seizures (with certain opioids or hypoxia)
  • Coma
  • Death

Prevention

  • Judicious prescribing of opioids.
  • Patient education on safe use, storage, and disposal.
  • Co-prescription of naloxone rescue kits for high-risk patients.
  • Awareness programs about risks of illicit opioids (heroin, fentanyl).
  • Harm reduction strategies (needle exchange, supervised consumption sites).
  • Treatment programs for opioid use disorder (e.g., methadone, buprenorphine).
  • Mental health support.

Patient education

  • Explain the cause of the overdose and the life-saving effect of naloxone.
  • Discuss the risks of opioid use/misuse.
  • Provide information and referral for substance use disorder treatment if appropriate.
  • Educate patient and family on recognizing overdose signs and using naloxone rescue kits if prescribed/available.

Uganda-specific notes

Commonly encountered opioids include codeine (in cough syrups), tramadol, morphine, pethidine, and increasingly heroin. Naloxone is the critical antidote and should be readily available. Availability of nasal naloxone may be limited. Emphasis is on basic airway management, assisted ventilation (BVM), and titrated naloxone administration. Remember tramadol can cause seizures which require benzodiazepines. Prolonged observation after naloxone is essential.

References

  • Uganda Clinical Guidelines (UCG) 2023

    Chapter 1, Section 1.3.9

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