Opioid Overdose
Mu-opioid receptor agonism blunts the brainstem's response to rising carbon dioxide, causing the respiratory depression that actually kills, and naloxone reverses this by displacing the opioid, but often for less time than the opioid itself remains active.
In a nutshell
Mu-opioid receptor agonism causes respiratory depression, miosis and reduced consciousness from one mechanism acting in three CNS locations. Naloxone competitively displaces the opioid from the receptor, but because its own duration of action is often shorter than the opioid's, respiratory depression can recur: the basis for repeat dosing, infusion and observation.
Classic presentation
A patient found with reduced respiratory rate, pinpoint pupils and reduced consciousness, with evidence of opioid use nearby or on examination.
Key points
- Airway and breathing support takes priority over naloxone administration. Do not delay ventilation.
- Naloxone is titrated to restore breathing, not full consciousness, to reduce the risk of precipitated withdrawal.
- Naloxone's shorter half-life relative to many opioids (especially long-acting agents and methadone) means re-sedation can occur: prolonged observation is required.
- Co-ingestion with other sedatives (benzodiazepines, alcohol) compounds respiratory depression and changes risk.
First-line investigation
Clinical assessment of airway, breathing rate/depth, oxygen saturation and pupils; blood glucose to exclude hypoglycaemia as a mimic.
First-line management
Support airway and breathing, then give titrated naloxone to restore adequate ventilation.
Exam traps
- Giving a single naloxone dose and discharging early risks missed re-sedation, particularly with long-acting opioids or methadone.
- Full-dose rapid reversal in a dependent patient can precipitate severe withdrawal: titration is the safer approach.
- Reduced consciousness with pinpoint pupils should not be assumed opioid-related until hypoglycaemia has been excluded.
Educational content pending clinical review. Not medical advice.