Overview
Definition
Life-threatening toxicity caused by excessive opioid receptor stimulation.
Epidemiology
A massive public health crisis. Driven heavily by synthetic opioids like Fentanyl.
Etiology & Risk Factors
- Excessive binding to mu-opioid receptors in the central nervous system, leading to profound respiratory depression.
- Common agents: Heroin, Fentanyl, Oxycodone, Morphine, Methadone.
Clinical Symptoms
- Classic Triad: Pinpoint pupils (Miosis), Respiratory Depression (RR < 12), and CNS Depression (Coma)
- Hypoxia and cyanosis
- Decreased bowel sounds
Clinical Approach
Diagnosis
- Clinical diagnosis (the triad of coma, miosis, and respiratory depression is highly specific)
- Response to Naloxone is diagnostic
- Urine drug screen is NOT helpful in the acute setting (takes too long, false negatives with synthetic opioids)
Management
- Supportive Care (ABCs): Bag-valve-mask ventilation for hypoxia/apnea
- Naloxone (Narcan): A competitive mu-opioid receptor antagonist. Can be given IV, IM, or Intranasally. Titrate to restore respiratory drive (not necessarily to full consciousness) to avoid precipitating acute withdrawal.
- Observation: Patients must be observed for at least 2-4 hours after naloxone, as the half-life of naloxone is often shorter than the opioid (especially methadone), risking re-sedation.
Complications
- Hypoxic brain injury
- Aspiration pneumonitis
- Death from respiratory arrest