Write a short note on opioid overdose and poisoning.

Introduction

Opioid poisoning occurs with heroin, morphine, tramadol (widely misused in India), codeine, fentanyl, methadone and buprenorphine, and with therapeutic opioids in the elderly or in renal impairment where accumulation occurs. It is a leading cause of preventable drug-related death, and is entirely reversible with a specific antidote.

Mechanism

Opioids act at mu, kappa and delta receptors. Toxicity results from mu receptor stimulation, causing depression of the brainstem respiratory centre with reduced responsiveness to carbon dioxide, along with sedation, analgesia and pupillary constriction. Death is from respiratory failure.

Clinical Features — the Classic Triad

1. Pinpoint pupils (miosis)

2. Respiratory depression — slow, shallow breathing, ultimately apnoea

3. Depressed consciousness — drowsiness to deep coma

Other features: hypotension, bradycardia, hypothermia, absent bowel sounds and constipation, urinary retention, and needle track marks in intravenous users.

Complications: non-cardiogenic pulmonary oedema (classically with heroin), aspiration pneumonia, hypoxic brain injury, rhabdomyolysis with acute kidney injury from prolonged immobility, compartment syndrome, and — with intravenous use — infective endocarditis, hepatitis B and C, HIV and skin infections.

Drug-specific caveats:

• Tramadol and pethidine may cause seizures and serotonin syndrome, and miosis may be absent.
• Fentanyl and its analogues are extremely potent, with rapid onset and chest wall rigidity; they may need much larger antidote doses.
• Methadone has a long half-life and causes QT prolongation with torsades; toxicity outlasts naloxone by many hours.
• Buprenorphine is a partial agonist and is only incompletely reversed by naloxone.

Investigations

Diagnosis is clinical and treatment must not be delayed. Supporting tests: capillary blood glucose (always, in any unconscious patient), arterial blood gas showing respiratory acidosis, urine toxicology screen (note that fentanyl, tramadol and synthetic opioids are frequently missed on standard immunoassays), creatine kinase for rhabdomyolysis, renal and liver function, ECG (QT with methadone), and chest X-ray for aspiration or pulmonary oedema.

Management

1. Airway and breathing first

• Open the airway, give high-flow oxygen, and provide bag-mask ventilation if breathing is inadequate. Oxygenation and ventilation save the patient — naloxone is an adjunct, not a substitute.

2. Naloxone — the specific antidote

• A competitive mu receptor antagonist with onset within 1–2 minutes intravenously.
• Titrate to adequate respiration, not to full consciousness. The aim is a patient who is breathing satisfactorily, not one who is awake, alert and in acute withdrawal.
• May be given intravenously, intramuscularly, subcutaneously or intranasally; intramuscular or intranasal routes are valuable in the pre-hospital setting and in community take-home kits.
• Its half-life is shorter than that of most opioids, so relapse into respiratory depression is common — the patient must be observed and a continuous infusion used for long-acting agents such as methadone.

3. Supportive care

• Intravenous fluids; treat hypothermia; correct hypoglycaemia; monitor for rhabdomyolysis with fluids and urine output.
• Manage aspiration pneumonia and non-cardiogenic pulmonary oedema with oxygen and ventilatory support.
• Observation period proportionate to the agent — several hours for heroin, considerably longer for methadone and sustained-release preparations.

4. Aftercare

Every case is an opportunity for intervention: assess for dependence, offer referral for opioid substitution therapy (buprenorphine or methadone), provide harm-reduction advice, immunise against hepatitis B, screen for HIV and hepatitis C, and consider take-home naloxone for the patient and family.