Comatose patient — ABCDE, GCS and reversible causes

Resuscitation first. Parallel ABCDE: open/protect airway (jaw thrust, NPA/OPA as appropriate), support ventilation with BVM aiming SpO2 94–98%, high-flow O2 initially given hypoventilation; IV access; cardiac monitor; full exposure for track marks/MedicAlert. Glucose is already normal — still recheck. Consider parenteral thiamine if alcohol/malnutrition likely — Wernicke encephalopathy is a life-threatening illness caused by thiamine deficiency.^[4]

GCS. Report components: E1 V1 M3 = total 5. Best motor is abnormal flexion (decorticate range) — prognostically concerning but may improve with reverse of toxin.^[1] Do not hand over "GCS 5" without E/V/M.

Diagnosis and antidote. Pinpoint pupils + hypoventilation + coma = opioid toxidrome until proven otherwise. Give low-dose naloxone (0.04 mg IV), titrated to reverse ventilatory depression (avoid precipitating acute withdrawal in dependent patients — titrate to ventilation, not full wakefulness). If long-acting opioid (methadone, oxycodone SR) or recurrent hypoventilation, consider a naloxone infusion per local protocol and observe for renarcotisation.^[3]

Intubation. GCS ≤8 with unprotected airway, or persistent hypoventilation/hypoxia despite naloxone and BVM, or other indication (aspiration risk, transfer needs) → RSI with preparation for difficult airway. If naloxone rapidly restores ventilation and protective reflexes, intubation may be avoided with close observation.^[2]

Disposition/workup. Observe for renarcotisation; screen for co-ingestions; CT if residual unexplained deficit after reverse or trauma/focal signs.^[2]