ICU · toxicology

Acute Carbon Monoxide Poisoning — Comprehensive ICU Management

Also known as Carbon monoxide poisoning · CO poisoning · Carboxyhaemoglobin (COHb) · Carboxyhemoglobin · Hyperbaric oxygen therapy (HBOT) · Delayed neurological sequelae (DNS) · Delayed encephalopathy · The great imitator (flu-like) · Cytochrome oxidase inhibition

Acute carbon monoxide (CO) poisoning — odourless, colourless gas of incomplete combustion (faulty heaters, house fires, exhausts, generators). CO binds haemoglobin with ~240x the affinity of oxygen, forming carboxyhaemoglobin (COHb), causing a TRIPLE insult: (1) functional anaemia (reduced O2 carrying capacity), (2) LEFT shift of the oxyhaemoglobin dissociation curve (residual O2 held too tightly — impaired tissue release), and (3) direct cellular hypoxia via binding myoglobin and inhibiting mitochondrial cytochrome c oxidase (cytochrome a3 / Complex IV) → histotoxic hypoxia + lactic acidosis. Clinical: headache, nausea, dizziness, confusion — 'flu-like symptoms in MULTIPLE people from the SAME household in WINTER = CO until proven otherwise.' Severe: syncope, seizures, coma, cardiovascular collapse. Cherry-red skin is a classical but RARE and LATE sign — do NOT rely on it. Diagnosis: COHb on venous blood gas (venous sample sufficient — arterial NOT required) — COHb 10% significant, 25% severe, 50% potentially fatal. CRITICAL: SpO2 by standard pulse oximetry is FALSELY NORMAL because it cannot distinguish COHb from oxyhaemoglobin. Management: 100% oxygen via non-rebreather mask immediately — reduces CO half-life from ~320 min (room air) to ~80 min; hyperbaric oxygen (HBO) at 2.5-3 atm reduces half-life to ~23 min — indicated (controversial) for COHb 25%, loss of consciousness, neurological signs, pregnancy, cardiac ischaemia. Delayed neurological sequelae (DNS) in 20-40% of severe cases at 2-40 days — cognitive impairment, parkinsonism — may be permanent; no proven prevention.