ICU · Toxicology

Carbon monoxide poisoning

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

Carbon monoxide (CO) is an odourless, colourless gas produced by incomplete combustion (faulty heaters, house fires, car exhausts, generators, barbecues used indoors). CO binds haemoglobin with 210x affinity of oxygen, forming carboxyhaemoglobin (COHb), causing tissue hypoxia via THREE mechanisms: (1) functional anaemia, (2) LEFT shift of oxyhaemoglobin dissociation curve (impaired tissue O2 release), (3) histotoxic hypoxia (CO binds myoglobin + inhibits mitochondrial cytochrome c oxidase / cytochrome a3 / Complex IV → anaerobic metabolism → lactate). Presentation: headache, nausea, dizziness, confusion (flu-like) — 'flu-like illness in MULTIPLE people from the SAME household in WINTER = CO until proven otherwise.' Severe: syncope, seizures, coma, cardiovascular collapse, death. Diagnosis: COHb level (venous blood gas — NOT SpO2 which is FALSELY NORMAL because pulse oximetry cannot distinguish COHb from oxyhaemoglobin). Treatment: 100% oxygen via non-rebreather (reduces CO half-life from about 5 hours on room air to about 1 hour). Hyperbaric oxygen (HBO) for severe cases (high COHb, unconscious, pregnant, cardiac ischaemia, neurological signs) — reduces CO half-life to about 20 minutes. Delayed neurological sequelae occur in 15-40% of patients after a lucid interval of days to weeks (cognitive impairment, parkinsonism) — may be permanent.