Carbon Monoxide Poisoning and Asphyxiant Gases — HbCO, Cherry-Red Lividity, Oxygen and Hyperbaric Treatment

Carbon monoxide (CO) is a colourless, odourless, tasteless and non-irritating gas, which is why exposure often goes unnoticed and diagnosis is delayed. It is produced by incomplete combustion of carbon-containing fuels in poorly ventilated spaces. Typical sources are faulty furnaces and space heaters, vehicle exhaust, generators and gas stoves, and smoke from fires. Tobacco smoke is the commonest source of chronic low-level exposure.

Two less obvious sources are worth remembering. Methylene chloride (dichloromethane, a paint stripper and solvent) is metabolised by hepatic CYP2E1 to CO, and because it accumulates in fat the COHb level can keep rising even after the patient is removed from the exposure. Endogenous CO arises from heme breakdown by heme oxygenase, giving a normal COHb of roughly 0.4 to 1.5%.

CO diffuses rapidly across the alveolar-capillary membrane and binds haemoglobin with an affinity approximately 200 to 250 times greater than oxygen, forming carboxyhaemoglobin (COHb). Three things follow: reduced oxygen-carrying capacity, a leftward shift of the oxyhaemoglobin dissociation curve so remaining oxygen is released poorly to tissues, and direct mitochondrial toxicity. The result is cellular hypoxia and metabolic acidosis.

Injury goes beyond hypoxia. CO-induced oxidative stress, lipid peroxidation and myeloperoxidase activity damage myelin and promote inflammation and delayed demyelination of cerebral white matter, the basis of delayed neurological sequelae. The brain and heart, with the highest oxygen demand, are the organs most vulnerable. Infants, pregnant women, older adults and people with cardiopulmonary disease are at higher risk.

Features are non-specific and mimic viral illness, intoxication or psychiatric disease. The commonest symptom is headache, followed by dizziness, weakness and nausea; confusion, poor concentration, breathlessness and visual disturbance may follow. Loss of consciousness is less common but strongly suggests significant toxicity. Tachycardia and tachypnoea are early; severe cases show hypotension, seizures, myocardial ischaemia, arrhythmia, coma and death. Symptoms correlate poorly with the COHb level.

• Delayed neurological sequelae (DNS) appear after a lucid interval of days to weeks: cognitive, behavioural and other neurological problems. Patients with any significant exposure should be counselled to return if new symptoms appear.
• Myocardial injury and arrhythmias can occur, because the heart is one of the organs most vulnerable to hypoxia.
• A pregnancy test is essential in women of childbearing age because a positive result changes management.
• Differential diagnosis includes cyanide poisoning (especially after fire smoke) and methaemoglobinaemia (cyanosis unresponsive to oxygen).

Standard pulse oximetry cannot distinguish oxyhaemoglobin from carboxyhaemoglobin and often gives a falsely reassuring SpO₂. The diagnostic standard is co-oximetry on a blood gas sample to measure COHb. Venous and arterial COHb correlate closely, so an arterial sample is not needed solely to measure COHb. Non-invasive pulse CO-oximeters exist but agree poorly with blood measurement and are not reliable for diagnosis.

• Arterial blood gas may show metabolic acidosis; lactate is often raised but is non-specific and does not track severity.
• In fire victims consider cyanide; take the blood gas before hydroxocobalamin, which can interfere with COHb measurement.
• In suspected deliberate exposure, add paracetamol, salicylate and urine drug screens.

Initial treatment is removal from the source and high-flow 100% oxygen by a non-rebreather mask (intubation and ventilation for impaired consciousness, airway compromise or respiratory failure). Oxygen competes with CO for haemoglobin and shortens the COHb half-life.

HBOT is considered for severe poisoning. Features commonly used to select patients include loss of consciousness, abnormal neurological findings, severe metabolic acidosis, cardiovascular dysfunction, age 36 years or above, prolonged or intermittent exposure, and a COHb of 25% or more; pregnancy also lowers the threshold. Only one rigorous double-blind trial showed fewer cognitive sequelae with 3 HBOT sessions within 24 hours compared with normobaric oxygen; other trials and the Cochrane review are inconsistent. Observational data suggest treatment within 6 hours does better than 6 to 24 hours. Risks include barotrauma and oxygen toxicity (seizures). ECMO is described only in case reports.

Simple asphyxiants are inert gases that act by displacing oxygen from inspired air, so the oxygen concentration falls. Chemical (tissue) asphyxiants interfere with oxygen transport or use even when oxygen is plentiful. Carbon monoxide, cyanide and hydrogen sulfide are the classic chemical asphyxiants.

• Cyanide is eliminated mainly as thiocyanate by rhodanese using thiosulfate. Cherry-red skin and a bitter-almond smell are classically taught but are unreliable. Diagnosis is clinical, supported by profound lactic acidosis.
• Hydrogen sulfide has a characteristic toxidrome: knockdown, pulmonary oedema, conjunctivitis ('gas eye') and odour perception followed by olfactory paralysis. It is a hazard to rescuers, who often become casualties.
• Sodium nitrite is less preferred in smoke inhalation because it causes hypotension and induces methaemoglobin.

• Affinity of CO for haemoglobin — about 200 times that of oxygen.
• Postmortem appearance — cherry-red lividity as the classic finding; living patients rarely look cherry red.
• Pulse oximetry — falsely normal; blood co-oximetry is the test.
• Treatment — 100% oxygen first; hyperbaric oxygen reduces COHb half-life from 4 to 6 hours to about 20 to 30 minutes.
• Delayed neurological sequelae after a lucid interval of days to weeks.
• Cyanide versus CO versus hydrogen sulfide — mechanisms and antidotes (hydroxocobalamin for cyanide).