CO Poisoning — UKMLA Guide 2026

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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.

Key points

CO binds haemoglobin with 240× greater affinity than O₂ → carboxyhaemoglobin (COHb) → tissue hypoxia
Sources: faulty gas appliances (boilers, heaters), house fires, car exhaust, barbecues in enclosed spaces
Symptoms: headache, nausea, dizziness, confusion, chest pain, seizures, coma, death. Suspect if multiple household members symptomatic
SpO₂ is UNRELIABLE — pulse oximetry cannot distinguish COHb from oxyhaemoglobin. Use ABG with co-oximetry
Treatment: 100% high-flow oxygen via non-rebreather mask — reduces COHb half-life from 4–6 h to 60–90 min
Hyperbaric oxygen: consider if COHb >25%, LOC, neurological/cardiac features, or pregnant. Half-life reduced to 20–30 min

Overview

Carbon monoxide (CO) is a colourless, odourless, tasteless gas produced by incomplete combustion of carbon-containing fuels. It causes poisoning by binding to haemoglobin with approximately 240 times the affinity of oxygen, forming carboxyhaemoglobin (COHb), which cannot carry oxygen. CO also binds to myoglobin (causing cardiac dysfunction), cytochrome oxidase (impairing cellular respiration), and triggers oxidative stress and inflammation, particularly in the brain. The net effect is both hypoxic and direct cellular toxicity. Delayed neuropsychiatric syndrome (DNS) can develop 2–40 days after apparent recovery, presenting with cognitive impairment, personality change, and movement disorders. Common sources include faulty gas boilers, house fires, car exhaust in enclosed spaces, and charcoal/gas barbecues used indoors. A key diagnostic clue is multiple household members presenting with similar symptoms simultaneously.

Epidemiology

CO poisoning causes approximately 30–50 deaths per year in the UK and an estimated 4,000 ED attendances. It is more common in winter (increased use of heating appliances). The Gas Safety (Installation and Use) Regulations require annual gas safety checks for rented properties. House fires account for the majority of severe/fatal cases. Unintentional CO exposure from faulty domestic appliances (boilers, gas fires, wood burners) is a common cause of subacute presentations. Students, tenants in older properties, and elderly living alone are at increased risk. Intentional CO poisoning (deliberate self-harm via car exhaust) has decreased with catalytic converters but still occurs.

Clinical Features

Symptoms

Headache — most common symptom (~90%). Often described as frontal, throbbing

Nausea, vomiting, dizziness

Confusion, impaired concentration, irritability

Chest pain, palpitations (CO-induced cardiac ischaemia)

Breathlessness

Seizures, reduced consciousness, coma

Symptoms improve when away from source (e.g. better when outdoors, recur when home)

Multiple household members/colleagues affected simultaneously

Signs

Cherry-red skin colour (classical but RARE and unreliable — usually only seen post-mortem)

Tachycardia

Altered consciousness, confusion

Hyperventilation

Normal or falsely normal SpO₂ (pulse oximeter cannot distinguish COHb from O₂Hb)

Cardiac arrhythmias, hypotension (severe)

Retinal haemorrhages (severe poisoning)

Investigations

First-line

ABG with co-oximetryCOHb level — DIAGNOSTIC. Normal non-smoker <3%, smoker <10%. Symptomatic usually >10%. Severe >25%. Note: level may have fallen by time of hospital arrival

ECGST changes (CO-induced myocardial ischaemia), arrhythmias. Troponin if cardiac symptoms

Second-line

FBC, U&Es, lactateMetabolic acidosis and raised lactate indicate severe tissue hypoxia

TroponinIf chest pain or ECG changes — CO causes myocardial injury even in young patients

Pregnancy testFetal haemoglobin has even higher affinity for CO — fetal COHb is 10–15% higher than maternal

Specialist

Neuropsychological testingAt follow-up — assess for delayed neuropsychiatric syndrome (DNS). Occurs in 10–30% at 2–40 days

MRI brainIf neurological deficits — may show globus pallidus and white matter changes

Management

NICE CKS — Carbon monoxide poisoning; Toxbase

Immediate

Remove from source — ensure scene safety (ventilate area, do not enter without appropriate safety equipment)
100% high-flow oxygen via tight-fitting non-rebreather mask at 15 L/min — continue until COHb <5% and symptoms resolved
High-flow O₂ reduces COHb half-life: room air 4–6 h → 100% O₂ 60–90 min → hyperbaric O₂ 20–30 min
Intubate and ventilate with 100% O₂ if GCS ≤8 or unable to protect airway
Cardiac monitoring — risk of arrhythmias and myocardial ischaemia

Hyperbaric oxygen therapy (HBO)

Consider if: COHb >25%, loss of consciousness at any point, neurological features (seizures, ataxia, cognitive impairment), cardiac ischaemia/arrhythmia, pregnant (lower threshold)
Contact nearest hyperbaric chamber (National Diving Accident Helpline / local protocol)
HBO reduces DNS risk — evidence debated but recommended for severe poisoning
Contraindications: untreated pneumothorax

Supportive and follow-up

Treat associated injuries (smoke inhalation, burns in house fire)
Alert gas emergency service (0800 111 999) if domestic appliance suspected — do not let patient return home until source identified and isolated
Environmental Health referral for rented properties
Advise CO alarm installation
Follow-up at 4–6 weeks: screen for delayed neuropsychiatric syndrome (personality change, memory impairment, movement disorders)

Complications

Delayed neuropsychiatric syndrome (DNS): Develops 2–40 days post-exposure in 10–30%. Cognitive impairment, personality change, parkinsonism, incontinence. May be permanent
Myocardial injury: Troponin elevation, arrhythmias, heart failure — even in young patients without coronary disease
Death: COHb >50% usually fatal. Death often occurs at scene (found dead)
Fetal harm: Fetal Hb has higher CO affinity — fetal COHb 10–15% higher than maternal. Risk of miscarriage, neurological damage, death

UKMLA Exam Tips

1SpO₂ is UNRELIABLE in CO poisoning — pulse oximeter reads COHb as O₂Hb and gives falsely normal reading. Use ABG with co-oximetry
2Cherry-red skin is RARE clinically — mostly a post-mortem finding. Do not rely on it
3Multiple household members with headache/nausea = CO poisoning until proven otherwise
4Treatment: 100% O₂ via NRB mask. Reduces COHb half-life from ~4–6 h to ~60–90 min
5Hyperbaric O₂: consider if LOC, neurological symptoms, COHb >25%, pregnant, cardiac features
6Delayed neuropsychiatric syndrome at 2–40 days: cognitive decline, personality change, parkinsonism. Follow up at 4–6 weeks
7Pregnant patients: lower threshold for HBO. Fetal Hb has even higher CO affinity

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