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Carbon monoxide poisoning

SNOMED: 1149330000784 words•Updated 03/03/2026
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Exam Tips

  • Use the COMA screen in OSCEs: Co-occupants, Outdoors better, Maintenance issues, Alarm present/absent.
  • A normal pulse oximeter reading does not exclude CO poisoning; request COHb measurement and blood gas.
  • Think CO when multiple people (or pets) in one property have similar non-specific symptoms that improve outside.
  • Pregnancy is high risk: fetal toxicity can be severe even when maternal symptoms or COHb appear moderate.
  • Long-term complications can be delayed by up to about 40 days; arrange follow-up advice for cognitive/psychiatric symptoms.

Definition

Carbon monoxide (CO) poisoning is a toxic hypoxic injury syndrome caused by inhalation of a colourless, odourless gas produced by incomplete combustion of carbon-based fuels. It causes reduced oxygen delivery and direct cellular toxicity, with particular risk to high-oxygen-demand organs (brain, heart) and can present acutely or after chronic low-level exposure with non-specific symptoms.

Pathophysiology

CO binds haemoglobin with approximately 240-fold greater affinity than oxygen, forming carboxyhaemoglobin and reducing blood oxygen-carrying capacity. It also shifts the oxyhaemoglobin dissociation curve to the left, impairing oxygen unloading to tissues. Beyond hypoxia, dissolved CO binds intracellular targets (including myoglobin, mitochondrial cytochromes, and guanylyl cyclase), promoting oxidative stress and cellular dysfunction. Severity depends on inspired concentration, duration of exposure, and minute ventilation; fetal toxicity may be disproportionate because fetal haemoglobin has high CO affinity and fetal elimination is slower than maternal elimination. See figure in standard physiology/toxicology texts showing carboxyhaemoglobin formation and left-shifted oxygen dissociation curve.

Risk Factors

  • Faulty, poorly ventilated, or poorly maintained fuel-burning appliances (boilers, heaters, cookers)
  • Blocked chimneys/flues or recent home ventilation changes (for example, tighter double glazing)
  • Using gas ovens for space heating, indoor barbecues, or shisha/hookah in enclosed spaces
  • Vehicle or generator exhaust exposure in enclosed spaces (garages, caravans, boats, tents)
  • Smoke inhalation from fires
  • Occupational exposure to fumes/exhaust (industrial settings, garages, enclosed engine use)
  • Intentional self-harm exposure (often with alcohol/sedatives co-ingestion)
  • Older age, cardiovascular disease, respiratory disease, anaemia
  • Pregnancy and childhood
  • Socioeconomic deprivation and winter-time indoor heating exposure

Clinical Features

Symptoms

  • Headache (most common)
  • Dizziness or vertigo
  • Nausea and vomiting
  • Flu-like malaise and fatigue
  • Myalgia
  • Confusion, poor concentration, memory disturbance
  • Personality or mood change, irritability
  • Visual disturbance
  • Dyspnoea or chest discomfort
  • Syncope or reduced consciousness in severe poisoning

Signs

  • Tachycardia
  • Hypotension
  • Neurological impairment (ataxia, focal deficits, seizures in severe cases)
  • Reduced Glasgow Coma Scale/coma
  • Signs of myocardial ischaemia or arrhythmia
  • Metabolic acidosis/respiratory failure in severe cases
  • Classical cherry-red skin is rare and late

Investigations

Venous or arterial carboxyhaemoglobin (COHb):Elevated COHb supports exposure, but level may be lower than expected if oxygen has already been given or exposure has ceased
Arterial/venous blood gas with lactate:Metabolic acidosis and raised lactate in moderate-severe poisoning
Pulse oximetry:May appear falsely normal; cannot reliably exclude CO poisoning
12-lead ECG and cardiac biomarkers (high-sensitivity troponin):May show myocardial ischaemia, arrhythmia, or myocardial injury
FBC:May identify anaemia, which increases vulnerability to hypoxia
U&Es, CK, LFTs, urinalysis:Assess end-organ injury (for example rhabdomyolysis, renal impairment)
Pregnancy test and urgent obstetric/fetal assessment when pregnant:Maternal COHb may underestimate fetal risk; fetal compromise can occur despite moderate maternal findings
Contextual exposure assessment (COMA history):Co-occupants/pets affected, improvement outdoors, poor appliance maintenance, absent alarm increase diagnostic probability

Management

Lifestyle Modifications

  • Immediately remove from source and move to fresh air; call emergency services
  • Stop exposure for all co-occupants and advise urgent building/appliance safety checks by qualified engineers
  • Do not re-enter potentially contaminated enclosed spaces until declared safe
  • Provide safety-net advice on CO alarms and correct appliance use/ventilation after acute care
  • In deliberate self-harm scenarios, complete psychosocial risk assessment before discharge

Pharmacological Treatment

Medicinal oxygen

  • Oxygen 100% via non-rebreather reservoir mask at 15 L/min immediately (adult and child emergency approach)

Continue high-concentration oxygen until clinical recovery and COHb has fallen to a safe range per local toxicology guidance. Oxygen shortens COHb half-life substantially. Safety: in patients at risk of hypercapnic respiratory failure (for example severe COPD), oxygen is still indicated in suspected CO poisoning, but monitor closely with blood gases and senior/critical care input.

Supportive symptom control

  • Ondansetron 4 mg IV/IM for significant nausea/vomiting (adult)
  • Paracetamol 1 g oral/IV every 4-6 hours, max 4 g/day (adult), for headache

These do not treat toxicity itself; definitive treatment is oxygen and source removal. Check standard contraindications (for example severe hepatic impairment for paracetamol dose adjustment).

Surgical / Interventional

  • Hyperbaric oxygen therapy (specialist chamber-based procedure) for selected severe cases, typically after toxicology consultation: examples include coma/neurological deficit, persistent severe symptoms, significant acidosis, myocardial ischaemia, very high COHb, or pregnancy with significant exposure. Contraindications/cautions include untreated pneumothorax and barotrauma risk.

Complications

  • Delayed neuropsychiatric sequelae (days to weeks): memory and concentration deficits, personality change, mood disturbance, parkinsonian features, psychosis
  • Persistent cognitive impairment
  • Myocardial infarction, arrhythmia, and chronic cardiac morbidity
  • Seizures, cerebral oedema, coma, and death
  • Rhabdomyolysis and acute kidney injury in severe poisoning
  • Pregnancy-related complications: fetal loss, preterm birth, low birth weight, congenital/neurodevelopmental harm

Prognosis

Most patients recover fully with early recognition and prompt oxygen therapy, but prognosis worsens with delayed diagnosis, prolonged exposure, loss of consciousness, cardiac injury, or severe acidosis. Delayed neurocognitive or psychiatric effects can occur up to several weeks later and may persist long term, so follow-up is important for symptomatic or high-risk patients.

Sources & References

✅NICE Guidelines(1)

📖Textbook References(14)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 267)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 389, 390)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 947, 948)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 946, 947)[context]
  • Emergencies in - Obstetrics and Gynaecology, Second Edition (Stergios K. Doumouchtsis, S. Arulkumaran) (Z-Library).pdf(pp. 361, 362)[context]
  • Emergencies in - Obstetrics and Gynaecology, Second Edition (Stergios K. Doumouchtsis, S. Arulkumaran) (Z-Library).pdf(pp. 97, 98)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 90, 91)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 795)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 496, 497)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 886, 887)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 176, 177)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 177)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 852, 853)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 794, 795)[context]

Sources

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