Carbon Monoxide Poisoning

Introduction

Carbon monoxide is a colourless, odourless gas produced by incomplete combustion of carbon-based fuels. It is a leading cause of accidental poisoning death in the UK, and its danger lies largely in how easily it is missed - the presentation is non-specific, standard monitoring equipment gives falsely reassuring readings, and the exposure itself is invisible.¹

Common sources include faulty or poorly ventilated gas boilers and heaters, blocked or damaged flues and chimneys, charcoal barbecues used indoors or in enclosed spaces (including tents), petrol generators run in enclosed areas, and smoke inhalation in house fires. Poisoning peaks in winter, when heating appliances are used more and ventilation is often reduced.

• Rented and poorly maintained accommodation, where appliance servicing may be overdue or neglected
• Recently arrived boilers, heaters or flues, or any appliance installed or serviced by someone who is not Gas Safe registered
• Camping and caravanning, particularly barbecues, gas stoves or heaters used inside a tent, caravan or poorly ventilated boat cabin
• Occupational exposure - workers using petrol-powered tools or generators in enclosed or poorly ventilated spaces
• Smokers and passengers in vehicles with a faulty exhaust system, which raise baseline carboxyhaemoglobin even without an acute exposure

Pathophysiology

Carbon monoxide binds haemoglobin with an affinity roughly 200-250 times greater than oxygen, forming carboxyhaemoglobin (COHb) and directly reducing the blood's oxygen-carrying capacity. It also shifts the oxygen-haemoglobin dissociation curve to the left, impairing the release of what oxygen remains bound to haemoglobin, and binds intracellular targets including myoglobin and cytochrome c oxidase, disrupting cellular respiration directly - which is why carbon monoxide toxicity is not fully explained by hypoxia alone and why tissues with the highest oxygen demand (brain and heart) are affected earliest and most severely.

Clinical features

Symptoms are notoriously non-specific and are frequently mistaken for a viral illness, migraine, or gastroenteritis, which is exactly why the diagnosis is so often missed on a first presentation.

Chronic low-level exposure

Not every presentation is a single acute exposure. Chronic low-level poisoning from a persistently faulty appliance can cause weeks or months of vague, fluctuating symptoms - fatigue, headache, poor concentration, low mood - that are often misattributed to stress, depression or a viral illness, sometimes across an entire household, and sometimes across repeated GP or emergency department attendances before the true cause is recognised. A history of symptoms that consistently improve at weekends, on holiday, or whenever the patient is away from a particular building is the key discriminator, and should prompt specific questioning about heating and cooking appliances at home or work.

Investigations

• Carboxyhaemoglobin level - measured by co-oximetry on a venous or arterial blood gas, not by standard pulse oximetry; normal is under 3% in non-smokers and up to around 10% in smokers, and levels above this support the diagnosis, though the level does not reliably correlate with clinical severity or predict delayed neurological sequelae, so treatment decisions are based on the clinical picture as much as the number
• ECG - look for ischaemic changes and arrhythmia, particularly in patients with chest pain or a significant exposure
• Troponin - if myocardial injury is suspected, since even patients without known coronary disease can sustain a hypoxic infarction
• Lactate and venous/arterial blood gas - to assess the severity of tissue hypoxia
• Pregnancy test - fetal haemoglobin has a higher affinity for carbon monoxide than adult haemoglobin, and the fetus is at particular risk even when the mother's symptoms are mild

Management

Remove the patient from the source of exposure and ensure the environment (and anyone else in it) is safe before treatment begins.

• High-flow 100% oxygen via a tight-fitting non-rebreathe mask, regardless of the pulse oximetry reading, continued until the carboxyhaemoglobin level normalises and symptoms resolve. High-flow oxygen reduces the COHb half-life from roughly 4-6 hours breathing room air to around 1 hour
• ABCDE support as needed - airway protection for reduced consciousness, seizure management, cardiac monitoring and treatment of arrhythmia
• Hyperbaric oxygen therapy is considered for severe poisoning - loss of consciousness at any point, neurological signs, cardiac ischaemia, a significantly raised COHb, or pregnancy - as it further accelerates COHb elimination and may reduce the risk of delayed neurological sequelae, though the supporting evidence is debated and access varies; discuss with a poisons information service or regional hyperbaric unit where the picture is severe²
• Admit for observation those with significant symptoms, cardiac involvement, or any loss of consciousness

Delayed neurological sequelae

A meaningful proportion of patients with significant poisoning develop delayed neurological sequelae - cognitive impairment, personality change, parkinsonism, or other neuropsychiatric symptoms - emerging days to weeks after apparent full recovery. The mechanism is thought to relate to delayed demyelination and is not reliably predicted by the peak carboxyhaemoglobin level or the severity of the initial presentation, which is why all patients with significant exposure need clear safety-netting advice and, ideally, follow-up.

Risk factors for delayed neurological sequelae include loss of consciousness at the time of exposure, older age, and a longer duration of exposure, though the association is imperfect enough that even apparently mild poisoning warrants a warning. Advise patients and families to seek review for new memory problems, personality or mood change, difficulty concentrating, or new movement symptoms in the weeks after exposure, rather than assuming full recovery is guaranteed simply because the acute symptoms have settled.

Public health and prevention

• Notify relevant authorities where appropriate, and advise the patient not to return home until the source has been identified and made safe - involve the fire service or a Gas Safe registered engineer
• Household screening - anyone else who lives in or has recently visited the property should also be assessed, since exposure is rarely limited to one person
• Advise on carbon monoxide alarms and regular servicing of gas appliances and flues as ongoing prevention
• Consider safeguarding where poisoning results from a deliberately unsafe living environment or possible self-harm

Differential diagnosis

• Viral illness or influenza - lacks the environmental clue and household clustering
• Migraine - recurrent, often with a personal history and typical aura, without an exposure pattern
• Gastroenteritis - prominent diarrhoea is uncommon in carbon monoxide poisoning
• Food poisoning affecting a household - consider alongside carbon monoxide when several people who share a meal or a house become unwell together

Red flags

Prognosis

Mild poisoning generally resolves completely with removal from exposure and oxygen therapy. Severe poisoning carries a risk of death from cardiac and neurological injury, and survivors of significant exposure remain at risk of delayed neurological sequelae for weeks afterwards, which is why follow-up and clear safety-netting advice matter as much as the acute treatment itself.