Carbon Monoxide Poisoning

Topic Overview

Summary

Carbon monoxide (CO) poisoning is a leading cause of fatal poisoning worldwide, resulting from inhalation of CO gas which binds haemoglobin with 200-250 times greater affinity than oxygen, forming carboxyhaemoglobin (COHb). This impairs oxygen delivery, shifts the oxygen-haemoglobin dissociation curve leftward, and directly inhibits cellular respiration through cytochrome oxidase binding. Common sources include faulty gas appliances, house fires, car exhaust in enclosed spaces, and portable generators. Clinical presentation is notoriously non-specific, ranging from headache and nausea to syncope, cardiac ischaemia, and death. The classic "cherry-red skin" is a late and rare finding. Diagnosis requires co-oximetry measurement of COHb levels, as standard pulse oximetry is unreliable. Treatment is immediate high-flow 100% oxygen; hyperbaric oxygen therapy (HBOT) is indicated for severe poisoning, neurological symptoms, cardiac involvement, or pregnancy. Delayed neuropsychiatric sequelae (DNS) can occur in 10-40% of survivors, manifesting days to weeks after exposure.

Key Facts

• Mechanism: CO binds haemoglobin → ↓ oxygen-carrying capacity + leftward shift of oxygen-dissociation curve → tissue hypoxia + direct cellular toxicity
• Sources: Faulty gas appliances (boilers, heaters), house fires, car exhaust, portable generators, BBQs/shisha indoors
• Symptoms: Headache (most common), nausea, dizziness, confusion, syncope — easily mistaken for viral illness
• Diagnosis: COHb level on arterial/venous blood gas with co-oximetry (> 3% non-smokers, > 10% smokers is abnormal)
• Pulse oximetry: Falsely normal — cannot distinguish COHb from oxyhaemoglobin
• Treatment: Remove from source + 100% high-flow oxygen (reduces half-life from ~5h to ~90min)
• Hyperbaric oxygen: Indicated for loss of consciousness, COHb > 20-25%, pregnancy, cardiac ischaemia, neurological signs (reduces half-life to ~20min)
• Delayed neuropsychiatric sequelae (DNS): Occurs in 10-40% — cognitive impairment, parkinsonism, personality change — onset 2-40 days post-exposure

Clinical Pearls

"Flu-like symptoms in winter with multiple household members affected" = CO poisoning until proven otherwise

Pulse oximetry may read 100% despite life-threatening COHb levels — always measure COHb with co-oximetry in suspected cases

"Cherry-red skin" is a rare, late sign (seen post-mortem) — absence does NOT exclude severe poisoning

Pregnant patients require HBOT regardless of COHb level — fetal haemoglobin has even higher CO affinity and slower elimination

Normal COHb does NOT exclude poisoning — if presentation delayed, COHb may have already declined but tissue injury persists

Why This Matters Clinically

CO poisoning is the leading cause of poisoning death worldwide, with significant morbidity from delayed neuropsychiatric sequelae. The diagnosis is frequently missed because symptoms mimic common illnesses (viral URTI, gastroenteritis, migraine). High index of suspicion is critical. Early recognition and treatment with 100% oxygen and appropriate HBOT can prevent long-term neurological disability. Public health measures (checking other household members, source investigation) prevent further exposure.

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Visual Summary

Visual assets to be added:

• CO pathophysiology: binding to haemoglobin, myoglobin, and cytochrome oxidase
• Leftward shift of oxygen-haemoglobin dissociation curve with COHb
• Common CO sources and scenarios
• Management algorithm: oxygen therapy decision pathway
• HBOT indications flowchart
• Delayed neuropsychiatric sequelae timeline

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Epidemiology

Incidence and Prevalence

United Kingdom:

• Approximately 4,000 emergency department (ED) attendances annually for CO poisoning [1]
• 40-50 deaths per year from accidental CO poisoning [1]
• Estimated 200 deaths annually when including fire-related CO poisoning [1]
• Suspected to be significantly under-diagnosed due to non-specific presentation

Global:

• Leading cause of poisoning-related mortality worldwide [2]
• United States: ~50,000 ED visits, ~1,500 deaths annually [3]
• Majority of deaths occur in house fires (smoke inhalation + CO)

Demographics and Seasonality

Age and Sex:

• All ages affected
• No significant sex predilection for accidental poisoning
• Intentional poisoning (suicide attempts) more common in males

Seasonality:

• Peak incidence in winter months (October-March) [1]
• Increased use of heating appliances and reduced ventilation
• Carbon monoxide accumulation in enclosed, poorly ventilated spaces

Sources of Exposure

Risk Factors

Environmental:

• Poor ventilation
• Blocked chimneys or flues
• Lack of carbon monoxide detectors
• Older, poorly maintained gas appliances

Individual:

• Infants and children (higher metabolic rate)
• Pregnancy (fetal vulnerability)
• Pre-existing cardiovascular or respiratory disease
• Anaemia (reduced oxygen-carrying capacity)
• Elderly (reduced physiological reserve)

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Pathophysiology

Molecular Mechanisms of Toxicity

Carbon monoxide exerts toxicity through multiple mechanisms:

1. Carboxyhaemoglobin Formation

• CO binds haemoglobin with 200-250 times greater affinity than oxygen [2]
• Forms carboxyhaemoglobin (COHb), which cannot carry oxygen
• Reduces oxygen-carrying capacity of blood

Key point: Even moderate COHb levels (e.g., 20%) dramatically impair oxygen delivery

2. Leftward Shift of Oxygen-Haemoglobin Dissociation Curve

• COHb binding to haemoglobin increases affinity of remaining sites for oxygen [2]
• Shifts dissociation curve to the left
• Result: Oxygen binds more tightly and is not released to tissues (Haldane effect)
• This mechanism contributes as much to toxicity as reduced oxygen-carrying capacity

3. Direct Cellular Toxicity

Cytochrome Oxidase Inhibition:

• CO binds mitochondrial cytochrome c oxidase (Complex IV of electron transport chain) [3]
• Directly impairs cellular respiration
• Particularly affects high-oxygen-demand organs: brain, heart, skeletal muscle

Myoglobin Binding:

• CO binds myoglobin in cardiac and skeletal muscle
• Impairs myocardial contractility
• Contributes to cardiac toxicity

4. Oxidative Stress and Inflammation

• CO exposure triggers lipid peroxidation and oxidative stress [3]
• Neutrophil activation and adhesion to vascular endothelium
• Inflammatory cascade contributes to delayed neurological injury
• May explain delayed neuropsychiatric sequelae (DNS)

Why Pulse Oximetry is Unreliable

Standard pulse oximetry measures only two wavelengths:

• Detects oxyhaemoglobin (HbO₂) and deoxyhaemoglobin (Hb)
• Cannot distinguish COHb from HbO₂ (similar light absorption)
• SpO₂ may read 98-100% despite life-threatening COHb levels [4]

Co-oximetry is required:

• Measures multiple wavelengths (typically 4-8)
• Directly measures COHb, methaemoglobin, oxyhaemoglobin, deoxyhaemoglobin
• Available on arterial/venous blood gas analysers

Carboxyhaemoglobin Kinetics

Half-life of COHb:

• Room air (21% O₂): ~5 hours [2]
• 100% oxygen (non-rebreather mask): ~90 minutes [2]
• Hyperbaric oxygen (2.5-3 ATA): ~20 minutes [2]

Clinical implications:

• Delayed presentation may show normal/low COHb despite significant prior exposure
• Treatment duration guided by symptoms and COHb levels
• Continue oxygen until COHb less than 3% and patient asymptomatic

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Clinical Presentation

Overview

CO poisoning presentation is notoriously non-specific, leading to frequent misdiagnosis. Symptoms depend on:

• COHb level
• Duration of exposure
• Individual susceptibility (age, comorbidities, pregnancy)

Symptoms by Severity

Mild Poisoning (COHb 10-20%)

Moderate Poisoning (COHb 20-40%)

• Confusion, impaired judgement
• Visual disturbances (blurred vision, scotomata)
• Chest pain (cardiac ischaemia — ominous sign)
• Dyspnoea
• Weakness
• Tachycardia, palpitations

Severe Poisoning (COHb > 40%)

• Syncope, loss of consciousness
• Seizures
• Arrhythmias
• Myocardial infarction
• Respiratory failure
• Cerebral oedema
• Coma
• Death (COHb > 60-70%)

Clinical Signs

General:

• Usually normal appearance in mild-moderate cases
• Reduced GCS in severe cases
• Tachycardia (compensatory)
• Hypotension (severe cases)

Skin:

• Cherry-red discolouration of skin and mucous membranes
  • Rare in living patients (more common post-mortem)
  • Indicates severe, often fatal poisoning
  • Absence does NOT exclude CO poisoning
• Cyanosis (severe cases with acidosis)

Cardiovascular:

• Tachycardia
• Hypotension (cardiogenic shock in severe cases)
• Arrhythmias
• Signs of myocardial ischaemia/infarction

Neurological:

• Confusion, agitation
• Focal neurological deficits (rare, but reported)
• Seizures
• Coma

Retinal examination:

• Retinal haemorrhages (rare)
• Cherry-red retinal vessels (rare)

Diagnostic Clues

Special Populations

Pregnancy

• Fetal haemoglobin has higher CO affinity than adult haemoglobin [5]
• Fetal COHb levels 10-15% higher than maternal levels [5]
• Fetal elimination slower (half-life longer)
• Increased risk of:
  • Fetal hypoxia and death
  • Preterm labour
  • Low birth weight
  • Neurodevelopmental impairment
• Maternal symptoms may be mild despite significant fetal toxicity
• HBOT indicated regardless of maternal COHb level [5]

Children

• Higher respiratory rate → greater CO uptake per unit time
• Higher metabolic rate → greater oxygen demand
• More vulnerable to neurological sequelae
• May present with non-specific symptoms (irritability, poor feeding)

Elderly and Cardiovascular Disease

• Pre-existing coronary artery disease → higher risk of myocardial ischaemia/infarction [6]
• Reduced physiological reserve
• Increased risk of arrhythmias
• Higher mortality

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Clinical Examination

ABCDE Assessment

Airway:

• Assess patency
• Consider intubation if GCS ≤8 or respiratory failure

Breathing:

• Respiratory rate (tachypnoea or respiratory depression)
• Oxygen saturation (pulse oximetry unreliable — use co-oximetry)
• Auscultate chest (pulmonary oedema in severe cases)

Circulation:

• Heart rate (tachycardia common)
• Blood pressure (hypotension in severe cases)
• Capillary refill time
• ECG monitoring (ischaemia, arrhythmias)

Disability:

• GCS assessment
• Pupillary reflexes (usually normal unless severe)
• Blood glucose (exclude hypoglycaemia)
• Focal neurological signs (rare, but exclude stroke)

Exposure:

• Skin examination (cherry-red discolouration rare)
• Core temperature

Systematic Examination

Cardiovascular:

• Tachycardia (compensatory)
• Signs of acute coronary syndrome (especially if chest pain)
• Arrhythmias
• Signs of heart failure (severe cases)

Respiratory:

• Tachypnoea
• Pulmonary oedema (severe cases)

Neurological:

• Mental status (confusion, agitation, coma)
• Cranial nerves (usually normal)
• Tone, power, reflexes (usually normal unless severe)
• Cerebellar signs (rare)
• Parkinsonian features (delayed, in DNS)

Other:

• Fundoscopy (retinal haemorrhages rare)
• Abdominal examination (non-specific tenderness)

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Investigations

Immediate Investigations

Blood Gas with Co-Oximetry — ESSENTIAL

Arterial or venous blood gas:

• Arterial and venous COHb levels are similar [7]
• Venous sample acceptable (less invasive)

COHb Level Interpretation:

CRITICAL POINT:

• COHb level may NOT correlate with severity in delayed presentations (half-life ~5h on room air)
• Clinical features and history take precedence over COHb level
• Normal COHb does NOT exclude CO poisoning if presentation is delayed

Metabolic parameters:

• Lactate: Elevated (tissue hypoxia, anaerobic metabolism) — marker of severity [8]
• pH: Metabolic acidosis in severe cases
• Base excess: Negative (metabolic acidosis)

Pulse Oximetry

• Unreliable and falsely reassuring [4]
• May read 98-100% despite COHb > 40%
• Do NOT use to exclude CO poisoning
• Always measure COHb with co-oximetry

Additional Investigations

Cardiac

Troponin:

• Elevated in ~35% of patients with moderate-severe CO poisoning [6]
• Marker of myocardial injury
• Strong predictor of mortality and morbidity [6]
• Consider in all patients with COHb > 10%, chest pain, or cardiovascular comorbidity

ECG:

• Sinus tachycardia (most common)
• ST-segment changes (ischaemia)
• Arrhythmias: atrial fibrillation, ventricular ectopics, VT/VF
• Prolonged QTc (increased arrhythmia risk)
• Consider serial ECGs if cardiac symptoms

Echocardiography:

• If suspected myocardial dysfunction or cardiogenic shock
• May show regional wall motion abnormalities

Haematology and Biochemistry

Full Blood Count:

• Usually normal
• Anaemia may exacerbate tissue hypoxia

Urea and Electrolytes:

• Baseline renal function
• Electrolyte disturbances (rare)

Creatine Kinase (CK):

• Rhabdomyolysis (if prolonged immobilisation/unconsciousness)
• Myoglobin binding to CO can contribute

Glucose:

• Exclude hypoglycaemia (alternative cause of reduced GCS)

Pregnancy test:

• All women of childbearing age (pregnancy changes management)

Neuroimaging

CT Head (non-contrast):

• Indicated if:
  • Severe poisoning with persistent reduced GCS
  • Focal neurological signs
  • Exclude alternative diagnoses (stroke, intracranial haemorrhage)
• Findings in severe CO poisoning:
  • Bilateral globus pallidus hypodensities (classic but rare)
  • Cerebral oedema
  • White matter changes

MRI Brain:

• More sensitive than CT
• T2/FLAIR hyperintensities:
  • Globus pallidus (most common)
  • White matter
  • Hippocampus, cerebellum, substantia nigra
• May predict delayed neuropsychiatric sequelae
• Not routinely required acutely (use for DNS evaluation)

Chest X-Ray

• Pulmonary oedema (severe cases)
• Aspiration pneumonia (if reduced GCS)
• Smoke inhalation injury (if fire exposure)

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Differential Diagnosis

Conditions Mimicking CO Poisoning

Other Toxicological Causes of Tissue Hypoxia

• Cyanide poisoning (smoke inhalation, industrial exposure)
• Hydrogen sulfide poisoning (sewers, industrial)
• Methemoglobinaemia (dapsone, nitrates, local anaesthetics)

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Management

Immediate Management — First 10 Minutes

Oxygen Therapy — Mainstay of Treatment

100% Normobaric Oxygen

Indications:

• All patients with suspected or confirmed CO poisoning

Mechanism:

• Accelerates dissociation of CO from haemoglobin
• Increases dissolved oxygen in plasma (compensates for reduced oxygen-carrying capacity)
• Reduces COHb half-life from ~5 hours to ~90 minutes [2]

Delivery:

• Non-rebreather mask at 15 L/min (provides ~85% FiO₂)
• Bag-valve-mask or endotracheal intubation if:
  • GCS ≤8
  • Respiratory failure
  • Unable to protect airway

Duration:

• Continue until:
  • COHb less than 3% (non-smokers) or less than 5% (smokers)
  • Patient asymptomatic
• Typically 6-12 hours minimum
• Longer if symptoms persist

Hyperbaric Oxygen Therapy (HBOT)

Mechanism:

• Delivers 100% oxygen at increased atmospheric pressure (typically 2.5-3 ATA)
• Reduces COHb half-life to ~20 minutes [2]
• Increases dissolved oxygen in plasma to therapeutic levels
• May reduce delayed neuropsychiatric sequelae (DNS) [9,10]

Evidence:

• Cochrane review: HBOT may reduce cognitive sequelae at 1 month (moderate-quality evidence) [9]
• Debate continues regarding benefit for DNS, but risk is low and potential benefit justifies use [10]

Indications for HBOT:

Refer for HBOT if ANY of the following:

Contraindications (relative):

• Untreated pneumothorax (absolute contraindication)
• COPD with CO₂ retention (relative)
• Claustrophobia, inability to equalize ear pressure (relative)
• Seizure disorder (relative)

Practical considerations:

• Not all centres have HBOT facilities
• Discuss with regional HBOT centre or toxicology service
• Do NOT delay normobaric 100% oxygen while arranging HBOT
• Transfer if HBOT indicated and patient stable

Regimen:

• Typically 2.5-3 ATA for 90-120 minutes
• May require repeat sessions (usually 1-3 total)
• Protocol varies by centre

Supportive Care

Airway and Breathing

• Intubation and mechanical ventilation if:
  • GCS ≤8
  • Respiratory failure
  • Inability to protect airway
• Ventilate with 100% FiO₂

Circulation

• IV fluids for hypotension (cardiogenic or distributive shock)
• Inotropes/vasopressors if refractory hypotension (ICU setting)
• Treat arrhythmias as per ACLS guidelines
• Avoid excessive fluids if pulmonary oedema present

Seizures

• Benzodiazepines (lorazepam 4 mg IV or diazepam 10 mg IV)
• Exclude/treat hypoglycaemia
• Ensure adequate oxygenation

Myocardial Ischaemia

• 100% oxygen (already in progress)
• Aspirin 300 mg (if no contraindications)
• Consider GTN if BP adequate
• Troponin and serial ECGs
• Cardiology consult if STEMI or ongoing ischaemia
• Caution with percutaneous coronary intervention (PCI) — ensure CO toxicity treated first

Rhabdomyolysis

• If CK markedly elevated (e.g., > 5,000 U/L):
  • IV fluid resuscitation
  • Monitor renal function, urine output
  • Urinary alkalinization if severe (sodium bicarbonate)

Public Health and Environmental Measures

Essential actions:

Disposition

Admission criteria:

Discharge criteria:

• COHb less than 5%
• Asymptomatic
• No cardiac or neurological features
• Reliable home environment (source addressed)
• Follow-up arranged

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Complications

Acute Complications

Delayed Neuropsychiatric Sequelae (DNS)

Incidence:

• Occurs in 10-40% of patients with significant CO poisoning [11]
• Higher risk with:
  • Loss of consciousness
  • Age > 36 years
  • Elevated lactate at presentation [12]
  • Abnormal brain imaging (MRI T2 hyperintensities)

Onset:

• Typically 2-40 days after exposure (median ~3 weeks)
• May occur after apparent full recovery (lucid interval)

Clinical features:

Prognosis:

• Variable: some patients improve over months, others have permanent disability
• Parkinsonism may be irreversible
• Majority improve within 1 year, but residual deficits common

Prevention:

• HBOT may reduce DNS risk (evidence moderate quality) [9,10]
• Early, aggressive oxygen therapy

Management:

• Neuropsychological assessment and rehabilitation
• Cognitive therapy, occupational therapy, physiotherapy
• Pharmacotherapy:
  • "Parkinsonian symptoms: levodopa (limited efficacy)"
  • "Depression/anxiety: SSRIs, psychological support"
• Serial MRI to assess structural changes
• Long-term follow-up (neurology/rehabilitation)

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Prognosis and Outcomes

Mortality

Overall:

• Accidental CO poisoning: 1-3% mortality with treatment [1]
• Fire-related CO poisoning: Higher mortality (~20-30%) due to smoke inhalation and burns

Risk factors for death:

• COHb > 40%
• Cardiac ischaemia or arrhythmias
• Severe metabolic acidosis (pH less than 7.1, lactate > 7 mmol/L)
• Age > 65 years
• Prolonged unconsciousness
• Delayed presentation (> 6 hours)

Morbidity

Delayed neuropsychiatric sequelae:

• 10-40% of survivors [11]
• Higher risk with severe initial poisoning

Cardiovascular:

• Increased risk of myocardial infarction in days-weeks post-exposure (especially if underlying CAD) [6]
• Long-term cardiovascular morbidity unclear

Recovery

Acute recovery:

• Most patients asymptomatic within 24-48 hours with appropriate oxygen therapy
• Symptoms may persist for several days

Long-term:

• Full recovery expected if:
  • No loss of consciousness
  • Prompt treatment with 100% oxygen
  • No cardiac or neurological complications
• DNS is the major concern for long-term morbidity

Follow-Up

All patients:

• GP follow-up within 1 week (assess symptoms, ensure source addressed)
• Advise on carbon monoxide alarm installation
• Counsel on symptoms of DNS (return if new cognitive/neurological symptoms)

Moderate-severe poisoning (COHb > 20%, loss of consciousness, HBOT):

• Neurology/toxicology follow-up at 4-6 weeks
• Neuropsychological testing if symptoms suggestive of DNS
• MRI brain if DNS suspected (T2/FLAIR for globus pallidus/white matter changes)
• Longer-term follow-up as needed (rehabilitation services)

Pregnancy:

• Obstetric follow-up with fetal monitoring
• Increased surveillance for fetal compromise
• Counsel on risk of neurodevelopmental effects

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Evidence and Guidelines

Key Guidelines

1. Undersea and Hyperbaric Medical Society (UHMS)

   • Indications for Hyperbaric Oxygen Therapy (14th Edition, 2019) [13]
   • Recommends HBOT for CO poisoning with loss of consciousness, neurological symptoms, cardiac involvement, COHb > 25%, pregnancy

2. National Poisons Information Service (NPIS) TOXBASE (UK)

   • Carbon Monoxide Poisoning Management
   • Comprehensive online resource for UK clinicians
   • Updated regularly with evidence-based recommendations

3. European Consensus Conference on Hyperbaric Medicine (2016) [14]

   • Type 1 recommendation (accepted indication) for HBOT in severe CO poisoning
   • Type 2 recommendation (HBOT should be considered) for moderate poisoning with risk factors

Key Studies and Reviews

Hyperbaric Oxygen Therapy:

4. Weaver LK et al. (2002) — Randomized trial of HBOT for acute CO poisoning

   • N Engl J Med 2002;347:1057-1067 [PMID: 12362006]
   • Found reduced cognitive sequelae at 6 and 12 months with HBOT

5. Cochrane Review: Buckley NA et al. (2011) — Hyperbaric oxygen for CO poisoning [9]

   • Cochrane Database Syst Rev 2011;(4):CD002041 [PMID: 21491385]
   • Concluded HBOT may reduce cognitive sequelae at 1 month (moderate-quality evidence)
   • Called for further high-quality trials

Pathophysiology and Clinical Features:

6. Rose JJ et al. (2017) — Comprehensive review of CO poisoning [2]

   • Am J Respir Crit Care Med 2017;195:596-606 [PMID: 27753502]
   • Detailed pathophysiology, clinical features, management

7. Weaver LK (2009) — Clinical review in NEJM [3]

   • N Engl J Med 2009;360:1217-1225 [PMID: 19297574]
   • Classic review article on CO poisoning

Cardiac Toxicity:

8. Henry CR et al. (2006) — Myocardial injury and long-term mortality [6]
   • JAMA 2006;295:398-402 [PMID: 16434630]
   • Troponin elevation predicts mortality

Delayed Neuropsychiatric Sequelae:

9. Ku HL et al. (2010) — Predictors of DNS
   • Clin Toxicol (Phila) 2010;48:755-761 [PMID: 20863206]
   • Loss of consciousness, age > 36, and elevated lactate predict DNS

Pregnancy:

10. Koren G et al. (1991) — Fetal outcomes after maternal CO poisoning [5]
    • Teratology 1991;44:225-228 [PMID: 1806148]
    • Fetal COHb levels exceed maternal; increased risk of death and neurodevelopmental impairment

Diagnosis:

11. Roth D et al. (2011) — Accuracy of pulse CO-oximetry
    • Ann Emerg Med 2011;58:74-79 [PMID: 21195507]
    • Non-invasive pulse CO-oximetry NOT sufficiently accurate; blood co-oximetry required

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Patient and Family Information

What is Carbon Monoxide Poisoning?

Carbon monoxide (CO) is a poisonous gas that you cannot see, smell, or taste. It is produced when fuels like gas, oil, coal, or wood do not burn completely. Common sources include faulty boilers, gas heaters, car exhaust, and house fires.

When you breathe in CO, it enters your bloodstream and stops your blood from carrying oxygen to your organs. This can make you very unwell and can be life-threatening.

What are the Symptoms?

Symptoms of CO poisoning include:

• Headache (often the first symptom)
• Feeling sick (nausea) and vomiting
• Dizziness and confusion
• Weakness and tiredness
• Chest pain
• Shortness of breath
• Collapse or loss of consciousness

These symptoms are similar to flu, but CO poisoning does not cause a high temperature (fever).

What Should I Do if I Suspect CO Poisoning?

1. Get fresh air immediately — leave the building and do not go back inside
2. Call 999 for an ambulance
3. Turn off gas appliances if safe to do so (but prioritize leaving the area)
4. Do not use the appliance or building until it has been checked by a qualified engineer

If multiple people in your home have similar symptoms, this is a major warning sign of CO poisoning.

How is it Diagnosed?

• A blood test measures the level of carbon monoxide in your blood (carboxyhaemoglobin)
• The test is quick and uses a small blood sample
• Standard "finger probe" oxygen monitors can be falsely normal, so a blood test is essential

How is it Treated?

• 100% oxygen through a tight-fitting mask
  • This helps remove CO from your blood
  • You may need oxygen for several hours
• Hyperbaric oxygen therapy (breathing 100% oxygen in a pressurized chamber)
  • Used for severe poisoning
  • Speeds up removal of CO from your body
  • May reduce long-term brain problems
• Admission to hospital for monitoring and treatment
• Treatment of complications (e.g., heart problems)

What are the Risks?

Immediate risks:

• Heart attack
• Brain damage
• Seizures
• Death (in severe cases)

Long-term risks:

• Delayed brain problems can occur 2-40 days after exposure, even if you initially felt better
• Symptoms include memory problems, difficulty concentrating, personality changes, and movement problems
• Affects 10-40% of people with moderate or severe poisoning

How Can I Prevent CO Poisoning?

1. Install carbon monoxide alarms

   • Place in hallways and near bedrooms
   • Test regularly and replace batteries annually
   • Replace alarms every 5-7 years

2. Have gas appliances serviced annually

   • Use a Gas Safe registered engineer (UK)
   • Check boilers, heaters, cookers, fires

3. Ensure adequate ventilation

   • Do not block air vents or flues
   • Keep chimneys clean and unblocked

4. Never use:

   • BBQs, camping stoves, or generators indoors
   • Petrol-powered equipment in enclosed spaces

5. Be aware of the symptoms

   • Seek help if multiple people in your home feel unwell

What Happens After Treatment?

• Most people make a full recovery if treated quickly
• You will need follow-up appointments to check for delayed brain problems
• If you were pregnant when poisoned, you will need extra monitoring of your baby
• Ensure the source of CO is fixed before returning home

Resources

• Gas Safe Register (UK): www.gassaferegister.co.uk — Find qualified engineers
• NHS Carbon Monoxide Poisoning: www.nhs.uk
• National Poisons Information Service (NPIS): For healthcare professionals — TOXBASE

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Examination Focus: MRCP PACES / Viva Scenarios

Scenario 1: Acute Presentation in ED

Viva Stem: "A 42-year-old woman presents to the emergency department in January with headache, nausea, and dizziness for 6 hours. Her husband and two children also have headaches. Their gas boiler was serviced yesterday. SpO₂ is 99% on air. What is your differential diagnosis and initial management?"

Model Answer:

Differential diagnosis:

1. Carbon monoxide poisoning (top differential)

   • Multiple household members affected
   • Recent boiler service (possible faulty installation)
   • Winter presentation
   • Non-specific symptoms (headache, nausea, dizziness)
   • SpO₂ is falsely reassuring (pulse oximetry cannot detect COHb)

2. Other considerations (less likely):

   • Viral gastroenteritis (but no fever, diarrhoea)
   • Food poisoning (would expect vomiting, diarrhoea)
   • Influenza (would expect fever)

Initial management:

1. Remove all household members from the property immediately
2. 100% high-flow oxygen via non-rebreather mask (15 L/min) for patient and all symptomatic family members
3. Blood gas with co-oximetry (arterial or venous) — measure COHb
4. IV access, bloods: FBC, U&E, glucose, troponin, lactate
5. ECG — assess for cardiac ischaemia
6. Pregnancy test (woman of childbearing age)
7. Monitor: continuous ECG, BP, GCS
8. Assess COHb levels and clinical severity to determine need for HBOT
9. Public health measures:
   • Contact Gas Safe engineer urgently
   • Evacuate building
   • Screen all household members (children too)

Key teaching point:

• Multiple household members with "flu-like" symptoms = CO poisoning until proven otherwise
• Pulse oximetry is unreliable — always measure COHb with co-oximetry

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Scenario 2: Hyperbaric Oxygen Decision

Viva Stem: "A 68-year-old man with ischaemic heart disease is brought to ED after being found unconscious next to his running car in a closed garage. On arrival, GCS is 12 (E3V4M5). SpO₂ 98% on 15L O₂. Blood gas shows COHb 32%, lactate 6.2 mmol/L, pH 7.28. ECG shows ST depression in leads V4-V6. Troponin is elevated. Does this patient require hyperbaric oxygen therapy?"

Model Answer:

Yes — multiple indications for HBOT:

1. Loss of consciousness (found unconscious, GCS 12)
2. COHb > 20% (32% in this case)
3. Cardiac ischaemia (ST depression, elevated troponin)
4. Metabolic acidosis (pH 7.28, lactate 6.2 mmol/L)

Any ONE of these is an indication for HBOT; this patient has FOUR.

Immediate actions:

1. Continue 100% oxygen (already in progress)
2. Contact regional HBOT centre urgently for transfer
3. Aspirin 300 mg (if no contraindications — cardiac ischaemia)
4. Monitor continuously: ECG, BP, GCS, oxygen saturation
5. Serial troponins and ECGs
6. Cardiology consultation (concurrent ACS management)
7. Repeat blood gas in 2-4 hours (assess COHb decline, lactate trend, pH)
8. ICU involvement (severe poisoning, cardiac ischaemia, impaired GCS)

Contraindications to HBOT?

• Untreated pneumothorax (absolute) — not present here
• Relative contraindications: COPD, claustrophobia — weigh risks vs benefits
• In this case, benefits clearly outweigh risks

Expected benefit:

• Reduces COHb half-life from ~90 min (on 100% O₂) to ~20 min (HBOT)
• May reduce delayed neuropsychiatric sequelae
• Improves tissue oxygenation in setting of cardiac ischaemia

Key teaching point:

• Do NOT delay transfer for HBOT if indicated
• Continue 100% normobaric oxygen until HBOT available
• Pre-existing cardiac disease increases risk — aggressive treatment essential

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Scenario 3: Pregnancy

Viva Stem: "A 28-year-old woman at 28 weeks' gestation presents with mild headache and nausea after her gas fire malfunctioned. She feels 'almost back to normal' now. COHb is 8%. Does she require hyperbaric oxygen therapy?"

Model Answer:

Yes — pregnancy is an absolute indication for HBOT regardless of COHb level or maternal symptoms.

Rationale:

1. Fetal haemoglobin has higher CO affinity than adult haemoglobin
2. Fetal COHb levels are 10-15% higher than maternal levels
3. Fetal elimination of CO is slower (longer half-life)
4. Maternal symptoms do NOT correlate with fetal toxicity
   • Mother may be mildly symptomatic or asymptomatic
   • Fetus may still have significant hypoxia
5. Risks of CO to fetus:
   • Fetal death
   • Preterm labour
   • Low birth weight
   • Neurodevelopmental impairment (cerebral palsy, cognitive impairment)

Management:

1. 100% high-flow oxygen immediately (non-rebreather mask, 15 L/min)
2. Contact HBOT centre for urgent transfer (pregnancy is priority indication)
3. Obstetric involvement:
   • Fetal heart rate monitoring (CTG)
   • Ultrasound assessment of fetal wellbeing
4. Continue oxygen therapy for longer duration than non-pregnant patients (aim for COHb less than 3% due to slower fetal elimination)
5. Admission for monitoring (minimum 24 hours)
6. Arrange follow-up with obstetrics for increased surveillance
7. Counsel regarding risks to fetus and importance of HBOT

Key teaching point:

• Pregnancy = HBOT regardless of COHb level or symptoms
• Fetal risk exceeds maternal risk
• Maternal COHb of 8% might seem "mild," but fetal COHb could be 18-20%

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Scenario 4: Delayed Presentation

Viva Stem: "A 55-year-old man presents 18 hours after exposure to car exhaust fumes in a suicide attempt. He was unconscious for an estimated 2 hours before being found. He is now alert (GCS 15) and asymptomatic. COHb is 4%. Should he be discharged?"

Model Answer:

No — this patient requires admission, monitoring, and likely HBOT despite low COHb and current clinical wellbeing.

Rationale:

1. COHb level does NOT reflect severity in delayed presentations
   • Half-life on room air ~5 hours
   • 18 hours post-exposure → COHb has largely cleared
   • Initial COHb was likely > 40% (given prolonged unconsciousness)
2. History of loss of consciousness is an indication for HBOT
   • Severe poisoning at time of exposure
   • High risk of delayed neuropsychiatric sequelae (DNS)
3. HBOT may reduce DNS risk, even if COHb now normal
4. Tissue injury may persist despite normal COHb

Management:

1. Admit (psychiatric and toxicology input)
2. Discuss with HBOT centre — HBOT may still be beneficial within 24 hours
3. Troponin, ECG (cardiac toxicity)
4. Lactate, pH (markers of tissue hypoxia)
5. Monitor for neurological/cardiac complications
6. Counsel regarding DNS:
   • May occur 2-40 days post-exposure
   • Symptoms: memory problems, personality change, Parkinsonism
   • Advise to return if symptoms develop
7. Psychiatric assessment (suicide attempt)
8. Arrange neurology follow-up (4-6 weeks) with neuropsychological testing

Key teaching point:

• Normal COHb in delayed presentation does NOT exclude severe poisoning
• History (loss of consciousness) takes precedence over delayed COHb level
• HBOT may still be beneficial within 24 hours of exposure

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Scenario 5: Differential Diagnosis Challenge

Viva Stem: "A 45-year-old smoker presents with headache, nausea, and confusion. You measure a COHb level of 8%. Can you exclude CO poisoning?"

Model Answer:

No — COHb of 8% does NOT exclude CO poisoning in a smoker.

Interpretation:

1. Smokers have baseline COHb levels of 3-10% depending on smoking habits
2. COHb of 8% could represent:
   • Baseline smoking (heavy smoker)
   • Mild CO poisoning superimposed on baseline (e.g., true COHb might be 15%, but smoking contributes 7%)
3. Clinical features take precedence over isolated COHb level

Approach:

1. Take detailed history:
   • Environmental clues (faulty appliances, multiple people affected, fire exposure)
   • Smoking history (how much, when last cigarette)
   • Timing of symptom onset
2. Measure COHb serially:
   • If true CO poisoning, COHb will decline with 100% oxygen therapy (half-life ~90 min)
   • If purely from smoking, COHb will not decline rapidly
3. Assess response to 100% oxygen:
   • Symptoms should improve with oxygen therapy if CO poisoning
4. Other investigations:
   • Lactate (elevated in CO poisoning)
   • Troponin, ECG (cardiac effects)
5. Environmental investigation:
   • Check CO levels in patient's home
   • Screen other household members
6. Treat as CO poisoning if:
   • Clinical suspicion high
   • Environmental clues present
   • Symptoms improve with oxygen

Key teaching point:

• Never exclude CO poisoning based solely on COHb level in smokers
• Serial COHb measurements and clinical correlation essential
• When in doubt, treat as CO poisoning (100% oxygen is harmless and life-saving if CO present)

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Special Considerations

Smoke Inhalation in House Fires

Combined toxicity:

• CO poisoning (incomplete combustion)
• Cyanide poisoning (combustion of synthetic materials — plastics, foams)
• Thermal injury to airway
• Particulate matter and chemical irritants

Clinical clues to cyanide co-poisoning:

• Severe metabolic acidosis (lactate > 10 mmol/L)
• Altered mental status out of proportion to COHb level
• Cardiovascular collapse
• Carboxyhaemoglobin may be normal or mildly elevated (cyanide acts at cellular level, not haemoglobin)

Management:

• 100% oxygen (treats both CO and cyanide)
• Consider hydroxocobalamin (cyanide antidote) if:
  • Severe acidosis (lactate > 10 mmol/L)
  • Altered mental status with low COHb
  • Enclosed-space fire with synthetic materials
• Early intubation for airway protection (thermal injury, oedema)
• HBOT if CO poisoning criteria met

Intentional CO Poisoning (Suicide Attempts)

Epidemiology:

• Car exhaust in enclosed garage (decreasing with catalytic converters)
• Charcoal burning (increasingly common method, especially in East Asia)

Management considerations:

• Often severe poisoning (prolonged exposure, high concentrations)
• High risk of HBOT indications (loss of consciousness, COHb > 40%)
• Psychiatric assessment and mental health act considerations
• One-to-one nursing (suicide precautions)
• Careful assessment for co-ingestions (other drugs/alcohol)

Chronic Low-Level CO Exposure

Presentation:

• Insidious onset of non-specific symptoms
• Chronic headaches, fatigue, poor concentration, irritability
• Often misdiagnosed as depression, chronic fatigue syndrome
• May not have elevated COHb at time of presentation (exposure intermittent, e.g., only when heating on)

Diagnosis:

• High index of suspicion based on history
• Measure CO levels in home environment
• Trial removal from environment (symptoms should improve)

Management:

• Identify and rectify source
• Prolonged recovery may be required (weeks to months)
• Neuropsychological assessment if cognitive symptoms persist

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Key Examination Themes

Common Viva Topics

1. Why is pulse oximetry unreliable in CO poisoning?

   • Standard pulse oximetry uses 2 wavelengths (red and infrared)
   • Cannot distinguish COHb (red) from oxyhaemoglobin (red)
   • SpO₂ may read 98-100% despite COHb > 40%
   • Co-oximetry (4-8 wavelengths) required to measure COHb directly

2. Describe the mechanisms of CO toxicity

   • High-affinity binding to haemoglobin → ↓ oxygen-carrying capacity
   • Leftward shift of oxygen-dissociation curve → oxygen not released to tissues (Haldane effect)
   • Binding to cytochrome oxidase → inhibits cellular respiration
   • Binding to myoglobin → myocardial dysfunction
   • Oxidative stress and inflammation → delayed neurological injury

3. What are the indications for hyperbaric oxygen therapy?

   • Loss of consciousness at any time
   • Neurological symptoms/signs (GCS less than 15, seizures, focal deficits)
   • Cardiac ischaemia/arrhythmias (troponin elevation, ECG changes)
   • COHb > 20-25%
   • Pregnancy (regardless of COHb level)
   • Metabolic acidosis (pH less than 7.1 or lactate > 7 mmol/L)
   • Failure to improve with normobaric oxygen after 4-6 hours

4. What is delayed neuropsychiatric sequelae (DNS)?

   • Neurological/psychiatric symptoms occurring 2-40 days post-exposure
   • Occurs in 10-40% of moderate-severe CO poisoning survivors
   • Manifests as cognitive impairment, personality change, Parkinsonism, psychiatric symptoms
   • May occur after initial apparent recovery (lucid interval)
   • Predictors: loss of consciousness, age > 36, elevated lactate
   • HBOT may reduce risk
   • Variable prognosis: some improve, others have permanent disability

5. How does CO poisoning affect pregnant patients differently?

   • Fetal haemoglobin has higher CO affinity than adult haemoglobin
   • Fetal COHb levels 10-15% higher than maternal
   • Fetal elimination slower (longer half-life)
   • Maternal symptoms do NOT predict fetal toxicity
   • Risks: fetal death, preterm labour, neurodevelopmental impairment
   • HBOT indicated regardless of maternal COHb level or symptoms

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References

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Document Control:

• Topic ID: carbon-monoxide-poisoning-adult
• Version: 2.0 (Gold Standard)
• Last Updated: 2026-01-07
• Next Review: 2027-01-07
• Evidence Level: High
• Citation Count: 20 PubMed-indexed sources