Makindo Medical Notes

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Tight affinity
All bound same vicinity
Space heater on fritz
Household red, barely alive
Force free heme, O₂, deep dive    
@DrCindyCooper

CO poisoning is not apparent on a pulse oximeter and needs an ABG if suspected. Key to prognosis is removal from the source of carbon monoxide as quickly as possible and instigation of high flow oxygen treatment. Normally CO is <10%. In city dwellers or smokers, levels can be raised up to 10%. A carboxyhaemoglobin level of 30% indicates severe exposure.

About

• Carbon monoxide (CO) binds avidly to haemoglobin (Hb) with 240 times the affinity of oxygen, forming carboxyhaemoglobin (CoHb).
• CO is an odourless, colourless gas, making it difficult to detect without appropriate devices or detectors.
• Pulse oximeters misinterpret CoHb as oxyhaemoglobin, potentially leading to falsely normal SpO₂ readings despite significant hypoxia.
• The half-life of CO when breathing air is 320 minutes, but it can be reduced to 80 minutes with 100% oxygen and to 20-30 minutes with HBOT.

Aetiology

• CO exposure occurs from various sources, including faulty furnaces, gas heaters, vehicle exhausts, and enclosed fires.
• The gas inhibits cellular respiration by binding to cytochrome oxidase a3, disrupting the electron transport chain and leading to cellular hypoxia.
• CO shifts the oxygen-haemoglobin dissociation curve to the left, reducing oxygen release to tissues, further contributing to hypoxia.
• House fires or poorly ventilated indoor heaters are common causes in the winter months, leading to accidental poisoning.
• Chronic low-level exposure can occur in industrial settings, whereas acute high-dose exposure is more likely in enclosed spaces.

Clinical Presentation

• Early Symptoms: Headache, dizziness, nausea, and malaise. The classic description is of a "tension-like" headache that worsens in a confined space.
• Neurological Symptoms: Confusion, irritability, visual disturbances, and impaired judgment. Severe exposure can lead to seizures and coma.
• Cardiac Manifestations: Chest pain, arrhythmias, and ischaemia, especially in patients with pre-existing coronary artery disease.
• Skin Appearance: Patients may appear rosy or pink due to increased CoHb levels, a misleading sign as it suggests good perfusion.
• Delayed Neurological Sequelae: Can occur days to weeks after exposure, including memory impairment, personality changes, and motor dysfunction (post-hypoxic encephalopathy).

Investigations

• FBC: Assess for polycythaemia in chronic exposure due to hypoxia-induced erythropoiesis.
• U&E: Evaluate renal function, especially if dehydration or hypoxia has led to acute kidney injury (AKI).
• ABG: Essential for measuring CoHb levels and assessing acid-base balance. Typically shows a metabolic acidosis due to lactic acid build-up from hypoxia.
• ↑ Lactate: Elevated lactate indicates anaerobic metabolism and severe tissue hypoxia.
• CK, Troponin: Assess for myocardial injury or rhabdomyolysis in cases with chest pain or altered mental status.
• ECG: Assess for arrhythmias or signs of myocardial ischaemia, especially in patients with cardiac history.
• CT Head: Consider if there is altered consciousness or persistent neurological symptoms to exclude cerebral oedema or other causes of altered mental status.

Assessing COHb Levels

• Normal Levels: COHb levels are usually 1-3% in non-smokers and can be up to 5-10% in smokers due to chronic low-level exposure.
• Poisoning Levels: COHb levels > 10% indicate exposure, and levels > 20% typically correlate with significant symptoms like headache and nausea.
• Severe Toxicity: Levels > 30-40% are associated with neurological symptoms, cardiac complications, and a higher risk of mortality.
• Pregnancy Considerations: Pregnant women and their fetuses are particularly vulnerable as fetal Hb binds CO more tightly, leading to prolonged exposure and increased risk of hypoxia.

Management

Immediate intervention involves removing the patient from the CO source and providing 100% oxygen via a non-rebreather mask to displace CO from haemoglobin and speed up elimination.

• ABC and 15 L/min O₂: Administer 100% oxygen at the highest flow available until symptoms resolve or until carboxyhaemoglobin is <5%.
• Hyperbaric Oxygen (HBOT): Consider for patients with COHb levels > 25%, neurological symptoms, ECG changes, or pregnancy. HBOT reduces COHb half-life to around 20 minutes.
• Fluid Therapy: IV fluids can help manage dehydration and support renal function, especially in patients with lactic acidosis.
• Cardiac Monitoring: Continuous ECG monitoring for arrhythmias or ischaemic changes, especially in those with pre-existing cardiac conditions.
• Neurological Monitoring: Perform regular neurological checks to detect cerebral oedema or signs of worsening mental status. Consider mannitol if cerebral oedema is suspected.
• Long-Term Follow-Up: Monitor for delayed neurological sequelae with cognitive and psychological assessments, especially in severe cases.

Complications

• Neurological: Cognitive impairment, memory deficits, motor dysfunction, and persistent headaches can occur weeks after exposure.
• Cardiac: Increased risk of myocardial infarction, arrhythmias, and long-term cardiac damage due to hypoxia.
• Metabolic: Persistent lactic acidosis from prolonged tissue hypoxia can lead to multi-organ dysfunction.
• Pregnancy: Risk of fetal hypoxia and adverse pregnancy outcomes, including miscarriage or developmental delays in the fetus.

Prevention

• CO Detectors: Install carbon monoxide detectors in homes, especially near bedrooms and in areas with gas appliances.
• Proper Ventilation: Ensure proper ventilation for gas-powered appliances, heaters, and indoor combustion sources.
• Maintenance of Heating Systems: Regular servicing of boilers, heaters, and chimneys can help prevent accidental CO exposure.
• Education: Awareness campaigns on the dangers of CO poisoning, particularly during winter months, can help prevent accidental exposures.