SN6
SHORT NOTE
5M
★ High-yield
Describe carbon monoxide poisoning.
Sources and Mechanism
- Carbon monoxide is a colourless, odourless, tasteless and non-irritant gas produced by the incomplete combustion of any carbon-containing fuel. Its complete absence of warning properties is what makes it dangerous — the victim has no reason to leave the room
- Sources — charcoal and coal braziers (angithi, sigri) used for heating in closed rooms in winter, which is the classical Indian setting and causes deaths of whole families every year; gas geysers in bathrooms, a recurring and preventable cause of death in young people; faulty heaters and chimneys; motor exhaust; and smoke inhalation in fires, which is much the commonest cause overall
- Mechanism — carbon monoxide binds haemoglobin with an affinity about 200 to 250 times that of oxygen, forming carboxyhaemoglobin; it also shifts the oxygen dissociation curve to the left, so that the remaining oxyhaemoglobin does not release its oxygen to the tissues; and it binds cytochrome oxidase and myoglobin, adding a histotoxic and a cardiac component. The tissue hypoxia is therefore far worse than the carboxyhaemoglobin figure alone suggests
| Carboxyhaemoglobin | Features |
|---|---|
| Up to 10% | Usually asymptomatic; found in smokers, which must be allowed for in interpretation |
| 10 to 30% | Headache (throbbing and frontal), dizziness, nausea, breathlessness on exertion and impaired judgement — readily mistaken for influenza or a viral illness, particularly when a whole household is affected |
| 30 to 50% | Severe headache, vomiting, confusion, ataxia, tachycardia, syncope, and muscular weakness which prevents escape even though the person understands the danger |
| 50 to 70% | Coma, convulsions, respiratory depression, cardiovascular collapse and death |
CLINICAL PEARL
A whole household with headache and nausea in winter is carbon monoxide until proved otherwise. The gas gives no warning, and the symptoms are exactly those of a viral illness — so families are treated for influenza and sent back to the same room. Ask what they are heating with, and note whether the symptoms improve away from the house and return on going back. That single question makes the diagnosis.
Findings, Investigation and Treatment
- The classical sign is cherry-pink discolouration of the skin, lividity, mucous membranes, blood, muscles and viscera — though it is often absent or unappreciated in life, and it appears reliably only at high saturations. The absence of cyanosis in a hypoxic patient is itself a clue
- Pulse oximetry IS falsely normal and is dangerously misleading, because the ordinary oximeter cannot distinguish carboxyhaemoglobin from oxyhaemoglobin and reports a high saturation in a profoundly hypoxic patient. A CO-oximeter or direct carboxyhaemoglobin estimation is required
- Delayed neuropsychiatric sequelae — occurring in a substantial minority days to weeks after apparent recovery: cognitive impairment, personality change, parkinsonism, incontinence and psychosis, with necrosis of the globus pallidus characteristically seen on imaging and at autopsy. This is what makes follow-up essential
- Postmortem — cherry-pink lividity, blood and viscera; the blood remains fluid and bright; and soot in the airway with burns where death occurred in a fire, which together with a raised carboxyhaemoglobin proves the person was alive and breathing in the fire
- Sampling — blood in a clean, airtight container, filled to the brim, with NO preservative, refrigerated
- Treatment — remove from exposure; 100% oxygen by tight-fitting mask, which reduces the half-life of carboxyhaemoglobin from about 4 to 5 hours in air to about 1 hour; and hyperbaric oxygen, which reduces it to about 20 minutes and is considered for severe poisoning, loss of consciousness, neurological signs, cardiac involvement and pregnancy — the fetus being especially vulnerable, since fetal haemoglobin binds carbon monoxide still more avidly
Applied Aspects
- Do not trust the pulse oximeter; it reads normal in carbon monoxide poisoning and has given false reassurance in fatal cases. Ask for a carboxyhaemoglobin
- Ask about the heating and the geyser in any winter cluster of headache and nausea, and about whether symptoms improve away from home
- Give high-flow oxygen immediately and continue it; it is the treatment, and it should not wait for confirmation
- Treat the pregnant patient more aggressively and consider hyperbaric oxygen; fetal haemoglobin binds carbon monoxide more strongly and the fetus is at greater risk than the mother
- Warn about delayed sequelae and arrange follow-up; a patient who recovers completely may deteriorate cognitively at two to four weeks, and the family must know to return
- Measure carboxyhaemoglobin in every fire death; a raised level with soot below the larynx proves the person was breathing in the fire, and a normal level in a burnt body suggests death occurred beforehand
- Allow for smoking when interpreting a modestly raised level, and for the time elapsed and any oxygen already given, which lower it rapidly
- Soot below the larynx with a raised carboxyhaemoglobin proves the person was alive and breathing in the fire
All questions in General Toxicology
- Q1Define poison. Describe the classification of poisons, the factors modifying their action and the laws relating to them. ★
- Q2Describe the diagnosis of poisoning in the living and in the dead. ★
- Q3Describe the general management of a case of acute poisoning including decontamination and antidotes. ★
- Q4Describe the duties of a doctor in a case of poisoning and the collection and preservation of viscera. ★
- Q5Describe the poisoning by arsenic, lead and mercury. ★
- SN1Describe the chelating agents with their uses and precautions. ★
- SN2Describe copper sulphate poisoning. ★
- SN3Describe iron poisoning with its stages and management. ★
- SN4Describe aluminium phosphide poisoning and the other rodenticides. ★
- SN5Describe food poisoning with its types and investigation. ★
- SN6Describe carbon monoxide poisoning. ★
- SN7Describe cyanide poisoning with its mechanism and treatment.