Acute carbon monoxide poisoning
د. حسين محمد جمعةاختصاصي الامراض الباطنة
البورد العربي
كلية طب الموصل
2010
After completing this module, you should know:
What the sources of carbon monoxide poisoning are The signs and symptoms of carbon monoxide poisoning.The factors that influence concentrations of endogenous carboxyhaemoglobin
What immediate action to take when you find a person with carbon monoxide poisoning, and what the subsequent treatment options are.
Why this module is important
Carbon monoxide is an odourless and colourless gas, and poisoning as a result of inhalation causes hypoxia, cell damage, and death. A person can die from carbon monoxide poisoning without noticing any symptoms, especially if the exposure occurs during the hours of sleep.Carbon monoxide is sometimes called "the great imitator" - because the non-specific symptoms are so similar to those of influenza, patients with mild to moderate carbon monoxide poisoning can be misdiagnosed as having the flu.
The symptoms of carbon monoxide poisoning are non-specific and varied, and they relate to the effects of carbon monoxide on the brain and heart. Because carbon monoxide competes with oxygen for binding to haemoglobin, tissues such as the brain and the heart which are most sensitive to oxygen deprivation are the first and worst affected.
The symptoms include:
Headache
Fatigue
Malaise
Confusion and trouble thinking
Nausea
Dizziness
Visual disturbances
Chest pain
Shortness of breath
Loss of consciousness
Seizures.
Cherry red lips are rarely seen, while seizures and loss of consciousness only occur in severe cases.
Learning bite: accidental carbon monoxide poisoning
Accidental carbon monoxide poisoning peaks during the winter months. The peak is associated with the increased use of indoor heating and petrol powered generators, as well as the reduced external ventilation that occurs in the winter.This seasonal rise in numbers coincides with the annual increase in influenza notifications. Given the similarity in symptoms, many patients with mild carbon monoxide poisoning are probably misdiagnosed with flu.
Although it is possible to confirm the diagnosis of carbon monoxide poisoning by detecting elevated concentrations of carboxyhaemoglobin,
a normal concentration does not rule out the diagnosis as the patient’s exposure to carbon monoxide may have ceased several hours before the test.
Learning bite: interpreting concentrations of carboxyhaemoglobin
The concentration of carboxyhaemoglobin is reduced by removing the patient from the source of the carbon monoxide. Any oxygen treatment given before measuring the percentage of carboxyhaemoglobin will also reduce the concentration. Using percentage carboxyhaemoglobin as a measure of the severity of carbon monoxide poisoning is limited.
Attempts have been made in the literature on the condition to divide carbon monoxide poisoning into mild, moderate, and severe based on the percentage of carboxyhaemoglobin concentration and clinical symptoms, but there is no clear clinical consensus or agreement on this issue.
Mild carbon monoxide poisoning has been described in the literature as a carboxyhaemoglobin concentration of greater than 10% in patients who do not have clinical signs or symptoms of carbon monoxide poisoning.
Moderate carbon monoxide poisoning has been described in the literature as a carboxyhaemoglobin concentration of greater than 10%, and a concentration of less than 20% to 25% in patients with minor clinical signs and symptoms of poisoning such as headache, lethargy, or fatigue.
Severe carbon monoxide poisoning has been described in the literature as a carboxyhaemoglobin concentration of greater than 20% to 25%, in addition to loss of consciousness, confusion, or signs of cardiac ischaemia, or all of these.
Learning bite: effect of smoking and urban living
Non-smokers living away from urban areas have carboxyhaemoglobin concentrations of between 0.4% and 1.0%. This reflects the endogenous production of carbon monoxide. In an urban or industrial setting, concentrations of up to 5% may be considered normal.Smokers are exposed to increased concentrations of carbon monoxide in cigarettes, and heavy smokers, who are otherwise healthy, can tolerate concentrations of carboxyhaemoglobin of
up to 15%.
Learning bite: risk of complications
People who are most at risk of complications as a result of carbon monoxide poisoning include:Those with coronary heart disease, vascular disease, or anaemia
Pregnant women and their fetuses
Infants
Elderly people.
Lengthy exposure to carbon monoxide, loss of consciousness, and advancing age are associated with a poor prognosis.
The prognosis for people resuscitated after experiencing cardiac arrest with carbon monoxide poisoning is also poor. Memory problems are common neurological sequelae of carbon monoxide poisoning.
You should check the patient’s airway and circulation as soon as they have been removed from the source of the carbon monoxide gas.
Learning bite: non-rebreather masks
A non-rebreather mask is usually a tight fitting mask with an oxygen reservoir bag attached and a one way valve that remains open during inspiration. The mask allows oxygen concentrations of 80% to 100% to be delivered when high concentrations of inspired oxygen are needed.Learning bite: oxygen treatment in carbon monoxide poisoning
Normobaric 100% oxygen reduces the half life of carboxyhaemoglobin and is considered to be effective, but studies proving the benefit compared with air or lower concentrations of oxygen have not been identified, and would be unethical.Paramedics use 28% oxygen and this is thought to be beneficial compared with air, but may be less effective than higher concentrations.
We don't yet know what the optimum duration of oxygen treatment is, but it is usually continued until carboxyhaemoglobin concentrations fall below 5%, or for at least six hours.
There is no evidence that the use of hyperbaric oxygen is more advantageous in terms of mortality and neurological sequelae when compared to normobaric 100% oxygen.
sometimes overlooked source of carbon monoxide is methylene chloride (dichloromethane), which is found in some paint strippers and sprays. Methylene chloride is readily absorbed through the skin and lungs and, once in the liver, is converted to carbon monoxide. Methylene chloride is stored in body tissues and released gradually.
Carbon monoxide is a byproduct of haem metabolism. In a condition like pernicious anaemia where haem metabolism is increased, higher levels than normal of carbon monoxide can be generated.
Carbon monoxide shifts the oxygen dissociation curve to the left. This is why tissue hypoxia develops in acute poisoning. The exhausts from newer car models emit far more carbon dioxide than carbon monoxide.
Carbon monoxide competes for oxygen sites on all haem proteins. In the developing fetus, oxygen is released at a lower oxygen partial pressure and fetal haemoglobin binds with carbon monoxide more quickly when compared with an adult.
Carbon monoxide may be a teratogen where there is a significant increase in maternal carboxyhaemoglobin or where there is moderate to severe maternal toxicity. It is important to realise that acute non-lethal maternal intoxication may result in fetal demise.
Learning bite: pregnancy
During pregnancy, a woman’s oxygen carrying capacity is reduced. This occurs because the production of endogenous carbon monoxide increases in pregnancy and, coupled with endogenous carbon monoxide from the developing fetus, this leads to an increased concentration of carboxyhaemoglobin. A higher ventilation rate during pregnancy will lead to an increased uptake of carbon monoxide at any given concentration of carbon monoxide.Key points
Many people with mild to moderate carbon monoxide poisoning are probably misdiagnosed.You should not ignore a history of known exposure to carbon monoxide and the presence of clinical signs and symptoms, even if the percentage carboxyhaemoglobin is low or within the normal range.
In suspected carbon monoxide poisoning, the most immediate and essential actions are to remove the person from the source of the carbon monoxide gas and to give oxygen, preferably 100%, through a non-rebreather mask.
There is no evidence that the use of hyperbaric oxygen reduces mortality or neurological sequelae when compared to normobaric 100% oxygen
