CO is a toxic gas generated in the burning of fuel. The sources of CO in the home are boilers and central heating systems, kitchens and grills, grills, homes and fireplaces. It is necessary that the owners of these devices have them checked by registered technicians, who follow the recommended instructions for each of them (usually once a year).
If the ventilation of these devices is blocked, it is normally operated in an environment without ventilation, dangerous levels of CO can accumulate in living spaces.
When inhaled in large quantities, CO enters the bloodstream and binds to hemoglobin molecules with an affinity much greater (230 times greater) than oxygen, forming carboxyhemoglobin. The binding of CO to hemoglobin causes the reduction of oxygen supply to tissues, which leads to ischemia.
Why is it not diagnosed?
The presentation of CO poisoning is not frequent enough to prioritize medical training in this condition, diagnostic performance, initial tests and publicity and public awareness.
Differential diagnoses include other common acute conditions such as influenza, viral gastroenteritis, tension and migraine headache and alcohol toxicity, which makes diagnosis difficult.
Establishing the severity of symptoms can be difficult since the symptoms are fluctuating in hours, slowing down and getting worse when approaching the source of CO. Apart from this, there is no established correlation between the levels of carboxyhemoglobin found in the analysis of blood gases, making it difficult to quantify CO poisoning.
In cigarette smokers there is greater tolerance to CO, which makes this cohort of patients particularly difficult to assess, since symptoms may appear only after an important CO exposure.
The major concern regarding the diagnostic omission of CO poisoning is the impact on the cardiovascular and neurological systems.
Different studies have shown the coexistence of CO poisoning in some patients hospitalized for unstable angina, decreased consciousness and epileptic seizures. Sources indicate that in several cases of chronic exposure from 3 weeks to 3 years, patients presented nonspecific symptoms such as physical pain, dyspnea, sleep disorders and nightmares, weight loss, tinnitus, muscle spasms, photophobia, ataxia, paranoia and loss of memory.
The diagnosis of CO requires obtaining a complete history to link any clinical symptom with the environment and exposure to CO.
Cardiovascular examination with electrocardiogram may reveal sinus tachycardia, but CO poisoning has also been associated with angina and cardiac ischemia.
The neurological examination may reveal nonspecific symptoms, such as a spectrum of sensory disturbances, lack of attention, memory disorders, confusion, ataxia and, in severe cases, seizures and decreased consciousness.
Carboxyhemoglobin has a brighter hue than oxyhemoglobin, which motivates conjunctival injection, as in the patient presented here. Textbooks often report elevated levels of carboxyhemoglobin that lead to a "cherry red" skin color. However, this seems to be unfounded and exceptionally rare.
The signs of the clinical examination of CO poisoning have little predictive value, which means that the key to the diagnosis is to relate the onset or worsening of symptoms with exposure to CO.
What are the initial tests?
Pulse oximetry, which is based on the absorption of infrared light by hemoglobin, is often falsely elevated in CO poisoning due to the similar properties of oxyhemoglobin and carboxyhemoglobin.
For the definitive diagnosis, it is necessary to measure the carboxyhemoglobin and make the gas analysis in venous or arterial blood. The toxic effects of CO poisoning are considered to originate in the accumulation of carboxyhemoglobin to a level of 15-20%.
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