Jordi Desola, MD, PhD.
Carbon monoxide poisoning is one of the best-established indications for Hyperbaric Oxygenation. A reasonable basis for therapeutics exists, a great number of observations from all over the world have been published, large and well-designed research projects have been conducted, and a few comparative studies have also been performed.
The indication of Hyperbaric Oxygenation for this intoxication is well accepted in some countries. In others, however, it is still controversial.
In Catalonia the incidence of carbon monoxide poisoning has decreased in recent years. In 1960 carbon monoxide poisoning accounted for 27 % of all poisonings, but in 1989 this incidence decreased to 4.9% .
The number of cases of carbon monoxide poisoning treated in our Hyperbaric Therapy Unit, however, has increased progressively since 1980, from 1 to 87 cases per year. That figure clearly shows that the indication of HBO for the treatment of carbon monoxide poisoning is fairly well accepted in general medical practice. However, much debate still remains and its acceptance is not unanimous.
This negative attitude is mainly due to ignorance about the most important aspects of the pathogenics of carbon monoxide poisoning and especially about the almost etiological mechanism of Hyperbaric Oxygenation in these cases.
Until june 1990, we have treated 348 cases of carbon monoxide poisoning, using a prospective method designed according to the basis established by the Committee on Hyperbaric Oxygenation of the Undersea and Hyperbaric Medical Society, and duplicating the protocol suggested for KINDWALL in Davis and Hunt's book.
The analysis of these data shows positive results in the majority of the cases, including the most serious ones, evaluated in terms of the mortality rate, the percentage of complications, and the carboxyhaemoglobin levels. The results do not vary significantly from those of similar reviews and are not the subject of this paper.
On the other hand, we have noticed a significant number of errors at patients' hospital admittance. They are not accidental because they appear consistently, and they can be classified into eight groups for study, which will be presented in their order of occurrence.
1.- DIAGNOSIS. Carbon monoxide poisoning is very often a hidden disaster. Only in catastrophic situations, or in cases where coal gas is obviously present, is the existence of carbon monoxide in the environment presumed.
Liquated gases from petroleum do not contain carbon monoxide, but they can form it if their combustion is inadequate.
2.- EVALUATION OF CARBOXYHAEMOGLOBIN LEVEL. Even when carbon monoxide poisoning is almost certain, some doctors only accept this diagnosis if the carboxyhaemoglobin is elevated. And even in these cases, they only consider an intoxication severe if the carboxyhaemoglobin elevation is high. This attitude implies a true ignorance about both the physiopathology of this intoxication, as well as the physiology of the haemoglobin oxygen transport and the carbon monoxide left deviation of the curve. Carboxyhaemoglobin only indicates the haemoglobin linked to carbon monoxide, but nothing is known about the plasmatic carbon monoxide levels. However, it is well known that in mild cases, patients often have important carboxyhaemoglobin elevations, while other patients in deep coma can have low levels. A carboxyhaemoglobin elevation only informs us that the patient has been exposed to carbon monoxide at some point during the preceding hours. The severity of the case cannot be deduced from this determination.
3.- EVALUATION OF GASOMETRICS. Patients poisoned by carbon monoxide often have nearly normal gasometric values. A mild hypoxemia may sometimes be observed even in seriously ill patients. . Analytical apparatuses only determine the oxygen transported by the normal haemoglobin, and the gasometrics may give a false normal result when the patient is really hypoxic with a high percentage of his total haemoglobin blocked by carbon monoxide. This is a typical gasometrics from a non extremely severe case. Only a Cooxymeter can determine the real oxygen content, but this apparatus is not available in all hospitals. When observing a severe hypoxemia in a patient affected by carbon monoxide poisoning, one must be aware of other coincidental respiratory pathologies, like smoke inhalation, or Adult Distress Respiratory Syndrome.
4.- INFREQUENT SYMPTOMS. Many books on internal medicine and on toxicology, explain that one of the most typical symptoms of carbon monoxide poisoning is the Pink Colour of the skin. These are the frequency of the symptoms observed in our series, where pink coloration of the skin has been found in only the 20.3% (twenty point three per cent) of the cases. This observation coincides with the results of other important casuistics published in recent years. On the other hand, vertigo, nausea or vomiting, headache, and loss of consciousness have been observed in our patients with higher frequency.
5.- INCORRECT DRUG TREATMENT. These patients are usually in real acidotic base-acid equilibrium, which may be much more relevant to the severity of the intoxication than, for instance, the carboxyhaemoglobin level. Clinicians usually try to "correct" this acidosis and very often patients develop alkalosis after having received unnecessary doses of bicarbonates. This metabolic acidosis is mainly related to the left deviation of the haemoglobin curve, and is, in fact, a defense mechanism against the hypoxia trying to achieve a more stable oxygen transference. Acidosis is a positive situation and need only be treated in extremely severe cases, when it may, by itself, cause major damage, possibly to a degree incompatible with life.
6.- INEFFICACY OF NORMOBARIC OXYGEN. Many patients start to improve from the moment of the rescue from the intoxication site. In fact, they frequently arrive at the hospital in nearly normal status. Applying normobaric oxygen may result in an apparent improvement in the less serious cases. But this amelioration does not correspond to an areal healing of the poisoning because carbon monoxide is completely separated from haemoglobin, and probably from the cells, only by Hyperbaric Oxygenation. This rejection of the Hyperbaric treatment after an apparent normobaric amelioration is very often related to the next error.
Theoretically, the half life of Carboxyhaemoglobin breathing normobaric oxygen is 80 minutes. But in practice this seems not be true. More than the half of our patients had received normobaric oxygen in other centres previously to be sent to us. The mean value of carboxyhaemoglobin in the moment of their arrival to our centre was however more than 19 %.
We had also the opportunity to treat 3 of the 5 patients from a collective carbon monoxide intoxication. That means that the time of exposition and the concentration of carbon-monoxide was the same for all the patients.
These were the mean values of carboxyhaemoglobin of our patients compared with those of the patients that received normobaric oxygen. The second determination of our patients was made about 2 hours after the first, having the patient received one session of Hyperbaric Oxygenation, and both were less than 1 %. The second determination of the patients who received normobaric oxygen in other hospitals were made 7 ours late, and the mean value were 18 %.
7.- IGNORANCE OF THE LATE NEUROLOGICAL SYNDROME. Not only are many general practitioners and hospital doctors unaware of the existence of this late syndrome, but also some hospital neurologists are equally uninformed. In fact, several well-known and internationally-accepted textbooks on internal medicine and even some books on toxicology do not mention this eventuality.
8.- DELAY OR NEGLIGENCE IN APPLYING HYPERBARIC OXYGENATION. Sometimes Hyperbaric Oxygenation is considered only for the most serious cases; that is, for the cases with high carboxyhaemoglobin elevations. In any case, hospitals wait for the result of this determination before deciding whether or not the patient must be treated in the chamber. Other hospitals consider that the less serious patients do not need treatment, and that the most serious cases are too serious to be transferred at that point. The patients are finally sent to the Hyperbaric Centres, often 12 to 24 hours after the time of diagnosis. Obviously, positive results are related to early treatment.
These are the clinical evolution of our patients. Only three of them evolved unfavourably. All three presented serious coincidental respiratory pathological findings. Two of them were heroin addicts rescued from a prison fire set by themselves; both were admitted after a delay of more than 24 hours.
Confusion about HBO may be exacerbated by badly-documented opinions or reviews that occasionally appear in newsletters. Recently even the important medical journal LANCET has published such an article.
Some basic textbooks on internal medicine claim in the chapter on carbon monoxide poisoning that there is no evidence that Hyperbaric Oxygen may have an advantage over normobaric oxygen.
All persons associated with Hyperbaric Medical Centres must accept this situation. Like it or not, it is the reality in which we work. We must counter these errors, not only for the welfare of our patients, that is, society as a whole, but also for our own benefit.
I am appealing to the chairman of this session, and through him, to the president of this Congress for an institutional communication to be sent to the main educational institutions, universities, medical editors, and biomedical newsletters, requesting more accurate information and education about this serious intoxication, which can only be cured by the timely and correct application of Hyperbaric Oxygenation.
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