Acta Clinica Belgica International Journal of Clinical and Laboratory Medicine
ISSN: 1784-3286 (Print) 2295-3337 (Online) Journal homepage: http://www.tandfonline.com/loi/yacb20
Carbon Monoxide Poisoning-Recent Advances A.T. Proudfoot To cite this article: A.T. Proudfoot (1990) Carbon Monoxide Poisoning-Recent Advances, Acta Clinica Belgica, 45:sup13, 61-68, DOI: 10.1080/17843286.1990.11718129 To link to this article: http://dx.doi.org/10.1080/17843286.1990.11718129
Published online: 16 May 2016.
Submit your article to this journal
View related articles
Citing articles: 3 View citing articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=yacb20 Download by: [Australian Catholic University]
Date: 24 August 2017, At: 15:14
61
Downloaded by [Australian Catholic University] at 15:14 24 August 2017
CARBON MONOXIDE POISONING - RECENT ADVANCES AT. Proudfoo t *
INTRODUCTION
'
1
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Carbon monoxide (CO) remains an important cause of deaths from acute poisoning throughout the world and in many countries it is numerically the single most important letha l toxin. Altough it has been claimed that th e great majority of the medical profession and the public a t large have forgotten about it, virtually every aspect of carbon monoxide poisoning has been the focus of research in rece nt years. The mechanism of toxicity (1)., haemodyn amic response to exposure (2), assessme nt of the severity of poisoning (3-7), delayed neurological sequ elae (8-12), computerised tomographic (13, 14) and magnetic resonance im aging (15) findings, non-ne urol ogica l complications (16-21), subacute and chronic poisoning (22-28), poisoning in children (28-30), poisoning in pregnancy (31-34) a nd forensic aspects (35) have all rece ived attention, not to me ntio n the rapidly grow ing literature on the role of hyperbaric oxygen (HBO) in treatme nt. While many of these a re of great interest, it is the latter which most concerns intensive care spec ialists.
• Director, Scottish Poi ons In forma tion Bureau , Royal Infirmary, Edinburgh, EH3 9YW Scotland
THE MECHANISM OF TOXICITY OF CARBON MONOXIDE The mechanism of toxicity of any sub tance is cl early importa nt in de te rmining ration al treatment for poisoning with it. There is no argument th at the major e ffect of CO is to re du ce oxygen delivery to tissues. Anaemic hypoxia is induced because CO combines with haemoglobin to form carboxyhaemoglobin (COHb) thus reducing th e amount hae moglobin available to carry oxygen. In addition, the formation of COHb shifts th e oxyhaemoglobin dissociation curve to th e le ft , the reby impairing liberation of oxygen to th e ce lls. If red uction of cardiac complicates intoxicatio n, oligaemic hypoxia is superimposed on anaemic hypoxi a, impairing tissue oxygenation even furth er, especially in vulnerable organs such as th e brain . In recent years, the view th at these were the only mechanisms of toxicity has bee n challenged. It is not known that CO also binds to myoglobin and various cytochrome oxidases and binding to the latte r has bee n inte rpreted as indicating th at CO poisons ce lls directly and impairs the ir ability to utilise the oxygen they receive . This view re mains controve rsial and th e arguments for and against it have been reviewed in detail by Pi antadosi (1 ). The existence of a toxic effect of CO on cells has bee n discounted
62
CARBON MONOXIDE POISONING - RECENT ADVANCE
Downloaded by [Australian Catholic University] at 15:14 24 August 2017
on . the grounds that the affinity of cytochrome oxidases for CO only exceeds that for oxygen under circumstances of extreme hypoxia. However, Piantadosi justifies the conclusion that inhibition of cytochrome oxidase (especially a, a3) may be more important than is generally appreciated, particularly in the brain, by adding to the effects of hypoxic and oligaemic hypoxia. HYP RBARI
OXYGEN TH RAPY
Normobaric oxygen (NBO) and, even more so, HBO improve oxygen delivery to cell in least two ways. They increase the dissolved oxygen content of plasma but, more importantly, they drastically shorten the half-life of OHb. The latter is of the order of 250 minutes when breathing air, 50 minutes when breathing 100 % (normobaric) oxygen, and a hort as 22 minutes when subjects are expo ed to HBO at 2.4 atmo phere (36). The effect of NBO and HBO on the cytochrome oxida e system are le ce rtain. On theoretical gr unds alone, therefore, the value of HBO in the management of 0 poi oning would eem unacute as ailable. Yet, after a careful review of the literature, Olson (37) co ncluded « ... it i not known if either 100 % oxygen or hyperbaric oxygen can actually alter mortality or improve neurological outcome in survivors. Carefully controlled prospective studies should be carried out to as e s the potential value of hyperbaric oxygen in 0 poi oning. » This suggestion received a sharp re pon e from Myers (38) who maintained th at « To a k for a clinical trial to prove th e effectiveness of oxygen or hyperbaric oxygen is like a king a surgeon to prove with a double-blind controlled trial that appendicectomy is the best trea tment for all ca es of acute appendiciti . » While the recommendations of Myers have been widely adopted, some later authors have come to the same conclusions as Olson (39, 40). Why then is there such a divergence of
views ? The matter is clearly of much more than academic importance as anyone who has tried to organise HBO treatment in countries where chambers are not readily accessible will testify. Clear evidence of reduction of mortality and prevention of delayed neurological sequelae would convince skeptics that the organisational difficulties and hazards of the procedure were justified. DOES HYPERBARIC OXYGEN REDUCE MORTALITY IN 0 POISONING ? One might have thought that it would be easy to produce evidence th at HBO treatment reduces the mortality from CO intoxication, but not so. Surprisingly, there are no animal studies to which one can refer and only a small number'()f se ries of human cases managed in this way have bee n published since the renewal of interest in HBO th erapy. Norkool and Kirkpatrick (41) treated 115 0-intoxicated patient with HBO. Eleven out of 44 patients who were uncon cious on arriva l at hospital died while there were no deaths among t those who were never unconscious or who had regained con ciou nes before reaching the eme rgency department. ight of the deaths were in the group of patients who had suffered from cardiorespiratory arrest at the scene of poisoning. Similarly, the four fatal cases out of 230 treated with HBO by Mathieu et al (42) occ,urred in patients who were unconscious on arrival at the emergency department and two of them had been resuscitated from cardiorespiratory arrest at the scene. That cardiorespiratory arrest should be an indicator of a poor prognosis · is hardly surprising. The e studies rai e two important issues. The first is the problem of trying to assess whether or not mortality was reduced by the treatm en t because they do not have control groups not given HBO. There are, of course, older published series not treated with HBO but their validity as « control » groups
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CARBON MONOXIDE POISONING - RECENT ADVANCE
Downloaded by [Australian Catholic University] at 15:14 24 August 2017
must be doubtful if only because standa rds of inte nsive care have advanced considerably and universally in th e last 10 - 15 years. For this reason even the recent Danish study reporting ' the outcome in 79 patie nts seve rely poisoned with CO and treated in an intensive care unit but without HBO is of doubtful value as a control group because it spa ns 15 years ( 43).
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The second probl e m perta in s to classification of the seve rity of CO poisoning so that different series can be usefull y compared . As indicated above, Norkool and Kirkpatrick cl assified their patients re latively simply according to whether or not coma had been present, ever, at th e scene of poisoning or on reaching hospital (4 1). Mathie u et al used a simil ar classification a nd extended it by grad ing patients unconscious in the e me rgency department according to the Glasgow coma scale (42). It shou ld be remembered, however, that this scale was introduced for the manageme nt of head injuries and later publications have suggested th at it is less satisfactory than others for the gradi ng of severity of poisoning ( 44). Krantz et a l ( 43) used G lasgowPittsburg cerebral performance categories while the Hyperbaric Cen ter Advisory Cornrnittee (45) used a comp licated system based on a number of clinical features in eludi ng responsiveness a nd orientation. Comparison or confirmation of th e benefits of one or different forms of treatment in subgroups of CO poisoning is therefo re likely to be impeded unless an internationally accepted system of grading is devised and agreed. THE PROBLEM OF SMOKE INHALATION
Inha latio n of smoke from fires is undoubtedly an important source of CO poisoning and cases which have been treated with HBO are included in ma ny of the published l series (Table 1). However, one must question th e wisdom of including the m along with other causes of CO poisoning since the (
i
toxicology of smoke inhalation is considerably more complicated than that of CO alon e. Even if one ignores the particle conte nt of smoke, the mate rials used for th e manufacture of prese nt-d ay furniture e nsure that it also co nta ins other irritant and toxic gases such as acrolein, hydroge n chloride and hydrogen cyanide ( 40). Postmorte m and othe r studies have clearly demonstrated the importance of these in both ad ults and childre n. Moreover, it is also well established th at adults who are the victims of smoke inhalation from domestic fires have significa nt conce ntrations of alcohol and psychotropic drugs in the ir blood (46). Unfortunate ly, most published series of CO poisoning, whether or not reporting the use of HBO, have not addressed these issues by appropriate laboratory investigation but me re ly concentrated on COHb conce ntrations. Only th e recent study by Raph ael et al (47) has attempted to tackle this problem but purists would maintain that they did not go far enough. There is no doubt that laboratory excl usio n of coexisting poisons would be a formidable task but to ignore such important factors is surely simplistic and must inevitably cast doubt on the va lidity of the results of the studies at fault. It would be bette r to co nside r smoke inhalation se parately from other causes of CO poisoning. DELAY D NEUROLOG ICAL FEATURES AFTER CO POISONING It has long bee n appreciated that the ce ntral nervous system was particularly vulnerable to CO intoxication. Parkinsonism, chorea, choreoathetosis, cortical blindness, muti sm, hemiplegia, peripheral neuropathy and a variety of other features and syndrom es have been repo rted. The development of these problems has been closely corre lated with th e lesion s demonstrated on computerised tomography and magne tic resonance imaging of the brain, particula rly those in the putamen and
64
CARBON MONOXIDE POISONING - RECENT A DVANCE
TABLE 1: SMOKE INHALATIONS INCLUDED IN PUBLISHED SERIES OF CARBON MONOXIDE POISONING
Downloaded by [Australian Catholic University] at 15:14 24 August 2017
SERIES Ziser et al (47) Goza! et al (30) Mathieu et al ( 42) Norkool & Kirkpatrick (41) Grube et al (39) Hyperbaric Center (45)
globus pallidus. In rece nt years, however, it has become apparent that some victims of CO poisoning who initially recover completely from the acute insult go on to develop symptoms and signs of ne urological damage days or weeks later. Jn such cases the damage is to the white ma tter of the brain. The characteristics of this delayed syndrome have now been defin ed in con iderab le detail , particul arly by workers in South Korea (8, 10). It should be no ted tha t the late r of the e report ( lO) is a n exte n ion of the first (8). The prevale nce of delayed neurological sequelae varies from one series to another but is of the order of 12 % (8, 10). Apathy, disorientation, a mn esia, a nd hypokinesia are almost in va ri able while urina ry and/or faeca l inco ntin e nce, irritability, easy distractibility, apraxia, increased muscle tone a nd behavioral ab normalities occur in over 70 % of victims. In almost half the patients developing th ese feat ures the onset is between two and four week after the acute incident while th e other cases a re about equ ally divided be tween starting earlie r or later. Unfortun ately, th e duration of coma does not corre la te with the development of delayed featu res. Two other important facts about the delayed yndrome have bee n established. The first is th at those who are affected are almost always adults over the age of 40 years and the second is that 75 - 80 % of
YEAR
TOTAL
SMOKE
1984 1985 1985 1985 1988 1988
6 6 230 115 10 81
4 2 3 29 10 43
them are e ith er completely recovered or conside rably improved within a year. Min (10) states that recovery is not affected by the sex of the victim, the interval between exposure a nd onset of delayed fea tures, the findings on EEG a nd brain CT, or by HBO therapy. DOES HYPE RBARIC OXYGEN T H E RAPY PREV ENT DELA YEO NEUROLOGICAL FEATURES? It is cl ear from the rece ntly reported series th at early HBO treatm ent of CO intoxication does not always prevent the developme nt of delayed neuropsychiatric problems. Comparison with older reports suggests th at the prevale nce is lowe red but one is again bound to question whether the use of « hi torica l » controls is valid. The most dramatic support for HBO preventing delayed seq uelae comes from Mye rs et al ( 48). None of th e 131 patie nts they treated with HBO developed de layed sequ elae while 10 out of 82 give n only NBO did . The difference is eve n more impre.ssive when one realises th at those who developed sequ elae were less seve rely poisoned th an the others, a t least as indicated by COHb conce ntrations. Such results will not be readily dismissed but such expe rie nce is not universal. Min (10) did not find that HBO made a differe nce to the development of sequ elae and is supported by Raphae l et al (47), the
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65
CARBON MONOXIDE POISONING - RECENT ADVANCE
only worke rs to have conducted a controlled trial of HBO. Th ey concluded that the num ber of deaths or serious sequelae was not influenced by two sessions of HBO. Fewer moderate sequelae developed in those given this treatment but th e diffe rence from th e control group was not significa nt. However, HBO enthusiasts will almost ce rtainly question these results because of the relatively low incide nce of severe morbidity.
Downloaded by [Australian Catholic University] at 15:14 24 August 2017
IS HYP ERBARIC O XYGEN OF VALU E ' IN THE TREATMENT O F DELAYE D NEUROPSYCHIATRIC ·SEQUELAE?
Controlled tri als of HBO in the treatm e nt of delayed ne urological seq uelae have not been carried out but anecdotal ev idence suggests th at it is not only effective but in some cases drama tica lly so, even days after the initial injury ( 49). In the opinion of th e writer, further studi es are req uired before these claims can be accepted without reservation. Moreover, one has to ask the nature of the ne urologica l lesion that is being corrected. Clearly, it ca nnot be a serio us ( structural one a nd the improvement with 1 HBO is perhaps due to its action in reduc( ing cerebral oedema. ARE THE ADVERSE EFFECTS
OF HY PERBAR IC OXYGEN { THERA PY IMPORTANT?
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Those who are skeptical of th e va lu e of HBO cite complications of treatment as reasons for caution . These have been reviewed in several papers (39, 45, 50) . Barotrauma to the ears is the commonest complication but perforation of the drum is rare, probably because myringotomy is commonly performed before treatment although it occasiona lly causes middle ear damage. Specialists in hyperbaric oxyge n therapy are unlikely to accept that these a re serious complications or sufficie nt for HBO to be reserved for only the most eriously poisoned patients but others cannot be dismissed lightly. Arrhythmias (3 cases), respiratory acidosis (2 cases), aspiration (2
cases), seizures, obstruction of an endotracheal tube, rupture of the cuff of the endotracheal tube a nd respiratory arrest (all 1 case each) occurred in chambers during a total of 92 treatme nts. OTH E R COMPLICATIONS RELATED TO HYPERBARIC OXYGEN TREATM ENT The complications foll owing HBO treatment have also been reported. Not surprisingly, respiratory complications, including delayed extuba tion , are more common amongst patie nts whose CO poisoning is th e result of smoke inh alation in fire s. In contrast, prolonged coma and confusion, increased intracra ni al pressure abnormal EEG and se izures tended to occur in patie nts without burns (45). CA RBON MONOXID E POISONING IN SPECIAL RISK GROUPS Pregnant women
There have been a number of recent reports of CO poisoning in pregnancy (31 34) a nd at least one study suggests that it is not an unco mmon occurrence while others indicate that the outcome for the pregnancy may be far from happy. In hum a ns it would be ext reme ly difficult, if not impossible, to study th e pathophysiology of maternal CO intoxica tion in the fet us. However, in vestigation s (51) in pregnant sheep show th at exposure of the mother to a constant inspired CO leve l produces a prompt increase in maternal COHb conce ntrations wh ich then plateau and decl ine exponen tially when exposure is stopped. In th e fetus, the rate of increase in COHb co nce ntrations is delayed compared with the mother but the plateau leve ls attain ed are some 10 - 15 % highe r. Similarly, fetal COHb disappears more slowly. Even under normal conditions, the fe tal oxyhaemoglobin dissociation curve is to th e left of the adult one and is moved even furth e r to the left after exposure to
CARBON MONOXIDE POISONING · RECENT ADVANCE
66 CQ. Bearing in mind th at the fetal arterial oxyge n tension is normally of the order of 30 mm Hg, th e upe rimposition of CO intoxication must create considerable feta l hypoxia a nd it i pe rhap not surprising that feta l death should occur. Limite d evidence suggests that pregna nt women tolerate HBO as we ll a a ny other group of patients (52, 53).
Downloaded by [Australian Catholic University] at 15:14 24 August 2017
Children
hildre n are also
ISSN: 1784-3286 (Print) 2295-3337 (Online) Journal homepage: http://www.tandfonline.com/loi/yacb20
Carbon Monoxide Poisoning-Recent Advances A.T. Proudfoot To cite this article: A.T. Proudfoot (1990) Carbon Monoxide Poisoning-Recent Advances, Acta Clinica Belgica, 45:sup13, 61-68, DOI: 10.1080/17843286.1990.11718129 To link to this article: http://dx.doi.org/10.1080/17843286.1990.11718129
Published online: 16 May 2016.
Submit your article to this journal
View related articles
Citing articles: 3 View citing articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=yacb20 Download by: [Australian Catholic University]
Date: 24 August 2017, At: 15:14
61
Downloaded by [Australian Catholic University] at 15:14 24 August 2017
CARBON MONOXIDE POISONING - RECENT ADVANCES AT. Proudfoo t *
INTRODUCTION
'
1
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(
Carbon monoxide (CO) remains an important cause of deaths from acute poisoning throughout the world and in many countries it is numerically the single most important letha l toxin. Altough it has been claimed that th e great majority of the medical profession and the public a t large have forgotten about it, virtually every aspect of carbon monoxide poisoning has been the focus of research in rece nt years. The mechanism of toxicity (1)., haemodyn amic response to exposure (2), assessme nt of the severity of poisoning (3-7), delayed neurological sequ elae (8-12), computerised tomographic (13, 14) and magnetic resonance im aging (15) findings, non-ne urol ogica l complications (16-21), subacute and chronic poisoning (22-28), poisoning in children (28-30), poisoning in pregnancy (31-34) a nd forensic aspects (35) have all rece ived attention, not to me ntio n the rapidly grow ing literature on the role of hyperbaric oxygen (HBO) in treatme nt. While many of these a re of great interest, it is the latter which most concerns intensive care spec ialists.
• Director, Scottish Poi ons In forma tion Bureau , Royal Infirmary, Edinburgh, EH3 9YW Scotland
THE MECHANISM OF TOXICITY OF CARBON MONOXIDE The mechanism of toxicity of any sub tance is cl early importa nt in de te rmining ration al treatment for poisoning with it. There is no argument th at the major e ffect of CO is to re du ce oxygen delivery to tissues. Anaemic hypoxia is induced because CO combines with haemoglobin to form carboxyhaemoglobin (COHb) thus reducing th e amount hae moglobin available to carry oxygen. In addition, the formation of COHb shifts th e oxyhaemoglobin dissociation curve to th e le ft , the reby impairing liberation of oxygen to th e ce lls. If red uction of cardiac complicates intoxicatio n, oligaemic hypoxia is superimposed on anaemic hypoxi a, impairing tissue oxygenation even furth er, especially in vulnerable organs such as th e brain . In recent years, the view th at these were the only mechanisms of toxicity has bee n challenged. It is not known that CO also binds to myoglobin and various cytochrome oxidases and binding to the latte r has bee n inte rpreted as indicating th at CO poisons ce lls directly and impairs the ir ability to utilise the oxygen they receive . This view re mains controve rsial and th e arguments for and against it have been reviewed in detail by Pi antadosi (1 ). The existence of a toxic effect of CO on cells has bee n discounted
62
CARBON MONOXIDE POISONING - RECENT ADVANCE
Downloaded by [Australian Catholic University] at 15:14 24 August 2017
on . the grounds that the affinity of cytochrome oxidases for CO only exceeds that for oxygen under circumstances of extreme hypoxia. However, Piantadosi justifies the conclusion that inhibition of cytochrome oxidase (especially a, a3) may be more important than is generally appreciated, particularly in the brain, by adding to the effects of hypoxic and oligaemic hypoxia. HYP RBARI
OXYGEN TH RAPY
Normobaric oxygen (NBO) and, even more so, HBO improve oxygen delivery to cell in least two ways. They increase the dissolved oxygen content of plasma but, more importantly, they drastically shorten the half-life of OHb. The latter is of the order of 250 minutes when breathing air, 50 minutes when breathing 100 % (normobaric) oxygen, and a hort as 22 minutes when subjects are expo ed to HBO at 2.4 atmo phere (36). The effect of NBO and HBO on the cytochrome oxida e system are le ce rtain. On theoretical gr unds alone, therefore, the value of HBO in the management of 0 poi oning would eem unacute as ailable. Yet, after a careful review of the literature, Olson (37) co ncluded « ... it i not known if either 100 % oxygen or hyperbaric oxygen can actually alter mortality or improve neurological outcome in survivors. Carefully controlled prospective studies should be carried out to as e s the potential value of hyperbaric oxygen in 0 poi oning. » This suggestion received a sharp re pon e from Myers (38) who maintained th at « To a k for a clinical trial to prove th e effectiveness of oxygen or hyperbaric oxygen is like a king a surgeon to prove with a double-blind controlled trial that appendicectomy is the best trea tment for all ca es of acute appendiciti . » While the recommendations of Myers have been widely adopted, some later authors have come to the same conclusions as Olson (39, 40). Why then is there such a divergence of
views ? The matter is clearly of much more than academic importance as anyone who has tried to organise HBO treatment in countries where chambers are not readily accessible will testify. Clear evidence of reduction of mortality and prevention of delayed neurological sequelae would convince skeptics that the organisational difficulties and hazards of the procedure were justified. DOES HYPERBARIC OXYGEN REDUCE MORTALITY IN 0 POISONING ? One might have thought that it would be easy to produce evidence th at HBO treatment reduces the mortality from CO intoxication, but not so. Surprisingly, there are no animal studies to which one can refer and only a small number'()f se ries of human cases managed in this way have bee n published since the renewal of interest in HBO th erapy. Norkool and Kirkpatrick (41) treated 115 0-intoxicated patient with HBO. Eleven out of 44 patients who were uncon cious on arriva l at hospital died while there were no deaths among t those who were never unconscious or who had regained con ciou nes before reaching the eme rgency department. ight of the deaths were in the group of patients who had suffered from cardiorespiratory arrest at the scene of poisoning. Similarly, the four fatal cases out of 230 treated with HBO by Mathieu et al (42) occ,urred in patients who were unconscious on arrival at the emergency department and two of them had been resuscitated from cardiorespiratory arrest at the scene. That cardiorespiratory arrest should be an indicator of a poor prognosis · is hardly surprising. The e studies rai e two important issues. The first is the problem of trying to assess whether or not mortality was reduced by the treatm en t because they do not have control groups not given HBO. There are, of course, older published series not treated with HBO but their validity as « control » groups
I J
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i
I [
~
63
CARBON MONOXIDE POISONING - RECENT ADVANCE
Downloaded by [Australian Catholic University] at 15:14 24 August 2017
must be doubtful if only because standa rds of inte nsive care have advanced considerably and universally in th e last 10 - 15 years. For this reason even the recent Danish study reporting ' the outcome in 79 patie nts seve rely poisoned with CO and treated in an intensive care unit but without HBO is of doubtful value as a control group because it spa ns 15 years ( 43).
'
I
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The second probl e m perta in s to classification of the seve rity of CO poisoning so that different series can be usefull y compared . As indicated above, Norkool and Kirkpatrick cl assified their patients re latively simply according to whether or not coma had been present, ever, at th e scene of poisoning or on reaching hospital (4 1). Mathie u et al used a simil ar classification a nd extended it by grad ing patients unconscious in the e me rgency department according to the Glasgow coma scale (42). It shou ld be remembered, however, that this scale was introduced for the manageme nt of head injuries and later publications have suggested th at it is less satisfactory than others for the gradi ng of severity of poisoning ( 44). Krantz et a l ( 43) used G lasgowPittsburg cerebral performance categories while the Hyperbaric Cen ter Advisory Cornrnittee (45) used a comp licated system based on a number of clinical features in eludi ng responsiveness a nd orientation. Comparison or confirmation of th e benefits of one or different forms of treatment in subgroups of CO poisoning is therefo re likely to be impeded unless an internationally accepted system of grading is devised and agreed. THE PROBLEM OF SMOKE INHALATION
Inha latio n of smoke from fires is undoubtedly an important source of CO poisoning and cases which have been treated with HBO are included in ma ny of the published l series (Table 1). However, one must question th e wisdom of including the m along with other causes of CO poisoning since the (
i
toxicology of smoke inhalation is considerably more complicated than that of CO alon e. Even if one ignores the particle conte nt of smoke, the mate rials used for th e manufacture of prese nt-d ay furniture e nsure that it also co nta ins other irritant and toxic gases such as acrolein, hydroge n chloride and hydrogen cyanide ( 40). Postmorte m and othe r studies have clearly demonstrated the importance of these in both ad ults and childre n. Moreover, it is also well established th at adults who are the victims of smoke inhalation from domestic fires have significa nt conce ntrations of alcohol and psychotropic drugs in the ir blood (46). Unfortunate ly, most published series of CO poisoning, whether or not reporting the use of HBO, have not addressed these issues by appropriate laboratory investigation but me re ly concentrated on COHb conce ntrations. Only th e recent study by Raph ael et al (47) has attempted to tackle this problem but purists would maintain that they did not go far enough. There is no doubt that laboratory excl usio n of coexisting poisons would be a formidable task but to ignore such important factors is surely simplistic and must inevitably cast doubt on the va lidity of the results of the studies at fault. It would be bette r to co nside r smoke inhalation se parately from other causes of CO poisoning. DELAY D NEUROLOG ICAL FEATURES AFTER CO POISONING It has long bee n appreciated that the ce ntral nervous system was particularly vulnerable to CO intoxication. Parkinsonism, chorea, choreoathetosis, cortical blindness, muti sm, hemiplegia, peripheral neuropathy and a variety of other features and syndrom es have been repo rted. The development of these problems has been closely corre lated with th e lesion s demonstrated on computerised tomography and magne tic resonance imaging of the brain, particula rly those in the putamen and
64
CARBON MONOXIDE POISONING - RECENT A DVANCE
TABLE 1: SMOKE INHALATIONS INCLUDED IN PUBLISHED SERIES OF CARBON MONOXIDE POISONING
Downloaded by [Australian Catholic University] at 15:14 24 August 2017
SERIES Ziser et al (47) Goza! et al (30) Mathieu et al ( 42) Norkool & Kirkpatrick (41) Grube et al (39) Hyperbaric Center (45)
globus pallidus. In rece nt years, however, it has become apparent that some victims of CO poisoning who initially recover completely from the acute insult go on to develop symptoms and signs of ne urological damage days or weeks later. Jn such cases the damage is to the white ma tter of the brain. The characteristics of this delayed syndrome have now been defin ed in con iderab le detail , particul arly by workers in South Korea (8, 10). It should be no ted tha t the late r of the e report ( lO) is a n exte n ion of the first (8). The prevale nce of delayed neurological sequelae varies from one series to another but is of the order of 12 % (8, 10). Apathy, disorientation, a mn esia, a nd hypokinesia are almost in va ri able while urina ry and/or faeca l inco ntin e nce, irritability, easy distractibility, apraxia, increased muscle tone a nd behavioral ab normalities occur in over 70 % of victims. In almost half the patients developing th ese feat ures the onset is between two and four week after the acute incident while th e other cases a re about equ ally divided be tween starting earlie r or later. Unfortun ately, th e duration of coma does not corre la te with the development of delayed featu res. Two other important facts about the delayed yndrome have bee n established. The first is th at those who are affected are almost always adults over the age of 40 years and the second is that 75 - 80 % of
YEAR
TOTAL
SMOKE
1984 1985 1985 1985 1988 1988
6 6 230 115 10 81
4 2 3 29 10 43
them are e ith er completely recovered or conside rably improved within a year. Min (10) states that recovery is not affected by the sex of the victim, the interval between exposure a nd onset of delayed fea tures, the findings on EEG a nd brain CT, or by HBO therapy. DOES HYPE RBARIC OXYGEN T H E RAPY PREV ENT DELA YEO NEUROLOGICAL FEATURES? It is cl ear from the rece ntly reported series th at early HBO treatm ent of CO intoxication does not always prevent the developme nt of delayed neuropsychiatric problems. Comparison with older reports suggests th at the prevale nce is lowe red but one is again bound to question whether the use of « hi torica l » controls is valid. The most dramatic support for HBO preventing delayed seq uelae comes from Mye rs et al ( 48). None of th e 131 patie nts they treated with HBO developed de layed sequ elae while 10 out of 82 give n only NBO did . The difference is eve n more impre.ssive when one realises th at those who developed sequ elae were less seve rely poisoned th an the others, a t least as indicated by COHb conce ntrations. Such results will not be readily dismissed but such expe rie nce is not universal. Min (10) did not find that HBO made a differe nce to the development of sequ elae and is supported by Raphae l et al (47), the
( \ ( /
l ( ·
r [
! 1
l
r
65
CARBON MONOXIDE POISONING - RECENT ADVANCE
only worke rs to have conducted a controlled trial of HBO. Th ey concluded that the num ber of deaths or serious sequelae was not influenced by two sessions of HBO. Fewer moderate sequelae developed in those given this treatment but th e diffe rence from th e control group was not significa nt. However, HBO enthusiasts will almost ce rtainly question these results because of the relatively low incide nce of severe morbidity.
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IS HYP ERBARIC O XYGEN OF VALU E ' IN THE TREATMENT O F DELAYE D NEUROPSYCHIATRIC ·SEQUELAE?
Controlled tri als of HBO in the treatm e nt of delayed ne urological seq uelae have not been carried out but anecdotal ev idence suggests th at it is not only effective but in some cases drama tica lly so, even days after the initial injury ( 49). In the opinion of th e writer, further studi es are req uired before these claims can be accepted without reservation. Moreover, one has to ask the nature of the ne urologica l lesion that is being corrected. Clearly, it ca nnot be a serio us ( structural one a nd the improvement with 1 HBO is perhaps due to its action in reduc( ing cerebral oedema. ARE THE ADVERSE EFFECTS
OF HY PERBAR IC OXYGEN { THERA PY IMPORTANT?
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Those who are skeptical of th e va lu e of HBO cite complications of treatment as reasons for caution . These have been reviewed in several papers (39, 45, 50) . Barotrauma to the ears is the commonest complication but perforation of the drum is rare, probably because myringotomy is commonly performed before treatment although it occasiona lly causes middle ear damage. Specialists in hyperbaric oxyge n therapy are unlikely to accept that these a re serious complications or sufficie nt for HBO to be reserved for only the most eriously poisoned patients but others cannot be dismissed lightly. Arrhythmias (3 cases), respiratory acidosis (2 cases), aspiration (2
cases), seizures, obstruction of an endotracheal tube, rupture of the cuff of the endotracheal tube a nd respiratory arrest (all 1 case each) occurred in chambers during a total of 92 treatme nts. OTH E R COMPLICATIONS RELATED TO HYPERBARIC OXYGEN TREATM ENT The complications foll owing HBO treatment have also been reported. Not surprisingly, respiratory complications, including delayed extuba tion , are more common amongst patie nts whose CO poisoning is th e result of smoke inh alation in fire s. In contrast, prolonged coma and confusion, increased intracra ni al pressure abnormal EEG and se izures tended to occur in patie nts without burns (45). CA RBON MONOXID E POISONING IN SPECIAL RISK GROUPS Pregnant women
There have been a number of recent reports of CO poisoning in pregnancy (31 34) a nd at least one study suggests that it is not an unco mmon occurrence while others indicate that the outcome for the pregnancy may be far from happy. In hum a ns it would be ext reme ly difficult, if not impossible, to study th e pathophysiology of maternal CO intoxica tion in the fet us. However, in vestigation s (51) in pregnant sheep show th at exposure of the mother to a constant inspired CO leve l produces a prompt increase in maternal COHb conce ntrations wh ich then plateau and decl ine exponen tially when exposure is stopped. In th e fetus, the rate of increase in COHb co nce ntrations is delayed compared with the mother but the plateau leve ls attain ed are some 10 - 15 % highe r. Similarly, fetal COHb disappears more slowly. Even under normal conditions, the fe tal oxyhaemoglobin dissociation curve is to th e left of the adult one and is moved even furth e r to the left after exposure to
CARBON MONOXIDE POISONING · RECENT ADVANCE
66 CQ. Bearing in mind th at the fetal arterial oxyge n tension is normally of the order of 30 mm Hg, th e upe rimposition of CO intoxication must create considerable feta l hypoxia a nd it i pe rhap not surprising that feta l death should occur. Limite d evidence suggests that pregna nt women tolerate HBO as we ll a a ny other group of patients (52, 53).
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