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Carbon Monoxide Poisoning 92 Turner, Hamilton-Farrell, Clark oxygen. Anecdotal reports of alternative ap- presented in this issue of the journal. One cer- proaches have not been followed up.'0 There is tainly wants to avoid the error of telling a little evidence from clinical studies that patient with undiagnosed carbon monoxide J Accid Emerg Med: first published as 10.1136/emj.16.2.92 on 1 March 1999. Downloaded from normobaric oxygen is effective, and even the poisoning to "go home and stay warm", with evidence concerning hyperbaric oxygen is dif- the result that they suffer even worse poison- ficult to interpret despite animal studies and ing. cellular research which provide strong evi- dence in its favour. One important factor is 1 Chief Medical Officer and Chief Nursing Officer. Carbon monoxide: the forgotten kilter. London: Department of that it reduces free radical concentrations, and Health, September 1998. this means that the benefit from hyperbaric 2 Chief Medical Officer. CO poisoning: pulse oximetry. oxygen may be far reaching. It provides an CMO's update 20. London: Department of Health, November 1998: 3. explanation why hyperbaric oxygen prevents 3 Carbon monoxide: health hazards and precautionary meas- the delayed manifestations of carbon monox- ures. Guidance note EH43. 2nd Ed. London: Health and Safety Executive, 1998. ide poisoning. 4 Smith JS, Brandon S. Morbidity from acute carbon monox- The presentation by Hamilton-Farrell ofthe ide poisoning at three year follow up. BMJ 1973;i:318-21. 5 Chale SN. Carbon monoxide poisoning. In: Vicciello P, ed. British Hyperbaric Association's carbon mon- Handbook ofmedical toxicology. Boston: Little, Brown 1993: oxide database (p98) provides an impressive 639-47. 6 Choi IS, Kim SK, Lee SS, et al. Evaluation of outcome of panorama of the use of hyperbaric oxygen in delayed neurologic sequelae after carbon monoxide poison- Britain." The indications for referral are ing by technetium 99m hexamethylpropylene amine oxime brain singe photon emission computed tomography. Eur clearly set out, and the reasons for delay to Neurol 1995;35: 137-42. referral and delay to arrival in a hyperbaric 7 Kirkpatrick JN. Occult carbon monoxide poisoning. West J7 facility are listed. Many of these can be Med 1987;146:52-6. 8 Turner M, Esaw M, Clark RJ. Carbon monoxide poisoning reduced by making a critical examination at a treated with hyperbaric oxygen: metabolic acidosis as a local level and addressing the deficiencies predictor of treatment requirements. J Accid Emerg Med 1999;16:96-8. identified. The rising number of referrals may 9 Turner M, Hamilton-Farrell MR, Clark RJ. Carbon monox- be a result of increased awareness, since the ide poisoning: an update. J Accid Emerg Med 1999;16: 92-6. number of cases of fatal poisoning is falling. It 10 Howard RJ, Lake DR, Pall H, et al. Allopurinol/N- has been suggested that this is due to the acetylcysteine for carbon monoxide poisoning. Lancet 1987;ii:628-9. introduction of catalytic converters in motor 11 Hamilton-Farrell MR. British Hyperbaric Association vehicles. 2 carbon dioxide database, 1993-96. Y Accid Emerg Med 1999;16:98-103. Those working in any branch of emergency 12 Kendell RE. Catalytic converters and prevention of suicide. medicine would do well to study the articles Lancet 1998;352:1525. Carbon monoxide poisoning: an update http://emj.bmj.com/ Mark Turner, Martin R Hamilton-Farrell, Robin J Clark Carbon monoxide is the major cause of death Death may be due to cardiac toxicity, from poisoning in the UK. In 1996 there were neurotoxicity, systemic acidosis, or respiratory on September 29, 2021 by guest. Protected copyright. 877 deaths from carbon monoxide poisoning arrest. (CMP) in England and Wales; the majority were suicides due to car exhaust fumes.' Pathophysiology The commonly held beliefthat CMP is mainly due to binding of haemoglobin was shown to Department of Causes be false over 20 years ago.6 Goldbaum et al Cardiology, Derriford The most common causes of CMP are demonstrated that exchange transfusion, using Hospital, Plymouth, deliberate attempted suicide using car exhaust a red cell concentrate with a carboxyhaemo- Devon PL6 8HD fumes, domestic heater malfunction, open globin (COHb) concentration of 80%, led to M Turner heating fires, burning buildings, and indefinite survival in one group of dogs, Whipps Cross accidental exposure to car exhaust. Rarer despite equilibrium COHb concentrations of Hospital, London causes include recreational boating,2 indoor 60%. The potential to endure a diminished M R Hamilton-Farrell burning of charcoal briquettes,' obstruction oxygen carrying capacity was demonstrated by snow of vehicle exhaust systems,4 and the when other dogs were venesected isovolaemi- Royal Naval Hospital hepatic metabolism of methylene chloride cally, reducing mean packed cell Haslar, Gosport volume by R J Clark from paint stripper fumes.5 The British 68%, and survived indefinitely. In contrast, Hyperbaric Association (BHA) CMP data- dogs in a third group inhaled 13% carbon Correspondence to: base suggests that, for cases managed with monoxide for 15 minutes, producing a mean Dr Turner, Specialist hyperbaric oxygen, approximately half are COHb of 65%, and all died. Goldbaum et al Registrar in Cardiology. deliberate and half accidental.5 This contrasts deduced that the slow rate of carbon monox- Accepted 10 September with the mortality figures, with 85% of CMP ide binding by haemoglobin led to blood 1998 deaths being due to deliberate poisoning. entering the systemic capillary beds with a Carbon monoxide poisoning 93 Clinical manifestations Box 1: Clinical manifestations of car- Severe CMP is characterised by neurological bon monoxide poisoning and cardiovascular manifestations (box 1). J Accid Emerg Med: first published as 10.1136/emj.16.2.92 on 1 March 1999. Downloaded from Neurological Unconsciousness is the most common neuro- * Loss of consciousness logical manifestation although memory loss, * Neurological and cognitive abnormality drowsiness, poor cognitive performance, and * Gait disturbance disturbance of balance or gait (including Cardiovascular cerebellar features) may be seen. Less severe * Hypotension cases may have non-specific symptoms includ- * Cardiac ischaemia ing headache, nausea, vomiting, and lethargy. * Arrhythmia In such cases a careful history should be taken Biochemical to identify potential exposure to carbon * Carboxyhaemoglobinaemia monoxide. It is possible that many mild cases * Metabolic acidosis are never diagnosed and there is evidence that much late morbidity from CMP goes unrecognised.'4 The commonly quoted cherry red discolora- tion mucous may be significant burden of dissolved carbon monox- of skin and membranes ide available for diffusion. Conversely, in the seen at autopsy but is extremely rare in patients exchange transfusion experiment described presenting with acute CMP.'5 The absence of above, minimal dissolved carbon monoxide the cherry red colour does nothing to exclude had been infused and the carbon monoxide the diagnosis.'6 was so tightly bound to haemoglobin that there was little tissue burden. The paper con- Clinical assessment cluded that the toxicity of carbon monoxide is A careful history, specifically seeking all of the predominantly a direct action on cells, rather possible manifestations listed above should be than mainly the denial of oxygen carriage by taken. The type of heating in the patient's haemoglobin. home should be established. A venous COHb The mechanism for tissue damage in CMP concentration should be performed if there is is the poisoning of intracellular oxygen any suspicion of the diagnosis. carrying haem proteins, such as cytochrome a, Even in obvious and severe cases, clinical and myoglobin. This leads to cellular history and examination are most important. dysfunction and produces the clinical mani- Specific features of the history should be festations most rapidly in tissues with high sought: cause, duration of exposure, loss of energy requirements (brain and heart). Fur- consciousness (even if transient), the ther injury is caused by radical oxygen species, possibility of other poisons (cyanide or drugs), including nitric oxide, produced locally by and chest pain. A history of possible chronic neutrophils.7 exposure should be sought in accidental cases, Hyperglycaemia and hypoglycaemia have an since this may have preceded the acute http://emj.bmj.com/ adverse effect in rats poisoned with carbon presentation. Neurological examination monoxide.8 Investigation of the brain energy should include assessment of cognitive func- metabolites ATP and phosphocreatine failed to tions and in particular memory; patients define clearly a mechanism for this finding, should all be asked to stand and walk, if they although lactate concentrations were lower in are able, because balance and gait disturbance the normoglycaemic animals than in those with may be the only abnormality in the physical hyperglycaemia.9 The role of plasma glucose in examination. on September 29, 2021 by guest. Protected copyright. humans has not been investigated, however it Most patients with severe poisoning will present with a reduced level of consciousness, would seem logical to maintain normoglycae- so bedside blood glucose analysis should be mia in patients. performed immediately to exclude hypoglycae- Ethanol has been shown to modify the mia, which may complicate CMP or may be severity of poisoning in mice.'0 Survival time the sole cause of unconsciousness. The COHb was improved in mice pretreated with
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