Effect of pretreatment with oral pyridostigmine.

CORRESPONDENCE MANAGEMENT OF CARBOXYHAEMOGLOBINAEMIA Sir,—Drs Vegfors and Lennmarken have demonstrated usefully how easy it is to be misled in the management of carbon monoxide poisoning [1]. Their case deserves further comment. Unfortunately, there is little information on the mechanism of cellular toxicity of carbon monoxide. Carbon monoxide binds to haem-containing enzymes such as cytochrome P450 [2]. Measurements of carboxyhaemoglobin concentration are not helpful in determining the degree of tissue poisoning [3]. In particular, the likelihood of late neuropsychiatric problems, such as memory disturbance, is difficult to predict [4]. Up to 43 % of survivors may have such sequelae if followed up for 3 years [5]. Vegfors and Lennmarken suggested that an elimination half-life of 2 h was sufficient. As they point out, the use of 100 % oxygen at ambient pressure and at 3 arm abs would have reduced this to 1 h and to 20 min, respectively. Intracellular concentrations of carbon monoxide cannot be measured at present, but it is assumed that oxygen therapy similarly increases the elimination from the tissues and so reduces tissue damage. Hyperbaric oxygen appears to reduce both acute symptoms and neuropsychiatric complications [2]; however, its exact role has yet to be determined. Members of the British Isles Group of Hyperbaric Therapists are planning a prospective controlled study which will look at this issue—with particular regard to long-term morbidity. In the meantime, every case of suspected carbon monoxide poisoning should be treated with 100% oxygen. Patients with evidence of severe poisoning should be referred for hyperbaric oxygen [6]. This Hyperbaric Unit will consider a patient who has any one of the following: loss of consciousness at any stage since exposure to carbon monoxide; neuropsychological symptoms other than a mild headache; cardiac complications, including ischacmia and arrhythmias; carboxyhaemoglobin concentration greater than 20% at any time; pregnancy. Acute carbon monoxide poisoning. Risk of late sequelae and treatment by hyperbaric oxygen. Morbidity from acute carbon monoxide poisoning: a three year follow-up. Sir,—Vegfors and Lennmarken confirm in a patient that pulse oximetry (SpoJ readings in cases of carbon monoxide poisoning mislead as to the fraction of blood haemoglobin present as oxyhaemoglobin (HbO). However, they also echo the misconception that pulse oximeters read carboxyhaemoglobin (HbCO) as HbO. A pulse oximeter [1] measures absorption of light of two wavelengths (660 and 940 run) during pulsatile expansion of tissue and establishes the ratio of these absorbances (A660: A940). At the factory, the …