5 November 1998
The Editor
The BMJ
BMA House,
Tavistock Square
London WC1H 9JR
Sir
Hyperbaric oxygen therapy; the XYZ of oxygen
Drs Leach et al (Oct 24, p 1140) 1 indicate the skepticism directed at hyperbaric oxygen therapy, but it is not difficult to understand why this is the case when they refer to "normobaric" or "hyperbaric" oxygen. The correct term is oxygenation and the oxygen provided in a hyperbaric chamber is no different to the oxygen in air. In the absence of pressure chamber oxygen dosage is limited by the ambient barometric pressure, which, at sea level in the UK, varies between 925 hPa (694 mm Hg) and 1054 hPa (791 mm Hg). Patients given 100% oxygen get less on a low pressure than a high-pressure day. Barometric pressure also falls with increasing altitude and a pressure chamber is needed for example, in Denver Colorado, to achieve what the authors refer to as "normobaric" oxygen at sea level. The accepted treatment for acute asphyxia is 100% oxygen, but barometric pressure is not considered. The use of a pressure chamber allows a much larger concentration to be given and if global oxygen depletion is corrected promptly this is life-saving. The window of opportunity for the resuscitation of cerebral tissue, even after circulatory arrest, may be much longer than currently recognized.
Human brain tissue removed up to eight hours after death has been found to function for up to 18 hours under hyperoxic conditions.2 Even after longer periods there may be recoverable tissue in the ischemic penumbra3 where, because of edema, sufficient oxygen may be present to prevent membrane failure, but not to allow function. Methods are now available to detect and even quantify tissue hypoxia.
For example, magnetic resonance spectroscopy has demonstrated hypoxia in many conditions from birth asphyxia4 to acute lesions in multiple sclerosis, 5 where studies of hyperbaric oxygen therapy have been limited to chronic stable patients. Should we be surprised that only a small number of these Trials have demonstrated significant benefit when most have recruited patients with disease durations in excess of ten years? To find any improvement in such patients indicates that oxygen should be used at the onset of symptoms, not when extensive scarring has occurred. Leach et al fail to mention a key property of oxygen in therapy; it is a vasoconstrictor and increasing the plasma oxygen tension uniquely allows a reduction of blood flow with an increase in oxygen delivery.
This science underpins the use of hyperbaric oxygenation in a wide variety of diseases. The mortality and morbidity of hypoxia is properly addressed by the administration of more oxygen. As JS Haldane stated many years ago, "lack of oxygen not only stops the machine it wrecks the machinery." There is no more critical, scientific and defensible action than to administer the correct dosage of oxygen in hypoxia to restore normal tissue values and this may require a hyperbaric chamber. We need to progress beyond the ABC of oxygen and this simple technology should be in every hospital.
Yours faithfully
Philip James M.D.
Senior Lecturer in Occupational Medicine
Reprinted with Permission
References
- Leach RM, Rees PJ, Wilmshurst P. ABC of oxygen hyperbaric oxygen therapy. Br Med J 1998;317:1140-1143.
- Neubauer RA, James PB.Cerebral oxygenation and the recoverable brain. Neurol Res 1998;20 (Suppl 1): 33-36.
- Dai J, Swaab DF, Buijs RM. Recovery of axonal transport in "dead neurons." Lancet 1998;351:499-500.
- Ashwal S, Holshouser BA, Tomasi LG, et al. 1H - magnetic resonance spectroscopy-determined cerebral lactate and poor neurological
outcomes in children with central nervous system disease. Ann Neurol 1997;41:470-481.
- Miller DH, Austin SJ, Connelly A, et al. Proton magnetic resonance spectroscopy of an acute and chronic lesion in multiple sclerosis. Lancet 1991;337:58-59.
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