Practice Uncertainties

Does routine oxygen supplementation in patients with acute stroke improve outcome?

BMJ 2012; 345 doi: http://dx.doi.org/10.1136/bmj.e6976 (Published 30 November 2012) Cite this as: BMJ 2012;345:e6976
  1. S J Pountain, study manager of the Stroke Oxygen Study1,
  2. C Roffe, consultant physician 1, professor of stroke medicine2
  1. 1Stoke Stroke Research Group, North Staffordshire Combined Healthcare NHS Trust, Stoke-on-Trent ST4 7LH, UK
  2. 2Institute for Science and Technology in Medicine, Keele University, Keele
  1. Correspondence to: christine.roffe{at}northstaffs.nhs.uk

Stroke is the third most common cause of death and the leading cause of long term disability in developed countries. Specialist care in stroke units is well established as being effective in preventing death and disability after stroke.1 However, which aspects of stroke care are crucial for improving outcome remains unclear. Patients in a stroke unit are more likely than those on a non-specialised general ward to receive oxygen.2 Bravata and colleagues found that treating all episodes of hypoxia with supplemental oxygen was one of three key processes associated with better outcome in acute stroke care.3 Mild hypoxia is common in patients with stroke and may have substantial adverse effects on an ischaemic brain after stroke. Whereas healthy adults with normal cerebral circulation can compensate for mild hypoxia by an increase in cerebral blood flow, this is not possible in patients whose brain is already ischaemic after stroke.4 Hypoxaemia in the first few hours after hospital admission is associated with an increased risk of death.5

Oxygen treatment is not without problems.6 The tubing that connects the patient to the oxygen source impedes early mobilisation and could pose an infection risk. Physiological changes associated with oxygen treatment can include absorption atelectasis; worsening of ventilation-perfusion mismatch; coronary, cerebral, and systemic vasoconstriction; and a reduction in cardiac output.7 Animal models and in vitro studies show that oxygen encourages the formation of toxic free radicals, leading to further damage to the ischaemic brain, especially during reperfusion. Oxidative stress has also been implicated in the activation of cell signalling pathways, which lead to apoptosis and neuronal cell death. Although some research points towards adverse effects of hyperoxia in the ischaemic brain, some evidence supports the notion that eubaric hyperoxia (hyperoxia induced by oxygen treatment at normal atmospheric pressure) …

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