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Oxygen therapy and inpatient mortality in COPD exacerbation
  1. Carlos Echevarria1,2,
  2. John Steer2,3,
  3. James Wason4,
  4. Stephen Bourke2,3
  1. 1Respiratory Department, Royal Victoria Infirmary, Newcastle upon Tyne, UK
  2. 2ICM, Newcastle University, Newcastle upon Tyne, UK
  3. 3Respiratory Department, North Tyneside General Hospital, North Shields, UK
  4. 4Population Health Sciences Institute, Newcastle University, Newcastle upon Tyne, UK
  1. Correspondence to Professor Stephen Bourke, North Tyneside General Hospital, North Shields NE29 8NH, UK; Stephen.Bourke{at}


Background In hospitalised patients with exacerbation of Chronic Obstructive Pulmonary Disease, European and British guidelines endorse oxygen target saturations of 88%–92%, with adjustment to 94%–98% if carbon dioxide levels are normal. We assessed the impact of admission oxygen saturation level and baseline carbon dioxide on inpatient mortality.

Methods Patients were identified from the prospective Dyspnoea, Eosinopenia, Consolidation, Acidaemia and Atrial Fibrillation (DECAF) derivation study (December 2008–June 2010) and the mixed methods DECAF validation study (January 2012 to May 2014). In six UK hospitals, of 2645 patients with COPD exacerbation, 1027 patients were in receipt of supplemental oxygen at admission. All had a clinical history of COPD and obstructive spirometry. These patients were subdivided into the following groups: admission oxygen saturations of 87% or less, 88%–92%, 93%–96% or 97%–100%. Inpatient mortality was calculated for each group and expressed as ORs. The DECAF score and National Early Warning Score 2 (excluding oxygen saturation) were used in binary logistic regression to adjust for baseline risk.

Results In patients with COPD receiving supplemental oxygen, oxygen saturations above 92% were associated with higher mortality and an adverse dose–response. Compared with the 88%–92% group, the adjusted risk of death (OR) in the 93%–96% and 97%–100% groups was 1.98 (95% CI 1.09 to 3.60, p=0.025) and 2.97 (95% CI 1.58 to 5.58, p=0.001). In the subgroup with normocapnia, the mortality signal remained significant in both the 93%–96% and 97%–100% groups.

Conclusions Inpatient mortality was lowest in those with oxygen saturations of 88%–92%. Even modest elevations in oxygen saturations above this range (93%–96%) were associated with an increased risk of death. A similar mortality trend was seen in both patients with hypercapnia and normocapnia. This shows that the practice of setting different target saturations based on carbon dioxide levels is not justified. Treating all patients with COPD with target saturations of 88%–92% will simplify prescribing and should improve outcome.

Trial registration number UKCRN ID 14214.

  • COPD
  • death/mortality
  • resuscitation
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  • Handling editor Richard John Parris

  • Contributors The study was conceived by SCB and designed by CE, JS and SCB. CE and JW performed statistical analyses. All authors contributed to data analysis and interpretation, and all were involved in drafting the manuscript and approving the final version. The corresponding author attests that all listed authors meet authorship criteria and that no others meeting the criteria have been omitted.

  • Funding This research was funded by the UK Department of Health, Northumbria NHS Foundation Trust TRF programme, Breathe North appeal, and Novartis Pharmaceuticals UK (reference RES 12-CO44).

  • Competing interests All authors declare: JS has no conflicts of interest to declare. CE reports grants from National Institute of Health Research, outside of the submitted work. SB reports grants from National Institute of Health Research, Philips Respironics and from Pfizer Open Air, personal fees from Pfizer, AstraZeneca, and ResMed, and non-financial support from Boehringer Ingelheim and GlaxoSmithKline outside the submitted work. No author has financial relationships with any organisation that might have an interest in the submitted work.

  • Patient consent for publication Not required.

  • Ethics approval Ethics approval was granted by NRES Committee North East, UK.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data availability statement Data are available upon reasonable request and after approval of the research team.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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