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Research paper
Hyperoxia may be related to delayed cerebral ischemia and poor outcome after subarachnoid haemorrhage
  1. Sang-Beom Jeon1,2,3,
  2. H Alex Choi2,3,
  3. Neeraj Badjatia3,4,
  4. J Michael Schmidt3,
  5. Hector Lantigua3,
  6. Jan Claassen3,
  7. E Sander Connolly5,
  8. Stephan A Mayer3,
  9. Kiwon Lee2,3
  1. 1Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea
  2. 2Departments of Neurology and Neurosurgery, The University of Texas Medical School at Houston, Houston, Texas, USA
  3. 3Department of Neurology, Columbia University College of Physicians and Surgeons, New York, New York, USA
  4. 4Department of Neurology, University of Maryland School of Medicine, Baltimore, Maryland, USA
  5. 5Departments of Neurosurgery, Columbia University College of Physicians and Surgeons, New York, New York, USA
  1. Correspondence to Dr Kiwon Lee, Departments of Neurology and Neurosurgery, The University of Texas Medical School at Houston, 6431 Fannin St., MSB 7.152, Houston, TX 77030, USA; Kiwon.Lee{at}uth.tmc.edu

Abstract

Objective To determine the association between exposure to hyperoxia and the risk of delayed cerebral ischaemia (DCI) after subarachnoid haemorrhage (SAH).

Methods We analysed data from a single centre, prospective, observational cohort database. Patient inclusion criteria were age ≥18 years, aneurysmal SAH, endotracheal intubation with mechanical ventilation, and arterial partial pressure of oxygen (PaO2) measurements. Hyperoxia was defined as the highest quartile of an area under the curve of PaO2, until the development of DCI (PaO2≥173 mm Hg). Poor outcome was defined as modified Rankin Scale 4–6 at 3 months after SAH.

Results Of 252 patients, there were no differences in baseline characteristics between the hyperoxia and control group. Ninety-seven (38.5%) patients developed DCI. The hyperoxia group had a higher incidence of DCI (p<0.001) and poor outcome (p=0.087). After adjusting for modified Fisher scale, rebleeding, global cerebral oedema, intracranial pressure crisis, pneumonia and sepsis, hyperoxia was independently associated with DCI (OR, 3.16; 95% CI 1.69 to 5.92; p<0.001). After adjusting for age, Hunt–Hess grade, aneurysm size, Acute Physiology and Chronic Health Evaluation II score, rebleeding, pneumonia and sepsis, hyperoxia was independently associated with poor outcome (OR, 2.30; 95% CI 1.03 to 5.12; p=0.042).

Conclusions In SAH patients, exposure to hyperoxia was associated with DCI. Our findings suggest that exposure to excess oxygen after SAH may represent a modifiable factor for morbidity and mortality in this population.

  • SUBARACHNOID HAEMORRHAGE

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