From: Bench-to-bedside review: the effects of hyperoxia during critical illness
Author | Country | Study type | Inclusion period | Subgroup | Sample size | Harm | Conclusions |
---|---|---|---|---|---|---|---|
Eastwood et al. [57] (2012) | Australia and New Zealand | Cohort | 2000–2009 | MV | 152,680 | – | Hypoxia in first 24 h of admission was associated with increased in-hospital mortality, but hyperoxia was not. |
de Jonge et al. [56] (2008) | The Netherlands | Cohort | 1999–2006 | MV | 36,307 | + | High FiO2 and both low PaO2 and high PaO2 in first 24 h of admission were associated with in-hospital mortality |
Suzuki et al. [96] (2014) | Australia | Before-after pilot | 2012 | MV | 105 | +/– | Conservative oxygen therapy in mechanically ventilated ICU patients was feasible and free of adverse biochemical, physiological, or clinical outcomes while allowing a marked decrease in excess oxygen exposure |
Aboab et al. [41] (2006) | France | Experimental | NA | ARDS | 14 | +/– | In mechanically ventilated patients with ARDS, the breathing of pure oxygen leads to alveolar derecruitment, which is prevented by high PEEP |
Austin et al. [53] (2010) | Australia | RCT | 2006–2007 | COPD | 405 | + | Titrated oxygen treatment significantly reduced mortality, hypercapnia, and respiratory acidosis compared with high-flow oxygen in acute exacerbations of COPD |
Cameron et al. [55] (2012) | New Zealand | Cohort | 2005–2008 | COPD | 180 | + | Serious adverse clinical outcomes are associated with both hypoxaemia and hyperoxaemia during acute exacerbations |
Perrin et al. [54] (2011) | New Zealand | RCT | 2007–2009 | Asthma | 106 | + | High-concentration oxygen therapy causes a clinically significant increase in transcutaneous CO2 during severe exacerbations |
Bellomo et al. [63] (2011) | Australia and New Zealand | Cohort | 2000–2009 | CA | 12,108 | – | Hyperoxia did not have a robust or consistently reproducible association with mortality |
Elmer et al. [62] (2014) | USA | Cohort | 2008–2010 | CA | 184 | + | Severe hyperoxia was independently associated with decreased survival to hospital discharge |
Ihle et al. [64] (2013) | Australia | Cohort | 2007–2011 | CA | 584 | – | Hyperoxia within the first 24 h was not associated with increased hospital mortality |
Janz et al. [61] (2012) | USA | Cohort | 2007–2012 | CA | 170 | + | Higher levels of the maximum measured PaO2 were associated with increased in-hospital mortality and poor neurological status on hospital discharge |
Kilgannon et al. [59] (2010) | USA | Cohort | 2001–2005 | CA | 6326 | + | Arterial hyperoxia was independently associated with increased in-hospital mortality compared with either hypoxia or normoxia |
Kilgannon et al. [60] (2011) | USA | Cohort substudy | 2001–2005 | CA | 4459 | + | Supranormal oxygen tension was dose-dependently associated with the risk of in-hospital death |
Kuisma et al. [69] (2006) | Finland | RCT pilot | NA | CA | 28 | – | No indication that 30 % oxygen with SpO2 monitoring did worse than the group receiving 100 % oxygen |
Lee et al. [65] (2014) | Korea | Cohort | 2008–2012 | CA | 213 | – | Mean PaO2 was not independently associated with in-hospital mortality |
Nelskyla et al. [112] (2013) | Australia | Cohort | 2008–2010 | CA | 122 | – | No statistically significant differences in numbers of patients discharged from the hospital and 30-day survival between patients with hyperoxia exposure and no exposure |
Spindelboeck et al. [67] (2013) | Austria | Cohort | 2003–2010 | CA | 145 | – | Increasing PaO2 was associated with a significantly increased rate of hospital admission and not with harmful effects |
Vaahersalo et al. [66] (2014) | Finland | Cohort | 2010–2011 | CA | 409 | – | Hypercapnia was associated with good 12-month outcome, but harm from hyperoxia exposure was not verified |
Minana et al. [113] (2011) | Spain | Cohort | 2003–2009 | ADHF | 588 | – | Admission PaO2 was not associated with all-cause long-term mortality |
Ranchord et al. [114] (2012) | New Zealand | RCT pilot | 2007–2009 | STEMI | 136 | – | No evidence of benefit or harm from high-concentration compared with titrated oxygen |
Stub et al. [78] (2012) | Australia | RCT | 2011–2014 | STEMI | 441 | + | Supplemental oxygen therapy in patients with STEMI but without hypoxia increased myocardial injury, recurrent myocardial infarction, and cardiac arrhythmia and was associated with larger myocardial infarct size at 6 months. Further results anticipated. |
Sutton et al. [115] (2014) | Australia and New Zealand | Cohort | 2003–2012 | Post cardiac surgery | 83,060 | – | No association between mortality and hyperoxia in the first 24 h in ICU after cardiac surgery |
Ukholkina et al. [80] (2005) | Russia | RCT | NA | AMI | 137 | – | Inhalation of 30–40 % oxygen within 30 min prior to endovascular myocardial reperfusion and within 4 h thereafter reduced the area of necrosis and peri-infarction area, improved central hemodynamics, and decreased the rate of post-operative rhythm disorders as compared with patients breathing ambient air |
Zughaft et al. [116] (2013) | Sweden | RCT | NA | ACS | 300 | – | The use of oxygen during PCI did not demonstrate any analgesic effect and no difference in myocardial injury measured with troponin- t or in the morphine dose |
Asher et al. [89] (2013) | USA | Cohort | NA | TBI | 193 | – | PaO2 threshold between 250 and 486 mm Hg during the first 72 h after injury was associated with improved all-cause survival independently of hypocarbia or hypercarbia |
Brenner et al. [88] (2012) | USA | Cohort | 2002–2007 | TBI | 1547 | + | Hyperoxia within the first 24 h of hospitalization was associated with worse short-term functional outcomes and higher mortality |
Davis et al. [87] (2009) | USA | Cohort | 1987–2003 | TBI | 3420 | + | Both hypoxemia and extreme hyperoxemia were associated with increased mortality and a decrease in good outcomes |
Quintard et al. [83] (2014) | Switzerland | Cohort | 2009–2013 | TBI | 36 | + | Incremental normobaric FiO2 levels were associated with increased cerebral excitotoxicity independently from brain tissue oxygen and other important cerebral and systemic determinants |
Raj et al. [90] (2013) | Finland | Cohort | 2003–2012 | TBI | 1116 | – | Hyperoxemia in the first 24 h of admission was not predictive of 6-month mortality |
Rincon et al. [92] (2013) | USA | Cohort | 2003–2008 | TBI | 1212 | + | Arterial hyperoxia was independently associated with higher in-hospital case fatality |
Jeon et al. [84] (2014) | USA | Cohort | 1996–2011 | Stroke | 252 | + | Exposure to hyperoxia was associated with delayed cerebral ischemia |
Rincon et al. [85] (2014) | USA | Cohort | 2003–2008 | Stroke | 2894 | + | Arterial hyperoxia was independently associated with in-hospital death as compared with either normoxia or hypoxia |
UK | RCT pilot | 2004–2008 | Stroke | 289 | – | Routine oxygen supplementation started within 24 h of hospital admission with acute stroke led to a small improvement in neurological recovery at 1 week, but no outcome differences were observed at 6 months | |
Ronning et al. [81] (1999) | Norway | Quasi-RCT | 1994–1995 | Stroke | 310 | + | Supplemental oxygen should not routinely be given to non-hypoxic patients with minor or moderate strokes |
Singhal et al. [118] (2005) | USA | RCT pilot | NA | Stroke | 16 | – | High-flow oxygen therapy is associated with a transient improvement of clinical deficits and MRI abnormalities |
Young et al. [91] (2012) | Australia and New Zealand | Cohort | 2000–2009 | Stroke | 2643 | – | Worst arterial oxygen tension in the first 24 h was not associated with outcome |
Stolmeijer et al. [119] (2014) | The Netherlands | Cohort | NA | Sepsis | 83 | – | No association between mortality and hyperoxia, nor between lower FiO2 and other detrimental effects |