Kyle Perrin

Pre‐hospital oxygen therapy in acute exacerbations of chronic obstructive pulmonary disease

Background: High concentration oxygen is commonly administered during acute exacerbations of chronic obstructive pulmonary disease (AECOPD). The aim of this study was to determine the association between oxygen, severity markers and poor outcomes in AECOPD.

The risk of asthma mortality with inhaled long acting β-agonists

This article reviews the available evidence as to whether inhaled long acting β-agonists (LABA) increase the risk of asthma mortality and considers the implications for the use of this treatment in the management of asthma. Randomised controlled trials suggest that LABAs prescribed as monotherapy may increase the risk of asthma death in certain circumstances, such as the unsupervised “off-label” use without concomitant inhaled corticosteroid (ICS) treatment in patients with unstable asthma. However, there is also evidence that the use of LABAs in conjunction with ICS treatment in adult asthma as recommended in current guidelines is not associated with an increased risk of asthma mortality. The only way in which a prescriber can ensure that a patient with asthma takes LABA treatment in conjunction with ICS is through a combination ICS/LABA product, an approach which may have additional therapeutic advantages. We propose that in the management of asthma, a case can now be made to limit the availability of LABAs to combination LABA/ICS therapy.

Epidemiology of Asthma Mortality

The epidemiology of asthma mortality has been controversial since Osler stated in the Principles and Practice of Medicine,published in 1901, that the “the asthmatic pants into old age” [1]. Certainly asthma deaths were rare in the first half of this century, although since this time, the patterns of asthma mortality have become considerably more complex. There have been epidemics of asthma deaths in six Western countries in the 1960s, and again in New Zealand in the 1970s. Another feature observed in many countries has been a more gradual increase in asthma mortality, which commenced in the 1940s and has been particularly marked in the 1970s and 1980s. During the 1990s, mortality has declined in some, but not in other countries. In this chapter, we commence by briefly considering issues relevant to the interpretation of long-term time trends in asthma mortality. We then discuss the international trends in asthma mortality throughout the 20th century, focusing primarily on the possible causes for the mortality epidemics and the gradual rise in asthma mortality which has occurred over recent decades. Finally, we review markers of an increased risk of asthma mortality, the characteristics of patients experiencing a fatal or near fatal attack of asthma, and factors that can provoke such episodes.

An audit of the effect of oxygen prescription charts on clinical practice

Problem The need to improve the prescription, administration and monitoring of oxygen therapy. Design An interventional, prospective audit. Background and setting Wellington Hospital, a teaching and tertiary referral hospital in New Zealand in 2007 and 2008. Key measures for improvement Demonstration of adequate oxygen prescribing, administration and monitoring of oxygen therapy. Strategies for improvement The introduction of a new drug chart with a specific oxygen prescription section. Targeted educational lectures primarily to medical staff. Effects of change 610 and 566 patients were reviewed in the first and second audits. After introduction of the new oxygen prescription section on the drug chart the proportion of patients whose oxygen therapy was prescribed increased from 15/85 (17.6%) to 39/98 (39.8%), relative risk 2.3 (95% CI 1.3 to 3.9). The proportion with adequate oxygen prescription, with documentation of device, flow rate or inspired oxygen concentration, and the target oxygen saturation increased from 5/85 (5.9%) to 36/98 (36.7%), relative risk 6.2 (95% CI 2.5 to 15.0). Introduction of the new charts was not associated with changes in clinical practice in terms of assessment of oxygen saturations on room air and commencement if ≤92%, or the titration of oxygen therapy in response to oxygen saturations ≤92%. Lessons learnt An oxygen prescription section on hospital drug charts improved the prescription of oxygen but did not improve clinical practice. Additional strategies are required to improve the administration of oxygen therapy in hospitals.

Oxygen therapy in acute exacerbations of chronic obstructive pulmonary disease

During the last decade, there have been major advances in knowledge of the effects of oxygen therapy in patients with acute exacerbations of chronic obstructive pulmonary disease. This includes a randomised controlled trial of oxygen therapy in the pre-hospital setting, which showed that high concentration oxygen therapy leads to a 2.4-fold increased risk of mortality compared with titrated oxygen therapy to maintain oxygen saturations (SpO2) within a target range of 88–92%. Professional guidelines now recommend the use of supplementary oxygen in acute exacerbations of chronic obstructive pulmonary disease only if the SpO2 is less than 88%, with titration to achieve an SpO2 of 88–92%, and the delivery of bronchodilators by air-driven nebulisation or metered dose inhaler with a spacer. The aim of this review is to provide an overview of the evidence base that underpins these recommendations. We suggest that their implementation will require important changes to current clinical practice in which there is an entrenched culture of the use of high concentration oxygen therapy.

Comparative audit of oxygen use in the prehospital setting, in acute COPD exacerbation, over 5 years

Background In 2009 the Wellington Free Ambulance implemented an education programme to reduce high concentration oxygen delivery to patients with an acute exacerbation of chronic obstructive pulmonary disease (AECOPD). The aim of this audit was to compare pre-hospital oxygen delivery to patients with AECOPD before and after the programme. Methods An audit of patients who presented to Wellington Regional Hospital by ambulance with an AECOPD in 2005 and then in 2010, after implementation of the education programme. Oxygen therapy was categorised as: HIGH, supplemental high concentration oxygen therapy ≥3u2005L/min and/or delivery via high concentration mask; NEB, high concentration oxygen only during nebuliser use; or LOW, neither of these. Results In 2005 those in the HIGH, NEB and LOW categories were 81 (75.0%), 18 (16.7%) and 9 (8.3%) of 108 identified patients. In 2010 those in the HIGH, NEB and LOW categories were 80 (44.0%), 61 (33.5%) and 41 (22.5%) of 182 identified patients. The proportions of patients in the three oxygen groups were significantly different between 2005 and 2010 (p<0.001). Conclusions The proportion of patients administered supplemental high concentration oxygen therapy markedly decreased between 2005 and 2010 following implementation of the education programme. However, in 2010 more than half of the patients not managed with high concentration oxygen therapy were still exposed to high concentration oxygen through the use of oxygen-driven nebulisers. To reduce exposure to high concentration oxygen in AECOPD the use of air-driven nebulisers or metered dose inhalers with spacers is required.

Authors' response: hyperoxia in acute asthma

We appreciate the comments by Snelson and Tunnicliffe1 regarding our study of the effects of high concentration oxygen therapy in acute exacerbations of asthma.2 We concur with the view that the effect of high concentration oxygen therapy on arterial carbon dioxide pressure (PaCO2) is not clinically relevant in all patients presenting to the emergency department (ED) with acute severe asthma. However, we consider that the 3.9-fold …

Reply: Letters to the Editor

We thank Wood-Baker and colleagues for highlighting their landmark randomised controlled trial (RCT). As discussed in the accompanying British Medical Journal editorial, there is now robust level 1 evidence that controlled oxygen therapy titrated to achieve oxygen saturations of 88 to 92% substantially reduces the risk of death associated with high concentration oxygen therapy in acute exacerbations of chronic obstructive pulmonary disease (AECOPD). However, there are two major obstacles to the implementation of this regimen. The first is to overcome the entrenched practice of delivering high concentration oxygen therapy in AECOPD. The extent of this behaviour was illustrated in the Australian RCT in which more than half of the patients with confirmed chronic obstructive pulmonary disease randomly assigned to the titrated oxygen group received high concentration oxygen at some stage during the ambulance transfer, in violation of the protocol, and despite 1 month of familiarisation and training of health professionals before commencement of data collection. The other obstacle is the delivery of high concentration oxygen through administration of bronchodilator through a nebuliser driven by oxygen. One alternative to this practice is to use air-driven nebulisers with titrated supplemental nasal oxygen, the regimen employed in the Australian RCT. We also thank Swain and colleagues for raising these and other issues relating to the interpretation of clinical data in our audit. We recognise that clinical documentation in emergency situations may not be ideal, but nevertheless, there was a significant association between increasing PaO2 at presentation to the emergency department and worse outcome in our audit. In regard to the strength of the association with oxygen administration, the odds ratio of 1.2 is per 1 L/min oxygen flow, which equates to an odds ratio of 3.0 per 6 L/min oxygen flow (the difference between 2 L and 8 L/min oxygen flow), which is similar to the odds ratios reported for other risk factors. In comparing odds ratios, another consideration is how common the risk factor occurs, and in this regard, 49% of patients in whom the oxygen flow rate was clearly documented had received oxygen 8 L/ min in our audit. In addition, some of the risk factors used to adjust the estimates for imbalance related to the non-experimental study design are not modifiable, whereas administration of oxygen is under the control of medical care. With regard to initial priorities, we do not concur with the view that measuring initial room air oxygen saturation would not be important when attending a patient suffering respiratory distress. It is a critical vital sign to both assess risk and enable a informed assessment of whether oxygen therapy is indicated. Looking forward, the challenge will be to achieve a paradigm shift in practice worldwide, so that titration of oxygen therapy to achieve an oxygen saturation target of 88 to 92% becomes the standard care in AECOPD, thereby minimising the risks of both hypoxaemia and hyperoxaemia.