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I read with interest the article published by Arbillaga-Etxarri et al.[1] titled “Socioenvironmental correlates of physical activity in patients with chronic obstructive pulmonary disease (COPD)”. In the introduction section, the authors stated that the current interventions (e.g., pharmacological treatment, rehabilitation, self-management) aiming to change physical activity behavior in COPD patients lack effectiveness, particularly in the long-term. The authors argue that this absence of effectiveness could be due to a lack of knowledge of physical activity determinants in this population. To address this issue, Arbillaga-Etxarri et al.[1] examined the socio-ecological determinants of active behaviours in 400 COPD patients and found that, after controlling potential confounders, having a dog and grandparenting were positively associated with physical activity; effects sizes were small, β = .19 and very small β = .08 for dog walking and grandparenting, respectively. The authors concluded that these two socio-environmental characteristics should be considered to promote physical activity both at the clinical level and in future research. This study is important because there is a lack of knowledge regarding the determinants of physical activity in this population.[2]
Nonetheless, there are some reservations regarding the clinical utility of physical activity socio-environmental correlates to design physical activity programs. Socioenvironmental correlates of physica...
I read with interest the article published by Arbillaga-Etxarri et al.[1] titled “Socioenvironmental correlates of physical activity in patients with chronic obstructive pulmonary disease (COPD)”. In the introduction section, the authors stated that the current interventions (e.g., pharmacological treatment, rehabilitation, self-management) aiming to change physical activity behavior in COPD patients lack effectiveness, particularly in the long-term. The authors argue that this absence of effectiveness could be due to a lack of knowledge of physical activity determinants in this population. To address this issue, Arbillaga-Etxarri et al.[1] examined the socio-ecological determinants of active behaviours in 400 COPD patients and found that, after controlling potential confounders, having a dog and grandparenting were positively associated with physical activity; effects sizes were small, β = .19 and very small β = .08 for dog walking and grandparenting, respectively. The authors concluded that these two socio-environmental characteristics should be considered to promote physical activity both at the clinical level and in future research. This study is important because there is a lack of knowledge regarding the determinants of physical activity in this population.[2]
Nonetheless, there are some reservations regarding the clinical utility of physical activity socio-environmental correlates to design physical activity programs. Socioenvironmental correlates of physical activity are often largely beyond participants’ control and thus non-modifiable during an intervention for a clinician, such as the ‘walkability’ of the environment. For example, in the current study, only 18 % of the sample had a dog and 12% of the participants reported walking it. The authors explained that patients could have concerns about dogs such as difficulties with controlling the animal, which could explain the lack of dog owners in the study. It could also be hypothesized that patients have a dog because they are already active and feel capable of owning a dog. Nevertheless, it could be difficult to use this leverage during a physical activity counseling intervention.
Physical activity is a complex behavior that may depend from many different factors, such as socio-environmental variables (e.g. age, family support), biological functions (e.g. functional capacity), or environmental factors (e.g. climatic conditions; ‘walkability’ of the environment). Among these potential predictors of physical activity there is an urgent need to identify factors that could be modifiable during an intervention. In this regard, the concept of motivation is an important target.
Motivation could be operationalized through different theoretical constructs, which have received different levels of empirical support regarding their associations with physical activity behaviour depending on the context [3]. These constructs could be clustered into (1) intentional processes (the development of objectives and intentions to be active), (2) affective judgments (feelings about physical activity) (3) self-perception of capability and opportunity (confidences in one’s capacity to be active) (4) self-regulation processes ( strategies used to maintain motivation and dealing with barriers) and (5) automatic or unconscious processes (physical activity habits driven by feelings about physical activity). Methodologically, these processes are often measured through either self-reported questionnaires [4] or computerized reaction-time tests.[5] To date, research dealing with motivational processes toward physical activity for patients with chronic respiratory disease are scarce. Selzler et al [6] found that stronger physical activity-specific self-efficacy was positively associated with exercise attendance, as well as 6-minute walk test improvement during pulmonary rehabilitation. Chevance et al [7] highlighted that unconscious feelings (measuring with computerized test) about physical activity prospectively predict self-reported physical activity at 6 months after pulmonary rehabilitation. These preliminary results are important because identifying modifiable determinants of physical activity could help (i) to motivate patient to integrate a program, or identify patient at risk to failing physical activity after an intervention and (ii) to design more effective evidence-based interventions regarding physical activity in COPD patients. In conclusion, future studies should consider the motivational determinants of physical activity as well as interventions to specifically enhance motivation.
Acknowledgments : I sincerely thank Anne-Marie Selzler for their comments
References
1. Arbillaga-Etxarri A, Gimeno-Santos E, Barberan-Garcia A, et al. Socio-environmental correlates of physical activity in patients with chronic obstructive pulmonary disease (COPD). Thorax, forthcoming. doi: 10.1136/thoraxjnl-2016-209209.
2. Gimeno-Santos E, Frei A, Steurer-Stey C, et al. Determinants and outcomes of physical activity in patients with COPD: a systematic review. Thorax, 2014;69: 731-39. doi: 10.1136/thoraxjnl-2013-204763.
3. Rhodes R. The Evolving Understanding of Physical Activity Behavior: A Multiprocess Action Control Approach. Advances in Motivation Science, 2017;4:171-205. doi: 10.1016/bs.adms.2016.11.001.
4. Rodgers W, Wilson P, Hall C, et al. Evidence for a Multidimensional Self-Efficacy for Exercise Scale. Res Q Exerc Sport, 2008;79:222-34. doi:10.1080/02701367.2008.10599485.
5. Chevance G, Heraud N, Guerrieri A, et al. Measuring implicit attitudes toward physical activity and sedentary behavior: Test-retest reliability of three scoring algorithms of the Implicit Association Test and Single Category-Implicit Association Test. Psychology of Sport and Exercise, 2017;31:70-8. doi: 10.1016/j.psychsport.2017.04.007.
6. Selzler A, Rodgers W, Berry T, et al. The importance of exercise selfefficacy for clinical outcomes in pulmonary rehabilitation. Rehabil Psychol, 2016;61:380-8. doi: 10.1037/rep0000106
7. Chevance G, Héraud N, Varray A, et al. Change in Explicit and Implicit Motivation toward Physical Activity and Sedentary Behavior in Pulmonary Rehabilitation and Associations with Postrehabilitation Behaviors. Rehabil Psychol, forthcoming. doi: 10.1037/rep0000137.
We commend Dr. Echevarria et al. for their excellent article, published in Thorax online (February 2017), concerning a new index (PEARL score) to predict the 90-day risk of death or readmission after hospitalization for an acute exacerbation of COPD (AECOPD). I agree with the authors on the relevance of 3 months’ prognosis after a hospitalization for AECOPD. Although policymakers usually consider 30-day readmissions as the marker of quality of care, only 36% of readmissions in COPD patients in this period are for a relapse, incomplete recovery, or a new COPD exacerbation. (1) The rest of readmissions in COPD patients are related with the deleterious complications associated with any hospitalization (post-hospital syndrome), especially in an aged population, with frequent comorbidities and often physical frailty. (2) In this sense, a 90-day time frame can probably better capture not only hospital and ambulatory quality of care, but also risk variables associated with readmissions in COPD patients. However, we believe that the article deserves some reflection.
First, the authors stated that no tool has previously been developed in COPD to predict short-term readmission or death. This is only partially true. As they themselves note later, the CODEX index was specifically developed and validated to evaluate the risk of mortality, readmission, and their combination in the short- (3 months) or medium-term (1-year) after hospital discharge for AECOPD. (3)
Second, the...
We commend Dr. Echevarria et al. for their excellent article, published in Thorax online (February 2017), concerning a new index (PEARL score) to predict the 90-day risk of death or readmission after hospitalization for an acute exacerbation of COPD (AECOPD). I agree with the authors on the relevance of 3 months’ prognosis after a hospitalization for AECOPD. Although policymakers usually consider 30-day readmissions as the marker of quality of care, only 36% of readmissions in COPD patients in this period are for a relapse, incomplete recovery, or a new COPD exacerbation. (1) The rest of readmissions in COPD patients are related with the deleterious complications associated with any hospitalization (post-hospital syndrome), especially in an aged population, with frequent comorbidities and often physical frailty. (2) In this sense, a 90-day time frame can probably better capture not only hospital and ambulatory quality of care, but also risk variables associated with readmissions in COPD patients. However, we believe that the article deserves some reflection.
First, the authors stated that no tool has previously been developed in COPD to predict short-term readmission or death. This is only partially true. As they themselves note later, the CODEX index was specifically developed and validated to evaluate the risk of mortality, readmission, and their combination in the short- (3 months) or medium-term (1-year) after hospital discharge for AECOPD. (3)
Second, the authors only analyse the combination of death or readmission. Clearly both are relevant events for the patients, but their impact is obviously different, and no data about mortality are detailed in the article. In our opinion, it would be more illustrative to analyse PEARL score separately for deaths, readmissions (excluding deceased patients without readmissions), and the combined variable. This is especially important in the follow-up at 1 year, represented in Figure3B of the article.
Third, the authors based the diagnosis of left ventricular failure (LVF) on echocardiographic results. However, heart failure is a clinical syndrome and not an echocardiographic diagnosis. This is especially important in heart failure with preserved ejection fraction, the most frequent cause of heart failure in aged patients with comorbidities. In these patients, echocardiographic evaluation is more difficult and less reliable. (4) The diagnosis of LVF based exclusively on echocardiographic results can exclude patients with heart failure without previous echocardiogram or with indeterminate results. This would explain the low prevalence of left ventricular failure observed in the present study compared with previous publications. (3,5)
Finally, the authors point out as a limitation of the CODEX and LACE indexes the requirement to calculate the Charlson index. We have doubts with this statement. The Charlson index is the most widely recognized prognostic index of comorbidity. It is easy and quick to calculate and in fact the variables included (previous chronic diseases) must be collected in any medical history.
1.-Jencks SF, Williams MV, Coleman EA. Rehospitalizations among patients in the Medicare fee-for-service program. N Engl J Med. 2009;360:1418-28.
2.-Krumholz HM. Post-hospital syndrome--an acquired, transient condition of generalized risk. N Engl J Med. 2013;368(2):100-2.
3.- Almagro P, Soriano JB, Cabrera FJ, et al. Short- and medium-term prognosis in patients hospitalized for COPD exacerbation: the CODEX index. Chest. 2014;145:972-80.
4.- Ponikowski P, Voors AA, Anker SD, et al.2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur J Heart Fail. 2016 ;18:891-975.
5.-Roversi S, Fabbri LM, Sin DD, Hawkins NM, Agustí A. Chronic obstructive pulmonary disease and cardiac diseases. An urgent need for integrated care. Am J Respir Crit Care Med. 2016;194:1319-1336.
We read the article by Hodgson LE, et al with interest. The authors examined the performance of National Early Warning Score (NEWS) for patients with an acute exacerbation of COPD. A limitation to this study was that the electronic scores (ward-based) were used as first NEWS - as the (paper) observations within the emergency department (ED) could not be included. We have reviewed data from our Hospital Trust of patients admitted with exacerbation of COPD (n=111), to determine whether NEWS scores from the ED department (paper records) differed from the first observation recorded on subsequent transfer to the acute medical wards (Electronic Patient Records). Admissions direct to ICU or HDU were excluded. Wilcoxon rank test was used to compare NEWS scores from ED to ward. Results are median (IQR).
NEWS in ED fell from 6 (4-8) to 4 (3-6) on the acute medical ward (P<0.0001) over a mean time interval of 377 (sd 182) mins. The change in NEWS was due to a reduction in scores for respiratory rate and heart rate. Improvement in score for oxygen saturations was offset by scoring for use of oxygen.
Not including the NEWS at presentation could underestimate risk of mortality, and hence contribute to the reduced sensitivity of NEWS that was observed in patients with COPD. Alternatively, utilising the NEWS at presentation to ED may lead to lower specificity in a patient with rapidly improving physiology.
Harmonisation of data collection between ED and the hospital...
We read the article by Hodgson LE, et al with interest. The authors examined the performance of National Early Warning Score (NEWS) for patients with an acute exacerbation of COPD. A limitation to this study was that the electronic scores (ward-based) were used as first NEWS - as the (paper) observations within the emergency department (ED) could not be included. We have reviewed data from our Hospital Trust of patients admitted with exacerbation of COPD (n=111), to determine whether NEWS scores from the ED department (paper records) differed from the first observation recorded on subsequent transfer to the acute medical wards (Electronic Patient Records). Admissions direct to ICU or HDU were excluded. Wilcoxon rank test was used to compare NEWS scores from ED to ward. Results are median (IQR).
NEWS in ED fell from 6 (4-8) to 4 (3-6) on the acute medical ward (P<0.0001) over a mean time interval of 377 (sd 182) mins. The change in NEWS was due to a reduction in scores for respiratory rate and heart rate. Improvement in score for oxygen saturations was offset by scoring for use of oxygen.
Not including the NEWS at presentation could underestimate risk of mortality, and hence contribute to the reduced sensitivity of NEWS that was observed in patients with COPD. Alternatively, utilising the NEWS at presentation to ED may lead to lower specificity in a patient with rapidly improving physiology.
Harmonisation of data collection between ED and the hospital ward is needed so that these questions may be addressed.
We thank Cardwell et al for their thoughtful comments on our paper.[1] The two alternative scoring systems did not demonstrate improved discrimination or calibration in our large dataset of AECOPD admissions. The authors suggest employing the Salford-NEWS only in patients ‘at risk’ of hypercapnic respiratory failure however, this introduces a subjective element that may negate the benefits of an objective physiological scoring system. As we emphasised in what we believe was a balanced discussion, patients with COPD should be managed in the right place by specialists and on-going education is crucial to avoid potential harms associated with misinterpretation of the NEWS alluded to by Cardwell and colleagues. Our article adds evidence that suggested RCP thresholds would indeed lead to unnecessary callouts in such patients. However, as we proposed, rather than abandon a scoring system that provides the significant advantages of standardisation and familiarity, it is possible to individualise patient management. For example, lowering observation frequency in a patient who is clinically ‘stable’, not increasing oxygen delivery if the prescribed target saturation is achieved, or taking into account prior/baseline physiology when deciding observation frequency and whether a senior review is required. Indeed a senior review may be appropriate to interpret whether the patient is at risk of hypercapnic respiratory failure and be able to advise on appropriate targets and level of mon...
We thank Cardwell et al for their thoughtful comments on our paper.[1] The two alternative scoring systems did not demonstrate improved discrimination or calibration in our large dataset of AECOPD admissions. The authors suggest employing the Salford-NEWS only in patients ‘at risk’ of hypercapnic respiratory failure however, this introduces a subjective element that may negate the benefits of an objective physiological scoring system. As we emphasised in what we believe was a balanced discussion, patients with COPD should be managed in the right place by specialists and on-going education is crucial to avoid potential harms associated with misinterpretation of the NEWS alluded to by Cardwell and colleagues. Our article adds evidence that suggested RCP thresholds would indeed lead to unnecessary callouts in such patients. However, as we proposed, rather than abandon a scoring system that provides the significant advantages of standardisation and familiarity, it is possible to individualise patient management. For example, lowering observation frequency in a patient who is clinically ‘stable’, not increasing oxygen delivery if the prescribed target saturation is achieved, or taking into account prior/baseline physiology when deciding observation frequency and whether a senior review is required. Indeed a senior review may be appropriate to interpret whether the patient is at risk of hypercapnic respiratory failure and be able to advise on appropriate targets and level of monitoring for the individual with subsequent avoidance of alarm fatigue.
1. Hodgson LE, Dimitrov BD, Congleton J, Venn R, Forni LG, Roderick PJ. A validation of the National Early Warning Score to predict outcome in patients with COPD exacerbation. Thorax 2017;72(1):23-30 doi: 10.1136/thoraxjnl-2016-208436.
2. Prytherch DR, Smith GB, Schmidt PE, Featherstone PI. ViEWS--Towards a national early warning score for detecting adult inpatient deterioration. Resuscitation 2010;81(8):932-7 doi: 10.1016/j.resuscitation.2010.04.014.
Dear Editors,
We are writing to comment on the work entitled “Alveolar macrophage-derived microvesicles mediate acute lung injury” published by Dr. Soni et al on Thorax 2016; 71:1020-1029[1].
Our group focuses on lung extracellular vesicle (EV) research and also studied the inhaled LPS-induced EVs in mouse models. Based on our experience, we raise the following comments to the work done by Dr. Soni et al and wish to draw attentions to future EV researchers. EV research is a novel field and carries a promising potential for the development of diagnostic and therapeutic agents. However, given the early stage of EV research, particular in the field of lung injury, the consistency of results relies largely on the precise techniques used in the isolation and characterization of these vesicles.
Briefly, EV is currently classified into three major categories per the definition of Society of extracellular vesicle research [2]. Apoptotic bodies (ABs) are the largest sizes of EVs usually larger than 1 µm and often resulted from cell death. Microvesicles (MVs) are the middle sized EVs (200 nm-1 µm) and are generated via plasma membrane budding. Exosomes (Exos) are the smallest EVs (less than 200 nm) and often generated from IVB-ER-Golgi system. Due to the different mechanisms of generation, MVs and Exos usually favor different compositions and subsequently may carry differential downstream biological functions[3 4]. For example, Exos have been reported to carry t...
Dear Editors,
We are writing to comment on the work entitled “Alveolar macrophage-derived microvesicles mediate acute lung injury” published by Dr. Soni et al on Thorax 2016; 71:1020-1029[1].
Our group focuses on lung extracellular vesicle (EV) research and also studied the inhaled LPS-induced EVs in mouse models. Based on our experience, we raise the following comments to the work done by Dr. Soni et al and wish to draw attentions to future EV researchers. EV research is a novel field and carries a promising potential for the development of diagnostic and therapeutic agents. However, given the early stage of EV research, particular in the field of lung injury, the consistency of results relies largely on the precise techniques used in the isolation and characterization of these vesicles.
Briefly, EV is currently classified into three major categories per the definition of Society of extracellular vesicle research [2]. Apoptotic bodies (ABs) are the largest sizes of EVs usually larger than 1 µm and often resulted from cell death. Microvesicles (MVs) are the middle sized EVs (200 nm-1 µm) and are generated via plasma membrane budding. Exosomes (Exos) are the smallest EVs (less than 200 nm) and often generated from IVB-ER-Golgi system. Due to the different mechanisms of generation, MVs and Exos usually favor different compositions and subsequently may carry differential downstream biological functions[3 4]. For example, Exos have been reported to carry the very minimal amount of popular microRNAs (miRNAs). Even for those most promising miRNA markers, less than 1 copy of miRNA can be found in each Exo[5]. This is part of the reason why the classification of EVs may be important.
In the work presented by Dr. Soni et al, a very large dose of LPS (20 μg per mouse) has been delivered to mice via intratracheal instillation. Certainly, different batch of LPS may carry different levels of potency. However, we found that the larger dose of LPS often quickly resulted in the release of ABs but rather than MVs by alveolar macrophages. In our experiences, as little as 1 μg LPS (Sigma-Aldrich, cat #L2630, St. Louis, MO, USA) resulted in the robust amount of MVs (about 50% in total EVs). However, a fair amount of Exos (about 25% in total EVs) is still mixed in the LPS-induced EVs. Additionally, the FACS analysis presented in figure 3 shows only one population of vesicles. This could be due to the overly too large dose of LPS and the detected EVs fall mainly on the range of ABs. In our experience, using a smaller dose of LPS, we often clearly observe two different population of EVs, one belongs to the larger size of ABs, and the other belongs to the smaller MVs.
We recognize that the variability of results could result from different technique, detecting apparatus, different batch of LPS and also different size/age/strain of mice. However, we would like to discuss our findings on this emerging novel topic and our comments may be found interesting and useful by other audience.
Thank you for your time and attention!
REFERENCES
1. Soni S, Wilson MR, O'Dea KP, et al. Alveolar macrophage-derived microvesicles mediate acute lung injury. Thorax 2016;71(11):1020-29. doi: 10.1136/thoraxjnl-2015-208032
2. Gyorgy B, Szabo TG, Pasztoi M, et al. Membrane vesicles, current state-of-the-art: emerging role of extracellular vesicles. Cell Mol Life Sci 2011;68(16):2667-88. doi: 10.1007/s00018-011-0689-3
3. Yanez-Mo M, Siljander PRM, Andreu Z, et al. Biological properties of extracellular vesicles and their physiological functions. J Extracell Vesicles 2015;4 doi: ARTN 27066
10.3402/jev.v4.27066
4. Raposo G, Stoorvogel W. Extracellular vesicles: Exosomes, microvesicles, and friends. J Cell Biol 2013;200(4):373-83. doi: 10.1083/jcb.201211138
5. Alexander M, Hu RZ, Runtsch MC, et al. Exosome-delivered microRNAs modulate the inflammatory response to endotoxin. Nat Commun 2015;6 doi: ARTN 7321
10.1038/ncomms8321
I enjoyed reading Hodgson et al’s validation study on Early Warning Scores (EWS) in patients admitted with an exacerbation of COPD. The current problem with EWS such as the National Early Warning Score (NEWS) in such patients is that the score is used in two contexts.
The first is in the initial triage of patients on arrival to hospital based on their early risk of death. NEWS is well validated in this context, and I wholeheartedly agree that NEWS is the best tool for this at present; patients at risk of type 2 respiratory failure, with target oxygen saturations of 88-92%, are at a high risk of death in hospital and identifying these patients early to enable senior review is entirely appropriate.
The problem comes with second use of NEWS – as a “track and trigger” tool used to monitor patients during their inpatient stay, with a rising score indicating deterioration, risk of death and the need for intervention. Hodgson et al have confirmed our finding that NEWS lacks specificity for patients with COPD. These patients will often have persistently high NEWS even when stable, well into their admission, and the actions this is supposed to trigger (hourly observations, senior review, etc.) are no longer appropriate. This leads to alarm fatigue, with high scores being ignored, increasing the risk of a true deterioration not being acted upon.
The proposals of Hodgson et al that such patients should have individually assigned observation frequencie...
I enjoyed reading Hodgson et al’s validation study on Early Warning Scores (EWS) in patients admitted with an exacerbation of COPD. The current problem with EWS such as the National Early Warning Score (NEWS) in such patients is that the score is used in two contexts.
The first is in the initial triage of patients on arrival to hospital based on their early risk of death. NEWS is well validated in this context, and I wholeheartedly agree that NEWS is the best tool for this at present; patients at risk of type 2 respiratory failure, with target oxygen saturations of 88-92%, are at a high risk of death in hospital and identifying these patients early to enable senior review is entirely appropriate.
The problem comes with second use of NEWS – as a “track and trigger” tool used to monitor patients during their inpatient stay, with a rising score indicating deterioration, risk of death and the need for intervention. Hodgson et al have confirmed our finding that NEWS lacks specificity for patients with COPD. These patients will often have persistently high NEWS even when stable, well into their admission, and the actions this is supposed to trigger (hourly observations, senior review, etc.) are no longer appropriate. This leads to alarm fatigue, with high scores being ignored, increasing the risk of a true deterioration not being acted upon.
The proposals of Hodgson et al that such patients should have individually assigned observation frequencies undermines the attraction of using EWS: consistency. If each patient has an individualised plan, often dependent on which individual healthcare professional has seen them, the consistency of response is lost. An on-call team member told of a score that has been individually put together cannot know what the urgency of response required is compared to a standardised score. Whilst there will be extreme cases where individualised plans are required, the population of patients with target oxygen saturations of 88-92%, make up a large enough proportion of the inpatient population to justify a standardised alternative score to suit their needs during the middle and latter portions of their admission. I would propose that NEWS is used at the “front door” for all patients to enable early senior review for these patients, but that once a senior clinical decision maker has prescribed target oxygen saturations of 88-92%, a standardised score for patients at risk of type 2 respiratory failure is a better method of monitoring these patients subsequently.
We read the paper of Hodgson and colleagues with interest.1 Unfortunately, we note that the Salford-NEWS system (observation chart based on target Oxygen saturation prescription) has been applied in this study to all patients with a diagnosis of acute exacerbation of COPD (AECOPD) whereas we proposed applying this system for all patients at risk of type 2 (hypercapnic) respiratory failure, a group which includes many but not all patients with AECOPD and a number of patients with other conditions.2 Around 86% of those prescribed the lower range of Oxygen saturation (88-92%) in Salford are COPD patients judged to be at risk of hypercapnia, the remainder have conditions such as morbid obesity, neuro-muscular disorders, or complex lung diseases.3 Given this key difference in rationale we suggest that the Salford-NEWS system has been inappropriately applied in this study; hence, the conclusions have to be interpreted with extreme caution.
When comparing NEWS with Salford-NEWS, it is clear that none of the systems had acceptable sensitivity at score thresholds of 5 and 7, and the most consistently reliable result from using either of them is the negative predictive value, which was similar. It was also evident that Salford-NEWS had better specificity at 91% and 95% compared to 57% and 80% for NEWS at score thresholds of 5 and 7 respectively. Since the increased sensitivity in NEWS is achieved at the expense of high “callout” rates, and low positive predictive value (8%...
We read the paper of Hodgson and colleagues with interest.1 Unfortunately, we note that the Salford-NEWS system (observation chart based on target Oxygen saturation prescription) has been applied in this study to all patients with a diagnosis of acute exacerbation of COPD (AECOPD) whereas we proposed applying this system for all patients at risk of type 2 (hypercapnic) respiratory failure, a group which includes many but not all patients with AECOPD and a number of patients with other conditions.2 Around 86% of those prescribed the lower range of Oxygen saturation (88-92%) in Salford are COPD patients judged to be at risk of hypercapnia, the remainder have conditions such as morbid obesity, neuro-muscular disorders, or complex lung diseases.3 Given this key difference in rationale we suggest that the Salford-NEWS system has been inappropriately applied in this study; hence, the conclusions have to be interpreted with extreme caution.
When comparing NEWS with Salford-NEWS, it is clear that none of the systems had acceptable sensitivity at score thresholds of 5 and 7, and the most consistently reliable result from using either of them is the negative predictive value, which was similar. It was also evident that Salford-NEWS had better specificity at 91% and 95% compared to 57% and 80% for NEWS at score thresholds of 5 and 7 respectively. Since the increased sensitivity in NEWS is achieved at the expense of high “callout” rates, and low positive predictive value (8%), clinicians would need to adjust the scoring parameters for almost half of patients with AECOPD to avoid repeated un-necessary “callouts”. Since there is no evidence-based system for making such adjustments, it may be worth considering the extension of the Salford-NEWS system to most patients with AECOPD as an interim solution.
This study does, however, demonstrate that the Salford-NEWS system, when applied blindly to all admitted patients with AECOPD (at risk of hypercapnia or not); at a score threshold of >5, generated fewer “alarms” requiring clinical callouts compared with the NEWS system, (the percent reduction is not revealed in the paper) but at the same time maintaining comparable positive and negative predicted values. Our previously published data, reported a “callout” rate of 56% for patients deemed to be at risk of hypercapnia when NEWS was used compared with 18% using the Salford-NEWS system.3 Such high “callout” rate would very quickly lead to “alarm fatigue”, as described by the authors, particularly at a time when hospital rotas are extremely pressurised. We note that similar concerns over NEWS and its tendency to trigger an increased volume of alerts in patients with AECOPD were raised by the authors in 2013. 4
Therefore, we would be concerned over the clinical appropriateness of keeping the NEWS score unadjusted for COPD patients, as suggested by Hodgson and colleagues, when the callout rate is as high as 44% with no evidence of improved outcomes in this cohort, particularly on reducing mortality through better and earlier identification of clinical deterioration leading to step-up in care; which can only be tested in a prospectively designed study. That said, the effort made by the investigators to extract evidence on such an important subject using retrospective data has to be applauded.
Furthermore, as it is known that the risk of death in AECOPD may be at least doubled if too much oxygen is given, 5, 6 we would argue strongly that bedside observation systems should help clinicians to identify patients with iatrogenic hyperoxaemia as well as identifying hypoxaemia. In addition to mortality benefit, evidence on COPD admission bundles demonstrates that when oxygen target ranges are assessed and documented correctly within 1 hour of admission, the mean length of stay is significantly reduced (LOS <5 days; OR 1.84(1.38-2.46)).6 Thus, in promoting more accurate assessments of oxygen target ranges, Salford-NEWS can be viewed as a better care-lower cost model of quality improvement.
The NEWS and CREWS systems do not flag hyperoxaemia although there are increasing safety concerns about this, not just in hypercapnic patients but also in a variety of medical conditions including myocardial infarction where Nehme et al. have reported an increase in infarct size of 17-21% associated with the unnecessary use of supplemental oxygen.7 Apart from patients at risk of hypercapnia, the Salford-NEWS system allocates one point for iatrogenic hyperoxaemia (target saturation is 94-98%, but patient is on Oxygen with measured saturation >98%) prompting nursing staff to titrate down un-necessary Oxygen. Bedside charts should not just predict risk of death but should also guide and facilitate best practice including the avoidance of hyperoxaemia, especially in oxygen sensitive patients.
References
1. Hodgson LE, Dimitrov BD, Congleton j et al . A validation of the National Early Warning Score to predict outcomes in patients with COPD exacerbation. Thorax 2016 In press
2. O’Driscoll BR, Bakerly ND, Murphy P et al. Concerns regarding the design of the bedside monitoring chart for use with the NEWS (National Early Warning System). Clinical Medicine 2013: 13:319-320
3. O’Driscoll BR, Grant K, Green D et al. Clinical and scientific letters: The national early warning score gives misleading scores for oxygen saturation in patients at risk of hypercapnia. Clinical Medicine 2014;14:695–696
4. Hodgson L, Bax S, Montefort M et al. The National Early Warning Score (NEWS) and iatrogenic harm – Could the NEWS for COPD patients be improved. Thorax. 2013;68:A37
5. Austin MA, Wills KE, Blizzard L, et al Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial. BMJ. 2010 Oct 18;341:c5462
6. Turner AM, Lim WS, Rodrigo C, et al. A care-bundles approach to improving standard of care in AECOPD admissions: results of a national project. Thorax. 2015 Oct;70(10):992-4.
7. Nehme Z, Stub D, Bernard S, et al. AVOID Investigators. Effect of supplemental oxygen exposure on myocardial injury in ST-elevation myocardial infarction. Heart. 2016 ;102:444-51
Dear Editor, We thank Dr Mansell for her comments regarding our
recently published trial. [1] We agree that there are different phenotypic
variations within the obesity hypoventilation syndrome (OHS), although it
remains to be determined whether OHS with co-existent obstructive sleep
apnoea (OSA) responds differently to treatment in comparison to OHS
without OSA. [2] Acknowledging that the presence and severity of OSA in...
Dear Editor, We thank Dr Mansell for her comments regarding our
recently published trial. [1] We agree that there are different phenotypic
variations within the obesity hypoventilation syndrome (OHS), although it
remains to be determined whether OHS with co-existent obstructive sleep
apnoea (OSA) responds differently to treatment in comparison to OHS
without OSA. [2] Acknowledging that the presence and severity of OSA in
OHS may impact on the response to CPAP or non-invasive ventilation (NIV),
clinical definitions and clinical trials in OHS have defined OHS as
obesity (BMI > 30 kg/m2) with chronic hypercapnia, irrespective of the
degree of co-existent OSA. [3] The degree of OSA in our study is in
keeping with the severity of OSA in previous clinical trial of OHS, [4,
5], although the degree of obesity, severity of baseline hypercapnia and
degree of pulmonary function impairment was substantially greater. All
three randomised controlled trials have found similar outcomes for CPAP
and NIV, and so do not support the routine use of NIV for all patients
with OHS. The predominant phenotype appears to be OHS in conjunction with
severe OSA, which comprised more than 70% of participants in the recent
manuscript from the Spanish Sleep Network. [6] In this subgroup they found
NIV provided greater improvement in respiratory failure and symptoms than
life style measure in OHS without OSA, however further results are awaited
to determine whether CPAP and NIV have different impacts in this subgroup.
We chose clinically significant outcomes and predictors of increased
mortality (hospital admission, persisting respiratory failure, non-
adherence and quality of life) as outcome measures rather than
polysomnographic variables. We did, however, use polysomnography to
titrate CPAP and NIV at the commencement of the project in order to
eliminate respiratory events and minimise persisting hypoxaemia and
hypoventilation. In terms of demonstrating laboratory effectiveness of
therapy, none of the participants required the addition of nocturnal
oxygen for persisting hypoxaemia on treatment, in contrast to other
trials, although we did not measure the apnoea hypopnoea index on the
final study settings. [5] We agree that assessment of long term outcomes,
including mortality is important and 12 month outcome data from this
cohort will be available shortly.
Some of the participants in our trial had treatment prior to trial
randomisation. The trial recruited OHS participants during acute hospital
admissions with respiratory failure as well as from ambulatory settings
that were the focus of previous trials. The design allowed for initial
treatment with NIV for correction of acute respiratory acidosis prior to
randomisation to CPAP or NIV. We acknowledge that this may have
influenced baseline measures, however it was not considered ethical to
withhold treatment in acutely unwell patients and there was no difference
in prior treatment use between the groups. Given the results from the
three published randomised controlled trials that have found similar
outcomes for CPAP and NIV in OHS, and in line with recent editorial
opinion, we believe that it is reasonable to use CPAP for treatment of OHS
following initial stabilisation of acute respiratory acidosis, with
careful observation of the response. [7], Further evidence may influence
optimal therapy in different OHS subgroups.
1.Howard ME, Piper AJ, Stevens B, et al. A randomised controlled trial of
CPAP versus non-invasive ventilation for initial treatment of obesity
hypoventilation syndrome. Thorax. 2016. Epub 2016/11/18.
2.Ojeda Castillejo
E, de Lucas Ramos P, Lopez Martin S, et al. Noninvasive mechanical ventilation in patients with obesity hypoventilation syndrome. Long-term outcome and prognostic factors. Arch Bronconeumol. 2015;51(2):61-8. Epub 2014/04/08.
3.Mokhlesi B, Tulaimat A. Recent Advances in Obesity
Hypoventilation Syndrome. Chest.2007;132(4):1322-36.
4.Piper AJ, Wang D, Yee BJ, et al. Randomised trial of CPAP vs bilevel support in the treatment of obesity hypoventilation syndrome without severe nocturnal
desaturation. Thorax. 2008;63(5):395-401. Epub 2008/01/22.
5.Masa JF,
Corral J, Alonso ML, et al. Efficacy of Different Treatment Alternatives
for Obesity Hypoventilation Syndrome. Pickwick Study. Am J Respir Crit
Care Med. 2015;192(1):86-95. Epub 2015/04/29.
6.Masa JF, Corral J,
Caballero C, et al. Non-invasive ventilation in obesity hypoventilation
syndrome without severe obstructive sleep apnoea. Thorax. 2016;71(10):899-
906. Epub 2016/07/14.
7.Noda JR, Masa JF, Mokhlesi B. CPAP or non-invasive
ventilation in obesity hypoventilation syndrome: does it matter which one
you start with? Thorax. 2017. Epub 2017/01/29.
Conflict of Interest:
MEH reports grants from Resmed Foundatio & non-financial support from Philips Respironics. AJP reports grants from Resmed Foundation, personal fees from ResMed, personal fees from Philips Respironics & personal fees from SenTec. DM reports grants from Resmed Foundation, National Health & Medical Research Council & Victoria Neurotrauma Initiative. BS, AEH, BJY, ED, ATB, DF, CB, LR, NS, DH and DJB report a grant from Resmed Foundation.
We read with great interest the article by Howard et al[1] and commend the authors on this excellent piece of work. However, we wish to raise several points for consideration of this work in a clinical context. Firstly, it is not clear whether the patients being treated were truly patients with obesity hypoventilation failure (OHS) or whether in fact they had hypercapnic obstructive sleep apnoea (OSA). There is in...
We read with great interest the article by Howard et al[1] and commend the authors on this excellent piece of work. However, we wish to raise several points for consideration of this work in a clinical context. Firstly, it is not clear whether the patients being treated were truly patients with obesity hypoventilation failure (OHS) or whether in fact they had hypercapnic obstructive sleep apnoea (OSA). There is increasing data to suggest the clinical entity of obesity related respiratory failure (ORRF) encompasses several different phenotypes including; hypercapnic OSA, OSA/OHS and lone OHS. The underlying pathophysiology is likely to differ between these phenotypes and will therefore respond differently to treatment[2]. Not all the participants underwent nocturnal respiratory polygraphy, and it is thus difficult to determine which clinical phenotype was being treated, especially given the wide standard deviation (for AHI mean = 82 events / hr (SD 45) and for SpO2 less than 90% mean = 67% of the sleep period (SD 31.4%). This is in keeping with data by Kawata et al[3], who also demonstrated that in patients with hypercapnic OSA, only half of patients responded to continuous positive airway pressure (CPAP) therapy. Those who failed to respond had a higher AHI and BMI, suggesting nocturnal polygraphy parameters may predict who will respond to CPAP therapy alone. More than 50% of patients had previously used either non-invasive ventilation (NIV) or CPAP therapy, it is unclear whether there was a wash out period and prior use of PAP therapy which may have affected compliance in these individuals and therefore outcomes. We note the mean CPAP was 15.2 cm H2O (SD 2.8); in our clinical experience we often find patients with OHS/OSA trialled on CPAP therapy who require higher CPAP pressures (>10cmH2O) have ongoing nocturnal events, particularly persistent hypoxia. The authors have not provided nocturnal data on PAP therapy, we are therefore unable to determine whether the CPAP group had a reduction in nocturnal events to within normal range. This is especially important given the fact that, although reduced, the PaCO2 in the CPAP group remained higher than the NIV group at three months. The authors also comment that PaCO2 at presentation was predictive of treatment failure, with an eightfold increase in risk when PaCO2 was greater than 62mmHg (8.27kPa). This is noteworthy since there is much debate about the diagnostic criteria for OHS[4-6], a cut-off level for PaCO2 to determine which patients may fail therapy would be clinically important in identifying patients who should be treated with NIV in the first instance. Lastly, only outcomes at 3 months have been presented. We wonder what the longer term outcomes for these patients would be; whether there would be an increase in the CPAP failure rate and, most importantly, a difference in mortality rates? We recognise the significance of this paper and acknowledge there may be a cohort of OHS/hypercapnic OSA patients who can be treated successfully with CPAP. However, this group is yet to be identified; much of this distinction may lie in a universal definition of OHS encompassing nocturnal and daytime parameters. We suggest that NIV is a safer treatment option until further phenotyping studies are conducted to comprehensively identify those patients requiring NIV and those for whom CPAP will be adequate.
References:
1. Howard ME, Piper AJ, Stevens B, et al. A randomised controlled trial of CPAP versus non-invasive ventilation for initial treatment of obesity hypoventilation syndrome. Thorax 2016 doi: 10.1136/thoraxjnl-2016-208559[published Online First: Epub Date]|.
2. Masa JF, Corral J, Caballero C, et al. Non-invasive ventilation in obesity hypoventilation syndrome without severe obstructive sleep apnoea. Thorax 2016:thoraxjnl-2016-208501
3. Kawata N, Tatsumi K, Terada J, et al. DAytime hypercapnia in obstructive sleep apnea syndrome*. Chest 2007;132(6):1832-38 doi: 10.1378/chest.07-0673[published Online First: Epub Date]|.
4. Manuel AR, Hart N, Stradling JR. Is a raised bicarbonate, without hypercapnia, part of the physiologic spectrum of obesity-related hypoventilation? CHEST Journal 2015;147(2):362-68
5. Murphy PB, Janssens J-P. NIV for OHS without severe OSAS: is it worth it? Thorax 2016 doi: 10.1136/thoraxjnl-2016-208986[published Online First: Epub Date]|.
6. Hart N, Mandal S, Manuel A, et al. Obesity hypoventilation syndrome: does the current definition need revisiting? Thorax 2014;69(1):83-4 doi: 10.1136/thoraxjnl-2013-204298[published Online First: Epub Date]|.
We thank Professors Lipworth and Anderson for their very thoughtful
comments in their response to our piece1, and for pointing out clear
strategies for treating obesity-associated asthma without expensive
therapies, e.g., with improved delivery of inhaled corticosteroids and/or
weight reduction.
It should be noted however, that the focus of the piece was on
mechanisms by which obesity might cause asthma,...
We thank Professors Lipworth and Anderson for their very thoughtful
comments in their response to our piece1, and for pointing out clear
strategies for treating obesity-associated asthma without expensive
therapies, e.g., with improved delivery of inhaled corticosteroids and/or
weight reduction.
It should be noted however, that the focus of the piece was on
mechanisms by which obesity might cause asthma, with the idea that a
greater understanding of disease mechanisms causing obesity-associated
asthma might lead to improved therapies, and possibly to even cost
effective ones. From a pathogenesis point of view, even pilot studies
showing the efficacy of any therapy might be extremely valuable in
identifying specific molecular mechanisms of disease. In that regard, the
impetus of the article was that obesity-associated asthma represents a
significant and growing unmet medical need, characterized by increased
healthcare utilization and reduced quality of life, and refractory to even
oral corticosteroid treatment and other current therapies. These current
therapies include inhaled corticosteroids and weight reduction programs,
although improved delivery or compliance with these measures, as suggested
by Professors Lipworth and Anderson, could improve the clinical result.
It is also worth mentioning that studies of obesity-associated
asthma, as mentioned in the piece1, indicate that there are at least two
forms of the disease, an early onset form and a late onset form, one of
which is much more responsive to weight reduction (late onset form) than
the other. We would therefore advocate further study of disease
mechanisms causing asthma in obese individuals, including subpopulations
thereof, along with improved implementation of current inexpensive
treatments, that might lead to an improved understanding and possibly to
new therapies for this very significant, growing and costly public heath
problem.
1. Umetsu, D.T. Mechanisms by which obesity impacts asthma. Thorax
(2016).
I read with interest the article published by Arbillaga-Etxarri et al.[1] titled “Socioenvironmental correlates of physical activity in patients with chronic obstructive pulmonary disease (COPD)”. In the introduction section, the authors stated that the current interventions (e.g., pharmacological treatment, rehabilitation, self-management) aiming to change physical activity behavior in COPD patients lack effectiveness, particularly in the long-term. The authors argue that this absence of effectiveness could be due to a lack of knowledge of physical activity determinants in this population. To address this issue, Arbillaga-Etxarri et al.[1] examined the socio-ecological determinants of active behaviours in 400 COPD patients and found that, after controlling potential confounders, having a dog and grandparenting were positively associated with physical activity; effects sizes were small, β = .19 and very small β = .08 for dog walking and grandparenting, respectively. The authors concluded that these two socio-environmental characteristics should be considered to promote physical activity both at the clinical level and in future research. This study is important because there is a lack of knowledge regarding the determinants of physical activity in this population.[2]
Nonetheless, there are some reservations regarding the clinical utility of physical activity socio-environmental correlates to design physical activity programs. Socioenvironmental correlates of physica...
Show MoreWe commend Dr. Echevarria et al. for their excellent article, published in Thorax online (February 2017), concerning a new index (PEARL score) to predict the 90-day risk of death or readmission after hospitalization for an acute exacerbation of COPD (AECOPD). I agree with the authors on the relevance of 3 months’ prognosis after a hospitalization for AECOPD. Although policymakers usually consider 30-day readmissions as the marker of quality of care, only 36% of readmissions in COPD patients in this period are for a relapse, incomplete recovery, or a new COPD exacerbation. (1) The rest of readmissions in COPD patients are related with the deleterious complications associated with any hospitalization (post-hospital syndrome), especially in an aged population, with frequent comorbidities and often physical frailty. (2) In this sense, a 90-day time frame can probably better capture not only hospital and ambulatory quality of care, but also risk variables associated with readmissions in COPD patients. However, we believe that the article deserves some reflection.
Show MoreFirst, the authors stated that no tool has previously been developed in COPD to predict short-term readmission or death. This is only partially true. As they themselves note later, the CODEX index was specifically developed and validated to evaluate the risk of mortality, readmission, and their combination in the short- (3 months) or medium-term (1-year) after hospital discharge for AECOPD. (3)
Second, the...
We read the article by Hodgson LE, et al with interest. The authors examined the performance of National Early Warning Score (NEWS) for patients with an acute exacerbation of COPD. A limitation to this study was that the electronic scores (ward-based) were used as first NEWS - as the (paper) observations within the emergency department (ED) could not be included. We have reviewed data from our Hospital Trust of patients admitted with exacerbation of COPD (n=111), to determine whether NEWS scores from the ED department (paper records) differed from the first observation recorded on subsequent transfer to the acute medical wards (Electronic Patient Records). Admissions direct to ICU or HDU were excluded. Wilcoxon rank test was used to compare NEWS scores from ED to ward. Results are median (IQR).
Show MoreNEWS in ED fell from 6 (4-8) to 4 (3-6) on the acute medical ward (P<0.0001) over a mean time interval of 377 (sd 182) mins. The change in NEWS was due to a reduction in scores for respiratory rate and heart rate. Improvement in score for oxygen saturations was offset by scoring for use of oxygen.
Not including the NEWS at presentation could underestimate risk of mortality, and hence contribute to the reduced sensitivity of NEWS that was observed in patients with COPD. Alternatively, utilising the NEWS at presentation to ED may lead to lower specificity in a patient with rapidly improving physiology.
Harmonisation of data collection between ED and the hospital...
We thank Cardwell et al for their thoughtful comments on our paper.[1] The two alternative scoring systems did not demonstrate improved discrimination or calibration in our large dataset of AECOPD admissions. The authors suggest employing the Salford-NEWS only in patients ‘at risk’ of hypercapnic respiratory failure however, this introduces a subjective element that may negate the benefits of an objective physiological scoring system. As we emphasised in what we believe was a balanced discussion, patients with COPD should be managed in the right place by specialists and on-going education is crucial to avoid potential harms associated with misinterpretation of the NEWS alluded to by Cardwell and colleagues. Our article adds evidence that suggested RCP thresholds would indeed lead to unnecessary callouts in such patients. However, as we proposed, rather than abandon a scoring system that provides the significant advantages of standardisation and familiarity, it is possible to individualise patient management. For example, lowering observation frequency in a patient who is clinically ‘stable’, not increasing oxygen delivery if the prescribed target saturation is achieved, or taking into account prior/baseline physiology when deciding observation frequency and whether a senior review is required. Indeed a senior review may be appropriate to interpret whether the patient is at risk of hypercapnic respiratory failure and be able to advise on appropriate targets and level of mon...
Show MoreDear Editors,
We are writing to comment on the work entitled “Alveolar macrophage-derived microvesicles mediate acute lung injury” published by Dr. Soni et al on Thorax 2016; 71:1020-1029[1].
Our group focuses on lung extracellular vesicle (EV) research and also studied the inhaled LPS-induced EVs in mouse models. Based on our experience, we raise the following comments to the work done by Dr. Soni et al and wish to draw attentions to future EV researchers. EV research is a novel field and carries a promising potential for the development of diagnostic and therapeutic agents. However, given the early stage of EV research, particular in the field of lung injury, the consistency of results relies largely on the precise techniques used in the isolation and characterization of these vesicles.
Briefly, EV is currently classified into three major categories per the definition of Society of extracellular vesicle research [2]. Apoptotic bodies (ABs) are the largest sizes of EVs usually larger than 1 µm and often resulted from cell death. Microvesicles (MVs) are the middle sized EVs (200 nm-1 µm) and are generated via plasma membrane budding. Exosomes (Exos) are the smallest EVs (less than 200 nm) and often generated from IVB-ER-Golgi system. Due to the different mechanisms of generation, MVs and Exos usually favor different compositions and subsequently may carry differential downstream biological functions[3 4]. For example, Exos have been reported to carry t...
Show MoreI enjoyed reading Hodgson et al’s validation study on Early Warning Scores (EWS) in patients admitted with an exacerbation of COPD. The current problem with EWS such as the National Early Warning Score (NEWS) in such patients is that the score is used in two contexts.
The first is in the initial triage of patients on arrival to hospital based on their early risk of death. NEWS is well validated in this context, and I wholeheartedly agree that NEWS is the best tool for this at present; patients at risk of type 2 respiratory failure, with target oxygen saturations of 88-92%, are at a high risk of death in hospital and identifying these patients early to enable senior review is entirely appropriate.
The problem comes with second use of NEWS – as a “track and trigger” tool used to monitor patients during their inpatient stay, with a rising score indicating deterioration, risk of death and the need for intervention. Hodgson et al have confirmed our finding that NEWS lacks specificity for patients with COPD. These patients will often have persistently high NEWS even when stable, well into their admission, and the actions this is supposed to trigger (hourly observations, senior review, etc.) are no longer appropriate. This leads to alarm fatigue, with high scores being ignored, increasing the risk of a true deterioration not being acted upon.
The proposals of Hodgson et al that such patients should have individually assigned observation frequencie...
Show MoreWe read the paper of Hodgson and colleagues with interest.1 Unfortunately, we note that the Salford-NEWS system (observation chart based on target Oxygen saturation prescription) has been applied in this study to all patients with a diagnosis of acute exacerbation of COPD (AECOPD) whereas we proposed applying this system for all patients at risk of type 2 (hypercapnic) respiratory failure, a group which includes many but not all patients with AECOPD and a number of patients with other conditions.2 Around 86% of those prescribed the lower range of Oxygen saturation (88-92%) in Salford are COPD patients judged to be at risk of hypercapnia, the remainder have conditions such as morbid obesity, neuro-muscular disorders, or complex lung diseases.3 Given this key difference in rationale we suggest that the Salford-NEWS system has been inappropriately applied in this study; hence, the conclusions have to be interpreted with extreme caution.
When comparing NEWS with Salford-NEWS, it is clear that none of the systems had acceptable sensitivity at score thresholds of 5 and 7, and the most consistently reliable result from using either of them is the negative predictive value, which was similar. It was also evident that Salford-NEWS had better specificity at 91% and 95% compared to 57% and 80% for NEWS at score thresholds of 5 and 7 respectively. Since the increased sensitivity in NEWS is achieved at the expense of high “callout” rates, and low positive predictive value (8%...
Show MoreDear Editor, We thank Dr Mansell for her comments regarding our recently published trial. [1] We agree that there are different phenotypic variations within the obesity hypoventilation syndrome (OHS), although it remains to be determined whether OHS with co-existent obstructive sleep apnoea (OSA) responds differently to treatment in comparison to OHS without OSA. [2] Acknowledging that the presence and severity of OSA in...
We read with great interest the article by Howard et al[1] and commend the authors on this excellent piece of work. However, we wish to raise several points for consideration of this work in a clinical context. Firstly, it is not clear whether the patients being treated were truly patients with obesity hypoventilation failure (OHS) or whether in fact they had hypercapnic obstructive sleep apnoea (OSA). There is in...
We thank Professors Lipworth and Anderson for their very thoughtful comments in their response to our piece1, and for pointing out clear strategies for treating obesity-associated asthma without expensive therapies, e.g., with improved delivery of inhaled corticosteroids and/or weight reduction.
It should be noted however, that the focus of the piece was on mechanisms by which obesity might cause asthma,...
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