News From CHEST Physician®

Ongoing hospital mergers, acquisitions, and closings demonstrate that reimbursement maximization and cost reduction are the twin sisters of health-care system reform. This focus is not going to change in the foreseeable future, as most experts now view “health system reform” as “health financing reform.”

Reports document that more than 50% of acute care hospitals in the United States experienced negative operating margins for the federal fiscal year ending September 30, 2017. Equally alarming is the increasing number of organizations either reducing or eliminating the roles of medical directors for clinical departments. Hospital and health system executives are increasingly engaging external consultants to find ways to decrease operating costs, with the caveat of maintaining or improving quality, safety, and patient satisfaction and engagement.

Given these cost reduction pressures, what can respiratory therapy medical directors and administrative directors do to ensure that quality and safety are ensured?

We believe that quality and safety can be maintained and improved in this bottom-line-focused environment if we collaborate with stakeholders and communicate the value of respiratory care services. Following are some examples of how to reinvigorate this collaboration. The list is far from complete, but we believe it is a good starting point for making a significant difference.
 

Science

We recognize that much of our practice is based on levels of evidence, and we must use this evidence as a basis for our services.

In talking and working with RT administrative directors across the country, we continue to see non-value-added “treatments” being provided, such as incentive spirometry and aerosolized acetylcysteine. Not only is this a waste of resources, but, because of it, our clinical RTs are not providing therapy.

One of the best opportunities to decrease cost is to eliminate waste. These services must be eliminated. For those patients who require secretion clearance/lung expansion, we can provide evidence-based services such as oscillating positive expiratory pressure.
 

Protocols

Respiratory care protocols have been around for decades, but surveys indicate that only half of all RT departments utilize them. Under the guidance of NAMDRC, the AARC has been educating RTs to transition from “treatments” to evidence-based protocols. Various barriers remain, and our challenge remains to implement proven care plans in every department.

Quality Assurance

The health-care industry made the transition from “Quality Control” to “Quality Assurance” several decades ago. However, many RT administrative directors lack the knowledge and/or resources necessary to create a comprehensive QA program, much less participate in clinical research. We suggest creating a standardized model to be adopted by RT departments across the country that would measure and communicate the value of respiratory care services.

Productivity/Staffing

An area where consultants and executives often focus their cost-saving efforts is staffing. Given that 50% to 60% of operating costs are personnel, this is to be expected.

Many organizations, however, are using the wrong metrics—such as procedures, CPT codes , and billables—to project staffing FTEs. Physicians and RTs understand that these metrics are not useful and must convince consultants and executives of this. The AARC Uniform Reporting Manual, which is currently being updated, is the best guide for determining appropriate staffing.

Education

Another common step in cost control has been the significant reduction or total elimination of education budgets.

During the past 5 years, RT leaders attending the AARC Summer Forum have been polled regarding whether they received financial assistance to attend the Management Section program. Sadly, the number attending on their own dime far surpasses those receiving financial assistance.

Additionally, the RT profession is witnessing more department-based education, which, in some cases, is not education at all, but marketing, cleverly packaged in the form of CEUs.

We fully understand these changes and recognize why they have occurred. However, we suggest the need to work together to differentiate marketing from education and ensure that clinical staff receive what is needed to ensure quality care.

It is vital for us to educate our physician leaders and pulmonary and critical care fellows on the science of respiratory care. There is a significant knowledge gap, and we have a great opportunity to improve the training of fellows. It is difficult to attract active medical directors if they don’t understand the science. We believe NAMDRC can play an important role by addressing these knowledge deficits.

Ongoing hospital mergers, acquisitions, and closings demonstrate that reimbursement maximization and cost reduction are the twin sisters of health-care system reform. This focus is not going to change in the foreseeable future, as most experts now view “health system reform” as “health financing reform.”

Reports document that more than 50% of acute care hospitals in the United States experienced negative operating margins for the federal fiscal year ending September 30, 2017. Equally alarming is the increasing number of organizations either reducing or eliminating the roles of medical directors for clinical departments. Hospital and health system executives are increasingly engaging external consultants to find ways to decrease operating costs, with the caveat of maintaining or improving quality, safety, and patient satisfaction and engagement.

Given these cost reduction pressures, what can respiratory therapy medical directors and administrative directors do to ensure that quality and safety are ensured?

We believe that quality and safety can be maintained and improved in this bottom-line-focused environment if we collaborate with stakeholders and communicate the value of respiratory care services. Following are some examples of how to reinvigorate this collaboration. The list is far from complete, but we believe it is a good starting point for making a significant difference.
 

Science

We recognize that much of our practice is based on levels of evidence, and we must use this evidence as a basis for our services.

In talking and working with RT administrative directors across the country, we continue to see non-value-added “treatments” being provided, such as incentive spirometry and aerosolized acetylcysteine. Not only is this a waste of resources, but, because of it, our clinical RTs are not providing therapy.

One of the best opportunities to decrease cost is to eliminate waste. These services must be eliminated. For those patients who require secretion clearance/lung expansion, we can provide evidence-based services such as oscillating positive expiratory pressure.
 

Protocols

Respiratory care protocols have been around for decades, but surveys indicate that only half of all RT departments utilize them. Under the guidance of NAMDRC, the AARC has been educating RTs to transition from “treatments” to evidence-based protocols. Various barriers remain, and our challenge remains to implement proven care plans in every department.

Quality Assurance

The health-care industry made the transition from “Quality Control” to “Quality Assurance” several decades ago. However, many RT administrative directors lack the knowledge and/or resources necessary to create a comprehensive QA program, much less participate in clinical research. We suggest creating a standardized model to be adopted by RT departments across the country that would measure and communicate the value of respiratory care services.

Productivity/Staffing

An area where consultants and executives often focus their cost-saving efforts is staffing. Given that 50% to 60% of operating costs are personnel, this is to be expected.

Many organizations, however, are using the wrong metrics—such as procedures, CPT codes , and billables—to project staffing FTEs. Physicians and RTs understand that these metrics are not useful and must convince consultants and executives of this. The AARC Uniform Reporting Manual, which is currently being updated, is the best guide for determining appropriate staffing.

Education

Another common step in cost control has been the significant reduction or total elimination of education budgets.

During the past 5 years, RT leaders attending the AARC Summer Forum have been polled regarding whether they received financial assistance to attend the Management Section program. Sadly, the number attending on their own dime far surpasses those receiving financial assistance.

Additionally, the RT profession is witnessing more department-based education, which, in some cases, is not education at all, but marketing, cleverly packaged in the form of CEUs.

We fully understand these changes and recognize why they have occurred. However, we suggest the need to work together to differentiate marketing from education and ensure that clinical staff receive what is needed to ensure quality care.

It is vital for us to educate our physician leaders and pulmonary and critical care fellows on the science of respiratory care. There is a significant knowledge gap, and we have a great opportunity to improve the training of fellows. It is difficult to attract active medical directors if they don’t understand the science. We believe NAMDRC can play an important role by addressing these knowledge deficits.

Ongoing hospital mergers, acquisitions, and closings demonstrate that reimbursement maximization and cost reduction are the twin sisters of health-care system reform. This focus is not going to change in the foreseeable future, as most experts now view “health system reform” as “health financing reform.”

Reports document that more than 50% of acute care hospitals in the United States experienced negative operating margins for the federal fiscal year ending September 30, 2017. Equally alarming is the increasing number of organizations either reducing or eliminating the roles of medical directors for clinical departments. Hospital and health system executives are increasingly engaging external consultants to find ways to decrease operating costs, with the caveat of maintaining or improving quality, safety, and patient satisfaction and engagement.

Given these cost reduction pressures, what can respiratory therapy medical directors and administrative directors do to ensure that quality and safety are ensured?

We believe that quality and safety can be maintained and improved in this bottom-line-focused environment if we collaborate with stakeholders and communicate the value of respiratory care services. Following are some examples of how to reinvigorate this collaboration. The list is far from complete, but we believe it is a good starting point for making a significant difference.
 

Science

We recognize that much of our practice is based on levels of evidence, and we must use this evidence as a basis for our services.

In talking and working with RT administrative directors across the country, we continue to see non-value-added “treatments” being provided, such as incentive spirometry and aerosolized acetylcysteine. Not only is this a waste of resources, but, because of it, our clinical RTs are not providing therapy.

One of the best opportunities to decrease cost is to eliminate waste. These services must be eliminated. For those patients who require secretion clearance/lung expansion, we can provide evidence-based services such as oscillating positive expiratory pressure.
 

Protocols

Respiratory care protocols have been around for decades, but surveys indicate that only half of all RT departments utilize them. Under the guidance of NAMDRC, the AARC has been educating RTs to transition from “treatments” to evidence-based protocols. Various barriers remain, and our challenge remains to implement proven care plans in every department.

Quality Assurance

The health-care industry made the transition from “Quality Control” to “Quality Assurance” several decades ago. However, many RT administrative directors lack the knowledge and/or resources necessary to create a comprehensive QA program, much less participate in clinical research. We suggest creating a standardized model to be adopted by RT departments across the country that would measure and communicate the value of respiratory care services.

Productivity/Staffing

An area where consultants and executives often focus their cost-saving efforts is staffing. Given that 50% to 60% of operating costs are personnel, this is to be expected.

Many organizations, however, are using the wrong metrics—such as procedures, CPT codes , and billables—to project staffing FTEs. Physicians and RTs understand that these metrics are not useful and must convince consultants and executives of this. The AARC Uniform Reporting Manual, which is currently being updated, is the best guide for determining appropriate staffing.

Education

Another common step in cost control has been the significant reduction or total elimination of education budgets.

During the past 5 years, RT leaders attending the AARC Summer Forum have been polled regarding whether they received financial assistance to attend the Management Section program. Sadly, the number attending on their own dime far surpasses those receiving financial assistance.

Additionally, the RT profession is witnessing more department-based education, which, in some cases, is not education at all, but marketing, cleverly packaged in the form of CEUs.

We fully understand these changes and recognize why they have occurred. However, we suggest the need to work together to differentiate marketing from education and ensure that clinical staff receive what is needed to ensure quality care.

It is vital for us to educate our physician leaders and pulmonary and critical care fellows on the science of respiratory care. There is a significant knowledge gap, and we have a great opportunity to improve the training of fellows. It is difficult to attract active medical directors if they don’t understand the science. We believe NAMDRC can play an important role by addressing these knowledge deficits.

The work of critical care clinicians can create a perfect storm for emotional exhaustion, depersonalization, and reduced self-efficacy – widely known as burnout. Burnout is occurring in record numbers among physicians in general – more than twice as frequently as for non-health-care workers – and intensivists top the chart. Clinicians from all specialties in medicine today experience the frustrations of workplace chaos and loss of control, displacement of meaningful work with menial work, and ever increasing documentation requirements and electronic health record challenges – all contributing to burnout. Intensivists and other ICU professionals, such as advanced practice providers and nurses, however, experience the added challenge of working in a highly stressful environment characterized by fast-paced high-stakes decision making, long and irregular hours, and end-of-life scenarios often clouded by moral distress. These and other drivers contribute to high rates of burnout.

Being burned out takes its toll on health-care workers, contributing to psychological and physical manifestations, alcohol or substance abuse, posttraumatic stress disorder, and even suicidal ideation. Additionally, burnout carries important negative consequences for the organization and directly to the patient, including higher rates of employee turnover, lower quality of work, more medical errors, and reduced patient satisfaction. Unfortunately, burnout rates continue to rise with alarming speed.

Fortunately, there is increasing attention paid to the magnitude and potential impact of burnout, compelling important organizations to highlight the problem and assist clinicians in combating burnout and its consequences. For example, the National Academy of Medicine (NAM) has convened an Action Collaborative on Clinician Well-Being and Resilience and invited more than 100 organizations to publish their statement of commitment to improve clinician well-being and reduce clinician burnout (https://nam.edu/initiatives/clinician-resilience-and-well-being/). The American Medical Association (AMA) has developed modules and tools to assist clinicians and administrators in taking important steps to prevent burnout (https://www.stepsforward.org/modules/physician-burnout).

CHEST has been an active participant in addressing burnout in ICU professionals, including in an important partnership with the American Association of Critical-Care Nurses (AACN), the American Thoracic Society (ATS), and the Society of Critical Care Medicine (SCCM) - the Critical Care Societies Collaborative (CCSC). The CCSC, whose members include greater than 150,000 critical care professionals in the United States, has established a principle goal of mitigating ICU burnout (#StopICUBurnout). One of the first CCSC efforts was to publish a white paper simultaneously in all four journals of the CCSC professional societies that provides the rationale and direction for a “call for action” to tackle ICU burnout (Moss M, Good VS, Gozal D, Kleinpell R, Sessler CN. Burnout syndrome in critical care health care professionals: A call for action. Chest. 2016;150[1]:17). Recently, the CCSC sponsored a National Summit on the Prevention and Management of Burnout in the ICU (http://ccsconline.org/optimizing-the-workforce/burnout). Fifty-five invited participants brought wide ranging expertise and substantial enthusiasm to the task of deconstructing ICU burnout and identifying knowledge gaps and future directions. Areas of focused discussion included factors influencing burnout, identifying individuals with burnout, the value of organizational and individual interventions to prevent and manage burnout, and translation of these discussions into a research agenda. CHEST and the CCSC are committed to the goals of enhancing clinician well-being and eliminating burnout in the ICU.

The work of critical care clinicians can create a perfect storm for emotional exhaustion, depersonalization, and reduced self-efficacy – widely known as burnout. Burnout is occurring in record numbers among physicians in general – more than twice as frequently as for non-health-care workers – and intensivists top the chart. Clinicians from all specialties in medicine today experience the frustrations of workplace chaos and loss of control, displacement of meaningful work with menial work, and ever increasing documentation requirements and electronic health record challenges – all contributing to burnout. Intensivists and other ICU professionals, such as advanced practice providers and nurses, however, experience the added challenge of working in a highly stressful environment characterized by fast-paced high-stakes decision making, long and irregular hours, and end-of-life scenarios often clouded by moral distress. These and other drivers contribute to high rates of burnout.

Being burned out takes its toll on health-care workers, contributing to psychological and physical manifestations, alcohol or substance abuse, posttraumatic stress disorder, and even suicidal ideation. Additionally, burnout carries important negative consequences for the organization and directly to the patient, including higher rates of employee turnover, lower quality of work, more medical errors, and reduced patient satisfaction. Unfortunately, burnout rates continue to rise with alarming speed.

Fortunately, there is increasing attention paid to the magnitude and potential impact of burnout, compelling important organizations to highlight the problem and assist clinicians in combating burnout and its consequences. For example, the National Academy of Medicine (NAM) has convened an Action Collaborative on Clinician Well-Being and Resilience and invited more than 100 organizations to publish their statement of commitment to improve clinician well-being and reduce clinician burnout (https://nam.edu/initiatives/clinician-resilience-and-well-being/). The American Medical Association (AMA) has developed modules and tools to assist clinicians and administrators in taking important steps to prevent burnout (https://www.stepsforward.org/modules/physician-burnout).

CHEST has been an active participant in addressing burnout in ICU professionals, including in an important partnership with the American Association of Critical-Care Nurses (AACN), the American Thoracic Society (ATS), and the Society of Critical Care Medicine (SCCM) - the Critical Care Societies Collaborative (CCSC). The CCSC, whose members include greater than 150,000 critical care professionals in the United States, has established a principle goal of mitigating ICU burnout (#StopICUBurnout). One of the first CCSC efforts was to publish a white paper simultaneously in all four journals of the CCSC professional societies that provides the rationale and direction for a “call for action” to tackle ICU burnout (Moss M, Good VS, Gozal D, Kleinpell R, Sessler CN. Burnout syndrome in critical care health care professionals: A call for action. Chest. 2016;150[1]:17). Recently, the CCSC sponsored a National Summit on the Prevention and Management of Burnout in the ICU (http://ccsconline.org/optimizing-the-workforce/burnout). Fifty-five invited participants brought wide ranging expertise and substantial enthusiasm to the task of deconstructing ICU burnout and identifying knowledge gaps and future directions. Areas of focused discussion included factors influencing burnout, identifying individuals with burnout, the value of organizational and individual interventions to prevent and manage burnout, and translation of these discussions into a research agenda. CHEST and the CCSC are committed to the goals of enhancing clinician well-being and eliminating burnout in the ICU.

The work of critical care clinicians can create a perfect storm for emotional exhaustion, depersonalization, and reduced self-efficacy – widely known as burnout. Burnout is occurring in record numbers among physicians in general – more than twice as frequently as for non-health-care workers – and intensivists top the chart. Clinicians from all specialties in medicine today experience the frustrations of workplace chaos and loss of control, displacement of meaningful work with menial work, and ever increasing documentation requirements and electronic health record challenges – all contributing to burnout. Intensivists and other ICU professionals, such as advanced practice providers and nurses, however, experience the added challenge of working in a highly stressful environment characterized by fast-paced high-stakes decision making, long and irregular hours, and end-of-life scenarios often clouded by moral distress. These and other drivers contribute to high rates of burnout.

Being burned out takes its toll on health-care workers, contributing to psychological and physical manifestations, alcohol or substance abuse, posttraumatic stress disorder, and even suicidal ideation. Additionally, burnout carries important negative consequences for the organization and directly to the patient, including higher rates of employee turnover, lower quality of work, more medical errors, and reduced patient satisfaction. Unfortunately, burnout rates continue to rise with alarming speed.

Fortunately, there is increasing attention paid to the magnitude and potential impact of burnout, compelling important organizations to highlight the problem and assist clinicians in combating burnout and its consequences. For example, the National Academy of Medicine (NAM) has convened an Action Collaborative on Clinician Well-Being and Resilience and invited more than 100 organizations to publish their statement of commitment to improve clinician well-being and reduce clinician burnout (https://nam.edu/initiatives/clinician-resilience-and-well-being/). The American Medical Association (AMA) has developed modules and tools to assist clinicians and administrators in taking important steps to prevent burnout (https://www.stepsforward.org/modules/physician-burnout).

CHEST has been an active participant in addressing burnout in ICU professionals, including in an important partnership with the American Association of Critical-Care Nurses (AACN), the American Thoracic Society (ATS), and the Society of Critical Care Medicine (SCCM) - the Critical Care Societies Collaborative (CCSC). The CCSC, whose members include greater than 150,000 critical care professionals in the United States, has established a principle goal of mitigating ICU burnout (#StopICUBurnout). One of the first CCSC efforts was to publish a white paper simultaneously in all four journals of the CCSC professional societies that provides the rationale and direction for a “call for action” to tackle ICU burnout (Moss M, Good VS, Gozal D, Kleinpell R, Sessler CN. Burnout syndrome in critical care health care professionals: A call for action. Chest. 2016;150[1]:17). Recently, the CCSC sponsored a National Summit on the Prevention and Management of Burnout in the ICU (http://ccsconline.org/optimizing-the-workforce/burnout). Fifty-five invited participants brought wide ranging expertise and substantial enthusiasm to the task of deconstructing ICU burnout and identifying knowledge gaps and future directions. Areas of focused discussion included factors influencing burnout, identifying individuals with burnout, the value of organizational and individual interventions to prevent and manage burnout, and translation of these discussions into a research agenda. CHEST and the CCSC are committed to the goals of enhancing clinician well-being and eliminating burnout in the ICU.

More than 95 cents of every dollar raised by the CHEST Foundation goes toward advancing our mission-based programming, ranging from clinical research grants, to global and local community service projects, to patient education and disease awareness campaigns.
 

DONATIONS BY THE NUMBERS in 2017

300% INCREASE

A gift at any level SUPPORTS these EFFORTS.

$100

provides four asthma training sessions for a community-based asthma educator.

$10,000

can fund clinical research that leads to advances in the diagnosis and treatment of obstructive sleep apnea in women.

$15,000

supports a lung health screening event for an underserved population at higher risk for COPD and other lung ailments.

$25,000

can help fund research investigating the factors that contribute to racial disparities in early palliative care among elderly patients with lung cancer.

Learn more and donate foundation.chestnet.org.

More than 95 cents of every dollar raised by the CHEST Foundation goes toward advancing our mission-based programming, ranging from clinical research grants, to global and local community service projects, to patient education and disease awareness campaigns.
 

DONATIONS BY THE NUMBERS in 2017

300% INCREASE

A gift at any level SUPPORTS these EFFORTS.

$100

provides four asthma training sessions for a community-based asthma educator.

$10,000

can fund clinical research that leads to advances in the diagnosis and treatment of obstructive sleep apnea in women.

$15,000

supports a lung health screening event for an underserved population at higher risk for COPD and other lung ailments.

$25,000

can help fund research investigating the factors that contribute to racial disparities in early palliative care among elderly patients with lung cancer.

Learn more and donate foundation.chestnet.org.

More than 95 cents of every dollar raised by the CHEST Foundation goes toward advancing our mission-based programming, ranging from clinical research grants, to global and local community service projects, to patient education and disease awareness campaigns.
 

DONATIONS BY THE NUMBERS in 2017

300% INCREASE

A gift at any level SUPPORTS these EFFORTS.

$100

provides four asthma training sessions for a community-based asthma educator.

$10,000

can fund clinical research that leads to advances in the diagnosis and treatment of obstructive sleep apnea in women.

$15,000

supports a lung health screening event for an underserved population at higher risk for COPD and other lung ailments.

$25,000

can help fund research investigating the factors that contribute to racial disparities in early palliative care among elderly patients with lung cancer.

Learn more and donate foundation.chestnet.org.

W. Gerald Rainer, MD, FCCP, died November 14, 2017, one day after his 90th birthday Dr. Rainer was President of the American College of Chest Physicians in 1982-1983. He practiced thoracic and cardiovascular surgery for 50 years with St. Joseph Hospital in Denver as his professional home. He was a respected leader, researcher, and educator, helping and mentoring countless residents, fellows, and many other health-care professionals. Dr. Rainer was a distinguished clinical professor of surgery at the University of Colorado School of Medicine and served on many University boards and committees. He published prolifically in many respected surgical journals and was able to masterfully blend his private practice with strong academic involvement. As President of the American College of Chest Physicians and many other respected medical and surgical organizations, he was also actively involved in international professional societies. CHEST extends its condolences to Dr. Rainer’s wife of 67 years, Lois, and to his family and friends.

W. Gerald Rainer, MD, FCCP, died November 14, 2017, one day after his 90th birthday Dr. Rainer was President of the American College of Chest Physicians in 1982-1983. He practiced thoracic and cardiovascular surgery for 50 years with St. Joseph Hospital in Denver as his professional home. He was a respected leader, researcher, and educator, helping and mentoring countless residents, fellows, and many other health-care professionals. Dr. Rainer was a distinguished clinical professor of surgery at the University of Colorado School of Medicine and served on many University boards and committees. He published prolifically in many respected surgical journals and was able to masterfully blend his private practice with strong academic involvement. As President of the American College of Chest Physicians and many other respected medical and surgical organizations, he was also actively involved in international professional societies. CHEST extends its condolences to Dr. Rainer’s wife of 67 years, Lois, and to his family and friends.

W. Gerald Rainer, MD, FCCP, died November 14, 2017, one day after his 90th birthday Dr. Rainer was President of the American College of Chest Physicians in 1982-1983. He practiced thoracic and cardiovascular surgery for 50 years with St. Joseph Hospital in Denver as his professional home. He was a respected leader, researcher, and educator, helping and mentoring countless residents, fellows, and many other health-care professionals. Dr. Rainer was a distinguished clinical professor of surgery at the University of Colorado School of Medicine and served on many University boards and committees. He published prolifically in many respected surgical journals and was able to masterfully blend his private practice with strong academic involvement. As President of the American College of Chest Physicians and many other respected medical and surgical organizations, he was also actively involved in international professional societies. CHEST extends its condolences to Dr. Rainer’s wife of 67 years, Lois, and to his family and friends.

Original Research

Community-Acquired Pneumonia Visualized on CT Scans but Not Chest Radiographs: Pathogens, Severity, and Clinical Outcomes. By Dr. C. P. Upchurch, et al.

Commentary

CHEST: Home of the Clinician-Educator. By Dr. W. F. Kelly and Dr. A. S. Niven, on behalf of the CHEST Education Committee.

Original Research

Community-Acquired Pneumonia Visualized on CT Scans but Not Chest Radiographs: Pathogens, Severity, and Clinical Outcomes. By Dr. C. P. Upchurch, et al.

Commentary

CHEST: Home of the Clinician-Educator. By Dr. W. F. Kelly and Dr. A. S. Niven, on behalf of the CHEST Education Committee.

Original Research

Community-Acquired Pneumonia Visualized on CT Scans but Not Chest Radiographs: Pathogens, Severity, and Clinical Outcomes. By Dr. C. P. Upchurch, et al.

Commentary

CHEST: Home of the Clinician-Educator. By Dr. W. F. Kelly and Dr. A. S. Niven, on behalf of the CHEST Education Committee.

Obstructive sleep apnea (OSA) contributes a major health burden to society due to its high prevalence and substantial neurocognitive and cardiovascular consequences. Estimates suggest that at least 10% of adults in North America are afflicted with OSA, making it probably the most common respiratory disease in the developed world (Peppard et al. Am J Epidemiol. 2013;177[9]:1006). Nasal CPAP is a highly efficacious therapy that has been shown to improve neurocognitive and cardiovascular outcomes. However, CPAP is not always well tolerated. Alternative therapies, such as oral appliances and upper airway surgery, have highly variable efficacy, and evidence of important clinical benefits are uncertain. Therefore, efforts are ongoing to determine optimal alternative strategies for therapy.

In order to treat any condition optimally, one needs to be able to predict who is at highest risk of developing the condition, then to assess the consequences if left untreated, and finally to be able to predict response to various treatment options. Currently, the OSA field is still in its early stages of our understanding. Clinically, we are often faced with patients who have varying presentations and manifestations, but, for reasons that are unclear. For instance, two individuals with the same body mass index may have very different clinical manifestations, one with severe OSA and one without any OSA. Similarly, two individuals with an apnea hypopnea index of 40 events per hour (ie, severe OSA) may have very different symptoms attributable to OSA, eg, one could be asymptomatic and the other could be debilitated from sleepiness. We and others have been making efforts to determine why these phenomenon occur. At present, the techniques to define mechanisms underlying OSA are labor-intensive, requiring one or two overnight experiments to gather meaningful data. Although we are gathering new insights based on these techniques, efforts are ongoing to simplify these approaches and to make assessment of pathophysiologic characteristics more accessible to the clinician (Orr et al. Am J Respir Crit Care Med. 2017 Nov 30. doi: 10.1164/rccm.201707-1357LE. [Epub ahead of print]).

We ultimately believe that a thorough analysis of a sleep recording combined with demographic data and other readily available clinical data (perhaps plasma biomarkers) may yield sufficient information for us to know why OSA is occurring and what interventions might be helpful for an individual patient. Currently, our use of the polysomnogram to derive only an apnea hypopnea index does not take full advantage of the available data. An apnea hypopnea index can be readily obtained from home sleep testing and does not truly provide much insight into why a given individual has OSA, what symptoms are attributable to OSA, and what interventions might be considered for the afflicted individual. By analogy, if the only useful data derived from an ECG were a heart rate, the test would rapidly become obsolete. Along these lines, if the only role for the sleep clinician was to prescribe CPAP to everyone with an AHI greater than 5/h, there would be little need or interest in specialized training. In contrast, we suggest that rich insights regarding pathophysiology and mechanisms should be gathered and may influence clinical management of patients afflicted with OSA. Thus, we encourage more thorough analyses of available data to maximize information gleaned and, ultimately, to optimize clinical outcomes.

Recent studies suggest that sleep apnea occurs for varying reasons, a concept that is now thought to be clinically important (Jordan et al. Lancet. 2014;383[9918]:736). We draw a crucial distinction between endotypes (mechanisms underlying disease) and phenotypes (clinical expression of disease). Important endotypes include compromised upper airway anatomy, dysfunction in pharyngeal dilator muscles, unstable ventilatory control (high loop gain), and low arousal threshold (wake up easily), among others. Important phenotypes of sleep apnea are emerging and still evolving to include minimally symptomatic OSA, OSA with daytime sleepiness, and OSA with major cardiometabolic risk, among others. Several important concepts have emerged regarding different OSA endotypes and phenotypes:

1 The mechanism underlying OSA may predict potential response to therapeutic interventions. For instance, the endotype of OSA with unstable ventilatory control (high loop gain) may respond to agents such as oxygen and acetazolamide, which serve to stabilize control of breathing. In patients with anatomical compromise at the level of the velopharynx, uvulopalatopharyngoplasty may be an effective intervention. For patients with multiple pathophysiologic abnormalities, combination therapy may be required to alleviate OSA (Edwards et al. Sleep. 2016;9[11]:1973).

2 Given that OSA has many underlying etiologies, efforts are underway to determine whether individuals with different risk factors for OSA develop their disease based on varying mechanisms. As an example, people with posttraumatic stress disorder (PTSD) may be at increased risk of OSA perhaps on the basis of a low threshold for arousal (Orr et al. JCSM. 2017, 13[1]: 57-63). Another example would be patients with neuromuscular disease who may be at risk of OSA primarily based on impaired pharyngeal dilator muscle function.

3 A new concept is emerging whereby endotypes of OSA may actually predict differing OSA phenotypes. In theory, loop gain-driven OSA may have different consequences from OSA driven by compromise of pharyngeal anatomy. To this point, data suggest that OSA in the elderly may not have as many consequences as OSA in younger people matched on severity of illness. OSA in the elderly has lower loop gain than OSA in younger people and is associated with less negative intrathoracic pressure at the time of arousal as compared with younger individuals with OSA (Kobayashi et al. Chest. 2010; 137[6]:1310). As such, the endotype of OSA in the elderly may explain why the clinical consequences are fewer than in the younger OSA counterparts.

4 The mechanism underlying OSA may be important in determining response to clinical interventions, such as nasal CPAP. Patients with a low arousal threshold may be prone to insomnia when placed on CPAP and could theoretically be poorly tolerant of therapy based on disrupted sleep architecture. Such patients may benefit from non-myorelaxant hypnotic therapy to consolidate sleep and improve CPAP adherence. In addition, patients with high loop gain (unstable ventilatory control) may be prone to develop central apneas when placed on CPAP therapy (Stanchina et al. Ann Am Thorac Soc. 2015;12[9]:1351). These patients may benefit from newer technologies, eg, auto or adaptive servo ventilation - ASV. High loop gain has also been shown to predict failure of upper airway surgery as a treatment for OSA by several groups (Li et al. JCSM. 2017;13[9]:1029). Such patients should, perhaps, undergo nonsurgical therapies for OSA.

We emphasize that some of the points being made are somewhat speculative and, thus, encourage further basic and clinical research to test our assumptions. Robust, multicenter clinical trials assessing hard outcomes will ultimately be required to change the current standard of care. Nonetheless, we believe that a more thorough understanding of OSA pathogenesis can help guide clinical care today and will be critical to the optimal treatment of afflicted individuals tomorrow.

Dr. Owens is Assistant Clinical Professor of Medicine; Dr. Deacon is a Post-Doctoral Research Scholar; and Dr. Malhotra is Kenneth M. Moser Professor of Medicine and Chief, Division of Pulmonary, Critical Care and Sleep Medicine, University of California San Diego.

Obstructive sleep apnea (OSA) contributes a major health burden to society due to its high prevalence and substantial neurocognitive and cardiovascular consequences. Estimates suggest that at least 10% of adults in North America are afflicted with OSA, making it probably the most common respiratory disease in the developed world (Peppard et al. Am J Epidemiol. 2013;177[9]:1006). Nasal CPAP is a highly efficacious therapy that has been shown to improve neurocognitive and cardiovascular outcomes. However, CPAP is not always well tolerated. Alternative therapies, such as oral appliances and upper airway surgery, have highly variable efficacy, and evidence of important clinical benefits are uncertain. Therefore, efforts are ongoing to determine optimal alternative strategies for therapy.

In order to treat any condition optimally, one needs to be able to predict who is at highest risk of developing the condition, then to assess the consequences if left untreated, and finally to be able to predict response to various treatment options. Currently, the OSA field is still in its early stages of our understanding. Clinically, we are often faced with patients who have varying presentations and manifestations, but, for reasons that are unclear. For instance, two individuals with the same body mass index may have very different clinical manifestations, one with severe OSA and one without any OSA. Similarly, two individuals with an apnea hypopnea index of 40 events per hour (ie, severe OSA) may have very different symptoms attributable to OSA, eg, one could be asymptomatic and the other could be debilitated from sleepiness. We and others have been making efforts to determine why these phenomenon occur. At present, the techniques to define mechanisms underlying OSA are labor-intensive, requiring one or two overnight experiments to gather meaningful data. Although we are gathering new insights based on these techniques, efforts are ongoing to simplify these approaches and to make assessment of pathophysiologic characteristics more accessible to the clinician (Orr et al. Am J Respir Crit Care Med. 2017 Nov 30. doi: 10.1164/rccm.201707-1357LE. [Epub ahead of print]).

We ultimately believe that a thorough analysis of a sleep recording combined with demographic data and other readily available clinical data (perhaps plasma biomarkers) may yield sufficient information for us to know why OSA is occurring and what interventions might be helpful for an individual patient. Currently, our use of the polysomnogram to derive only an apnea hypopnea index does not take full advantage of the available data. An apnea hypopnea index can be readily obtained from home sleep testing and does not truly provide much insight into why a given individual has OSA, what symptoms are attributable to OSA, and what interventions might be considered for the afflicted individual. By analogy, if the only useful data derived from an ECG were a heart rate, the test would rapidly become obsolete. Along these lines, if the only role for the sleep clinician was to prescribe CPAP to everyone with an AHI greater than 5/h, there would be little need or interest in specialized training. In contrast, we suggest that rich insights regarding pathophysiology and mechanisms should be gathered and may influence clinical management of patients afflicted with OSA. Thus, we encourage more thorough analyses of available data to maximize information gleaned and, ultimately, to optimize clinical outcomes.

Recent studies suggest that sleep apnea occurs for varying reasons, a concept that is now thought to be clinically important (Jordan et al. Lancet. 2014;383[9918]:736). We draw a crucial distinction between endotypes (mechanisms underlying disease) and phenotypes (clinical expression of disease). Important endotypes include compromised upper airway anatomy, dysfunction in pharyngeal dilator muscles, unstable ventilatory control (high loop gain), and low arousal threshold (wake up easily), among others. Important phenotypes of sleep apnea are emerging and still evolving to include minimally symptomatic OSA, OSA with daytime sleepiness, and OSA with major cardiometabolic risk, among others. Several important concepts have emerged regarding different OSA endotypes and phenotypes:

1 The mechanism underlying OSA may predict potential response to therapeutic interventions. For instance, the endotype of OSA with unstable ventilatory control (high loop gain) may respond to agents such as oxygen and acetazolamide, which serve to stabilize control of breathing. In patients with anatomical compromise at the level of the velopharynx, uvulopalatopharyngoplasty may be an effective intervention. For patients with multiple pathophysiologic abnormalities, combination therapy may be required to alleviate OSA (Edwards et al. Sleep. 2016;9[11]:1973).

2 Given that OSA has many underlying etiologies, efforts are underway to determine whether individuals with different risk factors for OSA develop their disease based on varying mechanisms. As an example, people with posttraumatic stress disorder (PTSD) may be at increased risk of OSA perhaps on the basis of a low threshold for arousal (Orr et al. JCSM. 2017, 13[1]: 57-63). Another example would be patients with neuromuscular disease who may be at risk of OSA primarily based on impaired pharyngeal dilator muscle function.

3 A new concept is emerging whereby endotypes of OSA may actually predict differing OSA phenotypes. In theory, loop gain-driven OSA may have different consequences from OSA driven by compromise of pharyngeal anatomy. To this point, data suggest that OSA in the elderly may not have as many consequences as OSA in younger people matched on severity of illness. OSA in the elderly has lower loop gain than OSA in younger people and is associated with less negative intrathoracic pressure at the time of arousal as compared with younger individuals with OSA (Kobayashi et al. Chest. 2010; 137[6]:1310). As such, the endotype of OSA in the elderly may explain why the clinical consequences are fewer than in the younger OSA counterparts.

4 The mechanism underlying OSA may be important in determining response to clinical interventions, such as nasal CPAP. Patients with a low arousal threshold may be prone to insomnia when placed on CPAP and could theoretically be poorly tolerant of therapy based on disrupted sleep architecture. Such patients may benefit from non-myorelaxant hypnotic therapy to consolidate sleep and improve CPAP adherence. In addition, patients with high loop gain (unstable ventilatory control) may be prone to develop central apneas when placed on CPAP therapy (Stanchina et al. Ann Am Thorac Soc. 2015;12[9]:1351). These patients may benefit from newer technologies, eg, auto or adaptive servo ventilation - ASV. High loop gain has also been shown to predict failure of upper airway surgery as a treatment for OSA by several groups (Li et al. JCSM. 2017;13[9]:1029). Such patients should, perhaps, undergo nonsurgical therapies for OSA.

We emphasize that some of the points being made are somewhat speculative and, thus, encourage further basic and clinical research to test our assumptions. Robust, multicenter clinical trials assessing hard outcomes will ultimately be required to change the current standard of care. Nonetheless, we believe that a more thorough understanding of OSA pathogenesis can help guide clinical care today and will be critical to the optimal treatment of afflicted individuals tomorrow.

Dr. Owens is Assistant Clinical Professor of Medicine; Dr. Deacon is a Post-Doctoral Research Scholar; and Dr. Malhotra is Kenneth M. Moser Professor of Medicine and Chief, Division of Pulmonary, Critical Care and Sleep Medicine, University of California San Diego.

Obstructive sleep apnea (OSA) contributes a major health burden to society due to its high prevalence and substantial neurocognitive and cardiovascular consequences. Estimates suggest that at least 10% of adults in North America are afflicted with OSA, making it probably the most common respiratory disease in the developed world (Peppard et al. Am J Epidemiol. 2013;177[9]:1006). Nasal CPAP is a highly efficacious therapy that has been shown to improve neurocognitive and cardiovascular outcomes. However, CPAP is not always well tolerated. Alternative therapies, such as oral appliances and upper airway surgery, have highly variable efficacy, and evidence of important clinical benefits are uncertain. Therefore, efforts are ongoing to determine optimal alternative strategies for therapy.

In order to treat any condition optimally, one needs to be able to predict who is at highest risk of developing the condition, then to assess the consequences if left untreated, and finally to be able to predict response to various treatment options. Currently, the OSA field is still in its early stages of our understanding. Clinically, we are often faced with patients who have varying presentations and manifestations, but, for reasons that are unclear. For instance, two individuals with the same body mass index may have very different clinical manifestations, one with severe OSA and one without any OSA. Similarly, two individuals with an apnea hypopnea index of 40 events per hour (ie, severe OSA) may have very different symptoms attributable to OSA, eg, one could be asymptomatic and the other could be debilitated from sleepiness. We and others have been making efforts to determine why these phenomenon occur. At present, the techniques to define mechanisms underlying OSA are labor-intensive, requiring one or two overnight experiments to gather meaningful data. Although we are gathering new insights based on these techniques, efforts are ongoing to simplify these approaches and to make assessment of pathophysiologic characteristics more accessible to the clinician (Orr et al. Am J Respir Crit Care Med. 2017 Nov 30. doi: 10.1164/rccm.201707-1357LE. [Epub ahead of print]).

We ultimately believe that a thorough analysis of a sleep recording combined with demographic data and other readily available clinical data (perhaps plasma biomarkers) may yield sufficient information for us to know why OSA is occurring and what interventions might be helpful for an individual patient. Currently, our use of the polysomnogram to derive only an apnea hypopnea index does not take full advantage of the available data. An apnea hypopnea index can be readily obtained from home sleep testing and does not truly provide much insight into why a given individual has OSA, what symptoms are attributable to OSA, and what interventions might be considered for the afflicted individual. By analogy, if the only useful data derived from an ECG were a heart rate, the test would rapidly become obsolete. Along these lines, if the only role for the sleep clinician was to prescribe CPAP to everyone with an AHI greater than 5/h, there would be little need or interest in specialized training. In contrast, we suggest that rich insights regarding pathophysiology and mechanisms should be gathered and may influence clinical management of patients afflicted with OSA. Thus, we encourage more thorough analyses of available data to maximize information gleaned and, ultimately, to optimize clinical outcomes.

Recent studies suggest that sleep apnea occurs for varying reasons, a concept that is now thought to be clinically important (Jordan et al. Lancet. 2014;383[9918]:736). We draw a crucial distinction between endotypes (mechanisms underlying disease) and phenotypes (clinical expression of disease). Important endotypes include compromised upper airway anatomy, dysfunction in pharyngeal dilator muscles, unstable ventilatory control (high loop gain), and low arousal threshold (wake up easily), among others. Important phenotypes of sleep apnea are emerging and still evolving to include minimally symptomatic OSA, OSA with daytime sleepiness, and OSA with major cardiometabolic risk, among others. Several important concepts have emerged regarding different OSA endotypes and phenotypes:

1 The mechanism underlying OSA may predict potential response to therapeutic interventions. For instance, the endotype of OSA with unstable ventilatory control (high loop gain) may respond to agents such as oxygen and acetazolamide, which serve to stabilize control of breathing. In patients with anatomical compromise at the level of the velopharynx, uvulopalatopharyngoplasty may be an effective intervention. For patients with multiple pathophysiologic abnormalities, combination therapy may be required to alleviate OSA (Edwards et al. Sleep. 2016;9[11]:1973).

2 Given that OSA has many underlying etiologies, efforts are underway to determine whether individuals with different risk factors for OSA develop their disease based on varying mechanisms. As an example, people with posttraumatic stress disorder (PTSD) may be at increased risk of OSA perhaps on the basis of a low threshold for arousal (Orr et al. JCSM. 2017, 13[1]: 57-63). Another example would be patients with neuromuscular disease who may be at risk of OSA primarily based on impaired pharyngeal dilator muscle function.

3 A new concept is emerging whereby endotypes of OSA may actually predict differing OSA phenotypes. In theory, loop gain-driven OSA may have different consequences from OSA driven by compromise of pharyngeal anatomy. To this point, data suggest that OSA in the elderly may not have as many consequences as OSA in younger people matched on severity of illness. OSA in the elderly has lower loop gain than OSA in younger people and is associated with less negative intrathoracic pressure at the time of arousal as compared with younger individuals with OSA (Kobayashi et al. Chest. 2010; 137[6]:1310). As such, the endotype of OSA in the elderly may explain why the clinical consequences are fewer than in the younger OSA counterparts.

4 The mechanism underlying OSA may be important in determining response to clinical interventions, such as nasal CPAP. Patients with a low arousal threshold may be prone to insomnia when placed on CPAP and could theoretically be poorly tolerant of therapy based on disrupted sleep architecture. Such patients may benefit from non-myorelaxant hypnotic therapy to consolidate sleep and improve CPAP adherence. In addition, patients with high loop gain (unstable ventilatory control) may be prone to develop central apneas when placed on CPAP therapy (Stanchina et al. Ann Am Thorac Soc. 2015;12[9]:1351). These patients may benefit from newer technologies, eg, auto or adaptive servo ventilation - ASV. High loop gain has also been shown to predict failure of upper airway surgery as a treatment for OSA by several groups (Li et al. JCSM. 2017;13[9]:1029). Such patients should, perhaps, undergo nonsurgical therapies for OSA.

We emphasize that some of the points being made are somewhat speculative and, thus, encourage further basic and clinical research to test our assumptions. Robust, multicenter clinical trials assessing hard outcomes will ultimately be required to change the current standard of care. Nonetheless, we believe that a more thorough understanding of OSA pathogenesis can help guide clinical care today and will be critical to the optimal treatment of afflicted individuals tomorrow.

Dr. Owens is Assistant Clinical Professor of Medicine; Dr. Deacon is a Post-Doctoral Research Scholar; and Dr. Malhotra is Kenneth M. Moser Professor of Medicine and Chief, Division of Pulmonary, Critical Care and Sleep Medicine, University of California San Diego.

Our CHEST Foundation grantees are doing amazing research and community service projects that are paving the way for change and improvements in chest medicine. How will you help champion lung health?

“This award carries great importance to me as a young clinician who is in the early phase of my career. I’m driven by my passion for researching this disease (PAH). This award helps establish me as a strong clinical researcher – where I see my career heading. It also helps us identify those clues that can lead to changing how this disease state is treated. Everything starts with an idea.”

Sandeep Sahay, MD, FCCP
Houston Methodist Hospital – Houston, Texas
CHEST Foundation Research Grant in Pulmonary Arterial Hypertension

Title: Alterations of Estrogen Metabolism in the Development of Portopulmonary Hypertension

Utilizing Medical-Legal Partnership to Promote Asthma Health Equity

Connecticut Children’s Medical Center – Hartford, Connecticut
CHEST Foundation Community Service Grant Honoring D. Robert McCaffree, MD, Master FCCP

Title: Haitian Pediatric Critical Care Collaborative Training Course

The CHEST Foundation is accepting grant applications now until March 31 in the following areas:



• CHEST Foundation Research Grant in Lung Cancer – $50,000 - $100,000 2-year grant*

• CHEST Foundation Research Grant in Asthma - $15,000 - $30,000 1-year grant*

• CHEST Foundation Research Grant in Pulmonary Arterial Hypertension - $25,000 - $50,000 1-year grant*

• CHEST Foundation and the Alpha-1 Foundation Research Grant in Alpha-1 Antitrypsin Deficiency - $25,000 1-year grant

• CHEST Foundation Research Grant in Pulmonary Fibrosis – $50,000 1-year grant

• CHEST Foundation Research Grant in Chronic Obstructive Pulmonary Disease – $50,000 1-year grant

• CHEST Foundation Research Grant in Venous Thromboembolism - $15,000 – $30,000 1-year grant*

• CHEST Foundation Research Grant in Nontuberculous Mycobacteria Disease - $30,000 1-year grant

• CHEST Foundation Research Grant in Women’s Lung Health - $10,000 1-year grant

• CHEST Foundation Research Grant in Cystic Fibrosis – $15,000 – $30,000 1-year grant

• CHEST Foundation Community Service Grant Honoring D. Robert McCaffree, MD, Master FCCP - $2,500- $15,000 1-year grant



*Amount contingent on funding.



Go to chestfoundation.org/grants to apply now.

Our CHEST Foundation grantees are doing amazing research and community service projects that are paving the way for change and improvements in chest medicine. How will you help champion lung health?

“This award carries great importance to me as a young clinician who is in the early phase of my career. I’m driven by my passion for researching this disease (PAH). This award helps establish me as a strong clinical researcher – where I see my career heading. It also helps us identify those clues that can lead to changing how this disease state is treated. Everything starts with an idea.”

Sandeep Sahay, MD, FCCP
Houston Methodist Hospital – Houston, Texas
CHEST Foundation Research Grant in Pulmonary Arterial Hypertension

Title: Alterations of Estrogen Metabolism in the Development of Portopulmonary Hypertension

Utilizing Medical-Legal Partnership to Promote Asthma Health Equity

Connecticut Children’s Medical Center – Hartford, Connecticut
CHEST Foundation Community Service Grant Honoring D. Robert McCaffree, MD, Master FCCP

Title: Haitian Pediatric Critical Care Collaborative Training Course

The CHEST Foundation is accepting grant applications now until March 31 in the following areas:



• CHEST Foundation Research Grant in Lung Cancer – $50,000 - $100,000 2-year grant*

• CHEST Foundation Research Grant in Asthma - $15,000 - $30,000 1-year grant*

• CHEST Foundation Research Grant in Pulmonary Arterial Hypertension - $25,000 - $50,000 1-year grant*

• CHEST Foundation and the Alpha-1 Foundation Research Grant in Alpha-1 Antitrypsin Deficiency - $25,000 1-year grant

• CHEST Foundation Research Grant in Pulmonary Fibrosis – $50,000 1-year grant

• CHEST Foundation Research Grant in Chronic Obstructive Pulmonary Disease – $50,000 1-year grant

• CHEST Foundation Research Grant in Venous Thromboembolism - $15,000 – $30,000 1-year grant*

• CHEST Foundation Research Grant in Nontuberculous Mycobacteria Disease - $30,000 1-year grant

• CHEST Foundation Research Grant in Women’s Lung Health - $10,000 1-year grant

• CHEST Foundation Research Grant in Cystic Fibrosis – $15,000 – $30,000 1-year grant

• CHEST Foundation Community Service Grant Honoring D. Robert McCaffree, MD, Master FCCP - $2,500- $15,000 1-year grant



*Amount contingent on funding.



Go to chestfoundation.org/grants to apply now.

Our CHEST Foundation grantees are doing amazing research and community service projects that are paving the way for change and improvements in chest medicine. How will you help champion lung health?

“This award carries great importance to me as a young clinician who is in the early phase of my career. I’m driven by my passion for researching this disease (PAH). This award helps establish me as a strong clinical researcher – where I see my career heading. It also helps us identify those clues that can lead to changing how this disease state is treated. Everything starts with an idea.”

Sandeep Sahay, MD, FCCP
Houston Methodist Hospital – Houston, Texas
CHEST Foundation Research Grant in Pulmonary Arterial Hypertension

Title: Alterations of Estrogen Metabolism in the Development of Portopulmonary Hypertension

Utilizing Medical-Legal Partnership to Promote Asthma Health Equity

Connecticut Children’s Medical Center – Hartford, Connecticut
CHEST Foundation Community Service Grant Honoring D. Robert McCaffree, MD, Master FCCP

Title: Haitian Pediatric Critical Care Collaborative Training Course

The CHEST Foundation is accepting grant applications now until March 31 in the following areas:



• CHEST Foundation Research Grant in Lung Cancer – $50,000 - $100,000 2-year grant*

• CHEST Foundation Research Grant in Asthma - $15,000 - $30,000 1-year grant*

• CHEST Foundation Research Grant in Pulmonary Arterial Hypertension - $25,000 - $50,000 1-year grant*

• CHEST Foundation and the Alpha-1 Foundation Research Grant in Alpha-1 Antitrypsin Deficiency - $25,000 1-year grant

• CHEST Foundation Research Grant in Pulmonary Fibrosis – $50,000 1-year grant

• CHEST Foundation Research Grant in Chronic Obstructive Pulmonary Disease – $50,000 1-year grant

• CHEST Foundation Research Grant in Venous Thromboembolism - $15,000 – $30,000 1-year grant*

• CHEST Foundation Research Grant in Nontuberculous Mycobacteria Disease - $30,000 1-year grant

• CHEST Foundation Research Grant in Women’s Lung Health - $10,000 1-year grant

• CHEST Foundation Research Grant in Cystic Fibrosis – $15,000 – $30,000 1-year grant

• CHEST Foundation Community Service Grant Honoring D. Robert McCaffree, MD, Master FCCP - $2,500- $15,000 1-year grant



*Amount contingent on funding.



Go to chestfoundation.org/grants to apply now.

Stephanie M. Levine, MD, FCCP, is an expert in lung transplantation, pulmonary and critical care issues in pregnancy and women’s lung health, and eosinophilic lung disorders. She is a Professor of Medicine in the Division of Pulmonary Diseases and Critical Care Medicine at the University of Texas Health Science Center in San Antonio, Texas; the Program Director of the Pulmonary and Critical Care Fellowship at the University of Texas Health Science Center; and the Director of the Medical Intensive Care Unit and Bronchoscopy Laboratory at the University Hospital. She also is a staff physician at the Audie Murphy Veteran Administration Hospital. Dr. Levine has authored or co-authored over 270 manuscripts, chapters, reviews, editorials, and abstracts, primarily in her major field of interest, lung transplantation. She has been Editor of both Critical Care SEEK and Pulmonary SEEK.

Stephanie M. Levine, MD, FCCP, is an expert in lung transplantation, pulmonary and critical care issues in pregnancy and women’s lung health, and eosinophilic lung disorders. She is a Professor of Medicine in the Division of Pulmonary Diseases and Critical Care Medicine at the University of Texas Health Science Center in San Antonio, Texas; the Program Director of the Pulmonary and Critical Care Fellowship at the University of Texas Health Science Center; and the Director of the Medical Intensive Care Unit and Bronchoscopy Laboratory at the University Hospital. She also is a staff physician at the Audie Murphy Veteran Administration Hospital. Dr. Levine has authored or co-authored over 270 manuscripts, chapters, reviews, editorials, and abstracts, primarily in her major field of interest, lung transplantation. She has been Editor of both Critical Care SEEK and Pulmonary SEEK.

Stephanie M. Levine, MD, FCCP, is an expert in lung transplantation, pulmonary and critical care issues in pregnancy and women’s lung health, and eosinophilic lung disorders. She is a Professor of Medicine in the Division of Pulmonary Diseases and Critical Care Medicine at the University of Texas Health Science Center in San Antonio, Texas; the Program Director of the Pulmonary and Critical Care Fellowship at the University of Texas Health Science Center; and the Director of the Medical Intensive Care Unit and Bronchoscopy Laboratory at the University Hospital. She also is a staff physician at the Audie Murphy Veteran Administration Hospital. Dr. Levine has authored or co-authored over 270 manuscripts, chapters, reviews, editorials, and abstracts, primarily in her major field of interest, lung transplantation. She has been Editor of both Critical Care SEEK and Pulmonary SEEK.

As I sit here and write this article, it is hard to fathom that a quarter of my year as the President of CHEST has passed by. Thanks again for this incredibly humbling opportunity to serve as your President.

I hope many who read this were able to get to Toronto and experience CHEST 2017. Special thanks to our Program Chair, Peter Mazzone, and to his Co-Chair Diane Lougheed from the Canadian Thoracic Society; the Scientific Program Committee; our excellent and committed CHEST 2017 faculty, who give their valuable time to ensure we are delivering the best clinical education possible; and our incredibly talented CHEST staff for all their work to make this meeting a reality.

1. The Editor in Chief Search Task Force, under the leadership of Dr.. David Gutterman and Nicki Augustyn, is hard at work with their diverse and talented colleagues on this critically important task.



2. The Scientific Program Committee, under Dr. David Schulman’s direction, is hard at work building October’s CHEST 2018 in San Antonio. It is so exciting to watch this group plan and create, in new and innovative ways, the content for this meeting to be held October 6-10.



3. By the publication date of this article, your Board of Regents most likely will have put the finishing touches, under the leadership of Jenny Nemkovich, our Chief of Staff, on our next 5-year strategic plan.



4. The Board of Regents is also moving forward with a uniform, business-like process and approach in delivering international education offerings and meeting opportunities. Special thanks to Bob Musacchio, our COO and the SVP of Strategy and Innovation, Sue Reimbold, wearing her hat of Market Growth; and Chad Jackson, VP of Innovation and Development, for their direction in this area.



5. Thanks to the Diversity/Inclusion Task Force for their continued work to ensure that the principles of diversity of thought and inclusion permeate all of our conversations and work on the volunteer and professional sides of CHEST.



6. Thanks also to our Training and Transitions Committee and their leadership, Drs. Gabe Bosslet and Matt Miles, and the support of Dr. Richard Irwin and our CHEST® journal for the introduction of the CHEST Teaching, Education, and Career Hub in the journal, which made its debut in January.



7. Also, emphasizing the critical importance of relationships, thanks to our colleagues and partners with so many sister societies with whom we are working closely to help advance the practice of chest medicine. I am confident that we are building better relationships built on common goals, transparency, communication, and trust than we have in many years.



8. Last, and certainly not least, one of the jobs of President I am most looking forward to is serving on the Board of Trustees of the CHEST Foundation as an ex officio member. Having served on this Board for about 10 years, I am so glad to be joining my CF family once again. What an amazing group of volunteers, leaders, and staff serving CHEST and our patients in such amazing ways.

These are but a few of so many things that are transpiring at CHEST. People have asked me if it is intimidating to take on this responsibility. With the support of such diversely talented leaders in our Presidential line; an incredibly mature and engaged BOR; and a CEO, senior leadership, and diverse and talented staff that we have at CHEST, all characterized by incredible intellect and energy, it is pretty easy to be just another member of a great team.

Thanks again for your unwavering support of CHEST and our mission.

As I sit here and write this article, it is hard to fathom that a quarter of my year as the President of CHEST has passed by. Thanks again for this incredibly humbling opportunity to serve as your President.

I hope many who read this were able to get to Toronto and experience CHEST 2017. Special thanks to our Program Chair, Peter Mazzone, and to his Co-Chair Diane Lougheed from the Canadian Thoracic Society; the Scientific Program Committee; our excellent and committed CHEST 2017 faculty, who give their valuable time to ensure we are delivering the best clinical education possible; and our incredibly talented CHEST staff for all their work to make this meeting a reality.

1. The Editor in Chief Search Task Force, under the leadership of Dr.. David Gutterman and Nicki Augustyn, is hard at work with their diverse and talented colleagues on this critically important task.



2. The Scientific Program Committee, under Dr. David Schulman’s direction, is hard at work building October’s CHEST 2018 in San Antonio. It is so exciting to watch this group plan and create, in new and innovative ways, the content for this meeting to be held October 6-10.



3. By the publication date of this article, your Board of Regents most likely will have put the finishing touches, under the leadership of Jenny Nemkovich, our Chief of Staff, on our next 5-year strategic plan.



4. The Board of Regents is also moving forward with a uniform, business-like process and approach in delivering international education offerings and meeting opportunities. Special thanks to Bob Musacchio, our COO and the SVP of Strategy and Innovation, Sue Reimbold, wearing her hat of Market Growth; and Chad Jackson, VP of Innovation and Development, for their direction in this area.



5. Thanks to the Diversity/Inclusion Task Force for their continued work to ensure that the principles of diversity of thought and inclusion permeate all of our conversations and work on the volunteer and professional sides of CHEST.



6. Thanks also to our Training and Transitions Committee and their leadership, Drs. Gabe Bosslet and Matt Miles, and the support of Dr. Richard Irwin and our CHEST® journal for the introduction of the CHEST Teaching, Education, and Career Hub in the journal, which made its debut in January.



7. Also, emphasizing the critical importance of relationships, thanks to our colleagues and partners with so many sister societies with whom we are working closely to help advance the practice of chest medicine. I am confident that we are building better relationships built on common goals, transparency, communication, and trust than we have in many years.



8. Last, and certainly not least, one of the jobs of President I am most looking forward to is serving on the Board of Trustees of the CHEST Foundation as an ex officio member. Having served on this Board for about 10 years, I am so glad to be joining my CF family once again. What an amazing group of volunteers, leaders, and staff serving CHEST and our patients in such amazing ways.

These are but a few of so many things that are transpiring at CHEST. People have asked me if it is intimidating to take on this responsibility. With the support of such diversely talented leaders in our Presidential line; an incredibly mature and engaged BOR; and a CEO, senior leadership, and diverse and talented staff that we have at CHEST, all characterized by incredible intellect and energy, it is pretty easy to be just another member of a great team.

Thanks again for your unwavering support of CHEST and our mission.

As I sit here and write this article, it is hard to fathom that a quarter of my year as the President of CHEST has passed by. Thanks again for this incredibly humbling opportunity to serve as your President.

I hope many who read this were able to get to Toronto and experience CHEST 2017. Special thanks to our Program Chair, Peter Mazzone, and to his Co-Chair Diane Lougheed from the Canadian Thoracic Society; the Scientific Program Committee; our excellent and committed CHEST 2017 faculty, who give their valuable time to ensure we are delivering the best clinical education possible; and our incredibly talented CHEST staff for all their work to make this meeting a reality.

1. The Editor in Chief Search Task Force, under the leadership of Dr.. David Gutterman and Nicki Augustyn, is hard at work with their diverse and talented colleagues on this critically important task.



2. The Scientific Program Committee, under Dr. David Schulman’s direction, is hard at work building October’s CHEST 2018 in San Antonio. It is so exciting to watch this group plan and create, in new and innovative ways, the content for this meeting to be held October 6-10.



3. By the publication date of this article, your Board of Regents most likely will have put the finishing touches, under the leadership of Jenny Nemkovich, our Chief of Staff, on our next 5-year strategic plan.



4. The Board of Regents is also moving forward with a uniform, business-like process and approach in delivering international education offerings and meeting opportunities. Special thanks to Bob Musacchio, our COO and the SVP of Strategy and Innovation, Sue Reimbold, wearing her hat of Market Growth; and Chad Jackson, VP of Innovation and Development, for their direction in this area.



5. Thanks to the Diversity/Inclusion Task Force for their continued work to ensure that the principles of diversity of thought and inclusion permeate all of our conversations and work on the volunteer and professional sides of CHEST.



6. Thanks also to our Training and Transitions Committee and their leadership, Drs. Gabe Bosslet and Matt Miles, and the support of Dr. Richard Irwin and our CHEST® journal for the introduction of the CHEST Teaching, Education, and Career Hub in the journal, which made its debut in January.



7. Also, emphasizing the critical importance of relationships, thanks to our colleagues and partners with so many sister societies with whom we are working closely to help advance the practice of chest medicine. I am confident that we are building better relationships built on common goals, transparency, communication, and trust than we have in many years.



8. Last, and certainly not least, one of the jobs of President I am most looking forward to is serving on the Board of Trustees of the CHEST Foundation as an ex officio member. Having served on this Board for about 10 years, I am so glad to be joining my CF family once again. What an amazing group of volunteers, leaders, and staff serving CHEST and our patients in such amazing ways.

These are but a few of so many things that are transpiring at CHEST. People have asked me if it is intimidating to take on this responsibility. With the support of such diversely talented leaders in our Presidential line; an incredibly mature and engaged BOR; and a CEO, senior leadership, and diverse and talented staff that we have at CHEST, all characterized by incredible intellect and energy, it is pretty easy to be just another member of a great team.

Thanks again for your unwavering support of CHEST and our mission.

Clinical Research

New guidelines for adult bronchiectasis

Clinically significant bronchiectasis is a combination of radiologic bronchial dilatation with clinical symptoms. Guidelines on management of adult bronchiectasis were recently published (Eur Respir J. 2017; Sep 10;50[3]).

For all adult patients with clinically significant bronchiectasis, the guidelines suggest standardized minimum testing with differential blood count, serum immunoglobulins, and testing for allergic bronchopulmonary aspergillosis with any further workup on an individual basis. Annual sputum surveillance is suggested for clinically stable adult patients; however, the evidence for this recommendation came from studies done on patients with cystic fibrosis.

Inhaled bronchodilators are suggested as the first-line treatment in symptomatic patients. Long-term antibiotics (greater than 3 months) are recommended in patients with greater than 3 exacerbations/year after optimizing airway clearance and disease-specific treatment. Pseudomonas aeruginosa infections are to be treated with inhaled antibiotics (colistin or gentamicin) (Charles SH, et al. Am J Respir Crit Care Med. 2014;189[8]975; Murray P, et al. Am J Respir Crit Care Med. 2011;183[4]:491; and nonpseudomonal infections are to be treated with macrolides (Conroy W, et al. Lancet. 2012;380[9842]:660; Altenburg J, et al. JAMA. 2013;309[12];1251), although interchangeable for intolerance. Sputum cultured early will guide therapy among poor responders. Long-term mucolytic agents are suggested in appropriate tolerating patients. Pulmonary rehabilitation for 6-8 weeks is strongly recommended in adult bronchiectasis with impaired exercise capacity. Surgical interventions for bronchiectasis are reserved for a small group of patients who have localized disease and high exacerbation rates despite maximal medical therapy. Inhaled corticosteroids are suggested not to be used in adult bronchiectasis. Guidelines recommend against the use of statins and recombinant human DNase as it increases exacerbations (Chest. 1998;113[5]:1329. The task force acknowledged the low quality of evidence for their recommendations requiring more research in the field of adult bronchiectasis.

Bharat Bajantri, MD
Fellow-in-Training Member

Airways Disorders

ICS/LABA combo therapy: black box warning removed

Publication of the Salmeterol Multicenter Asthma Research Trial (SMART) in 2006 caused panic among asthmatics and the physicians who treat them (Nelson et al. Chest. 2006;129[1]:15). The study suggested that the long-acting beta-2-agonist (LABA) salmeterol leads to an increased risk of asthma/respiratory-related deaths compared with placebo. This finding was more pronounced in the African American subpopulation. The study left many questions unanswered, including whether or not this risk is present when LABA therapy is combined with inhaled corticosteroids (ICS) (O’Byrne. Chest. 2006;129[1]:3). Subsequent meta-analyses confirmed the increased risk with LABA monotherapy but not with LABA/ICS (Salpeter et al. Ann Inter Med. 2006;144[12]: 904; Jaeschke et al. Am J Respir Crit Care Med. 2008;178[10]:1009). Still, a black box warning relating LABA to asthma-related death was applied to LABA/ICS products.

In 2011, the Food and Drug Administration (FDA) mandated large, randomized controlled trials be performed for LABA/ICS products to assess safety. These trials were recently completed, showing no difference in asthma-related deaths between LABA/ICS and ICS alone. There were 41, 297 patients across four trials, three included teenagers and adults (age ≥ 12) and one enrolled children (ages 4-11). These studies prompted the FDA to remove the black box warning from salmeterol/fluticasone, formoterol/budesonide, and formoterol/mometasone (https://wwwfdagov/downloads/Drugs/DrugSafety/UCM589997pdf).

Conclusion: Because LABA/ICS therapy is effective for asthma, most pulmonologists continue to prescribe it despite the SMART study results and FDA warning. In a practical sense, we don’t expect the FDA findings to radically change asthma care. Still, it seems we can finally put this question to rest – LABA/ICS is indeed safe for asthmatics. Most physicians will continue to avoid LABA monotherapy, and now that tiotropium is included in the 2017 GINA guidelines, it’s only matter of time before we’re debating whether LABA/long-acting muscarinic antagonist (LAMA) is safe for asthmatics.

Aaron Holley, MD, FCCP
Steering Committee Member

Navitha Ramesh, MD, MBBS
Fellow-in-Training Member

Critical Care

Standardized handoffs in the ICU: room for improvement?

Transitions in patient care are commonplace in the ICU. But handoffs are particularly susceptible to error given the complexity of the patient population. Impacts of less-than-ideal handoffs likely include adverse events, delays in medical diagnosis and treatment, redundant communications, redundant activities such as additional procedures and tests, lower provider and patient satisfaction, higher costs, longer hospital stays, more hospital admissions, and less effective training for health -care providers. Yet, there is great heterogeneity in handoff practiced, and the impact of standardized handoffs in the ICU is unclear (Cochran A. JAMA Surg. 2018 Jan 3. doi: 10.1001/jamasurg.2017.5468. [Epub ahead of print]).

In a survey of over 600 academic intensivists, 55% of the participants stated that attending handoffs in the ICU should be standardized, yet, only 13% of those participating in handoffs reported using a standardized process (Lane-Fall M. Crit Care Med. 2016;44[4]690). Clinician miscommunication contributes to an estimated 250,000 deaths in US hospitals per year (Makary M. BMJ. 2016 May 3;353:i2139. doi: 10.1136/bmj.i2139). Standardized handoffs may improve outcomes in the ICU.

In many ICUs that do use standardized sign-out templates, higher clinician satisfaction and fewer unexpected patient events have been reported (Bavare AC. J Healthc Qual. 2015;37[5]:267; Nanchal R. BMJ Qual Saf. 2017;26[12]:987). In a recent randomized controlled trial, use of a standardized handoff curriculum in the ICU resulted in a significant 3% decrease in communication errors, without any change in the duration of the handoff. There also was a clinician-reported improvement in team communication and patient safety; but no changes in ICU length of stay, duration of mechanical ventilation, or number of re-intubations were noted (JAMA Surg. 2018 Jan 3. doi: 10.1001/jamasurg.2017.5440. [Epub ahead of print]).

Unfortunately, despite interest in improving patient handoffs, there are few tools to evaluate the effectiveness of different handoff strategies. Most studies report clinician perceptions rather than patient-centered outcomes. Further research is required to examine the optimal approach to handover communication. However, based on the available evidence, a standardized approach to handoffs is likely better than a nonstandardized format.

Shruti Gadre, MD
Fellow-in-Training Member

Christopher Carroll, MD, FCCP
Vice-Chair

Home-Based Mechanical Ventilation and Neuromuscular Disease

Update on two recent FDA-approved therapies for ALS and SMA

Amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA) are neuromuscular diseases often deteriorating to progressive respiratory failure. Two medications received recent FDA approval and are now available in clinical practice – edaravone for ALS and nusinersen for SMA. We present a balanced overview of the favorable data along with realistic challenges.

Edaravone (Radicava) is the second FDA-approved medication for management of ALS (Riluzole was approved over 20 years ago). Edaravone is a free radical scavenger that reduces oxidative stress, resulting in a protective effect on neuronal cells. It originally showed promise in acute ischemic stroke in Japan and was subsequently studied for ALS. A phase 3 randomized, double-blind placebo-controlled study performed in Japan (Lancet Neurol. 2017;16[7]:505) compared ALSFRS-R scores of a specific subset of ALS patients receiving edaravone vs placebo. This study revealed that patients with early ALS (2 years duration or less) with rapid progression (ALSFRS-R score of 7.5 in 6 months) had a 33% decrease in their degree of progression (reducing their ALSFRS-R score to 5) in the edaravone group. Of note, there was also slowing in the decline of FVC, though not clinically significant. Although the drug was rapidly approved by the FDA, there are obvious challenges that must be recognized. First, it is unclear if patients will discern such a mild degree of slowing of disease progression. In addition, the annual cost may be prohibitive, and lifelong IV administration of the medication for 10 days every month may pose logistical barriers.

Nusinersen (Spinraza) is the first FDA-approved therapeutic medication for spinal muscular atrophy (SMA). SMA is a hereditary neuromuscular disorder leading to degeneration of motor neuron cells and ultimately diffuse muscle weakness and often respiratory failure. Nusinersen is an antisense oligonucleotide that modifies splicing of the SMN-2 gene to increase production of normal, full-length SMN protein, which is deficient in SMA. The ENDEAR trial (Finkel RS, et al. N Engl J Med. 2017;377[18]:1723) was a phase 3, multicenter, double-blind study that enrolled SMA infants to receive nusinersen vs sham. Infants who received treatment had improvements in motor milestones (41% vs 0%) and less permanent-assisted ventilation or death in the nusinersen group (39% vs 68%), a 47% reduction in risk of death. The therapy is safe and tolerable, although there is reported risk of bleeding abnormalities, renal toxicity, and constipation. Administered intrathecally, there is a series of four loading doses, followed by maintenance doses every 4 months – presumably lifelong. Although FDA approved all three SMA subtypes, the eventual impact is uncertain, especially in cases of advanced muscle weakness. There are realistic challenges: the high cost ($125,000/dose), limited longitudinal evidence, technical administration, and limited access.

Pulmonologists should be aware of both medications as new therapeutic options for ALS and SMA; however, the long-term impact is yet to be determined.

Ashraf Elsayegh, MD, FCCP
Steering Committee Member

Won Y. Lee, MD
Steering Committee Member

Interstitial and Diffuse Lung Disease

Frailty as a measure of disease activity in ILD

Frailty is a systemic geriatric syndrome characterized by age-related accumulation of physiologic deficits across several systems with an attenuated response to biological stress. Considering that interstitial lung disease (ILD), particularly, idiopathic pulmonary fibrosis (IPF), is a disease of the aging population, frailty is an emerging area of clinical interest. The biological pathways driving the association of frailty with worse prognosis are complex but hinge on cellular senescence, systemic inflammation, and sarcopenia.

There is a high prevalence of frailty in adults with chronic lung diseases and is associated with worse prognosis. The current literature, though, is mostly derived from patients with COPD. Frailty measured using the 42-item patient-reported frailty index is associated with dyspnea severity in patients with fibrotic ILD (Milne et al. Respirology. 2017;22[4]:728) and systemic sclerosis-associated ILD (Guler et al. Respir Med. 2017 Aug;129:1-7. doi: 10.1016/j.rmed.2017.05.012. Epub 2017 May 25.). The SHARE-Frailty and the Edmonton Frail Scale instruments utilized to measure frailty in the University of Alabama at Birmingham IPF cohort detected a high-percentage of frail and pre-frail patients (Luckhardt et al. Am J Respir Crit Care Med. 2017;195:A7012). However, there are differences in targeted domains between the various frailty instruments, and this could affect the identification of the frailty syndrome in patients.

Frailty as a measure of disease activity and progression is not currently employed in clinical trials for ILD, primarily due to lack of standardized tools for this patient population. Future studies designed to utilize the frailty syndrome as outcome measures may further our understanding of the clinical manifestations and underlying mechanisms, as well as identify potential therapeutic interventions for patients with ILD.

Tejaswini Kulkarni MD, MPH
Fellow-in-Training Member

Clinical Research

New guidelines for adult bronchiectasis

Clinically significant bronchiectasis is a combination of radiologic bronchial dilatation with clinical symptoms. Guidelines on management of adult bronchiectasis were recently published (Eur Respir J. 2017; Sep 10;50[3]).

For all adult patients with clinically significant bronchiectasis, the guidelines suggest standardized minimum testing with differential blood count, serum immunoglobulins, and testing for allergic bronchopulmonary aspergillosis with any further workup on an individual basis. Annual sputum surveillance is suggested for clinically stable adult patients; however, the evidence for this recommendation came from studies done on patients with cystic fibrosis.

Inhaled bronchodilators are suggested as the first-line treatment in symptomatic patients. Long-term antibiotics (greater than 3 months) are recommended in patients with greater than 3 exacerbations/year after optimizing airway clearance and disease-specific treatment. Pseudomonas aeruginosa infections are to be treated with inhaled antibiotics (colistin or gentamicin) (Charles SH, et al. Am J Respir Crit Care Med. 2014;189[8]975; Murray P, et al. Am J Respir Crit Care Med. 2011;183[4]:491; and nonpseudomonal infections are to be treated with macrolides (Conroy W, et al. Lancet. 2012;380[9842]:660; Altenburg J, et al. JAMA. 2013;309[12];1251), although interchangeable for intolerance. Sputum cultured early will guide therapy among poor responders. Long-term mucolytic agents are suggested in appropriate tolerating patients. Pulmonary rehabilitation for 6-8 weeks is strongly recommended in adult bronchiectasis with impaired exercise capacity. Surgical interventions for bronchiectasis are reserved for a small group of patients who have localized disease and high exacerbation rates despite maximal medical therapy. Inhaled corticosteroids are suggested not to be used in adult bronchiectasis. Guidelines recommend against the use of statins and recombinant human DNase as it increases exacerbations (Chest. 1998;113[5]:1329. The task force acknowledged the low quality of evidence for their recommendations requiring more research in the field of adult bronchiectasis.

Bharat Bajantri, MD
Fellow-in-Training Member

Airways Disorders

ICS/LABA combo therapy: black box warning removed

Publication of the Salmeterol Multicenter Asthma Research Trial (SMART) in 2006 caused panic among asthmatics and the physicians who treat them (Nelson et al. Chest. 2006;129[1]:15). The study suggested that the long-acting beta-2-agonist (LABA) salmeterol leads to an increased risk of asthma/respiratory-related deaths compared with placebo. This finding was more pronounced in the African American subpopulation. The study left many questions unanswered, including whether or not this risk is present when LABA therapy is combined with inhaled corticosteroids (ICS) (O’Byrne. Chest. 2006;129[1]:3). Subsequent meta-analyses confirmed the increased risk with LABA monotherapy but not with LABA/ICS (Salpeter et al. Ann Inter Med. 2006;144[12]: 904; Jaeschke et al. Am J Respir Crit Care Med. 2008;178[10]:1009). Still, a black box warning relating LABA to asthma-related death was applied to LABA/ICS products.

In 2011, the Food and Drug Administration (FDA) mandated large, randomized controlled trials be performed for LABA/ICS products to assess safety. These trials were recently completed, showing no difference in asthma-related deaths between LABA/ICS and ICS alone. There were 41, 297 patients across four trials, three included teenagers and adults (age ≥ 12) and one enrolled children (ages 4-11). These studies prompted the FDA to remove the black box warning from salmeterol/fluticasone, formoterol/budesonide, and formoterol/mometasone (https://wwwfdagov/downloads/Drugs/DrugSafety/UCM589997pdf).

Conclusion: Because LABA/ICS therapy is effective for asthma, most pulmonologists continue to prescribe it despite the SMART study results and FDA warning. In a practical sense, we don’t expect the FDA findings to radically change asthma care. Still, it seems we can finally put this question to rest – LABA/ICS is indeed safe for asthmatics. Most physicians will continue to avoid LABA monotherapy, and now that tiotropium is included in the 2017 GINA guidelines, it’s only matter of time before we’re debating whether LABA/long-acting muscarinic antagonist (LAMA) is safe for asthmatics.

Aaron Holley, MD, FCCP
Steering Committee Member

Navitha Ramesh, MD, MBBS
Fellow-in-Training Member

Critical Care

Standardized handoffs in the ICU: room for improvement?

Transitions in patient care are commonplace in the ICU. But handoffs are particularly susceptible to error given the complexity of the patient population. Impacts of less-than-ideal handoffs likely include adverse events, delays in medical diagnosis and treatment, redundant communications, redundant activities such as additional procedures and tests, lower provider and patient satisfaction, higher costs, longer hospital stays, more hospital admissions, and less effective training for health -care providers. Yet, there is great heterogeneity in handoff practiced, and the impact of standardized handoffs in the ICU is unclear (Cochran A. JAMA Surg. 2018 Jan 3. doi: 10.1001/jamasurg.2017.5468. [Epub ahead of print]).

In a survey of over 600 academic intensivists, 55% of the participants stated that attending handoffs in the ICU should be standardized, yet, only 13% of those participating in handoffs reported using a standardized process (Lane-Fall M. Crit Care Med. 2016;44[4]690). Clinician miscommunication contributes to an estimated 250,000 deaths in US hospitals per year (Makary M. BMJ. 2016 May 3;353:i2139. doi: 10.1136/bmj.i2139). Standardized handoffs may improve outcomes in the ICU.

In many ICUs that do use standardized sign-out templates, higher clinician satisfaction and fewer unexpected patient events have been reported (Bavare AC. J Healthc Qual. 2015;37[5]:267; Nanchal R. BMJ Qual Saf. 2017;26[12]:987). In a recent randomized controlled trial, use of a standardized handoff curriculum in the ICU resulted in a significant 3% decrease in communication errors, without any change in the duration of the handoff. There also was a clinician-reported improvement in team communication and patient safety; but no changes in ICU length of stay, duration of mechanical ventilation, or number of re-intubations were noted (JAMA Surg. 2018 Jan 3. doi: 10.1001/jamasurg.2017.5440. [Epub ahead of print]).

Unfortunately, despite interest in improving patient handoffs, there are few tools to evaluate the effectiveness of different handoff strategies. Most studies report clinician perceptions rather than patient-centered outcomes. Further research is required to examine the optimal approach to handover communication. However, based on the available evidence, a standardized approach to handoffs is likely better than a nonstandardized format.

Shruti Gadre, MD
Fellow-in-Training Member

Christopher Carroll, MD, FCCP
Vice-Chair

Home-Based Mechanical Ventilation and Neuromuscular Disease

Update on two recent FDA-approved therapies for ALS and SMA

Amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA) are neuromuscular diseases often deteriorating to progressive respiratory failure. Two medications received recent FDA approval and are now available in clinical practice – edaravone for ALS and nusinersen for SMA. We present a balanced overview of the favorable data along with realistic challenges.

Edaravone (Radicava) is the second FDA-approved medication for management of ALS (Riluzole was approved over 20 years ago). Edaravone is a free radical scavenger that reduces oxidative stress, resulting in a protective effect on neuronal cells. It originally showed promise in acute ischemic stroke in Japan and was subsequently studied for ALS. A phase 3 randomized, double-blind placebo-controlled study performed in Japan (Lancet Neurol. 2017;16[7]:505) compared ALSFRS-R scores of a specific subset of ALS patients receiving edaravone vs placebo. This study revealed that patients with early ALS (2 years duration or less) with rapid progression (ALSFRS-R score of 7.5 in 6 months) had a 33% decrease in their degree of progression (reducing their ALSFRS-R score to 5) in the edaravone group. Of note, there was also slowing in the decline of FVC, though not clinically significant. Although the drug was rapidly approved by the FDA, there are obvious challenges that must be recognized. First, it is unclear if patients will discern such a mild degree of slowing of disease progression. In addition, the annual cost may be prohibitive, and lifelong IV administration of the medication for 10 days every month may pose logistical barriers.

Nusinersen (Spinraza) is the first FDA-approved therapeutic medication for spinal muscular atrophy (SMA). SMA is a hereditary neuromuscular disorder leading to degeneration of motor neuron cells and ultimately diffuse muscle weakness and often respiratory failure. Nusinersen is an antisense oligonucleotide that modifies splicing of the SMN-2 gene to increase production of normal, full-length SMN protein, which is deficient in SMA. The ENDEAR trial (Finkel RS, et al. N Engl J Med. 2017;377[18]:1723) was a phase 3, multicenter, double-blind study that enrolled SMA infants to receive nusinersen vs sham. Infants who received treatment had improvements in motor milestones (41% vs 0%) and less permanent-assisted ventilation or death in the nusinersen group (39% vs 68%), a 47% reduction in risk of death. The therapy is safe and tolerable, although there is reported risk of bleeding abnormalities, renal toxicity, and constipation. Administered intrathecally, there is a series of four loading doses, followed by maintenance doses every 4 months – presumably lifelong. Although FDA approved all three SMA subtypes, the eventual impact is uncertain, especially in cases of advanced muscle weakness. There are realistic challenges: the high cost ($125,000/dose), limited longitudinal evidence, technical administration, and limited access.

Pulmonologists should be aware of both medications as new therapeutic options for ALS and SMA; however, the long-term impact is yet to be determined.

Ashraf Elsayegh, MD, FCCP
Steering Committee Member

Won Y. Lee, MD
Steering Committee Member

Interstitial and Diffuse Lung Disease

Frailty as a measure of disease activity in ILD

Frailty is a systemic geriatric syndrome characterized by age-related accumulation of physiologic deficits across several systems with an attenuated response to biological stress. Considering that interstitial lung disease (ILD), particularly, idiopathic pulmonary fibrosis (IPF), is a disease of the aging population, frailty is an emerging area of clinical interest. The biological pathways driving the association of frailty with worse prognosis are complex but hinge on cellular senescence, systemic inflammation, and sarcopenia.

There is a high prevalence of frailty in adults with chronic lung diseases and is associated with worse prognosis. The current literature, though, is mostly derived from patients with COPD. Frailty measured using the 42-item patient-reported frailty index is associated with dyspnea severity in patients with fibrotic ILD (Milne et al. Respirology. 2017;22[4]:728) and systemic sclerosis-associated ILD (Guler et al. Respir Med. 2017 Aug;129:1-7. doi: 10.1016/j.rmed.2017.05.012. Epub 2017 May 25.). The SHARE-Frailty and the Edmonton Frail Scale instruments utilized to measure frailty in the University of Alabama at Birmingham IPF cohort detected a high-percentage of frail and pre-frail patients (Luckhardt et al. Am J Respir Crit Care Med. 2017;195:A7012). However, there are differences in targeted domains between the various frailty instruments, and this could affect the identification of the frailty syndrome in patients.

Frailty as a measure of disease activity and progression is not currently employed in clinical trials for ILD, primarily due to lack of standardized tools for this patient population. Future studies designed to utilize the frailty syndrome as outcome measures may further our understanding of the clinical manifestations and underlying mechanisms, as well as identify potential therapeutic interventions for patients with ILD.

Tejaswini Kulkarni MD, MPH
Fellow-in-Training Member

Clinical Research

New guidelines for adult bronchiectasis

Clinically significant bronchiectasis is a combination of radiologic bronchial dilatation with clinical symptoms. Guidelines on management of adult bronchiectasis were recently published (Eur Respir J. 2017; Sep 10;50[3]).

For all adult patients with clinically significant bronchiectasis, the guidelines suggest standardized minimum testing with differential blood count, serum immunoglobulins, and testing for allergic bronchopulmonary aspergillosis with any further workup on an individual basis. Annual sputum surveillance is suggested for clinically stable adult patients; however, the evidence for this recommendation came from studies done on patients with cystic fibrosis.

Inhaled bronchodilators are suggested as the first-line treatment in symptomatic patients. Long-term antibiotics (greater than 3 months) are recommended in patients with greater than 3 exacerbations/year after optimizing airway clearance and disease-specific treatment. Pseudomonas aeruginosa infections are to be treated with inhaled antibiotics (colistin or gentamicin) (Charles SH, et al. Am J Respir Crit Care Med. 2014;189[8]975; Murray P, et al. Am J Respir Crit Care Med. 2011;183[4]:491; and nonpseudomonal infections are to be treated with macrolides (Conroy W, et al. Lancet. 2012;380[9842]:660; Altenburg J, et al. JAMA. 2013;309[12];1251), although interchangeable for intolerance. Sputum cultured early will guide therapy among poor responders. Long-term mucolytic agents are suggested in appropriate tolerating patients. Pulmonary rehabilitation for 6-8 weeks is strongly recommended in adult bronchiectasis with impaired exercise capacity. Surgical interventions for bronchiectasis are reserved for a small group of patients who have localized disease and high exacerbation rates despite maximal medical therapy. Inhaled corticosteroids are suggested not to be used in adult bronchiectasis. Guidelines recommend against the use of statins and recombinant human DNase as it increases exacerbations (Chest. 1998;113[5]:1329. The task force acknowledged the low quality of evidence for their recommendations requiring more research in the field of adult bronchiectasis.

Bharat Bajantri, MD
Fellow-in-Training Member

Airways Disorders

ICS/LABA combo therapy: black box warning removed

Publication of the Salmeterol Multicenter Asthma Research Trial (SMART) in 2006 caused panic among asthmatics and the physicians who treat them (Nelson et al. Chest. 2006;129[1]:15). The study suggested that the long-acting beta-2-agonist (LABA) salmeterol leads to an increased risk of asthma/respiratory-related deaths compared with placebo. This finding was more pronounced in the African American subpopulation. The study left many questions unanswered, including whether or not this risk is present when LABA therapy is combined with inhaled corticosteroids (ICS) (O’Byrne. Chest. 2006;129[1]:3). Subsequent meta-analyses confirmed the increased risk with LABA monotherapy but not with LABA/ICS (Salpeter et al. Ann Inter Med. 2006;144[12]: 904; Jaeschke et al. Am J Respir Crit Care Med. 2008;178[10]:1009). Still, a black box warning relating LABA to asthma-related death was applied to LABA/ICS products.

In 2011, the Food and Drug Administration (FDA) mandated large, randomized controlled trials be performed for LABA/ICS products to assess safety. These trials were recently completed, showing no difference in asthma-related deaths between LABA/ICS and ICS alone. There were 41, 297 patients across four trials, three included teenagers and adults (age ≥ 12) and one enrolled children (ages 4-11). These studies prompted the FDA to remove the black box warning from salmeterol/fluticasone, formoterol/budesonide, and formoterol/mometasone (https://wwwfdagov/downloads/Drugs/DrugSafety/UCM589997pdf).

Conclusion: Because LABA/ICS therapy is effective for asthma, most pulmonologists continue to prescribe it despite the SMART study results and FDA warning. In a practical sense, we don’t expect the FDA findings to radically change asthma care. Still, it seems we can finally put this question to rest – LABA/ICS is indeed safe for asthmatics. Most physicians will continue to avoid LABA monotherapy, and now that tiotropium is included in the 2017 GINA guidelines, it’s only matter of time before we’re debating whether LABA/long-acting muscarinic antagonist (LAMA) is safe for asthmatics.

Aaron Holley, MD, FCCP
Steering Committee Member

Navitha Ramesh, MD, MBBS
Fellow-in-Training Member

Critical Care

Standardized handoffs in the ICU: room for improvement?

Transitions in patient care are commonplace in the ICU. But handoffs are particularly susceptible to error given the complexity of the patient population. Impacts of less-than-ideal handoffs likely include adverse events, delays in medical diagnosis and treatment, redundant communications, redundant activities such as additional procedures and tests, lower provider and patient satisfaction, higher costs, longer hospital stays, more hospital admissions, and less effective training for health -care providers. Yet, there is great heterogeneity in handoff practiced, and the impact of standardized handoffs in the ICU is unclear (Cochran A. JAMA Surg. 2018 Jan 3. doi: 10.1001/jamasurg.2017.5468. [Epub ahead of print]).

In a survey of over 600 academic intensivists, 55% of the participants stated that attending handoffs in the ICU should be standardized, yet, only 13% of those participating in handoffs reported using a standardized process (Lane-Fall M. Crit Care Med. 2016;44[4]690). Clinician miscommunication contributes to an estimated 250,000 deaths in US hospitals per year (Makary M. BMJ. 2016 May 3;353:i2139. doi: 10.1136/bmj.i2139). Standardized handoffs may improve outcomes in the ICU.

In many ICUs that do use standardized sign-out templates, higher clinician satisfaction and fewer unexpected patient events have been reported (Bavare AC. J Healthc Qual. 2015;37[5]:267; Nanchal R. BMJ Qual Saf. 2017;26[12]:987). In a recent randomized controlled trial, use of a standardized handoff curriculum in the ICU resulted in a significant 3% decrease in communication errors, without any change in the duration of the handoff. There also was a clinician-reported improvement in team communication and patient safety; but no changes in ICU length of stay, duration of mechanical ventilation, or number of re-intubations were noted (JAMA Surg. 2018 Jan 3. doi: 10.1001/jamasurg.2017.5440. [Epub ahead of print]).

Unfortunately, despite interest in improving patient handoffs, there are few tools to evaluate the effectiveness of different handoff strategies. Most studies report clinician perceptions rather than patient-centered outcomes. Further research is required to examine the optimal approach to handover communication. However, based on the available evidence, a standardized approach to handoffs is likely better than a nonstandardized format.

Shruti Gadre, MD
Fellow-in-Training Member

Christopher Carroll, MD, FCCP
Vice-Chair

Home-Based Mechanical Ventilation and Neuromuscular Disease

Update on two recent FDA-approved therapies for ALS and SMA

Amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA) are neuromuscular diseases often deteriorating to progressive respiratory failure. Two medications received recent FDA approval and are now available in clinical practice – edaravone for ALS and nusinersen for SMA. We present a balanced overview of the favorable data along with realistic challenges.

Edaravone (Radicava) is the second FDA-approved medication for management of ALS (Riluzole was approved over 20 years ago). Edaravone is a free radical scavenger that reduces oxidative stress, resulting in a protective effect on neuronal cells. It originally showed promise in acute ischemic stroke in Japan and was subsequently studied for ALS. A phase 3 randomized, double-blind placebo-controlled study performed in Japan (Lancet Neurol. 2017;16[7]:505) compared ALSFRS-R scores of a specific subset of ALS patients receiving edaravone vs placebo. This study revealed that patients with early ALS (2 years duration or less) with rapid progression (ALSFRS-R score of 7.5 in 6 months) had a 33% decrease in their degree of progression (reducing their ALSFRS-R score to 5) in the edaravone group. Of note, there was also slowing in the decline of FVC, though not clinically significant. Although the drug was rapidly approved by the FDA, there are obvious challenges that must be recognized. First, it is unclear if patients will discern such a mild degree of slowing of disease progression. In addition, the annual cost may be prohibitive, and lifelong IV administration of the medication for 10 days every month may pose logistical barriers.

Nusinersen (Spinraza) is the first FDA-approved therapeutic medication for spinal muscular atrophy (SMA). SMA is a hereditary neuromuscular disorder leading to degeneration of motor neuron cells and ultimately diffuse muscle weakness and often respiratory failure. Nusinersen is an antisense oligonucleotide that modifies splicing of the SMN-2 gene to increase production of normal, full-length SMN protein, which is deficient in SMA. The ENDEAR trial (Finkel RS, et al. N Engl J Med. 2017;377[18]:1723) was a phase 3, multicenter, double-blind study that enrolled SMA infants to receive nusinersen vs sham. Infants who received treatment had improvements in motor milestones (41% vs 0%) and less permanent-assisted ventilation or death in the nusinersen group (39% vs 68%), a 47% reduction in risk of death. The therapy is safe and tolerable, although there is reported risk of bleeding abnormalities, renal toxicity, and constipation. Administered intrathecally, there is a series of four loading doses, followed by maintenance doses every 4 months – presumably lifelong. Although FDA approved all three SMA subtypes, the eventual impact is uncertain, especially in cases of advanced muscle weakness. There are realistic challenges: the high cost ($125,000/dose), limited longitudinal evidence, technical administration, and limited access.

Pulmonologists should be aware of both medications as new therapeutic options for ALS and SMA; however, the long-term impact is yet to be determined.

Ashraf Elsayegh, MD, FCCP
Steering Committee Member

Won Y. Lee, MD
Steering Committee Member

Interstitial and Diffuse Lung Disease

Frailty as a measure of disease activity in ILD

Frailty is a systemic geriatric syndrome characterized by age-related accumulation of physiologic deficits across several systems with an attenuated response to biological stress. Considering that interstitial lung disease (ILD), particularly, idiopathic pulmonary fibrosis (IPF), is a disease of the aging population, frailty is an emerging area of clinical interest. The biological pathways driving the association of frailty with worse prognosis are complex but hinge on cellular senescence, systemic inflammation, and sarcopenia.

There is a high prevalence of frailty in adults with chronic lung diseases and is associated with worse prognosis. The current literature, though, is mostly derived from patients with COPD. Frailty measured using the 42-item patient-reported frailty index is associated with dyspnea severity in patients with fibrotic ILD (Milne et al. Respirology. 2017;22[4]:728) and systemic sclerosis-associated ILD (Guler et al. Respir Med. 2017 Aug;129:1-7. doi: 10.1016/j.rmed.2017.05.012. Epub 2017 May 25.). The SHARE-Frailty and the Edmonton Frail Scale instruments utilized to measure frailty in the University of Alabama at Birmingham IPF cohort detected a high-percentage of frail and pre-frail patients (Luckhardt et al. Am J Respir Crit Care Med. 2017;195:A7012). However, there are differences in targeted domains between the various frailty instruments, and this could affect the identification of the frailty syndrome in patients.

Frailty as a measure of disease activity and progression is not currently employed in clinical trials for ILD, primarily due to lack of standardized tools for this patient population. Future studies designed to utilize the frailty syndrome as outcome measures may further our understanding of the clinical manifestations and underlying mechanisms, as well as identify potential therapeutic interventions for patients with ILD.

Tejaswini Kulkarni MD, MPH
Fellow-in-Training Member