could not be explored in this study. Within the group of patients with RA, further risk factors for developing mycobacterial infections included chronic kidney disease, asthma, and COPD. A relationship between end-stage renal disease and TB has long been known but has not been described previously in NTM. The link between COPD and NTM has been described previously,6-8 but a relationship with asthma is more novel, if confirmed in future studies. Some patients with COPD may have a component of bronchiectasis that predisposes to NTM infection, or the additional steroids used to treat COPD and asthma may contribute to increased susceptibility to infection. In this study, diabetes and HIV infection did not further amplify the risk accorded by RA. In the case of HIV, there may simply have been too few patients to detect an effect. Diabetes has been clearly shown to be a risk factor for TB, but the effect on NTM here may have been swamped by the immunosuppression associated with RA or its treatment. The current study does not address issues of treatment or the effect of treatment on outcomes. Given the increased risk of mortality the authors detected in patients with RA and NTM, this should be a subject of considerable concern and focus in the future. In general, treatment of NTM is often a complex and frustrating endeavor. Physicians often elect not to treat elderly patients with NTM (usually M avium complex) if their symptoms are limited to cough, which is commonly the case. If treatment is initiated, a three-drug regimen of a macrolide, a rifamycin (rifampin or rifabutin), and ethambutol is preferred, and in many patients this regimen can be given thrice weekly.9,10 No randomized trials have been done to evaluate this regimen, although observational studies have indicated clinical and microbiologic improvement with this regimen in a considerable number of patients. Conducting trials in patients with complex conditions such as those in this study should be a particular priority. The group, led by Dr Marras, the senior author on the current study,5 should be commended for their focus on NTM disease and for their many important insights. We anticipate further elucidation on this complex subject from them in the future.
References 1. Bodle EE, Cunningham JA, Della-Latta P, Schluger NW, Saiman L. Epidemiology of nontuberculous mycobacteria in patients without HIV infection, New York City. Emerg Infect Dis. 2008;14(3):390-396. 2. Kendall BA, Winthrop KL. Update on the epidemiology of pulmonary nontuberculous mycobacterial infections. Semin Respir Crit Care Med. 2013;34(1):87-94.
530 Editorials
3. Marras TK, Mendelson D, Marchand-Austin A, May K, Jamieson FB. Pulmonary nontuberculous mycobacterial disease, Ontario, Canada, 1998-2010. Emerg Infect Dis. 2013;19(11):1889-1891. 4. Keane J, Gershon S, Wise RP, et al. Tuberculosis associated with infliximab, a tumor necrosis factor alpha-neutralizing agent. N Engl J Med. 2001;345(15):1098-1104. 5. Brode SK, Jamieson FB, Ng R, et al. Risk of mycobacterial infections associated with rheumatoid arthritis in Ontario, Canada. Chest. 2014;146(3):563-572. 6. Huang CT, Tsai YJ, Wu HD, et al. Impact of non-tuberculous mycobacteria on pulmonary function decline in chronic obstructive pulmonary disease. Int J Tuberc Lung Dis. 2012;16(4):539-545. 7. Chan ED, Iseman MD. Underlying host risk factors for nontuberculous mycobacterial lung disease. Semin Respir Crit Care Med. 2013;34(1): 110-123. 8. de Mello KG, Mello FC, Borga L, et al. Clinical and therapeutic features of pulmonary nontuberculous mycobacterial disease, Brazil, 1993-2011. Emerg Infect Dis. 2013;19(3):393-399. 9. Wallace RJ Jr, Brown-Elliott BA, McNulty S, et al. Macrolide/azalide therapy for nodular/bronchiectatic: Mycobacterium avium complex lung disease. Chest. 2014;146(2):276-282. 10. Lam PK, Griffith DE, Aksamit TR, et al. Factors related to response to intermittent treatment of Mycobacterium avium complex lung disease. Am J Respir Crit Care Med. 2006;173(11):1283-1289.
Choose Wisely Endobronchial Ultrasound-Guided Transbronchial Needle Aspiration for Sarcoidosis Atul C. Mehta, MBBS, FCCP Francisco A. Almeida, MD, FCCP Cleveland, OH
You must choose. But choose wisely. Indiana Jones and the Last Crusade1
Confirming the diagnosis of sarcoidosis presents a plethora of options to the pulmonologist, ranging from a close follow-up to an open lung biopsy. Flexible bronchoscopy and conventional transbronchial needle aspiration (cTBNA) have empowered bronchoscopists in the confirmation of sarcoidosis since their introduction in the late 1960s and 1980s, respectively.2 The last decade has witnessed the addition of endobronchial AFFILIATIONS:
From the Department of Pulmonary Medicine, Respiratory Institute, Cleveland Clinic. FINANCIAL/NONFINANCIAL DISCLOSURES: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article. CORRESPONDENCE TO: Atul C. Mehta, MBBS, FCCP, Respiratory Institute, Cleveland Clinic, 9500 Euclid Ave, A-90, Cleveland, OH 44195; e-mail: [email protected] © 2014 AMERICAN COLLEGE OF CHEST PHYSICIANS. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details. DOI: 10.1378/chest.14-0374
[
146#3 CHEST SEPTEMBER 2014
]
ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) and esophageal ultrasound (EUS) to the bronchoscopist’s armamentarium for confirming sarcoidosis.3 In fact, some investigators now consider EBUS-TBNA and EUS-guided TBNA as the “only game in town” for the confirmation of sarcoidosis.3-5 We, however, believe that although EBUS-TBNA and EUSguided TBNA have an undisputed role in staging nonsmall cell lung carcinoma, its usefulness as an exclusive test for sarcoidosis warrants careful consideration. The elephant in the room is, “is it really essential to establish the diagnosis in all patients with suspected sarcoidosis?” In most cases, clinical presentation of stage I sarcoidosis is characteristic, and, hence, invasive diagnostic testing would be unnecessary. The astute remarks by Winterbauer and colleagues6 have withstood the test of time and are further corroborated by the statistical analysis of Reich and colleagues.6,7 Accordingly, one would have to perform . 10,000 invasive diagnostic procedures to identify no more than five alternative diagnoses in patients presenting with stage I sarcoidosis.7,8 Furthermore, close clinical follow-up in a majority of these patients can easily establish sarcoidosis without any intervention. Thus, the results of the endobronchial ultrasound (EBUS)- and EUS-related studies that have included stage I sarcoidosis should be interpreted with great caution.9 Additional parameters affecting the choice of a diagnostic procedure for confirming sarcoidosis include availability, affordability, accuracy, and safety in conjunction with the performer’s ability and competence.10 Currently, in developing countries, the availability and affordability of EBUS-TBNA remains questionable. In addition, training for EBUS-TBNA can be challenging and is complicated by lung ailments that mimic sarcoidosis, especially in developing countries.11 Moreover, incorporating EUS in the diagnostic algorithm further adds to competency problems all over the world.9 In this issue of CHEST (see page 547), Gupta and colleagues12 address the issue of accuracy and safety of EBUS-TBNA over cTBNA in patients suspected to have sarcoidosis, when performed in conjunction with conventional transbronchial and endobronchial biopsies. They make a convincing argument that even though individually EBUS-TBNA has the highest diagnostic yield in sarcoidosis, it should be combined with transbronchial lung biopsy for optimal results. Besides, the diagnostic yield of cTBNA plus endobronchial and transbronchial
journal.publications.chestnet.org
biopsies is similar to EBUS-TBNA plus the transbronchial lung biopsy. We applaud their efforts and agree with the conclusions. However, we would like to point out that . 50% of the patients in this study had pulmonary infiltrates, possibly explaining the lack of superiority of EBUS-TBNA compared with the transbronchial lung biopsy in detecting granulomas.13 Although this fact does not undermine the results, it reinforces the concept of “choosing wisely.” A very small number of individuals in this study were treated for or diagnosed with sarcoidosis in the absence of a pathologic confirmation. Perhaps in these patients bronchoscopy may not be necessary.14 On the other hand, considering the prevalence of TB in the community, it is possible that the samples obtained made the latter diagnosis less likely.13 From a pure clinical perspective, diagnostic uncertainty must be considered before subjecting a patient to an invasive diagnostic procedure.12 Thus, if the finding of a “good granuloma” (nonnecrotizing granuloma) will not change the management, invasive tests are not necessary.5,6 Second, the operator must be familiar with the yield of the chosen procedure for the specific diagnosis under consideration. To that end, we believe that a nondiagnostic bronchoscopy can be more harmful than the fear of complications. Therefore, the bronchoscopist must be equipped with the minimal necessary tools and skills to avoid a nondiagnostic outcome.9 Although no major adverse events were observed in this study, transbronchial lung biopsy is commonly associated with more complications compared with other bronchoscopic techniques.15,16 If a rapid on-site cytologic evaluation is available, EBUS-TBNA can avoid additional sampling (endobronchial and transbronchial biopsies) and related complications, especially among patients without parenchymal infiltrates.17,18 On the other hand, in patients with predominant pulmonary infiltrates from presumed sarcoidosis, rapid on-site cytologic evaluation has no benefit either with EBUS or cTBNA.13,19 From a global perspective, the cost and the required skills associated with EBUS, EUS, and rapid on-site cytologic evaluation can interfere with the worldwide use of these technologies in the near future.19 Thus, although the present study suggests that cTBNA in combination with endobronchial and transbronchial lung biopsies, and perhaps the latter alone in patients with parenchymal infiltrates, is sufficient to establish the diagnosis of sarcoidosis, we believe that unavailability of EBUS should not hinder an experienced bronchoscopist.
531
We, therefore, encourage standard bronchoscopy with conventional tools in the appropriate clinical setting and propose the notion of “choosing wisely,” wherein both pulmonologists and institutions select their techniques and investments based on their patient population and available skills.
Variability in Decisions to Limit Life-Sustaining Treatments
Acknowledgments
J. Randall Curtis, MD, MPH
Other contributions: We thank Nirupama Mulherkar, PhD, for writing assistance.
Seattle, WA
Is It All About the Physician? Amber E. Barnato, MD, MPH Pittsburgh, PA
References 1. Indiana Jones and the Last Crusade. Dir: Steven Spielberg. Paramount Pictures, 1989. Film. 2. Wang KP, Fuenning C, Johns CJ, Terry PB. Flexible transbronchial needle aspiration for the diagnosis of sarcoidosis. Ann Otol Rhinol Laryngol. 1989;98(4 pt 1):298-300. 3. von Bartheld MB, Dekkers OM, Szlubowski A, et al. Endosonography vs conventional bronchoscopy for the diagnosis of sarcoidosis: the GRANULOMA randomized clinical trial. JAMA. 2013;309(23):2457-2464. 4. Annema JT, van Meerbeeck JP, Rintoul RC, et al. Mediastinoscopy vs endosonography for mediastinal nodal staging of lung cancer: a randomized trial. JAMA. 2010;304(20):2245-2252. 5. Culver DA, Costabel U. EBUS-TBNA for the diagnosis of sarcoidosis: is it the only game in town? J Bronchology Interv Pulmonol. 2013;20(3):195-197. 6. Winterbauer RH, Belic N, Moores KD. Clinical interpretation of bilateral hilar adenopathy. Ann Intern Med. 1973;78(1):65-71. 7. Reich JM, Brouns MC, O’Connor EA, Edwards MJ. Mediastinoscopy in patients with presumptive stage I sarcoidosis: a risk/benefit, cost/benefit analysis. Chest. 1998;113(1):147-153. 8. Reich JM. Tissue confirmation of presumptive stage I sarcoidosis. J Bronchology Interv Pulmonol. 2013;20(2):103-105. 9. Narula T, Baughman RP, Mehta AC. “Sarcoidosis Americana-route Europa.” J Bronchology Interv Pulmonol. 2013;20(4):293-296. 10. Mehta AC, Mazzone PJ. An attempt to reach the galaxy of the pulmonary nodules. Am J Respir Crit Care Med. 2013;188(3): 264-265. 11. Mehta AC, Wang KP. Teaching conventional transbronchial needle aspiration. A continuum. Ann Am Thorac Soc. 2013;10(6): 685-689. 12. Gupta D, Dadhwal DS, Agarwal R, Gupta N, Bal A, Aggarwal AN. Endobronchial ultrasound-guided transbronchial needle aspiration vs conventional transbronchial needle aspiration in the diagnosis of sarcoidosis. Chest. 2014;146(3):547-556. 13. de Boer S, Milne DG, Zeng I, Wilsher ML. Does CT scanning predict the likelihood of a positive transbronchial biopsy in sarcoidosis? Thorax. 2009;64(5):436-439. 14. Ribeiro Neto ML, Culver DA, Mehta AC. Sarcoidosis—no business of the bronchoscopist. J Thorac Cardiovasc Surg. 2012;144(5):1276-1277. 15. Almeida FA, Casal RF, Jimenez CA, et al. Quality gaps and comparative effectiveness in lung cancer staging: the impact of test sequencing on outcomes. Chest. 2013;144(6):1776-1782. 16. Hernández Blasco L, Sánchez Hernández IM, Villena Garrido V, de Miguel Poch E, Nuñez Delgado M, Alfaro Abreu J. Safety of the transbronchial biopsy in outpatients. Chest. 1991;99(3):562-565. 17. Pue CA, Pacht ER. Complications of fiberoptic bronchoscopy at a university hospital. Chest. 1995;107(2):430-432. 18. Plit ML, Havryk AP, Hodgson A, et al. Rapid cytological analysis of endobronchial ultrasound-guided aspirates in sarcoidosis. Eur Respir J. 2013;42(5):1302-1308. 19. Cicenia J, Almeida F, Machuzak M, et al. The utility of rapid on-site evaluation (ROSE) in the detection of granulomas in mediastinal lymph nodes. Chest. 2013;144(4_MeetingAbstracts):797A.
532 Editorials
Approximately 20% of deaths in the United States occur in or shortly after a stay in the ICU, and the proportion of Medicare beneficiaries who spend time in the ICU in the last 30 days of their lives is increasing.1,2 Of the deaths occurring in the ICU, the majority involve decisions to withhold or withdraw life-sustaining treatments. Studies from the past century documented dramatic variability from ICU to ICU in the proportion of deaths preceded by withholding and withdrawing life-sustaining treatments.3 An article by Quill and colleagues4 in this issue of CHEST (see page 573) shows that dramatic variability persists—sixfold—in these decisions from ICU to ICU, even after adjusting for patient and ICU factors. Why might this variability exist? If such variability is explained by systematic variability from ICU to ICU in patient or family preferences for care at the end of life, it might be an indication of patient- and family-centered care. However, this is unlikely. Although there is regional variability in patient preferences for end-of-life care, the variability in intensity of care at the end of life is not explained by variability in patient preferences.5 Indeed, there is compelling evidence that considerable variability in decision-making about withdrawing life support in the ICU is explained by individual physicians, even after adjusting for patient characteristics.6 AFFILIATIONS:
From the Division of Pulmonary and Critical Care Medicine (Dr Curtis), Harborview Medical Center, University of Washington; and Division of General Internal Medicine (Dr Barnato), Department of Medicine, University of Pittsburgh. FINANCIAL/NONFINANCIAL DISCLOSURES: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article. CORRESPONDENCE TO: J. Randall Curtis, MD, MPH, Division of Pulmonary and Critical Care Medicine, Harborview Medical Center, University of Washington, Box 359762, 325 Ninth Ave, Seattle, WA 98104; e-mail: [email protected] © 2014 AMERICAN COLLEGE OF CHEST PHYSICIANS. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details. DOI: 10.1378/chest.14-0636
[
146#3 CHEST SEPTEMBER 2014
]
References 1. Bodle EE, Cunningham JA, Della-Latta P, Schluger NW, Saiman L. Epidemiology of nontuberculous mycobacteria in patients without HIV infection, New York City. Emerg Infect Dis. 2008;14(3):390-396. 2. Kendall BA, Winthrop KL. Update on the epidemiology of pulmonary nontuberculous mycobacterial infections. Semin Respir Crit Care Med. 2013;34(1):87-94.
530 Editorials
3. Marras TK, Mendelson D, Marchand-Austin A, May K, Jamieson FB. Pulmonary nontuberculous mycobacterial disease, Ontario, Canada, 1998-2010. Emerg Infect Dis. 2013;19(11):1889-1891. 4. Keane J, Gershon S, Wise RP, et al. Tuberculosis associated with infliximab, a tumor necrosis factor alpha-neutralizing agent. N Engl J Med. 2001;345(15):1098-1104. 5. Brode SK, Jamieson FB, Ng R, et al. Risk of mycobacterial infections associated with rheumatoid arthritis in Ontario, Canada. Chest. 2014;146(3):563-572. 6. Huang CT, Tsai YJ, Wu HD, et al. Impact of non-tuberculous mycobacteria on pulmonary function decline in chronic obstructive pulmonary disease. Int J Tuberc Lung Dis. 2012;16(4):539-545. 7. Chan ED, Iseman MD. Underlying host risk factors for nontuberculous mycobacterial lung disease. Semin Respir Crit Care Med. 2013;34(1): 110-123. 8. de Mello KG, Mello FC, Borga L, et al. Clinical and therapeutic features of pulmonary nontuberculous mycobacterial disease, Brazil, 1993-2011. Emerg Infect Dis. 2013;19(3):393-399. 9. Wallace RJ Jr, Brown-Elliott BA, McNulty S, et al. Macrolide/azalide therapy for nodular/bronchiectatic: Mycobacterium avium complex lung disease. Chest. 2014;146(2):276-282. 10. Lam PK, Griffith DE, Aksamit TR, et al. Factors related to response to intermittent treatment of Mycobacterium avium complex lung disease. Am J Respir Crit Care Med. 2006;173(11):1283-1289.
Choose Wisely Endobronchial Ultrasound-Guided Transbronchial Needle Aspiration for Sarcoidosis Atul C. Mehta, MBBS, FCCP Francisco A. Almeida, MD, FCCP Cleveland, OH
You must choose. But choose wisely. Indiana Jones and the Last Crusade1
Confirming the diagnosis of sarcoidosis presents a plethora of options to the pulmonologist, ranging from a close follow-up to an open lung biopsy. Flexible bronchoscopy and conventional transbronchial needle aspiration (cTBNA) have empowered bronchoscopists in the confirmation of sarcoidosis since their introduction in the late 1960s and 1980s, respectively.2 The last decade has witnessed the addition of endobronchial AFFILIATIONS:
From the Department of Pulmonary Medicine, Respiratory Institute, Cleveland Clinic. FINANCIAL/NONFINANCIAL DISCLOSURES: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article. CORRESPONDENCE TO: Atul C. Mehta, MBBS, FCCP, Respiratory Institute, Cleveland Clinic, 9500 Euclid Ave, A-90, Cleveland, OH 44195; e-mail: [email protected] © 2014 AMERICAN COLLEGE OF CHEST PHYSICIANS. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details. DOI: 10.1378/chest.14-0374
[
146#3 CHEST SEPTEMBER 2014
]
ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) and esophageal ultrasound (EUS) to the bronchoscopist’s armamentarium for confirming sarcoidosis.3 In fact, some investigators now consider EBUS-TBNA and EUS-guided TBNA as the “only game in town” for the confirmation of sarcoidosis.3-5 We, however, believe that although EBUS-TBNA and EUSguided TBNA have an undisputed role in staging nonsmall cell lung carcinoma, its usefulness as an exclusive test for sarcoidosis warrants careful consideration. The elephant in the room is, “is it really essential to establish the diagnosis in all patients with suspected sarcoidosis?” In most cases, clinical presentation of stage I sarcoidosis is characteristic, and, hence, invasive diagnostic testing would be unnecessary. The astute remarks by Winterbauer and colleagues6 have withstood the test of time and are further corroborated by the statistical analysis of Reich and colleagues.6,7 Accordingly, one would have to perform . 10,000 invasive diagnostic procedures to identify no more than five alternative diagnoses in patients presenting with stage I sarcoidosis.7,8 Furthermore, close clinical follow-up in a majority of these patients can easily establish sarcoidosis without any intervention. Thus, the results of the endobronchial ultrasound (EBUS)- and EUS-related studies that have included stage I sarcoidosis should be interpreted with great caution.9 Additional parameters affecting the choice of a diagnostic procedure for confirming sarcoidosis include availability, affordability, accuracy, and safety in conjunction with the performer’s ability and competence.10 Currently, in developing countries, the availability and affordability of EBUS-TBNA remains questionable. In addition, training for EBUS-TBNA can be challenging and is complicated by lung ailments that mimic sarcoidosis, especially in developing countries.11 Moreover, incorporating EUS in the diagnostic algorithm further adds to competency problems all over the world.9 In this issue of CHEST (see page 547), Gupta and colleagues12 address the issue of accuracy and safety of EBUS-TBNA over cTBNA in patients suspected to have sarcoidosis, when performed in conjunction with conventional transbronchial and endobronchial biopsies. They make a convincing argument that even though individually EBUS-TBNA has the highest diagnostic yield in sarcoidosis, it should be combined with transbronchial lung biopsy for optimal results. Besides, the diagnostic yield of cTBNA plus endobronchial and transbronchial
journal.publications.chestnet.org
biopsies is similar to EBUS-TBNA plus the transbronchial lung biopsy. We applaud their efforts and agree with the conclusions. However, we would like to point out that . 50% of the patients in this study had pulmonary infiltrates, possibly explaining the lack of superiority of EBUS-TBNA compared with the transbronchial lung biopsy in detecting granulomas.13 Although this fact does not undermine the results, it reinforces the concept of “choosing wisely.” A very small number of individuals in this study were treated for or diagnosed with sarcoidosis in the absence of a pathologic confirmation. Perhaps in these patients bronchoscopy may not be necessary.14 On the other hand, considering the prevalence of TB in the community, it is possible that the samples obtained made the latter diagnosis less likely.13 From a pure clinical perspective, diagnostic uncertainty must be considered before subjecting a patient to an invasive diagnostic procedure.12 Thus, if the finding of a “good granuloma” (nonnecrotizing granuloma) will not change the management, invasive tests are not necessary.5,6 Second, the operator must be familiar with the yield of the chosen procedure for the specific diagnosis under consideration. To that end, we believe that a nondiagnostic bronchoscopy can be more harmful than the fear of complications. Therefore, the bronchoscopist must be equipped with the minimal necessary tools and skills to avoid a nondiagnostic outcome.9 Although no major adverse events were observed in this study, transbronchial lung biopsy is commonly associated with more complications compared with other bronchoscopic techniques.15,16 If a rapid on-site cytologic evaluation is available, EBUS-TBNA can avoid additional sampling (endobronchial and transbronchial biopsies) and related complications, especially among patients without parenchymal infiltrates.17,18 On the other hand, in patients with predominant pulmonary infiltrates from presumed sarcoidosis, rapid on-site cytologic evaluation has no benefit either with EBUS or cTBNA.13,19 From a global perspective, the cost and the required skills associated with EBUS, EUS, and rapid on-site cytologic evaluation can interfere with the worldwide use of these technologies in the near future.19 Thus, although the present study suggests that cTBNA in combination with endobronchial and transbronchial lung biopsies, and perhaps the latter alone in patients with parenchymal infiltrates, is sufficient to establish the diagnosis of sarcoidosis, we believe that unavailability of EBUS should not hinder an experienced bronchoscopist.
531
We, therefore, encourage standard bronchoscopy with conventional tools in the appropriate clinical setting and propose the notion of “choosing wisely,” wherein both pulmonologists and institutions select their techniques and investments based on their patient population and available skills.
Variability in Decisions to Limit Life-Sustaining Treatments
Acknowledgments
J. Randall Curtis, MD, MPH
Other contributions: We thank Nirupama Mulherkar, PhD, for writing assistance.
Seattle, WA
Is It All About the Physician? Amber E. Barnato, MD, MPH Pittsburgh, PA
References 1. Indiana Jones and the Last Crusade. Dir: Steven Spielberg. Paramount Pictures, 1989. Film. 2. Wang KP, Fuenning C, Johns CJ, Terry PB. Flexible transbronchial needle aspiration for the diagnosis of sarcoidosis. Ann Otol Rhinol Laryngol. 1989;98(4 pt 1):298-300. 3. von Bartheld MB, Dekkers OM, Szlubowski A, et al. Endosonography vs conventional bronchoscopy for the diagnosis of sarcoidosis: the GRANULOMA randomized clinical trial. JAMA. 2013;309(23):2457-2464. 4. Annema JT, van Meerbeeck JP, Rintoul RC, et al. Mediastinoscopy vs endosonography for mediastinal nodal staging of lung cancer: a randomized trial. JAMA. 2010;304(20):2245-2252. 5. Culver DA, Costabel U. EBUS-TBNA for the diagnosis of sarcoidosis: is it the only game in town? J Bronchology Interv Pulmonol. 2013;20(3):195-197. 6. Winterbauer RH, Belic N, Moores KD. Clinical interpretation of bilateral hilar adenopathy. Ann Intern Med. 1973;78(1):65-71. 7. Reich JM, Brouns MC, O’Connor EA, Edwards MJ. Mediastinoscopy in patients with presumptive stage I sarcoidosis: a risk/benefit, cost/benefit analysis. Chest. 1998;113(1):147-153. 8. Reich JM. Tissue confirmation of presumptive stage I sarcoidosis. J Bronchology Interv Pulmonol. 2013;20(2):103-105. 9. Narula T, Baughman RP, Mehta AC. “Sarcoidosis Americana-route Europa.” J Bronchology Interv Pulmonol. 2013;20(4):293-296. 10. Mehta AC, Mazzone PJ. An attempt to reach the galaxy of the pulmonary nodules. Am J Respir Crit Care Med. 2013;188(3): 264-265. 11. Mehta AC, Wang KP. Teaching conventional transbronchial needle aspiration. A continuum. Ann Am Thorac Soc. 2013;10(6): 685-689. 12. Gupta D, Dadhwal DS, Agarwal R, Gupta N, Bal A, Aggarwal AN. Endobronchial ultrasound-guided transbronchial needle aspiration vs conventional transbronchial needle aspiration in the diagnosis of sarcoidosis. Chest. 2014;146(3):547-556. 13. de Boer S, Milne DG, Zeng I, Wilsher ML. Does CT scanning predict the likelihood of a positive transbronchial biopsy in sarcoidosis? Thorax. 2009;64(5):436-439. 14. Ribeiro Neto ML, Culver DA, Mehta AC. Sarcoidosis—no business of the bronchoscopist. J Thorac Cardiovasc Surg. 2012;144(5):1276-1277. 15. Almeida FA, Casal RF, Jimenez CA, et al. Quality gaps and comparative effectiveness in lung cancer staging: the impact of test sequencing on outcomes. Chest. 2013;144(6):1776-1782. 16. Hernández Blasco L, Sánchez Hernández IM, Villena Garrido V, de Miguel Poch E, Nuñez Delgado M, Alfaro Abreu J. Safety of the transbronchial biopsy in outpatients. Chest. 1991;99(3):562-565. 17. Pue CA, Pacht ER. Complications of fiberoptic bronchoscopy at a university hospital. Chest. 1995;107(2):430-432. 18. Plit ML, Havryk AP, Hodgson A, et al. Rapid cytological analysis of endobronchial ultrasound-guided aspirates in sarcoidosis. Eur Respir J. 2013;42(5):1302-1308. 19. Cicenia J, Almeida F, Machuzak M, et al. The utility of rapid on-site evaluation (ROSE) in the detection of granulomas in mediastinal lymph nodes. Chest. 2013;144(4_MeetingAbstracts):797A.
532 Editorials
Approximately 20% of deaths in the United States occur in or shortly after a stay in the ICU, and the proportion of Medicare beneficiaries who spend time in the ICU in the last 30 days of their lives is increasing.1,2 Of the deaths occurring in the ICU, the majority involve decisions to withhold or withdraw life-sustaining treatments. Studies from the past century documented dramatic variability from ICU to ICU in the proportion of deaths preceded by withholding and withdrawing life-sustaining treatments.3 An article by Quill and colleagues4 in this issue of CHEST (see page 573) shows that dramatic variability persists—sixfold—in these decisions from ICU to ICU, even after adjusting for patient and ICU factors. Why might this variability exist? If such variability is explained by systematic variability from ICU to ICU in patient or family preferences for care at the end of life, it might be an indication of patient- and family-centered care. However, this is unlikely. Although there is regional variability in patient preferences for end-of-life care, the variability in intensity of care at the end of life is not explained by variability in patient preferences.5 Indeed, there is compelling evidence that considerable variability in decision-making about withdrawing life support in the ICU is explained by individual physicians, even after adjusting for patient characteristics.6 AFFILIATIONS:
From the Division of Pulmonary and Critical Care Medicine (Dr Curtis), Harborview Medical Center, University of Washington; and Division of General Internal Medicine (Dr Barnato), Department of Medicine, University of Pittsburgh. FINANCIAL/NONFINANCIAL DISCLOSURES: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article. CORRESPONDENCE TO: J. Randall Curtis, MD, MPH, Division of Pulmonary and Critical Care Medicine, Harborview Medical Center, University of Washington, Box 359762, 325 Ninth Ave, Seattle, WA 98104; e-mail: [email protected] © 2014 AMERICAN COLLEGE OF CHEST PHYSICIANS. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details. DOI: 10.1378/chest.14-0636
[
146#3 CHEST SEPTEMBER 2014
]
