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Why do clinicians continue to order ‘routine preoperative tests’ despite the evidence?

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Why do clinicians continue to order ‘routine preoperative tests’ despite the evidence?

Guidelines and practice advisories issued by several medical societies, including the American Society of Anesthesiologists,1 American Heart Association (AHA) and American College of Cardiology (ACC),2 and Society of General Internal Medicine,3 advise against routine preoperative testing for patients undergoing low-risk surgical procedures. Such testing often includes routine blood chemistry, complete blood cell counts, measures of the clotting system, and cardiac stress testing.

See related article

In this issue of the Cleveland Clinic Journal of Medicine, Dr. Nathan Houchens reviews the evidence against these measures.4

Despite a substantial body of evidence going back more than 2 decades that includes prospective randomized controlled trials,5–10 physicians continue to order unnecessary, ineffective, and costly tests in the perioperative period.11 The process of abandoning current medical practice—a phenomenon known as medical reversal12—often takes years,13 because it is more difficult to convince physicians to discontinue a current behavior than to implement a new one.14 The study of what makes physicians accept new therapies and abandon old ones began more than half a century ago.15

More recently, Cabana et al16 created a framework to understand why physicians do not follow clinical practice guidelines. Among the reasons are lack of familiarity or agreement with the contents of the guideline, lack of outcome expectancy, inertia of previous practice, and external barriers to implementation.

It is harder to convince physicians to discontinue a current behavior than to implement a new one

The rapid proliferation of guidelines in the past 20 years has led to numerous conflicting recommendations, many of which are based primarily on expert opinion.17 Guidelines based solely on randomized trials have also come under fire.18,19

In the case of preoperative testing, the recommendations are generally evidence-based and consistent. Why then do physicians appear to disregard the evidence? We propose several reasons why they might do so.

SOME PHYSICIANS ARE UNFAMILIAR WITH THE EVIDENCE

The complexity of the evidence summarized in guidelines has increased exponentially in the last decade, but physician time to assess the evidence has not increased. For example, the number of references in the executive summary of the ACC/AHA perioperative guidelines increased from 96 in 2002 to 252 in 2014. Most of the recommendations are backed by substantial amounts of high-quality evidence. For example, there are 17 prospective and 13 retrospective studies demonstrating that routine testing with the prothrombin time and the partial thromboplastin time is not helpful in asymptomatic patients.20

Although compliance with medical evidence varies among specialties,21 most physicians do not have time to keep up with the ever-increasing amount of information. Specifically in the area of cardiac risk assessment, there has been a rapid proliferation of tests that can be used to assess cardiac risk.22–28 In a Harris Interactive survey from 2008, physicians reported not applying medical evidence routinely. One-third believed they would do it more if they had the time.29 Without information technology support to provide medical information at the point of care,30 especially in small practices, using evidence may not be practical. Simply making the information available online and not promoting it actively does not improve utilization.31

As a consequence, physicians continue to order unnecessary tests, even though they may not feel confident interpreting the results.32

PHYSICIANS MAY NOT BELIEVE THE EVIDENCE

A lack of transparency in evidence-based guidelines and, sometimes, a lack of flexibility and relevance to clinical practice are important barriers to physicians’ acceptance of and adherence to evidence-based clinical practice guidelines.30

Most physicians do not have time to keep up with the ever-increasing amount of information

Even experts who write guidelines may not be swayed by the evidence. For example, a randomized prospective trial of almost 6,000 patients reported that coronary artery revascularization before elective major vascular surgery does not affect long-term mortality rates.33 Based on this study, the 2014 ACC/AHA guidelines2 advised against revascularization before noncardiac surgery exclusively to reduce perioperative cardiac events. Yet the same guidelines do recommend assessing for myocardial ischemia in patients with elevated risk and poor or unknown functional capacity, using a pharmacologic stress test. Based on the extent of the stress test abnormalities, coronary angiography and revascularization are then suggested for patients willing to undergo coronary artery bypass grafting (CABG) or percutaneous coronary intervention.2

The 2014 European Society of Cardiology and European Society of Anaesthesiology guidelines directly recommend revascularization before high-risk surgery, depending on the extent of a stress-induced perfusion defect.34 This recommendation relies on data from the Coronary Artery Surgery Study registry, which included almost 25,000 patients who underwent coronary angiography from 1975 through 1979. At a mean follow-up of 4.1 years, 1,961 patients underwent high-risk surgery. In this observational cohort, patients who underwent CABG had a lower risk of death and myocardial infarction after surgery.35 The reliance of medical societies34 on data that are more than 30 years old—when operative mortality rates and the treatment of coronary artery disease have changed substantially in the interim and despite the fact that this study did not test whether preoperative revascularization can reduce postoperative mortality—reflects a certain resistance to accept the results of the more recent and relevant randomized trial.33

Other physicians may also prefer to rely on selective data or to simply defer to guidelines that support their beliefs. Some physicians find that evidence-based guidelines are impractical and rigid and reduce their autonomy.36 For many physicians, trials that use surrogate end points and short-term outcomes are not sufficiently compelling to make them abandon current practice.37 Finally, when members of the guideline committees have financial associations with the pharmaceutical industry, or when corporations interested in the outcomes provide financial support for a trial’s development, the likelihood of a recommendation being trusted and used by physicians is drastically reduced.38

 

 

PRACTICING DEFENSIVELY

Even if physicians are familiar with the evidence and believe it, they may choose not to act on it. One reason is fear of litigation.

In court, attorneys can use guidelines as well as articles from medical journals as both exculpatory and inculpatory evidence. But they more frequently rely on the standard of care, or what most physicians would do under similar circumstances. If a patient has a bad outcome, such as a perioperative myocardial infarction or life-threatening bleeding, the defendant may assert that testing was unwarranted because guidelines do not recommend it or because the probability of such an outcome was low. However, because the outcome occurred, the jury may not believe that the probability was low enough not to consider, especially if expert witnesses testify that the standard of care would be to order the test.

In areas of controversy, physicians generally believe that erring on the side of more testing is more defensible in court.39 Indeed, following established practice traditions, learned during residency,11,40 may absolve physicians in negligence claims if the way medical care was delivered is supported by recognized and respected physicians.41

Even physicians who write the guidelines may be unswayed by the evidence

As a consequence, physicians prefer to practice the same way their peers do rather than follow the evidence. Unfortunately, the more procedures physicians perform for low-risk patients, the more likely these tests will become accepted as the legal standard of care.42 In this vicious circle, the new standard of care can increase the risk of litigation for others.43 Although unnecessary testing that leads to harmful invasive tests or procedures can also result in malpractice litigation, physicians may not consider this possibility.

FINANCIAL INCENTIVES

The threat of malpractice litigation provides a negative financial incentive to keep performing unnecessary tests, but there are a number of positive incentives as well.

First, physicians often feel compelled to order tests when they believe that physicians referring the patients want the tests done, or when they fear that not completing the tests could delay or cancel the scheduled surgery.40 Refusing to order the test could result in a loss of future referrals. In contrast, ordering tests allows them to meet expectations, preserve trust, and appear more valuable to referring physicians and their patients.

Insurance companies are complicit in these practices. Paying for unnecessary tests can create direct financial incentives for physicians or institutions that own on-site laboratories or diagnostic imaging equipment. Evidence shows that under those circumstances physicians do order more tests. Self-referral and referral to facilities where physicians have a financial interest is associated with increased healthcare costs.44 In addition to direct revenues for the tests performed, physicians may also bill for test interpretation, follow-up visits, and additional procedures generated from test results.

This may be one explanation why the ordering of cardiac tests (stress testing, echocardiography, vascular ultrasonography) by US physicians varies widely from state to state.45

RECOMMENDATIONS TO REDUCE INAPPROPRIATE TESTING

To counter these influences, we propose a multifaceted intervention that includes the following:

  • Establish preoperative clinics staffed by experts. Despite the large volume of potentially relevant evidence, the number of articles directly supporting or refuting preoperative laboratory testing is small enough that physicians who routinely engage in preoperative assessment should easily master the evidence.
  • Identify local leaders who can convince colleagues of the evidence. Distribute evidence summaries or guidelines with references to major articles that support each recommendation.
  • Work with clinical practice committees to establish new standards of care within the hospital. Establish hospital care paths to dictate and support local standards of care. Measure individual physician performance and offer feedback with the goal of reducing utilization.
  • National societies should recommend that insurance companies remove inappropriate financial incentives. If companies deny payment for inappropriate testing, physicians will stop ordering it. Even requirements for preauthorization of tests should reduce utilization. The Choosing Wisely campaign (www.choosingwisely.org) would be a good place to start.
References
  1. Committee on Standards and Practice Parameters, Apfelbaum JL, Connis RT, Nickinovich DG, et al. Practice advisory for preanesthesia evaluation. An updated report by the American Society of Anesthesiologists Task Force on Preanesthesia Evaluation. Anesthesiology 2012; 116:522–538.
  2. Fleisher LA, Fleischmann KE, Auerbach AD, et al; American College of Cardiology and American Heart Association. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines. J Am Coll Cardiol 2014; 64:e77–e137.
  3. Society of General Internal Medicine. Don’t perform routine pre-operative testing before low-risk surgical procedures. Choosing Wisely. An initiative of the ABIM Foundation. September 12, 2013. www.choosingwisely.org/clinician-lists/society-general-internal-medicine-routine-preoperative-testing-before-low-risk-surgery/. Accessed August 31, 2015.
  4. Houchens N. Should healthy patients undergoing low-risk, elective, noncardiac surgery undergo routine preoperative laboratory testing? Cleve Clin J Med 2015; 82:664–666.
  5. Rohrer MJ, Michelotti MC, Nahrwold DL. A prospective evaluation of the efficacy of preoperative coagulation testing. Ann Surg 1988; 208:554–557.
  6. Eagle KA, Coley CM, Newell JB, et al. Combining clinical and thallium data optimizes preoperative assessment of cardiac risk before major vascular surgery. Ann Intern Med 1989; 110:859–866.
  7. Mangano DT, London MJ, Tubau JF, et al. Dipyridamole thallium-201 scintigraphy as a preoperative screening test. A reexamination of its predictive potential. Study of Perioperative Ischemia Research Group. Circulation 1991; 84:493–502.
  8. Stratmann HG, Younis LT, Wittry MD, Amato M, Mark AL, Miller DD. Dipyridamole technetium 99m sestamibi myocardial tomography for preoperative cardiac risk stratification before major or minor nonvascular surgery. Am Heart J 1996; 132:536–541.
  9. Schein OD, Katz J, Bass EB, et al. The value of routine preoperative medical testing before cataract surgery. Study of Medical Testing for Cataract Surgery. N Engl J Med 2000; 342:168–175.
  10. Hashimoto J, Nakahara T, Bai J, Kitamura N, Kasamatsu T, Kubo A. Preoperative risk stratification with myocardial perfusion imaging in intermediate and low-risk non-cardiac surgery. Circ J 2007; 71:1395–1400.
  11. Smetana GW. The conundrum of unnecessary preoperative testing. JAMA Intern Med 2015; 175:1359–1361.
  12. Prasad V, Cifu A. Medical reversal: why we must raise the bar before adopting new technologies. Yale J Biol Med 2011; 84:471–478.
  13. Tatsioni A, Bonitsis NG, Ioannidis JP. Persistence of contradicted claims in the literature. JAMA 2007; 298:2517–2526.
  14. Moscucci M. Medical reversal, clinical trials, and the “late” open artery hypothesis in acute myocardial infarction. Arch Intern Med 2011; 171:1643–1644.
  15. Coleman J, Menzel H, Katz E. Social processes in physicians’ adoption of a new drug. J Chronic Dis 1959; 9:1–19.
  16. Cabana MD, Rand CS, Powe NR, et al. Why don’t physicians follow clinical practice guidelines? A framework for improvement. JAMA 1999; 282:1458–1465.
  17. Tricoci P, Allen JM, Kramer JM, Califf RM, Smith SC Jr. Scientific evidence underlying the ACC/AHA clinical practice guidelines. JAMA 2009; 301:831–841.
  18. Moher D, Hopewell S, Schulz KF, et al; CONSORT. CONSORT 2010 explanation and elaboration: updated guidelines for reporting parallel group randomised trials. Int J Surg 2012; 10:28–55.
  19. Gattinoni L, Giomarelli P. Acquiring knowledge in intensive care: merits and pitfalls of randomized controlled trials. Intensive Care Med 2015; 41:1460–1464.
  20. Levy JH, Szlam F, Wolberg AS, Winkler A. Clinical use of the activated partial thromboplastin time and prothrombin time for screening: a review of the literature and current guidelines for testing. Clin Lab Med 2014; 34:453–477.
  21. Dale W, Hemmerich J, Moliski E, Schwarze ML, Tung A. Effect of specialty and recent experience on perioperative decision-making for abdominal aortic aneurysm repair. J Am Geriatr Soc 2012; 60:1889–1894.
  22. Underwood SR, Anagnostopoulos C, Cerqueira M, et al; British Cardiac Society, British Nuclear Cardiology Society, British Nuclear Medicine Society, Royal College of Physicians of London, Royal College of Physicians of London. Myocardial perfusion scintigraphy: the evidence. Eur J Nucl Med Mol Imaging 2004; 31:261–291.
  23. Das MK, Pellikka PA, Mahoney DW, et al. Assessment of cardiac risk before nonvascular surgery: dobutamine stress echocardiography in 530 patients. J Am Coll Cardiol 2000; 35:1647–1653.
  24. Meijboom WB, Mollet NR, Van Mieghem CA, et al. Pre-operative computed tomography coronary angiography to detect significant coronary artery disease in patients referred for cardiac valve surgery. J Am Coll Cardiol 2006; 48:1658–1665.
  25. Russo V, Gostoli V, Lovato L, et al. Clinical value of multidetector CT coronary angiography as a preoperative screening test before non-coronary cardiac surgery. Heart 2007; 93:1591–1598.
  26. Schuetz GM, Zacharopoulou NM, Schlattmann P, Dewey M. Meta-analysis: noninvasive coronary angiography using computed tomography versus magnetic resonance imaging. Ann Intern Med 2010; 152:167–177.
  27. Bluemke DA, Achenbach S, Budoff M, et al. Noninvasive coronary artery imaging: magnetic resonance angiography and multidetector computed tomography angiography: a scientific statement from the American Heart Association Committee on Cardiovascular Imaging and Intervention of the Council on Cardiovascular Radiology and Intervention, and the Councils on Clinical Cardiology and Cardiovascular Disease in the Young. Circulation 2008; 118:586–606.
  28. Nagel E, Lehmkuhl HB, Bocksch W, et al. Noninvasive diagnosis of ischemia-induced wall motion abnormalities with the use of high-dose dobutamine stress MRI: comparison with dobutamine stress echocardiography. Circulation 1999; 99:763–770.
  29. Taylor H. Physicians’ use of clinical guidelines—and how to increase it. Healthcare News 2008; 8:32–55. www.harrisinteractive.com/vault/HI_HealthCareNews2008Vol8_Iss04.pdf. Accessed August 31, 2015.
  30. Kenefick H, Lee J, Fleishman V. Improving physician adherence to clinical practice guidelines. Barriers and stragies for change. New England Healthcare Institute, February 2008. www.nehi.net/writable/publication_files/file/cpg_report_final.pdf. Accessed August 31, 2015.
  31. Williams J, Cheung WY, Price DE, et al. Clinical guidelines online: do they improve compliance? Postgrad Med J 2004; 80:415–419.
  32. Wians F. Clinical laboratory tests: which, why, and what do the results mean? Lab Medicine 2009; 40:105–113.
  33. McFalls EO, Ward HB, Moritz TE, et al. Coronary-artery revascularization before elective major vascular surgery. N Engl J Med 2004; 351:2795–2804.
  34. Kristensen SD, Knuuti J, Saraste A, et al; Authors/Task Force Members. 2014 ESC/ESA guidelines on non-cardiac surgery: cardiovascular assessment and management: The Joint Task Force on non-cardiac surgery: cardiovascular assessment and management of the European Society of Cardiology (ESC) and the European Society of Anaesthesiology (ESA). Eur Heart J 2014; 35:2383–2431.
  35. Eagle KA, Rihal CS, Mickel MC, Holmes DR, Foster ED, Gersh BJ. Cardiac risk of noncardiac surgery: influence of coronary disease and type of surgery in 3368 operations. CASS Investigators and University of Michigan Heart Care Program. Coronary Artery Surgery Study. Circulation 1997; 96:1882–1887.
  36. Farquhar CM, Kofa EW, Slutsky JR. Clinicians’ attitudes to clinical practice guidelines: a systematic review. Med J Aust 2002; 177:502–506.
  37. Prasad V, Cifu A, Ioannidis JP. Reversals of established medical practices: evidence to abandon ship. JAMA 2012; 307:37–38.
  38. Steinbrook R. Guidance for guidelines. N Engl J Med 2007; 356:331–333.
  39. Sirovich BE, Woloshin S, Schwartz LM. Too little? Too much? Primary care physicians’ views on US health care: a brief report. Arch Intern Med 2011; 171:1582–1585.
  40. Brown SR, Brown J. Why do physicians order unnecessary preoperative tests? A qualitative study. Fam Med 2011; 43:338–343.
  41. LeCraw LL. Use of clinical practice guidelines in medical malpractice litigation. J Oncol Pract 2007; 3:254.
  42. Studdert DM, Mello MM, Sage WM, et al. Defensive medicine among high-risk specialist physicians in a volatile malpractice environment. JAMA 2005; 293:2609–2617.
  43. Budetti PP. Tort reform and the patient safety movement: seeking common ground. JAMA 2005; 293:2660–2662.
  44. Bishop TF, Federman AD, Ross JS. Laboratory test ordering at physician offices with and without on-site laboratories. J Gen Intern Med 2010; 25:1057–1063.
  45. Rosenthal E. Medical costs rise as retirees winter in Florida. The New York Times, Jan 31, 2015. http://nyti.ms/1vmjfa5. Accessed August 31, 2015.
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Andrei Brateanu, MD
Department of Internal Medicine, Medicine Institute, Cleveland Clinic; Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Michael B. Rothberg, MD, MPH
Vice Chair for Research, Medicine Institute, Cleveland Clinic, Cleveland Clinic; Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Address: Andrei Brateanu, MD, Department of Medicine, NA10, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; e-mail: abratean@ccf.org

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Andrei Brateanu, MD
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Michael B. Rothberg, MD, MPH
Vice Chair for Research, Medicine Institute, Cleveland Clinic, Cleveland Clinic; Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Address: Andrei Brateanu, MD, Department of Medicine, NA10, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; e-mail: abratean@ccf.org

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Andrei Brateanu, MD
Department of Internal Medicine, Medicine Institute, Cleveland Clinic; Assistant Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Michael B. Rothberg, MD, MPH
Vice Chair for Research, Medicine Institute, Cleveland Clinic, Cleveland Clinic; Professor, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH

Address: Andrei Brateanu, MD, Department of Medicine, NA10, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; e-mail: abratean@ccf.org

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Related Articles

Guidelines and practice advisories issued by several medical societies, including the American Society of Anesthesiologists,1 American Heart Association (AHA) and American College of Cardiology (ACC),2 and Society of General Internal Medicine,3 advise against routine preoperative testing for patients undergoing low-risk surgical procedures. Such testing often includes routine blood chemistry, complete blood cell counts, measures of the clotting system, and cardiac stress testing.

See related article

In this issue of the Cleveland Clinic Journal of Medicine, Dr. Nathan Houchens reviews the evidence against these measures.4

Despite a substantial body of evidence going back more than 2 decades that includes prospective randomized controlled trials,5–10 physicians continue to order unnecessary, ineffective, and costly tests in the perioperative period.11 The process of abandoning current medical practice—a phenomenon known as medical reversal12—often takes years,13 because it is more difficult to convince physicians to discontinue a current behavior than to implement a new one.14 The study of what makes physicians accept new therapies and abandon old ones began more than half a century ago.15

More recently, Cabana et al16 created a framework to understand why physicians do not follow clinical practice guidelines. Among the reasons are lack of familiarity or agreement with the contents of the guideline, lack of outcome expectancy, inertia of previous practice, and external barriers to implementation.

It is harder to convince physicians to discontinue a current behavior than to implement a new one

The rapid proliferation of guidelines in the past 20 years has led to numerous conflicting recommendations, many of which are based primarily on expert opinion.17 Guidelines based solely on randomized trials have also come under fire.18,19

In the case of preoperative testing, the recommendations are generally evidence-based and consistent. Why then do physicians appear to disregard the evidence? We propose several reasons why they might do so.

SOME PHYSICIANS ARE UNFAMILIAR WITH THE EVIDENCE

The complexity of the evidence summarized in guidelines has increased exponentially in the last decade, but physician time to assess the evidence has not increased. For example, the number of references in the executive summary of the ACC/AHA perioperative guidelines increased from 96 in 2002 to 252 in 2014. Most of the recommendations are backed by substantial amounts of high-quality evidence. For example, there are 17 prospective and 13 retrospective studies demonstrating that routine testing with the prothrombin time and the partial thromboplastin time is not helpful in asymptomatic patients.20

Although compliance with medical evidence varies among specialties,21 most physicians do not have time to keep up with the ever-increasing amount of information. Specifically in the area of cardiac risk assessment, there has been a rapid proliferation of tests that can be used to assess cardiac risk.22–28 In a Harris Interactive survey from 2008, physicians reported not applying medical evidence routinely. One-third believed they would do it more if they had the time.29 Without information technology support to provide medical information at the point of care,30 especially in small practices, using evidence may not be practical. Simply making the information available online and not promoting it actively does not improve utilization.31

As a consequence, physicians continue to order unnecessary tests, even though they may not feel confident interpreting the results.32

PHYSICIANS MAY NOT BELIEVE THE EVIDENCE

A lack of transparency in evidence-based guidelines and, sometimes, a lack of flexibility and relevance to clinical practice are important barriers to physicians’ acceptance of and adherence to evidence-based clinical practice guidelines.30

Most physicians do not have time to keep up with the ever-increasing amount of information

Even experts who write guidelines may not be swayed by the evidence. For example, a randomized prospective trial of almost 6,000 patients reported that coronary artery revascularization before elective major vascular surgery does not affect long-term mortality rates.33 Based on this study, the 2014 ACC/AHA guidelines2 advised against revascularization before noncardiac surgery exclusively to reduce perioperative cardiac events. Yet the same guidelines do recommend assessing for myocardial ischemia in patients with elevated risk and poor or unknown functional capacity, using a pharmacologic stress test. Based on the extent of the stress test abnormalities, coronary angiography and revascularization are then suggested for patients willing to undergo coronary artery bypass grafting (CABG) or percutaneous coronary intervention.2

The 2014 European Society of Cardiology and European Society of Anaesthesiology guidelines directly recommend revascularization before high-risk surgery, depending on the extent of a stress-induced perfusion defect.34 This recommendation relies on data from the Coronary Artery Surgery Study registry, which included almost 25,000 patients who underwent coronary angiography from 1975 through 1979. At a mean follow-up of 4.1 years, 1,961 patients underwent high-risk surgery. In this observational cohort, patients who underwent CABG had a lower risk of death and myocardial infarction after surgery.35 The reliance of medical societies34 on data that are more than 30 years old—when operative mortality rates and the treatment of coronary artery disease have changed substantially in the interim and despite the fact that this study did not test whether preoperative revascularization can reduce postoperative mortality—reflects a certain resistance to accept the results of the more recent and relevant randomized trial.33

Other physicians may also prefer to rely on selective data or to simply defer to guidelines that support their beliefs. Some physicians find that evidence-based guidelines are impractical and rigid and reduce their autonomy.36 For many physicians, trials that use surrogate end points and short-term outcomes are not sufficiently compelling to make them abandon current practice.37 Finally, when members of the guideline committees have financial associations with the pharmaceutical industry, or when corporations interested in the outcomes provide financial support for a trial’s development, the likelihood of a recommendation being trusted and used by physicians is drastically reduced.38

 

 

PRACTICING DEFENSIVELY

Even if physicians are familiar with the evidence and believe it, they may choose not to act on it. One reason is fear of litigation.

In court, attorneys can use guidelines as well as articles from medical journals as both exculpatory and inculpatory evidence. But they more frequently rely on the standard of care, or what most physicians would do under similar circumstances. If a patient has a bad outcome, such as a perioperative myocardial infarction or life-threatening bleeding, the defendant may assert that testing was unwarranted because guidelines do not recommend it or because the probability of such an outcome was low. However, because the outcome occurred, the jury may not believe that the probability was low enough not to consider, especially if expert witnesses testify that the standard of care would be to order the test.

In areas of controversy, physicians generally believe that erring on the side of more testing is more defensible in court.39 Indeed, following established practice traditions, learned during residency,11,40 may absolve physicians in negligence claims if the way medical care was delivered is supported by recognized and respected physicians.41

Even physicians who write the guidelines may be unswayed by the evidence

As a consequence, physicians prefer to practice the same way their peers do rather than follow the evidence. Unfortunately, the more procedures physicians perform for low-risk patients, the more likely these tests will become accepted as the legal standard of care.42 In this vicious circle, the new standard of care can increase the risk of litigation for others.43 Although unnecessary testing that leads to harmful invasive tests or procedures can also result in malpractice litigation, physicians may not consider this possibility.

FINANCIAL INCENTIVES

The threat of malpractice litigation provides a negative financial incentive to keep performing unnecessary tests, but there are a number of positive incentives as well.

First, physicians often feel compelled to order tests when they believe that physicians referring the patients want the tests done, or when they fear that not completing the tests could delay or cancel the scheduled surgery.40 Refusing to order the test could result in a loss of future referrals. In contrast, ordering tests allows them to meet expectations, preserve trust, and appear more valuable to referring physicians and their patients.

Insurance companies are complicit in these practices. Paying for unnecessary tests can create direct financial incentives for physicians or institutions that own on-site laboratories or diagnostic imaging equipment. Evidence shows that under those circumstances physicians do order more tests. Self-referral and referral to facilities where physicians have a financial interest is associated with increased healthcare costs.44 In addition to direct revenues for the tests performed, physicians may also bill for test interpretation, follow-up visits, and additional procedures generated from test results.

This may be one explanation why the ordering of cardiac tests (stress testing, echocardiography, vascular ultrasonography) by US physicians varies widely from state to state.45

RECOMMENDATIONS TO REDUCE INAPPROPRIATE TESTING

To counter these influences, we propose a multifaceted intervention that includes the following:

  • Establish preoperative clinics staffed by experts. Despite the large volume of potentially relevant evidence, the number of articles directly supporting or refuting preoperative laboratory testing is small enough that physicians who routinely engage in preoperative assessment should easily master the evidence.
  • Identify local leaders who can convince colleagues of the evidence. Distribute evidence summaries or guidelines with references to major articles that support each recommendation.
  • Work with clinical practice committees to establish new standards of care within the hospital. Establish hospital care paths to dictate and support local standards of care. Measure individual physician performance and offer feedback with the goal of reducing utilization.
  • National societies should recommend that insurance companies remove inappropriate financial incentives. If companies deny payment for inappropriate testing, physicians will stop ordering it. Even requirements for preauthorization of tests should reduce utilization. The Choosing Wisely campaign (www.choosingwisely.org) would be a good place to start.

Guidelines and practice advisories issued by several medical societies, including the American Society of Anesthesiologists,1 American Heart Association (AHA) and American College of Cardiology (ACC),2 and Society of General Internal Medicine,3 advise against routine preoperative testing for patients undergoing low-risk surgical procedures. Such testing often includes routine blood chemistry, complete blood cell counts, measures of the clotting system, and cardiac stress testing.

See related article

In this issue of the Cleveland Clinic Journal of Medicine, Dr. Nathan Houchens reviews the evidence against these measures.4

Despite a substantial body of evidence going back more than 2 decades that includes prospective randomized controlled trials,5–10 physicians continue to order unnecessary, ineffective, and costly tests in the perioperative period.11 The process of abandoning current medical practice—a phenomenon known as medical reversal12—often takes years,13 because it is more difficult to convince physicians to discontinue a current behavior than to implement a new one.14 The study of what makes physicians accept new therapies and abandon old ones began more than half a century ago.15

More recently, Cabana et al16 created a framework to understand why physicians do not follow clinical practice guidelines. Among the reasons are lack of familiarity or agreement with the contents of the guideline, lack of outcome expectancy, inertia of previous practice, and external barriers to implementation.

It is harder to convince physicians to discontinue a current behavior than to implement a new one

The rapid proliferation of guidelines in the past 20 years has led to numerous conflicting recommendations, many of which are based primarily on expert opinion.17 Guidelines based solely on randomized trials have also come under fire.18,19

In the case of preoperative testing, the recommendations are generally evidence-based and consistent. Why then do physicians appear to disregard the evidence? We propose several reasons why they might do so.

SOME PHYSICIANS ARE UNFAMILIAR WITH THE EVIDENCE

The complexity of the evidence summarized in guidelines has increased exponentially in the last decade, but physician time to assess the evidence has not increased. For example, the number of references in the executive summary of the ACC/AHA perioperative guidelines increased from 96 in 2002 to 252 in 2014. Most of the recommendations are backed by substantial amounts of high-quality evidence. For example, there are 17 prospective and 13 retrospective studies demonstrating that routine testing with the prothrombin time and the partial thromboplastin time is not helpful in asymptomatic patients.20

Although compliance with medical evidence varies among specialties,21 most physicians do not have time to keep up with the ever-increasing amount of information. Specifically in the area of cardiac risk assessment, there has been a rapid proliferation of tests that can be used to assess cardiac risk.22–28 In a Harris Interactive survey from 2008, physicians reported not applying medical evidence routinely. One-third believed they would do it more if they had the time.29 Without information technology support to provide medical information at the point of care,30 especially in small practices, using evidence may not be practical. Simply making the information available online and not promoting it actively does not improve utilization.31

As a consequence, physicians continue to order unnecessary tests, even though they may not feel confident interpreting the results.32

PHYSICIANS MAY NOT BELIEVE THE EVIDENCE

A lack of transparency in evidence-based guidelines and, sometimes, a lack of flexibility and relevance to clinical practice are important barriers to physicians’ acceptance of and adherence to evidence-based clinical practice guidelines.30

Most physicians do not have time to keep up with the ever-increasing amount of information

Even experts who write guidelines may not be swayed by the evidence. For example, a randomized prospective trial of almost 6,000 patients reported that coronary artery revascularization before elective major vascular surgery does not affect long-term mortality rates.33 Based on this study, the 2014 ACC/AHA guidelines2 advised against revascularization before noncardiac surgery exclusively to reduce perioperative cardiac events. Yet the same guidelines do recommend assessing for myocardial ischemia in patients with elevated risk and poor or unknown functional capacity, using a pharmacologic stress test. Based on the extent of the stress test abnormalities, coronary angiography and revascularization are then suggested for patients willing to undergo coronary artery bypass grafting (CABG) or percutaneous coronary intervention.2

The 2014 European Society of Cardiology and European Society of Anaesthesiology guidelines directly recommend revascularization before high-risk surgery, depending on the extent of a stress-induced perfusion defect.34 This recommendation relies on data from the Coronary Artery Surgery Study registry, which included almost 25,000 patients who underwent coronary angiography from 1975 through 1979. At a mean follow-up of 4.1 years, 1,961 patients underwent high-risk surgery. In this observational cohort, patients who underwent CABG had a lower risk of death and myocardial infarction after surgery.35 The reliance of medical societies34 on data that are more than 30 years old—when operative mortality rates and the treatment of coronary artery disease have changed substantially in the interim and despite the fact that this study did not test whether preoperative revascularization can reduce postoperative mortality—reflects a certain resistance to accept the results of the more recent and relevant randomized trial.33

Other physicians may also prefer to rely on selective data or to simply defer to guidelines that support their beliefs. Some physicians find that evidence-based guidelines are impractical and rigid and reduce their autonomy.36 For many physicians, trials that use surrogate end points and short-term outcomes are not sufficiently compelling to make them abandon current practice.37 Finally, when members of the guideline committees have financial associations with the pharmaceutical industry, or when corporations interested in the outcomes provide financial support for a trial’s development, the likelihood of a recommendation being trusted and used by physicians is drastically reduced.38

 

 

PRACTICING DEFENSIVELY

Even if physicians are familiar with the evidence and believe it, they may choose not to act on it. One reason is fear of litigation.

In court, attorneys can use guidelines as well as articles from medical journals as both exculpatory and inculpatory evidence. But they more frequently rely on the standard of care, or what most physicians would do under similar circumstances. If a patient has a bad outcome, such as a perioperative myocardial infarction or life-threatening bleeding, the defendant may assert that testing was unwarranted because guidelines do not recommend it or because the probability of such an outcome was low. However, because the outcome occurred, the jury may not believe that the probability was low enough not to consider, especially if expert witnesses testify that the standard of care would be to order the test.

In areas of controversy, physicians generally believe that erring on the side of more testing is more defensible in court.39 Indeed, following established practice traditions, learned during residency,11,40 may absolve physicians in negligence claims if the way medical care was delivered is supported by recognized and respected physicians.41

Even physicians who write the guidelines may be unswayed by the evidence

As a consequence, physicians prefer to practice the same way their peers do rather than follow the evidence. Unfortunately, the more procedures physicians perform for low-risk patients, the more likely these tests will become accepted as the legal standard of care.42 In this vicious circle, the new standard of care can increase the risk of litigation for others.43 Although unnecessary testing that leads to harmful invasive tests or procedures can also result in malpractice litigation, physicians may not consider this possibility.

FINANCIAL INCENTIVES

The threat of malpractice litigation provides a negative financial incentive to keep performing unnecessary tests, but there are a number of positive incentives as well.

First, physicians often feel compelled to order tests when they believe that physicians referring the patients want the tests done, or when they fear that not completing the tests could delay or cancel the scheduled surgery.40 Refusing to order the test could result in a loss of future referrals. In contrast, ordering tests allows them to meet expectations, preserve trust, and appear more valuable to referring physicians and their patients.

Insurance companies are complicit in these practices. Paying for unnecessary tests can create direct financial incentives for physicians or institutions that own on-site laboratories or diagnostic imaging equipment. Evidence shows that under those circumstances physicians do order more tests. Self-referral and referral to facilities where physicians have a financial interest is associated with increased healthcare costs.44 In addition to direct revenues for the tests performed, physicians may also bill for test interpretation, follow-up visits, and additional procedures generated from test results.

This may be one explanation why the ordering of cardiac tests (stress testing, echocardiography, vascular ultrasonography) by US physicians varies widely from state to state.45

RECOMMENDATIONS TO REDUCE INAPPROPRIATE TESTING

To counter these influences, we propose a multifaceted intervention that includes the following:

  • Establish preoperative clinics staffed by experts. Despite the large volume of potentially relevant evidence, the number of articles directly supporting or refuting preoperative laboratory testing is small enough that physicians who routinely engage in preoperative assessment should easily master the evidence.
  • Identify local leaders who can convince colleagues of the evidence. Distribute evidence summaries or guidelines with references to major articles that support each recommendation.
  • Work with clinical practice committees to establish new standards of care within the hospital. Establish hospital care paths to dictate and support local standards of care. Measure individual physician performance and offer feedback with the goal of reducing utilization.
  • National societies should recommend that insurance companies remove inappropriate financial incentives. If companies deny payment for inappropriate testing, physicians will stop ordering it. Even requirements for preauthorization of tests should reduce utilization. The Choosing Wisely campaign (www.choosingwisely.org) would be a good place to start.
References
  1. Committee on Standards and Practice Parameters, Apfelbaum JL, Connis RT, Nickinovich DG, et al. Practice advisory for preanesthesia evaluation. An updated report by the American Society of Anesthesiologists Task Force on Preanesthesia Evaluation. Anesthesiology 2012; 116:522–538.
  2. Fleisher LA, Fleischmann KE, Auerbach AD, et al; American College of Cardiology and American Heart Association. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines. J Am Coll Cardiol 2014; 64:e77–e137.
  3. Society of General Internal Medicine. Don’t perform routine pre-operative testing before low-risk surgical procedures. Choosing Wisely. An initiative of the ABIM Foundation. September 12, 2013. www.choosingwisely.org/clinician-lists/society-general-internal-medicine-routine-preoperative-testing-before-low-risk-surgery/. Accessed August 31, 2015.
  4. Houchens N. Should healthy patients undergoing low-risk, elective, noncardiac surgery undergo routine preoperative laboratory testing? Cleve Clin J Med 2015; 82:664–666.
  5. Rohrer MJ, Michelotti MC, Nahrwold DL. A prospective evaluation of the efficacy of preoperative coagulation testing. Ann Surg 1988; 208:554–557.
  6. Eagle KA, Coley CM, Newell JB, et al. Combining clinical and thallium data optimizes preoperative assessment of cardiac risk before major vascular surgery. Ann Intern Med 1989; 110:859–866.
  7. Mangano DT, London MJ, Tubau JF, et al. Dipyridamole thallium-201 scintigraphy as a preoperative screening test. A reexamination of its predictive potential. Study of Perioperative Ischemia Research Group. Circulation 1991; 84:493–502.
  8. Stratmann HG, Younis LT, Wittry MD, Amato M, Mark AL, Miller DD. Dipyridamole technetium 99m sestamibi myocardial tomography for preoperative cardiac risk stratification before major or minor nonvascular surgery. Am Heart J 1996; 132:536–541.
  9. Schein OD, Katz J, Bass EB, et al. The value of routine preoperative medical testing before cataract surgery. Study of Medical Testing for Cataract Surgery. N Engl J Med 2000; 342:168–175.
  10. Hashimoto J, Nakahara T, Bai J, Kitamura N, Kasamatsu T, Kubo A. Preoperative risk stratification with myocardial perfusion imaging in intermediate and low-risk non-cardiac surgery. Circ J 2007; 71:1395–1400.
  11. Smetana GW. The conundrum of unnecessary preoperative testing. JAMA Intern Med 2015; 175:1359–1361.
  12. Prasad V, Cifu A. Medical reversal: why we must raise the bar before adopting new technologies. Yale J Biol Med 2011; 84:471–478.
  13. Tatsioni A, Bonitsis NG, Ioannidis JP. Persistence of contradicted claims in the literature. JAMA 2007; 298:2517–2526.
  14. Moscucci M. Medical reversal, clinical trials, and the “late” open artery hypothesis in acute myocardial infarction. Arch Intern Med 2011; 171:1643–1644.
  15. Coleman J, Menzel H, Katz E. Social processes in physicians’ adoption of a new drug. J Chronic Dis 1959; 9:1–19.
  16. Cabana MD, Rand CS, Powe NR, et al. Why don’t physicians follow clinical practice guidelines? A framework for improvement. JAMA 1999; 282:1458–1465.
  17. Tricoci P, Allen JM, Kramer JM, Califf RM, Smith SC Jr. Scientific evidence underlying the ACC/AHA clinical practice guidelines. JAMA 2009; 301:831–841.
  18. Moher D, Hopewell S, Schulz KF, et al; CONSORT. CONSORT 2010 explanation and elaboration: updated guidelines for reporting parallel group randomised trials. Int J Surg 2012; 10:28–55.
  19. Gattinoni L, Giomarelli P. Acquiring knowledge in intensive care: merits and pitfalls of randomized controlled trials. Intensive Care Med 2015; 41:1460–1464.
  20. Levy JH, Szlam F, Wolberg AS, Winkler A. Clinical use of the activated partial thromboplastin time and prothrombin time for screening: a review of the literature and current guidelines for testing. Clin Lab Med 2014; 34:453–477.
  21. Dale W, Hemmerich J, Moliski E, Schwarze ML, Tung A. Effect of specialty and recent experience on perioperative decision-making for abdominal aortic aneurysm repair. J Am Geriatr Soc 2012; 60:1889–1894.
  22. Underwood SR, Anagnostopoulos C, Cerqueira M, et al; British Cardiac Society, British Nuclear Cardiology Society, British Nuclear Medicine Society, Royal College of Physicians of London, Royal College of Physicians of London. Myocardial perfusion scintigraphy: the evidence. Eur J Nucl Med Mol Imaging 2004; 31:261–291.
  23. Das MK, Pellikka PA, Mahoney DW, et al. Assessment of cardiac risk before nonvascular surgery: dobutamine stress echocardiography in 530 patients. J Am Coll Cardiol 2000; 35:1647–1653.
  24. Meijboom WB, Mollet NR, Van Mieghem CA, et al. Pre-operative computed tomography coronary angiography to detect significant coronary artery disease in patients referred for cardiac valve surgery. J Am Coll Cardiol 2006; 48:1658–1665.
  25. Russo V, Gostoli V, Lovato L, et al. Clinical value of multidetector CT coronary angiography as a preoperative screening test before non-coronary cardiac surgery. Heart 2007; 93:1591–1598.
  26. Schuetz GM, Zacharopoulou NM, Schlattmann P, Dewey M. Meta-analysis: noninvasive coronary angiography using computed tomography versus magnetic resonance imaging. Ann Intern Med 2010; 152:167–177.
  27. Bluemke DA, Achenbach S, Budoff M, et al. Noninvasive coronary artery imaging: magnetic resonance angiography and multidetector computed tomography angiography: a scientific statement from the American Heart Association Committee on Cardiovascular Imaging and Intervention of the Council on Cardiovascular Radiology and Intervention, and the Councils on Clinical Cardiology and Cardiovascular Disease in the Young. Circulation 2008; 118:586–606.
  28. Nagel E, Lehmkuhl HB, Bocksch W, et al. Noninvasive diagnosis of ischemia-induced wall motion abnormalities with the use of high-dose dobutamine stress MRI: comparison with dobutamine stress echocardiography. Circulation 1999; 99:763–770.
  29. Taylor H. Physicians’ use of clinical guidelines—and how to increase it. Healthcare News 2008; 8:32–55. www.harrisinteractive.com/vault/HI_HealthCareNews2008Vol8_Iss04.pdf. Accessed August 31, 2015.
  30. Kenefick H, Lee J, Fleishman V. Improving physician adherence to clinical practice guidelines. Barriers and stragies for change. New England Healthcare Institute, February 2008. www.nehi.net/writable/publication_files/file/cpg_report_final.pdf. Accessed August 31, 2015.
  31. Williams J, Cheung WY, Price DE, et al. Clinical guidelines online: do they improve compliance? Postgrad Med J 2004; 80:415–419.
  32. Wians F. Clinical laboratory tests: which, why, and what do the results mean? Lab Medicine 2009; 40:105–113.
  33. McFalls EO, Ward HB, Moritz TE, et al. Coronary-artery revascularization before elective major vascular surgery. N Engl J Med 2004; 351:2795–2804.
  34. Kristensen SD, Knuuti J, Saraste A, et al; Authors/Task Force Members. 2014 ESC/ESA guidelines on non-cardiac surgery: cardiovascular assessment and management: The Joint Task Force on non-cardiac surgery: cardiovascular assessment and management of the European Society of Cardiology (ESC) and the European Society of Anaesthesiology (ESA). Eur Heart J 2014; 35:2383–2431.
  35. Eagle KA, Rihal CS, Mickel MC, Holmes DR, Foster ED, Gersh BJ. Cardiac risk of noncardiac surgery: influence of coronary disease and type of surgery in 3368 operations. CASS Investigators and University of Michigan Heart Care Program. Coronary Artery Surgery Study. Circulation 1997; 96:1882–1887.
  36. Farquhar CM, Kofa EW, Slutsky JR. Clinicians’ attitudes to clinical practice guidelines: a systematic review. Med J Aust 2002; 177:502–506.
  37. Prasad V, Cifu A, Ioannidis JP. Reversals of established medical practices: evidence to abandon ship. JAMA 2012; 307:37–38.
  38. Steinbrook R. Guidance for guidelines. N Engl J Med 2007; 356:331–333.
  39. Sirovich BE, Woloshin S, Schwartz LM. Too little? Too much? Primary care physicians’ views on US health care: a brief report. Arch Intern Med 2011; 171:1582–1585.
  40. Brown SR, Brown J. Why do physicians order unnecessary preoperative tests? A qualitative study. Fam Med 2011; 43:338–343.
  41. LeCraw LL. Use of clinical practice guidelines in medical malpractice litigation. J Oncol Pract 2007; 3:254.
  42. Studdert DM, Mello MM, Sage WM, et al. Defensive medicine among high-risk specialist physicians in a volatile malpractice environment. JAMA 2005; 293:2609–2617.
  43. Budetti PP. Tort reform and the patient safety movement: seeking common ground. JAMA 2005; 293:2660–2662.
  44. Bishop TF, Federman AD, Ross JS. Laboratory test ordering at physician offices with and without on-site laboratories. J Gen Intern Med 2010; 25:1057–1063.
  45. Rosenthal E. Medical costs rise as retirees winter in Florida. The New York Times, Jan 31, 2015. http://nyti.ms/1vmjfa5. Accessed August 31, 2015.
References
  1. Committee on Standards and Practice Parameters, Apfelbaum JL, Connis RT, Nickinovich DG, et al. Practice advisory for preanesthesia evaluation. An updated report by the American Society of Anesthesiologists Task Force on Preanesthesia Evaluation. Anesthesiology 2012; 116:522–538.
  2. Fleisher LA, Fleischmann KE, Auerbach AD, et al; American College of Cardiology and American Heart Association. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines. J Am Coll Cardiol 2014; 64:e77–e137.
  3. Society of General Internal Medicine. Don’t perform routine pre-operative testing before low-risk surgical procedures. Choosing Wisely. An initiative of the ABIM Foundation. September 12, 2013. www.choosingwisely.org/clinician-lists/society-general-internal-medicine-routine-preoperative-testing-before-low-risk-surgery/. Accessed August 31, 2015.
  4. Houchens N. Should healthy patients undergoing low-risk, elective, noncardiac surgery undergo routine preoperative laboratory testing? Cleve Clin J Med 2015; 82:664–666.
  5. Rohrer MJ, Michelotti MC, Nahrwold DL. A prospective evaluation of the efficacy of preoperative coagulation testing. Ann Surg 1988; 208:554–557.
  6. Eagle KA, Coley CM, Newell JB, et al. Combining clinical and thallium data optimizes preoperative assessment of cardiac risk before major vascular surgery. Ann Intern Med 1989; 110:859–866.
  7. Mangano DT, London MJ, Tubau JF, et al. Dipyridamole thallium-201 scintigraphy as a preoperative screening test. A reexamination of its predictive potential. Study of Perioperative Ischemia Research Group. Circulation 1991; 84:493–502.
  8. Stratmann HG, Younis LT, Wittry MD, Amato M, Mark AL, Miller DD. Dipyridamole technetium 99m sestamibi myocardial tomography for preoperative cardiac risk stratification before major or minor nonvascular surgery. Am Heart J 1996; 132:536–541.
  9. Schein OD, Katz J, Bass EB, et al. The value of routine preoperative medical testing before cataract surgery. Study of Medical Testing for Cataract Surgery. N Engl J Med 2000; 342:168–175.
  10. Hashimoto J, Nakahara T, Bai J, Kitamura N, Kasamatsu T, Kubo A. Preoperative risk stratification with myocardial perfusion imaging in intermediate and low-risk non-cardiac surgery. Circ J 2007; 71:1395–1400.
  11. Smetana GW. The conundrum of unnecessary preoperative testing. JAMA Intern Med 2015; 175:1359–1361.
  12. Prasad V, Cifu A. Medical reversal: why we must raise the bar before adopting new technologies. Yale J Biol Med 2011; 84:471–478.
  13. Tatsioni A, Bonitsis NG, Ioannidis JP. Persistence of contradicted claims in the literature. JAMA 2007; 298:2517–2526.
  14. Moscucci M. Medical reversal, clinical trials, and the “late” open artery hypothesis in acute myocardial infarction. Arch Intern Med 2011; 171:1643–1644.
  15. Coleman J, Menzel H, Katz E. Social processes in physicians’ adoption of a new drug. J Chronic Dis 1959; 9:1–19.
  16. Cabana MD, Rand CS, Powe NR, et al. Why don’t physicians follow clinical practice guidelines? A framework for improvement. JAMA 1999; 282:1458–1465.
  17. Tricoci P, Allen JM, Kramer JM, Califf RM, Smith SC Jr. Scientific evidence underlying the ACC/AHA clinical practice guidelines. JAMA 2009; 301:831–841.
  18. Moher D, Hopewell S, Schulz KF, et al; CONSORT. CONSORT 2010 explanation and elaboration: updated guidelines for reporting parallel group randomised trials. Int J Surg 2012; 10:28–55.
  19. Gattinoni L, Giomarelli P. Acquiring knowledge in intensive care: merits and pitfalls of randomized controlled trials. Intensive Care Med 2015; 41:1460–1464.
  20. Levy JH, Szlam F, Wolberg AS, Winkler A. Clinical use of the activated partial thromboplastin time and prothrombin time for screening: a review of the literature and current guidelines for testing. Clin Lab Med 2014; 34:453–477.
  21. Dale W, Hemmerich J, Moliski E, Schwarze ML, Tung A. Effect of specialty and recent experience on perioperative decision-making for abdominal aortic aneurysm repair. J Am Geriatr Soc 2012; 60:1889–1894.
  22. Underwood SR, Anagnostopoulos C, Cerqueira M, et al; British Cardiac Society, British Nuclear Cardiology Society, British Nuclear Medicine Society, Royal College of Physicians of London, Royal College of Physicians of London. Myocardial perfusion scintigraphy: the evidence. Eur J Nucl Med Mol Imaging 2004; 31:261–291.
  23. Das MK, Pellikka PA, Mahoney DW, et al. Assessment of cardiac risk before nonvascular surgery: dobutamine stress echocardiography in 530 patients. J Am Coll Cardiol 2000; 35:1647–1653.
  24. Meijboom WB, Mollet NR, Van Mieghem CA, et al. Pre-operative computed tomography coronary angiography to detect significant coronary artery disease in patients referred for cardiac valve surgery. J Am Coll Cardiol 2006; 48:1658–1665.
  25. Russo V, Gostoli V, Lovato L, et al. Clinical value of multidetector CT coronary angiography as a preoperative screening test before non-coronary cardiac surgery. Heart 2007; 93:1591–1598.
  26. Schuetz GM, Zacharopoulou NM, Schlattmann P, Dewey M. Meta-analysis: noninvasive coronary angiography using computed tomography versus magnetic resonance imaging. Ann Intern Med 2010; 152:167–177.
  27. Bluemke DA, Achenbach S, Budoff M, et al. Noninvasive coronary artery imaging: magnetic resonance angiography and multidetector computed tomography angiography: a scientific statement from the American Heart Association Committee on Cardiovascular Imaging and Intervention of the Council on Cardiovascular Radiology and Intervention, and the Councils on Clinical Cardiology and Cardiovascular Disease in the Young. Circulation 2008; 118:586–606.
  28. Nagel E, Lehmkuhl HB, Bocksch W, et al. Noninvasive diagnosis of ischemia-induced wall motion abnormalities with the use of high-dose dobutamine stress MRI: comparison with dobutamine stress echocardiography. Circulation 1999; 99:763–770.
  29. Taylor H. Physicians’ use of clinical guidelines—and how to increase it. Healthcare News 2008; 8:32–55. www.harrisinteractive.com/vault/HI_HealthCareNews2008Vol8_Iss04.pdf. Accessed August 31, 2015.
  30. Kenefick H, Lee J, Fleishman V. Improving physician adherence to clinical practice guidelines. Barriers and stragies for change. New England Healthcare Institute, February 2008. www.nehi.net/writable/publication_files/file/cpg_report_final.pdf. Accessed August 31, 2015.
  31. Williams J, Cheung WY, Price DE, et al. Clinical guidelines online: do they improve compliance? Postgrad Med J 2004; 80:415–419.
  32. Wians F. Clinical laboratory tests: which, why, and what do the results mean? Lab Medicine 2009; 40:105–113.
  33. McFalls EO, Ward HB, Moritz TE, et al. Coronary-artery revascularization before elective major vascular surgery. N Engl J Med 2004; 351:2795–2804.
  34. Kristensen SD, Knuuti J, Saraste A, et al; Authors/Task Force Members. 2014 ESC/ESA guidelines on non-cardiac surgery: cardiovascular assessment and management: The Joint Task Force on non-cardiac surgery: cardiovascular assessment and management of the European Society of Cardiology (ESC) and the European Society of Anaesthesiology (ESA). Eur Heart J 2014; 35:2383–2431.
  35. Eagle KA, Rihal CS, Mickel MC, Holmes DR, Foster ED, Gersh BJ. Cardiac risk of noncardiac surgery: influence of coronary disease and type of surgery in 3368 operations. CASS Investigators and University of Michigan Heart Care Program. Coronary Artery Surgery Study. Circulation 1997; 96:1882–1887.
  36. Farquhar CM, Kofa EW, Slutsky JR. Clinicians’ attitudes to clinical practice guidelines: a systematic review. Med J Aust 2002; 177:502–506.
  37. Prasad V, Cifu A, Ioannidis JP. Reversals of established medical practices: evidence to abandon ship. JAMA 2012; 307:37–38.
  38. Steinbrook R. Guidance for guidelines. N Engl J Med 2007; 356:331–333.
  39. Sirovich BE, Woloshin S, Schwartz LM. Too little? Too much? Primary care physicians’ views on US health care: a brief report. Arch Intern Med 2011; 171:1582–1585.
  40. Brown SR, Brown J. Why do physicians order unnecessary preoperative tests? A qualitative study. Fam Med 2011; 43:338–343.
  41. LeCraw LL. Use of clinical practice guidelines in medical malpractice litigation. J Oncol Pract 2007; 3:254.
  42. Studdert DM, Mello MM, Sage WM, et al. Defensive medicine among high-risk specialist physicians in a volatile malpractice environment. JAMA 2005; 293:2609–2617.
  43. Budetti PP. Tort reform and the patient safety movement: seeking common ground. JAMA 2005; 293:2660–2662.
  44. Bishop TF, Federman AD, Ross JS. Laboratory test ordering at physician offices with and without on-site laboratories. J Gen Intern Med 2010; 25:1057–1063.
  45. Rosenthal E. Medical costs rise as retirees winter in Florida. The New York Times, Jan 31, 2015. http://nyti.ms/1vmjfa5. Accessed August 31, 2015.
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Ischemic Stroke Workup

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Enough is enough? The changing world of ischemic stroke workup

After entertaining the possibility of acute intervention, the majority of hospitalists efforts in the management of patients with ischemic stroke involve identifying an etiology and initiating secondary prevention strategies. Other than evaluating stroke risk factors, workup has traditionally involved extracranial and intracranial vessel imaging, cardiac telemetry, and echocardiography. Even after exhaustive searches, no cause for stroke is found in nearly 25% of cases, leading to a recent focus on determining why these so‐called cryptogenic strokes happen and how to prevent their recurrence.[1, 2]

Echocardiography is commonly obtained in most patients with ischemic stroke, but its yield is probably modest at best. Although transesophageal echocardiography (TEE) may be superior to transthoracic echocardiography (TTE) for determining an etiology of stroke, whether these findings substantially change management remains debatable.[3, 4] In this issue of the Journal of Hospital Medicine, Marino and colleagues examined the yield of TEE in patients without a known cause of ischemic stroke following a normal TTE.[5] A possible cause of stroke was identified in 42%, including aortic plaques and patent foramen ovale (PFO), but in only 1 patient did this discovery change management.

Secondary prevention strategies in ischemic stroke outside of atrial fibrillation now almost exclusively involve antiplatelet medications.[6] Studies of secondary prevention in aortic arch atheromas, patients with depressed systolic function, and those with PFO have failed to demonstrate any strategy that is superior to antiplatelets, and therefore the bar is high to show that any TEE findings impact treatment other than obvious and rare smoking guns such as a rare valvular lesion, cardiac tumor, or atrial thrombus.[7, 8, 9]

What is more of a recent headline in stroke workup is the increasing emphasis on long‐term cardiac monitoring following discharge to detect those with atrial fibrillation, which likely comprise between 15% and 20% of cryptogenic stroke patients.[10] Finding atrial fibrillation clearly changes management and therefore has a higher yield than the vast majority of possible findings on echocardiography. Perhaps in patients in whom a TEE is being considered, extended monitoring should happen first as an outpatient, followed by TEE if the stroke etiology remains obscure. On the other hand, severe left atrial enlargement, thrombus in the atrium, or atrial spontaneous echo contrast (smoke) are features on echocardiography that might raise the suspicion of atrial fibrillation so high that anticoagulation could be considered while long‐term monitoring is being used to definitively prove an atrial arrhythmia.

The current study does have some limitations other than those inherent to its retrospective design. Patients were only included if they were older than 50 years. Some have advocated using TEE as the echocardiogram of choice in young stroke patients due to its perhaps higher yield in these individuals; this study does not address this strategy. At institutions such as ours, an abnormal TTE in a cryptogenic stroke patient is followed by a TEE, and this study again does not alter this approach, because only those with a normal TTE were included. The definition of a normal TTE used in the study was so narrow, including normal left ventricular systolic function, that a majority of stroke patients with vascular risk factors such as hypertension would have likely been excluded. Determining what features and quality of a TTE are so definitive that a TEE is not necessary will be an important thrust of additional research. However, because TEE shows a better view of the left atrial appendage, the aortic arch, and is probably a better shunt study compared with TTE, it is not clear if a normal TTE will ever be adequate to prevent this second more invasive study in selected patients.

At the heart of the matter for health systems is the cost‐effectiveness of any screening approach used to determine the etiology of acute ischemic stroke. Studies are underway that will likely demonstrate that long‐term monitoring for atrial fibrillation will be worth it. Although it is dubious that TEE would ever fall into the same category due to its low yield, one might imagine a scenario, as our workup for cryptogenic stroke becomes more and more complicated, where obtaining a TEE is cost‐effective simply because it gives an answer and therefore can halt further testing. Perhaps at the end of the day, a TEE will just allow us to say to our stroke patients that enough is enough.

Disclosures: Dr. Josephson receives personal compensation as Editor‐in‐Chief of the New England Journal of Medicine Journal Watch Neurology and in an editorial capacity for Continuum Audio.

References
  1. Hart RG, Diener HC, Coutts SB, et al. Embolic strokes of undetermined source: the case for a new clinical construct. Lancet Neurol. 2014;13:429438.
  2. Lin L, Yiin GS, Geraghty OC, et al. Incidence, outcome, risk factors, and long‐term prognosis of cryptogenic transient ischaemic attack and ischaemic stroke: a population‐based study. Lancet Neurol. 2015;14:903913.
  3. Bruijn SF, Agema WR, Lammers GJ, et al. Transesophageal echocardiography is superior to transthoracic echocardiography in management of patients of any age with transient ischemic attack or stroke. Stroke. 2006;37:25312534.
  4. McGrath ER, Paikin JS, Motlagh B, Salehian O, Kapral MK, O'Donnell MJ. Transesophageal echocardiography in patients with cryptogenic ischemic stroke: a systematic review. Am Heart J. 2014;168:706712.
  5. Marino B, Jaiswal A, Goldbarg S, Bernardini GL, Kerwin T. Impact of transesophageal echocardiography on clinical management of patients over age 50 with cryptogenic stroke and normal transthoracic echocardiogram. J Hosp Med. 2016;11(2):9598.
  6. Kernan WN, Ovbiagele B, Black HR, et al. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45:21602236.
  7. Amarenco P, Davis S, Jones EF, et al. Clopidogrel plus aspirin versus warfarin in patients with stroke and aortic arch plaques. Stroke. 2014;45:12481257.
  8. Homma S, Thompson JL, Pullicino PM, et al. Warfarin and aspirin in patients with heart failure and sinus rhythm. N Engl J Med. 2012;366:18591869.
  9. Furlan AJ, Reisman M, Massaro J, et al. Closure or medical therapy for cryptogenic stroke with patent foramen ovale. N Engl J Med. 2012;366:991999.
  10. Gladstone DJ, Spring M, Dorian P, et al. Atrial fibrillation in patients with cryptogenic stroke. N Engl J Med. 2014;370:24672477.
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After entertaining the possibility of acute intervention, the majority of hospitalists efforts in the management of patients with ischemic stroke involve identifying an etiology and initiating secondary prevention strategies. Other than evaluating stroke risk factors, workup has traditionally involved extracranial and intracranial vessel imaging, cardiac telemetry, and echocardiography. Even after exhaustive searches, no cause for stroke is found in nearly 25% of cases, leading to a recent focus on determining why these so‐called cryptogenic strokes happen and how to prevent their recurrence.[1, 2]

Echocardiography is commonly obtained in most patients with ischemic stroke, but its yield is probably modest at best. Although transesophageal echocardiography (TEE) may be superior to transthoracic echocardiography (TTE) for determining an etiology of stroke, whether these findings substantially change management remains debatable.[3, 4] In this issue of the Journal of Hospital Medicine, Marino and colleagues examined the yield of TEE in patients without a known cause of ischemic stroke following a normal TTE.[5] A possible cause of stroke was identified in 42%, including aortic plaques and patent foramen ovale (PFO), but in only 1 patient did this discovery change management.

Secondary prevention strategies in ischemic stroke outside of atrial fibrillation now almost exclusively involve antiplatelet medications.[6] Studies of secondary prevention in aortic arch atheromas, patients with depressed systolic function, and those with PFO have failed to demonstrate any strategy that is superior to antiplatelets, and therefore the bar is high to show that any TEE findings impact treatment other than obvious and rare smoking guns such as a rare valvular lesion, cardiac tumor, or atrial thrombus.[7, 8, 9]

What is more of a recent headline in stroke workup is the increasing emphasis on long‐term cardiac monitoring following discharge to detect those with atrial fibrillation, which likely comprise between 15% and 20% of cryptogenic stroke patients.[10] Finding atrial fibrillation clearly changes management and therefore has a higher yield than the vast majority of possible findings on echocardiography. Perhaps in patients in whom a TEE is being considered, extended monitoring should happen first as an outpatient, followed by TEE if the stroke etiology remains obscure. On the other hand, severe left atrial enlargement, thrombus in the atrium, or atrial spontaneous echo contrast (smoke) are features on echocardiography that might raise the suspicion of atrial fibrillation so high that anticoagulation could be considered while long‐term monitoring is being used to definitively prove an atrial arrhythmia.

The current study does have some limitations other than those inherent to its retrospective design. Patients were only included if they were older than 50 years. Some have advocated using TEE as the echocardiogram of choice in young stroke patients due to its perhaps higher yield in these individuals; this study does not address this strategy. At institutions such as ours, an abnormal TTE in a cryptogenic stroke patient is followed by a TEE, and this study again does not alter this approach, because only those with a normal TTE were included. The definition of a normal TTE used in the study was so narrow, including normal left ventricular systolic function, that a majority of stroke patients with vascular risk factors such as hypertension would have likely been excluded. Determining what features and quality of a TTE are so definitive that a TEE is not necessary will be an important thrust of additional research. However, because TEE shows a better view of the left atrial appendage, the aortic arch, and is probably a better shunt study compared with TTE, it is not clear if a normal TTE will ever be adequate to prevent this second more invasive study in selected patients.

At the heart of the matter for health systems is the cost‐effectiveness of any screening approach used to determine the etiology of acute ischemic stroke. Studies are underway that will likely demonstrate that long‐term monitoring for atrial fibrillation will be worth it. Although it is dubious that TEE would ever fall into the same category due to its low yield, one might imagine a scenario, as our workup for cryptogenic stroke becomes more and more complicated, where obtaining a TEE is cost‐effective simply because it gives an answer and therefore can halt further testing. Perhaps at the end of the day, a TEE will just allow us to say to our stroke patients that enough is enough.

Disclosures: Dr. Josephson receives personal compensation as Editor‐in‐Chief of the New England Journal of Medicine Journal Watch Neurology and in an editorial capacity for Continuum Audio.

After entertaining the possibility of acute intervention, the majority of hospitalists efforts in the management of patients with ischemic stroke involve identifying an etiology and initiating secondary prevention strategies. Other than evaluating stroke risk factors, workup has traditionally involved extracranial and intracranial vessel imaging, cardiac telemetry, and echocardiography. Even after exhaustive searches, no cause for stroke is found in nearly 25% of cases, leading to a recent focus on determining why these so‐called cryptogenic strokes happen and how to prevent their recurrence.[1, 2]

Echocardiography is commonly obtained in most patients with ischemic stroke, but its yield is probably modest at best. Although transesophageal echocardiography (TEE) may be superior to transthoracic echocardiography (TTE) for determining an etiology of stroke, whether these findings substantially change management remains debatable.[3, 4] In this issue of the Journal of Hospital Medicine, Marino and colleagues examined the yield of TEE in patients without a known cause of ischemic stroke following a normal TTE.[5] A possible cause of stroke was identified in 42%, including aortic plaques and patent foramen ovale (PFO), but in only 1 patient did this discovery change management.

Secondary prevention strategies in ischemic stroke outside of atrial fibrillation now almost exclusively involve antiplatelet medications.[6] Studies of secondary prevention in aortic arch atheromas, patients with depressed systolic function, and those with PFO have failed to demonstrate any strategy that is superior to antiplatelets, and therefore the bar is high to show that any TEE findings impact treatment other than obvious and rare smoking guns such as a rare valvular lesion, cardiac tumor, or atrial thrombus.[7, 8, 9]

What is more of a recent headline in stroke workup is the increasing emphasis on long‐term cardiac monitoring following discharge to detect those with atrial fibrillation, which likely comprise between 15% and 20% of cryptogenic stroke patients.[10] Finding atrial fibrillation clearly changes management and therefore has a higher yield than the vast majority of possible findings on echocardiography. Perhaps in patients in whom a TEE is being considered, extended monitoring should happen first as an outpatient, followed by TEE if the stroke etiology remains obscure. On the other hand, severe left atrial enlargement, thrombus in the atrium, or atrial spontaneous echo contrast (smoke) are features on echocardiography that might raise the suspicion of atrial fibrillation so high that anticoagulation could be considered while long‐term monitoring is being used to definitively prove an atrial arrhythmia.

The current study does have some limitations other than those inherent to its retrospective design. Patients were only included if they were older than 50 years. Some have advocated using TEE as the echocardiogram of choice in young stroke patients due to its perhaps higher yield in these individuals; this study does not address this strategy. At institutions such as ours, an abnormal TTE in a cryptogenic stroke patient is followed by a TEE, and this study again does not alter this approach, because only those with a normal TTE were included. The definition of a normal TTE used in the study was so narrow, including normal left ventricular systolic function, that a majority of stroke patients with vascular risk factors such as hypertension would have likely been excluded. Determining what features and quality of a TTE are so definitive that a TEE is not necessary will be an important thrust of additional research. However, because TEE shows a better view of the left atrial appendage, the aortic arch, and is probably a better shunt study compared with TTE, it is not clear if a normal TTE will ever be adequate to prevent this second more invasive study in selected patients.

At the heart of the matter for health systems is the cost‐effectiveness of any screening approach used to determine the etiology of acute ischemic stroke. Studies are underway that will likely demonstrate that long‐term monitoring for atrial fibrillation will be worth it. Although it is dubious that TEE would ever fall into the same category due to its low yield, one might imagine a scenario, as our workup for cryptogenic stroke becomes more and more complicated, where obtaining a TEE is cost‐effective simply because it gives an answer and therefore can halt further testing. Perhaps at the end of the day, a TEE will just allow us to say to our stroke patients that enough is enough.

Disclosures: Dr. Josephson receives personal compensation as Editor‐in‐Chief of the New England Journal of Medicine Journal Watch Neurology and in an editorial capacity for Continuum Audio.

References
  1. Hart RG, Diener HC, Coutts SB, et al. Embolic strokes of undetermined source: the case for a new clinical construct. Lancet Neurol. 2014;13:429438.
  2. Lin L, Yiin GS, Geraghty OC, et al. Incidence, outcome, risk factors, and long‐term prognosis of cryptogenic transient ischaemic attack and ischaemic stroke: a population‐based study. Lancet Neurol. 2015;14:903913.
  3. Bruijn SF, Agema WR, Lammers GJ, et al. Transesophageal echocardiography is superior to transthoracic echocardiography in management of patients of any age with transient ischemic attack or stroke. Stroke. 2006;37:25312534.
  4. McGrath ER, Paikin JS, Motlagh B, Salehian O, Kapral MK, O'Donnell MJ. Transesophageal echocardiography in patients with cryptogenic ischemic stroke: a systematic review. Am Heart J. 2014;168:706712.
  5. Marino B, Jaiswal A, Goldbarg S, Bernardini GL, Kerwin T. Impact of transesophageal echocardiography on clinical management of patients over age 50 with cryptogenic stroke and normal transthoracic echocardiogram. J Hosp Med. 2016;11(2):9598.
  6. Kernan WN, Ovbiagele B, Black HR, et al. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45:21602236.
  7. Amarenco P, Davis S, Jones EF, et al. Clopidogrel plus aspirin versus warfarin in patients with stroke and aortic arch plaques. Stroke. 2014;45:12481257.
  8. Homma S, Thompson JL, Pullicino PM, et al. Warfarin and aspirin in patients with heart failure and sinus rhythm. N Engl J Med. 2012;366:18591869.
  9. Furlan AJ, Reisman M, Massaro J, et al. Closure or medical therapy for cryptogenic stroke with patent foramen ovale. N Engl J Med. 2012;366:991999.
  10. Gladstone DJ, Spring M, Dorian P, et al. Atrial fibrillation in patients with cryptogenic stroke. N Engl J Med. 2014;370:24672477.
References
  1. Hart RG, Diener HC, Coutts SB, et al. Embolic strokes of undetermined source: the case for a new clinical construct. Lancet Neurol. 2014;13:429438.
  2. Lin L, Yiin GS, Geraghty OC, et al. Incidence, outcome, risk factors, and long‐term prognosis of cryptogenic transient ischaemic attack and ischaemic stroke: a population‐based study. Lancet Neurol. 2015;14:903913.
  3. Bruijn SF, Agema WR, Lammers GJ, et al. Transesophageal echocardiography is superior to transthoracic echocardiography in management of patients of any age with transient ischemic attack or stroke. Stroke. 2006;37:25312534.
  4. McGrath ER, Paikin JS, Motlagh B, Salehian O, Kapral MK, O'Donnell MJ. Transesophageal echocardiography in patients with cryptogenic ischemic stroke: a systematic review. Am Heart J. 2014;168:706712.
  5. Marino B, Jaiswal A, Goldbarg S, Bernardini GL, Kerwin T. Impact of transesophageal echocardiography on clinical management of patients over age 50 with cryptogenic stroke and normal transthoracic echocardiogram. J Hosp Med. 2016;11(2):9598.
  6. Kernan WN, Ovbiagele B, Black HR, et al. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45:21602236.
  7. Amarenco P, Davis S, Jones EF, et al. Clopidogrel plus aspirin versus warfarin in patients with stroke and aortic arch plaques. Stroke. 2014;45:12481257.
  8. Homma S, Thompson JL, Pullicino PM, et al. Warfarin and aspirin in patients with heart failure and sinus rhythm. N Engl J Med. 2012;366:18591869.
  9. Furlan AJ, Reisman M, Massaro J, et al. Closure or medical therapy for cryptogenic stroke with patent foramen ovale. N Engl J Med. 2012;366:991999.
  10. Gladstone DJ, Spring M, Dorian P, et al. Atrial fibrillation in patients with cryptogenic stroke. N Engl J Med. 2014;370:24672477.
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Enough is enough? The changing world of ischemic stroke workup
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Address for correspondence and reprint requests: S. Andrew Josephson, MD, Department of Neurology, Box 0114, 505 Parnassus Avenue, M‐798, San Francisco, CA 94143‐0114; Telephone: 415‐476‐9211; Fax: 415‐476‐8705; E‐mail: andrew.josephson@ucsf.edu
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Ultrabrief Delirium Assessments

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Ultrabrief delirium assessments—are they ready for primetime?

Delirium is a form of acute brain failure that affects up to 64% of older hospitalized patients and is associated with a multitude of adverse outcomes.[1] Healthcare providers, regardless of clinical setting, do not identify delirium in approximately 75% of cases.[2, 3] The paucity of brief and simple delirium assessment tools has been a barrier to improving delirium recognition.

To address this unmet need, several ultrabrief (30 seconds) delirium assessment tools have been recently studied. In this issue of the Journal of Hospital Medicine, Fick et al. evaluated 20 individual components of the 3‐minute diagnostic interview for delirium using the Confusion Assessment Method (3D‐CAM), which was recently validated in older hospitalized patients.[4, 5] They observed that the best‐performing single‐item delirium assessment was the months of the year backward (MOTYB) task from December to January. This task assesses for inattention, a cardinal feature of delirium. Using a cutoff of 1 or more errors, the MOTYB was 83% sensitive and 69% specific for delirium.[5] By adding name the day of the week, the sensitivity increased to 93% with similar specificity (64%). This supports research by O'Regan et al., who examined MOTYB, but defined a positive screen if they could not recite the months backward from December to July perfectly. They observed a sensitivity and specificity of 84% and 90%, respectively, in older hospitalized patients.[6]

The assessment of arousal, another feature of delirium, has also garnered significant interest as another ultrabrief delirium screening method. Arousal is the patient's responsiveness to the environment and can be assessed during routine clinical care. Fick et al. observed that impaired arousal using the 3D‐CAM was 19% sensitive for delirium. This is in contrast to others who have reported sensitivities of 64% to 84%.[7, 8, 9] The difference in sensitivity may in part be explained by the method used to detect arousal. The 3D‐CAM asks, Was the patient sleep/stuporous? or Was the patient hyperviglant? Previous studies used the Richmond Agitation Sedation Scale (RASS), an arousal scale based on eye contact and physical behaviors to assess patients from 5 (coma) to +4 (combative).[10] Therefore, it is important to consider the method of arousal assessment if using this feature for delirium screening.

These ultrabrief delirium assessments would be even more clinically useful if they identified patients at high risk for adverse outcomes. In this same journal issue, 2 studies evaluated the prognostic ability of several ultrabrief delirium assessments. Zadravecz et al. observed that an abnormal RASS was a moderately good predictor of 24‐hour mortality, with an area under the receiver operating characteristic curve of 0.82.[11] Yevchak et al. observed that an abnormal RASS or MOTYB was associated with longer hospital length of stays, increased in‐hospital mortality, and need for skilled nursing.[12]

Viewed as a whole, these studies represent a significant advancement in delirium measurement and have the potential to improve this quality‐of‐care issue. However, uncertainties still exist. (1) Can these ultrabrief delirium assessments be used as standalone assessments? Based upon current data, these assessments have a significant proportion of false negative and positive rates. The effect on such misclassification on patient outcomes and healthcare utilization needs to be clarified. Because of this concern, Fick et al. recommended performing a more specific delirium assessment in those who have a positive MOTYB screen.[5] (2) What is the optimal cutoff of the MOTYB task and does this cutoff vary in different patient populations? The optimal cutoff will depend on whether or not a more sensitive test (lower error threshold) or specific test (higher error threshold) is desired. The optimal cutoff may also depend on the patient population (eg, demented versus nondemented). (3) Most important to practicing hospitalist and patients, will introducing these ultrabrief delirium assessments improve delirium recognition and improve patient outcomes? The impetus for widespread implementation of these assessments would be strengthened if healthcare providers successfully applied these assessments in clinical practice and subsequently improved outcomes.

In conclusion, the MOTYB and the assessment of arousal may be reasonable alternatives to more conventional delirium screening, especially in clinical environments with significant time constraints. However, additional research is needed to better refine these instruments to the clinical environment they will be used and determine how they impact clinical care and patient outcomes.

Disclosures

Dr. Han is supported the National Heart, Lung, and Blood Institute (K12HL109019). Dr. Vasilevskis is supported by the National Institutes of Health (K23AG040157) and the Geriatric Research, Education and Clinical Center (GRECC). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health or the Department of Veterans Affairs. The authors report no conflicts of interest.

References
  1. Inouye SK, Westendorp RG, Saczynski JS. Delirium in elderly people. Lancet. 2014;383(9920):911922.
  2. Collins N, Blanchard MR, Tookman A, Sampson EL. Detection of delirium in the acute hospital. Age Ageing. 2010;39(1):131135.
  3. Han JH, Zimmerman EE, Cutler N, et al. Delirium in older emergency department patients: recognition, risk factors, and psychomotor subtypes. Acad Emerg Med. 2009;16(3):193200.
  4. Marcantonio ER, Ngo LH, O'Connor M, et al. 3D‐CAM: derivation and validation of a 3‐minute diagnostic interview for CAM‐defined delirium: a cross‐sectional diagnostic test study. Ann Intern Med. 2014;161(8):554561.
  5. Fick DM, Inouye SK, Guess J, et al. Preliminary development of an ultrabrief two‐item bedside test for delirium. J Hosp Med. 2015;10(00):000000.
  6. O'Regan NA, Ryan DJ, Boland E, et al. Attention! A good bedside test for delirium? J Neurol Neurosurg Psychiatry. 2014;85(10):11221131.
  7. Chester JG, Beth Harrington M, Rudolph JL, Delirium Working Group VA. Serial administration of a modified Richmond Agitation and Sedation Scale for delirium screening. J Hosp Med. 2012;7(5):450453.
  8. Tieges Z, McGrath A, Hall RJ, Maclullich AM. Abnormal level of arousal as a predictor of delirium and inattention: an exploratory study. Am J Geriatr Psychiatry. 2013;21(12):12441253.
  9. Han JH, Vasilevskis EE, Schnelle JF, et al. The diagnostic performance of the Richmond Agitation Sedation Scale for detecting delirium in older emergency department patients. Acad Emerg Med. 2015;22(7):878882.
  10. Sessler CN, Gosnell MS, Grap MJ, et al. The Richmond Agitation‐Sedation Scale: validity and reliability in adult intensive care unit patients. Am J Respir Crit Care Med. 2002;166(10):13381344.
  11. Zadravecz F, Tien L, Robertson‐Dick B, et al. Comparison of mental status scales for predicting mortality on the general wards. J Hosp Med. 2015;10(10):658663.
  12. Yevchak AM, Doherty K, Archambault E, Kelley KW, Fonda JR, Rudolph JL. The association between an ultrabrief cognitive screening in older adults and hospital outcomes. J Hosp Med. 2015;10(10):651657.
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Delirium is a form of acute brain failure that affects up to 64% of older hospitalized patients and is associated with a multitude of adverse outcomes.[1] Healthcare providers, regardless of clinical setting, do not identify delirium in approximately 75% of cases.[2, 3] The paucity of brief and simple delirium assessment tools has been a barrier to improving delirium recognition.

To address this unmet need, several ultrabrief (30 seconds) delirium assessment tools have been recently studied. In this issue of the Journal of Hospital Medicine, Fick et al. evaluated 20 individual components of the 3‐minute diagnostic interview for delirium using the Confusion Assessment Method (3D‐CAM), which was recently validated in older hospitalized patients.[4, 5] They observed that the best‐performing single‐item delirium assessment was the months of the year backward (MOTYB) task from December to January. This task assesses for inattention, a cardinal feature of delirium. Using a cutoff of 1 or more errors, the MOTYB was 83% sensitive and 69% specific for delirium.[5] By adding name the day of the week, the sensitivity increased to 93% with similar specificity (64%). This supports research by O'Regan et al., who examined MOTYB, but defined a positive screen if they could not recite the months backward from December to July perfectly. They observed a sensitivity and specificity of 84% and 90%, respectively, in older hospitalized patients.[6]

The assessment of arousal, another feature of delirium, has also garnered significant interest as another ultrabrief delirium screening method. Arousal is the patient's responsiveness to the environment and can be assessed during routine clinical care. Fick et al. observed that impaired arousal using the 3D‐CAM was 19% sensitive for delirium. This is in contrast to others who have reported sensitivities of 64% to 84%.[7, 8, 9] The difference in sensitivity may in part be explained by the method used to detect arousal. The 3D‐CAM asks, Was the patient sleep/stuporous? or Was the patient hyperviglant? Previous studies used the Richmond Agitation Sedation Scale (RASS), an arousal scale based on eye contact and physical behaviors to assess patients from 5 (coma) to +4 (combative).[10] Therefore, it is important to consider the method of arousal assessment if using this feature for delirium screening.

These ultrabrief delirium assessments would be even more clinically useful if they identified patients at high risk for adverse outcomes. In this same journal issue, 2 studies evaluated the prognostic ability of several ultrabrief delirium assessments. Zadravecz et al. observed that an abnormal RASS was a moderately good predictor of 24‐hour mortality, with an area under the receiver operating characteristic curve of 0.82.[11] Yevchak et al. observed that an abnormal RASS or MOTYB was associated with longer hospital length of stays, increased in‐hospital mortality, and need for skilled nursing.[12]

Viewed as a whole, these studies represent a significant advancement in delirium measurement and have the potential to improve this quality‐of‐care issue. However, uncertainties still exist. (1) Can these ultrabrief delirium assessments be used as standalone assessments? Based upon current data, these assessments have a significant proportion of false negative and positive rates. The effect on such misclassification on patient outcomes and healthcare utilization needs to be clarified. Because of this concern, Fick et al. recommended performing a more specific delirium assessment in those who have a positive MOTYB screen.[5] (2) What is the optimal cutoff of the MOTYB task and does this cutoff vary in different patient populations? The optimal cutoff will depend on whether or not a more sensitive test (lower error threshold) or specific test (higher error threshold) is desired. The optimal cutoff may also depend on the patient population (eg, demented versus nondemented). (3) Most important to practicing hospitalist and patients, will introducing these ultrabrief delirium assessments improve delirium recognition and improve patient outcomes? The impetus for widespread implementation of these assessments would be strengthened if healthcare providers successfully applied these assessments in clinical practice and subsequently improved outcomes.

In conclusion, the MOTYB and the assessment of arousal may be reasonable alternatives to more conventional delirium screening, especially in clinical environments with significant time constraints. However, additional research is needed to better refine these instruments to the clinical environment they will be used and determine how they impact clinical care and patient outcomes.

Disclosures

Dr. Han is supported the National Heart, Lung, and Blood Institute (K12HL109019). Dr. Vasilevskis is supported by the National Institutes of Health (K23AG040157) and the Geriatric Research, Education and Clinical Center (GRECC). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health or the Department of Veterans Affairs. The authors report no conflicts of interest.

Delirium is a form of acute brain failure that affects up to 64% of older hospitalized patients and is associated with a multitude of adverse outcomes.[1] Healthcare providers, regardless of clinical setting, do not identify delirium in approximately 75% of cases.[2, 3] The paucity of brief and simple delirium assessment tools has been a barrier to improving delirium recognition.

To address this unmet need, several ultrabrief (30 seconds) delirium assessment tools have been recently studied. In this issue of the Journal of Hospital Medicine, Fick et al. evaluated 20 individual components of the 3‐minute diagnostic interview for delirium using the Confusion Assessment Method (3D‐CAM), which was recently validated in older hospitalized patients.[4, 5] They observed that the best‐performing single‐item delirium assessment was the months of the year backward (MOTYB) task from December to January. This task assesses for inattention, a cardinal feature of delirium. Using a cutoff of 1 or more errors, the MOTYB was 83% sensitive and 69% specific for delirium.[5] By adding name the day of the week, the sensitivity increased to 93% with similar specificity (64%). This supports research by O'Regan et al., who examined MOTYB, but defined a positive screen if they could not recite the months backward from December to July perfectly. They observed a sensitivity and specificity of 84% and 90%, respectively, in older hospitalized patients.[6]

The assessment of arousal, another feature of delirium, has also garnered significant interest as another ultrabrief delirium screening method. Arousal is the patient's responsiveness to the environment and can be assessed during routine clinical care. Fick et al. observed that impaired arousal using the 3D‐CAM was 19% sensitive for delirium. This is in contrast to others who have reported sensitivities of 64% to 84%.[7, 8, 9] The difference in sensitivity may in part be explained by the method used to detect arousal. The 3D‐CAM asks, Was the patient sleep/stuporous? or Was the patient hyperviglant? Previous studies used the Richmond Agitation Sedation Scale (RASS), an arousal scale based on eye contact and physical behaviors to assess patients from 5 (coma) to +4 (combative).[10] Therefore, it is important to consider the method of arousal assessment if using this feature for delirium screening.

These ultrabrief delirium assessments would be even more clinically useful if they identified patients at high risk for adverse outcomes. In this same journal issue, 2 studies evaluated the prognostic ability of several ultrabrief delirium assessments. Zadravecz et al. observed that an abnormal RASS was a moderately good predictor of 24‐hour mortality, with an area under the receiver operating characteristic curve of 0.82.[11] Yevchak et al. observed that an abnormal RASS or MOTYB was associated with longer hospital length of stays, increased in‐hospital mortality, and need for skilled nursing.[12]

Viewed as a whole, these studies represent a significant advancement in delirium measurement and have the potential to improve this quality‐of‐care issue. However, uncertainties still exist. (1) Can these ultrabrief delirium assessments be used as standalone assessments? Based upon current data, these assessments have a significant proportion of false negative and positive rates. The effect on such misclassification on patient outcomes and healthcare utilization needs to be clarified. Because of this concern, Fick et al. recommended performing a more specific delirium assessment in those who have a positive MOTYB screen.[5] (2) What is the optimal cutoff of the MOTYB task and does this cutoff vary in different patient populations? The optimal cutoff will depend on whether or not a more sensitive test (lower error threshold) or specific test (higher error threshold) is desired. The optimal cutoff may also depend on the patient population (eg, demented versus nondemented). (3) Most important to practicing hospitalist and patients, will introducing these ultrabrief delirium assessments improve delirium recognition and improve patient outcomes? The impetus for widespread implementation of these assessments would be strengthened if healthcare providers successfully applied these assessments in clinical practice and subsequently improved outcomes.

In conclusion, the MOTYB and the assessment of arousal may be reasonable alternatives to more conventional delirium screening, especially in clinical environments with significant time constraints. However, additional research is needed to better refine these instruments to the clinical environment they will be used and determine how they impact clinical care and patient outcomes.

Disclosures

Dr. Han is supported the National Heart, Lung, and Blood Institute (K12HL109019). Dr. Vasilevskis is supported by the National Institutes of Health (K23AG040157) and the Geriatric Research, Education and Clinical Center (GRECC). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health or the Department of Veterans Affairs. The authors report no conflicts of interest.

References
  1. Inouye SK, Westendorp RG, Saczynski JS. Delirium in elderly people. Lancet. 2014;383(9920):911922.
  2. Collins N, Blanchard MR, Tookman A, Sampson EL. Detection of delirium in the acute hospital. Age Ageing. 2010;39(1):131135.
  3. Han JH, Zimmerman EE, Cutler N, et al. Delirium in older emergency department patients: recognition, risk factors, and psychomotor subtypes. Acad Emerg Med. 2009;16(3):193200.
  4. Marcantonio ER, Ngo LH, O'Connor M, et al. 3D‐CAM: derivation and validation of a 3‐minute diagnostic interview for CAM‐defined delirium: a cross‐sectional diagnostic test study. Ann Intern Med. 2014;161(8):554561.
  5. Fick DM, Inouye SK, Guess J, et al. Preliminary development of an ultrabrief two‐item bedside test for delirium. J Hosp Med. 2015;10(00):000000.
  6. O'Regan NA, Ryan DJ, Boland E, et al. Attention! A good bedside test for delirium? J Neurol Neurosurg Psychiatry. 2014;85(10):11221131.
  7. Chester JG, Beth Harrington M, Rudolph JL, Delirium Working Group VA. Serial administration of a modified Richmond Agitation and Sedation Scale for delirium screening. J Hosp Med. 2012;7(5):450453.
  8. Tieges Z, McGrath A, Hall RJ, Maclullich AM. Abnormal level of arousal as a predictor of delirium and inattention: an exploratory study. Am J Geriatr Psychiatry. 2013;21(12):12441253.
  9. Han JH, Vasilevskis EE, Schnelle JF, et al. The diagnostic performance of the Richmond Agitation Sedation Scale for detecting delirium in older emergency department patients. Acad Emerg Med. 2015;22(7):878882.
  10. Sessler CN, Gosnell MS, Grap MJ, et al. The Richmond Agitation‐Sedation Scale: validity and reliability in adult intensive care unit patients. Am J Respir Crit Care Med. 2002;166(10):13381344.
  11. Zadravecz F, Tien L, Robertson‐Dick B, et al. Comparison of mental status scales for predicting mortality on the general wards. J Hosp Med. 2015;10(10):658663.
  12. Yevchak AM, Doherty K, Archambault E, Kelley KW, Fonda JR, Rudolph JL. The association between an ultrabrief cognitive screening in older adults and hospital outcomes. J Hosp Med. 2015;10(10):651657.
References
  1. Inouye SK, Westendorp RG, Saczynski JS. Delirium in elderly people. Lancet. 2014;383(9920):911922.
  2. Collins N, Blanchard MR, Tookman A, Sampson EL. Detection of delirium in the acute hospital. Age Ageing. 2010;39(1):131135.
  3. Han JH, Zimmerman EE, Cutler N, et al. Delirium in older emergency department patients: recognition, risk factors, and psychomotor subtypes. Acad Emerg Med. 2009;16(3):193200.
  4. Marcantonio ER, Ngo LH, O'Connor M, et al. 3D‐CAM: derivation and validation of a 3‐minute diagnostic interview for CAM‐defined delirium: a cross‐sectional diagnostic test study. Ann Intern Med. 2014;161(8):554561.
  5. Fick DM, Inouye SK, Guess J, et al. Preliminary development of an ultrabrief two‐item bedside test for delirium. J Hosp Med. 2015;10(00):000000.
  6. O'Regan NA, Ryan DJ, Boland E, et al. Attention! A good bedside test for delirium? J Neurol Neurosurg Psychiatry. 2014;85(10):11221131.
  7. Chester JG, Beth Harrington M, Rudolph JL, Delirium Working Group VA. Serial administration of a modified Richmond Agitation and Sedation Scale for delirium screening. J Hosp Med. 2012;7(5):450453.
  8. Tieges Z, McGrath A, Hall RJ, Maclullich AM. Abnormal level of arousal as a predictor of delirium and inattention: an exploratory study. Am J Geriatr Psychiatry. 2013;21(12):12441253.
  9. Han JH, Vasilevskis EE, Schnelle JF, et al. The diagnostic performance of the Richmond Agitation Sedation Scale for detecting delirium in older emergency department patients. Acad Emerg Med. 2015;22(7):878882.
  10. Sessler CN, Gosnell MS, Grap MJ, et al. The Richmond Agitation‐Sedation Scale: validity and reliability in adult intensive care unit patients. Am J Respir Crit Care Med. 2002;166(10):13381344.
  11. Zadravecz F, Tien L, Robertson‐Dick B, et al. Comparison of mental status scales for predicting mortality on the general wards. J Hosp Med. 2015;10(10):658663.
  12. Yevchak AM, Doherty K, Archambault E, Kelley KW, Fonda JR, Rudolph JL. The association between an ultrabrief cognitive screening in older adults and hospital outcomes. J Hosp Med. 2015;10(10):651657.
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Things We Do for No Reason/

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In this issue of the Journal of Hospital Medicine, we introduce a new recurring feature, Choosing Wisely: Things We Do for No Reason. The series is based on a talk I have delivered for the past 4 years at the annual national meeting of the Society of Hospital Medicine, in which I highlight 4 diagnostic tests, therapies, or other clinical practices that are commonly performed even though they are of low value to our inpatients.

There are many reasons hospitalists order unnecessary tests or treatments, or employ unhelpful clinical practices. Unnecessary testing may occur when we are not familiar with the test itselfthe actual costs of the test, the operating characteristics of the test, or the evidence supporting its usefulness in specific situations. Some tests are ordered unnecessarily because we cannot retrieve usable results from a different hospital or even our own electronic medical records. We may order tests or treatments due to patient expectations, a perceived need to practice defensively, or economic incentives.

Finally, we may simply order tests because of our uncertainty in the absence of data or simply because they are traditional practices (the way we've always done it). Physicians often order tests and treatments and institute clinical practices learned in residency or fellowship training.[1, 2] Local norms and practices influence physician behavior.

We created Things We Do for No Reason (TWDFNR) as a platform for provocative discussions of practices that have become common parts of hospital care but have limited supporting evidence, or even have evidence refuting or justifiably challenging their value. Each article in TWDFNR will describe why the test, treatment, or other clinical practice is commonly employed, why it may not be of high value, in what circumstances it may actually be valuable, and what conclusions can be drawn from the evidence provided. TWDFNR pieces are not systematic reviews or meta‐analyses and do not represent black and white conclusions or clinical practice standards; they are meant as a starting place for research and active discussions among hospitalists and patients.

In many respects, the Choosing Wisely: Things We Do for No Reason series is an extension of the Choosing Wisely campaign created by the American Board of Internal Medicine Foundation. Like Choosing Wisely, we are focusing on individual tests, treatments, and other clinical practices that are not beneficial and are potentially harmful to patients. Practices discussed may not cause significant physical or financial harm at the time they are used, but they may have significant downstream effects.

The Choosing Wisely campaign has brilliantly identified 5 important hospital medicine low‐value practices, and we hope to identify many more. We hope this series will serve as a grassroots effort to uncover more Choosing Wisely‐type practices. As institutions create their own high‐value care committees, the Choosing Wisely: Things We Do for No Reason series can provide possible agenda items, or provide the opportunity for sites to carry out analyses of their own practices to see whether any of the TWDFNR topics provide local opportunities for implementing higher‐value practices.

Although we do not believe that reducing the low‐value practices that will appear in TWDFNR will, alone, solve our wasteful practices, we hope that highlighting them will remind individuals, institutions, and systems that targeting low‐value practices is a responsibility that we all must embrace. We accept that not everyone will agree that the practices we present are low value, but the conversation is important to have. We invite you to take part in the Choosing Wisely: Things We Do for No Reason conversation. Let us know whether you think the practices highlighted are low value or whether you disagree with the conclusions. We welcome unsolicited proposals for series topics submitted as a 500‐word prcis. Send us your prcis or ideas on low‐value adult or pediatric patient practices that we should highlight in this series by emailing us at twdfnr@hospitalmedicine.org.

Disclosure: Nothing to report.

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References
  1. Sirovich BE, Lipner RS, Johnston M, Holmboe ES. The association between residency training and internists' ability to practice conservatively. JAMA Intern Med. 2014;174:16401648.
  2. Chen C, Petterson S, Phillips R, Bazemore A, Mullan F. Spending patterns in region of residency training and subsequent expenditures for care provided by practicing physicians for Medicare beneficiaries. JAMA. 2014;312:23852393.
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In this issue of the Journal of Hospital Medicine, we introduce a new recurring feature, Choosing Wisely: Things We Do for No Reason. The series is based on a talk I have delivered for the past 4 years at the annual national meeting of the Society of Hospital Medicine, in which I highlight 4 diagnostic tests, therapies, or other clinical practices that are commonly performed even though they are of low value to our inpatients.

There are many reasons hospitalists order unnecessary tests or treatments, or employ unhelpful clinical practices. Unnecessary testing may occur when we are not familiar with the test itselfthe actual costs of the test, the operating characteristics of the test, or the evidence supporting its usefulness in specific situations. Some tests are ordered unnecessarily because we cannot retrieve usable results from a different hospital or even our own electronic medical records. We may order tests or treatments due to patient expectations, a perceived need to practice defensively, or economic incentives.

Finally, we may simply order tests because of our uncertainty in the absence of data or simply because they are traditional practices (the way we've always done it). Physicians often order tests and treatments and institute clinical practices learned in residency or fellowship training.[1, 2] Local norms and practices influence physician behavior.

We created Things We Do for No Reason (TWDFNR) as a platform for provocative discussions of practices that have become common parts of hospital care but have limited supporting evidence, or even have evidence refuting or justifiably challenging their value. Each article in TWDFNR will describe why the test, treatment, or other clinical practice is commonly employed, why it may not be of high value, in what circumstances it may actually be valuable, and what conclusions can be drawn from the evidence provided. TWDFNR pieces are not systematic reviews or meta‐analyses and do not represent black and white conclusions or clinical practice standards; they are meant as a starting place for research and active discussions among hospitalists and patients.

In many respects, the Choosing Wisely: Things We Do for No Reason series is an extension of the Choosing Wisely campaign created by the American Board of Internal Medicine Foundation. Like Choosing Wisely, we are focusing on individual tests, treatments, and other clinical practices that are not beneficial and are potentially harmful to patients. Practices discussed may not cause significant physical or financial harm at the time they are used, but they may have significant downstream effects.

The Choosing Wisely campaign has brilliantly identified 5 important hospital medicine low‐value practices, and we hope to identify many more. We hope this series will serve as a grassroots effort to uncover more Choosing Wisely‐type practices. As institutions create their own high‐value care committees, the Choosing Wisely: Things We Do for No Reason series can provide possible agenda items, or provide the opportunity for sites to carry out analyses of their own practices to see whether any of the TWDFNR topics provide local opportunities for implementing higher‐value practices.

Although we do not believe that reducing the low‐value practices that will appear in TWDFNR will, alone, solve our wasteful practices, we hope that highlighting them will remind individuals, institutions, and systems that targeting low‐value practices is a responsibility that we all must embrace. We accept that not everyone will agree that the practices we present are low value, but the conversation is important to have. We invite you to take part in the Choosing Wisely: Things We Do for No Reason conversation. Let us know whether you think the practices highlighted are low value or whether you disagree with the conclusions. We welcome unsolicited proposals for series topics submitted as a 500‐word prcis. Send us your prcis or ideas on low‐value adult or pediatric patient practices that we should highlight in this series by emailing us at twdfnr@hospitalmedicine.org.

Disclosure: Nothing to report.

In this issue of the Journal of Hospital Medicine, we introduce a new recurring feature, Choosing Wisely: Things We Do for No Reason. The series is based on a talk I have delivered for the past 4 years at the annual national meeting of the Society of Hospital Medicine, in which I highlight 4 diagnostic tests, therapies, or other clinical practices that are commonly performed even though they are of low value to our inpatients.

There are many reasons hospitalists order unnecessary tests or treatments, or employ unhelpful clinical practices. Unnecessary testing may occur when we are not familiar with the test itselfthe actual costs of the test, the operating characteristics of the test, or the evidence supporting its usefulness in specific situations. Some tests are ordered unnecessarily because we cannot retrieve usable results from a different hospital or even our own electronic medical records. We may order tests or treatments due to patient expectations, a perceived need to practice defensively, or economic incentives.

Finally, we may simply order tests because of our uncertainty in the absence of data or simply because they are traditional practices (the way we've always done it). Physicians often order tests and treatments and institute clinical practices learned in residency or fellowship training.[1, 2] Local norms and practices influence physician behavior.

We created Things We Do for No Reason (TWDFNR) as a platform for provocative discussions of practices that have become common parts of hospital care but have limited supporting evidence, or even have evidence refuting or justifiably challenging their value. Each article in TWDFNR will describe why the test, treatment, or other clinical practice is commonly employed, why it may not be of high value, in what circumstances it may actually be valuable, and what conclusions can be drawn from the evidence provided. TWDFNR pieces are not systematic reviews or meta‐analyses and do not represent black and white conclusions or clinical practice standards; they are meant as a starting place for research and active discussions among hospitalists and patients.

In many respects, the Choosing Wisely: Things We Do for No Reason series is an extension of the Choosing Wisely campaign created by the American Board of Internal Medicine Foundation. Like Choosing Wisely, we are focusing on individual tests, treatments, and other clinical practices that are not beneficial and are potentially harmful to patients. Practices discussed may not cause significant physical or financial harm at the time they are used, but they may have significant downstream effects.

The Choosing Wisely campaign has brilliantly identified 5 important hospital medicine low‐value practices, and we hope to identify many more. We hope this series will serve as a grassroots effort to uncover more Choosing Wisely‐type practices. As institutions create their own high‐value care committees, the Choosing Wisely: Things We Do for No Reason series can provide possible agenda items, or provide the opportunity for sites to carry out analyses of their own practices to see whether any of the TWDFNR topics provide local opportunities for implementing higher‐value practices.

Although we do not believe that reducing the low‐value practices that will appear in TWDFNR will, alone, solve our wasteful practices, we hope that highlighting them will remind individuals, institutions, and systems that targeting low‐value practices is a responsibility that we all must embrace. We accept that not everyone will agree that the practices we present are low value, but the conversation is important to have. We invite you to take part in the Choosing Wisely: Things We Do for No Reason conversation. Let us know whether you think the practices highlighted are low value or whether you disagree with the conclusions. We welcome unsolicited proposals for series topics submitted as a 500‐word prcis. Send us your prcis or ideas on low‐value adult or pediatric patient practices that we should highlight in this series by emailing us at twdfnr@hospitalmedicine.org.

Disclosure: Nothing to report.

References
  1. Sirovich BE, Lipner RS, Johnston M, Holmboe ES. The association between residency training and internists' ability to practice conservatively. JAMA Intern Med. 2014;174:16401648.
  2. Chen C, Petterson S, Phillips R, Bazemore A, Mullan F. Spending patterns in region of residency training and subsequent expenditures for care provided by practicing physicians for Medicare beneficiaries. JAMA. 2014;312:23852393.
References
  1. Sirovich BE, Lipner RS, Johnston M, Holmboe ES. The association between residency training and internists' ability to practice conservatively. JAMA Intern Med. 2014;174:16401648.
  2. Chen C, Petterson S, Phillips R, Bazemore A, Mullan F. Spending patterns in region of residency training and subsequent expenditures for care provided by practicing physicians for Medicare beneficiaries. JAMA. 2014;312:23852393.
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Postoperative troponin surveillance: A diagnostic dilemma

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A major goal of perioperative medicine is to prevent, detect, and treat postoperative complications—in particular, cardiovascular complications. In the Perioperative Ischemic Evaluation (POISE) study,1 the 30-day mortality rate was four times higher in patients who had a perioperative myocardial infarction (MI) than in those who did not.1 Yet fewer than half of patients who have a postoperative MI have ischemic symptoms, suggesting that routine monitoring of cardiac biomarkers could detect these events and allow early intervention.

See related article

From 10% to 20% of patients have troponin elevations after noncardiac surgery.2 But until recently, many of these elevations were thought to be of minor importance and were ignored unless the patient met diagnostic criteria for MI. A new entity called MINS (myocardial injury after noncardiac surgery)3 was defined as a troponin level exceeding the upper limit of normal with or without ischemic symptoms or electrocardiographic changes and excluding noncardiac causes such as stroke, sepsis, and pulmonary embolism. Because elevations of troponin at any level have been associated with increased 30-day mortality rates, the question of the value of routine screening of asymptomatic postoperative patients for troponin elevation has been raised.

In this issue of Cleveland Clinic Journal of Medicine, Horr et al4 review the controversy of postoperative screening using troponin measurement and propose an algorithm for management.

QUESTIONS TO CONSIDER

Before recommending screening asymptomatic patients for troponin elevation, we need to consider a number of questions:

  • Which patients should be screened?
  • How should troponin elevations be treated?
  • Would casting a wider net improve outcomes?
  • What are the possible harms of troponin screening?

The bottom line is, will postoperative troponin screening change management and result in improved outcomes?

WHICH PATIENTS SHOULD BE SCREENED?

Why routine screening may be indicated

Elevated or even just detectable troponin levels are associated with adverse outcomes. A systematic review and meta-analysis of 3,318 patients2 demonstrated that high troponin levels after noncardiac surgery were independently associated with a risk of death three times higher than in patients with normal troponin levels.

In the Vascular Events in Noncardiac Surgery Patients Cohort Evaluation (VISION) study,5 troponin T was measured in 15,133 patients after surgery. The overall mortality rate was 1.9%, and the higher the peak troponin T level the higher the risk of death.

Postoperative troponin elevations are linked to bad outcomes, but should we screen everyone?In a single-center Canadian retrospective cohort analysis of 51,701 consecutive patients by Beattie et al,6 the peak postoperative level of troponin I improved the ability of a multivariable model to predict the risk of death. As in the VISION study, the mortality rate rose with the troponin level.6

In a study by van Waes et al7 in 2,232 consecutive noncardiac surgery patients over age 60 at intermediate to high risk, the all-cause mortality rate was 3%, and troponin I was elevated in 19% of patients. As in VISION and the Canadian retrospective study, the mortality rate increased with the troponin level.

Why routine screening may not help

In VISION,5 the probability of detecting myocardial injury was three times higher if patients were screened for 3 days after surgery than if they were tested only if clinical signs or symptoms indicated it.

However, in deciding whether to screen troponin levels in postoperative patients, we must take into account the patient’s clinical risk as well as the risk of the surgical procedure. Troponin elevation in low-risk patients is associated with a low mortality rate, and troponin elevations often are secondary to causes other than myocardial ischemia. In the study by van Waes et al,7 the association was stronger with all-cause mortality than with myocardial infarction, and in VISION5 there were more nonvascular deaths than vascular deaths, suggesting that troponin elevation is a nonspecific marker of adverse events.

Beattie et al6 found that the probability that a patient’s postoperative troponin level would be elevated increased as the patient’s clinical risk increased, but the yield was very low and the mortality rate was less than 1% in patients in risk classes 1 through 3 (of a possible 5 classes). In risk class 4, troponin I was elevated in 21.8%, and the mortality rate was 2.5%; in risk class 5 troponin I was elevated in 18.6%, and the mortality rate was 11.9%. Analyzing the data according to the type of surgery, mortality rates were highest in patients undergoing vascular surgery, neurosurgery, general surgery, and thoracic procedures, with all-cause mortality rates ranging from 2.6% to 5.2%.6

Screening should depend on risk

If postoperative troponin screening is to be recommended, it should not be routine for all patients but should be restricted to those with high clinical risk and those undergoing high-risk surgical procedures.

Rodseth and Devereaux8 recommended routine postoperative troponin measurement not only after vascular surgery, but also after high-risk surgery (general, neurosurgery, emergency surgery), as well as in patients over age 65 and patients with established atherosclerotic disease or risk factors for it. However, I believe this latter group may not be at high enough risk to justify routine screening.

Beattie et al6 advocated limiting postoperative troponin screening to patients with at least a moderate risk of MI and also suggested an international consensus conference to define criteria for postoperative MI, populations who should have routine postoperative screening, and consensus on treatment of patients with troponin elevations but not meeting the criteria for MI. Without this consensus on treatment, it is unclear if protocols for universal postoperative screening would improve outcomes.

For these reasons, the 2014 joint guidelines of the American College of Cardiology and American Heart Association9 (ACC/AHA) stated that the benefit of postoperative screening of troponin levels in patients with a high perioperative risk of MI but no signs or symptoms of myocardial ischemia or MI is “uncertain in the absence of established risks and benefits of a defined management strategy.” This recommendation was given a class IIb rating (may be considered) and level of evidence B (usefulness or efficacy less well established). On the other hand, the guidelines recommend measuring troponin levels if signs or symptoms suggest myocardial ischemia or MI (class I recommendation, level of evidence A) but state there is no benefit in routine screening of unselected patients without signs or symptoms of ischemia (class III recommendation, level of evidence B).

HOW SHOULD ELEVATIONS BE TREATED?

Lacking evidence, we can only speculate whether troponin screening helps or harmsBecause a troponin elevation in a patient without signs or symptoms of ischemia does not predict a specific type of death, physicians need to treat patients individually. Perioperative ischemia and inflammation could lead to injury of other organs, and death could result from multiorgan injury rather than from myocardial injury. Treating these troponin elevations in the same way we treat MI—ie, with antiplatelet therapy and anticoagulation—may result in increased bleeding or unnecessary cardiac catheterization, and starting beta-blockers in the perioperative period may be harmful. Because it is unclear how to manage these patients, cardiac medications have not routinely been given in previous studies.

POISE provided some evidence that patients with postoperative MI who were given aspirin and a statin did better.1 And the results of a smaller study10 suggested that intensification of drug therapy (aspirin, statin, beta-blocker, angiotensin-converting enzyme inhibitor) in patients with postoperative troponin I elevations was associated with improved outcomes at 1 year. If the bleeding risk is low, I believe that there is potential benefit in prescribing aspirin and statins for these patients.

CASTING A WIDER NET

Further complicating matters in the near future is the issue of using fifth-generation high-sensitivity troponin T assays. The European Society of Cardiology guidelines11 are somewhat more liberal than the ACC/AHA guidelines, stating that measuring high-sensitivity troponin after surgery “may be considered in high-risk patients to improve risk stratification.” This is a class IIB recommendation, level of evidence B.

With fifth-generation high-sensitivity troponin assays, troponin may be elevated in as many as 20% of patients preoperatively and 40% postoperatively, significantly increasing the number of patients said to have a complication. Besides potentially subjecting these patients to unproven treatments, such results would give the false impression that hospitals and surgeons using the screening tools actually had higher complication rates than those that did not screen.

POSSIBLE HARMS OF SCREENING

Elevated postoperative troponin may identify patients at higher risk of any adverse event but not specifically of cardiac-specific events. In an editorial, Beckman12 stated that routine measurement of troponin “is more likely to cause harm than to provide benefit and should not be used as a screening modality” because of the lack of a proven beneficial treatment strategy, because of the possible harm from applying the standard treatment for type 1 MI, and because it could divert attention from a true cause of an adverse event to a false one—ie, from a nonvascular condition to MI.11

There is clearly a need for clinical trials to determine which treatment, if any, can improve outcomes in these patients, and several trials have been started. But until we have evidence, we can only speculate as to whether screening postoperative patients for troponin elevation is beneficial or detrimental.

References
  1. Devereaux PJ, Xavier D, Pogue J, et al. Characteristics and short-term prognosis of perioperative myocardial infarction in patients undergoing noncardiac surgery: a cohort study. Ann Intern Med 2011; 154:523–528.
  2. Levy M, Heels-Ansdell D, Hiralal R, et al. Prognostic value of troponin and creatine kinase muscle and brain isoenzyme measurement after noncardiac surgery: a systematic review and meta-analysis. Anesthesiology 2011; 114:796–806.
  3. Botto F, Alonso-Coello P, Chan MT, et al. Myocardial injury after noncardiac surgery: a large, international, prospective cohort study establishing diagnostic criteria, characteristics, predictors, and 30-day outcomes. Anesthesiology 2014; 120:564–578.
  4. Horr S, Reed G, Menon V. Troponin elevation after noncardiac surgery: significance and management. Cleve Clin J Med 2015; 82:595–602.
  5. Vascular Events In Noncardiac Surgery Patients Cohort Evaluation Study I, Devereaux PJ, Chan MT, Alonso-Coello P, et al. Association between postoperative troponin levels and 30-day mortality among patients undergoing noncardiac surgery. JAMA 2012; 307:2295–2304.
  6. Beattie WS, Karkouti K, Tait G, et al. Use of clinically based troponin underestimates the cardiac injury in non-cardiac surgery: a single-centre cohort study in 51,701 consecutive patients. Can J Anaesth 2012; 59:1013–1022.
  7. van Waes JA, Nathoe HM, de Graaff JC, et al. Myocardial injury after noncardiac surgery and its association with short-term mortality. Circulation 2013; 127:2264–2271.
  8. Rodseth R, Devereaux PJ. Should we measure troponin routinely in patients after vascular surgery? American College of Cardiology. www.acc.org/latest-in-cardiology/articles/2014/07/18/14/46/should-we-measure-troponin-routinely-in-patients-after-vascular-surgery?w_nav=LC. Accessed August 5, 2015.
  9. Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014; 64:e77–e137.
  10. Foucrier A, Rodseth R, Aissaoui M, et al. The long-term impact of early cardiovascular therapy intensification for postoperative troponin elevation after major vascular surgery. Anesth Analg 2014; 119:1053–1063.
  11. Kristensen SD, Knuuti J, Saraste A, et al. 2014 ESC/ESA Guidelines on non-cardiac surgery: cardiovascular assessment and management: The Joint Task Force on non-cardiac surgery: cardiovascular assessment and management of the European Society of Cardiology (ESC) and the European Society of Anaesthesiology (ESA). Eur Heart J 2014; 35:2383–2431.
  12. Beckman JA. Postoperative troponin screening: a cardiac Cassandra? Circulation 2013; 127:2253–2266.
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Related Articles

A major goal of perioperative medicine is to prevent, detect, and treat postoperative complications—in particular, cardiovascular complications. In the Perioperative Ischemic Evaluation (POISE) study,1 the 30-day mortality rate was four times higher in patients who had a perioperative myocardial infarction (MI) than in those who did not.1 Yet fewer than half of patients who have a postoperative MI have ischemic symptoms, suggesting that routine monitoring of cardiac biomarkers could detect these events and allow early intervention.

See related article

From 10% to 20% of patients have troponin elevations after noncardiac surgery.2 But until recently, many of these elevations were thought to be of minor importance and were ignored unless the patient met diagnostic criteria for MI. A new entity called MINS (myocardial injury after noncardiac surgery)3 was defined as a troponin level exceeding the upper limit of normal with or without ischemic symptoms or electrocardiographic changes and excluding noncardiac causes such as stroke, sepsis, and pulmonary embolism. Because elevations of troponin at any level have been associated with increased 30-day mortality rates, the question of the value of routine screening of asymptomatic postoperative patients for troponin elevation has been raised.

In this issue of Cleveland Clinic Journal of Medicine, Horr et al4 review the controversy of postoperative screening using troponin measurement and propose an algorithm for management.

QUESTIONS TO CONSIDER

Before recommending screening asymptomatic patients for troponin elevation, we need to consider a number of questions:

  • Which patients should be screened?
  • How should troponin elevations be treated?
  • Would casting a wider net improve outcomes?
  • What are the possible harms of troponin screening?

The bottom line is, will postoperative troponin screening change management and result in improved outcomes?

WHICH PATIENTS SHOULD BE SCREENED?

Why routine screening may be indicated

Elevated or even just detectable troponin levels are associated with adverse outcomes. A systematic review and meta-analysis of 3,318 patients2 demonstrated that high troponin levels after noncardiac surgery were independently associated with a risk of death three times higher than in patients with normal troponin levels.

In the Vascular Events in Noncardiac Surgery Patients Cohort Evaluation (VISION) study,5 troponin T was measured in 15,133 patients after surgery. The overall mortality rate was 1.9%, and the higher the peak troponin T level the higher the risk of death.

Postoperative troponin elevations are linked to bad outcomes, but should we screen everyone?In a single-center Canadian retrospective cohort analysis of 51,701 consecutive patients by Beattie et al,6 the peak postoperative level of troponin I improved the ability of a multivariable model to predict the risk of death. As in the VISION study, the mortality rate rose with the troponin level.6

In a study by van Waes et al7 in 2,232 consecutive noncardiac surgery patients over age 60 at intermediate to high risk, the all-cause mortality rate was 3%, and troponin I was elevated in 19% of patients. As in VISION and the Canadian retrospective study, the mortality rate increased with the troponin level.

Why routine screening may not help

In VISION,5 the probability of detecting myocardial injury was three times higher if patients were screened for 3 days after surgery than if they were tested only if clinical signs or symptoms indicated it.

However, in deciding whether to screen troponin levels in postoperative patients, we must take into account the patient’s clinical risk as well as the risk of the surgical procedure. Troponin elevation in low-risk patients is associated with a low mortality rate, and troponin elevations often are secondary to causes other than myocardial ischemia. In the study by van Waes et al,7 the association was stronger with all-cause mortality than with myocardial infarction, and in VISION5 there were more nonvascular deaths than vascular deaths, suggesting that troponin elevation is a nonspecific marker of adverse events.

Beattie et al6 found that the probability that a patient’s postoperative troponin level would be elevated increased as the patient’s clinical risk increased, but the yield was very low and the mortality rate was less than 1% in patients in risk classes 1 through 3 (of a possible 5 classes). In risk class 4, troponin I was elevated in 21.8%, and the mortality rate was 2.5%; in risk class 5 troponin I was elevated in 18.6%, and the mortality rate was 11.9%. Analyzing the data according to the type of surgery, mortality rates were highest in patients undergoing vascular surgery, neurosurgery, general surgery, and thoracic procedures, with all-cause mortality rates ranging from 2.6% to 5.2%.6

Screening should depend on risk

If postoperative troponin screening is to be recommended, it should not be routine for all patients but should be restricted to those with high clinical risk and those undergoing high-risk surgical procedures.

Rodseth and Devereaux8 recommended routine postoperative troponin measurement not only after vascular surgery, but also after high-risk surgery (general, neurosurgery, emergency surgery), as well as in patients over age 65 and patients with established atherosclerotic disease or risk factors for it. However, I believe this latter group may not be at high enough risk to justify routine screening.

Beattie et al6 advocated limiting postoperative troponin screening to patients with at least a moderate risk of MI and also suggested an international consensus conference to define criteria for postoperative MI, populations who should have routine postoperative screening, and consensus on treatment of patients with troponin elevations but not meeting the criteria for MI. Without this consensus on treatment, it is unclear if protocols for universal postoperative screening would improve outcomes.

For these reasons, the 2014 joint guidelines of the American College of Cardiology and American Heart Association9 (ACC/AHA) stated that the benefit of postoperative screening of troponin levels in patients with a high perioperative risk of MI but no signs or symptoms of myocardial ischemia or MI is “uncertain in the absence of established risks and benefits of a defined management strategy.” This recommendation was given a class IIb rating (may be considered) and level of evidence B (usefulness or efficacy less well established). On the other hand, the guidelines recommend measuring troponin levels if signs or symptoms suggest myocardial ischemia or MI (class I recommendation, level of evidence A) but state there is no benefit in routine screening of unselected patients without signs or symptoms of ischemia (class III recommendation, level of evidence B).

HOW SHOULD ELEVATIONS BE TREATED?

Lacking evidence, we can only speculate whether troponin screening helps or harmsBecause a troponin elevation in a patient without signs or symptoms of ischemia does not predict a specific type of death, physicians need to treat patients individually. Perioperative ischemia and inflammation could lead to injury of other organs, and death could result from multiorgan injury rather than from myocardial injury. Treating these troponin elevations in the same way we treat MI—ie, with antiplatelet therapy and anticoagulation—may result in increased bleeding or unnecessary cardiac catheterization, and starting beta-blockers in the perioperative period may be harmful. Because it is unclear how to manage these patients, cardiac medications have not routinely been given in previous studies.

POISE provided some evidence that patients with postoperative MI who were given aspirin and a statin did better.1 And the results of a smaller study10 suggested that intensification of drug therapy (aspirin, statin, beta-blocker, angiotensin-converting enzyme inhibitor) in patients with postoperative troponin I elevations was associated with improved outcomes at 1 year. If the bleeding risk is low, I believe that there is potential benefit in prescribing aspirin and statins for these patients.

CASTING A WIDER NET

Further complicating matters in the near future is the issue of using fifth-generation high-sensitivity troponin T assays. The European Society of Cardiology guidelines11 are somewhat more liberal than the ACC/AHA guidelines, stating that measuring high-sensitivity troponin after surgery “may be considered in high-risk patients to improve risk stratification.” This is a class IIB recommendation, level of evidence B.

With fifth-generation high-sensitivity troponin assays, troponin may be elevated in as many as 20% of patients preoperatively and 40% postoperatively, significantly increasing the number of patients said to have a complication. Besides potentially subjecting these patients to unproven treatments, such results would give the false impression that hospitals and surgeons using the screening tools actually had higher complication rates than those that did not screen.

POSSIBLE HARMS OF SCREENING

Elevated postoperative troponin may identify patients at higher risk of any adverse event but not specifically of cardiac-specific events. In an editorial, Beckman12 stated that routine measurement of troponin “is more likely to cause harm than to provide benefit and should not be used as a screening modality” because of the lack of a proven beneficial treatment strategy, because of the possible harm from applying the standard treatment for type 1 MI, and because it could divert attention from a true cause of an adverse event to a false one—ie, from a nonvascular condition to MI.11

There is clearly a need for clinical trials to determine which treatment, if any, can improve outcomes in these patients, and several trials have been started. But until we have evidence, we can only speculate as to whether screening postoperative patients for troponin elevation is beneficial or detrimental.

A major goal of perioperative medicine is to prevent, detect, and treat postoperative complications—in particular, cardiovascular complications. In the Perioperative Ischemic Evaluation (POISE) study,1 the 30-day mortality rate was four times higher in patients who had a perioperative myocardial infarction (MI) than in those who did not.1 Yet fewer than half of patients who have a postoperative MI have ischemic symptoms, suggesting that routine monitoring of cardiac biomarkers could detect these events and allow early intervention.

See related article

From 10% to 20% of patients have troponin elevations after noncardiac surgery.2 But until recently, many of these elevations were thought to be of minor importance and were ignored unless the patient met diagnostic criteria for MI. A new entity called MINS (myocardial injury after noncardiac surgery)3 was defined as a troponin level exceeding the upper limit of normal with or without ischemic symptoms or electrocardiographic changes and excluding noncardiac causes such as stroke, sepsis, and pulmonary embolism. Because elevations of troponin at any level have been associated with increased 30-day mortality rates, the question of the value of routine screening of asymptomatic postoperative patients for troponin elevation has been raised.

In this issue of Cleveland Clinic Journal of Medicine, Horr et al4 review the controversy of postoperative screening using troponin measurement and propose an algorithm for management.

QUESTIONS TO CONSIDER

Before recommending screening asymptomatic patients for troponin elevation, we need to consider a number of questions:

  • Which patients should be screened?
  • How should troponin elevations be treated?
  • Would casting a wider net improve outcomes?
  • What are the possible harms of troponin screening?

The bottom line is, will postoperative troponin screening change management and result in improved outcomes?

WHICH PATIENTS SHOULD BE SCREENED?

Why routine screening may be indicated

Elevated or even just detectable troponin levels are associated with adverse outcomes. A systematic review and meta-analysis of 3,318 patients2 demonstrated that high troponin levels after noncardiac surgery were independently associated with a risk of death three times higher than in patients with normal troponin levels.

In the Vascular Events in Noncardiac Surgery Patients Cohort Evaluation (VISION) study,5 troponin T was measured in 15,133 patients after surgery. The overall mortality rate was 1.9%, and the higher the peak troponin T level the higher the risk of death.

Postoperative troponin elevations are linked to bad outcomes, but should we screen everyone?In a single-center Canadian retrospective cohort analysis of 51,701 consecutive patients by Beattie et al,6 the peak postoperative level of troponin I improved the ability of a multivariable model to predict the risk of death. As in the VISION study, the mortality rate rose with the troponin level.6

In a study by van Waes et al7 in 2,232 consecutive noncardiac surgery patients over age 60 at intermediate to high risk, the all-cause mortality rate was 3%, and troponin I was elevated in 19% of patients. As in VISION and the Canadian retrospective study, the mortality rate increased with the troponin level.

Why routine screening may not help

In VISION,5 the probability of detecting myocardial injury was three times higher if patients were screened for 3 days after surgery than if they were tested only if clinical signs or symptoms indicated it.

However, in deciding whether to screen troponin levels in postoperative patients, we must take into account the patient’s clinical risk as well as the risk of the surgical procedure. Troponin elevation in low-risk patients is associated with a low mortality rate, and troponin elevations often are secondary to causes other than myocardial ischemia. In the study by van Waes et al,7 the association was stronger with all-cause mortality than with myocardial infarction, and in VISION5 there were more nonvascular deaths than vascular deaths, suggesting that troponin elevation is a nonspecific marker of adverse events.

Beattie et al6 found that the probability that a patient’s postoperative troponin level would be elevated increased as the patient’s clinical risk increased, but the yield was very low and the mortality rate was less than 1% in patients in risk classes 1 through 3 (of a possible 5 classes). In risk class 4, troponin I was elevated in 21.8%, and the mortality rate was 2.5%; in risk class 5 troponin I was elevated in 18.6%, and the mortality rate was 11.9%. Analyzing the data according to the type of surgery, mortality rates were highest in patients undergoing vascular surgery, neurosurgery, general surgery, and thoracic procedures, with all-cause mortality rates ranging from 2.6% to 5.2%.6

Screening should depend on risk

If postoperative troponin screening is to be recommended, it should not be routine for all patients but should be restricted to those with high clinical risk and those undergoing high-risk surgical procedures.

Rodseth and Devereaux8 recommended routine postoperative troponin measurement not only after vascular surgery, but also after high-risk surgery (general, neurosurgery, emergency surgery), as well as in patients over age 65 and patients with established atherosclerotic disease or risk factors for it. However, I believe this latter group may not be at high enough risk to justify routine screening.

Beattie et al6 advocated limiting postoperative troponin screening to patients with at least a moderate risk of MI and also suggested an international consensus conference to define criteria for postoperative MI, populations who should have routine postoperative screening, and consensus on treatment of patients with troponin elevations but not meeting the criteria for MI. Without this consensus on treatment, it is unclear if protocols for universal postoperative screening would improve outcomes.

For these reasons, the 2014 joint guidelines of the American College of Cardiology and American Heart Association9 (ACC/AHA) stated that the benefit of postoperative screening of troponin levels in patients with a high perioperative risk of MI but no signs or symptoms of myocardial ischemia or MI is “uncertain in the absence of established risks and benefits of a defined management strategy.” This recommendation was given a class IIb rating (may be considered) and level of evidence B (usefulness or efficacy less well established). On the other hand, the guidelines recommend measuring troponin levels if signs or symptoms suggest myocardial ischemia or MI (class I recommendation, level of evidence A) but state there is no benefit in routine screening of unselected patients without signs or symptoms of ischemia (class III recommendation, level of evidence B).

HOW SHOULD ELEVATIONS BE TREATED?

Lacking evidence, we can only speculate whether troponin screening helps or harmsBecause a troponin elevation in a patient without signs or symptoms of ischemia does not predict a specific type of death, physicians need to treat patients individually. Perioperative ischemia and inflammation could lead to injury of other organs, and death could result from multiorgan injury rather than from myocardial injury. Treating these troponin elevations in the same way we treat MI—ie, with antiplatelet therapy and anticoagulation—may result in increased bleeding or unnecessary cardiac catheterization, and starting beta-blockers in the perioperative period may be harmful. Because it is unclear how to manage these patients, cardiac medications have not routinely been given in previous studies.

POISE provided some evidence that patients with postoperative MI who were given aspirin and a statin did better.1 And the results of a smaller study10 suggested that intensification of drug therapy (aspirin, statin, beta-blocker, angiotensin-converting enzyme inhibitor) in patients with postoperative troponin I elevations was associated with improved outcomes at 1 year. If the bleeding risk is low, I believe that there is potential benefit in prescribing aspirin and statins for these patients.

CASTING A WIDER NET

Further complicating matters in the near future is the issue of using fifth-generation high-sensitivity troponin T assays. The European Society of Cardiology guidelines11 are somewhat more liberal than the ACC/AHA guidelines, stating that measuring high-sensitivity troponin after surgery “may be considered in high-risk patients to improve risk stratification.” This is a class IIB recommendation, level of evidence B.

With fifth-generation high-sensitivity troponin assays, troponin may be elevated in as many as 20% of patients preoperatively and 40% postoperatively, significantly increasing the number of patients said to have a complication. Besides potentially subjecting these patients to unproven treatments, such results would give the false impression that hospitals and surgeons using the screening tools actually had higher complication rates than those that did not screen.

POSSIBLE HARMS OF SCREENING

Elevated postoperative troponin may identify patients at higher risk of any adverse event but not specifically of cardiac-specific events. In an editorial, Beckman12 stated that routine measurement of troponin “is more likely to cause harm than to provide benefit and should not be used as a screening modality” because of the lack of a proven beneficial treatment strategy, because of the possible harm from applying the standard treatment for type 1 MI, and because it could divert attention from a true cause of an adverse event to a false one—ie, from a nonvascular condition to MI.11

There is clearly a need for clinical trials to determine which treatment, if any, can improve outcomes in these patients, and several trials have been started. But until we have evidence, we can only speculate as to whether screening postoperative patients for troponin elevation is beneficial or detrimental.

References
  1. Devereaux PJ, Xavier D, Pogue J, et al. Characteristics and short-term prognosis of perioperative myocardial infarction in patients undergoing noncardiac surgery: a cohort study. Ann Intern Med 2011; 154:523–528.
  2. Levy M, Heels-Ansdell D, Hiralal R, et al. Prognostic value of troponin and creatine kinase muscle and brain isoenzyme measurement after noncardiac surgery: a systematic review and meta-analysis. Anesthesiology 2011; 114:796–806.
  3. Botto F, Alonso-Coello P, Chan MT, et al. Myocardial injury after noncardiac surgery: a large, international, prospective cohort study establishing diagnostic criteria, characteristics, predictors, and 30-day outcomes. Anesthesiology 2014; 120:564–578.
  4. Horr S, Reed G, Menon V. Troponin elevation after noncardiac surgery: significance and management. Cleve Clin J Med 2015; 82:595–602.
  5. Vascular Events In Noncardiac Surgery Patients Cohort Evaluation Study I, Devereaux PJ, Chan MT, Alonso-Coello P, et al. Association between postoperative troponin levels and 30-day mortality among patients undergoing noncardiac surgery. JAMA 2012; 307:2295–2304.
  6. Beattie WS, Karkouti K, Tait G, et al. Use of clinically based troponin underestimates the cardiac injury in non-cardiac surgery: a single-centre cohort study in 51,701 consecutive patients. Can J Anaesth 2012; 59:1013–1022.
  7. van Waes JA, Nathoe HM, de Graaff JC, et al. Myocardial injury after noncardiac surgery and its association with short-term mortality. Circulation 2013; 127:2264–2271.
  8. Rodseth R, Devereaux PJ. Should we measure troponin routinely in patients after vascular surgery? American College of Cardiology. www.acc.org/latest-in-cardiology/articles/2014/07/18/14/46/should-we-measure-troponin-routinely-in-patients-after-vascular-surgery?w_nav=LC. Accessed August 5, 2015.
  9. Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014; 64:e77–e137.
  10. Foucrier A, Rodseth R, Aissaoui M, et al. The long-term impact of early cardiovascular therapy intensification for postoperative troponin elevation after major vascular surgery. Anesth Analg 2014; 119:1053–1063.
  11. Kristensen SD, Knuuti J, Saraste A, et al. 2014 ESC/ESA Guidelines on non-cardiac surgery: cardiovascular assessment and management: The Joint Task Force on non-cardiac surgery: cardiovascular assessment and management of the European Society of Cardiology (ESC) and the European Society of Anaesthesiology (ESA). Eur Heart J 2014; 35:2383–2431.
  12. Beckman JA. Postoperative troponin screening: a cardiac Cassandra? Circulation 2013; 127:2253–2266.
References
  1. Devereaux PJ, Xavier D, Pogue J, et al. Characteristics and short-term prognosis of perioperative myocardial infarction in patients undergoing noncardiac surgery: a cohort study. Ann Intern Med 2011; 154:523–528.
  2. Levy M, Heels-Ansdell D, Hiralal R, et al. Prognostic value of troponin and creatine kinase muscle and brain isoenzyme measurement after noncardiac surgery: a systematic review and meta-analysis. Anesthesiology 2011; 114:796–806.
  3. Botto F, Alonso-Coello P, Chan MT, et al. Myocardial injury after noncardiac surgery: a large, international, prospective cohort study establishing diagnostic criteria, characteristics, predictors, and 30-day outcomes. Anesthesiology 2014; 120:564–578.
  4. Horr S, Reed G, Menon V. Troponin elevation after noncardiac surgery: significance and management. Cleve Clin J Med 2015; 82:595–602.
  5. Vascular Events In Noncardiac Surgery Patients Cohort Evaluation Study I, Devereaux PJ, Chan MT, Alonso-Coello P, et al. Association between postoperative troponin levels and 30-day mortality among patients undergoing noncardiac surgery. JAMA 2012; 307:2295–2304.
  6. Beattie WS, Karkouti K, Tait G, et al. Use of clinically based troponin underestimates the cardiac injury in non-cardiac surgery: a single-centre cohort study in 51,701 consecutive patients. Can J Anaesth 2012; 59:1013–1022.
  7. van Waes JA, Nathoe HM, de Graaff JC, et al. Myocardial injury after noncardiac surgery and its association with short-term mortality. Circulation 2013; 127:2264–2271.
  8. Rodseth R, Devereaux PJ. Should we measure troponin routinely in patients after vascular surgery? American College of Cardiology. www.acc.org/latest-in-cardiology/articles/2014/07/18/14/46/should-we-measure-troponin-routinely-in-patients-after-vascular-surgery?w_nav=LC. Accessed August 5, 2015.
  9. Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014; 64:e77–e137.
  10. Foucrier A, Rodseth R, Aissaoui M, et al. The long-term impact of early cardiovascular therapy intensification for postoperative troponin elevation after major vascular surgery. Anesth Analg 2014; 119:1053–1063.
  11. Kristensen SD, Knuuti J, Saraste A, et al. 2014 ESC/ESA Guidelines on non-cardiac surgery: cardiovascular assessment and management: The Joint Task Force on non-cardiac surgery: cardiovascular assessment and management of the European Society of Cardiology (ESC) and the European Society of Anaesthesiology (ESA). Eur Heart J 2014; 35:2383–2431.
  12. Beckman JA. Postoperative troponin screening: a cardiac Cassandra? Circulation 2013; 127:2253–2266.
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The problems surrounding hospital observation care and associated audits by Recovery Audit Contractors are gaining increased attention from both Congress and the Centers for Medicare & Medicaid Services (CMS).[1, 2, 3, 4, 5] On August 6, 2015, President Obama signed the NOTICE (Notice of Observation Treatment and Implication for Care Eligibility) Act (P.L. 114‐42),[4] which will require all Medicare beneficiaries receiving observation services for over 24 hours to be informed of their outpatient status. However, providers and hospitals are currently unable to answer a question that patients will certainly ask: What will an observation stay cost me compared to the same stay billed as an inpatient?

In this issue of the Journal of Hospital Medicine, Kangovi et al.[6] get a step closer to answering this question. Using 2010 to 2012 Medicare data, Kangovi and colleagues studied patient out‐of‐pocket costs per Medicare benefit period and found that the mean financial self‐pay cost per beneficiary observation stay was less ($469.42) than the 2010 inpatient deductible ($1100),[7] although about 1 in 10 observation stays exceeded the inpatient deductible. For beneficiaries with multiple observation stays per benefit period, the mean cumulative self‐pay cost ($947.40) was also less than the inpatient deductible. However, for over a quarter of beneficiaries with multiple observation stays, the cumulative patient cost exceeded the inpatient deductible. The authors also found that black beneficiaries and those with more comorbidities were more likely to have multiple observation visits per benefit period, but higher out‐of‐pocket observation liability was associated with nonblack race, lower number of chronic conditions, and not being dual eligible.

Medicare beneficiaries hospitalized as inpatients are covered by Medicare Part A, with a single deductible per benefit period, and are eligible for skilled nursing facility (SNF) coverage after 3 consecutive inpatient midnights. Medicare patients hospitalized as outpatients, including those receiving observation services, are not eligible for SNF coverage, must pay the cost of many self‐administered pharmaceuticals, and are generally responsible for 20% of each service rendered, but with the per‐service out‐of‐pocket 20% deductible capped at the equivalent to the current Part A deductible. However, there is no cumulative limit on the total out‐of‐pocket cost for outpatient observation (Part B) hospitalizations.[8]

Put in a slightly different way, while [outpatient coverage] is designed to reflect the cost of caring for each individual beneficiary, [inpatient payment structure] is designed to reflect the cost of caring for an average beneficiary.[9] Because outpatient observation payments are made per service, Medicare and beneficiary payment amounts both increase as the number of services provided increases,[9] which creates a threshold where the number and complexity of outpatient services exceeds the average inpatient stay, resulting in out‐of‐pocket observation costs exceeding the inpatient deductible. It makes sense that this threshold is more likely to be reached when the costs of multiple observation stays are added. Therefore, we should not be surprised at the findings of Kangovi et al.,[6] nor at those of the Office of Inspector General (OIG)[9] using 2012 Medicare claims data, showing higher average out‐of‐pocket patient costs for short inpatient stays compared to observation stays, but with a significant minority of out‐of‐pocket observation patient stay costs exceeding the inpatient deductible.

Dr. Kangovi and colleagues should be applauded for their efforts to address this important Medicare beneficiary issue. Yet many questions remain. First, neither the OIG study nor Kangovi et al. fully included cost of self‐administered medications in calculating patients' out‐of‐pocket patient liability. Second, Kangovi and colleagues did not account for beneficiary posthospitalization SNF costs, which would be substantially higher for any patients who did not have a qualifying 3‐day inpatient stay, including all patients hospitalized under observation. Third, both reports used data predating the 2‐midnight rule, so it is unlikely that beneficiary costs are comparable under current policy. Fewer long (>48 hours) observation stays under the 2‐midnight rule should reduce beneficiary financial burden, though this is unconfirmed. However, certain shorter, high‐acuity, procedure‐based observation stays could be more costly for patients.[9] Fourth, Kangovi et al. also did not consider patients with both an inpatient stay and an observation stay in the same benefit period; these patients would be liable for both the inpatient deductible and the outpatient fees. Fifth, to be meaningful, comparison of beneficiary out‐of‐pocket liability for inpatient versus outpatient care must occur in the context of services rendered, similar to what was proposed by the House Ways and Means Subcommittee in their Hospital Improvements for Payment draft bill.[10] Absent this, we should not conclude from this study that observation care is delivered at a discounted rate for patients when it is possible that lower out‐of‐pocket payments simply reflect, on average, fewer services rendered per observation stay when compared to an inpatient stay. Finally, the association between race, socioeconomic status, chronic conditions, and inpatient and observation stays merits further investigation. How such hospitalizations may relate to larger costs associated with lack of appropriate follow‐up care, including costs for those who have adverse consequences when they curtail or forego SNF placement, must be considered.

Even if we accept these limitations and accede that out‐of‐pocket observation cost is, on average, less than inpatient, pitfalls of observation policy remain: a cap on out‐of‐pocket financial risk for hospital care and SNF coverage are protections only afforded to those Medicare beneficiaries hospitalized as inpatients. Although the aspect of CMS' 2‐midnight rule that presumes inpatient status if a there is a physician's expectation of a medically necessary hospitalization of 2 or more midnights mitigates, but does not eliminate, the observation policy problem of uncapped out‐of‐pocket financial liability, it does not address the lack of SNF coverage following outpatient hospitalization. Further action and answers need to come from both Congress and CMS. At a recent Senate Special Committee on Aging hearing, Elizabeth Warren emphasized that CMS must accurately determine Medicare beneficiary out‐of‐pocket cost for observation care so providers can answer this question that patients undoubtedly ask.[1] CMS should be called upon to make available estimates of beneficiary costs under the 2‐midnight rule that include pharmacy charges, copayments (in the context of services rendered), and SNF costs. In addition, data should extend past beneficiary liability to detail differences in outpatient versus inpatient hospital reimbursement, systematic recovery auditing costs, and the total financial impact of maintaining 2 distinct (inpatient and outpatient) hospital reimbursement systems.[11, 12]

Congress and CMS must ultimately go beyond cost estimates and actually reform the core problems in outpatient observation policy and the Recovery Audit program charged with enforcing status determinations. Congress should pass the Improving Access to Medicare Coverage Act of 2015 (H.R. 1571 and S. 843), which would guarantee SNF coverage for Medicare beneficiaries hospitalized for 3 consecutive midnights, regardless of whether those nights are inpatient or outpatient.[13] Recovery Audit reform bills in the House (H.R. 2156)[3] and under consideration in the Senate[2] should be strongly supported. In addition, Congress and CMS should consider legislation or regulation that would cap outpatient hospitalization out‐of‐pocket liability at the inpatient Medicare beneficiary deductible. Alternatively, policymakers could finally recognize the current observation versus inpatient system for what it is: a payment structure with little clinical relevance. When the same exact medical care has 2 different hospital reimbursement rates and 2 different patient out‐of‐pocket financial liabilities, it may be time for policymakers to eliminate the false distinction altogether.

Disclosure: Nothing to report.

Files
References
  1. Senate Special Committee on Aging hearing: challenging the status quo: solutions to the hospital observation stay crisis. May 20, 2015. Available at: http://www.aging.senate.gov/hearings/challenging‐the‐status‐quo_solutions‐to‐the‐hospital‐observation‐stay‐crisis. Accessed July 1, 2015.
  2. Senate Finance Committee Open Executive Session to consider an original bill entitled Audit 10(11):718723.
  3. Medicare general information, eligibility, and entitlement. Chapter 3—deductibles, coninsurance amounts, and payment limitations. Available at: http://www.cms.gov/Regulations‐and‐Guidance/Guidance/Manuals/downloads/ge101c03.pdf. Accessed July 5, 2015.
  4. What Medicare covers: find out if you're an inpatient or an outpatient—it affects what you pay. Available at: http://www.medicare.gov/what‐medicare‐covers/part‐a/inpatient‐or‐outpatient.html. Accessed July 10, 2015.
  5. Department of Health and Human Services. Office of Inspector General. Hospitals' use of observation stays and short inpatient stays for Medicare beneficiaries, OEI‐02‐12‐00040. July 29, 2013. Available at: https://oig.hhs.gov/oei/reports/oei‐02‐12‐00040.pdf. Accessed July 1, 2015.
  6. Association of American Medical Colleges. Washington Highlights: Ways and Means Committee releases Medicare hospital bill. Available at: https://www.aamc.org/advocacy/washhigh/highlights2014/415486/112114waysandmeanscommitteereleasesmedicarehospitalbill.html. Accessed July 10, 2015.
  7. Sheehy A, Graf B, Gangireddy S, et al. Hospitalized but not admitted: characteristics of patients with “observation status” at an academic medical center. JAMA Intern Med. 2013;173(21):19911998.
  8. Sheehy A, Locke C, Engel J, et al. Recovery audit contractor audits and appeals at three academic medical centers. J Hosp Med. 2015;10(4):212219.
  9. Improving Access to Medicare Coverage Act of 2015 (H.R. 1571/S. 843). Available at: https://www.congress.gov/bill/114th‐congress/house‐bill/1571. Accessed July 6, 2015.
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The problems surrounding hospital observation care and associated audits by Recovery Audit Contractors are gaining increased attention from both Congress and the Centers for Medicare & Medicaid Services (CMS).[1, 2, 3, 4, 5] On August 6, 2015, President Obama signed the NOTICE (Notice of Observation Treatment and Implication for Care Eligibility) Act (P.L. 114‐42),[4] which will require all Medicare beneficiaries receiving observation services for over 24 hours to be informed of their outpatient status. However, providers and hospitals are currently unable to answer a question that patients will certainly ask: What will an observation stay cost me compared to the same stay billed as an inpatient?

In this issue of the Journal of Hospital Medicine, Kangovi et al.[6] get a step closer to answering this question. Using 2010 to 2012 Medicare data, Kangovi and colleagues studied patient out‐of‐pocket costs per Medicare benefit period and found that the mean financial self‐pay cost per beneficiary observation stay was less ($469.42) than the 2010 inpatient deductible ($1100),[7] although about 1 in 10 observation stays exceeded the inpatient deductible. For beneficiaries with multiple observation stays per benefit period, the mean cumulative self‐pay cost ($947.40) was also less than the inpatient deductible. However, for over a quarter of beneficiaries with multiple observation stays, the cumulative patient cost exceeded the inpatient deductible. The authors also found that black beneficiaries and those with more comorbidities were more likely to have multiple observation visits per benefit period, but higher out‐of‐pocket observation liability was associated with nonblack race, lower number of chronic conditions, and not being dual eligible.

Medicare beneficiaries hospitalized as inpatients are covered by Medicare Part A, with a single deductible per benefit period, and are eligible for skilled nursing facility (SNF) coverage after 3 consecutive inpatient midnights. Medicare patients hospitalized as outpatients, including those receiving observation services, are not eligible for SNF coverage, must pay the cost of many self‐administered pharmaceuticals, and are generally responsible for 20% of each service rendered, but with the per‐service out‐of‐pocket 20% deductible capped at the equivalent to the current Part A deductible. However, there is no cumulative limit on the total out‐of‐pocket cost for outpatient observation (Part B) hospitalizations.[8]

Put in a slightly different way, while [outpatient coverage] is designed to reflect the cost of caring for each individual beneficiary, [inpatient payment structure] is designed to reflect the cost of caring for an average beneficiary.[9] Because outpatient observation payments are made per service, Medicare and beneficiary payment amounts both increase as the number of services provided increases,[9] which creates a threshold where the number and complexity of outpatient services exceeds the average inpatient stay, resulting in out‐of‐pocket observation costs exceeding the inpatient deductible. It makes sense that this threshold is more likely to be reached when the costs of multiple observation stays are added. Therefore, we should not be surprised at the findings of Kangovi et al.,[6] nor at those of the Office of Inspector General (OIG)[9] using 2012 Medicare claims data, showing higher average out‐of‐pocket patient costs for short inpatient stays compared to observation stays, but with a significant minority of out‐of‐pocket observation patient stay costs exceeding the inpatient deductible.

Dr. Kangovi and colleagues should be applauded for their efforts to address this important Medicare beneficiary issue. Yet many questions remain. First, neither the OIG study nor Kangovi et al. fully included cost of self‐administered medications in calculating patients' out‐of‐pocket patient liability. Second, Kangovi and colleagues did not account for beneficiary posthospitalization SNF costs, which would be substantially higher for any patients who did not have a qualifying 3‐day inpatient stay, including all patients hospitalized under observation. Third, both reports used data predating the 2‐midnight rule, so it is unlikely that beneficiary costs are comparable under current policy. Fewer long (>48 hours) observation stays under the 2‐midnight rule should reduce beneficiary financial burden, though this is unconfirmed. However, certain shorter, high‐acuity, procedure‐based observation stays could be more costly for patients.[9] Fourth, Kangovi et al. also did not consider patients with both an inpatient stay and an observation stay in the same benefit period; these patients would be liable for both the inpatient deductible and the outpatient fees. Fifth, to be meaningful, comparison of beneficiary out‐of‐pocket liability for inpatient versus outpatient care must occur in the context of services rendered, similar to what was proposed by the House Ways and Means Subcommittee in their Hospital Improvements for Payment draft bill.[10] Absent this, we should not conclude from this study that observation care is delivered at a discounted rate for patients when it is possible that lower out‐of‐pocket payments simply reflect, on average, fewer services rendered per observation stay when compared to an inpatient stay. Finally, the association between race, socioeconomic status, chronic conditions, and inpatient and observation stays merits further investigation. How such hospitalizations may relate to larger costs associated with lack of appropriate follow‐up care, including costs for those who have adverse consequences when they curtail or forego SNF placement, must be considered.

Even if we accept these limitations and accede that out‐of‐pocket observation cost is, on average, less than inpatient, pitfalls of observation policy remain: a cap on out‐of‐pocket financial risk for hospital care and SNF coverage are protections only afforded to those Medicare beneficiaries hospitalized as inpatients. Although the aspect of CMS' 2‐midnight rule that presumes inpatient status if a there is a physician's expectation of a medically necessary hospitalization of 2 or more midnights mitigates, but does not eliminate, the observation policy problem of uncapped out‐of‐pocket financial liability, it does not address the lack of SNF coverage following outpatient hospitalization. Further action and answers need to come from both Congress and CMS. At a recent Senate Special Committee on Aging hearing, Elizabeth Warren emphasized that CMS must accurately determine Medicare beneficiary out‐of‐pocket cost for observation care so providers can answer this question that patients undoubtedly ask.[1] CMS should be called upon to make available estimates of beneficiary costs under the 2‐midnight rule that include pharmacy charges, copayments (in the context of services rendered), and SNF costs. In addition, data should extend past beneficiary liability to detail differences in outpatient versus inpatient hospital reimbursement, systematic recovery auditing costs, and the total financial impact of maintaining 2 distinct (inpatient and outpatient) hospital reimbursement systems.[11, 12]

Congress and CMS must ultimately go beyond cost estimates and actually reform the core problems in outpatient observation policy and the Recovery Audit program charged with enforcing status determinations. Congress should pass the Improving Access to Medicare Coverage Act of 2015 (H.R. 1571 and S. 843), which would guarantee SNF coverage for Medicare beneficiaries hospitalized for 3 consecutive midnights, regardless of whether those nights are inpatient or outpatient.[13] Recovery Audit reform bills in the House (H.R. 2156)[3] and under consideration in the Senate[2] should be strongly supported. In addition, Congress and CMS should consider legislation or regulation that would cap outpatient hospitalization out‐of‐pocket liability at the inpatient Medicare beneficiary deductible. Alternatively, policymakers could finally recognize the current observation versus inpatient system for what it is: a payment structure with little clinical relevance. When the same exact medical care has 2 different hospital reimbursement rates and 2 different patient out‐of‐pocket financial liabilities, it may be time for policymakers to eliminate the false distinction altogether.

Disclosure: Nothing to report.

The problems surrounding hospital observation care and associated audits by Recovery Audit Contractors are gaining increased attention from both Congress and the Centers for Medicare & Medicaid Services (CMS).[1, 2, 3, 4, 5] On August 6, 2015, President Obama signed the NOTICE (Notice of Observation Treatment and Implication for Care Eligibility) Act (P.L. 114‐42),[4] which will require all Medicare beneficiaries receiving observation services for over 24 hours to be informed of their outpatient status. However, providers and hospitals are currently unable to answer a question that patients will certainly ask: What will an observation stay cost me compared to the same stay billed as an inpatient?

In this issue of the Journal of Hospital Medicine, Kangovi et al.[6] get a step closer to answering this question. Using 2010 to 2012 Medicare data, Kangovi and colleagues studied patient out‐of‐pocket costs per Medicare benefit period and found that the mean financial self‐pay cost per beneficiary observation stay was less ($469.42) than the 2010 inpatient deductible ($1100),[7] although about 1 in 10 observation stays exceeded the inpatient deductible. For beneficiaries with multiple observation stays per benefit period, the mean cumulative self‐pay cost ($947.40) was also less than the inpatient deductible. However, for over a quarter of beneficiaries with multiple observation stays, the cumulative patient cost exceeded the inpatient deductible. The authors also found that black beneficiaries and those with more comorbidities were more likely to have multiple observation visits per benefit period, but higher out‐of‐pocket observation liability was associated with nonblack race, lower number of chronic conditions, and not being dual eligible.

Medicare beneficiaries hospitalized as inpatients are covered by Medicare Part A, with a single deductible per benefit period, and are eligible for skilled nursing facility (SNF) coverage after 3 consecutive inpatient midnights. Medicare patients hospitalized as outpatients, including those receiving observation services, are not eligible for SNF coverage, must pay the cost of many self‐administered pharmaceuticals, and are generally responsible for 20% of each service rendered, but with the per‐service out‐of‐pocket 20% deductible capped at the equivalent to the current Part A deductible. However, there is no cumulative limit on the total out‐of‐pocket cost for outpatient observation (Part B) hospitalizations.[8]

Put in a slightly different way, while [outpatient coverage] is designed to reflect the cost of caring for each individual beneficiary, [inpatient payment structure] is designed to reflect the cost of caring for an average beneficiary.[9] Because outpatient observation payments are made per service, Medicare and beneficiary payment amounts both increase as the number of services provided increases,[9] which creates a threshold where the number and complexity of outpatient services exceeds the average inpatient stay, resulting in out‐of‐pocket observation costs exceeding the inpatient deductible. It makes sense that this threshold is more likely to be reached when the costs of multiple observation stays are added. Therefore, we should not be surprised at the findings of Kangovi et al.,[6] nor at those of the Office of Inspector General (OIG)[9] using 2012 Medicare claims data, showing higher average out‐of‐pocket patient costs for short inpatient stays compared to observation stays, but with a significant minority of out‐of‐pocket observation patient stay costs exceeding the inpatient deductible.

Dr. Kangovi and colleagues should be applauded for their efforts to address this important Medicare beneficiary issue. Yet many questions remain. First, neither the OIG study nor Kangovi et al. fully included cost of self‐administered medications in calculating patients' out‐of‐pocket patient liability. Second, Kangovi and colleagues did not account for beneficiary posthospitalization SNF costs, which would be substantially higher for any patients who did not have a qualifying 3‐day inpatient stay, including all patients hospitalized under observation. Third, both reports used data predating the 2‐midnight rule, so it is unlikely that beneficiary costs are comparable under current policy. Fewer long (>48 hours) observation stays under the 2‐midnight rule should reduce beneficiary financial burden, though this is unconfirmed. However, certain shorter, high‐acuity, procedure‐based observation stays could be more costly for patients.[9] Fourth, Kangovi et al. also did not consider patients with both an inpatient stay and an observation stay in the same benefit period; these patients would be liable for both the inpatient deductible and the outpatient fees. Fifth, to be meaningful, comparison of beneficiary out‐of‐pocket liability for inpatient versus outpatient care must occur in the context of services rendered, similar to what was proposed by the House Ways and Means Subcommittee in their Hospital Improvements for Payment draft bill.[10] Absent this, we should not conclude from this study that observation care is delivered at a discounted rate for patients when it is possible that lower out‐of‐pocket payments simply reflect, on average, fewer services rendered per observation stay when compared to an inpatient stay. Finally, the association between race, socioeconomic status, chronic conditions, and inpatient and observation stays merits further investigation. How such hospitalizations may relate to larger costs associated with lack of appropriate follow‐up care, including costs for those who have adverse consequences when they curtail or forego SNF placement, must be considered.

Even if we accept these limitations and accede that out‐of‐pocket observation cost is, on average, less than inpatient, pitfalls of observation policy remain: a cap on out‐of‐pocket financial risk for hospital care and SNF coverage are protections only afforded to those Medicare beneficiaries hospitalized as inpatients. Although the aspect of CMS' 2‐midnight rule that presumes inpatient status if a there is a physician's expectation of a medically necessary hospitalization of 2 or more midnights mitigates, but does not eliminate, the observation policy problem of uncapped out‐of‐pocket financial liability, it does not address the lack of SNF coverage following outpatient hospitalization. Further action and answers need to come from both Congress and CMS. At a recent Senate Special Committee on Aging hearing, Elizabeth Warren emphasized that CMS must accurately determine Medicare beneficiary out‐of‐pocket cost for observation care so providers can answer this question that patients undoubtedly ask.[1] CMS should be called upon to make available estimates of beneficiary costs under the 2‐midnight rule that include pharmacy charges, copayments (in the context of services rendered), and SNF costs. In addition, data should extend past beneficiary liability to detail differences in outpatient versus inpatient hospital reimbursement, systematic recovery auditing costs, and the total financial impact of maintaining 2 distinct (inpatient and outpatient) hospital reimbursement systems.[11, 12]

Congress and CMS must ultimately go beyond cost estimates and actually reform the core problems in outpatient observation policy and the Recovery Audit program charged with enforcing status determinations. Congress should pass the Improving Access to Medicare Coverage Act of 2015 (H.R. 1571 and S. 843), which would guarantee SNF coverage for Medicare beneficiaries hospitalized for 3 consecutive midnights, regardless of whether those nights are inpatient or outpatient.[13] Recovery Audit reform bills in the House (H.R. 2156)[3] and under consideration in the Senate[2] should be strongly supported. In addition, Congress and CMS should consider legislation or regulation that would cap outpatient hospitalization out‐of‐pocket liability at the inpatient Medicare beneficiary deductible. Alternatively, policymakers could finally recognize the current observation versus inpatient system for what it is: a payment structure with little clinical relevance. When the same exact medical care has 2 different hospital reimbursement rates and 2 different patient out‐of‐pocket financial liabilities, it may be time for policymakers to eliminate the false distinction altogether.

Disclosure: Nothing to report.

References
  1. Senate Special Committee on Aging hearing: challenging the status quo: solutions to the hospital observation stay crisis. May 20, 2015. Available at: http://www.aging.senate.gov/hearings/challenging‐the‐status‐quo_solutions‐to‐the‐hospital‐observation‐stay‐crisis. Accessed July 1, 2015.
  2. Senate Finance Committee Open Executive Session to consider an original bill entitled Audit 10(11):718723.
  3. Medicare general information, eligibility, and entitlement. Chapter 3—deductibles, coninsurance amounts, and payment limitations. Available at: http://www.cms.gov/Regulations‐and‐Guidance/Guidance/Manuals/downloads/ge101c03.pdf. Accessed July 5, 2015.
  4. What Medicare covers: find out if you're an inpatient or an outpatient—it affects what you pay. Available at: http://www.medicare.gov/what‐medicare‐covers/part‐a/inpatient‐or‐outpatient.html. Accessed July 10, 2015.
  5. Department of Health and Human Services. Office of Inspector General. Hospitals' use of observation stays and short inpatient stays for Medicare beneficiaries, OEI‐02‐12‐00040. July 29, 2013. Available at: https://oig.hhs.gov/oei/reports/oei‐02‐12‐00040.pdf. Accessed July 1, 2015.
  6. Association of American Medical Colleges. Washington Highlights: Ways and Means Committee releases Medicare hospital bill. Available at: https://www.aamc.org/advocacy/washhigh/highlights2014/415486/112114waysandmeanscommitteereleasesmedicarehospitalbill.html. Accessed July 10, 2015.
  7. Sheehy A, Graf B, Gangireddy S, et al. Hospitalized but not admitted: characteristics of patients with “observation status” at an academic medical center. JAMA Intern Med. 2013;173(21):19911998.
  8. Sheehy A, Locke C, Engel J, et al. Recovery audit contractor audits and appeals at three academic medical centers. J Hosp Med. 2015;10(4):212219.
  9. Improving Access to Medicare Coverage Act of 2015 (H.R. 1571/S. 843). Available at: https://www.congress.gov/bill/114th‐congress/house‐bill/1571. Accessed July 6, 2015.
References
  1. Senate Special Committee on Aging hearing: challenging the status quo: solutions to the hospital observation stay crisis. May 20, 2015. Available at: http://www.aging.senate.gov/hearings/challenging‐the‐status‐quo_solutions‐to‐the‐hospital‐observation‐stay‐crisis. Accessed July 1, 2015.
  2. Senate Finance Committee Open Executive Session to consider an original bill entitled Audit 10(11):718723.
  3. Medicare general information, eligibility, and entitlement. Chapter 3—deductibles, coninsurance amounts, and payment limitations. Available at: http://www.cms.gov/Regulations‐and‐Guidance/Guidance/Manuals/downloads/ge101c03.pdf. Accessed July 5, 2015.
  4. What Medicare covers: find out if you're an inpatient or an outpatient—it affects what you pay. Available at: http://www.medicare.gov/what‐medicare‐covers/part‐a/inpatient‐or‐outpatient.html. Accessed July 10, 2015.
  5. Department of Health and Human Services. Office of Inspector General. Hospitals' use of observation stays and short inpatient stays for Medicare beneficiaries, OEI‐02‐12‐00040. July 29, 2013. Available at: https://oig.hhs.gov/oei/reports/oei‐02‐12‐00040.pdf. Accessed July 1, 2015.
  6. Association of American Medical Colleges. Washington Highlights: Ways and Means Committee releases Medicare hospital bill. Available at: https://www.aamc.org/advocacy/washhigh/highlights2014/415486/112114waysandmeanscommitteereleasesmedicarehospitalbill.html. Accessed July 10, 2015.
  7. Sheehy A, Graf B, Gangireddy S, et al. Hospitalized but not admitted: characteristics of patients with “observation status” at an academic medical center. JAMA Intern Med. 2013;173(21):19911998.
  8. Sheehy A, Locke C, Engel J, et al. Recovery audit contractor audits and appeals at three academic medical centers. J Hosp Med. 2015;10(4):212219.
  9. Improving Access to Medicare Coverage Act of 2015 (H.R. 1571/S. 843). Available at: https://www.congress.gov/bill/114th‐congress/house‐bill/1571. Accessed July 6, 2015.
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Stenting may benefit select patients with severe renal artery stenosis

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Stenting may benefit select patients with severe renal artery stenosis

In their article in this issue of the Cleveland Clinic Journal of Medicine, Kabach et al answer no to the question of whether stenting of severe renal artery stenosis improves outcomes compared with medical therapy alone.1 They review the findings of four key studies2–5 published between 2003 and 2014 and conclude that, in patients with severe atherosclerotic renal artery stenosis and hypertension or chronic kidney disease, renal artery stenting with medical therapy can improve blood pressure control but has no significant impact on cardiovascular or mortality outcomes.1

See related article

Furthermore, the authors state that in view of the risk of complications associated with stenting, medical management should continue to be the first-line therapy.1 Indeed, the ASTRAL study (Angioplasty and Stenting for Renal Artery Lesions) investigators found substantial risks without evidence of a worthwhile clinical benefit from revascularization in patients with atherosclerotic renovascular disease.3

Nevertheless, I believe that this procedure may benefit certain patients.

MAYO CLINIC COHORT STUDY

In 2008, our group at Mayo Clinic Health system in Eau Claire, Wisconsin, published the results of a prospective cohort study in 26 patients with renal artery stenosis and chronic kidney disease who presented with rapidly worsening renal failure (defined as an increase in serum creatinine of ≥ 25%) while receiving an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin II receptor blocker (ARB).6,7

These drugs—inhibitors of the renin-angiotensin-aldosterone system—slow the progression of chronic kidney disease but can acutely worsen renal function, especially in patients with renal artery stenosis, and withdrawing them in this situation was the focus of our study.

The patients (10 men and 16 women) ranged in age from 63 to 87 (mean age 75.3).

At enrollment, the ACE inhibitors and ARBs were discontinued, standard nephrologic care was applied, and the glomerular filtration rate (estimated by the Modification of Diet in Renal Disease Study equation) was monitored. After at least 2 weeks, percutaneous renal angioplasty with stent placement was considered if the patient met any of the following criteria:

  • Persistence of renal failure
  • Flash pulmonary edema
  • Uncontrolled hypertension despite the use of at least three antihypertensive medications.

Figure 1. Changes in the estimated glomerular filtration rate (eGFR) after percutaneous transluminal angioplasty and stenting of the right renal artery in a 67-year-old woman with hypertension, bilateral renal artery stenosis, and atrophy of the left kidney. She presented in November 2002 with symptomatic acute exacerbation of chronic kidney disease.

Nine patients underwent percutaneous angioplasty and stenting and 17 did not. The procedure was done on one renal artery in 8 patients and both renal arteries in 1. Indications for the procedure were recent worsening of renal failure in 8 patients and recent worsening renal failure together with symptomatic flash pulmonary edema in 1 patient. (Flash pulmonary edema is the only class I recommendation for percutaneous renal angioplasty in the 2006 joint guidelines of the American College of Cardiology and the American Heart Association.8) As noted above, all the patients were experiencing acute exacerbation of chronic kidney disease at the time.

We found clear evidence of additional improved and sustained renal function in the patients who underwent percutaneous renal angioplasty and stenting compared with the patients who did not (Figures 1 and 2).6,7

Figure 2. Changes in the serum creatinine level after bilateral percutaneous transluminal angioplasty and renal artery stenting in a 70-year-old woman with hypertension and diabetes who presented in May 2004 with symptomatic acute exacerbation of chronic kidney disease in association with flash pulmonary edema.

In an editorial9 following publication of the ASTRAL study, our group reported a subsequent 82-month analysis of our 26-patient cohort completed in June 2009. In the 7 surviving patients who had undergone percutaneous renal angioplasty and stenting, the estimated glomerular filtration rate had increased from 27.4 mL/min/1.73 m2 (± 12.7, range 11–47) at baseline to 50.3 (± 21.7, range 23–68) (P = .018) after 46.9 months.

PATIENT NUMBER 13

To illustrate how percutaneous renal angioplasty and stenting can reverse recently worsening renal failure in renal artery stenosis, I would like to discuss in greater detail a patient from our two previous reports.6,7

Patient 13, a 67-year-old woman with hypertension, was referred to our nephrology service in September 2004 to consider starting hemodialysis for symptomatic renal failure. Her serum creatinine had increased to 3.4 mg/dL from a previous baseline level of 2.0 mg/dL, and she also had worsening anemia and hyperkalemia. She had been taking lisinopril 10 mg/day for the last 12 months. Magnetic resonance angiography revealed high-grade (> 95%) bilateral renal artery stenosis with an atrophic left kidney.

Lisinopril was promptly discontinued, and within 2 weeks her serum creatinine level had decreased by more than 0.5 mg/dL. In mid-November 2004, she underwent right renal artery angioplasty with stent placement. After that, her serum creatinine decreased further, and 3 months later it had dropped to 1.6 mg/dL. The value continued to improve, with the lowest measurement of 1.1 mg/dL, equivalent to an estimated glomerular filtration rate of 51 mL/min/1.73 m2. This was in May 2006, 19 months after stopping lisinopril and 17 months after angioplasty and stenting. The last available serum creatinine level (August 2006) was 1.2 mg/dL, equivalent to an estimated glomerular filtration rate of 45 mL/min/1.73 m2 (Figure 1). Unfortunately, the patient died of metastatic lung cancer in December of that year.

Also of note, the patient who underwent angioplasty because of recurrent flash pulmonary edema had no recurrences of it afterward.

We concluded that, in patients with hemodynamically significant renal artery stenosis presenting with acutely worsening renal failure, renal angioplasty with stenting has the potential to reverse renal failure, improve blood pressure control, and stop flash pulmonary edema.6–8

In severe renal artery stenosis, no one treatment fits all

Notably, all patients in our study who underwent renal angioplasty with stenting had new-onset acute renal injury as defined by an increase in the baseline serum creatinine of more than 25% during the 3 months before stent placement.6–8 Patients in the STAR,2 HERCULES,4 and CORAL5 studies had renal artery stenosis but otherwise stable chronic kidney disease at the time of enrollment. In the ASTRAL study,3 12% of the patients had acute kidney injury on study enrollment, defined as an increase in the serum creatinine level of more than 20% or of more than 1.13 mg/dL.3

While we strongly agree with aggressive yet monitored medical therapy for patients with hemodynamically significant renal artery stenosis, I posit that selected patients do indeed derive significant clinical benefits from renal angioplasty and stenting. Our group’s prospective individual-patient-level data support the paradigm that angioplasty with stenting is useful in patients with renal artery stenosis who experience “acute-on-chronic” kidney disease.

The pathophysiology of renal artery stenosis and the progression of chronic kidney disease are complex, and many factors affect patient outcomes and response to treatment. Thus, the message is that treatment of severe renal artery stenosis must be individualized.9–11 No one treatment fits all.10,11

References
  1. Kabach A, Agha OQ, Baibars M, Alraiyes AH, Alraies MC. Does stenting of severe renal artery stenosis improve outcomes compared with medical therapy alone? Cleve Clin J Med 2015; 82:491–494.
  2. Bax L, Mali WP, Buskens E, et al; STAR Study Group. The benefit of STent placement and blood pressure and lipid-lowering for the prevention of progression of renal dysfunction caused by Atherosclerotic ostial stenosis of the Renal artery. The STAR-study: rationale and study design. J Nephrol 2003; 16:807–812.
  3. ASTRAL Investigators; Wheatley K, Ives N, Gray R, et al. Revascularization versus medical therapy for renal-artery stenosis. N Engl J Med 2009; 361:1953–1962.
  4. Jaff MR, Bates M, Sullivan T, et al; HERCULES Investigators. Significant reduction in systolic blood pressure following renal artery stenting in patients with uncontrolled hypertension: results from the HERCULES trial. Catheter Cardiovasc Interv 2012; 80:343–350.
  5. Cooper CJ, Murphy TP, Cutlip DE, et al; CORAL Investigators. Stenting and medical therapy for atherosclerotic renal-artery stenosis. N Engl J Med 2014; 370:13–22.
  6. Onuigbo MAC, Onuigbo NTC. Worsening renal failure in older chronic kidney disease patients with renal artery stenosis concurrently on renin angiotensin aldosterone system blockade: a prospective 50-month Mayo Health System clinic analysis. QJM 2008; 101:519–527.
  7. Onuigbo MA, Onuigbo NT. Renal failure and concurrent RAAS blockade in older CKD patients with renal artery stenosis: an extended Mayo Clinic prospective 63-month experience. Ren Fail 2008; 30:363–371.
  8. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary. J Am Coll Cardiol 2006; 47:1239–1312.
  9. Onuigbo M, Frenandes R, Nijhawan V. The ASTRAL trial results revisited—to stent or not to stent in renal artery stenosis? QJM 2010; 103:357.
  10. Singh M, Kovacs DF, Singh A, Dhaliwal P, Khosla S. ACE inhibition and renal artery stenosis: what lessons have we learnt? A 21st century perspective. In: Onuigbo MAC, ed. ACE inhibitors: Medical Uses, Mechanisms of Action, Potential Adverse Effects and Related Topics. Volume 2. New York, NY: NOVA Publishers; 2013:203–218.
  11. Onuigbo MA, Onuigbo C, Onuigbo V, et al. The CKD enigma, reengineering CKD care, narrowing asymmetric information and confronting ethicomedicinomics in CKD care: the introduction of the new 'CKD express©' IT software program. In: Onuigbo MAC, ed. ACE Inhibitors: Medical Uses, Mechanisms of Action, Potential Adverse Effects and Related Topics. Volume 1. New York, NY: NOVA Publishers; 2013: 41–56.
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Address: Macaulay Amechi Chukwukadibia Onuigbo, MD, MSc, FWACP, FASN, MBA, Department of Nephrology, Mayo Clinic Health System, 1221 Whipple Street, Eau Claire, WI 54702; e-mail: onuigbo.macaulay@mayo.edu

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Address: Macaulay Amechi Chukwukadibia Onuigbo, MD, MSc, FWACP, FASN, MBA, Department of Nephrology, Mayo Clinic Health System, 1221 Whipple Street, Eau Claire, WI 54702; e-mail: onuigbo.macaulay@mayo.edu

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In their article in this issue of the Cleveland Clinic Journal of Medicine, Kabach et al answer no to the question of whether stenting of severe renal artery stenosis improves outcomes compared with medical therapy alone.1 They review the findings of four key studies2–5 published between 2003 and 2014 and conclude that, in patients with severe atherosclerotic renal artery stenosis and hypertension or chronic kidney disease, renal artery stenting with medical therapy can improve blood pressure control but has no significant impact on cardiovascular or mortality outcomes.1

See related article

Furthermore, the authors state that in view of the risk of complications associated with stenting, medical management should continue to be the first-line therapy.1 Indeed, the ASTRAL study (Angioplasty and Stenting for Renal Artery Lesions) investigators found substantial risks without evidence of a worthwhile clinical benefit from revascularization in patients with atherosclerotic renovascular disease.3

Nevertheless, I believe that this procedure may benefit certain patients.

MAYO CLINIC COHORT STUDY

In 2008, our group at Mayo Clinic Health system in Eau Claire, Wisconsin, published the results of a prospective cohort study in 26 patients with renal artery stenosis and chronic kidney disease who presented with rapidly worsening renal failure (defined as an increase in serum creatinine of ≥ 25%) while receiving an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin II receptor blocker (ARB).6,7

These drugs—inhibitors of the renin-angiotensin-aldosterone system—slow the progression of chronic kidney disease but can acutely worsen renal function, especially in patients with renal artery stenosis, and withdrawing them in this situation was the focus of our study.

The patients (10 men and 16 women) ranged in age from 63 to 87 (mean age 75.3).

At enrollment, the ACE inhibitors and ARBs were discontinued, standard nephrologic care was applied, and the glomerular filtration rate (estimated by the Modification of Diet in Renal Disease Study equation) was monitored. After at least 2 weeks, percutaneous renal angioplasty with stent placement was considered if the patient met any of the following criteria:

  • Persistence of renal failure
  • Flash pulmonary edema
  • Uncontrolled hypertension despite the use of at least three antihypertensive medications.

Figure 1. Changes in the estimated glomerular filtration rate (eGFR) after percutaneous transluminal angioplasty and stenting of the right renal artery in a 67-year-old woman with hypertension, bilateral renal artery stenosis, and atrophy of the left kidney. She presented in November 2002 with symptomatic acute exacerbation of chronic kidney disease.

Nine patients underwent percutaneous angioplasty and stenting and 17 did not. The procedure was done on one renal artery in 8 patients and both renal arteries in 1. Indications for the procedure were recent worsening of renal failure in 8 patients and recent worsening renal failure together with symptomatic flash pulmonary edema in 1 patient. (Flash pulmonary edema is the only class I recommendation for percutaneous renal angioplasty in the 2006 joint guidelines of the American College of Cardiology and the American Heart Association.8) As noted above, all the patients were experiencing acute exacerbation of chronic kidney disease at the time.

We found clear evidence of additional improved and sustained renal function in the patients who underwent percutaneous renal angioplasty and stenting compared with the patients who did not (Figures 1 and 2).6,7

Figure 2. Changes in the serum creatinine level after bilateral percutaneous transluminal angioplasty and renal artery stenting in a 70-year-old woman with hypertension and diabetes who presented in May 2004 with symptomatic acute exacerbation of chronic kidney disease in association with flash pulmonary edema.

In an editorial9 following publication of the ASTRAL study, our group reported a subsequent 82-month analysis of our 26-patient cohort completed in June 2009. In the 7 surviving patients who had undergone percutaneous renal angioplasty and stenting, the estimated glomerular filtration rate had increased from 27.4 mL/min/1.73 m2 (± 12.7, range 11–47) at baseline to 50.3 (± 21.7, range 23–68) (P = .018) after 46.9 months.

PATIENT NUMBER 13

To illustrate how percutaneous renal angioplasty and stenting can reverse recently worsening renal failure in renal artery stenosis, I would like to discuss in greater detail a patient from our two previous reports.6,7

Patient 13, a 67-year-old woman with hypertension, was referred to our nephrology service in September 2004 to consider starting hemodialysis for symptomatic renal failure. Her serum creatinine had increased to 3.4 mg/dL from a previous baseline level of 2.0 mg/dL, and she also had worsening anemia and hyperkalemia. She had been taking lisinopril 10 mg/day for the last 12 months. Magnetic resonance angiography revealed high-grade (> 95%) bilateral renal artery stenosis with an atrophic left kidney.

Lisinopril was promptly discontinued, and within 2 weeks her serum creatinine level had decreased by more than 0.5 mg/dL. In mid-November 2004, she underwent right renal artery angioplasty with stent placement. After that, her serum creatinine decreased further, and 3 months later it had dropped to 1.6 mg/dL. The value continued to improve, with the lowest measurement of 1.1 mg/dL, equivalent to an estimated glomerular filtration rate of 51 mL/min/1.73 m2. This was in May 2006, 19 months after stopping lisinopril and 17 months after angioplasty and stenting. The last available serum creatinine level (August 2006) was 1.2 mg/dL, equivalent to an estimated glomerular filtration rate of 45 mL/min/1.73 m2 (Figure 1). Unfortunately, the patient died of metastatic lung cancer in December of that year.

Also of note, the patient who underwent angioplasty because of recurrent flash pulmonary edema had no recurrences of it afterward.

We concluded that, in patients with hemodynamically significant renal artery stenosis presenting with acutely worsening renal failure, renal angioplasty with stenting has the potential to reverse renal failure, improve blood pressure control, and stop flash pulmonary edema.6–8

In severe renal artery stenosis, no one treatment fits all

Notably, all patients in our study who underwent renal angioplasty with stenting had new-onset acute renal injury as defined by an increase in the baseline serum creatinine of more than 25% during the 3 months before stent placement.6–8 Patients in the STAR,2 HERCULES,4 and CORAL5 studies had renal artery stenosis but otherwise stable chronic kidney disease at the time of enrollment. In the ASTRAL study,3 12% of the patients had acute kidney injury on study enrollment, defined as an increase in the serum creatinine level of more than 20% or of more than 1.13 mg/dL.3

While we strongly agree with aggressive yet monitored medical therapy for patients with hemodynamically significant renal artery stenosis, I posit that selected patients do indeed derive significant clinical benefits from renal angioplasty and stenting. Our group’s prospective individual-patient-level data support the paradigm that angioplasty with stenting is useful in patients with renal artery stenosis who experience “acute-on-chronic” kidney disease.

The pathophysiology of renal artery stenosis and the progression of chronic kidney disease are complex, and many factors affect patient outcomes and response to treatment. Thus, the message is that treatment of severe renal artery stenosis must be individualized.9–11 No one treatment fits all.10,11

In their article in this issue of the Cleveland Clinic Journal of Medicine, Kabach et al answer no to the question of whether stenting of severe renal artery stenosis improves outcomes compared with medical therapy alone.1 They review the findings of four key studies2–5 published between 2003 and 2014 and conclude that, in patients with severe atherosclerotic renal artery stenosis and hypertension or chronic kidney disease, renal artery stenting with medical therapy can improve blood pressure control but has no significant impact on cardiovascular or mortality outcomes.1

See related article

Furthermore, the authors state that in view of the risk of complications associated with stenting, medical management should continue to be the first-line therapy.1 Indeed, the ASTRAL study (Angioplasty and Stenting for Renal Artery Lesions) investigators found substantial risks without evidence of a worthwhile clinical benefit from revascularization in patients with atherosclerotic renovascular disease.3

Nevertheless, I believe that this procedure may benefit certain patients.

MAYO CLINIC COHORT STUDY

In 2008, our group at Mayo Clinic Health system in Eau Claire, Wisconsin, published the results of a prospective cohort study in 26 patients with renal artery stenosis and chronic kidney disease who presented with rapidly worsening renal failure (defined as an increase in serum creatinine of ≥ 25%) while receiving an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin II receptor blocker (ARB).6,7

These drugs—inhibitors of the renin-angiotensin-aldosterone system—slow the progression of chronic kidney disease but can acutely worsen renal function, especially in patients with renal artery stenosis, and withdrawing them in this situation was the focus of our study.

The patients (10 men and 16 women) ranged in age from 63 to 87 (mean age 75.3).

At enrollment, the ACE inhibitors and ARBs were discontinued, standard nephrologic care was applied, and the glomerular filtration rate (estimated by the Modification of Diet in Renal Disease Study equation) was monitored. After at least 2 weeks, percutaneous renal angioplasty with stent placement was considered if the patient met any of the following criteria:

  • Persistence of renal failure
  • Flash pulmonary edema
  • Uncontrolled hypertension despite the use of at least three antihypertensive medications.

Figure 1. Changes in the estimated glomerular filtration rate (eGFR) after percutaneous transluminal angioplasty and stenting of the right renal artery in a 67-year-old woman with hypertension, bilateral renal artery stenosis, and atrophy of the left kidney. She presented in November 2002 with symptomatic acute exacerbation of chronic kidney disease.

Nine patients underwent percutaneous angioplasty and stenting and 17 did not. The procedure was done on one renal artery in 8 patients and both renal arteries in 1. Indications for the procedure were recent worsening of renal failure in 8 patients and recent worsening renal failure together with symptomatic flash pulmonary edema in 1 patient. (Flash pulmonary edema is the only class I recommendation for percutaneous renal angioplasty in the 2006 joint guidelines of the American College of Cardiology and the American Heart Association.8) As noted above, all the patients were experiencing acute exacerbation of chronic kidney disease at the time.

We found clear evidence of additional improved and sustained renal function in the patients who underwent percutaneous renal angioplasty and stenting compared with the patients who did not (Figures 1 and 2).6,7

Figure 2. Changes in the serum creatinine level after bilateral percutaneous transluminal angioplasty and renal artery stenting in a 70-year-old woman with hypertension and diabetes who presented in May 2004 with symptomatic acute exacerbation of chronic kidney disease in association with flash pulmonary edema.

In an editorial9 following publication of the ASTRAL study, our group reported a subsequent 82-month analysis of our 26-patient cohort completed in June 2009. In the 7 surviving patients who had undergone percutaneous renal angioplasty and stenting, the estimated glomerular filtration rate had increased from 27.4 mL/min/1.73 m2 (± 12.7, range 11–47) at baseline to 50.3 (± 21.7, range 23–68) (P = .018) after 46.9 months.

PATIENT NUMBER 13

To illustrate how percutaneous renal angioplasty and stenting can reverse recently worsening renal failure in renal artery stenosis, I would like to discuss in greater detail a patient from our two previous reports.6,7

Patient 13, a 67-year-old woman with hypertension, was referred to our nephrology service in September 2004 to consider starting hemodialysis for symptomatic renal failure. Her serum creatinine had increased to 3.4 mg/dL from a previous baseline level of 2.0 mg/dL, and she also had worsening anemia and hyperkalemia. She had been taking lisinopril 10 mg/day for the last 12 months. Magnetic resonance angiography revealed high-grade (> 95%) bilateral renal artery stenosis with an atrophic left kidney.

Lisinopril was promptly discontinued, and within 2 weeks her serum creatinine level had decreased by more than 0.5 mg/dL. In mid-November 2004, she underwent right renal artery angioplasty with stent placement. After that, her serum creatinine decreased further, and 3 months later it had dropped to 1.6 mg/dL. The value continued to improve, with the lowest measurement of 1.1 mg/dL, equivalent to an estimated glomerular filtration rate of 51 mL/min/1.73 m2. This was in May 2006, 19 months after stopping lisinopril and 17 months after angioplasty and stenting. The last available serum creatinine level (August 2006) was 1.2 mg/dL, equivalent to an estimated glomerular filtration rate of 45 mL/min/1.73 m2 (Figure 1). Unfortunately, the patient died of metastatic lung cancer in December of that year.

Also of note, the patient who underwent angioplasty because of recurrent flash pulmonary edema had no recurrences of it afterward.

We concluded that, in patients with hemodynamically significant renal artery stenosis presenting with acutely worsening renal failure, renal angioplasty with stenting has the potential to reverse renal failure, improve blood pressure control, and stop flash pulmonary edema.6–8

In severe renal artery stenosis, no one treatment fits all

Notably, all patients in our study who underwent renal angioplasty with stenting had new-onset acute renal injury as defined by an increase in the baseline serum creatinine of more than 25% during the 3 months before stent placement.6–8 Patients in the STAR,2 HERCULES,4 and CORAL5 studies had renal artery stenosis but otherwise stable chronic kidney disease at the time of enrollment. In the ASTRAL study,3 12% of the patients had acute kidney injury on study enrollment, defined as an increase in the serum creatinine level of more than 20% or of more than 1.13 mg/dL.3

While we strongly agree with aggressive yet monitored medical therapy for patients with hemodynamically significant renal artery stenosis, I posit that selected patients do indeed derive significant clinical benefits from renal angioplasty and stenting. Our group’s prospective individual-patient-level data support the paradigm that angioplasty with stenting is useful in patients with renal artery stenosis who experience “acute-on-chronic” kidney disease.

The pathophysiology of renal artery stenosis and the progression of chronic kidney disease are complex, and many factors affect patient outcomes and response to treatment. Thus, the message is that treatment of severe renal artery stenosis must be individualized.9–11 No one treatment fits all.10,11

References
  1. Kabach A, Agha OQ, Baibars M, Alraiyes AH, Alraies MC. Does stenting of severe renal artery stenosis improve outcomes compared with medical therapy alone? Cleve Clin J Med 2015; 82:491–494.
  2. Bax L, Mali WP, Buskens E, et al; STAR Study Group. The benefit of STent placement and blood pressure and lipid-lowering for the prevention of progression of renal dysfunction caused by Atherosclerotic ostial stenosis of the Renal artery. The STAR-study: rationale and study design. J Nephrol 2003; 16:807–812.
  3. ASTRAL Investigators; Wheatley K, Ives N, Gray R, et al. Revascularization versus medical therapy for renal-artery stenosis. N Engl J Med 2009; 361:1953–1962.
  4. Jaff MR, Bates M, Sullivan T, et al; HERCULES Investigators. Significant reduction in systolic blood pressure following renal artery stenting in patients with uncontrolled hypertension: results from the HERCULES trial. Catheter Cardiovasc Interv 2012; 80:343–350.
  5. Cooper CJ, Murphy TP, Cutlip DE, et al; CORAL Investigators. Stenting and medical therapy for atherosclerotic renal-artery stenosis. N Engl J Med 2014; 370:13–22.
  6. Onuigbo MAC, Onuigbo NTC. Worsening renal failure in older chronic kidney disease patients with renal artery stenosis concurrently on renin angiotensin aldosterone system blockade: a prospective 50-month Mayo Health System clinic analysis. QJM 2008; 101:519–527.
  7. Onuigbo MA, Onuigbo NT. Renal failure and concurrent RAAS blockade in older CKD patients with renal artery stenosis: an extended Mayo Clinic prospective 63-month experience. Ren Fail 2008; 30:363–371.
  8. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary. J Am Coll Cardiol 2006; 47:1239–1312.
  9. Onuigbo M, Frenandes R, Nijhawan V. The ASTRAL trial results revisited—to stent or not to stent in renal artery stenosis? QJM 2010; 103:357.
  10. Singh M, Kovacs DF, Singh A, Dhaliwal P, Khosla S. ACE inhibition and renal artery stenosis: what lessons have we learnt? A 21st century perspective. In: Onuigbo MAC, ed. ACE inhibitors: Medical Uses, Mechanisms of Action, Potential Adverse Effects and Related Topics. Volume 2. New York, NY: NOVA Publishers; 2013:203–218.
  11. Onuigbo MA, Onuigbo C, Onuigbo V, et al. The CKD enigma, reengineering CKD care, narrowing asymmetric information and confronting ethicomedicinomics in CKD care: the introduction of the new 'CKD express©' IT software program. In: Onuigbo MAC, ed. ACE Inhibitors: Medical Uses, Mechanisms of Action, Potential Adverse Effects and Related Topics. Volume 1. New York, NY: NOVA Publishers; 2013: 41–56.
References
  1. Kabach A, Agha OQ, Baibars M, Alraiyes AH, Alraies MC. Does stenting of severe renal artery stenosis improve outcomes compared with medical therapy alone? Cleve Clin J Med 2015; 82:491–494.
  2. Bax L, Mali WP, Buskens E, et al; STAR Study Group. The benefit of STent placement and blood pressure and lipid-lowering for the prevention of progression of renal dysfunction caused by Atherosclerotic ostial stenosis of the Renal artery. The STAR-study: rationale and study design. J Nephrol 2003; 16:807–812.
  3. ASTRAL Investigators; Wheatley K, Ives N, Gray R, et al. Revascularization versus medical therapy for renal-artery stenosis. N Engl J Med 2009; 361:1953–1962.
  4. Jaff MR, Bates M, Sullivan T, et al; HERCULES Investigators. Significant reduction in systolic blood pressure following renal artery stenting in patients with uncontrolled hypertension: results from the HERCULES trial. Catheter Cardiovasc Interv 2012; 80:343–350.
  5. Cooper CJ, Murphy TP, Cutlip DE, et al; CORAL Investigators. Stenting and medical therapy for atherosclerotic renal-artery stenosis. N Engl J Med 2014; 370:13–22.
  6. Onuigbo MAC, Onuigbo NTC. Worsening renal failure in older chronic kidney disease patients with renal artery stenosis concurrently on renin angiotensin aldosterone system blockade: a prospective 50-month Mayo Health System clinic analysis. QJM 2008; 101:519–527.
  7. Onuigbo MA, Onuigbo NT. Renal failure and concurrent RAAS blockade in older CKD patients with renal artery stenosis: an extended Mayo Clinic prospective 63-month experience. Ren Fail 2008; 30:363–371.
  8. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary. J Am Coll Cardiol 2006; 47:1239–1312.
  9. Onuigbo M, Frenandes R, Nijhawan V. The ASTRAL trial results revisited—to stent or not to stent in renal artery stenosis? QJM 2010; 103:357.
  10. Singh M, Kovacs DF, Singh A, Dhaliwal P, Khosla S. ACE inhibition and renal artery stenosis: what lessons have we learnt? A 21st century perspective. In: Onuigbo MAC, ed. ACE inhibitors: Medical Uses, Mechanisms of Action, Potential Adverse Effects and Related Topics. Volume 2. New York, NY: NOVA Publishers; 2013:203–218.
  11. Onuigbo MA, Onuigbo C, Onuigbo V, et al. The CKD enigma, reengineering CKD care, narrowing asymmetric information and confronting ethicomedicinomics in CKD care: the introduction of the new 'CKD express©' IT software program. In: Onuigbo MAC, ed. ACE Inhibitors: Medical Uses, Mechanisms of Action, Potential Adverse Effects and Related Topics. Volume 1. New York, NY: NOVA Publishers; 2013: 41–56.
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Improving patient satisfaction: Timely feedback to specific physicians is essential for success

Patient satisfaction has received increased attention in recent years, which we believe is well deserved and long overdue. Anyone who has been hospitalized, or has had a loved one hospitalized, can appreciate that there is room to improve the patient experience. Dedicating time and effort to improving the patient experience is consistent with our professional commitment to comfort, empathize, and partner with our patients. Though patient satisfaction itself is an outcome worthy of our attention, it is also positively associated with measures related to patient safety and clinical effectiveness.[1, 2] Moreover, patient satisfaction is the only publicly reported measure that represents the patient's voice,[3] and accounts for a substantial portion of the Centers for Medicare and Medicaid Services payment adjustments under the Hospital Value Based Purchasing Program.[4]

However, all healthcare professionals should understand some key fundamental issues related to the measurement of patient satisfaction. The survey from which data are publicly reported and used for hospital payment adjustment is the Hospital Consumer Assessment of Healthcare Providers and Systems (HCAHPS) survey, developed by the Agency for Healthcare Research and Quality.[5, 6] HCAHPS is sent to a random sample of 40% of hospitalized patients between 48 hours and 6 weeks after discharge. The HCAHPS survey uses ordinal response scales (eg, never, sometimes, usually, always) that generate highly skewed results toward favorable responses. Therefore, results are reported as the percent top box (ie, the percentage of responses in the most favorable category) rather than as a median score. The skewed distribution of results indicates that most patients are generally satisfied with care (ie, most respondents do not have an axe to grind), but also makes meaningful improvement difficult to achieve. Prior to public reporting and determination of effect on hospital payment, results are adjusted for mode of survey administration and patient mix. The same is not true when patient satisfaction data are used for internal purposes. Hospital leaders typically do not perform statistical adjustment and therefore need to be careful not to make apples‐to‐orangestype comparisons. For example, obstetric patient satisfaction scores should not be compared to general medical patient satisfaction scores, as these populations tend to rate satisfaction differently.

The HCAHPS survey questions are organized into domains of care, including satisfaction with nurses and satisfaction with doctors. Importantly, other healthcare team members may influence patients' perception in these domains. For example, a patient responding to nurse communication questions may also reflect on experiences with patient care technicians, social workers, and therapists. A patient responding to physician communication questions might also reflect on experiences with advanced practice providers. A common mistake is the practice of attributing satisfaction with doctors to the individual who served as the discharge physician. Many readers have likely seen patient satisfaction reports broken out by discharge physician with the expectation that giving this information to individual physicians will serve as useful formative feedback. The reality is that patients see many doctors during a hospitalization. To illustrate this point, we analyzed data from 420 patients admitted to our nonteaching hospitalist service who had completed an HCAHPS survey in 2014. We found that the discharge hospitalist accounted for only 34% of all physician encounters. Furthermore, research has shown that patients' experiences with specialist physicians also have a strong influence on their overall satisfaction with physicians.[7]

Having reliable patient satisfaction data on specific individuals would be a truly powerful formative assessment tool. In this issue of the Journal of Hospital Medicine, Banka and colleagues report on an impressive approach incorporating such a tool to give constructive feedback to physicians.[8] Since 2006, the study site had administered surveys to hospitalized patients that assess their satisfaction with specific resident physicians.[9] However, residency programs only reviewed the survey results with resident physicians about twice a year. The multifaceted intervention developed by Banka and colleagues included directly emailing the survey results to internal medicine resident physicians in real time while they were in service, a 1‐hour conference on best communication practices, and a reward program in which 3 residents were identified monthly to receive department‐wide recognition via email and a generous movie package. Using difference‐in‐differences regression analysis, the investigators compared changes in patient satisfaction results for internal medicine residents to results for residents from other specialties (who were not part of the intervention). The percentage of patients who gave top box responses to all 3 physician‐related questions and to the overall hospital rating was significantly higher for the internal medicine residents.

The findings from this study are important, because no prior study of an intervention, to our knowledge, has shown a significant improvement in patient satisfaction scores. In this study, feedback was believed to be the most powerful factor. The importance of meaningful, timely feedback in medical education is well recognized.[10] Without feedback there is poor insight into how intended results from specific actions compare with actual results. When feedback is lacking from external sources (in this case the voice of the patient), an uncontested sense of mastery develops, allowing mistakes to go uncorrected. This false sense of mastery contributes to an emotional and defensive response when performance is finally revealed to be less than optimal. The simple act of giving more timely feedback in this study encouraged self‐motivated reflection and practice change aimed at improving patient satisfaction, with remarkable results.

The study should inspire physician leaders from various hospital settings, and researchers, to develop and evaluate similar programs to improve patient satisfaction. We agree with the investigators that the approach should be multifaceted. Feedback to specific physicians is a powerful motivator, but needs to be combined with strategies to enhance communication skills. Brief conferences are less likely to have a lasting impact on behaviors than strategies like coaching and simulation based training.[11] Interventions should include recognition and reward to acknowledge exceptional performance and build friendly competition.

The biggest challenge to adopting an intervention such as the one used in the Banka study relates to the feasibility of implementing physician‐specific patient satisfaction reporting. Several survey instruments are available for use as tools to assess satisfaction with specific physicians.[9, 12, 13] However, who will administer these instruments? Most hospitals do not have undergraduate students available. Hospitals could use their volunteers, but this is not likely to be a sustainable solution. Hospitals could consider administering the survey via email, but many hospitals are just starting to collect patient email addresses and many patients do not use email. Once data are collected, who will conduct analyses and create comparative reports? Press Ganey recently developed a survey assessing satisfaction with specific hospitalists, using photographs, and offers the ability to create comparative reports.[14] Their service addresses the analytic challenge, but the quandary of survey administration remains.

In conclusion, we encourage hospital medicine leaders to develop and evaluate multifaceted interventions to improve patient satisfaction such as the one reported by Banka et al. Timely, specific feedback to physicians is an essential feature. The collection of physician‐specific data is a major challenge, but not an insurmountable one. Novel use of personnel and/or technology is likely to play a role in these efforts.

Disclosure: Nothing to report.

References
  1. Doyle C, Lennox L, Bell D. A systematic review of evidence on the links between patient experience and clinical safety and effectiveness. BMJ Open. 2013;3(1).
  2. Jha AK, Orav EJ, Zheng J, Epstein AM. Patients' perception of hospital care in the United States. N Engl J Med. 2008;359(18):19211931.
  3. Medicare.gov. Hospital Compare. Available at: http://www.medicare.gov/hospitalcompare/search.html. Accessed April 27, 2015.
  4. Centers for Medicare 67(1):2737.
  5. Wild DM, Kwon N, Dutta S, et al. Who's behind an HCAHPS score? Jt Comm J Qual Patient Saf. 2011;37(10):461468.
  6. Banka G, Edington S, Kyulo N, et al. Improving patient satisfaction through physician education, feedback, and incentives. J Hosp Med. 2015;10(8):497502.
  7. Wen T, Huang B, Mosley V, Afsar‐Manesh N. Promoting patient‐centred care through trainee feedback: assessing residents' C‐I‐CARE (ARC) program. BMJ Qual Saf. 2012;21(3):225233.
  8. Ende J. Feedback in clinical medical education. JAMA. 1983;250(6):777781.
  9. O'Leary KJ, Darling TA, Rauworth J, Williams MV. Impact of hospitalist communication‐skills training on patient‐satisfaction scores. J Hosp Med. 2013;8(6):315320.
  10. Ferranti DE, Makoul G, Forth VE, Rauworth J, Lee J, Williams MV. Assessing patient perceptions of hospitalist communication skills using the Communication Assessment Tool (CAT). J Hosp Med. 2010;5(9):522527.
  11. Torok H, Ghazarian SR, Kotwal S, Landis R, Wright S, Howell E. Development and validation of the tool to assess inpatient satisfaction with care from hospitalists. J Hosp Med. 2014;9(9):553558.
  12. Press Ganey. A true performance solution for hospitalists. Available at: http://www.pressganey.com/ourSolutions/patient‐voice/census‐based‐surveying/hospitalist.aspx. Accessed April 27, 2015.
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Patient satisfaction has received increased attention in recent years, which we believe is well deserved and long overdue. Anyone who has been hospitalized, or has had a loved one hospitalized, can appreciate that there is room to improve the patient experience. Dedicating time and effort to improving the patient experience is consistent with our professional commitment to comfort, empathize, and partner with our patients. Though patient satisfaction itself is an outcome worthy of our attention, it is also positively associated with measures related to patient safety and clinical effectiveness.[1, 2] Moreover, patient satisfaction is the only publicly reported measure that represents the patient's voice,[3] and accounts for a substantial portion of the Centers for Medicare and Medicaid Services payment adjustments under the Hospital Value Based Purchasing Program.[4]

However, all healthcare professionals should understand some key fundamental issues related to the measurement of patient satisfaction. The survey from which data are publicly reported and used for hospital payment adjustment is the Hospital Consumer Assessment of Healthcare Providers and Systems (HCAHPS) survey, developed by the Agency for Healthcare Research and Quality.[5, 6] HCAHPS is sent to a random sample of 40% of hospitalized patients between 48 hours and 6 weeks after discharge. The HCAHPS survey uses ordinal response scales (eg, never, sometimes, usually, always) that generate highly skewed results toward favorable responses. Therefore, results are reported as the percent top box (ie, the percentage of responses in the most favorable category) rather than as a median score. The skewed distribution of results indicates that most patients are generally satisfied with care (ie, most respondents do not have an axe to grind), but also makes meaningful improvement difficult to achieve. Prior to public reporting and determination of effect on hospital payment, results are adjusted for mode of survey administration and patient mix. The same is not true when patient satisfaction data are used for internal purposes. Hospital leaders typically do not perform statistical adjustment and therefore need to be careful not to make apples‐to‐orangestype comparisons. For example, obstetric patient satisfaction scores should not be compared to general medical patient satisfaction scores, as these populations tend to rate satisfaction differently.

The HCAHPS survey questions are organized into domains of care, including satisfaction with nurses and satisfaction with doctors. Importantly, other healthcare team members may influence patients' perception in these domains. For example, a patient responding to nurse communication questions may also reflect on experiences with patient care technicians, social workers, and therapists. A patient responding to physician communication questions might also reflect on experiences with advanced practice providers. A common mistake is the practice of attributing satisfaction with doctors to the individual who served as the discharge physician. Many readers have likely seen patient satisfaction reports broken out by discharge physician with the expectation that giving this information to individual physicians will serve as useful formative feedback. The reality is that patients see many doctors during a hospitalization. To illustrate this point, we analyzed data from 420 patients admitted to our nonteaching hospitalist service who had completed an HCAHPS survey in 2014. We found that the discharge hospitalist accounted for only 34% of all physician encounters. Furthermore, research has shown that patients' experiences with specialist physicians also have a strong influence on their overall satisfaction with physicians.[7]

Having reliable patient satisfaction data on specific individuals would be a truly powerful formative assessment tool. In this issue of the Journal of Hospital Medicine, Banka and colleagues report on an impressive approach incorporating such a tool to give constructive feedback to physicians.[8] Since 2006, the study site had administered surveys to hospitalized patients that assess their satisfaction with specific resident physicians.[9] However, residency programs only reviewed the survey results with resident physicians about twice a year. The multifaceted intervention developed by Banka and colleagues included directly emailing the survey results to internal medicine resident physicians in real time while they were in service, a 1‐hour conference on best communication practices, and a reward program in which 3 residents were identified monthly to receive department‐wide recognition via email and a generous movie package. Using difference‐in‐differences regression analysis, the investigators compared changes in patient satisfaction results for internal medicine residents to results for residents from other specialties (who were not part of the intervention). The percentage of patients who gave top box responses to all 3 physician‐related questions and to the overall hospital rating was significantly higher for the internal medicine residents.

The findings from this study are important, because no prior study of an intervention, to our knowledge, has shown a significant improvement in patient satisfaction scores. In this study, feedback was believed to be the most powerful factor. The importance of meaningful, timely feedback in medical education is well recognized.[10] Without feedback there is poor insight into how intended results from specific actions compare with actual results. When feedback is lacking from external sources (in this case the voice of the patient), an uncontested sense of mastery develops, allowing mistakes to go uncorrected. This false sense of mastery contributes to an emotional and defensive response when performance is finally revealed to be less than optimal. The simple act of giving more timely feedback in this study encouraged self‐motivated reflection and practice change aimed at improving patient satisfaction, with remarkable results.

The study should inspire physician leaders from various hospital settings, and researchers, to develop and evaluate similar programs to improve patient satisfaction. We agree with the investigators that the approach should be multifaceted. Feedback to specific physicians is a powerful motivator, but needs to be combined with strategies to enhance communication skills. Brief conferences are less likely to have a lasting impact on behaviors than strategies like coaching and simulation based training.[11] Interventions should include recognition and reward to acknowledge exceptional performance and build friendly competition.

The biggest challenge to adopting an intervention such as the one used in the Banka study relates to the feasibility of implementing physician‐specific patient satisfaction reporting. Several survey instruments are available for use as tools to assess satisfaction with specific physicians.[9, 12, 13] However, who will administer these instruments? Most hospitals do not have undergraduate students available. Hospitals could use their volunteers, but this is not likely to be a sustainable solution. Hospitals could consider administering the survey via email, but many hospitals are just starting to collect patient email addresses and many patients do not use email. Once data are collected, who will conduct analyses and create comparative reports? Press Ganey recently developed a survey assessing satisfaction with specific hospitalists, using photographs, and offers the ability to create comparative reports.[14] Their service addresses the analytic challenge, but the quandary of survey administration remains.

In conclusion, we encourage hospital medicine leaders to develop and evaluate multifaceted interventions to improve patient satisfaction such as the one reported by Banka et al. Timely, specific feedback to physicians is an essential feature. The collection of physician‐specific data is a major challenge, but not an insurmountable one. Novel use of personnel and/or technology is likely to play a role in these efforts.

Disclosure: Nothing to report.

Patient satisfaction has received increased attention in recent years, which we believe is well deserved and long overdue. Anyone who has been hospitalized, or has had a loved one hospitalized, can appreciate that there is room to improve the patient experience. Dedicating time and effort to improving the patient experience is consistent with our professional commitment to comfort, empathize, and partner with our patients. Though patient satisfaction itself is an outcome worthy of our attention, it is also positively associated with measures related to patient safety and clinical effectiveness.[1, 2] Moreover, patient satisfaction is the only publicly reported measure that represents the patient's voice,[3] and accounts for a substantial portion of the Centers for Medicare and Medicaid Services payment adjustments under the Hospital Value Based Purchasing Program.[4]

However, all healthcare professionals should understand some key fundamental issues related to the measurement of patient satisfaction. The survey from which data are publicly reported and used for hospital payment adjustment is the Hospital Consumer Assessment of Healthcare Providers and Systems (HCAHPS) survey, developed by the Agency for Healthcare Research and Quality.[5, 6] HCAHPS is sent to a random sample of 40% of hospitalized patients between 48 hours and 6 weeks after discharge. The HCAHPS survey uses ordinal response scales (eg, never, sometimes, usually, always) that generate highly skewed results toward favorable responses. Therefore, results are reported as the percent top box (ie, the percentage of responses in the most favorable category) rather than as a median score. The skewed distribution of results indicates that most patients are generally satisfied with care (ie, most respondents do not have an axe to grind), but also makes meaningful improvement difficult to achieve. Prior to public reporting and determination of effect on hospital payment, results are adjusted for mode of survey administration and patient mix. The same is not true when patient satisfaction data are used for internal purposes. Hospital leaders typically do not perform statistical adjustment and therefore need to be careful not to make apples‐to‐orangestype comparisons. For example, obstetric patient satisfaction scores should not be compared to general medical patient satisfaction scores, as these populations tend to rate satisfaction differently.

The HCAHPS survey questions are organized into domains of care, including satisfaction with nurses and satisfaction with doctors. Importantly, other healthcare team members may influence patients' perception in these domains. For example, a patient responding to nurse communication questions may also reflect on experiences with patient care technicians, social workers, and therapists. A patient responding to physician communication questions might also reflect on experiences with advanced practice providers. A common mistake is the practice of attributing satisfaction with doctors to the individual who served as the discharge physician. Many readers have likely seen patient satisfaction reports broken out by discharge physician with the expectation that giving this information to individual physicians will serve as useful formative feedback. The reality is that patients see many doctors during a hospitalization. To illustrate this point, we analyzed data from 420 patients admitted to our nonteaching hospitalist service who had completed an HCAHPS survey in 2014. We found that the discharge hospitalist accounted for only 34% of all physician encounters. Furthermore, research has shown that patients' experiences with specialist physicians also have a strong influence on their overall satisfaction with physicians.[7]

Having reliable patient satisfaction data on specific individuals would be a truly powerful formative assessment tool. In this issue of the Journal of Hospital Medicine, Banka and colleagues report on an impressive approach incorporating such a tool to give constructive feedback to physicians.[8] Since 2006, the study site had administered surveys to hospitalized patients that assess their satisfaction with specific resident physicians.[9] However, residency programs only reviewed the survey results with resident physicians about twice a year. The multifaceted intervention developed by Banka and colleagues included directly emailing the survey results to internal medicine resident physicians in real time while they were in service, a 1‐hour conference on best communication practices, and a reward program in which 3 residents were identified monthly to receive department‐wide recognition via email and a generous movie package. Using difference‐in‐differences regression analysis, the investigators compared changes in patient satisfaction results for internal medicine residents to results for residents from other specialties (who were not part of the intervention). The percentage of patients who gave top box responses to all 3 physician‐related questions and to the overall hospital rating was significantly higher for the internal medicine residents.

The findings from this study are important, because no prior study of an intervention, to our knowledge, has shown a significant improvement in patient satisfaction scores. In this study, feedback was believed to be the most powerful factor. The importance of meaningful, timely feedback in medical education is well recognized.[10] Without feedback there is poor insight into how intended results from specific actions compare with actual results. When feedback is lacking from external sources (in this case the voice of the patient), an uncontested sense of mastery develops, allowing mistakes to go uncorrected. This false sense of mastery contributes to an emotional and defensive response when performance is finally revealed to be less than optimal. The simple act of giving more timely feedback in this study encouraged self‐motivated reflection and practice change aimed at improving patient satisfaction, with remarkable results.

The study should inspire physician leaders from various hospital settings, and researchers, to develop and evaluate similar programs to improve patient satisfaction. We agree with the investigators that the approach should be multifaceted. Feedback to specific physicians is a powerful motivator, but needs to be combined with strategies to enhance communication skills. Brief conferences are less likely to have a lasting impact on behaviors than strategies like coaching and simulation based training.[11] Interventions should include recognition and reward to acknowledge exceptional performance and build friendly competition.

The biggest challenge to adopting an intervention such as the one used in the Banka study relates to the feasibility of implementing physician‐specific patient satisfaction reporting. Several survey instruments are available for use as tools to assess satisfaction with specific physicians.[9, 12, 13] However, who will administer these instruments? Most hospitals do not have undergraduate students available. Hospitals could use their volunteers, but this is not likely to be a sustainable solution. Hospitals could consider administering the survey via email, but many hospitals are just starting to collect patient email addresses and many patients do not use email. Once data are collected, who will conduct analyses and create comparative reports? Press Ganey recently developed a survey assessing satisfaction with specific hospitalists, using photographs, and offers the ability to create comparative reports.[14] Their service addresses the analytic challenge, but the quandary of survey administration remains.

In conclusion, we encourage hospital medicine leaders to develop and evaluate multifaceted interventions to improve patient satisfaction such as the one reported by Banka et al. Timely, specific feedback to physicians is an essential feature. The collection of physician‐specific data is a major challenge, but not an insurmountable one. Novel use of personnel and/or technology is likely to play a role in these efforts.

Disclosure: Nothing to report.

References
  1. Doyle C, Lennox L, Bell D. A systematic review of evidence on the links between patient experience and clinical safety and effectiveness. BMJ Open. 2013;3(1).
  2. Jha AK, Orav EJ, Zheng J, Epstein AM. Patients' perception of hospital care in the United States. N Engl J Med. 2008;359(18):19211931.
  3. Medicare.gov. Hospital Compare. Available at: http://www.medicare.gov/hospitalcompare/search.html. Accessed April 27, 2015.
  4. Centers for Medicare 67(1):2737.
  5. Wild DM, Kwon N, Dutta S, et al. Who's behind an HCAHPS score? Jt Comm J Qual Patient Saf. 2011;37(10):461468.
  6. Banka G, Edington S, Kyulo N, et al. Improving patient satisfaction through physician education, feedback, and incentives. J Hosp Med. 2015;10(8):497502.
  7. Wen T, Huang B, Mosley V, Afsar‐Manesh N. Promoting patient‐centred care through trainee feedback: assessing residents' C‐I‐CARE (ARC) program. BMJ Qual Saf. 2012;21(3):225233.
  8. Ende J. Feedback in clinical medical education. JAMA. 1983;250(6):777781.
  9. O'Leary KJ, Darling TA, Rauworth J, Williams MV. Impact of hospitalist communication‐skills training on patient‐satisfaction scores. J Hosp Med. 2013;8(6):315320.
  10. Ferranti DE, Makoul G, Forth VE, Rauworth J, Lee J, Williams MV. Assessing patient perceptions of hospitalist communication skills using the Communication Assessment Tool (CAT). J Hosp Med. 2010;5(9):522527.
  11. Torok H, Ghazarian SR, Kotwal S, Landis R, Wright S, Howell E. Development and validation of the tool to assess inpatient satisfaction with care from hospitalists. J Hosp Med. 2014;9(9):553558.
  12. Press Ganey. A true performance solution for hospitalists. Available at: http://www.pressganey.com/ourSolutions/patient‐voice/census‐based‐surveying/hospitalist.aspx. Accessed April 27, 2015.
References
  1. Doyle C, Lennox L, Bell D. A systematic review of evidence on the links between patient experience and clinical safety and effectiveness. BMJ Open. 2013;3(1).
  2. Jha AK, Orav EJ, Zheng J, Epstein AM. Patients' perception of hospital care in the United States. N Engl J Med. 2008;359(18):19211931.
  3. Medicare.gov. Hospital Compare. Available at: http://www.medicare.gov/hospitalcompare/search.html. Accessed April 27, 2015.
  4. Centers for Medicare 67(1):2737.
  5. Wild DM, Kwon N, Dutta S, et al. Who's behind an HCAHPS score? Jt Comm J Qual Patient Saf. 2011;37(10):461468.
  6. Banka G, Edington S, Kyulo N, et al. Improving patient satisfaction through physician education, feedback, and incentives. J Hosp Med. 2015;10(8):497502.
  7. Wen T, Huang B, Mosley V, Afsar‐Manesh N. Promoting patient‐centred care through trainee feedback: assessing residents' C‐I‐CARE (ARC) program. BMJ Qual Saf. 2012;21(3):225233.
  8. Ende J. Feedback in clinical medical education. JAMA. 1983;250(6):777781.
  9. O'Leary KJ, Darling TA, Rauworth J, Williams MV. Impact of hospitalist communication‐skills training on patient‐satisfaction scores. J Hosp Med. 2013;8(6):315320.
  10. Ferranti DE, Makoul G, Forth VE, Rauworth J, Lee J, Williams MV. Assessing patient perceptions of hospitalist communication skills using the Communication Assessment Tool (CAT). J Hosp Med. 2010;5(9):522527.
  11. Torok H, Ghazarian SR, Kotwal S, Landis R, Wright S, Howell E. Development and validation of the tool to assess inpatient satisfaction with care from hospitalists. J Hosp Med. 2014;9(9):553558.
  12. Press Ganey. A true performance solution for hospitalists. Available at: http://www.pressganey.com/ourSolutions/patient‐voice/census‐based‐surveying/hospitalist.aspx. Accessed April 27, 2015.
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Address for correspondence and reprint requests: Kevin J. O'Leary, MD, Associate Professor of Medicine, Division of Hospital Medicine, Northwestern University Feinberg School of Medicine, 211 E. Ontario St., Chicago, IL 60611; Telephone: 312‐926‐5984; Fax: 312‐926‐4588; E‐mail: keoleary@nmh.org
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We specialize in change leadership: A call for hospitalists to lead the quest for workforce gender equity

From a new concept to 44,000 practitioners in just 18 years,[1] there is no doubt that the word hospitalist is synonymous with innovation, leadership, growth, and change. Yet 2 articles in this month's Journal of Hospital Medicine prove that even our new field faces age‐old problems. Although women comprise half of all academic hospitalist and general internal medicine faculty, Burden et al.[2] showed that female hospitalists are less likely than male hospitalists to be division or section heads of hospital medicine, speakers at national meetings, and first or last authors on both research publications and editorials. This is made more concerning given that women are more likely to choose academic hospital medicine careers,[3] as they represent one‐third of all hospitalists but half of the academic hospitalist workforce.[2, 3] Findings in general internal medicine were similar, except that equal numbers of women and men were national meeting speakers and first authors on research publications (but not editorials). Weaver et al.[4] shed even more light on this disparity, and found that female hospitalists made $14,581 less per year than their male counterparts, even after adjusting for relevant differences. Weaver and colleagues also found other gender‐specific differences: women worked more nights and had fewer billable encounters per hospitalist shift than men.

Unfortunately, these trends are not new or limited to hospital medicine. For decades, almost equal numbers of women and men have entered medical school,[5] yet women are under‐represented in high status specialties,[6] less likely to be first or senior authors on original research studies compared to men,[7] less likely to be promoted,[8] and women physicians are consistently paid less than men across specialties.[9, 10] Simple analyses have not yet explained these disparities. Compared with men, women have similar leadership aspirations[11, 12] and are at least as effective as leaders.[13, 14, 15] Yet equity has not been attained.

Implicit bias research suggests that gender stereotypes influence women at all career stages.[16, 17, 18] For example, an elegant study conducted by Correll et al. identified a motherhood penalty, where indicating membership in the elementary school parent‐teacher organization on one's curriculum vitae hurt women's chances of employment and pay, but actually helped men.[19] Gender stereotypes exist, even among those who do not support their content. The universal reinforcement of such stereotypes over time leads to implicit but prescriptive rules about how women and men should act.[20] In particular, communal behaviors, including being cooperative, kind, and understanding, are typically associated with women, and agentic behaviors, including being ambitious and acting as a leader, are considered appropriate for men.[21] This leads to the think leader, think male phenomena, where we automatically associate men with leadership and higher status tasks (like first authorship or speaker invitations).[22, 23] Furthermore, acting against the stereotype (eg, a woman showing anger[24] or negotiating for more pay[25] or a man showing sadness[26]) can negatively impact wage and employment. Expecting social censure for violating gender norms, women develop a fear of the backlash that alone may shape behavior such that women may not express interest in having a high salary or negotiate for a raise.[27, 28, 29]

The specific system and institutional barriers that prevent female hospitalists from receiving equal pay and opportunities for leadership are not known, but one can surmise they are similar to those found in other specialties.[10, 30, 31] The findings of the studies of Burden et al.[2] and Weaver et al.[4] invite investigation of new questions specific to hospital medicine. Why are women in hospital medicine working more night shifts? Does this impact leadership or scholarship opportunities? Why are women documenting less productivity? Are they spending more time with patients, as they do in other settings?[32] What influences their practice choice? We would like to believe that there is something about hospital medicine that can explain the gender differences identified in these 2 studies. However, these data should prompt a serious and thorough examination of our specialty. We must accept that despite being a new specialty and a change leader, hospital medicine may not have escaped systematic gender bias that constrains the full participation and advancement of women.

But we believe that hospitalistsinnovators and change leaders in medicinewill be spurred to action to address the possibility of gender inequities. We do not need to know all of the causes to begin to address disparities, of every type, on an individual, institutional, and national level. As individuals, we can acknowledge that there are implicit assumptions that influence our decision making. No matter how unintentional, and even conflicting with evidence, these assumptions can lead us to judge women as less capable leaders than men or to automatically envision a high salary for a woman and man as different amounts. However, these automatic gender biases function as habits of mind, so they can be broken like any other unwanted habit.[33] Institutionally, we can also hold ourselves accountable for transparency in mentorship, leadership, scholarship, promotions, and wages to ensure diverse representation. We should routinely examine our practices to ensure the equitable hiring, pay, and promotion of our workforce.[18] National organizations and their respective journals should actively pursue diverse representation in leadership and membership on boards and committees, award nominees and recipients, and opportunities for invited editorials. Hospital medicinebeing young, innovative, and committed to changeis uniquely well suited to lead the charge for workforce equity. We can, and will, show the rest of medicine how it is done.

Disclosure

Nothing to report.

Files
References
  1. Society of Hospital Medicine. Milestones in the hospital medicine movement. Available at: http://www.hospitalmedicine.org/Web/About_SHM/Industry/shm_History.aspx. Accessed March 23, 2015.
  2. Burden M, Frank M, Keniston A, et al. Gender disparities in leadership and scholarly productivity of academic hospitalists. J Hosp Med. 2015;10(X):000000.
  3. Hinami K, Whelan C, Miller J, Wolosin R, Wetterneck T. Job characteristics, satisfaction, and burnout across hospitalist practice models. J Hosp Med. 2012;7:402410.
  4. Weaver C, Wetterneck T, Whelan C, Hinami K. A matter of priorities? Exploring the persistent gender pay gap in hospital medicine. J Hosp Med. 2015;10(8):486490.
  5. Association of American Medical Colleges. Table 1: medical students, selected years, 1965–2013. Available at: https://www.aamc.org/download/411782/data/2014_table1.pdf. Accessed March 23, 2015.
  6. Jagsi R, Griffith K, DeCastro R, Ubel P. Sex, role models, and specialty choices among graduates of US medical schools in 2006‐2008. J Am Coll Surg. 2014;218(3):345352.
  7. Jagsi R, Guancial E, Worobey C, et al. The “Gender Gap” in authorship of academic medical literature—a 35‐year perspective. N Engl J Med. 2006;355(3):281287.
  8. Nonnemaker L. Women physicians in academic medicine. N Engl J Med. 2000;342(6):399405.
  9. Jagsi R, Griffith K, Stewart A, Sambuco D, DeCastro R, Ubel P. Gender differences in the salaries of physician researchers. JAMA. 2012;307(22):24102417.
  10. Sasso A, Richards M, Chou C, Gerber S. The $16,819 pay gap for newly trained physicians: the unexplained trend of men earning more than women. Health Affairs. 2011;30(2):193201.
  11. Pololi L, Civian J, Brennan R, Dottalo A, Krupat E. Experiencing the culture of academic medicine: gender matters, a national study. J Gen Intern Med. 2013;28(2):201207.
  12. Wright A, Schwindt L, Bassford T, et al. Gender differences in academic advancement: patterns, causes, and potential solutions in one US College of Medicine. Acad Med. 2003;78(5):500508.
  13. Rosser V. Faculty and staff members perceptions of effective leadership: are there differences between men and women leaders? Equity Excell Educ. 2003;36(1):7181.
  14. Eagly A, Johannesen‐Schmidt M, Engen M. Transformational, transactional, and lasissez‐faire leadership styles: a meta‐analysis comparing women and men. Psychol Bull. 2003;129(4):569591.
  15. Isaac C, Griffin L, Carnes M. A qualitative study of faculty members' views of women chairs. J Womens Health (Larchmt). 2010;19(3):533546.
  16. Kaatz A, Carnes M. Stuck in the out‐group: Jennifer can't grow up, Jane's invisible, and Janet's over the hill. J Womens Health (Larchmt). 2014;23(6):481484.
  17. Eagly A, Carli L. Women and the labyrinth of leadership. Harv Bus Rev. 2007;85(9):6271.
  18. Isaac C, Lee B, Carnes M. Interventions that affect gender bias in hiring: a systematic review. Acad Med. 2009;84(10):14401446.
  19. Correll S, Benard S, Paik I. Getting a job: is there a motherhood penalty? Am J Sociol. 2017;112(5):12971339.
  20. Kolehmainen C, Brennan M, Filut A, Isaac C, Carnes M. Afraid of being “witchy with a ‘b’”: a qualitative study of how gender influences residents' experiences leading cardiopulmonary resuscitation. Acad Med. 2014;89(9):12761281.
  21. Bem S. The measurement of psychological androgyny. J Consult Clin Psychol. 1974;42:155162.
  22. Schein V, Mueller R, Lituchy T, Liu J. Think manager—think male: A global phenomenon? J Organ Behav. 1996;17(1):3341.
  23. Koenig A, Eagly A, Mitchell A, Ristikari T. Are leader stereotypes masculine? A meta‐analysis of three research paradigms. Psychol Bull. 2011;137(4):616642.
  24. Brescoll V, Uhlmann E. Can an angry woman get ahead? Status conferral, gender, and expression of emotion in the workplace. Psychol Sci. 2008;19(3):268275.
  25. Bowles H, Babcock L, Lai L. Social incentives for gender differences in the propensity to initiate negations: sometimes it does hurt to ask. Organ Behav Hum Decis Process 2007;103:84103.
  26. Tiedens L. Anger and advancement versus sadness and subjugation: the effect of negative emotion expressions on social status conferral. J Pers Soc Psychol. 2001;80(1):8694.
  27. Kray L, Thompson L, Galinsky A. Battle of the sexes: gender stereotype confirmation and reactance in negotiations. J Pers Soc Psychol. 2001;80(6):942958.
  28. Phelan J, Rudman L. Prejudice toward female leaders: Backlash effects and women's impression management dilemma. Soc Personal Psychol Compass. 2010;4(10):807820.
  29. Carnes M. Commentary: deconstructing gender difference. Acad Med. 2010;85(4):575577.
  30. Shollen S, Bland C, Finstad D, Taylor A. Organizational climate and family life: how these factors affect the status of women faculty at one medical school. Acad Med. 2009;84(1):8794.
  31. Poppas A, Cummings J, Dorbala S, Douglas P, Foster E, Limacher M. Survey results: a decade of change in professional life in cardiology: a 2008 report of the ACC women in cardiology council. J Am Coll Cardiol. 2008;52(25):22152226.
  32. Jefferson L, Bloor K, Birks Y, Hewitt C, Bland M. Effect of physicians' gender on communication and consultation length: a systematic review and meta‐analysis. J Health Serv Res Policy. 2013;18:242248.
  33. Carnes M, Devine P, Baier Manwell L, et al. The effect of an intervention to break the gender bias habit for faculty at one institution: a cluster randomized, controlled trial. Acad Med. 2015;90(2):221230.
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From a new concept to 44,000 practitioners in just 18 years,[1] there is no doubt that the word hospitalist is synonymous with innovation, leadership, growth, and change. Yet 2 articles in this month's Journal of Hospital Medicine prove that even our new field faces age‐old problems. Although women comprise half of all academic hospitalist and general internal medicine faculty, Burden et al.[2] showed that female hospitalists are less likely than male hospitalists to be division or section heads of hospital medicine, speakers at national meetings, and first or last authors on both research publications and editorials. This is made more concerning given that women are more likely to choose academic hospital medicine careers,[3] as they represent one‐third of all hospitalists but half of the academic hospitalist workforce.[2, 3] Findings in general internal medicine were similar, except that equal numbers of women and men were national meeting speakers and first authors on research publications (but not editorials). Weaver et al.[4] shed even more light on this disparity, and found that female hospitalists made $14,581 less per year than their male counterparts, even after adjusting for relevant differences. Weaver and colleagues also found other gender‐specific differences: women worked more nights and had fewer billable encounters per hospitalist shift than men.

Unfortunately, these trends are not new or limited to hospital medicine. For decades, almost equal numbers of women and men have entered medical school,[5] yet women are under‐represented in high status specialties,[6] less likely to be first or senior authors on original research studies compared to men,[7] less likely to be promoted,[8] and women physicians are consistently paid less than men across specialties.[9, 10] Simple analyses have not yet explained these disparities. Compared with men, women have similar leadership aspirations[11, 12] and are at least as effective as leaders.[13, 14, 15] Yet equity has not been attained.

Implicit bias research suggests that gender stereotypes influence women at all career stages.[16, 17, 18] For example, an elegant study conducted by Correll et al. identified a motherhood penalty, where indicating membership in the elementary school parent‐teacher organization on one's curriculum vitae hurt women's chances of employment and pay, but actually helped men.[19] Gender stereotypes exist, even among those who do not support their content. The universal reinforcement of such stereotypes over time leads to implicit but prescriptive rules about how women and men should act.[20] In particular, communal behaviors, including being cooperative, kind, and understanding, are typically associated with women, and agentic behaviors, including being ambitious and acting as a leader, are considered appropriate for men.[21] This leads to the think leader, think male phenomena, where we automatically associate men with leadership and higher status tasks (like first authorship or speaker invitations).[22, 23] Furthermore, acting against the stereotype (eg, a woman showing anger[24] or negotiating for more pay[25] or a man showing sadness[26]) can negatively impact wage and employment. Expecting social censure for violating gender norms, women develop a fear of the backlash that alone may shape behavior such that women may not express interest in having a high salary or negotiate for a raise.[27, 28, 29]

The specific system and institutional barriers that prevent female hospitalists from receiving equal pay and opportunities for leadership are not known, but one can surmise they are similar to those found in other specialties.[10, 30, 31] The findings of the studies of Burden et al.[2] and Weaver et al.[4] invite investigation of new questions specific to hospital medicine. Why are women in hospital medicine working more night shifts? Does this impact leadership or scholarship opportunities? Why are women documenting less productivity? Are they spending more time with patients, as they do in other settings?[32] What influences their practice choice? We would like to believe that there is something about hospital medicine that can explain the gender differences identified in these 2 studies. However, these data should prompt a serious and thorough examination of our specialty. We must accept that despite being a new specialty and a change leader, hospital medicine may not have escaped systematic gender bias that constrains the full participation and advancement of women.

But we believe that hospitalistsinnovators and change leaders in medicinewill be spurred to action to address the possibility of gender inequities. We do not need to know all of the causes to begin to address disparities, of every type, on an individual, institutional, and national level. As individuals, we can acknowledge that there are implicit assumptions that influence our decision making. No matter how unintentional, and even conflicting with evidence, these assumptions can lead us to judge women as less capable leaders than men or to automatically envision a high salary for a woman and man as different amounts. However, these automatic gender biases function as habits of mind, so they can be broken like any other unwanted habit.[33] Institutionally, we can also hold ourselves accountable for transparency in mentorship, leadership, scholarship, promotions, and wages to ensure diverse representation. We should routinely examine our practices to ensure the equitable hiring, pay, and promotion of our workforce.[18] National organizations and their respective journals should actively pursue diverse representation in leadership and membership on boards and committees, award nominees and recipients, and opportunities for invited editorials. Hospital medicinebeing young, innovative, and committed to changeis uniquely well suited to lead the charge for workforce equity. We can, and will, show the rest of medicine how it is done.

Disclosure

Nothing to report.

From a new concept to 44,000 practitioners in just 18 years,[1] there is no doubt that the word hospitalist is synonymous with innovation, leadership, growth, and change. Yet 2 articles in this month's Journal of Hospital Medicine prove that even our new field faces age‐old problems. Although women comprise half of all academic hospitalist and general internal medicine faculty, Burden et al.[2] showed that female hospitalists are less likely than male hospitalists to be division or section heads of hospital medicine, speakers at national meetings, and first or last authors on both research publications and editorials. This is made more concerning given that women are more likely to choose academic hospital medicine careers,[3] as they represent one‐third of all hospitalists but half of the academic hospitalist workforce.[2, 3] Findings in general internal medicine were similar, except that equal numbers of women and men were national meeting speakers and first authors on research publications (but not editorials). Weaver et al.[4] shed even more light on this disparity, and found that female hospitalists made $14,581 less per year than their male counterparts, even after adjusting for relevant differences. Weaver and colleagues also found other gender‐specific differences: women worked more nights and had fewer billable encounters per hospitalist shift than men.

Unfortunately, these trends are not new or limited to hospital medicine. For decades, almost equal numbers of women and men have entered medical school,[5] yet women are under‐represented in high status specialties,[6] less likely to be first or senior authors on original research studies compared to men,[7] less likely to be promoted,[8] and women physicians are consistently paid less than men across specialties.[9, 10] Simple analyses have not yet explained these disparities. Compared with men, women have similar leadership aspirations[11, 12] and are at least as effective as leaders.[13, 14, 15] Yet equity has not been attained.

Implicit bias research suggests that gender stereotypes influence women at all career stages.[16, 17, 18] For example, an elegant study conducted by Correll et al. identified a motherhood penalty, where indicating membership in the elementary school parent‐teacher organization on one's curriculum vitae hurt women's chances of employment and pay, but actually helped men.[19] Gender stereotypes exist, even among those who do not support their content. The universal reinforcement of such stereotypes over time leads to implicit but prescriptive rules about how women and men should act.[20] In particular, communal behaviors, including being cooperative, kind, and understanding, are typically associated with women, and agentic behaviors, including being ambitious and acting as a leader, are considered appropriate for men.[21] This leads to the think leader, think male phenomena, where we automatically associate men with leadership and higher status tasks (like first authorship or speaker invitations).[22, 23] Furthermore, acting against the stereotype (eg, a woman showing anger[24] or negotiating for more pay[25] or a man showing sadness[26]) can negatively impact wage and employment. Expecting social censure for violating gender norms, women develop a fear of the backlash that alone may shape behavior such that women may not express interest in having a high salary or negotiate for a raise.[27, 28, 29]

The specific system and institutional barriers that prevent female hospitalists from receiving equal pay and opportunities for leadership are not known, but one can surmise they are similar to those found in other specialties.[10, 30, 31] The findings of the studies of Burden et al.[2] and Weaver et al.[4] invite investigation of new questions specific to hospital medicine. Why are women in hospital medicine working more night shifts? Does this impact leadership or scholarship opportunities? Why are women documenting less productivity? Are they spending more time with patients, as they do in other settings?[32] What influences their practice choice? We would like to believe that there is something about hospital medicine that can explain the gender differences identified in these 2 studies. However, these data should prompt a serious and thorough examination of our specialty. We must accept that despite being a new specialty and a change leader, hospital medicine may not have escaped systematic gender bias that constrains the full participation and advancement of women.

But we believe that hospitalistsinnovators and change leaders in medicinewill be spurred to action to address the possibility of gender inequities. We do not need to know all of the causes to begin to address disparities, of every type, on an individual, institutional, and national level. As individuals, we can acknowledge that there are implicit assumptions that influence our decision making. No matter how unintentional, and even conflicting with evidence, these assumptions can lead us to judge women as less capable leaders than men or to automatically envision a high salary for a woman and man as different amounts. However, these automatic gender biases function as habits of mind, so they can be broken like any other unwanted habit.[33] Institutionally, we can also hold ourselves accountable for transparency in mentorship, leadership, scholarship, promotions, and wages to ensure diverse representation. We should routinely examine our practices to ensure the equitable hiring, pay, and promotion of our workforce.[18] National organizations and their respective journals should actively pursue diverse representation in leadership and membership on boards and committees, award nominees and recipients, and opportunities for invited editorials. Hospital medicinebeing young, innovative, and committed to changeis uniquely well suited to lead the charge for workforce equity. We can, and will, show the rest of medicine how it is done.

Disclosure

Nothing to report.

References
  1. Society of Hospital Medicine. Milestones in the hospital medicine movement. Available at: http://www.hospitalmedicine.org/Web/About_SHM/Industry/shm_History.aspx. Accessed March 23, 2015.
  2. Burden M, Frank M, Keniston A, et al. Gender disparities in leadership and scholarly productivity of academic hospitalists. J Hosp Med. 2015;10(X):000000.
  3. Hinami K, Whelan C, Miller J, Wolosin R, Wetterneck T. Job characteristics, satisfaction, and burnout across hospitalist practice models. J Hosp Med. 2012;7:402410.
  4. Weaver C, Wetterneck T, Whelan C, Hinami K. A matter of priorities? Exploring the persistent gender pay gap in hospital medicine. J Hosp Med. 2015;10(8):486490.
  5. Association of American Medical Colleges. Table 1: medical students, selected years, 1965–2013. Available at: https://www.aamc.org/download/411782/data/2014_table1.pdf. Accessed March 23, 2015.
  6. Jagsi R, Griffith K, DeCastro R, Ubel P. Sex, role models, and specialty choices among graduates of US medical schools in 2006‐2008. J Am Coll Surg. 2014;218(3):345352.
  7. Jagsi R, Guancial E, Worobey C, et al. The “Gender Gap” in authorship of academic medical literature—a 35‐year perspective. N Engl J Med. 2006;355(3):281287.
  8. Nonnemaker L. Women physicians in academic medicine. N Engl J Med. 2000;342(6):399405.
  9. Jagsi R, Griffith K, Stewart A, Sambuco D, DeCastro R, Ubel P. Gender differences in the salaries of physician researchers. JAMA. 2012;307(22):24102417.
  10. Sasso A, Richards M, Chou C, Gerber S. The $16,819 pay gap for newly trained physicians: the unexplained trend of men earning more than women. Health Affairs. 2011;30(2):193201.
  11. Pololi L, Civian J, Brennan R, Dottalo A, Krupat E. Experiencing the culture of academic medicine: gender matters, a national study. J Gen Intern Med. 2013;28(2):201207.
  12. Wright A, Schwindt L, Bassford T, et al. Gender differences in academic advancement: patterns, causes, and potential solutions in one US College of Medicine. Acad Med. 2003;78(5):500508.
  13. Rosser V. Faculty and staff members perceptions of effective leadership: are there differences between men and women leaders? Equity Excell Educ. 2003;36(1):7181.
  14. Eagly A, Johannesen‐Schmidt M, Engen M. Transformational, transactional, and lasissez‐faire leadership styles: a meta‐analysis comparing women and men. Psychol Bull. 2003;129(4):569591.
  15. Isaac C, Griffin L, Carnes M. A qualitative study of faculty members' views of women chairs. J Womens Health (Larchmt). 2010;19(3):533546.
  16. Kaatz A, Carnes M. Stuck in the out‐group: Jennifer can't grow up, Jane's invisible, and Janet's over the hill. J Womens Health (Larchmt). 2014;23(6):481484.
  17. Eagly A, Carli L. Women and the labyrinth of leadership. Harv Bus Rev. 2007;85(9):6271.
  18. Isaac C, Lee B, Carnes M. Interventions that affect gender bias in hiring: a systematic review. Acad Med. 2009;84(10):14401446.
  19. Correll S, Benard S, Paik I. Getting a job: is there a motherhood penalty? Am J Sociol. 2017;112(5):12971339.
  20. Kolehmainen C, Brennan M, Filut A, Isaac C, Carnes M. Afraid of being “witchy with a ‘b’”: a qualitative study of how gender influences residents' experiences leading cardiopulmonary resuscitation. Acad Med. 2014;89(9):12761281.
  21. Bem S. The measurement of psychological androgyny. J Consult Clin Psychol. 1974;42:155162.
  22. Schein V, Mueller R, Lituchy T, Liu J. Think manager—think male: A global phenomenon? J Organ Behav. 1996;17(1):3341.
  23. Koenig A, Eagly A, Mitchell A, Ristikari T. Are leader stereotypes masculine? A meta‐analysis of three research paradigms. Psychol Bull. 2011;137(4):616642.
  24. Brescoll V, Uhlmann E. Can an angry woman get ahead? Status conferral, gender, and expression of emotion in the workplace. Psychol Sci. 2008;19(3):268275.
  25. Bowles H, Babcock L, Lai L. Social incentives for gender differences in the propensity to initiate negations: sometimes it does hurt to ask. Organ Behav Hum Decis Process 2007;103:84103.
  26. Tiedens L. Anger and advancement versus sadness and subjugation: the effect of negative emotion expressions on social status conferral. J Pers Soc Psychol. 2001;80(1):8694.
  27. Kray L, Thompson L, Galinsky A. Battle of the sexes: gender stereotype confirmation and reactance in negotiations. J Pers Soc Psychol. 2001;80(6):942958.
  28. Phelan J, Rudman L. Prejudice toward female leaders: Backlash effects and women's impression management dilemma. Soc Personal Psychol Compass. 2010;4(10):807820.
  29. Carnes M. Commentary: deconstructing gender difference. Acad Med. 2010;85(4):575577.
  30. Shollen S, Bland C, Finstad D, Taylor A. Organizational climate and family life: how these factors affect the status of women faculty at one medical school. Acad Med. 2009;84(1):8794.
  31. Poppas A, Cummings J, Dorbala S, Douglas P, Foster E, Limacher M. Survey results: a decade of change in professional life in cardiology: a 2008 report of the ACC women in cardiology council. J Am Coll Cardiol. 2008;52(25):22152226.
  32. Jefferson L, Bloor K, Birks Y, Hewitt C, Bland M. Effect of physicians' gender on communication and consultation length: a systematic review and meta‐analysis. J Health Serv Res Policy. 2013;18:242248.
  33. Carnes M, Devine P, Baier Manwell L, et al. The effect of an intervention to break the gender bias habit for faculty at one institution: a cluster randomized, controlled trial. Acad Med. 2015;90(2):221230.
References
  1. Society of Hospital Medicine. Milestones in the hospital medicine movement. Available at: http://www.hospitalmedicine.org/Web/About_SHM/Industry/shm_History.aspx. Accessed March 23, 2015.
  2. Burden M, Frank M, Keniston A, et al. Gender disparities in leadership and scholarly productivity of academic hospitalists. J Hosp Med. 2015;10(X):000000.
  3. Hinami K, Whelan C, Miller J, Wolosin R, Wetterneck T. Job characteristics, satisfaction, and burnout across hospitalist practice models. J Hosp Med. 2012;7:402410.
  4. Weaver C, Wetterneck T, Whelan C, Hinami K. A matter of priorities? Exploring the persistent gender pay gap in hospital medicine. J Hosp Med. 2015;10(8):486490.
  5. Association of American Medical Colleges. Table 1: medical students, selected years, 1965–2013. Available at: https://www.aamc.org/download/411782/data/2014_table1.pdf. Accessed March 23, 2015.
  6. Jagsi R, Griffith K, DeCastro R, Ubel P. Sex, role models, and specialty choices among graduates of US medical schools in 2006‐2008. J Am Coll Surg. 2014;218(3):345352.
  7. Jagsi R, Guancial E, Worobey C, et al. The “Gender Gap” in authorship of academic medical literature—a 35‐year perspective. N Engl J Med. 2006;355(3):281287.
  8. Nonnemaker L. Women physicians in academic medicine. N Engl J Med. 2000;342(6):399405.
  9. Jagsi R, Griffith K, Stewart A, Sambuco D, DeCastro R, Ubel P. Gender differences in the salaries of physician researchers. JAMA. 2012;307(22):24102417.
  10. Sasso A, Richards M, Chou C, Gerber S. The $16,819 pay gap for newly trained physicians: the unexplained trend of men earning more than women. Health Affairs. 2011;30(2):193201.
  11. Pololi L, Civian J, Brennan R, Dottalo A, Krupat E. Experiencing the culture of academic medicine: gender matters, a national study. J Gen Intern Med. 2013;28(2):201207.
  12. Wright A, Schwindt L, Bassford T, et al. Gender differences in academic advancement: patterns, causes, and potential solutions in one US College of Medicine. Acad Med. 2003;78(5):500508.
  13. Rosser V. Faculty and staff members perceptions of effective leadership: are there differences between men and women leaders? Equity Excell Educ. 2003;36(1):7181.
  14. Eagly A, Johannesen‐Schmidt M, Engen M. Transformational, transactional, and lasissez‐faire leadership styles: a meta‐analysis comparing women and men. Psychol Bull. 2003;129(4):569591.
  15. Isaac C, Griffin L, Carnes M. A qualitative study of faculty members' views of women chairs. J Womens Health (Larchmt). 2010;19(3):533546.
  16. Kaatz A, Carnes M. Stuck in the out‐group: Jennifer can't grow up, Jane's invisible, and Janet's over the hill. J Womens Health (Larchmt). 2014;23(6):481484.
  17. Eagly A, Carli L. Women and the labyrinth of leadership. Harv Bus Rev. 2007;85(9):6271.
  18. Isaac C, Lee B, Carnes M. Interventions that affect gender bias in hiring: a systematic review. Acad Med. 2009;84(10):14401446.
  19. Correll S, Benard S, Paik I. Getting a job: is there a motherhood penalty? Am J Sociol. 2017;112(5):12971339.
  20. Kolehmainen C, Brennan M, Filut A, Isaac C, Carnes M. Afraid of being “witchy with a ‘b’”: a qualitative study of how gender influences residents' experiences leading cardiopulmonary resuscitation. Acad Med. 2014;89(9):12761281.
  21. Bem S. The measurement of psychological androgyny. J Consult Clin Psychol. 1974;42:155162.
  22. Schein V, Mueller R, Lituchy T, Liu J. Think manager—think male: A global phenomenon? J Organ Behav. 1996;17(1):3341.
  23. Koenig A, Eagly A, Mitchell A, Ristikari T. Are leader stereotypes masculine? A meta‐analysis of three research paradigms. Psychol Bull. 2011;137(4):616642.
  24. Brescoll V, Uhlmann E. Can an angry woman get ahead? Status conferral, gender, and expression of emotion in the workplace. Psychol Sci. 2008;19(3):268275.
  25. Bowles H, Babcock L, Lai L. Social incentives for gender differences in the propensity to initiate negations: sometimes it does hurt to ask. Organ Behav Hum Decis Process 2007;103:84103.
  26. Tiedens L. Anger and advancement versus sadness and subjugation: the effect of negative emotion expressions on social status conferral. J Pers Soc Psychol. 2001;80(1):8694.
  27. Kray L, Thompson L, Galinsky A. Battle of the sexes: gender stereotype confirmation and reactance in negotiations. J Pers Soc Psychol. 2001;80(6):942958.
  28. Phelan J, Rudman L. Prejudice toward female leaders: Backlash effects and women's impression management dilemma. Soc Personal Psychol Compass. 2010;4(10):807820.
  29. Carnes M. Commentary: deconstructing gender difference. Acad Med. 2010;85(4):575577.
  30. Shollen S, Bland C, Finstad D, Taylor A. Organizational climate and family life: how these factors affect the status of women faculty at one medical school. Acad Med. 2009;84(1):8794.
  31. Poppas A, Cummings J, Dorbala S, Douglas P, Foster E, Limacher M. Survey results: a decade of change in professional life in cardiology: a 2008 report of the ACC women in cardiology council. J Am Coll Cardiol. 2008;52(25):22152226.
  32. Jefferson L, Bloor K, Birks Y, Hewitt C, Bland M. Effect of physicians' gender on communication and consultation length: a systematic review and meta‐analysis. J Health Serv Res Policy. 2013;18:242248.
  33. Carnes M, Devine P, Baier Manwell L, et al. The effect of an intervention to break the gender bias habit for faculty at one institution: a cluster randomized, controlled trial. Acad Med. 2015;90(2):221230.
Issue
Journal of Hospital Medicine - 10(8)
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551-552
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We specialize in change leadership: A call for hospitalists to lead the quest for workforce gender equity
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We specialize in change leadership: A call for hospitalists to lead the quest for workforce gender equity
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Address for correspondence and reprint requests: Ann M. Sheehy, MD, Department of Medicine, Division of Hospital Medicine, University of Wisconsin School of Medicine and Public Health, 1685 Highland Ave, MFCB 3126, Madison, Wisconsin 53705; Telephone: 608‐262‐2434; Fax: 608‐265‐1420; E‐mail: asr@medicine.wisc.edu
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Hospital Medicine in 2015

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Hospital medicine in 2015: Remarkable successes and a crucial crossroads

This year, we celebrate the 10th anniversary of this esteemed publication, and it is indeed an occasion for celebration. For those of us who were there at the creation of the hospitalist field, the establishment of a vibrant academic journal was a dream, one whose fulfillment was central to the legitimization of our field as a full‐fledged specialty. After a decade and 83 issues, the Journal of Hospital Medicine is a formidable source of information, cohesion, and pride.

The anniversary comes at a particularly interesting time for hospitals and hospitalists. Our field's lifeblood has been in trailblazing and continuous reinvention. We were the first physician specialty that embraced the mantra of systems thinking, as captured in our famous metaphor that we care for two sick patients: the person and the system. We were the first field that proudly, and without a hint of shame, allied ourselves with hospital leaders, believing that we were mutually dependent on one another, and that our ability to make change happen and stick was better if we were working with our institutions' leaders. In creating our professional society (and this journal), we took unusual pains to be inclusiveof academic and community‐based hospitalists, or hospitalists entering the field from a variety of backgrounds, of hospitalists caring for adults and kids, and of nonphysician providers.

Our efforts have paid off. Leaders as prominent as Don Berwick have observed that hospitalists have become the essential army of improvers in hospitals and healthcare systems. Hospitalists have made immense contributions at their own institutions, and are increasingly assuming leadership roles both locally and nationally. It is not a coincidence that Medicare's top physician (Patrick Conway) and the Surgeon General (Vivek Murthy) are both hospitalists. Although there have been a few bumps along the way, hospitalists are generally satisfied with their careers, respected by their colleagues, accepted by their patients, and pleased to be members of the fastest growing specialty in the history of modern medicine.

All of this should leave us all feeling warm, proud and more than a little nervous. We are now a mature medical specialty, no longer upstarts, and the natural inclination, in a changing world, will be to hunker down and protect what we have. Of course, some of that is reasonable and appropriate (for example, to fight for our fair share of a bundled payment pie),[1] but some of it will be wrong, even self‐defeating. The world of healthcare is changing fast, and our ability to stay relevant and indispensable will depend on our ability to evolve to meet new conditions and needs.

Let us consider some of the major trends playing out in healthcare. The biggest is the brisk and unmistakable shift from volume to value.[2] This is a trend we have been on top of, because this really has been our field's raison d'tre: improving value in the hospital by cutting costs and length of stay while improving (or at least keeping neutral) quality and safety.[3] However, a world under intense value pressure will work hard to move patients from hospital to less expensive postacute settings, and will insist on seamless handoffs between the hospital and such settings. Thoughtful hospital medicine groups are thinking hard about this trend, and many are placing colleagues in skilled nursing facilities, or at the very least tightening their connections to the postacute facilities in their healthcare ecosystem. We no longer have the luxury of confining our talents and energies to those things that take place within the 4 walls of the hospital.

Another trend is the digitization of healthcare, a trend turbocharged by $30 billion in federal incentive payments distributed between 2009 and 2014.[4] Here too, hospitalists have emerged as leaders in information technology (IT) implementations, and a disproportionate number of chief medical information officers and other IT leaders seem to be hospitalists. Splendid. But it is also up to us to help figure out how to use IT tools effectively. The notes have morphed into bloated, copy‐and‐pasteridden monstrosities: let us figure out what a good note should look like in the digital era, and then implement educational and system changes to create a new standard. We no longer go to radiology because we do not need to to see our films; let us think about what the loss of the collegial exchange with our radiology colleagues has cost, and then set out to develop new systems to reimagine it. Right now, big data are mostly hype and unrequited promise. Who better than hospitalists to dive in and start making sense of the data to predict risks or help point to better treatments?

Another trend is population health. Although I do not foresee a return to the Marcus Welby model of a kindly physician following the patient everywhere, I can imagine certain patients (mostly those with several social and clinical comorbidities and at least 3 admissions per year) who might be well served by a back‐to‐the‐future system in which a primary care provider follows them into the hospital, perhaps comanaging the patients with the on‐service hospitalist. David Meltzer, at the University of Chicago, is currently studying such a model, and I look forward to seeing his results.[5] Rather than rejecting such experiments as violating the usual hospitalist structure, we must embrace them, at least until the evidence is in.

In the end, the field of hospital medicine emerged and thrived because of the promise, and later the evidence, that our presence led to better quality, safety, patient experience, education, and efficiency. This mandate must remain our mantra, even if it means that we have to evolve our model in keeping with a changing healthcare landscape. The minute we stop evolving is the minute our field starts planting the seeds of its own destruction.

Disclosure

Dr. Wachter reports that he is a member of the board of directors of IPC Healthcare.

References
  1. Burns J. Bundled payment. Hospitals see the advantages but face big challenges, too. Hospitals 367:292295.
  2. Wachter RM, Goldman L. The emerging role of “hospitalists” in the American health care system. N Engl J Med. 1995;335:514517.
  3. Wachter RM. The Digital Doctor: Hope, Hype, and Harm at the Dawn of Medicine's Computer Age. New York, NY: McGraw‐Hill; 2015.
  4. Simmons J. Comprehensive care physicians: an emerging specialty for chronic care. Fierce Healthcare website. Available at: http://www.fiercehealthcare.com/story/comprehensivists‐close‐chronic‐care‐communication‐gaps/2011‐05‐02. Published May 2, 2011. Last accessed May 29, 2015.
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Issue
Journal of Hospital Medicine - 10(12)
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830-831
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This year, we celebrate the 10th anniversary of this esteemed publication, and it is indeed an occasion for celebration. For those of us who were there at the creation of the hospitalist field, the establishment of a vibrant academic journal was a dream, one whose fulfillment was central to the legitimization of our field as a full‐fledged specialty. After a decade and 83 issues, the Journal of Hospital Medicine is a formidable source of information, cohesion, and pride.

The anniversary comes at a particularly interesting time for hospitals and hospitalists. Our field's lifeblood has been in trailblazing and continuous reinvention. We were the first physician specialty that embraced the mantra of systems thinking, as captured in our famous metaphor that we care for two sick patients: the person and the system. We were the first field that proudly, and without a hint of shame, allied ourselves with hospital leaders, believing that we were mutually dependent on one another, and that our ability to make change happen and stick was better if we were working with our institutions' leaders. In creating our professional society (and this journal), we took unusual pains to be inclusiveof academic and community‐based hospitalists, or hospitalists entering the field from a variety of backgrounds, of hospitalists caring for adults and kids, and of nonphysician providers.

Our efforts have paid off. Leaders as prominent as Don Berwick have observed that hospitalists have become the essential army of improvers in hospitals and healthcare systems. Hospitalists have made immense contributions at their own institutions, and are increasingly assuming leadership roles both locally and nationally. It is not a coincidence that Medicare's top physician (Patrick Conway) and the Surgeon General (Vivek Murthy) are both hospitalists. Although there have been a few bumps along the way, hospitalists are generally satisfied with their careers, respected by their colleagues, accepted by their patients, and pleased to be members of the fastest growing specialty in the history of modern medicine.

All of this should leave us all feeling warm, proud and more than a little nervous. We are now a mature medical specialty, no longer upstarts, and the natural inclination, in a changing world, will be to hunker down and protect what we have. Of course, some of that is reasonable and appropriate (for example, to fight for our fair share of a bundled payment pie),[1] but some of it will be wrong, even self‐defeating. The world of healthcare is changing fast, and our ability to stay relevant and indispensable will depend on our ability to evolve to meet new conditions and needs.

Let us consider some of the major trends playing out in healthcare. The biggest is the brisk and unmistakable shift from volume to value.[2] This is a trend we have been on top of, because this really has been our field's raison d'tre: improving value in the hospital by cutting costs and length of stay while improving (or at least keeping neutral) quality and safety.[3] However, a world under intense value pressure will work hard to move patients from hospital to less expensive postacute settings, and will insist on seamless handoffs between the hospital and such settings. Thoughtful hospital medicine groups are thinking hard about this trend, and many are placing colleagues in skilled nursing facilities, or at the very least tightening their connections to the postacute facilities in their healthcare ecosystem. We no longer have the luxury of confining our talents and energies to those things that take place within the 4 walls of the hospital.

Another trend is the digitization of healthcare, a trend turbocharged by $30 billion in federal incentive payments distributed between 2009 and 2014.[4] Here too, hospitalists have emerged as leaders in information technology (IT) implementations, and a disproportionate number of chief medical information officers and other IT leaders seem to be hospitalists. Splendid. But it is also up to us to help figure out how to use IT tools effectively. The notes have morphed into bloated, copy‐and‐pasteridden monstrosities: let us figure out what a good note should look like in the digital era, and then implement educational and system changes to create a new standard. We no longer go to radiology because we do not need to to see our films; let us think about what the loss of the collegial exchange with our radiology colleagues has cost, and then set out to develop new systems to reimagine it. Right now, big data are mostly hype and unrequited promise. Who better than hospitalists to dive in and start making sense of the data to predict risks or help point to better treatments?

Another trend is population health. Although I do not foresee a return to the Marcus Welby model of a kindly physician following the patient everywhere, I can imagine certain patients (mostly those with several social and clinical comorbidities and at least 3 admissions per year) who might be well served by a back‐to‐the‐future system in which a primary care provider follows them into the hospital, perhaps comanaging the patients with the on‐service hospitalist. David Meltzer, at the University of Chicago, is currently studying such a model, and I look forward to seeing his results.[5] Rather than rejecting such experiments as violating the usual hospitalist structure, we must embrace them, at least until the evidence is in.

In the end, the field of hospital medicine emerged and thrived because of the promise, and later the evidence, that our presence led to better quality, safety, patient experience, education, and efficiency. This mandate must remain our mantra, even if it means that we have to evolve our model in keeping with a changing healthcare landscape. The minute we stop evolving is the minute our field starts planting the seeds of its own destruction.

Disclosure

Dr. Wachter reports that he is a member of the board of directors of IPC Healthcare.

This year, we celebrate the 10th anniversary of this esteemed publication, and it is indeed an occasion for celebration. For those of us who were there at the creation of the hospitalist field, the establishment of a vibrant academic journal was a dream, one whose fulfillment was central to the legitimization of our field as a full‐fledged specialty. After a decade and 83 issues, the Journal of Hospital Medicine is a formidable source of information, cohesion, and pride.

The anniversary comes at a particularly interesting time for hospitals and hospitalists. Our field's lifeblood has been in trailblazing and continuous reinvention. We were the first physician specialty that embraced the mantra of systems thinking, as captured in our famous metaphor that we care for two sick patients: the person and the system. We were the first field that proudly, and without a hint of shame, allied ourselves with hospital leaders, believing that we were mutually dependent on one another, and that our ability to make change happen and stick was better if we were working with our institutions' leaders. In creating our professional society (and this journal), we took unusual pains to be inclusiveof academic and community‐based hospitalists, or hospitalists entering the field from a variety of backgrounds, of hospitalists caring for adults and kids, and of nonphysician providers.

Our efforts have paid off. Leaders as prominent as Don Berwick have observed that hospitalists have become the essential army of improvers in hospitals and healthcare systems. Hospitalists have made immense contributions at their own institutions, and are increasingly assuming leadership roles both locally and nationally. It is not a coincidence that Medicare's top physician (Patrick Conway) and the Surgeon General (Vivek Murthy) are both hospitalists. Although there have been a few bumps along the way, hospitalists are generally satisfied with their careers, respected by their colleagues, accepted by their patients, and pleased to be members of the fastest growing specialty in the history of modern medicine.

All of this should leave us all feeling warm, proud and more than a little nervous. We are now a mature medical specialty, no longer upstarts, and the natural inclination, in a changing world, will be to hunker down and protect what we have. Of course, some of that is reasonable and appropriate (for example, to fight for our fair share of a bundled payment pie),[1] but some of it will be wrong, even self‐defeating. The world of healthcare is changing fast, and our ability to stay relevant and indispensable will depend on our ability to evolve to meet new conditions and needs.

Let us consider some of the major trends playing out in healthcare. The biggest is the brisk and unmistakable shift from volume to value.[2] This is a trend we have been on top of, because this really has been our field's raison d'tre: improving value in the hospital by cutting costs and length of stay while improving (or at least keeping neutral) quality and safety.[3] However, a world under intense value pressure will work hard to move patients from hospital to less expensive postacute settings, and will insist on seamless handoffs between the hospital and such settings. Thoughtful hospital medicine groups are thinking hard about this trend, and many are placing colleagues in skilled nursing facilities, or at the very least tightening their connections to the postacute facilities in their healthcare ecosystem. We no longer have the luxury of confining our talents and energies to those things that take place within the 4 walls of the hospital.

Another trend is the digitization of healthcare, a trend turbocharged by $30 billion in federal incentive payments distributed between 2009 and 2014.[4] Here too, hospitalists have emerged as leaders in information technology (IT) implementations, and a disproportionate number of chief medical information officers and other IT leaders seem to be hospitalists. Splendid. But it is also up to us to help figure out how to use IT tools effectively. The notes have morphed into bloated, copy‐and‐pasteridden monstrosities: let us figure out what a good note should look like in the digital era, and then implement educational and system changes to create a new standard. We no longer go to radiology because we do not need to to see our films; let us think about what the loss of the collegial exchange with our radiology colleagues has cost, and then set out to develop new systems to reimagine it. Right now, big data are mostly hype and unrequited promise. Who better than hospitalists to dive in and start making sense of the data to predict risks or help point to better treatments?

Another trend is population health. Although I do not foresee a return to the Marcus Welby model of a kindly physician following the patient everywhere, I can imagine certain patients (mostly those with several social and clinical comorbidities and at least 3 admissions per year) who might be well served by a back‐to‐the‐future system in which a primary care provider follows them into the hospital, perhaps comanaging the patients with the on‐service hospitalist. David Meltzer, at the University of Chicago, is currently studying such a model, and I look forward to seeing his results.[5] Rather than rejecting such experiments as violating the usual hospitalist structure, we must embrace them, at least until the evidence is in.

In the end, the field of hospital medicine emerged and thrived because of the promise, and later the evidence, that our presence led to better quality, safety, patient experience, education, and efficiency. This mandate must remain our mantra, even if it means that we have to evolve our model in keeping with a changing healthcare landscape. The minute we stop evolving is the minute our field starts planting the seeds of its own destruction.

Disclosure

Dr. Wachter reports that he is a member of the board of directors of IPC Healthcare.

References
  1. Burns J. Bundled payment. Hospitals see the advantages but face big challenges, too. Hospitals 367:292295.
  2. Wachter RM, Goldman L. The emerging role of “hospitalists” in the American health care system. N Engl J Med. 1995;335:514517.
  3. Wachter RM. The Digital Doctor: Hope, Hype, and Harm at the Dawn of Medicine's Computer Age. New York, NY: McGraw‐Hill; 2015.
  4. Simmons J. Comprehensive care physicians: an emerging specialty for chronic care. Fierce Healthcare website. Available at: http://www.fiercehealthcare.com/story/comprehensivists‐close‐chronic‐care‐communication‐gaps/2011‐05‐02. Published May 2, 2011. Last accessed May 29, 2015.
References
  1. Burns J. Bundled payment. Hospitals see the advantages but face big challenges, too. Hospitals 367:292295.
  2. Wachter RM, Goldman L. The emerging role of “hospitalists” in the American health care system. N Engl J Med. 1995;335:514517.
  3. Wachter RM. The Digital Doctor: Hope, Hype, and Harm at the Dawn of Medicine's Computer Age. New York, NY: McGraw‐Hill; 2015.
  4. Simmons J. Comprehensive care physicians: an emerging specialty for chronic care. Fierce Healthcare website. Available at: http://www.fiercehealthcare.com/story/comprehensivists‐close‐chronic‐care‐communication‐gaps/2011‐05‐02. Published May 2, 2011. Last accessed May 29, 2015.
Issue
Journal of Hospital Medicine - 10(12)
Issue
Journal of Hospital Medicine - 10(12)
Page Number
830-831
Page Number
830-831
Article Type
Display Headline
Hospital medicine in 2015: Remarkable successes and a crucial crossroads
Display Headline
Hospital medicine in 2015: Remarkable successes and a crucial crossroads
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© 2015 Society of Hospital Medicine
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Address for correspondence and reprint requests: Robert M. Wachter, MD, Department of Medicine, University of California, San Francisco, Room M994, 505 Parnassus Avenue, San Francisco, CA 94143‐0120; Telephone: 415‐476‐5632; Fax: 415‐502‐5869; E‐mail: bobw@medicine.ucsf.edu
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