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The stethoscope as metaphor

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The stethoscope as metaphor

“Those who advise that all stethoscopes should be ‘scrapped’ may be influenced by the fact that they do not know how to use their own.”

From Pulmonary Tuberculosis, 1921, by Sir James Kingston Fowler (1852–1934) of the Brompton Hospital, England

The commentary by Clark et al in this issue1 is a timely reminder of an important problem in modern medicine: the demise of the bedside. My only divergence from the authors is in their conclusion, since my Mediterranean pessimism leads me to believe that theirs is just a gallant attempt at rearguard action for a battle that, unfortunately, has long been lost.

More than half a century ago, Paul Wood warned us against the “danger of losing our clinical heritage and pinning too much faith in figures thrown out by machines,” thundering that “medicine must suffer if this tendency is not checked.”2 Well, that tendency was not checked, and medicine (and our wallets) have indeed suffered.

See related commentary

Still, technology is not the enemy. The misuse of technology is the problem.

Like Dr. Clark and his colleagues, I’ve seen many cases in which technology unguided by bedside skills took physicians down a path where tests begot tests and where, at the end, there was usually a surgeon, and often a lawyer. Sometimes even an undertaker. The deaths of Jonathan Larson (writer-composer of the musical Rent) and of his namesake, actor Jonathan (John) Ritter—who both succumbed to undiagnosed aortic dissection—make me wonder whether their pulses were ever checked.

Editorials have lamented the “hyposkillia” of our times,3 and the usual suspects have been already rounded up: our overreliance on tests, our ever-increasing fascination with the machine (what Erich Fromm called the necrophilia of our times),4 the loss of bedside teaching, and lastly, the lure of compensation. But one important player has so far gone unnoticed, despite being probably the major offender. In fact, it may even be responsible for the other disturbing trend in modern medicine: the loss of empathy.5

I’m referring to the disappearance of the humanities in both the undergraduate and the graduate curriculum. This is actually new. If we look, for example, at the great bedside diagnosticians of the past, we find that they were passionately interested in everything human. Most, if not all, were indeed humanists—lovers of the arts and literature, travelers and historians, poets and painters, curious of any field that could enrich the human spirit. Charcot, who single-handedly invented neurology, was not only a superb scientist, but also a talented artist who drew and painted (skills he considered fundamental for bedside observation) plus a bona-fide Beethoven fanatic who spent Thursday evenings on music, strictly forbidding any medical talk. Laënnec himself was a poet and musician who modeled his stethoscope after the flutes he made. And Charles Bell (of Bell palsy, phenomenon, and law) was a well-respected painter who soldiered with Wellington and left us incredible sketches of the Waterloo wounded and maimed. Even Osler, the pinnacle of 19th century humanistic medicine, believed so strongly in the value of a liberal education as to provide students with a list of 10 books (ranging from Plutarch and Montaigne to Marcus Aurelius and Shakespeare) to read for half an hour before going to sleep. Addressing the Classical Association just before his death, he lamented the “grievous damage” that had been done by regarding the humanities and science in any other light than complementary, while in reality they are “twin berries on one stem.”6

 

 

Until the 1870s, medicine was in fact a spin-off of the humanities. A solid humanistic education was deemed essential for admission to medical school. Then the German victory in the Franco-Prussian War shifted the axis from Paris to Berlin, and medicine went the German way. Never as touchy-feely as the French, and definitely more comfortable in the laboratory than at the bedside, the Germans produced giants like Koch, Virchow, and Roentgen, who gradually moved medicine away from the bedside and into the lab. In fact, medicine even adopted the uniform of the laboratory—the infamous white coat now banned by the British National Health system as a dirty carrier of bacteria.

Finding herself at a crossroads, America went the German way, mostly because of Flexner (himself the son of German immigrants), whose 1910 report totally changed the face of medical education. The “two cultures” were born—science was “in” and the humanities “out.”7

The result is what Lewis Thomas called the “baleful and malign” influence of the modern medical school on liberal-arts education.8 Michael Crichton put it even more bluntly. Explaining why he dropped out of medicine, he wrote, “My classmates [at Harvard] tended to think that literature, music, and art were irrelevant distractions. They held these “cultural” matters in the same intellectual contempt that a physicist holds astrology. Everything outside medicine was just a waste of time.”9

And since then, things have only worsened.10

Yet the link between humanities and the bedside remains crucial. I have had the privilege of meeting most of the clinicians who still contribute to physical diagnosis, and they are almost all humanists.

So why should the humanities nurture the bedside? For one, they may increase our tolerance of ambiguity, a trait sorely lacking in modern medicine. This makes sense, since decoding feeble sounds emanating from chests, palpating indistinct organs, and detecting bedside nuances are all painful reminders of the ambiguous in our craft, not to mention in life. And if unprepared by a humanistic education to deal with the uncertain, students may easily opt for the “certainties” of the laboratory or radiology suite.11 Once again, Osler comes to our rescue.

“A distressing feature in the life which you are about to enter” he told the graduating class of the University of Pennsylvania in 1889, “is the uncertainty which pertains not alone to our science and arts but to the very hopes and fears which make us men. In seeking absolute truth we aim at the unattainable, and must be content with finding broken portions.”12

The stethoscope is too closely bound with the doctor’s image not to be a metaphor for something larger. To me, it’s a metaphor for medicine as both an art and a science, wherein the humanities are—and of right ought to be—a fundamental part of the education. Hence, if we want to rekindle the bedside, we must rekindle the humanities. After all, this is what both Lewis Thomas8 and Sherwin Nuland13 have urged us to do. My hunch is that this would need to be done sooner rather than later, because if it is possible to make a scientist out of a humanist (it was done for centuries), it might be considerably harder to make a humanist out of a scientist. The experience of the past few decades seems to support this conclusion.

The alternative is a future full of tricorders and technicians, but sorely lacking in healers.

References
  1. Clark D, Ahmed MI, Dell’Italia LJ, Fan P, McGiffin DC. An argument for retrieving the disappearing skill of cardiac auscultation. Cleve Clin J Med 2012; 79:536544.
  2. Wood PH. Diseases of the Heart and Circulation. London: Eyre and Spottiswoode; 1950.
  3. Fred HL. Hyposkillia: deficiency of clinical skills. Tex Heart Inst J 2005; 32:255257.
  4. Fromm E. To Have or To Be? New York, NY: Harper & Row; 1976.
  5. Hojat M, Mangione S, Nasca TJ, Gonnella JS, Magee M. Empathy scores in medical school and ratings of empathic behavior in residency training 3 years later. J Soc Psychol 2005; 145:663672.
  6. Osler W. The old humanities and the new science: The presidential address delivered before the Classical Association at Oxford, May, 1919. Br Med J 1919; 2:17.
  7. Snow CP. The Two Cultures and the Scientific Revolution. London, England: Cambridge University Press; 1959.
  8. Thomas L. Notes of a biology-watcher. How to fix the premedical curriculum. N Engl J Med 1978; 298:11801181.
  9. Crichton M. Travels. New York, NY: Alfred A. Knopf, Inc; 1988:69.
  10. Gunderman RB, Kanter SL. Perspective: “How to fix the premedical curriculum” revisited. Acad Med 2008; 83:11581161.
  11. Nevalainen M, Kuikka L, Sjoberg L, Eriksson J, Pitkala K. Tolerance of uncertainty and fears of making mistakes among fifth-year medical students. Fam Med 2012; 44:240246.
  12. Osler W. Aequanimitas, with other addresses to medical students, nurses, and practitioners of medicine. May 1, 1889. www.medicalarchives.jhmi.edu/osler/aequessay.htm. Accessed June 26, 2012.
  13. Nuland SB. Where is Wisdom? Restraint in a Time of Biomedical Miracles. The Great Lectures Library. Chautauqua Institution; 2006.
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Address: Salvatore Mangione, MD, Department of Medicine and Clinical Skills Center, Thomas Jefferson University, 1001 Locust Street, Suite 309C, Philadelphia, PA 19096; e-mail [email protected]

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Address: Salvatore Mangione, MD, Department of Medicine and Clinical Skills Center, Thomas Jefferson University, 1001 Locust Street, Suite 309C, Philadelphia, PA 19096; e-mail [email protected]

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“Those who advise that all stethoscopes should be ‘scrapped’ may be influenced by the fact that they do not know how to use their own.”

From Pulmonary Tuberculosis, 1921, by Sir James Kingston Fowler (1852–1934) of the Brompton Hospital, England

The commentary by Clark et al in this issue1 is a timely reminder of an important problem in modern medicine: the demise of the bedside. My only divergence from the authors is in their conclusion, since my Mediterranean pessimism leads me to believe that theirs is just a gallant attempt at rearguard action for a battle that, unfortunately, has long been lost.

More than half a century ago, Paul Wood warned us against the “danger of losing our clinical heritage and pinning too much faith in figures thrown out by machines,” thundering that “medicine must suffer if this tendency is not checked.”2 Well, that tendency was not checked, and medicine (and our wallets) have indeed suffered.

See related commentary

Still, technology is not the enemy. The misuse of technology is the problem.

Like Dr. Clark and his colleagues, I’ve seen many cases in which technology unguided by bedside skills took physicians down a path where tests begot tests and where, at the end, there was usually a surgeon, and often a lawyer. Sometimes even an undertaker. The deaths of Jonathan Larson (writer-composer of the musical Rent) and of his namesake, actor Jonathan (John) Ritter—who both succumbed to undiagnosed aortic dissection—make me wonder whether their pulses were ever checked.

Editorials have lamented the “hyposkillia” of our times,3 and the usual suspects have been already rounded up: our overreliance on tests, our ever-increasing fascination with the machine (what Erich Fromm called the necrophilia of our times),4 the loss of bedside teaching, and lastly, the lure of compensation. But one important player has so far gone unnoticed, despite being probably the major offender. In fact, it may even be responsible for the other disturbing trend in modern medicine: the loss of empathy.5

I’m referring to the disappearance of the humanities in both the undergraduate and the graduate curriculum. This is actually new. If we look, for example, at the great bedside diagnosticians of the past, we find that they were passionately interested in everything human. Most, if not all, were indeed humanists—lovers of the arts and literature, travelers and historians, poets and painters, curious of any field that could enrich the human spirit. Charcot, who single-handedly invented neurology, was not only a superb scientist, but also a talented artist who drew and painted (skills he considered fundamental for bedside observation) plus a bona-fide Beethoven fanatic who spent Thursday evenings on music, strictly forbidding any medical talk. Laënnec himself was a poet and musician who modeled his stethoscope after the flutes he made. And Charles Bell (of Bell palsy, phenomenon, and law) was a well-respected painter who soldiered with Wellington and left us incredible sketches of the Waterloo wounded and maimed. Even Osler, the pinnacle of 19th century humanistic medicine, believed so strongly in the value of a liberal education as to provide students with a list of 10 books (ranging from Plutarch and Montaigne to Marcus Aurelius and Shakespeare) to read for half an hour before going to sleep. Addressing the Classical Association just before his death, he lamented the “grievous damage” that had been done by regarding the humanities and science in any other light than complementary, while in reality they are “twin berries on one stem.”6

 

 

Until the 1870s, medicine was in fact a spin-off of the humanities. A solid humanistic education was deemed essential for admission to medical school. Then the German victory in the Franco-Prussian War shifted the axis from Paris to Berlin, and medicine went the German way. Never as touchy-feely as the French, and definitely more comfortable in the laboratory than at the bedside, the Germans produced giants like Koch, Virchow, and Roentgen, who gradually moved medicine away from the bedside and into the lab. In fact, medicine even adopted the uniform of the laboratory—the infamous white coat now banned by the British National Health system as a dirty carrier of bacteria.

Finding herself at a crossroads, America went the German way, mostly because of Flexner (himself the son of German immigrants), whose 1910 report totally changed the face of medical education. The “two cultures” were born—science was “in” and the humanities “out.”7

The result is what Lewis Thomas called the “baleful and malign” influence of the modern medical school on liberal-arts education.8 Michael Crichton put it even more bluntly. Explaining why he dropped out of medicine, he wrote, “My classmates [at Harvard] tended to think that literature, music, and art were irrelevant distractions. They held these “cultural” matters in the same intellectual contempt that a physicist holds astrology. Everything outside medicine was just a waste of time.”9

And since then, things have only worsened.10

Yet the link between humanities and the bedside remains crucial. I have had the privilege of meeting most of the clinicians who still contribute to physical diagnosis, and they are almost all humanists.

So why should the humanities nurture the bedside? For one, they may increase our tolerance of ambiguity, a trait sorely lacking in modern medicine. This makes sense, since decoding feeble sounds emanating from chests, palpating indistinct organs, and detecting bedside nuances are all painful reminders of the ambiguous in our craft, not to mention in life. And if unprepared by a humanistic education to deal with the uncertain, students may easily opt for the “certainties” of the laboratory or radiology suite.11 Once again, Osler comes to our rescue.

“A distressing feature in the life which you are about to enter” he told the graduating class of the University of Pennsylvania in 1889, “is the uncertainty which pertains not alone to our science and arts but to the very hopes and fears which make us men. In seeking absolute truth we aim at the unattainable, and must be content with finding broken portions.”12

The stethoscope is too closely bound with the doctor’s image not to be a metaphor for something larger. To me, it’s a metaphor for medicine as both an art and a science, wherein the humanities are—and of right ought to be—a fundamental part of the education. Hence, if we want to rekindle the bedside, we must rekindle the humanities. After all, this is what both Lewis Thomas8 and Sherwin Nuland13 have urged us to do. My hunch is that this would need to be done sooner rather than later, because if it is possible to make a scientist out of a humanist (it was done for centuries), it might be considerably harder to make a humanist out of a scientist. The experience of the past few decades seems to support this conclusion.

The alternative is a future full of tricorders and technicians, but sorely lacking in healers.

“Those who advise that all stethoscopes should be ‘scrapped’ may be influenced by the fact that they do not know how to use their own.”

From Pulmonary Tuberculosis, 1921, by Sir James Kingston Fowler (1852–1934) of the Brompton Hospital, England

The commentary by Clark et al in this issue1 is a timely reminder of an important problem in modern medicine: the demise of the bedside. My only divergence from the authors is in their conclusion, since my Mediterranean pessimism leads me to believe that theirs is just a gallant attempt at rearguard action for a battle that, unfortunately, has long been lost.

More than half a century ago, Paul Wood warned us against the “danger of losing our clinical heritage and pinning too much faith in figures thrown out by machines,” thundering that “medicine must suffer if this tendency is not checked.”2 Well, that tendency was not checked, and medicine (and our wallets) have indeed suffered.

See related commentary

Still, technology is not the enemy. The misuse of technology is the problem.

Like Dr. Clark and his colleagues, I’ve seen many cases in which technology unguided by bedside skills took physicians down a path where tests begot tests and where, at the end, there was usually a surgeon, and often a lawyer. Sometimes even an undertaker. The deaths of Jonathan Larson (writer-composer of the musical Rent) and of his namesake, actor Jonathan (John) Ritter—who both succumbed to undiagnosed aortic dissection—make me wonder whether their pulses were ever checked.

Editorials have lamented the “hyposkillia” of our times,3 and the usual suspects have been already rounded up: our overreliance on tests, our ever-increasing fascination with the machine (what Erich Fromm called the necrophilia of our times),4 the loss of bedside teaching, and lastly, the lure of compensation. But one important player has so far gone unnoticed, despite being probably the major offender. In fact, it may even be responsible for the other disturbing trend in modern medicine: the loss of empathy.5

I’m referring to the disappearance of the humanities in both the undergraduate and the graduate curriculum. This is actually new. If we look, for example, at the great bedside diagnosticians of the past, we find that they were passionately interested in everything human. Most, if not all, were indeed humanists—lovers of the arts and literature, travelers and historians, poets and painters, curious of any field that could enrich the human spirit. Charcot, who single-handedly invented neurology, was not only a superb scientist, but also a talented artist who drew and painted (skills he considered fundamental for bedside observation) plus a bona-fide Beethoven fanatic who spent Thursday evenings on music, strictly forbidding any medical talk. Laënnec himself was a poet and musician who modeled his stethoscope after the flutes he made. And Charles Bell (of Bell palsy, phenomenon, and law) was a well-respected painter who soldiered with Wellington and left us incredible sketches of the Waterloo wounded and maimed. Even Osler, the pinnacle of 19th century humanistic medicine, believed so strongly in the value of a liberal education as to provide students with a list of 10 books (ranging from Plutarch and Montaigne to Marcus Aurelius and Shakespeare) to read for half an hour before going to sleep. Addressing the Classical Association just before his death, he lamented the “grievous damage” that had been done by regarding the humanities and science in any other light than complementary, while in reality they are “twin berries on one stem.”6

 

 

Until the 1870s, medicine was in fact a spin-off of the humanities. A solid humanistic education was deemed essential for admission to medical school. Then the German victory in the Franco-Prussian War shifted the axis from Paris to Berlin, and medicine went the German way. Never as touchy-feely as the French, and definitely more comfortable in the laboratory than at the bedside, the Germans produced giants like Koch, Virchow, and Roentgen, who gradually moved medicine away from the bedside and into the lab. In fact, medicine even adopted the uniform of the laboratory—the infamous white coat now banned by the British National Health system as a dirty carrier of bacteria.

Finding herself at a crossroads, America went the German way, mostly because of Flexner (himself the son of German immigrants), whose 1910 report totally changed the face of medical education. The “two cultures” were born—science was “in” and the humanities “out.”7

The result is what Lewis Thomas called the “baleful and malign” influence of the modern medical school on liberal-arts education.8 Michael Crichton put it even more bluntly. Explaining why he dropped out of medicine, he wrote, “My classmates [at Harvard] tended to think that literature, music, and art were irrelevant distractions. They held these “cultural” matters in the same intellectual contempt that a physicist holds astrology. Everything outside medicine was just a waste of time.”9

And since then, things have only worsened.10

Yet the link between humanities and the bedside remains crucial. I have had the privilege of meeting most of the clinicians who still contribute to physical diagnosis, and they are almost all humanists.

So why should the humanities nurture the bedside? For one, they may increase our tolerance of ambiguity, a trait sorely lacking in modern medicine. This makes sense, since decoding feeble sounds emanating from chests, palpating indistinct organs, and detecting bedside nuances are all painful reminders of the ambiguous in our craft, not to mention in life. And if unprepared by a humanistic education to deal with the uncertain, students may easily opt for the “certainties” of the laboratory or radiology suite.11 Once again, Osler comes to our rescue.

“A distressing feature in the life which you are about to enter” he told the graduating class of the University of Pennsylvania in 1889, “is the uncertainty which pertains not alone to our science and arts but to the very hopes and fears which make us men. In seeking absolute truth we aim at the unattainable, and must be content with finding broken portions.”12

The stethoscope is too closely bound with the doctor’s image not to be a metaphor for something larger. To me, it’s a metaphor for medicine as both an art and a science, wherein the humanities are—and of right ought to be—a fundamental part of the education. Hence, if we want to rekindle the bedside, we must rekindle the humanities. After all, this is what both Lewis Thomas8 and Sherwin Nuland13 have urged us to do. My hunch is that this would need to be done sooner rather than later, because if it is possible to make a scientist out of a humanist (it was done for centuries), it might be considerably harder to make a humanist out of a scientist. The experience of the past few decades seems to support this conclusion.

The alternative is a future full of tricorders and technicians, but sorely lacking in healers.

References
  1. Clark D, Ahmed MI, Dell’Italia LJ, Fan P, McGiffin DC. An argument for retrieving the disappearing skill of cardiac auscultation. Cleve Clin J Med 2012; 79:536544.
  2. Wood PH. Diseases of the Heart and Circulation. London: Eyre and Spottiswoode; 1950.
  3. Fred HL. Hyposkillia: deficiency of clinical skills. Tex Heart Inst J 2005; 32:255257.
  4. Fromm E. To Have or To Be? New York, NY: Harper & Row; 1976.
  5. Hojat M, Mangione S, Nasca TJ, Gonnella JS, Magee M. Empathy scores in medical school and ratings of empathic behavior in residency training 3 years later. J Soc Psychol 2005; 145:663672.
  6. Osler W. The old humanities and the new science: The presidential address delivered before the Classical Association at Oxford, May, 1919. Br Med J 1919; 2:17.
  7. Snow CP. The Two Cultures and the Scientific Revolution. London, England: Cambridge University Press; 1959.
  8. Thomas L. Notes of a biology-watcher. How to fix the premedical curriculum. N Engl J Med 1978; 298:11801181.
  9. Crichton M. Travels. New York, NY: Alfred A. Knopf, Inc; 1988:69.
  10. Gunderman RB, Kanter SL. Perspective: “How to fix the premedical curriculum” revisited. Acad Med 2008; 83:11581161.
  11. Nevalainen M, Kuikka L, Sjoberg L, Eriksson J, Pitkala K. Tolerance of uncertainty and fears of making mistakes among fifth-year medical students. Fam Med 2012; 44:240246.
  12. Osler W. Aequanimitas, with other addresses to medical students, nurses, and practitioners of medicine. May 1, 1889. www.medicalarchives.jhmi.edu/osler/aequessay.htm. Accessed June 26, 2012.
  13. Nuland SB. Where is Wisdom? Restraint in a Time of Biomedical Miracles. The Great Lectures Library. Chautauqua Institution; 2006.
References
  1. Clark D, Ahmed MI, Dell’Italia LJ, Fan P, McGiffin DC. An argument for retrieving the disappearing skill of cardiac auscultation. Cleve Clin J Med 2012; 79:536544.
  2. Wood PH. Diseases of the Heart and Circulation. London: Eyre and Spottiswoode; 1950.
  3. Fred HL. Hyposkillia: deficiency of clinical skills. Tex Heart Inst J 2005; 32:255257.
  4. Fromm E. To Have or To Be? New York, NY: Harper & Row; 1976.
  5. Hojat M, Mangione S, Nasca TJ, Gonnella JS, Magee M. Empathy scores in medical school and ratings of empathic behavior in residency training 3 years later. J Soc Psychol 2005; 145:663672.
  6. Osler W. The old humanities and the new science: The presidential address delivered before the Classical Association at Oxford, May, 1919. Br Med J 1919; 2:17.
  7. Snow CP. The Two Cultures and the Scientific Revolution. London, England: Cambridge University Press; 1959.
  8. Thomas L. Notes of a biology-watcher. How to fix the premedical curriculum. N Engl J Med 1978; 298:11801181.
  9. Crichton M. Travels. New York, NY: Alfred A. Knopf, Inc; 1988:69.
  10. Gunderman RB, Kanter SL. Perspective: “How to fix the premedical curriculum” revisited. Acad Med 2008; 83:11581161.
  11. Nevalainen M, Kuikka L, Sjoberg L, Eriksson J, Pitkala K. Tolerance of uncertainty and fears of making mistakes among fifth-year medical students. Fam Med 2012; 44:240246.
  12. Osler W. Aequanimitas, with other addresses to medical students, nurses, and practitioners of medicine. May 1, 1889. www.medicalarchives.jhmi.edu/osler/aequessay.htm. Accessed June 26, 2012.
  13. Nuland SB. Where is Wisdom? Restraint in a Time of Biomedical Miracles. The Great Lectures Library. Chautauqua Institution; 2006.
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Challenges in the management of aortic stenosis

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Challenges in the management of aortic stenosis

The classic case of aortic stenosis is in an otherwise healthy middle-aged patient with symptomatic severe disease who is referred to a cardiac surgeon for surgical aortic valve replacement. Unfortunately, physicians who manage valvular heart disease do not encounter this straightforward scenario on a regular basis. Rather, patients come with comorbidities such as advanced age, pulmonary disease, renal dysfunction, coronary artery disease, and significant left ventricular dysfunction. They also come with severe aortic stenosis without symptoms.

See related article

In this issue of the Cleveland Clinic Journal of Medicine, Sawaya and colleagues1 review the management of aortic stenosis, focusing on clinically challenging scenarios such as low-flow, low-gradient aortic stenosis, low-gradient severe aortic stenosis with a normal ejection fraction, aortic stenosis in elderly patients, moderate aortic stenosis in patients undergoing other cardiac surgery, and transcatheter aortic valve replacement, according to the guidelines from the American College of Cardiology and American Heart Association.2

In addition to the situations covered in their review, a few other complicated situations in patients with severe aortic stenosis also merit discussion. We discuss these below.

ASYMPTOMATIC SEVERE AORTIC STENOSIS AND A NORMAL EJECTION FRACTION

Patients with aortic stenosis may be unaware of their decline in functional capacity, since the illness is gradually progressive. In these patients, exercise testing is often done, as it can uncover limitations and determine the need for aortic valve replacement. Another group of patients with asymptomatic severe aortic stenosis who need aortic valve replacement are those whose ejection fraction is less than 50%.

However, many patients with asymptomatic aortic stenosis pass the stress test with flying colors—no symptoms, no blood pressure changes, no arrhythmias—and have a normal ejection fraction. Managing these patients can be more complicated.

Lancellotti et al3 described a group of patients with asymptomatic severe aortic stenosis, a normal ejection fraction, an aortic valve area smaller than 1 cm2, and normal results on exercise testing. Rates of the primary end point (cardiovascular death or need for aortic valve replacement due to symptoms or left ventricular dysfunction) were assessed in subsets of patients grouped on the basis of two variables:

  • Left ventricular stroke volume index (flow)—either normal or low (< 35 mL/m2) and
  • Mean gradient—either high or low (< 40 mm Hg).

The prevalence rates and 2-year event rates (which were substantial) were as follows:

  • Normal flow, high gradient—51% of patients; event rate 56%
  • Normal flow, low gradient—31% of patients; event rate 17%
  • Low flow, high gradient—10% of patients; event rate 70%
  • Low flow, low gradient—7% of patients; event rate 73%.

Mihaljevic et al4 at our institution found that left ventricular hypertrophy at the time of surgery for aortic stenosis may have lasting negative consequences. In an observational study of 3,049 patients who underwent aortic valve replacement, severe left ventricular hypertrophy preceded symptoms in 17%. Additionally, the survival rate at 10 years in the group whose left ventricular mass was greater than 185 g/m2 was 45% at 10 years, compared with 65% in patients whose left ventricular mass was less than 100 g/m2. Left ventricular hypertrophy may, therefore, eventually become another factor that we use in defining the appropriateness of surgery in patients with severe but asymptomatic aortic stenosis.

Comment. Not all patients who have severe aortic stenosis, no symptoms, and a “normal” ejection fraction are the same. Our view of what constitutes appropriate left ventricular function in aortic stenosis has changed and now encompasses diastolic filling values, myocardial velocity, and patterns of hypertrophy in addition to ejection fraction. Surgery is already considered reasonable for patients with asymptomatic but “extremely severe” aortic stenosis (aortic valve area < 0.6 cm2, jet velocity > 5 m/sec, mean gradient > 60 mm Hg), and it may improve long-term survival.2,5

However, closer inspection of left ventricular mechanics may also identify another group of patients whose prognosis is worse than in the rest. It is possible that a more thorough evaluation of left ventricular mechanics, including strain imaging, will provide a more elegant way to risk-stratify patients and help clinicians decide when to intervene in this difficult group of patients.6

While these factors are not yet a part of the diagnostic algorithm, the work by Lancellotti et al3 and Mihaljevic et al4 sheds light on the idea that evaluation of advanced echocardiographic variables may provide clinical insights into whether patients should undergo aortic valve replacement.

 

 

PCI FOR CONCOMITANT SEVERE CORONARY ARTERY DISEASE

The risk factors for aortic stenosis are similar to those for coronary artery disease, and many patients with moderate or severe aortic stenosis also have significant coronary disease. These patients are traditionally referred for combined surgical aortic valve replacement and coronary artery bypass grafting.

Patients who have the combination of both diseases have a worse prognosis, and adding coronary artery bypass grafting to surgical aortic valve replacement increases the perioperative mortality rate.7

With advances in transcatheter aortic valve replacement, attention has turned to managing concomitant coronary artery disease percutaneously as well. Until recently, however, there were few data on the safety of percutaneous coronary intervention (PCI) in patients with severe aortic stenosis.

Goel et al8 analyzed the outcomes of 254 patients with severe aortic stenosis who underwent PCI at our institution, compared with a propensity-matched group of 508 patients without aortic stenosis undergoing PCI. Overall, the 30-day mortality rate did not differ significantly between the two groups (4.3% vs 4.7%, P = .20), nor did the rate of complications such as contrast nephropathy, periprocedural myocardial infarction, and hemodynamic compromise during the procedure. In subgroup analysis, patients who had severe aortic stenosis and ejection fractions of 30% or less had a significantly higher risk of death than those with ejection fractions greater than 30% (15.4% vs 1.2%, P < .001).

Comment. This information is important, since many patients with severe aortic stenosis also have coronary artery disease. Certainly, for patients with significant coronary artery disease and severe aortic stenosis who cannot undergo surgery, the findings are especially encouraging with respect to the safety of PCI.

The findings also suggest that in patients for whom transcatheter aortic valve replacement can be performed in a timely fashion, a completely percutaneous approach to treating aortic stenosis and coronary artery disease may be reasonable. This hypothesis must be further investigated, but the preliminary data are encouraging.

TRANSCATHETER AORTIC VALVE REPLACEMENT IN LOWER-RISK PATIENTS

The PARTNER (Placement of Aortic Transcatheter Valves) trial showed that transcatheter aortic valve replacement was superior to medical therapy alone for patients who cannot undergo surgery, and not inferior to surgical aortic valve replacement for patients at high surgical risk, ie, a Society of Thoracic Surgeons (STS) mortality risk score greater than 10%.9

Given these encouraging results, the PARTNER II trial is now randomizing patients who are at moderate surgical risk (STS score > 4%) to surgical vs transcatheter aortic valve replacement.

Since transcatheter aortic valve replacement has been performed in Europe under the Conformité Européenne (CE) marking since 2007, diffusion of the procedure there has occurred in a more rapid fashion than in the United States. As a result, a number of patients with low or moderate surgical risk have undergone this procedure.

Lange et al10 summarized their experience at a single center in Munich, Germany, with an eye toward patient selection and surgical risk. Between 2007 and 2010, 420 patients underwent transcatheter aortic valve replacement. When the authors divided the cases into quartiles according to the sequence in which they were seen, they found a statistically significant decline in the STS score over time, from 7.1% in the earliest quartile to 4.8% in the latest quartile (P < .001), indicating the procedure was diffusing into lower-risk groups. With respect to outcome, the 6-month mortality rate declined from 23.5% to 12.4%; this was likely due to a combination of patient-related factors (more patients at lower risk over time), device advances, and greater operator experience. Also of note, only 70% of patients in the latest quartile were intubated for the procedure.

Comment. Diffusion of transcatheter aortic valve replacement in the United States is following a thoughtful path, with patients being assessed by “heart teams” of clinical cardiologists, interventional cardiologists, imaging cardiologists, and cardiac surgeons, and with strict criteria for site approval to perform commercial placement of the Edwards Sapien valve. In keeping with this controlled process, future randomized studies (such as PARTNER II) of transcatheter aortic valve replacement in lower-risk patients will be necessary before this procedure can be widely applied to this patient group. The results are, therefore, eagerly anticipated, but preliminary experience from Europe is encouraging.

 

 

BALLOON AORTIC VALVULOPLASTY IS SEEING A RESURGENCE

In large part due to rising interest in managing aortic stenosis and to the anticipated diffusion of transcatheter aortic valve replacement, balloon aortic valvuloplasty has seen a resurgence in recent years.

This procedure can be considered in a number of situations. In patients with severe aortic stenosis who are hemodynamically unstable and for whom urgent aortic valve replacement is not feasible, balloon valvuloplasty may serve as a “bridge” to valve replacement. Similarly, we have seen significant functional improvement in patients after balloon aortic valvuloplasty, so that some who initially were unable to undergo aortic valve replacement have improved to a point that either transcatheter or surgical replacement could be performed safely. In patients who need urgent noncardiac surgery, balloon valvuloplasty may be considered as a temporizing measure in the hope of reducing the risks of perioperative hemodynamic changes associated with anesthesia.

Many patients with severe aortic stenosis have comorbidities such as chronic obstructive pulmonary disease or liver or kidney disease that make it difficult to discern the degree to which aortic stenosis contributes to their symptoms. In such cases, the balloon procedure may provide a therapeutic answer; improvement of symptoms points to aortic stenosis as the driver of symptoms and may push for a more definitive valve replacement option.

Finally, in patients with no option for either transcatheter or surgical aortic valve replacement, balloon aortic valvuloplasty may be considered as a palliative measure.

The benefit of this procedure is only temporary, and restenosis generally occurs within 6 months. Therefore, its value as a stand-alone procedure is limited, and the overall survival rate is significantly improved only when it is used as a bridge to valve replacement.

It should be noted that balloon aortic valvuloplasty carries significant risk. The 30-day mortality rate may be as high as 10%, usually due to either aortic regurgitation (as a complication of the procedure) or persistent heart failure. Other complications occur in up to 15% of cases and include stroke, peripheral vascular complications (due to the size of the devices used and concomitant incidence of peripheral arterial disease), coronary occlusion, need for permanent pacemaker implantation, cardiac tamponade, and cardiac arrest. In patients who require a repeat procedure, it entails similar risks and outcomes as the first procedure.

Comment. Balloon aortic valvuloplasty holds an important place in the treatment of patients with severe aortic stenosis. In our experience, it is most often performed to bridge severely symptomatic patients to transcatheter or surgical aortic valve replacement, or to better understand the contribution of aortic stenosis to functional limitation in patients with multiple comorbidities. It has tremendous potential to alleviate symptoms and provide an opportunity for functional improvement, in turn allowing definitive treatment with aortic valve replacement and improved quality and quantity of life in patients with severe aortic stenosis.

MANAGING SEVERE STENOSIS IS FULFILLING, BUT CHALLENGING

Managing patients with severe aortic stenosis is very fulfilling but at the same time can be extraordinarily challenging. It requires a patient-by-patient analysis of clinical, echocardiographic, and hemodynamic data. In some cases, the relationship between aortic stenosis and current symptoms or future outcomes may be in doubt, and provocative testing or balloon aortic valvuloplasty may be necessary to provide further direction. A meticulous assessment, requiring the expertise of clinicians, imagers, interventionalists, and surgeons is often necessary to deliver optimal care to this group of patients.

References
  1. Sawaya F, Stewart J, Babaliaros V. Aortic stenosis: who should undergo surgery, transcatheter valve replacement? Cleve Clin J Med 2012; 79:487497.
  2. Bonow RO, Carabello BA, Chatterjee K, et al; 2006 Writing Committee Members; American College of Cardiology/American Heart Association Task Force. 2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation 2008; 118:e523e661
  3. Lancellotti P, Magne J, Donal E, et al. Clinical outcome in asymptomatic severe aortic stenosis: insights from the new proposed aortic stenosis grading classification. J Am Coll Cardiol 2012; 59:235243.
  4. Mihaljevic T, Nowicki ER, Rajeswaran J, et al. Survival after valve replacement for aortic stenosis: implications for decision making. J Thorac Cardiovasc Surg 2008; 135:12701278; discussion 1278–1279.
  5. Kang DH, Park SJ, Rim JH, et al. Early surgery versus conventional treatment in asymptomatic very severe aortic stenosis. Circulation 2010; 121:15021509.
  6. Ozkan A, Kapadia S, Tuzcu M, Marwick TH. Assessment of left ventricular function in aortic stenosis. Nat Rev Cardiol 2011; 8:494501.
  7. Nowicki ER, Birkmeyer NJ, Weintraub RW, et al; Northern New England Cardiovascular Disease Study Group and the Center for Evaluative Clinical Sciences, Dartmouth Medical School. Multivariable prediction of in-hospital mortality associated with aortic and mitral valve surgery in Northern New England. Ann Thorac Surg 2004; 77:19661977.
  8. Goel SS, Agarwal S, Tuzcu EM, et al. Percutaneous coronary intervention in patients with severe aortic stenosis: implications for transcatheter aortic valve replacement. Circulation 2012; 125:10051013.
  9. Smith CR, Leon MB, Mack MJ, et al; PARTNER Trial Investigators. Transcatheter versus surgical aortic-valve replacement in high-risk patients. N Engl J Med 2011; 364:21872198.
  10. Lange R, Bleiziffer S, Mazzitelli D, et al. Improvements in transcatheter aortic valve implantation outcomes in lower surgical risk patients: a glimpse into the future. J Am Coll Cardiol 2012; 59:280287.
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Related Articles

The classic case of aortic stenosis is in an otherwise healthy middle-aged patient with symptomatic severe disease who is referred to a cardiac surgeon for surgical aortic valve replacement. Unfortunately, physicians who manage valvular heart disease do not encounter this straightforward scenario on a regular basis. Rather, patients come with comorbidities such as advanced age, pulmonary disease, renal dysfunction, coronary artery disease, and significant left ventricular dysfunction. They also come with severe aortic stenosis without symptoms.

See related article

In this issue of the Cleveland Clinic Journal of Medicine, Sawaya and colleagues1 review the management of aortic stenosis, focusing on clinically challenging scenarios such as low-flow, low-gradient aortic stenosis, low-gradient severe aortic stenosis with a normal ejection fraction, aortic stenosis in elderly patients, moderate aortic stenosis in patients undergoing other cardiac surgery, and transcatheter aortic valve replacement, according to the guidelines from the American College of Cardiology and American Heart Association.2

In addition to the situations covered in their review, a few other complicated situations in patients with severe aortic stenosis also merit discussion. We discuss these below.

ASYMPTOMATIC SEVERE AORTIC STENOSIS AND A NORMAL EJECTION FRACTION

Patients with aortic stenosis may be unaware of their decline in functional capacity, since the illness is gradually progressive. In these patients, exercise testing is often done, as it can uncover limitations and determine the need for aortic valve replacement. Another group of patients with asymptomatic severe aortic stenosis who need aortic valve replacement are those whose ejection fraction is less than 50%.

However, many patients with asymptomatic aortic stenosis pass the stress test with flying colors—no symptoms, no blood pressure changes, no arrhythmias—and have a normal ejection fraction. Managing these patients can be more complicated.

Lancellotti et al3 described a group of patients with asymptomatic severe aortic stenosis, a normal ejection fraction, an aortic valve area smaller than 1 cm2, and normal results on exercise testing. Rates of the primary end point (cardiovascular death or need for aortic valve replacement due to symptoms or left ventricular dysfunction) were assessed in subsets of patients grouped on the basis of two variables:

  • Left ventricular stroke volume index (flow)—either normal or low (< 35 mL/m2) and
  • Mean gradient—either high or low (< 40 mm Hg).

The prevalence rates and 2-year event rates (which were substantial) were as follows:

  • Normal flow, high gradient—51% of patients; event rate 56%
  • Normal flow, low gradient—31% of patients; event rate 17%
  • Low flow, high gradient—10% of patients; event rate 70%
  • Low flow, low gradient—7% of patients; event rate 73%.

Mihaljevic et al4 at our institution found that left ventricular hypertrophy at the time of surgery for aortic stenosis may have lasting negative consequences. In an observational study of 3,049 patients who underwent aortic valve replacement, severe left ventricular hypertrophy preceded symptoms in 17%. Additionally, the survival rate at 10 years in the group whose left ventricular mass was greater than 185 g/m2 was 45% at 10 years, compared with 65% in patients whose left ventricular mass was less than 100 g/m2. Left ventricular hypertrophy may, therefore, eventually become another factor that we use in defining the appropriateness of surgery in patients with severe but asymptomatic aortic stenosis.

Comment. Not all patients who have severe aortic stenosis, no symptoms, and a “normal” ejection fraction are the same. Our view of what constitutes appropriate left ventricular function in aortic stenosis has changed and now encompasses diastolic filling values, myocardial velocity, and patterns of hypertrophy in addition to ejection fraction. Surgery is already considered reasonable for patients with asymptomatic but “extremely severe” aortic stenosis (aortic valve area < 0.6 cm2, jet velocity > 5 m/sec, mean gradient > 60 mm Hg), and it may improve long-term survival.2,5

However, closer inspection of left ventricular mechanics may also identify another group of patients whose prognosis is worse than in the rest. It is possible that a more thorough evaluation of left ventricular mechanics, including strain imaging, will provide a more elegant way to risk-stratify patients and help clinicians decide when to intervene in this difficult group of patients.6

While these factors are not yet a part of the diagnostic algorithm, the work by Lancellotti et al3 and Mihaljevic et al4 sheds light on the idea that evaluation of advanced echocardiographic variables may provide clinical insights into whether patients should undergo aortic valve replacement.

 

 

PCI FOR CONCOMITANT SEVERE CORONARY ARTERY DISEASE

The risk factors for aortic stenosis are similar to those for coronary artery disease, and many patients with moderate or severe aortic stenosis also have significant coronary disease. These patients are traditionally referred for combined surgical aortic valve replacement and coronary artery bypass grafting.

Patients who have the combination of both diseases have a worse prognosis, and adding coronary artery bypass grafting to surgical aortic valve replacement increases the perioperative mortality rate.7

With advances in transcatheter aortic valve replacement, attention has turned to managing concomitant coronary artery disease percutaneously as well. Until recently, however, there were few data on the safety of percutaneous coronary intervention (PCI) in patients with severe aortic stenosis.

Goel et al8 analyzed the outcomes of 254 patients with severe aortic stenosis who underwent PCI at our institution, compared with a propensity-matched group of 508 patients without aortic stenosis undergoing PCI. Overall, the 30-day mortality rate did not differ significantly between the two groups (4.3% vs 4.7%, P = .20), nor did the rate of complications such as contrast nephropathy, periprocedural myocardial infarction, and hemodynamic compromise during the procedure. In subgroup analysis, patients who had severe aortic stenosis and ejection fractions of 30% or less had a significantly higher risk of death than those with ejection fractions greater than 30% (15.4% vs 1.2%, P < .001).

Comment. This information is important, since many patients with severe aortic stenosis also have coronary artery disease. Certainly, for patients with significant coronary artery disease and severe aortic stenosis who cannot undergo surgery, the findings are especially encouraging with respect to the safety of PCI.

The findings also suggest that in patients for whom transcatheter aortic valve replacement can be performed in a timely fashion, a completely percutaneous approach to treating aortic stenosis and coronary artery disease may be reasonable. This hypothesis must be further investigated, but the preliminary data are encouraging.

TRANSCATHETER AORTIC VALVE REPLACEMENT IN LOWER-RISK PATIENTS

The PARTNER (Placement of Aortic Transcatheter Valves) trial showed that transcatheter aortic valve replacement was superior to medical therapy alone for patients who cannot undergo surgery, and not inferior to surgical aortic valve replacement for patients at high surgical risk, ie, a Society of Thoracic Surgeons (STS) mortality risk score greater than 10%.9

Given these encouraging results, the PARTNER II trial is now randomizing patients who are at moderate surgical risk (STS score > 4%) to surgical vs transcatheter aortic valve replacement.

Since transcatheter aortic valve replacement has been performed in Europe under the Conformité Européenne (CE) marking since 2007, diffusion of the procedure there has occurred in a more rapid fashion than in the United States. As a result, a number of patients with low or moderate surgical risk have undergone this procedure.

Lange et al10 summarized their experience at a single center in Munich, Germany, with an eye toward patient selection and surgical risk. Between 2007 and 2010, 420 patients underwent transcatheter aortic valve replacement. When the authors divided the cases into quartiles according to the sequence in which they were seen, they found a statistically significant decline in the STS score over time, from 7.1% in the earliest quartile to 4.8% in the latest quartile (P < .001), indicating the procedure was diffusing into lower-risk groups. With respect to outcome, the 6-month mortality rate declined from 23.5% to 12.4%; this was likely due to a combination of patient-related factors (more patients at lower risk over time), device advances, and greater operator experience. Also of note, only 70% of patients in the latest quartile were intubated for the procedure.

Comment. Diffusion of transcatheter aortic valve replacement in the United States is following a thoughtful path, with patients being assessed by “heart teams” of clinical cardiologists, interventional cardiologists, imaging cardiologists, and cardiac surgeons, and with strict criteria for site approval to perform commercial placement of the Edwards Sapien valve. In keeping with this controlled process, future randomized studies (such as PARTNER II) of transcatheter aortic valve replacement in lower-risk patients will be necessary before this procedure can be widely applied to this patient group. The results are, therefore, eagerly anticipated, but preliminary experience from Europe is encouraging.

 

 

BALLOON AORTIC VALVULOPLASTY IS SEEING A RESURGENCE

In large part due to rising interest in managing aortic stenosis and to the anticipated diffusion of transcatheter aortic valve replacement, balloon aortic valvuloplasty has seen a resurgence in recent years.

This procedure can be considered in a number of situations. In patients with severe aortic stenosis who are hemodynamically unstable and for whom urgent aortic valve replacement is not feasible, balloon valvuloplasty may serve as a “bridge” to valve replacement. Similarly, we have seen significant functional improvement in patients after balloon aortic valvuloplasty, so that some who initially were unable to undergo aortic valve replacement have improved to a point that either transcatheter or surgical replacement could be performed safely. In patients who need urgent noncardiac surgery, balloon valvuloplasty may be considered as a temporizing measure in the hope of reducing the risks of perioperative hemodynamic changes associated with anesthesia.

Many patients with severe aortic stenosis have comorbidities such as chronic obstructive pulmonary disease or liver or kidney disease that make it difficult to discern the degree to which aortic stenosis contributes to their symptoms. In such cases, the balloon procedure may provide a therapeutic answer; improvement of symptoms points to aortic stenosis as the driver of symptoms and may push for a more definitive valve replacement option.

Finally, in patients with no option for either transcatheter or surgical aortic valve replacement, balloon aortic valvuloplasty may be considered as a palliative measure.

The benefit of this procedure is only temporary, and restenosis generally occurs within 6 months. Therefore, its value as a stand-alone procedure is limited, and the overall survival rate is significantly improved only when it is used as a bridge to valve replacement.

It should be noted that balloon aortic valvuloplasty carries significant risk. The 30-day mortality rate may be as high as 10%, usually due to either aortic regurgitation (as a complication of the procedure) or persistent heart failure. Other complications occur in up to 15% of cases and include stroke, peripheral vascular complications (due to the size of the devices used and concomitant incidence of peripheral arterial disease), coronary occlusion, need for permanent pacemaker implantation, cardiac tamponade, and cardiac arrest. In patients who require a repeat procedure, it entails similar risks and outcomes as the first procedure.

Comment. Balloon aortic valvuloplasty holds an important place in the treatment of patients with severe aortic stenosis. In our experience, it is most often performed to bridge severely symptomatic patients to transcatheter or surgical aortic valve replacement, or to better understand the contribution of aortic stenosis to functional limitation in patients with multiple comorbidities. It has tremendous potential to alleviate symptoms and provide an opportunity for functional improvement, in turn allowing definitive treatment with aortic valve replacement and improved quality and quantity of life in patients with severe aortic stenosis.

MANAGING SEVERE STENOSIS IS FULFILLING, BUT CHALLENGING

Managing patients with severe aortic stenosis is very fulfilling but at the same time can be extraordinarily challenging. It requires a patient-by-patient analysis of clinical, echocardiographic, and hemodynamic data. In some cases, the relationship between aortic stenosis and current symptoms or future outcomes may be in doubt, and provocative testing or balloon aortic valvuloplasty may be necessary to provide further direction. A meticulous assessment, requiring the expertise of clinicians, imagers, interventionalists, and surgeons is often necessary to deliver optimal care to this group of patients.

The classic case of aortic stenosis is in an otherwise healthy middle-aged patient with symptomatic severe disease who is referred to a cardiac surgeon for surgical aortic valve replacement. Unfortunately, physicians who manage valvular heart disease do not encounter this straightforward scenario on a regular basis. Rather, patients come with comorbidities such as advanced age, pulmonary disease, renal dysfunction, coronary artery disease, and significant left ventricular dysfunction. They also come with severe aortic stenosis without symptoms.

See related article

In this issue of the Cleveland Clinic Journal of Medicine, Sawaya and colleagues1 review the management of aortic stenosis, focusing on clinically challenging scenarios such as low-flow, low-gradient aortic stenosis, low-gradient severe aortic stenosis with a normal ejection fraction, aortic stenosis in elderly patients, moderate aortic stenosis in patients undergoing other cardiac surgery, and transcatheter aortic valve replacement, according to the guidelines from the American College of Cardiology and American Heart Association.2

In addition to the situations covered in their review, a few other complicated situations in patients with severe aortic stenosis also merit discussion. We discuss these below.

ASYMPTOMATIC SEVERE AORTIC STENOSIS AND A NORMAL EJECTION FRACTION

Patients with aortic stenosis may be unaware of their decline in functional capacity, since the illness is gradually progressive. In these patients, exercise testing is often done, as it can uncover limitations and determine the need for aortic valve replacement. Another group of patients with asymptomatic severe aortic stenosis who need aortic valve replacement are those whose ejection fraction is less than 50%.

However, many patients with asymptomatic aortic stenosis pass the stress test with flying colors—no symptoms, no blood pressure changes, no arrhythmias—and have a normal ejection fraction. Managing these patients can be more complicated.

Lancellotti et al3 described a group of patients with asymptomatic severe aortic stenosis, a normal ejection fraction, an aortic valve area smaller than 1 cm2, and normal results on exercise testing. Rates of the primary end point (cardiovascular death or need for aortic valve replacement due to symptoms or left ventricular dysfunction) were assessed in subsets of patients grouped on the basis of two variables:

  • Left ventricular stroke volume index (flow)—either normal or low (< 35 mL/m2) and
  • Mean gradient—either high or low (< 40 mm Hg).

The prevalence rates and 2-year event rates (which were substantial) were as follows:

  • Normal flow, high gradient—51% of patients; event rate 56%
  • Normal flow, low gradient—31% of patients; event rate 17%
  • Low flow, high gradient—10% of patients; event rate 70%
  • Low flow, low gradient—7% of patients; event rate 73%.

Mihaljevic et al4 at our institution found that left ventricular hypertrophy at the time of surgery for aortic stenosis may have lasting negative consequences. In an observational study of 3,049 patients who underwent aortic valve replacement, severe left ventricular hypertrophy preceded symptoms in 17%. Additionally, the survival rate at 10 years in the group whose left ventricular mass was greater than 185 g/m2 was 45% at 10 years, compared with 65% in patients whose left ventricular mass was less than 100 g/m2. Left ventricular hypertrophy may, therefore, eventually become another factor that we use in defining the appropriateness of surgery in patients with severe but asymptomatic aortic stenosis.

Comment. Not all patients who have severe aortic stenosis, no symptoms, and a “normal” ejection fraction are the same. Our view of what constitutes appropriate left ventricular function in aortic stenosis has changed and now encompasses diastolic filling values, myocardial velocity, and patterns of hypertrophy in addition to ejection fraction. Surgery is already considered reasonable for patients with asymptomatic but “extremely severe” aortic stenosis (aortic valve area < 0.6 cm2, jet velocity > 5 m/sec, mean gradient > 60 mm Hg), and it may improve long-term survival.2,5

However, closer inspection of left ventricular mechanics may also identify another group of patients whose prognosis is worse than in the rest. It is possible that a more thorough evaluation of left ventricular mechanics, including strain imaging, will provide a more elegant way to risk-stratify patients and help clinicians decide when to intervene in this difficult group of patients.6

While these factors are not yet a part of the diagnostic algorithm, the work by Lancellotti et al3 and Mihaljevic et al4 sheds light on the idea that evaluation of advanced echocardiographic variables may provide clinical insights into whether patients should undergo aortic valve replacement.

 

 

PCI FOR CONCOMITANT SEVERE CORONARY ARTERY DISEASE

The risk factors for aortic stenosis are similar to those for coronary artery disease, and many patients with moderate or severe aortic stenosis also have significant coronary disease. These patients are traditionally referred for combined surgical aortic valve replacement and coronary artery bypass grafting.

Patients who have the combination of both diseases have a worse prognosis, and adding coronary artery bypass grafting to surgical aortic valve replacement increases the perioperative mortality rate.7

With advances in transcatheter aortic valve replacement, attention has turned to managing concomitant coronary artery disease percutaneously as well. Until recently, however, there were few data on the safety of percutaneous coronary intervention (PCI) in patients with severe aortic stenosis.

Goel et al8 analyzed the outcomes of 254 patients with severe aortic stenosis who underwent PCI at our institution, compared with a propensity-matched group of 508 patients without aortic stenosis undergoing PCI. Overall, the 30-day mortality rate did not differ significantly between the two groups (4.3% vs 4.7%, P = .20), nor did the rate of complications such as contrast nephropathy, periprocedural myocardial infarction, and hemodynamic compromise during the procedure. In subgroup analysis, patients who had severe aortic stenosis and ejection fractions of 30% or less had a significantly higher risk of death than those with ejection fractions greater than 30% (15.4% vs 1.2%, P < .001).

Comment. This information is important, since many patients with severe aortic stenosis also have coronary artery disease. Certainly, for patients with significant coronary artery disease and severe aortic stenosis who cannot undergo surgery, the findings are especially encouraging with respect to the safety of PCI.

The findings also suggest that in patients for whom transcatheter aortic valve replacement can be performed in a timely fashion, a completely percutaneous approach to treating aortic stenosis and coronary artery disease may be reasonable. This hypothesis must be further investigated, but the preliminary data are encouraging.

TRANSCATHETER AORTIC VALVE REPLACEMENT IN LOWER-RISK PATIENTS

The PARTNER (Placement of Aortic Transcatheter Valves) trial showed that transcatheter aortic valve replacement was superior to medical therapy alone for patients who cannot undergo surgery, and not inferior to surgical aortic valve replacement for patients at high surgical risk, ie, a Society of Thoracic Surgeons (STS) mortality risk score greater than 10%.9

Given these encouraging results, the PARTNER II trial is now randomizing patients who are at moderate surgical risk (STS score > 4%) to surgical vs transcatheter aortic valve replacement.

Since transcatheter aortic valve replacement has been performed in Europe under the Conformité Européenne (CE) marking since 2007, diffusion of the procedure there has occurred in a more rapid fashion than in the United States. As a result, a number of patients with low or moderate surgical risk have undergone this procedure.

Lange et al10 summarized their experience at a single center in Munich, Germany, with an eye toward patient selection and surgical risk. Between 2007 and 2010, 420 patients underwent transcatheter aortic valve replacement. When the authors divided the cases into quartiles according to the sequence in which they were seen, they found a statistically significant decline in the STS score over time, from 7.1% in the earliest quartile to 4.8% in the latest quartile (P < .001), indicating the procedure was diffusing into lower-risk groups. With respect to outcome, the 6-month mortality rate declined from 23.5% to 12.4%; this was likely due to a combination of patient-related factors (more patients at lower risk over time), device advances, and greater operator experience. Also of note, only 70% of patients in the latest quartile were intubated for the procedure.

Comment. Diffusion of transcatheter aortic valve replacement in the United States is following a thoughtful path, with patients being assessed by “heart teams” of clinical cardiologists, interventional cardiologists, imaging cardiologists, and cardiac surgeons, and with strict criteria for site approval to perform commercial placement of the Edwards Sapien valve. In keeping with this controlled process, future randomized studies (such as PARTNER II) of transcatheter aortic valve replacement in lower-risk patients will be necessary before this procedure can be widely applied to this patient group. The results are, therefore, eagerly anticipated, but preliminary experience from Europe is encouraging.

 

 

BALLOON AORTIC VALVULOPLASTY IS SEEING A RESURGENCE

In large part due to rising interest in managing aortic stenosis and to the anticipated diffusion of transcatheter aortic valve replacement, balloon aortic valvuloplasty has seen a resurgence in recent years.

This procedure can be considered in a number of situations. In patients with severe aortic stenosis who are hemodynamically unstable and for whom urgent aortic valve replacement is not feasible, balloon valvuloplasty may serve as a “bridge” to valve replacement. Similarly, we have seen significant functional improvement in patients after balloon aortic valvuloplasty, so that some who initially were unable to undergo aortic valve replacement have improved to a point that either transcatheter or surgical replacement could be performed safely. In patients who need urgent noncardiac surgery, balloon valvuloplasty may be considered as a temporizing measure in the hope of reducing the risks of perioperative hemodynamic changes associated with anesthesia.

Many patients with severe aortic stenosis have comorbidities such as chronic obstructive pulmonary disease or liver or kidney disease that make it difficult to discern the degree to which aortic stenosis contributes to their symptoms. In such cases, the balloon procedure may provide a therapeutic answer; improvement of symptoms points to aortic stenosis as the driver of symptoms and may push for a more definitive valve replacement option.

Finally, in patients with no option for either transcatheter or surgical aortic valve replacement, balloon aortic valvuloplasty may be considered as a palliative measure.

The benefit of this procedure is only temporary, and restenosis generally occurs within 6 months. Therefore, its value as a stand-alone procedure is limited, and the overall survival rate is significantly improved only when it is used as a bridge to valve replacement.

It should be noted that balloon aortic valvuloplasty carries significant risk. The 30-day mortality rate may be as high as 10%, usually due to either aortic regurgitation (as a complication of the procedure) or persistent heart failure. Other complications occur in up to 15% of cases and include stroke, peripheral vascular complications (due to the size of the devices used and concomitant incidence of peripheral arterial disease), coronary occlusion, need for permanent pacemaker implantation, cardiac tamponade, and cardiac arrest. In patients who require a repeat procedure, it entails similar risks and outcomes as the first procedure.

Comment. Balloon aortic valvuloplasty holds an important place in the treatment of patients with severe aortic stenosis. In our experience, it is most often performed to bridge severely symptomatic patients to transcatheter or surgical aortic valve replacement, or to better understand the contribution of aortic stenosis to functional limitation in patients with multiple comorbidities. It has tremendous potential to alleviate symptoms and provide an opportunity for functional improvement, in turn allowing definitive treatment with aortic valve replacement and improved quality and quantity of life in patients with severe aortic stenosis.

MANAGING SEVERE STENOSIS IS FULFILLING, BUT CHALLENGING

Managing patients with severe aortic stenosis is very fulfilling but at the same time can be extraordinarily challenging. It requires a patient-by-patient analysis of clinical, echocardiographic, and hemodynamic data. In some cases, the relationship between aortic stenosis and current symptoms or future outcomes may be in doubt, and provocative testing or balloon aortic valvuloplasty may be necessary to provide further direction. A meticulous assessment, requiring the expertise of clinicians, imagers, interventionalists, and surgeons is often necessary to deliver optimal care to this group of patients.

References
  1. Sawaya F, Stewart J, Babaliaros V. Aortic stenosis: who should undergo surgery, transcatheter valve replacement? Cleve Clin J Med 2012; 79:487497.
  2. Bonow RO, Carabello BA, Chatterjee K, et al; 2006 Writing Committee Members; American College of Cardiology/American Heart Association Task Force. 2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation 2008; 118:e523e661
  3. Lancellotti P, Magne J, Donal E, et al. Clinical outcome in asymptomatic severe aortic stenosis: insights from the new proposed aortic stenosis grading classification. J Am Coll Cardiol 2012; 59:235243.
  4. Mihaljevic T, Nowicki ER, Rajeswaran J, et al. Survival after valve replacement for aortic stenosis: implications for decision making. J Thorac Cardiovasc Surg 2008; 135:12701278; discussion 1278–1279.
  5. Kang DH, Park SJ, Rim JH, et al. Early surgery versus conventional treatment in asymptomatic very severe aortic stenosis. Circulation 2010; 121:15021509.
  6. Ozkan A, Kapadia S, Tuzcu M, Marwick TH. Assessment of left ventricular function in aortic stenosis. Nat Rev Cardiol 2011; 8:494501.
  7. Nowicki ER, Birkmeyer NJ, Weintraub RW, et al; Northern New England Cardiovascular Disease Study Group and the Center for Evaluative Clinical Sciences, Dartmouth Medical School. Multivariable prediction of in-hospital mortality associated with aortic and mitral valve surgery in Northern New England. Ann Thorac Surg 2004; 77:19661977.
  8. Goel SS, Agarwal S, Tuzcu EM, et al. Percutaneous coronary intervention in patients with severe aortic stenosis: implications for transcatheter aortic valve replacement. Circulation 2012; 125:10051013.
  9. Smith CR, Leon MB, Mack MJ, et al; PARTNER Trial Investigators. Transcatheter versus surgical aortic-valve replacement in high-risk patients. N Engl J Med 2011; 364:21872198.
  10. Lange R, Bleiziffer S, Mazzitelli D, et al. Improvements in transcatheter aortic valve implantation outcomes in lower surgical risk patients: a glimpse into the future. J Am Coll Cardiol 2012; 59:280287.
References
  1. Sawaya F, Stewart J, Babaliaros V. Aortic stenosis: who should undergo surgery, transcatheter valve replacement? Cleve Clin J Med 2012; 79:487497.
  2. Bonow RO, Carabello BA, Chatterjee K, et al; 2006 Writing Committee Members; American College of Cardiology/American Heart Association Task Force. 2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation 2008; 118:e523e661
  3. Lancellotti P, Magne J, Donal E, et al. Clinical outcome in asymptomatic severe aortic stenosis: insights from the new proposed aortic stenosis grading classification. J Am Coll Cardiol 2012; 59:235243.
  4. Mihaljevic T, Nowicki ER, Rajeswaran J, et al. Survival after valve replacement for aortic stenosis: implications for decision making. J Thorac Cardiovasc Surg 2008; 135:12701278; discussion 1278–1279.
  5. Kang DH, Park SJ, Rim JH, et al. Early surgery versus conventional treatment in asymptomatic very severe aortic stenosis. Circulation 2010; 121:15021509.
  6. Ozkan A, Kapadia S, Tuzcu M, Marwick TH. Assessment of left ventricular function in aortic stenosis. Nat Rev Cardiol 2011; 8:494501.
  7. Nowicki ER, Birkmeyer NJ, Weintraub RW, et al; Northern New England Cardiovascular Disease Study Group and the Center for Evaluative Clinical Sciences, Dartmouth Medical School. Multivariable prediction of in-hospital mortality associated with aortic and mitral valve surgery in Northern New England. Ann Thorac Surg 2004; 77:19661977.
  8. Goel SS, Agarwal S, Tuzcu EM, et al. Percutaneous coronary intervention in patients with severe aortic stenosis: implications for transcatheter aortic valve replacement. Circulation 2012; 125:10051013.
  9. Smith CR, Leon MB, Mack MJ, et al; PARTNER Trial Investigators. Transcatheter versus surgical aortic-valve replacement in high-risk patients. N Engl J Med 2011; 364:21872198.
  10. Lange R, Bleiziffer S, Mazzitelli D, et al. Improvements in transcatheter aortic valve implantation outcomes in lower surgical risk patients: a glimpse into the future. J Am Coll Cardiol 2012; 59:280287.
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Resistant hypertension has become the focus of intense medical interest. The most commonly accepted definition of resistant hypertension is uncontrolled blood pressure despite the use of drugs from three or more antihypertensive classes, one of which is a diuretic, at maximally tolerated doses. About 1 in 50 patients with a new diagnosis of hypertension will develop resistant hypertension.1

See related article

In the 1950s, surgical renal denervation was shown to be a highly effective treatment for resistant hypertension, but the procedure was abandoned because of intolerable side effects such as bladder dysfunction and orthostasis. More recently, carotid baroreceptor surgery for resistant hypertension was investigated; results were encouraging, but this currently remains a surgical procedure.2 Now, catheter-based renal denervation has emerged as a potential minimally invasive strategy to treat resistant hypertension.

In this issue of Cleveland Clinic Journal of Medicine, Thomas et al provide an elegant review of catheter-based renal denervation to treat resistant hypertension.3 The authors nicely summarize the available data for renal denervation for resistant hypertension. A reduction in office systolic blood pressure of about 30 mm Hg has been observed.4,5 In the published studies to date, there have been no major complications beyond those associated with any angiographic procedure.

Of note, this procedure is investigational in the United States, though it is available outside of research studies in other parts of the world. Symplicity HTN-3, a pivotal trial for potential US Food and Drug Administration approval of catheter-based renal denervation, is ongoing.6

The review by Thomas et al is relevant to primary care physicians, cardiologists, nephrologists, and endocrinologists, all of whom manage patients with resistant and refractory hypertension. It explains the potential indications and referral patterns for the procedure, if approved. This review brings clinicians quickly up to speed about the exciting developments in renal denervation.

UNANSWERED QUESTIONS

As should be evident, there are many unanswered questions about renal denervation.

The long-term durability of catheter-based renal denervation remains to be determined. The available data support a sustained effect out to at least 2 years.7 Further study will be necessary to determine if there are some patients in whom the effects wear out over time. But even if that happens, assuming the beneficial effect lasts at least a few years, it may be reasonable to repeat the procedure.

Another important question is whether the reductions in blood pressure with denervation translate into reductions in stroke, heart failure, renal failure, myocardial infarction, and death. It is logical to think that this relationship holds for catheter-based denervation as it does for medical therapy, though more study is needed to see if this is true.

CAVEATS

As with coronary artery disease, it will be important to ensure that patients labeled as having resistant hypertension truly have the disease. The diagnosis requires a careful history, evaluation of potential causes of secondary hypertension, and increased use of ambulatory blood pressure monitoring to rule out white-coat and masked hypertension.

If a patient truly has resistant hypertension, appropriate lifestyle modifications (primarily salt restriction to levels well below 2.4 g/day) and aggressive pharmacotherapy should first be attempted.8 Aldosterone blockade clearly has an important role, especially in obese patients, as it has been shown to markedly lower blood pressure in this phenotype.9

Imitation is the greatest form of flattery, and this is certainly true in the world of drugs and medical devices. Accordingly, a number of systems for renal denervation are being developed. This will likely spur further innovation and refinement in the technology.

On the other hand, as with coronary artery stents, it is important to realize that there is a fair amount of engineering sophistication behind catheter-based renal denervation. As has already happened in some parts of the world, taking a radiofrequency catheter designed for electrophysiology procedures and indiscriminately using it for renal denervation could be dangerous for patients.

Furthermore, if practitioners rapidly adopt this procedure but do not adhere to the indications and protocols used in the clinical trials, the outcomes could be worse, and the net result might be a setback for this promising field of research.

OTHER INDICATIONS AND BENEFITS?

As Thomas et al point out, in addition to resistant hypertension, renal denervation has also been studied in heart failure, chronic renal failure, diabetes mellitus, and sleep apnea.10–12 Sympathetic nerve overactivity appears to have a pathologic role in all these diseases. In small studies, renal denervation has already been shown to improve systolic and diastolic dysfunction, to cause regression of left ventricular hypertrophy, and to improve glycemic control. Since these cardiovascular risk factors often cluster in the same patient, a treatment that addresses several risk factors simultaneously would be expected to have a profound benefit on cardiovascular outcomes, though this remains to be established.

Several studies are under way. Symplicity-HF will study renal denervation in 40 patients with chronic heart failure and renal impairment. The Symplicity registry will follow more than 5,000 patients undergoing catheter-based renal denervation for resistant hypertension and other conditions marked by sympathetic nerve overactivity. If an important role for renal denervation is validated in Symplicity HTN-3, it would be easy to imagine trials of renal denervation in patients with lesser degrees of hypertension.

Only with further careful randomized trials of renal denervation will its full promise be realized.

References
  1. Daugherty SL, Powers JD, Magid DJ, et al. Incidence and prognosis of resistant hypertension in hypertensive patients. Circulation 2012; e-pub ahead of print.
  2. Bisognano JD, Bakris G, Nadim MK, et al. Baroreflex activation therapy lowers blood pressure in patients with resistant hypertension: results from the double-blind, randomized, placebo-controlled Rheos Pivotal Trial. J Am Coll Cardiol 2011; 58:765773.
  3. Thomas G, Shishehbor MH, Bravo EL, Nally JV. Renal denervation to treat resistant hypertension. Cleve Clin J Med 2012; 79:501510.
  4. Krum H, Schlaich M, Whitbourn R, et al. Catheter-based renal sympathetic denervation for resistant hypertension: a multicentre safety and proof-of-principle cohort study. Lancet 2009; 373:12751281.
  5. Esler MD, Krum H, Sobotka PA, Schlaich MP, Schmieder RE, Böhm M; Symplicity HTN-2 Investigators. Renal sympathetic denervation in patients with treatment-resistant hypertension (The Symplicity HTN-2 Trial): a randomised controlled trial. Lancet 2010; 376:19031909.
  6. Kandzari DE, Bhatt DL, Sobotka PA, et al. Catheter-based renal denervation for resistant hypertension: rationale and design of the SYMPLICITY HTN-3 Trial. Clin Cardiol 2012; in press.
  7. Symplicity HTN-1 Investigators. Catheter-based renal sympathetic denervation for resistant hypertension: durability of blood pressure reduction out to 24 months. Hypertension 2011; 57:911917.
  8. Chobanian AV, Bakris GL, Black HR, et al; Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003; 42:12061252.
  9. Calhoun DA, Jones D, Textor S, et al; American Heart Association Professional Education Committee. Resistant hypertension: diagnosis, evaluation, and treatment: a scientific statement from the American Heart Association Professional Education Committee of the Council for High Blood Pressure Research. Circulation 2008; 117:e510e526.
  10. Mahfoud F, Schlaich M, Kindermann I, et al. Effect of renal sympathetic denervation on glucose metabolism in patients with resistant hypertension: a pilot study. Circulation 2011; 123:19401946.
  11. Brandt MC, Mahfoud F, Reda S, et al. Renal sympathetic denervation reduces left ventricular hypertrophy and improves cardiac function in patients with resistant hypertension. J Am Coll Cardiol 2012; 59:901909.
  12. Witkowski A, Prejbisz A, Florczak E, et al. Effects of renal sympathetic denervation on blood pressure, sleep apnea course, and glycemic control in patients with resistant hypertension and sleep apnea. Hypertension 2011; 58:559565.
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Deepak L. Bhatt, MD, MPH, FACC, FAHA, FSCAI, FESC
Chief of Cardiology, VA Boston Healthcare System; Director, Integrated Interventional Cardiovascular Program, Brigham and Women’s Hospital & VA Boston Healthcare System; Senior Investigator, TIMI Study Group; and Associate Professor of Medicine, Harvard Medical School, Boston, MA

George L. Bakris, MD
Director, ASH Comprehensive Hypertension Center, The University of Chicago Medicine, and Professor of Medicine, University of Chicago, Chicago, IL

Address: Deepak L. Bhatt, MD, MPH, FACC, FAHA, FSCAI, FESC, VA Boston Healthcare System, 1400 VFW Parkway, Boston, MA 02132; e-mail: [email protected]

Dr. Bhatt has disclosed that he has received research grants from Amarin, AstraZeneca, Bristol-Myers Squibb, Eisai, Ethicon, Medtronic, sanofi-aventis, and The Medicines Company. He has received honoraria from WebMD. He serves as the co-principal investigator of the Symplicity HTN-3 trial, which is sponsored by Medtronic.

Dr. Bakris has disclosed that he has received research grants from Forest Labs, Relapsya, and WebMD and has served as a consultant to Abbott, Takeda, Johnson & Johnson, Daiichi-Sankyo, and Medtronic. He serves as the co-principal investigator of the Symplicity HTN-3 trial, which is sponsored by Medtronic.

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Author and Disclosure Information

Deepak L. Bhatt, MD, MPH, FACC, FAHA, FSCAI, FESC
Chief of Cardiology, VA Boston Healthcare System; Director, Integrated Interventional Cardiovascular Program, Brigham and Women’s Hospital & VA Boston Healthcare System; Senior Investigator, TIMI Study Group; and Associate Professor of Medicine, Harvard Medical School, Boston, MA

George L. Bakris, MD
Director, ASH Comprehensive Hypertension Center, The University of Chicago Medicine, and Professor of Medicine, University of Chicago, Chicago, IL

Address: Deepak L. Bhatt, MD, MPH, FACC, FAHA, FSCAI, FESC, VA Boston Healthcare System, 1400 VFW Parkway, Boston, MA 02132; e-mail: [email protected]

Dr. Bhatt has disclosed that he has received research grants from Amarin, AstraZeneca, Bristol-Myers Squibb, Eisai, Ethicon, Medtronic, sanofi-aventis, and The Medicines Company. He has received honoraria from WebMD. He serves as the co-principal investigator of the Symplicity HTN-3 trial, which is sponsored by Medtronic.

Dr. Bakris has disclosed that he has received research grants from Forest Labs, Relapsya, and WebMD and has served as a consultant to Abbott, Takeda, Johnson & Johnson, Daiichi-Sankyo, and Medtronic. He serves as the co-principal investigator of the Symplicity HTN-3 trial, which is sponsored by Medtronic.

Author and Disclosure Information

Deepak L. Bhatt, MD, MPH, FACC, FAHA, FSCAI, FESC
Chief of Cardiology, VA Boston Healthcare System; Director, Integrated Interventional Cardiovascular Program, Brigham and Women’s Hospital & VA Boston Healthcare System; Senior Investigator, TIMI Study Group; and Associate Professor of Medicine, Harvard Medical School, Boston, MA

George L. Bakris, MD
Director, ASH Comprehensive Hypertension Center, The University of Chicago Medicine, and Professor of Medicine, University of Chicago, Chicago, IL

Address: Deepak L. Bhatt, MD, MPH, FACC, FAHA, FSCAI, FESC, VA Boston Healthcare System, 1400 VFW Parkway, Boston, MA 02132; e-mail: [email protected]

Dr. Bhatt has disclosed that he has received research grants from Amarin, AstraZeneca, Bristol-Myers Squibb, Eisai, Ethicon, Medtronic, sanofi-aventis, and The Medicines Company. He has received honoraria from WebMD. He serves as the co-principal investigator of the Symplicity HTN-3 trial, which is sponsored by Medtronic.

Dr. Bakris has disclosed that he has received research grants from Forest Labs, Relapsya, and WebMD and has served as a consultant to Abbott, Takeda, Johnson & Johnson, Daiichi-Sankyo, and Medtronic. He serves as the co-principal investigator of the Symplicity HTN-3 trial, which is sponsored by Medtronic.

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Resistant hypertension has become the focus of intense medical interest. The most commonly accepted definition of resistant hypertension is uncontrolled blood pressure despite the use of drugs from three or more antihypertensive classes, one of which is a diuretic, at maximally tolerated doses. About 1 in 50 patients with a new diagnosis of hypertension will develop resistant hypertension.1

See related article

In the 1950s, surgical renal denervation was shown to be a highly effective treatment for resistant hypertension, but the procedure was abandoned because of intolerable side effects such as bladder dysfunction and orthostasis. More recently, carotid baroreceptor surgery for resistant hypertension was investigated; results were encouraging, but this currently remains a surgical procedure.2 Now, catheter-based renal denervation has emerged as a potential minimally invasive strategy to treat resistant hypertension.

In this issue of Cleveland Clinic Journal of Medicine, Thomas et al provide an elegant review of catheter-based renal denervation to treat resistant hypertension.3 The authors nicely summarize the available data for renal denervation for resistant hypertension. A reduction in office systolic blood pressure of about 30 mm Hg has been observed.4,5 In the published studies to date, there have been no major complications beyond those associated with any angiographic procedure.

Of note, this procedure is investigational in the United States, though it is available outside of research studies in other parts of the world. Symplicity HTN-3, a pivotal trial for potential US Food and Drug Administration approval of catheter-based renal denervation, is ongoing.6

The review by Thomas et al is relevant to primary care physicians, cardiologists, nephrologists, and endocrinologists, all of whom manage patients with resistant and refractory hypertension. It explains the potential indications and referral patterns for the procedure, if approved. This review brings clinicians quickly up to speed about the exciting developments in renal denervation.

UNANSWERED QUESTIONS

As should be evident, there are many unanswered questions about renal denervation.

The long-term durability of catheter-based renal denervation remains to be determined. The available data support a sustained effect out to at least 2 years.7 Further study will be necessary to determine if there are some patients in whom the effects wear out over time. But even if that happens, assuming the beneficial effect lasts at least a few years, it may be reasonable to repeat the procedure.

Another important question is whether the reductions in blood pressure with denervation translate into reductions in stroke, heart failure, renal failure, myocardial infarction, and death. It is logical to think that this relationship holds for catheter-based denervation as it does for medical therapy, though more study is needed to see if this is true.

CAVEATS

As with coronary artery disease, it will be important to ensure that patients labeled as having resistant hypertension truly have the disease. The diagnosis requires a careful history, evaluation of potential causes of secondary hypertension, and increased use of ambulatory blood pressure monitoring to rule out white-coat and masked hypertension.

If a patient truly has resistant hypertension, appropriate lifestyle modifications (primarily salt restriction to levels well below 2.4 g/day) and aggressive pharmacotherapy should first be attempted.8 Aldosterone blockade clearly has an important role, especially in obese patients, as it has been shown to markedly lower blood pressure in this phenotype.9

Imitation is the greatest form of flattery, and this is certainly true in the world of drugs and medical devices. Accordingly, a number of systems for renal denervation are being developed. This will likely spur further innovation and refinement in the technology.

On the other hand, as with coronary artery stents, it is important to realize that there is a fair amount of engineering sophistication behind catheter-based renal denervation. As has already happened in some parts of the world, taking a radiofrequency catheter designed for electrophysiology procedures and indiscriminately using it for renal denervation could be dangerous for patients.

Furthermore, if practitioners rapidly adopt this procedure but do not adhere to the indications and protocols used in the clinical trials, the outcomes could be worse, and the net result might be a setback for this promising field of research.

OTHER INDICATIONS AND BENEFITS?

As Thomas et al point out, in addition to resistant hypertension, renal denervation has also been studied in heart failure, chronic renal failure, diabetes mellitus, and sleep apnea.10–12 Sympathetic nerve overactivity appears to have a pathologic role in all these diseases. In small studies, renal denervation has already been shown to improve systolic and diastolic dysfunction, to cause regression of left ventricular hypertrophy, and to improve glycemic control. Since these cardiovascular risk factors often cluster in the same patient, a treatment that addresses several risk factors simultaneously would be expected to have a profound benefit on cardiovascular outcomes, though this remains to be established.

Several studies are under way. Symplicity-HF will study renal denervation in 40 patients with chronic heart failure and renal impairment. The Symplicity registry will follow more than 5,000 patients undergoing catheter-based renal denervation for resistant hypertension and other conditions marked by sympathetic nerve overactivity. If an important role for renal denervation is validated in Symplicity HTN-3, it would be easy to imagine trials of renal denervation in patients with lesser degrees of hypertension.

Only with further careful randomized trials of renal denervation will its full promise be realized.

Resistant hypertension has become the focus of intense medical interest. The most commonly accepted definition of resistant hypertension is uncontrolled blood pressure despite the use of drugs from three or more antihypertensive classes, one of which is a diuretic, at maximally tolerated doses. About 1 in 50 patients with a new diagnosis of hypertension will develop resistant hypertension.1

See related article

In the 1950s, surgical renal denervation was shown to be a highly effective treatment for resistant hypertension, but the procedure was abandoned because of intolerable side effects such as bladder dysfunction and orthostasis. More recently, carotid baroreceptor surgery for resistant hypertension was investigated; results were encouraging, but this currently remains a surgical procedure.2 Now, catheter-based renal denervation has emerged as a potential minimally invasive strategy to treat resistant hypertension.

In this issue of Cleveland Clinic Journal of Medicine, Thomas et al provide an elegant review of catheter-based renal denervation to treat resistant hypertension.3 The authors nicely summarize the available data for renal denervation for resistant hypertension. A reduction in office systolic blood pressure of about 30 mm Hg has been observed.4,5 In the published studies to date, there have been no major complications beyond those associated with any angiographic procedure.

Of note, this procedure is investigational in the United States, though it is available outside of research studies in other parts of the world. Symplicity HTN-3, a pivotal trial for potential US Food and Drug Administration approval of catheter-based renal denervation, is ongoing.6

The review by Thomas et al is relevant to primary care physicians, cardiologists, nephrologists, and endocrinologists, all of whom manage patients with resistant and refractory hypertension. It explains the potential indications and referral patterns for the procedure, if approved. This review brings clinicians quickly up to speed about the exciting developments in renal denervation.

UNANSWERED QUESTIONS

As should be evident, there are many unanswered questions about renal denervation.

The long-term durability of catheter-based renal denervation remains to be determined. The available data support a sustained effect out to at least 2 years.7 Further study will be necessary to determine if there are some patients in whom the effects wear out over time. But even if that happens, assuming the beneficial effect lasts at least a few years, it may be reasonable to repeat the procedure.

Another important question is whether the reductions in blood pressure with denervation translate into reductions in stroke, heart failure, renal failure, myocardial infarction, and death. It is logical to think that this relationship holds for catheter-based denervation as it does for medical therapy, though more study is needed to see if this is true.

CAVEATS

As with coronary artery disease, it will be important to ensure that patients labeled as having resistant hypertension truly have the disease. The diagnosis requires a careful history, evaluation of potential causes of secondary hypertension, and increased use of ambulatory blood pressure monitoring to rule out white-coat and masked hypertension.

If a patient truly has resistant hypertension, appropriate lifestyle modifications (primarily salt restriction to levels well below 2.4 g/day) and aggressive pharmacotherapy should first be attempted.8 Aldosterone blockade clearly has an important role, especially in obese patients, as it has been shown to markedly lower blood pressure in this phenotype.9

Imitation is the greatest form of flattery, and this is certainly true in the world of drugs and medical devices. Accordingly, a number of systems for renal denervation are being developed. This will likely spur further innovation and refinement in the technology.

On the other hand, as with coronary artery stents, it is important to realize that there is a fair amount of engineering sophistication behind catheter-based renal denervation. As has already happened in some parts of the world, taking a radiofrequency catheter designed for electrophysiology procedures and indiscriminately using it for renal denervation could be dangerous for patients.

Furthermore, if practitioners rapidly adopt this procedure but do not adhere to the indications and protocols used in the clinical trials, the outcomes could be worse, and the net result might be a setback for this promising field of research.

OTHER INDICATIONS AND BENEFITS?

As Thomas et al point out, in addition to resistant hypertension, renal denervation has also been studied in heart failure, chronic renal failure, diabetes mellitus, and sleep apnea.10–12 Sympathetic nerve overactivity appears to have a pathologic role in all these diseases. In small studies, renal denervation has already been shown to improve systolic and diastolic dysfunction, to cause regression of left ventricular hypertrophy, and to improve glycemic control. Since these cardiovascular risk factors often cluster in the same patient, a treatment that addresses several risk factors simultaneously would be expected to have a profound benefit on cardiovascular outcomes, though this remains to be established.

Several studies are under way. Symplicity-HF will study renal denervation in 40 patients with chronic heart failure and renal impairment. The Symplicity registry will follow more than 5,000 patients undergoing catheter-based renal denervation for resistant hypertension and other conditions marked by sympathetic nerve overactivity. If an important role for renal denervation is validated in Symplicity HTN-3, it would be easy to imagine trials of renal denervation in patients with lesser degrees of hypertension.

Only with further careful randomized trials of renal denervation will its full promise be realized.

References
  1. Daugherty SL, Powers JD, Magid DJ, et al. Incidence and prognosis of resistant hypertension in hypertensive patients. Circulation 2012; e-pub ahead of print.
  2. Bisognano JD, Bakris G, Nadim MK, et al. Baroreflex activation therapy lowers blood pressure in patients with resistant hypertension: results from the double-blind, randomized, placebo-controlled Rheos Pivotal Trial. J Am Coll Cardiol 2011; 58:765773.
  3. Thomas G, Shishehbor MH, Bravo EL, Nally JV. Renal denervation to treat resistant hypertension. Cleve Clin J Med 2012; 79:501510.
  4. Krum H, Schlaich M, Whitbourn R, et al. Catheter-based renal sympathetic denervation for resistant hypertension: a multicentre safety and proof-of-principle cohort study. Lancet 2009; 373:12751281.
  5. Esler MD, Krum H, Sobotka PA, Schlaich MP, Schmieder RE, Böhm M; Symplicity HTN-2 Investigators. Renal sympathetic denervation in patients with treatment-resistant hypertension (The Symplicity HTN-2 Trial): a randomised controlled trial. Lancet 2010; 376:19031909.
  6. Kandzari DE, Bhatt DL, Sobotka PA, et al. Catheter-based renal denervation for resistant hypertension: rationale and design of the SYMPLICITY HTN-3 Trial. Clin Cardiol 2012; in press.
  7. Symplicity HTN-1 Investigators. Catheter-based renal sympathetic denervation for resistant hypertension: durability of blood pressure reduction out to 24 months. Hypertension 2011; 57:911917.
  8. Chobanian AV, Bakris GL, Black HR, et al; Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003; 42:12061252.
  9. Calhoun DA, Jones D, Textor S, et al; American Heart Association Professional Education Committee. Resistant hypertension: diagnosis, evaluation, and treatment: a scientific statement from the American Heart Association Professional Education Committee of the Council for High Blood Pressure Research. Circulation 2008; 117:e510e526.
  10. Mahfoud F, Schlaich M, Kindermann I, et al. Effect of renal sympathetic denervation on glucose metabolism in patients with resistant hypertension: a pilot study. Circulation 2011; 123:19401946.
  11. Brandt MC, Mahfoud F, Reda S, et al. Renal sympathetic denervation reduces left ventricular hypertrophy and improves cardiac function in patients with resistant hypertension. J Am Coll Cardiol 2012; 59:901909.
  12. Witkowski A, Prejbisz A, Florczak E, et al. Effects of renal sympathetic denervation on blood pressure, sleep apnea course, and glycemic control in patients with resistant hypertension and sleep apnea. Hypertension 2011; 58:559565.
References
  1. Daugherty SL, Powers JD, Magid DJ, et al. Incidence and prognosis of resistant hypertension in hypertensive patients. Circulation 2012; e-pub ahead of print.
  2. Bisognano JD, Bakris G, Nadim MK, et al. Baroreflex activation therapy lowers blood pressure in patients with resistant hypertension: results from the double-blind, randomized, placebo-controlled Rheos Pivotal Trial. J Am Coll Cardiol 2011; 58:765773.
  3. Thomas G, Shishehbor MH, Bravo EL, Nally JV. Renal denervation to treat resistant hypertension. Cleve Clin J Med 2012; 79:501510.
  4. Krum H, Schlaich M, Whitbourn R, et al. Catheter-based renal sympathetic denervation for resistant hypertension: a multicentre safety and proof-of-principle cohort study. Lancet 2009; 373:12751281.
  5. Esler MD, Krum H, Sobotka PA, Schlaich MP, Schmieder RE, Böhm M; Symplicity HTN-2 Investigators. Renal sympathetic denervation in patients with treatment-resistant hypertension (The Symplicity HTN-2 Trial): a randomised controlled trial. Lancet 2010; 376:19031909.
  6. Kandzari DE, Bhatt DL, Sobotka PA, et al. Catheter-based renal denervation for resistant hypertension: rationale and design of the SYMPLICITY HTN-3 Trial. Clin Cardiol 2012; in press.
  7. Symplicity HTN-1 Investigators. Catheter-based renal sympathetic denervation for resistant hypertension: durability of blood pressure reduction out to 24 months. Hypertension 2011; 57:911917.
  8. Chobanian AV, Bakris GL, Black HR, et al; Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National Heart, Lung, and Blood Institute; National High Blood Pressure Education Program Coordinating Committee. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003; 42:12061252.
  9. Calhoun DA, Jones D, Textor S, et al; American Heart Association Professional Education Committee. Resistant hypertension: diagnosis, evaluation, and treatment: a scientific statement from the American Heart Association Professional Education Committee of the Council for High Blood Pressure Research. Circulation 2008; 117:e510e526.
  10. Mahfoud F, Schlaich M, Kindermann I, et al. Effect of renal sympathetic denervation on glucose metabolism in patients with resistant hypertension: a pilot study. Circulation 2011; 123:19401946.
  11. Brandt MC, Mahfoud F, Reda S, et al. Renal sympathetic denervation reduces left ventricular hypertrophy and improves cardiac function in patients with resistant hypertension. J Am Coll Cardiol 2012; 59:901909.
  12. Witkowski A, Prejbisz A, Florczak E, et al. Effects of renal sympathetic denervation on blood pressure, sleep apnea course, and glycemic control in patients with resistant hypertension and sleep apnea. Hypertension 2011; 58:559565.
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Preface

Antibiotic resistance is a particularly troublesome problem in healthcare institutions, and is clearly linked to antibiotic usage.12 The total annual cost of antimicrobial resistance was estimated to be as high as $35 billion or more in the United States in 1989,3 and much higher in current US dollars. Approximately 5 of every 100 patients admitted to a US hospital develops a nosocomial or hospital‐associated infection (HAI),4 and many of these infections involve bacteria resistant to 1 or more antibiotics.5 This is important because hospitalized patients infected with antibiotic‐resistant bacteria spend a longer time in the hospital, at increased cost, and are at higher risk of death compared to patients with similar infections due to antibiotic‐susceptible bacteria.6 Furthermore, choice of antimicrobial agents across all hospitalized patients is being driven by the concern for these resistant organisms, potentially contributing to medication costs and hospital length of stay.3

Awareness of the problem of HAIs and their frequent association with multidrug‐resistant pathogens, led The Joint Commission of the United States to identify reduction in risk of HAIs as one of their national patient safety goals.7 While The Joint Commission's primary focus is on infection control measures (eg, hand hygiene),7 antimicrobial stewardship can and should play a key role in reducing the emergence and subsequent transmission of antimicrobial‐resistant pathogens within the hospital or other healthcare settings.

Antimicrobial stewardship has been defined as the optimal selection, dose, and duration of an antimicrobial that results in the best clinical outcome for the treatment or prevention of infection, with minimal toxicity to the patient and minimal impact on subsequent resistance. Hospitalists will instinctively find the element of an antimicrobial stewardship to be inherently valuable to their clinical practice.8 By instituting and adhering to optimal antimicrobial usage within one's own practice and across their institutions, patient care is improved through better clinical outcomes, reduced microbial resistance, and shorter hospital stays.

This supplement of the Journal of Hospital Medicine examines key aspects of antimicrobial stewardship in 4 interrelated papers with respective focuses on appropriate initiation and selection of antibiotics (Dr Snydman), antimicrobial de‐escalation strategies (Dr Kaye), duration and cessation of treatment (Dr File), and the hospitalist's role in antimicrobial stewardship (Dr Rosenberg). Three case studies, interwoven through 3 of the 4 papers, are used to highlight the application of antimicrobial stewardship principles discussed in the respective papers, in patients commonly encountered in the hospital. The clinical cases deal with healthcare‐associated pneumonia, intra‐abdominal infections (diverticulitis), and central line‐associated bacteremia. The final paper by Rosenberg reviews trends in antimicrobial resistance, costs of hospital‐acquired infections, and lays out the argument for Hospitalist participation and, at times, leadership in antimicrobial stewardship programs.

Files
References
  1. Dellit TH,Owens RC,McGowan JE, et al.Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America guidelines for developing an institutional program to enhance antimicrobial stewardship.Clin Infect Dis.2007;44:159177.
  2. Tacconelli E.Antimicrobial use: risk driver of multidrug resistant microorganisms in healthcare settings.Curr Opin Infect Dis.2009;22:352358.
  3. Phelps CE.Bug/drug resistance: sometimes less is more.Med Care.1989;27:194203.
  4. Weinstein RA.Nosocomial infection update.Emerg Infect Dis.1998;4:416420.
  5. Hidron AI,Edwards JR,Patel J, et al.NHSN annual update: antimicrobial‐resistant pathogens associated with healthcare‐associated infections: annual summary of data reported to the National Healthcare Safety Network at the Centers for Disease Control and Prevention, 2006–2007.Infect Control Hosp Epidemiol.2008;29:9961011.
  6. Cosgrove SE.The relationship between antimicrobial resistance and patient outcomes: mortality, length of hospital stay, and health care costs.Clin Infect Dis.2006;42(suppl 2):S82S89.
  7. The Joint Commission. Accreditation Program: Hospital. National Patient Safety Goals. Effective January 1, 2011. Available at http://www.jointcommission.org/assets/1/6/2011_NPSGs_HAP.pdf. Accessed January 24, 2011.
  8. Gerding DN.The search for good antimicrobial stewardship.Jt Comm J Qual Improv.2001;27:403404.
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Antibiotic resistance is a particularly troublesome problem in healthcare institutions, and is clearly linked to antibiotic usage.12 The total annual cost of antimicrobial resistance was estimated to be as high as $35 billion or more in the United States in 1989,3 and much higher in current US dollars. Approximately 5 of every 100 patients admitted to a US hospital develops a nosocomial or hospital‐associated infection (HAI),4 and many of these infections involve bacteria resistant to 1 or more antibiotics.5 This is important because hospitalized patients infected with antibiotic‐resistant bacteria spend a longer time in the hospital, at increased cost, and are at higher risk of death compared to patients with similar infections due to antibiotic‐susceptible bacteria.6 Furthermore, choice of antimicrobial agents across all hospitalized patients is being driven by the concern for these resistant organisms, potentially contributing to medication costs and hospital length of stay.3

Awareness of the problem of HAIs and their frequent association with multidrug‐resistant pathogens, led The Joint Commission of the United States to identify reduction in risk of HAIs as one of their national patient safety goals.7 While The Joint Commission's primary focus is on infection control measures (eg, hand hygiene),7 antimicrobial stewardship can and should play a key role in reducing the emergence and subsequent transmission of antimicrobial‐resistant pathogens within the hospital or other healthcare settings.

Antimicrobial stewardship has been defined as the optimal selection, dose, and duration of an antimicrobial that results in the best clinical outcome for the treatment or prevention of infection, with minimal toxicity to the patient and minimal impact on subsequent resistance. Hospitalists will instinctively find the element of an antimicrobial stewardship to be inherently valuable to their clinical practice.8 By instituting and adhering to optimal antimicrobial usage within one's own practice and across their institutions, patient care is improved through better clinical outcomes, reduced microbial resistance, and shorter hospital stays.

This supplement of the Journal of Hospital Medicine examines key aspects of antimicrobial stewardship in 4 interrelated papers with respective focuses on appropriate initiation and selection of antibiotics (Dr Snydman), antimicrobial de‐escalation strategies (Dr Kaye), duration and cessation of treatment (Dr File), and the hospitalist's role in antimicrobial stewardship (Dr Rosenberg). Three case studies, interwoven through 3 of the 4 papers, are used to highlight the application of antimicrobial stewardship principles discussed in the respective papers, in patients commonly encountered in the hospital. The clinical cases deal with healthcare‐associated pneumonia, intra‐abdominal infections (diverticulitis), and central line‐associated bacteremia. The final paper by Rosenberg reviews trends in antimicrobial resistance, costs of hospital‐acquired infections, and lays out the argument for Hospitalist participation and, at times, leadership in antimicrobial stewardship programs.

Antibiotic resistance is a particularly troublesome problem in healthcare institutions, and is clearly linked to antibiotic usage.12 The total annual cost of antimicrobial resistance was estimated to be as high as $35 billion or more in the United States in 1989,3 and much higher in current US dollars. Approximately 5 of every 100 patients admitted to a US hospital develops a nosocomial or hospital‐associated infection (HAI),4 and many of these infections involve bacteria resistant to 1 or more antibiotics.5 This is important because hospitalized patients infected with antibiotic‐resistant bacteria spend a longer time in the hospital, at increased cost, and are at higher risk of death compared to patients with similar infections due to antibiotic‐susceptible bacteria.6 Furthermore, choice of antimicrobial agents across all hospitalized patients is being driven by the concern for these resistant organisms, potentially contributing to medication costs and hospital length of stay.3

Awareness of the problem of HAIs and their frequent association with multidrug‐resistant pathogens, led The Joint Commission of the United States to identify reduction in risk of HAIs as one of their national patient safety goals.7 While The Joint Commission's primary focus is on infection control measures (eg, hand hygiene),7 antimicrobial stewardship can and should play a key role in reducing the emergence and subsequent transmission of antimicrobial‐resistant pathogens within the hospital or other healthcare settings.

Antimicrobial stewardship has been defined as the optimal selection, dose, and duration of an antimicrobial that results in the best clinical outcome for the treatment or prevention of infection, with minimal toxicity to the patient and minimal impact on subsequent resistance. Hospitalists will instinctively find the element of an antimicrobial stewardship to be inherently valuable to their clinical practice.8 By instituting and adhering to optimal antimicrobial usage within one's own practice and across their institutions, patient care is improved through better clinical outcomes, reduced microbial resistance, and shorter hospital stays.

This supplement of the Journal of Hospital Medicine examines key aspects of antimicrobial stewardship in 4 interrelated papers with respective focuses on appropriate initiation and selection of antibiotics (Dr Snydman), antimicrobial de‐escalation strategies (Dr Kaye), duration and cessation of treatment (Dr File), and the hospitalist's role in antimicrobial stewardship (Dr Rosenberg). Three case studies, interwoven through 3 of the 4 papers, are used to highlight the application of antimicrobial stewardship principles discussed in the respective papers, in patients commonly encountered in the hospital. The clinical cases deal with healthcare‐associated pneumonia, intra‐abdominal infections (diverticulitis), and central line‐associated bacteremia. The final paper by Rosenberg reviews trends in antimicrobial resistance, costs of hospital‐acquired infections, and lays out the argument for Hospitalist participation and, at times, leadership in antimicrobial stewardship programs.

References
  1. Dellit TH,Owens RC,McGowan JE, et al.Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America guidelines for developing an institutional program to enhance antimicrobial stewardship.Clin Infect Dis.2007;44:159177.
  2. Tacconelli E.Antimicrobial use: risk driver of multidrug resistant microorganisms in healthcare settings.Curr Opin Infect Dis.2009;22:352358.
  3. Phelps CE.Bug/drug resistance: sometimes less is more.Med Care.1989;27:194203.
  4. Weinstein RA.Nosocomial infection update.Emerg Infect Dis.1998;4:416420.
  5. Hidron AI,Edwards JR,Patel J, et al.NHSN annual update: antimicrobial‐resistant pathogens associated with healthcare‐associated infections: annual summary of data reported to the National Healthcare Safety Network at the Centers for Disease Control and Prevention, 2006–2007.Infect Control Hosp Epidemiol.2008;29:9961011.
  6. Cosgrove SE.The relationship between antimicrobial resistance and patient outcomes: mortality, length of hospital stay, and health care costs.Clin Infect Dis.2006;42(suppl 2):S82S89.
  7. The Joint Commission. Accreditation Program: Hospital. National Patient Safety Goals. Effective January 1, 2011. Available at http://www.jointcommission.org/assets/1/6/2011_NPSGs_HAP.pdf. Accessed January 24, 2011.
  8. Gerding DN.The search for good antimicrobial stewardship.Jt Comm J Qual Improv.2001;27:403404.
References
  1. Dellit TH,Owens RC,McGowan JE, et al.Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America guidelines for developing an institutional program to enhance antimicrobial stewardship.Clin Infect Dis.2007;44:159177.
  2. Tacconelli E.Antimicrobial use: risk driver of multidrug resistant microorganisms in healthcare settings.Curr Opin Infect Dis.2009;22:352358.
  3. Phelps CE.Bug/drug resistance: sometimes less is more.Med Care.1989;27:194203.
  4. Weinstein RA.Nosocomial infection update.Emerg Infect Dis.1998;4:416420.
  5. Hidron AI,Edwards JR,Patel J, et al.NHSN annual update: antimicrobial‐resistant pathogens associated with healthcare‐associated infections: annual summary of data reported to the National Healthcare Safety Network at the Centers for Disease Control and Prevention, 2006–2007.Infect Control Hosp Epidemiol.2008;29:9961011.
  6. Cosgrove SE.The relationship between antimicrobial resistance and patient outcomes: mortality, length of hospital stay, and health care costs.Clin Infect Dis.2006;42(suppl 2):S82S89.
  7. The Joint Commission. Accreditation Program: Hospital. National Patient Safety Goals. Effective January 1, 2011. Available at http://www.jointcommission.org/assets/1/6/2011_NPSGs_HAP.pdf. Accessed January 24, 2011.
  8. Gerding DN.The search for good antimicrobial stewardship.Jt Comm J Qual Improv.2001;27:403404.
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Appropriate Loop Diuretic Dosing

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Appropriate diuretic dosing: Closed loop communication

Injectable furosemide was first approved for use by the US Food and Drug Administration in 1968.1 For more than 40 years, loop diuretics have been the mainstay of therapy for relief of congestion and fluid removal in patients admitted with acute decompensated heart failure (ADHF). Despite the widespread use of loop diuretics in clinical practice, robust data supporting their role is scarce. Furthermore, the optimal approach to the management of the patient with acute volume overload has not been well defined.

In this issue of the Journal of Hospital Medicine, Amer et al.2 present a meta‐analysis of randomized controlled trials comparing continuous infusion to bolus doses of furosemide in hospitalized patients with ADHF. The study demonstrates that continuous infusion is superior to bolus in terms of weight loss and urine output over 24 hours. Specifically, patients receiving a continuous infusion of furosemide had 240 mL/day (95% CI, 462.42 to 18.66) more urine and lost an additional 0.78 kg (95% CI, 1.54 to 0.03) in their hospital stay compared with patients receiving a bolus infusion. The heterogeneity in study designs for urine output and wide confidence intervals for urine output and weight loss create uncertainty about the superiority of continuous infusion. The small difference in daily urine output questions the clinical significance of the results. Many of the studies evaluated in the meta‐analysis lacked rigorous design and/or appropriately dosed furosemide.

Despite the shortcomings of the available studies, the authors have published a sound and reasonable meta‐analysis. This is the first meta‐analysis comparing the use of furosemide alone as a continuous infusion versus bolus dose in patients with ADHF. Additionally, Amer et al. are the first to include recent data from the DOSE trial,3 which showed no difference in volume loss between heart failure patients receiving bolus versus continuous infusions dosing of loop diuretics. Although the benefits of continuous infusion in the meta‐analysis by Amer et al. represent only a modest clinical advantage over bolus infusions, the authors should be commended for addressing an important controversy in the management of patients with volume overload.

Although the method of dose delivery is an important issue in the management of such patients, we believe that a number of critical factors must be taken into consideration to assure sufficient fluid removal and quick relief of congestion. Ensuring the delivery of an adequate loop diuretic dose is critical. Additionally, the dose response must be assessed at an appropriate interval so adjustments can be made in a timely manner. Using this method, diuretic dosing can be individualized based on response.

Current guidelines jointly published by the American Heart Association (AHA) and American College of Cardiology (ACC) do not provide clinicians with specific details about the optimal approach to volume‐overloaded patients.4 In a 2009 update, the ACC and AHA recommend diuretic use to optimize volume status and relieve signs and symptoms of congestion without inducing excessively rapid reduction in intravascular volume.4 They further recommend that patients already receiving a loop diuretic who present with volume overload should receive a dose of diuretic equal to or higher than the outpatient dose. Urine output and congestion should be reassessed serially, and diuretics should be titrated accordingly. Current guidelines do not adequately address several topics, including: (1) appropriate urine output in 24 hours, and how frequently urine output should be assessed; (2) optimal frequency of diuretic dosing; and (3) appropriate choice of diuretic.

An understanding of the pharmacokinetics of loop diuretics helps answer these questions. Intravenous furosemide and bumetanide have similar elimination half‐lives of 1 to 2 hours and peak intravenous action at 30 minutes.5, 6 Intravenous torsemide has not been widely available, but has a longer half‐life of 3 to 4 hours, with peak action in 1 to 2 hours.5, 6 The magnitude of a patient's diuretic response compared with the amount of drug administered is best represented by a sigmoid curve.5 Therefore, after a specific dose threshold, further natriuresis is not achieved. Based on the elimination half‐life, proper bolus dosing of furosemide or bumetanide should be every 4 to 8 hours in patients with volume overload and adequate blood pressure.6 The administration of a loading dose of loop diuretic is of paramount importance to rapidly achieve therapeutic levels immediately before initiating a continuous infusion. Without a proper loading dose, it can take up to 20 hours to achieve steady state serum levels of diuretic during continuous infusion.5 The ACC and AHA acknowledge this point in their guidelines for chronic heart failure by recommending a bolus dose before initiation of continuous infusion.7 The negative results of the DOSE trial may have been due to lack of a loading dose before infusion initiation.3 Additionally, the total volume loss during continuous infusion compared with bolus dosing might be greater if loading doses were consistently given before starting infusions in published studies. Overall, individual patient response to a diuretic dose is variable and dependent on several factors, including serum albumin level, renal and liver function, and diuretic resistance.5

Teamwork and collaboration are essential to overcome barriers to proper diuretic dosing and provide patients with safe and effective care. Closed loop communication between nurses, physicians, and pharmacists in structured daily interdisciplinary rounds appears to reduce adverse drug events in hospitalized patients.8 The increased mortality9, 10 associated with high doses of diuretic, as well as registry data suggesting that over 50% of patients are discharged with significant heart failure symptoms and minimal weight loss,11 call for a more structured approach toward fluid removal. A team‐based protocol that directs titration of medication, monitors response, and clearly outlines communication channels to adjust doses allows for more efficacious medication administration with lower rates of serious events. This method was used with a dosing algorithm for the administration of opioids for patients with acute pain syndromes.12 Serious or fatal opioid‐related adverse drug events were reduced to zero using this communication‐enhancing approach.12 A similar approach should be used for diuretic dosing in patients who are admitted with ADHF.

We believe frequent follow‐up of diuretic response is critical in the successful treatment of the volume‐overloaded patient. Many clinicians who treat hospitalized patients with ADHF prescribe a fixed daily diuretic dose and evaluate the natriuretic response based on 24‐hour urine output and weight loss. This can lead to unnecessary increases in length of hospital stay. We recommend using a protocol for diuretic administration that includes more frequent assessment and follow‐up of dose response. After a diuretic dose is given, nurses communicate with the physician about the amount of urine output after a prespecified time based on an understanding of the pharmacokinetics of the medication administered. If the urine output is not within the desired range, then the diuretic dose can be increased and immediately administered. If the urine output is above a desired range, doses can be decreased, delayed, or held. With optimal protocol dosing for loop diuretics, continuous infusion may be superfluous. In one study, Peacock et al.13 evaluated a diuretic protocol used to treat patients with ADHF who were admitted to an observation unit. This protocol set 2‐hour urine output goals after loop diuretic bolus doses were administered. If the urine output goals were not met, the diuretic dose was doubled and 2‐hour urine measurements were repeated.13 Limits were set on maximum dosing to ensure patient safety, and electrolytes and renal function were monitored. Using this protocol with other ADHF multidisciplinary interventions, 90‐day heart failure readmission rates decreased by 64% (P = 0.007) with a trend toward decreased 90‐day mortality.13 Although the multidisciplinary approach may have been the major contributor to these outcomes, the diuretic protocol allowed rapid achievement of euvolemia in an observation unit patient population with ADHF. Future investigation needs to specifically evaluate dosing protocols and patient safety because of the association between high doses of diuretics and increased mortality. However, studies showing that high diuretic doses are harmful may simply reflect the fact that patients who require high doses of diuretic have more advanced cardiac or renal disease. In such situations, the clinician needs to be aware of the possibility of decreased cardiac output, hypotension, and intrinsic renal disease as potential barriers to diuresis.

Currently, clinicians have no clear evidence‐based strategies for using diuretics to safely reduce congestion in patients with ADHF. As shown by Amer et al.,2 continuous furosemide infusion may provide more effective weight and volume loss than bolus injections. More rigorous studies comparing effectively dosed diuretics regimens are needed. These studies should optimize diuretic use by accounting for individual patient characteristics and drug pharmacokinetics, using a protocol that monitors response in an appropriate interval, and facilitates care team communication. Ultimately, the mode of diuretic administration is only 1 part of developing a process to remove fluid in patients with ADHF.

Acknowledgements

Disclosure: Nothing to report.

Files
References
  1. US Food and Drug Administration. FDA Approved Drug Products. Available at: http://www.accessdata.fda.gov/scripts/cder/drugsatfda/index.cfm?fuseaction=Search.DrugDetails. Accessed May 2, 2011.
  2. Amer M, Adomaityte J, Qayyum R. Continuous infusion with intermittent bolus injections of furosemide in patients hospitalized with acute decompensated heart failure: a metaanalysis of randomized control trials. J Hosp Med. 2011;7:270275.
  3. Felker GM, Lee KL, Bull DA, et al. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med. 2011;364:797805.
  4. Jessup M, Abraham WT, Casey DE, et al. 2009 focused update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation. Circulation 2009;119:19772016.
  5. Brater DC. Diuretic therapy. N Engl J Med. 1998;339:387395.
  6. Elsevier. Clinical Pharmacology. Available at: http://clinicalpharmacology‐ip.com/Default.aspx. Accessed April 18, 2011.
  7. Hunt SA. ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). J Am Coll Cardiol. 2005;46:e1e82.
  8. O'Leary KJ, Buck R, Fligiel HM, et al. Structured interdisciplinary rounds in a medical teaching unit: improving patient safety. Arch Intern Med. 2011;171:678684.
  9. Hasselblad V, Gattis Stough W, Shah MR, et al. Relation between dose of loop diuretics and outcomes in a heart failure population: results of the ESCAPE trial. Eur J Heart Fail. 2007;9:10641069.
  10. Peacock WF, Costanzo MR, De Marco T, et al. Impact of intravenous loop diuretics on outcomes of patients hospitalized with acute decompensated heart failure: insights from the ADHERE registry. Cardiology. 2009;113:1219.
  11. Yancy CW, Lopatin M, Stevenson LW, De Marco T, Fonarow GC. Clinical presentation, management, and in‐hospital outcomes of patients admitted with acute decompensated heart failure with preserved systolic function: a report from the Acute Decompensated Heart Failure National Registry (ADHERE) Database. J Am Coll Cardiol. 2006;47:7684.
  12. Belknap SM, Moore H, Lanzotti SA, et al. Application of software design principles and debugging methods to an analgesia prescription reduces risk of severe injury from medical use of opioids. Clin Pharmacol Ther. 2008;84:385392.
  13. Peacock WF, Remer EE, Aponte J, Moffa DA, Emerman CE, Albert NM. Effective observation unit treatment of decompensated heart failure. Congest Heart Fail. 2002;8:6873.
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Injectable furosemide was first approved for use by the US Food and Drug Administration in 1968.1 For more than 40 years, loop diuretics have been the mainstay of therapy for relief of congestion and fluid removal in patients admitted with acute decompensated heart failure (ADHF). Despite the widespread use of loop diuretics in clinical practice, robust data supporting their role is scarce. Furthermore, the optimal approach to the management of the patient with acute volume overload has not been well defined.

In this issue of the Journal of Hospital Medicine, Amer et al.2 present a meta‐analysis of randomized controlled trials comparing continuous infusion to bolus doses of furosemide in hospitalized patients with ADHF. The study demonstrates that continuous infusion is superior to bolus in terms of weight loss and urine output over 24 hours. Specifically, patients receiving a continuous infusion of furosemide had 240 mL/day (95% CI, 462.42 to 18.66) more urine and lost an additional 0.78 kg (95% CI, 1.54 to 0.03) in their hospital stay compared with patients receiving a bolus infusion. The heterogeneity in study designs for urine output and wide confidence intervals for urine output and weight loss create uncertainty about the superiority of continuous infusion. The small difference in daily urine output questions the clinical significance of the results. Many of the studies evaluated in the meta‐analysis lacked rigorous design and/or appropriately dosed furosemide.

Despite the shortcomings of the available studies, the authors have published a sound and reasonable meta‐analysis. This is the first meta‐analysis comparing the use of furosemide alone as a continuous infusion versus bolus dose in patients with ADHF. Additionally, Amer et al. are the first to include recent data from the DOSE trial,3 which showed no difference in volume loss between heart failure patients receiving bolus versus continuous infusions dosing of loop diuretics. Although the benefits of continuous infusion in the meta‐analysis by Amer et al. represent only a modest clinical advantage over bolus infusions, the authors should be commended for addressing an important controversy in the management of patients with volume overload.

Although the method of dose delivery is an important issue in the management of such patients, we believe that a number of critical factors must be taken into consideration to assure sufficient fluid removal and quick relief of congestion. Ensuring the delivery of an adequate loop diuretic dose is critical. Additionally, the dose response must be assessed at an appropriate interval so adjustments can be made in a timely manner. Using this method, diuretic dosing can be individualized based on response.

Current guidelines jointly published by the American Heart Association (AHA) and American College of Cardiology (ACC) do not provide clinicians with specific details about the optimal approach to volume‐overloaded patients.4 In a 2009 update, the ACC and AHA recommend diuretic use to optimize volume status and relieve signs and symptoms of congestion without inducing excessively rapid reduction in intravascular volume.4 They further recommend that patients already receiving a loop diuretic who present with volume overload should receive a dose of diuretic equal to or higher than the outpatient dose. Urine output and congestion should be reassessed serially, and diuretics should be titrated accordingly. Current guidelines do not adequately address several topics, including: (1) appropriate urine output in 24 hours, and how frequently urine output should be assessed; (2) optimal frequency of diuretic dosing; and (3) appropriate choice of diuretic.

An understanding of the pharmacokinetics of loop diuretics helps answer these questions. Intravenous furosemide and bumetanide have similar elimination half‐lives of 1 to 2 hours and peak intravenous action at 30 minutes.5, 6 Intravenous torsemide has not been widely available, but has a longer half‐life of 3 to 4 hours, with peak action in 1 to 2 hours.5, 6 The magnitude of a patient's diuretic response compared with the amount of drug administered is best represented by a sigmoid curve.5 Therefore, after a specific dose threshold, further natriuresis is not achieved. Based on the elimination half‐life, proper bolus dosing of furosemide or bumetanide should be every 4 to 8 hours in patients with volume overload and adequate blood pressure.6 The administration of a loading dose of loop diuretic is of paramount importance to rapidly achieve therapeutic levels immediately before initiating a continuous infusion. Without a proper loading dose, it can take up to 20 hours to achieve steady state serum levels of diuretic during continuous infusion.5 The ACC and AHA acknowledge this point in their guidelines for chronic heart failure by recommending a bolus dose before initiation of continuous infusion.7 The negative results of the DOSE trial may have been due to lack of a loading dose before infusion initiation.3 Additionally, the total volume loss during continuous infusion compared with bolus dosing might be greater if loading doses were consistently given before starting infusions in published studies. Overall, individual patient response to a diuretic dose is variable and dependent on several factors, including serum albumin level, renal and liver function, and diuretic resistance.5

Teamwork and collaboration are essential to overcome barriers to proper diuretic dosing and provide patients with safe and effective care. Closed loop communication between nurses, physicians, and pharmacists in structured daily interdisciplinary rounds appears to reduce adverse drug events in hospitalized patients.8 The increased mortality9, 10 associated with high doses of diuretic, as well as registry data suggesting that over 50% of patients are discharged with significant heart failure symptoms and minimal weight loss,11 call for a more structured approach toward fluid removal. A team‐based protocol that directs titration of medication, monitors response, and clearly outlines communication channels to adjust doses allows for more efficacious medication administration with lower rates of serious events. This method was used with a dosing algorithm for the administration of opioids for patients with acute pain syndromes.12 Serious or fatal opioid‐related adverse drug events were reduced to zero using this communication‐enhancing approach.12 A similar approach should be used for diuretic dosing in patients who are admitted with ADHF.

We believe frequent follow‐up of diuretic response is critical in the successful treatment of the volume‐overloaded patient. Many clinicians who treat hospitalized patients with ADHF prescribe a fixed daily diuretic dose and evaluate the natriuretic response based on 24‐hour urine output and weight loss. This can lead to unnecessary increases in length of hospital stay. We recommend using a protocol for diuretic administration that includes more frequent assessment and follow‐up of dose response. After a diuretic dose is given, nurses communicate with the physician about the amount of urine output after a prespecified time based on an understanding of the pharmacokinetics of the medication administered. If the urine output is not within the desired range, then the diuretic dose can be increased and immediately administered. If the urine output is above a desired range, doses can be decreased, delayed, or held. With optimal protocol dosing for loop diuretics, continuous infusion may be superfluous. In one study, Peacock et al.13 evaluated a diuretic protocol used to treat patients with ADHF who were admitted to an observation unit. This protocol set 2‐hour urine output goals after loop diuretic bolus doses were administered. If the urine output goals were not met, the diuretic dose was doubled and 2‐hour urine measurements were repeated.13 Limits were set on maximum dosing to ensure patient safety, and electrolytes and renal function were monitored. Using this protocol with other ADHF multidisciplinary interventions, 90‐day heart failure readmission rates decreased by 64% (P = 0.007) with a trend toward decreased 90‐day mortality.13 Although the multidisciplinary approach may have been the major contributor to these outcomes, the diuretic protocol allowed rapid achievement of euvolemia in an observation unit patient population with ADHF. Future investigation needs to specifically evaluate dosing protocols and patient safety because of the association between high doses of diuretics and increased mortality. However, studies showing that high diuretic doses are harmful may simply reflect the fact that patients who require high doses of diuretic have more advanced cardiac or renal disease. In such situations, the clinician needs to be aware of the possibility of decreased cardiac output, hypotension, and intrinsic renal disease as potential barriers to diuresis.

Currently, clinicians have no clear evidence‐based strategies for using diuretics to safely reduce congestion in patients with ADHF. As shown by Amer et al.,2 continuous furosemide infusion may provide more effective weight and volume loss than bolus injections. More rigorous studies comparing effectively dosed diuretics regimens are needed. These studies should optimize diuretic use by accounting for individual patient characteristics and drug pharmacokinetics, using a protocol that monitors response in an appropriate interval, and facilitates care team communication. Ultimately, the mode of diuretic administration is only 1 part of developing a process to remove fluid in patients with ADHF.

Acknowledgements

Disclosure: Nothing to report.

Injectable furosemide was first approved for use by the US Food and Drug Administration in 1968.1 For more than 40 years, loop diuretics have been the mainstay of therapy for relief of congestion and fluid removal in patients admitted with acute decompensated heart failure (ADHF). Despite the widespread use of loop diuretics in clinical practice, robust data supporting their role is scarce. Furthermore, the optimal approach to the management of the patient with acute volume overload has not been well defined.

In this issue of the Journal of Hospital Medicine, Amer et al.2 present a meta‐analysis of randomized controlled trials comparing continuous infusion to bolus doses of furosemide in hospitalized patients with ADHF. The study demonstrates that continuous infusion is superior to bolus in terms of weight loss and urine output over 24 hours. Specifically, patients receiving a continuous infusion of furosemide had 240 mL/day (95% CI, 462.42 to 18.66) more urine and lost an additional 0.78 kg (95% CI, 1.54 to 0.03) in their hospital stay compared with patients receiving a bolus infusion. The heterogeneity in study designs for urine output and wide confidence intervals for urine output and weight loss create uncertainty about the superiority of continuous infusion. The small difference in daily urine output questions the clinical significance of the results. Many of the studies evaluated in the meta‐analysis lacked rigorous design and/or appropriately dosed furosemide.

Despite the shortcomings of the available studies, the authors have published a sound and reasonable meta‐analysis. This is the first meta‐analysis comparing the use of furosemide alone as a continuous infusion versus bolus dose in patients with ADHF. Additionally, Amer et al. are the first to include recent data from the DOSE trial,3 which showed no difference in volume loss between heart failure patients receiving bolus versus continuous infusions dosing of loop diuretics. Although the benefits of continuous infusion in the meta‐analysis by Amer et al. represent only a modest clinical advantage over bolus infusions, the authors should be commended for addressing an important controversy in the management of patients with volume overload.

Although the method of dose delivery is an important issue in the management of such patients, we believe that a number of critical factors must be taken into consideration to assure sufficient fluid removal and quick relief of congestion. Ensuring the delivery of an adequate loop diuretic dose is critical. Additionally, the dose response must be assessed at an appropriate interval so adjustments can be made in a timely manner. Using this method, diuretic dosing can be individualized based on response.

Current guidelines jointly published by the American Heart Association (AHA) and American College of Cardiology (ACC) do not provide clinicians with specific details about the optimal approach to volume‐overloaded patients.4 In a 2009 update, the ACC and AHA recommend diuretic use to optimize volume status and relieve signs and symptoms of congestion without inducing excessively rapid reduction in intravascular volume.4 They further recommend that patients already receiving a loop diuretic who present with volume overload should receive a dose of diuretic equal to or higher than the outpatient dose. Urine output and congestion should be reassessed serially, and diuretics should be titrated accordingly. Current guidelines do not adequately address several topics, including: (1) appropriate urine output in 24 hours, and how frequently urine output should be assessed; (2) optimal frequency of diuretic dosing; and (3) appropriate choice of diuretic.

An understanding of the pharmacokinetics of loop diuretics helps answer these questions. Intravenous furosemide and bumetanide have similar elimination half‐lives of 1 to 2 hours and peak intravenous action at 30 minutes.5, 6 Intravenous torsemide has not been widely available, but has a longer half‐life of 3 to 4 hours, with peak action in 1 to 2 hours.5, 6 The magnitude of a patient's diuretic response compared with the amount of drug administered is best represented by a sigmoid curve.5 Therefore, after a specific dose threshold, further natriuresis is not achieved. Based on the elimination half‐life, proper bolus dosing of furosemide or bumetanide should be every 4 to 8 hours in patients with volume overload and adequate blood pressure.6 The administration of a loading dose of loop diuretic is of paramount importance to rapidly achieve therapeutic levels immediately before initiating a continuous infusion. Without a proper loading dose, it can take up to 20 hours to achieve steady state serum levels of diuretic during continuous infusion.5 The ACC and AHA acknowledge this point in their guidelines for chronic heart failure by recommending a bolus dose before initiation of continuous infusion.7 The negative results of the DOSE trial may have been due to lack of a loading dose before infusion initiation.3 Additionally, the total volume loss during continuous infusion compared with bolus dosing might be greater if loading doses were consistently given before starting infusions in published studies. Overall, individual patient response to a diuretic dose is variable and dependent on several factors, including serum albumin level, renal and liver function, and diuretic resistance.5

Teamwork and collaboration are essential to overcome barriers to proper diuretic dosing and provide patients with safe and effective care. Closed loop communication between nurses, physicians, and pharmacists in structured daily interdisciplinary rounds appears to reduce adverse drug events in hospitalized patients.8 The increased mortality9, 10 associated with high doses of diuretic, as well as registry data suggesting that over 50% of patients are discharged with significant heart failure symptoms and minimal weight loss,11 call for a more structured approach toward fluid removal. A team‐based protocol that directs titration of medication, monitors response, and clearly outlines communication channels to adjust doses allows for more efficacious medication administration with lower rates of serious events. This method was used with a dosing algorithm for the administration of opioids for patients with acute pain syndromes.12 Serious or fatal opioid‐related adverse drug events were reduced to zero using this communication‐enhancing approach.12 A similar approach should be used for diuretic dosing in patients who are admitted with ADHF.

We believe frequent follow‐up of diuretic response is critical in the successful treatment of the volume‐overloaded patient. Many clinicians who treat hospitalized patients with ADHF prescribe a fixed daily diuretic dose and evaluate the natriuretic response based on 24‐hour urine output and weight loss. This can lead to unnecessary increases in length of hospital stay. We recommend using a protocol for diuretic administration that includes more frequent assessment and follow‐up of dose response. After a diuretic dose is given, nurses communicate with the physician about the amount of urine output after a prespecified time based on an understanding of the pharmacokinetics of the medication administered. If the urine output is not within the desired range, then the diuretic dose can be increased and immediately administered. If the urine output is above a desired range, doses can be decreased, delayed, or held. With optimal protocol dosing for loop diuretics, continuous infusion may be superfluous. In one study, Peacock et al.13 evaluated a diuretic protocol used to treat patients with ADHF who were admitted to an observation unit. This protocol set 2‐hour urine output goals after loop diuretic bolus doses were administered. If the urine output goals were not met, the diuretic dose was doubled and 2‐hour urine measurements were repeated.13 Limits were set on maximum dosing to ensure patient safety, and electrolytes and renal function were monitored. Using this protocol with other ADHF multidisciplinary interventions, 90‐day heart failure readmission rates decreased by 64% (P = 0.007) with a trend toward decreased 90‐day mortality.13 Although the multidisciplinary approach may have been the major contributor to these outcomes, the diuretic protocol allowed rapid achievement of euvolemia in an observation unit patient population with ADHF. Future investigation needs to specifically evaluate dosing protocols and patient safety because of the association between high doses of diuretics and increased mortality. However, studies showing that high diuretic doses are harmful may simply reflect the fact that patients who require high doses of diuretic have more advanced cardiac or renal disease. In such situations, the clinician needs to be aware of the possibility of decreased cardiac output, hypotension, and intrinsic renal disease as potential barriers to diuresis.

Currently, clinicians have no clear evidence‐based strategies for using diuretics to safely reduce congestion in patients with ADHF. As shown by Amer et al.,2 continuous furosemide infusion may provide more effective weight and volume loss than bolus injections. More rigorous studies comparing effectively dosed diuretics regimens are needed. These studies should optimize diuretic use by accounting for individual patient characteristics and drug pharmacokinetics, using a protocol that monitors response in an appropriate interval, and facilitates care team communication. Ultimately, the mode of diuretic administration is only 1 part of developing a process to remove fluid in patients with ADHF.

Acknowledgements

Disclosure: Nothing to report.

References
  1. US Food and Drug Administration. FDA Approved Drug Products. Available at: http://www.accessdata.fda.gov/scripts/cder/drugsatfda/index.cfm?fuseaction=Search.DrugDetails. Accessed May 2, 2011.
  2. Amer M, Adomaityte J, Qayyum R. Continuous infusion with intermittent bolus injections of furosemide in patients hospitalized with acute decompensated heart failure: a metaanalysis of randomized control trials. J Hosp Med. 2011;7:270275.
  3. Felker GM, Lee KL, Bull DA, et al. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med. 2011;364:797805.
  4. Jessup M, Abraham WT, Casey DE, et al. 2009 focused update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation. Circulation 2009;119:19772016.
  5. Brater DC. Diuretic therapy. N Engl J Med. 1998;339:387395.
  6. Elsevier. Clinical Pharmacology. Available at: http://clinicalpharmacology‐ip.com/Default.aspx. Accessed April 18, 2011.
  7. Hunt SA. ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). J Am Coll Cardiol. 2005;46:e1e82.
  8. O'Leary KJ, Buck R, Fligiel HM, et al. Structured interdisciplinary rounds in a medical teaching unit: improving patient safety. Arch Intern Med. 2011;171:678684.
  9. Hasselblad V, Gattis Stough W, Shah MR, et al. Relation between dose of loop diuretics and outcomes in a heart failure population: results of the ESCAPE trial. Eur J Heart Fail. 2007;9:10641069.
  10. Peacock WF, Costanzo MR, De Marco T, et al. Impact of intravenous loop diuretics on outcomes of patients hospitalized with acute decompensated heart failure: insights from the ADHERE registry. Cardiology. 2009;113:1219.
  11. Yancy CW, Lopatin M, Stevenson LW, De Marco T, Fonarow GC. Clinical presentation, management, and in‐hospital outcomes of patients admitted with acute decompensated heart failure with preserved systolic function: a report from the Acute Decompensated Heart Failure National Registry (ADHERE) Database. J Am Coll Cardiol. 2006;47:7684.
  12. Belknap SM, Moore H, Lanzotti SA, et al. Application of software design principles and debugging methods to an analgesia prescription reduces risk of severe injury from medical use of opioids. Clin Pharmacol Ther. 2008;84:385392.
  13. Peacock WF, Remer EE, Aponte J, Moffa DA, Emerman CE, Albert NM. Effective observation unit treatment of decompensated heart failure. Congest Heart Fail. 2002;8:6873.
References
  1. US Food and Drug Administration. FDA Approved Drug Products. Available at: http://www.accessdata.fda.gov/scripts/cder/drugsatfda/index.cfm?fuseaction=Search.DrugDetails. Accessed May 2, 2011.
  2. Amer M, Adomaityte J, Qayyum R. Continuous infusion with intermittent bolus injections of furosemide in patients hospitalized with acute decompensated heart failure: a metaanalysis of randomized control trials. J Hosp Med. 2011;7:270275.
  3. Felker GM, Lee KL, Bull DA, et al. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med. 2011;364:797805.
  4. Jessup M, Abraham WT, Casey DE, et al. 2009 focused update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation. Circulation 2009;119:19772016.
  5. Brater DC. Diuretic therapy. N Engl J Med. 1998;339:387395.
  6. Elsevier. Clinical Pharmacology. Available at: http://clinicalpharmacology‐ip.com/Default.aspx. Accessed April 18, 2011.
  7. Hunt SA. ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure). J Am Coll Cardiol. 2005;46:e1e82.
  8. O'Leary KJ, Buck R, Fligiel HM, et al. Structured interdisciplinary rounds in a medical teaching unit: improving patient safety. Arch Intern Med. 2011;171:678684.
  9. Hasselblad V, Gattis Stough W, Shah MR, et al. Relation between dose of loop diuretics and outcomes in a heart failure population: results of the ESCAPE trial. Eur J Heart Fail. 2007;9:10641069.
  10. Peacock WF, Costanzo MR, De Marco T, et al. Impact of intravenous loop diuretics on outcomes of patients hospitalized with acute decompensated heart failure: insights from the ADHERE registry. Cardiology. 2009;113:1219.
  11. Yancy CW, Lopatin M, Stevenson LW, De Marco T, Fonarow GC. Clinical presentation, management, and in‐hospital outcomes of patients admitted with acute decompensated heart failure with preserved systolic function: a report from the Acute Decompensated Heart Failure National Registry (ADHERE) Database. J Am Coll Cardiol. 2006;47:7684.
  12. Belknap SM, Moore H, Lanzotti SA, et al. Application of software design principles and debugging methods to an analgesia prescription reduces risk of severe injury from medical use of opioids. Clin Pharmacol Ther. 2008;84:385392.
  13. Peacock WF, Remer EE, Aponte J, Moffa DA, Emerman CE, Albert NM. Effective observation unit treatment of decompensated heart failure. Congest Heart Fail. 2002;8:6873.
Issue
Journal of Hospital Medicine - 7(3)
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Journal of Hospital Medicine - 7(3)
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167-169
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Appropriate diuretic dosing: Closed loop communication
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Appropriate diuretic dosing: Closed loop communication
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Editor Transition/Williams

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Editor transition—Getting up off the couch and walking out the door

Beginning in January 2012, version 2.0 of the Journal of Hospital Medicine will begin with the talented and capable Andrew Auerbach, MD, MPH taking over as Editor‐in‐Chief. A premier hospital medicine researcher, he possesses experience as a journal editor and practicing hospitalist. With Andy at the helm, JHM will certainly get an upgrade. As my 7‐year tenure comes to an end, I look forward to moving on to new activities, but will dally a bit and reflect on this wonderful opportunity provided to me by the leadership of the Society of Hospital Medicine.

Undertaking with trepidation my role as the founding Editor‐in‐Chief in 2005, I recognized that a talented team of editors would be needed to achieve the expected goals for JHMindexing in MEDLINE (Medical Literature Analysis and Retrieval System Online) and selection for impact factor coverage by Thomson's Institute of Scientific Information (ISI) services. Thankfully, I learned from George Thibault, my egalitarian and brilliant residency program director at Massachusetts General Hospital, that successful leaders succeed by recruiting colleagues smarter than them. With no experience in journal editing beyond writing and reviewing articles, I leaned on numerous people more clever than me. Guided by Kathy Alexander and Vickie Thaw at Wiley‐Blackwell, we put together the framework for the journal. Fortunately, remarkable people agreed to serve as the founding Associate Editors. The abilities of Scott Flanders, Karen Hauer, Jean Kutner, James Pile, and Kaveh Shojania are reflected in their subsequent selection for leadership positions at their institutions and internationally.

JHM's leadership team evolved with replacements and the addition of superbly talented members: Thomas Baudendistel, Daniel Brotman, Vincent Chiang, Lakshmi Halasyamani, Brian Harte, Daniel Hunt, and Sunil Kripalani joined Jim Pile as Deputy Editors. Numerous Associate and Assistant Editors listed on our masthead also contributed their time and thoughtful reviews. Integral to our efforts, the exceptional Managing Editor Phaedra Cress kept us organized, cajoled everyone to meet deadlines, and offered a responsive and affable face to authors.

And succeed this team did! Midway through its second year of publication, JHM was selected for indexing and inclusion in the National Library of Medicine's MEDLINE. After just 2 years of publication, Thomson's ISI services selected JHM for impact factor coverage, and the journal received its first impact factor (3.163) in 2009. The nearly 100,000 article downloads this past year reflect JHM's acceptance beyond hospital medicine, becoming a valuable and respected resource across medicine.

In my first editorial, I remarked that the goal is for JHM to become the premier forum for peer‐reviewed research articles and evidence‐based reviews in the specialty of hospital medicine.1 This journal is on its way to achieving this ambition, possibly further and faster than expected, thanks to all the authors who confidently selected JHM as the publication venue for their scholarly work, the innumerable hours contributed by reviewers who volunteered their time and diligently evaluated thousands of manuscripts, and the terrific work by all the Deputy, Associate, and Assistant Editors. JHM never would have succeeded without their contributions, and I never will be able to thank them enough. Now trusted colleagues and lifelong friends, they deserve the bulk of the credit for JHM's success.

In my life, any accomplishments I achieve stem from the values and work ethic my father inculcated in me. Reportedly known as Bucket Seats by his Army Air Force colleagues because of his muscular size, required of a B‐24 bomber pilot who flew in World War II as a member of the 8th Army Air Force in Europe, a description of the B‐24 by Stephen Ambrose in The Blue Yonder aptly described my father's demeanor and power. It could be sternly unforgiving. It always required, and sometimes demanded, almost superhuman strength to fly. My siblings and I knew him as Smoky, a nickname attached to him by his military buddies after he fell asleep in bed with a cigarette setting his mattress on fire. Sadly, though he miraculously survived fighter plane bullets, flak and fire, unlike many of his fellow pilots and crew, kidney cancer ended his life before age 60, just after I finished my first year of medical school. The attentive and considerate hospital care he received, as well as compassionate care from my mother, who previously worked as a nurse and attended to him at home in his final months, influenced me throughout my career. I hope hospitalists everywhere never forget that patients and their caregivers should remain the primary focus of all our efforts. Document your work and share it with your colleagues through JHM, and all of us will benefit.

A 7‐year journey now ends for me, and I hope much less time sitting on the couch, as I will no longer be spending chunks of my weekends and evenings assigning work to the tireless editors of JHM, reviewing manuscripts, and editing articles. Coincidentally, our youngest child Caroline moved out this autumn, joining her older brothers Stephen and Jason to pursue their dreams. With an empty nest, my wife Karee and I look forward to exploring more of the world.

Lastly, I thank the members of the Society of Hospital Medicine and the readers of JHM, whose kind and frequent compliments provided the fuel for my efforts. Always grateful for this opportunity, I will never forget the unique and indescribable experience of serving as the founding editor of the Journal of Hospital Medicine. Take care, and best wishes to the new leadership as they upgrade the journal to the next level. Out the door I go, on to other endeavors.

References
  • Williams MV.Hospital medicine's evolution—the next step.J Hosp Med.2006;1:12.
Article PDF
Issue
Journal of Hospital Medicine - 6(9)
Page Number
485-486
Sections
Article PDF
Article PDF

Beginning in January 2012, version 2.0 of the Journal of Hospital Medicine will begin with the talented and capable Andrew Auerbach, MD, MPH taking over as Editor‐in‐Chief. A premier hospital medicine researcher, he possesses experience as a journal editor and practicing hospitalist. With Andy at the helm, JHM will certainly get an upgrade. As my 7‐year tenure comes to an end, I look forward to moving on to new activities, but will dally a bit and reflect on this wonderful opportunity provided to me by the leadership of the Society of Hospital Medicine.

Undertaking with trepidation my role as the founding Editor‐in‐Chief in 2005, I recognized that a talented team of editors would be needed to achieve the expected goals for JHMindexing in MEDLINE (Medical Literature Analysis and Retrieval System Online) and selection for impact factor coverage by Thomson's Institute of Scientific Information (ISI) services. Thankfully, I learned from George Thibault, my egalitarian and brilliant residency program director at Massachusetts General Hospital, that successful leaders succeed by recruiting colleagues smarter than them. With no experience in journal editing beyond writing and reviewing articles, I leaned on numerous people more clever than me. Guided by Kathy Alexander and Vickie Thaw at Wiley‐Blackwell, we put together the framework for the journal. Fortunately, remarkable people agreed to serve as the founding Associate Editors. The abilities of Scott Flanders, Karen Hauer, Jean Kutner, James Pile, and Kaveh Shojania are reflected in their subsequent selection for leadership positions at their institutions and internationally.

JHM's leadership team evolved with replacements and the addition of superbly talented members: Thomas Baudendistel, Daniel Brotman, Vincent Chiang, Lakshmi Halasyamani, Brian Harte, Daniel Hunt, and Sunil Kripalani joined Jim Pile as Deputy Editors. Numerous Associate and Assistant Editors listed on our masthead also contributed their time and thoughtful reviews. Integral to our efforts, the exceptional Managing Editor Phaedra Cress kept us organized, cajoled everyone to meet deadlines, and offered a responsive and affable face to authors.

And succeed this team did! Midway through its second year of publication, JHM was selected for indexing and inclusion in the National Library of Medicine's MEDLINE. After just 2 years of publication, Thomson's ISI services selected JHM for impact factor coverage, and the journal received its first impact factor (3.163) in 2009. The nearly 100,000 article downloads this past year reflect JHM's acceptance beyond hospital medicine, becoming a valuable and respected resource across medicine.

In my first editorial, I remarked that the goal is for JHM to become the premier forum for peer‐reviewed research articles and evidence‐based reviews in the specialty of hospital medicine.1 This journal is on its way to achieving this ambition, possibly further and faster than expected, thanks to all the authors who confidently selected JHM as the publication venue for their scholarly work, the innumerable hours contributed by reviewers who volunteered their time and diligently evaluated thousands of manuscripts, and the terrific work by all the Deputy, Associate, and Assistant Editors. JHM never would have succeeded without their contributions, and I never will be able to thank them enough. Now trusted colleagues and lifelong friends, they deserve the bulk of the credit for JHM's success.

In my life, any accomplishments I achieve stem from the values and work ethic my father inculcated in me. Reportedly known as Bucket Seats by his Army Air Force colleagues because of his muscular size, required of a B‐24 bomber pilot who flew in World War II as a member of the 8th Army Air Force in Europe, a description of the B‐24 by Stephen Ambrose in The Blue Yonder aptly described my father's demeanor and power. It could be sternly unforgiving. It always required, and sometimes demanded, almost superhuman strength to fly. My siblings and I knew him as Smoky, a nickname attached to him by his military buddies after he fell asleep in bed with a cigarette setting his mattress on fire. Sadly, though he miraculously survived fighter plane bullets, flak and fire, unlike many of his fellow pilots and crew, kidney cancer ended his life before age 60, just after I finished my first year of medical school. The attentive and considerate hospital care he received, as well as compassionate care from my mother, who previously worked as a nurse and attended to him at home in his final months, influenced me throughout my career. I hope hospitalists everywhere never forget that patients and their caregivers should remain the primary focus of all our efforts. Document your work and share it with your colleagues through JHM, and all of us will benefit.

A 7‐year journey now ends for me, and I hope much less time sitting on the couch, as I will no longer be spending chunks of my weekends and evenings assigning work to the tireless editors of JHM, reviewing manuscripts, and editing articles. Coincidentally, our youngest child Caroline moved out this autumn, joining her older brothers Stephen and Jason to pursue their dreams. With an empty nest, my wife Karee and I look forward to exploring more of the world.

Lastly, I thank the members of the Society of Hospital Medicine and the readers of JHM, whose kind and frequent compliments provided the fuel for my efforts. Always grateful for this opportunity, I will never forget the unique and indescribable experience of serving as the founding editor of the Journal of Hospital Medicine. Take care, and best wishes to the new leadership as they upgrade the journal to the next level. Out the door I go, on to other endeavors.

Beginning in January 2012, version 2.0 of the Journal of Hospital Medicine will begin with the talented and capable Andrew Auerbach, MD, MPH taking over as Editor‐in‐Chief. A premier hospital medicine researcher, he possesses experience as a journal editor and practicing hospitalist. With Andy at the helm, JHM will certainly get an upgrade. As my 7‐year tenure comes to an end, I look forward to moving on to new activities, but will dally a bit and reflect on this wonderful opportunity provided to me by the leadership of the Society of Hospital Medicine.

Undertaking with trepidation my role as the founding Editor‐in‐Chief in 2005, I recognized that a talented team of editors would be needed to achieve the expected goals for JHMindexing in MEDLINE (Medical Literature Analysis and Retrieval System Online) and selection for impact factor coverage by Thomson's Institute of Scientific Information (ISI) services. Thankfully, I learned from George Thibault, my egalitarian and brilliant residency program director at Massachusetts General Hospital, that successful leaders succeed by recruiting colleagues smarter than them. With no experience in journal editing beyond writing and reviewing articles, I leaned on numerous people more clever than me. Guided by Kathy Alexander and Vickie Thaw at Wiley‐Blackwell, we put together the framework for the journal. Fortunately, remarkable people agreed to serve as the founding Associate Editors. The abilities of Scott Flanders, Karen Hauer, Jean Kutner, James Pile, and Kaveh Shojania are reflected in their subsequent selection for leadership positions at their institutions and internationally.

JHM's leadership team evolved with replacements and the addition of superbly talented members: Thomas Baudendistel, Daniel Brotman, Vincent Chiang, Lakshmi Halasyamani, Brian Harte, Daniel Hunt, and Sunil Kripalani joined Jim Pile as Deputy Editors. Numerous Associate and Assistant Editors listed on our masthead also contributed their time and thoughtful reviews. Integral to our efforts, the exceptional Managing Editor Phaedra Cress kept us organized, cajoled everyone to meet deadlines, and offered a responsive and affable face to authors.

And succeed this team did! Midway through its second year of publication, JHM was selected for indexing and inclusion in the National Library of Medicine's MEDLINE. After just 2 years of publication, Thomson's ISI services selected JHM for impact factor coverage, and the journal received its first impact factor (3.163) in 2009. The nearly 100,000 article downloads this past year reflect JHM's acceptance beyond hospital medicine, becoming a valuable and respected resource across medicine.

In my first editorial, I remarked that the goal is for JHM to become the premier forum for peer‐reviewed research articles and evidence‐based reviews in the specialty of hospital medicine.1 This journal is on its way to achieving this ambition, possibly further and faster than expected, thanks to all the authors who confidently selected JHM as the publication venue for their scholarly work, the innumerable hours contributed by reviewers who volunteered their time and diligently evaluated thousands of manuscripts, and the terrific work by all the Deputy, Associate, and Assistant Editors. JHM never would have succeeded without their contributions, and I never will be able to thank them enough. Now trusted colleagues and lifelong friends, they deserve the bulk of the credit for JHM's success.

In my life, any accomplishments I achieve stem from the values and work ethic my father inculcated in me. Reportedly known as Bucket Seats by his Army Air Force colleagues because of his muscular size, required of a B‐24 bomber pilot who flew in World War II as a member of the 8th Army Air Force in Europe, a description of the B‐24 by Stephen Ambrose in The Blue Yonder aptly described my father's demeanor and power. It could be sternly unforgiving. It always required, and sometimes demanded, almost superhuman strength to fly. My siblings and I knew him as Smoky, a nickname attached to him by his military buddies after he fell asleep in bed with a cigarette setting his mattress on fire. Sadly, though he miraculously survived fighter plane bullets, flak and fire, unlike many of his fellow pilots and crew, kidney cancer ended his life before age 60, just after I finished my first year of medical school. The attentive and considerate hospital care he received, as well as compassionate care from my mother, who previously worked as a nurse and attended to him at home in his final months, influenced me throughout my career. I hope hospitalists everywhere never forget that patients and their caregivers should remain the primary focus of all our efforts. Document your work and share it with your colleagues through JHM, and all of us will benefit.

A 7‐year journey now ends for me, and I hope much less time sitting on the couch, as I will no longer be spending chunks of my weekends and evenings assigning work to the tireless editors of JHM, reviewing manuscripts, and editing articles. Coincidentally, our youngest child Caroline moved out this autumn, joining her older brothers Stephen and Jason to pursue their dreams. With an empty nest, my wife Karee and I look forward to exploring more of the world.

Lastly, I thank the members of the Society of Hospital Medicine and the readers of JHM, whose kind and frequent compliments provided the fuel for my efforts. Always grateful for this opportunity, I will never forget the unique and indescribable experience of serving as the founding editor of the Journal of Hospital Medicine. Take care, and best wishes to the new leadership as they upgrade the journal to the next level. Out the door I go, on to other endeavors.

References
  • Williams MV.Hospital medicine's evolution—the next step.J Hosp Med.2006;1:12.
References
  • Williams MV.Hospital medicine's evolution—the next step.J Hosp Med.2006;1:12.
Issue
Journal of Hospital Medicine - 6(9)
Issue
Journal of Hospital Medicine - 6(9)
Page Number
485-486
Page Number
485-486
Article Type
Display Headline
Editor transition—Getting up off the couch and walking out the door
Display Headline
Editor transition—Getting up off the couch and walking out the door
Sections
Article Source
Copyright © 2011 Society of Hospital Medicine
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Correspondence Location
211 E. Ontario Street; Suite 700; Chicago, IL 60611
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2.0

Article Type
Changed
Mon, 01/02/2017 - 19:34
Display Headline
JHM 2.0: The Journal of Hospital Medicine at its first transition

Ten years ago, leaders in Hospital Medicine saw the need for a peer‐reviewed Hospital Medicine journal, a key step in the growth of the field. However, there was no small amount of uncertainty as to whether there was room for another medical publication, or whether Hospital Medicine was ready for its own journal.

It's clear now that we should not have been worried. Our specialty has grown in size and influence, and the Journal of Hospital Medicine's growth has progressed along a similar track, linked to the success of the many leaders in our field, including the founders of the Society of Hospital Medicine: John Nelson, MD, MHM, Win Whitcomb, MD, MHM, and Bob Wachter, MD, MHM. Support from them in selecting the Founding Editor, Mark V. Williams, ensured his success in assembling an outstanding editorial team, developing JHM's editorial process, and setting this journal as the bestand not just the onlyjournal for hospitalists to publish their work. JHM serves as both a beacon and a mirror for the field of Hospital Medicine, and I am honored for the opportunity to lead this dynamic journal. I also owe special thanks to the Society of Hospital Medicine and the outstanding team at Wiley‐Blackwell, who have made my transition to this role a smooth one.

After the transition, JHM will continue to be a mirror for Hospital Medicine in that it will reflect the scholarship and innovation of hospitalists' scholarly work in research, quality improvement, education, and clinical excellence. From a practical standpoint, this means JHM will continue to do what it has done so successfully to date: provide fair, insightful, and rapid evaluation and publication of articles that are scientifically rigorous and have an impact on hospitalists and their patients. Being an effective mirror also means the journal will need to be in tune with technological advances in publication and learning. Few of us read paper journals any longer, and the move from print to digital and mobile media provides an important opportunity for this journal. Expanding the means by which we disseminate JHM's findings, highlight evidence, and promote knowledge that impacts our field is a clear direction for the journal.

At the transition from JHM 1.0 to JHM 2.0, the journal is positioned to be a beacon for the field by publishing papers that address new and rapidly evolving issues that will affect hospitalists and their patients. JHM and my editorial team eagerly seek submission of manuscripts on these issues delineated below.

Even if health care reform legislation evolves or changes after the 2012 elections, the need to improve health care value across multiple phases of care is unlikely to disappear. The medical home and accountable care organizations will prompt hospitalists to work with outpatient partners to achieve improvements; focus on readmissions and high‐utilization patients may catalyze integration even without larger changes. This evolution plays to hospitalists' traditional strengths as innovators and leaders of health system innovations while erasing the boundaries between inpatient and outpatient phases of care. How the field adapts toor even better, anticipateschanges in care delivery is a momentous opportunity.

Hospitalists will continue to be leaders in quality and safety improvement, but the need to develop innovations that are effective, scalable, and widely adoptable is growing even more acute. Stated alternately, we need to develop innovations quickly and rigorously, so that neither time nor resources are wasted. Fortunately, there is likely to be financial support for projects that link improvement and evaluation from the Center for Medicare and Medicaid Innovations (CMMI). It is a fair bet that a large number of the CMMI's target issues will be ones that hospitalists also find important, and which are ripe for inquiry.

Shifting from quality to outcomes will prompt a revisiting of how we measure our success as hospitalists. Achieving success in process benchmarks will no longer be sufficient, as our practices will increasingly be measured by our patients' experience, functional status, quality of life, and clinical events (of which measures of safety are a part)both within the walls of the hospital and afterwardrather than solely relying on whether patients appropriately received a drug or procedure during their stay. The need to improve outcomes will immediately bump up against the disappointingly small proportion of measures or evidence that apply to the typical Hospital Medicine patient. Developing these new measures, and the evidence for how to improve them, will be a key challenge for the field of Hospital Medicine. Outcome development and comparisons are a clear focus of the Patient‐Centered Outcomes Research Institute. Again, studies documenting such research will find a welcome home at JHM.

The role of information technology in how hospitalists provide care to patients, decide on best practices, communicate with physicians and patients, and manage their practices is becoming central. A huge, nationwide natural experiment is underway as health systems work to meet meaningful use criteria, and oftentimes hospitalists are central to these efforts. Disseminating best practices, implementing innovative systems, and creating workflows that meet the needs of hospitalists' patients is a key short‐term need, and one our field is uniquely positioned to address.

Finally, the practice of Hospital Medicine continues to evolve. In teaching centers, hospitalists are leading educators of medical students and residents; developing training models that reflect newer thinking about how to teach a 21st‐century physician is a key need for the field. The importance of adaptations to work‐hour reductions for residents cannot be overstated, but attention must be paid to how hospitalists' work hours impact patient care as well. Comanagement systemswhether for medical subspecialties (ie, cancer or heart failure) or surgical specialtieshave yet to fulfill their promise, yet demand for comanagement grows. How might comanagement systems be adapted and targeted so that they become more effective?

Not being a futurist or even slightly omniscient, I am sure this list is neither exhaustive nor final. In my 15 or so years in Hospital Medicine, I know firsthand that the field is vigorous, innovative, and full of surprises. Fortunately, JHM is attuned to changes happening now as well as issues on the horizon, and will always strive to be an even better messenger for Hospital Medicine as a professional and academic specialty.1 In that way, JHM 2.0 will be the same as JHM 1.0. I'm excited to shepherd JHM's ongoing growth and look forward to my years at the helm.

Acknowledgements

Funding Source: Dr. Auerbach is supported by National Heart, Lung, and Blood Institute Grant K24 K24HL098372.

Disclosure: The author discloses no relevant or financial conflicts of interest.

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References
  1. Williams MV.Editor transition—getting up off the couch and walking out the door.J Hosp Med.2011;6:485486.
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Ten years ago, leaders in Hospital Medicine saw the need for a peer‐reviewed Hospital Medicine journal, a key step in the growth of the field. However, there was no small amount of uncertainty as to whether there was room for another medical publication, or whether Hospital Medicine was ready for its own journal.

It's clear now that we should not have been worried. Our specialty has grown in size and influence, and the Journal of Hospital Medicine's growth has progressed along a similar track, linked to the success of the many leaders in our field, including the founders of the Society of Hospital Medicine: John Nelson, MD, MHM, Win Whitcomb, MD, MHM, and Bob Wachter, MD, MHM. Support from them in selecting the Founding Editor, Mark V. Williams, ensured his success in assembling an outstanding editorial team, developing JHM's editorial process, and setting this journal as the bestand not just the onlyjournal for hospitalists to publish their work. JHM serves as both a beacon and a mirror for the field of Hospital Medicine, and I am honored for the opportunity to lead this dynamic journal. I also owe special thanks to the Society of Hospital Medicine and the outstanding team at Wiley‐Blackwell, who have made my transition to this role a smooth one.

After the transition, JHM will continue to be a mirror for Hospital Medicine in that it will reflect the scholarship and innovation of hospitalists' scholarly work in research, quality improvement, education, and clinical excellence. From a practical standpoint, this means JHM will continue to do what it has done so successfully to date: provide fair, insightful, and rapid evaluation and publication of articles that are scientifically rigorous and have an impact on hospitalists and their patients. Being an effective mirror also means the journal will need to be in tune with technological advances in publication and learning. Few of us read paper journals any longer, and the move from print to digital and mobile media provides an important opportunity for this journal. Expanding the means by which we disseminate JHM's findings, highlight evidence, and promote knowledge that impacts our field is a clear direction for the journal.

At the transition from JHM 1.0 to JHM 2.0, the journal is positioned to be a beacon for the field by publishing papers that address new and rapidly evolving issues that will affect hospitalists and their patients. JHM and my editorial team eagerly seek submission of manuscripts on these issues delineated below.

Even if health care reform legislation evolves or changes after the 2012 elections, the need to improve health care value across multiple phases of care is unlikely to disappear. The medical home and accountable care organizations will prompt hospitalists to work with outpatient partners to achieve improvements; focus on readmissions and high‐utilization patients may catalyze integration even without larger changes. This evolution plays to hospitalists' traditional strengths as innovators and leaders of health system innovations while erasing the boundaries between inpatient and outpatient phases of care. How the field adapts toor even better, anticipateschanges in care delivery is a momentous opportunity.

Hospitalists will continue to be leaders in quality and safety improvement, but the need to develop innovations that are effective, scalable, and widely adoptable is growing even more acute. Stated alternately, we need to develop innovations quickly and rigorously, so that neither time nor resources are wasted. Fortunately, there is likely to be financial support for projects that link improvement and evaluation from the Center for Medicare and Medicaid Innovations (CMMI). It is a fair bet that a large number of the CMMI's target issues will be ones that hospitalists also find important, and which are ripe for inquiry.

Shifting from quality to outcomes will prompt a revisiting of how we measure our success as hospitalists. Achieving success in process benchmarks will no longer be sufficient, as our practices will increasingly be measured by our patients' experience, functional status, quality of life, and clinical events (of which measures of safety are a part)both within the walls of the hospital and afterwardrather than solely relying on whether patients appropriately received a drug or procedure during their stay. The need to improve outcomes will immediately bump up against the disappointingly small proportion of measures or evidence that apply to the typical Hospital Medicine patient. Developing these new measures, and the evidence for how to improve them, will be a key challenge for the field of Hospital Medicine. Outcome development and comparisons are a clear focus of the Patient‐Centered Outcomes Research Institute. Again, studies documenting such research will find a welcome home at JHM.

The role of information technology in how hospitalists provide care to patients, decide on best practices, communicate with physicians and patients, and manage their practices is becoming central. A huge, nationwide natural experiment is underway as health systems work to meet meaningful use criteria, and oftentimes hospitalists are central to these efforts. Disseminating best practices, implementing innovative systems, and creating workflows that meet the needs of hospitalists' patients is a key short‐term need, and one our field is uniquely positioned to address.

Finally, the practice of Hospital Medicine continues to evolve. In teaching centers, hospitalists are leading educators of medical students and residents; developing training models that reflect newer thinking about how to teach a 21st‐century physician is a key need for the field. The importance of adaptations to work‐hour reductions for residents cannot be overstated, but attention must be paid to how hospitalists' work hours impact patient care as well. Comanagement systemswhether for medical subspecialties (ie, cancer or heart failure) or surgical specialtieshave yet to fulfill their promise, yet demand for comanagement grows. How might comanagement systems be adapted and targeted so that they become more effective?

Not being a futurist or even slightly omniscient, I am sure this list is neither exhaustive nor final. In my 15 or so years in Hospital Medicine, I know firsthand that the field is vigorous, innovative, and full of surprises. Fortunately, JHM is attuned to changes happening now as well as issues on the horizon, and will always strive to be an even better messenger for Hospital Medicine as a professional and academic specialty.1 In that way, JHM 2.0 will be the same as JHM 1.0. I'm excited to shepherd JHM's ongoing growth and look forward to my years at the helm.

Acknowledgements

Funding Source: Dr. Auerbach is supported by National Heart, Lung, and Blood Institute Grant K24 K24HL098372.

Disclosure: The author discloses no relevant or financial conflicts of interest.

Ten years ago, leaders in Hospital Medicine saw the need for a peer‐reviewed Hospital Medicine journal, a key step in the growth of the field. However, there was no small amount of uncertainty as to whether there was room for another medical publication, or whether Hospital Medicine was ready for its own journal.

It's clear now that we should not have been worried. Our specialty has grown in size and influence, and the Journal of Hospital Medicine's growth has progressed along a similar track, linked to the success of the many leaders in our field, including the founders of the Society of Hospital Medicine: John Nelson, MD, MHM, Win Whitcomb, MD, MHM, and Bob Wachter, MD, MHM. Support from them in selecting the Founding Editor, Mark V. Williams, ensured his success in assembling an outstanding editorial team, developing JHM's editorial process, and setting this journal as the bestand not just the onlyjournal for hospitalists to publish their work. JHM serves as both a beacon and a mirror for the field of Hospital Medicine, and I am honored for the opportunity to lead this dynamic journal. I also owe special thanks to the Society of Hospital Medicine and the outstanding team at Wiley‐Blackwell, who have made my transition to this role a smooth one.

After the transition, JHM will continue to be a mirror for Hospital Medicine in that it will reflect the scholarship and innovation of hospitalists' scholarly work in research, quality improvement, education, and clinical excellence. From a practical standpoint, this means JHM will continue to do what it has done so successfully to date: provide fair, insightful, and rapid evaluation and publication of articles that are scientifically rigorous and have an impact on hospitalists and their patients. Being an effective mirror also means the journal will need to be in tune with technological advances in publication and learning. Few of us read paper journals any longer, and the move from print to digital and mobile media provides an important opportunity for this journal. Expanding the means by which we disseminate JHM's findings, highlight evidence, and promote knowledge that impacts our field is a clear direction for the journal.

At the transition from JHM 1.0 to JHM 2.0, the journal is positioned to be a beacon for the field by publishing papers that address new and rapidly evolving issues that will affect hospitalists and their patients. JHM and my editorial team eagerly seek submission of manuscripts on these issues delineated below.

Even if health care reform legislation evolves or changes after the 2012 elections, the need to improve health care value across multiple phases of care is unlikely to disappear. The medical home and accountable care organizations will prompt hospitalists to work with outpatient partners to achieve improvements; focus on readmissions and high‐utilization patients may catalyze integration even without larger changes. This evolution plays to hospitalists' traditional strengths as innovators and leaders of health system innovations while erasing the boundaries between inpatient and outpatient phases of care. How the field adapts toor even better, anticipateschanges in care delivery is a momentous opportunity.

Hospitalists will continue to be leaders in quality and safety improvement, but the need to develop innovations that are effective, scalable, and widely adoptable is growing even more acute. Stated alternately, we need to develop innovations quickly and rigorously, so that neither time nor resources are wasted. Fortunately, there is likely to be financial support for projects that link improvement and evaluation from the Center for Medicare and Medicaid Innovations (CMMI). It is a fair bet that a large number of the CMMI's target issues will be ones that hospitalists also find important, and which are ripe for inquiry.

Shifting from quality to outcomes will prompt a revisiting of how we measure our success as hospitalists. Achieving success in process benchmarks will no longer be sufficient, as our practices will increasingly be measured by our patients' experience, functional status, quality of life, and clinical events (of which measures of safety are a part)both within the walls of the hospital and afterwardrather than solely relying on whether patients appropriately received a drug or procedure during their stay. The need to improve outcomes will immediately bump up against the disappointingly small proportion of measures or evidence that apply to the typical Hospital Medicine patient. Developing these new measures, and the evidence for how to improve them, will be a key challenge for the field of Hospital Medicine. Outcome development and comparisons are a clear focus of the Patient‐Centered Outcomes Research Institute. Again, studies documenting such research will find a welcome home at JHM.

The role of information technology in how hospitalists provide care to patients, decide on best practices, communicate with physicians and patients, and manage their practices is becoming central. A huge, nationwide natural experiment is underway as health systems work to meet meaningful use criteria, and oftentimes hospitalists are central to these efforts. Disseminating best practices, implementing innovative systems, and creating workflows that meet the needs of hospitalists' patients is a key short‐term need, and one our field is uniquely positioned to address.

Finally, the practice of Hospital Medicine continues to evolve. In teaching centers, hospitalists are leading educators of medical students and residents; developing training models that reflect newer thinking about how to teach a 21st‐century physician is a key need for the field. The importance of adaptations to work‐hour reductions for residents cannot be overstated, but attention must be paid to how hospitalists' work hours impact patient care as well. Comanagement systemswhether for medical subspecialties (ie, cancer or heart failure) or surgical specialtieshave yet to fulfill their promise, yet demand for comanagement grows. How might comanagement systems be adapted and targeted so that they become more effective?

Not being a futurist or even slightly omniscient, I am sure this list is neither exhaustive nor final. In my 15 or so years in Hospital Medicine, I know firsthand that the field is vigorous, innovative, and full of surprises. Fortunately, JHM is attuned to changes happening now as well as issues on the horizon, and will always strive to be an even better messenger for Hospital Medicine as a professional and academic specialty.1 In that way, JHM 2.0 will be the same as JHM 1.0. I'm excited to shepherd JHM's ongoing growth and look forward to my years at the helm.

Acknowledgements

Funding Source: Dr. Auerbach is supported by National Heart, Lung, and Blood Institute Grant K24 K24HL098372.

Disclosure: The author discloses no relevant or financial conflicts of interest.

References
  1. Williams MV.Editor transition—getting up off the couch and walking out the door.J Hosp Med.2011;6:485486.
References
  1. Williams MV.Editor transition—getting up off the couch and walking out the door.J Hosp Med.2011;6:485486.
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JHM 2.0: The Journal of Hospital Medicine at its first transition
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A Grumpy Old Man

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A grumpy old man

Ms Chen acutely worse, altered, please assist, room 522Beth, chirped my pager. Ever increasing time pressures meant that hospitalists were supervising rounds almost daily. I had sent my resident, Beth, and the rest of the team to round separately that day, to foster their independence. It looked like we would be meeting ahead of schedule.

I'd received a similar page 2 years earlier when I was a junior resident myself. From the beginning of internship, our faculty never hesitated to challenge us. I will never forget when one of the hospitalists who had just come across an unresponsive patient tapped me on the shoulder and casually asked, Hey, you wanna run a code? and will never forget my inadequacy or the specific assistance I required in those tense few minutes. He, and the ICU team that arrived, gave me every chance to lead, and supported me each time I hesitated.

In similar fashion, I had sent my intern, David, to admit a patient with suspected CHF. I received his urgent update shortly after our patient arrived on the cardiology floor: Mr Johnson dropping sats, please help, room 207. I jogged to the patient's room, where I found David, 3 nurses, 2 medical students, and in the center, Mr Johnson: lethargic, gray, cachectic, and making no effort to rise from the 40 degree incline of his hospital bed. Weak respirations fogged his non‐rebreather mask about 28 times a minute.

David offered a quick report: 74‐year‐old male, CAD, hypertension, dementia CHF exacerbation hypertensive to 190. I think he needs IV nitroglycerin and another 80 of lasix.

I was pleased to hear him commit to a diagnosis and plan, but after sitting Mr Johnson up for a quick exam, I couldn't agree. Are you sure? He sounds more junky than crackly. Neck veins are flat.

His EF is 25% and he's been here 3 times with CHF.

Well, that won't protect him from anything else. Mr Johnson slumped forward, accessory muscles firing weakly, and only half‐opened his eyes to a loud command and vigorous shake. Well, let's get the diagnosis later, what does he need, now?

Well, the lasix and the nitro

Assuming this is CHF, looking at him now, will that work fast enough to prevent intubation? David shook his head no. He's full code, right? Let's just call a code before he gets any worse. Anyone disagree? A nurse made the call, then guarded the door to turn away everyone but anesthesia and the MICU as they arrived.

So what do you think it is? David asked.

This doesn't smell like failure. He's not anxious, he's more obtunded than dyspneic. He looks hypercarbic. He doesn't have COPD?

Nah, just vomiting, then weaker, more confused, restless.

Maybe he aspirated. We'll see. So what do you want to have ready for anesthesia?

Um, meds. An IV. Chest X‐ray ready.

Good they bring the meds he's got an IV how about we pull the bed from the wall and raise it up, get some suction ready, take the headboard off? Nurses sprang into action.

If he's hypercarbic, shouldn't we bag him? David asked.

Good point, I said. David took the mask from the bag of emergency gear from the wall and started to fit it on Mr Johnson. It's a 2‐person job, if you want to hold the mask2 hands, good. A nurse began ventilations, and I added some cricoid pressure. Keeps us from inflating his stomach.

Seconds later, anesthesia arrived, and David provided a concise, organized summary. Mr Johnson was intubated and whisked without incident to the MICU, where bronchoscopy extracted several mucus plugs. He was soon extubated, and later recovered from a delirium which began with promethazine for nausea. It was the last year before the 80‐hour workweek regulations, and not once in the entire processfrom admission, to emergency on the ward, to initial MICU managementdid I or my fellow residents think to call an attending, although I'm sure we would have learned something, as I hadn't suspected a mucous plug. We weren't hiding anything. We were just taking care of our patient.

Two years later, it didn't seem odd that my junior resident called me for assistance with Ms Cheninitially. In room 522, much as I found Mr Johnson, I found Ms Chen: elderly, lethargic, gray, frail, laboring to breathe, rhythmically fogging a non‐rebreather mask 30 times a minute, only half‐opening her eyes to a vigorous shake. It was day 4 of her fifth hospitalization for bronchiectasis‐related respiratory failure within 2 months.

She just got a treatment but she still sounds awful, offered Beth. Indeed, Ms Chen's chest was gurgly and wheezy throughout. We put her on a non‐rebreather, but that hasn't helped.

I glanced at her monitor. Sat's 99%. What was she before?

96%.

So hypoxia isn't the problemwho's this? I asked, as transportation staff arrived.

Stat head CT for Chen, he replied.

I'm sorry, she can't go off the floor right now. Thanks for coming, I apologized, and sent him away. Beth, can you lay her flat or send her off the unit right now?

She's altered and I need to rule out stroke.

Let's talk about that later. I did a quick neuro exam as I spoke: Besides, she resists weak but equal; pupils and face symmetricshe's not focal. What's a more likely cause?

Metabolic? We can repeat her morning labs

Will they be different? Why is she here? What's her exam telling you?

Beth took in the scene before her, as Ms Chen struggled weakly to ventilate her lungs, and after a brief pause she had it worked out. She's hypercarbic. She needs an ABG. You think she plugged? She shook her head, and grasped Ms Chen's hand in her own. But she really hates suctioning.

Well, she's DNI, and without it, she could die. Beth agreed; we also called for noninvasive ventilation. But the team missed much of the action. The medical student missed the entire eventaside from attempting to summarize it from second‐hand reports for rounds the following day. I realized only later that her intern had been pushed to the back of the room for the critical decisions (much like the students during Mr Johnson's emergency), and headed out midway to attend a mandatory teaching sessionthe chief residents had begun taking attendance. The resident soon left for noon conference and afternoon clinic, enlisting me to write transfer orders and call the family. Finished with her other work, and under pressure to bank time against work hour limitations, which she was at risk of violating, the intern signed her pager over to me and left in the early afternoon, after sheepishly asking me if I wouldn't mind keeping an eye on our patient.

Later, a translator and I met with the Chens to comfort them and plan care for the family matriarch, having found a quiet solarium we could use, with summery views of the city and ocean in the distance to belie the grim topic of discussion.

What is your understanding of her lung problem right now?

Nay yeega jee um'jee huigor fai ho jing yeung?

What were her hopes and fears about her health?

Nay jee um'jee huigor see seung hai mai ho tai hoi?

My mind drifted during the Cantonese as I thought about how I use the unique teaching opportunities offered by wholly translated meetings. Never check the time. This body language says I am listening. I am speaking to them, not the translator. I make notes because families don't remember much after the C‐word, I would whisper to trainees while families conversed with translators. Now, as I began to discuss hospice philosophy, I felt acutely alone.

My team had missed most of a great hospital medicine experience: applying knowledge to manage a physiologic crisis; using communication skills to ease the resulting human crisis. Recently, to manage the latest set of work hour restrictions, our residency program withdrew from medicine consultation at 2 of 3 sites, and from the medicine wards at the hospital that serves most of our insured, geriatric, and oncology patients. The cost of this experiment to the overall residency experience is unknown. But cases like Ms Chen's remind me how much I missed being the primary doctor. I do not mind the new tasks I perform for my trainees. But I worry about what they are missing: sufficient responsibility for making key clinical decisions while protected by supervision on demand. I am glad my internship challenged meit prepared me for residency, moonlighting, and attending positions. Without a doubt, residency remains challenging, but it seems that the greatestor firstchallenge imposed on residents is now to beat the clock, not to become a well‐rounded, capable, independent physician.

That night, I complained to my spouse, then a psychiatry intern: We weren't giving our trainees the best preparation for a career in medicine the lengthy shift I spent managing a hypotensive crisis would be forbidden now my pre‐work hours interns were much happier than their work hours successors a 4‐year residency must be around the corner. The response I got was more bemused smile than grave concern. You don't think that's important? I asked.

Of course I do. It's just that with all this talk about the days of the giants, he said gently, you're starting to sound like a grumpy old man. We chuckled. He was right. I expect a lot from myself, my trainees, and every clinician. I'd figured I'd be worthy of the title at some point.

But at 30?

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Ms Chen acutely worse, altered, please assist, room 522Beth, chirped my pager. Ever increasing time pressures meant that hospitalists were supervising rounds almost daily. I had sent my resident, Beth, and the rest of the team to round separately that day, to foster their independence. It looked like we would be meeting ahead of schedule.

I'd received a similar page 2 years earlier when I was a junior resident myself. From the beginning of internship, our faculty never hesitated to challenge us. I will never forget when one of the hospitalists who had just come across an unresponsive patient tapped me on the shoulder and casually asked, Hey, you wanna run a code? and will never forget my inadequacy or the specific assistance I required in those tense few minutes. He, and the ICU team that arrived, gave me every chance to lead, and supported me each time I hesitated.

In similar fashion, I had sent my intern, David, to admit a patient with suspected CHF. I received his urgent update shortly after our patient arrived on the cardiology floor: Mr Johnson dropping sats, please help, room 207. I jogged to the patient's room, where I found David, 3 nurses, 2 medical students, and in the center, Mr Johnson: lethargic, gray, cachectic, and making no effort to rise from the 40 degree incline of his hospital bed. Weak respirations fogged his non‐rebreather mask about 28 times a minute.

David offered a quick report: 74‐year‐old male, CAD, hypertension, dementia CHF exacerbation hypertensive to 190. I think he needs IV nitroglycerin and another 80 of lasix.

I was pleased to hear him commit to a diagnosis and plan, but after sitting Mr Johnson up for a quick exam, I couldn't agree. Are you sure? He sounds more junky than crackly. Neck veins are flat.

His EF is 25% and he's been here 3 times with CHF.

Well, that won't protect him from anything else. Mr Johnson slumped forward, accessory muscles firing weakly, and only half‐opened his eyes to a loud command and vigorous shake. Well, let's get the diagnosis later, what does he need, now?

Well, the lasix and the nitro

Assuming this is CHF, looking at him now, will that work fast enough to prevent intubation? David shook his head no. He's full code, right? Let's just call a code before he gets any worse. Anyone disagree? A nurse made the call, then guarded the door to turn away everyone but anesthesia and the MICU as they arrived.

So what do you think it is? David asked.

This doesn't smell like failure. He's not anxious, he's more obtunded than dyspneic. He looks hypercarbic. He doesn't have COPD?

Nah, just vomiting, then weaker, more confused, restless.

Maybe he aspirated. We'll see. So what do you want to have ready for anesthesia?

Um, meds. An IV. Chest X‐ray ready.

Good they bring the meds he's got an IV how about we pull the bed from the wall and raise it up, get some suction ready, take the headboard off? Nurses sprang into action.

If he's hypercarbic, shouldn't we bag him? David asked.

Good point, I said. David took the mask from the bag of emergency gear from the wall and started to fit it on Mr Johnson. It's a 2‐person job, if you want to hold the mask2 hands, good. A nurse began ventilations, and I added some cricoid pressure. Keeps us from inflating his stomach.

Seconds later, anesthesia arrived, and David provided a concise, organized summary. Mr Johnson was intubated and whisked without incident to the MICU, where bronchoscopy extracted several mucus plugs. He was soon extubated, and later recovered from a delirium which began with promethazine for nausea. It was the last year before the 80‐hour workweek regulations, and not once in the entire processfrom admission, to emergency on the ward, to initial MICU managementdid I or my fellow residents think to call an attending, although I'm sure we would have learned something, as I hadn't suspected a mucous plug. We weren't hiding anything. We were just taking care of our patient.

Two years later, it didn't seem odd that my junior resident called me for assistance with Ms Cheninitially. In room 522, much as I found Mr Johnson, I found Ms Chen: elderly, lethargic, gray, frail, laboring to breathe, rhythmically fogging a non‐rebreather mask 30 times a minute, only half‐opening her eyes to a vigorous shake. It was day 4 of her fifth hospitalization for bronchiectasis‐related respiratory failure within 2 months.

She just got a treatment but she still sounds awful, offered Beth. Indeed, Ms Chen's chest was gurgly and wheezy throughout. We put her on a non‐rebreather, but that hasn't helped.

I glanced at her monitor. Sat's 99%. What was she before?

96%.

So hypoxia isn't the problemwho's this? I asked, as transportation staff arrived.

Stat head CT for Chen, he replied.

I'm sorry, she can't go off the floor right now. Thanks for coming, I apologized, and sent him away. Beth, can you lay her flat or send her off the unit right now?

She's altered and I need to rule out stroke.

Let's talk about that later. I did a quick neuro exam as I spoke: Besides, she resists weak but equal; pupils and face symmetricshe's not focal. What's a more likely cause?

Metabolic? We can repeat her morning labs

Will they be different? Why is she here? What's her exam telling you?

Beth took in the scene before her, as Ms Chen struggled weakly to ventilate her lungs, and after a brief pause she had it worked out. She's hypercarbic. She needs an ABG. You think she plugged? She shook her head, and grasped Ms Chen's hand in her own. But she really hates suctioning.

Well, she's DNI, and without it, she could die. Beth agreed; we also called for noninvasive ventilation. But the team missed much of the action. The medical student missed the entire eventaside from attempting to summarize it from second‐hand reports for rounds the following day. I realized only later that her intern had been pushed to the back of the room for the critical decisions (much like the students during Mr Johnson's emergency), and headed out midway to attend a mandatory teaching sessionthe chief residents had begun taking attendance. The resident soon left for noon conference and afternoon clinic, enlisting me to write transfer orders and call the family. Finished with her other work, and under pressure to bank time against work hour limitations, which she was at risk of violating, the intern signed her pager over to me and left in the early afternoon, after sheepishly asking me if I wouldn't mind keeping an eye on our patient.

Later, a translator and I met with the Chens to comfort them and plan care for the family matriarch, having found a quiet solarium we could use, with summery views of the city and ocean in the distance to belie the grim topic of discussion.

What is your understanding of her lung problem right now?

Nay yeega jee um'jee huigor fai ho jing yeung?

What were her hopes and fears about her health?

Nay jee um'jee huigor see seung hai mai ho tai hoi?

My mind drifted during the Cantonese as I thought about how I use the unique teaching opportunities offered by wholly translated meetings. Never check the time. This body language says I am listening. I am speaking to them, not the translator. I make notes because families don't remember much after the C‐word, I would whisper to trainees while families conversed with translators. Now, as I began to discuss hospice philosophy, I felt acutely alone.

My team had missed most of a great hospital medicine experience: applying knowledge to manage a physiologic crisis; using communication skills to ease the resulting human crisis. Recently, to manage the latest set of work hour restrictions, our residency program withdrew from medicine consultation at 2 of 3 sites, and from the medicine wards at the hospital that serves most of our insured, geriatric, and oncology patients. The cost of this experiment to the overall residency experience is unknown. But cases like Ms Chen's remind me how much I missed being the primary doctor. I do not mind the new tasks I perform for my trainees. But I worry about what they are missing: sufficient responsibility for making key clinical decisions while protected by supervision on demand. I am glad my internship challenged meit prepared me for residency, moonlighting, and attending positions. Without a doubt, residency remains challenging, but it seems that the greatestor firstchallenge imposed on residents is now to beat the clock, not to become a well‐rounded, capable, independent physician.

That night, I complained to my spouse, then a psychiatry intern: We weren't giving our trainees the best preparation for a career in medicine the lengthy shift I spent managing a hypotensive crisis would be forbidden now my pre‐work hours interns were much happier than their work hours successors a 4‐year residency must be around the corner. The response I got was more bemused smile than grave concern. You don't think that's important? I asked.

Of course I do. It's just that with all this talk about the days of the giants, he said gently, you're starting to sound like a grumpy old man. We chuckled. He was right. I expect a lot from myself, my trainees, and every clinician. I'd figured I'd be worthy of the title at some point.

But at 30?

Ms Chen acutely worse, altered, please assist, room 522Beth, chirped my pager. Ever increasing time pressures meant that hospitalists were supervising rounds almost daily. I had sent my resident, Beth, and the rest of the team to round separately that day, to foster their independence. It looked like we would be meeting ahead of schedule.

I'd received a similar page 2 years earlier when I was a junior resident myself. From the beginning of internship, our faculty never hesitated to challenge us. I will never forget when one of the hospitalists who had just come across an unresponsive patient tapped me on the shoulder and casually asked, Hey, you wanna run a code? and will never forget my inadequacy or the specific assistance I required in those tense few minutes. He, and the ICU team that arrived, gave me every chance to lead, and supported me each time I hesitated.

In similar fashion, I had sent my intern, David, to admit a patient with suspected CHF. I received his urgent update shortly after our patient arrived on the cardiology floor: Mr Johnson dropping sats, please help, room 207. I jogged to the patient's room, where I found David, 3 nurses, 2 medical students, and in the center, Mr Johnson: lethargic, gray, cachectic, and making no effort to rise from the 40 degree incline of his hospital bed. Weak respirations fogged his non‐rebreather mask about 28 times a minute.

David offered a quick report: 74‐year‐old male, CAD, hypertension, dementia CHF exacerbation hypertensive to 190. I think he needs IV nitroglycerin and another 80 of lasix.

I was pleased to hear him commit to a diagnosis and plan, but after sitting Mr Johnson up for a quick exam, I couldn't agree. Are you sure? He sounds more junky than crackly. Neck veins are flat.

His EF is 25% and he's been here 3 times with CHF.

Well, that won't protect him from anything else. Mr Johnson slumped forward, accessory muscles firing weakly, and only half‐opened his eyes to a loud command and vigorous shake. Well, let's get the diagnosis later, what does he need, now?

Well, the lasix and the nitro

Assuming this is CHF, looking at him now, will that work fast enough to prevent intubation? David shook his head no. He's full code, right? Let's just call a code before he gets any worse. Anyone disagree? A nurse made the call, then guarded the door to turn away everyone but anesthesia and the MICU as they arrived.

So what do you think it is? David asked.

This doesn't smell like failure. He's not anxious, he's more obtunded than dyspneic. He looks hypercarbic. He doesn't have COPD?

Nah, just vomiting, then weaker, more confused, restless.

Maybe he aspirated. We'll see. So what do you want to have ready for anesthesia?

Um, meds. An IV. Chest X‐ray ready.

Good they bring the meds he's got an IV how about we pull the bed from the wall and raise it up, get some suction ready, take the headboard off? Nurses sprang into action.

If he's hypercarbic, shouldn't we bag him? David asked.

Good point, I said. David took the mask from the bag of emergency gear from the wall and started to fit it on Mr Johnson. It's a 2‐person job, if you want to hold the mask2 hands, good. A nurse began ventilations, and I added some cricoid pressure. Keeps us from inflating his stomach.

Seconds later, anesthesia arrived, and David provided a concise, organized summary. Mr Johnson was intubated and whisked without incident to the MICU, where bronchoscopy extracted several mucus plugs. He was soon extubated, and later recovered from a delirium which began with promethazine for nausea. It was the last year before the 80‐hour workweek regulations, and not once in the entire processfrom admission, to emergency on the ward, to initial MICU managementdid I or my fellow residents think to call an attending, although I'm sure we would have learned something, as I hadn't suspected a mucous plug. We weren't hiding anything. We were just taking care of our patient.

Two years later, it didn't seem odd that my junior resident called me for assistance with Ms Cheninitially. In room 522, much as I found Mr Johnson, I found Ms Chen: elderly, lethargic, gray, frail, laboring to breathe, rhythmically fogging a non‐rebreather mask 30 times a minute, only half‐opening her eyes to a vigorous shake. It was day 4 of her fifth hospitalization for bronchiectasis‐related respiratory failure within 2 months.

She just got a treatment but she still sounds awful, offered Beth. Indeed, Ms Chen's chest was gurgly and wheezy throughout. We put her on a non‐rebreather, but that hasn't helped.

I glanced at her monitor. Sat's 99%. What was she before?

96%.

So hypoxia isn't the problemwho's this? I asked, as transportation staff arrived.

Stat head CT for Chen, he replied.

I'm sorry, she can't go off the floor right now. Thanks for coming, I apologized, and sent him away. Beth, can you lay her flat or send her off the unit right now?

She's altered and I need to rule out stroke.

Let's talk about that later. I did a quick neuro exam as I spoke: Besides, she resists weak but equal; pupils and face symmetricshe's not focal. What's a more likely cause?

Metabolic? We can repeat her morning labs

Will they be different? Why is she here? What's her exam telling you?

Beth took in the scene before her, as Ms Chen struggled weakly to ventilate her lungs, and after a brief pause she had it worked out. She's hypercarbic. She needs an ABG. You think she plugged? She shook her head, and grasped Ms Chen's hand in her own. But she really hates suctioning.

Well, she's DNI, and without it, she could die. Beth agreed; we also called for noninvasive ventilation. But the team missed much of the action. The medical student missed the entire eventaside from attempting to summarize it from second‐hand reports for rounds the following day. I realized only later that her intern had been pushed to the back of the room for the critical decisions (much like the students during Mr Johnson's emergency), and headed out midway to attend a mandatory teaching sessionthe chief residents had begun taking attendance. The resident soon left for noon conference and afternoon clinic, enlisting me to write transfer orders and call the family. Finished with her other work, and under pressure to bank time against work hour limitations, which she was at risk of violating, the intern signed her pager over to me and left in the early afternoon, after sheepishly asking me if I wouldn't mind keeping an eye on our patient.

Later, a translator and I met with the Chens to comfort them and plan care for the family matriarch, having found a quiet solarium we could use, with summery views of the city and ocean in the distance to belie the grim topic of discussion.

What is your understanding of her lung problem right now?

Nay yeega jee um'jee huigor fai ho jing yeung?

What were her hopes and fears about her health?

Nay jee um'jee huigor see seung hai mai ho tai hoi?

My mind drifted during the Cantonese as I thought about how I use the unique teaching opportunities offered by wholly translated meetings. Never check the time. This body language says I am listening. I am speaking to them, not the translator. I make notes because families don't remember much after the C‐word, I would whisper to trainees while families conversed with translators. Now, as I began to discuss hospice philosophy, I felt acutely alone.

My team had missed most of a great hospital medicine experience: applying knowledge to manage a physiologic crisis; using communication skills to ease the resulting human crisis. Recently, to manage the latest set of work hour restrictions, our residency program withdrew from medicine consultation at 2 of 3 sites, and from the medicine wards at the hospital that serves most of our insured, geriatric, and oncology patients. The cost of this experiment to the overall residency experience is unknown. But cases like Ms Chen's remind me how much I missed being the primary doctor. I do not mind the new tasks I perform for my trainees. But I worry about what they are missing: sufficient responsibility for making key clinical decisions while protected by supervision on demand. I am glad my internship challenged meit prepared me for residency, moonlighting, and attending positions. Without a doubt, residency remains challenging, but it seems that the greatestor firstchallenge imposed on residents is now to beat the clock, not to become a well‐rounded, capable, independent physician.

That night, I complained to my spouse, then a psychiatry intern: We weren't giving our trainees the best preparation for a career in medicine the lengthy shift I spent managing a hypotensive crisis would be forbidden now my pre‐work hours interns were much happier than their work hours successors a 4‐year residency must be around the corner. The response I got was more bemused smile than grave concern. You don't think that's important? I asked.

Of course I do. It's just that with all this talk about the days of the giants, he said gently, you're starting to sound like a grumpy old man. We chuckled. He was right. I expect a lot from myself, my trainees, and every clinician. I'd figured I'd be worthy of the title at some point.

But at 30?

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Journal of Hospital Medicine - 7(2)
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Journal of Hospital Medicine - 7(2)
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154-155
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A grumpy old man
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Department of Medicine, University of California, San Diego Medical Center, 200 W Arbor Dr, MC 8485, San Diego, CA 92103
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Chief resident year as stepping stone to attending academic hospitalist

Academic hospitalists have multiple duties including direct patient care, hospital management, teaching, and scholarly productivity. We are frequently pulled in divergent directions, while attending to these responsibilities. Without a framework to manage these assorted tasks, we are at risk of subpar performance and career dissatisfaction. Alternatively, we often thrive in our roles as utility players when armed with a developed skill set. Our profession could benefit greatly from encouraging future academic hospitalists to obtain further training prior to starting as an attending. Although hospital medicine fellowship training exists, there are still relatively few programs available. A well‐crafted year spent as a chief medical resident (CMR) may be a viable alternative.

My year as CMR allowed me to develop the skills necessary for success as an academic hospitalist in a supportive setting, and has given me an advantage in accelerating my career. This experience provided me with important tools that my initial 3 years of internal medicine residency did not. Even during my final year of residency, I was focused mostly on obtaining medical knowledge, learning its clinical applications, and honing team leadership skills. My mind rarely trespassed into the broader concerns of quality improvement initiatives, educational enhancements, or hospital management issues. Although the American College of Graduate Medical Education (ACGME) core competencies are helping to better focus residents' attention to these more diverse aspects of healthcare, residents still spend the majority of their time providing direct patient care.1 Now in my fourth year as an attending academic hospitalist, I continue to appreciate how my chief experience provided the foundation for much of the work I perform today.

My motivations for becoming a CMR included a desire to spend more time teaching and learning medicine, and an interest in helping to improve the residency program itself. I did not appreciate how much of the job would be spent managing people, and evaluating systems of care within the hospital, while working closely with nurses and hospital administrators. However, the skills I learned while addressing those unexpected tasks are what continue to help me in my position as a multifaceted hospitalist today. CMRs have been described as middle managers, being pushed and pulled by the demands and requirements of the groups above, below and around them.2 Academic hospitalists who frequently wear administrative and educational hats are not dissimilar. Retrospectively, I realize how fortunate I was to be exposed to those aspects as a CMR, with many of the same responsibilities but without the full expectations of a more seasoned attending.

The most memorable interaction during my first day as junior ward attending was with a revered internist, himself a former CMR, who dryly commented, So, you're pretending now. It took me a moment to catch his play on words until he clarified, you are now a pre‐attending. The true meaning of this was elucidated over the next several weeks as I was expected to perform many of the same duties of a seasoned attending, but often had the sense that I was only pretending to be an attending and still had much to learn.

CMR positions vary in terms of clinical, educational, and administrative responsibilities. Moreover, many institutions mix inpatient and outpatient roles. My position was focused almost entirely on inpatient duties at a single hospital, which gave me an in‐depth and longitudinal view of how a hospital is managed. Like many other CMRs, much of my time was spent on educational activities, such as running morning report, preparing for chief of medicine rounds, coordinating noon teaching conferences, and spending time with the medical students. Administrative tasks included various institutional‐based meetings for student grading, educational review committees, and program scheduling. In addition, I spent 1 month as junior attending on a ward team. Many other programs' CMRs spend more time as junior attending; however, by offloading some of this ward service requirement, I feel fortunate to have had that time to use for my own scholarly activity and teaching/administrative opportunities. Perhaps unique to my CMR position, I also was involved with the daily running of the hospital by working with administrators to evaluate patient transfer requests and addressing provider work flow issues. These additional tasks provided an invaluable learning experience.

Organizing morning report, running physical diagnosis rounds, and preparing cases and speakers for Chair's Rounds allowed me to hone and expand my teaching skills in ways that 3 years of residency did not. Moreover, it put me in direct contact with an energetic, inspiring group of learners that challenged me to solidify my own medical knowledge. (Try explaining the delta‐delta equation to figure out if there are 2 metabolic processes going on, in front of a group of 20 residents, and you'll discover what I mean.) I quickly learned that the one doing the talking is the one doing the learning and changed my teaching style to better facilitate student learning. My bedside learning was further augmented by attending Masters' Rounds to which I owe my ongoing interests in physical diagnosis. Masters Rounds were given once a week by 2 master clinicians. It was only for chief residents and was directed at teaching us how to teach others the art of bedside physical diagnosis. The majority of physical exam teaching points I focus on today come from those sessions.

As chief, I felt like I had the pulse of the hospital at all times. Most of my mornings were spent on the wards floating between teams. I owe thanks to my predecessor who told me that the true sign of a good CMR was to never sit long enough in your chair to let it get warm. My office was located on the wards, between a team room and a double patient room. Aside from times when I was having confidential conversations with residents, the door was open. Nurses looking to vent, phlebotomists wanting to sit down, and attendings needing a break from their teams to get work done were common visitors. Administrative personnel were also frequent visitors, usually requesting me to disseminate new policies to the residents. Because of this, I learned to understand and better interact with the diverse group of people responsible for making a teaching hospital function. These are the same constituencies that I now sit down with on various committees to attempt to make my present hospital operate more smoothly.

Despite running morning report, attending rounds with teams, and developing plans for better patient flow, I had time for scholarly work and found easy mentorship. I was able to revive 2 projects I had started as a resident and bring them close to conclusion under the continued mentorship of my coinvestigators. Offers for career skill development were also abound, and I benefited greatly from one associate director's tutorials on preparing effective PowerPoint presentations. Another attending mentored me in student feedback skills, which have allowed me to become a much more effective educator. I was also able to model that mentorship and begin to build my own mentor relationships with my students. In fact, this mentorship has become one of the most fulfilling aspects of my job. I was fortunate to have that mentorship early on in my career, as similar mentorship becomes difficult to obtain once in an attending hospitalist position.3

In conclusion, although current internal medicine residency training provides intensive direct patient care experiences, it only allows glimpses into the other aspects of an academic hospitalist's job. Unfortunately, it does not adequately prepare one to begin this type of position with a full complement of skills. Only a minority of hospitalists pursue additional structured training directly after residency; the majority jump into hospitalist positions and opt for on‐the‐job training. While there is an early economic advantage to starting an attending position without delay, I believe that the skills learned during an additional year of dedicated training allow for a more meaningful work experience and, ultimately, a faster rise within the track of an academic hospitalist.

The tasks that residency programs and hospitals may give to CMRs provide fertile material for developing the skills necessary to become a productive academic hospitalist. I thrived on the multifaceted work of caring for a diverse group of patients, teaching different levels of learners, helping to manage various hospital systems, and better understanding the hospital as the sum of its parts. As noted above, this pre‐attending league gave me the exposure to more fully develop my academic hospitalist game in a supportive environment. A CMR year may be beneficial for residents entering any career in internal medicine; however, I believe it is most aptly suited as a stepping stone for future academic hospitalists. I strongly recommend that current residents interested in academic hospital medicine consider a CMR position, and encourage program directors to consider molding their inpatient CMR experiences to facilitate this. Moreover, unless fellowship training in hospital medicine becomes the norm, I propose that current academic hospitalists do more to closely court and usher these pretenders into our ranks.

Files
References
  1. Varkey P,Karlapudi S,Rose S,Nelson R,Warner M.A systems approach for implementing practice‐based learning and improvement and systems‐based practice in graduate medical education.Acad Med.2009;84(3):335339.
  2. Berg DN,Huot SJ.Middle manager role of the chief medical resident: an organizational psychologist's perspective.J Gen Intern Med.2007;22(12):17711774.
  3. Harrison R,Hunter AJ,Sharpe B,Auerbach AD.Survey of US academic hospitalist leaders about mentorship and academic activities in hospitalist groups.J Hosp Med.2011;6:59.
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Journal of Hospital Medicine - 6(9)
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Academic hospitalists have multiple duties including direct patient care, hospital management, teaching, and scholarly productivity. We are frequently pulled in divergent directions, while attending to these responsibilities. Without a framework to manage these assorted tasks, we are at risk of subpar performance and career dissatisfaction. Alternatively, we often thrive in our roles as utility players when armed with a developed skill set. Our profession could benefit greatly from encouraging future academic hospitalists to obtain further training prior to starting as an attending. Although hospital medicine fellowship training exists, there are still relatively few programs available. A well‐crafted year spent as a chief medical resident (CMR) may be a viable alternative.

My year as CMR allowed me to develop the skills necessary for success as an academic hospitalist in a supportive setting, and has given me an advantage in accelerating my career. This experience provided me with important tools that my initial 3 years of internal medicine residency did not. Even during my final year of residency, I was focused mostly on obtaining medical knowledge, learning its clinical applications, and honing team leadership skills. My mind rarely trespassed into the broader concerns of quality improvement initiatives, educational enhancements, or hospital management issues. Although the American College of Graduate Medical Education (ACGME) core competencies are helping to better focus residents' attention to these more diverse aspects of healthcare, residents still spend the majority of their time providing direct patient care.1 Now in my fourth year as an attending academic hospitalist, I continue to appreciate how my chief experience provided the foundation for much of the work I perform today.

My motivations for becoming a CMR included a desire to spend more time teaching and learning medicine, and an interest in helping to improve the residency program itself. I did not appreciate how much of the job would be spent managing people, and evaluating systems of care within the hospital, while working closely with nurses and hospital administrators. However, the skills I learned while addressing those unexpected tasks are what continue to help me in my position as a multifaceted hospitalist today. CMRs have been described as middle managers, being pushed and pulled by the demands and requirements of the groups above, below and around them.2 Academic hospitalists who frequently wear administrative and educational hats are not dissimilar. Retrospectively, I realize how fortunate I was to be exposed to those aspects as a CMR, with many of the same responsibilities but without the full expectations of a more seasoned attending.

The most memorable interaction during my first day as junior ward attending was with a revered internist, himself a former CMR, who dryly commented, So, you're pretending now. It took me a moment to catch his play on words until he clarified, you are now a pre‐attending. The true meaning of this was elucidated over the next several weeks as I was expected to perform many of the same duties of a seasoned attending, but often had the sense that I was only pretending to be an attending and still had much to learn.

CMR positions vary in terms of clinical, educational, and administrative responsibilities. Moreover, many institutions mix inpatient and outpatient roles. My position was focused almost entirely on inpatient duties at a single hospital, which gave me an in‐depth and longitudinal view of how a hospital is managed. Like many other CMRs, much of my time was spent on educational activities, such as running morning report, preparing for chief of medicine rounds, coordinating noon teaching conferences, and spending time with the medical students. Administrative tasks included various institutional‐based meetings for student grading, educational review committees, and program scheduling. In addition, I spent 1 month as junior attending on a ward team. Many other programs' CMRs spend more time as junior attending; however, by offloading some of this ward service requirement, I feel fortunate to have had that time to use for my own scholarly activity and teaching/administrative opportunities. Perhaps unique to my CMR position, I also was involved with the daily running of the hospital by working with administrators to evaluate patient transfer requests and addressing provider work flow issues. These additional tasks provided an invaluable learning experience.

Organizing morning report, running physical diagnosis rounds, and preparing cases and speakers for Chair's Rounds allowed me to hone and expand my teaching skills in ways that 3 years of residency did not. Moreover, it put me in direct contact with an energetic, inspiring group of learners that challenged me to solidify my own medical knowledge. (Try explaining the delta‐delta equation to figure out if there are 2 metabolic processes going on, in front of a group of 20 residents, and you'll discover what I mean.) I quickly learned that the one doing the talking is the one doing the learning and changed my teaching style to better facilitate student learning. My bedside learning was further augmented by attending Masters' Rounds to which I owe my ongoing interests in physical diagnosis. Masters Rounds were given once a week by 2 master clinicians. It was only for chief residents and was directed at teaching us how to teach others the art of bedside physical diagnosis. The majority of physical exam teaching points I focus on today come from those sessions.

As chief, I felt like I had the pulse of the hospital at all times. Most of my mornings were spent on the wards floating between teams. I owe thanks to my predecessor who told me that the true sign of a good CMR was to never sit long enough in your chair to let it get warm. My office was located on the wards, between a team room and a double patient room. Aside from times when I was having confidential conversations with residents, the door was open. Nurses looking to vent, phlebotomists wanting to sit down, and attendings needing a break from their teams to get work done were common visitors. Administrative personnel were also frequent visitors, usually requesting me to disseminate new policies to the residents. Because of this, I learned to understand and better interact with the diverse group of people responsible for making a teaching hospital function. These are the same constituencies that I now sit down with on various committees to attempt to make my present hospital operate more smoothly.

Despite running morning report, attending rounds with teams, and developing plans for better patient flow, I had time for scholarly work and found easy mentorship. I was able to revive 2 projects I had started as a resident and bring them close to conclusion under the continued mentorship of my coinvestigators. Offers for career skill development were also abound, and I benefited greatly from one associate director's tutorials on preparing effective PowerPoint presentations. Another attending mentored me in student feedback skills, which have allowed me to become a much more effective educator. I was also able to model that mentorship and begin to build my own mentor relationships with my students. In fact, this mentorship has become one of the most fulfilling aspects of my job. I was fortunate to have that mentorship early on in my career, as similar mentorship becomes difficult to obtain once in an attending hospitalist position.3

In conclusion, although current internal medicine residency training provides intensive direct patient care experiences, it only allows glimpses into the other aspects of an academic hospitalist's job. Unfortunately, it does not adequately prepare one to begin this type of position with a full complement of skills. Only a minority of hospitalists pursue additional structured training directly after residency; the majority jump into hospitalist positions and opt for on‐the‐job training. While there is an early economic advantage to starting an attending position without delay, I believe that the skills learned during an additional year of dedicated training allow for a more meaningful work experience and, ultimately, a faster rise within the track of an academic hospitalist.

The tasks that residency programs and hospitals may give to CMRs provide fertile material for developing the skills necessary to become a productive academic hospitalist. I thrived on the multifaceted work of caring for a diverse group of patients, teaching different levels of learners, helping to manage various hospital systems, and better understanding the hospital as the sum of its parts. As noted above, this pre‐attending league gave me the exposure to more fully develop my academic hospitalist game in a supportive environment. A CMR year may be beneficial for residents entering any career in internal medicine; however, I believe it is most aptly suited as a stepping stone for future academic hospitalists. I strongly recommend that current residents interested in academic hospital medicine consider a CMR position, and encourage program directors to consider molding their inpatient CMR experiences to facilitate this. Moreover, unless fellowship training in hospital medicine becomes the norm, I propose that current academic hospitalists do more to closely court and usher these pretenders into our ranks.

Academic hospitalists have multiple duties including direct patient care, hospital management, teaching, and scholarly productivity. We are frequently pulled in divergent directions, while attending to these responsibilities. Without a framework to manage these assorted tasks, we are at risk of subpar performance and career dissatisfaction. Alternatively, we often thrive in our roles as utility players when armed with a developed skill set. Our profession could benefit greatly from encouraging future academic hospitalists to obtain further training prior to starting as an attending. Although hospital medicine fellowship training exists, there are still relatively few programs available. A well‐crafted year spent as a chief medical resident (CMR) may be a viable alternative.

My year as CMR allowed me to develop the skills necessary for success as an academic hospitalist in a supportive setting, and has given me an advantage in accelerating my career. This experience provided me with important tools that my initial 3 years of internal medicine residency did not. Even during my final year of residency, I was focused mostly on obtaining medical knowledge, learning its clinical applications, and honing team leadership skills. My mind rarely trespassed into the broader concerns of quality improvement initiatives, educational enhancements, or hospital management issues. Although the American College of Graduate Medical Education (ACGME) core competencies are helping to better focus residents' attention to these more diverse aspects of healthcare, residents still spend the majority of their time providing direct patient care.1 Now in my fourth year as an attending academic hospitalist, I continue to appreciate how my chief experience provided the foundation for much of the work I perform today.

My motivations for becoming a CMR included a desire to spend more time teaching and learning medicine, and an interest in helping to improve the residency program itself. I did not appreciate how much of the job would be spent managing people, and evaluating systems of care within the hospital, while working closely with nurses and hospital administrators. However, the skills I learned while addressing those unexpected tasks are what continue to help me in my position as a multifaceted hospitalist today. CMRs have been described as middle managers, being pushed and pulled by the demands and requirements of the groups above, below and around them.2 Academic hospitalists who frequently wear administrative and educational hats are not dissimilar. Retrospectively, I realize how fortunate I was to be exposed to those aspects as a CMR, with many of the same responsibilities but without the full expectations of a more seasoned attending.

The most memorable interaction during my first day as junior ward attending was with a revered internist, himself a former CMR, who dryly commented, So, you're pretending now. It took me a moment to catch his play on words until he clarified, you are now a pre‐attending. The true meaning of this was elucidated over the next several weeks as I was expected to perform many of the same duties of a seasoned attending, but often had the sense that I was only pretending to be an attending and still had much to learn.

CMR positions vary in terms of clinical, educational, and administrative responsibilities. Moreover, many institutions mix inpatient and outpatient roles. My position was focused almost entirely on inpatient duties at a single hospital, which gave me an in‐depth and longitudinal view of how a hospital is managed. Like many other CMRs, much of my time was spent on educational activities, such as running morning report, preparing for chief of medicine rounds, coordinating noon teaching conferences, and spending time with the medical students. Administrative tasks included various institutional‐based meetings for student grading, educational review committees, and program scheduling. In addition, I spent 1 month as junior attending on a ward team. Many other programs' CMRs spend more time as junior attending; however, by offloading some of this ward service requirement, I feel fortunate to have had that time to use for my own scholarly activity and teaching/administrative opportunities. Perhaps unique to my CMR position, I also was involved with the daily running of the hospital by working with administrators to evaluate patient transfer requests and addressing provider work flow issues. These additional tasks provided an invaluable learning experience.

Organizing morning report, running physical diagnosis rounds, and preparing cases and speakers for Chair's Rounds allowed me to hone and expand my teaching skills in ways that 3 years of residency did not. Moreover, it put me in direct contact with an energetic, inspiring group of learners that challenged me to solidify my own medical knowledge. (Try explaining the delta‐delta equation to figure out if there are 2 metabolic processes going on, in front of a group of 20 residents, and you'll discover what I mean.) I quickly learned that the one doing the talking is the one doing the learning and changed my teaching style to better facilitate student learning. My bedside learning was further augmented by attending Masters' Rounds to which I owe my ongoing interests in physical diagnosis. Masters Rounds were given once a week by 2 master clinicians. It was only for chief residents and was directed at teaching us how to teach others the art of bedside physical diagnosis. The majority of physical exam teaching points I focus on today come from those sessions.

As chief, I felt like I had the pulse of the hospital at all times. Most of my mornings were spent on the wards floating between teams. I owe thanks to my predecessor who told me that the true sign of a good CMR was to never sit long enough in your chair to let it get warm. My office was located on the wards, between a team room and a double patient room. Aside from times when I was having confidential conversations with residents, the door was open. Nurses looking to vent, phlebotomists wanting to sit down, and attendings needing a break from their teams to get work done were common visitors. Administrative personnel were also frequent visitors, usually requesting me to disseminate new policies to the residents. Because of this, I learned to understand and better interact with the diverse group of people responsible for making a teaching hospital function. These are the same constituencies that I now sit down with on various committees to attempt to make my present hospital operate more smoothly.

Despite running morning report, attending rounds with teams, and developing plans for better patient flow, I had time for scholarly work and found easy mentorship. I was able to revive 2 projects I had started as a resident and bring them close to conclusion under the continued mentorship of my coinvestigators. Offers for career skill development were also abound, and I benefited greatly from one associate director's tutorials on preparing effective PowerPoint presentations. Another attending mentored me in student feedback skills, which have allowed me to become a much more effective educator. I was also able to model that mentorship and begin to build my own mentor relationships with my students. In fact, this mentorship has become one of the most fulfilling aspects of my job. I was fortunate to have that mentorship early on in my career, as similar mentorship becomes difficult to obtain once in an attending hospitalist position.3

In conclusion, although current internal medicine residency training provides intensive direct patient care experiences, it only allows glimpses into the other aspects of an academic hospitalist's job. Unfortunately, it does not adequately prepare one to begin this type of position with a full complement of skills. Only a minority of hospitalists pursue additional structured training directly after residency; the majority jump into hospitalist positions and opt for on‐the‐job training. While there is an early economic advantage to starting an attending position without delay, I believe that the skills learned during an additional year of dedicated training allow for a more meaningful work experience and, ultimately, a faster rise within the track of an academic hospitalist.

The tasks that residency programs and hospitals may give to CMRs provide fertile material for developing the skills necessary to become a productive academic hospitalist. I thrived on the multifaceted work of caring for a diverse group of patients, teaching different levels of learners, helping to manage various hospital systems, and better understanding the hospital as the sum of its parts. As noted above, this pre‐attending league gave me the exposure to more fully develop my academic hospitalist game in a supportive environment. A CMR year may be beneficial for residents entering any career in internal medicine; however, I believe it is most aptly suited as a stepping stone for future academic hospitalists. I strongly recommend that current residents interested in academic hospital medicine consider a CMR position, and encourage program directors to consider molding their inpatient CMR experiences to facilitate this. Moreover, unless fellowship training in hospital medicine becomes the norm, I propose that current academic hospitalists do more to closely court and usher these pretenders into our ranks.

References
  1. Varkey P,Karlapudi S,Rose S,Nelson R,Warner M.A systems approach for implementing practice‐based learning and improvement and systems‐based practice in graduate medical education.Acad Med.2009;84(3):335339.
  2. Berg DN,Huot SJ.Middle manager role of the chief medical resident: an organizational psychologist's perspective.J Gen Intern Med.2007;22(12):17711774.
  3. Harrison R,Hunter AJ,Sharpe B,Auerbach AD.Survey of US academic hospitalist leaders about mentorship and academic activities in hospitalist groups.J Hosp Med.2011;6:59.
References
  1. Varkey P,Karlapudi S,Rose S,Nelson R,Warner M.A systems approach for implementing practice‐based learning and improvement and systems‐based practice in graduate medical education.Acad Med.2009;84(3):335339.
  2. Berg DN,Huot SJ.Middle manager role of the chief medical resident: an organizational psychologist's perspective.J Gen Intern Med.2007;22(12):17711774.
  3. Harrison R,Hunter AJ,Sharpe B,Auerbach AD.Survey of US academic hospitalist leaders about mentorship and academic activities in hospitalist groups.J Hosp Med.2011;6:59.
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Too Many Cooks in the Kitchen?

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Hospitalists, PCPs, specialists, and non‐physicians: Too many cooks in the kitchen?

The tension between continuity of care and specialization is not new, but may have reached a tipping point when the hospitalist movement erupted onto the American medical scene in the late 1990s. By definition, when a hospitalist cares for an inpatient, there is some fragmentation of care, which is, at least in theory, avoidableif the primary care provider (PCP) can serve as attending physician in the hospital. Literature has since emerged suggesting that clinical and economic outcomes of care by hospitalists are at least as good as that provided by PCPs, and that patients are not, in general, opposed to hospitalist care.13

However, the degree of discontinuity is not just a feature of whether a hospitalist assumes care of the hospitalized patient. Discontinuity can be exacerbated by changing attendings throughout the hospital stay. And inpatient continuity is a potential issue for both the hospitalist model and traditional model of care (in which the PCP serves as inpatient attending physician). While one might assume that the hospitalist model fosters more inpatient discontinuity because most hospitalistswhether working a 7‐on7‐off schedule or another scheduledo not commit to caring for a patient throughout an entire hospitalization the way a PCP might, this question has not previously been examined. Even if the hospitalist model is a fait accompli in many hospitals, it is worth knowing how inpatient continuity differs between the 2 models.

In this issue of the Journal, Fletcher and colleagues4 used billing data to examine trends in inpatient continuity of care over a 10‐year period ending in 2006, and sought to determine: (1) whether inpatient care has become more fragmented over time (as defined by the number of generalists caring for a patient over the course of an average hospitalization), and (2) whether inpatient care provided by hospitalists tends to be more fragmented than care provided by PCPs. They found that continuity of inpatient care has indeed decreased over time. In 1996, just over 70% of patients received care from 1 generalist; this number declined to just under 60% a decade later, despite a decrease in length‐of‐stay during that period. However, and perhaps surprisingly, patients cared for exclusively by hospitalists saw fewer generalists in the hospital (ie, fewer different hospitalists) than those cared for exclusively by outpatient providers. The authors conclude that the doctorpatient continuity over the course of a hospital stay is not worse in the hospitalist model than in the traditional model. While reassuring, it is important to remember that the patient experience does not begin at admission or end at discharge, and a more patient‐centered analysis might take into account the outpatient providers too (ie, those seeing the patient before admission and after discharge), and would probably show that the hospitalist model indeed leads to more care fragmentation. After all, there are at least 2 providers involved in every patient's care when a hospitalist model is used, whereas a large subset of patients cared for by PCPs would have only 1 provider involved.

While not the primary focus of the analysis, Fletcher and colleagues4 identified additional predictors of inpatient continuity of care. Higher socioeconomic class and white race were associated with lower continuity. This suggests that care fragmentation is not a feature of inferior, or at least cheap, care. In keeping with this observation, there was also enormous geographic variation in inpatient care continuity, marked by greater fragmentation of care in the New England and the mid‐Atlantic regions than in other areas of the country, and more fragmentation in larger hospitals serving heavily populated metropolitan areas. This pattern is strikingly similar to the cost‐of‐care patterns observed by the Dartmouth Atlas researchers.5, 6 Densely populated areas tend to have more specialists per capita and also tend to deliver more expensive carewithout demonstrably higher quality. In parallel, it is easy to see how care fragmentation might increase length‐of‐stay7 and lead to excessive diagnostic testing and consultation. More cooks in the kitchen might make costlier stew.

How hospitalists tackle the issue of inpatient continuity is not only a matter of quality of care, but also a matter of job sustainability. The simple way to maximize continuityworking many consecutive dayscan lead to burnout if taken too far. But there are creative ways to assign admissions that maximize continuity for the average inpatient while allowing providers needed time off. The CICLE initiative (Creating Incentives and Continuity Leading to Efficiency in hospital medicine) at the Johns Hopkins Bayview Medical Center, for instance, assigns physicians to 4‐day cycles of clinical work; the first day of the cycle (a long‐call day) involves admitting a large number of patients during a busy shift, with no new patients admitted on the remaining days of the cycle. Thus, all patients whose length of stay is less than 5 days will have a single attending‐of‐record. Not only does this model increase continuity, it also incentivizes providers to augment throughput: more discharged patients on Tuesday means fewer patients to see on Wednesday, without any expectation to backfill. Other less aggressive but similar approaches are used elsewhere, such as exempting hospitalists from accepting new patients on the last 1 or 2 of the consecutive days they work. We eagerly await data on the impact of these programs on quality of care, patient satisfaction, and provider satisfaction.

The impact of other providers and staff cannot be ignored. While the most important handoff in many cases may indeed be between the PCP and attending hospitalist tasked with coordinating the overall care of the patient, for some patients, there may be a specialist who has known the patient for years who is driving the plan of care. For patients with severe chronic illnesses, such as end‐stage renal disease or asthma, a well‐structured specialty clinic may even serve as a patient‐centered medical home.8 And the current inpatient team includes night coverage physicians (whether moonlighters, house staff, or covering hospitalists), and an ever‐increasing number of non‐physicians who play a critical role in hospital care (non‐physician providers, nurses, social workers, pharmacists, case managers, physical therapists, and others). While it is tempting to focus on the attending physician as the main driver of healthcare quality, continuity, and the inpatient experience, this is an oversimplification.

If there is a take‐home message, it is probably that most hospitalized patients will be cared for by multiple providers and a team of non‐physicians. The Marcus Welby practice model may not be completely dead, but if Dr. Welby were still in practice, it would be a safe bet that he would be slower at computerized order entry than the average intern, that financial pressures would make it hard for him to attend to his hospitalized patients, and that he probably would have turned over much of his inpatient practice to the physicians and non‐physician caregivers who make the hospital their primary workplace.9 Going forward, research should examine ways to optimize care coordination under the hospitalist model,1013 rather than comparing it to the traditional model of inpatient care. The ingredients for success include coordinated care by a committee of caregivers, effective handoffs (throughout hospitalization and at discharge),12, 14 focused and deliberate multidisciplinary communication, and effective patient education,15 regardless of the attending‐du‐jour.

Files
References
  1. Coffman J,Rundall TG.The impact of hospitalists on the cost and quality of inpatient care in the United States: a research synthesis.Med Care Res Rev.2005;62:379406.
  2. Auerbach AD,Aronson MD,Davis RB,Phillips RS.How physicians perceive hospitalist services after implementation: anticipation vs reality.Arch Intern Med.2003;163:23302336.
  3. Lindenauer PK,Rothberg MB,Pekow PS,Kenwood C,Benjamin EM,Auerbach AD.Outcomes of care by hospitalists, general internists, and family physicians.N Engl J Med.2007;357:25892600.
  4. Fletcher K,Sharma G,Dong Z,Yong‐fang K,Goodwin J.Trends in inpatient continuity of care for a cohort of Medicare patients, 1996–2006.J Hosp Med.2011;6:438444.
  5. Fisher ES,Wennberg DE,Stukel TA,Gottlieb DJ,Lucas FL,Pinder EL.The implications of regional variations in Medicare spending. Part 2: health outcomes and satisfaction with care.Ann Intern Med.2003;138:288298.
  6. Fisher ES,Wennberg DE,Stukel TA,Gottlieb DJ,Lucas FL,Pinder EL.The implications of regional variations in Medicare spending. Part 1: the content, quality, and accessibility of care.Ann Intern Med.2003;138:273287.
  7. Epstein K,Juarez E,Epstein A,Loya K,Singer A.The impact of fragmentation of hospitalist care on length of stay.J Hosp Med.2010;5:335338.
  8. Kirschner N,Barr MS.Specialists/subspecialists and the patient‐centered medical home.Chest.2010;137:200204.
  9. Meltzer DO,Chung JW.U.S. trends in hospitalization and generalist physician workforce and the emergence of hospitalists.J Gen Intern Med.2010;25:453459.
  10. Hinami K,Farnan JM,Meltzer DO,Arora VM.Understanding communication during hospitalist service changes: a mixed methods study.J Hosp Med.2009;4:535540.
  11. Halasyamani L,Kripalani S,Coleman E, et al.Transition of care for hospitalized elderly patients—development of a discharge checklist for hospitalists.J Hosp Med.2006;1:354360.
  12. Arora VM,Manjarrez E,Dressler DD,Basaviah P,Halasyamani L,Kripalani S.Hospitalist handoffs: a systematic review and task force recommendations.J Hosp Med.2009;4:433440.
  13. Wachter RM.The hospitalist field turns 15: new opportunities and challenges.J Hosp Med.2011;6:E1E4.
  14. Snow V,Beck D,Budnitz T, et al.Transitions of Care Consensus Policy Statement American College of Physicians‐Society of General Internal Medicine‐Society of Hospital Medicine‐American Geriatrics Society‐American College of Emergency Physicians‐Society of Academic Emergency Medicine.J Gen Intern Med.2009;24:971976.
  15. Jack BW,Chetty VK,Anthony D, et al.A reengineered hospital discharge program to decrease rehospitalization: a randomized trial.Ann Intern Med.2009;150:178187.
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The tension between continuity of care and specialization is not new, but may have reached a tipping point when the hospitalist movement erupted onto the American medical scene in the late 1990s. By definition, when a hospitalist cares for an inpatient, there is some fragmentation of care, which is, at least in theory, avoidableif the primary care provider (PCP) can serve as attending physician in the hospital. Literature has since emerged suggesting that clinical and economic outcomes of care by hospitalists are at least as good as that provided by PCPs, and that patients are not, in general, opposed to hospitalist care.13

However, the degree of discontinuity is not just a feature of whether a hospitalist assumes care of the hospitalized patient. Discontinuity can be exacerbated by changing attendings throughout the hospital stay. And inpatient continuity is a potential issue for both the hospitalist model and traditional model of care (in which the PCP serves as inpatient attending physician). While one might assume that the hospitalist model fosters more inpatient discontinuity because most hospitalistswhether working a 7‐on7‐off schedule or another scheduledo not commit to caring for a patient throughout an entire hospitalization the way a PCP might, this question has not previously been examined. Even if the hospitalist model is a fait accompli in many hospitals, it is worth knowing how inpatient continuity differs between the 2 models.

In this issue of the Journal, Fletcher and colleagues4 used billing data to examine trends in inpatient continuity of care over a 10‐year period ending in 2006, and sought to determine: (1) whether inpatient care has become more fragmented over time (as defined by the number of generalists caring for a patient over the course of an average hospitalization), and (2) whether inpatient care provided by hospitalists tends to be more fragmented than care provided by PCPs. They found that continuity of inpatient care has indeed decreased over time. In 1996, just over 70% of patients received care from 1 generalist; this number declined to just under 60% a decade later, despite a decrease in length‐of‐stay during that period. However, and perhaps surprisingly, patients cared for exclusively by hospitalists saw fewer generalists in the hospital (ie, fewer different hospitalists) than those cared for exclusively by outpatient providers. The authors conclude that the doctorpatient continuity over the course of a hospital stay is not worse in the hospitalist model than in the traditional model. While reassuring, it is important to remember that the patient experience does not begin at admission or end at discharge, and a more patient‐centered analysis might take into account the outpatient providers too (ie, those seeing the patient before admission and after discharge), and would probably show that the hospitalist model indeed leads to more care fragmentation. After all, there are at least 2 providers involved in every patient's care when a hospitalist model is used, whereas a large subset of patients cared for by PCPs would have only 1 provider involved.

While not the primary focus of the analysis, Fletcher and colleagues4 identified additional predictors of inpatient continuity of care. Higher socioeconomic class and white race were associated with lower continuity. This suggests that care fragmentation is not a feature of inferior, or at least cheap, care. In keeping with this observation, there was also enormous geographic variation in inpatient care continuity, marked by greater fragmentation of care in the New England and the mid‐Atlantic regions than in other areas of the country, and more fragmentation in larger hospitals serving heavily populated metropolitan areas. This pattern is strikingly similar to the cost‐of‐care patterns observed by the Dartmouth Atlas researchers.5, 6 Densely populated areas tend to have more specialists per capita and also tend to deliver more expensive carewithout demonstrably higher quality. In parallel, it is easy to see how care fragmentation might increase length‐of‐stay7 and lead to excessive diagnostic testing and consultation. More cooks in the kitchen might make costlier stew.

How hospitalists tackle the issue of inpatient continuity is not only a matter of quality of care, but also a matter of job sustainability. The simple way to maximize continuityworking many consecutive dayscan lead to burnout if taken too far. But there are creative ways to assign admissions that maximize continuity for the average inpatient while allowing providers needed time off. The CICLE initiative (Creating Incentives and Continuity Leading to Efficiency in hospital medicine) at the Johns Hopkins Bayview Medical Center, for instance, assigns physicians to 4‐day cycles of clinical work; the first day of the cycle (a long‐call day) involves admitting a large number of patients during a busy shift, with no new patients admitted on the remaining days of the cycle. Thus, all patients whose length of stay is less than 5 days will have a single attending‐of‐record. Not only does this model increase continuity, it also incentivizes providers to augment throughput: more discharged patients on Tuesday means fewer patients to see on Wednesday, without any expectation to backfill. Other less aggressive but similar approaches are used elsewhere, such as exempting hospitalists from accepting new patients on the last 1 or 2 of the consecutive days they work. We eagerly await data on the impact of these programs on quality of care, patient satisfaction, and provider satisfaction.

The impact of other providers and staff cannot be ignored. While the most important handoff in many cases may indeed be between the PCP and attending hospitalist tasked with coordinating the overall care of the patient, for some patients, there may be a specialist who has known the patient for years who is driving the plan of care. For patients with severe chronic illnesses, such as end‐stage renal disease or asthma, a well‐structured specialty clinic may even serve as a patient‐centered medical home.8 And the current inpatient team includes night coverage physicians (whether moonlighters, house staff, or covering hospitalists), and an ever‐increasing number of non‐physicians who play a critical role in hospital care (non‐physician providers, nurses, social workers, pharmacists, case managers, physical therapists, and others). While it is tempting to focus on the attending physician as the main driver of healthcare quality, continuity, and the inpatient experience, this is an oversimplification.

If there is a take‐home message, it is probably that most hospitalized patients will be cared for by multiple providers and a team of non‐physicians. The Marcus Welby practice model may not be completely dead, but if Dr. Welby were still in practice, it would be a safe bet that he would be slower at computerized order entry than the average intern, that financial pressures would make it hard for him to attend to his hospitalized patients, and that he probably would have turned over much of his inpatient practice to the physicians and non‐physician caregivers who make the hospital their primary workplace.9 Going forward, research should examine ways to optimize care coordination under the hospitalist model,1013 rather than comparing it to the traditional model of inpatient care. The ingredients for success include coordinated care by a committee of caregivers, effective handoffs (throughout hospitalization and at discharge),12, 14 focused and deliberate multidisciplinary communication, and effective patient education,15 regardless of the attending‐du‐jour.

The tension between continuity of care and specialization is not new, but may have reached a tipping point when the hospitalist movement erupted onto the American medical scene in the late 1990s. By definition, when a hospitalist cares for an inpatient, there is some fragmentation of care, which is, at least in theory, avoidableif the primary care provider (PCP) can serve as attending physician in the hospital. Literature has since emerged suggesting that clinical and economic outcomes of care by hospitalists are at least as good as that provided by PCPs, and that patients are not, in general, opposed to hospitalist care.13

However, the degree of discontinuity is not just a feature of whether a hospitalist assumes care of the hospitalized patient. Discontinuity can be exacerbated by changing attendings throughout the hospital stay. And inpatient continuity is a potential issue for both the hospitalist model and traditional model of care (in which the PCP serves as inpatient attending physician). While one might assume that the hospitalist model fosters more inpatient discontinuity because most hospitalistswhether working a 7‐on7‐off schedule or another scheduledo not commit to caring for a patient throughout an entire hospitalization the way a PCP might, this question has not previously been examined. Even if the hospitalist model is a fait accompli in many hospitals, it is worth knowing how inpatient continuity differs between the 2 models.

In this issue of the Journal, Fletcher and colleagues4 used billing data to examine trends in inpatient continuity of care over a 10‐year period ending in 2006, and sought to determine: (1) whether inpatient care has become more fragmented over time (as defined by the number of generalists caring for a patient over the course of an average hospitalization), and (2) whether inpatient care provided by hospitalists tends to be more fragmented than care provided by PCPs. They found that continuity of inpatient care has indeed decreased over time. In 1996, just over 70% of patients received care from 1 generalist; this number declined to just under 60% a decade later, despite a decrease in length‐of‐stay during that period. However, and perhaps surprisingly, patients cared for exclusively by hospitalists saw fewer generalists in the hospital (ie, fewer different hospitalists) than those cared for exclusively by outpatient providers. The authors conclude that the doctorpatient continuity over the course of a hospital stay is not worse in the hospitalist model than in the traditional model. While reassuring, it is important to remember that the patient experience does not begin at admission or end at discharge, and a more patient‐centered analysis might take into account the outpatient providers too (ie, those seeing the patient before admission and after discharge), and would probably show that the hospitalist model indeed leads to more care fragmentation. After all, there are at least 2 providers involved in every patient's care when a hospitalist model is used, whereas a large subset of patients cared for by PCPs would have only 1 provider involved.

While not the primary focus of the analysis, Fletcher and colleagues4 identified additional predictors of inpatient continuity of care. Higher socioeconomic class and white race were associated with lower continuity. This suggests that care fragmentation is not a feature of inferior, or at least cheap, care. In keeping with this observation, there was also enormous geographic variation in inpatient care continuity, marked by greater fragmentation of care in the New England and the mid‐Atlantic regions than in other areas of the country, and more fragmentation in larger hospitals serving heavily populated metropolitan areas. This pattern is strikingly similar to the cost‐of‐care patterns observed by the Dartmouth Atlas researchers.5, 6 Densely populated areas tend to have more specialists per capita and also tend to deliver more expensive carewithout demonstrably higher quality. In parallel, it is easy to see how care fragmentation might increase length‐of‐stay7 and lead to excessive diagnostic testing and consultation. More cooks in the kitchen might make costlier stew.

How hospitalists tackle the issue of inpatient continuity is not only a matter of quality of care, but also a matter of job sustainability. The simple way to maximize continuityworking many consecutive dayscan lead to burnout if taken too far. But there are creative ways to assign admissions that maximize continuity for the average inpatient while allowing providers needed time off. The CICLE initiative (Creating Incentives and Continuity Leading to Efficiency in hospital medicine) at the Johns Hopkins Bayview Medical Center, for instance, assigns physicians to 4‐day cycles of clinical work; the first day of the cycle (a long‐call day) involves admitting a large number of patients during a busy shift, with no new patients admitted on the remaining days of the cycle. Thus, all patients whose length of stay is less than 5 days will have a single attending‐of‐record. Not only does this model increase continuity, it also incentivizes providers to augment throughput: more discharged patients on Tuesday means fewer patients to see on Wednesday, without any expectation to backfill. Other less aggressive but similar approaches are used elsewhere, such as exempting hospitalists from accepting new patients on the last 1 or 2 of the consecutive days they work. We eagerly await data on the impact of these programs on quality of care, patient satisfaction, and provider satisfaction.

The impact of other providers and staff cannot be ignored. While the most important handoff in many cases may indeed be between the PCP and attending hospitalist tasked with coordinating the overall care of the patient, for some patients, there may be a specialist who has known the patient for years who is driving the plan of care. For patients with severe chronic illnesses, such as end‐stage renal disease or asthma, a well‐structured specialty clinic may even serve as a patient‐centered medical home.8 And the current inpatient team includes night coverage physicians (whether moonlighters, house staff, or covering hospitalists), and an ever‐increasing number of non‐physicians who play a critical role in hospital care (non‐physician providers, nurses, social workers, pharmacists, case managers, physical therapists, and others). While it is tempting to focus on the attending physician as the main driver of healthcare quality, continuity, and the inpatient experience, this is an oversimplification.

If there is a take‐home message, it is probably that most hospitalized patients will be cared for by multiple providers and a team of non‐physicians. The Marcus Welby practice model may not be completely dead, but if Dr. Welby were still in practice, it would be a safe bet that he would be slower at computerized order entry than the average intern, that financial pressures would make it hard for him to attend to his hospitalized patients, and that he probably would have turned over much of his inpatient practice to the physicians and non‐physician caregivers who make the hospital their primary workplace.9 Going forward, research should examine ways to optimize care coordination under the hospitalist model,1013 rather than comparing it to the traditional model of inpatient care. The ingredients for success include coordinated care by a committee of caregivers, effective handoffs (throughout hospitalization and at discharge),12, 14 focused and deliberate multidisciplinary communication, and effective patient education,15 regardless of the attending‐du‐jour.

References
  1. Coffman J,Rundall TG.The impact of hospitalists on the cost and quality of inpatient care in the United States: a research synthesis.Med Care Res Rev.2005;62:379406.
  2. Auerbach AD,Aronson MD,Davis RB,Phillips RS.How physicians perceive hospitalist services after implementation: anticipation vs reality.Arch Intern Med.2003;163:23302336.
  3. Lindenauer PK,Rothberg MB,Pekow PS,Kenwood C,Benjamin EM,Auerbach AD.Outcomes of care by hospitalists, general internists, and family physicians.N Engl J Med.2007;357:25892600.
  4. Fletcher K,Sharma G,Dong Z,Yong‐fang K,Goodwin J.Trends in inpatient continuity of care for a cohort of Medicare patients, 1996–2006.J Hosp Med.2011;6:438444.
  5. Fisher ES,Wennberg DE,Stukel TA,Gottlieb DJ,Lucas FL,Pinder EL.The implications of regional variations in Medicare spending. Part 2: health outcomes and satisfaction with care.Ann Intern Med.2003;138:288298.
  6. Fisher ES,Wennberg DE,Stukel TA,Gottlieb DJ,Lucas FL,Pinder EL.The implications of regional variations in Medicare spending. Part 1: the content, quality, and accessibility of care.Ann Intern Med.2003;138:273287.
  7. Epstein K,Juarez E,Epstein A,Loya K,Singer A.The impact of fragmentation of hospitalist care on length of stay.J Hosp Med.2010;5:335338.
  8. Kirschner N,Barr MS.Specialists/subspecialists and the patient‐centered medical home.Chest.2010;137:200204.
  9. Meltzer DO,Chung JW.U.S. trends in hospitalization and generalist physician workforce and the emergence of hospitalists.J Gen Intern Med.2010;25:453459.
  10. Hinami K,Farnan JM,Meltzer DO,Arora VM.Understanding communication during hospitalist service changes: a mixed methods study.J Hosp Med.2009;4:535540.
  11. Halasyamani L,Kripalani S,Coleman E, et al.Transition of care for hospitalized elderly patients—development of a discharge checklist for hospitalists.J Hosp Med.2006;1:354360.
  12. Arora VM,Manjarrez E,Dressler DD,Basaviah P,Halasyamani L,Kripalani S.Hospitalist handoffs: a systematic review and task force recommendations.J Hosp Med.2009;4:433440.
  13. Wachter RM.The hospitalist field turns 15: new opportunities and challenges.J Hosp Med.2011;6:E1E4.
  14. Snow V,Beck D,Budnitz T, et al.Transitions of Care Consensus Policy Statement American College of Physicians‐Society of General Internal Medicine‐Society of Hospital Medicine‐American Geriatrics Society‐American College of Emergency Physicians‐Society of Academic Emergency Medicine.J Gen Intern Med.2009;24:971976.
  15. Jack BW,Chetty VK,Anthony D, et al.A reengineered hospital discharge program to decrease rehospitalization: a randomized trial.Ann Intern Med.2009;150:178187.
References
  1. Coffman J,Rundall TG.The impact of hospitalists on the cost and quality of inpatient care in the United States: a research synthesis.Med Care Res Rev.2005;62:379406.
  2. Auerbach AD,Aronson MD,Davis RB,Phillips RS.How physicians perceive hospitalist services after implementation: anticipation vs reality.Arch Intern Med.2003;163:23302336.
  3. Lindenauer PK,Rothberg MB,Pekow PS,Kenwood C,Benjamin EM,Auerbach AD.Outcomes of care by hospitalists, general internists, and family physicians.N Engl J Med.2007;357:25892600.
  4. Fletcher K,Sharma G,Dong Z,Yong‐fang K,Goodwin J.Trends in inpatient continuity of care for a cohort of Medicare patients, 1996–2006.J Hosp Med.2011;6:438444.
  5. Fisher ES,Wennberg DE,Stukel TA,Gottlieb DJ,Lucas FL,Pinder EL.The implications of regional variations in Medicare spending. Part 2: health outcomes and satisfaction with care.Ann Intern Med.2003;138:288298.
  6. Fisher ES,Wennberg DE,Stukel TA,Gottlieb DJ,Lucas FL,Pinder EL.The implications of regional variations in Medicare spending. Part 1: the content, quality, and accessibility of care.Ann Intern Med.2003;138:273287.
  7. Epstein K,Juarez E,Epstein A,Loya K,Singer A.The impact of fragmentation of hospitalist care on length of stay.J Hosp Med.2010;5:335338.
  8. Kirschner N,Barr MS.Specialists/subspecialists and the patient‐centered medical home.Chest.2010;137:200204.
  9. Meltzer DO,Chung JW.U.S. trends in hospitalization and generalist physician workforce and the emergence of hospitalists.J Gen Intern Med.2010;25:453459.
  10. Hinami K,Farnan JM,Meltzer DO,Arora VM.Understanding communication during hospitalist service changes: a mixed methods study.J Hosp Med.2009;4:535540.
  11. Halasyamani L,Kripalani S,Coleman E, et al.Transition of care for hospitalized elderly patients—development of a discharge checklist for hospitalists.J Hosp Med.2006;1:354360.
  12. Arora VM,Manjarrez E,Dressler DD,Basaviah P,Halasyamani L,Kripalani S.Hospitalist handoffs: a systematic review and task force recommendations.J Hosp Med.2009;4:433440.
  13. Wachter RM.The hospitalist field turns 15: new opportunities and challenges.J Hosp Med.2011;6:E1E4.
  14. Snow V,Beck D,Budnitz T, et al.Transitions of Care Consensus Policy Statement American College of Physicians‐Society of General Internal Medicine‐Society of Hospital Medicine‐American Geriatrics Society‐American College of Emergency Physicians‐Society of Academic Emergency Medicine.J Gen Intern Med.2009;24:971976.
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Issue
Journal of Hospital Medicine - 6(8)
Issue
Journal of Hospital Medicine - 6(8)
Page Number
433-434
Page Number
433-434
Article Type
Display Headline
Hospitalists, PCPs, specialists, and non‐physicians: Too many cooks in the kitchen?
Display Headline
Hospitalists, PCPs, specialists, and non‐physicians: Too many cooks in the kitchen?
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Article Source
Copyright © 2011 Society of Hospital Medicine
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Correspondence Location
Hospitalist Program, Johns Hopkins Hospital, 600 North Wolfe St/Park 307, Baltimore, MD 21287
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