Now that I have your attention, I hope no one thinks the “40 patients per day” suggestion is in any way SHM current policy. But it is becoming increasingly clear that demands for the hospitalist workforce and demands on ongoing accountability for performance will require a redefinition of the role the hospitalist should have in patient care.

This isn’t unique to HM. In many ways, the patient-centered medical home (PCMH) and accountable-care organizations (ACOs) will in their own ways redefine the physician’s role at many steps along the healthcare continuum. But, as usual, HM might very well be at the leading edge.

Scope of Practice

There just aren’t enough qualified hospitalists to do the work, let alone all of the things coming our way with an ever-expanding scope of practice. Sure, hospitalists will always have a central role in managing the acute care of most medical illnesses. We already manage more inpatient heart-failure patients and more chest pain than cardiologists; more seizures, strokes, and dementia than neurologists; and more diabetes than endocrinologists. In many hospitals, we have replaced PCPs in managing acutely ill patients on medical floors.

But in recent years, hospitalists have played an increasing role in comanaging orthopedic and other surgical patients, and are playing a larger role in the care of patients formerly managed solely by subspecialists. As neurologists have left the building, hospitalists have had to expand our management of patients with acute neurologic problems. And as the critical-care shortage expands, hospitalists are playing a greater role in our nation’s ICUs.

Forward-thinking hospitals are redefining the roles of ED physicians in an era of hospitalists. Patients who present with a temperature of 104, a BP of 90/60, and a pulmonary infiltrate get a 60-second evaluation in the ED and are quickly admitted upstairs to the hospitalists. No need for two to three hours of an ED workup for a patient everyone knows is coming into the house. More and more EDs are routinely using hospitalists as in-house consultants on difficult patient decisions.

As ACOs become commonplace and as hospitals become responsible for the gaps post-discharge, look for some HM groups to be asked to manage the subacute patient experience, those critical first post-hospital visits in the 30 days after hospitalization. PCPs and medical homes will have their own capacity issues and difficulties in managing these fragile patients just out of the hospital.

Add to this all the time hospitalists need to spend each day in developing and implementing performance improvement, and in creating and participating in the new hospital team, it is no wonder that a limited HM workforce is being stretched beyond its capacity.

Workforce Issues

In many ways, this is a blessing for an individual hospitalist, especially one with a track record of competency and skill. This is at least part of the reason that HM was one of only five medical specialties in which incomes increased in 2009, and why hospitals everywhere are looking for strategies to attract and retain the best talent.

While this trend might bode well for the individual hospitalist looking for career flexibility, the ever-enlarging specialty of HM cannot easily fill all the needs described above, even with a large influx of medical students or residents in internal medicine, family medicine, and pediatrics, or even with recruitment of additional nonphysician providers. The work is growing too fast and the people just aren’t available.

Job Description

It is time to rethink the job description for the physician hospitalists. How do we want to deploy the $100-plus-per-hour hospitalist, who is in short supply, to get the most out of this limited resource?

If we step back a minute and start to list all the roles hospitalists have played in patient care, we might see ways to involve existing health professionals, and we might also see a need to add some new players, to alter the current hierarchy and authority. If we keep the focus on always providing the best care for the patient and to only ask each member of the team to play roles consistent with their training and competencies, then we can come out the other side of all this in better shape than we are in now.

Hospitalists today are asked to take a detailed history, do a complete physical examination, review any old records, speak to the referring physicians, talk to the doctor and possibly the nurse in the ED, meet with the nurse on the floor, make an initial diagnosis, order initial and subsequent tests to confirm or deny each specific diagnosis, order initial therapies (pharmaceutical and other), adjust therapy as the tests clarify or muddy the diagnostic approach, order additional tests to make sure the therapies are helpful and not toxic, record all of these ideas, directions, assumptions, and guesses in the medical record, generate a bill to collect payment for care rendered, meet with the patient and possibly the family to educate them about the potential disease states and each therapy ordered, assess the home (or nonhospital) situation, and make plans and arrangements for discharge, round on the patient at least once daily to redo and revise many of these steps as the course of the disease and new information warrants, produce instructions at discharge to include a summary of the hospital course, new therapies, future testing at a level for the patient and their family, and also for the future physicians in compliance with the requirements for billing and in compliance with hospital regulations and the community standards, make sure your care elements are being documented for performance evaluations and to satisfy whatever alphabet soup is looking at measurement and accountability, and along the way figure out what information any consultants, comanagers, other hospitalists, nurses, etc. might need to know, and create a venue or process to communicate the information. And I am sure there are more roles I have left out.

The point is, do we really need an MD to do all of these things? Is it time to create a process, a trusted team, and a new way to deliver the best care and deploy our limited resources more economically and effectively?

What are the unique roles and skill sets that physician hospitalists can bring to their patients’ care? And, more important, what are the current roles that would be better handed off to another member of the team?

The hospitalist should be the integrator of information, who then works with the entire team to set a direction and plan for diagnosis and therapy. Most everything else could be delegated to someone else.

But that presupposes a trust in the competencies of the rest of the team. Do I believe the history and physical already performed in the ED, by the nurse, by the NPP, or by another physician, or do I need to repeat this again? Do I trust the pharmacist to select the correct agent and know how to monitor its effectiveness and potential toxicity, and to be prepared to transition to outpatient therapy? Do I trust that the nurse (and every nurse on every shift) will be able educate the patient about their disease and hospital course and to provide accurate and timely information about the patient? And on and on.

Some EDs right now have a new person, the scribe, who sees the patient side by side with the physician, transcribing the orders, writing the notes, and interfacing with the hospital’s electronic health record (EHR). Does this free up the ED physician to see more patients? Does this lead to better care? Does this lead to better payment collection or fewer liability suits?

And this is just replacing one element of the doctors’ job. Think how existing healthcare professionals and new ones on the horizon can change the workforce.

The point is, the role and the need for the unique skill set of the well-tuned hospitalist have grown too broad for us to continue with business as usual. It is time to systematically look at the tasks that need to be accomplished for each acutely ill patient and to evaluate the entire healthcare team available, their competencies and their skill sets, and to set a “new paradigm” for their deployment.

This will require some documentation of each professional’s competence and a trust that they can deliver on a daily basis. In this new world, the hospitalist moves from playing lead trumpet to being the conductor of the orchestra, to being the coxswain for a crew team, or the quarterback of a multiskilled team.

In this world, the hospitalist could oversee 40 patients a day in a very different role than occurs today. The team would be empowered by viewing the “hospitalist’s patients” as all of our patients, and the patients would benefit from an accountable team focused directly on them.

This is a world not taught in residency, but one that the future clamors for. There is not an easy path from today to the future, but as in many things in the last decade or so, I trust that the best of HM is up to the task of playing a leading role in designing and implementing the future of healthcare.

SHM will continue to do its part to help you at every step along the way. TH

Dr. Wellikson is CEO of SHM.

Now that I have your attention, I hope no one thinks the “40 patients per day” suggestion is in any way SHM current policy. But it is becoming increasingly clear that demands for the hospitalist workforce and demands on ongoing accountability for performance will require a redefinition of the role the hospitalist should have in patient care.

This isn’t unique to HM. In many ways, the patient-centered medical home (PCMH) and accountable-care organizations (ACOs) will in their own ways redefine the physician’s role at many steps along the healthcare continuum. But, as usual, HM might very well be at the leading edge.

Scope of Practice

There just aren’t enough qualified hospitalists to do the work, let alone all of the things coming our way with an ever-expanding scope of practice. Sure, hospitalists will always have a central role in managing the acute care of most medical illnesses. We already manage more inpatient heart-failure patients and more chest pain than cardiologists; more seizures, strokes, and dementia than neurologists; and more diabetes than endocrinologists. In many hospitals, we have replaced PCPs in managing acutely ill patients on medical floors.

But in recent years, hospitalists have played an increasing role in comanaging orthopedic and other surgical patients, and are playing a larger role in the care of patients formerly managed solely by subspecialists. As neurologists have left the building, hospitalists have had to expand our management of patients with acute neurologic problems. And as the critical-care shortage expands, hospitalists are playing a greater role in our nation’s ICUs.

Forward-thinking hospitals are redefining the roles of ED physicians in an era of hospitalists. Patients who present with a temperature of 104, a BP of 90/60, and a pulmonary infiltrate get a 60-second evaluation in the ED and are quickly admitted upstairs to the hospitalists. No need for two to three hours of an ED workup for a patient everyone knows is coming into the house. More and more EDs are routinely using hospitalists as in-house consultants on difficult patient decisions.

As ACOs become commonplace and as hospitals become responsible for the gaps post-discharge, look for some HM groups to be asked to manage the subacute patient experience, those critical first post-hospital visits in the 30 days after hospitalization. PCPs and medical homes will have their own capacity issues and difficulties in managing these fragile patients just out of the hospital.

Add to this all the time hospitalists need to spend each day in developing and implementing performance improvement, and in creating and participating in the new hospital team, it is no wonder that a limited HM workforce is being stretched beyond its capacity.

Workforce Issues

In many ways, this is a blessing for an individual hospitalist, especially one with a track record of competency and skill. This is at least part of the reason that HM was one of only five medical specialties in which incomes increased in 2009, and why hospitals everywhere are looking for strategies to attract and retain the best talent.

While this trend might bode well for the individual hospitalist looking for career flexibility, the ever-enlarging specialty of HM cannot easily fill all the needs described above, even with a large influx of medical students or residents in internal medicine, family medicine, and pediatrics, or even with recruitment of additional nonphysician providers. The work is growing too fast and the people just aren’t available.

Job Description

It is time to rethink the job description for the physician hospitalists. How do we want to deploy the $100-plus-per-hour hospitalist, who is in short supply, to get the most out of this limited resource?

If we step back a minute and start to list all the roles hospitalists have played in patient care, we might see ways to involve existing health professionals, and we might also see a need to add some new players, to alter the current hierarchy and authority. If we keep the focus on always providing the best care for the patient and to only ask each member of the team to play roles consistent with their training and competencies, then we can come out the other side of all this in better shape than we are in now.

Hospitalists today are asked to take a detailed history, do a complete physical examination, review any old records, speak to the referring physicians, talk to the doctor and possibly the nurse in the ED, meet with the nurse on the floor, make an initial diagnosis, order initial and subsequent tests to confirm or deny each specific diagnosis, order initial therapies (pharmaceutical and other), adjust therapy as the tests clarify or muddy the diagnostic approach, order additional tests to make sure the therapies are helpful and not toxic, record all of these ideas, directions, assumptions, and guesses in the medical record, generate a bill to collect payment for care rendered, meet with the patient and possibly the family to educate them about the potential disease states and each therapy ordered, assess the home (or nonhospital) situation, and make plans and arrangements for discharge, round on the patient at least once daily to redo and revise many of these steps as the course of the disease and new information warrants, produce instructions at discharge to include a summary of the hospital course, new therapies, future testing at a level for the patient and their family, and also for the future physicians in compliance with the requirements for billing and in compliance with hospital regulations and the community standards, make sure your care elements are being documented for performance evaluations and to satisfy whatever alphabet soup is looking at measurement and accountability, and along the way figure out what information any consultants, comanagers, other hospitalists, nurses, etc. might need to know, and create a venue or process to communicate the information. And I am sure there are more roles I have left out.

The point is, do we really need an MD to do all of these things? Is it time to create a process, a trusted team, and a new way to deliver the best care and deploy our limited resources more economically and effectively?

What are the unique roles and skill sets that physician hospitalists can bring to their patients’ care? And, more important, what are the current roles that would be better handed off to another member of the team?

The hospitalist should be the integrator of information, who then works with the entire team to set a direction and plan for diagnosis and therapy. Most everything else could be delegated to someone else.

But that presupposes a trust in the competencies of the rest of the team. Do I believe the history and physical already performed in the ED, by the nurse, by the NPP, or by another physician, or do I need to repeat this again? Do I trust the pharmacist to select the correct agent and know how to monitor its effectiveness and potential toxicity, and to be prepared to transition to outpatient therapy? Do I trust that the nurse (and every nurse on every shift) will be able educate the patient about their disease and hospital course and to provide accurate and timely information about the patient? And on and on.

Some EDs right now have a new person, the scribe, who sees the patient side by side with the physician, transcribing the orders, writing the notes, and interfacing with the hospital’s electronic health record (EHR). Does this free up the ED physician to see more patients? Does this lead to better care? Does this lead to better payment collection or fewer liability suits?

And this is just replacing one element of the doctors’ job. Think how existing healthcare professionals and new ones on the horizon can change the workforce.

The point is, the role and the need for the unique skill set of the well-tuned hospitalist have grown too broad for us to continue with business as usual. It is time to systematically look at the tasks that need to be accomplished for each acutely ill patient and to evaluate the entire healthcare team available, their competencies and their skill sets, and to set a “new paradigm” for their deployment.

This will require some documentation of each professional’s competence and a trust that they can deliver on a daily basis. In this new world, the hospitalist moves from playing lead trumpet to being the conductor of the orchestra, to being the coxswain for a crew team, or the quarterback of a multiskilled team.

In this world, the hospitalist could oversee 40 patients a day in a very different role than occurs today. The team would be empowered by viewing the “hospitalist’s patients” as all of our patients, and the patients would benefit from an accountable team focused directly on them.

This is a world not taught in residency, but one that the future clamors for. There is not an easy path from today to the future, but as in many things in the last decade or so, I trust that the best of HM is up to the task of playing a leading role in designing and implementing the future of healthcare.

SHM will continue to do its part to help you at every step along the way. TH

Dr. Wellikson is CEO of SHM.

Now that I have your attention, I hope no one thinks the “40 patients per day” suggestion is in any way SHM current policy. But it is becoming increasingly clear that demands for the hospitalist workforce and demands on ongoing accountability for performance will require a redefinition of the role the hospitalist should have in patient care.

This isn’t unique to HM. In many ways, the patient-centered medical home (PCMH) and accountable-care organizations (ACOs) will in their own ways redefine the physician’s role at many steps along the healthcare continuum. But, as usual, HM might very well be at the leading edge.

Scope of Practice

There just aren’t enough qualified hospitalists to do the work, let alone all of the things coming our way with an ever-expanding scope of practice. Sure, hospitalists will always have a central role in managing the acute care of most medical illnesses. We already manage more inpatient heart-failure patients and more chest pain than cardiologists; more seizures, strokes, and dementia than neurologists; and more diabetes than endocrinologists. In many hospitals, we have replaced PCPs in managing acutely ill patients on medical floors.

But in recent years, hospitalists have played an increasing role in comanaging orthopedic and other surgical patients, and are playing a larger role in the care of patients formerly managed solely by subspecialists. As neurologists have left the building, hospitalists have had to expand our management of patients with acute neurologic problems. And as the critical-care shortage expands, hospitalists are playing a greater role in our nation’s ICUs.

Forward-thinking hospitals are redefining the roles of ED physicians in an era of hospitalists. Patients who present with a temperature of 104, a BP of 90/60, and a pulmonary infiltrate get a 60-second evaluation in the ED and are quickly admitted upstairs to the hospitalists. No need for two to three hours of an ED workup for a patient everyone knows is coming into the house. More and more EDs are routinely using hospitalists as in-house consultants on difficult patient decisions.

As ACOs become commonplace and as hospitals become responsible for the gaps post-discharge, look for some HM groups to be asked to manage the subacute patient experience, those critical first post-hospital visits in the 30 days after hospitalization. PCPs and medical homes will have their own capacity issues and difficulties in managing these fragile patients just out of the hospital.

Add to this all the time hospitalists need to spend each day in developing and implementing performance improvement, and in creating and participating in the new hospital team, it is no wonder that a limited HM workforce is being stretched beyond its capacity.

Workforce Issues

In many ways, this is a blessing for an individual hospitalist, especially one with a track record of competency and skill. This is at least part of the reason that HM was one of only five medical specialties in which incomes increased in 2009, and why hospitals everywhere are looking for strategies to attract and retain the best talent.

While this trend might bode well for the individual hospitalist looking for career flexibility, the ever-enlarging specialty of HM cannot easily fill all the needs described above, even with a large influx of medical students or residents in internal medicine, family medicine, and pediatrics, or even with recruitment of additional nonphysician providers. The work is growing too fast and the people just aren’t available.

Job Description

It is time to rethink the job description for the physician hospitalists. How do we want to deploy the $100-plus-per-hour hospitalist, who is in short supply, to get the most out of this limited resource?

If we step back a minute and start to list all the roles hospitalists have played in patient care, we might see ways to involve existing health professionals, and we might also see a need to add some new players, to alter the current hierarchy and authority. If we keep the focus on always providing the best care for the patient and to only ask each member of the team to play roles consistent with their training and competencies, then we can come out the other side of all this in better shape than we are in now.

Hospitalists today are asked to take a detailed history, do a complete physical examination, review any old records, speak to the referring physicians, talk to the doctor and possibly the nurse in the ED, meet with the nurse on the floor, make an initial diagnosis, order initial and subsequent tests to confirm or deny each specific diagnosis, order initial therapies (pharmaceutical and other), adjust therapy as the tests clarify or muddy the diagnostic approach, order additional tests to make sure the therapies are helpful and not toxic, record all of these ideas, directions, assumptions, and guesses in the medical record, generate a bill to collect payment for care rendered, meet with the patient and possibly the family to educate them about the potential disease states and each therapy ordered, assess the home (or nonhospital) situation, and make plans and arrangements for discharge, round on the patient at least once daily to redo and revise many of these steps as the course of the disease and new information warrants, produce instructions at discharge to include a summary of the hospital course, new therapies, future testing at a level for the patient and their family, and also for the future physicians in compliance with the requirements for billing and in compliance with hospital regulations and the community standards, make sure your care elements are being documented for performance evaluations and to satisfy whatever alphabet soup is looking at measurement and accountability, and along the way figure out what information any consultants, comanagers, other hospitalists, nurses, etc. might need to know, and create a venue or process to communicate the information. And I am sure there are more roles I have left out.

The point is, do we really need an MD to do all of these things? Is it time to create a process, a trusted team, and a new way to deliver the best care and deploy our limited resources more economically and effectively?

What are the unique roles and skill sets that physician hospitalists can bring to their patients’ care? And, more important, what are the current roles that would be better handed off to another member of the team?

The hospitalist should be the integrator of information, who then works with the entire team to set a direction and plan for diagnosis and therapy. Most everything else could be delegated to someone else.

But that presupposes a trust in the competencies of the rest of the team. Do I believe the history and physical already performed in the ED, by the nurse, by the NPP, or by another physician, or do I need to repeat this again? Do I trust the pharmacist to select the correct agent and know how to monitor its effectiveness and potential toxicity, and to be prepared to transition to outpatient therapy? Do I trust that the nurse (and every nurse on every shift) will be able educate the patient about their disease and hospital course and to provide accurate and timely information about the patient? And on and on.

Some EDs right now have a new person, the scribe, who sees the patient side by side with the physician, transcribing the orders, writing the notes, and interfacing with the hospital’s electronic health record (EHR). Does this free up the ED physician to see more patients? Does this lead to better care? Does this lead to better payment collection or fewer liability suits?

And this is just replacing one element of the doctors’ job. Think how existing healthcare professionals and new ones on the horizon can change the workforce.

The point is, the role and the need for the unique skill set of the well-tuned hospitalist have grown too broad for us to continue with business as usual. It is time to systematically look at the tasks that need to be accomplished for each acutely ill patient and to evaluate the entire healthcare team available, their competencies and their skill sets, and to set a “new paradigm” for their deployment.

This will require some documentation of each professional’s competence and a trust that they can deliver on a daily basis. In this new world, the hospitalist moves from playing lead trumpet to being the conductor of the orchestra, to being the coxswain for a crew team, or the quarterback of a multiskilled team.

In this world, the hospitalist could oversee 40 patients a day in a very different role than occurs today. The team would be empowered by viewing the “hospitalist’s patients” as all of our patients, and the patients would benefit from an accountable team focused directly on them.

This is a world not taught in residency, but one that the future clamors for. There is not an easy path from today to the future, but as in many things in the last decade or so, I trust that the best of HM is up to the task of playing a leading role in designing and implementing the future of healthcare.

SHM will continue to do its part to help you at every step along the way. TH

Dr. Wellikson is CEO of SHM.

It’s fall. I know that because the leaves are turning, the nights are chillier, and my dogs have migrated back to the bed from a hot summer on the floor. Oh, and I again need to fill four positions for my hospitalist group.

A lot has changed in HM recruiting in the past few years. There was a feeding frenzy in the early part of the century, when I often joked that group leaders were so desperate for boots on the ground that my mom (who is not a physician, is retired, and struggles somewhat with the triple acid-base disorder) could have gotten a job as a hospitalist. I saw it in the number of reference calls for the residents in our program, their ever-increasing salary offers, and the breathless e-mails I’d receive from headhunters. Improbably, on occasion, their froth would even boil over to an offer for me, an academic. Now that’s desperation.

But things seem to be changing. The number of calls per resident is down and my inbox is filled with slightly less-winded recruiters. Maybe groups have finally matured and don’t need to hire; maybe the recession has induced an air of caution around growth; or maybe groups have uncovered the secret tonic to seeing more patients with fewer providers. Whatever it is, it seems that the job market has tightened ever so slightly.

And the job market has changed, especially on the academic side.

Work Harder for Less

In academics, we hire into jobs we describe as “clinician-something,” with the something reflecting what you do when you are not seeing patients, the thing that in most cases will get you promoted from instructor to assistant to associate to professor. Because HM is not a fellowship-driven field, primary researchers, called clinician-researchers, are rare. Most of the folks we hire fall into the clinician-educator mold—that is, they see patients and teach, develop curriculums, and produce scholarship, often around education.

And therein lies the problem.

We’re running out of educational opportunities. The demand for clinical work long ago outstripped the supply of teaching opportunities, resulting in many academic HM groups hiring hospitalists for clinical jobs without residents to teach. Much like a deep-sea diver miles below the surface who finds his oxygen tank is running low, we now find ourselves looking up at an ocean of patients and realize that our educational lifeline has been severed. And the dyspnea is becoming ever more uncomfortable.

Increasingly, here is the sell for many academic HM groups: “Come work for us, do the same work you’d do at a community hospital, in a less-efficient system, without residents, for a lot less money.” And because you are primarily a clinician, you probably won’t have protected time to develop an academic interest and, therefore, you won’t get promoted beyond the “instructor” level because you haven’t contributed to advancing your field of medicine.

Even my mom wouldn’t apply for that job.

Failure Does Matter

The academic hospitalist job circa 2010 is heavy on the hospitalist and light on the academic. This is bad. And it matters to all of us, community hospitalists included. Without a strong frontline of academic hospitalists, we will not develop this field beyond “doctors who work in a hospital.”

There is a science to our field and it needs to be further developed. It can be seen in the comparative-effectiveness research, which tells us the best way to manage common diagnoses, the translational research (i.e. getting that new drug from the bench to the bedside), and the systems-based improvements (e.g. ensuring every stroke patient gets thrombolytics within three hours).

Take readmissions. There is a lot of dyspepsia swirling around this issue, and it’s clear that we have to reduce them. In fact, without such reductions, our hospitals (and likely us) won’t get paid. How will we do that? Maybe Project RED, maybe Project BOOST, maybe the best solution hasn’t been found yet. We don’t know, and we won’t until academic hospitalists have studied it.

Moreover, if we don’t present learners with talented, satisfied, respected hospitalist role models, I guarantee you that the quantity and quality of residents graduating to academic and community HM programs will suffer. Think back to those people who lured you into your specialty. Were you inspired to pediatrics, family medicine, or internal medicine because you saw those providers toiling away unsated by themselves on the wards?

Academic HM has a problem. And we are working toward the solution.

Six months ago, 90 academic hospitalist leaders convened in Washington, D.C., for the first Academic Hospital Medicine Leadership Summit. The goal was to develop a vision and action plan for the future of academic HM. Three work groups tackled the research, educational, and clinical issues facing our field. The recommendations of these sessions were then transferred to SHM’s Academic Committee and its subcommittees for operationalization.

A Pipeline of Quality

The education work group identified a need to establish hospitalists as the teachers of quality and safety for students and residents. This included increasing the number of hospitalists in such educational leadership positions as program and clerkship directors, where they can visibly lead the educational infrastructure. In response, SHM will unfurl the Quality and Safety Educators Academy this spring with the goal of providing academic hospitalists the construct to teach quality and safety.

Additionally, SHM’s Education Committee is developing a “plug and play” quality-improvement (QI) curriculum for use by any hospitalist educator. These initiatives will build on the success of the Academic Hospitalist Academy, developed two years ago to provide early career direction to academic hospitalists.

The education work group also prioritized the development of a strong pipeline of interest in HM starting at the medical-student level. This recommendation was turned over to the newly minted Pipeline Committee, which has been working feverishly to develop and expand medical student Hospital Medicine Interest Groups, the development of HM residency tracks, and an extension of our partnerships with other educational groups.

Answers to Future Questions

On the research front, goals were set to better develop and support clinician-researchers. This includes better delineating HM core research strengths, devising methods to partner with other medical subspecialties to perform quality and safety research in their areas of content expertise, and to develop a pipeline of future researchers.

To this last point, SHM awarded its first set of $50,000 research awards to two burgeoning researchers earlier this year.

SHM also is partnering with the Association of Specialty Professors to offer career development grants in geriatric medicine through the new Grants for Early Medical and Surgical Subspecialists’ Transitions to Aging Research (GEMSSTAR) program. And for the rest of us, SHM has devised free, Web-based forums for young researchers to present their work to their peers nationally.

Productivity, Efficiency, and Promotion

On the clinical side, the needs addressed include identification of benchmarks for academic clinical productivity, pathways for academic promotion, a methodology to garner more support for nonclinical work, and expectations to improve workflow and efficiency in academic medical centers.

These important tasks were assigned to a newly created Academic Practice and Promotions Task Force. This group is actively developing a quantitative survey to evaluate these needs and plans to publish a white paper of their findings, along with recommendations for hospitalist program directors, their department chairs and deans, and the hospitals that fund their programs. The findings will be presented at the next summit—at HM11 on May 10, 2011, in Dallas—as we continue to chart the course for success in academic hospital medicine.

Until then, I need to get my tank refilled. TH

Dr. Glasheen is associate professor of medicine at the University of Colorado Denver, where he serves as director of the Hospital Medicine Program and the Hospitalist Training Program, and as associate program director of the Internal Medicine Residency Program.

It’s fall. I know that because the leaves are turning, the nights are chillier, and my dogs have migrated back to the bed from a hot summer on the floor. Oh, and I again need to fill four positions for my hospitalist group.

A lot has changed in HM recruiting in the past few years. There was a feeding frenzy in the early part of the century, when I often joked that group leaders were so desperate for boots on the ground that my mom (who is not a physician, is retired, and struggles somewhat with the triple acid-base disorder) could have gotten a job as a hospitalist. I saw it in the number of reference calls for the residents in our program, their ever-increasing salary offers, and the breathless e-mails I’d receive from headhunters. Improbably, on occasion, their froth would even boil over to an offer for me, an academic. Now that’s desperation.

But things seem to be changing. The number of calls per resident is down and my inbox is filled with slightly less-winded recruiters. Maybe groups have finally matured and don’t need to hire; maybe the recession has induced an air of caution around growth; or maybe groups have uncovered the secret tonic to seeing more patients with fewer providers. Whatever it is, it seems that the job market has tightened ever so slightly.

And the job market has changed, especially on the academic side.

Work Harder for Less

In academics, we hire into jobs we describe as “clinician-something,” with the something reflecting what you do when you are not seeing patients, the thing that in most cases will get you promoted from instructor to assistant to associate to professor. Because HM is not a fellowship-driven field, primary researchers, called clinician-researchers, are rare. Most of the folks we hire fall into the clinician-educator mold—that is, they see patients and teach, develop curriculums, and produce scholarship, often around education.

And therein lies the problem.

We’re running out of educational opportunities. The demand for clinical work long ago outstripped the supply of teaching opportunities, resulting in many academic HM groups hiring hospitalists for clinical jobs without residents to teach. Much like a deep-sea diver miles below the surface who finds his oxygen tank is running low, we now find ourselves looking up at an ocean of patients and realize that our educational lifeline has been severed. And the dyspnea is becoming ever more uncomfortable.

Increasingly, here is the sell for many academic HM groups: “Come work for us, do the same work you’d do at a community hospital, in a less-efficient system, without residents, for a lot less money.” And because you are primarily a clinician, you probably won’t have protected time to develop an academic interest and, therefore, you won’t get promoted beyond the “instructor” level because you haven’t contributed to advancing your field of medicine.

Even my mom wouldn’t apply for that job.

Failure Does Matter

The academic hospitalist job circa 2010 is heavy on the hospitalist and light on the academic. This is bad. And it matters to all of us, community hospitalists included. Without a strong frontline of academic hospitalists, we will not develop this field beyond “doctors who work in a hospital.”

There is a science to our field and it needs to be further developed. It can be seen in the comparative-effectiveness research, which tells us the best way to manage common diagnoses, the translational research (i.e. getting that new drug from the bench to the bedside), and the systems-based improvements (e.g. ensuring every stroke patient gets thrombolytics within three hours).

Take readmissions. There is a lot of dyspepsia swirling around this issue, and it’s clear that we have to reduce them. In fact, without such reductions, our hospitals (and likely us) won’t get paid. How will we do that? Maybe Project RED, maybe Project BOOST, maybe the best solution hasn’t been found yet. We don’t know, and we won’t until academic hospitalists have studied it.

Moreover, if we don’t present learners with talented, satisfied, respected hospitalist role models, I guarantee you that the quantity and quality of residents graduating to academic and community HM programs will suffer. Think back to those people who lured you into your specialty. Were you inspired to pediatrics, family medicine, or internal medicine because you saw those providers toiling away unsated by themselves on the wards?

Academic HM has a problem. And we are working toward the solution.

Six months ago, 90 academic hospitalist leaders convened in Washington, D.C., for the first Academic Hospital Medicine Leadership Summit. The goal was to develop a vision and action plan for the future of academic HM. Three work groups tackled the research, educational, and clinical issues facing our field. The recommendations of these sessions were then transferred to SHM’s Academic Committee and its subcommittees for operationalization.

A Pipeline of Quality

The education work group identified a need to establish hospitalists as the teachers of quality and safety for students and residents. This included increasing the number of hospitalists in such educational leadership positions as program and clerkship directors, where they can visibly lead the educational infrastructure. In response, SHM will unfurl the Quality and Safety Educators Academy this spring with the goal of providing academic hospitalists the construct to teach quality and safety.

Additionally, SHM’s Education Committee is developing a “plug and play” quality-improvement (QI) curriculum for use by any hospitalist educator. These initiatives will build on the success of the Academic Hospitalist Academy, developed two years ago to provide early career direction to academic hospitalists.

The education work group also prioritized the development of a strong pipeline of interest in HM starting at the medical-student level. This recommendation was turned over to the newly minted Pipeline Committee, which has been working feverishly to develop and expand medical student Hospital Medicine Interest Groups, the development of HM residency tracks, and an extension of our partnerships with other educational groups.

Answers to Future Questions

On the research front, goals were set to better develop and support clinician-researchers. This includes better delineating HM core research strengths, devising methods to partner with other medical subspecialties to perform quality and safety research in their areas of content expertise, and to develop a pipeline of future researchers.

To this last point, SHM awarded its first set of $50,000 research awards to two burgeoning researchers earlier this year.

SHM also is partnering with the Association of Specialty Professors to offer career development grants in geriatric medicine through the new Grants for Early Medical and Surgical Subspecialists’ Transitions to Aging Research (GEMSSTAR) program. And for the rest of us, SHM has devised free, Web-based forums for young researchers to present their work to their peers nationally.

Productivity, Efficiency, and Promotion

On the clinical side, the needs addressed include identification of benchmarks for academic clinical productivity, pathways for academic promotion, a methodology to garner more support for nonclinical work, and expectations to improve workflow and efficiency in academic medical centers.

These important tasks were assigned to a newly created Academic Practice and Promotions Task Force. This group is actively developing a quantitative survey to evaluate these needs and plans to publish a white paper of their findings, along with recommendations for hospitalist program directors, their department chairs and deans, and the hospitals that fund their programs. The findings will be presented at the next summit—at HM11 on May 10, 2011, in Dallas—as we continue to chart the course for success in academic hospital medicine.

Until then, I need to get my tank refilled. TH

Dr. Glasheen is associate professor of medicine at the University of Colorado Denver, where he serves as director of the Hospital Medicine Program and the Hospitalist Training Program, and as associate program director of the Internal Medicine Residency Program.

It’s fall. I know that because the leaves are turning, the nights are chillier, and my dogs have migrated back to the bed from a hot summer on the floor. Oh, and I again need to fill four positions for my hospitalist group.

A lot has changed in HM recruiting in the past few years. There was a feeding frenzy in the early part of the century, when I often joked that group leaders were so desperate for boots on the ground that my mom (who is not a physician, is retired, and struggles somewhat with the triple acid-base disorder) could have gotten a job as a hospitalist. I saw it in the number of reference calls for the residents in our program, their ever-increasing salary offers, and the breathless e-mails I’d receive from headhunters. Improbably, on occasion, their froth would even boil over to an offer for me, an academic. Now that’s desperation.

But things seem to be changing. The number of calls per resident is down and my inbox is filled with slightly less-winded recruiters. Maybe groups have finally matured and don’t need to hire; maybe the recession has induced an air of caution around growth; or maybe groups have uncovered the secret tonic to seeing more patients with fewer providers. Whatever it is, it seems that the job market has tightened ever so slightly.

And the job market has changed, especially on the academic side.

Work Harder for Less

In academics, we hire into jobs we describe as “clinician-something,” with the something reflecting what you do when you are not seeing patients, the thing that in most cases will get you promoted from instructor to assistant to associate to professor. Because HM is not a fellowship-driven field, primary researchers, called clinician-researchers, are rare. Most of the folks we hire fall into the clinician-educator mold—that is, they see patients and teach, develop curriculums, and produce scholarship, often around education.

And therein lies the problem.

We’re running out of educational opportunities. The demand for clinical work long ago outstripped the supply of teaching opportunities, resulting in many academic HM groups hiring hospitalists for clinical jobs without residents to teach. Much like a deep-sea diver miles below the surface who finds his oxygen tank is running low, we now find ourselves looking up at an ocean of patients and realize that our educational lifeline has been severed. And the dyspnea is becoming ever more uncomfortable.

Increasingly, here is the sell for many academic HM groups: “Come work for us, do the same work you’d do at a community hospital, in a less-efficient system, without residents, for a lot less money.” And because you are primarily a clinician, you probably won’t have protected time to develop an academic interest and, therefore, you won’t get promoted beyond the “instructor” level because you haven’t contributed to advancing your field of medicine.

Even my mom wouldn’t apply for that job.

Failure Does Matter

The academic hospitalist job circa 2010 is heavy on the hospitalist and light on the academic. This is bad. And it matters to all of us, community hospitalists included. Without a strong frontline of academic hospitalists, we will not develop this field beyond “doctors who work in a hospital.”

There is a science to our field and it needs to be further developed. It can be seen in the comparative-effectiveness research, which tells us the best way to manage common diagnoses, the translational research (i.e. getting that new drug from the bench to the bedside), and the systems-based improvements (e.g. ensuring every stroke patient gets thrombolytics within three hours).

Take readmissions. There is a lot of dyspepsia swirling around this issue, and it’s clear that we have to reduce them. In fact, without such reductions, our hospitals (and likely us) won’t get paid. How will we do that? Maybe Project RED, maybe Project BOOST, maybe the best solution hasn’t been found yet. We don’t know, and we won’t until academic hospitalists have studied it.

Moreover, if we don’t present learners with talented, satisfied, respected hospitalist role models, I guarantee you that the quantity and quality of residents graduating to academic and community HM programs will suffer. Think back to those people who lured you into your specialty. Were you inspired to pediatrics, family medicine, or internal medicine because you saw those providers toiling away unsated by themselves on the wards?

Academic HM has a problem. And we are working toward the solution.

Six months ago, 90 academic hospitalist leaders convened in Washington, D.C., for the first Academic Hospital Medicine Leadership Summit. The goal was to develop a vision and action plan for the future of academic HM. Three work groups tackled the research, educational, and clinical issues facing our field. The recommendations of these sessions were then transferred to SHM’s Academic Committee and its subcommittees for operationalization.

A Pipeline of Quality

The education work group identified a need to establish hospitalists as the teachers of quality and safety for students and residents. This included increasing the number of hospitalists in such educational leadership positions as program and clerkship directors, where they can visibly lead the educational infrastructure. In response, SHM will unfurl the Quality and Safety Educators Academy this spring with the goal of providing academic hospitalists the construct to teach quality and safety.

Additionally, SHM’s Education Committee is developing a “plug and play” quality-improvement (QI) curriculum for use by any hospitalist educator. These initiatives will build on the success of the Academic Hospitalist Academy, developed two years ago to provide early career direction to academic hospitalists.

The education work group also prioritized the development of a strong pipeline of interest in HM starting at the medical-student level. This recommendation was turned over to the newly minted Pipeline Committee, which has been working feverishly to develop and expand medical student Hospital Medicine Interest Groups, the development of HM residency tracks, and an extension of our partnerships with other educational groups.

Answers to Future Questions

On the research front, goals were set to better develop and support clinician-researchers. This includes better delineating HM core research strengths, devising methods to partner with other medical subspecialties to perform quality and safety research in their areas of content expertise, and to develop a pipeline of future researchers.

To this last point, SHM awarded its first set of $50,000 research awards to two burgeoning researchers earlier this year.

SHM also is partnering with the Association of Specialty Professors to offer career development grants in geriatric medicine through the new Grants for Early Medical and Surgical Subspecialists’ Transitions to Aging Research (GEMSSTAR) program. And for the rest of us, SHM has devised free, Web-based forums for young researchers to present their work to their peers nationally.

Productivity, Efficiency, and Promotion

On the clinical side, the needs addressed include identification of benchmarks for academic clinical productivity, pathways for academic promotion, a methodology to garner more support for nonclinical work, and expectations to improve workflow and efficiency in academic medical centers.

These important tasks were assigned to a newly created Academic Practice and Promotions Task Force. This group is actively developing a quantitative survey to evaluate these needs and plans to publish a white paper of their findings, along with recommendations for hospitalist program directors, their department chairs and deans, and the hospitals that fund their programs. The findings will be presented at the next summit—at HM11 on May 10, 2011, in Dallas—as we continue to chart the course for success in academic hospital medicine.

Until then, I need to get my tank refilled. TH

Dr. Glasheen is associate professor of medicine at the University of Colorado Denver, where he serves as director of the Hospital Medicine Program and the Hospitalist Training Program, and as associate program director of the Internal Medicine Residency Program.

The providers in every hospitalist practice should be a good fit for the practice’s culture. They should have reasonable relationships with their colleagues in the practice, patients and families, and other staff at the hospital.

I can’t imagine anyone arguing with this point of view. But in my work with hundreds of hospitalist practices over the past 15 years, I’ve found that many practices seem to have a hard time ensuring their providers meet that standard. I can think of lots of reasons for this. The first that comes to mind is the difficult HM recruiting environment. Almost all hospitalist practices needed to grow quickly, and many lowered the bar in the qualifications and the fit of the candidates they hired to make sure they filled all of their positions.

Even if it later becomes clear a provider isn’t a good fit for the group culture, or worse still lacks the knowledge base and judgment to perform well, many practices are reluctant to replace the hospitalist because it might be difficult to find a replacement—and there is no guarantee the new person will perform any better. Because of this, a number of practices have ended up with providers who in many cases have a negative influence on others in the practice, and both the practice and the problem provider would be better off if the provider went elsewhere.

The Problem Physician

To their credit, most practices do act when a provider simply lacks the skill and judgment to perform adequately. This can mean close proctoring/mentoring for an extended period, or requiring specific CME course work to correct a skill that is lacking. But it also means reassigning the person to a different job, or termination.

But in the case of someone with a toxic personality, practices often are more reluctant to act. I’ll often hear the leadership of a practice say something like, “We knew Alice wasn’t a good fit for our practice within a few weeks of her start date.” The start date was several years ago and nothing has been done about this. Not surprisingly, Alice still performs poorly.

I’m not talking about someone who has occasional problems. I’m talking about people who cause problems almost every time they show up to work. Here are some real anecdotes, with fictitious names to ensure anonymity for the person and institution:

• Dr. Lee routinely disappears for several hours, during which he doesn’t answer pages. This even happens when he is the only doctor covering the practice.
• Dr. Lifeson, while generally getting along well with his fellow hospitalists and the nursing staff, can be counted on to complain bitterly about all levels of the hospital administration and leadership. He never misses an opportunity to try to convince other hospitalists that the leadership is not only inept, but also clearly has a malicious intent toward hospitalists.
• Dr. Peart complains incessantly about even tiny inequities in the work schedule or patient load. Others in the group have found that it is easier to ensure he always has the best schedule and lightest patient load, hoping they won’t have to hear his constant complaining. But even that hasn’t stemmed the steady downpour of negativity from him.

In all three of these cases, it seemed clear that the doctor should be terminated. And while the practice leadership agreed with me, they offered several excuses for why they hadn’t taken this step.

• “Who knows if we can find a replacement who will be any better?”
• “But he’s actually a decent doctor and doesn’t get a lot of complaints from patients.”
• “He’s such an angry guy, we worry about litigation if we fire him.”

I can’t offer any clear rule about when a practice should stop trying to improve a provider’s behavior and recognize that it is time to terminate the provider. But it is worth remembering that waiting too long has many costs, including the satisfaction of others in the group. Everyone will think less of the practice they are part of if poor behavior is tolerated.

Assess the Situation, Then Take Action

Most doctors who serve as the lead physician for their group have little or no experience dealing with problem behavior, let alone experience ensuring that necessary steps are followed prior to disciplining or terminating someone. But every hospital has someone who is very knowledgeable about these things; they should be engaged for advice, and, in the case of hospital-employed groups, should participate in the process of counseling and/or termination. It is important to take advantage of the expertise that is available.

Of course, the best approach is to prevent such problems from coming up. The best way to do this is to be very careful when hiring new providers. Checking references carefully is probably the best way to get an idea about whether someone might have behavior or personality problems. There are “job fit” survey instruments that you can use, but I’m not sure how effective they are, or how much value they add for a hospitalist practice beyond other means of assessing the candidate. And in the process of hiring someone, be sure to set behavior expectations very clearly. A new candidate should know that you will not tolerate not living up to behavioral expectations.

When dealing with bad behavior, make sure that you follow a careful and well-documented process. If someone still makes it through the hiring process only to be revealed as a troublemaker soon after their start date, don’t wait to sit that person down for very clear counseling; insist that their behavior change. Take notes of each meeting, and consider having the problem doctor sign and date the notes. While it might be easier to just wait and see if the first instance of bad behavior was an anomaly, that usually is a bad idea.

You should consider bringing the problem provider into the tent. The root of some bad behavior (i.e. criticism of leadership) is a person’s insecurity and lack of a feeling of ownership or control of their role in the practice. In that case, it might be reasonable to invite such a person into a role of greater responsibility in the practice so that they feel more in control. For example, a doctor who constantly complains about the work schedule might be invited to join the group’s executive committee or take on some other formal leadership role in the practice. This could backfire, so it should be tried only in carefully selected cases, and with the problem doctor’s clear understanding that they are being given a chance to have a bigger role in the practice but must improve their behavior or face serious consequences that could include termination.

I have seen this work beautifully in some cases, curing the problem behavior and turning the doctor into a valuable asset. I only wish there were a reliable way to know when to try this strategy. Sadly, it just requires judgment and intuition. TH

Dr. Nelson has been a practicing hospitalist since 1988 and is co-founder and past president of SHM. He is a principal in Nelson Flores Hospital Medicine Consultants, a national hospitalist practice management consulting firm (www.nelsonflores.com). He is course co-director and faculty for SHM’s “Best Practices in Managing a Hospital Medicine Program.” This column represents his views and is not intended to reflect an official position of SHM.

The providers in every hospitalist practice should be a good fit for the practice’s culture. They should have reasonable relationships with their colleagues in the practice, patients and families, and other staff at the hospital.

I can’t imagine anyone arguing with this point of view. But in my work with hundreds of hospitalist practices over the past 15 years, I’ve found that many practices seem to have a hard time ensuring their providers meet that standard. I can think of lots of reasons for this. The first that comes to mind is the difficult HM recruiting environment. Almost all hospitalist practices needed to grow quickly, and many lowered the bar in the qualifications and the fit of the candidates they hired to make sure they filled all of their positions.

Even if it later becomes clear a provider isn’t a good fit for the group culture, or worse still lacks the knowledge base and judgment to perform well, many practices are reluctant to replace the hospitalist because it might be difficult to find a replacement—and there is no guarantee the new person will perform any better. Because of this, a number of practices have ended up with providers who in many cases have a negative influence on others in the practice, and both the practice and the problem provider would be better off if the provider went elsewhere.

The Problem Physician

To their credit, most practices do act when a provider simply lacks the skill and judgment to perform adequately. This can mean close proctoring/mentoring for an extended period, or requiring specific CME course work to correct a skill that is lacking. But it also means reassigning the person to a different job, or termination.

But in the case of someone with a toxic personality, practices often are more reluctant to act. I’ll often hear the leadership of a practice say something like, “We knew Alice wasn’t a good fit for our practice within a few weeks of her start date.” The start date was several years ago and nothing has been done about this. Not surprisingly, Alice still performs poorly.

I’m not talking about someone who has occasional problems. I’m talking about people who cause problems almost every time they show up to work. Here are some real anecdotes, with fictitious names to ensure anonymity for the person and institution:

• Dr. Lee routinely disappears for several hours, during which he doesn’t answer pages. This even happens when he is the only doctor covering the practice.
• Dr. Lifeson, while generally getting along well with his fellow hospitalists and the nursing staff, can be counted on to complain bitterly about all levels of the hospital administration and leadership. He never misses an opportunity to try to convince other hospitalists that the leadership is not only inept, but also clearly has a malicious intent toward hospitalists.
• Dr. Peart complains incessantly about even tiny inequities in the work schedule or patient load. Others in the group have found that it is easier to ensure he always has the best schedule and lightest patient load, hoping they won’t have to hear his constant complaining. But even that hasn’t stemmed the steady downpour of negativity from him.

In all three of these cases, it seemed clear that the doctor should be terminated. And while the practice leadership agreed with me, they offered several excuses for why they hadn’t taken this step.

• “Who knows if we can find a replacement who will be any better?”
• “But he’s actually a decent doctor and doesn’t get a lot of complaints from patients.”
• “He’s such an angry guy, we worry about litigation if we fire him.”

I can’t offer any clear rule about when a practice should stop trying to improve a provider’s behavior and recognize that it is time to terminate the provider. But it is worth remembering that waiting too long has many costs, including the satisfaction of others in the group. Everyone will think less of the practice they are part of if poor behavior is tolerated.

Assess the Situation, Then Take Action

Most doctors who serve as the lead physician for their group have little or no experience dealing with problem behavior, let alone experience ensuring that necessary steps are followed prior to disciplining or terminating someone. But every hospital has someone who is very knowledgeable about these things; they should be engaged for advice, and, in the case of hospital-employed groups, should participate in the process of counseling and/or termination. It is important to take advantage of the expertise that is available.

Of course, the best approach is to prevent such problems from coming up. The best way to do this is to be very careful when hiring new providers. Checking references carefully is probably the best way to get an idea about whether someone might have behavior or personality problems. There are “job fit” survey instruments that you can use, but I’m not sure how effective they are, or how much value they add for a hospitalist practice beyond other means of assessing the candidate. And in the process of hiring someone, be sure to set behavior expectations very clearly. A new candidate should know that you will not tolerate not living up to behavioral expectations.

When dealing with bad behavior, make sure that you follow a careful and well-documented process. If someone still makes it through the hiring process only to be revealed as a troublemaker soon after their start date, don’t wait to sit that person down for very clear counseling; insist that their behavior change. Take notes of each meeting, and consider having the problem doctor sign and date the notes. While it might be easier to just wait and see if the first instance of bad behavior was an anomaly, that usually is a bad idea.

You should consider bringing the problem provider into the tent. The root of some bad behavior (i.e. criticism of leadership) is a person’s insecurity and lack of a feeling of ownership or control of their role in the practice. In that case, it might be reasonable to invite such a person into a role of greater responsibility in the practice so that they feel more in control. For example, a doctor who constantly complains about the work schedule might be invited to join the group’s executive committee or take on some other formal leadership role in the practice. This could backfire, so it should be tried only in carefully selected cases, and with the problem doctor’s clear understanding that they are being given a chance to have a bigger role in the practice but must improve their behavior or face serious consequences that could include termination.

I have seen this work beautifully in some cases, curing the problem behavior and turning the doctor into a valuable asset. I only wish there were a reliable way to know when to try this strategy. Sadly, it just requires judgment and intuition. TH

Dr. Nelson has been a practicing hospitalist since 1988 and is co-founder and past president of SHM. He is a principal in Nelson Flores Hospital Medicine Consultants, a national hospitalist practice management consulting firm (www.nelsonflores.com). He is course co-director and faculty for SHM’s “Best Practices in Managing a Hospital Medicine Program.” This column represents his views and is not intended to reflect an official position of SHM.

The providers in every hospitalist practice should be a good fit for the practice’s culture. They should have reasonable relationships with their colleagues in the practice, patients and families, and other staff at the hospital.

I can’t imagine anyone arguing with this point of view. But in my work with hundreds of hospitalist practices over the past 15 years, I’ve found that many practices seem to have a hard time ensuring their providers meet that standard. I can think of lots of reasons for this. The first that comes to mind is the difficult HM recruiting environment. Almost all hospitalist practices needed to grow quickly, and many lowered the bar in the qualifications and the fit of the candidates they hired to make sure they filled all of their positions.

Even if it later becomes clear a provider isn’t a good fit for the group culture, or worse still lacks the knowledge base and judgment to perform well, many practices are reluctant to replace the hospitalist because it might be difficult to find a replacement—and there is no guarantee the new person will perform any better. Because of this, a number of practices have ended up with providers who in many cases have a negative influence on others in the practice, and both the practice and the problem provider would be better off if the provider went elsewhere.

The Problem Physician

To their credit, most practices do act when a provider simply lacks the skill and judgment to perform adequately. This can mean close proctoring/mentoring for an extended period, or requiring specific CME course work to correct a skill that is lacking. But it also means reassigning the person to a different job, or termination.

But in the case of someone with a toxic personality, practices often are more reluctant to act. I’ll often hear the leadership of a practice say something like, “We knew Alice wasn’t a good fit for our practice within a few weeks of her start date.” The start date was several years ago and nothing has been done about this. Not surprisingly, Alice still performs poorly.

I’m not talking about someone who has occasional problems. I’m talking about people who cause problems almost every time they show up to work. Here are some real anecdotes, with fictitious names to ensure anonymity for the person and institution:

• Dr. Lee routinely disappears for several hours, during which he doesn’t answer pages. This even happens when he is the only doctor covering the practice.
• Dr. Lifeson, while generally getting along well with his fellow hospitalists and the nursing staff, can be counted on to complain bitterly about all levels of the hospital administration and leadership. He never misses an opportunity to try to convince other hospitalists that the leadership is not only inept, but also clearly has a malicious intent toward hospitalists.
• Dr. Peart complains incessantly about even tiny inequities in the work schedule or patient load. Others in the group have found that it is easier to ensure he always has the best schedule and lightest patient load, hoping they won’t have to hear his constant complaining. But even that hasn’t stemmed the steady downpour of negativity from him.

In all three of these cases, it seemed clear that the doctor should be terminated. And while the practice leadership agreed with me, they offered several excuses for why they hadn’t taken this step.

• “Who knows if we can find a replacement who will be any better?”
• “But he’s actually a decent doctor and doesn’t get a lot of complaints from patients.”
• “He’s such an angry guy, we worry about litigation if we fire him.”

I can’t offer any clear rule about when a practice should stop trying to improve a provider’s behavior and recognize that it is time to terminate the provider. But it is worth remembering that waiting too long has many costs, including the satisfaction of others in the group. Everyone will think less of the practice they are part of if poor behavior is tolerated.

Assess the Situation, Then Take Action

Most doctors who serve as the lead physician for their group have little or no experience dealing with problem behavior, let alone experience ensuring that necessary steps are followed prior to disciplining or terminating someone. But every hospital has someone who is very knowledgeable about these things; they should be engaged for advice, and, in the case of hospital-employed groups, should participate in the process of counseling and/or termination. It is important to take advantage of the expertise that is available.

Of course, the best approach is to prevent such problems from coming up. The best way to do this is to be very careful when hiring new providers. Checking references carefully is probably the best way to get an idea about whether someone might have behavior or personality problems. There are “job fit” survey instruments that you can use, but I’m not sure how effective they are, or how much value they add for a hospitalist practice beyond other means of assessing the candidate. And in the process of hiring someone, be sure to set behavior expectations very clearly. A new candidate should know that you will not tolerate not living up to behavioral expectations.

When dealing with bad behavior, make sure that you follow a careful and well-documented process. If someone still makes it through the hiring process only to be revealed as a troublemaker soon after their start date, don’t wait to sit that person down for very clear counseling; insist that their behavior change. Take notes of each meeting, and consider having the problem doctor sign and date the notes. While it might be easier to just wait and see if the first instance of bad behavior was an anomaly, that usually is a bad idea.

You should consider bringing the problem provider into the tent. The root of some bad behavior (i.e. criticism of leadership) is a person’s insecurity and lack of a feeling of ownership or control of their role in the practice. In that case, it might be reasonable to invite such a person into a role of greater responsibility in the practice so that they feel more in control. For example, a doctor who constantly complains about the work schedule might be invited to join the group’s executive committee or take on some other formal leadership role in the practice. This could backfire, so it should be tried only in carefully selected cases, and with the problem doctor’s clear understanding that they are being given a chance to have a bigger role in the practice but must improve their behavior or face serious consequences that could include termination.

I have seen this work beautifully in some cases, curing the problem behavior and turning the doctor into a valuable asset. I only wish there were a reliable way to know when to try this strategy. Sadly, it just requires judgment and intuition. TH

Dr. Nelson has been a practicing hospitalist since 1988 and is co-founder and past president of SHM. He is a principal in Nelson Flores Hospital Medicine Consultants, a national hospitalist practice management consulting firm (www.nelsonflores.com). He is course co-director and faculty for SHM’s “Best Practices in Managing a Hospital Medicine Program.” This column represents his views and is not intended to reflect an official position of SHM.

Click here to listen to Bryn Nelson's interview with Robert Berenson, MD

Click here to listen to Bryn Nelson's interview with Stuart Guterman

Click here to listen to Bryn Nelson's interview with Robert Berenson, MD

Click here to listen to Bryn Nelson's interview with Stuart Guterman

Click here to listen to Bryn Nelson's interview with Robert Berenson, MD

Click here to listen to Bryn Nelson's interview with Stuart Guterman

Hillcrest Medical Center in Tulsa, Okla., went live with its ACE Demonstration on May 1, 2009. Over the next 15 months, scores on several quality metrics soared, supply costs plunged, patient volumes shot up, and the hospital saved Medicare $750,000 on 37 diagnosis-related groups (DRGs).

So what’s the problem?

For one thing, handling the bundled payment system required “massive” computer conversions, says Hillcrest CEO Steve Dobbs, and cash payments from CMS were significantly delayed, in part due to glitches over how discharges were handled. And then there was the confusion over processing supplemental Medicare plans.

Hillcrest’s first-year experience with bundled payments for orthopedics, cardiology, and cardiovascular surgery provides an illuminating window into what other hospitals might encounter as the concept of bundling expands beyond the first few pilot sites.

Because Hillcrest didn’t have a way to pay physician claims, it hired a third-party vendor, Texas-based Trailblazer, to manage them. Then Hillcrest set up two LLCs—one for orthopedics and one for cardiology—to receive the bundled payments. CMS required the hospital to establish a quality committee, finance committee, and board within each LLC, and report quarterly about the program. But Dobbs says the hospital has received no written feedback from CMS or any indications of how the ACE Demonstration has worked at two other sites that also started last year.

Through “trial by error,” the hospital has had to learn many of its lessons on its own, he says, explaining that “you just had to go make some mistakes and try something.” For example, the hospital began posting the Medicare rate for each of the demonstration’s 37 DRGs on its website after frequent updates to the rates led to widespread confusion among area physicians. Hillcrest also learned that it needed to set up a dedicated toll-free call center for people to get information about the program.

There have been triumphs, too. Scores on such metrics as antibiotics administered one hour prior to surgical start and antibiotics stopped 24 hours post-surgery have climbed significantly, perhaps by linking them to gainsharing incentives. When one heart valve vendor “wouldn’t play,” Dobbs says, the hospital switched to another, less expensive vendor. By involving its open-heart surgeons in scrutinizing supplies, the hospital saved 10% of the cost of sterile packs in the operating room.

Hillcrest’s orthopedic surgeons—an independent group—also combed through instruments and drugs to look for savings. For their efforts, the six orthopedists netted a combined $130,000 in incentive checks. For the hospital’s own cardiologists and cardiovascular surgeons, the bonus money went back into the practice.

Early in the demonstration project, Dobbs says, hospitalists saw a dip in the number of cases they were getting pulled in on. “Early on they called me and said, ‘What’s up, because we’re not getting as many referrals from orthopedics?’” Dobbs says. “I think it’s leveled out over time, and they really haven’t seen that big of a change.”

The hospital also is reaping the rewards of recent investments, including a new heart hospital, heavy investment in cardiology, and a three-year-old orthopedics unit. In the first year of its demonstration, the hospital saw a 24% gain in its cardiology and cardiovascular surgery volume, and a whopping 37% gain in orthopedics volume.

One facet of the project that has been less fruitful is the Medicare discount given to patients who have their orthopedic or cardiology procedure done at Hillcrest. “People are saying it’s nice to have, but that’s not why they chose the program, especially in cardiology,” Dobbs says. “You don’t have a heart attack and tell the ambulance driver, ‘Oh, by the way, I want to get my incentive check.’ ”

Hillcrest Medical Center in Tulsa, Okla., went live with its ACE Demonstration on May 1, 2009. Over the next 15 months, scores on several quality metrics soared, supply costs plunged, patient volumes shot up, and the hospital saved Medicare $750,000 on 37 diagnosis-related groups (DRGs).

So what’s the problem?

For one thing, handling the bundled payment system required “massive” computer conversions, says Hillcrest CEO Steve Dobbs, and cash payments from CMS were significantly delayed, in part due to glitches over how discharges were handled. And then there was the confusion over processing supplemental Medicare plans.

Hillcrest’s first-year experience with bundled payments for orthopedics, cardiology, and cardiovascular surgery provides an illuminating window into what other hospitals might encounter as the concept of bundling expands beyond the first few pilot sites.

Because Hillcrest didn’t have a way to pay physician claims, it hired a third-party vendor, Texas-based Trailblazer, to manage them. Then Hillcrest set up two LLCs—one for orthopedics and one for cardiology—to receive the bundled payments. CMS required the hospital to establish a quality committee, finance committee, and board within each LLC, and report quarterly about the program. But Dobbs says the hospital has received no written feedback from CMS or any indications of how the ACE Demonstration has worked at two other sites that also started last year.

Through “trial by error,” the hospital has had to learn many of its lessons on its own, he says, explaining that “you just had to go make some mistakes and try something.” For example, the hospital began posting the Medicare rate for each of the demonstration’s 37 DRGs on its website after frequent updates to the rates led to widespread confusion among area physicians. Hillcrest also learned that it needed to set up a dedicated toll-free call center for people to get information about the program.

There have been triumphs, too. Scores on such metrics as antibiotics administered one hour prior to surgical start and antibiotics stopped 24 hours post-surgery have climbed significantly, perhaps by linking them to gainsharing incentives. When one heart valve vendor “wouldn’t play,” Dobbs says, the hospital switched to another, less expensive vendor. By involving its open-heart surgeons in scrutinizing supplies, the hospital saved 10% of the cost of sterile packs in the operating room.

Hillcrest’s orthopedic surgeons—an independent group—also combed through instruments and drugs to look for savings. For their efforts, the six orthopedists netted a combined $130,000 in incentive checks. For the hospital’s own cardiologists and cardiovascular surgeons, the bonus money went back into the practice.

Early in the demonstration project, Dobbs says, hospitalists saw a dip in the number of cases they were getting pulled in on. “Early on they called me and said, ‘What’s up, because we’re not getting as many referrals from orthopedics?’” Dobbs says. “I think it’s leveled out over time, and they really haven’t seen that big of a change.”

The hospital also is reaping the rewards of recent investments, including a new heart hospital, heavy investment in cardiology, and a three-year-old orthopedics unit. In the first year of its demonstration, the hospital saw a 24% gain in its cardiology and cardiovascular surgery volume, and a whopping 37% gain in orthopedics volume.

One facet of the project that has been less fruitful is the Medicare discount given to patients who have their orthopedic or cardiology procedure done at Hillcrest. “People are saying it’s nice to have, but that’s not why they chose the program, especially in cardiology,” Dobbs says. “You don’t have a heart attack and tell the ambulance driver, ‘Oh, by the way, I want to get my incentive check.’ ”

Hillcrest Medical Center in Tulsa, Okla., went live with its ACE Demonstration on May 1, 2009. Over the next 15 months, scores on several quality metrics soared, supply costs plunged, patient volumes shot up, and the hospital saved Medicare $750,000 on 37 diagnosis-related groups (DRGs).

So what’s the problem?

For one thing, handling the bundled payment system required “massive” computer conversions, says Hillcrest CEO Steve Dobbs, and cash payments from CMS were significantly delayed, in part due to glitches over how discharges were handled. And then there was the confusion over processing supplemental Medicare plans.

Hillcrest’s first-year experience with bundled payments for orthopedics, cardiology, and cardiovascular surgery provides an illuminating window into what other hospitals might encounter as the concept of bundling expands beyond the first few pilot sites.

Because Hillcrest didn’t have a way to pay physician claims, it hired a third-party vendor, Texas-based Trailblazer, to manage them. Then Hillcrest set up two LLCs—one for orthopedics and one for cardiology—to receive the bundled payments. CMS required the hospital to establish a quality committee, finance committee, and board within each LLC, and report quarterly about the program. But Dobbs says the hospital has received no written feedback from CMS or any indications of how the ACE Demonstration has worked at two other sites that also started last year.

Through “trial by error,” the hospital has had to learn many of its lessons on its own, he says, explaining that “you just had to go make some mistakes and try something.” For example, the hospital began posting the Medicare rate for each of the demonstration’s 37 DRGs on its website after frequent updates to the rates led to widespread confusion among area physicians. Hillcrest also learned that it needed to set up a dedicated toll-free call center for people to get information about the program.

There have been triumphs, too. Scores on such metrics as antibiotics administered one hour prior to surgical start and antibiotics stopped 24 hours post-surgery have climbed significantly, perhaps by linking them to gainsharing incentives. When one heart valve vendor “wouldn’t play,” Dobbs says, the hospital switched to another, less expensive vendor. By involving its open-heart surgeons in scrutinizing supplies, the hospital saved 10% of the cost of sterile packs in the operating room.

Hillcrest’s orthopedic surgeons—an independent group—also combed through instruments and drugs to look for savings. For their efforts, the six orthopedists netted a combined $130,000 in incentive checks. For the hospital’s own cardiologists and cardiovascular surgeons, the bonus money went back into the practice.

Early in the demonstration project, Dobbs says, hospitalists saw a dip in the number of cases they were getting pulled in on. “Early on they called me and said, ‘What’s up, because we’re not getting as many referrals from orthopedics?’” Dobbs says. “I think it’s leveled out over time, and they really haven’t seen that big of a change.”

The hospital also is reaping the rewards of recent investments, including a new heart hospital, heavy investment in cardiology, and a three-year-old orthopedics unit. In the first year of its demonstration, the hospital saw a 24% gain in its cardiology and cardiovascular surgery volume, and a whopping 37% gain in orthopedics volume.

One facet of the project that has been less fruitful is the Medicare discount given to patients who have their orthopedic or cardiology procedure done at Hillcrest. “People are saying it’s nice to have, but that’s not why they chose the program, especially in cardiology,” Dobbs says. “You don’t have a heart attack and tell the ambulance driver, ‘Oh, by the way, I want to get my incentive check.’ ”

New clinical trials and observational studies are shedding light on ways to improve the health of elderly patients. Here is a brief summary of these trials and how they might influence your clinical practice.

EXERCISE HAS NEWLY DISCOVERED BENEFITS

According to government data,¹ exercise has a dose-dependent effect on rates of all-cause mortality: the more hours one exercises per week, the lower the risk of death. The difference in risk is most pronounced as one goes from no exercise to about 3 hours of exercise per week; above 3 hours per week, the curve flattens out but continues to decline. Hence, we advise patients to engage in about 30 minutes of moderate-intensity exercise every day.

Lately, physical exercise has been found to have other, unexpected benefits.

Exercise helps cognition

ERICKSON KI, PRAKASH RS, VOSS MW, ET AL. AEROBIC FITNESS IS ASSOCIATED WITH HIPPOCAMPAL VOLUME IN ELDERLY HUMANS. HIPPOCAMPUS 2009; 19:1030–1039.

ETGEN T, SANDER D, HUNTGEBURTH U, POPPERT H, FÖRSTL H, BICKEL H. PHYSICAL ACTIVITY AND INCIDENT COGNITIVE IMPAIRMENT IN ELDERLY PERSONS: THE INVADE STUDY. ARCH INTERN MED 2010; 170:186–193.

The hippocampus is a structure deep in the brain that is involved in short-term memory. It atrophies with age, more so with dementia. Erickson² found a correlation between aerobic fitness (as measured by maximum oxygen consumption), hippocampal volume, and spatial memory performance.

Etgen and colleagues³ studied nearly 4,000 older adults in Bavaria for 2 years. Among those reporting no physical activity, 21.4% had cognitive impairment at baseline, compared with 7.3% of those with high activity at baseline. Following those without cognitive impairment over a 2-year period, they found the incidence of new cognitive impairment was 13.9% in those with no physical activity at baseline, 6.7% in those with moderate activity, and 5.1% in those with high activity.

Exercise boosts the effect of influenza vaccine

WOODS JA, KEYLOCK KT, LOWDER T, ET AL. CARDIOVASCULAR EXERCISE TRAINING EXTENDS INFLUENZA VACCINE SEROPROTECTION IN SEDENTARY OLDER ADULTS: THE IMMUNE FUNCTION INTERVENTION TRIAL. J AM GERIATR SOC 2009; 57:2183–2191.

In a study in 144 sedentary but healthy older adults (ages 60 to 83), Woods et al⁴ randomized the participants to undergo either flexibility or cardiovascular training for 10 months, starting 4 months before their annual influenza shot. Exercise extended the duration of antibody protection, with more participants in the cardiovascular group than in the flexibility group showing protection at 24 weeks against all three strains covered by the vaccine: H1N1, H3N2, and influenza B.

PREVENTING FRACTURES

Each year, about 30% of people age 65 or older fall, sustaining serious injuries in 5% to 10% of cases. Unintentional falls are the main cause of hip fractures, which number 300,000 per year. They are also a common cause of death.

Vitamin D prevents fractures, but can there be too much of a good thing?

BISCHOFF-FERRARI HA, WILLETT WC, WONG JB, ET AL. PREVENTION OF NONVERTEBRAL FRACTURES WITH ORAL VITAMIN D AND DOSE DEPENDENCY: A META-ANALYSIS OF RANDOMIZED CONTROLLED TRIALS. ARCH INTERN MED 2009; 169:551–561.

SANDERS KM, STUART AL, WILLIAMSON EJ, ET AL. ANNUAL HIGH-DOSE ORAL VITAMIN D AND FALLS AND FRACTURES IN OLDER WOMEN: A RANDOMIZED CONTROLLED TRIAL. JAMA 2010; 303:1815–1822.

Bischoff-Ferrari⁵ performed a meta-analysis of 12 randomized controlled trials of oral supplemental vitamin D₃ for preventing nonvertebral fractures in people age 65 and older, and eight trials for preventing hip fractures in the same age group. They found that the higher the daily dose of vitamin D, the lower the relative risk of hip fracture. The threshold dose at which supplementation significantly reduced the risk of falling was about 400 units per day. Higher doses of vitamin D reduced both falls and hip fractures by about 20%. The maximal effect was seen with studies using the maximum daily doses, ie, 770 to 800 units per day—not megadoses, but more than most Americans are taking. The threshold serum level of vitamin D of significance was 60 nmol/L (24 ng/mL).

Of interest, the effect on fractures was independent of calcium supplementation. This is important because calcium supplementation over and above ordinary dietary intake may increase the risk of cardiovascular events.^6,7

Despite the benefits of vitamin D, too much may be too much of a good thing. Sanders et al⁸ performed a double-blind, placebo-controlled trial in 2,256 community-dwelling women, age 70 or older, who were considered to be at high risk for fractures. Half received a large oral dose (500,000 units) once a year for 3 to 5 years, and half got placebo. Their initial serum vitamin D level was 49 nmol/L; the level 30 days after a dose in the treatment group was 120 nmol/L.

Contrary to expectations, the incidence of falls was 15% higher in the vitamin D group than in the placebo group (P = .03), and the incidence of fractures was 26% higher (P = .047). The falls and fractures tended to cluster in the first 3 months after the dose in the active treatment group, when serum vitamin D levels were highest.

Comments. Unless future studies suggest a benefit to megadoses of vitamin D or prove calcium supplementation greater than 1,000 mg is safe, the optimal daily intake of vitamin D is likely 1,000 units, with approximately 200 units from diet and 800 units from supplements. A diet rich in low-fat dairy products may not require calcium supplementation. In those consuming a low-calcium diet, supplements of 500 to 1,000 mg/day are likely adequate.

Denosumab, a new drug for preventing fractures

CUMMINGS SR, SAN MARTIN J, MCCLUNG MR, ET AL; FREEDOM TRIAL. DENOSUMAB FOR PREVENTION OF FRACTURES IN POSTMENOPAUSAL WOMEN WITH OSTEOPOROSIS. N ENGL J MED 2009; 361:756–765.

SMITH MR, EGERDIE B, HERNÁNDEZ TORIZ N, ET AL; DENOSUMAB HALT PROSTATE CANCER STUDY GROUP. DENOSUMAB IN MEN RECEIVING ANDROGEN-DEPRIVATION THERAPY FOR PROSTATE CANCER. N ENGL J MED 2009; 361:745–755.

Denosumab (Prolia) is the first of a new class of drugs for the treatment of osteoporosis. It is a monoclonal antibody and member of the tumor necrosis factor superfamily that binds to the receptor activator nuclear factor kappa B (RANK) ligand. It has an antiresorptive effect, preventing osteoclast differentiation and activation. It is given by subcutaneous injection of 60 mg every 6 months; it is cleared by a nonrenal mechanism.

In a randomized controlled trial in 7,868 women between the ages of 60 and 90 who had osteoporosis, Cummings et al⁹ reported that denosumab reduced the 3-year incidence of vertebral fractures by 68% (P < .001), reduced the incidence of hip fractures by 40% (P = .01), and reduced the incidence of nonvertebral fractures by 20% (P = .01). In a trial in men receiving androgen deprivation therapy for prostate cancer, Smith et al¹⁰ reported that denosumab reduced the incidence of vertebral fracture by 62% (P = .006).

Comment. Denosumab was approved by the US Food and Drug Administration (FDA) on June 1, 2010, and is emerging in specialty clinics at the time of this publication. Its potential impact on clinical care is not yet known. It is costly—about $825 (average wholesale price) per injection—but since it is given by injection it may be easier than a yearly infusion of zoledronic acid (Reclast). It has the potential to suppress immune function, although this was not reported in the clinical trials. It may ultimately have a role in treating osteoporosis in men and women, prostate cancer following androgen deprivation, metastatic prostate cancer, metastatic breast cancer, osteoporosis with renal impairment, and other diseases.

DIALYSIS IN THE ELDERLY: A BLEAK STORY

KURELLA TAMURA M, COVINSKY KE, CHERTOW GM, YAFFE K, LANDEFELD CS, MCCOLLOCH CE. FUNCTIONAL STATUS OF ELDERLY ADULTS BEFORE AND AFTER INITIATION OF DIALYSIS. N ENGL J MED 2009; 361:1539–1547.

JASSAL SV, CHIU E, HLADUNEWITH M. LOSS OF INDEPENDENCE IN PATIENTS STARTING DIALYSIS AT 80 YEARS OF AGE OR OLDER (LETTER). N ENGL J MED 2009; 361:1612–1613.

Nursing home residents account for 4% of all patients in end-stage renal disease. However, the benefits of dialysis in older patients are uncertain. The mortality rate during the first year of dialysis is 35% in patients 70 years of age and older and 50% in patients 80 years and older.

Is dialysis helpful in the elderly, ie, does it improve survival and function?

Kurella Tamura et al¹¹ retrospectively identified 3,702 nursing home residents starting dialysis in whom functional assessments had been done. The numbers told a bleak story. Initiation of dialysis was associated with a sharp decline in functional status, as reflected in an increase of 2.8 points on the 28-point Minimum Data Set–Activities of Daily Living (MDS-ADL) scale (the higher the score, the worse the function). MDS-ADL scores stabilized at a plateau for about 6 months and then continued to decline. Moreover, at 12 months, 58% of the patients had died.

The MDS-ADL score is based on seven components: eating, bed mobility, locomotion, transferring, toileting, hygiene, and dressing; function declined in all of these areas when patients started dialysis.

Patients were more likely to decline in activities of daily living after starting dialysis if they were older, were white, had cerebrovascular disease, had a diagnosis of dementia, were hospitalized at the start of dialysis, or had a serum albumin level lower than 3.5 g/dL.

The same thing happens to elders living in the community when they start dialysis. Jassal and colleagues¹² reported that, of 97 community-dwelling patients (mean age 85), 46 (47%) were dead 2 years after starting dialysis. Although 76 (78%) had been living independently at the start of dialysis, only 11 (11%) were still doing so at 2 years.

Comment. These findings indicate that we do not know if hemodialysis improves survival. Hemodialysis may buy about 3 months of stable function, but it clearly does not restore function.

Is this the best we can do? Standard hemodialysis may have flaws, and nocturnal dialysis and peritoneal dialysis are used more in other countries. These dialysis techniques require more study in our older population. The lesson from these two publications on dialysis is that we should attend more carefully to slowing the decline in renal function before patients reach end-stage renal disease.

DABIGATRAN: AN ALTERNATIVE TO WARFARIN FOR ATRIAL FIBRILLATION

CONNOLLY SJ, EZEKOWITZ MD, YUSUF S, ET AL; RE-LY STEERING COMMITTEE AND INVESTIGATORS. DABIGATRAN VERSUS WARFARIN IN PATIENTS WITH ATRIAL FIBRILLATION. N ENGL J MED 2009; 361:1139–1151.

Atrial fibrillation is common, affecting 2.2 million adults. The median age of people who have atrial fibrillation is 75 years, and it is the most common arrhythmia in the elderly. Some 20% of ischemic strokes are attributed to it.^13–15

Warfarin (Coumadin) is still the mainstay of treatment to prevent stroke in patients with atrial fibrillation. In an analysis of pooled data from five clinical trials,¹⁶ the relative risk reduction with warfarin was about 68% in the overall population (number needed to treat 32), 51% in people older than 75 years with no other risk factors (number needed to treat 56), and 85% in people older than 75 years with one or more risk factors (number needed to treat 15).

But warfarin carries a risk of bleeding, and its dose must be periodically adjusted on the basis of the international normalized ratio (INR) of the prothrombin time, so it carries a burden of laboratory monitoring. It is less safe in people who eat erratically, resulting in wide fluctuations in the INR.

Dabigatran (Pradaxa), a direct thrombin inhibitor, is expected to become an alternative to warfarin. It has been approved in Europe but not yet in the United States.

Connolly et al,¹⁷ in a randomized, double-blind trial, assigned 18,113 patients who had atrial fibrillation to receive either dabigatran 110 or 150 mg twice daily or adjusted-dose warfarin in an unblinded fashion. At 2 years, the rates of stroke and systemic embolism were about the same with dabigatran 110 mg as with warfarin but were lower with dabigatran 150 mg (relative risk 0.66, 95% confidence interval [CI] 0.53–0.82, P < .001). The rate of major bleeding was lower with dabigatran 110 mg than with warfarin (2.71% per year vs 3.36% per year, P = .003), but it was similar with dabigatran 150 mg (3.11% per year). Rates of life-threatening bleeding were 1.80% with warfarin, 1.22% with dabigatran 110 mg (P < .05), and 1.45% with dabigatran 150 mg (P < .05).

Comment. I suspect that warfarin’s days are numbered. Dabigatran 110 or 150 mg was as safe and as effective as warfarin in clinical trials, and probably will be more effective than warfarin in clinical practice. It will also probably be safer than warfarin in clinical practice, particularly in challenging settings such as long-term care. On the other hand, it will likely be much more expensive than warfarin.

DEMENTIA

Adverse effects of cholinesterase inhibitors

GILL SS, ANDERSON GM, FISCHER HD, ET AL. SYNCOPE AND ITS CONSEQUENCES IN PATIENTS WITH DEMENTIA RECEIVING CHOLINESTERASE INHIBITORS: A POPULATION-BASED COHORT STUDY. ARCH INTERN MED 2009; 169:867–873.

Cholinesterase inhibitors, eg, donepezil (Aricept), galantamine (Razadyne), and rivastigmine (Exelon), are commonly used to treat Alzheimer disease. However, these drugs carry risks of serious adverse effects.

Gill et al¹⁸ retrospectively reviewed a database from Ontario, Canada, and identified about 20,000 community-dwelling elderly persons admitted to the hospital who had been prescribed cholinesterase inhibitors and about three times as many matched controls.

Several adverse events were more frequent in people receiving cholinesterase inhibitors. Findings (events per 1,000 person-years):

• Hospital visits for syncope: 31.5 vs 18.6, adjusted hazard ratio (HR) 1.76, 95% CI 1.57–1.98
• Hip fractures: 22.4 vs 19.8, HR 1.18, 85% CI 1.04–1.34
• Hospital visits for bradycardia: 6.9 vs 4.4, HR 1.69, 95% CI 1.32–2.15
• Permanent pacemaker insertion: 4.7 vs 3.3, HR 1.49, 95% CI 1.12–2.00.

Comment. This study adds to the concerns that cholinesterase inhibitors, which have only modest cognitive benefits, may increase the risk of falls, injury, and need for pacemaker placement in demented patients. A low threshold to stop medications in this class should be considered when a patient on a cholinesterase inhibitor presents with bradycardia, falls, and syncope.

IVERSON DJ, GRONSETH GS, REGER MA, ET AL; STANDARDS SUBCOMMITTEE OF THE AMERICAN ACADEMY OF NEUROLOGY. PRACTICE PARAMETER UPDATE: EVALUATION AND MANAGEMENT OF DRIVING RISK IN DEMENTIA: REPORT OF THE QUALITY STANDARDS SUBCOMMITTEE OF THE AMERICAN ACADEMY OF NEUROLOGY. NEUROLOGY 2010; 74:1316–1324.

The Clinical Dementia Rating (CDR) is a simple scale that should be applied by clinicians to describe stage of dementia in patients with Alzheimer disease. This scale can be useful in a variety of settings, from prescribing antidementia drugs to determining whether a patient should still drive. Although research protocols utilize a survey or semistructured interview to derive the stage, the clinician can estimate the stage easily in the office, particularly if there is an informant who can comment on performance outside the office.

There are four stages to the CDR¹⁹:

• 0: No dementia
• 0.5: Mild memory deficit but intact function
• 1.0: Moderate memory loss with mild functional impairment
• 2.0: Severe memory loss, moderate functional impairment
• 3.0: Severe memory loss, no significant function outside of the house.

Comment. The first stage (0.5, mild memory deficit but intact function) corresponds to “mild cognitive impairment.” In the clinic, these patients tend to take more notes. They come to the appointment with a little book and they write everything down so they don’t forget. They do arrive at their appointments on time; they are not crashing the car; they are paying their bills.

Patients with CDR stage 1.0 dementia (moderate memory loss with mild functional impairment) may miss appointments, they may confuse their medications, and they may have problems driving. They are still taking care of their basic needs, and they show up for appointments acceptably washed and dressed. However, they are likely having trouble shopping and managing their finances.

Patients with severe memory loss and moderate functional impairment (CDR stage 2.0) may not realize they haven’t bathed for a week or have worn the same clothes repeatedly. They are having trouble with basic activities of daily living, such as bathing and toilet hygiene. However, if you were to encounter them socially and didn’t talk to them for too long, you might think they were normal.

Those with severe memory loss and no significant function outside the house (CDR stage 3.0) are the most severely disabled. Dementia in these individuals is recognizable at a glance, from across the room.

Alzheimer patients progress through the stages, from CDR stage 0.5 at about 1 year to stage 1 by about 2 years, to stage 2 by 5 years, and to stage 3 at 8 or 9 years.²⁰

In prescribing antidementia medications. The CDR can help with prescribing antidementia drugs. No medications are approved by the FDA for stage 0 or 0.5. Cholinesterase inhibitors are approved for stages 1, 2, and 3; memantine (Namenda) is approved for stages 2 and 3.

Advising about driving. The CDR is the only risk predictor with a quality-of-evidence rating of A. More than half of people with stage 0.5 memory impairment are safe drivers; fewer than half of those with stage 1.0 are still safe drivers; and patients with stage 2.0 dementia should not be driving at all.²¹ An adverse rating by a caregiver carries a quality-of-evidence rating of B. Predictors of driving risk with a quality-of-evidence rating of C are decreased mileage due to self-restriction, agitation, or aggression; a crash in the past 1 to 5 years; a citation in the past 2 to 3 years; and a Folstein Mini-Mental State Examination score of 24 or less. Studies also show that a memory-impaired person’s self-rating of safe driving ability or of assurance that he or she avoids unsafe situations is not reliable.²¹

DELIRIUM

Delirium goes by a number of synonyms, eg, “sundowning,” acute confusional state, acute change in mental status, metabolic encephalopathy, toxic encephalopathy (psychosis), acute brain syndrome, and acute toxic psychosis.

Delirium is common in hospitalized elderly patients, occurring in 11% to 42% of elderly hospitalized patients overall, up to 53% of elderly surgical patients on regular hospital floors, 80% of elderly surgical patients in intensive care, and about half of elderly patients after undergoing coronary artery bypass grafting. Unfortunately, it is undiagnosed in 30% to 60% of cases.^22–24

Many pathways can lead to delirium, including hypoxemia, metabolic derangement, drug effects, systemic inflammation, and infection.²⁵

Outcomes can vary from full recovery to death. After 1 year, 50% of those who leave the hospital with some evidence of delirium have not regained their baseline function. Delirium also increases the cost of care and the risk of institutionalization.

Delirium can accelerate dementia

FONG TG, JONES RN, SHI P, ET AL. DELIRIUM ACCELERATES COGNITIVE DECLINE IN ALZHEIMER DISEASE. NEUROLOGY 2009; 72:1570–1575.

Delirium accelerates the course of dementia in patients who had some evidence of dementia before they entered the hospital. Often, the change is noticeable by the family.²⁶

Preventing delirium

INOUYE SK BOGARDUS ST JR, CHARPENTIER PA, ET AL. A MULTICOMPONENT INTERVENTION TO PREVENT DELIRIUM IN HOSPITALIZED OLDER PATIENTS. N ENGL J MED 1999; 340:669–676.

LUNDSTRÖM M, OLOFSSON B, STENVALL M, ET AL. POSTOPERATIVE DELIRIUM IN OLD PATIENTS WITH FEMORAL NECK FRACTURE: A RANDOMIZED INTERVENTION STUDY. AGING CLIN EXP RES 2007; 19:178–186.

Delirium can often be prevented. In a report published in 1999, Inouye et al²⁷ described the outcomes of a program to prevent delirium in hospitalized medically ill elderly patients. Interventions were aimed at optimizing cognitive function, preventing sleep deprivation, avoiding immobility, improving vision and hearing, and treating dehydration. The incidence of delirium was 9.9% in the intervention group vs 15% in the control group, a 40% reduction (P < .05).

Lundström et al²⁸ implemented a similar program for elderly patients with hip fractures. Interventions included staff education and teamwork; active prevention, detection, and treatment of delirium; transfusions if hemoglobin levels were less than 10 g/dL; prompt removal of indwelling urinary catheters, with screening for urinary retention; active prevention and treatment of constipation; and protein-enriched meals. The incidence of delirium was 55% in the intervention group vs 75% in the control group, a 27% reduction.

Comment. Although we have long known that the risk of delirium in medical and surgical patients can be reduced, most hospitals do not have systematic programs to detect delirium and reduce its incidence. Hopefully, reduction in delirium risk will also reduce its adverse consequences, including worsening of dementia and increased mortality.

New clinical trials and observational studies are shedding light on ways to improve the health of elderly patients. Here is a brief summary of these trials and how they might influence your clinical practice.

EXERCISE HAS NEWLY DISCOVERED BENEFITS

According to government data,¹ exercise has a dose-dependent effect on rates of all-cause mortality: the more hours one exercises per week, the lower the risk of death. The difference in risk is most pronounced as one goes from no exercise to about 3 hours of exercise per week; above 3 hours per week, the curve flattens out but continues to decline. Hence, we advise patients to engage in about 30 minutes of moderate-intensity exercise every day.

Lately, physical exercise has been found to have other, unexpected benefits.

Exercise helps cognition

ERICKSON KI, PRAKASH RS, VOSS MW, ET AL. AEROBIC FITNESS IS ASSOCIATED WITH HIPPOCAMPAL VOLUME IN ELDERLY HUMANS. HIPPOCAMPUS 2009; 19:1030–1039.

ETGEN T, SANDER D, HUNTGEBURTH U, POPPERT H, FÖRSTL H, BICKEL H. PHYSICAL ACTIVITY AND INCIDENT COGNITIVE IMPAIRMENT IN ELDERLY PERSONS: THE INVADE STUDY. ARCH INTERN MED 2010; 170:186–193.

The hippocampus is a structure deep in the brain that is involved in short-term memory. It atrophies with age, more so with dementia. Erickson² found a correlation between aerobic fitness (as measured by maximum oxygen consumption), hippocampal volume, and spatial memory performance.

Etgen and colleagues³ studied nearly 4,000 older adults in Bavaria for 2 years. Among those reporting no physical activity, 21.4% had cognitive impairment at baseline, compared with 7.3% of those with high activity at baseline. Following those without cognitive impairment over a 2-year period, they found the incidence of new cognitive impairment was 13.9% in those with no physical activity at baseline, 6.7% in those with moderate activity, and 5.1% in those with high activity.

Exercise boosts the effect of influenza vaccine

WOODS JA, KEYLOCK KT, LOWDER T, ET AL. CARDIOVASCULAR EXERCISE TRAINING EXTENDS INFLUENZA VACCINE SEROPROTECTION IN SEDENTARY OLDER ADULTS: THE IMMUNE FUNCTION INTERVENTION TRIAL. J AM GERIATR SOC 2009; 57:2183–2191.

In a study in 144 sedentary but healthy older adults (ages 60 to 83), Woods et al⁴ randomized the participants to undergo either flexibility or cardiovascular training for 10 months, starting 4 months before their annual influenza shot. Exercise extended the duration of antibody protection, with more participants in the cardiovascular group than in the flexibility group showing protection at 24 weeks against all three strains covered by the vaccine: H1N1, H3N2, and influenza B.

PREVENTING FRACTURES

Each year, about 30% of people age 65 or older fall, sustaining serious injuries in 5% to 10% of cases. Unintentional falls are the main cause of hip fractures, which number 300,000 per year. They are also a common cause of death.

Vitamin D prevents fractures, but can there be too much of a good thing?

BISCHOFF-FERRARI HA, WILLETT WC, WONG JB, ET AL. PREVENTION OF NONVERTEBRAL FRACTURES WITH ORAL VITAMIN D AND DOSE DEPENDENCY: A META-ANALYSIS OF RANDOMIZED CONTROLLED TRIALS. ARCH INTERN MED 2009; 169:551–561.

SANDERS KM, STUART AL, WILLIAMSON EJ, ET AL. ANNUAL HIGH-DOSE ORAL VITAMIN D AND FALLS AND FRACTURES IN OLDER WOMEN: A RANDOMIZED CONTROLLED TRIAL. JAMA 2010; 303:1815–1822.

Bischoff-Ferrari⁵ performed a meta-analysis of 12 randomized controlled trials of oral supplemental vitamin D₃ for preventing nonvertebral fractures in people age 65 and older, and eight trials for preventing hip fractures in the same age group. They found that the higher the daily dose of vitamin D, the lower the relative risk of hip fracture. The threshold dose at which supplementation significantly reduced the risk of falling was about 400 units per day. Higher doses of vitamin D reduced both falls and hip fractures by about 20%. The maximal effect was seen with studies using the maximum daily doses, ie, 770 to 800 units per day—not megadoses, but more than most Americans are taking. The threshold serum level of vitamin D of significance was 60 nmol/L (24 ng/mL).

Of interest, the effect on fractures was independent of calcium supplementation. This is important because calcium supplementation over and above ordinary dietary intake may increase the risk of cardiovascular events.^6,7

Despite the benefits of vitamin D, too much may be too much of a good thing. Sanders et al⁸ performed a double-blind, placebo-controlled trial in 2,256 community-dwelling women, age 70 or older, who were considered to be at high risk for fractures. Half received a large oral dose (500,000 units) once a year for 3 to 5 years, and half got placebo. Their initial serum vitamin D level was 49 nmol/L; the level 30 days after a dose in the treatment group was 120 nmol/L.

Contrary to expectations, the incidence of falls was 15% higher in the vitamin D group than in the placebo group (P = .03), and the incidence of fractures was 26% higher (P = .047). The falls and fractures tended to cluster in the first 3 months after the dose in the active treatment group, when serum vitamin D levels were highest.

Comments. Unless future studies suggest a benefit to megadoses of vitamin D or prove calcium supplementation greater than 1,000 mg is safe, the optimal daily intake of vitamin D is likely 1,000 units, with approximately 200 units from diet and 800 units from supplements. A diet rich in low-fat dairy products may not require calcium supplementation. In those consuming a low-calcium diet, supplements of 500 to 1,000 mg/day are likely adequate.

Denosumab, a new drug for preventing fractures

CUMMINGS SR, SAN MARTIN J, MCCLUNG MR, ET AL; FREEDOM TRIAL. DENOSUMAB FOR PREVENTION OF FRACTURES IN POSTMENOPAUSAL WOMEN WITH OSTEOPOROSIS. N ENGL J MED 2009; 361:756–765.

SMITH MR, EGERDIE B, HERNÁNDEZ TORIZ N, ET AL; DENOSUMAB HALT PROSTATE CANCER STUDY GROUP. DENOSUMAB IN MEN RECEIVING ANDROGEN-DEPRIVATION THERAPY FOR PROSTATE CANCER. N ENGL J MED 2009; 361:745–755.

Denosumab (Prolia) is the first of a new class of drugs for the treatment of osteoporosis. It is a monoclonal antibody and member of the tumor necrosis factor superfamily that binds to the receptor activator nuclear factor kappa B (RANK) ligand. It has an antiresorptive effect, preventing osteoclast differentiation and activation. It is given by subcutaneous injection of 60 mg every 6 months; it is cleared by a nonrenal mechanism.

In a randomized controlled trial in 7,868 women between the ages of 60 and 90 who had osteoporosis, Cummings et al⁹ reported that denosumab reduced the 3-year incidence of vertebral fractures by 68% (P < .001), reduced the incidence of hip fractures by 40% (P = .01), and reduced the incidence of nonvertebral fractures by 20% (P = .01). In a trial in men receiving androgen deprivation therapy for prostate cancer, Smith et al¹⁰ reported that denosumab reduced the incidence of vertebral fracture by 62% (P = .006).

Comment. Denosumab was approved by the US Food and Drug Administration (FDA) on June 1, 2010, and is emerging in specialty clinics at the time of this publication. Its potential impact on clinical care is not yet known. It is costly—about $825 (average wholesale price) per injection—but since it is given by injection it may be easier than a yearly infusion of zoledronic acid (Reclast). It has the potential to suppress immune function, although this was not reported in the clinical trials. It may ultimately have a role in treating osteoporosis in men and women, prostate cancer following androgen deprivation, metastatic prostate cancer, metastatic breast cancer, osteoporosis with renal impairment, and other diseases.

DIALYSIS IN THE ELDERLY: A BLEAK STORY

KURELLA TAMURA M, COVINSKY KE, CHERTOW GM, YAFFE K, LANDEFELD CS, MCCOLLOCH CE. FUNCTIONAL STATUS OF ELDERLY ADULTS BEFORE AND AFTER INITIATION OF DIALYSIS. N ENGL J MED 2009; 361:1539–1547.

JASSAL SV, CHIU E, HLADUNEWITH M. LOSS OF INDEPENDENCE IN PATIENTS STARTING DIALYSIS AT 80 YEARS OF AGE OR OLDER (LETTER). N ENGL J MED 2009; 361:1612–1613.

Nursing home residents account for 4% of all patients in end-stage renal disease. However, the benefits of dialysis in older patients are uncertain. The mortality rate during the first year of dialysis is 35% in patients 70 years of age and older and 50% in patients 80 years and older.

Is dialysis helpful in the elderly, ie, does it improve survival and function?

Kurella Tamura et al¹¹ retrospectively identified 3,702 nursing home residents starting dialysis in whom functional assessments had been done. The numbers told a bleak story. Initiation of dialysis was associated with a sharp decline in functional status, as reflected in an increase of 2.8 points on the 28-point Minimum Data Set–Activities of Daily Living (MDS-ADL) scale (the higher the score, the worse the function). MDS-ADL scores stabilized at a plateau for about 6 months and then continued to decline. Moreover, at 12 months, 58% of the patients had died.

The MDS-ADL score is based on seven components: eating, bed mobility, locomotion, transferring, toileting, hygiene, and dressing; function declined in all of these areas when patients started dialysis.

Patients were more likely to decline in activities of daily living after starting dialysis if they were older, were white, had cerebrovascular disease, had a diagnosis of dementia, were hospitalized at the start of dialysis, or had a serum albumin level lower than 3.5 g/dL.

The same thing happens to elders living in the community when they start dialysis. Jassal and colleagues¹² reported that, of 97 community-dwelling patients (mean age 85), 46 (47%) were dead 2 years after starting dialysis. Although 76 (78%) had been living independently at the start of dialysis, only 11 (11%) were still doing so at 2 years.

Comment. These findings indicate that we do not know if hemodialysis improves survival. Hemodialysis may buy about 3 months of stable function, but it clearly does not restore function.

Is this the best we can do? Standard hemodialysis may have flaws, and nocturnal dialysis and peritoneal dialysis are used more in other countries. These dialysis techniques require more study in our older population. The lesson from these two publications on dialysis is that we should attend more carefully to slowing the decline in renal function before patients reach end-stage renal disease.

DABIGATRAN: AN ALTERNATIVE TO WARFARIN FOR ATRIAL FIBRILLATION

CONNOLLY SJ, EZEKOWITZ MD, YUSUF S, ET AL; RE-LY STEERING COMMITTEE AND INVESTIGATORS. DABIGATRAN VERSUS WARFARIN IN PATIENTS WITH ATRIAL FIBRILLATION. N ENGL J MED 2009; 361:1139–1151.

Atrial fibrillation is common, affecting 2.2 million adults. The median age of people who have atrial fibrillation is 75 years, and it is the most common arrhythmia in the elderly. Some 20% of ischemic strokes are attributed to it.^13–15

Warfarin (Coumadin) is still the mainstay of treatment to prevent stroke in patients with atrial fibrillation. In an analysis of pooled data from five clinical trials,¹⁶ the relative risk reduction with warfarin was about 68% in the overall population (number needed to treat 32), 51% in people older than 75 years with no other risk factors (number needed to treat 56), and 85% in people older than 75 years with one or more risk factors (number needed to treat 15).

But warfarin carries a risk of bleeding, and its dose must be periodically adjusted on the basis of the international normalized ratio (INR) of the prothrombin time, so it carries a burden of laboratory monitoring. It is less safe in people who eat erratically, resulting in wide fluctuations in the INR.

Dabigatran (Pradaxa), a direct thrombin inhibitor, is expected to become an alternative to warfarin. It has been approved in Europe but not yet in the United States.

Connolly et al,¹⁷ in a randomized, double-blind trial, assigned 18,113 patients who had atrial fibrillation to receive either dabigatran 110 or 150 mg twice daily or adjusted-dose warfarin in an unblinded fashion. At 2 years, the rates of stroke and systemic embolism were about the same with dabigatran 110 mg as with warfarin but were lower with dabigatran 150 mg (relative risk 0.66, 95% confidence interval [CI] 0.53–0.82, P < .001). The rate of major bleeding was lower with dabigatran 110 mg than with warfarin (2.71% per year vs 3.36% per year, P = .003), but it was similar with dabigatran 150 mg (3.11% per year). Rates of life-threatening bleeding were 1.80% with warfarin, 1.22% with dabigatran 110 mg (P < .05), and 1.45% with dabigatran 150 mg (P < .05).

Comment. I suspect that warfarin’s days are numbered. Dabigatran 110 or 150 mg was as safe and as effective as warfarin in clinical trials, and probably will be more effective than warfarin in clinical practice. It will also probably be safer than warfarin in clinical practice, particularly in challenging settings such as long-term care. On the other hand, it will likely be much more expensive than warfarin.

DEMENTIA

Adverse effects of cholinesterase inhibitors

GILL SS, ANDERSON GM, FISCHER HD, ET AL. SYNCOPE AND ITS CONSEQUENCES IN PATIENTS WITH DEMENTIA RECEIVING CHOLINESTERASE INHIBITORS: A POPULATION-BASED COHORT STUDY. ARCH INTERN MED 2009; 169:867–873.

Cholinesterase inhibitors, eg, donepezil (Aricept), galantamine (Razadyne), and rivastigmine (Exelon), are commonly used to treat Alzheimer disease. However, these drugs carry risks of serious adverse effects.

Gill et al¹⁸ retrospectively reviewed a database from Ontario, Canada, and identified about 20,000 community-dwelling elderly persons admitted to the hospital who had been prescribed cholinesterase inhibitors and about three times as many matched controls.

Several adverse events were more frequent in people receiving cholinesterase inhibitors. Findings (events per 1,000 person-years):

• Hospital visits for syncope: 31.5 vs 18.6, adjusted hazard ratio (HR) 1.76, 95% CI 1.57–1.98
• Hip fractures: 22.4 vs 19.8, HR 1.18, 85% CI 1.04–1.34
• Hospital visits for bradycardia: 6.9 vs 4.4, HR 1.69, 95% CI 1.32–2.15
• Permanent pacemaker insertion: 4.7 vs 3.3, HR 1.49, 95% CI 1.12–2.00.

Comment. This study adds to the concerns that cholinesterase inhibitors, which have only modest cognitive benefits, may increase the risk of falls, injury, and need for pacemaker placement in demented patients. A low threshold to stop medications in this class should be considered when a patient on a cholinesterase inhibitor presents with bradycardia, falls, and syncope.

IVERSON DJ, GRONSETH GS, REGER MA, ET AL; STANDARDS SUBCOMMITTEE OF THE AMERICAN ACADEMY OF NEUROLOGY. PRACTICE PARAMETER UPDATE: EVALUATION AND MANAGEMENT OF DRIVING RISK IN DEMENTIA: REPORT OF THE QUALITY STANDARDS SUBCOMMITTEE OF THE AMERICAN ACADEMY OF NEUROLOGY. NEUROLOGY 2010; 74:1316–1324.

The Clinical Dementia Rating (CDR) is a simple scale that should be applied by clinicians to describe stage of dementia in patients with Alzheimer disease. This scale can be useful in a variety of settings, from prescribing antidementia drugs to determining whether a patient should still drive. Although research protocols utilize a survey or semistructured interview to derive the stage, the clinician can estimate the stage easily in the office, particularly if there is an informant who can comment on performance outside the office.

There are four stages to the CDR¹⁹:

• 0: No dementia
• 0.5: Mild memory deficit but intact function
• 1.0: Moderate memory loss with mild functional impairment
• 2.0: Severe memory loss, moderate functional impairment
• 3.0: Severe memory loss, no significant function outside of the house.

Comment. The first stage (0.5, mild memory deficit but intact function) corresponds to “mild cognitive impairment.” In the clinic, these patients tend to take more notes. They come to the appointment with a little book and they write everything down so they don’t forget. They do arrive at their appointments on time; they are not crashing the car; they are paying their bills.

Patients with CDR stage 1.0 dementia (moderate memory loss with mild functional impairment) may miss appointments, they may confuse their medications, and they may have problems driving. They are still taking care of their basic needs, and they show up for appointments acceptably washed and dressed. However, they are likely having trouble shopping and managing their finances.

Patients with severe memory loss and moderate functional impairment (CDR stage 2.0) may not realize they haven’t bathed for a week or have worn the same clothes repeatedly. They are having trouble with basic activities of daily living, such as bathing and toilet hygiene. However, if you were to encounter them socially and didn’t talk to them for too long, you might think they were normal.

Those with severe memory loss and no significant function outside the house (CDR stage 3.0) are the most severely disabled. Dementia in these individuals is recognizable at a glance, from across the room.

Alzheimer patients progress through the stages, from CDR stage 0.5 at about 1 year to stage 1 by about 2 years, to stage 2 by 5 years, and to stage 3 at 8 or 9 years.²⁰

In prescribing antidementia medications. The CDR can help with prescribing antidementia drugs. No medications are approved by the FDA for stage 0 or 0.5. Cholinesterase inhibitors are approved for stages 1, 2, and 3; memantine (Namenda) is approved for stages 2 and 3.

Advising about driving. The CDR is the only risk predictor with a quality-of-evidence rating of A. More than half of people with stage 0.5 memory impairment are safe drivers; fewer than half of those with stage 1.0 are still safe drivers; and patients with stage 2.0 dementia should not be driving at all.²¹ An adverse rating by a caregiver carries a quality-of-evidence rating of B. Predictors of driving risk with a quality-of-evidence rating of C are decreased mileage due to self-restriction, agitation, or aggression; a crash in the past 1 to 5 years; a citation in the past 2 to 3 years; and a Folstein Mini-Mental State Examination score of 24 or less. Studies also show that a memory-impaired person’s self-rating of safe driving ability or of assurance that he or she avoids unsafe situations is not reliable.²¹

DELIRIUM

Delirium goes by a number of synonyms, eg, “sundowning,” acute confusional state, acute change in mental status, metabolic encephalopathy, toxic encephalopathy (psychosis), acute brain syndrome, and acute toxic psychosis.

Delirium is common in hospitalized elderly patients, occurring in 11% to 42% of elderly hospitalized patients overall, up to 53% of elderly surgical patients on regular hospital floors, 80% of elderly surgical patients in intensive care, and about half of elderly patients after undergoing coronary artery bypass grafting. Unfortunately, it is undiagnosed in 30% to 60% of cases.^22–24

Many pathways can lead to delirium, including hypoxemia, metabolic derangement, drug effects, systemic inflammation, and infection.²⁵

Outcomes can vary from full recovery to death. After 1 year, 50% of those who leave the hospital with some evidence of delirium have not regained their baseline function. Delirium also increases the cost of care and the risk of institutionalization.

Delirium can accelerate dementia

FONG TG, JONES RN, SHI P, ET AL. DELIRIUM ACCELERATES COGNITIVE DECLINE IN ALZHEIMER DISEASE. NEUROLOGY 2009; 72:1570–1575.

Delirium accelerates the course of dementia in patients who had some evidence of dementia before they entered the hospital. Often, the change is noticeable by the family.²⁶

Preventing delirium

INOUYE SK BOGARDUS ST JR, CHARPENTIER PA, ET AL. A MULTICOMPONENT INTERVENTION TO PREVENT DELIRIUM IN HOSPITALIZED OLDER PATIENTS. N ENGL J MED 1999; 340:669–676.

LUNDSTRÖM M, OLOFSSON B, STENVALL M, ET AL. POSTOPERATIVE DELIRIUM IN OLD PATIENTS WITH FEMORAL NECK FRACTURE: A RANDOMIZED INTERVENTION STUDY. AGING CLIN EXP RES 2007; 19:178–186.

Delirium can often be prevented. In a report published in 1999, Inouye et al²⁷ described the outcomes of a program to prevent delirium in hospitalized medically ill elderly patients. Interventions were aimed at optimizing cognitive function, preventing sleep deprivation, avoiding immobility, improving vision and hearing, and treating dehydration. The incidence of delirium was 9.9% in the intervention group vs 15% in the control group, a 40% reduction (P < .05).

Lundström et al²⁸ implemented a similar program for elderly patients with hip fractures. Interventions included staff education and teamwork; active prevention, detection, and treatment of delirium; transfusions if hemoglobin levels were less than 10 g/dL; prompt removal of indwelling urinary catheters, with screening for urinary retention; active prevention and treatment of constipation; and protein-enriched meals. The incidence of delirium was 55% in the intervention group vs 75% in the control group, a 27% reduction.

Comment. Although we have long known that the risk of delirium in medical and surgical patients can be reduced, most hospitals do not have systematic programs to detect delirium and reduce its incidence. Hopefully, reduction in delirium risk will also reduce its adverse consequences, including worsening of dementia and increased mortality.

New clinical trials and observational studies are shedding light on ways to improve the health of elderly patients. Here is a brief summary of these trials and how they might influence your clinical practice.

EXERCISE HAS NEWLY DISCOVERED BENEFITS

According to government data,¹ exercise has a dose-dependent effect on rates of all-cause mortality: the more hours one exercises per week, the lower the risk of death. The difference in risk is most pronounced as one goes from no exercise to about 3 hours of exercise per week; above 3 hours per week, the curve flattens out but continues to decline. Hence, we advise patients to engage in about 30 minutes of moderate-intensity exercise every day.

Lately, physical exercise has been found to have other, unexpected benefits.

Exercise helps cognition

ERICKSON KI, PRAKASH RS, VOSS MW, ET AL. AEROBIC FITNESS IS ASSOCIATED WITH HIPPOCAMPAL VOLUME IN ELDERLY HUMANS. HIPPOCAMPUS 2009; 19:1030–1039.

ETGEN T, SANDER D, HUNTGEBURTH U, POPPERT H, FÖRSTL H, BICKEL H. PHYSICAL ACTIVITY AND INCIDENT COGNITIVE IMPAIRMENT IN ELDERLY PERSONS: THE INVADE STUDY. ARCH INTERN MED 2010; 170:186–193.

The hippocampus is a structure deep in the brain that is involved in short-term memory. It atrophies with age, more so with dementia. Erickson² found a correlation between aerobic fitness (as measured by maximum oxygen consumption), hippocampal volume, and spatial memory performance.

Etgen and colleagues³ studied nearly 4,000 older adults in Bavaria for 2 years. Among those reporting no physical activity, 21.4% had cognitive impairment at baseline, compared with 7.3% of those with high activity at baseline. Following those without cognitive impairment over a 2-year period, they found the incidence of new cognitive impairment was 13.9% in those with no physical activity at baseline, 6.7% in those with moderate activity, and 5.1% in those with high activity.

Exercise boosts the effect of influenza vaccine

WOODS JA, KEYLOCK KT, LOWDER T, ET AL. CARDIOVASCULAR EXERCISE TRAINING EXTENDS INFLUENZA VACCINE SEROPROTECTION IN SEDENTARY OLDER ADULTS: THE IMMUNE FUNCTION INTERVENTION TRIAL. J AM GERIATR SOC 2009; 57:2183–2191.

In a study in 144 sedentary but healthy older adults (ages 60 to 83), Woods et al⁴ randomized the participants to undergo either flexibility or cardiovascular training for 10 months, starting 4 months before their annual influenza shot. Exercise extended the duration of antibody protection, with more participants in the cardiovascular group than in the flexibility group showing protection at 24 weeks against all three strains covered by the vaccine: H1N1, H3N2, and influenza B.

PREVENTING FRACTURES

Each year, about 30% of people age 65 or older fall, sustaining serious injuries in 5% to 10% of cases. Unintentional falls are the main cause of hip fractures, which number 300,000 per year. They are also a common cause of death.

Vitamin D prevents fractures, but can there be too much of a good thing?

BISCHOFF-FERRARI HA, WILLETT WC, WONG JB, ET AL. PREVENTION OF NONVERTEBRAL FRACTURES WITH ORAL VITAMIN D AND DOSE DEPENDENCY: A META-ANALYSIS OF RANDOMIZED CONTROLLED TRIALS. ARCH INTERN MED 2009; 169:551–561.

SANDERS KM, STUART AL, WILLIAMSON EJ, ET AL. ANNUAL HIGH-DOSE ORAL VITAMIN D AND FALLS AND FRACTURES IN OLDER WOMEN: A RANDOMIZED CONTROLLED TRIAL. JAMA 2010; 303:1815–1822.

Bischoff-Ferrari⁵ performed a meta-analysis of 12 randomized controlled trials of oral supplemental vitamin D₃ for preventing nonvertebral fractures in people age 65 and older, and eight trials for preventing hip fractures in the same age group. They found that the higher the daily dose of vitamin D, the lower the relative risk of hip fracture. The threshold dose at which supplementation significantly reduced the risk of falling was about 400 units per day. Higher doses of vitamin D reduced both falls and hip fractures by about 20%. The maximal effect was seen with studies using the maximum daily doses, ie, 770 to 800 units per day—not megadoses, but more than most Americans are taking. The threshold serum level of vitamin D of significance was 60 nmol/L (24 ng/mL).

Of interest, the effect on fractures was independent of calcium supplementation. This is important because calcium supplementation over and above ordinary dietary intake may increase the risk of cardiovascular events.^6,7

Despite the benefits of vitamin D, too much may be too much of a good thing. Sanders et al⁸ performed a double-blind, placebo-controlled trial in 2,256 community-dwelling women, age 70 or older, who were considered to be at high risk for fractures. Half received a large oral dose (500,000 units) once a year for 3 to 5 years, and half got placebo. Their initial serum vitamin D level was 49 nmol/L; the level 30 days after a dose in the treatment group was 120 nmol/L.

Contrary to expectations, the incidence of falls was 15% higher in the vitamin D group than in the placebo group (P = .03), and the incidence of fractures was 26% higher (P = .047). The falls and fractures tended to cluster in the first 3 months after the dose in the active treatment group, when serum vitamin D levels were highest.

Comments. Unless future studies suggest a benefit to megadoses of vitamin D or prove calcium supplementation greater than 1,000 mg is safe, the optimal daily intake of vitamin D is likely 1,000 units, with approximately 200 units from diet and 800 units from supplements. A diet rich in low-fat dairy products may not require calcium supplementation. In those consuming a low-calcium diet, supplements of 500 to 1,000 mg/day are likely adequate.

Denosumab, a new drug for preventing fractures

CUMMINGS SR, SAN MARTIN J, MCCLUNG MR, ET AL; FREEDOM TRIAL. DENOSUMAB FOR PREVENTION OF FRACTURES IN POSTMENOPAUSAL WOMEN WITH OSTEOPOROSIS. N ENGL J MED 2009; 361:756–765.

SMITH MR, EGERDIE B, HERNÁNDEZ TORIZ N, ET AL; DENOSUMAB HALT PROSTATE CANCER STUDY GROUP. DENOSUMAB IN MEN RECEIVING ANDROGEN-DEPRIVATION THERAPY FOR PROSTATE CANCER. N ENGL J MED 2009; 361:745–755.

Denosumab (Prolia) is the first of a new class of drugs for the treatment of osteoporosis. It is a monoclonal antibody and member of the tumor necrosis factor superfamily that binds to the receptor activator nuclear factor kappa B (RANK) ligand. It has an antiresorptive effect, preventing osteoclast differentiation and activation. It is given by subcutaneous injection of 60 mg every 6 months; it is cleared by a nonrenal mechanism.

In a randomized controlled trial in 7,868 women between the ages of 60 and 90 who had osteoporosis, Cummings et al⁹ reported that denosumab reduced the 3-year incidence of vertebral fractures by 68% (P < .001), reduced the incidence of hip fractures by 40% (P = .01), and reduced the incidence of nonvertebral fractures by 20% (P = .01). In a trial in men receiving androgen deprivation therapy for prostate cancer, Smith et al¹⁰ reported that denosumab reduced the incidence of vertebral fracture by 62% (P = .006).

Comment. Denosumab was approved by the US Food and Drug Administration (FDA) on June 1, 2010, and is emerging in specialty clinics at the time of this publication. Its potential impact on clinical care is not yet known. It is costly—about $825 (average wholesale price) per injection—but since it is given by injection it may be easier than a yearly infusion of zoledronic acid (Reclast). It has the potential to suppress immune function, although this was not reported in the clinical trials. It may ultimately have a role in treating osteoporosis in men and women, prostate cancer following androgen deprivation, metastatic prostate cancer, metastatic breast cancer, osteoporosis with renal impairment, and other diseases.

DIALYSIS IN THE ELDERLY: A BLEAK STORY

KURELLA TAMURA M, COVINSKY KE, CHERTOW GM, YAFFE K, LANDEFELD CS, MCCOLLOCH CE. FUNCTIONAL STATUS OF ELDERLY ADULTS BEFORE AND AFTER INITIATION OF DIALYSIS. N ENGL J MED 2009; 361:1539–1547.

JASSAL SV, CHIU E, HLADUNEWITH M. LOSS OF INDEPENDENCE IN PATIENTS STARTING DIALYSIS AT 80 YEARS OF AGE OR OLDER (LETTER). N ENGL J MED 2009; 361:1612–1613.

Nursing home residents account for 4% of all patients in end-stage renal disease. However, the benefits of dialysis in older patients are uncertain. The mortality rate during the first year of dialysis is 35% in patients 70 years of age and older and 50% in patients 80 years and older.

Is dialysis helpful in the elderly, ie, does it improve survival and function?

Kurella Tamura et al¹¹ retrospectively identified 3,702 nursing home residents starting dialysis in whom functional assessments had been done. The numbers told a bleak story. Initiation of dialysis was associated with a sharp decline in functional status, as reflected in an increase of 2.8 points on the 28-point Minimum Data Set–Activities of Daily Living (MDS-ADL) scale (the higher the score, the worse the function). MDS-ADL scores stabilized at a plateau for about 6 months and then continued to decline. Moreover, at 12 months, 58% of the patients had died.

The MDS-ADL score is based on seven components: eating, bed mobility, locomotion, transferring, toileting, hygiene, and dressing; function declined in all of these areas when patients started dialysis.

Patients were more likely to decline in activities of daily living after starting dialysis if they were older, were white, had cerebrovascular disease, had a diagnosis of dementia, were hospitalized at the start of dialysis, or had a serum albumin level lower than 3.5 g/dL.

The same thing happens to elders living in the community when they start dialysis. Jassal and colleagues¹² reported that, of 97 community-dwelling patients (mean age 85), 46 (47%) were dead 2 years after starting dialysis. Although 76 (78%) had been living independently at the start of dialysis, only 11 (11%) were still doing so at 2 years.

Comment. These findings indicate that we do not know if hemodialysis improves survival. Hemodialysis may buy about 3 months of stable function, but it clearly does not restore function.

Is this the best we can do? Standard hemodialysis may have flaws, and nocturnal dialysis and peritoneal dialysis are used more in other countries. These dialysis techniques require more study in our older population. The lesson from these two publications on dialysis is that we should attend more carefully to slowing the decline in renal function before patients reach end-stage renal disease.

DABIGATRAN: AN ALTERNATIVE TO WARFARIN FOR ATRIAL FIBRILLATION

CONNOLLY SJ, EZEKOWITZ MD, YUSUF S, ET AL; RE-LY STEERING COMMITTEE AND INVESTIGATORS. DABIGATRAN VERSUS WARFARIN IN PATIENTS WITH ATRIAL FIBRILLATION. N ENGL J MED 2009; 361:1139–1151.

Atrial fibrillation is common, affecting 2.2 million adults. The median age of people who have atrial fibrillation is 75 years, and it is the most common arrhythmia in the elderly. Some 20% of ischemic strokes are attributed to it.^13–15

Warfarin (Coumadin) is still the mainstay of treatment to prevent stroke in patients with atrial fibrillation. In an analysis of pooled data from five clinical trials,¹⁶ the relative risk reduction with warfarin was about 68% in the overall population (number needed to treat 32), 51% in people older than 75 years with no other risk factors (number needed to treat 56), and 85% in people older than 75 years with one or more risk factors (number needed to treat 15).

But warfarin carries a risk of bleeding, and its dose must be periodically adjusted on the basis of the international normalized ratio (INR) of the prothrombin time, so it carries a burden of laboratory monitoring. It is less safe in people who eat erratically, resulting in wide fluctuations in the INR.

Dabigatran (Pradaxa), a direct thrombin inhibitor, is expected to become an alternative to warfarin. It has been approved in Europe but not yet in the United States.

Connolly et al,¹⁷ in a randomized, double-blind trial, assigned 18,113 patients who had atrial fibrillation to receive either dabigatran 110 or 150 mg twice daily or adjusted-dose warfarin in an unblinded fashion. At 2 years, the rates of stroke and systemic embolism were about the same with dabigatran 110 mg as with warfarin but were lower with dabigatran 150 mg (relative risk 0.66, 95% confidence interval [CI] 0.53–0.82, P < .001). The rate of major bleeding was lower with dabigatran 110 mg than with warfarin (2.71% per year vs 3.36% per year, P = .003), but it was similar with dabigatran 150 mg (3.11% per year). Rates of life-threatening bleeding were 1.80% with warfarin, 1.22% with dabigatran 110 mg (P < .05), and 1.45% with dabigatran 150 mg (P < .05).

Comment. I suspect that warfarin’s days are numbered. Dabigatran 110 or 150 mg was as safe and as effective as warfarin in clinical trials, and probably will be more effective than warfarin in clinical practice. It will also probably be safer than warfarin in clinical practice, particularly in challenging settings such as long-term care. On the other hand, it will likely be much more expensive than warfarin.

DEMENTIA

Adverse effects of cholinesterase inhibitors

GILL SS, ANDERSON GM, FISCHER HD, ET AL. SYNCOPE AND ITS CONSEQUENCES IN PATIENTS WITH DEMENTIA RECEIVING CHOLINESTERASE INHIBITORS: A POPULATION-BASED COHORT STUDY. ARCH INTERN MED 2009; 169:867–873.

Cholinesterase inhibitors, eg, donepezil (Aricept), galantamine (Razadyne), and rivastigmine (Exelon), are commonly used to treat Alzheimer disease. However, these drugs carry risks of serious adverse effects.

Gill et al¹⁸ retrospectively reviewed a database from Ontario, Canada, and identified about 20,000 community-dwelling elderly persons admitted to the hospital who had been prescribed cholinesterase inhibitors and about three times as many matched controls.

Several adverse events were more frequent in people receiving cholinesterase inhibitors. Findings (events per 1,000 person-years):

• Hospital visits for syncope: 31.5 vs 18.6, adjusted hazard ratio (HR) 1.76, 95% CI 1.57–1.98
• Hip fractures: 22.4 vs 19.8, HR 1.18, 85% CI 1.04–1.34
• Hospital visits for bradycardia: 6.9 vs 4.4, HR 1.69, 95% CI 1.32–2.15
• Permanent pacemaker insertion: 4.7 vs 3.3, HR 1.49, 95% CI 1.12–2.00.

Comment. This study adds to the concerns that cholinesterase inhibitors, which have only modest cognitive benefits, may increase the risk of falls, injury, and need for pacemaker placement in demented patients. A low threshold to stop medications in this class should be considered when a patient on a cholinesterase inhibitor presents with bradycardia, falls, and syncope.

IVERSON DJ, GRONSETH GS, REGER MA, ET AL; STANDARDS SUBCOMMITTEE OF THE AMERICAN ACADEMY OF NEUROLOGY. PRACTICE PARAMETER UPDATE: EVALUATION AND MANAGEMENT OF DRIVING RISK IN DEMENTIA: REPORT OF THE QUALITY STANDARDS SUBCOMMITTEE OF THE AMERICAN ACADEMY OF NEUROLOGY. NEUROLOGY 2010; 74:1316–1324.

The Clinical Dementia Rating (CDR) is a simple scale that should be applied by clinicians to describe stage of dementia in patients with Alzheimer disease. This scale can be useful in a variety of settings, from prescribing antidementia drugs to determining whether a patient should still drive. Although research protocols utilize a survey or semistructured interview to derive the stage, the clinician can estimate the stage easily in the office, particularly if there is an informant who can comment on performance outside the office.

There are four stages to the CDR¹⁹:

• 0: No dementia
• 0.5: Mild memory deficit but intact function
• 1.0: Moderate memory loss with mild functional impairment
• 2.0: Severe memory loss, moderate functional impairment
• 3.0: Severe memory loss, no significant function outside of the house.

Comment. The first stage (0.5, mild memory deficit but intact function) corresponds to “mild cognitive impairment.” In the clinic, these patients tend to take more notes. They come to the appointment with a little book and they write everything down so they don’t forget. They do arrive at their appointments on time; they are not crashing the car; they are paying their bills.

Patients with CDR stage 1.0 dementia (moderate memory loss with mild functional impairment) may miss appointments, they may confuse their medications, and they may have problems driving. They are still taking care of their basic needs, and they show up for appointments acceptably washed and dressed. However, they are likely having trouble shopping and managing their finances.

Patients with severe memory loss and moderate functional impairment (CDR stage 2.0) may not realize they haven’t bathed for a week or have worn the same clothes repeatedly. They are having trouble with basic activities of daily living, such as bathing and toilet hygiene. However, if you were to encounter them socially and didn’t talk to them for too long, you might think they were normal.

Those with severe memory loss and no significant function outside the house (CDR stage 3.0) are the most severely disabled. Dementia in these individuals is recognizable at a glance, from across the room.

Alzheimer patients progress through the stages, from CDR stage 0.5 at about 1 year to stage 1 by about 2 years, to stage 2 by 5 years, and to stage 3 at 8 or 9 years.²⁰

In prescribing antidementia medications. The CDR can help with prescribing antidementia drugs. No medications are approved by the FDA for stage 0 or 0.5. Cholinesterase inhibitors are approved for stages 1, 2, and 3; memantine (Namenda) is approved for stages 2 and 3.

Advising about driving. The CDR is the only risk predictor with a quality-of-evidence rating of A. More than half of people with stage 0.5 memory impairment are safe drivers; fewer than half of those with stage 1.0 are still safe drivers; and patients with stage 2.0 dementia should not be driving at all.²¹ An adverse rating by a caregiver carries a quality-of-evidence rating of B. Predictors of driving risk with a quality-of-evidence rating of C are decreased mileage due to self-restriction, agitation, or aggression; a crash in the past 1 to 5 years; a citation in the past 2 to 3 years; and a Folstein Mini-Mental State Examination score of 24 or less. Studies also show that a memory-impaired person’s self-rating of safe driving ability or of assurance that he or she avoids unsafe situations is not reliable.²¹

DELIRIUM

Delirium goes by a number of synonyms, eg, “sundowning,” acute confusional state, acute change in mental status, metabolic encephalopathy, toxic encephalopathy (psychosis), acute brain syndrome, and acute toxic psychosis.

Delirium is common in hospitalized elderly patients, occurring in 11% to 42% of elderly hospitalized patients overall, up to 53% of elderly surgical patients on regular hospital floors, 80% of elderly surgical patients in intensive care, and about half of elderly patients after undergoing coronary artery bypass grafting. Unfortunately, it is undiagnosed in 30% to 60% of cases.^22–24

Many pathways can lead to delirium, including hypoxemia, metabolic derangement, drug effects, systemic inflammation, and infection.²⁵

Outcomes can vary from full recovery to death. After 1 year, 50% of those who leave the hospital with some evidence of delirium have not regained their baseline function. Delirium also increases the cost of care and the risk of institutionalization.

Delirium can accelerate dementia

FONG TG, JONES RN, SHI P, ET AL. DELIRIUM ACCELERATES COGNITIVE DECLINE IN ALZHEIMER DISEASE. NEUROLOGY 2009; 72:1570–1575.

Delirium accelerates the course of dementia in patients who had some evidence of dementia before they entered the hospital. Often, the change is noticeable by the family.²⁶

Preventing delirium

INOUYE SK BOGARDUS ST JR, CHARPENTIER PA, ET AL. A MULTICOMPONENT INTERVENTION TO PREVENT DELIRIUM IN HOSPITALIZED OLDER PATIENTS. N ENGL J MED 1999; 340:669–676.

LUNDSTRÖM M, OLOFSSON B, STENVALL M, ET AL. POSTOPERATIVE DELIRIUM IN OLD PATIENTS WITH FEMORAL NECK FRACTURE: A RANDOMIZED INTERVENTION STUDY. AGING CLIN EXP RES 2007; 19:178–186.

Delirium can often be prevented. In a report published in 1999, Inouye et al²⁷ described the outcomes of a program to prevent delirium in hospitalized medically ill elderly patients. Interventions were aimed at optimizing cognitive function, preventing sleep deprivation, avoiding immobility, improving vision and hearing, and treating dehydration. The incidence of delirium was 9.9% in the intervention group vs 15% in the control group, a 40% reduction (P < .05).

Lundström et al²⁸ implemented a similar program for elderly patients with hip fractures. Interventions included staff education and teamwork; active prevention, detection, and treatment of delirium; transfusions if hemoglobin levels were less than 10 g/dL; prompt removal of indwelling urinary catheters, with screening for urinary retention; active prevention and treatment of constipation; and protein-enriched meals. The incidence of delirium was 55% in the intervention group vs 75% in the control group, a 27% reduction.

Comment. Although we have long known that the risk of delirium in medical and surgical patients can be reduced, most hospitals do not have systematic programs to detect delirium and reduce its incidence. Hopefully, reduction in delirium risk will also reduce its adverse consequences, including worsening of dementia and increased mortality.

Patients with an osteoporotic hip fracture suffer from profound morbidity and are at a heightened risk of death. It is therefore essential that they receive treatment with a bisphosphonate known to modify the subsequent risk of fracture at any site—eg, alendronate (Fosamax), risedronate (Actonel), or zoledronic acid (Reclast).

However, there is concern that starting a bisphosphonate too soon after surgery could disrupt bone remodeling and delay fracture repair.

Only one clinical study addressed the timing of bisphosphonate therapy after hip fracture repair. In this study, Eriksen et al¹ performed a post hoc analysis of data from the Health Outcomes and Reduced Incidence With Zoledronic Acid Once Yearly Recurrent Fracture Trial (HORIZON-RFT)² and concluded that the optimal time to give intravenous zoledronic acid is 2 to 12 weeks after surgical repair of the fracture.

In a frail, elderly patient with comorbidities, a single intravenous 5-mg dose of zoledronic acid guarantees adequate treatment, obviating issues of poor compliance and oral absorption and loss to follow-up. Sufficient levels of vitamin D and calcium should be ensured.

THE EVIDENCE

The original HORIZON-RFT study,² published in 2007, compared intravenous zoledronic acid against placebo in elderly patients with osteoporotic hip fracture. Most of the patients were white women; their mean age was 74; 1,065 received intravenous zoledronic acid, and 1,062 received placebo. All received vitamin D and calcium.

The trial showed a clear reduction in the rate of recurrent fractures at other sites (a primary end point) and a reduction in the rate of all-cause mortality in patients treated within 90 days of fracture. A total of 424 fractures occurred in 231 patients. The risk of any new clinical fracture was 35% lower with treatment than with placebo (occurring in 8.6% vs 13.9% of patients, P = .001), and the number of deaths due to any cause was 28% lower with treatment than with placebo (occurring in 101 vs 141, P = .01).²

The mean time to fracture was 39.8 months in the treated group vs 36.4 in the placebo group. The fracture risk reduction began to be apparent by 12 months, and the reduction in mortality rate by 16 months.²

In a post hoc analysis of the trial, Eriksen et al¹ attempted to ascertain the optimal time for therapy in terms of fracture risk and mortality reduction. Analyzing the data by 2-week intervals beginning after the surgical repair of the fracture, the authors found that only 56 patients (5.3%) had received zoledronic acid within 2 weeks of surgery and only 47 had received placebo, and they saw no advantage to intravenous zoledronic acid compared with placebo in these first 2 weeks with respect to bone mineral density, fracture risk, or risk of death. However, excluding this small subset, antifracture efficacy and reduction in mortality rate were present when patients were treated with zoledronic acid in the 2 to 12 weeks after hip fracture repair, and improvement in bone mineral density at the hip was noted at 12 months in all cohorts.

Colón-Emeric et al³ performed another post hoc analysis, attempting to explain the lower mortality rate seen in patients treated with zoledronic acid. It had been an unexpected finding, and determinants of mortality rate reduction were hampered by a limited knowledge of the true cause of death or the circumstances of care after fracture. The authors concluded that only 8% of the reduction in mortality rate evident early in the second year of treatment with zoledronic acid could be attributed to a reduction in fractures.³ Other mechanisms by which the mortality rate reduction occurred remained unclear.

Curiously, in another large randomized controlled trial of zoledronic acid, in women with postmenopausal osteoporosis, Black et al⁴ reported that more patients died in the treated group (130 of 3,862) than in the placebo group (112 of 3,852). This difference was not statistically significant, but neither was it explained.

A meta-analysis by Bolland et al⁵ examined the effect of other osteoporosis treatments on mortality rate, using randomized controlled trials that lasted more than 12 months and that reported more than 10 deaths. The authors concluded the following:

• In the trials in which bisphosphonates reduced the mortality rate, the mortality rate in the placebo group was higher than 10 per 1,000 patient-years
• The effect of osteoporosis treatment on the mortality rate in a frail, elderly population is evident using agents with proven efficacy in reducing vertebral and nonvertebral fractures, eg, alendronate, risedronate, and zoledronic acid.⁵

THE SCIENCE

Osteoporotic fractures occur with minimal trauma, with the failure of bone attributed to impaired integrity of bone microarchitecture. The ultimate goal of fracture repair is to restore bone size, shape, and tissue properties. The issue of when to treat with a bisphosphonate after hip fracture arises because bisphosphonates are known to disrupt bone remodeling and so delay fracture repair.

After fracture, both anabolic and catabolic phases occur.⁶ The final outcome depends on the following:

• The type of intervention to stabilize the fracture site (eg, surgical repair)
• The inflammatory cytokines and growth factors released by the cellular elements in bloody and disrupted tissue.

Oxygen tension, angiogenesis, and osteoblasts are critical to primary bone formation, and osteoclasts are essential in remodeling this initial bone deposition. These late phases of fracture repair are most vulnerable to the bisphosphonates, through suppression of osteoclast resorption and possibly through decreased angiogenesis.⁶ Callus formation is sustained, but bone remodeling is delayed.

Amanat et al⁷ examined the timing of a single dose of zoledronic acid after fracture repair in a rat model of diaphyseal fracture and found that the callus was larger and stronger if the bisphosphonate dose had been delayed 1 or 2 weeks. The animals treated with zoledronic acid showed a remarkable trabecular network of bone between the original femoral cortex and the new cortical bone that was not present in the control group, perhaps contributing to the enhanced mechanical properties of the callus. Other studies suggest single dosing rather than continuous dosing may be advantageous in fracture healing.⁸

THE REALITY

Healthy dogs or growing rats with linear diaphyseal fractures are imperfect models for elderly osteoporotic patients with hip fracture, as Dr. Herbert Fleisch noted in his editorial, “Can bisphosphonates be given to patients with fractures?”⁹ Still, if retained primary bone can be used in the process of fracture repair to gain an early mechanical advantage, then perhaps delayed remodeling will permit early mobilization and further fracture prevention in humans.

How soon after hip fracture surgery should a patient start a bisphosphonate? The only data we have are from a single randomized controlled trial designed to measure fracture risk reduction in osteoporotic patients with hip fracture using intravenous zoledronic acid 5 mg compared with placebo.² A post hoc analysis of this study¹ generated the limited clinical data we have on the optimal timing of the treatment. Linking these study data with the laboratory data, one would intuit that delaying the infusion of zoledronic acid for at least 2 weeks after hip fracture repair would offer a clinical reduction in fracture risk and improvement (or stabilization) in bone mineral density by 12 months, and a reduction in the rate of all-cause mortality beginning at 16 months.

Patients with an osteoporotic hip fracture suffer from profound morbidity and are at a heightened risk of death. It is therefore essential that they receive treatment with a bisphosphonate known to modify the subsequent risk of fracture at any site—eg, alendronate (Fosamax), risedronate (Actonel), or zoledronic acid (Reclast).

However, there is concern that starting a bisphosphonate too soon after surgery could disrupt bone remodeling and delay fracture repair.

Only one clinical study addressed the timing of bisphosphonate therapy after hip fracture repair. In this study, Eriksen et al¹ performed a post hoc analysis of data from the Health Outcomes and Reduced Incidence With Zoledronic Acid Once Yearly Recurrent Fracture Trial (HORIZON-RFT)² and concluded that the optimal time to give intravenous zoledronic acid is 2 to 12 weeks after surgical repair of the fracture.

In a frail, elderly patient with comorbidities, a single intravenous 5-mg dose of zoledronic acid guarantees adequate treatment, obviating issues of poor compliance and oral absorption and loss to follow-up. Sufficient levels of vitamin D and calcium should be ensured.

THE EVIDENCE

The original HORIZON-RFT study,² published in 2007, compared intravenous zoledronic acid against placebo in elderly patients with osteoporotic hip fracture. Most of the patients were white women; their mean age was 74; 1,065 received intravenous zoledronic acid, and 1,062 received placebo. All received vitamin D and calcium.

The trial showed a clear reduction in the rate of recurrent fractures at other sites (a primary end point) and a reduction in the rate of all-cause mortality in patients treated within 90 days of fracture. A total of 424 fractures occurred in 231 patients. The risk of any new clinical fracture was 35% lower with treatment than with placebo (occurring in 8.6% vs 13.9% of patients, P = .001), and the number of deaths due to any cause was 28% lower with treatment than with placebo (occurring in 101 vs 141, P = .01).²

The mean time to fracture was 39.8 months in the treated group vs 36.4 in the placebo group. The fracture risk reduction began to be apparent by 12 months, and the reduction in mortality rate by 16 months.²

In a post hoc analysis of the trial, Eriksen et al¹ attempted to ascertain the optimal time for therapy in terms of fracture risk and mortality reduction. Analyzing the data by 2-week intervals beginning after the surgical repair of the fracture, the authors found that only 56 patients (5.3%) had received zoledronic acid within 2 weeks of surgery and only 47 had received placebo, and they saw no advantage to intravenous zoledronic acid compared with placebo in these first 2 weeks with respect to bone mineral density, fracture risk, or risk of death. However, excluding this small subset, antifracture efficacy and reduction in mortality rate were present when patients were treated with zoledronic acid in the 2 to 12 weeks after hip fracture repair, and improvement in bone mineral density at the hip was noted at 12 months in all cohorts.

Colón-Emeric et al³ performed another post hoc analysis, attempting to explain the lower mortality rate seen in patients treated with zoledronic acid. It had been an unexpected finding, and determinants of mortality rate reduction were hampered by a limited knowledge of the true cause of death or the circumstances of care after fracture. The authors concluded that only 8% of the reduction in mortality rate evident early in the second year of treatment with zoledronic acid could be attributed to a reduction in fractures.³ Other mechanisms by which the mortality rate reduction occurred remained unclear.

Curiously, in another large randomized controlled trial of zoledronic acid, in women with postmenopausal osteoporosis, Black et al⁴ reported that more patients died in the treated group (130 of 3,862) than in the placebo group (112 of 3,852). This difference was not statistically significant, but neither was it explained.

A meta-analysis by Bolland et al⁵ examined the effect of other osteoporosis treatments on mortality rate, using randomized controlled trials that lasted more than 12 months and that reported more than 10 deaths. The authors concluded the following:

• In the trials in which bisphosphonates reduced the mortality rate, the mortality rate in the placebo group was higher than 10 per 1,000 patient-years
• The effect of osteoporosis treatment on the mortality rate in a frail, elderly population is evident using agents with proven efficacy in reducing vertebral and nonvertebral fractures, eg, alendronate, risedronate, and zoledronic acid.⁵

THE SCIENCE

Osteoporotic fractures occur with minimal trauma, with the failure of bone attributed to impaired integrity of bone microarchitecture. The ultimate goal of fracture repair is to restore bone size, shape, and tissue properties. The issue of when to treat with a bisphosphonate after hip fracture arises because bisphosphonates are known to disrupt bone remodeling and so delay fracture repair.

After fracture, both anabolic and catabolic phases occur.⁶ The final outcome depends on the following:

• The type of intervention to stabilize the fracture site (eg, surgical repair)
• The inflammatory cytokines and growth factors released by the cellular elements in bloody and disrupted tissue.

Oxygen tension, angiogenesis, and osteoblasts are critical to primary bone formation, and osteoclasts are essential in remodeling this initial bone deposition. These late phases of fracture repair are most vulnerable to the bisphosphonates, through suppression of osteoclast resorption and possibly through decreased angiogenesis.⁶ Callus formation is sustained, but bone remodeling is delayed.

Amanat et al⁷ examined the timing of a single dose of zoledronic acid after fracture repair in a rat model of diaphyseal fracture and found that the callus was larger and stronger if the bisphosphonate dose had been delayed 1 or 2 weeks. The animals treated with zoledronic acid showed a remarkable trabecular network of bone between the original femoral cortex and the new cortical bone that was not present in the control group, perhaps contributing to the enhanced mechanical properties of the callus. Other studies suggest single dosing rather than continuous dosing may be advantageous in fracture healing.⁸

THE REALITY

Healthy dogs or growing rats with linear diaphyseal fractures are imperfect models for elderly osteoporotic patients with hip fracture, as Dr. Herbert Fleisch noted in his editorial, “Can bisphosphonates be given to patients with fractures?”⁹ Still, if retained primary bone can be used in the process of fracture repair to gain an early mechanical advantage, then perhaps delayed remodeling will permit early mobilization and further fracture prevention in humans.

How soon after hip fracture surgery should a patient start a bisphosphonate? The only data we have are from a single randomized controlled trial designed to measure fracture risk reduction in osteoporotic patients with hip fracture using intravenous zoledronic acid 5 mg compared with placebo.² A post hoc analysis of this study¹ generated the limited clinical data we have on the optimal timing of the treatment. Linking these study data with the laboratory data, one would intuit that delaying the infusion of zoledronic acid for at least 2 weeks after hip fracture repair would offer a clinical reduction in fracture risk and improvement (or stabilization) in bone mineral density by 12 months, and a reduction in the rate of all-cause mortality beginning at 16 months.

Patients with an osteoporotic hip fracture suffer from profound morbidity and are at a heightened risk of death. It is therefore essential that they receive treatment with a bisphosphonate known to modify the subsequent risk of fracture at any site—eg, alendronate (Fosamax), risedronate (Actonel), or zoledronic acid (Reclast).

However, there is concern that starting a bisphosphonate too soon after surgery could disrupt bone remodeling and delay fracture repair.

Only one clinical study addressed the timing of bisphosphonate therapy after hip fracture repair. In this study, Eriksen et al¹ performed a post hoc analysis of data from the Health Outcomes and Reduced Incidence With Zoledronic Acid Once Yearly Recurrent Fracture Trial (HORIZON-RFT)² and concluded that the optimal time to give intravenous zoledronic acid is 2 to 12 weeks after surgical repair of the fracture.

In a frail, elderly patient with comorbidities, a single intravenous 5-mg dose of zoledronic acid guarantees adequate treatment, obviating issues of poor compliance and oral absorption and loss to follow-up. Sufficient levels of vitamin D and calcium should be ensured.

THE EVIDENCE

The original HORIZON-RFT study,² published in 2007, compared intravenous zoledronic acid against placebo in elderly patients with osteoporotic hip fracture. Most of the patients were white women; their mean age was 74; 1,065 received intravenous zoledronic acid, and 1,062 received placebo. All received vitamin D and calcium.

The trial showed a clear reduction in the rate of recurrent fractures at other sites (a primary end point) and a reduction in the rate of all-cause mortality in patients treated within 90 days of fracture. A total of 424 fractures occurred in 231 patients. The risk of any new clinical fracture was 35% lower with treatment than with placebo (occurring in 8.6% vs 13.9% of patients, P = .001), and the number of deaths due to any cause was 28% lower with treatment than with placebo (occurring in 101 vs 141, P = .01).²

The mean time to fracture was 39.8 months in the treated group vs 36.4 in the placebo group. The fracture risk reduction began to be apparent by 12 months, and the reduction in mortality rate by 16 months.²

In a post hoc analysis of the trial, Eriksen et al¹ attempted to ascertain the optimal time for therapy in terms of fracture risk and mortality reduction. Analyzing the data by 2-week intervals beginning after the surgical repair of the fracture, the authors found that only 56 patients (5.3%) had received zoledronic acid within 2 weeks of surgery and only 47 had received placebo, and they saw no advantage to intravenous zoledronic acid compared with placebo in these first 2 weeks with respect to bone mineral density, fracture risk, or risk of death. However, excluding this small subset, antifracture efficacy and reduction in mortality rate were present when patients were treated with zoledronic acid in the 2 to 12 weeks after hip fracture repair, and improvement in bone mineral density at the hip was noted at 12 months in all cohorts.

Colón-Emeric et al³ performed another post hoc analysis, attempting to explain the lower mortality rate seen in patients treated with zoledronic acid. It had been an unexpected finding, and determinants of mortality rate reduction were hampered by a limited knowledge of the true cause of death or the circumstances of care after fracture. The authors concluded that only 8% of the reduction in mortality rate evident early in the second year of treatment with zoledronic acid could be attributed to a reduction in fractures.³ Other mechanisms by which the mortality rate reduction occurred remained unclear.

Curiously, in another large randomized controlled trial of zoledronic acid, in women with postmenopausal osteoporosis, Black et al⁴ reported that more patients died in the treated group (130 of 3,862) than in the placebo group (112 of 3,852). This difference was not statistically significant, but neither was it explained.

A meta-analysis by Bolland et al⁵ examined the effect of other osteoporosis treatments on mortality rate, using randomized controlled trials that lasted more than 12 months and that reported more than 10 deaths. The authors concluded the following:

• In the trials in which bisphosphonates reduced the mortality rate, the mortality rate in the placebo group was higher than 10 per 1,000 patient-years
• The effect of osteoporosis treatment on the mortality rate in a frail, elderly population is evident using agents with proven efficacy in reducing vertebral and nonvertebral fractures, eg, alendronate, risedronate, and zoledronic acid.⁵

THE SCIENCE

Osteoporotic fractures occur with minimal trauma, with the failure of bone attributed to impaired integrity of bone microarchitecture. The ultimate goal of fracture repair is to restore bone size, shape, and tissue properties. The issue of when to treat with a bisphosphonate after hip fracture arises because bisphosphonates are known to disrupt bone remodeling and so delay fracture repair.

After fracture, both anabolic and catabolic phases occur.⁶ The final outcome depends on the following:

• The type of intervention to stabilize the fracture site (eg, surgical repair)
• The inflammatory cytokines and growth factors released by the cellular elements in bloody and disrupted tissue.

Oxygen tension, angiogenesis, and osteoblasts are critical to primary bone formation, and osteoclasts are essential in remodeling this initial bone deposition. These late phases of fracture repair are most vulnerable to the bisphosphonates, through suppression of osteoclast resorption and possibly through decreased angiogenesis.⁶ Callus formation is sustained, but bone remodeling is delayed.

Amanat et al⁷ examined the timing of a single dose of zoledronic acid after fracture repair in a rat model of diaphyseal fracture and found that the callus was larger and stronger if the bisphosphonate dose had been delayed 1 or 2 weeks. The animals treated with zoledronic acid showed a remarkable trabecular network of bone between the original femoral cortex and the new cortical bone that was not present in the control group, perhaps contributing to the enhanced mechanical properties of the callus. Other studies suggest single dosing rather than continuous dosing may be advantageous in fracture healing.⁸

THE REALITY

Healthy dogs or growing rats with linear diaphyseal fractures are imperfect models for elderly osteoporotic patients with hip fracture, as Dr. Herbert Fleisch noted in his editorial, “Can bisphosphonates be given to patients with fractures?”⁹ Still, if retained primary bone can be used in the process of fracture repair to gain an early mechanical advantage, then perhaps delayed remodeling will permit early mobilization and further fracture prevention in humans.

How soon after hip fracture surgery should a patient start a bisphosphonate? The only data we have are from a single randomized controlled trial designed to measure fracture risk reduction in osteoporotic patients with hip fracture using intravenous zoledronic acid 5 mg compared with placebo.² A post hoc analysis of this study¹ generated the limited clinical data we have on the optimal timing of the treatment. Linking these study data with the laboratory data, one would intuit that delaying the infusion of zoledronic acid for at least 2 weeks after hip fracture repair would offer a clinical reduction in fracture risk and improvement (or stabilization) in bone mineral density by 12 months, and a reduction in the rate of all-cause mortality beginning at 16 months.

Along with massive pulmonary embolism, the most feared thromboembolic event is the clot that migrates to the brain, resulting in life-altering stroke. We assess this risk in a semiquantitative manner in patients with atrial fibrillation using the CHADS₂ score, hoping to maximize the benefits of anticoagulation while reducing the risks. We recognize that patients at the greatest risk of stroke in this setting are those with a history of a prior stroke. Also, patients bedridden with a recent cerebrovascular accident (CVA) seem to be hypercoagulable, potentially adding risk to recent injury. Thus, we try to start anticoagulation as soon as feasible after the diagnosis of a possible thrombotic event.

But the decision to start or resume anticoagulation is especially agonizing in a patient who has suffered an intracerebral hemorrhage. In this issue of the Journal, Drs. Joshua Goldstein and Steven Greenberg and Dr. Franklin Michota provide a thoughtful discussion of the issues we need to consider in these patients.

While not contributing to the prevention of additional CVAs or other arterial thrombotic events, a modality often underused in the prevention of thrombotic disease is the application (not just the ordering) of compressive leg stockings to bedridden hospitalized patients who cannot, for any reason, be provided pharmacologic anticoagulation therapy. I just completed a stint of hospital consultation, and I was pleased to see the widespread integration of prophylactic anticoagulation therapy, but somewhat dismayed by the number of compressive stockings I watched pumping with vigor, but to no one’s benefit, as they were draped over a bed rail.

As we struggle with complex clinical decisions, we need to also be attentive to the simple and the seemingly mundane: using the foam dispenser at the door, offering the verbal greeting and patient touch at the bedside, and rewrapping the pneumatic stockings that have somehow migrated between mattress and footboard.

Along with massive pulmonary embolism, the most feared thromboembolic event is the clot that migrates to the brain, resulting in life-altering stroke. We assess this risk in a semiquantitative manner in patients with atrial fibrillation using the CHADS₂ score, hoping to maximize the benefits of anticoagulation while reducing the risks. We recognize that patients at the greatest risk of stroke in this setting are those with a history of a prior stroke. Also, patients bedridden with a recent cerebrovascular accident (CVA) seem to be hypercoagulable, potentially adding risk to recent injury. Thus, we try to start anticoagulation as soon as feasible after the diagnosis of a possible thrombotic event.

But the decision to start or resume anticoagulation is especially agonizing in a patient who has suffered an intracerebral hemorrhage. In this issue of the Journal, Drs. Joshua Goldstein and Steven Greenberg and Dr. Franklin Michota provide a thoughtful discussion of the issues we need to consider in these patients.

While not contributing to the prevention of additional CVAs or other arterial thrombotic events, a modality often underused in the prevention of thrombotic disease is the application (not just the ordering) of compressive leg stockings to bedridden hospitalized patients who cannot, for any reason, be provided pharmacologic anticoagulation therapy. I just completed a stint of hospital consultation, and I was pleased to see the widespread integration of prophylactic anticoagulation therapy, but somewhat dismayed by the number of compressive stockings I watched pumping with vigor, but to no one’s benefit, as they were draped over a bed rail.

As we struggle with complex clinical decisions, we need to also be attentive to the simple and the seemingly mundane: using the foam dispenser at the door, offering the verbal greeting and patient touch at the bedside, and rewrapping the pneumatic stockings that have somehow migrated between mattress and footboard.

Along with massive pulmonary embolism, the most feared thromboembolic event is the clot that migrates to the brain, resulting in life-altering stroke. We assess this risk in a semiquantitative manner in patients with atrial fibrillation using the CHADS₂ score, hoping to maximize the benefits of anticoagulation while reducing the risks. We recognize that patients at the greatest risk of stroke in this setting are those with a history of a prior stroke. Also, patients bedridden with a recent cerebrovascular accident (CVA) seem to be hypercoagulable, potentially adding risk to recent injury. Thus, we try to start anticoagulation as soon as feasible after the diagnosis of a possible thrombotic event.

But the decision to start or resume anticoagulation is especially agonizing in a patient who has suffered an intracerebral hemorrhage. In this issue of the Journal, Drs. Joshua Goldstein and Steven Greenberg and Dr. Franklin Michota provide a thoughtful discussion of the issues we need to consider in these patients.

While not contributing to the prevention of additional CVAs or other arterial thrombotic events, a modality often underused in the prevention of thrombotic disease is the application (not just the ordering) of compressive leg stockings to bedridden hospitalized patients who cannot, for any reason, be provided pharmacologic anticoagulation therapy. I just completed a stint of hospital consultation, and I was pleased to see the widespread integration of prophylactic anticoagulation therapy, but somewhat dismayed by the number of compressive stockings I watched pumping with vigor, but to no one’s benefit, as they were draped over a bed rail.

As we struggle with complex clinical decisions, we need to also be attentive to the simple and the seemingly mundane: using the foam dispenser at the door, offering the verbal greeting and patient touch at the bedside, and rewrapping the pneumatic stockings that have somehow migrated between mattress and footboard.

Anticoagulants have been helping patients at risk of thrombosis since the late 1930s.^1,2 Although the indications for these agents are many, the development of anticoagulants beyond oral vitamin K antagonists and parenteral heparin has been slow. In the United States, the vitamin K antagonist warfarin (Coumadin) is still the only oral anticoagulant available.

See related article

The major complication of anticoagulant therapy is bleeding, and vitamin K antagonists have proven challenging to use in clinical practice.^1,3 They have a narrow therapeutic window, they vary considerably in dose-response from patient to patient, and they are subject to significant interactions with other drugs and with foods. For these reasons, therapy must be monitored with laboratory testing, and good patient compliance and patient education are essential. Yet even with these measures, life-threatening hemorrhage still can occur.

In this issue of the Cleveland Clinic Journal of Medicine, Goldstein and Greenberg⁴ review warfarin-related intracerebral hemorrhage (ICH) and provide a framework for considering whether to resume anticoagulant therapy.

WHAT TO DO IN THE ACUTE PHASE

Goldstein and Greenberg divide the difficult clinical question of what to do after ICH into the acute phase and the chronic phase.

What to do in the acute phase appears straightforward, as the risk of hematoma expansion in the hours immediately after warfarin-related ICH outweighs the risk of arterial or venous thromboembolism. Anticoagulant reversal should be the primary consideration in the first 24 hours, and, assuming the patient does not have acute (< 4-week-old) deep vein thrombosis, intermittent pneumatic compression should be applied to the lower extremities to reduce the risk of venous thromboembolism associated with ICH.⁵

Prophylactic anticoagulation with subcutaneous fixed-dose heparin or low-molecular-weight heparin is recommended starting 72 hours after ICH is diagnosed, provided the patient is not underweight (< 50 kg), has relatively normal renal function (creatinine clearance > 30 mL/minute/1.73 m²) and normal platelet function, and does not have coagulopathy. ⁶ If any one of these criteria is not met, the risk of bleeding can be higher, even with only prophylactic doses of anticoagulant drugs. Prophylactic anticoagulation should be continued until hospital and rehabilitation discharge, typically 1 to 2 weeks after ICH, depending on the severity of the patient’s neurologic impairment.

If a patient with warfarin-related ICH has concomitant acute proximal deep vein thrombosis or pulmonary embolism (ie, < 4 weeks old), then caval interruption therapy would be indicated.⁷ Although retrievable inferior vena cava filters are increasingly preferred over permanent filters, it is important to recognize the relative lack of both longitudinal and prospective data on retrievable devices. Given that provoked venous thromboembolism requires a minimum of 3 months of anticoagulation, and retrievable filters generally need to be removed before 3 months, a retrievable filter should be chosen only if the clinician has already decided that oral anticoagulation will be restarted in the next 3 to 4 weeks after filter removal.

WHAT TO DO IN THE CHRONIC PHASE

A more difficult question in patients with warfarin-related ICH arises in the chronic phase: should oral anticoagulation be resumed at all?

Since the risk of ICH is related to the intensity of anticoagulation, a lower target international normalized ratio may be the best compromise, depending on the patient. Alternatively, antiplatelet therapy alone may offer some benefit with less risk of ICH.

THE NEWER ORAL ANTICOAGULANTS

As Goldstein and Greenberg mention, the ongoing development of new and potentially safer oral anticoagulants may affect how we approach these risk-benefit equations.

Three new oral anticoagulants—dabigatran (Pradaxa), apixaban, and rivaroxaban (Xarelto)—are being tested for various anticoagulant indications, and several phase III studies have recently closed or are nearing completion.

Dabigatran is an oral direct thrombin inhibitor currently available in Europe and Canada.

In the Randomized Evaluation of Long-term Anticoagulant Therapy (RE-LY) trial, the efficacy and safety of two different doses of dabigatran (110 mg twice daily or 150 mg twice daily) relative to warfarin were studied in more than 18,000 patients with atrial fibrillation. ⁹ The primary outcome measure was stroke or systemic embolism. Dabigatran 110 mg was not inferior to warfarin in terms of the primary outcome, while dabigatran 150 mg was superior. The rate of major bleeding was 3.36% per year in the warfarin group vs 2.71% in the 110-mg group (P = .003) and 3.11% in the 150-mg group (P not significant).

Additional safety data on this drug are available from the 2,500-patient RE-COVER trial.¹⁰ Dabigatran was not inferior to warfarin in the treatment of acute venous thromboembolism, with a similar rate of major bleeding and a lower rate of combined major plus nonmajor bleeding.

Apixaban, an oral direct factor Xa inhibitor, is in a phase III trial in patients with atrial fibrillation—Apixaban for Reduction in Stroke and Other Thromboembolic Events in Atrial Fibrillation (ARISTOTLE)¹¹—comparing apixaban vs warfarin. Another phase III trial, AVERROES,¹² was stopped early after a predefined interim analysis by the independent data-monitoring committee found clear evidence of benefit in the apixaban group.¹³ The AVERROES results were presented at the 2010 European Society of Cardiology Congress, August 28–September 1, Stockholm, Sweden.¹⁴

Rivaroxaban, another promising oral direct factor Xa inhibitor, is currently available in Europe and Canada for the prevention of thrombosis in orthopedic surgery patients. Rivaroxaban is also in large phase III trials for the treatment of acute venous thromboembolism^15–17 and for the prevention of stroke in atrial fibrillation.¹⁸

Newer agents have drawbacks, too

These new agents need no laboratory monitoring, and they do not appear to be subject to the dose variability and the interactions with drugs and foods seen with vitamin K antagonists. As a result, they may pose less risk of anticoagulant-related ICH.

The decision to resume anticoagulation after anticoagulant-associated intracranial hemorrhage should be based on the risk of rebleeding vs the risk of thrombosis. Patients determined to be at high risk of thrombosis and low risk of rebleeding are the best candidates for resuming anticoagulation.

Still, for patients who suffer an anticoagulant- or warfarin-related ICH, these new anticoagulants are not likely to simplify the issue of restarting anticoagulant therapy. Unlike vitamin K antagonists, dabigatran and the direct factor Xa inhibitors have no known antidote for their anticoagulant effects. Animal data suggest that factor Xa concentrates may help,¹⁹ but for patients at risk of a second anticoagulant-related ICH, this does not provide much reassurance.

As with all clinical decisions in medicine, the potential benefits of any therapy should outweigh the risks. In the case of warfarin-related ICH, resuming anticoagulant therapy requires careful consideration of many factors, including patient preferences and tolerance of different levels of risk. As new and perhaps safer anticoagulants become available, clinicians may face such difficult questions less and less. But in the meantime, doctors and their patients are left to pick their poison.

Anticoagulants have been helping patients at risk of thrombosis since the late 1930s.^1,2 Although the indications for these agents are many, the development of anticoagulants beyond oral vitamin K antagonists and parenteral heparin has been slow. In the United States, the vitamin K antagonist warfarin (Coumadin) is still the only oral anticoagulant available.

See related article

The major complication of anticoagulant therapy is bleeding, and vitamin K antagonists have proven challenging to use in clinical practice.^1,3 They have a narrow therapeutic window, they vary considerably in dose-response from patient to patient, and they are subject to significant interactions with other drugs and with foods. For these reasons, therapy must be monitored with laboratory testing, and good patient compliance and patient education are essential. Yet even with these measures, life-threatening hemorrhage still can occur.

In this issue of the Cleveland Clinic Journal of Medicine, Goldstein and Greenberg⁴ review warfarin-related intracerebral hemorrhage (ICH) and provide a framework for considering whether to resume anticoagulant therapy.

WHAT TO DO IN THE ACUTE PHASE

Goldstein and Greenberg divide the difficult clinical question of what to do after ICH into the acute phase and the chronic phase.

What to do in the acute phase appears straightforward, as the risk of hematoma expansion in the hours immediately after warfarin-related ICH outweighs the risk of arterial or venous thromboembolism. Anticoagulant reversal should be the primary consideration in the first 24 hours, and, assuming the patient does not have acute (< 4-week-old) deep vein thrombosis, intermittent pneumatic compression should be applied to the lower extremities to reduce the risk of venous thromboembolism associated with ICH.⁵

Prophylactic anticoagulation with subcutaneous fixed-dose heparin or low-molecular-weight heparin is recommended starting 72 hours after ICH is diagnosed, provided the patient is not underweight (< 50 kg), has relatively normal renal function (creatinine clearance > 30 mL/minute/1.73 m²) and normal platelet function, and does not have coagulopathy. ⁶ If any one of these criteria is not met, the risk of bleeding can be higher, even with only prophylactic doses of anticoagulant drugs. Prophylactic anticoagulation should be continued until hospital and rehabilitation discharge, typically 1 to 2 weeks after ICH, depending on the severity of the patient’s neurologic impairment.

If a patient with warfarin-related ICH has concomitant acute proximal deep vein thrombosis or pulmonary embolism (ie, < 4 weeks old), then caval interruption therapy would be indicated.⁷ Although retrievable inferior vena cava filters are increasingly preferred over permanent filters, it is important to recognize the relative lack of both longitudinal and prospective data on retrievable devices. Given that provoked venous thromboembolism requires a minimum of 3 months of anticoagulation, and retrievable filters generally need to be removed before 3 months, a retrievable filter should be chosen only if the clinician has already decided that oral anticoagulation will be restarted in the next 3 to 4 weeks after filter removal.

WHAT TO DO IN THE CHRONIC PHASE

A more difficult question in patients with warfarin-related ICH arises in the chronic phase: should oral anticoagulation be resumed at all?

Since the risk of ICH is related to the intensity of anticoagulation, a lower target international normalized ratio may be the best compromise, depending on the patient. Alternatively, antiplatelet therapy alone may offer some benefit with less risk of ICH.

THE NEWER ORAL ANTICOAGULANTS

As Goldstein and Greenberg mention, the ongoing development of new and potentially safer oral anticoagulants may affect how we approach these risk-benefit equations.

Three new oral anticoagulants—dabigatran (Pradaxa), apixaban, and rivaroxaban (Xarelto)—are being tested for various anticoagulant indications, and several phase III studies have recently closed or are nearing completion.

Dabigatran is an oral direct thrombin inhibitor currently available in Europe and Canada.

In the Randomized Evaluation of Long-term Anticoagulant Therapy (RE-LY) trial, the efficacy and safety of two different doses of dabigatran (110 mg twice daily or 150 mg twice daily) relative to warfarin were studied in more than 18,000 patients with atrial fibrillation. ⁹ The primary outcome measure was stroke or systemic embolism. Dabigatran 110 mg was not inferior to warfarin in terms of the primary outcome, while dabigatran 150 mg was superior. The rate of major bleeding was 3.36% per year in the warfarin group vs 2.71% in the 110-mg group (P = .003) and 3.11% in the 150-mg group (P not significant).

Additional safety data on this drug are available from the 2,500-patient RE-COVER trial.¹⁰ Dabigatran was not inferior to warfarin in the treatment of acute venous thromboembolism, with a similar rate of major bleeding and a lower rate of combined major plus nonmajor bleeding.

Apixaban, an oral direct factor Xa inhibitor, is in a phase III trial in patients with atrial fibrillation—Apixaban for Reduction in Stroke and Other Thromboembolic Events in Atrial Fibrillation (ARISTOTLE)¹¹—comparing apixaban vs warfarin. Another phase III trial, AVERROES,¹² was stopped early after a predefined interim analysis by the independent data-monitoring committee found clear evidence of benefit in the apixaban group.¹³ The AVERROES results were presented at the 2010 European Society of Cardiology Congress, August 28–September 1, Stockholm, Sweden.¹⁴

Rivaroxaban, another promising oral direct factor Xa inhibitor, is currently available in Europe and Canada for the prevention of thrombosis in orthopedic surgery patients. Rivaroxaban is also in large phase III trials for the treatment of acute venous thromboembolism^15–17 and for the prevention of stroke in atrial fibrillation.¹⁸

Newer agents have drawbacks, too

These new agents need no laboratory monitoring, and they do not appear to be subject to the dose variability and the interactions with drugs and foods seen with vitamin K antagonists. As a result, they may pose less risk of anticoagulant-related ICH.

The decision to resume anticoagulation after anticoagulant-associated intracranial hemorrhage should be based on the risk of rebleeding vs the risk of thrombosis. Patients determined to be at high risk of thrombosis and low risk of rebleeding are the best candidates for resuming anticoagulation.

Still, for patients who suffer an anticoagulant- or warfarin-related ICH, these new anticoagulants are not likely to simplify the issue of restarting anticoagulant therapy. Unlike vitamin K antagonists, dabigatran and the direct factor Xa inhibitors have no known antidote for their anticoagulant effects. Animal data suggest that factor Xa concentrates may help,¹⁹ but for patients at risk of a second anticoagulant-related ICH, this does not provide much reassurance.

As with all clinical decisions in medicine, the potential benefits of any therapy should outweigh the risks. In the case of warfarin-related ICH, resuming anticoagulant therapy requires careful consideration of many factors, including patient preferences and tolerance of different levels of risk. As new and perhaps safer anticoagulants become available, clinicians may face such difficult questions less and less. But in the meantime, doctors and their patients are left to pick their poison.

Anticoagulants have been helping patients at risk of thrombosis since the late 1930s.^1,2 Although the indications for these agents are many, the development of anticoagulants beyond oral vitamin K antagonists and parenteral heparin has been slow. In the United States, the vitamin K antagonist warfarin (Coumadin) is still the only oral anticoagulant available.

See related article

The major complication of anticoagulant therapy is bleeding, and vitamin K antagonists have proven challenging to use in clinical practice.^1,3 They have a narrow therapeutic window, they vary considerably in dose-response from patient to patient, and they are subject to significant interactions with other drugs and with foods. For these reasons, therapy must be monitored with laboratory testing, and good patient compliance and patient education are essential. Yet even with these measures, life-threatening hemorrhage still can occur.

In this issue of the Cleveland Clinic Journal of Medicine, Goldstein and Greenberg⁴ review warfarin-related intracerebral hemorrhage (ICH) and provide a framework for considering whether to resume anticoagulant therapy.

WHAT TO DO IN THE ACUTE PHASE

Goldstein and Greenberg divide the difficult clinical question of what to do after ICH into the acute phase and the chronic phase.

What to do in the acute phase appears straightforward, as the risk of hematoma expansion in the hours immediately after warfarin-related ICH outweighs the risk of arterial or venous thromboembolism. Anticoagulant reversal should be the primary consideration in the first 24 hours, and, assuming the patient does not have acute (< 4-week-old) deep vein thrombosis, intermittent pneumatic compression should be applied to the lower extremities to reduce the risk of venous thromboembolism associated with ICH.⁵

Prophylactic anticoagulation with subcutaneous fixed-dose heparin or low-molecular-weight heparin is recommended starting 72 hours after ICH is diagnosed, provided the patient is not underweight (< 50 kg), has relatively normal renal function (creatinine clearance > 30 mL/minute/1.73 m²) and normal platelet function, and does not have coagulopathy. ⁶ If any one of these criteria is not met, the risk of bleeding can be higher, even with only prophylactic doses of anticoagulant drugs. Prophylactic anticoagulation should be continued until hospital and rehabilitation discharge, typically 1 to 2 weeks after ICH, depending on the severity of the patient’s neurologic impairment.

If a patient with warfarin-related ICH has concomitant acute proximal deep vein thrombosis or pulmonary embolism (ie, < 4 weeks old), then caval interruption therapy would be indicated.⁷ Although retrievable inferior vena cava filters are increasingly preferred over permanent filters, it is important to recognize the relative lack of both longitudinal and prospective data on retrievable devices. Given that provoked venous thromboembolism requires a minimum of 3 months of anticoagulation, and retrievable filters generally need to be removed before 3 months, a retrievable filter should be chosen only if the clinician has already decided that oral anticoagulation will be restarted in the next 3 to 4 weeks after filter removal.

WHAT TO DO IN THE CHRONIC PHASE

A more difficult question in patients with warfarin-related ICH arises in the chronic phase: should oral anticoagulation be resumed at all?

Since the risk of ICH is related to the intensity of anticoagulation, a lower target international normalized ratio may be the best compromise, depending on the patient. Alternatively, antiplatelet therapy alone may offer some benefit with less risk of ICH.

THE NEWER ORAL ANTICOAGULANTS

As Goldstein and Greenberg mention, the ongoing development of new and potentially safer oral anticoagulants may affect how we approach these risk-benefit equations.

Three new oral anticoagulants—dabigatran (Pradaxa), apixaban, and rivaroxaban (Xarelto)—are being tested for various anticoagulant indications, and several phase III studies have recently closed or are nearing completion.

Dabigatran is an oral direct thrombin inhibitor currently available in Europe and Canada.

In the Randomized Evaluation of Long-term Anticoagulant Therapy (RE-LY) trial, the efficacy and safety of two different doses of dabigatran (110 mg twice daily or 150 mg twice daily) relative to warfarin were studied in more than 18,000 patients with atrial fibrillation. ⁹ The primary outcome measure was stroke or systemic embolism. Dabigatran 110 mg was not inferior to warfarin in terms of the primary outcome, while dabigatran 150 mg was superior. The rate of major bleeding was 3.36% per year in the warfarin group vs 2.71% in the 110-mg group (P = .003) and 3.11% in the 150-mg group (P not significant).

Additional safety data on this drug are available from the 2,500-patient RE-COVER trial.¹⁰ Dabigatran was not inferior to warfarin in the treatment of acute venous thromboembolism, with a similar rate of major bleeding and a lower rate of combined major plus nonmajor bleeding.

Apixaban, an oral direct factor Xa inhibitor, is in a phase III trial in patients with atrial fibrillation—Apixaban for Reduction in Stroke and Other Thromboembolic Events in Atrial Fibrillation (ARISTOTLE)¹¹—comparing apixaban vs warfarin. Another phase III trial, AVERROES,¹² was stopped early after a predefined interim analysis by the independent data-monitoring committee found clear evidence of benefit in the apixaban group.¹³ The AVERROES results were presented at the 2010 European Society of Cardiology Congress, August 28–September 1, Stockholm, Sweden.¹⁴

Rivaroxaban, another promising oral direct factor Xa inhibitor, is currently available in Europe and Canada for the prevention of thrombosis in orthopedic surgery patients. Rivaroxaban is also in large phase III trials for the treatment of acute venous thromboembolism^15–17 and for the prevention of stroke in atrial fibrillation.¹⁸

Newer agents have drawbacks, too

These new agents need no laboratory monitoring, and they do not appear to be subject to the dose variability and the interactions with drugs and foods seen with vitamin K antagonists. As a result, they may pose less risk of anticoagulant-related ICH.

The decision to resume anticoagulation after anticoagulant-associated intracranial hemorrhage should be based on the risk of rebleeding vs the risk of thrombosis. Patients determined to be at high risk of thrombosis and low risk of rebleeding are the best candidates for resuming anticoagulation.

Still, for patients who suffer an anticoagulant- or warfarin-related ICH, these new anticoagulants are not likely to simplify the issue of restarting anticoagulant therapy. Unlike vitamin K antagonists, dabigatran and the direct factor Xa inhibitors have no known antidote for their anticoagulant effects. Animal data suggest that factor Xa concentrates may help,¹⁹ but for patients at risk of a second anticoagulant-related ICH, this does not provide much reassurance.

As with all clinical decisions in medicine, the potential benefits of any therapy should outweigh the risks. In the case of warfarin-related ICH, resuming anticoagulant therapy requires careful consideration of many factors, including patient preferences and tolerance of different levels of risk. As new and perhaps safer anticoagulants become available, clinicians may face such difficult questions less and less. But in the meantime, doctors and their patients are left to pick their poison.