Salary One Part of the Compensation Package

I am a senior medical resident who intends to start a new job as a hospitalist later this year. I have been interviewing and feel fortunate to have several offers of employment. Is there anything I should be looking for in employment contracts?

M. Berkowitz, DO, Manchester, N.H.

Dr. Hospitalist responds:

Congratulations on your graduation, and welcome to the rest of your career. I have worked in HM for more than a decade. You have made a wonderful career choice; there is no better time to be a hospitalist.

Selecting the right job is important. I recognize it’s not easy to determine the best employer for you. All too often, I hear about physicians taking a job because the employer offered the highest salary. Money is important, but it’s not the only variable you should consider when sorting out offers. I have no formal training in human resources or employment law, but I have been hiring physicians for more than a decade, and I believe there are very important elements of compensation in any job offer aside from salary. For example, benefit packages and benefits costs to the employee and employer vary from job to job. Some employee benefits cost the HM group 25% of salary. Compare a job offer with paid benefits to a job offer with a similar salary and no paid benefits. When you do the math, you’ll understand why salary isn’t the only variable you should consider.

Take time to understand retirement plan offerings, including the short- and long-term implications. Some employers offer pension plans; most offer access to 401(k) or 403(b) plans. Some employers match employee contributions, while others do not. Over the long term, match programs offer a huge investment advantage. However, it is important to know the terms of the plan—namely, the vesting period. The vesting period is the number of months or years an individual must be employed to qualify for matching contributions. Ideally, you want a retirement plan that vests immediately.

Another important benefit is malpractice insurance. Do not assume that your employer will provide malpractice insurance at no additional cost to you. Do not assume that all malpractice insurance policies are the same. Most policies provide a monetary amount of coverage for each incident with an annual aggregate limit. For example, a 1/3 policy covers up to $1 million per incident and up to $3 million in annual aggregate. Higher amounts of coverage will offer greater protection against high-dollar verdicts but might make the insured an attractive candidate for litigation in the eyes of some plaintiffs.

Most hospitals require that physicians carry a medical malpractice policy with a minimum amount of coverage before they grant privileges. Some policies, such as occurrence policies, provide coverage for incidents that occur during your period of employment, even if you leave your job.

Claims-made medical malpractice policies typically are less expensive, but they will not provide coverage after you leave an employer unless the policy includes “tail coverage.” If you have a claims-made policy, I urge you to consider purchasing tail coverage. The take-home message is that medical malpractice insurance should be figured into your employment decision.

Also consider whether prospective employers offer signing bonuses; reimbursement for continuing medical education; and health, life, disability, and accidental death and dismemberment insurance coverage for you and your family. I suggest you examine the language of each individual insurance policy to understand what coverage is offered.

Perhaps the most important piece of advice I have for you is to retain the services of a healthcare attorney. Make sure this person is familiar with physician employment agreements in the state where you plan to work. TH

Salary One Part of the Compensation Package

I am a senior medical resident who intends to start a new job as a hospitalist later this year. I have been interviewing and feel fortunate to have several offers of employment. Is there anything I should be looking for in employment contracts?

M. Berkowitz, DO, Manchester, N.H.

Dr. Hospitalist responds:

Congratulations on your graduation, and welcome to the rest of your career. I have worked in HM for more than a decade. You have made a wonderful career choice; there is no better time to be a hospitalist.

Selecting the right job is important. I recognize it’s not easy to determine the best employer for you. All too often, I hear about physicians taking a job because the employer offered the highest salary. Money is important, but it’s not the only variable you should consider when sorting out offers. I have no formal training in human resources or employment law, but I have been hiring physicians for more than a decade, and I believe there are very important elements of compensation in any job offer aside from salary. For example, benefit packages and benefits costs to the employee and employer vary from job to job. Some employee benefits cost the HM group 25% of salary. Compare a job offer with paid benefits to a job offer with a similar salary and no paid benefits. When you do the math, you’ll understand why salary isn’t the only variable you should consider.

Take time to understand retirement plan offerings, including the short- and long-term implications. Some employers offer pension plans; most offer access to 401(k) or 403(b) plans. Some employers match employee contributions, while others do not. Over the long term, match programs offer a huge investment advantage. However, it is important to know the terms of the plan—namely, the vesting period. The vesting period is the number of months or years an individual must be employed to qualify for matching contributions. Ideally, you want a retirement plan that vests immediately.

Another important benefit is malpractice insurance. Do not assume that your employer will provide malpractice insurance at no additional cost to you. Do not assume that all malpractice insurance policies are the same. Most policies provide a monetary amount of coverage for each incident with an annual aggregate limit. For example, a 1/3 policy covers up to $1 million per incident and up to $3 million in annual aggregate. Higher amounts of coverage will offer greater protection against high-dollar verdicts but might make the insured an attractive candidate for litigation in the eyes of some plaintiffs.

Most hospitals require that physicians carry a medical malpractice policy with a minimum amount of coverage before they grant privileges. Some policies, such as occurrence policies, provide coverage for incidents that occur during your period of employment, even if you leave your job.

Claims-made medical malpractice policies typically are less expensive, but they will not provide coverage after you leave an employer unless the policy includes “tail coverage.” If you have a claims-made policy, I urge you to consider purchasing tail coverage. The take-home message is that medical malpractice insurance should be figured into your employment decision.

Also consider whether prospective employers offer signing bonuses; reimbursement for continuing medical education; and health, life, disability, and accidental death and dismemberment insurance coverage for you and your family. I suggest you examine the language of each individual insurance policy to understand what coverage is offered.

Perhaps the most important piece of advice I have for you is to retain the services of a healthcare attorney. Make sure this person is familiar with physician employment agreements in the state where you plan to work. TH

Salary One Part of the Compensation Package

I am a senior medical resident who intends to start a new job as a hospitalist later this year. I have been interviewing and feel fortunate to have several offers of employment. Is there anything I should be looking for in employment contracts?

M. Berkowitz, DO, Manchester, N.H.

Dr. Hospitalist responds:

Congratulations on your graduation, and welcome to the rest of your career. I have worked in HM for more than a decade. You have made a wonderful career choice; there is no better time to be a hospitalist.

Selecting the right job is important. I recognize it’s not easy to determine the best employer for you. All too often, I hear about physicians taking a job because the employer offered the highest salary. Money is important, but it’s not the only variable you should consider when sorting out offers. I have no formal training in human resources or employment law, but I have been hiring physicians for more than a decade, and I believe there are very important elements of compensation in any job offer aside from salary. For example, benefit packages and benefits costs to the employee and employer vary from job to job. Some employee benefits cost the HM group 25% of salary. Compare a job offer with paid benefits to a job offer with a similar salary and no paid benefits. When you do the math, you’ll understand why salary isn’t the only variable you should consider.

Take time to understand retirement plan offerings, including the short- and long-term implications. Some employers offer pension plans; most offer access to 401(k) or 403(b) plans. Some employers match employee contributions, while others do not. Over the long term, match programs offer a huge investment advantage. However, it is important to know the terms of the plan—namely, the vesting period. The vesting period is the number of months or years an individual must be employed to qualify for matching contributions. Ideally, you want a retirement plan that vests immediately.

Another important benefit is malpractice insurance. Do not assume that your employer will provide malpractice insurance at no additional cost to you. Do not assume that all malpractice insurance policies are the same. Most policies provide a monetary amount of coverage for each incident with an annual aggregate limit. For example, a 1/3 policy covers up to $1 million per incident and up to $3 million in annual aggregate. Higher amounts of coverage will offer greater protection against high-dollar verdicts but might make the insured an attractive candidate for litigation in the eyes of some plaintiffs.

Most hospitals require that physicians carry a medical malpractice policy with a minimum amount of coverage before they grant privileges. Some policies, such as occurrence policies, provide coverage for incidents that occur during your period of employment, even if you leave your job.

Claims-made medical malpractice policies typically are less expensive, but they will not provide coverage after you leave an employer unless the policy includes “tail coverage.” If you have a claims-made policy, I urge you to consider purchasing tail coverage. The take-home message is that medical malpractice insurance should be figured into your employment decision.

Also consider whether prospective employers offer signing bonuses; reimbursement for continuing medical education; and health, life, disability, and accidental death and dismemberment insurance coverage for you and your family. I suggest you examine the language of each individual insurance policy to understand what coverage is offered.

Perhaps the most important piece of advice I have for you is to retain the services of a healthcare attorney. Make sure this person is familiar with physician employment agreements in the state where you plan to work. TH

Hospitalist Stephanie Jackson, MD, medical director of patient safety at Sacred Heart Medical Center in Eugene, Ore., was preparing for SHM’s meeting with lawmakers in Washington, D.C., in March. As a member of SHM’s Public Policy Committee, she knew the annual powwow with Congressional leaders would be particularly sensitive this year as the economy continues to crater, healthcare reform hangs in political purgatory, and HM advocates look to insulate the industry from growing pressures.

But while she was prepping to tackle national issues, Dr. Jackson was dealing with serious problems closer to home. Her own hospital administrators were preparing to slash the safety initiatives she was championing, including an ambitious new bar-coding system to reduce medication errors and a long-planned information technology upgrade, from the budget. Hospital executives held emergency financial meetings two weeks running. At the time, Sacred Heart had less than 70 days’ cash on hand, compared with its usual 350-day buffer. In essence, the threat to her HM program had sprouted up so severely and quickly that Dr. Jackson was too busy batting them down to travel 3,000 miles to talk about the issues.

“It’s hard to leave when your organization is not doing well,” she says. “You need to be home. Our whole mission is to provide safe, high-quality, compassionate patient care. When budget cuts are made, it will affect patient care. There’s absolutely no way it can’t.”

It’s the new HM paradigm: a landscape in which hospitalists confront a growing confluence of threats to their livelihood. The pressures are rooted in the economic downturn, as hospitals nationwide face sagging revenues and daily fights to raise capital as investors lower their investment ratings. Questions abound:

• Will more primary-care physicians (PCPs) return to hospitals to supplement their practices, siphoning encounters from HM groups?
• Will an infusion of government money into community health centers draw patients away from hospital stays?
• Will HM’s workforce expansion continue as hospitals close or lose the ability to pay competitive subsidies? Even the Federal Reserve, in its latest Beige Book survey, reported falling patient volumes for elective procedures and an increase in emergency services.
• Will the very real fears of physician overload and burnout—and the possible departure of qualified hospitalists for other specialties or careers—grow as institutions cut ancillary medical staff and put more duties on the HM checklist?

The threats are real, of course, but HM advocates and practitioners say that, for now, they remain just that. HM groups continue to grow, and HM job postings are plenty. To date, hospital administrators have been mostly loathe to lay off the staffers they count on to lower costs through patient safety initiatives, reduced length of stay, and faster throughput. The most optimistic of hospitalists view the threats as opportunities to further establish themselves as thought leaders who can prove their worth through quantifiable metrics. Still, hospitals are increasingly in dire straits, and that means hospitalists could be in the same situation.

“The dilemma is that hospitalists are tied to the hospital as an institution,” says Larry Wellikson, MD, CEO of SHM. “It doesn’t really matter what causes the hospital to have less discretionary capital. … These things play against the hospitalist.”

Beyond Staff Cuts

Dr. Jackson’s case is typical. Her institution—a two-hospital center with 510 combined beds—recently eliminated 70 positions. None were physicians, but several care-management jobs were lost. Add in a local unemployment rate of almost 12%, and it’s no surprise the hospital is buckling under the weight of uncompensated charity care. And even though Sacred Heart lists patient safety initiatives as a top priority, “it always comes up that it can be cut,” Dr. Jackson says.

The bar-coding initiative was put on hold until the end of 2010, despite the hospital’s purchase of a packager that separates medications into individual packets. Dr. Jackson thinks the new technology could cut medication errors by at least 25%. Updates in information technology have been put on hold. And even if President Obama’s stimulus plan supplies money for electronic medical records (EMR), much of that money might not make it to the hospital-floor level for another 12 to 18 months.

Budget cuts aren’t relegated to large-scale initiatives, either. “Positions have been frozen, perks disappearing,” Dr. Jackson says. “At medical staff meetings, food is getting sparse. Educational opportunities that would have been there before, they’re not going to pay for that. My money to go to [HM09] is frozen right now.”

Stay the Course

Greg Maynard, MD, MS, clinical professor of medicine and chief of the division of hospital medicine at the University of California at San Diego Medical Center, also identifies the threats to HM in personal terms. Cutbacks on spending are hard to avoid in tough economic times, he reasons, but the key for hospitalists is to not allow those discussions to affect the interpersonal relationships between HM groups and hospital executives. He also echoes the sentiments of burnout fears and morale issues. In the past year, his 24-member HM group has added primary coverage of the adult oncology unit and adult cystic fibrosis patients, among other responsibilities. It also started night coverage shifts. All the while, Dr. Maynard and his staff have heard UC San Diego is having financial issues, including troubles with its pension investments. Budget discussions are more strained because of the overall economic crisis, which makes professional relationships even more important to maintain, he says.

“You have to empathize with the medical center administrators as they struggle,” he adds. “I think there’s a threat of a dialogue. When pressure comes on, debates can become contentious. It’s important to avoid that.”

Dr. Maynard blames some of the current friction between hospitals and hospitalists on HM’s growth—estimated at 28,000 physicians and still growing—and the lagging increases in Medicare, Medicaid, and private insurer reimbursement. A new reimbursement system is at the top of Obama’s agenda for national healthcare reform; however, the economy has slowed the advance of those initiatives. Obama has set aside roughly $20 billion in stimulus funding to encourage EMR programs.

Other plans are likely to gain momentum in coming months, with the expected confirmation of Kansas Gov. Kathleen Sebelius as secretary of the U.S. Department of Health and Human Services.

“You can’t grow and grow, and not grow the amount of money needed,” Dr. Maynard says.

Return of the PCP

Another oft-discussed threat to the HM model is the potential return of primary-care physicians (PCPs) to the hospital. PCPs pulling back to focus on their private outpatient practices helped birth the HM movement. Many of the nation’s uninsured forego primary care and instead seek care in the ED, which often leads to hospital admission and HM care. If PCPs return to the hospital, it could mean a decrease in hospitalist patient census.

The plight of the unemployed, which has ballooned to more than 500,000 per month since December 2008, is another consideration. Will PCPs need to fill an encounter gap when millions of American families lose their employee-funded medical benefits? And what about the billions being set aside to open new community health centers, which theoretically would siphon potential PCP patients—and revenue? Will these centers push PCPs to resume caring for hospitalized patients?

“The only threat to HM is if we had major healthcare reform that included comprehensiveness, that included something to make it worthwhile for the PCPs to take care of their patients in the hospital,” says Robert M. Centor, MD, FACP, associate dean and director of the division of general internal medicine at Huntsville Regional Medical Campus in Alabama. “For more and more family physicians … it doesn’t make financial sense to travel to the hospital.”

Gene “Rusty” Kallenberg, MD, chief of family medicine at UC San Diego’s School of Medicine, points out PCPs can hurt hospitalists without returning to the hospital. More patients treated in primary care means fewer patients whom hospitalists can charge. Should Obama extend healthcare coverage to the estimated 47 million uninsured people in the U.S., patients once treated in the ED and admitted through HM programs likely would seek primary care before heading to the hospital, further limiting billing opportunities for HM groups. The irony, Dr. Kallenberg says, is that what is best for the patient isn’t necessarily best for the industry—HM included—that treats them.

“If you reward PCPs for doing what’s right, then somebody has to pay for it,” he says. “The specialists are going to pay for it. If what happens is epidemiologically fine, that we lower the census … where is the money coming from?”

For the well-positioned HM group, the money will come from the savings it can prove to hospital administrators, says Dr. Centor, a nationally recognized voice in the debate on the value of hospitalists. He and Dr. Wellikson agree that hospitalists should be viewed as even more valuable to a hospital in financial trouble.

“Good hospitalists demonstrate their value with pay-for-performance-type things, with the avoidance of events, getting involved in quality committees,” Dr. Centor says. “A really good hospitalist program is worth its weight in gold and makes the hospital money. If you’re in a hospitalist group that is just churning out patients and isn’t involved in quality and isn’t considered good clinically, then you might be in danger.”

Integration Model

At Boston Medical Center, hospitalists have a more secure place—even in worsening economic times—through a vertical integration program that uses physicians hired through the Department of Family Medicine. The doctors split time between community health centers and hospital inpatient units, and work directly with hospitalists led by Jeffrey Greenwald, MD, HM director and associate professor of medicine at Boston University School of Medicine.

Larry Culpepper, MD, MPH, chairman of family medicine at Boston University School of Medicine and Boston Medical Center, says the vertical integration helps the family medicine physician and hospitalist to find efficiencies. “It has huge advantages,” Dr. Culpepper says. “They’re closely tied to the hospital this way. They’re not out in the community health center getting burned out and drifting away from mainstream medicine. … They see—face to face—the urologist or the cardiologist. They’ve got great communication that helps both ways.”

Collaborative programs are likely to crop up more in the next 12 to 18 months as HM leaders look for creative ways to justify their hospital support. More than 90% of HM groups receive hospital support payments, and the average subsidy is nearly $900,000 per year, according to SHM’s “2007-2008 Bi-Annual Survey on the State of Hospital Medicine.” Dr. Wellikson says hospitalists are establishing initiatives to demonstrate their value, but independent experts say more empirical data is needed to quantify that value.

“Many studies report that hospitalist care is associated with shorter lengths of stay and reduced costs,” say the authors of a recent study in the New England Journal of Medicine.1 “However, most studies were single-center, observational studies, and the results of the few available randomized trials have been mixed.”

Dr. Wellikson says recognition of the symbiotic relationship between hospitals and the hospitalists that work there is a major step in and of itself. HM leaders need to recognize and appreciate the litany of current statistics tied to hospitals. He frequently quotes recent hospital data that show 65% of institutions experienced both a drop in elective procedures and an uptick in charity care.

Combine that information with fact that many hospitals saw credit ratings downgraded and investment portfolios trimmed to the tune of $1 billion, and it’s clear hospitalists need to be cognizant of the threats to their livelihood. That means HM and hospitals need to work together, Dr. Wellikson says, to make both businesses financially viable. Thought leaders who take a long-term view, one that aligns HM fortunes with hospitals’ fate, would be in the strongest position moving forward, he says.

“In any cycle in any industry, you have fat times and lean times,” he says. “You have to manage in both times, and this is the first lean time. … Eventually, this recession will pass and the strong hospitals will survive. The better hospitalists will survive, because they’re going to be more valuable to their institution.” TH

Richard Quinn is a freelance writer based in New Jersey.

Reference

1. Hamel MB, Drazen JM, Epstein AM. The growth of hospitalists and the changing face of primary care. NEJM. 2009;360(11):1141-1143.

Hospitalist Stephanie Jackson, MD, medical director of patient safety at Sacred Heart Medical Center in Eugene, Ore., was preparing for SHM’s meeting with lawmakers in Washington, D.C., in March. As a member of SHM’s Public Policy Committee, she knew the annual powwow with Congressional leaders would be particularly sensitive this year as the economy continues to crater, healthcare reform hangs in political purgatory, and HM advocates look to insulate the industry from growing pressures.

But while she was prepping to tackle national issues, Dr. Jackson was dealing with serious problems closer to home. Her own hospital administrators were preparing to slash the safety initiatives she was championing, including an ambitious new bar-coding system to reduce medication errors and a long-planned information technology upgrade, from the budget. Hospital executives held emergency financial meetings two weeks running. At the time, Sacred Heart had less than 70 days’ cash on hand, compared with its usual 350-day buffer. In essence, the threat to her HM program had sprouted up so severely and quickly that Dr. Jackson was too busy batting them down to travel 3,000 miles to talk about the issues.

“It’s hard to leave when your organization is not doing well,” she says. “You need to be home. Our whole mission is to provide safe, high-quality, compassionate patient care. When budget cuts are made, it will affect patient care. There’s absolutely no way it can’t.”

It’s the new HM paradigm: a landscape in which hospitalists confront a growing confluence of threats to their livelihood. The pressures are rooted in the economic downturn, as hospitals nationwide face sagging revenues and daily fights to raise capital as investors lower their investment ratings. Questions abound:

• Will more primary-care physicians (PCPs) return to hospitals to supplement their practices, siphoning encounters from HM groups?
• Will an infusion of government money into community health centers draw patients away from hospital stays?
• Will HM’s workforce expansion continue as hospitals close or lose the ability to pay competitive subsidies? Even the Federal Reserve, in its latest Beige Book survey, reported falling patient volumes for elective procedures and an increase in emergency services.
• Will the very real fears of physician overload and burnout—and the possible departure of qualified hospitalists for other specialties or careers—grow as institutions cut ancillary medical staff and put more duties on the HM checklist?

The threats are real, of course, but HM advocates and practitioners say that, for now, they remain just that. HM groups continue to grow, and HM job postings are plenty. To date, hospital administrators have been mostly loathe to lay off the staffers they count on to lower costs through patient safety initiatives, reduced length of stay, and faster throughput. The most optimistic of hospitalists view the threats as opportunities to further establish themselves as thought leaders who can prove their worth through quantifiable metrics. Still, hospitals are increasingly in dire straits, and that means hospitalists could be in the same situation.

“The dilemma is that hospitalists are tied to the hospital as an institution,” says Larry Wellikson, MD, CEO of SHM. “It doesn’t really matter what causes the hospital to have less discretionary capital. … These things play against the hospitalist.”

Beyond Staff Cuts

Dr. Jackson’s case is typical. Her institution—a two-hospital center with 510 combined beds—recently eliminated 70 positions. None were physicians, but several care-management jobs were lost. Add in a local unemployment rate of almost 12%, and it’s no surprise the hospital is buckling under the weight of uncompensated charity care. And even though Sacred Heart lists patient safety initiatives as a top priority, “it always comes up that it can be cut,” Dr. Jackson says.

The bar-coding initiative was put on hold until the end of 2010, despite the hospital’s purchase of a packager that separates medications into individual packets. Dr. Jackson thinks the new technology could cut medication errors by at least 25%. Updates in information technology have been put on hold. And even if President Obama’s stimulus plan supplies money for electronic medical records (EMR), much of that money might not make it to the hospital-floor level for another 12 to 18 months.

Budget cuts aren’t relegated to large-scale initiatives, either. “Positions have been frozen, perks disappearing,” Dr. Jackson says. “At medical staff meetings, food is getting sparse. Educational opportunities that would have been there before, they’re not going to pay for that. My money to go to [HM09] is frozen right now.”

Stay the Course

Greg Maynard, MD, MS, clinical professor of medicine and chief of the division of hospital medicine at the University of California at San Diego Medical Center, also identifies the threats to HM in personal terms. Cutbacks on spending are hard to avoid in tough economic times, he reasons, but the key for hospitalists is to not allow those discussions to affect the interpersonal relationships between HM groups and hospital executives. He also echoes the sentiments of burnout fears and morale issues. In the past year, his 24-member HM group has added primary coverage of the adult oncology unit and adult cystic fibrosis patients, among other responsibilities. It also started night coverage shifts. All the while, Dr. Maynard and his staff have heard UC San Diego is having financial issues, including troubles with its pension investments. Budget discussions are more strained because of the overall economic crisis, which makes professional relationships even more important to maintain, he says.

“You have to empathize with the medical center administrators as they struggle,” he adds. “I think there’s a threat of a dialogue. When pressure comes on, debates can become contentious. It’s important to avoid that.”

Dr. Maynard blames some of the current friction between hospitals and hospitalists on HM’s growth—estimated at 28,000 physicians and still growing—and the lagging increases in Medicare, Medicaid, and private insurer reimbursement. A new reimbursement system is at the top of Obama’s agenda for national healthcare reform; however, the economy has slowed the advance of those initiatives. Obama has set aside roughly $20 billion in stimulus funding to encourage EMR programs.

Other plans are likely to gain momentum in coming months, with the expected confirmation of Kansas Gov. Kathleen Sebelius as secretary of the U.S. Department of Health and Human Services.

“You can’t grow and grow, and not grow the amount of money needed,” Dr. Maynard says.

Return of the PCP

Another oft-discussed threat to the HM model is the potential return of primary-care physicians (PCPs) to the hospital. PCPs pulling back to focus on their private outpatient practices helped birth the HM movement. Many of the nation’s uninsured forego primary care and instead seek care in the ED, which often leads to hospital admission and HM care. If PCPs return to the hospital, it could mean a decrease in hospitalist patient census.

The plight of the unemployed, which has ballooned to more than 500,000 per month since December 2008, is another consideration. Will PCPs need to fill an encounter gap when millions of American families lose their employee-funded medical benefits? And what about the billions being set aside to open new community health centers, which theoretically would siphon potential PCP patients—and revenue? Will these centers push PCPs to resume caring for hospitalized patients?

“The only threat to HM is if we had major healthcare reform that included comprehensiveness, that included something to make it worthwhile for the PCPs to take care of their patients in the hospital,” says Robert M. Centor, MD, FACP, associate dean and director of the division of general internal medicine at Huntsville Regional Medical Campus in Alabama. “For more and more family physicians … it doesn’t make financial sense to travel to the hospital.”

Gene “Rusty” Kallenberg, MD, chief of family medicine at UC San Diego’s School of Medicine, points out PCPs can hurt hospitalists without returning to the hospital. More patients treated in primary care means fewer patients whom hospitalists can charge. Should Obama extend healthcare coverage to the estimated 47 million uninsured people in the U.S., patients once treated in the ED and admitted through HM programs likely would seek primary care before heading to the hospital, further limiting billing opportunities for HM groups. The irony, Dr. Kallenberg says, is that what is best for the patient isn’t necessarily best for the industry—HM included—that treats them.

“If you reward PCPs for doing what’s right, then somebody has to pay for it,” he says. “The specialists are going to pay for it. If what happens is epidemiologically fine, that we lower the census … where is the money coming from?”

For the well-positioned HM group, the money will come from the savings it can prove to hospital administrators, says Dr. Centor, a nationally recognized voice in the debate on the value of hospitalists. He and Dr. Wellikson agree that hospitalists should be viewed as even more valuable to a hospital in financial trouble.

“Good hospitalists demonstrate their value with pay-for-performance-type things, with the avoidance of events, getting involved in quality committees,” Dr. Centor says. “A really good hospitalist program is worth its weight in gold and makes the hospital money. If you’re in a hospitalist group that is just churning out patients and isn’t involved in quality and isn’t considered good clinically, then you might be in danger.”

Integration Model

At Boston Medical Center, hospitalists have a more secure place—even in worsening economic times—through a vertical integration program that uses physicians hired through the Department of Family Medicine. The doctors split time between community health centers and hospital inpatient units, and work directly with hospitalists led by Jeffrey Greenwald, MD, HM director and associate professor of medicine at Boston University School of Medicine.

Larry Culpepper, MD, MPH, chairman of family medicine at Boston University School of Medicine and Boston Medical Center, says the vertical integration helps the family medicine physician and hospitalist to find efficiencies. “It has huge advantages,” Dr. Culpepper says. “They’re closely tied to the hospital this way. They’re not out in the community health center getting burned out and drifting away from mainstream medicine. … They see—face to face—the urologist or the cardiologist. They’ve got great communication that helps both ways.”

Collaborative programs are likely to crop up more in the next 12 to 18 months as HM leaders look for creative ways to justify their hospital support. More than 90% of HM groups receive hospital support payments, and the average subsidy is nearly $900,000 per year, according to SHM’s “2007-2008 Bi-Annual Survey on the State of Hospital Medicine.” Dr. Wellikson says hospitalists are establishing initiatives to demonstrate their value, but independent experts say more empirical data is needed to quantify that value.

“Many studies report that hospitalist care is associated with shorter lengths of stay and reduced costs,” say the authors of a recent study in the New England Journal of Medicine.1 “However, most studies were single-center, observational studies, and the results of the few available randomized trials have been mixed.”

Dr. Wellikson says recognition of the symbiotic relationship between hospitals and the hospitalists that work there is a major step in and of itself. HM leaders need to recognize and appreciate the litany of current statistics tied to hospitals. He frequently quotes recent hospital data that show 65% of institutions experienced both a drop in elective procedures and an uptick in charity care.

Combine that information with fact that many hospitals saw credit ratings downgraded and investment portfolios trimmed to the tune of $1 billion, and it’s clear hospitalists need to be cognizant of the threats to their livelihood. That means HM and hospitals need to work together, Dr. Wellikson says, to make both businesses financially viable. Thought leaders who take a long-term view, one that aligns HM fortunes with hospitals’ fate, would be in the strongest position moving forward, he says.

“In any cycle in any industry, you have fat times and lean times,” he says. “You have to manage in both times, and this is the first lean time. … Eventually, this recession will pass and the strong hospitals will survive. The better hospitalists will survive, because they’re going to be more valuable to their institution.” TH

Richard Quinn is a freelance writer based in New Jersey.

Reference

1. Hamel MB, Drazen JM, Epstein AM. The growth of hospitalists and the changing face of primary care. NEJM. 2009;360(11):1141-1143.

Hospitalist Stephanie Jackson, MD, medical director of patient safety at Sacred Heart Medical Center in Eugene, Ore., was preparing for SHM’s meeting with lawmakers in Washington, D.C., in March. As a member of SHM’s Public Policy Committee, she knew the annual powwow with Congressional leaders would be particularly sensitive this year as the economy continues to crater, healthcare reform hangs in political purgatory, and HM advocates look to insulate the industry from growing pressures.

But while she was prepping to tackle national issues, Dr. Jackson was dealing with serious problems closer to home. Her own hospital administrators were preparing to slash the safety initiatives she was championing, including an ambitious new bar-coding system to reduce medication errors and a long-planned information technology upgrade, from the budget. Hospital executives held emergency financial meetings two weeks running. At the time, Sacred Heart had less than 70 days’ cash on hand, compared with its usual 350-day buffer. In essence, the threat to her HM program had sprouted up so severely and quickly that Dr. Jackson was too busy batting them down to travel 3,000 miles to talk about the issues.

“It’s hard to leave when your organization is not doing well,” she says. “You need to be home. Our whole mission is to provide safe, high-quality, compassionate patient care. When budget cuts are made, it will affect patient care. There’s absolutely no way it can’t.”

It’s the new HM paradigm: a landscape in which hospitalists confront a growing confluence of threats to their livelihood. The pressures are rooted in the economic downturn, as hospitals nationwide face sagging revenues and daily fights to raise capital as investors lower their investment ratings. Questions abound:

• Will more primary-care physicians (PCPs) return to hospitals to supplement their practices, siphoning encounters from HM groups?
• Will an infusion of government money into community health centers draw patients away from hospital stays?
• Will HM’s workforce expansion continue as hospitals close or lose the ability to pay competitive subsidies? Even the Federal Reserve, in its latest Beige Book survey, reported falling patient volumes for elective procedures and an increase in emergency services.
• Will the very real fears of physician overload and burnout—and the possible departure of qualified hospitalists for other specialties or careers—grow as institutions cut ancillary medical staff and put more duties on the HM checklist?

The threats are real, of course, but HM advocates and practitioners say that, for now, they remain just that. HM groups continue to grow, and HM job postings are plenty. To date, hospital administrators have been mostly loathe to lay off the staffers they count on to lower costs through patient safety initiatives, reduced length of stay, and faster throughput. The most optimistic of hospitalists view the threats as opportunities to further establish themselves as thought leaders who can prove their worth through quantifiable metrics. Still, hospitals are increasingly in dire straits, and that means hospitalists could be in the same situation.

“The dilemma is that hospitalists are tied to the hospital as an institution,” says Larry Wellikson, MD, CEO of SHM. “It doesn’t really matter what causes the hospital to have less discretionary capital. … These things play against the hospitalist.”

Beyond Staff Cuts

Dr. Jackson’s case is typical. Her institution—a two-hospital center with 510 combined beds—recently eliminated 70 positions. None were physicians, but several care-management jobs were lost. Add in a local unemployment rate of almost 12%, and it’s no surprise the hospital is buckling under the weight of uncompensated charity care. And even though Sacred Heart lists patient safety initiatives as a top priority, “it always comes up that it can be cut,” Dr. Jackson says.

The bar-coding initiative was put on hold until the end of 2010, despite the hospital’s purchase of a packager that separates medications into individual packets. Dr. Jackson thinks the new technology could cut medication errors by at least 25%. Updates in information technology have been put on hold. And even if President Obama’s stimulus plan supplies money for electronic medical records (EMR), much of that money might not make it to the hospital-floor level for another 12 to 18 months.

Budget cuts aren’t relegated to large-scale initiatives, either. “Positions have been frozen, perks disappearing,” Dr. Jackson says. “At medical staff meetings, food is getting sparse. Educational opportunities that would have been there before, they’re not going to pay for that. My money to go to [HM09] is frozen right now.”

Stay the Course

Greg Maynard, MD, MS, clinical professor of medicine and chief of the division of hospital medicine at the University of California at San Diego Medical Center, also identifies the threats to HM in personal terms. Cutbacks on spending are hard to avoid in tough economic times, he reasons, but the key for hospitalists is to not allow those discussions to affect the interpersonal relationships between HM groups and hospital executives. He also echoes the sentiments of burnout fears and morale issues. In the past year, his 24-member HM group has added primary coverage of the adult oncology unit and adult cystic fibrosis patients, among other responsibilities. It also started night coverage shifts. All the while, Dr. Maynard and his staff have heard UC San Diego is having financial issues, including troubles with its pension investments. Budget discussions are more strained because of the overall economic crisis, which makes professional relationships even more important to maintain, he says.

“You have to empathize with the medical center administrators as they struggle,” he adds. “I think there’s a threat of a dialogue. When pressure comes on, debates can become contentious. It’s important to avoid that.”

Dr. Maynard blames some of the current friction between hospitals and hospitalists on HM’s growth—estimated at 28,000 physicians and still growing—and the lagging increases in Medicare, Medicaid, and private insurer reimbursement. A new reimbursement system is at the top of Obama’s agenda for national healthcare reform; however, the economy has slowed the advance of those initiatives. Obama has set aside roughly $20 billion in stimulus funding to encourage EMR programs.

Other plans are likely to gain momentum in coming months, with the expected confirmation of Kansas Gov. Kathleen Sebelius as secretary of the U.S. Department of Health and Human Services.

“You can’t grow and grow, and not grow the amount of money needed,” Dr. Maynard says.

Return of the PCP

Another oft-discussed threat to the HM model is the potential return of primary-care physicians (PCPs) to the hospital. PCPs pulling back to focus on their private outpatient practices helped birth the HM movement. Many of the nation’s uninsured forego primary care and instead seek care in the ED, which often leads to hospital admission and HM care. If PCPs return to the hospital, it could mean a decrease in hospitalist patient census.

The plight of the unemployed, which has ballooned to more than 500,000 per month since December 2008, is another consideration. Will PCPs need to fill an encounter gap when millions of American families lose their employee-funded medical benefits? And what about the billions being set aside to open new community health centers, which theoretically would siphon potential PCP patients—and revenue? Will these centers push PCPs to resume caring for hospitalized patients?

“The only threat to HM is if we had major healthcare reform that included comprehensiveness, that included something to make it worthwhile for the PCPs to take care of their patients in the hospital,” says Robert M. Centor, MD, FACP, associate dean and director of the division of general internal medicine at Huntsville Regional Medical Campus in Alabama. “For more and more family physicians … it doesn’t make financial sense to travel to the hospital.”

Gene “Rusty” Kallenberg, MD, chief of family medicine at UC San Diego’s School of Medicine, points out PCPs can hurt hospitalists without returning to the hospital. More patients treated in primary care means fewer patients whom hospitalists can charge. Should Obama extend healthcare coverage to the estimated 47 million uninsured people in the U.S., patients once treated in the ED and admitted through HM programs likely would seek primary care before heading to the hospital, further limiting billing opportunities for HM groups. The irony, Dr. Kallenberg says, is that what is best for the patient isn’t necessarily best for the industry—HM included—that treats them.

“If you reward PCPs for doing what’s right, then somebody has to pay for it,” he says. “The specialists are going to pay for it. If what happens is epidemiologically fine, that we lower the census … where is the money coming from?”

For the well-positioned HM group, the money will come from the savings it can prove to hospital administrators, says Dr. Centor, a nationally recognized voice in the debate on the value of hospitalists. He and Dr. Wellikson agree that hospitalists should be viewed as even more valuable to a hospital in financial trouble.

“Good hospitalists demonstrate their value with pay-for-performance-type things, with the avoidance of events, getting involved in quality committees,” Dr. Centor says. “A really good hospitalist program is worth its weight in gold and makes the hospital money. If you’re in a hospitalist group that is just churning out patients and isn’t involved in quality and isn’t considered good clinically, then you might be in danger.”

Integration Model

At Boston Medical Center, hospitalists have a more secure place—even in worsening economic times—through a vertical integration program that uses physicians hired through the Department of Family Medicine. The doctors split time between community health centers and hospital inpatient units, and work directly with hospitalists led by Jeffrey Greenwald, MD, HM director and associate professor of medicine at Boston University School of Medicine.

Larry Culpepper, MD, MPH, chairman of family medicine at Boston University School of Medicine and Boston Medical Center, says the vertical integration helps the family medicine physician and hospitalist to find efficiencies. “It has huge advantages,” Dr. Culpepper says. “They’re closely tied to the hospital this way. They’re not out in the community health center getting burned out and drifting away from mainstream medicine. … They see—face to face—the urologist or the cardiologist. They’ve got great communication that helps both ways.”

Collaborative programs are likely to crop up more in the next 12 to 18 months as HM leaders look for creative ways to justify their hospital support. More than 90% of HM groups receive hospital support payments, and the average subsidy is nearly $900,000 per year, according to SHM’s “2007-2008 Bi-Annual Survey on the State of Hospital Medicine.” Dr. Wellikson says hospitalists are establishing initiatives to demonstrate their value, but independent experts say more empirical data is needed to quantify that value.

“Many studies report that hospitalist care is associated with shorter lengths of stay and reduced costs,” say the authors of a recent study in the New England Journal of Medicine.1 “However, most studies were single-center, observational studies, and the results of the few available randomized trials have been mixed.”

Dr. Wellikson says recognition of the symbiotic relationship between hospitals and the hospitalists that work there is a major step in and of itself. HM leaders need to recognize and appreciate the litany of current statistics tied to hospitals. He frequently quotes recent hospital data that show 65% of institutions experienced both a drop in elective procedures and an uptick in charity care.

Combine that information with fact that many hospitals saw credit ratings downgraded and investment portfolios trimmed to the tune of $1 billion, and it’s clear hospitalists need to be cognizant of the threats to their livelihood. That means HM and hospitals need to work together, Dr. Wellikson says, to make both businesses financially viable. Thought leaders who take a long-term view, one that aligns HM fortunes with hospitals’ fate, would be in the strongest position moving forward, he says.

“In any cycle in any industry, you have fat times and lean times,” he says. “You have to manage in both times, and this is the first lean time. … Eventually, this recession will pass and the strong hospitals will survive. The better hospitalists will survive, because they’re going to be more valuable to their institution.” TH

Richard Quinn is a freelance writer based in New Jersey.

Reference

1. Hamel MB, Drazen JM, Epstein AM. The growth of hospitalists and the changing face of primary care. NEJM. 2009;360(11):1141-1143.

It wasn’t that long ago that SHM was pretty excited to see that the word “hospitalist” had been added to the dictionary, but to have hospitalists mentioned on Oprah Winfrey’s television show, on The Today Show, and in the New England Journal of Medicine (NEJM) all in the same week is a watershed moment. It’s further recognition that HM is part of the fabric of this country and an established specialty in America’s healthcare system.

It all started in March, when SHM President Pat Cawley, MD, was quoted in O, The Oprah Magazine, which has a circulation of more than 2 million. Later that month, Oprah had Dennis Quaid on her show to discuss the overdose of anticoagulant his newborn twins were given at a Los Angeles hospital. The conversation quickly turned to patient safety and performance expectations for hospitalized patients. Dr. Mehmet Oz, the resident medical guru for Oprah’s show, created a list of eight essential steps for hospitalized patients to take in order to have the best and safest hospital experience. No. 7 on this list was “Get to know your hospitalist.” It’s the kind of exposure that drives 10,000 to 20,000 people to go online and discover hospitalists.

That same week, The Today Show featured Geno Merli, MD, chief medical officer at Jefferson Medical College in Philadelphia, an SHM member, and our representative to the Coalition to Prevent DVT (www.preventDVT.org). Dr. Merli discussed deep-vein thrombosis (DVT) and pulmonary embolism (PE) prevention, as well as efforts to engage patients and their physicians in this effort. SHM has assumed a leadership role in this 60-group coalition, which is providing DVT awareness to millions of people.

And to top off a banner week, NEJM ran a story and editorial about the rapid growth of HM, based on a study analyzing Medicare data from 1997 to 2006. In “Growth in the Care of Older Patients by Hospitalists in the United States,” by Kuo et al, the main finding was the very rapid growth of HM. The editorial authors noted “the odds that a Medicare patient would be cared for by a hospitalist grew by 29% per year from 1997 through 2006.”

The cherry on the sundae was when other media outlets followed up on the Oprah story, and even more jumped on the NEJM article. Hundreds of media outlets seized the opportunity to tout the growth of HM and our role in patient safety and performance improvement. The reach of these messages, through a national consumer audience and through a prestigious medical journal, should not be underestimated. SHM couldn’t buy that kind of message and deliver it to our patients and their families.

No Slowing Down

It was interesting that I was at SHM’s Leadership Academy in Hawaii when all the stories broke, which made it seem more tangible and brought it home on a personal level as a hospitalist. Just being around 120 current and future HM leaders made me realize that we have the manpower (and womanpower) to continue to create the needed change for our health system.

Hospitalist leaders took a week off from their overwhelming, day-to-day responsibilities to learn how to be more effective leaders. This is the ninth time SHM has brought together more than 100 hospitalist leaders, and every time, we find bright, young—and some not-so-young—hospitalists who thirst for direction to manage their group of hospitalists, to create a team of health professionals, to reshape and fix the hospitals they work in, to move from volume to value, and to do all of the hundreds of other things hospitalist leaders get handed to them every day.

The energy in our specialty will also be felt at HM09. Despite the recession and the recent falloff in attendance at many medical meetings, SHM’s annual meeting—the largest gathering in HM, which will occur in Chicago this month—is having its best registration ever. More than 2,000 stakeholders will come together to network, train to be a better hospitalist, and learn how to effect real change at their hospitals.

As President Obama has mentioned time and again, there are plenty of companies and organizations that continue to produce the products and services that Americans want and need, and even though we are in tough times, those organizations will prevail. Hospitalists clearly are in demand. Even in tough economic times, hospitals, medical staffs, and our patients continue to look to us for answers.

HM is growing exponentially, even when many still know little about hospitalists and what we do. With voices like Oprah, Today, and NEJM highlighting our good work, more light will be shed on our specialty. And I believe we are ready for the scrutiny and the recognition.

Hospitalists earn their keep by taking over a greater share of the management of the acutely ill patient, in working with our primary-care physician, subspecialty, and surgical colleagues, and by being strong team members with our allied health professionals. In many ways, HM remains a work in progress. Although we have accomplished much in a little more than a decade, our best days are still ahead of us.

Just turn on the TV or open a magazine to hear all about it. TH

Dr. Wellikson is CEO of SHM.

It wasn’t that long ago that SHM was pretty excited to see that the word “hospitalist” had been added to the dictionary, but to have hospitalists mentioned on Oprah Winfrey’s television show, on The Today Show, and in the New England Journal of Medicine (NEJM) all in the same week is a watershed moment. It’s further recognition that HM is part of the fabric of this country and an established specialty in America’s healthcare system.

It all started in March, when SHM President Pat Cawley, MD, was quoted in O, The Oprah Magazine, which has a circulation of more than 2 million. Later that month, Oprah had Dennis Quaid on her show to discuss the overdose of anticoagulant his newborn twins were given at a Los Angeles hospital. The conversation quickly turned to patient safety and performance expectations for hospitalized patients. Dr. Mehmet Oz, the resident medical guru for Oprah’s show, created a list of eight essential steps for hospitalized patients to take in order to have the best and safest hospital experience. No. 7 on this list was “Get to know your hospitalist.” It’s the kind of exposure that drives 10,000 to 20,000 people to go online and discover hospitalists.

That same week, The Today Show featured Geno Merli, MD, chief medical officer at Jefferson Medical College in Philadelphia, an SHM member, and our representative to the Coalition to Prevent DVT (www.preventDVT.org). Dr. Merli discussed deep-vein thrombosis (DVT) and pulmonary embolism (PE) prevention, as well as efforts to engage patients and their physicians in this effort. SHM has assumed a leadership role in this 60-group coalition, which is providing DVT awareness to millions of people.

And to top off a banner week, NEJM ran a story and editorial about the rapid growth of HM, based on a study analyzing Medicare data from 1997 to 2006. In “Growth in the Care of Older Patients by Hospitalists in the United States,” by Kuo et al, the main finding was the very rapid growth of HM. The editorial authors noted “the odds that a Medicare patient would be cared for by a hospitalist grew by 29% per year from 1997 through 2006.”

The cherry on the sundae was when other media outlets followed up on the Oprah story, and even more jumped on the NEJM article. Hundreds of media outlets seized the opportunity to tout the growth of HM and our role in patient safety and performance improvement. The reach of these messages, through a national consumer audience and through a prestigious medical journal, should not be underestimated. SHM couldn’t buy that kind of message and deliver it to our patients and their families.

No Slowing Down

It was interesting that I was at SHM’s Leadership Academy in Hawaii when all the stories broke, which made it seem more tangible and brought it home on a personal level as a hospitalist. Just being around 120 current and future HM leaders made me realize that we have the manpower (and womanpower) to continue to create the needed change for our health system.

Hospitalist leaders took a week off from their overwhelming, day-to-day responsibilities to learn how to be more effective leaders. This is the ninth time SHM has brought together more than 100 hospitalist leaders, and every time, we find bright, young—and some not-so-young—hospitalists who thirst for direction to manage their group of hospitalists, to create a team of health professionals, to reshape and fix the hospitals they work in, to move from volume to value, and to do all of the hundreds of other things hospitalist leaders get handed to them every day.

The energy in our specialty will also be felt at HM09. Despite the recession and the recent falloff in attendance at many medical meetings, SHM’s annual meeting—the largest gathering in HM, which will occur in Chicago this month—is having its best registration ever. More than 2,000 stakeholders will come together to network, train to be a better hospitalist, and learn how to effect real change at their hospitals.

As President Obama has mentioned time and again, there are plenty of companies and organizations that continue to produce the products and services that Americans want and need, and even though we are in tough times, those organizations will prevail. Hospitalists clearly are in demand. Even in tough economic times, hospitals, medical staffs, and our patients continue to look to us for answers.

HM is growing exponentially, even when many still know little about hospitalists and what we do. With voices like Oprah, Today, and NEJM highlighting our good work, more light will be shed on our specialty. And I believe we are ready for the scrutiny and the recognition.

Hospitalists earn their keep by taking over a greater share of the management of the acutely ill patient, in working with our primary-care physician, subspecialty, and surgical colleagues, and by being strong team members with our allied health professionals. In many ways, HM remains a work in progress. Although we have accomplished much in a little more than a decade, our best days are still ahead of us.

Just turn on the TV or open a magazine to hear all about it. TH

Dr. Wellikson is CEO of SHM.

It wasn’t that long ago that SHM was pretty excited to see that the word “hospitalist” had been added to the dictionary, but to have hospitalists mentioned on Oprah Winfrey’s television show, on The Today Show, and in the New England Journal of Medicine (NEJM) all in the same week is a watershed moment. It’s further recognition that HM is part of the fabric of this country and an established specialty in America’s healthcare system.

It all started in March, when SHM President Pat Cawley, MD, was quoted in O, The Oprah Magazine, which has a circulation of more than 2 million. Later that month, Oprah had Dennis Quaid on her show to discuss the overdose of anticoagulant his newborn twins were given at a Los Angeles hospital. The conversation quickly turned to patient safety and performance expectations for hospitalized patients. Dr. Mehmet Oz, the resident medical guru for Oprah’s show, created a list of eight essential steps for hospitalized patients to take in order to have the best and safest hospital experience. No. 7 on this list was “Get to know your hospitalist.” It’s the kind of exposure that drives 10,000 to 20,000 people to go online and discover hospitalists.

That same week, The Today Show featured Geno Merli, MD, chief medical officer at Jefferson Medical College in Philadelphia, an SHM member, and our representative to the Coalition to Prevent DVT (www.preventDVT.org). Dr. Merli discussed deep-vein thrombosis (DVT) and pulmonary embolism (PE) prevention, as well as efforts to engage patients and their physicians in this effort. SHM has assumed a leadership role in this 60-group coalition, which is providing DVT awareness to millions of people.

And to top off a banner week, NEJM ran a story and editorial about the rapid growth of HM, based on a study analyzing Medicare data from 1997 to 2006. In “Growth in the Care of Older Patients by Hospitalists in the United States,” by Kuo et al, the main finding was the very rapid growth of HM. The editorial authors noted “the odds that a Medicare patient would be cared for by a hospitalist grew by 29% per year from 1997 through 2006.”

The cherry on the sundae was when other media outlets followed up on the Oprah story, and even more jumped on the NEJM article. Hundreds of media outlets seized the opportunity to tout the growth of HM and our role in patient safety and performance improvement. The reach of these messages, through a national consumer audience and through a prestigious medical journal, should not be underestimated. SHM couldn’t buy that kind of message and deliver it to our patients and their families.

No Slowing Down

It was interesting that I was at SHM’s Leadership Academy in Hawaii when all the stories broke, which made it seem more tangible and brought it home on a personal level as a hospitalist. Just being around 120 current and future HM leaders made me realize that we have the manpower (and womanpower) to continue to create the needed change for our health system.

Hospitalist leaders took a week off from their overwhelming, day-to-day responsibilities to learn how to be more effective leaders. This is the ninth time SHM has brought together more than 100 hospitalist leaders, and every time, we find bright, young—and some not-so-young—hospitalists who thirst for direction to manage their group of hospitalists, to create a team of health professionals, to reshape and fix the hospitals they work in, to move from volume to value, and to do all of the hundreds of other things hospitalist leaders get handed to them every day.

The energy in our specialty will also be felt at HM09. Despite the recession and the recent falloff in attendance at many medical meetings, SHM’s annual meeting—the largest gathering in HM, which will occur in Chicago this month—is having its best registration ever. More than 2,000 stakeholders will come together to network, train to be a better hospitalist, and learn how to effect real change at their hospitals.

As President Obama has mentioned time and again, there are plenty of companies and organizations that continue to produce the products and services that Americans want and need, and even though we are in tough times, those organizations will prevail. Hospitalists clearly are in demand. Even in tough economic times, hospitals, medical staffs, and our patients continue to look to us for answers.

HM is growing exponentially, even when many still know little about hospitalists and what we do. With voices like Oprah, Today, and NEJM highlighting our good work, more light will be shed on our specialty. And I believe we are ready for the scrutiny and the recognition.

Hospitalists earn their keep by taking over a greater share of the management of the acutely ill patient, in working with our primary-care physician, subspecialty, and surgical colleagues, and by being strong team members with our allied health professionals. In many ways, HM remains a work in progress. Although we have accomplished much in a little more than a decade, our best days are still ahead of us.

Just turn on the TV or open a magazine to hear all about it. TH

Dr. Wellikson is CEO of SHM.

Editor’s note: This is the first of a two-part series addressing large HM group issues.

In the mid-1990s, when I first became interested in how other hospitalist groups were organized, I started surveying by phone all the groups I could find. It was really unusual to find a group larger than four or five full-time equivalent (FTE) hospitalists. Since then, the size of a typical hospitalist group has grown steadily, and data reported in SHM’s “2007-2008 Bi-Annual Survey on the State of Hospital Medicine” shows the median number of FTE physicians in HM groups is 8.0 (mean of 9.75). So in just a few years, our field has grown in such a way that half of all groups in operation now have more than eight physician FTEs. I think most future growth in numbers of hospitalists will be due to individual practices getting larger, rather than new practices starting up.

I work regularly with groups that have more than 20 FTEs, and I have found that large groups tend to have a number of attributes in common.

Separate Daytime Admitter and Rounder Functions

Large groups almost always staff admitter and rounder functions with separate doctors around the clock. That means patients arriving during regular business hours are admitted by a different doctor (the admitter) than the doctor who will provide their care on Day Two and beyond (the rounder).

Although such a system is popular, I suggest every group challenge itself to think about whether it really is the best system. Most groups, regardless of size, have about a quarter to a third of their new admits and consults arrive between 7 a.m. and 5 p.m. If the group did away with a separate admitter during the day and moved all daytime admitters into additional rounder positions, all the daytime admissions could be rotated among all of the daytime doctors, and those patients would typically be seen by the same hospitalist the next day. That would improve hospitalist-patient continuity for the patients who arrive during the day, which might improve the group’s overall efficiency as well as quality and patient satisfaction. Each rounder would become responsible for seeing up to three new consults or admissions during the course of the daytime rounding shift, and the list of new patients to take over each morning—patients admitted by the evening and night admitters—would be smaller.

Of course, one significant benefit of having a separate admitter shift during the day is relieving the rounding doctors of the stress of interrupting rounds for an unpredictable number of new admissions each day. And if the new admissions arrive in the morning, throughput may suffer as it might mean the rounding doctor may see “dischargeable” patients later in the day.

I think there is room for debate about whether it is best for large groups to have a separate admitter during the day, but whatever approach a group chooses, it should acknowledge the costs of that approach and not just assume that it is the only one that is feasible or reasonable.

Who Is Caring for Whom?

The larger the hospitalist group, the more difficulty nurses and other staff have understanding exactly how patients are distributed among the doctors. When one hospitalist rotates “off service” to be replaced by another the next day, or when overnight admissions are “picked up” by a rounding doctor the next morning, it can be difficult for nurses to know which hospitalist is responsible for the patient at a given moment.

All groups, regardless of size, should ensure that the hospitalist who picks up patients from a colleague who has rotated off the day before writes an order in the chart indicating “change attending to Dr. Jones,” or clearly communicates who the new hospitalist is by some other means, such as an electronic medical record or a phone call from a clerk. It isn’t enough that patients are assigned to a particular team—say, the “white team” or the “green team”—for their entire stay. Nurses and other staff need to know which hospitalist is covering that team each day.

One test of how well your system is working is to assess how the nurse answers when a patient or family asks, “Which doctor will be in to see me today?” It isn’t good enough for the nurse to just say, “The green-team doctor will see you, but I don’t know who that is today.” The nurse needs to be able to provide the name of the doctor who will be in. If nurses at your hospital regularly page the wrong hospitalist, or must call around just to figure out who the attending hospitalist is for a particular patient, then you have an opportunity to improve how you communicate this information to the nurse and others.

Even if you have a system in which it is clear to everyone which hospitalist has taken over for one who has rotated off-service, you need to ensure that nurses can easily determine the attending hospitalist for patients admitted the night before. Night-shift staff not knowing which doctor will take over in the morning is an all-too-common problem, and it results in too many staffers not knowing who is caring for the patient from the time the night doctor goes off (e.g., 7 a.m.) until the rounder taking over gets to that patient on rounds. Having evening/night admitters assign attending, or rounder, hospitalists at the time of each admission is a great solution, and I’ll provide ideas about how to do this in next month’s column.

I worry about patient satisfaction if the evening/night admitter can’t tell the patient the name of the hospitalist who will take over in the morning. How can the patient feel that they’re getting personalized care when they’re told, “I don’t know which of my partners will take over your care tomorrow. They all get together and divide up the patients each morning and will assign a doctor to you then”? It’s different if the admitter tells the patient, “I’m on call for our group tonight, but will be home sleeping tomorrow and my colleague, Dr. Clapton, will take over your care in the morning.” I usually go on to say with a wink that the patient is getting an upgrade, because Dr. Clapton is so much smarter and better-looking than me. I’ll understand if the embellishment doesn’t feel right for you, but I think there is value in the admitter, or a hospitalist rotating off-service, taking a minute to say something nice about the hospitalist who will take over next.

Next month, I will continue to explore issues that are particularly problematic for larger groups. 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 Associates, a national hospitalist practice management consulting firm. He also is part of the faculty for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. This column represents his views and is not intended to reflect an official position of SHM.

Editor’s note: This is the first of a two-part series addressing large HM group issues.

In the mid-1990s, when I first became interested in how other hospitalist groups were organized, I started surveying by phone all the groups I could find. It was really unusual to find a group larger than four or five full-time equivalent (FTE) hospitalists. Since then, the size of a typical hospitalist group has grown steadily, and data reported in SHM’s “2007-2008 Bi-Annual Survey on the State of Hospital Medicine” shows the median number of FTE physicians in HM groups is 8.0 (mean of 9.75). So in just a few years, our field has grown in such a way that half of all groups in operation now have more than eight physician FTEs. I think most future growth in numbers of hospitalists will be due to individual practices getting larger, rather than new practices starting up.

I work regularly with groups that have more than 20 FTEs, and I have found that large groups tend to have a number of attributes in common.

Separate Daytime Admitter and Rounder Functions

Large groups almost always staff admitter and rounder functions with separate doctors around the clock. That means patients arriving during regular business hours are admitted by a different doctor (the admitter) than the doctor who will provide their care on Day Two and beyond (the rounder).

Although such a system is popular, I suggest every group challenge itself to think about whether it really is the best system. Most groups, regardless of size, have about a quarter to a third of their new admits and consults arrive between 7 a.m. and 5 p.m. If the group did away with a separate admitter during the day and moved all daytime admitters into additional rounder positions, all the daytime admissions could be rotated among all of the daytime doctors, and those patients would typically be seen by the same hospitalist the next day. That would improve hospitalist-patient continuity for the patients who arrive during the day, which might improve the group’s overall efficiency as well as quality and patient satisfaction. Each rounder would become responsible for seeing up to three new consults or admissions during the course of the daytime rounding shift, and the list of new patients to take over each morning—patients admitted by the evening and night admitters—would be smaller.

Of course, one significant benefit of having a separate admitter shift during the day is relieving the rounding doctors of the stress of interrupting rounds for an unpredictable number of new admissions each day. And if the new admissions arrive in the morning, throughput may suffer as it might mean the rounding doctor may see “dischargeable” patients later in the day.

I think there is room for debate about whether it is best for large groups to have a separate admitter during the day, but whatever approach a group chooses, it should acknowledge the costs of that approach and not just assume that it is the only one that is feasible or reasonable.

Who Is Caring for Whom?

The larger the hospitalist group, the more difficulty nurses and other staff have understanding exactly how patients are distributed among the doctors. When one hospitalist rotates “off service” to be replaced by another the next day, or when overnight admissions are “picked up” by a rounding doctor the next morning, it can be difficult for nurses to know which hospitalist is responsible for the patient at a given moment.

All groups, regardless of size, should ensure that the hospitalist who picks up patients from a colleague who has rotated off the day before writes an order in the chart indicating “change attending to Dr. Jones,” or clearly communicates who the new hospitalist is by some other means, such as an electronic medical record or a phone call from a clerk. It isn’t enough that patients are assigned to a particular team—say, the “white team” or the “green team”—for their entire stay. Nurses and other staff need to know which hospitalist is covering that team each day.

One test of how well your system is working is to assess how the nurse answers when a patient or family asks, “Which doctor will be in to see me today?” It isn’t good enough for the nurse to just say, “The green-team doctor will see you, but I don’t know who that is today.” The nurse needs to be able to provide the name of the doctor who will be in. If nurses at your hospital regularly page the wrong hospitalist, or must call around just to figure out who the attending hospitalist is for a particular patient, then you have an opportunity to improve how you communicate this information to the nurse and others.

Even if you have a system in which it is clear to everyone which hospitalist has taken over for one who has rotated off-service, you need to ensure that nurses can easily determine the attending hospitalist for patients admitted the night before. Night-shift staff not knowing which doctor will take over in the morning is an all-too-common problem, and it results in too many staffers not knowing who is caring for the patient from the time the night doctor goes off (e.g., 7 a.m.) until the rounder taking over gets to that patient on rounds. Having evening/night admitters assign attending, or rounder, hospitalists at the time of each admission is a great solution, and I’ll provide ideas about how to do this in next month’s column.

I worry about patient satisfaction if the evening/night admitter can’t tell the patient the name of the hospitalist who will take over in the morning. How can the patient feel that they’re getting personalized care when they’re told, “I don’t know which of my partners will take over your care tomorrow. They all get together and divide up the patients each morning and will assign a doctor to you then”? It’s different if the admitter tells the patient, “I’m on call for our group tonight, but will be home sleeping tomorrow and my colleague, Dr. Clapton, will take over your care in the morning.” I usually go on to say with a wink that the patient is getting an upgrade, because Dr. Clapton is so much smarter and better-looking than me. I’ll understand if the embellishment doesn’t feel right for you, but I think there is value in the admitter, or a hospitalist rotating off-service, taking a minute to say something nice about the hospitalist who will take over next.

Next month, I will continue to explore issues that are particularly problematic for larger groups. 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 Associates, a national hospitalist practice management consulting firm. He also is part of the faculty for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. This column represents his views and is not intended to reflect an official position of SHM.

Editor’s note: This is the first of a two-part series addressing large HM group issues.

In the mid-1990s, when I first became interested in how other hospitalist groups were organized, I started surveying by phone all the groups I could find. It was really unusual to find a group larger than four or five full-time equivalent (FTE) hospitalists. Since then, the size of a typical hospitalist group has grown steadily, and data reported in SHM’s “2007-2008 Bi-Annual Survey on the State of Hospital Medicine” shows the median number of FTE physicians in HM groups is 8.0 (mean of 9.75). So in just a few years, our field has grown in such a way that half of all groups in operation now have more than eight physician FTEs. I think most future growth in numbers of hospitalists will be due to individual practices getting larger, rather than new practices starting up.

I work regularly with groups that have more than 20 FTEs, and I have found that large groups tend to have a number of attributes in common.

Separate Daytime Admitter and Rounder Functions

Large groups almost always staff admitter and rounder functions with separate doctors around the clock. That means patients arriving during regular business hours are admitted by a different doctor (the admitter) than the doctor who will provide their care on Day Two and beyond (the rounder).

Although such a system is popular, I suggest every group challenge itself to think about whether it really is the best system. Most groups, regardless of size, have about a quarter to a third of their new admits and consults arrive between 7 a.m. and 5 p.m. If the group did away with a separate admitter during the day and moved all daytime admitters into additional rounder positions, all the daytime admissions could be rotated among all of the daytime doctors, and those patients would typically be seen by the same hospitalist the next day. That would improve hospitalist-patient continuity for the patients who arrive during the day, which might improve the group’s overall efficiency as well as quality and patient satisfaction. Each rounder would become responsible for seeing up to three new consults or admissions during the course of the daytime rounding shift, and the list of new patients to take over each morning—patients admitted by the evening and night admitters—would be smaller.

Of course, one significant benefit of having a separate admitter shift during the day is relieving the rounding doctors of the stress of interrupting rounds for an unpredictable number of new admissions each day. And if the new admissions arrive in the morning, throughput may suffer as it might mean the rounding doctor may see “dischargeable” patients later in the day.

I think there is room for debate about whether it is best for large groups to have a separate admitter during the day, but whatever approach a group chooses, it should acknowledge the costs of that approach and not just assume that it is the only one that is feasible or reasonable.

Who Is Caring for Whom?

The larger the hospitalist group, the more difficulty nurses and other staff have understanding exactly how patients are distributed among the doctors. When one hospitalist rotates “off service” to be replaced by another the next day, or when overnight admissions are “picked up” by a rounding doctor the next morning, it can be difficult for nurses to know which hospitalist is responsible for the patient at a given moment.

All groups, regardless of size, should ensure that the hospitalist who picks up patients from a colleague who has rotated off the day before writes an order in the chart indicating “change attending to Dr. Jones,” or clearly communicates who the new hospitalist is by some other means, such as an electronic medical record or a phone call from a clerk. It isn’t enough that patients are assigned to a particular team—say, the “white team” or the “green team”—for their entire stay. Nurses and other staff need to know which hospitalist is covering that team each day.

One test of how well your system is working is to assess how the nurse answers when a patient or family asks, “Which doctor will be in to see me today?” It isn’t good enough for the nurse to just say, “The green-team doctor will see you, but I don’t know who that is today.” The nurse needs to be able to provide the name of the doctor who will be in. If nurses at your hospital regularly page the wrong hospitalist, or must call around just to figure out who the attending hospitalist is for a particular patient, then you have an opportunity to improve how you communicate this information to the nurse and others.

Even if you have a system in which it is clear to everyone which hospitalist has taken over for one who has rotated off-service, you need to ensure that nurses can easily determine the attending hospitalist for patients admitted the night before. Night-shift staff not knowing which doctor will take over in the morning is an all-too-common problem, and it results in too many staffers not knowing who is caring for the patient from the time the night doctor goes off (e.g., 7 a.m.) until the rounder taking over gets to that patient on rounds. Having evening/night admitters assign attending, or rounder, hospitalists at the time of each admission is a great solution, and I’ll provide ideas about how to do this in next month’s column.

I worry about patient satisfaction if the evening/night admitter can’t tell the patient the name of the hospitalist who will take over in the morning. How can the patient feel that they’re getting personalized care when they’re told, “I don’t know which of my partners will take over your care tomorrow. They all get together and divide up the patients each morning and will assign a doctor to you then”? It’s different if the admitter tells the patient, “I’m on call for our group tonight, but will be home sleeping tomorrow and my colleague, Dr. Clapton, will take over your care in the morning.” I usually go on to say with a wink that the patient is getting an upgrade, because Dr. Clapton is so much smarter and better-looking than me. I’ll understand if the embellishment doesn’t feel right for you, but I think there is value in the admitter, or a hospitalist rotating off-service, taking a minute to say something nice about the hospitalist who will take over next.

Next month, I will continue to explore issues that are particularly problematic for larger groups. 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 Associates, a national hospitalist practice management consulting firm. He also is part of the faculty for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. This column represents his views and is not intended to reflect an official position of SHM.

In the aftermath of the recent shuttering of Colorado’s oldest newspaper, The Rocky Mountain News, a couple of colleagues and I were discussing how unlikely it seemed just a few months ago that this could happen. It wasn’t long until we made the theoretical leap to what it would take for our hospitalist group to go out of business. Of course, this seems highly unlikely, but then again, the closing of a 150-year-old metropolitan newspaper seemed a preposterous proposition.

In the course of this discussion, we conjured myriad internal or external factors that could adversely affect our program. Although this was a tangential, lunchtime discussion, it did reverberate against the tuning fork of a faltering U.S. economy, especially regarding the financial sector and the automotive industry.

With that as a frame, I thought I’d take a dip into Paranoia Pond and look at potential threats to the HM model. Let me start by saying that I believe—deeply—in the hospitalist movement, the strides we’ve made, and the bright path that lies before us. I am not stating that any of these potential perils will put hospitalists out of business. However, the list below includes several risks that, if not properly mitigated, could alter our future course.

Here are 10 potential threats to the HM business model that you should keep an eye on:

1. Failure to Embrace QI

Those who fundamentally improve outcomes will write the future of medicine. Hospitalists are perfectly positioned—and expected—to do this. I believe most hospital CEOs think this is part of the contract: funding for quality. A failure to live up to our end of the bargain puts us at great risk. If your group isn’t able to demonstrate measurable improvements in processes and clinical outcomes, then you are at risk of losing hospital funding. As the economy recedes further and hospital reimbursement is more closely tied to quality, this will quickly move beyond a potential threat to a reality.

2. Lack of New Data to Support the HM Model

A corollary of No. 1 is our ability to show how we work. This burden, by and large, falls to my academic colleagues. After a rash of early studies showed the benefits of the hospitalist model, more recent data has been less convincing. This doesn’t mean we aren’t improving outcomes; rather, it means we aren’t always measuring and proving it. HM must get past the easy-to-measure endpoints, such as length-of-stay reduction and cost savings, to more meaningful endpoints, such as readmission rates, mortality, and clinical improvements. Ultimately, HM depends on robust, published data that clearly illustrate our benefit to hospitals and patients. Anything short of that intensifies the pressure to achieve No. 1.

3. Decreased Admissions

Our mother ship is under fire. Each wound our hospitals suffer is a wound to us. Erosion of hospital margins likely will translate to decreased levels of support. Nearly 40% of hospitals are experiencing a decrease in admissions. Coupled with economy-induced increases in the number of uninsured patients, this looms as a major threat to our future stability.

4. Elective Procedures

Thirty-one percent of hospitals have witnessed a decrease in lucrative, elective procedures. It began with the rise of procedural centers (e.g., surgery, gastroenterology, radiology) and is being exacerbated by the wheezing U.S. economy. Each 1% increase in unemployment results in roughly 2.5 million Americans losing their employer-provided health benefits. That means fewer elective procedures, which directly threatens the profitability of HM groups who depend on co-management revenue.

5. Recruitment

For years, HM has battled a workforce shortage, which has stifled growth and pushed providers to the verge of exhaustion. This problem persists despite offers of lucrative salaries, significant free time, and specialty status. The continuing workforce shortage should serve as a call to arms to improve recruitment into the field. An inability to increase the flow of providers will limit growth and tax the hospitalists we have in place. Ultimately, we will retard our progress toward achieving the improved outcomes articulated in No. 1.

6. Retention

We must address burnout and career satisfaction issues. Although exact numbers are tough to come by, it’s clear that many hospitalists are exhausted and overworked. This should not come as a surprise, considering we are a rapidly growing field constantly tasked with seeing more patients and solving all of a hospital’s problems. However, an inability to keep our current workforce sated and in HM jobs will amplify the workforce shortage.

7. PCPs Return

One interesting theory is that the floundering economy could prompt primary-care physicians (PCPs), whose hospital exodus we backfilled, to return to inpatient care in order to supplement their income. This isn’t likely to happen unless outpatient providers see such a drop in business that they cannot field a large-enough insured panel of patients to make ends meet. The possibility of PCPs seeing insured inpatients and leaving hospitalists with a largely uninsured population would be a game-changer. In the face of a large PCP shortage, however, this seems an unlikely scenario.

8. PCP Payment Reform

It is more likely our primary-care colleagues will get an ever-so-deserved pay raise. This is central to the proposed medical-home model and a key point of many healthcare reform plans. To stay competitive, hospitalists might also see a resultant pay increase. Anything short of this could further strain HM recruitment, as working hospitalists and new grads might migrate back toward primary-care jobs.

9. Bundling

It’s too early to know the effects of the proposed bundling of physician and hospital payments into one fee, which would compensate both hospitals and physicians. On the one hand, it could be a boon, as HM efficiency could be rewarded in ways not currently allowed. On the other hand, if hospitals continue to struggle financially and we are completely dependent upon bundled payments for our revenue, it could be a financial calamity.

10. Healthcare Reform

Without a clear sense of President Obama’s plans for healthcare reform, it’s tough to predict the future. We could try to paint numerous rosy scenarios that derive from a plan that includes a universal payor, improved access, and increased technology. However, it’s possible this reform would hamstring our efforts through reduced reimbursement, increased regulation, and cumbersome federal mandates.

Final Thought

I believe HM is strong and will overcome future threats. But it pays to consider and mitigate the hazards we might confront. Still, after much deliberation, I just cannot conceive of a reasonable scenario that results in a future without hospitalists.

Then again, Henry Ford probably felt the same about cars. TH

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

In the aftermath of the recent shuttering of Colorado’s oldest newspaper, The Rocky Mountain News, a couple of colleagues and I were discussing how unlikely it seemed just a few months ago that this could happen. It wasn’t long until we made the theoretical leap to what it would take for our hospitalist group to go out of business. Of course, this seems highly unlikely, but then again, the closing of a 150-year-old metropolitan newspaper seemed a preposterous proposition.

In the course of this discussion, we conjured myriad internal or external factors that could adversely affect our program. Although this was a tangential, lunchtime discussion, it did reverberate against the tuning fork of a faltering U.S. economy, especially regarding the financial sector and the automotive industry.

With that as a frame, I thought I’d take a dip into Paranoia Pond and look at potential threats to the HM model. Let me start by saying that I believe—deeply—in the hospitalist movement, the strides we’ve made, and the bright path that lies before us. I am not stating that any of these potential perils will put hospitalists out of business. However, the list below includes several risks that, if not properly mitigated, could alter our future course.

Here are 10 potential threats to the HM business model that you should keep an eye on:

1. Failure to Embrace QI

Those who fundamentally improve outcomes will write the future of medicine. Hospitalists are perfectly positioned—and expected—to do this. I believe most hospital CEOs think this is part of the contract: funding for quality. A failure to live up to our end of the bargain puts us at great risk. If your group isn’t able to demonstrate measurable improvements in processes and clinical outcomes, then you are at risk of losing hospital funding. As the economy recedes further and hospital reimbursement is more closely tied to quality, this will quickly move beyond a potential threat to a reality.

2. Lack of New Data to Support the HM Model

A corollary of No. 1 is our ability to show how we work. This burden, by and large, falls to my academic colleagues. After a rash of early studies showed the benefits of the hospitalist model, more recent data has been less convincing. This doesn’t mean we aren’t improving outcomes; rather, it means we aren’t always measuring and proving it. HM must get past the easy-to-measure endpoints, such as length-of-stay reduction and cost savings, to more meaningful endpoints, such as readmission rates, mortality, and clinical improvements. Ultimately, HM depends on robust, published data that clearly illustrate our benefit to hospitals and patients. Anything short of that intensifies the pressure to achieve No. 1.

3. Decreased Admissions

Our mother ship is under fire. Each wound our hospitals suffer is a wound to us. Erosion of hospital margins likely will translate to decreased levels of support. Nearly 40% of hospitals are experiencing a decrease in admissions. Coupled with economy-induced increases in the number of uninsured patients, this looms as a major threat to our future stability.

4. Elective Procedures

Thirty-one percent of hospitals have witnessed a decrease in lucrative, elective procedures. It began with the rise of procedural centers (e.g., surgery, gastroenterology, radiology) and is being exacerbated by the wheezing U.S. economy. Each 1% increase in unemployment results in roughly 2.5 million Americans losing their employer-provided health benefits. That means fewer elective procedures, which directly threatens the profitability of HM groups who depend on co-management revenue.

5. Recruitment

For years, HM has battled a workforce shortage, which has stifled growth and pushed providers to the verge of exhaustion. This problem persists despite offers of lucrative salaries, significant free time, and specialty status. The continuing workforce shortage should serve as a call to arms to improve recruitment into the field. An inability to increase the flow of providers will limit growth and tax the hospitalists we have in place. Ultimately, we will retard our progress toward achieving the improved outcomes articulated in No. 1.

6. Retention

We must address burnout and career satisfaction issues. Although exact numbers are tough to come by, it’s clear that many hospitalists are exhausted and overworked. This should not come as a surprise, considering we are a rapidly growing field constantly tasked with seeing more patients and solving all of a hospital’s problems. However, an inability to keep our current workforce sated and in HM jobs will amplify the workforce shortage.

7. PCPs Return

One interesting theory is that the floundering economy could prompt primary-care physicians (PCPs), whose hospital exodus we backfilled, to return to inpatient care in order to supplement their income. This isn’t likely to happen unless outpatient providers see such a drop in business that they cannot field a large-enough insured panel of patients to make ends meet. The possibility of PCPs seeing insured inpatients and leaving hospitalists with a largely uninsured population would be a game-changer. In the face of a large PCP shortage, however, this seems an unlikely scenario.

8. PCP Payment Reform

It is more likely our primary-care colleagues will get an ever-so-deserved pay raise. This is central to the proposed medical-home model and a key point of many healthcare reform plans. To stay competitive, hospitalists might also see a resultant pay increase. Anything short of this could further strain HM recruitment, as working hospitalists and new grads might migrate back toward primary-care jobs.

9. Bundling

It’s too early to know the effects of the proposed bundling of physician and hospital payments into one fee, which would compensate both hospitals and physicians. On the one hand, it could be a boon, as HM efficiency could be rewarded in ways not currently allowed. On the other hand, if hospitals continue to struggle financially and we are completely dependent upon bundled payments for our revenue, it could be a financial calamity.

10. Healthcare Reform

Without a clear sense of President Obama’s plans for healthcare reform, it’s tough to predict the future. We could try to paint numerous rosy scenarios that derive from a plan that includes a universal payor, improved access, and increased technology. However, it’s possible this reform would hamstring our efforts through reduced reimbursement, increased regulation, and cumbersome federal mandates.

Final Thought

I believe HM is strong and will overcome future threats. But it pays to consider and mitigate the hazards we might confront. Still, after much deliberation, I just cannot conceive of a reasonable scenario that results in a future without hospitalists.

Then again, Henry Ford probably felt the same about cars. TH

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

In the aftermath of the recent shuttering of Colorado’s oldest newspaper, The Rocky Mountain News, a couple of colleagues and I were discussing how unlikely it seemed just a few months ago that this could happen. It wasn’t long until we made the theoretical leap to what it would take for our hospitalist group to go out of business. Of course, this seems highly unlikely, but then again, the closing of a 150-year-old metropolitan newspaper seemed a preposterous proposition.

In the course of this discussion, we conjured myriad internal or external factors that could adversely affect our program. Although this was a tangential, lunchtime discussion, it did reverberate against the tuning fork of a faltering U.S. economy, especially regarding the financial sector and the automotive industry.

With that as a frame, I thought I’d take a dip into Paranoia Pond and look at potential threats to the HM model. Let me start by saying that I believe—deeply—in the hospitalist movement, the strides we’ve made, and the bright path that lies before us. I am not stating that any of these potential perils will put hospitalists out of business. However, the list below includes several risks that, if not properly mitigated, could alter our future course.

Here are 10 potential threats to the HM business model that you should keep an eye on:

1. Failure to Embrace QI

Those who fundamentally improve outcomes will write the future of medicine. Hospitalists are perfectly positioned—and expected—to do this. I believe most hospital CEOs think this is part of the contract: funding for quality. A failure to live up to our end of the bargain puts us at great risk. If your group isn’t able to demonstrate measurable improvements in processes and clinical outcomes, then you are at risk of losing hospital funding. As the economy recedes further and hospital reimbursement is more closely tied to quality, this will quickly move beyond a potential threat to a reality.

2. Lack of New Data to Support the HM Model

A corollary of No. 1 is our ability to show how we work. This burden, by and large, falls to my academic colleagues. After a rash of early studies showed the benefits of the hospitalist model, more recent data has been less convincing. This doesn’t mean we aren’t improving outcomes; rather, it means we aren’t always measuring and proving it. HM must get past the easy-to-measure endpoints, such as length-of-stay reduction and cost savings, to more meaningful endpoints, such as readmission rates, mortality, and clinical improvements. Ultimately, HM depends on robust, published data that clearly illustrate our benefit to hospitals and patients. Anything short of that intensifies the pressure to achieve No. 1.

3. Decreased Admissions

Our mother ship is under fire. Each wound our hospitals suffer is a wound to us. Erosion of hospital margins likely will translate to decreased levels of support. Nearly 40% of hospitals are experiencing a decrease in admissions. Coupled with economy-induced increases in the number of uninsured patients, this looms as a major threat to our future stability.

4. Elective Procedures

Thirty-one percent of hospitals have witnessed a decrease in lucrative, elective procedures. It began with the rise of procedural centers (e.g., surgery, gastroenterology, radiology) and is being exacerbated by the wheezing U.S. economy. Each 1% increase in unemployment results in roughly 2.5 million Americans losing their employer-provided health benefits. That means fewer elective procedures, which directly threatens the profitability of HM groups who depend on co-management revenue.

5. Recruitment

For years, HM has battled a workforce shortage, which has stifled growth and pushed providers to the verge of exhaustion. This problem persists despite offers of lucrative salaries, significant free time, and specialty status. The continuing workforce shortage should serve as a call to arms to improve recruitment into the field. An inability to increase the flow of providers will limit growth and tax the hospitalists we have in place. Ultimately, we will retard our progress toward achieving the improved outcomes articulated in No. 1.

6. Retention

We must address burnout and career satisfaction issues. Although exact numbers are tough to come by, it’s clear that many hospitalists are exhausted and overworked. This should not come as a surprise, considering we are a rapidly growing field constantly tasked with seeing more patients and solving all of a hospital’s problems. However, an inability to keep our current workforce sated and in HM jobs will amplify the workforce shortage.

7. PCPs Return

One interesting theory is that the floundering economy could prompt primary-care physicians (PCPs), whose hospital exodus we backfilled, to return to inpatient care in order to supplement their income. This isn’t likely to happen unless outpatient providers see such a drop in business that they cannot field a large-enough insured panel of patients to make ends meet. The possibility of PCPs seeing insured inpatients and leaving hospitalists with a largely uninsured population would be a game-changer. In the face of a large PCP shortage, however, this seems an unlikely scenario.

8. PCP Payment Reform

It is more likely our primary-care colleagues will get an ever-so-deserved pay raise. This is central to the proposed medical-home model and a key point of many healthcare reform plans. To stay competitive, hospitalists might also see a resultant pay increase. Anything short of this could further strain HM recruitment, as working hospitalists and new grads might migrate back toward primary-care jobs.

9. Bundling

It’s too early to know the effects of the proposed bundling of physician and hospital payments into one fee, which would compensate both hospitals and physicians. On the one hand, it could be a boon, as HM efficiency could be rewarded in ways not currently allowed. On the other hand, if hospitals continue to struggle financially and we are completely dependent upon bundled payments for our revenue, it could be a financial calamity.

10. Healthcare Reform

Without a clear sense of President Obama’s plans for healthcare reform, it’s tough to predict the future. We could try to paint numerous rosy scenarios that derive from a plan that includes a universal payor, improved access, and increased technology. However, it’s possible this reform would hamstring our efforts through reduced reimbursement, increased regulation, and cumbersome federal mandates.

Final Thought

I believe HM is strong and will overcome future threats. But it pays to consider and mitigate the hazards we might confront. Still, after much deliberation, I just cannot conceive of a reasonable scenario that results in a future without hospitalists.

Then again, Henry Ford probably felt the same about cars. TH

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

A 74-year-old man is admitted to the hospital with a 7-day history of fever, rigors, chest pain, and general weakness. He underwent coronary artery bypass surgery 10 years ago.

After 2 weeks of intravenous ceftriaxone 2 g/day, the patient undergoes excision of the mycotic pseudoaneurysm of the descending aorta, with placement of an aortic homograft. Biopsy of the excised aortic segment shows calcified fibroatheromatous plaques with no evidence of cystic medial degeneration or granulomas.

DISCUSSION

Mycotic aneurysm is a localized and irreversible dilatation of an artery due to destruction of the vessel wall by an infection. The dilatation is at least one and one-half times the normal diameter of the affected artery. It may be a true aneurysm or a pseudoaneurysm, involving all or some layers of the arterial wall. It is a rare but life-threatening condition.

A mycotic aneurysm can develop from septic embolization to the vasa vasorum, hematogenous seeding of an existing aneurysm, or extension from a contiguous site of infection.^1,2 Mycotic infections of the aorta show a preference for male patients already infected with S enteritidis or S typhimurium. ³ Predisposing factors include rheumatic deformity of the valves, a bicuspid valve, impaired immunity,⁴ self-induced or iatrogenic arterial trauma,^5,6 atherosclerotic deposits and calcification of the endovascular structure,⁷ and, in elderly patients, Salmonella septicemia.^8,9 Computed tomography is the most useful imaging modality.^10,11 Surgical interventions, in addition to parenteral antibiotic therapy for at least 6 weeks,^11,12 are required to:

• Confirm the diagnosis
• Reconstruct the arterial vasculature
• Manage the complications of sepsis
• Start preventive measures (ie, cholecystectomy).²

A 74-year-old man is admitted to the hospital with a 7-day history of fever, rigors, chest pain, and general weakness. He underwent coronary artery bypass surgery 10 years ago.

After 2 weeks of intravenous ceftriaxone 2 g/day, the patient undergoes excision of the mycotic pseudoaneurysm of the descending aorta, with placement of an aortic homograft. Biopsy of the excised aortic segment shows calcified fibroatheromatous plaques with no evidence of cystic medial degeneration or granulomas.

DISCUSSION

Mycotic aneurysm is a localized and irreversible dilatation of an artery due to destruction of the vessel wall by an infection. The dilatation is at least one and one-half times the normal diameter of the affected artery. It may be a true aneurysm or a pseudoaneurysm, involving all or some layers of the arterial wall. It is a rare but life-threatening condition.

A mycotic aneurysm can develop from septic embolization to the vasa vasorum, hematogenous seeding of an existing aneurysm, or extension from a contiguous site of infection.^1,2 Mycotic infections of the aorta show a preference for male patients already infected with S enteritidis or S typhimurium. ³ Predisposing factors include rheumatic deformity of the valves, a bicuspid valve, impaired immunity,⁴ self-induced or iatrogenic arterial trauma,^5,6 atherosclerotic deposits and calcification of the endovascular structure,⁷ and, in elderly patients, Salmonella septicemia.^8,9 Computed tomography is the most useful imaging modality.^10,11 Surgical interventions, in addition to parenteral antibiotic therapy for at least 6 weeks,^11,12 are required to:

• Confirm the diagnosis
• Reconstruct the arterial vasculature
• Manage the complications of sepsis
• Start preventive measures (ie, cholecystectomy).²

A 74-year-old man is admitted to the hospital with a 7-day history of fever, rigors, chest pain, and general weakness. He underwent coronary artery bypass surgery 10 years ago.

After 2 weeks of intravenous ceftriaxone 2 g/day, the patient undergoes excision of the mycotic pseudoaneurysm of the descending aorta, with placement of an aortic homograft. Biopsy of the excised aortic segment shows calcified fibroatheromatous plaques with no evidence of cystic medial degeneration or granulomas.

DISCUSSION

Mycotic aneurysm is a localized and irreversible dilatation of an artery due to destruction of the vessel wall by an infection. The dilatation is at least one and one-half times the normal diameter of the affected artery. It may be a true aneurysm or a pseudoaneurysm, involving all or some layers of the arterial wall. It is a rare but life-threatening condition.

A mycotic aneurysm can develop from septic embolization to the vasa vasorum, hematogenous seeding of an existing aneurysm, or extension from a contiguous site of infection.^1,2 Mycotic infections of the aorta show a preference for male patients already infected with S enteritidis or S typhimurium. ³ Predisposing factors include rheumatic deformity of the valves, a bicuspid valve, impaired immunity,⁴ self-induced or iatrogenic arterial trauma,^5,6 atherosclerotic deposits and calcification of the endovascular structure,⁷ and, in elderly patients, Salmonella septicemia.^8,9 Computed tomography is the most useful imaging modality.^10,11 Surgical interventions, in addition to parenteral antibiotic therapy for at least 6 weeks,^11,12 are required to:

• Confirm the diagnosis
• Reconstruct the arterial vasculature
• Manage the complications of sepsis
• Start preventive measures (ie, cholecystectomy).²

A 70-year-old man falls in his bathroom and subsequently presents to an urgent care clinic. Among his complaints is right-sided chest pain. On physical examination he has point tenderness over the lateral right thorax with some superficial swelling and bruising. The chest is normal on auscultation.

Should this patient undergo imaging to determine if he has a rib fracture? And which imaging study would be appropriate?

This article outlines the use of various imaging tests in the evaluation of suspected rib fractures and recommends an approach to management. This article does not address fractures in children.

MANY CAUSES OF RIB FRACTURES

Trauma, the most common cause of rib fractures, includes penetrating injuries and blunt injury to the chest wall. Between 10% and 66% of traumatic injuries result in rib fractures. ¹ Traumatic injury can result from motor vehicle accidents, assault, sports, cardiopulmonary resuscitation, physical abuse (“nonaccidental” trauma), and, rarely, severe paroxysms of coughing.²

Cancer can cause pathologic fractures of the rib.

Stress fractures of the ribs are more likely to occur in high-level athletes whose activity involves repetitive musculoskeletal loading, although they can also occur in people with repetitive coughing paroxysms.³ Sports and activities that result in stress fractures include rowing, pitching or throwing, basketball, weight-lifting, ballet, golf, gymnastics, and swimming.⁴

WHICH RIB IS BROKEN?

The fourth through 10th ribs are the most often fractured. Fractures of the first through the third ribs can be associated with underlying nerve and vascular injuries, and fractures of the 10th through 12th ribs are associated with damage to abdominal organs,⁵ most commonly the liver, spleen, kidneys, and diaphragm.³

Fractures of the costal cartilage can occur by any of the mechanisms described above. The true incidence of costal cartilage fractures is not known because plain radiography, the traditional method of evaluation, does not reliably detect them.

WHY CONFIRM A RIB FRACTURE?

For many rib fractures without associated injury, a radiographic diagnosis has little impact on patient management, which consists mainly of pain control. But knowing whether a patient has a broken rib can often be important.

To detect associated injury. The rate of associated injury in patients with rib fractures is high.⁶ Potentially severe complications include:

• Pneumothorax
• Hemothorax
• Pulmonary contusion
• Flail chest
• Pneumonia
• Vascular and nerve damage (especially with trauma to the upper chest or the first through third ribs)
• Abdominal organ injury (particularly with trauma to the lower thorax or lower ribs).

The absence of a rib fracture does not preclude these conditions, however.

To prevent complications. Even in the absence of associated injuries, radiographic confirmation of a rib fracture can help prevent complications such as atelectasis and is particularly important in patients with comorbidities such as chronic obstructive pulmonary disease, cardiac disease, hepatic disease, renal disease, dementia, and coagulopathy.¹

To document the injury. Radiographic documentation of a rib fracture may be required for medical-legal issues in cases of assault, motor vehicle accident, occupational injury, and abuse.

To help manage pain. Confirmation of rib fracture can facilitate pain management, particularly in patients with undiagnosed fractures with long-standing refractory pain. For example, conservative pain control with nonsteroidal anti-inflammatory drugs may be sufficient for a soft-tissue injury but may not be enough for a rib fracture. Intravenous narcotics or nerve blocks might be preferable.^3,7 Controlling pain helps limit the incidence of associated complications.

To count how many ribs are broken. The more ribs broken, the greater the likelihood of illness and death in certain populations, such as the elderly. One study⁸ found that patients over age 45 with more than four broken ribs are at a significantly higher risk of prolonged stay in the intensive care unit, prolonged ventilator support, and prolonged overall hospital stay.

Knowing the number of ribs fractured may also influence other treatment decisions, such as whether to transfer the patient to a trauma center: a study showed that the more ribs broken, the greater the death rate, and that more than three rib fractures may indicate the need to transfer to a trauma center.⁶

HOW TO DIAGNOSE A BROKEN RIB

Signs and symptoms are unreliable but important

Clinical symptoms do not reliably tell us if a rib is broken.^9,10 Nevertheless, the history and physical examination can uncover possible complications or associated injuries,^10,11 such as flail chest, pneumothorax, or vascular injury.

Classic clinical signs and symptoms of rib fracture include point tenderness, focally referred pain with general chest compression, splinting, bony crepitus, and ecchymosis.⁹ A history of a motor vehicle accident (especially on a motorcycle) or other injury due to rapid deceleration, a fall from higher than 20 feet, a gunshot wound, assault, or a crushing injury would indicate a greater risk of complications.

Signs of complications may include decreased oxygen saturation, decreased or absent breath sounds, dullness or hyperresonance to percussion, tracheal deviation, hypotension, arrythmia, subcutaneous emphysema, neck vein distension, neck hematoma, a focal neurologic deficit below the clavicles or in the upper extremities, and flail chest.¹¹ Flail chest results from multiple fractures in the same rib, so that a segment of chest wall does not contribute to breathing.

Further research is needed into the correlation of clinical symptoms with rib fractures. Much of the evidence that clinical symptoms correlate poorly with fractures comes from studies that used plain radiography to detect the fractures. However, ultrasonography and computed tomography (CT) can detect fractures that plain radiography cannot, and studies using these newer imaging tests may reveal a better correlation between clinical symptoms and rib fracture than previously thought.⁶

Chest radiography may miss 50% of rib fractures, but is still useful

Plain radiography of the chest with or without oblique views and optimized by the technologist for bony detail (“bone technique”) has historically been the imaging test of choice. However, it may miss up to 50% of fractures.¹⁰ Furthermore, it is not sensitive for costal cartilage³ or stress fractures.

Despite these limitations, plain radiography is vitally important in diagnosing complications and associated injuries such as a pneumothorax, hemothorax, pulmonary contusion, pneumomediastinum, or pneumoperitoneum. Also, a widened mediastinum could indicate aortic injury.

Currently, a standard chest x-ray is often the initial study of choice in the evaluation of chest pain and in cases of minor blunt trauma. If rib fractures are suspected clinically, a rib series can be of benefit. A rib series consists of a marker placed over the region of interest, oblique views, and optimization of the radiograph by the technologist to highlight bony detail. The decision to image a rib fracture in the absence of other underlying abnormalities or associated injuries depends on the clinical scenario.

Computed tomography provides more detail

While CT appears to be the best imaging test for evaluating for rib fractures and associated injuries, it is relatively costly, is time-consuming, is not always available, and exposes the patient to a significant amount of radiation.

Also, while CT plays a vital role in major and penetrating trauma of the chest or abdomen, its use in other situations is more limited. Again, the issue of clinical impact of a diagnosis of rib fracture comes into play, and in this setting CT competes with plain radiography and ultrasonography, which are less costly and involve less or no radiation exposure.

Ultrasonography has advantages but is not widely used

Ultrasonography can be used to look for broken ribs and costal cartilage fractures. Associated injuries such as pneumothorax, hemothorax, and abdominal organ injury can also be evaluated. Studies have found it to be much more sensitive than plain radiography in detecting rib fractures,^3,15 whereas other studies have suggested it is only equally sensitive or slightly better.⁷ It also has the advantage of not using radiation.

Because of a number of disadvantages, ultrasonography is rarely used in the evaluation of rib fracture. It is time-consuming and more costly than plain radiography. It is often not readily available. It can be painful, making it impractical for trauma patients. Its results depend greatly on the skill of the technician, and it is unable to adequately assess certain portions of the thorax (eg, the first rib under the clavicle, and the upper ribs under the scapula).^7,15 Although able to detect some associated injuries, ultrasonography is not as sensitive and comprehensive as plain radiography and CT. Its role is therefore limited to situations in which the diagnosis of a rib fracture alone, in an accessible rib, is important.

Technetium Tc 99m methylene diphosphonate bone scanning can be used to look for bone pathology, including rib fractures. Bone scans are sensitive but not specific, and abnormal uptake generates an extensive differential diagnosis.¹⁶ Single-photon emission CT, or SPECT, can help localize the abnormality. ⁴ Because a hot spot on a bone scan can represent a number of conditions besides rib fractures, including cancer, focal sclerosis, and focal osteosclerosis, bone scanning is not routinely used for evaluating rib fractures, although it is very sensitive for stress fractures.

Occasionally, in a patient undergoing a bone scan as part of a workup for cancer, a scan shows a lesion that might be a rib fracture. In this case, one should correlate the results with those of plain radiography or CT.¹⁶

Magnetic resonance imaging: no role yet in rib fracture evaluation

MRI is not considered appropriate for evaluating rib fractures. It may be useful if there is concern about soft-tissue or vascular abnormalities. Beyond this, further research is needed to elucidate its role in rib fracture.

THE CHOICE OF TEST DEPENDS ON THE SITUATION

In patients with penetrating or major chest or abdominal trauma, CT is the study of choice. It provides the most information about associated injuries, and it accurately detects rib fractures. This helps target treatment of associated injuries, and helps identify patients at higher risk, such as those with significant vascular, pulmonary, or abdominal injuries and those with a greater number of fractures. An unstable, critically injured patient would not be a candidate for CT because of the risk of transport to the scanner; chest radiography would have to suffice in these cases.

In cases of minor blunt trauma when there is little suspicion of associated injuries or complications, plain radiography is likely sufficient. If there is suspicion of a rib fracture alone and confirmation is of clinical importance (eg, in the elderly or those with long-standing refractory pain, or when certain pain management treatments are being considered), then oblique radiographic views, bone technique, and marker placement over the concerning region are recommended. The role of ultrasonography in this setting is still up for debate.

In cases of suspected rib fracture with longstanding pain refractory to conservative pain management, plain radiography with oblique views, bone technique, and marker placement is useful. If the radiograph is negative or if there is a high suspicion of cartilage fracture, CT or ultrasonography may be of benefit only if the diagnosis will alter clinical management.

If stress fracture is suspected, a nuclear bone scan may be helpful to first detect an abnormality, and CT may then be used for correlation if needed.

CASE CONCLUDED: LIVING WITH UNCERTAINTY

As for the 70-year-old man presented at the beginning of this article, the first question is whether we suspect an associated injury on the basis of clinical features. If we had clinical findings suspicious for pneumothorax or hemothorax, plain radiography of the chest would be indicated. Since the patient was not involved in major trauma, a CT scan is not indicated as the first study.

Our patient has clinical findings suggesting a rib fracture without associated injury. In this setting, routine posteroanterior and lateral chest radiography would be useful to rule out major associated injuries and, perhaps, to find a rib fracture. If the chest film is normal and rib fracture is still suspected, we must decide whether the diagnosis would alter our clinical management. Our patient would likely be treated the same regardless of whether or not he has a fracture; therefore, we would prescribe pain management.

Chest radiography was performed to rule out associated injuries, especially since the patient was elderly, but the chest x-ray did not reveal anything. On follow-up approximately 1 month later, he appeared improved, with less pain and tenderness. This may be due to healing of a rib fracture or healing of his soft-tissue injury. We will never know whether he truly had a fracture, but it is irrelevant to his care.

A 70-year-old man falls in his bathroom and subsequently presents to an urgent care clinic. Among his complaints is right-sided chest pain. On physical examination he has point tenderness over the lateral right thorax with some superficial swelling and bruising. The chest is normal on auscultation.

Should this patient undergo imaging to determine if he has a rib fracture? And which imaging study would be appropriate?

This article outlines the use of various imaging tests in the evaluation of suspected rib fractures and recommends an approach to management. This article does not address fractures in children.

MANY CAUSES OF RIB FRACTURES

Trauma, the most common cause of rib fractures, includes penetrating injuries and blunt injury to the chest wall. Between 10% and 66% of traumatic injuries result in rib fractures. ¹ Traumatic injury can result from motor vehicle accidents, assault, sports, cardiopulmonary resuscitation, physical abuse (“nonaccidental” trauma), and, rarely, severe paroxysms of coughing.²

Cancer can cause pathologic fractures of the rib.

Stress fractures of the ribs are more likely to occur in high-level athletes whose activity involves repetitive musculoskeletal loading, although they can also occur in people with repetitive coughing paroxysms.³ Sports and activities that result in stress fractures include rowing, pitching or throwing, basketball, weight-lifting, ballet, golf, gymnastics, and swimming.⁴

WHICH RIB IS BROKEN?

The fourth through 10th ribs are the most often fractured. Fractures of the first through the third ribs can be associated with underlying nerve and vascular injuries, and fractures of the 10th through 12th ribs are associated with damage to abdominal organs,⁵ most commonly the liver, spleen, kidneys, and diaphragm.³

Fractures of the costal cartilage can occur by any of the mechanisms described above. The true incidence of costal cartilage fractures is not known because plain radiography, the traditional method of evaluation, does not reliably detect them.

WHY CONFIRM A RIB FRACTURE?

For many rib fractures without associated injury, a radiographic diagnosis has little impact on patient management, which consists mainly of pain control. But knowing whether a patient has a broken rib can often be important.

To detect associated injury. The rate of associated injury in patients with rib fractures is high.⁶ Potentially severe complications include:

• Pneumothorax
• Hemothorax
• Pulmonary contusion
• Flail chest
• Pneumonia
• Vascular and nerve damage (especially with trauma to the upper chest or the first through third ribs)
• Abdominal organ injury (particularly with trauma to the lower thorax or lower ribs).

The absence of a rib fracture does not preclude these conditions, however.

To prevent complications. Even in the absence of associated injuries, radiographic confirmation of a rib fracture can help prevent complications such as atelectasis and is particularly important in patients with comorbidities such as chronic obstructive pulmonary disease, cardiac disease, hepatic disease, renal disease, dementia, and coagulopathy.¹

To document the injury. Radiographic documentation of a rib fracture may be required for medical-legal issues in cases of assault, motor vehicle accident, occupational injury, and abuse.

To help manage pain. Confirmation of rib fracture can facilitate pain management, particularly in patients with undiagnosed fractures with long-standing refractory pain. For example, conservative pain control with nonsteroidal anti-inflammatory drugs may be sufficient for a soft-tissue injury but may not be enough for a rib fracture. Intravenous narcotics or nerve blocks might be preferable.^3,7 Controlling pain helps limit the incidence of associated complications.

To count how many ribs are broken. The more ribs broken, the greater the likelihood of illness and death in certain populations, such as the elderly. One study⁸ found that patients over age 45 with more than four broken ribs are at a significantly higher risk of prolonged stay in the intensive care unit, prolonged ventilator support, and prolonged overall hospital stay.

Knowing the number of ribs fractured may also influence other treatment decisions, such as whether to transfer the patient to a trauma center: a study showed that the more ribs broken, the greater the death rate, and that more than three rib fractures may indicate the need to transfer to a trauma center.⁶

HOW TO DIAGNOSE A BROKEN RIB

Signs and symptoms are unreliable but important

Clinical symptoms do not reliably tell us if a rib is broken.^9,10 Nevertheless, the history and physical examination can uncover possible complications or associated injuries,^10,11 such as flail chest, pneumothorax, or vascular injury.

Classic clinical signs and symptoms of rib fracture include point tenderness, focally referred pain with general chest compression, splinting, bony crepitus, and ecchymosis.⁹ A history of a motor vehicle accident (especially on a motorcycle) or other injury due to rapid deceleration, a fall from higher than 20 feet, a gunshot wound, assault, or a crushing injury would indicate a greater risk of complications.

Signs of complications may include decreased oxygen saturation, decreased or absent breath sounds, dullness or hyperresonance to percussion, tracheal deviation, hypotension, arrythmia, subcutaneous emphysema, neck vein distension, neck hematoma, a focal neurologic deficit below the clavicles or in the upper extremities, and flail chest.¹¹ Flail chest results from multiple fractures in the same rib, so that a segment of chest wall does not contribute to breathing.

Further research is needed into the correlation of clinical symptoms with rib fractures. Much of the evidence that clinical symptoms correlate poorly with fractures comes from studies that used plain radiography to detect the fractures. However, ultrasonography and computed tomography (CT) can detect fractures that plain radiography cannot, and studies using these newer imaging tests may reveal a better correlation between clinical symptoms and rib fracture than previously thought.⁶

Chest radiography may miss 50% of rib fractures, but is still useful

Plain radiography of the chest with or without oblique views and optimized by the technologist for bony detail (“bone technique”) has historically been the imaging test of choice. However, it may miss up to 50% of fractures.¹⁰ Furthermore, it is not sensitive for costal cartilage³ or stress fractures.

Despite these limitations, plain radiography is vitally important in diagnosing complications and associated injuries such as a pneumothorax, hemothorax, pulmonary contusion, pneumomediastinum, or pneumoperitoneum. Also, a widened mediastinum could indicate aortic injury.

Currently, a standard chest x-ray is often the initial study of choice in the evaluation of chest pain and in cases of minor blunt trauma. If rib fractures are suspected clinically, a rib series can be of benefit. A rib series consists of a marker placed over the region of interest, oblique views, and optimization of the radiograph by the technologist to highlight bony detail. The decision to image a rib fracture in the absence of other underlying abnormalities or associated injuries depends on the clinical scenario.

Computed tomography provides more detail

While CT appears to be the best imaging test for evaluating for rib fractures and associated injuries, it is relatively costly, is time-consuming, is not always available, and exposes the patient to a significant amount of radiation.

Also, while CT plays a vital role in major and penetrating trauma of the chest or abdomen, its use in other situations is more limited. Again, the issue of clinical impact of a diagnosis of rib fracture comes into play, and in this setting CT competes with plain radiography and ultrasonography, which are less costly and involve less or no radiation exposure.

Ultrasonography has advantages but is not widely used

Ultrasonography can be used to look for broken ribs and costal cartilage fractures. Associated injuries such as pneumothorax, hemothorax, and abdominal organ injury can also be evaluated. Studies have found it to be much more sensitive than plain radiography in detecting rib fractures,^3,15 whereas other studies have suggested it is only equally sensitive or slightly better.⁷ It also has the advantage of not using radiation.

Because of a number of disadvantages, ultrasonography is rarely used in the evaluation of rib fracture. It is time-consuming and more costly than plain radiography. It is often not readily available. It can be painful, making it impractical for trauma patients. Its results depend greatly on the skill of the technician, and it is unable to adequately assess certain portions of the thorax (eg, the first rib under the clavicle, and the upper ribs under the scapula).^7,15 Although able to detect some associated injuries, ultrasonography is not as sensitive and comprehensive as plain radiography and CT. Its role is therefore limited to situations in which the diagnosis of a rib fracture alone, in an accessible rib, is important.

Technetium Tc 99m methylene diphosphonate bone scanning can be used to look for bone pathology, including rib fractures. Bone scans are sensitive but not specific, and abnormal uptake generates an extensive differential diagnosis.¹⁶ Single-photon emission CT, or SPECT, can help localize the abnormality. ⁴ Because a hot spot on a bone scan can represent a number of conditions besides rib fractures, including cancer, focal sclerosis, and focal osteosclerosis, bone scanning is not routinely used for evaluating rib fractures, although it is very sensitive for stress fractures.

Occasionally, in a patient undergoing a bone scan as part of a workup for cancer, a scan shows a lesion that might be a rib fracture. In this case, one should correlate the results with those of plain radiography or CT.¹⁶

Magnetic resonance imaging: no role yet in rib fracture evaluation

MRI is not considered appropriate for evaluating rib fractures. It may be useful if there is concern about soft-tissue or vascular abnormalities. Beyond this, further research is needed to elucidate its role in rib fracture.

THE CHOICE OF TEST DEPENDS ON THE SITUATION

In patients with penetrating or major chest or abdominal trauma, CT is the study of choice. It provides the most information about associated injuries, and it accurately detects rib fractures. This helps target treatment of associated injuries, and helps identify patients at higher risk, such as those with significant vascular, pulmonary, or abdominal injuries and those with a greater number of fractures. An unstable, critically injured patient would not be a candidate for CT because of the risk of transport to the scanner; chest radiography would have to suffice in these cases.

In cases of minor blunt trauma when there is little suspicion of associated injuries or complications, plain radiography is likely sufficient. If there is suspicion of a rib fracture alone and confirmation is of clinical importance (eg, in the elderly or those with long-standing refractory pain, or when certain pain management treatments are being considered), then oblique radiographic views, bone technique, and marker placement over the concerning region are recommended. The role of ultrasonography in this setting is still up for debate.

In cases of suspected rib fracture with longstanding pain refractory to conservative pain management, plain radiography with oblique views, bone technique, and marker placement is useful. If the radiograph is negative or if there is a high suspicion of cartilage fracture, CT or ultrasonography may be of benefit only if the diagnosis will alter clinical management.

If stress fracture is suspected, a nuclear bone scan may be helpful to first detect an abnormality, and CT may then be used for correlation if needed.

CASE CONCLUDED: LIVING WITH UNCERTAINTY

As for the 70-year-old man presented at the beginning of this article, the first question is whether we suspect an associated injury on the basis of clinical features. If we had clinical findings suspicious for pneumothorax or hemothorax, plain radiography of the chest would be indicated. Since the patient was not involved in major trauma, a CT scan is not indicated as the first study.

Our patient has clinical findings suggesting a rib fracture without associated injury. In this setting, routine posteroanterior and lateral chest radiography would be useful to rule out major associated injuries and, perhaps, to find a rib fracture. If the chest film is normal and rib fracture is still suspected, we must decide whether the diagnosis would alter our clinical management. Our patient would likely be treated the same regardless of whether or not he has a fracture; therefore, we would prescribe pain management.

Chest radiography was performed to rule out associated injuries, especially since the patient was elderly, but the chest x-ray did not reveal anything. On follow-up approximately 1 month later, he appeared improved, with less pain and tenderness. This may be due to healing of a rib fracture or healing of his soft-tissue injury. We will never know whether he truly had a fracture, but it is irrelevant to his care.

A 70-year-old man falls in his bathroom and subsequently presents to an urgent care clinic. Among his complaints is right-sided chest pain. On physical examination he has point tenderness over the lateral right thorax with some superficial swelling and bruising. The chest is normal on auscultation.

Should this patient undergo imaging to determine if he has a rib fracture? And which imaging study would be appropriate?

This article outlines the use of various imaging tests in the evaluation of suspected rib fractures and recommends an approach to management. This article does not address fractures in children.

MANY CAUSES OF RIB FRACTURES

Trauma, the most common cause of rib fractures, includes penetrating injuries and blunt injury to the chest wall. Between 10% and 66% of traumatic injuries result in rib fractures. ¹ Traumatic injury can result from motor vehicle accidents, assault, sports, cardiopulmonary resuscitation, physical abuse (“nonaccidental” trauma), and, rarely, severe paroxysms of coughing.²

Cancer can cause pathologic fractures of the rib.

Stress fractures of the ribs are more likely to occur in high-level athletes whose activity involves repetitive musculoskeletal loading, although they can also occur in people with repetitive coughing paroxysms.³ Sports and activities that result in stress fractures include rowing, pitching or throwing, basketball, weight-lifting, ballet, golf, gymnastics, and swimming.⁴

WHICH RIB IS BROKEN?

The fourth through 10th ribs are the most often fractured. Fractures of the first through the third ribs can be associated with underlying nerve and vascular injuries, and fractures of the 10th through 12th ribs are associated with damage to abdominal organs,⁵ most commonly the liver, spleen, kidneys, and diaphragm.³

Fractures of the costal cartilage can occur by any of the mechanisms described above. The true incidence of costal cartilage fractures is not known because plain radiography, the traditional method of evaluation, does not reliably detect them.

WHY CONFIRM A RIB FRACTURE?

For many rib fractures without associated injury, a radiographic diagnosis has little impact on patient management, which consists mainly of pain control. But knowing whether a patient has a broken rib can often be important.

To detect associated injury. The rate of associated injury in patients with rib fractures is high.⁶ Potentially severe complications include:

• Pneumothorax
• Hemothorax
• Pulmonary contusion
• Flail chest
• Pneumonia
• Vascular and nerve damage (especially with trauma to the upper chest or the first through third ribs)
• Abdominal organ injury (particularly with trauma to the lower thorax or lower ribs).

The absence of a rib fracture does not preclude these conditions, however.

To prevent complications. Even in the absence of associated injuries, radiographic confirmation of a rib fracture can help prevent complications such as atelectasis and is particularly important in patients with comorbidities such as chronic obstructive pulmonary disease, cardiac disease, hepatic disease, renal disease, dementia, and coagulopathy.¹

To document the injury. Radiographic documentation of a rib fracture may be required for medical-legal issues in cases of assault, motor vehicle accident, occupational injury, and abuse.

To help manage pain. Confirmation of rib fracture can facilitate pain management, particularly in patients with undiagnosed fractures with long-standing refractory pain. For example, conservative pain control with nonsteroidal anti-inflammatory drugs may be sufficient for a soft-tissue injury but may not be enough for a rib fracture. Intravenous narcotics or nerve blocks might be preferable.^3,7 Controlling pain helps limit the incidence of associated complications.

To count how many ribs are broken. The more ribs broken, the greater the likelihood of illness and death in certain populations, such as the elderly. One study⁸ found that patients over age 45 with more than four broken ribs are at a significantly higher risk of prolonged stay in the intensive care unit, prolonged ventilator support, and prolonged overall hospital stay.

Knowing the number of ribs fractured may also influence other treatment decisions, such as whether to transfer the patient to a trauma center: a study showed that the more ribs broken, the greater the death rate, and that more than three rib fractures may indicate the need to transfer to a trauma center.⁶

HOW TO DIAGNOSE A BROKEN RIB

Signs and symptoms are unreliable but important

Clinical symptoms do not reliably tell us if a rib is broken.^9,10 Nevertheless, the history and physical examination can uncover possible complications or associated injuries,^10,11 such as flail chest, pneumothorax, or vascular injury.

Classic clinical signs and symptoms of rib fracture include point tenderness, focally referred pain with general chest compression, splinting, bony crepitus, and ecchymosis.⁹ A history of a motor vehicle accident (especially on a motorcycle) or other injury due to rapid deceleration, a fall from higher than 20 feet, a gunshot wound, assault, or a crushing injury would indicate a greater risk of complications.

Signs of complications may include decreased oxygen saturation, decreased or absent breath sounds, dullness or hyperresonance to percussion, tracheal deviation, hypotension, arrythmia, subcutaneous emphysema, neck vein distension, neck hematoma, a focal neurologic deficit below the clavicles or in the upper extremities, and flail chest.¹¹ Flail chest results from multiple fractures in the same rib, so that a segment of chest wall does not contribute to breathing.

Further research is needed into the correlation of clinical symptoms with rib fractures. Much of the evidence that clinical symptoms correlate poorly with fractures comes from studies that used plain radiography to detect the fractures. However, ultrasonography and computed tomography (CT) can detect fractures that plain radiography cannot, and studies using these newer imaging tests may reveal a better correlation between clinical symptoms and rib fracture than previously thought.⁶

Chest radiography may miss 50% of rib fractures, but is still useful

Plain radiography of the chest with or without oblique views and optimized by the technologist for bony detail (“bone technique”) has historically been the imaging test of choice. However, it may miss up to 50% of fractures.¹⁰ Furthermore, it is not sensitive for costal cartilage³ or stress fractures.

Despite these limitations, plain radiography is vitally important in diagnosing complications and associated injuries such as a pneumothorax, hemothorax, pulmonary contusion, pneumomediastinum, or pneumoperitoneum. Also, a widened mediastinum could indicate aortic injury.

Currently, a standard chest x-ray is often the initial study of choice in the evaluation of chest pain and in cases of minor blunt trauma. If rib fractures are suspected clinically, a rib series can be of benefit. A rib series consists of a marker placed over the region of interest, oblique views, and optimization of the radiograph by the technologist to highlight bony detail. The decision to image a rib fracture in the absence of other underlying abnormalities or associated injuries depends on the clinical scenario.

Computed tomography provides more detail

While CT appears to be the best imaging test for evaluating for rib fractures and associated injuries, it is relatively costly, is time-consuming, is not always available, and exposes the patient to a significant amount of radiation.

Also, while CT plays a vital role in major and penetrating trauma of the chest or abdomen, its use in other situations is more limited. Again, the issue of clinical impact of a diagnosis of rib fracture comes into play, and in this setting CT competes with plain radiography and ultrasonography, which are less costly and involve less or no radiation exposure.

Ultrasonography has advantages but is not widely used

Ultrasonography can be used to look for broken ribs and costal cartilage fractures. Associated injuries such as pneumothorax, hemothorax, and abdominal organ injury can also be evaluated. Studies have found it to be much more sensitive than plain radiography in detecting rib fractures,^3,15 whereas other studies have suggested it is only equally sensitive or slightly better.⁷ It also has the advantage of not using radiation.

Because of a number of disadvantages, ultrasonography is rarely used in the evaluation of rib fracture. It is time-consuming and more costly than plain radiography. It is often not readily available. It can be painful, making it impractical for trauma patients. Its results depend greatly on the skill of the technician, and it is unable to adequately assess certain portions of the thorax (eg, the first rib under the clavicle, and the upper ribs under the scapula).^7,15 Although able to detect some associated injuries, ultrasonography is not as sensitive and comprehensive as plain radiography and CT. Its role is therefore limited to situations in which the diagnosis of a rib fracture alone, in an accessible rib, is important.

Technetium Tc 99m methylene diphosphonate bone scanning can be used to look for bone pathology, including rib fractures. Bone scans are sensitive but not specific, and abnormal uptake generates an extensive differential diagnosis.¹⁶ Single-photon emission CT, or SPECT, can help localize the abnormality. ⁴ Because a hot spot on a bone scan can represent a number of conditions besides rib fractures, including cancer, focal sclerosis, and focal osteosclerosis, bone scanning is not routinely used for evaluating rib fractures, although it is very sensitive for stress fractures.

Occasionally, in a patient undergoing a bone scan as part of a workup for cancer, a scan shows a lesion that might be a rib fracture. In this case, one should correlate the results with those of plain radiography or CT.¹⁶

Magnetic resonance imaging: no role yet in rib fracture evaluation

MRI is not considered appropriate for evaluating rib fractures. It may be useful if there is concern about soft-tissue or vascular abnormalities. Beyond this, further research is needed to elucidate its role in rib fracture.

THE CHOICE OF TEST DEPENDS ON THE SITUATION

In patients with penetrating or major chest or abdominal trauma, CT is the study of choice. It provides the most information about associated injuries, and it accurately detects rib fractures. This helps target treatment of associated injuries, and helps identify patients at higher risk, such as those with significant vascular, pulmonary, or abdominal injuries and those with a greater number of fractures. An unstable, critically injured patient would not be a candidate for CT because of the risk of transport to the scanner; chest radiography would have to suffice in these cases.

In cases of minor blunt trauma when there is little suspicion of associated injuries or complications, plain radiography is likely sufficient. If there is suspicion of a rib fracture alone and confirmation is of clinical importance (eg, in the elderly or those with long-standing refractory pain, or when certain pain management treatments are being considered), then oblique radiographic views, bone technique, and marker placement over the concerning region are recommended. The role of ultrasonography in this setting is still up for debate.

In cases of suspected rib fracture with longstanding pain refractory to conservative pain management, plain radiography with oblique views, bone technique, and marker placement is useful. If the radiograph is negative or if there is a high suspicion of cartilage fracture, CT or ultrasonography may be of benefit only if the diagnosis will alter clinical management.

If stress fracture is suspected, a nuclear bone scan may be helpful to first detect an abnormality, and CT may then be used for correlation if needed.

CASE CONCLUDED: LIVING WITH UNCERTAINTY

As for the 70-year-old man presented at the beginning of this article, the first question is whether we suspect an associated injury on the basis of clinical features. If we had clinical findings suspicious for pneumothorax or hemothorax, plain radiography of the chest would be indicated. Since the patient was not involved in major trauma, a CT scan is not indicated as the first study.

Our patient has clinical findings suggesting a rib fracture without associated injury. In this setting, routine posteroanterior and lateral chest radiography would be useful to rule out major associated injuries and, perhaps, to find a rib fracture. If the chest film is normal and rib fracture is still suspected, we must decide whether the diagnosis would alter our clinical management. Our patient would likely be treated the same regardless of whether or not he has a fracture; therefore, we would prescribe pain management.

Chest radiography was performed to rule out associated injuries, especially since the patient was elderly, but the chest x-ray did not reveal anything. On follow-up approximately 1 month later, he appeared improved, with less pain and tenderness. This may be due to healing of a rib fracture or healing of his soft-tissue injury. We will never know whether he truly had a fracture, but it is irrelevant to his care.

With prolonged cellular telephone use, people may note the onset of aching, burning, numbness, or tingling in the ulnar forearm and hand. This constellation of symptoms, termed “cell phone elbow” by the lay press, is known medically as cubital tunnel syndrome—the second most common nerve compression syndrome in the upper extremities after carpal tunnel syndrome.

In most cases, treatment consists simply of modifying the activity and avoiding activities that aggravate the symptoms. Switching hands frequently while talking on the phone or using a hands-free headset can help. Other daily activities that produce cubital tunnel syndrome include leaning on an elbow while driving or working, and sitting at a computer workstation that requires elbow flexion greater than 90 degrees. Making ergonomic adjustments to these activities is beneficial.

For patients who have nocturnal symptoms, a simple elbow pad worn anteriorly or a towel wrapped around the elbow to prevent flexion while sleeping can be very efficacious. Occasionally, anti-inflammatory injections can be given to quiet an inflamed ulnar nerve and reduce symptoms.¹ Surgical interventions, discussed below, are available for patients with severe, persistent symptoms.

WHAT IS CUBITAL TUNNEL SYNDROME?

Cellular telephone use has increased exponentially, with 3.3 billion service contracts active worldwide—or about one for every two people on the planet. The exact incidence of cell phone elbow is not known, but anecdotal reports and our own clinical experience indicate that its incidence parallels the rise in the use of cell phones and computer workstations.

Cubital tunnel syndrome is caused by compression of the ulnar nerve as it traverses the posterior elbow, wrapping around the medial condyle of the humerus. When people hold their elbow flexed for a prolonged period, such as when speaking on the phone or sleeping at night, the ulnar nerve is placed in tension; the nerve itself can elongate 4.5 to 8 mm with elbow flexion.² Additionally, flexion of the elbow narrows the space available for the nerve² and can cause a sevenfold to 20-fold increase in the pressure within the cubital tunnel, depending on muscle contraction.³ This can be compounded by compression on the nerve, either from various fascial bands surrounding the nerve or from extrinsic sources of compression, such as leaning on one’s elbow while driving or talking. This increased pressure on the nerve leads to decreased blood flow and nerve ischemia; this in turn causes increased permeability of the epineurial vessels and nerve edema, enlarging the nerve and continuing the cycle. Less frequently, cubital tunnel symptoms can be caused by the ulnar nerve subluxing in and out of its groove in the posterior elbow, leading to nerve inflammation and swelling from the repetitive friction.

THE CLINICAL PRESENTATION

The clinical picture of cubital tunnel syndrome consists of numbness or paresthesias in the small and ring fingers. Dorsal ulnar hand numbness, which is not present if the ulnar nerve is compressed at Guyon’s canal, helps the clinician differentiate cubital tunnel nerve compression from distal ulnar nerve compression.

If ulnar nerve compression persists, symptoms may progress to hand fatigue and weakness, including difficulty opening bottles or jars. Chronic and severe compression may lead to permanent motor deficits, including an inability to adduct the small finger (Wartenberg sign) and severe clawing of the ring and small fingers (a hand posture of metacarpophalangeal extension and flexion of the proximal and distal interphalangeal joints due to dysfunction of the ulnar-innervated intrinsic hand musculature). Patients may be unable to grasp things in a key-pinch grip, using a fingertip grip instead (Froment sign).

THE DIAGNOSIS IS USUALLY CLINICAL

The diagnosis of cubital tunnel syndrome is first and foremost a clinical one based on a thorough history, including symptoms, duration, and aggravating activities and factors.

The physical examination should include evaluation of sensibility of the hand, including the Semmes-Weinstein monofilament test and vibratory perception test, which will be affected before the Weber two-point discrimination test. Sensibility of the entire hand should be assessed to differentiate focal ulnar deficits from more widespread peripheral neuropathies.

Motor function can be evaluated by asking the patient to hold the fingers abducted, testing key-pinch grip, or asking the patient to cross the middle finger over the index finger. This crossed-finger test is quite reliable, as it is difficult to “fake out” with other muscles.⁴

The examination should also evaluate the cervical spine and vascularity. Provocative maneuvers can be performed to elicit symptoms, including the Hoffman-Tinel test (tapping the ulnar nerve in its groove at the posterior medial elbow, eliciting electric shocks or tingling radiating into the small finger). The equivalent of the Phalen maneuver for carpal tunnel syndrome can be performed by having the patient sit with the elbow fully flexed for 30 seconds to see if symptoms are reproduced; this may be positive in 10% of normal individuals. ⁵ One can combine elbow flexion with compression over the proximal ulnar nerve; this maneuver has good sensitivity and specificity. ⁶ Early in the disease, these provocative maneuvers may be the only examination findings, since sensation and motor function are usually normal.

Ruling out other entities that can cause numbness in the distribution of the medial hand and forearm is also important. These entities include cervical spine conditions such as herniated disk impinging on the C8 nerve root, or a space-occupying lesion of the cervical spine such as a tumor or syrinx.

The neck should be examined for loss of motion. Also, a Spurling test of the cervical spine checks for foraminal nerve impingement: with the patient seated, the clinician extends the patient’s neck and rotates it toward the involved side, then presses down on the top of the patient’s head and asks if this reproduces or worsens the symptoms in the patient’s arm. Hyperreflexia of the upper extremities or the presence of a Hoffman sign should alert the clinician to a more central process. In unclear cases or in patients with known cervical disease, electromyography should be able to differentiate ulnar neuropathy from a C8 nerveroot impingement or confirm the presence of both conditions (a so-called “double crush” phenomenon).

Other less common entities that can present with hand tingling include an apical lung tumor compressing the lower brachial plexus, thoracic outlet syndrome, or peripheral neuropathy (diabetes, vitamin B₁₂ deficiency, hypothyroidism, alcoholism). Other conditions that can cause medial-sided elbow pain include elbow instability or medial epicondylitis (golfer’s elbow); however, these are not associated with numbness or tingling by themselves.

DIAGNOSTIC TESTS

Advanced diagnostic studies may help in certain cases, although they are not essential if the diagnosis is obvious on clinical examination.

Imaging studies may include plain radiography to look for osteophytes or bone fragments, which may impinge on the ulnar nerve, particularly in an arthritic or previously traumatized elbow. Magnetic resonance imaging is only indicated if a space-occupying lesion is suspected. Electrodiagnostic studies may help when findings are equivocal, when the site of compression is unclear, or when coexisting conditions such as diabetes or cervical spine disease make the diagnosis unclear. Nerve conduction studies may be unreliable early in cubital tunnel syndrome, as nondiseased nerve fibers may be tested, creating a false-negative result. Performing the study with the patient’s elbow flexed may increase the sensitivity of the test. Electromyography generally does not become positive until later in the disease, when more profound changes have occurred.

TREATMENT OF CELL PHONE ELBOW

As mentioned, changing how one uses a cell phone often helps, as does avoiding activities that require the elbow to remain flexed more than 90 degrees for extended periods. But when nonoperative means fail to reduce symptoms, surgery may be warranted.

Operative interventions include simple decompression or transposing the nerve from its usual course around the posterior elbow to a path anterior to the elbow, thus decreasing the tension on the nerve. This can be done either subcutaneously or by embedding the nerve in or under the muscles of the forearm.

In patients with coexisting medial epicondylitis or a subluxing nerve, the medial epicondyle can be excised. Techniques for minimally invasive or endoscopic ulnar nerve decompression have been recently introduced, but the long-term results with these are not yet known.

Overall, treatment for persistent paresthesias is successful even when patients present late, but those who present early have a better chance of full sensory and motor recovery.

With prolonged cellular telephone use, people may note the onset of aching, burning, numbness, or tingling in the ulnar forearm and hand. This constellation of symptoms, termed “cell phone elbow” by the lay press, is known medically as cubital tunnel syndrome—the second most common nerve compression syndrome in the upper extremities after carpal tunnel syndrome.

In most cases, treatment consists simply of modifying the activity and avoiding activities that aggravate the symptoms. Switching hands frequently while talking on the phone or using a hands-free headset can help. Other daily activities that produce cubital tunnel syndrome include leaning on an elbow while driving or working, and sitting at a computer workstation that requires elbow flexion greater than 90 degrees. Making ergonomic adjustments to these activities is beneficial.

For patients who have nocturnal symptoms, a simple elbow pad worn anteriorly or a towel wrapped around the elbow to prevent flexion while sleeping can be very efficacious. Occasionally, anti-inflammatory injections can be given to quiet an inflamed ulnar nerve and reduce symptoms.¹ Surgical interventions, discussed below, are available for patients with severe, persistent symptoms.

WHAT IS CUBITAL TUNNEL SYNDROME?

Cellular telephone use has increased exponentially, with 3.3 billion service contracts active worldwide—or about one for every two people on the planet. The exact incidence of cell phone elbow is not known, but anecdotal reports and our own clinical experience indicate that its incidence parallels the rise in the use of cell phones and computer workstations.

Cubital tunnel syndrome is caused by compression of the ulnar nerve as it traverses the posterior elbow, wrapping around the medial condyle of the humerus. When people hold their elbow flexed for a prolonged period, such as when speaking on the phone or sleeping at night, the ulnar nerve is placed in tension; the nerve itself can elongate 4.5 to 8 mm with elbow flexion.² Additionally, flexion of the elbow narrows the space available for the nerve² and can cause a sevenfold to 20-fold increase in the pressure within the cubital tunnel, depending on muscle contraction.³ This can be compounded by compression on the nerve, either from various fascial bands surrounding the nerve or from extrinsic sources of compression, such as leaning on one’s elbow while driving or talking. This increased pressure on the nerve leads to decreased blood flow and nerve ischemia; this in turn causes increased permeability of the epineurial vessels and nerve edema, enlarging the nerve and continuing the cycle. Less frequently, cubital tunnel symptoms can be caused by the ulnar nerve subluxing in and out of its groove in the posterior elbow, leading to nerve inflammation and swelling from the repetitive friction.

THE CLINICAL PRESENTATION

The clinical picture of cubital tunnel syndrome consists of numbness or paresthesias in the small and ring fingers. Dorsal ulnar hand numbness, which is not present if the ulnar nerve is compressed at Guyon’s canal, helps the clinician differentiate cubital tunnel nerve compression from distal ulnar nerve compression.

If ulnar nerve compression persists, symptoms may progress to hand fatigue and weakness, including difficulty opening bottles or jars. Chronic and severe compression may lead to permanent motor deficits, including an inability to adduct the small finger (Wartenberg sign) and severe clawing of the ring and small fingers (a hand posture of metacarpophalangeal extension and flexion of the proximal and distal interphalangeal joints due to dysfunction of the ulnar-innervated intrinsic hand musculature). Patients may be unable to grasp things in a key-pinch grip, using a fingertip grip instead (Froment sign).

THE DIAGNOSIS IS USUALLY CLINICAL

The diagnosis of cubital tunnel syndrome is first and foremost a clinical one based on a thorough history, including symptoms, duration, and aggravating activities and factors.

The physical examination should include evaluation of sensibility of the hand, including the Semmes-Weinstein monofilament test and vibratory perception test, which will be affected before the Weber two-point discrimination test. Sensibility of the entire hand should be assessed to differentiate focal ulnar deficits from more widespread peripheral neuropathies.

Motor function can be evaluated by asking the patient to hold the fingers abducted, testing key-pinch grip, or asking the patient to cross the middle finger over the index finger. This crossed-finger test is quite reliable, as it is difficult to “fake out” with other muscles.⁴

The examination should also evaluate the cervical spine and vascularity. Provocative maneuvers can be performed to elicit symptoms, including the Hoffman-Tinel test (tapping the ulnar nerve in its groove at the posterior medial elbow, eliciting electric shocks or tingling radiating into the small finger). The equivalent of the Phalen maneuver for carpal tunnel syndrome can be performed by having the patient sit with the elbow fully flexed for 30 seconds to see if symptoms are reproduced; this may be positive in 10% of normal individuals. ⁵ One can combine elbow flexion with compression over the proximal ulnar nerve; this maneuver has good sensitivity and specificity. ⁶ Early in the disease, these provocative maneuvers may be the only examination findings, since sensation and motor function are usually normal.

Ruling out other entities that can cause numbness in the distribution of the medial hand and forearm is also important. These entities include cervical spine conditions such as herniated disk impinging on the C8 nerve root, or a space-occupying lesion of the cervical spine such as a tumor or syrinx.

The neck should be examined for loss of motion. Also, a Spurling test of the cervical spine checks for foraminal nerve impingement: with the patient seated, the clinician extends the patient’s neck and rotates it toward the involved side, then presses down on the top of the patient’s head and asks if this reproduces or worsens the symptoms in the patient’s arm. Hyperreflexia of the upper extremities or the presence of a Hoffman sign should alert the clinician to a more central process. In unclear cases or in patients with known cervical disease, electromyography should be able to differentiate ulnar neuropathy from a C8 nerveroot impingement or confirm the presence of both conditions (a so-called “double crush” phenomenon).

Other less common entities that can present with hand tingling include an apical lung tumor compressing the lower brachial plexus, thoracic outlet syndrome, or peripheral neuropathy (diabetes, vitamin B₁₂ deficiency, hypothyroidism, alcoholism). Other conditions that can cause medial-sided elbow pain include elbow instability or medial epicondylitis (golfer’s elbow); however, these are not associated with numbness or tingling by themselves.

DIAGNOSTIC TESTS

Advanced diagnostic studies may help in certain cases, although they are not essential if the diagnosis is obvious on clinical examination.

Imaging studies may include plain radiography to look for osteophytes or bone fragments, which may impinge on the ulnar nerve, particularly in an arthritic or previously traumatized elbow. Magnetic resonance imaging is only indicated if a space-occupying lesion is suspected. Electrodiagnostic studies may help when findings are equivocal, when the site of compression is unclear, or when coexisting conditions such as diabetes or cervical spine disease make the diagnosis unclear. Nerve conduction studies may be unreliable early in cubital tunnel syndrome, as nondiseased nerve fibers may be tested, creating a false-negative result. Performing the study with the patient’s elbow flexed may increase the sensitivity of the test. Electromyography generally does not become positive until later in the disease, when more profound changes have occurred.

TREATMENT OF CELL PHONE ELBOW

As mentioned, changing how one uses a cell phone often helps, as does avoiding activities that require the elbow to remain flexed more than 90 degrees for extended periods. But when nonoperative means fail to reduce symptoms, surgery may be warranted.

Operative interventions include simple decompression or transposing the nerve from its usual course around the posterior elbow to a path anterior to the elbow, thus decreasing the tension on the nerve. This can be done either subcutaneously or by embedding the nerve in or under the muscles of the forearm.

In patients with coexisting medial epicondylitis or a subluxing nerve, the medial epicondyle can be excised. Techniques for minimally invasive or endoscopic ulnar nerve decompression have been recently introduced, but the long-term results with these are not yet known.

Overall, treatment for persistent paresthesias is successful even when patients present late, but those who present early have a better chance of full sensory and motor recovery.

With prolonged cellular telephone use, people may note the onset of aching, burning, numbness, or tingling in the ulnar forearm and hand. This constellation of symptoms, termed “cell phone elbow” by the lay press, is known medically as cubital tunnel syndrome—the second most common nerve compression syndrome in the upper extremities after carpal tunnel syndrome.

In most cases, treatment consists simply of modifying the activity and avoiding activities that aggravate the symptoms. Switching hands frequently while talking on the phone or using a hands-free headset can help. Other daily activities that produce cubital tunnel syndrome include leaning on an elbow while driving or working, and sitting at a computer workstation that requires elbow flexion greater than 90 degrees. Making ergonomic adjustments to these activities is beneficial.

For patients who have nocturnal symptoms, a simple elbow pad worn anteriorly or a towel wrapped around the elbow to prevent flexion while sleeping can be very efficacious. Occasionally, anti-inflammatory injections can be given to quiet an inflamed ulnar nerve and reduce symptoms.¹ Surgical interventions, discussed below, are available for patients with severe, persistent symptoms.

WHAT IS CUBITAL TUNNEL SYNDROME?

Cellular telephone use has increased exponentially, with 3.3 billion service contracts active worldwide—or about one for every two people on the planet. The exact incidence of cell phone elbow is not known, but anecdotal reports and our own clinical experience indicate that its incidence parallels the rise in the use of cell phones and computer workstations.

Cubital tunnel syndrome is caused by compression of the ulnar nerve as it traverses the posterior elbow, wrapping around the medial condyle of the humerus. When people hold their elbow flexed for a prolonged period, such as when speaking on the phone or sleeping at night, the ulnar nerve is placed in tension; the nerve itself can elongate 4.5 to 8 mm with elbow flexion.² Additionally, flexion of the elbow narrows the space available for the nerve² and can cause a sevenfold to 20-fold increase in the pressure within the cubital tunnel, depending on muscle contraction.³ This can be compounded by compression on the nerve, either from various fascial bands surrounding the nerve or from extrinsic sources of compression, such as leaning on one’s elbow while driving or talking. This increased pressure on the nerve leads to decreased blood flow and nerve ischemia; this in turn causes increased permeability of the epineurial vessels and nerve edema, enlarging the nerve and continuing the cycle. Less frequently, cubital tunnel symptoms can be caused by the ulnar nerve subluxing in and out of its groove in the posterior elbow, leading to nerve inflammation and swelling from the repetitive friction.

THE CLINICAL PRESENTATION

The clinical picture of cubital tunnel syndrome consists of numbness or paresthesias in the small and ring fingers. Dorsal ulnar hand numbness, which is not present if the ulnar nerve is compressed at Guyon’s canal, helps the clinician differentiate cubital tunnel nerve compression from distal ulnar nerve compression.

If ulnar nerve compression persists, symptoms may progress to hand fatigue and weakness, including difficulty opening bottles or jars. Chronic and severe compression may lead to permanent motor deficits, including an inability to adduct the small finger (Wartenberg sign) and severe clawing of the ring and small fingers (a hand posture of metacarpophalangeal extension and flexion of the proximal and distal interphalangeal joints due to dysfunction of the ulnar-innervated intrinsic hand musculature). Patients may be unable to grasp things in a key-pinch grip, using a fingertip grip instead (Froment sign).

THE DIAGNOSIS IS USUALLY CLINICAL

The diagnosis of cubital tunnel syndrome is first and foremost a clinical one based on a thorough history, including symptoms, duration, and aggravating activities and factors.

The physical examination should include evaluation of sensibility of the hand, including the Semmes-Weinstein monofilament test and vibratory perception test, which will be affected before the Weber two-point discrimination test. Sensibility of the entire hand should be assessed to differentiate focal ulnar deficits from more widespread peripheral neuropathies.

Motor function can be evaluated by asking the patient to hold the fingers abducted, testing key-pinch grip, or asking the patient to cross the middle finger over the index finger. This crossed-finger test is quite reliable, as it is difficult to “fake out” with other muscles.⁴

The examination should also evaluate the cervical spine and vascularity. Provocative maneuvers can be performed to elicit symptoms, including the Hoffman-Tinel test (tapping the ulnar nerve in its groove at the posterior medial elbow, eliciting electric shocks or tingling radiating into the small finger). The equivalent of the Phalen maneuver for carpal tunnel syndrome can be performed by having the patient sit with the elbow fully flexed for 30 seconds to see if symptoms are reproduced; this may be positive in 10% of normal individuals. ⁵ One can combine elbow flexion with compression over the proximal ulnar nerve; this maneuver has good sensitivity and specificity. ⁶ Early in the disease, these provocative maneuvers may be the only examination findings, since sensation and motor function are usually normal.

Ruling out other entities that can cause numbness in the distribution of the medial hand and forearm is also important. These entities include cervical spine conditions such as herniated disk impinging on the C8 nerve root, or a space-occupying lesion of the cervical spine such as a tumor or syrinx.

The neck should be examined for loss of motion. Also, a Spurling test of the cervical spine checks for foraminal nerve impingement: with the patient seated, the clinician extends the patient’s neck and rotates it toward the involved side, then presses down on the top of the patient’s head and asks if this reproduces or worsens the symptoms in the patient’s arm. Hyperreflexia of the upper extremities or the presence of a Hoffman sign should alert the clinician to a more central process. In unclear cases or in patients with known cervical disease, electromyography should be able to differentiate ulnar neuropathy from a C8 nerveroot impingement or confirm the presence of both conditions (a so-called “double crush” phenomenon).

Other less common entities that can present with hand tingling include an apical lung tumor compressing the lower brachial plexus, thoracic outlet syndrome, or peripheral neuropathy (diabetes, vitamin B₁₂ deficiency, hypothyroidism, alcoholism). Other conditions that can cause medial-sided elbow pain include elbow instability or medial epicondylitis (golfer’s elbow); however, these are not associated with numbness or tingling by themselves.

DIAGNOSTIC TESTS

Advanced diagnostic studies may help in certain cases, although they are not essential if the diagnosis is obvious on clinical examination.

Imaging studies may include plain radiography to look for osteophytes or bone fragments, which may impinge on the ulnar nerve, particularly in an arthritic or previously traumatized elbow. Magnetic resonance imaging is only indicated if a space-occupying lesion is suspected. Electrodiagnostic studies may help when findings are equivocal, when the site of compression is unclear, or when coexisting conditions such as diabetes or cervical spine disease make the diagnosis unclear. Nerve conduction studies may be unreliable early in cubital tunnel syndrome, as nondiseased nerve fibers may be tested, creating a false-negative result. Performing the study with the patient’s elbow flexed may increase the sensitivity of the test. Electromyography generally does not become positive until later in the disease, when more profound changes have occurred.

TREATMENT OF CELL PHONE ELBOW

As mentioned, changing how one uses a cell phone often helps, as does avoiding activities that require the elbow to remain flexed more than 90 degrees for extended periods. But when nonoperative means fail to reduce symptoms, surgery may be warranted.

Operative interventions include simple decompression or transposing the nerve from its usual course around the posterior elbow to a path anterior to the elbow, thus decreasing the tension on the nerve. This can be done either subcutaneously or by embedding the nerve in or under the muscles of the forearm.

In patients with coexisting medial epicondylitis or a subluxing nerve, the medial epicondyle can be excised. Techniques for minimally invasive or endoscopic ulnar nerve decompression have been recently introduced, but the long-term results with these are not yet known.

Overall, treatment for persistent paresthesias is successful even when patients present late, but those who present early have a better chance of full sensory and motor recovery.

In many of these patients, the findings on neurologic examination, nerve conduction studies, and electromyography are normal, although some may show signs of mild distal sensory loss on physical examination. The lack of objective findings on routine nerve conduction studies and electromyography may lead many physicians to attribute the symptoms to other disorders such as plantar fasciitis, vascular insufficiency, or degenerative lumbosacral spine disease.

The past 2 decades have seen the development of specialized tests that have greatly facilitated the diagnosis of small fiber neuropathy; these include skin biopsy to evaluate the density of nerve fibers in the epidermis and studies of autonomic nerve function. Common etiologies have been identified for small fiber neuropathy and can be specifically treated, which is critical for controlling progression of the disease. Pain management is becoming easier with more available options but is still quite challenging.

WHAT IS SMALL FIBER NEUROPATHY?

Peripheral nerve fibers can be classified according to size, which correlates with the degree of myelination.

• Large nerve fibers are heavily myelinated and include A-alpha fibers, which mediate motor strength, and A-beta fibers, which mediate vibratory and touch sensation.
• Medium-sized fibers, known as A-gamma fibers, are also myelinated and carry information to muscle spindles.
• Small fibers include myelinated A-delta fibers and unmyelinated C fibers, which innervate skin (somatic fibers) and involuntary muscles, including cardiac and smooth muscles (autonomic fibers). Together, they mediate pain, thermal sensation, and autonomic function.

Small fiber neuropathy results from selective impairment of small myelinated A-delta and unmyelinated C fibers.

Sensory symptoms: Pain, burning, tingling, numbness

Damage to or loss of small somatic nerve fibers results in pain, burning, tingling, or numbness that typically affects the limbs in a distal-to-proximal gradient. In rare cases, small fiber neuropathy follows a non-length-dependent distribution in which symptoms may be manifested predominantly in the arms, face, or trunk.

Symptoms may be mild initially, with some patients complaining of vague discomfort in one or both feet similar to the sensation of a sock gathering at the end of a shoe. Others report a wooden quality in their feet, numbness in their toes, or a feeling as if they are walking on pebbles, sand, or golf balls. The most bothersome and fairly typical symptom is burning pain in the feet that extends proximally in a stocking-glove distribution and is often accompanied by stabbing or aching pains, electric shock-like or pins-and-needles sensations, or cramping of the feet and calves.

Symptoms are usually worse at night and often affect sleep. Some patients say that their feet have become so exquisitely tender that they cannot bear having the bed sheets touch them, and so they sleep with their feet uncovered. A small number of patients do not have pain but report a feeling of tightness and swelling in their feet (even though the feet appear normal).

Examination often reveals allodynia (perception of nonpainful stimuli as being painful), hyperalgesia (perception of painful stimuli as being more painful than expected), or reduced pinprick and thermal sensation in the affected area. Vibratory sensation can be mildly reduced at the toes. Motor strength, tendon reflexes, and proprioception, however, are preserved because they are functions of large nerve fibers.

Autonomic symptoms

When autonomic fibers are affected, patients may experience dry eyes, dry mouth, orthostatic dizziness, constipation, bladder incontinence, sexual dysfunction, trouble sweating, or red or white skin discoloration.² Examination may show orthostatic hypotension and skin changes. The skin over the affected area may appear atrophic, dry, shiny, discolored, or mildly edematous as the result of sudomotor and vasomotor abnormalities.

WHAT CAUSES SMALL FIBER NEUROPATHY?

Small fiber neuropathy has been associated with many medical conditions, including glucose dysmetabolism,³ connective tissue disease,^4,5 dysthyroidism,⁶ vitamin B₁₂ deficiency, paraproteinemia, human immunodeficiency virus (HIV) infection,⁷ hepatitis C virus infection, celiac disease,⁸ restless legs syndrome,⁹ neurotoxic drug exposure, hereditary diseases, and paraneoplastic syndrome. While most of these conditions cause a length-dependent small fiber neuropathy, others (Sjögren disease, celiac disease, and paraneoplastic syndrome) can cause a form of small fiber neuropathy that is not length-dependent.^4,8,10

Diabetes and prediabetes

Glucose dysmetabolism, including diabetes and prediabetes with impaired oral glucose tolerance (a glucose level 140–199 mg/dL 2 hours after a 75-g oral dextrose load), is the most common identifiable associated condition, present in about one-third of patients with painful sensory neuropathy¹¹ and in nearly half of those with otherwise idiopathic small fiber neuropathy.^12–14

Research findings strongly suggest that even prediabetes is a risk factor for small fiber neuropathy, and that so-called “impaired glucose tolerance neuropathy” may represent the earliest stage of diabetic neuropathy. Several recent studies have found a high prevalence of impaired glucose tolerance in patients with sensory peripheral neuropathy,^12–14 with a rate of up to 42% in cases initially thought to be idiopathic¹⁴ compared with 14% in the general population.¹⁵ Also, a dose-response relationship between the severity of hyperglycemia and the degree of neuropathy was demonstrated in one study, in which patients with impaired glucose tolerance more often had small fiber neuropathy, whereas those with diabetes more often had polyneuropathy involving both small and large fibers.¹⁴ And studies in animals and cell cultures have shown that intermittent hyperglycemia, which can be seen in patients with impaired glucose tolerance, caused sensory neuron and nerve fiber damage and increased spontaneous C-fiber firing, resulting in neuropathic pain.^8,16,17

Metabolic syndrome

Insulin resistance with prediabetes and diabetes is a part of the metabolic syndrome, which also consists of hypertension, hyperlipidemia, and obesity. The individual components of the metabolic syndrome have been implicated as risk factors not only for cardiovascular and cerebrovascular disease but also for small fiber neuropathy.

One study in 548 patients with type 2 diabetes showed that those with the metabolic syndrome were twice as likely to have neuropathy as those without.¹⁸ Another study showed that in 1,200 patients with type 1 diabetes without neuropathy at baseline, hypertension, hyperlipidemia, and increased body mass index were each independently associated with a higher risk of developing neuropathy.¹⁹

A recent study of 219 patients with idiopathic distal symmetrical peripheral neuropathy and 175 diabetic patients without neuropathy found a higher prevalence of metabolic syndrome in patients with neuropathy than in normal populations. The prevalence of dyslipidemia (high levels of total and low-density lipoprotein cholesterol and triglycerides and low levels of high-density lipoprotein cholesterol), but not hypertension or obesity, was higher in patients with neuropathy than in patients with diabetes but no neuropathy.²⁰ The findings linked dyslipidemia to neuropathy and showed the need for further studies of the potential pathogenic role of dyslipidemia in neuropathy.

Hereditary causes

Hereditary causes of small fiber neuropathy are rare and include Fabry disease, Tangier disease, hereditary sensory autonomic neuropathy, and hereditary amyloidosis.

HOW DO YOU EVALUATE PATIENTS WITH SUSPECTED SMALL FIBER NEUROPATHY?

A thorough history should be taken to obtain details regarding onset and features of neuropathy symptoms, exacerbating factors, and progression. It is also important to ascertain whether the patient has any associated conditions as mentioned above, a family history of neuropathy, risk factors for HIV or hepatitis C virus infection, or a history of neurotoxic drug exposure.

Clinical suspicion of small fiber neuropathy should be high if a patient presents with predominant small fiber symptoms and signs with preserved large fiber functions.

Nerve conduction studies and electromyography

For diagnostic testing, routine nerve conduction studies and electromyography assess the function of large nerve fibers only and are thus normal in small fiber neuropathy. These tests should still be ordered to rule out subclinical involvement of large fibers, which may affect the diagnostic evaluation, prognosis, and treatment plan. However, if the results of these tests are normal, specialized studies are needed to evaluate small fibers.

Although several tests are available to evaluate somatic and autonomic small fibers, the two that have the highest diagnostic efficiency for small fiber neuropathy and that are used most often are skin biopsy, to evaluate intraepidermal nerve fiber density, and quantitative sudomotor axon reflex testing (QSART), to assess sudomotor autonomic function.^21–23

Skin biopsy

Skin biopsy is a minimally invasive procedure in which 3-mm-diameter punch biopsy specimens are taken from the distal leg, distal thigh, and proximal thigh of one lower limb. The procedure takes only 10 to 15 minutes.

Biopsy specimens are immunostained using an antibody against protein gene product 9.5, which is a panaxonal marker. Small nerve fibers in the epidermis are counted under a microscope, and intraepithelial nerve fiber densities are calculated and compared with established normative values. The diagnosis of small fiber neuropathy can be established if the intraepidermal nerve fiber density is lower than normal (Figure 1). Nerve fiber density may be normal in the early stage of small fiber neuropathy, but in this setting skin biopsy often shows abnormal morphologic changes in the small fibers, especially large swellings,²⁴ and repeat biopsy in 6 to 12 months may be considered.

The diagnostic efficiency of skin biopsy is about 88%.^21,23 For diagnosing small fiber neuropathy, it is more sensitive than quantitative sensory testing^21,25 and more sensitive and less invasive than sural nerve biopsy.²⁶ Intraepidermal nerve fiber density also correlates well with a variety of measures of severity of HIV distal sensory neuropathy and thus may be used to measure the severity and treatment response of small fiber neuropathy.²⁷

QSART is an autonomic study that measures sweat output in response to acetylcholine, which reflects the function of postganglionic sympathetic unmyelinated sudomotor nerve fibers. Electrodes are placed on the arms and legs to record the volume of sweat produced by acetylcholine iontophoresis, in which a mild electrical stimulation on the skin allows acetylcholine to stimulate the sweat glands. The output is compared with normative values.

One prospective study showed that 67 (72.8%) of 92 patients with painful feet had abnormal results on QSART, ie, low sweat output.²⁸ A retrospective study found that 77 (62%) of 125 patients with clinical features of distal small fiber neuropathy had a length-dependent pattern of QSART abnormalities.²² QSART abnormalities were detected in some patients without autonomic symptoms.

If these tests are not available

Skin biopsy and QSART are objective, reproducible, sensitive, and complementary in diagnosing small fiber neuropathy. One or both can be ordered, depending on whether the patient has somatic symptoms, autonomic symptoms, or both. However, these two tests are not widely available. Only a few laboratories in the country can process skin biopsy specimens to evaluate intraepidermal nerve fiber density. Nevertheless, it is easy to learn the skin punch biopsy procedure, and primary care physicians and neurologists can perform it after appropriate training. (A concern is avoiding damage to the epidermis.) They can then send specimens to one of the cutaneous nerve laboratories (but not to a routine reference laboratory).

A special technique, including unique fixative and cryoprotectant, is used to fix and process the biopsy specimens, because routine techniques for processing dermatologic punch biopsy specimens often result in lower intraepidermal nerve fiber densities. Therefore, it is very important to contact the laboratory regarding fixative and processing before performing a biopsy.

QSART requires specialized equipment and must be performed on site. In addition, the test is very sensitive to drugs that can affect sweating, such as antihistamines and antidepressants, and such drugs must be discontinued 48 hours before the study.

Basic laboratory tests to find the cause

Once the diagnosis of small fiber neuropathy is established, the next important step is to order a battery of laboratory tests to search for an underlying cause. The tests should include the following:

• Complete blood cell count
• Comprehensive metabolic panel
• Lipid panel
• Erythrocyte sedimentation rate
• Thyroid-stimulating hormone level
• Free thyroxine (T4) level
• Antinuclear antibody
• Extractable nuclear antigens
• Angiotensin-converting enzyme (ACE) level
• Serum and urine immunofixation tests
• Vitamin B₁₂ level
• 2-hour oral glucose tolerance test.

Oral glucose tolerance testing is much more sensitive than measuring the hemoglobin A_1c and fasting glucose levels in detecting diabetes and prediabetes. These two conditions were detected by oral glucose tolerance testing in more than 50% of patients with otherwise idiopathic sensory-predominant peripheral neuropathy and normal hemoglobin A_1c and fasting glucose levels.^13,14 Therefore, every patient with small fiber neuropathy without a known history of diabetes or prediabetes should have an oral glucose tolerance test.

Special laboratory tests in special cases

• If there is a history of gastrointestinal symptoms or herpetiform-like rash, then testing for gliadin antibody and tissue transglutaminase antibodies as well as small-bowel biopsy may be pursued to evaluate for celiac sprue.
• Serologic tests for HIV or hepatitis C should be ordered if the patient has risk factors.
• If there is a significant family history, further genetic testing should be considered.
• Lip biopsy or bone marrow biopsy should be considered if clinical suspicion is high for Sjögren disease, seronegative sicca syndrome, or amyloidosis.
• The serum ACE level has a low sensitivity and specificity; therefore, if sarcoid is suspected clinically, additional confirmatory testing, such as computed tomography of the chest, should be ordered despite a normal ACE value.

HOW DO YOU TREAT SMALL FIBER NEUROPATHY?

Treatment of small fiber neuropathy should target the underlying cause and neuropathic pain. Cause-specific treatment is a key in preventing small fiber neuropathy or slowing its progression.

Glucose control, weight control, and regular exercise

As glucose dysmetabolism is the condition most often associated with small fiber neuropathy (and since individual components of the metabolic syndrome are potential risk factors for it), tight glycemic control and lifestyle modification with diet control, weight control, and regular exercise are of paramount importance in patients with these conditions.

The Diabetic Prevention Program,²⁹ a study in 3,234 people with prediabetes, found that diet and exercise were more effective than metformin (Glucophage) in preventing full-blown diabetes. At an average of 2.8 years of follow-up, the incidence of diabetes was 11.0 cases per 100 patient-years in a group assigned to receive placebo, compared with 7.8 in those assigned to receive metformin (31% lower), and 4.8 (58% lower) in those who were assigned to undergo a lifestyle intervention that included at least 150 minutes of physical activity per week with a weight-loss goal of 7%. Put another way, to prevent one case of diabetes over 3 years, 6.9 patients would have to undergo the lifestyle intervention program, or 13.9 would have to receive metformin. Since impaired glucose tolerance neuropathy may represent the earliest stage of diabetic neuropathy, the neuropathy at this stage may be reversible with lifestyle intervention and improvement of impaired glucose tolerance.

This concept is supported by a 3-year study in 31 people, which showed that lifestyle intervention significantly improved impaired glucose tolerance, reduced the body mass index, and lowered total serum cholesterol levels.³⁰ Changes in these metabolic variables were accompanied by significant improvement of neuropathy as evidenced by significantly increased intraepidermal nerve fiber density, increased foot sweat volume, and decreased neuropathic pain.³⁰

It has also been reported that treatment of sarcoidosis, autoimmune diseases, and celiac disease improved the symptoms of small fiber neuropathy resulting from these conditions.^8,31 Therefore, it is important to identify the cause and treat it to prevent and slow the progression of small fiber neuropathy, and doing so may improve the disease in some mild cases.

Pain management

First-line choices of pain medications are the anticonvulsants gabapentin (Neurontin) and pregabalin (Lyrica), the tricyclic antidepressants amitriptyline (Elavil) and nortriptyline (Aventyl), a 5% lidocaine patch (Lidoderm), and the semisynthetic opioid analgesic tramadol (Ultram). These can be used alone or in combination.

Gabapentin is relatively well tolerated, but drowsiness can occur, especially with high starting doses. We usually start with 300 mg daily and increase it by 300 mg every week up to 1,200 mg three times a day as tolerated. Most patients need 600 to 900 mg three times a day.

Pregabalin is a newer antiepileptic drug, similar to gabapentin but less sedating. It can be started at 75 mg twice a day and gradually increased to 300 mg twice a day as needed. Weight gain and, rarely, swelling of the lower extremities may limit the use of both of these drugs.

Tricyclic antidepressants, such as amitriptyline, nortriptyline, and desipramine (Norpramin), are proven effective in controlling neuropathic pain, although no response with amitriptyline was seen in patients with painful HIV distal sensory neuropathy.³⁴

Lidocaine patch is preferred if the painful area is small. Patients should be instructed to use the patch to cover the painful area 12 hours on and 12 hours off. If it does not provide relief within 1 week, it should be discontinued.

Tramadol is also helpful in treating neuropathic pain. It can be started at 50 mg two to four times a day as needed.

Nonsteroidal anti-inflammatory drugs and selective serotonin reuptake inhibitors are typically less effective than the other drugs mentioned.

Opioids should be reserved for refractory cases, given the potential for addiction, but they are sometimes necessary in patients with disabling pain that does not respond to other drugs.

TENS may be of benefit. The patient controls a pocket-size device that sends electrical signals to leads placed on affected areas.

Alternative therapies for small fiber neuropathy, such as meditation, yoga, and acupuncture, have yet to be studied.

It is also important to explain to patients that the typical course of small fiber neuropathy is relatively benign, as many patients worry about developing weakness and eventually not being able to walk. These concerns and fears can aggravate pain and depression, which can make treatment difficult.

WHAT IS THE PROGNOSIS OF SMALL FIBER NEUROPATHY?

Most patients with small fiber neuropathy experience a slowly progressive course, with symptoms and signs spreading proximally over time.

In one study, only 13% of 124 patients with small fiber neuropathy showed evidence of large-fiber involvement over a 2-year period. ²¹ None went on to develop Charcot joints, foot ulcers, weakness, or sensory ataxia, as is often seen in patients with long-standing or severe large fiber neuropathy. Neuropathic pain worsened in 30% and resolved spontaneously in 11%.²¹

Most patients with small fiber neuropathy require chronic pain management. Again, treatment of the underlying cause is important and can improve the prognosis.

We believe that the overall progression of small fiber neuropathy is slow. A longitudinal study with a follow-up longer than 2 years would be useful to confirm this.

TAKE-HOME POINTS

As the population continues to age and as more patients develop diabetes and the metabolic syndrome, the prevalence of small fiber neuropathy will rise. Patients who present to their primary care physicians with painful, burning feet require a thorough diagnostic evaluation, which may include referral for specialized neurodiagnostic testing. Aggressive cause-specific treatment, lifestyle modification, and pain control are key elements of a team approach to managing small fiber neuropathy.

In many of these patients, the findings on neurologic examination, nerve conduction studies, and electromyography are normal, although some may show signs of mild distal sensory loss on physical examination. The lack of objective findings on routine nerve conduction studies and electromyography may lead many physicians to attribute the symptoms to other disorders such as plantar fasciitis, vascular insufficiency, or degenerative lumbosacral spine disease.

The past 2 decades have seen the development of specialized tests that have greatly facilitated the diagnosis of small fiber neuropathy; these include skin biopsy to evaluate the density of nerve fibers in the epidermis and studies of autonomic nerve function. Common etiologies have been identified for small fiber neuropathy and can be specifically treated, which is critical for controlling progression of the disease. Pain management is becoming easier with more available options but is still quite challenging.

WHAT IS SMALL FIBER NEUROPATHY?

Peripheral nerve fibers can be classified according to size, which correlates with the degree of myelination.

• Large nerve fibers are heavily myelinated and include A-alpha fibers, which mediate motor strength, and A-beta fibers, which mediate vibratory and touch sensation.
• Medium-sized fibers, known as A-gamma fibers, are also myelinated and carry information to muscle spindles.
• Small fibers include myelinated A-delta fibers and unmyelinated C fibers, which innervate skin (somatic fibers) and involuntary muscles, including cardiac and smooth muscles (autonomic fibers). Together, they mediate pain, thermal sensation, and autonomic function.

Small fiber neuropathy results from selective impairment of small myelinated A-delta and unmyelinated C fibers.

Sensory symptoms: Pain, burning, tingling, numbness

Damage to or loss of small somatic nerve fibers results in pain, burning, tingling, or numbness that typically affects the limbs in a distal-to-proximal gradient. In rare cases, small fiber neuropathy follows a non-length-dependent distribution in which symptoms may be manifested predominantly in the arms, face, or trunk.

Symptoms may be mild initially, with some patients complaining of vague discomfort in one or both feet similar to the sensation of a sock gathering at the end of a shoe. Others report a wooden quality in their feet, numbness in their toes, or a feeling as if they are walking on pebbles, sand, or golf balls. The most bothersome and fairly typical symptom is burning pain in the feet that extends proximally in a stocking-glove distribution and is often accompanied by stabbing or aching pains, electric shock-like or pins-and-needles sensations, or cramping of the feet and calves.

Symptoms are usually worse at night and often affect sleep. Some patients say that their feet have become so exquisitely tender that they cannot bear having the bed sheets touch them, and so they sleep with their feet uncovered. A small number of patients do not have pain but report a feeling of tightness and swelling in their feet (even though the feet appear normal).

Examination often reveals allodynia (perception of nonpainful stimuli as being painful), hyperalgesia (perception of painful stimuli as being more painful than expected), or reduced pinprick and thermal sensation in the affected area. Vibratory sensation can be mildly reduced at the toes. Motor strength, tendon reflexes, and proprioception, however, are preserved because they are functions of large nerve fibers.

Autonomic symptoms

When autonomic fibers are affected, patients may experience dry eyes, dry mouth, orthostatic dizziness, constipation, bladder incontinence, sexual dysfunction, trouble sweating, or red or white skin discoloration.² Examination may show orthostatic hypotension and skin changes. The skin over the affected area may appear atrophic, dry, shiny, discolored, or mildly edematous as the result of sudomotor and vasomotor abnormalities.

WHAT CAUSES SMALL FIBER NEUROPATHY?

Small fiber neuropathy has been associated with many medical conditions, including glucose dysmetabolism,³ connective tissue disease,^4,5 dysthyroidism,⁶ vitamin B₁₂ deficiency, paraproteinemia, human immunodeficiency virus (HIV) infection,⁷ hepatitis C virus infection, celiac disease,⁸ restless legs syndrome,⁹ neurotoxic drug exposure, hereditary diseases, and paraneoplastic syndrome. While most of these conditions cause a length-dependent small fiber neuropathy, others (Sjögren disease, celiac disease, and paraneoplastic syndrome) can cause a form of small fiber neuropathy that is not length-dependent.^4,8,10

Diabetes and prediabetes

Glucose dysmetabolism, including diabetes and prediabetes with impaired oral glucose tolerance (a glucose level 140–199 mg/dL 2 hours after a 75-g oral dextrose load), is the most common identifiable associated condition, present in about one-third of patients with painful sensory neuropathy¹¹ and in nearly half of those with otherwise idiopathic small fiber neuropathy.^12–14

Research findings strongly suggest that even prediabetes is a risk factor for small fiber neuropathy, and that so-called “impaired glucose tolerance neuropathy” may represent the earliest stage of diabetic neuropathy. Several recent studies have found a high prevalence of impaired glucose tolerance in patients with sensory peripheral neuropathy,^12–14 with a rate of up to 42% in cases initially thought to be idiopathic¹⁴ compared with 14% in the general population.¹⁵ Also, a dose-response relationship between the severity of hyperglycemia and the degree of neuropathy was demonstrated in one study, in which patients with impaired glucose tolerance more often had small fiber neuropathy, whereas those with diabetes more often had polyneuropathy involving both small and large fibers.¹⁴ And studies in animals and cell cultures have shown that intermittent hyperglycemia, which can be seen in patients with impaired glucose tolerance, caused sensory neuron and nerve fiber damage and increased spontaneous C-fiber firing, resulting in neuropathic pain.^8,16,17

Metabolic syndrome

Insulin resistance with prediabetes and diabetes is a part of the metabolic syndrome, which also consists of hypertension, hyperlipidemia, and obesity. The individual components of the metabolic syndrome have been implicated as risk factors not only for cardiovascular and cerebrovascular disease but also for small fiber neuropathy.

One study in 548 patients with type 2 diabetes showed that those with the metabolic syndrome were twice as likely to have neuropathy as those without.¹⁸ Another study showed that in 1,200 patients with type 1 diabetes without neuropathy at baseline, hypertension, hyperlipidemia, and increased body mass index were each independently associated with a higher risk of developing neuropathy.¹⁹

A recent study of 219 patients with idiopathic distal symmetrical peripheral neuropathy and 175 diabetic patients without neuropathy found a higher prevalence of metabolic syndrome in patients with neuropathy than in normal populations. The prevalence of dyslipidemia (high levels of total and low-density lipoprotein cholesterol and triglycerides and low levels of high-density lipoprotein cholesterol), but not hypertension or obesity, was higher in patients with neuropathy than in patients with diabetes but no neuropathy.²⁰ The findings linked dyslipidemia to neuropathy and showed the need for further studies of the potential pathogenic role of dyslipidemia in neuropathy.

Hereditary causes

Hereditary causes of small fiber neuropathy are rare and include Fabry disease, Tangier disease, hereditary sensory autonomic neuropathy, and hereditary amyloidosis.

HOW DO YOU EVALUATE PATIENTS WITH SUSPECTED SMALL FIBER NEUROPATHY?

A thorough history should be taken to obtain details regarding onset and features of neuropathy symptoms, exacerbating factors, and progression. It is also important to ascertain whether the patient has any associated conditions as mentioned above, a family history of neuropathy, risk factors for HIV or hepatitis C virus infection, or a history of neurotoxic drug exposure.

Clinical suspicion of small fiber neuropathy should be high if a patient presents with predominant small fiber symptoms and signs with preserved large fiber functions.

Nerve conduction studies and electromyography

For diagnostic testing, routine nerve conduction studies and electromyography assess the function of large nerve fibers only and are thus normal in small fiber neuropathy. These tests should still be ordered to rule out subclinical involvement of large fibers, which may affect the diagnostic evaluation, prognosis, and treatment plan. However, if the results of these tests are normal, specialized studies are needed to evaluate small fibers.

Although several tests are available to evaluate somatic and autonomic small fibers, the two that have the highest diagnostic efficiency for small fiber neuropathy and that are used most often are skin biopsy, to evaluate intraepidermal nerve fiber density, and quantitative sudomotor axon reflex testing (QSART), to assess sudomotor autonomic function.^21–23

Skin biopsy

Skin biopsy is a minimally invasive procedure in which 3-mm-diameter punch biopsy specimens are taken from the distal leg, distal thigh, and proximal thigh of one lower limb. The procedure takes only 10 to 15 minutes.

Biopsy specimens are immunostained using an antibody against protein gene product 9.5, which is a panaxonal marker. Small nerve fibers in the epidermis are counted under a microscope, and intraepithelial nerve fiber densities are calculated and compared with established normative values. The diagnosis of small fiber neuropathy can be established if the intraepidermal nerve fiber density is lower than normal (Figure 1). Nerve fiber density may be normal in the early stage of small fiber neuropathy, but in this setting skin biopsy often shows abnormal morphologic changes in the small fibers, especially large swellings,²⁴ and repeat biopsy in 6 to 12 months may be considered.

The diagnostic efficiency of skin biopsy is about 88%.^21,23 For diagnosing small fiber neuropathy, it is more sensitive than quantitative sensory testing^21,25 and more sensitive and less invasive than sural nerve biopsy.²⁶ Intraepidermal nerve fiber density also correlates well with a variety of measures of severity of HIV distal sensory neuropathy and thus may be used to measure the severity and treatment response of small fiber neuropathy.²⁷

QSART is an autonomic study that measures sweat output in response to acetylcholine, which reflects the function of postganglionic sympathetic unmyelinated sudomotor nerve fibers. Electrodes are placed on the arms and legs to record the volume of sweat produced by acetylcholine iontophoresis, in which a mild electrical stimulation on the skin allows acetylcholine to stimulate the sweat glands. The output is compared with normative values.

One prospective study showed that 67 (72.8%) of 92 patients with painful feet had abnormal results on QSART, ie, low sweat output.²⁸ A retrospective study found that 77 (62%) of 125 patients with clinical features of distal small fiber neuropathy had a length-dependent pattern of QSART abnormalities.²² QSART abnormalities were detected in some patients without autonomic symptoms.

If these tests are not available

Skin biopsy and QSART are objective, reproducible, sensitive, and complementary in diagnosing small fiber neuropathy. One or both can be ordered, depending on whether the patient has somatic symptoms, autonomic symptoms, or both. However, these two tests are not widely available. Only a few laboratories in the country can process skin biopsy specimens to evaluate intraepidermal nerve fiber density. Nevertheless, it is easy to learn the skin punch biopsy procedure, and primary care physicians and neurologists can perform it after appropriate training. (A concern is avoiding damage to the epidermis.) They can then send specimens to one of the cutaneous nerve laboratories (but not to a routine reference laboratory).

A special technique, including unique fixative and cryoprotectant, is used to fix and process the biopsy specimens, because routine techniques for processing dermatologic punch biopsy specimens often result in lower intraepidermal nerve fiber densities. Therefore, it is very important to contact the laboratory regarding fixative and processing before performing a biopsy.

QSART requires specialized equipment and must be performed on site. In addition, the test is very sensitive to drugs that can affect sweating, such as antihistamines and antidepressants, and such drugs must be discontinued 48 hours before the study.

Basic laboratory tests to find the cause

Once the diagnosis of small fiber neuropathy is established, the next important step is to order a battery of laboratory tests to search for an underlying cause. The tests should include the following:

• Complete blood cell count
• Comprehensive metabolic panel
• Lipid panel
• Erythrocyte sedimentation rate
• Thyroid-stimulating hormone level
• Free thyroxine (T4) level
• Antinuclear antibody
• Extractable nuclear antigens
• Angiotensin-converting enzyme (ACE) level
• Serum and urine immunofixation tests
• Vitamin B₁₂ level
• 2-hour oral glucose tolerance test.

Oral glucose tolerance testing is much more sensitive than measuring the hemoglobin A_1c and fasting glucose levels in detecting diabetes and prediabetes. These two conditions were detected by oral glucose tolerance testing in more than 50% of patients with otherwise idiopathic sensory-predominant peripheral neuropathy and normal hemoglobin A_1c and fasting glucose levels.^13,14 Therefore, every patient with small fiber neuropathy without a known history of diabetes or prediabetes should have an oral glucose tolerance test.

Special laboratory tests in special cases

• If there is a history of gastrointestinal symptoms or herpetiform-like rash, then testing for gliadin antibody and tissue transglutaminase antibodies as well as small-bowel biopsy may be pursued to evaluate for celiac sprue.
• Serologic tests for HIV or hepatitis C should be ordered if the patient has risk factors.
• If there is a significant family history, further genetic testing should be considered.
• Lip biopsy or bone marrow biopsy should be considered if clinical suspicion is high for Sjögren disease, seronegative sicca syndrome, or amyloidosis.
• The serum ACE level has a low sensitivity and specificity; therefore, if sarcoid is suspected clinically, additional confirmatory testing, such as computed tomography of the chest, should be ordered despite a normal ACE value.

HOW DO YOU TREAT SMALL FIBER NEUROPATHY?

Treatment of small fiber neuropathy should target the underlying cause and neuropathic pain. Cause-specific treatment is a key in preventing small fiber neuropathy or slowing its progression.

Glucose control, weight control, and regular exercise

As glucose dysmetabolism is the condition most often associated with small fiber neuropathy (and since individual components of the metabolic syndrome are potential risk factors for it), tight glycemic control and lifestyle modification with diet control, weight control, and regular exercise are of paramount importance in patients with these conditions.

The Diabetic Prevention Program,²⁹ a study in 3,234 people with prediabetes, found that diet and exercise were more effective than metformin (Glucophage) in preventing full-blown diabetes. At an average of 2.8 years of follow-up, the incidence of diabetes was 11.0 cases per 100 patient-years in a group assigned to receive placebo, compared with 7.8 in those assigned to receive metformin (31% lower), and 4.8 (58% lower) in those who were assigned to undergo a lifestyle intervention that included at least 150 minutes of physical activity per week with a weight-loss goal of 7%. Put another way, to prevent one case of diabetes over 3 years, 6.9 patients would have to undergo the lifestyle intervention program, or 13.9 would have to receive metformin. Since impaired glucose tolerance neuropathy may represent the earliest stage of diabetic neuropathy, the neuropathy at this stage may be reversible with lifestyle intervention and improvement of impaired glucose tolerance.

This concept is supported by a 3-year study in 31 people, which showed that lifestyle intervention significantly improved impaired glucose tolerance, reduced the body mass index, and lowered total serum cholesterol levels.³⁰ Changes in these metabolic variables were accompanied by significant improvement of neuropathy as evidenced by significantly increased intraepidermal nerve fiber density, increased foot sweat volume, and decreased neuropathic pain.³⁰

It has also been reported that treatment of sarcoidosis, autoimmune diseases, and celiac disease improved the symptoms of small fiber neuropathy resulting from these conditions.^8,31 Therefore, it is important to identify the cause and treat it to prevent and slow the progression of small fiber neuropathy, and doing so may improve the disease in some mild cases.

Pain management

First-line choices of pain medications are the anticonvulsants gabapentin (Neurontin) and pregabalin (Lyrica), the tricyclic antidepressants amitriptyline (Elavil) and nortriptyline (Aventyl), a 5% lidocaine patch (Lidoderm), and the semisynthetic opioid analgesic tramadol (Ultram). These can be used alone or in combination.

Gabapentin is relatively well tolerated, but drowsiness can occur, especially with high starting doses. We usually start with 300 mg daily and increase it by 300 mg every week up to 1,200 mg three times a day as tolerated. Most patients need 600 to 900 mg three times a day.

Pregabalin is a newer antiepileptic drug, similar to gabapentin but less sedating. It can be started at 75 mg twice a day and gradually increased to 300 mg twice a day as needed. Weight gain and, rarely, swelling of the lower extremities may limit the use of both of these drugs.

Tricyclic antidepressants, such as amitriptyline, nortriptyline, and desipramine (Norpramin), are proven effective in controlling neuropathic pain, although no response with amitriptyline was seen in patients with painful HIV distal sensory neuropathy.³⁴

Lidocaine patch is preferred if the painful area is small. Patients should be instructed to use the patch to cover the painful area 12 hours on and 12 hours off. If it does not provide relief within 1 week, it should be discontinued.

Tramadol is also helpful in treating neuropathic pain. It can be started at 50 mg two to four times a day as needed.

Nonsteroidal anti-inflammatory drugs and selective serotonin reuptake inhibitors are typically less effective than the other drugs mentioned.

Opioids should be reserved for refractory cases, given the potential for addiction, but they are sometimes necessary in patients with disabling pain that does not respond to other drugs.

TENS may be of benefit. The patient controls a pocket-size device that sends electrical signals to leads placed on affected areas.

Alternative therapies for small fiber neuropathy, such as meditation, yoga, and acupuncture, have yet to be studied.

It is also important to explain to patients that the typical course of small fiber neuropathy is relatively benign, as many patients worry about developing weakness and eventually not being able to walk. These concerns and fears can aggravate pain and depression, which can make treatment difficult.

WHAT IS THE PROGNOSIS OF SMALL FIBER NEUROPATHY?

Most patients with small fiber neuropathy experience a slowly progressive course, with symptoms and signs spreading proximally over time.

In one study, only 13% of 124 patients with small fiber neuropathy showed evidence of large-fiber involvement over a 2-year period. ²¹ None went on to develop Charcot joints, foot ulcers, weakness, or sensory ataxia, as is often seen in patients with long-standing or severe large fiber neuropathy. Neuropathic pain worsened in 30% and resolved spontaneously in 11%.²¹

Most patients with small fiber neuropathy require chronic pain management. Again, treatment of the underlying cause is important and can improve the prognosis.

We believe that the overall progression of small fiber neuropathy is slow. A longitudinal study with a follow-up longer than 2 years would be useful to confirm this.

TAKE-HOME POINTS

As the population continues to age and as more patients develop diabetes and the metabolic syndrome, the prevalence of small fiber neuropathy will rise. Patients who present to their primary care physicians with painful, burning feet require a thorough diagnostic evaluation, which may include referral for specialized neurodiagnostic testing. Aggressive cause-specific treatment, lifestyle modification, and pain control are key elements of a team approach to managing small fiber neuropathy.

In many of these patients, the findings on neurologic examination, nerve conduction studies, and electromyography are normal, although some may show signs of mild distal sensory loss on physical examination. The lack of objective findings on routine nerve conduction studies and electromyography may lead many physicians to attribute the symptoms to other disorders such as plantar fasciitis, vascular insufficiency, or degenerative lumbosacral spine disease.

The past 2 decades have seen the development of specialized tests that have greatly facilitated the diagnosis of small fiber neuropathy; these include skin biopsy to evaluate the density of nerve fibers in the epidermis and studies of autonomic nerve function. Common etiologies have been identified for small fiber neuropathy and can be specifically treated, which is critical for controlling progression of the disease. Pain management is becoming easier with more available options but is still quite challenging.

WHAT IS SMALL FIBER NEUROPATHY?

Peripheral nerve fibers can be classified according to size, which correlates with the degree of myelination.

• Large nerve fibers are heavily myelinated and include A-alpha fibers, which mediate motor strength, and A-beta fibers, which mediate vibratory and touch sensation.
• Medium-sized fibers, known as A-gamma fibers, are also myelinated and carry information to muscle spindles.
• Small fibers include myelinated A-delta fibers and unmyelinated C fibers, which innervate skin (somatic fibers) and involuntary muscles, including cardiac and smooth muscles (autonomic fibers). Together, they mediate pain, thermal sensation, and autonomic function.

Small fiber neuropathy results from selective impairment of small myelinated A-delta and unmyelinated C fibers.

Sensory symptoms: Pain, burning, tingling, numbness

Damage to or loss of small somatic nerve fibers results in pain, burning, tingling, or numbness that typically affects the limbs in a distal-to-proximal gradient. In rare cases, small fiber neuropathy follows a non-length-dependent distribution in which symptoms may be manifested predominantly in the arms, face, or trunk.

Symptoms may be mild initially, with some patients complaining of vague discomfort in one or both feet similar to the sensation of a sock gathering at the end of a shoe. Others report a wooden quality in their feet, numbness in their toes, or a feeling as if they are walking on pebbles, sand, or golf balls. The most bothersome and fairly typical symptom is burning pain in the feet that extends proximally in a stocking-glove distribution and is often accompanied by stabbing or aching pains, electric shock-like or pins-and-needles sensations, or cramping of the feet and calves.

Symptoms are usually worse at night and often affect sleep. Some patients say that their feet have become so exquisitely tender that they cannot bear having the bed sheets touch them, and so they sleep with their feet uncovered. A small number of patients do not have pain but report a feeling of tightness and swelling in their feet (even though the feet appear normal).

Examination often reveals allodynia (perception of nonpainful stimuli as being painful), hyperalgesia (perception of painful stimuli as being more painful than expected), or reduced pinprick and thermal sensation in the affected area. Vibratory sensation can be mildly reduced at the toes. Motor strength, tendon reflexes, and proprioception, however, are preserved because they are functions of large nerve fibers.

Autonomic symptoms

When autonomic fibers are affected, patients may experience dry eyes, dry mouth, orthostatic dizziness, constipation, bladder incontinence, sexual dysfunction, trouble sweating, or red or white skin discoloration.² Examination may show orthostatic hypotension and skin changes. The skin over the affected area may appear atrophic, dry, shiny, discolored, or mildly edematous as the result of sudomotor and vasomotor abnormalities.

WHAT CAUSES SMALL FIBER NEUROPATHY?

Small fiber neuropathy has been associated with many medical conditions, including glucose dysmetabolism,³ connective tissue disease,^4,5 dysthyroidism,⁶ vitamin B₁₂ deficiency, paraproteinemia, human immunodeficiency virus (HIV) infection,⁷ hepatitis C virus infection, celiac disease,⁸ restless legs syndrome,⁹ neurotoxic drug exposure, hereditary diseases, and paraneoplastic syndrome. While most of these conditions cause a length-dependent small fiber neuropathy, others (Sjögren disease, celiac disease, and paraneoplastic syndrome) can cause a form of small fiber neuropathy that is not length-dependent.^4,8,10

Diabetes and prediabetes

Glucose dysmetabolism, including diabetes and prediabetes with impaired oral glucose tolerance (a glucose level 140–199 mg/dL 2 hours after a 75-g oral dextrose load), is the most common identifiable associated condition, present in about one-third of patients with painful sensory neuropathy¹¹ and in nearly half of those with otherwise idiopathic small fiber neuropathy.^12–14

Research findings strongly suggest that even prediabetes is a risk factor for small fiber neuropathy, and that so-called “impaired glucose tolerance neuropathy” may represent the earliest stage of diabetic neuropathy. Several recent studies have found a high prevalence of impaired glucose tolerance in patients with sensory peripheral neuropathy,^12–14 with a rate of up to 42% in cases initially thought to be idiopathic¹⁴ compared with 14% in the general population.¹⁵ Also, a dose-response relationship between the severity of hyperglycemia and the degree of neuropathy was demonstrated in one study, in which patients with impaired glucose tolerance more often had small fiber neuropathy, whereas those with diabetes more often had polyneuropathy involving both small and large fibers.¹⁴ And studies in animals and cell cultures have shown that intermittent hyperglycemia, which can be seen in patients with impaired glucose tolerance, caused sensory neuron and nerve fiber damage and increased spontaneous C-fiber firing, resulting in neuropathic pain.^8,16,17

Metabolic syndrome

Insulin resistance with prediabetes and diabetes is a part of the metabolic syndrome, which also consists of hypertension, hyperlipidemia, and obesity. The individual components of the metabolic syndrome have been implicated as risk factors not only for cardiovascular and cerebrovascular disease but also for small fiber neuropathy.

One study in 548 patients with type 2 diabetes showed that those with the metabolic syndrome were twice as likely to have neuropathy as those without.¹⁸ Another study showed that in 1,200 patients with type 1 diabetes without neuropathy at baseline, hypertension, hyperlipidemia, and increased body mass index were each independently associated with a higher risk of developing neuropathy.¹⁹

A recent study of 219 patients with idiopathic distal symmetrical peripheral neuropathy and 175 diabetic patients without neuropathy found a higher prevalence of metabolic syndrome in patients with neuropathy than in normal populations. The prevalence of dyslipidemia (high levels of total and low-density lipoprotein cholesterol and triglycerides and low levels of high-density lipoprotein cholesterol), but not hypertension or obesity, was higher in patients with neuropathy than in patients with diabetes but no neuropathy.²⁰ The findings linked dyslipidemia to neuropathy and showed the need for further studies of the potential pathogenic role of dyslipidemia in neuropathy.

Hereditary causes

Hereditary causes of small fiber neuropathy are rare and include Fabry disease, Tangier disease, hereditary sensory autonomic neuropathy, and hereditary amyloidosis.

HOW DO YOU EVALUATE PATIENTS WITH SUSPECTED SMALL FIBER NEUROPATHY?

A thorough history should be taken to obtain details regarding onset and features of neuropathy symptoms, exacerbating factors, and progression. It is also important to ascertain whether the patient has any associated conditions as mentioned above, a family history of neuropathy, risk factors for HIV or hepatitis C virus infection, or a history of neurotoxic drug exposure.

Clinical suspicion of small fiber neuropathy should be high if a patient presents with predominant small fiber symptoms and signs with preserved large fiber functions.

Nerve conduction studies and electromyography

For diagnostic testing, routine nerve conduction studies and electromyography assess the function of large nerve fibers only and are thus normal in small fiber neuropathy. These tests should still be ordered to rule out subclinical involvement of large fibers, which may affect the diagnostic evaluation, prognosis, and treatment plan. However, if the results of these tests are normal, specialized studies are needed to evaluate small fibers.

Although several tests are available to evaluate somatic and autonomic small fibers, the two that have the highest diagnostic efficiency for small fiber neuropathy and that are used most often are skin biopsy, to evaluate intraepidermal nerve fiber density, and quantitative sudomotor axon reflex testing (QSART), to assess sudomotor autonomic function.^21–23

Skin biopsy

Skin biopsy is a minimally invasive procedure in which 3-mm-diameter punch biopsy specimens are taken from the distal leg, distal thigh, and proximal thigh of one lower limb. The procedure takes only 10 to 15 minutes.

Biopsy specimens are immunostained using an antibody against protein gene product 9.5, which is a panaxonal marker. Small nerve fibers in the epidermis are counted under a microscope, and intraepithelial nerve fiber densities are calculated and compared with established normative values. The diagnosis of small fiber neuropathy can be established if the intraepidermal nerve fiber density is lower than normal (Figure 1). Nerve fiber density may be normal in the early stage of small fiber neuropathy, but in this setting skin biopsy often shows abnormal morphologic changes in the small fibers, especially large swellings,²⁴ and repeat biopsy in 6 to 12 months may be considered.

The diagnostic efficiency of skin biopsy is about 88%.^21,23 For diagnosing small fiber neuropathy, it is more sensitive than quantitative sensory testing^21,25 and more sensitive and less invasive than sural nerve biopsy.²⁶ Intraepidermal nerve fiber density also correlates well with a variety of measures of severity of HIV distal sensory neuropathy and thus may be used to measure the severity and treatment response of small fiber neuropathy.²⁷

QSART is an autonomic study that measures sweat output in response to acetylcholine, which reflects the function of postganglionic sympathetic unmyelinated sudomotor nerve fibers. Electrodes are placed on the arms and legs to record the volume of sweat produced by acetylcholine iontophoresis, in which a mild electrical stimulation on the skin allows acetylcholine to stimulate the sweat glands. The output is compared with normative values.

One prospective study showed that 67 (72.8%) of 92 patients with painful feet had abnormal results on QSART, ie, low sweat output.²⁸ A retrospective study found that 77 (62%) of 125 patients with clinical features of distal small fiber neuropathy had a length-dependent pattern of QSART abnormalities.²² QSART abnormalities were detected in some patients without autonomic symptoms.

If these tests are not available

Skin biopsy and QSART are objective, reproducible, sensitive, and complementary in diagnosing small fiber neuropathy. One or both can be ordered, depending on whether the patient has somatic symptoms, autonomic symptoms, or both. However, these two tests are not widely available. Only a few laboratories in the country can process skin biopsy specimens to evaluate intraepidermal nerve fiber density. Nevertheless, it is easy to learn the skin punch biopsy procedure, and primary care physicians and neurologists can perform it after appropriate training. (A concern is avoiding damage to the epidermis.) They can then send specimens to one of the cutaneous nerve laboratories (but not to a routine reference laboratory).

A special technique, including unique fixative and cryoprotectant, is used to fix and process the biopsy specimens, because routine techniques for processing dermatologic punch biopsy specimens often result in lower intraepidermal nerve fiber densities. Therefore, it is very important to contact the laboratory regarding fixative and processing before performing a biopsy.

QSART requires specialized equipment and must be performed on site. In addition, the test is very sensitive to drugs that can affect sweating, such as antihistamines and antidepressants, and such drugs must be discontinued 48 hours before the study.

Basic laboratory tests to find the cause

Once the diagnosis of small fiber neuropathy is established, the next important step is to order a battery of laboratory tests to search for an underlying cause. The tests should include the following:

• Complete blood cell count
• Comprehensive metabolic panel
• Lipid panel
• Erythrocyte sedimentation rate
• Thyroid-stimulating hormone level
• Free thyroxine (T4) level
• Antinuclear antibody
• Extractable nuclear antigens
• Angiotensin-converting enzyme (ACE) level
• Serum and urine immunofixation tests
• Vitamin B₁₂ level
• 2-hour oral glucose tolerance test.

Oral glucose tolerance testing is much more sensitive than measuring the hemoglobin A_1c and fasting glucose levels in detecting diabetes and prediabetes. These two conditions were detected by oral glucose tolerance testing in more than 50% of patients with otherwise idiopathic sensory-predominant peripheral neuropathy and normal hemoglobin A_1c and fasting glucose levels.^13,14 Therefore, every patient with small fiber neuropathy without a known history of diabetes or prediabetes should have an oral glucose tolerance test.

Special laboratory tests in special cases

• If there is a history of gastrointestinal symptoms or herpetiform-like rash, then testing for gliadin antibody and tissue transglutaminase antibodies as well as small-bowel biopsy may be pursued to evaluate for celiac sprue.
• Serologic tests for HIV or hepatitis C should be ordered if the patient has risk factors.
• If there is a significant family history, further genetic testing should be considered.
• Lip biopsy or bone marrow biopsy should be considered if clinical suspicion is high for Sjögren disease, seronegative sicca syndrome, or amyloidosis.
• The serum ACE level has a low sensitivity and specificity; therefore, if sarcoid is suspected clinically, additional confirmatory testing, such as computed tomography of the chest, should be ordered despite a normal ACE value.

HOW DO YOU TREAT SMALL FIBER NEUROPATHY?

Treatment of small fiber neuropathy should target the underlying cause and neuropathic pain. Cause-specific treatment is a key in preventing small fiber neuropathy or slowing its progression.

Glucose control, weight control, and regular exercise

As glucose dysmetabolism is the condition most often associated with small fiber neuropathy (and since individual components of the metabolic syndrome are potential risk factors for it), tight glycemic control and lifestyle modification with diet control, weight control, and regular exercise are of paramount importance in patients with these conditions.

The Diabetic Prevention Program,²⁹ a study in 3,234 people with prediabetes, found that diet and exercise were more effective than metformin (Glucophage) in preventing full-blown diabetes. At an average of 2.8 years of follow-up, the incidence of diabetes was 11.0 cases per 100 patient-years in a group assigned to receive placebo, compared with 7.8 in those assigned to receive metformin (31% lower), and 4.8 (58% lower) in those who were assigned to undergo a lifestyle intervention that included at least 150 minutes of physical activity per week with a weight-loss goal of 7%. Put another way, to prevent one case of diabetes over 3 years, 6.9 patients would have to undergo the lifestyle intervention program, or 13.9 would have to receive metformin. Since impaired glucose tolerance neuropathy may represent the earliest stage of diabetic neuropathy, the neuropathy at this stage may be reversible with lifestyle intervention and improvement of impaired glucose tolerance.

This concept is supported by a 3-year study in 31 people, which showed that lifestyle intervention significantly improved impaired glucose tolerance, reduced the body mass index, and lowered total serum cholesterol levels.³⁰ Changes in these metabolic variables were accompanied by significant improvement of neuropathy as evidenced by significantly increased intraepidermal nerve fiber density, increased foot sweat volume, and decreased neuropathic pain.³⁰

It has also been reported that treatment of sarcoidosis, autoimmune diseases, and celiac disease improved the symptoms of small fiber neuropathy resulting from these conditions.^8,31 Therefore, it is important to identify the cause and treat it to prevent and slow the progression of small fiber neuropathy, and doing so may improve the disease in some mild cases.

Pain management

First-line choices of pain medications are the anticonvulsants gabapentin (Neurontin) and pregabalin (Lyrica), the tricyclic antidepressants amitriptyline (Elavil) and nortriptyline (Aventyl), a 5% lidocaine patch (Lidoderm), and the semisynthetic opioid analgesic tramadol (Ultram). These can be used alone or in combination.

Gabapentin is relatively well tolerated, but drowsiness can occur, especially with high starting doses. We usually start with 300 mg daily and increase it by 300 mg every week up to 1,200 mg three times a day as tolerated. Most patients need 600 to 900 mg three times a day.

Pregabalin is a newer antiepileptic drug, similar to gabapentin but less sedating. It can be started at 75 mg twice a day and gradually increased to 300 mg twice a day as needed. Weight gain and, rarely, swelling of the lower extremities may limit the use of both of these drugs.

Tricyclic antidepressants, such as amitriptyline, nortriptyline, and desipramine (Norpramin), are proven effective in controlling neuropathic pain, although no response with amitriptyline was seen in patients with painful HIV distal sensory neuropathy.³⁴

Lidocaine patch is preferred if the painful area is small. Patients should be instructed to use the patch to cover the painful area 12 hours on and 12 hours off. If it does not provide relief within 1 week, it should be discontinued.

Tramadol is also helpful in treating neuropathic pain. It can be started at 50 mg two to four times a day as needed.

Nonsteroidal anti-inflammatory drugs and selective serotonin reuptake inhibitors are typically less effective than the other drugs mentioned.

Opioids should be reserved for refractory cases, given the potential for addiction, but they are sometimes necessary in patients with disabling pain that does not respond to other drugs.

TENS may be of benefit. The patient controls a pocket-size device that sends electrical signals to leads placed on affected areas.

Alternative therapies for small fiber neuropathy, such as meditation, yoga, and acupuncture, have yet to be studied.

It is also important to explain to patients that the typical course of small fiber neuropathy is relatively benign, as many patients worry about developing weakness and eventually not being able to walk. These concerns and fears can aggravate pain and depression, which can make treatment difficult.

WHAT IS THE PROGNOSIS OF SMALL FIBER NEUROPATHY?

Most patients with small fiber neuropathy experience a slowly progressive course, with symptoms and signs spreading proximally over time.

In one study, only 13% of 124 patients with small fiber neuropathy showed evidence of large-fiber involvement over a 2-year period. ²¹ None went on to develop Charcot joints, foot ulcers, weakness, or sensory ataxia, as is often seen in patients with long-standing or severe large fiber neuropathy. Neuropathic pain worsened in 30% and resolved spontaneously in 11%.²¹

Most patients with small fiber neuropathy require chronic pain management. Again, treatment of the underlying cause is important and can improve the prognosis.

We believe that the overall progression of small fiber neuropathy is slow. A longitudinal study with a follow-up longer than 2 years would be useful to confirm this.

TAKE-HOME POINTS

As the population continues to age and as more patients develop diabetes and the metabolic syndrome, the prevalence of small fiber neuropathy will rise. Patients who present to their primary care physicians with painful, burning feet require a thorough diagnostic evaluation, which may include referral for specialized neurodiagnostic testing. Aggressive cause-specific treatment, lifestyle modification, and pain control are key elements of a team approach to managing small fiber neuropathy.

Mr. B., an 82-year-old retired accountant with hypertension, was diagnosed with early Alzheimer disease 6 years ago. He now needs supervision with bathing and dressing and no longer consistently recognizes family members. You are seeing him in the office today after a hospitalization for aspiration pneumonia, his second in the past 6 months.

See related editorial

In the hospital, a brain scan showed that atrophy had progressed and white-matter disease was more extensive than 3 years earlier. A barium swallow study showed esophageal dysmotility and aspiration. He was prescribed a “dysphagia diet,”¹ which he dislikes.

Since returning home, he has been disoriented, he has been wandering about the house, and he has fallen several times. He has lost 10 pounds in 6 months. Because of his confusion, his wife cannot take him out, and she is exhausted caring for him.

Reviewing his medical record, you note that 10 years ago, Mr. B. completed a living will and designated his wife as his proxy decision-maker via a medical power of attorney document.

PLANNING IS OFTEN NEGLECTED

Many clinicians and older patients feel a strong need to document, in advance, the patient’s wishes regarding medical care in the event the patient becomes seriously ill and unable to participate in treatment decisions. Professional societies such as the American Geriatrics Society promote advance care planning,² and some indices of the quality of medical care include whether advance directives have been discussed and completed.³

Yet, despite the high profile of advance care planning,⁴ few patients actually fill out advance directives,⁵ with completion rates that vary widely,^6–8 sometimes by ethnicity and sex.^9,10 Furthermore, in a crisis, these directives are seldom followed.¹¹

In this paper, we recommend an approach to advance care planning for older adults that redirects the focus from “signing away” interventions such as dialysis, mechanical ventilation, and tube feeding. Instead, the focus is on the goals of care. We also advocate naming a surrogate decision-maker, since the medical power of attorney is more flexible and more widely applicable than the living will.

START BY LISTENING

A change in function resulting from disease progression, hospitalization, trauma, or other reasons is an ideal opportunity to introduce the process of advance care planning.

The first step is to find out how well the patient and family understand the patient’s relevant medical conditions, and what their expectations, hopes, and concerns are. This listening phase can provide insight into the patient’s values and goals and how much the patient and family want to engage in these discussions.

In matters of health behavior (such as advance care planning), people change only when they are ready to change.^12,13 Thus, we advise physicians to defer extensive discussions of values and goals of care until patients and families are ready to listen, hear, and talk about these topics (often, after a change for the worse in prognosis).

And it is a process. Advance care directives are most likely to be set up and followed if the patient and doctor discuss this issue during multiple visits, rather than if the physician merely hands the patient a packet of forms and information.^14–16

CASE CONTINUED: A PEG TUBE REFUSED

Mrs. B. says that Mr. B. is in good health except for his memory: he does not have a serious condition such as diabetes, heart failure, or cancer. While Mr. B. was in the hospital, the hospitalist recommended placing a percutaneous endoscopic gastrostomy (PEG) tube, but Mrs. B. declined the recommendation because her husband had a living will that specified “no artificially or technologically supplied nutrition or hydration.”

At this point, Mrs. B. begins to cry. She has slept poorly because of his wandering. Also, her two daughters do not support her refusal of the PEG tube.

Comment. This brief conversation illuminates knowledge deficits in Mrs. B.’s understanding of Alzheimer disease and the circumstances in which the living will applies. Although one could argue that Mr. B.’s Alzheimer disease has advanced to the point that he is likely to die of a complication of that condition, he is not likely to die in the near future. If he is not considered by law and his physician to be terminally ill or permanently unconscious, a living will likely does not offer guidance about artificial feeding.

LIMITATIONS OF A LIVING WILL

A living will, a commonly used advance directive, states that the patient does not wish to receive life-sustaining treatment in the event that he or she suffers an incurable, irreversible disease and cannot give informed consent, and it often lists specific treatments that the patient does not want. However, we believe that approaching the patient with a list of life-sustaining measures to accept or reject, before discussing goals of care and prognosis, puts the cart before the horse. This approach threatens to distract from the need to ascertain values and offer appropriate care. Additionally, a living will is active only within a very limited scenario and does not address relatively routine but important decisions in a person’s care.

All ‘terminal illness’ isn’t the same

A living will goes into effect only if the patient either enters a permanent vegetative state following an event such as cardiac arrest or severe brain trauma, or is diagnosed with a terminal illness such as metastatic cancer, and lacks decision-making capacity.

But what is terminal illness? The definition differs from state to state, but it is generally defined as an irreversible condition leading to death in a relatively short time. The time may not be specified, as in Florida statute 765. In contrast, Ohio Revised Code 2133.01(AA) uses the phrase “relatively short,” while other states specify a time, such as within 6 months (Texas Health and Safety Code 166.002). The Medicare hospice benefit also carries a short time limit, usually less than 6 months.

The middle panel in Figure 1 depicts a more typical decline from serial organ insults such as stroke followed by infection from aspiration or followed by falls. Older adults with dementia or with multiple progressive diseases such as heart failure, diabetes, hypertension, or cancer decline in a trajectory such as in the bottom panel of Figure 1.

A living will might not be activated in the latter two scenarios until years into the condition because the patient would not be considered terminally ill—by state law, by the health care provider, or even by the patient.

The living will does not address routine interventions

In most states, living wills address only life-sustaining treatments such as dialysis, mechanical ventilation, and medically supplied nutrition and hydration. Living wills do not address relatively common diseases in older adults that could cause severe debility, such as a major stroke or advanced dementia.

If an older patient has dementia, a living will is unlikely to provide guidance about interventions such as intubation to get through an episode of potentially reversible respiratory failure, a feeding tube to correct weight loss, or cardiac catheterization or bypass surgery to treat angina. Yet these important decisions often arise as function declines and comorbidities progress.

Patients may change their minds

Many older adults are reluctant to sign documents to “micromanage” their future care if they should become ill.¹⁹ Many people change their mind as the situation changes.^11,20,21 Although few claim they would want burdensome interventions if they had dementia²² or if their prognosis were poor,²³ patients may tolerate more burdensome interventions if they are already receiving treatments for chronic illnesses such as end-stage renal disease.²⁴

Thus, a living will may help if unexpected trauma occurs in a healthy person, but not so much if chronic illness progresses over a period of years.

Advance directives may not be honored

Even if completed, written advance directives may not be followed, for a variety of reasons. Physicians may not know the patient has a living will, and fewer than one-third of people who actually complete an advance directive have discussed its content with a physician.²⁵ The people named as surrogate decision-makers may not know the patient’s wishes. Family members may disagree with the goals and plan of care and may interfere with implementation of the advance care plan. A patient may see multiple physicians at different institutions who may not communicate with each other about the patient’s wishes. Also, physicians and patients may interpret terms such as “terminally ill” differently, making it difficult to translate the documents into an action plan.

CASE CONTINUED: RELIEVING CAREGIVER STRESS

Returning to Mr. B., your first goal is to address care issues, including caregiver stress. Skilled services in the home are appropriate for him at this time (and Medicare will pay for them) because he is still homebound. These services could include physical therapy, occupational therapy, and speech (swallowing) therapy. A home care agency may also provide an aide for a few weeks to assist with bathing and other personal needs.

You strongly recommend that the family (including both daughters) participate in the Alzheimer’s Association educational programs. You recommend that Mrs. B. locate an adult day care program now so that when Mr. B. completes his home therapy course and is no longer homebound, he may attend. Day care would provide a therapeutic environment for him and respite for her.

You request that the home care agency provide a social worker to advise her on community resources. Meta-analysis suggests that structured, multicomponent interventions with caregivers of demented patients reduce several types of caregiver burden and delay institutionalization.²⁶

He improves with conservative measures

Three weeks later, Mr. B. is sleeping better and has stopped wandering. However, he dislikes the thickened liquids required by the dysphagia diet and has lost another 2 pounds. If his beverages are not thickened, he coughs profusely when he swallows. His daughters are still pressuring Mrs. B. for a PEG tube; one of them has angrily asserted that the doctors are going to allow her father to die.

You explain the burdens of PEG tubes: surgical risks, continued aspiration, disrupted bowel habits, the risk of the tube being accidentally or intentionally dislodged by the patient, and special binders (which may be uncomfortable) or restraints (which may cause further functional decline) that may be necessary to prevent this complication.

You request that the speech therapist work with the patient more aggressively in the use of swallowing techniques such as the chin tuck, which may be at least as effective as thickeners in preventing both aspiration pneumonia and dehydration.²⁷ The therapist will need to include Mrs. B. in these sessions, since she will be Mr. B.’s coach at mealtime.

With more aggressive speech therapy, the patient’s weight stabilizes over the next 4 weeks. He is in day care 3 days a week, and Mrs. B. is more rested and relaxed.

Cardiopulmonary resuscitation

You continue the advance care planning discussion and suggest that if Mr. B. aspirates, is hospitalized again, and declines further care, it would be helpful to delineate instructions for resuscitation. Right now, although his Alzheimer disease is advanced, he is not clearly terminal. Thus, his living will does not strictly apply and provides limited guidance about intubation, cardiopulmonary resuscitation (CPR), or medically supplied nutrition and hydration. However, because Mrs. B. is his agent in the medical power of attorney, this document enables her to make a wide spectrum of treatment decisions on his behalf.

Mrs. B. asks about her husband’s prognosis and why CPR would not be helpful.

Comment. Further discussion with her could be guided by an estimate of Mr. B.’s prognosis. Function-based tools^28,29 may also be useful. For example,^28,30 an 80-year-old man with high functional status might have a life expectancy of more than 10 years. Mr. B., with multiple medical problems and declining function, would have an estimated life expectancy of approximately 3 years. Even without specifically categorizing function, impaired cognition by itself predicted a shorter life expectancy in population-based studies.^31,32

Regarding CPR, patients and families may overestimate successful outcomes. A recent study³³ of 10 years of outcomes of in-hospital cardiac arrest found that only 6.6% of patients survived to discharge. The average age of the survivors was 59 years, and fewer than half of them survived 3 years after cardiac arrest. In eight studies of CPR outcomes in nursing homes,³⁴ three studies had no survivors, and all but one study had a survival rate below 5%.

PROVIDING APPROPRIATE CARE, NOT LIMITING TREATMENTS

In the case of Mr. B., as in many situations encountered with older patients, written advance directives provide little help or guidance. Instead, we recommend a model of advance care planning that takes place during multiple office visits over time, and that maintains a focus on providing appropriate care rather than on limiting life-sustaining treatments. We recommend providing estimates of prognosis and CPR outcomes when the family appeares ready to hear them. This approach should result in a care-oriented process while moving the family towards decisions regarding artificial feeding and CPR.

All patients, particularly those unwilling or unable to participate in advance care planning, are encouraged to identify one or more surrogate decision-makers and articulate how much flexibility that person should be given in important health care decisions. The medical power of attorney can be activated any time the patient lacks decision-making capacity and deactivated when decision-making capacity returns.^38,39

As in the case of Mr. B., a tailored approach to advance care planning requires clinicians to estimate life expectancy (more than 5 years, less than 5 years, or less than 1 year) and to determine the patient’s and the family’s readiness to focus on a values-oriented and goal-oriented care plan. Some patients are not receptive to advance care planning, and clinical time and effort are optimized by providing the right amount of information to patients when they are ready to receive it.

Figure 2 is the algorithm for older patients who are expected to live at least 5 years, ie, who are relatively healthy and functional. Patients with little or no interest in advance care planning can be asked about it annually, or sooner if their medical condition changes. Patients with limited interest can be given written information, specifically living will and medical power of attorney documents recognized in their state. Patients more open to advance care planning can be offered a values history form (Table 1), Web sites, and educational materials, with a plan to discuss them at future appointments.

Periodic reevaluation of values and goals of care is important. Patients may assert that particular interventions (eg, a PEG tube or dialysis) are “worse than death” when they are healthy, but they may change their views over time.²¹ Additionally, although a recent hospitalization or a decline in function may predispose patients to want to limit life-sustaining treatments, they may return to their earlier values and wishes a few months later, particularly if their medical condition stabilizes. ²⁰ Values and decisions should be reassessed not only when medical conditions deteriorate, but also when they improve.

For chronically ill patients

Caregiver stress is important to identify and address, since caregivers often neglect themselves.^40–42

For terminally ill patients

In this situation, patients and families need information about community resources that can assist them in the home. Some older adults with cognitive impairment may be exploited or neglect themselves, and referral to an adult protective services agency may be needed.

Treatment burden, particularly due to multiple prescribed medications, may be high and should be reassessed in light of the goals of treatment. Polypharmacy reduction is especially important at this stage in the illness, since the goals of care may be different than when the medications were prescribed.

Physical or psychosocial symptoms may be the cue to bring up the topic of palliative care. If the patient is expected to live less than 6 months, hospice referral is appropriate. With either palliative care or hospice, the focus of attention shifts explicitly from curing the disease to managing symptoms, and from the patient to the patient-family dyad. Interventions such as CPR and ventilatory support should be discussed and information from Table 2 provided to the patient and family.

Complete advance care planning incorporates taking a values history, estimating life expectancy, determining physical, psychosocial and spiritual needs, clarifying treatment goals, and estimating manageable treatment burden. Offering statistics on CPR and providing state-specific living will and medical power of attorney documents are important but are only one facet of effective advance care planning. In fact, shifting the emphasis of advance care planning from statistics and forms to values and goals of care may help in developing a more comprehensive care plan.

Goals of care range from curing the disease (with aggressive therapy, which may be burdensome) to simply improving function or decreasing pain. In the latter case, one may be able to discontinue some of the patient’s drugs, utilize medical and community resources more effectively, and better meet the patient’s needs.

Woven through all these discussions should be reassurance that the plan can be revisited and possibly revised, and that the physician will be there to help with those decisions.

Episodic, staged advance care planning is appropriate not only in the office but also in other settings such as assisted living and nursing facilities.

In the hospital, however, a different approach is needed, since patients are usually admitted because of an acute illness or sudden functional decline, or both. Decisions about technological interventions such as CPR, mechanical ventilation, or dialysis may be needed urgently. Often, patients are unable to provide guidance to physicians during acute illness because of delirium and other impediments. Developing a plan for care in the hospital may require urgent family meetings. However, if a surrogate decision-maker is in place, and if the patient has already participated in some form of advance care planning as an outpatient, the values and goals of care previously identified can contribute to decision-making during hospitalization.

As mentioned above, fragmentation of health care across providers and health care systems may limit the effectiveness of office-based advance care planning. It may be reasonable to train office staff to place advance care planning documentation in easily accessible sections of the patient’s medical record and to forward these to specialists involved in a patient’s care.

The patient and family should be encouraged and empowered to help with this process and should have updated advance care planning documentation readily available. In some states, comprehensive medical order sets, especially for end-of-life care, are portable across care settings and address CPR, medically supplied nutrition, hospital transfer, and antibiotic treatment.⁴³

Research suggests that health care systems are more likely to comply with patients’ end-of-life preferences when portable medical order forms are developed and disseminated.^44–44 Ultimately, major changes in health care delivery, including universal electronic health records, may be needed to implement and communicate patients’ advance care planning preferences across settings.

Mr. B., an 82-year-old retired accountant with hypertension, was diagnosed with early Alzheimer disease 6 years ago. He now needs supervision with bathing and dressing and no longer consistently recognizes family members. You are seeing him in the office today after a hospitalization for aspiration pneumonia, his second in the past 6 months.

See related editorial

In the hospital, a brain scan showed that atrophy had progressed and white-matter disease was more extensive than 3 years earlier. A barium swallow study showed esophageal dysmotility and aspiration. He was prescribed a “dysphagia diet,”¹ which he dislikes.

Since returning home, he has been disoriented, he has been wandering about the house, and he has fallen several times. He has lost 10 pounds in 6 months. Because of his confusion, his wife cannot take him out, and she is exhausted caring for him.

Reviewing his medical record, you note that 10 years ago, Mr. B. completed a living will and designated his wife as his proxy decision-maker via a medical power of attorney document.

PLANNING IS OFTEN NEGLECTED

Many clinicians and older patients feel a strong need to document, in advance, the patient’s wishes regarding medical care in the event the patient becomes seriously ill and unable to participate in treatment decisions. Professional societies such as the American Geriatrics Society promote advance care planning,² and some indices of the quality of medical care include whether advance directives have been discussed and completed.³

Yet, despite the high profile of advance care planning,⁴ few patients actually fill out advance directives,⁵ with completion rates that vary widely,^6–8 sometimes by ethnicity and sex.^9,10 Furthermore, in a crisis, these directives are seldom followed.¹¹

In this paper, we recommend an approach to advance care planning for older adults that redirects the focus from “signing away” interventions such as dialysis, mechanical ventilation, and tube feeding. Instead, the focus is on the goals of care. We also advocate naming a surrogate decision-maker, since the medical power of attorney is more flexible and more widely applicable than the living will.

START BY LISTENING

A change in function resulting from disease progression, hospitalization, trauma, or other reasons is an ideal opportunity to introduce the process of advance care planning.

The first step is to find out how well the patient and family understand the patient’s relevant medical conditions, and what their expectations, hopes, and concerns are. This listening phase can provide insight into the patient’s values and goals and how much the patient and family want to engage in these discussions.

In matters of health behavior (such as advance care planning), people change only when they are ready to change.^12,13 Thus, we advise physicians to defer extensive discussions of values and goals of care until patients and families are ready to listen, hear, and talk about these topics (often, after a change for the worse in prognosis).

And it is a process. Advance care directives are most likely to be set up and followed if the patient and doctor discuss this issue during multiple visits, rather than if the physician merely hands the patient a packet of forms and information.^14–16

CASE CONTINUED: A PEG TUBE REFUSED

Mrs. B. says that Mr. B. is in good health except for his memory: he does not have a serious condition such as diabetes, heart failure, or cancer. While Mr. B. was in the hospital, the hospitalist recommended placing a percutaneous endoscopic gastrostomy (PEG) tube, but Mrs. B. declined the recommendation because her husband had a living will that specified “no artificially or technologically supplied nutrition or hydration.”

At this point, Mrs. B. begins to cry. She has slept poorly because of his wandering. Also, her two daughters do not support her refusal of the PEG tube.

Comment. This brief conversation illuminates knowledge deficits in Mrs. B.’s understanding of Alzheimer disease and the circumstances in which the living will applies. Although one could argue that Mr. B.’s Alzheimer disease has advanced to the point that he is likely to die of a complication of that condition, he is not likely to die in the near future. If he is not considered by law and his physician to be terminally ill or permanently unconscious, a living will likely does not offer guidance about artificial feeding.

LIMITATIONS OF A LIVING WILL

A living will, a commonly used advance directive, states that the patient does not wish to receive life-sustaining treatment in the event that he or she suffers an incurable, irreversible disease and cannot give informed consent, and it often lists specific treatments that the patient does not want. However, we believe that approaching the patient with a list of life-sustaining measures to accept or reject, before discussing goals of care and prognosis, puts the cart before the horse. This approach threatens to distract from the need to ascertain values and offer appropriate care. Additionally, a living will is active only within a very limited scenario and does not address relatively routine but important decisions in a person’s care.

All ‘terminal illness’ isn’t the same

A living will goes into effect only if the patient either enters a permanent vegetative state following an event such as cardiac arrest or severe brain trauma, or is diagnosed with a terminal illness such as metastatic cancer, and lacks decision-making capacity.

But what is terminal illness? The definition differs from state to state, but it is generally defined as an irreversible condition leading to death in a relatively short time. The time may not be specified, as in Florida statute 765. In contrast, Ohio Revised Code 2133.01(AA) uses the phrase “relatively short,” while other states specify a time, such as within 6 months (Texas Health and Safety Code 166.002). The Medicare hospice benefit also carries a short time limit, usually less than 6 months.

The middle panel in Figure 1 depicts a more typical decline from serial organ insults such as stroke followed by infection from aspiration or followed by falls. Older adults with dementia or with multiple progressive diseases such as heart failure, diabetes, hypertension, or cancer decline in a trajectory such as in the bottom panel of Figure 1.

A living will might not be activated in the latter two scenarios until years into the condition because the patient would not be considered terminally ill—by state law, by the health care provider, or even by the patient.

The living will does not address routine interventions

In most states, living wills address only life-sustaining treatments such as dialysis, mechanical ventilation, and medically supplied nutrition and hydration. Living wills do not address relatively common diseases in older adults that could cause severe debility, such as a major stroke or advanced dementia.

If an older patient has dementia, a living will is unlikely to provide guidance about interventions such as intubation to get through an episode of potentially reversible respiratory failure, a feeding tube to correct weight loss, or cardiac catheterization or bypass surgery to treat angina. Yet these important decisions often arise as function declines and comorbidities progress.

Patients may change their minds

Many older adults are reluctant to sign documents to “micromanage” their future care if they should become ill.¹⁹ Many people change their mind as the situation changes.^11,20,21 Although few claim they would want burdensome interventions if they had dementia²² or if their prognosis were poor,²³ patients may tolerate more burdensome interventions if they are already receiving treatments for chronic illnesses such as end-stage renal disease.²⁴

Thus, a living will may help if unexpected trauma occurs in a healthy person, but not so much if chronic illness progresses over a period of years.

Advance directives may not be honored

Even if completed, written advance directives may not be followed, for a variety of reasons. Physicians may not know the patient has a living will, and fewer than one-third of people who actually complete an advance directive have discussed its content with a physician.²⁵ The people named as surrogate decision-makers may not know the patient’s wishes. Family members may disagree with the goals and plan of care and may interfere with implementation of the advance care plan. A patient may see multiple physicians at different institutions who may not communicate with each other about the patient’s wishes. Also, physicians and patients may interpret terms such as “terminally ill” differently, making it difficult to translate the documents into an action plan.

CASE CONTINUED: RELIEVING CAREGIVER STRESS

Returning to Mr. B., your first goal is to address care issues, including caregiver stress. Skilled services in the home are appropriate for him at this time (and Medicare will pay for them) because he is still homebound. These services could include physical therapy, occupational therapy, and speech (swallowing) therapy. A home care agency may also provide an aide for a few weeks to assist with bathing and other personal needs.

You strongly recommend that the family (including both daughters) participate in the Alzheimer’s Association educational programs. You recommend that Mrs. B. locate an adult day care program now so that when Mr. B. completes his home therapy course and is no longer homebound, he may attend. Day care would provide a therapeutic environment for him and respite for her.

You request that the home care agency provide a social worker to advise her on community resources. Meta-analysis suggests that structured, multicomponent interventions with caregivers of demented patients reduce several types of caregiver burden and delay institutionalization.²⁶

He improves with conservative measures

Three weeks later, Mr. B. is sleeping better and has stopped wandering. However, he dislikes the thickened liquids required by the dysphagia diet and has lost another 2 pounds. If his beverages are not thickened, he coughs profusely when he swallows. His daughters are still pressuring Mrs. B. for a PEG tube; one of them has angrily asserted that the doctors are going to allow her father to die.

You explain the burdens of PEG tubes: surgical risks, continued aspiration, disrupted bowel habits, the risk of the tube being accidentally or intentionally dislodged by the patient, and special binders (which may be uncomfortable) or restraints (which may cause further functional decline) that may be necessary to prevent this complication.

You request that the speech therapist work with the patient more aggressively in the use of swallowing techniques such as the chin tuck, which may be at least as effective as thickeners in preventing both aspiration pneumonia and dehydration.²⁷ The therapist will need to include Mrs. B. in these sessions, since she will be Mr. B.’s coach at mealtime.

With more aggressive speech therapy, the patient’s weight stabilizes over the next 4 weeks. He is in day care 3 days a week, and Mrs. B. is more rested and relaxed.

Cardiopulmonary resuscitation

You continue the advance care planning discussion and suggest that if Mr. B. aspirates, is hospitalized again, and declines further care, it would be helpful to delineate instructions for resuscitation. Right now, although his Alzheimer disease is advanced, he is not clearly terminal. Thus, his living will does not strictly apply and provides limited guidance about intubation, cardiopulmonary resuscitation (CPR), or medically supplied nutrition and hydration. However, because Mrs. B. is his agent in the medical power of attorney, this document enables her to make a wide spectrum of treatment decisions on his behalf.

Mrs. B. asks about her husband’s prognosis and why CPR would not be helpful.

Comment. Further discussion with her could be guided by an estimate of Mr. B.’s prognosis. Function-based tools^28,29 may also be useful. For example,^28,30 an 80-year-old man with high functional status might have a life expectancy of more than 10 years. Mr. B., with multiple medical problems and declining function, would have an estimated life expectancy of approximately 3 years. Even without specifically categorizing function, impaired cognition by itself predicted a shorter life expectancy in population-based studies.^31,32

Regarding CPR, patients and families may overestimate successful outcomes. A recent study³³ of 10 years of outcomes of in-hospital cardiac arrest found that only 6.6% of patients survived to discharge. The average age of the survivors was 59 years, and fewer than half of them survived 3 years after cardiac arrest. In eight studies of CPR outcomes in nursing homes,³⁴ three studies had no survivors, and all but one study had a survival rate below 5%.

PROVIDING APPROPRIATE CARE, NOT LIMITING TREATMENTS

In the case of Mr. B., as in many situations encountered with older patients, written advance directives provide little help or guidance. Instead, we recommend a model of advance care planning that takes place during multiple office visits over time, and that maintains a focus on providing appropriate care rather than on limiting life-sustaining treatments. We recommend providing estimates of prognosis and CPR outcomes when the family appeares ready to hear them. This approach should result in a care-oriented process while moving the family towards decisions regarding artificial feeding and CPR.

All patients, particularly those unwilling or unable to participate in advance care planning, are encouraged to identify one or more surrogate decision-makers and articulate how much flexibility that person should be given in important health care decisions. The medical power of attorney can be activated any time the patient lacks decision-making capacity and deactivated when decision-making capacity returns.^38,39

As in the case of Mr. B., a tailored approach to advance care planning requires clinicians to estimate life expectancy (more than 5 years, less than 5 years, or less than 1 year) and to determine the patient’s and the family’s readiness to focus on a values-oriented and goal-oriented care plan. Some patients are not receptive to advance care planning, and clinical time and effort are optimized by providing the right amount of information to patients when they are ready to receive it.

Figure 2 is the algorithm for older patients who are expected to live at least 5 years, ie, who are relatively healthy and functional. Patients with little or no interest in advance care planning can be asked about it annually, or sooner if their medical condition changes. Patients with limited interest can be given written information, specifically living will and medical power of attorney documents recognized in their state. Patients more open to advance care planning can be offered a values history form (Table 1), Web sites, and educational materials, with a plan to discuss them at future appointments.

Periodic reevaluation of values and goals of care is important. Patients may assert that particular interventions (eg, a PEG tube or dialysis) are “worse than death” when they are healthy, but they may change their views over time.²¹ Additionally, although a recent hospitalization or a decline in function may predispose patients to want to limit life-sustaining treatments, they may return to their earlier values and wishes a few months later, particularly if their medical condition stabilizes. ²⁰ Values and decisions should be reassessed not only when medical conditions deteriorate, but also when they improve.

For chronically ill patients

Caregiver stress is important to identify and address, since caregivers often neglect themselves.^40–42

For terminally ill patients

In this situation, patients and families need information about community resources that can assist them in the home. Some older adults with cognitive impairment may be exploited or neglect themselves, and referral to an adult protective services agency may be needed.

Treatment burden, particularly due to multiple prescribed medications, may be high and should be reassessed in light of the goals of treatment. Polypharmacy reduction is especially important at this stage in the illness, since the goals of care may be different than when the medications were prescribed.

Physical or psychosocial symptoms may be the cue to bring up the topic of palliative care. If the patient is expected to live less than 6 months, hospice referral is appropriate. With either palliative care or hospice, the focus of attention shifts explicitly from curing the disease to managing symptoms, and from the patient to the patient-family dyad. Interventions such as CPR and ventilatory support should be discussed and information from Table 2 provided to the patient and family.

Complete advance care planning incorporates taking a values history, estimating life expectancy, determining physical, psychosocial and spiritual needs, clarifying treatment goals, and estimating manageable treatment burden. Offering statistics on CPR and providing state-specific living will and medical power of attorney documents are important but are only one facet of effective advance care planning. In fact, shifting the emphasis of advance care planning from statistics and forms to values and goals of care may help in developing a more comprehensive care plan.

Goals of care range from curing the disease (with aggressive therapy, which may be burdensome) to simply improving function or decreasing pain. In the latter case, one may be able to discontinue some of the patient’s drugs, utilize medical and community resources more effectively, and better meet the patient’s needs.

Woven through all these discussions should be reassurance that the plan can be revisited and possibly revised, and that the physician will be there to help with those decisions.

Episodic, staged advance care planning is appropriate not only in the office but also in other settings such as assisted living and nursing facilities.

In the hospital, however, a different approach is needed, since patients are usually admitted because of an acute illness or sudden functional decline, or both. Decisions about technological interventions such as CPR, mechanical ventilation, or dialysis may be needed urgently. Often, patients are unable to provide guidance to physicians during acute illness because of delirium and other impediments. Developing a plan for care in the hospital may require urgent family meetings. However, if a surrogate decision-maker is in place, and if the patient has already participated in some form of advance care planning as an outpatient, the values and goals of care previously identified can contribute to decision-making during hospitalization.

As mentioned above, fragmentation of health care across providers and health care systems may limit the effectiveness of office-based advance care planning. It may be reasonable to train office staff to place advance care planning documentation in easily accessible sections of the patient’s medical record and to forward these to specialists involved in a patient’s care.

The patient and family should be encouraged and empowered to help with this process and should have updated advance care planning documentation readily available. In some states, comprehensive medical order sets, especially for end-of-life care, are portable across care settings and address CPR, medically supplied nutrition, hospital transfer, and antibiotic treatment.⁴³

Research suggests that health care systems are more likely to comply with patients’ end-of-life preferences when portable medical order forms are developed and disseminated.^44–44 Ultimately, major changes in health care delivery, including universal electronic health records, may be needed to implement and communicate patients’ advance care planning preferences across settings.

Mr. B., an 82-year-old retired accountant with hypertension, was diagnosed with early Alzheimer disease 6 years ago. He now needs supervision with bathing and dressing and no longer consistently recognizes family members. You are seeing him in the office today after a hospitalization for aspiration pneumonia, his second in the past 6 months.

See related editorial

In the hospital, a brain scan showed that atrophy had progressed and white-matter disease was more extensive than 3 years earlier. A barium swallow study showed esophageal dysmotility and aspiration. He was prescribed a “dysphagia diet,”¹ which he dislikes.

Since returning home, he has been disoriented, he has been wandering about the house, and he has fallen several times. He has lost 10 pounds in 6 months. Because of his confusion, his wife cannot take him out, and she is exhausted caring for him.

Reviewing his medical record, you note that 10 years ago, Mr. B. completed a living will and designated his wife as his proxy decision-maker via a medical power of attorney document.

PLANNING IS OFTEN NEGLECTED

Many clinicians and older patients feel a strong need to document, in advance, the patient’s wishes regarding medical care in the event the patient becomes seriously ill and unable to participate in treatment decisions. Professional societies such as the American Geriatrics Society promote advance care planning,² and some indices of the quality of medical care include whether advance directives have been discussed and completed.³

Yet, despite the high profile of advance care planning,⁴ few patients actually fill out advance directives,⁵ with completion rates that vary widely,^6–8 sometimes by ethnicity and sex.^9,10 Furthermore, in a crisis, these directives are seldom followed.¹¹

In this paper, we recommend an approach to advance care planning for older adults that redirects the focus from “signing away” interventions such as dialysis, mechanical ventilation, and tube feeding. Instead, the focus is on the goals of care. We also advocate naming a surrogate decision-maker, since the medical power of attorney is more flexible and more widely applicable than the living will.

START BY LISTENING

A change in function resulting from disease progression, hospitalization, trauma, or other reasons is an ideal opportunity to introduce the process of advance care planning.

The first step is to find out how well the patient and family understand the patient’s relevant medical conditions, and what their expectations, hopes, and concerns are. This listening phase can provide insight into the patient’s values and goals and how much the patient and family want to engage in these discussions.

In matters of health behavior (such as advance care planning), people change only when they are ready to change.^12,13 Thus, we advise physicians to defer extensive discussions of values and goals of care until patients and families are ready to listen, hear, and talk about these topics (often, after a change for the worse in prognosis).

And it is a process. Advance care directives are most likely to be set up and followed if the patient and doctor discuss this issue during multiple visits, rather than if the physician merely hands the patient a packet of forms and information.^14–16

CASE CONTINUED: A PEG TUBE REFUSED

Mrs. B. says that Mr. B. is in good health except for his memory: he does not have a serious condition such as diabetes, heart failure, or cancer. While Mr. B. was in the hospital, the hospitalist recommended placing a percutaneous endoscopic gastrostomy (PEG) tube, but Mrs. B. declined the recommendation because her husband had a living will that specified “no artificially or technologically supplied nutrition or hydration.”

At this point, Mrs. B. begins to cry. She has slept poorly because of his wandering. Also, her two daughters do not support her refusal of the PEG tube.

Comment. This brief conversation illuminates knowledge deficits in Mrs. B.’s understanding of Alzheimer disease and the circumstances in which the living will applies. Although one could argue that Mr. B.’s Alzheimer disease has advanced to the point that he is likely to die of a complication of that condition, he is not likely to die in the near future. If he is not considered by law and his physician to be terminally ill or permanently unconscious, a living will likely does not offer guidance about artificial feeding.

LIMITATIONS OF A LIVING WILL

A living will, a commonly used advance directive, states that the patient does not wish to receive life-sustaining treatment in the event that he or she suffers an incurable, irreversible disease and cannot give informed consent, and it often lists specific treatments that the patient does not want. However, we believe that approaching the patient with a list of life-sustaining measures to accept or reject, before discussing goals of care and prognosis, puts the cart before the horse. This approach threatens to distract from the need to ascertain values and offer appropriate care. Additionally, a living will is active only within a very limited scenario and does not address relatively routine but important decisions in a person’s care.

All ‘terminal illness’ isn’t the same

A living will goes into effect only if the patient either enters a permanent vegetative state following an event such as cardiac arrest or severe brain trauma, or is diagnosed with a terminal illness such as metastatic cancer, and lacks decision-making capacity.

But what is terminal illness? The definition differs from state to state, but it is generally defined as an irreversible condition leading to death in a relatively short time. The time may not be specified, as in Florida statute 765. In contrast, Ohio Revised Code 2133.01(AA) uses the phrase “relatively short,” while other states specify a time, such as within 6 months (Texas Health and Safety Code 166.002). The Medicare hospice benefit also carries a short time limit, usually less than 6 months.

The middle panel in Figure 1 depicts a more typical decline from serial organ insults such as stroke followed by infection from aspiration or followed by falls. Older adults with dementia or with multiple progressive diseases such as heart failure, diabetes, hypertension, or cancer decline in a trajectory such as in the bottom panel of Figure 1.

A living will might not be activated in the latter two scenarios until years into the condition because the patient would not be considered terminally ill—by state law, by the health care provider, or even by the patient.

The living will does not address routine interventions

In most states, living wills address only life-sustaining treatments such as dialysis, mechanical ventilation, and medically supplied nutrition and hydration. Living wills do not address relatively common diseases in older adults that could cause severe debility, such as a major stroke or advanced dementia.

If an older patient has dementia, a living will is unlikely to provide guidance about interventions such as intubation to get through an episode of potentially reversible respiratory failure, a feeding tube to correct weight loss, or cardiac catheterization or bypass surgery to treat angina. Yet these important decisions often arise as function declines and comorbidities progress.

Patients may change their minds

Many older adults are reluctant to sign documents to “micromanage” their future care if they should become ill.¹⁹ Many people change their mind as the situation changes.^11,20,21 Although few claim they would want burdensome interventions if they had dementia²² or if their prognosis were poor,²³ patients may tolerate more burdensome interventions if they are already receiving treatments for chronic illnesses such as end-stage renal disease.²⁴

Thus, a living will may help if unexpected trauma occurs in a healthy person, but not so much if chronic illness progresses over a period of years.

Advance directives may not be honored

Even if completed, written advance directives may not be followed, for a variety of reasons. Physicians may not know the patient has a living will, and fewer than one-third of people who actually complete an advance directive have discussed its content with a physician.²⁵ The people named as surrogate decision-makers may not know the patient’s wishes. Family members may disagree with the goals and plan of care and may interfere with implementation of the advance care plan. A patient may see multiple physicians at different institutions who may not communicate with each other about the patient’s wishes. Also, physicians and patients may interpret terms such as “terminally ill” differently, making it difficult to translate the documents into an action plan.

CASE CONTINUED: RELIEVING CAREGIVER STRESS

Returning to Mr. B., your first goal is to address care issues, including caregiver stress. Skilled services in the home are appropriate for him at this time (and Medicare will pay for them) because he is still homebound. These services could include physical therapy, occupational therapy, and speech (swallowing) therapy. A home care agency may also provide an aide for a few weeks to assist with bathing and other personal needs.

You strongly recommend that the family (including both daughters) participate in the Alzheimer’s Association educational programs. You recommend that Mrs. B. locate an adult day care program now so that when Mr. B. completes his home therapy course and is no longer homebound, he may attend. Day care would provide a therapeutic environment for him and respite for her.

You request that the home care agency provide a social worker to advise her on community resources. Meta-analysis suggests that structured, multicomponent interventions with caregivers of demented patients reduce several types of caregiver burden and delay institutionalization.²⁶

He improves with conservative measures

Three weeks later, Mr. B. is sleeping better and has stopped wandering. However, he dislikes the thickened liquids required by the dysphagia diet and has lost another 2 pounds. If his beverages are not thickened, he coughs profusely when he swallows. His daughters are still pressuring Mrs. B. for a PEG tube; one of them has angrily asserted that the doctors are going to allow her father to die.

You explain the burdens of PEG tubes: surgical risks, continued aspiration, disrupted bowel habits, the risk of the tube being accidentally or intentionally dislodged by the patient, and special binders (which may be uncomfortable) or restraints (which may cause further functional decline) that may be necessary to prevent this complication.

You request that the speech therapist work with the patient more aggressively in the use of swallowing techniques such as the chin tuck, which may be at least as effective as thickeners in preventing both aspiration pneumonia and dehydration.²⁷ The therapist will need to include Mrs. B. in these sessions, since she will be Mr. B.’s coach at mealtime.

With more aggressive speech therapy, the patient’s weight stabilizes over the next 4 weeks. He is in day care 3 days a week, and Mrs. B. is more rested and relaxed.

Cardiopulmonary resuscitation

You continue the advance care planning discussion and suggest that if Mr. B. aspirates, is hospitalized again, and declines further care, it would be helpful to delineate instructions for resuscitation. Right now, although his Alzheimer disease is advanced, he is not clearly terminal. Thus, his living will does not strictly apply and provides limited guidance about intubation, cardiopulmonary resuscitation (CPR), or medically supplied nutrition and hydration. However, because Mrs. B. is his agent in the medical power of attorney, this document enables her to make a wide spectrum of treatment decisions on his behalf.

Mrs. B. asks about her husband’s prognosis and why CPR would not be helpful.

Comment. Further discussion with her could be guided by an estimate of Mr. B.’s prognosis. Function-based tools^28,29 may also be useful. For example,^28,30 an 80-year-old man with high functional status might have a life expectancy of more than 10 years. Mr. B., with multiple medical problems and declining function, would have an estimated life expectancy of approximately 3 years. Even without specifically categorizing function, impaired cognition by itself predicted a shorter life expectancy in population-based studies.^31,32

Regarding CPR, patients and families may overestimate successful outcomes. A recent study³³ of 10 years of outcomes of in-hospital cardiac arrest found that only 6.6% of patients survived to discharge. The average age of the survivors was 59 years, and fewer than half of them survived 3 years after cardiac arrest. In eight studies of CPR outcomes in nursing homes,³⁴ three studies had no survivors, and all but one study had a survival rate below 5%.

PROVIDING APPROPRIATE CARE, NOT LIMITING TREATMENTS

In the case of Mr. B., as in many situations encountered with older patients, written advance directives provide little help or guidance. Instead, we recommend a model of advance care planning that takes place during multiple office visits over time, and that maintains a focus on providing appropriate care rather than on limiting life-sustaining treatments. We recommend providing estimates of prognosis and CPR outcomes when the family appeares ready to hear them. This approach should result in a care-oriented process while moving the family towards decisions regarding artificial feeding and CPR.

All patients, particularly those unwilling or unable to participate in advance care planning, are encouraged to identify one or more surrogate decision-makers and articulate how much flexibility that person should be given in important health care decisions. The medical power of attorney can be activated any time the patient lacks decision-making capacity and deactivated when decision-making capacity returns.^38,39

As in the case of Mr. B., a tailored approach to advance care planning requires clinicians to estimate life expectancy (more than 5 years, less than 5 years, or less than 1 year) and to determine the patient’s and the family’s readiness to focus on a values-oriented and goal-oriented care plan. Some patients are not receptive to advance care planning, and clinical time and effort are optimized by providing the right amount of information to patients when they are ready to receive it.

Figure 2 is the algorithm for older patients who are expected to live at least 5 years, ie, who are relatively healthy and functional. Patients with little or no interest in advance care planning can be asked about it annually, or sooner if their medical condition changes. Patients with limited interest can be given written information, specifically living will and medical power of attorney documents recognized in their state. Patients more open to advance care planning can be offered a values history form (Table 1), Web sites, and educational materials, with a plan to discuss them at future appointments.

Periodic reevaluation of values and goals of care is important. Patients may assert that particular interventions (eg, a PEG tube or dialysis) are “worse than death” when they are healthy, but they may change their views over time.²¹ Additionally, although a recent hospitalization or a decline in function may predispose patients to want to limit life-sustaining treatments, they may return to their earlier values and wishes a few months later, particularly if their medical condition stabilizes. ²⁰ Values and decisions should be reassessed not only when medical conditions deteriorate, but also when they improve.

For chronically ill patients

Caregiver stress is important to identify and address, since caregivers often neglect themselves.^40–42

For terminally ill patients

In this situation, patients and families need information about community resources that can assist them in the home. Some older adults with cognitive impairment may be exploited or neglect themselves, and referral to an adult protective services agency may be needed.

Treatment burden, particularly due to multiple prescribed medications, may be high and should be reassessed in light of the goals of treatment. Polypharmacy reduction is especially important at this stage in the illness, since the goals of care may be different than when the medications were prescribed.

Physical or psychosocial symptoms may be the cue to bring up the topic of palliative care. If the patient is expected to live less than 6 months, hospice referral is appropriate. With either palliative care or hospice, the focus of attention shifts explicitly from curing the disease to managing symptoms, and from the patient to the patient-family dyad. Interventions such as CPR and ventilatory support should be discussed and information from Table 2 provided to the patient and family.

Complete advance care planning incorporates taking a values history, estimating life expectancy, determining physical, psychosocial and spiritual needs, clarifying treatment goals, and estimating manageable treatment burden. Offering statistics on CPR and providing state-specific living will and medical power of attorney documents are important but are only one facet of effective advance care planning. In fact, shifting the emphasis of advance care planning from statistics and forms to values and goals of care may help in developing a more comprehensive care plan.

Goals of care range from curing the disease (with aggressive therapy, which may be burdensome) to simply improving function or decreasing pain. In the latter case, one may be able to discontinue some of the patient’s drugs, utilize medical and community resources more effectively, and better meet the patient’s needs.

Woven through all these discussions should be reassurance that the plan can be revisited and possibly revised, and that the physician will be there to help with those decisions.

Episodic, staged advance care planning is appropriate not only in the office but also in other settings such as assisted living and nursing facilities.

In the hospital, however, a different approach is needed, since patients are usually admitted because of an acute illness or sudden functional decline, or both. Decisions about technological interventions such as CPR, mechanical ventilation, or dialysis may be needed urgently. Often, patients are unable to provide guidance to physicians during acute illness because of delirium and other impediments. Developing a plan for care in the hospital may require urgent family meetings. However, if a surrogate decision-maker is in place, and if the patient has already participated in some form of advance care planning as an outpatient, the values and goals of care previously identified can contribute to decision-making during hospitalization.

As mentioned above, fragmentation of health care across providers and health care systems may limit the effectiveness of office-based advance care planning. It may be reasonable to train office staff to place advance care planning documentation in easily accessible sections of the patient’s medical record and to forward these to specialists involved in a patient’s care.

The patient and family should be encouraged and empowered to help with this process and should have updated advance care planning documentation readily available. In some states, comprehensive medical order sets, especially for end-of-life care, are portable across care settings and address CPR, medically supplied nutrition, hospital transfer, and antibiotic treatment.⁴³

Research suggests that health care systems are more likely to comply with patients’ end-of-life preferences when portable medical order forms are developed and disseminated.^44–44 Ultimately, major changes in health care delivery, including universal electronic health records, may be needed to implement and communicate patients’ advance care planning preferences across settings.