Dr. Brezina

The pharmaceutical industry is big business, and its goal is to make money. If the industry can convince physicians to prescribe its medicines, then it makes more money.

Although pharmaceutical representatives brief physicians on new medications in an effort to encourage the use of their brand-name products, they also provide substantive information on the drugs that serves an educational purpose.

In the past, pharmaceutical companies—along with the medical device and biotechnology industries—showered physicians with expensive gifts, raising ethical questions about physicians’ obligation to the drug companies. Fair enough. These excessive practices were identified and curtailed—to my knowledge—some years ago.

Dr. Brezina

Watchdog groups, however, have continued to call into question every suggestion of “being in the pay” of big pharma. Everything from a plastic pen to a piece of pizza is suspect. There is considerable concern that practicing clinicians are influenced by the smallest gesture, while many large medical institutions continue to accept pharmaceutical-company-funded research grants. If big-pharma investment in research does not corrupt institutions, why is it assumed that carrying a pharmaceutical pen has such a pernicious effect on clinicians?

As a corollary to this question, does anyone really want to discontinue these important research studies just because they are funded by industry dollars?

Listening to drug representatives—even being seen in the vicinity—raises the eyebrows of purists. Do we really want physicians completely divorced from all pharmaceutical company education and communication? Do we feel there is zero benefit to hearing about new medications from the company’s viewpoint?

If physicians completely shut out the representatives, it would be expected that pharmaceutical companies would direct their efforts elsewhere—most likely, to consumers. Is that a better and healthier scenario?

Clearly, there is potential for abuse in pharmaceutical gifts to physicians. The practice should be controlled and monitored. The suspicions raised by purist groups that physicians’ prescribing habits are unalterably biased after a five-minute pharmaceutical representative detail and a chicken sandwich is hyperbole. The voice of reason is silenced in the midst of the inquisition.

In the academic setting, fear of being accused of “bought bias” has physicians clearing their pockets of tainted pens and checking their desks for corrupting paraphernalia. The positive aspects of pharma-sponsored programs and medical lectures are lost for fear of appearing to be complicit with drug companies.

The Aristotelian Golden Mean is superior to extreme positions, and I submit that the best road is the center. Listen to what the drug company representatives have to say, just like you listen to a car salesman: You can learn from both—as long as you research the data and form your own opinion. TH

Dr. Brezina is a hospitalist at Durham Regional Hospital in North Carolina.

Dr. Brezina

The pharmaceutical industry is big business, and its goal is to make money. If the industry can convince physicians to prescribe its medicines, then it makes more money.

Although pharmaceutical representatives brief physicians on new medications in an effort to encourage the use of their brand-name products, they also provide substantive information on the drugs that serves an educational purpose.

In the past, pharmaceutical companies—along with the medical device and biotechnology industries—showered physicians with expensive gifts, raising ethical questions about physicians’ obligation to the drug companies. Fair enough. These excessive practices were identified and curtailed—to my knowledge—some years ago.

Dr. Brezina

Watchdog groups, however, have continued to call into question every suggestion of “being in the pay” of big pharma. Everything from a plastic pen to a piece of pizza is suspect. There is considerable concern that practicing clinicians are influenced by the smallest gesture, while many large medical institutions continue to accept pharmaceutical-company-funded research grants. If big-pharma investment in research does not corrupt institutions, why is it assumed that carrying a pharmaceutical pen has such a pernicious effect on clinicians?

As a corollary to this question, does anyone really want to discontinue these important research studies just because they are funded by industry dollars?

Listening to drug representatives—even being seen in the vicinity—raises the eyebrows of purists. Do we really want physicians completely divorced from all pharmaceutical company education and communication? Do we feel there is zero benefit to hearing about new medications from the company’s viewpoint?

If physicians completely shut out the representatives, it would be expected that pharmaceutical companies would direct their efforts elsewhere—most likely, to consumers. Is that a better and healthier scenario?

Clearly, there is potential for abuse in pharmaceutical gifts to physicians. The practice should be controlled and monitored. The suspicions raised by purist groups that physicians’ prescribing habits are unalterably biased after a five-minute pharmaceutical representative detail and a chicken sandwich is hyperbole. The voice of reason is silenced in the midst of the inquisition.

In the academic setting, fear of being accused of “bought bias” has physicians clearing their pockets of tainted pens and checking their desks for corrupting paraphernalia. The positive aspects of pharma-sponsored programs and medical lectures are lost for fear of appearing to be complicit with drug companies.

The Aristotelian Golden Mean is superior to extreme positions, and I submit that the best road is the center. Listen to what the drug company representatives have to say, just like you listen to a car salesman: You can learn from both—as long as you research the data and form your own opinion. TH

Dr. Brezina is a hospitalist at Durham Regional Hospital in North Carolina.

Dr. Brezina

The pharmaceutical industry is big business, and its goal is to make money. If the industry can convince physicians to prescribe its medicines, then it makes more money.

Although pharmaceutical representatives brief physicians on new medications in an effort to encourage the use of their brand-name products, they also provide substantive information on the drugs that serves an educational purpose.

In the past, pharmaceutical companies—along with the medical device and biotechnology industries—showered physicians with expensive gifts, raising ethical questions about physicians’ obligation to the drug companies. Fair enough. These excessive practices were identified and curtailed—to my knowledge—some years ago.

Dr. Brezina

Watchdog groups, however, have continued to call into question every suggestion of “being in the pay” of big pharma. Everything from a plastic pen to a piece of pizza is suspect. There is considerable concern that practicing clinicians are influenced by the smallest gesture, while many large medical institutions continue to accept pharmaceutical-company-funded research grants. If big-pharma investment in research does not corrupt institutions, why is it assumed that carrying a pharmaceutical pen has such a pernicious effect on clinicians?

As a corollary to this question, does anyone really want to discontinue these important research studies just because they are funded by industry dollars?

Listening to drug representatives—even being seen in the vicinity—raises the eyebrows of purists. Do we really want physicians completely divorced from all pharmaceutical company education and communication? Do we feel there is zero benefit to hearing about new medications from the company’s viewpoint?

If physicians completely shut out the representatives, it would be expected that pharmaceutical companies would direct their efforts elsewhere—most likely, to consumers. Is that a better and healthier scenario?

Clearly, there is potential for abuse in pharmaceutical gifts to physicians. The practice should be controlled and monitored. The suspicions raised by purist groups that physicians’ prescribing habits are unalterably biased after a five-minute pharmaceutical representative detail and a chicken sandwich is hyperbole. The voice of reason is silenced in the midst of the inquisition.

In the academic setting, fear of being accused of “bought bias” has physicians clearing their pockets of tainted pens and checking their desks for corrupting paraphernalia. The positive aspects of pharma-sponsored programs and medical lectures are lost for fear of appearing to be complicit with drug companies.

The Aristotelian Golden Mean is superior to extreme positions, and I submit that the best road is the center. Listen to what the drug company representatives have to say, just like you listen to a car salesman: You can learn from both—as long as you research the data and form your own opinion. TH

Dr. Brezina is a hospitalist at Durham Regional Hospital in North Carolina.

The challenges facing SHM are very different than they were 10 years ago. In the 1990s, the focus was on building a society that would represent the needs of the practicing hospitalist. Converting NAIP, with its 200 members, to SHM, with its now 10,000 members, was certainly no easy task, but the society then enjoyed some luxuries no longer afforded to an organization the size of the modern-day SHM. Early on, SHM was far from the public eye, escaping public scrutiny for each of its actions. With only a few hundred members, the society was intimate: Almost every member knew of every action before it happened. And the agenda, compared with today’s standards, was reasonably focused.

But times are different now. The organization is much larger and complex, and the challenges we now face are collectively a product of our success. SHM is squarely in the spotlight; every decision is closely monitored by the public eye. We now have a voice such that when we speak, people listen. But with greatness comes responsibility, and because we are in the spotlight, we must be especially careful in how we speak, lest the message be misunderstood. Further, with more than 10,000 members, 50 full-time staff, 44 committees, and nearly 500 physician volunteers, the organization no longer has the luxury of every action being known by every member prior to its enactment.

More challenging still is our agenda, which has grown to be a diverse and far-reaching strategy. While impressive and admirable, the size of this “footprint” creates new challenges in balancing the need to be “nimble” (i.e., being able to act quickly enough to be timely and effective) versus being “thorough” (i.e., ensuring that each action is appropriately vetted prior to execution).

I suspect that there are few practicing hospitalists who have not read To Err is Human or Crossing the Quality Chasm.^1,2 Both make this essential point about quality: In complex systems, mistakes are bound to happen. And when errors do occur, each member of the team must be ready to take responsibility for the mistake, and immediately begin seeking systematic solutions to ensure that it does not happen again. SHM’s focus is to advance quality for all hospitalized patients. But an organization can only be effective if it emulates the principles that it hopes its members will individually espouse.

So let me start with this: There have been mistakes along the way.

That’s the hard truth. I believe that none of the mistakes have been intentional; rather, these missteps have been a product of an organization that has grown so fast, and whose success has gained so much public attention, that its infrastructure has struggled to keep pace with its growth. Any hospitalist who has seen his or her service size double in the span of a year or two knows of what I speak: As growth occurs, the approach to dealing with daily business has to evolve to meet new demands. If it does not, errors result.

One of the areas in which SHM’s growth has outpaced its policies and procedures regards SHM’s relationship with industry. I will say from the outset that having relationships with industry is not in and of itself a mistake. The reality is that without such relationships, in the setting of a landscape where governmental and philanthropic funding is disproportionately in deficit to the need, it would be almost impossible to advance the quality initiatives that have defined SHM’s success. SHM has, and will likely continue to have, relationships with industry. But requisite for having these relationships, especially for an organization that is a national leader, is going above and beyond the minimum standards to ensure transparency and ethics.

Two years ago, SHM began the arduous process of reviewing its partnerships and how it interacts with industry. I am pleased to announce that this has culminated in the Council of Medical Specialty Societies (CMSS; www.cmss.org) asking SHM to apply to become an affiliate member. Acceptance of SHM into CMSS is evidence of SHM’s demonstrated compliance with CMSS’s requirements, with respect to industry relationships, disclosure of conflicts of interest, and other measures of organizational transparency, all of which can be found at www.hospitalmedicine.org/industry.

But meeting the minimum standards has never been sufficient for SHM. The cost of greatness is responsibility, and as a national leader, SHM has a responsibility to ensure that its approaches to potential conflicts of interest and external relationships are above reproach.

COI Disclosure

The conflict of interest statements for each board member have long been posted on the SHM website. In an effort to go above and beyond the minimum standards, the format of the disclosure form has been revised, making it the most compete and detailed COI disclosure form of any physician organization in the country. In the coming months, SHM will make even tighter restrictions regarding disclosing potential conflicts of interest. While board members are required to report any and all financial receipts, the amended version will require board members who receive any contribution in excess of $5,000 to provide a detailed narrative as to what was required in service for the receipt of those funds. Further, to ensure collective accountability, any board member may call upon any other board member to provide a similarly detailed description of any item on his or her COI disclosure form.

Recognizing that other leaders in the organization might also have influence over important decisions, thereby being at risk for a conflict of interest, SHM is one of the first physician organizations to require public reporting of COI disclosures for all editors, course directors, and senior staff.

Next year, all committee chairs and quality-improvement (QI) project leaders will be required to submit similar COI disclosures.

But reporting potential conflicts is one thing; ensuring that those with significant conflicts are not put in a position of inescapable conflict of interest by virtue of their appointments is another. To be proactive, the executive committee has a designated meeting each year to individually review each nominee being considered for election to the board, committee chairs, editors, and course directors prior to their appointment.

The society will enforce CMSS Standard 1.4, which prohibits key society leaders (president, past-president, president-elect, CEO, editors, course directors) from having direct financial relationships with companies during his or her term of service. All people seeking such positions will be required to attest, at the time of the nomination, to cease all direct financial relationships prior to seeking office; failure to do so will negate their candidacy for the position they seek.

External Communications Regarding Industry

It is one thing to have potential conflicts disclosed on a website; it is quite another to ensure, with 100% confidence, that all recipients of all communications from SHM are aware of this website. Reminding all representatives of SHM to alert communication recipients to our potential conflicts of interest is a good start, but in quality parlance, this is tantamount to “telling people to try harder,” which is rarely an effective strategy to ensure 100% compliance. In response, SHM has designed a fail-safe systems solution to ensure that every communication alerts the recipient to SHM’s potential conflicts of interest. Beginning this year, SHM letterheads and e-mail, used for all written communications with external parties, will carry the following statement on the bottom of each page: “To Learn More About SHM’s Relationship with Industry Partners, Visit www.hospitalmedicine.org/industry.”

One of SHM’s missteps over the years has been the failure to distinguish external communications regarding pharmaceuticals/devices as being different from the organization’s other nonpharmaceutical communications. This unintentional oversight has been a product of the exponential increase in the society’s external communications during the past 10 years. But nonetheless, the distinction between these types of communications is important, especially for a society that receives industry support for its quality initiatives.

At the August board meeting in Chicago, a special ad hoc committee was appointed to develop specific policies regarding SHM’s communication strategy. This committee will bring to the board in November the following policy for approval: “Before SHM makes a specific comment, writes a letter, or posts an official statement on the SHM website about a pharmaceutical agent, a medical device, a specific disease state, or any medical IT services or products, the communication must be approved by the Executive Committee and reflected in the minutes of the Executive Committee. At the President’s discretion, the proposed communication will be brought to the entire Board for discussion and approval.”

As noted below, all agendas and decisions by the executive committee are communicated to the board, further ensuring accountability and oversight for any such decision.

Choices and Definitions

In the early years, all external relationships were initiated by SHM. Because SHM was a relative unknown on the national scene, if a relationship was to be entertained, it was based on SHM’s initiative to do so. Naturally, the smaller number of relationships, and the fact that the choice and nature of the relationship were initiated by SHM, made it easier to define the scope of such relationships. But now things are different: SHM’s agenda now encompasses a vast set of domains, and SHM is regularly on the receiving end of invitations to establish relationships with other organizations. Once again, as a leader of medical specialty organizations, SHM’s policies and procedures have to adapt to fit the needs of a larger and more diverse organization.

An intense amount of work has been devoted to evolving the mechanism by which SHM chooses and defines its relationships. An ad hoc committee from the board of directors has defined the 10 principles of SHM’s business relationships (see “10 Principles of SHM Business Relationships,” p. 42). In November, the board will adopt policies and procedures that will ensure that SHM will continue to only enter into relationships with external organizations with which it shares common interests or goals for advancing the quality and safety of patient care. SHM will continue to avoid influence from external organizations with respect to the policies, conduct, actions, and priorities of SHM.

Further, by policy, SHM will continue to reserve absolute control over all content and speakers at its educational conferences; content will continue to not be influenced by brand or product consideration during development or revisions. All potential partners will be informed from the outset that a partnership with SHM does not imply that SHM endorses the policies, values, and missions of the partner organization; any significant deviation from the values and mission of SHM will dissolve the partnership. SHM will establish from the outset that a partnership does not imply SHM’s support or endorsement of any products from a partner. As noted above, transparency of these relationships will be of paramount importance: All relationships, including the dollar amounts received as a product of those relationships, will be posted on SHM’s website.

Transparency in Decision-Making

As noted from the outset, the benefit of small organizations with limited agendas is that every member knows every decision. With limited decisions to be made, the vetting and review process is virtually assured. As organizations grow, as agendas expand exponentially, and as the pace quickens, the multiperson review of each decision becomes difficult to assure. The result is that errors start to appear—not due to intentional wrongdoing, but because the luxury of intense oversight is lost as the organization expands. For an organization to grow and still maintain oversight of its decision-making process, it is vital that the organization evolve to develop new methods of accountability and transparency.

To meet this need, SHM has enacted a change in its communication infrastructure to ensure “double-checks” for all of the important organizational decisions. An SHM leadership and staff “wiki” has been developed to promote and ensure transparency of all organizational decisions. Because it is accessible only to the SHM staff, board, and committee chairs, the wiki is invisible to the SHM membership. Nonetheless, you should know of this important innovation.

The wiki requires that all committee chairs post the results of their committee activities. This ensures that staff and committee leadership are on the same page, ensures that other committees are not duplicating work, augments collaboration across committees, and, most importantly, ensures collective accountability for each decision made.

Technology-based innovations have been enacted to improve the transparency of the executive leadership of the organization. The board of directors meets four times a year; the purpose of the board is to ensure oversight for all SHM decisions. Because the board comprises exclusively volunteer members meeting only four times a year, it is practically impossible for the board to approve every decision made by an organization as large as SHM. To ensure the necessary efficiency and effectiveness (i.e., being sufficiently “nimble” to act on important issues in between scheduled board meetings), the executive committee (EC) was established years ago. The EC, comprised of the president, the past-president, the president-elect, and the CEO, meets every two weeks via teleconference to review and approve all essential SHM decisions.

As an innovation to augment accountability and transparency, the agenda and minutes of the EC are now posted on the SHM board portal, allowing all board members to review and comment upon the decisions made by the president, the CEO, or the EC as a whole. Any board member, at any time, can request that the full board be convened to review an agenda item or decision.

And underlying all of these initiatives to improve an already exceptional organization are the tireless efforts of the SHM staff. Though there are nearly 50 staff members now, each continues to do the work of multiple people. SHM is arguably the fastest-growing organization in history, and advancing the organization to level after level has been an exceptional challenge. But regardless of the challenge, SHM leadership and staff has come through. I have no doubt that during this next chapter in SHM’s history, the result will be the same.

SHM is committed to advancing quality. Intrinsic to the “culture of quality” is the commitment to honesty, transparency, and ethics. Any permutation of the society that does not fully exemplify these standards will be ineffective in accomplishing our wished-for goal. In short, the actions of the society must model those that we wish to inspire in the day-to-day practice of our members. Although the unprecedented growth of the society is responsible for errors in the past, the importance of admitting our shortcomings is no less significant. We’ve had some missteps along the way, and while these mistakes are a product of events preceding my tenure, it does not matter. As president of the organization, I am taking responsibility for them, with a pledge to devote all time and energy, with all due speed, to finding systematic solutions that will prevent these errors from happening again.

And let me be even more honest. As we go forward, there are probably going to be more missteps; such is the nature of a growing and active organization. I cannot promise an error-free organization, but I can promise that if and when errors are made in the future, the same intensity will be applied to seek systematic solutions to ensure that we continue to evolve in becoming an organization that is emblematic of quality. Such is the promise of SHM; such is the promise of the hospitalist. TH

Dr. Wiese is president of SHM.

References

1. Kohn LT, Corrigan JM, Donaldson MS, et al. To Err Is Human: Building a Safer Health System. Washington, D.C.: National Academies Press; 2000.
2. Institute of Medicine Committee on Quality Health Care in America. Crossing the Quality Chasm: A New Health System for the 21st Century. Washington, D.C.: National Academies Press; 2001.

The challenges facing SHM are very different than they were 10 years ago. In the 1990s, the focus was on building a society that would represent the needs of the practicing hospitalist. Converting NAIP, with its 200 members, to SHM, with its now 10,000 members, was certainly no easy task, but the society then enjoyed some luxuries no longer afforded to an organization the size of the modern-day SHM. Early on, SHM was far from the public eye, escaping public scrutiny for each of its actions. With only a few hundred members, the society was intimate: Almost every member knew of every action before it happened. And the agenda, compared with today’s standards, was reasonably focused.

But times are different now. The organization is much larger and complex, and the challenges we now face are collectively a product of our success. SHM is squarely in the spotlight; every decision is closely monitored by the public eye. We now have a voice such that when we speak, people listen. But with greatness comes responsibility, and because we are in the spotlight, we must be especially careful in how we speak, lest the message be misunderstood. Further, with more than 10,000 members, 50 full-time staff, 44 committees, and nearly 500 physician volunteers, the organization no longer has the luxury of every action being known by every member prior to its enactment.

More challenging still is our agenda, which has grown to be a diverse and far-reaching strategy. While impressive and admirable, the size of this “footprint” creates new challenges in balancing the need to be “nimble” (i.e., being able to act quickly enough to be timely and effective) versus being “thorough” (i.e., ensuring that each action is appropriately vetted prior to execution).

I suspect that there are few practicing hospitalists who have not read To Err is Human or Crossing the Quality Chasm.^1,2 Both make this essential point about quality: In complex systems, mistakes are bound to happen. And when errors do occur, each member of the team must be ready to take responsibility for the mistake, and immediately begin seeking systematic solutions to ensure that it does not happen again. SHM’s focus is to advance quality for all hospitalized patients. But an organization can only be effective if it emulates the principles that it hopes its members will individually espouse.

So let me start with this: There have been mistakes along the way.

That’s the hard truth. I believe that none of the mistakes have been intentional; rather, these missteps have been a product of an organization that has grown so fast, and whose success has gained so much public attention, that its infrastructure has struggled to keep pace with its growth. Any hospitalist who has seen his or her service size double in the span of a year or two knows of what I speak: As growth occurs, the approach to dealing with daily business has to evolve to meet new demands. If it does not, errors result.

One of the areas in which SHM’s growth has outpaced its policies and procedures regards SHM’s relationship with industry. I will say from the outset that having relationships with industry is not in and of itself a mistake. The reality is that without such relationships, in the setting of a landscape where governmental and philanthropic funding is disproportionately in deficit to the need, it would be almost impossible to advance the quality initiatives that have defined SHM’s success. SHM has, and will likely continue to have, relationships with industry. But requisite for having these relationships, especially for an organization that is a national leader, is going above and beyond the minimum standards to ensure transparency and ethics.

Two years ago, SHM began the arduous process of reviewing its partnerships and how it interacts with industry. I am pleased to announce that this has culminated in the Council of Medical Specialty Societies (CMSS; www.cmss.org) asking SHM to apply to become an affiliate member. Acceptance of SHM into CMSS is evidence of SHM’s demonstrated compliance with CMSS’s requirements, with respect to industry relationships, disclosure of conflicts of interest, and other measures of organizational transparency, all of which can be found at www.hospitalmedicine.org/industry.

But meeting the minimum standards has never been sufficient for SHM. The cost of greatness is responsibility, and as a national leader, SHM has a responsibility to ensure that its approaches to potential conflicts of interest and external relationships are above reproach.

COI Disclosure

The conflict of interest statements for each board member have long been posted on the SHM website. In an effort to go above and beyond the minimum standards, the format of the disclosure form has been revised, making it the most compete and detailed COI disclosure form of any physician organization in the country. In the coming months, SHM will make even tighter restrictions regarding disclosing potential conflicts of interest. While board members are required to report any and all financial receipts, the amended version will require board members who receive any contribution in excess of $5,000 to provide a detailed narrative as to what was required in service for the receipt of those funds. Further, to ensure collective accountability, any board member may call upon any other board member to provide a similarly detailed description of any item on his or her COI disclosure form.

Recognizing that other leaders in the organization might also have influence over important decisions, thereby being at risk for a conflict of interest, SHM is one of the first physician organizations to require public reporting of COI disclosures for all editors, course directors, and senior staff.

Next year, all committee chairs and quality-improvement (QI) project leaders will be required to submit similar COI disclosures.

But reporting potential conflicts is one thing; ensuring that those with significant conflicts are not put in a position of inescapable conflict of interest by virtue of their appointments is another. To be proactive, the executive committee has a designated meeting each year to individually review each nominee being considered for election to the board, committee chairs, editors, and course directors prior to their appointment.

The society will enforce CMSS Standard 1.4, which prohibits key society leaders (president, past-president, president-elect, CEO, editors, course directors) from having direct financial relationships with companies during his or her term of service. All people seeking such positions will be required to attest, at the time of the nomination, to cease all direct financial relationships prior to seeking office; failure to do so will negate their candidacy for the position they seek.

External Communications Regarding Industry

It is one thing to have potential conflicts disclosed on a website; it is quite another to ensure, with 100% confidence, that all recipients of all communications from SHM are aware of this website. Reminding all representatives of SHM to alert communication recipients to our potential conflicts of interest is a good start, but in quality parlance, this is tantamount to “telling people to try harder,” which is rarely an effective strategy to ensure 100% compliance. In response, SHM has designed a fail-safe systems solution to ensure that every communication alerts the recipient to SHM’s potential conflicts of interest. Beginning this year, SHM letterheads and e-mail, used for all written communications with external parties, will carry the following statement on the bottom of each page: “To Learn More About SHM’s Relationship with Industry Partners, Visit www.hospitalmedicine.org/industry.”

One of SHM’s missteps over the years has been the failure to distinguish external communications regarding pharmaceuticals/devices as being different from the organization’s other nonpharmaceutical communications. This unintentional oversight has been a product of the exponential increase in the society’s external communications during the past 10 years. But nonetheless, the distinction between these types of communications is important, especially for a society that receives industry support for its quality initiatives.

At the August board meeting in Chicago, a special ad hoc committee was appointed to develop specific policies regarding SHM’s communication strategy. This committee will bring to the board in November the following policy for approval: “Before SHM makes a specific comment, writes a letter, or posts an official statement on the SHM website about a pharmaceutical agent, a medical device, a specific disease state, or any medical IT services or products, the communication must be approved by the Executive Committee and reflected in the minutes of the Executive Committee. At the President’s discretion, the proposed communication will be brought to the entire Board for discussion and approval.”

As noted below, all agendas and decisions by the executive committee are communicated to the board, further ensuring accountability and oversight for any such decision.

Choices and Definitions

In the early years, all external relationships were initiated by SHM. Because SHM was a relative unknown on the national scene, if a relationship was to be entertained, it was based on SHM’s initiative to do so. Naturally, the smaller number of relationships, and the fact that the choice and nature of the relationship were initiated by SHM, made it easier to define the scope of such relationships. But now things are different: SHM’s agenda now encompasses a vast set of domains, and SHM is regularly on the receiving end of invitations to establish relationships with other organizations. Once again, as a leader of medical specialty organizations, SHM’s policies and procedures have to adapt to fit the needs of a larger and more diverse organization.

An intense amount of work has been devoted to evolving the mechanism by which SHM chooses and defines its relationships. An ad hoc committee from the board of directors has defined the 10 principles of SHM’s business relationships (see “10 Principles of SHM Business Relationships,” p. 42). In November, the board will adopt policies and procedures that will ensure that SHM will continue to only enter into relationships with external organizations with which it shares common interests or goals for advancing the quality and safety of patient care. SHM will continue to avoid influence from external organizations with respect to the policies, conduct, actions, and priorities of SHM.

Further, by policy, SHM will continue to reserve absolute control over all content and speakers at its educational conferences; content will continue to not be influenced by brand or product consideration during development or revisions. All potential partners will be informed from the outset that a partnership with SHM does not imply that SHM endorses the policies, values, and missions of the partner organization; any significant deviation from the values and mission of SHM will dissolve the partnership. SHM will establish from the outset that a partnership does not imply SHM’s support or endorsement of any products from a partner. As noted above, transparency of these relationships will be of paramount importance: All relationships, including the dollar amounts received as a product of those relationships, will be posted on SHM’s website.

Transparency in Decision-Making

As noted from the outset, the benefit of small organizations with limited agendas is that every member knows every decision. With limited decisions to be made, the vetting and review process is virtually assured. As organizations grow, as agendas expand exponentially, and as the pace quickens, the multiperson review of each decision becomes difficult to assure. The result is that errors start to appear—not due to intentional wrongdoing, but because the luxury of intense oversight is lost as the organization expands. For an organization to grow and still maintain oversight of its decision-making process, it is vital that the organization evolve to develop new methods of accountability and transparency.

To meet this need, SHM has enacted a change in its communication infrastructure to ensure “double-checks” for all of the important organizational decisions. An SHM leadership and staff “wiki” has been developed to promote and ensure transparency of all organizational decisions. Because it is accessible only to the SHM staff, board, and committee chairs, the wiki is invisible to the SHM membership. Nonetheless, you should know of this important innovation.

The wiki requires that all committee chairs post the results of their committee activities. This ensures that staff and committee leadership are on the same page, ensures that other committees are not duplicating work, augments collaboration across committees, and, most importantly, ensures collective accountability for each decision made.

Technology-based innovations have been enacted to improve the transparency of the executive leadership of the organization. The board of directors meets four times a year; the purpose of the board is to ensure oversight for all SHM decisions. Because the board comprises exclusively volunteer members meeting only four times a year, it is practically impossible for the board to approve every decision made by an organization as large as SHM. To ensure the necessary efficiency and effectiveness (i.e., being sufficiently “nimble” to act on important issues in between scheduled board meetings), the executive committee (EC) was established years ago. The EC, comprised of the president, the past-president, the president-elect, and the CEO, meets every two weeks via teleconference to review and approve all essential SHM decisions.

As an innovation to augment accountability and transparency, the agenda and minutes of the EC are now posted on the SHM board portal, allowing all board members to review and comment upon the decisions made by the president, the CEO, or the EC as a whole. Any board member, at any time, can request that the full board be convened to review an agenda item or decision.

And underlying all of these initiatives to improve an already exceptional organization are the tireless efforts of the SHM staff. Though there are nearly 50 staff members now, each continues to do the work of multiple people. SHM is arguably the fastest-growing organization in history, and advancing the organization to level after level has been an exceptional challenge. But regardless of the challenge, SHM leadership and staff has come through. I have no doubt that during this next chapter in SHM’s history, the result will be the same.

SHM is committed to advancing quality. Intrinsic to the “culture of quality” is the commitment to honesty, transparency, and ethics. Any permutation of the society that does not fully exemplify these standards will be ineffective in accomplishing our wished-for goal. In short, the actions of the society must model those that we wish to inspire in the day-to-day practice of our members. Although the unprecedented growth of the society is responsible for errors in the past, the importance of admitting our shortcomings is no less significant. We’ve had some missteps along the way, and while these mistakes are a product of events preceding my tenure, it does not matter. As president of the organization, I am taking responsibility for them, with a pledge to devote all time and energy, with all due speed, to finding systematic solutions that will prevent these errors from happening again.

And let me be even more honest. As we go forward, there are probably going to be more missteps; such is the nature of a growing and active organization. I cannot promise an error-free organization, but I can promise that if and when errors are made in the future, the same intensity will be applied to seek systematic solutions to ensure that we continue to evolve in becoming an organization that is emblematic of quality. Such is the promise of SHM; such is the promise of the hospitalist. TH

Dr. Wiese is president of SHM.

References

1. Kohn LT, Corrigan JM, Donaldson MS, et al. To Err Is Human: Building a Safer Health System. Washington, D.C.: National Academies Press; 2000.
2. Institute of Medicine Committee on Quality Health Care in America. Crossing the Quality Chasm: A New Health System for the 21st Century. Washington, D.C.: National Academies Press; 2001.

The challenges facing SHM are very different than they were 10 years ago. In the 1990s, the focus was on building a society that would represent the needs of the practicing hospitalist. Converting NAIP, with its 200 members, to SHM, with its now 10,000 members, was certainly no easy task, but the society then enjoyed some luxuries no longer afforded to an organization the size of the modern-day SHM. Early on, SHM was far from the public eye, escaping public scrutiny for each of its actions. With only a few hundred members, the society was intimate: Almost every member knew of every action before it happened. And the agenda, compared with today’s standards, was reasonably focused.

But times are different now. The organization is much larger and complex, and the challenges we now face are collectively a product of our success. SHM is squarely in the spotlight; every decision is closely monitored by the public eye. We now have a voice such that when we speak, people listen. But with greatness comes responsibility, and because we are in the spotlight, we must be especially careful in how we speak, lest the message be misunderstood. Further, with more than 10,000 members, 50 full-time staff, 44 committees, and nearly 500 physician volunteers, the organization no longer has the luxury of every action being known by every member prior to its enactment.

More challenging still is our agenda, which has grown to be a diverse and far-reaching strategy. While impressive and admirable, the size of this “footprint” creates new challenges in balancing the need to be “nimble” (i.e., being able to act quickly enough to be timely and effective) versus being “thorough” (i.e., ensuring that each action is appropriately vetted prior to execution).

I suspect that there are few practicing hospitalists who have not read To Err is Human or Crossing the Quality Chasm.^1,2 Both make this essential point about quality: In complex systems, mistakes are bound to happen. And when errors do occur, each member of the team must be ready to take responsibility for the mistake, and immediately begin seeking systematic solutions to ensure that it does not happen again. SHM’s focus is to advance quality for all hospitalized patients. But an organization can only be effective if it emulates the principles that it hopes its members will individually espouse.

So let me start with this: There have been mistakes along the way.

That’s the hard truth. I believe that none of the mistakes have been intentional; rather, these missteps have been a product of an organization that has grown so fast, and whose success has gained so much public attention, that its infrastructure has struggled to keep pace with its growth. Any hospitalist who has seen his or her service size double in the span of a year or two knows of what I speak: As growth occurs, the approach to dealing with daily business has to evolve to meet new demands. If it does not, errors result.

One of the areas in which SHM’s growth has outpaced its policies and procedures regards SHM’s relationship with industry. I will say from the outset that having relationships with industry is not in and of itself a mistake. The reality is that without such relationships, in the setting of a landscape where governmental and philanthropic funding is disproportionately in deficit to the need, it would be almost impossible to advance the quality initiatives that have defined SHM’s success. SHM has, and will likely continue to have, relationships with industry. But requisite for having these relationships, especially for an organization that is a national leader, is going above and beyond the minimum standards to ensure transparency and ethics.

Two years ago, SHM began the arduous process of reviewing its partnerships and how it interacts with industry. I am pleased to announce that this has culminated in the Council of Medical Specialty Societies (CMSS; www.cmss.org) asking SHM to apply to become an affiliate member. Acceptance of SHM into CMSS is evidence of SHM’s demonstrated compliance with CMSS’s requirements, with respect to industry relationships, disclosure of conflicts of interest, and other measures of organizational transparency, all of which can be found at www.hospitalmedicine.org/industry.

But meeting the minimum standards has never been sufficient for SHM. The cost of greatness is responsibility, and as a national leader, SHM has a responsibility to ensure that its approaches to potential conflicts of interest and external relationships are above reproach.

COI Disclosure

The conflict of interest statements for each board member have long been posted on the SHM website. In an effort to go above and beyond the minimum standards, the format of the disclosure form has been revised, making it the most compete and detailed COI disclosure form of any physician organization in the country. In the coming months, SHM will make even tighter restrictions regarding disclosing potential conflicts of interest. While board members are required to report any and all financial receipts, the amended version will require board members who receive any contribution in excess of $5,000 to provide a detailed narrative as to what was required in service for the receipt of those funds. Further, to ensure collective accountability, any board member may call upon any other board member to provide a similarly detailed description of any item on his or her COI disclosure form.

Recognizing that other leaders in the organization might also have influence over important decisions, thereby being at risk for a conflict of interest, SHM is one of the first physician organizations to require public reporting of COI disclosures for all editors, course directors, and senior staff.

Next year, all committee chairs and quality-improvement (QI) project leaders will be required to submit similar COI disclosures.

But reporting potential conflicts is one thing; ensuring that those with significant conflicts are not put in a position of inescapable conflict of interest by virtue of their appointments is another. To be proactive, the executive committee has a designated meeting each year to individually review each nominee being considered for election to the board, committee chairs, editors, and course directors prior to their appointment.

The society will enforce CMSS Standard 1.4, which prohibits key society leaders (president, past-president, president-elect, CEO, editors, course directors) from having direct financial relationships with companies during his or her term of service. All people seeking such positions will be required to attest, at the time of the nomination, to cease all direct financial relationships prior to seeking office; failure to do so will negate their candidacy for the position they seek.

External Communications Regarding Industry

It is one thing to have potential conflicts disclosed on a website; it is quite another to ensure, with 100% confidence, that all recipients of all communications from SHM are aware of this website. Reminding all representatives of SHM to alert communication recipients to our potential conflicts of interest is a good start, but in quality parlance, this is tantamount to “telling people to try harder,” which is rarely an effective strategy to ensure 100% compliance. In response, SHM has designed a fail-safe systems solution to ensure that every communication alerts the recipient to SHM’s potential conflicts of interest. Beginning this year, SHM letterheads and e-mail, used for all written communications with external parties, will carry the following statement on the bottom of each page: “To Learn More About SHM’s Relationship with Industry Partners, Visit www.hospitalmedicine.org/industry.”

One of SHM’s missteps over the years has been the failure to distinguish external communications regarding pharmaceuticals/devices as being different from the organization’s other nonpharmaceutical communications. This unintentional oversight has been a product of the exponential increase in the society’s external communications during the past 10 years. But nonetheless, the distinction between these types of communications is important, especially for a society that receives industry support for its quality initiatives.

At the August board meeting in Chicago, a special ad hoc committee was appointed to develop specific policies regarding SHM’s communication strategy. This committee will bring to the board in November the following policy for approval: “Before SHM makes a specific comment, writes a letter, or posts an official statement on the SHM website about a pharmaceutical agent, a medical device, a specific disease state, or any medical IT services or products, the communication must be approved by the Executive Committee and reflected in the minutes of the Executive Committee. At the President’s discretion, the proposed communication will be brought to the entire Board for discussion and approval.”

As noted below, all agendas and decisions by the executive committee are communicated to the board, further ensuring accountability and oversight for any such decision.

Choices and Definitions

In the early years, all external relationships were initiated by SHM. Because SHM was a relative unknown on the national scene, if a relationship was to be entertained, it was based on SHM’s initiative to do so. Naturally, the smaller number of relationships, and the fact that the choice and nature of the relationship were initiated by SHM, made it easier to define the scope of such relationships. But now things are different: SHM’s agenda now encompasses a vast set of domains, and SHM is regularly on the receiving end of invitations to establish relationships with other organizations. Once again, as a leader of medical specialty organizations, SHM’s policies and procedures have to adapt to fit the needs of a larger and more diverse organization.

An intense amount of work has been devoted to evolving the mechanism by which SHM chooses and defines its relationships. An ad hoc committee from the board of directors has defined the 10 principles of SHM’s business relationships (see “10 Principles of SHM Business Relationships,” p. 42). In November, the board will adopt policies and procedures that will ensure that SHM will continue to only enter into relationships with external organizations with which it shares common interests or goals for advancing the quality and safety of patient care. SHM will continue to avoid influence from external organizations with respect to the policies, conduct, actions, and priorities of SHM.

Further, by policy, SHM will continue to reserve absolute control over all content and speakers at its educational conferences; content will continue to not be influenced by brand or product consideration during development or revisions. All potential partners will be informed from the outset that a partnership with SHM does not imply that SHM endorses the policies, values, and missions of the partner organization; any significant deviation from the values and mission of SHM will dissolve the partnership. SHM will establish from the outset that a partnership does not imply SHM’s support or endorsement of any products from a partner. As noted above, transparency of these relationships will be of paramount importance: All relationships, including the dollar amounts received as a product of those relationships, will be posted on SHM’s website.

Transparency in Decision-Making

As noted from the outset, the benefit of small organizations with limited agendas is that every member knows every decision. With limited decisions to be made, the vetting and review process is virtually assured. As organizations grow, as agendas expand exponentially, and as the pace quickens, the multiperson review of each decision becomes difficult to assure. The result is that errors start to appear—not due to intentional wrongdoing, but because the luxury of intense oversight is lost as the organization expands. For an organization to grow and still maintain oversight of its decision-making process, it is vital that the organization evolve to develop new methods of accountability and transparency.

To meet this need, SHM has enacted a change in its communication infrastructure to ensure “double-checks” for all of the important organizational decisions. An SHM leadership and staff “wiki” has been developed to promote and ensure transparency of all organizational decisions. Because it is accessible only to the SHM staff, board, and committee chairs, the wiki is invisible to the SHM membership. Nonetheless, you should know of this important innovation.

The wiki requires that all committee chairs post the results of their committee activities. This ensures that staff and committee leadership are on the same page, ensures that other committees are not duplicating work, augments collaboration across committees, and, most importantly, ensures collective accountability for each decision made.

Technology-based innovations have been enacted to improve the transparency of the executive leadership of the organization. The board of directors meets four times a year; the purpose of the board is to ensure oversight for all SHM decisions. Because the board comprises exclusively volunteer members meeting only four times a year, it is practically impossible for the board to approve every decision made by an organization as large as SHM. To ensure the necessary efficiency and effectiveness (i.e., being sufficiently “nimble” to act on important issues in between scheduled board meetings), the executive committee (EC) was established years ago. The EC, comprised of the president, the past-president, the president-elect, and the CEO, meets every two weeks via teleconference to review and approve all essential SHM decisions.

As an innovation to augment accountability and transparency, the agenda and minutes of the EC are now posted on the SHM board portal, allowing all board members to review and comment upon the decisions made by the president, the CEO, or the EC as a whole. Any board member, at any time, can request that the full board be convened to review an agenda item or decision.

And underlying all of these initiatives to improve an already exceptional organization are the tireless efforts of the SHM staff. Though there are nearly 50 staff members now, each continues to do the work of multiple people. SHM is arguably the fastest-growing organization in history, and advancing the organization to level after level has been an exceptional challenge. But regardless of the challenge, SHM leadership and staff has come through. I have no doubt that during this next chapter in SHM’s history, the result will be the same.

SHM is committed to advancing quality. Intrinsic to the “culture of quality” is the commitment to honesty, transparency, and ethics. Any permutation of the society that does not fully exemplify these standards will be ineffective in accomplishing our wished-for goal. In short, the actions of the society must model those that we wish to inspire in the day-to-day practice of our members. Although the unprecedented growth of the society is responsible for errors in the past, the importance of admitting our shortcomings is no less significant. We’ve had some missteps along the way, and while these mistakes are a product of events preceding my tenure, it does not matter. As president of the organization, I am taking responsibility for them, with a pledge to devote all time and energy, with all due speed, to finding systematic solutions that will prevent these errors from happening again.

And let me be even more honest. As we go forward, there are probably going to be more missteps; such is the nature of a growing and active organization. I cannot promise an error-free organization, but I can promise that if and when errors are made in the future, the same intensity will be applied to seek systematic solutions to ensure that we continue to evolve in becoming an organization that is emblematic of quality. Such is the promise of SHM; such is the promise of the hospitalist. TH

Dr. Wiese is president of SHM.

References

1. Kohn LT, Corrigan JM, Donaldson MS, et al. To Err Is Human: Building a Safer Health System. Washington, D.C.: National Academies Press; 2000.
2. Institute of Medicine Committee on Quality Health Care in America. Crossing the Quality Chasm: A New Health System for the 21st Century. Washington, D.C.: National Academies Press; 2001.

How many people have to die before you’ll pay attention? Like many of you, I read the article but it didn’t really stick. Rather, I filed it in the “interesting tidbits” folder on my brain’s hard drive. Somehow 29,000 people with cancer just didn’t register as a big number.

Until I thought I could be one of them.

The Number

I was harried, running late for a meeting, questioning my decision to try to shoehorn a PCP appointment into my lunch break. Then again, this was a routine follow-up of some labs and I, of course, am the picture of health. Well, I am if you exclude my LDL. It turns out that on a check 12 months earlier, my LDL was found to be running a few heart attacks higher than normal. I took this as a sign, combined with my ballooning waist, middle-ish age, and nagging wife, that I needed to do something.

Still, I wasn’t ready for “something” to include an anticholesterol medication. Instead, I chose the masochistic route and hit the treadmill. And the bike. And a little less of the dinner plate. As a result, I had lost 30 pounds, a handful of pant sizes and, while I wasn’t exactly “in shape,” I did find myself shaped a little less like the Michelin Man.

Triumphantly, I was returning to vanquish my tormentor—the PCP who foolhardily recommended I start a medication.

Sitting in the office awaiting the news of my post-weight-loss cholesterol, my grin was wide and smug—and apparently still overflowing with LDL. I was devastated. 259? I lose weight and my LDL actually goes up!?! I could feel the foam cells in my coronary plaques twitch with delight as they mockingly gorged on chylomicrons.

Undeterred, I inquired what my options were, secretly hoping the answer would be more red wine. Emboldened by my supersaturated serum, my PCP declared it was time for a statin. Alternatively, he noted that I could get a CT angiogram of my coronaries and, if they were clean, I potentially could bypass drug therapy. Thoughts of avoided myalgias happily flittered across my mind until they stumbled onto the number 29,000. It was then that I recalled the recent Archives of Internal Medicine paper.¹

The Study

Using risk models based on the known biological effects of radiation, researchers estimated that approximately 29,000 people would develop cancer from the radiation associated with CT scans in 2007 alone. To arrive at this number, the authors used data showing that 1.5% to 2% of all U.S. cancers could be traced to the radiation from CT scans.

Not surprisingly, the most commonly utilized CT scans—namely, abdominal (14,000 a year), chest (4,100 a year), and head (4,000 a year)—accounted for the most morbidity. However, CT angiography, with its super-high dose of radiation, was projected to contribute 2,700 cancers a year. Apparently, my PCP didn’t read this article.

In terms of types of malignancy, lung cancer leads the list with 6,200 projected CT-induced cancers per year, followed by colon cancer (3,500 a year) and leukemia (2,800 a year).

The Names

If the numbers from this study hold, then about 1 in every 2,000 CT scans results in a new cancer. That would mean that I’ve dished out several cancers during my practice. In fact, I’ve ordered many thousand CT scans over my career—give or take a cancer. So my pen has, statistically, caused approximately three cancers.

I wondered which three patients it was. Was it Mr. Reynolds, who would’ve very likely died had we not diagnosed his post-operative abdominal abscess? Perhaps it was Mr. Jenson, who surely would have fared poorly if his pulmonary embolism had not been diagnosed and treated. Maybe it was Mrs. Hernandez, who wouldn’t have received thrombolytics for her stroke without a head CT.

Yes, I might have played a role in causing cancer in these three patients, but I did so knowing that I also saved, or at least improved, their lives. Most patients would accept that calculus.

But what if it were a different three? What if my cancer was that head CT I ordered for Mr. Davidson’s confusion, even though I know that head scans are rarely helpful in the evaluation of delirium? Perhaps my cancer-causer was that abdominal CT scan for Mrs. Ramirez’s chronic pain, which was clearly referable to her irritable bowel syndrome. Maybe it will be that CT scan I ordered last week because the patient insisted it be done, even though I strongly suspected, correctly, that it wouldn’t alter my management.

Which three would it be?

The Questions

This triggered more questions. How many of the 70 million-plus CT scans we order every year really are necessary? How many could be avoided by a robust physical examination, crisper clinical reasoning, or an alternate test? Do our patients really know the risk of these “innocuous” tests? Do we?

And, more personally, what if my PCP was still sitting on two? Would I be his number three?

Moving forward, I vow to remember 29,000. It will remain in the forefront of my mind, constantly badgering me about the next CT scan I order. To be sure, I will continue to order CTs—a lot of CTs. However, I will do so through the prism of the following query. If a patient developed a cancer from the CT scan I was about to order, could I sincerely look them in the eye and tell them I would do the test again?

And I’m agitated by one final question. How is that it took my own carcinogenic brush with CT scans for me to realize the gravity of 29,000? It’s not that 29,000 is not a big number. In fact, it’s precisely because it is a big number that we miss its importance. It’s too easy to hide behind the anonymity of the number. Because in the end, numbers don’t have names until the name is yours. TH

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

Reference

1. Berrington de González A, Mahesh M, Kim KP, et al. Projected cancer risks from computed tomographic scans performed in the United States in 2007. Arch Intern Med. 2009;169(22):2071-2077.

How many people have to die before you’ll pay attention? Like many of you, I read the article but it didn’t really stick. Rather, I filed it in the “interesting tidbits” folder on my brain’s hard drive. Somehow 29,000 people with cancer just didn’t register as a big number.

Until I thought I could be one of them.

The Number

I was harried, running late for a meeting, questioning my decision to try to shoehorn a PCP appointment into my lunch break. Then again, this was a routine follow-up of some labs and I, of course, am the picture of health. Well, I am if you exclude my LDL. It turns out that on a check 12 months earlier, my LDL was found to be running a few heart attacks higher than normal. I took this as a sign, combined with my ballooning waist, middle-ish age, and nagging wife, that I needed to do something.

Still, I wasn’t ready for “something” to include an anticholesterol medication. Instead, I chose the masochistic route and hit the treadmill. And the bike. And a little less of the dinner plate. As a result, I had lost 30 pounds, a handful of pant sizes and, while I wasn’t exactly “in shape,” I did find myself shaped a little less like the Michelin Man.

Triumphantly, I was returning to vanquish my tormentor—the PCP who foolhardily recommended I start a medication.

Sitting in the office awaiting the news of my post-weight-loss cholesterol, my grin was wide and smug—and apparently still overflowing with LDL. I was devastated. 259? I lose weight and my LDL actually goes up!?! I could feel the foam cells in my coronary plaques twitch with delight as they mockingly gorged on chylomicrons.

Undeterred, I inquired what my options were, secretly hoping the answer would be more red wine. Emboldened by my supersaturated serum, my PCP declared it was time for a statin. Alternatively, he noted that I could get a CT angiogram of my coronaries and, if they were clean, I potentially could bypass drug therapy. Thoughts of avoided myalgias happily flittered across my mind until they stumbled onto the number 29,000. It was then that I recalled the recent Archives of Internal Medicine paper.¹

The Study

Using risk models based on the known biological effects of radiation, researchers estimated that approximately 29,000 people would develop cancer from the radiation associated with CT scans in 2007 alone. To arrive at this number, the authors used data showing that 1.5% to 2% of all U.S. cancers could be traced to the radiation from CT scans.

Not surprisingly, the most commonly utilized CT scans—namely, abdominal (14,000 a year), chest (4,100 a year), and head (4,000 a year)—accounted for the most morbidity. However, CT angiography, with its super-high dose of radiation, was projected to contribute 2,700 cancers a year. Apparently, my PCP didn’t read this article.

In terms of types of malignancy, lung cancer leads the list with 6,200 projected CT-induced cancers per year, followed by colon cancer (3,500 a year) and leukemia (2,800 a year).

The Names

If the numbers from this study hold, then about 1 in every 2,000 CT scans results in a new cancer. That would mean that I’ve dished out several cancers during my practice. In fact, I’ve ordered many thousand CT scans over my career—give or take a cancer. So my pen has, statistically, caused approximately three cancers.

I wondered which three patients it was. Was it Mr. Reynolds, who would’ve very likely died had we not diagnosed his post-operative abdominal abscess? Perhaps it was Mr. Jenson, who surely would have fared poorly if his pulmonary embolism had not been diagnosed and treated. Maybe it was Mrs. Hernandez, who wouldn’t have received thrombolytics for her stroke without a head CT.

Yes, I might have played a role in causing cancer in these three patients, but I did so knowing that I also saved, or at least improved, their lives. Most patients would accept that calculus.

But what if it were a different three? What if my cancer was that head CT I ordered for Mr. Davidson’s confusion, even though I know that head scans are rarely helpful in the evaluation of delirium? Perhaps my cancer-causer was that abdominal CT scan for Mrs. Ramirez’s chronic pain, which was clearly referable to her irritable bowel syndrome. Maybe it will be that CT scan I ordered last week because the patient insisted it be done, even though I strongly suspected, correctly, that it wouldn’t alter my management.

Which three would it be?

The Questions

This triggered more questions. How many of the 70 million-plus CT scans we order every year really are necessary? How many could be avoided by a robust physical examination, crisper clinical reasoning, or an alternate test? Do our patients really know the risk of these “innocuous” tests? Do we?

And, more personally, what if my PCP was still sitting on two? Would I be his number three?

Moving forward, I vow to remember 29,000. It will remain in the forefront of my mind, constantly badgering me about the next CT scan I order. To be sure, I will continue to order CTs—a lot of CTs. However, I will do so through the prism of the following query. If a patient developed a cancer from the CT scan I was about to order, could I sincerely look them in the eye and tell them I would do the test again?

And I’m agitated by one final question. How is that it took my own carcinogenic brush with CT scans for me to realize the gravity of 29,000? It’s not that 29,000 is not a big number. In fact, it’s precisely because it is a big number that we miss its importance. It’s too easy to hide behind the anonymity of the number. Because in the end, numbers don’t have names until the name is yours. TH

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

Reference

1. Berrington de González A, Mahesh M, Kim KP, et al. Projected cancer risks from computed tomographic scans performed in the United States in 2007. Arch Intern Med. 2009;169(22):2071-2077.

How many people have to die before you’ll pay attention? Like many of you, I read the article but it didn’t really stick. Rather, I filed it in the “interesting tidbits” folder on my brain’s hard drive. Somehow 29,000 people with cancer just didn’t register as a big number.

Until I thought I could be one of them.

The Number

I was harried, running late for a meeting, questioning my decision to try to shoehorn a PCP appointment into my lunch break. Then again, this was a routine follow-up of some labs and I, of course, am the picture of health. Well, I am if you exclude my LDL. It turns out that on a check 12 months earlier, my LDL was found to be running a few heart attacks higher than normal. I took this as a sign, combined with my ballooning waist, middle-ish age, and nagging wife, that I needed to do something.

Still, I wasn’t ready for “something” to include an anticholesterol medication. Instead, I chose the masochistic route and hit the treadmill. And the bike. And a little less of the dinner plate. As a result, I had lost 30 pounds, a handful of pant sizes and, while I wasn’t exactly “in shape,” I did find myself shaped a little less like the Michelin Man.

Triumphantly, I was returning to vanquish my tormentor—the PCP who foolhardily recommended I start a medication.

Sitting in the office awaiting the news of my post-weight-loss cholesterol, my grin was wide and smug—and apparently still overflowing with LDL. I was devastated. 259? I lose weight and my LDL actually goes up!?! I could feel the foam cells in my coronary plaques twitch with delight as they mockingly gorged on chylomicrons.

Undeterred, I inquired what my options were, secretly hoping the answer would be more red wine. Emboldened by my supersaturated serum, my PCP declared it was time for a statin. Alternatively, he noted that I could get a CT angiogram of my coronaries and, if they were clean, I potentially could bypass drug therapy. Thoughts of avoided myalgias happily flittered across my mind until they stumbled onto the number 29,000. It was then that I recalled the recent Archives of Internal Medicine paper.¹

The Study

Using risk models based on the known biological effects of radiation, researchers estimated that approximately 29,000 people would develop cancer from the radiation associated with CT scans in 2007 alone. To arrive at this number, the authors used data showing that 1.5% to 2% of all U.S. cancers could be traced to the radiation from CT scans.

Not surprisingly, the most commonly utilized CT scans—namely, abdominal (14,000 a year), chest (4,100 a year), and head (4,000 a year)—accounted for the most morbidity. However, CT angiography, with its super-high dose of radiation, was projected to contribute 2,700 cancers a year. Apparently, my PCP didn’t read this article.

In terms of types of malignancy, lung cancer leads the list with 6,200 projected CT-induced cancers per year, followed by colon cancer (3,500 a year) and leukemia (2,800 a year).

The Names

If the numbers from this study hold, then about 1 in every 2,000 CT scans results in a new cancer. That would mean that I’ve dished out several cancers during my practice. In fact, I’ve ordered many thousand CT scans over my career—give or take a cancer. So my pen has, statistically, caused approximately three cancers.

I wondered which three patients it was. Was it Mr. Reynolds, who would’ve very likely died had we not diagnosed his post-operative abdominal abscess? Perhaps it was Mr. Jenson, who surely would have fared poorly if his pulmonary embolism had not been diagnosed and treated. Maybe it was Mrs. Hernandez, who wouldn’t have received thrombolytics for her stroke without a head CT.

Yes, I might have played a role in causing cancer in these three patients, but I did so knowing that I also saved, or at least improved, their lives. Most patients would accept that calculus.

But what if it were a different three? What if my cancer was that head CT I ordered for Mr. Davidson’s confusion, even though I know that head scans are rarely helpful in the evaluation of delirium? Perhaps my cancer-causer was that abdominal CT scan for Mrs. Ramirez’s chronic pain, which was clearly referable to her irritable bowel syndrome. Maybe it will be that CT scan I ordered last week because the patient insisted it be done, even though I strongly suspected, correctly, that it wouldn’t alter my management.

Which three would it be?

The Questions

This triggered more questions. How many of the 70 million-plus CT scans we order every year really are necessary? How many could be avoided by a robust physical examination, crisper clinical reasoning, or an alternate test? Do our patients really know the risk of these “innocuous” tests? Do we?

And, more personally, what if my PCP was still sitting on two? Would I be his number three?

Moving forward, I vow to remember 29,000. It will remain in the forefront of my mind, constantly badgering me about the next CT scan I order. To be sure, I will continue to order CTs—a lot of CTs. However, I will do so through the prism of the following query. If a patient developed a cancer from the CT scan I was about to order, could I sincerely look them in the eye and tell them I would do the test again?

And I’m agitated by one final question. How is that it took my own carcinogenic brush with CT scans for me to realize the gravity of 29,000? It’s not that 29,000 is not a big number. In fact, it’s precisely because it is a big number that we miss its importance. It’s too easy to hide behind the anonymity of the number. Because in the end, numbers don’t have names until the name is yours. TH

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

Reference

1. Berrington de González A, Mahesh M, Kim KP, et al. Projected cancer risks from computed tomographic scans performed in the United States in 2007. Arch Intern Med. 2009;169(22):2071-2077.

Last month I began looking at ways hospitalist practices can manage unpredictable increases in patient volume, also known as surge staffing. I provided my view of a “jeopardy” system and a patient volume cap for hospitalists. While both are potentially very effective, they have a high cost and in my view are imperfect solutions. This month I’ll examine some less common strategies to provide surge staffing. Although less popular, I think these options are more valuable.

Schedule More Providers

I’ve worked with a lot of practices and am struck by how patient volume for nearly all of them falls within a reasonably predictable range. While no one can predict with certainty which days will be unusually busy or slow, nearly all practices have a range of daily encounters that is roughly half to 1 1/2 of the mean. For example, if a practice has a mean of 60 billable encounters per day, it probably ranges from about 30 to 90 encounters on any given day. (The larger the practice, the more likely they are to conform to this range. Small practices, with average daily encounters fewer than 20, have a much wider range of daily volumes as a percent of the mean.)

Despite knowing that volumes will vary unpredictably, most practices provide the same fixed “dose” of provider staffing every day—that is, the single most common model for staffing and scheduling is to provide a fixed number of day-shift doctors (“rounders”) who work a fixed number of hours. For example, with an average of 60 billable encounters a day, a hospitalist group might decide to staff with four day-shift rounders working 12-hour shifts. This equates to a fixed 48 hours of daytime staffing. This is reasonable until the busy days arrive. Those four doctors will be much busier than average when there are 90 patients to see in a day, and will probably have a hard time seeing 22 or 23 patients each during their 12-hour shift. If such a busy day occurs more than a couple of times annually, then the practice should probably make some changes.

One approach to solving this type of staffing predicament is to add a fifth day-shift rounder. In other words, when making staffing decisions, consider giving more weight to the busiest days than the average day. This sounds fine until thinking about the practice budget. It will be pretty expensive to add doctors every day just so there are enough on duty when things get really busy. But if the hospitalists are willing to accept reduced compensation, then it might be financially reasonable to go ahead and add staff. This is easiest to do when the hospitalists are paid a significant (e.g. ≥50%) portion of their income based on their productivity, which will enable the hospitalists themselves to have a lot of say about when it is time to add staff. (Being paid on a nearly fixed annual salary means that it is the finance person who usually has the say about when it is time to add staff. And you can bet he’ll be making staffing decisions based on the average daily encounters, rather than the busy days.)

My own preference would be to do just that: Accept a reduction in compensation in return for protection against really busy and stressful days. I’m not suggesting others should agree with me, and in my experience, most don’t. (My own practice partners don’t agree with me on this one.) So I’m not really recommending it as a best practice, but I want to ensure that you don’t forget it is an option. And keep in mind you could adjust staffing by degrees; some settings might add a half-time physician or a nonphysician provider to try to find the sweet spot between having enough staff on duty every day to handle surges in volume and the cost of that staffing to the employer—or the hospitalists themselves.

Of course, if I were willing to reduce my compensation and average daily workload, then I would expect to be freed from the expectation that all rounding doctors work 12-hour shifts. Let’s turn our attention to the interplay between fixed day-shift durations and surge staffing.

Fixed-Shift Schedules Inhibit Surge Capacity

I think it usually is best to avoid fixed durations for day shifts. It might be necessary to require at least one daytime rounder to stay at least until a specified time (e.g. the arrival of the night-shift doctor), but in most cases it is reasonable for some rounders to leave when their work is done. They might need to continue responding to pages until the start of the night shift, but it usually isn’t necessary to have all rounders in the hospital until a predetermined end of the shift.

The problem is that when shifts have a fixed duration, the providers will focus on the start and stop time of their shift and might be unwilling to work beyond it. If instead there are no clearly fixed start and stop times for each day shift, then the hospitalists are likely to be willing to simply work longer on busy days, as long as they can work shorter on slow days. This is probably the most effective method of surge capacity, and it fits well with staffing each day with more providers than are required for the average patient volume.

Simply having the rounding doctors work longer on busy days must be done within reason. And there is a really wide range of opinion about what is reasonable. I think it is reasonable if a hospitalist works two or three hours longer than usual for three or four consecutive busy days, as long as the hospitalist is allowed to work less on days that are not very busy. But just what is a reasonable maximum daily amount of work for even one day is a topic that can lead to passionate debate. You’ll have to decide the details of what is and isn’t acceptable in your group.

Unit-Based Assignments

Aside from fixed-duration day shifts, unit-based assignment of hospitalists is the most common practice inhibiting surge capacity. Not long ago I worked with a practice that followed very strict unit-based assignments, which significantly inhibited “load-leveling,” and thus surge capacity. On any given day the patient volume for the whole practice might be very reasonable, but because it was never distributed evenly among the rounders, there was a very good chance that at least one doctor was drowning in work. And because of the strict approach, the other doctors didn’t come to the rescue.

I think the only reasonable approach is to deviate from such a strict unit-based assignment, at least a little. One rounder could be a utility doctor who doesn’t have her own unit and instead roams throughout the hospital, having been assigned patients based on the workload of each of her unit-based colleagues. TH

Dr. Nelson has been a practicing hospitalist since 1988 and is cofounder and past president of SHM. He is a principal in Nelson Flores Hospital Medicine Consultants (www.nelsonflores.com) and codirector and 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.

Last month I began looking at ways hospitalist practices can manage unpredictable increases in patient volume, also known as surge staffing. I provided my view of a “jeopardy” system and a patient volume cap for hospitalists. While both are potentially very effective, they have a high cost and in my view are imperfect solutions. This month I’ll examine some less common strategies to provide surge staffing. Although less popular, I think these options are more valuable.

Schedule More Providers

I’ve worked with a lot of practices and am struck by how patient volume for nearly all of them falls within a reasonably predictable range. While no one can predict with certainty which days will be unusually busy or slow, nearly all practices have a range of daily encounters that is roughly half to 1 1/2 of the mean. For example, if a practice has a mean of 60 billable encounters per day, it probably ranges from about 30 to 90 encounters on any given day. (The larger the practice, the more likely they are to conform to this range. Small practices, with average daily encounters fewer than 20, have a much wider range of daily volumes as a percent of the mean.)

Despite knowing that volumes will vary unpredictably, most practices provide the same fixed “dose” of provider staffing every day—that is, the single most common model for staffing and scheduling is to provide a fixed number of day-shift doctors (“rounders”) who work a fixed number of hours. For example, with an average of 60 billable encounters a day, a hospitalist group might decide to staff with four day-shift rounders working 12-hour shifts. This equates to a fixed 48 hours of daytime staffing. This is reasonable until the busy days arrive. Those four doctors will be much busier than average when there are 90 patients to see in a day, and will probably have a hard time seeing 22 or 23 patients each during their 12-hour shift. If such a busy day occurs more than a couple of times annually, then the practice should probably make some changes.

One approach to solving this type of staffing predicament is to add a fifth day-shift rounder. In other words, when making staffing decisions, consider giving more weight to the busiest days than the average day. This sounds fine until thinking about the practice budget. It will be pretty expensive to add doctors every day just so there are enough on duty when things get really busy. But if the hospitalists are willing to accept reduced compensation, then it might be financially reasonable to go ahead and add staff. This is easiest to do when the hospitalists are paid a significant (e.g. ≥50%) portion of their income based on their productivity, which will enable the hospitalists themselves to have a lot of say about when it is time to add staff. (Being paid on a nearly fixed annual salary means that it is the finance person who usually has the say about when it is time to add staff. And you can bet he’ll be making staffing decisions based on the average daily encounters, rather than the busy days.)

My own preference would be to do just that: Accept a reduction in compensation in return for protection against really busy and stressful days. I’m not suggesting others should agree with me, and in my experience, most don’t. (My own practice partners don’t agree with me on this one.) So I’m not really recommending it as a best practice, but I want to ensure that you don’t forget it is an option. And keep in mind you could adjust staffing by degrees; some settings might add a half-time physician or a nonphysician provider to try to find the sweet spot between having enough staff on duty every day to handle surges in volume and the cost of that staffing to the employer—or the hospitalists themselves.

Of course, if I were willing to reduce my compensation and average daily workload, then I would expect to be freed from the expectation that all rounding doctors work 12-hour shifts. Let’s turn our attention to the interplay between fixed day-shift durations and surge staffing.

Fixed-Shift Schedules Inhibit Surge Capacity

I think it usually is best to avoid fixed durations for day shifts. It might be necessary to require at least one daytime rounder to stay at least until a specified time (e.g. the arrival of the night-shift doctor), but in most cases it is reasonable for some rounders to leave when their work is done. They might need to continue responding to pages until the start of the night shift, but it usually isn’t necessary to have all rounders in the hospital until a predetermined end of the shift.

The problem is that when shifts have a fixed duration, the providers will focus on the start and stop time of their shift and might be unwilling to work beyond it. If instead there are no clearly fixed start and stop times for each day shift, then the hospitalists are likely to be willing to simply work longer on busy days, as long as they can work shorter on slow days. This is probably the most effective method of surge capacity, and it fits well with staffing each day with more providers than are required for the average patient volume.

Simply having the rounding doctors work longer on busy days must be done within reason. And there is a really wide range of opinion about what is reasonable. I think it is reasonable if a hospitalist works two or three hours longer than usual for three or four consecutive busy days, as long as the hospitalist is allowed to work less on days that are not very busy. But just what is a reasonable maximum daily amount of work for even one day is a topic that can lead to passionate debate. You’ll have to decide the details of what is and isn’t acceptable in your group.

Unit-Based Assignments

Aside from fixed-duration day shifts, unit-based assignment of hospitalists is the most common practice inhibiting surge capacity. Not long ago I worked with a practice that followed very strict unit-based assignments, which significantly inhibited “load-leveling,” and thus surge capacity. On any given day the patient volume for the whole practice might be very reasonable, but because it was never distributed evenly among the rounders, there was a very good chance that at least one doctor was drowning in work. And because of the strict approach, the other doctors didn’t come to the rescue.

I think the only reasonable approach is to deviate from such a strict unit-based assignment, at least a little. One rounder could be a utility doctor who doesn’t have her own unit and instead roams throughout the hospital, having been assigned patients based on the workload of each of her unit-based colleagues. TH

Dr. Nelson has been a practicing hospitalist since 1988 and is cofounder and past president of SHM. He is a principal in Nelson Flores Hospital Medicine Consultants (www.nelsonflores.com) and codirector and 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.

Last month I began looking at ways hospitalist practices can manage unpredictable increases in patient volume, also known as surge staffing. I provided my view of a “jeopardy” system and a patient volume cap for hospitalists. While both are potentially very effective, they have a high cost and in my view are imperfect solutions. This month I’ll examine some less common strategies to provide surge staffing. Although less popular, I think these options are more valuable.

Schedule More Providers

I’ve worked with a lot of practices and am struck by how patient volume for nearly all of them falls within a reasonably predictable range. While no one can predict with certainty which days will be unusually busy or slow, nearly all practices have a range of daily encounters that is roughly half to 1 1/2 of the mean. For example, if a practice has a mean of 60 billable encounters per day, it probably ranges from about 30 to 90 encounters on any given day. (The larger the practice, the more likely they are to conform to this range. Small practices, with average daily encounters fewer than 20, have a much wider range of daily volumes as a percent of the mean.)

Despite knowing that volumes will vary unpredictably, most practices provide the same fixed “dose” of provider staffing every day—that is, the single most common model for staffing and scheduling is to provide a fixed number of day-shift doctors (“rounders”) who work a fixed number of hours. For example, with an average of 60 billable encounters a day, a hospitalist group might decide to staff with four day-shift rounders working 12-hour shifts. This equates to a fixed 48 hours of daytime staffing. This is reasonable until the busy days arrive. Those four doctors will be much busier than average when there are 90 patients to see in a day, and will probably have a hard time seeing 22 or 23 patients each during their 12-hour shift. If such a busy day occurs more than a couple of times annually, then the practice should probably make some changes.

One approach to solving this type of staffing predicament is to add a fifth day-shift rounder. In other words, when making staffing decisions, consider giving more weight to the busiest days than the average day. This sounds fine until thinking about the practice budget. It will be pretty expensive to add doctors every day just so there are enough on duty when things get really busy. But if the hospitalists are willing to accept reduced compensation, then it might be financially reasonable to go ahead and add staff. This is easiest to do when the hospitalists are paid a significant (e.g. ≥50%) portion of their income based on their productivity, which will enable the hospitalists themselves to have a lot of say about when it is time to add staff. (Being paid on a nearly fixed annual salary means that it is the finance person who usually has the say about when it is time to add staff. And you can bet he’ll be making staffing decisions based on the average daily encounters, rather than the busy days.)

My own preference would be to do just that: Accept a reduction in compensation in return for protection against really busy and stressful days. I’m not suggesting others should agree with me, and in my experience, most don’t. (My own practice partners don’t agree with me on this one.) So I’m not really recommending it as a best practice, but I want to ensure that you don’t forget it is an option. And keep in mind you could adjust staffing by degrees; some settings might add a half-time physician or a nonphysician provider to try to find the sweet spot between having enough staff on duty every day to handle surges in volume and the cost of that staffing to the employer—or the hospitalists themselves.

Of course, if I were willing to reduce my compensation and average daily workload, then I would expect to be freed from the expectation that all rounding doctors work 12-hour shifts. Let’s turn our attention to the interplay between fixed day-shift durations and surge staffing.

Fixed-Shift Schedules Inhibit Surge Capacity

I think it usually is best to avoid fixed durations for day shifts. It might be necessary to require at least one daytime rounder to stay at least until a specified time (e.g. the arrival of the night-shift doctor), but in most cases it is reasonable for some rounders to leave when their work is done. They might need to continue responding to pages until the start of the night shift, but it usually isn’t necessary to have all rounders in the hospital until a predetermined end of the shift.

The problem is that when shifts have a fixed duration, the providers will focus on the start and stop time of their shift and might be unwilling to work beyond it. If instead there are no clearly fixed start and stop times for each day shift, then the hospitalists are likely to be willing to simply work longer on busy days, as long as they can work shorter on slow days. This is probably the most effective method of surge capacity, and it fits well with staffing each day with more providers than are required for the average patient volume.

Simply having the rounding doctors work longer on busy days must be done within reason. And there is a really wide range of opinion about what is reasonable. I think it is reasonable if a hospitalist works two or three hours longer than usual for three or four consecutive busy days, as long as the hospitalist is allowed to work less on days that are not very busy. But just what is a reasonable maximum daily amount of work for even one day is a topic that can lead to passionate debate. You’ll have to decide the details of what is and isn’t acceptable in your group.

Unit-Based Assignments

Aside from fixed-duration day shifts, unit-based assignment of hospitalists is the most common practice inhibiting surge capacity. Not long ago I worked with a practice that followed very strict unit-based assignments, which significantly inhibited “load-leveling,” and thus surge capacity. On any given day the patient volume for the whole practice might be very reasonable, but because it was never distributed evenly among the rounders, there was a very good chance that at least one doctor was drowning in work. And because of the strict approach, the other doctors didn’t come to the rescue.

I think the only reasonable approach is to deviate from such a strict unit-based assignment, at least a little. One rounder could be a utility doctor who doesn’t have her own unit and instead roams throughout the hospital, having been assigned patients based on the workload of each of her unit-based colleagues. TH

Dr. Nelson has been a practicing hospitalist since 1988 and is cofounder and past president of SHM. He is a principal in Nelson Flores Hospital Medicine Consultants (www.nelsonflores.com) and codirector and 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.

Did you happen to read a recent New York Times article (www.nytimes.com/2010/05/27/us/27hosp.html) about hospitalists? I thought the article was great, but I was surprised by some of the negative reader feedback. What did you think?

George Eppley, MD

Reed, Ga.

Dr. Hospitalist responds: I read the NYT article by Jane Gross, “New Breed of Specialist Steps in for Family Doctor,” which was published May 26. The accompanying reader comment section is available at http://newoldage.blogs.nytimes.com/2010/05/26/in-hospitals-new-fingers -on-the-pulse/?ref=us.

The article provides the statistics that all of us in HM have come to know: HM is the fastest-growing medical specialty in the U.S. and, over the past decade, the number of hospitalists in the U.S. has grown from hundreds to 30,000. Gross talks about the care a hospitalist at the Hospital of the University of Pennsylvania provides for her patient. She highlights the challenges of transitions of care and references the work being done by hospitalists and SHM to make sure patients are making safe transitions. While the article was largely supportive of HM, she does provide a shade of balance when she mentions the risks to the patient when hospitalists fail to do their job when it comes to communication.

As a practicing hospitalist, I kind of wished I had stopped reading at the end of the article. I honestly did not like most of what I read in the reader comment section. Although the article was a feel-good story, I think it is fair to say the reader comments were largely negative. I understand that readers with negative experiences with hospitalists might be more likely to post a comment; nevertheless, some of the comments are hard to ignore—mainly because I suspect some of it is true.

One reader from Raleigh, N.C., wrote, “Hospitalists proved inept at contacting the patients’ existing doctors or even talking to the patients. Then, on discharge to nursing homes for further recovery, the ball was dropped further, with very poor communication of medication dosages, etc.” Yikes! What happened to the communication and the medication reconciliation process?

A reader from Massachusetts wrote about “the hospitalist … (who) ordered five blood draws in the space of several hours to replicate tests that had already been taken by the primary-care physician before admission.” So, not only are hospitalists poor communicators and do not do a good job with transitions of care, but their care is also driving up the cost of healthcare needlessly?

The most positive comments seem to come from outpatient providers and, quite honestly, I found them lukewarm at best. A PCP from Charleston, S.C., wrote, “I no longer have to cancel the appointments of the patients at the last minute in order to attend to an emergency occurring outside my office. It is a very efficient system.” Glad to hear the hospitalist relationship is working out for you, Dr. PCP, but as a patient in the hospital, I am worried more about the competency of this doctor, whom I have never met before this hospitalization, as opposed to how this doctor is going to make you more “efficient” in your office practice.

I came away with several thoughts after reading the article and the comments.

First, we need to set the right expectations. Is this the equivalent of the star athlete who makes a brash statement followed shortly thereafter by the statement, “I was misquoted”? Well … maybe. Are we who we say we are? The headline is “New Breed of Specialist Steps in for Family Doctor.”

As a practicing hospitalist, I never describe myself as replacing the family doctor, because this is the worst position I could put myself in. A patient might have a relationship with a family doctor for three or four decades. This family doctor might not only care for this patient, but also his children and grandchildren. The patient visits the family doctor at least once a year for a checkup. But when the patient is as sick as they have ever been in their life and needs their family doctor whom they trust, I am supposed to “step in” for this family doctor? Good luck trying to meet that standard. It’s like putting me next to Justin Timberlake on stage at a teenybopper concert. Who do you think is going to look better in that sort of comparison?

We, as hospitalists, should never allow anyone to think we are replacing their family doctor. We are here to work with the family doctor to provide the best care possible. Do surgeons, medical subspecialists, or ED doctors “replace” the family doctor? No way! They are working with the family doctor. Perhaps the problem here is that we have not set the appropriate expectations for our patients.

Next, we need to be clear in saying what we say we do or doing we what we say we do. A line in this article bothers me more than any of the reader comments: “The most compelling argument in favor of hospitalists, who are now in 5,000 institutions, from academic giants like the Hospital of the University of Pennsylvania to small community hospitals to innovators like the Mayo and Cleveland Clinics—is that they are there all the time.”

Why does it bother me so much? It is troubling because it is misleading and might simply be untrue. Many hospitalists are not there “all the time.” While many of our hospitalist programs have providers in the hospital 24 hours a day, many do not. I know a number of hospitalists who make rounds at multiple hospitals throughout the day. Are they really hospitalists or are they inpatient rounders?

Hospitalists are physicians defined by their location, not unlike ED physicians. Do we have ED doctors going from hospital to hospital, leaving nurses alone to care for patients when they are at another hospital? So what do we expect from our hospitalists? Should they be in the hospital 24/7? That would seem to be more consistent with the thought that “they are there all the time.” Remember, Gross did not say hospitalists are “reachable” all the time. She did say hospitalists are “on top of everything that happens to a patient—from entry through treatment and discharge.” It is time that we, as hospitalists, uniformly meet those expectations. Patients all over the country are figuring out that not all hospitalists are doing what they are supposed to do when it comes to communications and establishing safe transitions of care. Remember the adage: It does not take many rotten apples to spoil the barrel.

Last, let us talk more about how hospitalists can provide patient-centric care, as opposed to cost savings and carrying out President Obama’s marching orders. The article describes how a study published in the Journal of the American Medical Association found that patients have a reduced length of stay in the hospital when cared for by hospitalists; how hospitalists are being viewed as leaders in healthcare reform; and how the hospitalist spends her nonclinical time “design(ing) computer programs to contain costs.” Do not get me wrong. I am supportive as anyone of the notion that hospitalists should provide cost-effective care. But the reality is that our patients’ No. 1 priority is to believe that their doctor is providing the best care possible. They do not want to feel someone is short-changing them.

Talk all you want to insurers and hospitals about cost savings, but when speaking with patients, I think it makes more sense to discuss the quality as opposed to cost of care. Ask your next patient whether they give a hoot what you do when you are not caring for them. TH

Did you happen to read a recent New York Times article (www.nytimes.com/2010/05/27/us/27hosp.html) about hospitalists? I thought the article was great, but I was surprised by some of the negative reader feedback. What did you think?

George Eppley, MD

Reed, Ga.

Dr. Hospitalist responds: I read the NYT article by Jane Gross, “New Breed of Specialist Steps in for Family Doctor,” which was published May 26. The accompanying reader comment section is available at http://newoldage.blogs.nytimes.com/2010/05/26/in-hospitals-new-fingers -on-the-pulse/?ref=us.

The article provides the statistics that all of us in HM have come to know: HM is the fastest-growing medical specialty in the U.S. and, over the past decade, the number of hospitalists in the U.S. has grown from hundreds to 30,000. Gross talks about the care a hospitalist at the Hospital of the University of Pennsylvania provides for her patient. She highlights the challenges of transitions of care and references the work being done by hospitalists and SHM to make sure patients are making safe transitions. While the article was largely supportive of HM, she does provide a shade of balance when she mentions the risks to the patient when hospitalists fail to do their job when it comes to communication.

As a practicing hospitalist, I kind of wished I had stopped reading at the end of the article. I honestly did not like most of what I read in the reader comment section. Although the article was a feel-good story, I think it is fair to say the reader comments were largely negative. I understand that readers with negative experiences with hospitalists might be more likely to post a comment; nevertheless, some of the comments are hard to ignore—mainly because I suspect some of it is true.

One reader from Raleigh, N.C., wrote, “Hospitalists proved inept at contacting the patients’ existing doctors or even talking to the patients. Then, on discharge to nursing homes for further recovery, the ball was dropped further, with very poor communication of medication dosages, etc.” Yikes! What happened to the communication and the medication reconciliation process?

A reader from Massachusetts wrote about “the hospitalist … (who) ordered five blood draws in the space of several hours to replicate tests that had already been taken by the primary-care physician before admission.” So, not only are hospitalists poor communicators and do not do a good job with transitions of care, but their care is also driving up the cost of healthcare needlessly?

The most positive comments seem to come from outpatient providers and, quite honestly, I found them lukewarm at best. A PCP from Charleston, S.C., wrote, “I no longer have to cancel the appointments of the patients at the last minute in order to attend to an emergency occurring outside my office. It is a very efficient system.” Glad to hear the hospitalist relationship is working out for you, Dr. PCP, but as a patient in the hospital, I am worried more about the competency of this doctor, whom I have never met before this hospitalization, as opposed to how this doctor is going to make you more “efficient” in your office practice.

I came away with several thoughts after reading the article and the comments.

First, we need to set the right expectations. Is this the equivalent of the star athlete who makes a brash statement followed shortly thereafter by the statement, “I was misquoted”? Well … maybe. Are we who we say we are? The headline is “New Breed of Specialist Steps in for Family Doctor.”

As a practicing hospitalist, I never describe myself as replacing the family doctor, because this is the worst position I could put myself in. A patient might have a relationship with a family doctor for three or four decades. This family doctor might not only care for this patient, but also his children and grandchildren. The patient visits the family doctor at least once a year for a checkup. But when the patient is as sick as they have ever been in their life and needs their family doctor whom they trust, I am supposed to “step in” for this family doctor? Good luck trying to meet that standard. It’s like putting me next to Justin Timberlake on stage at a teenybopper concert. Who do you think is going to look better in that sort of comparison?

We, as hospitalists, should never allow anyone to think we are replacing their family doctor. We are here to work with the family doctor to provide the best care possible. Do surgeons, medical subspecialists, or ED doctors “replace” the family doctor? No way! They are working with the family doctor. Perhaps the problem here is that we have not set the appropriate expectations for our patients.

Next, we need to be clear in saying what we say we do or doing we what we say we do. A line in this article bothers me more than any of the reader comments: “The most compelling argument in favor of hospitalists, who are now in 5,000 institutions, from academic giants like the Hospital of the University of Pennsylvania to small community hospitals to innovators like the Mayo and Cleveland Clinics—is that they are there all the time.”

Why does it bother me so much? It is troubling because it is misleading and might simply be untrue. Many hospitalists are not there “all the time.” While many of our hospitalist programs have providers in the hospital 24 hours a day, many do not. I know a number of hospitalists who make rounds at multiple hospitals throughout the day. Are they really hospitalists or are they inpatient rounders?

Hospitalists are physicians defined by their location, not unlike ED physicians. Do we have ED doctors going from hospital to hospital, leaving nurses alone to care for patients when they are at another hospital? So what do we expect from our hospitalists? Should they be in the hospital 24/7? That would seem to be more consistent with the thought that “they are there all the time.” Remember, Gross did not say hospitalists are “reachable” all the time. She did say hospitalists are “on top of everything that happens to a patient—from entry through treatment and discharge.” It is time that we, as hospitalists, uniformly meet those expectations. Patients all over the country are figuring out that not all hospitalists are doing what they are supposed to do when it comes to communications and establishing safe transitions of care. Remember the adage: It does not take many rotten apples to spoil the barrel.

Last, let us talk more about how hospitalists can provide patient-centric care, as opposed to cost savings and carrying out President Obama’s marching orders. The article describes how a study published in the Journal of the American Medical Association found that patients have a reduced length of stay in the hospital when cared for by hospitalists; how hospitalists are being viewed as leaders in healthcare reform; and how the hospitalist spends her nonclinical time “design(ing) computer programs to contain costs.” Do not get me wrong. I am supportive as anyone of the notion that hospitalists should provide cost-effective care. But the reality is that our patients’ No. 1 priority is to believe that their doctor is providing the best care possible. They do not want to feel someone is short-changing them.

Talk all you want to insurers and hospitals about cost savings, but when speaking with patients, I think it makes more sense to discuss the quality as opposed to cost of care. Ask your next patient whether they give a hoot what you do when you are not caring for them. TH

Did you happen to read a recent New York Times article (www.nytimes.com/2010/05/27/us/27hosp.html) about hospitalists? I thought the article was great, but I was surprised by some of the negative reader feedback. What did you think?

George Eppley, MD

Reed, Ga.

Dr. Hospitalist responds: I read the NYT article by Jane Gross, “New Breed of Specialist Steps in for Family Doctor,” which was published May 26. The accompanying reader comment section is available at http://newoldage.blogs.nytimes.com/2010/05/26/in-hospitals-new-fingers -on-the-pulse/?ref=us.

The article provides the statistics that all of us in HM have come to know: HM is the fastest-growing medical specialty in the U.S. and, over the past decade, the number of hospitalists in the U.S. has grown from hundreds to 30,000. Gross talks about the care a hospitalist at the Hospital of the University of Pennsylvania provides for her patient. She highlights the challenges of transitions of care and references the work being done by hospitalists and SHM to make sure patients are making safe transitions. While the article was largely supportive of HM, she does provide a shade of balance when she mentions the risks to the patient when hospitalists fail to do their job when it comes to communication.

As a practicing hospitalist, I kind of wished I had stopped reading at the end of the article. I honestly did not like most of what I read in the reader comment section. Although the article was a feel-good story, I think it is fair to say the reader comments were largely negative. I understand that readers with negative experiences with hospitalists might be more likely to post a comment; nevertheless, some of the comments are hard to ignore—mainly because I suspect some of it is true.

One reader from Raleigh, N.C., wrote, “Hospitalists proved inept at contacting the patients’ existing doctors or even talking to the patients. Then, on discharge to nursing homes for further recovery, the ball was dropped further, with very poor communication of medication dosages, etc.” Yikes! What happened to the communication and the medication reconciliation process?

A reader from Massachusetts wrote about “the hospitalist … (who) ordered five blood draws in the space of several hours to replicate tests that had already been taken by the primary-care physician before admission.” So, not only are hospitalists poor communicators and do not do a good job with transitions of care, but their care is also driving up the cost of healthcare needlessly?

The most positive comments seem to come from outpatient providers and, quite honestly, I found them lukewarm at best. A PCP from Charleston, S.C., wrote, “I no longer have to cancel the appointments of the patients at the last minute in order to attend to an emergency occurring outside my office. It is a very efficient system.” Glad to hear the hospitalist relationship is working out for you, Dr. PCP, but as a patient in the hospital, I am worried more about the competency of this doctor, whom I have never met before this hospitalization, as opposed to how this doctor is going to make you more “efficient” in your office practice.

I came away with several thoughts after reading the article and the comments.

First, we need to set the right expectations. Is this the equivalent of the star athlete who makes a brash statement followed shortly thereafter by the statement, “I was misquoted”? Well … maybe. Are we who we say we are? The headline is “New Breed of Specialist Steps in for Family Doctor.”

As a practicing hospitalist, I never describe myself as replacing the family doctor, because this is the worst position I could put myself in. A patient might have a relationship with a family doctor for three or four decades. This family doctor might not only care for this patient, but also his children and grandchildren. The patient visits the family doctor at least once a year for a checkup. But when the patient is as sick as they have ever been in their life and needs their family doctor whom they trust, I am supposed to “step in” for this family doctor? Good luck trying to meet that standard. It’s like putting me next to Justin Timberlake on stage at a teenybopper concert. Who do you think is going to look better in that sort of comparison?

We, as hospitalists, should never allow anyone to think we are replacing their family doctor. We are here to work with the family doctor to provide the best care possible. Do surgeons, medical subspecialists, or ED doctors “replace” the family doctor? No way! They are working with the family doctor. Perhaps the problem here is that we have not set the appropriate expectations for our patients.

Next, we need to be clear in saying what we say we do or doing we what we say we do. A line in this article bothers me more than any of the reader comments: “The most compelling argument in favor of hospitalists, who are now in 5,000 institutions, from academic giants like the Hospital of the University of Pennsylvania to small community hospitals to innovators like the Mayo and Cleveland Clinics—is that they are there all the time.”

Why does it bother me so much? It is troubling because it is misleading and might simply be untrue. Many hospitalists are not there “all the time.” While many of our hospitalist programs have providers in the hospital 24 hours a day, many do not. I know a number of hospitalists who make rounds at multiple hospitals throughout the day. Are they really hospitalists or are they inpatient rounders?

Hospitalists are physicians defined by their location, not unlike ED physicians. Do we have ED doctors going from hospital to hospital, leaving nurses alone to care for patients when they are at another hospital? So what do we expect from our hospitalists? Should they be in the hospital 24/7? That would seem to be more consistent with the thought that “they are there all the time.” Remember, Gross did not say hospitalists are “reachable” all the time. She did say hospitalists are “on top of everything that happens to a patient—from entry through treatment and discharge.” It is time that we, as hospitalists, uniformly meet those expectations. Patients all over the country are figuring out that not all hospitalists are doing what they are supposed to do when it comes to communications and establishing safe transitions of care. Remember the adage: It does not take many rotten apples to spoil the barrel.

Last, let us talk more about how hospitalists can provide patient-centric care, as opposed to cost savings and carrying out President Obama’s marching orders. The article describes how a study published in the Journal of the American Medical Association found that patients have a reduced length of stay in the hospital when cared for by hospitalists; how hospitalists are being viewed as leaders in healthcare reform; and how the hospitalist spends her nonclinical time “design(ing) computer programs to contain costs.” Do not get me wrong. I am supportive as anyone of the notion that hospitalists should provide cost-effective care. But the reality is that our patients’ No. 1 priority is to believe that their doctor is providing the best care possible. They do not want to feel someone is short-changing them.

Talk all you want to insurers and hospitals about cost savings, but when speaking with patients, I think it makes more sense to discuss the quality as opposed to cost of care. Ask your next patient whether they give a hoot what you do when you are not caring for them. TH

A 38-year-old woman presents with recurrent asymptomatic lesions on the palms and soles and on the sides of both feet. The lesions have been developing for 2 months, unaccompanied by fever or other systemic symptoms.

Laboratory tests of C-reactive protein, erythrocyte sedimentation rate, viral serologies, and antinuclear antibodies are normal. A pustule culture is negative, and a cutaneous biopsy shows parakeratosis and elongation of rete ridges, neutrophils migrating from papillary capillaries to the epidermis, and spongiform Kogoj pustule.

Q: Which is the most likely diagnosis?

• Pustular psoriasis
• Impetigo contagiosa
• Syndrome of synovitis, acne, pustulosis, hyperostosis, osteitis (SAPHO)
• Dyshidrotic eczema
• Acute exanthematous pustulosis (drug eruption)

A: SAPHO syndrome is the most likely diagnosis. The presence of pustules and aseptic osteitis of the anterior chest wall is compatible with SAPHO syndrome. Treatment with topical clobetasol propionate (Temovate) for pustules and NSAIDs for osteitis brought a good response.

Pustular psoriasis is an uncommon type of psoriasis characterized by erythema and pustules involving the flexural and anogenital areas. Cutaneous lesions of psoriasis vulgaris may be present before an acute pustular episode. Withdrawal of systemic corticosteroids in a patient with psoriasis has been reported as a precipitating factor.

Impetigo contagiosa is a superficial cutaneous infection characterized by an erythematous macule that evolves into a vesicle or pustule. These lesions are more common in children. Culture of the fluid usually reveals Staphylococcus aureus or S pyogenes.

Dyshidrotic eczema is a pruritic vesicular eruption of unknown cause on the palm and soles (bilateral and symmetric). The typical histologic findings are spongiotic and intraepidermal vesicles.

Acute exanthematous pustulosis is a drug-induced reaction characterized by confluent erythema, blisters, and pustules, mucous membrane erosions with fever, and lymphadenopathy. Cultures of the pustules are negative, and biopsy can help confirm the diagnosis of drug eruption.

SAPHO SYNDROME

SAPHO syndrome is a rare condition of unknown pathogenesis originally described by Chamot et al¹ in 1987. The onset is usually in young adulthood, and is similar in men and women. It is characterized by synovitis, acne, pustulosis, hyperostosis, and osteitis. Of paramount importance is the finding of a non-infectious inflammatory osteitis in a patient with skin lesions.

Clinical findings: Pustules plus rheumatic pain

SAPHO syndrome must be suspected when a patient is affected by a pustular skin disease associated with rheumatic pain. If examination shows that the pain is caused by a sterile inflammation of bone or joints, the diagnosis tends to be confirmed.²

Osteoarticular involvement tends to be limited to the anterior chest wall. It may include aseptic osteitis, hyperostosis, and symmetrical arthritis. Peripheral and axial osteitis is one of the main characteristics of the syndrome and is found in around 90% of cases.

Cutaneous manifestations are present in two-thirds of patients and consist chiefly of severe acne (acne fulminans, acne conglobata, and hidradenitis suppurativa), pustular psoriasis, and palmoplantar pustulosis. Neutrophilic dermatoses associated with this syndrome include Sweet syndrome and pyoderma gangrenosum. Acne lesions are usually seen in men, whereas palmoplantar pustulosis is seen in women,³ often accompanying osteoarticular manifestations.

Radiologic findings in the spine are spondylodiskitis, osteosclerosis, sacroiliac joint involvement, and paravertebral ossification. In anterior chest wall hyperostosis, common findings are bone hypertrophy and sclerosis with a soft-tissue component. Laboratory test results are uncharacteristic, with variable signs of inflammation, and the C-reactive protein and sedimentation rate are usually elevated in the absence of leukocytosis.

Pathogenesis remains elusive

The pathogenesis of this syndrome remains elusive. Since SAPHO syndrome usually involves the axial skeleton, some investigators have suggested a possible link between the SAPHO syndrome and the seronegative spondyloarthopathies.³ It has also been related to an infection by Propionibacterium acnes and Corynebacterium species,⁴ which have been isolated in cultures of bone and skin lesions. However, the fact that these bacteria are contaminant agents makes their involvement in the pathogenesis of this syndrome unlikely. More recently, high concentrations of tumor necrosis factor alpha in bone specimens of patients with SAPHO syndrome have been reported, thus highlighting the central role of this cytokine in maintaining inflammation.

Treatment is to relieve symptoms

Since understanding of the pathogenesis of SAPHO syndrome is limited, a wide range of therapies has been used,⁵ mostly to relieve symptoms. These include NSAIDs; steroids; antibiotics; bisphosphonates such as pamidronate (Aredia) and zoledronic acid (Reclast); and immunosuppressors and immunomodulators such as methotrexate (Trexall), leflunomide (Arava), sulfasalazine (Azulfidine), cyclosporine (Sandimmune). The results with these therapies have been quite varied. Good response has been reported with tumor necrosis factor alpha blockers—infliximab (Remicade), etanercept (Enbrel), and adalimumab (Humira).⁶

A 38-year-old woman presents with recurrent asymptomatic lesions on the palms and soles and on the sides of both feet. The lesions have been developing for 2 months, unaccompanied by fever or other systemic symptoms.

Laboratory tests of C-reactive protein, erythrocyte sedimentation rate, viral serologies, and antinuclear antibodies are normal. A pustule culture is negative, and a cutaneous biopsy shows parakeratosis and elongation of rete ridges, neutrophils migrating from papillary capillaries to the epidermis, and spongiform Kogoj pustule.

Q: Which is the most likely diagnosis?

• Pustular psoriasis
• Impetigo contagiosa
• Syndrome of synovitis, acne, pustulosis, hyperostosis, osteitis (SAPHO)
• Dyshidrotic eczema
• Acute exanthematous pustulosis (drug eruption)

A: SAPHO syndrome is the most likely diagnosis. The presence of pustules and aseptic osteitis of the anterior chest wall is compatible with SAPHO syndrome. Treatment with topical clobetasol propionate (Temovate) for pustules and NSAIDs for osteitis brought a good response.

Pustular psoriasis is an uncommon type of psoriasis characterized by erythema and pustules involving the flexural and anogenital areas. Cutaneous lesions of psoriasis vulgaris may be present before an acute pustular episode. Withdrawal of systemic corticosteroids in a patient with psoriasis has been reported as a precipitating factor.

Impetigo contagiosa is a superficial cutaneous infection characterized by an erythematous macule that evolves into a vesicle or pustule. These lesions are more common in children. Culture of the fluid usually reveals Staphylococcus aureus or S pyogenes.

Dyshidrotic eczema is a pruritic vesicular eruption of unknown cause on the palm and soles (bilateral and symmetric). The typical histologic findings are spongiotic and intraepidermal vesicles.

Acute exanthematous pustulosis is a drug-induced reaction characterized by confluent erythema, blisters, and pustules, mucous membrane erosions with fever, and lymphadenopathy. Cultures of the pustules are negative, and biopsy can help confirm the diagnosis of drug eruption.

SAPHO SYNDROME

SAPHO syndrome is a rare condition of unknown pathogenesis originally described by Chamot et al¹ in 1987. The onset is usually in young adulthood, and is similar in men and women. It is characterized by synovitis, acne, pustulosis, hyperostosis, and osteitis. Of paramount importance is the finding of a non-infectious inflammatory osteitis in a patient with skin lesions.

Clinical findings: Pustules plus rheumatic pain

SAPHO syndrome must be suspected when a patient is affected by a pustular skin disease associated with rheumatic pain. If examination shows that the pain is caused by a sterile inflammation of bone or joints, the diagnosis tends to be confirmed.²

Osteoarticular involvement tends to be limited to the anterior chest wall. It may include aseptic osteitis, hyperostosis, and symmetrical arthritis. Peripheral and axial osteitis is one of the main characteristics of the syndrome and is found in around 90% of cases.

Cutaneous manifestations are present in two-thirds of patients and consist chiefly of severe acne (acne fulminans, acne conglobata, and hidradenitis suppurativa), pustular psoriasis, and palmoplantar pustulosis. Neutrophilic dermatoses associated with this syndrome include Sweet syndrome and pyoderma gangrenosum. Acne lesions are usually seen in men, whereas palmoplantar pustulosis is seen in women,³ often accompanying osteoarticular manifestations.

Radiologic findings in the spine are spondylodiskitis, osteosclerosis, sacroiliac joint involvement, and paravertebral ossification. In anterior chest wall hyperostosis, common findings are bone hypertrophy and sclerosis with a soft-tissue component. Laboratory test results are uncharacteristic, with variable signs of inflammation, and the C-reactive protein and sedimentation rate are usually elevated in the absence of leukocytosis.

Pathogenesis remains elusive

The pathogenesis of this syndrome remains elusive. Since SAPHO syndrome usually involves the axial skeleton, some investigators have suggested a possible link between the SAPHO syndrome and the seronegative spondyloarthopathies.³ It has also been related to an infection by Propionibacterium acnes and Corynebacterium species,⁴ which have been isolated in cultures of bone and skin lesions. However, the fact that these bacteria are contaminant agents makes their involvement in the pathogenesis of this syndrome unlikely. More recently, high concentrations of tumor necrosis factor alpha in bone specimens of patients with SAPHO syndrome have been reported, thus highlighting the central role of this cytokine in maintaining inflammation.

Treatment is to relieve symptoms

Since understanding of the pathogenesis of SAPHO syndrome is limited, a wide range of therapies has been used,⁵ mostly to relieve symptoms. These include NSAIDs; steroids; antibiotics; bisphosphonates such as pamidronate (Aredia) and zoledronic acid (Reclast); and immunosuppressors and immunomodulators such as methotrexate (Trexall), leflunomide (Arava), sulfasalazine (Azulfidine), cyclosporine (Sandimmune). The results with these therapies have been quite varied. Good response has been reported with tumor necrosis factor alpha blockers—infliximab (Remicade), etanercept (Enbrel), and adalimumab (Humira).⁶

A 38-year-old woman presents with recurrent asymptomatic lesions on the palms and soles and on the sides of both feet. The lesions have been developing for 2 months, unaccompanied by fever or other systemic symptoms.

Laboratory tests of C-reactive protein, erythrocyte sedimentation rate, viral serologies, and antinuclear antibodies are normal. A pustule culture is negative, and a cutaneous biopsy shows parakeratosis and elongation of rete ridges, neutrophils migrating from papillary capillaries to the epidermis, and spongiform Kogoj pustule.

Q: Which is the most likely diagnosis?

• Pustular psoriasis
• Impetigo contagiosa
• Syndrome of synovitis, acne, pustulosis, hyperostosis, osteitis (SAPHO)
• Dyshidrotic eczema
• Acute exanthematous pustulosis (drug eruption)

A: SAPHO syndrome is the most likely diagnosis. The presence of pustules and aseptic osteitis of the anterior chest wall is compatible with SAPHO syndrome. Treatment with topical clobetasol propionate (Temovate) for pustules and NSAIDs for osteitis brought a good response.

Pustular psoriasis is an uncommon type of psoriasis characterized by erythema and pustules involving the flexural and anogenital areas. Cutaneous lesions of psoriasis vulgaris may be present before an acute pustular episode. Withdrawal of systemic corticosteroids in a patient with psoriasis has been reported as a precipitating factor.

Impetigo contagiosa is a superficial cutaneous infection characterized by an erythematous macule that evolves into a vesicle or pustule. These lesions are more common in children. Culture of the fluid usually reveals Staphylococcus aureus or S pyogenes.

Dyshidrotic eczema is a pruritic vesicular eruption of unknown cause on the palm and soles (bilateral and symmetric). The typical histologic findings are spongiotic and intraepidermal vesicles.

Acute exanthematous pustulosis is a drug-induced reaction characterized by confluent erythema, blisters, and pustules, mucous membrane erosions with fever, and lymphadenopathy. Cultures of the pustules are negative, and biopsy can help confirm the diagnosis of drug eruption.

SAPHO SYNDROME

SAPHO syndrome is a rare condition of unknown pathogenesis originally described by Chamot et al¹ in 1987. The onset is usually in young adulthood, and is similar in men and women. It is characterized by synovitis, acne, pustulosis, hyperostosis, and osteitis. Of paramount importance is the finding of a non-infectious inflammatory osteitis in a patient with skin lesions.

Clinical findings: Pustules plus rheumatic pain

SAPHO syndrome must be suspected when a patient is affected by a pustular skin disease associated with rheumatic pain. If examination shows that the pain is caused by a sterile inflammation of bone or joints, the diagnosis tends to be confirmed.²

Osteoarticular involvement tends to be limited to the anterior chest wall. It may include aseptic osteitis, hyperostosis, and symmetrical arthritis. Peripheral and axial osteitis is one of the main characteristics of the syndrome and is found in around 90% of cases.

Cutaneous manifestations are present in two-thirds of patients and consist chiefly of severe acne (acne fulminans, acne conglobata, and hidradenitis suppurativa), pustular psoriasis, and palmoplantar pustulosis. Neutrophilic dermatoses associated with this syndrome include Sweet syndrome and pyoderma gangrenosum. Acne lesions are usually seen in men, whereas palmoplantar pustulosis is seen in women,³ often accompanying osteoarticular manifestations.

Radiologic findings in the spine are spondylodiskitis, osteosclerosis, sacroiliac joint involvement, and paravertebral ossification. In anterior chest wall hyperostosis, common findings are bone hypertrophy and sclerosis with a soft-tissue component. Laboratory test results are uncharacteristic, with variable signs of inflammation, and the C-reactive protein and sedimentation rate are usually elevated in the absence of leukocytosis.

Pathogenesis remains elusive

The pathogenesis of this syndrome remains elusive. Since SAPHO syndrome usually involves the axial skeleton, some investigators have suggested a possible link between the SAPHO syndrome and the seronegative spondyloarthopathies.³ It has also been related to an infection by Propionibacterium acnes and Corynebacterium species,⁴ which have been isolated in cultures of bone and skin lesions. However, the fact that these bacteria are contaminant agents makes their involvement in the pathogenesis of this syndrome unlikely. More recently, high concentrations of tumor necrosis factor alpha in bone specimens of patients with SAPHO syndrome have been reported, thus highlighting the central role of this cytokine in maintaining inflammation.

Treatment is to relieve symptoms

Since understanding of the pathogenesis of SAPHO syndrome is limited, a wide range of therapies has been used,⁵ mostly to relieve symptoms. These include NSAIDs; steroids; antibiotics; bisphosphonates such as pamidronate (Aredia) and zoledronic acid (Reclast); and immunosuppressors and immunomodulators such as methotrexate (Trexall), leflunomide (Arava), sulfasalazine (Azulfidine), cyclosporine (Sandimmune). The results with these therapies have been quite varied. Good response has been reported with tumor necrosis factor alpha blockers—infliximab (Remicade), etanercept (Enbrel), and adalimumab (Humira).⁶

Noninvasive positive pressure ventilation (NIPPV) is any form of positive ventilatory support applied without an endotracheal tube, including continuous positive airway pressure (CPAP).¹ The role of NIPPV in acute care has been discussed in an earlier review in the Cleveland Clinic Journal of Medicine.²

NIPPV is also used at night in outpatients with stable chronic conditions, first used in the 1980s in the treatment of obstructive sleep apnea³ and neuromuscular diseases,⁴ and since then in several other conditions including sleep disorders associated with congestive heart failure (including sleep apnea and the Cheyne-Stokes respiration-central sleep apnea syndrome), chronic obstructive pulmonary disease (COPD), and the obesity-hypoventilation syndrome.

In this review, we discuss the different types of NIPPV, the specific conditions in which they can be used, and the indications, recommendations, and evidence supporting the efficacy of NIPPV in outpatients.

THE TYPES OF NIPPV AND THEIR USES

Although the conditions for which different types of NIPPV can be used overlap significantly, each type has general indications and different goals of treatment. This section begins with types of NIPPV that are predominantly used to treat sleep-disordered breathing, and then proceeds to those predominantly used for conditions associated with hypoventilation and hypercapnia.

Continuous positive airway pressure

CPAP, currently the most widely used form of NIPPV, applies a constant level of positive pressure at the airway opening during spontaneous breathing.

CPAP is commonly used to treat obstructive sleep-disordered breathing, with the goals of improving daytime sleepiness and reducing cardiovascular risk. It has also been used to treat sleep-disordered breathing associated with congestive heart failure.

CPAP’s role in the support of ventilation is limited and indirect. For instance, it has been used in the obesity-hypoventilation syndrome and in the “overlap” syndrome (in which both sleep apnea and COPD coexist). However, its benefits in those conditions are probably derived in large part from correction of underlying obstructive sleep apnea.

The mechanisms of action of CPAP include:

• Preventing intermittent narrowing and collapse of the airway in patients with obstructive sleep apnea-hypopnea syndrome by acting as a pneumatic splint during sleep^3,5,6
• Counteracting auto-positive end-expiratory pressure, thereby reducing respiratory muscle load, reducing the work of breathing, and lowering daytime Paco₂ in patients with coexistent COPD and obstructive sleep apnea-hypopnea syndrome (the overlap syndrome)^7–9
• Improving lung function (particularly the functional residual capacity) and daytime gas exchange in obstructive sleep apnea-hypopnea syndrome ¹⁰
• Improving left ventricular systolic function in patients with heart failure coexisting with obstructive sleep apnea-hypopnea syndrome.^11,12

Auto-CPAP is delivered via a self-titrating CPAP device, which uses algorithms to detect variations in the degree of obstruction and consequently adjusts the pressure level to restore normal breathing. Auto-CPAP therefore compensates for factors that modify the upper airway collapsibility, such as body posture during sleep, stage of sleep, use of alcohol, and drugs that affect upper airway muscle tone.¹³

Although one of the premises of using auto-CPAP is that it improves the patient’s satisfaction and compliance, several studies found it to be no more effective than fixed CPAP for treating obstructive sleep apnea-hypopnea syndrome.^14–16 Current guidelines of the American Academy of Sleep Medicine do not recommend self-titrating CPAP devices to diagnose obstructive sleep apnea or to treat patients with cardiopulmonary disorders or other conditions in which nocturnal desaturation may be unrelated to obstructive events.¹⁷

Adaptive servo-ventilation

Adaptive servo-ventilation was developed for Cheyne-Stokes respiration-central sleep apnea syndrome in patients with congestive heart failure, who may have periods of crescendo-decrescendo change in tidal volume (Cheyne-Stokes respiration) with possible intercalated episodes of central apnea or hypopnea. It is also applied in patients with the complex sleep apnea syndrome.

Adaptive servo-ventilation devices are usually set at an expiratory positive airway pressure (EPAP) level sufficient to control obstructive sleep apnea. The device then automatically adjusts the pressure support for each inspiration, within a prespecified range, to maintain a moving-target ventilation set at 90% of the patient’s recent average ventilation. The aim is to stabilize breathing and reduce respiratory alkalosis, which can trigger apnea reentry cycles.¹⁸

Bilevel positive airway pressure

Bilevel positive airway pressure (bilevel PAP) can be of use in sleep-disordered breathing (including cases associated with congestive heart failure), but it is predominantly applied in conditions associated with hypoventilation.

Bilevel PAP devices deliver a higher pressure during inspiration (inspiratory positive airway pressure, or IPAP) and a lower pressure during expiration (EPAP). The gradient between IPAP and EPAP is of key importance in maintaining alveolar ventilation and reducing Paco₂. The IPAP acts as pressure support to augment the patient’s effort, maintain adequate alveolar ventilation, unload respiratory muscles, decrease the work of breathing, and control obstructive hypopnea, whereas EPAP is set to maintain upper airway patency, control obstructive apnea, improve functional residual capacity, and prevent microatelectasis.

Although there is no evidence that bilevel PAP is better adhered to or more effective than CPAP, current guidelines propose it as an option for patients who require high pressures to control obstructive sleep apnea-hypopnea syndrome or for those who cannot tolerate exhaling against a high fixed CPAP pressure.¹⁹

Other, more-common uses of bilevel PAP are to treat coexisting central sleep apnea or hypoventilation,¹⁹ the obesity-hypoventilation syndrome with residual alveolar hypoventilation despite CPAP and control of concomitant obstructive sleep apnea-hypopnea syndrome,^5,20 severe stable COPD with significant nocturnal hypoventilation and daytime hypercarbia,²¹ and restrictive pulmonary diseases.²¹

Average volume-assured pressure support

CONDITIONS IN WHICH NOCTURNAL NIPPV IS USED IN OUT PATIENTS

Obstructive sleep apnea-hypopnea syndrome

Obstructive sleep apnea-hypopnea syndrome is estimated to affect 2% of women and 4% of men.²⁵ It is characterized by recurrent episodes of partial (hypopnea) or complete (apnea) upper airway obstruction during sleep despite ongoing inspiratory efforts, with associated episodes of arousal or desaturation or both. Corresponding symptoms include excessive daytime sleepiness, choking and gasping during sleep, recurrent awakenings from sleep, unrefreshing sleep, daytime fatigue, and impaired concentration that is not explained by other factors.²⁶

Current understanding of the pathophysiology of obstructive sleep apnea implicates an impairment in the balance between factors that promote collapsibility of the airway (including obesity and anatomic issues such as the volume of the soft-tissue structures surrounding the upper airway) and the compensatory neuromuscular response.^27,28

Long-standing obstructive sleep apnea-hypopnea syndrome has been linked in prospective studies to the development of hypertension,^29–31 coronary artery disease,^32,33 increased coagulation,^34,35 and stroke or death from any cause.^36,37 It is also associated with a greater rate and severity of motor vehicular accidents,³⁸ greater health care utilization, impaired work performance, and occupational injuries.³⁹

Strong evidence exists that NIPPV (most commonly CPAP) is beneficial in obstructive sleep apnea-hypopnea syndrome, improving sleep quality, sleepiness, cognitive impairment, and quality of life,^40,41 decreasing motor vehicle accidents,⁴² lowering blood pressure, ^43,44 and decreasing the rates of myocardial infarction,³² stroke,³² and death.⁴⁵

The American Academy of Sleep Medicine recommends CPAP as an optional adjunctive therapy to lower blood pressure in patients with obstructive sleep apnea-hypopnea syndrome with concomitant hypertension.¹⁹ This is supported by a recent study that suggested that CPAP may have additional benefits on blood pressure in a subgroup of patients with uncontrolled hypertension while on antihypertensive medications.⁴⁶ Indications with Medicare guidelines for reimbursement of CPAP devices are summarized in Table 2.

Complex sleep apnea syndrome

The complex sleep apnea syndrome is characterized by the emergence of significant central sleep apnea or Cheyne-Stokes respiration after obstructive events have been brought under control with NIPPV in patients who initially appear to have obstructive sleep apnea-hypopnea syndrome. A retrospective study of patients with the complex sleep apnea syndrome who continued their NIPPV use until a subsequent polysomnographic study and NIPPV titration showed that the syndrome may resolve spontaneously, but that 46% of patients had a persistently elevated apnea-hypopnea index with central apnea activity.⁴⁷

Restoration of upper airway patency by CPAP and dysregulation or delayed adaptation of chemosensitive ventilatory control to a changing Paco₂ level may be a key pathophysiologic mechanism of the complex sleep apnea syndrome.⁴⁸ In this mechanism, increased ventilation from restored airway patency and from an increase in the slope of the ventilatory response may intermittently draw the Paco₂ to below the hypocapnic apneic threshold and trigger episodes of central apnea.⁴⁸

The ideal NIPPV device for use in the complex sleep apnea syndrome should be able to provide enough pressure to resolve the obstructive sleep apnea-hypopnea syndrome while maintaining proper ventilatory support during central apnea episodes without fluctuations of Paco₂, which could further worsen the dysregulated ventilatory control. Currently, adaptive servo-ventilation appears to be superior to bilevel PAP and CPAP in the management of the complex sleep apnea syndrome.^49,50

Sleep disturbances associated with cardiac dysfunction

There are specific indications for NIPPV modes in the setting of respiratory sleep disturbances associated with heart failure.

Obstructive sleep apnea in congestive heart failure. The prevalence of obstructive sleep apnea in patients with impaired left ventricular ejection fraction is 11% to 53%.⁵¹ Obstructive sleep apnea-hypopnea syndrome can worsen congestive heart failure by causing a periodic increase in negative intrathoracic pressure from breathing against an occluded airway, by raising arterial blood pressure, and causing tachycardia from sympathetic nervous system stimulation from hypoxia, hypercarbia, and arousals.^52,53 Both heart failure and sleep apnea contribute in an additive manner to the increased sympathetic nervous activity.⁵⁴

Fortunately, treatment with CPAP has been found to reduce systolic blood pressure and improve left ventricular systolic function in medically treated patients with heart failure and coexisting obstructive sleep apnea.^11,12 Furthermore, in a randomized trial in patients with stable congestive heart failure and newly diagnosed obstructive sleep apnea-hypopnea syndrome, a greater improvement in cardiac function was observed in patients on bilevel PAP than in those on CPAP.⁵⁵ The authors speculated that bilevel PAP might provide more unloading of the respiratory muscles, reduce the work of breathing more, and result in less positive intrathoracic pressure than with CPAP, and that the higher intrathoracic pressure with CPAP could reduce the left ventricular ejection fraction in patients with low filling pressures (pulmonary capillary wedge pressure < 12 mm Hg) and low baseline left ventricular ejection fractions (< 30%).⁵⁵

Whether these interventions reduce the mortality rate is uncertain. In a prospective nonrandomized study, 9 (24%) of 37 patients who had heart failure with untreated obstructive sleep apnea died, compared with no deaths in 14 treated patients (P = .07).⁵⁶

Cheyne-Stokes respiration with central sleep apnea in congestive heart failure. A related but different situation is central apnea associated with congestive heart failure.

There are several pathophysiologic mechanisms of Cheyne-Stokes respiration with central sleep apnea. Specifically, the elevation of left ventricular filling pressures, end-diastolic volumes, and pulmonary congestion generate hyperventilation, chronic hypocapnia, and increased chemoreceptor responsiveness, which contribute to the development of central apnea by promoting a decrease in the Paco₂ during sleep to below the hypocapnic apneic threshold.^57,58 Additionally, an increase in circulation time may result in periodicity of breathing and hyperpnea.⁵⁹ Obstructive events can then occur at the end of the central events corresponding with the nadir of the inspiratory drive.^60,61

The Canadian Continuous Positive Airway Pressure for Patients With Central Sleep Apnea and Heart Failure (CANPAP) trial, a randomized trial of CPAP in this clinical setting, showed that compared with optimal medical therapy alone, CPAP plus optimal medical therapy improved the ejection fraction, reduced central sleep apnea, improved nocturnal oxygenation, and improved the 6-minute walking distance, but without a survival benefit.⁶² The disappointing survival results from CANPAP have to be interpreted in the context that CPAP may have failed to control the central apnea in some patients, such that the mean apnea-hypopnea index in treated patients (19 events/hour) remained above the entry criterion for recruitment (15 events/hour). In a post hoc analysis of this study, the heart-transplantation-free survival rate was significantly greater in the subgroup of patients in whom CPAP effectively suppressed central sleep apnea (< 15 events/hour).⁶³

Other NIPPV modes such as bilevel PAP with backup rate and adaptive servo-ventilation have been shown in some studies to be superior to CPAP in controlling respiratory events, with adaptive servo-ventilation being the most effective in controlling central, mixed, and complex sleep apnea in this setting. ^49,50 Whether more effective resolution of obstructive and central events with these treatment modes translates into improved mortality rates and transplantation-free survival rates remains to be determined.

 

 

Obesity-hypoventilation syndrome

Obesity-hypoventilation syndrome refers to daytime hypercapnia (Paco₂ > 45 mm Hg) in obese people when no other cause of hypoventilation is present.

The prevalence of obesity-hypoventilation syndrome among patients with obstructive sleep apnea-hypopnea syndrome is 20% to 30% and is greater in extremely obese patients (body mass index > 40 kg/m²).⁶⁴ However, about 10% of patients with obesity-hypoventilation syndrome do not have obstructive sleep apnea-hypopnea syndrome.⁶⁴ Additionally, nocturnal hypoxemia and diurnal hypercapnia persist in about 40% of patients with obesity-hypoventilation syndrome after CPAP eliminates their sleep apnea.⁶⁵ Therefore, factors other than sleep apnea contribute to the development of obesity-hypoventilation syndrome, and in a meta-analysis, factors associated with daytime hypercapnia included, in addition to body mass index and the apnea-hypopnea index, mean overnight oxygen saturation and severity of restrictive pulmonary function.⁶⁶ Predictors of success with CPAP include better spirometric findings, a higher apnea-hypopnea index, and adequate oxygenation.^67,68

Bilevel PAP therapy can be tried in patients in whom CPAP by itself fails. In a study of patients with obesity-hypoventilation syndrome in whom initial CPAP treatment failed, average volume-assured pressure support lowered Paco₂ compared to bilevel PAP alone, but did not further improve oxygenation, sleep quality, or quality of life.⁶⁹

Restrictive pulmonary diseases

Neuromuscular diseases and thoracic cage abnormalities. Noninvasive ventilation has been used in patients with progressive neuromuscular disorders or severe thoracic cage abnormalities, with recognized benefits including an improved survival rate and improved quality of life.^70,71 However, NIPPV is used in only 9% of patients with amyotrophic lateral sclerosis when clearly indicated.⁷² The indications and Medicare guidelines for reimbursement of NIPPV (with or without a backup rate) in this setting are shown in Table 2.

Potential contraindications to starting NIPPV in this population include upper airway obstruction, failure to clear secretions despite optimal noninvasive support, inability to achieve a mask fit, and intolerance of the intervention.^73,74

The mechanisms of benefit of NIPPV in these settings include improvements in daytime blood gas levels (including hypercapnia⁷⁵), a reduction in the oxygen cost of breathing,⁷⁶ an increase in the ventilatory response to carbon dioxide,⁷⁵ and improved lung compliance.⁷⁷

Chronic hypercapnic failure due to severe COPD

The use of NIPPV in chronic COPD is less well established than in patients with exacerbations of COPD,⁷⁸ and limitations in its use are reflected in the more stringent Medicare indications for NIPPV in this setting (Table 2).

A particular subset of patients with stable COPD who may benefit from NIPPV includes those with daytime hypercapnia and super-imposed nocturnal hypoventilation.⁷⁸ The potential benefits of NIPPV in these patients include improved daytime and nocturnal gas exchange, increased sleep duration, and improved quality of life.⁷⁸ Additionally, a recent randomized controlled trial of NIPPV plus long-term oxygen therapy compared with oxygen therapy alone in patients with severe COPD and a Paco₂ greater than 46 mm Hg demonstrated a survival benefit in favor of adding NIPPV (hazard ratio 0.6).⁷⁹

However, that study also found no reduction in hospitalization rates, an apparent worsening in general and mental health (as reflected on the 36-Item Short Form Health Survey or SF-36, a quality-of-life questionnaire), as well as increased confusion and bewilderment (reflected on the Profile of Mood States scale).⁷⁹ These potentially deleterious effects may explain why adherence to NIPPV is low in patients with stable COPD: only 37% to 57% of patients continued to use it in several reported studies.^79–81

A level of inspiratory pressure support that is insufficient to reduce hypercapnia may account for the low adherence rate and worsened quality of life in such patients. For instance, in a randomized trial,⁸² compared with low-intensity NIPPV (mean IPAP 14 cm H₂O, backup rate 8 per minute), settings that aimed to maximally reduce Paco₂ (mean IPAP 29 cm H₂O with a backup rate of 17.5 per minute) increased the daily use of NIPPV by 3.6 hours/day and improved exercise-related dyspnea, daytime Paco₂, forced expiratory volume in 1 second (FEV₁), vital capacity, and health-related quality of life.

The overlap syndrome was first described by Flenley in 1985 as a combination of chronic respiratory disease (more generally limited to COPD) and obstructive sleep apnea-hypopnea syndrome.⁸³ Epidemiologic studies do not consistently show a higher incidence of obstructive sleep apnea-hypopnea syndrome in patients with COPD, but the exaggerated oxygen desaturation during sleep in patients with this combination increases the risk of hypoxemia, hypercapnia, and pulmonary hypertension. ⁸⁴ In addition, there was evidence of higher risks of death and of hospitalization for COPD in patients with the overlap syndrome. ⁸⁵ NIPPV is the main treatment for obstructive sleep apnea-hypopnea syndrome with or without COPD.

A recent study by Marin et al⁸⁵ showed that CPAP was associated with improved survival and decreased hospitalization in patients with the overlap syndrome. However, polysomnography or nocturnal oximetry while on NIPPV alone must be done, as additional nocturnal oxygen therapy may be warranted when significant chronic respiratory illness coexists with sleep apnea.
 

Acknowledgment: The authors gratefully acknowledge the contribution of Scott Marlow, RRT, to Table 2 of this review.

Noninvasive positive pressure ventilation (NIPPV) is any form of positive ventilatory support applied without an endotracheal tube, including continuous positive airway pressure (CPAP).¹ The role of NIPPV in acute care has been discussed in an earlier review in the Cleveland Clinic Journal of Medicine.²

NIPPV is also used at night in outpatients with stable chronic conditions, first used in the 1980s in the treatment of obstructive sleep apnea³ and neuromuscular diseases,⁴ and since then in several other conditions including sleep disorders associated with congestive heart failure (including sleep apnea and the Cheyne-Stokes respiration-central sleep apnea syndrome), chronic obstructive pulmonary disease (COPD), and the obesity-hypoventilation syndrome.

In this review, we discuss the different types of NIPPV, the specific conditions in which they can be used, and the indications, recommendations, and evidence supporting the efficacy of NIPPV in outpatients.

THE TYPES OF NIPPV AND THEIR USES

Although the conditions for which different types of NIPPV can be used overlap significantly, each type has general indications and different goals of treatment. This section begins with types of NIPPV that are predominantly used to treat sleep-disordered breathing, and then proceeds to those predominantly used for conditions associated with hypoventilation and hypercapnia.

Continuous positive airway pressure

CPAP, currently the most widely used form of NIPPV, applies a constant level of positive pressure at the airway opening during spontaneous breathing.

CPAP is commonly used to treat obstructive sleep-disordered breathing, with the goals of improving daytime sleepiness and reducing cardiovascular risk. It has also been used to treat sleep-disordered breathing associated with congestive heart failure.

CPAP’s role in the support of ventilation is limited and indirect. For instance, it has been used in the obesity-hypoventilation syndrome and in the “overlap” syndrome (in which both sleep apnea and COPD coexist). However, its benefits in those conditions are probably derived in large part from correction of underlying obstructive sleep apnea.

The mechanisms of action of CPAP include:

• Preventing intermittent narrowing and collapse of the airway in patients with obstructive sleep apnea-hypopnea syndrome by acting as a pneumatic splint during sleep^3,5,6
• Counteracting auto-positive end-expiratory pressure, thereby reducing respiratory muscle load, reducing the work of breathing, and lowering daytime Paco₂ in patients with coexistent COPD and obstructive sleep apnea-hypopnea syndrome (the overlap syndrome)^7–9
• Improving lung function (particularly the functional residual capacity) and daytime gas exchange in obstructive sleep apnea-hypopnea syndrome ¹⁰
• Improving left ventricular systolic function in patients with heart failure coexisting with obstructive sleep apnea-hypopnea syndrome.^11,12

Auto-CPAP is delivered via a self-titrating CPAP device, which uses algorithms to detect variations in the degree of obstruction and consequently adjusts the pressure level to restore normal breathing. Auto-CPAP therefore compensates for factors that modify the upper airway collapsibility, such as body posture during sleep, stage of sleep, use of alcohol, and drugs that affect upper airway muscle tone.¹³

Although one of the premises of using auto-CPAP is that it improves the patient’s satisfaction and compliance, several studies found it to be no more effective than fixed CPAP for treating obstructive sleep apnea-hypopnea syndrome.^14–16 Current guidelines of the American Academy of Sleep Medicine do not recommend self-titrating CPAP devices to diagnose obstructive sleep apnea or to treat patients with cardiopulmonary disorders or other conditions in which nocturnal desaturation may be unrelated to obstructive events.¹⁷

Adaptive servo-ventilation

Adaptive servo-ventilation was developed for Cheyne-Stokes respiration-central sleep apnea syndrome in patients with congestive heart failure, who may have periods of crescendo-decrescendo change in tidal volume (Cheyne-Stokes respiration) with possible intercalated episodes of central apnea or hypopnea. It is also applied in patients with the complex sleep apnea syndrome.

Adaptive servo-ventilation devices are usually set at an expiratory positive airway pressure (EPAP) level sufficient to control obstructive sleep apnea. The device then automatically adjusts the pressure support for each inspiration, within a prespecified range, to maintain a moving-target ventilation set at 90% of the patient’s recent average ventilation. The aim is to stabilize breathing and reduce respiratory alkalosis, which can trigger apnea reentry cycles.¹⁸

Bilevel positive airway pressure

Bilevel positive airway pressure (bilevel PAP) can be of use in sleep-disordered breathing (including cases associated with congestive heart failure), but it is predominantly applied in conditions associated with hypoventilation.

Bilevel PAP devices deliver a higher pressure during inspiration (inspiratory positive airway pressure, or IPAP) and a lower pressure during expiration (EPAP). The gradient between IPAP and EPAP is of key importance in maintaining alveolar ventilation and reducing Paco₂. The IPAP acts as pressure support to augment the patient’s effort, maintain adequate alveolar ventilation, unload respiratory muscles, decrease the work of breathing, and control obstructive hypopnea, whereas EPAP is set to maintain upper airway patency, control obstructive apnea, improve functional residual capacity, and prevent microatelectasis.

Although there is no evidence that bilevel PAP is better adhered to or more effective than CPAP, current guidelines propose it as an option for patients who require high pressures to control obstructive sleep apnea-hypopnea syndrome or for those who cannot tolerate exhaling against a high fixed CPAP pressure.¹⁹

Other, more-common uses of bilevel PAP are to treat coexisting central sleep apnea or hypoventilation,¹⁹ the obesity-hypoventilation syndrome with residual alveolar hypoventilation despite CPAP and control of concomitant obstructive sleep apnea-hypopnea syndrome,^5,20 severe stable COPD with significant nocturnal hypoventilation and daytime hypercarbia,²¹ and restrictive pulmonary diseases.²¹

Average volume-assured pressure support

CONDITIONS IN WHICH NOCTURNAL NIPPV IS USED IN OUT PATIENTS

Obstructive sleep apnea-hypopnea syndrome

Obstructive sleep apnea-hypopnea syndrome is estimated to affect 2% of women and 4% of men.²⁵ It is characterized by recurrent episodes of partial (hypopnea) or complete (apnea) upper airway obstruction during sleep despite ongoing inspiratory efforts, with associated episodes of arousal or desaturation or both. Corresponding symptoms include excessive daytime sleepiness, choking and gasping during sleep, recurrent awakenings from sleep, unrefreshing sleep, daytime fatigue, and impaired concentration that is not explained by other factors.²⁶

Current understanding of the pathophysiology of obstructive sleep apnea implicates an impairment in the balance between factors that promote collapsibility of the airway (including obesity and anatomic issues such as the volume of the soft-tissue structures surrounding the upper airway) and the compensatory neuromuscular response.^27,28

Long-standing obstructive sleep apnea-hypopnea syndrome has been linked in prospective studies to the development of hypertension,^29–31 coronary artery disease,^32,33 increased coagulation,^34,35 and stroke or death from any cause.^36,37 It is also associated with a greater rate and severity of motor vehicular accidents,³⁸ greater health care utilization, impaired work performance, and occupational injuries.³⁹

Strong evidence exists that NIPPV (most commonly CPAP) is beneficial in obstructive sleep apnea-hypopnea syndrome, improving sleep quality, sleepiness, cognitive impairment, and quality of life,^40,41 decreasing motor vehicle accidents,⁴² lowering blood pressure, ^43,44 and decreasing the rates of myocardial infarction,³² stroke,³² and death.⁴⁵

The American Academy of Sleep Medicine recommends CPAP as an optional adjunctive therapy to lower blood pressure in patients with obstructive sleep apnea-hypopnea syndrome with concomitant hypertension.¹⁹ This is supported by a recent study that suggested that CPAP may have additional benefits on blood pressure in a subgroup of patients with uncontrolled hypertension while on antihypertensive medications.⁴⁶ Indications with Medicare guidelines for reimbursement of CPAP devices are summarized in Table 2.

Complex sleep apnea syndrome

The complex sleep apnea syndrome is characterized by the emergence of significant central sleep apnea or Cheyne-Stokes respiration after obstructive events have been brought under control with NIPPV in patients who initially appear to have obstructive sleep apnea-hypopnea syndrome. A retrospective study of patients with the complex sleep apnea syndrome who continued their NIPPV use until a subsequent polysomnographic study and NIPPV titration showed that the syndrome may resolve spontaneously, but that 46% of patients had a persistently elevated apnea-hypopnea index with central apnea activity.⁴⁷

Restoration of upper airway patency by CPAP and dysregulation or delayed adaptation of chemosensitive ventilatory control to a changing Paco₂ level may be a key pathophysiologic mechanism of the complex sleep apnea syndrome.⁴⁸ In this mechanism, increased ventilation from restored airway patency and from an increase in the slope of the ventilatory response may intermittently draw the Paco₂ to below the hypocapnic apneic threshold and trigger episodes of central apnea.⁴⁸

The ideal NIPPV device for use in the complex sleep apnea syndrome should be able to provide enough pressure to resolve the obstructive sleep apnea-hypopnea syndrome while maintaining proper ventilatory support during central apnea episodes without fluctuations of Paco₂, which could further worsen the dysregulated ventilatory control. Currently, adaptive servo-ventilation appears to be superior to bilevel PAP and CPAP in the management of the complex sleep apnea syndrome.^49,50

Sleep disturbances associated with cardiac dysfunction

There are specific indications for NIPPV modes in the setting of respiratory sleep disturbances associated with heart failure.

Obstructive sleep apnea in congestive heart failure. The prevalence of obstructive sleep apnea in patients with impaired left ventricular ejection fraction is 11% to 53%.⁵¹ Obstructive sleep apnea-hypopnea syndrome can worsen congestive heart failure by causing a periodic increase in negative intrathoracic pressure from breathing against an occluded airway, by raising arterial blood pressure, and causing tachycardia from sympathetic nervous system stimulation from hypoxia, hypercarbia, and arousals.^52,53 Both heart failure and sleep apnea contribute in an additive manner to the increased sympathetic nervous activity.⁵⁴

Fortunately, treatment with CPAP has been found to reduce systolic blood pressure and improve left ventricular systolic function in medically treated patients with heart failure and coexisting obstructive sleep apnea.^11,12 Furthermore, in a randomized trial in patients with stable congestive heart failure and newly diagnosed obstructive sleep apnea-hypopnea syndrome, a greater improvement in cardiac function was observed in patients on bilevel PAP than in those on CPAP.⁵⁵ The authors speculated that bilevel PAP might provide more unloading of the respiratory muscles, reduce the work of breathing more, and result in less positive intrathoracic pressure than with CPAP, and that the higher intrathoracic pressure with CPAP could reduce the left ventricular ejection fraction in patients with low filling pressures (pulmonary capillary wedge pressure < 12 mm Hg) and low baseline left ventricular ejection fractions (< 30%).⁵⁵

Whether these interventions reduce the mortality rate is uncertain. In a prospective nonrandomized study, 9 (24%) of 37 patients who had heart failure with untreated obstructive sleep apnea died, compared with no deaths in 14 treated patients (P = .07).⁵⁶

Cheyne-Stokes respiration with central sleep apnea in congestive heart failure. A related but different situation is central apnea associated with congestive heart failure.

There are several pathophysiologic mechanisms of Cheyne-Stokes respiration with central sleep apnea. Specifically, the elevation of left ventricular filling pressures, end-diastolic volumes, and pulmonary congestion generate hyperventilation, chronic hypocapnia, and increased chemoreceptor responsiveness, which contribute to the development of central apnea by promoting a decrease in the Paco₂ during sleep to below the hypocapnic apneic threshold.^57,58 Additionally, an increase in circulation time may result in periodicity of breathing and hyperpnea.⁵⁹ Obstructive events can then occur at the end of the central events corresponding with the nadir of the inspiratory drive.^60,61

The Canadian Continuous Positive Airway Pressure for Patients With Central Sleep Apnea and Heart Failure (CANPAP) trial, a randomized trial of CPAP in this clinical setting, showed that compared with optimal medical therapy alone, CPAP plus optimal medical therapy improved the ejection fraction, reduced central sleep apnea, improved nocturnal oxygenation, and improved the 6-minute walking distance, but without a survival benefit.⁶² The disappointing survival results from CANPAP have to be interpreted in the context that CPAP may have failed to control the central apnea in some patients, such that the mean apnea-hypopnea index in treated patients (19 events/hour) remained above the entry criterion for recruitment (15 events/hour). In a post hoc analysis of this study, the heart-transplantation-free survival rate was significantly greater in the subgroup of patients in whom CPAP effectively suppressed central sleep apnea (< 15 events/hour).⁶³

Other NIPPV modes such as bilevel PAP with backup rate and adaptive servo-ventilation have been shown in some studies to be superior to CPAP in controlling respiratory events, with adaptive servo-ventilation being the most effective in controlling central, mixed, and complex sleep apnea in this setting. ^49,50 Whether more effective resolution of obstructive and central events with these treatment modes translates into improved mortality rates and transplantation-free survival rates remains to be determined.

 

 

Obesity-hypoventilation syndrome

Obesity-hypoventilation syndrome refers to daytime hypercapnia (Paco₂ > 45 mm Hg) in obese people when no other cause of hypoventilation is present.

The prevalence of obesity-hypoventilation syndrome among patients with obstructive sleep apnea-hypopnea syndrome is 20% to 30% and is greater in extremely obese patients (body mass index > 40 kg/m²).⁶⁴ However, about 10% of patients with obesity-hypoventilation syndrome do not have obstructive sleep apnea-hypopnea syndrome.⁶⁴ Additionally, nocturnal hypoxemia and diurnal hypercapnia persist in about 40% of patients with obesity-hypoventilation syndrome after CPAP eliminates their sleep apnea.⁶⁵ Therefore, factors other than sleep apnea contribute to the development of obesity-hypoventilation syndrome, and in a meta-analysis, factors associated with daytime hypercapnia included, in addition to body mass index and the apnea-hypopnea index, mean overnight oxygen saturation and severity of restrictive pulmonary function.⁶⁶ Predictors of success with CPAP include better spirometric findings, a higher apnea-hypopnea index, and adequate oxygenation.^67,68

Bilevel PAP therapy can be tried in patients in whom CPAP by itself fails. In a study of patients with obesity-hypoventilation syndrome in whom initial CPAP treatment failed, average volume-assured pressure support lowered Paco₂ compared to bilevel PAP alone, but did not further improve oxygenation, sleep quality, or quality of life.⁶⁹

Restrictive pulmonary diseases

Neuromuscular diseases and thoracic cage abnormalities. Noninvasive ventilation has been used in patients with progressive neuromuscular disorders or severe thoracic cage abnormalities, with recognized benefits including an improved survival rate and improved quality of life.^70,71 However, NIPPV is used in only 9% of patients with amyotrophic lateral sclerosis when clearly indicated.⁷² The indications and Medicare guidelines for reimbursement of NIPPV (with or without a backup rate) in this setting are shown in Table 2.

Potential contraindications to starting NIPPV in this population include upper airway obstruction, failure to clear secretions despite optimal noninvasive support, inability to achieve a mask fit, and intolerance of the intervention.^73,74

The mechanisms of benefit of NIPPV in these settings include improvements in daytime blood gas levels (including hypercapnia⁷⁵), a reduction in the oxygen cost of breathing,⁷⁶ an increase in the ventilatory response to carbon dioxide,⁷⁵ and improved lung compliance.⁷⁷

Chronic hypercapnic failure due to severe COPD

The use of NIPPV in chronic COPD is less well established than in patients with exacerbations of COPD,⁷⁸ and limitations in its use are reflected in the more stringent Medicare indications for NIPPV in this setting (Table 2).

A particular subset of patients with stable COPD who may benefit from NIPPV includes those with daytime hypercapnia and super-imposed nocturnal hypoventilation.⁷⁸ The potential benefits of NIPPV in these patients include improved daytime and nocturnal gas exchange, increased sleep duration, and improved quality of life.⁷⁸ Additionally, a recent randomized controlled trial of NIPPV plus long-term oxygen therapy compared with oxygen therapy alone in patients with severe COPD and a Paco₂ greater than 46 mm Hg demonstrated a survival benefit in favor of adding NIPPV (hazard ratio 0.6).⁷⁹

However, that study also found no reduction in hospitalization rates, an apparent worsening in general and mental health (as reflected on the 36-Item Short Form Health Survey or SF-36, a quality-of-life questionnaire), as well as increased confusion and bewilderment (reflected on the Profile of Mood States scale).⁷⁹ These potentially deleterious effects may explain why adherence to NIPPV is low in patients with stable COPD: only 37% to 57% of patients continued to use it in several reported studies.^79–81

A level of inspiratory pressure support that is insufficient to reduce hypercapnia may account for the low adherence rate and worsened quality of life in such patients. For instance, in a randomized trial,⁸² compared with low-intensity NIPPV (mean IPAP 14 cm H₂O, backup rate 8 per minute), settings that aimed to maximally reduce Paco₂ (mean IPAP 29 cm H₂O with a backup rate of 17.5 per minute) increased the daily use of NIPPV by 3.6 hours/day and improved exercise-related dyspnea, daytime Paco₂, forced expiratory volume in 1 second (FEV₁), vital capacity, and health-related quality of life.

The overlap syndrome was first described by Flenley in 1985 as a combination of chronic respiratory disease (more generally limited to COPD) and obstructive sleep apnea-hypopnea syndrome.⁸³ Epidemiologic studies do not consistently show a higher incidence of obstructive sleep apnea-hypopnea syndrome in patients with COPD, but the exaggerated oxygen desaturation during sleep in patients with this combination increases the risk of hypoxemia, hypercapnia, and pulmonary hypertension. ⁸⁴ In addition, there was evidence of higher risks of death and of hospitalization for COPD in patients with the overlap syndrome. ⁸⁵ NIPPV is the main treatment for obstructive sleep apnea-hypopnea syndrome with or without COPD.

A recent study by Marin et al⁸⁵ showed that CPAP was associated with improved survival and decreased hospitalization in patients with the overlap syndrome. However, polysomnography or nocturnal oximetry while on NIPPV alone must be done, as additional nocturnal oxygen therapy may be warranted when significant chronic respiratory illness coexists with sleep apnea.
 

Acknowledgment: The authors gratefully acknowledge the contribution of Scott Marlow, RRT, to Table 2 of this review.

Noninvasive positive pressure ventilation (NIPPV) is any form of positive ventilatory support applied without an endotracheal tube, including continuous positive airway pressure (CPAP).¹ The role of NIPPV in acute care has been discussed in an earlier review in the Cleveland Clinic Journal of Medicine.²

NIPPV is also used at night in outpatients with stable chronic conditions, first used in the 1980s in the treatment of obstructive sleep apnea³ and neuromuscular diseases,⁴ and since then in several other conditions including sleep disorders associated with congestive heart failure (including sleep apnea and the Cheyne-Stokes respiration-central sleep apnea syndrome), chronic obstructive pulmonary disease (COPD), and the obesity-hypoventilation syndrome.

In this review, we discuss the different types of NIPPV, the specific conditions in which they can be used, and the indications, recommendations, and evidence supporting the efficacy of NIPPV in outpatients.

THE TYPES OF NIPPV AND THEIR USES

Although the conditions for which different types of NIPPV can be used overlap significantly, each type has general indications and different goals of treatment. This section begins with types of NIPPV that are predominantly used to treat sleep-disordered breathing, and then proceeds to those predominantly used for conditions associated with hypoventilation and hypercapnia.

Continuous positive airway pressure

CPAP, currently the most widely used form of NIPPV, applies a constant level of positive pressure at the airway opening during spontaneous breathing.

CPAP is commonly used to treat obstructive sleep-disordered breathing, with the goals of improving daytime sleepiness and reducing cardiovascular risk. It has also been used to treat sleep-disordered breathing associated with congestive heart failure.

CPAP’s role in the support of ventilation is limited and indirect. For instance, it has been used in the obesity-hypoventilation syndrome and in the “overlap” syndrome (in which both sleep apnea and COPD coexist). However, its benefits in those conditions are probably derived in large part from correction of underlying obstructive sleep apnea.

The mechanisms of action of CPAP include:

• Preventing intermittent narrowing and collapse of the airway in patients with obstructive sleep apnea-hypopnea syndrome by acting as a pneumatic splint during sleep^3,5,6
• Counteracting auto-positive end-expiratory pressure, thereby reducing respiratory muscle load, reducing the work of breathing, and lowering daytime Paco₂ in patients with coexistent COPD and obstructive sleep apnea-hypopnea syndrome (the overlap syndrome)^7–9
• Improving lung function (particularly the functional residual capacity) and daytime gas exchange in obstructive sleep apnea-hypopnea syndrome ¹⁰
• Improving left ventricular systolic function in patients with heart failure coexisting with obstructive sleep apnea-hypopnea syndrome.^11,12

Auto-CPAP is delivered via a self-titrating CPAP device, which uses algorithms to detect variations in the degree of obstruction and consequently adjusts the pressure level to restore normal breathing. Auto-CPAP therefore compensates for factors that modify the upper airway collapsibility, such as body posture during sleep, stage of sleep, use of alcohol, and drugs that affect upper airway muscle tone.¹³

Although one of the premises of using auto-CPAP is that it improves the patient’s satisfaction and compliance, several studies found it to be no more effective than fixed CPAP for treating obstructive sleep apnea-hypopnea syndrome.^14–16 Current guidelines of the American Academy of Sleep Medicine do not recommend self-titrating CPAP devices to diagnose obstructive sleep apnea or to treat patients with cardiopulmonary disorders or other conditions in which nocturnal desaturation may be unrelated to obstructive events.¹⁷

Adaptive servo-ventilation

Adaptive servo-ventilation was developed for Cheyne-Stokes respiration-central sleep apnea syndrome in patients with congestive heart failure, who may have periods of crescendo-decrescendo change in tidal volume (Cheyne-Stokes respiration) with possible intercalated episodes of central apnea or hypopnea. It is also applied in patients with the complex sleep apnea syndrome.

Adaptive servo-ventilation devices are usually set at an expiratory positive airway pressure (EPAP) level sufficient to control obstructive sleep apnea. The device then automatically adjusts the pressure support for each inspiration, within a prespecified range, to maintain a moving-target ventilation set at 90% of the patient’s recent average ventilation. The aim is to stabilize breathing and reduce respiratory alkalosis, which can trigger apnea reentry cycles.¹⁸

Bilevel positive airway pressure

Bilevel positive airway pressure (bilevel PAP) can be of use in sleep-disordered breathing (including cases associated with congestive heart failure), but it is predominantly applied in conditions associated with hypoventilation.

Bilevel PAP devices deliver a higher pressure during inspiration (inspiratory positive airway pressure, or IPAP) and a lower pressure during expiration (EPAP). The gradient between IPAP and EPAP is of key importance in maintaining alveolar ventilation and reducing Paco₂. The IPAP acts as pressure support to augment the patient’s effort, maintain adequate alveolar ventilation, unload respiratory muscles, decrease the work of breathing, and control obstructive hypopnea, whereas EPAP is set to maintain upper airway patency, control obstructive apnea, improve functional residual capacity, and prevent microatelectasis.

Although there is no evidence that bilevel PAP is better adhered to or more effective than CPAP, current guidelines propose it as an option for patients who require high pressures to control obstructive sleep apnea-hypopnea syndrome or for those who cannot tolerate exhaling against a high fixed CPAP pressure.¹⁹

Other, more-common uses of bilevel PAP are to treat coexisting central sleep apnea or hypoventilation,¹⁹ the obesity-hypoventilation syndrome with residual alveolar hypoventilation despite CPAP and control of concomitant obstructive sleep apnea-hypopnea syndrome,^5,20 severe stable COPD with significant nocturnal hypoventilation and daytime hypercarbia,²¹ and restrictive pulmonary diseases.²¹

Average volume-assured pressure support

CONDITIONS IN WHICH NOCTURNAL NIPPV IS USED IN OUT PATIENTS

Obstructive sleep apnea-hypopnea syndrome

Obstructive sleep apnea-hypopnea syndrome is estimated to affect 2% of women and 4% of men.²⁵ It is characterized by recurrent episodes of partial (hypopnea) or complete (apnea) upper airway obstruction during sleep despite ongoing inspiratory efforts, with associated episodes of arousal or desaturation or both. Corresponding symptoms include excessive daytime sleepiness, choking and gasping during sleep, recurrent awakenings from sleep, unrefreshing sleep, daytime fatigue, and impaired concentration that is not explained by other factors.²⁶

Current understanding of the pathophysiology of obstructive sleep apnea implicates an impairment in the balance between factors that promote collapsibility of the airway (including obesity and anatomic issues such as the volume of the soft-tissue structures surrounding the upper airway) and the compensatory neuromuscular response.^27,28

Long-standing obstructive sleep apnea-hypopnea syndrome has been linked in prospective studies to the development of hypertension,^29–31 coronary artery disease,^32,33 increased coagulation,^34,35 and stroke or death from any cause.^36,37 It is also associated with a greater rate and severity of motor vehicular accidents,³⁸ greater health care utilization, impaired work performance, and occupational injuries.³⁹

Strong evidence exists that NIPPV (most commonly CPAP) is beneficial in obstructive sleep apnea-hypopnea syndrome, improving sleep quality, sleepiness, cognitive impairment, and quality of life,^40,41 decreasing motor vehicle accidents,⁴² lowering blood pressure, ^43,44 and decreasing the rates of myocardial infarction,³² stroke,³² and death.⁴⁵

The American Academy of Sleep Medicine recommends CPAP as an optional adjunctive therapy to lower blood pressure in patients with obstructive sleep apnea-hypopnea syndrome with concomitant hypertension.¹⁹ This is supported by a recent study that suggested that CPAP may have additional benefits on blood pressure in a subgroup of patients with uncontrolled hypertension while on antihypertensive medications.⁴⁶ Indications with Medicare guidelines for reimbursement of CPAP devices are summarized in Table 2.

Complex sleep apnea syndrome

The complex sleep apnea syndrome is characterized by the emergence of significant central sleep apnea or Cheyne-Stokes respiration after obstructive events have been brought under control with NIPPV in patients who initially appear to have obstructive sleep apnea-hypopnea syndrome. A retrospective study of patients with the complex sleep apnea syndrome who continued their NIPPV use until a subsequent polysomnographic study and NIPPV titration showed that the syndrome may resolve spontaneously, but that 46% of patients had a persistently elevated apnea-hypopnea index with central apnea activity.⁴⁷

Restoration of upper airway patency by CPAP and dysregulation or delayed adaptation of chemosensitive ventilatory control to a changing Paco₂ level may be a key pathophysiologic mechanism of the complex sleep apnea syndrome.⁴⁸ In this mechanism, increased ventilation from restored airway patency and from an increase in the slope of the ventilatory response may intermittently draw the Paco₂ to below the hypocapnic apneic threshold and trigger episodes of central apnea.⁴⁸

The ideal NIPPV device for use in the complex sleep apnea syndrome should be able to provide enough pressure to resolve the obstructive sleep apnea-hypopnea syndrome while maintaining proper ventilatory support during central apnea episodes without fluctuations of Paco₂, which could further worsen the dysregulated ventilatory control. Currently, adaptive servo-ventilation appears to be superior to bilevel PAP and CPAP in the management of the complex sleep apnea syndrome.^49,50

Sleep disturbances associated with cardiac dysfunction

There are specific indications for NIPPV modes in the setting of respiratory sleep disturbances associated with heart failure.

Obstructive sleep apnea in congestive heart failure. The prevalence of obstructive sleep apnea in patients with impaired left ventricular ejection fraction is 11% to 53%.⁵¹ Obstructive sleep apnea-hypopnea syndrome can worsen congestive heart failure by causing a periodic increase in negative intrathoracic pressure from breathing against an occluded airway, by raising arterial blood pressure, and causing tachycardia from sympathetic nervous system stimulation from hypoxia, hypercarbia, and arousals.^52,53 Both heart failure and sleep apnea contribute in an additive manner to the increased sympathetic nervous activity.⁵⁴

Fortunately, treatment with CPAP has been found to reduce systolic blood pressure and improve left ventricular systolic function in medically treated patients with heart failure and coexisting obstructive sleep apnea.^11,12 Furthermore, in a randomized trial in patients with stable congestive heart failure and newly diagnosed obstructive sleep apnea-hypopnea syndrome, a greater improvement in cardiac function was observed in patients on bilevel PAP than in those on CPAP.⁵⁵ The authors speculated that bilevel PAP might provide more unloading of the respiratory muscles, reduce the work of breathing more, and result in less positive intrathoracic pressure than with CPAP, and that the higher intrathoracic pressure with CPAP could reduce the left ventricular ejection fraction in patients with low filling pressures (pulmonary capillary wedge pressure < 12 mm Hg) and low baseline left ventricular ejection fractions (< 30%).⁵⁵

Whether these interventions reduce the mortality rate is uncertain. In a prospective nonrandomized study, 9 (24%) of 37 patients who had heart failure with untreated obstructive sleep apnea died, compared with no deaths in 14 treated patients (P = .07).⁵⁶

Cheyne-Stokes respiration with central sleep apnea in congestive heart failure. A related but different situation is central apnea associated with congestive heart failure.

There are several pathophysiologic mechanisms of Cheyne-Stokes respiration with central sleep apnea. Specifically, the elevation of left ventricular filling pressures, end-diastolic volumes, and pulmonary congestion generate hyperventilation, chronic hypocapnia, and increased chemoreceptor responsiveness, which contribute to the development of central apnea by promoting a decrease in the Paco₂ during sleep to below the hypocapnic apneic threshold.^57,58 Additionally, an increase in circulation time may result in periodicity of breathing and hyperpnea.⁵⁹ Obstructive events can then occur at the end of the central events corresponding with the nadir of the inspiratory drive.^60,61

The Canadian Continuous Positive Airway Pressure for Patients With Central Sleep Apnea and Heart Failure (CANPAP) trial, a randomized trial of CPAP in this clinical setting, showed that compared with optimal medical therapy alone, CPAP plus optimal medical therapy improved the ejection fraction, reduced central sleep apnea, improved nocturnal oxygenation, and improved the 6-minute walking distance, but without a survival benefit.⁶² The disappointing survival results from CANPAP have to be interpreted in the context that CPAP may have failed to control the central apnea in some patients, such that the mean apnea-hypopnea index in treated patients (19 events/hour) remained above the entry criterion for recruitment (15 events/hour). In a post hoc analysis of this study, the heart-transplantation-free survival rate was significantly greater in the subgroup of patients in whom CPAP effectively suppressed central sleep apnea (< 15 events/hour).⁶³

Other NIPPV modes such as bilevel PAP with backup rate and adaptive servo-ventilation have been shown in some studies to be superior to CPAP in controlling respiratory events, with adaptive servo-ventilation being the most effective in controlling central, mixed, and complex sleep apnea in this setting. ^49,50 Whether more effective resolution of obstructive and central events with these treatment modes translates into improved mortality rates and transplantation-free survival rates remains to be determined.

 

 

Obesity-hypoventilation syndrome

Obesity-hypoventilation syndrome refers to daytime hypercapnia (Paco₂ > 45 mm Hg) in obese people when no other cause of hypoventilation is present.

The prevalence of obesity-hypoventilation syndrome among patients with obstructive sleep apnea-hypopnea syndrome is 20% to 30% and is greater in extremely obese patients (body mass index > 40 kg/m²).⁶⁴ However, about 10% of patients with obesity-hypoventilation syndrome do not have obstructive sleep apnea-hypopnea syndrome.⁶⁴ Additionally, nocturnal hypoxemia and diurnal hypercapnia persist in about 40% of patients with obesity-hypoventilation syndrome after CPAP eliminates their sleep apnea.⁶⁵ Therefore, factors other than sleep apnea contribute to the development of obesity-hypoventilation syndrome, and in a meta-analysis, factors associated with daytime hypercapnia included, in addition to body mass index and the apnea-hypopnea index, mean overnight oxygen saturation and severity of restrictive pulmonary function.⁶⁶ Predictors of success with CPAP include better spirometric findings, a higher apnea-hypopnea index, and adequate oxygenation.^67,68

Bilevel PAP therapy can be tried in patients in whom CPAP by itself fails. In a study of patients with obesity-hypoventilation syndrome in whom initial CPAP treatment failed, average volume-assured pressure support lowered Paco₂ compared to bilevel PAP alone, but did not further improve oxygenation, sleep quality, or quality of life.⁶⁹

Restrictive pulmonary diseases

Neuromuscular diseases and thoracic cage abnormalities. Noninvasive ventilation has been used in patients with progressive neuromuscular disorders or severe thoracic cage abnormalities, with recognized benefits including an improved survival rate and improved quality of life.^70,71 However, NIPPV is used in only 9% of patients with amyotrophic lateral sclerosis when clearly indicated.⁷² The indications and Medicare guidelines for reimbursement of NIPPV (with or without a backup rate) in this setting are shown in Table 2.

Potential contraindications to starting NIPPV in this population include upper airway obstruction, failure to clear secretions despite optimal noninvasive support, inability to achieve a mask fit, and intolerance of the intervention.^73,74

The mechanisms of benefit of NIPPV in these settings include improvements in daytime blood gas levels (including hypercapnia⁷⁵), a reduction in the oxygen cost of breathing,⁷⁶ an increase in the ventilatory response to carbon dioxide,⁷⁵ and improved lung compliance.⁷⁷

Chronic hypercapnic failure due to severe COPD

The use of NIPPV in chronic COPD is less well established than in patients with exacerbations of COPD,⁷⁸ and limitations in its use are reflected in the more stringent Medicare indications for NIPPV in this setting (Table 2).

A particular subset of patients with stable COPD who may benefit from NIPPV includes those with daytime hypercapnia and super-imposed nocturnal hypoventilation.⁷⁸ The potential benefits of NIPPV in these patients include improved daytime and nocturnal gas exchange, increased sleep duration, and improved quality of life.⁷⁸ Additionally, a recent randomized controlled trial of NIPPV plus long-term oxygen therapy compared with oxygen therapy alone in patients with severe COPD and a Paco₂ greater than 46 mm Hg demonstrated a survival benefit in favor of adding NIPPV (hazard ratio 0.6).⁷⁹

However, that study also found no reduction in hospitalization rates, an apparent worsening in general and mental health (as reflected on the 36-Item Short Form Health Survey or SF-36, a quality-of-life questionnaire), as well as increased confusion and bewilderment (reflected on the Profile of Mood States scale).⁷⁹ These potentially deleterious effects may explain why adherence to NIPPV is low in patients with stable COPD: only 37% to 57% of patients continued to use it in several reported studies.^79–81

A level of inspiratory pressure support that is insufficient to reduce hypercapnia may account for the low adherence rate and worsened quality of life in such patients. For instance, in a randomized trial,⁸² compared with low-intensity NIPPV (mean IPAP 14 cm H₂O, backup rate 8 per minute), settings that aimed to maximally reduce Paco₂ (mean IPAP 29 cm H₂O with a backup rate of 17.5 per minute) increased the daily use of NIPPV by 3.6 hours/day and improved exercise-related dyspnea, daytime Paco₂, forced expiratory volume in 1 second (FEV₁), vital capacity, and health-related quality of life.

The overlap syndrome was first described by Flenley in 1985 as a combination of chronic respiratory disease (more generally limited to COPD) and obstructive sleep apnea-hypopnea syndrome.⁸³ Epidemiologic studies do not consistently show a higher incidence of obstructive sleep apnea-hypopnea syndrome in patients with COPD, but the exaggerated oxygen desaturation during sleep in patients with this combination increases the risk of hypoxemia, hypercapnia, and pulmonary hypertension. ⁸⁴ In addition, there was evidence of higher risks of death and of hospitalization for COPD in patients with the overlap syndrome. ⁸⁵ NIPPV is the main treatment for obstructive sleep apnea-hypopnea syndrome with or without COPD.

A recent study by Marin et al⁸⁵ showed that CPAP was associated with improved survival and decreased hospitalization in patients with the overlap syndrome. However, polysomnography or nocturnal oximetry while on NIPPV alone must be done, as additional nocturnal oxygen therapy may be warranted when significant chronic respiratory illness coexists with sleep apnea.
 

Acknowledgment: The authors gratefully acknowledge the contribution of Scott Marlow, RRT, to Table 2 of this review.

The reality of blood pressure measurement is that human beings do not do it very well. The time has come to delegate this job to machines that can do it better.

Several automatic devices are available. Used in physicians’ offices and in patients’ homes, they can eliminate some types of observer error as well as the “white-coat effect,” ie, the tendency of some patients to have higher blood pressure when medical personnel are present than in their natural environment. Since a difference of only a few millimeters of mercury can affect the physician’s decision to start or to modify treatment, measurements that more accurately reflect a person’s average blood pressure are to be desired.

In the following pages, we review the problems that plague blood pressure measurement by human observers, and we describe the advantages of automatic devices.

SHORTCOMINGS OF OFFICE BLOOD PRESSURE MEASUREMENT

For decades, large surveys have provided invaluable information on the prevalence of hypertension, its relationship to cardiovascular disease, and the benefits of treating it.^1–3 Unfortunately, the percentage of hypertensive patients whose blood pressure is under control has remained low despite our increased knowledge about hypertension’s diagnosis and therapy.⁴

In these surveys, blood pressure was measured by auscultation by human observers using mercury or aneroid sphygmomanometers, and most physicians still use this method in clinical practice. But in spite of multiple guidelines for accurate measurement of blood pressure in the office, the overall accuracy and reproducibility of office blood pressure measurements remain poor.^5–7

The accuracy of blood pressure measurement with aneroid and mercury manometers is affected by a number of observer errors and patient factors.^8,9

Observer errors

Failure to prepare the patient. National guidelines⁵ state that before having their blood pressure taken, patients should be allowed to sit quietly for at least 5 minutes, which often does not happen. Another error is that clinicians rarely discourage patients from smoking cigarettes or drinking coffee in the 30 minutes prior to measurement.

Equipment and layout problems. Equipment should be properly calibrated and validated. ⁵ However, even if the sphygmomanometer is periodically calibrated, too often it is mounted on the wall adjacent to the examination table in the examination room, making it difficult to provide a comfortable seat with back and arm support during the reading. The measurement should be done with the patient sitting in a chair (not on an examination table), with feet on the floor and the arm supported at the level of the heart. If the forearm is not supported in the horizontal position and with the cuff at heart level, the blood pressure and heart rate tend to be higher.¹⁰ Further, the diastolic blood pressure and heart rate may be misleadingly low with the patient supine rather than seated,^11,12 so readings should be taken with the patient sitting.

Miscuffing, ie, the use of a blood pressure cuff that is too large or, more often, too small for the patient’s arm, is a common source of error. The cuff bladder should encircle at least 80% of the arm.⁵ However, some offices do not have a large blood pressure cuff for overweight patients or a pediatric cuff for children or adults with arms of small circumference. It is recommended that a large blood pressure cuff be used routinely in adults, since a smaller cuff gives falsely high readings in people with large upper arms (circumference > 29 cm).^13,14

Digit preference. Many physicians round off the blood pressure to the nearest 5 or 10 mm Hg. This problem may go along with:

Deflating the cuff too rapidly.

Talking to the patient while taking the blood pressure can contribute to higher readings.⁹

Not taking enough readings. Ideally, at the initial visit, blood pressure should be measured in both arms with the patient seated, and another reading should be taken with the patient standing. The arm with the higher pressure should be used for subsequent readings. Physicians should not make any treatment decisions based on blood pressure during an initial clinic visit, and at least two readings should be taken even on subsequent visits. However, owing to time constraints in busy clinical practices, treatment decisions are often based on single readings or on multiple readings on a single visit.

Discrepancies between observers. The blood pressure readings obtained by the nurse or medical assistant may differ significantly from those obtained by the physician. These differences can be large enough to affect treatment decisions,^15,16 and they can be partially corrected by adequate training of all medical personnel who take blood pressure, doctors as well as nurses.

Given that time is tight in busy clinical practices and a trained blood pressure nurse or technician is usually not available, we will probably not see any significant improvement in the accuracy of blood pressure measurement using older technology and current physician practices.

The white-coat effect

Most patients have a higher level of anxiety, and therefore higher blood pressure, in the physician’s office or clinic than in their normal environment (as revealed by ambulatory monitoring or home blood pressure measurements), a phenomenon commonly called the white-coat effect.

Several factors can increase this effect, such as observer-patient interaction during the measurement. The effect tends to be greatest in the initial measurement, but can persist through multiple readings by the doctor or nurse during the same visit.

Whether the white-coat effect is due purely to patient anxiety about an office visit or to a conditioned response has been a point of interest in clinical studies. Regardless, it may result in the misdiagnosis of hypertension or in overestimation of the severity of hypertension and may lead to overly aggressive therapy. Antihypertensive treatment may be unnecessary in the absence of concurrent cardiovascular risk factors.¹⁷

“White-coat hypertension” or “isolated office hypertension” is the condition in which a patient who is not on antihypertensive drug therapy has persistently elevated blood pressure in the clinic or office (> 140/90 mm Hg) but normal daytime ambulatory blood pressure (< 135/85 mm Hg).¹⁸ Since patients may have an elevated reading when seen for a first office visit, at least several visits are required to establish the diagnosis. Multiple studies have suggested that white-coat hypertension may account for 20% to 25% of the hypertensive population, particularly in older patients, mainly women.^19,20

Both white-coat hypertension and the white-coat effect can be avoided by using an automatic and programmable device that can take multiple readings after the clinician leaves the examination room (more about this below).²¹

MEASURING BLOOD PRESSURE OUTSIDE THE OFFICE

Recent studies have reported that the information obtained by 24-hour ambulatory blood pressure monitoring and by self-measurement of blood pressure in the home more accurately reflects the patient’s risk of future cardiovascular events than do conventional blood pressure measurements taken in the physician’s office. ^22–24 Current national guidelines recognize this pattern and the frequent measurement inaccuracies observed in clinical practice, and they are recommending including out-of-office measurements in the diagnosis of hypertension. ^25,26

Ambulatory monitoring provides the most accurate measurement of out-of-office blood pressure. With ambulatory monitoring, the normal mean daytime pressure is considered to be lower than 135/85 mm Hg, in contrast to the 140/90 mm Hg cutoff used in the physician’s office with standard aneroid or mercury devices.

Self-monitoring of blood pressure at home has now become widely available with single-measurement oscillometric devices. (Oscillometric means that these devices measure the blood pressure by sensing the oscillations in pressure in the cuff induced by the pulsation of the brachial artery, as opposed to auscultating the Korotkoff sounds.) Blood pressures lower than 135/85 mm Hg outside the clinician’s office are considered normal with these devices.

However, despite its proven value, ambulatory monitoring is neither widely available nor cost-effective for the long-term management of hypertension. Furthermore, few physicians recommend that patients take their blood pressure at home, although the information obtained can be of significant value in the patient’s long-term management.

AUTOMATED MEASUREMENT IN THE OFFICE

In recent years, several automated oscillometric sphygmomanometers have been developed for measuring blood pressure in the office, and more are on the way. These devices can be programmed to take multiple readings without a clinician observer in the examination room, thus reducing the white-coat response.

Omron (Kyoto, Japan) makes several devices, including the HEM-907 and the HEM-705, that have been used in the clinical setting. ^21,27–29 They can be programmed to take two or three readings at intervals of 1 to 2 minutes, with up to 5 minutes before the first reading. Unfortunately, data were not recorded with the patient alone in the room in many studies of the Omron devices, even though the devices meet national and international standards for accuracy.

The Microlife Watch BP Office (Microlife, Widnau, Switzerland) is currently undergoing development.³⁰

The BpTRU (BpTRU Medical Devices, Coquitlam, BC, Canada) has enjoyed greater clinical acceptance, since it can take up to five blood pressure readings at intervals of 1 to 5 minutes, and calculates the mean of all five readings, taken with the patient resting comfortably in a quiet room without a clinician present.

The accuracy and durability of the device has been well established. Since the BpTRU self-calibrates between every blood pressure measurement, periodic calibration has not been required. The device can be placed on a table, mounted on the wall, or mounted on a cart if used in several locations in the office.

At Cleveland Clinic, several departments are using the BpTRU on a daily basis. Soon, we will be able to transfer data directly from the BpTRU to our electronic medical record system.

Studies of the BpTRU device

To date, most of the studies of automated office blood pressure measurement have used the BpTRU with the recording interval set at 1 to 2 minutes.

Myers³¹ used the BpTRU device in 50 hypertensive patients. The physician took the patient’s blood pressure with a mercury sphygmomanometer while the BpTRU device made the first reading, and then he left the room. The next five readings were taken at 2-minute intervals with the patient alone in the room. The mean initial reading by the machine was 162/85 mm Hg; the reading by the physician was 163/86 mm Hg. The third automatic reading was the lowest (averaging 140/84 mm Hg), and the mean of the five automated readings was 142/80 mm Hg, which was significantly lower than the initial reading obtained by the physician (P < .001).

In another study, Myers et al³² compared the measurements obtained by 24-hour ambulatory monitoring and by the BpTRU device (the mean of five readings obtained at 1-minute or 2-minute intervals) in 309 hypertensive patients. The mean blood pressure with the Bp-TRU was 132/75 mm Hg, which correlated well with the mean awake ambulatory blood pressure (134/77 mm Hg; r = 0.62 for the systolic pressure and 0.72 for the diastolic pressure).

We recently reviewed the records of 278 patients seen in our preventive medicine clinic (D.G. Vidt, MD, unpublished data, November 2009). The group included patients with and without established hypertension, and among the hypertensive group, both treated and untreated individuals. We had initially set the device to take readings at 3-minute intervals following the initial nurse-initiated reading. But in view of the recent data on the Bp-TRU using shorter intervals, we also obtained readings in 51 patients with the device set to record at 2-minute intervals, and then in 72 additional patients at 1-minute intervals. In all three groups, blood pressure had stabilized by the third reading after the clinician had left the room. These observations support those reported by Myers et al.^31,32 Of particular importance is the observation that the white-coat effect dissipates within 2 to 3 minutes after the clinician leaves the room.³³

The shorter measurement intervals can add up in a busy office practice, in which the time relegated to taking blood pressure is often limited.

In fact, waiting 5 minutes between measurements may allow the patient to become too relaxed and the blood pressure to drop too low vis-a-vis the gold standard, ambulatory monitoring. Culleton and colleagues³⁴ compared the blood pressure in 107 hypertensive patients as measured four ways: by the referring physician, by a nurse who was trained to adhere to the protocol of the Canadian Hypertension Education Program, by 24-hour ambulatory monitoring, and by the BpTRU (the mean of five readings obtained at 5-minute intervals). The mean measured values were:

• 150/90 mm Hg by the referring physician
• 139/86 mm Hg by the nurse
• 142/85 mm Hg by ambulatory monitoring
• 132/82 mm Hg by the BpTRU device.

Although the BpTRU reduced the white-coat effect and white-coat hypertension, it underestimated the blood pressure, leading to misclassification of hypertension. Using 140/90 mm Hg as the cutoff for whether the patient was hypertensive and using ambulatory monitoring as the gold standard, the BpTRU misclassified more than half of the patients, agreeing with the classification of hypertensive or not hypertensive by ambulatory monitoring in only 48%. The authors recommended that the BpTRU not be set at 5-minute measurement intervals.³⁴

WHAT ROLE FOR AUTOMATED READINGS IN THE OFFICE?

Although automatic devices, by enabling the physician to leave the room, can eliminate the white-coat effect and white-coat hypertension, physicians must continue to take care to avoid the other potential errors of office blood pressure measurement addressed earlier in this review, for example, by positioning the patient correctly and using a cuff that is large enough. These issues can take on more importance as the clinician leaves the patient alone for brief periods during measurements.

In view of its perennial inaccuracies, some experts have suggested that we abandon routine office measurement of blood pressure.^35,36 In its place, ambulatory monitoring would be used for diagnosis and for periodic follow-up. In addition, patients would regularly take their pressure at home with approved, single-measurement oscillometric devices. Unfortunately, in our health care system, periodic ambulatory monitoring for hypertension management would impose a significant financial burden on patients at this time.³⁷

Of particular importance is the observation that the mean of five readings with the BpTRU device, obtained at 1- or 2-minute intervals, closely approximates the mean awake blood pressure obtained in the same patient with an ambulatory monitor.^32,38 The ability to obtain readings that correlate exceptionally well with mean daytime ambulatory pressure suggests that this device could well reduce the need for ambulatory monitoring, with its associated cost. The ability to negate the white-coat effect with the use of the BpTRU in the office setting also has particular importance, not only for patient office readings, but for the diagnosis and subsequent treatment of hypertension in individual patients.

Most clinical decisions about the treatment of hypertension are still made on the basis of office determinations of blood pressure. Most office practices still rely on the aneroid manometer or, decreasingly, mercury sphygmomanometers. As noted earlier, although auscultatory blood pressure measurement appears to be simple, it is fraught with a host of observer- or patient-induced errors that not only lead to inaccurate diagnoses, but may also result in the mismanagement of hypertension. Even single-measurement oscillometric devices, now used in a minority of clinical practices, are associated with many of the same measurement issues that lead to overestimation of blood pressure.

We believe the time has come for broader use of oscillometric devices in the outpatient setting. While many available oscillometric devices for use in the home could also be used in the physician’s office, they carry the similar disadvantage of providing only a single measurement. The major disadvantage of all single-measurement devices is the continued presence of the clinician during the reading and the associated white-coat effect observed in most patients.

It is highly likely that the next Joint National Committee Report on Hypertension will further emphasize the role of automated blood pressure devices in the outpatient setting.
 

Acknowledgment: The authors wish to acknowledge the contributions of Deborah McCoy, RN, and Maria Eckhouse, RN.

The reality of blood pressure measurement is that human beings do not do it very well. The time has come to delegate this job to machines that can do it better.

Several automatic devices are available. Used in physicians’ offices and in patients’ homes, they can eliminate some types of observer error as well as the “white-coat effect,” ie, the tendency of some patients to have higher blood pressure when medical personnel are present than in their natural environment. Since a difference of only a few millimeters of mercury can affect the physician’s decision to start or to modify treatment, measurements that more accurately reflect a person’s average blood pressure are to be desired.

In the following pages, we review the problems that plague blood pressure measurement by human observers, and we describe the advantages of automatic devices.

SHORTCOMINGS OF OFFICE BLOOD PRESSURE MEASUREMENT

For decades, large surveys have provided invaluable information on the prevalence of hypertension, its relationship to cardiovascular disease, and the benefits of treating it.^1–3 Unfortunately, the percentage of hypertensive patients whose blood pressure is under control has remained low despite our increased knowledge about hypertension’s diagnosis and therapy.⁴

In these surveys, blood pressure was measured by auscultation by human observers using mercury or aneroid sphygmomanometers, and most physicians still use this method in clinical practice. But in spite of multiple guidelines for accurate measurement of blood pressure in the office, the overall accuracy and reproducibility of office blood pressure measurements remain poor.^5–7

The accuracy of blood pressure measurement with aneroid and mercury manometers is affected by a number of observer errors and patient factors.^8,9

Observer errors

Failure to prepare the patient. National guidelines⁵ state that before having their blood pressure taken, patients should be allowed to sit quietly for at least 5 minutes, which often does not happen. Another error is that clinicians rarely discourage patients from smoking cigarettes or drinking coffee in the 30 minutes prior to measurement.

Equipment and layout problems. Equipment should be properly calibrated and validated. ⁵ However, even if the sphygmomanometer is periodically calibrated, too often it is mounted on the wall adjacent to the examination table in the examination room, making it difficult to provide a comfortable seat with back and arm support during the reading. The measurement should be done with the patient sitting in a chair (not on an examination table), with feet on the floor and the arm supported at the level of the heart. If the forearm is not supported in the horizontal position and with the cuff at heart level, the blood pressure and heart rate tend to be higher.¹⁰ Further, the diastolic blood pressure and heart rate may be misleadingly low with the patient supine rather than seated,^11,12 so readings should be taken with the patient sitting.

Miscuffing, ie, the use of a blood pressure cuff that is too large or, more often, too small for the patient’s arm, is a common source of error. The cuff bladder should encircle at least 80% of the arm.⁵ However, some offices do not have a large blood pressure cuff for overweight patients or a pediatric cuff for children or adults with arms of small circumference. It is recommended that a large blood pressure cuff be used routinely in adults, since a smaller cuff gives falsely high readings in people with large upper arms (circumference > 29 cm).^13,14

Digit preference. Many physicians round off the blood pressure to the nearest 5 or 10 mm Hg. This problem may go along with:

Deflating the cuff too rapidly.

Talking to the patient while taking the blood pressure can contribute to higher readings.⁹

Not taking enough readings. Ideally, at the initial visit, blood pressure should be measured in both arms with the patient seated, and another reading should be taken with the patient standing. The arm with the higher pressure should be used for subsequent readings. Physicians should not make any treatment decisions based on blood pressure during an initial clinic visit, and at least two readings should be taken even on subsequent visits. However, owing to time constraints in busy clinical practices, treatment decisions are often based on single readings or on multiple readings on a single visit.

Discrepancies between observers. The blood pressure readings obtained by the nurse or medical assistant may differ significantly from those obtained by the physician. These differences can be large enough to affect treatment decisions,^15,16 and they can be partially corrected by adequate training of all medical personnel who take blood pressure, doctors as well as nurses.

Given that time is tight in busy clinical practices and a trained blood pressure nurse or technician is usually not available, we will probably not see any significant improvement in the accuracy of blood pressure measurement using older technology and current physician practices.

The white-coat effect

Most patients have a higher level of anxiety, and therefore higher blood pressure, in the physician’s office or clinic than in their normal environment (as revealed by ambulatory monitoring or home blood pressure measurements), a phenomenon commonly called the white-coat effect.

Several factors can increase this effect, such as observer-patient interaction during the measurement. The effect tends to be greatest in the initial measurement, but can persist through multiple readings by the doctor or nurse during the same visit.

Whether the white-coat effect is due purely to patient anxiety about an office visit or to a conditioned response has been a point of interest in clinical studies. Regardless, it may result in the misdiagnosis of hypertension or in overestimation of the severity of hypertension and may lead to overly aggressive therapy. Antihypertensive treatment may be unnecessary in the absence of concurrent cardiovascular risk factors.¹⁷

“White-coat hypertension” or “isolated office hypertension” is the condition in which a patient who is not on antihypertensive drug therapy has persistently elevated blood pressure in the clinic or office (> 140/90 mm Hg) but normal daytime ambulatory blood pressure (< 135/85 mm Hg).¹⁸ Since patients may have an elevated reading when seen for a first office visit, at least several visits are required to establish the diagnosis. Multiple studies have suggested that white-coat hypertension may account for 20% to 25% of the hypertensive population, particularly in older patients, mainly women.^19,20

Both white-coat hypertension and the white-coat effect can be avoided by using an automatic and programmable device that can take multiple readings after the clinician leaves the examination room (more about this below).²¹

MEASURING BLOOD PRESSURE OUTSIDE THE OFFICE

Recent studies have reported that the information obtained by 24-hour ambulatory blood pressure monitoring and by self-measurement of blood pressure in the home more accurately reflects the patient’s risk of future cardiovascular events than do conventional blood pressure measurements taken in the physician’s office. ^22–24 Current national guidelines recognize this pattern and the frequent measurement inaccuracies observed in clinical practice, and they are recommending including out-of-office measurements in the diagnosis of hypertension. ^25,26

Ambulatory monitoring provides the most accurate measurement of out-of-office blood pressure. With ambulatory monitoring, the normal mean daytime pressure is considered to be lower than 135/85 mm Hg, in contrast to the 140/90 mm Hg cutoff used in the physician’s office with standard aneroid or mercury devices.

Self-monitoring of blood pressure at home has now become widely available with single-measurement oscillometric devices. (Oscillometric means that these devices measure the blood pressure by sensing the oscillations in pressure in the cuff induced by the pulsation of the brachial artery, as opposed to auscultating the Korotkoff sounds.) Blood pressures lower than 135/85 mm Hg outside the clinician’s office are considered normal with these devices.

However, despite its proven value, ambulatory monitoring is neither widely available nor cost-effective for the long-term management of hypertension. Furthermore, few physicians recommend that patients take their blood pressure at home, although the information obtained can be of significant value in the patient’s long-term management.

AUTOMATED MEASUREMENT IN THE OFFICE

In recent years, several automated oscillometric sphygmomanometers have been developed for measuring blood pressure in the office, and more are on the way. These devices can be programmed to take multiple readings without a clinician observer in the examination room, thus reducing the white-coat response.

Omron (Kyoto, Japan) makes several devices, including the HEM-907 and the HEM-705, that have been used in the clinical setting. ^21,27–29 They can be programmed to take two or three readings at intervals of 1 to 2 minutes, with up to 5 minutes before the first reading. Unfortunately, data were not recorded with the patient alone in the room in many studies of the Omron devices, even though the devices meet national and international standards for accuracy.

The Microlife Watch BP Office (Microlife, Widnau, Switzerland) is currently undergoing development.³⁰

The BpTRU (BpTRU Medical Devices, Coquitlam, BC, Canada) has enjoyed greater clinical acceptance, since it can take up to five blood pressure readings at intervals of 1 to 5 minutes, and calculates the mean of all five readings, taken with the patient resting comfortably in a quiet room without a clinician present.

The accuracy and durability of the device has been well established. Since the BpTRU self-calibrates between every blood pressure measurement, periodic calibration has not been required. The device can be placed on a table, mounted on the wall, or mounted on a cart if used in several locations in the office.

At Cleveland Clinic, several departments are using the BpTRU on a daily basis. Soon, we will be able to transfer data directly from the BpTRU to our electronic medical record system.

Studies of the BpTRU device

To date, most of the studies of automated office blood pressure measurement have used the BpTRU with the recording interval set at 1 to 2 minutes.

Myers³¹ used the BpTRU device in 50 hypertensive patients. The physician took the patient’s blood pressure with a mercury sphygmomanometer while the BpTRU device made the first reading, and then he left the room. The next five readings were taken at 2-minute intervals with the patient alone in the room. The mean initial reading by the machine was 162/85 mm Hg; the reading by the physician was 163/86 mm Hg. The third automatic reading was the lowest (averaging 140/84 mm Hg), and the mean of the five automated readings was 142/80 mm Hg, which was significantly lower than the initial reading obtained by the physician (P < .001).

In another study, Myers et al³² compared the measurements obtained by 24-hour ambulatory monitoring and by the BpTRU device (the mean of five readings obtained at 1-minute or 2-minute intervals) in 309 hypertensive patients. The mean blood pressure with the Bp-TRU was 132/75 mm Hg, which correlated well with the mean awake ambulatory blood pressure (134/77 mm Hg; r = 0.62 for the systolic pressure and 0.72 for the diastolic pressure).

We recently reviewed the records of 278 patients seen in our preventive medicine clinic (D.G. Vidt, MD, unpublished data, November 2009). The group included patients with and without established hypertension, and among the hypertensive group, both treated and untreated individuals. We had initially set the device to take readings at 3-minute intervals following the initial nurse-initiated reading. But in view of the recent data on the Bp-TRU using shorter intervals, we also obtained readings in 51 patients with the device set to record at 2-minute intervals, and then in 72 additional patients at 1-minute intervals. In all three groups, blood pressure had stabilized by the third reading after the clinician had left the room. These observations support those reported by Myers et al.^31,32 Of particular importance is the observation that the white-coat effect dissipates within 2 to 3 minutes after the clinician leaves the room.³³

The shorter measurement intervals can add up in a busy office practice, in which the time relegated to taking blood pressure is often limited.

In fact, waiting 5 minutes between measurements may allow the patient to become too relaxed and the blood pressure to drop too low vis-a-vis the gold standard, ambulatory monitoring. Culleton and colleagues³⁴ compared the blood pressure in 107 hypertensive patients as measured four ways: by the referring physician, by a nurse who was trained to adhere to the protocol of the Canadian Hypertension Education Program, by 24-hour ambulatory monitoring, and by the BpTRU (the mean of five readings obtained at 5-minute intervals). The mean measured values were:

• 150/90 mm Hg by the referring physician
• 139/86 mm Hg by the nurse
• 142/85 mm Hg by ambulatory monitoring
• 132/82 mm Hg by the BpTRU device.

Although the BpTRU reduced the white-coat effect and white-coat hypertension, it underestimated the blood pressure, leading to misclassification of hypertension. Using 140/90 mm Hg as the cutoff for whether the patient was hypertensive and using ambulatory monitoring as the gold standard, the BpTRU misclassified more than half of the patients, agreeing with the classification of hypertensive or not hypertensive by ambulatory monitoring in only 48%. The authors recommended that the BpTRU not be set at 5-minute measurement intervals.³⁴

WHAT ROLE FOR AUTOMATED READINGS IN THE OFFICE?

Although automatic devices, by enabling the physician to leave the room, can eliminate the white-coat effect and white-coat hypertension, physicians must continue to take care to avoid the other potential errors of office blood pressure measurement addressed earlier in this review, for example, by positioning the patient correctly and using a cuff that is large enough. These issues can take on more importance as the clinician leaves the patient alone for brief periods during measurements.

In view of its perennial inaccuracies, some experts have suggested that we abandon routine office measurement of blood pressure.^35,36 In its place, ambulatory monitoring would be used for diagnosis and for periodic follow-up. In addition, patients would regularly take their pressure at home with approved, single-measurement oscillometric devices. Unfortunately, in our health care system, periodic ambulatory monitoring for hypertension management would impose a significant financial burden on patients at this time.³⁷

Of particular importance is the observation that the mean of five readings with the BpTRU device, obtained at 1- or 2-minute intervals, closely approximates the mean awake blood pressure obtained in the same patient with an ambulatory monitor.^32,38 The ability to obtain readings that correlate exceptionally well with mean daytime ambulatory pressure suggests that this device could well reduce the need for ambulatory monitoring, with its associated cost. The ability to negate the white-coat effect with the use of the BpTRU in the office setting also has particular importance, not only for patient office readings, but for the diagnosis and subsequent treatment of hypertension in individual patients.

Most clinical decisions about the treatment of hypertension are still made on the basis of office determinations of blood pressure. Most office practices still rely on the aneroid manometer or, decreasingly, mercury sphygmomanometers. As noted earlier, although auscultatory blood pressure measurement appears to be simple, it is fraught with a host of observer- or patient-induced errors that not only lead to inaccurate diagnoses, but may also result in the mismanagement of hypertension. Even single-measurement oscillometric devices, now used in a minority of clinical practices, are associated with many of the same measurement issues that lead to overestimation of blood pressure.

We believe the time has come for broader use of oscillometric devices in the outpatient setting. While many available oscillometric devices for use in the home could also be used in the physician’s office, they carry the similar disadvantage of providing only a single measurement. The major disadvantage of all single-measurement devices is the continued presence of the clinician during the reading and the associated white-coat effect observed in most patients.

It is highly likely that the next Joint National Committee Report on Hypertension will further emphasize the role of automated blood pressure devices in the outpatient setting.
 

Acknowledgment: The authors wish to acknowledge the contributions of Deborah McCoy, RN, and Maria Eckhouse, RN.

The reality of blood pressure measurement is that human beings do not do it very well. The time has come to delegate this job to machines that can do it better.

Several automatic devices are available. Used in physicians’ offices and in patients’ homes, they can eliminate some types of observer error as well as the “white-coat effect,” ie, the tendency of some patients to have higher blood pressure when medical personnel are present than in their natural environment. Since a difference of only a few millimeters of mercury can affect the physician’s decision to start or to modify treatment, measurements that more accurately reflect a person’s average blood pressure are to be desired.

In the following pages, we review the problems that plague blood pressure measurement by human observers, and we describe the advantages of automatic devices.

SHORTCOMINGS OF OFFICE BLOOD PRESSURE MEASUREMENT

For decades, large surveys have provided invaluable information on the prevalence of hypertension, its relationship to cardiovascular disease, and the benefits of treating it.^1–3 Unfortunately, the percentage of hypertensive patients whose blood pressure is under control has remained low despite our increased knowledge about hypertension’s diagnosis and therapy.⁴

In these surveys, blood pressure was measured by auscultation by human observers using mercury or aneroid sphygmomanometers, and most physicians still use this method in clinical practice. But in spite of multiple guidelines for accurate measurement of blood pressure in the office, the overall accuracy and reproducibility of office blood pressure measurements remain poor.^5–7

The accuracy of blood pressure measurement with aneroid and mercury manometers is affected by a number of observer errors and patient factors.^8,9

Observer errors

Failure to prepare the patient. National guidelines⁵ state that before having their blood pressure taken, patients should be allowed to sit quietly for at least 5 minutes, which often does not happen. Another error is that clinicians rarely discourage patients from smoking cigarettes or drinking coffee in the 30 minutes prior to measurement.

Equipment and layout problems. Equipment should be properly calibrated and validated. ⁵ However, even if the sphygmomanometer is periodically calibrated, too often it is mounted on the wall adjacent to the examination table in the examination room, making it difficult to provide a comfortable seat with back and arm support during the reading. The measurement should be done with the patient sitting in a chair (not on an examination table), with feet on the floor and the arm supported at the level of the heart. If the forearm is not supported in the horizontal position and with the cuff at heart level, the blood pressure and heart rate tend to be higher.¹⁰ Further, the diastolic blood pressure and heart rate may be misleadingly low with the patient supine rather than seated,^11,12 so readings should be taken with the patient sitting.

Miscuffing, ie, the use of a blood pressure cuff that is too large or, more often, too small for the patient’s arm, is a common source of error. The cuff bladder should encircle at least 80% of the arm.⁵ However, some offices do not have a large blood pressure cuff for overweight patients or a pediatric cuff for children or adults with arms of small circumference. It is recommended that a large blood pressure cuff be used routinely in adults, since a smaller cuff gives falsely high readings in people with large upper arms (circumference > 29 cm).^13,14

Digit preference. Many physicians round off the blood pressure to the nearest 5 or 10 mm Hg. This problem may go along with:

Deflating the cuff too rapidly.

Talking to the patient while taking the blood pressure can contribute to higher readings.⁹

Not taking enough readings. Ideally, at the initial visit, blood pressure should be measured in both arms with the patient seated, and another reading should be taken with the patient standing. The arm with the higher pressure should be used for subsequent readings. Physicians should not make any treatment decisions based on blood pressure during an initial clinic visit, and at least two readings should be taken even on subsequent visits. However, owing to time constraints in busy clinical practices, treatment decisions are often based on single readings or on multiple readings on a single visit.

Discrepancies between observers. The blood pressure readings obtained by the nurse or medical assistant may differ significantly from those obtained by the physician. These differences can be large enough to affect treatment decisions,^15,16 and they can be partially corrected by adequate training of all medical personnel who take blood pressure, doctors as well as nurses.

Given that time is tight in busy clinical practices and a trained blood pressure nurse or technician is usually not available, we will probably not see any significant improvement in the accuracy of blood pressure measurement using older technology and current physician practices.

The white-coat effect

Most patients have a higher level of anxiety, and therefore higher blood pressure, in the physician’s office or clinic than in their normal environment (as revealed by ambulatory monitoring or home blood pressure measurements), a phenomenon commonly called the white-coat effect.

Several factors can increase this effect, such as observer-patient interaction during the measurement. The effect tends to be greatest in the initial measurement, but can persist through multiple readings by the doctor or nurse during the same visit.

Whether the white-coat effect is due purely to patient anxiety about an office visit or to a conditioned response has been a point of interest in clinical studies. Regardless, it may result in the misdiagnosis of hypertension or in overestimation of the severity of hypertension and may lead to overly aggressive therapy. Antihypertensive treatment may be unnecessary in the absence of concurrent cardiovascular risk factors.¹⁷

“White-coat hypertension” or “isolated office hypertension” is the condition in which a patient who is not on antihypertensive drug therapy has persistently elevated blood pressure in the clinic or office (> 140/90 mm Hg) but normal daytime ambulatory blood pressure (< 135/85 mm Hg).¹⁸ Since patients may have an elevated reading when seen for a first office visit, at least several visits are required to establish the diagnosis. Multiple studies have suggested that white-coat hypertension may account for 20% to 25% of the hypertensive population, particularly in older patients, mainly women.^19,20

Both white-coat hypertension and the white-coat effect can be avoided by using an automatic and programmable device that can take multiple readings after the clinician leaves the examination room (more about this below).²¹

MEASURING BLOOD PRESSURE OUTSIDE THE OFFICE

Recent studies have reported that the information obtained by 24-hour ambulatory blood pressure monitoring and by self-measurement of blood pressure in the home more accurately reflects the patient’s risk of future cardiovascular events than do conventional blood pressure measurements taken in the physician’s office. ^22–24 Current national guidelines recognize this pattern and the frequent measurement inaccuracies observed in clinical practice, and they are recommending including out-of-office measurements in the diagnosis of hypertension. ^25,26

Ambulatory monitoring provides the most accurate measurement of out-of-office blood pressure. With ambulatory monitoring, the normal mean daytime pressure is considered to be lower than 135/85 mm Hg, in contrast to the 140/90 mm Hg cutoff used in the physician’s office with standard aneroid or mercury devices.

Self-monitoring of blood pressure at home has now become widely available with single-measurement oscillometric devices. (Oscillometric means that these devices measure the blood pressure by sensing the oscillations in pressure in the cuff induced by the pulsation of the brachial artery, as opposed to auscultating the Korotkoff sounds.) Blood pressures lower than 135/85 mm Hg outside the clinician’s office are considered normal with these devices.

However, despite its proven value, ambulatory monitoring is neither widely available nor cost-effective for the long-term management of hypertension. Furthermore, few physicians recommend that patients take their blood pressure at home, although the information obtained can be of significant value in the patient’s long-term management.

AUTOMATED MEASUREMENT IN THE OFFICE

In recent years, several automated oscillometric sphygmomanometers have been developed for measuring blood pressure in the office, and more are on the way. These devices can be programmed to take multiple readings without a clinician observer in the examination room, thus reducing the white-coat response.

Omron (Kyoto, Japan) makes several devices, including the HEM-907 and the HEM-705, that have been used in the clinical setting. ^21,27–29 They can be programmed to take two or three readings at intervals of 1 to 2 minutes, with up to 5 minutes before the first reading. Unfortunately, data were not recorded with the patient alone in the room in many studies of the Omron devices, even though the devices meet national and international standards for accuracy.

The Microlife Watch BP Office (Microlife, Widnau, Switzerland) is currently undergoing development.³⁰

The BpTRU (BpTRU Medical Devices, Coquitlam, BC, Canada) has enjoyed greater clinical acceptance, since it can take up to five blood pressure readings at intervals of 1 to 5 minutes, and calculates the mean of all five readings, taken with the patient resting comfortably in a quiet room without a clinician present.

The accuracy and durability of the device has been well established. Since the BpTRU self-calibrates between every blood pressure measurement, periodic calibration has not been required. The device can be placed on a table, mounted on the wall, or mounted on a cart if used in several locations in the office.

At Cleveland Clinic, several departments are using the BpTRU on a daily basis. Soon, we will be able to transfer data directly from the BpTRU to our electronic medical record system.

Studies of the BpTRU device

To date, most of the studies of automated office blood pressure measurement have used the BpTRU with the recording interval set at 1 to 2 minutes.

Myers³¹ used the BpTRU device in 50 hypertensive patients. The physician took the patient’s blood pressure with a mercury sphygmomanometer while the BpTRU device made the first reading, and then he left the room. The next five readings were taken at 2-minute intervals with the patient alone in the room. The mean initial reading by the machine was 162/85 mm Hg; the reading by the physician was 163/86 mm Hg. The third automatic reading was the lowest (averaging 140/84 mm Hg), and the mean of the five automated readings was 142/80 mm Hg, which was significantly lower than the initial reading obtained by the physician (P < .001).

In another study, Myers et al³² compared the measurements obtained by 24-hour ambulatory monitoring and by the BpTRU device (the mean of five readings obtained at 1-minute or 2-minute intervals) in 309 hypertensive patients. The mean blood pressure with the Bp-TRU was 132/75 mm Hg, which correlated well with the mean awake ambulatory blood pressure (134/77 mm Hg; r = 0.62 for the systolic pressure and 0.72 for the diastolic pressure).

We recently reviewed the records of 278 patients seen in our preventive medicine clinic (D.G. Vidt, MD, unpublished data, November 2009). The group included patients with and without established hypertension, and among the hypertensive group, both treated and untreated individuals. We had initially set the device to take readings at 3-minute intervals following the initial nurse-initiated reading. But in view of the recent data on the Bp-TRU using shorter intervals, we also obtained readings in 51 patients with the device set to record at 2-minute intervals, and then in 72 additional patients at 1-minute intervals. In all three groups, blood pressure had stabilized by the third reading after the clinician had left the room. These observations support those reported by Myers et al.^31,32 Of particular importance is the observation that the white-coat effect dissipates within 2 to 3 minutes after the clinician leaves the room.³³

The shorter measurement intervals can add up in a busy office practice, in which the time relegated to taking blood pressure is often limited.

In fact, waiting 5 minutes between measurements may allow the patient to become too relaxed and the blood pressure to drop too low vis-a-vis the gold standard, ambulatory monitoring. Culleton and colleagues³⁴ compared the blood pressure in 107 hypertensive patients as measured four ways: by the referring physician, by a nurse who was trained to adhere to the protocol of the Canadian Hypertension Education Program, by 24-hour ambulatory monitoring, and by the BpTRU (the mean of five readings obtained at 5-minute intervals). The mean measured values were:

• 150/90 mm Hg by the referring physician
• 139/86 mm Hg by the nurse
• 142/85 mm Hg by ambulatory monitoring
• 132/82 mm Hg by the BpTRU device.

Although the BpTRU reduced the white-coat effect and white-coat hypertension, it underestimated the blood pressure, leading to misclassification of hypertension. Using 140/90 mm Hg as the cutoff for whether the patient was hypertensive and using ambulatory monitoring as the gold standard, the BpTRU misclassified more than half of the patients, agreeing with the classification of hypertensive or not hypertensive by ambulatory monitoring in only 48%. The authors recommended that the BpTRU not be set at 5-minute measurement intervals.³⁴

WHAT ROLE FOR AUTOMATED READINGS IN THE OFFICE?

Although automatic devices, by enabling the physician to leave the room, can eliminate the white-coat effect and white-coat hypertension, physicians must continue to take care to avoid the other potential errors of office blood pressure measurement addressed earlier in this review, for example, by positioning the patient correctly and using a cuff that is large enough. These issues can take on more importance as the clinician leaves the patient alone for brief periods during measurements.

In view of its perennial inaccuracies, some experts have suggested that we abandon routine office measurement of blood pressure.^35,36 In its place, ambulatory monitoring would be used for diagnosis and for periodic follow-up. In addition, patients would regularly take their pressure at home with approved, single-measurement oscillometric devices. Unfortunately, in our health care system, periodic ambulatory monitoring for hypertension management would impose a significant financial burden on patients at this time.³⁷

Of particular importance is the observation that the mean of five readings with the BpTRU device, obtained at 1- or 2-minute intervals, closely approximates the mean awake blood pressure obtained in the same patient with an ambulatory monitor.^32,38 The ability to obtain readings that correlate exceptionally well with mean daytime ambulatory pressure suggests that this device could well reduce the need for ambulatory monitoring, with its associated cost. The ability to negate the white-coat effect with the use of the BpTRU in the office setting also has particular importance, not only for patient office readings, but for the diagnosis and subsequent treatment of hypertension in individual patients.

Most clinical decisions about the treatment of hypertension are still made on the basis of office determinations of blood pressure. Most office practices still rely on the aneroid manometer or, decreasingly, mercury sphygmomanometers. As noted earlier, although auscultatory blood pressure measurement appears to be simple, it is fraught with a host of observer- or patient-induced errors that not only lead to inaccurate diagnoses, but may also result in the mismanagement of hypertension. Even single-measurement oscillometric devices, now used in a minority of clinical practices, are associated with many of the same measurement issues that lead to overestimation of blood pressure.

We believe the time has come for broader use of oscillometric devices in the outpatient setting. While many available oscillometric devices for use in the home could also be used in the physician’s office, they carry the similar disadvantage of providing only a single measurement. The major disadvantage of all single-measurement devices is the continued presence of the clinician during the reading and the associated white-coat effect observed in most patients.

It is highly likely that the next Joint National Committee Report on Hypertension will further emphasize the role of automated blood pressure devices in the outpatient setting.
 

Acknowledgment: The authors wish to acknowledge the contributions of Deborah McCoy, RN, and Maria Eckhouse, RN.