I always loved the game Hot Potato. A more stationary version of musical chairs, it involves the passing of the spud as the music plays or the clock ticks, then the last-minute handoff; the excitement of that game trained me for a life of brinkmanship.

The earliest version of the game involved passing a lit candle, with the loser holding the extinguished taper. I always enjoyed my cold war version, a wind-up fake bomb passed around the circle. Hot Potato was the name of a terrible Jim Kelly martial arts movie in 1976, and an even worse short-lived NBC game show in 1984. It is even a poorly rated video game. The newest “Hot Potato” is a computer routing system.

In the game Hot Potato, you never want to be the one with the spud when the music stops. Unfortunately, sometimes patients become that hot potato.

When I was a first-year medical student, I wanted my own patients. I shared the clinical experience with others grudgingly. Someone else would always ask the question I wanted to; they routinely heard the murmur first. Every patient was a new mystery to be solved, a reminder of how little I knew (and still don’t know). By my senior year of school, I still wanted my own patients, but I wanted the most exotic and difficult cases I could find, as a matter of principle.

By internship that glory had faded. I was harassed, sleep deprived, overworked, and underpaid, but otherwise I was OK. If I could avoid another admission, I was happy. New terminology entered my vocabulary. Expressions like “He’s a sieve” or “She’s a wall” described my coworkers in the emergency department (ED). Why would they admit that patient, were they crazy? Your chief resident was strong or weak based on turfing prowess. What could be sweeter than a bounce back to the other service?

Maybe Spud ended up on your service for a reason?

As a resident, I perfected what Samuel Shem (a.k.a., Stephen Bergman, MD) described in the classic The House of God as the “buff and turf.” Transfer to surgery, no problem. Patient wants to leave AMA, just have him sign the paperwork. This negative attitude was pervasive. A team was judged by the strength of the resident, and measured by the relative size of the census. Of course, residents today would never feel this way, given work hour limits. That was in the old days.

As a newly minted private practice internist, I wanted all the patients I could see. I took every ED admit, opened all my slots. I was building my practice. I was on a productivity formula and wanted to surpass my targets. I was incentivized. It seemed odd to be working so hard to get patients when I had done the opposite just one year earlier. My colleagues looked on in amazement as I said yes to everything. The best advice I was ever given was to say no, but I did not heed it.

After a few years in practice, I was well stocked with patients. I still accepted all Medicare patients; at the time, I was the only one in private practice who would do so secondary to the lower pay rate. I didn’t mind because of my interest in geriatrics. I enjoyed these old folks, plus they brought in the best homegrown produce. My kids grew sick of okra.

When the HMOs came to town, with their IPAs and IPOs, along with other alphabetic acronyms too fierce to mention, I was once again incentivized to not see patients. It was fine for me to capture their PMPM (per member per month) fee, but I wasn’t encouraged to actually see them, and hospitalization involved a tremendous amount of paperwork and psychological conflict with my IPA handlers. “Do you really need that MRI?” was the question of the day.

I spent a brief and disastrous year in the world of practice management groups, where patients were subsidiary to stock value and practice acquisition. I emerged bent but not broken. Well, maybe slightly broken. Yes, money is the root of all evil.

Next, I began to work for a community-based university practice, on a straight salary. My financial incentives were eliminated, I saw as many as I comfortably could, and I forgot about the money. Life was good. I had a few medical students and an intern. We saw a large but comfortable volume of patients, mostly geriatric. I always tried to see the people who needed to be seen, but not so many that a visit was too brief.

The dark side reared its head again when I got a new boss who wanted the community university practice to go on productivity. Once again I was back to the bean counting rat race: see more patients and squeeze in an extra three this afternoon. “What do you mean you want a day off?”

But then I became a hospitalist and all was right with the world again. It was an excellent consultative practice with ample opportunities for teaching and research. Unfortunately, when the resident hours rules began, we found ourselves staffing services formerly run by teaching teams. We also found ourselves in rotation with the remaining teams.

This was the moment of truth. Would I return to my long abandoned roots? Would I begin once again to order the “surf and turf” platter? Happily, the answer has been “No.” The fullness of time has helped me to realize that patients are not hot potatoes. There are days when I find myself watching the admit board intently or wondering why one service or another is not taking their bounce backs. I have found, however, that the mental energy that is wasted in playing Hot Potato is needed to care for the patients who seek our help. Would I want my mother sitting in an ED while three services did their best to not have her on their lists? OK, in my mom’s case, I could understand. (Just joking, Arlene.)

So, the next time you get the call from the ED and find yourself wondering what that patient is doing on your service, think about the game of Hot Potato. Perhaps when the music stops, you are the right one to have the spud in hand. TH

Jamie Newman, MD, FACP, is the physician editor of The Hospitalist, consultant, Hospital Internal Medicine, and assistant professor of internal medicine and medical history, Mayo Clinic College of Medicine, Rochester, Minn.

I always loved the game Hot Potato. A more stationary version of musical chairs, it involves the passing of the spud as the music plays or the clock ticks, then the last-minute handoff; the excitement of that game trained me for a life of brinkmanship.

The earliest version of the game involved passing a lit candle, with the loser holding the extinguished taper. I always enjoyed my cold war version, a wind-up fake bomb passed around the circle. Hot Potato was the name of a terrible Jim Kelly martial arts movie in 1976, and an even worse short-lived NBC game show in 1984. It is even a poorly rated video game. The newest “Hot Potato” is a computer routing system.

In the game Hot Potato, you never want to be the one with the spud when the music stops. Unfortunately, sometimes patients become that hot potato.

When I was a first-year medical student, I wanted my own patients. I shared the clinical experience with others grudgingly. Someone else would always ask the question I wanted to; they routinely heard the murmur first. Every patient was a new mystery to be solved, a reminder of how little I knew (and still don’t know). By my senior year of school, I still wanted my own patients, but I wanted the most exotic and difficult cases I could find, as a matter of principle.

By internship that glory had faded. I was harassed, sleep deprived, overworked, and underpaid, but otherwise I was OK. If I could avoid another admission, I was happy. New terminology entered my vocabulary. Expressions like “He’s a sieve” or “She’s a wall” described my coworkers in the emergency department (ED). Why would they admit that patient, were they crazy? Your chief resident was strong or weak based on turfing prowess. What could be sweeter than a bounce back to the other service?

Maybe Spud ended up on your service for a reason?

As a resident, I perfected what Samuel Shem (a.k.a., Stephen Bergman, MD) described in the classic The House of God as the “buff and turf.” Transfer to surgery, no problem. Patient wants to leave AMA, just have him sign the paperwork. This negative attitude was pervasive. A team was judged by the strength of the resident, and measured by the relative size of the census. Of course, residents today would never feel this way, given work hour limits. That was in the old days.

As a newly minted private practice internist, I wanted all the patients I could see. I took every ED admit, opened all my slots. I was building my practice. I was on a productivity formula and wanted to surpass my targets. I was incentivized. It seemed odd to be working so hard to get patients when I had done the opposite just one year earlier. My colleagues looked on in amazement as I said yes to everything. The best advice I was ever given was to say no, but I did not heed it.

After a few years in practice, I was well stocked with patients. I still accepted all Medicare patients; at the time, I was the only one in private practice who would do so secondary to the lower pay rate. I didn’t mind because of my interest in geriatrics. I enjoyed these old folks, plus they brought in the best homegrown produce. My kids grew sick of okra.

When the HMOs came to town, with their IPAs and IPOs, along with other alphabetic acronyms too fierce to mention, I was once again incentivized to not see patients. It was fine for me to capture their PMPM (per member per month) fee, but I wasn’t encouraged to actually see them, and hospitalization involved a tremendous amount of paperwork and psychological conflict with my IPA handlers. “Do you really need that MRI?” was the question of the day.

I spent a brief and disastrous year in the world of practice management groups, where patients were subsidiary to stock value and practice acquisition. I emerged bent but not broken. Well, maybe slightly broken. Yes, money is the root of all evil.

Next, I began to work for a community-based university practice, on a straight salary. My financial incentives were eliminated, I saw as many as I comfortably could, and I forgot about the money. Life was good. I had a few medical students and an intern. We saw a large but comfortable volume of patients, mostly geriatric. I always tried to see the people who needed to be seen, but not so many that a visit was too brief.

The dark side reared its head again when I got a new boss who wanted the community university practice to go on productivity. Once again I was back to the bean counting rat race: see more patients and squeeze in an extra three this afternoon. “What do you mean you want a day off?”

But then I became a hospitalist and all was right with the world again. It was an excellent consultative practice with ample opportunities for teaching and research. Unfortunately, when the resident hours rules began, we found ourselves staffing services formerly run by teaching teams. We also found ourselves in rotation with the remaining teams.

This was the moment of truth. Would I return to my long abandoned roots? Would I begin once again to order the “surf and turf” platter? Happily, the answer has been “No.” The fullness of time has helped me to realize that patients are not hot potatoes. There are days when I find myself watching the admit board intently or wondering why one service or another is not taking their bounce backs. I have found, however, that the mental energy that is wasted in playing Hot Potato is needed to care for the patients who seek our help. Would I want my mother sitting in an ED while three services did their best to not have her on their lists? OK, in my mom’s case, I could understand. (Just joking, Arlene.)

So, the next time you get the call from the ED and find yourself wondering what that patient is doing on your service, think about the game of Hot Potato. Perhaps when the music stops, you are the right one to have the spud in hand. TH

Jamie Newman, MD, FACP, is the physician editor of The Hospitalist, consultant, Hospital Internal Medicine, and assistant professor of internal medicine and medical history, Mayo Clinic College of Medicine, Rochester, Minn.

I always loved the game Hot Potato. A more stationary version of musical chairs, it involves the passing of the spud as the music plays or the clock ticks, then the last-minute handoff; the excitement of that game trained me for a life of brinkmanship.

The earliest version of the game involved passing a lit candle, with the loser holding the extinguished taper. I always enjoyed my cold war version, a wind-up fake bomb passed around the circle. Hot Potato was the name of a terrible Jim Kelly martial arts movie in 1976, and an even worse short-lived NBC game show in 1984. It is even a poorly rated video game. The newest “Hot Potato” is a computer routing system.

In the game Hot Potato, you never want to be the one with the spud when the music stops. Unfortunately, sometimes patients become that hot potato.

When I was a first-year medical student, I wanted my own patients. I shared the clinical experience with others grudgingly. Someone else would always ask the question I wanted to; they routinely heard the murmur first. Every patient was a new mystery to be solved, a reminder of how little I knew (and still don’t know). By my senior year of school, I still wanted my own patients, but I wanted the most exotic and difficult cases I could find, as a matter of principle.

By internship that glory had faded. I was harassed, sleep deprived, overworked, and underpaid, but otherwise I was OK. If I could avoid another admission, I was happy. New terminology entered my vocabulary. Expressions like “He’s a sieve” or “She’s a wall” described my coworkers in the emergency department (ED). Why would they admit that patient, were they crazy? Your chief resident was strong or weak based on turfing prowess. What could be sweeter than a bounce back to the other service?

Maybe Spud ended up on your service for a reason?

As a resident, I perfected what Samuel Shem (a.k.a., Stephen Bergman, MD) described in the classic The House of God as the “buff and turf.” Transfer to surgery, no problem. Patient wants to leave AMA, just have him sign the paperwork. This negative attitude was pervasive. A team was judged by the strength of the resident, and measured by the relative size of the census. Of course, residents today would never feel this way, given work hour limits. That was in the old days.

As a newly minted private practice internist, I wanted all the patients I could see. I took every ED admit, opened all my slots. I was building my practice. I was on a productivity formula and wanted to surpass my targets. I was incentivized. It seemed odd to be working so hard to get patients when I had done the opposite just one year earlier. My colleagues looked on in amazement as I said yes to everything. The best advice I was ever given was to say no, but I did not heed it.

After a few years in practice, I was well stocked with patients. I still accepted all Medicare patients; at the time, I was the only one in private practice who would do so secondary to the lower pay rate. I didn’t mind because of my interest in geriatrics. I enjoyed these old folks, plus they brought in the best homegrown produce. My kids grew sick of okra.

When the HMOs came to town, with their IPAs and IPOs, along with other alphabetic acronyms too fierce to mention, I was once again incentivized to not see patients. It was fine for me to capture their PMPM (per member per month) fee, but I wasn’t encouraged to actually see them, and hospitalization involved a tremendous amount of paperwork and psychological conflict with my IPA handlers. “Do you really need that MRI?” was the question of the day.

I spent a brief and disastrous year in the world of practice management groups, where patients were subsidiary to stock value and practice acquisition. I emerged bent but not broken. Well, maybe slightly broken. Yes, money is the root of all evil.

Next, I began to work for a community-based university practice, on a straight salary. My financial incentives were eliminated, I saw as many as I comfortably could, and I forgot about the money. Life was good. I had a few medical students and an intern. We saw a large but comfortable volume of patients, mostly geriatric. I always tried to see the people who needed to be seen, but not so many that a visit was too brief.

The dark side reared its head again when I got a new boss who wanted the community university practice to go on productivity. Once again I was back to the bean counting rat race: see more patients and squeeze in an extra three this afternoon. “What do you mean you want a day off?”

But then I became a hospitalist and all was right with the world again. It was an excellent consultative practice with ample opportunities for teaching and research. Unfortunately, when the resident hours rules began, we found ourselves staffing services formerly run by teaching teams. We also found ourselves in rotation with the remaining teams.

This was the moment of truth. Would I return to my long abandoned roots? Would I begin once again to order the “surf and turf” platter? Happily, the answer has been “No.” The fullness of time has helped me to realize that patients are not hot potatoes. There are days when I find myself watching the admit board intently or wondering why one service or another is not taking their bounce backs. I have found, however, that the mental energy that is wasted in playing Hot Potato is needed to care for the patients who seek our help. Would I want my mother sitting in an ED while three services did their best to not have her on their lists? OK, in my mom’s case, I could understand. (Just joking, Arlene.)

So, the next time you get the call from the ED and find yourself wondering what that patient is doing on your service, think about the game of Hot Potato. Perhaps when the music stops, you are the right one to have the spud in hand. TH

Jamie Newman, MD, FACP, is the physician editor of The Hospitalist, consultant, Hospital Internal Medicine, and assistant professor of internal medicine and medical history, Mayo Clinic College of Medicine, Rochester, Minn.

A few years ago, I cared for an unfortunate homeless patient who seemed incapable of managing his own affairs and was probably illiterate. When he left the hospital, I gave him a copy of his discharge summary and stressed that he should carry it around and always show it to anyone taking care of him. A lot went on in the hospital, and I worried he wouldn’t follow through with the subsequent care I had arranged and would instead wind up in another emergency department (ED) the next time he had a problem.

A few weeks later I got a call from another ED in the area and learned that the patient hadn’t been able to provide any meaningful details of his health history or where he had received care previously. But he did pull a wrinkled copy of the discharge summary from his pocket to show the staff. In our phone conversation, the ED doctor remarked how helpful it had been to have this information that he probably would have never found otherwise. It saved the need to pursue workup for things that I had already investigated.

I tell this story because I think it would be great for hospitalists to ensure that all, or nearly all, of their patients receive a copy of their discharge summary as they leave the hospital—or soon thereafter. In fact, I suspect that if this became common for hospitalists, the idea might become de rigueur for all patients in the hospital.

I’ve been providing a copy for many of my patients for several years. I first started doing this for patients I cared for who lived out of my area (e.g., a different state) and I couldn’t rely on the hospital getting a copy of the summary to the patient’s primary care physician (PCP) at home. That experience convinced me it could be a good idea to give it to nearly all patients.

Giving each patient a copy of selected parts of the medical record and, when requested by patients, all of the medical record, is not a new idea. I think it is great that a number of clinics and other providers mail test results to patients, and neater still are the organizations that encourage patients to “visit our Web site to review your test results” and other such information. However routinely encouraging them to review all of the test results and other records generated during a hospital stay may be an idea that isn’t yet ready for prime time. Instead, I think it is useful to give the patient a copy of the discharge summary, which highlights relevant test results with accompanying explanation and analysis.

There are many reasons this can be a good idea. Of course, a discharge summary can’t replace or reduce the need for the doctor to discuss diagnoses, treatment, and follow-up plans with the patient. Still, it is a great summary of the diagnoses, medications, and discharge instructions that the patient can review later. Research shows that many patients forget most of what they have been told by the time they get home, and my hope is that the discharge summary will serve as a reminder.

Think about the other caregivers who will see the patient after discharge. They benefit from having a discharge summary to review. Sure I’ll send a copy of the summary to the patient’s primary care doctor and to the cardiologist who consulted during the hospital stay. But what about the visiting nurse who will start seeing the patient the day after discharge? The patient can show the summary to the nurse instead of trying to recall what he was told about his illness and showing the nurse his pill bottles. Also, the patient may end up seeing doctors that I didn’t know about who won’t be getting a copy of the summary from me (my hospital). He may see other doctors in the community that he didn’t think to tell me about and can take a copy of the summary to those visits. This is why I usually tell patients to carry the summary around with them and show it to all the providers they see.

What about the patients with low health literacy? I think they might be the ones to benefit the most from getting the summary. A patient with low literacy may often get assistance from other and can show the report to these caregivers (often friends or family members). Not every patient will show the report to someone who can read it, but I think a lot of them will. So I think it’s worthwhile to give the report to everyone, just in case. If a patient is demented or otherwise incompetent, I try to get the summary into the hands of a family member or other caregiver. (Of course this can raise HIPAA-related privacy issues, and consent may be needed in some cases.)

I think that most lay people can make sense of most of what is in a discharge summary. As for the more challenging technical language in nearly every summary, sophisticated people can turn to the Internet for help. I want patients to have written reminders when they need things like a follow-up chest X-ray or results of tests that were pending at discharge. The need for specific follow-up like this gets reported directly to the PCP (via the copy of the discharge summary sent directly to him/her), and I hope that patients who have read the summary will help remind the PCP of these things.

There are two principle costs or barriers to making this standard practice. The first is that doctors tend to resist it. They worry that patients won’t understand the information or—worse—will become needlessly worried and stressed, and that the doctor will have to spend significant time “talking the patient down” from a worry that would never have arisen if the patient hadn’t been nosing around in a record that is written in “medicalese.” Or maybe the patient will read an unflattering portrayal of his situation and become angry at the doctor. (“He called me a drug seeker!”) Yet my experience shows that these are infrequent problems.

I can recall only one such incident out of the thousands of patients who have left my care with a copy of their discharge summary. One reason is that it’s now a habit for me to dictate each report while keeping in mind the idea that the patient is likely to read it. So instead of referring to a patient as a likely drug seeker, I’m apt to say something like “the patient had difficult pain management problems.” And isn’t this better language anyway? I might be wrong about his drug seeking, and any future provider who sees my report will probably still understand that drug seeking is a possibility. There are rare cases in which I think it is best not to automatically give the patient a copy of the report. These could include a proven unflattering diagnosis that the patient disputes. But remember, the patient may eventually end up seeing any report you create, so it’s worth keeping this in mind with all of your medical record documentation.

The second reason for resisting this idea is the perceived difficulty or cost of implementing it. I’m fortunate that most of my patients can get a paper copy of the discharge summary I’ve prepared as they are leaving the hospital. Of course, this requires that I dictate the report at the time of the discharge visit, and it is transcribed immediately. If you can’t pull this off, then I suggest that you have a copy mailed (or e-mailed if feasible) within a day or two of discharge. If the summary isn’t available when the patient is ready to leave, I wouldn’t have him stay and needlessly tie up a hospital bed. When this happens to my patients, I have them go ahead and leave, and a copy is mailed to them.

So I hope you will consider making this a routine practice in your hospital. The costs are small, and the potential benefit to quality of care and patient satisfaction could be significant. TH

Dr. Nelson has been a practicing hospitalist since 1988 and is a co-founder and past-president of SHM. He is a principal in Nelson/Flores Associates, a national hospitalist practice management consulting firm. This column represents his views and is not intended to reflect an official position of SHM.

A few years ago, I cared for an unfortunate homeless patient who seemed incapable of managing his own affairs and was probably illiterate. When he left the hospital, I gave him a copy of his discharge summary and stressed that he should carry it around and always show it to anyone taking care of him. A lot went on in the hospital, and I worried he wouldn’t follow through with the subsequent care I had arranged and would instead wind up in another emergency department (ED) the next time he had a problem.

A few weeks later I got a call from another ED in the area and learned that the patient hadn’t been able to provide any meaningful details of his health history or where he had received care previously. But he did pull a wrinkled copy of the discharge summary from his pocket to show the staff. In our phone conversation, the ED doctor remarked how helpful it had been to have this information that he probably would have never found otherwise. It saved the need to pursue workup for things that I had already investigated.

I tell this story because I think it would be great for hospitalists to ensure that all, or nearly all, of their patients receive a copy of their discharge summary as they leave the hospital—or soon thereafter. In fact, I suspect that if this became common for hospitalists, the idea might become de rigueur for all patients in the hospital.

I’ve been providing a copy for many of my patients for several years. I first started doing this for patients I cared for who lived out of my area (e.g., a different state) and I couldn’t rely on the hospital getting a copy of the summary to the patient’s primary care physician (PCP) at home. That experience convinced me it could be a good idea to give it to nearly all patients.

Giving each patient a copy of selected parts of the medical record and, when requested by patients, all of the medical record, is not a new idea. I think it is great that a number of clinics and other providers mail test results to patients, and neater still are the organizations that encourage patients to “visit our Web site to review your test results” and other such information. However routinely encouraging them to review all of the test results and other records generated during a hospital stay may be an idea that isn’t yet ready for prime time. Instead, I think it is useful to give the patient a copy of the discharge summary, which highlights relevant test results with accompanying explanation and analysis.

There are many reasons this can be a good idea. Of course, a discharge summary can’t replace or reduce the need for the doctor to discuss diagnoses, treatment, and follow-up plans with the patient. Still, it is a great summary of the diagnoses, medications, and discharge instructions that the patient can review later. Research shows that many patients forget most of what they have been told by the time they get home, and my hope is that the discharge summary will serve as a reminder.

Think about the other caregivers who will see the patient after discharge. They benefit from having a discharge summary to review. Sure I’ll send a copy of the summary to the patient’s primary care doctor and to the cardiologist who consulted during the hospital stay. But what about the visiting nurse who will start seeing the patient the day after discharge? The patient can show the summary to the nurse instead of trying to recall what he was told about his illness and showing the nurse his pill bottles. Also, the patient may end up seeing doctors that I didn’t know about who won’t be getting a copy of the summary from me (my hospital). He may see other doctors in the community that he didn’t think to tell me about and can take a copy of the summary to those visits. This is why I usually tell patients to carry the summary around with them and show it to all the providers they see.

What about the patients with low health literacy? I think they might be the ones to benefit the most from getting the summary. A patient with low literacy may often get assistance from other and can show the report to these caregivers (often friends or family members). Not every patient will show the report to someone who can read it, but I think a lot of them will. So I think it’s worthwhile to give the report to everyone, just in case. If a patient is demented or otherwise incompetent, I try to get the summary into the hands of a family member or other caregiver. (Of course this can raise HIPAA-related privacy issues, and consent may be needed in some cases.)

I think that most lay people can make sense of most of what is in a discharge summary. As for the more challenging technical language in nearly every summary, sophisticated people can turn to the Internet for help. I want patients to have written reminders when they need things like a follow-up chest X-ray or results of tests that were pending at discharge. The need for specific follow-up like this gets reported directly to the PCP (via the copy of the discharge summary sent directly to him/her), and I hope that patients who have read the summary will help remind the PCP of these things.

There are two principle costs or barriers to making this standard practice. The first is that doctors tend to resist it. They worry that patients won’t understand the information or—worse—will become needlessly worried and stressed, and that the doctor will have to spend significant time “talking the patient down” from a worry that would never have arisen if the patient hadn’t been nosing around in a record that is written in “medicalese.” Or maybe the patient will read an unflattering portrayal of his situation and become angry at the doctor. (“He called me a drug seeker!”) Yet my experience shows that these are infrequent problems.

I can recall only one such incident out of the thousands of patients who have left my care with a copy of their discharge summary. One reason is that it’s now a habit for me to dictate each report while keeping in mind the idea that the patient is likely to read it. So instead of referring to a patient as a likely drug seeker, I’m apt to say something like “the patient had difficult pain management problems.” And isn’t this better language anyway? I might be wrong about his drug seeking, and any future provider who sees my report will probably still understand that drug seeking is a possibility. There are rare cases in which I think it is best not to automatically give the patient a copy of the report. These could include a proven unflattering diagnosis that the patient disputes. But remember, the patient may eventually end up seeing any report you create, so it’s worth keeping this in mind with all of your medical record documentation.

The second reason for resisting this idea is the perceived difficulty or cost of implementing it. I’m fortunate that most of my patients can get a paper copy of the discharge summary I’ve prepared as they are leaving the hospital. Of course, this requires that I dictate the report at the time of the discharge visit, and it is transcribed immediately. If you can’t pull this off, then I suggest that you have a copy mailed (or e-mailed if feasible) within a day or two of discharge. If the summary isn’t available when the patient is ready to leave, I wouldn’t have him stay and needlessly tie up a hospital bed. When this happens to my patients, I have them go ahead and leave, and a copy is mailed to them.

So I hope you will consider making this a routine practice in your hospital. The costs are small, and the potential benefit to quality of care and patient satisfaction could be significant. TH

Dr. Nelson has been a practicing hospitalist since 1988 and is a co-founder and past-president of SHM. He is a principal in Nelson/Flores Associates, a national hospitalist practice management consulting firm. This column represents his views and is not intended to reflect an official position of SHM.

A few years ago, I cared for an unfortunate homeless patient who seemed incapable of managing his own affairs and was probably illiterate. When he left the hospital, I gave him a copy of his discharge summary and stressed that he should carry it around and always show it to anyone taking care of him. A lot went on in the hospital, and I worried he wouldn’t follow through with the subsequent care I had arranged and would instead wind up in another emergency department (ED) the next time he had a problem.

A few weeks later I got a call from another ED in the area and learned that the patient hadn’t been able to provide any meaningful details of his health history or where he had received care previously. But he did pull a wrinkled copy of the discharge summary from his pocket to show the staff. In our phone conversation, the ED doctor remarked how helpful it had been to have this information that he probably would have never found otherwise. It saved the need to pursue workup for things that I had already investigated.

I tell this story because I think it would be great for hospitalists to ensure that all, or nearly all, of their patients receive a copy of their discharge summary as they leave the hospital—or soon thereafter. In fact, I suspect that if this became common for hospitalists, the idea might become de rigueur for all patients in the hospital.

I’ve been providing a copy for many of my patients for several years. I first started doing this for patients I cared for who lived out of my area (e.g., a different state) and I couldn’t rely on the hospital getting a copy of the summary to the patient’s primary care physician (PCP) at home. That experience convinced me it could be a good idea to give it to nearly all patients.

Giving each patient a copy of selected parts of the medical record and, when requested by patients, all of the medical record, is not a new idea. I think it is great that a number of clinics and other providers mail test results to patients, and neater still are the organizations that encourage patients to “visit our Web site to review your test results” and other such information. However routinely encouraging them to review all of the test results and other records generated during a hospital stay may be an idea that isn’t yet ready for prime time. Instead, I think it is useful to give the patient a copy of the discharge summary, which highlights relevant test results with accompanying explanation and analysis.

There are many reasons this can be a good idea. Of course, a discharge summary can’t replace or reduce the need for the doctor to discuss diagnoses, treatment, and follow-up plans with the patient. Still, it is a great summary of the diagnoses, medications, and discharge instructions that the patient can review later. Research shows that many patients forget most of what they have been told by the time they get home, and my hope is that the discharge summary will serve as a reminder.

Think about the other caregivers who will see the patient after discharge. They benefit from having a discharge summary to review. Sure I’ll send a copy of the summary to the patient’s primary care doctor and to the cardiologist who consulted during the hospital stay. But what about the visiting nurse who will start seeing the patient the day after discharge? The patient can show the summary to the nurse instead of trying to recall what he was told about his illness and showing the nurse his pill bottles. Also, the patient may end up seeing doctors that I didn’t know about who won’t be getting a copy of the summary from me (my hospital). He may see other doctors in the community that he didn’t think to tell me about and can take a copy of the summary to those visits. This is why I usually tell patients to carry the summary around with them and show it to all the providers they see.

What about the patients with low health literacy? I think they might be the ones to benefit the most from getting the summary. A patient with low literacy may often get assistance from other and can show the report to these caregivers (often friends or family members). Not every patient will show the report to someone who can read it, but I think a lot of them will. So I think it’s worthwhile to give the report to everyone, just in case. If a patient is demented or otherwise incompetent, I try to get the summary into the hands of a family member or other caregiver. (Of course this can raise HIPAA-related privacy issues, and consent may be needed in some cases.)

I think that most lay people can make sense of most of what is in a discharge summary. As for the more challenging technical language in nearly every summary, sophisticated people can turn to the Internet for help. I want patients to have written reminders when they need things like a follow-up chest X-ray or results of tests that were pending at discharge. The need for specific follow-up like this gets reported directly to the PCP (via the copy of the discharge summary sent directly to him/her), and I hope that patients who have read the summary will help remind the PCP of these things.

There are two principle costs or barriers to making this standard practice. The first is that doctors tend to resist it. They worry that patients won’t understand the information or—worse—will become needlessly worried and stressed, and that the doctor will have to spend significant time “talking the patient down” from a worry that would never have arisen if the patient hadn’t been nosing around in a record that is written in “medicalese.” Or maybe the patient will read an unflattering portrayal of his situation and become angry at the doctor. (“He called me a drug seeker!”) Yet my experience shows that these are infrequent problems.

I can recall only one such incident out of the thousands of patients who have left my care with a copy of their discharge summary. One reason is that it’s now a habit for me to dictate each report while keeping in mind the idea that the patient is likely to read it. So instead of referring to a patient as a likely drug seeker, I’m apt to say something like “the patient had difficult pain management problems.” And isn’t this better language anyway? I might be wrong about his drug seeking, and any future provider who sees my report will probably still understand that drug seeking is a possibility. There are rare cases in which I think it is best not to automatically give the patient a copy of the report. These could include a proven unflattering diagnosis that the patient disputes. But remember, the patient may eventually end up seeing any report you create, so it’s worth keeping this in mind with all of your medical record documentation.

The second reason for resisting this idea is the perceived difficulty or cost of implementing it. I’m fortunate that most of my patients can get a paper copy of the discharge summary I’ve prepared as they are leaving the hospital. Of course, this requires that I dictate the report at the time of the discharge visit, and it is transcribed immediately. If you can’t pull this off, then I suggest that you have a copy mailed (or e-mailed if feasible) within a day or two of discharge. If the summary isn’t available when the patient is ready to leave, I wouldn’t have him stay and needlessly tie up a hospital bed. When this happens to my patients, I have them go ahead and leave, and a copy is mailed to them.

So I hope you will consider making this a routine practice in your hospital. The costs are small, and the potential benefit to quality of care and patient satisfaction could be significant. TH

Dr. Nelson has been a practicing hospitalist since 1988 and is a co-founder and past-president of SHM. He is a principal in Nelson/Flores Associates, a national hospitalist practice management consulting firm. This column represents his views and is not intended to reflect an official position of SHM.

Most hospitalist programs start when hospital administrators realize that having physicians dedicated exclusively to inpatient care is a great idea. Administrators then recruit a lead hospitalist—perhaps a stellar performer straight from residency, a community doctor closing his office, or a doctor located through a specialty staffing group.

Colorado Permanente Medical Group (CPMG), backed by a brand as powerful as Starbucks or Nordstrom, did things differently. So imbued with the Permanente culture are its physicians that its hospitalist group arose organically from physicians serving Denver’s Exempla St. Joseph Hospital and Boulder Community Hospital. (See “Kaiser Permanente Culture,” below.)

click for large version

“Thirty years ago Permanente explored building their own versus finding a cost-effective hospital. They chose us, and their clinic doctors rounded on what grew to 70% of our department of medicine patients,” says Robert Gibbons, MD, St. Joseph’s residency program director. “Then they saw they needed to provide full-time inpatient coverage—the advent of the hospitalist program. Soon many CPMG clinic doctors disappeared, but the quality of medicine remained the same.”

Regional Department Chief Lauren Fraser, MD, oversees the now-mature hospitalist program, which keeps growing in size, complexity, and competence. “We’re always a work in progress, and that’s good,” she says.

According to Joe Heaton, MD, currently a Good Samaritan hospitalist and formerly CPMG regional department chief, CPMG’s primary care departments targeted three areas for better care early in 1995: streamlining patient scheduling, developing a centralized call center, and starting a hospitalist program.

The hospitalist program aimed for cost neutrality by limiting staffing at both hospitals to the same full-time equivalents (FTEs). To avoid forcing physicians into unwelcome assignments, the department offered its 70 internal medicine and 30 family practice doctors four tracks:

1. Track A meant full-time hospital work;
2. Track B offered a 50-50 hospital-clinic split;
3. Track C provided for a 70% clinic, 30% hospital schedule; and
4. Track D was full-time clinic work.

The family medicine department opted out of hospital duty, while the internists tracked themselves as follows: eight each for full-time hospital and half-time hospital duty, 34 for 30% hospital time, and 20 for full-time clinic. Fortunately, the tracks chosen matched the hospitals’ needs, and the program was off and running by July 1995.

“At the time, our group’s size created one of the largest hospitalist programs, allowing us to provide 24/7 coverage with at least two physicians on site,” says Dr. Heaton of the launch.

The hospitalist program had immediate measurable impact. Average length of stay dropped by 15%, and Track A and C physicians had similar utilization measures, suggesting that the model of care delivery was the key driver—rather than the amount of time physicians spent in the hospital. Dr. Gibbons was impressed with the hospitalist group’s results, noting that St. Joseph’s average reduced length of stay of 0.7 to one full day was consistent with national benchmarks. Because CPMG sees only Permanente patients, St. Joseph eventually contracted with two other hospitalist groups: the Exempla Faculty Inpatient Team, which covers half of its unassigned patients, and Midtown Inpatient Medicine, private internists who cover the other half of the unassigned patients, co-manage with orthopedic surgeons, and cover for internal medicine groups that no longer make hospital rounds.

CPMG hospitalists also covered Boulder Community Hospital in Denver’s rapidly expanding suburbs until 2005, when CPMG’s contract expired. All six hospitalists moved to nearby Exempla’s new Good Samaritan Hospital, where patient volume grew quickly from 25-30 patients a day to 80; 90% of the patients are Permanente members. Hospitalist staffing jumped to 13 FTEs (19 physicians). “We recruited very aggressively, including lots of locum tenens and moonlighters to cover the booming volume,” explains Brian Thom, MD, assistant regional department chief, Good Samaritan Hospital.

click for large version

More Measures

In addition to length of stay, CPMG tracks the percentage of patients discharged in less than 24 hours, readmission rates, and disease-specific mortality by provider. All hospitalists get regular reports of department averages and statistical analyses of individual physicians. “This may be controversial, but we must look at outliers to see if [the problem is] case mix, such as many hospice patients, or something else,” says Dr. Heaton.

Striving for high levels of clinical expertise and consistency is a CPMG hallmark. Working for a medical behemoth in the Denver area, CPMG doctors—whether clinic-based or hospitalists—have a huge opportunity to integrate care and to co-manage many conditions with their colleagues. Hospitalists also staff the ICUs. In 2000, William Kinnard, MD, CPMG’s ICU co-director, commented that the group’s use of data-driven protocols allowed hospitalists to practice effectively in ICUs.

As for patient satisfaction, Dr. Heaton admits to “struggling for good measures,” noting that CPMG tackled it head-on in 1999 when Executive Medical Director Jack Cochran, MD, addressed the level of patient tenacity it took to navigate CPMG. Physician career satisfaction was sinking from long chaotic workdays that left both patients and doctors frustrated. By re-engineering scheduling and visit processes, Dr. Cochran made things run more smoothly. Other initiatives included an eight-hour physician-patient interaction course, video vignettes starring CPMG doctors illustrating communication techniques, and formal physician-to-physician coaching. Dr. Fraser still sends new hires to the course, recognizing that good communication satisfies both patients and physicians.

Scheduling: Every Program’s Mt. Everest

Because of the hospitalist program’s size and longevity, physicians have experimented extensively with scheduling. As do many groups, it started with seven 12-hour days on/seven days off blocks, which proved dissatisfying both personally and professionally.

“We experimented with scheduling to find what was sustainable for physicians and provided patient continuity,” says Dr. Fraser. “We’ve found that six eight-hour days in a row of rounding works best.”

Scheduling has evolved to the point that hospitalists provide the following to meet the hospitalist’s, the group’s, and the hospital’s needs: a dedicated triage physician 24/7 to handle calls from all sources of patient flow, two hospitalists on site at all times, eight-hour rounding days, and call physicians who admit and cross-cover after 4 p.m. Average daily census (ADC) is 10-12, plus one or two admissions. While that appears low, if CPMG hospitalists worked 12-hour shifts, their ADC would be 13-16, consistent with national norms.

“Dropping to eight-hour, as opposed to 12-hour, days keeps the job sustainable and helps doctors avoid burnout,” says Dr. Fraser. “However, we work more days per month, an average of 20-22.”

Overall, the scheduling strategy is working. “The majority of physicians who started over a decade ago remain, including many mid-life hospitalists in their 40s and 50s,” she adds. Physicians, rather than administrators, handle scheduling. Dr. Fraser has found that physicians can accept that third triage shift in a month (or an extra night shift when they’re short-handed) when another physician is filling the slots.

Other Features

All CPMG hospitalists can participate in St. Joseph’s residency program as “teaching attendings” for one month. From them, residents learn to co-manage care and participate in interdisciplinary rounds with nurses and social workers. Physicians note that residents make a hospitalist’s life smoother.

“At Good Sam, we do all our own procedures, unlike St. Joe’s, where they have residents. With our patient volumes, there’s little breathing room, especially when we have to cover non-Kaiser patients,” says Dr. Thom. Eventually, residents will rotate through Good Samaritan as well as St. Joseph.

One of the advantages of working in a brand-new hospital like Good Samaritan is establishing systems from scratch. That includes the new hospital’s electronic medical record (EMR), which is integrated with CPMG’s outpatient EMR. “We set up our own systems, complete with order sets and protocols,” explains Dr. Thom. “Considering that 90% of our patients are CPMG members, this gives us a high level of integration, clinically and electronically.”

Challenges Ahead

Despite CPMG’s size and stellar track record, challenges remain. Dr. Fraser identifies them as salaries that rank last within the group, making recruiting difficult; a hard time providing adequate back-up if a physician is unexpectedly absent; adjustments to fluctuations in patient census; time pressures of hospital committee work; and identification of an optimal scheduling model that fosters continuity of care yet provides a sustainable work life.

The group’s size has drawbacks, which Dr. Heaton identifies as the potential for a physician to not feel mission critical or to hide, and that communication and face-to-face meetings get complicated.

“Overall, the program can always use fine tuning, but we love who we work with and have the ultimate respect for our colleagues, which is the true benchmark of the quality of a medical career,” concludes Dr. Fraser. TH

Marlene Piturro regularly writes “Practice Profile.”

Most hospitalist programs start when hospital administrators realize that having physicians dedicated exclusively to inpatient care is a great idea. Administrators then recruit a lead hospitalist—perhaps a stellar performer straight from residency, a community doctor closing his office, or a doctor located through a specialty staffing group.

Colorado Permanente Medical Group (CPMG), backed by a brand as powerful as Starbucks or Nordstrom, did things differently. So imbued with the Permanente culture are its physicians that its hospitalist group arose organically from physicians serving Denver’s Exempla St. Joseph Hospital and Boulder Community Hospital. (See “Kaiser Permanente Culture,” below.)

click for large version

“Thirty years ago Permanente explored building their own versus finding a cost-effective hospital. They chose us, and their clinic doctors rounded on what grew to 70% of our department of medicine patients,” says Robert Gibbons, MD, St. Joseph’s residency program director. “Then they saw they needed to provide full-time inpatient coverage—the advent of the hospitalist program. Soon many CPMG clinic doctors disappeared, but the quality of medicine remained the same.”

Regional Department Chief Lauren Fraser, MD, oversees the now-mature hospitalist program, which keeps growing in size, complexity, and competence. “We’re always a work in progress, and that’s good,” she says.

According to Joe Heaton, MD, currently a Good Samaritan hospitalist and formerly CPMG regional department chief, CPMG’s primary care departments targeted three areas for better care early in 1995: streamlining patient scheduling, developing a centralized call center, and starting a hospitalist program.

The hospitalist program aimed for cost neutrality by limiting staffing at both hospitals to the same full-time equivalents (FTEs). To avoid forcing physicians into unwelcome assignments, the department offered its 70 internal medicine and 30 family practice doctors four tracks:

1. Track A meant full-time hospital work;
2. Track B offered a 50-50 hospital-clinic split;
3. Track C provided for a 70% clinic, 30% hospital schedule; and
4. Track D was full-time clinic work.

The family medicine department opted out of hospital duty, while the internists tracked themselves as follows: eight each for full-time hospital and half-time hospital duty, 34 for 30% hospital time, and 20 for full-time clinic. Fortunately, the tracks chosen matched the hospitals’ needs, and the program was off and running by July 1995.

“At the time, our group’s size created one of the largest hospitalist programs, allowing us to provide 24/7 coverage with at least two physicians on site,” says Dr. Heaton of the launch.

The hospitalist program had immediate measurable impact. Average length of stay dropped by 15%, and Track A and C physicians had similar utilization measures, suggesting that the model of care delivery was the key driver—rather than the amount of time physicians spent in the hospital. Dr. Gibbons was impressed with the hospitalist group’s results, noting that St. Joseph’s average reduced length of stay of 0.7 to one full day was consistent with national benchmarks. Because CPMG sees only Permanente patients, St. Joseph eventually contracted with two other hospitalist groups: the Exempla Faculty Inpatient Team, which covers half of its unassigned patients, and Midtown Inpatient Medicine, private internists who cover the other half of the unassigned patients, co-manage with orthopedic surgeons, and cover for internal medicine groups that no longer make hospital rounds.

CPMG hospitalists also covered Boulder Community Hospital in Denver’s rapidly expanding suburbs until 2005, when CPMG’s contract expired. All six hospitalists moved to nearby Exempla’s new Good Samaritan Hospital, where patient volume grew quickly from 25-30 patients a day to 80; 90% of the patients are Permanente members. Hospitalist staffing jumped to 13 FTEs (19 physicians). “We recruited very aggressively, including lots of locum tenens and moonlighters to cover the booming volume,” explains Brian Thom, MD, assistant regional department chief, Good Samaritan Hospital.

click for large version

More Measures

In addition to length of stay, CPMG tracks the percentage of patients discharged in less than 24 hours, readmission rates, and disease-specific mortality by provider. All hospitalists get regular reports of department averages and statistical analyses of individual physicians. “This may be controversial, but we must look at outliers to see if [the problem is] case mix, such as many hospice patients, or something else,” says Dr. Heaton.

Striving for high levels of clinical expertise and consistency is a CPMG hallmark. Working for a medical behemoth in the Denver area, CPMG doctors—whether clinic-based or hospitalists—have a huge opportunity to integrate care and to co-manage many conditions with their colleagues. Hospitalists also staff the ICUs. In 2000, William Kinnard, MD, CPMG’s ICU co-director, commented that the group’s use of data-driven protocols allowed hospitalists to practice effectively in ICUs.

As for patient satisfaction, Dr. Heaton admits to “struggling for good measures,” noting that CPMG tackled it head-on in 1999 when Executive Medical Director Jack Cochran, MD, addressed the level of patient tenacity it took to navigate CPMG. Physician career satisfaction was sinking from long chaotic workdays that left both patients and doctors frustrated. By re-engineering scheduling and visit processes, Dr. Cochran made things run more smoothly. Other initiatives included an eight-hour physician-patient interaction course, video vignettes starring CPMG doctors illustrating communication techniques, and formal physician-to-physician coaching. Dr. Fraser still sends new hires to the course, recognizing that good communication satisfies both patients and physicians.

Scheduling: Every Program’s Mt. Everest

Because of the hospitalist program’s size and longevity, physicians have experimented extensively with scheduling. As do many groups, it started with seven 12-hour days on/seven days off blocks, which proved dissatisfying both personally and professionally.

“We experimented with scheduling to find what was sustainable for physicians and provided patient continuity,” says Dr. Fraser. “We’ve found that six eight-hour days in a row of rounding works best.”

Scheduling has evolved to the point that hospitalists provide the following to meet the hospitalist’s, the group’s, and the hospital’s needs: a dedicated triage physician 24/7 to handle calls from all sources of patient flow, two hospitalists on site at all times, eight-hour rounding days, and call physicians who admit and cross-cover after 4 p.m. Average daily census (ADC) is 10-12, plus one or two admissions. While that appears low, if CPMG hospitalists worked 12-hour shifts, their ADC would be 13-16, consistent with national norms.

“Dropping to eight-hour, as opposed to 12-hour, days keeps the job sustainable and helps doctors avoid burnout,” says Dr. Fraser. “However, we work more days per month, an average of 20-22.”

Overall, the scheduling strategy is working. “The majority of physicians who started over a decade ago remain, including many mid-life hospitalists in their 40s and 50s,” she adds. Physicians, rather than administrators, handle scheduling. Dr. Fraser has found that physicians can accept that third triage shift in a month (or an extra night shift when they’re short-handed) when another physician is filling the slots.

Other Features

All CPMG hospitalists can participate in St. Joseph’s residency program as “teaching attendings” for one month. From them, residents learn to co-manage care and participate in interdisciplinary rounds with nurses and social workers. Physicians note that residents make a hospitalist’s life smoother.

“At Good Sam, we do all our own procedures, unlike St. Joe’s, where they have residents. With our patient volumes, there’s little breathing room, especially when we have to cover non-Kaiser patients,” says Dr. Thom. Eventually, residents will rotate through Good Samaritan as well as St. Joseph.

One of the advantages of working in a brand-new hospital like Good Samaritan is establishing systems from scratch. That includes the new hospital’s electronic medical record (EMR), which is integrated with CPMG’s outpatient EMR. “We set up our own systems, complete with order sets and protocols,” explains Dr. Thom. “Considering that 90% of our patients are CPMG members, this gives us a high level of integration, clinically and electronically.”

Challenges Ahead

Despite CPMG’s size and stellar track record, challenges remain. Dr. Fraser identifies them as salaries that rank last within the group, making recruiting difficult; a hard time providing adequate back-up if a physician is unexpectedly absent; adjustments to fluctuations in patient census; time pressures of hospital committee work; and identification of an optimal scheduling model that fosters continuity of care yet provides a sustainable work life.

The group’s size has drawbacks, which Dr. Heaton identifies as the potential for a physician to not feel mission critical or to hide, and that communication and face-to-face meetings get complicated.

“Overall, the program can always use fine tuning, but we love who we work with and have the ultimate respect for our colleagues, which is the true benchmark of the quality of a medical career,” concludes Dr. Fraser. TH

Marlene Piturro regularly writes “Practice Profile.”

Most hospitalist programs start when hospital administrators realize that having physicians dedicated exclusively to inpatient care is a great idea. Administrators then recruit a lead hospitalist—perhaps a stellar performer straight from residency, a community doctor closing his office, or a doctor located through a specialty staffing group.

Colorado Permanente Medical Group (CPMG), backed by a brand as powerful as Starbucks or Nordstrom, did things differently. So imbued with the Permanente culture are its physicians that its hospitalist group arose organically from physicians serving Denver’s Exempla St. Joseph Hospital and Boulder Community Hospital. (See “Kaiser Permanente Culture,” below.)

click for large version

“Thirty years ago Permanente explored building their own versus finding a cost-effective hospital. They chose us, and their clinic doctors rounded on what grew to 70% of our department of medicine patients,” says Robert Gibbons, MD, St. Joseph’s residency program director. “Then they saw they needed to provide full-time inpatient coverage—the advent of the hospitalist program. Soon many CPMG clinic doctors disappeared, but the quality of medicine remained the same.”

Regional Department Chief Lauren Fraser, MD, oversees the now-mature hospitalist program, which keeps growing in size, complexity, and competence. “We’re always a work in progress, and that’s good,” she says.

According to Joe Heaton, MD, currently a Good Samaritan hospitalist and formerly CPMG regional department chief, CPMG’s primary care departments targeted three areas for better care early in 1995: streamlining patient scheduling, developing a centralized call center, and starting a hospitalist program.

The hospitalist program aimed for cost neutrality by limiting staffing at both hospitals to the same full-time equivalents (FTEs). To avoid forcing physicians into unwelcome assignments, the department offered its 70 internal medicine and 30 family practice doctors four tracks:

1. Track A meant full-time hospital work;
2. Track B offered a 50-50 hospital-clinic split;
3. Track C provided for a 70% clinic, 30% hospital schedule; and
4. Track D was full-time clinic work.

The family medicine department opted out of hospital duty, while the internists tracked themselves as follows: eight each for full-time hospital and half-time hospital duty, 34 for 30% hospital time, and 20 for full-time clinic. Fortunately, the tracks chosen matched the hospitals’ needs, and the program was off and running by July 1995.

“At the time, our group’s size created one of the largest hospitalist programs, allowing us to provide 24/7 coverage with at least two physicians on site,” says Dr. Heaton of the launch.

The hospitalist program had immediate measurable impact. Average length of stay dropped by 15%, and Track A and C physicians had similar utilization measures, suggesting that the model of care delivery was the key driver—rather than the amount of time physicians spent in the hospital. Dr. Gibbons was impressed with the hospitalist group’s results, noting that St. Joseph’s average reduced length of stay of 0.7 to one full day was consistent with national benchmarks. Because CPMG sees only Permanente patients, St. Joseph eventually contracted with two other hospitalist groups: the Exempla Faculty Inpatient Team, which covers half of its unassigned patients, and Midtown Inpatient Medicine, private internists who cover the other half of the unassigned patients, co-manage with orthopedic surgeons, and cover for internal medicine groups that no longer make hospital rounds.

CPMG hospitalists also covered Boulder Community Hospital in Denver’s rapidly expanding suburbs until 2005, when CPMG’s contract expired. All six hospitalists moved to nearby Exempla’s new Good Samaritan Hospital, where patient volume grew quickly from 25-30 patients a day to 80; 90% of the patients are Permanente members. Hospitalist staffing jumped to 13 FTEs (19 physicians). “We recruited very aggressively, including lots of locum tenens and moonlighters to cover the booming volume,” explains Brian Thom, MD, assistant regional department chief, Good Samaritan Hospital.

click for large version

More Measures

In addition to length of stay, CPMG tracks the percentage of patients discharged in less than 24 hours, readmission rates, and disease-specific mortality by provider. All hospitalists get regular reports of department averages and statistical analyses of individual physicians. “This may be controversial, but we must look at outliers to see if [the problem is] case mix, such as many hospice patients, or something else,” says Dr. Heaton.

Striving for high levels of clinical expertise and consistency is a CPMG hallmark. Working for a medical behemoth in the Denver area, CPMG doctors—whether clinic-based or hospitalists—have a huge opportunity to integrate care and to co-manage many conditions with their colleagues. Hospitalists also staff the ICUs. In 2000, William Kinnard, MD, CPMG’s ICU co-director, commented that the group’s use of data-driven protocols allowed hospitalists to practice effectively in ICUs.

As for patient satisfaction, Dr. Heaton admits to “struggling for good measures,” noting that CPMG tackled it head-on in 1999 when Executive Medical Director Jack Cochran, MD, addressed the level of patient tenacity it took to navigate CPMG. Physician career satisfaction was sinking from long chaotic workdays that left both patients and doctors frustrated. By re-engineering scheduling and visit processes, Dr. Cochran made things run more smoothly. Other initiatives included an eight-hour physician-patient interaction course, video vignettes starring CPMG doctors illustrating communication techniques, and formal physician-to-physician coaching. Dr. Fraser still sends new hires to the course, recognizing that good communication satisfies both patients and physicians.

Scheduling: Every Program’s Mt. Everest

Because of the hospitalist program’s size and longevity, physicians have experimented extensively with scheduling. As do many groups, it started with seven 12-hour days on/seven days off blocks, which proved dissatisfying both personally and professionally.

“We experimented with scheduling to find what was sustainable for physicians and provided patient continuity,” says Dr. Fraser. “We’ve found that six eight-hour days in a row of rounding works best.”

Scheduling has evolved to the point that hospitalists provide the following to meet the hospitalist’s, the group’s, and the hospital’s needs: a dedicated triage physician 24/7 to handle calls from all sources of patient flow, two hospitalists on site at all times, eight-hour rounding days, and call physicians who admit and cross-cover after 4 p.m. Average daily census (ADC) is 10-12, plus one or two admissions. While that appears low, if CPMG hospitalists worked 12-hour shifts, their ADC would be 13-16, consistent with national norms.

“Dropping to eight-hour, as opposed to 12-hour, days keeps the job sustainable and helps doctors avoid burnout,” says Dr. Fraser. “However, we work more days per month, an average of 20-22.”

Overall, the scheduling strategy is working. “The majority of physicians who started over a decade ago remain, including many mid-life hospitalists in their 40s and 50s,” she adds. Physicians, rather than administrators, handle scheduling. Dr. Fraser has found that physicians can accept that third triage shift in a month (or an extra night shift when they’re short-handed) when another physician is filling the slots.

Other Features

All CPMG hospitalists can participate in St. Joseph’s residency program as “teaching attendings” for one month. From them, residents learn to co-manage care and participate in interdisciplinary rounds with nurses and social workers. Physicians note that residents make a hospitalist’s life smoother.

“At Good Sam, we do all our own procedures, unlike St. Joe’s, where they have residents. With our patient volumes, there’s little breathing room, especially when we have to cover non-Kaiser patients,” says Dr. Thom. Eventually, residents will rotate through Good Samaritan as well as St. Joseph.

One of the advantages of working in a brand-new hospital like Good Samaritan is establishing systems from scratch. That includes the new hospital’s electronic medical record (EMR), which is integrated with CPMG’s outpatient EMR. “We set up our own systems, complete with order sets and protocols,” explains Dr. Thom. “Considering that 90% of our patients are CPMG members, this gives us a high level of integration, clinically and electronically.”

Challenges Ahead

Despite CPMG’s size and stellar track record, challenges remain. Dr. Fraser identifies them as salaries that rank last within the group, making recruiting difficult; a hard time providing adequate back-up if a physician is unexpectedly absent; adjustments to fluctuations in patient census; time pressures of hospital committee work; and identification of an optimal scheduling model that fosters continuity of care yet provides a sustainable work life.

The group’s size has drawbacks, which Dr. Heaton identifies as the potential for a physician to not feel mission critical or to hide, and that communication and face-to-face meetings get complicated.

“Overall, the program can always use fine tuning, but we love who we work with and have the ultimate respect for our colleagues, which is the true benchmark of the quality of a medical career,” concludes Dr. Fraser. TH

Marlene Piturro regularly writes “Practice Profile.”

In July, a teenage mother-to-be entered a Madison, Wis., hospital to give birth. Within hours she was dead, though her baby survived.

An investigation by the Wisconsin State Department of Health revealed that the young woman had died after receiving an intravenous dose of an epidural anesthetic instead of the penicillin she was supposed to be given. Shortly after receiving the injection, the teenager had a seizure. She died less than two hours later.

In explaining what had happened, a nurse told investigators that the patient had been nervous about how she was to be anesthetized during the birth. To ease her concerns, the nurse brought out the epidural bag and told her how it worked. Unfortunately, it was one bag too many; the nurse later confused the epidural bag with the penicillin bag. The consequences were fatal.

The Human Toll

Such sentinel events are all too common. According to a just-released report, Preventing Medication Errors, prepared by the Institute of Medicine (IOM) at the behest of the Centers for Medicare and Medicaid Services, medication errors harm 1.5 million people yearly in the U.S. and kill thousands. The annual cost: at least $3.5 billion. But medication mistakes are just part of the picture.

Sentinel events—unexpected occurrences that result in death or serious physical or psychological injury, or the risk of their later occurrence—can happen anywhere along the healthcare continuum, in any setting. Statistics from the Joint Commission on Accreditation of Healthcare Organizations (JCAHO), however, show that 68% occur in general hospitals and another 11% in psychiatric hospitals. JCAHO tracked the sentinel events they reviewed from 1995 to March of 2006 and found that the most commonly reported sentinel events were patient suicide, wrong-site surgery, operative/postoperative complications, medication errors, and delay in treatment—in that order. Of the total number of cases reviewed, 73% resulted in the death of the patient and 10% in loss of function.

Hard-and-fast statistics on sentinel events are difficult to come by, however. Information from the JCAHO covers only the incidents reviewed by that organization, and experts agree that almost all types of sentinel events are under-reported. Researchers cite a number of reasons that many incidents go unreported; among them are lack of time, fear of punishment, and confusion about the severity of events that require notification. For example, do near misses count? (See “Near Misses,” The Hospitalist, May, p. 34.) Others see no benefit to themselves or their institutions from reporting.

Studies have attempted to define the true incidence of sentinel events, but a lack of consistent language and definitions makes it difficult to put the whole puzzle together, even when sentinel events do come to the surface.

Focus on Medication Errors

That said, we know that the incidence of sentinel events is much higher than it should be. As regularly reported by The Hospitalist, the problem most in the spotlight today—among researchers and the popular press—is medication errors. The IOM report says that, on average, a hospitalized patient is subject to at least one medication error per day, though error rates vary widely among hospitals. Fortunately, most errors cause no serious harm, but the costs for those that do are substantial. One study found that each preventable adverse drug event (ADE) costs a hospital approximately $8,750.

At least a quarter of medication-related injuries are preventable, according to the report. The irony is that many error-prevention methods are available today: “do not use” abbreviation lists; medication reconciliation (used to compare a patient’s medication orders with all other medications the patient is taking in order to avoid omissions, duplications, dosing errors, or drug interactions); and computerized physician order entry systems, to name a few.

With so much emphasis on patient safety and the increasing availability of sophisticated reporting and record-keeping technology, why haven’t incidence rates for ADEs and other sentinel events dropped dramatically? The answer is not that hospital personnel are lazy, incompetent, or indifferent to the safety of their patients. Experts agree that today’s doctors, nurses, pharmacists, and other medical staff are highly trained, dedicated professionals who want to practice the best medicine possible. The present system focuses on individual fault and does not foster disclosure that could lead to corrective procedures.

In fact, legal experts worry that JCAHO’s Sentinel Events Policy, which mandates self-reporting by hospitals accredited by the JCAHO, creates new problems. They suggest that self-reporting will have limited success in the absence of immunity from legal liability. One proposed solution calls for submitting self-regulatory reports to a neutral, nonsanctioning third-party entity. This approach has worked well for the airline industry.

New Patient-Care Focus

Abandoning a policy that concentrates on blame is at the heart of the improvements in patient safety proposed in the IOM report. Rather than pinpointing individual error, the new paradigm focuses on developing new systems of care that foster patient safety and help prevent sentinel events. In the absence of a finger-pointing environment, hospital personnel can freely examine what happened, discover the causes, and structure new procedures to prevent future occurrences – without fear of any retribution.

That’s the way they handle it at California Pacific Medical Center in San Francisco. In one case, when a nurse removed a dialysis catheter, the patient developed an air embolism and subsequently suffered a severe, permanently disabling stroke.

“When we investigated, we found that there was a written procedure in place to document a dialysis nurse’s credential,” says hospitalist Thomas E. Baudendistel, MD, FCAP, who is associate medical director of the hospital’s Internal Medicine Residency Program. “A, we weren’t aware of the credentialing procedure, and B, when we looked at it we weren’t sure it represented best practice. So we researched the literature and rewrote the policy. Now we schedule regular nursing education on pulling a dialysis catheter.”

In addition, the hospital set in place a follow-up plan to re-evaluate the procedure periodically. They also offer refresher training in catheter removal.

“We’ve used a similar approach in other situations,” says Dr. Baudendistel. “For example, our procedure with falls has changed. Now we use an event-based algorithm to determine whether a head CT scan is necessary.”

Hospitalists Can Lead

Hospital-based physicians are in an advantageous position to promote—as well as participate in—new initiatives for patient safety. Because they are involved in the day-to-day care of patients, hospitalists are firsthand observers when many errors occur. They have the experience and clinical judgment to give meaningful input to new incident-reporting protocols and to promote new policies through interdisciplinary teams that investigate and analyze adverse events.

Inevitably, electronic systems will replace paper-and-pen reporting and recordkeeping. Here hospitalists can take the lead, too. Unlike physicians who admit patients to multiple hospitals (each with a different information system), hospitalists practice in a single institution with only one system to learn. Hospitalists’ patient load may also help them to master new technology more quickly.

Surveys show that, while many hospitals have electronic ordering systems in place, relatively few physicians actually use them. In many cases, nurses or pharmacists place the electronic orders. Hospitalists who place their own orders can contribute to a reduction in medication errors by eliminating the pass-through of information that often causes misunderstandings.

Patient-Centric Healthcare: the New Paradigm

The traditional hospital system—and the healthcare system as a whole—are provider-oriented and provider-directed. Many patients, especially older ones, have a “doctor knows all” mindset, and they typically ask few questions—even when they don’t understand their treatment plans or exactly how they’re to take their medications when they go home. Case in point: A patient who was discharged from the hospital died at home shortly thereafter. The cause: His wife misunderstood the instructions for his pain medication and mistakenly applied six transdermal patches to his skin at one time instead of the single patch she should have applied. The multiple patches delivered a fatal overdose of the narcotic fentanyl.

Many experts believe that better informed—and empowered—patients are the key to reducing the number of sentinel events, including ADEs. The IOM report advocates a shift from a provider-centered to a patient-centered healthcare model. In this new paradigm, hospitalists would be much more expansive in their communications with patients. With regard to medications in particular, the report recommends that a physician:

• Review the patient’s medication list routinely and during care transitions.
• Review different treatment options.
• Review the names and purposes of all medications.
• Discuss when and how to take the medication.
• Discuss important and likely side effects and what to do about them.
• Discuss drug-drug, drug-food, and drug-disease interactions.
• Review the patient’s (or surrogate’s) role in appropriate medication use.
• Review the role of medications in the overall context of the patient’s health.

There are barriers to surmount before patients can become full partners in their healthcare. One of the most obvious is that patients need to be much better informed, and—when they are incapable of making appropriate decisions—they need surrogates to stand in for them. Patients need access to trustworthy and understandable information both online and in printed materials.

The IOM report recommends a government-sponsored national drug-information hotline; medication leaflets that provide standardized language in a manner that is appropriate for various age, literacy, and visual acuity levels; and development of personal health records.

PeaceHealth in Washington state took up the challenge of developing personal health records in 2001. PeaceHealth’s Project Manager, Mary Minniti, invited patients to design the system for self-management and communication among care team members. Today, the Shared Care Plan Personal Health Record is a reality, and Marc Pierson, MD, who is PeaceHealth’s regional vice president of Clinical Information and Special Projects, says “early evidence suggests that this type of tool promotes personal responsibility and positively affects patients’ confidence and active participation in their care.”

The tool is available on CD from www.peacehealth.org for those who would like to adopt it for their use.

Final Thought

The bad news is that sentinel events still take a staggering human and economic toll. The good news is that momentum is building for an important change in the way healthcare is delivered. Better communication, new technologies, and, perhaps most importantly, true provider-patient partnerships hold the promise of making hospital healthcare much safer. Hospitalists play a key role in this new scenario. TH

Joen Kinnan is a freelance medical writer based in Chicago.

In July, a teenage mother-to-be entered a Madison, Wis., hospital to give birth. Within hours she was dead, though her baby survived.

An investigation by the Wisconsin State Department of Health revealed that the young woman had died after receiving an intravenous dose of an epidural anesthetic instead of the penicillin she was supposed to be given. Shortly after receiving the injection, the teenager had a seizure. She died less than two hours later.

In explaining what had happened, a nurse told investigators that the patient had been nervous about how she was to be anesthetized during the birth. To ease her concerns, the nurse brought out the epidural bag and told her how it worked. Unfortunately, it was one bag too many; the nurse later confused the epidural bag with the penicillin bag. The consequences were fatal.

The Human Toll

Such sentinel events are all too common. According to a just-released report, Preventing Medication Errors, prepared by the Institute of Medicine (IOM) at the behest of the Centers for Medicare and Medicaid Services, medication errors harm 1.5 million people yearly in the U.S. and kill thousands. The annual cost: at least $3.5 billion. But medication mistakes are just part of the picture.

Sentinel events—unexpected occurrences that result in death or serious physical or psychological injury, or the risk of their later occurrence—can happen anywhere along the healthcare continuum, in any setting. Statistics from the Joint Commission on Accreditation of Healthcare Organizations (JCAHO), however, show that 68% occur in general hospitals and another 11% in psychiatric hospitals. JCAHO tracked the sentinel events they reviewed from 1995 to March of 2006 and found that the most commonly reported sentinel events were patient suicide, wrong-site surgery, operative/postoperative complications, medication errors, and delay in treatment—in that order. Of the total number of cases reviewed, 73% resulted in the death of the patient and 10% in loss of function.

Hard-and-fast statistics on sentinel events are difficult to come by, however. Information from the JCAHO covers only the incidents reviewed by that organization, and experts agree that almost all types of sentinel events are under-reported. Researchers cite a number of reasons that many incidents go unreported; among them are lack of time, fear of punishment, and confusion about the severity of events that require notification. For example, do near misses count? (See “Near Misses,” The Hospitalist, May, p. 34.) Others see no benefit to themselves or their institutions from reporting.

Studies have attempted to define the true incidence of sentinel events, but a lack of consistent language and definitions makes it difficult to put the whole puzzle together, even when sentinel events do come to the surface.

Focus on Medication Errors

That said, we know that the incidence of sentinel events is much higher than it should be. As regularly reported by The Hospitalist, the problem most in the spotlight today—among researchers and the popular press—is medication errors. The IOM report says that, on average, a hospitalized patient is subject to at least one medication error per day, though error rates vary widely among hospitals. Fortunately, most errors cause no serious harm, but the costs for those that do are substantial. One study found that each preventable adverse drug event (ADE) costs a hospital approximately $8,750.

At least a quarter of medication-related injuries are preventable, according to the report. The irony is that many error-prevention methods are available today: “do not use” abbreviation lists; medication reconciliation (used to compare a patient’s medication orders with all other medications the patient is taking in order to avoid omissions, duplications, dosing errors, or drug interactions); and computerized physician order entry systems, to name a few.

With so much emphasis on patient safety and the increasing availability of sophisticated reporting and record-keeping technology, why haven’t incidence rates for ADEs and other sentinel events dropped dramatically? The answer is not that hospital personnel are lazy, incompetent, or indifferent to the safety of their patients. Experts agree that today’s doctors, nurses, pharmacists, and other medical staff are highly trained, dedicated professionals who want to practice the best medicine possible. The present system focuses on individual fault and does not foster disclosure that could lead to corrective procedures.

In fact, legal experts worry that JCAHO’s Sentinel Events Policy, which mandates self-reporting by hospitals accredited by the JCAHO, creates new problems. They suggest that self-reporting will have limited success in the absence of immunity from legal liability. One proposed solution calls for submitting self-regulatory reports to a neutral, nonsanctioning third-party entity. This approach has worked well for the airline industry.

New Patient-Care Focus

Abandoning a policy that concentrates on blame is at the heart of the improvements in patient safety proposed in the IOM report. Rather than pinpointing individual error, the new paradigm focuses on developing new systems of care that foster patient safety and help prevent sentinel events. In the absence of a finger-pointing environment, hospital personnel can freely examine what happened, discover the causes, and structure new procedures to prevent future occurrences – without fear of any retribution.

That’s the way they handle it at California Pacific Medical Center in San Francisco. In one case, when a nurse removed a dialysis catheter, the patient developed an air embolism and subsequently suffered a severe, permanently disabling stroke.

“When we investigated, we found that there was a written procedure in place to document a dialysis nurse’s credential,” says hospitalist Thomas E. Baudendistel, MD, FCAP, who is associate medical director of the hospital’s Internal Medicine Residency Program. “A, we weren’t aware of the credentialing procedure, and B, when we looked at it we weren’t sure it represented best practice. So we researched the literature and rewrote the policy. Now we schedule regular nursing education on pulling a dialysis catheter.”

In addition, the hospital set in place a follow-up plan to re-evaluate the procedure periodically. They also offer refresher training in catheter removal.

“We’ve used a similar approach in other situations,” says Dr. Baudendistel. “For example, our procedure with falls has changed. Now we use an event-based algorithm to determine whether a head CT scan is necessary.”

Hospitalists Can Lead

Hospital-based physicians are in an advantageous position to promote—as well as participate in—new initiatives for patient safety. Because they are involved in the day-to-day care of patients, hospitalists are firsthand observers when many errors occur. They have the experience and clinical judgment to give meaningful input to new incident-reporting protocols and to promote new policies through interdisciplinary teams that investigate and analyze adverse events.

Inevitably, electronic systems will replace paper-and-pen reporting and recordkeeping. Here hospitalists can take the lead, too. Unlike physicians who admit patients to multiple hospitals (each with a different information system), hospitalists practice in a single institution with only one system to learn. Hospitalists’ patient load may also help them to master new technology more quickly.

Surveys show that, while many hospitals have electronic ordering systems in place, relatively few physicians actually use them. In many cases, nurses or pharmacists place the electronic orders. Hospitalists who place their own orders can contribute to a reduction in medication errors by eliminating the pass-through of information that often causes misunderstandings.

Patient-Centric Healthcare: the New Paradigm

The traditional hospital system—and the healthcare system as a whole—are provider-oriented and provider-directed. Many patients, especially older ones, have a “doctor knows all” mindset, and they typically ask few questions—even when they don’t understand their treatment plans or exactly how they’re to take their medications when they go home. Case in point: A patient who was discharged from the hospital died at home shortly thereafter. The cause: His wife misunderstood the instructions for his pain medication and mistakenly applied six transdermal patches to his skin at one time instead of the single patch she should have applied. The multiple patches delivered a fatal overdose of the narcotic fentanyl.

Many experts believe that better informed—and empowered—patients are the key to reducing the number of sentinel events, including ADEs. The IOM report advocates a shift from a provider-centered to a patient-centered healthcare model. In this new paradigm, hospitalists would be much more expansive in their communications with patients. With regard to medications in particular, the report recommends that a physician:

• Review the patient’s medication list routinely and during care transitions.
• Review different treatment options.
• Review the names and purposes of all medications.
• Discuss when and how to take the medication.
• Discuss important and likely side effects and what to do about them.
• Discuss drug-drug, drug-food, and drug-disease interactions.
• Review the patient’s (or surrogate’s) role in appropriate medication use.
• Review the role of medications in the overall context of the patient’s health.

There are barriers to surmount before patients can become full partners in their healthcare. One of the most obvious is that patients need to be much better informed, and—when they are incapable of making appropriate decisions—they need surrogates to stand in for them. Patients need access to trustworthy and understandable information both online and in printed materials.

The IOM report recommends a government-sponsored national drug-information hotline; medication leaflets that provide standardized language in a manner that is appropriate for various age, literacy, and visual acuity levels; and development of personal health records.

PeaceHealth in Washington state took up the challenge of developing personal health records in 2001. PeaceHealth’s Project Manager, Mary Minniti, invited patients to design the system for self-management and communication among care team members. Today, the Shared Care Plan Personal Health Record is a reality, and Marc Pierson, MD, who is PeaceHealth’s regional vice president of Clinical Information and Special Projects, says “early evidence suggests that this type of tool promotes personal responsibility and positively affects patients’ confidence and active participation in their care.”

The tool is available on CD from www.peacehealth.org for those who would like to adopt it for their use.

Final Thought

The bad news is that sentinel events still take a staggering human and economic toll. The good news is that momentum is building for an important change in the way healthcare is delivered. Better communication, new technologies, and, perhaps most importantly, true provider-patient partnerships hold the promise of making hospital healthcare much safer. Hospitalists play a key role in this new scenario. TH

Joen Kinnan is a freelance medical writer based in Chicago.

In July, a teenage mother-to-be entered a Madison, Wis., hospital to give birth. Within hours she was dead, though her baby survived.

An investigation by the Wisconsin State Department of Health revealed that the young woman had died after receiving an intravenous dose of an epidural anesthetic instead of the penicillin she was supposed to be given. Shortly after receiving the injection, the teenager had a seizure. She died less than two hours later.

In explaining what had happened, a nurse told investigators that the patient had been nervous about how she was to be anesthetized during the birth. To ease her concerns, the nurse brought out the epidural bag and told her how it worked. Unfortunately, it was one bag too many; the nurse later confused the epidural bag with the penicillin bag. The consequences were fatal.

The Human Toll

Such sentinel events are all too common. According to a just-released report, Preventing Medication Errors, prepared by the Institute of Medicine (IOM) at the behest of the Centers for Medicare and Medicaid Services, medication errors harm 1.5 million people yearly in the U.S. and kill thousands. The annual cost: at least $3.5 billion. But medication mistakes are just part of the picture.

Sentinel events—unexpected occurrences that result in death or serious physical or psychological injury, or the risk of their later occurrence—can happen anywhere along the healthcare continuum, in any setting. Statistics from the Joint Commission on Accreditation of Healthcare Organizations (JCAHO), however, show that 68% occur in general hospitals and another 11% in psychiatric hospitals. JCAHO tracked the sentinel events they reviewed from 1995 to March of 2006 and found that the most commonly reported sentinel events were patient suicide, wrong-site surgery, operative/postoperative complications, medication errors, and delay in treatment—in that order. Of the total number of cases reviewed, 73% resulted in the death of the patient and 10% in loss of function.

Hard-and-fast statistics on sentinel events are difficult to come by, however. Information from the JCAHO covers only the incidents reviewed by that organization, and experts agree that almost all types of sentinel events are under-reported. Researchers cite a number of reasons that many incidents go unreported; among them are lack of time, fear of punishment, and confusion about the severity of events that require notification. For example, do near misses count? (See “Near Misses,” The Hospitalist, May, p. 34.) Others see no benefit to themselves or their institutions from reporting.

Studies have attempted to define the true incidence of sentinel events, but a lack of consistent language and definitions makes it difficult to put the whole puzzle together, even when sentinel events do come to the surface.

Focus on Medication Errors

That said, we know that the incidence of sentinel events is much higher than it should be. As regularly reported by The Hospitalist, the problem most in the spotlight today—among researchers and the popular press—is medication errors. The IOM report says that, on average, a hospitalized patient is subject to at least one medication error per day, though error rates vary widely among hospitals. Fortunately, most errors cause no serious harm, but the costs for those that do are substantial. One study found that each preventable adverse drug event (ADE) costs a hospital approximately $8,750.

At least a quarter of medication-related injuries are preventable, according to the report. The irony is that many error-prevention methods are available today: “do not use” abbreviation lists; medication reconciliation (used to compare a patient’s medication orders with all other medications the patient is taking in order to avoid omissions, duplications, dosing errors, or drug interactions); and computerized physician order entry systems, to name a few.

With so much emphasis on patient safety and the increasing availability of sophisticated reporting and record-keeping technology, why haven’t incidence rates for ADEs and other sentinel events dropped dramatically? The answer is not that hospital personnel are lazy, incompetent, or indifferent to the safety of their patients. Experts agree that today’s doctors, nurses, pharmacists, and other medical staff are highly trained, dedicated professionals who want to practice the best medicine possible. The present system focuses on individual fault and does not foster disclosure that could lead to corrective procedures.

In fact, legal experts worry that JCAHO’s Sentinel Events Policy, which mandates self-reporting by hospitals accredited by the JCAHO, creates new problems. They suggest that self-reporting will have limited success in the absence of immunity from legal liability. One proposed solution calls for submitting self-regulatory reports to a neutral, nonsanctioning third-party entity. This approach has worked well for the airline industry.

New Patient-Care Focus

Abandoning a policy that concentrates on blame is at the heart of the improvements in patient safety proposed in the IOM report. Rather than pinpointing individual error, the new paradigm focuses on developing new systems of care that foster patient safety and help prevent sentinel events. In the absence of a finger-pointing environment, hospital personnel can freely examine what happened, discover the causes, and structure new procedures to prevent future occurrences – without fear of any retribution.

That’s the way they handle it at California Pacific Medical Center in San Francisco. In one case, when a nurse removed a dialysis catheter, the patient developed an air embolism and subsequently suffered a severe, permanently disabling stroke.

“When we investigated, we found that there was a written procedure in place to document a dialysis nurse’s credential,” says hospitalist Thomas E. Baudendistel, MD, FCAP, who is associate medical director of the hospital’s Internal Medicine Residency Program. “A, we weren’t aware of the credentialing procedure, and B, when we looked at it we weren’t sure it represented best practice. So we researched the literature and rewrote the policy. Now we schedule regular nursing education on pulling a dialysis catheter.”

In addition, the hospital set in place a follow-up plan to re-evaluate the procedure periodically. They also offer refresher training in catheter removal.

“We’ve used a similar approach in other situations,” says Dr. Baudendistel. “For example, our procedure with falls has changed. Now we use an event-based algorithm to determine whether a head CT scan is necessary.”

Hospitalists Can Lead

Hospital-based physicians are in an advantageous position to promote—as well as participate in—new initiatives for patient safety. Because they are involved in the day-to-day care of patients, hospitalists are firsthand observers when many errors occur. They have the experience and clinical judgment to give meaningful input to new incident-reporting protocols and to promote new policies through interdisciplinary teams that investigate and analyze adverse events.

Inevitably, electronic systems will replace paper-and-pen reporting and recordkeeping. Here hospitalists can take the lead, too. Unlike physicians who admit patients to multiple hospitals (each with a different information system), hospitalists practice in a single institution with only one system to learn. Hospitalists’ patient load may also help them to master new technology more quickly.

Surveys show that, while many hospitals have electronic ordering systems in place, relatively few physicians actually use them. In many cases, nurses or pharmacists place the electronic orders. Hospitalists who place their own orders can contribute to a reduction in medication errors by eliminating the pass-through of information that often causes misunderstandings.

Patient-Centric Healthcare: the New Paradigm

The traditional hospital system—and the healthcare system as a whole—are provider-oriented and provider-directed. Many patients, especially older ones, have a “doctor knows all” mindset, and they typically ask few questions—even when they don’t understand their treatment plans or exactly how they’re to take their medications when they go home. Case in point: A patient who was discharged from the hospital died at home shortly thereafter. The cause: His wife misunderstood the instructions for his pain medication and mistakenly applied six transdermal patches to his skin at one time instead of the single patch she should have applied. The multiple patches delivered a fatal overdose of the narcotic fentanyl.

Many experts believe that better informed—and empowered—patients are the key to reducing the number of sentinel events, including ADEs. The IOM report advocates a shift from a provider-centered to a patient-centered healthcare model. In this new paradigm, hospitalists would be much more expansive in their communications with patients. With regard to medications in particular, the report recommends that a physician:

• Review the patient’s medication list routinely and during care transitions.
• Review different treatment options.
• Review the names and purposes of all medications.
• Discuss when and how to take the medication.
• Discuss important and likely side effects and what to do about them.
• Discuss drug-drug, drug-food, and drug-disease interactions.
• Review the patient’s (or surrogate’s) role in appropriate medication use.
• Review the role of medications in the overall context of the patient’s health.

There are barriers to surmount before patients can become full partners in their healthcare. One of the most obvious is that patients need to be much better informed, and—when they are incapable of making appropriate decisions—they need surrogates to stand in for them. Patients need access to trustworthy and understandable information both online and in printed materials.

The IOM report recommends a government-sponsored national drug-information hotline; medication leaflets that provide standardized language in a manner that is appropriate for various age, literacy, and visual acuity levels; and development of personal health records.

PeaceHealth in Washington state took up the challenge of developing personal health records in 2001. PeaceHealth’s Project Manager, Mary Minniti, invited patients to design the system for self-management and communication among care team members. Today, the Shared Care Plan Personal Health Record is a reality, and Marc Pierson, MD, who is PeaceHealth’s regional vice president of Clinical Information and Special Projects, says “early evidence suggests that this type of tool promotes personal responsibility and positively affects patients’ confidence and active participation in their care.”

The tool is available on CD from www.peacehealth.org for those who would like to adopt it for their use.

Final Thought

The bad news is that sentinel events still take a staggering human and economic toll. The good news is that momentum is building for an important change in the way healthcare is delivered. Better communication, new technologies, and, perhaps most importantly, true provider-patient partnerships hold the promise of making hospital healthcare much safer. Hospitalists play a key role in this new scenario. TH

Joen Kinnan is a freelance medical writer based in Chicago.

If the secret to successful real estate investing is “location, location, location,” the key to maintaining good relationships with referring physicians is “communication, communication, communication.” While this may seem simplistic, the complexities of interpersonal communications can pose challenges even in the most straightforward of physician interchanges.

Recent studies and hospitalists consulted for this report maintain that hospitalists’ communications with referring physicians must be examined, practiced, and fine-tuned continually to ensure satisfaction for doctors—and their patients.

“It’s all about the communication,” says Bruce Becker, MD, chief medical officer at Medical Center Hospital in Odessa, Texas, and a family physician and professor of medicine for more than 20 years. “It’s sometimes not what you say, but how you say it.”

According to John Nelson, MD, medical director of the Hospitalist Practice at Overlake Hospital in Bellevue, Wash., a consultant for hospital medicine groups with Nelson/Flores Associates and a columnist for The Hospitalist (“Practice Management”), it is key for hospitalists to examine and revise oral and written communication processes—especially at critical points during patient handoffs—rather than to assume that good communication will just happen naturally.

Gaining Acceptance

Some primary care physicians (PCPs) are more willing than others to refer patients to a hospitalist. Initially, new programs may have to work hard to gain acceptance with referring physicians. Some referring physicians may not be ready to give up hospital visits and may want to maintain collegiality and control. On the other hand, some family physicians are “ready to step away from hospital practice,” says Dr. Becker, citing diminishing reimbursements due to diagnosis-related groups (DRGs) and managed care.

John A. Bolinger, DO, FACP, medical director of the Hospitalist Program at Terre Haute (Ind.) Regional Hospital, believes that one way to promote a hospitalist program to PCPs is to emphasize hospitalists’ levels of training and efficiency.

“I try to make them aware of how [our hospitalist program] can be advantageous to them,” he explains. “Even if they have only one patient in the hospital, by the time they drive there, get the chart, make the rounds, make their notes, and do the required paperwork, it may take them an hour to see one patient. It makes good economic sense for them to stay in their offices, where they can see a minimum of four patients in the same amount of time for equal or better reimbursements.”

When primary care physicians voice resistance to using a hospitalist program, Dr. Bolinger says he tries to impress upon them the fact that hospitalists do not have outside practices, they will “never try to steal patients,” they stay within referral patterns, and they will make sure that PCPs get pertinent records as soon as possible. Dr. Bolinger believes referring physicians’ biggest concern when dealing with hospitalists is that they “don’t want to lose control.” The way to address those fears is to make sure referring physicians are always kept in the communications loop regarding their patients’ progress.

The policy for Dr. Bolinger’s hospitalist program is to make sure all dictated reports are transcribed and faxed immediately to the referring physician’s office. All scheduled follow-up appointments and medication changes are included in discharge summaries. “If need be,” says Dr. Bolinger, “we will even hand deliver information to physicians’ offices, which we have done multiple times.”

Become User-Friendly

The methods Dr. Bolinger describes often result in referring physicians’ satisfaction with hospitalist services, followed by increased referrals. Hospitalists can ensure continued referrals from their PCPs if they remember hospital medicine’s cardinal rules of availability and prompt, thorough reporting, says Dr. Nelson. It can help to view the interface with the hospitalist service from the PCP’s point of view.

For instance, how can physicians quickly reach the hospitalist service? “If you’re a referring doctor and you’ve got a patient in your office whom you think should be admitted today, who do you call? This can actually be a little tricky for most practices,” says Dr. Nelson. “Every practice should give some thought to making that contact as easy for the referring doctors as possible.”

Some important questions to ask: When trying to reach a hospitalist, is it best to call the group’s main number? Will a voicemail message be returned within an hour? Two hours? Is it better to call the hospital operator and have the hospitalist paged? Or do PCPs have access to hospitalists’ cell phone numbers?

Dr. Nelson suggests that hospitalist groups also give thought to standardizing admission and discharge reports, as well as other forms. Often, individual members of a hospitalist group use slightly different formats for reporting to referring physicians. He points out that this can be less user friendly for the reader, who may have a harder time scanning the document quickly to find a particular piece of important information. Other useful suggestions for making reports user friendly: Use similar headings on all reports; avoid dense text; list pending tests in a prominent place in the report document; and consider highlighting or underlining key words.

Preference for In-Person Contact

For a new hospitalist practice, telephone communication between the hospitalist and the primary physician is valuable, and the hospitalist should “pick up the phone liberally,” says Dr. Nelson.

Dr. Becker believes the best way for physicians to communicate is one on one—in person. “Too often,” he says, “we get used to communicating through a third party—usually a unit clerk, a nurse, or a resident. I believe that physician-to-physician communication is the ideal. If the attending physician and the consultant [hospitalist or subspecialist] speak in person, they can explain their thinking to each other, and “within one minute of precious time, figure out which way to go.”

In this way, without wasting time, the physician gives the consultant guidance as to the appropriate track to take and can also listen to the consultant’s suggestions.

“I feel that medicine has perhaps gotten a little bit away from that communication link,” continues Dr. Becker. “When we get further away from that direct communication—whether it is between doctors and consultants, nurses and doctors, or doctors and family members—you take that little bit of risk that there will be a missed step, either on the part of the communicator or on the receiving end as the listener.”

In a study exploring barriers to effective patient handoffs, Solet and colleagues focused on the communication between physicians as a vital link in patient care continuity. The authors concluded that, regardless of the method of managing patient handoffs (e.g., computer-assisted or paper-based), the best way to ensure effective handoffs of hospitalized patients was “precise, unambiguous, face-to-face communication.”1

In a 2001 study by Hruby, Pantilat, and colleagues at UCSF, the authors found that, for the most part, hospitalized patients with PCPs wanted contact with their primary physicians even while in the hospital. Approximately half of the surveyed patients also believed that the PCP, rather than an inpatient physician, should be the first to discuss with them serious diagnoses or disease management choices.2 Preferences such as those expressed in this study may play into referring physicians’ reluctance to make use of hospitalist services, says Dr. Bolinger. They may fear that patients will feel abandoned by the primary physician. Dr. Bolinger’s response to those sentiments: “Initially, some patients [in our hospital] were a little guarded and were not sure what to expect. But after a day or two of having us there, they are generally very, very pleased to have us on board. We are part of their medical team now.”

A Need for Marketing?

Dr. Becker has been actively developing a hospital medicine program at Medical Center Hospital for the past two years and joined SHM as part of that effort. Familiarizing himself with the tenets of hospital medicine, he discovered that, as a family doctor, “unknowingly, I was actually practicing hospital medicine for 20 years!”

As part of the hospital medicine program development process, he has solicited input from local physicians as well as patients. A simple survey to assess interest in a hospitalist program asked potential referring physicians, Would you use a hospitalist? Would you use a hospitalist after waiting a while to see how the process goes? Or, would you not consider using a hospitalist?

In two years, says Dr. Becker, response from the referring physician community has changed from “bah, humbug” to one of readiness for the program.

A mass mailing can serve to introduce a hospital medicine program in a community. Dr. Bolinger’s group used this method and, in his experience, local subspecialists—orthopedists, cardiologists, endocrinologists, pulmonologists—have proved the biggest source of referrals to their program. But PCPs are starting to use the hospitalist service for vacations and call-coverage issues and are beginning to value hospitalists’ services. “Physicians like coming to the hospital, but they’re starting to realize that the hospitalist program is a better system,” says Dr. Bolinger.

Dr. Nelson has been a hospitalist for 18 years. For most of that time he has had no shortage of referred patients. In fact, the bigger problem has been finding enough doctors to join the group and handle the existing referral volume. In that situation, it has not made sense to undertake marketing with the goal of increasing referrals. However, he advises, “It is always worth spending time and energy trying to maintain good relationships with physicians with whom you regularly share patients, and perhaps this could be called ‘marketing.’”

To maintain good relationships with referring physicians, his group conducts a survey on a yearly basis. A survey, he suggests, should be very short, consisting of only a few key questions, such as:

• Do we send reports promptly to your practice?
• Are your patients satisfied with the care they receive from us?
• Do you have any comments or feedback for our group?

Although his group gains information from these surveys, Dr. Nelson notes that the greater value of conducting such surveys may be in building public relations capital. By conducting a survey, hospitalists demonstrate that they care enough to ask for their referring physicians’ input.

Another good marketing tool is a patient education brochure, given to referring physicians, that explains hospitalists and hospitalist care. These brochures can help referring physicians prepare their patients for seeing a hospitalist in the inpatient setting, thus easing the initial reluctance patients sometimes experience when encountering a new physician.

Conclusion

On the cusp of launching his medical center’s hospital medicine program, Dr. Becker sees that good communication between referring physicians and hospitalists will ensure the program’s success. He advises physicians to remember their classes in communication as third-year medical students, when most participate in videotaped patient encounters. It’s always instructive, he says, to see how we come across to others in conversation.

Both verbal and nonverbal cues play a part in good communication. A 2003 study by Griffith and colleagues concluded that better nonverbal communication skills are associated with greater patient satisfaction, and that formal instruction in nonverbal communication can be a good addition to residency training.3

“I find that doctors talk to each other, in general, very easily,” says Dr. Becker. Sometimes [good communication] is just a matter of opening that door and essentially keeping the former attending, the PCP, apprised of what is going on.”

When hospitalists attend to thorough communication and promptly deliver complete discharge summaries, family physicians can report to their patients that they know what happened in the hospital and poll their patients about their experiences in the hospital. In this way, hospitalists and referring physicians can cement their relationship as team members for the patient. The success of any hospitalist program, Dr. Becker believes, lies in “making sure you fulfill the promise of what hospital medicine generates, and that is a continuity of care … , obtaining front-end communication so that patients get the best care throughout their [hospital] stay, and then follow up with discharge summaries to the primary physician’s office.” TH

Gretchen Henkel is a regular contributor to The Hospitalist.

References

1. Solet DJ, Norvell JM, Rutan GH, et al. Lost in translation: challenges and opportunities in physician-to-physician communication during patient handoffs. Acad Med. 2005 Dec;80(12): 1094-1099.
2. Hruby M, Pantilat SZ, Lo B. How do patients view the role of the primary care physician in inpatient care? Am J Med. 2001;21;111(9B):21S-25S.
3. Griffith CH III, Wilson JF, Langer S, et al. House staff nonverbal communication skills and standardized patient satisfaction. J Gen Intern Med. 2003 Mar;18(3):170-174.

If the secret to successful real estate investing is “location, location, location,” the key to maintaining good relationships with referring physicians is “communication, communication, communication.” While this may seem simplistic, the complexities of interpersonal communications can pose challenges even in the most straightforward of physician interchanges.

Recent studies and hospitalists consulted for this report maintain that hospitalists’ communications with referring physicians must be examined, practiced, and fine-tuned continually to ensure satisfaction for doctors—and their patients.

“It’s all about the communication,” says Bruce Becker, MD, chief medical officer at Medical Center Hospital in Odessa, Texas, and a family physician and professor of medicine for more than 20 years. “It’s sometimes not what you say, but how you say it.”

According to John Nelson, MD, medical director of the Hospitalist Practice at Overlake Hospital in Bellevue, Wash., a consultant for hospital medicine groups with Nelson/Flores Associates and a columnist for The Hospitalist (“Practice Management”), it is key for hospitalists to examine and revise oral and written communication processes—especially at critical points during patient handoffs—rather than to assume that good communication will just happen naturally.

Gaining Acceptance

Some primary care physicians (PCPs) are more willing than others to refer patients to a hospitalist. Initially, new programs may have to work hard to gain acceptance with referring physicians. Some referring physicians may not be ready to give up hospital visits and may want to maintain collegiality and control. On the other hand, some family physicians are “ready to step away from hospital practice,” says Dr. Becker, citing diminishing reimbursements due to diagnosis-related groups (DRGs) and managed care.

John A. Bolinger, DO, FACP, medical director of the Hospitalist Program at Terre Haute (Ind.) Regional Hospital, believes that one way to promote a hospitalist program to PCPs is to emphasize hospitalists’ levels of training and efficiency.

“I try to make them aware of how [our hospitalist program] can be advantageous to them,” he explains. “Even if they have only one patient in the hospital, by the time they drive there, get the chart, make the rounds, make their notes, and do the required paperwork, it may take them an hour to see one patient. It makes good economic sense for them to stay in their offices, where they can see a minimum of four patients in the same amount of time for equal or better reimbursements.”

When primary care physicians voice resistance to using a hospitalist program, Dr. Bolinger says he tries to impress upon them the fact that hospitalists do not have outside practices, they will “never try to steal patients,” they stay within referral patterns, and they will make sure that PCPs get pertinent records as soon as possible. Dr. Bolinger believes referring physicians’ biggest concern when dealing with hospitalists is that they “don’t want to lose control.” The way to address those fears is to make sure referring physicians are always kept in the communications loop regarding their patients’ progress.

The policy for Dr. Bolinger’s hospitalist program is to make sure all dictated reports are transcribed and faxed immediately to the referring physician’s office. All scheduled follow-up appointments and medication changes are included in discharge summaries. “If need be,” says Dr. Bolinger, “we will even hand deliver information to physicians’ offices, which we have done multiple times.”

Become User-Friendly

The methods Dr. Bolinger describes often result in referring physicians’ satisfaction with hospitalist services, followed by increased referrals. Hospitalists can ensure continued referrals from their PCPs if they remember hospital medicine’s cardinal rules of availability and prompt, thorough reporting, says Dr. Nelson. It can help to view the interface with the hospitalist service from the PCP’s point of view.

For instance, how can physicians quickly reach the hospitalist service? “If you’re a referring doctor and you’ve got a patient in your office whom you think should be admitted today, who do you call? This can actually be a little tricky for most practices,” says Dr. Nelson. “Every practice should give some thought to making that contact as easy for the referring doctors as possible.”

Some important questions to ask: When trying to reach a hospitalist, is it best to call the group’s main number? Will a voicemail message be returned within an hour? Two hours? Is it better to call the hospital operator and have the hospitalist paged? Or do PCPs have access to hospitalists’ cell phone numbers?

Dr. Nelson suggests that hospitalist groups also give thought to standardizing admission and discharge reports, as well as other forms. Often, individual members of a hospitalist group use slightly different formats for reporting to referring physicians. He points out that this can be less user friendly for the reader, who may have a harder time scanning the document quickly to find a particular piece of important information. Other useful suggestions for making reports user friendly: Use similar headings on all reports; avoid dense text; list pending tests in a prominent place in the report document; and consider highlighting or underlining key words.

Preference for In-Person Contact

For a new hospitalist practice, telephone communication between the hospitalist and the primary physician is valuable, and the hospitalist should “pick up the phone liberally,” says Dr. Nelson.

Dr. Becker believes the best way for physicians to communicate is one on one—in person. “Too often,” he says, “we get used to communicating through a third party—usually a unit clerk, a nurse, or a resident. I believe that physician-to-physician communication is the ideal. If the attending physician and the consultant [hospitalist or subspecialist] speak in person, they can explain their thinking to each other, and “within one minute of precious time, figure out which way to go.”

In this way, without wasting time, the physician gives the consultant guidance as to the appropriate track to take and can also listen to the consultant’s suggestions.

“I feel that medicine has perhaps gotten a little bit away from that communication link,” continues Dr. Becker. “When we get further away from that direct communication—whether it is between doctors and consultants, nurses and doctors, or doctors and family members—you take that little bit of risk that there will be a missed step, either on the part of the communicator or on the receiving end as the listener.”

In a study exploring barriers to effective patient handoffs, Solet and colleagues focused on the communication between physicians as a vital link in patient care continuity. The authors concluded that, regardless of the method of managing patient handoffs (e.g., computer-assisted or paper-based), the best way to ensure effective handoffs of hospitalized patients was “precise, unambiguous, face-to-face communication.”1

In a 2001 study by Hruby, Pantilat, and colleagues at UCSF, the authors found that, for the most part, hospitalized patients with PCPs wanted contact with their primary physicians even while in the hospital. Approximately half of the surveyed patients also believed that the PCP, rather than an inpatient physician, should be the first to discuss with them serious diagnoses or disease management choices.2 Preferences such as those expressed in this study may play into referring physicians’ reluctance to make use of hospitalist services, says Dr. Bolinger. They may fear that patients will feel abandoned by the primary physician. Dr. Bolinger’s response to those sentiments: “Initially, some patients [in our hospital] were a little guarded and were not sure what to expect. But after a day or two of having us there, they are generally very, very pleased to have us on board. We are part of their medical team now.”

A Need for Marketing?

Dr. Becker has been actively developing a hospital medicine program at Medical Center Hospital for the past two years and joined SHM as part of that effort. Familiarizing himself with the tenets of hospital medicine, he discovered that, as a family doctor, “unknowingly, I was actually practicing hospital medicine for 20 years!”

As part of the hospital medicine program development process, he has solicited input from local physicians as well as patients. A simple survey to assess interest in a hospitalist program asked potential referring physicians, Would you use a hospitalist? Would you use a hospitalist after waiting a while to see how the process goes? Or, would you not consider using a hospitalist?

In two years, says Dr. Becker, response from the referring physician community has changed from “bah, humbug” to one of readiness for the program.

A mass mailing can serve to introduce a hospital medicine program in a community. Dr. Bolinger’s group used this method and, in his experience, local subspecialists—orthopedists, cardiologists, endocrinologists, pulmonologists—have proved the biggest source of referrals to their program. But PCPs are starting to use the hospitalist service for vacations and call-coverage issues and are beginning to value hospitalists’ services. “Physicians like coming to the hospital, but they’re starting to realize that the hospitalist program is a better system,” says Dr. Bolinger.

Dr. Nelson has been a hospitalist for 18 years. For most of that time he has had no shortage of referred patients. In fact, the bigger problem has been finding enough doctors to join the group and handle the existing referral volume. In that situation, it has not made sense to undertake marketing with the goal of increasing referrals. However, he advises, “It is always worth spending time and energy trying to maintain good relationships with physicians with whom you regularly share patients, and perhaps this could be called ‘marketing.’”

To maintain good relationships with referring physicians, his group conducts a survey on a yearly basis. A survey, he suggests, should be very short, consisting of only a few key questions, such as:

• Do we send reports promptly to your practice?
• Are your patients satisfied with the care they receive from us?
• Do you have any comments or feedback for our group?

Although his group gains information from these surveys, Dr. Nelson notes that the greater value of conducting such surveys may be in building public relations capital. By conducting a survey, hospitalists demonstrate that they care enough to ask for their referring physicians’ input.

Another good marketing tool is a patient education brochure, given to referring physicians, that explains hospitalists and hospitalist care. These brochures can help referring physicians prepare their patients for seeing a hospitalist in the inpatient setting, thus easing the initial reluctance patients sometimes experience when encountering a new physician.

Conclusion

On the cusp of launching his medical center’s hospital medicine program, Dr. Becker sees that good communication between referring physicians and hospitalists will ensure the program’s success. He advises physicians to remember their classes in communication as third-year medical students, when most participate in videotaped patient encounters. It’s always instructive, he says, to see how we come across to others in conversation.

Both verbal and nonverbal cues play a part in good communication. A 2003 study by Griffith and colleagues concluded that better nonverbal communication skills are associated with greater patient satisfaction, and that formal instruction in nonverbal communication can be a good addition to residency training.3

“I find that doctors talk to each other, in general, very easily,” says Dr. Becker. Sometimes [good communication] is just a matter of opening that door and essentially keeping the former attending, the PCP, apprised of what is going on.”

When hospitalists attend to thorough communication and promptly deliver complete discharge summaries, family physicians can report to their patients that they know what happened in the hospital and poll their patients about their experiences in the hospital. In this way, hospitalists and referring physicians can cement their relationship as team members for the patient. The success of any hospitalist program, Dr. Becker believes, lies in “making sure you fulfill the promise of what hospital medicine generates, and that is a continuity of care … , obtaining front-end communication so that patients get the best care throughout their [hospital] stay, and then follow up with discharge summaries to the primary physician’s office.” TH

Gretchen Henkel is a regular contributor to The Hospitalist.

References

1. Solet DJ, Norvell JM, Rutan GH, et al. Lost in translation: challenges and opportunities in physician-to-physician communication during patient handoffs. Acad Med. 2005 Dec;80(12): 1094-1099.
2. Hruby M, Pantilat SZ, Lo B. How do patients view the role of the primary care physician in inpatient care? Am J Med. 2001;21;111(9B):21S-25S.
3. Griffith CH III, Wilson JF, Langer S, et al. House staff nonverbal communication skills and standardized patient satisfaction. J Gen Intern Med. 2003 Mar;18(3):170-174.

If the secret to successful real estate investing is “location, location, location,” the key to maintaining good relationships with referring physicians is “communication, communication, communication.” While this may seem simplistic, the complexities of interpersonal communications can pose challenges even in the most straightforward of physician interchanges.

Recent studies and hospitalists consulted for this report maintain that hospitalists’ communications with referring physicians must be examined, practiced, and fine-tuned continually to ensure satisfaction for doctors—and their patients.

“It’s all about the communication,” says Bruce Becker, MD, chief medical officer at Medical Center Hospital in Odessa, Texas, and a family physician and professor of medicine for more than 20 years. “It’s sometimes not what you say, but how you say it.”

According to John Nelson, MD, medical director of the Hospitalist Practice at Overlake Hospital in Bellevue, Wash., a consultant for hospital medicine groups with Nelson/Flores Associates and a columnist for The Hospitalist (“Practice Management”), it is key for hospitalists to examine and revise oral and written communication processes—especially at critical points during patient handoffs—rather than to assume that good communication will just happen naturally.

Gaining Acceptance

Some primary care physicians (PCPs) are more willing than others to refer patients to a hospitalist. Initially, new programs may have to work hard to gain acceptance with referring physicians. Some referring physicians may not be ready to give up hospital visits and may want to maintain collegiality and control. On the other hand, some family physicians are “ready to step away from hospital practice,” says Dr. Becker, citing diminishing reimbursements due to diagnosis-related groups (DRGs) and managed care.

John A. Bolinger, DO, FACP, medical director of the Hospitalist Program at Terre Haute (Ind.) Regional Hospital, believes that one way to promote a hospitalist program to PCPs is to emphasize hospitalists’ levels of training and efficiency.

“I try to make them aware of how [our hospitalist program] can be advantageous to them,” he explains. “Even if they have only one patient in the hospital, by the time they drive there, get the chart, make the rounds, make their notes, and do the required paperwork, it may take them an hour to see one patient. It makes good economic sense for them to stay in their offices, where they can see a minimum of four patients in the same amount of time for equal or better reimbursements.”

When primary care physicians voice resistance to using a hospitalist program, Dr. Bolinger says he tries to impress upon them the fact that hospitalists do not have outside practices, they will “never try to steal patients,” they stay within referral patterns, and they will make sure that PCPs get pertinent records as soon as possible. Dr. Bolinger believes referring physicians’ biggest concern when dealing with hospitalists is that they “don’t want to lose control.” The way to address those fears is to make sure referring physicians are always kept in the communications loop regarding their patients’ progress.

The policy for Dr. Bolinger’s hospitalist program is to make sure all dictated reports are transcribed and faxed immediately to the referring physician’s office. All scheduled follow-up appointments and medication changes are included in discharge summaries. “If need be,” says Dr. Bolinger, “we will even hand deliver information to physicians’ offices, which we have done multiple times.”

Become User-Friendly

The methods Dr. Bolinger describes often result in referring physicians’ satisfaction with hospitalist services, followed by increased referrals. Hospitalists can ensure continued referrals from their PCPs if they remember hospital medicine’s cardinal rules of availability and prompt, thorough reporting, says Dr. Nelson. It can help to view the interface with the hospitalist service from the PCP’s point of view.

For instance, how can physicians quickly reach the hospitalist service? “If you’re a referring doctor and you’ve got a patient in your office whom you think should be admitted today, who do you call? This can actually be a little tricky for most practices,” says Dr. Nelson. “Every practice should give some thought to making that contact as easy for the referring doctors as possible.”

Some important questions to ask: When trying to reach a hospitalist, is it best to call the group’s main number? Will a voicemail message be returned within an hour? Two hours? Is it better to call the hospital operator and have the hospitalist paged? Or do PCPs have access to hospitalists’ cell phone numbers?

Dr. Nelson suggests that hospitalist groups also give thought to standardizing admission and discharge reports, as well as other forms. Often, individual members of a hospitalist group use slightly different formats for reporting to referring physicians. He points out that this can be less user friendly for the reader, who may have a harder time scanning the document quickly to find a particular piece of important information. Other useful suggestions for making reports user friendly: Use similar headings on all reports; avoid dense text; list pending tests in a prominent place in the report document; and consider highlighting or underlining key words.

Preference for In-Person Contact

For a new hospitalist practice, telephone communication between the hospitalist and the primary physician is valuable, and the hospitalist should “pick up the phone liberally,” says Dr. Nelson.

Dr. Becker believes the best way for physicians to communicate is one on one—in person. “Too often,” he says, “we get used to communicating through a third party—usually a unit clerk, a nurse, or a resident. I believe that physician-to-physician communication is the ideal. If the attending physician and the consultant [hospitalist or subspecialist] speak in person, they can explain their thinking to each other, and “within one minute of precious time, figure out which way to go.”

In this way, without wasting time, the physician gives the consultant guidance as to the appropriate track to take and can also listen to the consultant’s suggestions.

“I feel that medicine has perhaps gotten a little bit away from that communication link,” continues Dr. Becker. “When we get further away from that direct communication—whether it is between doctors and consultants, nurses and doctors, or doctors and family members—you take that little bit of risk that there will be a missed step, either on the part of the communicator or on the receiving end as the listener.”

In a study exploring barriers to effective patient handoffs, Solet and colleagues focused on the communication between physicians as a vital link in patient care continuity. The authors concluded that, regardless of the method of managing patient handoffs (e.g., computer-assisted or paper-based), the best way to ensure effective handoffs of hospitalized patients was “precise, unambiguous, face-to-face communication.”1

In a 2001 study by Hruby, Pantilat, and colleagues at UCSF, the authors found that, for the most part, hospitalized patients with PCPs wanted contact with their primary physicians even while in the hospital. Approximately half of the surveyed patients also believed that the PCP, rather than an inpatient physician, should be the first to discuss with them serious diagnoses or disease management choices.2 Preferences such as those expressed in this study may play into referring physicians’ reluctance to make use of hospitalist services, says Dr. Bolinger. They may fear that patients will feel abandoned by the primary physician. Dr. Bolinger’s response to those sentiments: “Initially, some patients [in our hospital] were a little guarded and were not sure what to expect. But after a day or two of having us there, they are generally very, very pleased to have us on board. We are part of their medical team now.”

A Need for Marketing?

Dr. Becker has been actively developing a hospital medicine program at Medical Center Hospital for the past two years and joined SHM as part of that effort. Familiarizing himself with the tenets of hospital medicine, he discovered that, as a family doctor, “unknowingly, I was actually practicing hospital medicine for 20 years!”

As part of the hospital medicine program development process, he has solicited input from local physicians as well as patients. A simple survey to assess interest in a hospitalist program asked potential referring physicians, Would you use a hospitalist? Would you use a hospitalist after waiting a while to see how the process goes? Or, would you not consider using a hospitalist?

In two years, says Dr. Becker, response from the referring physician community has changed from “bah, humbug” to one of readiness for the program.

A mass mailing can serve to introduce a hospital medicine program in a community. Dr. Bolinger’s group used this method and, in his experience, local subspecialists—orthopedists, cardiologists, endocrinologists, pulmonologists—have proved the biggest source of referrals to their program. But PCPs are starting to use the hospitalist service for vacations and call-coverage issues and are beginning to value hospitalists’ services. “Physicians like coming to the hospital, but they’re starting to realize that the hospitalist program is a better system,” says Dr. Bolinger.

Dr. Nelson has been a hospitalist for 18 years. For most of that time he has had no shortage of referred patients. In fact, the bigger problem has been finding enough doctors to join the group and handle the existing referral volume. In that situation, it has not made sense to undertake marketing with the goal of increasing referrals. However, he advises, “It is always worth spending time and energy trying to maintain good relationships with physicians with whom you regularly share patients, and perhaps this could be called ‘marketing.’”

To maintain good relationships with referring physicians, his group conducts a survey on a yearly basis. A survey, he suggests, should be very short, consisting of only a few key questions, such as:

• Do we send reports promptly to your practice?
• Are your patients satisfied with the care they receive from us?
• Do you have any comments or feedback for our group?

Although his group gains information from these surveys, Dr. Nelson notes that the greater value of conducting such surveys may be in building public relations capital. By conducting a survey, hospitalists demonstrate that they care enough to ask for their referring physicians’ input.

Another good marketing tool is a patient education brochure, given to referring physicians, that explains hospitalists and hospitalist care. These brochures can help referring physicians prepare their patients for seeing a hospitalist in the inpatient setting, thus easing the initial reluctance patients sometimes experience when encountering a new physician.

Conclusion

On the cusp of launching his medical center’s hospital medicine program, Dr. Becker sees that good communication between referring physicians and hospitalists will ensure the program’s success. He advises physicians to remember their classes in communication as third-year medical students, when most participate in videotaped patient encounters. It’s always instructive, he says, to see how we come across to others in conversation.

Both verbal and nonverbal cues play a part in good communication. A 2003 study by Griffith and colleagues concluded that better nonverbal communication skills are associated with greater patient satisfaction, and that formal instruction in nonverbal communication can be a good addition to residency training.3

“I find that doctors talk to each other, in general, very easily,” says Dr. Becker. Sometimes [good communication] is just a matter of opening that door and essentially keeping the former attending, the PCP, apprised of what is going on.”

When hospitalists attend to thorough communication and promptly deliver complete discharge summaries, family physicians can report to their patients that they know what happened in the hospital and poll their patients about their experiences in the hospital. In this way, hospitalists and referring physicians can cement their relationship as team members for the patient. The success of any hospitalist program, Dr. Becker believes, lies in “making sure you fulfill the promise of what hospital medicine generates, and that is a continuity of care … , obtaining front-end communication so that patients get the best care throughout their [hospital] stay, and then follow up with discharge summaries to the primary physician’s office.” TH

Gretchen Henkel is a regular contributor to The Hospitalist.

References

1. Solet DJ, Norvell JM, Rutan GH, et al. Lost in translation: challenges and opportunities in physician-to-physician communication during patient handoffs. Acad Med. 2005 Dec;80(12): 1094-1099.
2. Hruby M, Pantilat SZ, Lo B. How do patients view the role of the primary care physician in inpatient care? Am J Med. 2001;21;111(9B):21S-25S.
3. Griffith CH III, Wilson JF, Langer S, et al. House staff nonverbal communication skills and standardized patient satisfaction. J Gen Intern Med. 2003 Mar;18(3):170-174.

Hypertension during pregnancy, of which preeclampsia and eclampsia predominate, constitutes a significant health problem both because of its high incidence (4%-11% of pregnancies in developed countries) and due to the maternal and fetal health outcomes it creates.1 Hypertensive disorders are the second leading cause of maternal mortality.1 They cause 15% of all maternal deaths and constitute considerable morbidity both during and after pregnancy.2 Fetal outcomes include premature delivery, small-for-gestational-age (SGA) infants, and fetal mortality.

The long-term cardiovascular risks for mothers who suffer from the triad of hypertension during pregnancy, SGA infants, and pre-term delivery are approximately eight times higher than for individuals without these complications during pregnancy.

Hypertension observed during pregnancy is defined according to one of the following classifications:

1. Chronic hypertension, present prior to pregnancy;
2. Preeclampsia/eclampsia: development of hypertension, proteinuria, and edema during pregnancy;
3. Preeclampsia superimposed on preexisting renal disease; and
4. Gestational hypertension: either transient mild hypertension during the third trimester or mild hypertension detected during the third trimester that does not resolve by 12 weeks postpartum.

Diagnosing Preeclampsia/Eclampsia

Of these hypertensive entities, this article focuses on the most common and potentially serious one: preeclampsia/eclampsia. Preeclampsia is characterized by blood pressure over 140/90 mm Hg—measured on two separate occasions, and proteinuria greater than 300 mg/24 hours, occurring after 20 weeks gestation. Severe preeclampsia includes the same criteria, as well as proteinuria greater than 5,000 mg/24 hours; blood pressure higher than 160/110 mm Hg; or end-organ damage such as headaches, visual changes, renal dysfunction, hepatic dysfunction, or thrombocytopenia.

Historically, the term eclampsia has been reserved to describe the symptoms of preeclampsia combined with the occurrence of seizure activity. HELLP syndrome is a severe variant of preeclampsia that affects up to 1% of pregnancies and includes the constellation of hemolysis, elevated liver enzyme levels, and a low platelet count.

Given the potential risks for these disorders during pregnancy, it seems logical to target primarily those individuals at risk and attempt to prevent the disorder. Traditionally, the higher risk populations include patients experiencing primagravida pregnancies, those with a history of hypertension or renal disease, women who have had prior episodes of preeclampsia, and multiparous individuals with different paternal partners. Other less helpful or more expensive screening procedures include evaluation for inherited thrombophilias.

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Recommended Treatment

Several trials have attempted to prevent the development of preeclampsia using calcium supplementation or aspirin therapy, but current evidence demonstrates no benefit from these interventions except in selected populations.3,4 For the past several decades, the treatment for hypertension during pregnancy has consisted of either delivery of the fetus or bed rest combined with therapies involving alpha-methyl-DOPA, hydralazine, and intravenous magnesium sulfate, depending on the level of the patient’s blood pressure and proteinuria, as well as the stage of the pregnancy.

Because of the potential risks to the health of the infant (as well as that of the mother) generic interventional trials extrapolated from other hypertensive populations that may offer equivalent or more effective therapies have not been readily accomplished. In spite of this lack of clinical and outcomes studies, the following generalizations regarding care are currently advocated:

1. Continue anti-hypertensive therapy for chronic hypertension with a goal of maintaining blood pressure below 140/90 mm Hg. Though the risks of SGA infants and preeclampsia were not affected by therapy, the incidence of premature delivery was reduced. Nearly all anti-hypertensive drugs have been used in treating chronic hypertension in pregnancy, but angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are contraindicated because of teratogenecity. Diuretics and hydralazine may also have adverse outcomes on fetal and/or maternal health, respectively.

Though diuretics may reduce an already compromised placental blood flow by reducing intravascular volume, a number of randomized trials using diuretics have been reported. The population studied in these trials totaled approximately 7,000 individuals, and the results show no demonstrable adverse effects.5 Centrally acting alpha 2 adrenergic agonists (alpha-methyl-DOPA, clonidine), long-acting dihydropyridines (calcium channel blockers), and beta-adrenergic blockers with or without alpha-adrenergic blockade have been used successfully during pregnancy.6 Infants born to mothers receiving beta-blockers have a higher incidence of transient heart block and bradycardia. Newer agents, as opposed to alpha-methyl-DOPA and hydralazine, have not been shown to be more effective in controlling blood pressure but have demonstrated fewer adverse effects or events.

2. Mild preeclampsia may be treated using late-term delivery or bed rest before the pregnancy reaches 36 weeks. Close observation in a hospital is warranted until lack of progression to severe eclampsia is ensured.

3. Severe preeclampsia must be treated using either delivery or interventions to control blood pressure and prevent seizures while delivery is temporarily delayed to allow for fetal maturation. Intravenous magnesium sulfate (Mg2SO4), titrated to therapeutic concentrations of magnesium (4.5-8.5 mg/dl) along with suppression of deep tendon reflexes, has significantly lowered blood pressure and reduced the incidence of seizure activity. In direct comparison with intravenous phenytoin, there were no episodes of eclampsia in patients treated with magnesium (zero of 1,049 patients treated), while 10 of 1,089 individuals treated with phenytoin developed eclampsia.7 Similarly, Mg2SO4 decreased the incidence of eclampsia to 0.8% compared with 2.6% of individuals treated with nimodipine.8 Likewise, Mg2SO4 significantly reduced recurrent seizures compared to diazepam and phenytoin. In patients with renal insufficiency or other relative contraindications to Mg2SO4 therapy, the physician may treat the blood pressure with labetalol or a calcium channel antagonist and provide prophylaxis from seizures using phenytoin.

Because of the lack of a more complete understanding of the etiology (or etiologies) of preeclampsia/eclampsia, we are not fully able to identify individuals who are at risk. With further investigation, we will be able to provide more selective and effective interventions.

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Nitrous Oxide’s Vital Role in Pregnancy

In this regard, considerable investigation has been directed toward a better understanding of eclampsia/preeclampsia in the past 20 years. The current discussion will highlight three promising lines of inquiry. Before commenting on these three areas of investigation, we feel it is important to illustrate the fundamental defect observed in all models of preeclampsia. This unifying abnormality is the presence of a placenta with inadequate uterine blood flow.

In a normal pregnancy, after implantation in the uterine wall, cytotrophoblasts invade the uterine wall, undergo a transformation of cell adhesion molecules from epithelial to endothelial expression characteristics, and induce the deep invasion of the placenta by the spiral arteries, creating large vascular sinuses in the decidua (pseudovasculogenesis). Finally, beta human chorionic gonadotropin production by the placenta stimulates the release of relaxin from the corpus luteum. Many cytokines and growth factors contribute to this normal placental development, but vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) appear to be the most important.

VEGF and PlGF play an integral role in the inducement of conversion of the cytotrophoblast cell adhesion molecules from epithelial to endothelial expression, particularly integrins and cadherins. In models of preeclampsia, there is insufficient invasion of the spiral arteries and inadequate uterine blood flow, as well as a lack of alteration in adhesion molecules of cytotrophoblasts and failed pseudovasculogenesis.9

During normal pregnancy, intravascular volume increases, peripheral vascular resistance (PVR) decreases, and renal blood flow and glomerular filtration rate (GFR) increase. (See Figure 1, above left.) Concomitant with the increased plasma volume, the reduction of PVR (vasodilation) not only mitigates the effect of plasma volume on systemic blood pressure, but actually reduces the systemic blood pressure during normal pregnancy. (See Figure 2, below.) Based on seminal studies by Jeyabalan and colleagues, one explanation for the decline in PVR and blood pressure, along with the increased renal plasma flow and GFR, is the production and action of relaxin on vascular smooth muscle to stimulate gelatinase-A (matrix metalloproteinase-2), which cleaves bigET (endothelin precursor) to form ET1-32. (See Figure 3, above.) ET1-32 binds to the ETB receptor and increases nitrous oxide (NO) synthetase activity and NO production, leading to vasodilation.10

click for large version

The Pathophysiology of Preeclampsia

Based on this observation of normal pregnancy, the following three lines of investigation have furthered our understanding of the potential pathophysiology of pre-eclampsia.

1. Because NO appears to play an important role in the normal vasodilation of pregnancy, abnormalities in this vascular regulatory pathway may be critical to the development of hypertension. Asymmetric dimethylarginine (ADMA) competitively inhibits NO production from arginine by nitric oxide synthetase (NOS). Savvidou and colleagues showed that women with ultrasound evidence of low uterine blood flow were more likely to develop preeclampsia and exhibited higher ADMA levels.11 There was a strong inverse relationship between ADMA levels and flow-mediated vasodilation in women who developed preeclampsia.

Similarly, dimethylarginine dimethylaminohydrolase (DDAH II), an enzyme that metabolizes ADMA, is strongly expressed in placental tissue. In states of placental insufficiency, one might speculate that levels of DDAH II would be reduced, while ADMA levels would increase. Along this same line of investigation, Noris and colleagues have shown increased arginase II activity in placental tissue from preeclamptic individuals and subsequently reduced levels of L-arginine, a substrate for NO production.12

2. A second line of promising research involves the production of a circulating inhibitor of VEGF. The growth factors VEGF and PlGF are produced by the placenta and affect vascular function by binding to two high affinity receptor tyrosine kinases: kinase insert domain-containing region (KDR) and Fms-like tyrosine kinase 1 receptor (Flt-1). Alternative splicing results in the production of an endogenously secreted protein, soluble Fms-like tyrosine kinase 1 receptor (sFlt-1), which lacks the transmembrane and cytoplasmic region of the VEGF receptor and cannot become membrane bound, but that binds VEGF and PlGF. Once VEGF has bound to sFlt-1, normal binding to the membrane-bound receptor is inhibited; thus the effects of VEGF are inhibited.

Studies have found that infusion of sFlt-1 to nonpregnant animals causes glomerular endotheliosis and hypertension similar to those found in preeclampsia; these findings support the possibility that sFlt-1 contributes to preeclampsia. Further, Levine and colleagues have shown that plasma sFlt-1 levels increase more in women with preeclampsia and precede clinical findings compared with individuals with normal pregnancies.13 In addition, PlGF levels were decreased in women with preeclampsia compared with the levels found in those experiencing normal pregnancies.

The supposition from these studies is that increased plasma levels of sFlt-1 competitively inhibit VEGF binding to VEGF receptors on vascular tissue. This inhibition causes a lack of vasodilation and increased blood pressure, with the normal fluid retention and volume expansion of pregnancy. VEGF is difficult to accurately determine in plasma, but PlGF levels, which are affected similarly, are reduced in individuals suffering from or destined to develop preeclampsia. Furthermore, since VEGF is an important determinant of normal placental development, decreased cellular binding due to competitive inhibition could contribute to abnormal placental pseudovasculogenesis.

3. Finally, Vu and colleagues have shown that pregnant animals made hypertensive by a high salt diet and deoxycorticosterone administration exhibit a higher circulating level of the Na, K-ATPase inhibitor, marinobufagenin.14 Further, blood pressure is reduced by the administration of the inhibitor of this cardenolide compound, resibufogenin. Though this is not a model of spontaneous preeclampsia, many features are similar, including reduced placental blood flow in spite of volume expansion and proteinuria.

Treatment Recommendations

1. In individuals with hypertension prior to pregnancy, the physician may continue the same anti-hypertensive therapy used pre-pregnancy, with or without diuretics—except for angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. The goal is to maintain the blood pressure at or below a level of 140/90 mm Hg. The pregnancy should be monitored as a high-risk pregnancy, and urine protein excretion, blood pressure, and fetal health should be monitored frequently, particularly after the 24th week of gestation. Urine protein excretion is most easily monitored using a spot urine protein-to-creatinine ratio. A value of less than 0.3 is equivalent to a 24-hour urine excretion of less than 300 mg.

2. Monitor individuals who develop mild preeclampsia for 24-72 hours to assess for progression. If they remain stable, the decision analysis depends on the stage of pregnancy. After 32 weeks gestation, the physician can elect to continue the pregnancy while prescribing reduced activity or bed rest with or without anti-hypertensive therapy. If anti-hypertensive therapy is elected, optimal choices include the dihydropyridine class of calcium channel antagonists, centrally acting alpha 2 agonists such as clonidine, or beta-blockers.

Though diuretics appear safe, most obstetricians do not advocate their use. Most physicians choose to initiate pharmacologic therapy if preeclampsia occurs prior to 32 weeks, in order to allow further fetal development prior to delivery. Many obstetricians will induce labor if the pregnancy is beyond 36 weeks to avoid the complications of preeclampsia/eclampsia. Delivery usually resolves the syndrome of preeclampsia within a period of time that ranges from hours to days.

3. In patients with severe preeclampsia, the risks are greater. In these circumstances, physicians are more likely to induce delivery if gestation is greater than 32 weeks. However, in pregnancies beyond 36 weeks, a physician may choose to delay delivery in order to allow fetal lung maturation, using steroids while controlling blood pressure and preventing seizures with intravenous Mg2SO4. Other options include the use of intravenous labetalol, hydralazine, or even nitroprusside, while also treating the patient with phenytoin to prevent seizures.

4. The presence of the HELLP syndrome usually necessitates urgent delivery and may have prolonged effects on blood pressure, liver function, and compromised renal function after the pregnancy has ended.

As a better understanding of the pathogenesis of preeclampsia develops in the future, more selective and definitive preventive or interventional therapy is likely. As further investigation moves toward that goal, this serious health problem in an otherwise young and healthy population should be mitigated. TH

Dr. Beach is the Paul R. Stalnaker Distinguished Professor of Internal Medicine, director, Division of Nephrology and Hypertension, and scholar, John McGovern Academy of Oslerian Medicine.

References

1. Longo SA, Dola CP, Pridjian G. Preeclampsia and eclampsia revisited. South Med J. 2003 Sep;96(9): 891-899.
2. Irgens HU, Reisaeter L, Irgens LM, et al. Long-term mortality of mothers and fathers after pre-eclampsia: population based cohort study. BMJ. 2001 Nov 24;323(7323):1213-1217.
3. CLASP (Collaborative Low-dose Aspirin Study in Pregnancy) Collaborative Group. CLASP: a randomised trial of low-dose aspirin for the prevention and treatment of pre-eclampsia among 9364 pregnant women. Lancet. 1994;343:619-629.
4. Hofmeyer GJ, Atallah AN, Duley L. Calcium supplementation during pregnancy for preventing hypertensive disorders and related problems. Cochrane Database Sys Rev. 2000;3:CD001059.
5. Collins R, Yusuf S, Peto R. Overview of randomised trials of diuretics in pregnancy. Br Med J (Clin Res Ed). 1985 Jan 5;290 (6461):17-23.
6. Magee LA, Ornstein MP, von Dadelszen P. Fortnightly review: management of hypertension in pregnancy. BMJ. 1999 May 15;318 (7194):1332-1336.
7. Lucas MJ, Leveno KJ, Cunningham FG. A comparison of magnesium sulfate with phenytoin for the prevention of eclampsia. N Engl J Med. 1995 Jul 27;333 (4):201-205.
8. Belfort MA, Anthony J, Saade GR, et al. A comparison of magnesium sulfate and nimodipine for the prevention of eclampsia. N Engl J Med. 2003 Jan 23;348 (4):304-311.
9. Levine RJ, Karumanchi SA. Circulating angiogenic factors in preeclampsia. Clin Obstet Gynecol. 2005 Jun;48(2):372-386.
10. Jeyabalan A, Novak J, Danielson LA, et al. Essential role for vascular gelatinase activity in relaxin-induced renal vasodilation, hyperfiltration, and reduced myogenic reactivity of small arteries. Circ Res. 2003 Dec 12;93(12):1249-1257. Epub 2003 Oct 30.
11. Savvidou MD, Hingorani AD, Tsikas D, et al. Endothelial dysfunction and raised plasma concentrations of asymmetric dimethylarginine in pregnant women who subsequently develop pre-eclampsia. Lancet. 2003 May 3;361(9368):1511-1517.
12. Noris M, Todeschini M, Cassis P, et al. L-arginine depletion in preeclampsia orients nitric oxide synthase toward oxidant species. Hypertension. 2004 Mar;43(3):614-622. Epub 2004 Jan 26.
13. Levine RJ, Maynard SE, Qian C, et al. Circulating angiogenic factors and the risk of preeclampsia. N Engl J Med. 2004 Feb 12;350 (7):672-683. Epub 2004 Feb 5.
14. Vu H, Ianosi-Irimie M, Danchuk S, et al. Resibufogenin corrects hypertension in a rat model of human preeclampsia. Exp Biol Med (Maywood). 2006 Feb;231(2):215-220.

Hypertension during pregnancy, of which preeclampsia and eclampsia predominate, constitutes a significant health problem both because of its high incidence (4%-11% of pregnancies in developed countries) and due to the maternal and fetal health outcomes it creates.1 Hypertensive disorders are the second leading cause of maternal mortality.1 They cause 15% of all maternal deaths and constitute considerable morbidity both during and after pregnancy.2 Fetal outcomes include premature delivery, small-for-gestational-age (SGA) infants, and fetal mortality.

The long-term cardiovascular risks for mothers who suffer from the triad of hypertension during pregnancy, SGA infants, and pre-term delivery are approximately eight times higher than for individuals without these complications during pregnancy.

Hypertension observed during pregnancy is defined according to one of the following classifications:

1. Chronic hypertension, present prior to pregnancy;
2. Preeclampsia/eclampsia: development of hypertension, proteinuria, and edema during pregnancy;
3. Preeclampsia superimposed on preexisting renal disease; and
4. Gestational hypertension: either transient mild hypertension during the third trimester or mild hypertension detected during the third trimester that does not resolve by 12 weeks postpartum.

Diagnosing Preeclampsia/Eclampsia

Of these hypertensive entities, this article focuses on the most common and potentially serious one: preeclampsia/eclampsia. Preeclampsia is characterized by blood pressure over 140/90 mm Hg—measured on two separate occasions, and proteinuria greater than 300 mg/24 hours, occurring after 20 weeks gestation. Severe preeclampsia includes the same criteria, as well as proteinuria greater than 5,000 mg/24 hours; blood pressure higher than 160/110 mm Hg; or end-organ damage such as headaches, visual changes, renal dysfunction, hepatic dysfunction, or thrombocytopenia.

Historically, the term eclampsia has been reserved to describe the symptoms of preeclampsia combined with the occurrence of seizure activity. HELLP syndrome is a severe variant of preeclampsia that affects up to 1% of pregnancies and includes the constellation of hemolysis, elevated liver enzyme levels, and a low platelet count.

Given the potential risks for these disorders during pregnancy, it seems logical to target primarily those individuals at risk and attempt to prevent the disorder. Traditionally, the higher risk populations include patients experiencing primagravida pregnancies, those with a history of hypertension or renal disease, women who have had prior episodes of preeclampsia, and multiparous individuals with different paternal partners. Other less helpful or more expensive screening procedures include evaluation for inherited thrombophilias.

click for large version

Recommended Treatment

Several trials have attempted to prevent the development of preeclampsia using calcium supplementation or aspirin therapy, but current evidence demonstrates no benefit from these interventions except in selected populations.3,4 For the past several decades, the treatment for hypertension during pregnancy has consisted of either delivery of the fetus or bed rest combined with therapies involving alpha-methyl-DOPA, hydralazine, and intravenous magnesium sulfate, depending on the level of the patient’s blood pressure and proteinuria, as well as the stage of the pregnancy.

Because of the potential risks to the health of the infant (as well as that of the mother) generic interventional trials extrapolated from other hypertensive populations that may offer equivalent or more effective therapies have not been readily accomplished. In spite of this lack of clinical and outcomes studies, the following generalizations regarding care are currently advocated:

1. Continue anti-hypertensive therapy for chronic hypertension with a goal of maintaining blood pressure below 140/90 mm Hg. Though the risks of SGA infants and preeclampsia were not affected by therapy, the incidence of premature delivery was reduced. Nearly all anti-hypertensive drugs have been used in treating chronic hypertension in pregnancy, but angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are contraindicated because of teratogenecity. Diuretics and hydralazine may also have adverse outcomes on fetal and/or maternal health, respectively.

Though diuretics may reduce an already compromised placental blood flow by reducing intravascular volume, a number of randomized trials using diuretics have been reported. The population studied in these trials totaled approximately 7,000 individuals, and the results show no demonstrable adverse effects.5 Centrally acting alpha 2 adrenergic agonists (alpha-methyl-DOPA, clonidine), long-acting dihydropyridines (calcium channel blockers), and beta-adrenergic blockers with or without alpha-adrenergic blockade have been used successfully during pregnancy.6 Infants born to mothers receiving beta-blockers have a higher incidence of transient heart block and bradycardia. Newer agents, as opposed to alpha-methyl-DOPA and hydralazine, have not been shown to be more effective in controlling blood pressure but have demonstrated fewer adverse effects or events.

2. Mild preeclampsia may be treated using late-term delivery or bed rest before the pregnancy reaches 36 weeks. Close observation in a hospital is warranted until lack of progression to severe eclampsia is ensured.

3. Severe preeclampsia must be treated using either delivery or interventions to control blood pressure and prevent seizures while delivery is temporarily delayed to allow for fetal maturation. Intravenous magnesium sulfate (Mg2SO4), titrated to therapeutic concentrations of magnesium (4.5-8.5 mg/dl) along with suppression of deep tendon reflexes, has significantly lowered blood pressure and reduced the incidence of seizure activity. In direct comparison with intravenous phenytoin, there were no episodes of eclampsia in patients treated with magnesium (zero of 1,049 patients treated), while 10 of 1,089 individuals treated with phenytoin developed eclampsia.7 Similarly, Mg2SO4 decreased the incidence of eclampsia to 0.8% compared with 2.6% of individuals treated with nimodipine.8 Likewise, Mg2SO4 significantly reduced recurrent seizures compared to diazepam and phenytoin. In patients with renal insufficiency or other relative contraindications to Mg2SO4 therapy, the physician may treat the blood pressure with labetalol or a calcium channel antagonist and provide prophylaxis from seizures using phenytoin.

Because of the lack of a more complete understanding of the etiology (or etiologies) of preeclampsia/eclampsia, we are not fully able to identify individuals who are at risk. With further investigation, we will be able to provide more selective and effective interventions.

click for large version

Nitrous Oxide’s Vital Role in Pregnancy

In this regard, considerable investigation has been directed toward a better understanding of eclampsia/preeclampsia in the past 20 years. The current discussion will highlight three promising lines of inquiry. Before commenting on these three areas of investigation, we feel it is important to illustrate the fundamental defect observed in all models of preeclampsia. This unifying abnormality is the presence of a placenta with inadequate uterine blood flow.

In a normal pregnancy, after implantation in the uterine wall, cytotrophoblasts invade the uterine wall, undergo a transformation of cell adhesion molecules from epithelial to endothelial expression characteristics, and induce the deep invasion of the placenta by the spiral arteries, creating large vascular sinuses in the decidua (pseudovasculogenesis). Finally, beta human chorionic gonadotropin production by the placenta stimulates the release of relaxin from the corpus luteum. Many cytokines and growth factors contribute to this normal placental development, but vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) appear to be the most important.

VEGF and PlGF play an integral role in the inducement of conversion of the cytotrophoblast cell adhesion molecules from epithelial to endothelial expression, particularly integrins and cadherins. In models of preeclampsia, there is insufficient invasion of the spiral arteries and inadequate uterine blood flow, as well as a lack of alteration in adhesion molecules of cytotrophoblasts and failed pseudovasculogenesis.9

During normal pregnancy, intravascular volume increases, peripheral vascular resistance (PVR) decreases, and renal blood flow and glomerular filtration rate (GFR) increase. (See Figure 1, above left.) Concomitant with the increased plasma volume, the reduction of PVR (vasodilation) not only mitigates the effect of plasma volume on systemic blood pressure, but actually reduces the systemic blood pressure during normal pregnancy. (See Figure 2, below.) Based on seminal studies by Jeyabalan and colleagues, one explanation for the decline in PVR and blood pressure, along with the increased renal plasma flow and GFR, is the production and action of relaxin on vascular smooth muscle to stimulate gelatinase-A (matrix metalloproteinase-2), which cleaves bigET (endothelin precursor) to form ET1-32. (See Figure 3, above.) ET1-32 binds to the ETB receptor and increases nitrous oxide (NO) synthetase activity and NO production, leading to vasodilation.10

click for large version

The Pathophysiology of Preeclampsia

Based on this observation of normal pregnancy, the following three lines of investigation have furthered our understanding of the potential pathophysiology of pre-eclampsia.

1. Because NO appears to play an important role in the normal vasodilation of pregnancy, abnormalities in this vascular regulatory pathway may be critical to the development of hypertension. Asymmetric dimethylarginine (ADMA) competitively inhibits NO production from arginine by nitric oxide synthetase (NOS). Savvidou and colleagues showed that women with ultrasound evidence of low uterine blood flow were more likely to develop preeclampsia and exhibited higher ADMA levels.11 There was a strong inverse relationship between ADMA levels and flow-mediated vasodilation in women who developed preeclampsia.

Similarly, dimethylarginine dimethylaminohydrolase (DDAH II), an enzyme that metabolizes ADMA, is strongly expressed in placental tissue. In states of placental insufficiency, one might speculate that levels of DDAH II would be reduced, while ADMA levels would increase. Along this same line of investigation, Noris and colleagues have shown increased arginase II activity in placental tissue from preeclamptic individuals and subsequently reduced levels of L-arginine, a substrate for NO production.12

2. A second line of promising research involves the production of a circulating inhibitor of VEGF. The growth factors VEGF and PlGF are produced by the placenta and affect vascular function by binding to two high affinity receptor tyrosine kinases: kinase insert domain-containing region (KDR) and Fms-like tyrosine kinase 1 receptor (Flt-1). Alternative splicing results in the production of an endogenously secreted protein, soluble Fms-like tyrosine kinase 1 receptor (sFlt-1), which lacks the transmembrane and cytoplasmic region of the VEGF receptor and cannot become membrane bound, but that binds VEGF and PlGF. Once VEGF has bound to sFlt-1, normal binding to the membrane-bound receptor is inhibited; thus the effects of VEGF are inhibited.

Studies have found that infusion of sFlt-1 to nonpregnant animals causes glomerular endotheliosis and hypertension similar to those found in preeclampsia; these findings support the possibility that sFlt-1 contributes to preeclampsia. Further, Levine and colleagues have shown that plasma sFlt-1 levels increase more in women with preeclampsia and precede clinical findings compared with individuals with normal pregnancies.13 In addition, PlGF levels were decreased in women with preeclampsia compared with the levels found in those experiencing normal pregnancies.

The supposition from these studies is that increased plasma levels of sFlt-1 competitively inhibit VEGF binding to VEGF receptors on vascular tissue. This inhibition causes a lack of vasodilation and increased blood pressure, with the normal fluid retention and volume expansion of pregnancy. VEGF is difficult to accurately determine in plasma, but PlGF levels, which are affected similarly, are reduced in individuals suffering from or destined to develop preeclampsia. Furthermore, since VEGF is an important determinant of normal placental development, decreased cellular binding due to competitive inhibition could contribute to abnormal placental pseudovasculogenesis.

3. Finally, Vu and colleagues have shown that pregnant animals made hypertensive by a high salt diet and deoxycorticosterone administration exhibit a higher circulating level of the Na, K-ATPase inhibitor, marinobufagenin.14 Further, blood pressure is reduced by the administration of the inhibitor of this cardenolide compound, resibufogenin. Though this is not a model of spontaneous preeclampsia, many features are similar, including reduced placental blood flow in spite of volume expansion and proteinuria.

Treatment Recommendations

1. In individuals with hypertension prior to pregnancy, the physician may continue the same anti-hypertensive therapy used pre-pregnancy, with or without diuretics—except for angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. The goal is to maintain the blood pressure at or below a level of 140/90 mm Hg. The pregnancy should be monitored as a high-risk pregnancy, and urine protein excretion, blood pressure, and fetal health should be monitored frequently, particularly after the 24th week of gestation. Urine protein excretion is most easily monitored using a spot urine protein-to-creatinine ratio. A value of less than 0.3 is equivalent to a 24-hour urine excretion of less than 300 mg.

2. Monitor individuals who develop mild preeclampsia for 24-72 hours to assess for progression. If they remain stable, the decision analysis depends on the stage of pregnancy. After 32 weeks gestation, the physician can elect to continue the pregnancy while prescribing reduced activity or bed rest with or without anti-hypertensive therapy. If anti-hypertensive therapy is elected, optimal choices include the dihydropyridine class of calcium channel antagonists, centrally acting alpha 2 agonists such as clonidine, or beta-blockers.

Though diuretics appear safe, most obstetricians do not advocate their use. Most physicians choose to initiate pharmacologic therapy if preeclampsia occurs prior to 32 weeks, in order to allow further fetal development prior to delivery. Many obstetricians will induce labor if the pregnancy is beyond 36 weeks to avoid the complications of preeclampsia/eclampsia. Delivery usually resolves the syndrome of preeclampsia within a period of time that ranges from hours to days.

3. In patients with severe preeclampsia, the risks are greater. In these circumstances, physicians are more likely to induce delivery if gestation is greater than 32 weeks. However, in pregnancies beyond 36 weeks, a physician may choose to delay delivery in order to allow fetal lung maturation, using steroids while controlling blood pressure and preventing seizures with intravenous Mg2SO4. Other options include the use of intravenous labetalol, hydralazine, or even nitroprusside, while also treating the patient with phenytoin to prevent seizures.

4. The presence of the HELLP syndrome usually necessitates urgent delivery and may have prolonged effects on blood pressure, liver function, and compromised renal function after the pregnancy has ended.

As a better understanding of the pathogenesis of preeclampsia develops in the future, more selective and definitive preventive or interventional therapy is likely. As further investigation moves toward that goal, this serious health problem in an otherwise young and healthy population should be mitigated. TH

Dr. Beach is the Paul R. Stalnaker Distinguished Professor of Internal Medicine, director, Division of Nephrology and Hypertension, and scholar, John McGovern Academy of Oslerian Medicine.

References

1. Longo SA, Dola CP, Pridjian G. Preeclampsia and eclampsia revisited. South Med J. 2003 Sep;96(9): 891-899.
2. Irgens HU, Reisaeter L, Irgens LM, et al. Long-term mortality of mothers and fathers after pre-eclampsia: population based cohort study. BMJ. 2001 Nov 24;323(7323):1213-1217.
3. CLASP (Collaborative Low-dose Aspirin Study in Pregnancy) Collaborative Group. CLASP: a randomised trial of low-dose aspirin for the prevention and treatment of pre-eclampsia among 9364 pregnant women. Lancet. 1994;343:619-629.
4. Hofmeyer GJ, Atallah AN, Duley L. Calcium supplementation during pregnancy for preventing hypertensive disorders and related problems. Cochrane Database Sys Rev. 2000;3:CD001059.
5. Collins R, Yusuf S, Peto R. Overview of randomised trials of diuretics in pregnancy. Br Med J (Clin Res Ed). 1985 Jan 5;290 (6461):17-23.
6. Magee LA, Ornstein MP, von Dadelszen P. Fortnightly review: management of hypertension in pregnancy. BMJ. 1999 May 15;318 (7194):1332-1336.
7. Lucas MJ, Leveno KJ, Cunningham FG. A comparison of magnesium sulfate with phenytoin for the prevention of eclampsia. N Engl J Med. 1995 Jul 27;333 (4):201-205.
8. Belfort MA, Anthony J, Saade GR, et al. A comparison of magnesium sulfate and nimodipine for the prevention of eclampsia. N Engl J Med. 2003 Jan 23;348 (4):304-311.
9. Levine RJ, Karumanchi SA. Circulating angiogenic factors in preeclampsia. Clin Obstet Gynecol. 2005 Jun;48(2):372-386.
10. Jeyabalan A, Novak J, Danielson LA, et al. Essential role for vascular gelatinase activity in relaxin-induced renal vasodilation, hyperfiltration, and reduced myogenic reactivity of small arteries. Circ Res. 2003 Dec 12;93(12):1249-1257. Epub 2003 Oct 30.
11. Savvidou MD, Hingorani AD, Tsikas D, et al. Endothelial dysfunction and raised plasma concentrations of asymmetric dimethylarginine in pregnant women who subsequently develop pre-eclampsia. Lancet. 2003 May 3;361(9368):1511-1517.
12. Noris M, Todeschini M, Cassis P, et al. L-arginine depletion in preeclampsia orients nitric oxide synthase toward oxidant species. Hypertension. 2004 Mar;43(3):614-622. Epub 2004 Jan 26.
13. Levine RJ, Maynard SE, Qian C, et al. Circulating angiogenic factors and the risk of preeclampsia. N Engl J Med. 2004 Feb 12;350 (7):672-683. Epub 2004 Feb 5.
14. Vu H, Ianosi-Irimie M, Danchuk S, et al. Resibufogenin corrects hypertension in a rat model of human preeclampsia. Exp Biol Med (Maywood). 2006 Feb;231(2):215-220.

Hypertension during pregnancy, of which preeclampsia and eclampsia predominate, constitutes a significant health problem both because of its high incidence (4%-11% of pregnancies in developed countries) and due to the maternal and fetal health outcomes it creates.1 Hypertensive disorders are the second leading cause of maternal mortality.1 They cause 15% of all maternal deaths and constitute considerable morbidity both during and after pregnancy.2 Fetal outcomes include premature delivery, small-for-gestational-age (SGA) infants, and fetal mortality.

The long-term cardiovascular risks for mothers who suffer from the triad of hypertension during pregnancy, SGA infants, and pre-term delivery are approximately eight times higher than for individuals without these complications during pregnancy.

Hypertension observed during pregnancy is defined according to one of the following classifications:

1. Chronic hypertension, present prior to pregnancy;
2. Preeclampsia/eclampsia: development of hypertension, proteinuria, and edema during pregnancy;
3. Preeclampsia superimposed on preexisting renal disease; and
4. Gestational hypertension: either transient mild hypertension during the third trimester or mild hypertension detected during the third trimester that does not resolve by 12 weeks postpartum.

Diagnosing Preeclampsia/Eclampsia

Of these hypertensive entities, this article focuses on the most common and potentially serious one: preeclampsia/eclampsia. Preeclampsia is characterized by blood pressure over 140/90 mm Hg—measured on two separate occasions, and proteinuria greater than 300 mg/24 hours, occurring after 20 weeks gestation. Severe preeclampsia includes the same criteria, as well as proteinuria greater than 5,000 mg/24 hours; blood pressure higher than 160/110 mm Hg; or end-organ damage such as headaches, visual changes, renal dysfunction, hepatic dysfunction, or thrombocytopenia.

Historically, the term eclampsia has been reserved to describe the symptoms of preeclampsia combined with the occurrence of seizure activity. HELLP syndrome is a severe variant of preeclampsia that affects up to 1% of pregnancies and includes the constellation of hemolysis, elevated liver enzyme levels, and a low platelet count.

Given the potential risks for these disorders during pregnancy, it seems logical to target primarily those individuals at risk and attempt to prevent the disorder. Traditionally, the higher risk populations include patients experiencing primagravida pregnancies, those with a history of hypertension or renal disease, women who have had prior episodes of preeclampsia, and multiparous individuals with different paternal partners. Other less helpful or more expensive screening procedures include evaluation for inherited thrombophilias.

click for large version

Recommended Treatment

Several trials have attempted to prevent the development of preeclampsia using calcium supplementation or aspirin therapy, but current evidence demonstrates no benefit from these interventions except in selected populations.3,4 For the past several decades, the treatment for hypertension during pregnancy has consisted of either delivery of the fetus or bed rest combined with therapies involving alpha-methyl-DOPA, hydralazine, and intravenous magnesium sulfate, depending on the level of the patient’s blood pressure and proteinuria, as well as the stage of the pregnancy.

Because of the potential risks to the health of the infant (as well as that of the mother) generic interventional trials extrapolated from other hypertensive populations that may offer equivalent or more effective therapies have not been readily accomplished. In spite of this lack of clinical and outcomes studies, the following generalizations regarding care are currently advocated:

1. Continue anti-hypertensive therapy for chronic hypertension with a goal of maintaining blood pressure below 140/90 mm Hg. Though the risks of SGA infants and preeclampsia were not affected by therapy, the incidence of premature delivery was reduced. Nearly all anti-hypertensive drugs have been used in treating chronic hypertension in pregnancy, but angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are contraindicated because of teratogenecity. Diuretics and hydralazine may also have adverse outcomes on fetal and/or maternal health, respectively.

Though diuretics may reduce an already compromised placental blood flow by reducing intravascular volume, a number of randomized trials using diuretics have been reported. The population studied in these trials totaled approximately 7,000 individuals, and the results show no demonstrable adverse effects.5 Centrally acting alpha 2 adrenergic agonists (alpha-methyl-DOPA, clonidine), long-acting dihydropyridines (calcium channel blockers), and beta-adrenergic blockers with or without alpha-adrenergic blockade have been used successfully during pregnancy.6 Infants born to mothers receiving beta-blockers have a higher incidence of transient heart block and bradycardia. Newer agents, as opposed to alpha-methyl-DOPA and hydralazine, have not been shown to be more effective in controlling blood pressure but have demonstrated fewer adverse effects or events.

2. Mild preeclampsia may be treated using late-term delivery or bed rest before the pregnancy reaches 36 weeks. Close observation in a hospital is warranted until lack of progression to severe eclampsia is ensured.

3. Severe preeclampsia must be treated using either delivery or interventions to control blood pressure and prevent seizures while delivery is temporarily delayed to allow for fetal maturation. Intravenous magnesium sulfate (Mg2SO4), titrated to therapeutic concentrations of magnesium (4.5-8.5 mg/dl) along with suppression of deep tendon reflexes, has significantly lowered blood pressure and reduced the incidence of seizure activity. In direct comparison with intravenous phenytoin, there were no episodes of eclampsia in patients treated with magnesium (zero of 1,049 patients treated), while 10 of 1,089 individuals treated with phenytoin developed eclampsia.7 Similarly, Mg2SO4 decreased the incidence of eclampsia to 0.8% compared with 2.6% of individuals treated with nimodipine.8 Likewise, Mg2SO4 significantly reduced recurrent seizures compared to diazepam and phenytoin. In patients with renal insufficiency or other relative contraindications to Mg2SO4 therapy, the physician may treat the blood pressure with labetalol or a calcium channel antagonist and provide prophylaxis from seizures using phenytoin.

Because of the lack of a more complete understanding of the etiology (or etiologies) of preeclampsia/eclampsia, we are not fully able to identify individuals who are at risk. With further investigation, we will be able to provide more selective and effective interventions.

click for large version

Nitrous Oxide’s Vital Role in Pregnancy

In this regard, considerable investigation has been directed toward a better understanding of eclampsia/preeclampsia in the past 20 years. The current discussion will highlight three promising lines of inquiry. Before commenting on these three areas of investigation, we feel it is important to illustrate the fundamental defect observed in all models of preeclampsia. This unifying abnormality is the presence of a placenta with inadequate uterine blood flow.

In a normal pregnancy, after implantation in the uterine wall, cytotrophoblasts invade the uterine wall, undergo a transformation of cell adhesion molecules from epithelial to endothelial expression characteristics, and induce the deep invasion of the placenta by the spiral arteries, creating large vascular sinuses in the decidua (pseudovasculogenesis). Finally, beta human chorionic gonadotropin production by the placenta stimulates the release of relaxin from the corpus luteum. Many cytokines and growth factors contribute to this normal placental development, but vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) appear to be the most important.

VEGF and PlGF play an integral role in the inducement of conversion of the cytotrophoblast cell adhesion molecules from epithelial to endothelial expression, particularly integrins and cadherins. In models of preeclampsia, there is insufficient invasion of the spiral arteries and inadequate uterine blood flow, as well as a lack of alteration in adhesion molecules of cytotrophoblasts and failed pseudovasculogenesis.9

During normal pregnancy, intravascular volume increases, peripheral vascular resistance (PVR) decreases, and renal blood flow and glomerular filtration rate (GFR) increase. (See Figure 1, above left.) Concomitant with the increased plasma volume, the reduction of PVR (vasodilation) not only mitigates the effect of plasma volume on systemic blood pressure, but actually reduces the systemic blood pressure during normal pregnancy. (See Figure 2, below.) Based on seminal studies by Jeyabalan and colleagues, one explanation for the decline in PVR and blood pressure, along with the increased renal plasma flow and GFR, is the production and action of relaxin on vascular smooth muscle to stimulate gelatinase-A (matrix metalloproteinase-2), which cleaves bigET (endothelin precursor) to form ET1-32. (See Figure 3, above.) ET1-32 binds to the ETB receptor and increases nitrous oxide (NO) synthetase activity and NO production, leading to vasodilation.10

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The Pathophysiology of Preeclampsia

Based on this observation of normal pregnancy, the following three lines of investigation have furthered our understanding of the potential pathophysiology of pre-eclampsia.

1. Because NO appears to play an important role in the normal vasodilation of pregnancy, abnormalities in this vascular regulatory pathway may be critical to the development of hypertension. Asymmetric dimethylarginine (ADMA) competitively inhibits NO production from arginine by nitric oxide synthetase (NOS). Savvidou and colleagues showed that women with ultrasound evidence of low uterine blood flow were more likely to develop preeclampsia and exhibited higher ADMA levels.11 There was a strong inverse relationship between ADMA levels and flow-mediated vasodilation in women who developed preeclampsia.

Similarly, dimethylarginine dimethylaminohydrolase (DDAH II), an enzyme that metabolizes ADMA, is strongly expressed in placental tissue. In states of placental insufficiency, one might speculate that levels of DDAH II would be reduced, while ADMA levels would increase. Along this same line of investigation, Noris and colleagues have shown increased arginase II activity in placental tissue from preeclamptic individuals and subsequently reduced levels of L-arginine, a substrate for NO production.12

2. A second line of promising research involves the production of a circulating inhibitor of VEGF. The growth factors VEGF and PlGF are produced by the placenta and affect vascular function by binding to two high affinity receptor tyrosine kinases: kinase insert domain-containing region (KDR) and Fms-like tyrosine kinase 1 receptor (Flt-1). Alternative splicing results in the production of an endogenously secreted protein, soluble Fms-like tyrosine kinase 1 receptor (sFlt-1), which lacks the transmembrane and cytoplasmic region of the VEGF receptor and cannot become membrane bound, but that binds VEGF and PlGF. Once VEGF has bound to sFlt-1, normal binding to the membrane-bound receptor is inhibited; thus the effects of VEGF are inhibited.

Studies have found that infusion of sFlt-1 to nonpregnant animals causes glomerular endotheliosis and hypertension similar to those found in preeclampsia; these findings support the possibility that sFlt-1 contributes to preeclampsia. Further, Levine and colleagues have shown that plasma sFlt-1 levels increase more in women with preeclampsia and precede clinical findings compared with individuals with normal pregnancies.13 In addition, PlGF levels were decreased in women with preeclampsia compared with the levels found in those experiencing normal pregnancies.

The supposition from these studies is that increased plasma levels of sFlt-1 competitively inhibit VEGF binding to VEGF receptors on vascular tissue. This inhibition causes a lack of vasodilation and increased blood pressure, with the normal fluid retention and volume expansion of pregnancy. VEGF is difficult to accurately determine in plasma, but PlGF levels, which are affected similarly, are reduced in individuals suffering from or destined to develop preeclampsia. Furthermore, since VEGF is an important determinant of normal placental development, decreased cellular binding due to competitive inhibition could contribute to abnormal placental pseudovasculogenesis.

3. Finally, Vu and colleagues have shown that pregnant animals made hypertensive by a high salt diet and deoxycorticosterone administration exhibit a higher circulating level of the Na, K-ATPase inhibitor, marinobufagenin.14 Further, blood pressure is reduced by the administration of the inhibitor of this cardenolide compound, resibufogenin. Though this is not a model of spontaneous preeclampsia, many features are similar, including reduced placental blood flow in spite of volume expansion and proteinuria.

Treatment Recommendations

1. In individuals with hypertension prior to pregnancy, the physician may continue the same anti-hypertensive therapy used pre-pregnancy, with or without diuretics—except for angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. The goal is to maintain the blood pressure at or below a level of 140/90 mm Hg. The pregnancy should be monitored as a high-risk pregnancy, and urine protein excretion, blood pressure, and fetal health should be monitored frequently, particularly after the 24th week of gestation. Urine protein excretion is most easily monitored using a spot urine protein-to-creatinine ratio. A value of less than 0.3 is equivalent to a 24-hour urine excretion of less than 300 mg.

2. Monitor individuals who develop mild preeclampsia for 24-72 hours to assess for progression. If they remain stable, the decision analysis depends on the stage of pregnancy. After 32 weeks gestation, the physician can elect to continue the pregnancy while prescribing reduced activity or bed rest with or without anti-hypertensive therapy. If anti-hypertensive therapy is elected, optimal choices include the dihydropyridine class of calcium channel antagonists, centrally acting alpha 2 agonists such as clonidine, or beta-blockers.

Though diuretics appear safe, most obstetricians do not advocate their use. Most physicians choose to initiate pharmacologic therapy if preeclampsia occurs prior to 32 weeks, in order to allow further fetal development prior to delivery. Many obstetricians will induce labor if the pregnancy is beyond 36 weeks to avoid the complications of preeclampsia/eclampsia. Delivery usually resolves the syndrome of preeclampsia within a period of time that ranges from hours to days.

3. In patients with severe preeclampsia, the risks are greater. In these circumstances, physicians are more likely to induce delivery if gestation is greater than 32 weeks. However, in pregnancies beyond 36 weeks, a physician may choose to delay delivery in order to allow fetal lung maturation, using steroids while controlling blood pressure and preventing seizures with intravenous Mg2SO4. Other options include the use of intravenous labetalol, hydralazine, or even nitroprusside, while also treating the patient with phenytoin to prevent seizures.

4. The presence of the HELLP syndrome usually necessitates urgent delivery and may have prolonged effects on blood pressure, liver function, and compromised renal function after the pregnancy has ended.

As a better understanding of the pathogenesis of preeclampsia develops in the future, more selective and definitive preventive or interventional therapy is likely. As further investigation moves toward that goal, this serious health problem in an otherwise young and healthy population should be mitigated. TH

Dr. Beach is the Paul R. Stalnaker Distinguished Professor of Internal Medicine, director, Division of Nephrology and Hypertension, and scholar, John McGovern Academy of Oslerian Medicine.

References

1. Longo SA, Dola CP, Pridjian G. Preeclampsia and eclampsia revisited. South Med J. 2003 Sep;96(9): 891-899.
2. Irgens HU, Reisaeter L, Irgens LM, et al. Long-term mortality of mothers and fathers after pre-eclampsia: population based cohort study. BMJ. 2001 Nov 24;323(7323):1213-1217.
3. CLASP (Collaborative Low-dose Aspirin Study in Pregnancy) Collaborative Group. CLASP: a randomised trial of low-dose aspirin for the prevention and treatment of pre-eclampsia among 9364 pregnant women. Lancet. 1994;343:619-629.
4. Hofmeyer GJ, Atallah AN, Duley L. Calcium supplementation during pregnancy for preventing hypertensive disorders and related problems. Cochrane Database Sys Rev. 2000;3:CD001059.
5. Collins R, Yusuf S, Peto R. Overview of randomised trials of diuretics in pregnancy. Br Med J (Clin Res Ed). 1985 Jan 5;290 (6461):17-23.
6. Magee LA, Ornstein MP, von Dadelszen P. Fortnightly review: management of hypertension in pregnancy. BMJ. 1999 May 15;318 (7194):1332-1336.
7. Lucas MJ, Leveno KJ, Cunningham FG. A comparison of magnesium sulfate with phenytoin for the prevention of eclampsia. N Engl J Med. 1995 Jul 27;333 (4):201-205.
8. Belfort MA, Anthony J, Saade GR, et al. A comparison of magnesium sulfate and nimodipine for the prevention of eclampsia. N Engl J Med. 2003 Jan 23;348 (4):304-311.
9. Levine RJ, Karumanchi SA. Circulating angiogenic factors in preeclampsia. Clin Obstet Gynecol. 2005 Jun;48(2):372-386.
10. Jeyabalan A, Novak J, Danielson LA, et al. Essential role for vascular gelatinase activity in relaxin-induced renal vasodilation, hyperfiltration, and reduced myogenic reactivity of small arteries. Circ Res. 2003 Dec 12;93(12):1249-1257. Epub 2003 Oct 30.
11. Savvidou MD, Hingorani AD, Tsikas D, et al. Endothelial dysfunction and raised plasma concentrations of asymmetric dimethylarginine in pregnant women who subsequently develop pre-eclampsia. Lancet. 2003 May 3;361(9368):1511-1517.
12. Noris M, Todeschini M, Cassis P, et al. L-arginine depletion in preeclampsia orients nitric oxide synthase toward oxidant species. Hypertension. 2004 Mar;43(3):614-622. Epub 2004 Jan 26.
13. Levine RJ, Maynard SE, Qian C, et al. Circulating angiogenic factors and the risk of preeclampsia. N Engl J Med. 2004 Feb 12;350 (7):672-683. Epub 2004 Feb 5.
14. Vu H, Ianosi-Irimie M, Danchuk S, et al. Resibufogenin corrects hypertension in a rat model of human preeclampsia. Exp Biol Med (Maywood). 2006 Feb;231(2):215-220.

Diabetic foot infections are common, costly, and potentially catastrophic for patients. The average patient with a diabetic foot infection undergoes three surgical procedures, including toe amputation in 19% and leg amputation in 14%.1 The annual cost of diabetic foot osteomyelitis in the United States is $2.8 billion.2

Diabetics are uniquely predisposed to foot infections. Because of neuropathy, minor repetitive injury leads to large foot ulcers, especially over the metatarsal heads. Foot deformities result in soft tissue injury from poorly fitting shoes. Because of autonomic neuropathy, the diabetic foot sweats less, leading to dry, cracked skin for bacteria to invade. Resistance to infection is lower because of neutrophil dysfunction in hyperglycemia. Vascular insufficiency impairs both wound healing and the immune response.3

The major principles of therapy are as follows:

1. Use an empiric antibiotic regimen with broad coverage against gram-positive, gram-negative, and anaerobic organisms. Diabetic foot infections are usually polymicrobial. Except for mild infections, in which therapy directed at gram-positive organisms may suffice, initial therapy should cover streptococci, methicillin-sensitive Staphylococcus aureus, E. coli, Proteus, and anaerobes.

Many studies of antibiotic therapy in diabetic foot infections have been performed, without demonstrating a clear superiority for any one regimen. The 2004 guidelines of the Infectious Diseases Society of America list 13 acceptable regimens for moderate diabetic foot infections.4 Useful single drug regimens include ampicillin-sulbactam, piperacillin-tazobactam, levofloxacin, and cefoxitin. For the penicillin-allergic patient, clindamycin and ciprofloxacin is a useful combination. Empiric vancomycin should be reserved for patients with a history of MRSA, treatment failure, or severe infection. (I would also reserve carbapenems, such as imipenem-cilastatin, for more severe infections, to prevent antibiotic resistance against a class of drugs representing our last defense against highly resistant gram-negative organisms.)

Once the patient is clinically improved and results of adequate cultures are available, consideration can be given to narrowing the course of therapy. Most diabetic foot infections can be treated with some combination of intravenous and oral therapy.

2. Have a high clinical suspicion for osteomyelitis. Osteomyelitis is extremely common in diabetic foot infections due to plantar ulceration and poor soft tissue coverage. Cure rates are reduced in osteomyelitis because dead bone acts as a nidus for persistent infection. The most useful diagnostic maneuver for osteomyelitis is deep probing of the wound with a sterile swab at the bedside. If a gritty sensation is felt, osteomyelitis is likely, and further diagnostic testing is probably unnecessary.

If the physical examination is equivocal, plain radiographs should be obtained to look for bony erosions. If these are negative, MRI is the next most useful diagnostic step. Bone scans are of limited value due to their low specificity. (Charcot arthropathy is a common cause of false-positive bone scans in this setting.)

Because of the high prevalence of osteomyelitis in diabetic foot infections, my own practice is to err on the side of longer, rather than shorter, antibiotic therapy.

3. Surgical debridement is required for many diabetic foot infections. Develop a collaborative relationship with a vascular or orthopedic surgeon with interest and expertise in the management of diabetic foot infections. Necrotic and gangrenous material should be removed. Ideally, dead bone should be debrided, both therapeutically and to help establish a bacteriologic diagnosis. (When removal of dead bone would result in loss of function or might create a non-healing wound, the option of long-term antibiotic suppression could be explored with an infectious disease specialist.)

4. When osteomyelitis is present, bone cultures help to define the optimal antibiotic therapy. Recent studies have confirmed older data regarding the poor correlation between surface cultures and bone cultures. The latter are preferred, when feasible.

5. Consider revascularization. Most diabetic foot infections arise in the setting of vascular insufficiency. At a minimum, patients with diabetic foot infections should have ankle-brachial indices performed for screening. Because diabetics may have falsely elevated ankle pressures due to calcified and non-compressible arteries, additional diagnostic studies may be useful, such as segmental pressures and Doppler pulse volume recordings.

Measurement of the transcutaneous oxygen concentration (TcP02) has been recommended, particularly in assessing which patients may benefit from hyperbaric oxygen. However, the TcP02 is not widely available, and the benefit of hyperbaric oxygen in this setting remains controversial.

6. Patients should be educated in meticulous foot care to prevent recurrences and reinfections. A diabetic foot infection may indicate that the patient lacks the knowledge, resources, or motivation for proper foot care. It also suggests that something is seriously awry with the patient’s diabetic regimen, compliance, or both. Hospital admissions for diabetic foot infections provide an opportunity to revise the patient’s diabetic medications; to educate the patient regarding wound care, skin care, and daily foot self-examination; to provide additional resources such as visiting nurses; and to refer patients for podiatric care, including tailored shoes, orthotics, and, if necessary, casting to off-load ulcers. TH

Dr. Ross is an instructor in medicine at Harvard Medical School.

References

1. Hill SL, Holtzman GI, Buse R. The effects of peripheral vascular disease with osteomyelitis in the diabetic foot. Am J Surg. 1999 Apr;177(4):282-286.
2. Gordois A, Scuffham P, Shearer A, et al. The health care costs of diabetic peripheral neuropathy in the United States. Diabetes Care. 2003;26(6):1790-1795.
3. Lazzarini L, Mader JT, Calhoun JH. Diabetic foot infection. In: Calhoun JH, Mader JT, eds. Musculoskeletal Infections. New York, NY. Marcel Dekker. 2003.
4. Lipsky BA, Berendt AR, Deery HG, et al. Diagnosis and treatment of diabetic foot infections. Clin Infect Dis. 2004 Oct;39(7):885-910.

Diabetic foot infections are common, costly, and potentially catastrophic for patients. The average patient with a diabetic foot infection undergoes three surgical procedures, including toe amputation in 19% and leg amputation in 14%.1 The annual cost of diabetic foot osteomyelitis in the United States is $2.8 billion.2

Diabetics are uniquely predisposed to foot infections. Because of neuropathy, minor repetitive injury leads to large foot ulcers, especially over the metatarsal heads. Foot deformities result in soft tissue injury from poorly fitting shoes. Because of autonomic neuropathy, the diabetic foot sweats less, leading to dry, cracked skin for bacteria to invade. Resistance to infection is lower because of neutrophil dysfunction in hyperglycemia. Vascular insufficiency impairs both wound healing and the immune response.3

The major principles of therapy are as follows:

1. Use an empiric antibiotic regimen with broad coverage against gram-positive, gram-negative, and anaerobic organisms. Diabetic foot infections are usually polymicrobial. Except for mild infections, in which therapy directed at gram-positive organisms may suffice, initial therapy should cover streptococci, methicillin-sensitive Staphylococcus aureus, E. coli, Proteus, and anaerobes.

Many studies of antibiotic therapy in diabetic foot infections have been performed, without demonstrating a clear superiority for any one regimen. The 2004 guidelines of the Infectious Diseases Society of America list 13 acceptable regimens for moderate diabetic foot infections.4 Useful single drug regimens include ampicillin-sulbactam, piperacillin-tazobactam, levofloxacin, and cefoxitin. For the penicillin-allergic patient, clindamycin and ciprofloxacin is a useful combination. Empiric vancomycin should be reserved for patients with a history of MRSA, treatment failure, or severe infection. (I would also reserve carbapenems, such as imipenem-cilastatin, for more severe infections, to prevent antibiotic resistance against a class of drugs representing our last defense against highly resistant gram-negative organisms.)

Once the patient is clinically improved and results of adequate cultures are available, consideration can be given to narrowing the course of therapy. Most diabetic foot infections can be treated with some combination of intravenous and oral therapy.

2. Have a high clinical suspicion for osteomyelitis. Osteomyelitis is extremely common in diabetic foot infections due to plantar ulceration and poor soft tissue coverage. Cure rates are reduced in osteomyelitis because dead bone acts as a nidus for persistent infection. The most useful diagnostic maneuver for osteomyelitis is deep probing of the wound with a sterile swab at the bedside. If a gritty sensation is felt, osteomyelitis is likely, and further diagnostic testing is probably unnecessary.

If the physical examination is equivocal, plain radiographs should be obtained to look for bony erosions. If these are negative, MRI is the next most useful diagnostic step. Bone scans are of limited value due to their low specificity. (Charcot arthropathy is a common cause of false-positive bone scans in this setting.)

Because of the high prevalence of osteomyelitis in diabetic foot infections, my own practice is to err on the side of longer, rather than shorter, antibiotic therapy.

3. Surgical debridement is required for many diabetic foot infections. Develop a collaborative relationship with a vascular or orthopedic surgeon with interest and expertise in the management of diabetic foot infections. Necrotic and gangrenous material should be removed. Ideally, dead bone should be debrided, both therapeutically and to help establish a bacteriologic diagnosis. (When removal of dead bone would result in loss of function or might create a non-healing wound, the option of long-term antibiotic suppression could be explored with an infectious disease specialist.)

4. When osteomyelitis is present, bone cultures help to define the optimal antibiotic therapy. Recent studies have confirmed older data regarding the poor correlation between surface cultures and bone cultures. The latter are preferred, when feasible.

5. Consider revascularization. Most diabetic foot infections arise in the setting of vascular insufficiency. At a minimum, patients with diabetic foot infections should have ankle-brachial indices performed for screening. Because diabetics may have falsely elevated ankle pressures due to calcified and non-compressible arteries, additional diagnostic studies may be useful, such as segmental pressures and Doppler pulse volume recordings.

Measurement of the transcutaneous oxygen concentration (TcP02) has been recommended, particularly in assessing which patients may benefit from hyperbaric oxygen. However, the TcP02 is not widely available, and the benefit of hyperbaric oxygen in this setting remains controversial.

6. Patients should be educated in meticulous foot care to prevent recurrences and reinfections. A diabetic foot infection may indicate that the patient lacks the knowledge, resources, or motivation for proper foot care. It also suggests that something is seriously awry with the patient’s diabetic regimen, compliance, or both. Hospital admissions for diabetic foot infections provide an opportunity to revise the patient’s diabetic medications; to educate the patient regarding wound care, skin care, and daily foot self-examination; to provide additional resources such as visiting nurses; and to refer patients for podiatric care, including tailored shoes, orthotics, and, if necessary, casting to off-load ulcers. TH

Dr. Ross is an instructor in medicine at Harvard Medical School.

References

1. Hill SL, Holtzman GI, Buse R. The effects of peripheral vascular disease with osteomyelitis in the diabetic foot. Am J Surg. 1999 Apr;177(4):282-286.
2. Gordois A, Scuffham P, Shearer A, et al. The health care costs of diabetic peripheral neuropathy in the United States. Diabetes Care. 2003;26(6):1790-1795.
3. Lazzarini L, Mader JT, Calhoun JH. Diabetic foot infection. In: Calhoun JH, Mader JT, eds. Musculoskeletal Infections. New York, NY. Marcel Dekker. 2003.
4. Lipsky BA, Berendt AR, Deery HG, et al. Diagnosis and treatment of diabetic foot infections. Clin Infect Dis. 2004 Oct;39(7):885-910.

Diabetic foot infections are common, costly, and potentially catastrophic for patients. The average patient with a diabetic foot infection undergoes three surgical procedures, including toe amputation in 19% and leg amputation in 14%.1 The annual cost of diabetic foot osteomyelitis in the United States is $2.8 billion.2

Diabetics are uniquely predisposed to foot infections. Because of neuropathy, minor repetitive injury leads to large foot ulcers, especially over the metatarsal heads. Foot deformities result in soft tissue injury from poorly fitting shoes. Because of autonomic neuropathy, the diabetic foot sweats less, leading to dry, cracked skin for bacteria to invade. Resistance to infection is lower because of neutrophil dysfunction in hyperglycemia. Vascular insufficiency impairs both wound healing and the immune response.3

The major principles of therapy are as follows:

1. Use an empiric antibiotic regimen with broad coverage against gram-positive, gram-negative, and anaerobic organisms. Diabetic foot infections are usually polymicrobial. Except for mild infections, in which therapy directed at gram-positive organisms may suffice, initial therapy should cover streptococci, methicillin-sensitive Staphylococcus aureus, E. coli, Proteus, and anaerobes.

Many studies of antibiotic therapy in diabetic foot infections have been performed, without demonstrating a clear superiority for any one regimen. The 2004 guidelines of the Infectious Diseases Society of America list 13 acceptable regimens for moderate diabetic foot infections.4 Useful single drug regimens include ampicillin-sulbactam, piperacillin-tazobactam, levofloxacin, and cefoxitin. For the penicillin-allergic patient, clindamycin and ciprofloxacin is a useful combination. Empiric vancomycin should be reserved for patients with a history of MRSA, treatment failure, or severe infection. (I would also reserve carbapenems, such as imipenem-cilastatin, for more severe infections, to prevent antibiotic resistance against a class of drugs representing our last defense against highly resistant gram-negative organisms.)

Once the patient is clinically improved and results of adequate cultures are available, consideration can be given to narrowing the course of therapy. Most diabetic foot infections can be treated with some combination of intravenous and oral therapy.

2. Have a high clinical suspicion for osteomyelitis. Osteomyelitis is extremely common in diabetic foot infections due to plantar ulceration and poor soft tissue coverage. Cure rates are reduced in osteomyelitis because dead bone acts as a nidus for persistent infection. The most useful diagnostic maneuver for osteomyelitis is deep probing of the wound with a sterile swab at the bedside. If a gritty sensation is felt, osteomyelitis is likely, and further diagnostic testing is probably unnecessary.

If the physical examination is equivocal, plain radiographs should be obtained to look for bony erosions. If these are negative, MRI is the next most useful diagnostic step. Bone scans are of limited value due to their low specificity. (Charcot arthropathy is a common cause of false-positive bone scans in this setting.)

Because of the high prevalence of osteomyelitis in diabetic foot infections, my own practice is to err on the side of longer, rather than shorter, antibiotic therapy.

3. Surgical debridement is required for many diabetic foot infections. Develop a collaborative relationship with a vascular or orthopedic surgeon with interest and expertise in the management of diabetic foot infections. Necrotic and gangrenous material should be removed. Ideally, dead bone should be debrided, both therapeutically and to help establish a bacteriologic diagnosis. (When removal of dead bone would result in loss of function or might create a non-healing wound, the option of long-term antibiotic suppression could be explored with an infectious disease specialist.)

4. When osteomyelitis is present, bone cultures help to define the optimal antibiotic therapy. Recent studies have confirmed older data regarding the poor correlation between surface cultures and bone cultures. The latter are preferred, when feasible.

5. Consider revascularization. Most diabetic foot infections arise in the setting of vascular insufficiency. At a minimum, patients with diabetic foot infections should have ankle-brachial indices performed for screening. Because diabetics may have falsely elevated ankle pressures due to calcified and non-compressible arteries, additional diagnostic studies may be useful, such as segmental pressures and Doppler pulse volume recordings.

Measurement of the transcutaneous oxygen concentration (TcP02) has been recommended, particularly in assessing which patients may benefit from hyperbaric oxygen. However, the TcP02 is not widely available, and the benefit of hyperbaric oxygen in this setting remains controversial.

6. Patients should be educated in meticulous foot care to prevent recurrences and reinfections. A diabetic foot infection may indicate that the patient lacks the knowledge, resources, or motivation for proper foot care. It also suggests that something is seriously awry with the patient’s diabetic regimen, compliance, or both. Hospital admissions for diabetic foot infections provide an opportunity to revise the patient’s diabetic medications; to educate the patient regarding wound care, skin care, and daily foot self-examination; to provide additional resources such as visiting nurses; and to refer patients for podiatric care, including tailored shoes, orthotics, and, if necessary, casting to off-load ulcers. TH

Dr. Ross is an instructor in medicine at Harvard Medical School.

References

1. Hill SL, Holtzman GI, Buse R. The effects of peripheral vascular disease with osteomyelitis in the diabetic foot. Am J Surg. 1999 Apr;177(4):282-286.
2. Gordois A, Scuffham P, Shearer A, et al. The health care costs of diabetic peripheral neuropathy in the United States. Diabetes Care. 2003;26(6):1790-1795.
3. Lazzarini L, Mader JT, Calhoun JH. Diabetic foot infection. In: Calhoun JH, Mader JT, eds. Musculoskeletal Infections. New York, NY. Marcel Dekker. 2003.
4. Lipsky BA, Berendt AR, Deery HG, et al. Diagnosis and treatment of diabetic foot infections. Clin Infect Dis. 2004 Oct;39(7):885-910.

Acute decompensated heart failure (ADHF) remains one of the most common reasons for hospitalization. ADHF patients who have co-morbid conditions present stubborn challenges for hospitalists. And ADHF is frequently observed in patients 65 and older. The neurohormonal activation that results as a consequence of myocardial dysfunction leads to progressive cardiac deterioration and hemodynamic disturbances that ultimately become manifest as acute decompensated heart failure.

ADHG management goals include stabilizing the patient, managing acute hemodynamic abnormalities, reversing the symptoms of dyspnea caused by fluid overload, and initiating evidence-based therapies to decrease disease progression and improve survival.

In this article we present the case of a 26-year-old female with ADHF and highlight the management strategies that can result in stabilization and improved long-term outcome.

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Introduction

Despite major advances in the treatment of heart disease, heart failure remains a growing public health problem of epidemic proportions in the United States. Approximately five million Americans have heart failure, and more than 550,000 patients are diagnosed with the disease each year.1 The annual number of hospitalizations for heart failure as a primary diagnosis has increased from approximately 810,000 in 1990 to more than 1 million in 1999, and it is the most common discharge diagnosis-related group for patients 65 and older.2 Medicare spent more dollars on the diagnosis and treatment of heart failure than on any other diagnosis—more than $27.9 billion in 2005.1

Patients presenting to the emergency department (ED) with ADHF are often hemodynamically unstable, with severe symptoms of dyspnea and fluid overload. Rapid assessment and prompt initiation of appropriate interventions are necessary to achieve clinical stability and prevent prolonged hospital stay if hospitalization is required. The in-hospital mortality rate for ADHF is 5%-8%; median duration of hospitalization is five days, and the six-month re-hospitalization rate is about 50%.1,3 Thus, it is clear that improved recognition and treatment are of paramount importance. With these goals in mind, we present a recent case that highlights many of the concerns about and treatment options for ADHF.

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Case Presentation

Karen A. is a 26-year-old black female with stage III Hodgkin’s disease, diagnosed in 2000. She received chemotherapy (cisplatin, cytarabine, doxorubicin, rituxan, gemcitabine) and, as a result, in 2001 developed chemotherapy-induced cardiomyopathy with an ejection fraction of <20%. Her condition stabilized, and she remained in clinical remission until September 2002.

In 2003 she received an autologous stem cell transplant and subsequently presented to the ED with complaints of fatigue, progressive shortness of breath in the previous seven days, and lower extremity edema. She also reported right-sided pleuritic chest pain, but denied associated nausea, vomiting, or diaphoresis. In the three days preceding admission, she had gained 10 pounds. In the past six months, she had had multiple admissions for ADHF.

Her physical examination revealed an alert, obese female in moderate respiratory distress with dry mucous membranes. Her vital signs indicated a temperature of 36.5° C, a heart rate of 110 beats per minute, a respiratory rate of 20 breaths per minute, blood pressure measuring 111/73 mm Hg, and an oxygen saturation of 92%. She had no scleral icterus, but did have jugular venous distention to the angle of the mandible at 45° upright. Her cardiac examination indicated tachycardia with distant heart sounds and an audible third heart sound (S3), as well as a grade 2/6 systolic ejection murmur at the left sternal border. Her lung examination demonstrated diffuse crackles present in both lung fields, but no wheezes. Abdominal examination was notable for tenderness to palpation at the right hypogastric region and for hepatomegaly, her skin was warm and dry with no cyanosis, and her extremities demonstrated significant bilateral pitting pre-tibial edema to her knees.

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Her current medications included:

1. Furosemide, 60 mg by mouth two times daily;
2. Carvedilol, 12.5 mg by mouth in the morning, 6.25 mg in the evening;
3. Amiodarone, 200 mg by mouth daily; and
4. Digoxin, 0.125 mg by mouth daily.

Laboratory findings included normal electrolytes, blood urea nitrogen, and serum creatinine. Her hemoglobin was 11.3 gm/L, and her B-type natriuretic peptide (BNP) level was 4,837 pg/ml. Initial cardiac enzymes were negative (troponin I of <0. 03).

Her chest X-ray demonstrated moderate cardiac enlargement with bilateral thickening of subpleural septal lines and blurring of the pulmonary vasculature consistent with developing cardiogenic pulmonary edema. A 12-lead electrocardiogram indicated sinus tachycardia with a rate of 110 beats per minute and nonspecific ST-T wave changes in the inferior leads, but no Q waves were noted. Echocardiography showed severely reduced left ventricular systolic function with severe global hypokinesis of the left ventricle and a measured ejection fraction of 25%-30%. There was no pericardial effusion.

She was admitted to the telemetry floor with the diagnosis of ADHF. She was placed on supplemental oxygen and serial cardiac enzymes, and her electrocardiogram remained negative for injury or ischemia. Intravenous furosemide was initiated at 40 mg every 12 hours. After 24 hours, she was given a bolus of nesiritide (2 mcg/kg), followed by a continuous infusion at 0.01 mcg/kg/min. Cardiac medications were continued, and the dosage of carvedilol was reduced to 6.25 mg by mouth twice daily.

After a period of diuresis, the patient remained highly symptomatic; therefore, a right heart catheterization was done. The hemodynamics indicated a cardiac output of three liters per minute, a right atrial pressure of 20 mm Hg, a right ventricular pressure of 70/20 mm Hg, pulmonary artery pressure of 66/20 mm Hg with a mean pressure of 52 mm Hg, and a pulmonary capillary wedge pressure of 25 mm Hg. (See Figures 1 and 2, p. 23).

Over the next 24 hours, the patient had more than three liters of urine output and was significantly improved. The nesiritide infusion was discontinued after 48 hours of therapy, and the patient was weaned from supplemental oxygen. Lisinopril was started at 2.5 mg daily by mouth. On hospital day four, the patient walked around the nurses’ station without supplemental oxygen, and she was returned to the previous dose of furosemide, 60 mg twice daily.

The patient was enrolled in the Heart Success Program (HSP), a collaborative interdisciplinary program that is available in the institution for cancer patients with heart failure. She was provided with patient education materials that included educational videotapes on heart failure management, daily weight monitoring, diet, medications, exercise, and the emotional aspects of heart failure. Nurses with heart failure training were available to answer questions for the patient and to provide further instruction for follow-up after the patient’s discharge. The patient improved enough that she was able to enroll in a New York Heart Association (NYHA) class II and was discharged after five days, with a follow-up appointment to the outpatient clinic one week after hospital discharge.

Discussion

This case illustrates the challenges inherent in the diagnosis and management of ADHF in a cancer patient with a known history of heart failure. Rapid assessment is critical in establishing a diagnosis and initiating appropriate intervention. The goals of managing ADHF remain the same regardless of etiology. These include stabilizing the patient, managing acute hemodynamic abnormalities, reversing the symptoms of dyspnea caused by fluid overload, and initiating evidence-based therapies to decrease disease progression and improve survival. The same principles apply—even if the patient has a major comorbidity such as cancer, and suspicion for the diagnosis must remain high.

Initial Evaluation

Early diagnosis and effective management of ADHF are critically important, as these have been shown to reduce hospitalizations and intensive care unit admissions, to decrease length of stay, and to decrease cost of hospitalization.4 A comprehensive history and physical examination must be performed to identify signs and symptoms that lead to a heart failure diagnosis.

We must evaluate such potential risk factors as history of hypertension, dyslipidemia, diabetes mellitus, coronary artery disease, valvular disease, peripheral vascular disease, a family history of cardiomyopathy, smoking, alcohol use, thyroid problems, sleep apnea, and any recent history of infection (particularly upper respiratory tract infection, which can cause viral cardiomyopathy).

As part of further investigation with cancer patients, include the patient’s possible past exposure to cardiotoxic agents (e.g., anthracyclines, trastuzumab, high-dose cyclophosphamide) or mediastinal irradiation. Chemotherapy-induced cardiomyopathy is increasingly becoming an issue in heart failure management as a result of the growing number of long-term cancer survivors who have received treatment with anthracycline-containing chemotherapy or other aggressive therapy.

Focus on volume and perfusion status during the physical assessment of each patient. Most patients presenting to the ED with acute decompensation are volume overloaded. Volume overload is manifested by symptoms of dyspnea, orthopnea, and paroxysmal nocturnal dyspnea, as well as jugular venous distention, hepatojugular reflux, ascites, edema, and crackles in the lungs.5 Crackles are not always present in chronic heart failure patients, however, because of the continuous movement of fluid into the interstitium associated with increased lymphatic drainage, leaving the alveoli relatively dry.6

In addition to a comprehensive history and physical examination, several tests will help establish the diagnosis. (See Table 1, top left.) A measurement of a B-type natriuretic peptide (BNP) facilitates the diagnosis of ADHF. BNP is an endogenously generated natriuretic peptide that is activated in response to atrial or ventricular expansion due to volume overload and increased wall tension.7,8 Circulating levels of endogenous BNP are significantly elevated in ADHF patients and are a valuable tool for diagnosis of heart failure in the ED.9-11 In Karen A., the BNP level was 4,837 pg/mL, which is indicative of Stage D heart failure. This diagnosis was confirmed by chest X-ray findings of cardiogenic pulmonary edema in the setting of severe left ventricular hypokinesis and an ejection fraction of 25%-30%.

Although history and physical examination may provide important clues regarding the underlying cardiac abnormality, both invasive and noninvasive testing are necessary to provide a definitive diagnosis of heart failure and to evaluate potential exacerbating conditions. A two-dimensional echocardiogram with Doppler flow study is an essential diagnostic test for evaluating myocardial contractility or ejection fraction. Echocardiogram can also evaluate other structural components such as the pericardium, valvular status, and hemodynamic parameters that may contribute to the development of ADHF. In patients with cardiac risk factors, a myocardial perfusion stress test or catheterization may identify the presence of coronary artery disease as a contributor.

A 12-lead electrocardiogram is necessary to establish the rhythm and to show evidence of acute or prior myocardial infarction, pericarditis, conduction abnormalities, or left ventricular hypertrophy as a result of prolonged uncontrolled hypertension. It is known that rhythm disturbances such as atrial fibrillation can be a precipitating factor for ADHF.

A chest X-ray is needed to uncover pulmonary edema in cases of fluid overload and to show an enlarged cardiac silhouette in cases of dilated cardiomyopathy. Identification of a definitive cause or causes that precipitate the occurrence of ADHF is crucial in devising a management plan and initiating appropriate intervention. (See Table 2, p. 22.)

click for large version

Immediate Management of the ADHF

Newly developed clinical practice guidelines for the management of ADHF exist, but management is still based largely on empirical evidence.12 Begin ADHF treatment in the ED with intravenous diuretics (unless contraindicated). A majority of ADHF patients will respond to diuretics alone.13 If the patient responds poorly to diuretics, the use of nesiritide in conjunction with diuretics has proven beneficial, as shown in the analysis of data from the ADHERE registry indicating that patients treated with intravenous nesiritide had a lower hospital mortality rate than patients treated with milrinone or dobutamine.14 Other options include ultrafiltration, an intervention that has been noted to reduce lengths of stay and rehospitalization rates in patients with ADHF.

Nesiritide is a recombinant form of BNP without direct inotropic effects but with venous, arterial, and coronary vasodilatory properties that can improve symptoms in ADHF.15 The recommended dosage for nesiritide is an IV bolus of 2 mcg per kg, followed by a continuous infusion of 0.01 mcg/kg/min. In the setting of hypotension with a systolic blood pressure less than 100 mm Hg, however, an initial IV bolus dose is not recommended; instead, the patient may start with a continuous infusion of 0.01 mcg/kg/min, or consider other therapies.

In hemodynamically unstable patients with a systolic blood pressure less than 90 mm Hg, or in those with evidence of end organ hypoperfusion (cardiogenic shock), inotropic support may be considered until the patient is stabilized. (See Table 3, p. 22.) Recognize that inotropic agents have adverse effects on the neurohormonal system and are not recommended routinely but may be essential for temporary stabilization. (For more on pharmacologic management of ADHF, see Table 4, p. 24.)

click for large version

Subacute Management of ADHF

Once acute decompensation has been reversed and an euvolemic state has been achieved, shift therapy to a combination of three classes of medications: diuretics, angiotensin-converting enzyme (ACE) inhibitors, and beta-blockers, unless contraindicated. The benefits of these drugs have been established by evidence from numerous large-scale clinical trials.3,12

Start ACE inhibitors in all patients with heart failure due to left ventricular systolic dysfunction (unless contraindicated or if the patient is intolerant).3 Give ACE-I to patients who have experienced a recent episode of ADHF, along with diuretics to maintain sodium balance and to prevent peripheral and pulmonary edema. ACE inhibitors are contraindicated for patients who are pregnant and for those with childbearing potential, as well as for individuals with a prior history of angioedema or renal failure after receiving the drug. Instruct patients to avoid any sudden change of position, as they may experience orthostatic hypotension while taking ACE inhibitors.

Some patients are intolerant of ACE inhibitors due to a persistent cough that occurs in approximately 5% to 10% of Caucasian patients and in up to 50% of Chinese patients.16 Angiotensin receptor blockers (ARBs) are an established alternative.17 Two ARBs (candesartan and valsartan) are recommended for treatment of heart failure based on evidence from controlled clinical trials.17,18 These drugs have demonstrated a reduction in hospitalizations, and candesartan, when used as an alternative to ACE-I, has been shown to reduce mortality. Additionally, in patients with evidence of left ventricular dysfunction after myocardial infarction, valsartan provided a benefit that was not inferior to ACE inhibitors.17

Initiate beta-blockers at very low doses and gradually increased as tolerated. Monitor patients closely for symptoms of hypotension, significant weight gain, fluid retention, bradycardia, and heart block. In addition, inform patients that they may experience generalized fatigue or weakness with the initiation of beta-blockers. In a cancer patient it is difficult to differentiate between fatigue caused by the disease and the side effects of therapy. Fatigue associated with beta-blocker therapy usually resolves spontaneously within a few days. Make every effort to achieve optimum target beta-blocker dose.

An aldosterone antagonist, such as spironolactone or eplerenone, given at a daily dose of 12.5 to 25 mg in addition to standard therapy, effectively blocks the effects of aldosterone (RALES study) to achieve comprehensive neurohormonal blockade.19 When prescribing an aldosterone antagonist, especially in combination with ACE inhibitors and loop diuretics, it is important to monitor serum potassium levels because this combination can result in hyperkalemia.

click for large version

Disease Management Programs

Comprehensive management of heart failure is not only limited to hospital care during an episode of ADHF. In order to prevent repeated hospitalizations, implement additional measures through formal disease management programs. These disease management programs are often directed or coordinated by advanced practice nurses who address the comprehensive care of heart failure patients with emphasis on patient education and counseling to improve patient compliance.20

The non-pharmacologic treatment strategies emphasized in disease management programs have proven effective in achieving positive outcomes. These include counseling patients on dietary management, including encouraging a two-gram sodium diet, alcohol restriction, and adequate supplementation of electrolyte loss from diuretics. Keeping a diary of the patient’s daily weight at home and bringing it to office visits will help both the patient and the clinician monitor fluid retention efficiently.

Hypotension is a common side effect from the pharmacologic therapy for heart failure. Employ comprehensive education with both patient and family to avoid unnecessary discontinuation of the medications. A systolic blood pressure of 90 mm Hg is acceptable as long as there are no associated symptoms of dizziness or syncope.

Encourage activity guidelines, including participation in exercise programs. Attendance at support group meetings will provide a venue in which patients can share common problems and concerns with others in similar situations. One to two weeks after hospital discharge, schedule an outpatient follow-up in a heart failure clinic, where heart failure education is reinforced to prevent another episode of ADHF admission.

Summary

Despite the added challenges, managing ADHF in a patient with a serious comorbidity such as cancer involves the same goals as the treatment of ADHF in any other patient. With rapid assessment and appropriate intervention, the patient is given the best possible chance of survival. TH

The authors work at the University of Texas M.D. Anderson Cancer Center, Department of Cardiology, Houston.

References

1. American Heart Association. Heart Disease and Stroke Statistics—2005 Update. Dallas, Texas.: American Heart Association; 2005. Available at: www.americanheart.org/downloadable/heart/1105390918119HDSStats2005Update.pdf. Last accessed August 20, 2006.
2. Koelling TM, Chen RS, Lubwama RN, et al. The expanding national burden of heart failure in the United States: the influence of heart failure in women. Am Heart J. 2004 Jan;147(1):74-78.
3. Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society. Circulation. 2005 Sep 20;112(12):e154-235.Epub 2005 Sep 13.
4. Peacock WF IV, Emerman CL, Wynne J, for the ADHERE Scientific Advisory Committee and Investigators and the ADHERE Study Group. Early use of nesiritide in the emergency department is associated with improved outcome: an ADHERE registry analysis. Ann Emerg Med. 2004;44:S78.
5. Stevenson LW. Tailored therapy to hemodynamic goals for advanced heart failure. Eur J Heart Fail. 1999 Aug;1(3):251-257.
6. Stevenson LW, Perloff JK. The limited reliability of physical signs for estimating hemodynamics in chronic heart failure. JAMA. 1989;261:884-888.
7. Nakagawa O, Ogawa Y, Itoh H, et al. Rapid transcriptional activation and early mRNA turnover of brain natriuretic peptide in cardiocyte hypertrophy. Evidence for brain natriuretic peptide as an “emergency” cardiac hormone against ventricular overload. J Clin Invest. 1995 Sep;96(3):1280-1287.
8. Maeda K, Tsutamoto T, Wada A, et al. Plasma brain natriuretic peptide as a biochemical marker of high left ventricular end-diastolic pressure in patients with symptomatic left ventricular dysfunction. Am Heart J. 1998;135(5 Pt 1):825-832.
9. Burger AJ. A review of the renal and neurohormonal effects of B-type natriuretic peptide. Congest Heart Fail. 2005 Jan-Feb;11(1):30-38.
10. McCullough PA, Nowak RM, McCord J, et al. B-type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure: analysis from Breathing Not Properly (BNP) Multinational Study. Circulation. 2002 Jul;106(4):416-422.
11. Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002 Jul 18;347(3):161-167.
12. Adams KF, Lindenfeld J, Arnold JMO, et al. Executive Summary: HFSA 2006 Comprehensive Heart Failure Practice Guideline. J Card Fail. 2006 Feb;12(1):10-38.
13. Dec GW. Acute decompensated heart failure: the shrinking role of inotropic therapy. J Am Coll Cardiol. 2005 Jul;46(1):65-67.
14. Abraham WT, Adams KF, Fonarow GC, et al. In-hospital mortality in patients with acute decompensated heart failure requiring intravenous vasoactive medications: an analysis from the Acute Decompensated Heart Failure National Registry (ADHERE). J Am Coll Cardiol. 2005 Jul;46(1):57-64.
15. Burger AJ, Horton DP, LeJemtel T, et al. Effect of nesiritide (B-type natriuretic peptide) and dobutamine on ventricular arrhythmias in the treatment of patients with acutely decompensated congestive heart failure: the PRECEDENT study. Am Heart J. 2002 Dec;144(6):1102-1108.
16. Woo KS, Nicholls MG. High prevalence of persistent cough with angiotensin converting enzyme inhibitors in Chinese. Br J Clin Pharmacol. 1995 Aug;40(2):141-144.
17. Pfeffer MA, McMurray JJ, Velazquez EJ, et al. Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both. N Engl J Med. 2003 Nov 13;349(20):1893-1906. Epub 2003 Nov 10.
18. Granger CB, McMurray JJ, Yusuf S, et al. Effects of candesartan in patients with chronic heart failure and reduced left-ventricular systolic function intolerant to angiotensin-converting-enzyme inhibitors: the CHARM-Alternative trial. Lancet. 2003 Sep 6;362(9386):772-776.
19. Pitt B, Zannad F, Remme WJ, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med. 1999 Sep 2;341(10):709-717.
20. Albert NM, Eastwood CA, Edwards ML. Evidence-based practice for acute decompensated heart failure. Crit Care Nurse. 2004 Dec;24(6):14-16, 18-24, 26-29; quiz 30-31.

Acute decompensated heart failure (ADHF) remains one of the most common reasons for hospitalization. ADHF patients who have co-morbid conditions present stubborn challenges for hospitalists. And ADHF is frequently observed in patients 65 and older. The neurohormonal activation that results as a consequence of myocardial dysfunction leads to progressive cardiac deterioration and hemodynamic disturbances that ultimately become manifest as acute decompensated heart failure.

ADHG management goals include stabilizing the patient, managing acute hemodynamic abnormalities, reversing the symptoms of dyspnea caused by fluid overload, and initiating evidence-based therapies to decrease disease progression and improve survival.

In this article we present the case of a 26-year-old female with ADHF and highlight the management strategies that can result in stabilization and improved long-term outcome.

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Introduction

Despite major advances in the treatment of heart disease, heart failure remains a growing public health problem of epidemic proportions in the United States. Approximately five million Americans have heart failure, and more than 550,000 patients are diagnosed with the disease each year.1 The annual number of hospitalizations for heart failure as a primary diagnosis has increased from approximately 810,000 in 1990 to more than 1 million in 1999, and it is the most common discharge diagnosis-related group for patients 65 and older.2 Medicare spent more dollars on the diagnosis and treatment of heart failure than on any other diagnosis—more than $27.9 billion in 2005.1

Patients presenting to the emergency department (ED) with ADHF are often hemodynamically unstable, with severe symptoms of dyspnea and fluid overload. Rapid assessment and prompt initiation of appropriate interventions are necessary to achieve clinical stability and prevent prolonged hospital stay if hospitalization is required. The in-hospital mortality rate for ADHF is 5%-8%; median duration of hospitalization is five days, and the six-month re-hospitalization rate is about 50%.1,3 Thus, it is clear that improved recognition and treatment are of paramount importance. With these goals in mind, we present a recent case that highlights many of the concerns about and treatment options for ADHF.

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Case Presentation

Karen A. is a 26-year-old black female with stage III Hodgkin’s disease, diagnosed in 2000. She received chemotherapy (cisplatin, cytarabine, doxorubicin, rituxan, gemcitabine) and, as a result, in 2001 developed chemotherapy-induced cardiomyopathy with an ejection fraction of <20%. Her condition stabilized, and she remained in clinical remission until September 2002.

In 2003 she received an autologous stem cell transplant and subsequently presented to the ED with complaints of fatigue, progressive shortness of breath in the previous seven days, and lower extremity edema. She also reported right-sided pleuritic chest pain, but denied associated nausea, vomiting, or diaphoresis. In the three days preceding admission, she had gained 10 pounds. In the past six months, she had had multiple admissions for ADHF.

Her physical examination revealed an alert, obese female in moderate respiratory distress with dry mucous membranes. Her vital signs indicated a temperature of 36.5° C, a heart rate of 110 beats per minute, a respiratory rate of 20 breaths per minute, blood pressure measuring 111/73 mm Hg, and an oxygen saturation of 92%. She had no scleral icterus, but did have jugular venous distention to the angle of the mandible at 45° upright. Her cardiac examination indicated tachycardia with distant heart sounds and an audible third heart sound (S3), as well as a grade 2/6 systolic ejection murmur at the left sternal border. Her lung examination demonstrated diffuse crackles present in both lung fields, but no wheezes. Abdominal examination was notable for tenderness to palpation at the right hypogastric region and for hepatomegaly, her skin was warm and dry with no cyanosis, and her extremities demonstrated significant bilateral pitting pre-tibial edema to her knees.

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Her current medications included:

1. Furosemide, 60 mg by mouth two times daily;
2. Carvedilol, 12.5 mg by mouth in the morning, 6.25 mg in the evening;
3. Amiodarone, 200 mg by mouth daily; and
4. Digoxin, 0.125 mg by mouth daily.

Laboratory findings included normal electrolytes, blood urea nitrogen, and serum creatinine. Her hemoglobin was 11.3 gm/L, and her B-type natriuretic peptide (BNP) level was 4,837 pg/ml. Initial cardiac enzymes were negative (troponin I of <0. 03).

Her chest X-ray demonstrated moderate cardiac enlargement with bilateral thickening of subpleural septal lines and blurring of the pulmonary vasculature consistent with developing cardiogenic pulmonary edema. A 12-lead electrocardiogram indicated sinus tachycardia with a rate of 110 beats per minute and nonspecific ST-T wave changes in the inferior leads, but no Q waves were noted. Echocardiography showed severely reduced left ventricular systolic function with severe global hypokinesis of the left ventricle and a measured ejection fraction of 25%-30%. There was no pericardial effusion.

She was admitted to the telemetry floor with the diagnosis of ADHF. She was placed on supplemental oxygen and serial cardiac enzymes, and her electrocardiogram remained negative for injury or ischemia. Intravenous furosemide was initiated at 40 mg every 12 hours. After 24 hours, she was given a bolus of nesiritide (2 mcg/kg), followed by a continuous infusion at 0.01 mcg/kg/min. Cardiac medications were continued, and the dosage of carvedilol was reduced to 6.25 mg by mouth twice daily.

After a period of diuresis, the patient remained highly symptomatic; therefore, a right heart catheterization was done. The hemodynamics indicated a cardiac output of three liters per minute, a right atrial pressure of 20 mm Hg, a right ventricular pressure of 70/20 mm Hg, pulmonary artery pressure of 66/20 mm Hg with a mean pressure of 52 mm Hg, and a pulmonary capillary wedge pressure of 25 mm Hg. (See Figures 1 and 2, p. 23).

Over the next 24 hours, the patient had more than three liters of urine output and was significantly improved. The nesiritide infusion was discontinued after 48 hours of therapy, and the patient was weaned from supplemental oxygen. Lisinopril was started at 2.5 mg daily by mouth. On hospital day four, the patient walked around the nurses’ station without supplemental oxygen, and she was returned to the previous dose of furosemide, 60 mg twice daily.

The patient was enrolled in the Heart Success Program (HSP), a collaborative interdisciplinary program that is available in the institution for cancer patients with heart failure. She was provided with patient education materials that included educational videotapes on heart failure management, daily weight monitoring, diet, medications, exercise, and the emotional aspects of heart failure. Nurses with heart failure training were available to answer questions for the patient and to provide further instruction for follow-up after the patient’s discharge. The patient improved enough that she was able to enroll in a New York Heart Association (NYHA) class II and was discharged after five days, with a follow-up appointment to the outpatient clinic one week after hospital discharge.

Discussion

This case illustrates the challenges inherent in the diagnosis and management of ADHF in a cancer patient with a known history of heart failure. Rapid assessment is critical in establishing a diagnosis and initiating appropriate intervention. The goals of managing ADHF remain the same regardless of etiology. These include stabilizing the patient, managing acute hemodynamic abnormalities, reversing the symptoms of dyspnea caused by fluid overload, and initiating evidence-based therapies to decrease disease progression and improve survival. The same principles apply—even if the patient has a major comorbidity such as cancer, and suspicion for the diagnosis must remain high.

Initial Evaluation

Early diagnosis and effective management of ADHF are critically important, as these have been shown to reduce hospitalizations and intensive care unit admissions, to decrease length of stay, and to decrease cost of hospitalization.4 A comprehensive history and physical examination must be performed to identify signs and symptoms that lead to a heart failure diagnosis.

We must evaluate such potential risk factors as history of hypertension, dyslipidemia, diabetes mellitus, coronary artery disease, valvular disease, peripheral vascular disease, a family history of cardiomyopathy, smoking, alcohol use, thyroid problems, sleep apnea, and any recent history of infection (particularly upper respiratory tract infection, which can cause viral cardiomyopathy).

As part of further investigation with cancer patients, include the patient’s possible past exposure to cardiotoxic agents (e.g., anthracyclines, trastuzumab, high-dose cyclophosphamide) or mediastinal irradiation. Chemotherapy-induced cardiomyopathy is increasingly becoming an issue in heart failure management as a result of the growing number of long-term cancer survivors who have received treatment with anthracycline-containing chemotherapy or other aggressive therapy.

Focus on volume and perfusion status during the physical assessment of each patient. Most patients presenting to the ED with acute decompensation are volume overloaded. Volume overload is manifested by symptoms of dyspnea, orthopnea, and paroxysmal nocturnal dyspnea, as well as jugular venous distention, hepatojugular reflux, ascites, edema, and crackles in the lungs.5 Crackles are not always present in chronic heart failure patients, however, because of the continuous movement of fluid into the interstitium associated with increased lymphatic drainage, leaving the alveoli relatively dry.6

In addition to a comprehensive history and physical examination, several tests will help establish the diagnosis. (See Table 1, top left.) A measurement of a B-type natriuretic peptide (BNP) facilitates the diagnosis of ADHF. BNP is an endogenously generated natriuretic peptide that is activated in response to atrial or ventricular expansion due to volume overload and increased wall tension.7,8 Circulating levels of endogenous BNP are significantly elevated in ADHF patients and are a valuable tool for diagnosis of heart failure in the ED.9-11 In Karen A., the BNP level was 4,837 pg/mL, which is indicative of Stage D heart failure. This diagnosis was confirmed by chest X-ray findings of cardiogenic pulmonary edema in the setting of severe left ventricular hypokinesis and an ejection fraction of 25%-30%.

Although history and physical examination may provide important clues regarding the underlying cardiac abnormality, both invasive and noninvasive testing are necessary to provide a definitive diagnosis of heart failure and to evaluate potential exacerbating conditions. A two-dimensional echocardiogram with Doppler flow study is an essential diagnostic test for evaluating myocardial contractility or ejection fraction. Echocardiogram can also evaluate other structural components such as the pericardium, valvular status, and hemodynamic parameters that may contribute to the development of ADHF. In patients with cardiac risk factors, a myocardial perfusion stress test or catheterization may identify the presence of coronary artery disease as a contributor.

A 12-lead electrocardiogram is necessary to establish the rhythm and to show evidence of acute or prior myocardial infarction, pericarditis, conduction abnormalities, or left ventricular hypertrophy as a result of prolonged uncontrolled hypertension. It is known that rhythm disturbances such as atrial fibrillation can be a precipitating factor for ADHF.

A chest X-ray is needed to uncover pulmonary edema in cases of fluid overload and to show an enlarged cardiac silhouette in cases of dilated cardiomyopathy. Identification of a definitive cause or causes that precipitate the occurrence of ADHF is crucial in devising a management plan and initiating appropriate intervention. (See Table 2, p. 22.)

click for large version

Immediate Management of the ADHF

Newly developed clinical practice guidelines for the management of ADHF exist, but management is still based largely on empirical evidence.12 Begin ADHF treatment in the ED with intravenous diuretics (unless contraindicated). A majority of ADHF patients will respond to diuretics alone.13 If the patient responds poorly to diuretics, the use of nesiritide in conjunction with diuretics has proven beneficial, as shown in the analysis of data from the ADHERE registry indicating that patients treated with intravenous nesiritide had a lower hospital mortality rate than patients treated with milrinone or dobutamine.14 Other options include ultrafiltration, an intervention that has been noted to reduce lengths of stay and rehospitalization rates in patients with ADHF.

Nesiritide is a recombinant form of BNP without direct inotropic effects but with venous, arterial, and coronary vasodilatory properties that can improve symptoms in ADHF.15 The recommended dosage for nesiritide is an IV bolus of 2 mcg per kg, followed by a continuous infusion of 0.01 mcg/kg/min. In the setting of hypotension with a systolic blood pressure less than 100 mm Hg, however, an initial IV bolus dose is not recommended; instead, the patient may start with a continuous infusion of 0.01 mcg/kg/min, or consider other therapies.

In hemodynamically unstable patients with a systolic blood pressure less than 90 mm Hg, or in those with evidence of end organ hypoperfusion (cardiogenic shock), inotropic support may be considered until the patient is stabilized. (See Table 3, p. 22.) Recognize that inotropic agents have adverse effects on the neurohormonal system and are not recommended routinely but may be essential for temporary stabilization. (For more on pharmacologic management of ADHF, see Table 4, p. 24.)

click for large version

Subacute Management of ADHF

Once acute decompensation has been reversed and an euvolemic state has been achieved, shift therapy to a combination of three classes of medications: diuretics, angiotensin-converting enzyme (ACE) inhibitors, and beta-blockers, unless contraindicated. The benefits of these drugs have been established by evidence from numerous large-scale clinical trials.3,12

Start ACE inhibitors in all patients with heart failure due to left ventricular systolic dysfunction (unless contraindicated or if the patient is intolerant).3 Give ACE-I to patients who have experienced a recent episode of ADHF, along with diuretics to maintain sodium balance and to prevent peripheral and pulmonary edema. ACE inhibitors are contraindicated for patients who are pregnant and for those with childbearing potential, as well as for individuals with a prior history of angioedema or renal failure after receiving the drug. Instruct patients to avoid any sudden change of position, as they may experience orthostatic hypotension while taking ACE inhibitors.

Some patients are intolerant of ACE inhibitors due to a persistent cough that occurs in approximately 5% to 10% of Caucasian patients and in up to 50% of Chinese patients.16 Angiotensin receptor blockers (ARBs) are an established alternative.17 Two ARBs (candesartan and valsartan) are recommended for treatment of heart failure based on evidence from controlled clinical trials.17,18 These drugs have demonstrated a reduction in hospitalizations, and candesartan, when used as an alternative to ACE-I, has been shown to reduce mortality. Additionally, in patients with evidence of left ventricular dysfunction after myocardial infarction, valsartan provided a benefit that was not inferior to ACE inhibitors.17

Initiate beta-blockers at very low doses and gradually increased as tolerated. Monitor patients closely for symptoms of hypotension, significant weight gain, fluid retention, bradycardia, and heart block. In addition, inform patients that they may experience generalized fatigue or weakness with the initiation of beta-blockers. In a cancer patient it is difficult to differentiate between fatigue caused by the disease and the side effects of therapy. Fatigue associated with beta-blocker therapy usually resolves spontaneously within a few days. Make every effort to achieve optimum target beta-blocker dose.

An aldosterone antagonist, such as spironolactone or eplerenone, given at a daily dose of 12.5 to 25 mg in addition to standard therapy, effectively blocks the effects of aldosterone (RALES study) to achieve comprehensive neurohormonal blockade.19 When prescribing an aldosterone antagonist, especially in combination with ACE inhibitors and loop diuretics, it is important to monitor serum potassium levels because this combination can result in hyperkalemia.

click for large version

Disease Management Programs

Comprehensive management of heart failure is not only limited to hospital care during an episode of ADHF. In order to prevent repeated hospitalizations, implement additional measures through formal disease management programs. These disease management programs are often directed or coordinated by advanced practice nurses who address the comprehensive care of heart failure patients with emphasis on patient education and counseling to improve patient compliance.20

The non-pharmacologic treatment strategies emphasized in disease management programs have proven effective in achieving positive outcomes. These include counseling patients on dietary management, including encouraging a two-gram sodium diet, alcohol restriction, and adequate supplementation of electrolyte loss from diuretics. Keeping a diary of the patient’s daily weight at home and bringing it to office visits will help both the patient and the clinician monitor fluid retention efficiently.

Hypotension is a common side effect from the pharmacologic therapy for heart failure. Employ comprehensive education with both patient and family to avoid unnecessary discontinuation of the medications. A systolic blood pressure of 90 mm Hg is acceptable as long as there are no associated symptoms of dizziness or syncope.

Encourage activity guidelines, including participation in exercise programs. Attendance at support group meetings will provide a venue in which patients can share common problems and concerns with others in similar situations. One to two weeks after hospital discharge, schedule an outpatient follow-up in a heart failure clinic, where heart failure education is reinforced to prevent another episode of ADHF admission.

Summary

Despite the added challenges, managing ADHF in a patient with a serious comorbidity such as cancer involves the same goals as the treatment of ADHF in any other patient. With rapid assessment and appropriate intervention, the patient is given the best possible chance of survival. TH

The authors work at the University of Texas M.D. Anderson Cancer Center, Department of Cardiology, Houston.

References

1. American Heart Association. Heart Disease and Stroke Statistics—2005 Update. Dallas, Texas.: American Heart Association; 2005. Available at: www.americanheart.org/downloadable/heart/1105390918119HDSStats2005Update.pdf. Last accessed August 20, 2006.
2. Koelling TM, Chen RS, Lubwama RN, et al. The expanding national burden of heart failure in the United States: the influence of heart failure in women. Am Heart J. 2004 Jan;147(1):74-78.
3. Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society. Circulation. 2005 Sep 20;112(12):e154-235.Epub 2005 Sep 13.
4. Peacock WF IV, Emerman CL, Wynne J, for the ADHERE Scientific Advisory Committee and Investigators and the ADHERE Study Group. Early use of nesiritide in the emergency department is associated with improved outcome: an ADHERE registry analysis. Ann Emerg Med. 2004;44:S78.
5. Stevenson LW. Tailored therapy to hemodynamic goals for advanced heart failure. Eur J Heart Fail. 1999 Aug;1(3):251-257.
6. Stevenson LW, Perloff JK. The limited reliability of physical signs for estimating hemodynamics in chronic heart failure. JAMA. 1989;261:884-888.
7. Nakagawa O, Ogawa Y, Itoh H, et al. Rapid transcriptional activation and early mRNA turnover of brain natriuretic peptide in cardiocyte hypertrophy. Evidence for brain natriuretic peptide as an “emergency” cardiac hormone against ventricular overload. J Clin Invest. 1995 Sep;96(3):1280-1287.
8. Maeda K, Tsutamoto T, Wada A, et al. Plasma brain natriuretic peptide as a biochemical marker of high left ventricular end-diastolic pressure in patients with symptomatic left ventricular dysfunction. Am Heart J. 1998;135(5 Pt 1):825-832.
9. Burger AJ. A review of the renal and neurohormonal effects of B-type natriuretic peptide. Congest Heart Fail. 2005 Jan-Feb;11(1):30-38.
10. McCullough PA, Nowak RM, McCord J, et al. B-type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure: analysis from Breathing Not Properly (BNP) Multinational Study. Circulation. 2002 Jul;106(4):416-422.
11. Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002 Jul 18;347(3):161-167.
12. Adams KF, Lindenfeld J, Arnold JMO, et al. Executive Summary: HFSA 2006 Comprehensive Heart Failure Practice Guideline. J Card Fail. 2006 Feb;12(1):10-38.
13. Dec GW. Acute decompensated heart failure: the shrinking role of inotropic therapy. J Am Coll Cardiol. 2005 Jul;46(1):65-67.
14. Abraham WT, Adams KF, Fonarow GC, et al. In-hospital mortality in patients with acute decompensated heart failure requiring intravenous vasoactive medications: an analysis from the Acute Decompensated Heart Failure National Registry (ADHERE). J Am Coll Cardiol. 2005 Jul;46(1):57-64.
15. Burger AJ, Horton DP, LeJemtel T, et al. Effect of nesiritide (B-type natriuretic peptide) and dobutamine on ventricular arrhythmias in the treatment of patients with acutely decompensated congestive heart failure: the PRECEDENT study. Am Heart J. 2002 Dec;144(6):1102-1108.
16. Woo KS, Nicholls MG. High prevalence of persistent cough with angiotensin converting enzyme inhibitors in Chinese. Br J Clin Pharmacol. 1995 Aug;40(2):141-144.
17. Pfeffer MA, McMurray JJ, Velazquez EJ, et al. Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both. N Engl J Med. 2003 Nov 13;349(20):1893-1906. Epub 2003 Nov 10.
18. Granger CB, McMurray JJ, Yusuf S, et al. Effects of candesartan in patients with chronic heart failure and reduced left-ventricular systolic function intolerant to angiotensin-converting-enzyme inhibitors: the CHARM-Alternative trial. Lancet. 2003 Sep 6;362(9386):772-776.
19. Pitt B, Zannad F, Remme WJ, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med. 1999 Sep 2;341(10):709-717.
20. Albert NM, Eastwood CA, Edwards ML. Evidence-based practice for acute decompensated heart failure. Crit Care Nurse. 2004 Dec;24(6):14-16, 18-24, 26-29; quiz 30-31.

Acute decompensated heart failure (ADHF) remains one of the most common reasons for hospitalization. ADHF patients who have co-morbid conditions present stubborn challenges for hospitalists. And ADHF is frequently observed in patients 65 and older. The neurohormonal activation that results as a consequence of myocardial dysfunction leads to progressive cardiac deterioration and hemodynamic disturbances that ultimately become manifest as acute decompensated heart failure.

ADHG management goals include stabilizing the patient, managing acute hemodynamic abnormalities, reversing the symptoms of dyspnea caused by fluid overload, and initiating evidence-based therapies to decrease disease progression and improve survival.

In this article we present the case of a 26-year-old female with ADHF and highlight the management strategies that can result in stabilization and improved long-term outcome.

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Introduction

Despite major advances in the treatment of heart disease, heart failure remains a growing public health problem of epidemic proportions in the United States. Approximately five million Americans have heart failure, and more than 550,000 patients are diagnosed with the disease each year.1 The annual number of hospitalizations for heart failure as a primary diagnosis has increased from approximately 810,000 in 1990 to more than 1 million in 1999, and it is the most common discharge diagnosis-related group for patients 65 and older.2 Medicare spent more dollars on the diagnosis and treatment of heart failure than on any other diagnosis—more than $27.9 billion in 2005.1

Patients presenting to the emergency department (ED) with ADHF are often hemodynamically unstable, with severe symptoms of dyspnea and fluid overload. Rapid assessment and prompt initiation of appropriate interventions are necessary to achieve clinical stability and prevent prolonged hospital stay if hospitalization is required. The in-hospital mortality rate for ADHF is 5%-8%; median duration of hospitalization is five days, and the six-month re-hospitalization rate is about 50%.1,3 Thus, it is clear that improved recognition and treatment are of paramount importance. With these goals in mind, we present a recent case that highlights many of the concerns about and treatment options for ADHF.

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Case Presentation

Karen A. is a 26-year-old black female with stage III Hodgkin’s disease, diagnosed in 2000. She received chemotherapy (cisplatin, cytarabine, doxorubicin, rituxan, gemcitabine) and, as a result, in 2001 developed chemotherapy-induced cardiomyopathy with an ejection fraction of <20%. Her condition stabilized, and she remained in clinical remission until September 2002.

In 2003 she received an autologous stem cell transplant and subsequently presented to the ED with complaints of fatigue, progressive shortness of breath in the previous seven days, and lower extremity edema. She also reported right-sided pleuritic chest pain, but denied associated nausea, vomiting, or diaphoresis. In the three days preceding admission, she had gained 10 pounds. In the past six months, she had had multiple admissions for ADHF.

Her physical examination revealed an alert, obese female in moderate respiratory distress with dry mucous membranes. Her vital signs indicated a temperature of 36.5° C, a heart rate of 110 beats per minute, a respiratory rate of 20 breaths per minute, blood pressure measuring 111/73 mm Hg, and an oxygen saturation of 92%. She had no scleral icterus, but did have jugular venous distention to the angle of the mandible at 45° upright. Her cardiac examination indicated tachycardia with distant heart sounds and an audible third heart sound (S3), as well as a grade 2/6 systolic ejection murmur at the left sternal border. Her lung examination demonstrated diffuse crackles present in both lung fields, but no wheezes. Abdominal examination was notable for tenderness to palpation at the right hypogastric region and for hepatomegaly, her skin was warm and dry with no cyanosis, and her extremities demonstrated significant bilateral pitting pre-tibial edema to her knees.

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Her current medications included:

1. Furosemide, 60 mg by mouth two times daily;
2. Carvedilol, 12.5 mg by mouth in the morning, 6.25 mg in the evening;
3. Amiodarone, 200 mg by mouth daily; and
4. Digoxin, 0.125 mg by mouth daily.

Laboratory findings included normal electrolytes, blood urea nitrogen, and serum creatinine. Her hemoglobin was 11.3 gm/L, and her B-type natriuretic peptide (BNP) level was 4,837 pg/ml. Initial cardiac enzymes were negative (troponin I of <0. 03).

Her chest X-ray demonstrated moderate cardiac enlargement with bilateral thickening of subpleural septal lines and blurring of the pulmonary vasculature consistent with developing cardiogenic pulmonary edema. A 12-lead electrocardiogram indicated sinus tachycardia with a rate of 110 beats per minute and nonspecific ST-T wave changes in the inferior leads, but no Q waves were noted. Echocardiography showed severely reduced left ventricular systolic function with severe global hypokinesis of the left ventricle and a measured ejection fraction of 25%-30%. There was no pericardial effusion.

She was admitted to the telemetry floor with the diagnosis of ADHF. She was placed on supplemental oxygen and serial cardiac enzymes, and her electrocardiogram remained negative for injury or ischemia. Intravenous furosemide was initiated at 40 mg every 12 hours. After 24 hours, she was given a bolus of nesiritide (2 mcg/kg), followed by a continuous infusion at 0.01 mcg/kg/min. Cardiac medications were continued, and the dosage of carvedilol was reduced to 6.25 mg by mouth twice daily.

After a period of diuresis, the patient remained highly symptomatic; therefore, a right heart catheterization was done. The hemodynamics indicated a cardiac output of three liters per minute, a right atrial pressure of 20 mm Hg, a right ventricular pressure of 70/20 mm Hg, pulmonary artery pressure of 66/20 mm Hg with a mean pressure of 52 mm Hg, and a pulmonary capillary wedge pressure of 25 mm Hg. (See Figures 1 and 2, p. 23).

Over the next 24 hours, the patient had more than three liters of urine output and was significantly improved. The nesiritide infusion was discontinued after 48 hours of therapy, and the patient was weaned from supplemental oxygen. Lisinopril was started at 2.5 mg daily by mouth. On hospital day four, the patient walked around the nurses’ station without supplemental oxygen, and she was returned to the previous dose of furosemide, 60 mg twice daily.

The patient was enrolled in the Heart Success Program (HSP), a collaborative interdisciplinary program that is available in the institution for cancer patients with heart failure. She was provided with patient education materials that included educational videotapes on heart failure management, daily weight monitoring, diet, medications, exercise, and the emotional aspects of heart failure. Nurses with heart failure training were available to answer questions for the patient and to provide further instruction for follow-up after the patient’s discharge. The patient improved enough that she was able to enroll in a New York Heart Association (NYHA) class II and was discharged after five days, with a follow-up appointment to the outpatient clinic one week after hospital discharge.

Discussion

This case illustrates the challenges inherent in the diagnosis and management of ADHF in a cancer patient with a known history of heart failure. Rapid assessment is critical in establishing a diagnosis and initiating appropriate intervention. The goals of managing ADHF remain the same regardless of etiology. These include stabilizing the patient, managing acute hemodynamic abnormalities, reversing the symptoms of dyspnea caused by fluid overload, and initiating evidence-based therapies to decrease disease progression and improve survival. The same principles apply—even if the patient has a major comorbidity such as cancer, and suspicion for the diagnosis must remain high.

Initial Evaluation

Early diagnosis and effective management of ADHF are critically important, as these have been shown to reduce hospitalizations and intensive care unit admissions, to decrease length of stay, and to decrease cost of hospitalization.4 A comprehensive history and physical examination must be performed to identify signs and symptoms that lead to a heart failure diagnosis.

We must evaluate such potential risk factors as history of hypertension, dyslipidemia, diabetes mellitus, coronary artery disease, valvular disease, peripheral vascular disease, a family history of cardiomyopathy, smoking, alcohol use, thyroid problems, sleep apnea, and any recent history of infection (particularly upper respiratory tract infection, which can cause viral cardiomyopathy).

As part of further investigation with cancer patients, include the patient’s possible past exposure to cardiotoxic agents (e.g., anthracyclines, trastuzumab, high-dose cyclophosphamide) or mediastinal irradiation. Chemotherapy-induced cardiomyopathy is increasingly becoming an issue in heart failure management as a result of the growing number of long-term cancer survivors who have received treatment with anthracycline-containing chemotherapy or other aggressive therapy.

Focus on volume and perfusion status during the physical assessment of each patient. Most patients presenting to the ED with acute decompensation are volume overloaded. Volume overload is manifested by symptoms of dyspnea, orthopnea, and paroxysmal nocturnal dyspnea, as well as jugular venous distention, hepatojugular reflux, ascites, edema, and crackles in the lungs.5 Crackles are not always present in chronic heart failure patients, however, because of the continuous movement of fluid into the interstitium associated with increased lymphatic drainage, leaving the alveoli relatively dry.6

In addition to a comprehensive history and physical examination, several tests will help establish the diagnosis. (See Table 1, top left.) A measurement of a B-type natriuretic peptide (BNP) facilitates the diagnosis of ADHF. BNP is an endogenously generated natriuretic peptide that is activated in response to atrial or ventricular expansion due to volume overload and increased wall tension.7,8 Circulating levels of endogenous BNP are significantly elevated in ADHF patients and are a valuable tool for diagnosis of heart failure in the ED.9-11 In Karen A., the BNP level was 4,837 pg/mL, which is indicative of Stage D heart failure. This diagnosis was confirmed by chest X-ray findings of cardiogenic pulmonary edema in the setting of severe left ventricular hypokinesis and an ejection fraction of 25%-30%.

Although history and physical examination may provide important clues regarding the underlying cardiac abnormality, both invasive and noninvasive testing are necessary to provide a definitive diagnosis of heart failure and to evaluate potential exacerbating conditions. A two-dimensional echocardiogram with Doppler flow study is an essential diagnostic test for evaluating myocardial contractility or ejection fraction. Echocardiogram can also evaluate other structural components such as the pericardium, valvular status, and hemodynamic parameters that may contribute to the development of ADHF. In patients with cardiac risk factors, a myocardial perfusion stress test or catheterization may identify the presence of coronary artery disease as a contributor.

A 12-lead electrocardiogram is necessary to establish the rhythm and to show evidence of acute or prior myocardial infarction, pericarditis, conduction abnormalities, or left ventricular hypertrophy as a result of prolonged uncontrolled hypertension. It is known that rhythm disturbances such as atrial fibrillation can be a precipitating factor for ADHF.

A chest X-ray is needed to uncover pulmonary edema in cases of fluid overload and to show an enlarged cardiac silhouette in cases of dilated cardiomyopathy. Identification of a definitive cause or causes that precipitate the occurrence of ADHF is crucial in devising a management plan and initiating appropriate intervention. (See Table 2, p. 22.)

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Immediate Management of the ADHF

Newly developed clinical practice guidelines for the management of ADHF exist, but management is still based largely on empirical evidence.12 Begin ADHF treatment in the ED with intravenous diuretics (unless contraindicated). A majority of ADHF patients will respond to diuretics alone.13 If the patient responds poorly to diuretics, the use of nesiritide in conjunction with diuretics has proven beneficial, as shown in the analysis of data from the ADHERE registry indicating that patients treated with intravenous nesiritide had a lower hospital mortality rate than patients treated with milrinone or dobutamine.14 Other options include ultrafiltration, an intervention that has been noted to reduce lengths of stay and rehospitalization rates in patients with ADHF.

Nesiritide is a recombinant form of BNP without direct inotropic effects but with venous, arterial, and coronary vasodilatory properties that can improve symptoms in ADHF.15 The recommended dosage for nesiritide is an IV bolus of 2 mcg per kg, followed by a continuous infusion of 0.01 mcg/kg/min. In the setting of hypotension with a systolic blood pressure less than 100 mm Hg, however, an initial IV bolus dose is not recommended; instead, the patient may start with a continuous infusion of 0.01 mcg/kg/min, or consider other therapies.

In hemodynamically unstable patients with a systolic blood pressure less than 90 mm Hg, or in those with evidence of end organ hypoperfusion (cardiogenic shock), inotropic support may be considered until the patient is stabilized. (See Table 3, p. 22.) Recognize that inotropic agents have adverse effects on the neurohormonal system and are not recommended routinely but may be essential for temporary stabilization. (For more on pharmacologic management of ADHF, see Table 4, p. 24.)

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Subacute Management of ADHF

Once acute decompensation has been reversed and an euvolemic state has been achieved, shift therapy to a combination of three classes of medications: diuretics, angiotensin-converting enzyme (ACE) inhibitors, and beta-blockers, unless contraindicated. The benefits of these drugs have been established by evidence from numerous large-scale clinical trials.3,12

Start ACE inhibitors in all patients with heart failure due to left ventricular systolic dysfunction (unless contraindicated or if the patient is intolerant).3 Give ACE-I to patients who have experienced a recent episode of ADHF, along with diuretics to maintain sodium balance and to prevent peripheral and pulmonary edema. ACE inhibitors are contraindicated for patients who are pregnant and for those with childbearing potential, as well as for individuals with a prior history of angioedema or renal failure after receiving the drug. Instruct patients to avoid any sudden change of position, as they may experience orthostatic hypotension while taking ACE inhibitors.

Some patients are intolerant of ACE inhibitors due to a persistent cough that occurs in approximately 5% to 10% of Caucasian patients and in up to 50% of Chinese patients.16 Angiotensin receptor blockers (ARBs) are an established alternative.17 Two ARBs (candesartan and valsartan) are recommended for treatment of heart failure based on evidence from controlled clinical trials.17,18 These drugs have demonstrated a reduction in hospitalizations, and candesartan, when used as an alternative to ACE-I, has been shown to reduce mortality. Additionally, in patients with evidence of left ventricular dysfunction after myocardial infarction, valsartan provided a benefit that was not inferior to ACE inhibitors.17

Initiate beta-blockers at very low doses and gradually increased as tolerated. Monitor patients closely for symptoms of hypotension, significant weight gain, fluid retention, bradycardia, and heart block. In addition, inform patients that they may experience generalized fatigue or weakness with the initiation of beta-blockers. In a cancer patient it is difficult to differentiate between fatigue caused by the disease and the side effects of therapy. Fatigue associated with beta-blocker therapy usually resolves spontaneously within a few days. Make every effort to achieve optimum target beta-blocker dose.

An aldosterone antagonist, such as spironolactone or eplerenone, given at a daily dose of 12.5 to 25 mg in addition to standard therapy, effectively blocks the effects of aldosterone (RALES study) to achieve comprehensive neurohormonal blockade.19 When prescribing an aldosterone antagonist, especially in combination with ACE inhibitors and loop diuretics, it is important to monitor serum potassium levels because this combination can result in hyperkalemia.

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Disease Management Programs

Comprehensive management of heart failure is not only limited to hospital care during an episode of ADHF. In order to prevent repeated hospitalizations, implement additional measures through formal disease management programs. These disease management programs are often directed or coordinated by advanced practice nurses who address the comprehensive care of heart failure patients with emphasis on patient education and counseling to improve patient compliance.20

The non-pharmacologic treatment strategies emphasized in disease management programs have proven effective in achieving positive outcomes. These include counseling patients on dietary management, including encouraging a two-gram sodium diet, alcohol restriction, and adequate supplementation of electrolyte loss from diuretics. Keeping a diary of the patient’s daily weight at home and bringing it to office visits will help both the patient and the clinician monitor fluid retention efficiently.

Hypotension is a common side effect from the pharmacologic therapy for heart failure. Employ comprehensive education with both patient and family to avoid unnecessary discontinuation of the medications. A systolic blood pressure of 90 mm Hg is acceptable as long as there are no associated symptoms of dizziness or syncope.

Encourage activity guidelines, including participation in exercise programs. Attendance at support group meetings will provide a venue in which patients can share common problems and concerns with others in similar situations. One to two weeks after hospital discharge, schedule an outpatient follow-up in a heart failure clinic, where heart failure education is reinforced to prevent another episode of ADHF admission.

Summary

Despite the added challenges, managing ADHF in a patient with a serious comorbidity such as cancer involves the same goals as the treatment of ADHF in any other patient. With rapid assessment and appropriate intervention, the patient is given the best possible chance of survival. TH

The authors work at the University of Texas M.D. Anderson Cancer Center, Department of Cardiology, Houston.

References

1. American Heart Association. Heart Disease and Stroke Statistics—2005 Update. Dallas, Texas.: American Heart Association; 2005. Available at: www.americanheart.org/downloadable/heart/1105390918119HDSStats2005Update.pdf. Last accessed August 20, 2006.
2. Koelling TM, Chen RS, Lubwama RN, et al. The expanding national burden of heart failure in the United States: the influence of heart failure in women. Am Heart J. 2004 Jan;147(1):74-78.
3. Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society. Circulation. 2005 Sep 20;112(12):e154-235.Epub 2005 Sep 13.
4. Peacock WF IV, Emerman CL, Wynne J, for the ADHERE Scientific Advisory Committee and Investigators and the ADHERE Study Group. Early use of nesiritide in the emergency department is associated with improved outcome: an ADHERE registry analysis. Ann Emerg Med. 2004;44:S78.
5. Stevenson LW. Tailored therapy to hemodynamic goals for advanced heart failure. Eur J Heart Fail. 1999 Aug;1(3):251-257.
6. Stevenson LW, Perloff JK. The limited reliability of physical signs for estimating hemodynamics in chronic heart failure. JAMA. 1989;261:884-888.
7. Nakagawa O, Ogawa Y, Itoh H, et al. Rapid transcriptional activation and early mRNA turnover of brain natriuretic peptide in cardiocyte hypertrophy. Evidence for brain natriuretic peptide as an “emergency” cardiac hormone against ventricular overload. J Clin Invest. 1995 Sep;96(3):1280-1287.
8. Maeda K, Tsutamoto T, Wada A, et al. Plasma brain natriuretic peptide as a biochemical marker of high left ventricular end-diastolic pressure in patients with symptomatic left ventricular dysfunction. Am Heart J. 1998;135(5 Pt 1):825-832.
9. Burger AJ. A review of the renal and neurohormonal effects of B-type natriuretic peptide. Congest Heart Fail. 2005 Jan-Feb;11(1):30-38.
10. McCullough PA, Nowak RM, McCord J, et al. B-type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure: analysis from Breathing Not Properly (BNP) Multinational Study. Circulation. 2002 Jul;106(4):416-422.
11. Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002 Jul 18;347(3):161-167.
12. Adams KF, Lindenfeld J, Arnold JMO, et al. Executive Summary: HFSA 2006 Comprehensive Heart Failure Practice Guideline. J Card Fail. 2006 Feb;12(1):10-38.
13. Dec GW. Acute decompensated heart failure: the shrinking role of inotropic therapy. J Am Coll Cardiol. 2005 Jul;46(1):65-67.
14. Abraham WT, Adams KF, Fonarow GC, et al. In-hospital mortality in patients with acute decompensated heart failure requiring intravenous vasoactive medications: an analysis from the Acute Decompensated Heart Failure National Registry (ADHERE). J Am Coll Cardiol. 2005 Jul;46(1):57-64.
15. Burger AJ, Horton DP, LeJemtel T, et al. Effect of nesiritide (B-type natriuretic peptide) and dobutamine on ventricular arrhythmias in the treatment of patients with acutely decompensated congestive heart failure: the PRECEDENT study. Am Heart J. 2002 Dec;144(6):1102-1108.
16. Woo KS, Nicholls MG. High prevalence of persistent cough with angiotensin converting enzyme inhibitors in Chinese. Br J Clin Pharmacol. 1995 Aug;40(2):141-144.
17. Pfeffer MA, McMurray JJ, Velazquez EJ, et al. Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both. N Engl J Med. 2003 Nov 13;349(20):1893-1906. Epub 2003 Nov 10.
18. Granger CB, McMurray JJ, Yusuf S, et al. Effects of candesartan in patients with chronic heart failure and reduced left-ventricular systolic function intolerant to angiotensin-converting-enzyme inhibitors: the CHARM-Alternative trial. Lancet. 2003 Sep 6;362(9386):772-776.
19. Pitt B, Zannad F, Remme WJ, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med. 1999 Sep 2;341(10):709-717.
20. Albert NM, Eastwood CA, Edwards ML. Evidence-based practice for acute decompensated heart failure. Crit Care Nurse. 2004 Dec;24(6):14-16, 18-24, 26-29; quiz 30-31.

A72-year-old male with a history of renal transplantation underwent laparoscopic cholecystectomy for cholelithiasis. On post-operative day one, he developed worsening abdominal pain. An urgent exploratory laparotomy revealed no abnormalities. Over the next few days, he experienced worsening confusion and agitation. He developed respiratory failure, as well as a cutaneous eruption over the face, chest, abdomen, back, and upper extremities.

What is the most sensitive test for diagnosis of this eruption?

1. Tzanck smear;
2. Darkfield microscopy;
3. Direct fluorescent antibody testing;
4. Polymerase chain reaction; or
5. Viral culture.

Discussion

The answer is D: polymerase chain reaction. Varicella zoster virus (VZV) was detected by rapid polymerase chain reaction from a skin biopsy specimen and from a sample of cerebrospinal fluid. It was also detected by viral culture from tracheal secretions. The patient was diagnosed with disseminated herpes zoster with VZV encephalitis and pneumonitis. He was treated with intravenous acyclovir, 1 g every eight hours for 14 days. His respiratory function and mental status gradually improved.

Herpes zoster is a painful vesicular eruption confined to the distribution of a sensory dermatome. It is caused by the reactivation of latent VZV located in the dorsal root ganglion of the affected dermatome. Triggers for reactivation include stress, trauma, fever, radiation therapy, and immunosuppression. The reactivation of VZV can also present in a disseminated fashion. Herpes zoster is classified as disseminated when more than 20 vesicular lesions occur outside of the primary and adjacent dermatomes.1 Disseminated herpes zoster can occur in immunocompetent patients, but it usually occurs in the setting of immunosuppression.2 It is seen most often in the settings of HIV, malignancy, and immunosuppressive therapy.1

The cutaneous lesions of herpes zoster begin as erythematous macules and papules that progress to vesicles. The vesicular lesions can evolve into pustules. The vesicles become crusts after seven to 10 days. Intense pain often precedes the cutaneous eruption, which can lead to misdiagnosis as myocardial infarction, pleurisy, acute surgical abdomen, or herniated intervertebral disk.2

Disseminated herpes zoster can also involve the central nervous system, lungs, liver, heart, and gastrointestinal tract. Pulmonary involvement is the most common of the possible visceral manifestations. Visceral zoster occurs in 10% of immunocompromised patients with cutaneous zoster.1

The differential diagnosis of disseminated herpes zoster includes bullous impetigo, insect bites, erythema multiforme, papular urticaria, drug eruption, contact dermatitis, and other viral exanthems such as coxsackie virus, rickettsial pox, and smallpox. The best initial test is a Tzanck smear of a scraping from the base of a lesion. The presence of multinucleated giant cells and epithelial cells with acidophilic intranuclear inclusions provides a rapid diagnosis. The most sensitive test is polymerase chain reaction of vesicular fluid, but this test is not universally available.3 The diagnosis can also be made by viral culture, but this can be difficult because VZV is a labile virus.2,3 Other diagnostic tests include direct fluorescent antibody testing, serology, and immunohistochemical stains on a skin biopsy specimen.

Treatment with intravenous acyclovir is indicated in immunocompromised patients with disseminated VZV.1 Treatment should be started within 72 hours of the onset of the vesicular eruption. Acyclovir-resistant VZV should be treated with foscarnet.2 There are also reports of physicians combining acyclovir with plasma exchange, a treatment option that may be beneficial in decreasing the viral load.4 Varicella zoster virus is transmissible to susceptible individuals by direct contact or by respiratory transmission from a patient with pulmonary involvement. Airborne and contact precautions are recommended until all of the patient’s vesicles have crusted. TH

References

1. Stratman E. Visceral zoster as the presenting feature of disseminated herpes zoster. J Am Acad Dermatol. 2002;46(5):771-774.
2. McCrary ML, Severson J, Tyring SK. Varicella zoster virus. J Am Acad Dermatol. 1999;41(1):1-14.
3. Sauerbrei A, Eichhorn U, Schacke M, et al. Laboratory diagnosis of herpes zoster. J Clin Virol. 1999;14(1):31-36.
4. Lee C, Koike M, Oshimi K, et al. Acyclovir combined with plasma exchange for disseminated varicella-zoster virus infection after bone marrow transplantation [in Japanese]. Rinsho Ketsueki. 2006;47(3):210-213.

A72-year-old male with a history of renal transplantation underwent laparoscopic cholecystectomy for cholelithiasis. On post-operative day one, he developed worsening abdominal pain. An urgent exploratory laparotomy revealed no abnormalities. Over the next few days, he experienced worsening confusion and agitation. He developed respiratory failure, as well as a cutaneous eruption over the face, chest, abdomen, back, and upper extremities.

What is the most sensitive test for diagnosis of this eruption?

1. Tzanck smear;
2. Darkfield microscopy;
3. Direct fluorescent antibody testing;
4. Polymerase chain reaction; or
5. Viral culture.

Discussion

The answer is D: polymerase chain reaction. Varicella zoster virus (VZV) was detected by rapid polymerase chain reaction from a skin biopsy specimen and from a sample of cerebrospinal fluid. It was also detected by viral culture from tracheal secretions. The patient was diagnosed with disseminated herpes zoster with VZV encephalitis and pneumonitis. He was treated with intravenous acyclovir, 1 g every eight hours for 14 days. His respiratory function and mental status gradually improved.

Herpes zoster is a painful vesicular eruption confined to the distribution of a sensory dermatome. It is caused by the reactivation of latent VZV located in the dorsal root ganglion of the affected dermatome. Triggers for reactivation include stress, trauma, fever, radiation therapy, and immunosuppression. The reactivation of VZV can also present in a disseminated fashion. Herpes zoster is classified as disseminated when more than 20 vesicular lesions occur outside of the primary and adjacent dermatomes.1 Disseminated herpes zoster can occur in immunocompetent patients, but it usually occurs in the setting of immunosuppression.2 It is seen most often in the settings of HIV, malignancy, and immunosuppressive therapy.1

The cutaneous lesions of herpes zoster begin as erythematous macules and papules that progress to vesicles. The vesicular lesions can evolve into pustules. The vesicles become crusts after seven to 10 days. Intense pain often precedes the cutaneous eruption, which can lead to misdiagnosis as myocardial infarction, pleurisy, acute surgical abdomen, or herniated intervertebral disk.2

Disseminated herpes zoster can also involve the central nervous system, lungs, liver, heart, and gastrointestinal tract. Pulmonary involvement is the most common of the possible visceral manifestations. Visceral zoster occurs in 10% of immunocompromised patients with cutaneous zoster.1

The differential diagnosis of disseminated herpes zoster includes bullous impetigo, insect bites, erythema multiforme, papular urticaria, drug eruption, contact dermatitis, and other viral exanthems such as coxsackie virus, rickettsial pox, and smallpox. The best initial test is a Tzanck smear of a scraping from the base of a lesion. The presence of multinucleated giant cells and epithelial cells with acidophilic intranuclear inclusions provides a rapid diagnosis. The most sensitive test is polymerase chain reaction of vesicular fluid, but this test is not universally available.3 The diagnosis can also be made by viral culture, but this can be difficult because VZV is a labile virus.2,3 Other diagnostic tests include direct fluorescent antibody testing, serology, and immunohistochemical stains on a skin biopsy specimen.

Treatment with intravenous acyclovir is indicated in immunocompromised patients with disseminated VZV.1 Treatment should be started within 72 hours of the onset of the vesicular eruption. Acyclovir-resistant VZV should be treated with foscarnet.2 There are also reports of physicians combining acyclovir with plasma exchange, a treatment option that may be beneficial in decreasing the viral load.4 Varicella zoster virus is transmissible to susceptible individuals by direct contact or by respiratory transmission from a patient with pulmonary involvement. Airborne and contact precautions are recommended until all of the patient’s vesicles have crusted. TH

References

1. Stratman E. Visceral zoster as the presenting feature of disseminated herpes zoster. J Am Acad Dermatol. 2002;46(5):771-774.
2. McCrary ML, Severson J, Tyring SK. Varicella zoster virus. J Am Acad Dermatol. 1999;41(1):1-14.
3. Sauerbrei A, Eichhorn U, Schacke M, et al. Laboratory diagnosis of herpes zoster. J Clin Virol. 1999;14(1):31-36.
4. Lee C, Koike M, Oshimi K, et al. Acyclovir combined with plasma exchange for disseminated varicella-zoster virus infection after bone marrow transplantation [in Japanese]. Rinsho Ketsueki. 2006;47(3):210-213.

A72-year-old male with a history of renal transplantation underwent laparoscopic cholecystectomy for cholelithiasis. On post-operative day one, he developed worsening abdominal pain. An urgent exploratory laparotomy revealed no abnormalities. Over the next few days, he experienced worsening confusion and agitation. He developed respiratory failure, as well as a cutaneous eruption over the face, chest, abdomen, back, and upper extremities.

What is the most sensitive test for diagnosis of this eruption?

1. Tzanck smear;
2. Darkfield microscopy;
3. Direct fluorescent antibody testing;
4. Polymerase chain reaction; or
5. Viral culture.

Discussion

The answer is D: polymerase chain reaction. Varicella zoster virus (VZV) was detected by rapid polymerase chain reaction from a skin biopsy specimen and from a sample of cerebrospinal fluid. It was also detected by viral culture from tracheal secretions. The patient was diagnosed with disseminated herpes zoster with VZV encephalitis and pneumonitis. He was treated with intravenous acyclovir, 1 g every eight hours for 14 days. His respiratory function and mental status gradually improved.

Herpes zoster is a painful vesicular eruption confined to the distribution of a sensory dermatome. It is caused by the reactivation of latent VZV located in the dorsal root ganglion of the affected dermatome. Triggers for reactivation include stress, trauma, fever, radiation therapy, and immunosuppression. The reactivation of VZV can also present in a disseminated fashion. Herpes zoster is classified as disseminated when more than 20 vesicular lesions occur outside of the primary and adjacent dermatomes.1 Disseminated herpes zoster can occur in immunocompetent patients, but it usually occurs in the setting of immunosuppression.2 It is seen most often in the settings of HIV, malignancy, and immunosuppressive therapy.1

The cutaneous lesions of herpes zoster begin as erythematous macules and papules that progress to vesicles. The vesicular lesions can evolve into pustules. The vesicles become crusts after seven to 10 days. Intense pain often precedes the cutaneous eruption, which can lead to misdiagnosis as myocardial infarction, pleurisy, acute surgical abdomen, or herniated intervertebral disk.2

Disseminated herpes zoster can also involve the central nervous system, lungs, liver, heart, and gastrointestinal tract. Pulmonary involvement is the most common of the possible visceral manifestations. Visceral zoster occurs in 10% of immunocompromised patients with cutaneous zoster.1

The differential diagnosis of disseminated herpes zoster includes bullous impetigo, insect bites, erythema multiforme, papular urticaria, drug eruption, contact dermatitis, and other viral exanthems such as coxsackie virus, rickettsial pox, and smallpox. The best initial test is a Tzanck smear of a scraping from the base of a lesion. The presence of multinucleated giant cells and epithelial cells with acidophilic intranuclear inclusions provides a rapid diagnosis. The most sensitive test is polymerase chain reaction of vesicular fluid, but this test is not universally available.3 The diagnosis can also be made by viral culture, but this can be difficult because VZV is a labile virus.2,3 Other diagnostic tests include direct fluorescent antibody testing, serology, and immunohistochemical stains on a skin biopsy specimen.

Treatment with intravenous acyclovir is indicated in immunocompromised patients with disseminated VZV.1 Treatment should be started within 72 hours of the onset of the vesicular eruption. Acyclovir-resistant VZV should be treated with foscarnet.2 There are also reports of physicians combining acyclovir with plasma exchange, a treatment option that may be beneficial in decreasing the viral load.4 Varicella zoster virus is transmissible to susceptible individuals by direct contact or by respiratory transmission from a patient with pulmonary involvement. Airborne and contact precautions are recommended until all of the patient’s vesicles have crusted. TH

References

1. Stratman E. Visceral zoster as the presenting feature of disseminated herpes zoster. J Am Acad Dermatol. 2002;46(5):771-774.
2. McCrary ML, Severson J, Tyring SK. Varicella zoster virus. J Am Acad Dermatol. 1999;41(1):1-14.
3. Sauerbrei A, Eichhorn U, Schacke M, et al. Laboratory diagnosis of herpes zoster. J Clin Virol. 1999;14(1):31-36.
4. Lee C, Koike M, Oshimi K, et al. Acyclovir combined with plasma exchange for disseminated varicella-zoster virus infection after bone marrow transplantation [in Japanese]. Rinsho Ketsueki. 2006;47(3):210-213.

While pay-for-performance has become one of the hottest trends in healthcare, another program that would tie payment to performance is starting to get some notice. Gainsharing is on the horizon for hospitals and the physicians who work for them, but the advances made in this savings-sharing model are questionable.

Gainsharing Defined

What is gainsharing? It has to do with the sharing of gains—or of costs saved, to be more precise. Under a gainsharing model, a hospital will select specific best practices, including standard policies, procedures, and/or protocols that will improve quality of care and reduce financial costs. Any reduction in costs that results from physicians following these best practices is documented by the hospital over a specified period. After monitoring and noting that physicians met the predetermined benchmarks for quality of care, the hospital then pays a cash bonus to those who contributed to the cost reduction.

Gainsharing can take various forms, but generally the practice applies to services provided within a single clinical specialty such as oncology or cardiac surgery. “Gainsharing could affect anyone who cares for patients in a hospital if it became legal,” says Ron Greeno, MD, FCCP, chief medical officer, Cogent Healthcare, Irvine, Calif., “but hospitalists are the perfect group of doctors to take on projects like this.”

The most recent gainsharing programs have focused on the use of pre-approved medical devices, equipment, and supplies. For example, a hospital might recommend that physicians use less costly items with the same level of effectiveness, such as a knee-high sequential compression device rather than a thigh-high device.

How much money is involved in gainsharing? Of course, it depends on the program. “Gainsharing deals could include significant money depending on how they are structured,” explains Dr. Greeno, “if you did something that results in enough quality benefit.”

Example: A hospital asked a physician group to give an appropriate antibiotic to patients as soon as possible upon admission and was consequently able to show that they avoided a prolonged stay for five of those patients and that this saved the hospital $1 million in costs. “If the hospital gave 50% of that savings to 20 physicians who helped meet that goal, why would anyone want to regulate against that?” asks Dr. Greeno.

A Brief History of Gainsharing

There is a good reason you may not have heard much about gainsharing; the practice was banned in 1999 by the federal Office of Inspector General (OIG). The OIG was concerned that gainsharing could limit patient care and might lead to physicians “cherry picking” patients who are healthier, while sending seriously ill patients to a different hospital.

Only in September 2005 did the OIG carry out a half-hearted reversal, providing advisory opinions that allow pre-approved arrangements between individual hospitals and physician groups—as long as appropriate safeguards are adopted to protect against abuse.

“This was a very small change,” says Dr. Greeno. “Their approval is highly limited. They have basically agreed to very specific, very short trials of gainsharing, which they will approve one at a time.”

Dr. Greeno is frustrated by the baby step taken by the federal government. “The OIG equates gainsharing with denial of care,” he says. “Their limits are preventing a tremendous opportunity for hospitals and physicians to partner to provide quality care; they’re saying we can’t provide the right incentive scheme.”

The point that Dr. Greeno finds most frustrating is the vast difference of opinion on gainsharing versus another payment trend. “The irony is that all gainsharing is pay-for-performance,” says Dr. Greeno. “The difference is that instead of Medicare paying, it’s the individual hospital paying for performance. Even people who really understand healthcare haven’t connected the dots. They’re pushing for pay-for-performance, but telling hospitals they can’t do essentially the same thing. The hospital industry is developing a strategy to point that out to Capitol Hill, and in my opinion, SHM should develop a more formal approach to do the same.”

Current State of Gainsharing

There have been a few gainsharing programs that were approved by the OIG. “There are a couple of [pilot programs] that private hospitals have done,” says Dr. Greeno. “All the projects so far have targeted medical devices. One New Jersey hospital focused on the use of defibrillators. They spent a lot of money setting up the project, which only lasted one year. As I said, these [approved projects] are very limited.”

Gainsharing programs that focus on medical devices are simple because cost savings are easy to track; however, gainsharing could be built around quality indicators that are found in pay-for-performance programs. “Cutting costs is not the only way to improve quality,” says Dr. Greeno. “That’s not how you get the biggest bang for your buck. That comes when someone will invest in capabilities and processes that target the 30% of costs spent on each patient in the hospital that is waste.”

Pilot Programs Planned

Following the OIG reversal, Congress passed the Deficit Reduction Omnibus Reconciliation Act of 2005, which included funding for a gainsharing demonstration project. The Centers for Medicare and Medicaid Services (CMS) will establish six gainsharing pilot programs, including two in rural settings, by January 1, 2007. The bill states that these demonstration programs are intended to “test and evaluate methodologies and arrangements between hospitals and physicians designed to govern the utilization of inpatient hospital resources and physician work to improve quality and efficiency of care provided to Medicare beneficiaries.”

You can review details on the gainsharing demonstration on the CMS Web site at www.cms.hhs.gov/DemoProjectsEvalRpts/MD/itemdetail.asp?filterType=none&filterByDID=-99&sortByDID=3&sortOrder=ascending&itemID=CMS1186805.

A second new CMS demonstration program will go beyond the traditional concept of gainsharing. Under the program, known as the Physician-Hospital Collaboration Demonstration (PHCD), hospitals would be allowed to pay physicians a portion of the savings they reap from specific quality improvement and efficiency initiatives. This project, in particular, could eventually have direct implications for hospital medicine.

The SHM Public Policy Committee is urging members to consider soliciting involvement with PHCD, and possibly partnering with other physician groups and affiliated hospitals to compete for inclusion. You can find more on the PHCD online at www.cms.hhs.gov/DemoProjectsEvalRpts/MD/itemdetail.asp?filterType=none&filterByDID=99&sortByDID=3&sortOrder=ascending&itemID=CMS1186653. If you decide to submit a proposal to CMS for the PHCD, please let Joe Miller at SHM ([email protected]) know.

The Future of Gainsharing

Will the CMS gainsharing pilot programs lead to widespread trials? “Who knows?” asks Dr. Greeno. “It will be a slow crawl toward some type of application, but it will likely be too limited when it does happen.”

In the meantime, Dr. Greeno is urging SHM and individual physicians to keep pushing for some real advances in gainsharing. “Our best chance is to work with the hospital community to connect the dots for our federal lawmakers,” he says. “We want to work to allow hospitals to reward doctors for quality performance.” TH

Jane Jerrard regularly writes “Public Policy.”

While pay-for-performance has become one of the hottest trends in healthcare, another program that would tie payment to performance is starting to get some notice. Gainsharing is on the horizon for hospitals and the physicians who work for them, but the advances made in this savings-sharing model are questionable.

Gainsharing Defined

What is gainsharing? It has to do with the sharing of gains—or of costs saved, to be more precise. Under a gainsharing model, a hospital will select specific best practices, including standard policies, procedures, and/or protocols that will improve quality of care and reduce financial costs. Any reduction in costs that results from physicians following these best practices is documented by the hospital over a specified period. After monitoring and noting that physicians met the predetermined benchmarks for quality of care, the hospital then pays a cash bonus to those who contributed to the cost reduction.

Gainsharing can take various forms, but generally the practice applies to services provided within a single clinical specialty such as oncology or cardiac surgery. “Gainsharing could affect anyone who cares for patients in a hospital if it became legal,” says Ron Greeno, MD, FCCP, chief medical officer, Cogent Healthcare, Irvine, Calif., “but hospitalists are the perfect group of doctors to take on projects like this.”

The most recent gainsharing programs have focused on the use of pre-approved medical devices, equipment, and supplies. For example, a hospital might recommend that physicians use less costly items with the same level of effectiveness, such as a knee-high sequential compression device rather than a thigh-high device.

How much money is involved in gainsharing? Of course, it depends on the program. “Gainsharing deals could include significant money depending on how they are structured,” explains Dr. Greeno, “if you did something that results in enough quality benefit.”

Example: A hospital asked a physician group to give an appropriate antibiotic to patients as soon as possible upon admission and was consequently able to show that they avoided a prolonged stay for five of those patients and that this saved the hospital $1 million in costs. “If the hospital gave 50% of that savings to 20 physicians who helped meet that goal, why would anyone want to regulate against that?” asks Dr. Greeno.

A Brief History of Gainsharing

There is a good reason you may not have heard much about gainsharing; the practice was banned in 1999 by the federal Office of Inspector General (OIG). The OIG was concerned that gainsharing could limit patient care and might lead to physicians “cherry picking” patients who are healthier, while sending seriously ill patients to a different hospital.

Only in September 2005 did the OIG carry out a half-hearted reversal, providing advisory opinions that allow pre-approved arrangements between individual hospitals and physician groups—as long as appropriate safeguards are adopted to protect against abuse.

“This was a very small change,” says Dr. Greeno. “Their approval is highly limited. They have basically agreed to very specific, very short trials of gainsharing, which they will approve one at a time.”

Dr. Greeno is frustrated by the baby step taken by the federal government. “The OIG equates gainsharing with denial of care,” he says. “Their limits are preventing a tremendous opportunity for hospitals and physicians to partner to provide quality care; they’re saying we can’t provide the right incentive scheme.”

The point that Dr. Greeno finds most frustrating is the vast difference of opinion on gainsharing versus another payment trend. “The irony is that all gainsharing is pay-for-performance,” says Dr. Greeno. “The difference is that instead of Medicare paying, it’s the individual hospital paying for performance. Even people who really understand healthcare haven’t connected the dots. They’re pushing for pay-for-performance, but telling hospitals they can’t do essentially the same thing. The hospital industry is developing a strategy to point that out to Capitol Hill, and in my opinion, SHM should develop a more formal approach to do the same.”

Current State of Gainsharing

There have been a few gainsharing programs that were approved by the OIG. “There are a couple of [pilot programs] that private hospitals have done,” says Dr. Greeno. “All the projects so far have targeted medical devices. One New Jersey hospital focused on the use of defibrillators. They spent a lot of money setting up the project, which only lasted one year. As I said, these [approved projects] are very limited.”

Gainsharing programs that focus on medical devices are simple because cost savings are easy to track; however, gainsharing could be built around quality indicators that are found in pay-for-performance programs. “Cutting costs is not the only way to improve quality,” says Dr. Greeno. “That’s not how you get the biggest bang for your buck. That comes when someone will invest in capabilities and processes that target the 30% of costs spent on each patient in the hospital that is waste.”

Pilot Programs Planned

Following the OIG reversal, Congress passed the Deficit Reduction Omnibus Reconciliation Act of 2005, which included funding for a gainsharing demonstration project. The Centers for Medicare and Medicaid Services (CMS) will establish six gainsharing pilot programs, including two in rural settings, by January 1, 2007. The bill states that these demonstration programs are intended to “test and evaluate methodologies and arrangements between hospitals and physicians designed to govern the utilization of inpatient hospital resources and physician work to improve quality and efficiency of care provided to Medicare beneficiaries.”

You can review details on the gainsharing demonstration on the CMS Web site at www.cms.hhs.gov/DemoProjectsEvalRpts/MD/itemdetail.asp?filterType=none&filterByDID=-99&sortByDID=3&sortOrder=ascending&itemID=CMS1186805.

A second new CMS demonstration program will go beyond the traditional concept of gainsharing. Under the program, known as the Physician-Hospital Collaboration Demonstration (PHCD), hospitals would be allowed to pay physicians a portion of the savings they reap from specific quality improvement and efficiency initiatives. This project, in particular, could eventually have direct implications for hospital medicine.

The SHM Public Policy Committee is urging members to consider soliciting involvement with PHCD, and possibly partnering with other physician groups and affiliated hospitals to compete for inclusion. You can find more on the PHCD online at www.cms.hhs.gov/DemoProjectsEvalRpts/MD/itemdetail.asp?filterType=none&filterByDID=99&sortByDID=3&sortOrder=ascending&itemID=CMS1186653. If you decide to submit a proposal to CMS for the PHCD, please let Joe Miller at SHM ([email protected]) know.

The Future of Gainsharing

Will the CMS gainsharing pilot programs lead to widespread trials? “Who knows?” asks Dr. Greeno. “It will be a slow crawl toward some type of application, but it will likely be too limited when it does happen.”

In the meantime, Dr. Greeno is urging SHM and individual physicians to keep pushing for some real advances in gainsharing. “Our best chance is to work with the hospital community to connect the dots for our federal lawmakers,” he says. “We want to work to allow hospitals to reward doctors for quality performance.” TH

Jane Jerrard regularly writes “Public Policy.”

While pay-for-performance has become one of the hottest trends in healthcare, another program that would tie payment to performance is starting to get some notice. Gainsharing is on the horizon for hospitals and the physicians who work for them, but the advances made in this savings-sharing model are questionable.

Gainsharing Defined

What is gainsharing? It has to do with the sharing of gains—or of costs saved, to be more precise. Under a gainsharing model, a hospital will select specific best practices, including standard policies, procedures, and/or protocols that will improve quality of care and reduce financial costs. Any reduction in costs that results from physicians following these best practices is documented by the hospital over a specified period. After monitoring and noting that physicians met the predetermined benchmarks for quality of care, the hospital then pays a cash bonus to those who contributed to the cost reduction.

Gainsharing can take various forms, but generally the practice applies to services provided within a single clinical specialty such as oncology or cardiac surgery. “Gainsharing could affect anyone who cares for patients in a hospital if it became legal,” says Ron Greeno, MD, FCCP, chief medical officer, Cogent Healthcare, Irvine, Calif., “but hospitalists are the perfect group of doctors to take on projects like this.”

The most recent gainsharing programs have focused on the use of pre-approved medical devices, equipment, and supplies. For example, a hospital might recommend that physicians use less costly items with the same level of effectiveness, such as a knee-high sequential compression device rather than a thigh-high device.

How much money is involved in gainsharing? Of course, it depends on the program. “Gainsharing deals could include significant money depending on how they are structured,” explains Dr. Greeno, “if you did something that results in enough quality benefit.”

Example: A hospital asked a physician group to give an appropriate antibiotic to patients as soon as possible upon admission and was consequently able to show that they avoided a prolonged stay for five of those patients and that this saved the hospital $1 million in costs. “If the hospital gave 50% of that savings to 20 physicians who helped meet that goal, why would anyone want to regulate against that?” asks Dr. Greeno.

A Brief History of Gainsharing

There is a good reason you may not have heard much about gainsharing; the practice was banned in 1999 by the federal Office of Inspector General (OIG). The OIG was concerned that gainsharing could limit patient care and might lead to physicians “cherry picking” patients who are healthier, while sending seriously ill patients to a different hospital.

Only in September 2005 did the OIG carry out a half-hearted reversal, providing advisory opinions that allow pre-approved arrangements between individual hospitals and physician groups—as long as appropriate safeguards are adopted to protect against abuse.

“This was a very small change,” says Dr. Greeno. “Their approval is highly limited. They have basically agreed to very specific, very short trials of gainsharing, which they will approve one at a time.”

Dr. Greeno is frustrated by the baby step taken by the federal government. “The OIG equates gainsharing with denial of care,” he says. “Their limits are preventing a tremendous opportunity for hospitals and physicians to partner to provide quality care; they’re saying we can’t provide the right incentive scheme.”

The point that Dr. Greeno finds most frustrating is the vast difference of opinion on gainsharing versus another payment trend. “The irony is that all gainsharing is pay-for-performance,” says Dr. Greeno. “The difference is that instead of Medicare paying, it’s the individual hospital paying for performance. Even people who really understand healthcare haven’t connected the dots. They’re pushing for pay-for-performance, but telling hospitals they can’t do essentially the same thing. The hospital industry is developing a strategy to point that out to Capitol Hill, and in my opinion, SHM should develop a more formal approach to do the same.”

Current State of Gainsharing

There have been a few gainsharing programs that were approved by the OIG. “There are a couple of [pilot programs] that private hospitals have done,” says Dr. Greeno. “All the projects so far have targeted medical devices. One New Jersey hospital focused on the use of defibrillators. They spent a lot of money setting up the project, which only lasted one year. As I said, these [approved projects] are very limited.”

Gainsharing programs that focus on medical devices are simple because cost savings are easy to track; however, gainsharing could be built around quality indicators that are found in pay-for-performance programs. “Cutting costs is not the only way to improve quality,” says Dr. Greeno. “That’s not how you get the biggest bang for your buck. That comes when someone will invest in capabilities and processes that target the 30% of costs spent on each patient in the hospital that is waste.”

Pilot Programs Planned

Following the OIG reversal, Congress passed the Deficit Reduction Omnibus Reconciliation Act of 2005, which included funding for a gainsharing demonstration project. The Centers for Medicare and Medicaid Services (CMS) will establish six gainsharing pilot programs, including two in rural settings, by January 1, 2007. The bill states that these demonstration programs are intended to “test and evaluate methodologies and arrangements between hospitals and physicians designed to govern the utilization of inpatient hospital resources and physician work to improve quality and efficiency of care provided to Medicare beneficiaries.”

You can review details on the gainsharing demonstration on the CMS Web site at www.cms.hhs.gov/DemoProjectsEvalRpts/MD/itemdetail.asp?filterType=none&filterByDID=-99&sortByDID=3&sortOrder=ascending&itemID=CMS1186805.

A second new CMS demonstration program will go beyond the traditional concept of gainsharing. Under the program, known as the Physician-Hospital Collaboration Demonstration (PHCD), hospitals would be allowed to pay physicians a portion of the savings they reap from specific quality improvement and efficiency initiatives. This project, in particular, could eventually have direct implications for hospital medicine.

The SHM Public Policy Committee is urging members to consider soliciting involvement with PHCD, and possibly partnering with other physician groups and affiliated hospitals to compete for inclusion. You can find more on the PHCD online at www.cms.hhs.gov/DemoProjectsEvalRpts/MD/itemdetail.asp?filterType=none&filterByDID=99&sortByDID=3&sortOrder=ascending&itemID=CMS1186653. If you decide to submit a proposal to CMS for the PHCD, please let Joe Miller at SHM ([email protected]) know.

The Future of Gainsharing

Will the CMS gainsharing pilot programs lead to widespread trials? “Who knows?” asks Dr. Greeno. “It will be a slow crawl toward some type of application, but it will likely be too limited when it does happen.”

In the meantime, Dr. Greeno is urging SHM and individual physicians to keep pushing for some real advances in gainsharing. “Our best chance is to work with the hospital community to connect the dots for our federal lawmakers,” he says. “We want to work to allow hospitals to reward doctors for quality performance.” TH

Jane Jerrard regularly writes “Public Policy.”