Background Decision support interventions help patients who are facing difficult treatment decisions and improve shared decision making. There is little evidence of the economic impact of these interventions.

Objective To determine the costs of providing a decision support intervention in the form of consultation planning (CP) and consultation planning with recording and summary (CPRS) to women with breast cancer and to compare the cost benefit of CP and CPRS by telephone versus in person.

Methods Sixty-eight women with breast cancer who were being treated at a rural cancer resource center were randomized to CP in person or by telephone. All participants were then provided with an audio-recording of the physician consultation along with a typed summary for the full intervention (CPRS). Surveys completed by the participants and center staff provided data for measuring costs and willingness-to-pay (WTP) benefits. Societal perspective costs and incremental net benefit (INB) across delivery methods was determined.

Results Total CP costs were $208.72 for telephone and $264.00 for in-person delivery. Significantly lower telephone-group costs (P ˂ .001) were a result of lower participant travel expenses. Participants were willing to pay $154.12 for telephone and $144.03 for in-person CP (P = .85). WTP did not exceed costs of either delivery method compared with no intervention. INB of providing CP for telephone versus in person was $65.37, favoring telephone delivery. Sensitivity analysis revealed that with more efficient CP training, WTP became greater than the costs of delivering CP by telephone versus no intervention.

Limitations There may be some income distribution effects in the measurement of WTP.

Conclusions Providing CP by telephone was significantly less costly with no significant difference in benefit. Participants’ WTP only exceeded the full cost of CP with more efficient training or higher participant volume. A positive INB showed telephone delivery is efficient and may increase accessibility to decision support services, particularly in rural communities.


Click on the PDF icon at the top of this introduction to read the full article.



 

Background Decision support interventions help patients who are facing difficult treatment decisions and improve shared decision making. There is little evidence of the economic impact of these interventions.

Objective To determine the costs of providing a decision support intervention in the form of consultation planning (CP) and consultation planning with recording and summary (CPRS) to women with breast cancer and to compare the cost benefit of CP and CPRS by telephone versus in person.

Methods Sixty-eight women with breast cancer who were being treated at a rural cancer resource center were randomized to CP in person or by telephone. All participants were then provided with an audio-recording of the physician consultation along with a typed summary for the full intervention (CPRS). Surveys completed by the participants and center staff provided data for measuring costs and willingness-to-pay (WTP) benefits. Societal perspective costs and incremental net benefit (INB) across delivery methods was determined.

Results Total CP costs were $208.72 for telephone and $264.00 for in-person delivery. Significantly lower telephone-group costs (P ˂ .001) were a result of lower participant travel expenses. Participants were willing to pay $154.12 for telephone and $144.03 for in-person CP (P = .85). WTP did not exceed costs of either delivery method compared with no intervention. INB of providing CP for telephone versus in person was $65.37, favoring telephone delivery. Sensitivity analysis revealed that with more efficient CP training, WTP became greater than the costs of delivering CP by telephone versus no intervention.

Limitations There may be some income distribution effects in the measurement of WTP.

Conclusions Providing CP by telephone was significantly less costly with no significant difference in benefit. Participants’ WTP only exceeded the full cost of CP with more efficient training or higher participant volume. A positive INB showed telephone delivery is efficient and may increase accessibility to decision support services, particularly in rural communities.


Click on the PDF icon at the top of this introduction to read the full article.



 

Background Decision support interventions help patients who are facing difficult treatment decisions and improve shared decision making. There is little evidence of the economic impact of these interventions.

Objective To determine the costs of providing a decision support intervention in the form of consultation planning (CP) and consultation planning with recording and summary (CPRS) to women with breast cancer and to compare the cost benefit of CP and CPRS by telephone versus in person.

Methods Sixty-eight women with breast cancer who were being treated at a rural cancer resource center were randomized to CP in person or by telephone. All participants were then provided with an audio-recording of the physician consultation along with a typed summary for the full intervention (CPRS). Surveys completed by the participants and center staff provided data for measuring costs and willingness-to-pay (WTP) benefits. Societal perspective costs and incremental net benefit (INB) across delivery methods was determined.

Results Total CP costs were $208.72 for telephone and $264.00 for in-person delivery. Significantly lower telephone-group costs (P ˂ .001) were a result of lower participant travel expenses. Participants were willing to pay $154.12 for telephone and $144.03 for in-person CP (P = .85). WTP did not exceed costs of either delivery method compared with no intervention. INB of providing CP for telephone versus in person was $65.37, favoring telephone delivery. Sensitivity analysis revealed that with more efficient CP training, WTP became greater than the costs of delivering CP by telephone versus no intervention.

Limitations There may be some income distribution effects in the measurement of WTP.

Conclusions Providing CP by telephone was significantly less costly with no significant difference in benefit. Participants’ WTP only exceeded the full cost of CP with more efficient training or higher participant volume. A positive INB showed telephone delivery is efficient and may increase accessibility to decision support services, particularly in rural communities.


Click on the PDF icon at the top of this introduction to read the full article.



 

A healthy collaboration between hospitalists and pharmacists can generate cost savings and promote positive outcomes, such as preventing adverse drug events and improving care transitions, says Jonathan Edwards, PharmD, BCPS, a clinical pharmacy specialist at Huntsville Hospital in Alabama.

At the 2012 national conference of the American College of Clinical Pharmacy in Hollywood, Fla., Edwards presented a poster that detailed the effectiveness of such interdisciplinary collaboration at Huntsville Hospital, where pharmacists and physicians developed six order sets, a collaborative practice, and a patient interaction program from November 2011 to February 2012. During the study period, researchers documented a total cost savings of $9,825 resulting from 156 patient interventions.

Edwards’ collaborative study at Huntsville started with two physicians who had launched a service teaching hospitalists what pharmacists do, and how they could help in their efforts.

“We got together and developed an order set for treating acute alcohol withdrawal. That went well, so we did five more order sets,” Edwards says. “Then we thought: What if pharmacists got more involved by meeting directly with patients in the hospital to optimize their medication management and help them reach their goals for treatment? We now evaluate patients on the hospitalist service in three units.”

For Edwards, key factors that make the hospitalist-pharmacist relationship work include communicating the pharmacist’s availability to help with the hospitalist’s patients, identifying the physician’s openness to help, and clarifying how the physician prefers to be contacted.

Last October, the American Society of Health-System Pharmacists (ASHP) and the American Pharmacists Association (APhA) recognized eight care-transitions programs for best practices that improved patient outcomes and reduced hospital readmissions as part of the Medication Management in Care Transitions (MMCT) Project.

“The MMCT project highlights the valuable role pharmacists can play in addressing medication-related problems that can lead to hospital readmissions,” APhA chief executive officer Thomas E. Menighan, BSPharm, MBA, ScD (Hon), FAPhA, said in a news release. “By putting together these best practices, our goal is to provide a model for better coordination of care and better connectivity between pharmacists and healthcare providers in different practice settings that leads to improved patient health.”

Visit our website for more information about maximizing patient care through pharmacist-hospitalist collaboration.

Larry Beresford is a freelance writer in Oakland, Calif.

Articles first published in the Jan. 16, 2013, edition of The Hospitalist eWire.

A healthy collaboration between hospitalists and pharmacists can generate cost savings and promote positive outcomes, such as preventing adverse drug events and improving care transitions, says Jonathan Edwards, PharmD, BCPS, a clinical pharmacy specialist at Huntsville Hospital in Alabama.

At the 2012 national conference of the American College of Clinical Pharmacy in Hollywood, Fla., Edwards presented a poster that detailed the effectiveness of such interdisciplinary collaboration at Huntsville Hospital, where pharmacists and physicians developed six order sets, a collaborative practice, and a patient interaction program from November 2011 to February 2012. During the study period, researchers documented a total cost savings of $9,825 resulting from 156 patient interventions.

Edwards’ collaborative study at Huntsville started with two physicians who had launched a service teaching hospitalists what pharmacists do, and how they could help in their efforts.

“We got together and developed an order set for treating acute alcohol withdrawal. That went well, so we did five more order sets,” Edwards says. “Then we thought: What if pharmacists got more involved by meeting directly with patients in the hospital to optimize their medication management and help them reach their goals for treatment? We now evaluate patients on the hospitalist service in three units.”

For Edwards, key factors that make the hospitalist-pharmacist relationship work include communicating the pharmacist’s availability to help with the hospitalist’s patients, identifying the physician’s openness to help, and clarifying how the physician prefers to be contacted.

Last October, the American Society of Health-System Pharmacists (ASHP) and the American Pharmacists Association (APhA) recognized eight care-transitions programs for best practices that improved patient outcomes and reduced hospital readmissions as part of the Medication Management in Care Transitions (MMCT) Project.

“The MMCT project highlights the valuable role pharmacists can play in addressing medication-related problems that can lead to hospital readmissions,” APhA chief executive officer Thomas E. Menighan, BSPharm, MBA, ScD (Hon), FAPhA, said in a news release. “By putting together these best practices, our goal is to provide a model for better coordination of care and better connectivity between pharmacists and healthcare providers in different practice settings that leads to improved patient health.”

Visit our website for more information about maximizing patient care through pharmacist-hospitalist collaboration.

Larry Beresford is a freelance writer in Oakland, Calif.

Articles first published in the Jan. 16, 2013, edition of The Hospitalist eWire.

A healthy collaboration between hospitalists and pharmacists can generate cost savings and promote positive outcomes, such as preventing adverse drug events and improving care transitions, says Jonathan Edwards, PharmD, BCPS, a clinical pharmacy specialist at Huntsville Hospital in Alabama.

At the 2012 national conference of the American College of Clinical Pharmacy in Hollywood, Fla., Edwards presented a poster that detailed the effectiveness of such interdisciplinary collaboration at Huntsville Hospital, where pharmacists and physicians developed six order sets, a collaborative practice, and a patient interaction program from November 2011 to February 2012. During the study period, researchers documented a total cost savings of $9,825 resulting from 156 patient interventions.

Edwards’ collaborative study at Huntsville started with two physicians who had launched a service teaching hospitalists what pharmacists do, and how they could help in their efforts.

“We got together and developed an order set for treating acute alcohol withdrawal. That went well, so we did five more order sets,” Edwards says. “Then we thought: What if pharmacists got more involved by meeting directly with patients in the hospital to optimize their medication management and help them reach their goals for treatment? We now evaluate patients on the hospitalist service in three units.”

For Edwards, key factors that make the hospitalist-pharmacist relationship work include communicating the pharmacist’s availability to help with the hospitalist’s patients, identifying the physician’s openness to help, and clarifying how the physician prefers to be contacted.

Last October, the American Society of Health-System Pharmacists (ASHP) and the American Pharmacists Association (APhA) recognized eight care-transitions programs for best practices that improved patient outcomes and reduced hospital readmissions as part of the Medication Management in Care Transitions (MMCT) Project.

“The MMCT project highlights the valuable role pharmacists can play in addressing medication-related problems that can lead to hospital readmissions,” APhA chief executive officer Thomas E. Menighan, BSPharm, MBA, ScD (Hon), FAPhA, said in a news release. “By putting together these best practices, our goal is to provide a model for better coordination of care and better connectivity between pharmacists and healthcare providers in different practice settings that leads to improved patient health.”

Visit our website for more information about maximizing patient care through pharmacist-hospitalist collaboration.

Larry Beresford is a freelance writer in Oakland, Calif.

Articles first published in the Jan. 16, 2013, edition of The Hospitalist eWire.

Physicians who rank poorly in their communication skills with patients were associated with reduced rates of medication adherence in a new report.

A cross-sectional study of nearly 9,4000 patients in the Diabetes Study of Northern California (DISTANCE) found roughly 30% of patients who gave their physicians poor ratings when it came to involving them in decisions, understanding their problems with medications, and eliciting their trust were less likely to refill their cardiometabolic medications than those whose doctors were deemed to be good communicators, researchers found. For each 10-point decrease in the Consumer Assessment of Healthcare Providers and Systems Survey (CAHPS), the prevalence of poor medication adherence increased by 0.9% (P +0.1), the researchers added.

“One of the tricks is that medication adherence is an inherently physician-centric concept,” says lead author Neda Ratanawongsa, MD, MPH, assistant professor in the department of medicine at the University of California at San Francisco (UCSF). “We’re asking you to take medicine that we think will be best for you. That’s been the way that physicians operate for years, often appropriately so. But part of this is figuring out how to encourage the patients to disclose their decision that ‘Yes, I do want to take that medicine’ or ‘No, here’s why I don’t want to take that medicine.’”

Dr. Ratanawongsa adds that hospitalists and other physicians have to develop a sense of trust with patients to build relationships. Future studies could then track patient satisfaction and adherence over time to see if a corollary exists. Also, she says, hospitalists shouldn’t be discouraged that most of their relationships aren’t long-term ones like those found in other specialties.

“I wouldn’t underestimate the impact a hospitalist could have, whether one-time interaction or not, to change an existing therapy program,” Dr. Ratanawongsa says. “It’s important for hospitalists to understand the power of their words.”

Richard Quinn is a freelance writer in New Jersey.

Physicians who rank poorly in their communication skills with patients were associated with reduced rates of medication adherence in a new report.

A cross-sectional study of nearly 9,4000 patients in the Diabetes Study of Northern California (DISTANCE) found roughly 30% of patients who gave their physicians poor ratings when it came to involving them in decisions, understanding their problems with medications, and eliciting their trust were less likely to refill their cardiometabolic medications than those whose doctors were deemed to be good communicators, researchers found. For each 10-point decrease in the Consumer Assessment of Healthcare Providers and Systems Survey (CAHPS), the prevalence of poor medication adherence increased by 0.9% (P +0.1), the researchers added.

“One of the tricks is that medication adherence is an inherently physician-centric concept,” says lead author Neda Ratanawongsa, MD, MPH, assistant professor in the department of medicine at the University of California at San Francisco (UCSF). “We’re asking you to take medicine that we think will be best for you. That’s been the way that physicians operate for years, often appropriately so. But part of this is figuring out how to encourage the patients to disclose their decision that ‘Yes, I do want to take that medicine’ or ‘No, here’s why I don’t want to take that medicine.’”

Dr. Ratanawongsa adds that hospitalists and other physicians have to develop a sense of trust with patients to build relationships. Future studies could then track patient satisfaction and adherence over time to see if a corollary exists. Also, she says, hospitalists shouldn’t be discouraged that most of their relationships aren’t long-term ones like those found in other specialties.

“I wouldn’t underestimate the impact a hospitalist could have, whether one-time interaction or not, to change an existing therapy program,” Dr. Ratanawongsa says. “It’s important for hospitalists to understand the power of their words.”

Richard Quinn is a freelance writer in New Jersey.

Physicians who rank poorly in their communication skills with patients were associated with reduced rates of medication adherence in a new report.

A cross-sectional study of nearly 9,4000 patients in the Diabetes Study of Northern California (DISTANCE) found roughly 30% of patients who gave their physicians poor ratings when it came to involving them in decisions, understanding their problems with medications, and eliciting their trust were less likely to refill their cardiometabolic medications than those whose doctors were deemed to be good communicators, researchers found. For each 10-point decrease in the Consumer Assessment of Healthcare Providers and Systems Survey (CAHPS), the prevalence of poor medication adherence increased by 0.9% (P +0.1), the researchers added.

“One of the tricks is that medication adherence is an inherently physician-centric concept,” says lead author Neda Ratanawongsa, MD, MPH, assistant professor in the department of medicine at the University of California at San Francisco (UCSF). “We’re asking you to take medicine that we think will be best for you. That’s been the way that physicians operate for years, often appropriately so. But part of this is figuring out how to encourage the patients to disclose their decision that ‘Yes, I do want to take that medicine’ or ‘No, here’s why I don’t want to take that medicine.’”

Dr. Ratanawongsa adds that hospitalists and other physicians have to develop a sense of trust with patients to build relationships. Future studies could then track patient satisfaction and adherence over time to see if a corollary exists. Also, she says, hospitalists shouldn’t be discouraged that most of their relationships aren’t long-term ones like those found in other specialties.

“I wouldn’t underestimate the impact a hospitalist could have, whether one-time interaction or not, to change an existing therapy program,” Dr. Ratanawongsa says. “It’s important for hospitalists to understand the power of their words.”

Richard Quinn is a freelance writer in New Jersey.

Rajan Gurunathan, MD, was an undergraduate student at Johns Hopkins University in Baltimore in the early 1990s weighing his career options.

“I went through a lot of permutations, actually,” he says. “Scientist, clinical researcher, doctor, physician/scientist—all of those things entered my mind at some point.”

He applied to dual-track MD and PhD programs, but ultimately decided that interacting with people—patients in particular—was the goal for him. He earned his medical degree from UMDNJ-Robert Wood Johnson Medical School in Camden, N.J., and completed his internship in the department of medicine at St. Luke’s-Roosevelt Hospital Center in New York City, not far from where he grew up as a child in northern New Jersey.

And he never left.

I’ve always enjoyed the collegiality of a hospital environment in terms of multiple disciplines working together in ways to help care for patients. It’s a paradox in the sense that it’s fascinating to see disease and be able to be impactful in that way, but it’s also unfortunate sometimes to see what people have to go through.

—Anthony Back, MD, professor of medicine, University of Washington, Seattle

Dr. Gurunathan has risen through the ranks at St. Luke’s-Roosevelt, from resident to chief resident to chief of the section of hospital medicine. He is a faculty member for the Clinical Quality Fellowship Program at the Great New York Hospital Association and an assistant clinical professor of medicine at Columbia University College of Physicians and Surgeons in New York.

His long tenure at St. Luke’s-Roosevelt has been “an incredible experience because I really get a sense and feeling of commitment from the community,” he adds. “I’ve seen it grow over time and see how the needs have changed and how the service the hospital has been able to provide has only grown over time.”

After several years of presenting posters at SHM’s annual meetings, Dr. Gurunathan joined Team Hospitalist in April 2012 to become an even more active member of his specialty.

QUESTION: When you started as an intern 15 years ago, did you expect that you’d still be at the same institution?

Answer: No, I wouldn’t have expected that at all. In fact, there was a time where I was briefly considering a general medicine fellowship at Johns Hopkins, and I was prepared to go there. And family circumstances, etc., made me decide not to move on and to make a commitment and join the department as faculty, first as a chief and then as faculty. And I was really lucky to have those opportunities, because while my course didn’t go exactly the way that I’d planned, I wouldn’t have changed a thing.

Q: When you now deal with the residents and younger staff members, what’s that experience like for you?

A: It’s a really neat experience, and often brings a chuckle to my face when I see that they’re frustrated about the same things, because I can certainly commiserate. But I can really also see the value of what they provide every day, and having been in their shoes, I know a little bit about what they’ve been through and the work that they do. So I have a real appreciation for that.

Q: What brought you to hospital medicine?

A: I’ve always enjoyed the collegiality of a hospital environment in terms of multiple disciplines working together in ways to help care for patients. It’s a paradox in the sense that it’s fascinating to see disease and be able to be impactful in that way, but it’s also unfortunate sometimes to see what people have to go through.

Q: Is there something specific about the setting that’s kept you in the academic world?

A: A lot of things, actually. As I mentioned, hospitals in general should have a collegial nature. Again, it’s a really nice place where people share a unique common goal of banding together and fighting a goal, and academic departments are the same. So it’s being with people with like-minded intellectual interests. And we’re fortunate enough to have a number of strong mentors within the department who have had a lot of clinical training and bring a lot of experience and a wealth of knowledge, and being able to utilize their experience and draw from their experiences only makes people better clinicians. And we’re fortunate enough to have a pretty supportive department in general where there is a lot of collegiality and camaraderie.

Q: As an administrator, what is the value of being an SHM member, to you?

A: I think what I’ve seen administratively is the changing face of healthcare and how hospitals are going to need to continue to transform with time due to things that are both regulatory- and quality-of-care-based, in terms of improving outcomes and keeping people healthy. SHM has really embraced [those changes] and taken them head-on for really important reasons, not only in terms of helping people adapt to the changing landscape, but also training them in the ways that we need to be thinking about problems now and in the future.

Q: You’ve attended multiple annual meetings and presented posters. What value have you taken out of them, and would you recommend the experience to others?

A: Absolutely. I think as people develop, it’s good to always learn new skills, and my clinical research is an area that I would actually like to build up. So I’ve had a little bit of exposure, and it’s been nice to be able to draw from the resources of SHM and be able to partake. We presented something last year, which was a really neat experience, and we’re looking to bring some new faculty this year and encourage them to get involved in the scholarship process. These are the kinds of things that can really help hone skills, and that’s a good thing.

Q: Once you’re inside the doors of a New York City hospital, is daily practice much different than anywhere else?

A: I would say yes and no. I would say no in that I think all hospitals are really neat places and really incredible places. I heard somebody say once at a talk that hospitals were places of refuge, and I really do believe that. That being said, I think there is something slightly unique about New York City in a lot of ways. Certainly the challenges that New York City hospitals face are somewhat unique in terms of patient population, difficulty in socioeconomic factors, insurance issues. I think they are really fun places to work, but they’re not for the faint of heart.

Richard Quinn is a freelance writer in New Jersey.

Rajan Gurunathan, MD, was an undergraduate student at Johns Hopkins University in Baltimore in the early 1990s weighing his career options.

“I went through a lot of permutations, actually,” he says. “Scientist, clinical researcher, doctor, physician/scientist—all of those things entered my mind at some point.”

He applied to dual-track MD and PhD programs, but ultimately decided that interacting with people—patients in particular—was the goal for him. He earned his medical degree from UMDNJ-Robert Wood Johnson Medical School in Camden, N.J., and completed his internship in the department of medicine at St. Luke’s-Roosevelt Hospital Center in New York City, not far from where he grew up as a child in northern New Jersey.

And he never left.

I’ve always enjoyed the collegiality of a hospital environment in terms of multiple disciplines working together in ways to help care for patients. It’s a paradox in the sense that it’s fascinating to see disease and be able to be impactful in that way, but it’s also unfortunate sometimes to see what people have to go through.

—Anthony Back, MD, professor of medicine, University of Washington, Seattle

Dr. Gurunathan has risen through the ranks at St. Luke’s-Roosevelt, from resident to chief resident to chief of the section of hospital medicine. He is a faculty member for the Clinical Quality Fellowship Program at the Great New York Hospital Association and an assistant clinical professor of medicine at Columbia University College of Physicians and Surgeons in New York.

His long tenure at St. Luke’s-Roosevelt has been “an incredible experience because I really get a sense and feeling of commitment from the community,” he adds. “I’ve seen it grow over time and see how the needs have changed and how the service the hospital has been able to provide has only grown over time.”

After several years of presenting posters at SHM’s annual meetings, Dr. Gurunathan joined Team Hospitalist in April 2012 to become an even more active member of his specialty.

QUESTION: When you started as an intern 15 years ago, did you expect that you’d still be at the same institution?

Answer: No, I wouldn’t have expected that at all. In fact, there was a time where I was briefly considering a general medicine fellowship at Johns Hopkins, and I was prepared to go there. And family circumstances, etc., made me decide not to move on and to make a commitment and join the department as faculty, first as a chief and then as faculty. And I was really lucky to have those opportunities, because while my course didn’t go exactly the way that I’d planned, I wouldn’t have changed a thing.

Q: When you now deal with the residents and younger staff members, what’s that experience like for you?

A: It’s a really neat experience, and often brings a chuckle to my face when I see that they’re frustrated about the same things, because I can certainly commiserate. But I can really also see the value of what they provide every day, and having been in their shoes, I know a little bit about what they’ve been through and the work that they do. So I have a real appreciation for that.

Q: What brought you to hospital medicine?

A: I’ve always enjoyed the collegiality of a hospital environment in terms of multiple disciplines working together in ways to help care for patients. It’s a paradox in the sense that it’s fascinating to see disease and be able to be impactful in that way, but it’s also unfortunate sometimes to see what people have to go through.

Q: Is there something specific about the setting that’s kept you in the academic world?

A: A lot of things, actually. As I mentioned, hospitals in general should have a collegial nature. Again, it’s a really nice place where people share a unique common goal of banding together and fighting a goal, and academic departments are the same. So it’s being with people with like-minded intellectual interests. And we’re fortunate enough to have a number of strong mentors within the department who have had a lot of clinical training and bring a lot of experience and a wealth of knowledge, and being able to utilize their experience and draw from their experiences only makes people better clinicians. And we’re fortunate enough to have a pretty supportive department in general where there is a lot of collegiality and camaraderie.

Q: As an administrator, what is the value of being an SHM member, to you?

A: I think what I’ve seen administratively is the changing face of healthcare and how hospitals are going to need to continue to transform with time due to things that are both regulatory- and quality-of-care-based, in terms of improving outcomes and keeping people healthy. SHM has really embraced [those changes] and taken them head-on for really important reasons, not only in terms of helping people adapt to the changing landscape, but also training them in the ways that we need to be thinking about problems now and in the future.

Q: You’ve attended multiple annual meetings and presented posters. What value have you taken out of them, and would you recommend the experience to others?

A: Absolutely. I think as people develop, it’s good to always learn new skills, and my clinical research is an area that I would actually like to build up. So I’ve had a little bit of exposure, and it’s been nice to be able to draw from the resources of SHM and be able to partake. We presented something last year, which was a really neat experience, and we’re looking to bring some new faculty this year and encourage them to get involved in the scholarship process. These are the kinds of things that can really help hone skills, and that’s a good thing.

Q: Once you’re inside the doors of a New York City hospital, is daily practice much different than anywhere else?

A: I would say yes and no. I would say no in that I think all hospitals are really neat places and really incredible places. I heard somebody say once at a talk that hospitals were places of refuge, and I really do believe that. That being said, I think there is something slightly unique about New York City in a lot of ways. Certainly the challenges that New York City hospitals face are somewhat unique in terms of patient population, difficulty in socioeconomic factors, insurance issues. I think they are really fun places to work, but they’re not for the faint of heart.

Richard Quinn is a freelance writer in New Jersey.

Rajan Gurunathan, MD, was an undergraduate student at Johns Hopkins University in Baltimore in the early 1990s weighing his career options.

“I went through a lot of permutations, actually,” he says. “Scientist, clinical researcher, doctor, physician/scientist—all of those things entered my mind at some point.”

He applied to dual-track MD and PhD programs, but ultimately decided that interacting with people—patients in particular—was the goal for him. He earned his medical degree from UMDNJ-Robert Wood Johnson Medical School in Camden, N.J., and completed his internship in the department of medicine at St. Luke’s-Roosevelt Hospital Center in New York City, not far from where he grew up as a child in northern New Jersey.

And he never left.

I’ve always enjoyed the collegiality of a hospital environment in terms of multiple disciplines working together in ways to help care for patients. It’s a paradox in the sense that it’s fascinating to see disease and be able to be impactful in that way, but it’s also unfortunate sometimes to see what people have to go through.

—Anthony Back, MD, professor of medicine, University of Washington, Seattle

Dr. Gurunathan has risen through the ranks at St. Luke’s-Roosevelt, from resident to chief resident to chief of the section of hospital medicine. He is a faculty member for the Clinical Quality Fellowship Program at the Great New York Hospital Association and an assistant clinical professor of medicine at Columbia University College of Physicians and Surgeons in New York.

His long tenure at St. Luke’s-Roosevelt has been “an incredible experience because I really get a sense and feeling of commitment from the community,” he adds. “I’ve seen it grow over time and see how the needs have changed and how the service the hospital has been able to provide has only grown over time.”

After several years of presenting posters at SHM’s annual meetings, Dr. Gurunathan joined Team Hospitalist in April 2012 to become an even more active member of his specialty.

QUESTION: When you started as an intern 15 years ago, did you expect that you’d still be at the same institution?

Answer: No, I wouldn’t have expected that at all. In fact, there was a time where I was briefly considering a general medicine fellowship at Johns Hopkins, and I was prepared to go there. And family circumstances, etc., made me decide not to move on and to make a commitment and join the department as faculty, first as a chief and then as faculty. And I was really lucky to have those opportunities, because while my course didn’t go exactly the way that I’d planned, I wouldn’t have changed a thing.

Q: When you now deal with the residents and younger staff members, what’s that experience like for you?

A: It’s a really neat experience, and often brings a chuckle to my face when I see that they’re frustrated about the same things, because I can certainly commiserate. But I can really also see the value of what they provide every day, and having been in their shoes, I know a little bit about what they’ve been through and the work that they do. So I have a real appreciation for that.

Q: What brought you to hospital medicine?

A: I’ve always enjoyed the collegiality of a hospital environment in terms of multiple disciplines working together in ways to help care for patients. It’s a paradox in the sense that it’s fascinating to see disease and be able to be impactful in that way, but it’s also unfortunate sometimes to see what people have to go through.

Q: Is there something specific about the setting that’s kept you in the academic world?

A: A lot of things, actually. As I mentioned, hospitals in general should have a collegial nature. Again, it’s a really nice place where people share a unique common goal of banding together and fighting a goal, and academic departments are the same. So it’s being with people with like-minded intellectual interests. And we’re fortunate enough to have a number of strong mentors within the department who have had a lot of clinical training and bring a lot of experience and a wealth of knowledge, and being able to utilize their experience and draw from their experiences only makes people better clinicians. And we’re fortunate enough to have a pretty supportive department in general where there is a lot of collegiality and camaraderie.

Q: As an administrator, what is the value of being an SHM member, to you?

A: I think what I’ve seen administratively is the changing face of healthcare and how hospitals are going to need to continue to transform with time due to things that are both regulatory- and quality-of-care-based, in terms of improving outcomes and keeping people healthy. SHM has really embraced [those changes] and taken them head-on for really important reasons, not only in terms of helping people adapt to the changing landscape, but also training them in the ways that we need to be thinking about problems now and in the future.

Q: You’ve attended multiple annual meetings and presented posters. What value have you taken out of them, and would you recommend the experience to others?

A: Absolutely. I think as people develop, it’s good to always learn new skills, and my clinical research is an area that I would actually like to build up. So I’ve had a little bit of exposure, and it’s been nice to be able to draw from the resources of SHM and be able to partake. We presented something last year, which was a really neat experience, and we’re looking to bring some new faculty this year and encourage them to get involved in the scholarship process. These are the kinds of things that can really help hone skills, and that’s a good thing.

Q: Once you’re inside the doors of a New York City hospital, is daily practice much different than anywhere else?

A: I would say yes and no. I would say no in that I think all hospitals are really neat places and really incredible places. I heard somebody say once at a talk that hospitals were places of refuge, and I really do believe that. That being said, I think there is something slightly unique about New York City in a lot of ways. Certainly the challenges that New York City hospitals face are somewhat unique in terms of patient population, difficulty in socioeconomic factors, insurance issues. I think they are really fun places to work, but they’re not for the faint of heart.

Richard Quinn is a freelance writer in New Jersey.

New oral anticoagulants promise to impact hospitalists and their patients—but the question is how much

When the FDA gave the nod to factor Xa-inhibitor rivaroxaban in November for use in treating acute DVT and pulmonary embolism (PE), it was just the latest development in the swiftly evolving world of oral anticoagulants—a world that hospitalists had better get used to living in, and quick.

As many as 80% of the patients that hospitalists encounter are on some kind of anticoagulant, experts say. But the extent to which the emergence of the new drugs— particularly rivaroxaban, which also is approved for stroke prevention in nonvalvular atrial fibrillation (afib) and for DVT and PE prevention in knee and hip replacement patients—will affect the daily routines of hospitalists remains to be seen.

Hospitalists specializing in VTE prevention and vascular experts say that the new drugs will make life simpler for hospitalists in some ways, mainly because for some patients, a pill will replace the injectable enoxaparin that has been used to bridge patients to warfarin. But with more options available, things will become more complicated as well, they say.

Approvals for the new agents, which aim to replace warfarin and its need for constant monitoring and concern over drug and food interactions, have been coming rapid-fire. Along with rivaroxaban in the new oral anticoagulant group are dabigatran, approved in late 2010 for stroke prevention in nonvalvular afib, and apixaban, which is expected to be approved for the same indication this year.

“Of all three drugs, [rivaroxaban] has the broadest indications for use,” said Hiren Shah, MD, assistant professor of medicine at Northwestern University’s Feinberg School of Medicine and medical director of hospital medicine at Northwestern Memorial Hospital in Chicago. “Because of that, it’s likely that it’s going to be the agent that will be adopted much more broadly and more easily than dabigatran.”

But apixaban might come on strong in the U.S. when it’s approved because it shows better promise for patients with renal impairment and has a lower risk of intracranial hemorrhage, says Geno Merli, MD, director of the Jefferson Center for Vascular Disease and chief medical officer at Thomas Jefferson University Hospital in Philadelphia.

“I think the two other [manufacturers] are afraid of apixaban because apixaban’s safety profile was much better,” he says.

Steven Deitelzweig, MD, FACP, SFHM, secretary of the Gulf State chapter of SHM and a DVT prevention specialist at Ochsner Health System New Orleans, says hurdles to adoption of the new agents will include whether a system is integrated and can assure appropriate follow-up and concerns over proper patient selection and cost, as the cost-benefit analyses haven’t been done yet.

“The learning curve, or the adoption curve, is really going to be very variable around the country,” he says.

Experts agree changes are on the way as the new anticoagulants gain more traction. Here are some things they say hospitalists should watch out for.

Care and Discharge

Dr. Shah says the availability of the oral agents will streamline care and discharge of patients.

“The care and coordination process that needs to occur with the use of parenteral agents and warfarin is significantly more complex than the patient education and care coordination that will be required with the new oral anticoagulants,” he says. “That’s where there’s a significant time savings.”

Ian Jenkins, MD, assistant professor in the division of hospital medicine at the University of California at San Diego, says the windfall of time saved might not hit hospitalists directly, at least at some centers.

“The education is being done by pharmacy here for warfarin, and nurses handle enoxaparin injection teaching,” he says. “So the workload that benefits may be that of our colleagues.”

Dr. Shah notes that the responsibility in patient counseling ultimately falls within hospitalists’ purview, so he predicts that any greater simplicity in that regard would help hospitalists.

Who Ends up Hospitalized?

The option of oral agents might help diminish the number of patients who have to stay in the hospital for enoxaparin injections that bridge them to warfarin, a topic at a recent roundtable discussion Dr. Shah attended.

“It was shocking to me that I have many colleagues throughout the country who have patients who are in the hospital simply to get parenteral injections because they can’t take them themselves at home and have no loved ones or friends to help them,” he says.

Dr. Merli agrees that the new agents might affect hospitalists’ patient census. Many patients, he says, will be discharged straight from the ED.

“The DVT patients probably won’t get [admitted]. You’re going to put them on rivaroxaban and send them home,” he says. “You’re not going to get [admitted] with a DVT anymore, unless it’s extensive. And if it’s an extensive DVT, you’re not going to get rivaroxaban. You’re going to get enoxaparin or you’re going to get thrombolytics therapy followed by IV heparin followed by enoxaparin. So I don’t see rivaroxaban jumping into the marketplace and being a boon to hospitalists immediately.”

If patients skip hospitalization and are discharged straight from the ED, Dr. Deitelzweig says, “there will be patients who will backfill those spots.”

“I think most of the people will come in as observation status, if not inpatient,” he says, although simpler DVT patients will be likelier candidates for discharge from the ER. He predicts that stays might be shorter, though.

But Dr. Merli says hospitalists shouldn’t expect a big effect on length of stay.

“I don’t think you’re going to reduce dramatically length of stay because you have an oral pill,” he says.

QI Initiatives

What might be a boon, though, are opportunities for quality-improvement (QI) initiatives related to the new therapies, Dr. Jenkins says. “Many of these projects that are being done with anticoagulants … do focus on warfarin safety; it’s a frequent part of readmission and patient harm,” he says. “Having it much simpler to treat and educate these patients is actually going to be a boon, I think, for hospitalists working on quality-improvement projects, and for people who do that education, whether that is a hospitalist or a pharmacist or some other member of the staff.”

There are downsides, though, he notes. One is cost. Another is reversibility. Warfarin can be easily reversed in the event of a bleed, but that’s not the case with rivaroxaban and dabigatran. And none of the new therapies are suitable for patients with renal failure.

“Right now, we’re stuck with IV heparin and Coumadin in the hospital, and rivaroxaban won’t change this,” he says. “Rivaroxaban patients one might help with PCC; but with dabigatran, I don’t think much will help besides time and dialysis, which is dangerous in unstable anticoagulated patients.”

Dr. Shah, though, says he’s aware of only two times that bleeding reversal protocols—based on anecdotal evidence, because no method has been scientifically proven—had to be invoked at Northwestern in the past year.

It might be “more of a theoretical problem than one in reality,” he explains, “simply because we have not found the need to reverse oral anticoagulants very often given their short half-lives.”

The new agents, all the experts agree, will require hospitalists to stay on their toes.

“There are so many different facets in each case, whether it’s the age or the renal function or whether there’s a fall risk and what their compliance is, what their funding is, what the exact indication is,” Dr. Jenkins says. “Keeping up with those things is actually quite challenging.”

His main resources are the American College of Chest Physicians’ guidelines on anticoagulants, his center’s own protocols, and the primary literature for the main trials (see “Additional Reading,” right). He also looks to the inpatient pharmacist for guidance.

Dr. Shah says it is important to be aware of the patient-inclusion criteria, study design, and outcomes measured for each agent through their trials.

“There is a lot of information out there, and there are very subtle aspects of some of these trials and you’ve got to really understand: Does it apply to the patient that is front of me?” he said. “There’s a lot to know, there’s no doubt about it.”

Thomas R. Collins is a freelance writer in South Florida.

New oral anticoagulants promise to impact hospitalists and their patients—but the question is how much

When the FDA gave the nod to factor Xa-inhibitor rivaroxaban in November for use in treating acute DVT and pulmonary embolism (PE), it was just the latest development in the swiftly evolving world of oral anticoagulants—a world that hospitalists had better get used to living in, and quick.

As many as 80% of the patients that hospitalists encounter are on some kind of anticoagulant, experts say. But the extent to which the emergence of the new drugs— particularly rivaroxaban, which also is approved for stroke prevention in nonvalvular atrial fibrillation (afib) and for DVT and PE prevention in knee and hip replacement patients—will affect the daily routines of hospitalists remains to be seen.

Hospitalists specializing in VTE prevention and vascular experts say that the new drugs will make life simpler for hospitalists in some ways, mainly because for some patients, a pill will replace the injectable enoxaparin that has been used to bridge patients to warfarin. But with more options available, things will become more complicated as well, they say.

Approvals for the new agents, which aim to replace warfarin and its need for constant monitoring and concern over drug and food interactions, have been coming rapid-fire. Along with rivaroxaban in the new oral anticoagulant group are dabigatran, approved in late 2010 for stroke prevention in nonvalvular afib, and apixaban, which is expected to be approved for the same indication this year.

“Of all three drugs, [rivaroxaban] has the broadest indications for use,” said Hiren Shah, MD, assistant professor of medicine at Northwestern University’s Feinberg School of Medicine and medical director of hospital medicine at Northwestern Memorial Hospital in Chicago. “Because of that, it’s likely that it’s going to be the agent that will be adopted much more broadly and more easily than dabigatran.”

But apixaban might come on strong in the U.S. when it’s approved because it shows better promise for patients with renal impairment and has a lower risk of intracranial hemorrhage, says Geno Merli, MD, director of the Jefferson Center for Vascular Disease and chief medical officer at Thomas Jefferson University Hospital in Philadelphia.

“I think the two other [manufacturers] are afraid of apixaban because apixaban’s safety profile was much better,” he says.

Steven Deitelzweig, MD, FACP, SFHM, secretary of the Gulf State chapter of SHM and a DVT prevention specialist at Ochsner Health System New Orleans, says hurdles to adoption of the new agents will include whether a system is integrated and can assure appropriate follow-up and concerns over proper patient selection and cost, as the cost-benefit analyses haven’t been done yet.

“The learning curve, or the adoption curve, is really going to be very variable around the country,” he says.

Experts agree changes are on the way as the new anticoagulants gain more traction. Here are some things they say hospitalists should watch out for.

Care and Discharge

Dr. Shah says the availability of the oral agents will streamline care and discharge of patients.

“The care and coordination process that needs to occur with the use of parenteral agents and warfarin is significantly more complex than the patient education and care coordination that will be required with the new oral anticoagulants,” he says. “That’s where there’s a significant time savings.”

Ian Jenkins, MD, assistant professor in the division of hospital medicine at the University of California at San Diego, says the windfall of time saved might not hit hospitalists directly, at least at some centers.

“The education is being done by pharmacy here for warfarin, and nurses handle enoxaparin injection teaching,” he says. “So the workload that benefits may be that of our colleagues.”

Dr. Shah notes that the responsibility in patient counseling ultimately falls within hospitalists’ purview, so he predicts that any greater simplicity in that regard would help hospitalists.

Who Ends up Hospitalized?

The option of oral agents might help diminish the number of patients who have to stay in the hospital for enoxaparin injections that bridge them to warfarin, a topic at a recent roundtable discussion Dr. Shah attended.

“It was shocking to me that I have many colleagues throughout the country who have patients who are in the hospital simply to get parenteral injections because they can’t take them themselves at home and have no loved ones or friends to help them,” he says.

Dr. Merli agrees that the new agents might affect hospitalists’ patient census. Many patients, he says, will be discharged straight from the ED.

“The DVT patients probably won’t get [admitted]. You’re going to put them on rivaroxaban and send them home,” he says. “You’re not going to get [admitted] with a DVT anymore, unless it’s extensive. And if it’s an extensive DVT, you’re not going to get rivaroxaban. You’re going to get enoxaparin or you’re going to get thrombolytics therapy followed by IV heparin followed by enoxaparin. So I don’t see rivaroxaban jumping into the marketplace and being a boon to hospitalists immediately.”

If patients skip hospitalization and are discharged straight from the ED, Dr. Deitelzweig says, “there will be patients who will backfill those spots.”

“I think most of the people will come in as observation status, if not inpatient,” he says, although simpler DVT patients will be likelier candidates for discharge from the ER. He predicts that stays might be shorter, though.

But Dr. Merli says hospitalists shouldn’t expect a big effect on length of stay.

“I don’t think you’re going to reduce dramatically length of stay because you have an oral pill,” he says.

QI Initiatives

What might be a boon, though, are opportunities for quality-improvement (QI) initiatives related to the new therapies, Dr. Jenkins says. “Many of these projects that are being done with anticoagulants … do focus on warfarin safety; it’s a frequent part of readmission and patient harm,” he says. “Having it much simpler to treat and educate these patients is actually going to be a boon, I think, for hospitalists working on quality-improvement projects, and for people who do that education, whether that is a hospitalist or a pharmacist or some other member of the staff.”

There are downsides, though, he notes. One is cost. Another is reversibility. Warfarin can be easily reversed in the event of a bleed, but that’s not the case with rivaroxaban and dabigatran. And none of the new therapies are suitable for patients with renal failure.

“Right now, we’re stuck with IV heparin and Coumadin in the hospital, and rivaroxaban won’t change this,” he says. “Rivaroxaban patients one might help with PCC; but with dabigatran, I don’t think much will help besides time and dialysis, which is dangerous in unstable anticoagulated patients.”

Dr. Shah, though, says he’s aware of only two times that bleeding reversal protocols—based on anecdotal evidence, because no method has been scientifically proven—had to be invoked at Northwestern in the past year.

It might be “more of a theoretical problem than one in reality,” he explains, “simply because we have not found the need to reverse oral anticoagulants very often given their short half-lives.”

The new agents, all the experts agree, will require hospitalists to stay on their toes.

“There are so many different facets in each case, whether it’s the age or the renal function or whether there’s a fall risk and what their compliance is, what their funding is, what the exact indication is,” Dr. Jenkins says. “Keeping up with those things is actually quite challenging.”

His main resources are the American College of Chest Physicians’ guidelines on anticoagulants, his center’s own protocols, and the primary literature for the main trials (see “Additional Reading,” right). He also looks to the inpatient pharmacist for guidance.

Dr. Shah says it is important to be aware of the patient-inclusion criteria, study design, and outcomes measured for each agent through their trials.

“There is a lot of information out there, and there are very subtle aspects of some of these trials and you’ve got to really understand: Does it apply to the patient that is front of me?” he said. “There’s a lot to know, there’s no doubt about it.”

Thomas R. Collins is a freelance writer in South Florida.

New oral anticoagulants promise to impact hospitalists and their patients—but the question is how much

When the FDA gave the nod to factor Xa-inhibitor rivaroxaban in November for use in treating acute DVT and pulmonary embolism (PE), it was just the latest development in the swiftly evolving world of oral anticoagulants—a world that hospitalists had better get used to living in, and quick.

As many as 80% of the patients that hospitalists encounter are on some kind of anticoagulant, experts say. But the extent to which the emergence of the new drugs— particularly rivaroxaban, which also is approved for stroke prevention in nonvalvular atrial fibrillation (afib) and for DVT and PE prevention in knee and hip replacement patients—will affect the daily routines of hospitalists remains to be seen.

Hospitalists specializing in VTE prevention and vascular experts say that the new drugs will make life simpler for hospitalists in some ways, mainly because for some patients, a pill will replace the injectable enoxaparin that has been used to bridge patients to warfarin. But with more options available, things will become more complicated as well, they say.

Approvals for the new agents, which aim to replace warfarin and its need for constant monitoring and concern over drug and food interactions, have been coming rapid-fire. Along with rivaroxaban in the new oral anticoagulant group are dabigatran, approved in late 2010 for stroke prevention in nonvalvular afib, and apixaban, which is expected to be approved for the same indication this year.

“Of all three drugs, [rivaroxaban] has the broadest indications for use,” said Hiren Shah, MD, assistant professor of medicine at Northwestern University’s Feinberg School of Medicine and medical director of hospital medicine at Northwestern Memorial Hospital in Chicago. “Because of that, it’s likely that it’s going to be the agent that will be adopted much more broadly and more easily than dabigatran.”

But apixaban might come on strong in the U.S. when it’s approved because it shows better promise for patients with renal impairment and has a lower risk of intracranial hemorrhage, says Geno Merli, MD, director of the Jefferson Center for Vascular Disease and chief medical officer at Thomas Jefferson University Hospital in Philadelphia.

“I think the two other [manufacturers] are afraid of apixaban because apixaban’s safety profile was much better,” he says.

Steven Deitelzweig, MD, FACP, SFHM, secretary of the Gulf State chapter of SHM and a DVT prevention specialist at Ochsner Health System New Orleans, says hurdles to adoption of the new agents will include whether a system is integrated and can assure appropriate follow-up and concerns over proper patient selection and cost, as the cost-benefit analyses haven’t been done yet.

“The learning curve, or the adoption curve, is really going to be very variable around the country,” he says.

Experts agree changes are on the way as the new anticoagulants gain more traction. Here are some things they say hospitalists should watch out for.

Care and Discharge

Dr. Shah says the availability of the oral agents will streamline care and discharge of patients.

“The care and coordination process that needs to occur with the use of parenteral agents and warfarin is significantly more complex than the patient education and care coordination that will be required with the new oral anticoagulants,” he says. “That’s where there’s a significant time savings.”

Ian Jenkins, MD, assistant professor in the division of hospital medicine at the University of California at San Diego, says the windfall of time saved might not hit hospitalists directly, at least at some centers.

“The education is being done by pharmacy here for warfarin, and nurses handle enoxaparin injection teaching,” he says. “So the workload that benefits may be that of our colleagues.”

Dr. Shah notes that the responsibility in patient counseling ultimately falls within hospitalists’ purview, so he predicts that any greater simplicity in that regard would help hospitalists.

Who Ends up Hospitalized?

The option of oral agents might help diminish the number of patients who have to stay in the hospital for enoxaparin injections that bridge them to warfarin, a topic at a recent roundtable discussion Dr. Shah attended.

“It was shocking to me that I have many colleagues throughout the country who have patients who are in the hospital simply to get parenteral injections because they can’t take them themselves at home and have no loved ones or friends to help them,” he says.

Dr. Merli agrees that the new agents might affect hospitalists’ patient census. Many patients, he says, will be discharged straight from the ED.

“The DVT patients probably won’t get [admitted]. You’re going to put them on rivaroxaban and send them home,” he says. “You’re not going to get [admitted] with a DVT anymore, unless it’s extensive. And if it’s an extensive DVT, you’re not going to get rivaroxaban. You’re going to get enoxaparin or you’re going to get thrombolytics therapy followed by IV heparin followed by enoxaparin. So I don’t see rivaroxaban jumping into the marketplace and being a boon to hospitalists immediately.”

If patients skip hospitalization and are discharged straight from the ED, Dr. Deitelzweig says, “there will be patients who will backfill those spots.”

“I think most of the people will come in as observation status, if not inpatient,” he says, although simpler DVT patients will be likelier candidates for discharge from the ER. He predicts that stays might be shorter, though.

But Dr. Merli says hospitalists shouldn’t expect a big effect on length of stay.

“I don’t think you’re going to reduce dramatically length of stay because you have an oral pill,” he says.

QI Initiatives

What might be a boon, though, are opportunities for quality-improvement (QI) initiatives related to the new therapies, Dr. Jenkins says. “Many of these projects that are being done with anticoagulants … do focus on warfarin safety; it’s a frequent part of readmission and patient harm,” he says. “Having it much simpler to treat and educate these patients is actually going to be a boon, I think, for hospitalists working on quality-improvement projects, and for people who do that education, whether that is a hospitalist or a pharmacist or some other member of the staff.”

There are downsides, though, he notes. One is cost. Another is reversibility. Warfarin can be easily reversed in the event of a bleed, but that’s not the case with rivaroxaban and dabigatran. And none of the new therapies are suitable for patients with renal failure.

“Right now, we’re stuck with IV heparin and Coumadin in the hospital, and rivaroxaban won’t change this,” he says. “Rivaroxaban patients one might help with PCC; but with dabigatran, I don’t think much will help besides time and dialysis, which is dangerous in unstable anticoagulated patients.”

Dr. Shah, though, says he’s aware of only two times that bleeding reversal protocols—based on anecdotal evidence, because no method has been scientifically proven—had to be invoked at Northwestern in the past year.

It might be “more of a theoretical problem than one in reality,” he explains, “simply because we have not found the need to reverse oral anticoagulants very often given their short half-lives.”

The new agents, all the experts agree, will require hospitalists to stay on their toes.

“There are so many different facets in each case, whether it’s the age or the renal function or whether there’s a fall risk and what their compliance is, what their funding is, what the exact indication is,” Dr. Jenkins says. “Keeping up with those things is actually quite challenging.”

His main resources are the American College of Chest Physicians’ guidelines on anticoagulants, his center’s own protocols, and the primary literature for the main trials (see “Additional Reading,” right). He also looks to the inpatient pharmacist for guidance.

Dr. Shah says it is important to be aware of the patient-inclusion criteria, study design, and outcomes measured for each agent through their trials.

“There is a lot of information out there, and there are very subtle aspects of some of these trials and you’ve got to really understand: Does it apply to the patient that is front of me?” he said. “There’s a lot to know, there’s no doubt about it.”

Thomas R. Collins is a freelance writer in South Florida.

In November 2012, the Center for Medicare & Medicaid Services (CMS) finalized its 2013 physician fee schedule with two new transitional-care-management (TCM) codes, 99495 and 99496. These codes provide reimbursement for transitional-care services to patients for 30 days after hospital discharge. CMS estimates that two-thirds of the 10 million Medicare patients discharged annually from hospitals will have TCM services provided by an outpatient doctor. Why might hospitalists be interested in these outpatient codes? Read on.

As a post-discharge provider in a primary-care-based discharge clinic, I can say the new Medicare transitional codes read like our job description. Because I’ve worked in a post-discharge clinic for the past three years, I have learned that post-discharge care requires time and resource allocation beyond routine outpatient care. Because of the unique population we see, on average we bill at a higher level than the rest of the practice. Yet we, like all outpatient providers, remain constrained by the existing billing structure, which is intimately connected to physician face-to-face visits.

Here’s an illustration of a typical afternoon in the post-discharge clinic: A schizophrenic patient presents with renal failure, hypoglycemia, and confusion. Her home visiting nurse (VNA) administers her medications; the patient cannot tell you any of them. While you are calling the VNA to clarify her medications, trying to identify her healthcare proxy, and stopping her ACE inhibitor because her potassium is 5.6, the next patient arrives. She has end-stage liver disease and was recently in the hospital for liver failure, and now has worsening recurrent ascites. After clinic, you call interventional radiology to coordinate a therapeutic paracentesis and change diuretic doses after her labs return. Two weeks later, you arrange a repeat paracentesis, and subsequently a transition to comfort care in a hospice house. For this work, right now, you can at most bill a high-complexity office visit (99215), and the rest of the care coordination—by you, your nurse, or your administrative staff—is not compensated.

How Do the New Codes Work?

CMS created the new TCM codes to begin to change the outpatient fee schedule to emphasize primary care and care coordination for beneficiaries, particularly in the post-hospitalization period. The new TCM codes are a first step toward reimbursement for non-face-to-face activities, which are increasingly important in the evolving healthcare system.

The investment is estimated at more than $1 billion in 2013. The new codes are available to physicians, physician assistants, nurse practitioners, and other advanced-practice nurses only once within the 30 days after hospital discharge. During the 30 days after discharge, the two codes, 99495 and 99496, require a single face-to-face visit within seven days of discharge for the highest-risk patients and within 14 days of discharge for moderate-risk patients. The face-to-face visit is not billed separately. The codes also mandate telephone communication with the patient or caregiver within two business days of hospital discharge; the medical decision-making must be of either moderate or high complexity.

The average reimbursement for the codes will be $132.96 for 99495 and $231.11 for 99496, reflecting a higher wRVU than either hospital discharge day management or high-acuity outpatient visits. The code is billed at the end of the 30 days. The TCM code cannot be billed a second time if a patient is readmitted within the 30 days. Other E/M codes can be billed during the same time period for additional visits as necessary.

What’s the Impact on Hospitalists?

The new codes affect hospitalists in two ways. First, the hospitalists in the growing group of “transitionalists,” many of whom practice in outpatient clinics seeing patients after discharge, will be able to use these codes. As the codes require no pre-existing relationship with the patient, non-primary-care providers will be able to bill these codes, assuming that they fulfill the designated requirements. This concession enables hospitalists to fill a vital role for those patients who have inadequate access to immediate primary care post-hospitalization. It also provides a necessary bridge to appropriate primary care for those patients. This group of patients might be particularly vulnerable to adverse events, including hospital readmission, given their suboptimal connection with their primary-care providers.

Hospitalists who practice entirely as inpatient physicians will not be able to bill these new codes, but they will provide a valuable service to patients by helping identify the physicians who will provide their TCM and documenting this in the discharge documentation, already seen as a key element of discharge day management services.

Do These Codes Change the Business Case for Discharge Clinics?

Discharge clinics, either hospitalist-staffed or otherwise, have been actively discussed in the media in recent years.¹ Even without these transitional codes, discharge clinics have arisen where primary-care access is limited and as a potential, but as yet unproven, solution to high readmission rates. Despite this proliferation, discharge clinics have not yet proven to be cost-effective.

Implementation of these codes could change the calculus for organizations considering dedicating resources to a discharge clinic. The new codes could make discharge clinics more financially viable by increasing the reimbursement for care that often requires more than 30 minutes. However, based on the experience in our clinic, the increased revenue accurately reflects the intensity of service necessary to coordinate care in the post-discharge period.

The time intensity of care already is obvious from the structure of established discharge clinics. Examples include the comprehensive care centers at HealthCare Partners in Southern California, where multidisciplinary visits average 90 minutes, or at our clinic at Beth Israel Deaconess Medical Center in Boston.² While the visits in our clinic are less than half as long as those at HealthCare Partners, we are not including the time spent reviewing the discharge documentation, outstanding tests, and medication changes in advance of the visit, and the time spent after the visit, coordinating the patient’s care with visiting nurses and elder service agencies.³

What’s Next?

Whether these codes lead to an increased interest in hospitalist-staffed discharge clinics or to primary-care development of robust transitional-care structures, these new codes will help focus resources and attention on increasing services, with the goal of improving patient care during a period of extreme vulnerability. This alone is something to be grateful for, whether you are a transitionalist, hospitalist, primary-care doctor, caregiver, or patient.

Dr. Doctoroff is a hospitalist at Beth Israel Deaconess Medical Center in Boston and an instructor in medicine at Harvard Medical School. She is medical director of BIDMC’s Health Care Associates Post Discharge Clinic.

References

1. Andrews M. Post-discharge clinics try to cut hospital readmissions by helping patients. Washington Post website. Available at: http://articles.washingtonpost.com/2011-12-19/national/35288219_1_readmissions-discharge-vulnerable-patients. Accessed Jan. 7, 2013.
2. Feder JL. Predictive modeling and team care for high-need patients at HealthCare Partners. Health Aff (Millwood). 2011;30(3):416-418.
3. Doctoroff L. Interval examination: establishment of a hospitalist-staffed discharge clinic. J Gen Intern Med. 2012;27(10):1377-1382.

In November 2012, the Center for Medicare & Medicaid Services (CMS) finalized its 2013 physician fee schedule with two new transitional-care-management (TCM) codes, 99495 and 99496. These codes provide reimbursement for transitional-care services to patients for 30 days after hospital discharge. CMS estimates that two-thirds of the 10 million Medicare patients discharged annually from hospitals will have TCM services provided by an outpatient doctor. Why might hospitalists be interested in these outpatient codes? Read on.

As a post-discharge provider in a primary-care-based discharge clinic, I can say the new Medicare transitional codes read like our job description. Because I’ve worked in a post-discharge clinic for the past three years, I have learned that post-discharge care requires time and resource allocation beyond routine outpatient care. Because of the unique population we see, on average we bill at a higher level than the rest of the practice. Yet we, like all outpatient providers, remain constrained by the existing billing structure, which is intimately connected to physician face-to-face visits.

Here’s an illustration of a typical afternoon in the post-discharge clinic: A schizophrenic patient presents with renal failure, hypoglycemia, and confusion. Her home visiting nurse (VNA) administers her medications; the patient cannot tell you any of them. While you are calling the VNA to clarify her medications, trying to identify her healthcare proxy, and stopping her ACE inhibitor because her potassium is 5.6, the next patient arrives. She has end-stage liver disease and was recently in the hospital for liver failure, and now has worsening recurrent ascites. After clinic, you call interventional radiology to coordinate a therapeutic paracentesis and change diuretic doses after her labs return. Two weeks later, you arrange a repeat paracentesis, and subsequently a transition to comfort care in a hospice house. For this work, right now, you can at most bill a high-complexity office visit (99215), and the rest of the care coordination—by you, your nurse, or your administrative staff—is not compensated.

How Do the New Codes Work?

CMS created the new TCM codes to begin to change the outpatient fee schedule to emphasize primary care and care coordination for beneficiaries, particularly in the post-hospitalization period. The new TCM codes are a first step toward reimbursement for non-face-to-face activities, which are increasingly important in the evolving healthcare system.

The investment is estimated at more than $1 billion in 2013. The new codes are available to physicians, physician assistants, nurse practitioners, and other advanced-practice nurses only once within the 30 days after hospital discharge. During the 30 days after discharge, the two codes, 99495 and 99496, require a single face-to-face visit within seven days of discharge for the highest-risk patients and within 14 days of discharge for moderate-risk patients. The face-to-face visit is not billed separately. The codes also mandate telephone communication with the patient or caregiver within two business days of hospital discharge; the medical decision-making must be of either moderate or high complexity.

The average reimbursement for the codes will be $132.96 for 99495 and $231.11 for 99496, reflecting a higher wRVU than either hospital discharge day management or high-acuity outpatient visits. The code is billed at the end of the 30 days. The TCM code cannot be billed a second time if a patient is readmitted within the 30 days. Other E/M codes can be billed during the same time period for additional visits as necessary.

What’s the Impact on Hospitalists?

The new codes affect hospitalists in two ways. First, the hospitalists in the growing group of “transitionalists,” many of whom practice in outpatient clinics seeing patients after discharge, will be able to use these codes. As the codes require no pre-existing relationship with the patient, non-primary-care providers will be able to bill these codes, assuming that they fulfill the designated requirements. This concession enables hospitalists to fill a vital role for those patients who have inadequate access to immediate primary care post-hospitalization. It also provides a necessary bridge to appropriate primary care for those patients. This group of patients might be particularly vulnerable to adverse events, including hospital readmission, given their suboptimal connection with their primary-care providers.

Hospitalists who practice entirely as inpatient physicians will not be able to bill these new codes, but they will provide a valuable service to patients by helping identify the physicians who will provide their TCM and documenting this in the discharge documentation, already seen as a key element of discharge day management services.

Do These Codes Change the Business Case for Discharge Clinics?

Discharge clinics, either hospitalist-staffed or otherwise, have been actively discussed in the media in recent years.¹ Even without these transitional codes, discharge clinics have arisen where primary-care access is limited and as a potential, but as yet unproven, solution to high readmission rates. Despite this proliferation, discharge clinics have not yet proven to be cost-effective.

Implementation of these codes could change the calculus for organizations considering dedicating resources to a discharge clinic. The new codes could make discharge clinics more financially viable by increasing the reimbursement for care that often requires more than 30 minutes. However, based on the experience in our clinic, the increased revenue accurately reflects the intensity of service necessary to coordinate care in the post-discharge period.

The time intensity of care already is obvious from the structure of established discharge clinics. Examples include the comprehensive care centers at HealthCare Partners in Southern California, where multidisciplinary visits average 90 minutes, or at our clinic at Beth Israel Deaconess Medical Center in Boston.² While the visits in our clinic are less than half as long as those at HealthCare Partners, we are not including the time spent reviewing the discharge documentation, outstanding tests, and medication changes in advance of the visit, and the time spent after the visit, coordinating the patient’s care with visiting nurses and elder service agencies.³

What’s Next?

Whether these codes lead to an increased interest in hospitalist-staffed discharge clinics or to primary-care development of robust transitional-care structures, these new codes will help focus resources and attention on increasing services, with the goal of improving patient care during a period of extreme vulnerability. This alone is something to be grateful for, whether you are a transitionalist, hospitalist, primary-care doctor, caregiver, or patient.

Dr. Doctoroff is a hospitalist at Beth Israel Deaconess Medical Center in Boston and an instructor in medicine at Harvard Medical School. She is medical director of BIDMC’s Health Care Associates Post Discharge Clinic.

References

1. Andrews M. Post-discharge clinics try to cut hospital readmissions by helping patients. Washington Post website. Available at: http://articles.washingtonpost.com/2011-12-19/national/35288219_1_readmissions-discharge-vulnerable-patients. Accessed Jan. 7, 2013.
2. Feder JL. Predictive modeling and team care for high-need patients at HealthCare Partners. Health Aff (Millwood). 2011;30(3):416-418.
3. Doctoroff L. Interval examination: establishment of a hospitalist-staffed discharge clinic. J Gen Intern Med. 2012;27(10):1377-1382.

In November 2012, the Center for Medicare & Medicaid Services (CMS) finalized its 2013 physician fee schedule with two new transitional-care-management (TCM) codes, 99495 and 99496. These codes provide reimbursement for transitional-care services to patients for 30 days after hospital discharge. CMS estimates that two-thirds of the 10 million Medicare patients discharged annually from hospitals will have TCM services provided by an outpatient doctor. Why might hospitalists be interested in these outpatient codes? Read on.

As a post-discharge provider in a primary-care-based discharge clinic, I can say the new Medicare transitional codes read like our job description. Because I’ve worked in a post-discharge clinic for the past three years, I have learned that post-discharge care requires time and resource allocation beyond routine outpatient care. Because of the unique population we see, on average we bill at a higher level than the rest of the practice. Yet we, like all outpatient providers, remain constrained by the existing billing structure, which is intimately connected to physician face-to-face visits.

Here’s an illustration of a typical afternoon in the post-discharge clinic: A schizophrenic patient presents with renal failure, hypoglycemia, and confusion. Her home visiting nurse (VNA) administers her medications; the patient cannot tell you any of them. While you are calling the VNA to clarify her medications, trying to identify her healthcare proxy, and stopping her ACE inhibitor because her potassium is 5.6, the next patient arrives. She has end-stage liver disease and was recently in the hospital for liver failure, and now has worsening recurrent ascites. After clinic, you call interventional radiology to coordinate a therapeutic paracentesis and change diuretic doses after her labs return. Two weeks later, you arrange a repeat paracentesis, and subsequently a transition to comfort care in a hospice house. For this work, right now, you can at most bill a high-complexity office visit (99215), and the rest of the care coordination—by you, your nurse, or your administrative staff—is not compensated.

How Do the New Codes Work?

CMS created the new TCM codes to begin to change the outpatient fee schedule to emphasize primary care and care coordination for beneficiaries, particularly in the post-hospitalization period. The new TCM codes are a first step toward reimbursement for non-face-to-face activities, which are increasingly important in the evolving healthcare system.

The investment is estimated at more than $1 billion in 2013. The new codes are available to physicians, physician assistants, nurse practitioners, and other advanced-practice nurses only once within the 30 days after hospital discharge. During the 30 days after discharge, the two codes, 99495 and 99496, require a single face-to-face visit within seven days of discharge for the highest-risk patients and within 14 days of discharge for moderate-risk patients. The face-to-face visit is not billed separately. The codes also mandate telephone communication with the patient or caregiver within two business days of hospital discharge; the medical decision-making must be of either moderate or high complexity.

The average reimbursement for the codes will be $132.96 for 99495 and $231.11 for 99496, reflecting a higher wRVU than either hospital discharge day management or high-acuity outpatient visits. The code is billed at the end of the 30 days. The TCM code cannot be billed a second time if a patient is readmitted within the 30 days. Other E/M codes can be billed during the same time period for additional visits as necessary.

What’s the Impact on Hospitalists?

The new codes affect hospitalists in two ways. First, the hospitalists in the growing group of “transitionalists,” many of whom practice in outpatient clinics seeing patients after discharge, will be able to use these codes. As the codes require no pre-existing relationship with the patient, non-primary-care providers will be able to bill these codes, assuming that they fulfill the designated requirements. This concession enables hospitalists to fill a vital role for those patients who have inadequate access to immediate primary care post-hospitalization. It also provides a necessary bridge to appropriate primary care for those patients. This group of patients might be particularly vulnerable to adverse events, including hospital readmission, given their suboptimal connection with their primary-care providers.

Hospitalists who practice entirely as inpatient physicians will not be able to bill these new codes, but they will provide a valuable service to patients by helping identify the physicians who will provide their TCM and documenting this in the discharge documentation, already seen as a key element of discharge day management services.

Do These Codes Change the Business Case for Discharge Clinics?

Discharge clinics, either hospitalist-staffed or otherwise, have been actively discussed in the media in recent years.¹ Even without these transitional codes, discharge clinics have arisen where primary-care access is limited and as a potential, but as yet unproven, solution to high readmission rates. Despite this proliferation, discharge clinics have not yet proven to be cost-effective.

Implementation of these codes could change the calculus for organizations considering dedicating resources to a discharge clinic. The new codes could make discharge clinics more financially viable by increasing the reimbursement for care that often requires more than 30 minutes. However, based on the experience in our clinic, the increased revenue accurately reflects the intensity of service necessary to coordinate care in the post-discharge period.

The time intensity of care already is obvious from the structure of established discharge clinics. Examples include the comprehensive care centers at HealthCare Partners in Southern California, where multidisciplinary visits average 90 minutes, or at our clinic at Beth Israel Deaconess Medical Center in Boston.² While the visits in our clinic are less than half as long as those at HealthCare Partners, we are not including the time spent reviewing the discharge documentation, outstanding tests, and medication changes in advance of the visit, and the time spent after the visit, coordinating the patient’s care with visiting nurses and elder service agencies.³

What’s Next?

Whether these codes lead to an increased interest in hospitalist-staffed discharge clinics or to primary-care development of robust transitional-care structures, these new codes will help focus resources and attention on increasing services, with the goal of improving patient care during a period of extreme vulnerability. This alone is something to be grateful for, whether you are a transitionalist, hospitalist, primary-care doctor, caregiver, or patient.

Dr. Doctoroff is a hospitalist at Beth Israel Deaconess Medical Center in Boston and an instructor in medicine at Harvard Medical School. She is medical director of BIDMC’s Health Care Associates Post Discharge Clinic.

References

1. Andrews M. Post-discharge clinics try to cut hospital readmissions by helping patients. Washington Post website. Available at: http://articles.washingtonpost.com/2011-12-19/national/35288219_1_readmissions-discharge-vulnerable-patients. Accessed Jan. 7, 2013.
2. Feder JL. Predictive modeling and team care for high-need patients at HealthCare Partners. Health Aff (Millwood). 2011;30(3):416-418.
3. Doctoroff L. Interval examination: establishment of a hospitalist-staffed discharge clinic. J Gen Intern Med. 2012;27(10):1377-1382.

The autoimmune hemolytic anemias (AIHA) are rare but important hematologic diseases. They can range in severity from mildly symptomatic illness to a rapidly fatal syndrome. The incidence of AIHA is estimated to be between 0.6 and 3 cases per 100,000 persons. AIHA is mediated by antibodies, and in the majority of cases immunglobulin (Ig) G is the mediating antibody. This type of AIHA is referred to as "warm" AIHA because IgG antibodies bind best at body temperature. "Cold" AIHA is mediated by IgM antibodies, which bind maximally at temperatures below 37°C. This manual reviews the most common types of AIHA, with emphasis on diagnosis and treatment.

To read the full article in PDF:

Click here

The autoimmune hemolytic anemias (AIHA) are rare but important hematologic diseases. They can range in severity from mildly symptomatic illness to a rapidly fatal syndrome. The incidence of AIHA is estimated to be between 0.6 and 3 cases per 100,000 persons. AIHA is mediated by antibodies, and in the majority of cases immunglobulin (Ig) G is the mediating antibody. This type of AIHA is referred to as "warm" AIHA because IgG antibodies bind best at body temperature. "Cold" AIHA is mediated by IgM antibodies, which bind maximally at temperatures below 37°C. This manual reviews the most common types of AIHA, with emphasis on diagnosis and treatment.

To read the full article in PDF:

Click here

The autoimmune hemolytic anemias (AIHA) are rare but important hematologic diseases. They can range in severity from mildly symptomatic illness to a rapidly fatal syndrome. The incidence of AIHA is estimated to be between 0.6 and 3 cases per 100,000 persons. AIHA is mediated by antibodies, and in the majority of cases immunglobulin (Ig) G is the mediating antibody. This type of AIHA is referred to as "warm" AIHA because IgG antibodies bind best at body temperature. "Cold" AIHA is mediated by IgM antibodies, which bind maximally at temperatures below 37°C. This manual reviews the most common types of AIHA, with emphasis on diagnosis and treatment.

To read the full article in PDF:

Click here

Whenever a patient begins treatment with a glucocorticoid drug, we need to think about bone loss.

The American College of Rheumatology (ACR) issued recommendations for preventing and treating glucocorticoid-induced osteoporosis in 2010.¹ Compared with its previous guidelines,² the new ones are more tailored and nuanced but may be more difficult for physicians to follow. The guidelines call for assessing fracture risk using the computer-based Fracture Risk Assessment Tool, or FRAX (www/shef.ac.uk/FRAX), developed by the World Health Organization (WHO). For those without a computer or ready access to the Web, an application of FRAX is available for download on smartphones.

In this article, my purpose is to review the new recommendations and to offer my perspective, which does not necessarily reflect the opinions of the ACR.

DESPITE EVIDENCE, MANY PATIENTS RECEIVE NO INTERVENTION

Use of glucocorticoids is the most common cause of secondary osteoporosis. During the first 6 to 12 months of use, these drugs can cause a rapid loss of bone mass due to increased bone resorption; with continued use, they cause a slower but steady decline in bone mass due to reduced bone formation.³ Epidemiologic studies have found that the risk of fractures increases with dose, starting with doses as low as 2.5 mg per day of prednisone or its equivalent.⁴

Numerous clinical trials have evaluated the effect of bisphosphonates and teriparatide (Forteo) on bone mass and fracture risk in patients on glucocorticoid therapy. The bisphosphonates alendronate (Fosamax) and risedronate (Actonel) have both been shown to increase bone mass and reduce vertebral fracture risk in glucocorticoid recipients.^5–8 Zoledronic acid (Reclast), a parenteral bisphosphonate given in one annual dose, was shown to increase bone mass more than oral risedronate taken daily,⁹ and teriparatide, a formulation of parathyroid hormone, was better than alendronate.¹⁰

However, despite the known risk of fractures with glucocorticoid use and the demonstrated efficacy of available agents in preventing bone loss and fracture, many patients do not receive any intervention.^11,12

WHAT HAS HAPPENED SINCE 2001?

In the interval since 2001, several guidelines for managing glucocorticoid-induced osteoporosis have been published in other countries.^13–17 Broadly speaking, they recommend starting preventive drug therapy for patients at risk of fracture at the same time glucocorticoid drugs are started if the patient is expected to take glucocorticoids for more than 3 to 6 months in doses higher than 5 to 7.5 mg of prednisone or its equivalent daily.

Recommendations for patients who have been on glucocorticoids for longer than 3 to 6 months at initial evaluation have been based largely on T scores derived from dual-energy x-ray absorptiometry (DXA). Thresholds for initiating therapy have varied: the ACR in 2001 recommended preventive treatment if the T score is lower than −1.0, whereas British guidelines said −1.5 and Dutch guidelines said −2.5.

In the United States, since 2001 when the ACR published its last guidelines,² zoledronic acid and teriparatide have been approved for use in glucocorticoid-induced osteoporosis. In addition, guideline-development methodology has evolved and now is more scientifically rigorous. Finally, a risk-assessment tool has been developed that enables a more tailored approach (see below).

FRAX (www.shef.ac.uk/FRAX)

FRAX is a tool developed by the WHO to calculate the risk of fracture. If you go to the FRAX Web site and enter the required clinical information (race, age, sex, weight, height, previous fracture, family history of a fractured hip in a parent, current smoking, use of glucocorticoids, rheumatoid arthritis, secondary osteoporosis, consumption of three or more units of alcohol per day, and bone mineral density of the femoral neck), it will tell you the patient’s 10-year absolute (not relative) risk of major osteoporotic fracture and of hip fracture.

Since FRAX was unveiled in 2008, calculation of absolute fracture risk has become the standard method for making treatment decisions in patients with low bone mass who have not yet received any fracture-preventing treatment.¹⁸ The use of clinical risk factors in FRAX increases its ability to predict risk over and above the use of bone density by itself. And glucocorticoids are one of the clinical risk factors in FRAX.

But in which patients is treatment with a bisphosphonate or teriparatide cost-effective?

Thresholds for cost-effectiveness have been developed on the basis of economic assumptions that are country-specific. In the United States, the National Osteoporosis Foundation recommends drug therapy if the 10-year absolute risk of a major osteoporotic fracture of the hip, spine (clinical, not radiographic), wrist, or humerus is greater than 20% or if the risk of a hip fracture is greater than 3%.¹⁹

At equivalent bone densities, women taking glucocorticoids are at considerably higher risk of fracture than nonusers.²⁰ For example, consider a 65-year-old white woman, weight 59 kg, height 163 cm, no previous fractures, no parent with a fractured hip, no current smoking, no rheumatoid arthritis, no secondary osteoporosis, no excessive alcohol use, and a T score of −2.2 in the femoral neck. (Try this on the FRAX Web site.) If she does not use glucocorticoids, her 10-year risk of hip fracture is 2.0%; using glucocorticoids increases the risk to 3.6%. This is higher than the 3% National Osteoporosis Foundation guideline; thus, treatment would be recommended.

Also using FRAX, a 55-year-old white woman with a T score of −1.8 and on glucocorticoid therapy has a 67% higher risk of major osteoporotic fracture and an 80% higher risk of hip fracture.

For a third example, a white woman age 60, weight 70 kg, height 168 cm, negative for all the other risk factors but with a T score of −2.1 and on glucocorticoids has a calculated 10-year fracture risk of 2.1%, which is below the National Osteoporosis Foundation treatment threshold. However, most clinicians would probably recommend treatment for her, depending on the anticipated dose and duration of glucocorticoid therapy.

A caveat. In FRAX, glucocorticoid therapy is a categorical variable—a yes-or-no question—and yes is defined as having ever used a glucocorticoid in a dose greater than 5 mg for more than 3 months. Therefore, according to FRAX, a patient who took 5 mg of prednisone for 3 months 5 years ago has the same fracture risk as a patient on 60 mg of prednisone after a diagnosis of temporal arteritis. For this reason, the FRAX tool is likely to underestimate fracture risk, especially in patients currently taking glucocorticoids and those on higher doses of these drugs.

Kanis et al used the General Practice Research Database to adjust the fracture risk for glucocorticoid use in FRAX.²¹ At doses higher than 7.5 mg, the fracture risk had to be revised upward by 10% to 25% depending on the fracture site (hip vs any major osteoporotic fracture) and age (greater at age 40 than at age 90).

The underestimation of fracture risk led the ACR Expert Advisory Panel to create risk strata for major osteoporotic fractures, ie, low (< 10% risk per 10 years), medium (10%–20%), and high (> 20%) and uses these cut points to make treatment recommendations.

HOW THE 2010 GUIDELINES WERE DEVELOPED

Whereas the 2001 recommendations were based on a more informal consensus approach, the 2010 recommendations use a more scientifically rigorous methodology for guideline development, the Research and Development/University of California at Los Angeles (RAND/UCLA) Appropriateness Method. The RAND/UCLA method combines the best available scientific evidence with expert opinion to develop practice guidelines.

In drawing up the 2010 recommendations the ACR used three panels of experts. The Core Executive Panel conducted a systematic review of controlled clinical trials of therapies currently approved for treating glucocorticoid-induced osteoporosis in the United States, Canada, or the European Union. They found 53 articles meeting their inclusion criteria; an evidence report was produced that informed the development of the recommendations. This evidence report and guideline development process is available at http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)2151-4658. The Expert Advisory Panel framed the recommendations, and the Task Force Panel voted on them. The Core Executive Panel and Expert Advisory Panel constructed 48 patient-specific clinical scenarios using four variables: sex, age, race/ethnicity, and femoral neck T scores.

The members of the Task Force Panel were asked to use the evidence report and their expert judgment to vote on and rate the appropriateness of using a specific therapy in the context of each scenario on a 9-point Likert scale (1 = appropriate; 9 = not appropriate). Agreement occurred when 7 or more of the 10 panel members rated a scenario 1, 2, or 3. Disagreements were defined as 3 or more of the 10 members rating the scenario between 4 and 9 while the other members rated it lower.

Disagreements in voting were discussed in an attempt to achieve consensus, and a second vote was conducted which determined the final recommendations. If disagreement remained after the vote, no recommendation was made.

No attempt was made to assign priority of one drug over another when multiple drugs were deemed appropriate, although the final recommendations did differentiate drugs based on patient categories.

START WITH COUNSELING, ASSESSMENT

For patients starting or already on glucocorticoid therapy that is expected to last at least 3 months, the first step is to counsel them on lifestyle modifications (Table 1) and to assess their risk factors (Figure 1). Recommendations for monitoring patients receiving glucocorticoid therapy for at least 3 months are presented in Table 2.

These recommendations are based on literature review, and the strength of evidence is graded:

• Grade A—derived from multiple randomized controlled trials or a meta-analysis
• Grade B—derived from a single randomized controlled trial or nonrandomized study
• Grade C—derived from consensus, expert opinion, or case series.

This system is the same one used by the American College of Cardiology and is based on clinical trial data.²²

Recommendations for calcium intake and vitamin D supplementation were graded A; all other recommendations were graded C (Tables 1 and 2). It is important to note that practices that receive a grade of C may still be accepted as standard of care, such as fall assessment and smoking cessation.

FOR POSTMENOPAUSAL WOMEN AND FOR MEN AGE 50 AND OLDER

FRAX low-risk group

Recall that “low risk” based on the new ACR guidelines means that the 10-year absolute risk of a major osteoporotic fracture, as calculated with FRAX, is less than 10%.

• If glucocorticoid use is expected to last or has already lasted at least 3 months and the dose is less than 7.5 mg/day, no pharmacologic treatment is recommended.
• If glucocorticoid use is expected to last or has already lasted at least 3 months and the dose is 7.5 mg/day or higher, alendronate, risedronate, or zoledronic acid is recommended.

Comment. These are the most straightforward of the recommendations. All three bisphosphonates are recommended as treatment options if the glucocorticoid dose is at least 7.5 mg/day and the duration at least 3 months. Ibandronate (Boniva) was not included because it has no data from clinical trials.

“Medium risk” means that the 10-year absolute fracture risk of major osteoporotic fractures is 10% to 20%.

• If glucocorticoid use is anticipated to last or has lasted at least 3 months and the dose is less than 7.5 mg/day, alendronate or risedronate is recommended.
• If glucocorticoid use is anticipated to last or has lasted at least 3 months and the dose is 7.5 mg/day or higher, alendronate, risedronate, or zoledronic acid is recommended.

Comment. Treatment is recommended at all glucocorticoid doses for patients in the medium-risk category if the duration of glucocorticoid treatment is at least 3 months, with one difference: zoledronic acid is recommended only if the glucocorticoid dose is 7.5 mg/day or higher. This inconsistency persisted after a second round of voting by the Task Force Panel.

FRAX high-risk group

In this group, the 10-year risk of major osteoporotic fractures is higher than 20%.

• If the glucocorticoid dose is less than 5 mg/day for up to 1 month, alendronate, risedronate, or zoledronic acid is recommended.
• If the dose is 5 mg/day or more for up to 1 month, or any dose for more than 1 month, alendronate, risedronate, zoledronic acid or teriparatide is recommended.

Comment. Based on current National Osteoporosis Foundation guidelines, all patients with a 10-year risk greater than 20% are recommended for treatment for any duration and dose of glucocorticoid use. However, teriparatide is recommended only if the duration of glucocorticoid therapy is more than 1 month.

FOR PREMENOPAUSAL WOMEN AND FOR MEN YOUNGER THAN AGE 50

Use of FRAX is not appropriate in premenopausal women or in men younger than 50 years.

Younger patients with no prevalent fracture

For men younger than 50 and premenopausal women who have not had a previous fracture, data were considered inadequate to make a recommendation, and no votes were taken.

Prevalent fracture in premenopausal women of nonchildbearing potential

In premenopausal women of nonchildbearing potential who have had a fracture:

• If the glucocorticoid duration is 1 to 3 months and the dose is 5 mg/day or higher, alendronate or risedronate is recommended.
• If the duration is 1 to 3 months and the dose is 7.5 mg/day or higher, alendronate, risedronate, or zoledronic acid is recommended
• If the duration is more than 3 months, alendronate, risedronate, zoledronic acid, or teriparatide is recommended.

Comment. Treatment is recommended with any of the four medications in patients with a fracture and treated with glucocorticoids for more than 3 months. For shorter-duration glucocorticoid use (1–3 months) at 5 mg/day or higher, only alendronate and risedronate are recommended. If the dose is 7.5 mg/day or higher, any bisphosphonate is recommended. Zoledronic acid was consistently differentiated by the expert panel on the basis of dose and duration of glucocorticoid use, in view of its 1-year duration of effect after one dose.

Prevalent fracture in women of childbearing potential

• If the glucocorticoid duration is 1 to 3 months, there was no consensus (ie, voting disagreements could not be resolved).
• If the glucocorticoid duration is more than 3 months and the dose is 7.5 mg/day or more, alendronate, risedronate, or teriparatide is recommended.
• If the glucocorticoid duration is more than 3 months and the dose is less than 7.5 mg/day, there was no consensus.

Comment. Childbearing potential creates further complexities because of concern about fetal toxicity with bisphosphonates. For short-term glucocorticoid therapy at any dose and for therapy longer than 3 months at less than 7.5 mg, no consensus could be reached. For therapy longer than 3 months and with 7.5 mg/day or higher, treatment is recommended but not with zoledronic acid, based on the long half-life of the drug and concern for fetal toxicity.

Additional risk stratification

The panel recommended that if the following were present, a shift to a higher fracture risk category should be considered (low to medium, or medium to high):

• High daily dose of glucocorticoid
• High cumulative glucocorticoid dose
• Declining bone mineral density on serial DXA.

These are known risk factors that increase fracture risk but would not affect fracture risk in the FRAX model.

WHAT IS NEW IN THE 2010 RECOMMENDATIONS?

Recommendations for counseling now include fall risk assessment, height measurement, 25-hydroxyvitamin D measurement, and evaluation of patients for prevalent and incident fractures using vertebral fracture assessment by DXA or radiographic imaging of the spine.

Recommended drugs now include teriparatide and zoledronic acid, while estrogen and testosterone are no longer recommended as therapies for glucocorticoid-induced osteoporosis. Ibandronate is not included, since there have been no randomized controlled trials of this bisphosphonate in glucocorticoid-induced osteoporosis.

Recommendations for treatment in 2001 were based on T scores alone, while the 2010 recommendations use an assessment of absolute fracture risk based on FRAX for postmenopausal women and for men age 50 and older.

A clinician’s guide that summarizes the ACR recommendations is available at www.rheumatology.org/practice/clinical/guidelines/.

RECOMMENDATIONS DO NOT REPLACE CLINICAL JUDGMENT

Although the 2010 recommendations were more rigorous in their development process than those of 2001, they have limitations and they should not replace clinical judgment. Rather, they are intended to provide an evidence-based approach to guide clinicians in making treatment choices in patients on glucocorticoid therapy.

CONSIDERING ABSOLUTE FRACTURE RISK IN TREATMENT DECISIONS

The 2001 ACR guidelines recommended fracture-preventing treatment in all patients starting glucocorticoid therapy at more than 5 mg/day if the planned duration of treatment was at least 3 months, and in patients on long-term glucocorticoid therapy if the T score was less than −1.0. While these guidelines were simple and easy to use, they were not specific enough to provide useful guidance in specific scenarios.

A model of absolute fracture risk was not available in 2001. A 55-year old white woman with a T score of −1.1 who smoked, who had been using 5 mg of prednisone for the last 12 months, and who had stable bone mass on serial DXA scans would have been recommended for treatment based on the 2001 recommendations. If this patient’s FRAX-calculated 10-year absolute risk of a major osteoporotic fracture is less than 10%, that would be well below the National Osteoporosis Foundation’s cost-effective treatment threshold of 20%. The new guidelines suggest no treatment is needed, since the risk category is low and the dose is less than 7.5 mg. However, if on serial DXA this patient had a significant decline in bone mass, the guidelines suggest shifting the patient to a higher risk category, ie, from low to medium risk, which would result in a recommendation in favor of treatment.

The 2010 recommendations are not as simple to use as those from 2001. They encourage using FRAX to calculate fracture risk; thus, knowledge of the strengths and limitations of FRAX is required. Access to the internet in the examination room or use of the FRAX tool on a smartphone as well as willingness to spend a minute to calculate fracture risk are needed. For those who cannot or choose not to use the FRAX tool, the ACR publication provides tables for patient risk assessment based on age and T score. However, the tables would have to be readily available in the clinic, which may not be practical.

The 2010 recommendation provide a more nuanced approach to treatment in patients on glucocorticoid therapy and are likely to change treatment decisions based on their use, just as FRAX has altered treatment decisions in patients with primary osteoporosis.²³

FRAX has limitations

FRAX underestimates the effect of glucocorticoids on fracture risk because steroid use is a yes-or-no question and its weight represents the average risk in a population that has ever used steroids, most of whom were using doses between 2.5 and 7.5 mg.

The WHO recognized this limitation and suggested an upward adjustment of risk for patients on 7.5 mg or more, ranging from 10% to 25%.²¹ For patients on high doses of steroids, this adjustment is still likely to result in underestimation of fracture risk and undertreatment of glucocorticoid-treated patients.

The 2010 recommendations adjust for this limitation, recommending treatment in the low-risk and medium-risk categories if the glucocorticoid dose is 7.5 mg or higher. If a patient is using high daily doses of steroids or has a declining bone density, the 2010 recommendations suggest increasing the risk category from low to medium or medium to high.

FRAX risk factors are dichotomous (yes/no) and are not adjusted for dose effects such as multiple fractures (vs a single fracture), heavy smoking (vs light smoking), heavy alcohol use (6 units per day vs 3 units), or severe rheumatoid arthritis (vs mild disease). Family history of osteoporosis in the FRAX is limited to parents with a hip fracture—vertebral fractures in a family member do not count.

Since FRAX uses the bone mineral density in the hip, it underestimates fracture risk in patients with low spine density but normal hip density. It may also underestimate fracture risk in patients with declining bone mass; the 2010 recommendations suggest the clinician should increase the risk category in this situation.

LIMITATIONS OF THE GUIDELINES

The 2010 recommendations do not include several important groups in which steroids are used, including transplant recipients, children, and patients on inhaled corticosteroids. The panel thought that there were insufficient data to make recommendations for these populations, as well as for premenopausal women and men younger than 50 years who did not have a prevalent fracture. The absence of a recommendation in these situations should not be considered a recommendation for no treatment; it is an acknowledgment of a lack of evidence, a lack of consensus among experts, and the need for additional clinical trials.

For premenopausal women and men under age 50 with a fracture, the recommendations are complicated and not intuitive. Zoledronic acid is not recommended for women of non-childbearing potential with a glucocorticoid duration of 1 to 3 months unless the steroid dose is at least 7.5 mg. This recommendation was based on panel voting and consensus that giving zoledronic acid, a medication with a 1-year duration of effect, in a patient on steroids for only 1 to 3 months was not warranted.

Teriparatide was recommended only if glucocorticoids are used for at least 3 months, although anyone who already has a fracture might be considered at high enough risk to warrant anabolic therapy regardless of steroid use or duration.

Zoledronic acid was excluded in women of childbearing potential, based on panel voting and consensus that drugs given in smaller amounts over 1 year might be less harmful to a fetus than one with a longer half-life given in a larger bolus once a year.

The panel could reach no consensus on women of childbearing potential with a prevalent fracture who were using less than 7.5 mg/day of glucocorticoids. A lack of consensus was the result of insufficient data to make evidence-based decisions and a disagreement among experts on the correct treatment.

The guidelines do not address the duration of treatment with bisphosphonates, a topic of importance because of concern for the potential long-term side effects of these medications.

THE BOTTOM LINE

The 2010 recommendations add a degree of complexity, with different medications recommended on the basis of glucocorticoid dose and duration as well as patient age, menopausal status, and childbearing potential. Guideline developers and clinicians face a difficult trade-off: easy-to-follow guidelines or more targeted guidelines that are more complex and therefore more difficult to use than previous guidelines.

This criticism is reasonable. The complexity is a result of insufficient evidence from clinical trials to make more exact and user-friendly recommendations, and also a result of the RAND/UCLA methodology. In cases that lack sufficient evidence on which to make a decision, the guideline development uses voting among experts in an attempt to develop consensus. This often results in complexity, lack of consensus, or inconsistencies.

The guidelines are straightforward for postmenopausal women and men age 50 and older on at least 7.5 mg prednisone for more than 3 months.

Since there is substantial evidence that many patients on glucocorticoid therapy go untreated, the risk of fracture in this population would be substantially reduced if clinicians would adhere to the recommendations.

Whenever a patient begins treatment with a glucocorticoid drug, we need to think about bone loss.

The American College of Rheumatology (ACR) issued recommendations for preventing and treating glucocorticoid-induced osteoporosis in 2010.¹ Compared with its previous guidelines,² the new ones are more tailored and nuanced but may be more difficult for physicians to follow. The guidelines call for assessing fracture risk using the computer-based Fracture Risk Assessment Tool, or FRAX (www/shef.ac.uk/FRAX), developed by the World Health Organization (WHO). For those without a computer or ready access to the Web, an application of FRAX is available for download on smartphones.

In this article, my purpose is to review the new recommendations and to offer my perspective, which does not necessarily reflect the opinions of the ACR.

DESPITE EVIDENCE, MANY PATIENTS RECEIVE NO INTERVENTION

Use of glucocorticoids is the most common cause of secondary osteoporosis. During the first 6 to 12 months of use, these drugs can cause a rapid loss of bone mass due to increased bone resorption; with continued use, they cause a slower but steady decline in bone mass due to reduced bone formation.³ Epidemiologic studies have found that the risk of fractures increases with dose, starting with doses as low as 2.5 mg per day of prednisone or its equivalent.⁴

Numerous clinical trials have evaluated the effect of bisphosphonates and teriparatide (Forteo) on bone mass and fracture risk in patients on glucocorticoid therapy. The bisphosphonates alendronate (Fosamax) and risedronate (Actonel) have both been shown to increase bone mass and reduce vertebral fracture risk in glucocorticoid recipients.^5–8 Zoledronic acid (Reclast), a parenteral bisphosphonate given in one annual dose, was shown to increase bone mass more than oral risedronate taken daily,⁹ and teriparatide, a formulation of parathyroid hormone, was better than alendronate.¹⁰

However, despite the known risk of fractures with glucocorticoid use and the demonstrated efficacy of available agents in preventing bone loss and fracture, many patients do not receive any intervention.^11,12

WHAT HAS HAPPENED SINCE 2001?

In the interval since 2001, several guidelines for managing glucocorticoid-induced osteoporosis have been published in other countries.^13–17 Broadly speaking, they recommend starting preventive drug therapy for patients at risk of fracture at the same time glucocorticoid drugs are started if the patient is expected to take glucocorticoids for more than 3 to 6 months in doses higher than 5 to 7.5 mg of prednisone or its equivalent daily.

Recommendations for patients who have been on glucocorticoids for longer than 3 to 6 months at initial evaluation have been based largely on T scores derived from dual-energy x-ray absorptiometry (DXA). Thresholds for initiating therapy have varied: the ACR in 2001 recommended preventive treatment if the T score is lower than −1.0, whereas British guidelines said −1.5 and Dutch guidelines said −2.5.

In the United States, since 2001 when the ACR published its last guidelines,² zoledronic acid and teriparatide have been approved for use in glucocorticoid-induced osteoporosis. In addition, guideline-development methodology has evolved and now is more scientifically rigorous. Finally, a risk-assessment tool has been developed that enables a more tailored approach (see below).

FRAX (www.shef.ac.uk/FRAX)

FRAX is a tool developed by the WHO to calculate the risk of fracture. If you go to the FRAX Web site and enter the required clinical information (race, age, sex, weight, height, previous fracture, family history of a fractured hip in a parent, current smoking, use of glucocorticoids, rheumatoid arthritis, secondary osteoporosis, consumption of three or more units of alcohol per day, and bone mineral density of the femoral neck), it will tell you the patient’s 10-year absolute (not relative) risk of major osteoporotic fracture and of hip fracture.

Since FRAX was unveiled in 2008, calculation of absolute fracture risk has become the standard method for making treatment decisions in patients with low bone mass who have not yet received any fracture-preventing treatment.¹⁸ The use of clinical risk factors in FRAX increases its ability to predict risk over and above the use of bone density by itself. And glucocorticoids are one of the clinical risk factors in FRAX.

But in which patients is treatment with a bisphosphonate or teriparatide cost-effective?

Thresholds for cost-effectiveness have been developed on the basis of economic assumptions that are country-specific. In the United States, the National Osteoporosis Foundation recommends drug therapy if the 10-year absolute risk of a major osteoporotic fracture of the hip, spine (clinical, not radiographic), wrist, or humerus is greater than 20% or if the risk of a hip fracture is greater than 3%.¹⁹

At equivalent bone densities, women taking glucocorticoids are at considerably higher risk of fracture than nonusers.²⁰ For example, consider a 65-year-old white woman, weight 59 kg, height 163 cm, no previous fractures, no parent with a fractured hip, no current smoking, no rheumatoid arthritis, no secondary osteoporosis, no excessive alcohol use, and a T score of −2.2 in the femoral neck. (Try this on the FRAX Web site.) If she does not use glucocorticoids, her 10-year risk of hip fracture is 2.0%; using glucocorticoids increases the risk to 3.6%. This is higher than the 3% National Osteoporosis Foundation guideline; thus, treatment would be recommended.

Also using FRAX, a 55-year-old white woman with a T score of −1.8 and on glucocorticoid therapy has a 67% higher risk of major osteoporotic fracture and an 80% higher risk of hip fracture.

For a third example, a white woman age 60, weight 70 kg, height 168 cm, negative for all the other risk factors but with a T score of −2.1 and on glucocorticoids has a calculated 10-year fracture risk of 2.1%, which is below the National Osteoporosis Foundation treatment threshold. However, most clinicians would probably recommend treatment for her, depending on the anticipated dose and duration of glucocorticoid therapy.

A caveat. In FRAX, glucocorticoid therapy is a categorical variable—a yes-or-no question—and yes is defined as having ever used a glucocorticoid in a dose greater than 5 mg for more than 3 months. Therefore, according to FRAX, a patient who took 5 mg of prednisone for 3 months 5 years ago has the same fracture risk as a patient on 60 mg of prednisone after a diagnosis of temporal arteritis. For this reason, the FRAX tool is likely to underestimate fracture risk, especially in patients currently taking glucocorticoids and those on higher doses of these drugs.

Kanis et al used the General Practice Research Database to adjust the fracture risk for glucocorticoid use in FRAX.²¹ At doses higher than 7.5 mg, the fracture risk had to be revised upward by 10% to 25% depending on the fracture site (hip vs any major osteoporotic fracture) and age (greater at age 40 than at age 90).

The underestimation of fracture risk led the ACR Expert Advisory Panel to create risk strata for major osteoporotic fractures, ie, low (< 10% risk per 10 years), medium (10%–20%), and high (> 20%) and uses these cut points to make treatment recommendations.

HOW THE 2010 GUIDELINES WERE DEVELOPED

Whereas the 2001 recommendations were based on a more informal consensus approach, the 2010 recommendations use a more scientifically rigorous methodology for guideline development, the Research and Development/University of California at Los Angeles (RAND/UCLA) Appropriateness Method. The RAND/UCLA method combines the best available scientific evidence with expert opinion to develop practice guidelines.

In drawing up the 2010 recommendations the ACR used three panels of experts. The Core Executive Panel conducted a systematic review of controlled clinical trials of therapies currently approved for treating glucocorticoid-induced osteoporosis in the United States, Canada, or the European Union. They found 53 articles meeting their inclusion criteria; an evidence report was produced that informed the development of the recommendations. This evidence report and guideline development process is available at http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)2151-4658. The Expert Advisory Panel framed the recommendations, and the Task Force Panel voted on them. The Core Executive Panel and Expert Advisory Panel constructed 48 patient-specific clinical scenarios using four variables: sex, age, race/ethnicity, and femoral neck T scores.

The members of the Task Force Panel were asked to use the evidence report and their expert judgment to vote on and rate the appropriateness of using a specific therapy in the context of each scenario on a 9-point Likert scale (1 = appropriate; 9 = not appropriate). Agreement occurred when 7 or more of the 10 panel members rated a scenario 1, 2, or 3. Disagreements were defined as 3 or more of the 10 members rating the scenario between 4 and 9 while the other members rated it lower.

Disagreements in voting were discussed in an attempt to achieve consensus, and a second vote was conducted which determined the final recommendations. If disagreement remained after the vote, no recommendation was made.

No attempt was made to assign priority of one drug over another when multiple drugs were deemed appropriate, although the final recommendations did differentiate drugs based on patient categories.

START WITH COUNSELING, ASSESSMENT

For patients starting or already on glucocorticoid therapy that is expected to last at least 3 months, the first step is to counsel them on lifestyle modifications (Table 1) and to assess their risk factors (Figure 1). Recommendations for monitoring patients receiving glucocorticoid therapy for at least 3 months are presented in Table 2.

These recommendations are based on literature review, and the strength of evidence is graded:

• Grade A—derived from multiple randomized controlled trials or a meta-analysis
• Grade B—derived from a single randomized controlled trial or nonrandomized study
• Grade C—derived from consensus, expert opinion, or case series.

This system is the same one used by the American College of Cardiology and is based on clinical trial data.²²

Recommendations for calcium intake and vitamin D supplementation were graded A; all other recommendations were graded C (Tables 1 and 2). It is important to note that practices that receive a grade of C may still be accepted as standard of care, such as fall assessment and smoking cessation.

FOR POSTMENOPAUSAL WOMEN AND FOR MEN AGE 50 AND OLDER

FRAX low-risk group

Recall that “low risk” based on the new ACR guidelines means that the 10-year absolute risk of a major osteoporotic fracture, as calculated with FRAX, is less than 10%.

• If glucocorticoid use is expected to last or has already lasted at least 3 months and the dose is less than 7.5 mg/day, no pharmacologic treatment is recommended.
• If glucocorticoid use is expected to last or has already lasted at least 3 months and the dose is 7.5 mg/day or higher, alendronate, risedronate, or zoledronic acid is recommended.

Comment. These are the most straightforward of the recommendations. All three bisphosphonates are recommended as treatment options if the glucocorticoid dose is at least 7.5 mg/day and the duration at least 3 months. Ibandronate (Boniva) was not included because it has no data from clinical trials.

“Medium risk” means that the 10-year absolute fracture risk of major osteoporotic fractures is 10% to 20%.

• If glucocorticoid use is anticipated to last or has lasted at least 3 months and the dose is less than 7.5 mg/day, alendronate or risedronate is recommended.
• If glucocorticoid use is anticipated to last or has lasted at least 3 months and the dose is 7.5 mg/day or higher, alendronate, risedronate, or zoledronic acid is recommended.

Comment. Treatment is recommended at all glucocorticoid doses for patients in the medium-risk category if the duration of glucocorticoid treatment is at least 3 months, with one difference: zoledronic acid is recommended only if the glucocorticoid dose is 7.5 mg/day or higher. This inconsistency persisted after a second round of voting by the Task Force Panel.

FRAX high-risk group

In this group, the 10-year risk of major osteoporotic fractures is higher than 20%.

• If the glucocorticoid dose is less than 5 mg/day for up to 1 month, alendronate, risedronate, or zoledronic acid is recommended.
• If the dose is 5 mg/day or more for up to 1 month, or any dose for more than 1 month, alendronate, risedronate, zoledronic acid or teriparatide is recommended.

Comment. Based on current National Osteoporosis Foundation guidelines, all patients with a 10-year risk greater than 20% are recommended for treatment for any duration and dose of glucocorticoid use. However, teriparatide is recommended only if the duration of glucocorticoid therapy is more than 1 month.

FOR PREMENOPAUSAL WOMEN AND FOR MEN YOUNGER THAN AGE 50

Use of FRAX is not appropriate in premenopausal women or in men younger than 50 years.

Younger patients with no prevalent fracture

For men younger than 50 and premenopausal women who have not had a previous fracture, data were considered inadequate to make a recommendation, and no votes were taken.

Prevalent fracture in premenopausal women of nonchildbearing potential

In premenopausal women of nonchildbearing potential who have had a fracture:

• If the glucocorticoid duration is 1 to 3 months and the dose is 5 mg/day or higher, alendronate or risedronate is recommended.
• If the duration is 1 to 3 months and the dose is 7.5 mg/day or higher, alendronate, risedronate, or zoledronic acid is recommended
• If the duration is more than 3 months, alendronate, risedronate, zoledronic acid, or teriparatide is recommended.

Comment. Treatment is recommended with any of the four medications in patients with a fracture and treated with glucocorticoids for more than 3 months. For shorter-duration glucocorticoid use (1–3 months) at 5 mg/day or higher, only alendronate and risedronate are recommended. If the dose is 7.5 mg/day or higher, any bisphosphonate is recommended. Zoledronic acid was consistently differentiated by the expert panel on the basis of dose and duration of glucocorticoid use, in view of its 1-year duration of effect after one dose.

Prevalent fracture in women of childbearing potential

• If the glucocorticoid duration is 1 to 3 months, there was no consensus (ie, voting disagreements could not be resolved).
• If the glucocorticoid duration is more than 3 months and the dose is 7.5 mg/day or more, alendronate, risedronate, or teriparatide is recommended.
• If the glucocorticoid duration is more than 3 months and the dose is less than 7.5 mg/day, there was no consensus.

Comment. Childbearing potential creates further complexities because of concern about fetal toxicity with bisphosphonates. For short-term glucocorticoid therapy at any dose and for therapy longer than 3 months at less than 7.5 mg, no consensus could be reached. For therapy longer than 3 months and with 7.5 mg/day or higher, treatment is recommended but not with zoledronic acid, based on the long half-life of the drug and concern for fetal toxicity.

Additional risk stratification

The panel recommended that if the following were present, a shift to a higher fracture risk category should be considered (low to medium, or medium to high):

• High daily dose of glucocorticoid
• High cumulative glucocorticoid dose
• Declining bone mineral density on serial DXA.

These are known risk factors that increase fracture risk but would not affect fracture risk in the FRAX model.

WHAT IS NEW IN THE 2010 RECOMMENDATIONS?

Recommendations for counseling now include fall risk assessment, height measurement, 25-hydroxyvitamin D measurement, and evaluation of patients for prevalent and incident fractures using vertebral fracture assessment by DXA or radiographic imaging of the spine.

Recommended drugs now include teriparatide and zoledronic acid, while estrogen and testosterone are no longer recommended as therapies for glucocorticoid-induced osteoporosis. Ibandronate is not included, since there have been no randomized controlled trials of this bisphosphonate in glucocorticoid-induced osteoporosis.

Recommendations for treatment in 2001 were based on T scores alone, while the 2010 recommendations use an assessment of absolute fracture risk based on FRAX for postmenopausal women and for men age 50 and older.

A clinician’s guide that summarizes the ACR recommendations is available at www.rheumatology.org/practice/clinical/guidelines/.

RECOMMENDATIONS DO NOT REPLACE CLINICAL JUDGMENT

Although the 2010 recommendations were more rigorous in their development process than those of 2001, they have limitations and they should not replace clinical judgment. Rather, they are intended to provide an evidence-based approach to guide clinicians in making treatment choices in patients on glucocorticoid therapy.

CONSIDERING ABSOLUTE FRACTURE RISK IN TREATMENT DECISIONS

The 2001 ACR guidelines recommended fracture-preventing treatment in all patients starting glucocorticoid therapy at more than 5 mg/day if the planned duration of treatment was at least 3 months, and in patients on long-term glucocorticoid therapy if the T score was less than −1.0. While these guidelines were simple and easy to use, they were not specific enough to provide useful guidance in specific scenarios.

A model of absolute fracture risk was not available in 2001. A 55-year old white woman with a T score of −1.1 who smoked, who had been using 5 mg of prednisone for the last 12 months, and who had stable bone mass on serial DXA scans would have been recommended for treatment based on the 2001 recommendations. If this patient’s FRAX-calculated 10-year absolute risk of a major osteoporotic fracture is less than 10%, that would be well below the National Osteoporosis Foundation’s cost-effective treatment threshold of 20%. The new guidelines suggest no treatment is needed, since the risk category is low and the dose is less than 7.5 mg. However, if on serial DXA this patient had a significant decline in bone mass, the guidelines suggest shifting the patient to a higher risk category, ie, from low to medium risk, which would result in a recommendation in favor of treatment.

The 2010 recommendations are not as simple to use as those from 2001. They encourage using FRAX to calculate fracture risk; thus, knowledge of the strengths and limitations of FRAX is required. Access to the internet in the examination room or use of the FRAX tool on a smartphone as well as willingness to spend a minute to calculate fracture risk are needed. For those who cannot or choose not to use the FRAX tool, the ACR publication provides tables for patient risk assessment based on age and T score. However, the tables would have to be readily available in the clinic, which may not be practical.

The 2010 recommendation provide a more nuanced approach to treatment in patients on glucocorticoid therapy and are likely to change treatment decisions based on their use, just as FRAX has altered treatment decisions in patients with primary osteoporosis.²³

FRAX has limitations

FRAX underestimates the effect of glucocorticoids on fracture risk because steroid use is a yes-or-no question and its weight represents the average risk in a population that has ever used steroids, most of whom were using doses between 2.5 and 7.5 mg.

The WHO recognized this limitation and suggested an upward adjustment of risk for patients on 7.5 mg or more, ranging from 10% to 25%.²¹ For patients on high doses of steroids, this adjustment is still likely to result in underestimation of fracture risk and undertreatment of glucocorticoid-treated patients.

The 2010 recommendations adjust for this limitation, recommending treatment in the low-risk and medium-risk categories if the glucocorticoid dose is 7.5 mg or higher. If a patient is using high daily doses of steroids or has a declining bone density, the 2010 recommendations suggest increasing the risk category from low to medium or medium to high.

FRAX risk factors are dichotomous (yes/no) and are not adjusted for dose effects such as multiple fractures (vs a single fracture), heavy smoking (vs light smoking), heavy alcohol use (6 units per day vs 3 units), or severe rheumatoid arthritis (vs mild disease). Family history of osteoporosis in the FRAX is limited to parents with a hip fracture—vertebral fractures in a family member do not count.

Since FRAX uses the bone mineral density in the hip, it underestimates fracture risk in patients with low spine density but normal hip density. It may also underestimate fracture risk in patients with declining bone mass; the 2010 recommendations suggest the clinician should increase the risk category in this situation.

LIMITATIONS OF THE GUIDELINES

The 2010 recommendations do not include several important groups in which steroids are used, including transplant recipients, children, and patients on inhaled corticosteroids. The panel thought that there were insufficient data to make recommendations for these populations, as well as for premenopausal women and men younger than 50 years who did not have a prevalent fracture. The absence of a recommendation in these situations should not be considered a recommendation for no treatment; it is an acknowledgment of a lack of evidence, a lack of consensus among experts, and the need for additional clinical trials.

For premenopausal women and men under age 50 with a fracture, the recommendations are complicated and not intuitive. Zoledronic acid is not recommended for women of non-childbearing potential with a glucocorticoid duration of 1 to 3 months unless the steroid dose is at least 7.5 mg. This recommendation was based on panel voting and consensus that giving zoledronic acid, a medication with a 1-year duration of effect, in a patient on steroids for only 1 to 3 months was not warranted.

Teriparatide was recommended only if glucocorticoids are used for at least 3 months, although anyone who already has a fracture might be considered at high enough risk to warrant anabolic therapy regardless of steroid use or duration.

Zoledronic acid was excluded in women of childbearing potential, based on panel voting and consensus that drugs given in smaller amounts over 1 year might be less harmful to a fetus than one with a longer half-life given in a larger bolus once a year.

The panel could reach no consensus on women of childbearing potential with a prevalent fracture who were using less than 7.5 mg/day of glucocorticoids. A lack of consensus was the result of insufficient data to make evidence-based decisions and a disagreement among experts on the correct treatment.

The guidelines do not address the duration of treatment with bisphosphonates, a topic of importance because of concern for the potential long-term side effects of these medications.

THE BOTTOM LINE

The 2010 recommendations add a degree of complexity, with different medications recommended on the basis of glucocorticoid dose and duration as well as patient age, menopausal status, and childbearing potential. Guideline developers and clinicians face a difficult trade-off: easy-to-follow guidelines or more targeted guidelines that are more complex and therefore more difficult to use than previous guidelines.

This criticism is reasonable. The complexity is a result of insufficient evidence from clinical trials to make more exact and user-friendly recommendations, and also a result of the RAND/UCLA methodology. In cases that lack sufficient evidence on which to make a decision, the guideline development uses voting among experts in an attempt to develop consensus. This often results in complexity, lack of consensus, or inconsistencies.

The guidelines are straightforward for postmenopausal women and men age 50 and older on at least 7.5 mg prednisone for more than 3 months.

Since there is substantial evidence that many patients on glucocorticoid therapy go untreated, the risk of fracture in this population would be substantially reduced if clinicians would adhere to the recommendations.

Whenever a patient begins treatment with a glucocorticoid drug, we need to think about bone loss.

The American College of Rheumatology (ACR) issued recommendations for preventing and treating glucocorticoid-induced osteoporosis in 2010.¹ Compared with its previous guidelines,² the new ones are more tailored and nuanced but may be more difficult for physicians to follow. The guidelines call for assessing fracture risk using the computer-based Fracture Risk Assessment Tool, or FRAX (www/shef.ac.uk/FRAX), developed by the World Health Organization (WHO). For those without a computer or ready access to the Web, an application of FRAX is available for download on smartphones.

In this article, my purpose is to review the new recommendations and to offer my perspective, which does not necessarily reflect the opinions of the ACR.

DESPITE EVIDENCE, MANY PATIENTS RECEIVE NO INTERVENTION

Use of glucocorticoids is the most common cause of secondary osteoporosis. During the first 6 to 12 months of use, these drugs can cause a rapid loss of bone mass due to increased bone resorption; with continued use, they cause a slower but steady decline in bone mass due to reduced bone formation.³ Epidemiologic studies have found that the risk of fractures increases with dose, starting with doses as low as 2.5 mg per day of prednisone or its equivalent.⁴

Numerous clinical trials have evaluated the effect of bisphosphonates and teriparatide (Forteo) on bone mass and fracture risk in patients on glucocorticoid therapy. The bisphosphonates alendronate (Fosamax) and risedronate (Actonel) have both been shown to increase bone mass and reduce vertebral fracture risk in glucocorticoid recipients.^5–8 Zoledronic acid (Reclast), a parenteral bisphosphonate given in one annual dose, was shown to increase bone mass more than oral risedronate taken daily,⁹ and teriparatide, a formulation of parathyroid hormone, was better than alendronate.¹⁰

However, despite the known risk of fractures with glucocorticoid use and the demonstrated efficacy of available agents in preventing bone loss and fracture, many patients do not receive any intervention.^11,12

WHAT HAS HAPPENED SINCE 2001?

In the interval since 2001, several guidelines for managing glucocorticoid-induced osteoporosis have been published in other countries.^13–17 Broadly speaking, they recommend starting preventive drug therapy for patients at risk of fracture at the same time glucocorticoid drugs are started if the patient is expected to take glucocorticoids for more than 3 to 6 months in doses higher than 5 to 7.5 mg of prednisone or its equivalent daily.

Recommendations for patients who have been on glucocorticoids for longer than 3 to 6 months at initial evaluation have been based largely on T scores derived from dual-energy x-ray absorptiometry (DXA). Thresholds for initiating therapy have varied: the ACR in 2001 recommended preventive treatment if the T score is lower than −1.0, whereas British guidelines said −1.5 and Dutch guidelines said −2.5.

In the United States, since 2001 when the ACR published its last guidelines,² zoledronic acid and teriparatide have been approved for use in glucocorticoid-induced osteoporosis. In addition, guideline-development methodology has evolved and now is more scientifically rigorous. Finally, a risk-assessment tool has been developed that enables a more tailored approach (see below).

FRAX (www.shef.ac.uk/FRAX)

FRAX is a tool developed by the WHO to calculate the risk of fracture. If you go to the FRAX Web site and enter the required clinical information (race, age, sex, weight, height, previous fracture, family history of a fractured hip in a parent, current smoking, use of glucocorticoids, rheumatoid arthritis, secondary osteoporosis, consumption of three or more units of alcohol per day, and bone mineral density of the femoral neck), it will tell you the patient’s 10-year absolute (not relative) risk of major osteoporotic fracture and of hip fracture.

Since FRAX was unveiled in 2008, calculation of absolute fracture risk has become the standard method for making treatment decisions in patients with low bone mass who have not yet received any fracture-preventing treatment.¹⁸ The use of clinical risk factors in FRAX increases its ability to predict risk over and above the use of bone density by itself. And glucocorticoids are one of the clinical risk factors in FRAX.

But in which patients is treatment with a bisphosphonate or teriparatide cost-effective?

Thresholds for cost-effectiveness have been developed on the basis of economic assumptions that are country-specific. In the United States, the National Osteoporosis Foundation recommends drug therapy if the 10-year absolute risk of a major osteoporotic fracture of the hip, spine (clinical, not radiographic), wrist, or humerus is greater than 20% or if the risk of a hip fracture is greater than 3%.¹⁹

At equivalent bone densities, women taking glucocorticoids are at considerably higher risk of fracture than nonusers.²⁰ For example, consider a 65-year-old white woman, weight 59 kg, height 163 cm, no previous fractures, no parent with a fractured hip, no current smoking, no rheumatoid arthritis, no secondary osteoporosis, no excessive alcohol use, and a T score of −2.2 in the femoral neck. (Try this on the FRAX Web site.) If she does not use glucocorticoids, her 10-year risk of hip fracture is 2.0%; using glucocorticoids increases the risk to 3.6%. This is higher than the 3% National Osteoporosis Foundation guideline; thus, treatment would be recommended.

Also using FRAX, a 55-year-old white woman with a T score of −1.8 and on glucocorticoid therapy has a 67% higher risk of major osteoporotic fracture and an 80% higher risk of hip fracture.

For a third example, a white woman age 60, weight 70 kg, height 168 cm, negative for all the other risk factors but with a T score of −2.1 and on glucocorticoids has a calculated 10-year fracture risk of 2.1%, which is below the National Osteoporosis Foundation treatment threshold. However, most clinicians would probably recommend treatment for her, depending on the anticipated dose and duration of glucocorticoid therapy.

A caveat. In FRAX, glucocorticoid therapy is a categorical variable—a yes-or-no question—and yes is defined as having ever used a glucocorticoid in a dose greater than 5 mg for more than 3 months. Therefore, according to FRAX, a patient who took 5 mg of prednisone for 3 months 5 years ago has the same fracture risk as a patient on 60 mg of prednisone after a diagnosis of temporal arteritis. For this reason, the FRAX tool is likely to underestimate fracture risk, especially in patients currently taking glucocorticoids and those on higher doses of these drugs.

Kanis et al used the General Practice Research Database to adjust the fracture risk for glucocorticoid use in FRAX.²¹ At doses higher than 7.5 mg, the fracture risk had to be revised upward by 10% to 25% depending on the fracture site (hip vs any major osteoporotic fracture) and age (greater at age 40 than at age 90).

The underestimation of fracture risk led the ACR Expert Advisory Panel to create risk strata for major osteoporotic fractures, ie, low (< 10% risk per 10 years), medium (10%–20%), and high (> 20%) and uses these cut points to make treatment recommendations.

HOW THE 2010 GUIDELINES WERE DEVELOPED

Whereas the 2001 recommendations were based on a more informal consensus approach, the 2010 recommendations use a more scientifically rigorous methodology for guideline development, the Research and Development/University of California at Los Angeles (RAND/UCLA) Appropriateness Method. The RAND/UCLA method combines the best available scientific evidence with expert opinion to develop practice guidelines.

In drawing up the 2010 recommendations the ACR used three panels of experts. The Core Executive Panel conducted a systematic review of controlled clinical trials of therapies currently approved for treating glucocorticoid-induced osteoporosis in the United States, Canada, or the European Union. They found 53 articles meeting their inclusion criteria; an evidence report was produced that informed the development of the recommendations. This evidence report and guideline development process is available at http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)2151-4658. The Expert Advisory Panel framed the recommendations, and the Task Force Panel voted on them. The Core Executive Panel and Expert Advisory Panel constructed 48 patient-specific clinical scenarios using four variables: sex, age, race/ethnicity, and femoral neck T scores.

The members of the Task Force Panel were asked to use the evidence report and their expert judgment to vote on and rate the appropriateness of using a specific therapy in the context of each scenario on a 9-point Likert scale (1 = appropriate; 9 = not appropriate). Agreement occurred when 7 or more of the 10 panel members rated a scenario 1, 2, or 3. Disagreements were defined as 3 or more of the 10 members rating the scenario between 4 and 9 while the other members rated it lower.

Disagreements in voting were discussed in an attempt to achieve consensus, and a second vote was conducted which determined the final recommendations. If disagreement remained after the vote, no recommendation was made.

No attempt was made to assign priority of one drug over another when multiple drugs were deemed appropriate, although the final recommendations did differentiate drugs based on patient categories.

START WITH COUNSELING, ASSESSMENT

For patients starting or already on glucocorticoid therapy that is expected to last at least 3 months, the first step is to counsel them on lifestyle modifications (Table 1) and to assess their risk factors (Figure 1). Recommendations for monitoring patients receiving glucocorticoid therapy for at least 3 months are presented in Table 2.

These recommendations are based on literature review, and the strength of evidence is graded:

• Grade A—derived from multiple randomized controlled trials or a meta-analysis
• Grade B—derived from a single randomized controlled trial or nonrandomized study
• Grade C—derived from consensus, expert opinion, or case series.

This system is the same one used by the American College of Cardiology and is based on clinical trial data.²²

Recommendations for calcium intake and vitamin D supplementation were graded A; all other recommendations were graded C (Tables 1 and 2). It is important to note that practices that receive a grade of C may still be accepted as standard of care, such as fall assessment and smoking cessation.

FOR POSTMENOPAUSAL WOMEN AND FOR MEN AGE 50 AND OLDER

FRAX low-risk group

Recall that “low risk” based on the new ACR guidelines means that the 10-year absolute risk of a major osteoporotic fracture, as calculated with FRAX, is less than 10%.

• If glucocorticoid use is expected to last or has already lasted at least 3 months and the dose is less than 7.5 mg/day, no pharmacologic treatment is recommended.
• If glucocorticoid use is expected to last or has already lasted at least 3 months and the dose is 7.5 mg/day or higher, alendronate, risedronate, or zoledronic acid is recommended.

Comment. These are the most straightforward of the recommendations. All three bisphosphonates are recommended as treatment options if the glucocorticoid dose is at least 7.5 mg/day and the duration at least 3 months. Ibandronate (Boniva) was not included because it has no data from clinical trials.

“Medium risk” means that the 10-year absolute fracture risk of major osteoporotic fractures is 10% to 20%.

• If glucocorticoid use is anticipated to last or has lasted at least 3 months and the dose is less than 7.5 mg/day, alendronate or risedronate is recommended.
• If glucocorticoid use is anticipated to last or has lasted at least 3 months and the dose is 7.5 mg/day or higher, alendronate, risedronate, or zoledronic acid is recommended.

Comment. Treatment is recommended at all glucocorticoid doses for patients in the medium-risk category if the duration of glucocorticoid treatment is at least 3 months, with one difference: zoledronic acid is recommended only if the glucocorticoid dose is 7.5 mg/day or higher. This inconsistency persisted after a second round of voting by the Task Force Panel.

FRAX high-risk group

In this group, the 10-year risk of major osteoporotic fractures is higher than 20%.

• If the glucocorticoid dose is less than 5 mg/day for up to 1 month, alendronate, risedronate, or zoledronic acid is recommended.
• If the dose is 5 mg/day or more for up to 1 month, or any dose for more than 1 month, alendronate, risedronate, zoledronic acid or teriparatide is recommended.

Comment. Based on current National Osteoporosis Foundation guidelines, all patients with a 10-year risk greater than 20% are recommended for treatment for any duration and dose of glucocorticoid use. However, teriparatide is recommended only if the duration of glucocorticoid therapy is more than 1 month.

FOR PREMENOPAUSAL WOMEN AND FOR MEN YOUNGER THAN AGE 50

Use of FRAX is not appropriate in premenopausal women or in men younger than 50 years.

Younger patients with no prevalent fracture

For men younger than 50 and premenopausal women who have not had a previous fracture, data were considered inadequate to make a recommendation, and no votes were taken.

Prevalent fracture in premenopausal women of nonchildbearing potential

In premenopausal women of nonchildbearing potential who have had a fracture:

• If the glucocorticoid duration is 1 to 3 months and the dose is 5 mg/day or higher, alendronate or risedronate is recommended.
• If the duration is 1 to 3 months and the dose is 7.5 mg/day or higher, alendronate, risedronate, or zoledronic acid is recommended
• If the duration is more than 3 months, alendronate, risedronate, zoledronic acid, or teriparatide is recommended.

Comment. Treatment is recommended with any of the four medications in patients with a fracture and treated with glucocorticoids for more than 3 months. For shorter-duration glucocorticoid use (1–3 months) at 5 mg/day or higher, only alendronate and risedronate are recommended. If the dose is 7.5 mg/day or higher, any bisphosphonate is recommended. Zoledronic acid was consistently differentiated by the expert panel on the basis of dose and duration of glucocorticoid use, in view of its 1-year duration of effect after one dose.

Prevalent fracture in women of childbearing potential

• If the glucocorticoid duration is 1 to 3 months, there was no consensus (ie, voting disagreements could not be resolved).
• If the glucocorticoid duration is more than 3 months and the dose is 7.5 mg/day or more, alendronate, risedronate, or teriparatide is recommended.
• If the glucocorticoid duration is more than 3 months and the dose is less than 7.5 mg/day, there was no consensus.

Comment. Childbearing potential creates further complexities because of concern about fetal toxicity with bisphosphonates. For short-term glucocorticoid therapy at any dose and for therapy longer than 3 months at less than 7.5 mg, no consensus could be reached. For therapy longer than 3 months and with 7.5 mg/day or higher, treatment is recommended but not with zoledronic acid, based on the long half-life of the drug and concern for fetal toxicity.

Additional risk stratification

The panel recommended that if the following were present, a shift to a higher fracture risk category should be considered (low to medium, or medium to high):

• High daily dose of glucocorticoid
• High cumulative glucocorticoid dose
• Declining bone mineral density on serial DXA.

These are known risk factors that increase fracture risk but would not affect fracture risk in the FRAX model.

WHAT IS NEW IN THE 2010 RECOMMENDATIONS?

Recommendations for counseling now include fall risk assessment, height measurement, 25-hydroxyvitamin D measurement, and evaluation of patients for prevalent and incident fractures using vertebral fracture assessment by DXA or radiographic imaging of the spine.

Recommended drugs now include teriparatide and zoledronic acid, while estrogen and testosterone are no longer recommended as therapies for glucocorticoid-induced osteoporosis. Ibandronate is not included, since there have been no randomized controlled trials of this bisphosphonate in glucocorticoid-induced osteoporosis.

Recommendations for treatment in 2001 were based on T scores alone, while the 2010 recommendations use an assessment of absolute fracture risk based on FRAX for postmenopausal women and for men age 50 and older.

A clinician’s guide that summarizes the ACR recommendations is available at www.rheumatology.org/practice/clinical/guidelines/.

RECOMMENDATIONS DO NOT REPLACE CLINICAL JUDGMENT

Although the 2010 recommendations were more rigorous in their development process than those of 2001, they have limitations and they should not replace clinical judgment. Rather, they are intended to provide an evidence-based approach to guide clinicians in making treatment choices in patients on glucocorticoid therapy.

CONSIDERING ABSOLUTE FRACTURE RISK IN TREATMENT DECISIONS

The 2001 ACR guidelines recommended fracture-preventing treatment in all patients starting glucocorticoid therapy at more than 5 mg/day if the planned duration of treatment was at least 3 months, and in patients on long-term glucocorticoid therapy if the T score was less than −1.0. While these guidelines were simple and easy to use, they were not specific enough to provide useful guidance in specific scenarios.

A model of absolute fracture risk was not available in 2001. A 55-year old white woman with a T score of −1.1 who smoked, who had been using 5 mg of prednisone for the last 12 months, and who had stable bone mass on serial DXA scans would have been recommended for treatment based on the 2001 recommendations. If this patient’s FRAX-calculated 10-year absolute risk of a major osteoporotic fracture is less than 10%, that would be well below the National Osteoporosis Foundation’s cost-effective treatment threshold of 20%. The new guidelines suggest no treatment is needed, since the risk category is low and the dose is less than 7.5 mg. However, if on serial DXA this patient had a significant decline in bone mass, the guidelines suggest shifting the patient to a higher risk category, ie, from low to medium risk, which would result in a recommendation in favor of treatment.

The 2010 recommendations are not as simple to use as those from 2001. They encourage using FRAX to calculate fracture risk; thus, knowledge of the strengths and limitations of FRAX is required. Access to the internet in the examination room or use of the FRAX tool on a smartphone as well as willingness to spend a minute to calculate fracture risk are needed. For those who cannot or choose not to use the FRAX tool, the ACR publication provides tables for patient risk assessment based on age and T score. However, the tables would have to be readily available in the clinic, which may not be practical.

The 2010 recommendation provide a more nuanced approach to treatment in patients on glucocorticoid therapy and are likely to change treatment decisions based on their use, just as FRAX has altered treatment decisions in patients with primary osteoporosis.²³

FRAX has limitations

FRAX underestimates the effect of glucocorticoids on fracture risk because steroid use is a yes-or-no question and its weight represents the average risk in a population that has ever used steroids, most of whom were using doses between 2.5 and 7.5 mg.

The WHO recognized this limitation and suggested an upward adjustment of risk for patients on 7.5 mg or more, ranging from 10% to 25%.²¹ For patients on high doses of steroids, this adjustment is still likely to result in underestimation of fracture risk and undertreatment of glucocorticoid-treated patients.

The 2010 recommendations adjust for this limitation, recommending treatment in the low-risk and medium-risk categories if the glucocorticoid dose is 7.5 mg or higher. If a patient is using high daily doses of steroids or has a declining bone density, the 2010 recommendations suggest increasing the risk category from low to medium or medium to high.

FRAX risk factors are dichotomous (yes/no) and are not adjusted for dose effects such as multiple fractures (vs a single fracture), heavy smoking (vs light smoking), heavy alcohol use (6 units per day vs 3 units), or severe rheumatoid arthritis (vs mild disease). Family history of osteoporosis in the FRAX is limited to parents with a hip fracture—vertebral fractures in a family member do not count.

Since FRAX uses the bone mineral density in the hip, it underestimates fracture risk in patients with low spine density but normal hip density. It may also underestimate fracture risk in patients with declining bone mass; the 2010 recommendations suggest the clinician should increase the risk category in this situation.

LIMITATIONS OF THE GUIDELINES

The 2010 recommendations do not include several important groups in which steroids are used, including transplant recipients, children, and patients on inhaled corticosteroids. The panel thought that there were insufficient data to make recommendations for these populations, as well as for premenopausal women and men younger than 50 years who did not have a prevalent fracture. The absence of a recommendation in these situations should not be considered a recommendation for no treatment; it is an acknowledgment of a lack of evidence, a lack of consensus among experts, and the need for additional clinical trials.

For premenopausal women and men under age 50 with a fracture, the recommendations are complicated and not intuitive. Zoledronic acid is not recommended for women of non-childbearing potential with a glucocorticoid duration of 1 to 3 months unless the steroid dose is at least 7.5 mg. This recommendation was based on panel voting and consensus that giving zoledronic acid, a medication with a 1-year duration of effect, in a patient on steroids for only 1 to 3 months was not warranted.

Teriparatide was recommended only if glucocorticoids are used for at least 3 months, although anyone who already has a fracture might be considered at high enough risk to warrant anabolic therapy regardless of steroid use or duration.

Zoledronic acid was excluded in women of childbearing potential, based on panel voting and consensus that drugs given in smaller amounts over 1 year might be less harmful to a fetus than one with a longer half-life given in a larger bolus once a year.

The panel could reach no consensus on women of childbearing potential with a prevalent fracture who were using less than 7.5 mg/day of glucocorticoids. A lack of consensus was the result of insufficient data to make evidence-based decisions and a disagreement among experts on the correct treatment.

The guidelines do not address the duration of treatment with bisphosphonates, a topic of importance because of concern for the potential long-term side effects of these medications.

THE BOTTOM LINE

The 2010 recommendations add a degree of complexity, with different medications recommended on the basis of glucocorticoid dose and duration as well as patient age, menopausal status, and childbearing potential. Guideline developers and clinicians face a difficult trade-off: easy-to-follow guidelines or more targeted guidelines that are more complex and therefore more difficult to use than previous guidelines.

This criticism is reasonable. The complexity is a result of insufficient evidence from clinical trials to make more exact and user-friendly recommendations, and also a result of the RAND/UCLA methodology. In cases that lack sufficient evidence on which to make a decision, the guideline development uses voting among experts in an attempt to develop consensus. This often results in complexity, lack of consensus, or inconsistencies.

The guidelines are straightforward for postmenopausal women and men age 50 and older on at least 7.5 mg prednisone for more than 3 months.

Since there is substantial evidence that many patients on glucocorticoid therapy go untreated, the risk of fracture in this population would be substantially reduced if clinicians would adhere to the recommendations.

Cardiac tamponade is a life-threatening condition that can be palliated or cured, depending on its cause and on the timeliness of treatment. Making a timely diagnosis and providing the appropriate treatment can be gratifying for both patient and physician.

Cardiac tamponade occurs when fluid in the pericardial space reaches a pressure exceeding central venous pressure. This leads to jugular venous distention, visceral organ engorgement, edema, and elevated pulmonary venous pressure that causes dyspnea. Despite compensatory tachycardia, the decrease in cardiac filling leads to a fall in cardiac output and to arterial hypoperfusion of vital organs.

PEARL 1: SLOW ACCUMULATION LEADS TO EDEMA

The rate at which pericardial fluid accumulates influences the clinical presentation of cardiac tamponade, in particular whether or not there is edema. Whereas rapid accumulation is characterized more by hypotension than by edema, the slow accumulation of pericardial fluid affords the patient time to drink enough liquid to keep the central venous pressure higher than the rising pericardial pressure. Thus, edema and dyspnea are more prominent features of cardiac tamponade when there is a slow rise in pericardial pressure.

PEARL 2: EDEMA IS NOT ALWAYS TREATED WITH A DIURETIC

Edema is not always treated with a diuretic. In a patient who has a pericardial effusion that has developed slowly and who has been drinking enough fluid to keep the central venous pressure higher than the pericardial pressure, a diuretic can remove enough volume from the circulation to lower the central venous pressure below the intrapericardial pressure and thus convert a benign pericardial effusion to potentially lethal cardiac tamponade.

One must understand the cause of edema or low urine output before treating it. This underscores the importance of the history and the physical examination. All of the following must be assessed:

• Symptoms and time course of the illness
• Concurrent medical illnesses
• Neck veins
• Blood pressure and its response to inspiration
• Heart sounds
• Heart rate and rhythm
• Abdominal organ engorgement
• Edema (or its absence).

PEARL 3: UNDERSTANDING THE CAUSE IS ESSENTIAL

Understanding the cause of cardiac tamponade is essential.

A trauma patient first encountered in the emergency department may have an underlying disease, but the focus is squarely on the effects of trauma or violent injury. In a patient with multiple trauma, hypotension and tachycardia that do not respond to intravenous volume replacement when there is an obvious rise in central venous pressure should be clues to cardiac tamponade.¹

If the patient has recently undergone a cardiac procedure (for example, cardiac surgery, myocardial biopsy, coronary intervention, electrophysiologic study with intracardiac electrodes, transvenous pacemaker placement, pacemaker lead extraction, or radiofrequency ablation), knowing about the procedure narrows the differential diagnosis when hypotension, tachycardia, and jugular venous distention develop.

PEARL 4: CARDIAC OR AORTIC RUPTURE REQUIRES SURGERY

When the etiology of cardiac tamponade is cardiac or aortic rupture, the treatment is surgical.

Painful sudden causes of cardiac tamponade include hemopericardium due to rupture of the free wall after myocardial infarction, and spontaneous or posttraumatic dissection and rupture of the ascending aorta. Prompt diagnosis is necessary, but since these lesions will not close and heal spontaneously, the definitive treatment should be surgery. Moreover, needle removal of intrapericardial blood that has been opposing further bleeding is sure to permit bleeding to recur, often with lethal consequences.²

Causes of cardiac tamponade that have a less-acute onset are likely to be complications of medical problems. Medical illnesses known to be associated with cardiac tamponade include:

• Infectious disease (idiopathic or viral, associated with smallpox vaccination, mycobacterial, purulent bacterial, fungal)
• Metastatic cancer (lung, breast, esophagus, lymphoma, pancreas, liver, leukemia, stomach, melanoma)³
• Connective tissue disease (rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, scleroderma, Wegener granulomatosis, acute rheumatic fever)
• Endocrine disease (hypothyroidism)
• Drug side effects (procainamide, isoniazid, hydralazine, minoxidil, phenytoin, anticoagulants, methysergide)
• Inflammatory bowel disease (Crohn disease, ulcerative colitis)
• Congestive heart failure
• Uremia
• Radiation therapy
• Postmyocardial infarction syndrome (Dressler syndrome)
• Postpericardiotomy syndrome.

PEARL 5: REVIEW IMAGING BEFORE DIAGNOSING

What often brings a patient with cardiac tamponade to the attention of the physician is a finding on echocardiography, computed tomography, or magnetic resonance imaging of the chest.

Always review the imaging studies before making the diagnosis of cardiac tamponade. These tests must be reviewed to assess the anatomy and the size and location of the effusion. Particularly, one must look for atrial and right ventricular collapse and inferior vena caval plethora, which are echocardiographic signs of cardiac tamponade.⁴ Figures 1, 2, and 3 show imaging studies in a patient who presented with worsening cough 2 weeks after undergoing a cardiac procedure and who was found to have cardiac tamponade.

When the history and these imaging studies place cardiac tamponade high in the differential diagnosis as the cause of edema or dyspnea, it is time to reexamine the patient. The best first step is to measure pulsus paradoxus.

HOW PULSUS PARADOXUS OCCURS

To fully appreciate the subtleties of the next pearls, it is necessary to understand the pathophysiology of cardiac tamponade.

When pericardial fluid accumulation raises the pericardial pressure above the central venous pressure and pulmonary venous pressure (intravascular pressure), blood will not passively return to the right side of the heart from the venae cavae nor to the left side of the heart from the pulmonary veins unless it is influenced by the effects of respiration on intrathoracic pressure. During respiration, the right and left sides of the heart are alternately filled and deprived of their respective venous return.

During inspiration, as the intrathoracic pressure decreases, blood in the venae cavae empties into the right side of the heart, while blood in the pulmonary veins preferentially remains in the pulmonary veins, underfilling the left side of the heart. Since the right ventricle is more filled than the left ventricle during inspiration, the ventricular septum shifts from right to left, further opposing pulmonary venous return. As a result, during cardiac tamponade, the systemic blood pressure falls with inspiration.

During expiration the opposite occurs. Expiration decreases the intrathoracic volume, so the intrathoracic pressure rises. This tends to oppose vena caval return to the right side of the heart and to favor pulmonary venous return to the left side of the heart. The ventricular septum shifts from left to right, further accommodating left ventricular filling, raising stroke volume, and increasing blood pressure. This exaggerated alternate filling of the right and left sides of the heart during cardiac tamponade is what accounts for pulsus paradoxus, an inspiratory fall in systolic blood pressure of greater than 10 mm Hg.

If intravascular pressure is low (due to hemorrhage, dehydration, or diuretic therapy), the pressure in the pericardial space needed to oppose venous return is much less. In this low-pressure scenario, the results are low cardiac output and hypotension, which are treated by giving intravenous fluids to maintain intravascular volume.

PEARL 6: MEASURE PULSUS PARADOXUS

When cardiac tamponade is considered, one must always measure the pulsus paradoxus.

The term pulsus paradoxus was coined by Adolph Kussmaul in 1873, before physicians could even measure blood pressure. All they could do at that time was palpate the pulse and listen to the heart. Kussmaul described his observation as a conspicuous discrepancy between the cardiac action and the arterial pulse.

Although not described by Kussmaul, another explanation for this finding might be more suited to the use of the word “paradoxical.” When the pulse is palpated in a normal patient, with inspiration the pulse rate will increase via the Bainbridge reflex, and with expiration it will decrease. But in a patient with cardiac tamponade, there is a paradoxical inspiratory slowing of the pulse (because the decreased magnitude of the pulse at times makes it imperceptible) and an expiratory increase in pulse rate as the magnitude of the pulse again makes it palpable.

The magnitude of the fall in systolic blood pressure during inspiration has been used to estimate the level of hemodynamic impairment resulting from pericardial effusion.⁵ A rapidly accumulating pericardial effusion can have more hemodynamic impact than a much larger one that accumulates slowly. Thus, the intrapericardial pressure must be considered more than the volume of pericardial fluid.

When there is severe cardiac tamponade and overt pulsus paradoxus, simple palpation of a proximal arterial pulse can detect a marked inspiratory decrease or loss of the pulse, which returns with expiration. Tachycardia is almost always present, unless the cause is hypothyroidism.⁶

How to measure pulsus paradoxus with a manual sphygmomanometer

A stethoscope and manual sphygmomanometer are all that is needed to measure pulsus paradoxus. A noninvasive blood pressure monitor that averages multiple measurements cannot detect or quantify pulsus paradoxus.

The patient should be supine with the head elevated 30° to 45°, and the examiner should be seated comfortably at the patient’s side. The manometer should be on the opposite side of the patient in plain view of the examiner. Position the cuff on the arm above the elbow and place your stethoscope on the antecubital fossa. Then:

• Inflate the cuff 20 mm Hg above the highest systolic pressure previously auscultated.
• Slowly decrease the manometer pressure by 5 mm Hg and hold it there through two or three respiratory cycles while listening for the first Korotkoff (systolic) sound. Repeat this until you can hear the systolic sound (but only during expiration) and mentally note the pressure.
• Continue to decrease the manometer pressure by 5-mm Hg increments while listening. When the Korotkoff sounds no longer disappear with inspiration, mentally note this second value as well. The pulsus paradoxus is the difference between these values.
• When the Korotkoff sounds disappear as the manometer pressure is decreased, note this final value. This is the diastolic blood pressure.

PEARL 7: THE PLETHYSMOGRAM WAVE-FORM PARALLELS PULSUS PARADOXUS

Manual measurement of blood pressure and pulsus paradoxus can be difficult, especially in an obese patient or one with a fat-distorted arm on which the cuff does not maintain its position. In such patients, increased girth of the neck and abdomen also make it difficult to assess the jugular venous distention and visceral organ engorgement that characterize cardiac tamponade.

When the use of a sphygmomanometer is not possible, an arterial catheter can be inserted to demonstrate pulsus paradoxus. Simpler, however, is the novel use of another noninvasive instrument to detect and coarsely quantify pulsus paradoxus.⁷ The waveform on finger pulse oximetry can demonstrate pulsus paradoxus. The plethysmogram of the finger pulse oximeter can demonstrate the decrease in magnitude of the waveform with each inspiration (Figure 4).

Caution must be taken when interpreting this waveform, as with any measurement of pulsus paradoxus, to exclude a concomitant arrhythmia.

PEARL 8: PULSUS PARADOXUS WITHOUT CARDIAC TAMPONADE

Pulsus paradoxus can be present in the absence of cardiac tamponade. Once pulsus paradoxus of more than 10 mm Hg is measured, one must be sure the patient does not have a condition that can cause pulsus paradoxus without cardiac tamponade. Most of these are pulmonary conditions that necessitate an exaggerated inspiratory effort that can lower intrathoracic pressure sufficiently to oppose pulmonary venous return and cause a fall in systemic blood pressure:

• Chronic bronchitis
• Emphysema
• Mucus plug
• Pneumothorax
• Pulmonary embolism
• Stridor.

In these, there may be pulsus paradoxus, but not due to cardiac tamponade.

PEARL 9: CARDIAC TAMPONADE CAN BE PRESENT WITHOUT PULSUS PARADOXUS

Cardiac tamponade can be present without pulsus paradoxus. This occurs when certain conditions prevent inspiratory underfilling of the left ventricle relative to the filling of the right ventricle.⁸

How does this work? In cardiac tamponade, factors that drive the exaggerated fall in arterial pressure with inspiration (pulsus paradoxus) are the augmented right ventricular filling and the decreased left ventricular filling, both due to the lowering of the intrathoracic pressure. As the vena caval emptying is augmented, the right ventricular filling is increased, the ventricular septum shifts to the left, and pulmonary venous return to the heart is decreased.

Factors that can oppose pulsus paradoxus:

• Positive pressure ventilation prevents pulsus paradoxus by preventing the fall in intrathoracic pressure.
• Severe aortic regurgitation does not permit underfilling of the left ventricle during inspiration.
• An atrial septal defect will always equalize the right and left atrial pressures, preventing differential right ventricular and left ventricular filling with inspiration.
• Severe left ventricular hypertrophy does not permit the inspiratory shift of the ventricular septum from right to left that would otherwise lead to decreased left ventricular filling.
• Severe left ventricular dysfunction, with its low stroke volume and severe elevation of left ventricular end-diastolic pressure, never permits underfilling of the left ventricle, despite cardiac tamponade and an inspiratory decrease in intrathoracic pressure.
• Intravascular volume depletion due to hemorrhage, hemodialysis, or mistaken use of diuretics to treat edema can cause marked hypotension, making pulsus paradoxus impossible to detect.

Knowledge of underlying medical conditions, the likelihood of their causing cardiac tamponade, and the appearance of the echocardiogram prompt the physician to look further when the presence or absence of pulsus paradoxus does not fit with the working diagnosis.

The echocardiogram can give hints to the etiology of a pericardial effusion, such as clotted blood after trauma or a cardiac-perforating procedure, tumor studding of the epicardium,⁹ or fibrin strands indicating chronicity or an inflammatory process.¹⁰ Diastolic collapse of the right ventricle, more than collapse of the right atrium or left atrium, speaks for the severity of cardiac tamponade. With hemodynamically significant pericardial effusion and cardiac tamponade, the inferior vena cava is distended and does not decrease in size with inspiration unless there is severe intravascular volume depletion, at which time the inferior vena cava is underfilled throughout the respiratory cycle.

PEARL 10: PLAN HOW TO DRAIN

The size and location of the pericardial effusion and the patient’s hemodynamics must be integrated when deciding how to relieve cardiac tamponade. When cardiac tamponade is indeed severe and the patient and physician agree that it must be drained, the options are percutaneous needle aspiration (pericardiocentesis) and surgical pericardiostomy (creation of a pericardial window). Here again, as assessed by echocardiography, the access to the pericardial fluid should influence the choice.

Pericardiocentesis can be safely done if certain criteria are met. The patient must be able to lie still in the supine position, perhaps with the head of the bed elevated 30 degrees. Anticoagulation must be reversed or allowed time to resolve if drainage is not an emergency.

Pericardiocentesis can be risky or unsuccessful if there is not enough pericardial fluid to permit respiratory cardiac motion without perforating the heart with the needle; if the effusion is loculated (confined to a pocket) posteriorly; or if it is too far from the skin to permit precise control and placement of a spinal needle into the pericardial space. In cases of cardiac tamponade in which the anatomy indicates surgical pericardiostomy but severe hypotension prevents the induction of anesthesia and positive-pressure ventilation—which can result in profound, irreversible hypotension—percutaneous needle drainage (pericardiocentesis) should be performed in the operating room to relieve the tamponade before the induction of anesthesia and the surgical drainage.¹¹

To reiterate, a suspected cardiac or aortic rupture that causes cardiac tamponade is usually large and not apt to self-seal. In such cases, the halt in the accumulation of pericardial blood is due to hypotension and not due to spontaneous resolution. Open surgical drainage is required from the outset because an initial success of pericardiocentesis yields to the recurrence of cardiac tamponade.

PEARL 11: ANTICIPATE WHAT THE FLUID SHOULD LOOK LIKE

Before performing pericardiocentesis, anticipate the appearance of the pericardial fluid on the basis of the presumed etiology, ie:

• Sanguinous—trauma, heart surgery, cardiac perforation from a procedure, anticoagulation, uremia, or malignancy
• Serous—congestive heart failure, acute radiation therapy
• Purulent—infections (natural or postoperative)
• Turbid (like gold paint)—mycobacterial infection, rheumatoid arthritis, myxedema
• Chylous—pericardium fistulized to the thoracic duct by a natural or postsurgical cause.

Sanguinous pericardial effusion encountered during a pericardiocentesis, if not anticipated, can be daunting and can cause the operator to question if it is the result of inadvertent needle placement in a cardiac chamber. If the needle is indeed in the heart, blood often surges out under pressure in pulses, which strongly suggests that the needle is not in the pericardial space and should be removed; but if confirmation of the location is needed before removing the needle, it can be done by injecting 2 mL of agitated sterile saline through the pericardiocentesis needle during echocardiographic imaging.¹²

Before inserting the needle, the ideal access location and needle angle must be determined by the operator with echocardiographic transducer in hand. The distance from skin to a point just through the parietal pericardium can also be measured at this time.

Once the needle is in the pericardial fluid (and you are confident of its placement), removal of 50 to 100 mL of the fluid with a large syringe can be enough to afford the patient easier breathing, higher blood pressure, and lower pulsus paradoxus—and even the physician will breathe easier. The same syringe can be filled and emptied multiple times. Less traumatic and more complete removal of pericardial fluid requires insertion of a multihole pigtail catheter over a J-tipped guidewire that is introduced through the needle.

PEARL 12: DRAIN SLOWLY TO AVOID PULMONARY EDEMA

Pulmonary edema is an uncommon complication of pericardiocentesis that might be avoidable. Heralded by sudden coughing and pink, frothy sputum, it can rapidly deteriorate into respiratory failure. The mechanism has been attributed to a sudden increase in right ventricular stroke volume and resultant left ventricular filling after the excess pericardial fluid has been removed, before the systemic arteries, which constrict to keep the systemic blood pressure up during cardiac tamponade, have had time to relax.¹³

To avoid this complication, if the volume of pericardial fluid responsible for cardiac tamponade is large, it should be removed slowly,¹⁴ stopping for a several-minute rest after each 250 mL. Catheter removal of pericardial fluid by gravity drainage over 24 hours has been suggested.¹⁵ A drawback to this approach is catheter clotting or sludging before all the fluid has been removed. It is helpful to keep the drainage catheter close to the patient’s body temperature to make the fluid less viscous. Output should be monitored hourly.

When the pericardial fluid has been completely drained, one must decide how long to leave the catheter in. One reason to remove the catheter at this time is that it causes pleuritic pain; another is to avoid introducing infection. A reason to leave the catheter in is to observe the effect of medical treatment on the hourly pericardial fluid output. Nonsteroidal anti-inflammatory drugs are the drugs of first choice when treating pericardial inflammation and suppressing production of pericardial fluid.¹⁶ In most cases the catheter should not be left in place for more than 3 days.

Laboratory analysis of the pericardial fluid should shed light on its suspected cause. Analysis usually involves chemistry testing, microscopic inspection of blood cell smears, cytology, microbiologic stains and cultures, and immunologic tests. Results often take days. Meyers and colleagues¹⁷ expound on this subject.

Cardiac tamponade is a life-threatening condition that can be palliated or cured, depending on its cause and on the timeliness of treatment. Making a timely diagnosis and providing the appropriate treatment can be gratifying for both patient and physician.

Cardiac tamponade occurs when fluid in the pericardial space reaches a pressure exceeding central venous pressure. This leads to jugular venous distention, visceral organ engorgement, edema, and elevated pulmonary venous pressure that causes dyspnea. Despite compensatory tachycardia, the decrease in cardiac filling leads to a fall in cardiac output and to arterial hypoperfusion of vital organs.

PEARL 1: SLOW ACCUMULATION LEADS TO EDEMA

The rate at which pericardial fluid accumulates influences the clinical presentation of cardiac tamponade, in particular whether or not there is edema. Whereas rapid accumulation is characterized more by hypotension than by edema, the slow accumulation of pericardial fluid affords the patient time to drink enough liquid to keep the central venous pressure higher than the rising pericardial pressure. Thus, edema and dyspnea are more prominent features of cardiac tamponade when there is a slow rise in pericardial pressure.

PEARL 2: EDEMA IS NOT ALWAYS TREATED WITH A DIURETIC

Edema is not always treated with a diuretic. In a patient who has a pericardial effusion that has developed slowly and who has been drinking enough fluid to keep the central venous pressure higher than the pericardial pressure, a diuretic can remove enough volume from the circulation to lower the central venous pressure below the intrapericardial pressure and thus convert a benign pericardial effusion to potentially lethal cardiac tamponade.

One must understand the cause of edema or low urine output before treating it. This underscores the importance of the history and the physical examination. All of the following must be assessed:

• Symptoms and time course of the illness
• Concurrent medical illnesses
• Neck veins
• Blood pressure and its response to inspiration
• Heart sounds
• Heart rate and rhythm
• Abdominal organ engorgement
• Edema (or its absence).

PEARL 3: UNDERSTANDING THE CAUSE IS ESSENTIAL

Understanding the cause of cardiac tamponade is essential.

A trauma patient first encountered in the emergency department may have an underlying disease, but the focus is squarely on the effects of trauma or violent injury. In a patient with multiple trauma, hypotension and tachycardia that do not respond to intravenous volume replacement when there is an obvious rise in central venous pressure should be clues to cardiac tamponade.¹

If the patient has recently undergone a cardiac procedure (for example, cardiac surgery, myocardial biopsy, coronary intervention, electrophysiologic study with intracardiac electrodes, transvenous pacemaker placement, pacemaker lead extraction, or radiofrequency ablation), knowing about the procedure narrows the differential diagnosis when hypotension, tachycardia, and jugular venous distention develop.

PEARL 4: CARDIAC OR AORTIC RUPTURE REQUIRES SURGERY

When the etiology of cardiac tamponade is cardiac or aortic rupture, the treatment is surgical.

Painful sudden causes of cardiac tamponade include hemopericardium due to rupture of the free wall after myocardial infarction, and spontaneous or posttraumatic dissection and rupture of the ascending aorta. Prompt diagnosis is necessary, but since these lesions will not close and heal spontaneously, the definitive treatment should be surgery. Moreover, needle removal of intrapericardial blood that has been opposing further bleeding is sure to permit bleeding to recur, often with lethal consequences.²

Causes of cardiac tamponade that have a less-acute onset are likely to be complications of medical problems. Medical illnesses known to be associated with cardiac tamponade include:

• Infectious disease (idiopathic or viral, associated with smallpox vaccination, mycobacterial, purulent bacterial, fungal)
• Metastatic cancer (lung, breast, esophagus, lymphoma, pancreas, liver, leukemia, stomach, melanoma)³
• Connective tissue disease (rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, scleroderma, Wegener granulomatosis, acute rheumatic fever)
• Endocrine disease (hypothyroidism)
• Drug side effects (procainamide, isoniazid, hydralazine, minoxidil, phenytoin, anticoagulants, methysergide)
• Inflammatory bowel disease (Crohn disease, ulcerative colitis)
• Congestive heart failure
• Uremia
• Radiation therapy
• Postmyocardial infarction syndrome (Dressler syndrome)
• Postpericardiotomy syndrome.

PEARL 5: REVIEW IMAGING BEFORE DIAGNOSING

What often brings a patient with cardiac tamponade to the attention of the physician is a finding on echocardiography, computed tomography, or magnetic resonance imaging of the chest.

Always review the imaging studies before making the diagnosis of cardiac tamponade. These tests must be reviewed to assess the anatomy and the size and location of the effusion. Particularly, one must look for atrial and right ventricular collapse and inferior vena caval plethora, which are echocardiographic signs of cardiac tamponade.⁴ Figures 1, 2, and 3 show imaging studies in a patient who presented with worsening cough 2 weeks after undergoing a cardiac procedure and who was found to have cardiac tamponade.

When the history and these imaging studies place cardiac tamponade high in the differential diagnosis as the cause of edema or dyspnea, it is time to reexamine the patient. The best first step is to measure pulsus paradoxus.

HOW PULSUS PARADOXUS OCCURS

To fully appreciate the subtleties of the next pearls, it is necessary to understand the pathophysiology of cardiac tamponade.

When pericardial fluid accumulation raises the pericardial pressure above the central venous pressure and pulmonary venous pressure (intravascular pressure), blood will not passively return to the right side of the heart from the venae cavae nor to the left side of the heart from the pulmonary veins unless it is influenced by the effects of respiration on intrathoracic pressure. During respiration, the right and left sides of the heart are alternately filled and deprived of their respective venous return.

During inspiration, as the intrathoracic pressure decreases, blood in the venae cavae empties into the right side of the heart, while blood in the pulmonary veins preferentially remains in the pulmonary veins, underfilling the left side of the heart. Since the right ventricle is more filled than the left ventricle during inspiration, the ventricular septum shifts from right to left, further opposing pulmonary venous return. As a result, during cardiac tamponade, the systemic blood pressure falls with inspiration.

During expiration the opposite occurs. Expiration decreases the intrathoracic volume, so the intrathoracic pressure rises. This tends to oppose vena caval return to the right side of the heart and to favor pulmonary venous return to the left side of the heart. The ventricular septum shifts from left to right, further accommodating left ventricular filling, raising stroke volume, and increasing blood pressure. This exaggerated alternate filling of the right and left sides of the heart during cardiac tamponade is what accounts for pulsus paradoxus, an inspiratory fall in systolic blood pressure of greater than 10 mm Hg.

If intravascular pressure is low (due to hemorrhage, dehydration, or diuretic therapy), the pressure in the pericardial space needed to oppose venous return is much less. In this low-pressure scenario, the results are low cardiac output and hypotension, which are treated by giving intravenous fluids to maintain intravascular volume.

PEARL 6: MEASURE PULSUS PARADOXUS

When cardiac tamponade is considered, one must always measure the pulsus paradoxus.

The term pulsus paradoxus was coined by Adolph Kussmaul in 1873, before physicians could even measure blood pressure. All they could do at that time was palpate the pulse and listen to the heart. Kussmaul described his observation as a conspicuous discrepancy between the cardiac action and the arterial pulse.

Although not described by Kussmaul, another explanation for this finding might be more suited to the use of the word “paradoxical.” When the pulse is palpated in a normal patient, with inspiration the pulse rate will increase via the Bainbridge reflex, and with expiration it will decrease. But in a patient with cardiac tamponade, there is a paradoxical inspiratory slowing of the pulse (because the decreased magnitude of the pulse at times makes it imperceptible) and an expiratory increase in pulse rate as the magnitude of the pulse again makes it palpable.

The magnitude of the fall in systolic blood pressure during inspiration has been used to estimate the level of hemodynamic impairment resulting from pericardial effusion.⁵ A rapidly accumulating pericardial effusion can have more hemodynamic impact than a much larger one that accumulates slowly. Thus, the intrapericardial pressure must be considered more than the volume of pericardial fluid.

When there is severe cardiac tamponade and overt pulsus paradoxus, simple palpation of a proximal arterial pulse can detect a marked inspiratory decrease or loss of the pulse, which returns with expiration. Tachycardia is almost always present, unless the cause is hypothyroidism.⁶

How to measure pulsus paradoxus with a manual sphygmomanometer

A stethoscope and manual sphygmomanometer are all that is needed to measure pulsus paradoxus. A noninvasive blood pressure monitor that averages multiple measurements cannot detect or quantify pulsus paradoxus.

The patient should be supine with the head elevated 30° to 45°, and the examiner should be seated comfortably at the patient’s side. The manometer should be on the opposite side of the patient in plain view of the examiner. Position the cuff on the arm above the elbow and place your stethoscope on the antecubital fossa. Then:

• Inflate the cuff 20 mm Hg above the highest systolic pressure previously auscultated.
• Slowly decrease the manometer pressure by 5 mm Hg and hold it there through two or three respiratory cycles while listening for the first Korotkoff (systolic) sound. Repeat this until you can hear the systolic sound (but only during expiration) and mentally note the pressure.
• Continue to decrease the manometer pressure by 5-mm Hg increments while listening. When the Korotkoff sounds no longer disappear with inspiration, mentally note this second value as well. The pulsus paradoxus is the difference between these values.
• When the Korotkoff sounds disappear as the manometer pressure is decreased, note this final value. This is the diastolic blood pressure.

PEARL 7: THE PLETHYSMOGRAM WAVE-FORM PARALLELS PULSUS PARADOXUS

Manual measurement of blood pressure and pulsus paradoxus can be difficult, especially in an obese patient or one with a fat-distorted arm on which the cuff does not maintain its position. In such patients, increased girth of the neck and abdomen also make it difficult to assess the jugular venous distention and visceral organ engorgement that characterize cardiac tamponade.

When the use of a sphygmomanometer is not possible, an arterial catheter can be inserted to demonstrate pulsus paradoxus. Simpler, however, is the novel use of another noninvasive instrument to detect and coarsely quantify pulsus paradoxus.⁷ The waveform on finger pulse oximetry can demonstrate pulsus paradoxus. The plethysmogram of the finger pulse oximeter can demonstrate the decrease in magnitude of the waveform with each inspiration (Figure 4).

Caution must be taken when interpreting this waveform, as with any measurement of pulsus paradoxus, to exclude a concomitant arrhythmia.

PEARL 8: PULSUS PARADOXUS WITHOUT CARDIAC TAMPONADE

Pulsus paradoxus can be present in the absence of cardiac tamponade. Once pulsus paradoxus of more than 10 mm Hg is measured, one must be sure the patient does not have a condition that can cause pulsus paradoxus without cardiac tamponade. Most of these are pulmonary conditions that necessitate an exaggerated inspiratory effort that can lower intrathoracic pressure sufficiently to oppose pulmonary venous return and cause a fall in systemic blood pressure:

• Chronic bronchitis
• Emphysema
• Mucus plug
• Pneumothorax
• Pulmonary embolism
• Stridor.

In these, there may be pulsus paradoxus, but not due to cardiac tamponade.

PEARL 9: CARDIAC TAMPONADE CAN BE PRESENT WITHOUT PULSUS PARADOXUS

Cardiac tamponade can be present without pulsus paradoxus. This occurs when certain conditions prevent inspiratory underfilling of the left ventricle relative to the filling of the right ventricle.⁸

How does this work? In cardiac tamponade, factors that drive the exaggerated fall in arterial pressure with inspiration (pulsus paradoxus) are the augmented right ventricular filling and the decreased left ventricular filling, both due to the lowering of the intrathoracic pressure. As the vena caval emptying is augmented, the right ventricular filling is increased, the ventricular septum shifts to the left, and pulmonary venous return to the heart is decreased.

Factors that can oppose pulsus paradoxus:

• Positive pressure ventilation prevents pulsus paradoxus by preventing the fall in intrathoracic pressure.
• Severe aortic regurgitation does not permit underfilling of the left ventricle during inspiration.
• An atrial septal defect will always equalize the right and left atrial pressures, preventing differential right ventricular and left ventricular filling with inspiration.
• Severe left ventricular hypertrophy does not permit the inspiratory shift of the ventricular septum from right to left that would otherwise lead to decreased left ventricular filling.
• Severe left ventricular dysfunction, with its low stroke volume and severe elevation of left ventricular end-diastolic pressure, never permits underfilling of the left ventricle, despite cardiac tamponade and an inspiratory decrease in intrathoracic pressure.
• Intravascular volume depletion due to hemorrhage, hemodialysis, or mistaken use of diuretics to treat edema can cause marked hypotension, making pulsus paradoxus impossible to detect.

Knowledge of underlying medical conditions, the likelihood of their causing cardiac tamponade, and the appearance of the echocardiogram prompt the physician to look further when the presence or absence of pulsus paradoxus does not fit with the working diagnosis.

The echocardiogram can give hints to the etiology of a pericardial effusion, such as clotted blood after trauma or a cardiac-perforating procedure, tumor studding of the epicardium,⁹ or fibrin strands indicating chronicity or an inflammatory process.¹⁰ Diastolic collapse of the right ventricle, more than collapse of the right atrium or left atrium, speaks for the severity of cardiac tamponade. With hemodynamically significant pericardial effusion and cardiac tamponade, the inferior vena cava is distended and does not decrease in size with inspiration unless there is severe intravascular volume depletion, at which time the inferior vena cava is underfilled throughout the respiratory cycle.

PEARL 10: PLAN HOW TO DRAIN

The size and location of the pericardial effusion and the patient’s hemodynamics must be integrated when deciding how to relieve cardiac tamponade. When cardiac tamponade is indeed severe and the patient and physician agree that it must be drained, the options are percutaneous needle aspiration (pericardiocentesis) and surgical pericardiostomy (creation of a pericardial window). Here again, as assessed by echocardiography, the access to the pericardial fluid should influence the choice.

Pericardiocentesis can be safely done if certain criteria are met. The patient must be able to lie still in the supine position, perhaps with the head of the bed elevated 30 degrees. Anticoagulation must be reversed or allowed time to resolve if drainage is not an emergency.

Pericardiocentesis can be risky or unsuccessful if there is not enough pericardial fluid to permit respiratory cardiac motion without perforating the heart with the needle; if the effusion is loculated (confined to a pocket) posteriorly; or if it is too far from the skin to permit precise control and placement of a spinal needle into the pericardial space. In cases of cardiac tamponade in which the anatomy indicates surgical pericardiostomy but severe hypotension prevents the induction of anesthesia and positive-pressure ventilation—which can result in profound, irreversible hypotension—percutaneous needle drainage (pericardiocentesis) should be performed in the operating room to relieve the tamponade before the induction of anesthesia and the surgical drainage.¹¹

To reiterate, a suspected cardiac or aortic rupture that causes cardiac tamponade is usually large and not apt to self-seal. In such cases, the halt in the accumulation of pericardial blood is due to hypotension and not due to spontaneous resolution. Open surgical drainage is required from the outset because an initial success of pericardiocentesis yields to the recurrence of cardiac tamponade.

PEARL 11: ANTICIPATE WHAT THE FLUID SHOULD LOOK LIKE

Before performing pericardiocentesis, anticipate the appearance of the pericardial fluid on the basis of the presumed etiology, ie:

• Sanguinous—trauma, heart surgery, cardiac perforation from a procedure, anticoagulation, uremia, or malignancy
• Serous—congestive heart failure, acute radiation therapy
• Purulent—infections (natural or postoperative)
• Turbid (like gold paint)—mycobacterial infection, rheumatoid arthritis, myxedema
• Chylous—pericardium fistulized to the thoracic duct by a natural or postsurgical cause.

Sanguinous pericardial effusion encountered during a pericardiocentesis, if not anticipated, can be daunting and can cause the operator to question if it is the result of inadvertent needle placement in a cardiac chamber. If the needle is indeed in the heart, blood often surges out under pressure in pulses, which strongly suggests that the needle is not in the pericardial space and should be removed; but if confirmation of the location is needed before removing the needle, it can be done by injecting 2 mL of agitated sterile saline through the pericardiocentesis needle during echocardiographic imaging.¹²

Before inserting the needle, the ideal access location and needle angle must be determined by the operator with echocardiographic transducer in hand. The distance from skin to a point just through the parietal pericardium can also be measured at this time.

Once the needle is in the pericardial fluid (and you are confident of its placement), removal of 50 to 100 mL of the fluid with a large syringe can be enough to afford the patient easier breathing, higher blood pressure, and lower pulsus paradoxus—and even the physician will breathe easier. The same syringe can be filled and emptied multiple times. Less traumatic and more complete removal of pericardial fluid requires insertion of a multihole pigtail catheter over a J-tipped guidewire that is introduced through the needle.

PEARL 12: DRAIN SLOWLY TO AVOID PULMONARY EDEMA

Pulmonary edema is an uncommon complication of pericardiocentesis that might be avoidable. Heralded by sudden coughing and pink, frothy sputum, it can rapidly deteriorate into respiratory failure. The mechanism has been attributed to a sudden increase in right ventricular stroke volume and resultant left ventricular filling after the excess pericardial fluid has been removed, before the systemic arteries, which constrict to keep the systemic blood pressure up during cardiac tamponade, have had time to relax.¹³

To avoid this complication, if the volume of pericardial fluid responsible for cardiac tamponade is large, it should be removed slowly,¹⁴ stopping for a several-minute rest after each 250 mL. Catheter removal of pericardial fluid by gravity drainage over 24 hours has been suggested.¹⁵ A drawback to this approach is catheter clotting or sludging before all the fluid has been removed. It is helpful to keep the drainage catheter close to the patient’s body temperature to make the fluid less viscous. Output should be monitored hourly.

When the pericardial fluid has been completely drained, one must decide how long to leave the catheter in. One reason to remove the catheter at this time is that it causes pleuritic pain; another is to avoid introducing infection. A reason to leave the catheter in is to observe the effect of medical treatment on the hourly pericardial fluid output. Nonsteroidal anti-inflammatory drugs are the drugs of first choice when treating pericardial inflammation and suppressing production of pericardial fluid.¹⁶ In most cases the catheter should not be left in place for more than 3 days.

Laboratory analysis of the pericardial fluid should shed light on its suspected cause. Analysis usually involves chemistry testing, microscopic inspection of blood cell smears, cytology, microbiologic stains and cultures, and immunologic tests. Results often take days. Meyers and colleagues¹⁷ expound on this subject.

Cardiac tamponade is a life-threatening condition that can be palliated or cured, depending on its cause and on the timeliness of treatment. Making a timely diagnosis and providing the appropriate treatment can be gratifying for both patient and physician.

Cardiac tamponade occurs when fluid in the pericardial space reaches a pressure exceeding central venous pressure. This leads to jugular venous distention, visceral organ engorgement, edema, and elevated pulmonary venous pressure that causes dyspnea. Despite compensatory tachycardia, the decrease in cardiac filling leads to a fall in cardiac output and to arterial hypoperfusion of vital organs.

PEARL 1: SLOW ACCUMULATION LEADS TO EDEMA

The rate at which pericardial fluid accumulates influences the clinical presentation of cardiac tamponade, in particular whether or not there is edema. Whereas rapid accumulation is characterized more by hypotension than by edema, the slow accumulation of pericardial fluid affords the patient time to drink enough liquid to keep the central venous pressure higher than the rising pericardial pressure. Thus, edema and dyspnea are more prominent features of cardiac tamponade when there is a slow rise in pericardial pressure.

PEARL 2: EDEMA IS NOT ALWAYS TREATED WITH A DIURETIC

Edema is not always treated with a diuretic. In a patient who has a pericardial effusion that has developed slowly and who has been drinking enough fluid to keep the central venous pressure higher than the pericardial pressure, a diuretic can remove enough volume from the circulation to lower the central venous pressure below the intrapericardial pressure and thus convert a benign pericardial effusion to potentially lethal cardiac tamponade.

One must understand the cause of edema or low urine output before treating it. This underscores the importance of the history and the physical examination. All of the following must be assessed:

• Symptoms and time course of the illness
• Concurrent medical illnesses
• Neck veins
• Blood pressure and its response to inspiration
• Heart sounds
• Heart rate and rhythm
• Abdominal organ engorgement
• Edema (or its absence).

PEARL 3: UNDERSTANDING THE CAUSE IS ESSENTIAL

Understanding the cause of cardiac tamponade is essential.

A trauma patient first encountered in the emergency department may have an underlying disease, but the focus is squarely on the effects of trauma or violent injury. In a patient with multiple trauma, hypotension and tachycardia that do not respond to intravenous volume replacement when there is an obvious rise in central venous pressure should be clues to cardiac tamponade.¹

If the patient has recently undergone a cardiac procedure (for example, cardiac surgery, myocardial biopsy, coronary intervention, electrophysiologic study with intracardiac electrodes, transvenous pacemaker placement, pacemaker lead extraction, or radiofrequency ablation), knowing about the procedure narrows the differential diagnosis when hypotension, tachycardia, and jugular venous distention develop.

PEARL 4: CARDIAC OR AORTIC RUPTURE REQUIRES SURGERY

When the etiology of cardiac tamponade is cardiac or aortic rupture, the treatment is surgical.

Painful sudden causes of cardiac tamponade include hemopericardium due to rupture of the free wall after myocardial infarction, and spontaneous or posttraumatic dissection and rupture of the ascending aorta. Prompt diagnosis is necessary, but since these lesions will not close and heal spontaneously, the definitive treatment should be surgery. Moreover, needle removal of intrapericardial blood that has been opposing further bleeding is sure to permit bleeding to recur, often with lethal consequences.²

Causes of cardiac tamponade that have a less-acute onset are likely to be complications of medical problems. Medical illnesses known to be associated with cardiac tamponade include:

• Infectious disease (idiopathic or viral, associated with smallpox vaccination, mycobacterial, purulent bacterial, fungal)
• Metastatic cancer (lung, breast, esophagus, lymphoma, pancreas, liver, leukemia, stomach, melanoma)³
• Connective tissue disease (rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, scleroderma, Wegener granulomatosis, acute rheumatic fever)
• Endocrine disease (hypothyroidism)
• Drug side effects (procainamide, isoniazid, hydralazine, minoxidil, phenytoin, anticoagulants, methysergide)
• Inflammatory bowel disease (Crohn disease, ulcerative colitis)
• Congestive heart failure
• Uremia
• Radiation therapy
• Postmyocardial infarction syndrome (Dressler syndrome)
• Postpericardiotomy syndrome.

PEARL 5: REVIEW IMAGING BEFORE DIAGNOSING

What often brings a patient with cardiac tamponade to the attention of the physician is a finding on echocardiography, computed tomography, or magnetic resonance imaging of the chest.

Always review the imaging studies before making the diagnosis of cardiac tamponade. These tests must be reviewed to assess the anatomy and the size and location of the effusion. Particularly, one must look for atrial and right ventricular collapse and inferior vena caval plethora, which are echocardiographic signs of cardiac tamponade.⁴ Figures 1, 2, and 3 show imaging studies in a patient who presented with worsening cough 2 weeks after undergoing a cardiac procedure and who was found to have cardiac tamponade.

When the history and these imaging studies place cardiac tamponade high in the differential diagnosis as the cause of edema or dyspnea, it is time to reexamine the patient. The best first step is to measure pulsus paradoxus.

HOW PULSUS PARADOXUS OCCURS

To fully appreciate the subtleties of the next pearls, it is necessary to understand the pathophysiology of cardiac tamponade.

When pericardial fluid accumulation raises the pericardial pressure above the central venous pressure and pulmonary venous pressure (intravascular pressure), blood will not passively return to the right side of the heart from the venae cavae nor to the left side of the heart from the pulmonary veins unless it is influenced by the effects of respiration on intrathoracic pressure. During respiration, the right and left sides of the heart are alternately filled and deprived of their respective venous return.

During inspiration, as the intrathoracic pressure decreases, blood in the venae cavae empties into the right side of the heart, while blood in the pulmonary veins preferentially remains in the pulmonary veins, underfilling the left side of the heart. Since the right ventricle is more filled than the left ventricle during inspiration, the ventricular septum shifts from right to left, further opposing pulmonary venous return. As a result, during cardiac tamponade, the systemic blood pressure falls with inspiration.

During expiration the opposite occurs. Expiration decreases the intrathoracic volume, so the intrathoracic pressure rises. This tends to oppose vena caval return to the right side of the heart and to favor pulmonary venous return to the left side of the heart. The ventricular septum shifts from left to right, further accommodating left ventricular filling, raising stroke volume, and increasing blood pressure. This exaggerated alternate filling of the right and left sides of the heart during cardiac tamponade is what accounts for pulsus paradoxus, an inspiratory fall in systolic blood pressure of greater than 10 mm Hg.

If intravascular pressure is low (due to hemorrhage, dehydration, or diuretic therapy), the pressure in the pericardial space needed to oppose venous return is much less. In this low-pressure scenario, the results are low cardiac output and hypotension, which are treated by giving intravenous fluids to maintain intravascular volume.

PEARL 6: MEASURE PULSUS PARADOXUS

When cardiac tamponade is considered, one must always measure the pulsus paradoxus.

The term pulsus paradoxus was coined by Adolph Kussmaul in 1873, before physicians could even measure blood pressure. All they could do at that time was palpate the pulse and listen to the heart. Kussmaul described his observation as a conspicuous discrepancy between the cardiac action and the arterial pulse.

Although not described by Kussmaul, another explanation for this finding might be more suited to the use of the word “paradoxical.” When the pulse is palpated in a normal patient, with inspiration the pulse rate will increase via the Bainbridge reflex, and with expiration it will decrease. But in a patient with cardiac tamponade, there is a paradoxical inspiratory slowing of the pulse (because the decreased magnitude of the pulse at times makes it imperceptible) and an expiratory increase in pulse rate as the magnitude of the pulse again makes it palpable.

The magnitude of the fall in systolic blood pressure during inspiration has been used to estimate the level of hemodynamic impairment resulting from pericardial effusion.⁵ A rapidly accumulating pericardial effusion can have more hemodynamic impact than a much larger one that accumulates slowly. Thus, the intrapericardial pressure must be considered more than the volume of pericardial fluid.

When there is severe cardiac tamponade and overt pulsus paradoxus, simple palpation of a proximal arterial pulse can detect a marked inspiratory decrease or loss of the pulse, which returns with expiration. Tachycardia is almost always present, unless the cause is hypothyroidism.⁶

How to measure pulsus paradoxus with a manual sphygmomanometer

A stethoscope and manual sphygmomanometer are all that is needed to measure pulsus paradoxus. A noninvasive blood pressure monitor that averages multiple measurements cannot detect or quantify pulsus paradoxus.

The patient should be supine with the head elevated 30° to 45°, and the examiner should be seated comfortably at the patient’s side. The manometer should be on the opposite side of the patient in plain view of the examiner. Position the cuff on the arm above the elbow and place your stethoscope on the antecubital fossa. Then:

• Inflate the cuff 20 mm Hg above the highest systolic pressure previously auscultated.
• Slowly decrease the manometer pressure by 5 mm Hg and hold it there through two or three respiratory cycles while listening for the first Korotkoff (systolic) sound. Repeat this until you can hear the systolic sound (but only during expiration) and mentally note the pressure.
• Continue to decrease the manometer pressure by 5-mm Hg increments while listening. When the Korotkoff sounds no longer disappear with inspiration, mentally note this second value as well. The pulsus paradoxus is the difference between these values.
• When the Korotkoff sounds disappear as the manometer pressure is decreased, note this final value. This is the diastolic blood pressure.

PEARL 7: THE PLETHYSMOGRAM WAVE-FORM PARALLELS PULSUS PARADOXUS

Manual measurement of blood pressure and pulsus paradoxus can be difficult, especially in an obese patient or one with a fat-distorted arm on which the cuff does not maintain its position. In such patients, increased girth of the neck and abdomen also make it difficult to assess the jugular venous distention and visceral organ engorgement that characterize cardiac tamponade.

When the use of a sphygmomanometer is not possible, an arterial catheter can be inserted to demonstrate pulsus paradoxus. Simpler, however, is the novel use of another noninvasive instrument to detect and coarsely quantify pulsus paradoxus.⁷ The waveform on finger pulse oximetry can demonstrate pulsus paradoxus. The plethysmogram of the finger pulse oximeter can demonstrate the decrease in magnitude of the waveform with each inspiration (Figure 4).

Caution must be taken when interpreting this waveform, as with any measurement of pulsus paradoxus, to exclude a concomitant arrhythmia.

PEARL 8: PULSUS PARADOXUS WITHOUT CARDIAC TAMPONADE

Pulsus paradoxus can be present in the absence of cardiac tamponade. Once pulsus paradoxus of more than 10 mm Hg is measured, one must be sure the patient does not have a condition that can cause pulsus paradoxus without cardiac tamponade. Most of these are pulmonary conditions that necessitate an exaggerated inspiratory effort that can lower intrathoracic pressure sufficiently to oppose pulmonary venous return and cause a fall in systemic blood pressure:

• Chronic bronchitis
• Emphysema
• Mucus plug
• Pneumothorax
• Pulmonary embolism
• Stridor.

In these, there may be pulsus paradoxus, but not due to cardiac tamponade.

PEARL 9: CARDIAC TAMPONADE CAN BE PRESENT WITHOUT PULSUS PARADOXUS

Cardiac tamponade can be present without pulsus paradoxus. This occurs when certain conditions prevent inspiratory underfilling of the left ventricle relative to the filling of the right ventricle.⁸

How does this work? In cardiac tamponade, factors that drive the exaggerated fall in arterial pressure with inspiration (pulsus paradoxus) are the augmented right ventricular filling and the decreased left ventricular filling, both due to the lowering of the intrathoracic pressure. As the vena caval emptying is augmented, the right ventricular filling is increased, the ventricular septum shifts to the left, and pulmonary venous return to the heart is decreased.

Factors that can oppose pulsus paradoxus:

• Positive pressure ventilation prevents pulsus paradoxus by preventing the fall in intrathoracic pressure.
• Severe aortic regurgitation does not permit underfilling of the left ventricle during inspiration.
• An atrial septal defect will always equalize the right and left atrial pressures, preventing differential right ventricular and left ventricular filling with inspiration.
• Severe left ventricular hypertrophy does not permit the inspiratory shift of the ventricular septum from right to left that would otherwise lead to decreased left ventricular filling.
• Severe left ventricular dysfunction, with its low stroke volume and severe elevation of left ventricular end-diastolic pressure, never permits underfilling of the left ventricle, despite cardiac tamponade and an inspiratory decrease in intrathoracic pressure.
• Intravascular volume depletion due to hemorrhage, hemodialysis, or mistaken use of diuretics to treat edema can cause marked hypotension, making pulsus paradoxus impossible to detect.

Knowledge of underlying medical conditions, the likelihood of their causing cardiac tamponade, and the appearance of the echocardiogram prompt the physician to look further when the presence or absence of pulsus paradoxus does not fit with the working diagnosis.

The echocardiogram can give hints to the etiology of a pericardial effusion, such as clotted blood after trauma or a cardiac-perforating procedure, tumor studding of the epicardium,⁹ or fibrin strands indicating chronicity or an inflammatory process.¹⁰ Diastolic collapse of the right ventricle, more than collapse of the right atrium or left atrium, speaks for the severity of cardiac tamponade. With hemodynamically significant pericardial effusion and cardiac tamponade, the inferior vena cava is distended and does not decrease in size with inspiration unless there is severe intravascular volume depletion, at which time the inferior vena cava is underfilled throughout the respiratory cycle.

PEARL 10: PLAN HOW TO DRAIN

The size and location of the pericardial effusion and the patient’s hemodynamics must be integrated when deciding how to relieve cardiac tamponade. When cardiac tamponade is indeed severe and the patient and physician agree that it must be drained, the options are percutaneous needle aspiration (pericardiocentesis) and surgical pericardiostomy (creation of a pericardial window). Here again, as assessed by echocardiography, the access to the pericardial fluid should influence the choice.

Pericardiocentesis can be safely done if certain criteria are met. The patient must be able to lie still in the supine position, perhaps with the head of the bed elevated 30 degrees. Anticoagulation must be reversed or allowed time to resolve if drainage is not an emergency.

Pericardiocentesis can be risky or unsuccessful if there is not enough pericardial fluid to permit respiratory cardiac motion without perforating the heart with the needle; if the effusion is loculated (confined to a pocket) posteriorly; or if it is too far from the skin to permit precise control and placement of a spinal needle into the pericardial space. In cases of cardiac tamponade in which the anatomy indicates surgical pericardiostomy but severe hypotension prevents the induction of anesthesia and positive-pressure ventilation—which can result in profound, irreversible hypotension—percutaneous needle drainage (pericardiocentesis) should be performed in the operating room to relieve the tamponade before the induction of anesthesia and the surgical drainage.¹¹

To reiterate, a suspected cardiac or aortic rupture that causes cardiac tamponade is usually large and not apt to self-seal. In such cases, the halt in the accumulation of pericardial blood is due to hypotension and not due to spontaneous resolution. Open surgical drainage is required from the outset because an initial success of pericardiocentesis yields to the recurrence of cardiac tamponade.

PEARL 11: ANTICIPATE WHAT THE FLUID SHOULD LOOK LIKE

Before performing pericardiocentesis, anticipate the appearance of the pericardial fluid on the basis of the presumed etiology, ie:

• Sanguinous—trauma, heart surgery, cardiac perforation from a procedure, anticoagulation, uremia, or malignancy
• Serous—congestive heart failure, acute radiation therapy
• Purulent—infections (natural or postoperative)
• Turbid (like gold paint)—mycobacterial infection, rheumatoid arthritis, myxedema
• Chylous—pericardium fistulized to the thoracic duct by a natural or postsurgical cause.

Sanguinous pericardial effusion encountered during a pericardiocentesis, if not anticipated, can be daunting and can cause the operator to question if it is the result of inadvertent needle placement in a cardiac chamber. If the needle is indeed in the heart, blood often surges out under pressure in pulses, which strongly suggests that the needle is not in the pericardial space and should be removed; but if confirmation of the location is needed before removing the needle, it can be done by injecting 2 mL of agitated sterile saline through the pericardiocentesis needle during echocardiographic imaging.¹²

Before inserting the needle, the ideal access location and needle angle must be determined by the operator with echocardiographic transducer in hand. The distance from skin to a point just through the parietal pericardium can also be measured at this time.

Once the needle is in the pericardial fluid (and you are confident of its placement), removal of 50 to 100 mL of the fluid with a large syringe can be enough to afford the patient easier breathing, higher blood pressure, and lower pulsus paradoxus—and even the physician will breathe easier. The same syringe can be filled and emptied multiple times. Less traumatic and more complete removal of pericardial fluid requires insertion of a multihole pigtail catheter over a J-tipped guidewire that is introduced through the needle.

PEARL 12: DRAIN SLOWLY TO AVOID PULMONARY EDEMA

Pulmonary edema is an uncommon complication of pericardiocentesis that might be avoidable. Heralded by sudden coughing and pink, frothy sputum, it can rapidly deteriorate into respiratory failure. The mechanism has been attributed to a sudden increase in right ventricular stroke volume and resultant left ventricular filling after the excess pericardial fluid has been removed, before the systemic arteries, which constrict to keep the systemic blood pressure up during cardiac tamponade, have had time to relax.¹³

To avoid this complication, if the volume of pericardial fluid responsible for cardiac tamponade is large, it should be removed slowly,¹⁴ stopping for a several-minute rest after each 250 mL. Catheter removal of pericardial fluid by gravity drainage over 24 hours has been suggested.¹⁵ A drawback to this approach is catheter clotting or sludging before all the fluid has been removed. It is helpful to keep the drainage catheter close to the patient’s body temperature to make the fluid less viscous. Output should be monitored hourly.

When the pericardial fluid has been completely drained, one must decide how long to leave the catheter in. One reason to remove the catheter at this time is that it causes pleuritic pain; another is to avoid introducing infection. A reason to leave the catheter in is to observe the effect of medical treatment on the hourly pericardial fluid output. Nonsteroidal anti-inflammatory drugs are the drugs of first choice when treating pericardial inflammation and suppressing production of pericardial fluid.¹⁶ In most cases the catheter should not be left in place for more than 3 days.

Laboratory analysis of the pericardial fluid should shed light on its suspected cause. Analysis usually involves chemistry testing, microscopic inspection of blood cell smears, cytology, microbiologic stains and cultures, and immunologic tests. Results often take days. Meyers and colleagues¹⁷ expound on this subject.