Hospital Medicine

The Carl R. Darnall Army Medical Center at Fort Hood, Texas, is named in honor of Brigadier General Carl Rogers Darnall, a Texas native and career Army physician whose active-duty service spanned 35 years. Darnall, the oldest of 7 siblings, could not have imagined the enormity of the contributions that he would make and the lives that would be saved as he pursued a career in medicine.

Born on the family farm north of Dallas on Christmas Day in 1867, Darnall attended college in nearby Bonham and graduated from Transylvania University in Kentucky. He attended Jefferson Medical College in Philadelphia, Pennsylvania, graduating in 1890. Darnall spent several years in private practice before he joined the Army Medical Corps in 1896. He completed the Army Medical School in 1897. Opened in 1893, the Army Medical School was a 4-to-6-month course for civilian physicians entering active duty. The courses introduced physicians to the duties of medical officers as well as military surgery, medicine, and hygiene. It is considered by many to be the first school of public health in the U.S.

Darnall’s first assignments in Texas were followed by deployment to Cuba during the Spanish American War and then the Philippines, where he served as an operating surgeon and pathologist aboard the hospital ship, USS Relief. Darnall later accompanied an international expeditionary force to China in response to the Boxer Rebellion. In 1902, Darnall received an assignment to the Army Medical School in Washington, DC, that would change his life and the lives of millions around the world. Detailed as instructor for sanitary chemistry and operative surgery, he also served as secretary of the faculty. Just as Major Walter Reed and others before him, Darnall used his position at the Army Medical School to pursue important clinical research.

The complete story of the purification of drinking water is beyond the scope of this short biography. In brief, as early as 1894 the addition of chlorine to water was shown to render it “germ free.” In the 1890s, there were at least 2 attempts at water purification on a large scale with chlorine in European cities. One of the first uses of chlorine in the U.S. occurred in 1908 in Jersey City, New Jersey. At the Army Medical School, Darnall discovered the value of using compressed liquefied chlorine gas to purify water. He invented a mechanical liquid chlorine purifier in 1910 that became known as a chlorinator. In November 1911, Major Darnall authored a 15-page article concerning water purification.¹ Darnall also devised and patented a water filter, which the U.S. Army used for many years.

The principles of his chlorinator and use of anhydrous liquid chlorine were later applied to municipal water supplies throughout the world. The positive benefit of clean drinking water to improving public health is beyond measure. It has been said that more lives have been saved and more sickness prevented by Darnall’s contribution to sanitary water than by any other single achievement in medicine.

During World War I, Darnall was promoted to colonel and assigned to the Finance and Supply Division in the Office of the Surgeon General. After the war, he served as department surgeon in Hawaii. In 1925, he returned to the Office of the Surgeon General as executive officer. In November 1929, he was promoted to brigadier general and became the commanding general of the Army Medical Center and Walter Reed General Hospital, a position he held for 2 years until his retirement in 1931.Darnall died on January 18, 1941, at Walter Reed General Hospital just 6 days after his wife of 48 years had died at their home in Washington, DC. He is buried in Section 3 at Arlington National Cemetery. His 3 sons, Joseph Rogers, William Major, and Carl Robert, all served in some capacity in the Army.

Darnall Army Community Hospital opened in 1965, replacing the World War II-era hospital at Fort Hood. In 1984 a 5-year reconstruction project with additional floor space was completed. On May 1, 2006, the hospital was officially renamed the Carl R. Darnall Army Medical Center.

About this column
This column provides biographical sketches of the namesakes of military and VA health care facilities. To learn more about the individual your facility was named for or to offer a topic suggestion, contact us at [email protected] or on Facebook.

The Carl R. Darnall Army Medical Center at Fort Hood, Texas, is named in honor of Brigadier General Carl Rogers Darnall, a Texas native and career Army physician whose active-duty service spanned 35 years. Darnall, the oldest of 7 siblings, could not have imagined the enormity of the contributions that he would make and the lives that would be saved as he pursued a career in medicine.

Born on the family farm north of Dallas on Christmas Day in 1867, Darnall attended college in nearby Bonham and graduated from Transylvania University in Kentucky. He attended Jefferson Medical College in Philadelphia, Pennsylvania, graduating in 1890. Darnall spent several years in private practice before he joined the Army Medical Corps in 1896. He completed the Army Medical School in 1897. Opened in 1893, the Army Medical School was a 4-to-6-month course for civilian physicians entering active duty. The courses introduced physicians to the duties of medical officers as well as military surgery, medicine, and hygiene. It is considered by many to be the first school of public health in the U.S.

Darnall’s first assignments in Texas were followed by deployment to Cuba during the Spanish American War and then the Philippines, where he served as an operating surgeon and pathologist aboard the hospital ship, USS Relief. Darnall later accompanied an international expeditionary force to China in response to the Boxer Rebellion. In 1902, Darnall received an assignment to the Army Medical School in Washington, DC, that would change his life and the lives of millions around the world. Detailed as instructor for sanitary chemistry and operative surgery, he also served as secretary of the faculty. Just as Major Walter Reed and others before him, Darnall used his position at the Army Medical School to pursue important clinical research.

The complete story of the purification of drinking water is beyond the scope of this short biography. In brief, as early as 1894 the addition of chlorine to water was shown to render it “germ free.” In the 1890s, there were at least 2 attempts at water purification on a large scale with chlorine in European cities. One of the first uses of chlorine in the U.S. occurred in 1908 in Jersey City, New Jersey. At the Army Medical School, Darnall discovered the value of using compressed liquefied chlorine gas to purify water. He invented a mechanical liquid chlorine purifier in 1910 that became known as a chlorinator. In November 1911, Major Darnall authored a 15-page article concerning water purification.¹ Darnall also devised and patented a water filter, which the U.S. Army used for many years.

The principles of his chlorinator and use of anhydrous liquid chlorine were later applied to municipal water supplies throughout the world. The positive benefit of clean drinking water to improving public health is beyond measure. It has been said that more lives have been saved and more sickness prevented by Darnall’s contribution to sanitary water than by any other single achievement in medicine.

During World War I, Darnall was promoted to colonel and assigned to the Finance and Supply Division in the Office of the Surgeon General. After the war, he served as department surgeon in Hawaii. In 1925, he returned to the Office of the Surgeon General as executive officer. In November 1929, he was promoted to brigadier general and became the commanding general of the Army Medical Center and Walter Reed General Hospital, a position he held for 2 years until his retirement in 1931.Darnall died on January 18, 1941, at Walter Reed General Hospital just 6 days after his wife of 48 years had died at their home in Washington, DC. He is buried in Section 3 at Arlington National Cemetery. His 3 sons, Joseph Rogers, William Major, and Carl Robert, all served in some capacity in the Army.

Darnall Army Community Hospital opened in 1965, replacing the World War II-era hospital at Fort Hood. In 1984 a 5-year reconstruction project with additional floor space was completed. On May 1, 2006, the hospital was officially renamed the Carl R. Darnall Army Medical Center.

About this column
This column provides biographical sketches of the namesakes of military and VA health care facilities. To learn more about the individual your facility was named for or to offer a topic suggestion, contact us at [email protected] or on Facebook.

The Carl R. Darnall Army Medical Center at Fort Hood, Texas, is named in honor of Brigadier General Carl Rogers Darnall, a Texas native and career Army physician whose active-duty service spanned 35 years. Darnall, the oldest of 7 siblings, could not have imagined the enormity of the contributions that he would make and the lives that would be saved as he pursued a career in medicine.

Born on the family farm north of Dallas on Christmas Day in 1867, Darnall attended college in nearby Bonham and graduated from Transylvania University in Kentucky. He attended Jefferson Medical College in Philadelphia, Pennsylvania, graduating in 1890. Darnall spent several years in private practice before he joined the Army Medical Corps in 1896. He completed the Army Medical School in 1897. Opened in 1893, the Army Medical School was a 4-to-6-month course for civilian physicians entering active duty. The courses introduced physicians to the duties of medical officers as well as military surgery, medicine, and hygiene. It is considered by many to be the first school of public health in the U.S.

Darnall’s first assignments in Texas were followed by deployment to Cuba during the Spanish American War and then the Philippines, where he served as an operating surgeon and pathologist aboard the hospital ship, USS Relief. Darnall later accompanied an international expeditionary force to China in response to the Boxer Rebellion. In 1902, Darnall received an assignment to the Army Medical School in Washington, DC, that would change his life and the lives of millions around the world. Detailed as instructor for sanitary chemistry and operative surgery, he also served as secretary of the faculty. Just as Major Walter Reed and others before him, Darnall used his position at the Army Medical School to pursue important clinical research.

The complete story of the purification of drinking water is beyond the scope of this short biography. In brief, as early as 1894 the addition of chlorine to water was shown to render it “germ free.” In the 1890s, there were at least 2 attempts at water purification on a large scale with chlorine in European cities. One of the first uses of chlorine in the U.S. occurred in 1908 in Jersey City, New Jersey. At the Army Medical School, Darnall discovered the value of using compressed liquefied chlorine gas to purify water. He invented a mechanical liquid chlorine purifier in 1910 that became known as a chlorinator. In November 1911, Major Darnall authored a 15-page article concerning water purification.¹ Darnall also devised and patented a water filter, which the U.S. Army used for many years.

The principles of his chlorinator and use of anhydrous liquid chlorine were later applied to municipal water supplies throughout the world. The positive benefit of clean drinking water to improving public health is beyond measure. It has been said that more lives have been saved and more sickness prevented by Darnall’s contribution to sanitary water than by any other single achievement in medicine.

During World War I, Darnall was promoted to colonel and assigned to the Finance and Supply Division in the Office of the Surgeon General. After the war, he served as department surgeon in Hawaii. In 1925, he returned to the Office of the Surgeon General as executive officer. In November 1929, he was promoted to brigadier general and became the commanding general of the Army Medical Center and Walter Reed General Hospital, a position he held for 2 years until his retirement in 1931.Darnall died on January 18, 1941, at Walter Reed General Hospital just 6 days after his wife of 48 years had died at their home in Washington, DC. He is buried in Section 3 at Arlington National Cemetery. His 3 sons, Joseph Rogers, William Major, and Carl Robert, all served in some capacity in the Army.

Darnall Army Community Hospital opened in 1965, replacing the World War II-era hospital at Fort Hood. In 1984 a 5-year reconstruction project with additional floor space was completed. On May 1, 2006, the hospital was officially renamed the Carl R. Darnall Army Medical Center.

About this column
This column provides biographical sketches of the namesakes of military and VA health care facilities. To learn more about the individual your facility was named for or to offer a topic suggestion, contact us at [email protected] or on Facebook.

The landscape of postacute care in skilled nursing facilities (SNFs) in the United States is evolving. As the population ages, a growing number of elderly persons are being discharged to SNFs at an enormous cost and with clear evidence of disappointing outcomes. The reaction to these trends includes payment reforms that “bundle” hospital and postacute care, act as incentives to discourage SNFs, or penalize SNFs for undesired patient outcomes. Hospitalists are expected to increasingly feel the effect of these reforms.¹

Thus, hospitals are demonstrating renewed interest in reducing readmissions from SNFs. In this issue of Journal of Hospital Medicine, Rosen and colleagues present the results of the Enhanced Care Program (ECP), a multicomponent intervention consisting of 9 nurse practitioners (NPs), a pharmacist, a pharmacy technician, a nurse educator, a program administrator, and a medical director.² These providers are deployed to 8 SNFs around a large teaching hospital, providing direct clinical care as well as 24/7 call availability for enrolled patients, robust medication reconciliation, and monthly education for SNF nursing staff. A unique aspect of this model was that individual attending physicians in the associated SNFs could decide whether to enroll their patients in the model; patients not enrolled represented a contemporaneous control cohort. The authors found a nearly 30% reduction in the odds of 30-day readmission (OR 0.71 [0.60–0.85] after adjustment), which was robust to multiple sensitivity analyses, including a propensity-matched cohort comparison. The authors should be commended for working to mitigate these potential confounders, thereby strengthening their conclusions. Such a large reduction in readmissions reflects their high underlying prevalence (23% in the nonintervention cohort).

This report closely follows the evaluation of a similar program at the Cleveland Clinic called Connected Care Model (CCM), in which 4 physicians and 5 NPs or physician assistants provided care, including 24/7 call availability, in 7 associated SNFs.³ In a retrospective pre-post analysis comparing the 30-day readmission rates of these SNFs with those of others in the network, similar reductions in readmissions were observed. ECP and CCM represent important extensions of a much larger body of evidence, from the Evercare model⁴ to the Initiative to Reduce Avoidable Hospitalizations demonstration project, which suggests that adding NPs to nursing homes reduces hospitalizations.⁵

However, several factors have to be considered before disseminating ECP or CCM. First, other promising “proof of concept” quality improvement studies were not efficacious when rigorously tested in nursing homes.⁶ Second, these programs are representative of large academic medical centers, which may establish different relationships with different SNFs compared with smaller or less well-resourced hospitals. As the Initiative to Reduce Hospitalizations demonstrated, even a fundamentally similar intervention can have extremely different results depending on the nursing homes involved,⁵ and the science behind establishing effective hospital–SNF partnerships is still in its infancy.⁷ Third, both studies have significant methodological limitations, including most importantly that they are conducted within SNFs selected to be part of their hospitals’ network.

These significant early efforts also present an opportunity to reconsider the underlying assumption of these models: that adding more supervisory clinicians to SNFs is the right approach to reduce hospitalizations. Although adding resources is an attractive “plug and play” solution for many problems in healthcare delivery, placing only 1 NP in each of the 15,583 certified nursing facilities in the United States would employ fully 10% of the entire NP workforce. Amid rising concerns about costs related to our aging population, these interventions face substantial headwinds toward becoming the standard of care without demonstrating cost effectiveness. Furthermore, many SNF directors might suggest that hospitals and hospitalists working with them to address fundamental (but much more intransigent) problems in SNFs, such as high staff turnover, low concentration of highly skilled staff (RNs and MDs), regulatory burden, and hospitals using SNFs like stepdown units, could represent a generalizable and sustainable solution.

We realize that this argument is tricky for hospitalists because its underlying logic (care has become too complex, patients are too sick, and dedicated personnel are needed) also played a major role in establishing our existence. One possibility is that like hospitalists, NPs and a growing cadre of “SNFists” will become major drivers of quality improvement, education, and leadership locally at these facilities, thereby leading to sustainable change.⁸ Similarly, current conditions may drive recognition that a specific set of skills is required to function effectively in the SNF environment,⁹ just as we believe hospitalists need unique skills to excel in today’s hospital environment.

Studies such as that of Rosen et al. are valuable for JHM because they prompt us to recognize that we as hospitalists have much to share and learn from nursing homes and the dedicated practitioners who work there. In fact, we argue that few places in the healthcare system are more in need of innovation than hospital–nursing home relationships, and hospitalists do not just have a vested clinical interest; in many ways, we see a mirror of our own development as a “specialty.” We encourage hospitals and hospitalists to take up this challenge on behalf of some of the most vulnerable patients in our system during critical times in their care trajectory. As the Commission for Long-Term Care (www.ltccommission.org) wrote in its final report to Congress: “The need is great. The time to act is now.”

Disclosures

Dr. Burke is supported by a VA Health Services Research and Development (HSR&D) Career Development Award. All opinions are those of the authors and do not necessarily represent those of the Department of Veterans Affairs. Dr. Greysen has nothing to disclose.

The landscape of postacute care in skilled nursing facilities (SNFs) in the United States is evolving. As the population ages, a growing number of elderly persons are being discharged to SNFs at an enormous cost and with clear evidence of disappointing outcomes. The reaction to these trends includes payment reforms that “bundle” hospital and postacute care, act as incentives to discourage SNFs, or penalize SNFs for undesired patient outcomes. Hospitalists are expected to increasingly feel the effect of these reforms.¹

Thus, hospitals are demonstrating renewed interest in reducing readmissions from SNFs. In this issue of Journal of Hospital Medicine, Rosen and colleagues present the results of the Enhanced Care Program (ECP), a multicomponent intervention consisting of 9 nurse practitioners (NPs), a pharmacist, a pharmacy technician, a nurse educator, a program administrator, and a medical director.² These providers are deployed to 8 SNFs around a large teaching hospital, providing direct clinical care as well as 24/7 call availability for enrolled patients, robust medication reconciliation, and monthly education for SNF nursing staff. A unique aspect of this model was that individual attending physicians in the associated SNFs could decide whether to enroll their patients in the model; patients not enrolled represented a contemporaneous control cohort. The authors found a nearly 30% reduction in the odds of 30-day readmission (OR 0.71 [0.60–0.85] after adjustment), which was robust to multiple sensitivity analyses, including a propensity-matched cohort comparison. The authors should be commended for working to mitigate these potential confounders, thereby strengthening their conclusions. Such a large reduction in readmissions reflects their high underlying prevalence (23% in the nonintervention cohort).

This report closely follows the evaluation of a similar program at the Cleveland Clinic called Connected Care Model (CCM), in which 4 physicians and 5 NPs or physician assistants provided care, including 24/7 call availability, in 7 associated SNFs.³ In a retrospective pre-post analysis comparing the 30-day readmission rates of these SNFs with those of others in the network, similar reductions in readmissions were observed. ECP and CCM represent important extensions of a much larger body of evidence, from the Evercare model⁴ to the Initiative to Reduce Avoidable Hospitalizations demonstration project, which suggests that adding NPs to nursing homes reduces hospitalizations.⁵

However, several factors have to be considered before disseminating ECP or CCM. First, other promising “proof of concept” quality improvement studies were not efficacious when rigorously tested in nursing homes.⁶ Second, these programs are representative of large academic medical centers, which may establish different relationships with different SNFs compared with smaller or less well-resourced hospitals. As the Initiative to Reduce Hospitalizations demonstrated, even a fundamentally similar intervention can have extremely different results depending on the nursing homes involved,⁵ and the science behind establishing effective hospital–SNF partnerships is still in its infancy.⁷ Third, both studies have significant methodological limitations, including most importantly that they are conducted within SNFs selected to be part of their hospitals’ network.

These significant early efforts also present an opportunity to reconsider the underlying assumption of these models: that adding more supervisory clinicians to SNFs is the right approach to reduce hospitalizations. Although adding resources is an attractive “plug and play” solution for many problems in healthcare delivery, placing only 1 NP in each of the 15,583 certified nursing facilities in the United States would employ fully 10% of the entire NP workforce. Amid rising concerns about costs related to our aging population, these interventions face substantial headwinds toward becoming the standard of care without demonstrating cost effectiveness. Furthermore, many SNF directors might suggest that hospitals and hospitalists working with them to address fundamental (but much more intransigent) problems in SNFs, such as high staff turnover, low concentration of highly skilled staff (RNs and MDs), regulatory burden, and hospitals using SNFs like stepdown units, could represent a generalizable and sustainable solution.

We realize that this argument is tricky for hospitalists because its underlying logic (care has become too complex, patients are too sick, and dedicated personnel are needed) also played a major role in establishing our existence. One possibility is that like hospitalists, NPs and a growing cadre of “SNFists” will become major drivers of quality improvement, education, and leadership locally at these facilities, thereby leading to sustainable change.⁸ Similarly, current conditions may drive recognition that a specific set of skills is required to function effectively in the SNF environment,⁹ just as we believe hospitalists need unique skills to excel in today’s hospital environment.

Studies such as that of Rosen et al. are valuable for JHM because they prompt us to recognize that we as hospitalists have much to share and learn from nursing homes and the dedicated practitioners who work there. In fact, we argue that few places in the healthcare system are more in need of innovation than hospital–nursing home relationships, and hospitalists do not just have a vested clinical interest; in many ways, we see a mirror of our own development as a “specialty.” We encourage hospitals and hospitalists to take up this challenge on behalf of some of the most vulnerable patients in our system during critical times in their care trajectory. As the Commission for Long-Term Care (www.ltccommission.org) wrote in its final report to Congress: “The need is great. The time to act is now.”

Disclosures

Dr. Burke is supported by a VA Health Services Research and Development (HSR&D) Career Development Award. All opinions are those of the authors and do not necessarily represent those of the Department of Veterans Affairs. Dr. Greysen has nothing to disclose.

The landscape of postacute care in skilled nursing facilities (SNFs) in the United States is evolving. As the population ages, a growing number of elderly persons are being discharged to SNFs at an enormous cost and with clear evidence of disappointing outcomes. The reaction to these trends includes payment reforms that “bundle” hospital and postacute care, act as incentives to discourage SNFs, or penalize SNFs for undesired patient outcomes. Hospitalists are expected to increasingly feel the effect of these reforms.¹

Thus, hospitals are demonstrating renewed interest in reducing readmissions from SNFs. In this issue of Journal of Hospital Medicine, Rosen and colleagues present the results of the Enhanced Care Program (ECP), a multicomponent intervention consisting of 9 nurse practitioners (NPs), a pharmacist, a pharmacy technician, a nurse educator, a program administrator, and a medical director.² These providers are deployed to 8 SNFs around a large teaching hospital, providing direct clinical care as well as 24/7 call availability for enrolled patients, robust medication reconciliation, and monthly education for SNF nursing staff. A unique aspect of this model was that individual attending physicians in the associated SNFs could decide whether to enroll their patients in the model; patients not enrolled represented a contemporaneous control cohort. The authors found a nearly 30% reduction in the odds of 30-day readmission (OR 0.71 [0.60–0.85] after adjustment), which was robust to multiple sensitivity analyses, including a propensity-matched cohort comparison. The authors should be commended for working to mitigate these potential confounders, thereby strengthening their conclusions. Such a large reduction in readmissions reflects their high underlying prevalence (23% in the nonintervention cohort).

This report closely follows the evaluation of a similar program at the Cleveland Clinic called Connected Care Model (CCM), in which 4 physicians and 5 NPs or physician assistants provided care, including 24/7 call availability, in 7 associated SNFs.³ In a retrospective pre-post analysis comparing the 30-day readmission rates of these SNFs with those of others in the network, similar reductions in readmissions were observed. ECP and CCM represent important extensions of a much larger body of evidence, from the Evercare model⁴ to the Initiative to Reduce Avoidable Hospitalizations demonstration project, which suggests that adding NPs to nursing homes reduces hospitalizations.⁵

However, several factors have to be considered before disseminating ECP or CCM. First, other promising “proof of concept” quality improvement studies were not efficacious when rigorously tested in nursing homes.⁶ Second, these programs are representative of large academic medical centers, which may establish different relationships with different SNFs compared with smaller or less well-resourced hospitals. As the Initiative to Reduce Hospitalizations demonstrated, even a fundamentally similar intervention can have extremely different results depending on the nursing homes involved,⁵ and the science behind establishing effective hospital–SNF partnerships is still in its infancy.⁷ Third, both studies have significant methodological limitations, including most importantly that they are conducted within SNFs selected to be part of their hospitals’ network.

These significant early efforts also present an opportunity to reconsider the underlying assumption of these models: that adding more supervisory clinicians to SNFs is the right approach to reduce hospitalizations. Although adding resources is an attractive “plug and play” solution for many problems in healthcare delivery, placing only 1 NP in each of the 15,583 certified nursing facilities in the United States would employ fully 10% of the entire NP workforce. Amid rising concerns about costs related to our aging population, these interventions face substantial headwinds toward becoming the standard of care without demonstrating cost effectiveness. Furthermore, many SNF directors might suggest that hospitals and hospitalists working with them to address fundamental (but much more intransigent) problems in SNFs, such as high staff turnover, low concentration of highly skilled staff (RNs and MDs), regulatory burden, and hospitals using SNFs like stepdown units, could represent a generalizable and sustainable solution.

We realize that this argument is tricky for hospitalists because its underlying logic (care has become too complex, patients are too sick, and dedicated personnel are needed) also played a major role in establishing our existence. One possibility is that like hospitalists, NPs and a growing cadre of “SNFists” will become major drivers of quality improvement, education, and leadership locally at these facilities, thereby leading to sustainable change.⁸ Similarly, current conditions may drive recognition that a specific set of skills is required to function effectively in the SNF environment,⁹ just as we believe hospitalists need unique skills to excel in today’s hospital environment.

Studies such as that of Rosen et al. are valuable for JHM because they prompt us to recognize that we as hospitalists have much to share and learn from nursing homes and the dedicated practitioners who work there. In fact, we argue that few places in the healthcare system are more in need of innovation than hospital–nursing home relationships, and hospitalists do not just have a vested clinical interest; in many ways, we see a mirror of our own development as a “specialty.” We encourage hospitals and hospitalists to take up this challenge on behalf of some of the most vulnerable patients in our system during critical times in their care trajectory. As the Commission for Long-Term Care (www.ltccommission.org) wrote in its final report to Congress: “The need is great. The time to act is now.”

Disclosures

Dr. Burke is supported by a VA Health Services Research and Development (HSR&D) Career Development Award. All opinions are those of the authors and do not necessarily represent those of the Department of Veterans Affairs. Dr. Greysen has nothing to disclose.

The accountable care organization (ACO) concept, elucidated in 2006 as the development of partnerships between hospitals and physicians to coordinate and deliver efficient care,¹ seeks to remove existing barriers to improving value.² Some advocate this concept as a promising payment model that could successfully realign the current payment system to financially reward improvements in quality and efficiency that bend the cost curve.^3,4 Hospitalists fit well with this philosophy. As the fastest growing medical specialty in the history of American medicine, from a couple of thousand hospitalists in the mid-1990s to more than 50,000, the remarkable progression of hospitalists has ostensibly been driven partially by hospitals’ efforts to improve the value equation through enhanced efficiency in inpatient care. Importantly, hospitalists probably provide care for more than half of all hospitalized Medicare beneficiaries and increasingly patients in skilled nursing facilities (ie, SNFists).⁵ Along with primary care physicians, hospitalists thus represent an essential group of physicians needed to transform care delivery.

When the Affordable Care Act (ACA) established the Medicare Shared Savings Program (MSSP), ACOs leaped from being an intellectual concept^1,2 into a pragmatic health system strategy.^3,4 Following Medicare, various private health insurance plans and some state Medicaid programs entered into contracts with groups of healthcare providers (hospitals, physicians, or health systems) to serve as ACOs for their insured enrollees.⁶ Leavitt Partners’ ACO tracking database showed that the number of ACOs increased from 157 in March of 2012 to 782 in December of 2015.⁷

Until recently, the federal government’s commitment to having 50% of total Medicare spending via value-based payment models by 2018, coupled with endorsement from state Medicaid programs and commercial insurers, demonstrated strong support for continuation of ACOs. Unexpectedly on August 15, 2017, the Centers for Medicare & Medicaid Services (CMS) outlined a plan in its proposed rulemaking to cancel the Episode Payment Models and the Cardiac Rehabilitation incentive payment model, which were scheduled to commence on January 1, 2018. CMS also plans to scale back the mandatory Comprehensive Care for Joint Replacement (CCJR) bundled payment model from 67 selected geographic areas to 34. Although this proposed rulemaking created some equipoise in the healthcare industry regarding the future of value-based reimbursement approaches, cost containment and improved efficiency remain as major focuses of the federal government’s healthcare effort. Notably, CMS offers providers that are newly excluded from the CCJR model the opportunity to voluntarily participate in the program and is expected to increase opportunities for providers to participate in voluntary rather than large-scale mandatory episode payment model initiatives. In 2018, the agency also plans to develop new voluntary bundled payment models that will meet criteria to be considered an advanced alternative payment model for Quality Payment Program purposes.

Importantly, the value-based reimbursement movement was well underway before ACA legislation. Through ACA health reform, value-based reimbursement efforts were expanded through ACOs, bundled payments, value-based purchasing, the CMS Innovation Center and other initiatives. With health systems having an overflowing plate of activities, a wait-and-see attitude might seem reasonable at first. However, being unprepared for the inevitable shift to value-based reimbursement and reduced fee-for-service revenue places an organization at risk. A successful ACO requires system-level transformation, especially cultural and structural changes to achieve clinical integration. Being embedded in health system delivery, hospitalists can help shape a team-oriented culture and foster success in value-based payment models. This requires hospitalists to take a more active role in assessing and striking a balance between high-quality, cost-efficient care and financial risk inherent in ACO models.

The key to hospitalists fulfilling their value creation potential and becoming enablers for ACO success lies in developing a thorough understanding of the aspects of an ACO that promote efficient and effective care, while accounting for financial factors. Fundamentally, the ACO concept combines provider payment and delivery system reforms. Specifically, the definition of an ACO contains 3 factors: (1) a local healthcare organization (eg, hospital or multispecialty group of physicians) with a related set of providers that (2) can be held accountable for the cost and quality of care delivered to (3) a defined population. While the notion of accountability is not new, the locus of accountability is changed in the ACO model—emphasizing accountability at the level of actual care delivery with documentation of quality and cost outcomes. The ACO approach aims to address multiple, frequent, and recurring problems, including lack of financial incentives to improve quality and reduce cost, as well as the negative consequences of a pay-for-volume system—uncoordinated and fragmented care, overutilization of unnecessary tests and treatments, and poor patient experience all manifested as unwarranted geographic variation in practice patterns, clinical outcomes, and health spending. Participants in an ACO are rewarded financially if they can slow the growth of their patients’ healthcare costs while maintaining or improving the quality of care delivered. To succeed in this ACO world, hospitalists must assume greater prudence in the use of healthcare services while improving (or at a minimum, maintaining) patient outcomes, thus excising avoidable waste across the continuum of care.

More than half of ACOs include a hospital.⁸ However, whether hospital-led ACOs possess an advantage remains to be elucidated. Early reports indicated that physician-led ACOs saved more money.^9,10 However, others argue that hospitals¹¹ are better capitalized, have greater capacity for data sharing, and possess economies of scale that allow them to invest in more advanced technology, such as predictive modeling and/or simulation software. Such analytics can identify high-cost patients (ie, multiple comorbidities), super utilizers and populations lacking care, allowing ACOs to implement preventive measures to reduce unnecessary utilization. Recently released CMS MSSP 2016 performance data¹² showed that nearly half (45%) of physician-only ACOs earned shared savings, whereas 23% of ACOs that include hospitals earned shared savings. However, among all the ACOs that achieved savings, ACO entities that include hospitals generated the highest amount of shared savings (eg, Advocate, Hackensack Alliance, Cleveland Clinic, and AMITA Health). Notably, hospital-led ACOs tend to have much larger beneficiary populations than physician-led ACOs, which may create a scenario of higher risk but higher potential reward.

The emphasis on value over volume inherent in the development of ACOs occurs through employing care strategies implemented through changes in policies, and eventual structural and cultural changes. These changes require participating organizations to possess certain key competencies, including the following: 1) leadership that facilitates change; 2) organizational culture of teamwork; 3) collaborative relationships among providers; 4) information technology infrastructure for population management and care coordination; 5) infrastructure for monitoring, managing, and reporting quality; 6) ability to manage financial risk; 7) ability to receive and distribute payments or savings; and 8) resources for patient education and support.^2,3,13-16 Table 1 summarizes the broad range of roles that hospitalists can serve in delivering care to ACO populations.^17-19

Hospitalists’ active pursuit of nonclinical training and selection for administrative positions demonstrate their proclivity to provide these competencies. In addition to full-time clinician hospitalists, who can directly influence the delivery of high-value care to patients, hospitalists serve many other roles in hospitals and each can contribute differently based on their specialized expertise. Examples include the success of the Society of Hospital Medicine’s Leadership Academy; the acknowledged expertise of hospitalists in quality improvement (QI), informatics, teamwork, patient experience, care coordination and utilization; and advancement of hospitalists to senior leadership positions (eg, CQO, CMO, CEO). Given that nearly a third of healthcare expenditures are for hospital care,²⁰ hospitalists are in a unique position to foster ACO competencies while impacting the quality of care episodes associated with an index hospital stay.

Importantly, hospitalists cannot act as gatekeepers to restrict care. Managed care organizations and health maintenance organizations use of this approach in the 1990s to limit access to services in order to reduce costs led to unacceptable outcomes and numerous malpractice lawsuits. ACOs should aspire to deliver the most cost-effective high-quality care, and their performance should be monitored to ensure that they provide recommended services and timely access. The Medicare ACO contract holds the provider accountable for meeting 34 different quality measures (Supplemental Table 1), and hospitalists can influence outcomes for the majority. Especially through hospital and health system QI initiatives, hospitalists can directly impact and share accountability for measures ranging from care coordination to implementation of evidence-based care (eg, ACE inhibitors and beta blockers for heart failure) to patient and family caregiver experience.

Aligned with Medicare ACO quality measures, 5 high-impact target areas were identified for ACOs²¹: (1) Prevention and wellness; (2) Chronic conditions/care management; (3) Reduced hospitalizations; (4) Care transitions across the fragmented system; and (5) Multispecialty care coordination of complex patients. One essential element of a successful ACO is the ability to implement evidence-based medical guidelines and/or practices across the continuum of care for selected targeted initiatives. Optimizing care coordination/continuum requires team-based care, and hospitalists already routinely collaborate with nurses, social workers, case managers, pharmacists, and other stakeholders such as dieticians and physical therapists on inpatient care. Hospitalists are also experienced in facilitating communication and improving integration and coordination efficiencies among primary care providers and specialists, and between hospital care and post-acute care, as they coordinate post-hospital care and follow-up. This provides an opportunity to lead health system care coordination efforts, especially for complex and/or high-risk patients.^22,23 CMS MSSP 2016 performance data¹² showed that ACOs achieving shared savings had a decline in inpatient expenditures and utilization across several facility types (hospital, SNF, rehabilitation, long term). Postacute care management is critical to earning shared savings; SNF and Home Health expenditures fell by 18.3% and 9.7%, respectively, on average. We believe that hospitalists can have more influence over these cost areas by influencing treatment of hospitalized patients in a timely manner, discharge coordination, and selection of appropriate disposition locations. Hospitalists also play an integral role in ensuring the hospital performs well on quality metrics, including 30-day readmissions, hospital acquired conditions, and patient satisfaction. Examples below document the effectiveness of hospitalists in this new ACO era.

Care Transitions/Coordination

Before the Hospital Readmission Reduction Program (HRRP) delineated in the ACA, hospitalists developed Project BOOST (Better Outcomes by Optimizing Care Transitions) to improve hospital discharge care transition. The evidence-based foundation of this project led CMS to list Project BOOST as an example program that can reduce readmissions.²⁴ Through the dissemination and mentored implementation of Project BOOST to over 200 hospitals across the United States,²⁵ hospitalists contributed to the marked reduction in hospital readmission occurring since 2010.²⁶ Although hospital medicine began as a practice specific to the hospital setting, hospitalists’ skills generated growing demand for them in postacute facilities. SNF residents commonly come from hospitals postdischarge and suffer from multiple comorbidities and limitations in activities of daily living. Not surprisingly, SNF residents experience high rates of rehospitalizations.²⁷ Hospitalists can serve as a bridge between hospitals and SNFs and optimize this transition process to yield improved outcomes. Industry experts endorse this approach.²⁸ A recent study demonstrated a significant reduction in readmissions in 1 SNF (32.3% to 16.1%, odds ratio = 0.403, P < .001), by having a hospitalist-led team follow patients discharged from the hospital.²⁹

Chronic Conditions Management/High-Risk Patients

Interest in patients with multiple chronic comorbidities and social issues intensifies as healthcare systems focus limited resources on these high-risk patients to prevent the unnecessary use of costly services.^30,31 As health systems assume financial risk for health outcomes and costs of designated patient groups, they undertake efforts to understand the population they serve. Such efforts aim to identify patients with established high utilization patterns (or those at risk for high utilization). This knowledge enables targeted actions to provide access, treatment, and preventive interventions to avoid unneeded emergency and hospital services. Hospitalists commonly care for these patients and are positioned to lead the implementation of patient risk assessment and stratification, develop patient-centered care models across care settings, and act as a liaison with primary care. For frail elderly and seriously ill patients, the integration of hospitalists into palliative care provides several opportunities for improving the quality of care at the end of life.³² As patients and their family caregivers commonly do not address goals of care until faced with a life-threatening condition in the hospital, hospitalists represent ideal primary palliative care physicians to initiate these conversations.³³ A hospitalist communicating with a patient and/or their family caregiver about alleviating symptoms and clarifying patients’ preferences for care often yields decreases in ineffective healthcare utilization and better patient outcomes. The hospitalists’ ability to communicate with other providers within the hospital setting also allows them to better coordinate interdisciplinary care and prevent unnecessary and ineffective treatments and procedures.

De-Implementation/Waste Reduction

The largest inefficiencies in healthcare noted in the National Academy of Medicine report, Demanding Value from Our Health Care (2012), are failure to deliver known beneficial therapies or providing unnecessary or nonevidenced based services that do not improve outcomes, but come with associated risk and cost.³⁴ “De-implementation” of unnecessary diagnostic tests or ineffective or even harmful treatments by hospitalists represents a significant opportunity to reduce costs while maintaining or even improving the quality of care. The Society of Hospital Medicine joined the Choosing Wisely^® campaign and made 5 recommendations in adult care as an explicit starting point for eliminating waste in the hospital in 2013.³⁵ Since then, hospitalists have participated in multiple successful efforts to address overutilization of care; some published results include the following:

• decreased frequency of unnecessary common labs through a multifaceted hospitalist QI intervention;³⁶
• reduced length of stay and cost by appropriate use of telemetry;³⁷ and
• reduced unnecessary radiology testing by providing physicians with individualized audit and feedback reports.³⁸

Hundreds of ACOs now exist across the US, formed by a variety of providers including hospitals, physician groups, and integrated delivery systems. Provider groups range in size from primary care-focused physician groups with a handful of offices to large, multistate integrated delivery systems with dozens of hospitals and hundreds of office locations. Evaluations of ACO outcomes reveal mixed results.^9,39-53 Admittedly, assessments attempting to compare the magnitude of savings across ACO models are difficult given the variation in size, variability in specific efforts to influence utilization, and substantial turnover among participating beneficiaries.⁵⁴ Nonetheless, a newly published Office of Inspector General report⁵⁵ showed that most Medicare ACOs reduced spending and improved care quality (82% of the individual quality measures) over the first 3 years of the program, and savings increased with duration of an ACO program. The report also noted that considerable time and managerial resources are required to implement changes to improve quality and lower costs. While the political terrain ostensibly supports value-based care and the need to diminish the proportion of our nation’s gross domestic product dedicated to healthcare, health systems are navigating an environment that still largely rewards volume. Hospitalists may be ideal facilitators for this transitional period as they possess the clinical experience caring for complex patients with multiple comorbidities and quality improvement skills to lead efforts in this new ACO era.

Disclosures

The authors have nothing to disclose.

The accountable care organization (ACO) concept, elucidated in 2006 as the development of partnerships between hospitals and physicians to coordinate and deliver efficient care,¹ seeks to remove existing barriers to improving value.² Some advocate this concept as a promising payment model that could successfully realign the current payment system to financially reward improvements in quality and efficiency that bend the cost curve.^3,4 Hospitalists fit well with this philosophy. As the fastest growing medical specialty in the history of American medicine, from a couple of thousand hospitalists in the mid-1990s to more than 50,000, the remarkable progression of hospitalists has ostensibly been driven partially by hospitals’ efforts to improve the value equation through enhanced efficiency in inpatient care. Importantly, hospitalists probably provide care for more than half of all hospitalized Medicare beneficiaries and increasingly patients in skilled nursing facilities (ie, SNFists).⁵ Along with primary care physicians, hospitalists thus represent an essential group of physicians needed to transform care delivery.

When the Affordable Care Act (ACA) established the Medicare Shared Savings Program (MSSP), ACOs leaped from being an intellectual concept^1,2 into a pragmatic health system strategy.^3,4 Following Medicare, various private health insurance plans and some state Medicaid programs entered into contracts with groups of healthcare providers (hospitals, physicians, or health systems) to serve as ACOs for their insured enrollees.⁶ Leavitt Partners’ ACO tracking database showed that the number of ACOs increased from 157 in March of 2012 to 782 in December of 2015.⁷

Until recently, the federal government’s commitment to having 50% of total Medicare spending via value-based payment models by 2018, coupled with endorsement from state Medicaid programs and commercial insurers, demonstrated strong support for continuation of ACOs. Unexpectedly on August 15, 2017, the Centers for Medicare & Medicaid Services (CMS) outlined a plan in its proposed rulemaking to cancel the Episode Payment Models and the Cardiac Rehabilitation incentive payment model, which were scheduled to commence on January 1, 2018. CMS also plans to scale back the mandatory Comprehensive Care for Joint Replacement (CCJR) bundled payment model from 67 selected geographic areas to 34. Although this proposed rulemaking created some equipoise in the healthcare industry regarding the future of value-based reimbursement approaches, cost containment and improved efficiency remain as major focuses of the federal government’s healthcare effort. Notably, CMS offers providers that are newly excluded from the CCJR model the opportunity to voluntarily participate in the program and is expected to increase opportunities for providers to participate in voluntary rather than large-scale mandatory episode payment model initiatives. In 2018, the agency also plans to develop new voluntary bundled payment models that will meet criteria to be considered an advanced alternative payment model for Quality Payment Program purposes.

Importantly, the value-based reimbursement movement was well underway before ACA legislation. Through ACA health reform, value-based reimbursement efforts were expanded through ACOs, bundled payments, value-based purchasing, the CMS Innovation Center and other initiatives. With health systems having an overflowing plate of activities, a wait-and-see attitude might seem reasonable at first. However, being unprepared for the inevitable shift to value-based reimbursement and reduced fee-for-service revenue places an organization at risk. A successful ACO requires system-level transformation, especially cultural and structural changes to achieve clinical integration. Being embedded in health system delivery, hospitalists can help shape a team-oriented culture and foster success in value-based payment models. This requires hospitalists to take a more active role in assessing and striking a balance between high-quality, cost-efficient care and financial risk inherent in ACO models.

The key to hospitalists fulfilling their value creation potential and becoming enablers for ACO success lies in developing a thorough understanding of the aspects of an ACO that promote efficient and effective care, while accounting for financial factors. Fundamentally, the ACO concept combines provider payment and delivery system reforms. Specifically, the definition of an ACO contains 3 factors: (1) a local healthcare organization (eg, hospital or multispecialty group of physicians) with a related set of providers that (2) can be held accountable for the cost and quality of care delivered to (3) a defined population. While the notion of accountability is not new, the locus of accountability is changed in the ACO model—emphasizing accountability at the level of actual care delivery with documentation of quality and cost outcomes. The ACO approach aims to address multiple, frequent, and recurring problems, including lack of financial incentives to improve quality and reduce cost, as well as the negative consequences of a pay-for-volume system—uncoordinated and fragmented care, overutilization of unnecessary tests and treatments, and poor patient experience all manifested as unwarranted geographic variation in practice patterns, clinical outcomes, and health spending. Participants in an ACO are rewarded financially if they can slow the growth of their patients’ healthcare costs while maintaining or improving the quality of care delivered. To succeed in this ACO world, hospitalists must assume greater prudence in the use of healthcare services while improving (or at a minimum, maintaining) patient outcomes, thus excising avoidable waste across the continuum of care.

More than half of ACOs include a hospital.⁸ However, whether hospital-led ACOs possess an advantage remains to be elucidated. Early reports indicated that physician-led ACOs saved more money.^9,10 However, others argue that hospitals¹¹ are better capitalized, have greater capacity for data sharing, and possess economies of scale that allow them to invest in more advanced technology, such as predictive modeling and/or simulation software. Such analytics can identify high-cost patients (ie, multiple comorbidities), super utilizers and populations lacking care, allowing ACOs to implement preventive measures to reduce unnecessary utilization. Recently released CMS MSSP 2016 performance data¹² showed that nearly half (45%) of physician-only ACOs earned shared savings, whereas 23% of ACOs that include hospitals earned shared savings. However, among all the ACOs that achieved savings, ACO entities that include hospitals generated the highest amount of shared savings (eg, Advocate, Hackensack Alliance, Cleveland Clinic, and AMITA Health). Notably, hospital-led ACOs tend to have much larger beneficiary populations than physician-led ACOs, which may create a scenario of higher risk but higher potential reward.

The emphasis on value over volume inherent in the development of ACOs occurs through employing care strategies implemented through changes in policies, and eventual structural and cultural changes. These changes require participating organizations to possess certain key competencies, including the following: 1) leadership that facilitates change; 2) organizational culture of teamwork; 3) collaborative relationships among providers; 4) information technology infrastructure for population management and care coordination; 5) infrastructure for monitoring, managing, and reporting quality; 6) ability to manage financial risk; 7) ability to receive and distribute payments or savings; and 8) resources for patient education and support.^2,3,13-16 Table 1 summarizes the broad range of roles that hospitalists can serve in delivering care to ACO populations.^17-19

Hospitalists’ active pursuit of nonclinical training and selection for administrative positions demonstrate their proclivity to provide these competencies. In addition to full-time clinician hospitalists, who can directly influence the delivery of high-value care to patients, hospitalists serve many other roles in hospitals and each can contribute differently based on their specialized expertise. Examples include the success of the Society of Hospital Medicine’s Leadership Academy; the acknowledged expertise of hospitalists in quality improvement (QI), informatics, teamwork, patient experience, care coordination and utilization; and advancement of hospitalists to senior leadership positions (eg, CQO, CMO, CEO). Given that nearly a third of healthcare expenditures are for hospital care,²⁰ hospitalists are in a unique position to foster ACO competencies while impacting the quality of care episodes associated with an index hospital stay.

Importantly, hospitalists cannot act as gatekeepers to restrict care. Managed care organizations and health maintenance organizations use of this approach in the 1990s to limit access to services in order to reduce costs led to unacceptable outcomes and numerous malpractice lawsuits. ACOs should aspire to deliver the most cost-effective high-quality care, and their performance should be monitored to ensure that they provide recommended services and timely access. The Medicare ACO contract holds the provider accountable for meeting 34 different quality measures (Supplemental Table 1), and hospitalists can influence outcomes for the majority. Especially through hospital and health system QI initiatives, hospitalists can directly impact and share accountability for measures ranging from care coordination to implementation of evidence-based care (eg, ACE inhibitors and beta blockers for heart failure) to patient and family caregiver experience.

Aligned with Medicare ACO quality measures, 5 high-impact target areas were identified for ACOs²¹: (1) Prevention and wellness; (2) Chronic conditions/care management; (3) Reduced hospitalizations; (4) Care transitions across the fragmented system; and (5) Multispecialty care coordination of complex patients. One essential element of a successful ACO is the ability to implement evidence-based medical guidelines and/or practices across the continuum of care for selected targeted initiatives. Optimizing care coordination/continuum requires team-based care, and hospitalists already routinely collaborate with nurses, social workers, case managers, pharmacists, and other stakeholders such as dieticians and physical therapists on inpatient care. Hospitalists are also experienced in facilitating communication and improving integration and coordination efficiencies among primary care providers and specialists, and between hospital care and post-acute care, as they coordinate post-hospital care and follow-up. This provides an opportunity to lead health system care coordination efforts, especially for complex and/or high-risk patients.^22,23 CMS MSSP 2016 performance data¹² showed that ACOs achieving shared savings had a decline in inpatient expenditures and utilization across several facility types (hospital, SNF, rehabilitation, long term). Postacute care management is critical to earning shared savings; SNF and Home Health expenditures fell by 18.3% and 9.7%, respectively, on average. We believe that hospitalists can have more influence over these cost areas by influencing treatment of hospitalized patients in a timely manner, discharge coordination, and selection of appropriate disposition locations. Hospitalists also play an integral role in ensuring the hospital performs well on quality metrics, including 30-day readmissions, hospital acquired conditions, and patient satisfaction. Examples below document the effectiveness of hospitalists in this new ACO era.

Care Transitions/Coordination

Before the Hospital Readmission Reduction Program (HRRP) delineated in the ACA, hospitalists developed Project BOOST (Better Outcomes by Optimizing Care Transitions) to improve hospital discharge care transition. The evidence-based foundation of this project led CMS to list Project BOOST as an example program that can reduce readmissions.²⁴ Through the dissemination and mentored implementation of Project BOOST to over 200 hospitals across the United States,²⁵ hospitalists contributed to the marked reduction in hospital readmission occurring since 2010.²⁶ Although hospital medicine began as a practice specific to the hospital setting, hospitalists’ skills generated growing demand for them in postacute facilities. SNF residents commonly come from hospitals postdischarge and suffer from multiple comorbidities and limitations in activities of daily living. Not surprisingly, SNF residents experience high rates of rehospitalizations.²⁷ Hospitalists can serve as a bridge between hospitals and SNFs and optimize this transition process to yield improved outcomes. Industry experts endorse this approach.²⁸ A recent study demonstrated a significant reduction in readmissions in 1 SNF (32.3% to 16.1%, odds ratio = 0.403, P < .001), by having a hospitalist-led team follow patients discharged from the hospital.²⁹

Chronic Conditions Management/High-Risk Patients

Interest in patients with multiple chronic comorbidities and social issues intensifies as healthcare systems focus limited resources on these high-risk patients to prevent the unnecessary use of costly services.^30,31 As health systems assume financial risk for health outcomes and costs of designated patient groups, they undertake efforts to understand the population they serve. Such efforts aim to identify patients with established high utilization patterns (or those at risk for high utilization). This knowledge enables targeted actions to provide access, treatment, and preventive interventions to avoid unneeded emergency and hospital services. Hospitalists commonly care for these patients and are positioned to lead the implementation of patient risk assessment and stratification, develop patient-centered care models across care settings, and act as a liaison with primary care. For frail elderly and seriously ill patients, the integration of hospitalists into palliative care provides several opportunities for improving the quality of care at the end of life.³² As patients and their family caregivers commonly do not address goals of care until faced with a life-threatening condition in the hospital, hospitalists represent ideal primary palliative care physicians to initiate these conversations.³³ A hospitalist communicating with a patient and/or their family caregiver about alleviating symptoms and clarifying patients’ preferences for care often yields decreases in ineffective healthcare utilization and better patient outcomes. The hospitalists’ ability to communicate with other providers within the hospital setting also allows them to better coordinate interdisciplinary care and prevent unnecessary and ineffective treatments and procedures.

De-Implementation/Waste Reduction

The largest inefficiencies in healthcare noted in the National Academy of Medicine report, Demanding Value from Our Health Care (2012), are failure to deliver known beneficial therapies or providing unnecessary or nonevidenced based services that do not improve outcomes, but come with associated risk and cost.³⁴ “De-implementation” of unnecessary diagnostic tests or ineffective or even harmful treatments by hospitalists represents a significant opportunity to reduce costs while maintaining or even improving the quality of care. The Society of Hospital Medicine joined the Choosing Wisely^® campaign and made 5 recommendations in adult care as an explicit starting point for eliminating waste in the hospital in 2013.³⁵ Since then, hospitalists have participated in multiple successful efforts to address overutilization of care; some published results include the following:

• decreased frequency of unnecessary common labs through a multifaceted hospitalist QI intervention;³⁶
• reduced length of stay and cost by appropriate use of telemetry;³⁷ and
• reduced unnecessary radiology testing by providing physicians with individualized audit and feedback reports.³⁸

Hundreds of ACOs now exist across the US, formed by a variety of providers including hospitals, physician groups, and integrated delivery systems. Provider groups range in size from primary care-focused physician groups with a handful of offices to large, multistate integrated delivery systems with dozens of hospitals and hundreds of office locations. Evaluations of ACO outcomes reveal mixed results.^9,39-53 Admittedly, assessments attempting to compare the magnitude of savings across ACO models are difficult given the variation in size, variability in specific efforts to influence utilization, and substantial turnover among participating beneficiaries.⁵⁴ Nonetheless, a newly published Office of Inspector General report⁵⁵ showed that most Medicare ACOs reduced spending and improved care quality (82% of the individual quality measures) over the first 3 years of the program, and savings increased with duration of an ACO program. The report also noted that considerable time and managerial resources are required to implement changes to improve quality and lower costs. While the political terrain ostensibly supports value-based care and the need to diminish the proportion of our nation’s gross domestic product dedicated to healthcare, health systems are navigating an environment that still largely rewards volume. Hospitalists may be ideal facilitators for this transitional period as they possess the clinical experience caring for complex patients with multiple comorbidities and quality improvement skills to lead efforts in this new ACO era.

Disclosures

The authors have nothing to disclose.

The accountable care organization (ACO) concept, elucidated in 2006 as the development of partnerships between hospitals and physicians to coordinate and deliver efficient care,¹ seeks to remove existing barriers to improving value.² Some advocate this concept as a promising payment model that could successfully realign the current payment system to financially reward improvements in quality and efficiency that bend the cost curve.^3,4 Hospitalists fit well with this philosophy. As the fastest growing medical specialty in the history of American medicine, from a couple of thousand hospitalists in the mid-1990s to more than 50,000, the remarkable progression of hospitalists has ostensibly been driven partially by hospitals’ efforts to improve the value equation through enhanced efficiency in inpatient care. Importantly, hospitalists probably provide care for more than half of all hospitalized Medicare beneficiaries and increasingly patients in skilled nursing facilities (ie, SNFists).⁵ Along with primary care physicians, hospitalists thus represent an essential group of physicians needed to transform care delivery.

When the Affordable Care Act (ACA) established the Medicare Shared Savings Program (MSSP), ACOs leaped from being an intellectual concept^1,2 into a pragmatic health system strategy.^3,4 Following Medicare, various private health insurance plans and some state Medicaid programs entered into contracts with groups of healthcare providers (hospitals, physicians, or health systems) to serve as ACOs for their insured enrollees.⁶ Leavitt Partners’ ACO tracking database showed that the number of ACOs increased from 157 in March of 2012 to 782 in December of 2015.⁷

Until recently, the federal government’s commitment to having 50% of total Medicare spending via value-based payment models by 2018, coupled with endorsement from state Medicaid programs and commercial insurers, demonstrated strong support for continuation of ACOs. Unexpectedly on August 15, 2017, the Centers for Medicare & Medicaid Services (CMS) outlined a plan in its proposed rulemaking to cancel the Episode Payment Models and the Cardiac Rehabilitation incentive payment model, which were scheduled to commence on January 1, 2018. CMS also plans to scale back the mandatory Comprehensive Care for Joint Replacement (CCJR) bundled payment model from 67 selected geographic areas to 34. Although this proposed rulemaking created some equipoise in the healthcare industry regarding the future of value-based reimbursement approaches, cost containment and improved efficiency remain as major focuses of the federal government’s healthcare effort. Notably, CMS offers providers that are newly excluded from the CCJR model the opportunity to voluntarily participate in the program and is expected to increase opportunities for providers to participate in voluntary rather than large-scale mandatory episode payment model initiatives. In 2018, the agency also plans to develop new voluntary bundled payment models that will meet criteria to be considered an advanced alternative payment model for Quality Payment Program purposes.

Importantly, the value-based reimbursement movement was well underway before ACA legislation. Through ACA health reform, value-based reimbursement efforts were expanded through ACOs, bundled payments, value-based purchasing, the CMS Innovation Center and other initiatives. With health systems having an overflowing plate of activities, a wait-and-see attitude might seem reasonable at first. However, being unprepared for the inevitable shift to value-based reimbursement and reduced fee-for-service revenue places an organization at risk. A successful ACO requires system-level transformation, especially cultural and structural changes to achieve clinical integration. Being embedded in health system delivery, hospitalists can help shape a team-oriented culture and foster success in value-based payment models. This requires hospitalists to take a more active role in assessing and striking a balance between high-quality, cost-efficient care and financial risk inherent in ACO models.

The key to hospitalists fulfilling their value creation potential and becoming enablers for ACO success lies in developing a thorough understanding of the aspects of an ACO that promote efficient and effective care, while accounting for financial factors. Fundamentally, the ACO concept combines provider payment and delivery system reforms. Specifically, the definition of an ACO contains 3 factors: (1) a local healthcare organization (eg, hospital or multispecialty group of physicians) with a related set of providers that (2) can be held accountable for the cost and quality of care delivered to (3) a defined population. While the notion of accountability is not new, the locus of accountability is changed in the ACO model—emphasizing accountability at the level of actual care delivery with documentation of quality and cost outcomes. The ACO approach aims to address multiple, frequent, and recurring problems, including lack of financial incentives to improve quality and reduce cost, as well as the negative consequences of a pay-for-volume system—uncoordinated and fragmented care, overutilization of unnecessary tests and treatments, and poor patient experience all manifested as unwarranted geographic variation in practice patterns, clinical outcomes, and health spending. Participants in an ACO are rewarded financially if they can slow the growth of their patients’ healthcare costs while maintaining or improving the quality of care delivered. To succeed in this ACO world, hospitalists must assume greater prudence in the use of healthcare services while improving (or at a minimum, maintaining) patient outcomes, thus excising avoidable waste across the continuum of care.

More than half of ACOs include a hospital.⁸ However, whether hospital-led ACOs possess an advantage remains to be elucidated. Early reports indicated that physician-led ACOs saved more money.^9,10 However, others argue that hospitals¹¹ are better capitalized, have greater capacity for data sharing, and possess economies of scale that allow them to invest in more advanced technology, such as predictive modeling and/or simulation software. Such analytics can identify high-cost patients (ie, multiple comorbidities), super utilizers and populations lacking care, allowing ACOs to implement preventive measures to reduce unnecessary utilization. Recently released CMS MSSP 2016 performance data¹² showed that nearly half (45%) of physician-only ACOs earned shared savings, whereas 23% of ACOs that include hospitals earned shared savings. However, among all the ACOs that achieved savings, ACO entities that include hospitals generated the highest amount of shared savings (eg, Advocate, Hackensack Alliance, Cleveland Clinic, and AMITA Health). Notably, hospital-led ACOs tend to have much larger beneficiary populations than physician-led ACOs, which may create a scenario of higher risk but higher potential reward.

The emphasis on value over volume inherent in the development of ACOs occurs through employing care strategies implemented through changes in policies, and eventual structural and cultural changes. These changes require participating organizations to possess certain key competencies, including the following: 1) leadership that facilitates change; 2) organizational culture of teamwork; 3) collaborative relationships among providers; 4) information technology infrastructure for population management and care coordination; 5) infrastructure for monitoring, managing, and reporting quality; 6) ability to manage financial risk; 7) ability to receive and distribute payments or savings; and 8) resources for patient education and support.^2,3,13-16 Table 1 summarizes the broad range of roles that hospitalists can serve in delivering care to ACO populations.^17-19

Hospitalists’ active pursuit of nonclinical training and selection for administrative positions demonstrate their proclivity to provide these competencies. In addition to full-time clinician hospitalists, who can directly influence the delivery of high-value care to patients, hospitalists serve many other roles in hospitals and each can contribute differently based on their specialized expertise. Examples include the success of the Society of Hospital Medicine’s Leadership Academy; the acknowledged expertise of hospitalists in quality improvement (QI), informatics, teamwork, patient experience, care coordination and utilization; and advancement of hospitalists to senior leadership positions (eg, CQO, CMO, CEO). Given that nearly a third of healthcare expenditures are for hospital care,²⁰ hospitalists are in a unique position to foster ACO competencies while impacting the quality of care episodes associated with an index hospital stay.

Importantly, hospitalists cannot act as gatekeepers to restrict care. Managed care organizations and health maintenance organizations use of this approach in the 1990s to limit access to services in order to reduce costs led to unacceptable outcomes and numerous malpractice lawsuits. ACOs should aspire to deliver the most cost-effective high-quality care, and their performance should be monitored to ensure that they provide recommended services and timely access. The Medicare ACO contract holds the provider accountable for meeting 34 different quality measures (Supplemental Table 1), and hospitalists can influence outcomes for the majority. Especially through hospital and health system QI initiatives, hospitalists can directly impact and share accountability for measures ranging from care coordination to implementation of evidence-based care (eg, ACE inhibitors and beta blockers for heart failure) to patient and family caregiver experience.

Aligned with Medicare ACO quality measures, 5 high-impact target areas were identified for ACOs²¹: (1) Prevention and wellness; (2) Chronic conditions/care management; (3) Reduced hospitalizations; (4) Care transitions across the fragmented system; and (5) Multispecialty care coordination of complex patients. One essential element of a successful ACO is the ability to implement evidence-based medical guidelines and/or practices across the continuum of care for selected targeted initiatives. Optimizing care coordination/continuum requires team-based care, and hospitalists already routinely collaborate with nurses, social workers, case managers, pharmacists, and other stakeholders such as dieticians and physical therapists on inpatient care. Hospitalists are also experienced in facilitating communication and improving integration and coordination efficiencies among primary care providers and specialists, and between hospital care and post-acute care, as they coordinate post-hospital care and follow-up. This provides an opportunity to lead health system care coordination efforts, especially for complex and/or high-risk patients.^22,23 CMS MSSP 2016 performance data¹² showed that ACOs achieving shared savings had a decline in inpatient expenditures and utilization across several facility types (hospital, SNF, rehabilitation, long term). Postacute care management is critical to earning shared savings; SNF and Home Health expenditures fell by 18.3% and 9.7%, respectively, on average. We believe that hospitalists can have more influence over these cost areas by influencing treatment of hospitalized patients in a timely manner, discharge coordination, and selection of appropriate disposition locations. Hospitalists also play an integral role in ensuring the hospital performs well on quality metrics, including 30-day readmissions, hospital acquired conditions, and patient satisfaction. Examples below document the effectiveness of hospitalists in this new ACO era.

Care Transitions/Coordination

Before the Hospital Readmission Reduction Program (HRRP) delineated in the ACA, hospitalists developed Project BOOST (Better Outcomes by Optimizing Care Transitions) to improve hospital discharge care transition. The evidence-based foundation of this project led CMS to list Project BOOST as an example program that can reduce readmissions.²⁴ Through the dissemination and mentored implementation of Project BOOST to over 200 hospitals across the United States,²⁵ hospitalists contributed to the marked reduction in hospital readmission occurring since 2010.²⁶ Although hospital medicine began as a practice specific to the hospital setting, hospitalists’ skills generated growing demand for them in postacute facilities. SNF residents commonly come from hospitals postdischarge and suffer from multiple comorbidities and limitations in activities of daily living. Not surprisingly, SNF residents experience high rates of rehospitalizations.²⁷ Hospitalists can serve as a bridge between hospitals and SNFs and optimize this transition process to yield improved outcomes. Industry experts endorse this approach.²⁸ A recent study demonstrated a significant reduction in readmissions in 1 SNF (32.3% to 16.1%, odds ratio = 0.403, P < .001), by having a hospitalist-led team follow patients discharged from the hospital.²⁹

Chronic Conditions Management/High-Risk Patients

Interest in patients with multiple chronic comorbidities and social issues intensifies as healthcare systems focus limited resources on these high-risk patients to prevent the unnecessary use of costly services.^30,31 As health systems assume financial risk for health outcomes and costs of designated patient groups, they undertake efforts to understand the population they serve. Such efforts aim to identify patients with established high utilization patterns (or those at risk for high utilization). This knowledge enables targeted actions to provide access, treatment, and preventive interventions to avoid unneeded emergency and hospital services. Hospitalists commonly care for these patients and are positioned to lead the implementation of patient risk assessment and stratification, develop patient-centered care models across care settings, and act as a liaison with primary care. For frail elderly and seriously ill patients, the integration of hospitalists into palliative care provides several opportunities for improving the quality of care at the end of life.³² As patients and their family caregivers commonly do not address goals of care until faced with a life-threatening condition in the hospital, hospitalists represent ideal primary palliative care physicians to initiate these conversations.³³ A hospitalist communicating with a patient and/or their family caregiver about alleviating symptoms and clarifying patients’ preferences for care often yields decreases in ineffective healthcare utilization and better patient outcomes. The hospitalists’ ability to communicate with other providers within the hospital setting also allows them to better coordinate interdisciplinary care and prevent unnecessary and ineffective treatments and procedures.

De-Implementation/Waste Reduction

The largest inefficiencies in healthcare noted in the National Academy of Medicine report, Demanding Value from Our Health Care (2012), are failure to deliver known beneficial therapies or providing unnecessary or nonevidenced based services that do not improve outcomes, but come with associated risk and cost.³⁴ “De-implementation” of unnecessary diagnostic tests or ineffective or even harmful treatments by hospitalists represents a significant opportunity to reduce costs while maintaining or even improving the quality of care. The Society of Hospital Medicine joined the Choosing Wisely^® campaign and made 5 recommendations in adult care as an explicit starting point for eliminating waste in the hospital in 2013.³⁵ Since then, hospitalists have participated in multiple successful efforts to address overutilization of care; some published results include the following:

• decreased frequency of unnecessary common labs through a multifaceted hospitalist QI intervention;³⁶
• reduced length of stay and cost by appropriate use of telemetry;³⁷ and
• reduced unnecessary radiology testing by providing physicians with individualized audit and feedback reports.³⁸

Hundreds of ACOs now exist across the US, formed by a variety of providers including hospitals, physician groups, and integrated delivery systems. Provider groups range in size from primary care-focused physician groups with a handful of offices to large, multistate integrated delivery systems with dozens of hospitals and hundreds of office locations. Evaluations of ACO outcomes reveal mixed results.^9,39-53 Admittedly, assessments attempting to compare the magnitude of savings across ACO models are difficult given the variation in size, variability in specific efforts to influence utilization, and substantial turnover among participating beneficiaries.⁵⁴ Nonetheless, a newly published Office of Inspector General report⁵⁵ showed that most Medicare ACOs reduced spending and improved care quality (82% of the individual quality measures) over the first 3 years of the program, and savings increased with duration of an ACO program. The report also noted that considerable time and managerial resources are required to implement changes to improve quality and lower costs. While the political terrain ostensibly supports value-based care and the need to diminish the proportion of our nation’s gross domestic product dedicated to healthcare, health systems are navigating an environment that still largely rewards volume. Hospitalists may be ideal facilitators for this transitional period as they possess the clinical experience caring for complex patients with multiple comorbidities and quality improvement skills to lead efforts in this new ACO era.

Disclosures

The authors have nothing to disclose.

While patients may be newly exposed to opioids during medical and surgical hospitalization and the prescription of opioids at discharge is common,^1-5 prescribers of opioids at discharge may not intend to initiate long-term opioid (LTO) use. By understanding the frequency of progression to LTO use, hospitalists can better balance postdischarge pain treatment and the risk for unintended LTO initiation.

Estimates of LTO use rates following hospital discharge in selected populations^1,2,4-6 have varied depending on the population studied and the method of defining LTO use.⁷ Rates of LTO use following incident opioid prescription have not been directly compared at medical versus surgical discharge or compared with initiation in the ambulatory setting. We present the rates of LTO use following incident opioid exposure at surgical discharge and medical discharge and identify the factors associated with LTO use following surgical and medical discharge.

Data Sources

Veterans Health Administration (VHA) data were obtained through the Austin Information Technology Center for fiscal years (FYs) 2003 through 2012 (Austin, Texas). Decision support system national data extracts were used to identify prescription-dispensing events, and inpatient and outpatient medical SAS data sets were used to identify diagnostic codes. The study was approved by the University of Iowa Institutional Review Board and the Iowa City Veterans Affairs (VA) Health Care System Research and Development Committee.

Patients

We included all patients with an outpatient opioid prescription during FY 2011 that was preceded by a 1-year opioid-free period.⁷ Patients with broadly accepted indications for LTO use (eg, metastatic cancer, palliative care, or opioid-dependence treatment) were excluded.⁷

Opioid Exposure

We included all outpatient prescription fills for noninjectable dosage forms of butorphanol, fentanyl, hydrocodone, hydromorphone, levorphanol, meperidine, methadone, morphine, oxycodone, oxymorphone, pentazocine, and tramadol. Consistent with the Centers for Disease Control and Prevention and VA/Department of Defense guidelines, LTO use was defined conceptually as regular use for >90 days. Operationalizing this definition to pharmacy refill data was established by using a cabinet supply methodology,⁷ which allows for the construction of episodes of continuous medication therapy by estimating the medication supply available to a patient for each day during a defined period based on the pattern of observed refills. LTO use was defined as an episode of continuous opioid supply for >90 days and beginning within 30 days of the initial prescription. While some studies have defined LTO use based on onset within 1 year following surgery,⁵ the requirement for onset within 30 days of initiation was applied to more strongly tie the association of developing LTO use with the discharge event and minimize various forms of bias that are introduced with extended follow-up periods.

Clinical Characteristics

Patients were classified as being medical discharges, surgical discharges, or outpatient initiators. Patients with an opioid index date within 2 days following discharge were designated based on discharge bed section; additionally, if patients had a surgical bed section during hospitalization, they were assigned as surgical discharges. Demographic, diagnosis, and medication exposure variables that were previously associated with LTO use were selected.^8,9 Substance use disorder, chronic pain, anxiety disorder, and depressive disorder were based on International Classification of Diseases, 9th Revision (ICD-9) codes in the preceding year. The use of concurrent benzodiazepines, skeletal muscle relaxants, and antidepressants were determined at opioid initiation.¹⁰ Rural or urban residence was assigned by using the Rural-Urban Commuting Area Codes system and mapped with the zip code of a veteran’s residence.¹¹

Analysis

Bivariate and multivariable relationships were determined by using logistic regression. The multivariable model considered all pairwise interaction terms between inpatient service (surgery versus medicine) and each of the variables in the model. Statistically significant interaction terms (P < .05) were retained, and all others were omitted from the final model. The main effects for variables that were involved in a significant interaction term were not reported in the final multivariable model; instead, we created fully specified multivariable models for surgery service and medicine service and reported odds ratios (ORs) for the main effects. All analyses were conducted by using SAS version 9.4 (SAS Institute Inc, Cary, North Carolina).

The observation that subsequent LTO use occurs more frequently in discharged medical patients than surgical patients is consistent with the findings of Calcaterra et al.¹ that among patients with no surgery versus surgery during hospitalization, opioid receipt at discharge resulted in a higher adjusted OR (7.24 for no surgery versus 3.40 for surgery) for chronic opioid use at 1 year. One explanation for this finding may be an artifact of cohort selection in the study design: patients with prior opioid use are excluded from the cohort, and prior use may be more common among surgical patients presenting for elective inpatient surgery for painful conditions. Previous work suggests that opioid use preoperatively is a robust predictor of postoperative use, and rates of LTO use are low among patients without preoperative opioid exposure.⁶

Demographic characteristics associated with persistent opioid receipt were similar to those previously reported.^5,8,9 The inclusion of medication classes indicated in the treatment of mental health or pain conditions (ie, antidepressants, benzodiazepines, muscle relaxants, and nonopioid analgesics) resulted in diagnoses based on ICD-9 codes being no longer associated with LTO use. Severity or activity of illness, preferences regarding pharmacologic or nonpharmacologic treatment and undiagnosed or undocumented pain-comorbid conditions may all contribute to this finding. Future work studying opioid-related outcomes should include variables that reflect pharmacologic management of comorbid diagnoses in the cohort development or analytic design.

The strongest risk factors were potentially modifiable: days’ supply, dose, and concurrent medications. The measures of opioid quantity supplied are associated with subsequent ongoing use and are consistent with recent work based on prescription drug–monitoring data in a single state¹⁴ and in a nationally representative sample.¹⁵ That this relationship persists following hospital discharge, a scenario in which LTO use is unlikely to be initiated by a provider (who would be expected to subsequently titrate or monitor therapy), further supports the potential to curtail unintended LTO use through judicious early prescribing decisions.

We assessed only opioids that were supplied through a VA pharmacy, which may lead to the misclassification of patients as opioid naive for inclusion and an underestimation of the rate of opioid use following discharge. It is possible that differences in the rates of non-VA pharmacy use differ in medical and surgical populations in a nonrandom way. This study was performed in a large, integrated health system and may not be generalizable outside the VA system, where more discontinuities between hospital and ambulatory care may exist.

The initiation of LTO use at discharge is more common in veterans who are discharged from medical than surgical hospitalizations, likely reflecting differences in the patient population, pain conditions, and discharge prescribing decisions. While patient characteristics are associated with LTO use, the strongest associations are with increasing index dose and days’ supply; both represent potentially modifiable prescriber behaviors. These findings support policy changes and other efforts to minimize dose and days supplied when short-term use is intended as a means to address the current opioid epidemic.

Acknowledgments

The work reported here was supported by the Department of Veterans Affairs Office of Academic Affiliations and Office of Research and Development (Dr. Mosher and Dr. Hofmeyer), and Health Services Research and Development Service (HSR&D) through the Comprehensive Access and Delivery Research and Evaluation Center (CIN 13-412) and a Career Development Award (CDA 10-017; Dr. Lund).

Disclosures

The authors report no conflict of interest in regard to this study. The authors had full access to and take full responsibility for the integrity of the data. All analyses were conducted by using SAS version 9.2 (SAS Institute Inc, Cary, NC). This manuscript is not under review elsewhere, and there is no prior publication of the manuscript contents. The views expressed in this article are those of the authors and do not necessarily represent the views of the Department of Veterans Affairs. The study was approved by the University of Iowa Institutional Review Board and the Iowa City Healthcare System Research and Development Committee.

While patients may be newly exposed to opioids during medical and surgical hospitalization and the prescription of opioids at discharge is common,^1-5 prescribers of opioids at discharge may not intend to initiate long-term opioid (LTO) use. By understanding the frequency of progression to LTO use, hospitalists can better balance postdischarge pain treatment and the risk for unintended LTO initiation.

Estimates of LTO use rates following hospital discharge in selected populations^1,2,4-6 have varied depending on the population studied and the method of defining LTO use.⁷ Rates of LTO use following incident opioid prescription have not been directly compared at medical versus surgical discharge or compared with initiation in the ambulatory setting. We present the rates of LTO use following incident opioid exposure at surgical discharge and medical discharge and identify the factors associated with LTO use following surgical and medical discharge.

Data Sources

Veterans Health Administration (VHA) data were obtained through the Austin Information Technology Center for fiscal years (FYs) 2003 through 2012 (Austin, Texas). Decision support system national data extracts were used to identify prescription-dispensing events, and inpatient and outpatient medical SAS data sets were used to identify diagnostic codes. The study was approved by the University of Iowa Institutional Review Board and the Iowa City Veterans Affairs (VA) Health Care System Research and Development Committee.

Patients

We included all patients with an outpatient opioid prescription during FY 2011 that was preceded by a 1-year opioid-free period.⁷ Patients with broadly accepted indications for LTO use (eg, metastatic cancer, palliative care, or opioid-dependence treatment) were excluded.⁷

Opioid Exposure

We included all outpatient prescription fills for noninjectable dosage forms of butorphanol, fentanyl, hydrocodone, hydromorphone, levorphanol, meperidine, methadone, morphine, oxycodone, oxymorphone, pentazocine, and tramadol. Consistent with the Centers for Disease Control and Prevention and VA/Department of Defense guidelines, LTO use was defined conceptually as regular use for >90 days. Operationalizing this definition to pharmacy refill data was established by using a cabinet supply methodology,⁷ which allows for the construction of episodes of continuous medication therapy by estimating the medication supply available to a patient for each day during a defined period based on the pattern of observed refills. LTO use was defined as an episode of continuous opioid supply for >90 days and beginning within 30 days of the initial prescription. While some studies have defined LTO use based on onset within 1 year following surgery,⁵ the requirement for onset within 30 days of initiation was applied to more strongly tie the association of developing LTO use with the discharge event and minimize various forms of bias that are introduced with extended follow-up periods.

Clinical Characteristics

Patients were classified as being medical discharges, surgical discharges, or outpatient initiators. Patients with an opioid index date within 2 days following discharge were designated based on discharge bed section; additionally, if patients had a surgical bed section during hospitalization, they were assigned as surgical discharges. Demographic, diagnosis, and medication exposure variables that were previously associated with LTO use were selected.^8,9 Substance use disorder, chronic pain, anxiety disorder, and depressive disorder were based on International Classification of Diseases, 9th Revision (ICD-9) codes in the preceding year. The use of concurrent benzodiazepines, skeletal muscle relaxants, and antidepressants were determined at opioid initiation.¹⁰ Rural or urban residence was assigned by using the Rural-Urban Commuting Area Codes system and mapped with the zip code of a veteran’s residence.¹¹

Analysis

Bivariate and multivariable relationships were determined by using logistic regression. The multivariable model considered all pairwise interaction terms between inpatient service (surgery versus medicine) and each of the variables in the model. Statistically significant interaction terms (P < .05) were retained, and all others were omitted from the final model. The main effects for variables that were involved in a significant interaction term were not reported in the final multivariable model; instead, we created fully specified multivariable models for surgery service and medicine service and reported odds ratios (ORs) for the main effects. All analyses were conducted by using SAS version 9.4 (SAS Institute Inc, Cary, North Carolina).

The observation that subsequent LTO use occurs more frequently in discharged medical patients than surgical patients is consistent with the findings of Calcaterra et al.¹ that among patients with no surgery versus surgery during hospitalization, opioid receipt at discharge resulted in a higher adjusted OR (7.24 for no surgery versus 3.40 for surgery) for chronic opioid use at 1 year. One explanation for this finding may be an artifact of cohort selection in the study design: patients with prior opioid use are excluded from the cohort, and prior use may be more common among surgical patients presenting for elective inpatient surgery for painful conditions. Previous work suggests that opioid use preoperatively is a robust predictor of postoperative use, and rates of LTO use are low among patients without preoperative opioid exposure.⁶

Demographic characteristics associated with persistent opioid receipt were similar to those previously reported.^5,8,9 The inclusion of medication classes indicated in the treatment of mental health or pain conditions (ie, antidepressants, benzodiazepines, muscle relaxants, and nonopioid analgesics) resulted in diagnoses based on ICD-9 codes being no longer associated with LTO use. Severity or activity of illness, preferences regarding pharmacologic or nonpharmacologic treatment and undiagnosed or undocumented pain-comorbid conditions may all contribute to this finding. Future work studying opioid-related outcomes should include variables that reflect pharmacologic management of comorbid diagnoses in the cohort development or analytic design.

The strongest risk factors were potentially modifiable: days’ supply, dose, and concurrent medications. The measures of opioid quantity supplied are associated with subsequent ongoing use and are consistent with recent work based on prescription drug–monitoring data in a single state¹⁴ and in a nationally representative sample.¹⁵ That this relationship persists following hospital discharge, a scenario in which LTO use is unlikely to be initiated by a provider (who would be expected to subsequently titrate or monitor therapy), further supports the potential to curtail unintended LTO use through judicious early prescribing decisions.

We assessed only opioids that were supplied through a VA pharmacy, which may lead to the misclassification of patients as opioid naive for inclusion and an underestimation of the rate of opioid use following discharge. It is possible that differences in the rates of non-VA pharmacy use differ in medical and surgical populations in a nonrandom way. This study was performed in a large, integrated health system and may not be generalizable outside the VA system, where more discontinuities between hospital and ambulatory care may exist.

The initiation of LTO use at discharge is more common in veterans who are discharged from medical than surgical hospitalizations, likely reflecting differences in the patient population, pain conditions, and discharge prescribing decisions. While patient characteristics are associated with LTO use, the strongest associations are with increasing index dose and days’ supply; both represent potentially modifiable prescriber behaviors. These findings support policy changes and other efforts to minimize dose and days supplied when short-term use is intended as a means to address the current opioid epidemic.

Acknowledgments

The work reported here was supported by the Department of Veterans Affairs Office of Academic Affiliations and Office of Research and Development (Dr. Mosher and Dr. Hofmeyer), and Health Services Research and Development Service (HSR&D) through the Comprehensive Access and Delivery Research and Evaluation Center (CIN 13-412) and a Career Development Award (CDA 10-017; Dr. Lund).

Disclosures

The authors report no conflict of interest in regard to this study. The authors had full access to and take full responsibility for the integrity of the data. All analyses were conducted by using SAS version 9.2 (SAS Institute Inc, Cary, NC). This manuscript is not under review elsewhere, and there is no prior publication of the manuscript contents. The views expressed in this article are those of the authors and do not necessarily represent the views of the Department of Veterans Affairs. The study was approved by the University of Iowa Institutional Review Board and the Iowa City Healthcare System Research and Development Committee.

While patients may be newly exposed to opioids during medical and surgical hospitalization and the prescription of opioids at discharge is common,^1-5 prescribers of opioids at discharge may not intend to initiate long-term opioid (LTO) use. By understanding the frequency of progression to LTO use, hospitalists can better balance postdischarge pain treatment and the risk for unintended LTO initiation.

Estimates of LTO use rates following hospital discharge in selected populations^1,2,4-6 have varied depending on the population studied and the method of defining LTO use.⁷ Rates of LTO use following incident opioid prescription have not been directly compared at medical versus surgical discharge or compared with initiation in the ambulatory setting. We present the rates of LTO use following incident opioid exposure at surgical discharge and medical discharge and identify the factors associated with LTO use following surgical and medical discharge.

Data Sources

Veterans Health Administration (VHA) data were obtained through the Austin Information Technology Center for fiscal years (FYs) 2003 through 2012 (Austin, Texas). Decision support system national data extracts were used to identify prescription-dispensing events, and inpatient and outpatient medical SAS data sets were used to identify diagnostic codes. The study was approved by the University of Iowa Institutional Review Board and the Iowa City Veterans Affairs (VA) Health Care System Research and Development Committee.

Patients

We included all patients with an outpatient opioid prescription during FY 2011 that was preceded by a 1-year opioid-free period.⁷ Patients with broadly accepted indications for LTO use (eg, metastatic cancer, palliative care, or opioid-dependence treatment) were excluded.⁷

Opioid Exposure

We included all outpatient prescription fills for noninjectable dosage forms of butorphanol, fentanyl, hydrocodone, hydromorphone, levorphanol, meperidine, methadone, morphine, oxycodone, oxymorphone, pentazocine, and tramadol. Consistent with the Centers for Disease Control and Prevention and VA/Department of Defense guidelines, LTO use was defined conceptually as regular use for >90 days. Operationalizing this definition to pharmacy refill data was established by using a cabinet supply methodology,⁷ which allows for the construction of episodes of continuous medication therapy by estimating the medication supply available to a patient for each day during a defined period based on the pattern of observed refills. LTO use was defined as an episode of continuous opioid supply for >90 days and beginning within 30 days of the initial prescription. While some studies have defined LTO use based on onset within 1 year following surgery,⁵ the requirement for onset within 30 days of initiation was applied to more strongly tie the association of developing LTO use with the discharge event and minimize various forms of bias that are introduced with extended follow-up periods.

Clinical Characteristics

Patients were classified as being medical discharges, surgical discharges, or outpatient initiators. Patients with an opioid index date within 2 days following discharge were designated based on discharge bed section; additionally, if patients had a surgical bed section during hospitalization, they were assigned as surgical discharges. Demographic, diagnosis, and medication exposure variables that were previously associated with LTO use were selected.^8,9 Substance use disorder, chronic pain, anxiety disorder, and depressive disorder were based on International Classification of Diseases, 9th Revision (ICD-9) codes in the preceding year. The use of concurrent benzodiazepines, skeletal muscle relaxants, and antidepressants were determined at opioid initiation.¹⁰ Rural or urban residence was assigned by using the Rural-Urban Commuting Area Codes system and mapped with the zip code of a veteran’s residence.¹¹

Analysis

Bivariate and multivariable relationships were determined by using logistic regression. The multivariable model considered all pairwise interaction terms between inpatient service (surgery versus medicine) and each of the variables in the model. Statistically significant interaction terms (P < .05) were retained, and all others were omitted from the final model. The main effects for variables that were involved in a significant interaction term were not reported in the final multivariable model; instead, we created fully specified multivariable models for surgery service and medicine service and reported odds ratios (ORs) for the main effects. All analyses were conducted by using SAS version 9.4 (SAS Institute Inc, Cary, North Carolina).

The observation that subsequent LTO use occurs more frequently in discharged medical patients than surgical patients is consistent with the findings of Calcaterra et al.¹ that among patients with no surgery versus surgery during hospitalization, opioid receipt at discharge resulted in a higher adjusted OR (7.24 for no surgery versus 3.40 for surgery) for chronic opioid use at 1 year. One explanation for this finding may be an artifact of cohort selection in the study design: patients with prior opioid use are excluded from the cohort, and prior use may be more common among surgical patients presenting for elective inpatient surgery for painful conditions. Previous work suggests that opioid use preoperatively is a robust predictor of postoperative use, and rates of LTO use are low among patients without preoperative opioid exposure.⁶

Demographic characteristics associated with persistent opioid receipt were similar to those previously reported.^5,8,9 The inclusion of medication classes indicated in the treatment of mental health or pain conditions (ie, antidepressants, benzodiazepines, muscle relaxants, and nonopioid analgesics) resulted in diagnoses based on ICD-9 codes being no longer associated with LTO use. Severity or activity of illness, preferences regarding pharmacologic or nonpharmacologic treatment and undiagnosed or undocumented pain-comorbid conditions may all contribute to this finding. Future work studying opioid-related outcomes should include variables that reflect pharmacologic management of comorbid diagnoses in the cohort development or analytic design.

The strongest risk factors were potentially modifiable: days’ supply, dose, and concurrent medications. The measures of opioid quantity supplied are associated with subsequent ongoing use and are consistent with recent work based on prescription drug–monitoring data in a single state¹⁴ and in a nationally representative sample.¹⁵ That this relationship persists following hospital discharge, a scenario in which LTO use is unlikely to be initiated by a provider (who would be expected to subsequently titrate or monitor therapy), further supports the potential to curtail unintended LTO use through judicious early prescribing decisions.

We assessed only opioids that were supplied through a VA pharmacy, which may lead to the misclassification of patients as opioid naive for inclusion and an underestimation of the rate of opioid use following discharge. It is possible that differences in the rates of non-VA pharmacy use differ in medical and surgical populations in a nonrandom way. This study was performed in a large, integrated health system and may not be generalizable outside the VA system, where more discontinuities between hospital and ambulatory care may exist.

The initiation of LTO use at discharge is more common in veterans who are discharged from medical than surgical hospitalizations, likely reflecting differences in the patient population, pain conditions, and discharge prescribing decisions. While patient characteristics are associated with LTO use, the strongest associations are with increasing index dose and days’ supply; both represent potentially modifiable prescriber behaviors. These findings support policy changes and other efforts to minimize dose and days supplied when short-term use is intended as a means to address the current opioid epidemic.

Acknowledgments

The work reported here was supported by the Department of Veterans Affairs Office of Academic Affiliations and Office of Research and Development (Dr. Mosher and Dr. Hofmeyer), and Health Services Research and Development Service (HSR&D) through the Comprehensive Access and Delivery Research and Evaluation Center (CIN 13-412) and a Career Development Award (CDA 10-017; Dr. Lund).

Disclosures

The authors report no conflict of interest in regard to this study. The authors had full access to and take full responsibility for the integrity of the data. All analyses were conducted by using SAS version 9.2 (SAS Institute Inc, Cary, NC). This manuscript is not under review elsewhere, and there is no prior publication of the manuscript contents. The views expressed in this article are those of the authors and do not necessarily represent the views of the Department of Veterans Affairs. The study was approved by the University of Iowa Institutional Review Board and the Iowa City Healthcare System Research and Development Committee.

Delirium is an acute neurocognitive disorder¹ that affects up to 25% of older emergency department (ED) and hospitalized patients.^2-4 The relationship between delirium and adverse outcomes is well documented.^5-7 Delirium is a strong predictor of increased length of mechanical ventilation, longer intensive care unit and hospital stays, increased risk of falls, long-term cognitive impairment, and mortality.^8-13 Delirium is frequently missed by healthcare professionals^2,14-16 and goes undetected in up to 3 out of 4 patients by bedside nurses and medical practitioners in many hospital settings.^14,17-22 A significant barrier to recognizing delirium is the absence of brief delirium assessments.

In an effort to improve delirium recognition in the acute care setting, there has been a concerted effort to develop and validate brief delirium assessments. To address this unmet need, 4 ‘A’s Test (4AT), the Brief Confusion Assessment Method (bCAM), and the 3-minute diagnostic assessment for CAM-defined delirium (3D-CAM) are 1- to 3-minute delirium assessments that were validated in acutely ill older patients.²³ However, 1 to 3 minutes may still be too long in busy clinical environments, and briefer (<30 seconds) delirium assessments may be needed.

One potential more-rapid method to screen for delirium is to specifically test for the presence of inattention, which is a cardinal feature of delirium.^24,25 Inattention can be ascertained by having the patient recite the months backwards, recite the days of the week backwards, or spell a word backwards.²⁶ Recent studies have evaluated the diagnostic accuracy of reciting the months of the year backwards for delirium. O’Regan et al.²⁷ evaluated the diagnostic accuracy of the month of the year backwards from December to July (MOTYB-6) and observed that this task was 84% sensitive and 90% specific for delirium in older patients. However, they performed the reference standard delirium assessments in patients who had a positive MOTYB-6, which can overestimate sensitivity and underestimate specificity (verification bias).²⁸ Fick et al.²⁹ examined the diagnostic accuracy of 20 individual elements of the 3D-CAM and observed that reciting the months of the year backwards from December to January (MOTYB-12) was 83% sensitive and 69% specific for delirium. However, this was an exploratory study that was designed to identify an element of the 3D-CAM that had the best diagnostic accuracy.

To address these limitations, we sought to evaluate the diagnostic performance of the MOTYB-6 and MOTYB-12 for delirium as diagnosed by a reference standard. We also explored other brief tests of inattention such as spelling a word (“LUNCH”) backwards, reciting the days of the week backwards, 10-letter vigilance “A” task, and 5 picture recognition task.

Study Design and Setting

This was a preplanned secondary analysis of a prospective observational study that validated 3 delirium assessments.^30,31 This study was conducted at a tertiary care, academic ED. The local institutional review board (IRB) reviewed and approved this study. Informed consent from the patient or an authorized surrogate was obtained whenever possible. Because this was an observational study and posed minimal risk to the patient, the IRB granted a waiver of consent for patients who were both unable to provide consent and were without an authorized surrogate available in the ED or by phone.

Selection of Participants

We enrolled a convenience sample of patients between June 2010 and February 2012 Monday through Friday from 8 am to 4 pm. This enrollment window was based upon the psychiatrist’s availability. Because of the extensiveness of the psychiatric evaluations, we limited enrollment to 1 patient per day. Patients who were 65 years or older, not in a hallway bed, and in the ED for less than 12 hours at the time of enrollment were included. We used a 12-hour cutoff so that patients who presented in the evening and early morning hours could be included. Patients were excluded if they were previously enrolled, non-English speaking, deaf or blind, comatose, suffered from end-stage dementia, or were unable to complete all the study assessments. The rationale for excluding patients with end-stage dementia was that diagnosing delirium in this patient population is challenging.

Research assistants approached patients who met inclusion criteria and determined if any exclusion criteria were present. If none of the exclusion criteria were present, then the research assistant reviewed the informed consent document with the patient or authorized surrogate if the patient was not capable of providing consent. If a patient was not capable of providing consent and no authorized surrogate was available, then the patient was enrolled (under the waiver of consent) as long as the patient assented to be a part of the study. Once the patient was enrolled, the research assistant contacted the physician rater and reference standard psychiatrists to approach the patient.

Measures of Inattention

An emergency physician (JHH) who had no formal training in the mental status assessment of elders administered a cognitive battery to the patient, including tests of inattention. The following inattention tasks were administered:

• Spell the word “LUNCH” backwards.³⁰ Patients were initially allowed to spell the word “LUNCH” forwards. Patients who were unable to perform the task were assigned 5 errors.
• Recite the months of the year backwards from December to July.^{23,26,27,30,32} Patients who were unable to perform the task were assigned 6 errors.
• Recite the days of the week backwards.^23,26,33 Patients who were unable to perform the task were assigned 7 errors.
• Ten-letter vigilance “A” task.³⁴ The patient was given a series of 10 letters (“S-A-V-E-A-H-A-A-R-T”) every 3 seconds and was asked to squeeze the rater’s hand every time the patient heard the letter “A.” Patients who were unable to perform the task were assigned 10 errors.
• Five picture recognition task.³⁴ Patients were shown 5 objects on picture cards. Afterwards, patients were shown 10 pictures with the previously shown objects intermingled. The patient had to identify which objects were seen previously in the first 5 pictures. Patients who were unable to perform the task were assigned 10 errors.
• Recite the months of the year backwards from December to January.²⁹ Patients who were unable to perform the task were assigned 12 errors.

Reference Standard for Delirium

A comprehensive consultation-liaison psychiatrist assessment was the reference standard for delirium; the diagnosis of delirium was based on Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) criteria.³⁵ Three psychiatrists who each had an average of 11 years of clinical experience and regularly diagnosed delirium as part of their daily clinical practice were available to perform these assessments. To arrive at the diagnosis of delirium, they interviewed those who best understood the patient’s mental status (eg, the patient’s family members or caregivers, physician, and nurses). They also reviewed the patient’s medical record and radiology and laboratory test results. They performed bedside cognitive testing that included, but was not limited to, the Mini-Mental State Examination, Clock Drawing Test, Luria hand sequencing task, and tests for verbal fluency. A focused neurological examination was also performed (ie, screening for paraphasic errors, tremors, tone, asterixis, frontal release signs, etc.), and they also evaluated the patient for affective lability, hallucinations, and level of alertness. If the presence of delirium was still questionable, then confrontational naming, proverb interpretation or similarities, and assessments for apraxias were performed at the discretion of the psychiatrist. The psychiatrists were blinded to the physician’s assessments, and the assessments were conducted within 3 hours of each other.

Additional Variables Collected

Using medical record review, comorbidity burden, severity of illness, and premorbid cognition were ascertained. The Charlson Comorbidity Index, a weighted index that takes into account the number and seriousness of 19 preexisting comorbid conditions, was used to quantify comorbidity burden; higher scores indicate higher comorbid burden.^36,37 The Acute Physiology Score of the Acute Physiology and Chronic Health Evaluation II was used to quantify severity of illness.³⁸ This score is based upon the initial values of 12 routine physiologic measurements such as vital sign and laboratory abnormalities; higher scores represent higher severities of illness.³⁸ The medical record was reviewed to ascertain the presence of premorbid cognitive impairment; any documentation of dementia in the patient’s clinical problem list or physician history and physical examination from the outpatient or inpatient settings was considered positive. The medical record review was performed by a research assistant and was double-checked for accuracy by one of the investigators (JHH).

Data Analyses

Measures of central tendency and dispersion for continuous variables were reported as medians and interquartile ranges. Categorical variables were reported as proportions. Receiver operating characteristic curves were constructed for each inattention task. Area under the receiver operating characteristic curves (AUC) was reported to provide a global measure of diagnostic accuracy. Sensitivities, specificities, positive likelihood ratios (PLRs), and negative likelihood ratios (NLRs) with their 95% CIs were calculated using the psychiatrist’s assessment as the reference standard.³⁹ Cut-points with PLRs greater than 10 (strongly increased the likelihood of delirium) or NLRs less than 0.1 (strongly decreased the likelihood of delirium) were preferentially reported whenever possible.

All statistical analyses were performed with open source R statistical software version 3.0.1 (http://www.r-project.org/), SAS 9.4 (SAS Institute, Cary, NC), and Microsoft Excel 2010 (Microsoft Inc., Redmond, WA).

Delirium is frequently missed by healthcare providers because it is not routinely screened for in the acute care setting. To help address this deficiency of care, we evaluated several brief measures of inattention that take less than 30 seconds to complete. We observed that any errors made on the MOTYB-6 and MOTYB-12 tasks had very good sensitivities (80% and 84%) but were limited by their modest specificities (approximately 50%) for delirium. As a result, these assessments have limited clinical utility as standalone delirium screens. We also explored other commonly used brief measures of inattention and at a variety of error cutoffs. Reciting the days of the week backwards appeared to best balance sensitivity and specificity. None of the inattention measures could convincingly rule out delirium (NLR < 0.10), but the vigilance “A” and picture recognition tasks may have clinical utility in ruling in delirium (PLR > 10). Overall, all the inattention tasks, including MOTYB-6 and MOTYB-12, had very good diagnostic performances based upon their AUC. However, achieving a high sensitivity often had to be sacrificed for specificity or, alternatively, achieving a high specificity had to be sacrificed for sensitivity.

Inattention has been shown to be the cardinal feature for delirium,⁴⁰ and its assessment using cognitive testing has been recommended to help identify the presence of delirium according to an expert consensus panel.²⁶ The diagnostic performance of the MOTYB-12 observed in our study is similar to a study by Fick et al., who reported that MOTYB-12 had very good sensitivity (83%) but had modest specificity (69%) with a cutoff of 1 or more errors. Hendry et al. observed that the MOTYB-12 was 91% sensitive and 50% specific using a cutoff of 4 or more errors. With regard to the MOTYB-6, our reported specificity was different from what was observed by O’Regan et al.²⁷ Using 1 or more errors as a cutoff, they observed a much higher specificity for delirium than we did (90% vs 57%). Discordant observations regarding the diagnostic accuracy for other inattention tasks also exist. We observed that making any error on the days of the week backwards task was 84% sensitive and 82% specific for delirium, whereas Fick et al. observed a sensitivity and specificity of 50% and 94%, respectively. For the vigilance “A” task, we observed that making 2 or more errors over a series of 10 letters was 64.0% sensitive and 91.4% specific for delirium, whereas Pompei et al.⁴¹ observed that making 2 or more errors over a series of 60 letters was 51% sensitive and 77% specific for delirium.

The abovementioned discordant findings may be driven by spectrum bias, wherein the sensitivities and specificities for each inattention task may differ in different subgroups. As a result, differences in the age distribution, proportion of college graduates, history of dementia, and susceptibility to delirium can influence overall sensitivity and specificity. Objective measures of delirium, including the inattention screens studied, are particularly prone to spectrum bias.^31,34 However, the strength of this approach is that the assessment of inattention becomes less reliant upon clinical judgment and allows it to be used by raters from a wide range of clinical backgrounds. On the other hand, a subjective interpretation of these inattention tasks may allow the rater to capture the subtleties of inattention (ie, decreased speed of performance in a highly intelligent and well-educated patient without dementia). The disadvantage of this approach, however, is that it is more dependent on clinical judgment and may have decreased diagnostic accuracy in those with less clinical experience or with limited training.^14,42,43 These factors must be carefully considered when determining which delirium assessment to use.

Additional research is required to determine the clinical utility of these brief inattention assessments. These findings need to be further validated in larger studies, and the optimal cutoff of each task for different subgroup of patients (eg, demented vs nondemented) needs to be further clarified. It is not completely clear whether these inattention tests can serve as standalone assessments. Depending on the cutoff used, some of these assessments may have unacceptable false negative or false positive rates that may lead to increased adverse patient outcomes or increased resource utilization, respectively. Additional components or assessments may be needed to improve the diagnostic accuracy of these assessments. In addition to understanding these inattention assessments’ diagnostic accuracies, their ability to predict adverse outcomes also needs to be investigated. While a previous study observed that making any error on the MOTYB-12 task was associated with increased physical restraint use and prolonged hospital length of stay,⁴⁴ these assessments’ ability to prognosticate long-term outcomes such as mortality or long-term cognition or function need to be studied. Lastly, studies should also evaluate how easily implementable these assessments are and whether improved delirium recognition leads to improved patient outcomes.

This study has several notable limitations. Though planned a priori, this was a secondary analysis of a larger investigation designed to validate 3 delirium assessments. Our sample size was also relatively small, causing our 95% CIs to overlap in most cases and limiting the statistical power to truly determine whether one measure is better than the other. We also asked the patient to recite the months backwards from December to July as well as recite the months backwards from December to January. It is possible that the patient may have performed better at going from December to January because of learning effect. Our reference standard for delirium was based upon DSM-IV-TR criteria. The new DSM-V criteria may be more restrictive and may slightly change the sensitivities and specificities of the inattention tasks. We enrolled a convenience sample and enrolled patients who were more likely to be male, have cardiovascular chief complaints, and be admitted to the hospital; as a result, selection bias may have been introduced. Lastly, this study was conducted in a single center and enrolled patients who were 65 years and older. Our findings may not be generalizable to other settings and in those who are less than 65 years of age.

The MOTYB-6 and MOTYB-12 tasks had very good sensitivities but modest specificities (approximately 50%) using any error made as a cutoff; increasing cutoff to 2 errors and 3 errors, respectively, improved their specificities (approximately 70%) with minimal impact to their sensitivities. Reciting the days of the week backwards, spelling the word “LUNCH” backwards, and the 10-letter vigilance “A” task appeared to perform the best in ruling out delirium but only moderately decreased the likelihood of delirium. The 10-letter Vigilance “A” and picture recognition task appeared to perform the best in ruling in delirium. Days of the week backwards appeared to have the best combination of sensitivity and specificity.

Disclosure

This study was funded by the Emergency Medicine Foundation Career Development Award, National Institutes of Health K23AG032355, and National Center for Research Resources, Grant UL1 RR024975-01. The authors report no financial conflicts of interest.

Delirium is an acute neurocognitive disorder¹ that affects up to 25% of older emergency department (ED) and hospitalized patients.^2-4 The relationship between delirium and adverse outcomes is well documented.^5-7 Delirium is a strong predictor of increased length of mechanical ventilation, longer intensive care unit and hospital stays, increased risk of falls, long-term cognitive impairment, and mortality.^8-13 Delirium is frequently missed by healthcare professionals^2,14-16 and goes undetected in up to 3 out of 4 patients by bedside nurses and medical practitioners in many hospital settings.^14,17-22 A significant barrier to recognizing delirium is the absence of brief delirium assessments.

In an effort to improve delirium recognition in the acute care setting, there has been a concerted effort to develop and validate brief delirium assessments. To address this unmet need, 4 ‘A’s Test (4AT), the Brief Confusion Assessment Method (bCAM), and the 3-minute diagnostic assessment for CAM-defined delirium (3D-CAM) are 1- to 3-minute delirium assessments that were validated in acutely ill older patients.²³ However, 1 to 3 minutes may still be too long in busy clinical environments, and briefer (<30 seconds) delirium assessments may be needed.

One potential more-rapid method to screen for delirium is to specifically test for the presence of inattention, which is a cardinal feature of delirium.^24,25 Inattention can be ascertained by having the patient recite the months backwards, recite the days of the week backwards, or spell a word backwards.²⁶ Recent studies have evaluated the diagnostic accuracy of reciting the months of the year backwards for delirium. O’Regan et al.²⁷ evaluated the diagnostic accuracy of the month of the year backwards from December to July (MOTYB-6) and observed that this task was 84% sensitive and 90% specific for delirium in older patients. However, they performed the reference standard delirium assessments in patients who had a positive MOTYB-6, which can overestimate sensitivity and underestimate specificity (verification bias).²⁸ Fick et al.²⁹ examined the diagnostic accuracy of 20 individual elements of the 3D-CAM and observed that reciting the months of the year backwards from December to January (MOTYB-12) was 83% sensitive and 69% specific for delirium. However, this was an exploratory study that was designed to identify an element of the 3D-CAM that had the best diagnostic accuracy.

To address these limitations, we sought to evaluate the diagnostic performance of the MOTYB-6 and MOTYB-12 for delirium as diagnosed by a reference standard. We also explored other brief tests of inattention such as spelling a word (“LUNCH”) backwards, reciting the days of the week backwards, 10-letter vigilance “A” task, and 5 picture recognition task.

Study Design and Setting

This was a preplanned secondary analysis of a prospective observational study that validated 3 delirium assessments.^30,31 This study was conducted at a tertiary care, academic ED. The local institutional review board (IRB) reviewed and approved this study. Informed consent from the patient or an authorized surrogate was obtained whenever possible. Because this was an observational study and posed minimal risk to the patient, the IRB granted a waiver of consent for patients who were both unable to provide consent and were without an authorized surrogate available in the ED or by phone.

Selection of Participants

We enrolled a convenience sample of patients between June 2010 and February 2012 Monday through Friday from 8 am to 4 pm. This enrollment window was based upon the psychiatrist’s availability. Because of the extensiveness of the psychiatric evaluations, we limited enrollment to 1 patient per day. Patients who were 65 years or older, not in a hallway bed, and in the ED for less than 12 hours at the time of enrollment were included. We used a 12-hour cutoff so that patients who presented in the evening and early morning hours could be included. Patients were excluded if they were previously enrolled, non-English speaking, deaf or blind, comatose, suffered from end-stage dementia, or were unable to complete all the study assessments. The rationale for excluding patients with end-stage dementia was that diagnosing delirium in this patient population is challenging.

Research assistants approached patients who met inclusion criteria and determined if any exclusion criteria were present. If none of the exclusion criteria were present, then the research assistant reviewed the informed consent document with the patient or authorized surrogate if the patient was not capable of providing consent. If a patient was not capable of providing consent and no authorized surrogate was available, then the patient was enrolled (under the waiver of consent) as long as the patient assented to be a part of the study. Once the patient was enrolled, the research assistant contacted the physician rater and reference standard psychiatrists to approach the patient.

Measures of Inattention

An emergency physician (JHH) who had no formal training in the mental status assessment of elders administered a cognitive battery to the patient, including tests of inattention. The following inattention tasks were administered:

• Spell the word “LUNCH” backwards.³⁰ Patients were initially allowed to spell the word “LUNCH” forwards. Patients who were unable to perform the task were assigned 5 errors.
• Recite the months of the year backwards from December to July.^{23,26,27,30,32} Patients who were unable to perform the task were assigned 6 errors.
• Recite the days of the week backwards.^23,26,33 Patients who were unable to perform the task were assigned 7 errors.
• Ten-letter vigilance “A” task.³⁴ The patient was given a series of 10 letters (“S-A-V-E-A-H-A-A-R-T”) every 3 seconds and was asked to squeeze the rater’s hand every time the patient heard the letter “A.” Patients who were unable to perform the task were assigned 10 errors.
• Five picture recognition task.³⁴ Patients were shown 5 objects on picture cards. Afterwards, patients were shown 10 pictures with the previously shown objects intermingled. The patient had to identify which objects were seen previously in the first 5 pictures. Patients who were unable to perform the task were assigned 10 errors.
• Recite the months of the year backwards from December to January.²⁹ Patients who were unable to perform the task were assigned 12 errors.

Reference Standard for Delirium

A comprehensive consultation-liaison psychiatrist assessment was the reference standard for delirium; the diagnosis of delirium was based on Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) criteria.³⁵ Three psychiatrists who each had an average of 11 years of clinical experience and regularly diagnosed delirium as part of their daily clinical practice were available to perform these assessments. To arrive at the diagnosis of delirium, they interviewed those who best understood the patient’s mental status (eg, the patient’s family members or caregivers, physician, and nurses). They also reviewed the patient’s medical record and radiology and laboratory test results. They performed bedside cognitive testing that included, but was not limited to, the Mini-Mental State Examination, Clock Drawing Test, Luria hand sequencing task, and tests for verbal fluency. A focused neurological examination was also performed (ie, screening for paraphasic errors, tremors, tone, asterixis, frontal release signs, etc.), and they also evaluated the patient for affective lability, hallucinations, and level of alertness. If the presence of delirium was still questionable, then confrontational naming, proverb interpretation or similarities, and assessments for apraxias were performed at the discretion of the psychiatrist. The psychiatrists were blinded to the physician’s assessments, and the assessments were conducted within 3 hours of each other.

Additional Variables Collected

Using medical record review, comorbidity burden, severity of illness, and premorbid cognition were ascertained. The Charlson Comorbidity Index, a weighted index that takes into account the number and seriousness of 19 preexisting comorbid conditions, was used to quantify comorbidity burden; higher scores indicate higher comorbid burden.^36,37 The Acute Physiology Score of the Acute Physiology and Chronic Health Evaluation II was used to quantify severity of illness.³⁸ This score is based upon the initial values of 12 routine physiologic measurements such as vital sign and laboratory abnormalities; higher scores represent higher severities of illness.³⁸ The medical record was reviewed to ascertain the presence of premorbid cognitive impairment; any documentation of dementia in the patient’s clinical problem list or physician history and physical examination from the outpatient or inpatient settings was considered positive. The medical record review was performed by a research assistant and was double-checked for accuracy by one of the investigators (JHH).

Data Analyses

Measures of central tendency and dispersion for continuous variables were reported as medians and interquartile ranges. Categorical variables were reported as proportions. Receiver operating characteristic curves were constructed for each inattention task. Area under the receiver operating characteristic curves (AUC) was reported to provide a global measure of diagnostic accuracy. Sensitivities, specificities, positive likelihood ratios (PLRs), and negative likelihood ratios (NLRs) with their 95% CIs were calculated using the psychiatrist’s assessment as the reference standard.³⁹ Cut-points with PLRs greater than 10 (strongly increased the likelihood of delirium) or NLRs less than 0.1 (strongly decreased the likelihood of delirium) were preferentially reported whenever possible.

All statistical analyses were performed with open source R statistical software version 3.0.1 (http://www.r-project.org/), SAS 9.4 (SAS Institute, Cary, NC), and Microsoft Excel 2010 (Microsoft Inc., Redmond, WA).

Delirium is frequently missed by healthcare providers because it is not routinely screened for in the acute care setting. To help address this deficiency of care, we evaluated several brief measures of inattention that take less than 30 seconds to complete. We observed that any errors made on the MOTYB-6 and MOTYB-12 tasks had very good sensitivities (80% and 84%) but were limited by their modest specificities (approximately 50%) for delirium. As a result, these assessments have limited clinical utility as standalone delirium screens. We also explored other commonly used brief measures of inattention and at a variety of error cutoffs. Reciting the days of the week backwards appeared to best balance sensitivity and specificity. None of the inattention measures could convincingly rule out delirium (NLR < 0.10), but the vigilance “A” and picture recognition tasks may have clinical utility in ruling in delirium (PLR > 10). Overall, all the inattention tasks, including MOTYB-6 and MOTYB-12, had very good diagnostic performances based upon their AUC. However, achieving a high sensitivity often had to be sacrificed for specificity or, alternatively, achieving a high specificity had to be sacrificed for sensitivity.

Inattention has been shown to be the cardinal feature for delirium,⁴⁰ and its assessment using cognitive testing has been recommended to help identify the presence of delirium according to an expert consensus panel.²⁶ The diagnostic performance of the MOTYB-12 observed in our study is similar to a study by Fick et al., who reported that MOTYB-12 had very good sensitivity (83%) but had modest specificity (69%) with a cutoff of 1 or more errors. Hendry et al. observed that the MOTYB-12 was 91% sensitive and 50% specific using a cutoff of 4 or more errors. With regard to the MOTYB-6, our reported specificity was different from what was observed by O’Regan et al.²⁷ Using 1 or more errors as a cutoff, they observed a much higher specificity for delirium than we did (90% vs 57%). Discordant observations regarding the diagnostic accuracy for other inattention tasks also exist. We observed that making any error on the days of the week backwards task was 84% sensitive and 82% specific for delirium, whereas Fick et al. observed a sensitivity and specificity of 50% and 94%, respectively. For the vigilance “A” task, we observed that making 2 or more errors over a series of 10 letters was 64.0% sensitive and 91.4% specific for delirium, whereas Pompei et al.⁴¹ observed that making 2 or more errors over a series of 60 letters was 51% sensitive and 77% specific for delirium.

The abovementioned discordant findings may be driven by spectrum bias, wherein the sensitivities and specificities for each inattention task may differ in different subgroups. As a result, differences in the age distribution, proportion of college graduates, history of dementia, and susceptibility to delirium can influence overall sensitivity and specificity. Objective measures of delirium, including the inattention screens studied, are particularly prone to spectrum bias.^31,34 However, the strength of this approach is that the assessment of inattention becomes less reliant upon clinical judgment and allows it to be used by raters from a wide range of clinical backgrounds. On the other hand, a subjective interpretation of these inattention tasks may allow the rater to capture the subtleties of inattention (ie, decreased speed of performance in a highly intelligent and well-educated patient without dementia). The disadvantage of this approach, however, is that it is more dependent on clinical judgment and may have decreased diagnostic accuracy in those with less clinical experience or with limited training.^14,42,43 These factors must be carefully considered when determining which delirium assessment to use.

Additional research is required to determine the clinical utility of these brief inattention assessments. These findings need to be further validated in larger studies, and the optimal cutoff of each task for different subgroup of patients (eg, demented vs nondemented) needs to be further clarified. It is not completely clear whether these inattention tests can serve as standalone assessments. Depending on the cutoff used, some of these assessments may have unacceptable false negative or false positive rates that may lead to increased adverse patient outcomes or increased resource utilization, respectively. Additional components or assessments may be needed to improve the diagnostic accuracy of these assessments. In addition to understanding these inattention assessments’ diagnostic accuracies, their ability to predict adverse outcomes also needs to be investigated. While a previous study observed that making any error on the MOTYB-12 task was associated with increased physical restraint use and prolonged hospital length of stay,⁴⁴ these assessments’ ability to prognosticate long-term outcomes such as mortality or long-term cognition or function need to be studied. Lastly, studies should also evaluate how easily implementable these assessments are and whether improved delirium recognition leads to improved patient outcomes.

This study has several notable limitations. Though planned a priori, this was a secondary analysis of a larger investigation designed to validate 3 delirium assessments. Our sample size was also relatively small, causing our 95% CIs to overlap in most cases and limiting the statistical power to truly determine whether one measure is better than the other. We also asked the patient to recite the months backwards from December to July as well as recite the months backwards from December to January. It is possible that the patient may have performed better at going from December to January because of learning effect. Our reference standard for delirium was based upon DSM-IV-TR criteria. The new DSM-V criteria may be more restrictive and may slightly change the sensitivities and specificities of the inattention tasks. We enrolled a convenience sample and enrolled patients who were more likely to be male, have cardiovascular chief complaints, and be admitted to the hospital; as a result, selection bias may have been introduced. Lastly, this study was conducted in a single center and enrolled patients who were 65 years and older. Our findings may not be generalizable to other settings and in those who are less than 65 years of age.

The MOTYB-6 and MOTYB-12 tasks had very good sensitivities but modest specificities (approximately 50%) using any error made as a cutoff; increasing cutoff to 2 errors and 3 errors, respectively, improved their specificities (approximately 70%) with minimal impact to their sensitivities. Reciting the days of the week backwards, spelling the word “LUNCH” backwards, and the 10-letter vigilance “A” task appeared to perform the best in ruling out delirium but only moderately decreased the likelihood of delirium. The 10-letter Vigilance “A” and picture recognition task appeared to perform the best in ruling in delirium. Days of the week backwards appeared to have the best combination of sensitivity and specificity.

Disclosure

This study was funded by the Emergency Medicine Foundation Career Development Award, National Institutes of Health K23AG032355, and National Center for Research Resources, Grant UL1 RR024975-01. The authors report no financial conflicts of interest.

Delirium is an acute neurocognitive disorder¹ that affects up to 25% of older emergency department (ED) and hospitalized patients.^2-4 The relationship between delirium and adverse outcomes is well documented.^5-7 Delirium is a strong predictor of increased length of mechanical ventilation, longer intensive care unit and hospital stays, increased risk of falls, long-term cognitive impairment, and mortality.^8-13 Delirium is frequently missed by healthcare professionals^2,14-16 and goes undetected in up to 3 out of 4 patients by bedside nurses and medical practitioners in many hospital settings.^14,17-22 A significant barrier to recognizing delirium is the absence of brief delirium assessments.

In an effort to improve delirium recognition in the acute care setting, there has been a concerted effort to develop and validate brief delirium assessments. To address this unmet need, 4 ‘A’s Test (4AT), the Brief Confusion Assessment Method (bCAM), and the 3-minute diagnostic assessment for CAM-defined delirium (3D-CAM) are 1- to 3-minute delirium assessments that were validated in acutely ill older patients.²³ However, 1 to 3 minutes may still be too long in busy clinical environments, and briefer (<30 seconds) delirium assessments may be needed.

One potential more-rapid method to screen for delirium is to specifically test for the presence of inattention, which is a cardinal feature of delirium.^24,25 Inattention can be ascertained by having the patient recite the months backwards, recite the days of the week backwards, or spell a word backwards.²⁶ Recent studies have evaluated the diagnostic accuracy of reciting the months of the year backwards for delirium. O’Regan et al.²⁷ evaluated the diagnostic accuracy of the month of the year backwards from December to July (MOTYB-6) and observed that this task was 84% sensitive and 90% specific for delirium in older patients. However, they performed the reference standard delirium assessments in patients who had a positive MOTYB-6, which can overestimate sensitivity and underestimate specificity (verification bias).²⁸ Fick et al.²⁹ examined the diagnostic accuracy of 20 individual elements of the 3D-CAM and observed that reciting the months of the year backwards from December to January (MOTYB-12) was 83% sensitive and 69% specific for delirium. However, this was an exploratory study that was designed to identify an element of the 3D-CAM that had the best diagnostic accuracy.

To address these limitations, we sought to evaluate the diagnostic performance of the MOTYB-6 and MOTYB-12 for delirium as diagnosed by a reference standard. We also explored other brief tests of inattention such as spelling a word (“LUNCH”) backwards, reciting the days of the week backwards, 10-letter vigilance “A” task, and 5 picture recognition task.

Study Design and Setting

This was a preplanned secondary analysis of a prospective observational study that validated 3 delirium assessments.^30,31 This study was conducted at a tertiary care, academic ED. The local institutional review board (IRB) reviewed and approved this study. Informed consent from the patient or an authorized surrogate was obtained whenever possible. Because this was an observational study and posed minimal risk to the patient, the IRB granted a waiver of consent for patients who were both unable to provide consent and were without an authorized surrogate available in the ED or by phone.

Selection of Participants

We enrolled a convenience sample of patients between June 2010 and February 2012 Monday through Friday from 8 am to 4 pm. This enrollment window was based upon the psychiatrist’s availability. Because of the extensiveness of the psychiatric evaluations, we limited enrollment to 1 patient per day. Patients who were 65 years or older, not in a hallway bed, and in the ED for less than 12 hours at the time of enrollment were included. We used a 12-hour cutoff so that patients who presented in the evening and early morning hours could be included. Patients were excluded if they were previously enrolled, non-English speaking, deaf or blind, comatose, suffered from end-stage dementia, or were unable to complete all the study assessments. The rationale for excluding patients with end-stage dementia was that diagnosing delirium in this patient population is challenging.

Research assistants approached patients who met inclusion criteria and determined if any exclusion criteria were present. If none of the exclusion criteria were present, then the research assistant reviewed the informed consent document with the patient or authorized surrogate if the patient was not capable of providing consent. If a patient was not capable of providing consent and no authorized surrogate was available, then the patient was enrolled (under the waiver of consent) as long as the patient assented to be a part of the study. Once the patient was enrolled, the research assistant contacted the physician rater and reference standard psychiatrists to approach the patient.

Measures of Inattention

An emergency physician (JHH) who had no formal training in the mental status assessment of elders administered a cognitive battery to the patient, including tests of inattention. The following inattention tasks were administered:

• Spell the word “LUNCH” backwards.³⁰ Patients were initially allowed to spell the word “LUNCH” forwards. Patients who were unable to perform the task were assigned 5 errors.
• Recite the months of the year backwards from December to July.^{23,26,27,30,32} Patients who were unable to perform the task were assigned 6 errors.
• Recite the days of the week backwards.^23,26,33 Patients who were unable to perform the task were assigned 7 errors.
• Ten-letter vigilance “A” task.³⁴ The patient was given a series of 10 letters (“S-A-V-E-A-H-A-A-R-T”) every 3 seconds and was asked to squeeze the rater’s hand every time the patient heard the letter “A.” Patients who were unable to perform the task were assigned 10 errors.
• Five picture recognition task.³⁴ Patients were shown 5 objects on picture cards. Afterwards, patients were shown 10 pictures with the previously shown objects intermingled. The patient had to identify which objects were seen previously in the first 5 pictures. Patients who were unable to perform the task were assigned 10 errors.
• Recite the months of the year backwards from December to January.²⁹ Patients who were unable to perform the task were assigned 12 errors.

Reference Standard for Delirium

A comprehensive consultation-liaison psychiatrist assessment was the reference standard for delirium; the diagnosis of delirium was based on Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) criteria.³⁵ Three psychiatrists who each had an average of 11 years of clinical experience and regularly diagnosed delirium as part of their daily clinical practice were available to perform these assessments. To arrive at the diagnosis of delirium, they interviewed those who best understood the patient’s mental status (eg, the patient’s family members or caregivers, physician, and nurses). They also reviewed the patient’s medical record and radiology and laboratory test results. They performed bedside cognitive testing that included, but was not limited to, the Mini-Mental State Examination, Clock Drawing Test, Luria hand sequencing task, and tests for verbal fluency. A focused neurological examination was also performed (ie, screening for paraphasic errors, tremors, tone, asterixis, frontal release signs, etc.), and they also evaluated the patient for affective lability, hallucinations, and level of alertness. If the presence of delirium was still questionable, then confrontational naming, proverb interpretation or similarities, and assessments for apraxias were performed at the discretion of the psychiatrist. The psychiatrists were blinded to the physician’s assessments, and the assessments were conducted within 3 hours of each other.

Additional Variables Collected

Using medical record review, comorbidity burden, severity of illness, and premorbid cognition were ascertained. The Charlson Comorbidity Index, a weighted index that takes into account the number and seriousness of 19 preexisting comorbid conditions, was used to quantify comorbidity burden; higher scores indicate higher comorbid burden.^36,37 The Acute Physiology Score of the Acute Physiology and Chronic Health Evaluation II was used to quantify severity of illness.³⁸ This score is based upon the initial values of 12 routine physiologic measurements such as vital sign and laboratory abnormalities; higher scores represent higher severities of illness.³⁸ The medical record was reviewed to ascertain the presence of premorbid cognitive impairment; any documentation of dementia in the patient’s clinical problem list or physician history and physical examination from the outpatient or inpatient settings was considered positive. The medical record review was performed by a research assistant and was double-checked for accuracy by one of the investigators (JHH).

Data Analyses

Measures of central tendency and dispersion for continuous variables were reported as medians and interquartile ranges. Categorical variables were reported as proportions. Receiver operating characteristic curves were constructed for each inattention task. Area under the receiver operating characteristic curves (AUC) was reported to provide a global measure of diagnostic accuracy. Sensitivities, specificities, positive likelihood ratios (PLRs), and negative likelihood ratios (NLRs) with their 95% CIs were calculated using the psychiatrist’s assessment as the reference standard.³⁹ Cut-points with PLRs greater than 10 (strongly increased the likelihood of delirium) or NLRs less than 0.1 (strongly decreased the likelihood of delirium) were preferentially reported whenever possible.

All statistical analyses were performed with open source R statistical software version 3.0.1 (http://www.r-project.org/), SAS 9.4 (SAS Institute, Cary, NC), and Microsoft Excel 2010 (Microsoft Inc., Redmond, WA).

Delirium is frequently missed by healthcare providers because it is not routinely screened for in the acute care setting. To help address this deficiency of care, we evaluated several brief measures of inattention that take less than 30 seconds to complete. We observed that any errors made on the MOTYB-6 and MOTYB-12 tasks had very good sensitivities (80% and 84%) but were limited by their modest specificities (approximately 50%) for delirium. As a result, these assessments have limited clinical utility as standalone delirium screens. We also explored other commonly used brief measures of inattention and at a variety of error cutoffs. Reciting the days of the week backwards appeared to best balance sensitivity and specificity. None of the inattention measures could convincingly rule out delirium (NLR < 0.10), but the vigilance “A” and picture recognition tasks may have clinical utility in ruling in delirium (PLR > 10). Overall, all the inattention tasks, including MOTYB-6 and MOTYB-12, had very good diagnostic performances based upon their AUC. However, achieving a high sensitivity often had to be sacrificed for specificity or, alternatively, achieving a high specificity had to be sacrificed for sensitivity.

Inattention has been shown to be the cardinal feature for delirium,⁴⁰ and its assessment using cognitive testing has been recommended to help identify the presence of delirium according to an expert consensus panel.²⁶ The diagnostic performance of the MOTYB-12 observed in our study is similar to a study by Fick et al., who reported that MOTYB-12 had very good sensitivity (83%) but had modest specificity (69%) with a cutoff of 1 or more errors. Hendry et al. observed that the MOTYB-12 was 91% sensitive and 50% specific using a cutoff of 4 or more errors. With regard to the MOTYB-6, our reported specificity was different from what was observed by O’Regan et al.²⁷ Using 1 or more errors as a cutoff, they observed a much higher specificity for delirium than we did (90% vs 57%). Discordant observations regarding the diagnostic accuracy for other inattention tasks also exist. We observed that making any error on the days of the week backwards task was 84% sensitive and 82% specific for delirium, whereas Fick et al. observed a sensitivity and specificity of 50% and 94%, respectively. For the vigilance “A” task, we observed that making 2 or more errors over a series of 10 letters was 64.0% sensitive and 91.4% specific for delirium, whereas Pompei et al.⁴¹ observed that making 2 or more errors over a series of 60 letters was 51% sensitive and 77% specific for delirium.

The abovementioned discordant findings may be driven by spectrum bias, wherein the sensitivities and specificities for each inattention task may differ in different subgroups. As a result, differences in the age distribution, proportion of college graduates, history of dementia, and susceptibility to delirium can influence overall sensitivity and specificity. Objective measures of delirium, including the inattention screens studied, are particularly prone to spectrum bias.^31,34 However, the strength of this approach is that the assessment of inattention becomes less reliant upon clinical judgment and allows it to be used by raters from a wide range of clinical backgrounds. On the other hand, a subjective interpretation of these inattention tasks may allow the rater to capture the subtleties of inattention (ie, decreased speed of performance in a highly intelligent and well-educated patient without dementia). The disadvantage of this approach, however, is that it is more dependent on clinical judgment and may have decreased diagnostic accuracy in those with less clinical experience or with limited training.^14,42,43 These factors must be carefully considered when determining which delirium assessment to use.

Additional research is required to determine the clinical utility of these brief inattention assessments. These findings need to be further validated in larger studies, and the optimal cutoff of each task for different subgroup of patients (eg, demented vs nondemented) needs to be further clarified. It is not completely clear whether these inattention tests can serve as standalone assessments. Depending on the cutoff used, some of these assessments may have unacceptable false negative or false positive rates that may lead to increased adverse patient outcomes or increased resource utilization, respectively. Additional components or assessments may be needed to improve the diagnostic accuracy of these assessments. In addition to understanding these inattention assessments’ diagnostic accuracies, their ability to predict adverse outcomes also needs to be investigated. While a previous study observed that making any error on the MOTYB-12 task was associated with increased physical restraint use and prolonged hospital length of stay,⁴⁴ these assessments’ ability to prognosticate long-term outcomes such as mortality or long-term cognition or function need to be studied. Lastly, studies should also evaluate how easily implementable these assessments are and whether improved delirium recognition leads to improved patient outcomes.

This study has several notable limitations. Though planned a priori, this was a secondary analysis of a larger investigation designed to validate 3 delirium assessments. Our sample size was also relatively small, causing our 95% CIs to overlap in most cases and limiting the statistical power to truly determine whether one measure is better than the other. We also asked the patient to recite the months backwards from December to July as well as recite the months backwards from December to January. It is possible that the patient may have performed better at going from December to January because of learning effect. Our reference standard for delirium was based upon DSM-IV-TR criteria. The new DSM-V criteria may be more restrictive and may slightly change the sensitivities and specificities of the inattention tasks. We enrolled a convenience sample and enrolled patients who were more likely to be male, have cardiovascular chief complaints, and be admitted to the hospital; as a result, selection bias may have been introduced. Lastly, this study was conducted in a single center and enrolled patients who were 65 years and older. Our findings may not be generalizable to other settings and in those who are less than 65 years of age.

The MOTYB-6 and MOTYB-12 tasks had very good sensitivities but modest specificities (approximately 50%) using any error made as a cutoff; increasing cutoff to 2 errors and 3 errors, respectively, improved their specificities (approximately 70%) with minimal impact to their sensitivities. Reciting the days of the week backwards, spelling the word “LUNCH” backwards, and the 10-letter vigilance “A” task appeared to perform the best in ruling out delirium but only moderately decreased the likelihood of delirium. The 10-letter Vigilance “A” and picture recognition task appeared to perform the best in ruling in delirium. Days of the week backwards appeared to have the best combination of sensitivity and specificity.

Disclosure

This study was funded by the Emergency Medicine Foundation Career Development Award, National Institutes of Health K23AG032355, and National Center for Research Resources, Grant UL1 RR024975-01. The authors report no financial conflicts of interest.

As the heart goes, so go the kidneys—and vice versa. Cardiac and renal function are intricately interdependent, and failure of either organ causes injury to the other in a vicious circle of worsening function.¹

See related editorial

Here, we discuss acute cardiorenal syndrome, ie, acute exacerbation of heart failure leading to acute kidney injury, a common cause of hospitalization and admission to the intensive care unit. We examine its clinical definition, pathophysiology, hemodynamic derangements, clues that help in diagnosing it, and its treatment.

A GROUP OF LINKED DISORDERS

Two types of acute cardiac dysfunction

Although these definitions offer a good general description, further clarification of the nature of organ dysfunction is needed. Acute renal dysfunction can be unambiguously defined using the AKIN (Acute Kidney Injury Network) and RIFLE (risk, injury, failure, loss of kidney function, and end-stage kidney disease) classifications.³ Acute cardiac dysfunction, on the other hand, is an ambiguous term that encompasses 2 clinically and pathophysiologically distinct conditions: cardiogenic shock and acute heart failure.

Cardiogenic shock is characterized by a catastrophic compromise of cardiac pump function leading to global hypoperfusion severe enough to cause systemic organ damage.⁴ The cardiac index at which organs start to fail varies in different cases, but a value of less than 1.8 L/min/m² is typically used to define cardiogenic shock.⁴

Acute heart failure, on the other hand, is defined as gradually or rapidly worsening signs and symptoms of congestive heart failure due to worsening pulmonary or systemic congestion.⁵ Hypervolemia is the hallmark of acute heart failure, whereas patients with cardiogenic shock may be hypervolemic, normovolemic, or hypovolemic. Although cardiac output may be mildly reduced in some cases of acute heart failure, systemic perfusion is enough to maintain organ function.

These two conditions cause renal injury by distinct mechanisms and have entirely different therapeutic implications. As we discuss later, reduced renal perfusion due to renal venous congestion is now believed to be the major hemodynamic mechanism of renal injury in acute heart failure. On the other hand, in cardiogenic shock, renal perfusion is reduced due to a critical decline of cardiac pump function.

The ideal definition of acute cardiorenal syndrome should describe a distinct pathophysiology of the syndrome and offer distinct therapeutic options that counteract it. Hence, we propose that renal injury from cardiogenic shock should not be included in its definition, an approach that has been adopted in some of the recent reviews as well.⁶ Our discussion of acute cardiorenal syndrome is restricted to renal injury caused by acute heart failure.

PATHOPHYSIOLOGY OF ACUTE CARDIORENAL SYNDROME

Multiple mechanisms have been implicated in the pathophysiology of cardiorenal syndrome.^7,8

Sympathetic hyperactivity is a compensatory mechanism in heart failure and may be aggravated if cardiac output is further reduced. Its effects include constriction of afferent and efferent arterioles, causing reduced renal perfusion and increased tubular sodium and water reabsorption.⁷

The renin-angiotensin-aldosterone system is activated in patients with stable congestive heart failure and may be further stimulated in a state of reduced renal perfusion, which is a hallmark of acute cardiorenal syndrome. Its activation can cause further salt and water retention.

However, direct hemodynamic mechanisms likely play the most important role and have obvious diagnostic and therapeutic implications.

Elevated venous pressure, not reduced cardiac output, drives kidney injury

The classic view was that renal dysfunction in acute heart failure is caused by reduced renal blood flow due to failing cardiac pump function. Cardiac output may be reduced in acute heart failure for various reasons, such as atrial fibrillation, myocardial infarction, or other processes, but reduced cardiac output has a minimal role, if any, in the pathogenesis of renal injury in acute heart failure.

As evidence of this, acute heart failure is not always associated with reduced cardiac output.⁵ Even if the cardiac index (cardiac output divided by body surface area) is mildly reduced, renal blood flow is largely unaffected, thanks to effective renal autoregulatory mechanisms. Not until the mean arterial pressure falls below 70 mm Hg do these mechanisms fail and renal blood flow starts to drop.⁹ Hence, unless cardiac performance is compromised enough to cause cardiogenic shock, renal blood flow usually does not change significantly with mild reduction in cardiac output.

Hanberg et al¹⁰ performed a post hoc analysis of the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheter Effectiveness (ESCAPE) trial, in which 525 patients with advanced heart failure underwent pulmonary artery catheterization to measure their cardiac index. The authors found no association between the cardiac index and renal function in these patients.

In view of the current clinical evidence, the focus has shifted to renal venous congestion. According to Poiseuille’s law, blood flow through the kidneys depends on the pressure gradient—high pressure on the arterial side, low pressure on the venous side.⁸ Increased renal venous pressure causes reduced renal perfusion pressure, thereby affecting renal perfusion. This is now recognized as an important hemodynamic mechanism of acute cardiorenal syndrome.

Renal congestion can also affect renal function through indirect mechanisms. For example, it can cause renal interstitial edema that may then increase the intratubular pressure, thereby reducing the transglomerular pressure gradient.¹¹

Firth et al,¹⁴ in experiments in animals, found that increasing the renal venous pressure above 18.75 mm Hg significantly reduced the glomerular filtration rate, which completely resolved when renal venous pressure was restored to basal levels.

Mullens et al,¹⁵ in a study of 145 patients admitted with acute heart failure, reported that 58 (40%) developed acute kidney injury. Pulmonary artery catheterization revealed that elevated central venous pressure, rather than reduced cardiac index, was the primary hemodynamic factor driving renal dysfunction.

DIAGNOSIS AND CLINICAL ASSESSMENT

Patients with acute cardiorenal syndrome present with clinical features of pulmonary or systemic congestion (or both) and acute kidney injury.

Elevated left-sided pressures are usually but not always associated with elevated right-sided pressures. In a study of 1,000 patients with advanced heart failure, a pulmonary capillary wedge pressure of 22 mm Hg or higher had a positive predictive value of 88% for a right atrial pressure of 10 mm Hg or higher.¹⁶ Hence, the clinical presentation may vary depending on the location (pulmonary, systemic, or both) and degree of congestion.

Symptoms of pulmonary congestion include worsening exertional dyspnea and orthopnea; bilateral crackles may be heard on physical examination if pulmonary edema is present.

Systemic congestion can cause significant peripheral edema and weight gain. Jugular venous distention may be noted. Oliguria may be present due to renal dysfunction; patients on maintenance diuretic therapy often note its lack of efficacy.

Signs of acute heart failure

Wang et al,¹⁷ in a meta-analysis of 22 studies, concluded that the features that most strongly suggested acute heart failure were:

• History of paroxysmal nocturnal dyspnea
• A third heart sound
• Evidence of pulmonary venous congestion on chest radiography.

Features that most strongly suggested the patient did not have acute heart failure were:

• Absence of exertional dyspnea
• Absence of rales
• Absence of radiographic evidence of cardiomegaly.

Patients may present without some of these classic clinical features, and the diagnosis of acute heart failure may be challenging. For example, even if left-sided pressures are very high, pulmonary edema may be absent because of pulmonary vascular remodeling in chronic heart failure.¹⁸ Pulmonary artery catheterization reveals elevated cardiac filling pressures and can be used to guide therapy, but clinical evidence argues against its routine use.¹⁹

Urine electrolytes (fractional excretion of sodium < 1% and fractional excretion of urea < 35%) often suggest a prerenal form of acute kidney injury, since the hemodynamic derangements in acute cardiorenal syndrome reduce renal perfusion.

Biomarkers of cell-cycle arrest such as urine insulinlike growth factor-binding protein 7 and tissue inhibitor of metalloproteinase 2 have recently been shown to identify patients with acute heart failure at risk of developing acute cardiorenal syndrome.²⁰

Acute cardiorenal syndrome vs renal injury due to hypovolemia

The major alternative in the differential diagnosis of acute cardiorenal syndrome is renal injury due to hypovolemia. Patients with stable heart failure usually have mild hypervolemia at baseline, but they can become hypovolemic due to overaggressive diuretic therapy, severe diarrhea, or other causes.

Although the fluid status of patients in these 2 conditions is opposite, they can be difficult to distinguish. In both conditions, urine electrolytes suggest a prerenal acute kidney injury. A history of recent fluid losses or diuretic overuse may help identify hypovolemia. If available, analysis of the recent trend in weight can be vital in making the right diagnosis.

Misdiagnosis of acute cardiorenal syndrome as hypovolemia-induced acute kidney injury can be catastrophic. If volume depletion is erroneously judged to be the cause of acute kidney injury, fluid administration can further worsen both cardiac and renal function. This can perpetuate the vicious circle that is already in play. Lack of renal recovery may invite further fluid administration.

Fluid removal with diuresis or ultrafiltration is the cornerstone of treatment. Other treatments such as inotropes are reserved for patients with resistant disease.

Diuretics

The goal of therapy in acute cardiorenal syndrome is to achieve aggressive diuresis, typically using intravenous diuretics. Loop diuretics are the most potent class of diuretics and are the first-line drugs for this purpose. Other classes of diuretics can be used in conjunction with loop diuretics; however, using them by themselves is neither effective nor recommended.

Resistance to diuretics at usual doses is common in patients with acute cardiorenal syndrome. Several mechanisms contribute to diuretic resistance in these patients.²¹

Oral bioavailability of diuretics may be reduced due to intestinal edema.

Diuretic pharmacokinetics are significantly deranged in cardiorenal syndrome. All diuretics except mineralocorticoid antagonists (ie, spironolactone and eplerenone) act on targets on the luminal side of renal tubules, but are highly protein-bound and are hence not filtered at the glomerulus. Loop diuretics, thiazides, and carbonic anhydrase inhibitors are secreted in the proximal convoluted tubule via the organic anion transporter,²² whereas epithelial sodium channel inhibitors (amiloride and triamterene) are secreted via the organic cation transporter 2.²³ In renal dysfunction, various uremic toxins accumulate in the body and compete with diuretics for secretion into the proximal convoluted tubule via these transporters.²⁴

Finally, activation of the sympathetic nervous system and renin-angiotensin-aldosterone system leads to increased tubular sodium and water retention, thereby also blunting the diuretic response.

Diuretic dosage. In patients whose creatinine clearance is less than 15 mL/min, only 10% to 20% as much loop diuretic is secreted into the renal tubule as in normal individuals.²⁵ This effect warrants dose adjustment of diuretics during uremia.

Continuous infusion or bolus? Continuous infusion of loop diuretics is another strategy to optimize drug delivery. Compared with bolus therapy, continuous infusion provides more sustained and uniform drug delivery and prevents postdiuretic sodium retention.

The Diuretic Optimization Strategies Evaluation (DOSE) trial compared the efficacy and safety of continuous vs bolus furosemide therapy in 308 patients admitted with acute decompensated heart failure.²⁶ There was no difference in symptom control or net fluid loss at 72 hours in either group. Other studies have shown more diuresis with continuous infusion than with a similarly dosed bolus regimen.²⁷ However, definitive clinical evidence is lacking at this point to support routine use of continuous loop diuretic therapy.

Combination diuretic therapy. Sequential nephron blockade with combination diuretic therapy is an important therapeutic strategy against diuretic resistance. Notably, urine output-guided diuretic therapy has been shown to be superior to standard diuretic therapy.²⁸ Such therapeutic protocols may employ combination diuretic therapy as a next step when the desired diuretic response is not obtained with high doses of loop diuretic monotherapy.

The desired diuretic response depends on the clinical situation. For example, in patients with severe congestion, we would like the net fluid output to be at least 2 to 3 L more than the fluid intake after the first 24 hours. Sometimes, patients in the intensive care unit are on several essential drug infusions, so that their net intake amounts to 1 to 2 L. In these patients, the desired urine output would be even more than in patients not on these drug infusions.

Loop diuretics block sodium reabsorption at the thick ascending loop of Henle. This disrupts the countercurrent exchange mechanism and reduces renal medullary interstitial osmolarity; these effects prevent water reabsorption. However, the unresorbed sodium can be taken up by the sodium-chloride cotransporter and the epithelial sodium channel in the distal nephron, thereby blunting the diuretic effect. This is the rationale for combining loop diuretics with thiazides or potassium-sparing diuretics.

Similarly, carbonic anhydrase inhibitors (eg, acetazolamide) reduce sodium reabsorption from the proximal convoluted tubule, but most of this sodium is then reabsorbed distally. Hence, the combination of a loop diuretic and acetazolamide can also have a synergistic diuretic effect.

The most popular combination is a loop diuretic plus a thiazide, although no large-scale placebo-controlled trials have been performed.²⁹ Metolazone (a thiazidelike diuretic) is typically used due to its low cost and availability.³⁰ Metolazone has also been shown to block sodium reabsorption at the proximal tubule, which may contribute to its synergistic effect. Chlorothiazide is available in an intravenous formulation and has a faster onset of action than metolazone. However, studies have failed to detect any benefit of one over the other.³¹

The potential benefit of combining a loop diuretic with acetazolamide is a lower tendency to develop metabolic alkalosis, a potential side effect of loop diuretics and thiazides. Although data are limited, a recent study showed that adding acetazolamide to bumetanide led to significantly increased natriuresis.³²

In the Aldosterone Targeted Neurohormonal Combined With Natriuresis Therapy in Heart Failure (ATHENA-HF) trial, adding spironolactone in high doses to usual therapy was not found to cause any significant change in N-terminal pro-B-type natriuretic peptide level or net urine output.³³

Venovenous ultrafiltration (or aquapheresis) employs an extracorporeal circuit, similar to the one used in hemodialysis, which removes iso-osmolar fluid at a fixed rate.³⁴ Newer ultrafiltration systems are more portable, can be used with peripheral venous access, and require minimal nursing supervision.³⁵

Although ultrafiltration seems an attractive alternative to diuresis in acute heart failure, studies have been inconclusive. The Cardiorenal Rescue Study in Acute Decompensated Heart Failure (CARRESS-HF) trial compared ultrafiltration and diuresis in 188 patients with acute heart failure and acute cardiorenal syndrome.³⁶ Diuresis, performed according to an algorithm, was found to be superior to ultrafiltration in terms of a bivariate end point of change in weight and change in serum creatinine level at 96 hours. However, the level of cystatin C is thought to be a more accurate indicator of renal function, and the change in cystatin C level from baseline did not differ between the two treatment groups. Also, the ultrafiltration rate was 200 mL per hour, which, some argue, may have been excessive and may have caused intravascular depletion.

Although the ideal rate of fluid removal is unknown, it should be individualized and adjusted based on the patient’s renal function, volume status, and hemodynamic status. The initial rate should be based on the degree of fluid overload and the anticipated plasma refill rate from the interstitial fluid.³⁷ For example, a malnourished patient may have low serum oncotic pressure and hence have low plasma refill upon ultrafiltration. Disturbance of this delicate balance between the rates of ultrafiltration and plasma refill may lead to intravascular volume contraction.

In summary, although ultrafiltration is a valuable alternative to diuretics in resistant cases, its use as a primary decongestive therapy cannot be endorsed in view of the current data.

Inotropes

Inotropes such as dobutamine and milrinone are typically used in cases of cardiogenic shock to maintain organ perfusion. There is a physiologic rationale to using inotropes in acute cardiorenal syndrome as well, especially when the aforementioned strategies fail to overcome diuretic resistance.⁷

Inotropes increase cardiac output, improve renal blood flow, improve right ventricular output, and thereby relieve systemic congestion. These hemodynamic effects may improve renal perfusion and response to diuretics. However, clinical evidence to support this is lacking.

The Renal Optimization Strategies Evaluation (ROSE) trial enrolled 360 patients with acute heart failure and renal dysfunction. Adding dopamine in a low dose (2 μg/kg/min) to diuretic therapy had no significant effect on 72-hour cumulative urine output or renal function as measured by cystatin C levels.³⁸ However, acute kidney injury was not identified in this trial, and the renal function of many of these patients may have been at its baseline when they were admitted. In other words, this trial did not necessarily include patients with acute kidney injury along with acute heart failure. Hence, it did not necessarily include patients with acute cardiorenal syndrome.

Vasodilators

Vasodilators such as nitroglycerin, sodium nitroprusside, and hydralazine are commonly used in patients with acute heart failure, although the clinical evidence supporting their use is weak.

Physiologically, arterial dilation reduces afterload and can help relieve pulmonary congestion, and venodilation increases capacitance and reduces preload. In theory, venodilators such as nitroglycerin can relieve renal venous congestion in patients with acute cardiorenal syndrome, thereby improving renal perfusion.

However, the use of vasodilators is often limited by their adverse effects, the most important being hypotension. This is especially relevant in light of recent data identifying reduction in blood pressure during treatment of acute heart failure as an independent risk factor for worsening renal function.^39,40 It is important to note that in these studies, changes in cardiac index did not affect the propensity for developing worsening renal function. The precise mechanism of this finding is unclear but it is plausible that systemic vasodilation redistributes the cardiac output to nonrenal tissues, thereby overriding the renal autoregulatory mechanisms that are normally employed in low output states.

Preventive strategies

Various strategies can be used to prevent acute cardiorenal syndrome. An optimal outpatient diuretic regimen to avoid hypervolemia is essential. Patients with advanced congestive heart failure should be followed up closely in dedicated heart failure clinics until their diuretic regimen is optimized. Patients should be advised to check their weight on a regular basis and seek medical advice if they notice an increase in their weight or a reduction in their urine output.

TAKE-HOME POINTS

• A robust clinical definition of cardiorenal syndrome is lacking. Hence, recognition of this condition can be challenging.
• Volume overload is central to its pathogenesis, and accurate assessment of volume status is critical.
• Renal venous congestion is the major mechanism of type 1 cardiorenal syndrome.
• Misdiagnosis can have devastating consequences, as it may lead to an opposite therapeutic approach.
• Fluid removal by various strategies is the mainstay of treatment.
• Temporary inotropic support should be saved for the last resort.

As the heart goes, so go the kidneys—and vice versa. Cardiac and renal function are intricately interdependent, and failure of either organ causes injury to the other in a vicious circle of worsening function.¹

See related editorial

Here, we discuss acute cardiorenal syndrome, ie, acute exacerbation of heart failure leading to acute kidney injury, a common cause of hospitalization and admission to the intensive care unit. We examine its clinical definition, pathophysiology, hemodynamic derangements, clues that help in diagnosing it, and its treatment.

A GROUP OF LINKED DISORDERS

Two types of acute cardiac dysfunction

Although these definitions offer a good general description, further clarification of the nature of organ dysfunction is needed. Acute renal dysfunction can be unambiguously defined using the AKIN (Acute Kidney Injury Network) and RIFLE (risk, injury, failure, loss of kidney function, and end-stage kidney disease) classifications.³ Acute cardiac dysfunction, on the other hand, is an ambiguous term that encompasses 2 clinically and pathophysiologically distinct conditions: cardiogenic shock and acute heart failure.

Cardiogenic shock is characterized by a catastrophic compromise of cardiac pump function leading to global hypoperfusion severe enough to cause systemic organ damage.⁴ The cardiac index at which organs start to fail varies in different cases, but a value of less than 1.8 L/min/m² is typically used to define cardiogenic shock.⁴

Acute heart failure, on the other hand, is defined as gradually or rapidly worsening signs and symptoms of congestive heart failure due to worsening pulmonary or systemic congestion.⁵ Hypervolemia is the hallmark of acute heart failure, whereas patients with cardiogenic shock may be hypervolemic, normovolemic, or hypovolemic. Although cardiac output may be mildly reduced in some cases of acute heart failure, systemic perfusion is enough to maintain organ function.

These two conditions cause renal injury by distinct mechanisms and have entirely different therapeutic implications. As we discuss later, reduced renal perfusion due to renal venous congestion is now believed to be the major hemodynamic mechanism of renal injury in acute heart failure. On the other hand, in cardiogenic shock, renal perfusion is reduced due to a critical decline of cardiac pump function.

The ideal definition of acute cardiorenal syndrome should describe a distinct pathophysiology of the syndrome and offer distinct therapeutic options that counteract it. Hence, we propose that renal injury from cardiogenic shock should not be included in its definition, an approach that has been adopted in some of the recent reviews as well.⁶ Our discussion of acute cardiorenal syndrome is restricted to renal injury caused by acute heart failure.

PATHOPHYSIOLOGY OF ACUTE CARDIORENAL SYNDROME

Multiple mechanisms have been implicated in the pathophysiology of cardiorenal syndrome.^7,8

Sympathetic hyperactivity is a compensatory mechanism in heart failure and may be aggravated if cardiac output is further reduced. Its effects include constriction of afferent and efferent arterioles, causing reduced renal perfusion and increased tubular sodium and water reabsorption.⁷

The renin-angiotensin-aldosterone system is activated in patients with stable congestive heart failure and may be further stimulated in a state of reduced renal perfusion, which is a hallmark of acute cardiorenal syndrome. Its activation can cause further salt and water retention.

However, direct hemodynamic mechanisms likely play the most important role and have obvious diagnostic and therapeutic implications.

Elevated venous pressure, not reduced cardiac output, drives kidney injury

The classic view was that renal dysfunction in acute heart failure is caused by reduced renal blood flow due to failing cardiac pump function. Cardiac output may be reduced in acute heart failure for various reasons, such as atrial fibrillation, myocardial infarction, or other processes, but reduced cardiac output has a minimal role, if any, in the pathogenesis of renal injury in acute heart failure.

As evidence of this, acute heart failure is not always associated with reduced cardiac output.⁵ Even if the cardiac index (cardiac output divided by body surface area) is mildly reduced, renal blood flow is largely unaffected, thanks to effective renal autoregulatory mechanisms. Not until the mean arterial pressure falls below 70 mm Hg do these mechanisms fail and renal blood flow starts to drop.⁹ Hence, unless cardiac performance is compromised enough to cause cardiogenic shock, renal blood flow usually does not change significantly with mild reduction in cardiac output.

Hanberg et al¹⁰ performed a post hoc analysis of the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheter Effectiveness (ESCAPE) trial, in which 525 patients with advanced heart failure underwent pulmonary artery catheterization to measure their cardiac index. The authors found no association between the cardiac index and renal function in these patients.

In view of the current clinical evidence, the focus has shifted to renal venous congestion. According to Poiseuille’s law, blood flow through the kidneys depends on the pressure gradient—high pressure on the arterial side, low pressure on the venous side.⁸ Increased renal venous pressure causes reduced renal perfusion pressure, thereby affecting renal perfusion. This is now recognized as an important hemodynamic mechanism of acute cardiorenal syndrome.

Renal congestion can also affect renal function through indirect mechanisms. For example, it can cause renal interstitial edema that may then increase the intratubular pressure, thereby reducing the transglomerular pressure gradient.¹¹

Firth et al,¹⁴ in experiments in animals, found that increasing the renal venous pressure above 18.75 mm Hg significantly reduced the glomerular filtration rate, which completely resolved when renal venous pressure was restored to basal levels.

Mullens et al,¹⁵ in a study of 145 patients admitted with acute heart failure, reported that 58 (40%) developed acute kidney injury. Pulmonary artery catheterization revealed that elevated central venous pressure, rather than reduced cardiac index, was the primary hemodynamic factor driving renal dysfunction.

DIAGNOSIS AND CLINICAL ASSESSMENT

Patients with acute cardiorenal syndrome present with clinical features of pulmonary or systemic congestion (or both) and acute kidney injury.

Elevated left-sided pressures are usually but not always associated with elevated right-sided pressures. In a study of 1,000 patients with advanced heart failure, a pulmonary capillary wedge pressure of 22 mm Hg or higher had a positive predictive value of 88% for a right atrial pressure of 10 mm Hg or higher.¹⁶ Hence, the clinical presentation may vary depending on the location (pulmonary, systemic, or both) and degree of congestion.

Symptoms of pulmonary congestion include worsening exertional dyspnea and orthopnea; bilateral crackles may be heard on physical examination if pulmonary edema is present.

Systemic congestion can cause significant peripheral edema and weight gain. Jugular venous distention may be noted. Oliguria may be present due to renal dysfunction; patients on maintenance diuretic therapy often note its lack of efficacy.

Signs of acute heart failure

Wang et al,¹⁷ in a meta-analysis of 22 studies, concluded that the features that most strongly suggested acute heart failure were:

• History of paroxysmal nocturnal dyspnea
• A third heart sound
• Evidence of pulmonary venous congestion on chest radiography.

Features that most strongly suggested the patient did not have acute heart failure were:

• Absence of exertional dyspnea
• Absence of rales
• Absence of radiographic evidence of cardiomegaly.

Patients may present without some of these classic clinical features, and the diagnosis of acute heart failure may be challenging. For example, even if left-sided pressures are very high, pulmonary edema may be absent because of pulmonary vascular remodeling in chronic heart failure.¹⁸ Pulmonary artery catheterization reveals elevated cardiac filling pressures and can be used to guide therapy, but clinical evidence argues against its routine use.¹⁹

Urine electrolytes (fractional excretion of sodium < 1% and fractional excretion of urea < 35%) often suggest a prerenal form of acute kidney injury, since the hemodynamic derangements in acute cardiorenal syndrome reduce renal perfusion.

Biomarkers of cell-cycle arrest such as urine insulinlike growth factor-binding protein 7 and tissue inhibitor of metalloproteinase 2 have recently been shown to identify patients with acute heart failure at risk of developing acute cardiorenal syndrome.²⁰

Acute cardiorenal syndrome vs renal injury due to hypovolemia

The major alternative in the differential diagnosis of acute cardiorenal syndrome is renal injury due to hypovolemia. Patients with stable heart failure usually have mild hypervolemia at baseline, but they can become hypovolemic due to overaggressive diuretic therapy, severe diarrhea, or other causes.

Although the fluid status of patients in these 2 conditions is opposite, they can be difficult to distinguish. In both conditions, urine electrolytes suggest a prerenal acute kidney injury. A history of recent fluid losses or diuretic overuse may help identify hypovolemia. If available, analysis of the recent trend in weight can be vital in making the right diagnosis.

Misdiagnosis of acute cardiorenal syndrome as hypovolemia-induced acute kidney injury can be catastrophic. If volume depletion is erroneously judged to be the cause of acute kidney injury, fluid administration can further worsen both cardiac and renal function. This can perpetuate the vicious circle that is already in play. Lack of renal recovery may invite further fluid administration.

Fluid removal with diuresis or ultrafiltration is the cornerstone of treatment. Other treatments such as inotropes are reserved for patients with resistant disease.

Diuretics

The goal of therapy in acute cardiorenal syndrome is to achieve aggressive diuresis, typically using intravenous diuretics. Loop diuretics are the most potent class of diuretics and are the first-line drugs for this purpose. Other classes of diuretics can be used in conjunction with loop diuretics; however, using them by themselves is neither effective nor recommended.

Resistance to diuretics at usual doses is common in patients with acute cardiorenal syndrome. Several mechanisms contribute to diuretic resistance in these patients.²¹

Oral bioavailability of diuretics may be reduced due to intestinal edema.

Diuretic pharmacokinetics are significantly deranged in cardiorenal syndrome. All diuretics except mineralocorticoid antagonists (ie, spironolactone and eplerenone) act on targets on the luminal side of renal tubules, but are highly protein-bound and are hence not filtered at the glomerulus. Loop diuretics, thiazides, and carbonic anhydrase inhibitors are secreted in the proximal convoluted tubule via the organic anion transporter,²² whereas epithelial sodium channel inhibitors (amiloride and triamterene) are secreted via the organic cation transporter 2.²³ In renal dysfunction, various uremic toxins accumulate in the body and compete with diuretics for secretion into the proximal convoluted tubule via these transporters.²⁴

Finally, activation of the sympathetic nervous system and renin-angiotensin-aldosterone system leads to increased tubular sodium and water retention, thereby also blunting the diuretic response.

Diuretic dosage. In patients whose creatinine clearance is less than 15 mL/min, only 10% to 20% as much loop diuretic is secreted into the renal tubule as in normal individuals.²⁵ This effect warrants dose adjustment of diuretics during uremia.

Continuous infusion or bolus? Continuous infusion of loop diuretics is another strategy to optimize drug delivery. Compared with bolus therapy, continuous infusion provides more sustained and uniform drug delivery and prevents postdiuretic sodium retention.

The Diuretic Optimization Strategies Evaluation (DOSE) trial compared the efficacy and safety of continuous vs bolus furosemide therapy in 308 patients admitted with acute decompensated heart failure.²⁶ There was no difference in symptom control or net fluid loss at 72 hours in either group. Other studies have shown more diuresis with continuous infusion than with a similarly dosed bolus regimen.²⁷ However, definitive clinical evidence is lacking at this point to support routine use of continuous loop diuretic therapy.

Combination diuretic therapy. Sequential nephron blockade with combination diuretic therapy is an important therapeutic strategy against diuretic resistance. Notably, urine output-guided diuretic therapy has been shown to be superior to standard diuretic therapy.²⁸ Such therapeutic protocols may employ combination diuretic therapy as a next step when the desired diuretic response is not obtained with high doses of loop diuretic monotherapy.

The desired diuretic response depends on the clinical situation. For example, in patients with severe congestion, we would like the net fluid output to be at least 2 to 3 L more than the fluid intake after the first 24 hours. Sometimes, patients in the intensive care unit are on several essential drug infusions, so that their net intake amounts to 1 to 2 L. In these patients, the desired urine output would be even more than in patients not on these drug infusions.

Loop diuretics block sodium reabsorption at the thick ascending loop of Henle. This disrupts the countercurrent exchange mechanism and reduces renal medullary interstitial osmolarity; these effects prevent water reabsorption. However, the unresorbed sodium can be taken up by the sodium-chloride cotransporter and the epithelial sodium channel in the distal nephron, thereby blunting the diuretic effect. This is the rationale for combining loop diuretics with thiazides or potassium-sparing diuretics.

Similarly, carbonic anhydrase inhibitors (eg, acetazolamide) reduce sodium reabsorption from the proximal convoluted tubule, but most of this sodium is then reabsorbed distally. Hence, the combination of a loop diuretic and acetazolamide can also have a synergistic diuretic effect.

The most popular combination is a loop diuretic plus a thiazide, although no large-scale placebo-controlled trials have been performed.²⁹ Metolazone (a thiazidelike diuretic) is typically used due to its low cost and availability.³⁰ Metolazone has also been shown to block sodium reabsorption at the proximal tubule, which may contribute to its synergistic effect. Chlorothiazide is available in an intravenous formulation and has a faster onset of action than metolazone. However, studies have failed to detect any benefit of one over the other.³¹

The potential benefit of combining a loop diuretic with acetazolamide is a lower tendency to develop metabolic alkalosis, a potential side effect of loop diuretics and thiazides. Although data are limited, a recent study showed that adding acetazolamide to bumetanide led to significantly increased natriuresis.³²

In the Aldosterone Targeted Neurohormonal Combined With Natriuresis Therapy in Heart Failure (ATHENA-HF) trial, adding spironolactone in high doses to usual therapy was not found to cause any significant change in N-terminal pro-B-type natriuretic peptide level or net urine output.³³

Venovenous ultrafiltration (or aquapheresis) employs an extracorporeal circuit, similar to the one used in hemodialysis, which removes iso-osmolar fluid at a fixed rate.³⁴ Newer ultrafiltration systems are more portable, can be used with peripheral venous access, and require minimal nursing supervision.³⁵

Although ultrafiltration seems an attractive alternative to diuresis in acute heart failure, studies have been inconclusive. The Cardiorenal Rescue Study in Acute Decompensated Heart Failure (CARRESS-HF) trial compared ultrafiltration and diuresis in 188 patients with acute heart failure and acute cardiorenal syndrome.³⁶ Diuresis, performed according to an algorithm, was found to be superior to ultrafiltration in terms of a bivariate end point of change in weight and change in serum creatinine level at 96 hours. However, the level of cystatin C is thought to be a more accurate indicator of renal function, and the change in cystatin C level from baseline did not differ between the two treatment groups. Also, the ultrafiltration rate was 200 mL per hour, which, some argue, may have been excessive and may have caused intravascular depletion.

Although the ideal rate of fluid removal is unknown, it should be individualized and adjusted based on the patient’s renal function, volume status, and hemodynamic status. The initial rate should be based on the degree of fluid overload and the anticipated plasma refill rate from the interstitial fluid.³⁷ For example, a malnourished patient may have low serum oncotic pressure and hence have low plasma refill upon ultrafiltration. Disturbance of this delicate balance between the rates of ultrafiltration and plasma refill may lead to intravascular volume contraction.

In summary, although ultrafiltration is a valuable alternative to diuretics in resistant cases, its use as a primary decongestive therapy cannot be endorsed in view of the current data.

Inotropes

Inotropes such as dobutamine and milrinone are typically used in cases of cardiogenic shock to maintain organ perfusion. There is a physiologic rationale to using inotropes in acute cardiorenal syndrome as well, especially when the aforementioned strategies fail to overcome diuretic resistance.⁷

Inotropes increase cardiac output, improve renal blood flow, improve right ventricular output, and thereby relieve systemic congestion. These hemodynamic effects may improve renal perfusion and response to diuretics. However, clinical evidence to support this is lacking.

The Renal Optimization Strategies Evaluation (ROSE) trial enrolled 360 patients with acute heart failure and renal dysfunction. Adding dopamine in a low dose (2 μg/kg/min) to diuretic therapy had no significant effect on 72-hour cumulative urine output or renal function as measured by cystatin C levels.³⁸ However, acute kidney injury was not identified in this trial, and the renal function of many of these patients may have been at its baseline when they were admitted. In other words, this trial did not necessarily include patients with acute kidney injury along with acute heart failure. Hence, it did not necessarily include patients with acute cardiorenal syndrome.

Vasodilators

Vasodilators such as nitroglycerin, sodium nitroprusside, and hydralazine are commonly used in patients with acute heart failure, although the clinical evidence supporting their use is weak.

Physiologically, arterial dilation reduces afterload and can help relieve pulmonary congestion, and venodilation increases capacitance and reduces preload. In theory, venodilators such as nitroglycerin can relieve renal venous congestion in patients with acute cardiorenal syndrome, thereby improving renal perfusion.

However, the use of vasodilators is often limited by their adverse effects, the most important being hypotension. This is especially relevant in light of recent data identifying reduction in blood pressure during treatment of acute heart failure as an independent risk factor for worsening renal function.^39,40 It is important to note that in these studies, changes in cardiac index did not affect the propensity for developing worsening renal function. The precise mechanism of this finding is unclear but it is plausible that systemic vasodilation redistributes the cardiac output to nonrenal tissues, thereby overriding the renal autoregulatory mechanisms that are normally employed in low output states.

Preventive strategies

Various strategies can be used to prevent acute cardiorenal syndrome. An optimal outpatient diuretic regimen to avoid hypervolemia is essential. Patients with advanced congestive heart failure should be followed up closely in dedicated heart failure clinics until their diuretic regimen is optimized. Patients should be advised to check their weight on a regular basis and seek medical advice if they notice an increase in their weight or a reduction in their urine output.

TAKE-HOME POINTS

• A robust clinical definition of cardiorenal syndrome is lacking. Hence, recognition of this condition can be challenging.
• Volume overload is central to its pathogenesis, and accurate assessment of volume status is critical.
• Renal venous congestion is the major mechanism of type 1 cardiorenal syndrome.
• Misdiagnosis can have devastating consequences, as it may lead to an opposite therapeutic approach.
• Fluid removal by various strategies is the mainstay of treatment.
• Temporary inotropic support should be saved for the last resort.

As the heart goes, so go the kidneys—and vice versa. Cardiac and renal function are intricately interdependent, and failure of either organ causes injury to the other in a vicious circle of worsening function.¹

See related editorial

Here, we discuss acute cardiorenal syndrome, ie, acute exacerbation of heart failure leading to acute kidney injury, a common cause of hospitalization and admission to the intensive care unit. We examine its clinical definition, pathophysiology, hemodynamic derangements, clues that help in diagnosing it, and its treatment.

A GROUP OF LINKED DISORDERS

Two types of acute cardiac dysfunction

Although these definitions offer a good general description, further clarification of the nature of organ dysfunction is needed. Acute renal dysfunction can be unambiguously defined using the AKIN (Acute Kidney Injury Network) and RIFLE (risk, injury, failure, loss of kidney function, and end-stage kidney disease) classifications.³ Acute cardiac dysfunction, on the other hand, is an ambiguous term that encompasses 2 clinically and pathophysiologically distinct conditions: cardiogenic shock and acute heart failure.

Cardiogenic shock is characterized by a catastrophic compromise of cardiac pump function leading to global hypoperfusion severe enough to cause systemic organ damage.⁴ The cardiac index at which organs start to fail varies in different cases, but a value of less than 1.8 L/min/m² is typically used to define cardiogenic shock.⁴

Acute heart failure, on the other hand, is defined as gradually or rapidly worsening signs and symptoms of congestive heart failure due to worsening pulmonary or systemic congestion.⁵ Hypervolemia is the hallmark of acute heart failure, whereas patients with cardiogenic shock may be hypervolemic, normovolemic, or hypovolemic. Although cardiac output may be mildly reduced in some cases of acute heart failure, systemic perfusion is enough to maintain organ function.

These two conditions cause renal injury by distinct mechanisms and have entirely different therapeutic implications. As we discuss later, reduced renal perfusion due to renal venous congestion is now believed to be the major hemodynamic mechanism of renal injury in acute heart failure. On the other hand, in cardiogenic shock, renal perfusion is reduced due to a critical decline of cardiac pump function.

The ideal definition of acute cardiorenal syndrome should describe a distinct pathophysiology of the syndrome and offer distinct therapeutic options that counteract it. Hence, we propose that renal injury from cardiogenic shock should not be included in its definition, an approach that has been adopted in some of the recent reviews as well.⁶ Our discussion of acute cardiorenal syndrome is restricted to renal injury caused by acute heart failure.

PATHOPHYSIOLOGY OF ACUTE CARDIORENAL SYNDROME

Multiple mechanisms have been implicated in the pathophysiology of cardiorenal syndrome.^7,8

Sympathetic hyperactivity is a compensatory mechanism in heart failure and may be aggravated if cardiac output is further reduced. Its effects include constriction of afferent and efferent arterioles, causing reduced renal perfusion and increased tubular sodium and water reabsorption.⁷

The renin-angiotensin-aldosterone system is activated in patients with stable congestive heart failure and may be further stimulated in a state of reduced renal perfusion, which is a hallmark of acute cardiorenal syndrome. Its activation can cause further salt and water retention.

However, direct hemodynamic mechanisms likely play the most important role and have obvious diagnostic and therapeutic implications.

Elevated venous pressure, not reduced cardiac output, drives kidney injury

The classic view was that renal dysfunction in acute heart failure is caused by reduced renal blood flow due to failing cardiac pump function. Cardiac output may be reduced in acute heart failure for various reasons, such as atrial fibrillation, myocardial infarction, or other processes, but reduced cardiac output has a minimal role, if any, in the pathogenesis of renal injury in acute heart failure.

As evidence of this, acute heart failure is not always associated with reduced cardiac output.⁵ Even if the cardiac index (cardiac output divided by body surface area) is mildly reduced, renal blood flow is largely unaffected, thanks to effective renal autoregulatory mechanisms. Not until the mean arterial pressure falls below 70 mm Hg do these mechanisms fail and renal blood flow starts to drop.⁹ Hence, unless cardiac performance is compromised enough to cause cardiogenic shock, renal blood flow usually does not change significantly with mild reduction in cardiac output.

Hanberg et al¹⁰ performed a post hoc analysis of the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheter Effectiveness (ESCAPE) trial, in which 525 patients with advanced heart failure underwent pulmonary artery catheterization to measure their cardiac index. The authors found no association between the cardiac index and renal function in these patients.

In view of the current clinical evidence, the focus has shifted to renal venous congestion. According to Poiseuille’s law, blood flow through the kidneys depends on the pressure gradient—high pressure on the arterial side, low pressure on the venous side.⁸ Increased renal venous pressure causes reduced renal perfusion pressure, thereby affecting renal perfusion. This is now recognized as an important hemodynamic mechanism of acute cardiorenal syndrome.

Renal congestion can also affect renal function through indirect mechanisms. For example, it can cause renal interstitial edema that may then increase the intratubular pressure, thereby reducing the transglomerular pressure gradient.¹¹

Firth et al,¹⁴ in experiments in animals, found that increasing the renal venous pressure above 18.75 mm Hg significantly reduced the glomerular filtration rate, which completely resolved when renal venous pressure was restored to basal levels.

Mullens et al,¹⁵ in a study of 145 patients admitted with acute heart failure, reported that 58 (40%) developed acute kidney injury. Pulmonary artery catheterization revealed that elevated central venous pressure, rather than reduced cardiac index, was the primary hemodynamic factor driving renal dysfunction.

DIAGNOSIS AND CLINICAL ASSESSMENT

Patients with acute cardiorenal syndrome present with clinical features of pulmonary or systemic congestion (or both) and acute kidney injury.

Elevated left-sided pressures are usually but not always associated with elevated right-sided pressures. In a study of 1,000 patients with advanced heart failure, a pulmonary capillary wedge pressure of 22 mm Hg or higher had a positive predictive value of 88% for a right atrial pressure of 10 mm Hg or higher.¹⁶ Hence, the clinical presentation may vary depending on the location (pulmonary, systemic, or both) and degree of congestion.

Symptoms of pulmonary congestion include worsening exertional dyspnea and orthopnea; bilateral crackles may be heard on physical examination if pulmonary edema is present.

Systemic congestion can cause significant peripheral edema and weight gain. Jugular venous distention may be noted. Oliguria may be present due to renal dysfunction; patients on maintenance diuretic therapy often note its lack of efficacy.

Signs of acute heart failure

Wang et al,¹⁷ in a meta-analysis of 22 studies, concluded that the features that most strongly suggested acute heart failure were:

• History of paroxysmal nocturnal dyspnea
• A third heart sound
• Evidence of pulmonary venous congestion on chest radiography.

Features that most strongly suggested the patient did not have acute heart failure were:

• Absence of exertional dyspnea
• Absence of rales
• Absence of radiographic evidence of cardiomegaly.

Patients may present without some of these classic clinical features, and the diagnosis of acute heart failure may be challenging. For example, even if left-sided pressures are very high, pulmonary edema may be absent because of pulmonary vascular remodeling in chronic heart failure.¹⁸ Pulmonary artery catheterization reveals elevated cardiac filling pressures and can be used to guide therapy, but clinical evidence argues against its routine use.¹⁹

Urine electrolytes (fractional excretion of sodium < 1% and fractional excretion of urea < 35%) often suggest a prerenal form of acute kidney injury, since the hemodynamic derangements in acute cardiorenal syndrome reduce renal perfusion.

Biomarkers of cell-cycle arrest such as urine insulinlike growth factor-binding protein 7 and tissue inhibitor of metalloproteinase 2 have recently been shown to identify patients with acute heart failure at risk of developing acute cardiorenal syndrome.²⁰

Acute cardiorenal syndrome vs renal injury due to hypovolemia

The major alternative in the differential diagnosis of acute cardiorenal syndrome is renal injury due to hypovolemia. Patients with stable heart failure usually have mild hypervolemia at baseline, but they can become hypovolemic due to overaggressive diuretic therapy, severe diarrhea, or other causes.

Although the fluid status of patients in these 2 conditions is opposite, they can be difficult to distinguish. In both conditions, urine electrolytes suggest a prerenal acute kidney injury. A history of recent fluid losses or diuretic overuse may help identify hypovolemia. If available, analysis of the recent trend in weight can be vital in making the right diagnosis.

Misdiagnosis of acute cardiorenal syndrome as hypovolemia-induced acute kidney injury can be catastrophic. If volume depletion is erroneously judged to be the cause of acute kidney injury, fluid administration can further worsen both cardiac and renal function. This can perpetuate the vicious circle that is already in play. Lack of renal recovery may invite further fluid administration.

Fluid removal with diuresis or ultrafiltration is the cornerstone of treatment. Other treatments such as inotropes are reserved for patients with resistant disease.

Diuretics

The goal of therapy in acute cardiorenal syndrome is to achieve aggressive diuresis, typically using intravenous diuretics. Loop diuretics are the most potent class of diuretics and are the first-line drugs for this purpose. Other classes of diuretics can be used in conjunction with loop diuretics; however, using them by themselves is neither effective nor recommended.

Resistance to diuretics at usual doses is common in patients with acute cardiorenal syndrome. Several mechanisms contribute to diuretic resistance in these patients.²¹

Oral bioavailability of diuretics may be reduced due to intestinal edema.

Diuretic pharmacokinetics are significantly deranged in cardiorenal syndrome. All diuretics except mineralocorticoid antagonists (ie, spironolactone and eplerenone) act on targets on the luminal side of renal tubules, but are highly protein-bound and are hence not filtered at the glomerulus. Loop diuretics, thiazides, and carbonic anhydrase inhibitors are secreted in the proximal convoluted tubule via the organic anion transporter,²² whereas epithelial sodium channel inhibitors (amiloride and triamterene) are secreted via the organic cation transporter 2.²³ In renal dysfunction, various uremic toxins accumulate in the body and compete with diuretics for secretion into the proximal convoluted tubule via these transporters.²⁴

Finally, activation of the sympathetic nervous system and renin-angiotensin-aldosterone system leads to increased tubular sodium and water retention, thereby also blunting the diuretic response.

Diuretic dosage. In patients whose creatinine clearance is less than 15 mL/min, only 10% to 20% as much loop diuretic is secreted into the renal tubule as in normal individuals.²⁵ This effect warrants dose adjustment of diuretics during uremia.

Continuous infusion or bolus? Continuous infusion of loop diuretics is another strategy to optimize drug delivery. Compared with bolus therapy, continuous infusion provides more sustained and uniform drug delivery and prevents postdiuretic sodium retention.

The Diuretic Optimization Strategies Evaluation (DOSE) trial compared the efficacy and safety of continuous vs bolus furosemide therapy in 308 patients admitted with acute decompensated heart failure.²⁶ There was no difference in symptom control or net fluid loss at 72 hours in either group. Other studies have shown more diuresis with continuous infusion than with a similarly dosed bolus regimen.²⁷ However, definitive clinical evidence is lacking at this point to support routine use of continuous loop diuretic therapy.

Combination diuretic therapy. Sequential nephron blockade with combination diuretic therapy is an important therapeutic strategy against diuretic resistance. Notably, urine output-guided diuretic therapy has been shown to be superior to standard diuretic therapy.²⁸ Such therapeutic protocols may employ combination diuretic therapy as a next step when the desired diuretic response is not obtained with high doses of loop diuretic monotherapy.

The desired diuretic response depends on the clinical situation. For example, in patients with severe congestion, we would like the net fluid output to be at least 2 to 3 L more than the fluid intake after the first 24 hours. Sometimes, patients in the intensive care unit are on several essential drug infusions, so that their net intake amounts to 1 to 2 L. In these patients, the desired urine output would be even more than in patients not on these drug infusions.

Loop diuretics block sodium reabsorption at the thick ascending loop of Henle. This disrupts the countercurrent exchange mechanism and reduces renal medullary interstitial osmolarity; these effects prevent water reabsorption. However, the unresorbed sodium can be taken up by the sodium-chloride cotransporter and the epithelial sodium channel in the distal nephron, thereby blunting the diuretic effect. This is the rationale for combining loop diuretics with thiazides or potassium-sparing diuretics.

Similarly, carbonic anhydrase inhibitors (eg, acetazolamide) reduce sodium reabsorption from the proximal convoluted tubule, but most of this sodium is then reabsorbed distally. Hence, the combination of a loop diuretic and acetazolamide can also have a synergistic diuretic effect.

The most popular combination is a loop diuretic plus a thiazide, although no large-scale placebo-controlled trials have been performed.²⁹ Metolazone (a thiazidelike diuretic) is typically used due to its low cost and availability.³⁰ Metolazone has also been shown to block sodium reabsorption at the proximal tubule, which may contribute to its synergistic effect. Chlorothiazide is available in an intravenous formulation and has a faster onset of action than metolazone. However, studies have failed to detect any benefit of one over the other.³¹

The potential benefit of combining a loop diuretic with acetazolamide is a lower tendency to develop metabolic alkalosis, a potential side effect of loop diuretics and thiazides. Although data are limited, a recent study showed that adding acetazolamide to bumetanide led to significantly increased natriuresis.³²

In the Aldosterone Targeted Neurohormonal Combined With Natriuresis Therapy in Heart Failure (ATHENA-HF) trial, adding spironolactone in high doses to usual therapy was not found to cause any significant change in N-terminal pro-B-type natriuretic peptide level or net urine output.³³

Venovenous ultrafiltration (or aquapheresis) employs an extracorporeal circuit, similar to the one used in hemodialysis, which removes iso-osmolar fluid at a fixed rate.³⁴ Newer ultrafiltration systems are more portable, can be used with peripheral venous access, and require minimal nursing supervision.³⁵

Although ultrafiltration seems an attractive alternative to diuresis in acute heart failure, studies have been inconclusive. The Cardiorenal Rescue Study in Acute Decompensated Heart Failure (CARRESS-HF) trial compared ultrafiltration and diuresis in 188 patients with acute heart failure and acute cardiorenal syndrome.³⁶ Diuresis, performed according to an algorithm, was found to be superior to ultrafiltration in terms of a bivariate end point of change in weight and change in serum creatinine level at 96 hours. However, the level of cystatin C is thought to be a more accurate indicator of renal function, and the change in cystatin C level from baseline did not differ between the two treatment groups. Also, the ultrafiltration rate was 200 mL per hour, which, some argue, may have been excessive and may have caused intravascular depletion.

Although the ideal rate of fluid removal is unknown, it should be individualized and adjusted based on the patient’s renal function, volume status, and hemodynamic status. The initial rate should be based on the degree of fluid overload and the anticipated plasma refill rate from the interstitial fluid.³⁷ For example, a malnourished patient may have low serum oncotic pressure and hence have low plasma refill upon ultrafiltration. Disturbance of this delicate balance between the rates of ultrafiltration and plasma refill may lead to intravascular volume contraction.

In summary, although ultrafiltration is a valuable alternative to diuretics in resistant cases, its use as a primary decongestive therapy cannot be endorsed in view of the current data.

Inotropes

Inotropes such as dobutamine and milrinone are typically used in cases of cardiogenic shock to maintain organ perfusion. There is a physiologic rationale to using inotropes in acute cardiorenal syndrome as well, especially when the aforementioned strategies fail to overcome diuretic resistance.⁷

Inotropes increase cardiac output, improve renal blood flow, improve right ventricular output, and thereby relieve systemic congestion. These hemodynamic effects may improve renal perfusion and response to diuretics. However, clinical evidence to support this is lacking.

The Renal Optimization Strategies Evaluation (ROSE) trial enrolled 360 patients with acute heart failure and renal dysfunction. Adding dopamine in a low dose (2 μg/kg/min) to diuretic therapy had no significant effect on 72-hour cumulative urine output or renal function as measured by cystatin C levels.³⁸ However, acute kidney injury was not identified in this trial, and the renal function of many of these patients may have been at its baseline when they were admitted. In other words, this trial did not necessarily include patients with acute kidney injury along with acute heart failure. Hence, it did not necessarily include patients with acute cardiorenal syndrome.

Vasodilators

Vasodilators such as nitroglycerin, sodium nitroprusside, and hydralazine are commonly used in patients with acute heart failure, although the clinical evidence supporting their use is weak.

Physiologically, arterial dilation reduces afterload and can help relieve pulmonary congestion, and venodilation increases capacitance and reduces preload. In theory, venodilators such as nitroglycerin can relieve renal venous congestion in patients with acute cardiorenal syndrome, thereby improving renal perfusion.

However, the use of vasodilators is often limited by their adverse effects, the most important being hypotension. This is especially relevant in light of recent data identifying reduction in blood pressure during treatment of acute heart failure as an independent risk factor for worsening renal function.^39,40 It is important to note that in these studies, changes in cardiac index did not affect the propensity for developing worsening renal function. The precise mechanism of this finding is unclear but it is plausible that systemic vasodilation redistributes the cardiac output to nonrenal tissues, thereby overriding the renal autoregulatory mechanisms that are normally employed in low output states.

Preventive strategies

Various strategies can be used to prevent acute cardiorenal syndrome. An optimal outpatient diuretic regimen to avoid hypervolemia is essential. Patients with advanced congestive heart failure should be followed up closely in dedicated heart failure clinics until their diuretic regimen is optimized. Patients should be advised to check their weight on a regular basis and seek medical advice if they notice an increase in their weight or a reduction in their urine output.

TAKE-HOME POINTS

• A robust clinical definition of cardiorenal syndrome is lacking. Hence, recognition of this condition can be challenging.
• Volume overload is central to its pathogenesis, and accurate assessment of volume status is critical.
• Renal venous congestion is the major mechanism of type 1 cardiorenal syndrome.
• Misdiagnosis can have devastating consequences, as it may lead to an opposite therapeutic approach.
• Fluid removal by various strategies is the mainstay of treatment.
• Temporary inotropic support should be saved for the last resort.

In heart failure, the heart and the kidneys share a rocky relationship. Cardiac dysfunction can heighten renal dysfunction and vice versa—appropriately dubbed “cardiorenal syndrome.”

See related article

Although classically defined by a reduction in the glomerular filtration rate (GFR),¹ cardiorenal syndrome also encompasses complex neurohormonal, pharmacologic, and metabolic interactions affecting or affected by both glomerular and tubular function. Unfortunately, all of these maladaptive processes occur in heart failure and perpetuate a vicious circle of continued dual-organ dysfunction.

The central insult here is hemodynamic disarray from acute or chronic cardiac dysfunction, which can directly influence glomerular function. However, to understand the hemodynamic ramifications for glomerular function, we focus on the determinants of glomerular filtration.

DETERMINANTS OF GFR

The GFR is the rate of fluid flow between the glomerular capillaries and the Bowman capsule and is classically represented by the following equations²:

GFR = K_f × (P_G – P_B – π_G + π_B)

K_f = N × L_p × S

K_f is the filtration constant, N the number of functional nephrons, L_p the hydraulic conductivity of the glomerular capillary, S the filtration area, P_G the hydrostatic pressure in the glomerular capillaries, P_B the hydrostatic pressure in the Bowman capsule, and π_G and π_B the colloid osmotic pressures within the glomerular capillaries and Bowman space, respectively.

Based on this relationship, the GFR is reduced when P_G is reduced in the setting of hypovolemia, hypotension, or renin-angiotensin system antagonist use or when P_B is increased in the setting of elevated central venous pressure or elevated abdominal pressure—all common in heart failure. With this understanding, one would assume that strategies to increase P_G (improve perfusion) and reduce P_B (reduce congestion) might ameliorate ongoing renal dysfunction and improve the GFR in heart failure.

In this issue, Thind et al³ highlight the impact of hemodynamic derangements in heart failure with acute cardiorenal syndrome and provide an overview of its treatment. They review the complex relationship between progressive cardiac failure translating into accelerated neurohormonal responses (increases in sympathetic nervous system and renin-angiotensin-aldosterone system activation) and the impact of increased central venous pressure on progressive renal dysfunction. They also provide an overview of efforts to mitigate cardiorenal syndrome, after careful appraisal of volume status, through diuretic-mediated decongestion with aggressive use of loop diuretics (either in isolation or in the form of sequential nephron blockade with a thiazide or acetazolamide), and they highlight the lingering uncertainty regarding inotrope use.

Returning to the GFR equation, it is clear that an imbalance in P_G and P_B can worsen glomerular function. Because cardiac dysfunction can lead to both venous congestion and decreased cardiac output, this leads to the question, “Of these, which is the more important driver of this imbalance and its effects on renal function?”

A compelling argument can be made for each side. On one hand, experiments over a half-century old in human models of venous congestion highlighted the profound impact of elevated venous pressure, which decreases electrolyte excretion (sodium included) and diminishes urine flow.^4,5 This has been replicated in more-contemporary decompensated heart failure cohorts in which worsening renal function was more closely associated with elevated central venous pressure rather than cardiac output.^6,7 On the other hand, early landmark experiments and more recent cohorts with heart failure have also shown that reductions in effective arterial blood volume, renal blood flow, and cardiac output are also associated with reductions in GFR.^5,8,9

How then shall we reconcile whether cardiorenal syndrome is a “backward failure” (from central venous pressure) or a “forward failure” (from decreased perfusion) phenomenon?

The answer is complicated and is likely “both,” with the major component being increased central venous pressure. To understand this construct, we must first exclude frank cardiogenic shock—when the hydraulic function of the heart fails to provide enough flow, leading to a catastrophic drop in mean arterial pressure that supersedes the kidney’s ability to autoregulate renal blood flow.^10,11

In patients with chronic heart failure and congestion who are not in shock, historical observations suggest that both intra-abdominal pressure (which increases renal venous pressure) and central venous pressure lead to reduced renal blood flow and increased renal vasomotor resistance (increase in afferent, intrarenal, and efferent vascular tone).^12–14 More recent observations from epidemiologic studies have largely replicated these findings. Central venous pressure remains essential to impacting renal function in heart failure,^6,15 and the impact of cardiac output on renal function remains uncertain.¹⁶

The relationship of intracardiac hemodynamics may also play a role in modifying renal function. Several reports recently described the relationship between both right- and left-sided filling pressures as being associated with worse renal function in heart failure.^17–19 Patients with a disproportionately higher right atrial pressure to pulmonary capillary wedge pressure have higher serum creatinine during and after decongestive therapies. Therefore, the concept of “right-sided heart failure” expands beyond the simple representation of “backward congestion” at the level of venous return. In fact, a higher ratio of right atrial pressure to pulmonary capillary wedge pressure may point to an inability of the venous and pulmonary circulations to provide adequate left ventricular preload. Therefore, a relatively underfilled left ventricle in the face of biventricular dysfunction may result in worsening renal function.

The treatment of cardiorenal syndrome is challenging. It is often accompanied by heightened azotemia, diuretic resistance, electrolyte abnormalities, and a spectrum of hemodynamic disarray. As Thind et al point out, there is, unfortunately, no firmly established treatment. While “sequential nephron blockade” (pharmacologically blocking multiple sites on the nephron simultaneously) is theoretically promising, there are no rigorously studied therapeutic strategies with proven efficacy.

On the other hand, mechanical removal of isotonic fluid with ultrafiltration showed early promise in decompensated heart failure, but enthusiasm diminished with results from the Cardiorenal Rescue Study in Acute Decompensated Heart Failure (CARRESS-HF) trial.²⁰ Ultrafiltration was roughly equivalent to aggressive pharmacologic therapy for fluid loss, was associated with higher serum creatinine levels, and was more challenging to administer.

Equally uncertain is the benefit of inotropic or vasoactive therapy, which directly alters cardiac hemodynamics. Low-dose dopamine or low-dose nesiritide is of no benefit toward enhancement of decongestion or renal protection when added to standard diuretic therapy.²¹ Furthermore, routine use of ino­tropes is fraught with more arrhythmias and hypotension and is associated with dismal long-term outcomes.^22,23

Alternative therapies that act directly on renal physiology—eg, rolofylline, a selective adenosine A1 receptor antagonist that may enhance renal blood flow, augment natriuresis, and break diuretic resistance—have been similarly disappointing.²⁴

With so much uncertainty, more investigation into novel treatments for cardiorenal syndrome is clearly warranted.

However, because venous congestion is the hemodynamic hallmark of acute cardiorenal syndrome (increasing P_B), reducing central venous pressure remains the cornerstone treatment for cardiorenal syndrome. Additionally, efforts to preserve renal perfusion and avoid hypotension are prudent to maintain glomerular capillary hydrostatic pressure (P_G).

In light of these considerations, there is no “one size fits all” for the treatment of cardiorenal syndrome. Treatment should be based on thoughtful individualized strategies tailored to the underlying cardiorenal pathophysiology, and with the understanding that the kidney is at the heart of the matter.

In heart failure, the heart and the kidneys share a rocky relationship. Cardiac dysfunction can heighten renal dysfunction and vice versa—appropriately dubbed “cardiorenal syndrome.”

See related article

Although classically defined by a reduction in the glomerular filtration rate (GFR),¹ cardiorenal syndrome also encompasses complex neurohormonal, pharmacologic, and metabolic interactions affecting or affected by both glomerular and tubular function. Unfortunately, all of these maladaptive processes occur in heart failure and perpetuate a vicious circle of continued dual-organ dysfunction.

The central insult here is hemodynamic disarray from acute or chronic cardiac dysfunction, which can directly influence glomerular function. However, to understand the hemodynamic ramifications for glomerular function, we focus on the determinants of glomerular filtration.

DETERMINANTS OF GFR

The GFR is the rate of fluid flow between the glomerular capillaries and the Bowman capsule and is classically represented by the following equations²:

GFR = K_f × (P_G – P_B – π_G + π_B)

K_f = N × L_p × S

K_f is the filtration constant, N the number of functional nephrons, L_p the hydraulic conductivity of the glomerular capillary, S the filtration area, P_G the hydrostatic pressure in the glomerular capillaries, P_B the hydrostatic pressure in the Bowman capsule, and π_G and π_B the colloid osmotic pressures within the glomerular capillaries and Bowman space, respectively.

Based on this relationship, the GFR is reduced when P_G is reduced in the setting of hypovolemia, hypotension, or renin-angiotensin system antagonist use or when P_B is increased in the setting of elevated central venous pressure or elevated abdominal pressure—all common in heart failure. With this understanding, one would assume that strategies to increase P_G (improve perfusion) and reduce P_B (reduce congestion) might ameliorate ongoing renal dysfunction and improve the GFR in heart failure.

In this issue, Thind et al³ highlight the impact of hemodynamic derangements in heart failure with acute cardiorenal syndrome and provide an overview of its treatment. They review the complex relationship between progressive cardiac failure translating into accelerated neurohormonal responses (increases in sympathetic nervous system and renin-angiotensin-aldosterone system activation) and the impact of increased central venous pressure on progressive renal dysfunction. They also provide an overview of efforts to mitigate cardiorenal syndrome, after careful appraisal of volume status, through diuretic-mediated decongestion with aggressive use of loop diuretics (either in isolation or in the form of sequential nephron blockade with a thiazide or acetazolamide), and they highlight the lingering uncertainty regarding inotrope use.

Returning to the GFR equation, it is clear that an imbalance in P_G and P_B can worsen glomerular function. Because cardiac dysfunction can lead to both venous congestion and decreased cardiac output, this leads to the question, “Of these, which is the more important driver of this imbalance and its effects on renal function?”

A compelling argument can be made for each side. On one hand, experiments over a half-century old in human models of venous congestion highlighted the profound impact of elevated venous pressure, which decreases electrolyte excretion (sodium included) and diminishes urine flow.^4,5 This has been replicated in more-contemporary decompensated heart failure cohorts in which worsening renal function was more closely associated with elevated central venous pressure rather than cardiac output.^6,7 On the other hand, early landmark experiments and more recent cohorts with heart failure have also shown that reductions in effective arterial blood volume, renal blood flow, and cardiac output are also associated with reductions in GFR.^5,8,9

How then shall we reconcile whether cardiorenal syndrome is a “backward failure” (from central venous pressure) or a “forward failure” (from decreased perfusion) phenomenon?

The answer is complicated and is likely “both,” with the major component being increased central venous pressure. To understand this construct, we must first exclude frank cardiogenic shock—when the hydraulic function of the heart fails to provide enough flow, leading to a catastrophic drop in mean arterial pressure that supersedes the kidney’s ability to autoregulate renal blood flow.^10,11

In patients with chronic heart failure and congestion who are not in shock, historical observations suggest that both intra-abdominal pressure (which increases renal venous pressure) and central venous pressure lead to reduced renal blood flow and increased renal vasomotor resistance (increase in afferent, intrarenal, and efferent vascular tone).^12–14 More recent observations from epidemiologic studies have largely replicated these findings. Central venous pressure remains essential to impacting renal function in heart failure,^6,15 and the impact of cardiac output on renal function remains uncertain.¹⁶

The relationship of intracardiac hemodynamics may also play a role in modifying renal function. Several reports recently described the relationship between both right- and left-sided filling pressures as being associated with worse renal function in heart failure.^17–19 Patients with a disproportionately higher right atrial pressure to pulmonary capillary wedge pressure have higher serum creatinine during and after decongestive therapies. Therefore, the concept of “right-sided heart failure” expands beyond the simple representation of “backward congestion” at the level of venous return. In fact, a higher ratio of right atrial pressure to pulmonary capillary wedge pressure may point to an inability of the venous and pulmonary circulations to provide adequate left ventricular preload. Therefore, a relatively underfilled left ventricle in the face of biventricular dysfunction may result in worsening renal function.

The treatment of cardiorenal syndrome is challenging. It is often accompanied by heightened azotemia, diuretic resistance, electrolyte abnormalities, and a spectrum of hemodynamic disarray. As Thind et al point out, there is, unfortunately, no firmly established treatment. While “sequential nephron blockade” (pharmacologically blocking multiple sites on the nephron simultaneously) is theoretically promising, there are no rigorously studied therapeutic strategies with proven efficacy.

On the other hand, mechanical removal of isotonic fluid with ultrafiltration showed early promise in decompensated heart failure, but enthusiasm diminished with results from the Cardiorenal Rescue Study in Acute Decompensated Heart Failure (CARRESS-HF) trial.²⁰ Ultrafiltration was roughly equivalent to aggressive pharmacologic therapy for fluid loss, was associated with higher serum creatinine levels, and was more challenging to administer.

Equally uncertain is the benefit of inotropic or vasoactive therapy, which directly alters cardiac hemodynamics. Low-dose dopamine or low-dose nesiritide is of no benefit toward enhancement of decongestion or renal protection when added to standard diuretic therapy.²¹ Furthermore, routine use of ino­tropes is fraught with more arrhythmias and hypotension and is associated with dismal long-term outcomes.^22,23

Alternative therapies that act directly on renal physiology—eg, rolofylline, a selective adenosine A1 receptor antagonist that may enhance renal blood flow, augment natriuresis, and break diuretic resistance—have been similarly disappointing.²⁴

With so much uncertainty, more investigation into novel treatments for cardiorenal syndrome is clearly warranted.

However, because venous congestion is the hemodynamic hallmark of acute cardiorenal syndrome (increasing P_B), reducing central venous pressure remains the cornerstone treatment for cardiorenal syndrome. Additionally, efforts to preserve renal perfusion and avoid hypotension are prudent to maintain glomerular capillary hydrostatic pressure (P_G).

In light of these considerations, there is no “one size fits all” for the treatment of cardiorenal syndrome. Treatment should be based on thoughtful individualized strategies tailored to the underlying cardiorenal pathophysiology, and with the understanding that the kidney is at the heart of the matter.

In heart failure, the heart and the kidneys share a rocky relationship. Cardiac dysfunction can heighten renal dysfunction and vice versa—appropriately dubbed “cardiorenal syndrome.”

See related article

Although classically defined by a reduction in the glomerular filtration rate (GFR),¹ cardiorenal syndrome also encompasses complex neurohormonal, pharmacologic, and metabolic interactions affecting or affected by both glomerular and tubular function. Unfortunately, all of these maladaptive processes occur in heart failure and perpetuate a vicious circle of continued dual-organ dysfunction.

The central insult here is hemodynamic disarray from acute or chronic cardiac dysfunction, which can directly influence glomerular function. However, to understand the hemodynamic ramifications for glomerular function, we focus on the determinants of glomerular filtration.

DETERMINANTS OF GFR

The GFR is the rate of fluid flow between the glomerular capillaries and the Bowman capsule and is classically represented by the following equations²:

GFR = K_f × (P_G – P_B – π_G + π_B)

K_f = N × L_p × S

K_f is the filtration constant, N the number of functional nephrons, L_p the hydraulic conductivity of the glomerular capillary, S the filtration area, P_G the hydrostatic pressure in the glomerular capillaries, P_B the hydrostatic pressure in the Bowman capsule, and π_G and π_B the colloid osmotic pressures within the glomerular capillaries and Bowman space, respectively.

Based on this relationship, the GFR is reduced when P_G is reduced in the setting of hypovolemia, hypotension, or renin-angiotensin system antagonist use or when P_B is increased in the setting of elevated central venous pressure or elevated abdominal pressure—all common in heart failure. With this understanding, one would assume that strategies to increase P_G (improve perfusion) and reduce P_B (reduce congestion) might ameliorate ongoing renal dysfunction and improve the GFR in heart failure.

In this issue, Thind et al³ highlight the impact of hemodynamic derangements in heart failure with acute cardiorenal syndrome and provide an overview of its treatment. They review the complex relationship between progressive cardiac failure translating into accelerated neurohormonal responses (increases in sympathetic nervous system and renin-angiotensin-aldosterone system activation) and the impact of increased central venous pressure on progressive renal dysfunction. They also provide an overview of efforts to mitigate cardiorenal syndrome, after careful appraisal of volume status, through diuretic-mediated decongestion with aggressive use of loop diuretics (either in isolation or in the form of sequential nephron blockade with a thiazide or acetazolamide), and they highlight the lingering uncertainty regarding inotrope use.

Returning to the GFR equation, it is clear that an imbalance in P_G and P_B can worsen glomerular function. Because cardiac dysfunction can lead to both venous congestion and decreased cardiac output, this leads to the question, “Of these, which is the more important driver of this imbalance and its effects on renal function?”

A compelling argument can be made for each side. On one hand, experiments over a half-century old in human models of venous congestion highlighted the profound impact of elevated venous pressure, which decreases electrolyte excretion (sodium included) and diminishes urine flow.^4,5 This has been replicated in more-contemporary decompensated heart failure cohorts in which worsening renal function was more closely associated with elevated central venous pressure rather than cardiac output.^6,7 On the other hand, early landmark experiments and more recent cohorts with heart failure have also shown that reductions in effective arterial blood volume, renal blood flow, and cardiac output are also associated with reductions in GFR.^5,8,9

How then shall we reconcile whether cardiorenal syndrome is a “backward failure” (from central venous pressure) or a “forward failure” (from decreased perfusion) phenomenon?

The answer is complicated and is likely “both,” with the major component being increased central venous pressure. To understand this construct, we must first exclude frank cardiogenic shock—when the hydraulic function of the heart fails to provide enough flow, leading to a catastrophic drop in mean arterial pressure that supersedes the kidney’s ability to autoregulate renal blood flow.^10,11

In patients with chronic heart failure and congestion who are not in shock, historical observations suggest that both intra-abdominal pressure (which increases renal venous pressure) and central venous pressure lead to reduced renal blood flow and increased renal vasomotor resistance (increase in afferent, intrarenal, and efferent vascular tone).^12–14 More recent observations from epidemiologic studies have largely replicated these findings. Central venous pressure remains essential to impacting renal function in heart failure,^6,15 and the impact of cardiac output on renal function remains uncertain.¹⁶

The relationship of intracardiac hemodynamics may also play a role in modifying renal function. Several reports recently described the relationship between both right- and left-sided filling pressures as being associated with worse renal function in heart failure.^17–19 Patients with a disproportionately higher right atrial pressure to pulmonary capillary wedge pressure have higher serum creatinine during and after decongestive therapies. Therefore, the concept of “right-sided heart failure” expands beyond the simple representation of “backward congestion” at the level of venous return. In fact, a higher ratio of right atrial pressure to pulmonary capillary wedge pressure may point to an inability of the venous and pulmonary circulations to provide adequate left ventricular preload. Therefore, a relatively underfilled left ventricle in the face of biventricular dysfunction may result in worsening renal function.

The treatment of cardiorenal syndrome is challenging. It is often accompanied by heightened azotemia, diuretic resistance, electrolyte abnormalities, and a spectrum of hemodynamic disarray. As Thind et al point out, there is, unfortunately, no firmly established treatment. While “sequential nephron blockade” (pharmacologically blocking multiple sites on the nephron simultaneously) is theoretically promising, there are no rigorously studied therapeutic strategies with proven efficacy.

On the other hand, mechanical removal of isotonic fluid with ultrafiltration showed early promise in decompensated heart failure, but enthusiasm diminished with results from the Cardiorenal Rescue Study in Acute Decompensated Heart Failure (CARRESS-HF) trial.²⁰ Ultrafiltration was roughly equivalent to aggressive pharmacologic therapy for fluid loss, was associated with higher serum creatinine levels, and was more challenging to administer.

Equally uncertain is the benefit of inotropic or vasoactive therapy, which directly alters cardiac hemodynamics. Low-dose dopamine or low-dose nesiritide is of no benefit toward enhancement of decongestion or renal protection when added to standard diuretic therapy.²¹ Furthermore, routine use of ino­tropes is fraught with more arrhythmias and hypotension and is associated with dismal long-term outcomes.^22,23

Alternative therapies that act directly on renal physiology—eg, rolofylline, a selective adenosine A1 receptor antagonist that may enhance renal blood flow, augment natriuresis, and break diuretic resistance—have been similarly disappointing.²⁴

With so much uncertainty, more investigation into novel treatments for cardiorenal syndrome is clearly warranted.

However, because venous congestion is the hemodynamic hallmark of acute cardiorenal syndrome (increasing P_B), reducing central venous pressure remains the cornerstone treatment for cardiorenal syndrome. Additionally, efforts to preserve renal perfusion and avoid hypotension are prudent to maintain glomerular capillary hydrostatic pressure (P_G).

In light of these considerations, there is no “one size fits all” for the treatment of cardiorenal syndrome. Treatment should be based on thoughtful individualized strategies tailored to the underlying cardiorenal pathophysiology, and with the understanding that the kidney is at the heart of the matter.

Dramatic stories of disruptive physician behavior (DPB) appear occasionally in the news, such as the physician who shot and killed a colleague within hospital confines or the gynecologist who secretly took photographs using a camera disguised as a pen during pelvic examinations. More common in hospitals, however, are incidents of inappropriate behavior that may generate complaints from patients or other providers and at times snowball into administrative or legal challenges.

“Professionalism” is one of the six competencies listed by the Accreditation Council for Graduate Medical Education (ACGME)¹ and the American Board of Medical Specialties. Unfortunately, incidents of disruptive behavior can result in violation of the tenets of professionalism in the healthcare environment. These behaviors fall along a continuum ranging from outwardly aggressive and uncivil to overly passive and insidious. Although these behaviors can occur across all healthcare disciplines and settings and are not just limited to physicians, the behaviors of physicians often have a much greater impact on the healthcare system as a whole because of their positions of relative “power” within the system.² Hence, this problem requires greater awareness and education. In this context, the aim of this article is to discuss disruptive behaviors in physicians.

The AMA defines DPB as “personal conduct, verbal or physical that has the potential to negatively affect patient care or the ability to work with other members of the healthcare team.”³ The definition of DPB by the Joint Commission includes “all behaviors that undermine a culture of safety.”⁴ Both the Joint Commission and the AMA recognize the significance and patient safety implications of such behavior. Policy statements by both these organizations underscore the importance of confronting and remedying these potentially dangerous interpersonal behaviors.

Data regarding the prevalence of DPB have been inconsistent. One study estimated that 3%–5% of physicians demonstrate this behavior,⁵ whereas another study reported a DPB prevalence of 97% among physicians and nurses in the workplace.⁶ According to a 2004 survey of physician executives, more than 95% of them reported regular encounters of DPB.⁷

The etiology of such disruptive behaviors is multifactorial and complex. Explanations associated with ‘nature versus nurture’ have ranged from physician psychopathology to unhealthy modeling during training. Both extrinsic and intrinsic factors may also contribute to DPB. External stressors and negative experiences–professional and/or personal–can provoke disruptive behaviors. Overwork, fatigue, strife, and a dysfunctional environment that can arise in both work and home environments can contribute to the development of mental health problems. Stress, burnout, and depression have increasingly become prevalent among physicians and can play a significant role in causing impaired patterns of professional conduct.^{8, 9} These mental health problems can cause physicians to acquire maladaptive coping strategies such as substance abuse and drug or alcohol dependence. However, it is important to note that physician impairment and substance abuse are not the most frequent causes of DPB. In fact, fewer than 10% of physician behavior issues have been related to substance abuse.^{2, 5}

An institution’s organizational culture often has an impact on how DPB is addressed. Tolerance of such behavior can have far-reaching consequences. The central tenets of a “culture of safety and respect”–teamwork across disciplines and a blame-free environment in which every member of the healthcare team feels equally empowered to report errors and openly discuss safety issues–would be negatively impacted.

DPB can diminish the quality of care provided, increase the risk of medical errors, and adversely affect patient safety and satisfaction.^11-13 Such behavior can cause erosion of relationships and communication between individuals and contribute to a hostile work environment. For instance, nurses or trainees may be afraid to question a physician because of the fear of getting yelled at or being humiliated. Consequently, improperly written orders may be overlooked or a potentially “wrong-site” surgical procedure may not be questioned for fear of provoking a hostile response.

DPB can increase litigation risk and financial costs to institutions. Provider retention may be adversely affected; valued staff may leave hospitals and need to be replaced, and productivity may suffer. When physicians in training observe how their superiors model disruptive behaviors with impunity, a concerning problem that arises is that DPB becomes normalized in the workplace culture, especially if such behaviors are tolerated and result in a perceived gain.

Confrontation of DPB can be challenging without appropriate infrastructure. Healthcare facilities should have a fair system in place for reliable reporting and monitoring of DPB, including a complaints’ verification process, appeals process, and an option for fair hearing.

It is best to initially address the issue in a direct, timely, yet informal manner through counseling or a verbal warning. In several situations, such informal counseling opportunities create a mindful awareness of the problem and the problematic behavior ceases without the need for further action.

When informal intervention is either not appropriate (eg, if the alleged event involved an assault or other illegal behavior) or has already been offered in the past, more formal intervention is required. Institutional progressive disciplinary polices should be in place and adhered to. For example, repeat offenders may be issued written warnings or even temporary suspension of privileges.

Institutional resources such as human resources departments, office of general counsel, office of medical affairs, and the hospital’s medical board may be consulted. Some medical centers have “employee assistance programs” staffed with clinicians skilled in dealing with DPB. Individuals diagnosed with substance abuse or a mental health disorder may require consultation with mental health professionals.¹⁴

Special “Professionalism Committees” can be instituted and tasked with investigating complaints and making recommendations for the involvement of resources outside the institution, such as a state medical society.¹⁵

Although the vast majority of physicians are well-behaved, it is important to acknowledge that disruptive behaviors can occur in the healthcare environment. Such behaviors have a major impact on workplace culture and patient safety and must be recognized early. Hospital executives and leaders must ensure that appropriate interventions are undertaken—before the quality of patient care is affected and before lives are endangered.

Acknowledgment

The authors would like to thank Ansu John for providing editorial assistance with the manuscript.

Disclosures 

The authors have nothing to disclose (Conflict of Interest Form submitted as separate PDF document). Dr. Heitt consults with local hospitals, medical practices, and licensing boards regarding physicians and other healthcare practitioners who have been accused of engaging in disruptive behavior. In these situations he may be paid by the board, medical society, hospital, practice or the professional (patient).

Dramatic stories of disruptive physician behavior (DPB) appear occasionally in the news, such as the physician who shot and killed a colleague within hospital confines or the gynecologist who secretly took photographs using a camera disguised as a pen during pelvic examinations. More common in hospitals, however, are incidents of inappropriate behavior that may generate complaints from patients or other providers and at times snowball into administrative or legal challenges.

“Professionalism” is one of the six competencies listed by the Accreditation Council for Graduate Medical Education (ACGME)¹ and the American Board of Medical Specialties. Unfortunately, incidents of disruptive behavior can result in violation of the tenets of professionalism in the healthcare environment. These behaviors fall along a continuum ranging from outwardly aggressive and uncivil to overly passive and insidious. Although these behaviors can occur across all healthcare disciplines and settings and are not just limited to physicians, the behaviors of physicians often have a much greater impact on the healthcare system as a whole because of their positions of relative “power” within the system.² Hence, this problem requires greater awareness and education. In this context, the aim of this article is to discuss disruptive behaviors in physicians.

The AMA defines DPB as “personal conduct, verbal or physical that has the potential to negatively affect patient care or the ability to work with other members of the healthcare team.”³ The definition of DPB by the Joint Commission includes “all behaviors that undermine a culture of safety.”⁴ Both the Joint Commission and the AMA recognize the significance and patient safety implications of such behavior. Policy statements by both these organizations underscore the importance of confronting and remedying these potentially dangerous interpersonal behaviors.

Data regarding the prevalence of DPB have been inconsistent. One study estimated that 3%–5% of physicians demonstrate this behavior,⁵ whereas another study reported a DPB prevalence of 97% among physicians and nurses in the workplace.⁶ According to a 2004 survey of physician executives, more than 95% of them reported regular encounters of DPB.⁷

The etiology of such disruptive behaviors is multifactorial and complex. Explanations associated with ‘nature versus nurture’ have ranged from physician psychopathology to unhealthy modeling during training. Both extrinsic and intrinsic factors may also contribute to DPB. External stressors and negative experiences–professional and/or personal–can provoke disruptive behaviors. Overwork, fatigue, strife, and a dysfunctional environment that can arise in both work and home environments can contribute to the development of mental health problems. Stress, burnout, and depression have increasingly become prevalent among physicians and can play a significant role in causing impaired patterns of professional conduct.^{8, 9} These mental health problems can cause physicians to acquire maladaptive coping strategies such as substance abuse and drug or alcohol dependence. However, it is important to note that physician impairment and substance abuse are not the most frequent causes of DPB. In fact, fewer than 10% of physician behavior issues have been related to substance abuse.^{2, 5}

An institution’s organizational culture often has an impact on how DPB is addressed. Tolerance of such behavior can have far-reaching consequences. The central tenets of a “culture of safety and respect”–teamwork across disciplines and a blame-free environment in which every member of the healthcare team feels equally empowered to report errors and openly discuss safety issues–would be negatively impacted.

DPB can diminish the quality of care provided, increase the risk of medical errors, and adversely affect patient safety and satisfaction.^11-13 Such behavior can cause erosion of relationships and communication between individuals and contribute to a hostile work environment. For instance, nurses or trainees may be afraid to question a physician because of the fear of getting yelled at or being humiliated. Consequently, improperly written orders may be overlooked or a potentially “wrong-site” surgical procedure may not be questioned for fear of provoking a hostile response.

DPB can increase litigation risk and financial costs to institutions. Provider retention may be adversely affected; valued staff may leave hospitals and need to be replaced, and productivity may suffer. When physicians in training observe how their superiors model disruptive behaviors with impunity, a concerning problem that arises is that DPB becomes normalized in the workplace culture, especially if such behaviors are tolerated and result in a perceived gain.

Confrontation of DPB can be challenging without appropriate infrastructure. Healthcare facilities should have a fair system in place for reliable reporting and monitoring of DPB, including a complaints’ verification process, appeals process, and an option for fair hearing.

It is best to initially address the issue in a direct, timely, yet informal manner through counseling or a verbal warning. In several situations, such informal counseling opportunities create a mindful awareness of the problem and the problematic behavior ceases without the need for further action.

When informal intervention is either not appropriate (eg, if the alleged event involved an assault or other illegal behavior) or has already been offered in the past, more formal intervention is required. Institutional progressive disciplinary polices should be in place and adhered to. For example, repeat offenders may be issued written warnings or even temporary suspension of privileges.

Institutional resources such as human resources departments, office of general counsel, office of medical affairs, and the hospital’s medical board may be consulted. Some medical centers have “employee assistance programs” staffed with clinicians skilled in dealing with DPB. Individuals diagnosed with substance abuse or a mental health disorder may require consultation with mental health professionals.¹⁴

Special “Professionalism Committees” can be instituted and tasked with investigating complaints and making recommendations for the involvement of resources outside the institution, such as a state medical society.¹⁵

Although the vast majority of physicians are well-behaved, it is important to acknowledge that disruptive behaviors can occur in the healthcare environment. Such behaviors have a major impact on workplace culture and patient safety and must be recognized early. Hospital executives and leaders must ensure that appropriate interventions are undertaken—before the quality of patient care is affected and before lives are endangered.

Acknowledgment

The authors would like to thank Ansu John for providing editorial assistance with the manuscript.

Disclosures 

The authors have nothing to disclose (Conflict of Interest Form submitted as separate PDF document). Dr. Heitt consults with local hospitals, medical practices, and licensing boards regarding physicians and other healthcare practitioners who have been accused of engaging in disruptive behavior. In these situations he may be paid by the board, medical society, hospital, practice or the professional (patient).

Dramatic stories of disruptive physician behavior (DPB) appear occasionally in the news, such as the physician who shot and killed a colleague within hospital confines or the gynecologist who secretly took photographs using a camera disguised as a pen during pelvic examinations. More common in hospitals, however, are incidents of inappropriate behavior that may generate complaints from patients or other providers and at times snowball into administrative or legal challenges.

“Professionalism” is one of the six competencies listed by the Accreditation Council for Graduate Medical Education (ACGME)¹ and the American Board of Medical Specialties. Unfortunately, incidents of disruptive behavior can result in violation of the tenets of professionalism in the healthcare environment. These behaviors fall along a continuum ranging from outwardly aggressive and uncivil to overly passive and insidious. Although these behaviors can occur across all healthcare disciplines and settings and are not just limited to physicians, the behaviors of physicians often have a much greater impact on the healthcare system as a whole because of their positions of relative “power” within the system.² Hence, this problem requires greater awareness and education. In this context, the aim of this article is to discuss disruptive behaviors in physicians.

The AMA defines DPB as “personal conduct, verbal or physical that has the potential to negatively affect patient care or the ability to work with other members of the healthcare team.”³ The definition of DPB by the Joint Commission includes “all behaviors that undermine a culture of safety.”⁴ Both the Joint Commission and the AMA recognize the significance and patient safety implications of such behavior. Policy statements by both these organizations underscore the importance of confronting and remedying these potentially dangerous interpersonal behaviors.

Data regarding the prevalence of DPB have been inconsistent. One study estimated that 3%–5% of physicians demonstrate this behavior,⁵ whereas another study reported a DPB prevalence of 97% among physicians and nurses in the workplace.⁶ According to a 2004 survey of physician executives, more than 95% of them reported regular encounters of DPB.⁷

The etiology of such disruptive behaviors is multifactorial and complex. Explanations associated with ‘nature versus nurture’ have ranged from physician psychopathology to unhealthy modeling during training. Both extrinsic and intrinsic factors may also contribute to DPB. External stressors and negative experiences–professional and/or personal–can provoke disruptive behaviors. Overwork, fatigue, strife, and a dysfunctional environment that can arise in both work and home environments can contribute to the development of mental health problems. Stress, burnout, and depression have increasingly become prevalent among physicians and can play a significant role in causing impaired patterns of professional conduct.^{8, 9} These mental health problems can cause physicians to acquire maladaptive coping strategies such as substance abuse and drug or alcohol dependence. However, it is important to note that physician impairment and substance abuse are not the most frequent causes of DPB. In fact, fewer than 10% of physician behavior issues have been related to substance abuse.^{2, 5}

An institution’s organizational culture often has an impact on how DPB is addressed. Tolerance of such behavior can have far-reaching consequences. The central tenets of a “culture of safety and respect”–teamwork across disciplines and a blame-free environment in which every member of the healthcare team feels equally empowered to report errors and openly discuss safety issues–would be negatively impacted.

DPB can diminish the quality of care provided, increase the risk of medical errors, and adversely affect patient safety and satisfaction.^11-13 Such behavior can cause erosion of relationships and communication between individuals and contribute to a hostile work environment. For instance, nurses or trainees may be afraid to question a physician because of the fear of getting yelled at or being humiliated. Consequently, improperly written orders may be overlooked or a potentially “wrong-site” surgical procedure may not be questioned for fear of provoking a hostile response.

DPB can increase litigation risk and financial costs to institutions. Provider retention may be adversely affected; valued staff may leave hospitals and need to be replaced, and productivity may suffer. When physicians in training observe how their superiors model disruptive behaviors with impunity, a concerning problem that arises is that DPB becomes normalized in the workplace culture, especially if such behaviors are tolerated and result in a perceived gain.

Confrontation of DPB can be challenging without appropriate infrastructure. Healthcare facilities should have a fair system in place for reliable reporting and monitoring of DPB, including a complaints’ verification process, appeals process, and an option for fair hearing.

It is best to initially address the issue in a direct, timely, yet informal manner through counseling or a verbal warning. In several situations, such informal counseling opportunities create a mindful awareness of the problem and the problematic behavior ceases without the need for further action.

When informal intervention is either not appropriate (eg, if the alleged event involved an assault or other illegal behavior) or has already been offered in the past, more formal intervention is required. Institutional progressive disciplinary polices should be in place and adhered to. For example, repeat offenders may be issued written warnings or even temporary suspension of privileges.

Institutional resources such as human resources departments, office of general counsel, office of medical affairs, and the hospital’s medical board may be consulted. Some medical centers have “employee assistance programs” staffed with clinicians skilled in dealing with DPB. Individuals diagnosed with substance abuse or a mental health disorder may require consultation with mental health professionals.¹⁴

Special “Professionalism Committees” can be instituted and tasked with investigating complaints and making recommendations for the involvement of resources outside the institution, such as a state medical society.¹⁵

Although the vast majority of physicians are well-behaved, it is important to acknowledge that disruptive behaviors can occur in the healthcare environment. Such behaviors have a major impact on workplace culture and patient safety and must be recognized early. Hospital executives and leaders must ensure that appropriate interventions are undertaken—before the quality of patient care is affected and before lives are endangered.

Acknowledgment

The authors would like to thank Ansu John for providing editorial assistance with the manuscript.

Disclosures 

The authors have nothing to disclose (Conflict of Interest Form submitted as separate PDF document). Dr. Heitt consults with local hospitals, medical practices, and licensing boards regarding physicians and other healthcare practitioners who have been accused of engaging in disruptive behavior. In these situations he may be paid by the board, medical society, hospital, practice or the professional (patient).

We recently spoke with Denah Joseph, a clinical chaplain who works with the Palliative Care team to provide spiritual services to patients with serious illness. In addition, Denah leads efforts to address burnout among healthcare providers.

Denah, tell us about yourself.

My first career was actually in clinical psychology, but I’ve been a Palliative Care chaplain for 15 years. I also teach skill-building for providers around burnout and resilience.

What brought you to Palliative Care?

I’ve lost three sisters and a partner to breast cancer, and my dad died when I was quite young, so I’ve had a lot of exposure to loss. The other big thread in my life has been my spiritual practice. My father was an Orthodox Jew, but exceptionally ecumenical for his time. His first wife was Irish Catholic, and my father used to go to church, sit, kneel, and say the rosary, and light candles for his Catholic friends. Three hundred nuns from the local diocese all came to my dad’s funeral. It was really remarkable.

I’ve been a practicing Buddhist since I was 19. When I went back to school to become a chaplain I wanted to bring more of my spiritual interest into counseling work, so chaplaincy seemed like a really interesting way to do that.

Tell us more about what a chaplain actually does.

As a field, healthcare chaplaincy is relatively new. The old model was if a person was religious, somebody would arrange for a rabbi or an imam or a priest to come into the hospital and take care of the pastoral needs of that patient. In the last 10 to 15 years, the consensus guidelines for quality patient care now include addressing the spiritual dimension of patients’ lives. Instead of relying on volunteers from the community with no quality assurance, it’s required that any hospital over 200 beds have spiritual care available. In order to be a board-certified chaplain, you need to be endorsed by a faith community, and have an advanced degree in either Pastoral Counseling or Theology.

Everybody has spiritual needs even if they don’t use that word “spiritual.” We define it in terms of meaning, relationships, impact on one’s life, hope, fears, reconciliation issues, legacy issues, etc. Approximately 80% of patients want their physicians to understand a little bit about their spiritual/existential/emotional world, and only 20% of doctors ask—so there’s a really big gap. This can be a 5-minute conversation about who are you, what’s important to you, what’s the biggest struggle with your illness that is not medically oriented.

Can you share a patient encounter where you learned something?

Recently I cared for a patient whose wish was to survive to see his only son graduate from college. His wife and son both were like, “You’ve got to hang in there, Dad. You’ve got to hang in there.” He had very advanced pancreatic cancer, and the chances of him making it to graduation were exceedingly small, but nobody was dealing with this.

During the hospitalization, I went to the patient and his wife and I said, “We’re all hoping that you’re going to make it until the graduation but in the event you don’t, would you like to write a letter to your son?” In the Jewish tradition, it is called an ethical will. It’s the idea of legacy work. Just like you would make a will for your material possessions, an ethical will expresses what you value, what you hope for and dream for your beloved. He wanted to do it. His wife said, “Absolutely not, that’s like believing you’re not going to make it.” He was a very gentle guy. He would generally completely defer to his wife, but this time he said, “No, I want to do this.”

So I met with the patient and asked questions like, “What are the things you would hope to be remembered for? What are you most proud of that you want your son to know? What would you want your son to know if he became a father?”

I had him just talk, while I took notes. Later on, I wrote it up on official stationery and gave it to the patient.

What was his reaction when you gave the letter to him?

He started to cry. He said it was perfect. I usually read it to them so they can make edits if they want to. It sort of brings the grief forward when you imagine talking to a beloved that you’re leaving behind.

A few days later the patient died in the hospital surrounded by family members.

His wife, who had advocated so strongly against the letter, hugged me. She said, “That letter is the most important thing that happened here in the hospital.” I was shocked she said that, I had no idea he even shared it with her.

If people have the opportunity to share what’s important to them, particularly generationally, it could address a very deep need to be remembered.

Reflecting on it, I actually see myself as a healer and all my work is in healing, whether it’s working with physicians or working with patients or working with students or working with people in my private practice. It’s a theme that runs through everything. It’s not a word we hear often enough in medicine.

Why not?

The culture of medicine has lost its roots, in that sense. I hear a lot of people say, “There’s nothing we can do medically, so we’re just supporting them through this.” Supporting people through the experience is often seen as less valuable, but I think, particularly for serious, terminal illness, supporting people is not optional.

Switching gears a bit, tell us about the skill-building and resilience work you’ve done.

I think if you don’t proactively care for the rest of your life then your work life takes over. Although it’s pronounced in medicine, it’s in all fields. The pace and stress of our contemporary culture can be contrary to well-being in general.

When I first came to UCSF, I saw a culture of silence around stress, anxiety, and burnout. I started reading about burnout and the numbers of people who qualified to be burnt out at any given time, which may be at least 50% and trending upward. It just seemed to me that in any other profession if half the workforce was impaired, somebody would be doing something. I’ve really become passionate about this in the last couple of years.

So I developed a burnout prevention and resilience skills training class for providers. We work on mindfulness, social connection and support, positive psychology emotions like gratitude, appreciation, self-compassion, and humor, and delve into the sources of meaning in our work.

Based on your work, what would you say are the key stressors in medicine, generally?

Well there’s research on the electronic medical record and the increasing focus on metrics and “value-driven medicine,” which can lead to reduced connection with patients. I hope that what I’m doing makes some difference, but fundamentally, I believe there needs to be a real commitment on the part of the health system, to understand and make the changes that need to happen.

What is the fundamental problem? How do you define that?

Well I don’t think anybody knows. I think that’s what we’re saying. How can it be that so many people aren’t happy in such privileged work? It’s not clinical. It’s the system. It’s yet another flow sheet that you have to fill out; the actual amount of time spent with patients is low. No wonder we get burned out. We’re just doing orders all the time and answering phone calls.

It’s the loss of interconnectedness.

Yes, it’s the loss of connection. That goes back to even why chaplains may not be recognized as adding value. You can’t put a metric on connection. You can’t say, “I made 5 connections.”

Anything else you would like to share?

I don’t know how you feel about it, but I feel so grateful to have the opportunity to be in people’s lives in the intimate way we get to be and I, especially, get to be in a way sometimes even more than doctors. You get to be there, and you may even want to talk about the things that we were mentioning, but they’re asking you about their creatinine and their platelets and their urinary incontinence, so that’s what you’re having to talk about. I don’t have to do that, so I feel like I get the best seat in the house that way.

I think the seriously ill have so much to share and often are wise, particularly the young ones, from having dealt with illness. I’m really interested in that idea of wisdom and how you develop wisdom. Traditionally wisdom is associated with being an elder and having lived a long time and having a lot of experience. I think our work gives us that opportunity. We don’t have to necessarily live through everything to develop that kind of wisdom, but just to be with people who are living through these things.

So here I am, almost 70. I’m working harder than I’ve ever worked in my life. My partner is retired. She’s like, “Come on, let’s play.” She rides bikes, takes the dog out, cooks, reads. But I just can’t stop. I think it’s because I feel like, what else would I want to be doing with my time? I think that’s an amazing thing to be given that gift that I learn from my patients all the time and learn about what’s important. Obviously people are different, but it all boils down to relationships in the end.

That’s the promise of medicine, and I think that’s the great sadness of what’s going on with the epidemic of burnout. People lose connection to that.

There is some element to being present in these hard and difficult times that can bring perspective to life; and to know the sadness, in some ways

…is to know the joy.

Thank you, Denah, for sharing your thoughts with us.

We recently spoke with Denah Joseph, a clinical chaplain who works with the Palliative Care team to provide spiritual services to patients with serious illness. In addition, Denah leads efforts to address burnout among healthcare providers.

Denah, tell us about yourself.

My first career was actually in clinical psychology, but I’ve been a Palliative Care chaplain for 15 years. I also teach skill-building for providers around burnout and resilience.

What brought you to Palliative Care?

I’ve lost three sisters and a partner to breast cancer, and my dad died when I was quite young, so I’ve had a lot of exposure to loss. The other big thread in my life has been my spiritual practice. My father was an Orthodox Jew, but exceptionally ecumenical for his time. His first wife was Irish Catholic, and my father used to go to church, sit, kneel, and say the rosary, and light candles for his Catholic friends. Three hundred nuns from the local diocese all came to my dad’s funeral. It was really remarkable.

I’ve been a practicing Buddhist since I was 19. When I went back to school to become a chaplain I wanted to bring more of my spiritual interest into counseling work, so chaplaincy seemed like a really interesting way to do that.

Tell us more about what a chaplain actually does.

As a field, healthcare chaplaincy is relatively new. The old model was if a person was religious, somebody would arrange for a rabbi or an imam or a priest to come into the hospital and take care of the pastoral needs of that patient. In the last 10 to 15 years, the consensus guidelines for quality patient care now include addressing the spiritual dimension of patients’ lives. Instead of relying on volunteers from the community with no quality assurance, it’s required that any hospital over 200 beds have spiritual care available. In order to be a board-certified chaplain, you need to be endorsed by a faith community, and have an advanced degree in either Pastoral Counseling or Theology.

Everybody has spiritual needs even if they don’t use that word “spiritual.” We define it in terms of meaning, relationships, impact on one’s life, hope, fears, reconciliation issues, legacy issues, etc. Approximately 80% of patients want their physicians to understand a little bit about their spiritual/existential/emotional world, and only 20% of doctors ask—so there’s a really big gap. This can be a 5-minute conversation about who are you, what’s important to you, what’s the biggest struggle with your illness that is not medically oriented.

Can you share a patient encounter where you learned something?

Recently I cared for a patient whose wish was to survive to see his only son graduate from college. His wife and son both were like, “You’ve got to hang in there, Dad. You’ve got to hang in there.” He had very advanced pancreatic cancer, and the chances of him making it to graduation were exceedingly small, but nobody was dealing with this.

During the hospitalization, I went to the patient and his wife and I said, “We’re all hoping that you’re going to make it until the graduation but in the event you don’t, would you like to write a letter to your son?” In the Jewish tradition, it is called an ethical will. It’s the idea of legacy work. Just like you would make a will for your material possessions, an ethical will expresses what you value, what you hope for and dream for your beloved. He wanted to do it. His wife said, “Absolutely not, that’s like believing you’re not going to make it.” He was a very gentle guy. He would generally completely defer to his wife, but this time he said, “No, I want to do this.”

So I met with the patient and asked questions like, “What are the things you would hope to be remembered for? What are you most proud of that you want your son to know? What would you want your son to know if he became a father?”

I had him just talk, while I took notes. Later on, I wrote it up on official stationery and gave it to the patient.

What was his reaction when you gave the letter to him?

He started to cry. He said it was perfect. I usually read it to them so they can make edits if they want to. It sort of brings the grief forward when you imagine talking to a beloved that you’re leaving behind.

A few days later the patient died in the hospital surrounded by family members.

His wife, who had advocated so strongly against the letter, hugged me. She said, “That letter is the most important thing that happened here in the hospital.” I was shocked she said that, I had no idea he even shared it with her.

If people have the opportunity to share what’s important to them, particularly generationally, it could address a very deep need to be remembered.

Reflecting on it, I actually see myself as a healer and all my work is in healing, whether it’s working with physicians or working with patients or working with students or working with people in my private practice. It’s a theme that runs through everything. It’s not a word we hear often enough in medicine.

Why not?

The culture of medicine has lost its roots, in that sense. I hear a lot of people say, “There’s nothing we can do medically, so we’re just supporting them through this.” Supporting people through the experience is often seen as less valuable, but I think, particularly for serious, terminal illness, supporting people is not optional.

Switching gears a bit, tell us about the skill-building and resilience work you’ve done.

I think if you don’t proactively care for the rest of your life then your work life takes over. Although it’s pronounced in medicine, it’s in all fields. The pace and stress of our contemporary culture can be contrary to well-being in general.

When I first came to UCSF, I saw a culture of silence around stress, anxiety, and burnout. I started reading about burnout and the numbers of people who qualified to be burnt out at any given time, which may be at least 50% and trending upward. It just seemed to me that in any other profession if half the workforce was impaired, somebody would be doing something. I’ve really become passionate about this in the last couple of years.

So I developed a burnout prevention and resilience skills training class for providers. We work on mindfulness, social connection and support, positive psychology emotions like gratitude, appreciation, self-compassion, and humor, and delve into the sources of meaning in our work.

Based on your work, what would you say are the key stressors in medicine, generally?

Well there’s research on the electronic medical record and the increasing focus on metrics and “value-driven medicine,” which can lead to reduced connection with patients. I hope that what I’m doing makes some difference, but fundamentally, I believe there needs to be a real commitment on the part of the health system, to understand and make the changes that need to happen.

What is the fundamental problem? How do you define that?

Well I don’t think anybody knows. I think that’s what we’re saying. How can it be that so many people aren’t happy in such privileged work? It’s not clinical. It’s the system. It’s yet another flow sheet that you have to fill out; the actual amount of time spent with patients is low. No wonder we get burned out. We’re just doing orders all the time and answering phone calls.

It’s the loss of interconnectedness.

Yes, it’s the loss of connection. That goes back to even why chaplains may not be recognized as adding value. You can’t put a metric on connection. You can’t say, “I made 5 connections.”

Anything else you would like to share?

I don’t know how you feel about it, but I feel so grateful to have the opportunity to be in people’s lives in the intimate way we get to be and I, especially, get to be in a way sometimes even more than doctors. You get to be there, and you may even want to talk about the things that we were mentioning, but they’re asking you about their creatinine and their platelets and their urinary incontinence, so that’s what you’re having to talk about. I don’t have to do that, so I feel like I get the best seat in the house that way.

I think the seriously ill have so much to share and often are wise, particularly the young ones, from having dealt with illness. I’m really interested in that idea of wisdom and how you develop wisdom. Traditionally wisdom is associated with being an elder and having lived a long time and having a lot of experience. I think our work gives us that opportunity. We don’t have to necessarily live through everything to develop that kind of wisdom, but just to be with people who are living through these things.

So here I am, almost 70. I’m working harder than I’ve ever worked in my life. My partner is retired. She’s like, “Come on, let’s play.” She rides bikes, takes the dog out, cooks, reads. But I just can’t stop. I think it’s because I feel like, what else would I want to be doing with my time? I think that’s an amazing thing to be given that gift that I learn from my patients all the time and learn about what’s important. Obviously people are different, but it all boils down to relationships in the end.

That’s the promise of medicine, and I think that’s the great sadness of what’s going on with the epidemic of burnout. People lose connection to that.

There is some element to being present in these hard and difficult times that can bring perspective to life; and to know the sadness, in some ways

…is to know the joy.

Thank you, Denah, for sharing your thoughts with us.

We recently spoke with Denah Joseph, a clinical chaplain who works with the Palliative Care team to provide spiritual services to patients with serious illness. In addition, Denah leads efforts to address burnout among healthcare providers.

Denah, tell us about yourself.

My first career was actually in clinical psychology, but I’ve been a Palliative Care chaplain for 15 years. I also teach skill-building for providers around burnout and resilience.

What brought you to Palliative Care?

I’ve lost three sisters and a partner to breast cancer, and my dad died when I was quite young, so I’ve had a lot of exposure to loss. The other big thread in my life has been my spiritual practice. My father was an Orthodox Jew, but exceptionally ecumenical for his time. His first wife was Irish Catholic, and my father used to go to church, sit, kneel, and say the rosary, and light candles for his Catholic friends. Three hundred nuns from the local diocese all came to my dad’s funeral. It was really remarkable.

I’ve been a practicing Buddhist since I was 19. When I went back to school to become a chaplain I wanted to bring more of my spiritual interest into counseling work, so chaplaincy seemed like a really interesting way to do that.

Tell us more about what a chaplain actually does.

As a field, healthcare chaplaincy is relatively new. The old model was if a person was religious, somebody would arrange for a rabbi or an imam or a priest to come into the hospital and take care of the pastoral needs of that patient. In the last 10 to 15 years, the consensus guidelines for quality patient care now include addressing the spiritual dimension of patients’ lives. Instead of relying on volunteers from the community with no quality assurance, it’s required that any hospital over 200 beds have spiritual care available. In order to be a board-certified chaplain, you need to be endorsed by a faith community, and have an advanced degree in either Pastoral Counseling or Theology.

Everybody has spiritual needs even if they don’t use that word “spiritual.” We define it in terms of meaning, relationships, impact on one’s life, hope, fears, reconciliation issues, legacy issues, etc. Approximately 80% of patients want their physicians to understand a little bit about their spiritual/existential/emotional world, and only 20% of doctors ask—so there’s a really big gap. This can be a 5-minute conversation about who are you, what’s important to you, what’s the biggest struggle with your illness that is not medically oriented.

Can you share a patient encounter where you learned something?

Recently I cared for a patient whose wish was to survive to see his only son graduate from college. His wife and son both were like, “You’ve got to hang in there, Dad. You’ve got to hang in there.” He had very advanced pancreatic cancer, and the chances of him making it to graduation were exceedingly small, but nobody was dealing with this.

During the hospitalization, I went to the patient and his wife and I said, “We’re all hoping that you’re going to make it until the graduation but in the event you don’t, would you like to write a letter to your son?” In the Jewish tradition, it is called an ethical will. It’s the idea of legacy work. Just like you would make a will for your material possessions, an ethical will expresses what you value, what you hope for and dream for your beloved. He wanted to do it. His wife said, “Absolutely not, that’s like believing you’re not going to make it.” He was a very gentle guy. He would generally completely defer to his wife, but this time he said, “No, I want to do this.”

So I met with the patient and asked questions like, “What are the things you would hope to be remembered for? What are you most proud of that you want your son to know? What would you want your son to know if he became a father?”

I had him just talk, while I took notes. Later on, I wrote it up on official stationery and gave it to the patient.

What was his reaction when you gave the letter to him?

He started to cry. He said it was perfect. I usually read it to them so they can make edits if they want to. It sort of brings the grief forward when you imagine talking to a beloved that you’re leaving behind.

A few days later the patient died in the hospital surrounded by family members.

His wife, who had advocated so strongly against the letter, hugged me. She said, “That letter is the most important thing that happened here in the hospital.” I was shocked she said that, I had no idea he even shared it with her.

If people have the opportunity to share what’s important to them, particularly generationally, it could address a very deep need to be remembered.

Reflecting on it, I actually see myself as a healer and all my work is in healing, whether it’s working with physicians or working with patients or working with students or working with people in my private practice. It’s a theme that runs through everything. It’s not a word we hear often enough in medicine.

Why not?

The culture of medicine has lost its roots, in that sense. I hear a lot of people say, “There’s nothing we can do medically, so we’re just supporting them through this.” Supporting people through the experience is often seen as less valuable, but I think, particularly for serious, terminal illness, supporting people is not optional.

Switching gears a bit, tell us about the skill-building and resilience work you’ve done.

I think if you don’t proactively care for the rest of your life then your work life takes over. Although it’s pronounced in medicine, it’s in all fields. The pace and stress of our contemporary culture can be contrary to well-being in general.

When I first came to UCSF, I saw a culture of silence around stress, anxiety, and burnout. I started reading about burnout and the numbers of people who qualified to be burnt out at any given time, which may be at least 50% and trending upward. It just seemed to me that in any other profession if half the workforce was impaired, somebody would be doing something. I’ve really become passionate about this in the last couple of years.

So I developed a burnout prevention and resilience skills training class for providers. We work on mindfulness, social connection and support, positive psychology emotions like gratitude, appreciation, self-compassion, and humor, and delve into the sources of meaning in our work.

Based on your work, what would you say are the key stressors in medicine, generally?

Well there’s research on the electronic medical record and the increasing focus on metrics and “value-driven medicine,” which can lead to reduced connection with patients. I hope that what I’m doing makes some difference, but fundamentally, I believe there needs to be a real commitment on the part of the health system, to understand and make the changes that need to happen.

What is the fundamental problem? How do you define that?

Well I don’t think anybody knows. I think that’s what we’re saying. How can it be that so many people aren’t happy in such privileged work? It’s not clinical. It’s the system. It’s yet another flow sheet that you have to fill out; the actual amount of time spent with patients is low. No wonder we get burned out. We’re just doing orders all the time and answering phone calls.

It’s the loss of interconnectedness.

Yes, it’s the loss of connection. That goes back to even why chaplains may not be recognized as adding value. You can’t put a metric on connection. You can’t say, “I made 5 connections.”

Anything else you would like to share?

I don’t know how you feel about it, but I feel so grateful to have the opportunity to be in people’s lives in the intimate way we get to be and I, especially, get to be in a way sometimes even more than doctors. You get to be there, and you may even want to talk about the things that we were mentioning, but they’re asking you about their creatinine and their platelets and their urinary incontinence, so that’s what you’re having to talk about. I don’t have to do that, so I feel like I get the best seat in the house that way.

I think the seriously ill have so much to share and often are wise, particularly the young ones, from having dealt with illness. I’m really interested in that idea of wisdom and how you develop wisdom. Traditionally wisdom is associated with being an elder and having lived a long time and having a lot of experience. I think our work gives us that opportunity. We don’t have to necessarily live through everything to develop that kind of wisdom, but just to be with people who are living through these things.

So here I am, almost 70. I’m working harder than I’ve ever worked in my life. My partner is retired. She’s like, “Come on, let’s play.” She rides bikes, takes the dog out, cooks, reads. But I just can’t stop. I think it’s because I feel like, what else would I want to be doing with my time? I think that’s an amazing thing to be given that gift that I learn from my patients all the time and learn about what’s important. Obviously people are different, but it all boils down to relationships in the end.

That’s the promise of medicine, and I think that’s the great sadness of what’s going on with the epidemic of burnout. People lose connection to that.

There is some element to being present in these hard and difficult times that can bring perspective to life; and to know the sadness, in some ways

…is to know the joy.

Thank you, Denah, for sharing your thoughts with us.

The only real voyage of discovery consists not in seeking new landscapes but in having new eyes.

—Marcel Proust

Hospitals can be complex, challenging, and dehumanizing for both patients and practitioners. In a national survey, up to half of hospitalists were affected by burnout and scored highly on emotional exhaustion and depersonalization scales.¹

Yet hospitals are also ripe with meaningful stories. In addition to patients’ narratives, the stories of multidisciplinary team members who make quality patient care possible reveal that we are bound together in more ways than we realize. Now, we have the opportunity to tell these stories.

This issue of Journal of Hospital Medicine introduces a new series: In the Hospital. Through selected interviews we explore the day-to-day lives of members of our hospital team. Highlighting the “team” in healthcare has been a longstanding focus of JHM, but we also hope that this series will demonstrate how each individual we meet with is not only a critical part of how patients receive care but is also an important member of our community.

We invite readers to appreciate the common threads that bind these pieces together. These stories will introduce us to individuals who have discrete and often disparate job descriptions, but all of them care about patients and want the best for them. Some are frustrated with the health care system and the constraints it places on our efficiency. Many of them worry about how to balance the demands of work with the need to be available for their families and friends. Many are trying their best to maintain their humanism, build resilience, and sustain themselves in ways that meet their personal goals for excellence, empathy, and fulfillment.

This series begins with the story of a palliative-care clinical chaplain whose life experience and perspective brings to light issues of resilience, meaning, and purpose. Future stories in this series will include a variety of providers across a spectrum of practice environments. We look forward to engaging you in this journey and welcome feedback and contributions.

Disclosures

The authors have nothing to disclose.

The only real voyage of discovery consists not in seeking new landscapes but in having new eyes.

—Marcel Proust

Hospitals can be complex, challenging, and dehumanizing for both patients and practitioners. In a national survey, up to half of hospitalists were affected by burnout and scored highly on emotional exhaustion and depersonalization scales.¹

Yet hospitals are also ripe with meaningful stories. In addition to patients’ narratives, the stories of multidisciplinary team members who make quality patient care possible reveal that we are bound together in more ways than we realize. Now, we have the opportunity to tell these stories.

This issue of Journal of Hospital Medicine introduces a new series: In the Hospital. Through selected interviews we explore the day-to-day lives of members of our hospital team. Highlighting the “team” in healthcare has been a longstanding focus of JHM, but we also hope that this series will demonstrate how each individual we meet with is not only a critical part of how patients receive care but is also an important member of our community.

We invite readers to appreciate the common threads that bind these pieces together. These stories will introduce us to individuals who have discrete and often disparate job descriptions, but all of them care about patients and want the best for them. Some are frustrated with the health care system and the constraints it places on our efficiency. Many of them worry about how to balance the demands of work with the need to be available for their families and friends. Many are trying their best to maintain their humanism, build resilience, and sustain themselves in ways that meet their personal goals for excellence, empathy, and fulfillment.

This series begins with the story of a palliative-care clinical chaplain whose life experience and perspective brings to light issues of resilience, meaning, and purpose. Future stories in this series will include a variety of providers across a spectrum of practice environments. We look forward to engaging you in this journey and welcome feedback and contributions.

Disclosures

The authors have nothing to disclose.

The only real voyage of discovery consists not in seeking new landscapes but in having new eyes.

—Marcel Proust

Hospitals can be complex, challenging, and dehumanizing for both patients and practitioners. In a national survey, up to half of hospitalists were affected by burnout and scored highly on emotional exhaustion and depersonalization scales.¹

Yet hospitals are also ripe with meaningful stories. In addition to patients’ narratives, the stories of multidisciplinary team members who make quality patient care possible reveal that we are bound together in more ways than we realize. Now, we have the opportunity to tell these stories.

This issue of Journal of Hospital Medicine introduces a new series: In the Hospital. Through selected interviews we explore the day-to-day lives of members of our hospital team. Highlighting the “team” in healthcare has been a longstanding focus of JHM, but we also hope that this series will demonstrate how each individual we meet with is not only a critical part of how patients receive care but is also an important member of our community.

We invite readers to appreciate the common threads that bind these pieces together. These stories will introduce us to individuals who have discrete and often disparate job descriptions, but all of them care about patients and want the best for them. Some are frustrated with the health care system and the constraints it places on our efficiency. Many of them worry about how to balance the demands of work with the need to be available for their families and friends. Many are trying their best to maintain their humanism, build resilience, and sustain themselves in ways that meet their personal goals for excellence, empathy, and fulfillment.

This series begins with the story of a palliative-care clinical chaplain whose life experience and perspective brings to light issues of resilience, meaning, and purpose. Future stories in this series will include a variety of providers across a spectrum of practice environments. We look forward to engaging you in this journey and welcome feedback and contributions.

Disclosures

The authors have nothing to disclose.