Hospital Medicine

The care transition period between inpatient psychiatric hospitalization and initiation of outpatient mental health services is a time of extraordinarily heightened suicide risk that has been woefully neglected, according to speakers from the National Action Alliance for Suicide Prevention at the virtual annual meeting of the American Association of Suicidology.

This transition period traditionally has been a time when nobody really takes responsibility for patient care. In an effort to close this potentially deadly gap in services, the alliance recently has issued a report entitled, “Best Practices in Care Transitions for Individuals with Suicide Risk: Inpatient Care to Outpatient Care.” The recommendations focus on specific, innovative, evidence-based strategies that health care systems can use to prevent patients from falling through the cracks in care, mainly by implementing protocols aimed at fostering interorganizational teamwork between inpatient and outpatient behavioral health services.

“I believe that improving care transitions in the United States is the area where we can likely save the most lives. It’s within our grasp if we can just do this better,” declared Richard McKeon, PhD, MPH, chief of the Suicide Prevention Branch at the Center for Mental Health Services within SAMHSA, the Substance Abuse and Mental Health Services Administration.

He cited a recent meta-analysis that concluded that the risk of suicide during the first week post discharge after psychiatric hospitalization is a staggering 300 times greater than in the general population, while in the first month, the risk is increased 200-fold. The meta-analysis included 29 studies encompassing 3,551 suicides during the first month and 24 studies reporting 1,928 suicides during the first week post discharge (BMJ Open. 2019 Mar 23;9[3]:e023883. doi: 10.1136/bmjopen-2018-023883).

Everyone in the mental health field as well as patients and their families should know those statistics, but they don’t.

“I think it’s natural for people to think someone who’s been discharged from an inpatient unit or the emergency department is not at risk, when in reality it’s still a high-risk time. Suicide risk is not like a light switch that you can just switch off,” the clinical psychologist observed.

He cited other harrowing statistics that underscore the vast problem of poor care transitions. Nationally, fully one-third of patients don’t complete a single outpatient visit within the first 30 days after discharge from inpatient behavioral health care. And one in seven people who die by suicide have had contact with inpatient mental health services in the year before they died.

“That doesn’t mean that inpatient care did not do everything that they could do. What it does reflect is the need to make sure that there’s follow-up care after inpatient discharge. Too often, people don’t get the follow-up care that they need. And the research literature is clear that intervention can save lives,” Dr. McKeon said.

Panelist Becky Stoll, LCSW, vice president for crisis and disaster management at Centerstone Health in Nashville, Tenn., noted, “We see a lot of no-shows on the outpatient side, because nobody ever asked the patients if they can actually get to the outpatient appointment that’s been made.

“We have got to figure out this care transition and do better. The road to mental health is paved with Swiss cheese. There are so many holes to fall into, even if you know how to navigate the system – and most of the people we’re serving don’t know how,” observed Ms. Stoll, who, like Dr. McKeon, was among the coauthors of the alliance’s guidelines on best practices in care transitions. Ms. Stoll also serves on the AAS board as crisis services division chair.* 

The National Action Alliance for Suicide Prevention is a public/private partnership whose goal is to advance the National Strategy for Suicide Prevention, which was developed by the alliance and the U.S. Surgeon General. The alliance includes mental health professionals as well as influential leaders from the military, journalism, entertainment, railroad, health insurance, law enforcement, defense, education, technology, and other industries.

Dr. McKeon and Ms. Stall were joined by Karen Johnson, MSW, another coauthor of the guidelines. They shared highlights of the report.

Inpatient provider strategies

Discharge and crisis safety planning should begin upon admission, according to Ms. Johnson, senior vice president for clinical services and division compliance at Universal Health Services, which owns and operates more than 200 behavioral health facilities across the United States.

Inpatient and outpatient care providers need to sit down and develop collaborative protocols and negotiate a memorandum of understanding regarding expectations, which absolutely must include procedures to ensure timely electronic delivery of medical records and other key documents to the outpatient care providers. The inpatient providers need to work collaboratively with the patient, family, and community support resources to develop a safety plan – including reduced access to lethal mean – as part of predischarge planning.

Among the strategies routinely employed on the inpatient side at Universal Health Services are advance scheduling of an initial outpatient appointment within 24-72 hours post discharge. Also, someone on the inpatient team is tasked with connecting with the outpatient provider prior to discharge to develop rapport.

“If our outpatient providers are located in our facility, as many of them are, we ask them to come in and attend inpatient team meetings to identify and meet with patients who are appropriate for continuing care in outpatient settings,” she explained. “A soft, warm handoff is critical.”

At these team meetings, the appropriateness of step-down care in the form of partial hospitalization or intensive outpatient care is weighed. Someone from the inpatient side is charged with maintaining contact with the patient until after the first outpatient appointment. Ongoing caring contact in the form of brief, encouraging postcards, emails, or texts that do not require a response from the patient should be maintained for several months.
 

Strategies for outpatient providers

Ms. Stoll is a big believer in the guideline-recommended practice of notifying the inpatient provider that the patient kept the outpatient appointment, along with having a system for red-flagging no-shows for prompt follow-up by a crisis management team.

She and her colleagues at Centerstone Health have conducted two studies of an intensive patient outreach program designed for the first 30 days of the care transition. The program included many elements of the alliance’s best practices guidelines. The yearlong first study, funded by Blue Cross/Blue Shield of Tennessee, documented zero suicides and 92% freedom from emergency department visits during the care transition period, along with greater than $400,000 savings in health care costs, compared with usual care. The second study, funded by SAMHSA, showed much the same over a 2-year period.

She emphasized that this was not a high-tech, intensive intervention. She characterized it, instead as “high-touch follow-up.

“It’s some staff and a phone and a laptop, nothing fancy, just a person who’s competent and confident and skilled with a laptop. With that, you can do some pretty amazing stuff: Get people what they need, keep them alive, and oh, guess what? You can also save a lot of health care dollars that can be put back into the system,” Ms. Stoll said.

She recognizes that it’s a lot to ask busy outpatient providers to leave their practice during the workday to participate in inpatient team meetings addressing discharge planning, as recommended in the alliance guidelines. But in this regard, she sees a silver lining to the COVID-19 pandemic, in that it forces health professionals to rely upon newly opened channels of telemedicine.

“COVID-19 is giving us an opportunity to do things in a different way. Things don’t just have to be done in person. Now that we’ve opened up new channels of telehealth, I’m really excited that we’re almost in a beta test that we’ve dreamed about for decades, where we can do things in a more innovative way,” she said.

Dr. McKeon agreed that reimbursement issues have long impeded efforts to improve the inpatient to outpatient care transition. He added that it will be really important that adequate reimbursement of remote forms of care remain in place after COVID-19 fades.

“This is exactly the kind of thing that’s needed to improve care transitions,” according to Dr. McKeon.

*This story was updated 7/9/2020.

bjancin@mdedge.com

The care transition period between inpatient psychiatric hospitalization and initiation of outpatient mental health services is a time of extraordinarily heightened suicide risk that has been woefully neglected, according to speakers from the National Action Alliance for Suicide Prevention at the virtual annual meeting of the American Association of Suicidology.

This transition period traditionally has been a time when nobody really takes responsibility for patient care. In an effort to close this potentially deadly gap in services, the alliance recently has issued a report entitled, “Best Practices in Care Transitions for Individuals with Suicide Risk: Inpatient Care to Outpatient Care.” The recommendations focus on specific, innovative, evidence-based strategies that health care systems can use to prevent patients from falling through the cracks in care, mainly by implementing protocols aimed at fostering interorganizational teamwork between inpatient and outpatient behavioral health services.

“I believe that improving care transitions in the United States is the area where we can likely save the most lives. It’s within our grasp if we can just do this better,” declared Richard McKeon, PhD, MPH, chief of the Suicide Prevention Branch at the Center for Mental Health Services within SAMHSA, the Substance Abuse and Mental Health Services Administration.

He cited a recent meta-analysis that concluded that the risk of suicide during the first week post discharge after psychiatric hospitalization is a staggering 300 times greater than in the general population, while in the first month, the risk is increased 200-fold. The meta-analysis included 29 studies encompassing 3,551 suicides during the first month and 24 studies reporting 1,928 suicides during the first week post discharge (BMJ Open. 2019 Mar 23;9[3]:e023883. doi: 10.1136/bmjopen-2018-023883).

Everyone in the mental health field as well as patients and their families should know those statistics, but they don’t.

“I think it’s natural for people to think someone who’s been discharged from an inpatient unit or the emergency department is not at risk, when in reality it’s still a high-risk time. Suicide risk is not like a light switch that you can just switch off,” the clinical psychologist observed.

He cited other harrowing statistics that underscore the vast problem of poor care transitions. Nationally, fully one-third of patients don’t complete a single outpatient visit within the first 30 days after discharge from inpatient behavioral health care. And one in seven people who die by suicide have had contact with inpatient mental health services in the year before they died.

“That doesn’t mean that inpatient care did not do everything that they could do. What it does reflect is the need to make sure that there’s follow-up care after inpatient discharge. Too often, people don’t get the follow-up care that they need. And the research literature is clear that intervention can save lives,” Dr. McKeon said.

Panelist Becky Stoll, LCSW, vice president for crisis and disaster management at Centerstone Health in Nashville, Tenn., noted, “We see a lot of no-shows on the outpatient side, because nobody ever asked the patients if they can actually get to the outpatient appointment that’s been made.

“We have got to figure out this care transition and do better. The road to mental health is paved with Swiss cheese. There are so many holes to fall into, even if you know how to navigate the system – and most of the people we’re serving don’t know how,” observed Ms. Stoll, who, like Dr. McKeon, was among the coauthors of the alliance’s guidelines on best practices in care transitions. Ms. Stoll also serves on the AAS board as crisis services division chair.* 

The National Action Alliance for Suicide Prevention is a public/private partnership whose goal is to advance the National Strategy for Suicide Prevention, which was developed by the alliance and the U.S. Surgeon General. The alliance includes mental health professionals as well as influential leaders from the military, journalism, entertainment, railroad, health insurance, law enforcement, defense, education, technology, and other industries.

Dr. McKeon and Ms. Stall were joined by Karen Johnson, MSW, another coauthor of the guidelines. They shared highlights of the report.

Inpatient provider strategies

Discharge and crisis safety planning should begin upon admission, according to Ms. Johnson, senior vice president for clinical services and division compliance at Universal Health Services, which owns and operates more than 200 behavioral health facilities across the United States.

Inpatient and outpatient care providers need to sit down and develop collaborative protocols and negotiate a memorandum of understanding regarding expectations, which absolutely must include procedures to ensure timely electronic delivery of medical records and other key documents to the outpatient care providers. The inpatient providers need to work collaboratively with the patient, family, and community support resources to develop a safety plan – including reduced access to lethal mean – as part of predischarge planning.

Among the strategies routinely employed on the inpatient side at Universal Health Services are advance scheduling of an initial outpatient appointment within 24-72 hours post discharge. Also, someone on the inpatient team is tasked with connecting with the outpatient provider prior to discharge to develop rapport.

“If our outpatient providers are located in our facility, as many of them are, we ask them to come in and attend inpatient team meetings to identify and meet with patients who are appropriate for continuing care in outpatient settings,” she explained. “A soft, warm handoff is critical.”

At these team meetings, the appropriateness of step-down care in the form of partial hospitalization or intensive outpatient care is weighed. Someone from the inpatient side is charged with maintaining contact with the patient until after the first outpatient appointment. Ongoing caring contact in the form of brief, encouraging postcards, emails, or texts that do not require a response from the patient should be maintained for several months.
 

Strategies for outpatient providers

Ms. Stoll is a big believer in the guideline-recommended practice of notifying the inpatient provider that the patient kept the outpatient appointment, along with having a system for red-flagging no-shows for prompt follow-up by a crisis management team.

She and her colleagues at Centerstone Health have conducted two studies of an intensive patient outreach program designed for the first 30 days of the care transition. The program included many elements of the alliance’s best practices guidelines. The yearlong first study, funded by Blue Cross/Blue Shield of Tennessee, documented zero suicides and 92% freedom from emergency department visits during the care transition period, along with greater than $400,000 savings in health care costs, compared with usual care. The second study, funded by SAMHSA, showed much the same over a 2-year period.

She emphasized that this was not a high-tech, intensive intervention. She characterized it, instead as “high-touch follow-up.

“It’s some staff and a phone and a laptop, nothing fancy, just a person who’s competent and confident and skilled with a laptop. With that, you can do some pretty amazing stuff: Get people what they need, keep them alive, and oh, guess what? You can also save a lot of health care dollars that can be put back into the system,” Ms. Stoll said.

She recognizes that it’s a lot to ask busy outpatient providers to leave their practice during the workday to participate in inpatient team meetings addressing discharge planning, as recommended in the alliance guidelines. But in this regard, she sees a silver lining to the COVID-19 pandemic, in that it forces health professionals to rely upon newly opened channels of telemedicine.

“COVID-19 is giving us an opportunity to do things in a different way. Things don’t just have to be done in person. Now that we’ve opened up new channels of telehealth, I’m really excited that we’re almost in a beta test that we’ve dreamed about for decades, where we can do things in a more innovative way,” she said.

Dr. McKeon agreed that reimbursement issues have long impeded efforts to improve the inpatient to outpatient care transition. He added that it will be really important that adequate reimbursement of remote forms of care remain in place after COVID-19 fades.

“This is exactly the kind of thing that’s needed to improve care transitions,” according to Dr. McKeon.

*This story was updated 7/9/2020.

bjancin@mdedge.com

The care transition period between inpatient psychiatric hospitalization and initiation of outpatient mental health services is a time of extraordinarily heightened suicide risk that has been woefully neglected, according to speakers from the National Action Alliance for Suicide Prevention at the virtual annual meeting of the American Association of Suicidology.

This transition period traditionally has been a time when nobody really takes responsibility for patient care. In an effort to close this potentially deadly gap in services, the alliance recently has issued a report entitled, “Best Practices in Care Transitions for Individuals with Suicide Risk: Inpatient Care to Outpatient Care.” The recommendations focus on specific, innovative, evidence-based strategies that health care systems can use to prevent patients from falling through the cracks in care, mainly by implementing protocols aimed at fostering interorganizational teamwork between inpatient and outpatient behavioral health services.

“I believe that improving care transitions in the United States is the area where we can likely save the most lives. It’s within our grasp if we can just do this better,” declared Richard McKeon, PhD, MPH, chief of the Suicide Prevention Branch at the Center for Mental Health Services within SAMHSA, the Substance Abuse and Mental Health Services Administration.

He cited a recent meta-analysis that concluded that the risk of suicide during the first week post discharge after psychiatric hospitalization is a staggering 300 times greater than in the general population, while in the first month, the risk is increased 200-fold. The meta-analysis included 29 studies encompassing 3,551 suicides during the first month and 24 studies reporting 1,928 suicides during the first week post discharge (BMJ Open. 2019 Mar 23;9[3]:e023883. doi: 10.1136/bmjopen-2018-023883).

Everyone in the mental health field as well as patients and their families should know those statistics, but they don’t.

“I think it’s natural for people to think someone who’s been discharged from an inpatient unit or the emergency department is not at risk, when in reality it’s still a high-risk time. Suicide risk is not like a light switch that you can just switch off,” the clinical psychologist observed.

He cited other harrowing statistics that underscore the vast problem of poor care transitions. Nationally, fully one-third of patients don’t complete a single outpatient visit within the first 30 days after discharge from inpatient behavioral health care. And one in seven people who die by suicide have had contact with inpatient mental health services in the year before they died.

“That doesn’t mean that inpatient care did not do everything that they could do. What it does reflect is the need to make sure that there’s follow-up care after inpatient discharge. Too often, people don’t get the follow-up care that they need. And the research literature is clear that intervention can save lives,” Dr. McKeon said.

Panelist Becky Stoll, LCSW, vice president for crisis and disaster management at Centerstone Health in Nashville, Tenn., noted, “We see a lot of no-shows on the outpatient side, because nobody ever asked the patients if they can actually get to the outpatient appointment that’s been made.

“We have got to figure out this care transition and do better. The road to mental health is paved with Swiss cheese. There are so many holes to fall into, even if you know how to navigate the system – and most of the people we’re serving don’t know how,” observed Ms. Stoll, who, like Dr. McKeon, was among the coauthors of the alliance’s guidelines on best practices in care transitions. Ms. Stoll also serves on the AAS board as crisis services division chair.* 

The National Action Alliance for Suicide Prevention is a public/private partnership whose goal is to advance the National Strategy for Suicide Prevention, which was developed by the alliance and the U.S. Surgeon General. The alliance includes mental health professionals as well as influential leaders from the military, journalism, entertainment, railroad, health insurance, law enforcement, defense, education, technology, and other industries.

Dr. McKeon and Ms. Stall were joined by Karen Johnson, MSW, another coauthor of the guidelines. They shared highlights of the report.

Inpatient provider strategies

Discharge and crisis safety planning should begin upon admission, according to Ms. Johnson, senior vice president for clinical services and division compliance at Universal Health Services, which owns and operates more than 200 behavioral health facilities across the United States.

Inpatient and outpatient care providers need to sit down and develop collaborative protocols and negotiate a memorandum of understanding regarding expectations, which absolutely must include procedures to ensure timely electronic delivery of medical records and other key documents to the outpatient care providers. The inpatient providers need to work collaboratively with the patient, family, and community support resources to develop a safety plan – including reduced access to lethal mean – as part of predischarge planning.

Among the strategies routinely employed on the inpatient side at Universal Health Services are advance scheduling of an initial outpatient appointment within 24-72 hours post discharge. Also, someone on the inpatient team is tasked with connecting with the outpatient provider prior to discharge to develop rapport.

“If our outpatient providers are located in our facility, as many of them are, we ask them to come in and attend inpatient team meetings to identify and meet with patients who are appropriate for continuing care in outpatient settings,” she explained. “A soft, warm handoff is critical.”

At these team meetings, the appropriateness of step-down care in the form of partial hospitalization or intensive outpatient care is weighed. Someone from the inpatient side is charged with maintaining contact with the patient until after the first outpatient appointment. Ongoing caring contact in the form of brief, encouraging postcards, emails, or texts that do not require a response from the patient should be maintained for several months.
 

Strategies for outpatient providers

Ms. Stoll is a big believer in the guideline-recommended practice of notifying the inpatient provider that the patient kept the outpatient appointment, along with having a system for red-flagging no-shows for prompt follow-up by a crisis management team.

She and her colleagues at Centerstone Health have conducted two studies of an intensive patient outreach program designed for the first 30 days of the care transition. The program included many elements of the alliance’s best practices guidelines. The yearlong first study, funded by Blue Cross/Blue Shield of Tennessee, documented zero suicides and 92% freedom from emergency department visits during the care transition period, along with greater than $400,000 savings in health care costs, compared with usual care. The second study, funded by SAMHSA, showed much the same over a 2-year period.

She emphasized that this was not a high-tech, intensive intervention. She characterized it, instead as “high-touch follow-up.

“It’s some staff and a phone and a laptop, nothing fancy, just a person who’s competent and confident and skilled with a laptop. With that, you can do some pretty amazing stuff: Get people what they need, keep them alive, and oh, guess what? You can also save a lot of health care dollars that can be put back into the system,” Ms. Stoll said.

She recognizes that it’s a lot to ask busy outpatient providers to leave their practice during the workday to participate in inpatient team meetings addressing discharge planning, as recommended in the alliance guidelines. But in this regard, she sees a silver lining to the COVID-19 pandemic, in that it forces health professionals to rely upon newly opened channels of telemedicine.

“COVID-19 is giving us an opportunity to do things in a different way. Things don’t just have to be done in person. Now that we’ve opened up new channels of telehealth, I’m really excited that we’re almost in a beta test that we’ve dreamed about for decades, where we can do things in a more innovative way,” she said.

Dr. McKeon agreed that reimbursement issues have long impeded efforts to improve the inpatient to outpatient care transition. He added that it will be really important that adequate reimbursement of remote forms of care remain in place after COVID-19 fades.

“This is exactly the kind of thing that’s needed to improve care transitions,” according to Dr. McKeon.

*This story was updated 7/9/2020.

bjancin@mdedge.com

The Pediatric Hospital Medicine Core Competencies were first published in 2010 to help define a specific body of knowledge and measurable skills needed to practice high quality care for hospitalized pediatric patients across all practice settings.¹ Since then, the number of practicing pediatric hospitalists has grown to a conservative estimate of 3,000 physicians and the scope of practice among pediatric hospitalists has matured.² Pediatric hospitalists are increasingly leading or participating in organizational and national efforts that emphasize interprofessional collaboration and the delivery of high value care to hospitalized children and their caregivers—including innovative and family-centered care models, patient safety and quality improvement initiatives, and research and educational enterprises.^3-8 In response to these changes, the American Board of Medical Specialties designated Pediatric Hospital Medicine (PHM) as a pediatric subspecialty in 2016.

The field of PHM in the United States continues to be supported by three core societies—Society of Hospital Medicine (SHM), American Academy of Pediatrics (AAP), and Academic Pediatric Association (APA). Together, these societies serve as tri-sponsors of the annual Pediatric Hospital Medicine national conference, which now welcomes over 1,200 attendees from the United States and abroad.⁹ Each society also individually sponsors a variety of professional development and continuing medical education activities specific to PHM.

In addition, pediatric hospitalists often serve a pivotal role in teaching learners (medical students, residents, and other health profession students), physician colleagues, and other healthcare professionals on the hospital wards and via institutional educational programs. Nearly 50 institutions in the United States offer graduate medical education training in PHM.¹⁰ The PHM Fellowship Directors Council has developed a standardized curricular framework and entrustable professional activities, which reflect the tenets of competency-based medical education, for use in PHM training programs.^11-13

These changes in the practice environment of pediatric hospitalists, as well as the changing landscape of graduate and continuing medical education in PHM, have informed this revision of The PHM Core Competencies. The purpose of this article is to describe the methodology of the review and revision process.

Revision

The PHM Core Competencies: 2020 Revision provide a framework for graduate and continuing medical education that reflects the current roles and expectations for all pediatric hospitalists in the United States. The acuity and complexity of hospitalized children, the availability of pediatric subspecialty care and other resources, and the institutional orientation towards pediatric populations vary across community, tertiary, and children’s hospital settings. In order to unify the practice of PHM across these environments, The PHM Core Competencies: 2020 Revision address the fundamental and most common components of PHM which are encountered by the majority of practicing pediatric hospitalists, as opposed to an extensive review of all aspects of the field.

The compendium includes 66 chapters on both clinical and nonclinical topics, divided into four sections—Common Clinical Diagnoses and Conditions, Core Skills, Specialized Services, and Healthcare Systems: Supporting and Advancing Child Health (Table 1). Within each chapter is an introductory paragraph and learning objectives in three domains of educational outcomes—cognitive (knowledge), psychomotor (skills), and affective (attitudes)—as well as systems organization and improvement, to reflect the emphasis of PHM practice on improving healthcare systems. The objectives encompass a range of observable behaviors and other attributes, from foundational skills such as taking a history and performing a physical exam to more advanced actions such as participating in the development of care models to support the health of complex patient populations. Implicit in these objectives is the expectation that pediatric hospitalists build on experiences in medical school and residency training to attain a level of competency at the advanced levels of a developmental continuum, such as proficient, expert, or master.¹⁴

The objectives also balance specificity to the topic with a timeless quality, allowing for flexibility both as new information emerges and when applied to various educational activities and learner groups. Each chapter can stand alone, and thus themes recur if one reads the compendium in its entirety. However, in order to reflect related content among the chapters, the appendix contains a list of associated chapters (Chapter Links) for further exploration. In addition, a short reference list is provided in each chapter to reflect the literature and best practices at the time of publication.

Finally, The PHM Core Competencies: 2020 Revision reflect the status of children as a vulnerable population. Care for hospitalized children requires attention to many elements unique to the pediatric population. These include age-based differences in development, behavior, physiology, and prevalence of clinical conditions, the impact of acute and chronic disease states on child development, the use of medications and other medical interventions with limited investigative guidance, and the role of caregivers in decision-making and care delivery. Heightened awareness of these factors is required in the hospital setting, where diagnoses and interventions often include the use of high-risk modalities and require coordination of care across multiple providers.

Project Initiation

Revision of The PHM Core Competencies: 2020 Revision began in early 2017 following SHM’s work on The Core Competencies in Hospital Medicine 2017 Revision.¹⁵ The Executive Committee of the SHM Pediatrics Special Interest Group (SIG) supported the initiation of the revision. The 3 editors from the original compendium created an initial plan for the project that included a proposed timeline, processes for engagement of previously involved experts and new talent, and performance of a needs assessment to guide content selection. The Figure highlights these and other important steps in the revision process.

Editor and Associate Editor Selection

The above editors reviewed best practice examples of roles and responsibilities for editor and associate editor positions from relevant, leading societies and journals. From this review, the editors created an editorial structure specifically for The PHM Core Competencies: 2020 Revision. A new position of Contributing Editor was created to address the need for dedicated attention to the community site perspective and ensure review of all content, within and across chapters, by a pediatric hospitalist who is dedicated to this environment. Solicitation for additional editors and associate editors occurred via the SHM Pediatrics SIG to the wider SHM membership. The criteria for selection included active engagement in regional or national activities related to the growth and operations of PHM, strong organizational and leadership skills, including the ability to manage tasks and foster creativity, among others. In addition, a deliberate effort was made to recruit a diverse editorial cohort, considering geographic location, primary work environment, organizational affiliations, content expertise, time in practice, gender, and other factors.

Chapter Topic Selection

The editors conducted a two-pronged needs assessment related to optimal content for inclusion in The PHM Core Competencies: 2020 Revision. First, the editors reviewed content from conferences, textbooks, and handbooks specific to the field of PHM, including the conference programs for the most recent 5 years of both the annual PHM national conference and annual meetings of PHM’s 3 core societies in the United States—SHM, AAP, and APA. Second, the editors conducted a needs assessment survey with several stakeholder groups, including SHM’s Pediatrics and Medicine-Pediatrics SIGs, AAP Section on Hospital Medicine and its subcommittees, APA Hospital Medicine SIG, PHM Fellowship Directors Council, and PHM Division Directors, with encouragement to pass the survey link to others in the PHM community interested in providing input (Appendix Figure). The solicitation asked for comment on existing chapters and suggestions for new chapters. For any new chapter, respondents were asked to note the intended purpose of the chapter and the anticipated value that chapter would bring to our profession and the children and the caregivers served by pediatric hospitalists.

The entire editorial board then reviewed all of the needs assessment data and considered potential changes (additions or deletions) based on emerging trends in pediatric healthcare, the frequency, relevance, and value of the item across all environments in which pediatric hospitalists function, and the value to or impact on hospitalized children and caregivers. Almost all survey ratings and comments were either incorporated into an existing chapter or used to create a new chapter. There was a paucity of comments related to the deletion of chapters, and thus no chapters were entirely excluded. However, there were several comments supporting the exclusion of the suprapubic bladder tap procedure, and thus related content was eliminated from the relevant section in Core Skills. Of the 66 chapters in this revision, the needs assessment data directly informed the creation of 12 new chapters, as well as adjustments and/or additions to the titles of 7 chapters and the content of 29 chapters. In addition, the title of the Specialized Clinical Services section was changed to Specialized Services to represent that both clinical and nonclinical competencies reside in this section devoted to comprehensive management of these unique patient populations commonly encountered by pediatric hospitalists. Many of these changes are highlighted in Table 2.

Author selection

Authors from the initial work were invited to participate again as author of their given chapter. Subsequently, authors were identified for new chapters and chapters for which previous authors were no longer able to be engaged. Authors with content expertise were found by reviewing content from conferences, textbooks, and handbooks specific to the field of PHM. Any content expert who was not identified as a pediatric hospitalist was paired with a pediatric hospitalist as coauthor. In addition, as with the editorial board, a deliberate effort was made to recruit a diverse author cohort, considering geographic location, primary work environment, time in practice, gender, and other factors.

The editorial board held numerous conference calls to review potential authors, and the SHM Pediatrics SIG was directly engaged to ensure authorship opportunities were extended broadly. This vetting process resulted in a robust author list and included members of all three of PHM’s sponsoring societies in the United States. Once participation was confirmed, authors received an “author packet” detailing the process with the proposed timeline, resources related to writing learning objectives, the past chapter (if applicable), assigned associate editor, and other helpful resources.

Internal and External Review Process

After all chapters were drafted, the editorial board conducted a rigorous, internal review process. Each chapter was reviewed by at least one associate editor and two editors, with a focus on content, scope, and a standard approach to phrasing and formatting. In addition, the contributing editor reviewed all the chapters to ensure the community hospitalist perspective was adequately represented.

Thirty-two agencies and societies were solicited for external review, including both those involved in review of the previous edition and new stakeholder groups. External reviewers were first contacted to ascertain their interest in participating in the review process, and if interested, were provided with information on the review process. Robust feedback was received from the APA Hospital Medicine SIG, SHM Pediatrics and Medicine-Pediatrics SIGs, Association of Pediatric Program Directors Curriculum Committee, and 20 AAP committees, councils, and sections.

The feedback from the external reviewers and subsequent edits for each chapter were reviewed by at least one associate editor, two editors, and the contributing editor. Authors were engaged to address any salient changes recommended. As the final steps in the review process, the SHM Board of Directors approved the compendium and the APA provided their endorsement.

This second edition of The PHM Core Competencies: 2020 Revision addresses the knowledge, skills, attitudes, and systems organization and improvement objectives that define the field of pediatric hospital medicine and the leadership roles of pediatric hospitalists. This compendium reflects the recent changes in the practice and educational environments of pediatric hospitalists and can inform education, training, and career development for pediatric hospitalists across all environments in which comprehensive care is rendered for the hospitalized child. Future work at the local and national level can lead to development of associated curricula, conference content, and other training materials.

Acknowledgments

We wish to humbly and respectfully acknowledge the work of the authors, editors, and reviewers involved in the creation of the first edition, as well as this revision, of The PHM Core Competencies. In addition, we are grateful for the input of all pediatric hospitalists and other stakeholders who informed this compendium via contributions to the needs assessment survey, conference proceedings, publications, and other works. Finally, we acknowledge the support and work of SHM project coordinator, Nyla Nicholson, the SHM Pediatrics SIG, and the SHM Board of Directors.

Disclosures

SHM provided administrative support for project coordination (N. Nicholson). No author, editor, or other involved member received any compensation for efforts related to this work. There are no reported conflicts of interest.

The Pediatric Hospital Medicine Core Competencies were first published in 2010 to help define a specific body of knowledge and measurable skills needed to practice high quality care for hospitalized pediatric patients across all practice settings.¹ Since then, the number of practicing pediatric hospitalists has grown to a conservative estimate of 3,000 physicians and the scope of practice among pediatric hospitalists has matured.² Pediatric hospitalists are increasingly leading or participating in organizational and national efforts that emphasize interprofessional collaboration and the delivery of high value care to hospitalized children and their caregivers—including innovative and family-centered care models, patient safety and quality improvement initiatives, and research and educational enterprises.^3-8 In response to these changes, the American Board of Medical Specialties designated Pediatric Hospital Medicine (PHM) as a pediatric subspecialty in 2016.

The field of PHM in the United States continues to be supported by three core societies—Society of Hospital Medicine (SHM), American Academy of Pediatrics (AAP), and Academic Pediatric Association (APA). Together, these societies serve as tri-sponsors of the annual Pediatric Hospital Medicine national conference, which now welcomes over 1,200 attendees from the United States and abroad.⁹ Each society also individually sponsors a variety of professional development and continuing medical education activities specific to PHM.

In addition, pediatric hospitalists often serve a pivotal role in teaching learners (medical students, residents, and other health profession students), physician colleagues, and other healthcare professionals on the hospital wards and via institutional educational programs. Nearly 50 institutions in the United States offer graduate medical education training in PHM.¹⁰ The PHM Fellowship Directors Council has developed a standardized curricular framework and entrustable professional activities, which reflect the tenets of competency-based medical education, for use in PHM training programs.^11-13

These changes in the practice environment of pediatric hospitalists, as well as the changing landscape of graduate and continuing medical education in PHM, have informed this revision of The PHM Core Competencies. The purpose of this article is to describe the methodology of the review and revision process.

Revision

The PHM Core Competencies: 2020 Revision provide a framework for graduate and continuing medical education that reflects the current roles and expectations for all pediatric hospitalists in the United States. The acuity and complexity of hospitalized children, the availability of pediatric subspecialty care and other resources, and the institutional orientation towards pediatric populations vary across community, tertiary, and children’s hospital settings. In order to unify the practice of PHM across these environments, The PHM Core Competencies: 2020 Revision address the fundamental and most common components of PHM which are encountered by the majority of practicing pediatric hospitalists, as opposed to an extensive review of all aspects of the field.

The compendium includes 66 chapters on both clinical and nonclinical topics, divided into four sections—Common Clinical Diagnoses and Conditions, Core Skills, Specialized Services, and Healthcare Systems: Supporting and Advancing Child Health (Table 1). Within each chapter is an introductory paragraph and learning objectives in three domains of educational outcomes—cognitive (knowledge), psychomotor (skills), and affective (attitudes)—as well as systems organization and improvement, to reflect the emphasis of PHM practice on improving healthcare systems. The objectives encompass a range of observable behaviors and other attributes, from foundational skills such as taking a history and performing a physical exam to more advanced actions such as participating in the development of care models to support the health of complex patient populations. Implicit in these objectives is the expectation that pediatric hospitalists build on experiences in medical school and residency training to attain a level of competency at the advanced levels of a developmental continuum, such as proficient, expert, or master.¹⁴

The objectives also balance specificity to the topic with a timeless quality, allowing for flexibility both as new information emerges and when applied to various educational activities and learner groups. Each chapter can stand alone, and thus themes recur if one reads the compendium in its entirety. However, in order to reflect related content among the chapters, the appendix contains a list of associated chapters (Chapter Links) for further exploration. In addition, a short reference list is provided in each chapter to reflect the literature and best practices at the time of publication.

Finally, The PHM Core Competencies: 2020 Revision reflect the status of children as a vulnerable population. Care for hospitalized children requires attention to many elements unique to the pediatric population. These include age-based differences in development, behavior, physiology, and prevalence of clinical conditions, the impact of acute and chronic disease states on child development, the use of medications and other medical interventions with limited investigative guidance, and the role of caregivers in decision-making and care delivery. Heightened awareness of these factors is required in the hospital setting, where diagnoses and interventions often include the use of high-risk modalities and require coordination of care across multiple providers.

Project Initiation

Revision of The PHM Core Competencies: 2020 Revision began in early 2017 following SHM’s work on The Core Competencies in Hospital Medicine 2017 Revision.¹⁵ The Executive Committee of the SHM Pediatrics Special Interest Group (SIG) supported the initiation of the revision. The 3 editors from the original compendium created an initial plan for the project that included a proposed timeline, processes for engagement of previously involved experts and new talent, and performance of a needs assessment to guide content selection. The Figure highlights these and other important steps in the revision process.

Editor and Associate Editor Selection

The above editors reviewed best practice examples of roles and responsibilities for editor and associate editor positions from relevant, leading societies and journals. From this review, the editors created an editorial structure specifically for The PHM Core Competencies: 2020 Revision. A new position of Contributing Editor was created to address the need for dedicated attention to the community site perspective and ensure review of all content, within and across chapters, by a pediatric hospitalist who is dedicated to this environment. Solicitation for additional editors and associate editors occurred via the SHM Pediatrics SIG to the wider SHM membership. The criteria for selection included active engagement in regional or national activities related to the growth and operations of PHM, strong organizational and leadership skills, including the ability to manage tasks and foster creativity, among others. In addition, a deliberate effort was made to recruit a diverse editorial cohort, considering geographic location, primary work environment, organizational affiliations, content expertise, time in practice, gender, and other factors.

Chapter Topic Selection

The editors conducted a two-pronged needs assessment related to optimal content for inclusion in The PHM Core Competencies: 2020 Revision. First, the editors reviewed content from conferences, textbooks, and handbooks specific to the field of PHM, including the conference programs for the most recent 5 years of both the annual PHM national conference and annual meetings of PHM’s 3 core societies in the United States—SHM, AAP, and APA. Second, the editors conducted a needs assessment survey with several stakeholder groups, including SHM’s Pediatrics and Medicine-Pediatrics SIGs, AAP Section on Hospital Medicine and its subcommittees, APA Hospital Medicine SIG, PHM Fellowship Directors Council, and PHM Division Directors, with encouragement to pass the survey link to others in the PHM community interested in providing input (Appendix Figure). The solicitation asked for comment on existing chapters and suggestions for new chapters. For any new chapter, respondents were asked to note the intended purpose of the chapter and the anticipated value that chapter would bring to our profession and the children and the caregivers served by pediatric hospitalists.

The entire editorial board then reviewed all of the needs assessment data and considered potential changes (additions or deletions) based on emerging trends in pediatric healthcare, the frequency, relevance, and value of the item across all environments in which pediatric hospitalists function, and the value to or impact on hospitalized children and caregivers. Almost all survey ratings and comments were either incorporated into an existing chapter or used to create a new chapter. There was a paucity of comments related to the deletion of chapters, and thus no chapters were entirely excluded. However, there were several comments supporting the exclusion of the suprapubic bladder tap procedure, and thus related content was eliminated from the relevant section in Core Skills. Of the 66 chapters in this revision, the needs assessment data directly informed the creation of 12 new chapters, as well as adjustments and/or additions to the titles of 7 chapters and the content of 29 chapters. In addition, the title of the Specialized Clinical Services section was changed to Specialized Services to represent that both clinical and nonclinical competencies reside in this section devoted to comprehensive management of these unique patient populations commonly encountered by pediatric hospitalists. Many of these changes are highlighted in Table 2.

Author selection

Authors from the initial work were invited to participate again as author of their given chapter. Subsequently, authors were identified for new chapters and chapters for which previous authors were no longer able to be engaged. Authors with content expertise were found by reviewing content from conferences, textbooks, and handbooks specific to the field of PHM. Any content expert who was not identified as a pediatric hospitalist was paired with a pediatric hospitalist as coauthor. In addition, as with the editorial board, a deliberate effort was made to recruit a diverse author cohort, considering geographic location, primary work environment, time in practice, gender, and other factors.

The editorial board held numerous conference calls to review potential authors, and the SHM Pediatrics SIG was directly engaged to ensure authorship opportunities were extended broadly. This vetting process resulted in a robust author list and included members of all three of PHM’s sponsoring societies in the United States. Once participation was confirmed, authors received an “author packet” detailing the process with the proposed timeline, resources related to writing learning objectives, the past chapter (if applicable), assigned associate editor, and other helpful resources.

Internal and External Review Process

After all chapters were drafted, the editorial board conducted a rigorous, internal review process. Each chapter was reviewed by at least one associate editor and two editors, with a focus on content, scope, and a standard approach to phrasing and formatting. In addition, the contributing editor reviewed all the chapters to ensure the community hospitalist perspective was adequately represented.

Thirty-two agencies and societies were solicited for external review, including both those involved in review of the previous edition and new stakeholder groups. External reviewers were first contacted to ascertain their interest in participating in the review process, and if interested, were provided with information on the review process. Robust feedback was received from the APA Hospital Medicine SIG, SHM Pediatrics and Medicine-Pediatrics SIGs, Association of Pediatric Program Directors Curriculum Committee, and 20 AAP committees, councils, and sections.

The feedback from the external reviewers and subsequent edits for each chapter were reviewed by at least one associate editor, two editors, and the contributing editor. Authors were engaged to address any salient changes recommended. As the final steps in the review process, the SHM Board of Directors approved the compendium and the APA provided their endorsement.

This second edition of The PHM Core Competencies: 2020 Revision addresses the knowledge, skills, attitudes, and systems organization and improvement objectives that define the field of pediatric hospital medicine and the leadership roles of pediatric hospitalists. This compendium reflects the recent changes in the practice and educational environments of pediatric hospitalists and can inform education, training, and career development for pediatric hospitalists across all environments in which comprehensive care is rendered for the hospitalized child. Future work at the local and national level can lead to development of associated curricula, conference content, and other training materials.

Acknowledgments

We wish to humbly and respectfully acknowledge the work of the authors, editors, and reviewers involved in the creation of the first edition, as well as this revision, of The PHM Core Competencies. In addition, we are grateful for the input of all pediatric hospitalists and other stakeholders who informed this compendium via contributions to the needs assessment survey, conference proceedings, publications, and other works. Finally, we acknowledge the support and work of SHM project coordinator, Nyla Nicholson, the SHM Pediatrics SIG, and the SHM Board of Directors.

Disclosures

SHM provided administrative support for project coordination (N. Nicholson). No author, editor, or other involved member received any compensation for efforts related to this work. There are no reported conflicts of interest.

The Pediatric Hospital Medicine Core Competencies were first published in 2010 to help define a specific body of knowledge and measurable skills needed to practice high quality care for hospitalized pediatric patients across all practice settings.¹ Since then, the number of practicing pediatric hospitalists has grown to a conservative estimate of 3,000 physicians and the scope of practice among pediatric hospitalists has matured.² Pediatric hospitalists are increasingly leading or participating in organizational and national efforts that emphasize interprofessional collaboration and the delivery of high value care to hospitalized children and their caregivers—including innovative and family-centered care models, patient safety and quality improvement initiatives, and research and educational enterprises.^3-8 In response to these changes, the American Board of Medical Specialties designated Pediatric Hospital Medicine (PHM) as a pediatric subspecialty in 2016.

The field of PHM in the United States continues to be supported by three core societies—Society of Hospital Medicine (SHM), American Academy of Pediatrics (AAP), and Academic Pediatric Association (APA). Together, these societies serve as tri-sponsors of the annual Pediatric Hospital Medicine national conference, which now welcomes over 1,200 attendees from the United States and abroad.⁹ Each society also individually sponsors a variety of professional development and continuing medical education activities specific to PHM.

In addition, pediatric hospitalists often serve a pivotal role in teaching learners (medical students, residents, and other health profession students), physician colleagues, and other healthcare professionals on the hospital wards and via institutional educational programs. Nearly 50 institutions in the United States offer graduate medical education training in PHM.¹⁰ The PHM Fellowship Directors Council has developed a standardized curricular framework and entrustable professional activities, which reflect the tenets of competency-based medical education, for use in PHM training programs.^11-13

These changes in the practice environment of pediatric hospitalists, as well as the changing landscape of graduate and continuing medical education in PHM, have informed this revision of The PHM Core Competencies. The purpose of this article is to describe the methodology of the review and revision process.

Revision

The PHM Core Competencies: 2020 Revision provide a framework for graduate and continuing medical education that reflects the current roles and expectations for all pediatric hospitalists in the United States. The acuity and complexity of hospitalized children, the availability of pediatric subspecialty care and other resources, and the institutional orientation towards pediatric populations vary across community, tertiary, and children’s hospital settings. In order to unify the practice of PHM across these environments, The PHM Core Competencies: 2020 Revision address the fundamental and most common components of PHM which are encountered by the majority of practicing pediatric hospitalists, as opposed to an extensive review of all aspects of the field.

The compendium includes 66 chapters on both clinical and nonclinical topics, divided into four sections—Common Clinical Diagnoses and Conditions, Core Skills, Specialized Services, and Healthcare Systems: Supporting and Advancing Child Health (Table 1). Within each chapter is an introductory paragraph and learning objectives in three domains of educational outcomes—cognitive (knowledge), psychomotor (skills), and affective (attitudes)—as well as systems organization and improvement, to reflect the emphasis of PHM practice on improving healthcare systems. The objectives encompass a range of observable behaviors and other attributes, from foundational skills such as taking a history and performing a physical exam to more advanced actions such as participating in the development of care models to support the health of complex patient populations. Implicit in these objectives is the expectation that pediatric hospitalists build on experiences in medical school and residency training to attain a level of competency at the advanced levels of a developmental continuum, such as proficient, expert, or master.¹⁴

The objectives also balance specificity to the topic with a timeless quality, allowing for flexibility both as new information emerges and when applied to various educational activities and learner groups. Each chapter can stand alone, and thus themes recur if one reads the compendium in its entirety. However, in order to reflect related content among the chapters, the appendix contains a list of associated chapters (Chapter Links) for further exploration. In addition, a short reference list is provided in each chapter to reflect the literature and best practices at the time of publication.

Finally, The PHM Core Competencies: 2020 Revision reflect the status of children as a vulnerable population. Care for hospitalized children requires attention to many elements unique to the pediatric population. These include age-based differences in development, behavior, physiology, and prevalence of clinical conditions, the impact of acute and chronic disease states on child development, the use of medications and other medical interventions with limited investigative guidance, and the role of caregivers in decision-making and care delivery. Heightened awareness of these factors is required in the hospital setting, where diagnoses and interventions often include the use of high-risk modalities and require coordination of care across multiple providers.

Project Initiation

Revision of The PHM Core Competencies: 2020 Revision began in early 2017 following SHM’s work on The Core Competencies in Hospital Medicine 2017 Revision.¹⁵ The Executive Committee of the SHM Pediatrics Special Interest Group (SIG) supported the initiation of the revision. The 3 editors from the original compendium created an initial plan for the project that included a proposed timeline, processes for engagement of previously involved experts and new talent, and performance of a needs assessment to guide content selection. The Figure highlights these and other important steps in the revision process.

Editor and Associate Editor Selection

The above editors reviewed best practice examples of roles and responsibilities for editor and associate editor positions from relevant, leading societies and journals. From this review, the editors created an editorial structure specifically for The PHM Core Competencies: 2020 Revision. A new position of Contributing Editor was created to address the need for dedicated attention to the community site perspective and ensure review of all content, within and across chapters, by a pediatric hospitalist who is dedicated to this environment. Solicitation for additional editors and associate editors occurred via the SHM Pediatrics SIG to the wider SHM membership. The criteria for selection included active engagement in regional or national activities related to the growth and operations of PHM, strong organizational and leadership skills, including the ability to manage tasks and foster creativity, among others. In addition, a deliberate effort was made to recruit a diverse editorial cohort, considering geographic location, primary work environment, organizational affiliations, content expertise, time in practice, gender, and other factors.

Chapter Topic Selection

The editors conducted a two-pronged needs assessment related to optimal content for inclusion in The PHM Core Competencies: 2020 Revision. First, the editors reviewed content from conferences, textbooks, and handbooks specific to the field of PHM, including the conference programs for the most recent 5 years of both the annual PHM national conference and annual meetings of PHM’s 3 core societies in the United States—SHM, AAP, and APA. Second, the editors conducted a needs assessment survey with several stakeholder groups, including SHM’s Pediatrics and Medicine-Pediatrics SIGs, AAP Section on Hospital Medicine and its subcommittees, APA Hospital Medicine SIG, PHM Fellowship Directors Council, and PHM Division Directors, with encouragement to pass the survey link to others in the PHM community interested in providing input (Appendix Figure). The solicitation asked for comment on existing chapters and suggestions for new chapters. For any new chapter, respondents were asked to note the intended purpose of the chapter and the anticipated value that chapter would bring to our profession and the children and the caregivers served by pediatric hospitalists.

The entire editorial board then reviewed all of the needs assessment data and considered potential changes (additions or deletions) based on emerging trends in pediatric healthcare, the frequency, relevance, and value of the item across all environments in which pediatric hospitalists function, and the value to or impact on hospitalized children and caregivers. Almost all survey ratings and comments were either incorporated into an existing chapter or used to create a new chapter. There was a paucity of comments related to the deletion of chapters, and thus no chapters were entirely excluded. However, there were several comments supporting the exclusion of the suprapubic bladder tap procedure, and thus related content was eliminated from the relevant section in Core Skills. Of the 66 chapters in this revision, the needs assessment data directly informed the creation of 12 new chapters, as well as adjustments and/or additions to the titles of 7 chapters and the content of 29 chapters. In addition, the title of the Specialized Clinical Services section was changed to Specialized Services to represent that both clinical and nonclinical competencies reside in this section devoted to comprehensive management of these unique patient populations commonly encountered by pediatric hospitalists. Many of these changes are highlighted in Table 2.

Author selection

Authors from the initial work were invited to participate again as author of their given chapter. Subsequently, authors were identified for new chapters and chapters for which previous authors were no longer able to be engaged. Authors with content expertise were found by reviewing content from conferences, textbooks, and handbooks specific to the field of PHM. Any content expert who was not identified as a pediatric hospitalist was paired with a pediatric hospitalist as coauthor. In addition, as with the editorial board, a deliberate effort was made to recruit a diverse author cohort, considering geographic location, primary work environment, time in practice, gender, and other factors.

The editorial board held numerous conference calls to review potential authors, and the SHM Pediatrics SIG was directly engaged to ensure authorship opportunities were extended broadly. This vetting process resulted in a robust author list and included members of all three of PHM’s sponsoring societies in the United States. Once participation was confirmed, authors received an “author packet” detailing the process with the proposed timeline, resources related to writing learning objectives, the past chapter (if applicable), assigned associate editor, and other helpful resources.

Internal and External Review Process

After all chapters were drafted, the editorial board conducted a rigorous, internal review process. Each chapter was reviewed by at least one associate editor and two editors, with a focus on content, scope, and a standard approach to phrasing and formatting. In addition, the contributing editor reviewed all the chapters to ensure the community hospitalist perspective was adequately represented.

Thirty-two agencies and societies were solicited for external review, including both those involved in review of the previous edition and new stakeholder groups. External reviewers were first contacted to ascertain their interest in participating in the review process, and if interested, were provided with information on the review process. Robust feedback was received from the APA Hospital Medicine SIG, SHM Pediatrics and Medicine-Pediatrics SIGs, Association of Pediatric Program Directors Curriculum Committee, and 20 AAP committees, councils, and sections.

The feedback from the external reviewers and subsequent edits for each chapter were reviewed by at least one associate editor, two editors, and the contributing editor. Authors were engaged to address any salient changes recommended. As the final steps in the review process, the SHM Board of Directors approved the compendium and the APA provided their endorsement.

This second edition of The PHM Core Competencies: 2020 Revision addresses the knowledge, skills, attitudes, and systems organization and improvement objectives that define the field of pediatric hospital medicine and the leadership roles of pediatric hospitalists. This compendium reflects the recent changes in the practice and educational environments of pediatric hospitalists and can inform education, training, and career development for pediatric hospitalists across all environments in which comprehensive care is rendered for the hospitalized child. Future work at the local and national level can lead to development of associated curricula, conference content, and other training materials.

Acknowledgments

We wish to humbly and respectfully acknowledge the work of the authors, editors, and reviewers involved in the creation of the first edition, as well as this revision, of The PHM Core Competencies. In addition, we are grateful for the input of all pediatric hospitalists and other stakeholders who informed this compendium via contributions to the needs assessment survey, conference proceedings, publications, and other works. Finally, we acknowledge the support and work of SHM project coordinator, Nyla Nicholson, the SHM Pediatrics SIG, and the SHM Board of Directors.

Disclosures

SHM provided administrative support for project coordination (N. Nicholson). No author, editor, or other involved member received any compensation for efforts related to this work. There are no reported conflicts of interest.

“Nothing about us without us” (Latin: ”Nihil de nobis, sine nobis”)

Hospitalists are at the forefront of decisions, innovations, and system-improvement projects that impact hospitalized patients. However, many of our decisions—while centered on patient care—fail to include their perspectives or views.

In his book Total Leadership, Stewart Friedman describes the importance of identifying and engaging key stakeholders.¹ Friedman exhorts leaders to engage stakeholders in conversations to “confirm or correct your current understanding of stakeholder expectations.” In other words, instead of assuming what stakeholders want, ask and verify before proceeding.

Although hospitalists frequently include stakeholders such as nurses, pharmacists, and therapists in system-improvement initiatives, engaging patients is less common.

Why do we omit patients as stakeholders? There are considerable barriers to seeking patient input. The busy hospital environment or the acuity of a patient’s illness may, for instance, limit engagement between hospital caregivers and patients. Further, the power imbalance between physicians and patients may make it uncomfortable for the patient to offer direct feedback.

However, the importance of patient input is increasingly recognized by researchers. For example, community-based participatory research “involves community members or recipients of interventions in all phases of the research process.”² Similarly, we believe hospitalists should engage patients when designing new clinical initiatives.

Examples from some institutions provide further support of this concept. The Dana Farber Cancer Institute created a patient and family advisory council in response to the loss of trust over errors and in the face of community outrage over an impending joint venture. While the scope was initially limited to the collection of feedback regarding patient satisfaction and preferences, the council evolved to become an integral part of organizational decision making. Patient contributions were subsequently assimilated into policies, continuous improvement teams, and even search committees. Additional benefits included patient-generated initiatives such as “patient rounds.”³ Specifically soliciting input from hospitalized patients to inform hospital-based interventions may be uncommon, but this practice holds the potential to yield vital insights.⁴

We have experienced this benefit at our institution. For example, before implementing an inpatient addiction medicine consult service, we asked hospitalized patients struggling with addiction about their needs. The patient voice highlighted a lack of trust for hospital providers and led directly to the inclusion of peer-recovery mentors as part of the consulting team.⁵

Many organizations, including our own, have instituted a patient/family advisory committee comprising former patients and family members who participate voluntarily in projects and provide input. This resource can serve as an excellent platform for patient involvement. At the University of Michigan, the patient and family advisory council provides input on every major institutional decision, from the construction of a new building to the introduction of a new clinical service. This “hardwired” practice ensures that patients’ voices and views are incorporated into major health system decisions.

In order to engage patients as stakeholders, we recommend: (1) Be sensitive to the power imbalance between clinicians and patients and recognize that hospitalized patients may not feel comfortable providing direct feedback. (2) Familiarize yourself with your institution’s patient/family advisory committee. If one does not exist, consider soliciting responses from patients via interviews and/or postdischarge surveys. (3) Deliberately seek the opinions, experience, and values of patients or their representatives. (4) For projects aimed at improving patient experience, include patients among your key stakeholders.

Involving patients as stakeholders requires effort; however, it has potential to reap valuable rewards, making healthcare improvements more effective, inclusive, and healing.

The authors wish to thank Jeffrey S. Stewart for his contributions and feedback on this topic and manuscript.

The authors have nothing to disclose.

“Nothing about us without us” (Latin: ”Nihil de nobis, sine nobis”)

Hospitalists are at the forefront of decisions, innovations, and system-improvement projects that impact hospitalized patients. However, many of our decisions—while centered on patient care—fail to include their perspectives or views.

In his book Total Leadership, Stewart Friedman describes the importance of identifying and engaging key stakeholders.¹ Friedman exhorts leaders to engage stakeholders in conversations to “confirm or correct your current understanding of stakeholder expectations.” In other words, instead of assuming what stakeholders want, ask and verify before proceeding.

Although hospitalists frequently include stakeholders such as nurses, pharmacists, and therapists in system-improvement initiatives, engaging patients is less common.

Why do we omit patients as stakeholders? There are considerable barriers to seeking patient input. The busy hospital environment or the acuity of a patient’s illness may, for instance, limit engagement between hospital caregivers and patients. Further, the power imbalance between physicians and patients may make it uncomfortable for the patient to offer direct feedback.

However, the importance of patient input is increasingly recognized by researchers. For example, community-based participatory research “involves community members or recipients of interventions in all phases of the research process.”² Similarly, we believe hospitalists should engage patients when designing new clinical initiatives.

Examples from some institutions provide further support of this concept. The Dana Farber Cancer Institute created a patient and family advisory council in response to the loss of trust over errors and in the face of community outrage over an impending joint venture. While the scope was initially limited to the collection of feedback regarding patient satisfaction and preferences, the council evolved to become an integral part of organizational decision making. Patient contributions were subsequently assimilated into policies, continuous improvement teams, and even search committees. Additional benefits included patient-generated initiatives such as “patient rounds.”³ Specifically soliciting input from hospitalized patients to inform hospital-based interventions may be uncommon, but this practice holds the potential to yield vital insights.⁴

We have experienced this benefit at our institution. For example, before implementing an inpatient addiction medicine consult service, we asked hospitalized patients struggling with addiction about their needs. The patient voice highlighted a lack of trust for hospital providers and led directly to the inclusion of peer-recovery mentors as part of the consulting team.⁵

Many organizations, including our own, have instituted a patient/family advisory committee comprising former patients and family members who participate voluntarily in projects and provide input. This resource can serve as an excellent platform for patient involvement. At the University of Michigan, the patient and family advisory council provides input on every major institutional decision, from the construction of a new building to the introduction of a new clinical service. This “hardwired” practice ensures that patients’ voices and views are incorporated into major health system decisions.

In order to engage patients as stakeholders, we recommend: (1) Be sensitive to the power imbalance between clinicians and patients and recognize that hospitalized patients may not feel comfortable providing direct feedback. (2) Familiarize yourself with your institution’s patient/family advisory committee. If one does not exist, consider soliciting responses from patients via interviews and/or postdischarge surveys. (3) Deliberately seek the opinions, experience, and values of patients or their representatives. (4) For projects aimed at improving patient experience, include patients among your key stakeholders.

Involving patients as stakeholders requires effort; however, it has potential to reap valuable rewards, making healthcare improvements more effective, inclusive, and healing.

The authors wish to thank Jeffrey S. Stewart for his contributions and feedback on this topic and manuscript.

The authors have nothing to disclose.

“Nothing about us without us” (Latin: ”Nihil de nobis, sine nobis”)

Hospitalists are at the forefront of decisions, innovations, and system-improvement projects that impact hospitalized patients. However, many of our decisions—while centered on patient care—fail to include their perspectives or views.

In his book Total Leadership, Stewart Friedman describes the importance of identifying and engaging key stakeholders.¹ Friedman exhorts leaders to engage stakeholders in conversations to “confirm or correct your current understanding of stakeholder expectations.” In other words, instead of assuming what stakeholders want, ask and verify before proceeding.

Although hospitalists frequently include stakeholders such as nurses, pharmacists, and therapists in system-improvement initiatives, engaging patients is less common.

Why do we omit patients as stakeholders? There are considerable barriers to seeking patient input. The busy hospital environment or the acuity of a patient’s illness may, for instance, limit engagement between hospital caregivers and patients. Further, the power imbalance between physicians and patients may make it uncomfortable for the patient to offer direct feedback.

However, the importance of patient input is increasingly recognized by researchers. For example, community-based participatory research “involves community members or recipients of interventions in all phases of the research process.”² Similarly, we believe hospitalists should engage patients when designing new clinical initiatives.

Examples from some institutions provide further support of this concept. The Dana Farber Cancer Institute created a patient and family advisory council in response to the loss of trust over errors and in the face of community outrage over an impending joint venture. While the scope was initially limited to the collection of feedback regarding patient satisfaction and preferences, the council evolved to become an integral part of organizational decision making. Patient contributions were subsequently assimilated into policies, continuous improvement teams, and even search committees. Additional benefits included patient-generated initiatives such as “patient rounds.”³ Specifically soliciting input from hospitalized patients to inform hospital-based interventions may be uncommon, but this practice holds the potential to yield vital insights.⁴

We have experienced this benefit at our institution. For example, before implementing an inpatient addiction medicine consult service, we asked hospitalized patients struggling with addiction about their needs. The patient voice highlighted a lack of trust for hospital providers and led directly to the inclusion of peer-recovery mentors as part of the consulting team.⁵

Many organizations, including our own, have instituted a patient/family advisory committee comprising former patients and family members who participate voluntarily in projects and provide input. This resource can serve as an excellent platform for patient involvement. At the University of Michigan, the patient and family advisory council provides input on every major institutional decision, from the construction of a new building to the introduction of a new clinical service. This “hardwired” practice ensures that patients’ voices and views are incorporated into major health system decisions.

In order to engage patients as stakeholders, we recommend: (1) Be sensitive to the power imbalance between clinicians and patients and recognize that hospitalized patients may not feel comfortable providing direct feedback. (2) Familiarize yourself with your institution’s patient/family advisory committee. If one does not exist, consider soliciting responses from patients via interviews and/or postdischarge surveys. (3) Deliberately seek the opinions, experience, and values of patients or their representatives. (4) For projects aimed at improving patient experience, include patients among your key stakeholders.

Involving patients as stakeholders requires effort; however, it has potential to reap valuable rewards, making healthcare improvements more effective, inclusive, and healing.

The authors wish to thank Jeffrey S. Stewart for his contributions and feedback on this topic and manuscript.

The authors have nothing to disclose.

The ability to detect myocardial injury has never been more advanced. With the availability of high-­sensitivity troponin testing, microscopic evidence of myocyte death can now be detected, often within an hour or so of the inciting event. This, in turn, has facilitated quicker and more accurate identification and treatment of affected patients. However, these advances in detection have, in some cases, outstripped our understanding of the etiology and appropriate management of troponin elevation.

This dilemma is particularly apparent among patients undergoing noncardiac surgery. Annually, over 200 million of these surgeries occur worldwide, many in patients with elevated cardiac risk or overt cardiac disease. Naturally, physicians treating these patients are concerned that the stress of surgery will provoke myocardial injury. Since symptoms are often masked in the immediate postoperative period because of sedating or analgesic medications, many physicians rely on troponin testing to detect signs of myocardial injury. With the increased sensitivity of these assays, the prevalence of troponin elevation has increased, which currently affects nearly one in five postoperative patients. This knowledge, however, doesn’t lend itself to a clear management strategy, particularly in those patients with no other objective evidence of infarction. To paraphrase T.S. Eliot, have we lost the wisdom in our knowledge?

In this journal issue, Cohn and colleagues summarize the current information around this phenomenon of myocardial injury after noncardiac surgery, or MINS.¹ Consistent with the literature, they define MINS as an acute rise and/or fall in troponin (above the assay’s upper limit of normal) at any point in the 30 days following noncardiac surgery. Importantly, MINS is an umbrella term that can indicate either a myocardial infarction (MI) or nonischemic myocardial injury (NIMI). An MI exists if there are clinical signs of ischemia and/or objective evidence of infarction on imaging.

The authors found that MINS is highly prevalent (19.6%) and associated with both cardiac disease and perioperative hemodynamic stress. Between 2.9% and 13.5% of MINS patients experienced 30-day adverse cardiac events, with higher rates in patients with higher troponin elevations and/or accompanying ischemic symptoms. The authors suggested MINS management with standard cardio-protective medications, such as statins, beta-blockers, and angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers. For those patients at low bleeding risk, they also suggested dabigatran based on the recent MANAGE trial. Finally, they noted that US cardiac society guidelines suggested no screening for MINS, while the European and Canadian guidelines advocated for screening in patients at high risk for cardiac complications.

The authors are to be congratulated for highlighting an important and vexing area of postoperative management. To date, it has been difficult to chart the best path forward for these patients because we could “see” the issue, thanks to increasingly sensitive troponin assays, but we didn’t know what to do once we found it.

So what rationale exists to justify screening? Some advocate that the presence of MINS suggests a need for further imaging and closer monitoring of these patients to identify those with an MI. Indeed, several recent MINS registry studies have found that 20% to 40% of MINS patients had definitive evidence of MI.^2-4 But what about those patients with troponin elevation and no evidence of MI? A small, propensity-matched, observational study of MINS patients, including those without MI, noted positive associations between cardioprotective medications, such as aspirin and statins, and cardiac outcomes.⁵ In addition, the MANAGE trial suggested that MINS patients, with or without evidence of an MI, receiving dabigatran had reduced vascular events without increased bleeding complications.⁶ With this growing base of evidence, the rationale for systematic screening for MINS appears to be standing on stronger footing.

As noted by the authors, the recommendations for MINS screening differ across three major cardiovascular societies. How does the practicing clinician make sense of this discordant advice? Differences often occur when the evidence is of moderate or low quality, which means guideline committees must make their own interpretations of equivocal findings. Another driver of discordant recommendations is the timing of the guidelines. Both the US and European guidelines were published in 2014, while the Canadian guidelines were published in 2017. Over time, experience with postoperative troponin testing increased, which may have influenced the Canadian guidelines. Finally, many members of the Canadian guideline writing committee were the ones conducting the various studies identifying management options for MINS patients, which may have guided their ultimate recommendation. Regardless, practicing physicians should collectively view the guidelines as acceptable “guardrails” to guide their practice. Selection of the appropriate strategy can then be tailored to the individual patient’s risks and benefits, as well as available management options.

In this era of high-sensitivity troponin testing, we now possess an exquisite opportunity to “see” minute levels of myocardial injury among postoperative patients. Our growing ability to effectively act on this knowledge will enable us to make wise decisions with our patients to optimize their cardiac outcomes during the vulnerable postoperative period.

The ability to detect myocardial injury has never been more advanced. With the availability of high-­sensitivity troponin testing, microscopic evidence of myocyte death can now be detected, often within an hour or so of the inciting event. This, in turn, has facilitated quicker and more accurate identification and treatment of affected patients. However, these advances in detection have, in some cases, outstripped our understanding of the etiology and appropriate management of troponin elevation.

This dilemma is particularly apparent among patients undergoing noncardiac surgery. Annually, over 200 million of these surgeries occur worldwide, many in patients with elevated cardiac risk or overt cardiac disease. Naturally, physicians treating these patients are concerned that the stress of surgery will provoke myocardial injury. Since symptoms are often masked in the immediate postoperative period because of sedating or analgesic medications, many physicians rely on troponin testing to detect signs of myocardial injury. With the increased sensitivity of these assays, the prevalence of troponin elevation has increased, which currently affects nearly one in five postoperative patients. This knowledge, however, doesn’t lend itself to a clear management strategy, particularly in those patients with no other objective evidence of infarction. To paraphrase T.S. Eliot, have we lost the wisdom in our knowledge?

In this journal issue, Cohn and colleagues summarize the current information around this phenomenon of myocardial injury after noncardiac surgery, or MINS.¹ Consistent with the literature, they define MINS as an acute rise and/or fall in troponin (above the assay’s upper limit of normal) at any point in the 30 days following noncardiac surgery. Importantly, MINS is an umbrella term that can indicate either a myocardial infarction (MI) or nonischemic myocardial injury (NIMI). An MI exists if there are clinical signs of ischemia and/or objective evidence of infarction on imaging.

The authors found that MINS is highly prevalent (19.6%) and associated with both cardiac disease and perioperative hemodynamic stress. Between 2.9% and 13.5% of MINS patients experienced 30-day adverse cardiac events, with higher rates in patients with higher troponin elevations and/or accompanying ischemic symptoms. The authors suggested MINS management with standard cardio-protective medications, such as statins, beta-blockers, and angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers. For those patients at low bleeding risk, they also suggested dabigatran based on the recent MANAGE trial. Finally, they noted that US cardiac society guidelines suggested no screening for MINS, while the European and Canadian guidelines advocated for screening in patients at high risk for cardiac complications.

The authors are to be congratulated for highlighting an important and vexing area of postoperative management. To date, it has been difficult to chart the best path forward for these patients because we could “see” the issue, thanks to increasingly sensitive troponin assays, but we didn’t know what to do once we found it.

So what rationale exists to justify screening? Some advocate that the presence of MINS suggests a need for further imaging and closer monitoring of these patients to identify those with an MI. Indeed, several recent MINS registry studies have found that 20% to 40% of MINS patients had definitive evidence of MI.^2-4 But what about those patients with troponin elevation and no evidence of MI? A small, propensity-matched, observational study of MINS patients, including those without MI, noted positive associations between cardioprotective medications, such as aspirin and statins, and cardiac outcomes.⁵ In addition, the MANAGE trial suggested that MINS patients, with or without evidence of an MI, receiving dabigatran had reduced vascular events without increased bleeding complications.⁶ With this growing base of evidence, the rationale for systematic screening for MINS appears to be standing on stronger footing.

As noted by the authors, the recommendations for MINS screening differ across three major cardiovascular societies. How does the practicing clinician make sense of this discordant advice? Differences often occur when the evidence is of moderate or low quality, which means guideline committees must make their own interpretations of equivocal findings. Another driver of discordant recommendations is the timing of the guidelines. Both the US and European guidelines were published in 2014, while the Canadian guidelines were published in 2017. Over time, experience with postoperative troponin testing increased, which may have influenced the Canadian guidelines. Finally, many members of the Canadian guideline writing committee were the ones conducting the various studies identifying management options for MINS patients, which may have guided their ultimate recommendation. Regardless, practicing physicians should collectively view the guidelines as acceptable “guardrails” to guide their practice. Selection of the appropriate strategy can then be tailored to the individual patient’s risks and benefits, as well as available management options.

In this era of high-sensitivity troponin testing, we now possess an exquisite opportunity to “see” minute levels of myocardial injury among postoperative patients. Our growing ability to effectively act on this knowledge will enable us to make wise decisions with our patients to optimize their cardiac outcomes during the vulnerable postoperative period.

The ability to detect myocardial injury has never been more advanced. With the availability of high-­sensitivity troponin testing, microscopic evidence of myocyte death can now be detected, often within an hour or so of the inciting event. This, in turn, has facilitated quicker and more accurate identification and treatment of affected patients. However, these advances in detection have, in some cases, outstripped our understanding of the etiology and appropriate management of troponin elevation.

This dilemma is particularly apparent among patients undergoing noncardiac surgery. Annually, over 200 million of these surgeries occur worldwide, many in patients with elevated cardiac risk or overt cardiac disease. Naturally, physicians treating these patients are concerned that the stress of surgery will provoke myocardial injury. Since symptoms are often masked in the immediate postoperative period because of sedating or analgesic medications, many physicians rely on troponin testing to detect signs of myocardial injury. With the increased sensitivity of these assays, the prevalence of troponin elevation has increased, which currently affects nearly one in five postoperative patients. This knowledge, however, doesn’t lend itself to a clear management strategy, particularly in those patients with no other objective evidence of infarction. To paraphrase T.S. Eliot, have we lost the wisdom in our knowledge?

In this journal issue, Cohn and colleagues summarize the current information around this phenomenon of myocardial injury after noncardiac surgery, or MINS.¹ Consistent with the literature, they define MINS as an acute rise and/or fall in troponin (above the assay’s upper limit of normal) at any point in the 30 days following noncardiac surgery. Importantly, MINS is an umbrella term that can indicate either a myocardial infarction (MI) or nonischemic myocardial injury (NIMI). An MI exists if there are clinical signs of ischemia and/or objective evidence of infarction on imaging.

The authors found that MINS is highly prevalent (19.6%) and associated with both cardiac disease and perioperative hemodynamic stress. Between 2.9% and 13.5% of MINS patients experienced 30-day adverse cardiac events, with higher rates in patients with higher troponin elevations and/or accompanying ischemic symptoms. The authors suggested MINS management with standard cardio-protective medications, such as statins, beta-blockers, and angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers. For those patients at low bleeding risk, they also suggested dabigatran based on the recent MANAGE trial. Finally, they noted that US cardiac society guidelines suggested no screening for MINS, while the European and Canadian guidelines advocated for screening in patients at high risk for cardiac complications.

The authors are to be congratulated for highlighting an important and vexing area of postoperative management. To date, it has been difficult to chart the best path forward for these patients because we could “see” the issue, thanks to increasingly sensitive troponin assays, but we didn’t know what to do once we found it.

So what rationale exists to justify screening? Some advocate that the presence of MINS suggests a need for further imaging and closer monitoring of these patients to identify those with an MI. Indeed, several recent MINS registry studies have found that 20% to 40% of MINS patients had definitive evidence of MI.^2-4 But what about those patients with troponin elevation and no evidence of MI? A small, propensity-matched, observational study of MINS patients, including those without MI, noted positive associations between cardioprotective medications, such as aspirin and statins, and cardiac outcomes.⁵ In addition, the MANAGE trial suggested that MINS patients, with or without evidence of an MI, receiving dabigatran had reduced vascular events without increased bleeding complications.⁶ With this growing base of evidence, the rationale for systematic screening for MINS appears to be standing on stronger footing.

As noted by the authors, the recommendations for MINS screening differ across three major cardiovascular societies. How does the practicing clinician make sense of this discordant advice? Differences often occur when the evidence is of moderate or low quality, which means guideline committees must make their own interpretations of equivocal findings. Another driver of discordant recommendations is the timing of the guidelines. Both the US and European guidelines were published in 2014, while the Canadian guidelines were published in 2017. Over time, experience with postoperative troponin testing increased, which may have influenced the Canadian guidelines. Finally, many members of the Canadian guideline writing committee were the ones conducting the various studies identifying management options for MINS patients, which may have guided their ultimate recommendation. Regardless, practicing physicians should collectively view the guidelines as acceptable “guardrails” to guide their practice. Selection of the appropriate strategy can then be tailored to the individual patient’s risks and benefits, as well as available management options.

In this era of high-sensitivity troponin testing, we now possess an exquisite opportunity to “see” minute levels of myocardial injury among postoperative patients. Our growing ability to effectively act on this knowledge will enable us to make wise decisions with our patients to optimize their cardiac outcomes during the vulnerable postoperative period.

In this issue of the Journal of Hospital Medicine, Dr. Thomson and colleagues present an analysis of 4,700 hospitalizations in the Pediatric Health Information System (PHIS) database to compare the effectiveness of different antibiotic regimens for children with neurological impairment and aspiration pneumonia.¹ After adjusting for potential confounders, including illness severity markers and demographic factors, they observed that receiving anaerobic coverage was associated with improvements in rates of acute respiratory failure, intensive care unit (ICU) transfer frequency, and length of stay. Given that the authors used an administrative database, several considerations limit the generalizability of the current study. These limitations include that only patients hospitalized at freestanding children’s hospitals were included, the incomplete ability to assess illness severity, and the absence of validated clinical criteria for the diagnosis of aspiration pneumonia. Despite the limitations of a retrospective study using administrative data, the authors should be commended for their rigorous analyses and for their important contribution to the care of this understudied population.

Optimizing appropriate antibiotic therapy for children with suspected aspiration pneumonia is challenging for several reasons. First, previous epidemiological studies demonstrated that viruses cause most pediatric community-acquired pneumonia²; however, we lack tools to identify patients who do not require antibiotic therapy. Second, current clinical guidelines on community-acquired pneumonia do not address aspiration pneumonia diagnosis and management.³ Similar to community-acquired pneumonia, aspiration pneumonia is a clinical diagnosis supported by patient history and laboratory and radiographic data. Given the lack of a gold standard, diagnosis of aspiration pneumonia is difficult to confirm. Previous studies using the PHIS database have demonstrated that, compared with children with nonaspiration pneumonia, those with aspiration pneumonia International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) codes feature higher rates of mortality, ICU-level care, and 30-day readmission rates.^4,5 However, in these studies, patients with an ICD-9-CM code for aspiration pneumonia were also more medically complex, with a higher number of complex chronic conditions and rates of technology use. Lastly, aspiration pneumonia is occasionally synonymous with pneumonia in medically complex patients, which leads to the increased exposure to broad-­spectrum antibiotics. The exposure to broad-spectrum antibiotics causes complications, such as Clostridioides difficile infection and potential antibiotic resistance in a patient population that already experiences significant antibiotic exposure.

Growing concerns about antibiotic overuse and the declining prevalence of anaerobic isolates among adult pneumonia patients recently prompted the Infectious Diseases Society of America (IDSA) and the American Thoracic Society (ATS) to discourage routine anaerobic coverage among adults with suspected aspiration pneumonia and no abscess or empyema.⁶ These guidelines overturn years of habit for most adult hospitalists, although the IDSA and ATS acknowledge the extremely low quality of evidence informing the recommendation. Thus, the dilemma is whether the IDSA/ATS guidelines should be reconciled with the conclusions of Thomson et al. The answer is “not necessarily.” Fundamentally, different causes of neurological impairment, such as dementia and stroke, afflict elderly adults with aspiration pneumonia along with important differences in physiological and microbiological exposures. Instead, adult and pediatric hospitalists can find common ground around the shared uncertainty and variability in diagnosing aspiration pneumonia and the need for more credible evidence. Unfortunately, wide variation in diagnosis and coding practices might complicate the efforts to reproduce Thomson’s rigorous retrospective cohort study in large adult databases⁷ given that Medicare-quality comparison programs may have inadvertently encouraged changes in coding behaviors during the last decade. Attributing pneumonia cases to aspiration removed high-risk patients from reporting cohorts, thus improving a hospital’s apparent mortality rate for community-acquired pneumonia. Although the United States Centers for Medicare & Medicaid Services amended rules in 2017 to address this concern, years of overdiagnosis of aspiration pneumonia possibly biased adult administrative data sets.

Although the association between the use of anaerobic antibiotic coverage and improved pediatric outcomes is promising, these results also point out the need for rigorous prospective studies to improve the evidence base for the diagnosis and treatment of suspected aspiration pneumonia in hospitalized patients of all ages. Given the heterogeneity in the use of aspiration pneumonia diagnoses, foundational work might include assessing the factors that influence clinicians in deciding on the diagnosis of aspiration pneumonia (versus community-­acquired pneumonia). On the patient side, parallel trials may start with multicenter, prospective cohort studies to gain insights into the demographic, clinical, and laboratory factors that are associated with the diagnosis of aspiration pneumonia. This research direction may lead to the development and standardization of diagnostic criteria for aspiration pneumonia. Ultimately, prospective randomized controlled trials are needed to assess the comparative effectiveness of different antibiotic choices on clinical outcomes.

In this issue of the Journal of Hospital Medicine, Dr. Thomson and colleagues present an analysis of 4,700 hospitalizations in the Pediatric Health Information System (PHIS) database to compare the effectiveness of different antibiotic regimens for children with neurological impairment and aspiration pneumonia.¹ After adjusting for potential confounders, including illness severity markers and demographic factors, they observed that receiving anaerobic coverage was associated with improvements in rates of acute respiratory failure, intensive care unit (ICU) transfer frequency, and length of stay. Given that the authors used an administrative database, several considerations limit the generalizability of the current study. These limitations include that only patients hospitalized at freestanding children’s hospitals were included, the incomplete ability to assess illness severity, and the absence of validated clinical criteria for the diagnosis of aspiration pneumonia. Despite the limitations of a retrospective study using administrative data, the authors should be commended for their rigorous analyses and for their important contribution to the care of this understudied population.

Optimizing appropriate antibiotic therapy for children with suspected aspiration pneumonia is challenging for several reasons. First, previous epidemiological studies demonstrated that viruses cause most pediatric community-acquired pneumonia²; however, we lack tools to identify patients who do not require antibiotic therapy. Second, current clinical guidelines on community-acquired pneumonia do not address aspiration pneumonia diagnosis and management.³ Similar to community-acquired pneumonia, aspiration pneumonia is a clinical diagnosis supported by patient history and laboratory and radiographic data. Given the lack of a gold standard, diagnosis of aspiration pneumonia is difficult to confirm. Previous studies using the PHIS database have demonstrated that, compared with children with nonaspiration pneumonia, those with aspiration pneumonia International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) codes feature higher rates of mortality, ICU-level care, and 30-day readmission rates.^4,5 However, in these studies, patients with an ICD-9-CM code for aspiration pneumonia were also more medically complex, with a higher number of complex chronic conditions and rates of technology use. Lastly, aspiration pneumonia is occasionally synonymous with pneumonia in medically complex patients, which leads to the increased exposure to broad-­spectrum antibiotics. The exposure to broad-spectrum antibiotics causes complications, such as Clostridioides difficile infection and potential antibiotic resistance in a patient population that already experiences significant antibiotic exposure.

Growing concerns about antibiotic overuse and the declining prevalence of anaerobic isolates among adult pneumonia patients recently prompted the Infectious Diseases Society of America (IDSA) and the American Thoracic Society (ATS) to discourage routine anaerobic coverage among adults with suspected aspiration pneumonia and no abscess or empyema.⁶ These guidelines overturn years of habit for most adult hospitalists, although the IDSA and ATS acknowledge the extremely low quality of evidence informing the recommendation. Thus, the dilemma is whether the IDSA/ATS guidelines should be reconciled with the conclusions of Thomson et al. The answer is “not necessarily.” Fundamentally, different causes of neurological impairment, such as dementia and stroke, afflict elderly adults with aspiration pneumonia along with important differences in physiological and microbiological exposures. Instead, adult and pediatric hospitalists can find common ground around the shared uncertainty and variability in diagnosing aspiration pneumonia and the need for more credible evidence. Unfortunately, wide variation in diagnosis and coding practices might complicate the efforts to reproduce Thomson’s rigorous retrospective cohort study in large adult databases⁷ given that Medicare-quality comparison programs may have inadvertently encouraged changes in coding behaviors during the last decade. Attributing pneumonia cases to aspiration removed high-risk patients from reporting cohorts, thus improving a hospital’s apparent mortality rate for community-acquired pneumonia. Although the United States Centers for Medicare & Medicaid Services amended rules in 2017 to address this concern, years of overdiagnosis of aspiration pneumonia possibly biased adult administrative data sets.

Although the association between the use of anaerobic antibiotic coverage and improved pediatric outcomes is promising, these results also point out the need for rigorous prospective studies to improve the evidence base for the diagnosis and treatment of suspected aspiration pneumonia in hospitalized patients of all ages. Given the heterogeneity in the use of aspiration pneumonia diagnoses, foundational work might include assessing the factors that influence clinicians in deciding on the diagnosis of aspiration pneumonia (versus community-­acquired pneumonia). On the patient side, parallel trials may start with multicenter, prospective cohort studies to gain insights into the demographic, clinical, and laboratory factors that are associated with the diagnosis of aspiration pneumonia. This research direction may lead to the development and standardization of diagnostic criteria for aspiration pneumonia. Ultimately, prospective randomized controlled trials are needed to assess the comparative effectiveness of different antibiotic choices on clinical outcomes.

In this issue of the Journal of Hospital Medicine, Dr. Thomson and colleagues present an analysis of 4,700 hospitalizations in the Pediatric Health Information System (PHIS) database to compare the effectiveness of different antibiotic regimens for children with neurological impairment and aspiration pneumonia.¹ After adjusting for potential confounders, including illness severity markers and demographic factors, they observed that receiving anaerobic coverage was associated with improvements in rates of acute respiratory failure, intensive care unit (ICU) transfer frequency, and length of stay. Given that the authors used an administrative database, several considerations limit the generalizability of the current study. These limitations include that only patients hospitalized at freestanding children’s hospitals were included, the incomplete ability to assess illness severity, and the absence of validated clinical criteria for the diagnosis of aspiration pneumonia. Despite the limitations of a retrospective study using administrative data, the authors should be commended for their rigorous analyses and for their important contribution to the care of this understudied population.

Optimizing appropriate antibiotic therapy for children with suspected aspiration pneumonia is challenging for several reasons. First, previous epidemiological studies demonstrated that viruses cause most pediatric community-acquired pneumonia²; however, we lack tools to identify patients who do not require antibiotic therapy. Second, current clinical guidelines on community-acquired pneumonia do not address aspiration pneumonia diagnosis and management.³ Similar to community-acquired pneumonia, aspiration pneumonia is a clinical diagnosis supported by patient history and laboratory and radiographic data. Given the lack of a gold standard, diagnosis of aspiration pneumonia is difficult to confirm. Previous studies using the PHIS database have demonstrated that, compared with children with nonaspiration pneumonia, those with aspiration pneumonia International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) codes feature higher rates of mortality, ICU-level care, and 30-day readmission rates.^4,5 However, in these studies, patients with an ICD-9-CM code for aspiration pneumonia were also more medically complex, with a higher number of complex chronic conditions and rates of technology use. Lastly, aspiration pneumonia is occasionally synonymous with pneumonia in medically complex patients, which leads to the increased exposure to broad-­spectrum antibiotics. The exposure to broad-spectrum antibiotics causes complications, such as Clostridioides difficile infection and potential antibiotic resistance in a patient population that already experiences significant antibiotic exposure.

Growing concerns about antibiotic overuse and the declining prevalence of anaerobic isolates among adult pneumonia patients recently prompted the Infectious Diseases Society of America (IDSA) and the American Thoracic Society (ATS) to discourage routine anaerobic coverage among adults with suspected aspiration pneumonia and no abscess or empyema.⁶ These guidelines overturn years of habit for most adult hospitalists, although the IDSA and ATS acknowledge the extremely low quality of evidence informing the recommendation. Thus, the dilemma is whether the IDSA/ATS guidelines should be reconciled with the conclusions of Thomson et al. The answer is “not necessarily.” Fundamentally, different causes of neurological impairment, such as dementia and stroke, afflict elderly adults with aspiration pneumonia along with important differences in physiological and microbiological exposures. Instead, adult and pediatric hospitalists can find common ground around the shared uncertainty and variability in diagnosing aspiration pneumonia and the need for more credible evidence. Unfortunately, wide variation in diagnosis and coding practices might complicate the efforts to reproduce Thomson’s rigorous retrospective cohort study in large adult databases⁷ given that Medicare-quality comparison programs may have inadvertently encouraged changes in coding behaviors during the last decade. Attributing pneumonia cases to aspiration removed high-risk patients from reporting cohorts, thus improving a hospital’s apparent mortality rate for community-acquired pneumonia. Although the United States Centers for Medicare & Medicaid Services amended rules in 2017 to address this concern, years of overdiagnosis of aspiration pneumonia possibly biased adult administrative data sets.

Although the association between the use of anaerobic antibiotic coverage and improved pediatric outcomes is promising, these results also point out the need for rigorous prospective studies to improve the evidence base for the diagnosis and treatment of suspected aspiration pneumonia in hospitalized patients of all ages. Given the heterogeneity in the use of aspiration pneumonia diagnoses, foundational work might include assessing the factors that influence clinicians in deciding on the diagnosis of aspiration pneumonia (versus community-­acquired pneumonia). On the patient side, parallel trials may start with multicenter, prospective cohort studies to gain insights into the demographic, clinical, and laboratory factors that are associated with the diagnosis of aspiration pneumonia. This research direction may lead to the development and standardization of diagnostic criteria for aspiration pneumonia. Ultimately, prospective randomized controlled trials are needed to assess the comparative effectiveness of different antibiotic choices on clinical outcomes.

Core competencies are intended to provide defined expectations in a field of medicine. The newly published Pediatric Hospital Medicine (PHM) Core Competencies: 2020 Revision are an update of the original 2010 competencies¹ with added and restructured content based on relevance to current practice.^2,3 This is timely given the 2017 update to the Society of Hospital Medicine (SHM) core competencies⁴ and recent designation of PHM as a boarded subspecialty by the American Board of Pediatrics (ABP). The competencies help define the knowledge, skills, and attitudes of a pediatric hospital medicine specialist and inform curriculum development to achieve the determined expectations.

In this update to the PHM core competencies, key adjustments were made to the editorial process. Importantly, a community hospitalist was added to the editorial team; this change better reflects the proportion of care provided to hospitalized children at community sites nationwide.⁵ Content updates were considered using a two-pronged needs assessment: (1) review of recent PHM conference, textbook, and handbook content and (2) survey of the SHM, Academic Pediatric Association, and American Academy of Pediatrics stakeholder groups. These processes led to the addition of 12 chapters, the major revision of 7 chapters, and the addition of content to 29 of the original chapters.

The increased focus on mental health in the sections “Common Clinical Diagnoses and Conditions” and “Specialized Services” is a necessary update. Chapters on neonatal abstinence syndrome (NAS), substance abuse, and altered mental status were added to the “Common Clinical Diagnoses and Conditions” section. The increasing incidence of NAS has been well described, and the field of PHM has been instrumental in improving care for these patients.⁶ Children hospitalized with mental health diagnoses constitute a substantial portion of pediatric inpatient admissions,⁷ and we anticipate that it will be a continued area of need in PHM. Therefore, the addition of chapters on acute and chronic behavioral and psychiatric conditions in the “Specialized Services” section is noteworthy. In contrast, with the added chapters on constipation and gastrointestinal and digestive disorders, the gastrointestinal disorders may be disproportionately represented in the updated competencies and may be an area to streamline in future iterations.

Recognition of changing procedural needs in the inpatient pediatric setting, particularly with the growing population of children with medical complexity, resulted in removal of suprapubic bladder taps and addition of vesicostomy care to the “Core Skills” section. In future updates, it will be important to continue to remove practices that are no longer relevant or widespread and include advances in procedural skills applicable to PHM such as point-of-care ultrasound.⁸

The “Healthcare Systems” section highlights additional skills ranging from quality improvement and research to family-­centered care that PHM physicians bring to healthcare institutions. According to a recent survey of early-career hospitalists, skills in these areas are often not adequately developed during residency training.⁹ Therefore, the competencies outlined in this section are a key part of proposed PHM fellowship curricula¹⁰ and should be recognized as potential development opportunities for junior faculty in the field. This section also highlights the increasing medical complexity of patients and evolving role of PHM expertise in comanagement and consultation to improve quality and safety of care. Appreciating the unique needs of underserved communities is another important addition in the new chapter on family-centered care.

Looking ahead to future updates, we appreciate that the editors commented on diversity in both editorship and authorship. In line with the recent call for improved representation of women and racial and ethnic minorities in academic medicine by the Journal of Hospital Medicine,¹¹ future core competency publications should broadly consider diversity in editors, authors, and reviewers and more explicitly address methods for increasing diversity. We also anticipate that technological advances, such as telemedicine and remote patient monitoring, will be at the forefront in subsequent updates, which will allow higher levels of care to be provided outside of the traditional hospital structure. With the recent inauguration of the ABP PHM certification exam and the first cycle of Accreditation Council for Graduate Medical Education accreditation for PHM fellowships, these updated competencies are timely and relevant. The authors’ ongoing efforts are crucial for our young and evolving field as we strive to improve the health of all hospitalized children.

The authors have nothing to disclose.

Core competencies are intended to provide defined expectations in a field of medicine. The newly published Pediatric Hospital Medicine (PHM) Core Competencies: 2020 Revision are an update of the original 2010 competencies¹ with added and restructured content based on relevance to current practice.^2,3 This is timely given the 2017 update to the Society of Hospital Medicine (SHM) core competencies⁴ and recent designation of PHM as a boarded subspecialty by the American Board of Pediatrics (ABP). The competencies help define the knowledge, skills, and attitudes of a pediatric hospital medicine specialist and inform curriculum development to achieve the determined expectations.

In this update to the PHM core competencies, key adjustments were made to the editorial process. Importantly, a community hospitalist was added to the editorial team; this change better reflects the proportion of care provided to hospitalized children at community sites nationwide.⁵ Content updates were considered using a two-pronged needs assessment: (1) review of recent PHM conference, textbook, and handbook content and (2) survey of the SHM, Academic Pediatric Association, and American Academy of Pediatrics stakeholder groups. These processes led to the addition of 12 chapters, the major revision of 7 chapters, and the addition of content to 29 of the original chapters.

The increased focus on mental health in the sections “Common Clinical Diagnoses and Conditions” and “Specialized Services” is a necessary update. Chapters on neonatal abstinence syndrome (NAS), substance abuse, and altered mental status were added to the “Common Clinical Diagnoses and Conditions” section. The increasing incidence of NAS has been well described, and the field of PHM has been instrumental in improving care for these patients.⁶ Children hospitalized with mental health diagnoses constitute a substantial portion of pediatric inpatient admissions,⁷ and we anticipate that it will be a continued area of need in PHM. Therefore, the addition of chapters on acute and chronic behavioral and psychiatric conditions in the “Specialized Services” section is noteworthy. In contrast, with the added chapters on constipation and gastrointestinal and digestive disorders, the gastrointestinal disorders may be disproportionately represented in the updated competencies and may be an area to streamline in future iterations.

Recognition of changing procedural needs in the inpatient pediatric setting, particularly with the growing population of children with medical complexity, resulted in removal of suprapubic bladder taps and addition of vesicostomy care to the “Core Skills” section. In future updates, it will be important to continue to remove practices that are no longer relevant or widespread and include advances in procedural skills applicable to PHM such as point-of-care ultrasound.⁸

The “Healthcare Systems” section highlights additional skills ranging from quality improvement and research to family-­centered care that PHM physicians bring to healthcare institutions. According to a recent survey of early-career hospitalists, skills in these areas are often not adequately developed during residency training.⁹ Therefore, the competencies outlined in this section are a key part of proposed PHM fellowship curricula¹⁰ and should be recognized as potential development opportunities for junior faculty in the field. This section also highlights the increasing medical complexity of patients and evolving role of PHM expertise in comanagement and consultation to improve quality and safety of care. Appreciating the unique needs of underserved communities is another important addition in the new chapter on family-centered care.

Looking ahead to future updates, we appreciate that the editors commented on diversity in both editorship and authorship. In line with the recent call for improved representation of women and racial and ethnic minorities in academic medicine by the Journal of Hospital Medicine,¹¹ future core competency publications should broadly consider diversity in editors, authors, and reviewers and more explicitly address methods for increasing diversity. We also anticipate that technological advances, such as telemedicine and remote patient monitoring, will be at the forefront in subsequent updates, which will allow higher levels of care to be provided outside of the traditional hospital structure. With the recent inauguration of the ABP PHM certification exam and the first cycle of Accreditation Council for Graduate Medical Education accreditation for PHM fellowships, these updated competencies are timely and relevant. The authors’ ongoing efforts are crucial for our young and evolving field as we strive to improve the health of all hospitalized children.

The authors have nothing to disclose.

Core competencies are intended to provide defined expectations in a field of medicine. The newly published Pediatric Hospital Medicine (PHM) Core Competencies: 2020 Revision are an update of the original 2010 competencies¹ with added and restructured content based on relevance to current practice.^2,3 This is timely given the 2017 update to the Society of Hospital Medicine (SHM) core competencies⁴ and recent designation of PHM as a boarded subspecialty by the American Board of Pediatrics (ABP). The competencies help define the knowledge, skills, and attitudes of a pediatric hospital medicine specialist and inform curriculum development to achieve the determined expectations.

In this update to the PHM core competencies, key adjustments were made to the editorial process. Importantly, a community hospitalist was added to the editorial team; this change better reflects the proportion of care provided to hospitalized children at community sites nationwide.⁵ Content updates were considered using a two-pronged needs assessment: (1) review of recent PHM conference, textbook, and handbook content and (2) survey of the SHM, Academic Pediatric Association, and American Academy of Pediatrics stakeholder groups. These processes led to the addition of 12 chapters, the major revision of 7 chapters, and the addition of content to 29 of the original chapters.

The increased focus on mental health in the sections “Common Clinical Diagnoses and Conditions” and “Specialized Services” is a necessary update. Chapters on neonatal abstinence syndrome (NAS), substance abuse, and altered mental status were added to the “Common Clinical Diagnoses and Conditions” section. The increasing incidence of NAS has been well described, and the field of PHM has been instrumental in improving care for these patients.⁶ Children hospitalized with mental health diagnoses constitute a substantial portion of pediatric inpatient admissions,⁷ and we anticipate that it will be a continued area of need in PHM. Therefore, the addition of chapters on acute and chronic behavioral and psychiatric conditions in the “Specialized Services” section is noteworthy. In contrast, with the added chapters on constipation and gastrointestinal and digestive disorders, the gastrointestinal disorders may be disproportionately represented in the updated competencies and may be an area to streamline in future iterations.

Recognition of changing procedural needs in the inpatient pediatric setting, particularly with the growing population of children with medical complexity, resulted in removal of suprapubic bladder taps and addition of vesicostomy care to the “Core Skills” section. In future updates, it will be important to continue to remove practices that are no longer relevant or widespread and include advances in procedural skills applicable to PHM such as point-of-care ultrasound.⁸

The “Healthcare Systems” section highlights additional skills ranging from quality improvement and research to family-­centered care that PHM physicians bring to healthcare institutions. According to a recent survey of early-career hospitalists, skills in these areas are often not adequately developed during residency training.⁹ Therefore, the competencies outlined in this section are a key part of proposed PHM fellowship curricula¹⁰ and should be recognized as potential development opportunities for junior faculty in the field. This section also highlights the increasing medical complexity of patients and evolving role of PHM expertise in comanagement and consultation to improve quality and safety of care. Appreciating the unique needs of underserved communities is another important addition in the new chapter on family-centered care.

Looking ahead to future updates, we appreciate that the editors commented on diversity in both editorship and authorship. In line with the recent call for improved representation of women and racial and ethnic minorities in academic medicine by the Journal of Hospital Medicine,¹¹ future core competency publications should broadly consider diversity in editors, authors, and reviewers and more explicitly address methods for increasing diversity. We also anticipate that technological advances, such as telemedicine and remote patient monitoring, will be at the forefront in subsequent updates, which will allow higher levels of care to be provided outside of the traditional hospital structure. With the recent inauguration of the ABP PHM certification exam and the first cycle of Accreditation Council for Graduate Medical Education accreditation for PHM fellowships, these updated competencies are timely and relevant. The authors’ ongoing efforts are crucial for our young and evolving field as we strive to improve the health of all hospitalized children.

The authors have nothing to disclose.

Core values should reflect our fundamental beliefs and serve as the building blocks of our behaviors and actions. Health systems across the United States define themselves by a myriad of guiding principles, which include patient-centeredness, dignity, respect, safety, and teamwork. On the surface, medicine’s ties to such altruistic values make intuitive sense. However, as Black physicians, we are in a state of cognitive dissonance as we wrestle with healthcare’s real identity and the principles it espouses. We know that within this psychological tension lies the truth: the US healthcare system was not designed to live up to these ideals. This truth is most evident in health inequities that exist among Black people and other marginalized communities of color. It is also the undeniable reality of Black physicians whose professional role is juxtaposed with recurring experiences that signal to us that we do not belong.

Core values should reflect our fundamental beliefs and serve as the building blocks of our behaviors and actions. Health systems across the United States define themselves by a myriad of guiding principles, which include patient-centeredness, dignity, respect, safety, and teamwork. On the surface, medicine’s ties to such altruistic values make intuitive sense. However, as Black physicians, we are in a state of cognitive dissonance as we wrestle with healthcare’s real identity and the principles it espouses. We know that within this psychological tension lies the truth: the US healthcare system was not designed to live up to these ideals. This truth is most evident in health inequities that exist among Black people and other marginalized communities of color. It is also the undeniable reality of Black physicians whose professional role is juxtaposed with recurring experiences that signal to us that we do not belong.

Core values should reflect our fundamental beliefs and serve as the building blocks of our behaviors and actions. Health systems across the United States define themselves by a myriad of guiding principles, which include patient-centeredness, dignity, respect, safety, and teamwork. On the surface, medicine’s ties to such altruistic values make intuitive sense. However, as Black physicians, we are in a state of cognitive dissonance as we wrestle with healthcare’s real identity and the principles it espouses. We know that within this psychological tension lies the truth: the US healthcare system was not designed to live up to these ideals. This truth is most evident in health inequities that exist among Black people and other marginalized communities of color. It is also the undeniable reality of Black physicians whose professional role is juxtaposed with recurring experiences that signal to us that we do not belong.

A 62-year-old man with metastatic non–small cell lung cancer (NSCLC) presented to the Emergency Department with 3 days of progressive generalized weakness, anorexia, and nonbloody diarrhea. He denied fever, chills, nausea, vomiting, cough, shortness of breath, or abdominal pain. He had no sick contacts.

One diagnostic approach for patients with cancer who present with new symptoms is to consider diagnoses both related and unrelated to the cancer. Cancer-related diagnoses can include the broad categories of complications related to the tumor itself (such as mass effect), paraneoplastic phenomena, or treatment-related complications (such as infection from immunosuppression or chemotherapy toxicity).

For this patient with metastatic NSCLC, weakness, anorexia, and diarrhea are unlikely to be related to mass effect unless the patient has peritoneal metastases (an uncommon complication of NSCLC) with carcinomatosis-associated diarrhea.

Paraneoplastic phenomena, such as hypercalcemia or hyponatremia from the syndrome of inappropriate antidiuretic hormone (SIADH), are common with NSCLC and could both lead to weakness and anorexia. Hematologic consequences of NSCLC (or its treatment) include anemia, thrombosis, and thrombotic microangiopathy (TMA), though diarrhea, in the absence of abdominal pain or hematochezia, would be unexpected.

Weakness, anorexia, and diarrhea may also be symptoms of chemotherapy toxicity or an infection resulting from immunosuppression. It would be important to know what specific treatment the patient has received. Chemotherapy commonly causes neutropenia and predisposes to rapidly progressive infections, while immunotherapies have other toxicities. Diarrhea is a common toxicity of the checkpoint inhibitors and anaplastic lymphoma kinase (ALK) inhibitors that are frequently used to treat metastatic NSCLC. Checkpoint inhibitors also are known to cause a wide range of autoimmune phenomena including colitis.

Finally, the patient’s symptoms may be unrelated to the cancer. Weakness, anorexia, and nonbloody diarrhea could be signs of viral or bacterial gastroenteritis or Clostridioides difficile colitis particularly with frequent healthcare contact or antimicrobial use.

Two days prior, he had been diagnosed with nonsevere Clostridioides difficile colitis in an acute care clinic. He was started on oral metronidazole, but his diarrhea worsened over the next day and was accompanied by weakness and anorexia. Additional past medical history included untreated hepatitis C infection, chronic kidney disease stage 3, seizure disorder, and left lung NSCLC (adenocarcinoma). The lung cancer was diagnosed 8 months prior when he had presented with hemoptysis and 3 months of progressive constitutional symptoms. Imaging at that time revealed metastases to the contralateral lung and regional lymph nodes, as well as vertebrae, ribs, and pelvis. He had no abdominal metastases. He was initially treated with carboplatin and paclitaxel. After a partial response to initial chemotherapy, he developed peripheral neuropathy and was switched to gemcitabine 12 weeks ago. He received five cycles of gemcitabine over 10 weeks. He was last administered gemcitabine 2 weeks prior. He had not received any additional chemotherapy or immunotherapy. He had a 40 pack-year history of smoking, but quit when diagnosed with cancer. He did not drink alcohol. He had no recent travel or sick contacts. He was not on any medications. He was homeless but staying with family members in the area. Additional review of systems was negative for recent bleeding, bruising, hemoptysis, melena, hematochezia, or hematuria.

Recent treatment with gemcitabine could contribute to the presentation in a number of ways. First, gemcitabine is associated with myelosuppression and neutropenia that could predispose him to infectious colitis. Second, gemcitabine is known to cause anemia, anorexia, diarrhea, and fatigue. Third, gemcitabine may also cause renal injury that can contribute to worsening anemia. He may be at greater risk of anemia and renal toxicity because of preexisting chronic kidney disease. Finally, gemcitabine can rarely cause TMA with characteristics that mimic the hemolytic-uremic syndrome with microangiopathic hemolytic anemia, mild thrombocytopenia, and severe acute kidney injury (AKI).

In addition, worsening infectious colitis could certainly explain his presenting symptoms. At this point, local mass effect seems unlikely despite his metastatic disease. Lastly, it should be noted that, in an immunosuppressed cancer patient, multiple problems could be present at the same time. Laboratory testing should evaluate for hypercalcemia, SIADH, hematologic indexes, and renal function. If initial laboratory evaluation is unrevealing, abdominal imaging may be needed to assess for carcinomatosis, complications from colitis, typhlitis, abscess, or perforation.

On physical examination, the patient appeared fatigued. His temperature was 36.8°C, blood pressure 158/72 mm Hg, pulse 88 beats per minute, respiratory rate 16 breaths per minute, and oxygen saturation was 96% while breathing ambient air. There was neither scleral icterus nor conjunctival injection but he had mild conjunctival pallor. Cardiovascular and lung examinations were normal. Abdominal exam revealed normal bowel sounds without tenderness or organomegaly. He had no supraclavicular, axillary, or inguinal lymphadenopathy. He was alert and oriented. Cranial nerves II through XII were intact. He had decreased muscle bulk in his extremities without focal weakness. Gait and reflexes were not tested.

Initial laboratory testing revealed a white blood cell count of 5.5 K/mm³, hemoglobin of 5 g/dL (hemoglobin 1 month prior was 10.1 g/dL), and platelet count of 20 K/mm³ (platelet count 1 month prior was 246 K/mm³). Creatinine was 3.9 mg/dL (compared with a baseline of 1.8 mg/dL), and blood urea nitrogen was 39 mg/dL. His sodium was 137 mEq/L, potassium 4.2 mEq/L, chloride 105 mEq/L, bicarbonate 22 mEq/L, and thyroid stimulating hormone 0.9 mU/L. His total protein was 4.9 g/dL, albumin 2.1 g/dL, alkaline phosphatase 60 IU/L, alanine aminotransferase 17 IU/L, aspartate aminotransferase 60 IU/L, direct bilirubin 0.2 mg/dL, and total bilirubin 0.5 mg/dL. A chest x-ray showed no infiltrates.

The patient’s laboratory tests reveal several important new findings, including severe acute on chronic anemia, acute thrombocytopenia, and AKI, without clinical evidence of acute blood loss. These changes could be parts of a syndrome or multiple independent disorders. The most urgent priority is to evaluate for TMAs, many of which are fatal if not diagnosed and treated expeditiously. This includes thrombotic thrombocytopenic purpura (TTP), disseminated intravascular hemolysis (DIC), and atypical hemolytic uremic syndrome (aHUS). A manual review of a peripheral blood smear is required to evaluate for fragmented red blood cells (schistocytes). Thereafter, ancillary testing to confirm intravascular hemolysis would include measuring free plasma hemoglobin and lactate dehydrogenase (LDH). Additionally, in intravascular hemolysis, haptoglobin should be depleted and urinalysis should show heme-positive urine without RBCs. In this case the patient’s normal bilirubin studies argue against hemolysis; however, elevated bilirubin is variably present in hemolytic anemias depending on the liver’s ability to conjugate and excrete bilirubin, the relative degree of RBC turnover, and type of hemolysis. Patients with intravascular hemolysis lose hemoglobin directly into the urine leaving relatively little hemoglobin to be incorporated into bile once it has reached the reticuloendothelial system. This results in relatively normal bilirubin levels. More specific indicators of intravascular hemolysis include pink colored plasma on visual inspection (commonly done in the blood bank as part of assessing for hemolytic transfusion reactions), measuring plasma free hemoglobin, or by detecting hemoglobin in the urine.

If microangiopathic hemolytic anemia (MAHA) is excluded, then other causes of these laboratory abnormalities should be considered. Bleeding is the most common cause for anemia, and thrombocytopenia predisposes patients to bleeding. However, there is no evidence of bleeding in this patient, and such a rapid acute anemia is unlikely to be caused by occult blood loss alone. Concurrent anemia and thrombocytopenia could be evidence of bone marrow toxicity from chemotherapy or neoplastic infiltration. With marrow infiltration, there are typically signs on the peripheral smear of leukoerythroblastosis, with circulating nucleated red blood cells and early myeloid forms. Concurrent immune thrombocytopenia (ITP) and autoimmune hemolytic anemia (AIHA), or Evans’ Syndrome, should also be considered. AIHA would be suggested by spherocytes on the peripheral smear, elevated LDH and a positive direct antibody test (DAT).

Regarding the AKI, the patient has diarrhea, which could lead to prerenal azotemia and acute tubular necrosis. A formal urinalysis would evaluate for prerenal and intrinsic kidney disease. TMA can cause intrinsic kidney injury with a benign urinary sediment. The blood urea nitrogen-to-creatinine ratio is not elevated, but in a patient with malnutrition this may not indicate prerenal azotemia. In summary, to differentiate potential TMAs from other causes, the patient needs a blood smear, coagulation studies, and an evaluation for hemolysis, including a urinalysis for free heme and any evidence of intrinsic kidney disease.

Urinalysis showed amber-colored, dilute urine with no white blood cells, red blood cells, protein, or casts. It was positive for blood and negative for bilirubin and hemosiderin. LDH was 1,382 IU/L (reference range 135-225 IU/L), and haptoglobin was unmeasurably low. His ferritin was 2,267 ng/mL, serum iron was 57 mcg/dL, total iron-binding capacity was 241 mcg/dL, and transferrin was 162 mcg/dL. Reticulocyte count was 6% (reticulocyte index of 0.86). Vitamin B12 level was normal. DAT was negative; INR and aPTT were normal. Fibrinogen was 287 mg/dL (reference range 200-400 mg/dL), and D-dimer was 5,095 ng/mL (reference range 0-229 ng/mL).

The urinalysis shows no active sediment to suggest vasculitis or glomerulonephritis. The kidney injury could be the result of renal toxicity from free hemoglobin or as part of TMA caused by microvascular thrombosis. The dilute urine makes prerenal azotemia less likely.

There is clearly acute intravascular hemolysis occurring as evidenced by hemoglobinuria, very high LDH, and undetectable serum haptoglobin. The hemolysis is acute because chronic intravascular hemolysis would lead to positive urine hemosiderin via deposition in the renal tubules. Autoimmune hemolytic anemia is much less likely, but not ruled out, by a negative DAT.

This syndrome can be further refined from acute anemia to acute anemia with likely nonimmune intravascular hemolysis, acute thrombocytopenia, and AKI with hemoglobinuria and a bland urinary sediment. At this point, intravascular hemolysis and kidney injury could be part of a unifying diagnosis. However, this does not account for the patient’s thrombocytopenia, and TMA remains the best explanation for the constellation of findings. Review of the peripheral blood smear is urgent because evidence of MAHA would prompt urgent plasma exchange based on presumptive diagnosis of acquired TTP to later be confirmed with ADAMTS13 activity testing. Most TMAs are treated with supportive care only; TTP and aHUS have specific interventions that change the natural history of the disease (plasma exchange and anticomplement therapy, respectively). Given both the deadly natural history and opportunity to intervene with plasma exchange, patients with TMA should be treated with urgent plasma exchange until ADAMTS13 deficiency is confirmed or refuted. One TMA that can be excluded at this point is DIC. DIC in its acute and chronic forms nearly universally causes MAHA, thrombocytopenia, and consumptive coagulopathy including hypofibrinogenemia.

If MAHA is excluded, then other causes of intravascular hemolysis should be considered, along with causes of thrombocytopenia that might be occurring concurrently. Intravascular hemolysis can be further differentiated by etiologies primarily related to the RBC or whether the RBC is the innocent bystander amidst a systemic illness. RBC disorders include syndromes affecting RBC fragility like hereditary spherocytosis or RBC enzymopathies (G6PD deficiency), but these do not cause thrombocytopenia. One exception is an acquired membrane defect, paroxysmal nocturnal hemoglobinuria (PNH), in which RBCs and other blood cells become susceptible to complement-mediated lysis. Testing for PNH by peripheral blood flow cytometry should be considered if the blood film lacks schistocytes. Systemic disorders that cause intravascular hemolysis include severe burns (heat damage to RBCs), RBC trauma from “march hemoglobinuria” or mechanical heart valves, immune (antibody-mediated) hemolysis from Rh immune globulin administration, cold agglutinin disease or ABO mismatched transfusion, and infections including the intraerythrocyte parasites malaria, Bartonellosis, and Babesiosis, as well as organisms that induce RBC fragility such as Leishmaniasis, Clostridium perfringens, and Haemophilus influenzae B.

On review of additional history, the patient had not recently received blood products. He had received heparin during prior hospitalizations, but had no prior history of thrombosis. He had no history of tick exposure. Peripheral blood smear was obtained and reviewed by a hematopathologist. It showed no schistocytes or spherocytes, but demonstrated pyropoikilocytosis.

The blood smear helps narrow the differential further. The lack of schistocytes makes TMA far less likely and so plasma exchange is not urgently indicated. The differential still includes drug-­induced TMA (gemcitabine being a well-known cause for TMA) and cancer-associated TMA could still cause these findings, but plasma exchange does not improve outcomes. Acquired (immune) TTP is very unlikely unless the patient did not improve with supportive care or developed neurologic symptoms. Similarly, atypical (complement-driven) HUS would only be considered if renal failure did not improve with supportive care.

The blood smear does show a surprising finding of pyropoikilocytosis. Pyropoikilocytosis refers to changes in RBC shape (poikilocytosis) typically seen with thermal injury or rare RBC membrane structural defects. Hereditary pyropoikilocytosis, a very rare disease, is characterized by chronic hyperproliferative, compensated anemia, and occasional hemolytic crises. These crises are associated with splenomegaly, reticulocytosis, and elevated bilirubin with jaundice. As the patient has no history of similar episodes, the blood smear changes are not due to a hereditary cause and obviously not due to thermal injury (ie, severe burns). Pyropoikilocytosis has been rarely reported in drug-induced TMA and in severe bacterial bloodstream infections (most commonly Gram-negative bacilli). This patient has received gemcitabine (a known cause of drug-induced TMA) and has a recently diagnosed infection (C difficile colitis), either of which could be linked to this rare blood smear finding. Both of these syndromes would be treated with supportive care plus avoidance of future gemcitabine.

Transfusion of packed RBCs is indicated given his profound anemia and symptoms of fatigue. One should obtain further testing for cold agglutinins, PNH, and echocardiography to exclude endocarditis. If he were to become critically ill, anuric, or encephalopathic, then one could consider plasma exchange for treatment of TMA and hemoglobin-mediated AKI. Pyropoikilocytosis should be considered the result of drug-induced TMA, severe C difficile colitis, or an occult infection.

The patient was transfused packed RBCs. Because of a concern for an acute TMA such as TTP, both a hematopathologist and the consulting hematology/oncology team reviewed the peripheral blood morphology emergently. He was given aggressive fluid resuscitation and received 3 L of IV lactated ringers’ solution. An echocardiogram did not show valvular abnormalities. A renal biopsy was contraindicated because of the severe thrombocytopenia.

Given the recently confirmed C difficile colitis along with the findings of pyropoikilocytosis on the peripheral smear, toxin-mediated intravascular hemolysis from systemic C difficile infection became the leading diagnosis. Positing that the C difficile colitis was inadequately treated with oral metronidazole, aggressive treatment for C difficile was initiated with oral vancomycin in addition to intravenous metronidazole. Intravenous metronidazole was included given his elevated creatinine, presence of severe colitis on imaging, and concern he may be at risk for translocation of colonic C difficile or exotoxin into the bloodstream.

Over the course of the next 3 days, the patient’s platelet count normalized and his hemoglobin, creatinine, and symptoms of fatigue improved. Blood cultures remained negative. The patient’s rapid improvement with antibiotics supported our final diagnosis of toxin-mediated hemolysis caused by a systemic C difficile infection. On follow-up testing after hospital discharge, hemoglobin had returned to prior baseline and there was no recurrent hemolysis. Gemcitabine was considered to be a possible cause of his hemolytic anemia and was not continued in further treatment for his NSCLC.

When evaluating patients with cancer who present with fatigue, hospitalists should consider a broad list of potential causes. The differential should include etiologies directly related to the malignancy, paraneoplastic phenomena, treatment-related complications, and diseases unrelated to cancer. In addition, as the number of medications used for cancer proliferates, hospitalists must take a detailed history of the agents used and be aware of major side effects. Using this information, hospitalists may undertake a targeted approach to diagnostics while searching for a cause of fatigue.

When lab testing reveals profound anemia, hospitalists must consider syndromes that may require emergent management. Anemia can be caused by decreased RBC production, and acute anemia in the absence of clear blood loss suggests hemolysis. Moreover, the combination of elevated LDH and low haptoglobin is quite specific of hemolytic anemia.^1,2 Once hemolytic anemia is identified, DIC and TMA syndromes (such as TTP) need to be considered. The combination of hemolytic anemia and AKI may indicate a medical emergency and should prompt hospitalists to obtain an urgent peripheral blood smear to help narrow the differential.³

The absence of schistocytes on a blood smear does not rule out TTP or HUS, but does argue strongly against these diagnoses.^4,5 Of note, consultation with a hematopathologist and hematology subspecialist should be done to ensure appropriate and timely review of the peripheral blood smear.

In this case, the blood smear led to a very rare finding of pyropoikilocytosis. The unexpected result should prompt a broader review of the medical history particularly as it relates to the patient’s broader symptoms and laboratory abnormalities. Acquired pyropoikilocytosis is a very specific finding known to be associated only with hyperthermal injury (seen in burn patients), drug-induced TMA, and bacterial bloodstream infections, mainly Gram-negative toxins and Clostridioidal infections.^6-8 In this case, both drug-induced TMA and C difficile infection were considered.

Gemcitabine-induced TMA can occur with either short or long term use of the medication and can be difficult to distinguish from TTP. While both TTP and gemcitabine-induced TMA can cause thrombocytopenia, hemolytic anemia, and schistocytes on a blood smear, the latter causes acute kidney injury more frequently than TTP. In addition, gemcitabine-­induced TMA may not lead to severe decrease in ADAMTS13 activity. A kidney biopsy could confirm drug-induced TMA but was contraindicated in this case because of the thrombocytopenia. Gemcitabine should not be restarted if this side effect is suspected.

Given the continued rise in C difficile incidence, hospitalists should be aware that C difficile infection can cause extraintestinal illness.^9,10 Although uncommon, these extraintestinal complications are associated with high risk of mortality and frequently occur in those with a history of intestinal injury or inflammation and a concomitant bloodstream infection.¹⁰ Regarding the possibility of C difficile contributing to hemolysis in this case, the patient’s low blood counts and hemolysis improved concomitantly with more aggressive treatment of C difficile infection. Although his blood cultures were sterile, C difficile is notoriously difficult to culture. Prior case reports have associated C difficile with intravascular hemolysis, which leads to the possibility that the patient did have a very rare manifestation of this unfortunately common infection.¹¹

This case provides an excellent example of a diagnostic pivot point initiated by new information that fundamentally alters a patient’s diagnostic journey. Here, the finding of pyroipoikilocytes on peripheral smear led us to alter the differential diagnosis. Such pivots are often “surprises” that cause the care team to stop and reconsider their differential diagnosis because the problem representation has fundamentally changed. This patient’s unexpected fiery finding provided a pivot point that led to his effective treatment and recovery.

• In evaluating symptomatic cancer patients, providers must consider sequelae of the tumor, paraneoplastic phenomena, and treatment-related complications.
• Hemolytic anemia may represent a life-threatening emergency particularly when accompanied by AKI and requires urgent peripheral blood smear evaluation.
• Acquired pyropoikilocytosis is a specific finding known to be associated only with thermal injury, drug-induced TMA, and bacterial toxin–mediated hemolysis.

The authors have nothing to disclose.

A 62-year-old man with metastatic non–small cell lung cancer (NSCLC) presented to the Emergency Department with 3 days of progressive generalized weakness, anorexia, and nonbloody diarrhea. He denied fever, chills, nausea, vomiting, cough, shortness of breath, or abdominal pain. He had no sick contacts.

One diagnostic approach for patients with cancer who present with new symptoms is to consider diagnoses both related and unrelated to the cancer. Cancer-related diagnoses can include the broad categories of complications related to the tumor itself (such as mass effect), paraneoplastic phenomena, or treatment-related complications (such as infection from immunosuppression or chemotherapy toxicity).

For this patient with metastatic NSCLC, weakness, anorexia, and diarrhea are unlikely to be related to mass effect unless the patient has peritoneal metastases (an uncommon complication of NSCLC) with carcinomatosis-associated diarrhea.

Paraneoplastic phenomena, such as hypercalcemia or hyponatremia from the syndrome of inappropriate antidiuretic hormone (SIADH), are common with NSCLC and could both lead to weakness and anorexia. Hematologic consequences of NSCLC (or its treatment) include anemia, thrombosis, and thrombotic microangiopathy (TMA), though diarrhea, in the absence of abdominal pain or hematochezia, would be unexpected.

Weakness, anorexia, and diarrhea may also be symptoms of chemotherapy toxicity or an infection resulting from immunosuppression. It would be important to know what specific treatment the patient has received. Chemotherapy commonly causes neutropenia and predisposes to rapidly progressive infections, while immunotherapies have other toxicities. Diarrhea is a common toxicity of the checkpoint inhibitors and anaplastic lymphoma kinase (ALK) inhibitors that are frequently used to treat metastatic NSCLC. Checkpoint inhibitors also are known to cause a wide range of autoimmune phenomena including colitis.

Finally, the patient’s symptoms may be unrelated to the cancer. Weakness, anorexia, and nonbloody diarrhea could be signs of viral or bacterial gastroenteritis or Clostridioides difficile colitis particularly with frequent healthcare contact or antimicrobial use.

Two days prior, he had been diagnosed with nonsevere Clostridioides difficile colitis in an acute care clinic. He was started on oral metronidazole, but his diarrhea worsened over the next day and was accompanied by weakness and anorexia. Additional past medical history included untreated hepatitis C infection, chronic kidney disease stage 3, seizure disorder, and left lung NSCLC (adenocarcinoma). The lung cancer was diagnosed 8 months prior when he had presented with hemoptysis and 3 months of progressive constitutional symptoms. Imaging at that time revealed metastases to the contralateral lung and regional lymph nodes, as well as vertebrae, ribs, and pelvis. He had no abdominal metastases. He was initially treated with carboplatin and paclitaxel. After a partial response to initial chemotherapy, he developed peripheral neuropathy and was switched to gemcitabine 12 weeks ago. He received five cycles of gemcitabine over 10 weeks. He was last administered gemcitabine 2 weeks prior. He had not received any additional chemotherapy or immunotherapy. He had a 40 pack-year history of smoking, but quit when diagnosed with cancer. He did not drink alcohol. He had no recent travel or sick contacts. He was not on any medications. He was homeless but staying with family members in the area. Additional review of systems was negative for recent bleeding, bruising, hemoptysis, melena, hematochezia, or hematuria.

Recent treatment with gemcitabine could contribute to the presentation in a number of ways. First, gemcitabine is associated with myelosuppression and neutropenia that could predispose him to infectious colitis. Second, gemcitabine is known to cause anemia, anorexia, diarrhea, and fatigue. Third, gemcitabine may also cause renal injury that can contribute to worsening anemia. He may be at greater risk of anemia and renal toxicity because of preexisting chronic kidney disease. Finally, gemcitabine can rarely cause TMA with characteristics that mimic the hemolytic-uremic syndrome with microangiopathic hemolytic anemia, mild thrombocytopenia, and severe acute kidney injury (AKI).

In addition, worsening infectious colitis could certainly explain his presenting symptoms. At this point, local mass effect seems unlikely despite his metastatic disease. Lastly, it should be noted that, in an immunosuppressed cancer patient, multiple problems could be present at the same time. Laboratory testing should evaluate for hypercalcemia, SIADH, hematologic indexes, and renal function. If initial laboratory evaluation is unrevealing, abdominal imaging may be needed to assess for carcinomatosis, complications from colitis, typhlitis, abscess, or perforation.

On physical examination, the patient appeared fatigued. His temperature was 36.8°C, blood pressure 158/72 mm Hg, pulse 88 beats per minute, respiratory rate 16 breaths per minute, and oxygen saturation was 96% while breathing ambient air. There was neither scleral icterus nor conjunctival injection but he had mild conjunctival pallor. Cardiovascular and lung examinations were normal. Abdominal exam revealed normal bowel sounds without tenderness or organomegaly. He had no supraclavicular, axillary, or inguinal lymphadenopathy. He was alert and oriented. Cranial nerves II through XII were intact. He had decreased muscle bulk in his extremities without focal weakness. Gait and reflexes were not tested.

Initial laboratory testing revealed a white blood cell count of 5.5 K/mm³, hemoglobin of 5 g/dL (hemoglobin 1 month prior was 10.1 g/dL), and platelet count of 20 K/mm³ (platelet count 1 month prior was 246 K/mm³). Creatinine was 3.9 mg/dL (compared with a baseline of 1.8 mg/dL), and blood urea nitrogen was 39 mg/dL. His sodium was 137 mEq/L, potassium 4.2 mEq/L, chloride 105 mEq/L, bicarbonate 22 mEq/L, and thyroid stimulating hormone 0.9 mU/L. His total protein was 4.9 g/dL, albumin 2.1 g/dL, alkaline phosphatase 60 IU/L, alanine aminotransferase 17 IU/L, aspartate aminotransferase 60 IU/L, direct bilirubin 0.2 mg/dL, and total bilirubin 0.5 mg/dL. A chest x-ray showed no infiltrates.

The patient’s laboratory tests reveal several important new findings, including severe acute on chronic anemia, acute thrombocytopenia, and AKI, without clinical evidence of acute blood loss. These changes could be parts of a syndrome or multiple independent disorders. The most urgent priority is to evaluate for TMAs, many of which are fatal if not diagnosed and treated expeditiously. This includes thrombotic thrombocytopenic purpura (TTP), disseminated intravascular hemolysis (DIC), and atypical hemolytic uremic syndrome (aHUS). A manual review of a peripheral blood smear is required to evaluate for fragmented red blood cells (schistocytes). Thereafter, ancillary testing to confirm intravascular hemolysis would include measuring free plasma hemoglobin and lactate dehydrogenase (LDH). Additionally, in intravascular hemolysis, haptoglobin should be depleted and urinalysis should show heme-positive urine without RBCs. In this case the patient’s normal bilirubin studies argue against hemolysis; however, elevated bilirubin is variably present in hemolytic anemias depending on the liver’s ability to conjugate and excrete bilirubin, the relative degree of RBC turnover, and type of hemolysis. Patients with intravascular hemolysis lose hemoglobin directly into the urine leaving relatively little hemoglobin to be incorporated into bile once it has reached the reticuloendothelial system. This results in relatively normal bilirubin levels. More specific indicators of intravascular hemolysis include pink colored plasma on visual inspection (commonly done in the blood bank as part of assessing for hemolytic transfusion reactions), measuring plasma free hemoglobin, or by detecting hemoglobin in the urine.

If microangiopathic hemolytic anemia (MAHA) is excluded, then other causes of these laboratory abnormalities should be considered. Bleeding is the most common cause for anemia, and thrombocytopenia predisposes patients to bleeding. However, there is no evidence of bleeding in this patient, and such a rapid acute anemia is unlikely to be caused by occult blood loss alone. Concurrent anemia and thrombocytopenia could be evidence of bone marrow toxicity from chemotherapy or neoplastic infiltration. With marrow infiltration, there are typically signs on the peripheral smear of leukoerythroblastosis, with circulating nucleated red blood cells and early myeloid forms. Concurrent immune thrombocytopenia (ITP) and autoimmune hemolytic anemia (AIHA), or Evans’ Syndrome, should also be considered. AIHA would be suggested by spherocytes on the peripheral smear, elevated LDH and a positive direct antibody test (DAT).

Regarding the AKI, the patient has diarrhea, which could lead to prerenal azotemia and acute tubular necrosis. A formal urinalysis would evaluate for prerenal and intrinsic kidney disease. TMA can cause intrinsic kidney injury with a benign urinary sediment. The blood urea nitrogen-to-creatinine ratio is not elevated, but in a patient with malnutrition this may not indicate prerenal azotemia. In summary, to differentiate potential TMAs from other causes, the patient needs a blood smear, coagulation studies, and an evaluation for hemolysis, including a urinalysis for free heme and any evidence of intrinsic kidney disease.

Urinalysis showed amber-colored, dilute urine with no white blood cells, red blood cells, protein, or casts. It was positive for blood and negative for bilirubin and hemosiderin. LDH was 1,382 IU/L (reference range 135-225 IU/L), and haptoglobin was unmeasurably low. His ferritin was 2,267 ng/mL, serum iron was 57 mcg/dL, total iron-binding capacity was 241 mcg/dL, and transferrin was 162 mcg/dL. Reticulocyte count was 6% (reticulocyte index of 0.86). Vitamin B12 level was normal. DAT was negative; INR and aPTT were normal. Fibrinogen was 287 mg/dL (reference range 200-400 mg/dL), and D-dimer was 5,095 ng/mL (reference range 0-229 ng/mL).

The urinalysis shows no active sediment to suggest vasculitis or glomerulonephritis. The kidney injury could be the result of renal toxicity from free hemoglobin or as part of TMA caused by microvascular thrombosis. The dilute urine makes prerenal azotemia less likely.

There is clearly acute intravascular hemolysis occurring as evidenced by hemoglobinuria, very high LDH, and undetectable serum haptoglobin. The hemolysis is acute because chronic intravascular hemolysis would lead to positive urine hemosiderin via deposition in the renal tubules. Autoimmune hemolytic anemia is much less likely, but not ruled out, by a negative DAT.

This syndrome can be further refined from acute anemia to acute anemia with likely nonimmune intravascular hemolysis, acute thrombocytopenia, and AKI with hemoglobinuria and a bland urinary sediment. At this point, intravascular hemolysis and kidney injury could be part of a unifying diagnosis. However, this does not account for the patient’s thrombocytopenia, and TMA remains the best explanation for the constellation of findings. Review of the peripheral blood smear is urgent because evidence of MAHA would prompt urgent plasma exchange based on presumptive diagnosis of acquired TTP to later be confirmed with ADAMTS13 activity testing. Most TMAs are treated with supportive care only; TTP and aHUS have specific interventions that change the natural history of the disease (plasma exchange and anticomplement therapy, respectively). Given both the deadly natural history and opportunity to intervene with plasma exchange, patients with TMA should be treated with urgent plasma exchange until ADAMTS13 deficiency is confirmed or refuted. One TMA that can be excluded at this point is DIC. DIC in its acute and chronic forms nearly universally causes MAHA, thrombocytopenia, and consumptive coagulopathy including hypofibrinogenemia.

If MAHA is excluded, then other causes of intravascular hemolysis should be considered, along with causes of thrombocytopenia that might be occurring concurrently. Intravascular hemolysis can be further differentiated by etiologies primarily related to the RBC or whether the RBC is the innocent bystander amidst a systemic illness. RBC disorders include syndromes affecting RBC fragility like hereditary spherocytosis or RBC enzymopathies (G6PD deficiency), but these do not cause thrombocytopenia. One exception is an acquired membrane defect, paroxysmal nocturnal hemoglobinuria (PNH), in which RBCs and other blood cells become susceptible to complement-mediated lysis. Testing for PNH by peripheral blood flow cytometry should be considered if the blood film lacks schistocytes. Systemic disorders that cause intravascular hemolysis include severe burns (heat damage to RBCs), RBC trauma from “march hemoglobinuria” or mechanical heart valves, immune (antibody-mediated) hemolysis from Rh immune globulin administration, cold agglutinin disease or ABO mismatched transfusion, and infections including the intraerythrocyte parasites malaria, Bartonellosis, and Babesiosis, as well as organisms that induce RBC fragility such as Leishmaniasis, Clostridium perfringens, and Haemophilus influenzae B.

On review of additional history, the patient had not recently received blood products. He had received heparin during prior hospitalizations, but had no prior history of thrombosis. He had no history of tick exposure. Peripheral blood smear was obtained and reviewed by a hematopathologist. It showed no schistocytes or spherocytes, but demonstrated pyropoikilocytosis.

The blood smear helps narrow the differential further. The lack of schistocytes makes TMA far less likely and so plasma exchange is not urgently indicated. The differential still includes drug-­induced TMA (gemcitabine being a well-known cause for TMA) and cancer-associated TMA could still cause these findings, but plasma exchange does not improve outcomes. Acquired (immune) TTP is very unlikely unless the patient did not improve with supportive care or developed neurologic symptoms. Similarly, atypical (complement-driven) HUS would only be considered if renal failure did not improve with supportive care.

The blood smear does show a surprising finding of pyropoikilocytosis. Pyropoikilocytosis refers to changes in RBC shape (poikilocytosis) typically seen with thermal injury or rare RBC membrane structural defects. Hereditary pyropoikilocytosis, a very rare disease, is characterized by chronic hyperproliferative, compensated anemia, and occasional hemolytic crises. These crises are associated with splenomegaly, reticulocytosis, and elevated bilirubin with jaundice. As the patient has no history of similar episodes, the blood smear changes are not due to a hereditary cause and obviously not due to thermal injury (ie, severe burns). Pyropoikilocytosis has been rarely reported in drug-induced TMA and in severe bacterial bloodstream infections (most commonly Gram-negative bacilli). This patient has received gemcitabine (a known cause of drug-induced TMA) and has a recently diagnosed infection (C difficile colitis), either of which could be linked to this rare blood smear finding. Both of these syndromes would be treated with supportive care plus avoidance of future gemcitabine.

Transfusion of packed RBCs is indicated given his profound anemia and symptoms of fatigue. One should obtain further testing for cold agglutinins, PNH, and echocardiography to exclude endocarditis. If he were to become critically ill, anuric, or encephalopathic, then one could consider plasma exchange for treatment of TMA and hemoglobin-mediated AKI. Pyropoikilocytosis should be considered the result of drug-induced TMA, severe C difficile colitis, or an occult infection.

The patient was transfused packed RBCs. Because of a concern for an acute TMA such as TTP, both a hematopathologist and the consulting hematology/oncology team reviewed the peripheral blood morphology emergently. He was given aggressive fluid resuscitation and received 3 L of IV lactated ringers’ solution. An echocardiogram did not show valvular abnormalities. A renal biopsy was contraindicated because of the severe thrombocytopenia.

Given the recently confirmed C difficile colitis along with the findings of pyropoikilocytosis on the peripheral smear, toxin-mediated intravascular hemolysis from systemic C difficile infection became the leading diagnosis. Positing that the C difficile colitis was inadequately treated with oral metronidazole, aggressive treatment for C difficile was initiated with oral vancomycin in addition to intravenous metronidazole. Intravenous metronidazole was included given his elevated creatinine, presence of severe colitis on imaging, and concern he may be at risk for translocation of colonic C difficile or exotoxin into the bloodstream.

Over the course of the next 3 days, the patient’s platelet count normalized and his hemoglobin, creatinine, and symptoms of fatigue improved. Blood cultures remained negative. The patient’s rapid improvement with antibiotics supported our final diagnosis of toxin-mediated hemolysis caused by a systemic C difficile infection. On follow-up testing after hospital discharge, hemoglobin had returned to prior baseline and there was no recurrent hemolysis. Gemcitabine was considered to be a possible cause of his hemolytic anemia and was not continued in further treatment for his NSCLC.

When evaluating patients with cancer who present with fatigue, hospitalists should consider a broad list of potential causes. The differential should include etiologies directly related to the malignancy, paraneoplastic phenomena, treatment-related complications, and diseases unrelated to cancer. In addition, as the number of medications used for cancer proliferates, hospitalists must take a detailed history of the agents used and be aware of major side effects. Using this information, hospitalists may undertake a targeted approach to diagnostics while searching for a cause of fatigue.

When lab testing reveals profound anemia, hospitalists must consider syndromes that may require emergent management. Anemia can be caused by decreased RBC production, and acute anemia in the absence of clear blood loss suggests hemolysis. Moreover, the combination of elevated LDH and low haptoglobin is quite specific of hemolytic anemia.^1,2 Once hemolytic anemia is identified, DIC and TMA syndromes (such as TTP) need to be considered. The combination of hemolytic anemia and AKI may indicate a medical emergency and should prompt hospitalists to obtain an urgent peripheral blood smear to help narrow the differential.³

The absence of schistocytes on a blood smear does not rule out TTP or HUS, but does argue strongly against these diagnoses.^4,5 Of note, consultation with a hematopathologist and hematology subspecialist should be done to ensure appropriate and timely review of the peripheral blood smear.

In this case, the blood smear led to a very rare finding of pyropoikilocytosis. The unexpected result should prompt a broader review of the medical history particularly as it relates to the patient’s broader symptoms and laboratory abnormalities. Acquired pyropoikilocytosis is a very specific finding known to be associated only with hyperthermal injury (seen in burn patients), drug-induced TMA, and bacterial bloodstream infections, mainly Gram-negative toxins and Clostridioidal infections.^6-8 In this case, both drug-induced TMA and C difficile infection were considered.

Gemcitabine-induced TMA can occur with either short or long term use of the medication and can be difficult to distinguish from TTP. While both TTP and gemcitabine-induced TMA can cause thrombocytopenia, hemolytic anemia, and schistocytes on a blood smear, the latter causes acute kidney injury more frequently than TTP. In addition, gemcitabine-­induced TMA may not lead to severe decrease in ADAMTS13 activity. A kidney biopsy could confirm drug-induced TMA but was contraindicated in this case because of the thrombocytopenia. Gemcitabine should not be restarted if this side effect is suspected.

Given the continued rise in C difficile incidence, hospitalists should be aware that C difficile infection can cause extraintestinal illness.^9,10 Although uncommon, these extraintestinal complications are associated with high risk of mortality and frequently occur in those with a history of intestinal injury or inflammation and a concomitant bloodstream infection.¹⁰ Regarding the possibility of C difficile contributing to hemolysis in this case, the patient’s low blood counts and hemolysis improved concomitantly with more aggressive treatment of C difficile infection. Although his blood cultures were sterile, C difficile is notoriously difficult to culture. Prior case reports have associated C difficile with intravascular hemolysis, which leads to the possibility that the patient did have a very rare manifestation of this unfortunately common infection.¹¹

This case provides an excellent example of a diagnostic pivot point initiated by new information that fundamentally alters a patient’s diagnostic journey. Here, the finding of pyroipoikilocytes on peripheral smear led us to alter the differential diagnosis. Such pivots are often “surprises” that cause the care team to stop and reconsider their differential diagnosis because the problem representation has fundamentally changed. This patient’s unexpected fiery finding provided a pivot point that led to his effective treatment and recovery.

• In evaluating symptomatic cancer patients, providers must consider sequelae of the tumor, paraneoplastic phenomena, and treatment-related complications.
• Hemolytic anemia may represent a life-threatening emergency particularly when accompanied by AKI and requires urgent peripheral blood smear evaluation.
• Acquired pyropoikilocytosis is a specific finding known to be associated only with thermal injury, drug-induced TMA, and bacterial toxin–mediated hemolysis.

The authors have nothing to disclose.

A 62-year-old man with metastatic non–small cell lung cancer (NSCLC) presented to the Emergency Department with 3 days of progressive generalized weakness, anorexia, and nonbloody diarrhea. He denied fever, chills, nausea, vomiting, cough, shortness of breath, or abdominal pain. He had no sick contacts.

One diagnostic approach for patients with cancer who present with new symptoms is to consider diagnoses both related and unrelated to the cancer. Cancer-related diagnoses can include the broad categories of complications related to the tumor itself (such as mass effect), paraneoplastic phenomena, or treatment-related complications (such as infection from immunosuppression or chemotherapy toxicity).

For this patient with metastatic NSCLC, weakness, anorexia, and diarrhea are unlikely to be related to mass effect unless the patient has peritoneal metastases (an uncommon complication of NSCLC) with carcinomatosis-associated diarrhea.

Paraneoplastic phenomena, such as hypercalcemia or hyponatremia from the syndrome of inappropriate antidiuretic hormone (SIADH), are common with NSCLC and could both lead to weakness and anorexia. Hematologic consequences of NSCLC (or its treatment) include anemia, thrombosis, and thrombotic microangiopathy (TMA), though diarrhea, in the absence of abdominal pain or hematochezia, would be unexpected.

Weakness, anorexia, and diarrhea may also be symptoms of chemotherapy toxicity or an infection resulting from immunosuppression. It would be important to know what specific treatment the patient has received. Chemotherapy commonly causes neutropenia and predisposes to rapidly progressive infections, while immunotherapies have other toxicities. Diarrhea is a common toxicity of the checkpoint inhibitors and anaplastic lymphoma kinase (ALK) inhibitors that are frequently used to treat metastatic NSCLC. Checkpoint inhibitors also are known to cause a wide range of autoimmune phenomena including colitis.

Finally, the patient’s symptoms may be unrelated to the cancer. Weakness, anorexia, and nonbloody diarrhea could be signs of viral or bacterial gastroenteritis or Clostridioides difficile colitis particularly with frequent healthcare contact or antimicrobial use.

Two days prior, he had been diagnosed with nonsevere Clostridioides difficile colitis in an acute care clinic. He was started on oral metronidazole, but his diarrhea worsened over the next day and was accompanied by weakness and anorexia. Additional past medical history included untreated hepatitis C infection, chronic kidney disease stage 3, seizure disorder, and left lung NSCLC (adenocarcinoma). The lung cancer was diagnosed 8 months prior when he had presented with hemoptysis and 3 months of progressive constitutional symptoms. Imaging at that time revealed metastases to the contralateral lung and regional lymph nodes, as well as vertebrae, ribs, and pelvis. He had no abdominal metastases. He was initially treated with carboplatin and paclitaxel. After a partial response to initial chemotherapy, he developed peripheral neuropathy and was switched to gemcitabine 12 weeks ago. He received five cycles of gemcitabine over 10 weeks. He was last administered gemcitabine 2 weeks prior. He had not received any additional chemotherapy or immunotherapy. He had a 40 pack-year history of smoking, but quit when diagnosed with cancer. He did not drink alcohol. He had no recent travel or sick contacts. He was not on any medications. He was homeless but staying with family members in the area. Additional review of systems was negative for recent bleeding, bruising, hemoptysis, melena, hematochezia, or hematuria.

Recent treatment with gemcitabine could contribute to the presentation in a number of ways. First, gemcitabine is associated with myelosuppression and neutropenia that could predispose him to infectious colitis. Second, gemcitabine is known to cause anemia, anorexia, diarrhea, and fatigue. Third, gemcitabine may also cause renal injury that can contribute to worsening anemia. He may be at greater risk of anemia and renal toxicity because of preexisting chronic kidney disease. Finally, gemcitabine can rarely cause TMA with characteristics that mimic the hemolytic-uremic syndrome with microangiopathic hemolytic anemia, mild thrombocytopenia, and severe acute kidney injury (AKI).

In addition, worsening infectious colitis could certainly explain his presenting symptoms. At this point, local mass effect seems unlikely despite his metastatic disease. Lastly, it should be noted that, in an immunosuppressed cancer patient, multiple problems could be present at the same time. Laboratory testing should evaluate for hypercalcemia, SIADH, hematologic indexes, and renal function. If initial laboratory evaluation is unrevealing, abdominal imaging may be needed to assess for carcinomatosis, complications from colitis, typhlitis, abscess, or perforation.

On physical examination, the patient appeared fatigued. His temperature was 36.8°C, blood pressure 158/72 mm Hg, pulse 88 beats per minute, respiratory rate 16 breaths per minute, and oxygen saturation was 96% while breathing ambient air. There was neither scleral icterus nor conjunctival injection but he had mild conjunctival pallor. Cardiovascular and lung examinations were normal. Abdominal exam revealed normal bowel sounds without tenderness or organomegaly. He had no supraclavicular, axillary, or inguinal lymphadenopathy. He was alert and oriented. Cranial nerves II through XII were intact. He had decreased muscle bulk in his extremities without focal weakness. Gait and reflexes were not tested.

Initial laboratory testing revealed a white blood cell count of 5.5 K/mm³, hemoglobin of 5 g/dL (hemoglobin 1 month prior was 10.1 g/dL), and platelet count of 20 K/mm³ (platelet count 1 month prior was 246 K/mm³). Creatinine was 3.9 mg/dL (compared with a baseline of 1.8 mg/dL), and blood urea nitrogen was 39 mg/dL. His sodium was 137 mEq/L, potassium 4.2 mEq/L, chloride 105 mEq/L, bicarbonate 22 mEq/L, and thyroid stimulating hormone 0.9 mU/L. His total protein was 4.9 g/dL, albumin 2.1 g/dL, alkaline phosphatase 60 IU/L, alanine aminotransferase 17 IU/L, aspartate aminotransferase 60 IU/L, direct bilirubin 0.2 mg/dL, and total bilirubin 0.5 mg/dL. A chest x-ray showed no infiltrates.

The patient’s laboratory tests reveal several important new findings, including severe acute on chronic anemia, acute thrombocytopenia, and AKI, without clinical evidence of acute blood loss. These changes could be parts of a syndrome or multiple independent disorders. The most urgent priority is to evaluate for TMAs, many of which are fatal if not diagnosed and treated expeditiously. This includes thrombotic thrombocytopenic purpura (TTP), disseminated intravascular hemolysis (DIC), and atypical hemolytic uremic syndrome (aHUS). A manual review of a peripheral blood smear is required to evaluate for fragmented red blood cells (schistocytes). Thereafter, ancillary testing to confirm intravascular hemolysis would include measuring free plasma hemoglobin and lactate dehydrogenase (LDH). Additionally, in intravascular hemolysis, haptoglobin should be depleted and urinalysis should show heme-positive urine without RBCs. In this case the patient’s normal bilirubin studies argue against hemolysis; however, elevated bilirubin is variably present in hemolytic anemias depending on the liver’s ability to conjugate and excrete bilirubin, the relative degree of RBC turnover, and type of hemolysis. Patients with intravascular hemolysis lose hemoglobin directly into the urine leaving relatively little hemoglobin to be incorporated into bile once it has reached the reticuloendothelial system. This results in relatively normal bilirubin levels. More specific indicators of intravascular hemolysis include pink colored plasma on visual inspection (commonly done in the blood bank as part of assessing for hemolytic transfusion reactions), measuring plasma free hemoglobin, or by detecting hemoglobin in the urine.

If microangiopathic hemolytic anemia (MAHA) is excluded, then other causes of these laboratory abnormalities should be considered. Bleeding is the most common cause for anemia, and thrombocytopenia predisposes patients to bleeding. However, there is no evidence of bleeding in this patient, and such a rapid acute anemia is unlikely to be caused by occult blood loss alone. Concurrent anemia and thrombocytopenia could be evidence of bone marrow toxicity from chemotherapy or neoplastic infiltration. With marrow infiltration, there are typically signs on the peripheral smear of leukoerythroblastosis, with circulating nucleated red blood cells and early myeloid forms. Concurrent immune thrombocytopenia (ITP) and autoimmune hemolytic anemia (AIHA), or Evans’ Syndrome, should also be considered. AIHA would be suggested by spherocytes on the peripheral smear, elevated LDH and a positive direct antibody test (DAT).

Regarding the AKI, the patient has diarrhea, which could lead to prerenal azotemia and acute tubular necrosis. A formal urinalysis would evaluate for prerenal and intrinsic kidney disease. TMA can cause intrinsic kidney injury with a benign urinary sediment. The blood urea nitrogen-to-creatinine ratio is not elevated, but in a patient with malnutrition this may not indicate prerenal azotemia. In summary, to differentiate potential TMAs from other causes, the patient needs a blood smear, coagulation studies, and an evaluation for hemolysis, including a urinalysis for free heme and any evidence of intrinsic kidney disease.

Urinalysis showed amber-colored, dilute urine with no white blood cells, red blood cells, protein, or casts. It was positive for blood and negative for bilirubin and hemosiderin. LDH was 1,382 IU/L (reference range 135-225 IU/L), and haptoglobin was unmeasurably low. His ferritin was 2,267 ng/mL, serum iron was 57 mcg/dL, total iron-binding capacity was 241 mcg/dL, and transferrin was 162 mcg/dL. Reticulocyte count was 6% (reticulocyte index of 0.86). Vitamin B12 level was normal. DAT was negative; INR and aPTT were normal. Fibrinogen was 287 mg/dL (reference range 200-400 mg/dL), and D-dimer was 5,095 ng/mL (reference range 0-229 ng/mL).

The urinalysis shows no active sediment to suggest vasculitis or glomerulonephritis. The kidney injury could be the result of renal toxicity from free hemoglobin or as part of TMA caused by microvascular thrombosis. The dilute urine makes prerenal azotemia less likely.

There is clearly acute intravascular hemolysis occurring as evidenced by hemoglobinuria, very high LDH, and undetectable serum haptoglobin. The hemolysis is acute because chronic intravascular hemolysis would lead to positive urine hemosiderin via deposition in the renal tubules. Autoimmune hemolytic anemia is much less likely, but not ruled out, by a negative DAT.

This syndrome can be further refined from acute anemia to acute anemia with likely nonimmune intravascular hemolysis, acute thrombocytopenia, and AKI with hemoglobinuria and a bland urinary sediment. At this point, intravascular hemolysis and kidney injury could be part of a unifying diagnosis. However, this does not account for the patient’s thrombocytopenia, and TMA remains the best explanation for the constellation of findings. Review of the peripheral blood smear is urgent because evidence of MAHA would prompt urgent plasma exchange based on presumptive diagnosis of acquired TTP to later be confirmed with ADAMTS13 activity testing. Most TMAs are treated with supportive care only; TTP and aHUS have specific interventions that change the natural history of the disease (plasma exchange and anticomplement therapy, respectively). Given both the deadly natural history and opportunity to intervene with plasma exchange, patients with TMA should be treated with urgent plasma exchange until ADAMTS13 deficiency is confirmed or refuted. One TMA that can be excluded at this point is DIC. DIC in its acute and chronic forms nearly universally causes MAHA, thrombocytopenia, and consumptive coagulopathy including hypofibrinogenemia.

If MAHA is excluded, then other causes of intravascular hemolysis should be considered, along with causes of thrombocytopenia that might be occurring concurrently. Intravascular hemolysis can be further differentiated by etiologies primarily related to the RBC or whether the RBC is the innocent bystander amidst a systemic illness. RBC disorders include syndromes affecting RBC fragility like hereditary spherocytosis or RBC enzymopathies (G6PD deficiency), but these do not cause thrombocytopenia. One exception is an acquired membrane defect, paroxysmal nocturnal hemoglobinuria (PNH), in which RBCs and other blood cells become susceptible to complement-mediated lysis. Testing for PNH by peripheral blood flow cytometry should be considered if the blood film lacks schistocytes. Systemic disorders that cause intravascular hemolysis include severe burns (heat damage to RBCs), RBC trauma from “march hemoglobinuria” or mechanical heart valves, immune (antibody-mediated) hemolysis from Rh immune globulin administration, cold agglutinin disease or ABO mismatched transfusion, and infections including the intraerythrocyte parasites malaria, Bartonellosis, and Babesiosis, as well as organisms that induce RBC fragility such as Leishmaniasis, Clostridium perfringens, and Haemophilus influenzae B.

On review of additional history, the patient had not recently received blood products. He had received heparin during prior hospitalizations, but had no prior history of thrombosis. He had no history of tick exposure. Peripheral blood smear was obtained and reviewed by a hematopathologist. It showed no schistocytes or spherocytes, but demonstrated pyropoikilocytosis.

The blood smear helps narrow the differential further. The lack of schistocytes makes TMA far less likely and so plasma exchange is not urgently indicated. The differential still includes drug-­induced TMA (gemcitabine being a well-known cause for TMA) and cancer-associated TMA could still cause these findings, but plasma exchange does not improve outcomes. Acquired (immune) TTP is very unlikely unless the patient did not improve with supportive care or developed neurologic symptoms. Similarly, atypical (complement-driven) HUS would only be considered if renal failure did not improve with supportive care.

The blood smear does show a surprising finding of pyropoikilocytosis. Pyropoikilocytosis refers to changes in RBC shape (poikilocytosis) typically seen with thermal injury or rare RBC membrane structural defects. Hereditary pyropoikilocytosis, a very rare disease, is characterized by chronic hyperproliferative, compensated anemia, and occasional hemolytic crises. These crises are associated with splenomegaly, reticulocytosis, and elevated bilirubin with jaundice. As the patient has no history of similar episodes, the blood smear changes are not due to a hereditary cause and obviously not due to thermal injury (ie, severe burns). Pyropoikilocytosis has been rarely reported in drug-induced TMA and in severe bacterial bloodstream infections (most commonly Gram-negative bacilli). This patient has received gemcitabine (a known cause of drug-induced TMA) and has a recently diagnosed infection (C difficile colitis), either of which could be linked to this rare blood smear finding. Both of these syndromes would be treated with supportive care plus avoidance of future gemcitabine.

Transfusion of packed RBCs is indicated given his profound anemia and symptoms of fatigue. One should obtain further testing for cold agglutinins, PNH, and echocardiography to exclude endocarditis. If he were to become critically ill, anuric, or encephalopathic, then one could consider plasma exchange for treatment of TMA and hemoglobin-mediated AKI. Pyropoikilocytosis should be considered the result of drug-induced TMA, severe C difficile colitis, or an occult infection.

The patient was transfused packed RBCs. Because of a concern for an acute TMA such as TTP, both a hematopathologist and the consulting hematology/oncology team reviewed the peripheral blood morphology emergently. He was given aggressive fluid resuscitation and received 3 L of IV lactated ringers’ solution. An echocardiogram did not show valvular abnormalities. A renal biopsy was contraindicated because of the severe thrombocytopenia.

Given the recently confirmed C difficile colitis along with the findings of pyropoikilocytosis on the peripheral smear, toxin-mediated intravascular hemolysis from systemic C difficile infection became the leading diagnosis. Positing that the C difficile colitis was inadequately treated with oral metronidazole, aggressive treatment for C difficile was initiated with oral vancomycin in addition to intravenous metronidazole. Intravenous metronidazole was included given his elevated creatinine, presence of severe colitis on imaging, and concern he may be at risk for translocation of colonic C difficile or exotoxin into the bloodstream.

Over the course of the next 3 days, the patient’s platelet count normalized and his hemoglobin, creatinine, and symptoms of fatigue improved. Blood cultures remained negative. The patient’s rapid improvement with antibiotics supported our final diagnosis of toxin-mediated hemolysis caused by a systemic C difficile infection. On follow-up testing after hospital discharge, hemoglobin had returned to prior baseline and there was no recurrent hemolysis. Gemcitabine was considered to be a possible cause of his hemolytic anemia and was not continued in further treatment for his NSCLC.

When evaluating patients with cancer who present with fatigue, hospitalists should consider a broad list of potential causes. The differential should include etiologies directly related to the malignancy, paraneoplastic phenomena, treatment-related complications, and diseases unrelated to cancer. In addition, as the number of medications used for cancer proliferates, hospitalists must take a detailed history of the agents used and be aware of major side effects. Using this information, hospitalists may undertake a targeted approach to diagnostics while searching for a cause of fatigue.

When lab testing reveals profound anemia, hospitalists must consider syndromes that may require emergent management. Anemia can be caused by decreased RBC production, and acute anemia in the absence of clear blood loss suggests hemolysis. Moreover, the combination of elevated LDH and low haptoglobin is quite specific of hemolytic anemia.^1,2 Once hemolytic anemia is identified, DIC and TMA syndromes (such as TTP) need to be considered. The combination of hemolytic anemia and AKI may indicate a medical emergency and should prompt hospitalists to obtain an urgent peripheral blood smear to help narrow the differential.³

The absence of schistocytes on a blood smear does not rule out TTP or HUS, but does argue strongly against these diagnoses.^4,5 Of note, consultation with a hematopathologist and hematology subspecialist should be done to ensure appropriate and timely review of the peripheral blood smear.

In this case, the blood smear led to a very rare finding of pyropoikilocytosis. The unexpected result should prompt a broader review of the medical history particularly as it relates to the patient’s broader symptoms and laboratory abnormalities. Acquired pyropoikilocytosis is a very specific finding known to be associated only with hyperthermal injury (seen in burn patients), drug-induced TMA, and bacterial bloodstream infections, mainly Gram-negative toxins and Clostridioidal infections.^6-8 In this case, both drug-induced TMA and C difficile infection were considered.

Gemcitabine-induced TMA can occur with either short or long term use of the medication and can be difficult to distinguish from TTP. While both TTP and gemcitabine-induced TMA can cause thrombocytopenia, hemolytic anemia, and schistocytes on a blood smear, the latter causes acute kidney injury more frequently than TTP. In addition, gemcitabine-­induced TMA may not lead to severe decrease in ADAMTS13 activity. A kidney biopsy could confirm drug-induced TMA but was contraindicated in this case because of the thrombocytopenia. Gemcitabine should not be restarted if this side effect is suspected.

Given the continued rise in C difficile incidence, hospitalists should be aware that C difficile infection can cause extraintestinal illness.^9,10 Although uncommon, these extraintestinal complications are associated with high risk of mortality and frequently occur in those with a history of intestinal injury or inflammation and a concomitant bloodstream infection.¹⁰ Regarding the possibility of C difficile contributing to hemolysis in this case, the patient’s low blood counts and hemolysis improved concomitantly with more aggressive treatment of C difficile infection. Although his blood cultures were sterile, C difficile is notoriously difficult to culture. Prior case reports have associated C difficile with intravascular hemolysis, which leads to the possibility that the patient did have a very rare manifestation of this unfortunately common infection.¹¹

This case provides an excellent example of a diagnostic pivot point initiated by new information that fundamentally alters a patient’s diagnostic journey. Here, the finding of pyroipoikilocytes on peripheral smear led us to alter the differential diagnosis. Such pivots are often “surprises” that cause the care team to stop and reconsider their differential diagnosis because the problem representation has fundamentally changed. This patient’s unexpected fiery finding provided a pivot point that led to his effective treatment and recovery.

• In evaluating symptomatic cancer patients, providers must consider sequelae of the tumor, paraneoplastic phenomena, and treatment-related complications.
• Hemolytic anemia may represent a life-threatening emergency particularly when accompanied by AKI and requires urgent peripheral blood smear evaluation.
• Acquired pyropoikilocytosis is a specific finding known to be associated only with thermal injury, drug-induced TMA, and bacterial toxin–mediated hemolysis.

The authors have nothing to disclose.

More than 200 million patients worldwide undergo major noncardiac surgery each year. Of these, more than 10 million patients suffer a major adverse cardiovascular event (MACE) within 30 days of surgery.¹ Elevated troponins after noncardiac surgery have been associated with increased mortality, but the management of these patients and the indications for screening remain unclear. The nomenclature around myocardial injury also remains confusing. In this Progress Note, we aim to define myocardial injury after noncardiac surgery (MINS) and discuss the key questions on MINS and postoperative troponin elevation.

A PubMed search for medical subject headings and the terms “myocardial injury after noncardiac surgery,” “perioperative troponin,” and “postoperative troponin” restricted to humans, English language, and published in the past 5 years resulted in 144 articles. Articles most relevant to this progress note were included. Guidelines from major societies on perioperative cardiovascular assessment and management were also reviewed.

The Fourth Universal Definition of Myocardial Infarction ( UDMI 4) defines myocardial injury as detection of an elevated cardiac troponin above the 99th percentile upper reference limit (URL).² Different troponin assays are not comparable and institutions set their own thresholds for abnormal troponin. Per UDMI 4, myocardial injury is classified as (Figure)^2-4:

• Acute Myocardial Infarction (MI): This is defined as “detection of a rise and/or fall of cardiac troponin with ≥1 value above the 99th percentile URL and ≥1 of the following: symptoms of acute myocardial ischemia, new ischemic electrocardiographic changes, development of pathological Q waves, or imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology.” If these patients have an acute atherosclerotic plaque rupture, they are classified as Type 1 MI (T1MI), and if they have a mismatch between oxygen supply/demand, they are classified as Type 2 MI (T2MI).
• Acute Nonischemic Myocardial Injury (NIMI): This is defined as detection of both a rise and/or fall of cardiac troponin and one or more cardiac troponin values above the 99th percentile URL, but no overt clinical evidence of myocardial ischemia.
• Chronic Myocardial Injury: This is defined as one or more cardiac troponin values above the 99th percentile URL but without a rise and/or fall pattern.

MINS is defined as a rise and/or fall of cardiac biomarkers of presumed ischemic etiology within 30 days of noncardiac surgery that may occur with or without the clinical criteria necessary to fulfill the universal definition of MI (Figure).^5-8

A meta-analysis of 169 studies reported the overall incidence of MINS to be 17.9%; the incidence was 19.6% when systematic troponin screening was done versus 9.9% when troponins were ordered selectively based on the clinical context.⁵

That meta-analysis found that patients with MINS were more likely to be older, male, undergoing nonelective surgeries, and have hypertension, coronary artery disease (CAD), prior MI, heart failure, or kidney disease.⁵ Intraoperative hypotension (defined as systolic blood pressure <100 mm Hg or mean arterial pressure <55 mm Hg for up to 5 minutes or <60 mm Hg for 30 minutes or more) and intraoperative tachycardia (defined as heart rate >100 beats per minute) have been associated with MINS.^5,9 The relationship between anesthesia type and MINS is uncertain.

MINS is associated with an increased risk of 30-day mortality, nonfatal cardiac arrest, heart failure, and stroke.In the Vascular Events In Noncardiac Surgery Patients Cohort Evaluation (VISION) studies, the majority of patients did not have ischemic symptoms.^6,7 In this study, 30-day mortality rates were 8.5% to 13.5% in patients with ischemic symptoms or electrocardiographic changes and 2.9% to 7.7% in patients with asymptomatic troponin elevations. Among the patients without MINS, 30-day mortality was 0.6% to 1.1%. Higher levels of cardiac troponin were associated with higher mortality rates and shorter time to death.

The recommendations for perioperative screening for MINS vary from society to society. Although MINS is associated with worse outcomes, and most patients with MINS are asymptomatic, perioperative screening for MINS in the absence of clinical signs or symptoms is currently not recommended by the American College of Cardiology/American Heart Association (ACC/AHA).¹⁰

ACC/AHA

“The usefulness of postoperative screening with troponin levels in patients at high risk for perioperative MI, but without signs or symptoms suggestive of myocardial ischemia or MI, is uncertain in the absence of established risks and benefits of a defined management strategy (Class IIb; level of evidence [LOE]–B).”¹⁰

European Society of Cardiology

“Measurement of B-type natriuretic peptides (BNP) and high-sensitivity troponins (hsTn) after surgery may be considered in high-risk patients to improve risk stratification (Class IIb; LOE-B). Preoperatively and postoperatively, patients who could most benefit from BNP or hsTn measurements are those with metabolic equivalents (METs) ≤4 or those with a revised cardiac risk index (RCRI) score >1 for vascular surgery and >2 for nonvascular surgery. Postoperatively, patients with a surgical Apgar score <7 should also be monitored with BNP or hsTn to detect complications early, independent of their RCRI values.”¹¹

Canadian Cardiovascular Society

“We recommend obtaining daily troponins for 48-72 hours after noncardiac surgery in patients with a baseline risk of >5% for cardiovascular death or nonfatal MI at 30 days after surgery (ie, patients with an elevated N-terminal-proBNP (NT-proBNP)/BNP before surgery or, if there is no NT-proBNP/BNP before surgery, in those who have an RCRI score ≥1, age 45-64 years with significant cardiovascular disease, or age ≥65 years) (Strong recommendation; Moderate quality evidence).”¹

Currently, evidence-based therapies are well established only for T1MI. However, it is often challenging to differentiate T1MI from other causes of troponin elevation in the perioperative setting in which anesthesia, sedation, or analgesia may mask ischemic symptoms that typically prompt further investigation. While peak troponin levels may be higher in T1MI than they are in T2MI, the initial or delta change in the troponin may provide poor discrimination between T1MI and T2MI.² Management is complicated not only by the uncertainty about the underlying diagnosis (T1MI, T2MI, or NIMI) but also by the heterogeneity in the underlying pathophysiology of troponin elevation in patients with T2MI and NIMI. Patients with T2MI are generally sicker and have higher mortality than patients with T1MI, and management typically involves treating the underlying reason for oxygen supply/demand mismatch. Mortality in T2MI is more commonly caused by noncardiovascular causes, but underlying CAD is an independent predictor of cardiovascular death or recurrent MI in these patients.

The MANAGE trial (Management of Myocardial Injury After Noncardiac Surgery) had several methodological limitations to inform clinical practice but showed potential benefit of dabigatran in patients with MINS.¹² In this trial, patients on dabigatran had significantly lower rates of the primary efficacy outcome (composite of vascular mortality and nonfatal MI, nonhemorrhagic stroke, peripheral arterial thrombosis, amputation, and symptomatic venous thromboembolism) without a significant increase in life-threatening, major, or critical organ bleeding. Of the secondary efficacy outcomes, only nonhemorrhagic stroke was significantly reduced with dabigatran, but the event rate was low. In the subgroup analysis, patients randomized to dabigatran within 5 days of MINS and those meeting the criteria for MI had significantly lower rates of the primary efficacy outcome.

Patients with T2MI with known CAD may benefit from long-term risk reduction strategies for secondary prevention. There are no definitive management strategies in the literature for T2MI with unknown or no CAD. The SWEDEHEART registry (Swedish Web-System for Enhancement and Development of Evidence-Based Care in Heart Disease Evaluated According to Recommended Therapy) enrolled 9,136 patients with MI with nonobstructive coronary arteries (MINOCA).¹³ Though MINOCA may include T1MI patients, the majority of these patients are classified as T2MI under UDMI 4. Therefore, it has been proposed that data from this registry may inform management on T2MI.¹⁴ Data from this registry showed that statins and angiotensin-­converting enzyme inhibitors or angiotensin II receptor blockers were associated with lower incidence of MACE over a mean follow-up of 4.1 years. Dual-antiplatelet therapy or beta blockers did not significantly lower the incidence of MACE.¹³ In another study assessing 2-year mortality in patients with T2MI, beta blockers were beneficial.¹⁵

Who should be screened?

Screening can be performed if further risk stratification of high-risk patients or patients with poor functional status is desired. European Society of Cardiology and Canadian Cardiovascular Society guidelines provide guidance on the screening criteria. Troponin elevation in a low-risk group is associated with a low mortality rate, and many of these troponin elevations may be secondary to causes other than myocardial ischemia.

How should screening be conducted?

If planning to obtain postoperative troponins, then preoperative troponin should be obtained because 35% of the patients may have a chronic troponin elevation.

What is the risk if postoperative troponin screening is not performed?

Most patients with MINS are asymptomatic. Systematic screening with troponins (compared with selective screening based on clinical signs or symptoms) can detect T1MI that would otherwise remain occult and undiagnosed.

What is the risk if postoperative troponin screening is performed?

Detecting asymptomatic troponin elevations could lead to potentially harmful treatments (eg, increased risk of bleeding with antithrombotics in the postoperative setting, increased use of cardiac angiography, or addition of new medications such as statins and beta-blockers in the postoperative setting with the potential for adverse effects).

How should MINS be documented?

ST-elevation and non–ST elevation MI (STEMI and NSTEMI) should be reserved for T1MI only. T1MI should be documented when acute plaque rupture is strongly suspected. T2MI should be documented when oxygen supply/demand mismatch is strongly suspected as the etiology of acute MI (eg, T2MI secondary to tachyarrhythmia, hypertensive emergency, or septic shock). Documenting as “demand ischemia” or “unlikely acute coronary syndrome” for T2MI or NIMI should be avoided. Troponin elevations not meeting the criteria for acute MI should be documented as “non-MI troponin elevation” (eg, non-MI troponin elevation secondary to chronic kidney disease or left ventricular hypertrophy). Terms like “troponinitis” or “troponinemia” should be avoided.³

Can MINS be prevented?

There are no well-defined strategies for prevention of MINS, but cardiovascular risk factors should be optimized preoperatively for all patients. In a meta-analysis, preoperative aspirin was not associated with reduced incidence of MINS, and the role of preoperative statins remains speculative; however, nonacute initiation of beta-blockers preoperatively was associated with a lower incidence of MINS.⁵ Withholding angiotensin-­converting enzyme inhibitors or angiotensin II receptor blockers in the 24 hours prior to surgery has been associated with a lower incidence of MINS. Intraoperative hypotension or tachycardia should be avoided.

While MINS has been associated with increased 30-day mortality, there are currently no definitive evidence-based management strategies for these patients. Institutions should consider creating decision-support tools if considering screening for MINS based on patient- and surgery-specific risk factors.

The authors have nothing to disclose.

More than 200 million patients worldwide undergo major noncardiac surgery each year. Of these, more than 10 million patients suffer a major adverse cardiovascular event (MACE) within 30 days of surgery.¹ Elevated troponins after noncardiac surgery have been associated with increased mortality, but the management of these patients and the indications for screening remain unclear. The nomenclature around myocardial injury also remains confusing. In this Progress Note, we aim to define myocardial injury after noncardiac surgery (MINS) and discuss the key questions on MINS and postoperative troponin elevation.

A PubMed search for medical subject headings and the terms “myocardial injury after noncardiac surgery,” “perioperative troponin,” and “postoperative troponin” restricted to humans, English language, and published in the past 5 years resulted in 144 articles. Articles most relevant to this progress note were included. Guidelines from major societies on perioperative cardiovascular assessment and management were also reviewed.

The Fourth Universal Definition of Myocardial Infarction ( UDMI 4) defines myocardial injury as detection of an elevated cardiac troponin above the 99th percentile upper reference limit (URL).² Different troponin assays are not comparable and institutions set their own thresholds for abnormal troponin. Per UDMI 4, myocardial injury is classified as (Figure)^2-4:

• Acute Myocardial Infarction (MI): This is defined as “detection of a rise and/or fall of cardiac troponin with ≥1 value above the 99th percentile URL and ≥1 of the following: symptoms of acute myocardial ischemia, new ischemic electrocardiographic changes, development of pathological Q waves, or imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology.” If these patients have an acute atherosclerotic plaque rupture, they are classified as Type 1 MI (T1MI), and if they have a mismatch between oxygen supply/demand, they are classified as Type 2 MI (T2MI).
• Acute Nonischemic Myocardial Injury (NIMI): This is defined as detection of both a rise and/or fall of cardiac troponin and one or more cardiac troponin values above the 99th percentile URL, but no overt clinical evidence of myocardial ischemia.
• Chronic Myocardial Injury: This is defined as one or more cardiac troponin values above the 99th percentile URL but without a rise and/or fall pattern.

MINS is defined as a rise and/or fall of cardiac biomarkers of presumed ischemic etiology within 30 days of noncardiac surgery that may occur with or without the clinical criteria necessary to fulfill the universal definition of MI (Figure).^5-8

A meta-analysis of 169 studies reported the overall incidence of MINS to be 17.9%; the incidence was 19.6% when systematic troponin screening was done versus 9.9% when troponins were ordered selectively based on the clinical context.⁵

That meta-analysis found that patients with MINS were more likely to be older, male, undergoing nonelective surgeries, and have hypertension, coronary artery disease (CAD), prior MI, heart failure, or kidney disease.⁵ Intraoperative hypotension (defined as systolic blood pressure <100 mm Hg or mean arterial pressure <55 mm Hg for up to 5 minutes or <60 mm Hg for 30 minutes or more) and intraoperative tachycardia (defined as heart rate >100 beats per minute) have been associated with MINS.^5,9 The relationship between anesthesia type and MINS is uncertain.

MINS is associated with an increased risk of 30-day mortality, nonfatal cardiac arrest, heart failure, and stroke.In the Vascular Events In Noncardiac Surgery Patients Cohort Evaluation (VISION) studies, the majority of patients did not have ischemic symptoms.^6,7 In this study, 30-day mortality rates were 8.5% to 13.5% in patients with ischemic symptoms or electrocardiographic changes and 2.9% to 7.7% in patients with asymptomatic troponin elevations. Among the patients without MINS, 30-day mortality was 0.6% to 1.1%. Higher levels of cardiac troponin were associated with higher mortality rates and shorter time to death.

The recommendations for perioperative screening for MINS vary from society to society. Although MINS is associated with worse outcomes, and most patients with MINS are asymptomatic, perioperative screening for MINS in the absence of clinical signs or symptoms is currently not recommended by the American College of Cardiology/American Heart Association (ACC/AHA).¹⁰

ACC/AHA

“The usefulness of postoperative screening with troponin levels in patients at high risk for perioperative MI, but without signs or symptoms suggestive of myocardial ischemia or MI, is uncertain in the absence of established risks and benefits of a defined management strategy (Class IIb; level of evidence [LOE]–B).”¹⁰

European Society of Cardiology

“Measurement of B-type natriuretic peptides (BNP) and high-sensitivity troponins (hsTn) after surgery may be considered in high-risk patients to improve risk stratification (Class IIb; LOE-B). Preoperatively and postoperatively, patients who could most benefit from BNP or hsTn measurements are those with metabolic equivalents (METs) ≤4 or those with a revised cardiac risk index (RCRI) score >1 for vascular surgery and >2 for nonvascular surgery. Postoperatively, patients with a surgical Apgar score <7 should also be monitored with BNP or hsTn to detect complications early, independent of their RCRI values.”¹¹

Canadian Cardiovascular Society

“We recommend obtaining daily troponins for 48-72 hours after noncardiac surgery in patients with a baseline risk of >5% for cardiovascular death or nonfatal MI at 30 days after surgery (ie, patients with an elevated N-terminal-proBNP (NT-proBNP)/BNP before surgery or, if there is no NT-proBNP/BNP before surgery, in those who have an RCRI score ≥1, age 45-64 years with significant cardiovascular disease, or age ≥65 years) (Strong recommendation; Moderate quality evidence).”¹

Currently, evidence-based therapies are well established only for T1MI. However, it is often challenging to differentiate T1MI from other causes of troponin elevation in the perioperative setting in which anesthesia, sedation, or analgesia may mask ischemic symptoms that typically prompt further investigation. While peak troponin levels may be higher in T1MI than they are in T2MI, the initial or delta change in the troponin may provide poor discrimination between T1MI and T2MI.² Management is complicated not only by the uncertainty about the underlying diagnosis (T1MI, T2MI, or NIMI) but also by the heterogeneity in the underlying pathophysiology of troponin elevation in patients with T2MI and NIMI. Patients with T2MI are generally sicker and have higher mortality than patients with T1MI, and management typically involves treating the underlying reason for oxygen supply/demand mismatch. Mortality in T2MI is more commonly caused by noncardiovascular causes, but underlying CAD is an independent predictor of cardiovascular death or recurrent MI in these patients.

The MANAGE trial (Management of Myocardial Injury After Noncardiac Surgery) had several methodological limitations to inform clinical practice but showed potential benefit of dabigatran in patients with MINS.¹² In this trial, patients on dabigatran had significantly lower rates of the primary efficacy outcome (composite of vascular mortality and nonfatal MI, nonhemorrhagic stroke, peripheral arterial thrombosis, amputation, and symptomatic venous thromboembolism) without a significant increase in life-threatening, major, or critical organ bleeding. Of the secondary efficacy outcomes, only nonhemorrhagic stroke was significantly reduced with dabigatran, but the event rate was low. In the subgroup analysis, patients randomized to dabigatran within 5 days of MINS and those meeting the criteria for MI had significantly lower rates of the primary efficacy outcome.

Patients with T2MI with known CAD may benefit from long-term risk reduction strategies for secondary prevention. There are no definitive management strategies in the literature for T2MI with unknown or no CAD. The SWEDEHEART registry (Swedish Web-System for Enhancement and Development of Evidence-Based Care in Heart Disease Evaluated According to Recommended Therapy) enrolled 9,136 patients with MI with nonobstructive coronary arteries (MINOCA).¹³ Though MINOCA may include T1MI patients, the majority of these patients are classified as T2MI under UDMI 4. Therefore, it has been proposed that data from this registry may inform management on T2MI.¹⁴ Data from this registry showed that statins and angiotensin-­converting enzyme inhibitors or angiotensin II receptor blockers were associated with lower incidence of MACE over a mean follow-up of 4.1 years. Dual-antiplatelet therapy or beta blockers did not significantly lower the incidence of MACE.¹³ In another study assessing 2-year mortality in patients with T2MI, beta blockers were beneficial.¹⁵

Who should be screened?

Screening can be performed if further risk stratification of high-risk patients or patients with poor functional status is desired. European Society of Cardiology and Canadian Cardiovascular Society guidelines provide guidance on the screening criteria. Troponin elevation in a low-risk group is associated with a low mortality rate, and many of these troponin elevations may be secondary to causes other than myocardial ischemia.

How should screening be conducted?

If planning to obtain postoperative troponins, then preoperative troponin should be obtained because 35% of the patients may have a chronic troponin elevation.

What is the risk if postoperative troponin screening is not performed?

Most patients with MINS are asymptomatic. Systematic screening with troponins (compared with selective screening based on clinical signs or symptoms) can detect T1MI that would otherwise remain occult and undiagnosed.

What is the risk if postoperative troponin screening is performed?

Detecting asymptomatic troponin elevations could lead to potentially harmful treatments (eg, increased risk of bleeding with antithrombotics in the postoperative setting, increased use of cardiac angiography, or addition of new medications such as statins and beta-blockers in the postoperative setting with the potential for adverse effects).

How should MINS be documented?

ST-elevation and non–ST elevation MI (STEMI and NSTEMI) should be reserved for T1MI only. T1MI should be documented when acute plaque rupture is strongly suspected. T2MI should be documented when oxygen supply/demand mismatch is strongly suspected as the etiology of acute MI (eg, T2MI secondary to tachyarrhythmia, hypertensive emergency, or septic shock). Documenting as “demand ischemia” or “unlikely acute coronary syndrome” for T2MI or NIMI should be avoided. Troponin elevations not meeting the criteria for acute MI should be documented as “non-MI troponin elevation” (eg, non-MI troponin elevation secondary to chronic kidney disease or left ventricular hypertrophy). Terms like “troponinitis” or “troponinemia” should be avoided.³

Can MINS be prevented?

There are no well-defined strategies for prevention of MINS, but cardiovascular risk factors should be optimized preoperatively for all patients. In a meta-analysis, preoperative aspirin was not associated with reduced incidence of MINS, and the role of preoperative statins remains speculative; however, nonacute initiation of beta-blockers preoperatively was associated with a lower incidence of MINS.⁵ Withholding angiotensin-­converting enzyme inhibitors or angiotensin II receptor blockers in the 24 hours prior to surgery has been associated with a lower incidence of MINS. Intraoperative hypotension or tachycardia should be avoided.

While MINS has been associated with increased 30-day mortality, there are currently no definitive evidence-based management strategies for these patients. Institutions should consider creating decision-support tools if considering screening for MINS based on patient- and surgery-specific risk factors.

The authors have nothing to disclose.

More than 200 million patients worldwide undergo major noncardiac surgery each year. Of these, more than 10 million patients suffer a major adverse cardiovascular event (MACE) within 30 days of surgery.¹ Elevated troponins after noncardiac surgery have been associated with increased mortality, but the management of these patients and the indications for screening remain unclear. The nomenclature around myocardial injury also remains confusing. In this Progress Note, we aim to define myocardial injury after noncardiac surgery (MINS) and discuss the key questions on MINS and postoperative troponin elevation.

A PubMed search for medical subject headings and the terms “myocardial injury after noncardiac surgery,” “perioperative troponin,” and “postoperative troponin” restricted to humans, English language, and published in the past 5 years resulted in 144 articles. Articles most relevant to this progress note were included. Guidelines from major societies on perioperative cardiovascular assessment and management were also reviewed.

The Fourth Universal Definition of Myocardial Infarction ( UDMI 4) defines myocardial injury as detection of an elevated cardiac troponin above the 99th percentile upper reference limit (URL).² Different troponin assays are not comparable and institutions set their own thresholds for abnormal troponin. Per UDMI 4, myocardial injury is classified as (Figure)^2-4:

• Acute Myocardial Infarction (MI): This is defined as “detection of a rise and/or fall of cardiac troponin with ≥1 value above the 99th percentile URL and ≥1 of the following: symptoms of acute myocardial ischemia, new ischemic electrocardiographic changes, development of pathological Q waves, or imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology.” If these patients have an acute atherosclerotic plaque rupture, they are classified as Type 1 MI (T1MI), and if they have a mismatch between oxygen supply/demand, they are classified as Type 2 MI (T2MI).
• Acute Nonischemic Myocardial Injury (NIMI): This is defined as detection of both a rise and/or fall of cardiac troponin and one or more cardiac troponin values above the 99th percentile URL, but no overt clinical evidence of myocardial ischemia.
• Chronic Myocardial Injury: This is defined as one or more cardiac troponin values above the 99th percentile URL but without a rise and/or fall pattern.

MINS is defined as a rise and/or fall of cardiac biomarkers of presumed ischemic etiology within 30 days of noncardiac surgery that may occur with or without the clinical criteria necessary to fulfill the universal definition of MI (Figure).^5-8

A meta-analysis of 169 studies reported the overall incidence of MINS to be 17.9%; the incidence was 19.6% when systematic troponin screening was done versus 9.9% when troponins were ordered selectively based on the clinical context.⁵

That meta-analysis found that patients with MINS were more likely to be older, male, undergoing nonelective surgeries, and have hypertension, coronary artery disease (CAD), prior MI, heart failure, or kidney disease.⁵ Intraoperative hypotension (defined as systolic blood pressure <100 mm Hg or mean arterial pressure <55 mm Hg for up to 5 minutes or <60 mm Hg for 30 minutes or more) and intraoperative tachycardia (defined as heart rate >100 beats per minute) have been associated with MINS.^5,9 The relationship between anesthesia type and MINS is uncertain.

MINS is associated with an increased risk of 30-day mortality, nonfatal cardiac arrest, heart failure, and stroke.In the Vascular Events In Noncardiac Surgery Patients Cohort Evaluation (VISION) studies, the majority of patients did not have ischemic symptoms.^6,7 In this study, 30-day mortality rates were 8.5% to 13.5% in patients with ischemic symptoms or electrocardiographic changes and 2.9% to 7.7% in patients with asymptomatic troponin elevations. Among the patients without MINS, 30-day mortality was 0.6% to 1.1%. Higher levels of cardiac troponin were associated with higher mortality rates and shorter time to death.

The recommendations for perioperative screening for MINS vary from society to society. Although MINS is associated with worse outcomes, and most patients with MINS are asymptomatic, perioperative screening for MINS in the absence of clinical signs or symptoms is currently not recommended by the American College of Cardiology/American Heart Association (ACC/AHA).¹⁰

ACC/AHA

“The usefulness of postoperative screening with troponin levels in patients at high risk for perioperative MI, but without signs or symptoms suggestive of myocardial ischemia or MI, is uncertain in the absence of established risks and benefits of a defined management strategy (Class IIb; level of evidence [LOE]–B).”¹⁰

European Society of Cardiology

“Measurement of B-type natriuretic peptides (BNP) and high-sensitivity troponins (hsTn) after surgery may be considered in high-risk patients to improve risk stratification (Class IIb; LOE-B). Preoperatively and postoperatively, patients who could most benefit from BNP or hsTn measurements are those with metabolic equivalents (METs) ≤4 or those with a revised cardiac risk index (RCRI) score >1 for vascular surgery and >2 for nonvascular surgery. Postoperatively, patients with a surgical Apgar score <7 should also be monitored with BNP or hsTn to detect complications early, independent of their RCRI values.”¹¹

Canadian Cardiovascular Society

“We recommend obtaining daily troponins for 48-72 hours after noncardiac surgery in patients with a baseline risk of >5% for cardiovascular death or nonfatal MI at 30 days after surgery (ie, patients with an elevated N-terminal-proBNP (NT-proBNP)/BNP before surgery or, if there is no NT-proBNP/BNP before surgery, in those who have an RCRI score ≥1, age 45-64 years with significant cardiovascular disease, or age ≥65 years) (Strong recommendation; Moderate quality evidence).”¹

Currently, evidence-based therapies are well established only for T1MI. However, it is often challenging to differentiate T1MI from other causes of troponin elevation in the perioperative setting in which anesthesia, sedation, or analgesia may mask ischemic symptoms that typically prompt further investigation. While peak troponin levels may be higher in T1MI than they are in T2MI, the initial or delta change in the troponin may provide poor discrimination between T1MI and T2MI.² Management is complicated not only by the uncertainty about the underlying diagnosis (T1MI, T2MI, or NIMI) but also by the heterogeneity in the underlying pathophysiology of troponin elevation in patients with T2MI and NIMI. Patients with T2MI are generally sicker and have higher mortality than patients with T1MI, and management typically involves treating the underlying reason for oxygen supply/demand mismatch. Mortality in T2MI is more commonly caused by noncardiovascular causes, but underlying CAD is an independent predictor of cardiovascular death or recurrent MI in these patients.

The MANAGE trial (Management of Myocardial Injury After Noncardiac Surgery) had several methodological limitations to inform clinical practice but showed potential benefit of dabigatran in patients with MINS.¹² In this trial, patients on dabigatran had significantly lower rates of the primary efficacy outcome (composite of vascular mortality and nonfatal MI, nonhemorrhagic stroke, peripheral arterial thrombosis, amputation, and symptomatic venous thromboembolism) without a significant increase in life-threatening, major, or critical organ bleeding. Of the secondary efficacy outcomes, only nonhemorrhagic stroke was significantly reduced with dabigatran, but the event rate was low. In the subgroup analysis, patients randomized to dabigatran within 5 days of MINS and those meeting the criteria for MI had significantly lower rates of the primary efficacy outcome.

Patients with T2MI with known CAD may benefit from long-term risk reduction strategies for secondary prevention. There are no definitive management strategies in the literature for T2MI with unknown or no CAD. The SWEDEHEART registry (Swedish Web-System for Enhancement and Development of Evidence-Based Care in Heart Disease Evaluated According to Recommended Therapy) enrolled 9,136 patients with MI with nonobstructive coronary arteries (MINOCA).¹³ Though MINOCA may include T1MI patients, the majority of these patients are classified as T2MI under UDMI 4. Therefore, it has been proposed that data from this registry may inform management on T2MI.¹⁴ Data from this registry showed that statins and angiotensin-­converting enzyme inhibitors or angiotensin II receptor blockers were associated with lower incidence of MACE over a mean follow-up of 4.1 years. Dual-antiplatelet therapy or beta blockers did not significantly lower the incidence of MACE.¹³ In another study assessing 2-year mortality in patients with T2MI, beta blockers were beneficial.¹⁵

Who should be screened?

Screening can be performed if further risk stratification of high-risk patients or patients with poor functional status is desired. European Society of Cardiology and Canadian Cardiovascular Society guidelines provide guidance on the screening criteria. Troponin elevation in a low-risk group is associated with a low mortality rate, and many of these troponin elevations may be secondary to causes other than myocardial ischemia.

How should screening be conducted?

If planning to obtain postoperative troponins, then preoperative troponin should be obtained because 35% of the patients may have a chronic troponin elevation.

What is the risk if postoperative troponin screening is not performed?

Most patients with MINS are asymptomatic. Systematic screening with troponins (compared with selective screening based on clinical signs or symptoms) can detect T1MI that would otherwise remain occult and undiagnosed.

What is the risk if postoperative troponin screening is performed?

Detecting asymptomatic troponin elevations could lead to potentially harmful treatments (eg, increased risk of bleeding with antithrombotics in the postoperative setting, increased use of cardiac angiography, or addition of new medications such as statins and beta-blockers in the postoperative setting with the potential for adverse effects).

How should MINS be documented?

ST-elevation and non–ST elevation MI (STEMI and NSTEMI) should be reserved for T1MI only. T1MI should be documented when acute plaque rupture is strongly suspected. T2MI should be documented when oxygen supply/demand mismatch is strongly suspected as the etiology of acute MI (eg, T2MI secondary to tachyarrhythmia, hypertensive emergency, or septic shock). Documenting as “demand ischemia” or “unlikely acute coronary syndrome” for T2MI or NIMI should be avoided. Troponin elevations not meeting the criteria for acute MI should be documented as “non-MI troponin elevation” (eg, non-MI troponin elevation secondary to chronic kidney disease or left ventricular hypertrophy). Terms like “troponinitis” or “troponinemia” should be avoided.³

Can MINS be prevented?

There are no well-defined strategies for prevention of MINS, but cardiovascular risk factors should be optimized preoperatively for all patients. In a meta-analysis, preoperative aspirin was not associated with reduced incidence of MINS, and the role of preoperative statins remains speculative; however, nonacute initiation of beta-blockers preoperatively was associated with a lower incidence of MINS.⁵ Withholding angiotensin-­converting enzyme inhibitors or angiotensin II receptor blockers in the 24 hours prior to surgery has been associated with a lower incidence of MINS. Intraoperative hypotension or tachycardia should be avoided.

While MINS has been associated with increased 30-day mortality, there are currently no definitive evidence-based management strategies for these patients. Institutions should consider creating decision-support tools if considering screening for MINS based on patient- and surgery-specific risk factors.

The authors have nothing to disclose.

The Centers for Medicare & Medicaid Services (CMS) Hospital Compare overall hospital ratings was originally released in 2016 and was recently updated in February 2019.^1,2 The program is designed to provide a consumer-friendly global rating system for hospitals, with hospitals rated on a scale from one star (worst) to five stars (best). The ratings are based on a formula that combines scores on 57 performance measures into seven groups, with the groups of mortality, safety, readmission, and patient experience given weights of 22% each in the overall scoring, and groups of effectiveness of care, timeliness of care, and efficient use of medical imaging equally contributing to the rest of the score.

Concerns have been raised since the introduction of the program regarding the methodology and possible unfairly high or low star ratings for certain types of hospitals.^3,4 It has been noted that five-star hospitals are disproportionately small, specialty-focused hospitals that may not have Emergency Departments or significant volumes of Medicaid patients.⁵ Hospitals that report fewer measures and thus receive scores for fewer measure groups (in general, smaller or specialty hospitals) are more likely to receive higher star ratings than are hospitals that receive scores for all measure groups.^6,7 Teaching hospitals, on average, have received lower star ratings than nonteaching hospitals.^8,9

Multihospital systems generally designate one of their hospitals as a “flagship” hospital and often use the name of that hospital to identify the system as a whole (eg, Mayo Clinic Health System, University of Pittsburgh Medical Center). There is not a set of objective criteria to designate a “flagship” hospital of a multihospital health system. Flagships could be the founding hospitals of the systems or the largest hospitals in the systems, and they are usually (although not always) large teaching hospitals. There is therefore a potential paradox in which a set of hospitals that tend to get lower ratings in the CMS star rating system may also be the set frequently identified as system flagship hospitals and whose reputation is used as a brand identity for multihospital systems.

It is possible, though, that the hospitals designated as flagship hospitals in multihospital systems are exceptions to the general rule of lower star ratings for major teaching hospitals. The flagship designation may reflect excellence that is then reflected in the star rating system, or it may reflect some other kind of excellence (eg, reputation for research or teaching, diverse medical services provided) that is not reflected in the star rating system. The primary aim of this study was to compare the average star ratings and hospital characteristics of designated flagship hospitals in multihospital systems with those of (1) major teaching hospitals generally and (2) “nonflagship” hospitals across and within the same systems specifically. We sought to determine whether a flagship designation would be associated with higher star ratings than those of major teaching hospitals in general and with higher star ratings than other, nonflagship hospitals in the same system.

The use of a prestigious flagship hospital name to identify a multihospital system suggests that some aspects of high quality in the flagship are extended in some way to other hospitals in the system. If that is so, then the star ratings of hospitals in organized multihospital systems with a flagship may be more similar to each other than those of sets of hospitals selected at random. As a secondary aim, to determine whether this type of consistent quality throughout a system could be identified in the CMS hospital star rating system, we compared the variation in star ratings between organized multihospital systems with flagship hospitals to those of artificially created “pseudo systems” of unaffiliated hospitals.

We used the Agency for Healthcare Research and Quality (AHRQ) Compendium of U.S. Health Systems, 2016, database and hospital file to identify multihospital health systems and their member hospitals.¹⁰ The database also provides information about health system characteristics such as systemwide teaching intensity and total number of acute care hospitals. We linked the AHRQ files to the CMS Hospital Compare datasets and Hospital Inpatient Prospective Payment System (IPPS) 2018 Final Rule Impact File to obtain star ratings and other information about specific hospitals (eg, resident to bed ratio, uncompensated care payment). Throughout the study, we followed the AHRQ’s definition of “major teaching hospitals” as hospitals with a high resident to bed ratio (≥0.25).

For purposes of this study, the primary criterion for identification of flagship hospitals was an explicit designation by the parent health systems on their websites, in the systems’ official documents, or in press releases or through major media reports. In the few cases in which parent systems did not designate their flagships, we searched reliable online sources such as major newspapers and hospital reviews to see if there was an agreement among sources on the flagship status. If we could not unambiguously identify a flagship hospital in a multihospital system using these methods, the system was not included in the study. A health system could have more than one flagship hospital.

Because the concept of “flagship” often involves a role as a referral center for complex cases in a regional area small enough to have referrals from hospital to hospital within the same system, we excluded multistate national health systems (eg, Catholic Health Initiatives, Community Health Systems, Inc.) and health systems with no major teaching hospitals or no flagship(s) identified by the systems themselves. Non-acute care and stand-alone hospitals, hospitals with missing CMS Certification Numbers (CCNs) or unmatched CCNs or hospital types across different data files, and hospitals without a star rating, were excluded.

Our analyses were performed at both hospital and health system levels. In the hospital-level analysis, we grouped hospitals into “1-2 star,” “3 star,” and “4-5 star” rating categories. We first compared star ratings of flagship hospitals with those of major teaching hospitals in general (ie, hospitals in the CMS Hospital Compare database with resident to bed ratios ≥0.25 that were not designated as system flagship hospitals). We then compared the average flagship hospital and average nonflagship hospital star ratings pooled across all the health systems. To explore hospital-level characteristics that might be associated with flagship hospitals’ performance on star ratings, we compared hospitals’ teaching intensity, bed size, charity care, and disproportionate share hospital (DSH) patient percentage between flagship and major teaching hospitals and between flagship and nonflagship hospitals. Differences were tested using two-sample t test with equal variances. We also compared hospital characteristics among hospitals with 1-2 stars, 3 stars, and 4-5 stars with use of one-way analysis of variance (ANOVA) with Bonferroni adjustment for multiple comparisons.

In the system-level analysis, we examined flagship hospitals’ star ratings relative to the star ratings for other member hospitals in the same system. We assigned health systems to the following three groups according to their flagship hospitals’ star ratings in comparison to other hospitals within their own systems: health systems in which flagship hospitals were rated the lowest among all member hospitals, health systems in which flagship hospitals were rated neither highest nor lowest or all hospitals within the system had the same star rating, and health systems in which flagship hospitals were rated the highest among all member hospitals. We compared system-level characteristics of the three groups. We calculated the average differences in uncompensated care payment, resident to bed ratio, DSH patient percentage, and total beds between flagship hospitals and nonflagship hospitals of the same health systems, and we also compared the differences across the three health system groups defined previously. We conducted an analysis of covariance (ANCOVA) to take system-level factors into consideration, including system size (total number of acute care hospitals in the system), systemwide teaching intensity, and systemwide charity care. The Bonferroni correction was used to adjust for potential problems of multiple comparisons.

Finally, to compare the diversity of star ratings within health systems and the diversity of star ratings nationwide, we generated a set of 100 pseudo systems each comprising six member hospitals (corresponding to the average number of member hospitals per “true” health system included in the study) that were randomly selected from all hospitals excluded from this study. We calculated and compared the average standard deviations of star ratings between the true health systems and this set of pseudo systems. Differences were tested using two-sample t test with equal variances.

Data management and statistical analyses were conducted using Stata SE, version 13.0 (StataCorp LLC, College Station, Texas).

Our final analysis included 599 hospitals in 113 health systems; 119 hospitals were flagships (four health systems each had two flagship hospitals, and one health system had three flagship hospitals). All other hospitals (n = 480) were designated as nonflaghips. On average, each health system had 6 member hospitals with star ratings, with a range from 2 to 22.

Flagship hospitals did have higher average star ratings than major teaching hospitals (mean star rating, 2.8 vs 2.3, respectively; P < .01; Figure). A larger proportion of flagship hospitals received four or five stars than did major teaching hospitals (29% vs 20%, respectively), and a smaller proportion of them received one or two stars (44% vs 59%, respectively; P < .05).

Flagship hospitals had lower star ratings on average, across all systems, than did nonflagship hospitals (mean star rating, 2.8 vs 3.3, respectively; P < .001). A smaller proportion of flagships received four or five stars than did nonflagships (29% vs 44%, respectively), and a larger proportion of them received one or two stars (44% vs 23%, respectively; P < .001).

As expected, flagship hospitals had significantly higher teaching intensity, larger bed size, higher DSH patient percentage, and higher value of uncompensated care payments than did nonflagship hospitals (P < .001 for all). On average, flagship hospitals were significantly larger but had lower DSH patient percentage and lower value of uncompensated care payments than did major teaching hospitals in general (P < .01 for all). In all types of hospitals, four- or five-star hospitals consistently had significantly lower DSH patient percentage (P < .001) and lower value of uncompensated care payment per claim (P < .05) than did other hospitals (Table).

In half of all health systems (n = 56), flagship hospitals were rated the lowest of all hospitals within that system; in approximately 20% of all health systems (n = 22), flagship hospitals were rated the highest. Flagship hospitals were more likely to have the lowest star rating in the system if the within-system difference in DSH patient percentage between flagship and nonflagship hospitals was relatively large. Within-system DSH patient percentage differences between flagship and nonflagship hospitals were 12.4%, 5.4%, and 3.5% in “flagship rated lowest,” “flagship rated middle,” and “flagship rated highest” systems, respectively (P < .05).

Average standardized deviations of star ratings for the 113 true health systems and 100 randomly generated pseudo health systems were 0.86 and 0.97, respectively (P < .05).

System-designated flagship hospitals did not generally have higher star ratings than did the other, smaller, community hospitals, either on average or within their own systems. In fact, the most common pattern observed was the system-designated flagship hospitals had the lowest star rating in their system. Flagship hospitals in multihospital systems were, however, rated higher than major teaching hospitals in general. The safety-net role of many of the system flagship hospitals, as captured by relative DSH percentage, was the most important determinant of low star ratings. A high bed number and teaching status were not as strongly associated with low star ratings.

It is already well established that the CMS star rating system does not correspond to other global hospital ratings systems like those of US News & World Report, Healthgrades, or the Leapfrog Group.¹¹ Each global rating system uses a unique set of measures and weighting systems for those measures, so discrepancies among these systems are inevitable. Multihospital systems may feel that the positive reputation for tertiary care excellence held by a flagship hospital is captured in a rating system like US News that has an explicit reputation component¹² and that the US News rankings are more prominent in the public eye than are those of CMS. To the extent that the CMS star ratings do become more widely used by the public or by payers to establish narrow provider networks, the relatively low ratings of multisystem flagship hospitals may become a cause for concern for those hospitals and systems.

System-designated flagship hospitals are typically large teaching hospitals with higher levels of technology, more highly specialized services and medical staff, more extensive research programs and active clinical trials programs, and the ability to treat cases that are difficult or complex or instances of rare conditions. They are not generally, as it turns out, the hospitals in a given system that the CMS star rating system identifies as “best.” In a number of multihospital systems, the system name is derived from the name of the flagship hospital (eg, Yale New Haven Health System and Montefiore Health System), which suggests that the system finds a marketing or branding advantage in being publicly identified with the name and positive reputation of the flagship hospital. Flagship hospitals may be designated as such because they have other attributes that patients, the community, and the system value, which may not be represented by the CMS quality metrics summarized by star ratings.

We did find a somewhat lower level of variation in star ratings in actual multihospital systems than in a set of randomly created “pseudo systems,” suggesting the presence of some mechanism for quality management in those systems leading to a more similar set of star ratings than one would find in hospitals selected at random.

Our study has a few limitations. First, we excluded multihospital health systems without any major teaching member hospital, which was based on our observation that they do not usually designate their flagship hospitals or they do not have any identifiable flagship hospitals. There may be a small number of such health systems that have designated their flagship hospitals and were excluded from the study, but we do not believe it will change our key findings. Second, it was possible that multiple hospitals in the same health system reported under the same CCN (multicampuses will often use the flagship facility’s IDs for the purposes of claims processing or cost and measure reporting), and therefore, the star ratings for the flagship hospitals reflected the performance of both the flagship hospital and the other member hospitals sharing the same CCN. We cannot fix the underlying reporting issue, and as a result, part of our analysis was probably more of a comparison of the “financial” flagship with other more loosely associated hospitals in the system. We could have in fact overestimated the flagships’ star rating performance by including data of other better performing nonflagship hospitals.

System-designated flagship hospitals tended to have lower CMS Hospital Compare overall hospital quality star ratings than did nonflagship hospitals in the same multihospital systems. The characteristics of hospitals identified as system flagships do not seem well aligned with those associated with better performance in the star rating system.

The authors declared no conflicts of interest.

The Centers for Medicare & Medicaid Services (CMS) Hospital Compare overall hospital ratings was originally released in 2016 and was recently updated in February 2019.^1,2 The program is designed to provide a consumer-friendly global rating system for hospitals, with hospitals rated on a scale from one star (worst) to five stars (best). The ratings are based on a formula that combines scores on 57 performance measures into seven groups, with the groups of mortality, safety, readmission, and patient experience given weights of 22% each in the overall scoring, and groups of effectiveness of care, timeliness of care, and efficient use of medical imaging equally contributing to the rest of the score.

Concerns have been raised since the introduction of the program regarding the methodology and possible unfairly high or low star ratings for certain types of hospitals.^3,4 It has been noted that five-star hospitals are disproportionately small, specialty-focused hospitals that may not have Emergency Departments or significant volumes of Medicaid patients.⁵ Hospitals that report fewer measures and thus receive scores for fewer measure groups (in general, smaller or specialty hospitals) are more likely to receive higher star ratings than are hospitals that receive scores for all measure groups.^6,7 Teaching hospitals, on average, have received lower star ratings than nonteaching hospitals.^8,9

Multihospital systems generally designate one of their hospitals as a “flagship” hospital and often use the name of that hospital to identify the system as a whole (eg, Mayo Clinic Health System, University of Pittsburgh Medical Center). There is not a set of objective criteria to designate a “flagship” hospital of a multihospital health system. Flagships could be the founding hospitals of the systems or the largest hospitals in the systems, and they are usually (although not always) large teaching hospitals. There is therefore a potential paradox in which a set of hospitals that tend to get lower ratings in the CMS star rating system may also be the set frequently identified as system flagship hospitals and whose reputation is used as a brand identity for multihospital systems.

It is possible, though, that the hospitals designated as flagship hospitals in multihospital systems are exceptions to the general rule of lower star ratings for major teaching hospitals. The flagship designation may reflect excellence that is then reflected in the star rating system, or it may reflect some other kind of excellence (eg, reputation for research or teaching, diverse medical services provided) that is not reflected in the star rating system. The primary aim of this study was to compare the average star ratings and hospital characteristics of designated flagship hospitals in multihospital systems with those of (1) major teaching hospitals generally and (2) “nonflagship” hospitals across and within the same systems specifically. We sought to determine whether a flagship designation would be associated with higher star ratings than those of major teaching hospitals in general and with higher star ratings than other, nonflagship hospitals in the same system.

The use of a prestigious flagship hospital name to identify a multihospital system suggests that some aspects of high quality in the flagship are extended in some way to other hospitals in the system. If that is so, then the star ratings of hospitals in organized multihospital systems with a flagship may be more similar to each other than those of sets of hospitals selected at random. As a secondary aim, to determine whether this type of consistent quality throughout a system could be identified in the CMS hospital star rating system, we compared the variation in star ratings between organized multihospital systems with flagship hospitals to those of artificially created “pseudo systems” of unaffiliated hospitals.

We used the Agency for Healthcare Research and Quality (AHRQ) Compendium of U.S. Health Systems, 2016, database and hospital file to identify multihospital health systems and their member hospitals.¹⁰ The database also provides information about health system characteristics such as systemwide teaching intensity and total number of acute care hospitals. We linked the AHRQ files to the CMS Hospital Compare datasets and Hospital Inpatient Prospective Payment System (IPPS) 2018 Final Rule Impact File to obtain star ratings and other information about specific hospitals (eg, resident to bed ratio, uncompensated care payment). Throughout the study, we followed the AHRQ’s definition of “major teaching hospitals” as hospitals with a high resident to bed ratio (≥0.25).

For purposes of this study, the primary criterion for identification of flagship hospitals was an explicit designation by the parent health systems on their websites, in the systems’ official documents, or in press releases or through major media reports. In the few cases in which parent systems did not designate their flagships, we searched reliable online sources such as major newspapers and hospital reviews to see if there was an agreement among sources on the flagship status. If we could not unambiguously identify a flagship hospital in a multihospital system using these methods, the system was not included in the study. A health system could have more than one flagship hospital.

Because the concept of “flagship” often involves a role as a referral center for complex cases in a regional area small enough to have referrals from hospital to hospital within the same system, we excluded multistate national health systems (eg, Catholic Health Initiatives, Community Health Systems, Inc.) and health systems with no major teaching hospitals or no flagship(s) identified by the systems themselves. Non-acute care and stand-alone hospitals, hospitals with missing CMS Certification Numbers (CCNs) or unmatched CCNs or hospital types across different data files, and hospitals without a star rating, were excluded.

Our analyses were performed at both hospital and health system levels. In the hospital-level analysis, we grouped hospitals into “1-2 star,” “3 star,” and “4-5 star” rating categories. We first compared star ratings of flagship hospitals with those of major teaching hospitals in general (ie, hospitals in the CMS Hospital Compare database with resident to bed ratios ≥0.25 that were not designated as system flagship hospitals). We then compared the average flagship hospital and average nonflagship hospital star ratings pooled across all the health systems. To explore hospital-level characteristics that might be associated with flagship hospitals’ performance on star ratings, we compared hospitals’ teaching intensity, bed size, charity care, and disproportionate share hospital (DSH) patient percentage between flagship and major teaching hospitals and between flagship and nonflagship hospitals. Differences were tested using two-sample t test with equal variances. We also compared hospital characteristics among hospitals with 1-2 stars, 3 stars, and 4-5 stars with use of one-way analysis of variance (ANOVA) with Bonferroni adjustment for multiple comparisons.

In the system-level analysis, we examined flagship hospitals’ star ratings relative to the star ratings for other member hospitals in the same system. We assigned health systems to the following three groups according to their flagship hospitals’ star ratings in comparison to other hospitals within their own systems: health systems in which flagship hospitals were rated the lowest among all member hospitals, health systems in which flagship hospitals were rated neither highest nor lowest or all hospitals within the system had the same star rating, and health systems in which flagship hospitals were rated the highest among all member hospitals. We compared system-level characteristics of the three groups. We calculated the average differences in uncompensated care payment, resident to bed ratio, DSH patient percentage, and total beds between flagship hospitals and nonflagship hospitals of the same health systems, and we also compared the differences across the three health system groups defined previously. We conducted an analysis of covariance (ANCOVA) to take system-level factors into consideration, including system size (total number of acute care hospitals in the system), systemwide teaching intensity, and systemwide charity care. The Bonferroni correction was used to adjust for potential problems of multiple comparisons.

Finally, to compare the diversity of star ratings within health systems and the diversity of star ratings nationwide, we generated a set of 100 pseudo systems each comprising six member hospitals (corresponding to the average number of member hospitals per “true” health system included in the study) that were randomly selected from all hospitals excluded from this study. We calculated and compared the average standard deviations of star ratings between the true health systems and this set of pseudo systems. Differences were tested using two-sample t test with equal variances.

Data management and statistical analyses were conducted using Stata SE, version 13.0 (StataCorp LLC, College Station, Texas).

Our final analysis included 599 hospitals in 113 health systems; 119 hospitals were flagships (four health systems each had two flagship hospitals, and one health system had three flagship hospitals). All other hospitals (n = 480) were designated as nonflaghips. On average, each health system had 6 member hospitals with star ratings, with a range from 2 to 22.

Flagship hospitals did have higher average star ratings than major teaching hospitals (mean star rating, 2.8 vs 2.3, respectively; P < .01; Figure). A larger proportion of flagship hospitals received four or five stars than did major teaching hospitals (29% vs 20%, respectively), and a smaller proportion of them received one or two stars (44% vs 59%, respectively; P < .05).

Flagship hospitals had lower star ratings on average, across all systems, than did nonflagship hospitals (mean star rating, 2.8 vs 3.3, respectively; P < .001). A smaller proportion of flagships received four or five stars than did nonflagships (29% vs 44%, respectively), and a larger proportion of them received one or two stars (44% vs 23%, respectively; P < .001).

As expected, flagship hospitals had significantly higher teaching intensity, larger bed size, higher DSH patient percentage, and higher value of uncompensated care payments than did nonflagship hospitals (P < .001 for all). On average, flagship hospitals were significantly larger but had lower DSH patient percentage and lower value of uncompensated care payments than did major teaching hospitals in general (P < .01 for all). In all types of hospitals, four- or five-star hospitals consistently had significantly lower DSH patient percentage (P < .001) and lower value of uncompensated care payment per claim (P < .05) than did other hospitals (Table).

In half of all health systems (n = 56), flagship hospitals were rated the lowest of all hospitals within that system; in approximately 20% of all health systems (n = 22), flagship hospitals were rated the highest. Flagship hospitals were more likely to have the lowest star rating in the system if the within-system difference in DSH patient percentage between flagship and nonflagship hospitals was relatively large. Within-system DSH patient percentage differences between flagship and nonflagship hospitals were 12.4%, 5.4%, and 3.5% in “flagship rated lowest,” “flagship rated middle,” and “flagship rated highest” systems, respectively (P < .05).

Average standardized deviations of star ratings for the 113 true health systems and 100 randomly generated pseudo health systems were 0.86 and 0.97, respectively (P < .05).

System-designated flagship hospitals did not generally have higher star ratings than did the other, smaller, community hospitals, either on average or within their own systems. In fact, the most common pattern observed was the system-designated flagship hospitals had the lowest star rating in their system. Flagship hospitals in multihospital systems were, however, rated higher than major teaching hospitals in general. The safety-net role of many of the system flagship hospitals, as captured by relative DSH percentage, was the most important determinant of low star ratings. A high bed number and teaching status were not as strongly associated with low star ratings.

It is already well established that the CMS star rating system does not correspond to other global hospital ratings systems like those of US News & World Report, Healthgrades, or the Leapfrog Group.¹¹ Each global rating system uses a unique set of measures and weighting systems for those measures, so discrepancies among these systems are inevitable. Multihospital systems may feel that the positive reputation for tertiary care excellence held by a flagship hospital is captured in a rating system like US News that has an explicit reputation component¹² and that the US News rankings are more prominent in the public eye than are those of CMS. To the extent that the CMS star ratings do become more widely used by the public or by payers to establish narrow provider networks, the relatively low ratings of multisystem flagship hospitals may become a cause for concern for those hospitals and systems.

System-designated flagship hospitals are typically large teaching hospitals with higher levels of technology, more highly specialized services and medical staff, more extensive research programs and active clinical trials programs, and the ability to treat cases that are difficult or complex or instances of rare conditions. They are not generally, as it turns out, the hospitals in a given system that the CMS star rating system identifies as “best.” In a number of multihospital systems, the system name is derived from the name of the flagship hospital (eg, Yale New Haven Health System and Montefiore Health System), which suggests that the system finds a marketing or branding advantage in being publicly identified with the name and positive reputation of the flagship hospital. Flagship hospitals may be designated as such because they have other attributes that patients, the community, and the system value, which may not be represented by the CMS quality metrics summarized by star ratings.

We did find a somewhat lower level of variation in star ratings in actual multihospital systems than in a set of randomly created “pseudo systems,” suggesting the presence of some mechanism for quality management in those systems leading to a more similar set of star ratings than one would find in hospitals selected at random.

Our study has a few limitations. First, we excluded multihospital health systems without any major teaching member hospital, which was based on our observation that they do not usually designate their flagship hospitals or they do not have any identifiable flagship hospitals. There may be a small number of such health systems that have designated their flagship hospitals and were excluded from the study, but we do not believe it will change our key findings. Second, it was possible that multiple hospitals in the same health system reported under the same CCN (multicampuses will often use the flagship facility’s IDs for the purposes of claims processing or cost and measure reporting), and therefore, the star ratings for the flagship hospitals reflected the performance of both the flagship hospital and the other member hospitals sharing the same CCN. We cannot fix the underlying reporting issue, and as a result, part of our analysis was probably more of a comparison of the “financial” flagship with other more loosely associated hospitals in the system. We could have in fact overestimated the flagships’ star rating performance by including data of other better performing nonflagship hospitals.

System-designated flagship hospitals tended to have lower CMS Hospital Compare overall hospital quality star ratings than did nonflagship hospitals in the same multihospital systems. The characteristics of hospitals identified as system flagships do not seem well aligned with those associated with better performance in the star rating system.

The authors declared no conflicts of interest.

The Centers for Medicare & Medicaid Services (CMS) Hospital Compare overall hospital ratings was originally released in 2016 and was recently updated in February 2019.^1,2 The program is designed to provide a consumer-friendly global rating system for hospitals, with hospitals rated on a scale from one star (worst) to five stars (best). The ratings are based on a formula that combines scores on 57 performance measures into seven groups, with the groups of mortality, safety, readmission, and patient experience given weights of 22% each in the overall scoring, and groups of effectiveness of care, timeliness of care, and efficient use of medical imaging equally contributing to the rest of the score.

Concerns have been raised since the introduction of the program regarding the methodology and possible unfairly high or low star ratings for certain types of hospitals.^3,4 It has been noted that five-star hospitals are disproportionately small, specialty-focused hospitals that may not have Emergency Departments or significant volumes of Medicaid patients.⁵ Hospitals that report fewer measures and thus receive scores for fewer measure groups (in general, smaller or specialty hospitals) are more likely to receive higher star ratings than are hospitals that receive scores for all measure groups.^6,7 Teaching hospitals, on average, have received lower star ratings than nonteaching hospitals.^8,9

Multihospital systems generally designate one of their hospitals as a “flagship” hospital and often use the name of that hospital to identify the system as a whole (eg, Mayo Clinic Health System, University of Pittsburgh Medical Center). There is not a set of objective criteria to designate a “flagship” hospital of a multihospital health system. Flagships could be the founding hospitals of the systems or the largest hospitals in the systems, and they are usually (although not always) large teaching hospitals. There is therefore a potential paradox in which a set of hospitals that tend to get lower ratings in the CMS star rating system may also be the set frequently identified as system flagship hospitals and whose reputation is used as a brand identity for multihospital systems.

It is possible, though, that the hospitals designated as flagship hospitals in multihospital systems are exceptions to the general rule of lower star ratings for major teaching hospitals. The flagship designation may reflect excellence that is then reflected in the star rating system, or it may reflect some other kind of excellence (eg, reputation for research or teaching, diverse medical services provided) that is not reflected in the star rating system. The primary aim of this study was to compare the average star ratings and hospital characteristics of designated flagship hospitals in multihospital systems with those of (1) major teaching hospitals generally and (2) “nonflagship” hospitals across and within the same systems specifically. We sought to determine whether a flagship designation would be associated with higher star ratings than those of major teaching hospitals in general and with higher star ratings than other, nonflagship hospitals in the same system.

The use of a prestigious flagship hospital name to identify a multihospital system suggests that some aspects of high quality in the flagship are extended in some way to other hospitals in the system. If that is so, then the star ratings of hospitals in organized multihospital systems with a flagship may be more similar to each other than those of sets of hospitals selected at random. As a secondary aim, to determine whether this type of consistent quality throughout a system could be identified in the CMS hospital star rating system, we compared the variation in star ratings between organized multihospital systems with flagship hospitals to those of artificially created “pseudo systems” of unaffiliated hospitals.

We used the Agency for Healthcare Research and Quality (AHRQ) Compendium of U.S. Health Systems, 2016, database and hospital file to identify multihospital health systems and their member hospitals.¹⁰ The database also provides information about health system characteristics such as systemwide teaching intensity and total number of acute care hospitals. We linked the AHRQ files to the CMS Hospital Compare datasets and Hospital Inpatient Prospective Payment System (IPPS) 2018 Final Rule Impact File to obtain star ratings and other information about specific hospitals (eg, resident to bed ratio, uncompensated care payment). Throughout the study, we followed the AHRQ’s definition of “major teaching hospitals” as hospitals with a high resident to bed ratio (≥0.25).

For purposes of this study, the primary criterion for identification of flagship hospitals was an explicit designation by the parent health systems on their websites, in the systems’ official documents, or in press releases or through major media reports. In the few cases in which parent systems did not designate their flagships, we searched reliable online sources such as major newspapers and hospital reviews to see if there was an agreement among sources on the flagship status. If we could not unambiguously identify a flagship hospital in a multihospital system using these methods, the system was not included in the study. A health system could have more than one flagship hospital.

Because the concept of “flagship” often involves a role as a referral center for complex cases in a regional area small enough to have referrals from hospital to hospital within the same system, we excluded multistate national health systems (eg, Catholic Health Initiatives, Community Health Systems, Inc.) and health systems with no major teaching hospitals or no flagship(s) identified by the systems themselves. Non-acute care and stand-alone hospitals, hospitals with missing CMS Certification Numbers (CCNs) or unmatched CCNs or hospital types across different data files, and hospitals without a star rating, were excluded.

Our analyses were performed at both hospital and health system levels. In the hospital-level analysis, we grouped hospitals into “1-2 star,” “3 star,” and “4-5 star” rating categories. We first compared star ratings of flagship hospitals with those of major teaching hospitals in general (ie, hospitals in the CMS Hospital Compare database with resident to bed ratios ≥0.25 that were not designated as system flagship hospitals). We then compared the average flagship hospital and average nonflagship hospital star ratings pooled across all the health systems. To explore hospital-level characteristics that might be associated with flagship hospitals’ performance on star ratings, we compared hospitals’ teaching intensity, bed size, charity care, and disproportionate share hospital (DSH) patient percentage between flagship and major teaching hospitals and between flagship and nonflagship hospitals. Differences were tested using two-sample t test with equal variances. We also compared hospital characteristics among hospitals with 1-2 stars, 3 stars, and 4-5 stars with use of one-way analysis of variance (ANOVA) with Bonferroni adjustment for multiple comparisons.

In the system-level analysis, we examined flagship hospitals’ star ratings relative to the star ratings for other member hospitals in the same system. We assigned health systems to the following three groups according to their flagship hospitals’ star ratings in comparison to other hospitals within their own systems: health systems in which flagship hospitals were rated the lowest among all member hospitals, health systems in which flagship hospitals were rated neither highest nor lowest or all hospitals within the system had the same star rating, and health systems in which flagship hospitals were rated the highest among all member hospitals. We compared system-level characteristics of the three groups. We calculated the average differences in uncompensated care payment, resident to bed ratio, DSH patient percentage, and total beds between flagship hospitals and nonflagship hospitals of the same health systems, and we also compared the differences across the three health system groups defined previously. We conducted an analysis of covariance (ANCOVA) to take system-level factors into consideration, including system size (total number of acute care hospitals in the system), systemwide teaching intensity, and systemwide charity care. The Bonferroni correction was used to adjust for potential problems of multiple comparisons.

Finally, to compare the diversity of star ratings within health systems and the diversity of star ratings nationwide, we generated a set of 100 pseudo systems each comprising six member hospitals (corresponding to the average number of member hospitals per “true” health system included in the study) that were randomly selected from all hospitals excluded from this study. We calculated and compared the average standard deviations of star ratings between the true health systems and this set of pseudo systems. Differences were tested using two-sample t test with equal variances.

Data management and statistical analyses were conducted using Stata SE, version 13.0 (StataCorp LLC, College Station, Texas).

Our final analysis included 599 hospitals in 113 health systems; 119 hospitals were flagships (four health systems each had two flagship hospitals, and one health system had three flagship hospitals). All other hospitals (n = 480) were designated as nonflaghips. On average, each health system had 6 member hospitals with star ratings, with a range from 2 to 22.

Flagship hospitals did have higher average star ratings than major teaching hospitals (mean star rating, 2.8 vs 2.3, respectively; P < .01; Figure). A larger proportion of flagship hospitals received four or five stars than did major teaching hospitals (29% vs 20%, respectively), and a smaller proportion of them received one or two stars (44% vs 59%, respectively; P < .05).

Flagship hospitals had lower star ratings on average, across all systems, than did nonflagship hospitals (mean star rating, 2.8 vs 3.3, respectively; P < .001). A smaller proportion of flagships received four or five stars than did nonflagships (29% vs 44%, respectively), and a larger proportion of them received one or two stars (44% vs 23%, respectively; P < .001).

As expected, flagship hospitals had significantly higher teaching intensity, larger bed size, higher DSH patient percentage, and higher value of uncompensated care payments than did nonflagship hospitals (P < .001 for all). On average, flagship hospitals were significantly larger but had lower DSH patient percentage and lower value of uncompensated care payments than did major teaching hospitals in general (P < .01 for all). In all types of hospitals, four- or five-star hospitals consistently had significantly lower DSH patient percentage (P < .001) and lower value of uncompensated care payment per claim (P < .05) than did other hospitals (Table).

In half of all health systems (n = 56), flagship hospitals were rated the lowest of all hospitals within that system; in approximately 20% of all health systems (n = 22), flagship hospitals were rated the highest. Flagship hospitals were more likely to have the lowest star rating in the system if the within-system difference in DSH patient percentage between flagship and nonflagship hospitals was relatively large. Within-system DSH patient percentage differences between flagship and nonflagship hospitals were 12.4%, 5.4%, and 3.5% in “flagship rated lowest,” “flagship rated middle,” and “flagship rated highest” systems, respectively (P < .05).

Average standardized deviations of star ratings for the 113 true health systems and 100 randomly generated pseudo health systems were 0.86 and 0.97, respectively (P < .05).

System-designated flagship hospitals did not generally have higher star ratings than did the other, smaller, community hospitals, either on average or within their own systems. In fact, the most common pattern observed was the system-designated flagship hospitals had the lowest star rating in their system. Flagship hospitals in multihospital systems were, however, rated higher than major teaching hospitals in general. The safety-net role of many of the system flagship hospitals, as captured by relative DSH percentage, was the most important determinant of low star ratings. A high bed number and teaching status were not as strongly associated with low star ratings.

It is already well established that the CMS star rating system does not correspond to other global hospital ratings systems like those of US News & World Report, Healthgrades, or the Leapfrog Group.¹¹ Each global rating system uses a unique set of measures and weighting systems for those measures, so discrepancies among these systems are inevitable. Multihospital systems may feel that the positive reputation for tertiary care excellence held by a flagship hospital is captured in a rating system like US News that has an explicit reputation component¹² and that the US News rankings are more prominent in the public eye than are those of CMS. To the extent that the CMS star ratings do become more widely used by the public or by payers to establish narrow provider networks, the relatively low ratings of multisystem flagship hospitals may become a cause for concern for those hospitals and systems.

System-designated flagship hospitals are typically large teaching hospitals with higher levels of technology, more highly specialized services and medical staff, more extensive research programs and active clinical trials programs, and the ability to treat cases that are difficult or complex or instances of rare conditions. They are not generally, as it turns out, the hospitals in a given system that the CMS star rating system identifies as “best.” In a number of multihospital systems, the system name is derived from the name of the flagship hospital (eg, Yale New Haven Health System and Montefiore Health System), which suggests that the system finds a marketing or branding advantage in being publicly identified with the name and positive reputation of the flagship hospital. Flagship hospitals may be designated as such because they have other attributes that patients, the community, and the system value, which may not be represented by the CMS quality metrics summarized by star ratings.

We did find a somewhat lower level of variation in star ratings in actual multihospital systems than in a set of randomly created “pseudo systems,” suggesting the presence of some mechanism for quality management in those systems leading to a more similar set of star ratings than one would find in hospitals selected at random.

Our study has a few limitations. First, we excluded multihospital health systems without any major teaching member hospital, which was based on our observation that they do not usually designate their flagship hospitals or they do not have any identifiable flagship hospitals. There may be a small number of such health systems that have designated their flagship hospitals and were excluded from the study, but we do not believe it will change our key findings. Second, it was possible that multiple hospitals in the same health system reported under the same CCN (multicampuses will often use the flagship facility’s IDs for the purposes of claims processing or cost and measure reporting), and therefore, the star ratings for the flagship hospitals reflected the performance of both the flagship hospital and the other member hospitals sharing the same CCN. We cannot fix the underlying reporting issue, and as a result, part of our analysis was probably more of a comparison of the “financial” flagship with other more loosely associated hospitals in the system. We could have in fact overestimated the flagships’ star rating performance by including data of other better performing nonflagship hospitals.

System-designated flagship hospitals tended to have lower CMS Hospital Compare overall hospital quality star ratings than did nonflagship hospitals in the same multihospital systems. The characteristics of hospitals identified as system flagships do not seem well aligned with those associated with better performance in the star rating system.

The authors declared no conflicts of interest.