Hospital Medicine

While sick at home with a 26-day symptomatic course of COVID-19 in March 2020, I watched the surge unfold in my state and the hospital where I work as an inpatient adult medicine physician. Although the preponderance of my professional life is dedicated to leading teams in implementing delivery system transformation, the hat I wore in that moment involved living through and keeping up with the changes around me. Once I recovered and returned to the arena as a COVID doctor, I adapted to and made changes during constant shifts in how we provided care.

Looking back on those months during the worst of the COVID-19 hospital surge in my region, I reflect on the factors that helped me, as a frontline and shift-work clinician, adapt to and make those changes. In reflecting on the elements that were meaningful to me during the crisis, I recognize a set of change-enabling factors that have broad relevance for those of us who work to improve outcomes for patients and populations.

Confidence engendered by liberating data

In the early days of the surge, there was much uncertainty, and unfortunately, some seriously imperfect messaging. Trust was broken or badly bruised for many frontline clinicians. I share this painful phase not to criticize, but rather reflect on what mattered to me during that crisis of confidence. It was data. Raw, unadjusted, best-available data. Produced and pushed out. Available, trended over time, telling the story of where we are, now. Counts of tests, beds, and ventilators. The consistent, transparent availability of relevant and straightforward data provided an active antidote to a sense of uncertainty during a crisis of confidence.

Personal practice change stimulated by relevance and urgency

For half a decade, I have been encouraging interdisciplinary inpatient teams to identify and actively engage the family and/or care partner as a member of the care team. Despite even the American Association of Retired Persons mobilizing an impressive regulatory approach in 32 states to require that family and/or care partners are included as such, the practice change efforts continued on a slow and steady path. Why? We just didn’t believe it was of urgent, relevant, mission-critical importance to our daily practice to do so. That all changed in March 2020.

Without needing to be told, educated, or incentivized, my first night as a COVID doctor found me calling every single patient’s family upon admission, regardless of what time it was. It was critical to review the diagnosis, transparently discuss the uncertainty regarding the upcoming hours and days, review the potential contingencies, and ask, right there and then, whether intubation is consistent with goals of care. It was that urgent and relevant. Without exception, families were grateful for the effort and candor.

The significance of this practice—undoubtedly adopted by every inpatient provider who has worked a COVID surge—is rooted in decades of academic deliberation on which is the “right” doctor to have these discussions. None of that mattered. Historical opinions changed due to what was urgent and relevant given the situation at hand and the job we had to do. Imagine, for example, what we could do and how we could change if we now consider it urgent and relevant to identify and mobilize enhanced services and supports to patients who experience inequities because we believe it to be mission-critical to the job we show up to do every day.

Change fostered by a creative problem-solving ecosystem

Embracing personal practice change was made easier and implicitly affirmed by the creative problem solving that occurred everywhere. Tents, drive-throughs, and even college field houses were now settings of care. Primary care physicians, cardiologists, and gastrointestinal (GI) and postanesthesia care nurses staffed the COVID floors. Rolling stands held iPads so staff could communicate with patients without entering the room. This creative ecosystem fostered individual practice change. No debates were needed to recognize that standard processes were inadequate. No single role or service of any discipline was singularly asked to change to meet the needs of the moment. Because of this ecosystem of creative, active change, there was a much greater flexibility among individuals, role types, departments, and disciplines to change. This is particularly poignant to me in light of the work I lead to improve care for patients who experience systemic inequities in our health care system. When we ask a single role type or discipline to change, it can be met with resistance; far more success is achieved when we engage an interdisciplinary and interdepartmental approach to change. When surrounded by others making change, it makes us more willing to change, too.

It is so often invoked that health care is a team sport. In practicality, while we may aspire to work as a team, health care delivery is still all too often comprised of a set of individual actors with individualized responsibilities trying to communicate the best they can with each other.

What I experienced during the surge at my hospital was the very best version of teamwork I have ever been a part of in health care: empathetic, mutually interdependent strangers coming together during daily changes in staffing, processes, and resources. I will never forget nights walking into the pediatric floor or day surgery recovery area—now repurposed as a COVID unit—to entirely new faces comprised of GI suite nurses, outpatient doctors, and moonlighting intensivists.

We were all new to each other, all new to working in this setting, and all new to whatever the newest changes of the day brought. I will never forget how we greeted each other and introduced ourselves. We asked each other where we were “from,” and held a genuine appreciation to each other for being there. Imagine how this impacted how we worked together. Looking back on those night shifts, I remember us as a truly interdependent team. I will endeavor to bring that sense of mutual regard and interdependency into my work to foster effective interdisciplinary and cross-continuum teamwork.

Takeaways

As a student and practitioner of delivery system transformation, I am often in conversations about imperfect data, incomplete evidence, and role-specific and organizational resistance to change. As an acute care provider during the COVID-19 hospital surge in my region, the experiences I had as a participant in the COVID-related delivery system change will stay with me as I lead value-based delivery system change. What worked in an infectious disease crisis holds great relevance to our pressing, urgent, relevant work to create a more person-centered, equitable, and value-based delivery system.

I am confident that if those of us seeking to improve outcomes use visible and accessible data to engender confidence, clearly link practice change to the relevant and urgent issue at hand, promote broadly visible creative problem solving to foster an ecosystem of change, and cultivate empathy and mutual interdependence to promote the teamwork we aspire to have, that we will foster meaningful progress in our efforts to improve care for patients and populations.

Corresponding author: Amy Boutwell, MD, MPP, President, Collaborative Healthcare Strategies, Lexington, MA; amy@collaborativehealthcarestrategies.com.

Financial disclosures: None.

While sick at home with a 26-day symptomatic course of COVID-19 in March 2020, I watched the surge unfold in my state and the hospital where I work as an inpatient adult medicine physician. Although the preponderance of my professional life is dedicated to leading teams in implementing delivery system transformation, the hat I wore in that moment involved living through and keeping up with the changes around me. Once I recovered and returned to the arena as a COVID doctor, I adapted to and made changes during constant shifts in how we provided care.

Looking back on those months during the worst of the COVID-19 hospital surge in my region, I reflect on the factors that helped me, as a frontline and shift-work clinician, adapt to and make those changes. In reflecting on the elements that were meaningful to me during the crisis, I recognize a set of change-enabling factors that have broad relevance for those of us who work to improve outcomes for patients and populations.

Confidence engendered by liberating data

In the early days of the surge, there was much uncertainty, and unfortunately, some seriously imperfect messaging. Trust was broken or badly bruised for many frontline clinicians. I share this painful phase not to criticize, but rather reflect on what mattered to me during that crisis of confidence. It was data. Raw, unadjusted, best-available data. Produced and pushed out. Available, trended over time, telling the story of where we are, now. Counts of tests, beds, and ventilators. The consistent, transparent availability of relevant and straightforward data provided an active antidote to a sense of uncertainty during a crisis of confidence.

Personal practice change stimulated by relevance and urgency

For half a decade, I have been encouraging interdisciplinary inpatient teams to identify and actively engage the family and/or care partner as a member of the care team. Despite even the American Association of Retired Persons mobilizing an impressive regulatory approach in 32 states to require that family and/or care partners are included as such, the practice change efforts continued on a slow and steady path. Why? We just didn’t believe it was of urgent, relevant, mission-critical importance to our daily practice to do so. That all changed in March 2020.

Without needing to be told, educated, or incentivized, my first night as a COVID doctor found me calling every single patient’s family upon admission, regardless of what time it was. It was critical to review the diagnosis, transparently discuss the uncertainty regarding the upcoming hours and days, review the potential contingencies, and ask, right there and then, whether intubation is consistent with goals of care. It was that urgent and relevant. Without exception, families were grateful for the effort and candor.

The significance of this practice—undoubtedly adopted by every inpatient provider who has worked a COVID surge—is rooted in decades of academic deliberation on which is the “right” doctor to have these discussions. None of that mattered. Historical opinions changed due to what was urgent and relevant given the situation at hand and the job we had to do. Imagine, for example, what we could do and how we could change if we now consider it urgent and relevant to identify and mobilize enhanced services and supports to patients who experience inequities because we believe it to be mission-critical to the job we show up to do every day.

Change fostered by a creative problem-solving ecosystem

Embracing personal practice change was made easier and implicitly affirmed by the creative problem solving that occurred everywhere. Tents, drive-throughs, and even college field houses were now settings of care. Primary care physicians, cardiologists, and gastrointestinal (GI) and postanesthesia care nurses staffed the COVID floors. Rolling stands held iPads so staff could communicate with patients without entering the room. This creative ecosystem fostered individual practice change. No debates were needed to recognize that standard processes were inadequate. No single role or service of any discipline was singularly asked to change to meet the needs of the moment. Because of this ecosystem of creative, active change, there was a much greater flexibility among individuals, role types, departments, and disciplines to change. This is particularly poignant to me in light of the work I lead to improve care for patients who experience systemic inequities in our health care system. When we ask a single role type or discipline to change, it can be met with resistance; far more success is achieved when we engage an interdisciplinary and interdepartmental approach to change. When surrounded by others making change, it makes us more willing to change, too.

It is so often invoked that health care is a team sport. In practicality, while we may aspire to work as a team, health care delivery is still all too often comprised of a set of individual actors with individualized responsibilities trying to communicate the best they can with each other.

What I experienced during the surge at my hospital was the very best version of teamwork I have ever been a part of in health care: empathetic, mutually interdependent strangers coming together during daily changes in staffing, processes, and resources. I will never forget nights walking into the pediatric floor or day surgery recovery area—now repurposed as a COVID unit—to entirely new faces comprised of GI suite nurses, outpatient doctors, and moonlighting intensivists.

We were all new to each other, all new to working in this setting, and all new to whatever the newest changes of the day brought. I will never forget how we greeted each other and introduced ourselves. We asked each other where we were “from,” and held a genuine appreciation to each other for being there. Imagine how this impacted how we worked together. Looking back on those night shifts, I remember us as a truly interdependent team. I will endeavor to bring that sense of mutual regard and interdependency into my work to foster effective interdisciplinary and cross-continuum teamwork.

Takeaways

As a student and practitioner of delivery system transformation, I am often in conversations about imperfect data, incomplete evidence, and role-specific and organizational resistance to change. As an acute care provider during the COVID-19 hospital surge in my region, the experiences I had as a participant in the COVID-related delivery system change will stay with me as I lead value-based delivery system change. What worked in an infectious disease crisis holds great relevance to our pressing, urgent, relevant work to create a more person-centered, equitable, and value-based delivery system.

I am confident that if those of us seeking to improve outcomes use visible and accessible data to engender confidence, clearly link practice change to the relevant and urgent issue at hand, promote broadly visible creative problem solving to foster an ecosystem of change, and cultivate empathy and mutual interdependence to promote the teamwork we aspire to have, that we will foster meaningful progress in our efforts to improve care for patients and populations.

Corresponding author: Amy Boutwell, MD, MPP, President, Collaborative Healthcare Strategies, Lexington, MA; amy@collaborativehealthcarestrategies.com.

Financial disclosures: None.

While sick at home with a 26-day symptomatic course of COVID-19 in March 2020, I watched the surge unfold in my state and the hospital where I work as an inpatient adult medicine physician. Although the preponderance of my professional life is dedicated to leading teams in implementing delivery system transformation, the hat I wore in that moment involved living through and keeping up with the changes around me. Once I recovered and returned to the arena as a COVID doctor, I adapted to and made changes during constant shifts in how we provided care.

Looking back on those months during the worst of the COVID-19 hospital surge in my region, I reflect on the factors that helped me, as a frontline and shift-work clinician, adapt to and make those changes. In reflecting on the elements that were meaningful to me during the crisis, I recognize a set of change-enabling factors that have broad relevance for those of us who work to improve outcomes for patients and populations.

Confidence engendered by liberating data

In the early days of the surge, there was much uncertainty, and unfortunately, some seriously imperfect messaging. Trust was broken or badly bruised for many frontline clinicians. I share this painful phase not to criticize, but rather reflect on what mattered to me during that crisis of confidence. It was data. Raw, unadjusted, best-available data. Produced and pushed out. Available, trended over time, telling the story of where we are, now. Counts of tests, beds, and ventilators. The consistent, transparent availability of relevant and straightforward data provided an active antidote to a sense of uncertainty during a crisis of confidence.

Personal practice change stimulated by relevance and urgency

For half a decade, I have been encouraging interdisciplinary inpatient teams to identify and actively engage the family and/or care partner as a member of the care team. Despite even the American Association of Retired Persons mobilizing an impressive regulatory approach in 32 states to require that family and/or care partners are included as such, the practice change efforts continued on a slow and steady path. Why? We just didn’t believe it was of urgent, relevant, mission-critical importance to our daily practice to do so. That all changed in March 2020.

Without needing to be told, educated, or incentivized, my first night as a COVID doctor found me calling every single patient’s family upon admission, regardless of what time it was. It was critical to review the diagnosis, transparently discuss the uncertainty regarding the upcoming hours and days, review the potential contingencies, and ask, right there and then, whether intubation is consistent with goals of care. It was that urgent and relevant. Without exception, families were grateful for the effort and candor.

The significance of this practice—undoubtedly adopted by every inpatient provider who has worked a COVID surge—is rooted in decades of academic deliberation on which is the “right” doctor to have these discussions. None of that mattered. Historical opinions changed due to what was urgent and relevant given the situation at hand and the job we had to do. Imagine, for example, what we could do and how we could change if we now consider it urgent and relevant to identify and mobilize enhanced services and supports to patients who experience inequities because we believe it to be mission-critical to the job we show up to do every day.

Change fostered by a creative problem-solving ecosystem

Embracing personal practice change was made easier and implicitly affirmed by the creative problem solving that occurred everywhere. Tents, drive-throughs, and even college field houses were now settings of care. Primary care physicians, cardiologists, and gastrointestinal (GI) and postanesthesia care nurses staffed the COVID floors. Rolling stands held iPads so staff could communicate with patients without entering the room. This creative ecosystem fostered individual practice change. No debates were needed to recognize that standard processes were inadequate. No single role or service of any discipline was singularly asked to change to meet the needs of the moment. Because of this ecosystem of creative, active change, there was a much greater flexibility among individuals, role types, departments, and disciplines to change. This is particularly poignant to me in light of the work I lead to improve care for patients who experience systemic inequities in our health care system. When we ask a single role type or discipline to change, it can be met with resistance; far more success is achieved when we engage an interdisciplinary and interdepartmental approach to change. When surrounded by others making change, it makes us more willing to change, too.

It is so often invoked that health care is a team sport. In practicality, while we may aspire to work as a team, health care delivery is still all too often comprised of a set of individual actors with individualized responsibilities trying to communicate the best they can with each other.

What I experienced during the surge at my hospital was the very best version of teamwork I have ever been a part of in health care: empathetic, mutually interdependent strangers coming together during daily changes in staffing, processes, and resources. I will never forget nights walking into the pediatric floor or day surgery recovery area—now repurposed as a COVID unit—to entirely new faces comprised of GI suite nurses, outpatient doctors, and moonlighting intensivists.

We were all new to each other, all new to working in this setting, and all new to whatever the newest changes of the day brought. I will never forget how we greeted each other and introduced ourselves. We asked each other where we were “from,” and held a genuine appreciation to each other for being there. Imagine how this impacted how we worked together. Looking back on those night shifts, I remember us as a truly interdependent team. I will endeavor to bring that sense of mutual regard and interdependency into my work to foster effective interdisciplinary and cross-continuum teamwork.

Takeaways

As a student and practitioner of delivery system transformation, I am often in conversations about imperfect data, incomplete evidence, and role-specific and organizational resistance to change. As an acute care provider during the COVID-19 hospital surge in my region, the experiences I had as a participant in the COVID-related delivery system change will stay with me as I lead value-based delivery system change. What worked in an infectious disease crisis holds great relevance to our pressing, urgent, relevant work to create a more person-centered, equitable, and value-based delivery system.

I am confident that if those of us seeking to improve outcomes use visible and accessible data to engender confidence, clearly link practice change to the relevant and urgent issue at hand, promote broadly visible creative problem solving to foster an ecosystem of change, and cultivate empathy and mutual interdependence to promote the teamwork we aspire to have, that we will foster meaningful progress in our efforts to improve care for patients and populations.

Corresponding author: Amy Boutwell, MD, MPP, President, Collaborative Healthcare Strategies, Lexington, MA; amy@collaborativehealthcarestrategies.com.

Financial disclosures: None.

Study Overview

Objective. The objectives of this study were to (1) quantify the frequency of preoperative advance care planning (ACP) discussion and documentation for older adults undergoing major surgery in a national sample, and (2) characterize how surgical patients and their family members considered ACP after postoperative complications.

Design. A secondary analysis of data from a multisite randomized clinical trial testing the effects of a question prompt list intervention (a Question Problem List [QPL] brochure with 11 questions) given to patients aged 60 years or older undergoing high-risk surgery on preoperative communication with their surgeons.

Setting and participants. This multisite randomized controlled trial involved 5 study sites that encompassed distinct US geographic areas, including University of Wisconsin Hospital and Clinics (UWHC), Madison; the University of California, San Francisco, Medical Center (UCSF); Oregon Health & Science University (OHSU), Portland; the University Hospital of Rutgers New Jersey Medical School (Rutgers), Newark; and the Brigham and Women’s Hospital (BWH), Boston, Massachusetts. The study enrolled 40 surgeons who routinely performed high-risk oncological or vascular surgery via purposeful sampling; patients aged 60 years or older with at least 1 comorbidity and an oncological or vascular problem that were treatable with high-risk surgery; and 1 invited family member per enrolled patient to participate in open-ended interviews postsurgery. High-risk surgery was defined as an operation that has a 30-day in-hospital mortality rate greater than or equal to 1%. Data were collected from June 1, 2016, to November 30, 2018.

Main outcome measures. The frequency of preoperative discussions and documentation of ACP was determined. For patients who had major surgery, any mention of ACP (ie, mention of advance directive [AD], health care power of attorney, or preference for limitations of life-sustaining treatments) by the surgeon, patient or family member during the audio recorded, transcribed, and coded preoperative consultation was counted. The presence of a written AD in the medical record at the time of the initial consultation, filed between the consultation and the date of surgery, or added postoperatively, was recorded using a standardized abstraction form. Postoperative treatments administered and complications experienced within 6 weeks after surgery were recorded. Open-ended interviews with patients who experienced significant postoperative complications (eg, prolonged hospitalization > 8 days, intensive care unit stay > 3 days) and their family members were conducted 6 weeks after surgery. Information ascertained during interviews focused on treatment decisions, postoperative experiences, and interpersonal relationships among patients, families, and clinicians. Transcripts of these interviews were then subjected to qualitative content analysis.

Main results. A total of 446 patients were enrolled in the primary study. Of these patients, 213 (122 men [57%]; 91 women [43%]; mean [SD] age, 72 [7] years) underwent major surgery. Only 13 (6.1%) of those who had major surgery had any discussion related to ACP in the preoperative consultation. In this cohort, 141 (66%) patients did not have an AD on file before undergoing major surgery. The presence of AD was not associated with age (60-69 years, 26 [31%]; 70-79 years, 31 [33%]; ≥ 80 years, 15 [42%]; P = .55), number of comorbidities (1, 35 [32%]; 2, 18 [33%]; ≥ 3, 19 [40%]; P = .62), or type of procedure (oncological, 53 [32%]; vascular, 19 [42%]; P = .22). Moreover, there was no difference in preoperative communication about ACP or documentation of an AD for patients who were mailed a QPL brochure compared to those who received usual care (intervention, 38 [35%]; usual care, 34 [33%]; P = .77). Rates of AD documentation were associated with individual study sites with BWH and UWHC having higher rates of documentation (20 [50%] and 27 [44%], respectively) compared to OHSU, UCSF, or Rutgers (7 [17%], 17 [35%], and 1 [5%], respectively). Analysis from the interviews indicated that patients and families felt unprepared for serious surgical complications and had varied interpretations of ACP. Patients with complications were enthusiastic about ACP but did not think it was important to discuss their preferences for life-sustaining treatments with their surgeon preoperatively.

Conclusion. Although surgeons and patients report that they believe ACP is important, preoperative discussion of patient preferences rarely occurs. This study found that the frequency of ACP discussions or AD documentations among older patients undergoing high-risk oncologic or vascular surgery was low. Interventions that are aimed to increase rates of preoperative ACP discussions should be implemented to help prepare patients and their families for difficult decisions in the setting of serious surgical complications and could help decrease postoperative conflicts that result from unclear patient care goals.

Commentary

Surgeons and patients approach surgical interventions with optimistic outlooks while simultaneously preparing for unintended adverse outcomes. For patients, preoperative ACP discussions ease the burden on their families and ensure their wishes and care goals are communicated. For surgeons, these discussions inform them how best to support the values of the patient. Therefore, it is unsurprising that preoperative ACP is viewed favorably by both groups. Given the consensus that ACP is important in the care of older adults undergoing high-risk surgery, one would assume that preoperative ACP discussion is a standard of practice among surgeons and their aging patients. However, in a secondary analysis of a randomized control trial testing a patient-mediated intervention to improve preoperative communication, Kalbfell et al¹ showed that ACP discussions rarely take place prior to major surgery in older adults. This finding highlights the significant discrepancy between the belief that ACP is important, and the actual rate that it is practiced, in older patients undergoing high-risk surgery. This discordance is highly concerning because it suggests that surgeons who provide care to a very vulnerable subset of older patients may overlook an essential aspect of preoperative care and therefore lack a thorough and thoughtful understanding of the patient’s care goals. In practice, this omission can pose significant challenges associated with the surgeon and family’s decisions to use postoperative life-sustaining interventions or to manage unforeseen complications should a patient become unable to make medical decisions.

The barriers to conducting successful ACP discussions between surgeons and patients are multifactorial. Kalbfell et al¹ highlighted several of these barriers, including lack of patient efficacy, physician attitudes, and institutional values in older adults who require major surgeries. The inadequacy of patient efficacy in preoperative ACP is illustrated by findings from the primary, multisite trial of QPL intervention conducted by Schwarze et al. Interestingly, the authors found that patients who did not receive QPL brochure had no ACP discussions, and that QPL implementation did not significantly improve discussion rates despite its intent to encourage these discussions.² Possible explanations for this lack of engagement might be a lack of health literacy or patient efficacy in the study population. Qualitative data from the current study provided further evidence to support these explanations. For instance, some patients provided limited or incomplete information about their wishes for health care management while others felt it was unnecessary to have ACP discussions unless complications arose.¹ However, the latter example counters the purpose of ACP which is to enable patients to make plans about future health care and not reactive to a medical complication or emergency.

Surgeons bear a large responsibility in providing treatments that are consistent with the care goals of the patient. Thus, surgeons play a crucial role in engaging, guiding, and facilitating ACP discussions with patients. This role is even more critical when patients are unable or unwilling to initiate care goal discussions. Physician attitudes towards ACP, therefore, greatly influence the effectiveness of these discussions. In a study of self-administered surveys by vascular, neurologic, and cardiothoracic surgeons, greater than 90% of respondents viewed postoperative life-supporting therapy as necessary, and 54% would decline to operate on patients with an AD limiting life-supporting therapy.³ Moreover, the same study showed that 52% of respondents reported discussing AD before surgery, a figure that exceeded the actual rates at which ACP discussions occur in many other studies. In the current study, Kalbfell et al¹ also found that surgeons viewed ACP discussions largely in the context of AD creation and declined to investigate the full scope of patient preferences. These findings, when combined with other studies that indicate an incomplete understanding of ACP in some surgeons, suggest that not all physicians are able or willing to navigate these sometimes lengthy and difficult conversations with patients. This gap in practice provides opportunities for training in surgical specialties that center on optimizing preoperative ACP discussions to meet the care needs of older patients.

Institutional value and culture are important factors that impact physician behavior and the practice of ACP discussion. In the current study, the authors reported that the majority of ACP discussions were held by a minority of surgeons and that different institutions and study sites had vastly different rates of ACP documentation.¹ These results are further supported by findings of large variations between physicians and hospitals in ACP reporting in hospitalized frail older adults.⁴ These variations in practices at different institutions suggest that it is possible to improve rates of preoperative ACP discussion. Reasons for these differences need to be further investigated in order to identify strategies, resources, or trainings required by medical institutions to support surgeons to carry out ACP discussions with patients undergoing high-risk surgeries.

The study conducted by Kalbfell et al¹ has several strengths. For example, it included Spanish-speaking patients and the use of a Spanish version of the QPL intervention to account for cultural differences. The study also included multiple surgical specialties and institutions and captured a large and national sample, thus making its findings more generalizable. However, the lack of data on the duration of preoperative consultation visits in patients who completed ACP discussions poses a limitation to this study. This is relevant because surgeon availability to engage in lengthy ACP discussions may be limited due to busy clinical schedules. Additional data on the duration of preoperative visits inclusive of a thoughtfully conducted ACP discussion could help to modify clinical workflow to facilitate its uptake in surgical practices.

Applications for Clinical Practice

The findings from the current study indicate that patients and surgeons agree that preoperative ACP discussions are beneficial to the clinical care of older adults before high-risk surgeries. However, these important conversations do not occur frequently. Surgeons and health care institutions need to identify strategies to initiate, facilitate, and optimize productive preoperative ACP discussions to provide patient-centered care in vulnerable older surgical patients.

Financial disclosures: None.

Study Overview

Objective. The objectives of this study were to (1) quantify the frequency of preoperative advance care planning (ACP) discussion and documentation for older adults undergoing major surgery in a national sample, and (2) characterize how surgical patients and their family members considered ACP after postoperative complications.

Design. A secondary analysis of data from a multisite randomized clinical trial testing the effects of a question prompt list intervention (a Question Problem List [QPL] brochure with 11 questions) given to patients aged 60 years or older undergoing high-risk surgery on preoperative communication with their surgeons.

Setting and participants. This multisite randomized controlled trial involved 5 study sites that encompassed distinct US geographic areas, including University of Wisconsin Hospital and Clinics (UWHC), Madison; the University of California, San Francisco, Medical Center (UCSF); Oregon Health & Science University (OHSU), Portland; the University Hospital of Rutgers New Jersey Medical School (Rutgers), Newark; and the Brigham and Women’s Hospital (BWH), Boston, Massachusetts. The study enrolled 40 surgeons who routinely performed high-risk oncological or vascular surgery via purposeful sampling; patients aged 60 years or older with at least 1 comorbidity and an oncological or vascular problem that were treatable with high-risk surgery; and 1 invited family member per enrolled patient to participate in open-ended interviews postsurgery. High-risk surgery was defined as an operation that has a 30-day in-hospital mortality rate greater than or equal to 1%. Data were collected from June 1, 2016, to November 30, 2018.

Main outcome measures. The frequency of preoperative discussions and documentation of ACP was determined. For patients who had major surgery, any mention of ACP (ie, mention of advance directive [AD], health care power of attorney, or preference for limitations of life-sustaining treatments) by the surgeon, patient or family member during the audio recorded, transcribed, and coded preoperative consultation was counted. The presence of a written AD in the medical record at the time of the initial consultation, filed between the consultation and the date of surgery, or added postoperatively, was recorded using a standardized abstraction form. Postoperative treatments administered and complications experienced within 6 weeks after surgery were recorded. Open-ended interviews with patients who experienced significant postoperative complications (eg, prolonged hospitalization > 8 days, intensive care unit stay > 3 days) and their family members were conducted 6 weeks after surgery. Information ascertained during interviews focused on treatment decisions, postoperative experiences, and interpersonal relationships among patients, families, and clinicians. Transcripts of these interviews were then subjected to qualitative content analysis.

Main results. A total of 446 patients were enrolled in the primary study. Of these patients, 213 (122 men [57%]; 91 women [43%]; mean [SD] age, 72 [7] years) underwent major surgery. Only 13 (6.1%) of those who had major surgery had any discussion related to ACP in the preoperative consultation. In this cohort, 141 (66%) patients did not have an AD on file before undergoing major surgery. The presence of AD was not associated with age (60-69 years, 26 [31%]; 70-79 years, 31 [33%]; ≥ 80 years, 15 [42%]; P = .55), number of comorbidities (1, 35 [32%]; 2, 18 [33%]; ≥ 3, 19 [40%]; P = .62), or type of procedure (oncological, 53 [32%]; vascular, 19 [42%]; P = .22). Moreover, there was no difference in preoperative communication about ACP or documentation of an AD for patients who were mailed a QPL brochure compared to those who received usual care (intervention, 38 [35%]; usual care, 34 [33%]; P = .77). Rates of AD documentation were associated with individual study sites with BWH and UWHC having higher rates of documentation (20 [50%] and 27 [44%], respectively) compared to OHSU, UCSF, or Rutgers (7 [17%], 17 [35%], and 1 [5%], respectively). Analysis from the interviews indicated that patients and families felt unprepared for serious surgical complications and had varied interpretations of ACP. Patients with complications were enthusiastic about ACP but did not think it was important to discuss their preferences for life-sustaining treatments with their surgeon preoperatively.

Conclusion. Although surgeons and patients report that they believe ACP is important, preoperative discussion of patient preferences rarely occurs. This study found that the frequency of ACP discussions or AD documentations among older patients undergoing high-risk oncologic or vascular surgery was low. Interventions that are aimed to increase rates of preoperative ACP discussions should be implemented to help prepare patients and their families for difficult decisions in the setting of serious surgical complications and could help decrease postoperative conflicts that result from unclear patient care goals.

Commentary

Surgeons and patients approach surgical interventions with optimistic outlooks while simultaneously preparing for unintended adverse outcomes. For patients, preoperative ACP discussions ease the burden on their families and ensure their wishes and care goals are communicated. For surgeons, these discussions inform them how best to support the values of the patient. Therefore, it is unsurprising that preoperative ACP is viewed favorably by both groups. Given the consensus that ACP is important in the care of older adults undergoing high-risk surgery, one would assume that preoperative ACP discussion is a standard of practice among surgeons and their aging patients. However, in a secondary analysis of a randomized control trial testing a patient-mediated intervention to improve preoperative communication, Kalbfell et al¹ showed that ACP discussions rarely take place prior to major surgery in older adults. This finding highlights the significant discrepancy between the belief that ACP is important, and the actual rate that it is practiced, in older patients undergoing high-risk surgery. This discordance is highly concerning because it suggests that surgeons who provide care to a very vulnerable subset of older patients may overlook an essential aspect of preoperative care and therefore lack a thorough and thoughtful understanding of the patient’s care goals. In practice, this omission can pose significant challenges associated with the surgeon and family’s decisions to use postoperative life-sustaining interventions or to manage unforeseen complications should a patient become unable to make medical decisions.

The barriers to conducting successful ACP discussions between surgeons and patients are multifactorial. Kalbfell et al¹ highlighted several of these barriers, including lack of patient efficacy, physician attitudes, and institutional values in older adults who require major surgeries. The inadequacy of patient efficacy in preoperative ACP is illustrated by findings from the primary, multisite trial of QPL intervention conducted by Schwarze et al. Interestingly, the authors found that patients who did not receive QPL brochure had no ACP discussions, and that QPL implementation did not significantly improve discussion rates despite its intent to encourage these discussions.² Possible explanations for this lack of engagement might be a lack of health literacy or patient efficacy in the study population. Qualitative data from the current study provided further evidence to support these explanations. For instance, some patients provided limited or incomplete information about their wishes for health care management while others felt it was unnecessary to have ACP discussions unless complications arose.¹ However, the latter example counters the purpose of ACP which is to enable patients to make plans about future health care and not reactive to a medical complication or emergency.

Surgeons bear a large responsibility in providing treatments that are consistent with the care goals of the patient. Thus, surgeons play a crucial role in engaging, guiding, and facilitating ACP discussions with patients. This role is even more critical when patients are unable or unwilling to initiate care goal discussions. Physician attitudes towards ACP, therefore, greatly influence the effectiveness of these discussions. In a study of self-administered surveys by vascular, neurologic, and cardiothoracic surgeons, greater than 90% of respondents viewed postoperative life-supporting therapy as necessary, and 54% would decline to operate on patients with an AD limiting life-supporting therapy.³ Moreover, the same study showed that 52% of respondents reported discussing AD before surgery, a figure that exceeded the actual rates at which ACP discussions occur in many other studies. In the current study, Kalbfell et al¹ also found that surgeons viewed ACP discussions largely in the context of AD creation and declined to investigate the full scope of patient preferences. These findings, when combined with other studies that indicate an incomplete understanding of ACP in some surgeons, suggest that not all physicians are able or willing to navigate these sometimes lengthy and difficult conversations with patients. This gap in practice provides opportunities for training in surgical specialties that center on optimizing preoperative ACP discussions to meet the care needs of older patients.

Institutional value and culture are important factors that impact physician behavior and the practice of ACP discussion. In the current study, the authors reported that the majority of ACP discussions were held by a minority of surgeons and that different institutions and study sites had vastly different rates of ACP documentation.¹ These results are further supported by findings of large variations between physicians and hospitals in ACP reporting in hospitalized frail older adults.⁴ These variations in practices at different institutions suggest that it is possible to improve rates of preoperative ACP discussion. Reasons for these differences need to be further investigated in order to identify strategies, resources, or trainings required by medical institutions to support surgeons to carry out ACP discussions with patients undergoing high-risk surgeries.

The study conducted by Kalbfell et al¹ has several strengths. For example, it included Spanish-speaking patients and the use of a Spanish version of the QPL intervention to account for cultural differences. The study also included multiple surgical specialties and institutions and captured a large and national sample, thus making its findings more generalizable. However, the lack of data on the duration of preoperative consultation visits in patients who completed ACP discussions poses a limitation to this study. This is relevant because surgeon availability to engage in lengthy ACP discussions may be limited due to busy clinical schedules. Additional data on the duration of preoperative visits inclusive of a thoughtfully conducted ACP discussion could help to modify clinical workflow to facilitate its uptake in surgical practices.

Applications for Clinical Practice

The findings from the current study indicate that patients and surgeons agree that preoperative ACP discussions are beneficial to the clinical care of older adults before high-risk surgeries. However, these important conversations do not occur frequently. Surgeons and health care institutions need to identify strategies to initiate, facilitate, and optimize productive preoperative ACP discussions to provide patient-centered care in vulnerable older surgical patients.

Financial disclosures: None.

Study Overview

Objective. The objectives of this study were to (1) quantify the frequency of preoperative advance care planning (ACP) discussion and documentation for older adults undergoing major surgery in a national sample, and (2) characterize how surgical patients and their family members considered ACP after postoperative complications.

Design. A secondary analysis of data from a multisite randomized clinical trial testing the effects of a question prompt list intervention (a Question Problem List [QPL] brochure with 11 questions) given to patients aged 60 years or older undergoing high-risk surgery on preoperative communication with their surgeons.

Setting and participants. This multisite randomized controlled trial involved 5 study sites that encompassed distinct US geographic areas, including University of Wisconsin Hospital and Clinics (UWHC), Madison; the University of California, San Francisco, Medical Center (UCSF); Oregon Health & Science University (OHSU), Portland; the University Hospital of Rutgers New Jersey Medical School (Rutgers), Newark; and the Brigham and Women’s Hospital (BWH), Boston, Massachusetts. The study enrolled 40 surgeons who routinely performed high-risk oncological or vascular surgery via purposeful sampling; patients aged 60 years or older with at least 1 comorbidity and an oncological or vascular problem that were treatable with high-risk surgery; and 1 invited family member per enrolled patient to participate in open-ended interviews postsurgery. High-risk surgery was defined as an operation that has a 30-day in-hospital mortality rate greater than or equal to 1%. Data were collected from June 1, 2016, to November 30, 2018.

Main outcome measures. The frequency of preoperative discussions and documentation of ACP was determined. For patients who had major surgery, any mention of ACP (ie, mention of advance directive [AD], health care power of attorney, or preference for limitations of life-sustaining treatments) by the surgeon, patient or family member during the audio recorded, transcribed, and coded preoperative consultation was counted. The presence of a written AD in the medical record at the time of the initial consultation, filed between the consultation and the date of surgery, or added postoperatively, was recorded using a standardized abstraction form. Postoperative treatments administered and complications experienced within 6 weeks after surgery were recorded. Open-ended interviews with patients who experienced significant postoperative complications (eg, prolonged hospitalization > 8 days, intensive care unit stay > 3 days) and their family members were conducted 6 weeks after surgery. Information ascertained during interviews focused on treatment decisions, postoperative experiences, and interpersonal relationships among patients, families, and clinicians. Transcripts of these interviews were then subjected to qualitative content analysis.

Main results. A total of 446 patients were enrolled in the primary study. Of these patients, 213 (122 men [57%]; 91 women [43%]; mean [SD] age, 72 [7] years) underwent major surgery. Only 13 (6.1%) of those who had major surgery had any discussion related to ACP in the preoperative consultation. In this cohort, 141 (66%) patients did not have an AD on file before undergoing major surgery. The presence of AD was not associated with age (60-69 years, 26 [31%]; 70-79 years, 31 [33%]; ≥ 80 years, 15 [42%]; P = .55), number of comorbidities (1, 35 [32%]; 2, 18 [33%]; ≥ 3, 19 [40%]; P = .62), or type of procedure (oncological, 53 [32%]; vascular, 19 [42%]; P = .22). Moreover, there was no difference in preoperative communication about ACP or documentation of an AD for patients who were mailed a QPL brochure compared to those who received usual care (intervention, 38 [35%]; usual care, 34 [33%]; P = .77). Rates of AD documentation were associated with individual study sites with BWH and UWHC having higher rates of documentation (20 [50%] and 27 [44%], respectively) compared to OHSU, UCSF, or Rutgers (7 [17%], 17 [35%], and 1 [5%], respectively). Analysis from the interviews indicated that patients and families felt unprepared for serious surgical complications and had varied interpretations of ACP. Patients with complications were enthusiastic about ACP but did not think it was important to discuss their preferences for life-sustaining treatments with their surgeon preoperatively.

Conclusion. Although surgeons and patients report that they believe ACP is important, preoperative discussion of patient preferences rarely occurs. This study found that the frequency of ACP discussions or AD documentations among older patients undergoing high-risk oncologic or vascular surgery was low. Interventions that are aimed to increase rates of preoperative ACP discussions should be implemented to help prepare patients and their families for difficult decisions in the setting of serious surgical complications and could help decrease postoperative conflicts that result from unclear patient care goals.

Commentary

Surgeons and patients approach surgical interventions with optimistic outlooks while simultaneously preparing for unintended adverse outcomes. For patients, preoperative ACP discussions ease the burden on their families and ensure their wishes and care goals are communicated. For surgeons, these discussions inform them how best to support the values of the patient. Therefore, it is unsurprising that preoperative ACP is viewed favorably by both groups. Given the consensus that ACP is important in the care of older adults undergoing high-risk surgery, one would assume that preoperative ACP discussion is a standard of practice among surgeons and their aging patients. However, in a secondary analysis of a randomized control trial testing a patient-mediated intervention to improve preoperative communication, Kalbfell et al¹ showed that ACP discussions rarely take place prior to major surgery in older adults. This finding highlights the significant discrepancy between the belief that ACP is important, and the actual rate that it is practiced, in older patients undergoing high-risk surgery. This discordance is highly concerning because it suggests that surgeons who provide care to a very vulnerable subset of older patients may overlook an essential aspect of preoperative care and therefore lack a thorough and thoughtful understanding of the patient’s care goals. In practice, this omission can pose significant challenges associated with the surgeon and family’s decisions to use postoperative life-sustaining interventions or to manage unforeseen complications should a patient become unable to make medical decisions.

The barriers to conducting successful ACP discussions between surgeons and patients are multifactorial. Kalbfell et al¹ highlighted several of these barriers, including lack of patient efficacy, physician attitudes, and institutional values in older adults who require major surgeries. The inadequacy of patient efficacy in preoperative ACP is illustrated by findings from the primary, multisite trial of QPL intervention conducted by Schwarze et al. Interestingly, the authors found that patients who did not receive QPL brochure had no ACP discussions, and that QPL implementation did not significantly improve discussion rates despite its intent to encourage these discussions.² Possible explanations for this lack of engagement might be a lack of health literacy or patient efficacy in the study population. Qualitative data from the current study provided further evidence to support these explanations. For instance, some patients provided limited or incomplete information about their wishes for health care management while others felt it was unnecessary to have ACP discussions unless complications arose.¹ However, the latter example counters the purpose of ACP which is to enable patients to make plans about future health care and not reactive to a medical complication or emergency.

Surgeons bear a large responsibility in providing treatments that are consistent with the care goals of the patient. Thus, surgeons play a crucial role in engaging, guiding, and facilitating ACP discussions with patients. This role is even more critical when patients are unable or unwilling to initiate care goal discussions. Physician attitudes towards ACP, therefore, greatly influence the effectiveness of these discussions. In a study of self-administered surveys by vascular, neurologic, and cardiothoracic surgeons, greater than 90% of respondents viewed postoperative life-supporting therapy as necessary, and 54% would decline to operate on patients with an AD limiting life-supporting therapy.³ Moreover, the same study showed that 52% of respondents reported discussing AD before surgery, a figure that exceeded the actual rates at which ACP discussions occur in many other studies. In the current study, Kalbfell et al¹ also found that surgeons viewed ACP discussions largely in the context of AD creation and declined to investigate the full scope of patient preferences. These findings, when combined with other studies that indicate an incomplete understanding of ACP in some surgeons, suggest that not all physicians are able or willing to navigate these sometimes lengthy and difficult conversations with patients. This gap in practice provides opportunities for training in surgical specialties that center on optimizing preoperative ACP discussions to meet the care needs of older patients.

Institutional value and culture are important factors that impact physician behavior and the practice of ACP discussion. In the current study, the authors reported that the majority of ACP discussions were held by a minority of surgeons and that different institutions and study sites had vastly different rates of ACP documentation.¹ These results are further supported by findings of large variations between physicians and hospitals in ACP reporting in hospitalized frail older adults.⁴ These variations in practices at different institutions suggest that it is possible to improve rates of preoperative ACP discussion. Reasons for these differences need to be further investigated in order to identify strategies, resources, or trainings required by medical institutions to support surgeons to carry out ACP discussions with patients undergoing high-risk surgeries.

The study conducted by Kalbfell et al¹ has several strengths. For example, it included Spanish-speaking patients and the use of a Spanish version of the QPL intervention to account for cultural differences. The study also included multiple surgical specialties and institutions and captured a large and national sample, thus making its findings more generalizable. However, the lack of data on the duration of preoperative consultation visits in patients who completed ACP discussions poses a limitation to this study. This is relevant because surgeon availability to engage in lengthy ACP discussions may be limited due to busy clinical schedules. Additional data on the duration of preoperative visits inclusive of a thoughtfully conducted ACP discussion could help to modify clinical workflow to facilitate its uptake in surgical practices.

Applications for Clinical Practice

The findings from the current study indicate that patients and surgeons agree that preoperative ACP discussions are beneficial to the clinical care of older adults before high-risk surgeries. However, these important conversations do not occur frequently. Surgeons and health care institutions need to identify strategies to initiate, facilitate, and optimize productive preoperative ACP discussions to provide patient-centered care in vulnerable older surgical patients.

Financial disclosures: None.

Background

We sought to evaluate passive recruitment efforts of VA patients into a precision medicine research program. Access to clinical trials and other research opportunities is important to discovering new disease treatments and better ways to detect, diagnose, and reduce disease risk. The WISDOM (Women Informed to Screen Depending on Measures of risk) Study is a multi-site, pragmatic trial with webbased participation based at the University of California at San Francisco (UCSF) that aims to move breast cancer screening away from its current one-size-fitsall approach to one that is personalized based on each woman’s individual risk.

Methods

We created a hub and spoke recruitment model with the San Francisco VA Medical Center (SFVAMC) serving as the central hub of passive recruitment activities and eligible VA facilities that agreed to participate serving as the spoke recruitment sites. Eligible facilities had at least 3,000 women patients, VA clinical genetic services available, a site lead from the VA Women’s Health-Practice-Based Research Network, and mammography on site. Site participation involved permission for the research team to email eligible patients (women aged 40-74 without prior breast cancer diagnosis) about the WISDOM Study. We evaluated the effectiveness of the recruitment by assessing trends in enrollment and monitoring participation of VA patients in the WISDOM Study. Analysis: Pre/post frequencies of women consenting to participate in the WISDOM Study.

Results

From 5/24/2021 through 6/21/2021, we emailed 27,061 eligible VA patients from six participating VA facilities. Prior to the VA emailing, an average of 22 women per week consented to participating in the WISDOM Study and none were Veterans. After the first month of the VA emailing, an average of 186 women per week consented – a 7.5-fold increase. Additionally, during the first month of VA emailing, 81% of women registering with the WISDOM Study said they heard about the study from the VA.

Implications

The VA has recently approved of emailing as a method for recruiting research subjects. Our results demonstrate this is a feasible approach for precision medicine research, a growing area of research in VA and at academic affiliates.

Background

We sought to evaluate passive recruitment efforts of VA patients into a precision medicine research program. Access to clinical trials and other research opportunities is important to discovering new disease treatments and better ways to detect, diagnose, and reduce disease risk. The WISDOM (Women Informed to Screen Depending on Measures of risk) Study is a multi-site, pragmatic trial with webbased participation based at the University of California at San Francisco (UCSF) that aims to move breast cancer screening away from its current one-size-fitsall approach to one that is personalized based on each woman’s individual risk.

Methods

We created a hub and spoke recruitment model with the San Francisco VA Medical Center (SFVAMC) serving as the central hub of passive recruitment activities and eligible VA facilities that agreed to participate serving as the spoke recruitment sites. Eligible facilities had at least 3,000 women patients, VA clinical genetic services available, a site lead from the VA Women’s Health-Practice-Based Research Network, and mammography on site. Site participation involved permission for the research team to email eligible patients (women aged 40-74 without prior breast cancer diagnosis) about the WISDOM Study. We evaluated the effectiveness of the recruitment by assessing trends in enrollment and monitoring participation of VA patients in the WISDOM Study. Analysis: Pre/post frequencies of women consenting to participate in the WISDOM Study.

Results

From 5/24/2021 through 6/21/2021, we emailed 27,061 eligible VA patients from six participating VA facilities. Prior to the VA emailing, an average of 22 women per week consented to participating in the WISDOM Study and none were Veterans. After the first month of the VA emailing, an average of 186 women per week consented – a 7.5-fold increase. Additionally, during the first month of VA emailing, 81% of women registering with the WISDOM Study said they heard about the study from the VA.

Implications

The VA has recently approved of emailing as a method for recruiting research subjects. Our results demonstrate this is a feasible approach for precision medicine research, a growing area of research in VA and at academic affiliates.

Background

We sought to evaluate passive recruitment efforts of VA patients into a precision medicine research program. Access to clinical trials and other research opportunities is important to discovering new disease treatments and better ways to detect, diagnose, and reduce disease risk. The WISDOM (Women Informed to Screen Depending on Measures of risk) Study is a multi-site, pragmatic trial with webbased participation based at the University of California at San Francisco (UCSF) that aims to move breast cancer screening away from its current one-size-fitsall approach to one that is personalized based on each woman’s individual risk.

Methods

We created a hub and spoke recruitment model with the San Francisco VA Medical Center (SFVAMC) serving as the central hub of passive recruitment activities and eligible VA facilities that agreed to participate serving as the spoke recruitment sites. Eligible facilities had at least 3,000 women patients, VA clinical genetic services available, a site lead from the VA Women’s Health-Practice-Based Research Network, and mammography on site. Site participation involved permission for the research team to email eligible patients (women aged 40-74 without prior breast cancer diagnosis) about the WISDOM Study. We evaluated the effectiveness of the recruitment by assessing trends in enrollment and monitoring participation of VA patients in the WISDOM Study. Analysis: Pre/post frequencies of women consenting to participate in the WISDOM Study.

Results

From 5/24/2021 through 6/21/2021, we emailed 27,061 eligible VA patients from six participating VA facilities. Prior to the VA emailing, an average of 22 women per week consented to participating in the WISDOM Study and none were Veterans. After the first month of the VA emailing, an average of 186 women per week consented – a 7.5-fold increase. Additionally, during the first month of VA emailing, 81% of women registering with the WISDOM Study said they heard about the study from the VA.

Implications

The VA has recently approved of emailing as a method for recruiting research subjects. Our results demonstrate this is a feasible approach for precision medicine research, a growing area of research in VA and at academic affiliates.

High-value care (HVC) is a philosophy and approach to medicine that focuses on achieving the best patient outcomes through evidence-based practice while minimizing harm to patients, wasted healthcare resources, and costs. Incorporating HVC principles in pediatric clinical decision-making is particularly important owing to the harms of hospitalization, overutilization, and overdiagnosis, as well as rising costs of pediatric care.^1-4 How can we maintain these principles in the face of a global pandemic and new emerging syndrome, multisystem inflammatory syndrome in children (MIS-C), which has dramatically impacted healthcare systems for children?

In this article, we discuss the barriers and opportunities around practicing HVC in our evolving approach to novel COVID-19 management in hospitalized children. We also draw lessons from our experiences on how we can respond to future events that rapidly shift our approach to care.

As children’s hospitals and pediatric providers responded to the COVID-19 pandemic, practice recommendations were implemented rapidly and changed rapidly. A major challenge with an event like this is how we respond to the unknown and uncertainty, something most healthcare workers are not comfortable doing at baseline,^5,6 particularly trainees and early-career physicians.⁷ With the benefit of hindsight, many early clinical approaches to care may now be seen as low-value care (LVC). For example, COVID-19 test availability was initially limited, and many hospitals utilized respiratory viral panels (RVPs) to potentially eliminate COVID-19 as an etiology of symptoms. RVP use increased during this time⁸; however, studies have shown that the co-infection rate of SARS-CoV2 with other respiratory viruses varies widely, so a positive RVP was of uncertain benefit.⁹ In addition, routine RVP use is often low value and may lead to overdiagnosis, additional overtesting cascades, and, at times, false reassurance and premature closure of the diagnostic workup.¹⁰

As our understanding of COVID-19 has expanded, rapid changes in treatment have also occurred. Early data were often preliminary and based on small trials of adults, and treatments ranged from inexpensive and available (dexamethasone) to quite expensive (remdesivir, monoclonal antibodies). Pragmatic randomized controlled trials (RCTs) are an important tool that may have been underutilized in pediatrics. Similar to our adult hospitalist colleagues’ experience,¹¹ the rapid rise in cases provided an opportunity to collaborate across institutions to assess which treatments were most effective. In particular, the predictable rise in rates of MIS-C after a surge in COVID-19 cases could have provided an avenue to evaluate the relative effectiveness of the various treatments used.¹² However, there were limited pediatric RCTs and thus a missed opportunity to establish an evidence-based pediatric standard of care for COVID-19 and MIS-C. This resulted in the development and dissemination of care practices before they were fully tested in children.

Similarly, the medical community has become increasingly aware of laboratory findings that may be predictive of clinical course.¹³ The outcomes of COVID and MIS-C are potentially severe, so looking for “early warning signs” with diagnostic testing is appealing. Clinicians responding to early data, and with a fear of missing something, may order a full panel of bloodwork for admitted patients to assist with decision-making and may underestimate the perceived minor harms and cost of unnecessary testing/admissions.³ However, most of the evidence regarding lab values came from the adult population. There is little understanding of how lab values impact pediatric-specific outcomes.¹⁴ Even for MIS-C, a pediatric-specific condition, early protocols emphasize broad testing approaches.¹⁵ A focus on grave (but rare) outcomes from a novel virus may also distract from more common causes of symptoms and lead to missed common diagnoses that are less severe.¹⁶ For both testing and treatment, having this early information before clear evidence on how it guided care may have caused more harm than benefit. Again, RCTs may have helped guide MIS-C therapies and protocol development.

Changing workflows may also create new barriers to HVC. One of the recommendations from Choosing Wisely^® during the COVID-19 pandemic was to batch lab draws¹⁷ to reduce the risk of exposure to healthcare workers performing phlebotomy, as well as staff who transport, handle, and process bloodwork in the lab. This may inadvertently encourage the approach of getting a lab test “in case” we need it with a single daily blood draw. In trying to avoid multiple encounters (and conserve personal protective equipment [PPE]), we may be taking a less stepwise approach than in prepandemic times.

Finally, children’s hospitals witnessed significant financial challenges and reductions in patient volume related to the pandemic.¹⁸ Reductions in patient volume could present a potential opportunity for practicing HVC (eg, more time to discuss downstream effects) or alternatively could inadvertently incentivize low-value, low-priority care via messaging around preserving financial viability.

For clinicians and healthcare systems, these examples highlight why we may be predisposed to practicing LVC during a pandemic or similar emerging threat.

In light of these challenging clinical scenarios and nonclinical factors that predispose us to LVC, how can we reinforce a high-value approach to care during a pandemic or similar emerging threat? The following five specific concepts may help providers and organizations optimize HVC during this pandemic and in future situations:

1. Utilize pediatric RCTs to provide evidence-based recommendations. In the face of a novel virus with unclear manifestations, treatment options were rapidly implemented without time for careful evaluation. In the future, collaboratively utilizing shared resources in the research community could help rapidly and rigorously evaluate outcomes in the pursuit of evidence-based practice.
2. Use standardization as a tool to mitigate uncertainty. Knowing that uncertainty can be a driver of overuse and that during emerging threats, evidence is scarce and rapidly changing, a structured method for standardizing practice across your institution or multiple institutions can be helpful in many ways. Electronic health record–based orders and guidelines provide a standard of care to relieve uncertainty and have been shown to reduce overtesting.¹⁹ These resources can also be adapted rapidly as evidence emerges, reducing the burden on providers to know the latest evolving best practice. Experts who have reviewed the literature should have a method to quickly disseminate these findings through standardized practice, providing a venue for rapid learning and implementation.²⁰
3. Plan for active deimplementation from the outset. It is inevitable that some practices implemented early in pandemic response may need to be deimplemented later as the evidence and situation evolve. However, there is ample evidence that deimplementation can be difficult.²¹ Building in deimplementation mechanisms, such as standing educational sessions or hospital committees dedicated to value that review practices, from the beginning may ease these changes.
4. Take advantage of novel opportunities to improve value. Early stop-gap interventions may be wasteful, but the upheaval from major events may also create novel opportunities to improve value in other ways. Some of these efforts, like PPE conservation and as-needed follow-up visits, may become useful methods to improve value even after the pandemic ends.^22,23 The decreased pursuit of healthcare during the pandemic may also have given us an opportunity to better define when delayed diagnosis or even nondiagnosis for certain conditions is acceptable and when it may cause harm.
5. Highlight harms of overuse. While avoiding unnecessary costs is an important aspect of reducing overuse, often the other human-centered harms of overuse are better motivators for HVC. Especially during the response to an emerging threat, the impacts of overuse may be compounded. Laboratory resources that are strained to meet COVID-19 testing demand will be further stretched by overuse of other laboratory testing. Overuse of ineffective treatments adds stress to nurses, pharmacists, and other front-line staff taking care of ill patients. Side effects of unnecessary interventions, including those that could prolong hospitalization, would also increase strain on the system. Reducing overuse is also a way to reduce workload for hospital staff during a time of crisis. Improved efficiency of practice and less time spent on practices that do not add value to patient care can insulate staff against burnout.²⁴ Hospitalization and healthcare costs can add to the stress and financial burden of patients and families.²⁵ Clinicians can highlight harms of overuse through openly talking about it on rounds with the patients, families, and entire care team and incorporating it into health system–wide messaging.

As vaccine distribution continues, like many clinicians, we are hopeful that the worst days of the pandemic are behind us. The crucible of the COVID-19 pandemic has undoubtedly changed us as clinicians and impacted our future practice patterns. We believe there is a need to challenge ourselves to continue to think from a value mindset even in times of crisis. Furthermore, there are important opportunities to learn from our response to the COVID-19 pandemic and find strategies for minimizing LVC outside the pandemic. We believe the lessons learned around improving value during this pandemic can strengthen our response to the next novel, widespread threat and reduce waste in our care systems, with a potential to increase the resilience of systems in the future.

High-value care (HVC) is a philosophy and approach to medicine that focuses on achieving the best patient outcomes through evidence-based practice while minimizing harm to patients, wasted healthcare resources, and costs. Incorporating HVC principles in pediatric clinical decision-making is particularly important owing to the harms of hospitalization, overutilization, and overdiagnosis, as well as rising costs of pediatric care.^1-4 How can we maintain these principles in the face of a global pandemic and new emerging syndrome, multisystem inflammatory syndrome in children (MIS-C), which has dramatically impacted healthcare systems for children?

In this article, we discuss the barriers and opportunities around practicing HVC in our evolving approach to novel COVID-19 management in hospitalized children. We also draw lessons from our experiences on how we can respond to future events that rapidly shift our approach to care.

As children’s hospitals and pediatric providers responded to the COVID-19 pandemic, practice recommendations were implemented rapidly and changed rapidly. A major challenge with an event like this is how we respond to the unknown and uncertainty, something most healthcare workers are not comfortable doing at baseline,^5,6 particularly trainees and early-career physicians.⁷ With the benefit of hindsight, many early clinical approaches to care may now be seen as low-value care (LVC). For example, COVID-19 test availability was initially limited, and many hospitals utilized respiratory viral panels (RVPs) to potentially eliminate COVID-19 as an etiology of symptoms. RVP use increased during this time⁸; however, studies have shown that the co-infection rate of SARS-CoV2 with other respiratory viruses varies widely, so a positive RVP was of uncertain benefit.⁹ In addition, routine RVP use is often low value and may lead to overdiagnosis, additional overtesting cascades, and, at times, false reassurance and premature closure of the diagnostic workup.¹⁰

As our understanding of COVID-19 has expanded, rapid changes in treatment have also occurred. Early data were often preliminary and based on small trials of adults, and treatments ranged from inexpensive and available (dexamethasone) to quite expensive (remdesivir, monoclonal antibodies). Pragmatic randomized controlled trials (RCTs) are an important tool that may have been underutilized in pediatrics. Similar to our adult hospitalist colleagues’ experience,¹¹ the rapid rise in cases provided an opportunity to collaborate across institutions to assess which treatments were most effective. In particular, the predictable rise in rates of MIS-C after a surge in COVID-19 cases could have provided an avenue to evaluate the relative effectiveness of the various treatments used.¹² However, there were limited pediatric RCTs and thus a missed opportunity to establish an evidence-based pediatric standard of care for COVID-19 and MIS-C. This resulted in the development and dissemination of care practices before they were fully tested in children.

Similarly, the medical community has become increasingly aware of laboratory findings that may be predictive of clinical course.¹³ The outcomes of COVID and MIS-C are potentially severe, so looking for “early warning signs” with diagnostic testing is appealing. Clinicians responding to early data, and with a fear of missing something, may order a full panel of bloodwork for admitted patients to assist with decision-making and may underestimate the perceived minor harms and cost of unnecessary testing/admissions.³ However, most of the evidence regarding lab values came from the adult population. There is little understanding of how lab values impact pediatric-specific outcomes.¹⁴ Even for MIS-C, a pediatric-specific condition, early protocols emphasize broad testing approaches.¹⁵ A focus on grave (but rare) outcomes from a novel virus may also distract from more common causes of symptoms and lead to missed common diagnoses that are less severe.¹⁶ For both testing and treatment, having this early information before clear evidence on how it guided care may have caused more harm than benefit. Again, RCTs may have helped guide MIS-C therapies and protocol development.

Changing workflows may also create new barriers to HVC. One of the recommendations from Choosing Wisely^® during the COVID-19 pandemic was to batch lab draws¹⁷ to reduce the risk of exposure to healthcare workers performing phlebotomy, as well as staff who transport, handle, and process bloodwork in the lab. This may inadvertently encourage the approach of getting a lab test “in case” we need it with a single daily blood draw. In trying to avoid multiple encounters (and conserve personal protective equipment [PPE]), we may be taking a less stepwise approach than in prepandemic times.

Finally, children’s hospitals witnessed significant financial challenges and reductions in patient volume related to the pandemic.¹⁸ Reductions in patient volume could present a potential opportunity for practicing HVC (eg, more time to discuss downstream effects) or alternatively could inadvertently incentivize low-value, low-priority care via messaging around preserving financial viability.

For clinicians and healthcare systems, these examples highlight why we may be predisposed to practicing LVC during a pandemic or similar emerging threat.

In light of these challenging clinical scenarios and nonclinical factors that predispose us to LVC, how can we reinforce a high-value approach to care during a pandemic or similar emerging threat? The following five specific concepts may help providers and organizations optimize HVC during this pandemic and in future situations:

1. Utilize pediatric RCTs to provide evidence-based recommendations. In the face of a novel virus with unclear manifestations, treatment options were rapidly implemented without time for careful evaluation. In the future, collaboratively utilizing shared resources in the research community could help rapidly and rigorously evaluate outcomes in the pursuit of evidence-based practice.
2. Use standardization as a tool to mitigate uncertainty. Knowing that uncertainty can be a driver of overuse and that during emerging threats, evidence is scarce and rapidly changing, a structured method for standardizing practice across your institution or multiple institutions can be helpful in many ways. Electronic health record–based orders and guidelines provide a standard of care to relieve uncertainty and have been shown to reduce overtesting.¹⁹ These resources can also be adapted rapidly as evidence emerges, reducing the burden on providers to know the latest evolving best practice. Experts who have reviewed the literature should have a method to quickly disseminate these findings through standardized practice, providing a venue for rapid learning and implementation.²⁰
3. Plan for active deimplementation from the outset. It is inevitable that some practices implemented early in pandemic response may need to be deimplemented later as the evidence and situation evolve. However, there is ample evidence that deimplementation can be difficult.²¹ Building in deimplementation mechanisms, such as standing educational sessions or hospital committees dedicated to value that review practices, from the beginning may ease these changes.
4. Take advantage of novel opportunities to improve value. Early stop-gap interventions may be wasteful, but the upheaval from major events may also create novel opportunities to improve value in other ways. Some of these efforts, like PPE conservation and as-needed follow-up visits, may become useful methods to improve value even after the pandemic ends.^22,23 The decreased pursuit of healthcare during the pandemic may also have given us an opportunity to better define when delayed diagnosis or even nondiagnosis for certain conditions is acceptable and when it may cause harm.
5. Highlight harms of overuse. While avoiding unnecessary costs is an important aspect of reducing overuse, often the other human-centered harms of overuse are better motivators for HVC. Especially during the response to an emerging threat, the impacts of overuse may be compounded. Laboratory resources that are strained to meet COVID-19 testing demand will be further stretched by overuse of other laboratory testing. Overuse of ineffective treatments adds stress to nurses, pharmacists, and other front-line staff taking care of ill patients. Side effects of unnecessary interventions, including those that could prolong hospitalization, would also increase strain on the system. Reducing overuse is also a way to reduce workload for hospital staff during a time of crisis. Improved efficiency of practice and less time spent on practices that do not add value to patient care can insulate staff against burnout.²⁴ Hospitalization and healthcare costs can add to the stress and financial burden of patients and families.²⁵ Clinicians can highlight harms of overuse through openly talking about it on rounds with the patients, families, and entire care team and incorporating it into health system–wide messaging.

As vaccine distribution continues, like many clinicians, we are hopeful that the worst days of the pandemic are behind us. The crucible of the COVID-19 pandemic has undoubtedly changed us as clinicians and impacted our future practice patterns. We believe there is a need to challenge ourselves to continue to think from a value mindset even in times of crisis. Furthermore, there are important opportunities to learn from our response to the COVID-19 pandemic and find strategies for minimizing LVC outside the pandemic. We believe the lessons learned around improving value during this pandemic can strengthen our response to the next novel, widespread threat and reduce waste in our care systems, with a potential to increase the resilience of systems in the future.

High-value care (HVC) is a philosophy and approach to medicine that focuses on achieving the best patient outcomes through evidence-based practice while minimizing harm to patients, wasted healthcare resources, and costs. Incorporating HVC principles in pediatric clinical decision-making is particularly important owing to the harms of hospitalization, overutilization, and overdiagnosis, as well as rising costs of pediatric care.^1-4 How can we maintain these principles in the face of a global pandemic and new emerging syndrome, multisystem inflammatory syndrome in children (MIS-C), which has dramatically impacted healthcare systems for children?

In this article, we discuss the barriers and opportunities around practicing HVC in our evolving approach to novel COVID-19 management in hospitalized children. We also draw lessons from our experiences on how we can respond to future events that rapidly shift our approach to care.

As children’s hospitals and pediatric providers responded to the COVID-19 pandemic, practice recommendations were implemented rapidly and changed rapidly. A major challenge with an event like this is how we respond to the unknown and uncertainty, something most healthcare workers are not comfortable doing at baseline,^5,6 particularly trainees and early-career physicians.⁷ With the benefit of hindsight, many early clinical approaches to care may now be seen as low-value care (LVC). For example, COVID-19 test availability was initially limited, and many hospitals utilized respiratory viral panels (RVPs) to potentially eliminate COVID-19 as an etiology of symptoms. RVP use increased during this time⁸; however, studies have shown that the co-infection rate of SARS-CoV2 with other respiratory viruses varies widely, so a positive RVP was of uncertain benefit.⁹ In addition, routine RVP use is often low value and may lead to overdiagnosis, additional overtesting cascades, and, at times, false reassurance and premature closure of the diagnostic workup.¹⁰

As our understanding of COVID-19 has expanded, rapid changes in treatment have also occurred. Early data were often preliminary and based on small trials of adults, and treatments ranged from inexpensive and available (dexamethasone) to quite expensive (remdesivir, monoclonal antibodies). Pragmatic randomized controlled trials (RCTs) are an important tool that may have been underutilized in pediatrics. Similar to our adult hospitalist colleagues’ experience,¹¹ the rapid rise in cases provided an opportunity to collaborate across institutions to assess which treatments were most effective. In particular, the predictable rise in rates of MIS-C after a surge in COVID-19 cases could have provided an avenue to evaluate the relative effectiveness of the various treatments used.¹² However, there were limited pediatric RCTs and thus a missed opportunity to establish an evidence-based pediatric standard of care for COVID-19 and MIS-C. This resulted in the development and dissemination of care practices before they were fully tested in children.

Similarly, the medical community has become increasingly aware of laboratory findings that may be predictive of clinical course.¹³ The outcomes of COVID and MIS-C are potentially severe, so looking for “early warning signs” with diagnostic testing is appealing. Clinicians responding to early data, and with a fear of missing something, may order a full panel of bloodwork for admitted patients to assist with decision-making and may underestimate the perceived minor harms and cost of unnecessary testing/admissions.³ However, most of the evidence regarding lab values came from the adult population. There is little understanding of how lab values impact pediatric-specific outcomes.¹⁴ Even for MIS-C, a pediatric-specific condition, early protocols emphasize broad testing approaches.¹⁵ A focus on grave (but rare) outcomes from a novel virus may also distract from more common causes of symptoms and lead to missed common diagnoses that are less severe.¹⁶ For both testing and treatment, having this early information before clear evidence on how it guided care may have caused more harm than benefit. Again, RCTs may have helped guide MIS-C therapies and protocol development.

Changing workflows may also create new barriers to HVC. One of the recommendations from Choosing Wisely^® during the COVID-19 pandemic was to batch lab draws¹⁷ to reduce the risk of exposure to healthcare workers performing phlebotomy, as well as staff who transport, handle, and process bloodwork in the lab. This may inadvertently encourage the approach of getting a lab test “in case” we need it with a single daily blood draw. In trying to avoid multiple encounters (and conserve personal protective equipment [PPE]), we may be taking a less stepwise approach than in prepandemic times.

Finally, children’s hospitals witnessed significant financial challenges and reductions in patient volume related to the pandemic.¹⁸ Reductions in patient volume could present a potential opportunity for practicing HVC (eg, more time to discuss downstream effects) or alternatively could inadvertently incentivize low-value, low-priority care via messaging around preserving financial viability.

For clinicians and healthcare systems, these examples highlight why we may be predisposed to practicing LVC during a pandemic or similar emerging threat.

In light of these challenging clinical scenarios and nonclinical factors that predispose us to LVC, how can we reinforce a high-value approach to care during a pandemic or similar emerging threat? The following five specific concepts may help providers and organizations optimize HVC during this pandemic and in future situations:

1. Utilize pediatric RCTs to provide evidence-based recommendations. In the face of a novel virus with unclear manifestations, treatment options were rapidly implemented without time for careful evaluation. In the future, collaboratively utilizing shared resources in the research community could help rapidly and rigorously evaluate outcomes in the pursuit of evidence-based practice.
2. Use standardization as a tool to mitigate uncertainty. Knowing that uncertainty can be a driver of overuse and that during emerging threats, evidence is scarce and rapidly changing, a structured method for standardizing practice across your institution or multiple institutions can be helpful in many ways. Electronic health record–based orders and guidelines provide a standard of care to relieve uncertainty and have been shown to reduce overtesting.¹⁹ These resources can also be adapted rapidly as evidence emerges, reducing the burden on providers to know the latest evolving best practice. Experts who have reviewed the literature should have a method to quickly disseminate these findings through standardized practice, providing a venue for rapid learning and implementation.²⁰
3. Plan for active deimplementation from the outset. It is inevitable that some practices implemented early in pandemic response may need to be deimplemented later as the evidence and situation evolve. However, there is ample evidence that deimplementation can be difficult.²¹ Building in deimplementation mechanisms, such as standing educational sessions or hospital committees dedicated to value that review practices, from the beginning may ease these changes.
4. Take advantage of novel opportunities to improve value. Early stop-gap interventions may be wasteful, but the upheaval from major events may also create novel opportunities to improve value in other ways. Some of these efforts, like PPE conservation and as-needed follow-up visits, may become useful methods to improve value even after the pandemic ends.^22,23 The decreased pursuit of healthcare during the pandemic may also have given us an opportunity to better define when delayed diagnosis or even nondiagnosis for certain conditions is acceptable and when it may cause harm.
5. Highlight harms of overuse. While avoiding unnecessary costs is an important aspect of reducing overuse, often the other human-centered harms of overuse are better motivators for HVC. Especially during the response to an emerging threat, the impacts of overuse may be compounded. Laboratory resources that are strained to meet COVID-19 testing demand will be further stretched by overuse of other laboratory testing. Overuse of ineffective treatments adds stress to nurses, pharmacists, and other front-line staff taking care of ill patients. Side effects of unnecessary interventions, including those that could prolong hospitalization, would also increase strain on the system. Reducing overuse is also a way to reduce workload for hospital staff during a time of crisis. Improved efficiency of practice and less time spent on practices that do not add value to patient care can insulate staff against burnout.²⁴ Hospitalization and healthcare costs can add to the stress and financial burden of patients and families.²⁵ Clinicians can highlight harms of overuse through openly talking about it on rounds with the patients, families, and entire care team and incorporating it into health system–wide messaging.

As vaccine distribution continues, like many clinicians, we are hopeful that the worst days of the pandemic are behind us. The crucible of the COVID-19 pandemic has undoubtedly changed us as clinicians and impacted our future practice patterns. We believe there is a need to challenge ourselves to continue to think from a value mindset even in times of crisis. Furthermore, there are important opportunities to learn from our response to the COVID-19 pandemic and find strategies for minimizing LVC outside the pandemic. We believe the lessons learned around improving value during this pandemic can strengthen our response to the next novel, widespread threat and reduce waste in our care systems, with a potential to increase the resilience of systems in the future.

Inspired by the ABIM Foundation’s Choosing Wisely^® campaign, the “Things We Do for No Reason^™" (TWDFNR) series reviews practices that have become common parts of hospital care but may provide little value to our patients. Practices reviewed in the TWDFNR series do not represent clear-cut conclusions or clinical practice standards but are meant as a starting place for research and active discussions among hospitalists and patients. We invite you to be part of that discussion.

The hospitalist admits a 56-year-old anuric man with end-stage renal disease (ESRD) on maintenance hemodialysis (HD) for an acute coronary syndrome. He received his regularly scheduled HD the day before admission. Cardiology delays his coronary catheterization until nephrology can arrange for HD immediately after angiography. After angiography, the patient receives emergent HD even though he had acceptable metabolic parameters and did not show signs or symptoms of volume overload. The hospitalist wonders whether arranging emergent HD after the procedure with intravascular (IV) contrast was necessary for this patient.

Of the approximately 600 million radiological examinations performed annually, 75 million require iodinated contrast material (ICM).¹ ICM are small, highly diffusible, minimally protein-bound molecules. They are not metabolized by humans, with healthy kidneys excreting approximately 99.8% of the administered dose within 24 hours.² ICM has been associated with acute kidney injury (AKI), but its deleterious effects have not been thoroughly described, and the incidence and severity of contrast-associated nephropathy vary among studies.³ Not surprisingly, the strongest independent patient-related risk factor for developing contrast-induced AKI is preexisting chronic kidney disease.⁴ In patients with ESRD, the biliary system slowly clears the contrast, leading to long-standing retention. Newer low- or iso-osmolar contrast material is now used rather than older, conventional high-osmolality agents. These agents are less likely to lead to AKI.⁵

Recent studies have challenged the association between AKI and ICM administration.^6-8 In 2015, the American College of Radiology endorsed the terms contrast-associated acute kidney injury and contrast-induced acute kidney injury, instead of the contrast-induced nephropathy, to avoid the uncertainty about the causal relationship between AKI and ICM.⁹ ESRD patients have little or no functional renal tissue and are on renal replacement therapy, either HD or peritoneal dialysis. However, physicians apprehensive about the renal and cardiovascular toxicity caused by retained ICM might request postprocedural HD to promote quicker contrast clearance in patients with ESRD.

Clinicians divide patients with ESRD into two groups depending on their ability to produce urine. Those who produce urine have residual renal function (RRF), which independently predicts survival.¹⁰ Among a cohort of peritoneal and HD patients, Maiorca et al described a 40% reduction in the risk of death for each 1 mL/min increase in glomerular filtration rate (GFR).¹⁰ Therefore, patients on maintenance dialysis who have RRF are considered similar to patients with AKI and eGFR <30 mL/min/1.73 m².⁹ Clinicians might worry that contrast retention could reduce RRF by inducing AKI.^2,4,11

Volume overload is a second concern with ICM administration in ESRD patients. In mice, higher-osmolality ICM produced acute pulmonary edema, leading to death.¹² A rapid bolus of diatrizoate caused transient intravascular expansion as reflected by an average decrease in hemoglobin of 0.5 to 0.8 g/dL, depending on the osmolality of the agent.¹²

Conventional high-osmolar ICM also depresses myocardial contractile force, sinoatrial automaticity, and atrioventricular nodal conduction, resulting in bradycardia, transient heart blocks, and increased risk of ventricular fibrillation.¹² High-osmolar calcium-binding ICM transiently reduces systemic vascular resistance, resulting in transient hypotension and increased cardiac output. Researchers linked these adverse cardiac effects to the high-osmolality ionic ICM, not newer agents.¹² In one study of adverse outcomes linked to ICM, 36% of patients with normal kidney function exposed to contrast developed an adverse reaction; 2% of patients developed level 4 (severe) adverse reactions.¹³ The study noted a significantly increased risk of bradycardia (relative risk [RR], 17.9), hypotension (RR, 6.3), and angina (RR, 3.4) among those who received high-osmolality contrast agents.

HD removes 72% to 82% of ICM at 4 hours.¹⁴ Armed with data from mice or small-population studies that demonstrated the toxic effects of conventional high-osmolar ICM, many radiologists and clinicians recommend post-contrast HD for patients at high risk for contrast-induced AKI and chronic HD patients.² Moon et al suggested prophylactic HD for quicker removal of the iodinated contrast medium to prevent reduction in renal function among high-risk patients after angiographic interventions.¹⁵

Over the last 3 decades, we have transitioned from conventional radiocontrast to low-osmolality agents that are not directly toxic to the kidneys. Iodixanol, iohexol, and iopromide exposure during intravascular radiological procedures did not result in a decline of RRF among well-hydrated peritoneal dialysis patients with RRF.^16,17 The limited analysis of HD trials in the systematic review by Cruz et al concluded that periprocedural HD in patients with chronic kidney disease did not decrease the incidence of radiocontrast-associated nephropathy.¹⁸ A meta-analysis of nine studies (434 patients) concluded that ICM administration does not cause significant reduction of residual function in dialysis patients.¹⁹ Because anuric ESRD patients have no salvageable renal function and are on HD, managing AKI seems irrelevant.

Although volume overload is an important consideration, the theoretical increase in intravascular volume with administration of 100 mL of 1500 mOsm/L of conventional ICM to a 70 kg-patient is only 120 mL.¹⁴ More importantly, use of low-osmolar ICM substantially reduces any significant volume shifts.

Studies have not associated low-osmolality ICM with cardiovascular adverse effects.^20-23 A retrospective study by Takebayashi et al showed an absence of serious adverse reactions to low-osmolar contrast media when HD was performed on their regular HD schedule.²² Older, smaller prospective trials did not show a need for periprocedural HD after ICM exposure.^20,21,23 In a prospective study of 10 ESRD patients, Younathan et al assessed for postprocedural adverse effects of non-ionic contrast material and found that none required emergent HD.²³ Similarly, Hamani et al and Harasawa et al did not observe hemodynamic and cardiopulmonary effects of IV contrast in chronic HD patients (Table).^20,21 Injection of non-ionic contrast material in patients on chronic HD did not produce significant changes in blood pressure, electrocardiogram results, osmolality, extracellular fluid volume, or body weight.²³ Finally, the vasoconstrictor-mediated ischemic injury of ICM occurs within minutes of administration, making dialysis performed hours later of little benefit.

HD is associated with adverse effects, including hypotension, which can jeopardize cardiovascular recovery after a myocardial infarction.²⁴ The retrospective study performed by Fujimoto et al demonstrated dialytic complications in 24% of patients dialyzed the day of angiography.²⁵ They noted that the amount of contrast agent administered independently predicted intradialytic hypotension.^25,26

Delays in performing cardiac revascularizations are associated with an increase in 30-day mortality. The 30-day mortality rates of patients diagnosed with ST-elevation myocardial infarction who underwent revascularization in <60 minutes, 61 to 75 minutes, 76 to 90 minutes, and >90 minutes from study enrollment were 1%, 3.7%, 4%, and 6.7%, respectively.²⁷ Delayed diagnosis of pulmonary embolism or acute limb ischemia was associated with increased rates of complications and mortality.^28,29 The benefits of essential radiocontrast procedures outweigh the potential cardiovascular and cerebrovascular complications for HD patients. Considering the evidence, the American College of Radiology’s 2020 Manual on Contrast Media and the European Society for Urogenital Radiology’s 2018 guidelines on contrast medium administration in patients on HD concluded that an extra session or a change in the usual timing of HD is unnecessary.^13,30

HD performed post-contrast exposure does not provide any protective benefit, regardless of the degree of RRF (anuric ESRD or otherwise), making the timing of HD irrelevant. Do not delay studies that provide essential information for clinical management of high-risk conditions. The decision to perform HD in a patient who needs contrast-enhanced studies should be made independent of whether they will receive contrast.

• Immediate post-procedural HD after ICM exposure in ESRD patients is not required.
• Do not delay vital diagnostic or therapeutic procedures requiring ICM in ESRD patients.
• The indication for HD is independent of contrast exposure in ESRD patients.

The hospitalist did not need to arrange emergent post-procedural HD because it does not improve clinical outcomes. Delaying potentially lifesaving diagnostic and therapeutic measures involving the use of radiocontrast to secure post-radiocontrast HD could lead to worse outcomes.

Do you think this is a low-value practice? Is this truly a “Thing We Do for No Reason™”? Share what you do in your practice and join in the conversation online by retweeting it on Twitter (#TWDFNR) and liking it on Facebook. We invite you to propose ideas for other “Things We Do for No Reason™” topics by emailing TWDFNR@hospitalmedicine.org.

Inspired by the ABIM Foundation’s Choosing Wisely^® campaign, the “Things We Do for No Reason^™" (TWDFNR) series reviews practices that have become common parts of hospital care but may provide little value to our patients. Practices reviewed in the TWDFNR series do not represent clear-cut conclusions or clinical practice standards but are meant as a starting place for research and active discussions among hospitalists and patients. We invite you to be part of that discussion.

The hospitalist admits a 56-year-old anuric man with end-stage renal disease (ESRD) on maintenance hemodialysis (HD) for an acute coronary syndrome. He received his regularly scheduled HD the day before admission. Cardiology delays his coronary catheterization until nephrology can arrange for HD immediately after angiography. After angiography, the patient receives emergent HD even though he had acceptable metabolic parameters and did not show signs or symptoms of volume overload. The hospitalist wonders whether arranging emergent HD after the procedure with intravascular (IV) contrast was necessary for this patient.

Of the approximately 600 million radiological examinations performed annually, 75 million require iodinated contrast material (ICM).¹ ICM are small, highly diffusible, minimally protein-bound molecules. They are not metabolized by humans, with healthy kidneys excreting approximately 99.8% of the administered dose within 24 hours.² ICM has been associated with acute kidney injury (AKI), but its deleterious effects have not been thoroughly described, and the incidence and severity of contrast-associated nephropathy vary among studies.³ Not surprisingly, the strongest independent patient-related risk factor for developing contrast-induced AKI is preexisting chronic kidney disease.⁴ In patients with ESRD, the biliary system slowly clears the contrast, leading to long-standing retention. Newer low- or iso-osmolar contrast material is now used rather than older, conventional high-osmolality agents. These agents are less likely to lead to AKI.⁵

Recent studies have challenged the association between AKI and ICM administration.^6-8 In 2015, the American College of Radiology endorsed the terms contrast-associated acute kidney injury and contrast-induced acute kidney injury, instead of the contrast-induced nephropathy, to avoid the uncertainty about the causal relationship between AKI and ICM.⁹ ESRD patients have little or no functional renal tissue and are on renal replacement therapy, either HD or peritoneal dialysis. However, physicians apprehensive about the renal and cardiovascular toxicity caused by retained ICM might request postprocedural HD to promote quicker contrast clearance in patients with ESRD.

Clinicians divide patients with ESRD into two groups depending on their ability to produce urine. Those who produce urine have residual renal function (RRF), which independently predicts survival.¹⁰ Among a cohort of peritoneal and HD patients, Maiorca et al described a 40% reduction in the risk of death for each 1 mL/min increase in glomerular filtration rate (GFR).¹⁰ Therefore, patients on maintenance dialysis who have RRF are considered similar to patients with AKI and eGFR <30 mL/min/1.73 m².⁹ Clinicians might worry that contrast retention could reduce RRF by inducing AKI.^2,4,11

Volume overload is a second concern with ICM administration in ESRD patients. In mice, higher-osmolality ICM produced acute pulmonary edema, leading to death.¹² A rapid bolus of diatrizoate caused transient intravascular expansion as reflected by an average decrease in hemoglobin of 0.5 to 0.8 g/dL, depending on the osmolality of the agent.¹²

Conventional high-osmolar ICM also depresses myocardial contractile force, sinoatrial automaticity, and atrioventricular nodal conduction, resulting in bradycardia, transient heart blocks, and increased risk of ventricular fibrillation.¹² High-osmolar calcium-binding ICM transiently reduces systemic vascular resistance, resulting in transient hypotension and increased cardiac output. Researchers linked these adverse cardiac effects to the high-osmolality ionic ICM, not newer agents.¹² In one study of adverse outcomes linked to ICM, 36% of patients with normal kidney function exposed to contrast developed an adverse reaction; 2% of patients developed level 4 (severe) adverse reactions.¹³ The study noted a significantly increased risk of bradycardia (relative risk [RR], 17.9), hypotension (RR, 6.3), and angina (RR, 3.4) among those who received high-osmolality contrast agents.

HD removes 72% to 82% of ICM at 4 hours.¹⁴ Armed with data from mice or small-population studies that demonstrated the toxic effects of conventional high-osmolar ICM, many radiologists and clinicians recommend post-contrast HD for patients at high risk for contrast-induced AKI and chronic HD patients.² Moon et al suggested prophylactic HD for quicker removal of the iodinated contrast medium to prevent reduction in renal function among high-risk patients after angiographic interventions.¹⁵

Over the last 3 decades, we have transitioned from conventional radiocontrast to low-osmolality agents that are not directly toxic to the kidneys. Iodixanol, iohexol, and iopromide exposure during intravascular radiological procedures did not result in a decline of RRF among well-hydrated peritoneal dialysis patients with RRF.^16,17 The limited analysis of HD trials in the systematic review by Cruz et al concluded that periprocedural HD in patients with chronic kidney disease did not decrease the incidence of radiocontrast-associated nephropathy.¹⁸ A meta-analysis of nine studies (434 patients) concluded that ICM administration does not cause significant reduction of residual function in dialysis patients.¹⁹ Because anuric ESRD patients have no salvageable renal function and are on HD, managing AKI seems irrelevant.

Although volume overload is an important consideration, the theoretical increase in intravascular volume with administration of 100 mL of 1500 mOsm/L of conventional ICM to a 70 kg-patient is only 120 mL.¹⁴ More importantly, use of low-osmolar ICM substantially reduces any significant volume shifts.

Studies have not associated low-osmolality ICM with cardiovascular adverse effects.^20-23 A retrospective study by Takebayashi et al showed an absence of serious adverse reactions to low-osmolar contrast media when HD was performed on their regular HD schedule.²² Older, smaller prospective trials did not show a need for periprocedural HD after ICM exposure.^20,21,23 In a prospective study of 10 ESRD patients, Younathan et al assessed for postprocedural adverse effects of non-ionic contrast material and found that none required emergent HD.²³ Similarly, Hamani et al and Harasawa et al did not observe hemodynamic and cardiopulmonary effects of IV contrast in chronic HD patients (Table).^20,21 Injection of non-ionic contrast material in patients on chronic HD did not produce significant changes in blood pressure, electrocardiogram results, osmolality, extracellular fluid volume, or body weight.²³ Finally, the vasoconstrictor-mediated ischemic injury of ICM occurs within minutes of administration, making dialysis performed hours later of little benefit.

HD is associated with adverse effects, including hypotension, which can jeopardize cardiovascular recovery after a myocardial infarction.²⁴ The retrospective study performed by Fujimoto et al demonstrated dialytic complications in 24% of patients dialyzed the day of angiography.²⁵ They noted that the amount of contrast agent administered independently predicted intradialytic hypotension.^25,26

Delays in performing cardiac revascularizations are associated with an increase in 30-day mortality. The 30-day mortality rates of patients diagnosed with ST-elevation myocardial infarction who underwent revascularization in <60 minutes, 61 to 75 minutes, 76 to 90 minutes, and >90 minutes from study enrollment were 1%, 3.7%, 4%, and 6.7%, respectively.²⁷ Delayed diagnosis of pulmonary embolism or acute limb ischemia was associated with increased rates of complications and mortality.^28,29 The benefits of essential radiocontrast procedures outweigh the potential cardiovascular and cerebrovascular complications for HD patients. Considering the evidence, the American College of Radiology’s 2020 Manual on Contrast Media and the European Society for Urogenital Radiology’s 2018 guidelines on contrast medium administration in patients on HD concluded that an extra session or a change in the usual timing of HD is unnecessary.^13,30

HD performed post-contrast exposure does not provide any protective benefit, regardless of the degree of RRF (anuric ESRD or otherwise), making the timing of HD irrelevant. Do not delay studies that provide essential information for clinical management of high-risk conditions. The decision to perform HD in a patient who needs contrast-enhanced studies should be made independent of whether they will receive contrast.

• Immediate post-procedural HD after ICM exposure in ESRD patients is not required.
• Do not delay vital diagnostic or therapeutic procedures requiring ICM in ESRD patients.
• The indication for HD is independent of contrast exposure in ESRD patients.

The hospitalist did not need to arrange emergent post-procedural HD because it does not improve clinical outcomes. Delaying potentially lifesaving diagnostic and therapeutic measures involving the use of radiocontrast to secure post-radiocontrast HD could lead to worse outcomes.

Do you think this is a low-value practice? Is this truly a “Thing We Do for No Reason™”? Share what you do in your practice and join in the conversation online by retweeting it on Twitter (#TWDFNR) and liking it on Facebook. We invite you to propose ideas for other “Things We Do for No Reason™” topics by emailing TWDFNR@hospitalmedicine.org.

Inspired by the ABIM Foundation’s Choosing Wisely^® campaign, the “Things We Do for No Reason^™" (TWDFNR) series reviews practices that have become common parts of hospital care but may provide little value to our patients. Practices reviewed in the TWDFNR series do not represent clear-cut conclusions or clinical practice standards but are meant as a starting place for research and active discussions among hospitalists and patients. We invite you to be part of that discussion.

The hospitalist admits a 56-year-old anuric man with end-stage renal disease (ESRD) on maintenance hemodialysis (HD) for an acute coronary syndrome. He received his regularly scheduled HD the day before admission. Cardiology delays his coronary catheterization until nephrology can arrange for HD immediately after angiography. After angiography, the patient receives emergent HD even though he had acceptable metabolic parameters and did not show signs or symptoms of volume overload. The hospitalist wonders whether arranging emergent HD after the procedure with intravascular (IV) contrast was necessary for this patient.

Of the approximately 600 million radiological examinations performed annually, 75 million require iodinated contrast material (ICM).¹ ICM are small, highly diffusible, minimally protein-bound molecules. They are not metabolized by humans, with healthy kidneys excreting approximately 99.8% of the administered dose within 24 hours.² ICM has been associated with acute kidney injury (AKI), but its deleterious effects have not been thoroughly described, and the incidence and severity of contrast-associated nephropathy vary among studies.³ Not surprisingly, the strongest independent patient-related risk factor for developing contrast-induced AKI is preexisting chronic kidney disease.⁴ In patients with ESRD, the biliary system slowly clears the contrast, leading to long-standing retention. Newer low- or iso-osmolar contrast material is now used rather than older, conventional high-osmolality agents. These agents are less likely to lead to AKI.⁵

Recent studies have challenged the association between AKI and ICM administration.^6-8 In 2015, the American College of Radiology endorsed the terms contrast-associated acute kidney injury and contrast-induced acute kidney injury, instead of the contrast-induced nephropathy, to avoid the uncertainty about the causal relationship between AKI and ICM.⁹ ESRD patients have little or no functional renal tissue and are on renal replacement therapy, either HD or peritoneal dialysis. However, physicians apprehensive about the renal and cardiovascular toxicity caused by retained ICM might request postprocedural HD to promote quicker contrast clearance in patients with ESRD.

Clinicians divide patients with ESRD into two groups depending on their ability to produce urine. Those who produce urine have residual renal function (RRF), which independently predicts survival.¹⁰ Among a cohort of peritoneal and HD patients, Maiorca et al described a 40% reduction in the risk of death for each 1 mL/min increase in glomerular filtration rate (GFR).¹⁰ Therefore, patients on maintenance dialysis who have RRF are considered similar to patients with AKI and eGFR <30 mL/min/1.73 m².⁹ Clinicians might worry that contrast retention could reduce RRF by inducing AKI.^2,4,11

Volume overload is a second concern with ICM administration in ESRD patients. In mice, higher-osmolality ICM produced acute pulmonary edema, leading to death.¹² A rapid bolus of diatrizoate caused transient intravascular expansion as reflected by an average decrease in hemoglobin of 0.5 to 0.8 g/dL, depending on the osmolality of the agent.¹²

Conventional high-osmolar ICM also depresses myocardial contractile force, sinoatrial automaticity, and atrioventricular nodal conduction, resulting in bradycardia, transient heart blocks, and increased risk of ventricular fibrillation.¹² High-osmolar calcium-binding ICM transiently reduces systemic vascular resistance, resulting in transient hypotension and increased cardiac output. Researchers linked these adverse cardiac effects to the high-osmolality ionic ICM, not newer agents.¹² In one study of adverse outcomes linked to ICM, 36% of patients with normal kidney function exposed to contrast developed an adverse reaction; 2% of patients developed level 4 (severe) adverse reactions.¹³ The study noted a significantly increased risk of bradycardia (relative risk [RR], 17.9), hypotension (RR, 6.3), and angina (RR, 3.4) among those who received high-osmolality contrast agents.

HD removes 72% to 82% of ICM at 4 hours.¹⁴ Armed with data from mice or small-population studies that demonstrated the toxic effects of conventional high-osmolar ICM, many radiologists and clinicians recommend post-contrast HD for patients at high risk for contrast-induced AKI and chronic HD patients.² Moon et al suggested prophylactic HD for quicker removal of the iodinated contrast medium to prevent reduction in renal function among high-risk patients after angiographic interventions.¹⁵

Over the last 3 decades, we have transitioned from conventional radiocontrast to low-osmolality agents that are not directly toxic to the kidneys. Iodixanol, iohexol, and iopromide exposure during intravascular radiological procedures did not result in a decline of RRF among well-hydrated peritoneal dialysis patients with RRF.^16,17 The limited analysis of HD trials in the systematic review by Cruz et al concluded that periprocedural HD in patients with chronic kidney disease did not decrease the incidence of radiocontrast-associated nephropathy.¹⁸ A meta-analysis of nine studies (434 patients) concluded that ICM administration does not cause significant reduction of residual function in dialysis patients.¹⁹ Because anuric ESRD patients have no salvageable renal function and are on HD, managing AKI seems irrelevant.

Although volume overload is an important consideration, the theoretical increase in intravascular volume with administration of 100 mL of 1500 mOsm/L of conventional ICM to a 70 kg-patient is only 120 mL.¹⁴ More importantly, use of low-osmolar ICM substantially reduces any significant volume shifts.

Studies have not associated low-osmolality ICM with cardiovascular adverse effects.^20-23 A retrospective study by Takebayashi et al showed an absence of serious adverse reactions to low-osmolar contrast media when HD was performed on their regular HD schedule.²² Older, smaller prospective trials did not show a need for periprocedural HD after ICM exposure.^20,21,23 In a prospective study of 10 ESRD patients, Younathan et al assessed for postprocedural adverse effects of non-ionic contrast material and found that none required emergent HD.²³ Similarly, Hamani et al and Harasawa et al did not observe hemodynamic and cardiopulmonary effects of IV contrast in chronic HD patients (Table).^20,21 Injection of non-ionic contrast material in patients on chronic HD did not produce significant changes in blood pressure, electrocardiogram results, osmolality, extracellular fluid volume, or body weight.²³ Finally, the vasoconstrictor-mediated ischemic injury of ICM occurs within minutes of administration, making dialysis performed hours later of little benefit.

HD is associated with adverse effects, including hypotension, which can jeopardize cardiovascular recovery after a myocardial infarction.²⁴ The retrospective study performed by Fujimoto et al demonstrated dialytic complications in 24% of patients dialyzed the day of angiography.²⁵ They noted that the amount of contrast agent administered independently predicted intradialytic hypotension.^25,26

Delays in performing cardiac revascularizations are associated with an increase in 30-day mortality. The 30-day mortality rates of patients diagnosed with ST-elevation myocardial infarction who underwent revascularization in <60 minutes, 61 to 75 minutes, 76 to 90 minutes, and >90 minutes from study enrollment were 1%, 3.7%, 4%, and 6.7%, respectively.²⁷ Delayed diagnosis of pulmonary embolism or acute limb ischemia was associated with increased rates of complications and mortality.^28,29 The benefits of essential radiocontrast procedures outweigh the potential cardiovascular and cerebrovascular complications for HD patients. Considering the evidence, the American College of Radiology’s 2020 Manual on Contrast Media and the European Society for Urogenital Radiology’s 2018 guidelines on contrast medium administration in patients on HD concluded that an extra session or a change in the usual timing of HD is unnecessary.^13,30

HD performed post-contrast exposure does not provide any protective benefit, regardless of the degree of RRF (anuric ESRD or otherwise), making the timing of HD irrelevant. Do not delay studies that provide essential information for clinical management of high-risk conditions. The decision to perform HD in a patient who needs contrast-enhanced studies should be made independent of whether they will receive contrast.

• Immediate post-procedural HD after ICM exposure in ESRD patients is not required.
• Do not delay vital diagnostic or therapeutic procedures requiring ICM in ESRD patients.
• The indication for HD is independent of contrast exposure in ESRD patients.

The hospitalist did not need to arrange emergent post-procedural HD because it does not improve clinical outcomes. Delaying potentially lifesaving diagnostic and therapeutic measures involving the use of radiocontrast to secure post-radiocontrast HD could lead to worse outcomes.

Do you think this is a low-value practice? Is this truly a “Thing We Do for No Reason™”? Share what you do in your practice and join in the conversation online by retweeting it on Twitter (#TWDFNR) and liking it on Facebook. We invite you to propose ideas for other “Things We Do for No Reason™” topics by emailing TWDFNR@hospitalmedicine.org.

Inspired by the ABIM Foundation’s Choosing Wisely^® campaign, the “Things We Do for No Reason^™” (TWDFNR) series reviews practices that have become common parts of hospital care but may provide little value to our patients. Practices reviewed in the TWDFNR series do not represent clear-cut conclusions or clinical practice standards but are meant as a starting place for research and active discussions among hospitalists and patients. We invite you to be part of that discussion.

On teaching rounds, a medical student presents the following case to the attending hospitalist: “Mrs. L is a 54-year-old Black female with chronic kidney disease who was admitted with community-acquired pneumonia. She continues to improve symptomatically on ceftriaxone. Currently, she is afebrile and her vitals are stable. Supplemental oxygen has been weaned to 2 L/min by nasal cannula. Exam reveals improved crackles in the left lower chest without dullness to percussion. Labs are notable for down-trending leukocytosis and a stable serum creatinine of 2.8 mg/dL.” The hospitalist considers how including racial descriptors in clinical presentations may influence the care of the patient.

For decades, medical educators have taught learners to include sociopolitical constructs such as race in the opening sentence of the history of present illness (HPI). This practice presumably stems from the assumption that race accurately reflects biogenetic information about patients and serves as a key attribute in problem representations.¹ Proponents of including race in the HPI suggest doing so aids the clinical assessment of patients’ risks for particular diseases and may inform the selection of race-appropriate therapies.²

The construct of race does sometimes correlate with the risk of disease or response to therapies. For example, sickle cell disease (SCD) occurs more commonly among patients who identify as Black rather than White. Specifically, ancestry from African nations such as Nigeria or the Democratic Republic of Congo increases the likelihood of having the disease-associated hemoglobin gene variant HbS.¹ Popular genomic ancestry tests often report ancestral groupings that map to racial categories and may reinforce the perception that race has a genetic basis.³

Race, a construct of sociopolitical origins, incorrectly conflates skin color with genetic variation. Associations between race and disease have the potential to cause diagnostic and therapeutic errors and inequitable allocation of resources. Increased illness burden in minority populations results primarily from social factors such as environment, access to care, housing instability, food insecurity, and experiences of discrimination, rather than genetic differences. The resulting chronic and recurrent physiologic stress—known as allostatic load—also contributes to the inequitable health outcomes observed in vulnerable populations, including patients who identify as Black.⁴

Historically, race evolved as a sociopolitical framework stemming from colonialism, discrimination, and exploitation.⁵ Numerous studies reveal a lack of genetic precision in racial categories. In fact, genetic data compared across major continental groups found greater variation of microsatellite loci and restriction fragment length polymorphisms within racial groups than between them.⁶ The evidence indicates that racial categories do not reflect homogenous population groups but rather “arbitrary division[s] of continuous variation” that cannot serve as a surrogate to genetic diversity.⁵ Not only are racial categories genetically inaccurate, but data on race within the electronic health record often differ from patients’ self-description of race, underscoring the problematic nature of even identifying race.⁷ In one study, up to 41% of patients self-reported identification with at least one other racial or ethnic group than the race or ethnicity documented in their electronic health record.⁷

Additionally, conflating race with genetic variation can lead to diagnostic errors. As an example, the incidence of cystic fibrosis (CF) varies widely across populations of European ancestry. The primary focus on CF’s occurrence in patients of European descent may divert attention from the identification of mutations causing CF in populations of African descent or the decreased survival observed in the United States among CF patients of Hispanic descent.^8,9 Similarly, India represents one of the countries largely affected by SCD, suggesting that a myopic focus on SCD among those identifying as Black can lead to underdiagnosis of SCD among those with Indian ancestry.

Perhaps more insidiously, linking disease to race or other social constructs can result in differential support for affected individuals. SCD offers a striking illustration of this point. Reflecting the legacy of transatlantic slave trading, the majority of people with SCD in the United States are Black and face interpersonal and structural racism within society and healthcare that amplify the effects of this devastating illness.¹⁰ Compulsory screening programs for sickle cell trait introduced by many states in the 1970s targeted Black Americans and resulted in stigmatization and the denial of insurance, educational opportunities, and jobs for many identified with sickle cell trait. Federal funding for SCD research remains low, particularly in comparison to the tenfold higher funding for CF, which afflicts fewer, but primarily White, Americans.¹⁰

The incorporation of race into risk models and guidelines—alongside biologically relevant variables such as age and comorbid conditions—has received increasing attention for its potential to compound racial disparities in health outcomes. The American Heart Association Heart Failure Risk Score, for instance, may lead to the exclusion of some Black patients from necessary care because “Black” race, for no clear physiologic reason, serves as a protective factor against heart failure mortality.¹¹ Likewise, race adjustments in pulmonary function tests, breast cancer risk models, and estimated glomerular filtration rate calculations, among others, have limited biological basis and the potential to divert care disproportionately from minority populations.¹¹

Researchers have even called into question the application of race to pharmacotherapies. A 2001 investigation on geographic patterns of genetic variation in drug response concluded that common racial and ethnic labels were “insufficient and inaccurate representations” of the individual genetic clusters.¹² Further, numerous experts have criticized two landmark studies of vasodilators and angiotensin-converting enzyme inhibitors in Black patients with heart failure for inconsistent results and nonsignificant associations between race and major outcomes, such as the development of heart failure or death.¹³

Race-based labels can also divert attention from true causes of health inequities. The National Academy of Sciences concluded that social determinants of health and structural racism are the root causes of health inequities, rather than genetics.¹⁴ Medical professionals may perpetuate these disparities: Most US physicians demonstrate an unconscious preference—or implicit bias—for White Americans over Black Americans.¹⁵ Beyond obscuring the role of social determinants of health and structural racism in health outcomes, race-based labels may exacerbate the ways in which physicians’ implicit biases contribute to racial and ethnic health disparities, primarily affecting Black Americans.² In a recent study, clinicians documented race in the HPI for 33% of Black patients compared with 16% of White patients, and White clinicians were twice as likely to document race as Black physicians.¹⁶ Moreover, training medical students to view race as an independent risk factor of disease without discussing structural inequities can pathologize race and reinforce implicit biases linking race and disease.¹⁵

Based on the current evidence, we believe routine use of race-based labels in clinical presentations confuses providers at a minimum and potentially produces far more damage by obscuring or perpetuating the role of racism in health inequities.

Instead of routinely presenting race in the HPI, we recommend including racial or ethnic information in the social history only when the patient reports it as a meaningful identity or when it informs health disparities stemming from structural or interpersonal racism. Clinicians should include physical characteristics pertaining to race, such as skin tone, in the physical exam only if required to describe exam findings accurately. When presenting race, clinicians should explicitly justify its use and take care to avoid obfuscatory, inaccurate, or stigmatizing mention of associations between race and disease. Clinicians should not use race in clinical algorithms. Medical educators should emphasize the role of social determinants of health and structural racism in health outcomes to inform the use of race in medicine, in hopes that doing so will help students minimize implicit biases and learn to mitigate racial inequities in healthcare.^2,16 In short, clinicians and medical educators alike should ensure that clinical care and the medical curriculum avoid presenting race as a proxy for pathology.

There is little evidence to guide proper inclusion of race in clinical interviews. In the absence of clear guidance about how to approach patients about race, we suggest not asking about it unless there is a reasonable probability that doing so will improve clinical care. If a clinician decides to ask about race, it is important to provide a rationale—such as explaining that the information can be used to assure high-quality care for all patients—since many patients are uncomfortable with questions about race.¹⁷ If clinicians report information about race in the social history, we advise using the patient’s description of race rather than traditional racial categories.

Clinicians who ask their patients about race should approach every patient in a uniform manner to avoid perpetuating biases. We hope future studies will inform equitable, inclusive, and person-centered approaches to discussing race with patients and promote a shared understanding of how racism contributes to illness.

• Avoid using racial descriptors in the HPI.
• Include racial and ethnic information in the social history only when it serves as a meaningful identity or it informs disparities stemming from racism.
• If racial or ethnic information is asked for, explain to patients why and how it will be used.
• Mention physical characteristics such as skin tone, rather than race, in the physical exam if required to describe findings accurately.
• Advocate for the replacement of race or race-adjusted algorithms in patient care.
• Expand the medical curriculum in the social determinants of health and structural racism, and develop systems to avoid the use of stigmatizing, race-based labels.

Race, a sociopolitical construct, does not accurately represent genetic variation. The routine use of race in the HPI can perpetuate racial biases and muddle both diagnoses and treatment. Only mention race in the social history if it is meaningful to the patient’s self-identity or explains health disparities arising from racism. All documentation and presentations should avoid the use of stigmatizing, race-based labels.

In the clinical scenario mentioned earlier, the attending hospitalist raises the issue of race-based labels in patient care in a nonjudgmental fashion. To provide illustrative specificity, she notes how the incorporation of race in formulas of glomerular filtration rate can lead to under-referral for renal transplant. The hospitalist then facilitates an open and inclusive discussion with the team regarding the use of race in clinical presentations and its potential impact on health disparities.

Do you think this is a low-value practice? Is this truly a “Thing We Do for No Reason^™”? Let us know what you do in your practice and propose ideas for other “Things We Do for No Reason^™” topics. Please join in the conversation online at Twitter (#TWDFNR)/Facebook and don’t forget to “Like It” on Facebook or retweet it on Twitter.

Inspired by the ABIM Foundation’s Choosing Wisely^® campaign, the “Things We Do for No Reason^™” (TWDFNR) series reviews practices that have become common parts of hospital care but may provide little value to our patients. Practices reviewed in the TWDFNR series do not represent clear-cut conclusions or clinical practice standards but are meant as a starting place for research and active discussions among hospitalists and patients. We invite you to be part of that discussion.

On teaching rounds, a medical student presents the following case to the attending hospitalist: “Mrs. L is a 54-year-old Black female with chronic kidney disease who was admitted with community-acquired pneumonia. She continues to improve symptomatically on ceftriaxone. Currently, she is afebrile and her vitals are stable. Supplemental oxygen has been weaned to 2 L/min by nasal cannula. Exam reveals improved crackles in the left lower chest without dullness to percussion. Labs are notable for down-trending leukocytosis and a stable serum creatinine of 2.8 mg/dL.” The hospitalist considers how including racial descriptors in clinical presentations may influence the care of the patient.

For decades, medical educators have taught learners to include sociopolitical constructs such as race in the opening sentence of the history of present illness (HPI). This practice presumably stems from the assumption that race accurately reflects biogenetic information about patients and serves as a key attribute in problem representations.¹ Proponents of including race in the HPI suggest doing so aids the clinical assessment of patients’ risks for particular diseases and may inform the selection of race-appropriate therapies.²

The construct of race does sometimes correlate with the risk of disease or response to therapies. For example, sickle cell disease (SCD) occurs more commonly among patients who identify as Black rather than White. Specifically, ancestry from African nations such as Nigeria or the Democratic Republic of Congo increases the likelihood of having the disease-associated hemoglobin gene variant HbS.¹ Popular genomic ancestry tests often report ancestral groupings that map to racial categories and may reinforce the perception that race has a genetic basis.³

Race, a construct of sociopolitical origins, incorrectly conflates skin color with genetic variation. Associations between race and disease have the potential to cause diagnostic and therapeutic errors and inequitable allocation of resources. Increased illness burden in minority populations results primarily from social factors such as environment, access to care, housing instability, food insecurity, and experiences of discrimination, rather than genetic differences. The resulting chronic and recurrent physiologic stress—known as allostatic load—also contributes to the inequitable health outcomes observed in vulnerable populations, including patients who identify as Black.⁴

Historically, race evolved as a sociopolitical framework stemming from colonialism, discrimination, and exploitation.⁵ Numerous studies reveal a lack of genetic precision in racial categories. In fact, genetic data compared across major continental groups found greater variation of microsatellite loci and restriction fragment length polymorphisms within racial groups than between them.⁶ The evidence indicates that racial categories do not reflect homogenous population groups but rather “arbitrary division[s] of continuous variation” that cannot serve as a surrogate to genetic diversity.⁵ Not only are racial categories genetically inaccurate, but data on race within the electronic health record often differ from patients’ self-description of race, underscoring the problematic nature of even identifying race.⁷ In one study, up to 41% of patients self-reported identification with at least one other racial or ethnic group than the race or ethnicity documented in their electronic health record.⁷

Additionally, conflating race with genetic variation can lead to diagnostic errors. As an example, the incidence of cystic fibrosis (CF) varies widely across populations of European ancestry. The primary focus on CF’s occurrence in patients of European descent may divert attention from the identification of mutations causing CF in populations of African descent or the decreased survival observed in the United States among CF patients of Hispanic descent.^8,9 Similarly, India represents one of the countries largely affected by SCD, suggesting that a myopic focus on SCD among those identifying as Black can lead to underdiagnosis of SCD among those with Indian ancestry.

Perhaps more insidiously, linking disease to race or other social constructs can result in differential support for affected individuals. SCD offers a striking illustration of this point. Reflecting the legacy of transatlantic slave trading, the majority of people with SCD in the United States are Black and face interpersonal and structural racism within society and healthcare that amplify the effects of this devastating illness.¹⁰ Compulsory screening programs for sickle cell trait introduced by many states in the 1970s targeted Black Americans and resulted in stigmatization and the denial of insurance, educational opportunities, and jobs for many identified with sickle cell trait. Federal funding for SCD research remains low, particularly in comparison to the tenfold higher funding for CF, which afflicts fewer, but primarily White, Americans.¹⁰

The incorporation of race into risk models and guidelines—alongside biologically relevant variables such as age and comorbid conditions—has received increasing attention for its potential to compound racial disparities in health outcomes. The American Heart Association Heart Failure Risk Score, for instance, may lead to the exclusion of some Black patients from necessary care because “Black” race, for no clear physiologic reason, serves as a protective factor against heart failure mortality.¹¹ Likewise, race adjustments in pulmonary function tests, breast cancer risk models, and estimated glomerular filtration rate calculations, among others, have limited biological basis and the potential to divert care disproportionately from minority populations.¹¹

Researchers have even called into question the application of race to pharmacotherapies. A 2001 investigation on geographic patterns of genetic variation in drug response concluded that common racial and ethnic labels were “insufficient and inaccurate representations” of the individual genetic clusters.¹² Further, numerous experts have criticized two landmark studies of vasodilators and angiotensin-converting enzyme inhibitors in Black patients with heart failure for inconsistent results and nonsignificant associations between race and major outcomes, such as the development of heart failure or death.¹³

Race-based labels can also divert attention from true causes of health inequities. The National Academy of Sciences concluded that social determinants of health and structural racism are the root causes of health inequities, rather than genetics.¹⁴ Medical professionals may perpetuate these disparities: Most US physicians demonstrate an unconscious preference—or implicit bias—for White Americans over Black Americans.¹⁵ Beyond obscuring the role of social determinants of health and structural racism in health outcomes, race-based labels may exacerbate the ways in which physicians’ implicit biases contribute to racial and ethnic health disparities, primarily affecting Black Americans.² In a recent study, clinicians documented race in the HPI for 33% of Black patients compared with 16% of White patients, and White clinicians were twice as likely to document race as Black physicians.¹⁶ Moreover, training medical students to view race as an independent risk factor of disease without discussing structural inequities can pathologize race and reinforce implicit biases linking race and disease.¹⁵

Based on the current evidence, we believe routine use of race-based labels in clinical presentations confuses providers at a minimum and potentially produces far more damage by obscuring or perpetuating the role of racism in health inequities.

Instead of routinely presenting race in the HPI, we recommend including racial or ethnic information in the social history only when the patient reports it as a meaningful identity or when it informs health disparities stemming from structural or interpersonal racism. Clinicians should include physical characteristics pertaining to race, such as skin tone, in the physical exam only if required to describe exam findings accurately. When presenting race, clinicians should explicitly justify its use and take care to avoid obfuscatory, inaccurate, or stigmatizing mention of associations between race and disease. Clinicians should not use race in clinical algorithms. Medical educators should emphasize the role of social determinants of health and structural racism in health outcomes to inform the use of race in medicine, in hopes that doing so will help students minimize implicit biases and learn to mitigate racial inequities in healthcare.^2,16 In short, clinicians and medical educators alike should ensure that clinical care and the medical curriculum avoid presenting race as a proxy for pathology.

There is little evidence to guide proper inclusion of race in clinical interviews. In the absence of clear guidance about how to approach patients about race, we suggest not asking about it unless there is a reasonable probability that doing so will improve clinical care. If a clinician decides to ask about race, it is important to provide a rationale—such as explaining that the information can be used to assure high-quality care for all patients—since many patients are uncomfortable with questions about race.¹⁷ If clinicians report information about race in the social history, we advise using the patient’s description of race rather than traditional racial categories.

Clinicians who ask their patients about race should approach every patient in a uniform manner to avoid perpetuating biases. We hope future studies will inform equitable, inclusive, and person-centered approaches to discussing race with patients and promote a shared understanding of how racism contributes to illness.

• Avoid using racial descriptors in the HPI.
• Include racial and ethnic information in the social history only when it serves as a meaningful identity or it informs disparities stemming from racism.
• If racial or ethnic information is asked for, explain to patients why and how it will be used.
• Mention physical characteristics such as skin tone, rather than race, in the physical exam if required to describe findings accurately.
• Advocate for the replacement of race or race-adjusted algorithms in patient care.
• Expand the medical curriculum in the social determinants of health and structural racism, and develop systems to avoid the use of stigmatizing, race-based labels.

Race, a sociopolitical construct, does not accurately represent genetic variation. The routine use of race in the HPI can perpetuate racial biases and muddle both diagnoses and treatment. Only mention race in the social history if it is meaningful to the patient’s self-identity or explains health disparities arising from racism. All documentation and presentations should avoid the use of stigmatizing, race-based labels.

In the clinical scenario mentioned earlier, the attending hospitalist raises the issue of race-based labels in patient care in a nonjudgmental fashion. To provide illustrative specificity, she notes how the incorporation of race in formulas of glomerular filtration rate can lead to under-referral for renal transplant. The hospitalist then facilitates an open and inclusive discussion with the team regarding the use of race in clinical presentations and its potential impact on health disparities.

Do you think this is a low-value practice? Is this truly a “Thing We Do for No Reason^™”? Let us know what you do in your practice and propose ideas for other “Things We Do for No Reason^™” topics. Please join in the conversation online at Twitter (#TWDFNR)/Facebook and don’t forget to “Like It” on Facebook or retweet it on Twitter.

Inspired by the ABIM Foundation’s Choosing Wisely^® campaign, the “Things We Do for No Reason^™” (TWDFNR) series reviews practices that have become common parts of hospital care but may provide little value to our patients. Practices reviewed in the TWDFNR series do not represent clear-cut conclusions or clinical practice standards but are meant as a starting place for research and active discussions among hospitalists and patients. We invite you to be part of that discussion.

On teaching rounds, a medical student presents the following case to the attending hospitalist: “Mrs. L is a 54-year-old Black female with chronic kidney disease who was admitted with community-acquired pneumonia. She continues to improve symptomatically on ceftriaxone. Currently, she is afebrile and her vitals are stable. Supplemental oxygen has been weaned to 2 L/min by nasal cannula. Exam reveals improved crackles in the left lower chest without dullness to percussion. Labs are notable for down-trending leukocytosis and a stable serum creatinine of 2.8 mg/dL.” The hospitalist considers how including racial descriptors in clinical presentations may influence the care of the patient.

For decades, medical educators have taught learners to include sociopolitical constructs such as race in the opening sentence of the history of present illness (HPI). This practice presumably stems from the assumption that race accurately reflects biogenetic information about patients and serves as a key attribute in problem representations.¹ Proponents of including race in the HPI suggest doing so aids the clinical assessment of patients’ risks for particular diseases and may inform the selection of race-appropriate therapies.²

The construct of race does sometimes correlate with the risk of disease or response to therapies. For example, sickle cell disease (SCD) occurs more commonly among patients who identify as Black rather than White. Specifically, ancestry from African nations such as Nigeria or the Democratic Republic of Congo increases the likelihood of having the disease-associated hemoglobin gene variant HbS.¹ Popular genomic ancestry tests often report ancestral groupings that map to racial categories and may reinforce the perception that race has a genetic basis.³

Race, a construct of sociopolitical origins, incorrectly conflates skin color with genetic variation. Associations between race and disease have the potential to cause diagnostic and therapeutic errors and inequitable allocation of resources. Increased illness burden in minority populations results primarily from social factors such as environment, access to care, housing instability, food insecurity, and experiences of discrimination, rather than genetic differences. The resulting chronic and recurrent physiologic stress—known as allostatic load—also contributes to the inequitable health outcomes observed in vulnerable populations, including patients who identify as Black.⁴

Historically, race evolved as a sociopolitical framework stemming from colonialism, discrimination, and exploitation.⁵ Numerous studies reveal a lack of genetic precision in racial categories. In fact, genetic data compared across major continental groups found greater variation of microsatellite loci and restriction fragment length polymorphisms within racial groups than between them.⁶ The evidence indicates that racial categories do not reflect homogenous population groups but rather “arbitrary division[s] of continuous variation” that cannot serve as a surrogate to genetic diversity.⁵ Not only are racial categories genetically inaccurate, but data on race within the electronic health record often differ from patients’ self-description of race, underscoring the problematic nature of even identifying race.⁷ In one study, up to 41% of patients self-reported identification with at least one other racial or ethnic group than the race or ethnicity documented in their electronic health record.⁷

Additionally, conflating race with genetic variation can lead to diagnostic errors. As an example, the incidence of cystic fibrosis (CF) varies widely across populations of European ancestry. The primary focus on CF’s occurrence in patients of European descent may divert attention from the identification of mutations causing CF in populations of African descent or the decreased survival observed in the United States among CF patients of Hispanic descent.^8,9 Similarly, India represents one of the countries largely affected by SCD, suggesting that a myopic focus on SCD among those identifying as Black can lead to underdiagnosis of SCD among those with Indian ancestry.

Perhaps more insidiously, linking disease to race or other social constructs can result in differential support for affected individuals. SCD offers a striking illustration of this point. Reflecting the legacy of transatlantic slave trading, the majority of people with SCD in the United States are Black and face interpersonal and structural racism within society and healthcare that amplify the effects of this devastating illness.¹⁰ Compulsory screening programs for sickle cell trait introduced by many states in the 1970s targeted Black Americans and resulted in stigmatization and the denial of insurance, educational opportunities, and jobs for many identified with sickle cell trait. Federal funding for SCD research remains low, particularly in comparison to the tenfold higher funding for CF, which afflicts fewer, but primarily White, Americans.¹⁰

The incorporation of race into risk models and guidelines—alongside biologically relevant variables such as age and comorbid conditions—has received increasing attention for its potential to compound racial disparities in health outcomes. The American Heart Association Heart Failure Risk Score, for instance, may lead to the exclusion of some Black patients from necessary care because “Black” race, for no clear physiologic reason, serves as a protective factor against heart failure mortality.¹¹ Likewise, race adjustments in pulmonary function tests, breast cancer risk models, and estimated glomerular filtration rate calculations, among others, have limited biological basis and the potential to divert care disproportionately from minority populations.¹¹

Researchers have even called into question the application of race to pharmacotherapies. A 2001 investigation on geographic patterns of genetic variation in drug response concluded that common racial and ethnic labels were “insufficient and inaccurate representations” of the individual genetic clusters.¹² Further, numerous experts have criticized two landmark studies of vasodilators and angiotensin-converting enzyme inhibitors in Black patients with heart failure for inconsistent results and nonsignificant associations between race and major outcomes, such as the development of heart failure or death.¹³

Race-based labels can also divert attention from true causes of health inequities. The National Academy of Sciences concluded that social determinants of health and structural racism are the root causes of health inequities, rather than genetics.¹⁴ Medical professionals may perpetuate these disparities: Most US physicians demonstrate an unconscious preference—or implicit bias—for White Americans over Black Americans.¹⁵ Beyond obscuring the role of social determinants of health and structural racism in health outcomes, race-based labels may exacerbate the ways in which physicians’ implicit biases contribute to racial and ethnic health disparities, primarily affecting Black Americans.² In a recent study, clinicians documented race in the HPI for 33% of Black patients compared with 16% of White patients, and White clinicians were twice as likely to document race as Black physicians.¹⁶ Moreover, training medical students to view race as an independent risk factor of disease without discussing structural inequities can pathologize race and reinforce implicit biases linking race and disease.¹⁵

Based on the current evidence, we believe routine use of race-based labels in clinical presentations confuses providers at a minimum and potentially produces far more damage by obscuring or perpetuating the role of racism in health inequities.

Instead of routinely presenting race in the HPI, we recommend including racial or ethnic information in the social history only when the patient reports it as a meaningful identity or when it informs health disparities stemming from structural or interpersonal racism. Clinicians should include physical characteristics pertaining to race, such as skin tone, in the physical exam only if required to describe exam findings accurately. When presenting race, clinicians should explicitly justify its use and take care to avoid obfuscatory, inaccurate, or stigmatizing mention of associations between race and disease. Clinicians should not use race in clinical algorithms. Medical educators should emphasize the role of social determinants of health and structural racism in health outcomes to inform the use of race in medicine, in hopes that doing so will help students minimize implicit biases and learn to mitigate racial inequities in healthcare.^2,16 In short, clinicians and medical educators alike should ensure that clinical care and the medical curriculum avoid presenting race as a proxy for pathology.

There is little evidence to guide proper inclusion of race in clinical interviews. In the absence of clear guidance about how to approach patients about race, we suggest not asking about it unless there is a reasonable probability that doing so will improve clinical care. If a clinician decides to ask about race, it is important to provide a rationale—such as explaining that the information can be used to assure high-quality care for all patients—since many patients are uncomfortable with questions about race.¹⁷ If clinicians report information about race in the social history, we advise using the patient’s description of race rather than traditional racial categories.

Clinicians who ask their patients about race should approach every patient in a uniform manner to avoid perpetuating biases. We hope future studies will inform equitable, inclusive, and person-centered approaches to discussing race with patients and promote a shared understanding of how racism contributes to illness.

• Avoid using racial descriptors in the HPI.
• Include racial and ethnic information in the social history only when it serves as a meaningful identity or it informs disparities stemming from racism.
• If racial or ethnic information is asked for, explain to patients why and how it will be used.
• Mention physical characteristics such as skin tone, rather than race, in the physical exam if required to describe findings accurately.
• Advocate for the replacement of race or race-adjusted algorithms in patient care.
• Expand the medical curriculum in the social determinants of health and structural racism, and develop systems to avoid the use of stigmatizing, race-based labels.

Race, a sociopolitical construct, does not accurately represent genetic variation. The routine use of race in the HPI can perpetuate racial biases and muddle both diagnoses and treatment. Only mention race in the social history if it is meaningful to the patient’s self-identity or explains health disparities arising from racism. All documentation and presentations should avoid the use of stigmatizing, race-based labels.

In the clinical scenario mentioned earlier, the attending hospitalist raises the issue of race-based labels in patient care in a nonjudgmental fashion. To provide illustrative specificity, she notes how the incorporation of race in formulas of glomerular filtration rate can lead to under-referral for renal transplant. The hospitalist then facilitates an open and inclusive discussion with the team regarding the use of race in clinical presentations and its potential impact on health disparities.

Do you think this is a low-value practice? Is this truly a “Thing We Do for No Reason^™”? Let us know what you do in your practice and propose ideas for other “Things We Do for No Reason^™” topics. Please join in the conversation online at Twitter (#TWDFNR)/Facebook and don’t forget to “Like It” on Facebook or retweet it on Twitter.

Within the nationwide effort to combat the opioid epidemic and reduce opioid prescribing, researchers have described different prescribing patterns for non-White racial and ethnic groups, including Black and LatinX populations. This remains a largely unexplored area within hospital medicine. Earlier studies of racial disparities demonstrate how some patients are assessed less often for pain and prescribed fewer opioids from the emergency department, surgical settings, and outpatient primary care practices. Researchers also have documented racial and ethnic disparities in analgesia for cancer pain and chronic noncancer pain.^1-11 Studies have demonstrated that White patients are more likely to receive opioid prescriptions compared with Black patients. Even with similar documented pain scores, there is evidence that Black patients receive fewer analgesics compared with White patients. For example, a recent study found that Black and Hispanic patients presenting to the emergency room for renal colic received less opioid medication compared with White patients.³ A study across 22 sites in Northern California found that racial minorities with long-bone fractures received fewer opioids at discharge than White patients.¹

It is unknown whether differential prescribing patterns by race exist among patients hospitalized on general medicine services. The objective of our study was to assess whether race and ethnicity were associated with the likelihood of opioids being prescribed and the duration of opioids prescribed when these patients are discharged from the hospital. Quantifying and seeking to understand these differences are the first steps toward ensuring racial and ethnic health equity in patient care.

Study Population and Data Sources

We identified all adults (age ≥18 years) discharged from the acute care inpatient general medicine services between June 1, 2012, and November 30, 2018, at the University of California, San Francisco (UCSF) Helen Diller Medical Center at Parnassus Heights, a 785-bed urban academic teaching hospital. All data were obtained from the hospital’s Epic-based electronic medical record (Epic Systems Corporation). Data elements were extracted from Clarity, the relationship database that stores Epic inpatient data. Patients discharged from the inpatient cardiology or bone marrow transplant services were not included. We excluded patients who did not receive opioids in the last 24 hours of their hospitalization. Patients with cancer-related pain diagnoses or sickle cell disease pain crises and patients who were discharged to hospice or followed by palliative care were excluded from the study based on International Classification of Diseases, Tenth Revision (ICD-10) codes (available on request) or service codes, when available, or admitting provider electronic health record documentation (Appendix Figure 1). Palliative care and hospice patients have significantly different pain needs, with management often directed by specialists. Patients with sickle cell disease are disproportionately Black and have distinct opioid prescribing patterns.^12,13 We also excluded discharge opioid prescriptions that were a resumption of the patient’s opioid prescription before admission based on medication documentation. Only new prescriptions signed by the discharging hospitalist, including different doses and formulations, were included in this study.

We performed a subgroup analysis of patients who were not prescribed opioids before their admission based on medication reconciliation but were started on opioids while hospitalized.

Primary Outcomes

We examined two primary outcomes: whether a patient received an opioid prescription at discharge, and, for patients prescribed opioids, the number of days prescribed. Days of opioids at discharge were calculated as total morphine milligram equivalents (MMEs) prescribed divided by MMEs administered during the final 24 hours of hospitalization. This metric was used as a patient-specific approach to calculating how long an opioid prescription will last after discharge, standardized according to the actual opioid requirements from hospitalization.¹⁴ If a patient was discharged with prescriptions for several opioids, the longest single prescription duration was used.

Primary Predictors

The primary predictor was the patient’s primary self-reported race/ethnicity, categorized as White, Black, LatinX, Asian, Native Hawaiian or other Pacific Islander, American Indian or Alaska Native, and other/unknown. Other/unknown included patients who were listed as other, declined, or who were otherwise unspecified. Self-reported race/ethnicity is obtained through reporting to the registrar. These race/ethnicity groupings were done in concordance with US Census Bureau definitions. Researchers classified patients as LatinX if they had Hispanic documented as their ethnicity, no matter their racial identification. These categorizations were chosen to be consistent with the existing literature, recognizing the role of a combined race/ethnicity definition for Hispanic or LatinX populations.¹⁵ These definitions of race/ethnicity are self-reported and reflect socially—not genetically defined—groupings.¹⁶ This variable serves as a surrogate for the structural factors that contribute to racism, the determining factor for racially disparate outcomes.¹⁷

Covariate Data Collection

Additional data were obtained regarding patient demographics, hospitalization factors, and medical diagnoses. Demographic factors included age, sex, and limited English proficiency (LEP) status. LEP was defined as having a primary language other than English and requiring an interpreter. Hospitalization factors included length of stay, whether they required intensive care unit (ICU) management, average daily MMEs administered during their entire hospitalization, MMEs administered during the final 24 hours of their hospitalization, whether the patient was on a teaching service or direct-care hospitalist service, their disposition on discharge, and year. Medical diagnosis variables included the adjusted Elixhauser Comorbidity Index based on ICD-10 codes; whether the patient was taking opioids at admission; and specific diagnoses of cancer, posttraumatic stress disorder (PTSD), and mood, anxiety, or psychotic disorder based on ICD-10 documentation.¹⁸

Statistical Analysis

All statistical analyses were performed using Stata software version 16 (StataCorp LP). Baseline demographic variables, hospitalization factors, and medical diagnosis variables were stratified by race/ethnicity. Within group comparisons were performed using chi-square or analysis of varianace (ANOVA) testing. For regression analyses, we fit two models. First, we fit a multivariable logistic regression model on all patients who received opioids during the last 24 hours of their hospitalization to examine the association between patient race/ethnicity and whether a patient received opioids at discharge, adjusting for additional patient, hospitalization, and medical covariates. Then we fit a negative binomial regression model on patients who were prescribed opioids at discharge to examine the association between patient race/ethnicity and the amount of opioids prescribed at discharge, adjusting for covariates. We used a negative binomial model because of the overdispersed distribution of discharge opioid prescriptions and only examined patients with an opioid prescription at discharge. We included the listed variables in our model because they were all found a priori to be associated with discharge opioid prescriptions.¹⁹ Instead of using days of opioids based on the last 24 hours, we performed a secondary analysis using the actual days of opioids supplied as the outcome. For example, a prescription of 12 tablets with every 6 hours dosing would be 3 days’ duration.

For both models, subgroup analyses were performed using the adjusted models restricted to patients newly prescribed opioids during their hospitalization and who were not previously taking opioids based on admission medication reconciliation. After testing for effect modification, this subgroup analysis was performed to reduce selection bias associated with earlier opioid use.

For all models, we reported predicted population opioid prescribing rates from the average marginal effects (AME).²⁰ Marginal effects were used because ours was a population level study and the outcome of interest was relatively common, limiting the effective interpretation of odds ratios.²¹ Marginal effects allow us to observe the instantaneous effect a given independent variable has on a dependent variable, while holding all other variables constant. It is implemented using the margins command in Stata. Marginal effects enable us to present our results as differences in probabilities, which is a more accurate way to describe the differences found among patient groups. Further, marginal effects are less sensitive to changes in model specifications.²²The UCSF Institutional Review Board for Human Subjects Research approved this study with a waiver of informed consent.

Unadjusted Results

We identified 10,953 patients who received opioids during the last 24 hours of hospitalization (see Appendix Figure 1 for study consort diagram). The patient population was 52.2% White, 18.4% Black, 11.5% Latinx, 10.1% Asian, 6.2% other/unknown, 0.9% Native Hawaiian/Other Pacific Islander, and 0.8% American Indian/Alaska Native (Table 1, Appendix Table 1). Black patients had fewer cancer diagnoses and the highest rate of prescribed opioids on admission. Asian patients were older and more likely to be female, and had higher rates of cancer, the highest median comorbidity index, and the smallest median daily MME during both the last 24 hours and total duration of hospitalization. Representative of general medicine patients, the most common principal discharge diagnoses in our dataset were pneumonia, cellulitis, altered mental status, sepsis, and abdominal pain.

Overall, 5541 (50.6%) patients who received opioids in the last 24 hours of their hospitalization received an opioid prescription at discharge. There were significant differences among racial/ethnic groups receiving an opioid prescription at discharge. Black patients were less likely to be discharged with an opioid compared with White patients (47.7% vs 50.3%; P < .001) (Table 2). The median discharge prescription duration for all patients was 9.3 days (interquartile range [IQR], 3.8-20.0). Black patients received the fewest median days of opioids at 7.5 days (IQR, 3.2-16.7) compared with White patients at 8.8 days (IQR, 3.7-20.0; P < .001) (Table 2).

Adjusted Regression Results

Demographic, clinical, and diagnosis specific factors were significantly associated with opioid prescriptions, including previous opioid use, sex, and a concurrent cancer diagnosis. There were fewer opioid prescriptions over time (Figure).

Following multivariable logistic regression for the association between race/ethnicity and opioid on discharge and controlling for covariates, we found that Black patients were less likely to receive an opioid prescription on discharge compared with White patients (predicted population rate, 47.6% vs 50.7%; AME −3.1%; 95% CI, −5.5% to −0.8%). Asian patients were more likely to receive a prescription on discharge compared with White patients (predicted population rate, 55.6% vs 50.7%; AME +4.9; 95% CI, 1.5%-8.3%).

Following multivariable negative binomial regression for the association between race/ethnicity and the number of opioid days on discharge, we found that Black patients received a shorter duration of opioid days compared with White patients (predicted days of opioids on discharge, 15.7 days vs 17.8 days; AME −2.1 days; 95% CI, −3.3 to −0.87) (Table 3). There were no significant differences among patients and the other racial/ethnic groups.

Our secondary analysis from the negative binomial regression with the days of opioids supplied metric yielded similar results to our primary analysis showing that Black patients received statically significantly fewer days of opioid therapy compared with White patients (Appendix Table 2).

Subgroup Regression Results

After testing for effect modification, which was negative, we examined the relationships for patients started on opioids during their hospitalization (Appendix Table 3 and Appendix Table 4). There were 5101 patients with newly prescribed opioids during their hospitalization. Adjusting for covariates, we found that Black patients were less likely to receive opioids at discharge compared with White patients (predicted population rate, 34.9% vs 40.4%; AME −5.5%; 95% CI, −9.2% to −1.9%). American Indian or Alaska Native patients were more likely to receive opioids on discharge (predicted population rate, 58.3% vs 40.4%; AME +17.9%; 95% CI, 1.0%-34.8%). We also found that Asian patients received more days of opioids on discharge (predicted days of opioid on discharge, 16.7 vs 13.7 days; AME +3.0 days; 95% CI, 0.6-5.3 days) (Appendix Table 4, Appendix Figure 2).

We found that Black patients discharged from the general medicine service were less likely to receive opioids and received shorter courses on discharge compared with White patients, adjusting for demographic, hospitalization, and medical diagnosis variables. Asian patients were more likely to receive an opioid prescription at discharge—a finding not reported in the literature on opioid prescribing disparities in most other practice settings.¹

Previous studies have shown racial disparities in pain management in emergency and surgical settings, but these relationships have not been characterized in an inpatient medicine population. Medicine patients comprise the majority of admitted patients in the United States and reflect a wide diversity of medical conditions, many requiring opioids for pain management. Determining the etiology of these differential prescribing patterns was not within the scope of our study, but earlier studies demonstrate a number of reasons why these patterns exist across racial and ethnic groups in other practice settings.^23,24 These reports give us insight into potential mechanisms for our study population.

Differences in pain management likely represent the multiple structural mechanisms by which racism operates.¹⁷ Drawing from the existing literature and the socioecological model, we hypothesize the ways that individual, interpersonal relationships, organizations, communities, and public policy impact opioid prescribing.^25,26 Using this model and considering the framework of Critical Race Theory (CRT), we can work towards understanding how race and ethnicity stand in as surrogates for racism and how this manifests in different outcomes and identify areas for intervention. CRT draws attention to race consciousness, contemporary orientation, centering in the margins, and praxis. In the context of this analysis, we recognize race consciousness and the interactions among factors such as race/ethnicity, language, and diagnoses such as PTSD.²⁷ This approach is necessary because racism is a multilevel construct influenced by macrolevel factors.²⁸

Individually and interpersonally, there is clinician-driven bias in pain assessment, which is activated under times of stress and diagnostic uncertainty and is amplified by a lack of clear guidelines for pain management prescriptions.^23,29-32 Institutional and organizational culture contribute to disparities through ingrained culture, practice patterns, and resource allocation.^29,33 Last, public policy and the larger sociopolitical environment worsen disparities through nondiverse workforces, state and federal guidelines, criminal justice policy, supply chain regulation, and access to care.

As individual clinicians, departments, and health systems leaders, we must identify areas for intervention. At the individual and interpersonal levels, there is evidence that taking implicit association tests could help clinicians become more aware of their negative associations, and empathy-inducing, perspective-taking interventions can reduce pain treatment bias.^31,34 At the institutional level, we must report data on disparities, create guidelines for pain management, and reevaluate the educational curriculum and culture to assess how certain biases could be propagated. The lack of straightforward guidelines leads to unclear indications for opioid prescriptions, exacerbating provider-level differences in prescribing. At the policy level, legislation that promotes workplace diversity, increases training for and access to pain specialists, and incentivizes data collection and reporting could help reduce disparities.³⁵ Equitable access to prescriptions and care is essential. Pharmacies often understock opioids in minority neighborhoods, meaning that even if a patient is prescribed an opioid on discharge, he or she might have difficulty filling the prescription.³⁶

One could question whether fewer opioid prescriptions for Black patients protects against the harms of opioid overprescribing, and therefore is not reflective of harmful inequity.³⁷ Ongoing national programs aim to reduce the harmful effects of opioids, which is reflected in the reduction in opioid prescribing over time in our institution. Our point is that differences in prescribing could reflect practices that do result in patient harm, such as less adequately controlled pain among Black patients.^1,3 Undertreated pain has negative health and social consequences and further contributes to substance-use stigma within minority communities.³⁸ Moreover, Black people who describe more discrimination in medical settings were more likely to report subsequent opioid misuse.³⁹

Although the above mechanisms might partially explain our findings among Black patients, the higher rate of prescribing for Asian patients is more challenging to explain. Our models adjusted for clinical factors. Notably, our Asian patients had the highest baseline comorbidity index, oldest mean age, and highest cancer rates, and it is possible that we were unable to fully account for illness severity or related pain needs (Table 1). It also is possible—although speculative—that factors such as language, provider concordance, and the type of disease process all contribute.⁴⁰ Some researchers have proposed a “stereotype content model” that seeks to establish a pathway among social structure (status of a patient) to clinician stereotypes (is this patient warm and/or competent) to emotional prejudices (envy, pride) and ultimately to discrimination (active/passive, help/harm).²³Our study has limitations. Our model was limited by the available data collected on our patients. Covariates including primary care follow-up, pain scores, and overdose history were not available. Furthermore, our categorization of race/ethnicity was based on self-reported data. We had 676 patients with race/ethnicity specified as other/unknown. We recognize the heterogeneity within these racial/ethnic categorizations. For example, within the LatinX or Asian communities, there are large differences based on region, country, ethnic, or cultural groups. Our study only included patients presenting to a hospital in San Francisco, which is different from the racial/ethnic makeup of other cities across the nation. Our electronic health record capture of history of opioid use disorder and mood disorders is contingent on individual clinician documentation. We did not account for provider-level differences, which is an important part of variation in prescribing differences. We also did not examine differences at the diagnosis-specific level. Finally, we could not determine the indication or appropriateness of opioid prescriptions.

Future studies will be necessary to characterize this relationship at a diagnosis-specific level and to describe causal pathways. Within our own institution, these findings present an opportunity for positive change. We hope to continue to explore the etiology of these disparities and identify areas where differences could impact patient outcomes, such as pain control. It is essential to develop appropriate recommendations for inpatient and discharge opioid prescribing to help minimize disparities and to mitigate potential harms of overprescribing. All health systems should continue to collect data on their own disparities in opioid prescribing and educate clinicians on promoting more equitable practices.

The authors thank Sneha Daya, MD, Sachin Shah, MD, MPH, and the UCSF Division of Hospital Medicine Data Core.

Within the nationwide effort to combat the opioid epidemic and reduce opioid prescribing, researchers have described different prescribing patterns for non-White racial and ethnic groups, including Black and LatinX populations. This remains a largely unexplored area within hospital medicine. Earlier studies of racial disparities demonstrate how some patients are assessed less often for pain and prescribed fewer opioids from the emergency department, surgical settings, and outpatient primary care practices. Researchers also have documented racial and ethnic disparities in analgesia for cancer pain and chronic noncancer pain.^1-11 Studies have demonstrated that White patients are more likely to receive opioid prescriptions compared with Black patients. Even with similar documented pain scores, there is evidence that Black patients receive fewer analgesics compared with White patients. For example, a recent study found that Black and Hispanic patients presenting to the emergency room for renal colic received less opioid medication compared with White patients.³ A study across 22 sites in Northern California found that racial minorities with long-bone fractures received fewer opioids at discharge than White patients.¹

It is unknown whether differential prescribing patterns by race exist among patients hospitalized on general medicine services. The objective of our study was to assess whether race and ethnicity were associated with the likelihood of opioids being prescribed and the duration of opioids prescribed when these patients are discharged from the hospital. Quantifying and seeking to understand these differences are the first steps toward ensuring racial and ethnic health equity in patient care.

Study Population and Data Sources

We identified all adults (age ≥18 years) discharged from the acute care inpatient general medicine services between June 1, 2012, and November 30, 2018, at the University of California, San Francisco (UCSF) Helen Diller Medical Center at Parnassus Heights, a 785-bed urban academic teaching hospital. All data were obtained from the hospital’s Epic-based electronic medical record (Epic Systems Corporation). Data elements were extracted from Clarity, the relationship database that stores Epic inpatient data. Patients discharged from the inpatient cardiology or bone marrow transplant services were not included. We excluded patients who did not receive opioids in the last 24 hours of their hospitalization. Patients with cancer-related pain diagnoses or sickle cell disease pain crises and patients who were discharged to hospice or followed by palliative care were excluded from the study based on International Classification of Diseases, Tenth Revision (ICD-10) codes (available on request) or service codes, when available, or admitting provider electronic health record documentation (Appendix Figure 1). Palliative care and hospice patients have significantly different pain needs, with management often directed by specialists. Patients with sickle cell disease are disproportionately Black and have distinct opioid prescribing patterns.^12,13 We also excluded discharge opioid prescriptions that were a resumption of the patient’s opioid prescription before admission based on medication documentation. Only new prescriptions signed by the discharging hospitalist, including different doses and formulations, were included in this study.

We performed a subgroup analysis of patients who were not prescribed opioids before their admission based on medication reconciliation but were started on opioids while hospitalized.

Primary Outcomes

We examined two primary outcomes: whether a patient received an opioid prescription at discharge, and, for patients prescribed opioids, the number of days prescribed. Days of opioids at discharge were calculated as total morphine milligram equivalents (MMEs) prescribed divided by MMEs administered during the final 24 hours of hospitalization. This metric was used as a patient-specific approach to calculating how long an opioid prescription will last after discharge, standardized according to the actual opioid requirements from hospitalization.¹⁴ If a patient was discharged with prescriptions for several opioids, the longest single prescription duration was used.

Primary Predictors

The primary predictor was the patient’s primary self-reported race/ethnicity, categorized as White, Black, LatinX, Asian, Native Hawaiian or other Pacific Islander, American Indian or Alaska Native, and other/unknown. Other/unknown included patients who were listed as other, declined, or who were otherwise unspecified. Self-reported race/ethnicity is obtained through reporting to the registrar. These race/ethnicity groupings were done in concordance with US Census Bureau definitions. Researchers classified patients as LatinX if they had Hispanic documented as their ethnicity, no matter their racial identification. These categorizations were chosen to be consistent with the existing literature, recognizing the role of a combined race/ethnicity definition for Hispanic or LatinX populations.¹⁵ These definitions of race/ethnicity are self-reported and reflect socially—not genetically defined—groupings.¹⁶ This variable serves as a surrogate for the structural factors that contribute to racism, the determining factor for racially disparate outcomes.¹⁷

Covariate Data Collection

Additional data were obtained regarding patient demographics, hospitalization factors, and medical diagnoses. Demographic factors included age, sex, and limited English proficiency (LEP) status. LEP was defined as having a primary language other than English and requiring an interpreter. Hospitalization factors included length of stay, whether they required intensive care unit (ICU) management, average daily MMEs administered during their entire hospitalization, MMEs administered during the final 24 hours of their hospitalization, whether the patient was on a teaching service or direct-care hospitalist service, their disposition on discharge, and year. Medical diagnosis variables included the adjusted Elixhauser Comorbidity Index based on ICD-10 codes; whether the patient was taking opioids at admission; and specific diagnoses of cancer, posttraumatic stress disorder (PTSD), and mood, anxiety, or psychotic disorder based on ICD-10 documentation.¹⁸

Statistical Analysis

All statistical analyses were performed using Stata software version 16 (StataCorp LP). Baseline demographic variables, hospitalization factors, and medical diagnosis variables were stratified by race/ethnicity. Within group comparisons were performed using chi-square or analysis of varianace (ANOVA) testing. For regression analyses, we fit two models. First, we fit a multivariable logistic regression model on all patients who received opioids during the last 24 hours of their hospitalization to examine the association between patient race/ethnicity and whether a patient received opioids at discharge, adjusting for additional patient, hospitalization, and medical covariates. Then we fit a negative binomial regression model on patients who were prescribed opioids at discharge to examine the association between patient race/ethnicity and the amount of opioids prescribed at discharge, adjusting for covariates. We used a negative binomial model because of the overdispersed distribution of discharge opioid prescriptions and only examined patients with an opioid prescription at discharge. We included the listed variables in our model because they were all found a priori to be associated with discharge opioid prescriptions.¹⁹ Instead of using days of opioids based on the last 24 hours, we performed a secondary analysis using the actual days of opioids supplied as the outcome. For example, a prescription of 12 tablets with every 6 hours dosing would be 3 days’ duration.

For both models, subgroup analyses were performed using the adjusted models restricted to patients newly prescribed opioids during their hospitalization and who were not previously taking opioids based on admission medication reconciliation. After testing for effect modification, this subgroup analysis was performed to reduce selection bias associated with earlier opioid use.

For all models, we reported predicted population opioid prescribing rates from the average marginal effects (AME).²⁰ Marginal effects were used because ours was a population level study and the outcome of interest was relatively common, limiting the effective interpretation of odds ratios.²¹ Marginal effects allow us to observe the instantaneous effect a given independent variable has on a dependent variable, while holding all other variables constant. It is implemented using the margins command in Stata. Marginal effects enable us to present our results as differences in probabilities, which is a more accurate way to describe the differences found among patient groups. Further, marginal effects are less sensitive to changes in model specifications.²²The UCSF Institutional Review Board for Human Subjects Research approved this study with a waiver of informed consent.

Unadjusted Results

We identified 10,953 patients who received opioids during the last 24 hours of hospitalization (see Appendix Figure 1 for study consort diagram). The patient population was 52.2% White, 18.4% Black, 11.5% Latinx, 10.1% Asian, 6.2% other/unknown, 0.9% Native Hawaiian/Other Pacific Islander, and 0.8% American Indian/Alaska Native (Table 1, Appendix Table 1). Black patients had fewer cancer diagnoses and the highest rate of prescribed opioids on admission. Asian patients were older and more likely to be female, and had higher rates of cancer, the highest median comorbidity index, and the smallest median daily MME during both the last 24 hours and total duration of hospitalization. Representative of general medicine patients, the most common principal discharge diagnoses in our dataset were pneumonia, cellulitis, altered mental status, sepsis, and abdominal pain.

Overall, 5541 (50.6%) patients who received opioids in the last 24 hours of their hospitalization received an opioid prescription at discharge. There were significant differences among racial/ethnic groups receiving an opioid prescription at discharge. Black patients were less likely to be discharged with an opioid compared with White patients (47.7% vs 50.3%; P < .001) (Table 2). The median discharge prescription duration for all patients was 9.3 days (interquartile range [IQR], 3.8-20.0). Black patients received the fewest median days of opioids at 7.5 days (IQR, 3.2-16.7) compared with White patients at 8.8 days (IQR, 3.7-20.0; P < .001) (Table 2).

Adjusted Regression Results

Demographic, clinical, and diagnosis specific factors were significantly associated with opioid prescriptions, including previous opioid use, sex, and a concurrent cancer diagnosis. There were fewer opioid prescriptions over time (Figure).

Following multivariable logistic regression for the association between race/ethnicity and opioid on discharge and controlling for covariates, we found that Black patients were less likely to receive an opioid prescription on discharge compared with White patients (predicted population rate, 47.6% vs 50.7%; AME −3.1%; 95% CI, −5.5% to −0.8%). Asian patients were more likely to receive a prescription on discharge compared with White patients (predicted population rate, 55.6% vs 50.7%; AME +4.9; 95% CI, 1.5%-8.3%).

Following multivariable negative binomial regression for the association between race/ethnicity and the number of opioid days on discharge, we found that Black patients received a shorter duration of opioid days compared with White patients (predicted days of opioids on discharge, 15.7 days vs 17.8 days; AME −2.1 days; 95% CI, −3.3 to −0.87) (Table 3). There were no significant differences among patients and the other racial/ethnic groups.

Our secondary analysis from the negative binomial regression with the days of opioids supplied metric yielded similar results to our primary analysis showing that Black patients received statically significantly fewer days of opioid therapy compared with White patients (Appendix Table 2).

Subgroup Regression Results

After testing for effect modification, which was negative, we examined the relationships for patients started on opioids during their hospitalization (Appendix Table 3 and Appendix Table 4). There were 5101 patients with newly prescribed opioids during their hospitalization. Adjusting for covariates, we found that Black patients were less likely to receive opioids at discharge compared with White patients (predicted population rate, 34.9% vs 40.4%; AME −5.5%; 95% CI, −9.2% to −1.9%). American Indian or Alaska Native patients were more likely to receive opioids on discharge (predicted population rate, 58.3% vs 40.4%; AME +17.9%; 95% CI, 1.0%-34.8%). We also found that Asian patients received more days of opioids on discharge (predicted days of opioid on discharge, 16.7 vs 13.7 days; AME +3.0 days; 95% CI, 0.6-5.3 days) (Appendix Table 4, Appendix Figure 2).

We found that Black patients discharged from the general medicine service were less likely to receive opioids and received shorter courses on discharge compared with White patients, adjusting for demographic, hospitalization, and medical diagnosis variables. Asian patients were more likely to receive an opioid prescription at discharge—a finding not reported in the literature on opioid prescribing disparities in most other practice settings.¹

Previous studies have shown racial disparities in pain management in emergency and surgical settings, but these relationships have not been characterized in an inpatient medicine population. Medicine patients comprise the majority of admitted patients in the United States and reflect a wide diversity of medical conditions, many requiring opioids for pain management. Determining the etiology of these differential prescribing patterns was not within the scope of our study, but earlier studies demonstrate a number of reasons why these patterns exist across racial and ethnic groups in other practice settings.^23,24 These reports give us insight into potential mechanisms for our study population.

Differences in pain management likely represent the multiple structural mechanisms by which racism operates.¹⁷ Drawing from the existing literature and the socioecological model, we hypothesize the ways that individual, interpersonal relationships, organizations, communities, and public policy impact opioid prescribing.^25,26 Using this model and considering the framework of Critical Race Theory (CRT), we can work towards understanding how race and ethnicity stand in as surrogates for racism and how this manifests in different outcomes and identify areas for intervention. CRT draws attention to race consciousness, contemporary orientation, centering in the margins, and praxis. In the context of this analysis, we recognize race consciousness and the interactions among factors such as race/ethnicity, language, and diagnoses such as PTSD.²⁷ This approach is necessary because racism is a multilevel construct influenced by macrolevel factors.²⁸

Individually and interpersonally, there is clinician-driven bias in pain assessment, which is activated under times of stress and diagnostic uncertainty and is amplified by a lack of clear guidelines for pain management prescriptions.^23,29-32 Institutional and organizational culture contribute to disparities through ingrained culture, practice patterns, and resource allocation.^29,33 Last, public policy and the larger sociopolitical environment worsen disparities through nondiverse workforces, state and federal guidelines, criminal justice policy, supply chain regulation, and access to care.

As individual clinicians, departments, and health systems leaders, we must identify areas for intervention. At the individual and interpersonal levels, there is evidence that taking implicit association tests could help clinicians become more aware of their negative associations, and empathy-inducing, perspective-taking interventions can reduce pain treatment bias.^31,34 At the institutional level, we must report data on disparities, create guidelines for pain management, and reevaluate the educational curriculum and culture to assess how certain biases could be propagated. The lack of straightforward guidelines leads to unclear indications for opioid prescriptions, exacerbating provider-level differences in prescribing. At the policy level, legislation that promotes workplace diversity, increases training for and access to pain specialists, and incentivizes data collection and reporting could help reduce disparities.³⁵ Equitable access to prescriptions and care is essential. Pharmacies often understock opioids in minority neighborhoods, meaning that even if a patient is prescribed an opioid on discharge, he or she might have difficulty filling the prescription.³⁶

One could question whether fewer opioid prescriptions for Black patients protects against the harms of opioid overprescribing, and therefore is not reflective of harmful inequity.³⁷ Ongoing national programs aim to reduce the harmful effects of opioids, which is reflected in the reduction in opioid prescribing over time in our institution. Our point is that differences in prescribing could reflect practices that do result in patient harm, such as less adequately controlled pain among Black patients.^1,3 Undertreated pain has negative health and social consequences and further contributes to substance-use stigma within minority communities.³⁸ Moreover, Black people who describe more discrimination in medical settings were more likely to report subsequent opioid misuse.³⁹

Although the above mechanisms might partially explain our findings among Black patients, the higher rate of prescribing for Asian patients is more challenging to explain. Our models adjusted for clinical factors. Notably, our Asian patients had the highest baseline comorbidity index, oldest mean age, and highest cancer rates, and it is possible that we were unable to fully account for illness severity or related pain needs (Table 1). It also is possible—although speculative—that factors such as language, provider concordance, and the type of disease process all contribute.⁴⁰ Some researchers have proposed a “stereotype content model” that seeks to establish a pathway among social structure (status of a patient) to clinician stereotypes (is this patient warm and/or competent) to emotional prejudices (envy, pride) and ultimately to discrimination (active/passive, help/harm).²³Our study has limitations. Our model was limited by the available data collected on our patients. Covariates including primary care follow-up, pain scores, and overdose history were not available. Furthermore, our categorization of race/ethnicity was based on self-reported data. We had 676 patients with race/ethnicity specified as other/unknown. We recognize the heterogeneity within these racial/ethnic categorizations. For example, within the LatinX or Asian communities, there are large differences based on region, country, ethnic, or cultural groups. Our study only included patients presenting to a hospital in San Francisco, which is different from the racial/ethnic makeup of other cities across the nation. Our electronic health record capture of history of opioid use disorder and mood disorders is contingent on individual clinician documentation. We did not account for provider-level differences, which is an important part of variation in prescribing differences. We also did not examine differences at the diagnosis-specific level. Finally, we could not determine the indication or appropriateness of opioid prescriptions.

Future studies will be necessary to characterize this relationship at a diagnosis-specific level and to describe causal pathways. Within our own institution, these findings present an opportunity for positive change. We hope to continue to explore the etiology of these disparities and identify areas where differences could impact patient outcomes, such as pain control. It is essential to develop appropriate recommendations for inpatient and discharge opioid prescribing to help minimize disparities and to mitigate potential harms of overprescribing. All health systems should continue to collect data on their own disparities in opioid prescribing and educate clinicians on promoting more equitable practices.

The authors thank Sneha Daya, MD, Sachin Shah, MD, MPH, and the UCSF Division of Hospital Medicine Data Core.

Within the nationwide effort to combat the opioid epidemic and reduce opioid prescribing, researchers have described different prescribing patterns for non-White racial and ethnic groups, including Black and LatinX populations. This remains a largely unexplored area within hospital medicine. Earlier studies of racial disparities demonstrate how some patients are assessed less often for pain and prescribed fewer opioids from the emergency department, surgical settings, and outpatient primary care practices. Researchers also have documented racial and ethnic disparities in analgesia for cancer pain and chronic noncancer pain.^1-11 Studies have demonstrated that White patients are more likely to receive opioid prescriptions compared with Black patients. Even with similar documented pain scores, there is evidence that Black patients receive fewer analgesics compared with White patients. For example, a recent study found that Black and Hispanic patients presenting to the emergency room for renal colic received less opioid medication compared with White patients.³ A study across 22 sites in Northern California found that racial minorities with long-bone fractures received fewer opioids at discharge than White patients.¹

It is unknown whether differential prescribing patterns by race exist among patients hospitalized on general medicine services. The objective of our study was to assess whether race and ethnicity were associated with the likelihood of opioids being prescribed and the duration of opioids prescribed when these patients are discharged from the hospital. Quantifying and seeking to understand these differences are the first steps toward ensuring racial and ethnic health equity in patient care.

Study Population and Data Sources

We identified all adults (age ≥18 years) discharged from the acute care inpatient general medicine services between June 1, 2012, and November 30, 2018, at the University of California, San Francisco (UCSF) Helen Diller Medical Center at Parnassus Heights, a 785-bed urban academic teaching hospital. All data were obtained from the hospital’s Epic-based electronic medical record (Epic Systems Corporation). Data elements were extracted from Clarity, the relationship database that stores Epic inpatient data. Patients discharged from the inpatient cardiology or bone marrow transplant services were not included. We excluded patients who did not receive opioids in the last 24 hours of their hospitalization. Patients with cancer-related pain diagnoses or sickle cell disease pain crises and patients who were discharged to hospice or followed by palliative care were excluded from the study based on International Classification of Diseases, Tenth Revision (ICD-10) codes (available on request) or service codes, when available, or admitting provider electronic health record documentation (Appendix Figure 1). Palliative care and hospice patients have significantly different pain needs, with management often directed by specialists. Patients with sickle cell disease are disproportionately Black and have distinct opioid prescribing patterns.^12,13 We also excluded discharge opioid prescriptions that were a resumption of the patient’s opioid prescription before admission based on medication documentation. Only new prescriptions signed by the discharging hospitalist, including different doses and formulations, were included in this study.

We performed a subgroup analysis of patients who were not prescribed opioids before their admission based on medication reconciliation but were started on opioids while hospitalized.

Primary Outcomes

We examined two primary outcomes: whether a patient received an opioid prescription at discharge, and, for patients prescribed opioids, the number of days prescribed. Days of opioids at discharge were calculated as total morphine milligram equivalents (MMEs) prescribed divided by MMEs administered during the final 24 hours of hospitalization. This metric was used as a patient-specific approach to calculating how long an opioid prescription will last after discharge, standardized according to the actual opioid requirements from hospitalization.¹⁴ If a patient was discharged with prescriptions for several opioids, the longest single prescription duration was used.

Primary Predictors

The primary predictor was the patient’s primary self-reported race/ethnicity, categorized as White, Black, LatinX, Asian, Native Hawaiian or other Pacific Islander, American Indian or Alaska Native, and other/unknown. Other/unknown included patients who were listed as other, declined, or who were otherwise unspecified. Self-reported race/ethnicity is obtained through reporting to the registrar. These race/ethnicity groupings were done in concordance with US Census Bureau definitions. Researchers classified patients as LatinX if they had Hispanic documented as their ethnicity, no matter their racial identification. These categorizations were chosen to be consistent with the existing literature, recognizing the role of a combined race/ethnicity definition for Hispanic or LatinX populations.¹⁵ These definitions of race/ethnicity are self-reported and reflect socially—not genetically defined—groupings.¹⁶ This variable serves as a surrogate for the structural factors that contribute to racism, the determining factor for racially disparate outcomes.¹⁷

Covariate Data Collection

Additional data were obtained regarding patient demographics, hospitalization factors, and medical diagnoses. Demographic factors included age, sex, and limited English proficiency (LEP) status. LEP was defined as having a primary language other than English and requiring an interpreter. Hospitalization factors included length of stay, whether they required intensive care unit (ICU) management, average daily MMEs administered during their entire hospitalization, MMEs administered during the final 24 hours of their hospitalization, whether the patient was on a teaching service or direct-care hospitalist service, their disposition on discharge, and year. Medical diagnosis variables included the adjusted Elixhauser Comorbidity Index based on ICD-10 codes; whether the patient was taking opioids at admission; and specific diagnoses of cancer, posttraumatic stress disorder (PTSD), and mood, anxiety, or psychotic disorder based on ICD-10 documentation.¹⁸

Statistical Analysis

All statistical analyses were performed using Stata software version 16 (StataCorp LP). Baseline demographic variables, hospitalization factors, and medical diagnosis variables were stratified by race/ethnicity. Within group comparisons were performed using chi-square or analysis of varianace (ANOVA) testing. For regression analyses, we fit two models. First, we fit a multivariable logistic regression model on all patients who received opioids during the last 24 hours of their hospitalization to examine the association between patient race/ethnicity and whether a patient received opioids at discharge, adjusting for additional patient, hospitalization, and medical covariates. Then we fit a negative binomial regression model on patients who were prescribed opioids at discharge to examine the association between patient race/ethnicity and the amount of opioids prescribed at discharge, adjusting for covariates. We used a negative binomial model because of the overdispersed distribution of discharge opioid prescriptions and only examined patients with an opioid prescription at discharge. We included the listed variables in our model because they were all found a priori to be associated with discharge opioid prescriptions.¹⁹ Instead of using days of opioids based on the last 24 hours, we performed a secondary analysis using the actual days of opioids supplied as the outcome. For example, a prescription of 12 tablets with every 6 hours dosing would be 3 days’ duration.

For both models, subgroup analyses were performed using the adjusted models restricted to patients newly prescribed opioids during their hospitalization and who were not previously taking opioids based on admission medication reconciliation. After testing for effect modification, this subgroup analysis was performed to reduce selection bias associated with earlier opioid use.

For all models, we reported predicted population opioid prescribing rates from the average marginal effects (AME).²⁰ Marginal effects were used because ours was a population level study and the outcome of interest was relatively common, limiting the effective interpretation of odds ratios.²¹ Marginal effects allow us to observe the instantaneous effect a given independent variable has on a dependent variable, while holding all other variables constant. It is implemented using the margins command in Stata. Marginal effects enable us to present our results as differences in probabilities, which is a more accurate way to describe the differences found among patient groups. Further, marginal effects are less sensitive to changes in model specifications.²²The UCSF Institutional Review Board for Human Subjects Research approved this study with a waiver of informed consent.

Unadjusted Results

We identified 10,953 patients who received opioids during the last 24 hours of hospitalization (see Appendix Figure 1 for study consort diagram). The patient population was 52.2% White, 18.4% Black, 11.5% Latinx, 10.1% Asian, 6.2% other/unknown, 0.9% Native Hawaiian/Other Pacific Islander, and 0.8% American Indian/Alaska Native (Table 1, Appendix Table 1). Black patients had fewer cancer diagnoses and the highest rate of prescribed opioids on admission. Asian patients were older and more likely to be female, and had higher rates of cancer, the highest median comorbidity index, and the smallest median daily MME during both the last 24 hours and total duration of hospitalization. Representative of general medicine patients, the most common principal discharge diagnoses in our dataset were pneumonia, cellulitis, altered mental status, sepsis, and abdominal pain.

Overall, 5541 (50.6%) patients who received opioids in the last 24 hours of their hospitalization received an opioid prescription at discharge. There were significant differences among racial/ethnic groups receiving an opioid prescription at discharge. Black patients were less likely to be discharged with an opioid compared with White patients (47.7% vs 50.3%; P < .001) (Table 2). The median discharge prescription duration for all patients was 9.3 days (interquartile range [IQR], 3.8-20.0). Black patients received the fewest median days of opioids at 7.5 days (IQR, 3.2-16.7) compared with White patients at 8.8 days (IQR, 3.7-20.0; P < .001) (Table 2).

Adjusted Regression Results

Demographic, clinical, and diagnosis specific factors were significantly associated with opioid prescriptions, including previous opioid use, sex, and a concurrent cancer diagnosis. There were fewer opioid prescriptions over time (Figure).

Following multivariable logistic regression for the association between race/ethnicity and opioid on discharge and controlling for covariates, we found that Black patients were less likely to receive an opioid prescription on discharge compared with White patients (predicted population rate, 47.6% vs 50.7%; AME −3.1%; 95% CI, −5.5% to −0.8%). Asian patients were more likely to receive a prescription on discharge compared with White patients (predicted population rate, 55.6% vs 50.7%; AME +4.9; 95% CI, 1.5%-8.3%).

Following multivariable negative binomial regression for the association between race/ethnicity and the number of opioid days on discharge, we found that Black patients received a shorter duration of opioid days compared with White patients (predicted days of opioids on discharge, 15.7 days vs 17.8 days; AME −2.1 days; 95% CI, −3.3 to −0.87) (Table 3). There were no significant differences among patients and the other racial/ethnic groups.

Our secondary analysis from the negative binomial regression with the days of opioids supplied metric yielded similar results to our primary analysis showing that Black patients received statically significantly fewer days of opioid therapy compared with White patients (Appendix Table 2).

Subgroup Regression Results

After testing for effect modification, which was negative, we examined the relationships for patients started on opioids during their hospitalization (Appendix Table 3 and Appendix Table 4). There were 5101 patients with newly prescribed opioids during their hospitalization. Adjusting for covariates, we found that Black patients were less likely to receive opioids at discharge compared with White patients (predicted population rate, 34.9% vs 40.4%; AME −5.5%; 95% CI, −9.2% to −1.9%). American Indian or Alaska Native patients were more likely to receive opioids on discharge (predicted population rate, 58.3% vs 40.4%; AME +17.9%; 95% CI, 1.0%-34.8%). We also found that Asian patients received more days of opioids on discharge (predicted days of opioid on discharge, 16.7 vs 13.7 days; AME +3.0 days; 95% CI, 0.6-5.3 days) (Appendix Table 4, Appendix Figure 2).

We found that Black patients discharged from the general medicine service were less likely to receive opioids and received shorter courses on discharge compared with White patients, adjusting for demographic, hospitalization, and medical diagnosis variables. Asian patients were more likely to receive an opioid prescription at discharge—a finding not reported in the literature on opioid prescribing disparities in most other practice settings.¹

Previous studies have shown racial disparities in pain management in emergency and surgical settings, but these relationships have not been characterized in an inpatient medicine population. Medicine patients comprise the majority of admitted patients in the United States and reflect a wide diversity of medical conditions, many requiring opioids for pain management. Determining the etiology of these differential prescribing patterns was not within the scope of our study, but earlier studies demonstrate a number of reasons why these patterns exist across racial and ethnic groups in other practice settings.^23,24 These reports give us insight into potential mechanisms for our study population.

Differences in pain management likely represent the multiple structural mechanisms by which racism operates.¹⁷ Drawing from the existing literature and the socioecological model, we hypothesize the ways that individual, interpersonal relationships, organizations, communities, and public policy impact opioid prescribing.^25,26 Using this model and considering the framework of Critical Race Theory (CRT), we can work towards understanding how race and ethnicity stand in as surrogates for racism and how this manifests in different outcomes and identify areas for intervention. CRT draws attention to race consciousness, contemporary orientation, centering in the margins, and praxis. In the context of this analysis, we recognize race consciousness and the interactions among factors such as race/ethnicity, language, and diagnoses such as PTSD.²⁷ This approach is necessary because racism is a multilevel construct influenced by macrolevel factors.²⁸

Individually and interpersonally, there is clinician-driven bias in pain assessment, which is activated under times of stress and diagnostic uncertainty and is amplified by a lack of clear guidelines for pain management prescriptions.^23,29-32 Institutional and organizational culture contribute to disparities through ingrained culture, practice patterns, and resource allocation.^29,33 Last, public policy and the larger sociopolitical environment worsen disparities through nondiverse workforces, state and federal guidelines, criminal justice policy, supply chain regulation, and access to care.

As individual clinicians, departments, and health systems leaders, we must identify areas for intervention. At the individual and interpersonal levels, there is evidence that taking implicit association tests could help clinicians become more aware of their negative associations, and empathy-inducing, perspective-taking interventions can reduce pain treatment bias.^31,34 At the institutional level, we must report data on disparities, create guidelines for pain management, and reevaluate the educational curriculum and culture to assess how certain biases could be propagated. The lack of straightforward guidelines leads to unclear indications for opioid prescriptions, exacerbating provider-level differences in prescribing. At the policy level, legislation that promotes workplace diversity, increases training for and access to pain specialists, and incentivizes data collection and reporting could help reduce disparities.³⁵ Equitable access to prescriptions and care is essential. Pharmacies often understock opioids in minority neighborhoods, meaning that even if a patient is prescribed an opioid on discharge, he or she might have difficulty filling the prescription.³⁶

One could question whether fewer opioid prescriptions for Black patients protects against the harms of opioid overprescribing, and therefore is not reflective of harmful inequity.³⁷ Ongoing national programs aim to reduce the harmful effects of opioids, which is reflected in the reduction in opioid prescribing over time in our institution. Our point is that differences in prescribing could reflect practices that do result in patient harm, such as less adequately controlled pain among Black patients.^1,3 Undertreated pain has negative health and social consequences and further contributes to substance-use stigma within minority communities.³⁸ Moreover, Black people who describe more discrimination in medical settings were more likely to report subsequent opioid misuse.³⁹

Although the above mechanisms might partially explain our findings among Black patients, the higher rate of prescribing for Asian patients is more challenging to explain. Our models adjusted for clinical factors. Notably, our Asian patients had the highest baseline comorbidity index, oldest mean age, and highest cancer rates, and it is possible that we were unable to fully account for illness severity or related pain needs (Table 1). It also is possible—although speculative—that factors such as language, provider concordance, and the type of disease process all contribute.⁴⁰ Some researchers have proposed a “stereotype content model” that seeks to establish a pathway among social structure (status of a patient) to clinician stereotypes (is this patient warm and/or competent) to emotional prejudices (envy, pride) and ultimately to discrimination (active/passive, help/harm).²³Our study has limitations. Our model was limited by the available data collected on our patients. Covariates including primary care follow-up, pain scores, and overdose history were not available. Furthermore, our categorization of race/ethnicity was based on self-reported data. We had 676 patients with race/ethnicity specified as other/unknown. We recognize the heterogeneity within these racial/ethnic categorizations. For example, within the LatinX or Asian communities, there are large differences based on region, country, ethnic, or cultural groups. Our study only included patients presenting to a hospital in San Francisco, which is different from the racial/ethnic makeup of other cities across the nation. Our electronic health record capture of history of opioid use disorder and mood disorders is contingent on individual clinician documentation. We did not account for provider-level differences, which is an important part of variation in prescribing differences. We also did not examine differences at the diagnosis-specific level. Finally, we could not determine the indication or appropriateness of opioid prescriptions.

Future studies will be necessary to characterize this relationship at a diagnosis-specific level and to describe causal pathways. Within our own institution, these findings present an opportunity for positive change. We hope to continue to explore the etiology of these disparities and identify areas where differences could impact patient outcomes, such as pain control. It is essential to develop appropriate recommendations for inpatient and discharge opioid prescribing to help minimize disparities and to mitigate potential harms of overprescribing. All health systems should continue to collect data on their own disparities in opioid prescribing and educate clinicians on promoting more equitable practices.

The authors thank Sneha Daya, MD, Sachin Shah, MD, MPH, and the UCSF Division of Hospital Medicine Data Core.

Communication has always played a central role in facilitating technological advances and social progress. The printing press, mail, telegraph, radio, television, electronic mail, and social media have all allowed for the exchange of ideas that led to progress, and have done so with increasing speed. But some people are beginning to question whether we are experiencing diminishing returns from making such communication easier, faster, and more widespread. Disinformation, conspiracies, inappropriate messages, and personal attacks are just as easy to communicate as truth, good ideas, and empathy. In many cases, truth and falsehood are nearly indistinguishable. Raw, nasty emotions contained in personal attacks are often provocative, thus generating even more engagement, which many people view as the purpose of social media. In this context, it is more important than ever for trusted voices, such as those of scientists and physicians, to play a role in the public sphere.

In this essay, we offer our personal recommendations on how healthcare professionals, who in our view have outsized authority and responsibility on healthcare topics, might improve communication on social media. We focus particularly on Twitter given its prominent role in the public exchange of ideas and its recognized benefits (and challenges) for scientific communication.¹ We make these recommendations with some trepidation because we are sure readers will be able to find times when we have not followed our own advice. And we are sure many will disagree or feel that our advice raises the bar too high. We divide our recommendations into lists of Do’s and Don’ts. Let’s start with the Do’s.

DO separate facts from inferences, ideally labeling them as such. For example, you can report that public health has found five cases of the delta variant in people in a specific nursing home as a fact. You might then infer that the variant is widespread in that facility, and that community spread in the region is likely. Stating the source of your facts helps the reader evaluate their reliability and precision.

DO state when you are quoting preliminary evidence. If posting a preprint, press release, or other non-peer-reviewed paper (even if it is your own!), make its preliminary status clear to the reader (Figure, part A).

DO read the full article before posting. If you are posting an article, make sure you understand the whole context of any results you are highlighting. Avoid exaggerating, fear-mongering, or selectively picking facts or results to bolster your opinion.DO seek to add value to the public discourse. Rather than simply retweeting popular posts, consider taking the time to collate evidence (including contrary evidence) into a thread if seeking to prove a point or to teach, especially when it relates to something in your field. You likely are more knowledgeable about topics in your field than 99% of readers; use Twitter to spread your expertise. Clinical “tweetorials,” such as those popularized by @tony_breu, can be very effective teaching tools (Figure, part B).

DO make recommendations as specific as possible. If your goal is to improve adherence to evidence-based medicine or support disadvantaged people, be explicit about how you would achieve these goals. Tell readers exactly what you have in mind so that individuals and leaders can operationalize the recommendations. Use threads to expand on your advice and its rationale.

DO consider engaging with misinformation. We suggest doing so if the misinformation is posted by someone prominent who is likely to have broad reach, but only once per post and in a factual manner. You are unlikely to convince persons who post disinformation that they are wrong; extended arguments are unhelpful. Your role here is simply to inform readers of the post, who may be more open to reason. Occasionally, you may even convince the initial poster, as seen in Figure, part C, to delete certain misinformation. But don’t count on it.

DO consider your obligation to the general public. It is fine to engage explicitly with the medical community (ie, through tweetchats),² but also consider that your comments will be accessible to everyone. Now more than ever the public is looking to healthcare professionals for clarity, reassurance, and evidence about medical matters.

DO acknowledge when you were wrong. Update your opinions as facts change or when you realize you made a mistake. The COVID-19 pandemic has brought home the rapidity with which we can gain scientific knowledge. Many of the things we thought were right early on—and posted about on Twitter—we now know to be wrong. Be forthright about this, while making it clear that the fact that we know more now doesn’t mean no information can be trusted. (A corollary: Don’t overstate what we know to be true at any time, so that it does not feel as much of a surprise if we later learn more and need to revise an opinion or a statement.)

DO be kind. This is perhaps the most important thing. We are all experiencing stress as physicians, parents, children, and colleagues. Spend your time focusing on people’s actions rather than impugning their motives or intelligence. Most of the time you don’t really know what their motives are. We recognize that kindness may not generate the same amount of engagement as sarcasm, but at least take time to consider whether you want to be seen as mean-spirited forever.

DO pause before sending. Twitter creates a false perception of the need for speed (and doesn’t really lend itself to revising drafts). But in reality, there is no rush. The torrent of Twitter posts means that people typically only see what has been posted around the time they log in; an early post is not necessarily more likely to be noticed. So, take your time and avoid falling into a trap of writing something you will regret, or, in extreme cases, that will get you fired or otherwise ruin your career. There is no rush to be first; Twitter will still be there tomorrow.

For some time, mentors have warned physicians (and others whose careers depend on their reputation) to be careful in their use of social media. Electronic dissemination of inappropriate words or images can come back to haunt people—sometimes immediately, sometimes many years later.³ Physicians are also at risk of falling into some pitfalls specific to the profession. That said, here are some Don’ts to avoid or be cautious about.

DON’T reveal information about patients in a recognizable fashion. Journals ask for written consent from patients when authors submit a manuscript about individual cases so readers can be sure consent has been obtained. The same standard should apply to social media; if not, you are clearly violating a professional standard. Yet, on Twitter, people may assume you have not obtained consent, conveying a false sense of invasion of privacy and undermining confidence in the profession. The safest thing to do is not tell stories about patients, or to completely disguise the story so even the patients can’t recognize themselves. If you do choose to post about a patient, obtain written permission that you save, and clearly indicate that you have that permission in the Tweet.

DON’T claim to have expertise in areas where you have little training or education. For example, just because you are an expert in critical care and have seen the ravages of COVID-19 on your patients doesn’t mean you are an expert in how to stop a pandemic, though your observations may be helpful to those who are. This does not mean you shouldn’t speak out on important moral issues like climate change, nuclear war, or injustices, which clearly reflect personal opinion and values. Rather, be cautious about commenting authoritatively on areas in which the lay reader might mistakenly think you have specific expertise.

DON’T make yourself the hero of every story. Implicitly seeking praise for doing your job (Look at me, I’m working on Christmas!) may breed resentment and undercut professionalism. Rather, state what it is about your job that works well and what doesn’t (for example, teaching tips, wellness advice, and organizational strategies) in a way that helps others emulate your successes.

DON’T let emotions get the better of you. This past year has been full of outrageous and appalling events and behavior. We do not suggest that you ignore these. Rather, make sure that if you are blaming an individual for something that it really was their fault, because they had control of the factors that led to the disastrous outcome. Consider focusing on systemic and structural explanations for unacceptable phenomena to minimize defensiveness and maximize the potential for identifying solutions. And yes, sometimes you just have to let it rip, but be selective—maybe show your post to someone else and sleep on it before you send it.

We hope that you will find these suggestions helpful in both creating and reading social media posts on important topics. We recognize that some people like the spontaneity of the social media platform and will thus find our suggestions stunting. But at least everyone ought to consider what they are trying to achieve when they make public statements. The exchange of ideas has always been a key ingredient in creating progress. Let’s optimize the usefulness of those exchanges for that purpose, and to promote knowledge and science in a way that helps us all live healthier and happier lives.

Communication has always played a central role in facilitating technological advances and social progress. The printing press, mail, telegraph, radio, television, electronic mail, and social media have all allowed for the exchange of ideas that led to progress, and have done so with increasing speed. But some people are beginning to question whether we are experiencing diminishing returns from making such communication easier, faster, and more widespread. Disinformation, conspiracies, inappropriate messages, and personal attacks are just as easy to communicate as truth, good ideas, and empathy. In many cases, truth and falsehood are nearly indistinguishable. Raw, nasty emotions contained in personal attacks are often provocative, thus generating even more engagement, which many people view as the purpose of social media. In this context, it is more important than ever for trusted voices, such as those of scientists and physicians, to play a role in the public sphere.

In this essay, we offer our personal recommendations on how healthcare professionals, who in our view have outsized authority and responsibility on healthcare topics, might improve communication on social media. We focus particularly on Twitter given its prominent role in the public exchange of ideas and its recognized benefits (and challenges) for scientific communication.¹ We make these recommendations with some trepidation because we are sure readers will be able to find times when we have not followed our own advice. And we are sure many will disagree or feel that our advice raises the bar too high. We divide our recommendations into lists of Do’s and Don’ts. Let’s start with the Do’s.

DO separate facts from inferences, ideally labeling them as such. For example, you can report that public health has found five cases of the delta variant in people in a specific nursing home as a fact. You might then infer that the variant is widespread in that facility, and that community spread in the region is likely. Stating the source of your facts helps the reader evaluate their reliability and precision.

DO state when you are quoting preliminary evidence. If posting a preprint, press release, or other non-peer-reviewed paper (even if it is your own!), make its preliminary status clear to the reader (Figure, part A).

DO read the full article before posting. If you are posting an article, make sure you understand the whole context of any results you are highlighting. Avoid exaggerating, fear-mongering, or selectively picking facts or results to bolster your opinion.DO seek to add value to the public discourse. Rather than simply retweeting popular posts, consider taking the time to collate evidence (including contrary evidence) into a thread if seeking to prove a point or to teach, especially when it relates to something in your field. You likely are more knowledgeable about topics in your field than 99% of readers; use Twitter to spread your expertise. Clinical “tweetorials,” such as those popularized by @tony_breu, can be very effective teaching tools (Figure, part B).

DO make recommendations as specific as possible. If your goal is to improve adherence to evidence-based medicine or support disadvantaged people, be explicit about how you would achieve these goals. Tell readers exactly what you have in mind so that individuals and leaders can operationalize the recommendations. Use threads to expand on your advice and its rationale.

DO consider engaging with misinformation. We suggest doing so if the misinformation is posted by someone prominent who is likely to have broad reach, but only once per post and in a factual manner. You are unlikely to convince persons who post disinformation that they are wrong; extended arguments are unhelpful. Your role here is simply to inform readers of the post, who may be more open to reason. Occasionally, you may even convince the initial poster, as seen in Figure, part C, to delete certain misinformation. But don’t count on it.

DO consider your obligation to the general public. It is fine to engage explicitly with the medical community (ie, through tweetchats),² but also consider that your comments will be accessible to everyone. Now more than ever the public is looking to healthcare professionals for clarity, reassurance, and evidence about medical matters.

DO acknowledge when you were wrong. Update your opinions as facts change or when you realize you made a mistake. The COVID-19 pandemic has brought home the rapidity with which we can gain scientific knowledge. Many of the things we thought were right early on—and posted about on Twitter—we now know to be wrong. Be forthright about this, while making it clear that the fact that we know more now doesn’t mean no information can be trusted. (A corollary: Don’t overstate what we know to be true at any time, so that it does not feel as much of a surprise if we later learn more and need to revise an opinion or a statement.)

DO be kind. This is perhaps the most important thing. We are all experiencing stress as physicians, parents, children, and colleagues. Spend your time focusing on people’s actions rather than impugning their motives or intelligence. Most of the time you don’t really know what their motives are. We recognize that kindness may not generate the same amount of engagement as sarcasm, but at least take time to consider whether you want to be seen as mean-spirited forever.

DO pause before sending. Twitter creates a false perception of the need for speed (and doesn’t really lend itself to revising drafts). But in reality, there is no rush. The torrent of Twitter posts means that people typically only see what has been posted around the time they log in; an early post is not necessarily more likely to be noticed. So, take your time and avoid falling into a trap of writing something you will regret, or, in extreme cases, that will get you fired or otherwise ruin your career. There is no rush to be first; Twitter will still be there tomorrow.

For some time, mentors have warned physicians (and others whose careers depend on their reputation) to be careful in their use of social media. Electronic dissemination of inappropriate words or images can come back to haunt people—sometimes immediately, sometimes many years later.³ Physicians are also at risk of falling into some pitfalls specific to the profession. That said, here are some Don’ts to avoid or be cautious about.

DON’T reveal information about patients in a recognizable fashion. Journals ask for written consent from patients when authors submit a manuscript about individual cases so readers can be sure consent has been obtained. The same standard should apply to social media; if not, you are clearly violating a professional standard. Yet, on Twitter, people may assume you have not obtained consent, conveying a false sense of invasion of privacy and undermining confidence in the profession. The safest thing to do is not tell stories about patients, or to completely disguise the story so even the patients can’t recognize themselves. If you do choose to post about a patient, obtain written permission that you save, and clearly indicate that you have that permission in the Tweet.

DON’T claim to have expertise in areas where you have little training or education. For example, just because you are an expert in critical care and have seen the ravages of COVID-19 on your patients doesn’t mean you are an expert in how to stop a pandemic, though your observations may be helpful to those who are. This does not mean you shouldn’t speak out on important moral issues like climate change, nuclear war, or injustices, which clearly reflect personal opinion and values. Rather, be cautious about commenting authoritatively on areas in which the lay reader might mistakenly think you have specific expertise.

DON’T make yourself the hero of every story. Implicitly seeking praise for doing your job (Look at me, I’m working on Christmas!) may breed resentment and undercut professionalism. Rather, state what it is about your job that works well and what doesn’t (for example, teaching tips, wellness advice, and organizational strategies) in a way that helps others emulate your successes.

DON’T let emotions get the better of you. This past year has been full of outrageous and appalling events and behavior. We do not suggest that you ignore these. Rather, make sure that if you are blaming an individual for something that it really was their fault, because they had control of the factors that led to the disastrous outcome. Consider focusing on systemic and structural explanations for unacceptable phenomena to minimize defensiveness and maximize the potential for identifying solutions. And yes, sometimes you just have to let it rip, but be selective—maybe show your post to someone else and sleep on it before you send it.

We hope that you will find these suggestions helpful in both creating and reading social media posts on important topics. We recognize that some people like the spontaneity of the social media platform and will thus find our suggestions stunting. But at least everyone ought to consider what they are trying to achieve when they make public statements. The exchange of ideas has always been a key ingredient in creating progress. Let’s optimize the usefulness of those exchanges for that purpose, and to promote knowledge and science in a way that helps us all live healthier and happier lives.

Communication has always played a central role in facilitating technological advances and social progress. The printing press, mail, telegraph, radio, television, electronic mail, and social media have all allowed for the exchange of ideas that led to progress, and have done so with increasing speed. But some people are beginning to question whether we are experiencing diminishing returns from making such communication easier, faster, and more widespread. Disinformation, conspiracies, inappropriate messages, and personal attacks are just as easy to communicate as truth, good ideas, and empathy. In many cases, truth and falsehood are nearly indistinguishable. Raw, nasty emotions contained in personal attacks are often provocative, thus generating even more engagement, which many people view as the purpose of social media. In this context, it is more important than ever for trusted voices, such as those of scientists and physicians, to play a role in the public sphere.

In this essay, we offer our personal recommendations on how healthcare professionals, who in our view have outsized authority and responsibility on healthcare topics, might improve communication on social media. We focus particularly on Twitter given its prominent role in the public exchange of ideas and its recognized benefits (and challenges) for scientific communication.¹ We make these recommendations with some trepidation because we are sure readers will be able to find times when we have not followed our own advice. And we are sure many will disagree or feel that our advice raises the bar too high. We divide our recommendations into lists of Do’s and Don’ts. Let’s start with the Do’s.

DO separate facts from inferences, ideally labeling them as such. For example, you can report that public health has found five cases of the delta variant in people in a specific nursing home as a fact. You might then infer that the variant is widespread in that facility, and that community spread in the region is likely. Stating the source of your facts helps the reader evaluate their reliability and precision.

DO state when you are quoting preliminary evidence. If posting a preprint, press release, or other non-peer-reviewed paper (even if it is your own!), make its preliminary status clear to the reader (Figure, part A).

DO read the full article before posting. If you are posting an article, make sure you understand the whole context of any results you are highlighting. Avoid exaggerating, fear-mongering, or selectively picking facts or results to bolster your opinion.DO seek to add value to the public discourse. Rather than simply retweeting popular posts, consider taking the time to collate evidence (including contrary evidence) into a thread if seeking to prove a point or to teach, especially when it relates to something in your field. You likely are more knowledgeable about topics in your field than 99% of readers; use Twitter to spread your expertise. Clinical “tweetorials,” such as those popularized by @tony_breu, can be very effective teaching tools (Figure, part B).

DO make recommendations as specific as possible. If your goal is to improve adherence to evidence-based medicine or support disadvantaged people, be explicit about how you would achieve these goals. Tell readers exactly what you have in mind so that individuals and leaders can operationalize the recommendations. Use threads to expand on your advice and its rationale.

DO consider engaging with misinformation. We suggest doing so if the misinformation is posted by someone prominent who is likely to have broad reach, but only once per post and in a factual manner. You are unlikely to convince persons who post disinformation that they are wrong; extended arguments are unhelpful. Your role here is simply to inform readers of the post, who may be more open to reason. Occasionally, you may even convince the initial poster, as seen in Figure, part C, to delete certain misinformation. But don’t count on it.

DO consider your obligation to the general public. It is fine to engage explicitly with the medical community (ie, through tweetchats),² but also consider that your comments will be accessible to everyone. Now more than ever the public is looking to healthcare professionals for clarity, reassurance, and evidence about medical matters.

DO acknowledge when you were wrong. Update your opinions as facts change or when you realize you made a mistake. The COVID-19 pandemic has brought home the rapidity with which we can gain scientific knowledge. Many of the things we thought were right early on—and posted about on Twitter—we now know to be wrong. Be forthright about this, while making it clear that the fact that we know more now doesn’t mean no information can be trusted. (A corollary: Don’t overstate what we know to be true at any time, so that it does not feel as much of a surprise if we later learn more and need to revise an opinion or a statement.)

DO be kind. This is perhaps the most important thing. We are all experiencing stress as physicians, parents, children, and colleagues. Spend your time focusing on people’s actions rather than impugning their motives or intelligence. Most of the time you don’t really know what their motives are. We recognize that kindness may not generate the same amount of engagement as sarcasm, but at least take time to consider whether you want to be seen as mean-spirited forever.

DO pause before sending. Twitter creates a false perception of the need for speed (and doesn’t really lend itself to revising drafts). But in reality, there is no rush. The torrent of Twitter posts means that people typically only see what has been posted around the time they log in; an early post is not necessarily more likely to be noticed. So, take your time and avoid falling into a trap of writing something you will regret, or, in extreme cases, that will get you fired or otherwise ruin your career. There is no rush to be first; Twitter will still be there tomorrow.

For some time, mentors have warned physicians (and others whose careers depend on their reputation) to be careful in their use of social media. Electronic dissemination of inappropriate words or images can come back to haunt people—sometimes immediately, sometimes many years later.³ Physicians are also at risk of falling into some pitfalls specific to the profession. That said, here are some Don’ts to avoid or be cautious about.

DON’T reveal information about patients in a recognizable fashion. Journals ask for written consent from patients when authors submit a manuscript about individual cases so readers can be sure consent has been obtained. The same standard should apply to social media; if not, you are clearly violating a professional standard. Yet, on Twitter, people may assume you have not obtained consent, conveying a false sense of invasion of privacy and undermining confidence in the profession. The safest thing to do is not tell stories about patients, or to completely disguise the story so even the patients can’t recognize themselves. If you do choose to post about a patient, obtain written permission that you save, and clearly indicate that you have that permission in the Tweet.

DON’T claim to have expertise in areas where you have little training or education. For example, just because you are an expert in critical care and have seen the ravages of COVID-19 on your patients doesn’t mean you are an expert in how to stop a pandemic, though your observations may be helpful to those who are. This does not mean you shouldn’t speak out on important moral issues like climate change, nuclear war, or injustices, which clearly reflect personal opinion and values. Rather, be cautious about commenting authoritatively on areas in which the lay reader might mistakenly think you have specific expertise.

DON’T make yourself the hero of every story. Implicitly seeking praise for doing your job (Look at me, I’m working on Christmas!) may breed resentment and undercut professionalism. Rather, state what it is about your job that works well and what doesn’t (for example, teaching tips, wellness advice, and organizational strategies) in a way that helps others emulate your successes.

DON’T let emotions get the better of you. This past year has been full of outrageous and appalling events and behavior. We do not suggest that you ignore these. Rather, make sure that if you are blaming an individual for something that it really was their fault, because they had control of the factors that led to the disastrous outcome. Consider focusing on systemic and structural explanations for unacceptable phenomena to minimize defensiveness and maximize the potential for identifying solutions. And yes, sometimes you just have to let it rip, but be selective—maybe show your post to someone else and sleep on it before you send it.

We hope that you will find these suggestions helpful in both creating and reading social media posts on important topics. We recognize that some people like the spontaneity of the social media platform and will thus find our suggestions stunting. But at least everyone ought to consider what they are trying to achieve when they make public statements. The exchange of ideas has always been a key ingredient in creating progress. Let’s optimize the usefulness of those exchanges for that purpose, and to promote knowledge and science in a way that helps us all live healthier and happier lives.

This icon represents the patient’s case. Each paragraph that follows represents the discussant’s thoughts.

A 32-year-old, previously healthy woman presented to the emergency department (ED) with 3 days of nasal pain, congestion, and cough. A day prior, she had consulted with her primary care provider by phone and had been prescribed amoxicillin-clavulanate for presumed bacterial sinusitis. She subsequently developed fever (39 oC) and pleuritic, left-upper-quadrant abdominal pain. In the ED, chest radiograph demonstrated right hilar opacification. Laboratory studies and computed tomography (CT) of the abdomen and pelvis did not identify a cause for her pain. Given the pleuritic nature of her left-upper-quadrant pain, CT pulmonary angiography was ordered. The CT revealed “mass-like” right hilar opacification and lymphadenopathy. No pulmonary emboli were identified. Levofloxacin was prescribed for presumed pneumonia, and the patient was discharged home. The following week, mediastinal biopsy was arranged for evaluation of the right hilar abnormality.

This is a young woman presenting with upper respiratory symptoms, abdominal pain, fever, and hilar lymphadenopathy. Upper respiratory symptoms are common and usually indicate an inflammatory response to allergens or infection, though autoimmune disorders may affect the upper airways. Fever and hilar lymphadenopathy likely also signify an inflammatory response. Taken together, these findings can be associated with mycobacterial or fungal infection, malignancy, and, particularly in a young woman, sarcoidosis, which could explain her abdominal pain if her presentation included splenomegaly. At this point she likely has a systemic illness involving at least the upper, and possibly the lower, respiratory tract.

Within days, her symptoms resolved. Mediastinal biopsy of the hilar node revealed scant pus. Pathology demonstrated suppurative granulomata. Gram stain; bacterial, mycobacterial, and fungal cultures; and 16S ribosomal analyses for bacteria and fungi from the biopsy were unrevealing. For unclear reasons, prior to the biopsy, she was given intramuscular Haemophilus influenzae type B and tetanus, diphtheria, and pertussis vaccines. Two weeks later, she presented again with fever and left-upper-quadrant pain as well as painful skin nodules at her biopsy and vaccination sites. She was admitted for further evaluation. Chest CT showed expansion of the mediastinal lesion and splenic enlargement. Biopsy of a skin lesion revealed suppurative granulomatous dermatitis and panniculitis. Repeat blood cultures were negative, though serum β-D-glucan was weakly positive at 173 pg/mL (reference range, <60 pg/mL). Tissue cultures and Gram, acid-fast, Fite, and Warthin-Starry stains from the skin biopsy were negative. She was discharged on fluconazole and then readmitted 2 days later with dyspnea, fever, and leukocytosis.

The young woman’s symptoms resolved, only to recur days later; her granulomatous hilar lesions grew larger, and new cutaneous and splenic findings appeared. The granulomatous lesions prompt consideration of infectious, malignant, and immune-mediated processes. The negative cultures make infection less likely, although the elevated β-D-glucan may suggest fungal infection. By description, the skin lesions are consistent with pathergy, a phenomenon characterized by trauma-provoked cutaneous lesions or ulcers, which is associated with numerous syndromes, including Behçet syndrome, inflammatory bowel disease, and neutrophilic dermatoses such as pyoderma gangrenosum (PG) and Sweet syndrome. In addition to details about her medical history, it is important to seek evidence of oral ulcers or vasculitis, as Behçet syndrome may be associated with cutaneous, visceral, and ophthalmologic vasculitis.

Her medical history included hypertension and active, 10-pack-year cigarette use. During childhood, she had occasional ingrown hairs and folliculitis. She did not take medications prior to this acute illness. Family history was notable for cardiovascular disease. She rarely consumed alcohol and did not use illicit drugs. She lived in a rural town in the mid–Willamette Valley of Oregon and worked as an administrative assistant. She spent time outdoors, including trail running and golfing. A case of tularemia was recently reported in an area near her home. Her only travel outside of Oregon was to Puerto Vallarta, Mexico, 16 years previously. She grew up on a farm and had no known tuberculosis exposure.

Tularemia is an interesting diagnostic consideration and could explain her fever, cutaneous lesions, and hilar adenopathy. It is plausible that she had clinically mild pneumonic tularemia at the outset and that her cutaneous lesions are variants of ulceroglandular tularemia. Positive antibodies for Francisella tularensis would be expected if this were the cause of her illness. The ingrown hairs raise the possibility of a primary immune deficiency syndrome predisposing her to abscesses. However, they seem to have been of trivial significance to her, making an immune deficiency syndrome unlikely.

On readmission, she was afebrile, normotensive, and tachycardic (114 beats/min), with a normal respiratory rate and oxygen saturation. She was not ill appearing. She had noninjected conjunctiva and no oral lesions. Apart from tachycardia, cardiovascular examination was unremarkable. Abdominal examination was notable for mild distension and a palpable, tender spleen. Musculoskeletal and neurologic examinations were normal. Her skin was notable for various sized (8 cm × 4 cm to 10 cm × 15 cm) painful ulcers with violaceous, friable borders—some with fluctuance and purulent drainage—on her right hand, bilateral arms, right axilla, sternum, and legs (Figure 1).

Laboratory studies were notable for normocytic anemia (hemoglobin, 8.9 g/dL; range, 12.0-16.0 g/dL), leukocytosis (white blood cells, 24,900/µL; range, 4500-11,000/µL), thrombocytosis (platelet count, 690,000/µL; range, 150,000-400,000/µL), and elevated inflammatory markers (C-reactive protein, 33 mg/dL; range, <0.5 mg/dL; erythrocyte sedimentation rate, 78 mm/h; range, <20 mm/h). A complete metabolic panel was within normal limits. Repeat blood cultures and β -D-glucan and 16S ribosomal assays were negative. Polymerase chain reaction testing for Bartonella henselae was negative. Urine probes for Neisseria gonorrhoeae and Chlamydia trachomatis were negative. Rapid plasma regain (RPR) was negative. Antibodies to toxoplasmosis, histoplasmosis, blastomycosis, and aspergillosis were unrevealing. A Coccidioides test by immunodiffusion was negative. Serum antigen tests for Cryptococcus and Epstein-Barr virus (EBV) were negative. EBV, HIV, and hepatitis antibody tests were negative. Rheumatologic studies, including antinuclear, anti-double-stranded DNA, anti-Smith, anti–Sjögren syndrome antigens A and B, anticentromere, anti-topoisomerase (anti-Scl-70), anti-histidyl-transfer-RNA-synthetase (anti-Jo-1), and anti-nucleosome (anti-chromatic) antibodies, were unrevealing. Levels of angiotensin-converting enzyme, rheumatoid factor, complement, cytoplasmic, and perinuclear antineutrophil cytoplasmic antibodies were also normal. A neutrophil oxidative burst test was negative. In addition, peripheral flow cytology and serum and urine protein electrophoresis were negative. Chest CT revealed bilateral lower lobe consolidations concerning for necrotizing pneumonia, splenic enlargement, numerous hypodense splenic lesions, and a 1.3-cm right hilar node, which had decreased in size compared with 1 month prior.

In summary, the patient presented with recurrent upper respiratory symptoms, fever, and abdominal pain; expanding granulomatous hilar lesions, splenomegaly, and cutaneous lesions consistent with pathergy; elevated inflammatory markers and leukocytosis; and a possible exposure to F tularensis. She has had extensive negative infectious workups, except for a weakly positive β-D-glucan, and completed several courses of apparently unhelpful antimicrobials. At this point, the most notable findings are her splenomegaly and inflammatory masses suggesting an inflammatory process, which may be autoimmune in nature. Both vasculitis and sarcoidosis remain possibilities, and malignancy is possible. Given her possible exposure to F tularensis, obtaining serum antibodies to F tularensis, in addition to biopsies of the skin lesions, is advisable.

Laboratory studies revealed a positive F tularensis antibody with a titer of 1:320 and an IgM of 7 U/mL and IgG of 30 U/mL. This was repeated, revealing a titer of 1:540 and an IgM and IgG of 5 U/mL and 20 U/mL, respectively. Given the potential exposure history, the clinical syndrome compatible with tularemia, and an otherwise extensive yet unrevealing evaluation, she was treated with a 10-day course of streptomycin. Her fever persisted, and the splenic lesions increased in size and number, prompting addition of moxifloxacin without apparent benefit. Skin biopsies taken from the patient’s arm were notable for nodular, suppurative, neutrophilic infiltrates and histiocytes in the medium and deep dermis without multinucleated histiocytes or evidence of vasculitis. Fungal, mycobacterial, and bacterial stains from the biopsy were negative. The findings were consistent with but not diagnostic of an acute neutrophilic dermatosis.

At this point, the patient has a confirmed exposure to F tularensis; she also has persistent fever, progressive splenomegaly, and new skin biopsies consistent with neutrophilic dermatosis. Despite the F tularensis antibody positivity, her negative cultures and lack of improvement with multiple courses of antimicrobials argue against an infectious etiology. Accordingly, malignancy should be considered but seems less likely given that no laboratory, imaging, or tissue samples support it. This leaves immune-mediated etiologies, especially autoimmune conditions associated with neutrophilic dermatoses, as the most likely explanation of her inflammatory syndrome. Neutrophilic dermatoses include some vasculitides, Sweet syndrome, PG, Behçet syndrome, and other inflammatory entities. She has no evidence of vasculitis on biopsy. Given the evidence of inflammation and the history of pathergy, Behçet syndrome and PG should be seriously considered.

She underwent incision and drainage of the left leg and mediastinal lesions. A follow-up chest CT revealed stable cutaneous and deep tissue lesions and continued splenic enlargement. She was started on prednisone and dapsone for presumed cutaneous and visceral PG. The lesions improved dramatically and, following a month-long hospitalization, she was discharged on dapsone and a slow prednisone taper. Three weeks after discharge, while on dapsone and prednisone, she developed a new skin lesion. Cyclosporine was added, with improvement. Eight weeks after discharge, she developed fever, acute left-upper-quadrant pain, and marked splenomegaly with abscesses seen on CT imaging (Figure 2).

This continues to be a very puzzling case, and it is worth revisiting her clinical course once again. This is a previously healthy 32-year-old woman with multiple hospital presentations for upper-respiratory symptoms, persistent fever, abdominal pain, and painful cutaneous lesions consistent with pathergy; she was found to have granulomatous hilar lesions, progressive splenomegaly, and skin biopsies consistent with neutrophilic dermatosis. Exhaustive infectious and rheumatologic workup was negative, and no evident malignancy was found. Finally, despite multiple courses of antimicrobials, including standard treatments for tularemia (for which she had positive antibodies), her clinical course failed to improve until the addition of systemic anti-inflammatory agents, which resulted in rapid improvement. She then presented 8 weeks later with recurrent fever and splenomegaly. Given the recurrence and the severity of the splenic pathology, a diagnostic splenectomy is advisable for what appears to be visceral PG. In addition, attempting to identify a trigger of her syndrome is important. PG can be associated with inflammatory bowel disease, hematologic disorders (eg, leukemia, myeloma, myelodysplastic syndrome, and myelofibrosis), and autoimmune diseases, especially inflammatory arthritis.¹ Therefore, a diagnostic colonoscopy and bone marrow biopsy should be considered. With no history or examination supporting inflammatory arthritis and a broad, unrevealing workup, her rheumatologic evaluation is sufficient.

The patient underwent splenectomy. Gross description of the spleen was notable for multiple abscesses, consisting on microscopy of large areas of necrosis with islands of dense neutrophil collections (Figure 3). Microscopic examination failed to demonstrate microorganisms on multiple stains, and there was no microscopic or flow cytometric evidence of lymphoma. The final pathologic diagnosis was multiple sterile splenic abscesses with siderosis, which, in the context of her overall syndrome, was consistent with an entity termed aseptic abscess syndrome (AAS). After discharge, she underwent a slow steroid taper and was ultimately maintained on daily low-dose prednisone. Cyclosporine and dapsone were discontinued in favor of infliximab infusions. She underwent additional diagnostic workup, including an unremarkable colonoscopy and a bone marrow biopsy, which showed monoclonal gammopathy of undetermined significance (MGUS) with an insignificant IgA monoclonal gammopathy. All cutaneous lesions healed. Three years after the splenectomy, while still on infliximab and prednisone, she developed a new aseptic lung abscess, which resolved after increasing her prednisone dose. Six years after splenectomy, she developed an aseptic liver abscess, which resolved after again increasing the frequency of her infliximab infusions.

Diagnostic uncertainty is an intrinsic feature of medical practice—in part because patients often present with undifferentiated and evolving symptoms.² When faced with uncertainty, clinicians are well served by prioritizing a thoughtful differential diagnosis, adopting a stepwise management strategy, and engaging in iterative reassessments of the patient. In this case, a 32-year-old, previously healthy woman presented with an array of symptoms, including abdominal pain, fever, leukocytosis, necrotic skin lesions, necrotizing mediastinal lymphadenitis, pathergy, and splenomegaly. Elements of the history, examination, and diagnostic studies supported a differential diagnosis of tularemia, PG, and AAS. Through stepwise management and ongoing reassessment, she was ultimately diagnosed with AAS.

Tularemia was initially an important diagnostic consideration in this patient, given her potential exposure and positive F tularensis serum antibodies. Francisella tularensis is a Gram-negative coccobacillus found in more than 250 species of fish, ticks, birds, and mammals. In humans, an incubation period of 3 to 5 days is typical. Although clinical manifestations vary, they often include fever, headache, and malaise.³ Other findings may include lymphadenopathy with or without ulcerative cutaneous lesions (glandular or ulceroglandular tularemia) and cough, dyspnea, pleuritic chest pain, and hilar adenopathy (pneumonic tularemia). As noted by the discussant, a pneumonic tularemia syndrome could have explained this patient’s fever, respiratory symptoms, and hilar adenopathy; ulceroglandular tularemia might have explained her cutaneous lesions. Since splenomegaly may be seen in tularemia, this finding was also consistent with the diagnosis. Serum antibody testing is supportive of the diagnosis, while culture confirms it. Standard treatment consists of a 10- to 14-day course of streptomycin, and combination therapy with a fluoroquinolone is recommended in severe cases.⁴ In this patient, however, F tularensis was not demonstrated on culture. Furthermore, she did not experience the expected clinical improvement with treatment. Finally, because both IgG and IgM tularemia antibodies may co-occur up to 10 years following infection, her positive F tularensis serum antibodies did not provide evidence of acute infection.⁵

Recognizing inconsistencies in the diagnosis of tularemia, the focus shifted to PG owing to the patient’s neutrophilic cutaneous lesions, negative infectious workup, and pathergy. Pyoderma gangrenosum is a neutrophilic dermatosis—one of a heterogeneous group of skin conditions characterized by perivascular and diffuse neutrophilic infiltrates without an identifiable infectious agent.⁶ It is a chronic, recurrent cutaneous disease with several variants.⁷ The classic presentation includes painful lower-extremity ulcers with violaceous undermined borders and may be associated with pathergy. Guiding principles for the management of PG include controlling inflammation, optimizing wound healing, and minimizing exacerbating factors.¹ As such, treatment mainstays include local and systemic anti-inflammatory agents and wound care. As the discussant highlighted, in this case the inflammatory skin lesions were suggestive of PG. However, other features of the case, notably, splenomegaly, splenic abscesses, and necrotizing mediastinal lymphadenitis, were more consistent with another diagnosis: AAS. Aseptic abscess syndrome is an autoinflammatory disorder defined by deep, noninfectious abscesses that preferentially affect the spleen.⁸ Additional clinical manifestations include weight loss, fever, abdominal pain, and leukocytosis. Lesions may also affect bone, kidney, liver, lung, lymph node, and skin. In one case series, neutrophilic dermatoses were seen in 20% of AAS cases.⁸ In all cases of AAS, extensive infectious workup is unrevealing, and antibiotics are ineffective. The pathophysiology of AAS is unknown.

Similar to PG, the majority of AAS cases are associated with inflammatory bowel disease, especially Crohn disease.⁹ However, AAS also has associations with conditions such as MGUS, rheumatoid arthritis, spondyloarthritis, and relapsing polychondritis. Histologically, early lesions demonstrate a necrotic core of neutrophils, with or without surrounding palisading histiocytes, and giant cells. In older lesions, neutrophils may be absent; fibrous tissue may be present.⁸ Treatment regimens include splenectomy, corticosteroids, colchicine, thalidomide, tumor necrosis factor (TNF) antagonists, and cyclophosphamide. The discussant astutely recommended a splenectomy for this patient, which was both diagnostic and therapeutic. As in this case, relapse is common. Optimal maintenance therapy is yet to be determined.⁹

Given the overlapping clinical manifestations, shared disease associations, and similar responsiveness to immunosuppression, it is unclear whether AAS represents a new disease entity or a variant of known autoinflammatory disorders. Aseptic abscess syndrome is likely part of a spectrum of autoinflammatory disorders with inflammatory bowel diseases, neutrophilic dermatoses, and other similar diseases.⁸ While infectious visceral abscesses remain more common, this case highlights the clinical manifestation of an emerging and likely underrecognized entity.

• Aseptic abscess syndrome should be considered in patients who present with visceral (particularly splenic) abscesses and negative infectious workup.
• Aseptic abscess syndrome is commonly associated with other autoinflammatory disorders; the majority of reported cases are associated with inflammatory bowel disease, especially Crohn disease.
• Up to 20% of AAS cases are associated with neutrophilic dermatoses such as PG.
• The initial treatment for this syndrome is high-dose intravenous glucocorticoids; maintenance treatment regimens include corticosteroids, colchicine, thalidomide, TNF antagonists, and cyclophosphamide.

The authors would thank Dr Bob Pelz and Dr John Townes for their contributions to the case.

This icon represents the patient’s case. Each paragraph that follows represents the discussant’s thoughts.

A 32-year-old, previously healthy woman presented to the emergency department (ED) with 3 days of nasal pain, congestion, and cough. A day prior, she had consulted with her primary care provider by phone and had been prescribed amoxicillin-clavulanate for presumed bacterial sinusitis. She subsequently developed fever (39 oC) and pleuritic, left-upper-quadrant abdominal pain. In the ED, chest radiograph demonstrated right hilar opacification. Laboratory studies and computed tomography (CT) of the abdomen and pelvis did not identify a cause for her pain. Given the pleuritic nature of her left-upper-quadrant pain, CT pulmonary angiography was ordered. The CT revealed “mass-like” right hilar opacification and lymphadenopathy. No pulmonary emboli were identified. Levofloxacin was prescribed for presumed pneumonia, and the patient was discharged home. The following week, mediastinal biopsy was arranged for evaluation of the right hilar abnormality.

This is a young woman presenting with upper respiratory symptoms, abdominal pain, fever, and hilar lymphadenopathy. Upper respiratory symptoms are common and usually indicate an inflammatory response to allergens or infection, though autoimmune disorders may affect the upper airways. Fever and hilar lymphadenopathy likely also signify an inflammatory response. Taken together, these findings can be associated with mycobacterial or fungal infection, malignancy, and, particularly in a young woman, sarcoidosis, which could explain her abdominal pain if her presentation included splenomegaly. At this point she likely has a systemic illness involving at least the upper, and possibly the lower, respiratory tract.

Within days, her symptoms resolved. Mediastinal biopsy of the hilar node revealed scant pus. Pathology demonstrated suppurative granulomata. Gram stain; bacterial, mycobacterial, and fungal cultures; and 16S ribosomal analyses for bacteria and fungi from the biopsy were unrevealing. For unclear reasons, prior to the biopsy, she was given intramuscular Haemophilus influenzae type B and tetanus, diphtheria, and pertussis vaccines. Two weeks later, she presented again with fever and left-upper-quadrant pain as well as painful skin nodules at her biopsy and vaccination sites. She was admitted for further evaluation. Chest CT showed expansion of the mediastinal lesion and splenic enlargement. Biopsy of a skin lesion revealed suppurative granulomatous dermatitis and panniculitis. Repeat blood cultures were negative, though serum β-D-glucan was weakly positive at 173 pg/mL (reference range, <60 pg/mL). Tissue cultures and Gram, acid-fast, Fite, and Warthin-Starry stains from the skin biopsy were negative. She was discharged on fluconazole and then readmitted 2 days later with dyspnea, fever, and leukocytosis.

The young woman’s symptoms resolved, only to recur days later; her granulomatous hilar lesions grew larger, and new cutaneous and splenic findings appeared. The granulomatous lesions prompt consideration of infectious, malignant, and immune-mediated processes. The negative cultures make infection less likely, although the elevated β-D-glucan may suggest fungal infection. By description, the skin lesions are consistent with pathergy, a phenomenon characterized by trauma-provoked cutaneous lesions or ulcers, which is associated with numerous syndromes, including Behçet syndrome, inflammatory bowel disease, and neutrophilic dermatoses such as pyoderma gangrenosum (PG) and Sweet syndrome. In addition to details about her medical history, it is important to seek evidence of oral ulcers or vasculitis, as Behçet syndrome may be associated with cutaneous, visceral, and ophthalmologic vasculitis.

Her medical history included hypertension and active, 10-pack-year cigarette use. During childhood, she had occasional ingrown hairs and folliculitis. She did not take medications prior to this acute illness. Family history was notable for cardiovascular disease. She rarely consumed alcohol and did not use illicit drugs. She lived in a rural town in the mid–Willamette Valley of Oregon and worked as an administrative assistant. She spent time outdoors, including trail running and golfing. A case of tularemia was recently reported in an area near her home. Her only travel outside of Oregon was to Puerto Vallarta, Mexico, 16 years previously. She grew up on a farm and had no known tuberculosis exposure.

Tularemia is an interesting diagnostic consideration and could explain her fever, cutaneous lesions, and hilar adenopathy. It is plausible that she had clinically mild pneumonic tularemia at the outset and that her cutaneous lesions are variants of ulceroglandular tularemia. Positive antibodies for Francisella tularensis would be expected if this were the cause of her illness. The ingrown hairs raise the possibility of a primary immune deficiency syndrome predisposing her to abscesses. However, they seem to have been of trivial significance to her, making an immune deficiency syndrome unlikely.

On readmission, she was afebrile, normotensive, and tachycardic (114 beats/min), with a normal respiratory rate and oxygen saturation. She was not ill appearing. She had noninjected conjunctiva and no oral lesions. Apart from tachycardia, cardiovascular examination was unremarkable. Abdominal examination was notable for mild distension and a palpable, tender spleen. Musculoskeletal and neurologic examinations were normal. Her skin was notable for various sized (8 cm × 4 cm to 10 cm × 15 cm) painful ulcers with violaceous, friable borders—some with fluctuance and purulent drainage—on her right hand, bilateral arms, right axilla, sternum, and legs (Figure 1).

Laboratory studies were notable for normocytic anemia (hemoglobin, 8.9 g/dL; range, 12.0-16.0 g/dL), leukocytosis (white blood cells, 24,900/µL; range, 4500-11,000/µL), thrombocytosis (platelet count, 690,000/µL; range, 150,000-400,000/µL), and elevated inflammatory markers (C-reactive protein, 33 mg/dL; range, <0.5 mg/dL; erythrocyte sedimentation rate, 78 mm/h; range, <20 mm/h). A complete metabolic panel was within normal limits. Repeat blood cultures and β -D-glucan and 16S ribosomal assays were negative. Polymerase chain reaction testing for Bartonella henselae was negative. Urine probes for Neisseria gonorrhoeae and Chlamydia trachomatis were negative. Rapid plasma regain (RPR) was negative. Antibodies to toxoplasmosis, histoplasmosis, blastomycosis, and aspergillosis were unrevealing. A Coccidioides test by immunodiffusion was negative. Serum antigen tests for Cryptococcus and Epstein-Barr virus (EBV) were negative. EBV, HIV, and hepatitis antibody tests were negative. Rheumatologic studies, including antinuclear, anti-double-stranded DNA, anti-Smith, anti–Sjögren syndrome antigens A and B, anticentromere, anti-topoisomerase (anti-Scl-70), anti-histidyl-transfer-RNA-synthetase (anti-Jo-1), and anti-nucleosome (anti-chromatic) antibodies, were unrevealing. Levels of angiotensin-converting enzyme, rheumatoid factor, complement, cytoplasmic, and perinuclear antineutrophil cytoplasmic antibodies were also normal. A neutrophil oxidative burst test was negative. In addition, peripheral flow cytology and serum and urine protein electrophoresis were negative. Chest CT revealed bilateral lower lobe consolidations concerning for necrotizing pneumonia, splenic enlargement, numerous hypodense splenic lesions, and a 1.3-cm right hilar node, which had decreased in size compared with 1 month prior.

In summary, the patient presented with recurrent upper respiratory symptoms, fever, and abdominal pain; expanding granulomatous hilar lesions, splenomegaly, and cutaneous lesions consistent with pathergy; elevated inflammatory markers and leukocytosis; and a possible exposure to F tularensis. She has had extensive negative infectious workups, except for a weakly positive β-D-glucan, and completed several courses of apparently unhelpful antimicrobials. At this point, the most notable findings are her splenomegaly and inflammatory masses suggesting an inflammatory process, which may be autoimmune in nature. Both vasculitis and sarcoidosis remain possibilities, and malignancy is possible. Given her possible exposure to F tularensis, obtaining serum antibodies to F tularensis, in addition to biopsies of the skin lesions, is advisable.

Laboratory studies revealed a positive F tularensis antibody with a titer of 1:320 and an IgM of 7 U/mL and IgG of 30 U/mL. This was repeated, revealing a titer of 1:540 and an IgM and IgG of 5 U/mL and 20 U/mL, respectively. Given the potential exposure history, the clinical syndrome compatible with tularemia, and an otherwise extensive yet unrevealing evaluation, she was treated with a 10-day course of streptomycin. Her fever persisted, and the splenic lesions increased in size and number, prompting addition of moxifloxacin without apparent benefit. Skin biopsies taken from the patient’s arm were notable for nodular, suppurative, neutrophilic infiltrates and histiocytes in the medium and deep dermis without multinucleated histiocytes or evidence of vasculitis. Fungal, mycobacterial, and bacterial stains from the biopsy were negative. The findings were consistent with but not diagnostic of an acute neutrophilic dermatosis.

At this point, the patient has a confirmed exposure to F tularensis; she also has persistent fever, progressive splenomegaly, and new skin biopsies consistent with neutrophilic dermatosis. Despite the F tularensis antibody positivity, her negative cultures and lack of improvement with multiple courses of antimicrobials argue against an infectious etiology. Accordingly, malignancy should be considered but seems less likely given that no laboratory, imaging, or tissue samples support it. This leaves immune-mediated etiologies, especially autoimmune conditions associated with neutrophilic dermatoses, as the most likely explanation of her inflammatory syndrome. Neutrophilic dermatoses include some vasculitides, Sweet syndrome, PG, Behçet syndrome, and other inflammatory entities. She has no evidence of vasculitis on biopsy. Given the evidence of inflammation and the history of pathergy, Behçet syndrome and PG should be seriously considered.

She underwent incision and drainage of the left leg and mediastinal lesions. A follow-up chest CT revealed stable cutaneous and deep tissue lesions and continued splenic enlargement. She was started on prednisone and dapsone for presumed cutaneous and visceral PG. The lesions improved dramatically and, following a month-long hospitalization, she was discharged on dapsone and a slow prednisone taper. Three weeks after discharge, while on dapsone and prednisone, she developed a new skin lesion. Cyclosporine was added, with improvement. Eight weeks after discharge, she developed fever, acute left-upper-quadrant pain, and marked splenomegaly with abscesses seen on CT imaging (Figure 2).

This continues to be a very puzzling case, and it is worth revisiting her clinical course once again. This is a previously healthy 32-year-old woman with multiple hospital presentations for upper-respiratory symptoms, persistent fever, abdominal pain, and painful cutaneous lesions consistent with pathergy; she was found to have granulomatous hilar lesions, progressive splenomegaly, and skin biopsies consistent with neutrophilic dermatosis. Exhaustive infectious and rheumatologic workup was negative, and no evident malignancy was found. Finally, despite multiple courses of antimicrobials, including standard treatments for tularemia (for which she had positive antibodies), her clinical course failed to improve until the addition of systemic anti-inflammatory agents, which resulted in rapid improvement. She then presented 8 weeks later with recurrent fever and splenomegaly. Given the recurrence and the severity of the splenic pathology, a diagnostic splenectomy is advisable for what appears to be visceral PG. In addition, attempting to identify a trigger of her syndrome is important. PG can be associated with inflammatory bowel disease, hematologic disorders (eg, leukemia, myeloma, myelodysplastic syndrome, and myelofibrosis), and autoimmune diseases, especially inflammatory arthritis.¹ Therefore, a diagnostic colonoscopy and bone marrow biopsy should be considered. With no history or examination supporting inflammatory arthritis and a broad, unrevealing workup, her rheumatologic evaluation is sufficient.

The patient underwent splenectomy. Gross description of the spleen was notable for multiple abscesses, consisting on microscopy of large areas of necrosis with islands of dense neutrophil collections (Figure 3). Microscopic examination failed to demonstrate microorganisms on multiple stains, and there was no microscopic or flow cytometric evidence of lymphoma. The final pathologic diagnosis was multiple sterile splenic abscesses with siderosis, which, in the context of her overall syndrome, was consistent with an entity termed aseptic abscess syndrome (AAS). After discharge, she underwent a slow steroid taper and was ultimately maintained on daily low-dose prednisone. Cyclosporine and dapsone were discontinued in favor of infliximab infusions. She underwent additional diagnostic workup, including an unremarkable colonoscopy and a bone marrow biopsy, which showed monoclonal gammopathy of undetermined significance (MGUS) with an insignificant IgA monoclonal gammopathy. All cutaneous lesions healed. Three years after the splenectomy, while still on infliximab and prednisone, she developed a new aseptic lung abscess, which resolved after increasing her prednisone dose. Six years after splenectomy, she developed an aseptic liver abscess, which resolved after again increasing the frequency of her infliximab infusions.

Diagnostic uncertainty is an intrinsic feature of medical practice—in part because patients often present with undifferentiated and evolving symptoms.² When faced with uncertainty, clinicians are well served by prioritizing a thoughtful differential diagnosis, adopting a stepwise management strategy, and engaging in iterative reassessments of the patient. In this case, a 32-year-old, previously healthy woman presented with an array of symptoms, including abdominal pain, fever, leukocytosis, necrotic skin lesions, necrotizing mediastinal lymphadenitis, pathergy, and splenomegaly. Elements of the history, examination, and diagnostic studies supported a differential diagnosis of tularemia, PG, and AAS. Through stepwise management and ongoing reassessment, she was ultimately diagnosed with AAS.

Tularemia was initially an important diagnostic consideration in this patient, given her potential exposure and positive F tularensis serum antibodies. Francisella tularensis is a Gram-negative coccobacillus found in more than 250 species of fish, ticks, birds, and mammals. In humans, an incubation period of 3 to 5 days is typical. Although clinical manifestations vary, they often include fever, headache, and malaise.³ Other findings may include lymphadenopathy with or without ulcerative cutaneous lesions (glandular or ulceroglandular tularemia) and cough, dyspnea, pleuritic chest pain, and hilar adenopathy (pneumonic tularemia). As noted by the discussant, a pneumonic tularemia syndrome could have explained this patient’s fever, respiratory symptoms, and hilar adenopathy; ulceroglandular tularemia might have explained her cutaneous lesions. Since splenomegaly may be seen in tularemia, this finding was also consistent with the diagnosis. Serum antibody testing is supportive of the diagnosis, while culture confirms it. Standard treatment consists of a 10- to 14-day course of streptomycin, and combination therapy with a fluoroquinolone is recommended in severe cases.⁴ In this patient, however, F tularensis was not demonstrated on culture. Furthermore, she did not experience the expected clinical improvement with treatment. Finally, because both IgG and IgM tularemia antibodies may co-occur up to 10 years following infection, her positive F tularensis serum antibodies did not provide evidence of acute infection.⁵

Recognizing inconsistencies in the diagnosis of tularemia, the focus shifted to PG owing to the patient’s neutrophilic cutaneous lesions, negative infectious workup, and pathergy. Pyoderma gangrenosum is a neutrophilic dermatosis—one of a heterogeneous group of skin conditions characterized by perivascular and diffuse neutrophilic infiltrates without an identifiable infectious agent.⁶ It is a chronic, recurrent cutaneous disease with several variants.⁷ The classic presentation includes painful lower-extremity ulcers with violaceous undermined borders and may be associated with pathergy. Guiding principles for the management of PG include controlling inflammation, optimizing wound healing, and minimizing exacerbating factors.¹ As such, treatment mainstays include local and systemic anti-inflammatory agents and wound care. As the discussant highlighted, in this case the inflammatory skin lesions were suggestive of PG. However, other features of the case, notably, splenomegaly, splenic abscesses, and necrotizing mediastinal lymphadenitis, were more consistent with another diagnosis: AAS. Aseptic abscess syndrome is an autoinflammatory disorder defined by deep, noninfectious abscesses that preferentially affect the spleen.⁸ Additional clinical manifestations include weight loss, fever, abdominal pain, and leukocytosis. Lesions may also affect bone, kidney, liver, lung, lymph node, and skin. In one case series, neutrophilic dermatoses were seen in 20% of AAS cases.⁸ In all cases of AAS, extensive infectious workup is unrevealing, and antibiotics are ineffective. The pathophysiology of AAS is unknown.

Similar to PG, the majority of AAS cases are associated with inflammatory bowel disease, especially Crohn disease.⁹ However, AAS also has associations with conditions such as MGUS, rheumatoid arthritis, spondyloarthritis, and relapsing polychondritis. Histologically, early lesions demonstrate a necrotic core of neutrophils, with or without surrounding palisading histiocytes, and giant cells. In older lesions, neutrophils may be absent; fibrous tissue may be present.⁸ Treatment regimens include splenectomy, corticosteroids, colchicine, thalidomide, tumor necrosis factor (TNF) antagonists, and cyclophosphamide. The discussant astutely recommended a splenectomy for this patient, which was both diagnostic and therapeutic. As in this case, relapse is common. Optimal maintenance therapy is yet to be determined.⁹

Given the overlapping clinical manifestations, shared disease associations, and similar responsiveness to immunosuppression, it is unclear whether AAS represents a new disease entity or a variant of known autoinflammatory disorders. Aseptic abscess syndrome is likely part of a spectrum of autoinflammatory disorders with inflammatory bowel diseases, neutrophilic dermatoses, and other similar diseases.⁸ While infectious visceral abscesses remain more common, this case highlights the clinical manifestation of an emerging and likely underrecognized entity.

• Aseptic abscess syndrome should be considered in patients who present with visceral (particularly splenic) abscesses and negative infectious workup.
• Aseptic abscess syndrome is commonly associated with other autoinflammatory disorders; the majority of reported cases are associated with inflammatory bowel disease, especially Crohn disease.
• Up to 20% of AAS cases are associated with neutrophilic dermatoses such as PG.
• The initial treatment for this syndrome is high-dose intravenous glucocorticoids; maintenance treatment regimens include corticosteroids, colchicine, thalidomide, TNF antagonists, and cyclophosphamide.

The authors would thank Dr Bob Pelz and Dr John Townes for their contributions to the case.

This icon represents the patient’s case. Each paragraph that follows represents the discussant’s thoughts.

A 32-year-old, previously healthy woman presented to the emergency department (ED) with 3 days of nasal pain, congestion, and cough. A day prior, she had consulted with her primary care provider by phone and had been prescribed amoxicillin-clavulanate for presumed bacterial sinusitis. She subsequently developed fever (39 oC) and pleuritic, left-upper-quadrant abdominal pain. In the ED, chest radiograph demonstrated right hilar opacification. Laboratory studies and computed tomography (CT) of the abdomen and pelvis did not identify a cause for her pain. Given the pleuritic nature of her left-upper-quadrant pain, CT pulmonary angiography was ordered. The CT revealed “mass-like” right hilar opacification and lymphadenopathy. No pulmonary emboli were identified. Levofloxacin was prescribed for presumed pneumonia, and the patient was discharged home. The following week, mediastinal biopsy was arranged for evaluation of the right hilar abnormality.

This is a young woman presenting with upper respiratory symptoms, abdominal pain, fever, and hilar lymphadenopathy. Upper respiratory symptoms are common and usually indicate an inflammatory response to allergens or infection, though autoimmune disorders may affect the upper airways. Fever and hilar lymphadenopathy likely also signify an inflammatory response. Taken together, these findings can be associated with mycobacterial or fungal infection, malignancy, and, particularly in a young woman, sarcoidosis, which could explain her abdominal pain if her presentation included splenomegaly. At this point she likely has a systemic illness involving at least the upper, and possibly the lower, respiratory tract.

Within days, her symptoms resolved. Mediastinal biopsy of the hilar node revealed scant pus. Pathology demonstrated suppurative granulomata. Gram stain; bacterial, mycobacterial, and fungal cultures; and 16S ribosomal analyses for bacteria and fungi from the biopsy were unrevealing. For unclear reasons, prior to the biopsy, she was given intramuscular Haemophilus influenzae type B and tetanus, diphtheria, and pertussis vaccines. Two weeks later, she presented again with fever and left-upper-quadrant pain as well as painful skin nodules at her biopsy and vaccination sites. She was admitted for further evaluation. Chest CT showed expansion of the mediastinal lesion and splenic enlargement. Biopsy of a skin lesion revealed suppurative granulomatous dermatitis and panniculitis. Repeat blood cultures were negative, though serum β-D-glucan was weakly positive at 173 pg/mL (reference range, <60 pg/mL). Tissue cultures and Gram, acid-fast, Fite, and Warthin-Starry stains from the skin biopsy were negative. She was discharged on fluconazole and then readmitted 2 days later with dyspnea, fever, and leukocytosis.

The young woman’s symptoms resolved, only to recur days later; her granulomatous hilar lesions grew larger, and new cutaneous and splenic findings appeared. The granulomatous lesions prompt consideration of infectious, malignant, and immune-mediated processes. The negative cultures make infection less likely, although the elevated β-D-glucan may suggest fungal infection. By description, the skin lesions are consistent with pathergy, a phenomenon characterized by trauma-provoked cutaneous lesions or ulcers, which is associated with numerous syndromes, including Behçet syndrome, inflammatory bowel disease, and neutrophilic dermatoses such as pyoderma gangrenosum (PG) and Sweet syndrome. In addition to details about her medical history, it is important to seek evidence of oral ulcers or vasculitis, as Behçet syndrome may be associated with cutaneous, visceral, and ophthalmologic vasculitis.

Her medical history included hypertension and active, 10-pack-year cigarette use. During childhood, she had occasional ingrown hairs and folliculitis. She did not take medications prior to this acute illness. Family history was notable for cardiovascular disease. She rarely consumed alcohol and did not use illicit drugs. She lived in a rural town in the mid–Willamette Valley of Oregon and worked as an administrative assistant. She spent time outdoors, including trail running and golfing. A case of tularemia was recently reported in an area near her home. Her only travel outside of Oregon was to Puerto Vallarta, Mexico, 16 years previously. She grew up on a farm and had no known tuberculosis exposure.

Tularemia is an interesting diagnostic consideration and could explain her fever, cutaneous lesions, and hilar adenopathy. It is plausible that she had clinically mild pneumonic tularemia at the outset and that her cutaneous lesions are variants of ulceroglandular tularemia. Positive antibodies for Francisella tularensis would be expected if this were the cause of her illness. The ingrown hairs raise the possibility of a primary immune deficiency syndrome predisposing her to abscesses. However, they seem to have been of trivial significance to her, making an immune deficiency syndrome unlikely.

On readmission, she was afebrile, normotensive, and tachycardic (114 beats/min), with a normal respiratory rate and oxygen saturation. She was not ill appearing. She had noninjected conjunctiva and no oral lesions. Apart from tachycardia, cardiovascular examination was unremarkable. Abdominal examination was notable for mild distension and a palpable, tender spleen. Musculoskeletal and neurologic examinations were normal. Her skin was notable for various sized (8 cm × 4 cm to 10 cm × 15 cm) painful ulcers with violaceous, friable borders—some with fluctuance and purulent drainage—on her right hand, bilateral arms, right axilla, sternum, and legs (Figure 1).

Laboratory studies were notable for normocytic anemia (hemoglobin, 8.9 g/dL; range, 12.0-16.0 g/dL), leukocytosis (white blood cells, 24,900/µL; range, 4500-11,000/µL), thrombocytosis (platelet count, 690,000/µL; range, 150,000-400,000/µL), and elevated inflammatory markers (C-reactive protein, 33 mg/dL; range, <0.5 mg/dL; erythrocyte sedimentation rate, 78 mm/h; range, <20 mm/h). A complete metabolic panel was within normal limits. Repeat blood cultures and β -D-glucan and 16S ribosomal assays were negative. Polymerase chain reaction testing for Bartonella henselae was negative. Urine probes for Neisseria gonorrhoeae and Chlamydia trachomatis were negative. Rapid plasma regain (RPR) was negative. Antibodies to toxoplasmosis, histoplasmosis, blastomycosis, and aspergillosis were unrevealing. A Coccidioides test by immunodiffusion was negative. Serum antigen tests for Cryptococcus and Epstein-Barr virus (EBV) were negative. EBV, HIV, and hepatitis antibody tests were negative. Rheumatologic studies, including antinuclear, anti-double-stranded DNA, anti-Smith, anti–Sjögren syndrome antigens A and B, anticentromere, anti-topoisomerase (anti-Scl-70), anti-histidyl-transfer-RNA-synthetase (anti-Jo-1), and anti-nucleosome (anti-chromatic) antibodies, were unrevealing. Levels of angiotensin-converting enzyme, rheumatoid factor, complement, cytoplasmic, and perinuclear antineutrophil cytoplasmic antibodies were also normal. A neutrophil oxidative burst test was negative. In addition, peripheral flow cytology and serum and urine protein electrophoresis were negative. Chest CT revealed bilateral lower lobe consolidations concerning for necrotizing pneumonia, splenic enlargement, numerous hypodense splenic lesions, and a 1.3-cm right hilar node, which had decreased in size compared with 1 month prior.

In summary, the patient presented with recurrent upper respiratory symptoms, fever, and abdominal pain; expanding granulomatous hilar lesions, splenomegaly, and cutaneous lesions consistent with pathergy; elevated inflammatory markers and leukocytosis; and a possible exposure to F tularensis. She has had extensive negative infectious workups, except for a weakly positive β-D-glucan, and completed several courses of apparently unhelpful antimicrobials. At this point, the most notable findings are her splenomegaly and inflammatory masses suggesting an inflammatory process, which may be autoimmune in nature. Both vasculitis and sarcoidosis remain possibilities, and malignancy is possible. Given her possible exposure to F tularensis, obtaining serum antibodies to F tularensis, in addition to biopsies of the skin lesions, is advisable.

Laboratory studies revealed a positive F tularensis antibody with a titer of 1:320 and an IgM of 7 U/mL and IgG of 30 U/mL. This was repeated, revealing a titer of 1:540 and an IgM and IgG of 5 U/mL and 20 U/mL, respectively. Given the potential exposure history, the clinical syndrome compatible with tularemia, and an otherwise extensive yet unrevealing evaluation, she was treated with a 10-day course of streptomycin. Her fever persisted, and the splenic lesions increased in size and number, prompting addition of moxifloxacin without apparent benefit. Skin biopsies taken from the patient’s arm were notable for nodular, suppurative, neutrophilic infiltrates and histiocytes in the medium and deep dermis without multinucleated histiocytes or evidence of vasculitis. Fungal, mycobacterial, and bacterial stains from the biopsy were negative. The findings were consistent with but not diagnostic of an acute neutrophilic dermatosis.

At this point, the patient has a confirmed exposure to F tularensis; she also has persistent fever, progressive splenomegaly, and new skin biopsies consistent with neutrophilic dermatosis. Despite the F tularensis antibody positivity, her negative cultures and lack of improvement with multiple courses of antimicrobials argue against an infectious etiology. Accordingly, malignancy should be considered but seems less likely given that no laboratory, imaging, or tissue samples support it. This leaves immune-mediated etiologies, especially autoimmune conditions associated with neutrophilic dermatoses, as the most likely explanation of her inflammatory syndrome. Neutrophilic dermatoses include some vasculitides, Sweet syndrome, PG, Behçet syndrome, and other inflammatory entities. She has no evidence of vasculitis on biopsy. Given the evidence of inflammation and the history of pathergy, Behçet syndrome and PG should be seriously considered.

She underwent incision and drainage of the left leg and mediastinal lesions. A follow-up chest CT revealed stable cutaneous and deep tissue lesions and continued splenic enlargement. She was started on prednisone and dapsone for presumed cutaneous and visceral PG. The lesions improved dramatically and, following a month-long hospitalization, she was discharged on dapsone and a slow prednisone taper. Three weeks after discharge, while on dapsone and prednisone, she developed a new skin lesion. Cyclosporine was added, with improvement. Eight weeks after discharge, she developed fever, acute left-upper-quadrant pain, and marked splenomegaly with abscesses seen on CT imaging (Figure 2).

This continues to be a very puzzling case, and it is worth revisiting her clinical course once again. This is a previously healthy 32-year-old woman with multiple hospital presentations for upper-respiratory symptoms, persistent fever, abdominal pain, and painful cutaneous lesions consistent with pathergy; she was found to have granulomatous hilar lesions, progressive splenomegaly, and skin biopsies consistent with neutrophilic dermatosis. Exhaustive infectious and rheumatologic workup was negative, and no evident malignancy was found. Finally, despite multiple courses of antimicrobials, including standard treatments for tularemia (for which she had positive antibodies), her clinical course failed to improve until the addition of systemic anti-inflammatory agents, which resulted in rapid improvement. She then presented 8 weeks later with recurrent fever and splenomegaly. Given the recurrence and the severity of the splenic pathology, a diagnostic splenectomy is advisable for what appears to be visceral PG. In addition, attempting to identify a trigger of her syndrome is important. PG can be associated with inflammatory bowel disease, hematologic disorders (eg, leukemia, myeloma, myelodysplastic syndrome, and myelofibrosis), and autoimmune diseases, especially inflammatory arthritis.¹ Therefore, a diagnostic colonoscopy and bone marrow biopsy should be considered. With no history or examination supporting inflammatory arthritis and a broad, unrevealing workup, her rheumatologic evaluation is sufficient.

The patient underwent splenectomy. Gross description of the spleen was notable for multiple abscesses, consisting on microscopy of large areas of necrosis with islands of dense neutrophil collections (Figure 3). Microscopic examination failed to demonstrate microorganisms on multiple stains, and there was no microscopic or flow cytometric evidence of lymphoma. The final pathologic diagnosis was multiple sterile splenic abscesses with siderosis, which, in the context of her overall syndrome, was consistent with an entity termed aseptic abscess syndrome (AAS). After discharge, she underwent a slow steroid taper and was ultimately maintained on daily low-dose prednisone. Cyclosporine and dapsone were discontinued in favor of infliximab infusions. She underwent additional diagnostic workup, including an unremarkable colonoscopy and a bone marrow biopsy, which showed monoclonal gammopathy of undetermined significance (MGUS) with an insignificant IgA monoclonal gammopathy. All cutaneous lesions healed. Three years after the splenectomy, while still on infliximab and prednisone, she developed a new aseptic lung abscess, which resolved after increasing her prednisone dose. Six years after splenectomy, she developed an aseptic liver abscess, which resolved after again increasing the frequency of her infliximab infusions.

Diagnostic uncertainty is an intrinsic feature of medical practice—in part because patients often present with undifferentiated and evolving symptoms.² When faced with uncertainty, clinicians are well served by prioritizing a thoughtful differential diagnosis, adopting a stepwise management strategy, and engaging in iterative reassessments of the patient. In this case, a 32-year-old, previously healthy woman presented with an array of symptoms, including abdominal pain, fever, leukocytosis, necrotic skin lesions, necrotizing mediastinal lymphadenitis, pathergy, and splenomegaly. Elements of the history, examination, and diagnostic studies supported a differential diagnosis of tularemia, PG, and AAS. Through stepwise management and ongoing reassessment, she was ultimately diagnosed with AAS.

Tularemia was initially an important diagnostic consideration in this patient, given her potential exposure and positive F tularensis serum antibodies. Francisella tularensis is a Gram-negative coccobacillus found in more than 250 species of fish, ticks, birds, and mammals. In humans, an incubation period of 3 to 5 days is typical. Although clinical manifestations vary, they often include fever, headache, and malaise.³ Other findings may include lymphadenopathy with or without ulcerative cutaneous lesions (glandular or ulceroglandular tularemia) and cough, dyspnea, pleuritic chest pain, and hilar adenopathy (pneumonic tularemia). As noted by the discussant, a pneumonic tularemia syndrome could have explained this patient’s fever, respiratory symptoms, and hilar adenopathy; ulceroglandular tularemia might have explained her cutaneous lesions. Since splenomegaly may be seen in tularemia, this finding was also consistent with the diagnosis. Serum antibody testing is supportive of the diagnosis, while culture confirms it. Standard treatment consists of a 10- to 14-day course of streptomycin, and combination therapy with a fluoroquinolone is recommended in severe cases.⁴ In this patient, however, F tularensis was not demonstrated on culture. Furthermore, she did not experience the expected clinical improvement with treatment. Finally, because both IgG and IgM tularemia antibodies may co-occur up to 10 years following infection, her positive F tularensis serum antibodies did not provide evidence of acute infection.⁵

Recognizing inconsistencies in the diagnosis of tularemia, the focus shifted to PG owing to the patient’s neutrophilic cutaneous lesions, negative infectious workup, and pathergy. Pyoderma gangrenosum is a neutrophilic dermatosis—one of a heterogeneous group of skin conditions characterized by perivascular and diffuse neutrophilic infiltrates without an identifiable infectious agent.⁶ It is a chronic, recurrent cutaneous disease with several variants.⁷ The classic presentation includes painful lower-extremity ulcers with violaceous undermined borders and may be associated with pathergy. Guiding principles for the management of PG include controlling inflammation, optimizing wound healing, and minimizing exacerbating factors.¹ As such, treatment mainstays include local and systemic anti-inflammatory agents and wound care. As the discussant highlighted, in this case the inflammatory skin lesions were suggestive of PG. However, other features of the case, notably, splenomegaly, splenic abscesses, and necrotizing mediastinal lymphadenitis, were more consistent with another diagnosis: AAS. Aseptic abscess syndrome is an autoinflammatory disorder defined by deep, noninfectious abscesses that preferentially affect the spleen.⁸ Additional clinical manifestations include weight loss, fever, abdominal pain, and leukocytosis. Lesions may also affect bone, kidney, liver, lung, lymph node, and skin. In one case series, neutrophilic dermatoses were seen in 20% of AAS cases.⁸ In all cases of AAS, extensive infectious workup is unrevealing, and antibiotics are ineffective. The pathophysiology of AAS is unknown.

Similar to PG, the majority of AAS cases are associated with inflammatory bowel disease, especially Crohn disease.⁹ However, AAS also has associations with conditions such as MGUS, rheumatoid arthritis, spondyloarthritis, and relapsing polychondritis. Histologically, early lesions demonstrate a necrotic core of neutrophils, with or without surrounding palisading histiocytes, and giant cells. In older lesions, neutrophils may be absent; fibrous tissue may be present.⁸ Treatment regimens include splenectomy, corticosteroids, colchicine, thalidomide, tumor necrosis factor (TNF) antagonists, and cyclophosphamide. The discussant astutely recommended a splenectomy for this patient, which was both diagnostic and therapeutic. As in this case, relapse is common. Optimal maintenance therapy is yet to be determined.⁹

Given the overlapping clinical manifestations, shared disease associations, and similar responsiveness to immunosuppression, it is unclear whether AAS represents a new disease entity or a variant of known autoinflammatory disorders. Aseptic abscess syndrome is likely part of a spectrum of autoinflammatory disorders with inflammatory bowel diseases, neutrophilic dermatoses, and other similar diseases.⁸ While infectious visceral abscesses remain more common, this case highlights the clinical manifestation of an emerging and likely underrecognized entity.

• Aseptic abscess syndrome should be considered in patients who present with visceral (particularly splenic) abscesses and negative infectious workup.
• Aseptic abscess syndrome is commonly associated with other autoinflammatory disorders; the majority of reported cases are associated with inflammatory bowel disease, especially Crohn disease.
• Up to 20% of AAS cases are associated with neutrophilic dermatoses such as PG.
• The initial treatment for this syndrome is high-dose intravenous glucocorticoids; maintenance treatment regimens include corticosteroids, colchicine, thalidomide, TNF antagonists, and cyclophosphamide.

The authors would thank Dr Bob Pelz and Dr John Townes for their contributions to the case.