Hospital Medicine

Personal health records (PHRs) are a broad group of applications “through which individuals can access, manage, and share their health information,” and are intended as a means to increase consumer health awareness, activation, safety, and self-efficacy.¹ Patient portals—PHRs that are tethered to an electronic health record (EHR)—have expanded over the past decade, driven in part by the “Meaningful Use” EHR Incentive Program of the Centers for Medicare and Medicaid Services.² This has been particularly true in the outpatient setting. Unfortunately, despite increased adoption and a large number of research studies, it is not clear whether outpatient portal use is associated with improved clinical outcomes.³

Both the use of portals in the inpatient setting and the research thereof are at a more nascent stage. In this issue of the Journal of Hospital Medicine, Kelly et al.⁴ provide a systematic review of the existing research on the implementation of inpatient portals. The authors identified 17 studies and categorized the papers’ findings into the following 3 themes: design, use and usability, and impact. Most of the studies elicited feedback from patients, caregivers, and/or providers – sometimes in multiple phases as portals were redesigned – allowing the authors to offer the following recommendations for inpatient portal design: portals should present timely information, include the care plan in ways patients can understand, and facilitate identification and communication with the care team.⁴ Most of the included studies focused on portal design and use, thereby limiting knowledge regarding impact on the outcomes portals are intended to target. All findings should be interpreted with caution, as many of the included studies were small and qualitative, most of them used convenience samples and subject-reported outcomes, and all were conducted at a single center. Many sites also used customized portals, thus limiting generalizability.

Participants often found portals to be useful, but this finding is of uncertain value in the absence of robust evidence on outcomes. In addition, providers included in the reviewed studies expressed concerns that have not yet been well studied, such as the potential impact of portals on workload and on patient anxiety. Some studies reported that provider concerns lessened following a portal rollout, but few studies evaluated physician input on features such as direct communication and test result reporting in active use. The outpatient portal literature suggests potential harm related to how results are delivered, thus placing importance on conducting additional inpatient studies. Patients value online access to their health information⁵ and in previous literature have indicated a preference for immediate access to results even if abnormal results would then be given without explanation.⁶ However, in a recent study, even normal findings delivered without context were a cause of negative emotions and increased calls to physicians.⁷ This effect could be more pronounced in inpatient settings, given the large volume of tests and abnormal results, the rapidly evolving treatment plans, and generally higher acuity and medical uncertainty.

This review and other current literature highlight challenges for vendors and hospitals. Vendors must ensure that patient health information is contextualized and delivered in a manner that meets individual learning styles.⁸ Patients and caregivers need clinical decision support to process today’s large amount of data, just as providers do. We must be careful not to implement patient portals in ways that increase cognitive load and generate anxiety and confusion. Hospitals have infrastructural challenges if portals are to be successful. Care provider information must be accurately registered in the EHR to route patient-to-provider communications, a difficult task across frequent handoffs and staffing changes.

We now have the beginnings of an informed vision for inpatient portal design. Future research and industry directions include greater exploration of recognized concerns and how to best reconcile these concerns with the benefits of portals espoused by consumer health advocates and experienced by patients, caregivers, and providers in the reviewed studies. Specifically, we need a better understanding of how best to incorporate inpatient portals into routine care delivery in ways that are useful to both patients and providers. We also need a better understanding of why patients opt out of portal use. Most of the studies to date report on the set of patients who decided to use the portals, leaving a knowledge gap in design and use implications for patients who opted out. Studies should include comparisons of patient outcomes between users and nonusers. Although inpatient portals show promise, many questions remain.

Disclosures

The authors declare no conflicts of interest.

Personal health records (PHRs) are a broad group of applications “through which individuals can access, manage, and share their health information,” and are intended as a means to increase consumer health awareness, activation, safety, and self-efficacy.¹ Patient portals—PHRs that are tethered to an electronic health record (EHR)—have expanded over the past decade, driven in part by the “Meaningful Use” EHR Incentive Program of the Centers for Medicare and Medicaid Services.² This has been particularly true in the outpatient setting. Unfortunately, despite increased adoption and a large number of research studies, it is not clear whether outpatient portal use is associated with improved clinical outcomes.³

Both the use of portals in the inpatient setting and the research thereof are at a more nascent stage. In this issue of the Journal of Hospital Medicine, Kelly et al.⁴ provide a systematic review of the existing research on the implementation of inpatient portals. The authors identified 17 studies and categorized the papers’ findings into the following 3 themes: design, use and usability, and impact. Most of the studies elicited feedback from patients, caregivers, and/or providers – sometimes in multiple phases as portals were redesigned – allowing the authors to offer the following recommendations for inpatient portal design: portals should present timely information, include the care plan in ways patients can understand, and facilitate identification and communication with the care team.⁴ Most of the included studies focused on portal design and use, thereby limiting knowledge regarding impact on the outcomes portals are intended to target. All findings should be interpreted with caution, as many of the included studies were small and qualitative, most of them used convenience samples and subject-reported outcomes, and all were conducted at a single center. Many sites also used customized portals, thus limiting generalizability.

Participants often found portals to be useful, but this finding is of uncertain value in the absence of robust evidence on outcomes. In addition, providers included in the reviewed studies expressed concerns that have not yet been well studied, such as the potential impact of portals on workload and on patient anxiety. Some studies reported that provider concerns lessened following a portal rollout, but few studies evaluated physician input on features such as direct communication and test result reporting in active use. The outpatient portal literature suggests potential harm related to how results are delivered, thus placing importance on conducting additional inpatient studies. Patients value online access to their health information⁵ and in previous literature have indicated a preference for immediate access to results even if abnormal results would then be given without explanation.⁶ However, in a recent study, even normal findings delivered without context were a cause of negative emotions and increased calls to physicians.⁷ This effect could be more pronounced in inpatient settings, given the large volume of tests and abnormal results, the rapidly evolving treatment plans, and generally higher acuity and medical uncertainty.

This review and other current literature highlight challenges for vendors and hospitals. Vendors must ensure that patient health information is contextualized and delivered in a manner that meets individual learning styles.⁸ Patients and caregivers need clinical decision support to process today’s large amount of data, just as providers do. We must be careful not to implement patient portals in ways that increase cognitive load and generate anxiety and confusion. Hospitals have infrastructural challenges if portals are to be successful. Care provider information must be accurately registered in the EHR to route patient-to-provider communications, a difficult task across frequent handoffs and staffing changes.

We now have the beginnings of an informed vision for inpatient portal design. Future research and industry directions include greater exploration of recognized concerns and how to best reconcile these concerns with the benefits of portals espoused by consumer health advocates and experienced by patients, caregivers, and providers in the reviewed studies. Specifically, we need a better understanding of how best to incorporate inpatient portals into routine care delivery in ways that are useful to both patients and providers. We also need a better understanding of why patients opt out of portal use. Most of the studies to date report on the set of patients who decided to use the portals, leaving a knowledge gap in design and use implications for patients who opted out. Studies should include comparisons of patient outcomes between users and nonusers. Although inpatient portals show promise, many questions remain.

Disclosures

The authors declare no conflicts of interest.

Personal health records (PHRs) are a broad group of applications “through which individuals can access, manage, and share their health information,” and are intended as a means to increase consumer health awareness, activation, safety, and self-efficacy.¹ Patient portals—PHRs that are tethered to an electronic health record (EHR)—have expanded over the past decade, driven in part by the “Meaningful Use” EHR Incentive Program of the Centers for Medicare and Medicaid Services.² This has been particularly true in the outpatient setting. Unfortunately, despite increased adoption and a large number of research studies, it is not clear whether outpatient portal use is associated with improved clinical outcomes.³

Both the use of portals in the inpatient setting and the research thereof are at a more nascent stage. In this issue of the Journal of Hospital Medicine, Kelly et al.⁴ provide a systematic review of the existing research on the implementation of inpatient portals. The authors identified 17 studies and categorized the papers’ findings into the following 3 themes: design, use and usability, and impact. Most of the studies elicited feedback from patients, caregivers, and/or providers – sometimes in multiple phases as portals were redesigned – allowing the authors to offer the following recommendations for inpatient portal design: portals should present timely information, include the care plan in ways patients can understand, and facilitate identification and communication with the care team.⁴ Most of the included studies focused on portal design and use, thereby limiting knowledge regarding impact on the outcomes portals are intended to target. All findings should be interpreted with caution, as many of the included studies were small and qualitative, most of them used convenience samples and subject-reported outcomes, and all were conducted at a single center. Many sites also used customized portals, thus limiting generalizability.

Participants often found portals to be useful, but this finding is of uncertain value in the absence of robust evidence on outcomes. In addition, providers included in the reviewed studies expressed concerns that have not yet been well studied, such as the potential impact of portals on workload and on patient anxiety. Some studies reported that provider concerns lessened following a portal rollout, but few studies evaluated physician input on features such as direct communication and test result reporting in active use. The outpatient portal literature suggests potential harm related to how results are delivered, thus placing importance on conducting additional inpatient studies. Patients value online access to their health information⁵ and in previous literature have indicated a preference for immediate access to results even if abnormal results would then be given without explanation.⁶ However, in a recent study, even normal findings delivered without context were a cause of negative emotions and increased calls to physicians.⁷ This effect could be more pronounced in inpatient settings, given the large volume of tests and abnormal results, the rapidly evolving treatment plans, and generally higher acuity and medical uncertainty.

This review and other current literature highlight challenges for vendors and hospitals. Vendors must ensure that patient health information is contextualized and delivered in a manner that meets individual learning styles.⁸ Patients and caregivers need clinical decision support to process today’s large amount of data, just as providers do. We must be careful not to implement patient portals in ways that increase cognitive load and generate anxiety and confusion. Hospitals have infrastructural challenges if portals are to be successful. Care provider information must be accurately registered in the EHR to route patient-to-provider communications, a difficult task across frequent handoffs and staffing changes.

We now have the beginnings of an informed vision for inpatient portal design. Future research and industry directions include greater exploration of recognized concerns and how to best reconcile these concerns with the benefits of portals espoused by consumer health advocates and experienced by patients, caregivers, and providers in the reviewed studies. Specifically, we need a better understanding of how best to incorporate inpatient portals into routine care delivery in ways that are useful to both patients and providers. We also need a better understanding of why patients opt out of portal use. Most of the studies to date report on the set of patients who decided to use the portals, leaving a knowledge gap in design and use implications for patients who opted out. Studies should include comparisons of patient outcomes between users and nonusers. Although inpatient portals show promise, many questions remain.

Disclosures

The authors declare no conflicts of interest.

^“Am I supposed to have such a hard time feeling the kidneys?” “I think I’m doing it wrong,” echoed another classmate. The frustration of these first-year students, who were already overwhelmed by the three pages of physical exam techniques that they were responsible for, became increasingly visible as they palpated the abdomens of their standardized patients. Then, they asked the dreaded question: “How often do you do this on real patients?”

When we teach first-year medical students the physical exam, these students are already aware that they have never observed physicians perform these maneuvers in their own medical care. “How come I’ve never seen my doctor do this before?” is a common question that we are often asked. We as faculty struggle with demonstrating and defending techniques that we hardly ever use given their variable utility in daily clinical practice. However, students are told that they must be familiar with the various “tools” in the repertoire, and they are led to believe that these skills will be a fundamental part of their future practice as physicians. Of course, when they begin their clerkships, the truth is revealed: the currency on the wards revolves around the computer. The experienced and passionate clinicians who may astonish them with the bedside exam are the exception and are hardly the rule.

In this issue of Journal of Hospital Medicine, Bergl et al.¹ found that when medical students rotated on their internal medicine clerkship, patients were rarely examined during attending rounds and were even examined less often when these rounds were not at the bedside. Although the students themselves consistently incorporated the physical exam into patient assessments and presentations, neither their findings nor those of the residents were ever validated by the attending physician or by others. Notably, the physical exam did not influence clinical decision making as much as one might expect.

These findings should not come as a surprise. The current generation of residents and junior attendings today are more accustomed to emphasizing labs, imaging studies, pathology reports, and other data within the electronic health record (EHR) and with formulating initial plans before having met the patient.² Physicians become uneasy when asked to decide without the reassurance of daily lab results, as if the information in the EHR is highly fundamental to patient care. Caring for the “iPatient” often trumps revisiting and reexamining the real patient.³ Medical teams are also bombarded with increasing demands for their attention and time and are pushed to expedite patient discharges while constantly responding to documentation queries in the EHR. Emphasis on patient throughput, quality metrics, and multidisciplinary communication is essential to provide effective patient care but often feels at odds with opportunities for bedside teaching.

Although discussions on these obstacles have increased in recent years, time-motion studies spanning decades and even preceding the duty-hours era have consistently shown that physicians reserve little time for physical examination and direct patient care.⁴ In other words, the challenges in bringing physicians to the bedside might have less to do with environmental barriers than we think.

Much of what we teach about physical diagnosis is imperfect,⁵ and the routine annual exam might well be eliminated given its low yield.⁶ Nevertheless, we cannot discount the importance of the physical exam in fostering the bond between the patient and the healthcare provider, particularly in patients with acute illnesses, and in making the interaction meaningful to the practitioner.

Many of us can easily recall embarrassing examples of obvious physical exam findings that were critical and overlooked with consequences – the missed incarcerated hernia in a patient labeled with gastritis and vomiting, or the patient with chest pain who had to undergo catheterization because the shingles rash was missed. The confidence in normal findings that might save a patient from unnecessary lab tests, imaging, or consultation is often not discussed. The burden is on us to retire maneuvers that have outlived their usefulness and to demonstrate to students the hazards and consequences of poor examination skills. We must also further what we know and understand about the physical exam as Osler, Laennec, and others before us once did. Point-of-care ultrasound is only one example of how innovation can bring trainees to the bedside, excite learners, engage patients, and affect care in a meaningful way while enhancing the nonultrasound-based skills of practitioners.⁷

It is promising that the students in this study consistently examined their patients each day. As future physicians, they can be very enthusiastic learners eager to apply the physical exam skills they have recently acquired during their early years of training. However, this excitement can taper off if not actively encouraged and reinforced, especially if role models are unintentionally sending the message that the physical exam does not matter or emphasizing exam maneuvers that do not serve a meaningful purpose. New technology will hopefully help us develop novel exam skills. If we can advance what we can diagnose at the bedside, students will remain motivated to improve and learn exam skills that truly affect patient-care decisions. After all, one day, they too will serve as role models for the next generation of physicians and hopefully will be the ones taking care of us at the bedside.

Disclosures 

The authors declare no conflicts of interest.

^“Am I supposed to have such a hard time feeling the kidneys?” “I think I’m doing it wrong,” echoed another classmate. The frustration of these first-year students, who were already overwhelmed by the three pages of physical exam techniques that they were responsible for, became increasingly visible as they palpated the abdomens of their standardized patients. Then, they asked the dreaded question: “How often do you do this on real patients?”

When we teach first-year medical students the physical exam, these students are already aware that they have never observed physicians perform these maneuvers in their own medical care. “How come I’ve never seen my doctor do this before?” is a common question that we are often asked. We as faculty struggle with demonstrating and defending techniques that we hardly ever use given their variable utility in daily clinical practice. However, students are told that they must be familiar with the various “tools” in the repertoire, and they are led to believe that these skills will be a fundamental part of their future practice as physicians. Of course, when they begin their clerkships, the truth is revealed: the currency on the wards revolves around the computer. The experienced and passionate clinicians who may astonish them with the bedside exam are the exception and are hardly the rule.

In this issue of Journal of Hospital Medicine, Bergl et al.¹ found that when medical students rotated on their internal medicine clerkship, patients were rarely examined during attending rounds and were even examined less often when these rounds were not at the bedside. Although the students themselves consistently incorporated the physical exam into patient assessments and presentations, neither their findings nor those of the residents were ever validated by the attending physician or by others. Notably, the physical exam did not influence clinical decision making as much as one might expect.

These findings should not come as a surprise. The current generation of residents and junior attendings today are more accustomed to emphasizing labs, imaging studies, pathology reports, and other data within the electronic health record (EHR) and with formulating initial plans before having met the patient.² Physicians become uneasy when asked to decide without the reassurance of daily lab results, as if the information in the EHR is highly fundamental to patient care. Caring for the “iPatient” often trumps revisiting and reexamining the real patient.³ Medical teams are also bombarded with increasing demands for their attention and time and are pushed to expedite patient discharges while constantly responding to documentation queries in the EHR. Emphasis on patient throughput, quality metrics, and multidisciplinary communication is essential to provide effective patient care but often feels at odds with opportunities for bedside teaching.

Although discussions on these obstacles have increased in recent years, time-motion studies spanning decades and even preceding the duty-hours era have consistently shown that physicians reserve little time for physical examination and direct patient care.⁴ In other words, the challenges in bringing physicians to the bedside might have less to do with environmental barriers than we think.

Much of what we teach about physical diagnosis is imperfect,⁵ and the routine annual exam might well be eliminated given its low yield.⁶ Nevertheless, we cannot discount the importance of the physical exam in fostering the bond between the patient and the healthcare provider, particularly in patients with acute illnesses, and in making the interaction meaningful to the practitioner.

Many of us can easily recall embarrassing examples of obvious physical exam findings that were critical and overlooked with consequences – the missed incarcerated hernia in a patient labeled with gastritis and vomiting, or the patient with chest pain who had to undergo catheterization because the shingles rash was missed. The confidence in normal findings that might save a patient from unnecessary lab tests, imaging, or consultation is often not discussed. The burden is on us to retire maneuvers that have outlived their usefulness and to demonstrate to students the hazards and consequences of poor examination skills. We must also further what we know and understand about the physical exam as Osler, Laennec, and others before us once did. Point-of-care ultrasound is only one example of how innovation can bring trainees to the bedside, excite learners, engage patients, and affect care in a meaningful way while enhancing the nonultrasound-based skills of practitioners.⁷

It is promising that the students in this study consistently examined their patients each day. As future physicians, they can be very enthusiastic learners eager to apply the physical exam skills they have recently acquired during their early years of training. However, this excitement can taper off if not actively encouraged and reinforced, especially if role models are unintentionally sending the message that the physical exam does not matter or emphasizing exam maneuvers that do not serve a meaningful purpose. New technology will hopefully help us develop novel exam skills. If we can advance what we can diagnose at the bedside, students will remain motivated to improve and learn exam skills that truly affect patient-care decisions. After all, one day, they too will serve as role models for the next generation of physicians and hopefully will be the ones taking care of us at the bedside.

Disclosures 

The authors declare no conflicts of interest.

^“Am I supposed to have such a hard time feeling the kidneys?” “I think I’m doing it wrong,” echoed another classmate. The frustration of these first-year students, who were already overwhelmed by the three pages of physical exam techniques that they were responsible for, became increasingly visible as they palpated the abdomens of their standardized patients. Then, they asked the dreaded question: “How often do you do this on real patients?”

When we teach first-year medical students the physical exam, these students are already aware that they have never observed physicians perform these maneuvers in their own medical care. “How come I’ve never seen my doctor do this before?” is a common question that we are often asked. We as faculty struggle with demonstrating and defending techniques that we hardly ever use given their variable utility in daily clinical practice. However, students are told that they must be familiar with the various “tools” in the repertoire, and they are led to believe that these skills will be a fundamental part of their future practice as physicians. Of course, when they begin their clerkships, the truth is revealed: the currency on the wards revolves around the computer. The experienced and passionate clinicians who may astonish them with the bedside exam are the exception and are hardly the rule.

In this issue of Journal of Hospital Medicine, Bergl et al.¹ found that when medical students rotated on their internal medicine clerkship, patients were rarely examined during attending rounds and were even examined less often when these rounds were not at the bedside. Although the students themselves consistently incorporated the physical exam into patient assessments and presentations, neither their findings nor those of the residents were ever validated by the attending physician or by others. Notably, the physical exam did not influence clinical decision making as much as one might expect.

These findings should not come as a surprise. The current generation of residents and junior attendings today are more accustomed to emphasizing labs, imaging studies, pathology reports, and other data within the electronic health record (EHR) and with formulating initial plans before having met the patient.² Physicians become uneasy when asked to decide without the reassurance of daily lab results, as if the information in the EHR is highly fundamental to patient care. Caring for the “iPatient” often trumps revisiting and reexamining the real patient.³ Medical teams are also bombarded with increasing demands for their attention and time and are pushed to expedite patient discharges while constantly responding to documentation queries in the EHR. Emphasis on patient throughput, quality metrics, and multidisciplinary communication is essential to provide effective patient care but often feels at odds with opportunities for bedside teaching.

Although discussions on these obstacles have increased in recent years, time-motion studies spanning decades and even preceding the duty-hours era have consistently shown that physicians reserve little time for physical examination and direct patient care.⁴ In other words, the challenges in bringing physicians to the bedside might have less to do with environmental barriers than we think.

Much of what we teach about physical diagnosis is imperfect,⁵ and the routine annual exam might well be eliminated given its low yield.⁶ Nevertheless, we cannot discount the importance of the physical exam in fostering the bond between the patient and the healthcare provider, particularly in patients with acute illnesses, and in making the interaction meaningful to the practitioner.

Many of us can easily recall embarrassing examples of obvious physical exam findings that were critical and overlooked with consequences – the missed incarcerated hernia in a patient labeled with gastritis and vomiting, or the patient with chest pain who had to undergo catheterization because the shingles rash was missed. The confidence in normal findings that might save a patient from unnecessary lab tests, imaging, or consultation is often not discussed. The burden is on us to retire maneuvers that have outlived their usefulness and to demonstrate to students the hazards and consequences of poor examination skills. We must also further what we know and understand about the physical exam as Osler, Laennec, and others before us once did. Point-of-care ultrasound is only one example of how innovation can bring trainees to the bedside, excite learners, engage patients, and affect care in a meaningful way while enhancing the nonultrasound-based skills of practitioners.⁷

It is promising that the students in this study consistently examined their patients each day. As future physicians, they can be very enthusiastic learners eager to apply the physical exam skills they have recently acquired during their early years of training. However, this excitement can taper off if not actively encouraged and reinforced, especially if role models are unintentionally sending the message that the physical exam does not matter or emphasizing exam maneuvers that do not serve a meaningful purpose. New technology will hopefully help us develop novel exam skills. If we can advance what we can diagnose at the bedside, students will remain motivated to improve and learn exam skills that truly affect patient-care decisions. After all, one day, they too will serve as role models for the next generation of physicians and hopefully will be the ones taking care of us at the bedside.

Disclosures 

The authors declare no conflicts of interest.

Over the past two decades, the field of hospital medicine has gone from relative obscurity to a viable career pathway for approximately 50,000 physicians in this country.¹ A subset of hospitalists pursue careers in academic medicine, which is a pathway that traditionally includes education and scholarship in addition to patient care. While the academic career pathway is well paved in many clinical specialties, it is still relatively underdeveloped for academic hospitalists, and thus what defines career success for this group is even less clear.

In this issue of the Journal of Hospital Medicine, Cumbler et al. performed a qualitative analysis to explore how early career academic hospitalists self-define and perceive their career success.² Drawing on interviews with 17 early-career hospitalists at 3 academic medical centers, the authors created a theoretical framework organized around a traditional conceptual model of career success that is divided into intrinsic and extrinsic motivating factors. They found that early-career academic hospitalists, (clinician-educators in first 2-5 years), defined their career success almost exclusively around factors intrinsic to their day-to-day job. These factors included such things as excitement about their daily work, developing proficiency in the delivery of high-quality clinical care, and passion for doing work that is meaningful to them. In addition to these immediate job satisfiers, many hospitalists emphasized long-term career success factors such as becoming an expert in a particular domain of hospital medicine and gaining respect and recognition within their local or national environment. Surprisingly, compensation and career advancement through promotion, two traditional external career success factors, were not uniformly valued.

These findings come at a critical time for our field in which early-career faculty outnumber mid- and late-career faculty by an order of magnitude. Indeed, how to develop, promote, sustain, and retain young hospitalists is a topic on the minds of most hospital medicine group directors. Putting aside the impact of hospitalist turnover on productivity, patient care outcomes, and morale within an individual hospital medicine group, we agree with the authors that understanding and cultivating career success for academic hospitalists is imperative for the future of our field. For this reason, we launched a formal faculty development program at Penn this year, which focuses on supporting the growth of hospitalists in their first two years on faculty. The findings of this study provide interesting new perspectives and encourage us to continue our focus on early-career academic hospitalists. We laud the previous efforts in this area and hope that the paper by Cumbler et al. encourages and inspires other programs to start or accelerate their hospitalist faculty development efforts.^3-5

However, some findings from this study are somewhat perplexing or even a bit discouraging for those who are invested in faculty development in academia. For example, the authors raise the possibility that there may be a disconnect in the minds of early-career hospitalists as it pertains to their thoughts on career success. On the one hand, the hospitalists interviewed in this study are happy doing their clinical work and cite this as a primary driver of their career success. On the other hand, they equate career success with things such as developing expertise within a particular domain of hospital medicine, acquiring leadership roles, collaborating academically with other specialties or professions, or developing new innovations. Presumably this is part of the reason that they selected a job in an academic setting as opposed to a community setting. However, in order to achieve these goals, one must devote time and effort to purposefully developing them. Therefore, identifying and developing mentors who can assist early-career hospitalists with identifying, articulating, and developing strategies to achieve both their short- and long-term career goals is critical. One mentor–mentee conversation may reveal that an individual hospitalist values being an excellent clinician and has little interest in developing a niche within hospital medicine; another may reveal a lack of awareness of available professional development resources; still another may uncover a lack of realism regarding the time or skills it takes to achieve a particular career goal. These realities highlight an imperative for our field to develop robust and sustainable mentorship programs for not only early-career hospitalists but also some mid-career hospitalists whose careers may not yet be fully developed. Indeed, one of the biggest challenges that have emerged in our experience with a faculty development program at Penn is creating meaningful mentorship and career development advice for mid-career hospitalists (late assistant or early associate professors who are typically 5-10 years into their careers).

We found it interesting that the hospitalists interviewed did not mention three of the four pillars of career satisfaction outlined in the white paper on Hospitalist Career Satisfaction from the Society for Hospital Medicine: workload schedule, autonomy control, and community/environment.⁶ Perhaps this is because hospitalists, like many other professionals, recognize that feeling satisfied in one’s career is not the same as feeling successful. Satisfaction in one’s career refers to the foundational needs that one requires in order to feel content, whereas success is more often equated with achievement, even if that achievement is simply the acquisition of one’s goals for themselves. The reality is that given the constant growth and change within teaching hospitals, and therefore academic hospital medicine groups, tending to the satisfiers for hospitalists (eg, schedule and workload) often takes a front seat to assisting faculty in achieving their individual career potential. We assert that despite the inherent difficulty, academic hospital medicine group leaders need to focus their attention on both the satisfaction and career success of their early-career faculty.

Finally, this paper raises many interesting questions for researchers interested in the professional development of hospitalists. Are the career success perspectives of an early-career academic hospitalist different from those of an early-career intensivist or emergency medicine physician in an academic setting? Hospital medicine has historically been likened to both fields given the similar intensity of clinical work and the fact that all three fields were created around the need for specialists in a care setting as opposed to a disease state. It is possible that the vision of success for young academic physicians as a whole has changed with the millennial generation entering the workforce. Do early-career hospitalists look different from early-career general internists in academic settings? The latter group has more promoted faculty in their division to serve as role models and mentors and who have demonstrated more success in a variety of replicable career pathways. The fact that the definition of career success may evolve over time also emerged as a theme from this paper. Do mid-career academic hospitalists find that the excitement for daily clinical work wanes over time leaving them feeling less successful and looking for something more?

In conclusion, the findings of Cumbler et al. should promote unrest among leaders of academic hospital medicine groups and their departments of medicine. While it is inspiring to see so many early-career hospitalists focused on their daily happiness at work, we are unsure about whether they have the knowledge, tools, and guidance to achieve their self-professed academic goals, which many equate with career success. Given the continued growth of the hospital medicine workforce, we view this important new work as a national call to arms for the purposeful development of academic hospitalist faculty development programs.

Disclosures

Dr. Myers and Dr. Greysen have nothing to disclose.

Over the past two decades, the field of hospital medicine has gone from relative obscurity to a viable career pathway for approximately 50,000 physicians in this country.¹ A subset of hospitalists pursue careers in academic medicine, which is a pathway that traditionally includes education and scholarship in addition to patient care. While the academic career pathway is well paved in many clinical specialties, it is still relatively underdeveloped for academic hospitalists, and thus what defines career success for this group is even less clear.

In this issue of the Journal of Hospital Medicine, Cumbler et al. performed a qualitative analysis to explore how early career academic hospitalists self-define and perceive their career success.² Drawing on interviews with 17 early-career hospitalists at 3 academic medical centers, the authors created a theoretical framework organized around a traditional conceptual model of career success that is divided into intrinsic and extrinsic motivating factors. They found that early-career academic hospitalists, (clinician-educators in first 2-5 years), defined their career success almost exclusively around factors intrinsic to their day-to-day job. These factors included such things as excitement about their daily work, developing proficiency in the delivery of high-quality clinical care, and passion for doing work that is meaningful to them. In addition to these immediate job satisfiers, many hospitalists emphasized long-term career success factors such as becoming an expert in a particular domain of hospital medicine and gaining respect and recognition within their local or national environment. Surprisingly, compensation and career advancement through promotion, two traditional external career success factors, were not uniformly valued.

These findings come at a critical time for our field in which early-career faculty outnumber mid- and late-career faculty by an order of magnitude. Indeed, how to develop, promote, sustain, and retain young hospitalists is a topic on the minds of most hospital medicine group directors. Putting aside the impact of hospitalist turnover on productivity, patient care outcomes, and morale within an individual hospital medicine group, we agree with the authors that understanding and cultivating career success for academic hospitalists is imperative for the future of our field. For this reason, we launched a formal faculty development program at Penn this year, which focuses on supporting the growth of hospitalists in their first two years on faculty. The findings of this study provide interesting new perspectives and encourage us to continue our focus on early-career academic hospitalists. We laud the previous efforts in this area and hope that the paper by Cumbler et al. encourages and inspires other programs to start or accelerate their hospitalist faculty development efforts.^3-5

However, some findings from this study are somewhat perplexing or even a bit discouraging for those who are invested in faculty development in academia. For example, the authors raise the possibility that there may be a disconnect in the minds of early-career hospitalists as it pertains to their thoughts on career success. On the one hand, the hospitalists interviewed in this study are happy doing their clinical work and cite this as a primary driver of their career success. On the other hand, they equate career success with things such as developing expertise within a particular domain of hospital medicine, acquiring leadership roles, collaborating academically with other specialties or professions, or developing new innovations. Presumably this is part of the reason that they selected a job in an academic setting as opposed to a community setting. However, in order to achieve these goals, one must devote time and effort to purposefully developing them. Therefore, identifying and developing mentors who can assist early-career hospitalists with identifying, articulating, and developing strategies to achieve both their short- and long-term career goals is critical. One mentor–mentee conversation may reveal that an individual hospitalist values being an excellent clinician and has little interest in developing a niche within hospital medicine; another may reveal a lack of awareness of available professional development resources; still another may uncover a lack of realism regarding the time or skills it takes to achieve a particular career goal. These realities highlight an imperative for our field to develop robust and sustainable mentorship programs for not only early-career hospitalists but also some mid-career hospitalists whose careers may not yet be fully developed. Indeed, one of the biggest challenges that have emerged in our experience with a faculty development program at Penn is creating meaningful mentorship and career development advice for mid-career hospitalists (late assistant or early associate professors who are typically 5-10 years into their careers).

We found it interesting that the hospitalists interviewed did not mention three of the four pillars of career satisfaction outlined in the white paper on Hospitalist Career Satisfaction from the Society for Hospital Medicine: workload schedule, autonomy control, and community/environment.⁶ Perhaps this is because hospitalists, like many other professionals, recognize that feeling satisfied in one’s career is not the same as feeling successful. Satisfaction in one’s career refers to the foundational needs that one requires in order to feel content, whereas success is more often equated with achievement, even if that achievement is simply the acquisition of one’s goals for themselves. The reality is that given the constant growth and change within teaching hospitals, and therefore academic hospital medicine groups, tending to the satisfiers for hospitalists (eg, schedule and workload) often takes a front seat to assisting faculty in achieving their individual career potential. We assert that despite the inherent difficulty, academic hospital medicine group leaders need to focus their attention on both the satisfaction and career success of their early-career faculty.

Finally, this paper raises many interesting questions for researchers interested in the professional development of hospitalists. Are the career success perspectives of an early-career academic hospitalist different from those of an early-career intensivist or emergency medicine physician in an academic setting? Hospital medicine has historically been likened to both fields given the similar intensity of clinical work and the fact that all three fields were created around the need for specialists in a care setting as opposed to a disease state. It is possible that the vision of success for young academic physicians as a whole has changed with the millennial generation entering the workforce. Do early-career hospitalists look different from early-career general internists in academic settings? The latter group has more promoted faculty in their division to serve as role models and mentors and who have demonstrated more success in a variety of replicable career pathways. The fact that the definition of career success may evolve over time also emerged as a theme from this paper. Do mid-career academic hospitalists find that the excitement for daily clinical work wanes over time leaving them feeling less successful and looking for something more?

In conclusion, the findings of Cumbler et al. should promote unrest among leaders of academic hospital medicine groups and their departments of medicine. While it is inspiring to see so many early-career hospitalists focused on their daily happiness at work, we are unsure about whether they have the knowledge, tools, and guidance to achieve their self-professed academic goals, which many equate with career success. Given the continued growth of the hospital medicine workforce, we view this important new work as a national call to arms for the purposeful development of academic hospitalist faculty development programs.

Disclosures

Dr. Myers and Dr. Greysen have nothing to disclose.

Over the past two decades, the field of hospital medicine has gone from relative obscurity to a viable career pathway for approximately 50,000 physicians in this country.¹ A subset of hospitalists pursue careers in academic medicine, which is a pathway that traditionally includes education and scholarship in addition to patient care. While the academic career pathway is well paved in many clinical specialties, it is still relatively underdeveloped for academic hospitalists, and thus what defines career success for this group is even less clear.

In this issue of the Journal of Hospital Medicine, Cumbler et al. performed a qualitative analysis to explore how early career academic hospitalists self-define and perceive their career success.² Drawing on interviews with 17 early-career hospitalists at 3 academic medical centers, the authors created a theoretical framework organized around a traditional conceptual model of career success that is divided into intrinsic and extrinsic motivating factors. They found that early-career academic hospitalists, (clinician-educators in first 2-5 years), defined their career success almost exclusively around factors intrinsic to their day-to-day job. These factors included such things as excitement about their daily work, developing proficiency in the delivery of high-quality clinical care, and passion for doing work that is meaningful to them. In addition to these immediate job satisfiers, many hospitalists emphasized long-term career success factors such as becoming an expert in a particular domain of hospital medicine and gaining respect and recognition within their local or national environment. Surprisingly, compensation and career advancement through promotion, two traditional external career success factors, were not uniformly valued.

These findings come at a critical time for our field in which early-career faculty outnumber mid- and late-career faculty by an order of magnitude. Indeed, how to develop, promote, sustain, and retain young hospitalists is a topic on the minds of most hospital medicine group directors. Putting aside the impact of hospitalist turnover on productivity, patient care outcomes, and morale within an individual hospital medicine group, we agree with the authors that understanding and cultivating career success for academic hospitalists is imperative for the future of our field. For this reason, we launched a formal faculty development program at Penn this year, which focuses on supporting the growth of hospitalists in their first two years on faculty. The findings of this study provide interesting new perspectives and encourage us to continue our focus on early-career academic hospitalists. We laud the previous efforts in this area and hope that the paper by Cumbler et al. encourages and inspires other programs to start or accelerate their hospitalist faculty development efforts.^3-5

However, some findings from this study are somewhat perplexing or even a bit discouraging for those who are invested in faculty development in academia. For example, the authors raise the possibility that there may be a disconnect in the minds of early-career hospitalists as it pertains to their thoughts on career success. On the one hand, the hospitalists interviewed in this study are happy doing their clinical work and cite this as a primary driver of their career success. On the other hand, they equate career success with things such as developing expertise within a particular domain of hospital medicine, acquiring leadership roles, collaborating academically with other specialties or professions, or developing new innovations. Presumably this is part of the reason that they selected a job in an academic setting as opposed to a community setting. However, in order to achieve these goals, one must devote time and effort to purposefully developing them. Therefore, identifying and developing mentors who can assist early-career hospitalists with identifying, articulating, and developing strategies to achieve both their short- and long-term career goals is critical. One mentor–mentee conversation may reveal that an individual hospitalist values being an excellent clinician and has little interest in developing a niche within hospital medicine; another may reveal a lack of awareness of available professional development resources; still another may uncover a lack of realism regarding the time or skills it takes to achieve a particular career goal. These realities highlight an imperative for our field to develop robust and sustainable mentorship programs for not only early-career hospitalists but also some mid-career hospitalists whose careers may not yet be fully developed. Indeed, one of the biggest challenges that have emerged in our experience with a faculty development program at Penn is creating meaningful mentorship and career development advice for mid-career hospitalists (late assistant or early associate professors who are typically 5-10 years into their careers).

We found it interesting that the hospitalists interviewed did not mention three of the four pillars of career satisfaction outlined in the white paper on Hospitalist Career Satisfaction from the Society for Hospital Medicine: workload schedule, autonomy control, and community/environment.⁶ Perhaps this is because hospitalists, like many other professionals, recognize that feeling satisfied in one’s career is not the same as feeling successful. Satisfaction in one’s career refers to the foundational needs that one requires in order to feel content, whereas success is more often equated with achievement, even if that achievement is simply the acquisition of one’s goals for themselves. The reality is that given the constant growth and change within teaching hospitals, and therefore academic hospital medicine groups, tending to the satisfiers for hospitalists (eg, schedule and workload) often takes a front seat to assisting faculty in achieving their individual career potential. We assert that despite the inherent difficulty, academic hospital medicine group leaders need to focus their attention on both the satisfaction and career success of their early-career faculty.

Finally, this paper raises many interesting questions for researchers interested in the professional development of hospitalists. Are the career success perspectives of an early-career academic hospitalist different from those of an early-career intensivist or emergency medicine physician in an academic setting? Hospital medicine has historically been likened to both fields given the similar intensity of clinical work and the fact that all three fields were created around the need for specialists in a care setting as opposed to a disease state. It is possible that the vision of success for young academic physicians as a whole has changed with the millennial generation entering the workforce. Do early-career hospitalists look different from early-career general internists in academic settings? The latter group has more promoted faculty in their division to serve as role models and mentors and who have demonstrated more success in a variety of replicable career pathways. The fact that the definition of career success may evolve over time also emerged as a theme from this paper. Do mid-career academic hospitalists find that the excitement for daily clinical work wanes over time leaving them feeling less successful and looking for something more?

In conclusion, the findings of Cumbler et al. should promote unrest among leaders of academic hospital medicine groups and their departments of medicine. While it is inspiring to see so many early-career hospitalists focused on their daily happiness at work, we are unsure about whether they have the knowledge, tools, and guidance to achieve their self-professed academic goals, which many equate with career success. Given the continued growth of the hospital medicine workforce, we view this important new work as a national call to arms for the purposeful development of academic hospitalist faculty development programs.

Disclosures

Dr. Myers and Dr. Greysen have nothing to disclose.

¹Medical College of Wisconsin Affiliated Hospitals, Milwaukee, Wisconsin. At the time of this study, Dr. Bergl was with the Division of General Internal Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin. ²Medical College of Wisconsin, Milwaukee, Wisconsin.Physical examination (PE) is a core clinical skill in undergraduate medical education.¹ Although the optimal approach to teaching clinical skills is debated, robust preclinical curricula should generally be followed by iterative skill development during clinical rotations.^2,3

The internal medicine rotation represents a critical time to enhance PE skills. Diagnostic decision making and PE are highly prioritized competencies for the internal medicine clerkship,⁴ and students will likely utilize many core examination skills^1,2 during this time. Bedside teaching of PE during the internal medicine service also provides an opportunity for students to receive feedback based on direct observation,⁵ a sine qua non of competency-based assessment.

Unfortunately, current internal medicine training environments limit opportunities for workplace-based instruction in PE. Recent studies suggest diminishing time spent on bedside patient care and teaching, with computer-based “indirect patient care” dominating much of the clinical workday of internal medicine services.^6-8 However, the literature does not delineate how often medical students are enhancing their PE skills during clinical rotations or describe how the educational environment may influence PE teaching.

We aimed to describe the content and context of PE instruction during the internal medicine clerkship workflow. Specifically, we sought to explore what strategies physician team members used to teach PE to students. We also sought to describe factors in the inpatient learning environment that might explain why physical examination (PE) instruction occurs infrequently.

We conducted a prospective mixed-methods study using time motion analysis, checklists on clinical teaching, and daily open-ended observations written by a trained observer from June through August 2015 at a single academic medical center. Subjects were recruited from internal medicine teaching teams and were allowed to opt out. Teaching teams had 2 formats: (1) traditional team with an attending physician (hospitalist or general internist), a senior resident, 2 interns, a fourth-year medical student, and 2 third-year students or (2) hospitalist team in which a third-year student works directly with a hospitalist and advanced practitioner. The proposal was submitted to the Medical College of Wisconsin Institutional Review Board and deemed exempt from further review.

All observations were carried out by a single investigator (A.T.), who was a second-year medical student at the time. To train this observer and to pilot the data collection instruments, our lead investigator (P.B.) directly supervised our observer on 4 separate occasions, totaling over 12 hours of mentored co-observation. Immediately after each training session, both investigators (A.T. and P.B.) debriefed to compare notes, to review checklists on recorded observations, and to discuss areas of uncertainty. During the training period, formal metrics of agreement (eg, kappa coefficients) were not gathered, as data collection instruments were still being refined.

Observation periods were centered on third-year medical students and their interactions with patients and members of the teaching team. Observed activities included pre-rounding, teaching rounds with the attending physician, and new patient admissions during call days. Observations generally occurred between the hours of 7 AM and 6 PM, and we limited periods of observation to 3 consecutive hours to minimize observer fatigue. Observation periods were selected to maximize the number of subjects and teams observed, to adequately capture pre-rounding and new admissions activities, and to account for variations in rounding styles throughout the call cycle. Teams were excluded if a member of the study team was an attending physician on the clinical team or if any member of the patient care team had opted out of the study.

Data were collected on paper checklists that included idealized bedside teaching activities around PE. Teaching activities were identified through a review of relevant literature^9,10 and were further informed by our senior investigator’s own experience with faculty development in this area¹¹ and team members’ attendance at bedside teaching workshops. At the end of each day, our observer also wrote brief observations that summarized factors affecting bedside teaching of PE. Checklist data were transferred to an Excel file (Microsoft), and written observations were imported into NVivo 10 (QRS International, Melbourne, Australia) for coding and analysis.

Checklist data were analyzed using simple descriptive statistics. We compared time spent on various types of rounding using ANOVA, and we used a Student two-tailed t-test to compare the amount of time students spent examining patients on pre-rounds versus new admissions. To ascertain differences in the frequency of PE teaching activities by location, we used chi-squared tests. Statistical analysis was performed using embedded statistics functions in Microsoft Excel. A P value of <.05 was used as the cut-off for significance.

We analyzed the written observations using conventional qualitative content analysis. Two investigators (A.T. and P.B.) reviewed the written comments and used open coding to devise a preliminary inductive coding scheme. Codes were refined iteratively, and a schema of categories and nodes was outlined in a codebook that was periodically reviewed by the entire research team. The coding investigators met regularly to ensure consistency in coding, and a third team member remained available to reconcile significant disagreements in code definitions.

Eighty-one subjects participated in the study: 21 were attending physicians, 12 residents, 21 interns, 11 senior medical students, and 26 junior medical students. We observed 16 distinct inpatient teaching teams and 329 unique patient-related events (discussions and/or patient-clinician encounters), with most events being observed during attending rounds (269/329, or 82%). There were 123 encounters at the bedside, averaging 7 minutes; 43 encounters occurred in the hallway, averaging 8 minutes each; and 163 encounters occurred in a workroom and averaged 7 minutes per patient discussion. We also observed 28 student-patient encounters during pre-round activities and 30 student-patient encounters during new admissions.

Teaching and Direct Observation

During 28 pre-rounding encounters, students usually examined the patient (26 out of 28 instances, 93%) but were observed only 4 times doing so (out of 26 instances, or 15%). During 30 new patient admissions, students examined 27 patients (90%) and had their PE observed 6 times (out of 27 instances, or 22%). There were no significant differences in frequency of these activities (P > .05, chi-squared) between pre-rounds or new admissions.

Observations on Teaching Strategies

In the written observations, we categorized various methods being used to teach PE. Bedside teaching of PE most often involved teachers simply describing or discussing physical findings (42 mentions in observations) or verifying a student’s reported findings (15 mentions). Teachers were also observed to use bedside teaching to contextualize findings (13 mentions), such as relating the quality of bowel sounds to the patient’s constipation or to discuss expected pupillary light reflexes in a neurologically intact patient. Less commonly, attending physicians narrated steps in their PE technique (9 mentions). Students were infrequently encouraged to practice a specific PE skill again (7 mentions) or allowed to re-examine and reconsider their initial interpretations (5 mentions).

This observational study of clinical teaching on internal medicine teaching services demonstrates that PE teaching is most likely to occur during bedside rounding. However, even in bedside encounters, most PE instruction is limited to physician team members pointing out significant findings. Although physical findings were mentioned for the majority of patients seen on rounds, attending physicians infrequently verified students’ or residents’ findings, demonstrated technique, or incorporated PE into clinical decision making. We witnessed an alarming dearth of direct observation of students and almost no real-time feedback in performing and teaching PE. Thus, students rarely had opportunities to engage in higher-order learning activities related to PE on the internal medicine rotation.

We posit that the learning environment influenced PE instruction on the internal medicine rotation. To optimize inpatient teaching of PE, attending physicians need to consider the factors we identified in Table 2. Such teaching may be effective with a more limited number of participants and without distraction from technology. Time constraints are one of the major perceived barriers to bedside teaching of PE, and our data support this concern, as teams spent an average of only 7 minutes on each bedside encounter. However, many of the strategies observed to be used in real-time PE instruction, such as validating the learners’ findings or examining patients as a team, naturally fit into clinical routines and generally do not require extra thought or preparation.

One of the key strengths of our study is the use of direct observation of students and their teachers. This study is unique in its exclusive focus on PE and its description of factors affecting PE teaching activities on an internal medicine service. This observational, descriptive study also has obvious limitations. The study was conducted at a single institution during a limited time period. Moreover, the study period June through August, which was chosen based on our observer’s availability, includes the transition to a new academic year (July 1, 2015) when medical students and residents were becoming acclimated to their new roles. Additionally, the data were collected by a single researcher, and observer bias may affect the results of qualitative analysis of journal entries.

In conclusion, this study highlights the infrequency of applied PE skills in the daily clinical and educational workflow of internal medicine teaching teams. These findings may reflect a more widespread problem in clinical education, and replication of our findings at other teaching centers could galvanize faculty development around bedside PE teaching.

Disclosures

Dr. Bergl has nothing to disclose. Ms. Taylor reports grant support from the Cohen Endowment for Medical Student Research at the Medical College of Wisconsin during the conduct of the study. Mrs. Klumb, Ms. Quirk, Dr. Muntz, and Dr. Fletcher have nothing to disclose.

Funding

This work was funded in part by the Cohen Endowment for Medical Student Research at the Medical College of Wisconsin.

¹Medical College of Wisconsin Affiliated Hospitals, Milwaukee, Wisconsin. At the time of this study, Dr. Bergl was with the Division of General Internal Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin. ²Medical College of Wisconsin, Milwaukee, Wisconsin.Physical examination (PE) is a core clinical skill in undergraduate medical education.¹ Although the optimal approach to teaching clinical skills is debated, robust preclinical curricula should generally be followed by iterative skill development during clinical rotations.^2,3

The internal medicine rotation represents a critical time to enhance PE skills. Diagnostic decision making and PE are highly prioritized competencies for the internal medicine clerkship,⁴ and students will likely utilize many core examination skills^1,2 during this time. Bedside teaching of PE during the internal medicine service also provides an opportunity for students to receive feedback based on direct observation,⁵ a sine qua non of competency-based assessment.

Unfortunately, current internal medicine training environments limit opportunities for workplace-based instruction in PE. Recent studies suggest diminishing time spent on bedside patient care and teaching, with computer-based “indirect patient care” dominating much of the clinical workday of internal medicine services.^6-8 However, the literature does not delineate how often medical students are enhancing their PE skills during clinical rotations or describe how the educational environment may influence PE teaching.

We aimed to describe the content and context of PE instruction during the internal medicine clerkship workflow. Specifically, we sought to explore what strategies physician team members used to teach PE to students. We also sought to describe factors in the inpatient learning environment that might explain why physical examination (PE) instruction occurs infrequently.

We conducted a prospective mixed-methods study using time motion analysis, checklists on clinical teaching, and daily open-ended observations written by a trained observer from June through August 2015 at a single academic medical center. Subjects were recruited from internal medicine teaching teams and were allowed to opt out. Teaching teams had 2 formats: (1) traditional team with an attending physician (hospitalist or general internist), a senior resident, 2 interns, a fourth-year medical student, and 2 third-year students or (2) hospitalist team in which a third-year student works directly with a hospitalist and advanced practitioner. The proposal was submitted to the Medical College of Wisconsin Institutional Review Board and deemed exempt from further review.

All observations were carried out by a single investigator (A.T.), who was a second-year medical student at the time. To train this observer and to pilot the data collection instruments, our lead investigator (P.B.) directly supervised our observer on 4 separate occasions, totaling over 12 hours of mentored co-observation. Immediately after each training session, both investigators (A.T. and P.B.) debriefed to compare notes, to review checklists on recorded observations, and to discuss areas of uncertainty. During the training period, formal metrics of agreement (eg, kappa coefficients) were not gathered, as data collection instruments were still being refined.

Observation periods were centered on third-year medical students and their interactions with patients and members of the teaching team. Observed activities included pre-rounding, teaching rounds with the attending physician, and new patient admissions during call days. Observations generally occurred between the hours of 7 AM and 6 PM, and we limited periods of observation to 3 consecutive hours to minimize observer fatigue. Observation periods were selected to maximize the number of subjects and teams observed, to adequately capture pre-rounding and new admissions activities, and to account for variations in rounding styles throughout the call cycle. Teams were excluded if a member of the study team was an attending physician on the clinical team or if any member of the patient care team had opted out of the study.

Data were collected on paper checklists that included idealized bedside teaching activities around PE. Teaching activities were identified through a review of relevant literature^9,10 and were further informed by our senior investigator’s own experience with faculty development in this area¹¹ and team members’ attendance at bedside teaching workshops. At the end of each day, our observer also wrote brief observations that summarized factors affecting bedside teaching of PE. Checklist data were transferred to an Excel file (Microsoft), and written observations were imported into NVivo 10 (QRS International, Melbourne, Australia) for coding and analysis.

Checklist data were analyzed using simple descriptive statistics. We compared time spent on various types of rounding using ANOVA, and we used a Student two-tailed t-test to compare the amount of time students spent examining patients on pre-rounds versus new admissions. To ascertain differences in the frequency of PE teaching activities by location, we used chi-squared tests. Statistical analysis was performed using embedded statistics functions in Microsoft Excel. A P value of <.05 was used as the cut-off for significance.

We analyzed the written observations using conventional qualitative content analysis. Two investigators (A.T. and P.B.) reviewed the written comments and used open coding to devise a preliminary inductive coding scheme. Codes were refined iteratively, and a schema of categories and nodes was outlined in a codebook that was periodically reviewed by the entire research team. The coding investigators met regularly to ensure consistency in coding, and a third team member remained available to reconcile significant disagreements in code definitions.

Eighty-one subjects participated in the study: 21 were attending physicians, 12 residents, 21 interns, 11 senior medical students, and 26 junior medical students. We observed 16 distinct inpatient teaching teams and 329 unique patient-related events (discussions and/or patient-clinician encounters), with most events being observed during attending rounds (269/329, or 82%). There were 123 encounters at the bedside, averaging 7 minutes; 43 encounters occurred in the hallway, averaging 8 minutes each; and 163 encounters occurred in a workroom and averaged 7 minutes per patient discussion. We also observed 28 student-patient encounters during pre-round activities and 30 student-patient encounters during new admissions.

Teaching and Direct Observation

During 28 pre-rounding encounters, students usually examined the patient (26 out of 28 instances, 93%) but were observed only 4 times doing so (out of 26 instances, or 15%). During 30 new patient admissions, students examined 27 patients (90%) and had their PE observed 6 times (out of 27 instances, or 22%). There were no significant differences in frequency of these activities (P > .05, chi-squared) between pre-rounds or new admissions.

Observations on Teaching Strategies

In the written observations, we categorized various methods being used to teach PE. Bedside teaching of PE most often involved teachers simply describing or discussing physical findings (42 mentions in observations) or verifying a student’s reported findings (15 mentions). Teachers were also observed to use bedside teaching to contextualize findings (13 mentions), such as relating the quality of bowel sounds to the patient’s constipation or to discuss expected pupillary light reflexes in a neurologically intact patient. Less commonly, attending physicians narrated steps in their PE technique (9 mentions). Students were infrequently encouraged to practice a specific PE skill again (7 mentions) or allowed to re-examine and reconsider their initial interpretations (5 mentions).

This observational study of clinical teaching on internal medicine teaching services demonstrates that PE teaching is most likely to occur during bedside rounding. However, even in bedside encounters, most PE instruction is limited to physician team members pointing out significant findings. Although physical findings were mentioned for the majority of patients seen on rounds, attending physicians infrequently verified students’ or residents’ findings, demonstrated technique, or incorporated PE into clinical decision making. We witnessed an alarming dearth of direct observation of students and almost no real-time feedback in performing and teaching PE. Thus, students rarely had opportunities to engage in higher-order learning activities related to PE on the internal medicine rotation.

We posit that the learning environment influenced PE instruction on the internal medicine rotation. To optimize inpatient teaching of PE, attending physicians need to consider the factors we identified in Table 2. Such teaching may be effective with a more limited number of participants and without distraction from technology. Time constraints are one of the major perceived barriers to bedside teaching of PE, and our data support this concern, as teams spent an average of only 7 minutes on each bedside encounter. However, many of the strategies observed to be used in real-time PE instruction, such as validating the learners’ findings or examining patients as a team, naturally fit into clinical routines and generally do not require extra thought or preparation.

One of the key strengths of our study is the use of direct observation of students and their teachers. This study is unique in its exclusive focus on PE and its description of factors affecting PE teaching activities on an internal medicine service. This observational, descriptive study also has obvious limitations. The study was conducted at a single institution during a limited time period. Moreover, the study period June through August, which was chosen based on our observer’s availability, includes the transition to a new academic year (July 1, 2015) when medical students and residents were becoming acclimated to their new roles. Additionally, the data were collected by a single researcher, and observer bias may affect the results of qualitative analysis of journal entries.

In conclusion, this study highlights the infrequency of applied PE skills in the daily clinical and educational workflow of internal medicine teaching teams. These findings may reflect a more widespread problem in clinical education, and replication of our findings at other teaching centers could galvanize faculty development around bedside PE teaching.

Disclosures

Dr. Bergl has nothing to disclose. Ms. Taylor reports grant support from the Cohen Endowment for Medical Student Research at the Medical College of Wisconsin during the conduct of the study. Mrs. Klumb, Ms. Quirk, Dr. Muntz, and Dr. Fletcher have nothing to disclose.

Funding

This work was funded in part by the Cohen Endowment for Medical Student Research at the Medical College of Wisconsin.

¹Medical College of Wisconsin Affiliated Hospitals, Milwaukee, Wisconsin. At the time of this study, Dr. Bergl was with the Division of General Internal Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin. ²Medical College of Wisconsin, Milwaukee, Wisconsin.Physical examination (PE) is a core clinical skill in undergraduate medical education.¹ Although the optimal approach to teaching clinical skills is debated, robust preclinical curricula should generally be followed by iterative skill development during clinical rotations.^2,3

The internal medicine rotation represents a critical time to enhance PE skills. Diagnostic decision making and PE are highly prioritized competencies for the internal medicine clerkship,⁴ and students will likely utilize many core examination skills^1,2 during this time. Bedside teaching of PE during the internal medicine service also provides an opportunity for students to receive feedback based on direct observation,⁵ a sine qua non of competency-based assessment.

Unfortunately, current internal medicine training environments limit opportunities for workplace-based instruction in PE. Recent studies suggest diminishing time spent on bedside patient care and teaching, with computer-based “indirect patient care” dominating much of the clinical workday of internal medicine services.^6-8 However, the literature does not delineate how often medical students are enhancing their PE skills during clinical rotations or describe how the educational environment may influence PE teaching.

We aimed to describe the content and context of PE instruction during the internal medicine clerkship workflow. Specifically, we sought to explore what strategies physician team members used to teach PE to students. We also sought to describe factors in the inpatient learning environment that might explain why physical examination (PE) instruction occurs infrequently.

We conducted a prospective mixed-methods study using time motion analysis, checklists on clinical teaching, and daily open-ended observations written by a trained observer from June through August 2015 at a single academic medical center. Subjects were recruited from internal medicine teaching teams and were allowed to opt out. Teaching teams had 2 formats: (1) traditional team with an attending physician (hospitalist or general internist), a senior resident, 2 interns, a fourth-year medical student, and 2 third-year students or (2) hospitalist team in which a third-year student works directly with a hospitalist and advanced practitioner. The proposal was submitted to the Medical College of Wisconsin Institutional Review Board and deemed exempt from further review.

All observations were carried out by a single investigator (A.T.), who was a second-year medical student at the time. To train this observer and to pilot the data collection instruments, our lead investigator (P.B.) directly supervised our observer on 4 separate occasions, totaling over 12 hours of mentored co-observation. Immediately after each training session, both investigators (A.T. and P.B.) debriefed to compare notes, to review checklists on recorded observations, and to discuss areas of uncertainty. During the training period, formal metrics of agreement (eg, kappa coefficients) were not gathered, as data collection instruments were still being refined.

Observation periods were centered on third-year medical students and their interactions with patients and members of the teaching team. Observed activities included pre-rounding, teaching rounds with the attending physician, and new patient admissions during call days. Observations generally occurred between the hours of 7 AM and 6 PM, and we limited periods of observation to 3 consecutive hours to minimize observer fatigue. Observation periods were selected to maximize the number of subjects and teams observed, to adequately capture pre-rounding and new admissions activities, and to account for variations in rounding styles throughout the call cycle. Teams were excluded if a member of the study team was an attending physician on the clinical team or if any member of the patient care team had opted out of the study.

Data were collected on paper checklists that included idealized bedside teaching activities around PE. Teaching activities were identified through a review of relevant literature^9,10 and were further informed by our senior investigator’s own experience with faculty development in this area¹¹ and team members’ attendance at bedside teaching workshops. At the end of each day, our observer also wrote brief observations that summarized factors affecting bedside teaching of PE. Checklist data were transferred to an Excel file (Microsoft), and written observations were imported into NVivo 10 (QRS International, Melbourne, Australia) for coding and analysis.

Checklist data were analyzed using simple descriptive statistics. We compared time spent on various types of rounding using ANOVA, and we used a Student two-tailed t-test to compare the amount of time students spent examining patients on pre-rounds versus new admissions. To ascertain differences in the frequency of PE teaching activities by location, we used chi-squared tests. Statistical analysis was performed using embedded statistics functions in Microsoft Excel. A P value of <.05 was used as the cut-off for significance.

We analyzed the written observations using conventional qualitative content analysis. Two investigators (A.T. and P.B.) reviewed the written comments and used open coding to devise a preliminary inductive coding scheme. Codes were refined iteratively, and a schema of categories and nodes was outlined in a codebook that was periodically reviewed by the entire research team. The coding investigators met regularly to ensure consistency in coding, and a third team member remained available to reconcile significant disagreements in code definitions.

Eighty-one subjects participated in the study: 21 were attending physicians, 12 residents, 21 interns, 11 senior medical students, and 26 junior medical students. We observed 16 distinct inpatient teaching teams and 329 unique patient-related events (discussions and/or patient-clinician encounters), with most events being observed during attending rounds (269/329, or 82%). There were 123 encounters at the bedside, averaging 7 minutes; 43 encounters occurred in the hallway, averaging 8 minutes each; and 163 encounters occurred in a workroom and averaged 7 minutes per patient discussion. We also observed 28 student-patient encounters during pre-round activities and 30 student-patient encounters during new admissions.

Teaching and Direct Observation

During 28 pre-rounding encounters, students usually examined the patient (26 out of 28 instances, 93%) but were observed only 4 times doing so (out of 26 instances, or 15%). During 30 new patient admissions, students examined 27 patients (90%) and had their PE observed 6 times (out of 27 instances, or 22%). There were no significant differences in frequency of these activities (P > .05, chi-squared) between pre-rounds or new admissions.

Observations on Teaching Strategies

In the written observations, we categorized various methods being used to teach PE. Bedside teaching of PE most often involved teachers simply describing or discussing physical findings (42 mentions in observations) or verifying a student’s reported findings (15 mentions). Teachers were also observed to use bedside teaching to contextualize findings (13 mentions), such as relating the quality of bowel sounds to the patient’s constipation or to discuss expected pupillary light reflexes in a neurologically intact patient. Less commonly, attending physicians narrated steps in their PE technique (9 mentions). Students were infrequently encouraged to practice a specific PE skill again (7 mentions) or allowed to re-examine and reconsider their initial interpretations (5 mentions).

This observational study of clinical teaching on internal medicine teaching services demonstrates that PE teaching is most likely to occur during bedside rounding. However, even in bedside encounters, most PE instruction is limited to physician team members pointing out significant findings. Although physical findings were mentioned for the majority of patients seen on rounds, attending physicians infrequently verified students’ or residents’ findings, demonstrated technique, or incorporated PE into clinical decision making. We witnessed an alarming dearth of direct observation of students and almost no real-time feedback in performing and teaching PE. Thus, students rarely had opportunities to engage in higher-order learning activities related to PE on the internal medicine rotation.

We posit that the learning environment influenced PE instruction on the internal medicine rotation. To optimize inpatient teaching of PE, attending physicians need to consider the factors we identified in Table 2. Such teaching may be effective with a more limited number of participants and without distraction from technology. Time constraints are one of the major perceived barriers to bedside teaching of PE, and our data support this concern, as teams spent an average of only 7 minutes on each bedside encounter. However, many of the strategies observed to be used in real-time PE instruction, such as validating the learners’ findings or examining patients as a team, naturally fit into clinical routines and generally do not require extra thought or preparation.

One of the key strengths of our study is the use of direct observation of students and their teachers. This study is unique in its exclusive focus on PE and its description of factors affecting PE teaching activities on an internal medicine service. This observational, descriptive study also has obvious limitations. The study was conducted at a single institution during a limited time period. Moreover, the study period June through August, which was chosen based on our observer’s availability, includes the transition to a new academic year (July 1, 2015) when medical students and residents were becoming acclimated to their new roles. Additionally, the data were collected by a single researcher, and observer bias may affect the results of qualitative analysis of journal entries.

In conclusion, this study highlights the infrequency of applied PE skills in the daily clinical and educational workflow of internal medicine teaching teams. These findings may reflect a more widespread problem in clinical education, and replication of our findings at other teaching centers could galvanize faculty development around bedside PE teaching.

Disclosures

Dr. Bergl has nothing to disclose. Ms. Taylor reports grant support from the Cohen Endowment for Medical Student Research at the Medical College of Wisconsin during the conduct of the study. Mrs. Klumb, Ms. Quirk, Dr. Muntz, and Dr. Fletcher have nothing to disclose.

Funding

This work was funded in part by the Cohen Endowment for Medical Student Research at the Medical College of Wisconsin.

After discharge from the hospital, patients have a significantly elevated risk for adverse events, including emergency department use, hospital readmission, and death. More than 1 in 3 patients discharged from the hospital require acute care in the month after hospital discharge, and more than 1 in 6 require readmission, with readmission diagnoses frequently differing from those of the preceding hospitalization.^1-4 This heightened susceptibility to adverse events persists beyond 30 days but levels off by 7 weeks after discharge, suggesting that the period of increased risk is transient and dynamic.⁵

The term posthospital syndrome (PHS) describes this period of vulnerability to major adverse events following hospitalization.⁶ In addition to increased risk for readmission and mortality, patients in this period often show evidence of generalized dysfunction with new cognitive impairment, mobility disability, or functional decline.^7-12 To date, the etiology of this vulnerability is neither well understood nor effectively addressed by transitional care interventions.¹³

One hypothesis to explain PHS is that stressors associated with the experience of hospitalization contribute to transient multisystem dysfunction that induces susceptibility to a broad range of medical maladies. These stressors include frequent sleep disruption, noxious sounds, painful stimuli, mobility restrictions, and poor nutrition.¹² The stress hypothesis as a cause of PHS is therefore based, in large part, on evidence about allostasis and the deleterious effects of allostatic overload.

Allostasis defines a system functioning within normal stress-response parameters to promote adaptation and survival.¹⁴ In allostasis, the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic and parasympathetic branches of the autonomic nervous system (ANS) exist in homeostatic balance and respond to environmental stimuli within a range of healthy physiologic parameters. The hallmark of a system in allostasis is the ability to rapidly activate, then successfully deactivate, a stress response once the stressor (ie, threat) has resolved.^14,15 To promote survival and potentiate “fight or flight” mechanisms, an appropriate stress response necessarily impacts multiple physiologic systems that result in hemodynamic augmentation and gluconeogenesis to support the anticipated action of large muscle groups, heightened vigilance and memory capabilities to improve rapid decision-making, and enhancement of innate and adaptive immune capabilities to prepare for wound repair and infection defense.^14-16 The stress response is subsequently terminated by negative feedback mechanisms of glucocorticoids as well as a shift of the ANS from sympathetic to parasympathetic tone.^17,18

Extended or repetitive stress exposure, however, leads to dysregulation of allostatic mechanisms responsible for stress adaptation and hinders an efficient and effective stress response. After extended stress exposure, baseline (ie, resting) HPA activity resets, causing a disruption of normal diurnal cortisol rhythm and an increase in total cortisol concentration. Moreover, in response to stress, HPA and ANS system excitation becomes impaired, and negative feedback properties are undermined.^14,15 This maladaptive state, known as allostatic overload, disrupts the finely tuned mechanisms that are the foundation of mind-body balance and yields pathophysiologic consequences to multiple organ systems. Downstream ramifications of allostatic overload include cognitive deterioration, cardiovascular and immune system dysfunction, and functional decline.^14,15,19

Although a stress response is an expected and necessary aspect of acute illness that promotes survival, the central thesis of this work is that additional environmental and social stressors inherent in hospitalization may unnecessarily compound stress and increase the risk of HPA axis dysfunction, allostatic overload, and subsequent multisystem dysfunction, predisposing individuals to adverse outcomes after hospital discharge. Based on data from both human subjects and animal models, we present a possible pathophysiologic mechanism for the postdischarge vulnerability of PHS, encourage critical contemplation of traditional hospitalization, and suggest interventions that might improve outcomes.

Posthospital syndrome (PHS) describes a transient period of vulnerability after hospitalization during which patients are at elevated risk for adverse events from a broad range of conditions. In support of this characterization, epidemiologic data have demonstrated high rates of adverse outcomes following hospitalization. For example, data have shown that more than 1 in 6 older adults is readmitted to the hospital within 30 days of discharge.²⁰ Death is also common in this first month, during which rates of postdischarge mortality may exceed initial inpatient mortality.^21,22 Elevated vulnerability after hospitalization is not restricted to older adults, as readmission risk among younger patients 18 to 64 years of age may be even higher for selected conditions, such as heart failure.^3,23

Vulnerability after hospitalization is broad. In patients over age 65 initially admitted for heart failure or acute myocardial infarction, only 35% and 10% of readmissions are for recurrent heart failure or reinfarction, respectively.¹ Nearly half of readmissions are for noncardiovascular causes.¹ Similarly, following hospitalization for pneumonia, more than 60 percent of readmissions are for nonpulmonary etiologies. Moreover, the risk for all these causes of readmission is much higher than baseline risk, indicating an extended period of lack of resilience to many types of illness.²⁴ These patterns of broad susceptibility also extend to younger adults hospitalized with common medical conditions.³

Accumulating evidence suggests that hospitalized patients face functional decline, debility, and risk for adverse events despite resolution of the presenting illness, implying perhaps that the hospital environment itself is hazardous to patients’ health. In 1993, Creditor hypothesized that the “hazards of hospitalization,” including enforced bed-rest, sensory deprivation, social isolation, and malnutrition lead to a “cascade of dependency” in which a collection of small insults to multiple organ systems precipitates loss of function and debility despite cure or resolution of presenting illness.¹² Covinsky (2011) later defined hospitalization-associated disability as an iatrogenic hospital-related “disorder” characterized by new impairments in abilities to perform basic activities of daily living such as bathing, feeding, toileting, dressing, transferring, and walking at the time of hospital discharge.¹¹ Others have described a postintensive-care syndrome (PICS),²⁵ characterized by cognitive, psychiatric, and physical impairments acquired during hospitalization for critical illness that persist postdischarge and increase the long-term risk for adverse outcomes, including elevated mortality rates,^26,27 readmission rates,²⁸ and physical disabilities.²⁹ Similar to the “hazards of hospitalization,” PICS is thought to be related to common experiences of ICU stays, including mobility restriction, sensory deprivation, sleep disruption, sedation, malnutrition, and polypharmacy.^30-33

Taken together, these data suggest that adverse health consequences attributable to hospitalization extend across the spectrum of age, presenting disease severity, and hospital treatment location. As detailed below, the PHS hypothesis is rooted in a mechanistic understanding of the role of exogenous stressors in producing physiologic dysregulation and subsequent adverse health effects across multiple organ systems.

Nature of Stress in the Hospital

Compounding the stress of acute illness, hospitalized patients are routinely and repetitively exposed to a wide variety of environmental stressors that may have downstream adverse consequences (Table 1). In the absence of overt clinical manifestations of harm, the possible subclinical physiologic dysfunction generated by the following stress exposures may increase patients’ susceptibility to the manifestations of PHS.

Sleep Disruption

Sleep disruptions trigger potent stress responses,^34,35 yet they are common occurrences during hospitalization. In surveys, about half of patients report poor sleep quality during hospitalization that persists for many months after discharge.³⁶ In a simulated hospital setting, test subjects exposed to typical hospital sounds (paging system, machine alarms, etc.) experienced significant sleep-wake cycle abnormalities.³⁷ Although no work has yet focused specifically on the physiologic consequences of sleep disruption and stress in hospitalized patients, in healthy humans, mild sleep disruption has clear effects on allostasis by disrupting HPA activity, raising cortisol levels, diminishing parasympathetic tone, and impairing cognitive performance.^{18,34,35,38,39}

Malnourishment

Malnourishment in hospitalized patients is common, with one-fifth of hospitalized patients receiving nothing per mouth or clear liquid diets for more than 3 continuous days,⁴⁰ and one-fifth of hospitalized elderly patients receiving less than half of their calculated nutrition requirements.⁴¹ Although the relationship between food restriction, cortisol levels, and postdischarge outcomes has not been fully explored, in healthy humans, meal anticipation, meal withdrawal (withholding an expected meal), and self-reported dietary restraint are known to generate stress responses.^42,43 Furthermore, malnourishment during hospitalization is associated with increased 90-day and 1-year mortality after discharge,⁴⁴ adding malnourishment to the list of plausible components of hospital-related stress.

Mobility Restriction

Physical activity counterbalances stress responses and minimizes downstream consequences of allostatic load,¹⁵ yet mobility limitations via physical and chemical restraints are common in hospitalized patients, particularly among the elderly.^45-47 Many patients are tethered to devices that make ambulation hazardous, such as urinary catheters and infusion pumps. Even without physical or chemical restraints or a limited mobility order, patients may be hesitant to leave the room so as not to miss transport to a diagnostic study or an unscheduled physician’s visit. Indeed, mobility limitations of hospitalized patients increase the risk for adverse events after discharge, while interventions designed to encourage mobility are associated with improved postdischarge outcomes.^47,48

Other Stressors

Other hospital-related aversive stimuli are less commonly quantified, but clearly exist. According to surveys of hospitalized patients, sources of emotional stress include social isolation; loss of autonomy and privacy; fear of serious illness; lack of control over activities of daily living; lack of clear communication between treatment team and patients; and death of a patient roommate.^49,50 Furthermore, consider the physical discomfort and emotional distress of patients with urinary incontinence awaiting assistance for a diaper or bedding change or the pain of repetitive blood draws or other invasive testing. Although individualized, the subjective discomfort and emotional distress associated with these experiences undoubtedly contribute to the stress of hospitalization.

Animal Models of Stress

Laboratory techniques reminiscent of the numerous environmental stressors associated with hospitalization have been used to reliably trigger allostatic overload in healthy young animals.⁵¹ These techniques include sequential exposure to aversive stimuli, including food and water deprivation, continuous overnight illumination, paired housing with known and unknown cagemates, mobility restriction, soiled cage conditions, and continuous noise. All of these techniques have been shown to cause HPA axis and ANS dysfunction, allostatic overload, and subsequent stress-mediated consequences to multiple organ systems.^19,52-54 Given the remarkable similarity of these protocols to common experiences during hospitalization, animal models of stress may be useful in understanding the spectrum of maladaptive consequences experienced by patients within the hospital (Figure 1).

These animal models of stress have resulted in a number of instructive findings. For example, in rodents, extended stress exposure induces structural and functional remodeling of neuronal networks that precipitate learning and memory, working memory, and attention impairments.^55-57 These exposures also result in cardiovascular abnormalities, including dyslipidemia, progressive atherosclerosis,^58,59 and enhanced inflammatory cytokine expression,⁶⁰ all of which increase both atherosclerotic burden and susceptibility to plaque rupture, leading to elevated risk for major cardiovascular adverse events. Moreover, these extended stress exposures in animals increase susceptibility to both bacterial and viral infections and increase their severity.^16,61 This outcome appears to be driven by a stress-induced elevation of glucocorticoid levels, decreased leukocyte proliferation, altered leukocyte trafficking, and a transition to a proinflammatory cytokine environment.^{16, 61} Allostatic overload has also been shown to contribute to metabolic dysregulation involving insulin resistance, persistence of hyperglycemia, dyslipidemia, catabolism of lean muscle, and visceral adipose tissue deposition.^62-64 In addition to cardiovascular, immune, and metabolic consequences of allostatic overload, the spectrum of physiologic dysfunction in animal models is broad and includes mood disorder symptoms,⁶⁵ intestinal barrier abnormalities,⁶⁶ airway reactivity exacerbation,⁶⁷ and enhanced tumor growth.⁶⁸

Although the majority of this research highlights the multisystem effects of variable stress exposure in healthy animals, preliminary evidence suggests that aged or diseased animals subjected to additional stressors display a heightened inflammatory cytokine response that contributes to exaggerated sickness behavior and greater and prolonged cognitive deficits.⁶⁹ Future studies exploring the consequences of extended stress exposure in animals with existing disease or debility may therefore more closely simulate the experience of hospitalized patients and perhaps further our understanding of PHS.

Hospitalized Patients

While no intervention studies have examined the effects of potential hospital stressors on the development of allostatic overload, there is evidence from small studies that dysregulated stress responses during hospitalization are associated with adverse events. For example, high serum cortisol, catecholamine, and proinflammatory cytokine levels during hospitalization have individually been associated with the development of cognitive dysfunction,^70-72 increased risk of cardiovascular events such as myocardial infarction and stroke in the year following discharge,^73-76 and the development of wound infections after discharge.⁷⁷ Moreover, elevated plasma glucose during admission for myocardial infarction in patients with or without diabetes has been associated with greater in-hospital and 1-year mortality,⁷⁸ with a similar relationship seen between elevated plasma glucose and survival after admission for stroke⁷⁹ and pneumonia.⁸⁰ Furthermore, in addition to atherothrombosis, stress may contribute to the risk for venous thromboembolism,⁸¹ resulting in readmissions for deep vein thrombosis or pulmonary embolism posthospitalization. Although potentially surrogate markers of illness acuity, a handful of studies have shown that these stress biomarkers are actually only weakly correlated with,⁸² or independent of,^72,76 disease severity. As discussed in detail below, future studies utilizing a summative measure of multisystem physiologic dysfunction as opposed to individual biomarkers may more accurately reflect the cumulative stress effects of hospitalization and subsequent risk for adverse events.

Additional Considerations

Elderly patients, in particular, may have heightened susceptibility to the consequences of allostatic overload due to common geriatric issues such as multimorbidity and frailty. Patients with chronic diseases display both baseline HPA axis abnormalities as well as dysregulated stress responses and may therefore be more vulnerable to hospitalization-related stress. For example, when subjected to psychosocial stress, patients with chronic conditions such as diabetes, heart failure, or atherosclerosis demonstrate elevated cortisol levels, increased circulating markers of inflammation, as well as prolonged hemodynamic recovery after stress resolution compared with normal controls.^83-85 Additionally, frailty may affect an individual’s susceptibility to exogenous stress. Indeed, frailty identified on hospital admission increases the risk for adverse outcomes during hospitalization and postdischarge.⁸⁶ Although the specific etiology of this relationship is unclear, persons with frailty are known to have elevated levels of cortisol and other inflammatory markers,^87,88 which may contribute to adverse outcomes in the face of additional stressors.

A large body of evidence stretching from bench to bedside suggests that environmental stressors associated with hospitalization are toxic. Understanding PHS within the context of hospital-induced allostatic overload presents a unifying theory for the interrelated multisystem dysfunction and increased susceptibility to adverse events that patients experience after discharge (Figure 2). Furthermore, it defines a potential pathophysiological mechanism for the cognitive impairment, elevated cardiovascular risk, immune system dysfunction, metabolic derangements, and functional decline associated with PHS. Additionally, this theory highlights environmental interventions to limit PHS development and suggests mechanisms to promote stress resilience. Although it is difficult to disentangle the consequences of the endogenous stress triggered by an acute illness from the exogenous stressors related to hospitalization, it is likely that the 2 simultaneous exposures compound risk for stress system dysregulation and allostatic overload. Moreover, hospitalized patients with preexisting HPA axis dysfunction at baseline from chronic disease or advancing age may be even more susceptible to these adverse outcomes. If this hypothesis is true, a reduction in PHS would require mitigation of the modifiable environmental stressors encountered by patients during hospitalization. Directed efforts to diminish ambient noise, limit nighttime disruptions, thoughtfully plan procedures, consider ongoing nutritional status, and promote opportunities for patients to exert some control over their environment may diminish the burden of extrinsic stressors encountered by all patients in the hospital and improve outcomes after discharge.

Hospitals are increasingly recognizing the importance of improving patients’ experience of hospitalization by reducing exposure to potential toxicities. For example, many hospitals are now attempting to reduce sleep disturbances and sleep latency through reduced nighttime noise and light levels, fewer nighttime interruptions for vital signs checks and medication administration, and commonsensical interventions like massages, herbal teas, and warm milk prior to bedtime.⁸⁹ Likewise, intensive care units are targeting environmental and physical stressors with a multifaceted approach to decrease sedative use, promote healthy sleep cycles, and encourage exercise and ambulation even in those patients who are mechanically ventilated.³⁰ Another promising development has been the increase of Hospital at Home programs. In these programs, patients who meet the criteria for inpatient admission are instead comprehensively managed at home for their acute illness through a multidisciplinary effort between physicians, nurses, social workers, physical therapists, and others. Patients hospitalized at home report higher levels of satisfaction and have modest functional gains, improved health-related quality of life, and decreased risk of mortality at 6 months compared with hospitalized patients.^90,91 With some admitting diagnoses (eg, heart failure), hospitalization at home may be associated with decreased readmission risk.⁹² Although not yet investigated on a physiologic level, perhaps the benefits of hospital at home are partially due to the dramatic difference in exposure to environmental stressors.

A tool that quantifies hospital-associated stress may help health providers appreciate the experience of patients and better target interventions to aspects of their structure and process that contribute to allostatic overload. Importantly, allostatic overload cannot be identified by one biomarker of stress but instead requires evidence of dysregulation across inflammatory, neuroendocrine, hormonal, and cardiometabolic systems. Future studies to address the burden of stress faced by hospitalized patients should consider a summative measure of multisystem dysregulation as opposed to isolated assessments of individual biomarkers. Allostatic load has previously been operationalized as the summation of a variety of hemodynamic, hormonal, and metabolic factors, including blood pressure, lipid profile, glycosylated hemoglobin, cortisol, catecholamine levels, and inflammatory markers.⁹³ To develop a hospital-associated allostatic load index, models should ideally be adjusted for acute illness severity, patient-reported stress, and capacity for stress resilience. This tool could then be used to quantify hospitalization-related allostatic load and identify those at greatest risk for adverse events after discharge, as well as measure the effectiveness of strategic environmental interventions (Table 2). A natural first experiment may be a comparison of the allostatic load of hospitalized patients versus those hospitalized at home.

After discharge from the hospital, patients have a significantly elevated risk for adverse events, including emergency department use, hospital readmission, and death. More than 1 in 3 patients discharged from the hospital require acute care in the month after hospital discharge, and more than 1 in 6 require readmission, with readmission diagnoses frequently differing from those of the preceding hospitalization.^1-4 This heightened susceptibility to adverse events persists beyond 30 days but levels off by 7 weeks after discharge, suggesting that the period of increased risk is transient and dynamic.⁵

The term posthospital syndrome (PHS) describes this period of vulnerability to major adverse events following hospitalization.⁶ In addition to increased risk for readmission and mortality, patients in this period often show evidence of generalized dysfunction with new cognitive impairment, mobility disability, or functional decline.^7-12 To date, the etiology of this vulnerability is neither well understood nor effectively addressed by transitional care interventions.¹³

One hypothesis to explain PHS is that stressors associated with the experience of hospitalization contribute to transient multisystem dysfunction that induces susceptibility to a broad range of medical maladies. These stressors include frequent sleep disruption, noxious sounds, painful stimuli, mobility restrictions, and poor nutrition.¹² The stress hypothesis as a cause of PHS is therefore based, in large part, on evidence about allostasis and the deleterious effects of allostatic overload.

Allostasis defines a system functioning within normal stress-response parameters to promote adaptation and survival.¹⁴ In allostasis, the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic and parasympathetic branches of the autonomic nervous system (ANS) exist in homeostatic balance and respond to environmental stimuli within a range of healthy physiologic parameters. The hallmark of a system in allostasis is the ability to rapidly activate, then successfully deactivate, a stress response once the stressor (ie, threat) has resolved.^14,15 To promote survival and potentiate “fight or flight” mechanisms, an appropriate stress response necessarily impacts multiple physiologic systems that result in hemodynamic augmentation and gluconeogenesis to support the anticipated action of large muscle groups, heightened vigilance and memory capabilities to improve rapid decision-making, and enhancement of innate and adaptive immune capabilities to prepare for wound repair and infection defense.^14-16 The stress response is subsequently terminated by negative feedback mechanisms of glucocorticoids as well as a shift of the ANS from sympathetic to parasympathetic tone.^17,18

Extended or repetitive stress exposure, however, leads to dysregulation of allostatic mechanisms responsible for stress adaptation and hinders an efficient and effective stress response. After extended stress exposure, baseline (ie, resting) HPA activity resets, causing a disruption of normal diurnal cortisol rhythm and an increase in total cortisol concentration. Moreover, in response to stress, HPA and ANS system excitation becomes impaired, and negative feedback properties are undermined.^14,15 This maladaptive state, known as allostatic overload, disrupts the finely tuned mechanisms that are the foundation of mind-body balance and yields pathophysiologic consequences to multiple organ systems. Downstream ramifications of allostatic overload include cognitive deterioration, cardiovascular and immune system dysfunction, and functional decline.^14,15,19

Although a stress response is an expected and necessary aspect of acute illness that promotes survival, the central thesis of this work is that additional environmental and social stressors inherent in hospitalization may unnecessarily compound stress and increase the risk of HPA axis dysfunction, allostatic overload, and subsequent multisystem dysfunction, predisposing individuals to adverse outcomes after hospital discharge. Based on data from both human subjects and animal models, we present a possible pathophysiologic mechanism for the postdischarge vulnerability of PHS, encourage critical contemplation of traditional hospitalization, and suggest interventions that might improve outcomes.

Posthospital syndrome (PHS) describes a transient period of vulnerability after hospitalization during which patients are at elevated risk for adverse events from a broad range of conditions. In support of this characterization, epidemiologic data have demonstrated high rates of adverse outcomes following hospitalization. For example, data have shown that more than 1 in 6 older adults is readmitted to the hospital within 30 days of discharge.²⁰ Death is also common in this first month, during which rates of postdischarge mortality may exceed initial inpatient mortality.^21,22 Elevated vulnerability after hospitalization is not restricted to older adults, as readmission risk among younger patients 18 to 64 years of age may be even higher for selected conditions, such as heart failure.^3,23

Vulnerability after hospitalization is broad. In patients over age 65 initially admitted for heart failure or acute myocardial infarction, only 35% and 10% of readmissions are for recurrent heart failure or reinfarction, respectively.¹ Nearly half of readmissions are for noncardiovascular causes.¹ Similarly, following hospitalization for pneumonia, more than 60 percent of readmissions are for nonpulmonary etiologies. Moreover, the risk for all these causes of readmission is much higher than baseline risk, indicating an extended period of lack of resilience to many types of illness.²⁴ These patterns of broad susceptibility also extend to younger adults hospitalized with common medical conditions.³

Accumulating evidence suggests that hospitalized patients face functional decline, debility, and risk for adverse events despite resolution of the presenting illness, implying perhaps that the hospital environment itself is hazardous to patients’ health. In 1993, Creditor hypothesized that the “hazards of hospitalization,” including enforced bed-rest, sensory deprivation, social isolation, and malnutrition lead to a “cascade of dependency” in which a collection of small insults to multiple organ systems precipitates loss of function and debility despite cure or resolution of presenting illness.¹² Covinsky (2011) later defined hospitalization-associated disability as an iatrogenic hospital-related “disorder” characterized by new impairments in abilities to perform basic activities of daily living such as bathing, feeding, toileting, dressing, transferring, and walking at the time of hospital discharge.¹¹ Others have described a postintensive-care syndrome (PICS),²⁵ characterized by cognitive, psychiatric, and physical impairments acquired during hospitalization for critical illness that persist postdischarge and increase the long-term risk for adverse outcomes, including elevated mortality rates,^26,27 readmission rates,²⁸ and physical disabilities.²⁹ Similar to the “hazards of hospitalization,” PICS is thought to be related to common experiences of ICU stays, including mobility restriction, sensory deprivation, sleep disruption, sedation, malnutrition, and polypharmacy.^30-33

Taken together, these data suggest that adverse health consequences attributable to hospitalization extend across the spectrum of age, presenting disease severity, and hospital treatment location. As detailed below, the PHS hypothesis is rooted in a mechanistic understanding of the role of exogenous stressors in producing physiologic dysregulation and subsequent adverse health effects across multiple organ systems.

Nature of Stress in the Hospital

Compounding the stress of acute illness, hospitalized patients are routinely and repetitively exposed to a wide variety of environmental stressors that may have downstream adverse consequences (Table 1). In the absence of overt clinical manifestations of harm, the possible subclinical physiologic dysfunction generated by the following stress exposures may increase patients’ susceptibility to the manifestations of PHS.

Sleep Disruption

Sleep disruptions trigger potent stress responses,^34,35 yet they are common occurrences during hospitalization. In surveys, about half of patients report poor sleep quality during hospitalization that persists for many months after discharge.³⁶ In a simulated hospital setting, test subjects exposed to typical hospital sounds (paging system, machine alarms, etc.) experienced significant sleep-wake cycle abnormalities.³⁷ Although no work has yet focused specifically on the physiologic consequences of sleep disruption and stress in hospitalized patients, in healthy humans, mild sleep disruption has clear effects on allostasis by disrupting HPA activity, raising cortisol levels, diminishing parasympathetic tone, and impairing cognitive performance.^{18,34,35,38,39}

Malnourishment

Malnourishment in hospitalized patients is common, with one-fifth of hospitalized patients receiving nothing per mouth or clear liquid diets for more than 3 continuous days,⁴⁰ and one-fifth of hospitalized elderly patients receiving less than half of their calculated nutrition requirements.⁴¹ Although the relationship between food restriction, cortisol levels, and postdischarge outcomes has not been fully explored, in healthy humans, meal anticipation, meal withdrawal (withholding an expected meal), and self-reported dietary restraint are known to generate stress responses.^42,43 Furthermore, malnourishment during hospitalization is associated with increased 90-day and 1-year mortality after discharge,⁴⁴ adding malnourishment to the list of plausible components of hospital-related stress.

Mobility Restriction

Physical activity counterbalances stress responses and minimizes downstream consequences of allostatic load,¹⁵ yet mobility limitations via physical and chemical restraints are common in hospitalized patients, particularly among the elderly.^45-47 Many patients are tethered to devices that make ambulation hazardous, such as urinary catheters and infusion pumps. Even without physical or chemical restraints or a limited mobility order, patients may be hesitant to leave the room so as not to miss transport to a diagnostic study or an unscheduled physician’s visit. Indeed, mobility limitations of hospitalized patients increase the risk for adverse events after discharge, while interventions designed to encourage mobility are associated with improved postdischarge outcomes.^47,48

Other Stressors

Other hospital-related aversive stimuli are less commonly quantified, but clearly exist. According to surveys of hospitalized patients, sources of emotional stress include social isolation; loss of autonomy and privacy; fear of serious illness; lack of control over activities of daily living; lack of clear communication between treatment team and patients; and death of a patient roommate.^49,50 Furthermore, consider the physical discomfort and emotional distress of patients with urinary incontinence awaiting assistance for a diaper or bedding change or the pain of repetitive blood draws or other invasive testing. Although individualized, the subjective discomfort and emotional distress associated with these experiences undoubtedly contribute to the stress of hospitalization.

Animal Models of Stress

Laboratory techniques reminiscent of the numerous environmental stressors associated with hospitalization have been used to reliably trigger allostatic overload in healthy young animals.⁵¹ These techniques include sequential exposure to aversive stimuli, including food and water deprivation, continuous overnight illumination, paired housing with known and unknown cagemates, mobility restriction, soiled cage conditions, and continuous noise. All of these techniques have been shown to cause HPA axis and ANS dysfunction, allostatic overload, and subsequent stress-mediated consequences to multiple organ systems.^19,52-54 Given the remarkable similarity of these protocols to common experiences during hospitalization, animal models of stress may be useful in understanding the spectrum of maladaptive consequences experienced by patients within the hospital (Figure 1).

These animal models of stress have resulted in a number of instructive findings. For example, in rodents, extended stress exposure induces structural and functional remodeling of neuronal networks that precipitate learning and memory, working memory, and attention impairments.^55-57 These exposures also result in cardiovascular abnormalities, including dyslipidemia, progressive atherosclerosis,^58,59 and enhanced inflammatory cytokine expression,⁶⁰ all of which increase both atherosclerotic burden and susceptibility to plaque rupture, leading to elevated risk for major cardiovascular adverse events. Moreover, these extended stress exposures in animals increase susceptibility to both bacterial and viral infections and increase their severity.^16,61 This outcome appears to be driven by a stress-induced elevation of glucocorticoid levels, decreased leukocyte proliferation, altered leukocyte trafficking, and a transition to a proinflammatory cytokine environment.^{16, 61} Allostatic overload has also been shown to contribute to metabolic dysregulation involving insulin resistance, persistence of hyperglycemia, dyslipidemia, catabolism of lean muscle, and visceral adipose tissue deposition.^62-64 In addition to cardiovascular, immune, and metabolic consequences of allostatic overload, the spectrum of physiologic dysfunction in animal models is broad and includes mood disorder symptoms,⁶⁵ intestinal barrier abnormalities,⁶⁶ airway reactivity exacerbation,⁶⁷ and enhanced tumor growth.⁶⁸

Although the majority of this research highlights the multisystem effects of variable stress exposure in healthy animals, preliminary evidence suggests that aged or diseased animals subjected to additional stressors display a heightened inflammatory cytokine response that contributes to exaggerated sickness behavior and greater and prolonged cognitive deficits.⁶⁹ Future studies exploring the consequences of extended stress exposure in animals with existing disease or debility may therefore more closely simulate the experience of hospitalized patients and perhaps further our understanding of PHS.

Hospitalized Patients

While no intervention studies have examined the effects of potential hospital stressors on the development of allostatic overload, there is evidence from small studies that dysregulated stress responses during hospitalization are associated with adverse events. For example, high serum cortisol, catecholamine, and proinflammatory cytokine levels during hospitalization have individually been associated with the development of cognitive dysfunction,^70-72 increased risk of cardiovascular events such as myocardial infarction and stroke in the year following discharge,^73-76 and the development of wound infections after discharge.⁷⁷ Moreover, elevated plasma glucose during admission for myocardial infarction in patients with or without diabetes has been associated with greater in-hospital and 1-year mortality,⁷⁸ with a similar relationship seen between elevated plasma glucose and survival after admission for stroke⁷⁹ and pneumonia.⁸⁰ Furthermore, in addition to atherothrombosis, stress may contribute to the risk for venous thromboembolism,⁸¹ resulting in readmissions for deep vein thrombosis or pulmonary embolism posthospitalization. Although potentially surrogate markers of illness acuity, a handful of studies have shown that these stress biomarkers are actually only weakly correlated with,⁸² or independent of,^72,76 disease severity. As discussed in detail below, future studies utilizing a summative measure of multisystem physiologic dysfunction as opposed to individual biomarkers may more accurately reflect the cumulative stress effects of hospitalization and subsequent risk for adverse events.

Additional Considerations

Elderly patients, in particular, may have heightened susceptibility to the consequences of allostatic overload due to common geriatric issues such as multimorbidity and frailty. Patients with chronic diseases display both baseline HPA axis abnormalities as well as dysregulated stress responses and may therefore be more vulnerable to hospitalization-related stress. For example, when subjected to psychosocial stress, patients with chronic conditions such as diabetes, heart failure, or atherosclerosis demonstrate elevated cortisol levels, increased circulating markers of inflammation, as well as prolonged hemodynamic recovery after stress resolution compared with normal controls.^83-85 Additionally, frailty may affect an individual’s susceptibility to exogenous stress. Indeed, frailty identified on hospital admission increases the risk for adverse outcomes during hospitalization and postdischarge.⁸⁶ Although the specific etiology of this relationship is unclear, persons with frailty are known to have elevated levels of cortisol and other inflammatory markers,^87,88 which may contribute to adverse outcomes in the face of additional stressors.

A large body of evidence stretching from bench to bedside suggests that environmental stressors associated with hospitalization are toxic. Understanding PHS within the context of hospital-induced allostatic overload presents a unifying theory for the interrelated multisystem dysfunction and increased susceptibility to adverse events that patients experience after discharge (Figure 2). Furthermore, it defines a potential pathophysiological mechanism for the cognitive impairment, elevated cardiovascular risk, immune system dysfunction, metabolic derangements, and functional decline associated with PHS. Additionally, this theory highlights environmental interventions to limit PHS development and suggests mechanisms to promote stress resilience. Although it is difficult to disentangle the consequences of the endogenous stress triggered by an acute illness from the exogenous stressors related to hospitalization, it is likely that the 2 simultaneous exposures compound risk for stress system dysregulation and allostatic overload. Moreover, hospitalized patients with preexisting HPA axis dysfunction at baseline from chronic disease or advancing age may be even more susceptible to these adverse outcomes. If this hypothesis is true, a reduction in PHS would require mitigation of the modifiable environmental stressors encountered by patients during hospitalization. Directed efforts to diminish ambient noise, limit nighttime disruptions, thoughtfully plan procedures, consider ongoing nutritional status, and promote opportunities for patients to exert some control over their environment may diminish the burden of extrinsic stressors encountered by all patients in the hospital and improve outcomes after discharge.

Hospitals are increasingly recognizing the importance of improving patients’ experience of hospitalization by reducing exposure to potential toxicities. For example, many hospitals are now attempting to reduce sleep disturbances and sleep latency through reduced nighttime noise and light levels, fewer nighttime interruptions for vital signs checks and medication administration, and commonsensical interventions like massages, herbal teas, and warm milk prior to bedtime.⁸⁹ Likewise, intensive care units are targeting environmental and physical stressors with a multifaceted approach to decrease sedative use, promote healthy sleep cycles, and encourage exercise and ambulation even in those patients who are mechanically ventilated.³⁰ Another promising development has been the increase of Hospital at Home programs. In these programs, patients who meet the criteria for inpatient admission are instead comprehensively managed at home for their acute illness through a multidisciplinary effort between physicians, nurses, social workers, physical therapists, and others. Patients hospitalized at home report higher levels of satisfaction and have modest functional gains, improved health-related quality of life, and decreased risk of mortality at 6 months compared with hospitalized patients.^90,91 With some admitting diagnoses (eg, heart failure), hospitalization at home may be associated with decreased readmission risk.⁹² Although not yet investigated on a physiologic level, perhaps the benefits of hospital at home are partially due to the dramatic difference in exposure to environmental stressors.

A tool that quantifies hospital-associated stress may help health providers appreciate the experience of patients and better target interventions to aspects of their structure and process that contribute to allostatic overload. Importantly, allostatic overload cannot be identified by one biomarker of stress but instead requires evidence of dysregulation across inflammatory, neuroendocrine, hormonal, and cardiometabolic systems. Future studies to address the burden of stress faced by hospitalized patients should consider a summative measure of multisystem dysregulation as opposed to isolated assessments of individual biomarkers. Allostatic load has previously been operationalized as the summation of a variety of hemodynamic, hormonal, and metabolic factors, including blood pressure, lipid profile, glycosylated hemoglobin, cortisol, catecholamine levels, and inflammatory markers.⁹³ To develop a hospital-associated allostatic load index, models should ideally be adjusted for acute illness severity, patient-reported stress, and capacity for stress resilience. This tool could then be used to quantify hospitalization-related allostatic load and identify those at greatest risk for adverse events after discharge, as well as measure the effectiveness of strategic environmental interventions (Table 2). A natural first experiment may be a comparison of the allostatic load of hospitalized patients versus those hospitalized at home.

After discharge from the hospital, patients have a significantly elevated risk for adverse events, including emergency department use, hospital readmission, and death. More than 1 in 3 patients discharged from the hospital require acute care in the month after hospital discharge, and more than 1 in 6 require readmission, with readmission diagnoses frequently differing from those of the preceding hospitalization.^1-4 This heightened susceptibility to adverse events persists beyond 30 days but levels off by 7 weeks after discharge, suggesting that the period of increased risk is transient and dynamic.⁵

The term posthospital syndrome (PHS) describes this period of vulnerability to major adverse events following hospitalization.⁶ In addition to increased risk for readmission and mortality, patients in this period often show evidence of generalized dysfunction with new cognitive impairment, mobility disability, or functional decline.^7-12 To date, the etiology of this vulnerability is neither well understood nor effectively addressed by transitional care interventions.¹³

One hypothesis to explain PHS is that stressors associated with the experience of hospitalization contribute to transient multisystem dysfunction that induces susceptibility to a broad range of medical maladies. These stressors include frequent sleep disruption, noxious sounds, painful stimuli, mobility restrictions, and poor nutrition.¹² The stress hypothesis as a cause of PHS is therefore based, in large part, on evidence about allostasis and the deleterious effects of allostatic overload.

Allostasis defines a system functioning within normal stress-response parameters to promote adaptation and survival.¹⁴ In allostasis, the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic and parasympathetic branches of the autonomic nervous system (ANS) exist in homeostatic balance and respond to environmental stimuli within a range of healthy physiologic parameters. The hallmark of a system in allostasis is the ability to rapidly activate, then successfully deactivate, a stress response once the stressor (ie, threat) has resolved.^14,15 To promote survival and potentiate “fight or flight” mechanisms, an appropriate stress response necessarily impacts multiple physiologic systems that result in hemodynamic augmentation and gluconeogenesis to support the anticipated action of large muscle groups, heightened vigilance and memory capabilities to improve rapid decision-making, and enhancement of innate and adaptive immune capabilities to prepare for wound repair and infection defense.^14-16 The stress response is subsequently terminated by negative feedback mechanisms of glucocorticoids as well as a shift of the ANS from sympathetic to parasympathetic tone.^17,18

Extended or repetitive stress exposure, however, leads to dysregulation of allostatic mechanisms responsible for stress adaptation and hinders an efficient and effective stress response. After extended stress exposure, baseline (ie, resting) HPA activity resets, causing a disruption of normal diurnal cortisol rhythm and an increase in total cortisol concentration. Moreover, in response to stress, HPA and ANS system excitation becomes impaired, and negative feedback properties are undermined.^14,15 This maladaptive state, known as allostatic overload, disrupts the finely tuned mechanisms that are the foundation of mind-body balance and yields pathophysiologic consequences to multiple organ systems. Downstream ramifications of allostatic overload include cognitive deterioration, cardiovascular and immune system dysfunction, and functional decline.^14,15,19

Although a stress response is an expected and necessary aspect of acute illness that promotes survival, the central thesis of this work is that additional environmental and social stressors inherent in hospitalization may unnecessarily compound stress and increase the risk of HPA axis dysfunction, allostatic overload, and subsequent multisystem dysfunction, predisposing individuals to adverse outcomes after hospital discharge. Based on data from both human subjects and animal models, we present a possible pathophysiologic mechanism for the postdischarge vulnerability of PHS, encourage critical contemplation of traditional hospitalization, and suggest interventions that might improve outcomes.

Posthospital syndrome (PHS) describes a transient period of vulnerability after hospitalization during which patients are at elevated risk for adverse events from a broad range of conditions. In support of this characterization, epidemiologic data have demonstrated high rates of adverse outcomes following hospitalization. For example, data have shown that more than 1 in 6 older adults is readmitted to the hospital within 30 days of discharge.²⁰ Death is also common in this first month, during which rates of postdischarge mortality may exceed initial inpatient mortality.^21,22 Elevated vulnerability after hospitalization is not restricted to older adults, as readmission risk among younger patients 18 to 64 years of age may be even higher for selected conditions, such as heart failure.^3,23

Vulnerability after hospitalization is broad. In patients over age 65 initially admitted for heart failure or acute myocardial infarction, only 35% and 10% of readmissions are for recurrent heart failure or reinfarction, respectively.¹ Nearly half of readmissions are for noncardiovascular causes.¹ Similarly, following hospitalization for pneumonia, more than 60 percent of readmissions are for nonpulmonary etiologies. Moreover, the risk for all these causes of readmission is much higher than baseline risk, indicating an extended period of lack of resilience to many types of illness.²⁴ These patterns of broad susceptibility also extend to younger adults hospitalized with common medical conditions.³

Accumulating evidence suggests that hospitalized patients face functional decline, debility, and risk for adverse events despite resolution of the presenting illness, implying perhaps that the hospital environment itself is hazardous to patients’ health. In 1993, Creditor hypothesized that the “hazards of hospitalization,” including enforced bed-rest, sensory deprivation, social isolation, and malnutrition lead to a “cascade of dependency” in which a collection of small insults to multiple organ systems precipitates loss of function and debility despite cure or resolution of presenting illness.¹² Covinsky (2011) later defined hospitalization-associated disability as an iatrogenic hospital-related “disorder” characterized by new impairments in abilities to perform basic activities of daily living such as bathing, feeding, toileting, dressing, transferring, and walking at the time of hospital discharge.¹¹ Others have described a postintensive-care syndrome (PICS),²⁵ characterized by cognitive, psychiatric, and physical impairments acquired during hospitalization for critical illness that persist postdischarge and increase the long-term risk for adverse outcomes, including elevated mortality rates,^26,27 readmission rates,²⁸ and physical disabilities.²⁹ Similar to the “hazards of hospitalization,” PICS is thought to be related to common experiences of ICU stays, including mobility restriction, sensory deprivation, sleep disruption, sedation, malnutrition, and polypharmacy.^30-33

Taken together, these data suggest that adverse health consequences attributable to hospitalization extend across the spectrum of age, presenting disease severity, and hospital treatment location. As detailed below, the PHS hypothesis is rooted in a mechanistic understanding of the role of exogenous stressors in producing physiologic dysregulation and subsequent adverse health effects across multiple organ systems.

Nature of Stress in the Hospital

Compounding the stress of acute illness, hospitalized patients are routinely and repetitively exposed to a wide variety of environmental stressors that may have downstream adverse consequences (Table 1). In the absence of overt clinical manifestations of harm, the possible subclinical physiologic dysfunction generated by the following stress exposures may increase patients’ susceptibility to the manifestations of PHS.

Sleep Disruption

Sleep disruptions trigger potent stress responses,^34,35 yet they are common occurrences during hospitalization. In surveys, about half of patients report poor sleep quality during hospitalization that persists for many months after discharge.³⁶ In a simulated hospital setting, test subjects exposed to typical hospital sounds (paging system, machine alarms, etc.) experienced significant sleep-wake cycle abnormalities.³⁷ Although no work has yet focused specifically on the physiologic consequences of sleep disruption and stress in hospitalized patients, in healthy humans, mild sleep disruption has clear effects on allostasis by disrupting HPA activity, raising cortisol levels, diminishing parasympathetic tone, and impairing cognitive performance.^{18,34,35,38,39}

Malnourishment

Malnourishment in hospitalized patients is common, with one-fifth of hospitalized patients receiving nothing per mouth or clear liquid diets for more than 3 continuous days,⁴⁰ and one-fifth of hospitalized elderly patients receiving less than half of their calculated nutrition requirements.⁴¹ Although the relationship between food restriction, cortisol levels, and postdischarge outcomes has not been fully explored, in healthy humans, meal anticipation, meal withdrawal (withholding an expected meal), and self-reported dietary restraint are known to generate stress responses.^42,43 Furthermore, malnourishment during hospitalization is associated with increased 90-day and 1-year mortality after discharge,⁴⁴ adding malnourishment to the list of plausible components of hospital-related stress.

Mobility Restriction

Physical activity counterbalances stress responses and minimizes downstream consequences of allostatic load,¹⁵ yet mobility limitations via physical and chemical restraints are common in hospitalized patients, particularly among the elderly.^45-47 Many patients are tethered to devices that make ambulation hazardous, such as urinary catheters and infusion pumps. Even without physical or chemical restraints or a limited mobility order, patients may be hesitant to leave the room so as not to miss transport to a diagnostic study or an unscheduled physician’s visit. Indeed, mobility limitations of hospitalized patients increase the risk for adverse events after discharge, while interventions designed to encourage mobility are associated with improved postdischarge outcomes.^47,48

Other Stressors

Other hospital-related aversive stimuli are less commonly quantified, but clearly exist. According to surveys of hospitalized patients, sources of emotional stress include social isolation; loss of autonomy and privacy; fear of serious illness; lack of control over activities of daily living; lack of clear communication between treatment team and patients; and death of a patient roommate.^49,50 Furthermore, consider the physical discomfort and emotional distress of patients with urinary incontinence awaiting assistance for a diaper or bedding change or the pain of repetitive blood draws or other invasive testing. Although individualized, the subjective discomfort and emotional distress associated with these experiences undoubtedly contribute to the stress of hospitalization.

Animal Models of Stress

Laboratory techniques reminiscent of the numerous environmental stressors associated with hospitalization have been used to reliably trigger allostatic overload in healthy young animals.⁵¹ These techniques include sequential exposure to aversive stimuli, including food and water deprivation, continuous overnight illumination, paired housing with known and unknown cagemates, mobility restriction, soiled cage conditions, and continuous noise. All of these techniques have been shown to cause HPA axis and ANS dysfunction, allostatic overload, and subsequent stress-mediated consequences to multiple organ systems.^19,52-54 Given the remarkable similarity of these protocols to common experiences during hospitalization, animal models of stress may be useful in understanding the spectrum of maladaptive consequences experienced by patients within the hospital (Figure 1).

These animal models of stress have resulted in a number of instructive findings. For example, in rodents, extended stress exposure induces structural and functional remodeling of neuronal networks that precipitate learning and memory, working memory, and attention impairments.^55-57 These exposures also result in cardiovascular abnormalities, including dyslipidemia, progressive atherosclerosis,^58,59 and enhanced inflammatory cytokine expression,⁶⁰ all of which increase both atherosclerotic burden and susceptibility to plaque rupture, leading to elevated risk for major cardiovascular adverse events. Moreover, these extended stress exposures in animals increase susceptibility to both bacterial and viral infections and increase their severity.^16,61 This outcome appears to be driven by a stress-induced elevation of glucocorticoid levels, decreased leukocyte proliferation, altered leukocyte trafficking, and a transition to a proinflammatory cytokine environment.^{16, 61} Allostatic overload has also been shown to contribute to metabolic dysregulation involving insulin resistance, persistence of hyperglycemia, dyslipidemia, catabolism of lean muscle, and visceral adipose tissue deposition.^62-64 In addition to cardiovascular, immune, and metabolic consequences of allostatic overload, the spectrum of physiologic dysfunction in animal models is broad and includes mood disorder symptoms,⁶⁵ intestinal barrier abnormalities,⁶⁶ airway reactivity exacerbation,⁶⁷ and enhanced tumor growth.⁶⁸

Although the majority of this research highlights the multisystem effects of variable stress exposure in healthy animals, preliminary evidence suggests that aged or diseased animals subjected to additional stressors display a heightened inflammatory cytokine response that contributes to exaggerated sickness behavior and greater and prolonged cognitive deficits.⁶⁹ Future studies exploring the consequences of extended stress exposure in animals with existing disease or debility may therefore more closely simulate the experience of hospitalized patients and perhaps further our understanding of PHS.

Hospitalized Patients

While no intervention studies have examined the effects of potential hospital stressors on the development of allostatic overload, there is evidence from small studies that dysregulated stress responses during hospitalization are associated with adverse events. For example, high serum cortisol, catecholamine, and proinflammatory cytokine levels during hospitalization have individually been associated with the development of cognitive dysfunction,^70-72 increased risk of cardiovascular events such as myocardial infarction and stroke in the year following discharge,^73-76 and the development of wound infections after discharge.⁷⁷ Moreover, elevated plasma glucose during admission for myocardial infarction in patients with or without diabetes has been associated with greater in-hospital and 1-year mortality,⁷⁸ with a similar relationship seen between elevated plasma glucose and survival after admission for stroke⁷⁹ and pneumonia.⁸⁰ Furthermore, in addition to atherothrombosis, stress may contribute to the risk for venous thromboembolism,⁸¹ resulting in readmissions for deep vein thrombosis or pulmonary embolism posthospitalization. Although potentially surrogate markers of illness acuity, a handful of studies have shown that these stress biomarkers are actually only weakly correlated with,⁸² or independent of,^72,76 disease severity. As discussed in detail below, future studies utilizing a summative measure of multisystem physiologic dysfunction as opposed to individual biomarkers may more accurately reflect the cumulative stress effects of hospitalization and subsequent risk for adverse events.

Additional Considerations

Elderly patients, in particular, may have heightened susceptibility to the consequences of allostatic overload due to common geriatric issues such as multimorbidity and frailty. Patients with chronic diseases display both baseline HPA axis abnormalities as well as dysregulated stress responses and may therefore be more vulnerable to hospitalization-related stress. For example, when subjected to psychosocial stress, patients with chronic conditions such as diabetes, heart failure, or atherosclerosis demonstrate elevated cortisol levels, increased circulating markers of inflammation, as well as prolonged hemodynamic recovery after stress resolution compared with normal controls.^83-85 Additionally, frailty may affect an individual’s susceptibility to exogenous stress. Indeed, frailty identified on hospital admission increases the risk for adverse outcomes during hospitalization and postdischarge.⁸⁶ Although the specific etiology of this relationship is unclear, persons with frailty are known to have elevated levels of cortisol and other inflammatory markers,^87,88 which may contribute to adverse outcomes in the face of additional stressors.

A large body of evidence stretching from bench to bedside suggests that environmental stressors associated with hospitalization are toxic. Understanding PHS within the context of hospital-induced allostatic overload presents a unifying theory for the interrelated multisystem dysfunction and increased susceptibility to adverse events that patients experience after discharge (Figure 2). Furthermore, it defines a potential pathophysiological mechanism for the cognitive impairment, elevated cardiovascular risk, immune system dysfunction, metabolic derangements, and functional decline associated with PHS. Additionally, this theory highlights environmental interventions to limit PHS development and suggests mechanisms to promote stress resilience. Although it is difficult to disentangle the consequences of the endogenous stress triggered by an acute illness from the exogenous stressors related to hospitalization, it is likely that the 2 simultaneous exposures compound risk for stress system dysregulation and allostatic overload. Moreover, hospitalized patients with preexisting HPA axis dysfunction at baseline from chronic disease or advancing age may be even more susceptible to these adverse outcomes. If this hypothesis is true, a reduction in PHS would require mitigation of the modifiable environmental stressors encountered by patients during hospitalization. Directed efforts to diminish ambient noise, limit nighttime disruptions, thoughtfully plan procedures, consider ongoing nutritional status, and promote opportunities for patients to exert some control over their environment may diminish the burden of extrinsic stressors encountered by all patients in the hospital and improve outcomes after discharge.

Hospitals are increasingly recognizing the importance of improving patients’ experience of hospitalization by reducing exposure to potential toxicities. For example, many hospitals are now attempting to reduce sleep disturbances and sleep latency through reduced nighttime noise and light levels, fewer nighttime interruptions for vital signs checks and medication administration, and commonsensical interventions like massages, herbal teas, and warm milk prior to bedtime.⁸⁹ Likewise, intensive care units are targeting environmental and physical stressors with a multifaceted approach to decrease sedative use, promote healthy sleep cycles, and encourage exercise and ambulation even in those patients who are mechanically ventilated.³⁰ Another promising development has been the increase of Hospital at Home programs. In these programs, patients who meet the criteria for inpatient admission are instead comprehensively managed at home for their acute illness through a multidisciplinary effort between physicians, nurses, social workers, physical therapists, and others. Patients hospitalized at home report higher levels of satisfaction and have modest functional gains, improved health-related quality of life, and decreased risk of mortality at 6 months compared with hospitalized patients.^90,91 With some admitting diagnoses (eg, heart failure), hospitalization at home may be associated with decreased readmission risk.⁹² Although not yet investigated on a physiologic level, perhaps the benefits of hospital at home are partially due to the dramatic difference in exposure to environmental stressors.

A tool that quantifies hospital-associated stress may help health providers appreciate the experience of patients and better target interventions to aspects of their structure and process that contribute to allostatic overload. Importantly, allostatic overload cannot be identified by one biomarker of stress but instead requires evidence of dysregulation across inflammatory, neuroendocrine, hormonal, and cardiometabolic systems. Future studies to address the burden of stress faced by hospitalized patients should consider a summative measure of multisystem dysregulation as opposed to isolated assessments of individual biomarkers. Allostatic load has previously been operationalized as the summation of a variety of hemodynamic, hormonal, and metabolic factors, including blood pressure, lipid profile, glycosylated hemoglobin, cortisol, catecholamine levels, and inflammatory markers.⁹³ To develop a hospital-associated allostatic load index, models should ideally be adjusted for acute illness severity, patient-reported stress, and capacity for stress resilience. This tool could then be used to quantify hospitalization-related allostatic load and identify those at greatest risk for adverse events after discharge, as well as measure the effectiveness of strategic environmental interventions (Table 2). A natural first experiment may be a comparison of the allostatic load of hospitalized patients versus those hospitalized at home.

The Substance Abuse and Mental Health Services Administration (SAMHSA) has launched a new Resource Center, aiming to give communities, clinicians, policy makers, and others the tools they need to put evidence-based information into practice.

The Evidence-Based Resource Center (www.samhsa.gov/ebp-resource-center) provides new or updated Treatment Improvement Protocols, tool kits, resource guides, clinical practice guidelines , and other science-based resources. The website has an easy-to-use point-and-click system. Users can search by topic, resource, target population, and target audience. The site also includes an opioid-specific resources section.

The center is part of a new comprehensive approach that allows rapid development and dissemination of the latest expert consensus on prevention, treatment, and recovery, SAMHSA says. It also provides communities and practitioners with tools to facilitate comprehensive needs assessment, match interventions to those needs, support implementation, and evaluate and incorporate continuous quality improvement as they translate science into action.

The Substance Abuse and Mental Health Services Administration (SAMHSA) has launched a new Resource Center, aiming to give communities, clinicians, policy makers, and others the tools they need to put evidence-based information into practice.

The Evidence-Based Resource Center (www.samhsa.gov/ebp-resource-center) provides new or updated Treatment Improvement Protocols, tool kits, resource guides, clinical practice guidelines , and other science-based resources. The website has an easy-to-use point-and-click system. Users can search by topic, resource, target population, and target audience. The site also includes an opioid-specific resources section.

The center is part of a new comprehensive approach that allows rapid development and dissemination of the latest expert consensus on prevention, treatment, and recovery, SAMHSA says. It also provides communities and practitioners with tools to facilitate comprehensive needs assessment, match interventions to those needs, support implementation, and evaluate and incorporate continuous quality improvement as they translate science into action.

The Substance Abuse and Mental Health Services Administration (SAMHSA) has launched a new Resource Center, aiming to give communities, clinicians, policy makers, and others the tools they need to put evidence-based information into practice.

The Evidence-Based Resource Center (www.samhsa.gov/ebp-resource-center) provides new or updated Treatment Improvement Protocols, tool kits, resource guides, clinical practice guidelines , and other science-based resources. The website has an easy-to-use point-and-click system. Users can search by topic, resource, target population, and target audience. The site also includes an opioid-specific resources section.

The center is part of a new comprehensive approach that allows rapid development and dissemination of the latest expert consensus on prevention, treatment, and recovery, SAMHSA says. It also provides communities and practitioners with tools to facilitate comprehensive needs assessment, match interventions to those needs, support implementation, and evaluate and incorporate continuous quality improvement as they translate science into action.

See related editorial

WHAT IS ‘EARLY’ SURGERY?

More than 50% of patients with infective endocarditis undergo cardiac surgery during their initial presentation.¹

The 2017 guidelines of the American Association for Thoracic Surgery (AATS) recommend surgery once a surgical indication has been established and effective antimicrobial therapy has been started.²

The American Heart Association/American College of Cardiology (ACC/AHA) guidelines recommend surgery during the initial hospitalization before completion of a full course of antibiotics.³

The European Society of Cardiology guidelines define surgery according to the time since the patient received intravenous antibiotic therapy: emergency surgery is performed within 24 hours of therapy, urgent surgery is performed within a few days, and elective surgery is performed after at least 1 to 2 weeks.⁴

These slight differences are due to the dearth of large randomized trials addressing this question.

INDICATIONS FOR EARLY SURGERY

Left ventricular dysfunction and heart failure

Of all the complications of infectious endocarditis, concomitant heart failure has the greatest impact on prognosis⁵ and is one of the most frequent indications for surgery.⁶

The guidelines recommend emergency surgery during the initial hospitalization for all patients with infective endocarditis who present with refractory pulmonary edema, worsening left ventricular dysfunction, or cardiogenic shock, regardless of whether they have completed a full course of antibiotics. This applies to both native valve endocarditis and prosthetic valve endocarditis.

Uncontrolled persistent infection

Persistent infection is defined as fever and positive cultures persisting after 1 week of appropriate antibiotic treatment.⁴ However, 1 week is a long time. Persistence of positive blood cultures more than 48 to 72 hours after starting antibiotic therapy is associated with poor outcome and is an independent predictor of in-hospital mortality.⁷

The ACC/AHA guidelines recommend early surgery in patients with left-sided infective endocarditis caused by fungi or highly resistant organisms such as vancomycin-resistant enterococci or multidrug-resistant gram-negative bacilli.³ Nonetheless, antibiotic resistance is an unusual reason for expediting surgery unless there are additional indications for it.

Extension of the infection beyond the valve annulus, which occurs in about 30% of cases of native valve endocarditis and 50% of cases of prosthetic valve endocarditis,⁸ is considered a more valid reason to expedite surgery. Similarly, urgent surgery should be considered if there is any evidence of locally uncontrolled infection causing perivalvular abscess, fistula, pseudoaneurysm, or conduction system abnormalities causing atrioventricular nodal block.^2–4

Some authors suggest reviewing the surgical pathology and microbial sequencing of excised cardiac valves after surgery to confirm the diagnosis and identify the culprit pathogen.^9,10

Right-sided infective endocarditis has a more favorable prognosis than left-sided infective endocarditis and usually responds well to medical therapy.¹¹

Nevertheless, surgery for right-sided infective endocarditis should be expedited in patients with right heart failure secondary to severe tricuspid regurgitation with poor response to medical therapy or in the case of large tricuspid valve vegetations.¹² Likewise, recurrent septic pulmonary emboli can be encountered in the setting of right-sided infective endocarditis and are an indication for early surgery.^4,12

Since many patients with right-sided infective endocarditis acquire the infection by intravenous drug use, there is often a reluctance to recommend surgery, given the risk of prosthetic valve infection if they continue to use intravenous drugs.^4,12 One study showed that the risk of death or reoperation between 3 and 6 months after surgery for infective endocarditis was 10 times higher in intravenous drug users. Yet their survival after surgery beyond this period was similar to that of patients with endocarditis who did not inject drugs.¹³ Therefore, the AATS guidelines recommend applying normal indications for surgery to those patients, with emphasis on the need for strict follow-up aimed at addiction treatment.²

Prevention of embolic events

Neurologic embolic events are a frequent complication of infective endocarditis, with the highest risk during the first few days after antibiotics are started. However, this risk decreases significantly after 2 weeks.¹⁴

The timing of surgery largely depends on whether the patient has had previous neurologic embolic events and on the size and mobility of the vegetation. The current guidelines recommend early surgery for recurrent emboli and persistent or enlarging vegetations despite appropriate antibiotic therapy, or in case of large vegetations (> 10 mm) on a native valve even in the absence of embolic events.⁴

A randomized trial by Kang et al¹⁵ demonstrated that, compared with conventional care, early surgery (within 48 hours of diagnosis) in patients with native valve endocarditis with large vegetations (> 10 mm) and severe valve dysfunction was associated with a significant reduction in the risk of death and embolic events.

Timing of surgery after a neurologic complication

Determining the right time for surgery is challenging in patients with infective endocarditis who have had neurologic complications, given the risk of hemorrhagic conversion of existing stroke with anticoagulation or exacerbation of cerebral ischemia in case of intraoperative hypotension. The decision should take into account the severity of cardiac decompensation, weighed against the severity of neurologic symptoms.

In general, surgery should be postponed for at least 4 weeks after intracerebral hemorrhage. However, it should be expedited in the event of silent cerebral embolism or transient ischemic attack, or in patients with infective endocarditis with stroke who have other indications for early surgery, as long as cerebral hemorrhage has been excluded by appropriate imaging.⁴

Early surgery for prosthetic valve endocarditis

The timing of surgery for prosthetic valve endocarditis follows the same general principles as for native valve endocarditis.^2–4,12

One study showed that early surgery for prosthetic valve endocarditis was not associated with lower in-hospital and 1-year mortality rates compared with medical therapy.¹⁶ On the other hand, a subgroup analysis demonstrated surgery to be significantly beneficial in those with the strongest indications for surgery, including severe valve regurgitation, heart failure, paravalvular abscess, fistula, or prosthetic valve dehiscence.

The decision to proceed with surgery in prosthetic valve endocarditis should be weighed carefully, taking into consideration the patient’s overall clinical condition and estimated surgical risk.¹⁶

COLLABORATION IS HELPFUL

Early surgery is indicated for infective endocarditis patients presenting with:

• Refractory heart failure symptoms
• Persistent infection
• Large vegetations with a high risk of embolism.

Expeditious and successful treatment entails multidisciplinary collaboration among experts in cardiology and infectious diseases with access to cardiac surgery input early in the evaluation.

See related editorial

WHAT IS ‘EARLY’ SURGERY?

More than 50% of patients with infective endocarditis undergo cardiac surgery during their initial presentation.¹

The 2017 guidelines of the American Association for Thoracic Surgery (AATS) recommend surgery once a surgical indication has been established and effective antimicrobial therapy has been started.²

The American Heart Association/American College of Cardiology (ACC/AHA) guidelines recommend surgery during the initial hospitalization before completion of a full course of antibiotics.³

The European Society of Cardiology guidelines define surgery according to the time since the patient received intravenous antibiotic therapy: emergency surgery is performed within 24 hours of therapy, urgent surgery is performed within a few days, and elective surgery is performed after at least 1 to 2 weeks.⁴

These slight differences are due to the dearth of large randomized trials addressing this question.

INDICATIONS FOR EARLY SURGERY

Left ventricular dysfunction and heart failure

Of all the complications of infectious endocarditis, concomitant heart failure has the greatest impact on prognosis⁵ and is one of the most frequent indications for surgery.⁶

The guidelines recommend emergency surgery during the initial hospitalization for all patients with infective endocarditis who present with refractory pulmonary edema, worsening left ventricular dysfunction, or cardiogenic shock, regardless of whether they have completed a full course of antibiotics. This applies to both native valve endocarditis and prosthetic valve endocarditis.

Uncontrolled persistent infection

Persistent infection is defined as fever and positive cultures persisting after 1 week of appropriate antibiotic treatment.⁴ However, 1 week is a long time. Persistence of positive blood cultures more than 48 to 72 hours after starting antibiotic therapy is associated with poor outcome and is an independent predictor of in-hospital mortality.⁷

The ACC/AHA guidelines recommend early surgery in patients with left-sided infective endocarditis caused by fungi or highly resistant organisms such as vancomycin-resistant enterococci or multidrug-resistant gram-negative bacilli.³ Nonetheless, antibiotic resistance is an unusual reason for expediting surgery unless there are additional indications for it.

Extension of the infection beyond the valve annulus, which occurs in about 30% of cases of native valve endocarditis and 50% of cases of prosthetic valve endocarditis,⁸ is considered a more valid reason to expedite surgery. Similarly, urgent surgery should be considered if there is any evidence of locally uncontrolled infection causing perivalvular abscess, fistula, pseudoaneurysm, or conduction system abnormalities causing atrioventricular nodal block.^2–4

Some authors suggest reviewing the surgical pathology and microbial sequencing of excised cardiac valves after surgery to confirm the diagnosis and identify the culprit pathogen.^9,10

Right-sided infective endocarditis has a more favorable prognosis than left-sided infective endocarditis and usually responds well to medical therapy.¹¹

Nevertheless, surgery for right-sided infective endocarditis should be expedited in patients with right heart failure secondary to severe tricuspid regurgitation with poor response to medical therapy or in the case of large tricuspid valve vegetations.¹² Likewise, recurrent septic pulmonary emboli can be encountered in the setting of right-sided infective endocarditis and are an indication for early surgery.^4,12

Since many patients with right-sided infective endocarditis acquire the infection by intravenous drug use, there is often a reluctance to recommend surgery, given the risk of prosthetic valve infection if they continue to use intravenous drugs.^4,12 One study showed that the risk of death or reoperation between 3 and 6 months after surgery for infective endocarditis was 10 times higher in intravenous drug users. Yet their survival after surgery beyond this period was similar to that of patients with endocarditis who did not inject drugs.¹³ Therefore, the AATS guidelines recommend applying normal indications for surgery to those patients, with emphasis on the need for strict follow-up aimed at addiction treatment.²

Prevention of embolic events

Neurologic embolic events are a frequent complication of infective endocarditis, with the highest risk during the first few days after antibiotics are started. However, this risk decreases significantly after 2 weeks.¹⁴

The timing of surgery largely depends on whether the patient has had previous neurologic embolic events and on the size and mobility of the vegetation. The current guidelines recommend early surgery for recurrent emboli and persistent or enlarging vegetations despite appropriate antibiotic therapy, or in case of large vegetations (> 10 mm) on a native valve even in the absence of embolic events.⁴

A randomized trial by Kang et al¹⁵ demonstrated that, compared with conventional care, early surgery (within 48 hours of diagnosis) in patients with native valve endocarditis with large vegetations (> 10 mm) and severe valve dysfunction was associated with a significant reduction in the risk of death and embolic events.

Timing of surgery after a neurologic complication

Determining the right time for surgery is challenging in patients with infective endocarditis who have had neurologic complications, given the risk of hemorrhagic conversion of existing stroke with anticoagulation or exacerbation of cerebral ischemia in case of intraoperative hypotension. The decision should take into account the severity of cardiac decompensation, weighed against the severity of neurologic symptoms.

In general, surgery should be postponed for at least 4 weeks after intracerebral hemorrhage. However, it should be expedited in the event of silent cerebral embolism or transient ischemic attack, or in patients with infective endocarditis with stroke who have other indications for early surgery, as long as cerebral hemorrhage has been excluded by appropriate imaging.⁴

Early surgery for prosthetic valve endocarditis

The timing of surgery for prosthetic valve endocarditis follows the same general principles as for native valve endocarditis.^2–4,12

One study showed that early surgery for prosthetic valve endocarditis was not associated with lower in-hospital and 1-year mortality rates compared with medical therapy.¹⁶ On the other hand, a subgroup analysis demonstrated surgery to be significantly beneficial in those with the strongest indications for surgery, including severe valve regurgitation, heart failure, paravalvular abscess, fistula, or prosthetic valve dehiscence.

The decision to proceed with surgery in prosthetic valve endocarditis should be weighed carefully, taking into consideration the patient’s overall clinical condition and estimated surgical risk.¹⁶

COLLABORATION IS HELPFUL

Early surgery is indicated for infective endocarditis patients presenting with:

• Refractory heart failure symptoms
• Persistent infection
• Large vegetations with a high risk of embolism.

Expeditious and successful treatment entails multidisciplinary collaboration among experts in cardiology and infectious diseases with access to cardiac surgery input early in the evaluation.

See related editorial

WHAT IS ‘EARLY’ SURGERY?

More than 50% of patients with infective endocarditis undergo cardiac surgery during their initial presentation.¹

The 2017 guidelines of the American Association for Thoracic Surgery (AATS) recommend surgery once a surgical indication has been established and effective antimicrobial therapy has been started.²

The American Heart Association/American College of Cardiology (ACC/AHA) guidelines recommend surgery during the initial hospitalization before completion of a full course of antibiotics.³

The European Society of Cardiology guidelines define surgery according to the time since the patient received intravenous antibiotic therapy: emergency surgery is performed within 24 hours of therapy, urgent surgery is performed within a few days, and elective surgery is performed after at least 1 to 2 weeks.⁴

These slight differences are due to the dearth of large randomized trials addressing this question.

INDICATIONS FOR EARLY SURGERY

Left ventricular dysfunction and heart failure

Of all the complications of infectious endocarditis, concomitant heart failure has the greatest impact on prognosis⁵ and is one of the most frequent indications for surgery.⁶

The guidelines recommend emergency surgery during the initial hospitalization for all patients with infective endocarditis who present with refractory pulmonary edema, worsening left ventricular dysfunction, or cardiogenic shock, regardless of whether they have completed a full course of antibiotics. This applies to both native valve endocarditis and prosthetic valve endocarditis.

Uncontrolled persistent infection

Persistent infection is defined as fever and positive cultures persisting after 1 week of appropriate antibiotic treatment.⁴ However, 1 week is a long time. Persistence of positive blood cultures more than 48 to 72 hours after starting antibiotic therapy is associated with poor outcome and is an independent predictor of in-hospital mortality.⁷

The ACC/AHA guidelines recommend early surgery in patients with left-sided infective endocarditis caused by fungi or highly resistant organisms such as vancomycin-resistant enterococci or multidrug-resistant gram-negative bacilli.³ Nonetheless, antibiotic resistance is an unusual reason for expediting surgery unless there are additional indications for it.

Extension of the infection beyond the valve annulus, which occurs in about 30% of cases of native valve endocarditis and 50% of cases of prosthetic valve endocarditis,⁸ is considered a more valid reason to expedite surgery. Similarly, urgent surgery should be considered if there is any evidence of locally uncontrolled infection causing perivalvular abscess, fistula, pseudoaneurysm, or conduction system abnormalities causing atrioventricular nodal block.^2–4

Some authors suggest reviewing the surgical pathology and microbial sequencing of excised cardiac valves after surgery to confirm the diagnosis and identify the culprit pathogen.^9,10

Right-sided infective endocarditis has a more favorable prognosis than left-sided infective endocarditis and usually responds well to medical therapy.¹¹

Nevertheless, surgery for right-sided infective endocarditis should be expedited in patients with right heart failure secondary to severe tricuspid regurgitation with poor response to medical therapy or in the case of large tricuspid valve vegetations.¹² Likewise, recurrent septic pulmonary emboli can be encountered in the setting of right-sided infective endocarditis and are an indication for early surgery.^4,12

Since many patients with right-sided infective endocarditis acquire the infection by intravenous drug use, there is often a reluctance to recommend surgery, given the risk of prosthetic valve infection if they continue to use intravenous drugs.^4,12 One study showed that the risk of death or reoperation between 3 and 6 months after surgery for infective endocarditis was 10 times higher in intravenous drug users. Yet their survival after surgery beyond this period was similar to that of patients with endocarditis who did not inject drugs.¹³ Therefore, the AATS guidelines recommend applying normal indications for surgery to those patients, with emphasis on the need for strict follow-up aimed at addiction treatment.²

Prevention of embolic events

Neurologic embolic events are a frequent complication of infective endocarditis, with the highest risk during the first few days after antibiotics are started. However, this risk decreases significantly after 2 weeks.¹⁴

The timing of surgery largely depends on whether the patient has had previous neurologic embolic events and on the size and mobility of the vegetation. The current guidelines recommend early surgery for recurrent emboli and persistent or enlarging vegetations despite appropriate antibiotic therapy, or in case of large vegetations (> 10 mm) on a native valve even in the absence of embolic events.⁴

A randomized trial by Kang et al¹⁵ demonstrated that, compared with conventional care, early surgery (within 48 hours of diagnosis) in patients with native valve endocarditis with large vegetations (> 10 mm) and severe valve dysfunction was associated with a significant reduction in the risk of death and embolic events.

Timing of surgery after a neurologic complication

Determining the right time for surgery is challenging in patients with infective endocarditis who have had neurologic complications, given the risk of hemorrhagic conversion of existing stroke with anticoagulation or exacerbation of cerebral ischemia in case of intraoperative hypotension. The decision should take into account the severity of cardiac decompensation, weighed against the severity of neurologic symptoms.

In general, surgery should be postponed for at least 4 weeks after intracerebral hemorrhage. However, it should be expedited in the event of silent cerebral embolism or transient ischemic attack, or in patients with infective endocarditis with stroke who have other indications for early surgery, as long as cerebral hemorrhage has been excluded by appropriate imaging.⁴

Early surgery for prosthetic valve endocarditis

The timing of surgery for prosthetic valve endocarditis follows the same general principles as for native valve endocarditis.^2–4,12

One study showed that early surgery for prosthetic valve endocarditis was not associated with lower in-hospital and 1-year mortality rates compared with medical therapy.¹⁶ On the other hand, a subgroup analysis demonstrated surgery to be significantly beneficial in those with the strongest indications for surgery, including severe valve regurgitation, heart failure, paravalvular abscess, fistula, or prosthetic valve dehiscence.

The decision to proceed with surgery in prosthetic valve endocarditis should be weighed carefully, taking into consideration the patient’s overall clinical condition and estimated surgical risk.¹⁶

COLLABORATION IS HELPFUL

Early surgery is indicated for infective endocarditis patients presenting with:

• Refractory heart failure symptoms
• Persistent infection
• Large vegetations with a high risk of embolism.

Expeditious and successful treatment entails multidisciplinary collaboration among experts in cardiology and infectious diseases with access to cardiac surgery input early in the evaluation.