The goal of this article is to explain how the first in a series of online resource rooms provides trainees and hospitalists with quality improvement tools that can be applied locally to improve inpatient care.1 During the emergence and explosive growth of hospital medicine, the SHM recognized the need to revise training relating to inpatient care and hospital process design to meet the evolving expectation of hospitalists that their performance will be measured, to actively set quality parameters, and to lead multidisciplinary teams to improve hospital performance.2 Armed with the appropriate skill set, hospitalists would be uniquely situated to lead and manage improvements in processes in the hospitals in which they work.

The content of the first Society of Hospital Medicine (SHM) Quality Improvement Resource Room (QI RR) supports hospitalists leading a multidisciplinary team dedicated to improving inpatient outcomes by preventing hospital‐acquired venous thromboembolism (VTE), a common cause of morbidity and mortality in hospitalized patients.3 The SHM developed this educational resource in the context of numerous reports on the incidence of medical errors in US hospitals and calls for action to improve the quality of health care.'47 Hospital report cards on quality measures are now public record, and hospitals will require uniformity in practice among physicians. Hospitalists are increasingly expected to lead initiatives that will implement national standards in key practices such as VTE prophylaxis2.

The QI RRs of the SHM are a collection of electronic tools accessible through the SHM Web site. They are designed to enhance the readiness of hospitalists and members of the multidisciplinary inpatient team to redesign care at the institutional level. Although all performance improvement is ultimately occurs locally, many QI methods and tools transcend hospital geography and disease topic. Leveraging a Web‐based platform, the SHM QI RRs present hospitalists with a general approach to QI, enriched by customizable workbooks that can be downloaded to best meet user needs. This resource is an innovation in practice‐based learning, quality improvement, and systems‐based practice.

METHODS

Development of the first QI RR followed a series of steps described in Curriculum Development for Medical Education8 (for process and timeline, see Table 1). Inadequate VTE prophylaxis was identified as an ongoing widespread problem of health care underutilization despite randomized clinical trials supporting the efficacy of prophylaxis.9, 10 Mirroring the AHRQ's assessment of underutilization of VTE prophylaxis as the single most important safety priority,6 the first QI RR focused on VTE, with plans to cover additional clinical conditions over time. As experts in the care of inpatients, hospitalists should be able to take custody of predictable complications of serious illness, identify and lower barriers to prevention, critically review prophylaxis options, utilize hospital‐specific data, and devise strategies to bridge the gap between knowledge and practice. Already leaders of multidisciplinary care teams, hospitalists are primed to lead multidisciplinary improvement teams as well.

Available data on the demographics of hospitalists and feedback from the SHM membership, leadership, and committees indicated that most learners would have minimal previous exposure to QI concepts and only a few years of management experience. Any previous quality improvement initiatives would tend to have been isolated, experimental, or smaller in scale. The resource rooms are designed to facilitate quality improvement learning among hospitalists that is practice‐based and immediately relevant to patient care. Measurable improvement in particular care processes or outcomes should correlate with actual learning.

The educational strategy of the SHM was predicated on ensuring that a quality and patient safety curriculum would retain clinical applicability in the hospital setting. This approach, grounded in adult learning principles and common to medical education, teaches general principles by framing the learning experience as problem centered.11 Several domains were identified as universally important to any quality improvement effort: raising awareness of a local performance gap, applying the best current evidence to practice, tapping the experience of others leading QI efforts, and using measurements derived from rapid‐cycle tests of change. Such a template delineates the components of successful QI planning, implementation, and evaluation and provides users with a familiar RR format applicable to improving any care process, not just VTE.

The Internet was chosen as the mechanism for delivering training on the basis of previous surveys of the SHM membership in which members expressed a preference for electronic and Web‐based forms of educational content delivery. Drawing from the example of other organizations teaching quality improvement, including the Institute for Healthcare Improvement and Intermountain Health Care, the SHM valued the ubiquity of a Web‐based educational resource. To facilitate on‐the‐job training, the first SHM QI RR provides a comprehensive tool kit to guide hospitalists through the process of advocating, developing, implementing, and evaluating a QI initiative for VTE.

Prior to launching the resource room, formative input was collected from SHM leaders, a panel of education and QI experts, and attendees of the society's annual meetings. Such input followed each significant step in the development of the RR curricula. For example, visitors at a kiosk at the 2005 SHM annual meeting completed surveys as they navigated through the VTE QI RR. This focused feedback shaped prelaunch development. The ultimate performance evaluation and feedback for the QI RR curricula will be gauged by user reports of measurable improvement in specific hospital process or outcomes measures. The VTE QI RR was launched in August 2005 and promoted at the SHM Web site.

RESULTS

The content and layout of the VTE QI RR are depicted in Figure 1. The self‐directed learner may navigate through the entire resource room or just select areas for study. Those likely to visit only a single area are individuals looking for guidance to support discrete roles on the improvement team: champion, clinical leader, facilitator of the QI process, or educator of staff or patient audiences (see Figure 2).

Figure 1

Figure 2

DISCUSSION

A case example, shown in Figure 3, demonstrates how content accessible through the SHM VTE QI RR may be used to catalyze a local quality improvement effort.

Figure 3

Hospitals will be measured on rates of VTE prophylaxis on medical and surgical services. Failure to standardize prophylaxis among different physician groups may adversely affect overall performance, with implications for both patient care and accreditation. The lack of a agreed‐on gold standard of what constitutes appropriate prophylaxis for a given patient does not absolve an institution of the duty to implement its own standards. The challenge of achieving local consensus on appropriate prophylaxis should not outweigh the urgency to address preventable in‐hospital deaths. In caring for increasing numbers of general medical and surgical patients, hospitalists are likely to be asked to develop and implement a protocol for VTE prophylaxis that can be used hospitalwide. In many instances hospitalists will accept this charge in the aftermath of previous hospital failures in which admission order sets or VTE assessment protocols were launched but never widely implemented. As the National Quality Forum or JCAHO regulations for uniformity among hospitals shift VTE prophylaxis from being voluntary to compulsory, hospitalists will need to develop improvement strategies that have greater reliability.

Hospitalists with no formal training in either vascular medicine or quality improvement may not be able to immediately cite the most current data about VTE prophylaxis rates and regimens and may not have the time to enroll in a training course on quality improvement. How would hospitalists determine baseline rates of appropriate VTE prophylaxis? How can medical education be used to build consensus and recruit support from other physicians? What should be the scope of the QI initiative, and what patient population should be targeted for intervention?

The goal of the SHM QI RR is to provide the tools and the framework to help hospitalists develop, implement, and manage a VTE prophylaxis quality improvement initiative. Suggested Steps to Action in the Awareness section depict exactly how a hospital medicine service can use the campaign's materials to raise institutional support for tackling this preventable problem. Hospital quality officers can direct the hospital's public relations department to the Awareness section for DVT Awareness Month materials, including public service announcements in audio, visual, and print formats. The hold music at the hospital can be temporarily replaced, television kiosks can be set up to run video loops, and banners can be printed and hung in central locations, all to get out the message simultaneously to patients and medical staff.

The Evidence section of the VTE QI RR references a key benchmark study, the DVT‐Free Prospective Registry.9 This study reported that at 183 sites in North America and Europe, more than twice as many medical patients as surgical patients failed to receive prophylaxis. The Evidence section includes the 7th American College of Chest Physicians Consensus Conference on Antithrombotic and Thrombolytic Therapy and also highlights 3 randomized placebo‐controlled clinical trials (MEDENOX 1999, ARTEMIS 2003, and PREVENT 2004) that have reported significant reduction of risk of VTE (50%‐60%) from pharmacologic prophylaxis in moderate‐risk medical inpatients.1315 Review of the data helps to determine which patient population to study first, which prophylaxis options a hospital could deploy appropriately, and the expected magnitude of the effect. Because the literature has already been narrowed and is kept current, hospitalists can save time in answering a range of questions, from the most commonly agreed‐on factors to stratify risk to which populations require alternative interventions.

The Experience section references the first clinical trial demonstrating improved patient outcomes from a quality improvement initiative aimed at improving utilization of VTE prophylaxis.10 At the large teaching hospital where the electronic alerts were studied, a preexisting wealth of educational information on the hospital Web site, in the form of multiple seminars and lectures on VTE prophylaxis by opinion leaders and international experts, had little impact on practice. For this reason, the investigators implemented a trial of how to change physician behavior by introducing a point‐of‐care intervention, the computer alerts. Clinicians prompted by an electronic alert to consider DVT prophylaxis for at‐risk patients employed nearly double the rate of pharmacologic prophylaxis and reduced the incidence of DVT or pulmonary embolism (PE) by 41%. This study suggests that a change introduced to the clinical workflow can improve evidence‐based VTE prophylaxis and also can reduce the incidence of VTE in acutely ill hospitalized patients.

We believe that if hospitalists use the current evidence and experience assembled in the VTE QI RR, they could develop and lead a systematic approach to improving utilization of VTE prophylaxis. Although there is no gold standard method for integrating VTE risk assessment into clinical workflow, the VTE QI RR presents key lessons both from the literature and real world experiences. The crucial take‐home message is that hospitalists can facilitate implementation of VTE risk assessments if they stress simplicity (ie, the sick, old, surgery benefit), link the risk assessment to a menu of evidence‐based prophylaxis options, and require assessment of VTE risk as part of a regular routine (on admission and at regular intervals). Although many hospitals do not yet have computerized entry of physician orders, the simple 4‐point VTE risk assessment described by Kucher et al might be applied to other hospitals.10 The 4‐point system would identify the patients at highest risk, a reasonable starting point for a QI initiative. Whatever the modelCPOE alerts of very high‐risk patients, CPOE‐forced VTE risk assessments, nursing assessments, or paper‐based order setsregular VTE risk assessment can be incorporated into the daily routine of hospital care.

The QI workbook sequences the steps of a multidisciplinary improvement team and prompts users to set specific goals, collect practical metrics, and conduct plan‐do‐study‐act (PDSA) cycles of learning and action (Figure 4). Hospitalists and other team members can use the information in the workbook to estimate the prevalence of use of the appropriate VTE prophylaxis and the incidence of hospital‐acquired VTE at their medical centers, develop a suitable VTE risk assessment model, and plan interventions. Starting with all patients admitted to one nurse on one unit, then expanding to an entire nursing unit, an improvement team could implement rapid PDSA cycles to iron out the wrinkles of a risk assessment protocol. After demonstrating a measurable benefit for the patients at highest risk, the team would then be expected to capture more patients at risk for VTE by modifying the risk assessment protocol to identify moderate‐risk patients (hospitalized patients with one risk factor), as in the MEDENOX, ARTEMIS, and PREVENT clinical trials. Within the first several months, the QI intervention could be expanded to more nursing units. An improvement report profiling a clinically important increase in the rate of appropriate VTE prophylaxis would advocate for additional local resources and projects.

Figure 4

As questions arise in assembling an improvement team, setting useful aims and metrics, choosing interventions, implementing and studying change, or collecting performance data, hospitalists can review answers to questions already posted and post their own questions in the Ask the Expert area. For example, one user asked whether there was a standard risk assessment tool for identifying patients at high risk of VTE. Another asked about the use of unfractionated heparin as a low‐cost alternative to low‐molecular‐weight heparin. Both these questions were answered within 24 hours by the content editor of the VTE QI RR and, for one question, also by 2 pharmacists and an international expert in VTE.

As other hospitalists begin de novo efforts of their own, success stories and strategies posted in the online forums of the VTE QI RR will be an evolving resource for basic know‐how and innovation.

Suggestions from a community of resource room users will be solicited, evaluated, and incorporated into the QI RR in order to improve its educational value and utility. The curricula could also be adapted or refined by others with an interest in systems‐based care or practice‐based learning, such as directors of residency training programs.

CONCLUSIONS

The QI RRs bring QI theory and practice to the hospitalist, when and wherever it is wanted, minimizing time away from patient care. The workbook links theory to practice and can be used to launch, sustain, and document a local VTE‐specific QI initiative. A range of experience is accommodated. Content is provided in a way that enables the user to immediately apply and adapt it to a local contextusers can access and download the subset of tools that best meet their needs. For practicing hospitalists, this QI resource offers an opportunity to bridge the training gap in systems‐based hospital care and should increase the quality and quantity of and support for opportunities to lead successful QI projects.

The Accreditation Council of Graduate Medical Education (ACGME) now requires education in health care systems, a requirement not previously mandated for traditional medical residency programs.17 Because the resource rooms should increase the number of hospitalists competently leading local efforts that achieve measurable gains in hospital outcomes, a wider potential constituency also includes residency program directors, internal medicine residents, physician assistants and nurse‐practitioners, nurses, hospital quality officers, and hospital medicine practice leaders.

Further research is needed to determine the clinical impact of the VTE QI workbook on outcomes for hospitalized patients. The effectiveness of such an educational method should be evaluated, at least in part, by documenting changes in clinically important process and outcome measures, in this case those specific to hospital‐acquired VTE. Investigation also will need to generate an impact assessment to see if the curricula are effective in meeting the strategic educational goals of the Society of Hospital Medicine. Further investigation will examine whether this resource can help residency training programs achieve ACGME goals for practice‐based learning and systems‐based care.

The goal of this article is to explain how the first in a series of online resource rooms provides trainees and hospitalists with quality improvement tools that can be applied locally to improve inpatient care.1 During the emergence and explosive growth of hospital medicine, the SHM recognized the need to revise training relating to inpatient care and hospital process design to meet the evolving expectation of hospitalists that their performance will be measured, to actively set quality parameters, and to lead multidisciplinary teams to improve hospital performance.2 Armed with the appropriate skill set, hospitalists would be uniquely situated to lead and manage improvements in processes in the hospitals in which they work.

The content of the first Society of Hospital Medicine (SHM) Quality Improvement Resource Room (QI RR) supports hospitalists leading a multidisciplinary team dedicated to improving inpatient outcomes by preventing hospital‐acquired venous thromboembolism (VTE), a common cause of morbidity and mortality in hospitalized patients.3 The SHM developed this educational resource in the context of numerous reports on the incidence of medical errors in US hospitals and calls for action to improve the quality of health care.'47 Hospital report cards on quality measures are now public record, and hospitals will require uniformity in practice among physicians. Hospitalists are increasingly expected to lead initiatives that will implement national standards in key practices such as VTE prophylaxis2.

The QI RRs of the SHM are a collection of electronic tools accessible through the SHM Web site. They are designed to enhance the readiness of hospitalists and members of the multidisciplinary inpatient team to redesign care at the institutional level. Although all performance improvement is ultimately occurs locally, many QI methods and tools transcend hospital geography and disease topic. Leveraging a Web‐based platform, the SHM QI RRs present hospitalists with a general approach to QI, enriched by customizable workbooks that can be downloaded to best meet user needs. This resource is an innovation in practice‐based learning, quality improvement, and systems‐based practice.

METHODS

Development of the first QI RR followed a series of steps described in Curriculum Development for Medical Education8 (for process and timeline, see Table 1). Inadequate VTE prophylaxis was identified as an ongoing widespread problem of health care underutilization despite randomized clinical trials supporting the efficacy of prophylaxis.9, 10 Mirroring the AHRQ's assessment of underutilization of VTE prophylaxis as the single most important safety priority,6 the first QI RR focused on VTE, with plans to cover additional clinical conditions over time. As experts in the care of inpatients, hospitalists should be able to take custody of predictable complications of serious illness, identify and lower barriers to prevention, critically review prophylaxis options, utilize hospital‐specific data, and devise strategies to bridge the gap between knowledge and practice. Already leaders of multidisciplinary care teams, hospitalists are primed to lead multidisciplinary improvement teams as well.

Available data on the demographics of hospitalists and feedback from the SHM membership, leadership, and committees indicated that most learners would have minimal previous exposure to QI concepts and only a few years of management experience. Any previous quality improvement initiatives would tend to have been isolated, experimental, or smaller in scale. The resource rooms are designed to facilitate quality improvement learning among hospitalists that is practice‐based and immediately relevant to patient care. Measurable improvement in particular care processes or outcomes should correlate with actual learning.

The educational strategy of the SHM was predicated on ensuring that a quality and patient safety curriculum would retain clinical applicability in the hospital setting. This approach, grounded in adult learning principles and common to medical education, teaches general principles by framing the learning experience as problem centered.11 Several domains were identified as universally important to any quality improvement effort: raising awareness of a local performance gap, applying the best current evidence to practice, tapping the experience of others leading QI efforts, and using measurements derived from rapid‐cycle tests of change. Such a template delineates the components of successful QI planning, implementation, and evaluation and provides users with a familiar RR format applicable to improving any care process, not just VTE.

The Internet was chosen as the mechanism for delivering training on the basis of previous surveys of the SHM membership in which members expressed a preference for electronic and Web‐based forms of educational content delivery. Drawing from the example of other organizations teaching quality improvement, including the Institute for Healthcare Improvement and Intermountain Health Care, the SHM valued the ubiquity of a Web‐based educational resource. To facilitate on‐the‐job training, the first SHM QI RR provides a comprehensive tool kit to guide hospitalists through the process of advocating, developing, implementing, and evaluating a QI initiative for VTE.

Prior to launching the resource room, formative input was collected from SHM leaders, a panel of education and QI experts, and attendees of the society's annual meetings. Such input followed each significant step in the development of the RR curricula. For example, visitors at a kiosk at the 2005 SHM annual meeting completed surveys as they navigated through the VTE QI RR. This focused feedback shaped prelaunch development. The ultimate performance evaluation and feedback for the QI RR curricula will be gauged by user reports of measurable improvement in specific hospital process or outcomes measures. The VTE QI RR was launched in August 2005 and promoted at the SHM Web site.

RESULTS

The content and layout of the VTE QI RR are depicted in Figure 1. The self‐directed learner may navigate through the entire resource room or just select areas for study. Those likely to visit only a single area are individuals looking for guidance to support discrete roles on the improvement team: champion, clinical leader, facilitator of the QI process, or educator of staff or patient audiences (see Figure 2).

Figure 1

Figure 2

DISCUSSION

A case example, shown in Figure 3, demonstrates how content accessible through the SHM VTE QI RR may be used to catalyze a local quality improvement effort.

Figure 3

Hospitals will be measured on rates of VTE prophylaxis on medical and surgical services. Failure to standardize prophylaxis among different physician groups may adversely affect overall performance, with implications for both patient care and accreditation. The lack of a agreed‐on gold standard of what constitutes appropriate prophylaxis for a given patient does not absolve an institution of the duty to implement its own standards. The challenge of achieving local consensus on appropriate prophylaxis should not outweigh the urgency to address preventable in‐hospital deaths. In caring for increasing numbers of general medical and surgical patients, hospitalists are likely to be asked to develop and implement a protocol for VTE prophylaxis that can be used hospitalwide. In many instances hospitalists will accept this charge in the aftermath of previous hospital failures in which admission order sets or VTE assessment protocols were launched but never widely implemented. As the National Quality Forum or JCAHO regulations for uniformity among hospitals shift VTE prophylaxis from being voluntary to compulsory, hospitalists will need to develop improvement strategies that have greater reliability.

Hospitalists with no formal training in either vascular medicine or quality improvement may not be able to immediately cite the most current data about VTE prophylaxis rates and regimens and may not have the time to enroll in a training course on quality improvement. How would hospitalists determine baseline rates of appropriate VTE prophylaxis? How can medical education be used to build consensus and recruit support from other physicians? What should be the scope of the QI initiative, and what patient population should be targeted for intervention?

The goal of the SHM QI RR is to provide the tools and the framework to help hospitalists develop, implement, and manage a VTE prophylaxis quality improvement initiative. Suggested Steps to Action in the Awareness section depict exactly how a hospital medicine service can use the campaign's materials to raise institutional support for tackling this preventable problem. Hospital quality officers can direct the hospital's public relations department to the Awareness section for DVT Awareness Month materials, including public service announcements in audio, visual, and print formats. The hold music at the hospital can be temporarily replaced, television kiosks can be set up to run video loops, and banners can be printed and hung in central locations, all to get out the message simultaneously to patients and medical staff.

The Evidence section of the VTE QI RR references a key benchmark study, the DVT‐Free Prospective Registry.9 This study reported that at 183 sites in North America and Europe, more than twice as many medical patients as surgical patients failed to receive prophylaxis. The Evidence section includes the 7th American College of Chest Physicians Consensus Conference on Antithrombotic and Thrombolytic Therapy and also highlights 3 randomized placebo‐controlled clinical trials (MEDENOX 1999, ARTEMIS 2003, and PREVENT 2004) that have reported significant reduction of risk of VTE (50%‐60%) from pharmacologic prophylaxis in moderate‐risk medical inpatients.1315 Review of the data helps to determine which patient population to study first, which prophylaxis options a hospital could deploy appropriately, and the expected magnitude of the effect. Because the literature has already been narrowed and is kept current, hospitalists can save time in answering a range of questions, from the most commonly agreed‐on factors to stratify risk to which populations require alternative interventions.

The Experience section references the first clinical trial demonstrating improved patient outcomes from a quality improvement initiative aimed at improving utilization of VTE prophylaxis.10 At the large teaching hospital where the electronic alerts were studied, a preexisting wealth of educational information on the hospital Web site, in the form of multiple seminars and lectures on VTE prophylaxis by opinion leaders and international experts, had little impact on practice. For this reason, the investigators implemented a trial of how to change physician behavior by introducing a point‐of‐care intervention, the computer alerts. Clinicians prompted by an electronic alert to consider DVT prophylaxis for at‐risk patients employed nearly double the rate of pharmacologic prophylaxis and reduced the incidence of DVT or pulmonary embolism (PE) by 41%. This study suggests that a change introduced to the clinical workflow can improve evidence‐based VTE prophylaxis and also can reduce the incidence of VTE in acutely ill hospitalized patients.

We believe that if hospitalists use the current evidence and experience assembled in the VTE QI RR, they could develop and lead a systematic approach to improving utilization of VTE prophylaxis. Although there is no gold standard method for integrating VTE risk assessment into clinical workflow, the VTE QI RR presents key lessons both from the literature and real world experiences. The crucial take‐home message is that hospitalists can facilitate implementation of VTE risk assessments if they stress simplicity (ie, the sick, old, surgery benefit), link the risk assessment to a menu of evidence‐based prophylaxis options, and require assessment of VTE risk as part of a regular routine (on admission and at regular intervals). Although many hospitals do not yet have computerized entry of physician orders, the simple 4‐point VTE risk assessment described by Kucher et al might be applied to other hospitals.10 The 4‐point system would identify the patients at highest risk, a reasonable starting point for a QI initiative. Whatever the modelCPOE alerts of very high‐risk patients, CPOE‐forced VTE risk assessments, nursing assessments, or paper‐based order setsregular VTE risk assessment can be incorporated into the daily routine of hospital care.

The QI workbook sequences the steps of a multidisciplinary improvement team and prompts users to set specific goals, collect practical metrics, and conduct plan‐do‐study‐act (PDSA) cycles of learning and action (Figure 4). Hospitalists and other team members can use the information in the workbook to estimate the prevalence of use of the appropriate VTE prophylaxis and the incidence of hospital‐acquired VTE at their medical centers, develop a suitable VTE risk assessment model, and plan interventions. Starting with all patients admitted to one nurse on one unit, then expanding to an entire nursing unit, an improvement team could implement rapid PDSA cycles to iron out the wrinkles of a risk assessment protocol. After demonstrating a measurable benefit for the patients at highest risk, the team would then be expected to capture more patients at risk for VTE by modifying the risk assessment protocol to identify moderate‐risk patients (hospitalized patients with one risk factor), as in the MEDENOX, ARTEMIS, and PREVENT clinical trials. Within the first several months, the QI intervention could be expanded to more nursing units. An improvement report profiling a clinically important increase in the rate of appropriate VTE prophylaxis would advocate for additional local resources and projects.

Figure 4

As questions arise in assembling an improvement team, setting useful aims and metrics, choosing interventions, implementing and studying change, or collecting performance data, hospitalists can review answers to questions already posted and post their own questions in the Ask the Expert area. For example, one user asked whether there was a standard risk assessment tool for identifying patients at high risk of VTE. Another asked about the use of unfractionated heparin as a low‐cost alternative to low‐molecular‐weight heparin. Both these questions were answered within 24 hours by the content editor of the VTE QI RR and, for one question, also by 2 pharmacists and an international expert in VTE.

As other hospitalists begin de novo efforts of their own, success stories and strategies posted in the online forums of the VTE QI RR will be an evolving resource for basic know‐how and innovation.

Suggestions from a community of resource room users will be solicited, evaluated, and incorporated into the QI RR in order to improve its educational value and utility. The curricula could also be adapted or refined by others with an interest in systems‐based care or practice‐based learning, such as directors of residency training programs.

CONCLUSIONS

The QI RRs bring QI theory and practice to the hospitalist, when and wherever it is wanted, minimizing time away from patient care. The workbook links theory to practice and can be used to launch, sustain, and document a local VTE‐specific QI initiative. A range of experience is accommodated. Content is provided in a way that enables the user to immediately apply and adapt it to a local contextusers can access and download the subset of tools that best meet their needs. For practicing hospitalists, this QI resource offers an opportunity to bridge the training gap in systems‐based hospital care and should increase the quality and quantity of and support for opportunities to lead successful QI projects.

The Accreditation Council of Graduate Medical Education (ACGME) now requires education in health care systems, a requirement not previously mandated for traditional medical residency programs.17 Because the resource rooms should increase the number of hospitalists competently leading local efforts that achieve measurable gains in hospital outcomes, a wider potential constituency also includes residency program directors, internal medicine residents, physician assistants and nurse‐practitioners, nurses, hospital quality officers, and hospital medicine practice leaders.

Further research is needed to determine the clinical impact of the VTE QI workbook on outcomes for hospitalized patients. The effectiveness of such an educational method should be evaluated, at least in part, by documenting changes in clinically important process and outcome measures, in this case those specific to hospital‐acquired VTE. Investigation also will need to generate an impact assessment to see if the curricula are effective in meeting the strategic educational goals of the Society of Hospital Medicine. Further investigation will examine whether this resource can help residency training programs achieve ACGME goals for practice‐based learning and systems‐based care.

The goal of this article is to explain how the first in a series of online resource rooms provides trainees and hospitalists with quality improvement tools that can be applied locally to improve inpatient care.1 During the emergence and explosive growth of hospital medicine, the SHM recognized the need to revise training relating to inpatient care and hospital process design to meet the evolving expectation of hospitalists that their performance will be measured, to actively set quality parameters, and to lead multidisciplinary teams to improve hospital performance.2 Armed with the appropriate skill set, hospitalists would be uniquely situated to lead and manage improvements in processes in the hospitals in which they work.

The content of the first Society of Hospital Medicine (SHM) Quality Improvement Resource Room (QI RR) supports hospitalists leading a multidisciplinary team dedicated to improving inpatient outcomes by preventing hospital‐acquired venous thromboembolism (VTE), a common cause of morbidity and mortality in hospitalized patients.3 The SHM developed this educational resource in the context of numerous reports on the incidence of medical errors in US hospitals and calls for action to improve the quality of health care.'47 Hospital report cards on quality measures are now public record, and hospitals will require uniformity in practice among physicians. Hospitalists are increasingly expected to lead initiatives that will implement national standards in key practices such as VTE prophylaxis2.

The QI RRs of the SHM are a collection of electronic tools accessible through the SHM Web site. They are designed to enhance the readiness of hospitalists and members of the multidisciplinary inpatient team to redesign care at the institutional level. Although all performance improvement is ultimately occurs locally, many QI methods and tools transcend hospital geography and disease topic. Leveraging a Web‐based platform, the SHM QI RRs present hospitalists with a general approach to QI, enriched by customizable workbooks that can be downloaded to best meet user needs. This resource is an innovation in practice‐based learning, quality improvement, and systems‐based practice.

METHODS

Development of the first QI RR followed a series of steps described in Curriculum Development for Medical Education8 (for process and timeline, see Table 1). Inadequate VTE prophylaxis was identified as an ongoing widespread problem of health care underutilization despite randomized clinical trials supporting the efficacy of prophylaxis.9, 10 Mirroring the AHRQ's assessment of underutilization of VTE prophylaxis as the single most important safety priority,6 the first QI RR focused on VTE, with plans to cover additional clinical conditions over time. As experts in the care of inpatients, hospitalists should be able to take custody of predictable complications of serious illness, identify and lower barriers to prevention, critically review prophylaxis options, utilize hospital‐specific data, and devise strategies to bridge the gap between knowledge and practice. Already leaders of multidisciplinary care teams, hospitalists are primed to lead multidisciplinary improvement teams as well.

Available data on the demographics of hospitalists and feedback from the SHM membership, leadership, and committees indicated that most learners would have minimal previous exposure to QI concepts and only a few years of management experience. Any previous quality improvement initiatives would tend to have been isolated, experimental, or smaller in scale. The resource rooms are designed to facilitate quality improvement learning among hospitalists that is practice‐based and immediately relevant to patient care. Measurable improvement in particular care processes or outcomes should correlate with actual learning.

The educational strategy of the SHM was predicated on ensuring that a quality and patient safety curriculum would retain clinical applicability in the hospital setting. This approach, grounded in adult learning principles and common to medical education, teaches general principles by framing the learning experience as problem centered.11 Several domains were identified as universally important to any quality improvement effort: raising awareness of a local performance gap, applying the best current evidence to practice, tapping the experience of others leading QI efforts, and using measurements derived from rapid‐cycle tests of change. Such a template delineates the components of successful QI planning, implementation, and evaluation and provides users with a familiar RR format applicable to improving any care process, not just VTE.

The Internet was chosen as the mechanism for delivering training on the basis of previous surveys of the SHM membership in which members expressed a preference for electronic and Web‐based forms of educational content delivery. Drawing from the example of other organizations teaching quality improvement, including the Institute for Healthcare Improvement and Intermountain Health Care, the SHM valued the ubiquity of a Web‐based educational resource. To facilitate on‐the‐job training, the first SHM QI RR provides a comprehensive tool kit to guide hospitalists through the process of advocating, developing, implementing, and evaluating a QI initiative for VTE.

Prior to launching the resource room, formative input was collected from SHM leaders, a panel of education and QI experts, and attendees of the society's annual meetings. Such input followed each significant step in the development of the RR curricula. For example, visitors at a kiosk at the 2005 SHM annual meeting completed surveys as they navigated through the VTE QI RR. This focused feedback shaped prelaunch development. The ultimate performance evaluation and feedback for the QI RR curricula will be gauged by user reports of measurable improvement in specific hospital process or outcomes measures. The VTE QI RR was launched in August 2005 and promoted at the SHM Web site.

RESULTS

The content and layout of the VTE QI RR are depicted in Figure 1. The self‐directed learner may navigate through the entire resource room or just select areas for study. Those likely to visit only a single area are individuals looking for guidance to support discrete roles on the improvement team: champion, clinical leader, facilitator of the QI process, or educator of staff or patient audiences (see Figure 2).

Figure 1

Figure 2

DISCUSSION

A case example, shown in Figure 3, demonstrates how content accessible through the SHM VTE QI RR may be used to catalyze a local quality improvement effort.

Figure 3

Hospitals will be measured on rates of VTE prophylaxis on medical and surgical services. Failure to standardize prophylaxis among different physician groups may adversely affect overall performance, with implications for both patient care and accreditation. The lack of a agreed‐on gold standard of what constitutes appropriate prophylaxis for a given patient does not absolve an institution of the duty to implement its own standards. The challenge of achieving local consensus on appropriate prophylaxis should not outweigh the urgency to address preventable in‐hospital deaths. In caring for increasing numbers of general medical and surgical patients, hospitalists are likely to be asked to develop and implement a protocol for VTE prophylaxis that can be used hospitalwide. In many instances hospitalists will accept this charge in the aftermath of previous hospital failures in which admission order sets or VTE assessment protocols were launched but never widely implemented. As the National Quality Forum or JCAHO regulations for uniformity among hospitals shift VTE prophylaxis from being voluntary to compulsory, hospitalists will need to develop improvement strategies that have greater reliability.

Hospitalists with no formal training in either vascular medicine or quality improvement may not be able to immediately cite the most current data about VTE prophylaxis rates and regimens and may not have the time to enroll in a training course on quality improvement. How would hospitalists determine baseline rates of appropriate VTE prophylaxis? How can medical education be used to build consensus and recruit support from other physicians? What should be the scope of the QI initiative, and what patient population should be targeted for intervention?

The goal of the SHM QI RR is to provide the tools and the framework to help hospitalists develop, implement, and manage a VTE prophylaxis quality improvement initiative. Suggested Steps to Action in the Awareness section depict exactly how a hospital medicine service can use the campaign's materials to raise institutional support for tackling this preventable problem. Hospital quality officers can direct the hospital's public relations department to the Awareness section for DVT Awareness Month materials, including public service announcements in audio, visual, and print formats. The hold music at the hospital can be temporarily replaced, television kiosks can be set up to run video loops, and banners can be printed and hung in central locations, all to get out the message simultaneously to patients and medical staff.

The Evidence section of the VTE QI RR references a key benchmark study, the DVT‐Free Prospective Registry.9 This study reported that at 183 sites in North America and Europe, more than twice as many medical patients as surgical patients failed to receive prophylaxis. The Evidence section includes the 7th American College of Chest Physicians Consensus Conference on Antithrombotic and Thrombolytic Therapy and also highlights 3 randomized placebo‐controlled clinical trials (MEDENOX 1999, ARTEMIS 2003, and PREVENT 2004) that have reported significant reduction of risk of VTE (50%‐60%) from pharmacologic prophylaxis in moderate‐risk medical inpatients.1315 Review of the data helps to determine which patient population to study first, which prophylaxis options a hospital could deploy appropriately, and the expected magnitude of the effect. Because the literature has already been narrowed and is kept current, hospitalists can save time in answering a range of questions, from the most commonly agreed‐on factors to stratify risk to which populations require alternative interventions.

The Experience section references the first clinical trial demonstrating improved patient outcomes from a quality improvement initiative aimed at improving utilization of VTE prophylaxis.10 At the large teaching hospital where the electronic alerts were studied, a preexisting wealth of educational information on the hospital Web site, in the form of multiple seminars and lectures on VTE prophylaxis by opinion leaders and international experts, had little impact on practice. For this reason, the investigators implemented a trial of how to change physician behavior by introducing a point‐of‐care intervention, the computer alerts. Clinicians prompted by an electronic alert to consider DVT prophylaxis for at‐risk patients employed nearly double the rate of pharmacologic prophylaxis and reduced the incidence of DVT or pulmonary embolism (PE) by 41%. This study suggests that a change introduced to the clinical workflow can improve evidence‐based VTE prophylaxis and also can reduce the incidence of VTE in acutely ill hospitalized patients.

We believe that if hospitalists use the current evidence and experience assembled in the VTE QI RR, they could develop and lead a systematic approach to improving utilization of VTE prophylaxis. Although there is no gold standard method for integrating VTE risk assessment into clinical workflow, the VTE QI RR presents key lessons both from the literature and real world experiences. The crucial take‐home message is that hospitalists can facilitate implementation of VTE risk assessments if they stress simplicity (ie, the sick, old, surgery benefit), link the risk assessment to a menu of evidence‐based prophylaxis options, and require assessment of VTE risk as part of a regular routine (on admission and at regular intervals). Although many hospitals do not yet have computerized entry of physician orders, the simple 4‐point VTE risk assessment described by Kucher et al might be applied to other hospitals.10 The 4‐point system would identify the patients at highest risk, a reasonable starting point for a QI initiative. Whatever the modelCPOE alerts of very high‐risk patients, CPOE‐forced VTE risk assessments, nursing assessments, or paper‐based order setsregular VTE risk assessment can be incorporated into the daily routine of hospital care.

The QI workbook sequences the steps of a multidisciplinary improvement team and prompts users to set specific goals, collect practical metrics, and conduct plan‐do‐study‐act (PDSA) cycles of learning and action (Figure 4). Hospitalists and other team members can use the information in the workbook to estimate the prevalence of use of the appropriate VTE prophylaxis and the incidence of hospital‐acquired VTE at their medical centers, develop a suitable VTE risk assessment model, and plan interventions. Starting with all patients admitted to one nurse on one unit, then expanding to an entire nursing unit, an improvement team could implement rapid PDSA cycles to iron out the wrinkles of a risk assessment protocol. After demonstrating a measurable benefit for the patients at highest risk, the team would then be expected to capture more patients at risk for VTE by modifying the risk assessment protocol to identify moderate‐risk patients (hospitalized patients with one risk factor), as in the MEDENOX, ARTEMIS, and PREVENT clinical trials. Within the first several months, the QI intervention could be expanded to more nursing units. An improvement report profiling a clinically important increase in the rate of appropriate VTE prophylaxis would advocate for additional local resources and projects.

Figure 4

As questions arise in assembling an improvement team, setting useful aims and metrics, choosing interventions, implementing and studying change, or collecting performance data, hospitalists can review answers to questions already posted and post their own questions in the Ask the Expert area. For example, one user asked whether there was a standard risk assessment tool for identifying patients at high risk of VTE. Another asked about the use of unfractionated heparin as a low‐cost alternative to low‐molecular‐weight heparin. Both these questions were answered within 24 hours by the content editor of the VTE QI RR and, for one question, also by 2 pharmacists and an international expert in VTE.

As other hospitalists begin de novo efforts of their own, success stories and strategies posted in the online forums of the VTE QI RR will be an evolving resource for basic know‐how and innovation.

Suggestions from a community of resource room users will be solicited, evaluated, and incorporated into the QI RR in order to improve its educational value and utility. The curricula could also be adapted or refined by others with an interest in systems‐based care or practice‐based learning, such as directors of residency training programs.

CONCLUSIONS

The QI RRs bring QI theory and practice to the hospitalist, when and wherever it is wanted, minimizing time away from patient care. The workbook links theory to practice and can be used to launch, sustain, and document a local VTE‐specific QI initiative. A range of experience is accommodated. Content is provided in a way that enables the user to immediately apply and adapt it to a local contextusers can access and download the subset of tools that best meet their needs. For practicing hospitalists, this QI resource offers an opportunity to bridge the training gap in systems‐based hospital care and should increase the quality and quantity of and support for opportunities to lead successful QI projects.

The Accreditation Council of Graduate Medical Education (ACGME) now requires education in health care systems, a requirement not previously mandated for traditional medical residency programs.17 Because the resource rooms should increase the number of hospitalists competently leading local efforts that achieve measurable gains in hospital outcomes, a wider potential constituency also includes residency program directors, internal medicine residents, physician assistants and nurse‐practitioners, nurses, hospital quality officers, and hospital medicine practice leaders.

Further research is needed to determine the clinical impact of the VTE QI workbook on outcomes for hospitalized patients. The effectiveness of such an educational method should be evaluated, at least in part, by documenting changes in clinically important process and outcome measures, in this case those specific to hospital‐acquired VTE. Investigation also will need to generate an impact assessment to see if the curricula are effective in meeting the strategic educational goals of the Society of Hospital Medicine. Further investigation will examine whether this resource can help residency training programs achieve ACGME goals for practice‐based learning and systems‐based care.

A 46‐year‐old African American man presented to the emergency department with severe chest pain that awakened him from sleep. The pain was substernal, radiated to the neck and back, and was continuous, lasting approximately 1 hour. It was associated with nausea, diaphoresis, and dizziness. The patient denied dyspnea, orthopnea, paroxysmal nocturnal dyspnea, dysphagia, odynophagia, vomiting, fever, chills, or headache. He denied recent recreational drug use. He works as a landscaper.

Substernal chest pain radiating to the neck and back implicates structures in the middle mediastinum, chiefly the heart, aorta, esophagus, pulmonary arteries, and mediastinal pleura. The presence of nausea and diaphoresis suggests a vagal response to pain.

The sudden onset of symptoms and the lack of fevers and chills make infectious causes in the mediastinum such as mediastinitis and pneumonia less likely. Acute pulmonary embolism often presents with pleuritic pain and dyspnea, features not present in this patient.

The absence of odynophagia and dysphagia makes esophageal rupture or perforation of esophageal diverticula unlikely. Likewise, the absence of dyspnea, orthopnea, and paroxysmal nocturnal dyspnea makes it unlikely to be acute left ventricular failure from a sudden rise in left atrial pressure. Such a scenario may occur in the setting of a myocardial infarction or rupture of a papillary muscle, chordae tendineae, or sinus of Valsalva.

Dissection of the aorta with or without involvement of the aortic root merits strong consideration. Dissection involving the carotid or vertebral arteries could explain the patient's dizziness. Physical stresses in a landscaper may contribute to elevation in blood pressure and set the stage for an aortic dissection, especially with other risk factors.

The patient has a history of a positive PPD and was treated with isoniazid for 6 months. His mother had a history of hypertension and died from a myocardial infarction at age 64. His father's medical history is unknown. He has a history of alcohol abuse but has been abstinent for more than a year. He smoked marijuana and tobacco occasionally, with a 15 pack‐year cigarette history. He also stated that the last time he used cocaine was 1 year prior to admission.

That his mother succumbed to a myocardial infarction as well as having been hypertensive could be important family history risk factors given the patient's symptoms. Furthermore, the concurrent use of alcohol and tobacco by the patient increases his risk of developing severe hypertension. The use of cocaine is associated with sudden elevations in systemic blood pressure, which predispose to intimal damage in the aorta, especially if other risk factors are present. Marijuana smoking has been implicated in pulmonary aspergillosis, but this sudden presentation in the absence of pulmonary symptoms makes it most unlikely. Optimal therapy of a positive PPD should not predispose the patient to acute exudative pericarditis. Thus far the features suggest an acute vascular episode without significant compromise of cardiac output.

The patient was alert and in mild distress from chest discomfort. He was afebrile, with a blood pressure of 136/64 in the right arm and 139/63 in the left arm. Heart rate was 60 beats per minute, and the respiratory rate was 12 beats per minute, with an oxygen saturation of 99% while breathing room air. Examination of the head and neck revealed no signs of trauma. Jugular venous waveforms were normal, and carotid artery pulsations had normal strength and upstroke without audible bruits. The lungs were clear to auscultation. Heart sounds were notable for a 3/6 diastolic murmur heard best at the right sternal border. Rate and rhythm were regular, and the apical impulse was sustained but not displaced. The peripheral pulses were present and equal in quality throughout. The findings of the abdominal exam were normal, and the digital rectal examination was negative for occult blood. The findings of the neurologic, musculoskeletal, and dermatologic exams also were normal.

A slightly elevated pulse pressure without a significant difference in upper extremity blood pressure could be a result of aortic regurgitation, sinus of Valsalva rupture, or a high‐cardiac‐output state, as seen in thyrotoxicosis, anemia, or arteriovenous fistula.

The presence of a 3/6 diastolic murmur at the sternal border, however, favors conditions that cause aortic valve regurgitation and, less commonly, pulmonary valve regurgitation, or turbulent flow across the tricuspid valve. The murmur of pulmonary and aortic valve regurgitation can be difficult to distinguish by auscultation; however, the absence of other findings such as a right ventricular heave, elevated jugular venous pressure, or primary lung disease do not support a pulmonary valve etiology. Turbulent flow across the tricuspid valve can be seen in high‐output states, large atrial septal defects, and tricuspid stenosis. This type of murmur is heard best at the lower sternal border and tends to increase with inspiration. An early diastolic murmur would suggest aortic regurgitation, either from aortic valve or aortic root pathology. Aortic regurgitation would contribute to a sustained apical impulse.

Clear lungs and the absence of tachycardia suggest that left ventricle function is not severely compromised. These findings argue against acute rupture of the sinus of Valsalva, a condition that normally causes biventricular failure. The presence of equal peripheral pulses does not exclude the diagnosis of aortic dissection, as the dissection may have occurred proximal to the origins of the right innominate and the left subclavian arteries.

Initial laboratory studies revealed a hematocrit of 34.9, a leukocyte count of 6800/mm³, and a platelet count of 195 000/mm³. The levels of serum electrolytes, serum creatinine, blood urea nitrogen, and initial cardiac enzymes were normal. The urine drug screen was negative. The electrocardiogram showed evidence of left ventricular hypertrophy (Figure 1), and portable chest radiography revealed an enlarged cardiac silhouette and a widened mediastinum (Figure 2).

Figure 1

Figure 2

The presence of a widened mediastinum is consistent with aortic dissection but may also suggest a mass, aortic aneurysm, infiltrative disease, or a collection of fluid (eg, blood). A normal level of cardiac enzymes and the absence of ischemic findings on electrocardiography make myocardial infarction less likely. Given his hemodynamic stability, he is unlikely to have suffered cardiac rupture; however, he may still have a dissection of the aorta or a rupture of the sinus of Valsalva. The slight decline in hematocrit is compatible with either a mediastinal or pericardial collection of blood.

The patient was emergently sent for computerized axial tomography of the chest, which revealed a dilated aortic root at 6 cm but no evidence of aortic dissection (Figure 3). The lung fields were normal.

Figure 3

Despite a negative test, the presence of severe acute chest pain in the presence of a widened mediastinum is still concerning for aortic dissection. If the dissection involved the aortic valve annulus, the resulting acute regurgitation can not be severe, given the absence of left ventricular heart failure. Likewise, the presence of normal lung fields suggests the patient has no acute elevation of left ventricular end diastolic pressures such as is seen in ventricle septal defect, papillary muscle dysfunction, or acute mitral valvular lesion.

Cardiology consultants were emergently consulted and performed a transesophageal echocardiogram that confirmed a dilated aortic root (6.3 cm) without evidence of dissection. The patient was noted to have moderate to severe aortic regurgitation and a dilated left ventricle with moderate hypertrophy. A trace effusion was noted, and the left ventricular ejection fraction was estimated to be 50%.

The presence of moderate to severe aortic regurgitation with a dilated aortic root suggests 3 possibilities: undiagnosed dissection of the aortic root with preexisting aortic insufficiency (eg, bicuspid aortic valve, rheumatic valve disease, previous endocarditis); infectious (eg, syphilitic) or noninfectious (eg, ankylosing spondylitis, Takayasu's arteritis) meso‐aortitis causing aortic dilatation and subsequent regurgitation; or, finally, connective tissue diseases (eg, Marfan's syndrome, Ehlers‐Danlos), which can cause premature degeneration of the aortic media. The acuity of the patient's symptoms and the lack of systemic findings make a connective tissue or inflammatory disease unlikely. The clinical index of suspicion for aortic dissection needs to remain very high, as failure to make an expedient diagnosis may lead to complications and a deleterious outcome. Aortography may help to define this lesion.

The cardiothoracic surgical team was consulted and recommended aortic root and valve replacement. The patient was observed overnight and scheduled for preoperative cardiac catheterization the following morning. Aortogram revealed moderate to severe aortic insufficiency and a small dissection flap on the lesser curvature of the aorta, above the left coronary ostia (Figure 4). Coronary angiography revealed a 50% stenosis of the ostia of the first and second diagonal arteries, with no other flow‐limiting lesions.

Figure 4

The study has clearly demonstrated that the patient suffered an acute aortic dissection without involvement of the aortic annulus. Given the absence of left ventricular failure, it appears the aortic regurgitation was chronic and secondary to a previously existing aortic aneurysm. Asymptomatic congenital defects of the meso‐aorta such as cystic medical necrosis can predispose to aortic dissection at a relatively young age. However, this patient's condition may have been aggravated by drug abuse, paroxysmal elevation of blood pressure during landscaping, or other risk factors. Surgical correction of the dissection and aortic regurgitation is necessary.

The patient underwent aortic valve replacement with a 25‐mm St. Jude mechanical valve and an ascending aortic transection repair with a 32‐mm Dacron tube graft. On postoperative day 9, the patient was discharged home in stable condition.

COMMENTARY

Ensuring both accuracy and efficiency when making a diagnosis can be difficult, particularly when patients present in an atypical fashion or when diagnostic testing yields inconclusive results. Thus, a physician must sift through each clinical clue, remembering that although certain findings are pathognomonic for a disease process, a constellation of signs and symptoms when present can be equally diagnostic.

The initial likelihood of disease (ie, pretest probability) is generated by the history and physical and laboratory examinations. If the pretest probability is high and the subsequent diagnostic test is positive, the modified likelihood of disease (post‐test probability) is nearly 100%. If, however, the pretest probability is high and the diagnostic test is negative, the likelihood of disease is less clear. In these situations, the physician can either review the initial findings that generated the pretest probability or perform an additional diagnostic test of higher sensitivity.

In this exercise, a 46‐year‐old man presented to the emergency department with severe chest pain and findings characteristic of aortic dissection. The physicians appropriately sent him for chest computerized tomography (CT) because of a high pretest likelihood of aortic dissection. Because this test did not confirm the presence of aortic dissection, the patient underwent transesophageal echocardiography (TEE), a test of equal or greater sensitivity.1, 2 This test was also negative; however, a small dissection flap was subsequently found during cardiac catheterization. In this case, a test of lower sensitivity and specificity confirmed the diagnosis of dissection,3 demonstrating the possibility that either CT or TEE can be misinterpreted. Indeed, a final review of the TEE, showed the dissection flap, albeit small, had been missed. In this case, a diagnostic error was made that delayed the diagnosis when sufficient information was available earlier. Diagnostic errors are prevalent in medical practice and are commonly the result of numerous factors, though cognitive problems appear to be the largest contributor to this process.4 In particular, faulty synthesis of information, rather than inadequate medical knowledge, is the most common cause of cognitive medical errors. The error made in this case likely falls under the subcategory of faulty test detection or perception and subsequent premature closure (failure to consider other possibilities once an initial diagnosis of uncomplicated aortic aneurysm had been reached).4

Though medical errors cannot be completely eliminated, cases such as this should be reviewed to understand the cognitive processes that may lead to an erroneous diagnosis. In addition to the false‐negative TEE finding, this patient also had a coexisting condition that may have preoccupied the medical team. The thoracic aortic aneurysm seen by all imaging modalities was large and required intervention regardless of the presence of a dissection. However, this chronic condition became the focus of treatment, and the acute event that precipitated admission was missed. Perhaps if the primary team maintained a very high index of suspicion for dissection and conveyed this to the cardiology consultants, a meticulous review of the TEE would have then followed that may have uncovered the subtle findings of the dissection flap.

Fortunately, definitive treatment with surgical aortic root and valve replacement was performed in a timely manner, as the consequences of a delayed diagnosis in this situation could have been catastrophic. The mortality rate of a type A dissection is extremely high initially (1%‐2% per hour),5, 6 and thus surgical intervention is typically performed immediately after the diagnosis and the extent of this disease is established, rather than the following morning.7

This case highlights not only the problems resulting in diagnostic errors but also exemplifies the thought process required to make a challenging diagnosis. Our case discussant was able to avoid cognitive pitfalls by presenting a broad differential diagnosis and reevaluating the diagnosis with each additional piece of information provided.8 An experienced clinician should realize that patients with an extremely high pretest probability of disease and a negative diagnostic test should be further investigated, regardless of the test sensitivity. Furthermore, time‐honored methods such as history taking, physical examination. and thoughtful analyses should remain critical tools in the process of reaching an accurate diagnosis despite technological advances in diagnostic testing.

A 46‐year‐old African American man presented to the emergency department with severe chest pain that awakened him from sleep. The pain was substernal, radiated to the neck and back, and was continuous, lasting approximately 1 hour. It was associated with nausea, diaphoresis, and dizziness. The patient denied dyspnea, orthopnea, paroxysmal nocturnal dyspnea, dysphagia, odynophagia, vomiting, fever, chills, or headache. He denied recent recreational drug use. He works as a landscaper.

Substernal chest pain radiating to the neck and back implicates structures in the middle mediastinum, chiefly the heart, aorta, esophagus, pulmonary arteries, and mediastinal pleura. The presence of nausea and diaphoresis suggests a vagal response to pain.

The sudden onset of symptoms and the lack of fevers and chills make infectious causes in the mediastinum such as mediastinitis and pneumonia less likely. Acute pulmonary embolism often presents with pleuritic pain and dyspnea, features not present in this patient.

The absence of odynophagia and dysphagia makes esophageal rupture or perforation of esophageal diverticula unlikely. Likewise, the absence of dyspnea, orthopnea, and paroxysmal nocturnal dyspnea makes it unlikely to be acute left ventricular failure from a sudden rise in left atrial pressure. Such a scenario may occur in the setting of a myocardial infarction or rupture of a papillary muscle, chordae tendineae, or sinus of Valsalva.

Dissection of the aorta with or without involvement of the aortic root merits strong consideration. Dissection involving the carotid or vertebral arteries could explain the patient's dizziness. Physical stresses in a landscaper may contribute to elevation in blood pressure and set the stage for an aortic dissection, especially with other risk factors.

The patient has a history of a positive PPD and was treated with isoniazid for 6 months. His mother had a history of hypertension and died from a myocardial infarction at age 64. His father's medical history is unknown. He has a history of alcohol abuse but has been abstinent for more than a year. He smoked marijuana and tobacco occasionally, with a 15 pack‐year cigarette history. He also stated that the last time he used cocaine was 1 year prior to admission.

That his mother succumbed to a myocardial infarction as well as having been hypertensive could be important family history risk factors given the patient's symptoms. Furthermore, the concurrent use of alcohol and tobacco by the patient increases his risk of developing severe hypertension. The use of cocaine is associated with sudden elevations in systemic blood pressure, which predispose to intimal damage in the aorta, especially if other risk factors are present. Marijuana smoking has been implicated in pulmonary aspergillosis, but this sudden presentation in the absence of pulmonary symptoms makes it most unlikely. Optimal therapy of a positive PPD should not predispose the patient to acute exudative pericarditis. Thus far the features suggest an acute vascular episode without significant compromise of cardiac output.

The patient was alert and in mild distress from chest discomfort. He was afebrile, with a blood pressure of 136/64 in the right arm and 139/63 in the left arm. Heart rate was 60 beats per minute, and the respiratory rate was 12 beats per minute, with an oxygen saturation of 99% while breathing room air. Examination of the head and neck revealed no signs of trauma. Jugular venous waveforms were normal, and carotid artery pulsations had normal strength and upstroke without audible bruits. The lungs were clear to auscultation. Heart sounds were notable for a 3/6 diastolic murmur heard best at the right sternal border. Rate and rhythm were regular, and the apical impulse was sustained but not displaced. The peripheral pulses were present and equal in quality throughout. The findings of the abdominal exam were normal, and the digital rectal examination was negative for occult blood. The findings of the neurologic, musculoskeletal, and dermatologic exams also were normal.

A slightly elevated pulse pressure without a significant difference in upper extremity blood pressure could be a result of aortic regurgitation, sinus of Valsalva rupture, or a high‐cardiac‐output state, as seen in thyrotoxicosis, anemia, or arteriovenous fistula.

The presence of a 3/6 diastolic murmur at the sternal border, however, favors conditions that cause aortic valve regurgitation and, less commonly, pulmonary valve regurgitation, or turbulent flow across the tricuspid valve. The murmur of pulmonary and aortic valve regurgitation can be difficult to distinguish by auscultation; however, the absence of other findings such as a right ventricular heave, elevated jugular venous pressure, or primary lung disease do not support a pulmonary valve etiology. Turbulent flow across the tricuspid valve can be seen in high‐output states, large atrial septal defects, and tricuspid stenosis. This type of murmur is heard best at the lower sternal border and tends to increase with inspiration. An early diastolic murmur would suggest aortic regurgitation, either from aortic valve or aortic root pathology. Aortic regurgitation would contribute to a sustained apical impulse.

Clear lungs and the absence of tachycardia suggest that left ventricle function is not severely compromised. These findings argue against acute rupture of the sinus of Valsalva, a condition that normally causes biventricular failure. The presence of equal peripheral pulses does not exclude the diagnosis of aortic dissection, as the dissection may have occurred proximal to the origins of the right innominate and the left subclavian arteries.

Initial laboratory studies revealed a hematocrit of 34.9, a leukocyte count of 6800/mm³, and a platelet count of 195 000/mm³. The levels of serum electrolytes, serum creatinine, blood urea nitrogen, and initial cardiac enzymes were normal. The urine drug screen was negative. The electrocardiogram showed evidence of left ventricular hypertrophy (Figure 1), and portable chest radiography revealed an enlarged cardiac silhouette and a widened mediastinum (Figure 2).

Figure 1

Figure 2

The presence of a widened mediastinum is consistent with aortic dissection but may also suggest a mass, aortic aneurysm, infiltrative disease, or a collection of fluid (eg, blood). A normal level of cardiac enzymes and the absence of ischemic findings on electrocardiography make myocardial infarction less likely. Given his hemodynamic stability, he is unlikely to have suffered cardiac rupture; however, he may still have a dissection of the aorta or a rupture of the sinus of Valsalva. The slight decline in hematocrit is compatible with either a mediastinal or pericardial collection of blood.

The patient was emergently sent for computerized axial tomography of the chest, which revealed a dilated aortic root at 6 cm but no evidence of aortic dissection (Figure 3). The lung fields were normal.

Figure 3

Despite a negative test, the presence of severe acute chest pain in the presence of a widened mediastinum is still concerning for aortic dissection. If the dissection involved the aortic valve annulus, the resulting acute regurgitation can not be severe, given the absence of left ventricular heart failure. Likewise, the presence of normal lung fields suggests the patient has no acute elevation of left ventricular end diastolic pressures such as is seen in ventricle septal defect, papillary muscle dysfunction, or acute mitral valvular lesion.

Cardiology consultants were emergently consulted and performed a transesophageal echocardiogram that confirmed a dilated aortic root (6.3 cm) without evidence of dissection. The patient was noted to have moderate to severe aortic regurgitation and a dilated left ventricle with moderate hypertrophy. A trace effusion was noted, and the left ventricular ejection fraction was estimated to be 50%.

The presence of moderate to severe aortic regurgitation with a dilated aortic root suggests 3 possibilities: undiagnosed dissection of the aortic root with preexisting aortic insufficiency (eg, bicuspid aortic valve, rheumatic valve disease, previous endocarditis); infectious (eg, syphilitic) or noninfectious (eg, ankylosing spondylitis, Takayasu's arteritis) meso‐aortitis causing aortic dilatation and subsequent regurgitation; or, finally, connective tissue diseases (eg, Marfan's syndrome, Ehlers‐Danlos), which can cause premature degeneration of the aortic media. The acuity of the patient's symptoms and the lack of systemic findings make a connective tissue or inflammatory disease unlikely. The clinical index of suspicion for aortic dissection needs to remain very high, as failure to make an expedient diagnosis may lead to complications and a deleterious outcome. Aortography may help to define this lesion.

The cardiothoracic surgical team was consulted and recommended aortic root and valve replacement. The patient was observed overnight and scheduled for preoperative cardiac catheterization the following morning. Aortogram revealed moderate to severe aortic insufficiency and a small dissection flap on the lesser curvature of the aorta, above the left coronary ostia (Figure 4). Coronary angiography revealed a 50% stenosis of the ostia of the first and second diagonal arteries, with no other flow‐limiting lesions.

Figure 4

The study has clearly demonstrated that the patient suffered an acute aortic dissection without involvement of the aortic annulus. Given the absence of left ventricular failure, it appears the aortic regurgitation was chronic and secondary to a previously existing aortic aneurysm. Asymptomatic congenital defects of the meso‐aorta such as cystic medical necrosis can predispose to aortic dissection at a relatively young age. However, this patient's condition may have been aggravated by drug abuse, paroxysmal elevation of blood pressure during landscaping, or other risk factors. Surgical correction of the dissection and aortic regurgitation is necessary.

The patient underwent aortic valve replacement with a 25‐mm St. Jude mechanical valve and an ascending aortic transection repair with a 32‐mm Dacron tube graft. On postoperative day 9, the patient was discharged home in stable condition.

COMMENTARY

Ensuring both accuracy and efficiency when making a diagnosis can be difficult, particularly when patients present in an atypical fashion or when diagnostic testing yields inconclusive results. Thus, a physician must sift through each clinical clue, remembering that although certain findings are pathognomonic for a disease process, a constellation of signs and symptoms when present can be equally diagnostic.

The initial likelihood of disease (ie, pretest probability) is generated by the history and physical and laboratory examinations. If the pretest probability is high and the subsequent diagnostic test is positive, the modified likelihood of disease (post‐test probability) is nearly 100%. If, however, the pretest probability is high and the diagnostic test is negative, the likelihood of disease is less clear. In these situations, the physician can either review the initial findings that generated the pretest probability or perform an additional diagnostic test of higher sensitivity.

In this exercise, a 46‐year‐old man presented to the emergency department with severe chest pain and findings characteristic of aortic dissection. The physicians appropriately sent him for chest computerized tomography (CT) because of a high pretest likelihood of aortic dissection. Because this test did not confirm the presence of aortic dissection, the patient underwent transesophageal echocardiography (TEE), a test of equal or greater sensitivity.1, 2 This test was also negative; however, a small dissection flap was subsequently found during cardiac catheterization. In this case, a test of lower sensitivity and specificity confirmed the diagnosis of dissection,3 demonstrating the possibility that either CT or TEE can be misinterpreted. Indeed, a final review of the TEE, showed the dissection flap, albeit small, had been missed. In this case, a diagnostic error was made that delayed the diagnosis when sufficient information was available earlier. Diagnostic errors are prevalent in medical practice and are commonly the result of numerous factors, though cognitive problems appear to be the largest contributor to this process.4 In particular, faulty synthesis of information, rather than inadequate medical knowledge, is the most common cause of cognitive medical errors. The error made in this case likely falls under the subcategory of faulty test detection or perception and subsequent premature closure (failure to consider other possibilities once an initial diagnosis of uncomplicated aortic aneurysm had been reached).4

Though medical errors cannot be completely eliminated, cases such as this should be reviewed to understand the cognitive processes that may lead to an erroneous diagnosis. In addition to the false‐negative TEE finding, this patient also had a coexisting condition that may have preoccupied the medical team. The thoracic aortic aneurysm seen by all imaging modalities was large and required intervention regardless of the presence of a dissection. However, this chronic condition became the focus of treatment, and the acute event that precipitated admission was missed. Perhaps if the primary team maintained a very high index of suspicion for dissection and conveyed this to the cardiology consultants, a meticulous review of the TEE would have then followed that may have uncovered the subtle findings of the dissection flap.

Fortunately, definitive treatment with surgical aortic root and valve replacement was performed in a timely manner, as the consequences of a delayed diagnosis in this situation could have been catastrophic. The mortality rate of a type A dissection is extremely high initially (1%‐2% per hour),5, 6 and thus surgical intervention is typically performed immediately after the diagnosis and the extent of this disease is established, rather than the following morning.7

This case highlights not only the problems resulting in diagnostic errors but also exemplifies the thought process required to make a challenging diagnosis. Our case discussant was able to avoid cognitive pitfalls by presenting a broad differential diagnosis and reevaluating the diagnosis with each additional piece of information provided.8 An experienced clinician should realize that patients with an extremely high pretest probability of disease and a negative diagnostic test should be further investigated, regardless of the test sensitivity. Furthermore, time‐honored methods such as history taking, physical examination. and thoughtful analyses should remain critical tools in the process of reaching an accurate diagnosis despite technological advances in diagnostic testing.

A 46‐year‐old African American man presented to the emergency department with severe chest pain that awakened him from sleep. The pain was substernal, radiated to the neck and back, and was continuous, lasting approximately 1 hour. It was associated with nausea, diaphoresis, and dizziness. The patient denied dyspnea, orthopnea, paroxysmal nocturnal dyspnea, dysphagia, odynophagia, vomiting, fever, chills, or headache. He denied recent recreational drug use. He works as a landscaper.

Substernal chest pain radiating to the neck and back implicates structures in the middle mediastinum, chiefly the heart, aorta, esophagus, pulmonary arteries, and mediastinal pleura. The presence of nausea and diaphoresis suggests a vagal response to pain.

The sudden onset of symptoms and the lack of fevers and chills make infectious causes in the mediastinum such as mediastinitis and pneumonia less likely. Acute pulmonary embolism often presents with pleuritic pain and dyspnea, features not present in this patient.

The absence of odynophagia and dysphagia makes esophageal rupture or perforation of esophageal diverticula unlikely. Likewise, the absence of dyspnea, orthopnea, and paroxysmal nocturnal dyspnea makes it unlikely to be acute left ventricular failure from a sudden rise in left atrial pressure. Such a scenario may occur in the setting of a myocardial infarction or rupture of a papillary muscle, chordae tendineae, or sinus of Valsalva.

Dissection of the aorta with or without involvement of the aortic root merits strong consideration. Dissection involving the carotid or vertebral arteries could explain the patient's dizziness. Physical stresses in a landscaper may contribute to elevation in blood pressure and set the stage for an aortic dissection, especially with other risk factors.

The patient has a history of a positive PPD and was treated with isoniazid for 6 months. His mother had a history of hypertension and died from a myocardial infarction at age 64. His father's medical history is unknown. He has a history of alcohol abuse but has been abstinent for more than a year. He smoked marijuana and tobacco occasionally, with a 15 pack‐year cigarette history. He also stated that the last time he used cocaine was 1 year prior to admission.

That his mother succumbed to a myocardial infarction as well as having been hypertensive could be important family history risk factors given the patient's symptoms. Furthermore, the concurrent use of alcohol and tobacco by the patient increases his risk of developing severe hypertension. The use of cocaine is associated with sudden elevations in systemic blood pressure, which predispose to intimal damage in the aorta, especially if other risk factors are present. Marijuana smoking has been implicated in pulmonary aspergillosis, but this sudden presentation in the absence of pulmonary symptoms makes it most unlikely. Optimal therapy of a positive PPD should not predispose the patient to acute exudative pericarditis. Thus far the features suggest an acute vascular episode without significant compromise of cardiac output.

The patient was alert and in mild distress from chest discomfort. He was afebrile, with a blood pressure of 136/64 in the right arm and 139/63 in the left arm. Heart rate was 60 beats per minute, and the respiratory rate was 12 beats per minute, with an oxygen saturation of 99% while breathing room air. Examination of the head and neck revealed no signs of trauma. Jugular venous waveforms were normal, and carotid artery pulsations had normal strength and upstroke without audible bruits. The lungs were clear to auscultation. Heart sounds were notable for a 3/6 diastolic murmur heard best at the right sternal border. Rate and rhythm were regular, and the apical impulse was sustained but not displaced. The peripheral pulses were present and equal in quality throughout. The findings of the abdominal exam were normal, and the digital rectal examination was negative for occult blood. The findings of the neurologic, musculoskeletal, and dermatologic exams also were normal.

A slightly elevated pulse pressure without a significant difference in upper extremity blood pressure could be a result of aortic regurgitation, sinus of Valsalva rupture, or a high‐cardiac‐output state, as seen in thyrotoxicosis, anemia, or arteriovenous fistula.

The presence of a 3/6 diastolic murmur at the sternal border, however, favors conditions that cause aortic valve regurgitation and, less commonly, pulmonary valve regurgitation, or turbulent flow across the tricuspid valve. The murmur of pulmonary and aortic valve regurgitation can be difficult to distinguish by auscultation; however, the absence of other findings such as a right ventricular heave, elevated jugular venous pressure, or primary lung disease do not support a pulmonary valve etiology. Turbulent flow across the tricuspid valve can be seen in high‐output states, large atrial septal defects, and tricuspid stenosis. This type of murmur is heard best at the lower sternal border and tends to increase with inspiration. An early diastolic murmur would suggest aortic regurgitation, either from aortic valve or aortic root pathology. Aortic regurgitation would contribute to a sustained apical impulse.

Clear lungs and the absence of tachycardia suggest that left ventricle function is not severely compromised. These findings argue against acute rupture of the sinus of Valsalva, a condition that normally causes biventricular failure. The presence of equal peripheral pulses does not exclude the diagnosis of aortic dissection, as the dissection may have occurred proximal to the origins of the right innominate and the left subclavian arteries.

Initial laboratory studies revealed a hematocrit of 34.9, a leukocyte count of 6800/mm³, and a platelet count of 195 000/mm³. The levels of serum electrolytes, serum creatinine, blood urea nitrogen, and initial cardiac enzymes were normal. The urine drug screen was negative. The electrocardiogram showed evidence of left ventricular hypertrophy (Figure 1), and portable chest radiography revealed an enlarged cardiac silhouette and a widened mediastinum (Figure 2).

Figure 1

Figure 2

The presence of a widened mediastinum is consistent with aortic dissection but may also suggest a mass, aortic aneurysm, infiltrative disease, or a collection of fluid (eg, blood). A normal level of cardiac enzymes and the absence of ischemic findings on electrocardiography make myocardial infarction less likely. Given his hemodynamic stability, he is unlikely to have suffered cardiac rupture; however, he may still have a dissection of the aorta or a rupture of the sinus of Valsalva. The slight decline in hematocrit is compatible with either a mediastinal or pericardial collection of blood.

The patient was emergently sent for computerized axial tomography of the chest, which revealed a dilated aortic root at 6 cm but no evidence of aortic dissection (Figure 3). The lung fields were normal.

Figure 3

Despite a negative test, the presence of severe acute chest pain in the presence of a widened mediastinum is still concerning for aortic dissection. If the dissection involved the aortic valve annulus, the resulting acute regurgitation can not be severe, given the absence of left ventricular heart failure. Likewise, the presence of normal lung fields suggests the patient has no acute elevation of left ventricular end diastolic pressures such as is seen in ventricle septal defect, papillary muscle dysfunction, or acute mitral valvular lesion.

Cardiology consultants were emergently consulted and performed a transesophageal echocardiogram that confirmed a dilated aortic root (6.3 cm) without evidence of dissection. The patient was noted to have moderate to severe aortic regurgitation and a dilated left ventricle with moderate hypertrophy. A trace effusion was noted, and the left ventricular ejection fraction was estimated to be 50%.

The presence of moderate to severe aortic regurgitation with a dilated aortic root suggests 3 possibilities: undiagnosed dissection of the aortic root with preexisting aortic insufficiency (eg, bicuspid aortic valve, rheumatic valve disease, previous endocarditis); infectious (eg, syphilitic) or noninfectious (eg, ankylosing spondylitis, Takayasu's arteritis) meso‐aortitis causing aortic dilatation and subsequent regurgitation; or, finally, connective tissue diseases (eg, Marfan's syndrome, Ehlers‐Danlos), which can cause premature degeneration of the aortic media. The acuity of the patient's symptoms and the lack of systemic findings make a connective tissue or inflammatory disease unlikely. The clinical index of suspicion for aortic dissection needs to remain very high, as failure to make an expedient diagnosis may lead to complications and a deleterious outcome. Aortography may help to define this lesion.

The cardiothoracic surgical team was consulted and recommended aortic root and valve replacement. The patient was observed overnight and scheduled for preoperative cardiac catheterization the following morning. Aortogram revealed moderate to severe aortic insufficiency and a small dissection flap on the lesser curvature of the aorta, above the left coronary ostia (Figure 4). Coronary angiography revealed a 50% stenosis of the ostia of the first and second diagonal arteries, with no other flow‐limiting lesions.

Figure 4

The study has clearly demonstrated that the patient suffered an acute aortic dissection without involvement of the aortic annulus. Given the absence of left ventricular failure, it appears the aortic regurgitation was chronic and secondary to a previously existing aortic aneurysm. Asymptomatic congenital defects of the meso‐aorta such as cystic medical necrosis can predispose to aortic dissection at a relatively young age. However, this patient's condition may have been aggravated by drug abuse, paroxysmal elevation of blood pressure during landscaping, or other risk factors. Surgical correction of the dissection and aortic regurgitation is necessary.

The patient underwent aortic valve replacement with a 25‐mm St. Jude mechanical valve and an ascending aortic transection repair with a 32‐mm Dacron tube graft. On postoperative day 9, the patient was discharged home in stable condition.

COMMENTARY

Ensuring both accuracy and efficiency when making a diagnosis can be difficult, particularly when patients present in an atypical fashion or when diagnostic testing yields inconclusive results. Thus, a physician must sift through each clinical clue, remembering that although certain findings are pathognomonic for a disease process, a constellation of signs and symptoms when present can be equally diagnostic.

The initial likelihood of disease (ie, pretest probability) is generated by the history and physical and laboratory examinations. If the pretest probability is high and the subsequent diagnostic test is positive, the modified likelihood of disease (post‐test probability) is nearly 100%. If, however, the pretest probability is high and the diagnostic test is negative, the likelihood of disease is less clear. In these situations, the physician can either review the initial findings that generated the pretest probability or perform an additional diagnostic test of higher sensitivity.

In this exercise, a 46‐year‐old man presented to the emergency department with severe chest pain and findings characteristic of aortic dissection. The physicians appropriately sent him for chest computerized tomography (CT) because of a high pretest likelihood of aortic dissection. Because this test did not confirm the presence of aortic dissection, the patient underwent transesophageal echocardiography (TEE), a test of equal or greater sensitivity.1, 2 This test was also negative; however, a small dissection flap was subsequently found during cardiac catheterization. In this case, a test of lower sensitivity and specificity confirmed the diagnosis of dissection,3 demonstrating the possibility that either CT or TEE can be misinterpreted. Indeed, a final review of the TEE, showed the dissection flap, albeit small, had been missed. In this case, a diagnostic error was made that delayed the diagnosis when sufficient information was available earlier. Diagnostic errors are prevalent in medical practice and are commonly the result of numerous factors, though cognitive problems appear to be the largest contributor to this process.4 In particular, faulty synthesis of information, rather than inadequate medical knowledge, is the most common cause of cognitive medical errors. The error made in this case likely falls under the subcategory of faulty test detection or perception and subsequent premature closure (failure to consider other possibilities once an initial diagnosis of uncomplicated aortic aneurysm had been reached).4

Though medical errors cannot be completely eliminated, cases such as this should be reviewed to understand the cognitive processes that may lead to an erroneous diagnosis. In addition to the false‐negative TEE finding, this patient also had a coexisting condition that may have preoccupied the medical team. The thoracic aortic aneurysm seen by all imaging modalities was large and required intervention regardless of the presence of a dissection. However, this chronic condition became the focus of treatment, and the acute event that precipitated admission was missed. Perhaps if the primary team maintained a very high index of suspicion for dissection and conveyed this to the cardiology consultants, a meticulous review of the TEE would have then followed that may have uncovered the subtle findings of the dissection flap.

Fortunately, definitive treatment with surgical aortic root and valve replacement was performed in a timely manner, as the consequences of a delayed diagnosis in this situation could have been catastrophic. The mortality rate of a type A dissection is extremely high initially (1%‐2% per hour),5, 6 and thus surgical intervention is typically performed immediately after the diagnosis and the extent of this disease is established, rather than the following morning.7

This case highlights not only the problems resulting in diagnostic errors but also exemplifies the thought process required to make a challenging diagnosis. Our case discussant was able to avoid cognitive pitfalls by presenting a broad differential diagnosis and reevaluating the diagnosis with each additional piece of information provided.8 An experienced clinician should realize that patients with an extremely high pretest probability of disease and a negative diagnostic test should be further investigated, regardless of the test sensitivity. Furthermore, time‐honored methods such as history taking, physical examination. and thoughtful analyses should remain critical tools in the process of reaching an accurate diagnosis despite technological advances in diagnostic testing.

Background

Influenza viruses are among the most common respiratory viral infections in humans. There are two major types of human influenza viruses, A and B, with influenza A strains responsible for seasonal or pandemic influenza. Influenza illness is characterized by fever, lower respiratory and often upper respiratory symptoms, myalgia, and malaise and occurs seasonally in temperate climates between late fall and early spring. The average flu season in the United States is marked by 30,000‐40,000 deaths, primarily in elderly patients with significant comorbidity and in the very young. Many of these deaths are caused by secondary bacterial pneumonias. Long interpandemic periods, including the current one of almost 40 years, involve minor mutations of the predominant influenza strain from year to year. Typically, adequate time exists to predict the prevailing strain with reasonable accuracy and to tailor a vaccine accordingly. Periodically an influenza pandemic involving a novel influenza strain emerges, attended by greater‐than‐expected morbidity and mortality.

All influenza viruses are subtyped on the basis of two surface glycoproteins. One of these, hemagglutinin (H), is responsible for viral cell entry; whereas the other, neuraminidase (N), facilitates release of the virus from infected cells, thus allowing perpetuation and amplification of infection. Antigenic drift is the ongoing process of genetic mutations that lead to new strains demonstrating variable change in antigenicity and is the basis for the annual updating of vaccine strains. Antigenic shift is the emergence of a novel influenza A subtype among humans, usually as the result of a recombination event. This radical change is necessary but not sufficient to initiate pandemic influenza, with efficient transmission from person to person also a critical feature. Pandemic influenza strains arise in 1 of 2 fashions. Genetic reassortment may occur when a mammalian host (human or porcine) is infected with both an avian and a human influenza virus, with subsequent dramatic movement into human populations, the source of the 1957 and 1968 pandemics. Alternatively, a novel virus may, after sufficient mutation, move directly from the avian population to humans, as appears to have occurred in 1918.

The 1918‐19 Pandemic

Abruptly in 1918, an influenza pandemic of seemingly unprecedented severity swept the world. Although disagreement remains regarding the source of the outbreak (China, the front lines of World War I, and even the United States have all been suggested), within 6‐9 months essentially the entire globe had been affected. Unlike more typical influenza seasons, the virus preferentially infected previously healthy young individuals, with those aged 15‐40 bearing the brunt of the illness. US military training installations, overcrowded with troops staging for service on the European front, played a particularly ill‐fated role in the pandemic as it swept through the United States.

Estimates of the pandemic's worldwide impact on mortality are sketchy at best, but many authorities believe that at least 50 million deaths resulted, with some suggesting a figure as high as 100 million. In the United States the virus was responsible for an estimated 700,000 deaths, with an untold burden of morbidity. Economic and social disruption was the norm in many areas, with widespread closure of businesses and schools and suspension of public gatherings of any kind. Many communities were simply overwhelmed by the sheer numbers of dying individuals. In Philadelphia, steam shovels were used to dig mass graves for influenza victims.1 The pandemic's effect on the health care system was likewise profound. Most hospitals counted their own physicians and nurses among those who died during the pandemic, and many of the health care workers who succumbed were infected in the course of caring for influenza patients. Overall, an estimated 2%‐3% of those infected with the virus died, a far higher percentage than is seen during interpandemic seasons. Strikingly, the vast majority of deaths do not appear to have resulted from secondary bacterial pneumonias, but rather to have been directly virally mediated through ARDS, a necrotizing viral pneumonia, or both.

The mystery of the 1918 pandemic has recently been partially unlocked, with the successful sequencing of the entire RNA genome of strains recovered from pathology tissue of two soldiers, as well as from lung tissue of a victim frozen in Alaskan permafrost since 1918.2, 3 The data suggest that the 1918 virus was derived from an avian source. Notably, some of the same changes in the polymerase proteins have been found in the highly pathogenic H5N1 viruses.

Avian Influenza Viruses

Influenza viruses that primarily infect birds are characterized as avian influenza viruses. These are always type A and are classified as either of low or high pathogenicity on the basis of the severity of the illness they cause in birds. The currently circulating H5N1 avian viruses are highly pathogenic.

Avian influenza viruses do not usually infect humans; however, several instances of human infections have been reported since 1997. The 1997 Hong Kong outbreak of avian (H5N1) influenza in 18 humans resulted in 6 deaths and was a seminal event that provided evidence that avian influenza viruses can infect people. It also provided the epidemiologic link between avian influenza infection in poultry with disease in humans and was proclaimed as a pandemic warning. These sentinel human infections led to the culling of the entire Hong Kong poultry population, with no subsequent human infection reported at that time. In 2003, more than 80 cases of avian influenza A (H7N7) illness occurred in the Netherlands among persons who handled infected poultry. Sustained human‐to‐human transmission did not occur in this or other outbreaks of avian influenza to date.

Since 2003, sporadic human cases of H5N1 have occurred, most recently reported from Turkey and Iraq. Human cases have also occurred in Vietnam, China, Cambodia, Thailand, and Indonesia, with a total of 173 reported cases and a case fatality rate exceeding 50% as of this writing.4 This mortality rate may be artificially inflated, as less severe cases have certainly gone unreported. All countries reporting human avian influenza diseases since 2003 have had concurrent epizoonotics in birds (both poultry and migratory birds).

Human cases of H5N1 influenza illness have been characterized by high fever and symptoms in the lower respiratory tract, as would be expected. Less predictable has been the presence of watery diarrhea in many patients and of abdominal and pleuritic pain and bleeding from the nose and gums in some. Sputum production has been variably present, and hemoptysis has been seen in some individuals. Most patients have had clinical and radiological evidence of pneumonia at the time they sought medical care, and progression to ARDS and multiorgan failure has been common. The majority of patients to date have required the initiation of mechanical ventilation early in their hospital course. Laboratory studies have typically shown lymphopenia, thrombocytopenia, and, in many cases, modestly elevated transaminase levels.5 Notably, the currently predominant strain of H5N1 (Z strain) is resistant to the M2 ion channel inhibitors amantadine and rimantadine but is susceptible to the newer class of neuraminidase inhibitors, zanamivir (Relenza) and oseltamivir (Tamiflu). Neuraminidase inhibitors and corticosteroids have been used to treat patients, although their efficacy in this setting is unclear. To date, virtually all cases appear to have been transmitted directly from poultry, although person‐to‐person transmission appears likely to have occurred in at least one family in Thailand.6 A recent study of the 14 clusters of avian influenza among humans emphasized the lack of sustained person‐to‐person transmission of H5N1 to date.7

Three factors are necessary for the emergence of a pandemic influenza strain: the ability to infect humans, a novel genetic makeup, and the ability for sustained transmission between people. A virus that in addition proves highly virulent, as did the 1918‐19 H1N1 strain, essentially creates the perfect storm. H5N1 influenza has currently fulfilled 2 of these 3 criteria. The virus is highly pathogenic, although how much of this fitness would be sacrificed with mutation to a more transmissible strain is uncertain. As many have observed, whether there will be another influenza pandemic does not seem in doubt; rather, it is when such a pandemic will occur and whether the pandemic will be caused by H5N1 or another influenza virus, that are the questions.

Potential Effects of the Next Pandemic

The global and national effects of an influenza pandemic will vary in direct proportion to the virulence of the circulating viral strain, but if such a virus is highly virulent, significant and perhaps severe economic and social disruption are likely.

The global economic impact has been estimated to be $800 billion with anticipated quarantines and interruption in global trade. On a national level, it has been estimated that in the United States a pandemic virus whose severity is comparable to that of the 1968 Hong Kong influenza pandemic would lead to approximately 200,000 deaths and 700,000 hospitalizations, of which roughly 100,000 would require treatment in intensive care unit settings. A more virulent strain, similar to that of the 1918‐19 pandemic, might easily result in 1 million deaths; with the number of patients hospitalized approaching 10 million, well over 1 million of which would require ICU‐level care. As an estimated 75% of the 105,000 ventilators in this country are in use at any given time under normal circumstances, the potential for demand to greatly outstrip supply is evident.8 Depending on the severity of a pandemic, suspension or curtailment of international trade and travel could be reasonably likely. Although the World Health Organization has recommended against closing borders or quarantining countries even in the throes of a pandemic, the prospect of this occurring does not seem implausible. In a worst‐case scenario, even the type of national and international chaos envisioned in the Dark Winter smallpox planning exercise might occur.9

Fortress America Versus Containment Strategies

Although the pandemic influenza plan calls for stockpiling antiviral drugs and increasing vaccine production capabilities, the most effective plan for pandemic preparedness may involve a surveillance and containment strategy. No country has enough medicines or vaccines to control a widespread outbreak of pandemic avian influenza. The best solution to prevention of a pandemic is stopping any virus from spreading in the first place. Increased surveillance for avian influenza among poultry and migratory birds in key Asian countries, along with provision of funds to compensate farmers for culling of potentially infected flocks, would align incentives for early detection and eradication. Containing an initial outbreak wherever it occurs is the best defense against a pandemic. Notably, China is thought to be a potential hot zone for emergence of pandemic avian influenza. China is not only the most populous nation in the world but has one quarter of the world's chickens, two thirds of the world's domesticated ducks, and 90% of the world's domesticated geese.

The challenges of biosecurity (protecting humans against animal‐borne diseases such as bird flu) in developing countries include the reality that populations living in close proximity to poultry are also the most illiterate and impoverished, with the most limited access to health care. The recent introduction of H5N1 into Europe has heightened surveillance efforts in the United States. The introduction of H5N1 into the United States may occur through movement of migratory birds and/or importation of exotic birds. The surveillance system has been expanded to include sampling for the influenza virus not only in poultry but also in bodies of water, as the virus is shed in bird feces.

Pandemic Planning

In the setting of a severe pandemic, hospitals will face an enormous burden of patients, with a huge influx of individuals requiring both intensive care unit as well as regular nursing floor care. At the local height of such a pandemic, the ability to successfully discharge every patient whose condition will permit this to the community or elsewhere will be critical, and almost certainly hospitals will need to expand to accept more patients than they are normally configured to hold. Hospitals staffs, particularly nurses and physicians, will be required to handle very large patient censuses. Among medical staffs, emergency physicians, hospitalists, critical care specialists, and infectious disease specialists will certainly be called on to play leading roles, much as they were during and in the aftermath of Hurricane Katrina recently. Despite all of the above, the ability of existing hospitals to accommodate all gravely ill patients may be outstripped, and auxiliary hospitals in schools and other public edifices may need to be established. Hospitalists are likely to be called on to play a major role in such temporary hospitals. The frustration and anguish of not being able to provide a standard level of care to patients (for example, being forced to triage which patients are most deserving of mechanical ventilation) should not be underestimated.

Although characterized by a relatively limited number of patients, the 2003 severe acute respiratory syndrome (SARS) outbreak in Toronto, Ontario, Canada, presented some of the same challenges that will be encountered in a virulent influenza pandemic. These include the need to quickly and drastically modify the usual emergency department and inpatient procedures, as hospitals initially serve to amplify the epidemic, as well as the additional stressor of health care workers becoming ill as a result of work‐related exposure. That fewer than 400 cases of SARS pushed the medical system of one of North America's largest cities nearly to its breaking point is both sobering and instructive.10, 11 Interested readers are directed to an excellent summary of lessons learned from the SARS outbreak, most of which are widely applicable to preparations for future infectious epidemics.12

Infection Control

Although the CDC and other Web sites currently recommend airborne isolation (respiratory personal protection) for avian influenza in humans, there is not strong epidemiologic evidence of transmission other than via droplets (the transmission mode of human influenza). The emergence of a limited number of cases of avian influenza in the United States would allow employment of airborne isolation measures; but in the event of a larger outbreak, the use of surgical masks and the practice of good hand hygiene would be sufficient by health care workers caring for persons with suspected or proven disease.

The CDC recently released proposed changes to help prevent disease outbreaks from contacts of those exposed to ill persons on airplanes. Proposed guidelines would require airlines to maintain computerized lists of passengers taken at point of departure in order to facilitate tracking of contacts and implementation of quarantine if necessary. These measures are part of pandemic planning and result from problems in tracking passengers on planes with SARS cases. By executive order, imposition of quarantine is limited to 9 diseases: cholera, diphtheria, smallpox, yellow fever, viral hemorrhagic fevers (eg, Ebola), plague, infectious tuberculosis, SARS and influenza caused by new strains with pandemic potential.

What Can Be Done?

Although valuable time has elapsed to prepare for the possibility of an H5N1 influenza pandemic, the US and global communities are presently taking the threat seriously and are engaging in a variety of activities to prepare for such an eventuality. Although currently available influenza vaccines do not provide any appreciable protection against H5N1, significant work is under way to develop an effective vaccine; with Chiron and sanofi pasteur preparing vaccine trials in association with the National Institute of Allergy and Infectious Diseases. Current influenza vaccine production is hampered by use of obsolete egg‐based manufacturing processes requiring 6 months, along with a limited capacity to manufacture adequate vaccine supplies even in many usual influenza seasons. The herculean task of providing hundreds of millions of doses of vaccine as soon as possible after the emergence of a pandemic strain, as daunting as it is, is further complicated by the fact that a successful H5N1 vaccine would not necessarily be effective against a strain that mutated sufficiently to move efficiently from person to person. Nonetheless, even partially solving these problems will pay dividends, whether or not H5N1 proves to be responsible for the next pandemic.

Given these difficulties with vaccine development and production, the backbone of any successful early response to a pandemic in the near future will be development of an adequate stockpile of antiviral medication, accompanied by a successful plan to distribute the drug when and where disease erupts. Despite uncertainties regarding their effectiveness as well as questions regarding optimal dose and duration in the setting of avian influenza, the neuraminidase inhibitors are the current drugs of choice. Of the 2 currently available agents, oseltamivir is the preferred drug for pandemic use, given its oral administration,. Unfortunately, the ability to manufacture the drug in sufficient quantities to stockpile has thus far proved problematic. Roche, the manufacturer of Tamiflu, has recently opened a new manufacturing plant and has stated that it can increase its current production of 55 million doses per year to 300 million doses by 2007. We do not recommend a role for personal stockpiling of neuraminidase inhibitors. Concerns include a shortage of the drug for seasonal influenza, absence of a pandemic at present, ignorance regarding the efficacy and optimal dose for H5N1, inappropriate use by individuals, and inequitable distribution. Recent case reports of oseltamivir resistance emerging during prophylaxis13 and treatment14 are of potential concern but do not alter current recommendations.

What can be done locally and specifically, and what can hospitalists do to prepare? First, although we are not sure that Dr Michael Osterholm's goal that planning for a pandemic must be on the agenda of every public health agency, school board, manufacturing plant, investment firm, mortuary, state legislature, and food distributor8 is entirely realistic, every hospital clearly needs to include pandemic influenza as a significant part of its disaster preparedness plan. Such planning will have broad overlap with planning for other potential disasters, including bioterrorist attacks, SARS outbreaks, and others. Hospitals must develop a plan for surge capacity, and such a plan should include not only coordination with other local hospitals, but also planning with local communities to identify sites where temporary flu hospitals can be established. Within hospital medicine groups, emergency staffing plans should be established before pandemic influenza (or another disaster) strikes. Such staffing plans need to include the ability to care for a much higher than normal number of patients for an extended period. Conceivably, a large number of patients will need to be manually ventilated for prolonged periods, which of course will tax the resources of any institution. Prompt discharge of all patients stable enough to leave the hospital will be critical, and given the investment of most hospital medicine groups in hospital throughput issues under normal conditions, much of the responsibility for helping to create beds during a crisis will inevitably fall on the shoulders of hospitalists.

Experiences during and shortly after Hurricane Katrina served to underscore that issues such as physical and mental fatigue, concern for the safety of family members, lack of supplies, communication difficulties, and absenteeism all add additional layers of complexity to the task of providing hospital care under extraordinary conditions such as during a natural disaster. These lessons can and should be extended to a major epidemic. This disaster also showed the importance of military involvement in the response to disasters that exceed local and state capabilities. The primary objective of the federal government in responding to disaster is to maintain security and essential services while preventing chaos. A pandemic of virulent influenza will raise the stakes still further, as physicians and nurses become casualties themselves. Despite these challenges, we are confident that the vast majority of hospitalists and other health care workers will rise to the occasion, and just as during the peri‐Katrina period, stories of selflessness and heroism will be de rigueur. Appropriate advance planning on all levels will serve to reduce the morbidity and mortality associated with the next pandemic and will help to ensure that health care workers do not sacrifice needlessly.0

Background

Influenza viruses are among the most common respiratory viral infections in humans. There are two major types of human influenza viruses, A and B, with influenza A strains responsible for seasonal or pandemic influenza. Influenza illness is characterized by fever, lower respiratory and often upper respiratory symptoms, myalgia, and malaise and occurs seasonally in temperate climates between late fall and early spring. The average flu season in the United States is marked by 30,000‐40,000 deaths, primarily in elderly patients with significant comorbidity and in the very young. Many of these deaths are caused by secondary bacterial pneumonias. Long interpandemic periods, including the current one of almost 40 years, involve minor mutations of the predominant influenza strain from year to year. Typically, adequate time exists to predict the prevailing strain with reasonable accuracy and to tailor a vaccine accordingly. Periodically an influenza pandemic involving a novel influenza strain emerges, attended by greater‐than‐expected morbidity and mortality.

All influenza viruses are subtyped on the basis of two surface glycoproteins. One of these, hemagglutinin (H), is responsible for viral cell entry; whereas the other, neuraminidase (N), facilitates release of the virus from infected cells, thus allowing perpetuation and amplification of infection. Antigenic drift is the ongoing process of genetic mutations that lead to new strains demonstrating variable change in antigenicity and is the basis for the annual updating of vaccine strains. Antigenic shift is the emergence of a novel influenza A subtype among humans, usually as the result of a recombination event. This radical change is necessary but not sufficient to initiate pandemic influenza, with efficient transmission from person to person also a critical feature. Pandemic influenza strains arise in 1 of 2 fashions. Genetic reassortment may occur when a mammalian host (human or porcine) is infected with both an avian and a human influenza virus, with subsequent dramatic movement into human populations, the source of the 1957 and 1968 pandemics. Alternatively, a novel virus may, after sufficient mutation, move directly from the avian population to humans, as appears to have occurred in 1918.

The 1918‐19 Pandemic

Abruptly in 1918, an influenza pandemic of seemingly unprecedented severity swept the world. Although disagreement remains regarding the source of the outbreak (China, the front lines of World War I, and even the United States have all been suggested), within 6‐9 months essentially the entire globe had been affected. Unlike more typical influenza seasons, the virus preferentially infected previously healthy young individuals, with those aged 15‐40 bearing the brunt of the illness. US military training installations, overcrowded with troops staging for service on the European front, played a particularly ill‐fated role in the pandemic as it swept through the United States.

Estimates of the pandemic's worldwide impact on mortality are sketchy at best, but many authorities believe that at least 50 million deaths resulted, with some suggesting a figure as high as 100 million. In the United States the virus was responsible for an estimated 700,000 deaths, with an untold burden of morbidity. Economic and social disruption was the norm in many areas, with widespread closure of businesses and schools and suspension of public gatherings of any kind. Many communities were simply overwhelmed by the sheer numbers of dying individuals. In Philadelphia, steam shovels were used to dig mass graves for influenza victims.1 The pandemic's effect on the health care system was likewise profound. Most hospitals counted their own physicians and nurses among those who died during the pandemic, and many of the health care workers who succumbed were infected in the course of caring for influenza patients. Overall, an estimated 2%‐3% of those infected with the virus died, a far higher percentage than is seen during interpandemic seasons. Strikingly, the vast majority of deaths do not appear to have resulted from secondary bacterial pneumonias, but rather to have been directly virally mediated through ARDS, a necrotizing viral pneumonia, or both.

The mystery of the 1918 pandemic has recently been partially unlocked, with the successful sequencing of the entire RNA genome of strains recovered from pathology tissue of two soldiers, as well as from lung tissue of a victim frozen in Alaskan permafrost since 1918.2, 3 The data suggest that the 1918 virus was derived from an avian source. Notably, some of the same changes in the polymerase proteins have been found in the highly pathogenic H5N1 viruses.

Avian Influenza Viruses

Influenza viruses that primarily infect birds are characterized as avian influenza viruses. These are always type A and are classified as either of low or high pathogenicity on the basis of the severity of the illness they cause in birds. The currently circulating H5N1 avian viruses are highly pathogenic.

Avian influenza viruses do not usually infect humans; however, several instances of human infections have been reported since 1997. The 1997 Hong Kong outbreak of avian (H5N1) influenza in 18 humans resulted in 6 deaths and was a seminal event that provided evidence that avian influenza viruses can infect people. It also provided the epidemiologic link between avian influenza infection in poultry with disease in humans and was proclaimed as a pandemic warning. These sentinel human infections led to the culling of the entire Hong Kong poultry population, with no subsequent human infection reported at that time. In 2003, more than 80 cases of avian influenza A (H7N7) illness occurred in the Netherlands among persons who handled infected poultry. Sustained human‐to‐human transmission did not occur in this or other outbreaks of avian influenza to date.

Since 2003, sporadic human cases of H5N1 have occurred, most recently reported from Turkey and Iraq. Human cases have also occurred in Vietnam, China, Cambodia, Thailand, and Indonesia, with a total of 173 reported cases and a case fatality rate exceeding 50% as of this writing.4 This mortality rate may be artificially inflated, as less severe cases have certainly gone unreported. All countries reporting human avian influenza diseases since 2003 have had concurrent epizoonotics in birds (both poultry and migratory birds).

Human cases of H5N1 influenza illness have been characterized by high fever and symptoms in the lower respiratory tract, as would be expected. Less predictable has been the presence of watery diarrhea in many patients and of abdominal and pleuritic pain and bleeding from the nose and gums in some. Sputum production has been variably present, and hemoptysis has been seen in some individuals. Most patients have had clinical and radiological evidence of pneumonia at the time they sought medical care, and progression to ARDS and multiorgan failure has been common. The majority of patients to date have required the initiation of mechanical ventilation early in their hospital course. Laboratory studies have typically shown lymphopenia, thrombocytopenia, and, in many cases, modestly elevated transaminase levels.5 Notably, the currently predominant strain of H5N1 (Z strain) is resistant to the M2 ion channel inhibitors amantadine and rimantadine but is susceptible to the newer class of neuraminidase inhibitors, zanamivir (Relenza) and oseltamivir (Tamiflu). Neuraminidase inhibitors and corticosteroids have been used to treat patients, although their efficacy in this setting is unclear. To date, virtually all cases appear to have been transmitted directly from poultry, although person‐to‐person transmission appears likely to have occurred in at least one family in Thailand.6 A recent study of the 14 clusters of avian influenza among humans emphasized the lack of sustained person‐to‐person transmission of H5N1 to date.7

Three factors are necessary for the emergence of a pandemic influenza strain: the ability to infect humans, a novel genetic makeup, and the ability for sustained transmission between people. A virus that in addition proves highly virulent, as did the 1918‐19 H1N1 strain, essentially creates the perfect storm. H5N1 influenza has currently fulfilled 2 of these 3 criteria. The virus is highly pathogenic, although how much of this fitness would be sacrificed with mutation to a more transmissible strain is uncertain. As many have observed, whether there will be another influenza pandemic does not seem in doubt; rather, it is when such a pandemic will occur and whether the pandemic will be caused by H5N1 or another influenza virus, that are the questions.

Potential Effects of the Next Pandemic

The global and national effects of an influenza pandemic will vary in direct proportion to the virulence of the circulating viral strain, but if such a virus is highly virulent, significant and perhaps severe economic and social disruption are likely.

The global economic impact has been estimated to be $800 billion with anticipated quarantines and interruption in global trade. On a national level, it has been estimated that in the United States a pandemic virus whose severity is comparable to that of the 1968 Hong Kong influenza pandemic would lead to approximately 200,000 deaths and 700,000 hospitalizations, of which roughly 100,000 would require treatment in intensive care unit settings. A more virulent strain, similar to that of the 1918‐19 pandemic, might easily result in 1 million deaths; with the number of patients hospitalized approaching 10 million, well over 1 million of which would require ICU‐level care. As an estimated 75% of the 105,000 ventilators in this country are in use at any given time under normal circumstances, the potential for demand to greatly outstrip supply is evident.8 Depending on the severity of a pandemic, suspension or curtailment of international trade and travel could be reasonably likely. Although the World Health Organization has recommended against closing borders or quarantining countries even in the throes of a pandemic, the prospect of this occurring does not seem implausible. In a worst‐case scenario, even the type of national and international chaos envisioned in the Dark Winter smallpox planning exercise might occur.9

Fortress America Versus Containment Strategies

Although the pandemic influenza plan calls for stockpiling antiviral drugs and increasing vaccine production capabilities, the most effective plan for pandemic preparedness may involve a surveillance and containment strategy. No country has enough medicines or vaccines to control a widespread outbreak of pandemic avian influenza. The best solution to prevention of a pandemic is stopping any virus from spreading in the first place. Increased surveillance for avian influenza among poultry and migratory birds in key Asian countries, along with provision of funds to compensate farmers for culling of potentially infected flocks, would align incentives for early detection and eradication. Containing an initial outbreak wherever it occurs is the best defense against a pandemic. Notably, China is thought to be a potential hot zone for emergence of pandemic avian influenza. China is not only the most populous nation in the world but has one quarter of the world's chickens, two thirds of the world's domesticated ducks, and 90% of the world's domesticated geese.

The challenges of biosecurity (protecting humans against animal‐borne diseases such as bird flu) in developing countries include the reality that populations living in close proximity to poultry are also the most illiterate and impoverished, with the most limited access to health care. The recent introduction of H5N1 into Europe has heightened surveillance efforts in the United States. The introduction of H5N1 into the United States may occur through movement of migratory birds and/or importation of exotic birds. The surveillance system has been expanded to include sampling for the influenza virus not only in poultry but also in bodies of water, as the virus is shed in bird feces.

Pandemic Planning

In the setting of a severe pandemic, hospitals will face an enormous burden of patients, with a huge influx of individuals requiring both intensive care unit as well as regular nursing floor care. At the local height of such a pandemic, the ability to successfully discharge every patient whose condition will permit this to the community or elsewhere will be critical, and almost certainly hospitals will need to expand to accept more patients than they are normally configured to hold. Hospitals staffs, particularly nurses and physicians, will be required to handle very large patient censuses. Among medical staffs, emergency physicians, hospitalists, critical care specialists, and infectious disease specialists will certainly be called on to play leading roles, much as they were during and in the aftermath of Hurricane Katrina recently. Despite all of the above, the ability of existing hospitals to accommodate all gravely ill patients may be outstripped, and auxiliary hospitals in schools and other public edifices may need to be established. Hospitalists are likely to be called on to play a major role in such temporary hospitals. The frustration and anguish of not being able to provide a standard level of care to patients (for example, being forced to triage which patients are most deserving of mechanical ventilation) should not be underestimated.

Although characterized by a relatively limited number of patients, the 2003 severe acute respiratory syndrome (SARS) outbreak in Toronto, Ontario, Canada, presented some of the same challenges that will be encountered in a virulent influenza pandemic. These include the need to quickly and drastically modify the usual emergency department and inpatient procedures, as hospitals initially serve to amplify the epidemic, as well as the additional stressor of health care workers becoming ill as a result of work‐related exposure. That fewer than 400 cases of SARS pushed the medical system of one of North America's largest cities nearly to its breaking point is both sobering and instructive.10, 11 Interested readers are directed to an excellent summary of lessons learned from the SARS outbreak, most of which are widely applicable to preparations for future infectious epidemics.12

Infection Control

Although the CDC and other Web sites currently recommend airborne isolation (respiratory personal protection) for avian influenza in humans, there is not strong epidemiologic evidence of transmission other than via droplets (the transmission mode of human influenza). The emergence of a limited number of cases of avian influenza in the United States would allow employment of airborne isolation measures; but in the event of a larger outbreak, the use of surgical masks and the practice of good hand hygiene would be sufficient by health care workers caring for persons with suspected or proven disease.

The CDC recently released proposed changes to help prevent disease outbreaks from contacts of those exposed to ill persons on airplanes. Proposed guidelines would require airlines to maintain computerized lists of passengers taken at point of departure in order to facilitate tracking of contacts and implementation of quarantine if necessary. These measures are part of pandemic planning and result from problems in tracking passengers on planes with SARS cases. By executive order, imposition of quarantine is limited to 9 diseases: cholera, diphtheria, smallpox, yellow fever, viral hemorrhagic fevers (eg, Ebola), plague, infectious tuberculosis, SARS and influenza caused by new strains with pandemic potential.

What Can Be Done?

Although valuable time has elapsed to prepare for the possibility of an H5N1 influenza pandemic, the US and global communities are presently taking the threat seriously and are engaging in a variety of activities to prepare for such an eventuality. Although currently available influenza vaccines do not provide any appreciable protection against H5N1, significant work is under way to develop an effective vaccine; with Chiron and sanofi pasteur preparing vaccine trials in association with the National Institute of Allergy and Infectious Diseases. Current influenza vaccine production is hampered by use of obsolete egg‐based manufacturing processes requiring 6 months, along with a limited capacity to manufacture adequate vaccine supplies even in many usual influenza seasons. The herculean task of providing hundreds of millions of doses of vaccine as soon as possible after the emergence of a pandemic strain, as daunting as it is, is further complicated by the fact that a successful H5N1 vaccine would not necessarily be effective against a strain that mutated sufficiently to move efficiently from person to person. Nonetheless, even partially solving these problems will pay dividends, whether or not H5N1 proves to be responsible for the next pandemic.

Given these difficulties with vaccine development and production, the backbone of any successful early response to a pandemic in the near future will be development of an adequate stockpile of antiviral medication, accompanied by a successful plan to distribute the drug when and where disease erupts. Despite uncertainties regarding their effectiveness as well as questions regarding optimal dose and duration in the setting of avian influenza, the neuraminidase inhibitors are the current drugs of choice. Of the 2 currently available agents, oseltamivir is the preferred drug for pandemic use, given its oral administration,. Unfortunately, the ability to manufacture the drug in sufficient quantities to stockpile has thus far proved problematic. Roche, the manufacturer of Tamiflu, has recently opened a new manufacturing plant and has stated that it can increase its current production of 55 million doses per year to 300 million doses by 2007. We do not recommend a role for personal stockpiling of neuraminidase inhibitors. Concerns include a shortage of the drug for seasonal influenza, absence of a pandemic at present, ignorance regarding the efficacy and optimal dose for H5N1, inappropriate use by individuals, and inequitable distribution. Recent case reports of oseltamivir resistance emerging during prophylaxis13 and treatment14 are of potential concern but do not alter current recommendations.

What can be done locally and specifically, and what can hospitalists do to prepare? First, although we are not sure that Dr Michael Osterholm's goal that planning for a pandemic must be on the agenda of every public health agency, school board, manufacturing plant, investment firm, mortuary, state legislature, and food distributor8 is entirely realistic, every hospital clearly needs to include pandemic influenza as a significant part of its disaster preparedness plan. Such planning will have broad overlap with planning for other potential disasters, including bioterrorist attacks, SARS outbreaks, and others. Hospitals must develop a plan for surge capacity, and such a plan should include not only coordination with other local hospitals, but also planning with local communities to identify sites where temporary flu hospitals can be established. Within hospital medicine groups, emergency staffing plans should be established before pandemic influenza (or another disaster) strikes. Such staffing plans need to include the ability to care for a much higher than normal number of patients for an extended period. Conceivably, a large number of patients will need to be manually ventilated for prolonged periods, which of course will tax the resources of any institution. Prompt discharge of all patients stable enough to leave the hospital will be critical, and given the investment of most hospital medicine groups in hospital throughput issues under normal conditions, much of the responsibility for helping to create beds during a crisis will inevitably fall on the shoulders of hospitalists.

Experiences during and shortly after Hurricane Katrina served to underscore that issues such as physical and mental fatigue, concern for the safety of family members, lack of supplies, communication difficulties, and absenteeism all add additional layers of complexity to the task of providing hospital care under extraordinary conditions such as during a natural disaster. These lessons can and should be extended to a major epidemic. This disaster also showed the importance of military involvement in the response to disasters that exceed local and state capabilities. The primary objective of the federal government in responding to disaster is to maintain security and essential services while preventing chaos. A pandemic of virulent influenza will raise the stakes still further, as physicians and nurses become casualties themselves. Despite these challenges, we are confident that the vast majority of hospitalists and other health care workers will rise to the occasion, and just as during the peri‐Katrina period, stories of selflessness and heroism will be de rigueur. Appropriate advance planning on all levels will serve to reduce the morbidity and mortality associated with the next pandemic and will help to ensure that health care workers do not sacrifice needlessly.0

Background

Influenza viruses are among the most common respiratory viral infections in humans. There are two major types of human influenza viruses, A and B, with influenza A strains responsible for seasonal or pandemic influenza. Influenza illness is characterized by fever, lower respiratory and often upper respiratory symptoms, myalgia, and malaise and occurs seasonally in temperate climates between late fall and early spring. The average flu season in the United States is marked by 30,000‐40,000 deaths, primarily in elderly patients with significant comorbidity and in the very young. Many of these deaths are caused by secondary bacterial pneumonias. Long interpandemic periods, including the current one of almost 40 years, involve minor mutations of the predominant influenza strain from year to year. Typically, adequate time exists to predict the prevailing strain with reasonable accuracy and to tailor a vaccine accordingly. Periodically an influenza pandemic involving a novel influenza strain emerges, attended by greater‐than‐expected morbidity and mortality.

All influenza viruses are subtyped on the basis of two surface glycoproteins. One of these, hemagglutinin (H), is responsible for viral cell entry; whereas the other, neuraminidase (N), facilitates release of the virus from infected cells, thus allowing perpetuation and amplification of infection. Antigenic drift is the ongoing process of genetic mutations that lead to new strains demonstrating variable change in antigenicity and is the basis for the annual updating of vaccine strains. Antigenic shift is the emergence of a novel influenza A subtype among humans, usually as the result of a recombination event. This radical change is necessary but not sufficient to initiate pandemic influenza, with efficient transmission from person to person also a critical feature. Pandemic influenza strains arise in 1 of 2 fashions. Genetic reassortment may occur when a mammalian host (human or porcine) is infected with both an avian and a human influenza virus, with subsequent dramatic movement into human populations, the source of the 1957 and 1968 pandemics. Alternatively, a novel virus may, after sufficient mutation, move directly from the avian population to humans, as appears to have occurred in 1918.

The 1918‐19 Pandemic

Abruptly in 1918, an influenza pandemic of seemingly unprecedented severity swept the world. Although disagreement remains regarding the source of the outbreak (China, the front lines of World War I, and even the United States have all been suggested), within 6‐9 months essentially the entire globe had been affected. Unlike more typical influenza seasons, the virus preferentially infected previously healthy young individuals, with those aged 15‐40 bearing the brunt of the illness. US military training installations, overcrowded with troops staging for service on the European front, played a particularly ill‐fated role in the pandemic as it swept through the United States.

Estimates of the pandemic's worldwide impact on mortality are sketchy at best, but many authorities believe that at least 50 million deaths resulted, with some suggesting a figure as high as 100 million. In the United States the virus was responsible for an estimated 700,000 deaths, with an untold burden of morbidity. Economic and social disruption was the norm in many areas, with widespread closure of businesses and schools and suspension of public gatherings of any kind. Many communities were simply overwhelmed by the sheer numbers of dying individuals. In Philadelphia, steam shovels were used to dig mass graves for influenza victims.1 The pandemic's effect on the health care system was likewise profound. Most hospitals counted their own physicians and nurses among those who died during the pandemic, and many of the health care workers who succumbed were infected in the course of caring for influenza patients. Overall, an estimated 2%‐3% of those infected with the virus died, a far higher percentage than is seen during interpandemic seasons. Strikingly, the vast majority of deaths do not appear to have resulted from secondary bacterial pneumonias, but rather to have been directly virally mediated through ARDS, a necrotizing viral pneumonia, or both.

The mystery of the 1918 pandemic has recently been partially unlocked, with the successful sequencing of the entire RNA genome of strains recovered from pathology tissue of two soldiers, as well as from lung tissue of a victim frozen in Alaskan permafrost since 1918.2, 3 The data suggest that the 1918 virus was derived from an avian source. Notably, some of the same changes in the polymerase proteins have been found in the highly pathogenic H5N1 viruses.

Avian Influenza Viruses

Influenza viruses that primarily infect birds are characterized as avian influenza viruses. These are always type A and are classified as either of low or high pathogenicity on the basis of the severity of the illness they cause in birds. The currently circulating H5N1 avian viruses are highly pathogenic.

Avian influenza viruses do not usually infect humans; however, several instances of human infections have been reported since 1997. The 1997 Hong Kong outbreak of avian (H5N1) influenza in 18 humans resulted in 6 deaths and was a seminal event that provided evidence that avian influenza viruses can infect people. It also provided the epidemiologic link between avian influenza infection in poultry with disease in humans and was proclaimed as a pandemic warning. These sentinel human infections led to the culling of the entire Hong Kong poultry population, with no subsequent human infection reported at that time. In 2003, more than 80 cases of avian influenza A (H7N7) illness occurred in the Netherlands among persons who handled infected poultry. Sustained human‐to‐human transmission did not occur in this or other outbreaks of avian influenza to date.

Since 2003, sporadic human cases of H5N1 have occurred, most recently reported from Turkey and Iraq. Human cases have also occurred in Vietnam, China, Cambodia, Thailand, and Indonesia, with a total of 173 reported cases and a case fatality rate exceeding 50% as of this writing.4 This mortality rate may be artificially inflated, as less severe cases have certainly gone unreported. All countries reporting human avian influenza diseases since 2003 have had concurrent epizoonotics in birds (both poultry and migratory birds).

Human cases of H5N1 influenza illness have been characterized by high fever and symptoms in the lower respiratory tract, as would be expected. Less predictable has been the presence of watery diarrhea in many patients and of abdominal and pleuritic pain and bleeding from the nose and gums in some. Sputum production has been variably present, and hemoptysis has been seen in some individuals. Most patients have had clinical and radiological evidence of pneumonia at the time they sought medical care, and progression to ARDS and multiorgan failure has been common. The majority of patients to date have required the initiation of mechanical ventilation early in their hospital course. Laboratory studies have typically shown lymphopenia, thrombocytopenia, and, in many cases, modestly elevated transaminase levels.5 Notably, the currently predominant strain of H5N1 (Z strain) is resistant to the M2 ion channel inhibitors amantadine and rimantadine but is susceptible to the newer class of neuraminidase inhibitors, zanamivir (Relenza) and oseltamivir (Tamiflu). Neuraminidase inhibitors and corticosteroids have been used to treat patients, although their efficacy in this setting is unclear. To date, virtually all cases appear to have been transmitted directly from poultry, although person‐to‐person transmission appears likely to have occurred in at least one family in Thailand.6 A recent study of the 14 clusters of avian influenza among humans emphasized the lack of sustained person‐to‐person transmission of H5N1 to date.7

Three factors are necessary for the emergence of a pandemic influenza strain: the ability to infect humans, a novel genetic makeup, and the ability for sustained transmission between people. A virus that in addition proves highly virulent, as did the 1918‐19 H1N1 strain, essentially creates the perfect storm. H5N1 influenza has currently fulfilled 2 of these 3 criteria. The virus is highly pathogenic, although how much of this fitness would be sacrificed with mutation to a more transmissible strain is uncertain. As many have observed, whether there will be another influenza pandemic does not seem in doubt; rather, it is when such a pandemic will occur and whether the pandemic will be caused by H5N1 or another influenza virus, that are the questions.

Potential Effects of the Next Pandemic

The global and national effects of an influenza pandemic will vary in direct proportion to the virulence of the circulating viral strain, but if such a virus is highly virulent, significant and perhaps severe economic and social disruption are likely.

The global economic impact has been estimated to be $800 billion with anticipated quarantines and interruption in global trade. On a national level, it has been estimated that in the United States a pandemic virus whose severity is comparable to that of the 1968 Hong Kong influenza pandemic would lead to approximately 200,000 deaths and 700,000 hospitalizations, of which roughly 100,000 would require treatment in intensive care unit settings. A more virulent strain, similar to that of the 1918‐19 pandemic, might easily result in 1 million deaths; with the number of patients hospitalized approaching 10 million, well over 1 million of which would require ICU‐level care. As an estimated 75% of the 105,000 ventilators in this country are in use at any given time under normal circumstances, the potential for demand to greatly outstrip supply is evident.8 Depending on the severity of a pandemic, suspension or curtailment of international trade and travel could be reasonably likely. Although the World Health Organization has recommended against closing borders or quarantining countries even in the throes of a pandemic, the prospect of this occurring does not seem implausible. In a worst‐case scenario, even the type of national and international chaos envisioned in the Dark Winter smallpox planning exercise might occur.9

Fortress America Versus Containment Strategies

Although the pandemic influenza plan calls for stockpiling antiviral drugs and increasing vaccine production capabilities, the most effective plan for pandemic preparedness may involve a surveillance and containment strategy. No country has enough medicines or vaccines to control a widespread outbreak of pandemic avian influenza. The best solution to prevention of a pandemic is stopping any virus from spreading in the first place. Increased surveillance for avian influenza among poultry and migratory birds in key Asian countries, along with provision of funds to compensate farmers for culling of potentially infected flocks, would align incentives for early detection and eradication. Containing an initial outbreak wherever it occurs is the best defense against a pandemic. Notably, China is thought to be a potential hot zone for emergence of pandemic avian influenza. China is not only the most populous nation in the world but has one quarter of the world's chickens, two thirds of the world's domesticated ducks, and 90% of the world's domesticated geese.

The challenges of biosecurity (protecting humans against animal‐borne diseases such as bird flu) in developing countries include the reality that populations living in close proximity to poultry are also the most illiterate and impoverished, with the most limited access to health care. The recent introduction of H5N1 into Europe has heightened surveillance efforts in the United States. The introduction of H5N1 into the United States may occur through movement of migratory birds and/or importation of exotic birds. The surveillance system has been expanded to include sampling for the influenza virus not only in poultry but also in bodies of water, as the virus is shed in bird feces.

Pandemic Planning

In the setting of a severe pandemic, hospitals will face an enormous burden of patients, with a huge influx of individuals requiring both intensive care unit as well as regular nursing floor care. At the local height of such a pandemic, the ability to successfully discharge every patient whose condition will permit this to the community or elsewhere will be critical, and almost certainly hospitals will need to expand to accept more patients than they are normally configured to hold. Hospitals staffs, particularly nurses and physicians, will be required to handle very large patient censuses. Among medical staffs, emergency physicians, hospitalists, critical care specialists, and infectious disease specialists will certainly be called on to play leading roles, much as they were during and in the aftermath of Hurricane Katrina recently. Despite all of the above, the ability of existing hospitals to accommodate all gravely ill patients may be outstripped, and auxiliary hospitals in schools and other public edifices may need to be established. Hospitalists are likely to be called on to play a major role in such temporary hospitals. The frustration and anguish of not being able to provide a standard level of care to patients (for example, being forced to triage which patients are most deserving of mechanical ventilation) should not be underestimated.

Although characterized by a relatively limited number of patients, the 2003 severe acute respiratory syndrome (SARS) outbreak in Toronto, Ontario, Canada, presented some of the same challenges that will be encountered in a virulent influenza pandemic. These include the need to quickly and drastically modify the usual emergency department and inpatient procedures, as hospitals initially serve to amplify the epidemic, as well as the additional stressor of health care workers becoming ill as a result of work‐related exposure. That fewer than 400 cases of SARS pushed the medical system of one of North America's largest cities nearly to its breaking point is both sobering and instructive.10, 11 Interested readers are directed to an excellent summary of lessons learned from the SARS outbreak, most of which are widely applicable to preparations for future infectious epidemics.12

Infection Control

Although the CDC and other Web sites currently recommend airborne isolation (respiratory personal protection) for avian influenza in humans, there is not strong epidemiologic evidence of transmission other than via droplets (the transmission mode of human influenza). The emergence of a limited number of cases of avian influenza in the United States would allow employment of airborne isolation measures; but in the event of a larger outbreak, the use of surgical masks and the practice of good hand hygiene would be sufficient by health care workers caring for persons with suspected or proven disease.

The CDC recently released proposed changes to help prevent disease outbreaks from contacts of those exposed to ill persons on airplanes. Proposed guidelines would require airlines to maintain computerized lists of passengers taken at point of departure in order to facilitate tracking of contacts and implementation of quarantine if necessary. These measures are part of pandemic planning and result from problems in tracking passengers on planes with SARS cases. By executive order, imposition of quarantine is limited to 9 diseases: cholera, diphtheria, smallpox, yellow fever, viral hemorrhagic fevers (eg, Ebola), plague, infectious tuberculosis, SARS and influenza caused by new strains with pandemic potential.

What Can Be Done?

Although valuable time has elapsed to prepare for the possibility of an H5N1 influenza pandemic, the US and global communities are presently taking the threat seriously and are engaging in a variety of activities to prepare for such an eventuality. Although currently available influenza vaccines do not provide any appreciable protection against H5N1, significant work is under way to develop an effective vaccine; with Chiron and sanofi pasteur preparing vaccine trials in association with the National Institute of Allergy and Infectious Diseases. Current influenza vaccine production is hampered by use of obsolete egg‐based manufacturing processes requiring 6 months, along with a limited capacity to manufacture adequate vaccine supplies even in many usual influenza seasons. The herculean task of providing hundreds of millions of doses of vaccine as soon as possible after the emergence of a pandemic strain, as daunting as it is, is further complicated by the fact that a successful H5N1 vaccine would not necessarily be effective against a strain that mutated sufficiently to move efficiently from person to person. Nonetheless, even partially solving these problems will pay dividends, whether or not H5N1 proves to be responsible for the next pandemic.

Given these difficulties with vaccine development and production, the backbone of any successful early response to a pandemic in the near future will be development of an adequate stockpile of antiviral medication, accompanied by a successful plan to distribute the drug when and where disease erupts. Despite uncertainties regarding their effectiveness as well as questions regarding optimal dose and duration in the setting of avian influenza, the neuraminidase inhibitors are the current drugs of choice. Of the 2 currently available agents, oseltamivir is the preferred drug for pandemic use, given its oral administration,. Unfortunately, the ability to manufacture the drug in sufficient quantities to stockpile has thus far proved problematic. Roche, the manufacturer of Tamiflu, has recently opened a new manufacturing plant and has stated that it can increase its current production of 55 million doses per year to 300 million doses by 2007. We do not recommend a role for personal stockpiling of neuraminidase inhibitors. Concerns include a shortage of the drug for seasonal influenza, absence of a pandemic at present, ignorance regarding the efficacy and optimal dose for H5N1, inappropriate use by individuals, and inequitable distribution. Recent case reports of oseltamivir resistance emerging during prophylaxis13 and treatment14 are of potential concern but do not alter current recommendations.

What can be done locally and specifically, and what can hospitalists do to prepare? First, although we are not sure that Dr Michael Osterholm's goal that planning for a pandemic must be on the agenda of every public health agency, school board, manufacturing plant, investment firm, mortuary, state legislature, and food distributor8 is entirely realistic, every hospital clearly needs to include pandemic influenza as a significant part of its disaster preparedness plan. Such planning will have broad overlap with planning for other potential disasters, including bioterrorist attacks, SARS outbreaks, and others. Hospitals must develop a plan for surge capacity, and such a plan should include not only coordination with other local hospitals, but also planning with local communities to identify sites where temporary flu hospitals can be established. Within hospital medicine groups, emergency staffing plans should be established before pandemic influenza (or another disaster) strikes. Such staffing plans need to include the ability to care for a much higher than normal number of patients for an extended period. Conceivably, a large number of patients will need to be manually ventilated for prolonged periods, which of course will tax the resources of any institution. Prompt discharge of all patients stable enough to leave the hospital will be critical, and given the investment of most hospital medicine groups in hospital throughput issues under normal conditions, much of the responsibility for helping to create beds during a crisis will inevitably fall on the shoulders of hospitalists.

Experiences during and shortly after Hurricane Katrina served to underscore that issues such as physical and mental fatigue, concern for the safety of family members, lack of supplies, communication difficulties, and absenteeism all add additional layers of complexity to the task of providing hospital care under extraordinary conditions such as during a natural disaster. These lessons can and should be extended to a major epidemic. This disaster also showed the importance of military involvement in the response to disasters that exceed local and state capabilities. The primary objective of the federal government in responding to disaster is to maintain security and essential services while preventing chaos. A pandemic of virulent influenza will raise the stakes still further, as physicians and nurses become casualties themselves. Despite these challenges, we are confident that the vast majority of hospitalists and other health care workers will rise to the occasion, and just as during the peri‐Katrina period, stories of selflessness and heroism will be de rigueur. Appropriate advance planning on all levels will serve to reduce the morbidity and mortality associated with the next pandemic and will help to ensure that health care workers do not sacrifice needlessly.0

She is not, however, without a certain, well, grim sense of humor.

The voice throws you at first. It's deceptively mild and calm, more Gwyneth Paltrow than James Earl Jones. To the best of my knowledge, however, Gwyneth Paltrow has never shown up in a patient's room wearing a hooded black robe and sporting a scythe.

Hmm, bad case of sepsis, huh? she asked.

I was still cleaning up from the central line, so I tried to get rid of her gracefully. Now's not really a good time. That line always seems to work with pesky administrators.

Death, however, would not be dissuaded. HIV positive for nearly 10 years now, flirting with CD4 counts in double digits, rising viral load the past 3 years. Picked a bad time to have her gallbladder go bad on her, didn't she?

Or a bad time to pick a surgeon who was less than fastidious about his sterile fields, I muttered.

Death, however, chose to ignore me. Ventilator, pressors, antibiotics. She reached for the girl's right hand, attached as it was to an arterial line blood pressure monitor, and somethingdamn, if it didn't look like a scarabfell out of the robe and then scrambled across my patient's chest, right next to my newly placed and oh‐so‐deftly sutured plastic catheter, ducking away from the light.

Hey, that was my sterile field, I complained. I, unlike the aforementioned surgeon, had been fastidious about it. I hoped the scarab was sterile, at least.

Splinter hemorrhages, Death noted with obvious glee, taking particular interest in the little streaks of blood under my patient's fingernails. Septic emboli. Death seems to have Gwnyeth Paltrow's laugh along with her voice. It's a light and airy thing, almost like a favorite wind chime. That laugh could almost make you think Death had a heart. Endocarditis, she said fondly. One of my favorites.

Almost make you think she had a heart.

Go away. I tried to look more busy than worried, but I didn't think she was buying it.

It's been a good month for me here in the ICU. Heck, you yourself have 4 kills. Why don't you throw in this one and call yourself an ace?

Very funny. Now get out. I would imagine it's best not to lose your temper with Death. Or with any of the other three Horsemen of the Apocalypse, for that matter. Didn't anyone ever tell you it's poor form to make fun of your host? You're in Donna Smith's house now, buddy. Don't be dissin' my nurse manager.

Come on, she pushed. She's pathetic, she's tired, she lives alone in a tiny room in a forgotten crack house that she pretends is her apartment, and her parents haven't taken her calls for years.

Donna? I asked. That was some serious disrespect.

Don't go all medical student on me. I was talking about your patient, she explained evenly. She'd be better off with me anyway. You know that.

She can be persuasive when she might be right. Death and I have been having similar conversations all the way back to my surgical rotation as a third‐year medical student. Although she has never been above making the easy score, she typically only makes serious plays for patients who, in all honesty, just might be better off heading with her beyond the vale. That's not my decision to make, I told Death, tweaking the pressors. I have this thing about systolic blood pressure less than room temperature. By being here, she's placed her life in my hands, I said, staring down into what almost looked like a lifeless face. Until and unless I have a compelling reason to do otherwise, I will do whatever is necessary to ensure she comes out of this thing as well as she can. I turned to look Death in those beady little eyes. Even go 15 rounds with you, if that's what it takes.

There was a moment of silence, during which I began to think that perhaps I had made my point. Rock, paper, scissors? Death asked with a hopeful lilt.

I sighed. Damn, but she was persistent. I don't gamble with death. That's something my mommy taught me, way back when I used to think I'd be able to fly if I jumped from that really tall tree on the hill.

Oh, come on. Your patient in the next bed did. Overdosed on Ativan with a fifth of Johnny Walker Black as a chaser? Now there's a lifestyle choice I can find myself endorsing.

I was out of witty comebacks. Everyone deserves another chance, I told her, my eyes fixed now on the hollowed, closed eyes of my patient in the ICU bed. Evenor maybe even especiallymy patient in the next bed. I don't know what it was about his life that had driven him to the lifestyle choices he had made. There's a part of every physician that thinks that he or she can make that difference in a patient's life. All too often, though, we see enough repeat business to learn, the hard way, that we rarely make the kind of differences we'd like to. With a little luck, and no small amount of medical diligence, both my patients would survive this hospitalization.

But would they survive their next?

Would there be a next?

Would this be the time they'd turn the corner?

I had to hope so, because I still consider myself far too young to be any more cynical than I already am.

What about your partner? Death asked suddenly.

No, I said with something I hoped sounded like authority. You can't have her either.

No, I meanhow about I work a deal with her? She's young, she's impressionable, she's idealisticwe could make it not your fault.

She's got enough to do; please just leave her alone.

The hood shook slowly back and forth, so I assumed she was shaking her head. Or her skull. Whichever. Look, you wouldn't even have to do anything, that sweet, seductive voice told me. Just head back to your call room for a few minutes. Turn off your pager.

I don't know why we're even having this conversation, I groaned. We both know that you're just a hallucination caused by way too little sleep and way too much caffeine. Last call night I caught myself discussing the relative merits of high‐frequency jet ventilation with Galen.

Galen, Death reflected, suddenly nostalgic. Highly overrated, a positive trait in a doctor if you don't mind my saying so. Has an ego that would make an orthopedist seem humble.

You're lying, I decided.

Yes, I am. And you're stalling. Her voice suddenly became a whole lot more James Earl Jonesish. I'm taking the septic chick with endocarditis. You can lose all the sleep you want, she still goes Home with me.

I glanced over the drips one more time. I've just added norepi. That's a whole bag full of bite me that says differently. So back off, sweetheart.

As with most true medical emergencies, I was too busy thinking ahead to realize just how much trouble my patient could have been in at that moment.

Now morning, like her fever, has broken.

The sun, for those that haven't noticed, gives off a beautiful red glow as it rises over Boot Hill. I got to see it from the rocking chair in my patient's room. Nurse Donna was finishing the night's vital sign flow sheet, politely pretending she hadn't heard me snoring away the past 15 minutes. I was trying to decide if that odor drifting into the room was someone's attempt at coffee or melana. Donna smiled politely at me as I rubbed the Sandman's crud out of my eyes. It was a very Chicago Hope kinda moment.

If I'd been playing a doctor on TV, I'd have made some reassuring comment about how my patient had made it through the night, and so she was now out of the woods. Uh‐huh. With Death sneaking up behind me, my bite‐me norepinephrine wasn't going to be weaned just yet.

Good morning, I greeted.

She seemed a bit put off that I had heard her sneaking in. But then, Death is not exactly graced with kitty‐cat feet.

You never turned your pager off. She said it like an accusation. The way my wife does.

Never do. An answer my wife doesn't appreciate, either. My patient's still with me, I said, managing to keep the victory dance out of my voice. Pressure is better, heart rate is lower, fever seems to have broken.

Death is patient, death is kind, she warned.

It took my postcall mind a moment to wrap itself around that one. Isn't that supposed to be Love? I asked her.

The shoulders of the robe shrugged. Love gets all the cool lines, she complained. What do I get? Be not proud, nothing's for sure but me and taxes, Yea, though I walk through the valley of the shadow of me, give me liberty or give me me. She turned to face me. I like that one, by the way.

Never fails to bring a tear to my eye. I'd give her that. She had lost the patient, I could afford to be gracious and throw her a bone. As long as said bone didn't belong to one of my patients.

Death was silent for a long moment. Well, I'm outta here, she finally decided. What about you?

I've got a few more hours. Rounds, orders, more rounds, discussions with families, likely more rounds

I thought I could hear a wry grin in her voice. Well, you be careful driving home, she suggested. It'd be a shame if you fell asleep at the wheel. And then ended up on my doorstep.

Damn.

She is not, however, without a certain, well, grim sense of humor.

The voice throws you at first. It's deceptively mild and calm, more Gwyneth Paltrow than James Earl Jones. To the best of my knowledge, however, Gwyneth Paltrow has never shown up in a patient's room wearing a hooded black robe and sporting a scythe.

Hmm, bad case of sepsis, huh? she asked.

I was still cleaning up from the central line, so I tried to get rid of her gracefully. Now's not really a good time. That line always seems to work with pesky administrators.

Death, however, would not be dissuaded. HIV positive for nearly 10 years now, flirting with CD4 counts in double digits, rising viral load the past 3 years. Picked a bad time to have her gallbladder go bad on her, didn't she?

Or a bad time to pick a surgeon who was less than fastidious about his sterile fields, I muttered.

Death, however, chose to ignore me. Ventilator, pressors, antibiotics. She reached for the girl's right hand, attached as it was to an arterial line blood pressure monitor, and somethingdamn, if it didn't look like a scarabfell out of the robe and then scrambled across my patient's chest, right next to my newly placed and oh‐so‐deftly sutured plastic catheter, ducking away from the light.

Hey, that was my sterile field, I complained. I, unlike the aforementioned surgeon, had been fastidious about it. I hoped the scarab was sterile, at least.

Splinter hemorrhages, Death noted with obvious glee, taking particular interest in the little streaks of blood under my patient's fingernails. Septic emboli. Death seems to have Gwnyeth Paltrow's laugh along with her voice. It's a light and airy thing, almost like a favorite wind chime. That laugh could almost make you think Death had a heart. Endocarditis, she said fondly. One of my favorites.

Almost make you think she had a heart.

Go away. I tried to look more busy than worried, but I didn't think she was buying it.

It's been a good month for me here in the ICU. Heck, you yourself have 4 kills. Why don't you throw in this one and call yourself an ace?

Very funny. Now get out. I would imagine it's best not to lose your temper with Death. Or with any of the other three Horsemen of the Apocalypse, for that matter. Didn't anyone ever tell you it's poor form to make fun of your host? You're in Donna Smith's house now, buddy. Don't be dissin' my nurse manager.

Come on, she pushed. She's pathetic, she's tired, she lives alone in a tiny room in a forgotten crack house that she pretends is her apartment, and her parents haven't taken her calls for years.

Donna? I asked. That was some serious disrespect.

Don't go all medical student on me. I was talking about your patient, she explained evenly. She'd be better off with me anyway. You know that.

She can be persuasive when she might be right. Death and I have been having similar conversations all the way back to my surgical rotation as a third‐year medical student. Although she has never been above making the easy score, she typically only makes serious plays for patients who, in all honesty, just might be better off heading with her beyond the vale. That's not my decision to make, I told Death, tweaking the pressors. I have this thing about systolic blood pressure less than room temperature. By being here, she's placed her life in my hands, I said, staring down into what almost looked like a lifeless face. Until and unless I have a compelling reason to do otherwise, I will do whatever is necessary to ensure she comes out of this thing as well as she can. I turned to look Death in those beady little eyes. Even go 15 rounds with you, if that's what it takes.

There was a moment of silence, during which I began to think that perhaps I had made my point. Rock, paper, scissors? Death asked with a hopeful lilt.

I sighed. Damn, but she was persistent. I don't gamble with death. That's something my mommy taught me, way back when I used to think I'd be able to fly if I jumped from that really tall tree on the hill.

Oh, come on. Your patient in the next bed did. Overdosed on Ativan with a fifth of Johnny Walker Black as a chaser? Now there's a lifestyle choice I can find myself endorsing.

I was out of witty comebacks. Everyone deserves another chance, I told her, my eyes fixed now on the hollowed, closed eyes of my patient in the ICU bed. Evenor maybe even especiallymy patient in the next bed. I don't know what it was about his life that had driven him to the lifestyle choices he had made. There's a part of every physician that thinks that he or she can make that difference in a patient's life. All too often, though, we see enough repeat business to learn, the hard way, that we rarely make the kind of differences we'd like to. With a little luck, and no small amount of medical diligence, both my patients would survive this hospitalization.

But would they survive their next?

Would there be a next?

Would this be the time they'd turn the corner?

I had to hope so, because I still consider myself far too young to be any more cynical than I already am.

What about your partner? Death asked suddenly.

No, I said with something I hoped sounded like authority. You can't have her either.

No, I meanhow about I work a deal with her? She's young, she's impressionable, she's idealisticwe could make it not your fault.

She's got enough to do; please just leave her alone.

The hood shook slowly back and forth, so I assumed she was shaking her head. Or her skull. Whichever. Look, you wouldn't even have to do anything, that sweet, seductive voice told me. Just head back to your call room for a few minutes. Turn off your pager.

I don't know why we're even having this conversation, I groaned. We both know that you're just a hallucination caused by way too little sleep and way too much caffeine. Last call night I caught myself discussing the relative merits of high‐frequency jet ventilation with Galen.

Galen, Death reflected, suddenly nostalgic. Highly overrated, a positive trait in a doctor if you don't mind my saying so. Has an ego that would make an orthopedist seem humble.

You're lying, I decided.

Yes, I am. And you're stalling. Her voice suddenly became a whole lot more James Earl Jonesish. I'm taking the septic chick with endocarditis. You can lose all the sleep you want, she still goes Home with me.

I glanced over the drips one more time. I've just added norepi. That's a whole bag full of bite me that says differently. So back off, sweetheart.

As with most true medical emergencies, I was too busy thinking ahead to realize just how much trouble my patient could have been in at that moment.

Now morning, like her fever, has broken.

The sun, for those that haven't noticed, gives off a beautiful red glow as it rises over Boot Hill. I got to see it from the rocking chair in my patient's room. Nurse Donna was finishing the night's vital sign flow sheet, politely pretending she hadn't heard me snoring away the past 15 minutes. I was trying to decide if that odor drifting into the room was someone's attempt at coffee or melana. Donna smiled politely at me as I rubbed the Sandman's crud out of my eyes. It was a very Chicago Hope kinda moment.

If I'd been playing a doctor on TV, I'd have made some reassuring comment about how my patient had made it through the night, and so she was now out of the woods. Uh‐huh. With Death sneaking up behind me, my bite‐me norepinephrine wasn't going to be weaned just yet.

Good morning, I greeted.

She seemed a bit put off that I had heard her sneaking in. But then, Death is not exactly graced with kitty‐cat feet.

You never turned your pager off. She said it like an accusation. The way my wife does.

Never do. An answer my wife doesn't appreciate, either. My patient's still with me, I said, managing to keep the victory dance out of my voice. Pressure is better, heart rate is lower, fever seems to have broken.

Death is patient, death is kind, she warned.

It took my postcall mind a moment to wrap itself around that one. Isn't that supposed to be Love? I asked her.

The shoulders of the robe shrugged. Love gets all the cool lines, she complained. What do I get? Be not proud, nothing's for sure but me and taxes, Yea, though I walk through the valley of the shadow of me, give me liberty or give me me. She turned to face me. I like that one, by the way.

Never fails to bring a tear to my eye. I'd give her that. She had lost the patient, I could afford to be gracious and throw her a bone. As long as said bone didn't belong to one of my patients.

Death was silent for a long moment. Well, I'm outta here, she finally decided. What about you?

I've got a few more hours. Rounds, orders, more rounds, discussions with families, likely more rounds

I thought I could hear a wry grin in her voice. Well, you be careful driving home, she suggested. It'd be a shame if you fell asleep at the wheel. And then ended up on my doorstep.

Damn.

She is not, however, without a certain, well, grim sense of humor.

The voice throws you at first. It's deceptively mild and calm, more Gwyneth Paltrow than James Earl Jones. To the best of my knowledge, however, Gwyneth Paltrow has never shown up in a patient's room wearing a hooded black robe and sporting a scythe.

Hmm, bad case of sepsis, huh? she asked.

I was still cleaning up from the central line, so I tried to get rid of her gracefully. Now's not really a good time. That line always seems to work with pesky administrators.

Death, however, would not be dissuaded. HIV positive for nearly 10 years now, flirting with CD4 counts in double digits, rising viral load the past 3 years. Picked a bad time to have her gallbladder go bad on her, didn't she?

Or a bad time to pick a surgeon who was less than fastidious about his sterile fields, I muttered.

Death, however, chose to ignore me. Ventilator, pressors, antibiotics. She reached for the girl's right hand, attached as it was to an arterial line blood pressure monitor, and somethingdamn, if it didn't look like a scarabfell out of the robe and then scrambled across my patient's chest, right next to my newly placed and oh‐so‐deftly sutured plastic catheter, ducking away from the light.

Hey, that was my sterile field, I complained. I, unlike the aforementioned surgeon, had been fastidious about it. I hoped the scarab was sterile, at least.

Splinter hemorrhages, Death noted with obvious glee, taking particular interest in the little streaks of blood under my patient's fingernails. Septic emboli. Death seems to have Gwnyeth Paltrow's laugh along with her voice. It's a light and airy thing, almost like a favorite wind chime. That laugh could almost make you think Death had a heart. Endocarditis, she said fondly. One of my favorites.

Almost make you think she had a heart.

Go away. I tried to look more busy than worried, but I didn't think she was buying it.

It's been a good month for me here in the ICU. Heck, you yourself have 4 kills. Why don't you throw in this one and call yourself an ace?

Very funny. Now get out. I would imagine it's best not to lose your temper with Death. Or with any of the other three Horsemen of the Apocalypse, for that matter. Didn't anyone ever tell you it's poor form to make fun of your host? You're in Donna Smith's house now, buddy. Don't be dissin' my nurse manager.

Come on, she pushed. She's pathetic, she's tired, she lives alone in a tiny room in a forgotten crack house that she pretends is her apartment, and her parents haven't taken her calls for years.

Donna? I asked. That was some serious disrespect.

Don't go all medical student on me. I was talking about your patient, she explained evenly. She'd be better off with me anyway. You know that.

She can be persuasive when she might be right. Death and I have been having similar conversations all the way back to my surgical rotation as a third‐year medical student. Although she has never been above making the easy score, she typically only makes serious plays for patients who, in all honesty, just might be better off heading with her beyond the vale. That's not my decision to make, I told Death, tweaking the pressors. I have this thing about systolic blood pressure less than room temperature. By being here, she's placed her life in my hands, I said, staring down into what almost looked like a lifeless face. Until and unless I have a compelling reason to do otherwise, I will do whatever is necessary to ensure she comes out of this thing as well as she can. I turned to look Death in those beady little eyes. Even go 15 rounds with you, if that's what it takes.

There was a moment of silence, during which I began to think that perhaps I had made my point. Rock, paper, scissors? Death asked with a hopeful lilt.

I sighed. Damn, but she was persistent. I don't gamble with death. That's something my mommy taught me, way back when I used to think I'd be able to fly if I jumped from that really tall tree on the hill.

Oh, come on. Your patient in the next bed did. Overdosed on Ativan with a fifth of Johnny Walker Black as a chaser? Now there's a lifestyle choice I can find myself endorsing.

I was out of witty comebacks. Everyone deserves another chance, I told her, my eyes fixed now on the hollowed, closed eyes of my patient in the ICU bed. Evenor maybe even especiallymy patient in the next bed. I don't know what it was about his life that had driven him to the lifestyle choices he had made. There's a part of every physician that thinks that he or she can make that difference in a patient's life. All too often, though, we see enough repeat business to learn, the hard way, that we rarely make the kind of differences we'd like to. With a little luck, and no small amount of medical diligence, both my patients would survive this hospitalization.

But would they survive their next?

Would there be a next?

Would this be the time they'd turn the corner?

I had to hope so, because I still consider myself far too young to be any more cynical than I already am.

What about your partner? Death asked suddenly.

No, I said with something I hoped sounded like authority. You can't have her either.

No, I meanhow about I work a deal with her? She's young, she's impressionable, she's idealisticwe could make it not your fault.

She's got enough to do; please just leave her alone.

The hood shook slowly back and forth, so I assumed she was shaking her head. Or her skull. Whichever. Look, you wouldn't even have to do anything, that sweet, seductive voice told me. Just head back to your call room for a few minutes. Turn off your pager.

I don't know why we're even having this conversation, I groaned. We both know that you're just a hallucination caused by way too little sleep and way too much caffeine. Last call night I caught myself discussing the relative merits of high‐frequency jet ventilation with Galen.

Galen, Death reflected, suddenly nostalgic. Highly overrated, a positive trait in a doctor if you don't mind my saying so. Has an ego that would make an orthopedist seem humble.

You're lying, I decided.

Yes, I am. And you're stalling. Her voice suddenly became a whole lot more James Earl Jonesish. I'm taking the septic chick with endocarditis. You can lose all the sleep you want, she still goes Home with me.

I glanced over the drips one more time. I've just added norepi. That's a whole bag full of bite me that says differently. So back off, sweetheart.

As with most true medical emergencies, I was too busy thinking ahead to realize just how much trouble my patient could have been in at that moment.

Now morning, like her fever, has broken.

The sun, for those that haven't noticed, gives off a beautiful red glow as it rises over Boot Hill. I got to see it from the rocking chair in my patient's room. Nurse Donna was finishing the night's vital sign flow sheet, politely pretending she hadn't heard me snoring away the past 15 minutes. I was trying to decide if that odor drifting into the room was someone's attempt at coffee or melana. Donna smiled politely at me as I rubbed the Sandman's crud out of my eyes. It was a very Chicago Hope kinda moment.

If I'd been playing a doctor on TV, I'd have made some reassuring comment about how my patient had made it through the night, and so she was now out of the woods. Uh‐huh. With Death sneaking up behind me, my bite‐me norepinephrine wasn't going to be weaned just yet.

Good morning, I greeted.

She seemed a bit put off that I had heard her sneaking in. But then, Death is not exactly graced with kitty‐cat feet.

You never turned your pager off. She said it like an accusation. The way my wife does.

Never do. An answer my wife doesn't appreciate, either. My patient's still with me, I said, managing to keep the victory dance out of my voice. Pressure is better, heart rate is lower, fever seems to have broken.

Death is patient, death is kind, she warned.

It took my postcall mind a moment to wrap itself around that one. Isn't that supposed to be Love? I asked her.

The shoulders of the robe shrugged. Love gets all the cool lines, she complained. What do I get? Be not proud, nothing's for sure but me and taxes, Yea, though I walk through the valley of the shadow of me, give me liberty or give me me. She turned to face me. I like that one, by the way.

Never fails to bring a tear to my eye. I'd give her that. She had lost the patient, I could afford to be gracious and throw her a bone. As long as said bone didn't belong to one of my patients.

Death was silent for a long moment. Well, I'm outta here, she finally decided. What about you?

I've got a few more hours. Rounds, orders, more rounds, discussions with families, likely more rounds

I thought I could hear a wry grin in her voice. Well, you be careful driving home, she suggested. It'd be a shame if you fell asleep at the wheel. And then ended up on my doorstep.

Damn.

The hospitalist model of care has experienced dramatic growth. In 2003 it was estimated that there were 8000 US hospitalists, a number projected to ultimately reach more than 19 000.1, 2 This rapid growth has largely been driven by improvements in clinical efficiency as a result of hospitalist programs. There is a substantial body of evidence showing that hospitalists reduce length of stay and inpatient costs.3 Despite the rapid growth and proven benefit to clinical efficiency, no studies have evaluated the type and frequency of activities that hospitalists perform during routine work. Although the use of hospitalists improves clinical efficiency for the hospital, relatively little is known about how the hospital can improve efficiency for the hospitalist.

Our institution greatly expanded our hospitalist program in June 2003 to create a resident‐uncovered hospitalist service. The impetus for this change was the need to comply with newly revised Accreditation Council for Graduate Medicine Education (ACGME) program requirements regarding resident duty hours. Many teaching hospitals have implemented similar resident‐uncovered hospitalist services.4 Inefficiencies in their work activities quickly became apparent to our hospitalists. Furthermore, our hospitalists believed that they frequently performed simultaneous activities and that they were excessively interrupted by pages.

To evaluate the type and frequency of activities that the hospitalists performed during routine work, we performed a time‐motion study of hospitalist physicians on the resident‐uncovered hospitalist service. Our goal was to identify areas for systems improvements and activities that were better suited for nonphysician providers and to quantify the time spent multitasking and the frequency of paging interruptions.

METHODS

Northwestern Memorial Hospital (NMH) is a 753‐bed hospital in Chicago, Illinois. NMH is the primary teaching hospital affiliated with the Feinberg School of Medicine of Northwestern University. There are 2 general medicine services at NMH: a traditional resident‐covered ward service and the resident‐uncovered hospitalist service. Patients are admitted to one of these 2 services on the basis of, in order of importance, capacity of the services, preference of the outpatient physician, and potential educational value of the admission. Patients admitted to the hospitalist service are preferentially given beds on specific wards intended for hospitalist service patients. Fourth‐year medical students are frequently paired with hospitalists during their medicine subinternship.

The resident‐uncovered hospitalist service comprises 5 daytime hospitalists on duty at a time. The hospitalists are on service for 7 consecutive days, usually followed by 7 consecutive days off. Hospitalists pick up new patients from the night float hospitalist each morning. Daytime admitting duties rotate on a daily basis. One hospitalist accepts new admissions each morning from 7:00 _AM until noon. Two hospitalists accept admissions from noon until 5:00 _PM. One hospitalist accepts admissions from 5:00 _PM until 9:00 _PM. One hospitalist is free from accepting new admissions each day. All daytime hospitalists begin the workday at 7:00 AM and leave when their duties are completed for the day. One night float hospitalist is on duty each night of the week. The night float hospitalist performs admissions and all cross cover activities from 7:00 _PM until 7:00 _AM.

We first conducted a pilot study to help identify specific activities that our hospitalists routinely perform. Broad categories and subcategories of activities were created based on the results of our pilot study, and a published time‐motion study performed on emergency medicine physicians5 (Table 1). Once activities were defined and codes established, our research assistant unobtrusively shadowed hospitalist physicians for periods lasting 3‐5 hours. The observation periods were distributed in order to sample all activities that a daytime hospitalist would perform throughout a typical week. Observation periods included 2 morning admitting periods, 4 morning nonadmitting periods, 4 afternoon admitting periods, 4 afternoon nonadmitting periods, and 2 admitting periods from 5:00 _PM to 9:00 _PM. Activities were recorded on a standardized data collection form in 1‐minute intervals. When multiple activities were performed at the same time, all activities were recorded in the same 1‐minute interval. Incoming pages were recorded as well. To minimize the possibility that observation would affect hospitalist behavior, the research assistant was instructed not to initiate conversation with the hospitalists.

The data collection forms were manually abstracted and minutes tallied for each category and subcategory, for which summary statistics were converted to percentage of total minutes.

RESULTS

Ten hospitalists were shadowed by a single research assistant for a total of 4467 minutes. Seven hospitalists were male and 3 were female. The hospitalists were a mean age of 31 1.6 years of age and had been practicing as a hospitalist for a mean of 2.1 1.0 years. The hospitalists saw an average of 9.4 4.0 patients on the days they were shadowed by the research assistant. Because simultaneous activities were recorded, a total of 5557 minutes of activities were recorded.

The distribution of total minutes recorded in each activity category is shown in Figure 1. Hospitalists spent 18% of their time doing direct patient care, 69% on indirect patient care, 4% on personal activities, and 3% each on professional development, education, and travel.

Figure 1

Of the time hospitalists directly cared for patients, 18% was spent obtaining histories and performing physical examinations on new patients, 53% seeing patients in follow‐up visits, 16% going over discharge instructions, and 13% in family meetings (Figure 2). Of the time hospitalists spent doing indirect patient care, 37% was taken up by documentation, 21% by reviewing results, 7% by orders, and 35% by communication (Figure 2).

Figure 2

As just explained, communication accounted for 35% of indirect patient care activities; it also accounted for 24% of the total activity minutes. The time spent by hospitalists on communication was further broken down as 23% paging other physicians, 31% returning pages, 34% in face‐to‐face communication, 5% taking report on new admissions, 4% on sign‐out to the night float hospitalist, and 3% receiving sign‐out from the night float hospitalist.

Multitasking, performing more than 1 activity at the same time, was done 21% of the time. Hospitalists received an average of 3.4 1.5 pages per hour, and 7% of total activity time was spent returning pages. Other forms of interruption were not evaluated.

DISCUSSION

Our study had several important findings. First, hospitalists spent most of their time on indirect patient care activities and relatively little time on direct patient care. Time‐motion studies of nonhospitalist physicians have reported similar findings.5, 6 A considerable amount of hospitalist time was spent on documentation. This finding also has been reported in studies of nonhospitalist physicians.5, 7

A unique finding in our study was the large amount of time, 24% of total minutes, spent on communication. A study of emergency medicine physicians by Hollingsworth found that 13% of their time was spent on communication activities.5 The large amount of time spent on communication in our study underscores the need for hospitalists to have outstanding communication skills and systems that support efficient communication. Hospitalists spent 6% of their total time paging other physicians and 7% returning pages. Improvements in the efficiency of paging communication could greatly reduce the amount of time communicating by page. Our paging system provides unidirectional alphanumeric paging. In an effort to improve the efficiency of paging, we have asked nurses and consultants to include FYI and callback in the text of the page so it is clear whether the person who has paged the hospitalist needs to be called back. This simple solution to help reduce the number of unnecessary callbacks has previously been proposed by others.8

Another part of solving this problem is adopting the use of 2‐way pagers instead of alphanumeric pagers. Two‐way paging can increase the efficiency of communication even further. For example, a nurse sends a hospitalist a page that asks if the previous diet orders for a patient just returned from a procedure can be resumed. This hospitalist is on another floor in another patient's room. Rather than spending time leaving the other patient's room, finding a phone, calling the floor, waiting for an answer, and then waiting on hold, the hospitalist simply texts a 1‐word answer, Yes, in the 2‐way paging system. In addition to the time occupied by paging activities, hospitalists spent a large amount of time in face‐to‐face communication (8% of total activity time). On the one hand, having hospitalists discuss patient care with consultants and nurses in person on an ongoing basis throughout the day may improve clinical efficiency. On the other hand, the constant potential for interruption may be problematic. Similarly, 2‐way paging could facilitate communication to such a degree that it could actually increase the frequency of interruptions. Research on improvements in communications systems, interventions to improve communication skills, and team‐based care is warranted in order to evaluate the impact on hospitalist workflow.

An important finding in our study was that multitasking and paging interruptions were common. Although this may come as no surprise to practicing hospitalists, the distraction caused by interruptions and multitasking is an important potential cause of medical errors.911 A thorough examination of the types of activities performed simultaneously and whether they contributed to medical error was beyond the scope of our study. Some activities, such as documenting a note on a patient while reviewing the patient's lab results, are concordant (ie, conducted for the same patient) and therefore may be unlikely to contribute to medical error. Other combinations of activities, such as returning a page about one patient while documenting a note on a different patient or having face‐to‐face communication about one patient while entering an order on another patient, are discordant. Discordant activities may contribute to medical error. Further research of the effect of hospitalist multitasking and interruption on medical error is warranted and should be conducted within the framework of concordant versus discordant activities.

We had hoped to find activities that could be performed by non‐physician providers. No high impact activities were discovered that would be better suited for a non‐physician provider in this study. Clerical tasks, such as calling for radiology orders or obtaining medical records, amounted to a small percentage of hospitalist time (less than 1% combined). We did identify several activities in which automation or process improvement would be helpful. Hospitalists spent 5% of time on the combined activity of documenting discharge instructions and writing out prescriptions. Our institution is in the process of implementing an electronic medical record and computerized physician order entry. We are currently working on an automated process to generate printed discharge instructions and prescriptions. This has the potential not only to improve efficiency, but also to eliminate medication errors, as care is transitioned to the outpatient setting.

Our study had several limitations. First, our findings reflect the experience at one institution. Hospitalist practices vary widely in their staffing and scheduling models as well as in their organizational support. The amount of time that hospitalists spend on activities may differ between practices and between individual hospitalists in the same practice. Another limitation to our study pertains to the workflow of our hospitalists and the locations of their patients. As discussed earlier, patients were assigned to a hospitalist according to time of admission, not location of admission. Because of this, the hospitalists were caring for patients on as many as 5 wards. Although travel time amounted to only 3% of total minutes, it is possible that communication time could have been reduced if patients were distributed to hospitalists on the basis of patient location rather than time of admission of patient. For example, physicians and nurses might spend less time communicating in person compared to communicating via unidirectional paging, which frequently requires waiting for a callback. Finally, our study only observed activities performed by the daytime hospitalists at our hospital. The distribution and types of activities performed by nighttime hospitalists may be somewhat different.

Our study may serve as a model for hospitalist time‐motion studies in other settings. Our findings are of particular importance to resident‐uncovered hospitalist programs in academic hospitals, a setting in which operational inefficiencies may be abundant as house staff members have been poorly positioned in the hospital organization to lobby for process change. We hope that our study is a precursor to research evaluating modifications to the environments and systems in which hospitalists work. Such modifications have the potential to improve productivity and work conditions and promote career satisfaction.

The hospitalist model of care has experienced dramatic growth. In 2003 it was estimated that there were 8000 US hospitalists, a number projected to ultimately reach more than 19 000.1, 2 This rapid growth has largely been driven by improvements in clinical efficiency as a result of hospitalist programs. There is a substantial body of evidence showing that hospitalists reduce length of stay and inpatient costs.3 Despite the rapid growth and proven benefit to clinical efficiency, no studies have evaluated the type and frequency of activities that hospitalists perform during routine work. Although the use of hospitalists improves clinical efficiency for the hospital, relatively little is known about how the hospital can improve efficiency for the hospitalist.

Our institution greatly expanded our hospitalist program in June 2003 to create a resident‐uncovered hospitalist service. The impetus for this change was the need to comply with newly revised Accreditation Council for Graduate Medicine Education (ACGME) program requirements regarding resident duty hours. Many teaching hospitals have implemented similar resident‐uncovered hospitalist services.4 Inefficiencies in their work activities quickly became apparent to our hospitalists. Furthermore, our hospitalists believed that they frequently performed simultaneous activities and that they were excessively interrupted by pages.

To evaluate the type and frequency of activities that the hospitalists performed during routine work, we performed a time‐motion study of hospitalist physicians on the resident‐uncovered hospitalist service. Our goal was to identify areas for systems improvements and activities that were better suited for nonphysician providers and to quantify the time spent multitasking and the frequency of paging interruptions.

METHODS

Northwestern Memorial Hospital (NMH) is a 753‐bed hospital in Chicago, Illinois. NMH is the primary teaching hospital affiliated with the Feinberg School of Medicine of Northwestern University. There are 2 general medicine services at NMH: a traditional resident‐covered ward service and the resident‐uncovered hospitalist service. Patients are admitted to one of these 2 services on the basis of, in order of importance, capacity of the services, preference of the outpatient physician, and potential educational value of the admission. Patients admitted to the hospitalist service are preferentially given beds on specific wards intended for hospitalist service patients. Fourth‐year medical students are frequently paired with hospitalists during their medicine subinternship.

The resident‐uncovered hospitalist service comprises 5 daytime hospitalists on duty at a time. The hospitalists are on service for 7 consecutive days, usually followed by 7 consecutive days off. Hospitalists pick up new patients from the night float hospitalist each morning. Daytime admitting duties rotate on a daily basis. One hospitalist accepts new admissions each morning from 7:00 _AM until noon. Two hospitalists accept admissions from noon until 5:00 _PM. One hospitalist accepts admissions from 5:00 _PM until 9:00 _PM. One hospitalist is free from accepting new admissions each day. All daytime hospitalists begin the workday at 7:00 AM and leave when their duties are completed for the day. One night float hospitalist is on duty each night of the week. The night float hospitalist performs admissions and all cross cover activities from 7:00 _PM until 7:00 _AM.

We first conducted a pilot study to help identify specific activities that our hospitalists routinely perform. Broad categories and subcategories of activities were created based on the results of our pilot study, and a published time‐motion study performed on emergency medicine physicians5 (Table 1). Once activities were defined and codes established, our research assistant unobtrusively shadowed hospitalist physicians for periods lasting 3‐5 hours. The observation periods were distributed in order to sample all activities that a daytime hospitalist would perform throughout a typical week. Observation periods included 2 morning admitting periods, 4 morning nonadmitting periods, 4 afternoon admitting periods, 4 afternoon nonadmitting periods, and 2 admitting periods from 5:00 _PM to 9:00 _PM. Activities were recorded on a standardized data collection form in 1‐minute intervals. When multiple activities were performed at the same time, all activities were recorded in the same 1‐minute interval. Incoming pages were recorded as well. To minimize the possibility that observation would affect hospitalist behavior, the research assistant was instructed not to initiate conversation with the hospitalists.

The data collection forms were manually abstracted and minutes tallied for each category and subcategory, for which summary statistics were converted to percentage of total minutes.

RESULTS

Ten hospitalists were shadowed by a single research assistant for a total of 4467 minutes. Seven hospitalists were male and 3 were female. The hospitalists were a mean age of 31 1.6 years of age and had been practicing as a hospitalist for a mean of 2.1 1.0 years. The hospitalists saw an average of 9.4 4.0 patients on the days they were shadowed by the research assistant. Because simultaneous activities were recorded, a total of 5557 minutes of activities were recorded.

The distribution of total minutes recorded in each activity category is shown in Figure 1. Hospitalists spent 18% of their time doing direct patient care, 69% on indirect patient care, 4% on personal activities, and 3% each on professional development, education, and travel.

Figure 1

Of the time hospitalists directly cared for patients, 18% was spent obtaining histories and performing physical examinations on new patients, 53% seeing patients in follow‐up visits, 16% going over discharge instructions, and 13% in family meetings (Figure 2). Of the time hospitalists spent doing indirect patient care, 37% was taken up by documentation, 21% by reviewing results, 7% by orders, and 35% by communication (Figure 2).

Figure 2

As just explained, communication accounted for 35% of indirect patient care activities; it also accounted for 24% of the total activity minutes. The time spent by hospitalists on communication was further broken down as 23% paging other physicians, 31% returning pages, 34% in face‐to‐face communication, 5% taking report on new admissions, 4% on sign‐out to the night float hospitalist, and 3% receiving sign‐out from the night float hospitalist.

Multitasking, performing more than 1 activity at the same time, was done 21% of the time. Hospitalists received an average of 3.4 1.5 pages per hour, and 7% of total activity time was spent returning pages. Other forms of interruption were not evaluated.

DISCUSSION

Our study had several important findings. First, hospitalists spent most of their time on indirect patient care activities and relatively little time on direct patient care. Time‐motion studies of nonhospitalist physicians have reported similar findings.5, 6 A considerable amount of hospitalist time was spent on documentation. This finding also has been reported in studies of nonhospitalist physicians.5, 7

A unique finding in our study was the large amount of time, 24% of total minutes, spent on communication. A study of emergency medicine physicians by Hollingsworth found that 13% of their time was spent on communication activities.5 The large amount of time spent on communication in our study underscores the need for hospitalists to have outstanding communication skills and systems that support efficient communication. Hospitalists spent 6% of their total time paging other physicians and 7% returning pages. Improvements in the efficiency of paging communication could greatly reduce the amount of time communicating by page. Our paging system provides unidirectional alphanumeric paging. In an effort to improve the efficiency of paging, we have asked nurses and consultants to include FYI and callback in the text of the page so it is clear whether the person who has paged the hospitalist needs to be called back. This simple solution to help reduce the number of unnecessary callbacks has previously been proposed by others.8

Another part of solving this problem is adopting the use of 2‐way pagers instead of alphanumeric pagers. Two‐way paging can increase the efficiency of communication even further. For example, a nurse sends a hospitalist a page that asks if the previous diet orders for a patient just returned from a procedure can be resumed. This hospitalist is on another floor in another patient's room. Rather than spending time leaving the other patient's room, finding a phone, calling the floor, waiting for an answer, and then waiting on hold, the hospitalist simply texts a 1‐word answer, Yes, in the 2‐way paging system. In addition to the time occupied by paging activities, hospitalists spent a large amount of time in face‐to‐face communication (8% of total activity time). On the one hand, having hospitalists discuss patient care with consultants and nurses in person on an ongoing basis throughout the day may improve clinical efficiency. On the other hand, the constant potential for interruption may be problematic. Similarly, 2‐way paging could facilitate communication to such a degree that it could actually increase the frequency of interruptions. Research on improvements in communications systems, interventions to improve communication skills, and team‐based care is warranted in order to evaluate the impact on hospitalist workflow.

An important finding in our study was that multitasking and paging interruptions were common. Although this may come as no surprise to practicing hospitalists, the distraction caused by interruptions and multitasking is an important potential cause of medical errors.911 A thorough examination of the types of activities performed simultaneously and whether they contributed to medical error was beyond the scope of our study. Some activities, such as documenting a note on a patient while reviewing the patient's lab results, are concordant (ie, conducted for the same patient) and therefore may be unlikely to contribute to medical error. Other combinations of activities, such as returning a page about one patient while documenting a note on a different patient or having face‐to‐face communication about one patient while entering an order on another patient, are discordant. Discordant activities may contribute to medical error. Further research of the effect of hospitalist multitasking and interruption on medical error is warranted and should be conducted within the framework of concordant versus discordant activities.

We had hoped to find activities that could be performed by non‐physician providers. No high impact activities were discovered that would be better suited for a non‐physician provider in this study. Clerical tasks, such as calling for radiology orders or obtaining medical records, amounted to a small percentage of hospitalist time (less than 1% combined). We did identify several activities in which automation or process improvement would be helpful. Hospitalists spent 5% of time on the combined activity of documenting discharge instructions and writing out prescriptions. Our institution is in the process of implementing an electronic medical record and computerized physician order entry. We are currently working on an automated process to generate printed discharge instructions and prescriptions. This has the potential not only to improve efficiency, but also to eliminate medication errors, as care is transitioned to the outpatient setting.

Our study had several limitations. First, our findings reflect the experience at one institution. Hospitalist practices vary widely in their staffing and scheduling models as well as in their organizational support. The amount of time that hospitalists spend on activities may differ between practices and between individual hospitalists in the same practice. Another limitation to our study pertains to the workflow of our hospitalists and the locations of their patients. As discussed earlier, patients were assigned to a hospitalist according to time of admission, not location of admission. Because of this, the hospitalists were caring for patients on as many as 5 wards. Although travel time amounted to only 3% of total minutes, it is possible that communication time could have been reduced if patients were distributed to hospitalists on the basis of patient location rather than time of admission of patient. For example, physicians and nurses might spend less time communicating in person compared to communicating via unidirectional paging, which frequently requires waiting for a callback. Finally, our study only observed activities performed by the daytime hospitalists at our hospital. The distribution and types of activities performed by nighttime hospitalists may be somewhat different.

Our study may serve as a model for hospitalist time‐motion studies in other settings. Our findings are of particular importance to resident‐uncovered hospitalist programs in academic hospitals, a setting in which operational inefficiencies may be abundant as house staff members have been poorly positioned in the hospital organization to lobby for process change. We hope that our study is a precursor to research evaluating modifications to the environments and systems in which hospitalists work. Such modifications have the potential to improve productivity and work conditions and promote career satisfaction.

The hospitalist model of care has experienced dramatic growth. In 2003 it was estimated that there were 8000 US hospitalists, a number projected to ultimately reach more than 19 000.1, 2 This rapid growth has largely been driven by improvements in clinical efficiency as a result of hospitalist programs. There is a substantial body of evidence showing that hospitalists reduce length of stay and inpatient costs.3 Despite the rapid growth and proven benefit to clinical efficiency, no studies have evaluated the type and frequency of activities that hospitalists perform during routine work. Although the use of hospitalists improves clinical efficiency for the hospital, relatively little is known about how the hospital can improve efficiency for the hospitalist.

Our institution greatly expanded our hospitalist program in June 2003 to create a resident‐uncovered hospitalist service. The impetus for this change was the need to comply with newly revised Accreditation Council for Graduate Medicine Education (ACGME) program requirements regarding resident duty hours. Many teaching hospitals have implemented similar resident‐uncovered hospitalist services.4 Inefficiencies in their work activities quickly became apparent to our hospitalists. Furthermore, our hospitalists believed that they frequently performed simultaneous activities and that they were excessively interrupted by pages.

To evaluate the type and frequency of activities that the hospitalists performed during routine work, we performed a time‐motion study of hospitalist physicians on the resident‐uncovered hospitalist service. Our goal was to identify areas for systems improvements and activities that were better suited for nonphysician providers and to quantify the time spent multitasking and the frequency of paging interruptions.

METHODS

Northwestern Memorial Hospital (NMH) is a 753‐bed hospital in Chicago, Illinois. NMH is the primary teaching hospital affiliated with the Feinberg School of Medicine of Northwestern University. There are 2 general medicine services at NMH: a traditional resident‐covered ward service and the resident‐uncovered hospitalist service. Patients are admitted to one of these 2 services on the basis of, in order of importance, capacity of the services, preference of the outpatient physician, and potential educational value of the admission. Patients admitted to the hospitalist service are preferentially given beds on specific wards intended for hospitalist service patients. Fourth‐year medical students are frequently paired with hospitalists during their medicine subinternship.

The resident‐uncovered hospitalist service comprises 5 daytime hospitalists on duty at a time. The hospitalists are on service for 7 consecutive days, usually followed by 7 consecutive days off. Hospitalists pick up new patients from the night float hospitalist each morning. Daytime admitting duties rotate on a daily basis. One hospitalist accepts new admissions each morning from 7:00 _AM until noon. Two hospitalists accept admissions from noon until 5:00 _PM. One hospitalist accepts admissions from 5:00 _PM until 9:00 _PM. One hospitalist is free from accepting new admissions each day. All daytime hospitalists begin the workday at 7:00 AM and leave when their duties are completed for the day. One night float hospitalist is on duty each night of the week. The night float hospitalist performs admissions and all cross cover activities from 7:00 _PM until 7:00 _AM.

We first conducted a pilot study to help identify specific activities that our hospitalists routinely perform. Broad categories and subcategories of activities were created based on the results of our pilot study, and a published time‐motion study performed on emergency medicine physicians5 (Table 1). Once activities were defined and codes established, our research assistant unobtrusively shadowed hospitalist physicians for periods lasting 3‐5 hours. The observation periods were distributed in order to sample all activities that a daytime hospitalist would perform throughout a typical week. Observation periods included 2 morning admitting periods, 4 morning nonadmitting periods, 4 afternoon admitting periods, 4 afternoon nonadmitting periods, and 2 admitting periods from 5:00 _PM to 9:00 _PM. Activities were recorded on a standardized data collection form in 1‐minute intervals. When multiple activities were performed at the same time, all activities were recorded in the same 1‐minute interval. Incoming pages were recorded as well. To minimize the possibility that observation would affect hospitalist behavior, the research assistant was instructed not to initiate conversation with the hospitalists.

The data collection forms were manually abstracted and minutes tallied for each category and subcategory, for which summary statistics were converted to percentage of total minutes.

RESULTS

Ten hospitalists were shadowed by a single research assistant for a total of 4467 minutes. Seven hospitalists were male and 3 were female. The hospitalists were a mean age of 31 1.6 years of age and had been practicing as a hospitalist for a mean of 2.1 1.0 years. The hospitalists saw an average of 9.4 4.0 patients on the days they were shadowed by the research assistant. Because simultaneous activities were recorded, a total of 5557 minutes of activities were recorded.

The distribution of total minutes recorded in each activity category is shown in Figure 1. Hospitalists spent 18% of their time doing direct patient care, 69% on indirect patient care, 4% on personal activities, and 3% each on professional development, education, and travel.

Figure 1

Of the time hospitalists directly cared for patients, 18% was spent obtaining histories and performing physical examinations on new patients, 53% seeing patients in follow‐up visits, 16% going over discharge instructions, and 13% in family meetings (Figure 2). Of the time hospitalists spent doing indirect patient care, 37% was taken up by documentation, 21% by reviewing results, 7% by orders, and 35% by communication (Figure 2).

Figure 2

As just explained, communication accounted for 35% of indirect patient care activities; it also accounted for 24% of the total activity minutes. The time spent by hospitalists on communication was further broken down as 23% paging other physicians, 31% returning pages, 34% in face‐to‐face communication, 5% taking report on new admissions, 4% on sign‐out to the night float hospitalist, and 3% receiving sign‐out from the night float hospitalist.

Multitasking, performing more than 1 activity at the same time, was done 21% of the time. Hospitalists received an average of 3.4 1.5 pages per hour, and 7% of total activity time was spent returning pages. Other forms of interruption were not evaluated.

DISCUSSION

Our study had several important findings. First, hospitalists spent most of their time on indirect patient care activities and relatively little time on direct patient care. Time‐motion studies of nonhospitalist physicians have reported similar findings.5, 6 A considerable amount of hospitalist time was spent on documentation. This finding also has been reported in studies of nonhospitalist physicians.5, 7

A unique finding in our study was the large amount of time, 24% of total minutes, spent on communication. A study of emergency medicine physicians by Hollingsworth found that 13% of their time was spent on communication activities.5 The large amount of time spent on communication in our study underscores the need for hospitalists to have outstanding communication skills and systems that support efficient communication. Hospitalists spent 6% of their total time paging other physicians and 7% returning pages. Improvements in the efficiency of paging communication could greatly reduce the amount of time communicating by page. Our paging system provides unidirectional alphanumeric paging. In an effort to improve the efficiency of paging, we have asked nurses and consultants to include FYI and callback in the text of the page so it is clear whether the person who has paged the hospitalist needs to be called back. This simple solution to help reduce the number of unnecessary callbacks has previously been proposed by others.8

Another part of solving this problem is adopting the use of 2‐way pagers instead of alphanumeric pagers. Two‐way paging can increase the efficiency of communication even further. For example, a nurse sends a hospitalist a page that asks if the previous diet orders for a patient just returned from a procedure can be resumed. This hospitalist is on another floor in another patient's room. Rather than spending time leaving the other patient's room, finding a phone, calling the floor, waiting for an answer, and then waiting on hold, the hospitalist simply texts a 1‐word answer, Yes, in the 2‐way paging system. In addition to the time occupied by paging activities, hospitalists spent a large amount of time in face‐to‐face communication (8% of total activity time). On the one hand, having hospitalists discuss patient care with consultants and nurses in person on an ongoing basis throughout the day may improve clinical efficiency. On the other hand, the constant potential for interruption may be problematic. Similarly, 2‐way paging could facilitate communication to such a degree that it could actually increase the frequency of interruptions. Research on improvements in communications systems, interventions to improve communication skills, and team‐based care is warranted in order to evaluate the impact on hospitalist workflow.

An important finding in our study was that multitasking and paging interruptions were common. Although this may come as no surprise to practicing hospitalists, the distraction caused by interruptions and multitasking is an important potential cause of medical errors.911 A thorough examination of the types of activities performed simultaneously and whether they contributed to medical error was beyond the scope of our study. Some activities, such as documenting a note on a patient while reviewing the patient's lab results, are concordant (ie, conducted for the same patient) and therefore may be unlikely to contribute to medical error. Other combinations of activities, such as returning a page about one patient while documenting a note on a different patient or having face‐to‐face communication about one patient while entering an order on another patient, are discordant. Discordant activities may contribute to medical error. Further research of the effect of hospitalist multitasking and interruption on medical error is warranted and should be conducted within the framework of concordant versus discordant activities.

We had hoped to find activities that could be performed by non‐physician providers. No high impact activities were discovered that would be better suited for a non‐physician provider in this study. Clerical tasks, such as calling for radiology orders or obtaining medical records, amounted to a small percentage of hospitalist time (less than 1% combined). We did identify several activities in which automation or process improvement would be helpful. Hospitalists spent 5% of time on the combined activity of documenting discharge instructions and writing out prescriptions. Our institution is in the process of implementing an electronic medical record and computerized physician order entry. We are currently working on an automated process to generate printed discharge instructions and prescriptions. This has the potential not only to improve efficiency, but also to eliminate medication errors, as care is transitioned to the outpatient setting.

Our study had several limitations. First, our findings reflect the experience at one institution. Hospitalist practices vary widely in their staffing and scheduling models as well as in their organizational support. The amount of time that hospitalists spend on activities may differ between practices and between individual hospitalists in the same practice. Another limitation to our study pertains to the workflow of our hospitalists and the locations of their patients. As discussed earlier, patients were assigned to a hospitalist according to time of admission, not location of admission. Because of this, the hospitalists were caring for patients on as many as 5 wards. Although travel time amounted to only 3% of total minutes, it is possible that communication time could have been reduced if patients were distributed to hospitalists on the basis of patient location rather than time of admission of patient. For example, physicians and nurses might spend less time communicating in person compared to communicating via unidirectional paging, which frequently requires waiting for a callback. Finally, our study only observed activities performed by the daytime hospitalists at our hospital. The distribution and types of activities performed by nighttime hospitalists may be somewhat different.

Our study may serve as a model for hospitalist time‐motion studies in other settings. Our findings are of particular importance to resident‐uncovered hospitalist programs in academic hospitals, a setting in which operational inefficiencies may be abundant as house staff members have been poorly positioned in the hospital organization to lobby for process change. We hope that our study is a precursor to research evaluating modifications to the environments and systems in which hospitalists work. Such modifications have the potential to improve productivity and work conditions and promote career satisfaction.

Aortic dissection is an uncommon but highly lethal disease with an incidence of approximately 2,000 cases per year in the United States.1 It is often mistaken for less serious pathology. In one series, aortic dissection was missed in 38% of patients at presentation, with 28% of patients first diagnosed at autopsy.2 Early recognition and management are crucial. If untreated, the mortality rate for acute aortic dissection increases by approximately 1% per hour over the first 48 hours and may reach 70% at 1 week. As many as 90% of untreated patients who suffer aortic dissection die within 3 months of presentation.3, 4 Generally, cardiothoracic surgeons or cardiologists experienced with managing aortic dissection should direct patient evaluation and treatment. Hospitalists, however, are increasingly assuming responsibility for the initial triage and management of patients with acute chest pain syndromes and therefore must be able to rapidly identify aortic dissection, initiate supportive therapy, and refer patients to appropriate specialty care.

PATHOPHYSIOLOGY

Aortic dissection occurs when layers of the aortic wall separate because of infiltration of high‐pressure arterial blood. The proximate causes are elevated shear stress across the aortic lumen in the setting of a concomitant defect in the aortic media. Shear stress is caused by the rapid increase in luminal pressure per unit of time (dP/dt) that results from cardiac systole. As the aorta traverses away from the heart, an increasing proportion of the kinetic energy of left ventricular systole is stored in the aortic wall as potential energy, which facilitates anterograde propagation of cardiac output during diastole. This conversion of kinetic to potential energy also attenuates shear stress. As the proximal aorta is subject to the steepest fluctuations in pressure, it is at the highest risk of dissection. Degeneration of the aortic media is part of the normal aging process but is accelerated in persons with a bicuspid aortic valve, Turner's syndrome, inflammatory arteritis, or inherited diseases of collagen formation.

Once the aortic intima is compromised, blood dissects longitudinally through the aortic media and propagates proximally or distally, creating a false lumen that may communicate with the true lumen of the aorta. Blood may flow through the true lumen, the false lumen, or both. Propagation of the dissection causes much of the morbidity associated with aortic dissection by disrupting blood flow across branch vessels or by directly compromising the pericardium or aortic valve. Over time, the dissection may traverse the entire aortic wall, causing aortic rupture and exsanguination.

CLASSIFICATION

Acute aortic dissection is classified as any aortic dissection diagnosed within 2 weeks of the onset of symptoms, which is the period of highest risk of mortality. Patients who survive more than 2 weeks without treatment are considered to have chronic dissection. Aortic dissections are further classified according to their anatomic location. The fundamental distinction is whether the dissection is proximal (involving the aortic root or ascending aorta) or distal (below the left subclavian artery). The Stanford and DeBakey classification systems are the classification systems most commonly used (Figure 1).

Figure 1

Some variants of aortic dissection are not described in either the Stanford or DeBakey systems. Aortic intramural hematomas (IMH) are caused by intramural hemorrhage of the vasa vasorum without an identifiable intimal tear.57 Penetrating atherosclerotic ulcers (PAUs) are focal defects in the aortic wall with surrounding hematoma but no longitudinal dissection across tissue planes, typically resulting from advanced atherosclerotic disease.8 The pathophysiologic distinctions between IMH, PAU, and classic aortic dissection remain somewhat controversial. Both IMH and PAU may progress to aortic aneurysm formation, frank dissection, or aortic rupture, suggesting that these entities represent a spectrum of diseases with broad overlap (Table 1).9, 10

EPIDEMIOLOGY

Aortic dissection is a rare disease, with an estimated incidence of approximately 5‐30 cases per 1 million people per year.1114 Fewer than 0.5% of patients presenting to an emergency department with chest or back pain suffer from aortic dissection.15 Two thirds of patients are male, with an average age at presentation of approximately 65 years. A history of systemic hypertension, found in up to 72% of patients, is by far the most common risk factor.2, 14, 16 Atherosclerosis, a history of prior cardiac surgery, and known aortic aneurysm are other major risk factors.14 The epidemiology of aortic dissection is substantially different in young patients (<40 years of age). Hypertension and atherosclerosis become significantly less common, as other risk factors, such as Marfan syndrome, take precedence17 (Table 2). Other risk factors for aortic dissection include:

• Collagen diseases (eg, Marfan syndrome and Ehlers‐Danlos): In the International Registry of Acute Aortic Dissection (IRAD), the largest prospective analysis of aortic dissection to date, 50% of the young patients presenting with aortic dissection had Marfan syndrome.17

• Bicuspid aortic valve (BAV): Individuals with BAV are 5‐18 times more likely to suffer aortic dissection than those with a trileaflet valve.18, 19 In one survey, 52% of asymptomatic young men with BAV were found to have aortic root dilatation, a frequent precursor of dissection.20 Vascular tissue in individuals with BAV has been found to have increased levels of matrix metalloproteinases, which may degrade elastic matrix components and accelerate medial necrosis.21

• Aortic coarctation: Aortic coarctation is associated with upper extremity hypertension, BAV and aortic dilatation, all of which predispose to aortic dissection.

• Turner syndrome: Aortic root dilatation with or without dissection has been incidentally noted in 6%‐9% of patients with Turner syndrome.22, 23

• Strenuous exercise: Multiple case reports have associated aortic dissection with high‐intensity weightlifting. Many affected individuals were subsequently found to have at least one other risk factor, including hypertension, anabolic steroid abuse, and cocaine abuse.2426

• Large vessel arteritis: Large vessel arteritides, specifically giant cell arteritis, Takayasu's disease, and tertiary syphilis have long been associated with aortic dilatation and dissection.

• Cocaine and methamphetamine ingestion: Sympathomimetic drugs cause rapid increases in heart rate and blood pressure, markedly increasing aortic intraluminal shear stress. Furthermore, cocaine is thought to be directly toxic to vascular endothelium and may accelerate medial necrosis.2730

• Third trimester pregnancy, especially in patients with diseases of collagen31; The significance of pregnancy has recently been called into question by data from the IRAD trial. Of 346 enrolled women with aortic dissection, only 2 were pregnant, suggesting that the previously held association of pregnancy with aortic dissection may be an artifact of selective reporting.1

• Blunt chest trauma or high‐speed deceleration injury.

• Iatrogenic injury, typically from intra‐aortic catheterization.

INITIAL EVALUATION

The differential diagnosis for acute aortic dissection includes acute coronary syndrome, pulmonary embolus, pneumothorax, pneumonia, musculoskeletal pain, acute cholecystitis, esophageal spasm or rupture, acute pancreatitis, and acute pericarditis. Acute aortic dissections are rarely asymptomatic; in fact, the absence of sudden‐onset chest pain decreases the likelihood of dissection (negative LR 0.3).32 In the IRAD trial, approximately 95% of patients with aortic dissection complained of pain in the chest, back, or abdomen, with 90% characterizing their pain as either severe or the worst ever and 64% describing it as sharp.14 Although the presence of tearing or ripping chest or back pain suggests aortic dissection (positive LR 1.2‐10.8), its absence does not reliably exclude this diagnosis.32 The wide variability in the presentation of aortic dissection increases the challenge of establishing a diagnosis. Clinical findings depend largely on the anatomical location of the dissection and may include pulse deficits, neurologic deficits, hypotension, hypertension, and end‐organ ischemia. Women who develop aortic dissection are generally older and present later than men. Their symptoms are less typical and are likely to be confounded by altered mental status.1 A diagnosis of aortic dissection should be strongly considered for patients presenting with acute chest or back pain and otherwise unexplained aortic insufficiency, focal neurologic deficits, pulse deficits, or end‐organ injury (Table 3).

Electrocardiogram: Electrocardiographic abnormalities are commonly seen in aortic dissection and may include ST‐segment or T‐wave abnormalities or left ventricular hypertrophy.14 Proximal aortic dissections may compromise coronary artery perfusion, generating electrocardiogram (ECG) findings compatible with acute myocardial infarction, which may lead the clinician to diagnose and treat myocardial infarction while missing the underlying diagnosis.33 In a recent survey, 9 of 44 patients (21%) presenting with acute aortic dissection were initially diagnosed with acute coronary syndrome and anticoagulated, with 2 deaths.34 ECGs must therefore be interpreted with extreme caution in aortic dissection.

Chest x‐ray: In the emergency department, chest radiography is a mainstay of the evaluation of acute chest pain. Unfortunately, plain‐film radiography has limited utility for diagnosing aortic dissection.35 In the IRAD trial, mediastinal widening (>8 cm) and abnormal aortic contour, the classic radiographic findings in aortic dissection, were present in only 50%‐60% of cases. Twelve percent of patients had a completely normal chest x‐ray.14 A pooled analysis of previous studies demonstrated that the sensitivity of widened mediastinum and abnormal aortic contour was 65% and 71%, respectively.32 Nonspecific radiographic findings, most notably pleural effusion, were common.36 Thus, if the index of suspicion for aortic dissection is elevated, a confirmatory study must be obtained (Figure 2).

Figure 2

CONFIRMATORY IMAGING STUDIES

The ideal confirmatory imaging modality should identify aortic dissection with high sensitivity and specificity. It should also identify the entry and exit points of the dissection and provide information about the extent of compromise of the aortic valve, pericardium, and great vessels. Four imaging modalities sufficiently meet these criteria in order to be considered diagnostically useful.

Aortography: Previously the gold standard for diagnosing aortic dissection, aortography is no longer a first‐line imaging modality. The sensitivity and specificity of aortography are at best equivalent and probably inferior to less invasive imaging modalities.37, 38 False negatives may occur if both the true and false lumens opacify equally with contrast, or if the false lumen is sufficiently thrombosed to preclude any instillation of contrast. Aortography cannot identify aortic intramural hematomas, is invasive and highly operator dependent, requires nephrotoxic contrast, and generally takes longer to obtain than other modalities.39

Aortography uniquely offers excellent visualization of the coronary arteries and great vessels and is preferred when such information is necessary. Percutaneous aortic endovascular stent grafting has been recently employed to repair distal aortic dissections.4043 As a result, aortography is gaining new life as a therapeutic modality.

CT angiography: Spiral CT angiography (CTA) is the most commonly used modality for diagnosing aortic dissection.44 It is emergently available at most hospitals, and images can be obtained in minutes. Sensitivity and specificity may approach 100%, and CTA may be more sensitive than MRA or TEE in evaluating arch vessel involvement.4547 Like conventional angiography, CTA requires administration of nephrotoxic contrast. It frequently cannot visualize the entry and exit sites (intimal flaps) of a dissection and provides limited information about the coronary arteries and no information about the competency of the aortic valve.48, 49 Thus, if aortic dissection is identified by CTA, a second study may be needed to provide further diagnostic information and to guide surgical intervention (Figures 3 and 4).

Figure 3

Figure 4

Magnetic Resonance Angiography: Magnetic resonance angiography (MRA) offers excellent noninvasive evaluation of the thoracic aorta. Sensitivity and specificity are probably superior to spiral CTA, and MRA generally identifies the location of the intimal tear and provides some functional information about the aortic valve.44, 50, 51 MRA is not emergently available at many hospitals. Scanning is time intensive, requiring the patient to remain motionless and relatively inaccessible for up to an hour. Furthermore, patient claustrophobia and the presence of implanted devices such as pacemakers or ferromagnetic foreign bodies may preclude MRA.

Transesophageal echocardiography: The sensitivity and specificity of transesophageal echocardiography (TEE) are also excellenton a par with CTA and MRA. In addition to providing excellent visualization of the thoracic aorta, TEE provides superb images of the pericardium and detailed assessment of aortic valve function.52 It also is extremely effective at visualizing the aortic intimal flap.44, 49, 53 A significant advantage of TEE is its portability, allowing rapid diagnosis at the bedside. For this reason, it is particularly useful for evaluation of patients who are hemodynamically unstable and are suspected to have an aortic dissection. Because of the anatomic relationship of the aorta with the esophagus and the trachea, TEE more effectively identifies proximal than distal dissections.43 TEE is also somewhat invasive, usually requires patient sedation, and is highly operator dependent, requiring the availability of an experienced and technically skilled operator (Figure 5).

Figure 5

Transthoracic echocardiography: Although it is an excellent tool for the evaluation of many aspects of cardiac anatomy and function, surface echocardiography can reliably visualize only limited portions of the ascending and descending aorta.54, 55 As a consequence, it is neither sensitive nor specific enough to diagnose aortic dissection. Transthoracic echocardiography (TTE) does, however, play a role in rapidly assessing patients at the bedside for aortic valve or pericardial compromise when these complications are suspected.

Recommendations

CTA, MRA, and TEE are all highly sensitive and specific modalities for diagnosing aortic dissection. Therefore, the condition of the patient, the information needed, and the resources and expertise immediately available should drive the choice of study. MRA is considered the gold standard diagnostic study and is the preferred modality for hemodynamically stable patients with suspected aortic dissection. Because of slow data acquisition and the inaccessibility of patients in the scanner, it is generally unsuited for unstable patients, including those with ongoing pain. Bedside TEE is an excellent choice for patients who are too unstable for MRA but is less effective at visualizing distal dissections. Arch aortography is generally reserved for the confirmation of questionable diagnoses or to image specific branch arteries (Tables 4 and 5).

Table 4.Comparative Sensitivities of Imaging Modalities in Aortic Dissection

	Overall	Proximal	Distal
Adapted from Moore et al.43
TEE	88%	90%	80%
CTA	93%	93%	93%
MRA	100%	100%	100%
Aortogram	87%	87%	87%

Table 5.Comparative Diagnostic Utility of Imaging Techniques in Aortic Dissection

	TEE	CTA	MRA	Aortography
Adapted from recommendations of the task force on aortic dissection, European Society of Cardiology.61
Sensitivity	++	++	+++	++
Specificity	+++	++	+++	++
Classification	+++	++	++	+
Intimal flap	+++	‐	++	+
Aortic regurgitation	+++		++	++
Pericardial effusion	+++	++	++
Branch vessel involvement	+	++	++	+++
Coronary artery involvement	++	+	+	+++

Most trials comparing CTA, MRA, and TEE were performed in the early 1990s. Computed tomography has evolved significantly over the intervening decade, and some of the diagnostic limitations previously ascribed to CTA, such as the inability to generate 3‐D reconstructed images, no longer exist. Furthermore, CT angiography is widely available and is gaining increasing acceptance as a first‐line imaging modality for patients with noncardiac chest pain.48 Medical centers that maintain round‐the‐clock CT capability may have limited or delayed access to TEE, MRA, or aortography. Given the potential for rapid and dramatic patient deterioration, it is imperative that a diagnosis be established quickly when aortic dissection is suspected. Thus, when the choice is obtaining an immediate CTA or a delayed TEE or MRA, CTA is generally the better choice (Figure 6).

Figure 6

MANAGEMENT

PROGNOSIS

Despite significant medical and surgical advances, aortic dissection remains exceptionally lethal. Patients with proximal dissections are more likely to die than those with distal dissections. Using data from the IRAD trial, Mehta et al determined that age 70 years (OR, 1.70), abrupt onset of chest pain (OR 2.60), hypotension/shock/tamponade (OR, 2.97), renal failure (OR, 4.77), pulse deficit (OR, 2.03), and abnormal ECG (OR, 1.77) were independent determinants of death.59 Medical treatment of proximal dissection is generally reserved for patients too ill, unstable, or frail to undergo surgery. In contrast, most patients with distal dissection are managed medically, with surgery generally reserved for those with acute complications. Hence, patients with proximal dissections who are managed medically and those with distal dissections who are managed surgically have the worst outcomes. Outcomes for women are worse than those for men, which is probably attributable to several factors. Women dissect at an older age, present later after the onset of symptoms, and are more likely to have confounding symptoms that may delay timely diagnosis1 (Table 7).

CONCLUSION

Aortic dissection is a rare and acutely life‐threatening cause of acute chest and back pain. Delays in diagnosis and misdiagnoses are common, frequently with catastrophic consequences. The key to diagnosis is maintaining a high index of suspicion for dissection, especially in patients who present with acute severe chest, back, or abdominal pain in the setting of unexplained acute pulse deficits, neurologic deficits, or acute end‐organ injury. Three clinical findings have been shown to be diagnostically useful: immediate onset of tearing or ripping chest or back pain, mediastinal widening or abnormal aortic contour on chest radiograph, and peripheral pulse deficits or variable pulse pressure (>20 mm Hg). If all 3 findings are absent, acute aortic dissection is unlikely. The presence of any of these findings should prompt further workup. A normal chest radiograph does not rule out aortic dissection. Only TEE, CT, and MR angiography are sufficiently specific to rule out dissection. Aortography is rarely used as a first‐line diagnostic tool but may be useful as a confirmatory test or to provide additional anatomic information. Patients who present with proximal aortic dissection or with any aortic dissection with concomitant hypotension are at exceptionally high risk of death and should be immediately referred for surgical evaluation. Beta‐blockers are the mainstay of acute and chronic therapy of aortic dissection. Survivors of aortic dissection are at a markedly elevated risk for further aortic events and should be followed vigilantly posthospitalization.

Aortic dissection is an uncommon but highly lethal disease with an incidence of approximately 2,000 cases per year in the United States.1 It is often mistaken for less serious pathology. In one series, aortic dissection was missed in 38% of patients at presentation, with 28% of patients first diagnosed at autopsy.2 Early recognition and management are crucial. If untreated, the mortality rate for acute aortic dissection increases by approximately 1% per hour over the first 48 hours and may reach 70% at 1 week. As many as 90% of untreated patients who suffer aortic dissection die within 3 months of presentation.3, 4 Generally, cardiothoracic surgeons or cardiologists experienced with managing aortic dissection should direct patient evaluation and treatment. Hospitalists, however, are increasingly assuming responsibility for the initial triage and management of patients with acute chest pain syndromes and therefore must be able to rapidly identify aortic dissection, initiate supportive therapy, and refer patients to appropriate specialty care.

PATHOPHYSIOLOGY

Aortic dissection occurs when layers of the aortic wall separate because of infiltration of high‐pressure arterial blood. The proximate causes are elevated shear stress across the aortic lumen in the setting of a concomitant defect in the aortic media. Shear stress is caused by the rapid increase in luminal pressure per unit of time (dP/dt) that results from cardiac systole. As the aorta traverses away from the heart, an increasing proportion of the kinetic energy of left ventricular systole is stored in the aortic wall as potential energy, which facilitates anterograde propagation of cardiac output during diastole. This conversion of kinetic to potential energy also attenuates shear stress. As the proximal aorta is subject to the steepest fluctuations in pressure, it is at the highest risk of dissection. Degeneration of the aortic media is part of the normal aging process but is accelerated in persons with a bicuspid aortic valve, Turner's syndrome, inflammatory arteritis, or inherited diseases of collagen formation.

Once the aortic intima is compromised, blood dissects longitudinally through the aortic media and propagates proximally or distally, creating a false lumen that may communicate with the true lumen of the aorta. Blood may flow through the true lumen, the false lumen, or both. Propagation of the dissection causes much of the morbidity associated with aortic dissection by disrupting blood flow across branch vessels or by directly compromising the pericardium or aortic valve. Over time, the dissection may traverse the entire aortic wall, causing aortic rupture and exsanguination.

CLASSIFICATION

Acute aortic dissection is classified as any aortic dissection diagnosed within 2 weeks of the onset of symptoms, which is the period of highest risk of mortality. Patients who survive more than 2 weeks without treatment are considered to have chronic dissection. Aortic dissections are further classified according to their anatomic location. The fundamental distinction is whether the dissection is proximal (involving the aortic root or ascending aorta) or distal (below the left subclavian artery). The Stanford and DeBakey classification systems are the classification systems most commonly used (Figure 1).

Figure 1

Some variants of aortic dissection are not described in either the Stanford or DeBakey systems. Aortic intramural hematomas (IMH) are caused by intramural hemorrhage of the vasa vasorum without an identifiable intimal tear.57 Penetrating atherosclerotic ulcers (PAUs) are focal defects in the aortic wall with surrounding hematoma but no longitudinal dissection across tissue planes, typically resulting from advanced atherosclerotic disease.8 The pathophysiologic distinctions between IMH, PAU, and classic aortic dissection remain somewhat controversial. Both IMH and PAU may progress to aortic aneurysm formation, frank dissection, or aortic rupture, suggesting that these entities represent a spectrum of diseases with broad overlap (Table 1).9, 10

EPIDEMIOLOGY

Aortic dissection is a rare disease, with an estimated incidence of approximately 5‐30 cases per 1 million people per year.1114 Fewer than 0.5% of patients presenting to an emergency department with chest or back pain suffer from aortic dissection.15 Two thirds of patients are male, with an average age at presentation of approximately 65 years. A history of systemic hypertension, found in up to 72% of patients, is by far the most common risk factor.2, 14, 16 Atherosclerosis, a history of prior cardiac surgery, and known aortic aneurysm are other major risk factors.14 The epidemiology of aortic dissection is substantially different in young patients (<40 years of age). Hypertension and atherosclerosis become significantly less common, as other risk factors, such as Marfan syndrome, take precedence17 (Table 2). Other risk factors for aortic dissection include:

• Collagen diseases (eg, Marfan syndrome and Ehlers‐Danlos): In the International Registry of Acute Aortic Dissection (IRAD), the largest prospective analysis of aortic dissection to date, 50% of the young patients presenting with aortic dissection had Marfan syndrome.17

• Bicuspid aortic valve (BAV): Individuals with BAV are 5‐18 times more likely to suffer aortic dissection than those with a trileaflet valve.18, 19 In one survey, 52% of asymptomatic young men with BAV were found to have aortic root dilatation, a frequent precursor of dissection.20 Vascular tissue in individuals with BAV has been found to have increased levels of matrix metalloproteinases, which may degrade elastic matrix components and accelerate medial necrosis.21

• Aortic coarctation: Aortic coarctation is associated with upper extremity hypertension, BAV and aortic dilatation, all of which predispose to aortic dissection.

• Turner syndrome: Aortic root dilatation with or without dissection has been incidentally noted in 6%‐9% of patients with Turner syndrome.22, 23

• Strenuous exercise: Multiple case reports have associated aortic dissection with high‐intensity weightlifting. Many affected individuals were subsequently found to have at least one other risk factor, including hypertension, anabolic steroid abuse, and cocaine abuse.2426

• Large vessel arteritis: Large vessel arteritides, specifically giant cell arteritis, Takayasu's disease, and tertiary syphilis have long been associated with aortic dilatation and dissection.

• Cocaine and methamphetamine ingestion: Sympathomimetic drugs cause rapid increases in heart rate and blood pressure, markedly increasing aortic intraluminal shear stress. Furthermore, cocaine is thought to be directly toxic to vascular endothelium and may accelerate medial necrosis.2730

• Third trimester pregnancy, especially in patients with diseases of collagen31; The significance of pregnancy has recently been called into question by data from the IRAD trial. Of 346 enrolled women with aortic dissection, only 2 were pregnant, suggesting that the previously held association of pregnancy with aortic dissection may be an artifact of selective reporting.1

• Blunt chest trauma or high‐speed deceleration injury.

• Iatrogenic injury, typically from intra‐aortic catheterization.

INITIAL EVALUATION

The differential diagnosis for acute aortic dissection includes acute coronary syndrome, pulmonary embolus, pneumothorax, pneumonia, musculoskeletal pain, acute cholecystitis, esophageal spasm or rupture, acute pancreatitis, and acute pericarditis. Acute aortic dissections are rarely asymptomatic; in fact, the absence of sudden‐onset chest pain decreases the likelihood of dissection (negative LR 0.3).32 In the IRAD trial, approximately 95% of patients with aortic dissection complained of pain in the chest, back, or abdomen, with 90% characterizing their pain as either severe or the worst ever and 64% describing it as sharp.14 Although the presence of tearing or ripping chest or back pain suggests aortic dissection (positive LR 1.2‐10.8), its absence does not reliably exclude this diagnosis.32 The wide variability in the presentation of aortic dissection increases the challenge of establishing a diagnosis. Clinical findings depend largely on the anatomical location of the dissection and may include pulse deficits, neurologic deficits, hypotension, hypertension, and end‐organ ischemia. Women who develop aortic dissection are generally older and present later than men. Their symptoms are less typical and are likely to be confounded by altered mental status.1 A diagnosis of aortic dissection should be strongly considered for patients presenting with acute chest or back pain and otherwise unexplained aortic insufficiency, focal neurologic deficits, pulse deficits, or end‐organ injury (Table 3).

Electrocardiogram: Electrocardiographic abnormalities are commonly seen in aortic dissection and may include ST‐segment or T‐wave abnormalities or left ventricular hypertrophy.14 Proximal aortic dissections may compromise coronary artery perfusion, generating electrocardiogram (ECG) findings compatible with acute myocardial infarction, which may lead the clinician to diagnose and treat myocardial infarction while missing the underlying diagnosis.33 In a recent survey, 9 of 44 patients (21%) presenting with acute aortic dissection were initially diagnosed with acute coronary syndrome and anticoagulated, with 2 deaths.34 ECGs must therefore be interpreted with extreme caution in aortic dissection.

Chest x‐ray: In the emergency department, chest radiography is a mainstay of the evaluation of acute chest pain. Unfortunately, plain‐film radiography has limited utility for diagnosing aortic dissection.35 In the IRAD trial, mediastinal widening (>8 cm) and abnormal aortic contour, the classic radiographic findings in aortic dissection, were present in only 50%‐60% of cases. Twelve percent of patients had a completely normal chest x‐ray.14 A pooled analysis of previous studies demonstrated that the sensitivity of widened mediastinum and abnormal aortic contour was 65% and 71%, respectively.32 Nonspecific radiographic findings, most notably pleural effusion, were common.36 Thus, if the index of suspicion for aortic dissection is elevated, a confirmatory study must be obtained (Figure 2).

Figure 2

CONFIRMATORY IMAGING STUDIES

The ideal confirmatory imaging modality should identify aortic dissection with high sensitivity and specificity. It should also identify the entry and exit points of the dissection and provide information about the extent of compromise of the aortic valve, pericardium, and great vessels. Four imaging modalities sufficiently meet these criteria in order to be considered diagnostically useful.

Aortography: Previously the gold standard for diagnosing aortic dissection, aortography is no longer a first‐line imaging modality. The sensitivity and specificity of aortography are at best equivalent and probably inferior to less invasive imaging modalities.37, 38 False negatives may occur if both the true and false lumens opacify equally with contrast, or if the false lumen is sufficiently thrombosed to preclude any instillation of contrast. Aortography cannot identify aortic intramural hematomas, is invasive and highly operator dependent, requires nephrotoxic contrast, and generally takes longer to obtain than other modalities.39

Aortography uniquely offers excellent visualization of the coronary arteries and great vessels and is preferred when such information is necessary. Percutaneous aortic endovascular stent grafting has been recently employed to repair distal aortic dissections.4043 As a result, aortography is gaining new life as a therapeutic modality.

CT angiography: Spiral CT angiography (CTA) is the most commonly used modality for diagnosing aortic dissection.44 It is emergently available at most hospitals, and images can be obtained in minutes. Sensitivity and specificity may approach 100%, and CTA may be more sensitive than MRA or TEE in evaluating arch vessel involvement.4547 Like conventional angiography, CTA requires administration of nephrotoxic contrast. It frequently cannot visualize the entry and exit sites (intimal flaps) of a dissection and provides limited information about the coronary arteries and no information about the competency of the aortic valve.48, 49 Thus, if aortic dissection is identified by CTA, a second study may be needed to provide further diagnostic information and to guide surgical intervention (Figures 3 and 4).

Figure 3

Figure 4

Magnetic Resonance Angiography: Magnetic resonance angiography (MRA) offers excellent noninvasive evaluation of the thoracic aorta. Sensitivity and specificity are probably superior to spiral CTA, and MRA generally identifies the location of the intimal tear and provides some functional information about the aortic valve.44, 50, 51 MRA is not emergently available at many hospitals. Scanning is time intensive, requiring the patient to remain motionless and relatively inaccessible for up to an hour. Furthermore, patient claustrophobia and the presence of implanted devices such as pacemakers or ferromagnetic foreign bodies may preclude MRA.

Transesophageal echocardiography: The sensitivity and specificity of transesophageal echocardiography (TEE) are also excellenton a par with CTA and MRA. In addition to providing excellent visualization of the thoracic aorta, TEE provides superb images of the pericardium and detailed assessment of aortic valve function.52 It also is extremely effective at visualizing the aortic intimal flap.44, 49, 53 A significant advantage of TEE is its portability, allowing rapid diagnosis at the bedside. For this reason, it is particularly useful for evaluation of patients who are hemodynamically unstable and are suspected to have an aortic dissection. Because of the anatomic relationship of the aorta with the esophagus and the trachea, TEE more effectively identifies proximal than distal dissections.43 TEE is also somewhat invasive, usually requires patient sedation, and is highly operator dependent, requiring the availability of an experienced and technically skilled operator (Figure 5).

Figure 5

Transthoracic echocardiography: Although it is an excellent tool for the evaluation of many aspects of cardiac anatomy and function, surface echocardiography can reliably visualize only limited portions of the ascending and descending aorta.54, 55 As a consequence, it is neither sensitive nor specific enough to diagnose aortic dissection. Transthoracic echocardiography (TTE) does, however, play a role in rapidly assessing patients at the bedside for aortic valve or pericardial compromise when these complications are suspected.

Recommendations

CTA, MRA, and TEE are all highly sensitive and specific modalities for diagnosing aortic dissection. Therefore, the condition of the patient, the information needed, and the resources and expertise immediately available should drive the choice of study. MRA is considered the gold standard diagnostic study and is the preferred modality for hemodynamically stable patients with suspected aortic dissection. Because of slow data acquisition and the inaccessibility of patients in the scanner, it is generally unsuited for unstable patients, including those with ongoing pain. Bedside TEE is an excellent choice for patients who are too unstable for MRA but is less effective at visualizing distal dissections. Arch aortography is generally reserved for the confirmation of questionable diagnoses or to image specific branch arteries (Tables 4 and 5).

Table 4.Comparative Sensitivities of Imaging Modalities in Aortic Dissection

	Overall	Proximal	Distal
Adapted from Moore et al.43
TEE	88%	90%	80%
CTA	93%	93%	93%
MRA	100%	100%	100%
Aortogram	87%	87%	87%

Table 5.Comparative Diagnostic Utility of Imaging Techniques in Aortic Dissection

	TEE	CTA	MRA	Aortography
Adapted from recommendations of the task force on aortic dissection, European Society of Cardiology.61
Sensitivity	++	++	+++	++
Specificity	+++	++	+++	++
Classification	+++	++	++	+
Intimal flap	+++	‐	++	+
Aortic regurgitation	+++		++	++
Pericardial effusion	+++	++	++
Branch vessel involvement	+	++	++	+++
Coronary artery involvement	++	+	+	+++

Most trials comparing CTA, MRA, and TEE were performed in the early 1990s. Computed tomography has evolved significantly over the intervening decade, and some of the diagnostic limitations previously ascribed to CTA, such as the inability to generate 3‐D reconstructed images, no longer exist. Furthermore, CT angiography is widely available and is gaining increasing acceptance as a first‐line imaging modality for patients with noncardiac chest pain.48 Medical centers that maintain round‐the‐clock CT capability may have limited or delayed access to TEE, MRA, or aortography. Given the potential for rapid and dramatic patient deterioration, it is imperative that a diagnosis be established quickly when aortic dissection is suspected. Thus, when the choice is obtaining an immediate CTA or a delayed TEE or MRA, CTA is generally the better choice (Figure 6).

Figure 6

MANAGEMENT

PROGNOSIS

Despite significant medical and surgical advances, aortic dissection remains exceptionally lethal. Patients with proximal dissections are more likely to die than those with distal dissections. Using data from the IRAD trial, Mehta et al determined that age 70 years (OR, 1.70), abrupt onset of chest pain (OR 2.60), hypotension/shock/tamponade (OR, 2.97), renal failure (OR, 4.77), pulse deficit (OR, 2.03), and abnormal ECG (OR, 1.77) were independent determinants of death.59 Medical treatment of proximal dissection is generally reserved for patients too ill, unstable, or frail to undergo surgery. In contrast, most patients with distal dissection are managed medically, with surgery generally reserved for those with acute complications. Hence, patients with proximal dissections who are managed medically and those with distal dissections who are managed surgically have the worst outcomes. Outcomes for women are worse than those for men, which is probably attributable to several factors. Women dissect at an older age, present later after the onset of symptoms, and are more likely to have confounding symptoms that may delay timely diagnosis1 (Table 7).

CONCLUSION

Aortic dissection is a rare and acutely life‐threatening cause of acute chest and back pain. Delays in diagnosis and misdiagnoses are common, frequently with catastrophic consequences. The key to diagnosis is maintaining a high index of suspicion for dissection, especially in patients who present with acute severe chest, back, or abdominal pain in the setting of unexplained acute pulse deficits, neurologic deficits, or acute end‐organ injury. Three clinical findings have been shown to be diagnostically useful: immediate onset of tearing or ripping chest or back pain, mediastinal widening or abnormal aortic contour on chest radiograph, and peripheral pulse deficits or variable pulse pressure (>20 mm Hg). If all 3 findings are absent, acute aortic dissection is unlikely. The presence of any of these findings should prompt further workup. A normal chest radiograph does not rule out aortic dissection. Only TEE, CT, and MR angiography are sufficiently specific to rule out dissection. Aortography is rarely used as a first‐line diagnostic tool but may be useful as a confirmatory test or to provide additional anatomic information. Patients who present with proximal aortic dissection or with any aortic dissection with concomitant hypotension are at exceptionally high risk of death and should be immediately referred for surgical evaluation. Beta‐blockers are the mainstay of acute and chronic therapy of aortic dissection. Survivors of aortic dissection are at a markedly elevated risk for further aortic events and should be followed vigilantly posthospitalization.

Aortic dissection is an uncommon but highly lethal disease with an incidence of approximately 2,000 cases per year in the United States.1 It is often mistaken for less serious pathology. In one series, aortic dissection was missed in 38% of patients at presentation, with 28% of patients first diagnosed at autopsy.2 Early recognition and management are crucial. If untreated, the mortality rate for acute aortic dissection increases by approximately 1% per hour over the first 48 hours and may reach 70% at 1 week. As many as 90% of untreated patients who suffer aortic dissection die within 3 months of presentation.3, 4 Generally, cardiothoracic surgeons or cardiologists experienced with managing aortic dissection should direct patient evaluation and treatment. Hospitalists, however, are increasingly assuming responsibility for the initial triage and management of patients with acute chest pain syndromes and therefore must be able to rapidly identify aortic dissection, initiate supportive therapy, and refer patients to appropriate specialty care.

PATHOPHYSIOLOGY

Aortic dissection occurs when layers of the aortic wall separate because of infiltration of high‐pressure arterial blood. The proximate causes are elevated shear stress across the aortic lumen in the setting of a concomitant defect in the aortic media. Shear stress is caused by the rapid increase in luminal pressure per unit of time (dP/dt) that results from cardiac systole. As the aorta traverses away from the heart, an increasing proportion of the kinetic energy of left ventricular systole is stored in the aortic wall as potential energy, which facilitates anterograde propagation of cardiac output during diastole. This conversion of kinetic to potential energy also attenuates shear stress. As the proximal aorta is subject to the steepest fluctuations in pressure, it is at the highest risk of dissection. Degeneration of the aortic media is part of the normal aging process but is accelerated in persons with a bicuspid aortic valve, Turner's syndrome, inflammatory arteritis, or inherited diseases of collagen formation.

Once the aortic intima is compromised, blood dissects longitudinally through the aortic media and propagates proximally or distally, creating a false lumen that may communicate with the true lumen of the aorta. Blood may flow through the true lumen, the false lumen, or both. Propagation of the dissection causes much of the morbidity associated with aortic dissection by disrupting blood flow across branch vessels or by directly compromising the pericardium or aortic valve. Over time, the dissection may traverse the entire aortic wall, causing aortic rupture and exsanguination.

CLASSIFICATION

Acute aortic dissection is classified as any aortic dissection diagnosed within 2 weeks of the onset of symptoms, which is the period of highest risk of mortality. Patients who survive more than 2 weeks without treatment are considered to have chronic dissection. Aortic dissections are further classified according to their anatomic location. The fundamental distinction is whether the dissection is proximal (involving the aortic root or ascending aorta) or distal (below the left subclavian artery). The Stanford and DeBakey classification systems are the classification systems most commonly used (Figure 1).

Figure 1

Some variants of aortic dissection are not described in either the Stanford or DeBakey systems. Aortic intramural hematomas (IMH) are caused by intramural hemorrhage of the vasa vasorum without an identifiable intimal tear.57 Penetrating atherosclerotic ulcers (PAUs) are focal defects in the aortic wall with surrounding hematoma but no longitudinal dissection across tissue planes, typically resulting from advanced atherosclerotic disease.8 The pathophysiologic distinctions between IMH, PAU, and classic aortic dissection remain somewhat controversial. Both IMH and PAU may progress to aortic aneurysm formation, frank dissection, or aortic rupture, suggesting that these entities represent a spectrum of diseases with broad overlap (Table 1).9, 10

EPIDEMIOLOGY

Aortic dissection is a rare disease, with an estimated incidence of approximately 5‐30 cases per 1 million people per year.1114 Fewer than 0.5% of patients presenting to an emergency department with chest or back pain suffer from aortic dissection.15 Two thirds of patients are male, with an average age at presentation of approximately 65 years. A history of systemic hypertension, found in up to 72% of patients, is by far the most common risk factor.2, 14, 16 Atherosclerosis, a history of prior cardiac surgery, and known aortic aneurysm are other major risk factors.14 The epidemiology of aortic dissection is substantially different in young patients (<40 years of age). Hypertension and atherosclerosis become significantly less common, as other risk factors, such as Marfan syndrome, take precedence17 (Table 2). Other risk factors for aortic dissection include:

• Collagen diseases (eg, Marfan syndrome and Ehlers‐Danlos): In the International Registry of Acute Aortic Dissection (IRAD), the largest prospective analysis of aortic dissection to date, 50% of the young patients presenting with aortic dissection had Marfan syndrome.17

• Bicuspid aortic valve (BAV): Individuals with BAV are 5‐18 times more likely to suffer aortic dissection than those with a trileaflet valve.18, 19 In one survey, 52% of asymptomatic young men with BAV were found to have aortic root dilatation, a frequent precursor of dissection.20 Vascular tissue in individuals with BAV has been found to have increased levels of matrix metalloproteinases, which may degrade elastic matrix components and accelerate medial necrosis.21

• Aortic coarctation: Aortic coarctation is associated with upper extremity hypertension, BAV and aortic dilatation, all of which predispose to aortic dissection.

• Turner syndrome: Aortic root dilatation with or without dissection has been incidentally noted in 6%‐9% of patients with Turner syndrome.22, 23

• Strenuous exercise: Multiple case reports have associated aortic dissection with high‐intensity weightlifting. Many affected individuals were subsequently found to have at least one other risk factor, including hypertension, anabolic steroid abuse, and cocaine abuse.2426

• Large vessel arteritis: Large vessel arteritides, specifically giant cell arteritis, Takayasu's disease, and tertiary syphilis have long been associated with aortic dilatation and dissection.

• Cocaine and methamphetamine ingestion: Sympathomimetic drugs cause rapid increases in heart rate and blood pressure, markedly increasing aortic intraluminal shear stress. Furthermore, cocaine is thought to be directly toxic to vascular endothelium and may accelerate medial necrosis.2730

• Third trimester pregnancy, especially in patients with diseases of collagen31; The significance of pregnancy has recently been called into question by data from the IRAD trial. Of 346 enrolled women with aortic dissection, only 2 were pregnant, suggesting that the previously held association of pregnancy with aortic dissection may be an artifact of selective reporting.1

• Blunt chest trauma or high‐speed deceleration injury.

• Iatrogenic injury, typically from intra‐aortic catheterization.

INITIAL EVALUATION

The differential diagnosis for acute aortic dissection includes acute coronary syndrome, pulmonary embolus, pneumothorax, pneumonia, musculoskeletal pain, acute cholecystitis, esophageal spasm or rupture, acute pancreatitis, and acute pericarditis. Acute aortic dissections are rarely asymptomatic; in fact, the absence of sudden‐onset chest pain decreases the likelihood of dissection (negative LR 0.3).32 In the IRAD trial, approximately 95% of patients with aortic dissection complained of pain in the chest, back, or abdomen, with 90% characterizing their pain as either severe or the worst ever and 64% describing it as sharp.14 Although the presence of tearing or ripping chest or back pain suggests aortic dissection (positive LR 1.2‐10.8), its absence does not reliably exclude this diagnosis.32 The wide variability in the presentation of aortic dissection increases the challenge of establishing a diagnosis. Clinical findings depend largely on the anatomical location of the dissection and may include pulse deficits, neurologic deficits, hypotension, hypertension, and end‐organ ischemia. Women who develop aortic dissection are generally older and present later than men. Their symptoms are less typical and are likely to be confounded by altered mental status.1 A diagnosis of aortic dissection should be strongly considered for patients presenting with acute chest or back pain and otherwise unexplained aortic insufficiency, focal neurologic deficits, pulse deficits, or end‐organ injury (Table 3).

Electrocardiogram: Electrocardiographic abnormalities are commonly seen in aortic dissection and may include ST‐segment or T‐wave abnormalities or left ventricular hypertrophy.14 Proximal aortic dissections may compromise coronary artery perfusion, generating electrocardiogram (ECG) findings compatible with acute myocardial infarction, which may lead the clinician to diagnose and treat myocardial infarction while missing the underlying diagnosis.33 In a recent survey, 9 of 44 patients (21%) presenting with acute aortic dissection were initially diagnosed with acute coronary syndrome and anticoagulated, with 2 deaths.34 ECGs must therefore be interpreted with extreme caution in aortic dissection.

Chest x‐ray: In the emergency department, chest radiography is a mainstay of the evaluation of acute chest pain. Unfortunately, plain‐film radiography has limited utility for diagnosing aortic dissection.35 In the IRAD trial, mediastinal widening (>8 cm) and abnormal aortic contour, the classic radiographic findings in aortic dissection, were present in only 50%‐60% of cases. Twelve percent of patients had a completely normal chest x‐ray.14 A pooled analysis of previous studies demonstrated that the sensitivity of widened mediastinum and abnormal aortic contour was 65% and 71%, respectively.32 Nonspecific radiographic findings, most notably pleural effusion, were common.36 Thus, if the index of suspicion for aortic dissection is elevated, a confirmatory study must be obtained (Figure 2).

Figure 2

CONFIRMATORY IMAGING STUDIES

The ideal confirmatory imaging modality should identify aortic dissection with high sensitivity and specificity. It should also identify the entry and exit points of the dissection and provide information about the extent of compromise of the aortic valve, pericardium, and great vessels. Four imaging modalities sufficiently meet these criteria in order to be considered diagnostically useful.

Aortography: Previously the gold standard for diagnosing aortic dissection, aortography is no longer a first‐line imaging modality. The sensitivity and specificity of aortography are at best equivalent and probably inferior to less invasive imaging modalities.37, 38 False negatives may occur if both the true and false lumens opacify equally with contrast, or if the false lumen is sufficiently thrombosed to preclude any instillation of contrast. Aortography cannot identify aortic intramural hematomas, is invasive and highly operator dependent, requires nephrotoxic contrast, and generally takes longer to obtain than other modalities.39

Aortography uniquely offers excellent visualization of the coronary arteries and great vessels and is preferred when such information is necessary. Percutaneous aortic endovascular stent grafting has been recently employed to repair distal aortic dissections.4043 As a result, aortography is gaining new life as a therapeutic modality.

CT angiography: Spiral CT angiography (CTA) is the most commonly used modality for diagnosing aortic dissection.44 It is emergently available at most hospitals, and images can be obtained in minutes. Sensitivity and specificity may approach 100%, and CTA may be more sensitive than MRA or TEE in evaluating arch vessel involvement.4547 Like conventional angiography, CTA requires administration of nephrotoxic contrast. It frequently cannot visualize the entry and exit sites (intimal flaps) of a dissection and provides limited information about the coronary arteries and no information about the competency of the aortic valve.48, 49 Thus, if aortic dissection is identified by CTA, a second study may be needed to provide further diagnostic information and to guide surgical intervention (Figures 3 and 4).

Figure 3

Figure 4

Magnetic Resonance Angiography: Magnetic resonance angiography (MRA) offers excellent noninvasive evaluation of the thoracic aorta. Sensitivity and specificity are probably superior to spiral CTA, and MRA generally identifies the location of the intimal tear and provides some functional information about the aortic valve.44, 50, 51 MRA is not emergently available at many hospitals. Scanning is time intensive, requiring the patient to remain motionless and relatively inaccessible for up to an hour. Furthermore, patient claustrophobia and the presence of implanted devices such as pacemakers or ferromagnetic foreign bodies may preclude MRA.

Transesophageal echocardiography: The sensitivity and specificity of transesophageal echocardiography (TEE) are also excellenton a par with CTA and MRA. In addition to providing excellent visualization of the thoracic aorta, TEE provides superb images of the pericardium and detailed assessment of aortic valve function.52 It also is extremely effective at visualizing the aortic intimal flap.44, 49, 53 A significant advantage of TEE is its portability, allowing rapid diagnosis at the bedside. For this reason, it is particularly useful for evaluation of patients who are hemodynamically unstable and are suspected to have an aortic dissection. Because of the anatomic relationship of the aorta with the esophagus and the trachea, TEE more effectively identifies proximal than distal dissections.43 TEE is also somewhat invasive, usually requires patient sedation, and is highly operator dependent, requiring the availability of an experienced and technically skilled operator (Figure 5).

Figure 5

Transthoracic echocardiography: Although it is an excellent tool for the evaluation of many aspects of cardiac anatomy and function, surface echocardiography can reliably visualize only limited portions of the ascending and descending aorta.54, 55 As a consequence, it is neither sensitive nor specific enough to diagnose aortic dissection. Transthoracic echocardiography (TTE) does, however, play a role in rapidly assessing patients at the bedside for aortic valve or pericardial compromise when these complications are suspected.

Recommendations

CTA, MRA, and TEE are all highly sensitive and specific modalities for diagnosing aortic dissection. Therefore, the condition of the patient, the information needed, and the resources and expertise immediately available should drive the choice of study. MRA is considered the gold standard diagnostic study and is the preferred modality for hemodynamically stable patients with suspected aortic dissection. Because of slow data acquisition and the inaccessibility of patients in the scanner, it is generally unsuited for unstable patients, including those with ongoing pain. Bedside TEE is an excellent choice for patients who are too unstable for MRA but is less effective at visualizing distal dissections. Arch aortography is generally reserved for the confirmation of questionable diagnoses or to image specific branch arteries (Tables 4 and 5).

Table 4.Comparative Sensitivities of Imaging Modalities in Aortic Dissection

	Overall	Proximal	Distal
Adapted from Moore et al.43
TEE	88%	90%	80%
CTA	93%	93%	93%
MRA	100%	100%	100%
Aortogram	87%	87%	87%

Table 5.Comparative Diagnostic Utility of Imaging Techniques in Aortic Dissection

	TEE	CTA	MRA	Aortography
Adapted from recommendations of the task force on aortic dissection, European Society of Cardiology.61
Sensitivity	++	++	+++	++
Specificity	+++	++	+++	++
Classification	+++	++	++	+
Intimal flap	+++	‐	++	+
Aortic regurgitation	+++		++	++
Pericardial effusion	+++	++	++
Branch vessel involvement	+	++	++	+++
Coronary artery involvement	++	+	+	+++

Most trials comparing CTA, MRA, and TEE were performed in the early 1990s. Computed tomography has evolved significantly over the intervening decade, and some of the diagnostic limitations previously ascribed to CTA, such as the inability to generate 3‐D reconstructed images, no longer exist. Furthermore, CT angiography is widely available and is gaining increasing acceptance as a first‐line imaging modality for patients with noncardiac chest pain.48 Medical centers that maintain round‐the‐clock CT capability may have limited or delayed access to TEE, MRA, or aortography. Given the potential for rapid and dramatic patient deterioration, it is imperative that a diagnosis be established quickly when aortic dissection is suspected. Thus, when the choice is obtaining an immediate CTA or a delayed TEE or MRA, CTA is generally the better choice (Figure 6).

Figure 6

MANAGEMENT

PROGNOSIS

Despite significant medical and surgical advances, aortic dissection remains exceptionally lethal. Patients with proximal dissections are more likely to die than those with distal dissections. Using data from the IRAD trial, Mehta et al determined that age 70 years (OR, 1.70), abrupt onset of chest pain (OR 2.60), hypotension/shock/tamponade (OR, 2.97), renal failure (OR, 4.77), pulse deficit (OR, 2.03), and abnormal ECG (OR, 1.77) were independent determinants of death.59 Medical treatment of proximal dissection is generally reserved for patients too ill, unstable, or frail to undergo surgery. In contrast, most patients with distal dissection are managed medically, with surgery generally reserved for those with acute complications. Hence, patients with proximal dissections who are managed medically and those with distal dissections who are managed surgically have the worst outcomes. Outcomes for women are worse than those for men, which is probably attributable to several factors. Women dissect at an older age, present later after the onset of symptoms, and are more likely to have confounding symptoms that may delay timely diagnosis1 (Table 7).

CONCLUSION

Aortic dissection is a rare and acutely life‐threatening cause of acute chest and back pain. Delays in diagnosis and misdiagnoses are common, frequently with catastrophic consequences. The key to diagnosis is maintaining a high index of suspicion for dissection, especially in patients who present with acute severe chest, back, or abdominal pain in the setting of unexplained acute pulse deficits, neurologic deficits, or acute end‐organ injury. Three clinical findings have been shown to be diagnostically useful: immediate onset of tearing or ripping chest or back pain, mediastinal widening or abnormal aortic contour on chest radiograph, and peripheral pulse deficits or variable pulse pressure (>20 mm Hg). If all 3 findings are absent, acute aortic dissection is unlikely. The presence of any of these findings should prompt further workup. A normal chest radiograph does not rule out aortic dissection. Only TEE, CT, and MR angiography are sufficiently specific to rule out dissection. Aortography is rarely used as a first‐line diagnostic tool but may be useful as a confirmatory test or to provide additional anatomic information. Patients who present with proximal aortic dissection or with any aortic dissection with concomitant hypotension are at exceptionally high risk of death and should be immediately referred for surgical evaluation. Beta‐blockers are the mainstay of acute and chronic therapy of aortic dissection. Survivors of aortic dissection are at a markedly elevated risk for further aortic events and should be followed vigilantly posthospitalization.