Vikas I. Parekh, MD

The growth of academic hospital medicine has been driven by multiple factors including expanding clinical needs, housestaff duty hours' limitations, and an increasing focus on quality and patient safety.1 Hospitalists at academic medical centers frequently assume roles that differ substantially from traditional faculty positions. Academic hospitalists may have predominantly clinical positions, and may be involved in quality improvement and patient safety projects.24 Because of these commitments, many academic hospitalists spend less time on research or educational efforts.1, 5 Many have raised concerns that these unique job descriptions might lead to less time to devote to scholarship and academic pursuits, and consequently greater challenges in the promotions process.2, 5

There are little published data on promotion and tenure in academics, and even less specifically focused on the promotion of hospitalists. Theoretically, promotion should recognize an individual's contribution to his or her institution and field. However, each institution has unique criteria though which faculty achieve promotion. Previous articles addressing specific groups, such as part‐time,6 clinical faculty,79 or clinician‐educators10 may be relevant to hospitalists, as hospitalists may be more likely to fall into these categories. These reports suggest general agreement that promotion committees should consider and weigh clinical and educational work (in addition to scholarly publications) in the promotions process, but assessment methods vary across institutions and the contribution of activities, such as quality improvement, remain unclear. The educator's portfolio has gained momentum as a way to document valued teaching in many institutions,11, 12 but academic hospitalist participation in education may be limited.13

Literature related to the development of Divisions of General Internal Medicine is relevant insofar as similar concerns for promotion were expressed with the growth of their faculty.14, 15 However, its applicability may be limited by differences between roles of hospitalists and more traditional general medicine faculty.

To better understand the factors influencing promotion for academic hospitalists, the Society of General Internal Medicine (SGIM) Academic Hospitalist Task Force (AHTF) undertook a survey of promoted hospitalists who had successfully reached the rank of Associate Professor or higher.

Methods

Results

Of the 33 hospitalists who received the survey, 26 responded (response rate of 79%). Of these, 25 completed the survey in its entirely and were included in our analysis; 1 did not submit details regarding specific promotion‐related activities. General information regarding the respondents and their programs at the time of their promotion is contained in Table 1.

The seven nonrespondents were from seven different institutions; however two of these institutions were represented by respondents. One nonrespondent had achieved a rank of Professor (through general medicine); the rest had been promoted to Associate Professor. One nonrespondent is known by the authors to hold a research position.

Ten respondents identified themselves as clinician‐educators (40%), ten as clinician‐administrators (40%), and five as clinician‐researchers (20%). Seventeen (68%) of the promoted hospitalists were not on a tenure track (as defined by them); they were more likely to have administrative or educational roles than a research appointment. Though the majority of self‐identified researchers were among the earliest to have been promoted, there were no statistically significant differences in self‐defined job description between more and less recently promoted hospitalists.

Promoted hospitalists were involved in a diverse range of activities which supported their promotion, including service (eg, institutional committees), education, research, and quality improvement. Nearly all hospitalists surveyed listed teaching and educational activities, and almost all had disseminated scholarly output and some degree of grant funding. Table 2 lists the specific activities in which respondents reported being engaged in each of these domains.

A range of individuals assisted the respondents in the promotion process. Twenty‐three (92%) respondents identified the individuals who supported their promotion, and all listed more than one person. Respondents most commonly credited their Section or Division Chief (43%) with facilitating their promotion, followed by Departmental Chairs or Vice/Associate Chairs (22%). Mentors (13%) or peers (8%) were also named. Four respondents (17%) named themselves as the person providing most guidance through the promotions process.

No consistent themes regarding obstacles emerged from free‐text responses to questions about the promotions process. One respondent felt that high clinical expectations made participation in other academic activities a challenge. The only other barriers noted were not being on the radar screen of the Division Chief of GIM, and difficulty identifying external, senior hospitalists to write letters in support of promotion.

When asked about the most important activities supporting their promotion, 24 respondents listed one to two key activities, detailed in Table 3. The most common response was peer‐reviewed publications (33%). Activities related to education and/or teaching were the next most common response (29%), specifically teaching, educational activities, curriculum design, or program director. Research or research funding represented 26% of responses. Valued activities outside of the respondent's institution included national reputation (21%) and service in professional societies (16%). Service or administrative responsibilities were mentioned by 25% of respondents.

Discussion

We conducted a unique and comprehensive survey of academic hospitalists who have been promoted since 1995. We identified the most common and important activities contributing to promotion. Contrary to our expectations, survey respondents generally did not report being a hospitalist was a barrier in the promotions process.

Respondents were engaged in a diverse range of activities, including service, education, and research. Interestingly, no one identified him or herself primarily as a clinician. Teaching appeared to be a core component for all surveyed, regardless of academic appointment. Only one felt that her clinical workload as a hospitalist was an obstacle that prevented her from being engaged in other activities important for promotion. With more programs potentially evolving to separate divisions, the issue of being on the radar screen of a General Internal Medicine Division Chief may become less common over time. We hope that as programs mature and the numbers of associate and full professors increase, there will not be difficulty obtaining outside letters.

Although only 23% self‐identified as clinician‐researchers, nearly all had peer‐reviewed publications and other evidence of disseminated scholarly work. Grant funding, both federal and nonfederal, was also common among this group. This finding is consistent with self‐reported activities of a cohort of junior internal medicine faculty followed over three years who were eventually promoted, though the majority of those participants were classified as having either traditional clinician‐educator or clinician‐researcher positions.16

Despite outlining a seemingly clear pathway to promotion for hospitalists, concerns remain. Most importantly, those surveyed seem to have achieved promotion through relatively traditional academic job descriptions. Obtaining or maintaining these types of positions may be difficult as clinical needs at academic centers increase. According to a recent survey of hospitalist faculty,13 over one‐third spend more than 60% of their time on nonteaching clinical services. In that survey, over half of respondents had little or no protected time for scholarly activities. The contrast between this survey's findings and ours raises the question of whether our promoted sample had positions similar to those of most academic hospitalists. Given that the majority of our respondents noted peer‐reviewed publications and grant funding to be among the most important activities for promotion, there may be a dangerous disconnect for junior academic hospitalists who spend the majority of their time in direct patient care. Moreover, the promoted hospitalists in our survey reported relatively less participation in quality improvement/patient safety activities, in contrast to both anecdotal and survey reports that these activities are a major component of many academic hospitalist positions.5, 17 Most academic medical centers do not yet consider achievements in this area in their promotions criteria, potentially creating a barrier for the ranks of clinician quality improvers.1 Thus, significant obstacles to promotion of academic hospitalists may exist.

Leaders in academic hospital medicine are recognizing these potential barriers. A diverse group from major professional societies recently published a summary of the challenges and opportunities for the field of academic hospital medicine.1 Several needs and areas for intervention were identified, including enhanced faculty development and improved documentation of quality improvement activities. The SGIM, the SHM, and the Association of Chiefs and Leaders of General Internal Medicine (ACLGIM) recently cosponsored an intensive four‐day faculty development course for junior faculty to promote skills necessary for academic hospitalist success. Early reports indicate that this was a success.1820

In addition, the AHTF has developed a Quality Portfolio, paralleling the Educator's Portfolio, that can be used as a tool for documenting quality improvement and patient safety activities in a way that can be useful for career development and promotion.4 Lastly, the Society of Hospital Medicine has hosted the inaugural Academic Hospital Medicine Leadership Summit as part of the national meeting to provide mentorship and professional development opportunities for junior faculty. Our hope is that these opportunities, coupled with the growth of mid‐level and senior leaders in hospital medicine, will provide greater infrastructure for the development and promotion of junior faculty.

Our results may have relevance beyond hospitalist groups. With anticipated further limits on housestaff duty hours, more academic physicians may be asked to fill predominantly clinical roles. In addition, a growing emphasis on quality and patient safety may lead to a more general expansion of academicians who focus on these areas.15

Our survey and methodology have limitations. By including only promoted individuals, we did not survey hospitalists with the most difficulties in the promotions processthose who were not promoted. Thus, we are unable to directly compare successful versus unsuccessful strategies. Identifying nonpromoted academic hospitalists to understand the reasons they were not (or have not yet been) promoted could be a next step in this line of inquiry. Additionally, understanding the attitudes of promotions committees regarding hospitalists, and the clinical and quality improvement roles in which they are engaged, could enhance our current results. Finally, we surveyed a convenience sample of a limited numbers of hospitalists and institutions, and were unable to systematically account for variations in promotions criteria across institutions. However, to our knowledge, this is the most comprehensive study of promotions among academic hospitalists to date. Given the common themes that emerged in terms of activities that supported promotion, mentors, and advice, we believe that our sample was sufficient to identify important themes and advance our understanding of this nascent specialty.

In conclusion, our survey of promoted hospital medicine faculty provides valuable information for junior faculty and hospitalist leaders. Success was found through engaging in a diverse set of activities in the traditional areas of education, service, and scholarship, frequently in conjunction with developing recognition outside of their institutions. While all respondents were clinically active, none described themselves as having purely clinical roles. As academic hospitalist roles evolve, academic leaders will need to provide adequate mentorship, create time for scholarly pursuits, and promote documentation and recognition of nontraditional activities that may nonetheless be worthy of promotion.

The growth of academic hospital medicine has been driven by multiple factors including expanding clinical needs, housestaff duty hours' limitations, and an increasing focus on quality and patient safety.1 Hospitalists at academic medical centers frequently assume roles that differ substantially from traditional faculty positions. Academic hospitalists may have predominantly clinical positions, and may be involved in quality improvement and patient safety projects.24 Because of these commitments, many academic hospitalists spend less time on research or educational efforts.1, 5 Many have raised concerns that these unique job descriptions might lead to less time to devote to scholarship and academic pursuits, and consequently greater challenges in the promotions process.2, 5

There are little published data on promotion and tenure in academics, and even less specifically focused on the promotion of hospitalists. Theoretically, promotion should recognize an individual's contribution to his or her institution and field. However, each institution has unique criteria though which faculty achieve promotion. Previous articles addressing specific groups, such as part‐time,6 clinical faculty,79 or clinician‐educators10 may be relevant to hospitalists, as hospitalists may be more likely to fall into these categories. These reports suggest general agreement that promotion committees should consider and weigh clinical and educational work (in addition to scholarly publications) in the promotions process, but assessment methods vary across institutions and the contribution of activities, such as quality improvement, remain unclear. The educator's portfolio has gained momentum as a way to document valued teaching in many institutions,11, 12 but academic hospitalist participation in education may be limited.13

Literature related to the development of Divisions of General Internal Medicine is relevant insofar as similar concerns for promotion were expressed with the growth of their faculty.14, 15 However, its applicability may be limited by differences between roles of hospitalists and more traditional general medicine faculty.

To better understand the factors influencing promotion for academic hospitalists, the Society of General Internal Medicine (SGIM) Academic Hospitalist Task Force (AHTF) undertook a survey of promoted hospitalists who had successfully reached the rank of Associate Professor or higher.

Methods

Results

Of the 33 hospitalists who received the survey, 26 responded (response rate of 79%). Of these, 25 completed the survey in its entirely and were included in our analysis; 1 did not submit details regarding specific promotion‐related activities. General information regarding the respondents and their programs at the time of their promotion is contained in Table 1.

The seven nonrespondents were from seven different institutions; however two of these institutions were represented by respondents. One nonrespondent had achieved a rank of Professor (through general medicine); the rest had been promoted to Associate Professor. One nonrespondent is known by the authors to hold a research position.

Ten respondents identified themselves as clinician‐educators (40%), ten as clinician‐administrators (40%), and five as clinician‐researchers (20%). Seventeen (68%) of the promoted hospitalists were not on a tenure track (as defined by them); they were more likely to have administrative or educational roles than a research appointment. Though the majority of self‐identified researchers were among the earliest to have been promoted, there were no statistically significant differences in self‐defined job description between more and less recently promoted hospitalists.

Promoted hospitalists were involved in a diverse range of activities which supported their promotion, including service (eg, institutional committees), education, research, and quality improvement. Nearly all hospitalists surveyed listed teaching and educational activities, and almost all had disseminated scholarly output and some degree of grant funding. Table 2 lists the specific activities in which respondents reported being engaged in each of these domains.

A range of individuals assisted the respondents in the promotion process. Twenty‐three (92%) respondents identified the individuals who supported their promotion, and all listed more than one person. Respondents most commonly credited their Section or Division Chief (43%) with facilitating their promotion, followed by Departmental Chairs or Vice/Associate Chairs (22%). Mentors (13%) or peers (8%) were also named. Four respondents (17%) named themselves as the person providing most guidance through the promotions process.

No consistent themes regarding obstacles emerged from free‐text responses to questions about the promotions process. One respondent felt that high clinical expectations made participation in other academic activities a challenge. The only other barriers noted were not being on the radar screen of the Division Chief of GIM, and difficulty identifying external, senior hospitalists to write letters in support of promotion.

When asked about the most important activities supporting their promotion, 24 respondents listed one to two key activities, detailed in Table 3. The most common response was peer‐reviewed publications (33%). Activities related to education and/or teaching were the next most common response (29%), specifically teaching, educational activities, curriculum design, or program director. Research or research funding represented 26% of responses. Valued activities outside of the respondent's institution included national reputation (21%) and service in professional societies (16%). Service or administrative responsibilities were mentioned by 25% of respondents.

Discussion

We conducted a unique and comprehensive survey of academic hospitalists who have been promoted since 1995. We identified the most common and important activities contributing to promotion. Contrary to our expectations, survey respondents generally did not report being a hospitalist was a barrier in the promotions process.

Respondents were engaged in a diverse range of activities, including service, education, and research. Interestingly, no one identified him or herself primarily as a clinician. Teaching appeared to be a core component for all surveyed, regardless of academic appointment. Only one felt that her clinical workload as a hospitalist was an obstacle that prevented her from being engaged in other activities important for promotion. With more programs potentially evolving to separate divisions, the issue of being on the radar screen of a General Internal Medicine Division Chief may become less common over time. We hope that as programs mature and the numbers of associate and full professors increase, there will not be difficulty obtaining outside letters.

Although only 23% self‐identified as clinician‐researchers, nearly all had peer‐reviewed publications and other evidence of disseminated scholarly work. Grant funding, both federal and nonfederal, was also common among this group. This finding is consistent with self‐reported activities of a cohort of junior internal medicine faculty followed over three years who were eventually promoted, though the majority of those participants were classified as having either traditional clinician‐educator or clinician‐researcher positions.16

Despite outlining a seemingly clear pathway to promotion for hospitalists, concerns remain. Most importantly, those surveyed seem to have achieved promotion through relatively traditional academic job descriptions. Obtaining or maintaining these types of positions may be difficult as clinical needs at academic centers increase. According to a recent survey of hospitalist faculty,13 over one‐third spend more than 60% of their time on nonteaching clinical services. In that survey, over half of respondents had little or no protected time for scholarly activities. The contrast between this survey's findings and ours raises the question of whether our promoted sample had positions similar to those of most academic hospitalists. Given that the majority of our respondents noted peer‐reviewed publications and grant funding to be among the most important activities for promotion, there may be a dangerous disconnect for junior academic hospitalists who spend the majority of their time in direct patient care. Moreover, the promoted hospitalists in our survey reported relatively less participation in quality improvement/patient safety activities, in contrast to both anecdotal and survey reports that these activities are a major component of many academic hospitalist positions.5, 17 Most academic medical centers do not yet consider achievements in this area in their promotions criteria, potentially creating a barrier for the ranks of clinician quality improvers.1 Thus, significant obstacles to promotion of academic hospitalists may exist.

Leaders in academic hospital medicine are recognizing these potential barriers. A diverse group from major professional societies recently published a summary of the challenges and opportunities for the field of academic hospital medicine.1 Several needs and areas for intervention were identified, including enhanced faculty development and improved documentation of quality improvement activities. The SGIM, the SHM, and the Association of Chiefs and Leaders of General Internal Medicine (ACLGIM) recently cosponsored an intensive four‐day faculty development course for junior faculty to promote skills necessary for academic hospitalist success. Early reports indicate that this was a success.1820

In addition, the AHTF has developed a Quality Portfolio, paralleling the Educator's Portfolio, that can be used as a tool for documenting quality improvement and patient safety activities in a way that can be useful for career development and promotion.4 Lastly, the Society of Hospital Medicine has hosted the inaugural Academic Hospital Medicine Leadership Summit as part of the national meeting to provide mentorship and professional development opportunities for junior faculty. Our hope is that these opportunities, coupled with the growth of mid‐level and senior leaders in hospital medicine, will provide greater infrastructure for the development and promotion of junior faculty.

Our results may have relevance beyond hospitalist groups. With anticipated further limits on housestaff duty hours, more academic physicians may be asked to fill predominantly clinical roles. In addition, a growing emphasis on quality and patient safety may lead to a more general expansion of academicians who focus on these areas.15

Our survey and methodology have limitations. By including only promoted individuals, we did not survey hospitalists with the most difficulties in the promotions processthose who were not promoted. Thus, we are unable to directly compare successful versus unsuccessful strategies. Identifying nonpromoted academic hospitalists to understand the reasons they were not (or have not yet been) promoted could be a next step in this line of inquiry. Additionally, understanding the attitudes of promotions committees regarding hospitalists, and the clinical and quality improvement roles in which they are engaged, could enhance our current results. Finally, we surveyed a convenience sample of a limited numbers of hospitalists and institutions, and were unable to systematically account for variations in promotions criteria across institutions. However, to our knowledge, this is the most comprehensive study of promotions among academic hospitalists to date. Given the common themes that emerged in terms of activities that supported promotion, mentors, and advice, we believe that our sample was sufficient to identify important themes and advance our understanding of this nascent specialty.

In conclusion, our survey of promoted hospital medicine faculty provides valuable information for junior faculty and hospitalist leaders. Success was found through engaging in a diverse set of activities in the traditional areas of education, service, and scholarship, frequently in conjunction with developing recognition outside of their institutions. While all respondents were clinically active, none described themselves as having purely clinical roles. As academic hospitalist roles evolve, academic leaders will need to provide adequate mentorship, create time for scholarly pursuits, and promote documentation and recognition of nontraditional activities that may nonetheless be worthy of promotion.

The growth of academic hospital medicine has been driven by multiple factors including expanding clinical needs, housestaff duty hours' limitations, and an increasing focus on quality and patient safety.1 Hospitalists at academic medical centers frequently assume roles that differ substantially from traditional faculty positions. Academic hospitalists may have predominantly clinical positions, and may be involved in quality improvement and patient safety projects.24 Because of these commitments, many academic hospitalists spend less time on research or educational efforts.1, 5 Many have raised concerns that these unique job descriptions might lead to less time to devote to scholarship and academic pursuits, and consequently greater challenges in the promotions process.2, 5

There are little published data on promotion and tenure in academics, and even less specifically focused on the promotion of hospitalists. Theoretically, promotion should recognize an individual's contribution to his or her institution and field. However, each institution has unique criteria though which faculty achieve promotion. Previous articles addressing specific groups, such as part‐time,6 clinical faculty,79 or clinician‐educators10 may be relevant to hospitalists, as hospitalists may be more likely to fall into these categories. These reports suggest general agreement that promotion committees should consider and weigh clinical and educational work (in addition to scholarly publications) in the promotions process, but assessment methods vary across institutions and the contribution of activities, such as quality improvement, remain unclear. The educator's portfolio has gained momentum as a way to document valued teaching in many institutions,11, 12 but academic hospitalist participation in education may be limited.13

Literature related to the development of Divisions of General Internal Medicine is relevant insofar as similar concerns for promotion were expressed with the growth of their faculty.14, 15 However, its applicability may be limited by differences between roles of hospitalists and more traditional general medicine faculty.

To better understand the factors influencing promotion for academic hospitalists, the Society of General Internal Medicine (SGIM) Academic Hospitalist Task Force (AHTF) undertook a survey of promoted hospitalists who had successfully reached the rank of Associate Professor or higher.

Methods

Results

Of the 33 hospitalists who received the survey, 26 responded (response rate of 79%). Of these, 25 completed the survey in its entirely and were included in our analysis; 1 did not submit details regarding specific promotion‐related activities. General information regarding the respondents and their programs at the time of their promotion is contained in Table 1.

The seven nonrespondents were from seven different institutions; however two of these institutions were represented by respondents. One nonrespondent had achieved a rank of Professor (through general medicine); the rest had been promoted to Associate Professor. One nonrespondent is known by the authors to hold a research position.

Ten respondents identified themselves as clinician‐educators (40%), ten as clinician‐administrators (40%), and five as clinician‐researchers (20%). Seventeen (68%) of the promoted hospitalists were not on a tenure track (as defined by them); they were more likely to have administrative or educational roles than a research appointment. Though the majority of self‐identified researchers were among the earliest to have been promoted, there were no statistically significant differences in self‐defined job description between more and less recently promoted hospitalists.

Promoted hospitalists were involved in a diverse range of activities which supported their promotion, including service (eg, institutional committees), education, research, and quality improvement. Nearly all hospitalists surveyed listed teaching and educational activities, and almost all had disseminated scholarly output and some degree of grant funding. Table 2 lists the specific activities in which respondents reported being engaged in each of these domains.

A range of individuals assisted the respondents in the promotion process. Twenty‐three (92%) respondents identified the individuals who supported their promotion, and all listed more than one person. Respondents most commonly credited their Section or Division Chief (43%) with facilitating their promotion, followed by Departmental Chairs or Vice/Associate Chairs (22%). Mentors (13%) or peers (8%) were also named. Four respondents (17%) named themselves as the person providing most guidance through the promotions process.

No consistent themes regarding obstacles emerged from free‐text responses to questions about the promotions process. One respondent felt that high clinical expectations made participation in other academic activities a challenge. The only other barriers noted were not being on the radar screen of the Division Chief of GIM, and difficulty identifying external, senior hospitalists to write letters in support of promotion.

When asked about the most important activities supporting their promotion, 24 respondents listed one to two key activities, detailed in Table 3. The most common response was peer‐reviewed publications (33%). Activities related to education and/or teaching were the next most common response (29%), specifically teaching, educational activities, curriculum design, or program director. Research or research funding represented 26% of responses. Valued activities outside of the respondent's institution included national reputation (21%) and service in professional societies (16%). Service or administrative responsibilities were mentioned by 25% of respondents.

Discussion

We conducted a unique and comprehensive survey of academic hospitalists who have been promoted since 1995. We identified the most common and important activities contributing to promotion. Contrary to our expectations, survey respondents generally did not report being a hospitalist was a barrier in the promotions process.

Respondents were engaged in a diverse range of activities, including service, education, and research. Interestingly, no one identified him or herself primarily as a clinician. Teaching appeared to be a core component for all surveyed, regardless of academic appointment. Only one felt that her clinical workload as a hospitalist was an obstacle that prevented her from being engaged in other activities important for promotion. With more programs potentially evolving to separate divisions, the issue of being on the radar screen of a General Internal Medicine Division Chief may become less common over time. We hope that as programs mature and the numbers of associate and full professors increase, there will not be difficulty obtaining outside letters.

Although only 23% self‐identified as clinician‐researchers, nearly all had peer‐reviewed publications and other evidence of disseminated scholarly work. Grant funding, both federal and nonfederal, was also common among this group. This finding is consistent with self‐reported activities of a cohort of junior internal medicine faculty followed over three years who were eventually promoted, though the majority of those participants were classified as having either traditional clinician‐educator or clinician‐researcher positions.16

Despite outlining a seemingly clear pathway to promotion for hospitalists, concerns remain. Most importantly, those surveyed seem to have achieved promotion through relatively traditional academic job descriptions. Obtaining or maintaining these types of positions may be difficult as clinical needs at academic centers increase. According to a recent survey of hospitalist faculty,13 over one‐third spend more than 60% of their time on nonteaching clinical services. In that survey, over half of respondents had little or no protected time for scholarly activities. The contrast between this survey's findings and ours raises the question of whether our promoted sample had positions similar to those of most academic hospitalists. Given that the majority of our respondents noted peer‐reviewed publications and grant funding to be among the most important activities for promotion, there may be a dangerous disconnect for junior academic hospitalists who spend the majority of their time in direct patient care. Moreover, the promoted hospitalists in our survey reported relatively less participation in quality improvement/patient safety activities, in contrast to both anecdotal and survey reports that these activities are a major component of many academic hospitalist positions.5, 17 Most academic medical centers do not yet consider achievements in this area in their promotions criteria, potentially creating a barrier for the ranks of clinician quality improvers.1 Thus, significant obstacles to promotion of academic hospitalists may exist.

Leaders in academic hospital medicine are recognizing these potential barriers. A diverse group from major professional societies recently published a summary of the challenges and opportunities for the field of academic hospital medicine.1 Several needs and areas for intervention were identified, including enhanced faculty development and improved documentation of quality improvement activities. The SGIM, the SHM, and the Association of Chiefs and Leaders of General Internal Medicine (ACLGIM) recently cosponsored an intensive four‐day faculty development course for junior faculty to promote skills necessary for academic hospitalist success. Early reports indicate that this was a success.1820

In addition, the AHTF has developed a Quality Portfolio, paralleling the Educator's Portfolio, that can be used as a tool for documenting quality improvement and patient safety activities in a way that can be useful for career development and promotion.4 Lastly, the Society of Hospital Medicine has hosted the inaugural Academic Hospital Medicine Leadership Summit as part of the national meeting to provide mentorship and professional development opportunities for junior faculty. Our hope is that these opportunities, coupled with the growth of mid‐level and senior leaders in hospital medicine, will provide greater infrastructure for the development and promotion of junior faculty.

Our results may have relevance beyond hospitalist groups. With anticipated further limits on housestaff duty hours, more academic physicians may be asked to fill predominantly clinical roles. In addition, a growing emphasis on quality and patient safety may lead to a more general expansion of academicians who focus on these areas.15

Our survey and methodology have limitations. By including only promoted individuals, we did not survey hospitalists with the most difficulties in the promotions processthose who were not promoted. Thus, we are unable to directly compare successful versus unsuccessful strategies. Identifying nonpromoted academic hospitalists to understand the reasons they were not (or have not yet been) promoted could be a next step in this line of inquiry. Additionally, understanding the attitudes of promotions committees regarding hospitalists, and the clinical and quality improvement roles in which they are engaged, could enhance our current results. Finally, we surveyed a convenience sample of a limited numbers of hospitalists and institutions, and were unable to systematically account for variations in promotions criteria across institutions. However, to our knowledge, this is the most comprehensive study of promotions among academic hospitalists to date. Given the common themes that emerged in terms of activities that supported promotion, mentors, and advice, we believe that our sample was sufficient to identify important themes and advance our understanding of this nascent specialty.

In conclusion, our survey of promoted hospital medicine faculty provides valuable information for junior faculty and hospitalist leaders. Success was found through engaging in a diverse set of activities in the traditional areas of education, service, and scholarship, frequently in conjunction with developing recognition outside of their institutions. While all respondents were clinically active, none described themselves as having purely clinical roles. As academic hospitalist roles evolve, academic leaders will need to provide adequate mentorship, create time for scholarly pursuits, and promote documentation and recognition of nontraditional activities that may nonetheless be worthy of promotion.

A 66‐year‐old man presented to the emergency department with 3 weeks of progressive exertional dyspnea. He also reported a single episode of chest pain 1 day prior to admission.

Cardiac and pulmonary causes of dyspnea are the most common. Other causes include anemia or a neuromuscular process. Given the recent episode of chest pain, coronary ischemia, congestive heart failure, chronic obstructive pulmonary disease (COPD), pulmonary embolism, and pericardial effusion must be considered.

Up until 3 weeks ago, he had no exercise intolerance, and had been relatively active. He began noticing progressive dyspnea to the point where he had considerable difficulty walking up stairs, and performing minor household chores. He also complained of orthopnea and paroxysmal nocturnal dyspnea for the last 3 weeks.He denied chest pain at presentation, but 24 hours prior, he experienced one episode of sharp, left‐sided, nonradiating, nonpositional chest pain that occurred at rest. It lasted approximately 20 minutes and was not associated with diaphoresis, nausea, vomiting, or palpitations. He had never experienced chest discomfort prior to this episode. He denied fever, chills, cough, or wheezing.

Progressive dyspnea on exertion with associated orthopnea and paroxysmal nocturnal dyspnea is classically seen in patients with heart failure and is typically associated with left ventricular failure. However, paroxysmal nocturnal dyspnea and orthopnea are only moderately specific for heart failure. Orthopnea can also be seen in pericardial disease, and in numerous pulmonary diseases, including asthma, COPD, pulmonary hypertension, diaphragmatic weakness, pleural effusion, pulmonary embolism, and any apical lung process including lung cancer or pneumonia. Paroxysmal nocturnal dyspnea can be seen in many of the same disorders and can also be reported in obstructive sleep apnea.

His past medical history was remarkable for two episodes of syncope, occurring 5 and 3 years ago, both while working outside in warm weather. Neither was associated with chest pain, diaphoresis, palpitations, or post‐ictal symptoms. He was diagnosed with prostate cancer 8 years ago, and underwent 2 years of androgen‐deprivation therapy with goserelin along with local radiation therapy. Medications included subcutaneous goserelin every 3 months and daily omeprazole. He denied any other prescription, over‐the‐counter, or herbal medications. He reported a 50‐pack‐year history of smoking, but denied alcohol or illicit drug abuse. He denied any travel history or recent immobilization. He had no children, and there was no known history of heart disease in his family.

The past medical history of two episodes of likely exertional syncope is interesting, but the episodes were sporadic and in the distant past, arguing against a serious and ongoing process. Nonetheless, this history still raises the possibility of cardiac causes of syncope, especially causes such as hypertrophic obstructive cardiomyopathy or aortic stenosis which are classically associated with exertional syncope. Either of these two conditions can result in heart failure if untreated. The history of goserelin therapy does make the possibility of heart failure higher, as there has been an association reported between use of this drug and heart failure. His history of tobacco use is a risk factor for coronary artery disease (CAD) and COPD. An active cancer history is also a risk factor for thromboembolic disease, which remains a consideration.

On admission, his temperature was 36.9C, heart rate 94 bpm, respiratory rate 22 breaths per minute, blood pressure 200/108 mmHg, and oxygen saturation 93% breathing ambient air. He was a thin man in no acute distress. Cardiovascular examination was significant for normal first and second heart sounds, with a soft left‐sided S3; the point of maximal impulse was diffuse, but displaced laterally. His jugular venous pressure was estimated at 9 cm of H₂O while positioned at a 45‐degree angle. Rales were heard at the lung bases bilaterally. Abdominal exam was normal. His lower extremities were without edema. There were no focal neurological deficits appreciated. Skin examination was unremarkable.

His combination of physical exam findings strongly suggests heart failure, most likely related to a dilated cardiomyopathy and left ventricular dysfunction. The presence of a left‐sided S3 and rales, and the lack of markedly elevated central venous pressure and peripheral edema, suggest heart failure predominantly due to left ventricular dysfunction. Of note, he is very hypertensive. This would not be the typical finding with severely decompensated heart failure. It would be important to determine whether his elevated blood pressure is due to an acute, reversible cause (e.g., pain, dyspnea, anxiety) or whether cocaine use, psychotropic agents, rare causes such as catecholamine‐producing tumors, other neuroendocrine tumors or thyroid toxic states are at play. In addition, one might see hypertension early in the course of heart failure, from a left ventricular outflow obstructive etiology such as severe aortic stenosis or hypertrophic obstructive cardiomyopathy.

Laboratory evaluation revealed a white blood cell count of 8900/mm³, with a normal differential; hemoglobin was 13.9 g/dL; platelet count was 264,000/mm³. Serum electrolytes and liver enzymes were unremarkable, with serum creatinine 1.1 mg/dL and blood urea nitrogen 7 mg/dL. Serial cardiac troponin‐I levels drawn 8 hours apart were 0.04, 0.07, 0.08, and 0.04 ng/mL (normal <0.04). Brain natriuretic peptide was 1420 pg/mL (normal <100). Thyroid stimulating hormone was 1.19 uIU/mL (normal 0.34‐5.60). Chest radiography revealed mild cardiomegaly, with peripheral interstitial opacities in the mid and lower lobes bilaterally, with fluid within the minor fissure. A 12‐lead electrocardiogram (ECG) revealed normal sinus rhythm at 95 bpm with left anterior fascicular block; intraventricular conduction delay was present (QRS width 106 ms) and QS complexes were present in V1‐V3. In addition, there was a left atrial abnormality and voltage criteria for left ventricular hypertrophy with secondary T‐wave inversions laterally (Figure 1). No previous ECGs were available for comparison. A chest computed tomography scan with contrast showed no evidence of pulmonary embolus. It did show interlobular septal thickening and small bilateral pleural effusions, consistent with left ventricular dysfunction.

Figure 1

The patient's initial lab, imaging, and diagnostic work‐up continues to be consistent with the diagnosis of heart failure. The patient appears to have cardiomegaly and mild pulmonary edema by imaging. The etiology of heart failure remains unknown, but ischemia remains in the differential, given the mildly elevated troponins initially and the ECG findings of left anterior fascicular block and T‐wave inversions in the lateral leads. Left anterior fascicular block can be seen with ischemic heart disease (especially involving the left anterior descending coronary artery), hypertensive heart disease, valvular disease, and some infiltrative cardiac processes. The lateral T‐wave inversions are likely secondary to left ventricular hypertrophy (a so‐called strain pattern), rather than ischemia. Left ventricular hypertrophy is consistent with his hypertension, suggesting that it is chronic; his presentation may be due to hypertensive heart disease with new onset heart failure.

He was admitted to the hospital, and metoprolol, lisinopril, and intravenous furosemide were given. Transthoracic echocardiography demonstrated severe global hypokinesis with a left ventricular ejection fraction of 10%. There was no evidence of ventricular thrombus or valvular disease; however, prominent left ventricular trabeculation with deep recesses was noted (see Figure 2).

Figure 2

The echocardiographic findings of deep recesses and prominent left ventricular trabeculation are seen in only a few disorders. Sometimes these findings are thought to be due to hypertrophic obstructive cardiomyopathy. The deep trabeculations can be seen in patients with some forms of congenital heart disease associated with ventricular pressure overload during fetal development. The other cause is left ventricular noncompaction, a genetic cardiomyopathy which is becoming increasingly recognized. The disorder, along with causing heart failure, is associated with a high risk of ventricular thrombus and thromboembolic events, and a high risk of arrhythmias and sudden death. The overall prognosis appears to be poor, compared to some other cardiomyopathies. The imaging findings of left ventricular noncompaction are nearly pathognomonic, and experienced echocardiographers can usually make the diagnosis. Finally, left heart catheterization or noninvasive stress testing should be part of the workup to definitively exclude an ischemic cardiomyopathy, even in the setting of noncompaction, and especially given his recent history of chest pain.

A left heart catheterization with coronary arteriography demonstrated no angiographic evidence of obstructive coronary disease. Left ventriculography revealed severe global hypokinesis. The patient was diagnosed with left ventricular noncompaction.

The initial medical management centers upon the treatment of heart failure with a beta‐blocker, ACE‐inhibitor, and diuretics for fluid management. Patients with left ventricular noncompaction are at particularly high risk of both embolic events (thought due to propensity to develop left ventricular clots within the deep recesses of the endocardium) and sudden death from arrhythmias. Thus, anticoagulation with warfarin is often indicated and would be reasonable in this patient, given the extremely low ejection fraction. The patient does meet established criteria for primary prophylaxis of sudden death with an implantable cardioverter‐defibrillator in nonischemic cardiomyopathy (left ventricular ejection fraction <35% and New York Heart Association class II failure), and this would also be appropriate therapy as well, given the high‐risk profile of this patient population.

He was discharged in stable condition with a medical regimen consisting of diuretics, metoprolol, and lisinopril. Given the risk for thromboembolism, he was started on warfarin. On subsequent follow‐up, repeat echocardiogram revealed a persistently low left ventricular ejection fraction at 10%. Despite his marked improvement in exercise tolerance and overall well‐being after 4 months of treatment, his ejection fraction did not improve. As a result, he was evaluated and counseled for placement of an implantable cardioverter‐defibrillator, and received a dual‐chamber device shortly afterward.

COMMENTARY

Left ventricular noncompaction is a form of cardiomyopathy increasingly recognized in both pediatric and adult populations. The hallmark features are a pattern of prominent trabeculations and deep recesses in the left ventricular wall. During normal gestation, the myocardium compacts and matures while deep recesses evolve into capillary precursors of the coronary circulation. Left ventricular noncompaction may result from an arrest in this process, with cardiac myofibers failing to compact from their initial spongiform architecture into a developed endocardium.1 Restrictive relaxation from persistent trabeculae predisposes to diastolic dysfunction, while systolic dysfunction may be related to subendocardial hypoperfusion and mechanical dyssynchrony between compacted and noncompacted myocardium.2

Differentiation of left ventricular noncompaction from other cardiomyopathies, based on history and physical examination alone, is essentially impossible. There is high variability and lack of specificity in both clinical profile and onset of symptoms. Electrocardiographic findings are also nonspecific, and the diagnosis typically becomes evident only with transthoracic echocardiography. Current diagnostic criteria include: 1) absence of coexisting cardiac abnormalities; 2) a two‐layer structure with >2:1 ratio of noncompacted to compacted myocardium; 3) predominant involvement of the apical segment of myocardium; and 4) deep intertrabecular recesses demonstrated on Doppler imaging.2, 3 Although echocardiography remains the standard in clinical practice, cardiac magnetic resonance imaging is being increasingly employed as well.4

With more awareness of the disease and the development of higher resolution imaging, the reported incidence has risen. In one single‐center study performed at a heart failure/transplant clinic, 3% of 960 patients referred to heart failure clinic were diagnosed with left ventricular noncompaction, a prevalence similar to hypertensive disease and hypertrophic cardiomyopathy.5 In another community‐hospitalbased study of 4929 adult patients referred for echocardiography, 3.7% of those with systolic dysfunction were diagnosed with noncompaction.6

Left ventricular noncompaction is considered a genetic cardiomyopathy; a family history of heart failure is often present.7 Despite its congenital origin and genetic involvement,2 it is unclear why symptoms may first present at an advanced age. Chest pain and shortness of breath are common complaints, and approximately 62% of patients will have congestive heart failure at presentation.8

Tachyarrhythmia and ventricular tachycardia are commonly seen, as are systemic embolic events and pulmonary embolism. Significant predictors of death include New York Heart Association class III‐IV, sustained ventricular arrhythmias, and increased left atrial size.9

Management is focused on the treatment of arrhythmias, heart failure, and thromboembolic events. The use of standard medical therapy for heart failure (including ACE‐inhibitors and beta‐blockers) is not based on large‐scale studies, yet remains the cornerstone of therapy. An implantable cardioverter‐defibrillator is indicated after hemodynamically compromising sustained ventricular tachycardia or aborted sudden cardiac death, but there are no guidelines for primary prophylaxis outside of patients with heart failure and a depressed ejection fraction.10 Cardiac resynchronization therapy has been successful in some patients with isolated left ventricular noncompaction. Long‐term oral anticoagulation is recommended, especially when impaired left ventricular function, thrombi, or atrial fibrillation have been documented. Patients with left ventricular dysfunction in concert with left ventricular noncompaction are at 10% higher risk for embolic complications when compared to those without noncompaction.11 Familial screening with echocardiography is indicated once the diagnosis has been made.2

In this Clinical Care Conundrum, we describe a rare but increasingly recognized condition, and highlight the importance of delineating the underlying cause of cardiomyopathy when possible. Treatment of heart failure in the hospital setting is sometimes more focused on initiation of diuresis and further stabilization of the patient, and less focused on elucidation of the etiology. While recognition of left ventricular failure led to early treatment with standard therapy in this case, identification of the underlying cause allowed for targeted interventions directed at cardiac arrhythmias, embolic events, and familial screening. Of note, the discussant was careful not to let the prior history of syncopal events distract him from the central issues in this case.

This case also serves as a reminder that congenital anomalies should remain on the differential diagnosis when evaluating new complaints in adult patients. The discussant approached the presentation of new‐onset left ventricular dysfunction in a thorough manner, weighing the likelihood of ischemic and nonischemic causes in the context of the history and physical examination. Careful consideration of the patient's new clinical manifestationscoupled with characteristic echocardiographic findings and normal coronary anatomysolidified the diagnosis. By developing a broad differential, the discussant and clinical team arrived at a diagnosis that for this 66‐year‐old gentleman was a lifetime in the making.

A 66‐year‐old man presented to the emergency department with 3 weeks of progressive exertional dyspnea. He also reported a single episode of chest pain 1 day prior to admission.

Cardiac and pulmonary causes of dyspnea are the most common. Other causes include anemia or a neuromuscular process. Given the recent episode of chest pain, coronary ischemia, congestive heart failure, chronic obstructive pulmonary disease (COPD), pulmonary embolism, and pericardial effusion must be considered.

Up until 3 weeks ago, he had no exercise intolerance, and had been relatively active. He began noticing progressive dyspnea to the point where he had considerable difficulty walking up stairs, and performing minor household chores. He also complained of orthopnea and paroxysmal nocturnal dyspnea for the last 3 weeks.He denied chest pain at presentation, but 24 hours prior, he experienced one episode of sharp, left‐sided, nonradiating, nonpositional chest pain that occurred at rest. It lasted approximately 20 minutes and was not associated with diaphoresis, nausea, vomiting, or palpitations. He had never experienced chest discomfort prior to this episode. He denied fever, chills, cough, or wheezing.

Progressive dyspnea on exertion with associated orthopnea and paroxysmal nocturnal dyspnea is classically seen in patients with heart failure and is typically associated with left ventricular failure. However, paroxysmal nocturnal dyspnea and orthopnea are only moderately specific for heart failure. Orthopnea can also be seen in pericardial disease, and in numerous pulmonary diseases, including asthma, COPD, pulmonary hypertension, diaphragmatic weakness, pleural effusion, pulmonary embolism, and any apical lung process including lung cancer or pneumonia. Paroxysmal nocturnal dyspnea can be seen in many of the same disorders and can also be reported in obstructive sleep apnea.

His past medical history was remarkable for two episodes of syncope, occurring 5 and 3 years ago, both while working outside in warm weather. Neither was associated with chest pain, diaphoresis, palpitations, or post‐ictal symptoms. He was diagnosed with prostate cancer 8 years ago, and underwent 2 years of androgen‐deprivation therapy with goserelin along with local radiation therapy. Medications included subcutaneous goserelin every 3 months and daily omeprazole. He denied any other prescription, over‐the‐counter, or herbal medications. He reported a 50‐pack‐year history of smoking, but denied alcohol or illicit drug abuse. He denied any travel history or recent immobilization. He had no children, and there was no known history of heart disease in his family.

The past medical history of two episodes of likely exertional syncope is interesting, but the episodes were sporadic and in the distant past, arguing against a serious and ongoing process. Nonetheless, this history still raises the possibility of cardiac causes of syncope, especially causes such as hypertrophic obstructive cardiomyopathy or aortic stenosis which are classically associated with exertional syncope. Either of these two conditions can result in heart failure if untreated. The history of goserelin therapy does make the possibility of heart failure higher, as there has been an association reported between use of this drug and heart failure. His history of tobacco use is a risk factor for coronary artery disease (CAD) and COPD. An active cancer history is also a risk factor for thromboembolic disease, which remains a consideration.

On admission, his temperature was 36.9C, heart rate 94 bpm, respiratory rate 22 breaths per minute, blood pressure 200/108 mmHg, and oxygen saturation 93% breathing ambient air. He was a thin man in no acute distress. Cardiovascular examination was significant for normal first and second heart sounds, with a soft left‐sided S3; the point of maximal impulse was diffuse, but displaced laterally. His jugular venous pressure was estimated at 9 cm of H₂O while positioned at a 45‐degree angle. Rales were heard at the lung bases bilaterally. Abdominal exam was normal. His lower extremities were without edema. There were no focal neurological deficits appreciated. Skin examination was unremarkable.

His combination of physical exam findings strongly suggests heart failure, most likely related to a dilated cardiomyopathy and left ventricular dysfunction. The presence of a left‐sided S3 and rales, and the lack of markedly elevated central venous pressure and peripheral edema, suggest heart failure predominantly due to left ventricular dysfunction. Of note, he is very hypertensive. This would not be the typical finding with severely decompensated heart failure. It would be important to determine whether his elevated blood pressure is due to an acute, reversible cause (e.g., pain, dyspnea, anxiety) or whether cocaine use, psychotropic agents, rare causes such as catecholamine‐producing tumors, other neuroendocrine tumors or thyroid toxic states are at play. In addition, one might see hypertension early in the course of heart failure, from a left ventricular outflow obstructive etiology such as severe aortic stenosis or hypertrophic obstructive cardiomyopathy.

Laboratory evaluation revealed a white blood cell count of 8900/mm³, with a normal differential; hemoglobin was 13.9 g/dL; platelet count was 264,000/mm³. Serum electrolytes and liver enzymes were unremarkable, with serum creatinine 1.1 mg/dL and blood urea nitrogen 7 mg/dL. Serial cardiac troponin‐I levels drawn 8 hours apart were 0.04, 0.07, 0.08, and 0.04 ng/mL (normal <0.04). Brain natriuretic peptide was 1420 pg/mL (normal <100). Thyroid stimulating hormone was 1.19 uIU/mL (normal 0.34‐5.60). Chest radiography revealed mild cardiomegaly, with peripheral interstitial opacities in the mid and lower lobes bilaterally, with fluid within the minor fissure. A 12‐lead electrocardiogram (ECG) revealed normal sinus rhythm at 95 bpm with left anterior fascicular block; intraventricular conduction delay was present (QRS width 106 ms) and QS complexes were present in V1‐V3. In addition, there was a left atrial abnormality and voltage criteria for left ventricular hypertrophy with secondary T‐wave inversions laterally (Figure 1). No previous ECGs were available for comparison. A chest computed tomography scan with contrast showed no evidence of pulmonary embolus. It did show interlobular septal thickening and small bilateral pleural effusions, consistent with left ventricular dysfunction.

Figure 1

The patient's initial lab, imaging, and diagnostic work‐up continues to be consistent with the diagnosis of heart failure. The patient appears to have cardiomegaly and mild pulmonary edema by imaging. The etiology of heart failure remains unknown, but ischemia remains in the differential, given the mildly elevated troponins initially and the ECG findings of left anterior fascicular block and T‐wave inversions in the lateral leads. Left anterior fascicular block can be seen with ischemic heart disease (especially involving the left anterior descending coronary artery), hypertensive heart disease, valvular disease, and some infiltrative cardiac processes. The lateral T‐wave inversions are likely secondary to left ventricular hypertrophy (a so‐called strain pattern), rather than ischemia. Left ventricular hypertrophy is consistent with his hypertension, suggesting that it is chronic; his presentation may be due to hypertensive heart disease with new onset heart failure.

He was admitted to the hospital, and metoprolol, lisinopril, and intravenous furosemide were given. Transthoracic echocardiography demonstrated severe global hypokinesis with a left ventricular ejection fraction of 10%. There was no evidence of ventricular thrombus or valvular disease; however, prominent left ventricular trabeculation with deep recesses was noted (see Figure 2).

Figure 2

The echocardiographic findings of deep recesses and prominent left ventricular trabeculation are seen in only a few disorders. Sometimes these findings are thought to be due to hypertrophic obstructive cardiomyopathy. The deep trabeculations can be seen in patients with some forms of congenital heart disease associated with ventricular pressure overload during fetal development. The other cause is left ventricular noncompaction, a genetic cardiomyopathy which is becoming increasingly recognized. The disorder, along with causing heart failure, is associated with a high risk of ventricular thrombus and thromboembolic events, and a high risk of arrhythmias and sudden death. The overall prognosis appears to be poor, compared to some other cardiomyopathies. The imaging findings of left ventricular noncompaction are nearly pathognomonic, and experienced echocardiographers can usually make the diagnosis. Finally, left heart catheterization or noninvasive stress testing should be part of the workup to definitively exclude an ischemic cardiomyopathy, even in the setting of noncompaction, and especially given his recent history of chest pain.

A left heart catheterization with coronary arteriography demonstrated no angiographic evidence of obstructive coronary disease. Left ventriculography revealed severe global hypokinesis. The patient was diagnosed with left ventricular noncompaction.

The initial medical management centers upon the treatment of heart failure with a beta‐blocker, ACE‐inhibitor, and diuretics for fluid management. Patients with left ventricular noncompaction are at particularly high risk of both embolic events (thought due to propensity to develop left ventricular clots within the deep recesses of the endocardium) and sudden death from arrhythmias. Thus, anticoagulation with warfarin is often indicated and would be reasonable in this patient, given the extremely low ejection fraction. The patient does meet established criteria for primary prophylaxis of sudden death with an implantable cardioverter‐defibrillator in nonischemic cardiomyopathy (left ventricular ejection fraction <35% and New York Heart Association class II failure), and this would also be appropriate therapy as well, given the high‐risk profile of this patient population.

He was discharged in stable condition with a medical regimen consisting of diuretics, metoprolol, and lisinopril. Given the risk for thromboembolism, he was started on warfarin. On subsequent follow‐up, repeat echocardiogram revealed a persistently low left ventricular ejection fraction at 10%. Despite his marked improvement in exercise tolerance and overall well‐being after 4 months of treatment, his ejection fraction did not improve. As a result, he was evaluated and counseled for placement of an implantable cardioverter‐defibrillator, and received a dual‐chamber device shortly afterward.

COMMENTARY

Left ventricular noncompaction is a form of cardiomyopathy increasingly recognized in both pediatric and adult populations. The hallmark features are a pattern of prominent trabeculations and deep recesses in the left ventricular wall. During normal gestation, the myocardium compacts and matures while deep recesses evolve into capillary precursors of the coronary circulation. Left ventricular noncompaction may result from an arrest in this process, with cardiac myofibers failing to compact from their initial spongiform architecture into a developed endocardium.1 Restrictive relaxation from persistent trabeculae predisposes to diastolic dysfunction, while systolic dysfunction may be related to subendocardial hypoperfusion and mechanical dyssynchrony between compacted and noncompacted myocardium.2

Differentiation of left ventricular noncompaction from other cardiomyopathies, based on history and physical examination alone, is essentially impossible. There is high variability and lack of specificity in both clinical profile and onset of symptoms. Electrocardiographic findings are also nonspecific, and the diagnosis typically becomes evident only with transthoracic echocardiography. Current diagnostic criteria include: 1) absence of coexisting cardiac abnormalities; 2) a two‐layer structure with >2:1 ratio of noncompacted to compacted myocardium; 3) predominant involvement of the apical segment of myocardium; and 4) deep intertrabecular recesses demonstrated on Doppler imaging.2, 3 Although echocardiography remains the standard in clinical practice, cardiac magnetic resonance imaging is being increasingly employed as well.4

With more awareness of the disease and the development of higher resolution imaging, the reported incidence has risen. In one single‐center study performed at a heart failure/transplant clinic, 3% of 960 patients referred to heart failure clinic were diagnosed with left ventricular noncompaction, a prevalence similar to hypertensive disease and hypertrophic cardiomyopathy.5 In another community‐hospitalbased study of 4929 adult patients referred for echocardiography, 3.7% of those with systolic dysfunction were diagnosed with noncompaction.6

Left ventricular noncompaction is considered a genetic cardiomyopathy; a family history of heart failure is often present.7 Despite its congenital origin and genetic involvement,2 it is unclear why symptoms may first present at an advanced age. Chest pain and shortness of breath are common complaints, and approximately 62% of patients will have congestive heart failure at presentation.8

Tachyarrhythmia and ventricular tachycardia are commonly seen, as are systemic embolic events and pulmonary embolism. Significant predictors of death include New York Heart Association class III‐IV, sustained ventricular arrhythmias, and increased left atrial size.9

Management is focused on the treatment of arrhythmias, heart failure, and thromboembolic events. The use of standard medical therapy for heart failure (including ACE‐inhibitors and beta‐blockers) is not based on large‐scale studies, yet remains the cornerstone of therapy. An implantable cardioverter‐defibrillator is indicated after hemodynamically compromising sustained ventricular tachycardia or aborted sudden cardiac death, but there are no guidelines for primary prophylaxis outside of patients with heart failure and a depressed ejection fraction.10 Cardiac resynchronization therapy has been successful in some patients with isolated left ventricular noncompaction. Long‐term oral anticoagulation is recommended, especially when impaired left ventricular function, thrombi, or atrial fibrillation have been documented. Patients with left ventricular dysfunction in concert with left ventricular noncompaction are at 10% higher risk for embolic complications when compared to those without noncompaction.11 Familial screening with echocardiography is indicated once the diagnosis has been made.2

In this Clinical Care Conundrum, we describe a rare but increasingly recognized condition, and highlight the importance of delineating the underlying cause of cardiomyopathy when possible. Treatment of heart failure in the hospital setting is sometimes more focused on initiation of diuresis and further stabilization of the patient, and less focused on elucidation of the etiology. While recognition of left ventricular failure led to early treatment with standard therapy in this case, identification of the underlying cause allowed for targeted interventions directed at cardiac arrhythmias, embolic events, and familial screening. Of note, the discussant was careful not to let the prior history of syncopal events distract him from the central issues in this case.

This case also serves as a reminder that congenital anomalies should remain on the differential diagnosis when evaluating new complaints in adult patients. The discussant approached the presentation of new‐onset left ventricular dysfunction in a thorough manner, weighing the likelihood of ischemic and nonischemic causes in the context of the history and physical examination. Careful consideration of the patient's new clinical manifestationscoupled with characteristic echocardiographic findings and normal coronary anatomysolidified the diagnosis. By developing a broad differential, the discussant and clinical team arrived at a diagnosis that for this 66‐year‐old gentleman was a lifetime in the making.

A 66‐year‐old man presented to the emergency department with 3 weeks of progressive exertional dyspnea. He also reported a single episode of chest pain 1 day prior to admission.

Cardiac and pulmonary causes of dyspnea are the most common. Other causes include anemia or a neuromuscular process. Given the recent episode of chest pain, coronary ischemia, congestive heart failure, chronic obstructive pulmonary disease (COPD), pulmonary embolism, and pericardial effusion must be considered.

Up until 3 weeks ago, he had no exercise intolerance, and had been relatively active. He began noticing progressive dyspnea to the point where he had considerable difficulty walking up stairs, and performing minor household chores. He also complained of orthopnea and paroxysmal nocturnal dyspnea for the last 3 weeks.He denied chest pain at presentation, but 24 hours prior, he experienced one episode of sharp, left‐sided, nonradiating, nonpositional chest pain that occurred at rest. It lasted approximately 20 minutes and was not associated with diaphoresis, nausea, vomiting, or palpitations. He had never experienced chest discomfort prior to this episode. He denied fever, chills, cough, or wheezing.

Progressive dyspnea on exertion with associated orthopnea and paroxysmal nocturnal dyspnea is classically seen in patients with heart failure and is typically associated with left ventricular failure. However, paroxysmal nocturnal dyspnea and orthopnea are only moderately specific for heart failure. Orthopnea can also be seen in pericardial disease, and in numerous pulmonary diseases, including asthma, COPD, pulmonary hypertension, diaphragmatic weakness, pleural effusion, pulmonary embolism, and any apical lung process including lung cancer or pneumonia. Paroxysmal nocturnal dyspnea can be seen in many of the same disorders and can also be reported in obstructive sleep apnea.

His past medical history was remarkable for two episodes of syncope, occurring 5 and 3 years ago, both while working outside in warm weather. Neither was associated with chest pain, diaphoresis, palpitations, or post‐ictal symptoms. He was diagnosed with prostate cancer 8 years ago, and underwent 2 years of androgen‐deprivation therapy with goserelin along with local radiation therapy. Medications included subcutaneous goserelin every 3 months and daily omeprazole. He denied any other prescription, over‐the‐counter, or herbal medications. He reported a 50‐pack‐year history of smoking, but denied alcohol or illicit drug abuse. He denied any travel history or recent immobilization. He had no children, and there was no known history of heart disease in his family.

The past medical history of two episodes of likely exertional syncope is interesting, but the episodes were sporadic and in the distant past, arguing against a serious and ongoing process. Nonetheless, this history still raises the possibility of cardiac causes of syncope, especially causes such as hypertrophic obstructive cardiomyopathy or aortic stenosis which are classically associated with exertional syncope. Either of these two conditions can result in heart failure if untreated. The history of goserelin therapy does make the possibility of heart failure higher, as there has been an association reported between use of this drug and heart failure. His history of tobacco use is a risk factor for coronary artery disease (CAD) and COPD. An active cancer history is also a risk factor for thromboembolic disease, which remains a consideration.

On admission, his temperature was 36.9C, heart rate 94 bpm, respiratory rate 22 breaths per minute, blood pressure 200/108 mmHg, and oxygen saturation 93% breathing ambient air. He was a thin man in no acute distress. Cardiovascular examination was significant for normal first and second heart sounds, with a soft left‐sided S3; the point of maximal impulse was diffuse, but displaced laterally. His jugular venous pressure was estimated at 9 cm of H₂O while positioned at a 45‐degree angle. Rales were heard at the lung bases bilaterally. Abdominal exam was normal. His lower extremities were without edema. There were no focal neurological deficits appreciated. Skin examination was unremarkable.

His combination of physical exam findings strongly suggests heart failure, most likely related to a dilated cardiomyopathy and left ventricular dysfunction. The presence of a left‐sided S3 and rales, and the lack of markedly elevated central venous pressure and peripheral edema, suggest heart failure predominantly due to left ventricular dysfunction. Of note, he is very hypertensive. This would not be the typical finding with severely decompensated heart failure. It would be important to determine whether his elevated blood pressure is due to an acute, reversible cause (e.g., pain, dyspnea, anxiety) or whether cocaine use, psychotropic agents, rare causes such as catecholamine‐producing tumors, other neuroendocrine tumors or thyroid toxic states are at play. In addition, one might see hypertension early in the course of heart failure, from a left ventricular outflow obstructive etiology such as severe aortic stenosis or hypertrophic obstructive cardiomyopathy.

Laboratory evaluation revealed a white blood cell count of 8900/mm³, with a normal differential; hemoglobin was 13.9 g/dL; platelet count was 264,000/mm³. Serum electrolytes and liver enzymes were unremarkable, with serum creatinine 1.1 mg/dL and blood urea nitrogen 7 mg/dL. Serial cardiac troponin‐I levels drawn 8 hours apart were 0.04, 0.07, 0.08, and 0.04 ng/mL (normal <0.04). Brain natriuretic peptide was 1420 pg/mL (normal <100). Thyroid stimulating hormone was 1.19 uIU/mL (normal 0.34‐5.60). Chest radiography revealed mild cardiomegaly, with peripheral interstitial opacities in the mid and lower lobes bilaterally, with fluid within the minor fissure. A 12‐lead electrocardiogram (ECG) revealed normal sinus rhythm at 95 bpm with left anterior fascicular block; intraventricular conduction delay was present (QRS width 106 ms) and QS complexes were present in V1‐V3. In addition, there was a left atrial abnormality and voltage criteria for left ventricular hypertrophy with secondary T‐wave inversions laterally (Figure 1). No previous ECGs were available for comparison. A chest computed tomography scan with contrast showed no evidence of pulmonary embolus. It did show interlobular septal thickening and small bilateral pleural effusions, consistent with left ventricular dysfunction.

Figure 1

The patient's initial lab, imaging, and diagnostic work‐up continues to be consistent with the diagnosis of heart failure. The patient appears to have cardiomegaly and mild pulmonary edema by imaging. The etiology of heart failure remains unknown, but ischemia remains in the differential, given the mildly elevated troponins initially and the ECG findings of left anterior fascicular block and T‐wave inversions in the lateral leads. Left anterior fascicular block can be seen with ischemic heart disease (especially involving the left anterior descending coronary artery), hypertensive heart disease, valvular disease, and some infiltrative cardiac processes. The lateral T‐wave inversions are likely secondary to left ventricular hypertrophy (a so‐called strain pattern), rather than ischemia. Left ventricular hypertrophy is consistent with his hypertension, suggesting that it is chronic; his presentation may be due to hypertensive heart disease with new onset heart failure.

He was admitted to the hospital, and metoprolol, lisinopril, and intravenous furosemide were given. Transthoracic echocardiography demonstrated severe global hypokinesis with a left ventricular ejection fraction of 10%. There was no evidence of ventricular thrombus or valvular disease; however, prominent left ventricular trabeculation with deep recesses was noted (see Figure 2).

Figure 2

The echocardiographic findings of deep recesses and prominent left ventricular trabeculation are seen in only a few disorders. Sometimes these findings are thought to be due to hypertrophic obstructive cardiomyopathy. The deep trabeculations can be seen in patients with some forms of congenital heart disease associated with ventricular pressure overload during fetal development. The other cause is left ventricular noncompaction, a genetic cardiomyopathy which is becoming increasingly recognized. The disorder, along with causing heart failure, is associated with a high risk of ventricular thrombus and thromboembolic events, and a high risk of arrhythmias and sudden death. The overall prognosis appears to be poor, compared to some other cardiomyopathies. The imaging findings of left ventricular noncompaction are nearly pathognomonic, and experienced echocardiographers can usually make the diagnosis. Finally, left heart catheterization or noninvasive stress testing should be part of the workup to definitively exclude an ischemic cardiomyopathy, even in the setting of noncompaction, and especially given his recent history of chest pain.

A left heart catheterization with coronary arteriography demonstrated no angiographic evidence of obstructive coronary disease. Left ventriculography revealed severe global hypokinesis. The patient was diagnosed with left ventricular noncompaction.

The initial medical management centers upon the treatment of heart failure with a beta‐blocker, ACE‐inhibitor, and diuretics for fluid management. Patients with left ventricular noncompaction are at particularly high risk of both embolic events (thought due to propensity to develop left ventricular clots within the deep recesses of the endocardium) and sudden death from arrhythmias. Thus, anticoagulation with warfarin is often indicated and would be reasonable in this patient, given the extremely low ejection fraction. The patient does meet established criteria for primary prophylaxis of sudden death with an implantable cardioverter‐defibrillator in nonischemic cardiomyopathy (left ventricular ejection fraction <35% and New York Heart Association class II failure), and this would also be appropriate therapy as well, given the high‐risk profile of this patient population.

He was discharged in stable condition with a medical regimen consisting of diuretics, metoprolol, and lisinopril. Given the risk for thromboembolism, he was started on warfarin. On subsequent follow‐up, repeat echocardiogram revealed a persistently low left ventricular ejection fraction at 10%. Despite his marked improvement in exercise tolerance and overall well‐being after 4 months of treatment, his ejection fraction did not improve. As a result, he was evaluated and counseled for placement of an implantable cardioverter‐defibrillator, and received a dual‐chamber device shortly afterward.

COMMENTARY

Left ventricular noncompaction is a form of cardiomyopathy increasingly recognized in both pediatric and adult populations. The hallmark features are a pattern of prominent trabeculations and deep recesses in the left ventricular wall. During normal gestation, the myocardium compacts and matures while deep recesses evolve into capillary precursors of the coronary circulation. Left ventricular noncompaction may result from an arrest in this process, with cardiac myofibers failing to compact from their initial spongiform architecture into a developed endocardium.1 Restrictive relaxation from persistent trabeculae predisposes to diastolic dysfunction, while systolic dysfunction may be related to subendocardial hypoperfusion and mechanical dyssynchrony between compacted and noncompacted myocardium.2

Differentiation of left ventricular noncompaction from other cardiomyopathies, based on history and physical examination alone, is essentially impossible. There is high variability and lack of specificity in both clinical profile and onset of symptoms. Electrocardiographic findings are also nonspecific, and the diagnosis typically becomes evident only with transthoracic echocardiography. Current diagnostic criteria include: 1) absence of coexisting cardiac abnormalities; 2) a two‐layer structure with >2:1 ratio of noncompacted to compacted myocardium; 3) predominant involvement of the apical segment of myocardium; and 4) deep intertrabecular recesses demonstrated on Doppler imaging.2, 3 Although echocardiography remains the standard in clinical practice, cardiac magnetic resonance imaging is being increasingly employed as well.4

With more awareness of the disease and the development of higher resolution imaging, the reported incidence has risen. In one single‐center study performed at a heart failure/transplant clinic, 3% of 960 patients referred to heart failure clinic were diagnosed with left ventricular noncompaction, a prevalence similar to hypertensive disease and hypertrophic cardiomyopathy.5 In another community‐hospitalbased study of 4929 adult patients referred for echocardiography, 3.7% of those with systolic dysfunction were diagnosed with noncompaction.6

Left ventricular noncompaction is considered a genetic cardiomyopathy; a family history of heart failure is often present.7 Despite its congenital origin and genetic involvement,2 it is unclear why symptoms may first present at an advanced age. Chest pain and shortness of breath are common complaints, and approximately 62% of patients will have congestive heart failure at presentation.8

Tachyarrhythmia and ventricular tachycardia are commonly seen, as are systemic embolic events and pulmonary embolism. Significant predictors of death include New York Heart Association class III‐IV, sustained ventricular arrhythmias, and increased left atrial size.9

Management is focused on the treatment of arrhythmias, heart failure, and thromboembolic events. The use of standard medical therapy for heart failure (including ACE‐inhibitors and beta‐blockers) is not based on large‐scale studies, yet remains the cornerstone of therapy. An implantable cardioverter‐defibrillator is indicated after hemodynamically compromising sustained ventricular tachycardia or aborted sudden cardiac death, but there are no guidelines for primary prophylaxis outside of patients with heart failure and a depressed ejection fraction.10 Cardiac resynchronization therapy has been successful in some patients with isolated left ventricular noncompaction. Long‐term oral anticoagulation is recommended, especially when impaired left ventricular function, thrombi, or atrial fibrillation have been documented. Patients with left ventricular dysfunction in concert with left ventricular noncompaction are at 10% higher risk for embolic complications when compared to those without noncompaction.11 Familial screening with echocardiography is indicated once the diagnosis has been made.2

In this Clinical Care Conundrum, we describe a rare but increasingly recognized condition, and highlight the importance of delineating the underlying cause of cardiomyopathy when possible. Treatment of heart failure in the hospital setting is sometimes more focused on initiation of diuresis and further stabilization of the patient, and less focused on elucidation of the etiology. While recognition of left ventricular failure led to early treatment with standard therapy in this case, identification of the underlying cause allowed for targeted interventions directed at cardiac arrhythmias, embolic events, and familial screening. Of note, the discussant was careful not to let the prior history of syncopal events distract him from the central issues in this case.

This case also serves as a reminder that congenital anomalies should remain on the differential diagnosis when evaluating new complaints in adult patients. The discussant approached the presentation of new‐onset left ventricular dysfunction in a thorough manner, weighing the likelihood of ischemic and nonischemic causes in the context of the history and physical examination. Careful consideration of the patient's new clinical manifestationscoupled with characteristic echocardiographic findings and normal coronary anatomysolidified the diagnosis. By developing a broad differential, the discussant and clinical team arrived at a diagnosis that for this 66‐year‐old gentleman was a lifetime in the making.

Ford and Britting's1 editorial in this month's Journal of Hospital Medicine raises important questions concerning the use of nonphysician providers in hospital medicine. They focus primarily on the use of mid‐level providers (MLPs), namely physician‐assistants (PAs) and nurse practitioners (NPs), as a potential solution to the current physician workforce shortages in our field. While we acknowledge the challenges of meeting workforce needs, we also believe that much is unknown about the optimal use of MLPs on inpatient general medicine services and it is premature to tout MLPs as the solution to hospital medicine staffing problems. This is especially true in those hospitals where hospitalists care for complex, general medical patients with a wide variety of medical conditions, a trend that is especially common in academic medical centers.2

This article discusses the current literature, our own experiences with MLPs, and suggests some future initiatives that might help better integrate MLPs into hospital medicine.

The Literature on MLPs in Inpatient Venues

The existing literature on the use of MLPs in inpatient venues is quite limited, and a recent review, while suggesting that the existing literature does describe benefits of MLPs in the inpatient setting, also states that the overall quality of the evidence is quite poor and that many studies suffer from significant limitations, including small populations, limited patient mixes, use of selected settings, and short durations of outcome assessment.3

Ford and Britting,1 in their article, cite several studies46 as evidence that a MLP model of care either improved outcomes or provided cost benefits. Each of these studies has important limitations that are worth examining.

The study by Myers et al.4 described the use of MLPs in a chest pain unit. NPs partnered with hospitalists to care for a low‐acuity chest pain population. In addition, 5 NPs only staffed the unit during daytime weekday hours. Off‐hour and weekend staffing was accomplished through the use of resident physicians. Notably, the work suggests the service only admitted 113 low‐risk patients over 10 months. The service was staffed by 3 full‐time equivalent (FTE) NPs in addition to involving hospitalists during the day. It is not surprising, given the extremely low volume of patients coupled with a daytime‐only focus, that this service showed efficiency gains. In addition, given the service was only staffed by NPs 40 hours a week and by resident physicians on nights and weekends, the true cost of such an intervention needs to take into account the full cost of 24/7 coverage. In addition, the model of using residents to cover nonteaching patients is no longer permitted by the current Accreditation Council for Graduate Medical Education (ACGME) Internal Medicine Residency Requirements7 and thus implementation of a model such as this in 2009 would require alternative means of nighttime coverage.

The study by Nishimura et al.,5 also describing the use of MLPs in cardiovascular care, has important caveats that make full assessment of the model impossible. The model describes the implementation of a care team consisting of an attending, a fellow, and MLPs to replace a traditional teaching team of an attending, senior resident, and 2 interns. The study states that the model resulted in a lower length of stay (LOS) and lower costs per case. Importantly, the new MLP‐based team only admitted during the hours of 7 _AM to 2 _PM. The study does not fully describe the number of MLPs required nor does it fully describe the role of cardiovascular fellows in the model. The study does state that the cost savings offset the cost of the MLPs but it is not clear if this cost analysis took into account the cost of the fellow's daytime involvement or if it measured attending time required before and after the implementation of the new model. In addition, this model presumes the availability of other services to admit patients during afternoon and nighttime hours and so may not be generalizable to other settings.

The final study by Cowan et al.6 describes the addition of a NP, a hospitalist medical director, and daily multidisciplinary rounds to a traditional teaching service model. Importantly, the NP was not involved in the admission process nor were they the primary providers for day‐to‐day medical care but rather they focused on implementation of care protocols, multidisciplinary coordination of care and discharge planning, and postdischarge follow‐up. In addition, the NP worked only weekdays for about 40 hours a week. It is not surprising that adding multiple additional resources to existing care models might provide benefits but this does not address any issues in terms of the workforce since the care in this model required a higher total input of providers than the usual care model being studied. Cost savings from such a model may make it cost‐effective but it does not represent a workforce solution.

There have been other studies examining the use of MLPs in the inpatient setting in internal medicine. Some of these studies have suggested that MLP‐based models result in equivalent outcomes and efficiency810 to traditional teaching or nonteaching physician‐only models. There are 2 important caveats, however, that must be considered. The total resources required for such models may be quite high, especially taking into account the costs of 24/7 coverage and physician backup of the MLPs, and most importantly there is almost no literature that robustly examines ultimate clinical outcomes in these models. We do note that a recent study11 did show a lower inpatient mortality rate over a 2‐year period of time after substituting a PA‐hospitalist model for a traditional academic medicine residency model in a community hospital. Importantly, however, the new model also added 24/7 hospitalist physicians and night and weekend intensivists that were not present in the prior residency‐based model. Thus, the lower mortality rate could be attributed to the addition of hospitalists or the more robust in‐house physician coverage during off‐hours rather than the use of MLPs.

Notably, while the evidence base in internal medicine is not robust, many studies have described successful use of MLPs in non‐internal medicine inpatient settings.1214 The reasons for this success is debatable, but it may be that MLPs are more successful in settings where the care is either more protocol‐driven or where there is less diagnostic and therapeutic complexity.

Recent Experiences with MLPs in Academic Hospital Medicine

Given the paucity of data, it is clear that further research is needed on the role of MLPs in hospital medicine. While waiting for such evidence to appear, it may be worthwhile to reflect on the recent experience of 3 major medical centers. A recent article described 5 hospitalist models at major academic medical centers across the country. Two of the institutions described at the time (University of Michigan Health System, Ann Arbor, MI; and Brigham and Women's Hospital, Boston, MA) utilized MLPs as a major element of their staffing of nonresident hospitalist services while another (University of California, San Francisco [UCSF] Medical Center at Mt. Zion, San Francisco, CA) had previously used MLPs as part of its model but phased them out about 1 year prior to publication of the article.2 The model used by the Brigham and Women's Hospital was later described in more detail in a subsequent publication.8 Recently 1 of these institutions (Michigan) has chosen to phase out MLPs. At Michigan, a 4‐year experience with PAs on a general‐medicine focused hospitalist service eventually led to the conclusion that continued use of PAs was not cost‐effective. Significant barriers to success included a steep learning curve and the significant time required before PAs developed sufficient autonomy and efficiency in caring for a highly complex heterogeneous patient population. In the Michigan experience, PAs took up to 2 years to attain a significant level of autonomy and efficiency and even then some PAs still required a significant amount of physician oversight. Similar concerns at UCSF Mt. Zion led to the elimination of their MLP program as well. At Brigham and Women's, the MLP service continues but has required additional hospitalist staffing due to difficulties recruiting qualified MLPs with appropriate inpatient experience. In all cases, the models were challenged by high costs and the difficulty of developing MLPs to attain the level of autonomy and efficiency needed to justify their continued use. A key point is that in each institution, MLPs continue to play an important role in some specialty inpatient areas such as Hematology/Oncology and Bone Marrow Transplant, which is where MLPs have traditionally found their niche in inpatient Internal Medicine. These focus shops allow MLPs to develop a niche and expertise in a specialized area, where they may become more autonomous and efficient than house staff. Thus these settings may be more appropriate for MLPs than a heterogeneous general medicine inpatient setting.

Reviewing the Financial Case

In their article, Ford and Britting1 cite potential financial advantages for the use of MLPs in hospital medicine by comparing the relative salaries of MLPs to Hospitalists. What was missing in their analysis was the relative productivity of the 2 types of providers. We do have some limited data from the Society of Hospital Medicine (SHM) annual survey that looks at MLPs in hospital medicine but, again, the number of respondents for most data elements is less than 70, making generalizability difficult. Nonetheless, the data suggest that MLPs in hospital medicine average about 60% to 75% of the productivity of a physician when measured by encounters, although there is wide variability depending on the employment model (academic vs. multispecialty group).15 Importantly, the existing data do not provide any measure of how much physician input is provided to these MLPs but we suspect that in most models there is some physician time and input. If we presume that the MLPs bill independently and collect 85% of the physician fee schedule for a Medicare population, then collections would be about 50% to 65% of a typical physician. Given that median total compensation including benefits from the SHM survey was $120,000 for MLPs and $216,000 for physiciansabout a 55% ratiothis would argue for potential financial neutrality when substituting MLPs for physicians in a 2:1 ratio but only if we presume they require no physician supervision, which in our own experience is not likely in a general medicine population. In an alternative model, in which the physician sees every patient with the MLP and the physician bills, one would need to see roughly 50% more patients to achieve a financially neutral situation. In our experience at our own institutions, this level of increased productivity was not achievable. It is important to note that our figures are median compensation and benefit cost figures and local markets vary widely. We know that in major east and west coast cities MLPs may command far higher salaries while early career hospitalist physicians may be paid somewhat less than the reported medians. Recent market changes have significantly pressured MLP salaries,15, 16 further impacting the financial equation and perhaps tilting it farther against a financial benefit for MLPs. Furthermore, night coverage for MLP services should always be considered in a financial analysis and is not captured in this simple analysis.

Next Steps

Given the current shortage of physicians, we imagine that many hospitalist groups will consider the use of MLPs as a solution to the current workforce issues. However, data on how best to utilize MLPs and the true impact on both the cost and quality of such models is lacking. In addition to urging increased publication and dissemination of existing experiences with NP and PAs, we strongly suggest that groups considering starting a MLP model do so in a way which would facilitate robust analysis and comparison of the model with alternatives. We also suggest that SHM consider the following: modifying its biennial survey to better capture the nuances of MLP productivity (such as assessing the amount of physician input and supervision required); targeting MLPs so as to increase the number of respondents; and doing an additional survey to capture demographics and basic data on existing MLP models given the lack of published literature.

In addition to gathering more data on effective models, a critical gap that we have identified is the development of models for the training and development of MLPs interested in hospital medicine. It would be a mistake to believe that MLPs could function in a manner similar to residency‐trained physicians if they do not undergo similar training. NP/PA programs generally do not have a significant inpatient internal medicine focus and so newly minted graduates often lack the skills needed to succeed in hospital medicine.17 Some hospitalist programs train their MLPs on the job, but many programs cannot afford the amount of time and effort required to do this on their own. There are a small number of advanced training options for MLPs in hospital medicine18 but it is not likely such models will proliferate given the inherent opportunity costs that exist for extended training in the current competitive job market for MLPs. Instead we think that very motivated hospital medicine groups may develop training relationships with PA and NP schools in an effort to train their own. In addition, national initiatives such as the Hospital Medicine Boot Camp for NPs and PAs, which is cosponsored by SHM, the American Association of Physician Assistants (AAPA), and the American Academy of Nurse Practitioners (AANP),19 can help fill the educational needs for MLPs who are already in practice.

Conclusions

While some literature exists that suggests that MLPs can successfully be used in the inpatient internal medicine setting, it is important to note that the evidence is quite limited and cannot be generalized across all care settings and patient populations. There is an urgent need to gather more data and share our collective experiences to better inform our decision‐making before we state that MLPs are the solution to workforce shortages in hospital medicine. In addition, existing data and experience suggest that MLPs may not be a cost‐effective workforce solution for complex general medical patients who require significant physician input. We believe that redesigning the clinical training of MLPs to focus on inpatient skills may hold promise and encourage interested parties to consider developing partnerships with MLP training programs and hospital medicine groups, as a way to build a more robust and successful hospital medicine MLP workforce.

Ford and Britting's1 editorial in this month's Journal of Hospital Medicine raises important questions concerning the use of nonphysician providers in hospital medicine. They focus primarily on the use of mid‐level providers (MLPs), namely physician‐assistants (PAs) and nurse practitioners (NPs), as a potential solution to the current physician workforce shortages in our field. While we acknowledge the challenges of meeting workforce needs, we also believe that much is unknown about the optimal use of MLPs on inpatient general medicine services and it is premature to tout MLPs as the solution to hospital medicine staffing problems. This is especially true in those hospitals where hospitalists care for complex, general medical patients with a wide variety of medical conditions, a trend that is especially common in academic medical centers.2

This article discusses the current literature, our own experiences with MLPs, and suggests some future initiatives that might help better integrate MLPs into hospital medicine.

The Literature on MLPs in Inpatient Venues

The existing literature on the use of MLPs in inpatient venues is quite limited, and a recent review, while suggesting that the existing literature does describe benefits of MLPs in the inpatient setting, also states that the overall quality of the evidence is quite poor and that many studies suffer from significant limitations, including small populations, limited patient mixes, use of selected settings, and short durations of outcome assessment.3

Ford and Britting,1 in their article, cite several studies46 as evidence that a MLP model of care either improved outcomes or provided cost benefits. Each of these studies has important limitations that are worth examining.

The study by Myers et al.4 described the use of MLPs in a chest pain unit. NPs partnered with hospitalists to care for a low‐acuity chest pain population. In addition, 5 NPs only staffed the unit during daytime weekday hours. Off‐hour and weekend staffing was accomplished through the use of resident physicians. Notably, the work suggests the service only admitted 113 low‐risk patients over 10 months. The service was staffed by 3 full‐time equivalent (FTE) NPs in addition to involving hospitalists during the day. It is not surprising, given the extremely low volume of patients coupled with a daytime‐only focus, that this service showed efficiency gains. In addition, given the service was only staffed by NPs 40 hours a week and by resident physicians on nights and weekends, the true cost of such an intervention needs to take into account the full cost of 24/7 coverage. In addition, the model of using residents to cover nonteaching patients is no longer permitted by the current Accreditation Council for Graduate Medical Education (ACGME) Internal Medicine Residency Requirements7 and thus implementation of a model such as this in 2009 would require alternative means of nighttime coverage.

The study by Nishimura et al.,5 also describing the use of MLPs in cardiovascular care, has important caveats that make full assessment of the model impossible. The model describes the implementation of a care team consisting of an attending, a fellow, and MLPs to replace a traditional teaching team of an attending, senior resident, and 2 interns. The study states that the model resulted in a lower length of stay (LOS) and lower costs per case. Importantly, the new MLP‐based team only admitted during the hours of 7 _AM to 2 _PM. The study does not fully describe the number of MLPs required nor does it fully describe the role of cardiovascular fellows in the model. The study does state that the cost savings offset the cost of the MLPs but it is not clear if this cost analysis took into account the cost of the fellow's daytime involvement or if it measured attending time required before and after the implementation of the new model. In addition, this model presumes the availability of other services to admit patients during afternoon and nighttime hours and so may not be generalizable to other settings.

The final study by Cowan et al.6 describes the addition of a NP, a hospitalist medical director, and daily multidisciplinary rounds to a traditional teaching service model. Importantly, the NP was not involved in the admission process nor were they the primary providers for day‐to‐day medical care but rather they focused on implementation of care protocols, multidisciplinary coordination of care and discharge planning, and postdischarge follow‐up. In addition, the NP worked only weekdays for about 40 hours a week. It is not surprising that adding multiple additional resources to existing care models might provide benefits but this does not address any issues in terms of the workforce since the care in this model required a higher total input of providers than the usual care model being studied. Cost savings from such a model may make it cost‐effective but it does not represent a workforce solution.

There have been other studies examining the use of MLPs in the inpatient setting in internal medicine. Some of these studies have suggested that MLP‐based models result in equivalent outcomes and efficiency810 to traditional teaching or nonteaching physician‐only models. There are 2 important caveats, however, that must be considered. The total resources required for such models may be quite high, especially taking into account the costs of 24/7 coverage and physician backup of the MLPs, and most importantly there is almost no literature that robustly examines ultimate clinical outcomes in these models. We do note that a recent study11 did show a lower inpatient mortality rate over a 2‐year period of time after substituting a PA‐hospitalist model for a traditional academic medicine residency model in a community hospital. Importantly, however, the new model also added 24/7 hospitalist physicians and night and weekend intensivists that were not present in the prior residency‐based model. Thus, the lower mortality rate could be attributed to the addition of hospitalists or the more robust in‐house physician coverage during off‐hours rather than the use of MLPs.

Notably, while the evidence base in internal medicine is not robust, many studies have described successful use of MLPs in non‐internal medicine inpatient settings.1214 The reasons for this success is debatable, but it may be that MLPs are more successful in settings where the care is either more protocol‐driven or where there is less diagnostic and therapeutic complexity.

Recent Experiences with MLPs in Academic Hospital Medicine

Given the paucity of data, it is clear that further research is needed on the role of MLPs in hospital medicine. While waiting for such evidence to appear, it may be worthwhile to reflect on the recent experience of 3 major medical centers. A recent article described 5 hospitalist models at major academic medical centers across the country. Two of the institutions described at the time (University of Michigan Health System, Ann Arbor, MI; and Brigham and Women's Hospital, Boston, MA) utilized MLPs as a major element of their staffing of nonresident hospitalist services while another (University of California, San Francisco [UCSF] Medical Center at Mt. Zion, San Francisco, CA) had previously used MLPs as part of its model but phased them out about 1 year prior to publication of the article.2 The model used by the Brigham and Women's Hospital was later described in more detail in a subsequent publication.8 Recently 1 of these institutions (Michigan) has chosen to phase out MLPs. At Michigan, a 4‐year experience with PAs on a general‐medicine focused hospitalist service eventually led to the conclusion that continued use of PAs was not cost‐effective. Significant barriers to success included a steep learning curve and the significant time required before PAs developed sufficient autonomy and efficiency in caring for a highly complex heterogeneous patient population. In the Michigan experience, PAs took up to 2 years to attain a significant level of autonomy and efficiency and even then some PAs still required a significant amount of physician oversight. Similar concerns at UCSF Mt. Zion led to the elimination of their MLP program as well. At Brigham and Women's, the MLP service continues but has required additional hospitalist staffing due to difficulties recruiting qualified MLPs with appropriate inpatient experience. In all cases, the models were challenged by high costs and the difficulty of developing MLPs to attain the level of autonomy and efficiency needed to justify their continued use. A key point is that in each institution, MLPs continue to play an important role in some specialty inpatient areas such as Hematology/Oncology and Bone Marrow Transplant, which is where MLPs have traditionally found their niche in inpatient Internal Medicine. These focus shops allow MLPs to develop a niche and expertise in a specialized area, where they may become more autonomous and efficient than house staff. Thus these settings may be more appropriate for MLPs than a heterogeneous general medicine inpatient setting.

Reviewing the Financial Case

In their article, Ford and Britting1 cite potential financial advantages for the use of MLPs in hospital medicine by comparing the relative salaries of MLPs to Hospitalists. What was missing in their analysis was the relative productivity of the 2 types of providers. We do have some limited data from the Society of Hospital Medicine (SHM) annual survey that looks at MLPs in hospital medicine but, again, the number of respondents for most data elements is less than 70, making generalizability difficult. Nonetheless, the data suggest that MLPs in hospital medicine average about 60% to 75% of the productivity of a physician when measured by encounters, although there is wide variability depending on the employment model (academic vs. multispecialty group).15 Importantly, the existing data do not provide any measure of how much physician input is provided to these MLPs but we suspect that in most models there is some physician time and input. If we presume that the MLPs bill independently and collect 85% of the physician fee schedule for a Medicare population, then collections would be about 50% to 65% of a typical physician. Given that median total compensation including benefits from the SHM survey was $120,000 for MLPs and $216,000 for physiciansabout a 55% ratiothis would argue for potential financial neutrality when substituting MLPs for physicians in a 2:1 ratio but only if we presume they require no physician supervision, which in our own experience is not likely in a general medicine population. In an alternative model, in which the physician sees every patient with the MLP and the physician bills, one would need to see roughly 50% more patients to achieve a financially neutral situation. In our experience at our own institutions, this level of increased productivity was not achievable. It is important to note that our figures are median compensation and benefit cost figures and local markets vary widely. We know that in major east and west coast cities MLPs may command far higher salaries while early career hospitalist physicians may be paid somewhat less than the reported medians. Recent market changes have significantly pressured MLP salaries,15, 16 further impacting the financial equation and perhaps tilting it farther against a financial benefit for MLPs. Furthermore, night coverage for MLP services should always be considered in a financial analysis and is not captured in this simple analysis.

Next Steps

Given the current shortage of physicians, we imagine that many hospitalist groups will consider the use of MLPs as a solution to the current workforce issues. However, data on how best to utilize MLPs and the true impact on both the cost and quality of such models is lacking. In addition to urging increased publication and dissemination of existing experiences with NP and PAs, we strongly suggest that groups considering starting a MLP model do so in a way which would facilitate robust analysis and comparison of the model with alternatives. We also suggest that SHM consider the following: modifying its biennial survey to better capture the nuances of MLP productivity (such as assessing the amount of physician input and supervision required); targeting MLPs so as to increase the number of respondents; and doing an additional survey to capture demographics and basic data on existing MLP models given the lack of published literature.

In addition to gathering more data on effective models, a critical gap that we have identified is the development of models for the training and development of MLPs interested in hospital medicine. It would be a mistake to believe that MLPs could function in a manner similar to residency‐trained physicians if they do not undergo similar training. NP/PA programs generally do not have a significant inpatient internal medicine focus and so newly minted graduates often lack the skills needed to succeed in hospital medicine.17 Some hospitalist programs train their MLPs on the job, but many programs cannot afford the amount of time and effort required to do this on their own. There are a small number of advanced training options for MLPs in hospital medicine18 but it is not likely such models will proliferate given the inherent opportunity costs that exist for extended training in the current competitive job market for MLPs. Instead we think that very motivated hospital medicine groups may develop training relationships with PA and NP schools in an effort to train their own. In addition, national initiatives such as the Hospital Medicine Boot Camp for NPs and PAs, which is cosponsored by SHM, the American Association of Physician Assistants (AAPA), and the American Academy of Nurse Practitioners (AANP),19 can help fill the educational needs for MLPs who are already in practice.

Conclusions

While some literature exists that suggests that MLPs can successfully be used in the inpatient internal medicine setting, it is important to note that the evidence is quite limited and cannot be generalized across all care settings and patient populations. There is an urgent need to gather more data and share our collective experiences to better inform our decision‐making before we state that MLPs are the solution to workforce shortages in hospital medicine. In addition, existing data and experience suggest that MLPs may not be a cost‐effective workforce solution for complex general medical patients who require significant physician input. We believe that redesigning the clinical training of MLPs to focus on inpatient skills may hold promise and encourage interested parties to consider developing partnerships with MLP training programs and hospital medicine groups, as a way to build a more robust and successful hospital medicine MLP workforce.

Ford and Britting's1 editorial in this month's Journal of Hospital Medicine raises important questions concerning the use of nonphysician providers in hospital medicine. They focus primarily on the use of mid‐level providers (MLPs), namely physician‐assistants (PAs) and nurse practitioners (NPs), as a potential solution to the current physician workforce shortages in our field. While we acknowledge the challenges of meeting workforce needs, we also believe that much is unknown about the optimal use of MLPs on inpatient general medicine services and it is premature to tout MLPs as the solution to hospital medicine staffing problems. This is especially true in those hospitals where hospitalists care for complex, general medical patients with a wide variety of medical conditions, a trend that is especially common in academic medical centers.2

This article discusses the current literature, our own experiences with MLPs, and suggests some future initiatives that might help better integrate MLPs into hospital medicine.

The Literature on MLPs in Inpatient Venues

The existing literature on the use of MLPs in inpatient venues is quite limited, and a recent review, while suggesting that the existing literature does describe benefits of MLPs in the inpatient setting, also states that the overall quality of the evidence is quite poor and that many studies suffer from significant limitations, including small populations, limited patient mixes, use of selected settings, and short durations of outcome assessment.3

Ford and Britting,1 in their article, cite several studies46 as evidence that a MLP model of care either improved outcomes or provided cost benefits. Each of these studies has important limitations that are worth examining.

The study by Myers et al.4 described the use of MLPs in a chest pain unit. NPs partnered with hospitalists to care for a low‐acuity chest pain population. In addition, 5 NPs only staffed the unit during daytime weekday hours. Off‐hour and weekend staffing was accomplished through the use of resident physicians. Notably, the work suggests the service only admitted 113 low‐risk patients over 10 months. The service was staffed by 3 full‐time equivalent (FTE) NPs in addition to involving hospitalists during the day. It is not surprising, given the extremely low volume of patients coupled with a daytime‐only focus, that this service showed efficiency gains. In addition, given the service was only staffed by NPs 40 hours a week and by resident physicians on nights and weekends, the true cost of such an intervention needs to take into account the full cost of 24/7 coverage. In addition, the model of using residents to cover nonteaching patients is no longer permitted by the current Accreditation Council for Graduate Medical Education (ACGME) Internal Medicine Residency Requirements7 and thus implementation of a model such as this in 2009 would require alternative means of nighttime coverage.

The study by Nishimura et al.,5 also describing the use of MLPs in cardiovascular care, has important caveats that make full assessment of the model impossible. The model describes the implementation of a care team consisting of an attending, a fellow, and MLPs to replace a traditional teaching team of an attending, senior resident, and 2 interns. The study states that the model resulted in a lower length of stay (LOS) and lower costs per case. Importantly, the new MLP‐based team only admitted during the hours of 7 _AM to 2 _PM. The study does not fully describe the number of MLPs required nor does it fully describe the role of cardiovascular fellows in the model. The study does state that the cost savings offset the cost of the MLPs but it is not clear if this cost analysis took into account the cost of the fellow's daytime involvement or if it measured attending time required before and after the implementation of the new model. In addition, this model presumes the availability of other services to admit patients during afternoon and nighttime hours and so may not be generalizable to other settings.

The final study by Cowan et al.6 describes the addition of a NP, a hospitalist medical director, and daily multidisciplinary rounds to a traditional teaching service model. Importantly, the NP was not involved in the admission process nor were they the primary providers for day‐to‐day medical care but rather they focused on implementation of care protocols, multidisciplinary coordination of care and discharge planning, and postdischarge follow‐up. In addition, the NP worked only weekdays for about 40 hours a week. It is not surprising that adding multiple additional resources to existing care models might provide benefits but this does not address any issues in terms of the workforce since the care in this model required a higher total input of providers than the usual care model being studied. Cost savings from such a model may make it cost‐effective but it does not represent a workforce solution.

There have been other studies examining the use of MLPs in the inpatient setting in internal medicine. Some of these studies have suggested that MLP‐based models result in equivalent outcomes and efficiency810 to traditional teaching or nonteaching physician‐only models. There are 2 important caveats, however, that must be considered. The total resources required for such models may be quite high, especially taking into account the costs of 24/7 coverage and physician backup of the MLPs, and most importantly there is almost no literature that robustly examines ultimate clinical outcomes in these models. We do note that a recent study11 did show a lower inpatient mortality rate over a 2‐year period of time after substituting a PA‐hospitalist model for a traditional academic medicine residency model in a community hospital. Importantly, however, the new model also added 24/7 hospitalist physicians and night and weekend intensivists that were not present in the prior residency‐based model. Thus, the lower mortality rate could be attributed to the addition of hospitalists or the more robust in‐house physician coverage during off‐hours rather than the use of MLPs.

Notably, while the evidence base in internal medicine is not robust, many studies have described successful use of MLPs in non‐internal medicine inpatient settings.1214 The reasons for this success is debatable, but it may be that MLPs are more successful in settings where the care is either more protocol‐driven or where there is less diagnostic and therapeutic complexity.

Recent Experiences with MLPs in Academic Hospital Medicine

Given the paucity of data, it is clear that further research is needed on the role of MLPs in hospital medicine. While waiting for such evidence to appear, it may be worthwhile to reflect on the recent experience of 3 major medical centers. A recent article described 5 hospitalist models at major academic medical centers across the country. Two of the institutions described at the time (University of Michigan Health System, Ann Arbor, MI; and Brigham and Women's Hospital, Boston, MA) utilized MLPs as a major element of their staffing of nonresident hospitalist services while another (University of California, San Francisco [UCSF] Medical Center at Mt. Zion, San Francisco, CA) had previously used MLPs as part of its model but phased them out about 1 year prior to publication of the article.2 The model used by the Brigham and Women's Hospital was later described in more detail in a subsequent publication.8 Recently 1 of these institutions (Michigan) has chosen to phase out MLPs. At Michigan, a 4‐year experience with PAs on a general‐medicine focused hospitalist service eventually led to the conclusion that continued use of PAs was not cost‐effective. Significant barriers to success included a steep learning curve and the significant time required before PAs developed sufficient autonomy and efficiency in caring for a highly complex heterogeneous patient population. In the Michigan experience, PAs took up to 2 years to attain a significant level of autonomy and efficiency and even then some PAs still required a significant amount of physician oversight. Similar concerns at UCSF Mt. Zion led to the elimination of their MLP program as well. At Brigham and Women's, the MLP service continues but has required additional hospitalist staffing due to difficulties recruiting qualified MLPs with appropriate inpatient experience. In all cases, the models were challenged by high costs and the difficulty of developing MLPs to attain the level of autonomy and efficiency needed to justify their continued use. A key point is that in each institution, MLPs continue to play an important role in some specialty inpatient areas such as Hematology/Oncology and Bone Marrow Transplant, which is where MLPs have traditionally found their niche in inpatient Internal Medicine. These focus shops allow MLPs to develop a niche and expertise in a specialized area, where they may become more autonomous and efficient than house staff. Thus these settings may be more appropriate for MLPs than a heterogeneous general medicine inpatient setting.

Reviewing the Financial Case

In their article, Ford and Britting1 cite potential financial advantages for the use of MLPs in hospital medicine by comparing the relative salaries of MLPs to Hospitalists. What was missing in their analysis was the relative productivity of the 2 types of providers. We do have some limited data from the Society of Hospital Medicine (SHM) annual survey that looks at MLPs in hospital medicine but, again, the number of respondents for most data elements is less than 70, making generalizability difficult. Nonetheless, the data suggest that MLPs in hospital medicine average about 60% to 75% of the productivity of a physician when measured by encounters, although there is wide variability depending on the employment model (academic vs. multispecialty group).15 Importantly, the existing data do not provide any measure of how much physician input is provided to these MLPs but we suspect that in most models there is some physician time and input. If we presume that the MLPs bill independently and collect 85% of the physician fee schedule for a Medicare population, then collections would be about 50% to 65% of a typical physician. Given that median total compensation including benefits from the SHM survey was $120,000 for MLPs and $216,000 for physiciansabout a 55% ratiothis would argue for potential financial neutrality when substituting MLPs for physicians in a 2:1 ratio but only if we presume they require no physician supervision, which in our own experience is not likely in a general medicine population. In an alternative model, in which the physician sees every patient with the MLP and the physician bills, one would need to see roughly 50% more patients to achieve a financially neutral situation. In our experience at our own institutions, this level of increased productivity was not achievable. It is important to note that our figures are median compensation and benefit cost figures and local markets vary widely. We know that in major east and west coast cities MLPs may command far higher salaries while early career hospitalist physicians may be paid somewhat less than the reported medians. Recent market changes have significantly pressured MLP salaries,15, 16 further impacting the financial equation and perhaps tilting it farther against a financial benefit for MLPs. Furthermore, night coverage for MLP services should always be considered in a financial analysis and is not captured in this simple analysis.

Next Steps

Given the current shortage of physicians, we imagine that many hospitalist groups will consider the use of MLPs as a solution to the current workforce issues. However, data on how best to utilize MLPs and the true impact on both the cost and quality of such models is lacking. In addition to urging increased publication and dissemination of existing experiences with NP and PAs, we strongly suggest that groups considering starting a MLP model do so in a way which would facilitate robust analysis and comparison of the model with alternatives. We also suggest that SHM consider the following: modifying its biennial survey to better capture the nuances of MLP productivity (such as assessing the amount of physician input and supervision required); targeting MLPs so as to increase the number of respondents; and doing an additional survey to capture demographics and basic data on existing MLP models given the lack of published literature.

In addition to gathering more data on effective models, a critical gap that we have identified is the development of models for the training and development of MLPs interested in hospital medicine. It would be a mistake to believe that MLPs could function in a manner similar to residency‐trained physicians if they do not undergo similar training. NP/PA programs generally do not have a significant inpatient internal medicine focus and so newly minted graduates often lack the skills needed to succeed in hospital medicine.17 Some hospitalist programs train their MLPs on the job, but many programs cannot afford the amount of time and effort required to do this on their own. There are a small number of advanced training options for MLPs in hospital medicine18 but it is not likely such models will proliferate given the inherent opportunity costs that exist for extended training in the current competitive job market for MLPs. Instead we think that very motivated hospital medicine groups may develop training relationships with PA and NP schools in an effort to train their own. In addition, national initiatives such as the Hospital Medicine Boot Camp for NPs and PAs, which is cosponsored by SHM, the American Association of Physician Assistants (AAPA), and the American Academy of Nurse Practitioners (AANP),19 can help fill the educational needs for MLPs who are already in practice.

Conclusions

While some literature exists that suggests that MLPs can successfully be used in the inpatient internal medicine setting, it is important to note that the evidence is quite limited and cannot be generalized across all care settings and patient populations. There is an urgent need to gather more data and share our collective experiences to better inform our decision‐making before we state that MLPs are the solution to workforce shortages in hospital medicine. In addition, existing data and experience suggest that MLPs may not be a cost‐effective workforce solution for complex general medical patients who require significant physician input. We believe that redesigning the clinical training of MLPs to focus on inpatient skills may hold promise and encourage interested parties to consider developing partnerships with MLP training programs and hospital medicine groups, as a way to build a more robust and successful hospital medicine MLP workforce.

Many academic medical centers (AMCs) have developed nonhousestaff services to provide clinical care once provided by physicians‐in‐training. These services, often staffed by hospitalists and/or midlevel providers, have experienced tremendous growth in the past few years, yet very little exists in the literature about their development, structure, efficacy, or impact on hospitals, patients, and hospital medicine programs. The primary forces driving this growth include Accreditation Council for Graduate Medical Education (ACGME) resident duty hour restrictions,1 growth of the hospitalist movement,2 and the emphasis on simultaneously improving financial performance and quality of care in AMCs.3

Resident Duty Hour Restrictions

In 2003, the ACGME mandated restrictions on resident work hours, limiting trainees to 80 hours per week.1 Many training programs struggled with how to provide important clinical services while complying with the new restrictionscreating numerous models that bridged care between different shifts of residents.45 Implementation of day floats (a dedicated resident who rounds with the postcall team), night floats (a dedicated overnight resident who admits and cross‐covers patients), or some variation of both was common.6 No guidelines accompanied the ACGME mandate, leaving institutions to independently structure their programs without a known best practice.

Subsequent literature carefully addressed how the duty hour restrictions affect residents' lives and education but failed to discuss models for providing care.711 Training programs began to institute necessary changes but in doing so, created greater patient discontinuity and increased handoffs between residents, elevating the potential for adverse patient outcomes.12 Recent large‐scale studies indicate that inpatient care is the same or improved since adoption of the duty hour restrictions,1316 but controversy continues, with several editorials debating the issue.1719

Because increasing the volume of patients on housestaff services was not a viable option,20 many AMCs created nonhousestaff services and hired midlevel providers (nurse practitioners and physician assistants) to offset resident workloads and comply with the new restrictions. However, this strategy represented a very expensive alternative.21 Moreover, the current 80‐hour work limits may be revised downward, particularly given the lower restrictions in other countries,22 and this will further drive the demand for nonhousestaff services. Hospitalists, with their documented impact on efficiency and return on investment,23 represent a solution to fill these needs and have quickly become the predominant approach at AMCs.

The Hospitalist Movement

Since the term hospitalist was first coined in 1996,24 the remarkable growth of the number of practicing hospitalists emphasizes how first community hospitals and now AMCs have embraced this approach.25 With more than 20,000 nationwide and projections that the field will grow to 30,000 by 2010,26 hospitalists are becoming the primary providers for in‐patients.2 This growth was further catalyzed when widely expressed concerns about safety and quality became public,2728 and hospitalists incorporated patient safety and quality improvement activities into their efforts.3 The confluence of these factors also prompted emergence of hospital medicine programs at AMCs, a growth that came with anticipated dangers.29 Reflecting the recognition that hospital medicine is becoming a separate specialty30 and is integral to the functioning of an AMC, institutions now operate dedicated divisions of hospital medicine.

AMCs and Hospital Performance

AMCs operate 3 related enterprises: a medical school that trains future physicians, a research arena that promotes basic and clinical investigation, and health care services that often encompass both hospitals and clinics. The financial viability of AMCs has always been a topic of debate, largely because of the different missions they pursue and the financial means by which they survive.3133 Over the past decade, cuts in Medicare reimbursement, challenges in balancing bed availability with occupancy rates, and a growing emphasis on cost reduction have created a more competitive health care environment, but without the predicted demise of AMCs.34 Because education and research generally fail to bolster the bottom line, AMCs have focused on optimizing clinical services to promote financial viability.

Hospitalists are uniquely positioned to help this bottom line, just as they do at community hospitals. Their involvement in patient care may produce reductions in length of stay, greater efficiency in discharge planning, and significant cost savings.3537 Hospitalists may also improve throughput in emergency departments and decrease wait times, leading to more efficient bed utilization.38 This leads to a potential for greater hospital revenue by increasing both the number of admissions, particularly surgical cases, and staffed inpatient beds, the latter a premium, as AMCs continue to expand their bed capacity almost annually. Finally, hospitalists may serve as change agents in improving the quality and safety of care delivered, an increasingly important metric given the desire for and expansion of publicly reported measures.

From a financial standpoint, Medicare support to AMCs for training residents now subsidizes fewer clinical care hours. Hospitalist‐driven nonhousestaff services will continue to fulfill a need created by this marked change in residency training. The tension of who pays for nonhousestaff servicesincreased federal support, financial backing from AMCs, or academic department fundsposes an ongoing struggle. In fact, this may be the most important issue currently debated among hospital administrators and department chairs. Regardless, AMCs continue to view hospitalists as a mechanism (or even solution) to maintaining their financial bottom line through improving care delivery systems, adhering to resident work hour restrictions, leading quality and safety improvement initiatives, and improving clinical patient outcomes.

MODELS FOR NONHOUSESTAFF MEDICAL SERVICES

For AMCs developing nonhousestaff services, the process begins by addressing a series of important questions (Table 1). How these questions are answered is often driven by local factors such as the vision of local leadership and the availability of important resources. Nonetheless, it is important for hospitals to share their experiences because best practices remain unclear. Table 2 provides a tabular snapshot of nonhousestaff medicine services at 5 AMCs to highlight similarities and differences. Data in the table were compiled by having a representative from each AMC report the different attributes, which reflects each program as of July 2007. Table 2 provides no data on the quality or efficiency of housestaff versus nonhousestaff services, though this type of investigation is underway and will be critical in future planning.3940

Table 2 does illustrate several important considerations in structuring nonhousestaff services. For example, if a nonhousestaff service operates at a different physical location, careful triage of patients is necessary. Resources, including the availability of subspecialty and surgical consultants, may differ, and thus patient complexity and acuity may dictate whether a patient gets admitted to the nonhousestaff service. These triage factors were a major challenge in the design of UCSF's nonhousestaff service. The other nonhousestaff services handle overflow admissions after the housestaff service reaches a census or admission cap; transfers between services rarely occur, and resources are similar.

Other observations include that hospitalists work a similar number of hours each year and cover 50% of weekends but with differing shift lengths and sequences. Each service also provides night coverage but only Emory, the University of Michigan, and Northwestern utilize dedicated nocturnists. The University of Michigan and Brigham & Women's Hospital are the only sites that employ midlevel providers who work closely with hospitalists. In terms of group structure, Northwestern's hospitalists are the most integrated, with each hospitalist sharing equal responsibility for nonhousestaff coverage. In contrast, the other programs use selected hospitalists or a dedicated core of hospitalists to provide nonhousestaff services. Compensation models also vary, with certain groups salaried and others having incentive systems, although all receive hospital‐based funding support. Hospital‐based funding support ranges from 40% to 100% of total program costs across sites, creating similar variance in a given program's deficit risk. Finally, most programs do compensate nonhousestaff services at higher rates.

All the decisions captured in Table 2 have implications for costs, recruitment, and service structure. Furthermore, the striking variations demonstrate how different academic hospitalist positions can occur both within a hospital medicine group and across institutions. Of note, Table 2 only characterizes nonhousestaff medicine services, not the growing number of comanagement (eg, orthopedics, neurosurgery, or hematology/oncology) and other clinical services (eg, observation unit or preoperative medicine clinic) also staffed by hospitalists at AMCs.

CHALLENGES

Hospital medicine programs and AMCs face several challenges in building non‐housestaff services, but these will likely become less daunting as programs learn from their own experiences, from those of colleagues at other institutions, and from future investigations of these care models. We highlight a few issues below that warrant important consideration.

FUTURE DIRECTIONS

Many lament that the milieu for academic hospitalists raises more challenges than solutions, but we believe the current era is one of excitement and opportunity. In the coming years, we will experience continued growth of nonhousestaff services, including greater comanagement with our surgical and medical specialty colleagues. These opportunities will create new relationships and increase our visibility in AMCs. However, we must remain committed to studying nonhousestaff services and determine if and how they differ from their housestaff and community counterparts, as this will be an important step toward addressing current challenges.

As hospitalists take on increasingly diverse roles,45 we must also lead initiatives to better train, recruit, and retain those interested in our specialty. Promoting our field and recruiting future faculty should occur through local hospitalist career nights, events at national meetings (targeting students, housestaff, and fellows), and other mechanisms utilized by our subspecialty colleagues. For housestaff interested in fellowship training, the growing number of hospitalist fellowships can provide skills in teaching and quality improvement.46 For trainees committed to research, we should work with existing general medicine research fellowships and partner to provide hospitalist mentorship.

Hospitalists are in a unique position to influence the delivery of clinical services, shape the future of residency training, guide quality and safety improvement initiatives, and take on leadership roles through our departments, universities, and medical centers. With the growing number of clinical services being added to our portfolio, we will need careful planning and evaluation of our efforts to build successful partnerships and develop faculty roles that balance clinical and academic pursuits to sustain long‐term and satisfying hospitalist careers.

Many academic medical centers (AMCs) have developed nonhousestaff services to provide clinical care once provided by physicians‐in‐training. These services, often staffed by hospitalists and/or midlevel providers, have experienced tremendous growth in the past few years, yet very little exists in the literature about their development, structure, efficacy, or impact on hospitals, patients, and hospital medicine programs. The primary forces driving this growth include Accreditation Council for Graduate Medical Education (ACGME) resident duty hour restrictions,1 growth of the hospitalist movement,2 and the emphasis on simultaneously improving financial performance and quality of care in AMCs.3

Resident Duty Hour Restrictions

In 2003, the ACGME mandated restrictions on resident work hours, limiting trainees to 80 hours per week.1 Many training programs struggled with how to provide important clinical services while complying with the new restrictionscreating numerous models that bridged care between different shifts of residents.45 Implementation of day floats (a dedicated resident who rounds with the postcall team), night floats (a dedicated overnight resident who admits and cross‐covers patients), or some variation of both was common.6 No guidelines accompanied the ACGME mandate, leaving institutions to independently structure their programs without a known best practice.

Subsequent literature carefully addressed how the duty hour restrictions affect residents' lives and education but failed to discuss models for providing care.711 Training programs began to institute necessary changes but in doing so, created greater patient discontinuity and increased handoffs between residents, elevating the potential for adverse patient outcomes.12 Recent large‐scale studies indicate that inpatient care is the same or improved since adoption of the duty hour restrictions,1316 but controversy continues, with several editorials debating the issue.1719

Because increasing the volume of patients on housestaff services was not a viable option,20 many AMCs created nonhousestaff services and hired midlevel providers (nurse practitioners and physician assistants) to offset resident workloads and comply with the new restrictions. However, this strategy represented a very expensive alternative.21 Moreover, the current 80‐hour work limits may be revised downward, particularly given the lower restrictions in other countries,22 and this will further drive the demand for nonhousestaff services. Hospitalists, with their documented impact on efficiency and return on investment,23 represent a solution to fill these needs and have quickly become the predominant approach at AMCs.

The Hospitalist Movement

Since the term hospitalist was first coined in 1996,24 the remarkable growth of the number of practicing hospitalists emphasizes how first community hospitals and now AMCs have embraced this approach.25 With more than 20,000 nationwide and projections that the field will grow to 30,000 by 2010,26 hospitalists are becoming the primary providers for in‐patients.2 This growth was further catalyzed when widely expressed concerns about safety and quality became public,2728 and hospitalists incorporated patient safety and quality improvement activities into their efforts.3 The confluence of these factors also prompted emergence of hospital medicine programs at AMCs, a growth that came with anticipated dangers.29 Reflecting the recognition that hospital medicine is becoming a separate specialty30 and is integral to the functioning of an AMC, institutions now operate dedicated divisions of hospital medicine.

AMCs and Hospital Performance

AMCs operate 3 related enterprises: a medical school that trains future physicians, a research arena that promotes basic and clinical investigation, and health care services that often encompass both hospitals and clinics. The financial viability of AMCs has always been a topic of debate, largely because of the different missions they pursue and the financial means by which they survive.3133 Over the past decade, cuts in Medicare reimbursement, challenges in balancing bed availability with occupancy rates, and a growing emphasis on cost reduction have created a more competitive health care environment, but without the predicted demise of AMCs.34 Because education and research generally fail to bolster the bottom line, AMCs have focused on optimizing clinical services to promote financial viability.

Hospitalists are uniquely positioned to help this bottom line, just as they do at community hospitals. Their involvement in patient care may produce reductions in length of stay, greater efficiency in discharge planning, and significant cost savings.3537 Hospitalists may also improve throughput in emergency departments and decrease wait times, leading to more efficient bed utilization.38 This leads to a potential for greater hospital revenue by increasing both the number of admissions, particularly surgical cases, and staffed inpatient beds, the latter a premium, as AMCs continue to expand their bed capacity almost annually. Finally, hospitalists may serve as change agents in improving the quality and safety of care delivered, an increasingly important metric given the desire for and expansion of publicly reported measures.

From a financial standpoint, Medicare support to AMCs for training residents now subsidizes fewer clinical care hours. Hospitalist‐driven nonhousestaff services will continue to fulfill a need created by this marked change in residency training. The tension of who pays for nonhousestaff servicesincreased federal support, financial backing from AMCs, or academic department fundsposes an ongoing struggle. In fact, this may be the most important issue currently debated among hospital administrators and department chairs. Regardless, AMCs continue to view hospitalists as a mechanism (or even solution) to maintaining their financial bottom line through improving care delivery systems, adhering to resident work hour restrictions, leading quality and safety improvement initiatives, and improving clinical patient outcomes.

MODELS FOR NONHOUSESTAFF MEDICAL SERVICES

For AMCs developing nonhousestaff services, the process begins by addressing a series of important questions (Table 1). How these questions are answered is often driven by local factors such as the vision of local leadership and the availability of important resources. Nonetheless, it is important for hospitals to share their experiences because best practices remain unclear. Table 2 provides a tabular snapshot of nonhousestaff medicine services at 5 AMCs to highlight similarities and differences. Data in the table were compiled by having a representative from each AMC report the different attributes, which reflects each program as of July 2007. Table 2 provides no data on the quality or efficiency of housestaff versus nonhousestaff services, though this type of investigation is underway and will be critical in future planning.3940

Table 2 does illustrate several important considerations in structuring nonhousestaff services. For example, if a nonhousestaff service operates at a different physical location, careful triage of patients is necessary. Resources, including the availability of subspecialty and surgical consultants, may differ, and thus patient complexity and acuity may dictate whether a patient gets admitted to the nonhousestaff service. These triage factors were a major challenge in the design of UCSF's nonhousestaff service. The other nonhousestaff services handle overflow admissions after the housestaff service reaches a census or admission cap; transfers between services rarely occur, and resources are similar.

Other observations include that hospitalists work a similar number of hours each year and cover 50% of weekends but with differing shift lengths and sequences. Each service also provides night coverage but only Emory, the University of Michigan, and Northwestern utilize dedicated nocturnists. The University of Michigan and Brigham & Women's Hospital are the only sites that employ midlevel providers who work closely with hospitalists. In terms of group structure, Northwestern's hospitalists are the most integrated, with each hospitalist sharing equal responsibility for nonhousestaff coverage. In contrast, the other programs use selected hospitalists or a dedicated core of hospitalists to provide nonhousestaff services. Compensation models also vary, with certain groups salaried and others having incentive systems, although all receive hospital‐based funding support. Hospital‐based funding support ranges from 40% to 100% of total program costs across sites, creating similar variance in a given program's deficit risk. Finally, most programs do compensate nonhousestaff services at higher rates.

All the decisions captured in Table 2 have implications for costs, recruitment, and service structure. Furthermore, the striking variations demonstrate how different academic hospitalist positions can occur both within a hospital medicine group and across institutions. Of note, Table 2 only characterizes nonhousestaff medicine services, not the growing number of comanagement (eg, orthopedics, neurosurgery, or hematology/oncology) and other clinical services (eg, observation unit or preoperative medicine clinic) also staffed by hospitalists at AMCs.

CHALLENGES

Hospital medicine programs and AMCs face several challenges in building non‐housestaff services, but these will likely become less daunting as programs learn from their own experiences, from those of colleagues at other institutions, and from future investigations of these care models. We highlight a few issues below that warrant important consideration.

FUTURE DIRECTIONS

Many lament that the milieu for academic hospitalists raises more challenges than solutions, but we believe the current era is one of excitement and opportunity. In the coming years, we will experience continued growth of nonhousestaff services, including greater comanagement with our surgical and medical specialty colleagues. These opportunities will create new relationships and increase our visibility in AMCs. However, we must remain committed to studying nonhousestaff services and determine if and how they differ from their housestaff and community counterparts, as this will be an important step toward addressing current challenges.

As hospitalists take on increasingly diverse roles,45 we must also lead initiatives to better train, recruit, and retain those interested in our specialty. Promoting our field and recruiting future faculty should occur through local hospitalist career nights, events at national meetings (targeting students, housestaff, and fellows), and other mechanisms utilized by our subspecialty colleagues. For housestaff interested in fellowship training, the growing number of hospitalist fellowships can provide skills in teaching and quality improvement.46 For trainees committed to research, we should work with existing general medicine research fellowships and partner to provide hospitalist mentorship.

Hospitalists are in a unique position to influence the delivery of clinical services, shape the future of residency training, guide quality and safety improvement initiatives, and take on leadership roles through our departments, universities, and medical centers. With the growing number of clinical services being added to our portfolio, we will need careful planning and evaluation of our efforts to build successful partnerships and develop faculty roles that balance clinical and academic pursuits to sustain long‐term and satisfying hospitalist careers.

Many academic medical centers (AMCs) have developed nonhousestaff services to provide clinical care once provided by physicians‐in‐training. These services, often staffed by hospitalists and/or midlevel providers, have experienced tremendous growth in the past few years, yet very little exists in the literature about their development, structure, efficacy, or impact on hospitals, patients, and hospital medicine programs. The primary forces driving this growth include Accreditation Council for Graduate Medical Education (ACGME) resident duty hour restrictions,1 growth of the hospitalist movement,2 and the emphasis on simultaneously improving financial performance and quality of care in AMCs.3

Resident Duty Hour Restrictions

In 2003, the ACGME mandated restrictions on resident work hours, limiting trainees to 80 hours per week.1 Many training programs struggled with how to provide important clinical services while complying with the new restrictionscreating numerous models that bridged care between different shifts of residents.45 Implementation of day floats (a dedicated resident who rounds with the postcall team), night floats (a dedicated overnight resident who admits and cross‐covers patients), or some variation of both was common.6 No guidelines accompanied the ACGME mandate, leaving institutions to independently structure their programs without a known best practice.

Subsequent literature carefully addressed how the duty hour restrictions affect residents' lives and education but failed to discuss models for providing care.711 Training programs began to institute necessary changes but in doing so, created greater patient discontinuity and increased handoffs between residents, elevating the potential for adverse patient outcomes.12 Recent large‐scale studies indicate that inpatient care is the same or improved since adoption of the duty hour restrictions,1316 but controversy continues, with several editorials debating the issue.1719

Because increasing the volume of patients on housestaff services was not a viable option,20 many AMCs created nonhousestaff services and hired midlevel providers (nurse practitioners and physician assistants) to offset resident workloads and comply with the new restrictions. However, this strategy represented a very expensive alternative.21 Moreover, the current 80‐hour work limits may be revised downward, particularly given the lower restrictions in other countries,22 and this will further drive the demand for nonhousestaff services. Hospitalists, with their documented impact on efficiency and return on investment,23 represent a solution to fill these needs and have quickly become the predominant approach at AMCs.

The Hospitalist Movement

Since the term hospitalist was first coined in 1996,24 the remarkable growth of the number of practicing hospitalists emphasizes how first community hospitals and now AMCs have embraced this approach.25 With more than 20,000 nationwide and projections that the field will grow to 30,000 by 2010,26 hospitalists are becoming the primary providers for in‐patients.2 This growth was further catalyzed when widely expressed concerns about safety and quality became public,2728 and hospitalists incorporated patient safety and quality improvement activities into their efforts.3 The confluence of these factors also prompted emergence of hospital medicine programs at AMCs, a growth that came with anticipated dangers.29 Reflecting the recognition that hospital medicine is becoming a separate specialty30 and is integral to the functioning of an AMC, institutions now operate dedicated divisions of hospital medicine.

AMCs and Hospital Performance

AMCs operate 3 related enterprises: a medical school that trains future physicians, a research arena that promotes basic and clinical investigation, and health care services that often encompass both hospitals and clinics. The financial viability of AMCs has always been a topic of debate, largely because of the different missions they pursue and the financial means by which they survive.3133 Over the past decade, cuts in Medicare reimbursement, challenges in balancing bed availability with occupancy rates, and a growing emphasis on cost reduction have created a more competitive health care environment, but without the predicted demise of AMCs.34 Because education and research generally fail to bolster the bottom line, AMCs have focused on optimizing clinical services to promote financial viability.

Hospitalists are uniquely positioned to help this bottom line, just as they do at community hospitals. Their involvement in patient care may produce reductions in length of stay, greater efficiency in discharge planning, and significant cost savings.3537 Hospitalists may also improve throughput in emergency departments and decrease wait times, leading to more efficient bed utilization.38 This leads to a potential for greater hospital revenue by increasing both the number of admissions, particularly surgical cases, and staffed inpatient beds, the latter a premium, as AMCs continue to expand their bed capacity almost annually. Finally, hospitalists may serve as change agents in improving the quality and safety of care delivered, an increasingly important metric given the desire for and expansion of publicly reported measures.

From a financial standpoint, Medicare support to AMCs for training residents now subsidizes fewer clinical care hours. Hospitalist‐driven nonhousestaff services will continue to fulfill a need created by this marked change in residency training. The tension of who pays for nonhousestaff servicesincreased federal support, financial backing from AMCs, or academic department fundsposes an ongoing struggle. In fact, this may be the most important issue currently debated among hospital administrators and department chairs. Regardless, AMCs continue to view hospitalists as a mechanism (or even solution) to maintaining their financial bottom line through improving care delivery systems, adhering to resident work hour restrictions, leading quality and safety improvement initiatives, and improving clinical patient outcomes.

MODELS FOR NONHOUSESTAFF MEDICAL SERVICES

For AMCs developing nonhousestaff services, the process begins by addressing a series of important questions (Table 1). How these questions are answered is often driven by local factors such as the vision of local leadership and the availability of important resources. Nonetheless, it is important for hospitals to share their experiences because best practices remain unclear. Table 2 provides a tabular snapshot of nonhousestaff medicine services at 5 AMCs to highlight similarities and differences. Data in the table were compiled by having a representative from each AMC report the different attributes, which reflects each program as of July 2007. Table 2 provides no data on the quality or efficiency of housestaff versus nonhousestaff services, though this type of investigation is underway and will be critical in future planning.3940

Table 2 does illustrate several important considerations in structuring nonhousestaff services. For example, if a nonhousestaff service operates at a different physical location, careful triage of patients is necessary. Resources, including the availability of subspecialty and surgical consultants, may differ, and thus patient complexity and acuity may dictate whether a patient gets admitted to the nonhousestaff service. These triage factors were a major challenge in the design of UCSF's nonhousestaff service. The other nonhousestaff services handle overflow admissions after the housestaff service reaches a census or admission cap; transfers between services rarely occur, and resources are similar.

Other observations include that hospitalists work a similar number of hours each year and cover 50% of weekends but with differing shift lengths and sequences. Each service also provides night coverage but only Emory, the University of Michigan, and Northwestern utilize dedicated nocturnists. The University of Michigan and Brigham & Women's Hospital are the only sites that employ midlevel providers who work closely with hospitalists. In terms of group structure, Northwestern's hospitalists are the most integrated, with each hospitalist sharing equal responsibility for nonhousestaff coverage. In contrast, the other programs use selected hospitalists or a dedicated core of hospitalists to provide nonhousestaff services. Compensation models also vary, with certain groups salaried and others having incentive systems, although all receive hospital‐based funding support. Hospital‐based funding support ranges from 40% to 100% of total program costs across sites, creating similar variance in a given program's deficit risk. Finally, most programs do compensate nonhousestaff services at higher rates.

All the decisions captured in Table 2 have implications for costs, recruitment, and service structure. Furthermore, the striking variations demonstrate how different academic hospitalist positions can occur both within a hospital medicine group and across institutions. Of note, Table 2 only characterizes nonhousestaff medicine services, not the growing number of comanagement (eg, orthopedics, neurosurgery, or hematology/oncology) and other clinical services (eg, observation unit or preoperative medicine clinic) also staffed by hospitalists at AMCs.

CHALLENGES

Hospital medicine programs and AMCs face several challenges in building non‐housestaff services, but these will likely become less daunting as programs learn from their own experiences, from those of colleagues at other institutions, and from future investigations of these care models. We highlight a few issues below that warrant important consideration.

FUTURE DIRECTIONS

Many lament that the milieu for academic hospitalists raises more challenges than solutions, but we believe the current era is one of excitement and opportunity. In the coming years, we will experience continued growth of nonhousestaff services, including greater comanagement with our surgical and medical specialty colleagues. These opportunities will create new relationships and increase our visibility in AMCs. However, we must remain committed to studying nonhousestaff services and determine if and how they differ from their housestaff and community counterparts, as this will be an important step toward addressing current challenges.

As hospitalists take on increasingly diverse roles,45 we must also lead initiatives to better train, recruit, and retain those interested in our specialty. Promoting our field and recruiting future faculty should occur through local hospitalist career nights, events at national meetings (targeting students, housestaff, and fellows), and other mechanisms utilized by our subspecialty colleagues. For housestaff interested in fellowship training, the growing number of hospitalist fellowships can provide skills in teaching and quality improvement.46 For trainees committed to research, we should work with existing general medicine research fellowships and partner to provide hospitalist mentorship.

Hospitalists are in a unique position to influence the delivery of clinical services, shape the future of residency training, guide quality and safety improvement initiatives, and take on leadership roles through our departments, universities, and medical centers. With the growing number of clinical services being added to our portfolio, we will need careful planning and evaluation of our efforts to build successful partnerships and develop faculty roles that balance clinical and academic pursuits to sustain long‐term and satisfying hospitalist careers.

A 49‐year‐old man presented with 2 days of chills, fever, anorexia, and increased cough and dyspnea. The patient had a history of chronic obstructive pulmonary disease (COPD) and noted that his cough and dyspnea had increased above normal for several days. He was now dyspneic with minimal activity and had slept at a 45‐degree incline the night prior to evaluation due to dyspnea. He noted less improvement than usual with the use of his metered dose inhaler. His cough was occasionally productive of small amounts of white phlegm. He had vomited once. During a coughing episode the patient experienced a sudden onset of sharp right upper quadrant abdominal pain that worsened with coughing and sudden position changes. The patient denied a prior history of abdominal pain or surgery. The patient's last bowel movement was 2 days prior to admission. He denied melena or bright red blood per rectum.

My initial differential diagnosis for this patient's dyspnea and cough is pneumonia, acute exacerbation of COPD, or congestive heart failure. The presence of fever and anorexia increases the likelihood of infectious etiologies, whereas the presence of orthopnea points toward congestive heart failure. Noncardiac processessuch as a large pleural effusion or apical lung diseasecould also cause orthopnea. His abdominal pain could be a result of pneumonia alone (perhaps in the right lower lobe with diaphragmatic irritation), but I am also considering complications of pneumonia such as empyema. Although his abdominal pain, dyspnea, and cough could also be a result of hepatobiliary disease, a perforated viscus, or pancreatitis, we currently have little reason to suspect a direct abdominal etiology. My top diagnosis is community‐acquired pneumonia, perhaps accompanied by pleural effusion.

His medical history was significant for dilated cardiomyopathy and heavy alcohol use. His medications included various meter‐dosed inhalers, bupropion, digoxin, spironolactone, lisinopril, and metoprolol. He had never received corticosteroid therapy and had not previously been hospitalized for COPD‐related problems. He had smoked one pack of cigarettes daily for 40 years.

Heavy alcohol use is associated with an increased risk of several pulmonary infections such as gram‐negative necrotizing pneumonia (classically, Klebsiella pneumoniae), pneumococcal pneumonia, aspiration pneumonia, anaerobic lung abscesses, and tuberculosis. Given his right upper quadrant pain, acute alcoholic hepatitis and alcohol‐related pancreatitis enter the differential. His history of cardiomyopathy makes me consider congestive heart failure as more likely than before, and perhaps his abdominal pain is a result of hepatic congestion from right heart failure. His fever, however, cannot be attributed to cardiac failure. Less likely diagnoses include ischemic conditions related to his cardiomyopathy such as mesenteric ischemia from low perfusion or embolism from a cardiac thrombus. A pulmonary infection remains the most likely diagnosis.

He was an ill‐appearing man in moderate respiratory distress, looking older than his stated age. His temperature was 38.4C, heart rate 129 beats/minute, blood pressure 85/56 mm Hg, respiratory rate 24 breaths/minute, and oxygen saturation 92% on room air. A cardiovascular exam revealed no murmur, gallop, or rub. The jugular venous pulse was not elevated. His lungs were clear to auscultation. Abdominal exam revealed right‐sided abdominal tenderness that appeared to localize to the rectus sheath. Otherwise, the abdomen was soft, with normal bowel sounds and no organomegaly. Rectal examination revealed guaiac negative stool and no focal tenderness. His extremities were normal.

His vital signs are worrisome for impending cardiovascular collapse and shock, possibly due to sepsis. The relatively nonfocal cardiopulmonary exam is surprising given his initial symptoms and makes me wonder if his dyspnea is primarily related to an abdominal process leading to diaphragmatic irritation rather than to a thoracic process. Congestive heart failure seems unlikely given the lack of supportive physical examination findings. His abdominal exam findings are puzzling. Although his abdominal wall tenderness could be benignperhaps from muscular strain or a tear from coughingit could represent a more worrisome process such as infection or a hematoma in the abdominal wall muscles. Mesenteric ischemia is still possible, as the exam is often unimpressive. A hepatic abscess or subphrenic abscess should be considered, as physical exam findings in these conditions can be subtle.

My differential remains relatively unchanged, but I have now put consideration of a hepatic or subphrenic abscess higher on my list. Early empiric broad‐spectrum antibiotics seem necessary.

He had a white blood cell count of 26,700/mL with 92% neutrophils, a hemoglobin of 14.6 g/dL, and a platelet count of 312,000/mL. Sodium was 134 mmol/L, potassium was 4.3 mmol/L, chloride was 94 mmol/L, bicarbonate was 23 mmol/L, blood urea nitrogen was 23 mg/dL, and creatinine was 2.1 mg/dL. The results of the calcium, protein, albumin, and liver function tests were normal. Urinalysis was negative for protein and red blood cells. An electrocardiogram revealed sinus tachycardia. A chest radiograph at admission revealed mild opacities in both lower lobes and the right middle lobe consistent with either atelectasis or pneumonia (Fig. 1). A very small left effusion was also identified.

Figure 1

The additional data reinforce my clinical impression that this process is likely to be infectious. The chest radiograph is consistent with community‐acquired pneumonia, possibly from an atypical pathogen. Given his elevated creatinine, I am also considering a pulmonary‐renal syndrome such as vasculitis, though hematuria was not present. A subphrenic abscess, mesenteric ischemia, or an abdominal wall process (because his abdominal tenderness on exam still needs an explanation) remain possibilities; my suspicion would increase if he does not respond appropriately to therapy for community‐acquired pneumonia.

The clinical team's working diagnosis also was community‐acquired pneumonia. Blood and sputum cultures were obtained, and the patient was treated with intravenous ceftriaxone, azithromycin, and intravenous fluid. By the second day, his creatinine had normalized; however, his hypoxemia had worsened, and he now required supplemental oxygen. His temperature was 39.3C, and his heart rate was 150 beats/minute. The findings of an abdominal ultrasound of the kidneys, spleen, and right upper quadrant were normal.

It is too early to say the patient has failed therapy because a patient can get worse before getting better during the course of antibiotic therapy for community‐acquired pneumonia. Fever, for example, may take up to 7 days to resolve, depending on host factors and the pathogen. Though I typically wait about 72 hours before assuming a patient is not appropriately responding to therapy, the additional information has made me concerned. The degree of tachycardia is significant and warrants an EKG to exclude an arrthymia. I would also repeat the chest radiograph to evaluate for worsening infiltrates or increased pleural effusion.

On the third hospital day, the patient's abdominal pain had decreased with analgesia, but his fever, cough, and dyspnea remained largely unchanged. Antibiotics were changed to intravenous levofloxacin. A repeat chest radiograph revealed elevation of the right hemidiaphragm and bilateral effusions (Fig. 2). An electrocardiogram revealed sinus tachycardia. Blood cultures revealed no growth, and sputum cultures grew oral flora.

Figure 2

A significantly elevated right hemidiaphragm makes me reconsider the diagnosis of simple community‐acquired pneumonia. The differential diagnosis for an elevated hemidiaphragm is best considered by location in relation to the diaphragm. Causes above the diaphragm include rib fracture, atelectasis, pleural thickening, and volume loss of the lung for another reason (e.g., surgery, bronchial obstruction due to tumor or mucus plugging), as well as mimics such as a densely consolidated pneumonia, pulmonary infarction, or a subpulmonary effusion. Diaphragmatic causes include eventration, rupture, phrenic nerve weakness, and intrinsic weakness because of neuromuscular disease (usually bilateral). Causes below the diaphragm that must be considered are subphrenic or liver abscess, liver (and other abdominal) malignancy, pancreatic pseudocyst, and distended bowel. Given the clinical picture, I am focusing below the diaphragmespecially on a possible hepatic or subphrenic abscess (which could be missed on ultrasound) and mimics of it such as dense consolidation or a subpulmonary effusion. Given the lack of response to antibiotics, I need to consider an infection that is not being treated, either because of location (abscess, effusion) or microbiology (tuberculosis, a parasite, a fungus, resistant bacteria). After confirming that the patient has a substantive pleural effusion, he needs a thoracentesis.

On the fourth hospital day, his temperature was 38.8C, and his white blood cell count was 21,000/mL. A right‐sided thoracentesis was performed; approximately 250 cc of fluid was obtained. Pleural fluid analysis revealed bloody fluid, with a white blood cell count of 16,750/mL with 94% neutrophils, 40,000 red blood cells/mL, lactate dehydrogenase of 278 U/L (normal serum value 80200 U/L), protein of 3.7 g/dL, and glucose of 81 mg/dL. A pleural fluid pH was not obtained. A gram stain revealed many white blood cells with no organisms noted. Serum protein was 7.4 g/dL. These results were thought to represent an exudative parapneumonic effusion; levofloxacin and supplemental oxygen were continued.

The pleural fluid appears exudative, but I am not sure this man has a parapneumonic effusion because, despite clinical deterioration, an obvious infiltrate is not seen on interval chest radiography. We must look closely at the fluid because this is a bloody effusion and somewhat atypical for a parapneumonic effusion. Also, the effusion does not appear large enough to explain why he has not improved on the current antibiotics. We should thus reconsider our diagnosis and management. I would obtain additional imaging (such as an abdominal and chest computed tomography [CT]) and perhaps obtain a consultation from the pulmonary team regarding the postulated initial diagnosis of pneumonia with effusion.

On the fifth day of hospitalization, the patient's dyspnea and cough persisted but were improved. His abdominal pain was minimal and felt improved with flatus. Fever continued to 38.8C, and the white blood cell count was 20,000/mL. On examination the patient had decreased breath sounds at the right base and bibasilar crackles. His abdomen was soft, with tenderness in his right upper quadrant only with deep palpation; bowel sounds remained. An ultrasound of the chest was performed to look for a loculated effusion; however, no fluid was identified. The pulmonary consultant thought it likely that the patient had a subpulmonic effusion and recommended CT of the abdomen and chest.

His right upper quadrant tenderness is still unexplained. I would agree with the CT, primarily to evaluate other causes of his elevated diaphragm such as subphrenic or hepatic abscess. For now, I would make no change in antibiotic therapy.

On the sixth hospital day, the patient had an episode of bilious emesis. Chest and abdominal CT revealed collapse of the right middle and lower lobes with a small adjacent effusion, and a 6 6 16 cm abscess intimately opposed to the right lobe of the liver. Extending from the inferior extent of the abscess was a tubular thick‐walled structure connecting to the cecum that was suspicious of a thickened inflamed appendix. There was periappendiceal stranding suggesting inflammation. The small bowel was diffusely dilated up to 4.5 cm, suggesting a small bowel obstruction.

I suspect that his abscess is related to a perforated appendix and that the dilated small bowel is most likely a result of localized irritation of the bowel by the abscess and appendicitis. The collapsed lung is most likely due to local inflammation from the subdiaphragmatic abscess. Treatment should now be changed substantially. I would ask a surgeon to evaluate the patient because the most likely diagnosis is perforated appendicitis with abscess formation.

When the periappendiceal abscess was drained percutaneously, 190 mL of purulent fluid was removed. The cultures were positive for Klebsiella pneumonia, Enterococcus faecalis,and Streptococcus milleri. The patient was given 6 weeks of intravenous antibiotics with improvement in his clinical symptoms. During the interval the findings on his chest radiograph resolved completely. A laproscopic appendectomy 3 months later revealed significant right lower quadrant adhesions. The pathology specimen identified a distorted appendix with regeneration consistent with prior appendicitis. The patient was contacted 4 months after his surgery, and he reported that he was doing well, with no cardiopulmonary or gastrointestinal symptoms.

COMMENTARY

Community‐acquired pneumonia (CAP) is a common cause of acute illness and accounts for nearly 1 million admissions per year in the United States.1 The diagnosis of CAP is made when symptoms including dyspnea, fever, cough, or leukocytosis are present, with confirmation provided by a chest radiograph. Often the diagnosis is clear; however, there is no pathognomonic constellation of signs or symptoms that establish the diagnosis with certainty.2 Many physicians learn that pneumoniaespecially lower‐lobe pneumoniacan lead to abdominal findings such as upper quadrant pain, vomiting, and tenderness to palpation. Conversely, the patient discussed above illustrates that a primary abdominal process can also result in a symptom complex that mimics pneumonia.

The prevalence of CAP coupled with the inherent uncertainty of a clinical diagnosis of CAP leads to an important question: How long is too long before questioning the diagnosis? An analysis of the pneumonia Patient Outcomes Research Trial (PORT) limited to inpatients with CAP examined time to clinical stability. For the majority of patients, abnormal vital signs resolved within 23 days.3 In this study, 29% of patients had severe disease, and not surprisingly, these patients took longer to improve. Using the pneumonia severity index score, which accounts for age, comorbidity, abnormal vital signs, and laboratory data, the patient described in this article would be considered at high risk for death and complication with an estimated mortality of 9%.4 Using a combination of defervescence, resolution of tachycardia, tachypnea, and hypoxemia as markers of clinical stability, a patient like ours should respond within 4 days (with a range of 27 days). On the basis of these dataand the discrepancy between the patient's severe illness and relatively minor pulmonary infiltratesit seems reasonable to have considered this patient as failing CAP therapy as early as the fourth day of hospitalization.

In approximately 10% of hospitalized patients with CAP, the clinical course is protracted.5 When patients do not improve as quickly as expected, the reasons that could explain this should be investigated. In a cohort of 49 patients with CAP who failed therapy the most common reasons for failure to improve were severity of the pneumonia and drug resistance.6 A multicenter study found that the incidence of resistance to penicillin by Streptococcus pneumoniae, the most common bacterial pathogen in CAP, was 30%, with a 4% in vitro resistance rate to ceftriaxone.7 How well in vitro resistance predicts clinical response, however, is unclear. Risk factors for antibiotic resistance include close exposure to children, recent antibiotic use, and recent hospitalization. Immunosuppressive conditions should also be considered in patients who fail to improve. Suppurative complications of pneumoniasuch as empyema, parapneumonic effusion, and lung abscessalso delay recovery.

Another consideration in a patient with what appears to be a nonresolving pneumonia with pleural effusion is that the initial diagnosis is incorrect and the cause is extrathoracic. Pulmonary and cardiac diseases account for more than 90% of effusions, whereas less than 5% of pleural effusions result from intraabdominal causes.8 When should intraabdominal diseases be sought in patients with an effusion, fever, dyspnea, and cough? Light suggests that intraabdominal pathology should be investigated in patients who have pleural effusions without significant parenchymal disease.8 This point is underscored by the experience of our patient, whose chest radiographs showed, despite clinical decline, minimal airspace disease.

Several abdominal entities cause pleural effusion. Pancreatitis, either acute or chronic, with pseudocyst formation is the most common abdominal cause of exudative pleural effusions. Approximately 10% of patients with pancreatic disease will develop effusions, usually left‐sided.9 These left‐sided effusions are also seen in splenic abscesses, usually as a result of endocarditis. Intrahepatic abscess is associated with effusions in 20% of patients.10 A subphrenic abscess, as seen in our patient, is an uncommon cause of exudative pleural effusions. Historically, subphrenic abscesses resulted from a perforated viscus, with ruptured appendicitis the most common cause,11 followed by perforated peptic ulcers and biliary tract disease. With the advent of antibiotics, the causes of subphrenic abscess changed considerably, with the majority of current cases resulting from postsurgical complications.12 The findings of a chest radiograph are abnormal in 80% of patients with subphrenic abscess;1214 an elevated hemidiaphragm and pleural effusion are found in the majority of cases. The symptoms of a subphrenic abscess are nonspecific, and patient's complaints are equally split between predominantly thoracic and predomninantly abdominal complaints.15

Appendicitis, a common disease predominantly of the young, may lead to atypical presentations in older individuals. In a retrospective analysis of 113 patients older than 60 years with appendicitis, 70% presented in an atypical fashion.16 Typical symptoms include right lower quadrant pain, fever, anorexia and a white blood cell count greater than 10,000/mL. Fever was the most frequently absent symptom, seen in only 37% of older patients. In this cohort, approximately one third of older patients waited more than 48 hours prior to presentation. The time between symptom onset and clinical presentation is a strong predictor of perforation risk.17 As in this case, roughly 2% of patients with acute appendicitis will present with perforation and abscess formation.18 In such patients the management is initially conservative. Percutaneous drainage and broad spectrum antibiotics are the treatment of choice, followed by an interval appendectomy in 612 weeks.19 The rationale for delayed surgery is that earlier surgery may disseminate a localized inflammatory process.20

Community‐acquired pneumonia is a more frequent cause of hospital admission than is intraabdominal abscess. Physicians often face the dilemma of when to pursue alternative diagnoses after a patient who is thought to have an atypical presentation of a common disease (ie, CAP) fails to respond to conventional therapy. Although clinicians learn that right upper quadrant pain may be a symptom of pneumonia, our patient revealed that abdominal causes may mimic pneumonia and produce a pleural effusion. Determining whether the primary disease originates above or below the diaphragm is critical to guiding therapy. When patients fail to respond adequately to therapy, clinicians should set a low threshold for deciding to image the abdomen in a patient with modest pulmonary infiltrates, pleural effusion, and abdominal pain.

A 49‐year‐old man presented with 2 days of chills, fever, anorexia, and increased cough and dyspnea. The patient had a history of chronic obstructive pulmonary disease (COPD) and noted that his cough and dyspnea had increased above normal for several days. He was now dyspneic with minimal activity and had slept at a 45‐degree incline the night prior to evaluation due to dyspnea. He noted less improvement than usual with the use of his metered dose inhaler. His cough was occasionally productive of small amounts of white phlegm. He had vomited once. During a coughing episode the patient experienced a sudden onset of sharp right upper quadrant abdominal pain that worsened with coughing and sudden position changes. The patient denied a prior history of abdominal pain or surgery. The patient's last bowel movement was 2 days prior to admission. He denied melena or bright red blood per rectum.

My initial differential diagnosis for this patient's dyspnea and cough is pneumonia, acute exacerbation of COPD, or congestive heart failure. The presence of fever and anorexia increases the likelihood of infectious etiologies, whereas the presence of orthopnea points toward congestive heart failure. Noncardiac processessuch as a large pleural effusion or apical lung diseasecould also cause orthopnea. His abdominal pain could be a result of pneumonia alone (perhaps in the right lower lobe with diaphragmatic irritation), but I am also considering complications of pneumonia such as empyema. Although his abdominal pain, dyspnea, and cough could also be a result of hepatobiliary disease, a perforated viscus, or pancreatitis, we currently have little reason to suspect a direct abdominal etiology. My top diagnosis is community‐acquired pneumonia, perhaps accompanied by pleural effusion.

His medical history was significant for dilated cardiomyopathy and heavy alcohol use. His medications included various meter‐dosed inhalers, bupropion, digoxin, spironolactone, lisinopril, and metoprolol. He had never received corticosteroid therapy and had not previously been hospitalized for COPD‐related problems. He had smoked one pack of cigarettes daily for 40 years.

Heavy alcohol use is associated with an increased risk of several pulmonary infections such as gram‐negative necrotizing pneumonia (classically, Klebsiella pneumoniae), pneumococcal pneumonia, aspiration pneumonia, anaerobic lung abscesses, and tuberculosis. Given his right upper quadrant pain, acute alcoholic hepatitis and alcohol‐related pancreatitis enter the differential. His history of cardiomyopathy makes me consider congestive heart failure as more likely than before, and perhaps his abdominal pain is a result of hepatic congestion from right heart failure. His fever, however, cannot be attributed to cardiac failure. Less likely diagnoses include ischemic conditions related to his cardiomyopathy such as mesenteric ischemia from low perfusion or embolism from a cardiac thrombus. A pulmonary infection remains the most likely diagnosis.

He was an ill‐appearing man in moderate respiratory distress, looking older than his stated age. His temperature was 38.4C, heart rate 129 beats/minute, blood pressure 85/56 mm Hg, respiratory rate 24 breaths/minute, and oxygen saturation 92% on room air. A cardiovascular exam revealed no murmur, gallop, or rub. The jugular venous pulse was not elevated. His lungs were clear to auscultation. Abdominal exam revealed right‐sided abdominal tenderness that appeared to localize to the rectus sheath. Otherwise, the abdomen was soft, with normal bowel sounds and no organomegaly. Rectal examination revealed guaiac negative stool and no focal tenderness. His extremities were normal.

His vital signs are worrisome for impending cardiovascular collapse and shock, possibly due to sepsis. The relatively nonfocal cardiopulmonary exam is surprising given his initial symptoms and makes me wonder if his dyspnea is primarily related to an abdominal process leading to diaphragmatic irritation rather than to a thoracic process. Congestive heart failure seems unlikely given the lack of supportive physical examination findings. His abdominal exam findings are puzzling. Although his abdominal wall tenderness could be benignperhaps from muscular strain or a tear from coughingit could represent a more worrisome process such as infection or a hematoma in the abdominal wall muscles. Mesenteric ischemia is still possible, as the exam is often unimpressive. A hepatic abscess or subphrenic abscess should be considered, as physical exam findings in these conditions can be subtle.

My differential remains relatively unchanged, but I have now put consideration of a hepatic or subphrenic abscess higher on my list. Early empiric broad‐spectrum antibiotics seem necessary.

He had a white blood cell count of 26,700/mL with 92% neutrophils, a hemoglobin of 14.6 g/dL, and a platelet count of 312,000/mL. Sodium was 134 mmol/L, potassium was 4.3 mmol/L, chloride was 94 mmol/L, bicarbonate was 23 mmol/L, blood urea nitrogen was 23 mg/dL, and creatinine was 2.1 mg/dL. The results of the calcium, protein, albumin, and liver function tests were normal. Urinalysis was negative for protein and red blood cells. An electrocardiogram revealed sinus tachycardia. A chest radiograph at admission revealed mild opacities in both lower lobes and the right middle lobe consistent with either atelectasis or pneumonia (Fig. 1). A very small left effusion was also identified.

Figure 1

The additional data reinforce my clinical impression that this process is likely to be infectious. The chest radiograph is consistent with community‐acquired pneumonia, possibly from an atypical pathogen. Given his elevated creatinine, I am also considering a pulmonary‐renal syndrome such as vasculitis, though hematuria was not present. A subphrenic abscess, mesenteric ischemia, or an abdominal wall process (because his abdominal tenderness on exam still needs an explanation) remain possibilities; my suspicion would increase if he does not respond appropriately to therapy for community‐acquired pneumonia.

The clinical team's working diagnosis also was community‐acquired pneumonia. Blood and sputum cultures were obtained, and the patient was treated with intravenous ceftriaxone, azithromycin, and intravenous fluid. By the second day, his creatinine had normalized; however, his hypoxemia had worsened, and he now required supplemental oxygen. His temperature was 39.3C, and his heart rate was 150 beats/minute. The findings of an abdominal ultrasound of the kidneys, spleen, and right upper quadrant were normal.

It is too early to say the patient has failed therapy because a patient can get worse before getting better during the course of antibiotic therapy for community‐acquired pneumonia. Fever, for example, may take up to 7 days to resolve, depending on host factors and the pathogen. Though I typically wait about 72 hours before assuming a patient is not appropriately responding to therapy, the additional information has made me concerned. The degree of tachycardia is significant and warrants an EKG to exclude an arrthymia. I would also repeat the chest radiograph to evaluate for worsening infiltrates or increased pleural effusion.

On the third hospital day, the patient's abdominal pain had decreased with analgesia, but his fever, cough, and dyspnea remained largely unchanged. Antibiotics were changed to intravenous levofloxacin. A repeat chest radiograph revealed elevation of the right hemidiaphragm and bilateral effusions (Fig. 2). An electrocardiogram revealed sinus tachycardia. Blood cultures revealed no growth, and sputum cultures grew oral flora.

Figure 2

A significantly elevated right hemidiaphragm makes me reconsider the diagnosis of simple community‐acquired pneumonia. The differential diagnosis for an elevated hemidiaphragm is best considered by location in relation to the diaphragm. Causes above the diaphragm include rib fracture, atelectasis, pleural thickening, and volume loss of the lung for another reason (e.g., surgery, bronchial obstruction due to tumor or mucus plugging), as well as mimics such as a densely consolidated pneumonia, pulmonary infarction, or a subpulmonary effusion. Diaphragmatic causes include eventration, rupture, phrenic nerve weakness, and intrinsic weakness because of neuromuscular disease (usually bilateral). Causes below the diaphragm that must be considered are subphrenic or liver abscess, liver (and other abdominal) malignancy, pancreatic pseudocyst, and distended bowel. Given the clinical picture, I am focusing below the diaphragmespecially on a possible hepatic or subphrenic abscess (which could be missed on ultrasound) and mimics of it such as dense consolidation or a subpulmonary effusion. Given the lack of response to antibiotics, I need to consider an infection that is not being treated, either because of location (abscess, effusion) or microbiology (tuberculosis, a parasite, a fungus, resistant bacteria). After confirming that the patient has a substantive pleural effusion, he needs a thoracentesis.

On the fourth hospital day, his temperature was 38.8C, and his white blood cell count was 21,000/mL. A right‐sided thoracentesis was performed; approximately 250 cc of fluid was obtained. Pleural fluid analysis revealed bloody fluid, with a white blood cell count of 16,750/mL with 94% neutrophils, 40,000 red blood cells/mL, lactate dehydrogenase of 278 U/L (normal serum value 80200 U/L), protein of 3.7 g/dL, and glucose of 81 mg/dL. A pleural fluid pH was not obtained. A gram stain revealed many white blood cells with no organisms noted. Serum protein was 7.4 g/dL. These results were thought to represent an exudative parapneumonic effusion; levofloxacin and supplemental oxygen were continued.

The pleural fluid appears exudative, but I am not sure this man has a parapneumonic effusion because, despite clinical deterioration, an obvious infiltrate is not seen on interval chest radiography. We must look closely at the fluid because this is a bloody effusion and somewhat atypical for a parapneumonic effusion. Also, the effusion does not appear large enough to explain why he has not improved on the current antibiotics. We should thus reconsider our diagnosis and management. I would obtain additional imaging (such as an abdominal and chest computed tomography [CT]) and perhaps obtain a consultation from the pulmonary team regarding the postulated initial diagnosis of pneumonia with effusion.

On the fifth day of hospitalization, the patient's dyspnea and cough persisted but were improved. His abdominal pain was minimal and felt improved with flatus. Fever continued to 38.8C, and the white blood cell count was 20,000/mL. On examination the patient had decreased breath sounds at the right base and bibasilar crackles. His abdomen was soft, with tenderness in his right upper quadrant only with deep palpation; bowel sounds remained. An ultrasound of the chest was performed to look for a loculated effusion; however, no fluid was identified. The pulmonary consultant thought it likely that the patient had a subpulmonic effusion and recommended CT of the abdomen and chest.

His right upper quadrant tenderness is still unexplained. I would agree with the CT, primarily to evaluate other causes of his elevated diaphragm such as subphrenic or hepatic abscess. For now, I would make no change in antibiotic therapy.

On the sixth hospital day, the patient had an episode of bilious emesis. Chest and abdominal CT revealed collapse of the right middle and lower lobes with a small adjacent effusion, and a 6 6 16 cm abscess intimately opposed to the right lobe of the liver. Extending from the inferior extent of the abscess was a tubular thick‐walled structure connecting to the cecum that was suspicious of a thickened inflamed appendix. There was periappendiceal stranding suggesting inflammation. The small bowel was diffusely dilated up to 4.5 cm, suggesting a small bowel obstruction.

I suspect that his abscess is related to a perforated appendix and that the dilated small bowel is most likely a result of localized irritation of the bowel by the abscess and appendicitis. The collapsed lung is most likely due to local inflammation from the subdiaphragmatic abscess. Treatment should now be changed substantially. I would ask a surgeon to evaluate the patient because the most likely diagnosis is perforated appendicitis with abscess formation.

When the periappendiceal abscess was drained percutaneously, 190 mL of purulent fluid was removed. The cultures were positive for Klebsiella pneumonia, Enterococcus faecalis,and Streptococcus milleri. The patient was given 6 weeks of intravenous antibiotics with improvement in his clinical symptoms. During the interval the findings on his chest radiograph resolved completely. A laproscopic appendectomy 3 months later revealed significant right lower quadrant adhesions. The pathology specimen identified a distorted appendix with regeneration consistent with prior appendicitis. The patient was contacted 4 months after his surgery, and he reported that he was doing well, with no cardiopulmonary or gastrointestinal symptoms.

COMMENTARY

Community‐acquired pneumonia (CAP) is a common cause of acute illness and accounts for nearly 1 million admissions per year in the United States.1 The diagnosis of CAP is made when symptoms including dyspnea, fever, cough, or leukocytosis are present, with confirmation provided by a chest radiograph. Often the diagnosis is clear; however, there is no pathognomonic constellation of signs or symptoms that establish the diagnosis with certainty.2 Many physicians learn that pneumoniaespecially lower‐lobe pneumoniacan lead to abdominal findings such as upper quadrant pain, vomiting, and tenderness to palpation. Conversely, the patient discussed above illustrates that a primary abdominal process can also result in a symptom complex that mimics pneumonia.

The prevalence of CAP coupled with the inherent uncertainty of a clinical diagnosis of CAP leads to an important question: How long is too long before questioning the diagnosis? An analysis of the pneumonia Patient Outcomes Research Trial (PORT) limited to inpatients with CAP examined time to clinical stability. For the majority of patients, abnormal vital signs resolved within 23 days.3 In this study, 29% of patients had severe disease, and not surprisingly, these patients took longer to improve. Using the pneumonia severity index score, which accounts for age, comorbidity, abnormal vital signs, and laboratory data, the patient described in this article would be considered at high risk for death and complication with an estimated mortality of 9%.4 Using a combination of defervescence, resolution of tachycardia, tachypnea, and hypoxemia as markers of clinical stability, a patient like ours should respond within 4 days (with a range of 27 days). On the basis of these dataand the discrepancy between the patient's severe illness and relatively minor pulmonary infiltratesit seems reasonable to have considered this patient as failing CAP therapy as early as the fourth day of hospitalization.

In approximately 10% of hospitalized patients with CAP, the clinical course is protracted.5 When patients do not improve as quickly as expected, the reasons that could explain this should be investigated. In a cohort of 49 patients with CAP who failed therapy the most common reasons for failure to improve were severity of the pneumonia and drug resistance.6 A multicenter study found that the incidence of resistance to penicillin by Streptococcus pneumoniae, the most common bacterial pathogen in CAP, was 30%, with a 4% in vitro resistance rate to ceftriaxone.7 How well in vitro resistance predicts clinical response, however, is unclear. Risk factors for antibiotic resistance include close exposure to children, recent antibiotic use, and recent hospitalization. Immunosuppressive conditions should also be considered in patients who fail to improve. Suppurative complications of pneumoniasuch as empyema, parapneumonic effusion, and lung abscessalso delay recovery.

Another consideration in a patient with what appears to be a nonresolving pneumonia with pleural effusion is that the initial diagnosis is incorrect and the cause is extrathoracic. Pulmonary and cardiac diseases account for more than 90% of effusions, whereas less than 5% of pleural effusions result from intraabdominal causes.8 When should intraabdominal diseases be sought in patients with an effusion, fever, dyspnea, and cough? Light suggests that intraabdominal pathology should be investigated in patients who have pleural effusions without significant parenchymal disease.8 This point is underscored by the experience of our patient, whose chest radiographs showed, despite clinical decline, minimal airspace disease.

Several abdominal entities cause pleural effusion. Pancreatitis, either acute or chronic, with pseudocyst formation is the most common abdominal cause of exudative pleural effusions. Approximately 10% of patients with pancreatic disease will develop effusions, usually left‐sided.9 These left‐sided effusions are also seen in splenic abscesses, usually as a result of endocarditis. Intrahepatic abscess is associated with effusions in 20% of patients.10 A subphrenic abscess, as seen in our patient, is an uncommon cause of exudative pleural effusions. Historically, subphrenic abscesses resulted from a perforated viscus, with ruptured appendicitis the most common cause,11 followed by perforated peptic ulcers and biliary tract disease. With the advent of antibiotics, the causes of subphrenic abscess changed considerably, with the majority of current cases resulting from postsurgical complications.12 The findings of a chest radiograph are abnormal in 80% of patients with subphrenic abscess;1214 an elevated hemidiaphragm and pleural effusion are found in the majority of cases. The symptoms of a subphrenic abscess are nonspecific, and patient's complaints are equally split between predominantly thoracic and predomninantly abdominal complaints.15

Appendicitis, a common disease predominantly of the young, may lead to atypical presentations in older individuals. In a retrospective analysis of 113 patients older than 60 years with appendicitis, 70% presented in an atypical fashion.16 Typical symptoms include right lower quadrant pain, fever, anorexia and a white blood cell count greater than 10,000/mL. Fever was the most frequently absent symptom, seen in only 37% of older patients. In this cohort, approximately one third of older patients waited more than 48 hours prior to presentation. The time between symptom onset and clinical presentation is a strong predictor of perforation risk.17 As in this case, roughly 2% of patients with acute appendicitis will present with perforation and abscess formation.18 In such patients the management is initially conservative. Percutaneous drainage and broad spectrum antibiotics are the treatment of choice, followed by an interval appendectomy in 612 weeks.19 The rationale for delayed surgery is that earlier surgery may disseminate a localized inflammatory process.20

Community‐acquired pneumonia is a more frequent cause of hospital admission than is intraabdominal abscess. Physicians often face the dilemma of when to pursue alternative diagnoses after a patient who is thought to have an atypical presentation of a common disease (ie, CAP) fails to respond to conventional therapy. Although clinicians learn that right upper quadrant pain may be a symptom of pneumonia, our patient revealed that abdominal causes may mimic pneumonia and produce a pleural effusion. Determining whether the primary disease originates above or below the diaphragm is critical to guiding therapy. When patients fail to respond adequately to therapy, clinicians should set a low threshold for deciding to image the abdomen in a patient with modest pulmonary infiltrates, pleural effusion, and abdominal pain.

A 49‐year‐old man presented with 2 days of chills, fever, anorexia, and increased cough and dyspnea. The patient had a history of chronic obstructive pulmonary disease (COPD) and noted that his cough and dyspnea had increased above normal for several days. He was now dyspneic with minimal activity and had slept at a 45‐degree incline the night prior to evaluation due to dyspnea. He noted less improvement than usual with the use of his metered dose inhaler. His cough was occasionally productive of small amounts of white phlegm. He had vomited once. During a coughing episode the patient experienced a sudden onset of sharp right upper quadrant abdominal pain that worsened with coughing and sudden position changes. The patient denied a prior history of abdominal pain or surgery. The patient's last bowel movement was 2 days prior to admission. He denied melena or bright red blood per rectum.

My initial differential diagnosis for this patient's dyspnea and cough is pneumonia, acute exacerbation of COPD, or congestive heart failure. The presence of fever and anorexia increases the likelihood of infectious etiologies, whereas the presence of orthopnea points toward congestive heart failure. Noncardiac processessuch as a large pleural effusion or apical lung diseasecould also cause orthopnea. His abdominal pain could be a result of pneumonia alone (perhaps in the right lower lobe with diaphragmatic irritation), but I am also considering complications of pneumonia such as empyema. Although his abdominal pain, dyspnea, and cough could also be a result of hepatobiliary disease, a perforated viscus, or pancreatitis, we currently have little reason to suspect a direct abdominal etiology. My top diagnosis is community‐acquired pneumonia, perhaps accompanied by pleural effusion.

His medical history was significant for dilated cardiomyopathy and heavy alcohol use. His medications included various meter‐dosed inhalers, bupropion, digoxin, spironolactone, lisinopril, and metoprolol. He had never received corticosteroid therapy and had not previously been hospitalized for COPD‐related problems. He had smoked one pack of cigarettes daily for 40 years.

Heavy alcohol use is associated with an increased risk of several pulmonary infections such as gram‐negative necrotizing pneumonia (classically, Klebsiella pneumoniae), pneumococcal pneumonia, aspiration pneumonia, anaerobic lung abscesses, and tuberculosis. Given his right upper quadrant pain, acute alcoholic hepatitis and alcohol‐related pancreatitis enter the differential. His history of cardiomyopathy makes me consider congestive heart failure as more likely than before, and perhaps his abdominal pain is a result of hepatic congestion from right heart failure. His fever, however, cannot be attributed to cardiac failure. Less likely diagnoses include ischemic conditions related to his cardiomyopathy such as mesenteric ischemia from low perfusion or embolism from a cardiac thrombus. A pulmonary infection remains the most likely diagnosis.

He was an ill‐appearing man in moderate respiratory distress, looking older than his stated age. His temperature was 38.4C, heart rate 129 beats/minute, blood pressure 85/56 mm Hg, respiratory rate 24 breaths/minute, and oxygen saturation 92% on room air. A cardiovascular exam revealed no murmur, gallop, or rub. The jugular venous pulse was not elevated. His lungs were clear to auscultation. Abdominal exam revealed right‐sided abdominal tenderness that appeared to localize to the rectus sheath. Otherwise, the abdomen was soft, with normal bowel sounds and no organomegaly. Rectal examination revealed guaiac negative stool and no focal tenderness. His extremities were normal.

His vital signs are worrisome for impending cardiovascular collapse and shock, possibly due to sepsis. The relatively nonfocal cardiopulmonary exam is surprising given his initial symptoms and makes me wonder if his dyspnea is primarily related to an abdominal process leading to diaphragmatic irritation rather than to a thoracic process. Congestive heart failure seems unlikely given the lack of supportive physical examination findings. His abdominal exam findings are puzzling. Although his abdominal wall tenderness could be benignperhaps from muscular strain or a tear from coughingit could represent a more worrisome process such as infection or a hematoma in the abdominal wall muscles. Mesenteric ischemia is still possible, as the exam is often unimpressive. A hepatic abscess or subphrenic abscess should be considered, as physical exam findings in these conditions can be subtle.

My differential remains relatively unchanged, but I have now put consideration of a hepatic or subphrenic abscess higher on my list. Early empiric broad‐spectrum antibiotics seem necessary.

He had a white blood cell count of 26,700/mL with 92% neutrophils, a hemoglobin of 14.6 g/dL, and a platelet count of 312,000/mL. Sodium was 134 mmol/L, potassium was 4.3 mmol/L, chloride was 94 mmol/L, bicarbonate was 23 mmol/L, blood urea nitrogen was 23 mg/dL, and creatinine was 2.1 mg/dL. The results of the calcium, protein, albumin, and liver function tests were normal. Urinalysis was negative for protein and red blood cells. An electrocardiogram revealed sinus tachycardia. A chest radiograph at admission revealed mild opacities in both lower lobes and the right middle lobe consistent with either atelectasis or pneumonia (Fig. 1). A very small left effusion was also identified.

Figure 1

The additional data reinforce my clinical impression that this process is likely to be infectious. The chest radiograph is consistent with community‐acquired pneumonia, possibly from an atypical pathogen. Given his elevated creatinine, I am also considering a pulmonary‐renal syndrome such as vasculitis, though hematuria was not present. A subphrenic abscess, mesenteric ischemia, or an abdominal wall process (because his abdominal tenderness on exam still needs an explanation) remain possibilities; my suspicion would increase if he does not respond appropriately to therapy for community‐acquired pneumonia.

The clinical team's working diagnosis also was community‐acquired pneumonia. Blood and sputum cultures were obtained, and the patient was treated with intravenous ceftriaxone, azithromycin, and intravenous fluid. By the second day, his creatinine had normalized; however, his hypoxemia had worsened, and he now required supplemental oxygen. His temperature was 39.3C, and his heart rate was 150 beats/minute. The findings of an abdominal ultrasound of the kidneys, spleen, and right upper quadrant were normal.

It is too early to say the patient has failed therapy because a patient can get worse before getting better during the course of antibiotic therapy for community‐acquired pneumonia. Fever, for example, may take up to 7 days to resolve, depending on host factors and the pathogen. Though I typically wait about 72 hours before assuming a patient is not appropriately responding to therapy, the additional information has made me concerned. The degree of tachycardia is significant and warrants an EKG to exclude an arrthymia. I would also repeat the chest radiograph to evaluate for worsening infiltrates or increased pleural effusion.

On the third hospital day, the patient's abdominal pain had decreased with analgesia, but his fever, cough, and dyspnea remained largely unchanged. Antibiotics were changed to intravenous levofloxacin. A repeat chest radiograph revealed elevation of the right hemidiaphragm and bilateral effusions (Fig. 2). An electrocardiogram revealed sinus tachycardia. Blood cultures revealed no growth, and sputum cultures grew oral flora.

Figure 2

A significantly elevated right hemidiaphragm makes me reconsider the diagnosis of simple community‐acquired pneumonia. The differential diagnosis for an elevated hemidiaphragm is best considered by location in relation to the diaphragm. Causes above the diaphragm include rib fracture, atelectasis, pleural thickening, and volume loss of the lung for another reason (e.g., surgery, bronchial obstruction due to tumor or mucus plugging), as well as mimics such as a densely consolidated pneumonia, pulmonary infarction, or a subpulmonary effusion. Diaphragmatic causes include eventration, rupture, phrenic nerve weakness, and intrinsic weakness because of neuromuscular disease (usually bilateral). Causes below the diaphragm that must be considered are subphrenic or liver abscess, liver (and other abdominal) malignancy, pancreatic pseudocyst, and distended bowel. Given the clinical picture, I am focusing below the diaphragmespecially on a possible hepatic or subphrenic abscess (which could be missed on ultrasound) and mimics of it such as dense consolidation or a subpulmonary effusion. Given the lack of response to antibiotics, I need to consider an infection that is not being treated, either because of location (abscess, effusion) or microbiology (tuberculosis, a parasite, a fungus, resistant bacteria). After confirming that the patient has a substantive pleural effusion, he needs a thoracentesis.

On the fourth hospital day, his temperature was 38.8C, and his white blood cell count was 21,000/mL. A right‐sided thoracentesis was performed; approximately 250 cc of fluid was obtained. Pleural fluid analysis revealed bloody fluid, with a white blood cell count of 16,750/mL with 94% neutrophils, 40,000 red blood cells/mL, lactate dehydrogenase of 278 U/L (normal serum value 80200 U/L), protein of 3.7 g/dL, and glucose of 81 mg/dL. A pleural fluid pH was not obtained. A gram stain revealed many white blood cells with no organisms noted. Serum protein was 7.4 g/dL. These results were thought to represent an exudative parapneumonic effusion; levofloxacin and supplemental oxygen were continued.

The pleural fluid appears exudative, but I am not sure this man has a parapneumonic effusion because, despite clinical deterioration, an obvious infiltrate is not seen on interval chest radiography. We must look closely at the fluid because this is a bloody effusion and somewhat atypical for a parapneumonic effusion. Also, the effusion does not appear large enough to explain why he has not improved on the current antibiotics. We should thus reconsider our diagnosis and management. I would obtain additional imaging (such as an abdominal and chest computed tomography [CT]) and perhaps obtain a consultation from the pulmonary team regarding the postulated initial diagnosis of pneumonia with effusion.

On the fifth day of hospitalization, the patient's dyspnea and cough persisted but were improved. His abdominal pain was minimal and felt improved with flatus. Fever continued to 38.8C, and the white blood cell count was 20,000/mL. On examination the patient had decreased breath sounds at the right base and bibasilar crackles. His abdomen was soft, with tenderness in his right upper quadrant only with deep palpation; bowel sounds remained. An ultrasound of the chest was performed to look for a loculated effusion; however, no fluid was identified. The pulmonary consultant thought it likely that the patient had a subpulmonic effusion and recommended CT of the abdomen and chest.

His right upper quadrant tenderness is still unexplained. I would agree with the CT, primarily to evaluate other causes of his elevated diaphragm such as subphrenic or hepatic abscess. For now, I would make no change in antibiotic therapy.

On the sixth hospital day, the patient had an episode of bilious emesis. Chest and abdominal CT revealed collapse of the right middle and lower lobes with a small adjacent effusion, and a 6 6 16 cm abscess intimately opposed to the right lobe of the liver. Extending from the inferior extent of the abscess was a tubular thick‐walled structure connecting to the cecum that was suspicious of a thickened inflamed appendix. There was periappendiceal stranding suggesting inflammation. The small bowel was diffusely dilated up to 4.5 cm, suggesting a small bowel obstruction.

I suspect that his abscess is related to a perforated appendix and that the dilated small bowel is most likely a result of localized irritation of the bowel by the abscess and appendicitis. The collapsed lung is most likely due to local inflammation from the subdiaphragmatic abscess. Treatment should now be changed substantially. I would ask a surgeon to evaluate the patient because the most likely diagnosis is perforated appendicitis with abscess formation.

When the periappendiceal abscess was drained percutaneously, 190 mL of purulent fluid was removed. The cultures were positive for Klebsiella pneumonia, Enterococcus faecalis,and Streptococcus milleri. The patient was given 6 weeks of intravenous antibiotics with improvement in his clinical symptoms. During the interval the findings on his chest radiograph resolved completely. A laproscopic appendectomy 3 months later revealed significant right lower quadrant adhesions. The pathology specimen identified a distorted appendix with regeneration consistent with prior appendicitis. The patient was contacted 4 months after his surgery, and he reported that he was doing well, with no cardiopulmonary or gastrointestinal symptoms.

COMMENTARY

Community‐acquired pneumonia (CAP) is a common cause of acute illness and accounts for nearly 1 million admissions per year in the United States.1 The diagnosis of CAP is made when symptoms including dyspnea, fever, cough, or leukocytosis are present, with confirmation provided by a chest radiograph. Often the diagnosis is clear; however, there is no pathognomonic constellation of signs or symptoms that establish the diagnosis with certainty.2 Many physicians learn that pneumoniaespecially lower‐lobe pneumoniacan lead to abdominal findings such as upper quadrant pain, vomiting, and tenderness to palpation. Conversely, the patient discussed above illustrates that a primary abdominal process can also result in a symptom complex that mimics pneumonia.

The prevalence of CAP coupled with the inherent uncertainty of a clinical diagnosis of CAP leads to an important question: How long is too long before questioning the diagnosis? An analysis of the pneumonia Patient Outcomes Research Trial (PORT) limited to inpatients with CAP examined time to clinical stability. For the majority of patients, abnormal vital signs resolved within 23 days.3 In this study, 29% of patients had severe disease, and not surprisingly, these patients took longer to improve. Using the pneumonia severity index score, which accounts for age, comorbidity, abnormal vital signs, and laboratory data, the patient described in this article would be considered at high risk for death and complication with an estimated mortality of 9%.4 Using a combination of defervescence, resolution of tachycardia, tachypnea, and hypoxemia as markers of clinical stability, a patient like ours should respond within 4 days (with a range of 27 days). On the basis of these dataand the discrepancy between the patient's severe illness and relatively minor pulmonary infiltratesit seems reasonable to have considered this patient as failing CAP therapy as early as the fourth day of hospitalization.

In approximately 10% of hospitalized patients with CAP, the clinical course is protracted.5 When patients do not improve as quickly as expected, the reasons that could explain this should be investigated. In a cohort of 49 patients with CAP who failed therapy the most common reasons for failure to improve were severity of the pneumonia and drug resistance.6 A multicenter study found that the incidence of resistance to penicillin by Streptococcus pneumoniae, the most common bacterial pathogen in CAP, was 30%, with a 4% in vitro resistance rate to ceftriaxone.7 How well in vitro resistance predicts clinical response, however, is unclear. Risk factors for antibiotic resistance include close exposure to children, recent antibiotic use, and recent hospitalization. Immunosuppressive conditions should also be considered in patients who fail to improve. Suppurative complications of pneumoniasuch as empyema, parapneumonic effusion, and lung abscessalso delay recovery.

Another consideration in a patient with what appears to be a nonresolving pneumonia with pleural effusion is that the initial diagnosis is incorrect and the cause is extrathoracic. Pulmonary and cardiac diseases account for more than 90% of effusions, whereas less than 5% of pleural effusions result from intraabdominal causes.8 When should intraabdominal diseases be sought in patients with an effusion, fever, dyspnea, and cough? Light suggests that intraabdominal pathology should be investigated in patients who have pleural effusions without significant parenchymal disease.8 This point is underscored by the experience of our patient, whose chest radiographs showed, despite clinical decline, minimal airspace disease.

Several abdominal entities cause pleural effusion. Pancreatitis, either acute or chronic, with pseudocyst formation is the most common abdominal cause of exudative pleural effusions. Approximately 10% of patients with pancreatic disease will develop effusions, usually left‐sided.9 These left‐sided effusions are also seen in splenic abscesses, usually as a result of endocarditis. Intrahepatic abscess is associated with effusions in 20% of patients.10 A subphrenic abscess, as seen in our patient, is an uncommon cause of exudative pleural effusions. Historically, subphrenic abscesses resulted from a perforated viscus, with ruptured appendicitis the most common cause,11 followed by perforated peptic ulcers and biliary tract disease. With the advent of antibiotics, the causes of subphrenic abscess changed considerably, with the majority of current cases resulting from postsurgical complications.12 The findings of a chest radiograph are abnormal in 80% of patients with subphrenic abscess;1214 an elevated hemidiaphragm and pleural effusion are found in the majority of cases. The symptoms of a subphrenic abscess are nonspecific, and patient's complaints are equally split between predominantly thoracic and predomninantly abdominal complaints.15

Appendicitis, a common disease predominantly of the young, may lead to atypical presentations in older individuals. In a retrospective analysis of 113 patients older than 60 years with appendicitis, 70% presented in an atypical fashion.16 Typical symptoms include right lower quadrant pain, fever, anorexia and a white blood cell count greater than 10,000/mL. Fever was the most frequently absent symptom, seen in only 37% of older patients. In this cohort, approximately one third of older patients waited more than 48 hours prior to presentation. The time between symptom onset and clinical presentation is a strong predictor of perforation risk.17 As in this case, roughly 2% of patients with acute appendicitis will present with perforation and abscess formation.18 In such patients the management is initially conservative. Percutaneous drainage and broad spectrum antibiotics are the treatment of choice, followed by an interval appendectomy in 612 weeks.19 The rationale for delayed surgery is that earlier surgery may disseminate a localized inflammatory process.20

Community‐acquired pneumonia is a more frequent cause of hospital admission than is intraabdominal abscess. Physicians often face the dilemma of when to pursue alternative diagnoses after a patient who is thought to have an atypical presentation of a common disease (ie, CAP) fails to respond to conventional therapy. Although clinicians learn that right upper quadrant pain may be a symptom of pneumonia, our patient revealed that abdominal causes may mimic pneumonia and produce a pleural effusion. Determining whether the primary disease originates above or below the diaphragm is critical to guiding therapy. When patients fail to respond adequately to therapy, clinicians should set a low threshold for deciding to image the abdomen in a patient with modest pulmonary infiltrates, pleural effusion, and abdominal pain.