The demand for hospital medicine specialists continues to grow at nearly an exponential pace.1 Society of Hospital Medicine (SHM) practice estimates rose from 2000 in 1998 to 15,000 in 2005, with a projection of 30,000 for 2010.2 Most new positions are filled by graduates of internal medicine and pediatric residencies without postgraduate fellowship training. However, as hospital medicine specialists increasingly provide not only direct care but also team leadership and quality improvement, basic residency training alone may not suffice to provide the required skill sets. In addition, the career satisfaction of hospitalists depends in large part on the esteem of colleagues in other specialties. Ready availability for emergency department admissions and inpatient consults, coupled with an absence of postgraduate clinical training and board certification,3 may promote a view of the hospitalist as a perpetual resident‐like workhorse rather than as a professional peer.

Clinical hospital medicine fellowships could address the needs both to expand skill sets and to elevate the perceived stature of the profession. To date, only a small number of hospital medicine fellowships have been created,4 and all but a few are intended to train academic educators rather than produce hospitalists for the emerging clinical marketplace.5 Furthermore, a fellowship curriculum would incorporate the advanced training in group dynamics and interpersonal communication needed to lead the increasing number of increasingly diverse hospitalist groups.1

In considering a clinical hospital fellowship for the reasons above, the University of Nevada School of Medicine sought first to address several potential obstacles:

• 1

  Curriculum. What is the proper balance of mentored clinical service and didactic coursework? How should quality improvement be taught? What emphasis should be placed on business and medicolegal aspects of the profession?

• 2

  Salary. Would a prospective fellow be willing to defer practice income during the training period? Will future employers compensate for this by rewarding clinical fellowshiptrained hospitalists with bonuses, higher initial salaries, or leadership positions?

• 3

  Reality check. Do practicing hospitalists regret not having had the opportunity to train in a clinical fellowship environment? Will current residents in training actually apply for such fellowships?

METHODS

Over the course of 7 months in late 2005 and early 2006, we administered a linked sequence of three nation‐wide surveys: Survey I to hospitalist employers, Survey II to practicing hospitalists, and Survey III to internal medicine residents. Although we roughed out the general structure of all surveys in advance, we awaited the main results of the first survey to be incorporated into the second, and the results of the first two into the third (see below). All surveys were created using PHP as the interface language between the user and a MySQL relational database running on our university server, conducted over secure encrypted Web connections. Surveys I‐III were field‐tested and amended based on the responses of focus groups of local employers, hospitalists, and residents, respectively. In addition to required responses targeting the perspectives of the recipient, all surveys requested optional demographic information. Although the surveys were anonymous, an option was provided for respondents to receive a compilation of the results of all 3 surveys by E‐mail. The proposal was screened by our university institutional review board and determined to be exempt from human subjects review.

RESULTS

Survey II (Hospitalists)

Demographics.

One hundred and one practicing hospitalists responded to the SHM E‐mail request. The SHM membership office estimates that the survey was sent to deliverable E‐mail addresses of approximately 2300 physicians, of whom approximately 68% (1560) were internists; based on this, our response rate was approximately 6.5%.

Table 3 shows that practicing hospitalists were predominantly internists (88%). They were evenly distributed across the nation and between hospital‐owned groups (46%) and privately owned groups (46%); the latter included medical school practice plans (18% of respondents). Of the respondents, 75% were full‐time hospitalists, and only 1 worked less than 0.25 the equivalent of full‐time. They had graduated a median of 8 years earlier (interquartile range, 6 years; range, 1970‐2005).

Table 3.Characteristics of Hospitalists (Survey II)

Category	n	(%)
* Median year of graduation was 1998; range 1970‐2005.
Practice region
East	32	(31.7)
South	21	(20.8)
Midwest	22	(21.8)
West	26	(25.7)
Ownership of employing organization
HOSPITAL OWNERSHIP	46	(45.5)
For‐profit hospital ownership	4	(4.0)
Not‐for‐profit hospital ownership	42	(41.6)
PRACTICE OWNERSHIP	46	(45.5)
Hospitalist‐only private practice group	7	(6.9)
Hospitalists within primary care private practice group	9	(8.9)
Multispecialty private practice group	12	(11.9)
Medical school practice plan	18	(17.8)
OTHER	9	(8.9)
Professional effort as hospitalist
100% FTE	76	(75.3)
75% FTE	13	(12.9)
50% FTE	6	(5.9)
25% FTE	5	(5.0)
<25% FTE	1	(1.0)
Residency Training*
Internal medicine	89	(88.1)
Pediatrics	6	(5.9)
Family medicine	5	(5.0)
Other	1	(1.0)

Primary Measures.

On average, practicing hospitalists ranked essentially all 12 curricular topics between moderate and high priority. Figure 1 displays the scores sorted by means with standard deviations; any pairwise difference between 2 means greater than 0.286 corresponds to a Bonferroni‐corrected P value < .05. Communication, leadership, and coding skills averaged above 2.5 (ie, closer to high than moderate priority), and bioethics ranked the lowest. There was no overall obvious clustering of topics, with administrative and clinical topics interspersed across the ratings. Respondents offered no separate topics in their open‐ended responses, but recommended subtopics to be included, such as contract negotiation, training for effective committee involvement, dealing with families, consultative medicine, and ICU comanagement. Several respondents also suggested tailoring the weighting of the curricular emphasis according to the needs and experience of individual fellows in each cohort.

Figure 1

Of the practicing hospitalists, 81% believed that clinical fellowship could be a good career move (Table 4), and 59% believed that graduating residents probably or strongly should consider such fellowship training. The median response to the question of minimum salary we should offer a hospitalist fellow was $70,000, with 80% of responses between $50,000 and $90,000.

Table 4.Perspectives of Hospitalists (Survey II)

Category	n	(%)
* Minimum annual salary, assuming 50% clinical load during fellowship; mean $68,900 $11,400.
Strength of recommendation to pursue fellowship
RECOMMEND	92	(91.1)
Possibly a good career move	33	(32.7)
Probably a good career move	37	(36.6)
Strongly recommend	22	(21.8)
DON'T RECOMMEND	9	(8.9)
Fellowship salary*
$50,000	11	(10.9)
$60,000	24	(23.8)
$70,000	30	(29.7)
$80,000	20	(19.8)
$90,000	8	(7.9)
$100,000	8	(7.9)
Likelihood of practicing hospital medicine in 5 years
Very likely	69	(68.3)
Somewhat likely	17	(16.8)
Somewhat unlikely	10	(9.9)
Very unlikely	5	(5.0)
Perceived reasons for job dissatisfaction
INTERNAL FACTORS	166	(71.0)
Excess workload	80	(34.2)
Scheduling frustrations	32	(13.7)
Organizational leadership and administrative problems	24	(10.2)
Inadequate salary	16	(6.8)
Productivity pressures	14	(6.0)
EXTERNAL FACTORS	78	(29.0)
Interaction, communication problems within hospital	29	(12.4)
Mistreatment, lack of professional respect	28	(12.0)
Other	11	(4.7)

When asked about their future plans, 69% were very likely to be practicing hospital medicine in 5 years (Table 4). Major reasons for career dissatisfaction were aggregated into 5 categories, 3 of which pertained to internal group management (accounting for 71% of concerns) and the others to external interactions in the hospital milieu (Table 4).

Survey III (Residents)

Demographics.

Two hundred and seventy‐nine categorical medicine residents responded to the survey link forwarded by their program director, 43% of whom requested a follow‐up summary of overall survey findings. Based on a total of 385 medicine program directors sent an E‐mail request and the E‐mail domain servers of the respondents, we estimate that about 70 program directors (18%) forwarded surveys to their residents.

Without respect to subspecialty choice, 75% of the 279 categorical residents planned to stay in their region after graduation; among the 25% planning to relocate, most were moving from the East or South to the West or Southwest (Table 5). Interestingly, no residents in the Southwest and the West planned to leave their region of current training. Overall, 40% were academically oriented. About 35% planned to work for a hospital entity, and about 20% planned to work in a private group.

Table 5.Characteristics and Plans of Categorical Residents (Survey III)

Category	n	(%)
* No residents in the Southwest and the West planned to leave their region.
Present residency program location
East	129	(46.2)
Midwest	92	(33.0)
South	20	(7.2)
Southwest*	3	(1.1)
West*	35	(12.5)
Anticipated future practice location
Eastern	95	(34.1)
Midwest	78	(28.0)
South	36	(12.9)
Southwest*	14	(5.0)
West*	56	(20.1)
Probably or definitely will do hospitalist career
PGY1 (n = 76)	36	(47.3)
PGY2 (n = 95)	37	(38.9)
PGY3 (n = 96)	44	(45.8)
Chiefs (n = 12)	6	(50.0)
Overall (n = 279)	123	(44.1)
Probably or definitely will do hospitalist career AND probably or definitely will do fellowship
PGY1 (n = 76)	24	(31.6)
PGY2 (n = 95)	24	(25.3)
PGY3 (n = 96)	21	(21.9)
Chiefs (n = 12)	1	(8.3)
Overall (n = 279)	70	(25.1)

Primary Measures.

One hundred and twenty‐three of the 279 categorical residents (44%) were strongly considering a hospitalist career. There was no significant difference in the proportion of interest across PGY 1‐3 level (P = .48). Seventy of these 123 (57%) would likely pursue a clinical hospital medicine fellowship if it was available to them. Although there was increasing fellowship interest, with interest by PGY1 residents greater than that of PGY2 residents, which was greater than of PGY3 residents, but this trend did not reach statistical significance (Cochrane linear trend, P = .15).

One hundred and forty‐seven of the 279 categorical residents (53%) offered reasons for interest (or lack of interest) in a hospital medicine career (Fig. 2). The predominant attractions (Fig. 2A) were the intellectual challenge and variety of cases encountered in general acute care (49%) and the flexibility in work scheduling and time off (37%). Reasons offered for not pursuing hospital medicine were mainly the intention to purse subspecialty or primary care medicine; remaining factors (from a relatively small number of responders) included perceptions of a lack of professional respect and unfavorable salary or scheduling (Fig. 2B).

Figure 2

DISCUSSION

The increasing demand for hospitalist care has outstripped the supply of physicians available to do the job and as a result of the unmet demand; in our study, two‐thirds of employers were willing to pay more, either through a signing bonus or a starting salary increase of at least $10,000 to fellowship graduates (with more than 20% willing to pay at least $20,000 above the initial salary). The value of enhancing organizational and communication skills was also recognized, as shown by the readiness of about 70% of employers to offer leadership positions to clinical fellowshiptrained hospitalists.

Residents drawn to hospital medicine were mainly attracted by the flexible scheduling and intellectual challenge (Fig. 2). Lack of interest mainly reflected plans to enter other subspecialties or primary care, rather than apprehension about professional frustrations. Practicing hospitalists, however, related substantial professional concerns arising from both internal factors (predominantly excessive workload) and external sources (respect from other physicians and interdisciplinary hospital communication issues). An alarming 31% were not very likely to remain in the practice of hospital medicine beyond the next 5 years. Fellowship training could indirectly address workload issues by creating leaders skilled in scheduling and team building and could directly enhance communication and team‐building skills and generate esteem among professional peers.

Would residents forgo a year of greater salary to pursue a fellowship? Based on the SHM estimate of a median salary of $169,000 and a leadership salary gradient of $12,0006 and Survey III median recommendation for a fellowship salary of $70,000, a 1‐year fellow would face a potential loss of income of about $100,000. Using the Survey I findings above and the leadership gradient, this could be recouped within about 5 years. Of course, it is difficult to assign a dollar value to the additional intangible benefits attributable to enhanced career satisfaction and greater effectiveness in affecting hospital care dynamics. The $70,000 salary proposed (higher than most traditional fellowships offer) corresponds to revenue collected from the proposed clinical workload of 50% that of a full‐time hospitalist; programs would thus need to identify other sources to cover supervisory and teaching overhead. Residents considering a hospital medicine career apparently did appreciate the deferred value of an investment in hospital fellowship: having been provided the results of the employer and hospitalist surveys, 57% would likely pursue a clinical fellowship if available. Extrapolating to the national pool of about 6600 annual graduates of internal medicine residencies, a 44% overall rate of hospital medicine career interest, with 57% fellowship interest, would yield about 550 fellowship candidates annually (this is an upper bound overestimate, given the relatively large proportion of our respondents with interest in an academic career).

The validity of the 12 proposed curricular topics is supported by the rating of all topics as moderate to high priority by practicing hospitalists (Fig. 1) and is consistent with the recently published SHM Core Competencies.7 Significant differences were found for topics rated in the lower versus upper half of the response range, without obvious clustering of clinical or administrative topics. Communication, leadership, and billing and coding were rated as top priorities, training in quality metrics and consultation were intermediate, and bioethics was given the lowest relative priority (although still considered moderately important). Although no novel additional topics were generated in open‐ended responses, several suggested tailoring the curricular emphasis according to the needs and prior experience of individual fellows in a cohort.

Generalization of our findings is limited by the low response rates of both hospitalist and resident physicians. It is likely that responding hospitalists were more interested than nonresponders in the concept of clinical hospital medicine fellowships. The strength of recommendation of fellowship training should therefore be considered an upper bound. The other main questions, pertaining to salary and curriculum, would presume a sufficient interest among responders and thus be less susceptible to sampling bias. Regarding resident response, we do not know the number of questionnaires actually forwarded by program directors to their residents. However, given that most responding residents were not planning to be hospitalists, we have at least a relatively representative sample of the attitudes of both uninterested and interested residents.

In summary, the results of our national surveys of hospitalist employers, practicing hospitalists, and current internal medicine residents reveals a potentially unmet demand for the provision of clinical hospital medicine fellowships. Curricular development under the leadership of organizations such as the Society of Hospital Medicine could hasten this development.

The demand for hospital medicine specialists continues to grow at nearly an exponential pace.1 Society of Hospital Medicine (SHM) practice estimates rose from 2000 in 1998 to 15,000 in 2005, with a projection of 30,000 for 2010.2 Most new positions are filled by graduates of internal medicine and pediatric residencies without postgraduate fellowship training. However, as hospital medicine specialists increasingly provide not only direct care but also team leadership and quality improvement, basic residency training alone may not suffice to provide the required skill sets. In addition, the career satisfaction of hospitalists depends in large part on the esteem of colleagues in other specialties. Ready availability for emergency department admissions and inpatient consults, coupled with an absence of postgraduate clinical training and board certification,3 may promote a view of the hospitalist as a perpetual resident‐like workhorse rather than as a professional peer.

Clinical hospital medicine fellowships could address the needs both to expand skill sets and to elevate the perceived stature of the profession. To date, only a small number of hospital medicine fellowships have been created,4 and all but a few are intended to train academic educators rather than produce hospitalists for the emerging clinical marketplace.5 Furthermore, a fellowship curriculum would incorporate the advanced training in group dynamics and interpersonal communication needed to lead the increasing number of increasingly diverse hospitalist groups.1

In considering a clinical hospital fellowship for the reasons above, the University of Nevada School of Medicine sought first to address several potential obstacles:

• 1

  Curriculum. What is the proper balance of mentored clinical service and didactic coursework? How should quality improvement be taught? What emphasis should be placed on business and medicolegal aspects of the profession?

• 2

  Salary. Would a prospective fellow be willing to defer practice income during the training period? Will future employers compensate for this by rewarding clinical fellowshiptrained hospitalists with bonuses, higher initial salaries, or leadership positions?

• 3

  Reality check. Do practicing hospitalists regret not having had the opportunity to train in a clinical fellowship environment? Will current residents in training actually apply for such fellowships?

METHODS

Over the course of 7 months in late 2005 and early 2006, we administered a linked sequence of three nation‐wide surveys: Survey I to hospitalist employers, Survey II to practicing hospitalists, and Survey III to internal medicine residents. Although we roughed out the general structure of all surveys in advance, we awaited the main results of the first survey to be incorporated into the second, and the results of the first two into the third (see below). All surveys were created using PHP as the interface language between the user and a MySQL relational database running on our university server, conducted over secure encrypted Web connections. Surveys I‐III were field‐tested and amended based on the responses of focus groups of local employers, hospitalists, and residents, respectively. In addition to required responses targeting the perspectives of the recipient, all surveys requested optional demographic information. Although the surveys were anonymous, an option was provided for respondents to receive a compilation of the results of all 3 surveys by E‐mail. The proposal was screened by our university institutional review board and determined to be exempt from human subjects review.

RESULTS

Survey II (Hospitalists)

Demographics.

One hundred and one practicing hospitalists responded to the SHM E‐mail request. The SHM membership office estimates that the survey was sent to deliverable E‐mail addresses of approximately 2300 physicians, of whom approximately 68% (1560) were internists; based on this, our response rate was approximately 6.5%.

Table 3 shows that practicing hospitalists were predominantly internists (88%). They were evenly distributed across the nation and between hospital‐owned groups (46%) and privately owned groups (46%); the latter included medical school practice plans (18% of respondents). Of the respondents, 75% were full‐time hospitalists, and only 1 worked less than 0.25 the equivalent of full‐time. They had graduated a median of 8 years earlier (interquartile range, 6 years; range, 1970‐2005).

Table 3.Characteristics of Hospitalists (Survey II)

Category	n	(%)
* Median year of graduation was 1998; range 1970‐2005.
Practice region
East	32	(31.7)
South	21	(20.8)
Midwest	22	(21.8)
West	26	(25.7)
Ownership of employing organization
HOSPITAL OWNERSHIP	46	(45.5)
For‐profit hospital ownership	4	(4.0)
Not‐for‐profit hospital ownership	42	(41.6)
PRACTICE OWNERSHIP	46	(45.5)
Hospitalist‐only private practice group	7	(6.9)
Hospitalists within primary care private practice group	9	(8.9)
Multispecialty private practice group	12	(11.9)
Medical school practice plan	18	(17.8)
OTHER	9	(8.9)
Professional effort as hospitalist
100% FTE	76	(75.3)
75% FTE	13	(12.9)
50% FTE	6	(5.9)
25% FTE	5	(5.0)
<25% FTE	1	(1.0)
Residency Training*
Internal medicine	89	(88.1)
Pediatrics	6	(5.9)
Family medicine	5	(5.0)
Other	1	(1.0)

Primary Measures.

On average, practicing hospitalists ranked essentially all 12 curricular topics between moderate and high priority. Figure 1 displays the scores sorted by means with standard deviations; any pairwise difference between 2 means greater than 0.286 corresponds to a Bonferroni‐corrected P value < .05. Communication, leadership, and coding skills averaged above 2.5 (ie, closer to high than moderate priority), and bioethics ranked the lowest. There was no overall obvious clustering of topics, with administrative and clinical topics interspersed across the ratings. Respondents offered no separate topics in their open‐ended responses, but recommended subtopics to be included, such as contract negotiation, training for effective committee involvement, dealing with families, consultative medicine, and ICU comanagement. Several respondents also suggested tailoring the weighting of the curricular emphasis according to the needs and experience of individual fellows in each cohort.

Figure 1

Of the practicing hospitalists, 81% believed that clinical fellowship could be a good career move (Table 4), and 59% believed that graduating residents probably or strongly should consider such fellowship training. The median response to the question of minimum salary we should offer a hospitalist fellow was $70,000, with 80% of responses between $50,000 and $90,000.

Table 4.Perspectives of Hospitalists (Survey II)

Category	n	(%)
* Minimum annual salary, assuming 50% clinical load during fellowship; mean $68,900 $11,400.
Strength of recommendation to pursue fellowship
RECOMMEND	92	(91.1)
Possibly a good career move	33	(32.7)
Probably a good career move	37	(36.6)
Strongly recommend	22	(21.8)
DON'T RECOMMEND	9	(8.9)
Fellowship salary*
$50,000	11	(10.9)
$60,000	24	(23.8)
$70,000	30	(29.7)
$80,000	20	(19.8)
$90,000	8	(7.9)
$100,000	8	(7.9)
Likelihood of practicing hospital medicine in 5 years
Very likely	69	(68.3)
Somewhat likely	17	(16.8)
Somewhat unlikely	10	(9.9)
Very unlikely	5	(5.0)
Perceived reasons for job dissatisfaction
INTERNAL FACTORS	166	(71.0)
Excess workload	80	(34.2)
Scheduling frustrations	32	(13.7)
Organizational leadership and administrative problems	24	(10.2)
Inadequate salary	16	(6.8)
Productivity pressures	14	(6.0)
EXTERNAL FACTORS	78	(29.0)
Interaction, communication problems within hospital	29	(12.4)
Mistreatment, lack of professional respect	28	(12.0)
Other	11	(4.7)

When asked about their future plans, 69% were very likely to be practicing hospital medicine in 5 years (Table 4). Major reasons for career dissatisfaction were aggregated into 5 categories, 3 of which pertained to internal group management (accounting for 71% of concerns) and the others to external interactions in the hospital milieu (Table 4).

Survey III (Residents)

Demographics.

Two hundred and seventy‐nine categorical medicine residents responded to the survey link forwarded by their program director, 43% of whom requested a follow‐up summary of overall survey findings. Based on a total of 385 medicine program directors sent an E‐mail request and the E‐mail domain servers of the respondents, we estimate that about 70 program directors (18%) forwarded surveys to their residents.

Without respect to subspecialty choice, 75% of the 279 categorical residents planned to stay in their region after graduation; among the 25% planning to relocate, most were moving from the East or South to the West or Southwest (Table 5). Interestingly, no residents in the Southwest and the West planned to leave their region of current training. Overall, 40% were academically oriented. About 35% planned to work for a hospital entity, and about 20% planned to work in a private group.

Table 5.Characteristics and Plans of Categorical Residents (Survey III)

Category	n	(%)
* No residents in the Southwest and the West planned to leave their region.
Present residency program location
East	129	(46.2)
Midwest	92	(33.0)
South	20	(7.2)
Southwest*	3	(1.1)
West*	35	(12.5)
Anticipated future practice location
Eastern	95	(34.1)
Midwest	78	(28.0)
South	36	(12.9)
Southwest*	14	(5.0)
West*	56	(20.1)
Probably or definitely will do hospitalist career
PGY1 (n = 76)	36	(47.3)
PGY2 (n = 95)	37	(38.9)
PGY3 (n = 96)	44	(45.8)
Chiefs (n = 12)	6	(50.0)
Overall (n = 279)	123	(44.1)
Probably or definitely will do hospitalist career AND probably or definitely will do fellowship
PGY1 (n = 76)	24	(31.6)
PGY2 (n = 95)	24	(25.3)
PGY3 (n = 96)	21	(21.9)
Chiefs (n = 12)	1	(8.3)
Overall (n = 279)	70	(25.1)

Primary Measures.

One hundred and twenty‐three of the 279 categorical residents (44%) were strongly considering a hospitalist career. There was no significant difference in the proportion of interest across PGY 1‐3 level (P = .48). Seventy of these 123 (57%) would likely pursue a clinical hospital medicine fellowship if it was available to them. Although there was increasing fellowship interest, with interest by PGY1 residents greater than that of PGY2 residents, which was greater than of PGY3 residents, but this trend did not reach statistical significance (Cochrane linear trend, P = .15).

One hundred and forty‐seven of the 279 categorical residents (53%) offered reasons for interest (or lack of interest) in a hospital medicine career (Fig. 2). The predominant attractions (Fig. 2A) were the intellectual challenge and variety of cases encountered in general acute care (49%) and the flexibility in work scheduling and time off (37%). Reasons offered for not pursuing hospital medicine were mainly the intention to purse subspecialty or primary care medicine; remaining factors (from a relatively small number of responders) included perceptions of a lack of professional respect and unfavorable salary or scheduling (Fig. 2B).

Figure 2

DISCUSSION

The increasing demand for hospitalist care has outstripped the supply of physicians available to do the job and as a result of the unmet demand; in our study, two‐thirds of employers were willing to pay more, either through a signing bonus or a starting salary increase of at least $10,000 to fellowship graduates (with more than 20% willing to pay at least $20,000 above the initial salary). The value of enhancing organizational and communication skills was also recognized, as shown by the readiness of about 70% of employers to offer leadership positions to clinical fellowshiptrained hospitalists.

Residents drawn to hospital medicine were mainly attracted by the flexible scheduling and intellectual challenge (Fig. 2). Lack of interest mainly reflected plans to enter other subspecialties or primary care, rather than apprehension about professional frustrations. Practicing hospitalists, however, related substantial professional concerns arising from both internal factors (predominantly excessive workload) and external sources (respect from other physicians and interdisciplinary hospital communication issues). An alarming 31% were not very likely to remain in the practice of hospital medicine beyond the next 5 years. Fellowship training could indirectly address workload issues by creating leaders skilled in scheduling and team building and could directly enhance communication and team‐building skills and generate esteem among professional peers.

Would residents forgo a year of greater salary to pursue a fellowship? Based on the SHM estimate of a median salary of $169,000 and a leadership salary gradient of $12,0006 and Survey III median recommendation for a fellowship salary of $70,000, a 1‐year fellow would face a potential loss of income of about $100,000. Using the Survey I findings above and the leadership gradient, this could be recouped within about 5 years. Of course, it is difficult to assign a dollar value to the additional intangible benefits attributable to enhanced career satisfaction and greater effectiveness in affecting hospital care dynamics. The $70,000 salary proposed (higher than most traditional fellowships offer) corresponds to revenue collected from the proposed clinical workload of 50% that of a full‐time hospitalist; programs would thus need to identify other sources to cover supervisory and teaching overhead. Residents considering a hospital medicine career apparently did appreciate the deferred value of an investment in hospital fellowship: having been provided the results of the employer and hospitalist surveys, 57% would likely pursue a clinical fellowship if available. Extrapolating to the national pool of about 6600 annual graduates of internal medicine residencies, a 44% overall rate of hospital medicine career interest, with 57% fellowship interest, would yield about 550 fellowship candidates annually (this is an upper bound overestimate, given the relatively large proportion of our respondents with interest in an academic career).

The validity of the 12 proposed curricular topics is supported by the rating of all topics as moderate to high priority by practicing hospitalists (Fig. 1) and is consistent with the recently published SHM Core Competencies.7 Significant differences were found for topics rated in the lower versus upper half of the response range, without obvious clustering of clinical or administrative topics. Communication, leadership, and billing and coding were rated as top priorities, training in quality metrics and consultation were intermediate, and bioethics was given the lowest relative priority (although still considered moderately important). Although no novel additional topics were generated in open‐ended responses, several suggested tailoring the curricular emphasis according to the needs and prior experience of individual fellows in a cohort.

Generalization of our findings is limited by the low response rates of both hospitalist and resident physicians. It is likely that responding hospitalists were more interested than nonresponders in the concept of clinical hospital medicine fellowships. The strength of recommendation of fellowship training should therefore be considered an upper bound. The other main questions, pertaining to salary and curriculum, would presume a sufficient interest among responders and thus be less susceptible to sampling bias. Regarding resident response, we do not know the number of questionnaires actually forwarded by program directors to their residents. However, given that most responding residents were not planning to be hospitalists, we have at least a relatively representative sample of the attitudes of both uninterested and interested residents.

In summary, the results of our national surveys of hospitalist employers, practicing hospitalists, and current internal medicine residents reveals a potentially unmet demand for the provision of clinical hospital medicine fellowships. Curricular development under the leadership of organizations such as the Society of Hospital Medicine could hasten this development.

The demand for hospital medicine specialists continues to grow at nearly an exponential pace.1 Society of Hospital Medicine (SHM) practice estimates rose from 2000 in 1998 to 15,000 in 2005, with a projection of 30,000 for 2010.2 Most new positions are filled by graduates of internal medicine and pediatric residencies without postgraduate fellowship training. However, as hospital medicine specialists increasingly provide not only direct care but also team leadership and quality improvement, basic residency training alone may not suffice to provide the required skill sets. In addition, the career satisfaction of hospitalists depends in large part on the esteem of colleagues in other specialties. Ready availability for emergency department admissions and inpatient consults, coupled with an absence of postgraduate clinical training and board certification,3 may promote a view of the hospitalist as a perpetual resident‐like workhorse rather than as a professional peer.

Clinical hospital medicine fellowships could address the needs both to expand skill sets and to elevate the perceived stature of the profession. To date, only a small number of hospital medicine fellowships have been created,4 and all but a few are intended to train academic educators rather than produce hospitalists for the emerging clinical marketplace.5 Furthermore, a fellowship curriculum would incorporate the advanced training in group dynamics and interpersonal communication needed to lead the increasing number of increasingly diverse hospitalist groups.1

In considering a clinical hospital fellowship for the reasons above, the University of Nevada School of Medicine sought first to address several potential obstacles:

• 1

  Curriculum. What is the proper balance of mentored clinical service and didactic coursework? How should quality improvement be taught? What emphasis should be placed on business and medicolegal aspects of the profession?

• 2

  Salary. Would a prospective fellow be willing to defer practice income during the training period? Will future employers compensate for this by rewarding clinical fellowshiptrained hospitalists with bonuses, higher initial salaries, or leadership positions?

• 3

  Reality check. Do practicing hospitalists regret not having had the opportunity to train in a clinical fellowship environment? Will current residents in training actually apply for such fellowships?

METHODS

Over the course of 7 months in late 2005 and early 2006, we administered a linked sequence of three nation‐wide surveys: Survey I to hospitalist employers, Survey II to practicing hospitalists, and Survey III to internal medicine residents. Although we roughed out the general structure of all surveys in advance, we awaited the main results of the first survey to be incorporated into the second, and the results of the first two into the third (see below). All surveys were created using PHP as the interface language between the user and a MySQL relational database running on our university server, conducted over secure encrypted Web connections. Surveys I‐III were field‐tested and amended based on the responses of focus groups of local employers, hospitalists, and residents, respectively. In addition to required responses targeting the perspectives of the recipient, all surveys requested optional demographic information. Although the surveys were anonymous, an option was provided for respondents to receive a compilation of the results of all 3 surveys by E‐mail. The proposal was screened by our university institutional review board and determined to be exempt from human subjects review.

RESULTS

Survey II (Hospitalists)

Demographics.

One hundred and one practicing hospitalists responded to the SHM E‐mail request. The SHM membership office estimates that the survey was sent to deliverable E‐mail addresses of approximately 2300 physicians, of whom approximately 68% (1560) were internists; based on this, our response rate was approximately 6.5%.

Table 3 shows that practicing hospitalists were predominantly internists (88%). They were evenly distributed across the nation and between hospital‐owned groups (46%) and privately owned groups (46%); the latter included medical school practice plans (18% of respondents). Of the respondents, 75% were full‐time hospitalists, and only 1 worked less than 0.25 the equivalent of full‐time. They had graduated a median of 8 years earlier (interquartile range, 6 years; range, 1970‐2005).

Table 3.Characteristics of Hospitalists (Survey II)

Category	n	(%)
* Median year of graduation was 1998; range 1970‐2005.
Practice region
East	32	(31.7)
South	21	(20.8)
Midwest	22	(21.8)
West	26	(25.7)
Ownership of employing organization
HOSPITAL OWNERSHIP	46	(45.5)
For‐profit hospital ownership	4	(4.0)
Not‐for‐profit hospital ownership	42	(41.6)
PRACTICE OWNERSHIP	46	(45.5)
Hospitalist‐only private practice group	7	(6.9)
Hospitalists within primary care private practice group	9	(8.9)
Multispecialty private practice group	12	(11.9)
Medical school practice plan	18	(17.8)
OTHER	9	(8.9)
Professional effort as hospitalist
100% FTE	76	(75.3)
75% FTE	13	(12.9)
50% FTE	6	(5.9)
25% FTE	5	(5.0)
<25% FTE	1	(1.0)
Residency Training*
Internal medicine	89	(88.1)
Pediatrics	6	(5.9)
Family medicine	5	(5.0)
Other	1	(1.0)

Primary Measures.

On average, practicing hospitalists ranked essentially all 12 curricular topics between moderate and high priority. Figure 1 displays the scores sorted by means with standard deviations; any pairwise difference between 2 means greater than 0.286 corresponds to a Bonferroni‐corrected P value < .05. Communication, leadership, and coding skills averaged above 2.5 (ie, closer to high than moderate priority), and bioethics ranked the lowest. There was no overall obvious clustering of topics, with administrative and clinical topics interspersed across the ratings. Respondents offered no separate topics in their open‐ended responses, but recommended subtopics to be included, such as contract negotiation, training for effective committee involvement, dealing with families, consultative medicine, and ICU comanagement. Several respondents also suggested tailoring the weighting of the curricular emphasis according to the needs and experience of individual fellows in each cohort.

Figure 1

Of the practicing hospitalists, 81% believed that clinical fellowship could be a good career move (Table 4), and 59% believed that graduating residents probably or strongly should consider such fellowship training. The median response to the question of minimum salary we should offer a hospitalist fellow was $70,000, with 80% of responses between $50,000 and $90,000.

Table 4.Perspectives of Hospitalists (Survey II)

Category	n	(%)
* Minimum annual salary, assuming 50% clinical load during fellowship; mean $68,900 $11,400.
Strength of recommendation to pursue fellowship
RECOMMEND	92	(91.1)
Possibly a good career move	33	(32.7)
Probably a good career move	37	(36.6)
Strongly recommend	22	(21.8)
DON'T RECOMMEND	9	(8.9)
Fellowship salary*
$50,000	11	(10.9)
$60,000	24	(23.8)
$70,000	30	(29.7)
$80,000	20	(19.8)
$90,000	8	(7.9)
$100,000	8	(7.9)
Likelihood of practicing hospital medicine in 5 years
Very likely	69	(68.3)
Somewhat likely	17	(16.8)
Somewhat unlikely	10	(9.9)
Very unlikely	5	(5.0)
Perceived reasons for job dissatisfaction
INTERNAL FACTORS	166	(71.0)
Excess workload	80	(34.2)
Scheduling frustrations	32	(13.7)
Organizational leadership and administrative problems	24	(10.2)
Inadequate salary	16	(6.8)
Productivity pressures	14	(6.0)
EXTERNAL FACTORS	78	(29.0)
Interaction, communication problems within hospital	29	(12.4)
Mistreatment, lack of professional respect	28	(12.0)
Other	11	(4.7)

When asked about their future plans, 69% were very likely to be practicing hospital medicine in 5 years (Table 4). Major reasons for career dissatisfaction were aggregated into 5 categories, 3 of which pertained to internal group management (accounting for 71% of concerns) and the others to external interactions in the hospital milieu (Table 4).

Survey III (Residents)

Demographics.

Two hundred and seventy‐nine categorical medicine residents responded to the survey link forwarded by their program director, 43% of whom requested a follow‐up summary of overall survey findings. Based on a total of 385 medicine program directors sent an E‐mail request and the E‐mail domain servers of the respondents, we estimate that about 70 program directors (18%) forwarded surveys to their residents.

Without respect to subspecialty choice, 75% of the 279 categorical residents planned to stay in their region after graduation; among the 25% planning to relocate, most were moving from the East or South to the West or Southwest (Table 5). Interestingly, no residents in the Southwest and the West planned to leave their region of current training. Overall, 40% were academically oriented. About 35% planned to work for a hospital entity, and about 20% planned to work in a private group.

Table 5.Characteristics and Plans of Categorical Residents (Survey III)

Category	n	(%)
* No residents in the Southwest and the West planned to leave their region.
Present residency program location
East	129	(46.2)
Midwest	92	(33.0)
South	20	(7.2)
Southwest*	3	(1.1)
West*	35	(12.5)
Anticipated future practice location
Eastern	95	(34.1)
Midwest	78	(28.0)
South	36	(12.9)
Southwest*	14	(5.0)
West*	56	(20.1)
Probably or definitely will do hospitalist career
PGY1 (n = 76)	36	(47.3)
PGY2 (n = 95)	37	(38.9)
PGY3 (n = 96)	44	(45.8)
Chiefs (n = 12)	6	(50.0)
Overall (n = 279)	123	(44.1)
Probably or definitely will do hospitalist career AND probably or definitely will do fellowship
PGY1 (n = 76)	24	(31.6)
PGY2 (n = 95)	24	(25.3)
PGY3 (n = 96)	21	(21.9)
Chiefs (n = 12)	1	(8.3)
Overall (n = 279)	70	(25.1)

Primary Measures.

One hundred and twenty‐three of the 279 categorical residents (44%) were strongly considering a hospitalist career. There was no significant difference in the proportion of interest across PGY 1‐3 level (P = .48). Seventy of these 123 (57%) would likely pursue a clinical hospital medicine fellowship if it was available to them. Although there was increasing fellowship interest, with interest by PGY1 residents greater than that of PGY2 residents, which was greater than of PGY3 residents, but this trend did not reach statistical significance (Cochrane linear trend, P = .15).

One hundred and forty‐seven of the 279 categorical residents (53%) offered reasons for interest (or lack of interest) in a hospital medicine career (Fig. 2). The predominant attractions (Fig. 2A) were the intellectual challenge and variety of cases encountered in general acute care (49%) and the flexibility in work scheduling and time off (37%). Reasons offered for not pursuing hospital medicine were mainly the intention to purse subspecialty or primary care medicine; remaining factors (from a relatively small number of responders) included perceptions of a lack of professional respect and unfavorable salary or scheduling (Fig. 2B).

Figure 2

DISCUSSION

The increasing demand for hospitalist care has outstripped the supply of physicians available to do the job and as a result of the unmet demand; in our study, two‐thirds of employers were willing to pay more, either through a signing bonus or a starting salary increase of at least $10,000 to fellowship graduates (with more than 20% willing to pay at least $20,000 above the initial salary). The value of enhancing organizational and communication skills was also recognized, as shown by the readiness of about 70% of employers to offer leadership positions to clinical fellowshiptrained hospitalists.

Residents drawn to hospital medicine were mainly attracted by the flexible scheduling and intellectual challenge (Fig. 2). Lack of interest mainly reflected plans to enter other subspecialties or primary care, rather than apprehension about professional frustrations. Practicing hospitalists, however, related substantial professional concerns arising from both internal factors (predominantly excessive workload) and external sources (respect from other physicians and interdisciplinary hospital communication issues). An alarming 31% were not very likely to remain in the practice of hospital medicine beyond the next 5 years. Fellowship training could indirectly address workload issues by creating leaders skilled in scheduling and team building and could directly enhance communication and team‐building skills and generate esteem among professional peers.

Would residents forgo a year of greater salary to pursue a fellowship? Based on the SHM estimate of a median salary of $169,000 and a leadership salary gradient of $12,0006 and Survey III median recommendation for a fellowship salary of $70,000, a 1‐year fellow would face a potential loss of income of about $100,000. Using the Survey I findings above and the leadership gradient, this could be recouped within about 5 years. Of course, it is difficult to assign a dollar value to the additional intangible benefits attributable to enhanced career satisfaction and greater effectiveness in affecting hospital care dynamics. The $70,000 salary proposed (higher than most traditional fellowships offer) corresponds to revenue collected from the proposed clinical workload of 50% that of a full‐time hospitalist; programs would thus need to identify other sources to cover supervisory and teaching overhead. Residents considering a hospital medicine career apparently did appreciate the deferred value of an investment in hospital fellowship: having been provided the results of the employer and hospitalist surveys, 57% would likely pursue a clinical fellowship if available. Extrapolating to the national pool of about 6600 annual graduates of internal medicine residencies, a 44% overall rate of hospital medicine career interest, with 57% fellowship interest, would yield about 550 fellowship candidates annually (this is an upper bound overestimate, given the relatively large proportion of our respondents with interest in an academic career).

The validity of the 12 proposed curricular topics is supported by the rating of all topics as moderate to high priority by practicing hospitalists (Fig. 1) and is consistent with the recently published SHM Core Competencies.7 Significant differences were found for topics rated in the lower versus upper half of the response range, without obvious clustering of clinical or administrative topics. Communication, leadership, and billing and coding were rated as top priorities, training in quality metrics and consultation were intermediate, and bioethics was given the lowest relative priority (although still considered moderately important). Although no novel additional topics were generated in open‐ended responses, several suggested tailoring the curricular emphasis according to the needs and prior experience of individual fellows in a cohort.

Generalization of our findings is limited by the low response rates of both hospitalist and resident physicians. It is likely that responding hospitalists were more interested than nonresponders in the concept of clinical hospital medicine fellowships. The strength of recommendation of fellowship training should therefore be considered an upper bound. The other main questions, pertaining to salary and curriculum, would presume a sufficient interest among responders and thus be less susceptible to sampling bias. Regarding resident response, we do not know the number of questionnaires actually forwarded by program directors to their residents. However, given that most responding residents were not planning to be hospitalists, we have at least a relatively representative sample of the attitudes of both uninterested and interested residents.

In summary, the results of our national surveys of hospitalist employers, practicing hospitalists, and current internal medicine residents reveals a potentially unmet demand for the provision of clinical hospital medicine fellowships. Curricular development under the leadership of organizations such as the Society of Hospital Medicine could hasten this development.

A 28‐year‐old man with sickle cell anemia was admitted with generalized pain. He noted an upper lip lesion 2 weeks prior to admission. He subsequently developed generalized pain in his legs, chest, and back typical of his pain crises. At admission he noted subjective fevers without chills for a week. Vital signs revealed a blood pressure of 135/80, a pulse of 81, a respiratory rate of 16, and an initial temperature of 37.7C. On examination he had scleral icterus and a large upper lip ulcer (Fig. 1). His hospital course was complicated by persistent fevers, a hepatic sequestration crisis, persistent hemolytic anemia requiring blood transfusion, and ultimately the identification of iris‐shaped targetoid lesions on the palms (Fig. 2).These lesions were believed to be consistent with erythema multiforme (EM) secondary to his recent HSV labialis, confirmed by a herpes culture. The patient recovered uneventfully after a 10‐day hospitalization. Erythema multiforme is an acute, self‐limited, but sometimes recurrent dermatologic condition considered to be a distinct hypersensitivity reaction.1 It is associated with certain infections such as herpes simplex 1 and 2, Mycoplasma pneumoniae and fungal infections, and a number of medications in the classes barbiturates, nonsteroidal anti‐inflammatory drugs, penicillins, hydantoins, phenothiazines, and sulfonamides.2 EM is diagnosed clinically by the characteristic rash on the hands and feet, with some cases involving the oral cavity. Treatment is typically focused on resolving the underlying infection or removing the offending drug. Dermatologic manifestations usually improve over 3‐5 weeks without residual sequelae.

Figure 1

Figure 2

A 28‐year‐old man with sickle cell anemia was admitted with generalized pain. He noted an upper lip lesion 2 weeks prior to admission. He subsequently developed generalized pain in his legs, chest, and back typical of his pain crises. At admission he noted subjective fevers without chills for a week. Vital signs revealed a blood pressure of 135/80, a pulse of 81, a respiratory rate of 16, and an initial temperature of 37.7C. On examination he had scleral icterus and a large upper lip ulcer (Fig. 1). His hospital course was complicated by persistent fevers, a hepatic sequestration crisis, persistent hemolytic anemia requiring blood transfusion, and ultimately the identification of iris‐shaped targetoid lesions on the palms (Fig. 2).These lesions were believed to be consistent with erythema multiforme (EM) secondary to his recent HSV labialis, confirmed by a herpes culture. The patient recovered uneventfully after a 10‐day hospitalization. Erythema multiforme is an acute, self‐limited, but sometimes recurrent dermatologic condition considered to be a distinct hypersensitivity reaction.1 It is associated with certain infections such as herpes simplex 1 and 2, Mycoplasma pneumoniae and fungal infections, and a number of medications in the classes barbiturates, nonsteroidal anti‐inflammatory drugs, penicillins, hydantoins, phenothiazines, and sulfonamides.2 EM is diagnosed clinically by the characteristic rash on the hands and feet, with some cases involving the oral cavity. Treatment is typically focused on resolving the underlying infection or removing the offending drug. Dermatologic manifestations usually improve over 3‐5 weeks without residual sequelae.

Figure 1

Figure 2

A 28‐year‐old man with sickle cell anemia was admitted with generalized pain. He noted an upper lip lesion 2 weeks prior to admission. He subsequently developed generalized pain in his legs, chest, and back typical of his pain crises. At admission he noted subjective fevers without chills for a week. Vital signs revealed a blood pressure of 135/80, a pulse of 81, a respiratory rate of 16, and an initial temperature of 37.7C. On examination he had scleral icterus and a large upper lip ulcer (Fig. 1). His hospital course was complicated by persistent fevers, a hepatic sequestration crisis, persistent hemolytic anemia requiring blood transfusion, and ultimately the identification of iris‐shaped targetoid lesions on the palms (Fig. 2).These lesions were believed to be consistent with erythema multiforme (EM) secondary to his recent HSV labialis, confirmed by a herpes culture. The patient recovered uneventfully after a 10‐day hospitalization. Erythema multiforme is an acute, self‐limited, but sometimes recurrent dermatologic condition considered to be a distinct hypersensitivity reaction.1 It is associated with certain infections such as herpes simplex 1 and 2, Mycoplasma pneumoniae and fungal infections, and a number of medications in the classes barbiturates, nonsteroidal anti‐inflammatory drugs, penicillins, hydantoins, phenothiazines, and sulfonamides.2 EM is diagnosed clinically by the characteristic rash on the hands and feet, with some cases involving the oral cavity. Treatment is typically focused on resolving the underlying infection or removing the offending drug. Dermatologic manifestations usually improve over 3‐5 weeks without residual sequelae.

Figure 1

Figure 2

The cornerstones of American medical ethics include respect for patient autonomy and beneficence. Although informed consent is required for surgical procedures and transfusion of blood products, the overwhelming majority of medical treatments administered by physicians to hospitalized patients are given without discussing risks, benefits, and alternatives. Although patients may sign a general permission‐to‐treat form on admission to the hospital, informed consent for medical treatments is generally ad hoc, and there are no national standards or mandates. We hypothesized that given the choice, hospitalized patients would want to participate in informed decision making, especially for therapies associated with substantial risks and benefits.

METHODS

The Institutional Review Board of Bridgeport Hospital approved this study. Each day between June and August 2006, the hospital's admitting department provided investigators with a list that included names and locations of all patients admitted to the Department of Medicine inpatient service. All the patients were eligible for participation in the study. Patients were excluded if they were in a comatose state, were encephalopathic, or were judged to be severely demented. In addition, patients were assessed during the scripted intervention to ascertain whether they had the capacity to make informed decisions based on their ability: (a) to understand the presented information, (b) to consider the information in relation to their personal values, and (c) to communicate their wishes. If personnel doubted an individual's capacity in any of these 3 areas, they were not included in the study.

Study personnel read directly from the script (see Appendix) and recorded answers. Study personnel were permitted to reread questions but did not provide additional guidance beyond the questionnaire. Patients whose primary language was not English were interviewed through in‐house or 3‐way telephone (remote) translators.

Statistical analyses included the chi‐square test to examine responses across the 3 categories of answers (ie, always consent, qualified consent, waive consent) and simple comparisons of percentages. A P value < .05 was considered statistically significant.

RESULTS

A total of 634 patients were admitted to the medicine service during the study period June‐August 2006. Of these, 158 were judged to lack sufficient capacity by study personnel and were excluded from the study. Ninety‐five refused to participate, and 171 were discharged before the questionnaire could be administered. Two hundred and ten patients answered the questionnaire. They ranged in age from 18 to 96 years (mean age standard error, 63.3 1.1 years). One hundred and three (49%) were men, and 107 (51%) were women. A majority (67.5%) were white, 20% (42) were African American, and 11.9% (25) were Hispanic. Most (87.6%) had at least a high school education, and 35% had a college‐/graduate‐level education. Sixty‐seven percent had at least 2 comorbid conditions in addition to their principal reason for hospitalization. Their average acute physiology and chronic health care evaluation (APACHE II) score was 7.5 0.3 (median 7; range 0‐22).

Figure 1 shows the distribution of answers to each of the 4 questions.

Figure 1

DISCUSSION

The principal finding of this study is that most medical patients prefer to participate in making decisions about their medical care during acute hospitalization, even for relatively low‐risk treatments like potassium supplementation and administration of diuretics. Very few patients were prepared to waive consent and grant their physicians the absolute right to administer therapies such as thrombolysis, even if the risk of bleeding was estimated to be less than 5%. Whereas the elderly patients were less likely to prefer being asked to consent to treatments than were younger patients, most would want to be informed of even trivial therapies if time allowed.

In some situations older patients (65 years old) were more likely than younger patients (<65 years old) to allow their physicians to make unilateral decisions regarding their health care. This could be explained by those age 65 and older having grown up when physician paternalism was more prevalent in American medicine. In the 1970s physician paternalism waned, and respect for patient autonomy emerged as the dominant physicianpatient model. Patients who became adults after 1970 know only this relationship with their physician, and so it makes sense that they would be more inclined to prefer a participatory model.

These data complement and extend a series of studies we conducted with patients admitted to Bridgeport Hospital. Our data suggest that our patients wish to consent for end‐of‐life decisions,1, 2 invasive procedures,3 and, now, to be apprised of medical therapies administered during hospitalization. At the same time, we have found that consent practices at many centers are not consistent with these patient predilections.1, 2, 4 Our study suffered from having a small sample size obtained in one geographic location; so results should be generalized cautiously. Nonetheless, insofar as the expectations of patients for participation are not being met by the health care system in Connecticut (and we suspect elsewhere), clinicians, hospital administrators, and health care policy makers might consider whether more rigorous and explicit consent practices and policies are required. Another important limitation of the study was that patients included may not have entirely understood the implications of their answers (ie, how cumbersome to the system and bothersome to the patient seeking consent for every therapy could become). In fact, we cannot be certain that all patients truly understood the questions, some of which were complex. Nonetheless, these results support that considered in the abstract, most patients prefer to consent for medical therapies. Had the implications for safety and expediency been explained in detail, it is possible that patients would have waived the need to give consent for treatments with minimal risk. The questionnaire also presents an abbreviated list of risks and benefits for each intervention, and although it refers to the formal process of informed consent in its preamble, it uses terminology (ie, permission) that may not reflect the complexity of informed consent. Nonetheless, our goal was to examine the degree to which patients wished to participate in their medical decision making. Notwithstanding these weaknesses of the survey instrument, the data suggest patients want to be in the loop whenever possible.

There are no national standards of consent for medical treatments. The Veterans' Administration, which has led the way in many areas of patients' rights, has a policy:

Compliance with this standard (ie, consent for every new medication) is not routine in most acute care hospitals. Although some clinicians obtain formal consent for high‐risk therapies (perhaps out of respect for autonomy, perhaps to reduce medical‐legal liability), there are no explicit decision rules to guide clinicians regarding for which treatments they should obtain formal consent. Accordingly, some might obtain formal consent for thrombolysis for massive pulmonary embolus, and others might not. It is not clear that the consent‐to‐treat form signed during hospital admission would legally cover all medical therapies during hospitalization. The legal standard for informed consent is what any reasonable patient would want to consent for. Our data suggest that most reasonable patients wish to at least assent and perhaps consent for much of what they receive during hospitalization. Although we have been unable to find case law predicated entirely on failure to obtain consent prior to administration of a therapy that caused a complication, it is plausible that the reasonable patient standard could be used in this manner. Regardless, it is impractical to require consent for the thousands of medical therapies administered each day in hospitals. Requiring consent for all therapies, if respected rigidly, would threaten the safety and efficiency of American hospitals. Naturally, a balance betweem respect for autonomy, that is, informed consent for the riskiest therapies, and efficiency is necessary. Explicit guidelines issued by accrediting agencies or the federal government would be helpful. The rules for consent (and/or assent) should be more explicit and less arbitrary, that is, determined independently by each clinician.

In conclusion, these data demonstrate that when considered in the abstract, that is, without explaining the logistical hurdles that it would create, inpatients wish to participate in decision making for both low‐ and high‐risk treatments. Clinicians are faced with demands and obligations that preclude full consent for the myriad low‐risk treatments administered daily to hospitalized patients. Some treatments are likely to be covered implicitly under the general consent‐to‐treat process and paperwork. Nonetheless, clinicians should consider explaining the principal risks and benefits of moderate‐risk treatments in order to secure informed assent. Full informed consent may be most appropriate for very high‐risk therapies. Patients expect and deserve frequent communication with caregivers that balances their safety with their right to self‐determination.

The cornerstones of American medical ethics include respect for patient autonomy and beneficence. Although informed consent is required for surgical procedures and transfusion of blood products, the overwhelming majority of medical treatments administered by physicians to hospitalized patients are given without discussing risks, benefits, and alternatives. Although patients may sign a general permission‐to‐treat form on admission to the hospital, informed consent for medical treatments is generally ad hoc, and there are no national standards or mandates. We hypothesized that given the choice, hospitalized patients would want to participate in informed decision making, especially for therapies associated with substantial risks and benefits.

METHODS

The Institutional Review Board of Bridgeport Hospital approved this study. Each day between June and August 2006, the hospital's admitting department provided investigators with a list that included names and locations of all patients admitted to the Department of Medicine inpatient service. All the patients were eligible for participation in the study. Patients were excluded if they were in a comatose state, were encephalopathic, or were judged to be severely demented. In addition, patients were assessed during the scripted intervention to ascertain whether they had the capacity to make informed decisions based on their ability: (a) to understand the presented information, (b) to consider the information in relation to their personal values, and (c) to communicate their wishes. If personnel doubted an individual's capacity in any of these 3 areas, they were not included in the study.

Study personnel read directly from the script (see Appendix) and recorded answers. Study personnel were permitted to reread questions but did not provide additional guidance beyond the questionnaire. Patients whose primary language was not English were interviewed through in‐house or 3‐way telephone (remote) translators.

Statistical analyses included the chi‐square test to examine responses across the 3 categories of answers (ie, always consent, qualified consent, waive consent) and simple comparisons of percentages. A P value < .05 was considered statistically significant.

RESULTS

A total of 634 patients were admitted to the medicine service during the study period June‐August 2006. Of these, 158 were judged to lack sufficient capacity by study personnel and were excluded from the study. Ninety‐five refused to participate, and 171 were discharged before the questionnaire could be administered. Two hundred and ten patients answered the questionnaire. They ranged in age from 18 to 96 years (mean age standard error, 63.3 1.1 years). One hundred and three (49%) were men, and 107 (51%) were women. A majority (67.5%) were white, 20% (42) were African American, and 11.9% (25) were Hispanic. Most (87.6%) had at least a high school education, and 35% had a college‐/graduate‐level education. Sixty‐seven percent had at least 2 comorbid conditions in addition to their principal reason for hospitalization. Their average acute physiology and chronic health care evaluation (APACHE II) score was 7.5 0.3 (median 7; range 0‐22).

Figure 1 shows the distribution of answers to each of the 4 questions.

Figure 1

DISCUSSION

The principal finding of this study is that most medical patients prefer to participate in making decisions about their medical care during acute hospitalization, even for relatively low‐risk treatments like potassium supplementation and administration of diuretics. Very few patients were prepared to waive consent and grant their physicians the absolute right to administer therapies such as thrombolysis, even if the risk of bleeding was estimated to be less than 5%. Whereas the elderly patients were less likely to prefer being asked to consent to treatments than were younger patients, most would want to be informed of even trivial therapies if time allowed.

In some situations older patients (65 years old) were more likely than younger patients (<65 years old) to allow their physicians to make unilateral decisions regarding their health care. This could be explained by those age 65 and older having grown up when physician paternalism was more prevalent in American medicine. In the 1970s physician paternalism waned, and respect for patient autonomy emerged as the dominant physicianpatient model. Patients who became adults after 1970 know only this relationship with their physician, and so it makes sense that they would be more inclined to prefer a participatory model.

These data complement and extend a series of studies we conducted with patients admitted to Bridgeport Hospital. Our data suggest that our patients wish to consent for end‐of‐life decisions,1, 2 invasive procedures,3 and, now, to be apprised of medical therapies administered during hospitalization. At the same time, we have found that consent practices at many centers are not consistent with these patient predilections.1, 2, 4 Our study suffered from having a small sample size obtained in one geographic location; so results should be generalized cautiously. Nonetheless, insofar as the expectations of patients for participation are not being met by the health care system in Connecticut (and we suspect elsewhere), clinicians, hospital administrators, and health care policy makers might consider whether more rigorous and explicit consent practices and policies are required. Another important limitation of the study was that patients included may not have entirely understood the implications of their answers (ie, how cumbersome to the system and bothersome to the patient seeking consent for every therapy could become). In fact, we cannot be certain that all patients truly understood the questions, some of which were complex. Nonetheless, these results support that considered in the abstract, most patients prefer to consent for medical therapies. Had the implications for safety and expediency been explained in detail, it is possible that patients would have waived the need to give consent for treatments with minimal risk. The questionnaire also presents an abbreviated list of risks and benefits for each intervention, and although it refers to the formal process of informed consent in its preamble, it uses terminology (ie, permission) that may not reflect the complexity of informed consent. Nonetheless, our goal was to examine the degree to which patients wished to participate in their medical decision making. Notwithstanding these weaknesses of the survey instrument, the data suggest patients want to be in the loop whenever possible.

There are no national standards of consent for medical treatments. The Veterans' Administration, which has led the way in many areas of patients' rights, has a policy:

Compliance with this standard (ie, consent for every new medication) is not routine in most acute care hospitals. Although some clinicians obtain formal consent for high‐risk therapies (perhaps out of respect for autonomy, perhaps to reduce medical‐legal liability), there are no explicit decision rules to guide clinicians regarding for which treatments they should obtain formal consent. Accordingly, some might obtain formal consent for thrombolysis for massive pulmonary embolus, and others might not. It is not clear that the consent‐to‐treat form signed during hospital admission would legally cover all medical therapies during hospitalization. The legal standard for informed consent is what any reasonable patient would want to consent for. Our data suggest that most reasonable patients wish to at least assent and perhaps consent for much of what they receive during hospitalization. Although we have been unable to find case law predicated entirely on failure to obtain consent prior to administration of a therapy that caused a complication, it is plausible that the reasonable patient standard could be used in this manner. Regardless, it is impractical to require consent for the thousands of medical therapies administered each day in hospitals. Requiring consent for all therapies, if respected rigidly, would threaten the safety and efficiency of American hospitals. Naturally, a balance betweem respect for autonomy, that is, informed consent for the riskiest therapies, and efficiency is necessary. Explicit guidelines issued by accrediting agencies or the federal government would be helpful. The rules for consent (and/or assent) should be more explicit and less arbitrary, that is, determined independently by each clinician.

In conclusion, these data demonstrate that when considered in the abstract, that is, without explaining the logistical hurdles that it would create, inpatients wish to participate in decision making for both low‐ and high‐risk treatments. Clinicians are faced with demands and obligations that preclude full consent for the myriad low‐risk treatments administered daily to hospitalized patients. Some treatments are likely to be covered implicitly under the general consent‐to‐treat process and paperwork. Nonetheless, clinicians should consider explaining the principal risks and benefits of moderate‐risk treatments in order to secure informed assent. Full informed consent may be most appropriate for very high‐risk therapies. Patients expect and deserve frequent communication with caregivers that balances their safety with their right to self‐determination.

The cornerstones of American medical ethics include respect for patient autonomy and beneficence. Although informed consent is required for surgical procedures and transfusion of blood products, the overwhelming majority of medical treatments administered by physicians to hospitalized patients are given without discussing risks, benefits, and alternatives. Although patients may sign a general permission‐to‐treat form on admission to the hospital, informed consent for medical treatments is generally ad hoc, and there are no national standards or mandates. We hypothesized that given the choice, hospitalized patients would want to participate in informed decision making, especially for therapies associated with substantial risks and benefits.

METHODS

The Institutional Review Board of Bridgeport Hospital approved this study. Each day between June and August 2006, the hospital's admitting department provided investigators with a list that included names and locations of all patients admitted to the Department of Medicine inpatient service. All the patients were eligible for participation in the study. Patients were excluded if they were in a comatose state, were encephalopathic, or were judged to be severely demented. In addition, patients were assessed during the scripted intervention to ascertain whether they had the capacity to make informed decisions based on their ability: (a) to understand the presented information, (b) to consider the information in relation to their personal values, and (c) to communicate their wishes. If personnel doubted an individual's capacity in any of these 3 areas, they were not included in the study.

Study personnel read directly from the script (see Appendix) and recorded answers. Study personnel were permitted to reread questions but did not provide additional guidance beyond the questionnaire. Patients whose primary language was not English were interviewed through in‐house or 3‐way telephone (remote) translators.

Statistical analyses included the chi‐square test to examine responses across the 3 categories of answers (ie, always consent, qualified consent, waive consent) and simple comparisons of percentages. A P value < .05 was considered statistically significant.

RESULTS

A total of 634 patients were admitted to the medicine service during the study period June‐August 2006. Of these, 158 were judged to lack sufficient capacity by study personnel and were excluded from the study. Ninety‐five refused to participate, and 171 were discharged before the questionnaire could be administered. Two hundred and ten patients answered the questionnaire. They ranged in age from 18 to 96 years (mean age standard error, 63.3 1.1 years). One hundred and three (49%) were men, and 107 (51%) were women. A majority (67.5%) were white, 20% (42) were African American, and 11.9% (25) were Hispanic. Most (87.6%) had at least a high school education, and 35% had a college‐/graduate‐level education. Sixty‐seven percent had at least 2 comorbid conditions in addition to their principal reason for hospitalization. Their average acute physiology and chronic health care evaluation (APACHE II) score was 7.5 0.3 (median 7; range 0‐22).

Figure 1 shows the distribution of answers to each of the 4 questions.

Figure 1

DISCUSSION

The principal finding of this study is that most medical patients prefer to participate in making decisions about their medical care during acute hospitalization, even for relatively low‐risk treatments like potassium supplementation and administration of diuretics. Very few patients were prepared to waive consent and grant their physicians the absolute right to administer therapies such as thrombolysis, even if the risk of bleeding was estimated to be less than 5%. Whereas the elderly patients were less likely to prefer being asked to consent to treatments than were younger patients, most would want to be informed of even trivial therapies if time allowed.

In some situations older patients (65 years old) were more likely than younger patients (<65 years old) to allow their physicians to make unilateral decisions regarding their health care. This could be explained by those age 65 and older having grown up when physician paternalism was more prevalent in American medicine. In the 1970s physician paternalism waned, and respect for patient autonomy emerged as the dominant physicianpatient model. Patients who became adults after 1970 know only this relationship with their physician, and so it makes sense that they would be more inclined to prefer a participatory model.

These data complement and extend a series of studies we conducted with patients admitted to Bridgeport Hospital. Our data suggest that our patients wish to consent for end‐of‐life decisions,1, 2 invasive procedures,3 and, now, to be apprised of medical therapies administered during hospitalization. At the same time, we have found that consent practices at many centers are not consistent with these patient predilections.1, 2, 4 Our study suffered from having a small sample size obtained in one geographic location; so results should be generalized cautiously. Nonetheless, insofar as the expectations of patients for participation are not being met by the health care system in Connecticut (and we suspect elsewhere), clinicians, hospital administrators, and health care policy makers might consider whether more rigorous and explicit consent practices and policies are required. Another important limitation of the study was that patients included may not have entirely understood the implications of their answers (ie, how cumbersome to the system and bothersome to the patient seeking consent for every therapy could become). In fact, we cannot be certain that all patients truly understood the questions, some of which were complex. Nonetheless, these results support that considered in the abstract, most patients prefer to consent for medical therapies. Had the implications for safety and expediency been explained in detail, it is possible that patients would have waived the need to give consent for treatments with minimal risk. The questionnaire also presents an abbreviated list of risks and benefits for each intervention, and although it refers to the formal process of informed consent in its preamble, it uses terminology (ie, permission) that may not reflect the complexity of informed consent. Nonetheless, our goal was to examine the degree to which patients wished to participate in their medical decision making. Notwithstanding these weaknesses of the survey instrument, the data suggest patients want to be in the loop whenever possible.

There are no national standards of consent for medical treatments. The Veterans' Administration, which has led the way in many areas of patients' rights, has a policy:

Compliance with this standard (ie, consent for every new medication) is not routine in most acute care hospitals. Although some clinicians obtain formal consent for high‐risk therapies (perhaps out of respect for autonomy, perhaps to reduce medical‐legal liability), there are no explicit decision rules to guide clinicians regarding for which treatments they should obtain formal consent. Accordingly, some might obtain formal consent for thrombolysis for massive pulmonary embolus, and others might not. It is not clear that the consent‐to‐treat form signed during hospital admission would legally cover all medical therapies during hospitalization. The legal standard for informed consent is what any reasonable patient would want to consent for. Our data suggest that most reasonable patients wish to at least assent and perhaps consent for much of what they receive during hospitalization. Although we have been unable to find case law predicated entirely on failure to obtain consent prior to administration of a therapy that caused a complication, it is plausible that the reasonable patient standard could be used in this manner. Regardless, it is impractical to require consent for the thousands of medical therapies administered each day in hospitals. Requiring consent for all therapies, if respected rigidly, would threaten the safety and efficiency of American hospitals. Naturally, a balance betweem respect for autonomy, that is, informed consent for the riskiest therapies, and efficiency is necessary. Explicit guidelines issued by accrediting agencies or the federal government would be helpful. The rules for consent (and/or assent) should be more explicit and less arbitrary, that is, determined independently by each clinician.

In conclusion, these data demonstrate that when considered in the abstract, that is, without explaining the logistical hurdles that it would create, inpatients wish to participate in decision making for both low‐ and high‐risk treatments. Clinicians are faced with demands and obligations that preclude full consent for the myriad low‐risk treatments administered daily to hospitalized patients. Some treatments are likely to be covered implicitly under the general consent‐to‐treat process and paperwork. Nonetheless, clinicians should consider explaining the principal risks and benefits of moderate‐risk treatments in order to secure informed assent. Full informed consent may be most appropriate for very high‐risk therapies. Patients expect and deserve frequent communication with caregivers that balances their safety with their right to self‐determination.

Two years ago we published the first issue of the Journal of Hospital Medicine and declared, Our goal is that JHM become the premier forum for peer‐reviewed research articles and evidence‐based reviews in the specialty of hospital medicine.1 That first issue was just one of many steps toward this ambition. At the completion of its first year, JHM was selected for indexing and inclusion in the National Library of Medicine's Medical Literature Analysis and Retrieval System Online (MEDLINE), the primary component of PubMed. Following this huge step, we welcomed a remarkable increase in submissions and will have exceeded 300 in our second year, an approximately 50% increase from our first year!

As important, JHM quickly became a valuable benefit of membership in the Society of Hospital Medicine, and the innumerable compliments received by the staff reflect the diligent efforts of a remarkable editorial staff and work by our reviewers. With profound gratitude we list on page 86 these 325 reviewers who donated their priceless time and expertise to enhancing the quality of the manuscripts. To handle the marked increase in submissions, we are expanding and modifying our editorial staff. Please welcome Sunil Kripalani (Vanderbilt) and Daniel Brotman (Johns Hopkins), who join our previous six associate editors and all eight will now serve as JHM's deputy editors. Seven new associate editors also join our team. Among them, Tom Baudendistel (California Pacific Medical Center, San Francisco), Eric Alper (UMass Memorial Health Care, Worcester), Brian Harte (Cleveland Clinic), and Rehan Qayyum (Johns Hopkins) will all focus on optimizing content for practicing hospitalists. Paul Aronowitz will continue to develop our Images section as an associate editor. Recognizing the growing number of pediatric hospitalists, Lisa Zauotis (Childrens Hospital of Philadelphia) and Erin Stucky (Children's Hospital San Diego) join JHM as the other 2 new associate editors. Finally, we welcome new Editorial Board members Mary C. Ottolini (Children's National Medical Center), Douglas Carlson (St. Louis Children's Hospital), and Daniel Rauch (NYU Children's Hospital). The welcome addition of these nationally recognized academicians prepares us for continued growth in manuscript submissions to JHM.

Although we could not excel without the editors, reviewers and our terrific new managing editor, Phaedra McGuinness, we would not survive without the authors who submit their manuscripts to JHMthey are responsible for the caliber of the journal, and we are immensely indebted to them. Originally, we hoped to include individuals involved in all aspects of hospital care,1 and fortunately this is now happening. Complementing hospitalists are nurses and pharmacists2 who recognize the importance of teamwork in the care of hospitalized patients. I encourage all members of the hospital care team to send us the results of their research, teaching, and quality improvement efforts.

As the specialty of hospital medicine continues to evolve, now with more than 20,000 hospitalists, JHM will develop with it. I am honored and grateful to collaborate with such a remarkable group of colleagues as we build the premier journal for the fastest growing specialty in the history of medicine in the United States. On to year 3!

Two years ago we published the first issue of the Journal of Hospital Medicine and declared, Our goal is that JHM become the premier forum for peer‐reviewed research articles and evidence‐based reviews in the specialty of hospital medicine.1 That first issue was just one of many steps toward this ambition. At the completion of its first year, JHM was selected for indexing and inclusion in the National Library of Medicine's Medical Literature Analysis and Retrieval System Online (MEDLINE), the primary component of PubMed. Following this huge step, we welcomed a remarkable increase in submissions and will have exceeded 300 in our second year, an approximately 50% increase from our first year!

As important, JHM quickly became a valuable benefit of membership in the Society of Hospital Medicine, and the innumerable compliments received by the staff reflect the diligent efforts of a remarkable editorial staff and work by our reviewers. With profound gratitude we list on page 86 these 325 reviewers who donated their priceless time and expertise to enhancing the quality of the manuscripts. To handle the marked increase in submissions, we are expanding and modifying our editorial staff. Please welcome Sunil Kripalani (Vanderbilt) and Daniel Brotman (Johns Hopkins), who join our previous six associate editors and all eight will now serve as JHM's deputy editors. Seven new associate editors also join our team. Among them, Tom Baudendistel (California Pacific Medical Center, San Francisco), Eric Alper (UMass Memorial Health Care, Worcester), Brian Harte (Cleveland Clinic), and Rehan Qayyum (Johns Hopkins) will all focus on optimizing content for practicing hospitalists. Paul Aronowitz will continue to develop our Images section as an associate editor. Recognizing the growing number of pediatric hospitalists, Lisa Zauotis (Childrens Hospital of Philadelphia) and Erin Stucky (Children's Hospital San Diego) join JHM as the other 2 new associate editors. Finally, we welcome new Editorial Board members Mary C. Ottolini (Children's National Medical Center), Douglas Carlson (St. Louis Children's Hospital), and Daniel Rauch (NYU Children's Hospital). The welcome addition of these nationally recognized academicians prepares us for continued growth in manuscript submissions to JHM.

Although we could not excel without the editors, reviewers and our terrific new managing editor, Phaedra McGuinness, we would not survive without the authors who submit their manuscripts to JHMthey are responsible for the caliber of the journal, and we are immensely indebted to them. Originally, we hoped to include individuals involved in all aspects of hospital care,1 and fortunately this is now happening. Complementing hospitalists are nurses and pharmacists2 who recognize the importance of teamwork in the care of hospitalized patients. I encourage all members of the hospital care team to send us the results of their research, teaching, and quality improvement efforts.

As the specialty of hospital medicine continues to evolve, now with more than 20,000 hospitalists, JHM will develop with it. I am honored and grateful to collaborate with such a remarkable group of colleagues as we build the premier journal for the fastest growing specialty in the history of medicine in the United States. On to year 3!

Two years ago we published the first issue of the Journal of Hospital Medicine and declared, Our goal is that JHM become the premier forum for peer‐reviewed research articles and evidence‐based reviews in the specialty of hospital medicine.1 That first issue was just one of many steps toward this ambition. At the completion of its first year, JHM was selected for indexing and inclusion in the National Library of Medicine's Medical Literature Analysis and Retrieval System Online (MEDLINE), the primary component of PubMed. Following this huge step, we welcomed a remarkable increase in submissions and will have exceeded 300 in our second year, an approximately 50% increase from our first year!

As important, JHM quickly became a valuable benefit of membership in the Society of Hospital Medicine, and the innumerable compliments received by the staff reflect the diligent efforts of a remarkable editorial staff and work by our reviewers. With profound gratitude we list on page 86 these 325 reviewers who donated their priceless time and expertise to enhancing the quality of the manuscripts. To handle the marked increase in submissions, we are expanding and modifying our editorial staff. Please welcome Sunil Kripalani (Vanderbilt) and Daniel Brotman (Johns Hopkins), who join our previous six associate editors and all eight will now serve as JHM's deputy editors. Seven new associate editors also join our team. Among them, Tom Baudendistel (California Pacific Medical Center, San Francisco), Eric Alper (UMass Memorial Health Care, Worcester), Brian Harte (Cleveland Clinic), and Rehan Qayyum (Johns Hopkins) will all focus on optimizing content for practicing hospitalists. Paul Aronowitz will continue to develop our Images section as an associate editor. Recognizing the growing number of pediatric hospitalists, Lisa Zauotis (Childrens Hospital of Philadelphia) and Erin Stucky (Children's Hospital San Diego) join JHM as the other 2 new associate editors. Finally, we welcome new Editorial Board members Mary C. Ottolini (Children's National Medical Center), Douglas Carlson (St. Louis Children's Hospital), and Daniel Rauch (NYU Children's Hospital). The welcome addition of these nationally recognized academicians prepares us for continued growth in manuscript submissions to JHM.

Although we could not excel without the editors, reviewers and our terrific new managing editor, Phaedra McGuinness, we would not survive without the authors who submit their manuscripts to JHMthey are responsible for the caliber of the journal, and we are immensely indebted to them. Originally, we hoped to include individuals involved in all aspects of hospital care,1 and fortunately this is now happening. Complementing hospitalists are nurses and pharmacists2 who recognize the importance of teamwork in the care of hospitalized patients. I encourage all members of the hospital care team to send us the results of their research, teaching, and quality improvement efforts.

As the specialty of hospital medicine continues to evolve, now with more than 20,000 hospitalists, JHM will develop with it. I am honored and grateful to collaborate with such a remarkable group of colleagues as we build the premier journal for the fastest growing specialty in the history of medicine in the United States. On to year 3!

A 65‐year‐old man was referred for evaluation of worsening ascites and end‐stage liver disease. The patient had been well until 1 year ago, when he developed lower extremity edema and abdominal distention. After evaluation by his primary care physician, he was given a diagnosis of cryptogenic cirrhosis. He underwent several paracenteses and was placed on furosemide and spironolactone. The patient had been stable on his diuretic regimen until 2 weeks previously, when he suddenly developed worsening edema and ascites, along with dizziness, nausea, and hypotension. His physician stopped the diuretics and referred him to the hospital.

Before diagnosing a patient with cryptogenic cirrhosis, it is necessary to exclude common etiologies of cirrhosis such as alcohol, viral hepatitis, and non‐alcoholic fatty liver disease and numerous uncommon causes, including Wilson's disease, hemochromatosis, Budd‐Chiari, and biliary cirrhosis. It is also important to remember that patients with liver disease are not immune to extrahepatic causes of ascites, such as peritoneal carcinomatosis and tuberculous ascites. Simultaneously, reasons for chronic liver disease decompensating acutely must be considered: medication nonadherence, excess salt intake, hepatotoxicity from acetaminophen or alcohol, and other acute insults, such as hepatocellular carcinoma, an intervening infection (especially spontaneous bacterial peritonitis), ascending cholangitis, or a flare of chronic viral hepatitis.

Past medical and surgical history included diabetes mellitus (diagnosed 10 years previously), obstructive sleep apnea, hypertension, hypothyroidism, and mild chronic kidney disease. Medications included levothyroxine, lactulose, sulfamethoxazole, pioglitazone (started 4 months prior), and ibuprofen. Furosemide and spironolactone had been discontinued 2 weeks previously. He currently resided in the Central Valley of California. He had lived in Thailand from age 7 to 17 and traveled to India more than 1 year ago. He did not smoke and had never used intravenous drugs or received a blood transfusion. He rarely drank alcohol. He worked as a chemist. There was no family history of liver disease.

There is no obvious explanation for the underlying liver disease or the acute decompensation. Sulfamethoxazole is a rare cause of allergic or granulomatous hepatitis. Pioglitazone is a thiazolinedione which in earlier formulations was linked to hepatitis but can be excluded as a cause of this patient's cirrhosis because it was started after liver disease was detected. As a chemist, he might have been exposed to carbon tetrachloride, a known hepatotoxin. Obstructive sleep apnea causes pulmonary hypertension, but severe ascites and acute hepatic decompensation would be unusual. Ibuprofen might precipitate worsening renal function and fluid accumulation. Time in Thailand and India raises the possibility of tuberculous ascites.

The patient had no headache, vision changes, abdominal pain, emesis, melena, hematochezia, chest pain, palpitations, dysuria, polyuria, pruritus, dark urine, or rashes. He reported difficulty with concentration when lactulose was decreased. He noted worsening exercise tolerance with dyspnea after 10 steps and reported a weight gain of 12 pounds in the past 2 weeks.

On examination, temperature was 36.8C; blood pressure, 129/87 mm Hg; heart rate, 85 beats per minute; respirations, 20 per minute; and oxygen saturation, 94% on room air. He was uncomfortable but alert. There was no scleral icterus or conjunctival pallor. Jugular venous pressure was elevated. The lungs were clear, and the heart was regular, with no murmur, rub, or gallops. The abdomen was massively distended with a fluid wave; the liver and spleen could not be palpated. There was pitting edema of the sacrum and lower extremities. There was no asterixis, palmar erythema, spider angiomata, or skin discoloration.

The additional history and physical exam suggest that the primary problem may lie outside the liver, especially as signs of advanced liver disease (other than ascites) are absent. Dyspnea on exertion is consistent with the physical stress of a large volume of ascites or could be secondary to several pulmonary complications associated with liver disease, including portopulmonary hypertension, hepatopulmonary syndrome, or hepatic hydrothorax. Alternatively, the dyspnea raises the possibility that the ascites is not related to a primary liver disorder but rather to anemia or to a cardiac disorder, such as chronic left ventricular failure, isolated right‐sided heart failure, or constrictive pericarditis. These diagnoses are suggested by the elevated jugular venous pressure, which is atypical in cirrhosis.

Although portal hypertension accounts for most cases of ascites, peritoneal fluid should be examined to exclude peritoneal carcinomatosis and tuberculous ascites. I am interested in the results of an echocardiogram.

Initial laboratory studies demonstrated a sodium concentration of 136 mEq/dL; potassium, 4.7 mEq/dL; chloride, 99 mEq/dL; bicarbonate, 24 mEq/dL; blood urea nitrogen, 54 mg/dL; creatinine, 3.3 mg/dL (increased from baseline of 1.6 mg/dL 4 months previously); white cell count, 7000/mm³; hemoglobin, 10.5 g/dL; MCV, 89 fL; platelet count, 205,000/mm³; bilirubin, 0.6 mg/dL; aspartate aminotransferase, 15 U/L; alanine aminotransferase, 8 U/L; alkaline phosphatase, 102 U/L; albumin, 4.2 g/dL; total protein, 8.2 g/dL; international normalized ratio, 1.2; and partial thromboplastin time, 31.8 seconds. A urine dipstick demonstrated 1+ protein. The chest radiograph was normal. Electrocardiogram had borderline low voltage with nonspecific T‐wave abnormalities. Additional studies showed a serum iron concentration of 49 mg/dL, transferrin saturation of 16%, total iron binding capacity of 310 mg/dL, and ferritin of 247 mg/mL. Hemoglobin A1c was 7.0%. Acute and chronic antibodies to hepatitis A, B, and C viruses were negative. The following study results were normal or negative: antinuclear antibody, alpha‐1‐antitrypsin, ceruloplasmin, alpha‐fetoprotein, carcinoembryonic antigen, and 24‐hour urinary copper. The thyroid function studies were normal. A purified protein derivative (PPD) skin test was nonreactive.

There continues to be a paucity of evidence of a primary liver disorder. The hepatic enzymes and tests of liver synthetic function are normal, and there is no pancytopenia, as might result from hypersplenism. I remain most suspicious of either a primary cardiac or pericardial disorder with secondary hepatic congestion or a disease that simultaneously affects the heart and liver.

The reasons for the low voltage on the electrocardiogram include processes that infiltrate the myocardium (amyloidosis, sarcoidosis, hemochromatosis, and myxedema fluid) and processes that increase the distance between the myocardium and surface electrodes, such as adipose tissue, air (from emphysema or pneumothorax), or pericardial effusion. Pericardial effusion may present subacutely with predominant features of right ventricular failure. Low voltage, liver disease, and possible heart failure raise the possibility of amyloidosis or hemochromatosis. The low transferrin saturation renders hemochromatosis unlikely. Although normal alkaline phosphatase and serum albumin are not characteristic when AL amyloid affects the liver and kidneys, serum and urine protein electrophoresis and immunofixation should be considered.

With paracentesis 3.5 L of ascitic fluid was removed. The red cell count was 4000/mm³, and white blood cell count was 505/mm³, of which 25% were polymorphonuclear cells, 22% were lymphocytes, and 53% were monocytes. Additional peritoneal fluid chemistries included albumin of 3.0 g/dL and total protein of 5.3 g/dL. Abdominal ultrasound with Doppler demonstrated a liver of normal size and echogenicity with patent hepatic arteries, hepatic veins, and portal vein. There was mild splenomegaly with normal kidneys. Evaluation for a possible liver transplant was initiated. Blood, urine, and peritoneal fluid cultures demonstrated no growth. Echocardiography demonstrated borderline concentric left ventricular hypertrophy, normal right and left ventricular function, dilated superior and inferior vena cavae, and no pericardial effusion or thickening.

The serum‐ascites albumin gradient (SAAG) of 1.2 is consistent with portal hypertension as the cause of the ascites. The Doppler findings exclude postsinusoidal causes of portal hypertension from hepatic vein obstruction or thrombosis. The combination of the elevated SAAG, elevated jugular venous pressure, borderline low voltage on ECG, and elevated peritoneal total protein make cardiac and pericardial disease the leading considerations. Given the normal ventricular function, I am concerned about elevated intracardiac pressures resulting from pericardial disease or restrictive cardiomyopathy. At this point, right heart catheterization would be useful for assessing intracardiac pressures.

On the fourth hospital day, paracentesis was repeated, and 15 L of fluid was removed. A transjugular liver biopsy demonstrated diffuse patchy fibrosis consistent with early cirrhosis and minor intralobular changes with minimal ballooning. There was no steatosis, active inflammation, granulomata, iron deposition, or evidence of viral hepatitis. Right heart catheterization revealed a right atrial pressure of 18 cm H₂0, right ventricular pressure of 34/20 cm H₂0, pulmonary artery pressure of 34/18 cm H₂0 (mean 25), pulmonary capillary wedge pressure of 20 cm H₂0, cardiac output of 5.8 L/min, and cardiac index of 2.5 L/min/m².

The mild hepatic histologic abnormalities do not support an intrinsic liver disease as the cause of his massive ascites and end‐stage liver disease physiology. Cardiac catheterization demonstrates equalization of diastolic pressures, which suggests constrictive pericarditis or restrictive cardiomyopathy. Despite the normal chest radiograph and nonreactive PPD, tuberculosis would be my leading explanation for constrictive pericarditis given the time spent in areas endemic with TB. Although lateral chest radiography may demonstrate pericardial calcifications, magnetic resonance imaging (MRI) is the best imaging modality to detect constrictive pericarditis. Alternately, cardiac amyloidosis could cause restrictive cardiomyopathy and has not been definitively excluded. A cardiac MRI to assess the pericardium would be my next test, and I would request Congo red stains of the liver biopsy. If these tests are unrevealing, endomyocardial biopsy may be necessary.

The cardiac MRI revealed a severely thickened 7‐mm pericardium (normal < 3 mm) most prominent over the right atrium and ventricle. The right ventricle was described as bullet‐shaped, suggesting constrictive pericardial disease (Fig. 1). Left heart catheterization to evaluate coronary anatomy and left ventricular pressures revealed no significant coronary arterial disease and demonstrated an elevated left ventricular end‐diastolic pressure consistent with constrictive pericarditis. Endomyocardial biopsy showed no evidence of infiltrative disease, granulomata, or other significant abnormality. The following day the patient underwent pericardiectomy. Postoperatively, his ascites was easily managed with low doses of diuretics. The pericardial tissue revealed chronic inflammatory cells and dense collagenous fibrosis characteristic of constrictive pericarditis without evidence of malignancy or granulomatous disease. Pericardial cultures were negative for bacteria, viruses, fungi, and mycobacteria.

Figure 1

DISCUSSION

Constrictive pericarditis is characterized by chronic fibrous thickening of the once‐elastic pericardial sac and can occur following any disease process that affects the pericardium (Table 1).1, 2 The challenge in the diagnosis of constrictive pericarditis lies in the recognition of this slowly progressive and uncommon disease. In many cases, nonspecific symptoms of reduced cardiac output and insidious right‐sided heart failure are present for 12 months or longer before a diagnosis is established.1, 3 A typical presentation of constrictive pericarditis is peripheral edema, ascites, and hepatomegaly, a combination that may understandably lead to a misdiagnosis of chronic liver disease and even subject a patient to the unnecessary risk of a liver biopsy, as in this case.

Cryptogenic cirrhosis, the initial diagnosis of this patient, is a term used only after excluding the common and uncommon causes of cirrhosis (Table 2).46 With expanded knowledge of the causes of cirrhosis, especially nonalcoholic fatty liver disease, the number of cases of cirrhosis considered to be cryptogenic has decreased from nearly one‐third of all cases in 1960 to approximately 5% in a modern series.7, 8 Chronic or repetitive heart failure can lead to progressive hepatic fibrosis and cirrhosis. Distinguishing features compared to other causes of cirrhosis include an ascitic protein concentration greater than 2.5 g/dL, relatively preserved synthetic function, and infrequent stigmata of end‐stage liver disease such as spider angiomata or pronounced jaundice.9, 10

A key exam feature that distinguishes cardiac cirrhosis from other causes of liver failure is an elevated jugular venous pressure. Hepatic causes of cirrhosis induce increased nitric oxide production, which leads to splanchnic and peripheral arterial vasodilatation with a reduced effective circulating volume and normal or low jugular venous pressure.11, 12 Therefore, a patient with cirrhosis and ascites having an elevated jugular venous pressure should prompt echocardiographic evaluation.13 When echocardiography excludes ventricular dysfunction, valvular abnormalities, and pulmonary hypertension, constrictive pericarditis and restrictive cardiomyopathy remain important diagnostic considerations.

In both constrictive pericarditis and restrictive cardiomyopathy, ventricular filling is limited. Pressures in the chambers rise abruptly and rapidly during ventricular filling until equilibrium is reached in early diastole. This can be conceptualized as the cardiac chambers being constrained by the limitations of a rigid external box. In constrictive pericarditis, the rigid external box is the fibrosed and thickened pericardial sac, which loses its elasticity and impairs filling of the ventricles. In restrictive cardiomyopathy, the stiff myocardium limits ventricular filling.

There is considerable overlap in the clinical, echocardiographic, and hemodynamic findings of constrictive pericarditis and restrictive cardiomyopathy.14 Both may present insidiously with progressive heart failure. Echocardiography demonstrates impaired diastolic function. Cardiac hemodynamics demonstrate abrupt and rapid early diastolic filling, elevated and equal ventricular end‐diastolic pressures, and reduced stroke volume and cardiac output. A diagnosis of constrictive pericarditis is favored when a marked inspiratory increase in right ventricular pressures and decrease in left ventricular pressures are seen on heart catheterization or a similar inspiratory increase in transvalvular flow velocities across the tricuspid valve compared with the mitral valve is shown by echocardiography. This finding results from normal inspiratory increases in intrathoracic pressures, which are unable to be transmitted through the rigid pericardium but continue to augment venous return to the right side of the heart. As many as one‐third of patients with pericardial constriction lack these characteristic findings on echocardiogram.14

The results of pericardial imaging may suggest a diagnosis of constrictive pericarditis. Lateral chest radiography demonstrates pericardial calcifications in less than 30% of cases.15 Cardiac computed tomography (CT) and MRI are the best imaging modalities for detecting an increase in pericardial thickness (3 mm or greater).16 However, in as many as 20% of patients with surgically confirmed constrictive pericarditis, CT and MRI will demonstrate a pericardium of normal thickness.17

When faced with the diagnostic conundrum of constrictive pericarditis versus restrictive cardiomyopathy, strong clinical suspicion, thorough echocardiography, careful hemodynamic assessment with right and left heart catheterization,14, 18 pericardial imaging, and sometimes endomyocardial biopsy to exclude restrictive cardiomyopathy are often needed before proceeding to pericardiectomy, which carries a significant surgical risk but can also be curative.

This case highlights many of the features of constrictive pericarditis, the challenges and delay in its diagnosis, and its occasional misdiagnosis as chronic liver disease. Clinicians may recognize the typical combination of cirrhosis (or suspected cirrhosis), high SAAG ascites, and edema as characteristic of advanced intrinsic liver disease. However, they must not be seduced into immediate pattern recognition when contrary evidencesuch as elevated neck veins, elevated ascitic total protein, or relatively preserved hepatic synthetic functionaccompanies that picture. Under such circumstances, they must remember to think outside the box and bear in mind that the heart may be trapped inside a box.

A 65‐year‐old man was referred for evaluation of worsening ascites and end‐stage liver disease. The patient had been well until 1 year ago, when he developed lower extremity edema and abdominal distention. After evaluation by his primary care physician, he was given a diagnosis of cryptogenic cirrhosis. He underwent several paracenteses and was placed on furosemide and spironolactone. The patient had been stable on his diuretic regimen until 2 weeks previously, when he suddenly developed worsening edema and ascites, along with dizziness, nausea, and hypotension. His physician stopped the diuretics and referred him to the hospital.

Before diagnosing a patient with cryptogenic cirrhosis, it is necessary to exclude common etiologies of cirrhosis such as alcohol, viral hepatitis, and non‐alcoholic fatty liver disease and numerous uncommon causes, including Wilson's disease, hemochromatosis, Budd‐Chiari, and biliary cirrhosis. It is also important to remember that patients with liver disease are not immune to extrahepatic causes of ascites, such as peritoneal carcinomatosis and tuberculous ascites. Simultaneously, reasons for chronic liver disease decompensating acutely must be considered: medication nonadherence, excess salt intake, hepatotoxicity from acetaminophen or alcohol, and other acute insults, such as hepatocellular carcinoma, an intervening infection (especially spontaneous bacterial peritonitis), ascending cholangitis, or a flare of chronic viral hepatitis.

Past medical and surgical history included diabetes mellitus (diagnosed 10 years previously), obstructive sleep apnea, hypertension, hypothyroidism, and mild chronic kidney disease. Medications included levothyroxine, lactulose, sulfamethoxazole, pioglitazone (started 4 months prior), and ibuprofen. Furosemide and spironolactone had been discontinued 2 weeks previously. He currently resided in the Central Valley of California. He had lived in Thailand from age 7 to 17 and traveled to India more than 1 year ago. He did not smoke and had never used intravenous drugs or received a blood transfusion. He rarely drank alcohol. He worked as a chemist. There was no family history of liver disease.

There is no obvious explanation for the underlying liver disease or the acute decompensation. Sulfamethoxazole is a rare cause of allergic or granulomatous hepatitis. Pioglitazone is a thiazolinedione which in earlier formulations was linked to hepatitis but can be excluded as a cause of this patient's cirrhosis because it was started after liver disease was detected. As a chemist, he might have been exposed to carbon tetrachloride, a known hepatotoxin. Obstructive sleep apnea causes pulmonary hypertension, but severe ascites and acute hepatic decompensation would be unusual. Ibuprofen might precipitate worsening renal function and fluid accumulation. Time in Thailand and India raises the possibility of tuberculous ascites.

The patient had no headache, vision changes, abdominal pain, emesis, melena, hematochezia, chest pain, palpitations, dysuria, polyuria, pruritus, dark urine, or rashes. He reported difficulty with concentration when lactulose was decreased. He noted worsening exercise tolerance with dyspnea after 10 steps and reported a weight gain of 12 pounds in the past 2 weeks.

On examination, temperature was 36.8C; blood pressure, 129/87 mm Hg; heart rate, 85 beats per minute; respirations, 20 per minute; and oxygen saturation, 94% on room air. He was uncomfortable but alert. There was no scleral icterus or conjunctival pallor. Jugular venous pressure was elevated. The lungs were clear, and the heart was regular, with no murmur, rub, or gallops. The abdomen was massively distended with a fluid wave; the liver and spleen could not be palpated. There was pitting edema of the sacrum and lower extremities. There was no asterixis, palmar erythema, spider angiomata, or skin discoloration.

The additional history and physical exam suggest that the primary problem may lie outside the liver, especially as signs of advanced liver disease (other than ascites) are absent. Dyspnea on exertion is consistent with the physical stress of a large volume of ascites or could be secondary to several pulmonary complications associated with liver disease, including portopulmonary hypertension, hepatopulmonary syndrome, or hepatic hydrothorax. Alternatively, the dyspnea raises the possibility that the ascites is not related to a primary liver disorder but rather to anemia or to a cardiac disorder, such as chronic left ventricular failure, isolated right‐sided heart failure, or constrictive pericarditis. These diagnoses are suggested by the elevated jugular venous pressure, which is atypical in cirrhosis.

Although portal hypertension accounts for most cases of ascites, peritoneal fluid should be examined to exclude peritoneal carcinomatosis and tuberculous ascites. I am interested in the results of an echocardiogram.

Initial laboratory studies demonstrated a sodium concentration of 136 mEq/dL; potassium, 4.7 mEq/dL; chloride, 99 mEq/dL; bicarbonate, 24 mEq/dL; blood urea nitrogen, 54 mg/dL; creatinine, 3.3 mg/dL (increased from baseline of 1.6 mg/dL 4 months previously); white cell count, 7000/mm³; hemoglobin, 10.5 g/dL; MCV, 89 fL; platelet count, 205,000/mm³; bilirubin, 0.6 mg/dL; aspartate aminotransferase, 15 U/L; alanine aminotransferase, 8 U/L; alkaline phosphatase, 102 U/L; albumin, 4.2 g/dL; total protein, 8.2 g/dL; international normalized ratio, 1.2; and partial thromboplastin time, 31.8 seconds. A urine dipstick demonstrated 1+ protein. The chest radiograph was normal. Electrocardiogram had borderline low voltage with nonspecific T‐wave abnormalities. Additional studies showed a serum iron concentration of 49 mg/dL, transferrin saturation of 16%, total iron binding capacity of 310 mg/dL, and ferritin of 247 mg/mL. Hemoglobin A1c was 7.0%. Acute and chronic antibodies to hepatitis A, B, and C viruses were negative. The following study results were normal or negative: antinuclear antibody, alpha‐1‐antitrypsin, ceruloplasmin, alpha‐fetoprotein, carcinoembryonic antigen, and 24‐hour urinary copper. The thyroid function studies were normal. A purified protein derivative (PPD) skin test was nonreactive.

There continues to be a paucity of evidence of a primary liver disorder. The hepatic enzymes and tests of liver synthetic function are normal, and there is no pancytopenia, as might result from hypersplenism. I remain most suspicious of either a primary cardiac or pericardial disorder with secondary hepatic congestion or a disease that simultaneously affects the heart and liver.

The reasons for the low voltage on the electrocardiogram include processes that infiltrate the myocardium (amyloidosis, sarcoidosis, hemochromatosis, and myxedema fluid) and processes that increase the distance between the myocardium and surface electrodes, such as adipose tissue, air (from emphysema or pneumothorax), or pericardial effusion. Pericardial effusion may present subacutely with predominant features of right ventricular failure. Low voltage, liver disease, and possible heart failure raise the possibility of amyloidosis or hemochromatosis. The low transferrin saturation renders hemochromatosis unlikely. Although normal alkaline phosphatase and serum albumin are not characteristic when AL amyloid affects the liver and kidneys, serum and urine protein electrophoresis and immunofixation should be considered.

With paracentesis 3.5 L of ascitic fluid was removed. The red cell count was 4000/mm³, and white blood cell count was 505/mm³, of which 25% were polymorphonuclear cells, 22% were lymphocytes, and 53% were monocytes. Additional peritoneal fluid chemistries included albumin of 3.0 g/dL and total protein of 5.3 g/dL. Abdominal ultrasound with Doppler demonstrated a liver of normal size and echogenicity with patent hepatic arteries, hepatic veins, and portal vein. There was mild splenomegaly with normal kidneys. Evaluation for a possible liver transplant was initiated. Blood, urine, and peritoneal fluid cultures demonstrated no growth. Echocardiography demonstrated borderline concentric left ventricular hypertrophy, normal right and left ventricular function, dilated superior and inferior vena cavae, and no pericardial effusion or thickening.

The serum‐ascites albumin gradient (SAAG) of 1.2 is consistent with portal hypertension as the cause of the ascites. The Doppler findings exclude postsinusoidal causes of portal hypertension from hepatic vein obstruction or thrombosis. The combination of the elevated SAAG, elevated jugular venous pressure, borderline low voltage on ECG, and elevated peritoneal total protein make cardiac and pericardial disease the leading considerations. Given the normal ventricular function, I am concerned about elevated intracardiac pressures resulting from pericardial disease or restrictive cardiomyopathy. At this point, right heart catheterization would be useful for assessing intracardiac pressures.

On the fourth hospital day, paracentesis was repeated, and 15 L of fluid was removed. A transjugular liver biopsy demonstrated diffuse patchy fibrosis consistent with early cirrhosis and minor intralobular changes with minimal ballooning. There was no steatosis, active inflammation, granulomata, iron deposition, or evidence of viral hepatitis. Right heart catheterization revealed a right atrial pressure of 18 cm H₂0, right ventricular pressure of 34/20 cm H₂0, pulmonary artery pressure of 34/18 cm H₂0 (mean 25), pulmonary capillary wedge pressure of 20 cm H₂0, cardiac output of 5.8 L/min, and cardiac index of 2.5 L/min/m².

The mild hepatic histologic abnormalities do not support an intrinsic liver disease as the cause of his massive ascites and end‐stage liver disease physiology. Cardiac catheterization demonstrates equalization of diastolic pressures, which suggests constrictive pericarditis or restrictive cardiomyopathy. Despite the normal chest radiograph and nonreactive PPD, tuberculosis would be my leading explanation for constrictive pericarditis given the time spent in areas endemic with TB. Although lateral chest radiography may demonstrate pericardial calcifications, magnetic resonance imaging (MRI) is the best imaging modality to detect constrictive pericarditis. Alternately, cardiac amyloidosis could cause restrictive cardiomyopathy and has not been definitively excluded. A cardiac MRI to assess the pericardium would be my next test, and I would request Congo red stains of the liver biopsy. If these tests are unrevealing, endomyocardial biopsy may be necessary.

The cardiac MRI revealed a severely thickened 7‐mm pericardium (normal < 3 mm) most prominent over the right atrium and ventricle. The right ventricle was described as bullet‐shaped, suggesting constrictive pericardial disease (Fig. 1). Left heart catheterization to evaluate coronary anatomy and left ventricular pressures revealed no significant coronary arterial disease and demonstrated an elevated left ventricular end‐diastolic pressure consistent with constrictive pericarditis. Endomyocardial biopsy showed no evidence of infiltrative disease, granulomata, or other significant abnormality. The following day the patient underwent pericardiectomy. Postoperatively, his ascites was easily managed with low doses of diuretics. The pericardial tissue revealed chronic inflammatory cells and dense collagenous fibrosis characteristic of constrictive pericarditis without evidence of malignancy or granulomatous disease. Pericardial cultures were negative for bacteria, viruses, fungi, and mycobacteria.

Figure 1

DISCUSSION

Constrictive pericarditis is characterized by chronic fibrous thickening of the once‐elastic pericardial sac and can occur following any disease process that affects the pericardium (Table 1).1, 2 The challenge in the diagnosis of constrictive pericarditis lies in the recognition of this slowly progressive and uncommon disease. In many cases, nonspecific symptoms of reduced cardiac output and insidious right‐sided heart failure are present for 12 months or longer before a diagnosis is established.1, 3 A typical presentation of constrictive pericarditis is peripheral edema, ascites, and hepatomegaly, a combination that may understandably lead to a misdiagnosis of chronic liver disease and even subject a patient to the unnecessary risk of a liver biopsy, as in this case.

Cryptogenic cirrhosis, the initial diagnosis of this patient, is a term used only after excluding the common and uncommon causes of cirrhosis (Table 2).46 With expanded knowledge of the causes of cirrhosis, especially nonalcoholic fatty liver disease, the number of cases of cirrhosis considered to be cryptogenic has decreased from nearly one‐third of all cases in 1960 to approximately 5% in a modern series.7, 8 Chronic or repetitive heart failure can lead to progressive hepatic fibrosis and cirrhosis. Distinguishing features compared to other causes of cirrhosis include an ascitic protein concentration greater than 2.5 g/dL, relatively preserved synthetic function, and infrequent stigmata of end‐stage liver disease such as spider angiomata or pronounced jaundice.9, 10

A key exam feature that distinguishes cardiac cirrhosis from other causes of liver failure is an elevated jugular venous pressure. Hepatic causes of cirrhosis induce increased nitric oxide production, which leads to splanchnic and peripheral arterial vasodilatation with a reduced effective circulating volume and normal or low jugular venous pressure.11, 12 Therefore, a patient with cirrhosis and ascites having an elevated jugular venous pressure should prompt echocardiographic evaluation.13 When echocardiography excludes ventricular dysfunction, valvular abnormalities, and pulmonary hypertension, constrictive pericarditis and restrictive cardiomyopathy remain important diagnostic considerations.

In both constrictive pericarditis and restrictive cardiomyopathy, ventricular filling is limited. Pressures in the chambers rise abruptly and rapidly during ventricular filling until equilibrium is reached in early diastole. This can be conceptualized as the cardiac chambers being constrained by the limitations of a rigid external box. In constrictive pericarditis, the rigid external box is the fibrosed and thickened pericardial sac, which loses its elasticity and impairs filling of the ventricles. In restrictive cardiomyopathy, the stiff myocardium limits ventricular filling.

There is considerable overlap in the clinical, echocardiographic, and hemodynamic findings of constrictive pericarditis and restrictive cardiomyopathy.14 Both may present insidiously with progressive heart failure. Echocardiography demonstrates impaired diastolic function. Cardiac hemodynamics demonstrate abrupt and rapid early diastolic filling, elevated and equal ventricular end‐diastolic pressures, and reduced stroke volume and cardiac output. A diagnosis of constrictive pericarditis is favored when a marked inspiratory increase in right ventricular pressures and decrease in left ventricular pressures are seen on heart catheterization or a similar inspiratory increase in transvalvular flow velocities across the tricuspid valve compared with the mitral valve is shown by echocardiography. This finding results from normal inspiratory increases in intrathoracic pressures, which are unable to be transmitted through the rigid pericardium but continue to augment venous return to the right side of the heart. As many as one‐third of patients with pericardial constriction lack these characteristic findings on echocardiogram.14

The results of pericardial imaging may suggest a diagnosis of constrictive pericarditis. Lateral chest radiography demonstrates pericardial calcifications in less than 30% of cases.15 Cardiac computed tomography (CT) and MRI are the best imaging modalities for detecting an increase in pericardial thickness (3 mm or greater).16 However, in as many as 20% of patients with surgically confirmed constrictive pericarditis, CT and MRI will demonstrate a pericardium of normal thickness.17

When faced with the diagnostic conundrum of constrictive pericarditis versus restrictive cardiomyopathy, strong clinical suspicion, thorough echocardiography, careful hemodynamic assessment with right and left heart catheterization,14, 18 pericardial imaging, and sometimes endomyocardial biopsy to exclude restrictive cardiomyopathy are often needed before proceeding to pericardiectomy, which carries a significant surgical risk but can also be curative.

This case highlights many of the features of constrictive pericarditis, the challenges and delay in its diagnosis, and its occasional misdiagnosis as chronic liver disease. Clinicians may recognize the typical combination of cirrhosis (or suspected cirrhosis), high SAAG ascites, and edema as characteristic of advanced intrinsic liver disease. However, they must not be seduced into immediate pattern recognition when contrary evidencesuch as elevated neck veins, elevated ascitic total protein, or relatively preserved hepatic synthetic functionaccompanies that picture. Under such circumstances, they must remember to think outside the box and bear in mind that the heart may be trapped inside a box.

A 65‐year‐old man was referred for evaluation of worsening ascites and end‐stage liver disease. The patient had been well until 1 year ago, when he developed lower extremity edema and abdominal distention. After evaluation by his primary care physician, he was given a diagnosis of cryptogenic cirrhosis. He underwent several paracenteses and was placed on furosemide and spironolactone. The patient had been stable on his diuretic regimen until 2 weeks previously, when he suddenly developed worsening edema and ascites, along with dizziness, nausea, and hypotension. His physician stopped the diuretics and referred him to the hospital.

Before diagnosing a patient with cryptogenic cirrhosis, it is necessary to exclude common etiologies of cirrhosis such as alcohol, viral hepatitis, and non‐alcoholic fatty liver disease and numerous uncommon causes, including Wilson's disease, hemochromatosis, Budd‐Chiari, and biliary cirrhosis. It is also important to remember that patients with liver disease are not immune to extrahepatic causes of ascites, such as peritoneal carcinomatosis and tuberculous ascites. Simultaneously, reasons for chronic liver disease decompensating acutely must be considered: medication nonadherence, excess salt intake, hepatotoxicity from acetaminophen or alcohol, and other acute insults, such as hepatocellular carcinoma, an intervening infection (especially spontaneous bacterial peritonitis), ascending cholangitis, or a flare of chronic viral hepatitis.

Past medical and surgical history included diabetes mellitus (diagnosed 10 years previously), obstructive sleep apnea, hypertension, hypothyroidism, and mild chronic kidney disease. Medications included levothyroxine, lactulose, sulfamethoxazole, pioglitazone (started 4 months prior), and ibuprofen. Furosemide and spironolactone had been discontinued 2 weeks previously. He currently resided in the Central Valley of California. He had lived in Thailand from age 7 to 17 and traveled to India more than 1 year ago. He did not smoke and had never used intravenous drugs or received a blood transfusion. He rarely drank alcohol. He worked as a chemist. There was no family history of liver disease.

There is no obvious explanation for the underlying liver disease or the acute decompensation. Sulfamethoxazole is a rare cause of allergic or granulomatous hepatitis. Pioglitazone is a thiazolinedione which in earlier formulations was linked to hepatitis but can be excluded as a cause of this patient's cirrhosis because it was started after liver disease was detected. As a chemist, he might have been exposed to carbon tetrachloride, a known hepatotoxin. Obstructive sleep apnea causes pulmonary hypertension, but severe ascites and acute hepatic decompensation would be unusual. Ibuprofen might precipitate worsening renal function and fluid accumulation. Time in Thailand and India raises the possibility of tuberculous ascites.

The patient had no headache, vision changes, abdominal pain, emesis, melena, hematochezia, chest pain, palpitations, dysuria, polyuria, pruritus, dark urine, or rashes. He reported difficulty with concentration when lactulose was decreased. He noted worsening exercise tolerance with dyspnea after 10 steps and reported a weight gain of 12 pounds in the past 2 weeks.

On examination, temperature was 36.8C; blood pressure, 129/87 mm Hg; heart rate, 85 beats per minute; respirations, 20 per minute; and oxygen saturation, 94% on room air. He was uncomfortable but alert. There was no scleral icterus or conjunctival pallor. Jugular venous pressure was elevated. The lungs were clear, and the heart was regular, with no murmur, rub, or gallops. The abdomen was massively distended with a fluid wave; the liver and spleen could not be palpated. There was pitting edema of the sacrum and lower extremities. There was no asterixis, palmar erythema, spider angiomata, or skin discoloration.

The additional history and physical exam suggest that the primary problem may lie outside the liver, especially as signs of advanced liver disease (other than ascites) are absent. Dyspnea on exertion is consistent with the physical stress of a large volume of ascites or could be secondary to several pulmonary complications associated with liver disease, including portopulmonary hypertension, hepatopulmonary syndrome, or hepatic hydrothorax. Alternatively, the dyspnea raises the possibility that the ascites is not related to a primary liver disorder but rather to anemia or to a cardiac disorder, such as chronic left ventricular failure, isolated right‐sided heart failure, or constrictive pericarditis. These diagnoses are suggested by the elevated jugular venous pressure, which is atypical in cirrhosis.

Although portal hypertension accounts for most cases of ascites, peritoneal fluid should be examined to exclude peritoneal carcinomatosis and tuberculous ascites. I am interested in the results of an echocardiogram.

Initial laboratory studies demonstrated a sodium concentration of 136 mEq/dL; potassium, 4.7 mEq/dL; chloride, 99 mEq/dL; bicarbonate, 24 mEq/dL; blood urea nitrogen, 54 mg/dL; creatinine, 3.3 mg/dL (increased from baseline of 1.6 mg/dL 4 months previously); white cell count, 7000/mm³; hemoglobin, 10.5 g/dL; MCV, 89 fL; platelet count, 205,000/mm³; bilirubin, 0.6 mg/dL; aspartate aminotransferase, 15 U/L; alanine aminotransferase, 8 U/L; alkaline phosphatase, 102 U/L; albumin, 4.2 g/dL; total protein, 8.2 g/dL; international normalized ratio, 1.2; and partial thromboplastin time, 31.8 seconds. A urine dipstick demonstrated 1+ protein. The chest radiograph was normal. Electrocardiogram had borderline low voltage with nonspecific T‐wave abnormalities. Additional studies showed a serum iron concentration of 49 mg/dL, transferrin saturation of 16%, total iron binding capacity of 310 mg/dL, and ferritin of 247 mg/mL. Hemoglobin A1c was 7.0%. Acute and chronic antibodies to hepatitis A, B, and C viruses were negative. The following study results were normal or negative: antinuclear antibody, alpha‐1‐antitrypsin, ceruloplasmin, alpha‐fetoprotein, carcinoembryonic antigen, and 24‐hour urinary copper. The thyroid function studies were normal. A purified protein derivative (PPD) skin test was nonreactive.

There continues to be a paucity of evidence of a primary liver disorder. The hepatic enzymes and tests of liver synthetic function are normal, and there is no pancytopenia, as might result from hypersplenism. I remain most suspicious of either a primary cardiac or pericardial disorder with secondary hepatic congestion or a disease that simultaneously affects the heart and liver.

The reasons for the low voltage on the electrocardiogram include processes that infiltrate the myocardium (amyloidosis, sarcoidosis, hemochromatosis, and myxedema fluid) and processes that increase the distance between the myocardium and surface electrodes, such as adipose tissue, air (from emphysema or pneumothorax), or pericardial effusion. Pericardial effusion may present subacutely with predominant features of right ventricular failure. Low voltage, liver disease, and possible heart failure raise the possibility of amyloidosis or hemochromatosis. The low transferrin saturation renders hemochromatosis unlikely. Although normal alkaline phosphatase and serum albumin are not characteristic when AL amyloid affects the liver and kidneys, serum and urine protein electrophoresis and immunofixation should be considered.

With paracentesis 3.5 L of ascitic fluid was removed. The red cell count was 4000/mm³, and white blood cell count was 505/mm³, of which 25% were polymorphonuclear cells, 22% were lymphocytes, and 53% were monocytes. Additional peritoneal fluid chemistries included albumin of 3.0 g/dL and total protein of 5.3 g/dL. Abdominal ultrasound with Doppler demonstrated a liver of normal size and echogenicity with patent hepatic arteries, hepatic veins, and portal vein. There was mild splenomegaly with normal kidneys. Evaluation for a possible liver transplant was initiated. Blood, urine, and peritoneal fluid cultures demonstrated no growth. Echocardiography demonstrated borderline concentric left ventricular hypertrophy, normal right and left ventricular function, dilated superior and inferior vena cavae, and no pericardial effusion or thickening.

The serum‐ascites albumin gradient (SAAG) of 1.2 is consistent with portal hypertension as the cause of the ascites. The Doppler findings exclude postsinusoidal causes of portal hypertension from hepatic vein obstruction or thrombosis. The combination of the elevated SAAG, elevated jugular venous pressure, borderline low voltage on ECG, and elevated peritoneal total protein make cardiac and pericardial disease the leading considerations. Given the normal ventricular function, I am concerned about elevated intracardiac pressures resulting from pericardial disease or restrictive cardiomyopathy. At this point, right heart catheterization would be useful for assessing intracardiac pressures.

On the fourth hospital day, paracentesis was repeated, and 15 L of fluid was removed. A transjugular liver biopsy demonstrated diffuse patchy fibrosis consistent with early cirrhosis and minor intralobular changes with minimal ballooning. There was no steatosis, active inflammation, granulomata, iron deposition, or evidence of viral hepatitis. Right heart catheterization revealed a right atrial pressure of 18 cm H₂0, right ventricular pressure of 34/20 cm H₂0, pulmonary artery pressure of 34/18 cm H₂0 (mean 25), pulmonary capillary wedge pressure of 20 cm H₂0, cardiac output of 5.8 L/min, and cardiac index of 2.5 L/min/m².

The mild hepatic histologic abnormalities do not support an intrinsic liver disease as the cause of his massive ascites and end‐stage liver disease physiology. Cardiac catheterization demonstrates equalization of diastolic pressures, which suggests constrictive pericarditis or restrictive cardiomyopathy. Despite the normal chest radiograph and nonreactive PPD, tuberculosis would be my leading explanation for constrictive pericarditis given the time spent in areas endemic with TB. Although lateral chest radiography may demonstrate pericardial calcifications, magnetic resonance imaging (MRI) is the best imaging modality to detect constrictive pericarditis. Alternately, cardiac amyloidosis could cause restrictive cardiomyopathy and has not been definitively excluded. A cardiac MRI to assess the pericardium would be my next test, and I would request Congo red stains of the liver biopsy. If these tests are unrevealing, endomyocardial biopsy may be necessary.

The cardiac MRI revealed a severely thickened 7‐mm pericardium (normal < 3 mm) most prominent over the right atrium and ventricle. The right ventricle was described as bullet‐shaped, suggesting constrictive pericardial disease (Fig. 1). Left heart catheterization to evaluate coronary anatomy and left ventricular pressures revealed no significant coronary arterial disease and demonstrated an elevated left ventricular end‐diastolic pressure consistent with constrictive pericarditis. Endomyocardial biopsy showed no evidence of infiltrative disease, granulomata, or other significant abnormality. The following day the patient underwent pericardiectomy. Postoperatively, his ascites was easily managed with low doses of diuretics. The pericardial tissue revealed chronic inflammatory cells and dense collagenous fibrosis characteristic of constrictive pericarditis without evidence of malignancy or granulomatous disease. Pericardial cultures were negative for bacteria, viruses, fungi, and mycobacteria.

Figure 1

DISCUSSION

Constrictive pericarditis is characterized by chronic fibrous thickening of the once‐elastic pericardial sac and can occur following any disease process that affects the pericardium (Table 1).1, 2 The challenge in the diagnosis of constrictive pericarditis lies in the recognition of this slowly progressive and uncommon disease. In many cases, nonspecific symptoms of reduced cardiac output and insidious right‐sided heart failure are present for 12 months or longer before a diagnosis is established.1, 3 A typical presentation of constrictive pericarditis is peripheral edema, ascites, and hepatomegaly, a combination that may understandably lead to a misdiagnosis of chronic liver disease and even subject a patient to the unnecessary risk of a liver biopsy, as in this case.

Cryptogenic cirrhosis, the initial diagnosis of this patient, is a term used only after excluding the common and uncommon causes of cirrhosis (Table 2).46 With expanded knowledge of the causes of cirrhosis, especially nonalcoholic fatty liver disease, the number of cases of cirrhosis considered to be cryptogenic has decreased from nearly one‐third of all cases in 1960 to approximately 5% in a modern series.7, 8 Chronic or repetitive heart failure can lead to progressive hepatic fibrosis and cirrhosis. Distinguishing features compared to other causes of cirrhosis include an ascitic protein concentration greater than 2.5 g/dL, relatively preserved synthetic function, and infrequent stigmata of end‐stage liver disease such as spider angiomata or pronounced jaundice.9, 10