In the United States, candida now accounts for between 8% and 12% of all catheter‐associated blood stream infections (BSIs).1 Additionally, crude mortality rates in candidemia exceed 40%, and a recent systematic review demonstrated that the attributable mortality of candidemia ranges from 5% to 71%.2 Candidal BSIs also affect resource utilization. These infections independently increase length of stay and result in substantial excess costs.3 Most cases of candidemia arise in noncritically ill patients and thus may be managed by hospitalists.

Historically, the majority of candidal BSIs were caused by C. albicans. Presently, C. albicans accounts for only half of all yeast BSIs, and approximately 20% of these infections are caused by organisms such as C. glabrata and C. krusei.4 These 2 organisms have either variable or no susceptibility to agents, such as fluconazole, empirically employed against yeast. Parallel with the evolution in microbiology of candidemia has been recognition that inappropriate treatment of these infections independently increases mortality.5 These factors underscore the need for the clinician to treat suspected candidal BSIs aggressively in order to avoid the risks associated with inappropriate treatment.

Efforts to enhance rates of initial appropriate therapy for bacterial infections have encompassed the realization that health care‐associated infections (HAIs) represent a distinct syndrome.6, 7 Traditionally, infections were considered either community‐acquired or nosocomial in origin. However, with the spread of health care delivery beyond the hospital, multiple studies indicate that patients may now present to the emergency department with infections caused by pathogens such as Methicillin‐resistant Staphylococcus aureus (MRSA) and P. aeruginosaorganisms that were previously thought limited to hospital‐acquired processes.69 Furthermore, hospitalists often encounter subjects presenting to the hospital with suspected BSIs who have an active and ongoing interaction with the healthcare system.

The importance of candida as a health care‐associated pathogen in BSI remains unclear. We hypothesized that health care‐associated candidemia (HCAC) represented a distinct clinical entity. In order to confirm our theory, we conducted a retrospective analysis of all cases of candidal BSI at our institution over a 3‐year period.

Methods

We reviewed the records of all patients diagnosed with candidemia at our hospital between January 1, 2004 and December 31, 2006. Our institutional review board approved this study. We included adult patients diagnosed with candidemia. The diagnosis of candidemia was based on the isolation of yeast from the blood in at least one blood culture. We employ the BACTEC 9240 blood Culture System (Becton Dickinson Microbiology Systems, Sparks, MD). We excluded subjects who were admitted to the hospital within one month of a known diagnosis of candidemia.

We defined a nosocomial candidal BSI as the diagnosis of candidemia based on cultures drawn after the patient had been hospitalized for >48 hours. We considered HCAC to be present based on previously employed criteria for identifying HAI.69 Specifically, for patients with candidemia based on blood cultures obtained within 48 hours of hospitalization, a patient had to meet at least 1 of the following criteria: (1) receipt of intravenous therapy outside the hospital, (2) end stage renal disease necessitating hemodialysis (ESRD requiring HD), (3) hospitalization within previous 30 days, (4) residence in a nursing home or long term care facility, or (5) underwent an invasive procedure as an outpatient within 30 days of presentation. Community‐acquired candidemia was restricted to patients whose index culture was drawn within 48 hours of admission but who failed to meet the definition for HCAC.

The prevalence of the various forms of candidemia served as our primary endpoint. In addition, we compared patients with respect to demographic factors, comorbidities, and severity of illness. Severity of illness was calculated based on the Acute Physiology and Chronic Health Evaluation (APACHE) II score. We further noted rates of immune suppression in the cohort and defined this as treatment with corticosteroids (10 mg of prednisone or equivalent daily for more than 30 consecutive days), other immunosuppressants (eg, methotrexate), or chemotherapy. Those with acquired immune deficiency syndrome (AIDS) or another immunodeficiency syndrome were defined as immunosuppressed as well. We examined the distribution of yeast species across the 3 forms of candidemia. Finally, we assessed the prevalence of fluconazole resistance. Fluconazole susceptibilities were determined based on Etest (AB BIODISK, Solna, Sweden). An isolate was considered resistant to fluconazole if the minimum inhibitory concentration was >64 g/mL.

We compared categorical variables with the Fisher's exact test. Continuous variables were analyzed with either the Student's t‐test or a Mann‐Whitney test, as appropriate. All tests were 2 tailed and a P value of <0.05 was assumed to represent statistical significance. Analyses were performed with Stata 9.1 (Stata Corp., College Station, TX).

Results

The final cohort included 223 subjects. The mean age of the patients was 59.6 15.7 years and 49% were male. Nearly one quarter (n = 55) fulfilled our criteria for HCAC. The remainder met the definition for nosocomial candidemia. We observed no cases of community‐acquired candidemia. Most (n = 33) patients with HCAC had exposure to more than 1 health care‐related source and many were initially admitted to the medicine/hospitalist service as opposed to the intensive care unit (ICU). The most common criteria leading to categorization as HCAC was recent hospitalization (n = 30, 54.5% of all HCAC). The median time from recent hospitalization to admission was 17 days (Range: 5‐28 days). Other common reasons for classification as HCAC included ESRD requiring HD (30.9%), residence in a nursing home (25.5%), and undergoing an invasive outpatient procedure (16.4%). More than 75% of subjects with HCAC (n = 42) had central venous catheters in place at presentation. Between 2004 and 2006, the proportion of all candidemia due to HCAC increased from 20.9% to 26.9%, but this difference was not statistically significant.

Patients with HCAC were similar to those with nosocomial candidemia (Table 1). There was no difference in either severity of illness or the frequency of neutropenia. The prevalence of most comorbidities did not differ between those with nosocomial candidemia and persons with HCAC. However, immunosuppression was more prevalent among patients with HCAC (prevalence ratio, 1.67; 95% CI, 1.13‐3.08; P = 0.004). In part this finding is expected given that our definition of HCAC includes exposure to agents which may lead to immunosuppression, such as chemotherapy. Of patients with HCAC, the majority (n = 38, 69.1%) were initially admitted to the general medicine service and not to the ICU.

A multitude of various yeast species were recovered (Figure 1). Overall, nonalbicans candida were responsible for nearly 60% of all infections. Nonalbicans yeast were as likely to be recovered in HCAC as in nosocomial yeast infection. Among both types of Candidemia, C. krusei was a rare culprit accounting for fewer than 2% of infections. C. glabrata, however, occurred more often in HCAC. Specifically, C. glabrata represented 1 in 5 cases of HCAC as opposed to approximately 10% of all nosocomial yeast BSIs (P = 0.05). In part reflecting this, fluconazole resistance was noted more often in HCAC (18.2% of patients vs. 7.7% among nosocomial candidemia, P = 0.036). There was no difference in the eventual diagnosis of deep‐seeded yeast infections (ie, endocarditis, endopthlamitis, or osteomyelitis) between those with HCAC and persons with nosocomial candidemia (3 cases in each group).

Figure 1

Discussion

This analysis demonstrates that HCAC accounts for approximately a quarter of all candidemia. Our findings underscore that candidemia can present to the emergency department as an HAI and may potentially be initially cared for by a hospitalist. In addition, patients with HCAC and nosocomial candidemia share many attributes. Furthermore, nonalbicans yeast are as prevalent in HCAC as in nosocomial candidal infection. Nonetheless, there appear to be important differences in these syndromes. Immunosuppression appears to be more common in HCAC as does infection due to C. glabrata.

Others have explored the concept of HCAC. Kung et al.10 described community‐onset candidemia at a single center over a 10‐year period. They described 56 patients and noted that the majority had been recently hospitalized or had ongoing interaction with the healthcare system. Sofair et al.11 followed subjects presenting to emergency departments with candidemia. Overall, more than one‐third met criteria for community‐onset infection. In this analysis, though, Sofair et al.11 did not distinguish between community‐acquired processes and HCAC. From a population perspective, Chen et al.12 explored candidemia in Australia. Among over 1000 patients, the noted that 11.6% represented HCAC and, as we note, that select nonalbicans yeast occurred more often in HCAC than in nosocomial candidemia. Our project builds on and adds to these earlier efforts. First, we confirm the general observation that candidemia is no longer solely a nosocomial pathogen. Second, unlike several of these earlier reports we examined a larger cohort of candidemia. Third, beyond the observations of Chen et al.,12 we note that currently, the proportion of Candidal BSI classified as HACA relative to nosocomial candidemia seems larger than reported in the past. Finally, a unique aspect of our report is that we employed express criteria to define HAI.

Our findings have several implications. First, hospitalists and emergency department physicians, along with others, must remain vigilant when approaching patients presenting to the hospital with signs and symptoms of BSI and multiple risk factors for candidal BSI. The fact that the patient has not been hospitalized should not preclude consideration of and treatment for candidemia. The current evidence does not support broad, empiric use of antifungal agents, as this would lead to excessive costs and potentially expose many patients to unnecessary antifungal coverage. On the other hand, given the association between delayed antifungal therapy and the risk for death in candidemia, failure to consider this infection in at‐risk subjects may have adverse consequences. Second, our observations emphasize the need for clinical risk stratification schemes and rapid diagnostic modalities. Such tools are urgently needed if physicians hope to target antifungal therapies more appropriately. Third, if the clinician opts to initiate therapy for possible HCAC, reliance on fluconazole alone may prove inadequate. As the generalizability of our conclusions is necessarily limited, we recommend that infection control practitioners review local epidemiologic data regarding HCAC so that physicians can have the best available guidance.

Our study has several important limitations. Its retrospective nature exposes it to several forms of bias. The single center design limits the generalizability of our findings. Prospective, multicenter studies are needed to validate our results. Additionally, no universally accepted criteria exist to define HAI syndromes. Nonetheless, the criteria we employed have been used by others. We also lacked data on exposure to recent broad spectrum antimicrobials. Selection pressure via exposure to such agents is a risk factor for candidemia and without this data we cannot gauge the impact of this on our findings. Finally, we cannot control for the possibility that some patients were miscategorized. This could have arisen because of: (1) either limitations inherent in the definition of HCAC or (2) because the clinician delayed the decision to obtain blood cultures. Some patients classified as nosocomial may actually have had HCAC or community‐acquired diseasebut for some reason blood cultures were not drawn at time of admission but were deferred until later. Although a difficult issue to address in any study of the epidemiology of infection, the significance of this misclassification bias must be considered a significant concern.

In summary, Candidemia can be the cause of BSI presenting to the hospital. Moreover, HCAC represents a significant proportion of all Candidemia. Although patients with HCAC and nosocomial candidemia share select characteristics, there appear to be some differences in the microbiology of these syndromes.

In the United States, candida now accounts for between 8% and 12% of all catheter‐associated blood stream infections (BSIs).1 Additionally, crude mortality rates in candidemia exceed 40%, and a recent systematic review demonstrated that the attributable mortality of candidemia ranges from 5% to 71%.2 Candidal BSIs also affect resource utilization. These infections independently increase length of stay and result in substantial excess costs.3 Most cases of candidemia arise in noncritically ill patients and thus may be managed by hospitalists.

Historically, the majority of candidal BSIs were caused by C. albicans. Presently, C. albicans accounts for only half of all yeast BSIs, and approximately 20% of these infections are caused by organisms such as C. glabrata and C. krusei.4 These 2 organisms have either variable or no susceptibility to agents, such as fluconazole, empirically employed against yeast. Parallel with the evolution in microbiology of candidemia has been recognition that inappropriate treatment of these infections independently increases mortality.5 These factors underscore the need for the clinician to treat suspected candidal BSIs aggressively in order to avoid the risks associated with inappropriate treatment.

Efforts to enhance rates of initial appropriate therapy for bacterial infections have encompassed the realization that health care‐associated infections (HAIs) represent a distinct syndrome.6, 7 Traditionally, infections were considered either community‐acquired or nosocomial in origin. However, with the spread of health care delivery beyond the hospital, multiple studies indicate that patients may now present to the emergency department with infections caused by pathogens such as Methicillin‐resistant Staphylococcus aureus (MRSA) and P. aeruginosaorganisms that were previously thought limited to hospital‐acquired processes.69 Furthermore, hospitalists often encounter subjects presenting to the hospital with suspected BSIs who have an active and ongoing interaction with the healthcare system.

The importance of candida as a health care‐associated pathogen in BSI remains unclear. We hypothesized that health care‐associated candidemia (HCAC) represented a distinct clinical entity. In order to confirm our theory, we conducted a retrospective analysis of all cases of candidal BSI at our institution over a 3‐year period.

Methods

We reviewed the records of all patients diagnosed with candidemia at our hospital between January 1, 2004 and December 31, 2006. Our institutional review board approved this study. We included adult patients diagnosed with candidemia. The diagnosis of candidemia was based on the isolation of yeast from the blood in at least one blood culture. We employ the BACTEC 9240 blood Culture System (Becton Dickinson Microbiology Systems, Sparks, MD). We excluded subjects who were admitted to the hospital within one month of a known diagnosis of candidemia.

We defined a nosocomial candidal BSI as the diagnosis of candidemia based on cultures drawn after the patient had been hospitalized for >48 hours. We considered HCAC to be present based on previously employed criteria for identifying HAI.69 Specifically, for patients with candidemia based on blood cultures obtained within 48 hours of hospitalization, a patient had to meet at least 1 of the following criteria: (1) receipt of intravenous therapy outside the hospital, (2) end stage renal disease necessitating hemodialysis (ESRD requiring HD), (3) hospitalization within previous 30 days, (4) residence in a nursing home or long term care facility, or (5) underwent an invasive procedure as an outpatient within 30 days of presentation. Community‐acquired candidemia was restricted to patients whose index culture was drawn within 48 hours of admission but who failed to meet the definition for HCAC.

The prevalence of the various forms of candidemia served as our primary endpoint. In addition, we compared patients with respect to demographic factors, comorbidities, and severity of illness. Severity of illness was calculated based on the Acute Physiology and Chronic Health Evaluation (APACHE) II score. We further noted rates of immune suppression in the cohort and defined this as treatment with corticosteroids (10 mg of prednisone or equivalent daily for more than 30 consecutive days), other immunosuppressants (eg, methotrexate), or chemotherapy. Those with acquired immune deficiency syndrome (AIDS) or another immunodeficiency syndrome were defined as immunosuppressed as well. We examined the distribution of yeast species across the 3 forms of candidemia. Finally, we assessed the prevalence of fluconazole resistance. Fluconazole susceptibilities were determined based on Etest (AB BIODISK, Solna, Sweden). An isolate was considered resistant to fluconazole if the minimum inhibitory concentration was >64 g/mL.

We compared categorical variables with the Fisher's exact test. Continuous variables were analyzed with either the Student's t‐test or a Mann‐Whitney test, as appropriate. All tests were 2 tailed and a P value of <0.05 was assumed to represent statistical significance. Analyses were performed with Stata 9.1 (Stata Corp., College Station, TX).

Results

The final cohort included 223 subjects. The mean age of the patients was 59.6 15.7 years and 49% were male. Nearly one quarter (n = 55) fulfilled our criteria for HCAC. The remainder met the definition for nosocomial candidemia. We observed no cases of community‐acquired candidemia. Most (n = 33) patients with HCAC had exposure to more than 1 health care‐related source and many were initially admitted to the medicine/hospitalist service as opposed to the intensive care unit (ICU). The most common criteria leading to categorization as HCAC was recent hospitalization (n = 30, 54.5% of all HCAC). The median time from recent hospitalization to admission was 17 days (Range: 5‐28 days). Other common reasons for classification as HCAC included ESRD requiring HD (30.9%), residence in a nursing home (25.5%), and undergoing an invasive outpatient procedure (16.4%). More than 75% of subjects with HCAC (n = 42) had central venous catheters in place at presentation. Between 2004 and 2006, the proportion of all candidemia due to HCAC increased from 20.9% to 26.9%, but this difference was not statistically significant.

Patients with HCAC were similar to those with nosocomial candidemia (Table 1). There was no difference in either severity of illness or the frequency of neutropenia. The prevalence of most comorbidities did not differ between those with nosocomial candidemia and persons with HCAC. However, immunosuppression was more prevalent among patients with HCAC (prevalence ratio, 1.67; 95% CI, 1.13‐3.08; P = 0.004). In part this finding is expected given that our definition of HCAC includes exposure to agents which may lead to immunosuppression, such as chemotherapy. Of patients with HCAC, the majority (n = 38, 69.1%) were initially admitted to the general medicine service and not to the ICU.

A multitude of various yeast species were recovered (Figure 1). Overall, nonalbicans candida were responsible for nearly 60% of all infections. Nonalbicans yeast were as likely to be recovered in HCAC as in nosocomial yeast infection. Among both types of Candidemia, C. krusei was a rare culprit accounting for fewer than 2% of infections. C. glabrata, however, occurred more often in HCAC. Specifically, C. glabrata represented 1 in 5 cases of HCAC as opposed to approximately 10% of all nosocomial yeast BSIs (P = 0.05). In part reflecting this, fluconazole resistance was noted more often in HCAC (18.2% of patients vs. 7.7% among nosocomial candidemia, P = 0.036). There was no difference in the eventual diagnosis of deep‐seeded yeast infections (ie, endocarditis, endopthlamitis, or osteomyelitis) between those with HCAC and persons with nosocomial candidemia (3 cases in each group).

Figure 1

Discussion

This analysis demonstrates that HCAC accounts for approximately a quarter of all candidemia. Our findings underscore that candidemia can present to the emergency department as an HAI and may potentially be initially cared for by a hospitalist. In addition, patients with HCAC and nosocomial candidemia share many attributes. Furthermore, nonalbicans yeast are as prevalent in HCAC as in nosocomial candidal infection. Nonetheless, there appear to be important differences in these syndromes. Immunosuppression appears to be more common in HCAC as does infection due to C. glabrata.

Others have explored the concept of HCAC. Kung et al.10 described community‐onset candidemia at a single center over a 10‐year period. They described 56 patients and noted that the majority had been recently hospitalized or had ongoing interaction with the healthcare system. Sofair et al.11 followed subjects presenting to emergency departments with candidemia. Overall, more than one‐third met criteria for community‐onset infection. In this analysis, though, Sofair et al.11 did not distinguish between community‐acquired processes and HCAC. From a population perspective, Chen et al.12 explored candidemia in Australia. Among over 1000 patients, the noted that 11.6% represented HCAC and, as we note, that select nonalbicans yeast occurred more often in HCAC than in nosocomial candidemia. Our project builds on and adds to these earlier efforts. First, we confirm the general observation that candidemia is no longer solely a nosocomial pathogen. Second, unlike several of these earlier reports we examined a larger cohort of candidemia. Third, beyond the observations of Chen et al.,12 we note that currently, the proportion of Candidal BSI classified as HACA relative to nosocomial candidemia seems larger than reported in the past. Finally, a unique aspect of our report is that we employed express criteria to define HAI.

Our findings have several implications. First, hospitalists and emergency department physicians, along with others, must remain vigilant when approaching patients presenting to the hospital with signs and symptoms of BSI and multiple risk factors for candidal BSI. The fact that the patient has not been hospitalized should not preclude consideration of and treatment for candidemia. The current evidence does not support broad, empiric use of antifungal agents, as this would lead to excessive costs and potentially expose many patients to unnecessary antifungal coverage. On the other hand, given the association between delayed antifungal therapy and the risk for death in candidemia, failure to consider this infection in at‐risk subjects may have adverse consequences. Second, our observations emphasize the need for clinical risk stratification schemes and rapid diagnostic modalities. Such tools are urgently needed if physicians hope to target antifungal therapies more appropriately. Third, if the clinician opts to initiate therapy for possible HCAC, reliance on fluconazole alone may prove inadequate. As the generalizability of our conclusions is necessarily limited, we recommend that infection control practitioners review local epidemiologic data regarding HCAC so that physicians can have the best available guidance.

Our study has several important limitations. Its retrospective nature exposes it to several forms of bias. The single center design limits the generalizability of our findings. Prospective, multicenter studies are needed to validate our results. Additionally, no universally accepted criteria exist to define HAI syndromes. Nonetheless, the criteria we employed have been used by others. We also lacked data on exposure to recent broad spectrum antimicrobials. Selection pressure via exposure to such agents is a risk factor for candidemia and without this data we cannot gauge the impact of this on our findings. Finally, we cannot control for the possibility that some patients were miscategorized. This could have arisen because of: (1) either limitations inherent in the definition of HCAC or (2) because the clinician delayed the decision to obtain blood cultures. Some patients classified as nosocomial may actually have had HCAC or community‐acquired diseasebut for some reason blood cultures were not drawn at time of admission but were deferred until later. Although a difficult issue to address in any study of the epidemiology of infection, the significance of this misclassification bias must be considered a significant concern.

In summary, Candidemia can be the cause of BSI presenting to the hospital. Moreover, HCAC represents a significant proportion of all Candidemia. Although patients with HCAC and nosocomial candidemia share select characteristics, there appear to be some differences in the microbiology of these syndromes.

In the United States, candida now accounts for between 8% and 12% of all catheter‐associated blood stream infections (BSIs).1 Additionally, crude mortality rates in candidemia exceed 40%, and a recent systematic review demonstrated that the attributable mortality of candidemia ranges from 5% to 71%.2 Candidal BSIs also affect resource utilization. These infections independently increase length of stay and result in substantial excess costs.3 Most cases of candidemia arise in noncritically ill patients and thus may be managed by hospitalists.

Historically, the majority of candidal BSIs were caused by C. albicans. Presently, C. albicans accounts for only half of all yeast BSIs, and approximately 20% of these infections are caused by organisms such as C. glabrata and C. krusei.4 These 2 organisms have either variable or no susceptibility to agents, such as fluconazole, empirically employed against yeast. Parallel with the evolution in microbiology of candidemia has been recognition that inappropriate treatment of these infections independently increases mortality.5 These factors underscore the need for the clinician to treat suspected candidal BSIs aggressively in order to avoid the risks associated with inappropriate treatment.

Efforts to enhance rates of initial appropriate therapy for bacterial infections have encompassed the realization that health care‐associated infections (HAIs) represent a distinct syndrome.6, 7 Traditionally, infections were considered either community‐acquired or nosocomial in origin. However, with the spread of health care delivery beyond the hospital, multiple studies indicate that patients may now present to the emergency department with infections caused by pathogens such as Methicillin‐resistant Staphylococcus aureus (MRSA) and P. aeruginosaorganisms that were previously thought limited to hospital‐acquired processes.69 Furthermore, hospitalists often encounter subjects presenting to the hospital with suspected BSIs who have an active and ongoing interaction with the healthcare system.

The importance of candida as a health care‐associated pathogen in BSI remains unclear. We hypothesized that health care‐associated candidemia (HCAC) represented a distinct clinical entity. In order to confirm our theory, we conducted a retrospective analysis of all cases of candidal BSI at our institution over a 3‐year period.

Methods

We reviewed the records of all patients diagnosed with candidemia at our hospital between January 1, 2004 and December 31, 2006. Our institutional review board approved this study. We included adult patients diagnosed with candidemia. The diagnosis of candidemia was based on the isolation of yeast from the blood in at least one blood culture. We employ the BACTEC 9240 blood Culture System (Becton Dickinson Microbiology Systems, Sparks, MD). We excluded subjects who were admitted to the hospital within one month of a known diagnosis of candidemia.

We defined a nosocomial candidal BSI as the diagnosis of candidemia based on cultures drawn after the patient had been hospitalized for >48 hours. We considered HCAC to be present based on previously employed criteria for identifying HAI.69 Specifically, for patients with candidemia based on blood cultures obtained within 48 hours of hospitalization, a patient had to meet at least 1 of the following criteria: (1) receipt of intravenous therapy outside the hospital, (2) end stage renal disease necessitating hemodialysis (ESRD requiring HD), (3) hospitalization within previous 30 days, (4) residence in a nursing home or long term care facility, or (5) underwent an invasive procedure as an outpatient within 30 days of presentation. Community‐acquired candidemia was restricted to patients whose index culture was drawn within 48 hours of admission but who failed to meet the definition for HCAC.

The prevalence of the various forms of candidemia served as our primary endpoint. In addition, we compared patients with respect to demographic factors, comorbidities, and severity of illness. Severity of illness was calculated based on the Acute Physiology and Chronic Health Evaluation (APACHE) II score. We further noted rates of immune suppression in the cohort and defined this as treatment with corticosteroids (10 mg of prednisone or equivalent daily for more than 30 consecutive days), other immunosuppressants (eg, methotrexate), or chemotherapy. Those with acquired immune deficiency syndrome (AIDS) or another immunodeficiency syndrome were defined as immunosuppressed as well. We examined the distribution of yeast species across the 3 forms of candidemia. Finally, we assessed the prevalence of fluconazole resistance. Fluconazole susceptibilities were determined based on Etest (AB BIODISK, Solna, Sweden). An isolate was considered resistant to fluconazole if the minimum inhibitory concentration was >64 g/mL.

We compared categorical variables with the Fisher's exact test. Continuous variables were analyzed with either the Student's t‐test or a Mann‐Whitney test, as appropriate. All tests were 2 tailed and a P value of <0.05 was assumed to represent statistical significance. Analyses were performed with Stata 9.1 (Stata Corp., College Station, TX).

Results

The final cohort included 223 subjects. The mean age of the patients was 59.6 15.7 years and 49% were male. Nearly one quarter (n = 55) fulfilled our criteria for HCAC. The remainder met the definition for nosocomial candidemia. We observed no cases of community‐acquired candidemia. Most (n = 33) patients with HCAC had exposure to more than 1 health care‐related source and many were initially admitted to the medicine/hospitalist service as opposed to the intensive care unit (ICU). The most common criteria leading to categorization as HCAC was recent hospitalization (n = 30, 54.5% of all HCAC). The median time from recent hospitalization to admission was 17 days (Range: 5‐28 days). Other common reasons for classification as HCAC included ESRD requiring HD (30.9%), residence in a nursing home (25.5%), and undergoing an invasive outpatient procedure (16.4%). More than 75% of subjects with HCAC (n = 42) had central venous catheters in place at presentation. Between 2004 and 2006, the proportion of all candidemia due to HCAC increased from 20.9% to 26.9%, but this difference was not statistically significant.

Patients with HCAC were similar to those with nosocomial candidemia (Table 1). There was no difference in either severity of illness or the frequency of neutropenia. The prevalence of most comorbidities did not differ between those with nosocomial candidemia and persons with HCAC. However, immunosuppression was more prevalent among patients with HCAC (prevalence ratio, 1.67; 95% CI, 1.13‐3.08; P = 0.004). In part this finding is expected given that our definition of HCAC includes exposure to agents which may lead to immunosuppression, such as chemotherapy. Of patients with HCAC, the majority (n = 38, 69.1%) were initially admitted to the general medicine service and not to the ICU.

A multitude of various yeast species were recovered (Figure 1). Overall, nonalbicans candida were responsible for nearly 60% of all infections. Nonalbicans yeast were as likely to be recovered in HCAC as in nosocomial yeast infection. Among both types of Candidemia, C. krusei was a rare culprit accounting for fewer than 2% of infections. C. glabrata, however, occurred more often in HCAC. Specifically, C. glabrata represented 1 in 5 cases of HCAC as opposed to approximately 10% of all nosocomial yeast BSIs (P = 0.05). In part reflecting this, fluconazole resistance was noted more often in HCAC (18.2% of patients vs. 7.7% among nosocomial candidemia, P = 0.036). There was no difference in the eventual diagnosis of deep‐seeded yeast infections (ie, endocarditis, endopthlamitis, or osteomyelitis) between those with HCAC and persons with nosocomial candidemia (3 cases in each group).

Figure 1

Discussion

This analysis demonstrates that HCAC accounts for approximately a quarter of all candidemia. Our findings underscore that candidemia can present to the emergency department as an HAI and may potentially be initially cared for by a hospitalist. In addition, patients with HCAC and nosocomial candidemia share many attributes. Furthermore, nonalbicans yeast are as prevalent in HCAC as in nosocomial candidal infection. Nonetheless, there appear to be important differences in these syndromes. Immunosuppression appears to be more common in HCAC as does infection due to C. glabrata.

Others have explored the concept of HCAC. Kung et al.10 described community‐onset candidemia at a single center over a 10‐year period. They described 56 patients and noted that the majority had been recently hospitalized or had ongoing interaction with the healthcare system. Sofair et al.11 followed subjects presenting to emergency departments with candidemia. Overall, more than one‐third met criteria for community‐onset infection. In this analysis, though, Sofair et al.11 did not distinguish between community‐acquired processes and HCAC. From a population perspective, Chen et al.12 explored candidemia in Australia. Among over 1000 patients, the noted that 11.6% represented HCAC and, as we note, that select nonalbicans yeast occurred more often in HCAC than in nosocomial candidemia. Our project builds on and adds to these earlier efforts. First, we confirm the general observation that candidemia is no longer solely a nosocomial pathogen. Second, unlike several of these earlier reports we examined a larger cohort of candidemia. Third, beyond the observations of Chen et al.,12 we note that currently, the proportion of Candidal BSI classified as HACA relative to nosocomial candidemia seems larger than reported in the past. Finally, a unique aspect of our report is that we employed express criteria to define HAI.

Our findings have several implications. First, hospitalists and emergency department physicians, along with others, must remain vigilant when approaching patients presenting to the hospital with signs and symptoms of BSI and multiple risk factors for candidal BSI. The fact that the patient has not been hospitalized should not preclude consideration of and treatment for candidemia. The current evidence does not support broad, empiric use of antifungal agents, as this would lead to excessive costs and potentially expose many patients to unnecessary antifungal coverage. On the other hand, given the association between delayed antifungal therapy and the risk for death in candidemia, failure to consider this infection in at‐risk subjects may have adverse consequences. Second, our observations emphasize the need for clinical risk stratification schemes and rapid diagnostic modalities. Such tools are urgently needed if physicians hope to target antifungal therapies more appropriately. Third, if the clinician opts to initiate therapy for possible HCAC, reliance on fluconazole alone may prove inadequate. As the generalizability of our conclusions is necessarily limited, we recommend that infection control practitioners review local epidemiologic data regarding HCAC so that physicians can have the best available guidance.

Our study has several important limitations. Its retrospective nature exposes it to several forms of bias. The single center design limits the generalizability of our findings. Prospective, multicenter studies are needed to validate our results. Additionally, no universally accepted criteria exist to define HAI syndromes. Nonetheless, the criteria we employed have been used by others. We also lacked data on exposure to recent broad spectrum antimicrobials. Selection pressure via exposure to such agents is a risk factor for candidemia and without this data we cannot gauge the impact of this on our findings. Finally, we cannot control for the possibility that some patients were miscategorized. This could have arisen because of: (1) either limitations inherent in the definition of HCAC or (2) because the clinician delayed the decision to obtain blood cultures. Some patients classified as nosocomial may actually have had HCAC or community‐acquired diseasebut for some reason blood cultures were not drawn at time of admission but were deferred until later. Although a difficult issue to address in any study of the epidemiology of infection, the significance of this misclassification bias must be considered a significant concern.

In summary, Candidemia can be the cause of BSI presenting to the hospital. Moreover, HCAC represents a significant proportion of all Candidemia. Although patients with HCAC and nosocomial candidemia share select characteristics, there appear to be some differences in the microbiology of these syndromes.

Patients who leave a hospital against medical advice (AMA) have increased risks of negative clinical outcomes. Leaving a hospital AMA has been associated with increased risks of emergency department and hospital readmission, longer lengths of stay upon hospital readmission, increased risk of morbidities, and increased mortality.13 Ibrahim et al.4 estimated that 1.44% of all hospitalizations for adults in the United States end with the patient leaving AMA. Prior research, however, has shown that specific patient populations may experience greater AMA discharge rates, as up to 4.9% of asthma‐related hospitalizations,2 13% of human immunodeficiency virus (HIV)‐related hospitalizations,1 and 30% of psychiatric‐related hospitalizations have been shown to end with the patient leaving AMA.5

A small body of research examines the reasons that patients leave AMA. In prior studies, dissatisfaction with care and conflicts with medical staff were among the most commonly cited reasons given by patients.2, 6 In a study of healthcare provider reflections on recent patients who left AMA, providers identified patient mistrust, suboptimal physician‐patient communication, and physician‐patient conflict as important contributors to the patient leaving AMA.7

Sickle‐cell disease (SCD) is a painful genetic condition which in the United States affects mostly African Americans and leads to frequent hospital utilization. Patients with SCD frequently report having poor‐quality interpersonal relations with health care providers when the patient seeks treatment for his or her pain.8 Patients often report that their health care providers do not believe the patient's reports of pain, providers do not involve the patient to his or her satisfaction in setting the course of care, and providers typically stigmatize the patient as having a substance abuse problem.817 Indeed, a recent systematic review has shown that there is a high level of evidence that negative health care provider attitudes serve as a barrier to appropriate pain management in SCD.18

To our knowledge, the only study to date of hospital self‐discharge history among adults with SCD was conducted in the United Kingdom by Elander et al.19 These investigators found that 14% of their sample of patients reported ever having discharged themselves from a hospital. The most common reasons for this behavior given by these patients were that they grew tired of waiting for relief of their pain, there were other conflicts that occurred on the medical ward, and because they just simply wanted to go home.

Given the interpersonal conflicts and poor‐quality pain management often found in SCD care, additional examinations of hospital self‐discharge in this population are warranted. We hypothesized that SCD patient reports of interpersonal conflict during previous health care encounters would have an independent association with the likelihood of the patient having ever self‐discharged from a hospital. We also hypothesized that there would be an independent association between a patient's level of trust in the medical profession and their self‐discharge history. The aim of this study was to test these hypotheses.

Methods

Results

Discussion

In this study, we found that a high proportion of patients with SCD had a history of hospital self‐discharge. Patients with lower trust, and those who reported difficulty in persuading medical staff about sickle‐cell pain, were more likely to report having ever self‐discharged from a hospital, even after controlling for self‐reported hospital utilization for sickle‐cell pain, and the patient's 5‐year toxicology screen history. Because hospital self‐discharge is potentially dangerous,13 our study reveals an understudied aspect of how low trust and poor health care experiences may put patients with SCD at risk for poor outcomes.

In our study, 46.5% of our sample reported ever having self‐discharged from a hospital, which is much higher than the 14% found by Elander et al.19 in their United Kingdom (London‐based) sample. Other differences in our 2 patient populations may account for this discrepancy. Compared to the Elander sample, a much greater percentage of our patients reported ever having difficulty persuading medical staff about their pain (65% vs. 39%). As difficulty persuading medical staff about pain was independently associated with an increased hospital self‐discharge history in our study, one might expect that our sample, which had a higher percentage of patients reporting difficulty, would also be found to have a higher percentage of patients reporting a history of hospital self‐discharge. A second difference between the two patient samples is that our sample of patients experienced a greater number of hospital visits in the 12 months preceding the study compared to the Elander et al.19 sample. If this difference reflects an underlying difference in the overall hospital utilization experiences of the 2 groups, then our sample of adults would have greater opportunities, on average, than the Elander et al.19 sample to experience hospital self‐discharge. Other factors, such as patient behavioral or cultural differences between patients in the United Kingdom (with a national health system) and the United States (without a national health system), might be explored in future studies.

It is important to note that the wording of the hospital self‐discharge item as used both in our study and by Elander et al.19 would not only capture AMA discharges, but additionally may capture other sudden decisions about hospital discharge made by patients. A national‐level study of AMA discharges among adults with SCD in the United States that uses hospital records and/or chart review is needed in order to provide a more generalizable estimate of the prevalence of AMA discharge among this patient population in the United States.

Elander et al.19 suggest that while hospital self‐discharge among SCD patients may be interpreted by many as a sign that the patient engages in problematic use of opioids or other substances, it may be more appropriate to view this behavior as a sign that the patient has received inadequate management of their pain.19 In our study, hospital self‐discharge tended to be associated with having a history of substance abuse as operationalized by a positive toxicology screen for cocaine or marijuana use during any admission in the previous 5 years. Elander et al.19 found that hospital self‐discharge and other so‐called concern raising behaviors such as use of illicit substances were found to be significantly associated with patient attempts to obtain relief from their pain, but were not significantly associated with symptoms of actual substance dependence or addiction. For example, each instance of illicit substance use reported by the patients in the Elander et al.19 study described patient attempts to use marijuana in efforts to manage pain, to relax, or as alternatives to prescribed analgesics. Clinicians in the United States who observe positive toxicology screen results for SCD patients may see these results as casting doubt upon the legitimacy of the patient's pain reports, thus causing a reduction in the amount of pain medicine provided to the patient, when in fact, a substantial percentage of these results may reflect SCD patients attempts to manage their pain outside of a hospital setting. This potential discrepancy between clinician interpretations of the meaning of positive toxicology screen results for SCD patients, and the actual significance of these results for many patients as reflecting attempts to manage pain, could contribute to interpersonal conflicts between the clinicians and patients, and ultimately, patient self‐discharge and decreases in patient trust in clinicians. Further, to the extent that SCD patient positive toxicology screen results reflect use of illicit substances for reasons other than attempts to manage pain, this should signal for clinicians a need to refer the patient for substance abuse treatment and counseling in addition to (and not instead of) efforts to manage the patient's pain.

Our study is among the first to show empirically that persons with a history of hospital self‐discharge have lower levels of trust in the medical profession. Discharging himself or herself from a hospital could cause a patient to view future health care experiences in a more negative light, and cause the patient to have lower trust in the medical profession. Healthcare providers often label patients with a history of leaving AMA as challenging patients. Seeing in the medical record that a patient has left AMA before may bias the provider to view the patient in a more negative light, and consequently affect the quality of their communication with the patient, leading to lower patient trust. Alternatively, a patient could already possess lower trust in the medical profession due to poor‐quality interpersonal experiences, and thus be more likely to self‐discharge from a hospital during a future acute care visit due to a heightened wariness or greater level of anxiety.

The most consistent and robust predictors of trust found across studies in the literature are the quality of previous interactions with medical care.23 Poor physician communication, and experiences of conflict with staff have been associated with lower ratings of trust among a wide variety of patient populations.2427 Interestingly, we found a relationship between trust and hospital self‐discharge even after controlling for the quality of previous interpersonal experiences as measured by prior difficulty persuading staff about pain. Future studies should examine the relationship between trust and hospital self‐discharge history while controlling for other measures of previous interpersonal healthcare experiences among this patient population.

There are limitations to the current study that must be considered. First, as a single‐institution study, these results may not be generalizable to patients with SCD seeking care at other institutions. Also, we did not assess the actual reasons why patients chose to self‐discharge. Thus, while our data suggests that patient perceptions of poor‐quality care contributed to this behavior, we cannot state this definitively. The validity of a self‐reported annual hospital utilization measure as used in this study may be limited by inaccurate patient recall. However, we compared our patient's self‐report of annual hospital utilization with chart documented hospital utilization in the previous 12 months and found that the 2 measures were correlated in the appropriate direction, thereby giving us greater confidence in the validity of our self‐reported measure. Finally, the cross‐sectional nature of the data in this study makes it impossible to specify with certainty the causal directionality of the associations found here. Prospective research must be conducted to help tease apart the potentially complex relationships among trust, interpersonal experiences with care, and hospital self‐discharge.

Adults with SCD who have ever self‐discharged from a hospital have lower trust in the medical profession, and are more likely to report having had prior difficulty persuading medical staff about their sickle‐cell pain. The clinical consequences of hospital self‐discharge in this patient population must be examined, and the specific reasons behind this behavior must be further elucidated, so that clinicians and researchers may be able to design interventions to mitigate the occurrence of this potentially dangerous phenomenon.

Patients who leave a hospital against medical advice (AMA) have increased risks of negative clinical outcomes. Leaving a hospital AMA has been associated with increased risks of emergency department and hospital readmission, longer lengths of stay upon hospital readmission, increased risk of morbidities, and increased mortality.13 Ibrahim et al.4 estimated that 1.44% of all hospitalizations for adults in the United States end with the patient leaving AMA. Prior research, however, has shown that specific patient populations may experience greater AMA discharge rates, as up to 4.9% of asthma‐related hospitalizations,2 13% of human immunodeficiency virus (HIV)‐related hospitalizations,1 and 30% of psychiatric‐related hospitalizations have been shown to end with the patient leaving AMA.5

A small body of research examines the reasons that patients leave AMA. In prior studies, dissatisfaction with care and conflicts with medical staff were among the most commonly cited reasons given by patients.2, 6 In a study of healthcare provider reflections on recent patients who left AMA, providers identified patient mistrust, suboptimal physician‐patient communication, and physician‐patient conflict as important contributors to the patient leaving AMA.7

Sickle‐cell disease (SCD) is a painful genetic condition which in the United States affects mostly African Americans and leads to frequent hospital utilization. Patients with SCD frequently report having poor‐quality interpersonal relations with health care providers when the patient seeks treatment for his or her pain.8 Patients often report that their health care providers do not believe the patient's reports of pain, providers do not involve the patient to his or her satisfaction in setting the course of care, and providers typically stigmatize the patient as having a substance abuse problem.817 Indeed, a recent systematic review has shown that there is a high level of evidence that negative health care provider attitudes serve as a barrier to appropriate pain management in SCD.18

To our knowledge, the only study to date of hospital self‐discharge history among adults with SCD was conducted in the United Kingdom by Elander et al.19 These investigators found that 14% of their sample of patients reported ever having discharged themselves from a hospital. The most common reasons for this behavior given by these patients were that they grew tired of waiting for relief of their pain, there were other conflicts that occurred on the medical ward, and because they just simply wanted to go home.

Given the interpersonal conflicts and poor‐quality pain management often found in SCD care, additional examinations of hospital self‐discharge in this population are warranted. We hypothesized that SCD patient reports of interpersonal conflict during previous health care encounters would have an independent association with the likelihood of the patient having ever self‐discharged from a hospital. We also hypothesized that there would be an independent association between a patient's level of trust in the medical profession and their self‐discharge history. The aim of this study was to test these hypotheses.

Methods

Results

Discussion

In this study, we found that a high proportion of patients with SCD had a history of hospital self‐discharge. Patients with lower trust, and those who reported difficulty in persuading medical staff about sickle‐cell pain, were more likely to report having ever self‐discharged from a hospital, even after controlling for self‐reported hospital utilization for sickle‐cell pain, and the patient's 5‐year toxicology screen history. Because hospital self‐discharge is potentially dangerous,13 our study reveals an understudied aspect of how low trust and poor health care experiences may put patients with SCD at risk for poor outcomes.

In our study, 46.5% of our sample reported ever having self‐discharged from a hospital, which is much higher than the 14% found by Elander et al.19 in their United Kingdom (London‐based) sample. Other differences in our 2 patient populations may account for this discrepancy. Compared to the Elander sample, a much greater percentage of our patients reported ever having difficulty persuading medical staff about their pain (65% vs. 39%). As difficulty persuading medical staff about pain was independently associated with an increased hospital self‐discharge history in our study, one might expect that our sample, which had a higher percentage of patients reporting difficulty, would also be found to have a higher percentage of patients reporting a history of hospital self‐discharge. A second difference between the two patient samples is that our sample of patients experienced a greater number of hospital visits in the 12 months preceding the study compared to the Elander et al.19 sample. If this difference reflects an underlying difference in the overall hospital utilization experiences of the 2 groups, then our sample of adults would have greater opportunities, on average, than the Elander et al.19 sample to experience hospital self‐discharge. Other factors, such as patient behavioral or cultural differences between patients in the United Kingdom (with a national health system) and the United States (without a national health system), might be explored in future studies.

It is important to note that the wording of the hospital self‐discharge item as used both in our study and by Elander et al.19 would not only capture AMA discharges, but additionally may capture other sudden decisions about hospital discharge made by patients. A national‐level study of AMA discharges among adults with SCD in the United States that uses hospital records and/or chart review is needed in order to provide a more generalizable estimate of the prevalence of AMA discharge among this patient population in the United States.

Elander et al.19 suggest that while hospital self‐discharge among SCD patients may be interpreted by many as a sign that the patient engages in problematic use of opioids or other substances, it may be more appropriate to view this behavior as a sign that the patient has received inadequate management of their pain.19 In our study, hospital self‐discharge tended to be associated with having a history of substance abuse as operationalized by a positive toxicology screen for cocaine or marijuana use during any admission in the previous 5 years. Elander et al.19 found that hospital self‐discharge and other so‐called concern raising behaviors such as use of illicit substances were found to be significantly associated with patient attempts to obtain relief from their pain, but were not significantly associated with symptoms of actual substance dependence or addiction. For example, each instance of illicit substance use reported by the patients in the Elander et al.19 study described patient attempts to use marijuana in efforts to manage pain, to relax, or as alternatives to prescribed analgesics. Clinicians in the United States who observe positive toxicology screen results for SCD patients may see these results as casting doubt upon the legitimacy of the patient's pain reports, thus causing a reduction in the amount of pain medicine provided to the patient, when in fact, a substantial percentage of these results may reflect SCD patients attempts to manage their pain outside of a hospital setting. This potential discrepancy between clinician interpretations of the meaning of positive toxicology screen results for SCD patients, and the actual significance of these results for many patients as reflecting attempts to manage pain, could contribute to interpersonal conflicts between the clinicians and patients, and ultimately, patient self‐discharge and decreases in patient trust in clinicians. Further, to the extent that SCD patient positive toxicology screen results reflect use of illicit substances for reasons other than attempts to manage pain, this should signal for clinicians a need to refer the patient for substance abuse treatment and counseling in addition to (and not instead of) efforts to manage the patient's pain.

Our study is among the first to show empirically that persons with a history of hospital self‐discharge have lower levels of trust in the medical profession. Discharging himself or herself from a hospital could cause a patient to view future health care experiences in a more negative light, and cause the patient to have lower trust in the medical profession. Healthcare providers often label patients with a history of leaving AMA as challenging patients. Seeing in the medical record that a patient has left AMA before may bias the provider to view the patient in a more negative light, and consequently affect the quality of their communication with the patient, leading to lower patient trust. Alternatively, a patient could already possess lower trust in the medical profession due to poor‐quality interpersonal experiences, and thus be more likely to self‐discharge from a hospital during a future acute care visit due to a heightened wariness or greater level of anxiety.

The most consistent and robust predictors of trust found across studies in the literature are the quality of previous interactions with medical care.23 Poor physician communication, and experiences of conflict with staff have been associated with lower ratings of trust among a wide variety of patient populations.2427 Interestingly, we found a relationship between trust and hospital self‐discharge even after controlling for the quality of previous interpersonal experiences as measured by prior difficulty persuading staff about pain. Future studies should examine the relationship between trust and hospital self‐discharge history while controlling for other measures of previous interpersonal healthcare experiences among this patient population.

There are limitations to the current study that must be considered. First, as a single‐institution study, these results may not be generalizable to patients with SCD seeking care at other institutions. Also, we did not assess the actual reasons why patients chose to self‐discharge. Thus, while our data suggests that patient perceptions of poor‐quality care contributed to this behavior, we cannot state this definitively. The validity of a self‐reported annual hospital utilization measure as used in this study may be limited by inaccurate patient recall. However, we compared our patient's self‐report of annual hospital utilization with chart documented hospital utilization in the previous 12 months and found that the 2 measures were correlated in the appropriate direction, thereby giving us greater confidence in the validity of our self‐reported measure. Finally, the cross‐sectional nature of the data in this study makes it impossible to specify with certainty the causal directionality of the associations found here. Prospective research must be conducted to help tease apart the potentially complex relationships among trust, interpersonal experiences with care, and hospital self‐discharge.

Adults with SCD who have ever self‐discharged from a hospital have lower trust in the medical profession, and are more likely to report having had prior difficulty persuading medical staff about their sickle‐cell pain. The clinical consequences of hospital self‐discharge in this patient population must be examined, and the specific reasons behind this behavior must be further elucidated, so that clinicians and researchers may be able to design interventions to mitigate the occurrence of this potentially dangerous phenomenon.

Patients who leave a hospital against medical advice (AMA) have increased risks of negative clinical outcomes. Leaving a hospital AMA has been associated with increased risks of emergency department and hospital readmission, longer lengths of stay upon hospital readmission, increased risk of morbidities, and increased mortality.13 Ibrahim et al.4 estimated that 1.44% of all hospitalizations for adults in the United States end with the patient leaving AMA. Prior research, however, has shown that specific patient populations may experience greater AMA discharge rates, as up to 4.9% of asthma‐related hospitalizations,2 13% of human immunodeficiency virus (HIV)‐related hospitalizations,1 and 30% of psychiatric‐related hospitalizations have been shown to end with the patient leaving AMA.5

A small body of research examines the reasons that patients leave AMA. In prior studies, dissatisfaction with care and conflicts with medical staff were among the most commonly cited reasons given by patients.2, 6 In a study of healthcare provider reflections on recent patients who left AMA, providers identified patient mistrust, suboptimal physician‐patient communication, and physician‐patient conflict as important contributors to the patient leaving AMA.7

Sickle‐cell disease (SCD) is a painful genetic condition which in the United States affects mostly African Americans and leads to frequent hospital utilization. Patients with SCD frequently report having poor‐quality interpersonal relations with health care providers when the patient seeks treatment for his or her pain.8 Patients often report that their health care providers do not believe the patient's reports of pain, providers do not involve the patient to his or her satisfaction in setting the course of care, and providers typically stigmatize the patient as having a substance abuse problem.817 Indeed, a recent systematic review has shown that there is a high level of evidence that negative health care provider attitudes serve as a barrier to appropriate pain management in SCD.18

To our knowledge, the only study to date of hospital self‐discharge history among adults with SCD was conducted in the United Kingdom by Elander et al.19 These investigators found that 14% of their sample of patients reported ever having discharged themselves from a hospital. The most common reasons for this behavior given by these patients were that they grew tired of waiting for relief of their pain, there were other conflicts that occurred on the medical ward, and because they just simply wanted to go home.

Given the interpersonal conflicts and poor‐quality pain management often found in SCD care, additional examinations of hospital self‐discharge in this population are warranted. We hypothesized that SCD patient reports of interpersonal conflict during previous health care encounters would have an independent association with the likelihood of the patient having ever self‐discharged from a hospital. We also hypothesized that there would be an independent association between a patient's level of trust in the medical profession and their self‐discharge history. The aim of this study was to test these hypotheses.

Methods

Results

Discussion

In this study, we found that a high proportion of patients with SCD had a history of hospital self‐discharge. Patients with lower trust, and those who reported difficulty in persuading medical staff about sickle‐cell pain, were more likely to report having ever self‐discharged from a hospital, even after controlling for self‐reported hospital utilization for sickle‐cell pain, and the patient's 5‐year toxicology screen history. Because hospital self‐discharge is potentially dangerous,13 our study reveals an understudied aspect of how low trust and poor health care experiences may put patients with SCD at risk for poor outcomes.

In our study, 46.5% of our sample reported ever having self‐discharged from a hospital, which is much higher than the 14% found by Elander et al.19 in their United Kingdom (London‐based) sample. Other differences in our 2 patient populations may account for this discrepancy. Compared to the Elander sample, a much greater percentage of our patients reported ever having difficulty persuading medical staff about their pain (65% vs. 39%). As difficulty persuading medical staff about pain was independently associated with an increased hospital self‐discharge history in our study, one might expect that our sample, which had a higher percentage of patients reporting difficulty, would also be found to have a higher percentage of patients reporting a history of hospital self‐discharge. A second difference between the two patient samples is that our sample of patients experienced a greater number of hospital visits in the 12 months preceding the study compared to the Elander et al.19 sample. If this difference reflects an underlying difference in the overall hospital utilization experiences of the 2 groups, then our sample of adults would have greater opportunities, on average, than the Elander et al.19 sample to experience hospital self‐discharge. Other factors, such as patient behavioral or cultural differences between patients in the United Kingdom (with a national health system) and the United States (without a national health system), might be explored in future studies.

It is important to note that the wording of the hospital self‐discharge item as used both in our study and by Elander et al.19 would not only capture AMA discharges, but additionally may capture other sudden decisions about hospital discharge made by patients. A national‐level study of AMA discharges among adults with SCD in the United States that uses hospital records and/or chart review is needed in order to provide a more generalizable estimate of the prevalence of AMA discharge among this patient population in the United States.

Elander et al.19 suggest that while hospital self‐discharge among SCD patients may be interpreted by many as a sign that the patient engages in problematic use of opioids or other substances, it may be more appropriate to view this behavior as a sign that the patient has received inadequate management of their pain.19 In our study, hospital self‐discharge tended to be associated with having a history of substance abuse as operationalized by a positive toxicology screen for cocaine or marijuana use during any admission in the previous 5 years. Elander et al.19 found that hospital self‐discharge and other so‐called concern raising behaviors such as use of illicit substances were found to be significantly associated with patient attempts to obtain relief from their pain, but were not significantly associated with symptoms of actual substance dependence or addiction. For example, each instance of illicit substance use reported by the patients in the Elander et al.19 study described patient attempts to use marijuana in efforts to manage pain, to relax, or as alternatives to prescribed analgesics. Clinicians in the United States who observe positive toxicology screen results for SCD patients may see these results as casting doubt upon the legitimacy of the patient's pain reports, thus causing a reduction in the amount of pain medicine provided to the patient, when in fact, a substantial percentage of these results may reflect SCD patients attempts to manage their pain outside of a hospital setting. This potential discrepancy between clinician interpretations of the meaning of positive toxicology screen results for SCD patients, and the actual significance of these results for many patients as reflecting attempts to manage pain, could contribute to interpersonal conflicts between the clinicians and patients, and ultimately, patient self‐discharge and decreases in patient trust in clinicians. Further, to the extent that SCD patient positive toxicology screen results reflect use of illicit substances for reasons other than attempts to manage pain, this should signal for clinicians a need to refer the patient for substance abuse treatment and counseling in addition to (and not instead of) efforts to manage the patient's pain.

Our study is among the first to show empirically that persons with a history of hospital self‐discharge have lower levels of trust in the medical profession. Discharging himself or herself from a hospital could cause a patient to view future health care experiences in a more negative light, and cause the patient to have lower trust in the medical profession. Healthcare providers often label patients with a history of leaving AMA as challenging patients. Seeing in the medical record that a patient has left AMA before may bias the provider to view the patient in a more negative light, and consequently affect the quality of their communication with the patient, leading to lower patient trust. Alternatively, a patient could already possess lower trust in the medical profession due to poor‐quality interpersonal experiences, and thus be more likely to self‐discharge from a hospital during a future acute care visit due to a heightened wariness or greater level of anxiety.

The most consistent and robust predictors of trust found across studies in the literature are the quality of previous interactions with medical care.23 Poor physician communication, and experiences of conflict with staff have been associated with lower ratings of trust among a wide variety of patient populations.2427 Interestingly, we found a relationship between trust and hospital self‐discharge even after controlling for the quality of previous interpersonal experiences as measured by prior difficulty persuading staff about pain. Future studies should examine the relationship between trust and hospital self‐discharge history while controlling for other measures of previous interpersonal healthcare experiences among this patient population.

There are limitations to the current study that must be considered. First, as a single‐institution study, these results may not be generalizable to patients with SCD seeking care at other institutions. Also, we did not assess the actual reasons why patients chose to self‐discharge. Thus, while our data suggests that patient perceptions of poor‐quality care contributed to this behavior, we cannot state this definitively. The validity of a self‐reported annual hospital utilization measure as used in this study may be limited by inaccurate patient recall. However, we compared our patient's self‐report of annual hospital utilization with chart documented hospital utilization in the previous 12 months and found that the 2 measures were correlated in the appropriate direction, thereby giving us greater confidence in the validity of our self‐reported measure. Finally, the cross‐sectional nature of the data in this study makes it impossible to specify with certainty the causal directionality of the associations found here. Prospective research must be conducted to help tease apart the potentially complex relationships among trust, interpersonal experiences with care, and hospital self‐discharge.

Adults with SCD who have ever self‐discharged from a hospital have lower trust in the medical profession, and are more likely to report having had prior difficulty persuading medical staff about their sickle‐cell pain. The clinical consequences of hospital self‐discharge in this patient population must be examined, and the specific reasons behind this behavior must be further elucidated, so that clinicians and researchers may be able to design interventions to mitigate the occurrence of this potentially dangerous phenomenon.

A previously healthy 21‐year‐old man presented with 6 weeks of low‐grade fever, sore throat, red eyes, and hematuria. Physical examination revealed episcleral injection consistent with episcleritis (Figure 1), oral ulcers (Figure 2, black arrows), diffuse fine crackles on chest auscultation and testicular tenderness. Laboratory workup was significant for leukocytosis (14,000 cell/mL), hematuria with red blood cell (RBC) casts and serum creatinine level of 2.1 mg/dL, which subsequently rose rapidly to 4.1 mg/dL. Test for cytoplasmic‐stainingantineutrophil cytoplasmic antibody (C‐ANCA) was positive. Antiproteinase 3 (PR3) antibodies were also positive. Chest x‐ray showed bilateral pulmonary opacities and sinus computed tomography (CT) scan showed mucosal thickening of the sinuses consistent with sinusitis (Figure 3). Renal biopsy revealed segmental necrotizing glomerulonephritis that was pauci‐immune on immunofluorescence staining. The patient was diagnosed with Wegener's granulomatosis with rapidly progressive glomerulonephritis. He was treated with intravenous corticosteroids, cyclophosphamide, and trimethoprim‐sulfamethoxazole. The patient's symptoms and acute renal failure resolved with this medical regimen.

Figure 1

Figure 2

Figure 3

A previously healthy 21‐year‐old man presented with 6 weeks of low‐grade fever, sore throat, red eyes, and hematuria. Physical examination revealed episcleral injection consistent with episcleritis (Figure 1), oral ulcers (Figure 2, black arrows), diffuse fine crackles on chest auscultation and testicular tenderness. Laboratory workup was significant for leukocytosis (14,000 cell/mL), hematuria with red blood cell (RBC) casts and serum creatinine level of 2.1 mg/dL, which subsequently rose rapidly to 4.1 mg/dL. Test for cytoplasmic‐stainingantineutrophil cytoplasmic antibody (C‐ANCA) was positive. Antiproteinase 3 (PR3) antibodies were also positive. Chest x‐ray showed bilateral pulmonary opacities and sinus computed tomography (CT) scan showed mucosal thickening of the sinuses consistent with sinusitis (Figure 3). Renal biopsy revealed segmental necrotizing glomerulonephritis that was pauci‐immune on immunofluorescence staining. The patient was diagnosed with Wegener's granulomatosis with rapidly progressive glomerulonephritis. He was treated with intravenous corticosteroids, cyclophosphamide, and trimethoprim‐sulfamethoxazole. The patient's symptoms and acute renal failure resolved with this medical regimen.

Figure 1

Figure 2

Figure 3

A previously healthy 21‐year‐old man presented with 6 weeks of low‐grade fever, sore throat, red eyes, and hematuria. Physical examination revealed episcleral injection consistent with episcleritis (Figure 1), oral ulcers (Figure 2, black arrows), diffuse fine crackles on chest auscultation and testicular tenderness. Laboratory workup was significant for leukocytosis (14,000 cell/mL), hematuria with red blood cell (RBC) casts and serum creatinine level of 2.1 mg/dL, which subsequently rose rapidly to 4.1 mg/dL. Test for cytoplasmic‐stainingantineutrophil cytoplasmic antibody (C‐ANCA) was positive. Antiproteinase 3 (PR3) antibodies were also positive. Chest x‐ray showed bilateral pulmonary opacities and sinus computed tomography (CT) scan showed mucosal thickening of the sinuses consistent with sinusitis (Figure 3). Renal biopsy revealed segmental necrotizing glomerulonephritis that was pauci‐immune on immunofluorescence staining. The patient was diagnosed with Wegener's granulomatosis with rapidly progressive glomerulonephritis. He was treated with intravenous corticosteroids, cyclophosphamide, and trimethoprim‐sulfamethoxazole. The patient's symptoms and acute renal failure resolved with this medical regimen.

Figure 1

Figure 2

Figure 3

A 51‐year‐old African American woman with medical history of essential hypertension and chronic obstructive pulmonary disease (COPD) presented to the hospital with chest pain and shortness of breath. The chest pain was retrosternal and radiated to the back. It lasted for about an hour and resolved without any intervention. After some time, she again felt discomfort in the chest, which was a constant and dull ache.

She had similar episodes of chest pain 1 week prior, although less severe in intensity, for which she went to an outside hospital before coming to our hospital. Acute coronary syndrome was ruled out with serial cardiac enzymes measurements. An exercise stress test was also performed at that time, which failed to show any stress‐induced ischemia.

Her medications included lisinopril for hypertension and aspirin, which had been started 1 week prior to admission. She gave a 10‐pack‐year history of smoking tobacco. Family history was significant for hypertension in her father and coronary artery disease in her mother at the age of 58 years. A review of systems was negative for fever, cough, orthopnea, wheezing, palpitations, nausea, vomiting, recent surgery, or any significant trauma.

Assessment

The patient's physical examination was only remarkable for a blood pressure (BP) of 181/100 mm Hg. She did not have Marfanoid features, hyperflexible joints, or easy bruisability. Laboratory tests, including complete blood count, comprehensive metabolic panel, and cardiac enzymes, were within normal limits. A contrast‐enhanced computed tomography (CT) of the chest showed a linear hypodense area in the left lateral aspect of the main pulmonary trunk, which suggested an intimal dissection of the main pulmonary artery. Magnetic resonance angiography/emmaging (MRA/MRI) confirmed dissection of the main pulmonary artery extending into the proximal left pulmonary artery and associated with a 12 8 mm² aneurysm (Figures 1 and 2). The entry site of dissection was located in the main pulmonary artery just after its origin and the exit site was located in the left pulmonary artery 5 mm distal to the bifurcation of main pulmonary artery. The pulmonary artery diameter at the dissection was 27 mm.

Figure 1

Figure 2

Diagnosis

To investigate possible etiologies, a transthoracic echocardiogram with Doppler was done to look for pulmonary hypertension. The echocardiogram showed normal pulmonary artery pressure with normal right ventricular systolic pressure. There was no evidence of pericardial effusion or structural cardiac abnormality on echocardiogram. Further investigations including work up for connective tissue diseases and infectious etiologies (Table 1) were normal.

According to Shilkin et al.,1 Helmbrecht first reported pulmonary artery dissection (PAD) in 1842. PAD is very rare and is usually diagnosed at autopsy. There are 71 other cases of PAD reported in the English literature, of which 16 cases are in living patients.217 Unlike aortic dissection, which is fairly common, the reentry circuit for PAD is formed by the rupture of the free wall of the pulmonary artery leading to hemopericardium, cardiac tamponade, and sudden death.2, 8, 9 There is wide variation in age of incidence, ranging from 26 to 85 years of age, with a slightly higher prevalence in females (male‐to‐female ratio 1:1.2).1, 2 The main pulmonary artery is usually involved, with or without involvement of its branches. Isolated left and right pulmonary artery involvement is seen in 6% and 4% of cases, respectively.2

Pulmonary hypertension, either primary or secondary (collagen vascular diseases, COPD, congenital heart diseases, etc.), is the most common underlying etiology. Other less common, but well‐described etiologies include: Marfan's syndrome, instrumentation of pulmonary artery, tuberculosis, syphilis, pregnancy, idiopathic cystic medial necrosis, and amyloidosis.2, 8

As noted earlier, underlying pulmonary hypertension is usually a major risk factor for PAD. More than 75% of the patients have underlying acute or chronic pulmonary hypertension.2 Our patient had COPD without pulmonary hypertension. Despite extensive investigation, no underlying cause of her pulmonary dissection was identified. The differential diagnosis includes cryptogenic cystic medionecrosis; however, because the patient refused surgery the diagnosis remains unknown. As in our case, idiopathic PAD is extremely rare, and only 4 other cases have been described in the literature.2 Underlying etiologies should always be ruled out to identify correctable causes such as congenital abnormalities of the heart leading to pulmonary hypertension.

Chest pain is a very common presenting complaint in the emergency department. Although rare, PAD should be suspected in a patient with retrosternal chest pain when other common causes of chest pain are excluded. Some of the more suggestive findings are the presence of a new diastolic murmur, a wide mediastinum on chest x‐ray, and CT scan of chest showing an intimal flap.2, 8 CT scan of the chest is an acceptable imaging modality to diagnose PAD.18 According to Neimatallah et al.,18 there are only 5 cases in the literature reported with detailed CT scans demonstrating PAD. If the diagnosis remains uncertain, it should be confirmed by MRI/MRA.16 Transthoracic echocardiography can be used for diagnosis and follow‐up of conservatively managed patients with PAD.3, 8, 19 The echocardiographic findings suggestive of PAD include direct or indirect evidence of pulmonary artery hypertension, with a large main pulmonary artery and an intimal flap across the pulmonary trunk.

Management

No consensus strategy is available for the management of PAD because of the rarity of this condition. In general, operative repair is the treatment of choice for PAD.2, 8, 9, 11 There are 16 cases diagnosed in living patients, out of which 6 were managed medically, 8 were managed surgically, and management was not discussed in 2 of the case reports (Table 2). In these case reports, medically managed patients were treated with oxygen, vasodilators (nitrates, angiotensin‐converting enzyme [ACE] inhibitors, dihydropyridine calcium channel blockers, sildenafil), diuretics and beta‐blockers. These patients did well on follow‐up, ranging from 3 weeks to 4 years, except for 1 who died on day 4 in the intensive care unit (ICU).

Conservative management may be tried in patients who are hemodynamically stable and do not have pericardial effusion.2, 9 The aim of conservative management is to decrease right ventricular preload and afterload. Preload reduction can be dangerous in patients with PAD and should be done in the intensive care setting as this can lead to profound hypotension. Nitrates for preload reduction should be used cautiously in patients taking sildenafil or similar agents for erectile dysfunction or pulmonary artery hypertension because of significant risk of cardiovascular collapse. The American Heart Association and American College of Cardiology both recommend that there should be a time gap of at least 24 hours between the last dose of sildenafil and the first dose of nitrates. Conservatively managed patients should be followed with interval CT scans2, 9, 18 or echocardiography.3, 19 In addition, the underlying etiology should always be investigated to predict prognosis and recommend future management strategies.

The patient was offered surgical repair but she declined. She was managed conservatively with nitrates and beta‐blockers and was pain free within 24 hours. Her BP was brought down to a systolic BP range of 130140 mm Hg. A repeat CT scan of the chest at 1‐month follow up was unchanged. The patient was doing well at 6‐month follow‐up.

Conclusions

PAD is an extremely rare cause of chest pain and a rare antemortem diagnosis. It is usually associated with underlying pulmonary hypertension. This case describes a patient with PAD in the absence of pulmonary hypertension. The patient was managed with conservative medical therapy and did well at 6‐month follow‐up. There are a total of 6 other case reports of patients with PAD managed conservatively, out of which 5 patients did well at follow‐up and 1 patient died. More case reports and longer follow‐up are needed to assess the effectiveness of conservative medical therapy in patients with PAD. To our knowledge, this is the first case report of idiopathic PAD diagnosed in a living patient and managed conservatively. This case also highlights better prognosis for patients with PAD without underlying pulmonary hypertension.

A 51‐year‐old African American woman with medical history of essential hypertension and chronic obstructive pulmonary disease (COPD) presented to the hospital with chest pain and shortness of breath. The chest pain was retrosternal and radiated to the back. It lasted for about an hour and resolved without any intervention. After some time, she again felt discomfort in the chest, which was a constant and dull ache.

She had similar episodes of chest pain 1 week prior, although less severe in intensity, for which she went to an outside hospital before coming to our hospital. Acute coronary syndrome was ruled out with serial cardiac enzymes measurements. An exercise stress test was also performed at that time, which failed to show any stress‐induced ischemia.

Her medications included lisinopril for hypertension and aspirin, which had been started 1 week prior to admission. She gave a 10‐pack‐year history of smoking tobacco. Family history was significant for hypertension in her father and coronary artery disease in her mother at the age of 58 years. A review of systems was negative for fever, cough, orthopnea, wheezing, palpitations, nausea, vomiting, recent surgery, or any significant trauma.

Assessment

The patient's physical examination was only remarkable for a blood pressure (BP) of 181/100 mm Hg. She did not have Marfanoid features, hyperflexible joints, or easy bruisability. Laboratory tests, including complete blood count, comprehensive metabolic panel, and cardiac enzymes, were within normal limits. A contrast‐enhanced computed tomography (CT) of the chest showed a linear hypodense area in the left lateral aspect of the main pulmonary trunk, which suggested an intimal dissection of the main pulmonary artery. Magnetic resonance angiography/emmaging (MRA/MRI) confirmed dissection of the main pulmonary artery extending into the proximal left pulmonary artery and associated with a 12 8 mm² aneurysm (Figures 1 and 2). The entry site of dissection was located in the main pulmonary artery just after its origin and the exit site was located in the left pulmonary artery 5 mm distal to the bifurcation of main pulmonary artery. The pulmonary artery diameter at the dissection was 27 mm.

Figure 1

Figure 2

Diagnosis

To investigate possible etiologies, a transthoracic echocardiogram with Doppler was done to look for pulmonary hypertension. The echocardiogram showed normal pulmonary artery pressure with normal right ventricular systolic pressure. There was no evidence of pericardial effusion or structural cardiac abnormality on echocardiogram. Further investigations including work up for connective tissue diseases and infectious etiologies (Table 1) were normal.

According to Shilkin et al.,1 Helmbrecht first reported pulmonary artery dissection (PAD) in 1842. PAD is very rare and is usually diagnosed at autopsy. There are 71 other cases of PAD reported in the English literature, of which 16 cases are in living patients.217 Unlike aortic dissection, which is fairly common, the reentry circuit for PAD is formed by the rupture of the free wall of the pulmonary artery leading to hemopericardium, cardiac tamponade, and sudden death.2, 8, 9 There is wide variation in age of incidence, ranging from 26 to 85 years of age, with a slightly higher prevalence in females (male‐to‐female ratio 1:1.2).1, 2 The main pulmonary artery is usually involved, with or without involvement of its branches. Isolated left and right pulmonary artery involvement is seen in 6% and 4% of cases, respectively.2

Pulmonary hypertension, either primary or secondary (collagen vascular diseases, COPD, congenital heart diseases, etc.), is the most common underlying etiology. Other less common, but well‐described etiologies include: Marfan's syndrome, instrumentation of pulmonary artery, tuberculosis, syphilis, pregnancy, idiopathic cystic medial necrosis, and amyloidosis.2, 8

As noted earlier, underlying pulmonary hypertension is usually a major risk factor for PAD. More than 75% of the patients have underlying acute or chronic pulmonary hypertension.2 Our patient had COPD without pulmonary hypertension. Despite extensive investigation, no underlying cause of her pulmonary dissection was identified. The differential diagnosis includes cryptogenic cystic medionecrosis; however, because the patient refused surgery the diagnosis remains unknown. As in our case, idiopathic PAD is extremely rare, and only 4 other cases have been described in the literature.2 Underlying etiologies should always be ruled out to identify correctable causes such as congenital abnormalities of the heart leading to pulmonary hypertension.

Chest pain is a very common presenting complaint in the emergency department. Although rare, PAD should be suspected in a patient with retrosternal chest pain when other common causes of chest pain are excluded. Some of the more suggestive findings are the presence of a new diastolic murmur, a wide mediastinum on chest x‐ray, and CT scan of chest showing an intimal flap.2, 8 CT scan of the chest is an acceptable imaging modality to diagnose PAD.18 According to Neimatallah et al.,18 there are only 5 cases in the literature reported with detailed CT scans demonstrating PAD. If the diagnosis remains uncertain, it should be confirmed by MRI/MRA.16 Transthoracic echocardiography can be used for diagnosis and follow‐up of conservatively managed patients with PAD.3, 8, 19 The echocardiographic findings suggestive of PAD include direct or indirect evidence of pulmonary artery hypertension, with a large main pulmonary artery and an intimal flap across the pulmonary trunk.

Management

No consensus strategy is available for the management of PAD because of the rarity of this condition. In general, operative repair is the treatment of choice for PAD.2, 8, 9, 11 There are 16 cases diagnosed in living patients, out of which 6 were managed medically, 8 were managed surgically, and management was not discussed in 2 of the case reports (Table 2). In these case reports, medically managed patients were treated with oxygen, vasodilators (nitrates, angiotensin‐converting enzyme [ACE] inhibitors, dihydropyridine calcium channel blockers, sildenafil), diuretics and beta‐blockers. These patients did well on follow‐up, ranging from 3 weeks to 4 years, except for 1 who died on day 4 in the intensive care unit (ICU).

Conservative management may be tried in patients who are hemodynamically stable and do not have pericardial effusion.2, 9 The aim of conservative management is to decrease right ventricular preload and afterload. Preload reduction can be dangerous in patients with PAD and should be done in the intensive care setting as this can lead to profound hypotension. Nitrates for preload reduction should be used cautiously in patients taking sildenafil or similar agents for erectile dysfunction or pulmonary artery hypertension because of significant risk of cardiovascular collapse. The American Heart Association and American College of Cardiology both recommend that there should be a time gap of at least 24 hours between the last dose of sildenafil and the first dose of nitrates. Conservatively managed patients should be followed with interval CT scans2, 9, 18 or echocardiography.3, 19 In addition, the underlying etiology should always be investigated to predict prognosis and recommend future management strategies.

The patient was offered surgical repair but she declined. She was managed conservatively with nitrates and beta‐blockers and was pain free within 24 hours. Her BP was brought down to a systolic BP range of 130140 mm Hg. A repeat CT scan of the chest at 1‐month follow up was unchanged. The patient was doing well at 6‐month follow‐up.

Conclusions

PAD is an extremely rare cause of chest pain and a rare antemortem diagnosis. It is usually associated with underlying pulmonary hypertension. This case describes a patient with PAD in the absence of pulmonary hypertension. The patient was managed with conservative medical therapy and did well at 6‐month follow‐up. There are a total of 6 other case reports of patients with PAD managed conservatively, out of which 5 patients did well at follow‐up and 1 patient died. More case reports and longer follow‐up are needed to assess the effectiveness of conservative medical therapy in patients with PAD. To our knowledge, this is the first case report of idiopathic PAD diagnosed in a living patient and managed conservatively. This case also highlights better prognosis for patients with PAD without underlying pulmonary hypertension.

A 51‐year‐old African American woman with medical history of essential hypertension and chronic obstructive pulmonary disease (COPD) presented to the hospital with chest pain and shortness of breath. The chest pain was retrosternal and radiated to the back. It lasted for about an hour and resolved without any intervention. After some time, she again felt discomfort in the chest, which was a constant and dull ache.

She had similar episodes of chest pain 1 week prior, although less severe in intensity, for which she went to an outside hospital before coming to our hospital. Acute coronary syndrome was ruled out with serial cardiac enzymes measurements. An exercise stress test was also performed at that time, which failed to show any stress‐induced ischemia.

Her medications included lisinopril for hypertension and aspirin, which had been started 1 week prior to admission. She gave a 10‐pack‐year history of smoking tobacco. Family history was significant for hypertension in her father and coronary artery disease in her mother at the age of 58 years. A review of systems was negative for fever, cough, orthopnea, wheezing, palpitations, nausea, vomiting, recent surgery, or any significant trauma.

Assessment

The patient's physical examination was only remarkable for a blood pressure (BP) of 181/100 mm Hg. She did not have Marfanoid features, hyperflexible joints, or easy bruisability. Laboratory tests, including complete blood count, comprehensive metabolic panel, and cardiac enzymes, were within normal limits. A contrast‐enhanced computed tomography (CT) of the chest showed a linear hypodense area in the left lateral aspect of the main pulmonary trunk, which suggested an intimal dissection of the main pulmonary artery. Magnetic resonance angiography/emmaging (MRA/MRI) confirmed dissection of the main pulmonary artery extending into the proximal left pulmonary artery and associated with a 12 8 mm² aneurysm (Figures 1 and 2). The entry site of dissection was located in the main pulmonary artery just after its origin and the exit site was located in the left pulmonary artery 5 mm distal to the bifurcation of main pulmonary artery. The pulmonary artery diameter at the dissection was 27 mm.

Figure 1

Figure 2

Diagnosis

To investigate possible etiologies, a transthoracic echocardiogram with Doppler was done to look for pulmonary hypertension. The echocardiogram showed normal pulmonary artery pressure with normal right ventricular systolic pressure. There was no evidence of pericardial effusion or structural cardiac abnormality on echocardiogram. Further investigations including work up for connective tissue diseases and infectious etiologies (Table 1) were normal.

According to Shilkin et al.,1 Helmbrecht first reported pulmonary artery dissection (PAD) in 1842. PAD is very rare and is usually diagnosed at autopsy. There are 71 other cases of PAD reported in the English literature, of which 16 cases are in living patients.217 Unlike aortic dissection, which is fairly common, the reentry circuit for PAD is formed by the rupture of the free wall of the pulmonary artery leading to hemopericardium, cardiac tamponade, and sudden death.2, 8, 9 There is wide variation in age of incidence, ranging from 26 to 85 years of age, with a slightly higher prevalence in females (male‐to‐female ratio 1:1.2).1, 2 The main pulmonary artery is usually involved, with or without involvement of its branches. Isolated left and right pulmonary artery involvement is seen in 6% and 4% of cases, respectively.2

Pulmonary hypertension, either primary or secondary (collagen vascular diseases, COPD, congenital heart diseases, etc.), is the most common underlying etiology. Other less common, but well‐described etiologies include: Marfan's syndrome, instrumentation of pulmonary artery, tuberculosis, syphilis, pregnancy, idiopathic cystic medial necrosis, and amyloidosis.2, 8

As noted earlier, underlying pulmonary hypertension is usually a major risk factor for PAD. More than 75% of the patients have underlying acute or chronic pulmonary hypertension.2 Our patient had COPD without pulmonary hypertension. Despite extensive investigation, no underlying cause of her pulmonary dissection was identified. The differential diagnosis includes cryptogenic cystic medionecrosis; however, because the patient refused surgery the diagnosis remains unknown. As in our case, idiopathic PAD is extremely rare, and only 4 other cases have been described in the literature.2 Underlying etiologies should always be ruled out to identify correctable causes such as congenital abnormalities of the heart leading to pulmonary hypertension.

Chest pain is a very common presenting complaint in the emergency department. Although rare, PAD should be suspected in a patient with retrosternal chest pain when other common causes of chest pain are excluded. Some of the more suggestive findings are the presence of a new diastolic murmur, a wide mediastinum on chest x‐ray, and CT scan of chest showing an intimal flap.2, 8 CT scan of the chest is an acceptable imaging modality to diagnose PAD.18 According to Neimatallah et al.,18 there are only 5 cases in the literature reported with detailed CT scans demonstrating PAD. If the diagnosis remains uncertain, it should be confirmed by MRI/MRA.16 Transthoracic echocardiography can be used for diagnosis and follow‐up of conservatively managed patients with PAD.3, 8, 19 The echocardiographic findings suggestive of PAD include direct or indirect evidence of pulmonary artery hypertension, with a large main pulmonary artery and an intimal flap across the pulmonary trunk.

Management

No consensus strategy is available for the management of PAD because of the rarity of this condition. In general, operative repair is the treatment of choice for PAD.2, 8, 9, 11 There are 16 cases diagnosed in living patients, out of which 6 were managed medically, 8 were managed surgically, and management was not discussed in 2 of the case reports (Table 2). In these case reports, medically managed patients were treated with oxygen, vasodilators (nitrates, angiotensin‐converting enzyme [ACE] inhibitors, dihydropyridine calcium channel blockers, sildenafil), diuretics and beta‐blockers. These patients did well on follow‐up, ranging from 3 weeks to 4 years, except for 1 who died on day 4 in the intensive care unit (ICU).

Conservative management may be tried in patients who are hemodynamically stable and do not have pericardial effusion.2, 9 The aim of conservative management is to decrease right ventricular preload and afterload. Preload reduction can be dangerous in patients with PAD and should be done in the intensive care setting as this can lead to profound hypotension. Nitrates for preload reduction should be used cautiously in patients taking sildenafil or similar agents for erectile dysfunction or pulmonary artery hypertension because of significant risk of cardiovascular collapse. The American Heart Association and American College of Cardiology both recommend that there should be a time gap of at least 24 hours between the last dose of sildenafil and the first dose of nitrates. Conservatively managed patients should be followed with interval CT scans2, 9, 18 or echocardiography.3, 19 In addition, the underlying etiology should always be investigated to predict prognosis and recommend future management strategies.

The patient was offered surgical repair but she declined. She was managed conservatively with nitrates and beta‐blockers and was pain free within 24 hours. Her BP was brought down to a systolic BP range of 130140 mm Hg. A repeat CT scan of the chest at 1‐month follow up was unchanged. The patient was doing well at 6‐month follow‐up.

Conclusions

PAD is an extremely rare cause of chest pain and a rare antemortem diagnosis. It is usually associated with underlying pulmonary hypertension. This case describes a patient with PAD in the absence of pulmonary hypertension. The patient was managed with conservative medical therapy and did well at 6‐month follow‐up. There are a total of 6 other case reports of patients with PAD managed conservatively, out of which 5 patients did well at follow‐up and 1 patient died. More case reports and longer follow‐up are needed to assess the effectiveness of conservative medical therapy in patients with PAD. To our knowledge, this is the first case report of idiopathic PAD diagnosed in a living patient and managed conservatively. This case also highlights better prognosis for patients with PAD without underlying pulmonary hypertension.

With the United States mired in its most severe recession in decades, stories of hospital struggles have emerged. Beaumont Hospital, located near the headquarters of major automakers and several assembly plants outside Detroit, recently cut hundreds of jobs and put major construction on indefinite hold.1 The CEO of Boston's Beth Israel Deaconess Medical Center made an agreement with employees to take large cuts in pay and vacation time to prevent laying off 10% of the staff.2 The University of Chicago Medical Center made plans to limit the number of emergency room beds, thereby decreasing low‐reimbursing emergency admissions while making beds available for higher‐paying elective hospitalizations.3

What is surprising about these stories is that hospitals have long been considered recession‐proof. Yet, with one‐half of US hospitals having reduced their staff to balance their budgets4 and with hospitals' financial margins falling dramatically,5 economic struggles are now a widespread problem.

Furthermore, it is difficult to determine if hospitals' clinical care has been damaged by the recession. The measurement of hospital quality is new and still under‐developed: there is virtually no reliable information on hospital quality from previous recessions, and even now it will be difficult to assess quality in real time.

Critics of waste and excess in the US health care system may see tough economic times as a Darwinian proving ground for hospitals, through which efficiency will improve and poor performers will close their doors. But more likely, hospital cutbacks will risk the quality and safety of health care delivery. For reasons of both public health and fiscal impact on communities, state and federal leaders may need to watch these trends closely to design and to be ready to implement potential government remedies for hospitals' fiscal woes.

In this commentary, we describe how hospitals have fared historically during recessions, how this recession could have different effectsfirst fiscally, then clinically, and we examine policy options to mitigate these untoward effects.

Decades of Recession‐Proof Hospitals

During the Great Depression, hospital insolvency was a national problem that prompted federal and state aid. Keeping hospitals alive was a critical policy goal and proved central to the early development of health insurance that focused on payment for hospital care.6

Since WWII, growth in America's hospitals has been only loosely related to national macroeconomic trends, with other changes like technological innovations and the advent of managed care far more influential to hospital finances. In fact, during recessions, hospital care spending growth often escalates in tandem with worsening unemployment (Figure 1). One explanation for this phenomenon is that economic pressures lead to declining primary care utilization, with adverse consequences for individuals' health.7

Figure 1

Hospitals' Current Fiscal Vulnerability

However, the current recession is the worst in 70 years. Every method of income generation available to hospitals appears at risk, including reimbursement per discharge (70% of hospitals report moderate or significant increases in uncompensated care), number of inpatient admissions (over one‐half report a moderate or significant decrease), difficulty obtaining bonds (60% report at least significant problems), and charitable donations.4 Over 50% of US hospitals had negative margins in the fourth quarter of 2008, though there has been some improvement since that time.8

Future hospital stability concerns remain. Growth in revenue per discharge is still below the norm.5 Because employment lags a recovering economy, further reimbursement decreases are possible from increasing proportions of patients with low‐reimbursing insurers or no coverage at all, decreasing payment rates from all payers, and decreasing elective care. The lower‐reimbursing payers, like state Medicaid programs, are experiencing increased enrollment as Americans lose their jobs and their better‐paying, employer‐sponsored private insurance.9 There's also evidence that reimbursement rates are declining from both Medicare and private insurers,10 which threatens the fragile cost‐shift through which hospitals have long used private insurance reimbursement to subsidize government reimbursements.11

Hospitals' specific financial challenges will likely vary across markets. The authors' state of Michigan has been hit particularly long and hard by the current recession. Unemployment rates exceeding 11% are expected to cause dramatic losses in private health insurance.9 Patients' increasing need with decreasing ability to pay will make markets in the deepest recession particularly vulnerable.

A Possible Stimulus: Investing in Quality Initiatives at Fiscally Vulnerable Hospitals

It is not enough to keep hospitals' doors open in a recession. Hospitals must continue to improve the quality and safety of the care they delivervital for their future patients and also for their communities who depend on them as anchors of health systems. We believe there is a need for a new, federally supported alignment of hospital finance and hospital quality that can limit damage to hospitals, help community employment, and improve patient safety.

Timely, structural quality measures could speed the introduction of functional value‐based purchasing, promote hospital safety, and help local economies at the same time. There are many simple structural measures that could be examined, such as development of discharge coordinators, promoting effective nurse‐to‐patient ratios, and encouraging health information technology (IT). Importantly, this would not duplicate efforts already underway to promote quality with process measures. With effective financial monitoring in real time, these measures could focus on high‐risk, fiscally disadvantaged hospitals.

To its credit, the Obama administration has already reached out to support hospitals, although aid has not been targeted specifically to hospitals in the most dire financial circumstances. Along with support for Medicaid and community health centers to improve primary care during the recession, the administration has provided a $268 million increase in Disproportionate Share Hospital payments towards hospitals that care for vulnerable patients, an increase of about 3%.17 Concurrently, the Centers for Medicare and Medicaid Services are implementing a value‐based purchasing program that starts with a 5% withhold in reimbursement that institutions need to earn back through a combination of mortality, process, and patient satisfaction metrics.18 The administration also reserved $19 billion to promote improvement of health IT for American medicine.19

Using health IT investment to help hospitals is an appealing concept, but for many institutions the infrastructure required to make that transition directly competes with other patient needs, including bedside patient care. IT investments have large initial costs, at a time when bank loans are difficult to acquire and few organizations can make expensive capital improvements. In fact, one‐quarter of hospitals report scaling back health IT investments that they had already started, in spite of the stimulus funds available.4

Instead, the administration may have more influence on improving care delivery by focusing on connecting hospital safety with hospital financial stability, by appropriating stimulus funds to center on quality and safety programs like those described above. Here is how: a hospital that would receive stimulus money for employing nurse discharge advocates would preserve employment while advancing patient safety, as would a hospital that retains a nurse‐to‐patient ratio above a specified threshold. By focusing on measures of structural quality, the government could improve care in ways that are easy to measure and maximize local economic stimulus without difficult outcomes assessment, insurance reform, or duplicating process measure efforts. There could even be an innovation differential (ie, payment/reward) for hospitals that improve quality while holding flat or lowering overall costs.

Equally important is to use this national financial crisis as an opportunity to improve monitoring of hospital quality. While quality assessment of hospitals is difficult, increased federal awareness of local medical need, hospital financial stability, and government awareness of emergency services overcrowding, nurse‐to‐patient ratios, and IT utilization are all valuable and easy to measure.

None of these quality‐focused fiscal interventions would be guaranteed to prevent hospital closure. Especially in small population centers, hospital closures can affect an entire community's financial growth and clinical safety net,20 while leaving hundreds or even thousands unemployed. Hospital closure should be assessed by state and federal government officials in these larger terms, perhaps even encouraging closure when appropriate, and helping prevent it when necessary.

Conclusion

Hospitals, as complex pieces of America's health care system, are central to communities' safety and economic growth. While national health coverage reform, as currently being discussed in Washington, would make hospital infrastructure less sensitive to macroeconomic changes, major reform would not come fast enough if hospitals start closing. While the worst of the recession may be over, recovery and the continuing rise in unemployment is a tenuous lifeline for hospitals on the financial brink.

We are not arguing against all hospital layoffs, or even closures. Indeed, this recession is a lean time for most industries and is likely to lead to closures for hospitals that cannot compete on efficiency or quality. But a hospital closure is a major event for a community and should not be permitted to occur without thorough consideration of alternatives. Current data on hospitals' financial status and clinical safety are limited, potentially biased, and not timely enough for this rapidly changing economic crisis. Therefore, state and federal government officials should assess whether hospitals would be eligible not just for possible emergency loans, but for linking loans to quality of care and community need. In so doing, this difficult time could be an opportunity to help hospitals improve their care, rather than watching it diminish.

With the United States mired in its most severe recession in decades, stories of hospital struggles have emerged. Beaumont Hospital, located near the headquarters of major automakers and several assembly plants outside Detroit, recently cut hundreds of jobs and put major construction on indefinite hold.1 The CEO of Boston's Beth Israel Deaconess Medical Center made an agreement with employees to take large cuts in pay and vacation time to prevent laying off 10% of the staff.2 The University of Chicago Medical Center made plans to limit the number of emergency room beds, thereby decreasing low‐reimbursing emergency admissions while making beds available for higher‐paying elective hospitalizations.3

What is surprising about these stories is that hospitals have long been considered recession‐proof. Yet, with one‐half of US hospitals having reduced their staff to balance their budgets4 and with hospitals' financial margins falling dramatically,5 economic struggles are now a widespread problem.

Furthermore, it is difficult to determine if hospitals' clinical care has been damaged by the recession. The measurement of hospital quality is new and still under‐developed: there is virtually no reliable information on hospital quality from previous recessions, and even now it will be difficult to assess quality in real time.

Critics of waste and excess in the US health care system may see tough economic times as a Darwinian proving ground for hospitals, through which efficiency will improve and poor performers will close their doors. But more likely, hospital cutbacks will risk the quality and safety of health care delivery. For reasons of both public health and fiscal impact on communities, state and federal leaders may need to watch these trends closely to design and to be ready to implement potential government remedies for hospitals' fiscal woes.

In this commentary, we describe how hospitals have fared historically during recessions, how this recession could have different effectsfirst fiscally, then clinically, and we examine policy options to mitigate these untoward effects.

Decades of Recession‐Proof Hospitals

During the Great Depression, hospital insolvency was a national problem that prompted federal and state aid. Keeping hospitals alive was a critical policy goal and proved central to the early development of health insurance that focused on payment for hospital care.6

Since WWII, growth in America's hospitals has been only loosely related to national macroeconomic trends, with other changes like technological innovations and the advent of managed care far more influential to hospital finances. In fact, during recessions, hospital care spending growth often escalates in tandem with worsening unemployment (Figure 1). One explanation for this phenomenon is that economic pressures lead to declining primary care utilization, with adverse consequences for individuals' health.7

Figure 1

Hospitals' Current Fiscal Vulnerability

However, the current recession is the worst in 70 years. Every method of income generation available to hospitals appears at risk, including reimbursement per discharge (70% of hospitals report moderate or significant increases in uncompensated care), number of inpatient admissions (over one‐half report a moderate or significant decrease), difficulty obtaining bonds (60% report at least significant problems), and charitable donations.4 Over 50% of US hospitals had negative margins in the fourth quarter of 2008, though there has been some improvement since that time.8

Future hospital stability concerns remain. Growth in revenue per discharge is still below the norm.5 Because employment lags a recovering economy, further reimbursement decreases are possible from increasing proportions of patients with low‐reimbursing insurers or no coverage at all, decreasing payment rates from all payers, and decreasing elective care. The lower‐reimbursing payers, like state Medicaid programs, are experiencing increased enrollment as Americans lose their jobs and their better‐paying, employer‐sponsored private insurance.9 There's also evidence that reimbursement rates are declining from both Medicare and private insurers,10 which threatens the fragile cost‐shift through which hospitals have long used private insurance reimbursement to subsidize government reimbursements.11

Hospitals' specific financial challenges will likely vary across markets. The authors' state of Michigan has been hit particularly long and hard by the current recession. Unemployment rates exceeding 11% are expected to cause dramatic losses in private health insurance.9 Patients' increasing need with decreasing ability to pay will make markets in the deepest recession particularly vulnerable.

A Possible Stimulus: Investing in Quality Initiatives at Fiscally Vulnerable Hospitals

It is not enough to keep hospitals' doors open in a recession. Hospitals must continue to improve the quality and safety of the care they delivervital for their future patients and also for their communities who depend on them as anchors of health systems. We believe there is a need for a new, federally supported alignment of hospital finance and hospital quality that can limit damage to hospitals, help community employment, and improve patient safety.

Timely, structural quality measures could speed the introduction of functional value‐based purchasing, promote hospital safety, and help local economies at the same time. There are many simple structural measures that could be examined, such as development of discharge coordinators, promoting effective nurse‐to‐patient ratios, and encouraging health information technology (IT). Importantly, this would not duplicate efforts already underway to promote quality with process measures. With effective financial monitoring in real time, these measures could focus on high‐risk, fiscally disadvantaged hospitals.

To its credit, the Obama administration has already reached out to support hospitals, although aid has not been targeted specifically to hospitals in the most dire financial circumstances. Along with support for Medicaid and community health centers to improve primary care during the recession, the administration has provided a $268 million increase in Disproportionate Share Hospital payments towards hospitals that care for vulnerable patients, an increase of about 3%.17 Concurrently, the Centers for Medicare and Medicaid Services are implementing a value‐based purchasing program that starts with a 5% withhold in reimbursement that institutions need to earn back through a combination of mortality, process, and patient satisfaction metrics.18 The administration also reserved $19 billion to promote improvement of health IT for American medicine.19

Using health IT investment to help hospitals is an appealing concept, but for many institutions the infrastructure required to make that transition directly competes with other patient needs, including bedside patient care. IT investments have large initial costs, at a time when bank loans are difficult to acquire and few organizations can make expensive capital improvements. In fact, one‐quarter of hospitals report scaling back health IT investments that they had already started, in spite of the stimulus funds available.4

Instead, the administration may have more influence on improving care delivery by focusing on connecting hospital safety with hospital financial stability, by appropriating stimulus funds to center on quality and safety programs like those described above. Here is how: a hospital that would receive stimulus money for employing nurse discharge advocates would preserve employment while advancing patient safety, as would a hospital that retains a nurse‐to‐patient ratio above a specified threshold. By focusing on measures of structural quality, the government could improve care in ways that are easy to measure and maximize local economic stimulus without difficult outcomes assessment, insurance reform, or duplicating process measure efforts. There could even be an innovation differential (ie, payment/reward) for hospitals that improve quality while holding flat or lowering overall costs.

Equally important is to use this national financial crisis as an opportunity to improve monitoring of hospital quality. While quality assessment of hospitals is difficult, increased federal awareness of local medical need, hospital financial stability, and government awareness of emergency services overcrowding, nurse‐to‐patient ratios, and IT utilization are all valuable and easy to measure.

None of these quality‐focused fiscal interventions would be guaranteed to prevent hospital closure. Especially in small population centers, hospital closures can affect an entire community's financial growth and clinical safety net,20 while leaving hundreds or even thousands unemployed. Hospital closure should be assessed by state and federal government officials in these larger terms, perhaps even encouraging closure when appropriate, and helping prevent it when necessary.

Conclusion

Hospitals, as complex pieces of America's health care system, are central to communities' safety and economic growth. While national health coverage reform, as currently being discussed in Washington, would make hospital infrastructure less sensitive to macroeconomic changes, major reform would not come fast enough if hospitals start closing. While the worst of the recession may be over, recovery and the continuing rise in unemployment is a tenuous lifeline for hospitals on the financial brink.

We are not arguing against all hospital layoffs, or even closures. Indeed, this recession is a lean time for most industries and is likely to lead to closures for hospitals that cannot compete on efficiency or quality. But a hospital closure is a major event for a community and should not be permitted to occur without thorough consideration of alternatives. Current data on hospitals' financial status and clinical safety are limited, potentially biased, and not timely enough for this rapidly changing economic crisis. Therefore, state and federal government officials should assess whether hospitals would be eligible not just for possible emergency loans, but for linking loans to quality of care and community need. In so doing, this difficult time could be an opportunity to help hospitals improve their care, rather than watching it diminish.

With the United States mired in its most severe recession in decades, stories of hospital struggles have emerged. Beaumont Hospital, located near the headquarters of major automakers and several assembly plants outside Detroit, recently cut hundreds of jobs and put major construction on indefinite hold.1 The CEO of Boston's Beth Israel Deaconess Medical Center made an agreement with employees to take large cuts in pay and vacation time to prevent laying off 10% of the staff.2 The University of Chicago Medical Center made plans to limit the number of emergency room beds, thereby decreasing low‐reimbursing emergency admissions while making beds available for higher‐paying elective hospitalizations.3

What is surprising about these stories is that hospitals have long been considered recession‐proof. Yet, with one‐half of US hospitals having reduced their staff to balance their budgets4 and with hospitals' financial margins falling dramatically,5 economic struggles are now a widespread problem.

Furthermore, it is difficult to determine if hospitals' clinical care has been damaged by the recession. The measurement of hospital quality is new and still under‐developed: there is virtually no reliable information on hospital quality from previous recessions, and even now it will be difficult to assess quality in real time.

Critics of waste and excess in the US health care system may see tough economic times as a Darwinian proving ground for hospitals, through which efficiency will improve and poor performers will close their doors. But more likely, hospital cutbacks will risk the quality and safety of health care delivery. For reasons of both public health and fiscal impact on communities, state and federal leaders may need to watch these trends closely to design and to be ready to implement potential government remedies for hospitals' fiscal woes.

In this commentary, we describe how hospitals have fared historically during recessions, how this recession could have different effectsfirst fiscally, then clinically, and we examine policy options to mitigate these untoward effects.

Decades of Recession‐Proof Hospitals

During the Great Depression, hospital insolvency was a national problem that prompted federal and state aid. Keeping hospitals alive was a critical policy goal and proved central to the early development of health insurance that focused on payment for hospital care.6

Since WWII, growth in America's hospitals has been only loosely related to national macroeconomic trends, with other changes like technological innovations and the advent of managed care far more influential to hospital finances. In fact, during recessions, hospital care spending growth often escalates in tandem with worsening unemployment (Figure 1). One explanation for this phenomenon is that economic pressures lead to declining primary care utilization, with adverse consequences for individuals' health.7

Figure 1

Hospitals' Current Fiscal Vulnerability

However, the current recession is the worst in 70 years. Every method of income generation available to hospitals appears at risk, including reimbursement per discharge (70% of hospitals report moderate or significant increases in uncompensated care), number of inpatient admissions (over one‐half report a moderate or significant decrease), difficulty obtaining bonds (60% report at least significant problems), and charitable donations.4 Over 50% of US hospitals had negative margins in the fourth quarter of 2008, though there has been some improvement since that time.8

Future hospital stability concerns remain. Growth in revenue per discharge is still below the norm.5 Because employment lags a recovering economy, further reimbursement decreases are possible from increasing proportions of patients with low‐reimbursing insurers or no coverage at all, decreasing payment rates from all payers, and decreasing elective care. The lower‐reimbursing payers, like state Medicaid programs, are experiencing increased enrollment as Americans lose their jobs and their better‐paying, employer‐sponsored private insurance.9 There's also evidence that reimbursement rates are declining from both Medicare and private insurers,10 which threatens the fragile cost‐shift through which hospitals have long used private insurance reimbursement to subsidize government reimbursements.11

Hospitals' specific financial challenges will likely vary across markets. The authors' state of Michigan has been hit particularly long and hard by the current recession. Unemployment rates exceeding 11% are expected to cause dramatic losses in private health insurance.9 Patients' increasing need with decreasing ability to pay will make markets in the deepest recession particularly vulnerable.

A Possible Stimulus: Investing in Quality Initiatives at Fiscally Vulnerable Hospitals

It is not enough to keep hospitals' doors open in a recession. Hospitals must continue to improve the quality and safety of the care they delivervital for their future patients and also for their communities who depend on them as anchors of health systems. We believe there is a need for a new, federally supported alignment of hospital finance and hospital quality that can limit damage to hospitals, help community employment, and improve patient safety.

Timely, structural quality measures could speed the introduction of functional value‐based purchasing, promote hospital safety, and help local economies at the same time. There are many simple structural measures that could be examined, such as development of discharge coordinators, promoting effective nurse‐to‐patient ratios, and encouraging health information technology (IT). Importantly, this would not duplicate efforts already underway to promote quality with process measures. With effective financial monitoring in real time, these measures could focus on high‐risk, fiscally disadvantaged hospitals.

To its credit, the Obama administration has already reached out to support hospitals, although aid has not been targeted specifically to hospitals in the most dire financial circumstances. Along with support for Medicaid and community health centers to improve primary care during the recession, the administration has provided a $268 million increase in Disproportionate Share Hospital payments towards hospitals that care for vulnerable patients, an increase of about 3%.17 Concurrently, the Centers for Medicare and Medicaid Services are implementing a value‐based purchasing program that starts with a 5% withhold in reimbursement that institutions need to earn back through a combination of mortality, process, and patient satisfaction metrics.18 The administration also reserved $19 billion to promote improvement of health IT for American medicine.19

Using health IT investment to help hospitals is an appealing concept, but for many institutions the infrastructure required to make that transition directly competes with other patient needs, including bedside patient care. IT investments have large initial costs, at a time when bank loans are difficult to acquire and few organizations can make expensive capital improvements. In fact, one‐quarter of hospitals report scaling back health IT investments that they had already started, in spite of the stimulus funds available.4

Instead, the administration may have more influence on improving care delivery by focusing on connecting hospital safety with hospital financial stability, by appropriating stimulus funds to center on quality and safety programs like those described above. Here is how: a hospital that would receive stimulus money for employing nurse discharge advocates would preserve employment while advancing patient safety, as would a hospital that retains a nurse‐to‐patient ratio above a specified threshold. By focusing on measures of structural quality, the government could improve care in ways that are easy to measure and maximize local economic stimulus without difficult outcomes assessment, insurance reform, or duplicating process measure efforts. There could even be an innovation differential (ie, payment/reward) for hospitals that improve quality while holding flat or lowering overall costs.

Equally important is to use this national financial crisis as an opportunity to improve monitoring of hospital quality. While quality assessment of hospitals is difficult, increased federal awareness of local medical need, hospital financial stability, and government awareness of emergency services overcrowding, nurse‐to‐patient ratios, and IT utilization are all valuable and easy to measure.

None of these quality‐focused fiscal interventions would be guaranteed to prevent hospital closure. Especially in small population centers, hospital closures can affect an entire community's financial growth and clinical safety net,20 while leaving hundreds or even thousands unemployed. Hospital closure should be assessed by state and federal government officials in these larger terms, perhaps even encouraging closure when appropriate, and helping prevent it when necessary.

Conclusion

Hospitals, as complex pieces of America's health care system, are central to communities' safety and economic growth. While national health coverage reform, as currently being discussed in Washington, would make hospital infrastructure less sensitive to macroeconomic changes, major reform would not come fast enough if hospitals start closing. While the worst of the recession may be over, recovery and the continuing rise in unemployment is a tenuous lifeline for hospitals on the financial brink.

We are not arguing against all hospital layoffs, or even closures. Indeed, this recession is a lean time for most industries and is likely to lead to closures for hospitals that cannot compete on efficiency or quality. But a hospital closure is a major event for a community and should not be permitted to occur without thorough consideration of alternatives. Current data on hospitals' financial status and clinical safety are limited, potentially biased, and not timely enough for this rapidly changing economic crisis. Therefore, state and federal government officials should assess whether hospitals would be eligible not just for possible emergency loans, but for linking loans to quality of care and community need. In so doing, this difficult time could be an opportunity to help hospitals improve their care, rather than watching it diminish.