Recently, there has been an increased focus on improving communication during care transitions for older patients as they leave the hospital. One reason for this focus is the increasing utilization of hospitalists, or hospital‐based physicians, caring for patients in the United States.1 As a result, many primary care physicians (PCPs) no longer care for their patients while in the hospital and may not be informed of their patients' hospitalization.2 Additionally, with an emphasis on shorter lengths of hospital stay, more extensive post‐discharge follow‐up is often warranted for patients, which often becomes the responsibility of a patient's PCP. Recently 6 societies (American College of Physicians, Society of General Internal Medicine, Society of Hospital Medicine, American Geriatrics Society, American College of Emergency Physicians, and Society of Academic Emergency Medicine) have recommended that a patient's PCP is notified during all steps in care transitions and that patient‐centered approaches are employed.3 Despite the increased need for improved inpatient‐ambulatory care transitions, the communication between hospitalists and PCPs has been characterized as being poor and ineffective.4 Prior studies have shown that PCPs are not aware of test results that require follow‐up, may not receive timely or high quality discharge materials, and have an overall poor perception of the quality of communication.46 Ensuring adequate communication is considered important due to the increased risk of adverse events that patients experience after discharge from the hospital.79 Furthermore, recent studies have shown that patients are often able to identify and report adverse events that would not be detected by medical record review alone.10, 11 Eliciting patient perspectives on their experiences after discharge and their expectations of communication between PCPs and hospital physicians can help clinical teams design more patient‐centered solutions for care transitions.

The aim of this study is to report older patients' experiences with problems after hospital discharge and their understanding and expectation of communication between hospital physicians and their PCP. We also explored the relationship between patient experiences and whether their PCPs were aware of their hospitalization.

Methods

Results

Of the 114 eligible patients recruited between February and July 2008, 64 patient interviews were completed (56%). The average patient age was 73 years. Most patients were female (69%), African American (70%), live at home (75%), and have a PCP located at the University of Chicago (70%). There were also several who were low income (23% below a median yearly income of $15,000), and did not attend any college (52%). These patients had an average length of stay of 5.3 days, nearly half (48%) having been hospitalized in the past year, and 6 patients (9%) required a proxy to complete the interview (Table 1). There were no significant differences between responders and nonresponders with respect to race, gender, education, income, admission in the past 12 months, residence, PCP location, mental status, length of stay, or discharge status. Responders were more likely to be older than nonresponders (73 years [95% confidence interval {CI} 6976 years] vs. 63 years for nonresponders [95% CI 5769 years]; [P < 0.01]).

Forty‐two percent (27) of patients reported experiencing a post‐discharge problem. These 27 patients reported 42 distinct problems, each of which fell into 1 of 5 broad categories (Table 2). The most common of these were patients having difficulty obtaining follow‐up tests or appointments. These patients either had delay in getting, or were unable to get, follow‐up appointments, or follow‐up tests and test results. There were also many patients who needed reevaluation and thus, were either readmitted to the hospital or had to return to the Emergency Department. Another major category was those who had problems getting medication or therapy. For example, one of (the patients) treatment medswas very hard to find and it delayed us giving her her meds. Others reported they were not properly prepared for discharge. Most of these patients did not receive proper discharge materials which then caused other issues. As one proxy reported, The services were supposed to be provided for (the patient) through her social worker, no one has been informed to her being discharged or her being sent home. We have not gotten any services. Lastly, a few patients reported having hospital complications, such as post‐procedural complications, or questions, such as diagnosis questions.0

Patients were often uncertain of whether and how communication between the inpatient physician and PCP (Table 3) took place. One patient said, I don't know what the procedure is as far as giving him the message. Does she fax it to him? I don't know She told me that she was going to call and inform him on everything that happened. I don't know anything from there. The second most commonly expressed perception was from patients who assumed good communication had taken place between his or her physicians. This assumption was grounded in a belief that good communication naturally occurred between physicians. For example 1 patient expressed: (doctors) let the other doctors in too. That's the way to take care of stuff. Lastly, many patients expressed the feeling that their physicians were obligated to communicate with each other. As 1 patient reported, I think that they should have let (my PCP) know that I was in the hospital.

Two new themes emerged from the inductive analysis (Table 4). Forty‐five percent of patients reported experiencing negative emotions. These negative emotions were most often expressed as frustration or confusion. For example, 1 patient expressed confusion by saying, When I usually have lab work done I have prescription signedmaybe they changed the way of doing it. Now the pharmacy called me. But I'm supposed to have a note or something. Patients who reported a post‐discharge problem were more likely to report negative emotions (67% vs. 26%, P < 0.01). Feelings of empowerment were reported by 31% of patients. Empowerment was expressed most often as the patient being proactive in communicating with the PCP. One patient reported, We informed (my PCP) and we filled in all of the information that we wanted him to know about. Empowerment was also expressed as being proactive in advocating for communication between the inpatient team and the PCP (Table 3). Some patients expressed feeling empowered through the support of a third party, such as a home nurse. In addition, patients who have a third party advocate are more likely to report being empowered. Empowerment was expressed by 26% of patients with no third party advocate compared with 71% of patients with a third party advocate (P = 0.02).

From our sample of patients who completed a 2‐week post‐discharge interview, we were able to obtain PCP surveys for 40 (63%) of these patients (Figure 1). Thirty percent (12) of PCPs reported being unaware of the hospitalization. In all but 4 cases, PCPs had communicated with the medical team during hospitalization. Examining the association between PCP knowledge and patient reported post‐discharge problems showed that patients whose PCPs were not aware of the hospitalization were 2 times more likely to report a post‐discharge problem. A post‐discharge problem was reported by 67% of patients whose PCP was not aware of the hospitalization, while a post‐discharge problem was reported by 32% of patients whose PCP was aware (P < 0.05). Six patients reported returning to the ED or being readmitted. Four patients (33%) of PCPs who were unaware of hospitalization reported returning for reevaluation whereas 7% (n = 2) of patients whose PCP was aware of hospitalization reported returning for evaluation (P = 0.055). Interestingly, patients whose PCPs were not aware of the hospitalization reported feeling more empowered (58%) than those patients whose PCP were aware of the hospitalization (21%, P = 0.03). Because of possible confounding (patient report of problems post‐discharge problems may be affected by PCP awareness of hospitalization), we examined whether patients whose PCPs were aware of their hospitalization differed from those that did not. Patients whose PCPs were aware of their hospitalization were often older (75 vs. 69 years old), white (80% white vs. 65% nonwhite) and female (75% female vs. 54% male). While this small sample size prohibits examining for statistical significance, the magnitude of these differences suggests the need for a larger study to examine patient predictors of PCP awareness of hospitalization.

Figure 1

Discussion

In this sample of frail, older hospitalized patients, nearly half reported at least 1 post‐discharge problem. Most patients have perceptions of what communication did or did not take place between their physicians. While most do not understand the communication process, many expect good communication to occur, and feel that physicians are obligated to communicate with each other. However, patients' perceptions of communication highlight that patient expectations are far from the actual practice in some cases. Nearly half of patients reported feeling negative emotions, such as confusion and frustration, and patients were more likely to experience negative emotions when they also reported a post‐discharge problem. One‐third of patients reported feeling empowered. Empowerment was associated with having a third party who helped advocate for them. Paradoxically, patients whose PCP were not aware of their hospitalization were more likely to feel empowered. Lastly, more patients reported a post‐discharge problem when their PCP was not aware of the hospitalization.

Because this is predominantly a qualitative observational study, it is important to consider the mechanism for these findings since we cannot assume causal relationships. The association of negative emotions, like confusion and frustration, with post‐discharge problems could be explained due to additional stress of the problem itself or that a distressed frame of mind is associated with reporting more problems that may have been overlooked otherwise. In addition, the association between patient empowerment and lack of PCP awareness could be due to the fact that patients are forced to assume a more proactive role in contacting their PCP if they feel that their PCP was not aware. It is equally possible that PCP communication is selectively initiated by hospital physicians when the patients are least empowered. For example, our comparison of demographics for patients whose PCP was aware versus those that were not do suggest that patient characteristics might play a role in whether a patient's PCP is contacted. The association between a third party advocate and patient empowerment is likely explained as the third party is able to keep the patient informed and empowered.

This study has implications for efforts to design a more patient‐centered care transition for hospitalized older patients. First, patients and their proxies should be advocates for good communication to avoid the risks of care transitions. Prior interventions such as use of coaches to boost patient empowerment have had positive results for hospitalized older patients. Moreover, hospitals should keep in mind that problems after discharge are common and are linked to negative emotions, which may lower patient satisfaction or increase liability risk. Similarly, these findings also highlight the importance of keeping PCPs aware of patient hospitalization. For example, PCPs that are aware of hospitalization are better prepared to properly follow‐up on medications, tests, and appointments. The PCP can also help to better prepare the patient for discharge and ease the transition for the patient.

There are several limitations to our study. First and foremost, our small sample size limits our ability to examine statistical significance. This study was part of a short planning grant to design interventions to improve communication with PCPs during hospitalization. Efforts are currently underway to design a communication solution and educational intervention to highlight the importance of contacting PCPs during hospitalization. Because these patients were hospitalized on the teaching service, the resident with the guidance of the teaching attending is responsible for communicating with the PCP. The teaching attending was either a generalist, hospitalist, or specialist who routinely had no a priori relationship with patients prior to the hospitalization. Only 53% of patients were reached by telephone which raises the concern for nonresponse bias. Our low response rate highlights the challenge of doing this type of work with recently discharge patients in low income, underserved areas. In comparing responders and nonresponders, the only difference between the 2 groups was that responders were more likely to be older. One possible reason for this difference may be that older people are more likely to be at home and easier to contact over the phone. Similarly, since data were collected through interviews and adverse events were discussed, these results are subject to recall bias. Efforts were made to reduce this by calling within 2 to 3 weeks after discharge. Lastly, these findings are limited by generalizability. All the patients included in this study were from the University of Chicago Medical Center, which serves largely underserved, African American patients. The experiences of these patients may be unique to this site. In addition, we only studied patients who had a PCP, excluding a population of patients that are at inherent risk due to lack of a coordinating physician to guide ongoing care.

In conclusion, this study suggests that many frail, older patients reported experiencing a post‐discharge problem and patients whose PCPs did not know about their admission were more likely to report a post‐discharge problem. Systematic interventions to improve communications with PCPs during patient care transitions in and out of the hospital are needed.

Recently, there has been an increased focus on improving communication during care transitions for older patients as they leave the hospital. One reason for this focus is the increasing utilization of hospitalists, or hospital‐based physicians, caring for patients in the United States.1 As a result, many primary care physicians (PCPs) no longer care for their patients while in the hospital and may not be informed of their patients' hospitalization.2 Additionally, with an emphasis on shorter lengths of hospital stay, more extensive post‐discharge follow‐up is often warranted for patients, which often becomes the responsibility of a patient's PCP. Recently 6 societies (American College of Physicians, Society of General Internal Medicine, Society of Hospital Medicine, American Geriatrics Society, American College of Emergency Physicians, and Society of Academic Emergency Medicine) have recommended that a patient's PCP is notified during all steps in care transitions and that patient‐centered approaches are employed.3 Despite the increased need for improved inpatient‐ambulatory care transitions, the communication between hospitalists and PCPs has been characterized as being poor and ineffective.4 Prior studies have shown that PCPs are not aware of test results that require follow‐up, may not receive timely or high quality discharge materials, and have an overall poor perception of the quality of communication.46 Ensuring adequate communication is considered important due to the increased risk of adverse events that patients experience after discharge from the hospital.79 Furthermore, recent studies have shown that patients are often able to identify and report adverse events that would not be detected by medical record review alone.10, 11 Eliciting patient perspectives on their experiences after discharge and their expectations of communication between PCPs and hospital physicians can help clinical teams design more patient‐centered solutions for care transitions.

The aim of this study is to report older patients' experiences with problems after hospital discharge and their understanding and expectation of communication between hospital physicians and their PCP. We also explored the relationship between patient experiences and whether their PCPs were aware of their hospitalization.

Methods

Results

Of the 114 eligible patients recruited between February and July 2008, 64 patient interviews were completed (56%). The average patient age was 73 years. Most patients were female (69%), African American (70%), live at home (75%), and have a PCP located at the University of Chicago (70%). There were also several who were low income (23% below a median yearly income of $15,000), and did not attend any college (52%). These patients had an average length of stay of 5.3 days, nearly half (48%) having been hospitalized in the past year, and 6 patients (9%) required a proxy to complete the interview (Table 1). There were no significant differences between responders and nonresponders with respect to race, gender, education, income, admission in the past 12 months, residence, PCP location, mental status, length of stay, or discharge status. Responders were more likely to be older than nonresponders (73 years [95% confidence interval {CI} 6976 years] vs. 63 years for nonresponders [95% CI 5769 years]; [P < 0.01]).

Forty‐two percent (27) of patients reported experiencing a post‐discharge problem. These 27 patients reported 42 distinct problems, each of which fell into 1 of 5 broad categories (Table 2). The most common of these were patients having difficulty obtaining follow‐up tests or appointments. These patients either had delay in getting, or were unable to get, follow‐up appointments, or follow‐up tests and test results. There were also many patients who needed reevaluation and thus, were either readmitted to the hospital or had to return to the Emergency Department. Another major category was those who had problems getting medication or therapy. For example, one of (the patients) treatment medswas very hard to find and it delayed us giving her her meds. Others reported they were not properly prepared for discharge. Most of these patients did not receive proper discharge materials which then caused other issues. As one proxy reported, The services were supposed to be provided for (the patient) through her social worker, no one has been informed to her being discharged or her being sent home. We have not gotten any services. Lastly, a few patients reported having hospital complications, such as post‐procedural complications, or questions, such as diagnosis questions.0

Patients were often uncertain of whether and how communication between the inpatient physician and PCP (Table 3) took place. One patient said, I don't know what the procedure is as far as giving him the message. Does she fax it to him? I don't know She told me that she was going to call and inform him on everything that happened. I don't know anything from there. The second most commonly expressed perception was from patients who assumed good communication had taken place between his or her physicians. This assumption was grounded in a belief that good communication naturally occurred between physicians. For example 1 patient expressed: (doctors) let the other doctors in too. That's the way to take care of stuff. Lastly, many patients expressed the feeling that their physicians were obligated to communicate with each other. As 1 patient reported, I think that they should have let (my PCP) know that I was in the hospital.

Two new themes emerged from the inductive analysis (Table 4). Forty‐five percent of patients reported experiencing negative emotions. These negative emotions were most often expressed as frustration or confusion. For example, 1 patient expressed confusion by saying, When I usually have lab work done I have prescription signedmaybe they changed the way of doing it. Now the pharmacy called me. But I'm supposed to have a note or something. Patients who reported a post‐discharge problem were more likely to report negative emotions (67% vs. 26%, P < 0.01). Feelings of empowerment were reported by 31% of patients. Empowerment was expressed most often as the patient being proactive in communicating with the PCP. One patient reported, We informed (my PCP) and we filled in all of the information that we wanted him to know about. Empowerment was also expressed as being proactive in advocating for communication between the inpatient team and the PCP (Table 3). Some patients expressed feeling empowered through the support of a third party, such as a home nurse. In addition, patients who have a third party advocate are more likely to report being empowered. Empowerment was expressed by 26% of patients with no third party advocate compared with 71% of patients with a third party advocate (P = 0.02).

From our sample of patients who completed a 2‐week post‐discharge interview, we were able to obtain PCP surveys for 40 (63%) of these patients (Figure 1). Thirty percent (12) of PCPs reported being unaware of the hospitalization. In all but 4 cases, PCPs had communicated with the medical team during hospitalization. Examining the association between PCP knowledge and patient reported post‐discharge problems showed that patients whose PCPs were not aware of the hospitalization were 2 times more likely to report a post‐discharge problem. A post‐discharge problem was reported by 67% of patients whose PCP was not aware of the hospitalization, while a post‐discharge problem was reported by 32% of patients whose PCP was aware (P < 0.05). Six patients reported returning to the ED or being readmitted. Four patients (33%) of PCPs who were unaware of hospitalization reported returning for reevaluation whereas 7% (n = 2) of patients whose PCP was aware of hospitalization reported returning for evaluation (P = 0.055). Interestingly, patients whose PCPs were not aware of the hospitalization reported feeling more empowered (58%) than those patients whose PCP were aware of the hospitalization (21%, P = 0.03). Because of possible confounding (patient report of problems post‐discharge problems may be affected by PCP awareness of hospitalization), we examined whether patients whose PCPs were aware of their hospitalization differed from those that did not. Patients whose PCPs were aware of their hospitalization were often older (75 vs. 69 years old), white (80% white vs. 65% nonwhite) and female (75% female vs. 54% male). While this small sample size prohibits examining for statistical significance, the magnitude of these differences suggests the need for a larger study to examine patient predictors of PCP awareness of hospitalization.

Figure 1

Discussion

In this sample of frail, older hospitalized patients, nearly half reported at least 1 post‐discharge problem. Most patients have perceptions of what communication did or did not take place between their physicians. While most do not understand the communication process, many expect good communication to occur, and feel that physicians are obligated to communicate with each other. However, patients' perceptions of communication highlight that patient expectations are far from the actual practice in some cases. Nearly half of patients reported feeling negative emotions, such as confusion and frustration, and patients were more likely to experience negative emotions when they also reported a post‐discharge problem. One‐third of patients reported feeling empowered. Empowerment was associated with having a third party who helped advocate for them. Paradoxically, patients whose PCP were not aware of their hospitalization were more likely to feel empowered. Lastly, more patients reported a post‐discharge problem when their PCP was not aware of the hospitalization.

Because this is predominantly a qualitative observational study, it is important to consider the mechanism for these findings since we cannot assume causal relationships. The association of negative emotions, like confusion and frustration, with post‐discharge problems could be explained due to additional stress of the problem itself or that a distressed frame of mind is associated with reporting more problems that may have been overlooked otherwise. In addition, the association between patient empowerment and lack of PCP awareness could be due to the fact that patients are forced to assume a more proactive role in contacting their PCP if they feel that their PCP was not aware. It is equally possible that PCP communication is selectively initiated by hospital physicians when the patients are least empowered. For example, our comparison of demographics for patients whose PCP was aware versus those that were not do suggest that patient characteristics might play a role in whether a patient's PCP is contacted. The association between a third party advocate and patient empowerment is likely explained as the third party is able to keep the patient informed and empowered.

This study has implications for efforts to design a more patient‐centered care transition for hospitalized older patients. First, patients and their proxies should be advocates for good communication to avoid the risks of care transitions. Prior interventions such as use of coaches to boost patient empowerment have had positive results for hospitalized older patients. Moreover, hospitals should keep in mind that problems after discharge are common and are linked to negative emotions, which may lower patient satisfaction or increase liability risk. Similarly, these findings also highlight the importance of keeping PCPs aware of patient hospitalization. For example, PCPs that are aware of hospitalization are better prepared to properly follow‐up on medications, tests, and appointments. The PCP can also help to better prepare the patient for discharge and ease the transition for the patient.

There are several limitations to our study. First and foremost, our small sample size limits our ability to examine statistical significance. This study was part of a short planning grant to design interventions to improve communication with PCPs during hospitalization. Efforts are currently underway to design a communication solution and educational intervention to highlight the importance of contacting PCPs during hospitalization. Because these patients were hospitalized on the teaching service, the resident with the guidance of the teaching attending is responsible for communicating with the PCP. The teaching attending was either a generalist, hospitalist, or specialist who routinely had no a priori relationship with patients prior to the hospitalization. Only 53% of patients were reached by telephone which raises the concern for nonresponse bias. Our low response rate highlights the challenge of doing this type of work with recently discharge patients in low income, underserved areas. In comparing responders and nonresponders, the only difference between the 2 groups was that responders were more likely to be older. One possible reason for this difference may be that older people are more likely to be at home and easier to contact over the phone. Similarly, since data were collected through interviews and adverse events were discussed, these results are subject to recall bias. Efforts were made to reduce this by calling within 2 to 3 weeks after discharge. Lastly, these findings are limited by generalizability. All the patients included in this study were from the University of Chicago Medical Center, which serves largely underserved, African American patients. The experiences of these patients may be unique to this site. In addition, we only studied patients who had a PCP, excluding a population of patients that are at inherent risk due to lack of a coordinating physician to guide ongoing care.

In conclusion, this study suggests that many frail, older patients reported experiencing a post‐discharge problem and patients whose PCPs did not know about their admission were more likely to report a post‐discharge problem. Systematic interventions to improve communications with PCPs during patient care transitions in and out of the hospital are needed.

Recently, there has been an increased focus on improving communication during care transitions for older patients as they leave the hospital. One reason for this focus is the increasing utilization of hospitalists, or hospital‐based physicians, caring for patients in the United States.1 As a result, many primary care physicians (PCPs) no longer care for their patients while in the hospital and may not be informed of their patients' hospitalization.2 Additionally, with an emphasis on shorter lengths of hospital stay, more extensive post‐discharge follow‐up is often warranted for patients, which often becomes the responsibility of a patient's PCP. Recently 6 societies (American College of Physicians, Society of General Internal Medicine, Society of Hospital Medicine, American Geriatrics Society, American College of Emergency Physicians, and Society of Academic Emergency Medicine) have recommended that a patient's PCP is notified during all steps in care transitions and that patient‐centered approaches are employed.3 Despite the increased need for improved inpatient‐ambulatory care transitions, the communication between hospitalists and PCPs has been characterized as being poor and ineffective.4 Prior studies have shown that PCPs are not aware of test results that require follow‐up, may not receive timely or high quality discharge materials, and have an overall poor perception of the quality of communication.46 Ensuring adequate communication is considered important due to the increased risk of adverse events that patients experience after discharge from the hospital.79 Furthermore, recent studies have shown that patients are often able to identify and report adverse events that would not be detected by medical record review alone.10, 11 Eliciting patient perspectives on their experiences after discharge and their expectations of communication between PCPs and hospital physicians can help clinical teams design more patient‐centered solutions for care transitions.

The aim of this study is to report older patients' experiences with problems after hospital discharge and their understanding and expectation of communication between hospital physicians and their PCP. We also explored the relationship between patient experiences and whether their PCPs were aware of their hospitalization.

Methods

Results

Of the 114 eligible patients recruited between February and July 2008, 64 patient interviews were completed (56%). The average patient age was 73 years. Most patients were female (69%), African American (70%), live at home (75%), and have a PCP located at the University of Chicago (70%). There were also several who were low income (23% below a median yearly income of $15,000), and did not attend any college (52%). These patients had an average length of stay of 5.3 days, nearly half (48%) having been hospitalized in the past year, and 6 patients (9%) required a proxy to complete the interview (Table 1). There were no significant differences between responders and nonresponders with respect to race, gender, education, income, admission in the past 12 months, residence, PCP location, mental status, length of stay, or discharge status. Responders were more likely to be older than nonresponders (73 years [95% confidence interval {CI} 6976 years] vs. 63 years for nonresponders [95% CI 5769 years]; [P < 0.01]).

Forty‐two percent (27) of patients reported experiencing a post‐discharge problem. These 27 patients reported 42 distinct problems, each of which fell into 1 of 5 broad categories (Table 2). The most common of these were patients having difficulty obtaining follow‐up tests or appointments. These patients either had delay in getting, or were unable to get, follow‐up appointments, or follow‐up tests and test results. There were also many patients who needed reevaluation and thus, were either readmitted to the hospital or had to return to the Emergency Department. Another major category was those who had problems getting medication or therapy. For example, one of (the patients) treatment medswas very hard to find and it delayed us giving her her meds. Others reported they were not properly prepared for discharge. Most of these patients did not receive proper discharge materials which then caused other issues. As one proxy reported, The services were supposed to be provided for (the patient) through her social worker, no one has been informed to her being discharged or her being sent home. We have not gotten any services. Lastly, a few patients reported having hospital complications, such as post‐procedural complications, or questions, such as diagnosis questions.0

Patients were often uncertain of whether and how communication between the inpatient physician and PCP (Table 3) took place. One patient said, I don't know what the procedure is as far as giving him the message. Does she fax it to him? I don't know She told me that she was going to call and inform him on everything that happened. I don't know anything from there. The second most commonly expressed perception was from patients who assumed good communication had taken place between his or her physicians. This assumption was grounded in a belief that good communication naturally occurred between physicians. For example 1 patient expressed: (doctors) let the other doctors in too. That's the way to take care of stuff. Lastly, many patients expressed the feeling that their physicians were obligated to communicate with each other. As 1 patient reported, I think that they should have let (my PCP) know that I was in the hospital.

Two new themes emerged from the inductive analysis (Table 4). Forty‐five percent of patients reported experiencing negative emotions. These negative emotions were most often expressed as frustration or confusion. For example, 1 patient expressed confusion by saying, When I usually have lab work done I have prescription signedmaybe they changed the way of doing it. Now the pharmacy called me. But I'm supposed to have a note or something. Patients who reported a post‐discharge problem were more likely to report negative emotions (67% vs. 26%, P < 0.01). Feelings of empowerment were reported by 31% of patients. Empowerment was expressed most often as the patient being proactive in communicating with the PCP. One patient reported, We informed (my PCP) and we filled in all of the information that we wanted him to know about. Empowerment was also expressed as being proactive in advocating for communication between the inpatient team and the PCP (Table 3). Some patients expressed feeling empowered through the support of a third party, such as a home nurse. In addition, patients who have a third party advocate are more likely to report being empowered. Empowerment was expressed by 26% of patients with no third party advocate compared with 71% of patients with a third party advocate (P = 0.02).

From our sample of patients who completed a 2‐week post‐discharge interview, we were able to obtain PCP surveys for 40 (63%) of these patients (Figure 1). Thirty percent (12) of PCPs reported being unaware of the hospitalization. In all but 4 cases, PCPs had communicated with the medical team during hospitalization. Examining the association between PCP knowledge and patient reported post‐discharge problems showed that patients whose PCPs were not aware of the hospitalization were 2 times more likely to report a post‐discharge problem. A post‐discharge problem was reported by 67% of patients whose PCP was not aware of the hospitalization, while a post‐discharge problem was reported by 32% of patients whose PCP was aware (P < 0.05). Six patients reported returning to the ED or being readmitted. Four patients (33%) of PCPs who were unaware of hospitalization reported returning for reevaluation whereas 7% (n = 2) of patients whose PCP was aware of hospitalization reported returning for evaluation (P = 0.055). Interestingly, patients whose PCPs were not aware of the hospitalization reported feeling more empowered (58%) than those patients whose PCP were aware of the hospitalization (21%, P = 0.03). Because of possible confounding (patient report of problems post‐discharge problems may be affected by PCP awareness of hospitalization), we examined whether patients whose PCPs were aware of their hospitalization differed from those that did not. Patients whose PCPs were aware of their hospitalization were often older (75 vs. 69 years old), white (80% white vs. 65% nonwhite) and female (75% female vs. 54% male). While this small sample size prohibits examining for statistical significance, the magnitude of these differences suggests the need for a larger study to examine patient predictors of PCP awareness of hospitalization.

Figure 1

Discussion

In this sample of frail, older hospitalized patients, nearly half reported at least 1 post‐discharge problem. Most patients have perceptions of what communication did or did not take place between their physicians. While most do not understand the communication process, many expect good communication to occur, and feel that physicians are obligated to communicate with each other. However, patients' perceptions of communication highlight that patient expectations are far from the actual practice in some cases. Nearly half of patients reported feeling negative emotions, such as confusion and frustration, and patients were more likely to experience negative emotions when they also reported a post‐discharge problem. One‐third of patients reported feeling empowered. Empowerment was associated with having a third party who helped advocate for them. Paradoxically, patients whose PCP were not aware of their hospitalization were more likely to feel empowered. Lastly, more patients reported a post‐discharge problem when their PCP was not aware of the hospitalization.

Because this is predominantly a qualitative observational study, it is important to consider the mechanism for these findings since we cannot assume causal relationships. The association of negative emotions, like confusion and frustration, with post‐discharge problems could be explained due to additional stress of the problem itself or that a distressed frame of mind is associated with reporting more problems that may have been overlooked otherwise. In addition, the association between patient empowerment and lack of PCP awareness could be due to the fact that patients are forced to assume a more proactive role in contacting their PCP if they feel that their PCP was not aware. It is equally possible that PCP communication is selectively initiated by hospital physicians when the patients are least empowered. For example, our comparison of demographics for patients whose PCP was aware versus those that were not do suggest that patient characteristics might play a role in whether a patient's PCP is contacted. The association between a third party advocate and patient empowerment is likely explained as the third party is able to keep the patient informed and empowered.

This study has implications for efforts to design a more patient‐centered care transition for hospitalized older patients. First, patients and their proxies should be advocates for good communication to avoid the risks of care transitions. Prior interventions such as use of coaches to boost patient empowerment have had positive results for hospitalized older patients. Moreover, hospitals should keep in mind that problems after discharge are common and are linked to negative emotions, which may lower patient satisfaction or increase liability risk. Similarly, these findings also highlight the importance of keeping PCPs aware of patient hospitalization. For example, PCPs that are aware of hospitalization are better prepared to properly follow‐up on medications, tests, and appointments. The PCP can also help to better prepare the patient for discharge and ease the transition for the patient.

There are several limitations to our study. First and foremost, our small sample size limits our ability to examine statistical significance. This study was part of a short planning grant to design interventions to improve communication with PCPs during hospitalization. Efforts are currently underway to design a communication solution and educational intervention to highlight the importance of contacting PCPs during hospitalization. Because these patients were hospitalized on the teaching service, the resident with the guidance of the teaching attending is responsible for communicating with the PCP. The teaching attending was either a generalist, hospitalist, or specialist who routinely had no a priori relationship with patients prior to the hospitalization. Only 53% of patients were reached by telephone which raises the concern for nonresponse bias. Our low response rate highlights the challenge of doing this type of work with recently discharge patients in low income, underserved areas. In comparing responders and nonresponders, the only difference between the 2 groups was that responders were more likely to be older. One possible reason for this difference may be that older people are more likely to be at home and easier to contact over the phone. Similarly, since data were collected through interviews and adverse events were discussed, these results are subject to recall bias. Efforts were made to reduce this by calling within 2 to 3 weeks after discharge. Lastly, these findings are limited by generalizability. All the patients included in this study were from the University of Chicago Medical Center, which serves largely underserved, African American patients. The experiences of these patients may be unique to this site. In addition, we only studied patients who had a PCP, excluding a population of patients that are at inherent risk due to lack of a coordinating physician to guide ongoing care.

In conclusion, this study suggests that many frail, older patients reported experiencing a post‐discharge problem and patients whose PCPs did not know about their admission were more likely to report a post‐discharge problem. Systematic interventions to improve communications with PCPs during patient care transitions in and out of the hospital are needed.

Narrative Description

This Case Report reviews the presentation, the differential diagnosis and the treatment modalities used to treat calciphylaxis. It emphasizes the poor prognosis and that there is inadequate clinical experience to guide a physician as to what the most appropriate treatment is despite promising anecdotal reports about a variety of agents. The report demonstrates that intravenous sodium thiosulfate is tolerated.

Key Points

• Calciphylaxis occurs in 1 to 4% of patients with end stage renal failure.

• Two patterns of presentation are generally recognizedcentral and peripheral.

• Pain is a prominent symptom and eschar formation is usually present.

• The role of surgery is controversial.

• Several promising modalities for the treatment of this condition have been described in anecdotal reports.

Calciphylaxis is a rare condition. It is seen most frequently in patients with chronic kidney disease and can affect any part of the body.14 Calciphylaxis is increasingly being referred to as calcific uremic arteriolopathy as this term more accurately reflects the histology of vascular calcification in small‐ and medium‐sized arteries, intimal arterial hypertrophy, and small vessel thrombosis associated with panniculitis, dermal necrosis, and eschar formation.5 Pain is a prominent symptom. The most effective treatment for this condition remains uncertain.

Case Report

A 68‐year‐old female presented with an 8‐month history of increasing lower extremity edema, and numerous large, painful, necrotic ulcers with an associated foul odor. She had a past medical history of type 2 diabetes mellitus, hypertension, end stage renal disease requiring hemodialysis 3 times a week for the previous 6 months, severe peripheral vascular disease, coronary artery disease for which she had previously undergone coronary artery bypass surgery, multiple myocardial infarctions, and congestive heart failure with an ejection fraction of 20%. She had also suffered from numerous infections including septicemia, endocarditis, and a sternal wound infection in the past with no current evidence of septicemia or endocarditis. The patient was not on calcium supplements, Vitamin D, warfarin or calcium‐containing phosphate binders.

Eight months prior to admission she developed vesicles on the left thigh that slowly progressed to large, extremely painful, violaceous, indurated plaques with central ulceration and eschar (Figure 1). She subsequently developed several smaller lesions with similar morphology on her legs and feet and gangrene of her left big toe (Figure 2). A biopsy from the left thigh was consistent with calciphylaxis with associated necrosis of the deep dermis and subcutaneous tissues. The patient's lesions were aggressively debrided, broad spectrum antibiotics given, and the patient dialyzed with low calcium dialysates. Ultimately intravenous sodium thiosulfate (25 g intravenously, over 60 minutes), was given which she tolerated with no side effect. Sodium thiosulfate is thought to act by forming highly soluble calcium thiosulfate salts and therefore mobilizing tissue calcium.5 Hyperbaric oxygen was contraindicated because of the patient's left ventricular ejection fraction (LVEF) of 20% and previous history of congestive heart failure as this treatment modality may precipitate congestive heart failure in a patient with a low LVEF particularly with a past history of congestive heart failure. Her condition continued to deteriorate and she died a few days after initiation of intravenous sodium thiosulfate infusion secondary to a massive gastrointestinal bleed.

Figure 1

Figure 2

Discussion

The differential diagnosis for painful necrotic cutaneous ulcerations with eschar formation includes: calciphylaxis, cryoglobulinemia, cryofibrinogenema, peripheral vascular disease, embolic phenomenon (endocarditis, septic, cholesterol), warfarin skin necrosis, brown recluse spider bites, hypercoagulable states, hyperoxaluria, and necrotizing vasculitis.14

Calciphylaxis is a rare entity that affects approximately 1% to 4% of end stage renal failure patients.1, 3 The typical patient is a morbidly obese, female with longstanding end stage renal disease, diabetes, hyperphosphatemia and an elevated calcium‐phosphate product usually greater than 60 mg²/dL².1, 3 It has also been described in patients with alcoholic cirrhosis and acute reversible renal failure,6 primary and secondary hyperparathyroidism,7 and metastatic breast cancer.8

Patients typically present with symmetric lesions that evolve from erythematous to violaceous, livedo‐reticularis like patches or plaques with occasional bullae to painful, indurated, necrotic plaques that subsequently ulcerate. The ulcerations are slow to heal and covered with eschar.4, 9

There are 2 patterns of involvement. The central/proximal pattern involves the abdomen, gluteal region, and thighs while the peripheral/distal pattern involves the extremities distal to the elbows and knees.1, 2, 4 The central pattern tends to carry a worse prognosis,9, 10 though this has not been validated in all reports and recent literature suggests that patients with both patterns have the worst prognosis.11

A biopsy may be required to exclude other diagnoses. The histology demonstrates an obliterative vasculopathy secondary to the vascular intimal changes and endovascular fibrosis.12 A suggestive finding is calcification of the medial wall of small‐ and medium‐sized arteries and arterioles with associated intimal hyperplasia and fibrosis. Necrosis of the surrounding tissue, panniculitis, and soft tissue calcification are often present.9, 13 The trauma of the biopsy can lead to worsening of the disease.

Secondary to its association with end stage renal disease, laboratory data often reveals elevated blood urea nitrogen (BUN), creatinine, parathyroid hormone, and calcium‐phosphate product. Bone scans show increased uptake in the subcutaneous calcified plaques.14 X‐rays utilizing mammogram technique have demonstrated arteriolar calcification.15

Besides chronic kidney disease, other potential risk factors include protein C and S deficiencies, obesity, warfarin use, high calcium containing dialysates, liver disease, and systemic corticosteroids.4, 9, 11, 16

Calciphylaxis is a difficult disease to treat with a mortality of 60% to 70%9 and a 1‐year survival rate of 45.8%.11 There is no consistently effective treatment.5 Therapy therefore, is focused on symptom control, debridement, and treatment of infection. Mortality is most commonly due to wound infections and resulting septicemia. Meticulous wound care is important with any infection treated early and aggressively. Though trauma and surgical procedures have been known to precipitate ulcerations, given their high rate of infection early surgical debridement of wounds is often required and has been shown to improve mortality.11, 17 Because of the poor healing of the involved tissues, wounds are often left to close by secondary intention or in some circumstances with vacuum assistance.2

As secondary hyperparathyroidism is common, attempts are often made to lower the calcium‐phosphate product. This often requires parathyroidectomy.18 Calcium containing phosphate binders are avoided and low calcium dialysate used.19 However, the above interventions do not consistently improve mortality.5, 11

Other potential treatments include: hyperbaric oxygen therapy,20 intravenous sodium thiosulfate,14 low‐dose tissue plasminogen activator,21 cinacalcet,22 etidronate disodium,23 and maggots.24 Because of the rarity of the condition, most of the literature to date is anecdotal and based on case reports and small retrospective studies.

Conclusions

As the number of patients who develop chronic kidney disease and require hemodialysis increases, it is likely that the number of patients who develop calciphylaxis will also increase. Hospitalists, besides nephrologists, should therefore become familiar with the presentation of this disease as it is possible, although unproven, that treatment in the early stage of the disease may result in a better response. Although several treatment modalities have been used to treat calcific uremic arteriolopathy or calciphylaxis, it remains unclear what is the best treatment for these patients. Carefully done clinical trials using some of the treatment modalities mentioned will help physicians decide what the most appropriate treatment is for patients with this debilitating and often fatal disease.

Narrative Description

This Case Report reviews the presentation, the differential diagnosis and the treatment modalities used to treat calciphylaxis. It emphasizes the poor prognosis and that there is inadequate clinical experience to guide a physician as to what the most appropriate treatment is despite promising anecdotal reports about a variety of agents. The report demonstrates that intravenous sodium thiosulfate is tolerated.

Key Points

• Calciphylaxis occurs in 1 to 4% of patients with end stage renal failure.

• Two patterns of presentation are generally recognizedcentral and peripheral.

• Pain is a prominent symptom and eschar formation is usually present.

• The role of surgery is controversial.

• Several promising modalities for the treatment of this condition have been described in anecdotal reports.

Calciphylaxis is a rare condition. It is seen most frequently in patients with chronic kidney disease and can affect any part of the body.14 Calciphylaxis is increasingly being referred to as calcific uremic arteriolopathy as this term more accurately reflects the histology of vascular calcification in small‐ and medium‐sized arteries, intimal arterial hypertrophy, and small vessel thrombosis associated with panniculitis, dermal necrosis, and eschar formation.5 Pain is a prominent symptom. The most effective treatment for this condition remains uncertain.

Case Report

A 68‐year‐old female presented with an 8‐month history of increasing lower extremity edema, and numerous large, painful, necrotic ulcers with an associated foul odor. She had a past medical history of type 2 diabetes mellitus, hypertension, end stage renal disease requiring hemodialysis 3 times a week for the previous 6 months, severe peripheral vascular disease, coronary artery disease for which she had previously undergone coronary artery bypass surgery, multiple myocardial infarctions, and congestive heart failure with an ejection fraction of 20%. She had also suffered from numerous infections including septicemia, endocarditis, and a sternal wound infection in the past with no current evidence of septicemia or endocarditis. The patient was not on calcium supplements, Vitamin D, warfarin or calcium‐containing phosphate binders.

Eight months prior to admission she developed vesicles on the left thigh that slowly progressed to large, extremely painful, violaceous, indurated plaques with central ulceration and eschar (Figure 1). She subsequently developed several smaller lesions with similar morphology on her legs and feet and gangrene of her left big toe (Figure 2). A biopsy from the left thigh was consistent with calciphylaxis with associated necrosis of the deep dermis and subcutaneous tissues. The patient's lesions were aggressively debrided, broad spectrum antibiotics given, and the patient dialyzed with low calcium dialysates. Ultimately intravenous sodium thiosulfate (25 g intravenously, over 60 minutes), was given which she tolerated with no side effect. Sodium thiosulfate is thought to act by forming highly soluble calcium thiosulfate salts and therefore mobilizing tissue calcium.5 Hyperbaric oxygen was contraindicated because of the patient's left ventricular ejection fraction (LVEF) of 20% and previous history of congestive heart failure as this treatment modality may precipitate congestive heart failure in a patient with a low LVEF particularly with a past history of congestive heart failure. Her condition continued to deteriorate and she died a few days after initiation of intravenous sodium thiosulfate infusion secondary to a massive gastrointestinal bleed.

Figure 1

Figure 2

Discussion

The differential diagnosis for painful necrotic cutaneous ulcerations with eschar formation includes: calciphylaxis, cryoglobulinemia, cryofibrinogenema, peripheral vascular disease, embolic phenomenon (endocarditis, septic, cholesterol), warfarin skin necrosis, brown recluse spider bites, hypercoagulable states, hyperoxaluria, and necrotizing vasculitis.14

Calciphylaxis is a rare entity that affects approximately 1% to 4% of end stage renal failure patients.1, 3 The typical patient is a morbidly obese, female with longstanding end stage renal disease, diabetes, hyperphosphatemia and an elevated calcium‐phosphate product usually greater than 60 mg²/dL².1, 3 It has also been described in patients with alcoholic cirrhosis and acute reversible renal failure,6 primary and secondary hyperparathyroidism,7 and metastatic breast cancer.8

Patients typically present with symmetric lesions that evolve from erythematous to violaceous, livedo‐reticularis like patches or plaques with occasional bullae to painful, indurated, necrotic plaques that subsequently ulcerate. The ulcerations are slow to heal and covered with eschar.4, 9

There are 2 patterns of involvement. The central/proximal pattern involves the abdomen, gluteal region, and thighs while the peripheral/distal pattern involves the extremities distal to the elbows and knees.1, 2, 4 The central pattern tends to carry a worse prognosis,9, 10 though this has not been validated in all reports and recent literature suggests that patients with both patterns have the worst prognosis.11

A biopsy may be required to exclude other diagnoses. The histology demonstrates an obliterative vasculopathy secondary to the vascular intimal changes and endovascular fibrosis.12 A suggestive finding is calcification of the medial wall of small‐ and medium‐sized arteries and arterioles with associated intimal hyperplasia and fibrosis. Necrosis of the surrounding tissue, panniculitis, and soft tissue calcification are often present.9, 13 The trauma of the biopsy can lead to worsening of the disease.

Secondary to its association with end stage renal disease, laboratory data often reveals elevated blood urea nitrogen (BUN), creatinine, parathyroid hormone, and calcium‐phosphate product. Bone scans show increased uptake in the subcutaneous calcified plaques.14 X‐rays utilizing mammogram technique have demonstrated arteriolar calcification.15

Besides chronic kidney disease, other potential risk factors include protein C and S deficiencies, obesity, warfarin use, high calcium containing dialysates, liver disease, and systemic corticosteroids.4, 9, 11, 16

Calciphylaxis is a difficult disease to treat with a mortality of 60% to 70%9 and a 1‐year survival rate of 45.8%.11 There is no consistently effective treatment.5 Therapy therefore, is focused on symptom control, debridement, and treatment of infection. Mortality is most commonly due to wound infections and resulting septicemia. Meticulous wound care is important with any infection treated early and aggressively. Though trauma and surgical procedures have been known to precipitate ulcerations, given their high rate of infection early surgical debridement of wounds is often required and has been shown to improve mortality.11, 17 Because of the poor healing of the involved tissues, wounds are often left to close by secondary intention or in some circumstances with vacuum assistance.2

As secondary hyperparathyroidism is common, attempts are often made to lower the calcium‐phosphate product. This often requires parathyroidectomy.18 Calcium containing phosphate binders are avoided and low calcium dialysate used.19 However, the above interventions do not consistently improve mortality.5, 11

Other potential treatments include: hyperbaric oxygen therapy,20 intravenous sodium thiosulfate,14 low‐dose tissue plasminogen activator,21 cinacalcet,22 etidronate disodium,23 and maggots.24 Because of the rarity of the condition, most of the literature to date is anecdotal and based on case reports and small retrospective studies.

Conclusions

As the number of patients who develop chronic kidney disease and require hemodialysis increases, it is likely that the number of patients who develop calciphylaxis will also increase. Hospitalists, besides nephrologists, should therefore become familiar with the presentation of this disease as it is possible, although unproven, that treatment in the early stage of the disease may result in a better response. Although several treatment modalities have been used to treat calcific uremic arteriolopathy or calciphylaxis, it remains unclear what is the best treatment for these patients. Carefully done clinical trials using some of the treatment modalities mentioned will help physicians decide what the most appropriate treatment is for patients with this debilitating and often fatal disease.

Narrative Description

This Case Report reviews the presentation, the differential diagnosis and the treatment modalities used to treat calciphylaxis. It emphasizes the poor prognosis and that there is inadequate clinical experience to guide a physician as to what the most appropriate treatment is despite promising anecdotal reports about a variety of agents. The report demonstrates that intravenous sodium thiosulfate is tolerated.

Key Points

• Calciphylaxis occurs in 1 to 4% of patients with end stage renal failure.

• Two patterns of presentation are generally recognizedcentral and peripheral.

• Pain is a prominent symptom and eschar formation is usually present.

• The role of surgery is controversial.

• Several promising modalities for the treatment of this condition have been described in anecdotal reports.

Calciphylaxis is a rare condition. It is seen most frequently in patients with chronic kidney disease and can affect any part of the body.14 Calciphylaxis is increasingly being referred to as calcific uremic arteriolopathy as this term more accurately reflects the histology of vascular calcification in small‐ and medium‐sized arteries, intimal arterial hypertrophy, and small vessel thrombosis associated with panniculitis, dermal necrosis, and eschar formation.5 Pain is a prominent symptom. The most effective treatment for this condition remains uncertain.

Case Report

A 68‐year‐old female presented with an 8‐month history of increasing lower extremity edema, and numerous large, painful, necrotic ulcers with an associated foul odor. She had a past medical history of type 2 diabetes mellitus, hypertension, end stage renal disease requiring hemodialysis 3 times a week for the previous 6 months, severe peripheral vascular disease, coronary artery disease for which she had previously undergone coronary artery bypass surgery, multiple myocardial infarctions, and congestive heart failure with an ejection fraction of 20%. She had also suffered from numerous infections including septicemia, endocarditis, and a sternal wound infection in the past with no current evidence of septicemia or endocarditis. The patient was not on calcium supplements, Vitamin D, warfarin or calcium‐containing phosphate binders.

Eight months prior to admission she developed vesicles on the left thigh that slowly progressed to large, extremely painful, violaceous, indurated plaques with central ulceration and eschar (Figure 1). She subsequently developed several smaller lesions with similar morphology on her legs and feet and gangrene of her left big toe (Figure 2). A biopsy from the left thigh was consistent with calciphylaxis with associated necrosis of the deep dermis and subcutaneous tissues. The patient's lesions were aggressively debrided, broad spectrum antibiotics given, and the patient dialyzed with low calcium dialysates. Ultimately intravenous sodium thiosulfate (25 g intravenously, over 60 minutes), was given which she tolerated with no side effect. Sodium thiosulfate is thought to act by forming highly soluble calcium thiosulfate salts and therefore mobilizing tissue calcium.5 Hyperbaric oxygen was contraindicated because of the patient's left ventricular ejection fraction (LVEF) of 20% and previous history of congestive heart failure as this treatment modality may precipitate congestive heart failure in a patient with a low LVEF particularly with a past history of congestive heart failure. Her condition continued to deteriorate and she died a few days after initiation of intravenous sodium thiosulfate infusion secondary to a massive gastrointestinal bleed.

Figure 1

Figure 2

Discussion

The differential diagnosis for painful necrotic cutaneous ulcerations with eschar formation includes: calciphylaxis, cryoglobulinemia, cryofibrinogenema, peripheral vascular disease, embolic phenomenon (endocarditis, septic, cholesterol), warfarin skin necrosis, brown recluse spider bites, hypercoagulable states, hyperoxaluria, and necrotizing vasculitis.14

Calciphylaxis is a rare entity that affects approximately 1% to 4% of end stage renal failure patients.1, 3 The typical patient is a morbidly obese, female with longstanding end stage renal disease, diabetes, hyperphosphatemia and an elevated calcium‐phosphate product usually greater than 60 mg²/dL².1, 3 It has also been described in patients with alcoholic cirrhosis and acute reversible renal failure,6 primary and secondary hyperparathyroidism,7 and metastatic breast cancer.8

Patients typically present with symmetric lesions that evolve from erythematous to violaceous, livedo‐reticularis like patches or plaques with occasional bullae to painful, indurated, necrotic plaques that subsequently ulcerate. The ulcerations are slow to heal and covered with eschar.4, 9

There are 2 patterns of involvement. The central/proximal pattern involves the abdomen, gluteal region, and thighs while the peripheral/distal pattern involves the extremities distal to the elbows and knees.1, 2, 4 The central pattern tends to carry a worse prognosis,9, 10 though this has not been validated in all reports and recent literature suggests that patients with both patterns have the worst prognosis.11

A biopsy may be required to exclude other diagnoses. The histology demonstrates an obliterative vasculopathy secondary to the vascular intimal changes and endovascular fibrosis.12 A suggestive finding is calcification of the medial wall of small‐ and medium‐sized arteries and arterioles with associated intimal hyperplasia and fibrosis. Necrosis of the surrounding tissue, panniculitis, and soft tissue calcification are often present.9, 13 The trauma of the biopsy can lead to worsening of the disease.

Secondary to its association with end stage renal disease, laboratory data often reveals elevated blood urea nitrogen (BUN), creatinine, parathyroid hormone, and calcium‐phosphate product. Bone scans show increased uptake in the subcutaneous calcified plaques.14 X‐rays utilizing mammogram technique have demonstrated arteriolar calcification.15

Besides chronic kidney disease, other potential risk factors include protein C and S deficiencies, obesity, warfarin use, high calcium containing dialysates, liver disease, and systemic corticosteroids.4, 9, 11, 16

Calciphylaxis is a difficult disease to treat with a mortality of 60% to 70%9 and a 1‐year survival rate of 45.8%.11 There is no consistently effective treatment.5 Therapy therefore, is focused on symptom control, debridement, and treatment of infection. Mortality is most commonly due to wound infections and resulting septicemia. Meticulous wound care is important with any infection treated early and aggressively. Though trauma and surgical procedures have been known to precipitate ulcerations, given their high rate of infection early surgical debridement of wounds is often required and has been shown to improve mortality.11, 17 Because of the poor healing of the involved tissues, wounds are often left to close by secondary intention or in some circumstances with vacuum assistance.2

As secondary hyperparathyroidism is common, attempts are often made to lower the calcium‐phosphate product. This often requires parathyroidectomy.18 Calcium containing phosphate binders are avoided and low calcium dialysate used.19 However, the above interventions do not consistently improve mortality.5, 11

Other potential treatments include: hyperbaric oxygen therapy,20 intravenous sodium thiosulfate,14 low‐dose tissue plasminogen activator,21 cinacalcet,22 etidronate disodium,23 and maggots.24 Because of the rarity of the condition, most of the literature to date is anecdotal and based on case reports and small retrospective studies.

Conclusions

As the number of patients who develop chronic kidney disease and require hemodialysis increases, it is likely that the number of patients who develop calciphylaxis will also increase. Hospitalists, besides nephrologists, should therefore become familiar with the presentation of this disease as it is possible, although unproven, that treatment in the early stage of the disease may result in a better response. Although several treatment modalities have been used to treat calcific uremic arteriolopathy or calciphylaxis, it remains unclear what is the best treatment for these patients. Carefully done clinical trials using some of the treatment modalities mentioned will help physicians decide what the most appropriate treatment is for patients with this debilitating and often fatal disease.

Presentation

An 84 year‐old male with past history of osteoarthritis, extensive degenerative spine disease with spinal stenosis presented to the emergency room with left groin pain accompanied by a foul‐smelling discharge from the acupuncture site. He had been receiving regular physical therapy and acupuncture sessions for the past 6 months prior to his presentation. One and a half weeks prior to presentation, needles were inserted over the left groin as part of his acupuncture regimen. The patient described the acupuncture needles originating from a single use, unopened package. Additionally, the patient states his skin was cleaned with an antiseptic solution prior to insertion. Within 3 days, he developed generalized weakness, malaise with localized swelling, erythema, and warmth over the left groin area. His primary care physician performed an incision and drainage and prescribed ciprofloxacin. The patient continued to experience worsening fatigue, difficulty ambulating, ongoing purulent drainage, and consequently presented to the hospital for further evaluation. The patient has an allergy to penicillin but no history of diabetes. He quit smoking 40 years ago and has occasional alcohol intake. Surgical history includes bilateral knee replacement 15 years ago for osteoarthritis and right inguinal hernia repair and appendectomy 60 years ago.

On physical examination the patient had a temperature of 96.8F, pulse of 88 beats per minute, blood pressure of 97/63 mm Hg, and an oxygen saturation of 98% on room air. There was extensive swelling, erythema, and induration of the left anterior and proximal inguinal area, with a 2‐cm malodorous ulcer over the midline thigh. No crepitation or mass was palpable. Range of motion at the hip on the affected limb was limited due to pain. Distal pulses on the lower extremity were present and equal bilaterally. Laboratory examination revealed white blood cell (WBC) = 16.4 with 41% bands. Blood cultures were sent and intravenous vancomycin, ciprofloxacin, clindamycin, and metronidazole were started. A computed tomography (CT)‐scan of the left lower extremity was performed and revealed skin thickening and reticulation of the subcutaneous tissues edema extending from the left groin to the left buttock. Several foci of gas were present within the soft tissues with the largest in the lateral aspect of the buttocks of gas in the soft tissues (Figure 1). The Laboratory Risk Indicator for Necrotizing Fasciitis, the patient scored a 3 out of a possible 13 points. The diagnosis of necrotizing fasciitis was made based on clinical findings and radiographic imaging.

Figure 1

Assessment

Patient became significantly hypotensive which required vasopressor support. He underwent surgical exploration of the left inguinal area. During surgery, tender crepitation of the antero‐lateral aspect of the thigh was noted. Extensive debridement with fasciotomy was performed. Tissue was sent for histopathological analysis and gram‐stain. A negative‐pressure wound dressing was placed over the defect. Post‐operatively, patient required intubation and continued vasopressor support. On post‐operative day 3, patient was extubated. Wound culture report revealed gram negative rods and Enterococcus faecalis which was sensitive to the patients' current antibiotic regimen. Clindamycin was discontinued. The patient was discharged to a subacute rehabilitation facility and returned for a split thickness skin graft 2 months after initial presentation.

Necrotizing fasciitis is a deep‐seated infection of the subcutaneous tissue that results in progressive destruction of fascia and fat. Presenting symptoms include pain, erythema, or bullae formation at the site of infection. Systemic symptoms such as fever, malaise, and myalgias may also be present at the time of presentation. Two types of necrotizing fasciitis are noted to occur. Type 1 is a mixed infection with a predominance of anaerobes1 and carries a 21% mortality.2 It is common post‐operatively and in patients with diabetes. In type 2 necrotizing fasciitis, Group‐A streptococcus was the most common cause of monomicrobial necrotizing fasciitis2 and mortality can be as high as 30%.3 Risk factors for the development of fasciitis include immunosuppression, diabetes, surgery, or penetrating injuries. Gas on soft tissue x‐rays, CT scan, or magnetic resonance imaging (MRI) is a highly specific but insensitive finding and is common in type I necrotizing fasciitis.

The patient in this case likely developed type I necrotizing fasciitis due to the presence of gas on CT scan and polymicrobial culture findings.

Diagnosis

A PubMed search of necrotizing fasciitis and acupuncture reveals only one case report, in which a diabetic patient underwent an unsterile acupuncture consultation.4 To our knowledge, we are the first to describe necrotizing fasciitis occurring in a nondiabetic patient who underwent a sterile acupuncture technique.

Given the lack of an explainable causal relationship regarding the pathogenesis of necrotizing fasciitis in our patient, it appears to be due to the acupuncture needle placement. The patient had no other history of abscesses, trauma and other portals of entry. The patient's presentation, temporal relation of the site of acupuncture, and the development of infection prompted a high index of suspicion as acupuncture as the main etiology.

Management

Treatment of necrotizing fasciitis includes early and aggressive surgical debridement. Multiple antibiotic regimens may be necessary due to the polymicrobial nature of the infection. In our patient, ciprofloxacin was initiated for broadened gram negative coverage, vancomycin for community acquired methicillin‐resistant Staphylococcus aureus (MRSA) and metronidazole for anaerobic coverage. Clindamycin was initiated due to concerns of toxin production, but was discontinued as the patient's condition improved.

Although complications of acupuncture may be rare, there exists the potential to cause life threatening complications. Necrotizing fasciitis has been observed as an adverse effect of acupuncture in a single diabetic patient,4 but can develop in nondiabetic individuals, such as in our patient.

Presentation

An 84 year‐old male with past history of osteoarthritis, extensive degenerative spine disease with spinal stenosis presented to the emergency room with left groin pain accompanied by a foul‐smelling discharge from the acupuncture site. He had been receiving regular physical therapy and acupuncture sessions for the past 6 months prior to his presentation. One and a half weeks prior to presentation, needles were inserted over the left groin as part of his acupuncture regimen. The patient described the acupuncture needles originating from a single use, unopened package. Additionally, the patient states his skin was cleaned with an antiseptic solution prior to insertion. Within 3 days, he developed generalized weakness, malaise with localized swelling, erythema, and warmth over the left groin area. His primary care physician performed an incision and drainage and prescribed ciprofloxacin. The patient continued to experience worsening fatigue, difficulty ambulating, ongoing purulent drainage, and consequently presented to the hospital for further evaluation. The patient has an allergy to penicillin but no history of diabetes. He quit smoking 40 years ago and has occasional alcohol intake. Surgical history includes bilateral knee replacement 15 years ago for osteoarthritis and right inguinal hernia repair and appendectomy 60 years ago.

On physical examination the patient had a temperature of 96.8F, pulse of 88 beats per minute, blood pressure of 97/63 mm Hg, and an oxygen saturation of 98% on room air. There was extensive swelling, erythema, and induration of the left anterior and proximal inguinal area, with a 2‐cm malodorous ulcer over the midline thigh. No crepitation or mass was palpable. Range of motion at the hip on the affected limb was limited due to pain. Distal pulses on the lower extremity were present and equal bilaterally. Laboratory examination revealed white blood cell (WBC) = 16.4 with 41% bands. Blood cultures were sent and intravenous vancomycin, ciprofloxacin, clindamycin, and metronidazole were started. A computed tomography (CT)‐scan of the left lower extremity was performed and revealed skin thickening and reticulation of the subcutaneous tissues edema extending from the left groin to the left buttock. Several foci of gas were present within the soft tissues with the largest in the lateral aspect of the buttocks of gas in the soft tissues (Figure 1). The Laboratory Risk Indicator for Necrotizing Fasciitis, the patient scored a 3 out of a possible 13 points. The diagnosis of necrotizing fasciitis was made based on clinical findings and radiographic imaging.

Figure 1

Assessment

Patient became significantly hypotensive which required vasopressor support. He underwent surgical exploration of the left inguinal area. During surgery, tender crepitation of the antero‐lateral aspect of the thigh was noted. Extensive debridement with fasciotomy was performed. Tissue was sent for histopathological analysis and gram‐stain. A negative‐pressure wound dressing was placed over the defect. Post‐operatively, patient required intubation and continued vasopressor support. On post‐operative day 3, patient was extubated. Wound culture report revealed gram negative rods and Enterococcus faecalis which was sensitive to the patients' current antibiotic regimen. Clindamycin was discontinued. The patient was discharged to a subacute rehabilitation facility and returned for a split thickness skin graft 2 months after initial presentation.

Necrotizing fasciitis is a deep‐seated infection of the subcutaneous tissue that results in progressive destruction of fascia and fat. Presenting symptoms include pain, erythema, or bullae formation at the site of infection. Systemic symptoms such as fever, malaise, and myalgias may also be present at the time of presentation. Two types of necrotizing fasciitis are noted to occur. Type 1 is a mixed infection with a predominance of anaerobes1 and carries a 21% mortality.2 It is common post‐operatively and in patients with diabetes. In type 2 necrotizing fasciitis, Group‐A streptococcus was the most common cause of monomicrobial necrotizing fasciitis2 and mortality can be as high as 30%.3 Risk factors for the development of fasciitis include immunosuppression, diabetes, surgery, or penetrating injuries. Gas on soft tissue x‐rays, CT scan, or magnetic resonance imaging (MRI) is a highly specific but insensitive finding and is common in type I necrotizing fasciitis.

The patient in this case likely developed type I necrotizing fasciitis due to the presence of gas on CT scan and polymicrobial culture findings.

Diagnosis

A PubMed search of necrotizing fasciitis and acupuncture reveals only one case report, in which a diabetic patient underwent an unsterile acupuncture consultation.4 To our knowledge, we are the first to describe necrotizing fasciitis occurring in a nondiabetic patient who underwent a sterile acupuncture technique.

Given the lack of an explainable causal relationship regarding the pathogenesis of necrotizing fasciitis in our patient, it appears to be due to the acupuncture needle placement. The patient had no other history of abscesses, trauma and other portals of entry. The patient's presentation, temporal relation of the site of acupuncture, and the development of infection prompted a high index of suspicion as acupuncture as the main etiology.

Management

Treatment of necrotizing fasciitis includes early and aggressive surgical debridement. Multiple antibiotic regimens may be necessary due to the polymicrobial nature of the infection. In our patient, ciprofloxacin was initiated for broadened gram negative coverage, vancomycin for community acquired methicillin‐resistant Staphylococcus aureus (MRSA) and metronidazole for anaerobic coverage. Clindamycin was initiated due to concerns of toxin production, but was discontinued as the patient's condition improved.

Although complications of acupuncture may be rare, there exists the potential to cause life threatening complications. Necrotizing fasciitis has been observed as an adverse effect of acupuncture in a single diabetic patient,4 but can develop in nondiabetic individuals, such as in our patient.

Presentation

An 84 year‐old male with past history of osteoarthritis, extensive degenerative spine disease with spinal stenosis presented to the emergency room with left groin pain accompanied by a foul‐smelling discharge from the acupuncture site. He had been receiving regular physical therapy and acupuncture sessions for the past 6 months prior to his presentation. One and a half weeks prior to presentation, needles were inserted over the left groin as part of his acupuncture regimen. The patient described the acupuncture needles originating from a single use, unopened package. Additionally, the patient states his skin was cleaned with an antiseptic solution prior to insertion. Within 3 days, he developed generalized weakness, malaise with localized swelling, erythema, and warmth over the left groin area. His primary care physician performed an incision and drainage and prescribed ciprofloxacin. The patient continued to experience worsening fatigue, difficulty ambulating, ongoing purulent drainage, and consequently presented to the hospital for further evaluation. The patient has an allergy to penicillin but no history of diabetes. He quit smoking 40 years ago and has occasional alcohol intake. Surgical history includes bilateral knee replacement 15 years ago for osteoarthritis and right inguinal hernia repair and appendectomy 60 years ago.

On physical examination the patient had a temperature of 96.8F, pulse of 88 beats per minute, blood pressure of 97/63 mm Hg, and an oxygen saturation of 98% on room air. There was extensive swelling, erythema, and induration of the left anterior and proximal inguinal area, with a 2‐cm malodorous ulcer over the midline thigh. No crepitation or mass was palpable. Range of motion at the hip on the affected limb was limited due to pain. Distal pulses on the lower extremity were present and equal bilaterally. Laboratory examination revealed white blood cell (WBC) = 16.4 with 41% bands. Blood cultures were sent and intravenous vancomycin, ciprofloxacin, clindamycin, and metronidazole were started. A computed tomography (CT)‐scan of the left lower extremity was performed and revealed skin thickening and reticulation of the subcutaneous tissues edema extending from the left groin to the left buttock. Several foci of gas were present within the soft tissues with the largest in the lateral aspect of the buttocks of gas in the soft tissues (Figure 1). The Laboratory Risk Indicator for Necrotizing Fasciitis, the patient scored a 3 out of a possible 13 points. The diagnosis of necrotizing fasciitis was made based on clinical findings and radiographic imaging.

Figure 1

Assessment

Patient became significantly hypotensive which required vasopressor support. He underwent surgical exploration of the left inguinal area. During surgery, tender crepitation of the antero‐lateral aspect of the thigh was noted. Extensive debridement with fasciotomy was performed. Tissue was sent for histopathological analysis and gram‐stain. A negative‐pressure wound dressing was placed over the defect. Post‐operatively, patient required intubation and continued vasopressor support. On post‐operative day 3, patient was extubated. Wound culture report revealed gram negative rods and Enterococcus faecalis which was sensitive to the patients' current antibiotic regimen. Clindamycin was discontinued. The patient was discharged to a subacute rehabilitation facility and returned for a split thickness skin graft 2 months after initial presentation.

Necrotizing fasciitis is a deep‐seated infection of the subcutaneous tissue that results in progressive destruction of fascia and fat. Presenting symptoms include pain, erythema, or bullae formation at the site of infection. Systemic symptoms such as fever, malaise, and myalgias may also be present at the time of presentation. Two types of necrotizing fasciitis are noted to occur. Type 1 is a mixed infection with a predominance of anaerobes1 and carries a 21% mortality.2 It is common post‐operatively and in patients with diabetes. In type 2 necrotizing fasciitis, Group‐A streptococcus was the most common cause of monomicrobial necrotizing fasciitis2 and mortality can be as high as 30%.3 Risk factors for the development of fasciitis include immunosuppression, diabetes, surgery, or penetrating injuries. Gas on soft tissue x‐rays, CT scan, or magnetic resonance imaging (MRI) is a highly specific but insensitive finding and is common in type I necrotizing fasciitis.

The patient in this case likely developed type I necrotizing fasciitis due to the presence of gas on CT scan and polymicrobial culture findings.

Diagnosis

A PubMed search of necrotizing fasciitis and acupuncture reveals only one case report, in which a diabetic patient underwent an unsterile acupuncture consultation.4 To our knowledge, we are the first to describe necrotizing fasciitis occurring in a nondiabetic patient who underwent a sterile acupuncture technique.

Given the lack of an explainable causal relationship regarding the pathogenesis of necrotizing fasciitis in our patient, it appears to be due to the acupuncture needle placement. The patient had no other history of abscesses, trauma and other portals of entry. The patient's presentation, temporal relation of the site of acupuncture, and the development of infection prompted a high index of suspicion as acupuncture as the main etiology.

Management

Treatment of necrotizing fasciitis includes early and aggressive surgical debridement. Multiple antibiotic regimens may be necessary due to the polymicrobial nature of the infection. In our patient, ciprofloxacin was initiated for broadened gram negative coverage, vancomycin for community acquired methicillin‐resistant Staphylococcus aureus (MRSA) and metronidazole for anaerobic coverage. Clindamycin was initiated due to concerns of toxin production, but was discontinued as the patient's condition improved.

Although complications of acupuncture may be rare, there exists the potential to cause life threatening complications. Necrotizing fasciitis has been observed as an adverse effect of acupuncture in a single diabetic patient,4 but can develop in nondiabetic individuals, such as in our patient.

Patients without a spleen have a diminished host immune defense in response to bacteria.1 Especially in the first 2 years after surgery there is a risk for severe infection, mostly with encapsulated bacteria such as Streptococcus pneumoniae.2 This syndrome is called post‐splenectomy sepsis (PSS), and although the incidence is estimated to be low, it is associated with a high mortality of 50% to 70%.2 Importantly, PSS can largely be prevented if protective measures such as immunization and the prescription of antibiotics are taken. Several relevant organizations and committees have developed guidelines for prevention of infections in this group of patients.3 The recommendations by the British Committee for Standards in Haematology are currently considered to reflect best practice4, 5 and consist of the key‐elements shown in Box 1.

Unfortunately, adherence to guidelines is generally considered to be low.6 One of the most consistent findings in health services research is the gap between best practice and actual clinical care.7, 8 We have shown earlier that management of splenectomized patients in the Netherlands is not optimal (Lammers et al., Management of post‐splenectomy patients in the Netherlands, EJCMID, in press, DOI: 10.1007/s10096‐009‐0870‐x).

Several studies demonstrate that performance of hospitals is related to structural characteristics such as teaching status and practice organization.911 A large review showed that teaching hospitals in general offer better care than nonteaching hospitals. Furthermore, major teaching hospitals perform better than minor and nonteaching hospitals.12, 13

The aim of the present study was to investigate whether or not hospital structural characteristics of care delivery are associated with better compliance with best‐practice guidelines for preventing infections in splenectomized patients in Dutch hospitals. Our research questions were two‐fold: (1) are teaching hospitals delivering better quality of care in the prevention of infections in splenectomized patients than nonteaching hospitals and (2) is there an association between characteristics of practice organization (ie, the size of the surgical staff, the availability of a protocol for post‐splenectomy management, and the use of a complication registry by the department of surgery) and quality of care. Quality of care parameters were defined as outcome of adherence to the prevention guidelines of the British Committee for Standards in Haematology.

Methods

Results

We included 28 of 93 Dutch hospitals (30%), containing a total of 536 splenectomized patients (Table 1.) Five hospitals were excluded because they refused cooperation, and were subsequently replaced by comparable hospitals in their category.

Discussion

Conclusion

University hospitals offer higher guideline adherence in preventing infections after splenectomy than other teaching and nonteaching hospitals. For all Dutch hospitals there is room for improving the quality of post‐splenectomy patient care. The results of this study suggest that the difference in performance may be related to several characteristics of hospital practice organization. Future research should further investigate these hospital characteristics and their influence on performance.

Patients without a spleen have a diminished host immune defense in response to bacteria.1 Especially in the first 2 years after surgery there is a risk for severe infection, mostly with encapsulated bacteria such as Streptococcus pneumoniae.2 This syndrome is called post‐splenectomy sepsis (PSS), and although the incidence is estimated to be low, it is associated with a high mortality of 50% to 70%.2 Importantly, PSS can largely be prevented if protective measures such as immunization and the prescription of antibiotics are taken. Several relevant organizations and committees have developed guidelines for prevention of infections in this group of patients.3 The recommendations by the British Committee for Standards in Haematology are currently considered to reflect best practice4, 5 and consist of the key‐elements shown in Box 1.

Unfortunately, adherence to guidelines is generally considered to be low.6 One of the most consistent findings in health services research is the gap between best practice and actual clinical care.7, 8 We have shown earlier that management of splenectomized patients in the Netherlands is not optimal (Lammers et al., Management of post‐splenectomy patients in the Netherlands, EJCMID, in press, DOI: 10.1007/s10096‐009‐0870‐x).

Several studies demonstrate that performance of hospitals is related to structural characteristics such as teaching status and practice organization.911 A large review showed that teaching hospitals in general offer better care than nonteaching hospitals. Furthermore, major teaching hospitals perform better than minor and nonteaching hospitals.12, 13

The aim of the present study was to investigate whether or not hospital structural characteristics of care delivery are associated with better compliance with best‐practice guidelines for preventing infections in splenectomized patients in Dutch hospitals. Our research questions were two‐fold: (1) are teaching hospitals delivering better quality of care in the prevention of infections in splenectomized patients than nonteaching hospitals and (2) is there an association between characteristics of practice organization (ie, the size of the surgical staff, the availability of a protocol for post‐splenectomy management, and the use of a complication registry by the department of surgery) and quality of care. Quality of care parameters were defined as outcome of adherence to the prevention guidelines of the British Committee for Standards in Haematology.

Methods

Results

We included 28 of 93 Dutch hospitals (30%), containing a total of 536 splenectomized patients (Table 1.) Five hospitals were excluded because they refused cooperation, and were subsequently replaced by comparable hospitals in their category.

Discussion

Conclusion

University hospitals offer higher guideline adherence in preventing infections after splenectomy than other teaching and nonteaching hospitals. For all Dutch hospitals there is room for improving the quality of post‐splenectomy patient care. The results of this study suggest that the difference in performance may be related to several characteristics of hospital practice organization. Future research should further investigate these hospital characteristics and their influence on performance.

Patients without a spleen have a diminished host immune defense in response to bacteria.1 Especially in the first 2 years after surgery there is a risk for severe infection, mostly with encapsulated bacteria such as Streptococcus pneumoniae.2 This syndrome is called post‐splenectomy sepsis (PSS), and although the incidence is estimated to be low, it is associated with a high mortality of 50% to 70%.2 Importantly, PSS can largely be prevented if protective measures such as immunization and the prescription of antibiotics are taken. Several relevant organizations and committees have developed guidelines for prevention of infections in this group of patients.3 The recommendations by the British Committee for Standards in Haematology are currently considered to reflect best practice4, 5 and consist of the key‐elements shown in Box 1.

Unfortunately, adherence to guidelines is generally considered to be low.6 One of the most consistent findings in health services research is the gap between best practice and actual clinical care.7, 8 We have shown earlier that management of splenectomized patients in the Netherlands is not optimal (Lammers et al., Management of post‐splenectomy patients in the Netherlands, EJCMID, in press, DOI: 10.1007/s10096‐009‐0870‐x).

Several studies demonstrate that performance of hospitals is related to structural characteristics such as teaching status and practice organization.911 A large review showed that teaching hospitals in general offer better care than nonteaching hospitals. Furthermore, major teaching hospitals perform better than minor and nonteaching hospitals.12, 13

The aim of the present study was to investigate whether or not hospital structural characteristics of care delivery are associated with better compliance with best‐practice guidelines for preventing infections in splenectomized patients in Dutch hospitals. Our research questions were two‐fold: (1) are teaching hospitals delivering better quality of care in the prevention of infections in splenectomized patients than nonteaching hospitals and (2) is there an association between characteristics of practice organization (ie, the size of the surgical staff, the availability of a protocol for post‐splenectomy management, and the use of a complication registry by the department of surgery) and quality of care. Quality of care parameters were defined as outcome of adherence to the prevention guidelines of the British Committee for Standards in Haematology.

Methods

Results

We included 28 of 93 Dutch hospitals (30%), containing a total of 536 splenectomized patients (Table 1.) Five hospitals were excluded because they refused cooperation, and were subsequently replaced by comparable hospitals in their category.

Discussion

Conclusion

University hospitals offer higher guideline adherence in preventing infections after splenectomy than other teaching and nonteaching hospitals. For all Dutch hospitals there is room for improving the quality of post‐splenectomy patient care. The results of this study suggest that the difference in performance may be related to several characteristics of hospital practice organization. Future research should further investigate these hospital characteristics and their influence on performance.

A 62‐year‐old woman with an extensive medical and surgical history presented with complaints of 2 days of weakness. Physical examination demonstrated a lethargic, but arousable woman in no distress. Her lower extremity motor strength was 4/5 bilaterally. The patient's electrocardiogram (ECG) demonstrated peaked T waves (Figure 1, arrow), absence of P waves, poor R wave progression and QRS interval widening (Figure 1, 2‐headed arrow.) Serum chemistries revealed a potassium level of 10.4 mmol/L and a creatinine of 0.9 mg/dL.

Figure 1

One ampule of D50, 10 units of insulin, 1 ampule of Calcium gluconate and 1 ampule of sodium bicarbonate were given intravenously along with oral Kayexalate. A repeat ECG showed a return of P waves, narrowing of the QRS interval, improved R wave progression and less peaking of the T waves (Figure 2). A repeat potassium level at that time was 9.2 mmol/L.

Figure 2

Despite continued therapy to lower the potassium, another ECG showed a return of peaked T waves, a prolonged PR interval and marked widening of the QRS interval to 205 msec; the potassium level was now 10.0 mmol/L (Figure 3).

Figure 3

Despite the patient's renal function being normal, she was emergently dialyzed. After a single dialysis, the patient's potassium level remained normal for the remainder of the hospitalization and a follow‐up ECG returned to baseline (Figure 4). No physiologic explanation was found for her hyperkalemia and it was concluded, despite her denials, that she had taken large quantities of exogenous potassium she had available from previous prescriptions.

Figure 4

A 62‐year‐old woman with an extensive medical and surgical history presented with complaints of 2 days of weakness. Physical examination demonstrated a lethargic, but arousable woman in no distress. Her lower extremity motor strength was 4/5 bilaterally. The patient's electrocardiogram (ECG) demonstrated peaked T waves (Figure 1, arrow), absence of P waves, poor R wave progression and QRS interval widening (Figure 1, 2‐headed arrow.) Serum chemistries revealed a potassium level of 10.4 mmol/L and a creatinine of 0.9 mg/dL.

Figure 1

One ampule of D50, 10 units of insulin, 1 ampule of Calcium gluconate and 1 ampule of sodium bicarbonate were given intravenously along with oral Kayexalate. A repeat ECG showed a return of P waves, narrowing of the QRS interval, improved R wave progression and less peaking of the T waves (Figure 2). A repeat potassium level at that time was 9.2 mmol/L.

Figure 2

Despite continued therapy to lower the potassium, another ECG showed a return of peaked T waves, a prolonged PR interval and marked widening of the QRS interval to 205 msec; the potassium level was now 10.0 mmol/L (Figure 3).

Figure 3

Despite the patient's renal function being normal, she was emergently dialyzed. After a single dialysis, the patient's potassium level remained normal for the remainder of the hospitalization and a follow‐up ECG returned to baseline (Figure 4). No physiologic explanation was found for her hyperkalemia and it was concluded, despite her denials, that she had taken large quantities of exogenous potassium she had available from previous prescriptions.

Figure 4

A 62‐year‐old woman with an extensive medical and surgical history presented with complaints of 2 days of weakness. Physical examination demonstrated a lethargic, but arousable woman in no distress. Her lower extremity motor strength was 4/5 bilaterally. The patient's electrocardiogram (ECG) demonstrated peaked T waves (Figure 1, arrow), absence of P waves, poor R wave progression and QRS interval widening (Figure 1, 2‐headed arrow.) Serum chemistries revealed a potassium level of 10.4 mmol/L and a creatinine of 0.9 mg/dL.

Figure 1

One ampule of D50, 10 units of insulin, 1 ampule of Calcium gluconate and 1 ampule of sodium bicarbonate were given intravenously along with oral Kayexalate. A repeat ECG showed a return of P waves, narrowing of the QRS interval, improved R wave progression and less peaking of the T waves (Figure 2). A repeat potassium level at that time was 9.2 mmol/L.

Figure 2

Despite continued therapy to lower the potassium, another ECG showed a return of peaked T waves, a prolonged PR interval and marked widening of the QRS interval to 205 msec; the potassium level was now 10.0 mmol/L (Figure 3).

Figure 3

Despite the patient's renal function being normal, she was emergently dialyzed. After a single dialysis, the patient's potassium level remained normal for the remainder of the hospitalization and a follow‐up ECG returned to baseline (Figure 4). No physiologic explanation was found for her hyperkalemia and it was concluded, despite her denials, that she had taken large quantities of exogenous potassium she had available from previous prescriptions.

Figure 4

Hospitalists frequently diagnose and treat lower extremity deep venous thrombosis (DVT). Patients presenting with acute DVT or chronic venous stasis of the left leg can have an underlying anatomic anomaly known as iliac vein compression syndrome (ICS), May‐Thurner syndrome, or Cockett syndrome in Europe. In this condition, the right iliac artery overlies the left iliac vein, causing extrinsic compression of the vein (Figure 1). 1 This compression and accompanying intraluminal changes predisposes patients to left‐sided lower extremity DVT.2 Failure to recognize and treat this anomaly in patients with acute thrombosis can result in serious vascular sequelae and chronic left leg symptoms.3 A high clinical suspicion should be maintained in young individuals presenting with proximal left leg DVT with or without hypercoagulable risk factors. The following report is a case of ICS in a young male recognized and treated early by aggressive diagnostic and therapeutic interventions.

Figure 1

Case Report

A 19‐year‐old man presented to the ER with sudden onset of left lower extremity swelling and pain 5 days after a fall. He had no known risk factors for DVT. On physical examination his left leg was dusky, swollen, and tender from his groin to his ankle, with good arterial pulses. Duplex ultra‐sonogram of the leg showed a clot in the femoral vein extending up the popliteal vein. Following a venogram, he underwent mechanical thrombectomy and regional thrombolysis. A repeat venogram showed an irregular narrowing of the left iliac vein and a tubular filling defect at the junction of the inferior vena cava and common iliac veins, suggestive of external compression from the right common iliac artery. The patient underwent successful angioplasty and stenting of the common iliac vein. He was treated with intravenous heparin, warfarin and clopidogrel. His hypercoagulable work‐up was inconclusive.

Discussion

In 1956, May and Thurner 1 brought clinical attention to ICS. They hypothesized that an abnormal compression of the left iliac vein by an overriding right iliac arterypresent in 22% of a series of 430 cadaversled to an intraluminal filling defect in the vein. The chronic extrinsic compression and pulsing force from the overlying artery results in endothelial irritation and formation of venous spurs (fibrous vascular lesions) in the intimal layer of the vein.1 Following the principles of Virchow's triad, this endothelial injury propagates the formation of a thrombus. Subsequent studies by Kim et al.4 suggest that there are 3 stages involved in the pathogenesis of thrombosis in ICS: asymptomatic vein compression, venous spur formation, and finally DVT formation.4, 5 It is estimated that 1 to 3 out of 1000 individuals with this malformation develop DVT each year.5, 6

Patients with ICS may present to the emergency or ambulatory setting in either an acute or chronic phase. The acute phase is the actual episode of thrombosis. Symptoms include left leg pain and swelling up to the groin. In rare cases, pulmonary emboli may be the initial presentation. A lifelong chronic phase can follow if undiagnosed, resulting in pain and swelling of the entire left leg, venous claudication, recurrent thrombosis, pigmentation changes, and ulceration. 3

The typical ICS patient is a woman between 18 and 30 years old, 3 possibly due to the developmental changes in the pelvic structures in preparation for child‐bearing.2 Many patients also present after pregnancy; increased lordosis during pregnancy may put additional strain on the anatomic lesion.3 Nevertheless, Steinberg and Jacocks7 reported that out of 127 patients, 38 (30%) were male. Thus, it is critical not to overlook ICS as a possible cause of thrombosis in male patients.

The urgency in diagnosing this anatomic variation lies in the distinct need for more aggressive treatment than that required for a typical DVT. While Doppler ultrasound is typically the first diagnostic test performed in this patient population, it is not specific. For patients with physical exam findings highly suspicious of ICS, venography and magnetic resonance venography are superior modalities to make a definitive diagnosis of the syndrome. 8 In ICS, these studies will reveal left common iliac vein narrowing with intraluminal changes suggestive of spur formation.2

Due to the mechanical nature of ICS pathology, anticoagulation therapy alone is ineffective. ICS prevents recanalization in 70% to 80% of patients and up to 40% will have continued clot propagation. 5, 7 More aggressive treatment using endovascular techniques such as the combination of thrombectomy, angioplasty, and intraluminal stenting have proven to be the most efficacious treatment modality for ICS.9 A study by AbuRahma et al.10 demonstrated that one year following this aggressive combination, patency rate was 83% (vs. 24% following thrombectomy alone).

Conclusion

The anatomic anomaly present in ICS was identified by CT in as many as two‐thirds of an asymptomatic patient population studied by Kibbe et al. 12 Although a common structural anomaly, it is important to note that only 1 to 3 out of 1000 individuals with this malformation develop DVT annually. ICS should be included in the differential diagnosis of all young individuals presenting with proximal left leg DVT with or without hypercoagulable risk factors. If the mechanical compression is not diagnosed and treated, the syndrome can develop into a life‐long chronic phase with multiple complications.2 It is therefore critical that aggressive diagnostic and therapeutic interventions be implemented immediately upon suspicion of ICS.

Hospitalists frequently diagnose and treat lower extremity deep venous thrombosis (DVT). Patients presenting with acute DVT or chronic venous stasis of the left leg can have an underlying anatomic anomaly known as iliac vein compression syndrome (ICS), May‐Thurner syndrome, or Cockett syndrome in Europe. In this condition, the right iliac artery overlies the left iliac vein, causing extrinsic compression of the vein (Figure 1). 1 This compression and accompanying intraluminal changes predisposes patients to left‐sided lower extremity DVT.2 Failure to recognize and treat this anomaly in patients with acute thrombosis can result in serious vascular sequelae and chronic left leg symptoms.3 A high clinical suspicion should be maintained in young individuals presenting with proximal left leg DVT with or without hypercoagulable risk factors. The following report is a case of ICS in a young male recognized and treated early by aggressive diagnostic and therapeutic interventions.

Figure 1

Case Report

A 19‐year‐old man presented to the ER with sudden onset of left lower extremity swelling and pain 5 days after a fall. He had no known risk factors for DVT. On physical examination his left leg was dusky, swollen, and tender from his groin to his ankle, with good arterial pulses. Duplex ultra‐sonogram of the leg showed a clot in the femoral vein extending up the popliteal vein. Following a venogram, he underwent mechanical thrombectomy and regional thrombolysis. A repeat venogram showed an irregular narrowing of the left iliac vein and a tubular filling defect at the junction of the inferior vena cava and common iliac veins, suggestive of external compression from the right common iliac artery. The patient underwent successful angioplasty and stenting of the common iliac vein. He was treated with intravenous heparin, warfarin and clopidogrel. His hypercoagulable work‐up was inconclusive.

Discussion

In 1956, May and Thurner 1 brought clinical attention to ICS. They hypothesized that an abnormal compression of the left iliac vein by an overriding right iliac arterypresent in 22% of a series of 430 cadaversled to an intraluminal filling defect in the vein. The chronic extrinsic compression and pulsing force from the overlying artery results in endothelial irritation and formation of venous spurs (fibrous vascular lesions) in the intimal layer of the vein.1 Following the principles of Virchow's triad, this endothelial injury propagates the formation of a thrombus. Subsequent studies by Kim et al.4 suggest that there are 3 stages involved in the pathogenesis of thrombosis in ICS: asymptomatic vein compression, venous spur formation, and finally DVT formation.4, 5 It is estimated that 1 to 3 out of 1000 individuals with this malformation develop DVT each year.5, 6

Patients with ICS may present to the emergency or ambulatory setting in either an acute or chronic phase. The acute phase is the actual episode of thrombosis. Symptoms include left leg pain and swelling up to the groin. In rare cases, pulmonary emboli may be the initial presentation. A lifelong chronic phase can follow if undiagnosed, resulting in pain and swelling of the entire left leg, venous claudication, recurrent thrombosis, pigmentation changes, and ulceration. 3

The typical ICS patient is a woman between 18 and 30 years old, 3 possibly due to the developmental changes in the pelvic structures in preparation for child‐bearing.2 Many patients also present after pregnancy; increased lordosis during pregnancy may put additional strain on the anatomic lesion.3 Nevertheless, Steinberg and Jacocks7 reported that out of 127 patients, 38 (30%) were male. Thus, it is critical not to overlook ICS as a possible cause of thrombosis in male patients.

The urgency in diagnosing this anatomic variation lies in the distinct need for more aggressive treatment than that required for a typical DVT. While Doppler ultrasound is typically the first diagnostic test performed in this patient population, it is not specific. For patients with physical exam findings highly suspicious of ICS, venography and magnetic resonance venography are superior modalities to make a definitive diagnosis of the syndrome. 8 In ICS, these studies will reveal left common iliac vein narrowing with intraluminal changes suggestive of spur formation.2

Due to the mechanical nature of ICS pathology, anticoagulation therapy alone is ineffective. ICS prevents recanalization in 70% to 80% of patients and up to 40% will have continued clot propagation. 5, 7 More aggressive treatment using endovascular techniques such as the combination of thrombectomy, angioplasty, and intraluminal stenting have proven to be the most efficacious treatment modality for ICS.9 A study by AbuRahma et al.10 demonstrated that one year following this aggressive combination, patency rate was 83% (vs. 24% following thrombectomy alone).

Conclusion

The anatomic anomaly present in ICS was identified by CT in as many as two‐thirds of an asymptomatic patient population studied by Kibbe et al. 12 Although a common structural anomaly, it is important to note that only 1 to 3 out of 1000 individuals with this malformation develop DVT annually. ICS should be included in the differential diagnosis of all young individuals presenting with proximal left leg DVT with or without hypercoagulable risk factors. If the mechanical compression is not diagnosed and treated, the syndrome can develop into a life‐long chronic phase with multiple complications.2 It is therefore critical that aggressive diagnostic and therapeutic interventions be implemented immediately upon suspicion of ICS.

Hospitalists frequently diagnose and treat lower extremity deep venous thrombosis (DVT). Patients presenting with acute DVT or chronic venous stasis of the left leg can have an underlying anatomic anomaly known as iliac vein compression syndrome (ICS), May‐Thurner syndrome, or Cockett syndrome in Europe. In this condition, the right iliac artery overlies the left iliac vein, causing extrinsic compression of the vein (Figure 1). 1 This compression and accompanying intraluminal changes predisposes patients to left‐sided lower extremity DVT.2 Failure to recognize and treat this anomaly in patients with acute thrombosis can result in serious vascular sequelae and chronic left leg symptoms.3 A high clinical suspicion should be maintained in young individuals presenting with proximal left leg DVT with or without hypercoagulable risk factors. The following report is a case of ICS in a young male recognized and treated early by aggressive diagnostic and therapeutic interventions.

Figure 1

Case Report

A 19‐year‐old man presented to the ER with sudden onset of left lower extremity swelling and pain 5 days after a fall. He had no known risk factors for DVT. On physical examination his left leg was dusky, swollen, and tender from his groin to his ankle, with good arterial pulses. Duplex ultra‐sonogram of the leg showed a clot in the femoral vein extending up the popliteal vein. Following a venogram, he underwent mechanical thrombectomy and regional thrombolysis. A repeat venogram showed an irregular narrowing of the left iliac vein and a tubular filling defect at the junction of the inferior vena cava and common iliac veins, suggestive of external compression from the right common iliac artery. The patient underwent successful angioplasty and stenting of the common iliac vein. He was treated with intravenous heparin, warfarin and clopidogrel. His hypercoagulable work‐up was inconclusive.

Discussion

In 1956, May and Thurner 1 brought clinical attention to ICS. They hypothesized that an abnormal compression of the left iliac vein by an overriding right iliac arterypresent in 22% of a series of 430 cadaversled to an intraluminal filling defect in the vein. The chronic extrinsic compression and pulsing force from the overlying artery results in endothelial irritation and formation of venous spurs (fibrous vascular lesions) in the intimal layer of the vein.1 Following the principles of Virchow's triad, this endothelial injury propagates the formation of a thrombus. Subsequent studies by Kim et al.4 suggest that there are 3 stages involved in the pathogenesis of thrombosis in ICS: asymptomatic vein compression, venous spur formation, and finally DVT formation.4, 5 It is estimated that 1 to 3 out of 1000 individuals with this malformation develop DVT each year.5, 6

Patients with ICS may present to the emergency or ambulatory setting in either an acute or chronic phase. The acute phase is the actual episode of thrombosis. Symptoms include left leg pain and swelling up to the groin. In rare cases, pulmonary emboli may be the initial presentation. A lifelong chronic phase can follow if undiagnosed, resulting in pain and swelling of the entire left leg, venous claudication, recurrent thrombosis, pigmentation changes, and ulceration. 3

The typical ICS patient is a woman between 18 and 30 years old, 3 possibly due to the developmental changes in the pelvic structures in preparation for child‐bearing.2 Many patients also present after pregnancy; increased lordosis during pregnancy may put additional strain on the anatomic lesion.3 Nevertheless, Steinberg and Jacocks7 reported that out of 127 patients, 38 (30%) were male. Thus, it is critical not to overlook ICS as a possible cause of thrombosis in male patients.

The urgency in diagnosing this anatomic variation lies in the distinct need for more aggressive treatment than that required for a typical DVT. While Doppler ultrasound is typically the first diagnostic test performed in this patient population, it is not specific. For patients with physical exam findings highly suspicious of ICS, venography and magnetic resonance venography are superior modalities to make a definitive diagnosis of the syndrome. 8 In ICS, these studies will reveal left common iliac vein narrowing with intraluminal changes suggestive of spur formation.2

Due to the mechanical nature of ICS pathology, anticoagulation therapy alone is ineffective. ICS prevents recanalization in 70% to 80% of patients and up to 40% will have continued clot propagation. 5, 7 More aggressive treatment using endovascular techniques such as the combination of thrombectomy, angioplasty, and intraluminal stenting have proven to be the most efficacious treatment modality for ICS.9 A study by AbuRahma et al.10 demonstrated that one year following this aggressive combination, patency rate was 83% (vs. 24% following thrombectomy alone).

Conclusion

The anatomic anomaly present in ICS was identified by CT in as many as two‐thirds of an asymptomatic patient population studied by Kibbe et al. 12 Although a common structural anomaly, it is important to note that only 1 to 3 out of 1000 individuals with this malformation develop DVT annually. ICS should be included in the differential diagnosis of all young individuals presenting with proximal left leg DVT with or without hypercoagulable risk factors. If the mechanical compression is not diagnosed and treated, the syndrome can develop into a life‐long chronic phase with multiple complications.2 It is therefore critical that aggressive diagnostic and therapeutic interventions be implemented immediately upon suspicion of ICS.

A 15‐year‐old male was hospitalized with painful blisters on the lips and ulcers in the oral mucosa that were preceded by upper respiratory infection symptoms for 1 week. He had not been treated with antimicrobials. He subsequently developed conjunctival injection and painful blisters at the urethral meatus and symmetric scattered target lesions in the extremities. Examination demonstrated low‐grade fever, mild conjunctival injection (Figure 2), and oral vesicular lesions affecting the lips (Figure 1) and both the hard and soft palate; he had vesicular lesions affecting the glans penis, a ruptured vesicle at the urethral meatus and target lesions in the arms (Figure 3) and legs (Figure 4). His cardiopulmonary exam was normal. He was started on acyclovir and azithromycin, and symptomatic treatment with oral lidocaine and morphine. Serologies for Epstein‐Barr virus (EBV), cytomegalovirus (CMV) and Coxsackievirus and cultures for herpes simplex virus (HSV) were negative. Mycoplasma pneumoniae immunoglobulin G (IgG) and IgM titers were significantly elevated (>4‐fold) and the diagnosis made of Stevens‐Johnson syndrome (SJS) secondary to Mycoplasma pneumoniae infection. He was able to tolerate oral intake after a 1‐week hospital course.

M. pneumoniae infection can cause mucocutaneous involvement varying from mild mucositis to SJS with significant morbidity and mortality, 1, 2 mostly in the pediatric population. The differential diagnosis includes HSV, Kawasaki, and Streptococcal toxic shock syndrome, as well as other viral infections (eg, Coxsackievirus).3 Pharmacologic causesespecially antibiotics, non steroidal anti‐inflammatory drug (NSAIDS) and anticonvulsantsshould also be considered in the etiology of SJS4 especially in the adult population.

Figure 1

Figure 2

Figure 3

Figure 4

A 15‐year‐old male was hospitalized with painful blisters on the lips and ulcers in the oral mucosa that were preceded by upper respiratory infection symptoms for 1 week. He had not been treated with antimicrobials. He subsequently developed conjunctival injection and painful blisters at the urethral meatus and symmetric scattered target lesions in the extremities. Examination demonstrated low‐grade fever, mild conjunctival injection (Figure 2), and oral vesicular lesions affecting the lips (Figure 1) and both the hard and soft palate; he had vesicular lesions affecting the glans penis, a ruptured vesicle at the urethral meatus and target lesions in the arms (Figure 3) and legs (Figure 4). His cardiopulmonary exam was normal. He was started on acyclovir and azithromycin, and symptomatic treatment with oral lidocaine and morphine. Serologies for Epstein‐Barr virus (EBV), cytomegalovirus (CMV) and Coxsackievirus and cultures for herpes simplex virus (HSV) were negative. Mycoplasma pneumoniae immunoglobulin G (IgG) and IgM titers were significantly elevated (>4‐fold) and the diagnosis made of Stevens‐Johnson syndrome (SJS) secondary to Mycoplasma pneumoniae infection. He was able to tolerate oral intake after a 1‐week hospital course.

M. pneumoniae infection can cause mucocutaneous involvement varying from mild mucositis to SJS with significant morbidity and mortality, 1, 2 mostly in the pediatric population. The differential diagnosis includes HSV, Kawasaki, and Streptococcal toxic shock syndrome, as well as other viral infections (eg, Coxsackievirus).3 Pharmacologic causesespecially antibiotics, non steroidal anti‐inflammatory drug (NSAIDS) and anticonvulsantsshould also be considered in the etiology of SJS4 especially in the adult population.

Figure 1

Figure 2

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Figure 4

A 15‐year‐old male was hospitalized with painful blisters on the lips and ulcers in the oral mucosa that were preceded by upper respiratory infection symptoms for 1 week. He had not been treated with antimicrobials. He subsequently developed conjunctival injection and painful blisters at the urethral meatus and symmetric scattered target lesions in the extremities. Examination demonstrated low‐grade fever, mild conjunctival injection (Figure 2), and oral vesicular lesions affecting the lips (Figure 1) and both the hard and soft palate; he had vesicular lesions affecting the glans penis, a ruptured vesicle at the urethral meatus and target lesions in the arms (Figure 3) and legs (Figure 4). His cardiopulmonary exam was normal. He was started on acyclovir and azithromycin, and symptomatic treatment with oral lidocaine and morphine. Serologies for Epstein‐Barr virus (EBV), cytomegalovirus (CMV) and Coxsackievirus and cultures for herpes simplex virus (HSV) were negative. Mycoplasma pneumoniae immunoglobulin G (IgG) and IgM titers were significantly elevated (>4‐fold) and the diagnosis made of Stevens‐Johnson syndrome (SJS) secondary to Mycoplasma pneumoniae infection. He was able to tolerate oral intake after a 1‐week hospital course.

M. pneumoniae infection can cause mucocutaneous involvement varying from mild mucositis to SJS with significant morbidity and mortality, 1, 2 mostly in the pediatric population. The differential diagnosis includes HSV, Kawasaki, and Streptococcal toxic shock syndrome, as well as other viral infections (eg, Coxsackievirus).3 Pharmacologic causesespecially antibiotics, non steroidal anti‐inflammatory drug (NSAIDS) and anticonvulsantsshould also be considered in the etiology of SJS4 especially in the adult population.

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With about 1 in 5 working‐age Americans (age 18‐64 years) currently uninsured and a large number relying on Medicaid, adequate access to quality health care services is becoming increasingly difficult.1 Substantial literature has accumulated over the years suggesting that access and quality in health care are closely linked to an individual's health insurance status.211 Some studies indicate that being uninsured or publicly insured is associated with negative health consequences.12, 13 Although the Medicaid program has improved access for qualifying low‐income individuals, significant gaps in access and quality remain.2, 5, 11, 1419 These issues are likely to become more pervasive should there be further modifications to state Medicaid funding in response to the unfolding economic crisis.

Although numerous studies have focused on insurance‐related disparities in the outpatient setting, few nationally representative studies have examined such disparities among hospitalized patients. A cross‐sectional study of a large hospital database from 1987 reported higher risk‐adjusted in‐hospital mortality, shorter length of stay (LOS), and lower procedure use among uninsured patients.9 A more recent analysis, limited to patients admitted with stroke, reported significant variation in hospital care associated with insurance status.15 Other studies reporting myocardial infarction registry and quality improvement program data are biased by the self‐selection of large urban teaching hospitals.1618 To our knowledge, no nationally representative study has focused on the impact of insurance coverage on hospital care for common medical conditions among working‐age Americans, the fastest growing segment of the uninsured population.

To address this gap in knowledge, we analyzed a nationally representative hospital database to determine whether there are significant insurance‐related disparities in in‐hospital mortality, LOS, and cost per hospitalization for 3 common medical conditions among working‐age adults, and, if present, to determine whether these disparities are due to differences in disease severity and comorbidities, and whether these disparities are affected by the proportion of uninsured and Medicaid patients receiving care in each hospital.

Methods

Results