0

Figure 1

Stolen Kisses (by Emily Osborn)

Poetry, without question, is a tricky thing. For many Americans it is an unapproachable art form that resides in a fortress guarded by elite intellectuals. For the minority of Americans who read it, it is a personal thingtough to define what works for some readers and tougher to understand for most. For the occasional reader of poetry, the favorite poem is usually something that sparks a familiar memory and puts it in perspectivea first love, the sight of the moon rising over a ridge in the mountains in the winter, or the memory of a summer night in youth. For those of us who don't read much poetry, it is the commonality of experience buried in the words speaking to something deep down inside our common existence as humans that tends to attract us to a poemthe I've been there or I've felt that experience.

Although the language in many of the poems in Body Language is striking, what draws in the physician‐reader more than anything else is the commonality of experiences inherent in these works. There are many remarkable landscapes in these poems, from the struggle to understand the intricate detail of the human body in anatomy class to the indelible memories of the patients who are manic or hopelessly depressed during the psychiatry core clerkship. It is mostly all here, the things we have experienced, in the form of poetry, evoking those moments that most of us painfully internalized or stepped around or ignored for lack of time to pay any attention to. For some of us, both the subtle and more profound experiences have become shadows or scars and for many, things we just never understood very well to begin with and try not to think about any more. These are our stories almost as much as they are those of the physician and medical student poets who wrote them. This book brings our experiences back, whether sadly, bluntly, humorously, or subtly, in a way that reminds us of all the things we've been blessed and cursed to see and be part of.

Body Language was the brain child of Neeta Jain, when she was still a medical student at the University of Rochester. She collaborated with another medical student from Yale University, Dagan Coppock, with the support of her University of Rochester faculty adviser, Stephanie Brown Clark. During the waning months of medical school, they solicited submissions from students, residents, and attending physicians from throughout the United States. Out of hundreds of submissions, they chose approximately 90 poems to create this anthology.

Perhaps I am cynical or perhaps I just don't really believe that given the frantic nature of modern medicine, there are many doctors who can devote the time to polishing their poetry in the tradition of William Carlos Williams, a New Jersey general practitioner who practiced before the era of information overload. Williams wrote on a typewriter between patients, during the time we reserve for looking up a question on Up‐to‐Date or answering a 1‐week old e‐mail.

But I was wrong. I came home from work exhausted one evening and picked up the book to discover another world, however familiar that world was. In that world are poems that occasionally jump off the page. Many of these poems were written by serious poets, poets published long before this book came along, and some are written by relative novices. But what unites these poems is the powerthe raw emotionof so many of the experiences described. We're reminded of overwhelming fatigue so harsh one envies the dead or the mundane call to pronounce a patient's death before fading back into the halls of the hospital. It is all here, our experiences in training and in the practice of medicine.

The anthology is divided into 6 sections: medical student, first year; medical student, second year; medical student, clinical years; intern; resident; and attending. It is almost impossible not to find a situation or emotion in a poem in each section that all physicians have experienced at some point in our lives. For example, life that occasionally interjects itself into the mind‐numbing lecture hall of our preclinical years of medical school (Richard M. Berlin):

Medical School Lovers

And for residents, the soft admit in the night (Mindy Shah):

MAO

After reading this book cover to cover, I was not surprised to learn that Garrison Keillor had asked permission to read some of its contents on his radio show. It is great stuff that speaks about many of the things we've been through that we're too tired or too busy or too afraid to stop and ponder over our years of practicing medicine. This anthology is easily worth the $15 it costs, if only because it repays us as a guide through the remarkable landscapes we have known.

0

Figure 1

Stolen Kisses (by Emily Osborn)

Poetry, without question, is a tricky thing. For many Americans it is an unapproachable art form that resides in a fortress guarded by elite intellectuals. For the minority of Americans who read it, it is a personal thingtough to define what works for some readers and tougher to understand for most. For the occasional reader of poetry, the favorite poem is usually something that sparks a familiar memory and puts it in perspectivea first love, the sight of the moon rising over a ridge in the mountains in the winter, or the memory of a summer night in youth. For those of us who don't read much poetry, it is the commonality of experience buried in the words speaking to something deep down inside our common existence as humans that tends to attract us to a poemthe I've been there or I've felt that experience.

Although the language in many of the poems in Body Language is striking, what draws in the physician‐reader more than anything else is the commonality of experiences inherent in these works. There are many remarkable landscapes in these poems, from the struggle to understand the intricate detail of the human body in anatomy class to the indelible memories of the patients who are manic or hopelessly depressed during the psychiatry core clerkship. It is mostly all here, the things we have experienced, in the form of poetry, evoking those moments that most of us painfully internalized or stepped around or ignored for lack of time to pay any attention to. For some of us, both the subtle and more profound experiences have become shadows or scars and for many, things we just never understood very well to begin with and try not to think about any more. These are our stories almost as much as they are those of the physician and medical student poets who wrote them. This book brings our experiences back, whether sadly, bluntly, humorously, or subtly, in a way that reminds us of all the things we've been blessed and cursed to see and be part of.

Body Language was the brain child of Neeta Jain, when she was still a medical student at the University of Rochester. She collaborated with another medical student from Yale University, Dagan Coppock, with the support of her University of Rochester faculty adviser, Stephanie Brown Clark. During the waning months of medical school, they solicited submissions from students, residents, and attending physicians from throughout the United States. Out of hundreds of submissions, they chose approximately 90 poems to create this anthology.

Perhaps I am cynical or perhaps I just don't really believe that given the frantic nature of modern medicine, there are many doctors who can devote the time to polishing their poetry in the tradition of William Carlos Williams, a New Jersey general practitioner who practiced before the era of information overload. Williams wrote on a typewriter between patients, during the time we reserve for looking up a question on Up‐to‐Date or answering a 1‐week old e‐mail.

But I was wrong. I came home from work exhausted one evening and picked up the book to discover another world, however familiar that world was. In that world are poems that occasionally jump off the page. Many of these poems were written by serious poets, poets published long before this book came along, and some are written by relative novices. But what unites these poems is the powerthe raw emotionof so many of the experiences described. We're reminded of overwhelming fatigue so harsh one envies the dead or the mundane call to pronounce a patient's death before fading back into the halls of the hospital. It is all here, our experiences in training and in the practice of medicine.

The anthology is divided into 6 sections: medical student, first year; medical student, second year; medical student, clinical years; intern; resident; and attending. It is almost impossible not to find a situation or emotion in a poem in each section that all physicians have experienced at some point in our lives. For example, life that occasionally interjects itself into the mind‐numbing lecture hall of our preclinical years of medical school (Richard M. Berlin):

Medical School Lovers

And for residents, the soft admit in the night (Mindy Shah):

MAO

After reading this book cover to cover, I was not surprised to learn that Garrison Keillor had asked permission to read some of its contents on his radio show. It is great stuff that speaks about many of the things we've been through that we're too tired or too busy or too afraid to stop and ponder over our years of practicing medicine. This anthology is easily worth the $15 it costs, if only because it repays us as a guide through the remarkable landscapes we have known.

0

Figure 1

Stolen Kisses (by Emily Osborn)

Poetry, without question, is a tricky thing. For many Americans it is an unapproachable art form that resides in a fortress guarded by elite intellectuals. For the minority of Americans who read it, it is a personal thingtough to define what works for some readers and tougher to understand for most. For the occasional reader of poetry, the favorite poem is usually something that sparks a familiar memory and puts it in perspectivea first love, the sight of the moon rising over a ridge in the mountains in the winter, or the memory of a summer night in youth. For those of us who don't read much poetry, it is the commonality of experience buried in the words speaking to something deep down inside our common existence as humans that tends to attract us to a poemthe I've been there or I've felt that experience.

Although the language in many of the poems in Body Language is striking, what draws in the physician‐reader more than anything else is the commonality of experiences inherent in these works. There are many remarkable landscapes in these poems, from the struggle to understand the intricate detail of the human body in anatomy class to the indelible memories of the patients who are manic or hopelessly depressed during the psychiatry core clerkship. It is mostly all here, the things we have experienced, in the form of poetry, evoking those moments that most of us painfully internalized or stepped around or ignored for lack of time to pay any attention to. For some of us, both the subtle and more profound experiences have become shadows or scars and for many, things we just never understood very well to begin with and try not to think about any more. These are our stories almost as much as they are those of the physician and medical student poets who wrote them. This book brings our experiences back, whether sadly, bluntly, humorously, or subtly, in a way that reminds us of all the things we've been blessed and cursed to see and be part of.

Body Language was the brain child of Neeta Jain, when she was still a medical student at the University of Rochester. She collaborated with another medical student from Yale University, Dagan Coppock, with the support of her University of Rochester faculty adviser, Stephanie Brown Clark. During the waning months of medical school, they solicited submissions from students, residents, and attending physicians from throughout the United States. Out of hundreds of submissions, they chose approximately 90 poems to create this anthology.

Perhaps I am cynical or perhaps I just don't really believe that given the frantic nature of modern medicine, there are many doctors who can devote the time to polishing their poetry in the tradition of William Carlos Williams, a New Jersey general practitioner who practiced before the era of information overload. Williams wrote on a typewriter between patients, during the time we reserve for looking up a question on Up‐to‐Date or answering a 1‐week old e‐mail.

But I was wrong. I came home from work exhausted one evening and picked up the book to discover another world, however familiar that world was. In that world are poems that occasionally jump off the page. Many of these poems were written by serious poets, poets published long before this book came along, and some are written by relative novices. But what unites these poems is the powerthe raw emotionof so many of the experiences described. We're reminded of overwhelming fatigue so harsh one envies the dead or the mundane call to pronounce a patient's death before fading back into the halls of the hospital. It is all here, our experiences in training and in the practice of medicine.

The anthology is divided into 6 sections: medical student, first year; medical student, second year; medical student, clinical years; intern; resident; and attending. It is almost impossible not to find a situation or emotion in a poem in each section that all physicians have experienced at some point in our lives. For example, life that occasionally interjects itself into the mind‐numbing lecture hall of our preclinical years of medical school (Richard M. Berlin):

Medical School Lovers

And for residents, the soft admit in the night (Mindy Shah):

MAO

After reading this book cover to cover, I was not surprised to learn that Garrison Keillor had asked permission to read some of its contents on his radio show. It is great stuff that speaks about many of the things we've been through that we're too tired or too busy or too afraid to stop and ponder over our years of practicing medicine. This anthology is easily worth the $15 it costs, if only because it repays us as a guide through the remarkable landscapes we have known.

Transitions from the acute hospital to other sites of care are critical and potentially dangerous times for patients. Improving coordination of care among health care settings is a major area of emphasis in the Institute of Medicine publication, Crossing the Quality Chasm: A New Health System for the 21st Century.1 System factors such as poor information transmission processes, inadequate training of discharging staff, and inadequate time for discharge teaching can prevent patients from having the information they need when being discharged home. Patient factors such as nervousness, home distractions, and poor health literacy further limit the implementation of discharge plans. Misalignment of system and patient factors can result in a bewildered patient with a failed discharge process that subverts the intentions of even the best posthospital plan. Regardless of whether system and/or patient factors underlie the problem, the perception of that bewildered patient is that of receiving inadequate instruction for self‐care after discharge from the hospital. As self‐care and medication compliance play an important role in health outcomes and whether patients are readmitted, such a perceived (or actual) lack of instruction can have important implications for future health, physical function, and quality of life. Patients cared for in settings where health literacy is generally low and socioeconomic conditions poor may be at especially high risk of problems with communication of the discharge plan.

The objectives of this study were to (1) describe patient recall regarding pre‐discharge communication between hospital staff and patients regarding discharge instructions, and (2) to demonstrate that a post‐hospitalization survey was both feasible and revealing in an urban, public hospital setting.

METHODS

This cross‐sectional survey of older inpatients discharged from Grady Memorial Hospital, an academically affiliated, 953‐bed public teaching hospital in downtown Atlanta, Georgia, was conducted by telephone.

RESULTS

We found the survey to be feasible and easily administered. Over the study period the mean length of stay of the respondents was 5.6 days (range, 056 days), and the mean number of times admitted was 1.6 (range, 17). Interviews were conducted an average of 3 days after discharge (range, 110 days). Other demographic information on the respondents is summarized in Table 1.

Most of those surveyed (81.8%, or 242 respondents) were able to answer the question Can you tell me what was explained to you [about why you were hospitalized]? The results of the content analysis of the answers to this open‐ended question are summarized in Table 2. The self‐reported problem area most frequently mentioned was the heart. Responses to questions about instructions and education received while in the hospital are reported in Table 3.

A correlation was found between providing information in written and verbal fashion and self‐reported understanding of the instructions. For example, of the 103 respondents who answered affirmatively to Did anyone talk with you about how to care for yourself at home after this hospitalization? and also recalled the source of that information, 66.0% (n = 68) reported receiving instructions verbally, 10.7% (n = 11) reported receiving them in writing, and 23.3% (n = 24) reported receiving both. Patients who received both verbal and written instructions were more likely to report that they understood the care instructions very well versus somewhat or very little (² = 29.612, df = 4, P = .000).

The association between the perceived provision of information to patients and effective use of that information was explored. For example, perceived medication compliance and instruction on medication use had a positive association. Among those who recalled receiving instruction on how to take their medications (n = 88), 76 (86.4%) stated that they were taking them correctly, 8 (9.1%) that they were not taking them correctly, and 4 (4.5%) were unsure. Among those who said that they did not receive instruction or did not recall being instructed on how to take their medications (n = 26), 16 (61.5%) believed that they were taking their mediations correctly, 4 (15.4%) that they were not taking them correctly, and 5 (19.2%) were unsure. Respondents who recalled receiving medication instruction were more likely to comply with taking medication. (² = 7.321, P = .026)

There was also a positive association between being told what to do if problems were experienced at home and calling about problems after arriving home. Among those who believed they were instructed on what to do if problems were experienced at home (N = 86), 23 (26.7%) reported they called about a problem. Among those who did not recall being instructed about what to do if problems were experienced at home (N = 183), only 13 (7.1%) reported calling about a problem. Respondents who believed they had been instructed on what to do at home were significantly more likely to call from home about problems (² = 16.740, df = 2, P = .000).

DISCUSSION

According to Bull and Roberts,2 there are 3 types of communication gaps in discharge planning: (1) gaps between health care providers in the hospital and those involved in the hospital‐community interface, (2) gaps between providers and patients, and (3) gaps between health care providers and family caregivers for elders. The present study focuses on the latter 2 types of communication gaps. In discharge planning it is critical not only to transmit information, but also to make sure that patients understand that information in the way health care providers intended. Systemic, cultural, emotional, and cognitive barriers may interact to limit the effectiveness of this communication.

In the present study, a large number of patients discharged from an academically affiliated public hospital were unaware of important discharge information, even though according to hospital protocol, all patients are given a discharge information sheet. Approximately 15% did not know why they were hospitalized. About 20% of those who reported their medications were changed in the hospital could not recall anyone explaining how to take these medications. More than half of respondents did not recall anyone speaking with them about how to take care of themselves following hospitalization. More than 60% of respondents did not recall getting information on what to do if they had a problem after being discharge home.

That patients were unaware of information that had been provided to them has significant implications for successful implementation of the spirit of the Joint Commission on Accreditation of Healthcare Organizations standards. These disease‐specific standards as well as medication standards are generally written as process measures. Although requiring that routine and clear standards of information be provided to patients is a significant step forward in patient safety, surveys such as the present one, done over time, should be an important part of any ongoing quality improvement process. As evident by the high response rate in our study and others,3 patients and their proxies are very willing to participate in such surveys. The results of the Consumer Assessment of Healthcare Providers and Systems (CHAMPS) survey,4 which will be published, should provide an important impetus for this ongoing quality improvement process. Interestingly, 2 of the CHAMPS questionsDuring this hospital stay, did doctors, nurses, or other hospital staff talk with you about whether you would have the help you needed when you left the hospital? and During this hospital stay, did you get information in writing about what symptoms or health problems to look out for after you left the hospital?are very similar to questions used in the present study. In our health system, site of the present study, these data have prompted a complete revision of the discharge instruction sheet, creation of a care transitions task force, and initiation of a pilot care transitions project. Follow‐up surveys will be performed to evaluate whether these changes have been effective in improving discharge information transfer and, more importantly, in patient outcomes.

The present study had several limitations. First, although the results are inconsistent with the findings of other studies, the present study took place at a single urban institution most of whose patients socioeconomically disadvantaged. Second, patient responses were combined with caregiver responses (elicited when a patient was unable to respond to the survey questions). Although it is not proven that these 2 groups are equivalent, from a practical point of view this was justified because the clinical issue is whether the person taking care of the patient (be it patient or caregiver) has the critical information needed after discharge from the hospital. Third, only those who could be reached by phone were included. This is likely to bias the results in a more favorable direction, given that the socioeconomic implications of not having a phone and/or the cognitive implications of not being able to use a phone would likely be reflected in even greater impediments to communication. Fourth, no attempt was made to evaluate the cognitive status or health literacy of either the subjects or their proxies. Fifth, generalizability of the survey to other research groups is unclear, as no additional attempt was made to define the interrater reliability of the survey. Finally, although it seems reasonable to presume that simpler discharge plans would be more effectively communicated, this study did not define the complexity of each discharge plan. Strengths of the study include a single trained interviewer, relatively rapid follow‐up of patients, and large sample size.

Effective communication during the care transition is important for improving patient outcomes and satisfaction. One study of 40 patient‐caregiver dyads showed that patients had a lower rate of medical problems postdischarge when they and their caregivers received verbal and/or printed information about activity and complications that could occur at home.5 Indeed, a study of 134 elder/family caregiver dyads interviewed 2 weeks after hospitalization found that receipt of information about the patient's condition, medications, and activities was an important contributor to both patient and family caregiver satisfaction with discharge care.6

At first glance, these findings may seem surprising, given that all patients discharged from the hospital should receive (by protocol) a discharge information sheet with postdischarge instructions. This study did not define what exactly transpired between hospital staff and patients, review discharge sheets, or validate the extent to which these instruction sheets are completely filled out and adequately reviewed with patients. The results of previous studies suggest that even when conversations are verified to have occurred, transmission is often inadequate. One study of 54 adult patients discharged after being hospitalized for pneumonia or acute myocardial infarction found that physicians believed that 88.9% of patients understood potential side effects of postdischarge medications, but only 57.4% of patients reported that they did understand instructions about side effects (P < .001).7 Another study of 47 patients discharged from a municipal teaching hospital in New York City showed that only 42% were able to state their diagnoses and only 28% were able to list all their medicines.8

The solutions to these problems may be as unapparent as they are difficult, and many of the challenges as well as some potential solutions have been recently reviewed.9 Arguing that physicians and/or hospital staff should spend more time with all their patients oversimplifies the problem and is not likely to occur. The present study confirmed earlier findings that providing verbal and written health information on hospital discharge significantly increases the knowledge of patients and caregivers.10 Risk stratificationtargeting those most at risk of medication noncompliance to receive augmented medication compliance instruction, such as the scheme suggested by Rosenow11has significant merit and warrants extension to discharge instructions in general and to prospective testing.

Discharge teaching videos have been shown to have some effectiveness in the emergency room setting12 and along with an audio‐only or CD option could be developed to supplement the written discharge information provided to patients. Calling patients after discharge to make sure they understand their prescribed medical regimen, have their prescriptions and home health equipment, and have a follow‐up visit scheduled with their doctors has been identified as a key characteristic of high‐achieving hospitalist programs. One care site found that 80% of patients have questions about their follow‐up care that could jeopardize their recovery.13 This strategy could just as well be implemented by a case manager or health educator. Follow‐up phone contact combined with Telecare has been shown to be effective in reducing hospital readmissions, emergency visits, and cost of care for patients with heart failure.14 Formal care transition instruments and interventions show promise for enabling patients and caregivers to take a more active role during care transition processes and improve outcomes. Whether this approach will be widely generalizable awaits demonstration.15

CONCLUSIONS

In summary, we found that a posthospitalization survey was both feasible and revealing and had a high acceptance rate in this urban public hospital population. Furthermore, subject recall about predischarge communication from hospital staff regarding discharge instructions demonstrated significant gaps about transfer of information. If these findings prove to be applicable to the large numbers of older as well as younger patients discharged from the hospital each year, the implications for patients health, safety, and satisfaction are enormous. It should not be assumed that this is a problem limited to older patients. As health care systems build bridges across gaps in the quality chasm, developing and testing more effective communication strategies for patients is imperative.

Transitions from the acute hospital to other sites of care are critical and potentially dangerous times for patients. Improving coordination of care among health care settings is a major area of emphasis in the Institute of Medicine publication, Crossing the Quality Chasm: A New Health System for the 21st Century.1 System factors such as poor information transmission processes, inadequate training of discharging staff, and inadequate time for discharge teaching can prevent patients from having the information they need when being discharged home. Patient factors such as nervousness, home distractions, and poor health literacy further limit the implementation of discharge plans. Misalignment of system and patient factors can result in a bewildered patient with a failed discharge process that subverts the intentions of even the best posthospital plan. Regardless of whether system and/or patient factors underlie the problem, the perception of that bewildered patient is that of receiving inadequate instruction for self‐care after discharge from the hospital. As self‐care and medication compliance play an important role in health outcomes and whether patients are readmitted, such a perceived (or actual) lack of instruction can have important implications for future health, physical function, and quality of life. Patients cared for in settings where health literacy is generally low and socioeconomic conditions poor may be at especially high risk of problems with communication of the discharge plan.

The objectives of this study were to (1) describe patient recall regarding pre‐discharge communication between hospital staff and patients regarding discharge instructions, and (2) to demonstrate that a post‐hospitalization survey was both feasible and revealing in an urban, public hospital setting.

METHODS

This cross‐sectional survey of older inpatients discharged from Grady Memorial Hospital, an academically affiliated, 953‐bed public teaching hospital in downtown Atlanta, Georgia, was conducted by telephone.

RESULTS

We found the survey to be feasible and easily administered. Over the study period the mean length of stay of the respondents was 5.6 days (range, 056 days), and the mean number of times admitted was 1.6 (range, 17). Interviews were conducted an average of 3 days after discharge (range, 110 days). Other demographic information on the respondents is summarized in Table 1.

Most of those surveyed (81.8%, or 242 respondents) were able to answer the question Can you tell me what was explained to you [about why you were hospitalized]? The results of the content analysis of the answers to this open‐ended question are summarized in Table 2. The self‐reported problem area most frequently mentioned was the heart. Responses to questions about instructions and education received while in the hospital are reported in Table 3.

A correlation was found between providing information in written and verbal fashion and self‐reported understanding of the instructions. For example, of the 103 respondents who answered affirmatively to Did anyone talk with you about how to care for yourself at home after this hospitalization? and also recalled the source of that information, 66.0% (n = 68) reported receiving instructions verbally, 10.7% (n = 11) reported receiving them in writing, and 23.3% (n = 24) reported receiving both. Patients who received both verbal and written instructions were more likely to report that they understood the care instructions very well versus somewhat or very little (² = 29.612, df = 4, P = .000).

The association between the perceived provision of information to patients and effective use of that information was explored. For example, perceived medication compliance and instruction on medication use had a positive association. Among those who recalled receiving instruction on how to take their medications (n = 88), 76 (86.4%) stated that they were taking them correctly, 8 (9.1%) that they were not taking them correctly, and 4 (4.5%) were unsure. Among those who said that they did not receive instruction or did not recall being instructed on how to take their medications (n = 26), 16 (61.5%) believed that they were taking their mediations correctly, 4 (15.4%) that they were not taking them correctly, and 5 (19.2%) were unsure. Respondents who recalled receiving medication instruction were more likely to comply with taking medication. (² = 7.321, P = .026)

There was also a positive association between being told what to do if problems were experienced at home and calling about problems after arriving home. Among those who believed they were instructed on what to do if problems were experienced at home (N = 86), 23 (26.7%) reported they called about a problem. Among those who did not recall being instructed about what to do if problems were experienced at home (N = 183), only 13 (7.1%) reported calling about a problem. Respondents who believed they had been instructed on what to do at home were significantly more likely to call from home about problems (² = 16.740, df = 2, P = .000).

DISCUSSION

According to Bull and Roberts,2 there are 3 types of communication gaps in discharge planning: (1) gaps between health care providers in the hospital and those involved in the hospital‐community interface, (2) gaps between providers and patients, and (3) gaps between health care providers and family caregivers for elders. The present study focuses on the latter 2 types of communication gaps. In discharge planning it is critical not only to transmit information, but also to make sure that patients understand that information in the way health care providers intended. Systemic, cultural, emotional, and cognitive barriers may interact to limit the effectiveness of this communication.

In the present study, a large number of patients discharged from an academically affiliated public hospital were unaware of important discharge information, even though according to hospital protocol, all patients are given a discharge information sheet. Approximately 15% did not know why they were hospitalized. About 20% of those who reported their medications were changed in the hospital could not recall anyone explaining how to take these medications. More than half of respondents did not recall anyone speaking with them about how to take care of themselves following hospitalization. More than 60% of respondents did not recall getting information on what to do if they had a problem after being discharge home.

That patients were unaware of information that had been provided to them has significant implications for successful implementation of the spirit of the Joint Commission on Accreditation of Healthcare Organizations standards. These disease‐specific standards as well as medication standards are generally written as process measures. Although requiring that routine and clear standards of information be provided to patients is a significant step forward in patient safety, surveys such as the present one, done over time, should be an important part of any ongoing quality improvement process. As evident by the high response rate in our study and others,3 patients and their proxies are very willing to participate in such surveys. The results of the Consumer Assessment of Healthcare Providers and Systems (CHAMPS) survey,4 which will be published, should provide an important impetus for this ongoing quality improvement process. Interestingly, 2 of the CHAMPS questionsDuring this hospital stay, did doctors, nurses, or other hospital staff talk with you about whether you would have the help you needed when you left the hospital? and During this hospital stay, did you get information in writing about what symptoms or health problems to look out for after you left the hospital?are very similar to questions used in the present study. In our health system, site of the present study, these data have prompted a complete revision of the discharge instruction sheet, creation of a care transitions task force, and initiation of a pilot care transitions project. Follow‐up surveys will be performed to evaluate whether these changes have been effective in improving discharge information transfer and, more importantly, in patient outcomes.

The present study had several limitations. First, although the results are inconsistent with the findings of other studies, the present study took place at a single urban institution most of whose patients socioeconomically disadvantaged. Second, patient responses were combined with caregiver responses (elicited when a patient was unable to respond to the survey questions). Although it is not proven that these 2 groups are equivalent, from a practical point of view this was justified because the clinical issue is whether the person taking care of the patient (be it patient or caregiver) has the critical information needed after discharge from the hospital. Third, only those who could be reached by phone were included. This is likely to bias the results in a more favorable direction, given that the socioeconomic implications of not having a phone and/or the cognitive implications of not being able to use a phone would likely be reflected in even greater impediments to communication. Fourth, no attempt was made to evaluate the cognitive status or health literacy of either the subjects or their proxies. Fifth, generalizability of the survey to other research groups is unclear, as no additional attempt was made to define the interrater reliability of the survey. Finally, although it seems reasonable to presume that simpler discharge plans would be more effectively communicated, this study did not define the complexity of each discharge plan. Strengths of the study include a single trained interviewer, relatively rapid follow‐up of patients, and large sample size.

Effective communication during the care transition is important for improving patient outcomes and satisfaction. One study of 40 patient‐caregiver dyads showed that patients had a lower rate of medical problems postdischarge when they and their caregivers received verbal and/or printed information about activity and complications that could occur at home.5 Indeed, a study of 134 elder/family caregiver dyads interviewed 2 weeks after hospitalization found that receipt of information about the patient's condition, medications, and activities was an important contributor to both patient and family caregiver satisfaction with discharge care.6

At first glance, these findings may seem surprising, given that all patients discharged from the hospital should receive (by protocol) a discharge information sheet with postdischarge instructions. This study did not define what exactly transpired between hospital staff and patients, review discharge sheets, or validate the extent to which these instruction sheets are completely filled out and adequately reviewed with patients. The results of previous studies suggest that even when conversations are verified to have occurred, transmission is often inadequate. One study of 54 adult patients discharged after being hospitalized for pneumonia or acute myocardial infarction found that physicians believed that 88.9% of patients understood potential side effects of postdischarge medications, but only 57.4% of patients reported that they did understand instructions about side effects (P < .001).7 Another study of 47 patients discharged from a municipal teaching hospital in New York City showed that only 42% were able to state their diagnoses and only 28% were able to list all their medicines.8

The solutions to these problems may be as unapparent as they are difficult, and many of the challenges as well as some potential solutions have been recently reviewed.9 Arguing that physicians and/or hospital staff should spend more time with all their patients oversimplifies the problem and is not likely to occur. The present study confirmed earlier findings that providing verbal and written health information on hospital discharge significantly increases the knowledge of patients and caregivers.10 Risk stratificationtargeting those most at risk of medication noncompliance to receive augmented medication compliance instruction, such as the scheme suggested by Rosenow11has significant merit and warrants extension to discharge instructions in general and to prospective testing.

Discharge teaching videos have been shown to have some effectiveness in the emergency room setting12 and along with an audio‐only or CD option could be developed to supplement the written discharge information provided to patients. Calling patients after discharge to make sure they understand their prescribed medical regimen, have their prescriptions and home health equipment, and have a follow‐up visit scheduled with their doctors has been identified as a key characteristic of high‐achieving hospitalist programs. One care site found that 80% of patients have questions about their follow‐up care that could jeopardize their recovery.13 This strategy could just as well be implemented by a case manager or health educator. Follow‐up phone contact combined with Telecare has been shown to be effective in reducing hospital readmissions, emergency visits, and cost of care for patients with heart failure.14 Formal care transition instruments and interventions show promise for enabling patients and caregivers to take a more active role during care transition processes and improve outcomes. Whether this approach will be widely generalizable awaits demonstration.15

CONCLUSIONS

In summary, we found that a posthospitalization survey was both feasible and revealing and had a high acceptance rate in this urban public hospital population. Furthermore, subject recall about predischarge communication from hospital staff regarding discharge instructions demonstrated significant gaps about transfer of information. If these findings prove to be applicable to the large numbers of older as well as younger patients discharged from the hospital each year, the implications for patients health, safety, and satisfaction are enormous. It should not be assumed that this is a problem limited to older patients. As health care systems build bridges across gaps in the quality chasm, developing and testing more effective communication strategies for patients is imperative.

Transitions from the acute hospital to other sites of care are critical and potentially dangerous times for patients. Improving coordination of care among health care settings is a major area of emphasis in the Institute of Medicine publication, Crossing the Quality Chasm: A New Health System for the 21st Century.1 System factors such as poor information transmission processes, inadequate training of discharging staff, and inadequate time for discharge teaching can prevent patients from having the information they need when being discharged home. Patient factors such as nervousness, home distractions, and poor health literacy further limit the implementation of discharge plans. Misalignment of system and patient factors can result in a bewildered patient with a failed discharge process that subverts the intentions of even the best posthospital plan. Regardless of whether system and/or patient factors underlie the problem, the perception of that bewildered patient is that of receiving inadequate instruction for self‐care after discharge from the hospital. As self‐care and medication compliance play an important role in health outcomes and whether patients are readmitted, such a perceived (or actual) lack of instruction can have important implications for future health, physical function, and quality of life. Patients cared for in settings where health literacy is generally low and socioeconomic conditions poor may be at especially high risk of problems with communication of the discharge plan.

The objectives of this study were to (1) describe patient recall regarding pre‐discharge communication between hospital staff and patients regarding discharge instructions, and (2) to demonstrate that a post‐hospitalization survey was both feasible and revealing in an urban, public hospital setting.

METHODS

This cross‐sectional survey of older inpatients discharged from Grady Memorial Hospital, an academically affiliated, 953‐bed public teaching hospital in downtown Atlanta, Georgia, was conducted by telephone.

RESULTS

We found the survey to be feasible and easily administered. Over the study period the mean length of stay of the respondents was 5.6 days (range, 056 days), and the mean number of times admitted was 1.6 (range, 17). Interviews were conducted an average of 3 days after discharge (range, 110 days). Other demographic information on the respondents is summarized in Table 1.

Most of those surveyed (81.8%, or 242 respondents) were able to answer the question Can you tell me what was explained to you [about why you were hospitalized]? The results of the content analysis of the answers to this open‐ended question are summarized in Table 2. The self‐reported problem area most frequently mentioned was the heart. Responses to questions about instructions and education received while in the hospital are reported in Table 3.

A correlation was found between providing information in written and verbal fashion and self‐reported understanding of the instructions. For example, of the 103 respondents who answered affirmatively to Did anyone talk with you about how to care for yourself at home after this hospitalization? and also recalled the source of that information, 66.0% (n = 68) reported receiving instructions verbally, 10.7% (n = 11) reported receiving them in writing, and 23.3% (n = 24) reported receiving both. Patients who received both verbal and written instructions were more likely to report that they understood the care instructions very well versus somewhat or very little (² = 29.612, df = 4, P = .000).

The association between the perceived provision of information to patients and effective use of that information was explored. For example, perceived medication compliance and instruction on medication use had a positive association. Among those who recalled receiving instruction on how to take their medications (n = 88), 76 (86.4%) stated that they were taking them correctly, 8 (9.1%) that they were not taking them correctly, and 4 (4.5%) were unsure. Among those who said that they did not receive instruction or did not recall being instructed on how to take their medications (n = 26), 16 (61.5%) believed that they were taking their mediations correctly, 4 (15.4%) that they were not taking them correctly, and 5 (19.2%) were unsure. Respondents who recalled receiving medication instruction were more likely to comply with taking medication. (² = 7.321, P = .026)

There was also a positive association between being told what to do if problems were experienced at home and calling about problems after arriving home. Among those who believed they were instructed on what to do if problems were experienced at home (N = 86), 23 (26.7%) reported they called about a problem. Among those who did not recall being instructed about what to do if problems were experienced at home (N = 183), only 13 (7.1%) reported calling about a problem. Respondents who believed they had been instructed on what to do at home were significantly more likely to call from home about problems (² = 16.740, df = 2, P = .000).

DISCUSSION

According to Bull and Roberts,2 there are 3 types of communication gaps in discharge planning: (1) gaps between health care providers in the hospital and those involved in the hospital‐community interface, (2) gaps between providers and patients, and (3) gaps between health care providers and family caregivers for elders. The present study focuses on the latter 2 types of communication gaps. In discharge planning it is critical not only to transmit information, but also to make sure that patients understand that information in the way health care providers intended. Systemic, cultural, emotional, and cognitive barriers may interact to limit the effectiveness of this communication.

In the present study, a large number of patients discharged from an academically affiliated public hospital were unaware of important discharge information, even though according to hospital protocol, all patients are given a discharge information sheet. Approximately 15% did not know why they were hospitalized. About 20% of those who reported their medications were changed in the hospital could not recall anyone explaining how to take these medications. More than half of respondents did not recall anyone speaking with them about how to take care of themselves following hospitalization. More than 60% of respondents did not recall getting information on what to do if they had a problem after being discharge home.

That patients were unaware of information that had been provided to them has significant implications for successful implementation of the spirit of the Joint Commission on Accreditation of Healthcare Organizations standards. These disease‐specific standards as well as medication standards are generally written as process measures. Although requiring that routine and clear standards of information be provided to patients is a significant step forward in patient safety, surveys such as the present one, done over time, should be an important part of any ongoing quality improvement process. As evident by the high response rate in our study and others,3 patients and their proxies are very willing to participate in such surveys. The results of the Consumer Assessment of Healthcare Providers and Systems (CHAMPS) survey,4 which will be published, should provide an important impetus for this ongoing quality improvement process. Interestingly, 2 of the CHAMPS questionsDuring this hospital stay, did doctors, nurses, or other hospital staff talk with you about whether you would have the help you needed when you left the hospital? and During this hospital stay, did you get information in writing about what symptoms or health problems to look out for after you left the hospital?are very similar to questions used in the present study. In our health system, site of the present study, these data have prompted a complete revision of the discharge instruction sheet, creation of a care transitions task force, and initiation of a pilot care transitions project. Follow‐up surveys will be performed to evaluate whether these changes have been effective in improving discharge information transfer and, more importantly, in patient outcomes.

The present study had several limitations. First, although the results are inconsistent with the findings of other studies, the present study took place at a single urban institution most of whose patients socioeconomically disadvantaged. Second, patient responses were combined with caregiver responses (elicited when a patient was unable to respond to the survey questions). Although it is not proven that these 2 groups are equivalent, from a practical point of view this was justified because the clinical issue is whether the person taking care of the patient (be it patient or caregiver) has the critical information needed after discharge from the hospital. Third, only those who could be reached by phone were included. This is likely to bias the results in a more favorable direction, given that the socioeconomic implications of not having a phone and/or the cognitive implications of not being able to use a phone would likely be reflected in even greater impediments to communication. Fourth, no attempt was made to evaluate the cognitive status or health literacy of either the subjects or their proxies. Fifth, generalizability of the survey to other research groups is unclear, as no additional attempt was made to define the interrater reliability of the survey. Finally, although it seems reasonable to presume that simpler discharge plans would be more effectively communicated, this study did not define the complexity of each discharge plan. Strengths of the study include a single trained interviewer, relatively rapid follow‐up of patients, and large sample size.

Effective communication during the care transition is important for improving patient outcomes and satisfaction. One study of 40 patient‐caregiver dyads showed that patients had a lower rate of medical problems postdischarge when they and their caregivers received verbal and/or printed information about activity and complications that could occur at home.5 Indeed, a study of 134 elder/family caregiver dyads interviewed 2 weeks after hospitalization found that receipt of information about the patient's condition, medications, and activities was an important contributor to both patient and family caregiver satisfaction with discharge care.6

At first glance, these findings may seem surprising, given that all patients discharged from the hospital should receive (by protocol) a discharge information sheet with postdischarge instructions. This study did not define what exactly transpired between hospital staff and patients, review discharge sheets, or validate the extent to which these instruction sheets are completely filled out and adequately reviewed with patients. The results of previous studies suggest that even when conversations are verified to have occurred, transmission is often inadequate. One study of 54 adult patients discharged after being hospitalized for pneumonia or acute myocardial infarction found that physicians believed that 88.9% of patients understood potential side effects of postdischarge medications, but only 57.4% of patients reported that they did understand instructions about side effects (P < .001).7 Another study of 47 patients discharged from a municipal teaching hospital in New York City showed that only 42% were able to state their diagnoses and only 28% were able to list all their medicines.8

The solutions to these problems may be as unapparent as they are difficult, and many of the challenges as well as some potential solutions have been recently reviewed.9 Arguing that physicians and/or hospital staff should spend more time with all their patients oversimplifies the problem and is not likely to occur. The present study confirmed earlier findings that providing verbal and written health information on hospital discharge significantly increases the knowledge of patients and caregivers.10 Risk stratificationtargeting those most at risk of medication noncompliance to receive augmented medication compliance instruction, such as the scheme suggested by Rosenow11has significant merit and warrants extension to discharge instructions in general and to prospective testing.

Discharge teaching videos have been shown to have some effectiveness in the emergency room setting12 and along with an audio‐only or CD option could be developed to supplement the written discharge information provided to patients. Calling patients after discharge to make sure they understand their prescribed medical regimen, have their prescriptions and home health equipment, and have a follow‐up visit scheduled with their doctors has been identified as a key characteristic of high‐achieving hospitalist programs. One care site found that 80% of patients have questions about their follow‐up care that could jeopardize their recovery.13 This strategy could just as well be implemented by a case manager or health educator. Follow‐up phone contact combined with Telecare has been shown to be effective in reducing hospital readmissions, emergency visits, and cost of care for patients with heart failure.14 Formal care transition instruments and interventions show promise for enabling patients and caregivers to take a more active role during care transition processes and improve outcomes. Whether this approach will be widely generalizable awaits demonstration.15

CONCLUSIONS

In summary, we found that a posthospitalization survey was both feasible and revealing and had a high acceptance rate in this urban public hospital population. Furthermore, subject recall about predischarge communication from hospital staff regarding discharge instructions demonstrated significant gaps about transfer of information. If these findings prove to be applicable to the large numbers of older as well as younger patients discharged from the hospital each year, the implications for patients health, safety, and satisfaction are enormous. It should not be assumed that this is a problem limited to older patients. As health care systems build bridges across gaps in the quality chasm, developing and testing more effective communication strategies for patients is imperative.

A 77‐year‐old woman with hypothyroidism presented with a 2‐week history of head, neck, jaw, and tongue pain. She had also developed slurred speech and difficulty chewing. On examination she had a temperature of 38.0C. She was without neurological deficits. However, she did have difficulty protruding her tongue, which had a cyanotic appearance and was painful. Laboratory findings showed an erythrocyte sedimentation rate of 68 mm/hr. Temporal arteritis was suspected, and the patient was started on corticosteroids. A subsequent temporal artery biopsy revealed inflammation and thrombus formation consistent with temporal arteritis. On hospital day 3, she developed unilateral ischemia in her tongue, which eventually became necrotic (Fig. 1). Although tongue necrosis is rare, temporal arteritis is the most frequent cause. It is usually unilateral and caused by compromised blood supply as a result of vasculitis in one of the lingual arteries. Other causes of tongue necrosis such as embolus, abscess, syphilis, tongue carcinoma, and Hodgkin's disease should be excluded.1, 2 Although necrotic tongue tissue must sometimes be extensively debrided or resected, our patient required minimal debridement. At follow‐up 1 month later, she was recovering at home with ongoing speech therapy and a corticosteroid taper.

Figure 1

A 77‐year‐old woman with hypothyroidism presented with a 2‐week history of head, neck, jaw, and tongue pain. She had also developed slurred speech and difficulty chewing. On examination she had a temperature of 38.0C. She was without neurological deficits. However, she did have difficulty protruding her tongue, which had a cyanotic appearance and was painful. Laboratory findings showed an erythrocyte sedimentation rate of 68 mm/hr. Temporal arteritis was suspected, and the patient was started on corticosteroids. A subsequent temporal artery biopsy revealed inflammation and thrombus formation consistent with temporal arteritis. On hospital day 3, she developed unilateral ischemia in her tongue, which eventually became necrotic (Fig. 1). Although tongue necrosis is rare, temporal arteritis is the most frequent cause. It is usually unilateral and caused by compromised blood supply as a result of vasculitis in one of the lingual arteries. Other causes of tongue necrosis such as embolus, abscess, syphilis, tongue carcinoma, and Hodgkin's disease should be excluded.1, 2 Although necrotic tongue tissue must sometimes be extensively debrided or resected, our patient required minimal debridement. At follow‐up 1 month later, she was recovering at home with ongoing speech therapy and a corticosteroid taper.

Figure 1

A 77‐year‐old woman with hypothyroidism presented with a 2‐week history of head, neck, jaw, and tongue pain. She had also developed slurred speech and difficulty chewing. On examination she had a temperature of 38.0C. She was without neurological deficits. However, she did have difficulty protruding her tongue, which had a cyanotic appearance and was painful. Laboratory findings showed an erythrocyte sedimentation rate of 68 mm/hr. Temporal arteritis was suspected, and the patient was started on corticosteroids. A subsequent temporal artery biopsy revealed inflammation and thrombus formation consistent with temporal arteritis. On hospital day 3, she developed unilateral ischemia in her tongue, which eventually became necrotic (Fig. 1). Although tongue necrosis is rare, temporal arteritis is the most frequent cause. It is usually unilateral and caused by compromised blood supply as a result of vasculitis in one of the lingual arteries. Other causes of tongue necrosis such as embolus, abscess, syphilis, tongue carcinoma, and Hodgkin's disease should be excluded.1, 2 Although necrotic tongue tissue must sometimes be extensively debrided or resected, our patient required minimal debridement. At follow‐up 1 month later, she was recovering at home with ongoing speech therapy and a corticosteroid taper.

Figure 1

Enterococci are a leading cause of endocarditis and nosocomial infections. Vancomycin‐resistant enterococci (VRE) emerged in the 1980s and now represent most nosocomial isolates in the United States. The first case of VRE endocarditis was reported in 1996.1 Although increasing enterococcal antibiotic resistance has prompted increasing reliance on newer antibiotics,2 a recent review of VRE endocarditis noted that survival rates were similar to those for vancomycin‐sensitive enterococcal endocarditis.1 Cure was achieved in several patients with bacteriostatic agents in the absence of valve replacement, but no patients were infected with truly linezolid‐resistant organisms. This case of linezolid‐resistant VRE endocarditis represents the first reported cure of infective endocarditis with a tigecycline‐containing regimen.

CASE REPORT

A 62‐year‐old man presented with hypoglycemia and delirium. His medical history included diabetes mellitus, coronary and peripheral arterial disease, and end‐stage renal disease. He had had endocarditis of an unknown type 12 years prior to admission. He had recently developed septic shock because of a Candida parapsilosis, Enterobacter cloacae, and Staphylococcus epidermidis infection of a peripherally inserted central catheter (PICC) and received 14 days of vancomycin, meropenem, and fluconazole administered through a new PICC. This catheter was not removed, and 39 days after completion of the antibiotic therapy, he developed hypoglycemia, which was attributed to weight loss without adjustment of his insulin regimen. He was afebrile; examination revealed a new 3/6 holosystolic murmur radiating to the axilla. There were no other stigmata of infective endocarditis, and his PICC and arteriovenous fistula sites appeared normal. Delirium resolved after administration of intravenous glucose.

E. faecium grew from all 6 initial blood cultures. A transesophageal echocardiogram revealed a new 3‐mm mitral valve vegetation with perforation and severe regurgitation. He had definite endocarditis on the basis of 2 major criteria.3 He was given vancomycin (1 g IV, then administered by levels), then switched to linezolid (600 mg orally every 12 hours), and finally tigecycline (100 mg IV followed by 50 mg IV every 12 hours) plus daptomycin (6 mg/kg IV every 48 hours) as further sensitivity data became available.

The organism was resistant to ampicillin, chloramphenicol, and linezolid (MIC > 20 g/mL), as well as vancomycin (MIC > 50 g/mL), quinupristin/dalfopristin (MIC 2.5 g/mL), and gentamicin (MIC > 200 g/mL), and demonstrated high‐level streptomycin resistance (>2000 g/mL). It was intermediate to doxycycline (MIC 5 g/mL). It was susceptible to daptomycin (MIC 4 g/mL) and tigecycline (MIC 0.06 g/mL).

Blood cultures done on hospital days 1, 4, 6, and 7 (day 1 of tigecycline) were positive, and multiple cultures were negative from day 10 on. Because of the lack of experience with tigecycline in infective endocarditis, unrevascularized left‐main coronary artery disease, and severe mitral regurgitation, the patient was advised to undergo valve replacement and coronary artery bypass surgery after antibiotic therapy. Because he feared surgical complications, he refused and received 70 days of tigecycline plus daptomycin therapy, which was complicated only by nausea. He remained clinically well and had negative blood cultures 16 weeks after completion of therapy.

DISCUSSION

Tigecycline, the first available glycylcycline, is a minocycline‐derived antibiotic that remains active in the presence of the ribosomal modifications and efflux pumps that mediate tetracycline resistance. Thus, it possesses broad‐spectrum bacteriostatic activity, including activity against VRE. A PubMed search revealed no published data about the use of tigecycline for endocarditis in humans. However, tetracyclines have been used to treat endocarditis due to such organisms as Bartonella, Coxiella burnetti, or methicillin‐resistant Staphylococcus aureus (MRSA), frequently for prolonged courses. Tetracyclines were combined with other antibiotics in 5 published cases of VRE endocarditis. All patients survived; 3 were cured with the tetracycline regimen and 2 with other antimicrobials.1 In animal models of endocarditis, tigecycline stabilized vegetation counts of E. faecalis and reduced vegetation counts of MRSA and 1 strain of E. faecium.4

Daptomycin, the first available cyclic lipopeptide, kills by nonlytic depolarization of the bacterial cell membrane. In a recent study, daptomycin was non‐inferior to vancomycin or antistaphylococcal penicillins for S. aureus bacteremia or endocarditis. Although a few patients had left‐sided endocarditis, only 1 of them experienced a successful outcome with daptomycin therapy, and daptomycin displayed a trend toward higher rates of persistent or relapsing infection.5 Less evidence supports the use of daptomycin for serious enterococcal infections.2 One report noted the deaths of 6 of 10 patients treated with daptomycin for VRE bacteremia, including both patients with endocarditis.6 Daptomycin was used successfully in a case of VRE endocarditis in combination with gentamicin and rifampin for 11 weeks1 and at least 6 other reported cases of VRE bacteremia.7, 8

In summary, despite tigecycline's lack of bactericidal activity or proven efficacy in endocarditis, daptomycin's prior performance in VRE bacteremia, and the isolate's borderline daptomycin susceptibility, prolonged combination therapy resulted in a cure of VRE endocarditis. This success extends the experience with using both agents in the treatment of resistant infections. As linezolid‐resistant VRE and other resistant pathogens become more common, the need for research on treatment options becomes more urgent, and familiarity with novel and lesser‐used antibiotics becomes more crucial for hospitalists.

Enterococci are a leading cause of endocarditis and nosocomial infections. Vancomycin‐resistant enterococci (VRE) emerged in the 1980s and now represent most nosocomial isolates in the United States. The first case of VRE endocarditis was reported in 1996.1 Although increasing enterococcal antibiotic resistance has prompted increasing reliance on newer antibiotics,2 a recent review of VRE endocarditis noted that survival rates were similar to those for vancomycin‐sensitive enterococcal endocarditis.1 Cure was achieved in several patients with bacteriostatic agents in the absence of valve replacement, but no patients were infected with truly linezolid‐resistant organisms. This case of linezolid‐resistant VRE endocarditis represents the first reported cure of infective endocarditis with a tigecycline‐containing regimen.

CASE REPORT

A 62‐year‐old man presented with hypoglycemia and delirium. His medical history included diabetes mellitus, coronary and peripheral arterial disease, and end‐stage renal disease. He had had endocarditis of an unknown type 12 years prior to admission. He had recently developed septic shock because of a Candida parapsilosis, Enterobacter cloacae, and Staphylococcus epidermidis infection of a peripherally inserted central catheter (PICC) and received 14 days of vancomycin, meropenem, and fluconazole administered through a new PICC. This catheter was not removed, and 39 days after completion of the antibiotic therapy, he developed hypoglycemia, which was attributed to weight loss without adjustment of his insulin regimen. He was afebrile; examination revealed a new 3/6 holosystolic murmur radiating to the axilla. There were no other stigmata of infective endocarditis, and his PICC and arteriovenous fistula sites appeared normal. Delirium resolved after administration of intravenous glucose.

E. faecium grew from all 6 initial blood cultures. A transesophageal echocardiogram revealed a new 3‐mm mitral valve vegetation with perforation and severe regurgitation. He had definite endocarditis on the basis of 2 major criteria.3 He was given vancomycin (1 g IV, then administered by levels), then switched to linezolid (600 mg orally every 12 hours), and finally tigecycline (100 mg IV followed by 50 mg IV every 12 hours) plus daptomycin (6 mg/kg IV every 48 hours) as further sensitivity data became available.

The organism was resistant to ampicillin, chloramphenicol, and linezolid (MIC > 20 g/mL), as well as vancomycin (MIC > 50 g/mL), quinupristin/dalfopristin (MIC 2.5 g/mL), and gentamicin (MIC > 200 g/mL), and demonstrated high‐level streptomycin resistance (>2000 g/mL). It was intermediate to doxycycline (MIC 5 g/mL). It was susceptible to daptomycin (MIC 4 g/mL) and tigecycline (MIC 0.06 g/mL).

Blood cultures done on hospital days 1, 4, 6, and 7 (day 1 of tigecycline) were positive, and multiple cultures were negative from day 10 on. Because of the lack of experience with tigecycline in infective endocarditis, unrevascularized left‐main coronary artery disease, and severe mitral regurgitation, the patient was advised to undergo valve replacement and coronary artery bypass surgery after antibiotic therapy. Because he feared surgical complications, he refused and received 70 days of tigecycline plus daptomycin therapy, which was complicated only by nausea. He remained clinically well and had negative blood cultures 16 weeks after completion of therapy.

DISCUSSION

Tigecycline, the first available glycylcycline, is a minocycline‐derived antibiotic that remains active in the presence of the ribosomal modifications and efflux pumps that mediate tetracycline resistance. Thus, it possesses broad‐spectrum bacteriostatic activity, including activity against VRE. A PubMed search revealed no published data about the use of tigecycline for endocarditis in humans. However, tetracyclines have been used to treat endocarditis due to such organisms as Bartonella, Coxiella burnetti, or methicillin‐resistant Staphylococcus aureus (MRSA), frequently for prolonged courses. Tetracyclines were combined with other antibiotics in 5 published cases of VRE endocarditis. All patients survived; 3 were cured with the tetracycline regimen and 2 with other antimicrobials.1 In animal models of endocarditis, tigecycline stabilized vegetation counts of E. faecalis and reduced vegetation counts of MRSA and 1 strain of E. faecium.4

Daptomycin, the first available cyclic lipopeptide, kills by nonlytic depolarization of the bacterial cell membrane. In a recent study, daptomycin was non‐inferior to vancomycin or antistaphylococcal penicillins for S. aureus bacteremia or endocarditis. Although a few patients had left‐sided endocarditis, only 1 of them experienced a successful outcome with daptomycin therapy, and daptomycin displayed a trend toward higher rates of persistent or relapsing infection.5 Less evidence supports the use of daptomycin for serious enterococcal infections.2 One report noted the deaths of 6 of 10 patients treated with daptomycin for VRE bacteremia, including both patients with endocarditis.6 Daptomycin was used successfully in a case of VRE endocarditis in combination with gentamicin and rifampin for 11 weeks1 and at least 6 other reported cases of VRE bacteremia.7, 8

In summary, despite tigecycline's lack of bactericidal activity or proven efficacy in endocarditis, daptomycin's prior performance in VRE bacteremia, and the isolate's borderline daptomycin susceptibility, prolonged combination therapy resulted in a cure of VRE endocarditis. This success extends the experience with using both agents in the treatment of resistant infections. As linezolid‐resistant VRE and other resistant pathogens become more common, the need for research on treatment options becomes more urgent, and familiarity with novel and lesser‐used antibiotics becomes more crucial for hospitalists.

Enterococci are a leading cause of endocarditis and nosocomial infections. Vancomycin‐resistant enterococci (VRE) emerged in the 1980s and now represent most nosocomial isolates in the United States. The first case of VRE endocarditis was reported in 1996.1 Although increasing enterococcal antibiotic resistance has prompted increasing reliance on newer antibiotics,2 a recent review of VRE endocarditis noted that survival rates were similar to those for vancomycin‐sensitive enterococcal endocarditis.1 Cure was achieved in several patients with bacteriostatic agents in the absence of valve replacement, but no patients were infected with truly linezolid‐resistant organisms. This case of linezolid‐resistant VRE endocarditis represents the first reported cure of infective endocarditis with a tigecycline‐containing regimen.

CASE REPORT

A 62‐year‐old man presented with hypoglycemia and delirium. His medical history included diabetes mellitus, coronary and peripheral arterial disease, and end‐stage renal disease. He had had endocarditis of an unknown type 12 years prior to admission. He had recently developed septic shock because of a Candida parapsilosis, Enterobacter cloacae, and Staphylococcus epidermidis infection of a peripherally inserted central catheter (PICC) and received 14 days of vancomycin, meropenem, and fluconazole administered through a new PICC. This catheter was not removed, and 39 days after completion of the antibiotic therapy, he developed hypoglycemia, which was attributed to weight loss without adjustment of his insulin regimen. He was afebrile; examination revealed a new 3/6 holosystolic murmur radiating to the axilla. There were no other stigmata of infective endocarditis, and his PICC and arteriovenous fistula sites appeared normal. Delirium resolved after administration of intravenous glucose.

E. faecium grew from all 6 initial blood cultures. A transesophageal echocardiogram revealed a new 3‐mm mitral valve vegetation with perforation and severe regurgitation. He had definite endocarditis on the basis of 2 major criteria.3 He was given vancomycin (1 g IV, then administered by levels), then switched to linezolid (600 mg orally every 12 hours), and finally tigecycline (100 mg IV followed by 50 mg IV every 12 hours) plus daptomycin (6 mg/kg IV every 48 hours) as further sensitivity data became available.

The organism was resistant to ampicillin, chloramphenicol, and linezolid (MIC > 20 g/mL), as well as vancomycin (MIC > 50 g/mL), quinupristin/dalfopristin (MIC 2.5 g/mL), and gentamicin (MIC > 200 g/mL), and demonstrated high‐level streptomycin resistance (>2000 g/mL). It was intermediate to doxycycline (MIC 5 g/mL). It was susceptible to daptomycin (MIC 4 g/mL) and tigecycline (MIC 0.06 g/mL).

Blood cultures done on hospital days 1, 4, 6, and 7 (day 1 of tigecycline) were positive, and multiple cultures were negative from day 10 on. Because of the lack of experience with tigecycline in infective endocarditis, unrevascularized left‐main coronary artery disease, and severe mitral regurgitation, the patient was advised to undergo valve replacement and coronary artery bypass surgery after antibiotic therapy. Because he feared surgical complications, he refused and received 70 days of tigecycline plus daptomycin therapy, which was complicated only by nausea. He remained clinically well and had negative blood cultures 16 weeks after completion of therapy.

DISCUSSION

Tigecycline, the first available glycylcycline, is a minocycline‐derived antibiotic that remains active in the presence of the ribosomal modifications and efflux pumps that mediate tetracycline resistance. Thus, it possesses broad‐spectrum bacteriostatic activity, including activity against VRE. A PubMed search revealed no published data about the use of tigecycline for endocarditis in humans. However, tetracyclines have been used to treat endocarditis due to such organisms as Bartonella, Coxiella burnetti, or methicillin‐resistant Staphylococcus aureus (MRSA), frequently for prolonged courses. Tetracyclines were combined with other antibiotics in 5 published cases of VRE endocarditis. All patients survived; 3 were cured with the tetracycline regimen and 2 with other antimicrobials.1 In animal models of endocarditis, tigecycline stabilized vegetation counts of E. faecalis and reduced vegetation counts of MRSA and 1 strain of E. faecium.4

Daptomycin, the first available cyclic lipopeptide, kills by nonlytic depolarization of the bacterial cell membrane. In a recent study, daptomycin was non‐inferior to vancomycin or antistaphylococcal penicillins for S. aureus bacteremia or endocarditis. Although a few patients had left‐sided endocarditis, only 1 of them experienced a successful outcome with daptomycin therapy, and daptomycin displayed a trend toward higher rates of persistent or relapsing infection.5 Less evidence supports the use of daptomycin for serious enterococcal infections.2 One report noted the deaths of 6 of 10 patients treated with daptomycin for VRE bacteremia, including both patients with endocarditis.6 Daptomycin was used successfully in a case of VRE endocarditis in combination with gentamicin and rifampin for 11 weeks1 and at least 6 other reported cases of VRE bacteremia.7, 8

In summary, despite tigecycline's lack of bactericidal activity or proven efficacy in endocarditis, daptomycin's prior performance in VRE bacteremia, and the isolate's borderline daptomycin susceptibility, prolonged combination therapy resulted in a cure of VRE endocarditis. This success extends the experience with using both agents in the treatment of resistant infections. As linezolid‐resistant VRE and other resistant pathogens become more common, the need for research on treatment options becomes more urgent, and familiarity with novel and lesser‐used antibiotics becomes more crucial for hospitalists.

A 54‐year‐old man with hypertension and type 2 diabetes mellitus entered the Chest Pain Evaluation Unit of a teaching hospital after 12 hours of intermittent thoracic discomfort. The pain began during dinner and was sharp, bandlike, and located beneath the sternum and across the entire chest. He had dyspnea but no diaphoresis or nausea. A recumbent position relieved the pain after dinner, but it recurred during the night and again the following morning. He did not smoke and had no family history of coronary artery disease.

A useful approach in evaluating acute chest pain is to employ a hierarchical differential diagnosis that emphasizes life‐threatening disorders requiring prompt recognition and intervention. Most prominent are cardiac ischemia, pericardial tamponade, pneumothorax, pulmonary embolus, esophageal rupture, and aortic dissection. The concurrent dyspnea and retrosternal location and intermittent nature of the pain that this patient has are consistent with myocardial ischemia, but the sharp quality of the pain and the relief gained by being recumbent are atypical. Pain with pericarditis is characteristically pleuritic and often worse when lying down. The pain of pneumothorax is typically unilateral, not intermittent, and unlikely to improve with recumbency. Although pain during eating suggests the possibility of an esophageal source, spontaneous rupture usually follows vomiting. The pain is typically continuous and severe. The pain of pulmonary embolism may be unilateral and pleuritic but often is more diffuse. Relief by recumbency is unusual, but the intermittent nature could suggest recurrent emboli. The patient has a history of hypertension, which predisposes him to aortic dissection, in which the pain is typically sharp, continuous, and severe but occasionally intermittent. Among numerous less urgent diagnoses are esophagitis and thoracic diabetic radiculopathy.

Important features to look for during this patient's examination include: disappearance of the radial pulse during inhalation, a simple screening test that is insensitive but very specific for pericardial tamponade; elevated neck veins, which can occur with tension pneumothorax, massive pulmonary embolism, and pericardial tamponade; pericardial and pleural friction rubs; discrepant blood pressures in the 2 arms, sometimes a sign of aortic dissection; local thoracic tenderness from chest wall disorders; and sensory examination of the chest surface, which is often abnormal in diabetic thoracic radiculopathy. Given this patient's age and history of diabetes, I am most concerned about myocardial ischemia. The most appropriate diagnostic tests include an electrocardiogram and a chest radiograph.

The patient appeared apprehensive but reported no pain. He had a temperature of 36.0 C, heart rate of 95 beats/minute, blood pressure of 138/77 mm Hg, respiratory rate of 16/minute, and oxygen saturation of 99% while breathing ambient air. Blood pressures were equal in both arms. Jugular venous distention was absent, and the lung and cardiac examinations had normal results. His pain did not increase on chest wall palpation. Examination of the abdomen, extremities, and the neurologic system showed normal results.

The results of laboratory tests showed a leukocyte count of 12,700/cm³, with 85% neutrophils, 8% lymphocytes, 6% monocytes, and 1% eosinophils. The hematocrit was 45%, and the platelet count was 172,000/cm³. The results of his chemistry panel were remarkable only for a glucose of 225 mg/dL. An electrocardiogram (ECG) showed a normal sinus rhythm and left anterior fascicular block without acute ST‐ or T‐wave changes. Prior ECGs were unavailable. An anteroposterior radiograph disclosed low lung volumes and bibasilar opacities. No pleural effusion was noted. Serial serum troponin and creatine kinase levels were normal. A Tc‐99m tetrofosmin cardiac nuclear perfusion test performed at rest demonstrated a moderate area of mildly decreased uptake along the inferior wall extending to the apex. An exercise treadmill test, terminated after 1 minute, 45 seconds because of chest pain, provoked no ECG changes diagnostic of ischemic disease.

The absence of elevated jugular venous pressure virtually eliminates pericardial tamponade as a diagnosis, and the chest film excludes pneumothorax. The intermittent nature of the chest pain, the absence on the chest radiograph of such findings as mediastinal gas, left pneumothorax, or hydropneumothorax, and the lack of a predisposing cause make esophageal rupture unlikely. Pulmonary emboli remain a consideration despite the normal oxygen saturation because there is no hypoxemia in a substantial minority of such cases. The normal cardiac enzyme levels and the lack of significant changes on the ECG exclude that a myocardial infarction has recently occurred, but cardiac ischemia remains a possibility, especially because the patient had chest pain on exercise and the nuclear scan indicated diminished blood flow to the inferior left ventricle. Aortic dissection still lurks as a possibility. The inferior wall abnormalities seen on the scan could result from dissection into the right coronary artery, which is more frequently involved than the left, or compression of it by an enlarged aorta, but they also may be artifacts. The leukocytosis may be a nonspecific response to stress but could indicate, although unlikely, infections such as mediastinitis from esophageal rupture or bacterial aortitis.

A conscientious clinician would repeat the history, reexamine the patient, and scrutinize the chest film to determine what the bilateral opacities represent. Given the story so far, however, I might consider a thoracic computed tomography (CT) angiogram because I am most concerned about pulmonary emboli and aortic dissection.

On hospital day 3, the patient had worsening dyspnea and persistent chest pain. His temperature was 39.3C, and his oxygen saturation decreased to 89% while breathing room air. Repeat chest radiography showed new bilateral pleural effusions and increased bibasilar opacification (Fig. 1). His leukocyte count was 19,000/cm³, with 88% neutrophils, 6% lymphocytes, 5% monocytes, and 1% eosinophils. Care was transferred from the chest pain team to an inpatient general medicine ward team. A pulmonary CT angiogram showed no large central clots but suggested emboli in the right superior subsegmental artery and a right upper lobe subsegmental artery. Bilateral pleural effusions were observed, as were bilateral pleural‐based atelectasis or infiltrates in the lower lungs. A hiatal hernia was noted, but no aortic dissection. The patient received supplemental oxygen, intravenous levofloxacin, and unfractionated heparin by continuous infusion.

Figure 1

Without other information, I will assume that the fever is part of the patient's original disease and not a nosocomial infection or drug fever. At this point, a crucial part of the evaluation is examining the CT scan with experienced radiologists to determine whether the abnormalities noted are genuinely convincing for pulmonary emboli. If the findings are equivocal, the next step might be a pulmonary angiogram or the indirect approach of evaluating the leg veins with ultrasound, reasoning that the presence of proximal leg vein thromboses would require anticoagulation in any event.

The patient's worsening chest pain and hypoxemia are consistent with multiple pulmonary emboli. Bilateral pleural effusions and leukocytosis can occur but are uncommon. Because of the fever, another possibility is septic pulmonary emboli, but he has no evidence of suppurative thrombophlebitis of the peripheral veins, apparent infection elsewhere, or previous intravenous drug abuse causing right‐sided endocarditis. An alternative diagnosis is infection of an initially bland pulmonary infarct.

An important consideration is a thoracentesis, depending on how persuasive the CT diagnosis of pulmonary embolism is and the size of the pleural effusions. It should be done before instituting antimicrobial therapy, which may decrease the yield of the cultures, and before starting heparin, which increases the risk of bleeding and occasionally causes a substantial, even fatal hemothorax.

The patient's oxygenation and dyspnea did not improve. Over the next day, he repeatedly mentioned that swallowing, particularly solid foods, worsened his chest pain. He had a temperature of 39.9C, a heart rate of 121 beats/minute, blood pressure of 149/94 mm Hg, a respiratory rate of 28/minute, and oxygen saturation of 93% while breathing 40% oxygen. He had inspiratory splinting, percussive dullness at both lung bases, and distant heart sounds. A contrast esophagogram showed distal narrowing that prevented solid contrast from passing, but no hiatal hernia. Blood and urine cultures obtained before antibiotic therapy were sterile. Duplex ultrasonography of bilateral lower extremities showed no evidence of deep venous thrombosis. A pulmonary angiogram revealed no emboli, and heparin was discontinued. Bilateral thoracentesis yielded grossly bloody fluid. Repeat chest CT (Fig. 2) demonstrated large bilateral effusions, a new large pericardial effusion, and a prominence at the gastroesophageal junction more concerning for a soft‐tissue mass than for a hiatal hernia, although the quality of the study was suboptimal because of an absence of oral contrast.

Figure 2

The CT scan suggests a paraesophageal abscess from an esophageal rupture. As mentioned earlier, if rupture occurs spontaneously, it typically follows retching or vomiting and is called Boerhaave's syndrome. Another consideration is a rupture secondary to an external insult, such as trauma or ingestion of a caustic substance. In evaluating these possibilities, the patient should have been asked 4 questions at the initial interview that I neglected to explicitly highlight earlier. First, what was he eating when he developed the chest pain? Second, did the pain begin during swallowing? Third, did he have previous symptoms suggesting an esophageal disorder such as dysphagia, odynophagia, or heartburn? These might indicate a cancer that could perforate or another problem such as a stricture or disordered esophageal motility that might have caused a swallowed item to lodge in the esophagus. Finally, did he have retching or vomiting? Though not routinely part of the review of systems, the former 2 questions are an appropriate history‐prompted line of questioning of a patient with onset of chest pain while eating.

At this point, a reasonable approach would be an esophagoscopy to delineate any intraluminal problems, such as a cancer or a foreign body. The apparent obstruction seen on barium swallow may be from extrinsic pressure from a paraesophageal abscess. The patient should receive broad‐spectrum antimicrobial therapy effective against oral anaerobes. Although occasionally patients recover with antibiotics alone, surgery is usually required. I am surprised that the original CT scan did not show evidence of an esophageal perforation. Possibly, the hiatal hernia was a paraesophageal abscess poorly characterized because of the lack of oral contrast.

The team, concerned about esophageal perforation, began the patient on intravenous clindamycin. The patient underwent video‐assisted thoracoscopic drainage, which yielded a moderate amount of turbid, bloody fluid from each hemithorax. The pericardium contained approximately 500 cm³ of turbid fluid. Gram stain and culture of these fluids were negative. No esophageal or mediastinal mass was noted during surgery. Intraoperative esophagogastroduodenoscopy with endoscopic ultrasound showed a healing linear mucosal tear in the distal esophagus (Fig. 3) as well as air/fluid collection in the esophageal soft tissue (not shown).

Figure 3

On further questioning postoperatively, the patient reported eating bony fish during the dinner when he first experienced chest pain. The patient received a 21‐day course of oral clindamycin and completely recovered. Five weeks later, a chest CT showed decreased distal esophageal thickening and no mediastinal air.

COMMENTARY

Esophageal perforation is an uncommon but life‐threatening cause of chest pain. In most series iatrogenic injury accounts for more than 70% of cases, whereas most of the other cases have spontaneous (5%20%) or traumatic (4%10%) causes (Table 1).14 Perforation as a complication of ingesting fish bones, although rare, is well described and continues to be reported.57

Diagnosis of esophageal perforation secondary to a foreign body may be difficult because of the considerable overlap of symptoms with other causes of chest pain and failure to consider this infrequent condition in the absence of a classic history of retching. To diagnose such a disease, physicians must gather data from various sourcesespecially the history, physical examination, and medical recordformulate hypotheses, integrate results from diagnostic tests, and then assess the importance of the available information in the context of a differential diagnosis. Incorrectly evaluating or failing to obtain essential data can lead to incorrect or delayed diagnoses.

A 54‐year‐old man with hypertension and type 2 diabetes mellitus entered the Chest Pain Evaluation Unit of a teaching hospital after 12 hours of intermittent thoracic discomfort. The pain began during dinner and was sharp, bandlike, and located beneath the sternum and across the entire chest. He had dyspnea but no diaphoresis or nausea. A recumbent position relieved the pain after dinner, but it recurred during the night and again the following morning. He did not smoke and had no family history of coronary artery disease.

A useful approach in evaluating acute chest pain is to employ a hierarchical differential diagnosis that emphasizes life‐threatening disorders requiring prompt recognition and intervention. Most prominent are cardiac ischemia, pericardial tamponade, pneumothorax, pulmonary embolus, esophageal rupture, and aortic dissection. The concurrent dyspnea and retrosternal location and intermittent nature of the pain that this patient has are consistent with myocardial ischemia, but the sharp quality of the pain and the relief gained by being recumbent are atypical. Pain with pericarditis is characteristically pleuritic and often worse when lying down. The pain of pneumothorax is typically unilateral, not intermittent, and unlikely to improve with recumbency. Although pain during eating suggests the possibility of an esophageal source, spontaneous rupture usually follows vomiting. The pain is typically continuous and severe. The pain of pulmonary embolism may be unilateral and pleuritic but often is more diffuse. Relief by recumbency is unusual, but the intermittent nature could suggest recurrent emboli. The patient has a history of hypertension, which predisposes him to aortic dissection, in which the pain is typically sharp, continuous, and severe but occasionally intermittent. Among numerous less urgent diagnoses are esophagitis and thoracic diabetic radiculopathy.

Important features to look for during this patient's examination include: disappearance of the radial pulse during inhalation, a simple screening test that is insensitive but very specific for pericardial tamponade; elevated neck veins, which can occur with tension pneumothorax, massive pulmonary embolism, and pericardial tamponade; pericardial and pleural friction rubs; discrepant blood pressures in the 2 arms, sometimes a sign of aortic dissection; local thoracic tenderness from chest wall disorders; and sensory examination of the chest surface, which is often abnormal in diabetic thoracic radiculopathy. Given this patient's age and history of diabetes, I am most concerned about myocardial ischemia. The most appropriate diagnostic tests include an electrocardiogram and a chest radiograph.

The patient appeared apprehensive but reported no pain. He had a temperature of 36.0 C, heart rate of 95 beats/minute, blood pressure of 138/77 mm Hg, respiratory rate of 16/minute, and oxygen saturation of 99% while breathing ambient air. Blood pressures were equal in both arms. Jugular venous distention was absent, and the lung and cardiac examinations had normal results. His pain did not increase on chest wall palpation. Examination of the abdomen, extremities, and the neurologic system showed normal results.

The results of laboratory tests showed a leukocyte count of 12,700/cm³, with 85% neutrophils, 8% lymphocytes, 6% monocytes, and 1% eosinophils. The hematocrit was 45%, and the platelet count was 172,000/cm³. The results of his chemistry panel were remarkable only for a glucose of 225 mg/dL. An electrocardiogram (ECG) showed a normal sinus rhythm and left anterior fascicular block without acute ST‐ or T‐wave changes. Prior ECGs were unavailable. An anteroposterior radiograph disclosed low lung volumes and bibasilar opacities. No pleural effusion was noted. Serial serum troponin and creatine kinase levels were normal. A Tc‐99m tetrofosmin cardiac nuclear perfusion test performed at rest demonstrated a moderate area of mildly decreased uptake along the inferior wall extending to the apex. An exercise treadmill test, terminated after 1 minute, 45 seconds because of chest pain, provoked no ECG changes diagnostic of ischemic disease.

The absence of elevated jugular venous pressure virtually eliminates pericardial tamponade as a diagnosis, and the chest film excludes pneumothorax. The intermittent nature of the chest pain, the absence on the chest radiograph of such findings as mediastinal gas, left pneumothorax, or hydropneumothorax, and the lack of a predisposing cause make esophageal rupture unlikely. Pulmonary emboli remain a consideration despite the normal oxygen saturation because there is no hypoxemia in a substantial minority of such cases. The normal cardiac enzyme levels and the lack of significant changes on the ECG exclude that a myocardial infarction has recently occurred, but cardiac ischemia remains a possibility, especially because the patient had chest pain on exercise and the nuclear scan indicated diminished blood flow to the inferior left ventricle. Aortic dissection still lurks as a possibility. The inferior wall abnormalities seen on the scan could result from dissection into the right coronary artery, which is more frequently involved than the left, or compression of it by an enlarged aorta, but they also may be artifacts. The leukocytosis may be a nonspecific response to stress but could indicate, although unlikely, infections such as mediastinitis from esophageal rupture or bacterial aortitis.

A conscientious clinician would repeat the history, reexamine the patient, and scrutinize the chest film to determine what the bilateral opacities represent. Given the story so far, however, I might consider a thoracic computed tomography (CT) angiogram because I am most concerned about pulmonary emboli and aortic dissection.

On hospital day 3, the patient had worsening dyspnea and persistent chest pain. His temperature was 39.3C, and his oxygen saturation decreased to 89% while breathing room air. Repeat chest radiography showed new bilateral pleural effusions and increased bibasilar opacification (Fig. 1). His leukocyte count was 19,000/cm³, with 88% neutrophils, 6% lymphocytes, 5% monocytes, and 1% eosinophils. Care was transferred from the chest pain team to an inpatient general medicine ward team. A pulmonary CT angiogram showed no large central clots but suggested emboli in the right superior subsegmental artery and a right upper lobe subsegmental artery. Bilateral pleural effusions were observed, as were bilateral pleural‐based atelectasis or infiltrates in the lower lungs. A hiatal hernia was noted, but no aortic dissection. The patient received supplemental oxygen, intravenous levofloxacin, and unfractionated heparin by continuous infusion.

Figure 1

Without other information, I will assume that the fever is part of the patient's original disease and not a nosocomial infection or drug fever. At this point, a crucial part of the evaluation is examining the CT scan with experienced radiologists to determine whether the abnormalities noted are genuinely convincing for pulmonary emboli. If the findings are equivocal, the next step might be a pulmonary angiogram or the indirect approach of evaluating the leg veins with ultrasound, reasoning that the presence of proximal leg vein thromboses would require anticoagulation in any event.

The patient's worsening chest pain and hypoxemia are consistent with multiple pulmonary emboli. Bilateral pleural effusions and leukocytosis can occur but are uncommon. Because of the fever, another possibility is septic pulmonary emboli, but he has no evidence of suppurative thrombophlebitis of the peripheral veins, apparent infection elsewhere, or previous intravenous drug abuse causing right‐sided endocarditis. An alternative diagnosis is infection of an initially bland pulmonary infarct.

An important consideration is a thoracentesis, depending on how persuasive the CT diagnosis of pulmonary embolism is and the size of the pleural effusions. It should be done before instituting antimicrobial therapy, which may decrease the yield of the cultures, and before starting heparin, which increases the risk of bleeding and occasionally causes a substantial, even fatal hemothorax.

The patient's oxygenation and dyspnea did not improve. Over the next day, he repeatedly mentioned that swallowing, particularly solid foods, worsened his chest pain. He had a temperature of 39.9C, a heart rate of 121 beats/minute, blood pressure of 149/94 mm Hg, a respiratory rate of 28/minute, and oxygen saturation of 93% while breathing 40% oxygen. He had inspiratory splinting, percussive dullness at both lung bases, and distant heart sounds. A contrast esophagogram showed distal narrowing that prevented solid contrast from passing, but no hiatal hernia. Blood and urine cultures obtained before antibiotic therapy were sterile. Duplex ultrasonography of bilateral lower extremities showed no evidence of deep venous thrombosis. A pulmonary angiogram revealed no emboli, and heparin was discontinued. Bilateral thoracentesis yielded grossly bloody fluid. Repeat chest CT (Fig. 2) demonstrated large bilateral effusions, a new large pericardial effusion, and a prominence at the gastroesophageal junction more concerning for a soft‐tissue mass than for a hiatal hernia, although the quality of the study was suboptimal because of an absence of oral contrast.

Figure 2

The CT scan suggests a paraesophageal abscess from an esophageal rupture. As mentioned earlier, if rupture occurs spontaneously, it typically follows retching or vomiting and is called Boerhaave's syndrome. Another consideration is a rupture secondary to an external insult, such as trauma or ingestion of a caustic substance. In evaluating these possibilities, the patient should have been asked 4 questions at the initial interview that I neglected to explicitly highlight earlier. First, what was he eating when he developed the chest pain? Second, did the pain begin during swallowing? Third, did he have previous symptoms suggesting an esophageal disorder such as dysphagia, odynophagia, or heartburn? These might indicate a cancer that could perforate or another problem such as a stricture or disordered esophageal motility that might have caused a swallowed item to lodge in the esophagus. Finally, did he have retching or vomiting? Though not routinely part of the review of systems, the former 2 questions are an appropriate history‐prompted line of questioning of a patient with onset of chest pain while eating.

At this point, a reasonable approach would be an esophagoscopy to delineate any intraluminal problems, such as a cancer or a foreign body. The apparent obstruction seen on barium swallow may be from extrinsic pressure from a paraesophageal abscess. The patient should receive broad‐spectrum antimicrobial therapy effective against oral anaerobes. Although occasionally patients recover with antibiotics alone, surgery is usually required. I am surprised that the original CT scan did not show evidence of an esophageal perforation. Possibly, the hiatal hernia was a paraesophageal abscess poorly characterized because of the lack of oral contrast.

The team, concerned about esophageal perforation, began the patient on intravenous clindamycin. The patient underwent video‐assisted thoracoscopic drainage, which yielded a moderate amount of turbid, bloody fluid from each hemithorax. The pericardium contained approximately 500 cm³ of turbid fluid. Gram stain and culture of these fluids were negative. No esophageal or mediastinal mass was noted during surgery. Intraoperative esophagogastroduodenoscopy with endoscopic ultrasound showed a healing linear mucosal tear in the distal esophagus (Fig. 3) as well as air/fluid collection in the esophageal soft tissue (not shown).

Figure 3

On further questioning postoperatively, the patient reported eating bony fish during the dinner when he first experienced chest pain. The patient received a 21‐day course of oral clindamycin and completely recovered. Five weeks later, a chest CT showed decreased distal esophageal thickening and no mediastinal air.

COMMENTARY

Esophageal perforation is an uncommon but life‐threatening cause of chest pain. In most series iatrogenic injury accounts for more than 70% of cases, whereas most of the other cases have spontaneous (5%20%) or traumatic (4%10%) causes (Table 1).14 Perforation as a complication of ingesting fish bones, although rare, is well described and continues to be reported.57

Diagnosis of esophageal perforation secondary to a foreign body may be difficult because of the considerable overlap of symptoms with other causes of chest pain and failure to consider this infrequent condition in the absence of a classic history of retching. To diagnose such a disease, physicians must gather data from various sourcesespecially the history, physical examination, and medical recordformulate hypotheses, integrate results from diagnostic tests, and then assess the importance of the available information in the context of a differential diagnosis. Incorrectly evaluating or failing to obtain essential data can lead to incorrect or delayed diagnoses.

A 54‐year‐old man with hypertension and type 2 diabetes mellitus entered the Chest Pain Evaluation Unit of a teaching hospital after 12 hours of intermittent thoracic discomfort. The pain began during dinner and was sharp, bandlike, and located beneath the sternum and across the entire chest. He had dyspnea but no diaphoresis or nausea. A recumbent position relieved the pain after dinner, but it recurred during the night and again the following morning. He did not smoke and had no family history of coronary artery disease.

A useful approach in evaluating acute chest pain is to employ a hierarchical differential diagnosis that emphasizes life‐threatening disorders requiring prompt recognition and intervention. Most prominent are cardiac ischemia, pericardial tamponade, pneumothorax, pulmonary embolus, esophageal rupture, and aortic dissection. The concurrent dyspnea and retrosternal location and intermittent nature of the pain that this patient has are consistent with myocardial ischemia, but the sharp quality of the pain and the relief gained by being recumbent are atypical. Pain with pericarditis is characteristically pleuritic and often worse when lying down. The pain of pneumothorax is typically unilateral, not intermittent, and unlikely to improve with recumbency. Although pain during eating suggests the possibility of an esophageal source, spontaneous rupture usually follows vomiting. The pain is typically continuous and severe. The pain of pulmonary embolism may be unilateral and pleuritic but often is more diffuse. Relief by recumbency is unusual, but the intermittent nature could suggest recurrent emboli. The patient has a history of hypertension, which predisposes him to aortic dissection, in which the pain is typically sharp, continuous, and severe but occasionally intermittent. Among numerous less urgent diagnoses are esophagitis and thoracic diabetic radiculopathy.

Important features to look for during this patient's examination include: disappearance of the radial pulse during inhalation, a simple screening test that is insensitive but very specific for pericardial tamponade; elevated neck veins, which can occur with tension pneumothorax, massive pulmonary embolism, and pericardial tamponade; pericardial and pleural friction rubs; discrepant blood pressures in the 2 arms, sometimes a sign of aortic dissection; local thoracic tenderness from chest wall disorders; and sensory examination of the chest surface, which is often abnormal in diabetic thoracic radiculopathy. Given this patient's age and history of diabetes, I am most concerned about myocardial ischemia. The most appropriate diagnostic tests include an electrocardiogram and a chest radiograph.

The patient appeared apprehensive but reported no pain. He had a temperature of 36.0 C, heart rate of 95 beats/minute, blood pressure of 138/77 mm Hg, respiratory rate of 16/minute, and oxygen saturation of 99% while breathing ambient air. Blood pressures were equal in both arms. Jugular venous distention was absent, and the lung and cardiac examinations had normal results. His pain did not increase on chest wall palpation. Examination of the abdomen, extremities, and the neurologic system showed normal results.

The results of laboratory tests showed a leukocyte count of 12,700/cm³, with 85% neutrophils, 8% lymphocytes, 6% monocytes, and 1% eosinophils. The hematocrit was 45%, and the platelet count was 172,000/cm³. The results of his chemistry panel were remarkable only for a glucose of 225 mg/dL. An electrocardiogram (ECG) showed a normal sinus rhythm and left anterior fascicular block without acute ST‐ or T‐wave changes. Prior ECGs were unavailable. An anteroposterior radiograph disclosed low lung volumes and bibasilar opacities. No pleural effusion was noted. Serial serum troponin and creatine kinase levels were normal. A Tc‐99m tetrofosmin cardiac nuclear perfusion test performed at rest demonstrated a moderate area of mildly decreased uptake along the inferior wall extending to the apex. An exercise treadmill test, terminated after 1 minute, 45 seconds because of chest pain, provoked no ECG changes diagnostic of ischemic disease.

The absence of elevated jugular venous pressure virtually eliminates pericardial tamponade as a diagnosis, and the chest film excludes pneumothorax. The intermittent nature of the chest pain, the absence on the chest radiograph of such findings as mediastinal gas, left pneumothorax, or hydropneumothorax, and the lack of a predisposing cause make esophageal rupture unlikely. Pulmonary emboli remain a consideration despite the normal oxygen saturation because there is no hypoxemia in a substantial minority of such cases. The normal cardiac enzyme levels and the lack of significant changes on the ECG exclude that a myocardial infarction has recently occurred, but cardiac ischemia remains a possibility, especially because the patient had chest pain on exercise and the nuclear scan indicated diminished blood flow to the inferior left ventricle. Aortic dissection still lurks as a possibility. The inferior wall abnormalities seen on the scan could result from dissection into the right coronary artery, which is more frequently involved than the left, or compression of it by an enlarged aorta, but they also may be artifacts. The leukocytosis may be a nonspecific response to stress but could indicate, although unlikely, infections such as mediastinitis from esophageal rupture or bacterial aortitis.

A conscientious clinician would repeat the history, reexamine the patient, and scrutinize the chest film to determine what the bilateral opacities represent. Given the story so far, however, I might consider a thoracic computed tomography (CT) angiogram because I am most concerned about pulmonary emboli and aortic dissection.

On hospital day 3, the patient had worsening dyspnea and persistent chest pain. His temperature was 39.3C, and his oxygen saturation decreased to 89% while breathing room air. Repeat chest radiography showed new bilateral pleural effusions and increased bibasilar opacification (Fig. 1). His leukocyte count was 19,000/cm³, with 88% neutrophils, 6% lymphocytes, 5% monocytes, and 1% eosinophils. Care was transferred from the chest pain team to an inpatient general medicine ward team. A pulmonary CT angiogram showed no large central clots but suggested emboli in the right superior subsegmental artery and a right upper lobe subsegmental artery. Bilateral pleural effusions were observed, as were bilateral pleural‐based atelectasis or infiltrates in the lower lungs. A hiatal hernia was noted, but no aortic dissection. The patient received supplemental oxygen, intravenous levofloxacin, and unfractionated heparin by continuous infusion.

Figure 1

Without other information, I will assume that the fever is part of the patient's original disease and not a nosocomial infection or drug fever. At this point, a crucial part of the evaluation is examining the CT scan with experienced radiologists to determine whether the abnormalities noted are genuinely convincing for pulmonary emboli. If the findings are equivocal, the next step might be a pulmonary angiogram or the indirect approach of evaluating the leg veins with ultrasound, reasoning that the presence of proximal leg vein thromboses would require anticoagulation in any event.

The patient's worsening chest pain and hypoxemia are consistent with multiple pulmonary emboli. Bilateral pleural effusions and leukocytosis can occur but are uncommon. Because of the fever, another possibility is septic pulmonary emboli, but he has no evidence of suppurative thrombophlebitis of the peripheral veins, apparent infection elsewhere, or previous intravenous drug abuse causing right‐sided endocarditis. An alternative diagnosis is infection of an initially bland pulmonary infarct.

An important consideration is a thoracentesis, depending on how persuasive the CT diagnosis of pulmonary embolism is and the size of the pleural effusions. It should be done before instituting antimicrobial therapy, which may decrease the yield of the cultures, and before starting heparin, which increases the risk of bleeding and occasionally causes a substantial, even fatal hemothorax.

The patient's oxygenation and dyspnea did not improve. Over the next day, he repeatedly mentioned that swallowing, particularly solid foods, worsened his chest pain. He had a temperature of 39.9C, a heart rate of 121 beats/minute, blood pressure of 149/94 mm Hg, a respiratory rate of 28/minute, and oxygen saturation of 93% while breathing 40% oxygen. He had inspiratory splinting, percussive dullness at both lung bases, and distant heart sounds. A contrast esophagogram showed distal narrowing that prevented solid contrast from passing, but no hiatal hernia. Blood and urine cultures obtained before antibiotic therapy were sterile. Duplex ultrasonography of bilateral lower extremities showed no evidence of deep venous thrombosis. A pulmonary angiogram revealed no emboli, and heparin was discontinued. Bilateral thoracentesis yielded grossly bloody fluid. Repeat chest CT (Fig. 2) demonstrated large bilateral effusions, a new large pericardial effusion, and a prominence at the gastroesophageal junction more concerning for a soft‐tissue mass than for a hiatal hernia, although the quality of the study was suboptimal because of an absence of oral contrast.

Figure 2

The CT scan suggests a paraesophageal abscess from an esophageal rupture. As mentioned earlier, if rupture occurs spontaneously, it typically follows retching or vomiting and is called Boerhaave's syndrome. Another consideration is a rupture secondary to an external insult, such as trauma or ingestion of a caustic substance. In evaluating these possibilities, the patient should have been asked 4 questions at the initial interview that I neglected to explicitly highlight earlier. First, what was he eating when he developed the chest pain? Second, did the pain begin during swallowing? Third, did he have previous symptoms suggesting an esophageal disorder such as dysphagia, odynophagia, or heartburn? These might indicate a cancer that could perforate or another problem such as a stricture or disordered esophageal motility that might have caused a swallowed item to lodge in the esophagus. Finally, did he have retching or vomiting? Though not routinely part of the review of systems, the former 2 questions are an appropriate history‐prompted line of questioning of a patient with onset of chest pain while eating.

At this point, a reasonable approach would be an esophagoscopy to delineate any intraluminal problems, such as a cancer or a foreign body. The apparent obstruction seen on barium swallow may be from extrinsic pressure from a paraesophageal abscess. The patient should receive broad‐spectrum antimicrobial therapy effective against oral anaerobes. Although occasionally patients recover with antibiotics alone, surgery is usually required. I am surprised that the original CT scan did not show evidence of an esophageal perforation. Possibly, the hiatal hernia was a paraesophageal abscess poorly characterized because of the lack of oral contrast.

The team, concerned about esophageal perforation, began the patient on intravenous clindamycin. The patient underwent video‐assisted thoracoscopic drainage, which yielded a moderate amount of turbid, bloody fluid from each hemithorax. The pericardium contained approximately 500 cm³ of turbid fluid. Gram stain and culture of these fluids were negative. No esophageal or mediastinal mass was noted during surgery. Intraoperative esophagogastroduodenoscopy with endoscopic ultrasound showed a healing linear mucosal tear in the distal esophagus (Fig. 3) as well as air/fluid collection in the esophageal soft tissue (not shown).