Educating patients about smoking cessation when they are hospitalized for acute coronary syndrome results in a 57% 1‐year quit rate.1 This rate is far higher than the typical 15%‐30% 1‐year quit rates observed with smoking cessation programs administered in the outpatient setting24 and suggests that hospitalized patients may be uniquely motivated to respond to health education.

Kerzman and colleagues5 found that 42% of hospitalized patients expressed a wish to receive more comprehensive counseling about their medications before being discharged from the hospital. And although the Joint Commission on Hospital Accreditation and the Centers for Medicare and Medicaid Services have established core quality measures mandating that patients hospitalized with congestive heart failure receive education as one component of a high‐quality discharge process,6, 7 approximately one third of patients nationally do not receive adequate patient education.8

Barber‐Parker9 suggested that because patient acuity in hospitals was so high and patients were so commonly absent from their nursing units for testing and treatment, there was little time available for health education during their hospitalization. Anecdotal observations in our institution suggested, however, that adult patients hospitalized on the general Internal Medicine service spent much of their day doing little more than lying in bed watching television. Accordingly, we hypothesized that considerable time might be available for patient education during a hospitalization. We therefore sought to quantify the fraction of time patients were not involved in treatment activities, diagnostic testing, or other evaluations and to determine whether during these times they wanted and were feeling well enough to participate in educational activities. We also sought to determine what patients wanted to know about their health problems and what types of educational activities they most preferred.

MATERIALS AND METHODS

We conducted a time‐motion and survey study from June 25, 2005, to August 15, 2005, at Denver Health Medical Center, an academic public safety‐net hospital affiliated with the University of Colorado School of Medicine. All patients older than 18 years of age who spoke English or Spanish and were admitted to the general Internal Medicine service were candidates for enrollment. Exclusion criteria were being admitted to the intensive care unit, having an inability to communicate, being in contact precautions, and being previously enrolled. The study was approved by the Colorado Multiple Institutional Review Board. Written informed consent was obtained for all study participants.

At 8:00 _AM, all patients admitted during the previous 15 hours were assigned a random number from a random number table and were approached for consent in numeric order. With 2 data collectors working daily, a maximum of 12 patients could be enrolled each day. Consenting subjects who passed a vision test were given the Test of Functional Health Literacy in Adults at the time of enrollment and a written questionnaire (in either English or Spanish) on a daily basis for a maximum of 6 days. Some of these patients also participated in a structured interview that was designed to elicit their views on health education topics and formats for education of hospitalized patients. Others, again determined by random number, were subjects of a time‐motion study.

Demographic data collected included age, sex, language, race, comorbidities, insurance status, and discharge diagnosis.

RESULTS

Patient selection is described in Figure 1, and patient demographics are summarized in Tables 2 and 3.

Figure 1

Time‐Motion Study

Thirteen patients were studied. Of the 315 patient‐hours observed, 71% were categorized as downtime, 15% as provider time, and 14% as busy time. The proportion of downtime ranged from a low of 0.65 (SE 0.04) on hospital Day 2 to a high of 0.76 (SE 0.06) on hospital Day 4, but the differences in downtime proportions by day did not reach statistical significance (P = .65; Fig. 2). The lowest percentage of downtime observed in any patient on any day was 39%. The 125 hours of downtime observed consisted of 1317 separate blocks of time, 80% of which were less than 15 minutes in duration, 14% of which were 15 to 30 minutes in duration, and 6% of which exceeded 30 minutes in duration.

Figure 2

Thirty‐six full days of observation, defined as greater than 7 hours of observation in 1 day, were used to assess the amount of time spent with providers. Of the 60 minutes/day (IQR = 44) that patients spent with health care providers, 21 minutes/day (IQR = 34) was spent with phlebotomists, physical or occupational therapists, dieticians, or social workers, 25 minutes/day (IQR = 25) was spent with patients' nurses, and a median of only 9 minutes/day (IQR = 11) was spent with their physicians.

Questionnaire

A total of 311 questionnaires were administered to the 138 consenting participants. Irrespective of the day of testing, 79% to 97% strongly agreed or agreed with the 4 statements (Fig. 3). In response to the first statementI feel well enough to learnpatient scores increased steadily over the 6 days of hospitalization patients were surveyed (coefficient = 0.15, P = .004). On hospital day 1, the mean score was 3.85 (SE 0.08), and by day 6 the mean score had increased to 4.75 (SE 0.08) However, there was no significant change over time in patients' desire to learn, self‐perceived time available to learn, or importance placed on learning during their hospital stay.

Figure 3

DISCUSSION

The important findings of this study are that hospitalized patients have a substantial amount of time available for health education and a considerable willingness and interest in participating in health educational activities. We found that although there was a great deal of time available on all days of hospitalization studied, patients felt increasingly well enough to participate in educational activities through their hospital stay.

We are unaware of other studies that have attempted to quantify the amount of time hospitalized patients are available for educational activities or whether they feel capable of participating in these activities. McBride10 found that 95% of hospitalized patients supported a health‐promoting hospital and that almost 80% wanted to modify at least 1 aspect of their lifestyle. Martin and colleagues11 found that patient satisfaction was improved by a patient‐centered unit incorporating dedicated nursing staff to promote patient involvement and provide personalized care and education. Barber‐Parker9 suggested that high patient acuity, short durations of hospitalization, and lack of patient availability because of testing and treatment limited the opportunities that patients had for health education during their hospitalization. These conclusions were reached on the basis of surveys of nurses' perceptions, however, rather than on direct observations or assessments of patients' perceptions.

Our findings suggest that many types of patient educational approaches may be needed to achieve maximal effectiveness and that regardless of the specific approach employed, the focus should be on the primary reason for a patient's hospitalization, what the hospitalization meant, why it happened and what the patient can do to prevent hospitalization from occurring in the future.

Transitions in care have been identified as periods in which communication lapses occur and outcomes can be adversely affected.12 A recent study by Epstein and colleagues13 found that almost 12% of patients had new or worsening symptoms of disease within the first few days after discharge from the hospital and that 22% either did not pick up their medications or understand how to take them (consistent with the observations of Kerzman and colleagues).5 The most common action taken in response to these findings was nurse‐mediated patient education. Our study indicates there is potential for further educational processes in hospitals, which may improve the safety of transitions from a hospital setting to outpatient care.

Although many disease management programs have been studied in the outpatient setting,1417 very few have been extended into hospitals. Accordingly, hospitalists are ideally suited to develop and implement disease management programs in concert with outpatient efforts.18 Our study suggests there is an underutilized opportunity for hospital‐based physicians and other health care providers to work with patients at a time when they are uniquely focused on their own health and free from many of the time constraints of their normal lives.

Although JCAHO mandates that hospitalized patients receive education and training specific to the patient's needs and as appropriate to the care, treatment and services provided,19 there is a paucity of data describing the educational processes in US hospitals. Johansson and colleagues20 conducted a survey in a Finnish hospital where patient education is also mandated. Written materials were given to about 55% of the patients. Demonstration and practice were used with about one third, whereas the Internet and videotapes were used for fewer than 10%. Although patients underwent educational activities throughout their hospitalization, and most were satisfied with the process, Johansson and colleagues found that only 59% felt that what they knew about their care was sufficient, almost a third felt they did not know enough about the side effects of their medical care, and almost half felt they did not have sufficient input into what they were being taught.

Although we found a large amount of time that might be used for patient education during a hospitalization, this time was commonly limited to 15‐minute blocks, as has been noted previously.9 This observation implies that educational activities should be designed so they can be conducted over short periods and/or stopped for short periods when interruptions occur or that the processes of care during a hospitalization should be altered to create larger blocks of continuous time available for educational activities.

A number of issues could have biased our results. Only 66% of the patients who were approached to participate agreed to do so. Because those declining may have been sicker and because sicker patients may require more diagnostic testing or more invasive treatment, we may have overestimated both the amount of downtime available and the willingness of patients to participate in educational activities. If we assume, however, that all patients who refused to participate either disagreed or strongly disagreed with the statements in the questionnaire regarding their interest in educational activities, the fraction of patients agreeing or strongly agreeing with idea that they were well enough and interested would still be 57% to 75% of the population sampled. Accordingly, this potential bias, if it occurred, would not alter our conclusions.

The time‐motion studies were only performed between 8:00 _AM and 5:00 _PM, such that the resulting data do not reflect any diagnostic testing, therapeutic interventions, or contact with health care providers that occurred at other times. This may have contributed to the strikingly small amount of time that patients spent with their physicians and nurses. If patient time after 5:00 _PM and before 8:00 _AM had been observed and included, it is likely that the absolute amount of time spent with physicians and nurses would increase, whereas the overall proportion of patient time spent with providers would decrease.

We were also only able to collect data on 13 time‐motion subjects. This limited sample size from a single institution may not be representative of all hospitalized non‐ICU patients on general medical wards. Accordingly, we make no claims that our data can be generalized to the entire population of patients admitted to non‐ICU medical services. However, the results of our surveys, which sampled a much broader patient population and supported our time‐motion findings, suggest that our time‐motion findings are likely to be representative of significant underutilized time and motivation for patient education in the hospital setting.

Also, it is important to note that although the time‐motion studies were only done with 13 patients, these studies are extremely labor intensive and are rarely done with much larger samples. In addition, the SDs on the data collected from the time‐motion studies were quite small. It is possible that if a larger sample were studied, the percentage of free time might be larger or smaller than what we observed for the 13 patients we studied. However, it would be quite unlikely that the amount of free time would be so small (eg, 10%‐15%) that it would invalidate our conclusion that considerable time is available for patient education over and above what currently occurs in most hospital settings.

A patient's self‐perception of his or her ability to learn may not reflect that patient's true cognitive readiness to do so. JCAHO requirements mandate that nurses be trained to assess patients for their ability to learn and to do so as part of the admission process. After reviewing all day 1 patient responses to our questionnaires, in no instance did a nurse assess a patient as having a barrier to learning when the patient had reported feeling well enough to learn. Accordingly, although we performed no direct tests of patients' ability to learn, this retrospective independent assessment did not suggest that patients systematically overestimated their ability to learn.

Finding that hospitalized patients are unoccupied for approximately 70% of their daytime hours and that most patients are both highly motivated to learn and have few barriers to doing so indicates that educational activities during hospitalizations have substantial potential for expansion. The current structure for educating hospitalized patients should be supplemented to take these findings into account.

Educating patients about smoking cessation when they are hospitalized for acute coronary syndrome results in a 57% 1‐year quit rate.1 This rate is far higher than the typical 15%‐30% 1‐year quit rates observed with smoking cessation programs administered in the outpatient setting24 and suggests that hospitalized patients may be uniquely motivated to respond to health education.

Kerzman and colleagues5 found that 42% of hospitalized patients expressed a wish to receive more comprehensive counseling about their medications before being discharged from the hospital. And although the Joint Commission on Hospital Accreditation and the Centers for Medicare and Medicaid Services have established core quality measures mandating that patients hospitalized with congestive heart failure receive education as one component of a high‐quality discharge process,6, 7 approximately one third of patients nationally do not receive adequate patient education.8

Barber‐Parker9 suggested that because patient acuity in hospitals was so high and patients were so commonly absent from their nursing units for testing and treatment, there was little time available for health education during their hospitalization. Anecdotal observations in our institution suggested, however, that adult patients hospitalized on the general Internal Medicine service spent much of their day doing little more than lying in bed watching television. Accordingly, we hypothesized that considerable time might be available for patient education during a hospitalization. We therefore sought to quantify the fraction of time patients were not involved in treatment activities, diagnostic testing, or other evaluations and to determine whether during these times they wanted and were feeling well enough to participate in educational activities. We also sought to determine what patients wanted to know about their health problems and what types of educational activities they most preferred.

MATERIALS AND METHODS

We conducted a time‐motion and survey study from June 25, 2005, to August 15, 2005, at Denver Health Medical Center, an academic public safety‐net hospital affiliated with the University of Colorado School of Medicine. All patients older than 18 years of age who spoke English or Spanish and were admitted to the general Internal Medicine service were candidates for enrollment. Exclusion criteria were being admitted to the intensive care unit, having an inability to communicate, being in contact precautions, and being previously enrolled. The study was approved by the Colorado Multiple Institutional Review Board. Written informed consent was obtained for all study participants.

At 8:00 _AM, all patients admitted during the previous 15 hours were assigned a random number from a random number table and were approached for consent in numeric order. With 2 data collectors working daily, a maximum of 12 patients could be enrolled each day. Consenting subjects who passed a vision test were given the Test of Functional Health Literacy in Adults at the time of enrollment and a written questionnaire (in either English or Spanish) on a daily basis for a maximum of 6 days. Some of these patients also participated in a structured interview that was designed to elicit their views on health education topics and formats for education of hospitalized patients. Others, again determined by random number, were subjects of a time‐motion study.

Demographic data collected included age, sex, language, race, comorbidities, insurance status, and discharge diagnosis.

RESULTS

Patient selection is described in Figure 1, and patient demographics are summarized in Tables 2 and 3.

Figure 1

Time‐Motion Study

Thirteen patients were studied. Of the 315 patient‐hours observed, 71% were categorized as downtime, 15% as provider time, and 14% as busy time. The proportion of downtime ranged from a low of 0.65 (SE 0.04) on hospital Day 2 to a high of 0.76 (SE 0.06) on hospital Day 4, but the differences in downtime proportions by day did not reach statistical significance (P = .65; Fig. 2). The lowest percentage of downtime observed in any patient on any day was 39%. The 125 hours of downtime observed consisted of 1317 separate blocks of time, 80% of which were less than 15 minutes in duration, 14% of which were 15 to 30 minutes in duration, and 6% of which exceeded 30 minutes in duration.

Figure 2

Thirty‐six full days of observation, defined as greater than 7 hours of observation in 1 day, were used to assess the amount of time spent with providers. Of the 60 minutes/day (IQR = 44) that patients spent with health care providers, 21 minutes/day (IQR = 34) was spent with phlebotomists, physical or occupational therapists, dieticians, or social workers, 25 minutes/day (IQR = 25) was spent with patients' nurses, and a median of only 9 minutes/day (IQR = 11) was spent with their physicians.

Questionnaire

A total of 311 questionnaires were administered to the 138 consenting participants. Irrespective of the day of testing, 79% to 97% strongly agreed or agreed with the 4 statements (Fig. 3). In response to the first statementI feel well enough to learnpatient scores increased steadily over the 6 days of hospitalization patients were surveyed (coefficient = 0.15, P = .004). On hospital day 1, the mean score was 3.85 (SE 0.08), and by day 6 the mean score had increased to 4.75 (SE 0.08) However, there was no significant change over time in patients' desire to learn, self‐perceived time available to learn, or importance placed on learning during their hospital stay.

Figure 3

DISCUSSION

The important findings of this study are that hospitalized patients have a substantial amount of time available for health education and a considerable willingness and interest in participating in health educational activities. We found that although there was a great deal of time available on all days of hospitalization studied, patients felt increasingly well enough to participate in educational activities through their hospital stay.

We are unaware of other studies that have attempted to quantify the amount of time hospitalized patients are available for educational activities or whether they feel capable of participating in these activities. McBride10 found that 95% of hospitalized patients supported a health‐promoting hospital and that almost 80% wanted to modify at least 1 aspect of their lifestyle. Martin and colleagues11 found that patient satisfaction was improved by a patient‐centered unit incorporating dedicated nursing staff to promote patient involvement and provide personalized care and education. Barber‐Parker9 suggested that high patient acuity, short durations of hospitalization, and lack of patient availability because of testing and treatment limited the opportunities that patients had for health education during their hospitalization. These conclusions were reached on the basis of surveys of nurses' perceptions, however, rather than on direct observations or assessments of patients' perceptions.

Our findings suggest that many types of patient educational approaches may be needed to achieve maximal effectiveness and that regardless of the specific approach employed, the focus should be on the primary reason for a patient's hospitalization, what the hospitalization meant, why it happened and what the patient can do to prevent hospitalization from occurring in the future.

Transitions in care have been identified as periods in which communication lapses occur and outcomes can be adversely affected.12 A recent study by Epstein and colleagues13 found that almost 12% of patients had new or worsening symptoms of disease within the first few days after discharge from the hospital and that 22% either did not pick up their medications or understand how to take them (consistent with the observations of Kerzman and colleagues).5 The most common action taken in response to these findings was nurse‐mediated patient education. Our study indicates there is potential for further educational processes in hospitals, which may improve the safety of transitions from a hospital setting to outpatient care.

Although many disease management programs have been studied in the outpatient setting,1417 very few have been extended into hospitals. Accordingly, hospitalists are ideally suited to develop and implement disease management programs in concert with outpatient efforts.18 Our study suggests there is an underutilized opportunity for hospital‐based physicians and other health care providers to work with patients at a time when they are uniquely focused on their own health and free from many of the time constraints of their normal lives.

Although JCAHO mandates that hospitalized patients receive education and training specific to the patient's needs and as appropriate to the care, treatment and services provided,19 there is a paucity of data describing the educational processes in US hospitals. Johansson and colleagues20 conducted a survey in a Finnish hospital where patient education is also mandated. Written materials were given to about 55% of the patients. Demonstration and practice were used with about one third, whereas the Internet and videotapes were used for fewer than 10%. Although patients underwent educational activities throughout their hospitalization, and most were satisfied with the process, Johansson and colleagues found that only 59% felt that what they knew about their care was sufficient, almost a third felt they did not know enough about the side effects of their medical care, and almost half felt they did not have sufficient input into what they were being taught.

Although we found a large amount of time that might be used for patient education during a hospitalization, this time was commonly limited to 15‐minute blocks, as has been noted previously.9 This observation implies that educational activities should be designed so they can be conducted over short periods and/or stopped for short periods when interruptions occur or that the processes of care during a hospitalization should be altered to create larger blocks of continuous time available for educational activities.

A number of issues could have biased our results. Only 66% of the patients who were approached to participate agreed to do so. Because those declining may have been sicker and because sicker patients may require more diagnostic testing or more invasive treatment, we may have overestimated both the amount of downtime available and the willingness of patients to participate in educational activities. If we assume, however, that all patients who refused to participate either disagreed or strongly disagreed with the statements in the questionnaire regarding their interest in educational activities, the fraction of patients agreeing or strongly agreeing with idea that they were well enough and interested would still be 57% to 75% of the population sampled. Accordingly, this potential bias, if it occurred, would not alter our conclusions.

The time‐motion studies were only performed between 8:00 _AM and 5:00 _PM, such that the resulting data do not reflect any diagnostic testing, therapeutic interventions, or contact with health care providers that occurred at other times. This may have contributed to the strikingly small amount of time that patients spent with their physicians and nurses. If patient time after 5:00 _PM and before 8:00 _AM had been observed and included, it is likely that the absolute amount of time spent with physicians and nurses would increase, whereas the overall proportion of patient time spent with providers would decrease.

We were also only able to collect data on 13 time‐motion subjects. This limited sample size from a single institution may not be representative of all hospitalized non‐ICU patients on general medical wards. Accordingly, we make no claims that our data can be generalized to the entire population of patients admitted to non‐ICU medical services. However, the results of our surveys, which sampled a much broader patient population and supported our time‐motion findings, suggest that our time‐motion findings are likely to be representative of significant underutilized time and motivation for patient education in the hospital setting.

Also, it is important to note that although the time‐motion studies were only done with 13 patients, these studies are extremely labor intensive and are rarely done with much larger samples. In addition, the SDs on the data collected from the time‐motion studies were quite small. It is possible that if a larger sample were studied, the percentage of free time might be larger or smaller than what we observed for the 13 patients we studied. However, it would be quite unlikely that the amount of free time would be so small (eg, 10%‐15%) that it would invalidate our conclusion that considerable time is available for patient education over and above what currently occurs in most hospital settings.

A patient's self‐perception of his or her ability to learn may not reflect that patient's true cognitive readiness to do so. JCAHO requirements mandate that nurses be trained to assess patients for their ability to learn and to do so as part of the admission process. After reviewing all day 1 patient responses to our questionnaires, in no instance did a nurse assess a patient as having a barrier to learning when the patient had reported feeling well enough to learn. Accordingly, although we performed no direct tests of patients' ability to learn, this retrospective independent assessment did not suggest that patients systematically overestimated their ability to learn.

Finding that hospitalized patients are unoccupied for approximately 70% of their daytime hours and that most patients are both highly motivated to learn and have few barriers to doing so indicates that educational activities during hospitalizations have substantial potential for expansion. The current structure for educating hospitalized patients should be supplemented to take these findings into account.

Educating patients about smoking cessation when they are hospitalized for acute coronary syndrome results in a 57% 1‐year quit rate.1 This rate is far higher than the typical 15%‐30% 1‐year quit rates observed with smoking cessation programs administered in the outpatient setting24 and suggests that hospitalized patients may be uniquely motivated to respond to health education.

Kerzman and colleagues5 found that 42% of hospitalized patients expressed a wish to receive more comprehensive counseling about their medications before being discharged from the hospital. And although the Joint Commission on Hospital Accreditation and the Centers for Medicare and Medicaid Services have established core quality measures mandating that patients hospitalized with congestive heart failure receive education as one component of a high‐quality discharge process,6, 7 approximately one third of patients nationally do not receive adequate patient education.8

Barber‐Parker9 suggested that because patient acuity in hospitals was so high and patients were so commonly absent from their nursing units for testing and treatment, there was little time available for health education during their hospitalization. Anecdotal observations in our institution suggested, however, that adult patients hospitalized on the general Internal Medicine service spent much of their day doing little more than lying in bed watching television. Accordingly, we hypothesized that considerable time might be available for patient education during a hospitalization. We therefore sought to quantify the fraction of time patients were not involved in treatment activities, diagnostic testing, or other evaluations and to determine whether during these times they wanted and were feeling well enough to participate in educational activities. We also sought to determine what patients wanted to know about their health problems and what types of educational activities they most preferred.

MATERIALS AND METHODS

We conducted a time‐motion and survey study from June 25, 2005, to August 15, 2005, at Denver Health Medical Center, an academic public safety‐net hospital affiliated with the University of Colorado School of Medicine. All patients older than 18 years of age who spoke English or Spanish and were admitted to the general Internal Medicine service were candidates for enrollment. Exclusion criteria were being admitted to the intensive care unit, having an inability to communicate, being in contact precautions, and being previously enrolled. The study was approved by the Colorado Multiple Institutional Review Board. Written informed consent was obtained for all study participants.

At 8:00 _AM, all patients admitted during the previous 15 hours were assigned a random number from a random number table and were approached for consent in numeric order. With 2 data collectors working daily, a maximum of 12 patients could be enrolled each day. Consenting subjects who passed a vision test were given the Test of Functional Health Literacy in Adults at the time of enrollment and a written questionnaire (in either English or Spanish) on a daily basis for a maximum of 6 days. Some of these patients also participated in a structured interview that was designed to elicit their views on health education topics and formats for education of hospitalized patients. Others, again determined by random number, were subjects of a time‐motion study.

Demographic data collected included age, sex, language, race, comorbidities, insurance status, and discharge diagnosis.

RESULTS

Patient selection is described in Figure 1, and patient demographics are summarized in Tables 2 and 3.

Figure 1

Time‐Motion Study

Thirteen patients were studied. Of the 315 patient‐hours observed, 71% were categorized as downtime, 15% as provider time, and 14% as busy time. The proportion of downtime ranged from a low of 0.65 (SE 0.04) on hospital Day 2 to a high of 0.76 (SE 0.06) on hospital Day 4, but the differences in downtime proportions by day did not reach statistical significance (P = .65; Fig. 2). The lowest percentage of downtime observed in any patient on any day was 39%. The 125 hours of downtime observed consisted of 1317 separate blocks of time, 80% of which were less than 15 minutes in duration, 14% of which were 15 to 30 minutes in duration, and 6% of which exceeded 30 minutes in duration.

Figure 2

Thirty‐six full days of observation, defined as greater than 7 hours of observation in 1 day, were used to assess the amount of time spent with providers. Of the 60 minutes/day (IQR = 44) that patients spent with health care providers, 21 minutes/day (IQR = 34) was spent with phlebotomists, physical or occupational therapists, dieticians, or social workers, 25 minutes/day (IQR = 25) was spent with patients' nurses, and a median of only 9 minutes/day (IQR = 11) was spent with their physicians.

Questionnaire

A total of 311 questionnaires were administered to the 138 consenting participants. Irrespective of the day of testing, 79% to 97% strongly agreed or agreed with the 4 statements (Fig. 3). In response to the first statementI feel well enough to learnpatient scores increased steadily over the 6 days of hospitalization patients were surveyed (coefficient = 0.15, P = .004). On hospital day 1, the mean score was 3.85 (SE 0.08), and by day 6 the mean score had increased to 4.75 (SE 0.08) However, there was no significant change over time in patients' desire to learn, self‐perceived time available to learn, or importance placed on learning during their hospital stay.

Figure 3

DISCUSSION

The important findings of this study are that hospitalized patients have a substantial amount of time available for health education and a considerable willingness and interest in participating in health educational activities. We found that although there was a great deal of time available on all days of hospitalization studied, patients felt increasingly well enough to participate in educational activities through their hospital stay.

We are unaware of other studies that have attempted to quantify the amount of time hospitalized patients are available for educational activities or whether they feel capable of participating in these activities. McBride10 found that 95% of hospitalized patients supported a health‐promoting hospital and that almost 80% wanted to modify at least 1 aspect of their lifestyle. Martin and colleagues11 found that patient satisfaction was improved by a patient‐centered unit incorporating dedicated nursing staff to promote patient involvement and provide personalized care and education. Barber‐Parker9 suggested that high patient acuity, short durations of hospitalization, and lack of patient availability because of testing and treatment limited the opportunities that patients had for health education during their hospitalization. These conclusions were reached on the basis of surveys of nurses' perceptions, however, rather than on direct observations or assessments of patients' perceptions.

Our findings suggest that many types of patient educational approaches may be needed to achieve maximal effectiveness and that regardless of the specific approach employed, the focus should be on the primary reason for a patient's hospitalization, what the hospitalization meant, why it happened and what the patient can do to prevent hospitalization from occurring in the future.

Transitions in care have been identified as periods in which communication lapses occur and outcomes can be adversely affected.12 A recent study by Epstein and colleagues13 found that almost 12% of patients had new or worsening symptoms of disease within the first few days after discharge from the hospital and that 22% either did not pick up their medications or understand how to take them (consistent with the observations of Kerzman and colleagues).5 The most common action taken in response to these findings was nurse‐mediated patient education. Our study indicates there is potential for further educational processes in hospitals, which may improve the safety of transitions from a hospital setting to outpatient care.

Although many disease management programs have been studied in the outpatient setting,1417 very few have been extended into hospitals. Accordingly, hospitalists are ideally suited to develop and implement disease management programs in concert with outpatient efforts.18 Our study suggests there is an underutilized opportunity for hospital‐based physicians and other health care providers to work with patients at a time when they are uniquely focused on their own health and free from many of the time constraints of their normal lives.

Although JCAHO mandates that hospitalized patients receive education and training specific to the patient's needs and as appropriate to the care, treatment and services provided,19 there is a paucity of data describing the educational processes in US hospitals. Johansson and colleagues20 conducted a survey in a Finnish hospital where patient education is also mandated. Written materials were given to about 55% of the patients. Demonstration and practice were used with about one third, whereas the Internet and videotapes were used for fewer than 10%. Although patients underwent educational activities throughout their hospitalization, and most were satisfied with the process, Johansson and colleagues found that only 59% felt that what they knew about their care was sufficient, almost a third felt they did not know enough about the side effects of their medical care, and almost half felt they did not have sufficient input into what they were being taught.

Although we found a large amount of time that might be used for patient education during a hospitalization, this time was commonly limited to 15‐minute blocks, as has been noted previously.9 This observation implies that educational activities should be designed so they can be conducted over short periods and/or stopped for short periods when interruptions occur or that the processes of care during a hospitalization should be altered to create larger blocks of continuous time available for educational activities.

A number of issues could have biased our results. Only 66% of the patients who were approached to participate agreed to do so. Because those declining may have been sicker and because sicker patients may require more diagnostic testing or more invasive treatment, we may have overestimated both the amount of downtime available and the willingness of patients to participate in educational activities. If we assume, however, that all patients who refused to participate either disagreed or strongly disagreed with the statements in the questionnaire regarding their interest in educational activities, the fraction of patients agreeing or strongly agreeing with idea that they were well enough and interested would still be 57% to 75% of the population sampled. Accordingly, this potential bias, if it occurred, would not alter our conclusions.

The time‐motion studies were only performed between 8:00 _AM and 5:00 _PM, such that the resulting data do not reflect any diagnostic testing, therapeutic interventions, or contact with health care providers that occurred at other times. This may have contributed to the strikingly small amount of time that patients spent with their physicians and nurses. If patient time after 5:00 _PM and before 8:00 _AM had been observed and included, it is likely that the absolute amount of time spent with physicians and nurses would increase, whereas the overall proportion of patient time spent with providers would decrease.

We were also only able to collect data on 13 time‐motion subjects. This limited sample size from a single institution may not be representative of all hospitalized non‐ICU patients on general medical wards. Accordingly, we make no claims that our data can be generalized to the entire population of patients admitted to non‐ICU medical services. However, the results of our surveys, which sampled a much broader patient population and supported our time‐motion findings, suggest that our time‐motion findings are likely to be representative of significant underutilized time and motivation for patient education in the hospital setting.

Also, it is important to note that although the time‐motion studies were only done with 13 patients, these studies are extremely labor intensive and are rarely done with much larger samples. In addition, the SDs on the data collected from the time‐motion studies were quite small. It is possible that if a larger sample were studied, the percentage of free time might be larger or smaller than what we observed for the 13 patients we studied. However, it would be quite unlikely that the amount of free time would be so small (eg, 10%‐15%) that it would invalidate our conclusion that considerable time is available for patient education over and above what currently occurs in most hospital settings.

A patient's self‐perception of his or her ability to learn may not reflect that patient's true cognitive readiness to do so. JCAHO requirements mandate that nurses be trained to assess patients for their ability to learn and to do so as part of the admission process. After reviewing all day 1 patient responses to our questionnaires, in no instance did a nurse assess a patient as having a barrier to learning when the patient had reported feeling well enough to learn. Accordingly, although we performed no direct tests of patients' ability to learn, this retrospective independent assessment did not suggest that patients systematically overestimated their ability to learn.

Finding that hospitalized patients are unoccupied for approximately 70% of their daytime hours and that most patients are both highly motivated to learn and have few barriers to doing so indicates that educational activities during hospitalizations have substantial potential for expansion. The current structure for educating hospitalized patients should be supplemented to take these findings into account.

Esophagogastroduodenoscopy (EGD) carries a small but serious risk of esophageal perforation.13 With its potential for sepsis and fatal mediastinitis, prompt recognition and treatment are essential for favorable outcomes. The risk of perforation with diagnostic flexible EGD is 0.03%, which is an improvement from the 0.1%0.4% risk associated with rigid endoscopy.4 However, the risk of perforation can dramatically increase to 17% depending on the methods of therapeutic intervention and underlying risk factors (Table 1).1, 57

It is estimated that 33%75% of all esophageal perforations are iatrogenic.8 Of those caused by EGD, therapeutic interventions portend an increased risk compared with the risk of diagnostic endoscopy alone (Table 2).4 With the expanding role of flexible EGD and the increasing number of procedures performed, this modest risk per procedure still translates into a sizable number of perforations with their ensuing complications.4, 7 Mortality rates following esophageal perforation may approach 25%.9

ANATOMY AND PATHOPHYSIOLOGY

The most common site of perforation is at the level of the cricopharyngeus, as it is a narrow introitus leading to the esophagus. The risk of perforation at this location is further increased with the presence of a Zenker's diverticulum or cervical osteophytes. The second most common site is proximal to the lower esophageal sphincter because of the angulation of the hiatus and the high frequency of esophageal webs, rings, reflux strictures, and hiatal hernias. The relatively straight middle esophagus is an uncommon site for perforations.

Cervical perforations are less commonly caused by organic lesions of the esophagus. Often, they are the result of technique and manipulation of the endoscope, or of certain conditions associated with the jaw, neck, or spinal column that are unfavorable for endoscopy. The risk of cervical perforation increases with the presence of bony spurs, as the upper esophagus is compressed over the underlying spinal column. Thoracic perforations, however, are more commonly seen with organic esophageal obstruction. These obstructions may be caused by an underlying inflammatory process, benign stricture, or neoplasm. In these cases, the risk of thoracic perforation is increased with blind procedures. Thoracic perforations carry a worse prognosis if diagnosis is delayed, or if the underlying obstruction cannot be removed.10

Esophageal perforation leads to periesophageal tissues being contaminated by food, secretions, air, or gastric contents and may be followed by chemical tissue injury and infection. The nature and extent of infection depend on the site of esophageal perforation. Cervical esophageal perforation can cause retropharyngeal space infection, which has the potential to extend directly into the posterior mediastinum via the danger space, which is between the retropharyngeal and prevertebral spaces and extends from the base of the skull descending freely throughout the entire length of the posterior mediastinum. With thoracic perforations, esophageal contents can enter the pleural space by negative intrathoracic pressure with subsequent pleural contamination and empyema.8, 1113

Pathogens responsible for infections after esophageal perforation vary based on several factors including site of perforation, clinical status of patient when perforation occurs (hospitalized versus not hospitalized, critically ill versus healthy), receipt of enteral nutrition, gastric acid suppression with H2‐receptor antagonists or proton‐pump inhibitors, immunosuppression, and recent (or current) receipt of antimicrobials. In nonintubated, healthy adults not on antimicrobial therapy, organisms in the upper esophagus are essentially identical to those in the oropharynx and include viridans streptococci, Haemophilus species, and anaerobes. During critical illness and following antibiotic therapy, the normal oral flora is rapidly replaced by aerobic Gram‐negative bacilli, Staphylococcus aureus, and yeast.14 The stomach, which is normally devoid of bacteria, can likewise be colonized with pathogenic organisms in the setting of gastric acid suppression and enteral nutrition.15, 16

SIGNS AND SYMPTOMS

Esophageal perforation should be considered after EGD, dilation, sclerotherapy, variceal banding, and esophageal stenting. However, perforation can also result from other invasive procedures such as insertion of feeding and nasogastric tubes, rapid sequence intubation, and transesophageal echocardiography.

The clinical triad of esophageal perforation includes pain, fever, and subcutaneous air.17 In a study by Wychulis et al., among 33 patients with esophageal perforation, 75% demonstrated all 3 findings.10 Pain is the most sensitive finding and occurs in nearly all patients identified with esophageal perforation. Crepitation, which results from air dissecting along soft tissue planes of the mediastinum and into the neck, occurs in up to 70% with cervical perforation and 30% with thoracic perforation.8, 10, 18

Clinical presentation and outcomes vary depending on the location of the perforation (Table 3).8 Cervical perforation is usually associated with anterior neck pain, located at the anterior border of the sternocleidomastoid muscle. Movement of the neck and palpation typically aggravate the pain. Thoracic perforation typically presents as substernal chest pain, often with a component of pleurisy. Pleural effusions are present in 50% of thoracic perforations, and mediastinitis is more likely to occur.19 Hamman's sign, a finding characterized by an audible crunch with chest auscultation, is suggestive of mediastinal emphysema. Perforation of the intra‐abdominal esophagus can result in epigastric pain and signs of acute abdomen.10, 17 Subcutaneous emphysema occurs more frequently with cervical perforation but can be present regardless of location.10 Secondary infections following esophageal perforation can manifest with an accelerated clinical course leading to sepsis and shock.

DIAGNOSIS

Clinical suspicion of esophageal perforation should prompt necessary radiographic studies to establish the diagnosis.18, 20 Contrast‐enhanced computed tomography (CT) scans of the neck and chest are preferable because of their increased sensitivity in localizing the site and showing the extent of perforation and abscess. CT scans may reveal subcutaneous or mediastinal air, abscess cavities adjacent to the esophagus, and fistulas between the esophagus and mediastinum (Figs. 1 and 2).2022 Results of contrast studies may be negative and warrant repeating within several hours.19

Figure 1

Figure 2

If CT scans cannot be performed, neck (soft‐tissue) and chest x‐rays may be useful. Although plain films have limited value in evaluating the retropharyngeal space, they can reveal soft‐tissue emphysema, a widened mediastinum, pulmonary infiltrates or effusions, neck abscess, and mediastinal air‐fluid levels. In cervical perforation, a lateral film of the neck can show air in deep cervical tissue before clinical signs are apparent.

Swallow studies with Gastrografin (meglumine diatrizoate) are useful in defining the exact location of the perforation (Fig. 3). However, the false‐negative rate of swallow studies can exceed 10%, especially if the patient is upright during the study. When the contrast propagates past the site of perforation too quickly, it may not extravasate.23 Although barium may provide slightly greater contrast, it may add to the problem of foreign body reaction in the area of perforation.18 An additional complication of barium is that once it has extravasated, it is not readily absorbed. The persistence of extravasated barium makes it difficult to assess the resolution of an esophageal tear on subsequent fluoroscopic or CT exams. Hence, our institution avoids using barium to evaluate esophageal perforation, unless Gastrografin swallow has excluded any major esophageal perforation. Barium swallow may then be used to exclude small mural tears. Some medical centers elect to routinely screen their high‐risk patients with swallow evaluations after an EGD, although this is not common practice.8, 24

Figure 3

If the above workup is negative, the use of EGD may be considered for establishing the diagnosis if a high index of suspicion remains. However, the risks of EGD in this situation include extension of the perforation, further extravasation of esophageal contents, and difficulty with subsequent radiographic studies to visualize the perforation.19

MANAGEMENT

Once the diagnosis of esophageal perforation has been established, treatment options are individualized based on the clinical scenario. Currently, there are no established guidelines, and large randomized clinical trials comparing outcomes of operative versus nonoperative management have not been conducted (Fig. 4).25, 26 Outcomes associated with esophageal perforations depend on preoperative clinical condition, comorbidities, location and size of the perforation, nature of underlying esophageal disease (if any), and time to establish the diagnosis and initiate therapy.10 Delay in patient presentation or diagnosis beyond 24 hours following esophageal perforation has been associated with adverse outcomes.18, 27, 28

Figure 4

A conservative approach is appropriate when clinically stable patients with minimal symptoms have well‐contained, nontransmural tears. Management entails broad‐spectrum antibiotics, nothing by mouth, nasogastric suction, and parenteral nutrition.24 Early surgical consultation is recommended in all cases. Serial CT scanning is useful for following the resolution of fistulas and tears. An oral diet can be resumed when contrast or swallow studies show no extravasation of dye. Cervical perforations typically fare well with this approach.26, 29

Surgical therapy is recommended for patients with large or uncontained esophageal perforations, mediastinal abscesses, and/or sepsis.25, 27 Surgical options include esophageal diversion, esophagectomy, or drainage with or without primary repair. Drainage with primary repair is considered the treatment of choice, regardless of time to presentation. Esophagectomy is considered in cases of delayed or neglected perforations, extensive transmural necrosis or underlying cancer.30 Operative mortality is 0%30% when treated within 24 hours. This rate increases to 26%64% when treatment is delayed beyond 24 hours, reaffirming the importance of making a prompt diagnosis.8

Endoscopic intervention is gaining recognition for its role in the management of esophageal perforations, especially when the risks make surgery prohibitive. Therapeutic options include stenting and clipping a perforation, as well as debriding and draining an abscess. Endoscopists can successfully treat traumatic nonmalignant esophageal perforations smaller than 50% to 70% of the circumference with self‐expanding plastic stents.26 Another option is to use metallic clipping devices to treat small esophageal perforations (<1 cm).3133 Combined with medical management and appropriate patient selection, the benefits of an endoscopic approach may potentially outweigh the risks of surgery.26, 29, 33, 34

Regardless of treatment approach, the appropriate and timely selection of empiric antibiotic therapy improves outcomes. Empiric antimicrobial therapy for esophageal perforation will depend on several host factors as well as the site of perforation. In healthy nonhospitalized adults, ampicillin‐sulbactam, clindamycin, and penicillin G plus metronidazole are good choices because of their excellent activity against oral microflora. In patients who are critically ill, are hospitalized, are immunosuppressed, or have gastric acid suppression, initial broad‐spectrum antimicrobials such as piperacillin‐tazobactam, imipenem, meropenem, or a third‐generation cephalosporin plus metronidazole (or clindamycin) should be initiated. Additional therapy against methicillin‐resistant Staphylococcus aureus or Candida sp. should be considered if the patient is critically ill or is known to be colonized with these organisms. Initial empiric therapy should be modified as necessary based on culture results. Total duration of therapy will vary based on location and magnitude of the infection, adjunctive surgical debridement, and pathogens involved.

SUMMARY

Despite being an extremely safe procedure, EGD carries a known serious risk of esophageal perforation. Mortality after esophageal perforation can approach 25%. Although diagnostic endoscopy has a perforation rate of less than 0.03%, the risk can approach 17% with therapeutic interventions such as stent placement and esophageal dilation. Factors influencing the risks of perforation include procedural complexity, operator experience, and underlying esophageal and systemic diseases. Furthermore, perforations complicated by infection can lead to fatal mediastinitis and sepsis. The clinical triad of esophageal perforation is fever, neck pain, and crepitus. The optimal diagnostic study is CT scan of the neck and thorax with water‐soluble oral contrast. Treatment options range from conservative management with broad‐spectrum antibiotics to surgery. Diagnosis of esophageal perforation within 24 hours is essential for favorable outcomes.

Esophagogastroduodenoscopy (EGD) carries a small but serious risk of esophageal perforation.13 With its potential for sepsis and fatal mediastinitis, prompt recognition and treatment are essential for favorable outcomes. The risk of perforation with diagnostic flexible EGD is 0.03%, which is an improvement from the 0.1%0.4% risk associated with rigid endoscopy.4 However, the risk of perforation can dramatically increase to 17% depending on the methods of therapeutic intervention and underlying risk factors (Table 1).1, 57

It is estimated that 33%75% of all esophageal perforations are iatrogenic.8 Of those caused by EGD, therapeutic interventions portend an increased risk compared with the risk of diagnostic endoscopy alone (Table 2).4 With the expanding role of flexible EGD and the increasing number of procedures performed, this modest risk per procedure still translates into a sizable number of perforations with their ensuing complications.4, 7 Mortality rates following esophageal perforation may approach 25%.9

ANATOMY AND PATHOPHYSIOLOGY

The most common site of perforation is at the level of the cricopharyngeus, as it is a narrow introitus leading to the esophagus. The risk of perforation at this location is further increased with the presence of a Zenker's diverticulum or cervical osteophytes. The second most common site is proximal to the lower esophageal sphincter because of the angulation of the hiatus and the high frequency of esophageal webs, rings, reflux strictures, and hiatal hernias. The relatively straight middle esophagus is an uncommon site for perforations.

Cervical perforations are less commonly caused by organic lesions of the esophagus. Often, they are the result of technique and manipulation of the endoscope, or of certain conditions associated with the jaw, neck, or spinal column that are unfavorable for endoscopy. The risk of cervical perforation increases with the presence of bony spurs, as the upper esophagus is compressed over the underlying spinal column. Thoracic perforations, however, are more commonly seen with organic esophageal obstruction. These obstructions may be caused by an underlying inflammatory process, benign stricture, or neoplasm. In these cases, the risk of thoracic perforation is increased with blind procedures. Thoracic perforations carry a worse prognosis if diagnosis is delayed, or if the underlying obstruction cannot be removed.10

Esophageal perforation leads to periesophageal tissues being contaminated by food, secretions, air, or gastric contents and may be followed by chemical tissue injury and infection. The nature and extent of infection depend on the site of esophageal perforation. Cervical esophageal perforation can cause retropharyngeal space infection, which has the potential to extend directly into the posterior mediastinum via the danger space, which is between the retropharyngeal and prevertebral spaces and extends from the base of the skull descending freely throughout the entire length of the posterior mediastinum. With thoracic perforations, esophageal contents can enter the pleural space by negative intrathoracic pressure with subsequent pleural contamination and empyema.8, 1113

Pathogens responsible for infections after esophageal perforation vary based on several factors including site of perforation, clinical status of patient when perforation occurs (hospitalized versus not hospitalized, critically ill versus healthy), receipt of enteral nutrition, gastric acid suppression with H2‐receptor antagonists or proton‐pump inhibitors, immunosuppression, and recent (or current) receipt of antimicrobials. In nonintubated, healthy adults not on antimicrobial therapy, organisms in the upper esophagus are essentially identical to those in the oropharynx and include viridans streptococci, Haemophilus species, and anaerobes. During critical illness and following antibiotic therapy, the normal oral flora is rapidly replaced by aerobic Gram‐negative bacilli, Staphylococcus aureus, and yeast.14 The stomach, which is normally devoid of bacteria, can likewise be colonized with pathogenic organisms in the setting of gastric acid suppression and enteral nutrition.15, 16

SIGNS AND SYMPTOMS

Esophageal perforation should be considered after EGD, dilation, sclerotherapy, variceal banding, and esophageal stenting. However, perforation can also result from other invasive procedures such as insertion of feeding and nasogastric tubes, rapid sequence intubation, and transesophageal echocardiography.

The clinical triad of esophageal perforation includes pain, fever, and subcutaneous air.17 In a study by Wychulis et al., among 33 patients with esophageal perforation, 75% demonstrated all 3 findings.10 Pain is the most sensitive finding and occurs in nearly all patients identified with esophageal perforation. Crepitation, which results from air dissecting along soft tissue planes of the mediastinum and into the neck, occurs in up to 70% with cervical perforation and 30% with thoracic perforation.8, 10, 18

Clinical presentation and outcomes vary depending on the location of the perforation (Table 3).8 Cervical perforation is usually associated with anterior neck pain, located at the anterior border of the sternocleidomastoid muscle. Movement of the neck and palpation typically aggravate the pain. Thoracic perforation typically presents as substernal chest pain, often with a component of pleurisy. Pleural effusions are present in 50% of thoracic perforations, and mediastinitis is more likely to occur.19 Hamman's sign, a finding characterized by an audible crunch with chest auscultation, is suggestive of mediastinal emphysema. Perforation of the intra‐abdominal esophagus can result in epigastric pain and signs of acute abdomen.10, 17 Subcutaneous emphysema occurs more frequently with cervical perforation but can be present regardless of location.10 Secondary infections following esophageal perforation can manifest with an accelerated clinical course leading to sepsis and shock.

DIAGNOSIS

Clinical suspicion of esophageal perforation should prompt necessary radiographic studies to establish the diagnosis.18, 20 Contrast‐enhanced computed tomography (CT) scans of the neck and chest are preferable because of their increased sensitivity in localizing the site and showing the extent of perforation and abscess. CT scans may reveal subcutaneous or mediastinal air, abscess cavities adjacent to the esophagus, and fistulas between the esophagus and mediastinum (Figs. 1 and 2).2022 Results of contrast studies may be negative and warrant repeating within several hours.19

Figure 1

Figure 2

If CT scans cannot be performed, neck (soft‐tissue) and chest x‐rays may be useful. Although plain films have limited value in evaluating the retropharyngeal space, they can reveal soft‐tissue emphysema, a widened mediastinum, pulmonary infiltrates or effusions, neck abscess, and mediastinal air‐fluid levels. In cervical perforation, a lateral film of the neck can show air in deep cervical tissue before clinical signs are apparent.

Swallow studies with Gastrografin (meglumine diatrizoate) are useful in defining the exact location of the perforation (Fig. 3). However, the false‐negative rate of swallow studies can exceed 10%, especially if the patient is upright during the study. When the contrast propagates past the site of perforation too quickly, it may not extravasate.23 Although barium may provide slightly greater contrast, it may add to the problem of foreign body reaction in the area of perforation.18 An additional complication of barium is that once it has extravasated, it is not readily absorbed. The persistence of extravasated barium makes it difficult to assess the resolution of an esophageal tear on subsequent fluoroscopic or CT exams. Hence, our institution avoids using barium to evaluate esophageal perforation, unless Gastrografin swallow has excluded any major esophageal perforation. Barium swallow may then be used to exclude small mural tears. Some medical centers elect to routinely screen their high‐risk patients with swallow evaluations after an EGD, although this is not common practice.8, 24

Figure 3

If the above workup is negative, the use of EGD may be considered for establishing the diagnosis if a high index of suspicion remains. However, the risks of EGD in this situation include extension of the perforation, further extravasation of esophageal contents, and difficulty with subsequent radiographic studies to visualize the perforation.19

MANAGEMENT

Once the diagnosis of esophageal perforation has been established, treatment options are individualized based on the clinical scenario. Currently, there are no established guidelines, and large randomized clinical trials comparing outcomes of operative versus nonoperative management have not been conducted (Fig. 4).25, 26 Outcomes associated with esophageal perforations depend on preoperative clinical condition, comorbidities, location and size of the perforation, nature of underlying esophageal disease (if any), and time to establish the diagnosis and initiate therapy.10 Delay in patient presentation or diagnosis beyond 24 hours following esophageal perforation has been associated with adverse outcomes.18, 27, 28

Figure 4

A conservative approach is appropriate when clinically stable patients with minimal symptoms have well‐contained, nontransmural tears. Management entails broad‐spectrum antibiotics, nothing by mouth, nasogastric suction, and parenteral nutrition.24 Early surgical consultation is recommended in all cases. Serial CT scanning is useful for following the resolution of fistulas and tears. An oral diet can be resumed when contrast or swallow studies show no extravasation of dye. Cervical perforations typically fare well with this approach.26, 29

Surgical therapy is recommended for patients with large or uncontained esophageal perforations, mediastinal abscesses, and/or sepsis.25, 27 Surgical options include esophageal diversion, esophagectomy, or drainage with or without primary repair. Drainage with primary repair is considered the treatment of choice, regardless of time to presentation. Esophagectomy is considered in cases of delayed or neglected perforations, extensive transmural necrosis or underlying cancer.30 Operative mortality is 0%30% when treated within 24 hours. This rate increases to 26%64% when treatment is delayed beyond 24 hours, reaffirming the importance of making a prompt diagnosis.8

Endoscopic intervention is gaining recognition for its role in the management of esophageal perforations, especially when the risks make surgery prohibitive. Therapeutic options include stenting and clipping a perforation, as well as debriding and draining an abscess. Endoscopists can successfully treat traumatic nonmalignant esophageal perforations smaller than 50% to 70% of the circumference with self‐expanding plastic stents.26 Another option is to use metallic clipping devices to treat small esophageal perforations (<1 cm).3133 Combined with medical management and appropriate patient selection, the benefits of an endoscopic approach may potentially outweigh the risks of surgery.26, 29, 33, 34

Regardless of treatment approach, the appropriate and timely selection of empiric antibiotic therapy improves outcomes. Empiric antimicrobial therapy for esophageal perforation will depend on several host factors as well as the site of perforation. In healthy nonhospitalized adults, ampicillin‐sulbactam, clindamycin, and penicillin G plus metronidazole are good choices because of their excellent activity against oral microflora. In patients who are critically ill, are hospitalized, are immunosuppressed, or have gastric acid suppression, initial broad‐spectrum antimicrobials such as piperacillin‐tazobactam, imipenem, meropenem, or a third‐generation cephalosporin plus metronidazole (or clindamycin) should be initiated. Additional therapy against methicillin‐resistant Staphylococcus aureus or Candida sp. should be considered if the patient is critically ill or is known to be colonized with these organisms. Initial empiric therapy should be modified as necessary based on culture results. Total duration of therapy will vary based on location and magnitude of the infection, adjunctive surgical debridement, and pathogens involved.

SUMMARY

Despite being an extremely safe procedure, EGD carries a known serious risk of esophageal perforation. Mortality after esophageal perforation can approach 25%. Although diagnostic endoscopy has a perforation rate of less than 0.03%, the risk can approach 17% with therapeutic interventions such as stent placement and esophageal dilation. Factors influencing the risks of perforation include procedural complexity, operator experience, and underlying esophageal and systemic diseases. Furthermore, perforations complicated by infection can lead to fatal mediastinitis and sepsis. The clinical triad of esophageal perforation is fever, neck pain, and crepitus. The optimal diagnostic study is CT scan of the neck and thorax with water‐soluble oral contrast. Treatment options range from conservative management with broad‐spectrum antibiotics to surgery. Diagnosis of esophageal perforation within 24 hours is essential for favorable outcomes.

Esophagogastroduodenoscopy (EGD) carries a small but serious risk of esophageal perforation.13 With its potential for sepsis and fatal mediastinitis, prompt recognition and treatment are essential for favorable outcomes. The risk of perforation with diagnostic flexible EGD is 0.03%, which is an improvement from the 0.1%0.4% risk associated with rigid endoscopy.4 However, the risk of perforation can dramatically increase to 17% depending on the methods of therapeutic intervention and underlying risk factors (Table 1).1, 57

It is estimated that 33%75% of all esophageal perforations are iatrogenic.8 Of those caused by EGD, therapeutic interventions portend an increased risk compared with the risk of diagnostic endoscopy alone (Table 2).4 With the expanding role of flexible EGD and the increasing number of procedures performed, this modest risk per procedure still translates into a sizable number of perforations with their ensuing complications.4, 7 Mortality rates following esophageal perforation may approach 25%.9

ANATOMY AND PATHOPHYSIOLOGY

The most common site of perforation is at the level of the cricopharyngeus, as it is a narrow introitus leading to the esophagus. The risk of perforation at this location is further increased with the presence of a Zenker's diverticulum or cervical osteophytes. The second most common site is proximal to the lower esophageal sphincter because of the angulation of the hiatus and the high frequency of esophageal webs, rings, reflux strictures, and hiatal hernias. The relatively straight middle esophagus is an uncommon site for perforations.

Cervical perforations are less commonly caused by organic lesions of the esophagus. Often, they are the result of technique and manipulation of the endoscope, or of certain conditions associated with the jaw, neck, or spinal column that are unfavorable for endoscopy. The risk of cervical perforation increases with the presence of bony spurs, as the upper esophagus is compressed over the underlying spinal column. Thoracic perforations, however, are more commonly seen with organic esophageal obstruction. These obstructions may be caused by an underlying inflammatory process, benign stricture, or neoplasm. In these cases, the risk of thoracic perforation is increased with blind procedures. Thoracic perforations carry a worse prognosis if diagnosis is delayed, or if the underlying obstruction cannot be removed.10

Esophageal perforation leads to periesophageal tissues being contaminated by food, secretions, air, or gastric contents and may be followed by chemical tissue injury and infection. The nature and extent of infection depend on the site of esophageal perforation. Cervical esophageal perforation can cause retropharyngeal space infection, which has the potential to extend directly into the posterior mediastinum via the danger space, which is between the retropharyngeal and prevertebral spaces and extends from the base of the skull descending freely throughout the entire length of the posterior mediastinum. With thoracic perforations, esophageal contents can enter the pleural space by negative intrathoracic pressure with subsequent pleural contamination and empyema.8, 1113

Pathogens responsible for infections after esophageal perforation vary based on several factors including site of perforation, clinical status of patient when perforation occurs (hospitalized versus not hospitalized, critically ill versus healthy), receipt of enteral nutrition, gastric acid suppression with H2‐receptor antagonists or proton‐pump inhibitors, immunosuppression, and recent (or current) receipt of antimicrobials. In nonintubated, healthy adults not on antimicrobial therapy, organisms in the upper esophagus are essentially identical to those in the oropharynx and include viridans streptococci, Haemophilus species, and anaerobes. During critical illness and following antibiotic therapy, the normal oral flora is rapidly replaced by aerobic Gram‐negative bacilli, Staphylococcus aureus, and yeast.14 The stomach, which is normally devoid of bacteria, can likewise be colonized with pathogenic organisms in the setting of gastric acid suppression and enteral nutrition.15, 16

SIGNS AND SYMPTOMS

Esophageal perforation should be considered after EGD, dilation, sclerotherapy, variceal banding, and esophageal stenting. However, perforation can also result from other invasive procedures such as insertion of feeding and nasogastric tubes, rapid sequence intubation, and transesophageal echocardiography.

The clinical triad of esophageal perforation includes pain, fever, and subcutaneous air.17 In a study by Wychulis et al., among 33 patients with esophageal perforation, 75% demonstrated all 3 findings.10 Pain is the most sensitive finding and occurs in nearly all patients identified with esophageal perforation. Crepitation, which results from air dissecting along soft tissue planes of the mediastinum and into the neck, occurs in up to 70% with cervical perforation and 30% with thoracic perforation.8, 10, 18

Clinical presentation and outcomes vary depending on the location of the perforation (Table 3).8 Cervical perforation is usually associated with anterior neck pain, located at the anterior border of the sternocleidomastoid muscle. Movement of the neck and palpation typically aggravate the pain. Thoracic perforation typically presents as substernal chest pain, often with a component of pleurisy. Pleural effusions are present in 50% of thoracic perforations, and mediastinitis is more likely to occur.19 Hamman's sign, a finding characterized by an audible crunch with chest auscultation, is suggestive of mediastinal emphysema. Perforation of the intra‐abdominal esophagus can result in epigastric pain and signs of acute abdomen.10, 17 Subcutaneous emphysema occurs more frequently with cervical perforation but can be present regardless of location.10 Secondary infections following esophageal perforation can manifest with an accelerated clinical course leading to sepsis and shock.

DIAGNOSIS

Clinical suspicion of esophageal perforation should prompt necessary radiographic studies to establish the diagnosis.18, 20 Contrast‐enhanced computed tomography (CT) scans of the neck and chest are preferable because of their increased sensitivity in localizing the site and showing the extent of perforation and abscess. CT scans may reveal subcutaneous or mediastinal air, abscess cavities adjacent to the esophagus, and fistulas between the esophagus and mediastinum (Figs. 1 and 2).2022 Results of contrast studies may be negative and warrant repeating within several hours.19

Figure 1

Figure 2

If CT scans cannot be performed, neck (soft‐tissue) and chest x‐rays may be useful. Although plain films have limited value in evaluating the retropharyngeal space, they can reveal soft‐tissue emphysema, a widened mediastinum, pulmonary infiltrates or effusions, neck abscess, and mediastinal air‐fluid levels. In cervical perforation, a lateral film of the neck can show air in deep cervical tissue before clinical signs are apparent.

Swallow studies with Gastrografin (meglumine diatrizoate) are useful in defining the exact location of the perforation (Fig. 3). However, the false‐negative rate of swallow studies can exceed 10%, especially if the patient is upright during the study. When the contrast propagates past the site of perforation too quickly, it may not extravasate.23 Although barium may provide slightly greater contrast, it may add to the problem of foreign body reaction in the area of perforation.18 An additional complication of barium is that once it has extravasated, it is not readily absorbed. The persistence of extravasated barium makes it difficult to assess the resolution of an esophageal tear on subsequent fluoroscopic or CT exams. Hence, our institution avoids using barium to evaluate esophageal perforation, unless Gastrografin swallow has excluded any major esophageal perforation. Barium swallow may then be used to exclude small mural tears. Some medical centers elect to routinely screen their high‐risk patients with swallow evaluations after an EGD, although this is not common practice.8, 24

Figure 3

If the above workup is negative, the use of EGD may be considered for establishing the diagnosis if a high index of suspicion remains. However, the risks of EGD in this situation include extension of the perforation, further extravasation of esophageal contents, and difficulty with subsequent radiographic studies to visualize the perforation.19

MANAGEMENT

Once the diagnosis of esophageal perforation has been established, treatment options are individualized based on the clinical scenario. Currently, there are no established guidelines, and large randomized clinical trials comparing outcomes of operative versus nonoperative management have not been conducted (Fig. 4).25, 26 Outcomes associated with esophageal perforations depend on preoperative clinical condition, comorbidities, location and size of the perforation, nature of underlying esophageal disease (if any), and time to establish the diagnosis and initiate therapy.10 Delay in patient presentation or diagnosis beyond 24 hours following esophageal perforation has been associated with adverse outcomes.18, 27, 28

Figure 4

A conservative approach is appropriate when clinically stable patients with minimal symptoms have well‐contained, nontransmural tears. Management entails broad‐spectrum antibiotics, nothing by mouth, nasogastric suction, and parenteral nutrition.24 Early surgical consultation is recommended in all cases. Serial CT scanning is useful for following the resolution of fistulas and tears. An oral diet can be resumed when contrast or swallow studies show no extravasation of dye. Cervical perforations typically fare well with this approach.26, 29

Surgical therapy is recommended for patients with large or uncontained esophageal perforations, mediastinal abscesses, and/or sepsis.25, 27 Surgical options include esophageal diversion, esophagectomy, or drainage with or without primary repair. Drainage with primary repair is considered the treatment of choice, regardless of time to presentation. Esophagectomy is considered in cases of delayed or neglected perforations, extensive transmural necrosis or underlying cancer.30 Operative mortality is 0%30% when treated within 24 hours. This rate increases to 26%64% when treatment is delayed beyond 24 hours, reaffirming the importance of making a prompt diagnosis.8

Endoscopic intervention is gaining recognition for its role in the management of esophageal perforations, especially when the risks make surgery prohibitive. Therapeutic options include stenting and clipping a perforation, as well as debriding and draining an abscess. Endoscopists can successfully treat traumatic nonmalignant esophageal perforations smaller than 50% to 70% of the circumference with self‐expanding plastic stents.26 Another option is to use metallic clipping devices to treat small esophageal perforations (<1 cm).3133 Combined with medical management and appropriate patient selection, the benefits of an endoscopic approach may potentially outweigh the risks of surgery.26, 29, 33, 34

Regardless of treatment approach, the appropriate and timely selection of empiric antibiotic therapy improves outcomes. Empiric antimicrobial therapy for esophageal perforation will depend on several host factors as well as the site of perforation. In healthy nonhospitalized adults, ampicillin‐sulbactam, clindamycin, and penicillin G plus metronidazole are good choices because of their excellent activity against oral microflora. In patients who are critically ill, are hospitalized, are immunosuppressed, or have gastric acid suppression, initial broad‐spectrum antimicrobials such as piperacillin‐tazobactam, imipenem, meropenem, or a third‐generation cephalosporin plus metronidazole (or clindamycin) should be initiated. Additional therapy against methicillin‐resistant Staphylococcus aureus or Candida sp. should be considered if the patient is critically ill or is known to be colonized with these organisms. Initial empiric therapy should be modified as necessary based on culture results. Total duration of therapy will vary based on location and magnitude of the infection, adjunctive surgical debridement, and pathogens involved.

SUMMARY

Despite being an extremely safe procedure, EGD carries a known serious risk of esophageal perforation. Mortality after esophageal perforation can approach 25%. Although diagnostic endoscopy has a perforation rate of less than 0.03%, the risk can approach 17% with therapeutic interventions such as stent placement and esophageal dilation. Factors influencing the risks of perforation include procedural complexity, operator experience, and underlying esophageal and systemic diseases. Furthermore, perforations complicated by infection can lead to fatal mediastinitis and sepsis. The clinical triad of esophageal perforation is fever, neck pain, and crepitus. The optimal diagnostic study is CT scan of the neck and thorax with water‐soluble oral contrast. Treatment options range from conservative management with broad‐spectrum antibiotics to surgery. Diagnosis of esophageal perforation within 24 hours is essential for favorable outcomes.

A 109‐year‐old woman was admitted to the hospital for mild congestive heart failure and bradycardia. She scored 30 out of 30 on the Mini‐mental status exam. Further conversations revealed that she was a native of San Francisco and that she was 9 years old during the earthquake of 1906. She was 109 years old during hospitalization (Fig. 1). About 5 months after the hospitalization, she celebrated her 110th birthday (Fig. 2).

Figure 1

Figure 2

A centenarian is a person who has lived to the age of 100, and a supercentenarian is a person who has reached the age of 110. The number of centenarians in the United States was counted as 50,454 in the 2000 Census, increased from the 37,306 reported in 1990.1 The US Census Bureau estimates the current number of centenarians to be 79,682 and projects an increase to 580,605 by the year 2040.2 The number of supercentenarians was reported as 1400 in the 2000 Census.3

Hospital physicians can expect to see a growing number of centenarians in their practice as this segment of the population continues to increase.

A 109‐year‐old woman was admitted to the hospital for mild congestive heart failure and bradycardia. She scored 30 out of 30 on the Mini‐mental status exam. Further conversations revealed that she was a native of San Francisco and that she was 9 years old during the earthquake of 1906. She was 109 years old during hospitalization (Fig. 1). About 5 months after the hospitalization, she celebrated her 110th birthday (Fig. 2).

Figure 1

Figure 2

A centenarian is a person who has lived to the age of 100, and a supercentenarian is a person who has reached the age of 110. The number of centenarians in the United States was counted as 50,454 in the 2000 Census, increased from the 37,306 reported in 1990.1 The US Census Bureau estimates the current number of centenarians to be 79,682 and projects an increase to 580,605 by the year 2040.2 The number of supercentenarians was reported as 1400 in the 2000 Census.3

Hospital physicians can expect to see a growing number of centenarians in their practice as this segment of the population continues to increase.

A 109‐year‐old woman was admitted to the hospital for mild congestive heart failure and bradycardia. She scored 30 out of 30 on the Mini‐mental status exam. Further conversations revealed that she was a native of San Francisco and that she was 9 years old during the earthquake of 1906. She was 109 years old during hospitalization (Fig. 1). About 5 months after the hospitalization, she celebrated her 110th birthday (Fig. 2).

Figure 1

Figure 2

A centenarian is a person who has lived to the age of 100, and a supercentenarian is a person who has reached the age of 110. The number of centenarians in the United States was counted as 50,454 in the 2000 Census, increased from the 37,306 reported in 1990.1 The US Census Bureau estimates the current number of centenarians to be 79,682 and projects an increase to 580,605 by the year 2040.2 The number of supercentenarians was reported as 1400 in the 2000 Census.3

Hospital physicians can expect to see a growing number of centenarians in their practice as this segment of the population continues to increase.

Stroke is a leading cause of disability and the third leading cause of death in the United States.1 Transient ischemic attack (TIA) carries a substantial short‐term risk for stroke.1 The risk of stroke following TIA ranges from 2% to 5% within 48 hours, is 10.5% within 90 days, and ranges from 24% to 29% within 5 years.24 Among the 780,000 new or recurrent strokes that occur each year, 180,000 are recurrent attacks.1, 5 Several evidence‐based guidelines for secondary prevention of stroke are available. To reduce variability in the assessment, diagnostic evaluation, and treatment of patients with TIA in actual clinical practice and to simplify the management of TIA or ischemic stroke, this article will review the available guidelines for secondary prevention of stroke and the data from clinical trials that support these guidelines.

PATHOPHYSIOLOGY AND SUBTYPES/CLASSIFICATION

Stroke is broadly classified as hemorrhagic or ischemic stroke. Hemorrhagic stroke, including intraparenchymal and subarachnoid hemorrhage, accounts for 13% of strokes and ischemic stroke for 87%.1 Ischemic stroke is caused by inadequate cerebral blood flow as a result of either stenosis or occlusion of the vessels supplying the brain.6 The average rate of cerebral blood flow is 50 mL/100 g a minute. Flow rates below 2025 mL/100 g a minute are usually associated with cerebral impairment, and rates below 10 mL/100 g a minute are associated with irreversible brain damage.

Approximately 20% of ischemic strokes are of cardioembolic origin; 25% are a result of atherosclerotic cerebrovascular disease; 20% are a result of penetrating artery disease (lacunes); 5% are due to other causes, such as hypercoagulable states, including protein S and C deficiency, sickle cell disease, and various types of vasculitis; and 30% are cryptogenic.7, 8 Cardioembolic stroke can be a manifestation of atrial fibrillation, valvular disease, ventricular thrombi, and other cardiac conditions.9 Large arteries, such as the carotid arteries and the proximal aorta, are a source of atherogenic emboli.10 Atherosclerotic plaques in the arteries may narrow the lumen of the blood vessel or produce emboli, which results in occlusion of the distal arteries, causing a stroke.

RISK FACTORS

Several risk factors, both nonmodifiable and modifiable, predispose individuals to stroke. Nonmodifiable risk factors include age, sex, race, and family or personal history of stroke or myocardial infarction (MI).1, 5 After the age of 55, the stroke rate doubles for every 10‐year increase in age.1 African Americans have a 50% greater risk of death due to stroke than whites.1 The appropriate management of modifiable risk factors can significantly reduce the risk of recurrent stroke and improve survival. The many modifiable factors include hypertension, heart disease, smoking, diabetes, atrial fibrillation, dyslipidemia, obesity, and alcohol abuse.1, 5 The mechanisms of how these factors increase the risk for stroke and management of these factors are discussed later in this article. It is important to educate individuals, particularly those who also have nonmodifiable risk factors, about modifiable risk factors in order to enable early and appropriate intervention.

DIAGNOSIS

Most patients with TIA are asymptomatic when they present to the emergency department (ED). The risk of stroke following an episode of TIA has been found to be 3.5% within 48 hours in a meta‐analysis based on a random effects model;11 therefore, it is critical to quickly identify patients with high short‐term risk for recurrent stroke.12 The ABCD2 score was recently validated in TIA patients to estimate the near‐term risk of completed stroke.13 Patients with a score of 03 on the ABCD2 are at low risk, those with a score of 4 or 5 are at moderate risk, and those with a score 6 or 7 are at severe risk for recurrent stroke (Table 1).13 Risk scores, although highly predictive, should complement clinical judgment in the assessment of individual stroke risk.

Currently, there are no specific guidelines for the diagnostic evaluation of patients with suspected TIA. However, the following approach, including elements of acute evaluation for both stroke and TIA as well as risk factor identification that may aid in choosing specifics of secondary prevention, may be adopted in the management of patients with TIA (Table 2).14, 15

A computed tomography (CT) scan of the head or magnetic resonance imaging (MRI) of the brain should be performed as soon as possible to distinguish between ischemic and hemorrhagic stroke, eliminate other pathologies that mimic TIA or stroke, and guide selection of the appropriate treatment approach. CT scanning is often the best initial imaging choice because it reliably excludes intracranial hemorrhage and is rapidly available in most settings. For those for whom the diagnosis is uncertain, diffusion‐weighted MRI may be more helpful. Because of the time issues surrounding the use of tissue plasminogen activator, waiting for an MRI may not always be the best choice, although some institutions are now able to provide quick access to MRI imaging. Imaging can detect silent cerebral infarcts associated with an increased risk of stroke. In patients with previous TIA and/or stroke, MRI is more sensitive than CT in detecting small, old infarcts (although most are seen on CT) and in visualizing the posterior fossa (cerebellum and brain stem).12

Holter electrocardiography or inpatient telemetry monitoring can be performed to identify atrial fibrillation, a known risk factor for stroke or TIA.16 Transesophageal echocardiography (TEE) has been reported to be more sensitive than transthoracic echocardiography (TTE) for detecting cardioembolic sources of TIA or ischemic stroke across multiple age groups.17 TEE has several advantages over TTE, such as the creation of clearer images of the aorta, the pulmonary artery, valves of the heart, both atria, the atrial septum, and the left atrial appendage.

Cerebral angiography is indicated in several instances, including in children or young patients with ischemic stroke because vascular abnormalities and cerebral vasculitis are relatively more common causes in patients in these age groups.18 Furthermore, in centers in which intra‐arterial procedures are frequently performed, angiography is indicated to confirm the suspicion of posterior circulation vessel (ie, vertebral or basilar artery) occlusion prior to intervention. Angiography has the highest diagnostic validity compared with other noninvasive techniques and may be indicated if cerebral vasculitis or nonatherosclerotic disease of extracranial arteries (eg, dissections, vascular malformations) is suspected. Angiography of intracranial vessels is the gold standard for the study of cerebral aneurysms and is recommended in patients with subarachnoid hemorrhage, but there is evidence that magnetic resonance angiography (MRA) and digital subtraction angiography have better discriminatory ability in the 70%99% range of stenosis compared with duplex ultrasonography (DUS) for determining candidacy for carotid endarterectomy (CEA) or stenting.19, 20

The MRA and CT angiography (CTA) are generally used to visualize the intracranial and extracranialboth anterior and posteriorcerebral circulation. The use of MRA or CTA to image cerebral circulation has generally supplanted the use of carotid and transcranial ultrasonography and obviated the need for catheter angiography in investigating the etiology of most ischemic strokes and TIAs. The degree of carotid stenosis should be primarily estimated using noninvasive techniques (DUS, MRA, CTA).21 Duplex ultrasonography is recommended after CEA 6 months and every 1 2 years after the procedure in order to monitor recurrent stenosis.22 Angiography should be performed when the results of noninvasive examinations are discordant; when significant atherosclerotic disease of intracranial arteries is suspected, especially in vertebrobasilar arteries; or when MRA or CT angiography provides technically poor images.23

Transcranial Doppler ultrasonography and color Doppler ultrasound (TCD) are used to evaluate the intracranial vessels and may provide additional information on patency of cerebral vessels, recanalization, and collateral pathways. Compared with the gold standard of conventional angiography, TCD has a positive predictive value of 36% and a negative predictive value of 86% for a diagnosis of intracranial stenosis.24 This technique also can be used as a complementary examination in patients undergoing CEA in order to aid in preoperative evaluation and intraoperative monitoring of blood flow in the territory of the operated artery.12

TREATMENT

The management of ischemic stroke or TIA includes lifestyle modifications, reduction of modifiable risk factors, and appropriate surgical and medical intervention.12

SUMMARY OF GUIDELINES FOR SECONDARY PREVENTION OF STROKE

The AHA/ASA, American College of Chest Physicians (ACCP), and National Stroke Association (NSA) have developed and published practice guidelines for the management of TIA, with detailed information on secondary prevention of stroke.5, 79, 80 The key recommendations from these 3 organizations are summarized in Table 5 .5, 79, 80 This section summarizes the current guidelines regarding the use of antiplatelets and anticoagulants for the secondary prevention of stroke.

FUTURE DEVELOPMENTS

One of the largest stroke prevention trials currently ongoing is the Prevention Regimen for Effectively avoiding Second Strokes (PRoFESS) study. The PRoFESS trial is a large (N = 20,333), randomized, double‐blind, placebo‐controlled, multinational study comparing the efficacy and safety of aspirin plus ER‐DP with that of clopidogrel and the efficacy of telmisartan versus placebo in the presence of background blood pressure treatments in preventing recurrent stroke.86 The primary outcome of the study is time to first recurrent stroke. Recently, the baseline demographics were published.86 The mean age of patients was 66.1 years at enrollment, 36% of patients were women, and mean time from event to randomization was 15 days (40% randomized within 10 days). Most participants had had a stroke of arterial origin (29% large vessel disease and 52% small vessel disease), whereas 2% had had a stroke due to cardioembolism and 18% due to other causes. These baseline data suggest that the trial involves a representative international population of patients with stroke. The PRoFESS trial will provide additional insight into the benefits of the combination of aspirin plus ER‐DP for secondary prevention of stroke in addition to providing direct comparison of efficacy with clopidogrel. The latest information on this and other ongoing stroke prevention trials can be accessed at http://www.strokecenter.org/trials/.

Stroke is a leading cause of disability and the third leading cause of death in the United States.1 Transient ischemic attack (TIA) carries a substantial short‐term risk for stroke.1 The risk of stroke following TIA ranges from 2% to 5% within 48 hours, is 10.5% within 90 days, and ranges from 24% to 29% within 5 years.24 Among the 780,000 new or recurrent strokes that occur each year, 180,000 are recurrent attacks.1, 5 Several evidence‐based guidelines for secondary prevention of stroke are available. To reduce variability in the assessment, diagnostic evaluation, and treatment of patients with TIA in actual clinical practice and to simplify the management of TIA or ischemic stroke, this article will review the available guidelines for secondary prevention of stroke and the data from clinical trials that support these guidelines.

PATHOPHYSIOLOGY AND SUBTYPES/CLASSIFICATION

Stroke is broadly classified as hemorrhagic or ischemic stroke. Hemorrhagic stroke, including intraparenchymal and subarachnoid hemorrhage, accounts for 13% of strokes and ischemic stroke for 87%.1 Ischemic stroke is caused by inadequate cerebral blood flow as a result of either stenosis or occlusion of the vessels supplying the brain.6 The average rate of cerebral blood flow is 50 mL/100 g a minute. Flow rates below 2025 mL/100 g a minute are usually associated with cerebral impairment, and rates below 10 mL/100 g a minute are associated with irreversible brain damage.

Approximately 20% of ischemic strokes are of cardioembolic origin; 25% are a result of atherosclerotic cerebrovascular disease; 20% are a result of penetrating artery disease (lacunes); 5% are due to other causes, such as hypercoagulable states, including protein S and C deficiency, sickle cell disease, and various types of vasculitis; and 30% are cryptogenic.7, 8 Cardioembolic stroke can be a manifestation of atrial fibrillation, valvular disease, ventricular thrombi, and other cardiac conditions.9 Large arteries, such as the carotid arteries and the proximal aorta, are a source of atherogenic emboli.10 Atherosclerotic plaques in the arteries may narrow the lumen of the blood vessel or produce emboli, which results in occlusion of the distal arteries, causing a stroke.

RISK FACTORS

Several risk factors, both nonmodifiable and modifiable, predispose individuals to stroke. Nonmodifiable risk factors include age, sex, race, and family or personal history of stroke or myocardial infarction (MI).1, 5 After the age of 55, the stroke rate doubles for every 10‐year increase in age.1 African Americans have a 50% greater risk of death due to stroke than whites.1 The appropriate management of modifiable risk factors can significantly reduce the risk of recurrent stroke and improve survival. The many modifiable factors include hypertension, heart disease, smoking, diabetes, atrial fibrillation, dyslipidemia, obesity, and alcohol abuse.1, 5 The mechanisms of how these factors increase the risk for stroke and management of these factors are discussed later in this article. It is important to educate individuals, particularly those who also have nonmodifiable risk factors, about modifiable risk factors in order to enable early and appropriate intervention.

DIAGNOSIS

Most patients with TIA are asymptomatic when they present to the emergency department (ED). The risk of stroke following an episode of TIA has been found to be 3.5% within 48 hours in a meta‐analysis based on a random effects model;11 therefore, it is critical to quickly identify patients with high short‐term risk for recurrent stroke.12 The ABCD2 score was recently validated in TIA patients to estimate the near‐term risk of completed stroke.13 Patients with a score of 03 on the ABCD2 are at low risk, those with a score of 4 or 5 are at moderate risk, and those with a score 6 or 7 are at severe risk for recurrent stroke (Table 1).13 Risk scores, although highly predictive, should complement clinical judgment in the assessment of individual stroke risk.

Currently, there are no specific guidelines for the diagnostic evaluation of patients with suspected TIA. However, the following approach, including elements of acute evaluation for both stroke and TIA as well as risk factor identification that may aid in choosing specifics of secondary prevention, may be adopted in the management of patients with TIA (Table 2).14, 15

A computed tomography (CT) scan of the head or magnetic resonance imaging (MRI) of the brain should be performed as soon as possible to distinguish between ischemic and hemorrhagic stroke, eliminate other pathologies that mimic TIA or stroke, and guide selection of the appropriate treatment approach. CT scanning is often the best initial imaging choice because it reliably excludes intracranial hemorrhage and is rapidly available in most settings. For those for whom the diagnosis is uncertain, diffusion‐weighted MRI may be more helpful. Because of the time issues surrounding the use of tissue plasminogen activator, waiting for an MRI may not always be the best choice, although some institutions are now able to provide quick access to MRI imaging. Imaging can detect silent cerebral infarcts associated with an increased risk of stroke. In patients with previous TIA and/or stroke, MRI is more sensitive than CT in detecting small, old infarcts (although most are seen on CT) and in visualizing the posterior fossa (cerebellum and brain stem).12

Holter electrocardiography or inpatient telemetry monitoring can be performed to identify atrial fibrillation, a known risk factor for stroke or TIA.16 Transesophageal echocardiography (TEE) has been reported to be more sensitive than transthoracic echocardiography (TTE) for detecting cardioembolic sources of TIA or ischemic stroke across multiple age groups.17 TEE has several advantages over TTE, such as the creation of clearer images of the aorta, the pulmonary artery, valves of the heart, both atria, the atrial septum, and the left atrial appendage.

Cerebral angiography is indicated in several instances, including in children or young patients with ischemic stroke because vascular abnormalities and cerebral vasculitis are relatively more common causes in patients in these age groups.18 Furthermore, in centers in which intra‐arterial procedures are frequently performed, angiography is indicated to confirm the suspicion of posterior circulation vessel (ie, vertebral or basilar artery) occlusion prior to intervention. Angiography has the highest diagnostic validity compared with other noninvasive techniques and may be indicated if cerebral vasculitis or nonatherosclerotic disease of extracranial arteries (eg, dissections, vascular malformations) is suspected. Angiography of intracranial vessels is the gold standard for the study of cerebral aneurysms and is recommended in patients with subarachnoid hemorrhage, but there is evidence that magnetic resonance angiography (MRA) and digital subtraction angiography have better discriminatory ability in the 70%99% range of stenosis compared with duplex ultrasonography (DUS) for determining candidacy for carotid endarterectomy (CEA) or stenting.19, 20

The MRA and CT angiography (CTA) are generally used to visualize the intracranial and extracranialboth anterior and posteriorcerebral circulation. The use of MRA or CTA to image cerebral circulation has generally supplanted the use of carotid and transcranial ultrasonography and obviated the need for catheter angiography in investigating the etiology of most ischemic strokes and TIAs. The degree of carotid stenosis should be primarily estimated using noninvasive techniques (DUS, MRA, CTA).21 Duplex ultrasonography is recommended after CEA 6 months and every 1 2 years after the procedure in order to monitor recurrent stenosis.22 Angiography should be performed when the results of noninvasive examinations are discordant; when significant atherosclerotic disease of intracranial arteries is suspected, especially in vertebrobasilar arteries; or when MRA or CT angiography provides technically poor images.23

Transcranial Doppler ultrasonography and color Doppler ultrasound (TCD) are used to evaluate the intracranial vessels and may provide additional information on patency of cerebral vessels, recanalization, and collateral pathways. Compared with the gold standard of conventional angiography, TCD has a positive predictive value of 36% and a negative predictive value of 86% for a diagnosis of intracranial stenosis.24 This technique also can be used as a complementary examination in patients undergoing CEA in order to aid in preoperative evaluation and intraoperative monitoring of blood flow in the territory of the operated artery.12

TREATMENT

The management of ischemic stroke or TIA includes lifestyle modifications, reduction of modifiable risk factors, and appropriate surgical and medical intervention.12

SUMMARY OF GUIDELINES FOR SECONDARY PREVENTION OF STROKE

The AHA/ASA, American College of Chest Physicians (ACCP), and National Stroke Association (NSA) have developed and published practice guidelines for the management of TIA, with detailed information on secondary prevention of stroke.5, 79, 80 The key recommendations from these 3 organizations are summarized in Table 5 .5, 79, 80 This section summarizes the current guidelines regarding the use of antiplatelets and anticoagulants for the secondary prevention of stroke.

FUTURE DEVELOPMENTS

One of the largest stroke prevention trials currently ongoing is the Prevention Regimen for Effectively avoiding Second Strokes (PRoFESS) study. The PRoFESS trial is a large (N = 20,333), randomized, double‐blind, placebo‐controlled, multinational study comparing the efficacy and safety of aspirin plus ER‐DP with that of clopidogrel and the efficacy of telmisartan versus placebo in the presence of background blood pressure treatments in preventing recurrent stroke.86 The primary outcome of the study is time to first recurrent stroke. Recently, the baseline demographics were published.86 The mean age of patients was 66.1 years at enrollment, 36% of patients were women, and mean time from event to randomization was 15 days (40% randomized within 10 days). Most participants had had a stroke of arterial origin (29% large vessel disease and 52% small vessel disease), whereas 2% had had a stroke due to cardioembolism and 18% due to other causes. These baseline data suggest that the trial involves a representative international population of patients with stroke. The PRoFESS trial will provide additional insight into the benefits of the combination of aspirin plus ER‐DP for secondary prevention of stroke in addition to providing direct comparison of efficacy with clopidogrel. The latest information on this and other ongoing stroke prevention trials can be accessed at http://www.strokecenter.org/trials/.

Stroke is a leading cause of disability and the third leading cause of death in the United States.1 Transient ischemic attack (TIA) carries a substantial short‐term risk for stroke.1 The risk of stroke following TIA ranges from 2% to 5% within 48 hours, is 10.5% within 90 days, and ranges from 24% to 29% within 5 years.24 Among the 780,000 new or recurrent strokes that occur each year, 180,000 are recurrent attacks.1, 5 Several evidence‐based guidelines for secondary prevention of stroke are available. To reduce variability in the assessment, diagnostic evaluation, and treatment of patients with TIA in actual clinical practice and to simplify the management of TIA or ischemic stroke, this article will review the available guidelines for secondary prevention of stroke and the data from clinical trials that support these guidelines.

PATHOPHYSIOLOGY AND SUBTYPES/CLASSIFICATION

Stroke is broadly classified as hemorrhagic or ischemic stroke. Hemorrhagic stroke, including intraparenchymal and subarachnoid hemorrhage, accounts for 13% of strokes and ischemic stroke for 87%.1 Ischemic stroke is caused by inadequate cerebral blood flow as a result of either stenosis or occlusion of the vessels supplying the brain.6 The average rate of cerebral blood flow is 50 mL/100 g a minute. Flow rates below 2025 mL/100 g a minute are usually associated with cerebral impairment, and rates below 10 mL/100 g a minute are associated with irreversible brain damage.

Approximately 20% of ischemic strokes are of cardioembolic origin; 25% are a result of atherosclerotic cerebrovascular disease; 20% are a result of penetrating artery disease (lacunes); 5% are due to other causes, such as hypercoagulable states, including protein S and C deficiency, sickle cell disease, and various types of vasculitis; and 30% are cryptogenic.7, 8 Cardioembolic stroke can be a manifestation of atrial fibrillation, valvular disease, ventricular thrombi, and other cardiac conditions.9 Large arteries, such as the carotid arteries and the proximal aorta, are a source of atherogenic emboli.10 Atherosclerotic plaques in the arteries may narrow the lumen of the blood vessel or produce emboli, which results in occlusion of the distal arteries, causing a stroke.

RISK FACTORS

Several risk factors, both nonmodifiable and modifiable, predispose individuals to stroke. Nonmodifiable risk factors include age, sex, race, and family or personal history of stroke or myocardial infarction (MI).1, 5 After the age of 55, the stroke rate doubles for every 10‐year increase in age.1 African Americans have a 50% greater risk of death due to stroke than whites.1 The appropriate management of modifiable risk factors can significantly reduce the risk of recurrent stroke and improve survival. The many modifiable factors include hypertension, heart disease, smoking, diabetes, atrial fibrillation, dyslipidemia, obesity, and alcohol abuse.1, 5 The mechanisms of how these factors increase the risk for stroke and management of these factors are discussed later in this article. It is important to educate individuals, particularly those who also have nonmodifiable risk factors, about modifiable risk factors in order to enable early and appropriate intervention.

DIAGNOSIS

Most patients with TIA are asymptomatic when they present to the emergency department (ED). The risk of stroke following an episode of TIA has been found to be 3.5% within 48 hours in a meta‐analysis based on a random effects model;11 therefore, it is critical to quickly identify patients with high short‐term risk for recurrent stroke.12 The ABCD2 score was recently validated in TIA patients to estimate the near‐term risk of completed stroke.13 Patients with a score of 03 on the ABCD2 are at low risk, those with a score of 4 or 5 are at moderate risk, and those with a score 6 or 7 are at severe risk for recurrent stroke (Table 1).13 Risk scores, although highly predictive, should complement clinical judgment in the assessment of individual stroke risk.

Currently, there are no specific guidelines for the diagnostic evaluation of patients with suspected TIA. However, the following approach, including elements of acute evaluation for both stroke and TIA as well as risk factor identification that may aid in choosing specifics of secondary prevention, may be adopted in the management of patients with TIA (Table 2).14, 15

A computed tomography (CT) scan of the head or magnetic resonance imaging (MRI) of the brain should be performed as soon as possible to distinguish between ischemic and hemorrhagic stroke, eliminate other pathologies that mimic TIA or stroke, and guide selection of the appropriate treatment approach. CT scanning is often the best initial imaging choice because it reliably excludes intracranial hemorrhage and is rapidly available in most settings. For those for whom the diagnosis is uncertain, diffusion‐weighted MRI may be more helpful. Because of the time issues surrounding the use of tissue plasminogen activator, waiting for an MRI may not always be the best choice, although some institutions are now able to provide quick access to MRI imaging. Imaging can detect silent cerebral infarcts associated with an increased risk of stroke. In patients with previous TIA and/or stroke, MRI is more sensitive than CT in detecting small, old infarcts (although most are seen on CT) and in visualizing the posterior fossa (cerebellum and brain stem).12

Holter electrocardiography or inpatient telemetry monitoring can be performed to identify atrial fibrillation, a known risk factor for stroke or TIA.16 Transesophageal echocardiography (TEE) has been reported to be more sensitive than transthoracic echocardiography (TTE) for detecting cardioembolic sources of TIA or ischemic stroke across multiple age groups.17 TEE has several advantages over TTE, such as the creation of clearer images of the aorta, the pulmonary artery, valves of the heart, both atria, the atrial septum, and the left atrial appendage.

Cerebral angiography is indicated in several instances, including in children or young patients with ischemic stroke because vascular abnormalities and cerebral vasculitis are relatively more common causes in patients in these age groups.18 Furthermore, in centers in which intra‐arterial procedures are frequently performed, angiography is indicated to confirm the suspicion of posterior circulation vessel (ie, vertebral or basilar artery) occlusion prior to intervention. Angiography has the highest diagnostic validity compared with other noninvasive techniques and may be indicated if cerebral vasculitis or nonatherosclerotic disease of extracranial arteries (eg, dissections, vascular malformations) is suspected. Angiography of intracranial vessels is the gold standard for the study of cerebral aneurysms and is recommended in patients with subarachnoid hemorrhage, but there is evidence that magnetic resonance angiography (MRA) and digital subtraction angiography have better discriminatory ability in the 70%99% range of stenosis compared with duplex ultrasonography (DUS) for determining candidacy for carotid endarterectomy (CEA) or stenting.19, 20

The MRA and CT angiography (CTA) are generally used to visualize the intracranial and extracranialboth anterior and posteriorcerebral circulation. The use of MRA or CTA to image cerebral circulation has generally supplanted the use of carotid and transcranial ultrasonography and obviated the need for catheter angiography in investigating the etiology of most ischemic strokes and TIAs. The degree of carotid stenosis should be primarily estimated using noninvasive techniques (DUS, MRA, CTA).21 Duplex ultrasonography is recommended after CEA 6 months and every 1 2 years after the procedure in order to monitor recurrent stenosis.22 Angiography should be performed when the results of noninvasive examinations are discordant; when significant atherosclerotic disease of intracranial arteries is suspected, especially in vertebrobasilar arteries; or when MRA or CT angiography provides technically poor images.23

Transcranial Doppler ultrasonography and color Doppler ultrasound (TCD) are used to evaluate the intracranial vessels and may provide additional information on patency of cerebral vessels, recanalization, and collateral pathways. Compared with the gold standard of conventional angiography, TCD has a positive predictive value of 36% and a negative predictive value of 86% for a diagnosis of intracranial stenosis.24 This technique also can be used as a complementary examination in patients undergoing CEA in order to aid in preoperative evaluation and intraoperative monitoring of blood flow in the territory of the operated artery.12

TREATMENT

The management of ischemic stroke or TIA includes lifestyle modifications, reduction of modifiable risk factors, and appropriate surgical and medical intervention.12

SUMMARY OF GUIDELINES FOR SECONDARY PREVENTION OF STROKE

The AHA/ASA, American College of Chest Physicians (ACCP), and National Stroke Association (NSA) have developed and published practice guidelines for the management of TIA, with detailed information on secondary prevention of stroke.5, 79, 80 The key recommendations from these 3 organizations are summarized in Table 5 .5, 79, 80 This section summarizes the current guidelines regarding the use of antiplatelets and anticoagulants for the secondary prevention of stroke.

FUTURE DEVELOPMENTS

One of the largest stroke prevention trials currently ongoing is the Prevention Regimen for Effectively avoiding Second Strokes (PRoFESS) study. The PRoFESS trial is a large (N = 20,333), randomized, double‐blind, placebo‐controlled, multinational study comparing the efficacy and safety of aspirin plus ER‐DP with that of clopidogrel and the efficacy of telmisartan versus placebo in the presence of background blood pressure treatments in preventing recurrent stroke.86 The primary outcome of the study is time to first recurrent stroke. Recently, the baseline demographics were published.86 The mean age of patients was 66.1 years at enrollment, 36% of patients were women, and mean time from event to randomization was 15 days (40% randomized within 10 days). Most participants had had a stroke of arterial origin (29% large vessel disease and 52% small vessel disease), whereas 2% had had a stroke due to cardioembolism and 18% due to other causes. These baseline data suggest that the trial involves a representative international population of patients with stroke. The PRoFESS trial will provide additional insight into the benefits of the combination of aspirin plus ER‐DP for secondary prevention of stroke in addition to providing direct comparison of efficacy with clopidogrel. The latest information on this and other ongoing stroke prevention trials can be accessed at http://www.strokecenter.org/trials/.