The ubiquitous urinary catheter is associated with 80% of hospital‐acquired urinary tract infections (UTIs)1estimated to number one million annuallyaccounting for 40% of all nosocomial infections.2, 3 The clinical consequences of these catheter‐associated urinary tract infections (CAUTIs) are substantial and include prolonged hospital stay, bacteremia, and death.4 Despite the known risks of CAUTIs, it is estimated that 25% of hospitalized patients receive urinary catheters and that inappropriate urinary catheter use is widespread.5 Among catheterized patients, catheter duration is the most important modifiable risk factor for CAUTI. The excess risk of any bacteriuria accrues at a rate of 5% per catheter‐day beyond the first 48 hours of catheterization.6, 7 The reduction of catheter‐days for a given patient is an important component of quality improvement efforts to reduce CAUTIs. Unfortunately, as of a 2005 survey, most hospitals do not systematically track urinary catheter insertions and removals.8

The above concerns are highlighted for surgical patients among whom indwelling urinary catheter use is particularly high. In a 2001 sample of Medicare beneficiaries, 85% of major surgical patients had perioperative urinary catheters.9 In this population, postoperative catheter duration exceeded 48 hours in nearly 50%, despite concern that the risks of infection offset the benefits of continued catheterization after 24 hours to 48 hours postoperatively.4, 7, 10 Patients with catheters greater than 2 postoperative days had a 21% increased likelihood of in‐hospital UTI, increased 30‐day mortality, and decreased odds of discharge to home.9

To address the risk of CAUTI associated with excess urinary catheter days, The Centers for Medicare and Medicaid Services' (CMS) Surgical Care Improvement Project (SCIP) added catheter removal on postoperative day 1 or 2 to its process measure set beginning in October 2009. SCIP is 1 of several high‐profile surgical quality improvement programs that employs performance audit and feedback of patient‐level process or outcome measures to address deficiencies in surgical care.11, 12 In addition, audit and feedback of CAUTI rates has been used to successfully reduce CAUTIs in medical‐surgical patients.13 The goal of our study was to audit patient‐level postoperative urinary catheter duration and measure the impact of its feedback to nursing staff on postoperative catheter duration, CAUTI rates, and nurse's attitudes about CAUTI prevention.

Methods

Results

During the study period there were a total of 1657 surgeries on the 2 study units during the baseline and follow‐up periods. After exclusions for urologic or gynecologic surgery (271), no indwelling catheter for surgery (505), or first surgery of 2 or more during the hospitalization (31), there were 846 eligible surgeries (51%).

Table 1 describes the population for the baseline and follow‐up periods for orthopedic and general surgery patients. Within each unit, the surgical populations were comparable during the baseline and follow‐up periods with the exception that the mean length of stay for eligible general surgery patients was significantly shorter in the baseline period as compared to the follow‐up period (6.6 vs. 8.5 days, P = 0.02). Cases on the orthopedic surgery unit were predominantly knee, hip and spine surgeries (85.9%), while those on the general surgery unit were predominantly gut and other gastrointestinal (GI) procedures (80.3%).

BaselineFollow‐Up Comparison

Table 3 describes the measures of urinary catheter use for each surgical population for both data collection periods. On both units, measures of catheter duration were improved following the education and feedback intervention. For the orthopedic unit, mean postoperative catheter duration was reduced from 1.7 to 1.4 days (P = 0.01) and the proportion of patients with catheter removal before day 3 was increased from 86% to 92% (P = 0.04). For the general surgery unit, mean postoperative catheter duration was reduced from 2.6 to 2.2 days (P = 0.01) and the proportion of patients with catheter removal before day 3 was increased from 56% to 63% (P = 0.14). When the general surgery measures were adjusted to account for the difference in length of stay between the 2 time periods, the odds of meeting the performance measure at follow‐up compared to baseline increased from unadjusted odds of 1.38 (P = 0.14) to adjusted odds of 1.69 (P = 0.02).

Table 3.Measures of Indwelling Urinary Catheter Duration and CAUTI Rates

Measure	Orthopedic Surgery			General Surgery
	Baseline, n = 206	Follow‐Up, n = 290	P Value	Baseline, n = 167	Follow‐Up, n = 183	P Value
Abbreviations: CAUTI, catheter‐associated urinary tract infection; ns, not sufficient; SD, standard deviation.
Postoperative catheter duration in days (mean, SD)	1.70 (1.24)	1.44 (0.85)	0.01	2.64 (1.85)	2.19 (1.40)	0.01
Postoperative catheter duration performance measure (%)	86	92	0.04	56	63	0.14
Total catheter days	350	418		441	401
Catheter days/1000 hospital days	423	394	ns*	398	259	s*
Catheter‐associated UTIs	3	0		3	3
Catheter‐associated UTI rate (infections/1000 device days)	8.6	0	ns*	6.8	7.5	ns*

Figure 1a and b are histograms of the frequency of cases having a given postoperative catheter duration in days. The dark bars show the baseline distribution and the light bars show the follow‐up distribution. Although the number of patients in the follow‐up period is greater than for the baseline period for the orthopedic surgery cohort, the images are instructive. In both groups of patients, but most notably in the general surgery population, the reduction in catheter measures resulted from a left shift in the frequency distribution, both for the longer duration outliers (removing the tail of each plot) and for the shorter duration catheters (3 days), increasing the proportion of catheters removed on postoperative day 1.

Figure 1

Discussion

This preobservational and postobservational study found that audit and feedback of patient‐level postoperative urinary catheter duration delivered in the context of an educational intervention and brainstorming session was temporally associated with clinically meaningful reductions in urinary catheter duration. In so doing, we demonstrated the feasibility of collecting patient level urinary catheter duration, and delivering it in a manner that had utility for frontline staff. Our results are consistent with the quality improvement literature which demonstrates that audit and feedback is a successful quality improvement strategy in many contexts and may be as good as more complex interventions at increasing adherence to the performance of process measures for surgical infection prevention.14 Two large national programs, the VA National Surgical Quality Improvement Program (NSQIP) and SCIP, use audit and feedback as the backbone of their large‐scale quality improvement strategies with promising results.11, 12

Given that the 2 study units were so different in practice patterns regarding urinary catheter management and nursing‐identified barriers to evidence‐based care, this work suggests that urinary catheter management may pose unique challenges for different clinical areas and provides a caution that one‐size‐fits‐all interventions for the rationalization of urinary catheter management and reduction of CAUTIs may be of limited effectiveness in the absence of local tailoring. As such, audit and feedback is well‐suited to this purpose as more proscriptive quality improvement strategies may meet with a variety of implementation challenges.

The impact of our intervention on CAUTI rates was not significant. There are several possible explanations for this finding. First, the study was not powered to detect a difference in CAUTI rates given the low infection rate at our institution. However, we cannot exclude the possibility that a reduction in mean catheter duration of one‐third to one‐half of a day is insufficient to impact CAUTI rates in postoperative patients, particularly when many of the follow‐up patients still had postoperative catheter duration 2 daysthe timeframe beyond which bacterial colonization of the catheter begins. While both study units had similar increases in postoperative catheter duration, the UTI rate was only decreased in the orthopedic surgery group which had much higher rates of postoperative catheter duration 2 days at baseline.

In recent years, there has been a renewed focus on the eradication of hospital‐acquired infections prompted by intense interest from the public, federal and state legislators, and others.15, 16 The CMS has recently used the revamping of the Inpatient Prospective Payment System (IPPS) as an opportunity to align financial incentives so that reimbursements for claims with certain hospital‐acquired conditions, including CAUTIs, will be reduced to that of the reimbursement of the same claim without the presence of the complication.17 This move is just one of several strategies to motivate hospitals and clinicians to address the pervasive problem of hospital‐acquired infection.

As urinary catheters are intimately linked to hospital‐acquired UTI, a focus of reduction efforts on catheter use is appropriate. The National Quality Forum (NQF) endorsed a postoperative catheter duration quality measure which was incorporated by the CMS's SCIP in late 2009.18 As a result, every hospital in the country that performs surgery and participates in the Medicare program is now tasked with determining patient‐level urinary catheter duration for selected surgical patients. This move represents a departure from current recommendations from the Centers for Disease Control and Prevention (CDC) and its National Healthcare Safety Network19, 20 which endorse the measurement of a catheter utilization ratio (urinary catheter days/patient days) for patient care units, but does not endorse any patient‐level utilization measures. In this instance, the use of patient‐level data may be better suited to quality improvement interventions such as audit and feedback because of its clinical relevance to frontline providers. However, it may also increase the data collection burden on hospitals. Notably, the measurement of postoperative catheter duration in this study was semiautomated using queries of an EHR. Such an approach can significantly reduce the data collection burden for this process measure and is consistent with national initiatives to integrate EHRs with quality improvement initiatives going forward.21

Our study has several limitations. This study took place in the year following the announcement of a high profile Medicare rule change regarding payment for hospital‐acquired harms. Certainly, the uncontrolled prestudy and poststudy design does not allow for the assessment of the impact of our intervention independent of this context. We are unable, therefore, to attribute the observed reduction solely to the intervention. Additionally, we did not follow postoperative urinary catheter duration beyond the immediate follow‐up period. It is anticipated that the impact of an audit and feedback intervention may diminish over time without a mechanism for repeated feedback. Certainly the sustainability of such repeated feedback in a single institution would be improved with an appropriately configured EHR.

In addition, we have reliable data on catheter reinsertions only from the follow‐up period. While the rates of reinsertions we recorded (0.7% on orthopedic surgery and 2.7% on general surgery) were lower than expected based on the literature,22 we are unable to determine if our intervention led to increases in postoperative urinary retention.

This study was limited to 2 surgical units of a single academic medical center and therefore the urinary catheter utilization patterns may not be representative of other patient populations at other institutions. However, the urinary catheter patterns were comparable to those identified in our prior work in a national sample of Medicare patients undergoing elective surgery.9

Finally, the field of CAUTI prevention has evolved rapidly since this study was performed. In particular, the surveillance definition of CAUTI was altered twice by the CDC in December of 2008 and March of 2009. In addition, the Infectious Diseases Society of America issued a new definition of CAUTI in February of 2010.23 All of these changes highlight the difference between asymptomatic bateriuria (ASB) and symptomatic CAUTI. However, the surveillance definition in use at the time of this study did not make this distinction. Therefore, we are unable to comment on the relative occurrence of ASB versus symptomatic CAUTI under the new definitions.

Rational urinary catheter use is a central component of CAUTI prevention efforts.24 We describe the use of patient‐level urinary catheter use in an audit and feedback intervention to frontline staff that was associated with reductions in urinary catheter duration. To do so, we employed a methodology for tracking urinary catheter use patterns that can provide important data for infection preventionists and frontline providers in efforts to improve urinary output management. This promising approach merits further study as an adjunct to current efforts to rationalize urinary catheter utilization and reduce CAUTIs. In the current environment, having the right data is a powerful aide for ongoing performance improvement.

The ubiquitous urinary catheter is associated with 80% of hospital‐acquired urinary tract infections (UTIs)1estimated to number one million annuallyaccounting for 40% of all nosocomial infections.2, 3 The clinical consequences of these catheter‐associated urinary tract infections (CAUTIs) are substantial and include prolonged hospital stay, bacteremia, and death.4 Despite the known risks of CAUTIs, it is estimated that 25% of hospitalized patients receive urinary catheters and that inappropriate urinary catheter use is widespread.5 Among catheterized patients, catheter duration is the most important modifiable risk factor for CAUTI. The excess risk of any bacteriuria accrues at a rate of 5% per catheter‐day beyond the first 48 hours of catheterization.6, 7 The reduction of catheter‐days for a given patient is an important component of quality improvement efforts to reduce CAUTIs. Unfortunately, as of a 2005 survey, most hospitals do not systematically track urinary catheter insertions and removals.8

The above concerns are highlighted for surgical patients among whom indwelling urinary catheter use is particularly high. In a 2001 sample of Medicare beneficiaries, 85% of major surgical patients had perioperative urinary catheters.9 In this population, postoperative catheter duration exceeded 48 hours in nearly 50%, despite concern that the risks of infection offset the benefits of continued catheterization after 24 hours to 48 hours postoperatively.4, 7, 10 Patients with catheters greater than 2 postoperative days had a 21% increased likelihood of in‐hospital UTI, increased 30‐day mortality, and decreased odds of discharge to home.9

To address the risk of CAUTI associated with excess urinary catheter days, The Centers for Medicare and Medicaid Services' (CMS) Surgical Care Improvement Project (SCIP) added catheter removal on postoperative day 1 or 2 to its process measure set beginning in October 2009. SCIP is 1 of several high‐profile surgical quality improvement programs that employs performance audit and feedback of patient‐level process or outcome measures to address deficiencies in surgical care.11, 12 In addition, audit and feedback of CAUTI rates has been used to successfully reduce CAUTIs in medical‐surgical patients.13 The goal of our study was to audit patient‐level postoperative urinary catheter duration and measure the impact of its feedback to nursing staff on postoperative catheter duration, CAUTI rates, and nurse's attitudes about CAUTI prevention.

Methods

Results

During the study period there were a total of 1657 surgeries on the 2 study units during the baseline and follow‐up periods. After exclusions for urologic or gynecologic surgery (271), no indwelling catheter for surgery (505), or first surgery of 2 or more during the hospitalization (31), there were 846 eligible surgeries (51%).

Table 1 describes the population for the baseline and follow‐up periods for orthopedic and general surgery patients. Within each unit, the surgical populations were comparable during the baseline and follow‐up periods with the exception that the mean length of stay for eligible general surgery patients was significantly shorter in the baseline period as compared to the follow‐up period (6.6 vs. 8.5 days, P = 0.02). Cases on the orthopedic surgery unit were predominantly knee, hip and spine surgeries (85.9%), while those on the general surgery unit were predominantly gut and other gastrointestinal (GI) procedures (80.3%).

BaselineFollow‐Up Comparison

Table 3 describes the measures of urinary catheter use for each surgical population for both data collection periods. On both units, measures of catheter duration were improved following the education and feedback intervention. For the orthopedic unit, mean postoperative catheter duration was reduced from 1.7 to 1.4 days (P = 0.01) and the proportion of patients with catheter removal before day 3 was increased from 86% to 92% (P = 0.04). For the general surgery unit, mean postoperative catheter duration was reduced from 2.6 to 2.2 days (P = 0.01) and the proportion of patients with catheter removal before day 3 was increased from 56% to 63% (P = 0.14). When the general surgery measures were adjusted to account for the difference in length of stay between the 2 time periods, the odds of meeting the performance measure at follow‐up compared to baseline increased from unadjusted odds of 1.38 (P = 0.14) to adjusted odds of 1.69 (P = 0.02).

Table 3.Measures of Indwelling Urinary Catheter Duration and CAUTI Rates

Measure	Orthopedic Surgery			General Surgery
	Baseline, n = 206	Follow‐Up, n = 290	P Value	Baseline, n = 167	Follow‐Up, n = 183	P Value
Abbreviations: CAUTI, catheter‐associated urinary tract infection; ns, not sufficient; SD, standard deviation.
Postoperative catheter duration in days (mean, SD)	1.70 (1.24)	1.44 (0.85)	0.01	2.64 (1.85)	2.19 (1.40)	0.01
Postoperative catheter duration performance measure (%)	86	92	0.04	56	63	0.14
Total catheter days	350	418		441	401
Catheter days/1000 hospital days	423	394	ns*	398	259	s*
Catheter‐associated UTIs	3	0		3	3
Catheter‐associated UTI rate (infections/1000 device days)	8.6	0	ns*	6.8	7.5	ns*

Figure 1a and b are histograms of the frequency of cases having a given postoperative catheter duration in days. The dark bars show the baseline distribution and the light bars show the follow‐up distribution. Although the number of patients in the follow‐up period is greater than for the baseline period for the orthopedic surgery cohort, the images are instructive. In both groups of patients, but most notably in the general surgery population, the reduction in catheter measures resulted from a left shift in the frequency distribution, both for the longer duration outliers (removing the tail of each plot) and for the shorter duration catheters (3 days), increasing the proportion of catheters removed on postoperative day 1.

Figure 1

Discussion

This preobservational and postobservational study found that audit and feedback of patient‐level postoperative urinary catheter duration delivered in the context of an educational intervention and brainstorming session was temporally associated with clinically meaningful reductions in urinary catheter duration. In so doing, we demonstrated the feasibility of collecting patient level urinary catheter duration, and delivering it in a manner that had utility for frontline staff. Our results are consistent with the quality improvement literature which demonstrates that audit and feedback is a successful quality improvement strategy in many contexts and may be as good as more complex interventions at increasing adherence to the performance of process measures for surgical infection prevention.14 Two large national programs, the VA National Surgical Quality Improvement Program (NSQIP) and SCIP, use audit and feedback as the backbone of their large‐scale quality improvement strategies with promising results.11, 12

Given that the 2 study units were so different in practice patterns regarding urinary catheter management and nursing‐identified barriers to evidence‐based care, this work suggests that urinary catheter management may pose unique challenges for different clinical areas and provides a caution that one‐size‐fits‐all interventions for the rationalization of urinary catheter management and reduction of CAUTIs may be of limited effectiveness in the absence of local tailoring. As such, audit and feedback is well‐suited to this purpose as more proscriptive quality improvement strategies may meet with a variety of implementation challenges.

The impact of our intervention on CAUTI rates was not significant. There are several possible explanations for this finding. First, the study was not powered to detect a difference in CAUTI rates given the low infection rate at our institution. However, we cannot exclude the possibility that a reduction in mean catheter duration of one‐third to one‐half of a day is insufficient to impact CAUTI rates in postoperative patients, particularly when many of the follow‐up patients still had postoperative catheter duration 2 daysthe timeframe beyond which bacterial colonization of the catheter begins. While both study units had similar increases in postoperative catheter duration, the UTI rate was only decreased in the orthopedic surgery group which had much higher rates of postoperative catheter duration 2 days at baseline.

In recent years, there has been a renewed focus on the eradication of hospital‐acquired infections prompted by intense interest from the public, federal and state legislators, and others.15, 16 The CMS has recently used the revamping of the Inpatient Prospective Payment System (IPPS) as an opportunity to align financial incentives so that reimbursements for claims with certain hospital‐acquired conditions, including CAUTIs, will be reduced to that of the reimbursement of the same claim without the presence of the complication.17 This move is just one of several strategies to motivate hospitals and clinicians to address the pervasive problem of hospital‐acquired infection.

As urinary catheters are intimately linked to hospital‐acquired UTI, a focus of reduction efforts on catheter use is appropriate. The National Quality Forum (NQF) endorsed a postoperative catheter duration quality measure which was incorporated by the CMS's SCIP in late 2009.18 As a result, every hospital in the country that performs surgery and participates in the Medicare program is now tasked with determining patient‐level urinary catheter duration for selected surgical patients. This move represents a departure from current recommendations from the Centers for Disease Control and Prevention (CDC) and its National Healthcare Safety Network19, 20 which endorse the measurement of a catheter utilization ratio (urinary catheter days/patient days) for patient care units, but does not endorse any patient‐level utilization measures. In this instance, the use of patient‐level data may be better suited to quality improvement interventions such as audit and feedback because of its clinical relevance to frontline providers. However, it may also increase the data collection burden on hospitals. Notably, the measurement of postoperative catheter duration in this study was semiautomated using queries of an EHR. Such an approach can significantly reduce the data collection burden for this process measure and is consistent with national initiatives to integrate EHRs with quality improvement initiatives going forward.21

Our study has several limitations. This study took place in the year following the announcement of a high profile Medicare rule change regarding payment for hospital‐acquired harms. Certainly, the uncontrolled prestudy and poststudy design does not allow for the assessment of the impact of our intervention independent of this context. We are unable, therefore, to attribute the observed reduction solely to the intervention. Additionally, we did not follow postoperative urinary catheter duration beyond the immediate follow‐up period. It is anticipated that the impact of an audit and feedback intervention may diminish over time without a mechanism for repeated feedback. Certainly the sustainability of such repeated feedback in a single institution would be improved with an appropriately configured EHR.

In addition, we have reliable data on catheter reinsertions only from the follow‐up period. While the rates of reinsertions we recorded (0.7% on orthopedic surgery and 2.7% on general surgery) were lower than expected based on the literature,22 we are unable to determine if our intervention led to increases in postoperative urinary retention.

This study was limited to 2 surgical units of a single academic medical center and therefore the urinary catheter utilization patterns may not be representative of other patient populations at other institutions. However, the urinary catheter patterns were comparable to those identified in our prior work in a national sample of Medicare patients undergoing elective surgery.9

Finally, the field of CAUTI prevention has evolved rapidly since this study was performed. In particular, the surveillance definition of CAUTI was altered twice by the CDC in December of 2008 and March of 2009. In addition, the Infectious Diseases Society of America issued a new definition of CAUTI in February of 2010.23 All of these changes highlight the difference between asymptomatic bateriuria (ASB) and symptomatic CAUTI. However, the surveillance definition in use at the time of this study did not make this distinction. Therefore, we are unable to comment on the relative occurrence of ASB versus symptomatic CAUTI under the new definitions.

Rational urinary catheter use is a central component of CAUTI prevention efforts.24 We describe the use of patient‐level urinary catheter use in an audit and feedback intervention to frontline staff that was associated with reductions in urinary catheter duration. To do so, we employed a methodology for tracking urinary catheter use patterns that can provide important data for infection preventionists and frontline providers in efforts to improve urinary output management. This promising approach merits further study as an adjunct to current efforts to rationalize urinary catheter utilization and reduce CAUTIs. In the current environment, having the right data is a powerful aide for ongoing performance improvement.

The ubiquitous urinary catheter is associated with 80% of hospital‐acquired urinary tract infections (UTIs)1estimated to number one million annuallyaccounting for 40% of all nosocomial infections.2, 3 The clinical consequences of these catheter‐associated urinary tract infections (CAUTIs) are substantial and include prolonged hospital stay, bacteremia, and death.4 Despite the known risks of CAUTIs, it is estimated that 25% of hospitalized patients receive urinary catheters and that inappropriate urinary catheter use is widespread.5 Among catheterized patients, catheter duration is the most important modifiable risk factor for CAUTI. The excess risk of any bacteriuria accrues at a rate of 5% per catheter‐day beyond the first 48 hours of catheterization.6, 7 The reduction of catheter‐days for a given patient is an important component of quality improvement efforts to reduce CAUTIs. Unfortunately, as of a 2005 survey, most hospitals do not systematically track urinary catheter insertions and removals.8

The above concerns are highlighted for surgical patients among whom indwelling urinary catheter use is particularly high. In a 2001 sample of Medicare beneficiaries, 85% of major surgical patients had perioperative urinary catheters.9 In this population, postoperative catheter duration exceeded 48 hours in nearly 50%, despite concern that the risks of infection offset the benefits of continued catheterization after 24 hours to 48 hours postoperatively.4, 7, 10 Patients with catheters greater than 2 postoperative days had a 21% increased likelihood of in‐hospital UTI, increased 30‐day mortality, and decreased odds of discharge to home.9

To address the risk of CAUTI associated with excess urinary catheter days, The Centers for Medicare and Medicaid Services' (CMS) Surgical Care Improvement Project (SCIP) added catheter removal on postoperative day 1 or 2 to its process measure set beginning in October 2009. SCIP is 1 of several high‐profile surgical quality improvement programs that employs performance audit and feedback of patient‐level process or outcome measures to address deficiencies in surgical care.11, 12 In addition, audit and feedback of CAUTI rates has been used to successfully reduce CAUTIs in medical‐surgical patients.13 The goal of our study was to audit patient‐level postoperative urinary catheter duration and measure the impact of its feedback to nursing staff on postoperative catheter duration, CAUTI rates, and nurse's attitudes about CAUTI prevention.

Methods

Results

During the study period there were a total of 1657 surgeries on the 2 study units during the baseline and follow‐up periods. After exclusions for urologic or gynecologic surgery (271), no indwelling catheter for surgery (505), or first surgery of 2 or more during the hospitalization (31), there were 846 eligible surgeries (51%).

Table 1 describes the population for the baseline and follow‐up periods for orthopedic and general surgery patients. Within each unit, the surgical populations were comparable during the baseline and follow‐up periods with the exception that the mean length of stay for eligible general surgery patients was significantly shorter in the baseline period as compared to the follow‐up period (6.6 vs. 8.5 days, P = 0.02). Cases on the orthopedic surgery unit were predominantly knee, hip and spine surgeries (85.9%), while those on the general surgery unit were predominantly gut and other gastrointestinal (GI) procedures (80.3%).

BaselineFollow‐Up Comparison

Table 3 describes the measures of urinary catheter use for each surgical population for both data collection periods. On both units, measures of catheter duration were improved following the education and feedback intervention. For the orthopedic unit, mean postoperative catheter duration was reduced from 1.7 to 1.4 days (P = 0.01) and the proportion of patients with catheter removal before day 3 was increased from 86% to 92% (P = 0.04). For the general surgery unit, mean postoperative catheter duration was reduced from 2.6 to 2.2 days (P = 0.01) and the proportion of patients with catheter removal before day 3 was increased from 56% to 63% (P = 0.14). When the general surgery measures were adjusted to account for the difference in length of stay between the 2 time periods, the odds of meeting the performance measure at follow‐up compared to baseline increased from unadjusted odds of 1.38 (P = 0.14) to adjusted odds of 1.69 (P = 0.02).

Table 3.Measures of Indwelling Urinary Catheter Duration and CAUTI Rates

Measure	Orthopedic Surgery			General Surgery
	Baseline, n = 206	Follow‐Up, n = 290	P Value	Baseline, n = 167	Follow‐Up, n = 183	P Value
Abbreviations: CAUTI, catheter‐associated urinary tract infection; ns, not sufficient; SD, standard deviation.
Postoperative catheter duration in days (mean, SD)	1.70 (1.24)	1.44 (0.85)	0.01	2.64 (1.85)	2.19 (1.40)	0.01
Postoperative catheter duration performance measure (%)	86	92	0.04	56	63	0.14
Total catheter days	350	418		441	401
Catheter days/1000 hospital days	423	394	ns*	398	259	s*
Catheter‐associated UTIs	3	0		3	3
Catheter‐associated UTI rate (infections/1000 device days)	8.6	0	ns*	6.8	7.5	ns*

Figure 1a and b are histograms of the frequency of cases having a given postoperative catheter duration in days. The dark bars show the baseline distribution and the light bars show the follow‐up distribution. Although the number of patients in the follow‐up period is greater than for the baseline period for the orthopedic surgery cohort, the images are instructive. In both groups of patients, but most notably in the general surgery population, the reduction in catheter measures resulted from a left shift in the frequency distribution, both for the longer duration outliers (removing the tail of each plot) and for the shorter duration catheters (3 days), increasing the proportion of catheters removed on postoperative day 1.

Figure 1

Discussion

This preobservational and postobservational study found that audit and feedback of patient‐level postoperative urinary catheter duration delivered in the context of an educational intervention and brainstorming session was temporally associated with clinically meaningful reductions in urinary catheter duration. In so doing, we demonstrated the feasibility of collecting patient level urinary catheter duration, and delivering it in a manner that had utility for frontline staff. Our results are consistent with the quality improvement literature which demonstrates that audit and feedback is a successful quality improvement strategy in many contexts and may be as good as more complex interventions at increasing adherence to the performance of process measures for surgical infection prevention.14 Two large national programs, the VA National Surgical Quality Improvement Program (NSQIP) and SCIP, use audit and feedback as the backbone of their large‐scale quality improvement strategies with promising results.11, 12

Given that the 2 study units were so different in practice patterns regarding urinary catheter management and nursing‐identified barriers to evidence‐based care, this work suggests that urinary catheter management may pose unique challenges for different clinical areas and provides a caution that one‐size‐fits‐all interventions for the rationalization of urinary catheter management and reduction of CAUTIs may be of limited effectiveness in the absence of local tailoring. As such, audit and feedback is well‐suited to this purpose as more proscriptive quality improvement strategies may meet with a variety of implementation challenges.

The impact of our intervention on CAUTI rates was not significant. There are several possible explanations for this finding. First, the study was not powered to detect a difference in CAUTI rates given the low infection rate at our institution. However, we cannot exclude the possibility that a reduction in mean catheter duration of one‐third to one‐half of a day is insufficient to impact CAUTI rates in postoperative patients, particularly when many of the follow‐up patients still had postoperative catheter duration 2 daysthe timeframe beyond which bacterial colonization of the catheter begins. While both study units had similar increases in postoperative catheter duration, the UTI rate was only decreased in the orthopedic surgery group which had much higher rates of postoperative catheter duration 2 days at baseline.

In recent years, there has been a renewed focus on the eradication of hospital‐acquired infections prompted by intense interest from the public, federal and state legislators, and others.15, 16 The CMS has recently used the revamping of the Inpatient Prospective Payment System (IPPS) as an opportunity to align financial incentives so that reimbursements for claims with certain hospital‐acquired conditions, including CAUTIs, will be reduced to that of the reimbursement of the same claim without the presence of the complication.17 This move is just one of several strategies to motivate hospitals and clinicians to address the pervasive problem of hospital‐acquired infection.

As urinary catheters are intimately linked to hospital‐acquired UTI, a focus of reduction efforts on catheter use is appropriate. The National Quality Forum (NQF) endorsed a postoperative catheter duration quality measure which was incorporated by the CMS's SCIP in late 2009.18 As a result, every hospital in the country that performs surgery and participates in the Medicare program is now tasked with determining patient‐level urinary catheter duration for selected surgical patients. This move represents a departure from current recommendations from the Centers for Disease Control and Prevention (CDC) and its National Healthcare Safety Network19, 20 which endorse the measurement of a catheter utilization ratio (urinary catheter days/patient days) for patient care units, but does not endorse any patient‐level utilization measures. In this instance, the use of patient‐level data may be better suited to quality improvement interventions such as audit and feedback because of its clinical relevance to frontline providers. However, it may also increase the data collection burden on hospitals. Notably, the measurement of postoperative catheter duration in this study was semiautomated using queries of an EHR. Such an approach can significantly reduce the data collection burden for this process measure and is consistent with national initiatives to integrate EHRs with quality improvement initiatives going forward.21

Our study has several limitations. This study took place in the year following the announcement of a high profile Medicare rule change regarding payment for hospital‐acquired harms. Certainly, the uncontrolled prestudy and poststudy design does not allow for the assessment of the impact of our intervention independent of this context. We are unable, therefore, to attribute the observed reduction solely to the intervention. Additionally, we did not follow postoperative urinary catheter duration beyond the immediate follow‐up period. It is anticipated that the impact of an audit and feedback intervention may diminish over time without a mechanism for repeated feedback. Certainly the sustainability of such repeated feedback in a single institution would be improved with an appropriately configured EHR.

In addition, we have reliable data on catheter reinsertions only from the follow‐up period. While the rates of reinsertions we recorded (0.7% on orthopedic surgery and 2.7% on general surgery) were lower than expected based on the literature,22 we are unable to determine if our intervention led to increases in postoperative urinary retention.

This study was limited to 2 surgical units of a single academic medical center and therefore the urinary catheter utilization patterns may not be representative of other patient populations at other institutions. However, the urinary catheter patterns were comparable to those identified in our prior work in a national sample of Medicare patients undergoing elective surgery.9

Finally, the field of CAUTI prevention has evolved rapidly since this study was performed. In particular, the surveillance definition of CAUTI was altered twice by the CDC in December of 2008 and March of 2009. In addition, the Infectious Diseases Society of America issued a new definition of CAUTI in February of 2010.23 All of these changes highlight the difference between asymptomatic bateriuria (ASB) and symptomatic CAUTI. However, the surveillance definition in use at the time of this study did not make this distinction. Therefore, we are unable to comment on the relative occurrence of ASB versus symptomatic CAUTI under the new definitions.

Rational urinary catheter use is a central component of CAUTI prevention efforts.24 We describe the use of patient‐level urinary catheter use in an audit and feedback intervention to frontline staff that was associated with reductions in urinary catheter duration. To do so, we employed a methodology for tracking urinary catheter use patterns that can provide important data for infection preventionists and frontline providers in efforts to improve urinary output management. This promising approach merits further study as an adjunct to current efforts to rationalize urinary catheter utilization and reduce CAUTIs. In the current environment, having the right data is a powerful aide for ongoing performance improvement.

Many people date the start of the hospitalist field to my 1996 New England Journal of Medicine article,1 which first introduced the concept to a broad audience. That makes 2011 the field's 15th year, andif you have kidsyou know this is a tough and exciting age. The cuteness of childhood has faded, and bad decisions can no longer be excused as youthful indiscretions.

That's an apt metaphor for our field as we celebrate our 15th birthday. We are now an established part of the health care landscape, with a clear place in the House of Medicine. All of the measures of a successful specialty are ours: a thriving professional society, high‐quality training programs, increasingly robust research, a flourishing journal, and more. The field has truly arrived.

But these successes are also tempered by several challenges that have become more evident in recent years. In this article, I'll reflect on some of these successes and challenges.

The Hospitalist Field's Successes and Growth

In our 1996 article, Goldman and I1 wrote about the forces promoting the hospitalist model:

When we cited the search for value as a driving force in 1996, we were a bit ahead of our time, since there was relatively little skin in this game at the time. Remember that when our field launched, none of these value‐promoting forces existed: robust unannounced hospital inspections by the Joint Commission, public reporting of quality data, pay for performance, no pay for errors, state reporting of sentinel events, and more. In other words, until recently, neither a hospital's income stream nor its reputation was threatened by poor performance.

But this landscape is undergoing a sea change. By 2015, fully 9% of a hospital's Medicare reimbursements will be at risk through a variety of initiatives, including value‐based purchasing and meaningful use standards. And private payers are beginning to replicate Medicare's standards, particularly when they perceive that they may lead to both improved quality and lower costs.

Hospitals and health systems increasingly recognize how indispensable hospitalists can be as they demonstrate that their presence improves value. But this is only one of the forces driving the fieldalready the fastest growing specialty in medical historyto even higher levels of growth. These others include: the exodus of primary care physicians from the hospital, the fact that the specialists have left the building, comanagement of nonmedical patients, new opportunities in systems leadership, and dealing with housestaff duty hours reductions. I'll say a word about each.

Challenges for Hospitalist Programs

These powerful forces promoting the growth in the hospitalist field continue to ensure that hospitalists are in high demand. As a practical matter, this has resulted in increasing salaries and improved job conditions for hospitalists.

But this growth brings many challenges. Many hospitalist programs are poorly managed, often because the leaders lack the training and experience to effectively run such a rapidly growing and complex enterprise. One manifestation of these leadership challenges is that schedules are often created around the convenience and desires of the physicians rather than the needs of the patients. For example, the increasingly prevalent seven‐days‐on, seven‐days‐off schedule often leads to burnout and a feeling by the hospitalists that they are working too hard. Yet many groups are unwilling to consider modifications to the schedule that might decrease the intensity, if the cost is fewer days off.

On the other hand, some groups pay little attention to patient continuity in constructing their schedules. I know of programs that schedule their hospitalists in 24‐hour shifts (followed by a few days off), which means that admitted patients will see a different hospitalist every day. I see this as highly problematic, particularly because the most common complaint I hear from patients about hospitalist programs is that I saw a different doctor every day.

Many of the field's challenges stem from hospitalists' near‐total dependency on hospital funding to create sustainable job descriptions.11 While I continue to believe that this bit of financial happenstance has been good for both hospitalists and hospitalssince it has driven uncommon degrees of interdependency and alignmentit does mean that a difficult budget battle is virtually assured every year. As hospital finances become tighter, one can expect these battles to grow even more heated. Speaking for hospitalists, I am not too worried about the outcomes of these battles, since hospitalists provide a mission‐critical service at a fair price, there are no viable lower‐priced replacements (expect perhaps for nonphysician providers such as nurse practitioners for the less‐complex patients), and hospitalists are extraordinarily mobilethere are virtually no barriers for a hospitalist, or an entire group, to transfer to another institution. Nevertheless, it seems inevitable that these battles will leave scars, scars that may ultimately compromise the crucial collaboration that both hospitalists and hospitals depend on.

The Bottom Line

Even at age 15, an age at which many adolescents are irredeemably cynical, the hospitalist field retains much of its sense of limitless possibility and exuberance. This is not because things are perfectthey are not. Some hospitalist jobs are poorly constructed, some groups have poor leadership, some hospitalists are burning out, there are examples of spotty quality and collaboration, and hospitalists continue to have to work to earn the respect of colleagues and patients that other specialists take for granted.

That said, the field of hospital medicine remains uniquely exciting, in part because it is so tightly linked to the broader changes in the health care policy landscape. Many other specialties see the profound changes underway in health care as an existential threat to their professional values and incomes. Hospitalists, on the other hand, see these changes as raising the pressure on hospitals to deliver the highest quality, most satisfying, and safest care at the lowest cost. Framed this way, forward‐thinking hospitalists quite naturally see these changes as yet another catalyst for the growth and indispensability of their field.

Many people date the start of the hospitalist field to my 1996 New England Journal of Medicine article,1 which first introduced the concept to a broad audience. That makes 2011 the field's 15th year, andif you have kidsyou know this is a tough and exciting age. The cuteness of childhood has faded, and bad decisions can no longer be excused as youthful indiscretions.

That's an apt metaphor for our field as we celebrate our 15th birthday. We are now an established part of the health care landscape, with a clear place in the House of Medicine. All of the measures of a successful specialty are ours: a thriving professional society, high‐quality training programs, increasingly robust research, a flourishing journal, and more. The field has truly arrived.

But these successes are also tempered by several challenges that have become more evident in recent years. In this article, I'll reflect on some of these successes and challenges.

The Hospitalist Field's Successes and Growth

In our 1996 article, Goldman and I1 wrote about the forces promoting the hospitalist model:

When we cited the search for value as a driving force in 1996, we were a bit ahead of our time, since there was relatively little skin in this game at the time. Remember that when our field launched, none of these value‐promoting forces existed: robust unannounced hospital inspections by the Joint Commission, public reporting of quality data, pay for performance, no pay for errors, state reporting of sentinel events, and more. In other words, until recently, neither a hospital's income stream nor its reputation was threatened by poor performance.

But this landscape is undergoing a sea change. By 2015, fully 9% of a hospital's Medicare reimbursements will be at risk through a variety of initiatives, including value‐based purchasing and meaningful use standards. And private payers are beginning to replicate Medicare's standards, particularly when they perceive that they may lead to both improved quality and lower costs.

Hospitals and health systems increasingly recognize how indispensable hospitalists can be as they demonstrate that their presence improves value. But this is only one of the forces driving the fieldalready the fastest growing specialty in medical historyto even higher levels of growth. These others include: the exodus of primary care physicians from the hospital, the fact that the specialists have left the building, comanagement of nonmedical patients, new opportunities in systems leadership, and dealing with housestaff duty hours reductions. I'll say a word about each.

Challenges for Hospitalist Programs

These powerful forces promoting the growth in the hospitalist field continue to ensure that hospitalists are in high demand. As a practical matter, this has resulted in increasing salaries and improved job conditions for hospitalists.

But this growth brings many challenges. Many hospitalist programs are poorly managed, often because the leaders lack the training and experience to effectively run such a rapidly growing and complex enterprise. One manifestation of these leadership challenges is that schedules are often created around the convenience and desires of the physicians rather than the needs of the patients. For example, the increasingly prevalent seven‐days‐on, seven‐days‐off schedule often leads to burnout and a feeling by the hospitalists that they are working too hard. Yet many groups are unwilling to consider modifications to the schedule that might decrease the intensity, if the cost is fewer days off.

On the other hand, some groups pay little attention to patient continuity in constructing their schedules. I know of programs that schedule their hospitalists in 24‐hour shifts (followed by a few days off), which means that admitted patients will see a different hospitalist every day. I see this as highly problematic, particularly because the most common complaint I hear from patients about hospitalist programs is that I saw a different doctor every day.

Many of the field's challenges stem from hospitalists' near‐total dependency on hospital funding to create sustainable job descriptions.11 While I continue to believe that this bit of financial happenstance has been good for both hospitalists and hospitalssince it has driven uncommon degrees of interdependency and alignmentit does mean that a difficult budget battle is virtually assured every year. As hospital finances become tighter, one can expect these battles to grow even more heated. Speaking for hospitalists, I am not too worried about the outcomes of these battles, since hospitalists provide a mission‐critical service at a fair price, there are no viable lower‐priced replacements (expect perhaps for nonphysician providers such as nurse practitioners for the less‐complex patients), and hospitalists are extraordinarily mobilethere are virtually no barriers for a hospitalist, or an entire group, to transfer to another institution. Nevertheless, it seems inevitable that these battles will leave scars, scars that may ultimately compromise the crucial collaboration that both hospitalists and hospitals depend on.

The Bottom Line

Even at age 15, an age at which many adolescents are irredeemably cynical, the hospitalist field retains much of its sense of limitless possibility and exuberance. This is not because things are perfectthey are not. Some hospitalist jobs are poorly constructed, some groups have poor leadership, some hospitalists are burning out, there are examples of spotty quality and collaboration, and hospitalists continue to have to work to earn the respect of colleagues and patients that other specialists take for granted.

That said, the field of hospital medicine remains uniquely exciting, in part because it is so tightly linked to the broader changes in the health care policy landscape. Many other specialties see the profound changes underway in health care as an existential threat to their professional values and incomes. Hospitalists, on the other hand, see these changes as raising the pressure on hospitals to deliver the highest quality, most satisfying, and safest care at the lowest cost. Framed this way, forward‐thinking hospitalists quite naturally see these changes as yet another catalyst for the growth and indispensability of their field.

Many people date the start of the hospitalist field to my 1996 New England Journal of Medicine article,1 which first introduced the concept to a broad audience. That makes 2011 the field's 15th year, andif you have kidsyou know this is a tough and exciting age. The cuteness of childhood has faded, and bad decisions can no longer be excused as youthful indiscretions.

That's an apt metaphor for our field as we celebrate our 15th birthday. We are now an established part of the health care landscape, with a clear place in the House of Medicine. All of the measures of a successful specialty are ours: a thriving professional society, high‐quality training programs, increasingly robust research, a flourishing journal, and more. The field has truly arrived.

But these successes are also tempered by several challenges that have become more evident in recent years. In this article, I'll reflect on some of these successes and challenges.

The Hospitalist Field's Successes and Growth

In our 1996 article, Goldman and I1 wrote about the forces promoting the hospitalist model:

When we cited the search for value as a driving force in 1996, we were a bit ahead of our time, since there was relatively little skin in this game at the time. Remember that when our field launched, none of these value‐promoting forces existed: robust unannounced hospital inspections by the Joint Commission, public reporting of quality data, pay for performance, no pay for errors, state reporting of sentinel events, and more. In other words, until recently, neither a hospital's income stream nor its reputation was threatened by poor performance.

But this landscape is undergoing a sea change. By 2015, fully 9% of a hospital's Medicare reimbursements will be at risk through a variety of initiatives, including value‐based purchasing and meaningful use standards. And private payers are beginning to replicate Medicare's standards, particularly when they perceive that they may lead to both improved quality and lower costs.

Hospitals and health systems increasingly recognize how indispensable hospitalists can be as they demonstrate that their presence improves value. But this is only one of the forces driving the fieldalready the fastest growing specialty in medical historyto even higher levels of growth. These others include: the exodus of primary care physicians from the hospital, the fact that the specialists have left the building, comanagement of nonmedical patients, new opportunities in systems leadership, and dealing with housestaff duty hours reductions. I'll say a word about each.

Challenges for Hospitalist Programs

These powerful forces promoting the growth in the hospitalist field continue to ensure that hospitalists are in high demand. As a practical matter, this has resulted in increasing salaries and improved job conditions for hospitalists.

But this growth brings many challenges. Many hospitalist programs are poorly managed, often because the leaders lack the training and experience to effectively run such a rapidly growing and complex enterprise. One manifestation of these leadership challenges is that schedules are often created around the convenience and desires of the physicians rather than the needs of the patients. For example, the increasingly prevalent seven‐days‐on, seven‐days‐off schedule often leads to burnout and a feeling by the hospitalists that they are working too hard. Yet many groups are unwilling to consider modifications to the schedule that might decrease the intensity, if the cost is fewer days off.

On the other hand, some groups pay little attention to patient continuity in constructing their schedules. I know of programs that schedule their hospitalists in 24‐hour shifts (followed by a few days off), which means that admitted patients will see a different hospitalist every day. I see this as highly problematic, particularly because the most common complaint I hear from patients about hospitalist programs is that I saw a different doctor every day.

Many of the field's challenges stem from hospitalists' near‐total dependency on hospital funding to create sustainable job descriptions.11 While I continue to believe that this bit of financial happenstance has been good for both hospitalists and hospitalssince it has driven uncommon degrees of interdependency and alignmentit does mean that a difficult budget battle is virtually assured every year. As hospital finances become tighter, one can expect these battles to grow even more heated. Speaking for hospitalists, I am not too worried about the outcomes of these battles, since hospitalists provide a mission‐critical service at a fair price, there are no viable lower‐priced replacements (expect perhaps for nonphysician providers such as nurse practitioners for the less‐complex patients), and hospitalists are extraordinarily mobilethere are virtually no barriers for a hospitalist, or an entire group, to transfer to another institution. Nevertheless, it seems inevitable that these battles will leave scars, scars that may ultimately compromise the crucial collaboration that both hospitalists and hospitals depend on.

The Bottom Line

Even at age 15, an age at which many adolescents are irredeemably cynical, the hospitalist field retains much of its sense of limitless possibility and exuberance. This is not because things are perfectthey are not. Some hospitalist jobs are poorly constructed, some groups have poor leadership, some hospitalists are burning out, there are examples of spotty quality and collaboration, and hospitalists continue to have to work to earn the respect of colleagues and patients that other specialists take for granted.

That said, the field of hospital medicine remains uniquely exciting, in part because it is so tightly linked to the broader changes in the health care policy landscape. Many other specialties see the profound changes underway in health care as an existential threat to their professional values and incomes. Hospitalists, on the other hand, see these changes as raising the pressure on hospitals to deliver the highest quality, most satisfying, and safest care at the lowest cost. Framed this way, forward‐thinking hospitalists quite naturally see these changes as yet another catalyst for the growth and indispensability of their field.

Venous thromboembolic events (VTE) are a significant cause of mortality in hospitalized medical and surgical patients.1, 2 The incidence of hospital‐acquired deep vein thrombosis (DVT) is 1040% among medical or general surgical patients in the absence of VTE prophylaxis.3 Approximately 5075% of these cases are preventable with appropriate prophylaxis.3, 4 To reduce hospital‐acquired VTE, the American College of Chest Physicians (ACCP) has published VTE prevention guidelines regularly since 1986. The latest version of the ACCP guidelines recommends that every hospital have an institution‐wide policy that encourages use of VTE prevention strategies. Nevertheless, current evidence demonstrates that VTE prophylaxis remains underutilized in at‐risk patients.5, 6 For example, the ENDORSE study showed that only 39% of at‐risk medical patients received appropriate VTE prophylaxis.6 A more recent study estimated that 58% of hospital‐acquired VTEs were preventable with appropriate prophylaxis utilization.7

Such data demonstrate that a quality gap exists between VTE prophylaxis guideline recommendations and actual practice. Such a gap highlights the need to identify barriers to appropriate implementation of systems‐based strategies aimed at preventing VTE. A presumed barrier for adherence to any VTE protocol is the complexity involved in performing individualized risk assessments.810 All VTE prophylaxis strategies require the clinician to risk‐stratify each patient, identify contraindications to a prophylaxis strategy, and select an accepted strategy. While many VTE risk assessment protocols exist, they tend to fall into two categories: 1) a point‐based system, and 2) a simplified tiered system. Point‐based clinical prediction rules have been advocated by Caprini and others.1115 Such approaches require the clinician to assign points during the identification of VTE risk factors. The clinician must add the points to determine a patient's cumulative VTE risk and use the points to classify that risk as low, moderate, or high. Such point‐based systems are generally considered complex and may underestimate VTE risk, potentially leading to underutilization of prophylaxis strategies.16

Studies have demonstrated that complexity introduces variation into the decision‐making process.17 As a result, both the ACCP and SHM advocate for simplifying the VTE risk assessment process.4, 18 To date, several studies have demonstrated that attending physicians and nurses can reliably apply a VTE risk assessment tool, but none that measure how reliably residents can perform this task when using a point‐based tool.18, 19 For academic medical centers, information about the reliability of such tools is especially important, since they will often be applied by physicians‐in‐training, who have limited knowledge and experience with VTE guidelines and risk assessment. The goal of our study, therefore, was to use clinical vignettes to determine the reliability and protocol adherence of medical residents' application of an adapted point‐based VTE risk assessment tool, independent of other interventions.

Methods

Development of the Risk Assessment Tool

A multispecialty team adapted existing individualized VTE risk assessment tools based on one developed by Caprini.11 The VTE tool (Fig. 1) was designed to assist residents in making two essential determinations prior to ordering a prophylaxis plan. The first determination was the calculation of a total risk score (070 points). This score was determined by identifying and assigning a point value to all medical and surgical risk factors, and summing the points into 3 categories: low (01 point), moderate (24 points), and high (>4 points) VTE risk. The second determination was to identify any contraindications to pharmacological prophylaxis. Like other nonvalidated tools, our tool divided contraindications into absolute or relative. After making these two determinations, residents were encouraged to order 1 of 6 VTE prophylaxis plans. These plans were intended to balance VTE risk against risk factors for bleeding due to prophylaxis.

Figure 1

Results

Twenty‐six medical residents attended the conference. Three residents left without submitting their assessments and were excluded from the analysis. Of the 23 residents included in the analysis, 15 (65%) were interns, 5 (22%) second‐year residents, and 3 (13%) third‐year residents. A maximum of 483 observations (21 clinical vignettes and 23 residents) was possible. Six (1%) risk stratifications were missing, and 14 (3%) VTE prophylaxis plans were missing. Therefore, out of a possible 483 paired assessments and plans, complete data existed for 95% (469) of the observations. Residents risk‐stratified the vignettes as low risk for 27% of cases, moderate risk for 38%, and high risk 34%. These differed from those of the lead author, who stratified proportionately more vignettes as high risk (Table 1).

Of those vignette patients stratified as high risk, 77% (128/166) received some form of prophylaxis. Of those stratified as moderate risk, 66% (121/183) received some form of prophylaxis. Finally, of those stratified as low risk, 15% (20/130) received some form of prophylaxis. To explore the impact of the disparity in risk assessments between residents and attending physicians, we used the lead author's assessments as the standard for comparison, and determined that only 64% (309/479) of the observations were risk‐stratified correctly. To emphasize further the potential negative impact of these misclassifications, we determined that appropriate plans would have occurred only 47% of the time. Analysis of these data via risk category showed that low‐risk patients received appropriate prophylaxis 84% of the time. However, protocol adherence for moderate and high‐risk patients occurred only 33 and 40% of the time, respectively (Table 2). Making the assumption that those vignette patients at moderate and high risk who only received mechanical prophylaxis had appropriate contraindications to heparin prophylaxis, protocol adherence remained low at 54 and 58%, respectively.

The ICC for the total risk score was 0.66, and the kappa coefficient for risk stratification was 0.51 (95% CI 0.50, 0.53), both of which represent moderate agreement. Absolute and relative contraindications were identified 12% (57/483) and 13% (61/483) of the time, respectively. The kappa scores for absolute and relative contraindications were 0.29 and 0.23, respectively. The kappa score for the VTE plan was 0.28 and represents only fair agreement (Table 2).

Subgroup analysis of the 15 intern participants for ICC for the risk score was 0.63. The kappa scores for risk stratification and VTE plan were 0.47 and 0.23, respectively. The kappa scores for senior residents represent aggregate data of 168 observations of second‐ and third‐year residents. For senior residents, the kappa scores for risk stratification and VTE plan were 0.61 and 0.35, respectively (Table 3).

Discussion

We performed this study to determine how reliably our medical residents could apply a point‐based VTE risk assessment tool, similar to those published previously.11 We observed that early in the academic year, our residents were not able to use this tool reliably. While our study does not evaluate the effects of audit and feedback, reminder alerts, or educational interventions, an important first step toward quality improvement in VTE prophylaxis is to reduce variability in risk assessment and decision making. In this endeavor, our results differ markedly from those in the literature. For instance, one study used 3 trained nurses to employ a similar risk assessment tool, and found an ICC of 0.98 for overall assessments of VTE risk, but did not report protocol adherence.19 Another study found inter‐rater reliability to be high among 5 physician observers (kappa scores of 0.81 and 0.90 for risk stratification and VTE plan, respectively).18 These two studies evaluated the performance of experienced evaluators who employed different and simpler VTE risk assessment tools. Our study determined that the inter‐rater reliability of risk assessment and VTE plan between residents using a point‐based VTE risk assessment tool was significantly lower, at 0.51 and 0.28, respectively. There was marked disparity between the lead author's and residents' risk assessments of those deemed to be at low and high risk (Table 1). While both determined approximately one‐third of the patient vignettes to be at moderate risk, the residents misclassified those at high risk in comparison with the author's assessments. This underestimation of VTE risk could lead to profound underprophylaxis in at‐risk patients. To the extent that our findings represent those in other teaching hospitals, such errors could hinder VTE quality improvement efforts in such institutions.

Previous studies that successfully improved VTE prophylaxis rates coupled a risk assessment tool with provider education as well as audit‐and‐feedback interventions.25, 26 In one study, provider education occurred on the first day of every month with an orientation to the hospital's recommended VTE prevention strategies.26 Another study sought to improve the rates of VTE prophylaxis in medical intensive care (MICU) patients without performing individualized risk assessment.27 Using only weekly graphic feedback and verbal reminders to the medical team, it showed an improvement in VTE prophylaxis for 1 year. A third study improved VTE prophylaxis adherence and reduced VTE at 90 days using only reminder alerts.28 Interestingly, several studies reduced the incidence of VTE without employing any patient risk stratification.29 These studies suggest that improvement in VTE prophylaxis rates could have occurred as result of audit‐and‐feedback or reminder systems and perhaps independent of the reliable application of a risk assessment tool.29 The studies that used risk assessment tools with layered interventions make it difficult to interpret whether the tool or the layered interventions were responsible for the improvement in VTE outcomes. Ours is the first study to evaluate how reliably residents can apply a tool independent of other interventions. With only fair to moderate resident agreement in patient risk assessment and VTE plan, our study suggests that the complexity of a point‐based risk assessment protocol (as opposed to a simplified three‐tiered approach) may affect resident prescriptive behavior.

As a result, our study corroborates two things: first, in medical centers that rely on residents to perform VTE prevention using individualized risk assessment, a multilayered approach for VTE prevention must occur. Second, a passively disseminated VTE protocol in the form of a pocket card will most likely not create a sustained improvement in VTE prophylaxis rates or reduce VTE.3035

When addressing certain aspects of quality improvement and safety, teaching hospitals must recognize that their efforts largely rely on resident performance. The 2009 National Resident Matching Program data indicate that there are 22,427 intern positions available in the United States. Often it is the resident's responsibility to perform risk assessments and provide prophylaxis, possibly using a tool that is too complex to apply reliably. Several studies have determined that 65% of medical errors were committed by interns and that 35‐44% of those errors resulted from knowledge deficits.3638 In order to best improve adherence to clinical guidelines, strategies that result in changing physician behavior need to be implemented, and can include but are not limited to the ones found in Figure 2.39 Ideally, teaching centers with computerized order entry should embed the risk assessment process as part of an admission/transfer order set, with a reminder alert. The alert would be activated when at‐risk patients do not receive appropriate prophylaxis. Most alert systems require hospitals to have computerized order entry, which has achieved only 20% market penetration in US hospitals.40, 41 Therefore, some hospitals employ, or intend to employ, passively disseminated risk assessment tools in the form of pocket cards or preprinted forms. These methods are estimated to improve prophylaxis by only 50% and are therefore not considered to be highly reliable strategies.3135

Figure 2

Our study demonstrates only fair to moderate reliability of a point‐based VTE risk assessment tool when used by residents independent of other strategies. It also suggests that residents underestimate those at high risk. In addition, our residents' protocol adherence was suboptimal and would have resulted in appropriate prophylaxis approximately 50% of the time in patients at moderate or high VTE risk. Therefore, when risk assessment tools such as ours are used, it is imperative that frequent education be combined with real‐time patient identification strategies as well as audit and feedback, a process called measure‐vention.13, 14 This is especially true when the risk assessment process is not linked to a reminder system as part of computer‐assisted order entry protocols.

A limitation of our study was the lack of a control group. Since all the residents in attendance received the same clinical vignettes, it would have been of interest to see how the risk assessment tool performed compared with residents who did not have access to the tool. However, based on average noon conference attendance, it would have been difficult to achieve an adequate number of observations to calculate credible ICC and kappa scores. Other limitations include the high number of interns who completed the vignettes compared with senior residents, and the lack of additional attending reviewers to score the vignettes prior to the session. Ideally, in determining the accuracy of protocol adherence, we would have compared residents' determinations with those of several experts who had used an adjudication process in the event of disagreement. In our ongoing work, we are collecting data from a representative sample of attending physicians at our hospital to compare their assessments both with each other and with those of the residents.

Another issue in our design was that the study presented only a limited amount of medical information in the vignettes. In actual clinical circumstances, the amount of historical information is greater and more complicated. One could argue that the artificiality of clinical vignettes is not an accurate representation of resident performance when ordering VTE prophylaxis. However, this approach limits case‐mix variation, so residents should have been able to reach similar conclusions with the information given. Thus the limited information should have maximized residents' intentions to prescribe VTE prophylaxis, and kappa scores would likely be lower in real clinical settings. Finally, our kappa scores were calculated based on aggregate data of interns and residents; however, interns comprised almost two‐thirds of the resident participants. As reported in the results section, intern inter‐rater reliability was slightly lower compared with the senior resident subgroup, suggesting that the variability may be a result of less clinical experience of the interns. However, the study was not powered to assess differences in kappa scores for level of training.

In conclusion, we determined the inter‐rater reliability of an individualized, point‐based VTE risk assessment tool when used by medical residents unfamiliar with its use. Our study showed that under conditions of minimal education, a point‐based VTE assessment tool achieves only fair to moderate reliability. It also suggests that as a stand‐alone tool without a reminder alert, adherence to VTE prevention guidelines is suboptimal and might result in underprophylaxis of hospitalized medical patients at moderate or high VTE risk. In fact, with appropriate prophylaxis, rates were maximally estimated to be 55% (Table 2). Because of the high percentage of interns in the study, these results approximate intern application of a VTE prevention protocol independent of other interventions. Comparing reliability data from our study with those of others raises the question of whether the observed differences in kappa score are because other studies used highly trained observers or because their protocols were less complex. However, a recent study validated a simpler method of VTE risk grouping that performs well regardless of clinical experience.20 Future studies are needed to determine whether there is improved resident inter‐rater reliability using a point‐based risk assessment tool that is embedded into a computerized order entry system with electronic reminder alerts. Finally, in actual clinical settings, the question remains of whether kappa scores correlate with protocol adherence, prophylaxis rates, and VTE reduction when using point‐based tools. If not, then the use of simplified risk‐stratification tools and VTE measure‐vention strategies should be implemented.

Venous thromboembolic events (VTE) are a significant cause of mortality in hospitalized medical and surgical patients.1, 2 The incidence of hospital‐acquired deep vein thrombosis (DVT) is 1040% among medical or general surgical patients in the absence of VTE prophylaxis.3 Approximately 5075% of these cases are preventable with appropriate prophylaxis.3, 4 To reduce hospital‐acquired VTE, the American College of Chest Physicians (ACCP) has published VTE prevention guidelines regularly since 1986. The latest version of the ACCP guidelines recommends that every hospital have an institution‐wide policy that encourages use of VTE prevention strategies. Nevertheless, current evidence demonstrates that VTE prophylaxis remains underutilized in at‐risk patients.5, 6 For example, the ENDORSE study showed that only 39% of at‐risk medical patients received appropriate VTE prophylaxis.6 A more recent study estimated that 58% of hospital‐acquired VTEs were preventable with appropriate prophylaxis utilization.7

Such data demonstrate that a quality gap exists between VTE prophylaxis guideline recommendations and actual practice. Such a gap highlights the need to identify barriers to appropriate implementation of systems‐based strategies aimed at preventing VTE. A presumed barrier for adherence to any VTE protocol is the complexity involved in performing individualized risk assessments.810 All VTE prophylaxis strategies require the clinician to risk‐stratify each patient, identify contraindications to a prophylaxis strategy, and select an accepted strategy. While many VTE risk assessment protocols exist, they tend to fall into two categories: 1) a point‐based system, and 2) a simplified tiered system. Point‐based clinical prediction rules have been advocated by Caprini and others.1115 Such approaches require the clinician to assign points during the identification of VTE risk factors. The clinician must add the points to determine a patient's cumulative VTE risk and use the points to classify that risk as low, moderate, or high. Such point‐based systems are generally considered complex and may underestimate VTE risk, potentially leading to underutilization of prophylaxis strategies.16

Studies have demonstrated that complexity introduces variation into the decision‐making process.17 As a result, both the ACCP and SHM advocate for simplifying the VTE risk assessment process.4, 18 To date, several studies have demonstrated that attending physicians and nurses can reliably apply a VTE risk assessment tool, but none that measure how reliably residents can perform this task when using a point‐based tool.18, 19 For academic medical centers, information about the reliability of such tools is especially important, since they will often be applied by physicians‐in‐training, who have limited knowledge and experience with VTE guidelines and risk assessment. The goal of our study, therefore, was to use clinical vignettes to determine the reliability and protocol adherence of medical residents' application of an adapted point‐based VTE risk assessment tool, independent of other interventions.

Methods

Development of the Risk Assessment Tool

A multispecialty team adapted existing individualized VTE risk assessment tools based on one developed by Caprini.11 The VTE tool (Fig. 1) was designed to assist residents in making two essential determinations prior to ordering a prophylaxis plan. The first determination was the calculation of a total risk score (070 points). This score was determined by identifying and assigning a point value to all medical and surgical risk factors, and summing the points into 3 categories: low (01 point), moderate (24 points), and high (>4 points) VTE risk. The second determination was to identify any contraindications to pharmacological prophylaxis. Like other nonvalidated tools, our tool divided contraindications into absolute or relative. After making these two determinations, residents were encouraged to order 1 of 6 VTE prophylaxis plans. These plans were intended to balance VTE risk against risk factors for bleeding due to prophylaxis.

Figure 1

Results

Twenty‐six medical residents attended the conference. Three residents left without submitting their assessments and were excluded from the analysis. Of the 23 residents included in the analysis, 15 (65%) were interns, 5 (22%) second‐year residents, and 3 (13%) third‐year residents. A maximum of 483 observations (21 clinical vignettes and 23 residents) was possible. Six (1%) risk stratifications were missing, and 14 (3%) VTE prophylaxis plans were missing. Therefore, out of a possible 483 paired assessments and plans, complete data existed for 95% (469) of the observations. Residents risk‐stratified the vignettes as low risk for 27% of cases, moderate risk for 38%, and high risk 34%. These differed from those of the lead author, who stratified proportionately more vignettes as high risk (Table 1).

Of those vignette patients stratified as high risk, 77% (128/166) received some form of prophylaxis. Of those stratified as moderate risk, 66% (121/183) received some form of prophylaxis. Finally, of those stratified as low risk, 15% (20/130) received some form of prophylaxis. To explore the impact of the disparity in risk assessments between residents and attending physicians, we used the lead author's assessments as the standard for comparison, and determined that only 64% (309/479) of the observations were risk‐stratified correctly. To emphasize further the potential negative impact of these misclassifications, we determined that appropriate plans would have occurred only 47% of the time. Analysis of these data via risk category showed that low‐risk patients received appropriate prophylaxis 84% of the time. However, protocol adherence for moderate and high‐risk patients occurred only 33 and 40% of the time, respectively (Table 2). Making the assumption that those vignette patients at moderate and high risk who only received mechanical prophylaxis had appropriate contraindications to heparin prophylaxis, protocol adherence remained low at 54 and 58%, respectively.

The ICC for the total risk score was 0.66, and the kappa coefficient for risk stratification was 0.51 (95% CI 0.50, 0.53), both of which represent moderate agreement. Absolute and relative contraindications were identified 12% (57/483) and 13% (61/483) of the time, respectively. The kappa scores for absolute and relative contraindications were 0.29 and 0.23, respectively. The kappa score for the VTE plan was 0.28 and represents only fair agreement (Table 2).

Subgroup analysis of the 15 intern participants for ICC for the risk score was 0.63. The kappa scores for risk stratification and VTE plan were 0.47 and 0.23, respectively. The kappa scores for senior residents represent aggregate data of 168 observations of second‐ and third‐year residents. For senior residents, the kappa scores for risk stratification and VTE plan were 0.61 and 0.35, respectively (Table 3).

Discussion

We performed this study to determine how reliably our medical residents could apply a point‐based VTE risk assessment tool, similar to those published previously.11 We observed that early in the academic year, our residents were not able to use this tool reliably. While our study does not evaluate the effects of audit and feedback, reminder alerts, or educational interventions, an important first step toward quality improvement in VTE prophylaxis is to reduce variability in risk assessment and decision making. In this endeavor, our results differ markedly from those in the literature. For instance, one study used 3 trained nurses to employ a similar risk assessment tool, and found an ICC of 0.98 for overall assessments of VTE risk, but did not report protocol adherence.19 Another study found inter‐rater reliability to be high among 5 physician observers (kappa scores of 0.81 and 0.90 for risk stratification and VTE plan, respectively).18 These two studies evaluated the performance of experienced evaluators who employed different and simpler VTE risk assessment tools. Our study determined that the inter‐rater reliability of risk assessment and VTE plan between residents using a point‐based VTE risk assessment tool was significantly lower, at 0.51 and 0.28, respectively. There was marked disparity between the lead author's and residents' risk assessments of those deemed to be at low and high risk (Table 1). While both determined approximately one‐third of the patient vignettes to be at moderate risk, the residents misclassified those at high risk in comparison with the author's assessments. This underestimation of VTE risk could lead to profound underprophylaxis in at‐risk patients. To the extent that our findings represent those in other teaching hospitals, such errors could hinder VTE quality improvement efforts in such institutions.

Previous studies that successfully improved VTE prophylaxis rates coupled a risk assessment tool with provider education as well as audit‐and‐feedback interventions.25, 26 In one study, provider education occurred on the first day of every month with an orientation to the hospital's recommended VTE prevention strategies.26 Another study sought to improve the rates of VTE prophylaxis in medical intensive care (MICU) patients without performing individualized risk assessment.27 Using only weekly graphic feedback and verbal reminders to the medical team, it showed an improvement in VTE prophylaxis for 1 year. A third study improved VTE prophylaxis adherence and reduced VTE at 90 days using only reminder alerts.28 Interestingly, several studies reduced the incidence of VTE without employing any patient risk stratification.29 These studies suggest that improvement in VTE prophylaxis rates could have occurred as result of audit‐and‐feedback or reminder systems and perhaps independent of the reliable application of a risk assessment tool.29 The studies that used risk assessment tools with layered interventions make it difficult to interpret whether the tool or the layered interventions were responsible for the improvement in VTE outcomes. Ours is the first study to evaluate how reliably residents can apply a tool independent of other interventions. With only fair to moderate resident agreement in patient risk assessment and VTE plan, our study suggests that the complexity of a point‐based risk assessment protocol (as opposed to a simplified three‐tiered approach) may affect resident prescriptive behavior.

As a result, our study corroborates two things: first, in medical centers that rely on residents to perform VTE prevention using individualized risk assessment, a multilayered approach for VTE prevention must occur. Second, a passively disseminated VTE protocol in the form of a pocket card will most likely not create a sustained improvement in VTE prophylaxis rates or reduce VTE.3035

When addressing certain aspects of quality improvement and safety, teaching hospitals must recognize that their efforts largely rely on resident performance. The 2009 National Resident Matching Program data indicate that there are 22,427 intern positions available in the United States. Often it is the resident's responsibility to perform risk assessments and provide prophylaxis, possibly using a tool that is too complex to apply reliably. Several studies have determined that 65% of medical errors were committed by interns and that 35‐44% of those errors resulted from knowledge deficits.3638 In order to best improve adherence to clinical guidelines, strategies that result in changing physician behavior need to be implemented, and can include but are not limited to the ones found in Figure 2.39 Ideally, teaching centers with computerized order entry should embed the risk assessment process as part of an admission/transfer order set, with a reminder alert. The alert would be activated when at‐risk patients do not receive appropriate prophylaxis. Most alert systems require hospitals to have computerized order entry, which has achieved only 20% market penetration in US hospitals.40, 41 Therefore, some hospitals employ, or intend to employ, passively disseminated risk assessment tools in the form of pocket cards or preprinted forms. These methods are estimated to improve prophylaxis by only 50% and are therefore not considered to be highly reliable strategies.3135

Figure 2

Our study demonstrates only fair to moderate reliability of a point‐based VTE risk assessment tool when used by residents independent of other strategies. It also suggests that residents underestimate those at high risk. In addition, our residents' protocol adherence was suboptimal and would have resulted in appropriate prophylaxis approximately 50% of the time in patients at moderate or high VTE risk. Therefore, when risk assessment tools such as ours are used, it is imperative that frequent education be combined with real‐time patient identification strategies as well as audit and feedback, a process called measure‐vention.13, 14 This is especially true when the risk assessment process is not linked to a reminder system as part of computer‐assisted order entry protocols.

A limitation of our study was the lack of a control group. Since all the residents in attendance received the same clinical vignettes, it would have been of interest to see how the risk assessment tool performed compared with residents who did not have access to the tool. However, based on average noon conference attendance, it would have been difficult to achieve an adequate number of observations to calculate credible ICC and kappa scores. Other limitations include the high number of interns who completed the vignettes compared with senior residents, and the lack of additional attending reviewers to score the vignettes prior to the session. Ideally, in determining the accuracy of protocol adherence, we would have compared residents' determinations with those of several experts who had used an adjudication process in the event of disagreement. In our ongoing work, we are collecting data from a representative sample of attending physicians at our hospital to compare their assessments both with each other and with those of the residents.

Another issue in our design was that the study presented only a limited amount of medical information in the vignettes. In actual clinical circumstances, the amount of historical information is greater and more complicated. One could argue that the artificiality of clinical vignettes is not an accurate representation of resident performance when ordering VTE prophylaxis. However, this approach limits case‐mix variation, so residents should have been able to reach similar conclusions with the information given. Thus the limited information should have maximized residents' intentions to prescribe VTE prophylaxis, and kappa scores would likely be lower in real clinical settings. Finally, our kappa scores were calculated based on aggregate data of interns and residents; however, interns comprised almost two‐thirds of the resident participants. As reported in the results section, intern inter‐rater reliability was slightly lower compared with the senior resident subgroup, suggesting that the variability may be a result of less clinical experience of the interns. However, the study was not powered to assess differences in kappa scores for level of training.

In conclusion, we determined the inter‐rater reliability of an individualized, point‐based VTE risk assessment tool when used by medical residents unfamiliar with its use. Our study showed that under conditions of minimal education, a point‐based VTE assessment tool achieves only fair to moderate reliability. It also suggests that as a stand‐alone tool without a reminder alert, adherence to VTE prevention guidelines is suboptimal and might result in underprophylaxis of hospitalized medical patients at moderate or high VTE risk. In fact, with appropriate prophylaxis, rates were maximally estimated to be 55% (Table 2). Because of the high percentage of interns in the study, these results approximate intern application of a VTE prevention protocol independent of other interventions. Comparing reliability data from our study with those of others raises the question of whether the observed differences in kappa score are because other studies used highly trained observers or because their protocols were less complex. However, a recent study validated a simpler method of VTE risk grouping that performs well regardless of clinical experience.20 Future studies are needed to determine whether there is improved resident inter‐rater reliability using a point‐based risk assessment tool that is embedded into a computerized order entry system with electronic reminder alerts. Finally, in actual clinical settings, the question remains of whether kappa scores correlate with protocol adherence, prophylaxis rates, and VTE reduction when using point‐based tools. If not, then the use of simplified risk‐stratification tools and VTE measure‐vention strategies should be implemented.

Venous thromboembolic events (VTE) are a significant cause of mortality in hospitalized medical and surgical patients.1, 2 The incidence of hospital‐acquired deep vein thrombosis (DVT) is 1040% among medical or general surgical patients in the absence of VTE prophylaxis.3 Approximately 5075% of these cases are preventable with appropriate prophylaxis.3, 4 To reduce hospital‐acquired VTE, the American College of Chest Physicians (ACCP) has published VTE prevention guidelines regularly since 1986. The latest version of the ACCP guidelines recommends that every hospital have an institution‐wide policy that encourages use of VTE prevention strategies. Nevertheless, current evidence demonstrates that VTE prophylaxis remains underutilized in at‐risk patients.5, 6 For example, the ENDORSE study showed that only 39% of at‐risk medical patients received appropriate VTE prophylaxis.6 A more recent study estimated that 58% of hospital‐acquired VTEs were preventable with appropriate prophylaxis utilization.7

Such data demonstrate that a quality gap exists between VTE prophylaxis guideline recommendations and actual practice. Such a gap highlights the need to identify barriers to appropriate implementation of systems‐based strategies aimed at preventing VTE. A presumed barrier for adherence to any VTE protocol is the complexity involved in performing individualized risk assessments.810 All VTE prophylaxis strategies require the clinician to risk‐stratify each patient, identify contraindications to a prophylaxis strategy, and select an accepted strategy. While many VTE risk assessment protocols exist, they tend to fall into two categories: 1) a point‐based system, and 2) a simplified tiered system. Point‐based clinical prediction rules have been advocated by Caprini and others.1115 Such approaches require the clinician to assign points during the identification of VTE risk factors. The clinician must add the points to determine a patient's cumulative VTE risk and use the points to classify that risk as low, moderate, or high. Such point‐based systems are generally considered complex and may underestimate VTE risk, potentially leading to underutilization of prophylaxis strategies.16

Studies have demonstrated that complexity introduces variation into the decision‐making process.17 As a result, both the ACCP and SHM advocate for simplifying the VTE risk assessment process.4, 18 To date, several studies have demonstrated that attending physicians and nurses can reliably apply a VTE risk assessment tool, but none that measure how reliably residents can perform this task when using a point‐based tool.18, 19 For academic medical centers, information about the reliability of such tools is especially important, since they will often be applied by physicians‐in‐training, who have limited knowledge and experience with VTE guidelines and risk assessment. The goal of our study, therefore, was to use clinical vignettes to determine the reliability and protocol adherence of medical residents' application of an adapted point‐based VTE risk assessment tool, independent of other interventions.

Methods

Development of the Risk Assessment Tool

A multispecialty team adapted existing individualized VTE risk assessment tools based on one developed by Caprini.11 The VTE tool (Fig. 1) was designed to assist residents in making two essential determinations prior to ordering a prophylaxis plan. The first determination was the calculation of a total risk score (070 points). This score was determined by identifying and assigning a point value to all medical and surgical risk factors, and summing the points into 3 categories: low (01 point), moderate (24 points), and high (>4 points) VTE risk. The second determination was to identify any contraindications to pharmacological prophylaxis. Like other nonvalidated tools, our tool divided contraindications into absolute or relative. After making these two determinations, residents were encouraged to order 1 of 6 VTE prophylaxis plans. These plans were intended to balance VTE risk against risk factors for bleeding due to prophylaxis.

Figure 1

Results

Twenty‐six medical residents attended the conference. Three residents left without submitting their assessments and were excluded from the analysis. Of the 23 residents included in the analysis, 15 (65%) were interns, 5 (22%) second‐year residents, and 3 (13%) third‐year residents. A maximum of 483 observations (21 clinical vignettes and 23 residents) was possible. Six (1%) risk stratifications were missing, and 14 (3%) VTE prophylaxis plans were missing. Therefore, out of a possible 483 paired assessments and plans, complete data existed for 95% (469) of the observations. Residents risk‐stratified the vignettes as low risk for 27% of cases, moderate risk for 38%, and high risk 34%. These differed from those of the lead author, who stratified proportionately more vignettes as high risk (Table 1).

Of those vignette patients stratified as high risk, 77% (128/166) received some form of prophylaxis. Of those stratified as moderate risk, 66% (121/183) received some form of prophylaxis. Finally, of those stratified as low risk, 15% (20/130) received some form of prophylaxis. To explore the impact of the disparity in risk assessments between residents and attending physicians, we used the lead author's assessments as the standard for comparison, and determined that only 64% (309/479) of the observations were risk‐stratified correctly. To emphasize further the potential negative impact of these misclassifications, we determined that appropriate plans would have occurred only 47% of the time. Analysis of these data via risk category showed that low‐risk patients received appropriate prophylaxis 84% of the time. However, protocol adherence for moderate and high‐risk patients occurred only 33 and 40% of the time, respectively (Table 2). Making the assumption that those vignette patients at moderate and high risk who only received mechanical prophylaxis had appropriate contraindications to heparin prophylaxis, protocol adherence remained low at 54 and 58%, respectively.

The ICC for the total risk score was 0.66, and the kappa coefficient for risk stratification was 0.51 (95% CI 0.50, 0.53), both of which represent moderate agreement. Absolute and relative contraindications were identified 12% (57/483) and 13% (61/483) of the time, respectively. The kappa scores for absolute and relative contraindications were 0.29 and 0.23, respectively. The kappa score for the VTE plan was 0.28 and represents only fair agreement (Table 2).

Subgroup analysis of the 15 intern participants for ICC for the risk score was 0.63. The kappa scores for risk stratification and VTE plan were 0.47 and 0.23, respectively. The kappa scores for senior residents represent aggregate data of 168 observations of second‐ and third‐year residents. For senior residents, the kappa scores for risk stratification and VTE plan were 0.61 and 0.35, respectively (Table 3).

Discussion

We performed this study to determine how reliably our medical residents could apply a point‐based VTE risk assessment tool, similar to those published previously.11 We observed that early in the academic year, our residents were not able to use this tool reliably. While our study does not evaluate the effects of audit and feedback, reminder alerts, or educational interventions, an important first step toward quality improvement in VTE prophylaxis is to reduce variability in risk assessment and decision making. In this endeavor, our results differ markedly from those in the literature. For instance, one study used 3 trained nurses to employ a similar risk assessment tool, and found an ICC of 0.98 for overall assessments of VTE risk, but did not report protocol adherence.19 Another study found inter‐rater reliability to be high among 5 physician observers (kappa scores of 0.81 and 0.90 for risk stratification and VTE plan, respectively).18 These two studies evaluated the performance of experienced evaluators who employed different and simpler VTE risk assessment tools. Our study determined that the inter‐rater reliability of risk assessment and VTE plan between residents using a point‐based VTE risk assessment tool was significantly lower, at 0.51 and 0.28, respectively. There was marked disparity between the lead author's and residents' risk assessments of those deemed to be at low and high risk (Table 1). While both determined approximately one‐third of the patient vignettes to be at moderate risk, the residents misclassified those at high risk in comparison with the author's assessments. This underestimation of VTE risk could lead to profound underprophylaxis in at‐risk patients. To the extent that our findings represent those in other teaching hospitals, such errors could hinder VTE quality improvement efforts in such institutions.

Previous studies that successfully improved VTE prophylaxis rates coupled a risk assessment tool with provider education as well as audit‐and‐feedback interventions.25, 26 In one study, provider education occurred on the first day of every month with an orientation to the hospital's recommended VTE prevention strategies.26 Another study sought to improve the rates of VTE prophylaxis in medical intensive care (MICU) patients without performing individualized risk assessment.27 Using only weekly graphic feedback and verbal reminders to the medical team, it showed an improvement in VTE prophylaxis for 1 year. A third study improved VTE prophylaxis adherence and reduced VTE at 90 days using only reminder alerts.28 Interestingly, several studies reduced the incidence of VTE without employing any patient risk stratification.29 These studies suggest that improvement in VTE prophylaxis rates could have occurred as result of audit‐and‐feedback or reminder systems and perhaps independent of the reliable application of a risk assessment tool.29 The studies that used risk assessment tools with layered interventions make it difficult to interpret whether the tool or the layered interventions were responsible for the improvement in VTE outcomes. Ours is the first study to evaluate how reliably residents can apply a tool independent of other interventions. With only fair to moderate resident agreement in patient risk assessment and VTE plan, our study suggests that the complexity of a point‐based risk assessment protocol (as opposed to a simplified three‐tiered approach) may affect resident prescriptive behavior.

As a result, our study corroborates two things: first, in medical centers that rely on residents to perform VTE prevention using individualized risk assessment, a multilayered approach for VTE prevention must occur. Second, a passively disseminated VTE protocol in the form of a pocket card will most likely not create a sustained improvement in VTE prophylaxis rates or reduce VTE.3035

When addressing certain aspects of quality improvement and safety, teaching hospitals must recognize that their efforts largely rely on resident performance. The 2009 National Resident Matching Program data indicate that there are 22,427 intern positions available in the United States. Often it is the resident's responsibility to perform risk assessments and provide prophylaxis, possibly using a tool that is too complex to apply reliably. Several studies have determined that 65% of medical errors were committed by interns and that 35‐44% of those errors resulted from knowledge deficits.3638 In order to best improve adherence to clinical guidelines, strategies that result in changing physician behavior need to be implemented, and can include but are not limited to the ones found in Figure 2.39 Ideally, teaching centers with computerized order entry should embed the risk assessment process as part of an admission/transfer order set, with a reminder alert. The alert would be activated when at‐risk patients do not receive appropriate prophylaxis. Most alert systems require hospitals to have computerized order entry, which has achieved only 20% market penetration in US hospitals.40, 41 Therefore, some hospitals employ, or intend to employ, passively disseminated risk assessment tools in the form of pocket cards or preprinted forms. These methods are estimated to improve prophylaxis by only 50% and are therefore not considered to be highly reliable strategies.3135

Figure 2

Our study demonstrates only fair to moderate reliability of a point‐based VTE risk assessment tool when used by residents independent of other strategies. It also suggests that residents underestimate those at high risk. In addition, our residents' protocol adherence was suboptimal and would have resulted in appropriate prophylaxis approximately 50% of the time in patients at moderate or high VTE risk. Therefore, when risk assessment tools such as ours are used, it is imperative that frequent education be combined with real‐time patient identification strategies as well as audit and feedback, a process called measure‐vention.13, 14 This is especially true when the risk assessment process is not linked to a reminder system as part of computer‐assisted order entry protocols.

A limitation of our study was the lack of a control group. Since all the residents in attendance received the same clinical vignettes, it would have been of interest to see how the risk assessment tool performed compared with residents who did not have access to the tool. However, based on average noon conference attendance, it would have been difficult to achieve an adequate number of observations to calculate credible ICC and kappa scores. Other limitations include the high number of interns who completed the vignettes compared with senior residents, and the lack of additional attending reviewers to score the vignettes prior to the session. Ideally, in determining the accuracy of protocol adherence, we would have compared residents' determinations with those of several experts who had used an adjudication process in the event of disagreement. In our ongoing work, we are collecting data from a representative sample of attending physicians at our hospital to compare their assessments both with each other and with those of the residents.

Another issue in our design was that the study presented only a limited amount of medical information in the vignettes. In actual clinical circumstances, the amount of historical information is greater and more complicated. One could argue that the artificiality of clinical vignettes is not an accurate representation of resident performance when ordering VTE prophylaxis. However, this approach limits case‐mix variation, so residents should have been able to reach similar conclusions with the information given. Thus the limited information should have maximized residents' intentions to prescribe VTE prophylaxis, and kappa scores would likely be lower in real clinical settings. Finally, our kappa scores were calculated based on aggregate data of interns and residents; however, interns comprised almost two‐thirds of the resident participants. As reported in the results section, intern inter‐rater reliability was slightly lower compared with the senior resident subgroup, suggesting that the variability may be a result of less clinical experience of the interns. However, the study was not powered to assess differences in kappa scores for level of training.

In conclusion, we determined the inter‐rater reliability of an individualized, point‐based VTE risk assessment tool when used by medical residents unfamiliar with its use. Our study showed that under conditions of minimal education, a point‐based VTE assessment tool achieves only fair to moderate reliability. It also suggests that as a stand‐alone tool without a reminder alert, adherence to VTE prevention guidelines is suboptimal and might result in underprophylaxis of hospitalized medical patients at moderate or high VTE risk. In fact, with appropriate prophylaxis, rates were maximally estimated to be 55% (Table 2). Because of the high percentage of interns in the study, these results approximate intern application of a VTE prevention protocol independent of other interventions. Comparing reliability data from our study with those of others raises the question of whether the observed differences in kappa score are because other studies used highly trained observers or because their protocols were less complex. However, a recent study validated a simpler method of VTE risk grouping that performs well regardless of clinical experience.20 Future studies are needed to determine whether there is improved resident inter‐rater reliability using a point‐based risk assessment tool that is embedded into a computerized order entry system with electronic reminder alerts. Finally, in actual clinical settings, the question remains of whether kappa scores correlate with protocol adherence, prophylaxis rates, and VTE reduction when using point‐based tools. If not, then the use of simplified risk‐stratification tools and VTE measure‐vention strategies should be implemented.

In October, a 36‐year‐old woman with no significant past medical history presented to the Emergency Department (ED) with a 3‐day history of headache and fever. The headache was severe, throbbing, and frontal in location. She also complained of daily fevers measured up to 103F, generalized malaise, and fatigue. She did not report neck stiffness or photophobia. She felt better after receiving intravenous fluids and was discharged home with a diagnosis of a nonspecific viral illness. Two days later, she returned to the ED with worsening headache, fever, mild photophobia, and poor oral intake. She also complained of a dry cough that made her headache worse, as did bending over. She did not report confusion, neck stiffness, shortness of breath, sore throat, runny nose, abdominal symptoms, or rash.

This patient presents a second time to the ED with worsening headache and fever raising concerns about meningitis. At the time of her first ED visit, it can be assumed that she had a nontoxic appearance because she was discharged shortly thereafter. Thus, acute bacterial meningitis seems less likely, but occasionally patients with meningococcal meningitis may not appear significantly ill until later in the process. Nonetheless, acute meningitis, possibly viral, is the initial concern. The time of the year is an important variable because many viral infections are seasonal. Enteroviruses are the most common cause of viral meningitis in the United States, particularly in the summer and fall. In contrast, mumps, measles, and varicella zoster viruses occur more commonly in winter and spring. Herpetic meningoencephalitis is a life‐threatening condition with a guarded prognosis. Therefore, early recognition and treatment is necessary to decrease morbidity and mortality. Drugs such as nonsteroidal anti‐inflammatory agents, trimethoprim‐sulfamethoxazole, amoxicillin, and rarely vaccines can also cause aseptic meningitis. Infections from fungi, spirochetes, mycobacteria, and rarely parasites also cause meningitis, but would be of greater concern in a patient with risk factors such as recent travel or an immunocompromised state.

Increased headache with bending and cough might indicate elevated intracranial pressure. However, this is a nonspecific complaint, and headache is often worse with the Valsalva maneuver. Because she reports a cough, a chest x‐ray would be useful. In addition to routine initial tests, cerebrospinal fluid (CSF) analysis and human immunodeficiency virus (HIV) testing is recommended.

Her past medical history was notable for depression. Her medications included bupropion, multivitamins, and fish oil. She was also taking milk thistle pills daily to protect her liver because she had been drinking alcohol heavily for the past 2 weeks since her husband left her. She smoked 1 pack of cigarettes daily. She had not traveled recently. She reported no recent animal or wildlife exposure but did recall falling into a midwestern river while canoeing 2 weeks prior to presentation. She worked as a hairstylist and described no sick contacts or risk factors for HIV disease.

An important new historical element is that the patient fell into a river. If she swallowed a significant amount of water during her fall overboard, meningitis from waterborne infections such as Aeromonas, Acanthamoeba, and Naegleria need to be considered. Fortunately, these are rare in the Midwest. Her canoeing history may suggest exposure to wooded areas. Certainly, tickborne infections such as ehrlichiosis, babesiosis, Lyme disease, and Rocky Mountain spotted fever can also cause meningitis. Histoplasmosis and blastomycosis are also endemic to the midwestern United States and can disseminate and cause central nervous system disease.

At this time, viral and bacterial infections are highest on the differential diagnosis. However, the microbiology laboratory needs to be alerted to the possibility of fungal or parasitic organisms depending on the initial CSF analysis results.

The patient was a Caucasian woman who appeared comfortable. Her blood pressure was 130/62 mm Hg, heart rate was 83 beats per minute, respiratory rate was 18 per minute, temperature was 100.8F, and oxygen saturation was 98% on room air. She was fully alert and oriented. Her pupils were bilaterally equal, reactive to light and accommodation with intact extraocular movement and no nystagmus. There was conjunctival injection bilaterally without noticeable pallor or icterus. Fundoscopic examination, which the patient tolerated without difficulty, was normal. Inspection of the oral cavity showed mild tonsillar enlargement. The neck was supple with no stiffness. No cervical, axillary, or inguinal lymph nodes were palpable. Faint bilateral basilar crackles were audible over the posterior chest. There was very mild right upper quadrant abdominal tenderness without guarding. The liver and spleen were normal size and bowel sounds were present. No rash, peripheral edema, or spinal tenderness was noted. A complete neurological examination was normal.

Her general appearance and vital signs seem reassuring. Conjunctival injection and mild tonsillar enlargement are nonspecific findings and may occur in systemic inflammatory states especially viral infections. Atelectasis may account for faint bilateral basilar crackles especially if associated with post‐tussive change. Her alcohol use puts her at risk of aspiration. A right lower lobe process (pneumonia) can sometimes present with right upper quadrant tenderness. However, this tenderness may also represent muscle soreness from repeated coughing, liver, or gallbladder disease. The same infectious process affecting the central nervous system and possibly her lungs, may also be affecting the liver.

A complete blood count revealed a white blood cell count of 3000/mm³ (79% neutrophils, 15% lymphocytes, 5% monocytes), hemoglobin of 11.7 g/dL, and platelets of 110,000/mm³. The serum sodium was 133 mmol/L, potassium was 3.7 mmol/L, bicarbonate was 22 mmol/L, and blood urea nitrogen was 20 mg/dL. The serum creatinine was 1.5 compared to 1.0 mg/dL on testing 2 days prior. A liver function panel showed protein of 5.1 g/dL, albumin of 3 g/dL, aspartate aminotransferase (AST) of 576 IU/L, alanine aminotransferase (ALT) of 584 IU/L, alkaline phosphatase of 282 IU/L, and total bilirubin of 1 mg/dL. The coagulation profile, creatinine phosphokinase, acetaminophen level, urine pregnancy test, urine drug screen, and urinalysis (including urine microscopy) were normal.

The CSF opening pressure was 13 cm H₂O. CSF analysis showed 4 mononuclear leukocytes per high‐power field, CSF protein was 27 mg/dL, and glucose was 76 mg/dL. No organisms were noted on gram stain. A chest x‐ray showed focal airspace opacity in the left lower lobe (Figure 1) and the patient was hospitalized for further management.

Figure 1

The normal CSF analysis makes acute meningitis much less likely. It is interesting to note that the aminotransferase levels are nearly equal. Usually, in viral and many other causes of hepatitis, the ALT is higher than the AST, whereas the contrary is true in alcoholic hepatitis. Because the patient has been consuming significant amounts of alcohol recently, these levels may become equal in the setting of another primary liver process. The elevation in liver enzymes also raises the possibility of autoimmune hepatitis secondary to a systemic vasculitis such as systemic lupus erythematosus. Nonetheless, the focus should be on infectious causes of hepatitis such as hepatitis C, adenovirus, parvovirus, Epstein‐Barr virus (EBV), cytomegalovirus, and herpes simplex virus that can cause pneumonia either as a primary or secondary infection. Acute HIV infection can also present in this fashion, and anti‐HIV antibody testing may be negative early in the disease. In the setting of a normal urinalysis and bland urine sediment, prerenal azotemia is the most likely cause of her acute renal injury and can be confirmed by testing the urinary sodium and creatinine. A peripheral smear should be reviewed to evaluate the pancytopenia.

Severe headache, fever, conjunctival injection, pancytopenia, acute kidney injury, hepatitis, and pneumonia may occur in leptospirosis, particularly in a patient with recent freshwater exposure. Alternatively, ehrlichiosis can also account for fever, headache, pancytopenia, renal failure, hepatitis, and pneumonia, but conjunctival suffusion is not often present. At this time, treatment for community‐acquired pneumonia that includes coverage for leptospirosis should be started.

The patient was hydrated with intravenous fluids and treated with intravenous ceftriaxone and azithromycin for community‐acquired pneumonia. An abdominal ultrasound was normal. The serologic assays for acute hepatitis A, B, and C infection were negative. The following morning, she reported worsening headache, increased cough now productive of whitish‐yellow sputum, and diffuse body aches. She appeared more lethargic and toxic. Her blood pressure was 100/83 mm Hg, heart rate was 84 beats per minute, respiratory rate was 24 per minute, and temperature was 101.3F. She had increased crackles on chest auscultation bilaterally and required supplemental oxygen at 4 L/minute by nasal cannula. Examination of both legs now revealed multiple scattered, faintly erythematous, 2‐cm‐sized patches overlying tender subtle subcutaneous nodules. Additionally, a mildly pruritic, V‐shaped area of blanchable erythema was also seen on her chest. The white blood cell count was 2500/mm³ (77% neutrophils, 15% lymphocytes), serum creatinine was 1.8 mg/dL, AST was 351 IU/L, and ALT was 485 IU/L. Blood cultures showed no growth and a peripheral smear examination was unrevealing. A noncontrast chest computed tomographic scan showed findings consistent with multifocal pneumonia (Figure 2).

Figure 2

It would be prudent at this time to expand her antimicrobial coverage (such as with vancomycin and piperacillin‐tazobactam) for activity against methicillin‐resistant Staphylococcus aureus and Pseudomonas because of her clinical worsening. Although ceftriaxone or piperacillin would cover leptospirosis, given the possibility of ehrlichiosis, the addition of doxycycline should be strongly considered.

The description of the rash on her legs seems consistent with erythema nodosum, which is associated with a number of infections (streptococcal, fungal, syphilis, EBV, cat‐scratch disease, tuberculosis), inflammatory conditions (inflammatory bowel disease, autoimmune disease, malignancy), and pregnancy. The blanchable rash on the chest is also a cause of concern for a possible drug reaction (ceftriaxone). A Jarisch‐Herxheimer reaction is possible given her acute worsening of symptoms with initiation of antibiotic therapy.

An antineutrophil cytoplasmic antibodyassociated vasculitis or another autoimmune condition such as systemic lupus erythematosus can account for erythema nodosum, rash, pancytopenia, and hepatitis. This diagnosis might also fit if she had a vasculitic pulmonary hemorrhage that caused her lung infiltrates and worsening hypoxia. A complete antinuclear antibody panel, antineutrophil cytoplasmic antibody, and antismooth muscle antibody testing is recommended. A skin and bronchoscopic biopsy should be considered.

Her dose of ceftriaxone was increased for possible severe pneumococcal pneumonia. The dermatology consultant felt that her leg lesions were consistent with erythema nodosum and the chest rash consistent with cutaneous photodamage. Bronchoscopic examination was normal and a bronchoalveolar lavage sample showed 2905 red blood cells/mm³ and 605 white blood cells/mm³ (70% neutrophils, 7% lymphocytes, 16% histiocytes), normal cytology, and negative cultures. There was no significant clinical improvement by the fourth hospital day and oral doxycycline was started. The next day, her skin lesions had resolved and she felt better. The serologic tests for Legionella, Mycoplasma, cytomegalovirus, EBV, Toxoplasma, Chlamydophila, Ehrlichia, Leptospira, Q‐fever, parvovirus, and adenovirus were negative. A fungal serology panel, HIV polymerase chain reaction, cryoglobulin level, and several rheumatologic tests (antinuclear antibody, extractable nuclear antigen panel, rheumatoid factor, antineutrophil cytoplasmic antibody, antiproteinase 3, and antiglomerular basement membrane antibodies) were normal. Blood cultures continued to show no growth.

The apparent response to doxycycline suggests she might have ehrlichiosis. A buffy coat review for morulae should be done. It is also possible that she may have improved on her initial therapy alone before starting doxycycline and her clinical worsening (including the chest rash) was due to a Jarisch‐Herxheimer reaction. Serologic tests for leptospirosis and ehrlichiosis should be repeated in 12 weeks because such infections may not cause detectable antibody levels early in the illness.

Ceftriaxone and doxycycline were continued and she showed rapid and significant clinical improvement. She was discharged 4 days later with instructions to complete a 10‐day course of antibiotics. At her 3‐month follow‐up, she was doing well and a repeat Leptospira antibody test by the Indirect Hemagglutination Assay (MRL Diagnostics, Cypress, California; normal titer <1:50) was positive at a titer of 1:100, which is highly suggestive of leptospirosis.

Commentary

Leptospirosis is a zoonotic infection caused by spirochetes of the genus Leptospira. The infection is usually transmitted indirectly to humans through contact with water, food, or soil contaminated with the urine of infected mammals.1 Risk factors for infection include participation in recreational activities (such as freshwater swimming, canoeing, and camping), occupational exposure, and exposure to infected pets or domesticated livestock. Approximately 100200 cases are identified annually in the United States, and approximately half occur in the state of Hawaii.2 Outbreaks of leptospirosis have been reported previously in the Midwest.3 These organisms inoculate humans through contact with mucous membranes or broken skin, or enter by swallowing infected food or water. A large number of these infections remain subclinical or result in a very mild illness with spontaneous clearance by the host's immune mechanism. Following an incubation period of 230 days, infected individuals may develop clinically significant disease (Table 1). Clinical presentations may overlap as the disease progresses. Although much remains to be learned about the exact pathogenic mechanism, disruption of the cell membranes of small vessel endothelia (a toxin‐like effect), and cytokine‐mediated tissue injury are believed to cause organ hemorrhage and ischemia.4

The clinical diagnosis of leptospirosis is difficult because of its protean manifestations. Although nonspecific, 2 clinical features may provide a clue to the clinical diagnosis. First, the presence of conjunctival suffusion occurs in the early stage of the disease and is often associated with subconjunctival hemorrhage. Second, severe myalgia, commonly involving the lower limbs, is also characteristically present.1, 5 In 1 series of 58 patients with acute leptospirosis, conjunctival suffusion was observed in 50% of cases, and subconjunctival hemorrhage in 29%. Body ache and muscle tenderness was described in almost all cases.6

As seen in this case, the presence of a rash may pose a clinical challenge. A transient macular, maculopapular, purpuric, or urticarial rash may be seen in acute leptospirosis, but rashes may also be representative of a complication of treatment.1 First described in 1895 in patients with syphilis treated with mercury, the Jarisch‐Herxheimer reaction typically occurs within a few hours of antimicrobial treatment of spirochete infections and often presents with a rash, headache, fever, rigors, hypotension, sweating, and worsening symptoms of the underlying illness.7 Other skin findings such as the occurrence of erythema nodosum have been previously reported in cases of leptospirosis.8

Human ehrlichiosis (HE) is caused by tickborne, obligatory intracellular bacteria that infect leukocytes. There are 3 distinct clinical conditions: human monocytic ehrlichiosis (HME, caused by Ehrlichia chaffeensis), human granulocytic anaplasmosis (HGA, caused by Anaplasma phagocytophilum), and human ewingii ehrlichiosis (HEE, caused by E. ewingii). Although most cases of HME and HEE are seen in the southeastern and south‐central United States and California, the highest incidence of HGA is reported in the northeastern and upper Midwest regions.9 As with leptospirosis, the clinical range of HE spans from asymptomatic infection to life‐threatening illness. Following an incubation period of 12 weeks, symptomatic cases usually present with nonspecific complaints such as high fevers, chills, headache, nausea, arthralgia, myalgia, and malaise.10 The majority of cases will report a tick bite or an exposure to ticks. Laboratory tests often reveal leukopenia (white blood cell count < 4000/mm³), thrombocytopenia, hyponatremia, and elevated AST and ALT. Patients with severe disease may develop renal, respiratory, and hepatic failure. Thus, differentiating ehrlichiosis from leptospirosis is often challenging for the clinician.

However, there are a few clinical clues that help distinguish between these illnesses in this case. HGA as a cause of HE would be more likely in the Midwest. Although a rash is present in one‐third of patients with HME, it is seldom present in HGA unless coinfected with Borrelia burgdorferi, the causative agent for Lyme disease. Additionally, her history of freshwater exposure and the absence of a history of a tick bite also favor leptospirosis. As noted previously, conjunctival suffusion, a characteristic clinical feature of leptospirosis, has only been described in case reports of HE.11, 12

Serologic tests are often used to establish the diagnosis of leptospirosis and ehrlichiosis. Leptospires are fastidious organisms that are difficult to isolate on inoculated growth media. The microscopic agglutination test for leptospirosis is considered the diagnostic gold standard due to its high specificity, but its use is limited by its technical complexity, lack of availability (other than in reference laboratories), and low sensitivity early in the disease (antibody levels detected by this method usually do not appear until 7 days after symptom onset).13 A variety of rapid serologic assays are also available. Although these tests have good overall sensitivity (ranging between 79% and 93%), they perform relatively poorly for acute‐phase sera (sensitivity of 38.5%52.7%).13 The high early false negative rate is believed to be a result of inadequate Leptospira antibody titers in the acute phase of the illness. Seroconversion or a 4‐fold rise between acute and convalescent‐phase antibody titers is the most definitive criterion for the diagnosis of leptospirosis. However, without paired sera samples, a single high microscopic agglutination test titer can be taken as diagnostic for leptospirosis depending on the degree of regional endemicity.14

Similarly, currently available serologic assays for ehrlichiosis produce negative results in most patients in the first week of illness, and it is important to obtain a convalescent phase serum specimen for confirmatory diagnosis of HME and HGA. Seroconversion or a 4‐fold increase in titer between acute and convalescent phase sera is considered diagnostic. The sensitivity of finding morulae (intracytoplasmic vacuolar microcolonies of Ehrlichia) on a peripheral smear is unknown, and data suggest that this finding is more common in cases of HGA compared to HME.15

Although doxycycline is the drug of choice for the treatment of ehrlichiosis, Leptospira is susceptible to a wide variety of antibiotics because it exhibits a double membrane surface architecture with components common to both gram‐negative and gram‐positive bacteria.1 Recommended treatment regimens for severe leptospirosis include the use of high‐dose intravenous penicillin or a third‐generation cephalosporin. Less severe cases can be treated with oral amoxicillin or doxycycline.16 The fact that this patient's clinical improvement appeared to lag after initiation of ceftriaxone does not necessarily indicate a lack of efficacy but perhaps a Jarisch‐Herxheimer reaction in response to appropriate antibiotic therapy.

In October, a 36‐year‐old woman with no significant past medical history presented to the Emergency Department (ED) with a 3‐day history of headache and fever. The headache was severe, throbbing, and frontal in location. She also complained of daily fevers measured up to 103F, generalized malaise, and fatigue. She did not report neck stiffness or photophobia. She felt better after receiving intravenous fluids and was discharged home with a diagnosis of a nonspecific viral illness. Two days later, she returned to the ED with worsening headache, fever, mild photophobia, and poor oral intake. She also complained of a dry cough that made her headache worse, as did bending over. She did not report confusion, neck stiffness, shortness of breath, sore throat, runny nose, abdominal symptoms, or rash.

This patient presents a second time to the ED with worsening headache and fever raising concerns about meningitis. At the time of her first ED visit, it can be assumed that she had a nontoxic appearance because she was discharged shortly thereafter. Thus, acute bacterial meningitis seems less likely, but occasionally patients with meningococcal meningitis may not appear significantly ill until later in the process. Nonetheless, acute meningitis, possibly viral, is the initial concern. The time of the year is an important variable because many viral infections are seasonal. Enteroviruses are the most common cause of viral meningitis in the United States, particularly in the summer and fall. In contrast, mumps, measles, and varicella zoster viruses occur more commonly in winter and spring. Herpetic meningoencephalitis is a life‐threatening condition with a guarded prognosis. Therefore, early recognition and treatment is necessary to decrease morbidity and mortality. Drugs such as nonsteroidal anti‐inflammatory agents, trimethoprim‐sulfamethoxazole, amoxicillin, and rarely vaccines can also cause aseptic meningitis. Infections from fungi, spirochetes, mycobacteria, and rarely parasites also cause meningitis, but would be of greater concern in a patient with risk factors such as recent travel or an immunocompromised state.

Increased headache with bending and cough might indicate elevated intracranial pressure. However, this is a nonspecific complaint, and headache is often worse with the Valsalva maneuver. Because she reports a cough, a chest x‐ray would be useful. In addition to routine initial tests, cerebrospinal fluid (CSF) analysis and human immunodeficiency virus (HIV) testing is recommended.

Her past medical history was notable for depression. Her medications included bupropion, multivitamins, and fish oil. She was also taking milk thistle pills daily to protect her liver because she had been drinking alcohol heavily for the past 2 weeks since her husband left her. She smoked 1 pack of cigarettes daily. She had not traveled recently. She reported no recent animal or wildlife exposure but did recall falling into a midwestern river while canoeing 2 weeks prior to presentation. She worked as a hairstylist and described no sick contacts or risk factors for HIV disease.

An important new historical element is that the patient fell into a river. If she swallowed a significant amount of water during her fall overboard, meningitis from waterborne infections such as Aeromonas, Acanthamoeba, and Naegleria need to be considered. Fortunately, these are rare in the Midwest. Her canoeing history may suggest exposure to wooded areas. Certainly, tickborne infections such as ehrlichiosis, babesiosis, Lyme disease, and Rocky Mountain spotted fever can also cause meningitis. Histoplasmosis and blastomycosis are also endemic to the midwestern United States and can disseminate and cause central nervous system disease.

At this time, viral and bacterial infections are highest on the differential diagnosis. However, the microbiology laboratory needs to be alerted to the possibility of fungal or parasitic organisms depending on the initial CSF analysis results.

The patient was a Caucasian woman who appeared comfortable. Her blood pressure was 130/62 mm Hg, heart rate was 83 beats per minute, respiratory rate was 18 per minute, temperature was 100.8F, and oxygen saturation was 98% on room air. She was fully alert and oriented. Her pupils were bilaterally equal, reactive to light and accommodation with intact extraocular movement and no nystagmus. There was conjunctival injection bilaterally without noticeable pallor or icterus. Fundoscopic examination, which the patient tolerated without difficulty, was normal. Inspection of the oral cavity showed mild tonsillar enlargement. The neck was supple with no stiffness. No cervical, axillary, or inguinal lymph nodes were palpable. Faint bilateral basilar crackles were audible over the posterior chest. There was very mild right upper quadrant abdominal tenderness without guarding. The liver and spleen were normal size and bowel sounds were present. No rash, peripheral edema, or spinal tenderness was noted. A complete neurological examination was normal.

Her general appearance and vital signs seem reassuring. Conjunctival injection and mild tonsillar enlargement are nonspecific findings and may occur in systemic inflammatory states especially viral infections. Atelectasis may account for faint bilateral basilar crackles especially if associated with post‐tussive change. Her alcohol use puts her at risk of aspiration. A right lower lobe process (pneumonia) can sometimes present with right upper quadrant tenderness. However, this tenderness may also represent muscle soreness from repeated coughing, liver, or gallbladder disease. The same infectious process affecting the central nervous system and possibly her lungs, may also be affecting the liver.

A complete blood count revealed a white blood cell count of 3000/mm³ (79% neutrophils, 15% lymphocytes, 5% monocytes), hemoglobin of 11.7 g/dL, and platelets of 110,000/mm³. The serum sodium was 133 mmol/L, potassium was 3.7 mmol/L, bicarbonate was 22 mmol/L, and blood urea nitrogen was 20 mg/dL. The serum creatinine was 1.5 compared to 1.0 mg/dL on testing 2 days prior. A liver function panel showed protein of 5.1 g/dL, albumin of 3 g/dL, aspartate aminotransferase (AST) of 576 IU/L, alanine aminotransferase (ALT) of 584 IU/L, alkaline phosphatase of 282 IU/L, and total bilirubin of 1 mg/dL. The coagulation profile, creatinine phosphokinase, acetaminophen level, urine pregnancy test, urine drug screen, and urinalysis (including urine microscopy) were normal.

The CSF opening pressure was 13 cm H₂O. CSF analysis showed 4 mononuclear leukocytes per high‐power field, CSF protein was 27 mg/dL, and glucose was 76 mg/dL. No organisms were noted on gram stain. A chest x‐ray showed focal airspace opacity in the left lower lobe (Figure 1) and the patient was hospitalized for further management.

Figure 1

The normal CSF analysis makes acute meningitis much less likely. It is interesting to note that the aminotransferase levels are nearly equal. Usually, in viral and many other causes of hepatitis, the ALT is higher than the AST, whereas the contrary is true in alcoholic hepatitis. Because the patient has been consuming significant amounts of alcohol recently, these levels may become equal in the setting of another primary liver process. The elevation in liver enzymes also raises the possibility of autoimmune hepatitis secondary to a systemic vasculitis such as systemic lupus erythematosus. Nonetheless, the focus should be on infectious causes of hepatitis such as hepatitis C, adenovirus, parvovirus, Epstein‐Barr virus (EBV), cytomegalovirus, and herpes simplex virus that can cause pneumonia either as a primary or secondary infection. Acute HIV infection can also present in this fashion, and anti‐HIV antibody testing may be negative early in the disease. In the setting of a normal urinalysis and bland urine sediment, prerenal azotemia is the most likely cause of her acute renal injury and can be confirmed by testing the urinary sodium and creatinine. A peripheral smear should be reviewed to evaluate the pancytopenia.

Severe headache, fever, conjunctival injection, pancytopenia, acute kidney injury, hepatitis, and pneumonia may occur in leptospirosis, particularly in a patient with recent freshwater exposure. Alternatively, ehrlichiosis can also account for fever, headache, pancytopenia, renal failure, hepatitis, and pneumonia, but conjunctival suffusion is not often present. At this time, treatment for community‐acquired pneumonia that includes coverage for leptospirosis should be started.

The patient was hydrated with intravenous fluids and treated with intravenous ceftriaxone and azithromycin for community‐acquired pneumonia. An abdominal ultrasound was normal. The serologic assays for acute hepatitis A, B, and C infection were negative. The following morning, she reported worsening headache, increased cough now productive of whitish‐yellow sputum, and diffuse body aches. She appeared more lethargic and toxic. Her blood pressure was 100/83 mm Hg, heart rate was 84 beats per minute, respiratory rate was 24 per minute, and temperature was 101.3F. She had increased crackles on chest auscultation bilaterally and required supplemental oxygen at 4 L/minute by nasal cannula. Examination of both legs now revealed multiple scattered, faintly erythematous, 2‐cm‐sized patches overlying tender subtle subcutaneous nodules. Additionally, a mildly pruritic, V‐shaped area of blanchable erythema was also seen on her chest. The white blood cell count was 2500/mm³ (77% neutrophils, 15% lymphocytes), serum creatinine was 1.8 mg/dL, AST was 351 IU/L, and ALT was 485 IU/L. Blood cultures showed no growth and a peripheral smear examination was unrevealing. A noncontrast chest computed tomographic scan showed findings consistent with multifocal pneumonia (Figure 2).

Figure 2

It would be prudent at this time to expand her antimicrobial coverage (such as with vancomycin and piperacillin‐tazobactam) for activity against methicillin‐resistant Staphylococcus aureus and Pseudomonas because of her clinical worsening. Although ceftriaxone or piperacillin would cover leptospirosis, given the possibility of ehrlichiosis, the addition of doxycycline should be strongly considered.

The description of the rash on her legs seems consistent with erythema nodosum, which is associated with a number of infections (streptococcal, fungal, syphilis, EBV, cat‐scratch disease, tuberculosis), inflammatory conditions (inflammatory bowel disease, autoimmune disease, malignancy), and pregnancy. The blanchable rash on the chest is also a cause of concern for a possible drug reaction (ceftriaxone). A Jarisch‐Herxheimer reaction is possible given her acute worsening of symptoms with initiation of antibiotic therapy.

An antineutrophil cytoplasmic antibodyassociated vasculitis or another autoimmune condition such as systemic lupus erythematosus can account for erythema nodosum, rash, pancytopenia, and hepatitis. This diagnosis might also fit if she had a vasculitic pulmonary hemorrhage that caused her lung infiltrates and worsening hypoxia. A complete antinuclear antibody panel, antineutrophil cytoplasmic antibody, and antismooth muscle antibody testing is recommended. A skin and bronchoscopic biopsy should be considered.

Her dose of ceftriaxone was increased for possible severe pneumococcal pneumonia. The dermatology consultant felt that her leg lesions were consistent with erythema nodosum and the chest rash consistent with cutaneous photodamage. Bronchoscopic examination was normal and a bronchoalveolar lavage sample showed 2905 red blood cells/mm³ and 605 white blood cells/mm³ (70% neutrophils, 7% lymphocytes, 16% histiocytes), normal cytology, and negative cultures. There was no significant clinical improvement by the fourth hospital day and oral doxycycline was started. The next day, her skin lesions had resolved and she felt better. The serologic tests for Legionella, Mycoplasma, cytomegalovirus, EBV, Toxoplasma, Chlamydophila, Ehrlichia, Leptospira, Q‐fever, parvovirus, and adenovirus were negative. A fungal serology panel, HIV polymerase chain reaction, cryoglobulin level, and several rheumatologic tests (antinuclear antibody, extractable nuclear antigen panel, rheumatoid factor, antineutrophil cytoplasmic antibody, antiproteinase 3, and antiglomerular basement membrane antibodies) were normal. Blood cultures continued to show no growth.

The apparent response to doxycycline suggests she might have ehrlichiosis. A buffy coat review for morulae should be done. It is also possible that she may have improved on her initial therapy alone before starting doxycycline and her clinical worsening (including the chest rash) was due to a Jarisch‐Herxheimer reaction. Serologic tests for leptospirosis and ehrlichiosis should be repeated in 12 weeks because such infections may not cause detectable antibody levels early in the illness.

Ceftriaxone and doxycycline were continued and she showed rapid and significant clinical improvement. She was discharged 4 days later with instructions to complete a 10‐day course of antibiotics. At her 3‐month follow‐up, she was doing well and a repeat Leptospira antibody test by the Indirect Hemagglutination Assay (MRL Diagnostics, Cypress, California; normal titer <1:50) was positive at a titer of 1:100, which is highly suggestive of leptospirosis.

Commentary

Leptospirosis is a zoonotic infection caused by spirochetes of the genus Leptospira. The infection is usually transmitted indirectly to humans through contact with water, food, or soil contaminated with the urine of infected mammals.1 Risk factors for infection include participation in recreational activities (such as freshwater swimming, canoeing, and camping), occupational exposure, and exposure to infected pets or domesticated livestock. Approximately 100200 cases are identified annually in the United States, and approximately half occur in the state of Hawaii.2 Outbreaks of leptospirosis have been reported previously in the Midwest.3 These organisms inoculate humans through contact with mucous membranes or broken skin, or enter by swallowing infected food or water. A large number of these infections remain subclinical or result in a very mild illness with spontaneous clearance by the host's immune mechanism. Following an incubation period of 230 days, infected individuals may develop clinically significant disease (Table 1). Clinical presentations may overlap as the disease progresses. Although much remains to be learned about the exact pathogenic mechanism, disruption of the cell membranes of small vessel endothelia (a toxin‐like effect), and cytokine‐mediated tissue injury are believed to cause organ hemorrhage and ischemia.4

The clinical diagnosis of leptospirosis is difficult because of its protean manifestations. Although nonspecific, 2 clinical features may provide a clue to the clinical diagnosis. First, the presence of conjunctival suffusion occurs in the early stage of the disease and is often associated with subconjunctival hemorrhage. Second, severe myalgia, commonly involving the lower limbs, is also characteristically present.1, 5 In 1 series of 58 patients with acute leptospirosis, conjunctival suffusion was observed in 50% of cases, and subconjunctival hemorrhage in 29%. Body ache and muscle tenderness was described in almost all cases.6

As seen in this case, the presence of a rash may pose a clinical challenge. A transient macular, maculopapular, purpuric, or urticarial rash may be seen in acute leptospirosis, but rashes may also be representative of a complication of treatment.1 First described in 1895 in patients with syphilis treated with mercury, the Jarisch‐Herxheimer reaction typically occurs within a few hours of antimicrobial treatment of spirochete infections and often presents with a rash, headache, fever, rigors, hypotension, sweating, and worsening symptoms of the underlying illness.7 Other skin findings such as the occurrence of erythema nodosum have been previously reported in cases of leptospirosis.8

Human ehrlichiosis (HE) is caused by tickborne, obligatory intracellular bacteria that infect leukocytes. There are 3 distinct clinical conditions: human monocytic ehrlichiosis (HME, caused by Ehrlichia chaffeensis), human granulocytic anaplasmosis (HGA, caused by Anaplasma phagocytophilum), and human ewingii ehrlichiosis (HEE, caused by E. ewingii). Although most cases of HME and HEE are seen in the southeastern and south‐central United States and California, the highest incidence of HGA is reported in the northeastern and upper Midwest regions.9 As with leptospirosis, the clinical range of HE spans from asymptomatic infection to life‐threatening illness. Following an incubation period of 12 weeks, symptomatic cases usually present with nonspecific complaints such as high fevers, chills, headache, nausea, arthralgia, myalgia, and malaise.10 The majority of cases will report a tick bite or an exposure to ticks. Laboratory tests often reveal leukopenia (white blood cell count < 4000/mm³), thrombocytopenia, hyponatremia, and elevated AST and ALT. Patients with severe disease may develop renal, respiratory, and hepatic failure. Thus, differentiating ehrlichiosis from leptospirosis is often challenging for the clinician.

However, there are a few clinical clues that help distinguish between these illnesses in this case. HGA as a cause of HE would be more likely in the Midwest. Although a rash is present in one‐third of patients with HME, it is seldom present in HGA unless coinfected with Borrelia burgdorferi, the causative agent for Lyme disease. Additionally, her history of freshwater exposure and the absence of a history of a tick bite also favor leptospirosis. As noted previously, conjunctival suffusion, a characteristic clinical feature of leptospirosis, has only been described in case reports of HE.11, 12

Serologic tests are often used to establish the diagnosis of leptospirosis and ehrlichiosis. Leptospires are fastidious organisms that are difficult to isolate on inoculated growth media. The microscopic agglutination test for leptospirosis is considered the diagnostic gold standard due to its high specificity, but its use is limited by its technical complexity, lack of availability (other than in reference laboratories), and low sensitivity early in the disease (antibody levels detected by this method usually do not appear until 7 days after symptom onset).13 A variety of rapid serologic assays are also available. Although these tests have good overall sensitivity (ranging between 79% and 93%), they perform relatively poorly for acute‐phase sera (sensitivity of 38.5%52.7%).13 The high early false negative rate is believed to be a result of inadequate Leptospira antibody titers in the acute phase of the illness. Seroconversion or a 4‐fold rise between acute and convalescent‐phase antibody titers is the most definitive criterion for the diagnosis of leptospirosis. However, without paired sera samples, a single high microscopic agglutination test titer can be taken as diagnostic for leptospirosis depending on the degree of regional endemicity.14

Similarly, currently available serologic assays for ehrlichiosis produce negative results in most patients in the first week of illness, and it is important to obtain a convalescent phase serum specimen for confirmatory diagnosis of HME and HGA. Seroconversion or a 4‐fold increase in titer between acute and convalescent phase sera is considered diagnostic. The sensitivity of finding morulae (intracytoplasmic vacuolar microcolonies of Ehrlichia) on a peripheral smear is unknown, and data suggest that this finding is more common in cases of HGA compared to HME.15

Although doxycycline is the drug of choice for the treatment of ehrlichiosis, Leptospira is susceptible to a wide variety of antibiotics because it exhibits a double membrane surface architecture with components common to both gram‐negative and gram‐positive bacteria.1 Recommended treatment regimens for severe leptospirosis include the use of high‐dose intravenous penicillin or a third‐generation cephalosporin. Less severe cases can be treated with oral amoxicillin or doxycycline.16 The fact that this patient's clinical improvement appeared to lag after initiation of ceftriaxone does not necessarily indicate a lack of efficacy but perhaps a Jarisch‐Herxheimer reaction in response to appropriate antibiotic therapy.

In October, a 36‐year‐old woman with no significant past medical history presented to the Emergency Department (ED) with a 3‐day history of headache and fever. The headache was severe, throbbing, and frontal in location. She also complained of daily fevers measured up to 103F, generalized malaise, and fatigue. She did not report neck stiffness or photophobia. She felt better after receiving intravenous fluids and was discharged home with a diagnosis of a nonspecific viral illness. Two days later, she returned to the ED with worsening headache, fever, mild photophobia, and poor oral intake. She also complained of a dry cough that made her headache worse, as did bending over. She did not report confusion, neck stiffness, shortness of breath, sore throat, runny nose, abdominal symptoms, or rash.

This patient presents a second time to the ED with worsening headache and fever raising concerns about meningitis. At the time of her first ED visit, it can be assumed that she had a nontoxic appearance because she was discharged shortly thereafter. Thus, acute bacterial meningitis seems less likely, but occasionally patients with meningococcal meningitis may not appear significantly ill until later in the process. Nonetheless, acute meningitis, possibly viral, is the initial concern. The time of the year is an important variable because many viral infections are seasonal. Enteroviruses are the most common cause of viral meningitis in the United States, particularly in the summer and fall. In contrast, mumps, measles, and varicella zoster viruses occur more commonly in winter and spring. Herpetic meningoencephalitis is a life‐threatening condition with a guarded prognosis. Therefore, early recognition and treatment is necessary to decrease morbidity and mortality. Drugs such as nonsteroidal anti‐inflammatory agents, trimethoprim‐sulfamethoxazole, amoxicillin, and rarely vaccines can also cause aseptic meningitis. Infections from fungi, spirochetes, mycobacteria, and rarely parasites also cause meningitis, but would be of greater concern in a patient with risk factors such as recent travel or an immunocompromised state.

Increased headache with bending and cough might indicate elevated intracranial pressure. However, this is a nonspecific complaint, and headache is often worse with the Valsalva maneuver. Because she reports a cough, a chest x‐ray would be useful. In addition to routine initial tests, cerebrospinal fluid (CSF) analysis and human immunodeficiency virus (HIV) testing is recommended.

Her past medical history was notable for depression. Her medications included bupropion, multivitamins, and fish oil. She was also taking milk thistle pills daily to protect her liver because she had been drinking alcohol heavily for the past 2 weeks since her husband left her. She smoked 1 pack of cigarettes daily. She had not traveled recently. She reported no recent animal or wildlife exposure but did recall falling into a midwestern river while canoeing 2 weeks prior to presentation. She worked as a hairstylist and described no sick contacts or risk factors for HIV disease.

An important new historical element is that the patient fell into a river. If she swallowed a significant amount of water during her fall overboard, meningitis from waterborne infections such as Aeromonas, Acanthamoeba, and Naegleria need to be considered. Fortunately, these are rare in the Midwest. Her canoeing history may suggest exposure to wooded areas. Certainly, tickborne infections such as ehrlichiosis, babesiosis, Lyme disease, and Rocky Mountain spotted fever can also cause meningitis. Histoplasmosis and blastomycosis are also endemic to the midwestern United States and can disseminate and cause central nervous system disease.

At this time, viral and bacterial infections are highest on the differential diagnosis. However, the microbiology laboratory needs to be alerted to the possibility of fungal or parasitic organisms depending on the initial CSF analysis results.

The patient was a Caucasian woman who appeared comfortable. Her blood pressure was 130/62 mm Hg, heart rate was 83 beats per minute, respiratory rate was 18 per minute, temperature was 100.8F, and oxygen saturation was 98% on room air. She was fully alert and oriented. Her pupils were bilaterally equal, reactive to light and accommodation with intact extraocular movement and no nystagmus. There was conjunctival injection bilaterally without noticeable pallor or icterus. Fundoscopic examination, which the patient tolerated without difficulty, was normal. Inspection of the oral cavity showed mild tonsillar enlargement. The neck was supple with no stiffness. No cervical, axillary, or inguinal lymph nodes were palpable. Faint bilateral basilar crackles were audible over the posterior chest. There was very mild right upper quadrant abdominal tenderness without guarding. The liver and spleen were normal size and bowel sounds were present. No rash, peripheral edema, or spinal tenderness was noted. A complete neurological examination was normal.

Her general appearance and vital signs seem reassuring. Conjunctival injection and mild tonsillar enlargement are nonspecific findings and may occur in systemic inflammatory states especially viral infections. Atelectasis may account for faint bilateral basilar crackles especially if associated with post‐tussive change. Her alcohol use puts her at risk of aspiration. A right lower lobe process (pneumonia) can sometimes present with right upper quadrant tenderness. However, this tenderness may also represent muscle soreness from repeated coughing, liver, or gallbladder disease. The same infectious process affecting the central nervous system and possibly her lungs, may also be affecting the liver.

A complete blood count revealed a white blood cell count of 3000/mm³ (79% neutrophils, 15% lymphocytes, 5% monocytes), hemoglobin of 11.7 g/dL, and platelets of 110,000/mm³. The serum sodium was 133 mmol/L, potassium was 3.7 mmol/L, bicarbonate was 22 mmol/L, and blood urea nitrogen was 20 mg/dL. The serum creatinine was 1.5 compared to 1.0 mg/dL on testing 2 days prior. A liver function panel showed protein of 5.1 g/dL, albumin of 3 g/dL, aspartate aminotransferase (AST) of 576 IU/L, alanine aminotransferase (ALT) of 584 IU/L, alkaline phosphatase of 282 IU/L, and total bilirubin of 1 mg/dL. The coagulation profile, creatinine phosphokinase, acetaminophen level, urine pregnancy test, urine drug screen, and urinalysis (including urine microscopy) were normal.

The CSF opening pressure was 13 cm H₂O. CSF analysis showed 4 mononuclear leukocytes per high‐power field, CSF protein was 27 mg/dL, and glucose was 76 mg/dL. No organisms were noted on gram stain. A chest x‐ray showed focal airspace opacity in the left lower lobe (Figure 1) and the patient was hospitalized for further management.

Figure 1

The normal CSF analysis makes acute meningitis much less likely. It is interesting to note that the aminotransferase levels are nearly equal. Usually, in viral and many other causes of hepatitis, the ALT is higher than the AST, whereas the contrary is true in alcoholic hepatitis. Because the patient has been consuming significant amounts of alcohol recently, these levels may become equal in the setting of another primary liver process. The elevation in liver enzymes also raises the possibility of autoimmune hepatitis secondary to a systemic vasculitis such as systemic lupus erythematosus. Nonetheless, the focus should be on infectious causes of hepatitis such as hepatitis C, adenovirus, parvovirus, Epstein‐Barr virus (EBV), cytomegalovirus, and herpes simplex virus that can cause pneumonia either as a primary or secondary infection. Acute HIV infection can also present in this fashion, and anti‐HIV antibody testing may be negative early in the disease. In the setting of a normal urinalysis and bland urine sediment, prerenal azotemia is the most likely cause of her acute renal injury and can be confirmed by testing the urinary sodium and creatinine. A peripheral smear should be reviewed to evaluate the pancytopenia.

Severe headache, fever, conjunctival injection, pancytopenia, acute kidney injury, hepatitis, and pneumonia may occur in leptospirosis, particularly in a patient with recent freshwater exposure. Alternatively, ehrlichiosis can also account for fever, headache, pancytopenia, renal failure, hepatitis, and pneumonia, but conjunctival suffusion is not often present. At this time, treatment for community‐acquired pneumonia that includes coverage for leptospirosis should be started.

The patient was hydrated with intravenous fluids and treated with intravenous ceftriaxone and azithromycin for community‐acquired pneumonia. An abdominal ultrasound was normal. The serologic assays for acute hepatitis A, B, and C infection were negative. The following morning, she reported worsening headache, increased cough now productive of whitish‐yellow sputum, and diffuse body aches. She appeared more lethargic and toxic. Her blood pressure was 100/83 mm Hg, heart rate was 84 beats per minute, respiratory rate was 24 per minute, and temperature was 101.3F. She had increased crackles on chest auscultation bilaterally and required supplemental oxygen at 4 L/minute by nasal cannula. Examination of both legs now revealed multiple scattered, faintly erythematous, 2‐cm‐sized patches overlying tender subtle subcutaneous nodules. Additionally, a mildly pruritic, V‐shaped area of blanchable erythema was also seen on her chest. The white blood cell count was 2500/mm³ (77% neutrophils, 15% lymphocytes), serum creatinine was 1.8 mg/dL, AST was 351 IU/L, and ALT was 485 IU/L. Blood cultures showed no growth and a peripheral smear examination was unrevealing. A noncontrast chest computed tomographic scan showed findings consistent with multifocal pneumonia (Figure 2).

Figure 2

It would be prudent at this time to expand her antimicrobial coverage (such as with vancomycin and piperacillin‐tazobactam) for activity against methicillin‐resistant Staphylococcus aureus and Pseudomonas because of her clinical worsening. Although ceftriaxone or piperacillin would cover leptospirosis, given the possibility of ehrlichiosis, the addition of doxycycline should be strongly considered.

The description of the rash on her legs seems consistent with erythema nodosum, which is associated with a number of infections (streptococcal, fungal, syphilis, EBV, cat‐scratch disease, tuberculosis), inflammatory conditions (inflammatory bowel disease, autoimmune disease, malignancy), and pregnancy. The blanchable rash on the chest is also a cause of concern for a possible drug reaction (ceftriaxone). A Jarisch‐Herxheimer reaction is possible given her acute worsening of symptoms with initiation of antibiotic therapy.

An antineutrophil cytoplasmic antibodyassociated vasculitis or another autoimmune condition such as systemic lupus erythematosus can account for erythema nodosum, rash, pancytopenia, and hepatitis. This diagnosis might also fit if she had a vasculitic pulmonary hemorrhage that caused her lung infiltrates and worsening hypoxia. A complete antinuclear antibody panel, antineutrophil cytoplasmic antibody, and antismooth muscle antibody testing is recommended. A skin and bronchoscopic biopsy should be considered.

Her dose of ceftriaxone was increased for possible severe pneumococcal pneumonia. The dermatology consultant felt that her leg lesions were consistent with erythema nodosum and the chest rash consistent with cutaneous photodamage. Bronchoscopic examination was normal and a bronchoalveolar lavage sample showed 2905 red blood cells/mm³ and 605 white blood cells/mm³ (70% neutrophils, 7% lymphocytes, 16% histiocytes), normal cytology, and negative cultures. There was no significant clinical improvement by the fourth hospital day and oral doxycycline was started. The next day, her skin lesions had resolved and she felt better. The serologic tests for Legionella, Mycoplasma, cytomegalovirus, EBV, Toxoplasma, Chlamydophila, Ehrlichia, Leptospira, Q‐fever, parvovirus, and adenovirus were negative. A fungal serology panel, HIV polymerase chain reaction, cryoglobulin level, and several rheumatologic tests (antinuclear antibody, extractable nuclear antigen panel, rheumatoid factor, antineutrophil cytoplasmic antibody, antiproteinase 3, and antiglomerular basement membrane antibodies) were normal. Blood cultures continued to show no growth.

The apparent response to doxycycline suggests she might have ehrlichiosis. A buffy coat review for morulae should be done. It is also possible that she may have improved on her initial therapy alone before starting doxycycline and her clinical worsening (including the chest rash) was due to a Jarisch‐Herxheimer reaction. Serologic tests for leptospirosis and ehrlichiosis should be repeated in 12 weeks because such infections may not cause detectable antibody levels early in the illness.

Ceftriaxone and doxycycline were continued and she showed rapid and significant clinical improvement. She was discharged 4 days later with instructions to complete a 10‐day course of antibiotics. At her 3‐month follow‐up, she was doing well and a repeat Leptospira antibody test by the Indirect Hemagglutination Assay (MRL Diagnostics, Cypress, California; normal titer <1:50) was positive at a titer of 1:100, which is highly suggestive of leptospirosis.

Commentary

Leptospirosis is a zoonotic infection caused by spirochetes of the genus Leptospira. The infection is usually transmitted indirectly to humans through contact with water, food, or soil contaminated with the urine of infected mammals.1 Risk factors for infection include participation in recreational activities (such as freshwater swimming, canoeing, and camping), occupational exposure, and exposure to infected pets or domesticated livestock. Approximately 100200 cases are identified annually in the United States, and approximately half occur in the state of Hawaii.2 Outbreaks of leptospirosis have been reported previously in the Midwest.3 These organisms inoculate humans through contact with mucous membranes or broken skin, or enter by swallowing infected food or water. A large number of these infections remain subclinical or result in a very mild illness with spontaneous clearance by the host's immune mechanism. Following an incubation period of 230 days, infected individuals may develop clinically significant disease (Table 1). Clinical presentations may overlap as the disease progresses. Although much remains to be learned about the exact pathogenic mechanism, disruption of the cell membranes of small vessel endothelia (a toxin‐like effect), and cytokine‐mediated tissue injury are believed to cause organ hemorrhage and ischemia.4

The clinical diagnosis of leptospirosis is difficult because of its protean manifestations. Although nonspecific, 2 clinical features may provide a clue to the clinical diagnosis. First, the presence of conjunctival suffusion occurs in the early stage of the disease and is often associated with subconjunctival hemorrhage. Second, severe myalgia, commonly involving the lower limbs, is also characteristically present.1, 5 In 1 series of 58 patients with acute leptospirosis, conjunctival suffusion was observed in 50% of cases, and subconjunctival hemorrhage in 29%. Body ache and muscle tenderness was described in almost all cases.6

As seen in this case, the presence of a rash may pose a clinical challenge. A transient macular, maculopapular, purpuric, or urticarial rash may be seen in acute leptospirosis, but rashes may also be representative of a complication of treatment.1 First described in 1895 in patients with syphilis treated with mercury, the Jarisch‐Herxheimer reaction typically occurs within a few hours of antimicrobial treatment of spirochete infections and often presents with a rash, headache, fever, rigors, hypotension, sweating, and worsening symptoms of the underlying illness.7 Other skin findings such as the occurrence of erythema nodosum have been previously reported in cases of leptospirosis.8

Human ehrlichiosis (HE) is caused by tickborne, obligatory intracellular bacteria that infect leukocytes. There are 3 distinct clinical conditions: human monocytic ehrlichiosis (HME, caused by Ehrlichia chaffeensis), human granulocytic anaplasmosis (HGA, caused by Anaplasma phagocytophilum), and human ewingii ehrlichiosis (HEE, caused by E. ewingii). Although most cases of HME and HEE are seen in the southeastern and south‐central United States and California, the highest incidence of HGA is reported in the northeastern and upper Midwest regions.9 As with leptospirosis, the clinical range of HE spans from asymptomatic infection to life‐threatening illness. Following an incubation period of 12 weeks, symptomatic cases usually present with nonspecific complaints such as high fevers, chills, headache, nausea, arthralgia, myalgia, and malaise.10 The majority of cases will report a tick bite or an exposure to ticks. Laboratory tests often reveal leukopenia (white blood cell count < 4000/mm³), thrombocytopenia, hyponatremia, and elevated AST and ALT. Patients with severe disease may develop renal, respiratory, and hepatic failure. Thus, differentiating ehrlichiosis from leptospirosis is often challenging for the clinician.

However, there are a few clinical clues that help distinguish between these illnesses in this case. HGA as a cause of HE would be more likely in the Midwest. Although a rash is present in one‐third of patients with HME, it is seldom present in HGA unless coinfected with Borrelia burgdorferi, the causative agent for Lyme disease. Additionally, her history of freshwater exposure and the absence of a history of a tick bite also favor leptospirosis. As noted previously, conjunctival suffusion, a characteristic clinical feature of leptospirosis, has only been described in case reports of HE.11, 12

Serologic tests are often used to establish the diagnosis of leptospirosis and ehrlichiosis. Leptospires are fastidious organisms that are difficult to isolate on inoculated growth media. The microscopic agglutination test for leptospirosis is considered the diagnostic gold standard due to its high specificity, but its use is limited by its technical complexity, lack of availability (other than in reference laboratories), and low sensitivity early in the disease (antibody levels detected by this method usually do not appear until 7 days after symptom onset).13 A variety of rapid serologic assays are also available. Although these tests have good overall sensitivity (ranging between 79% and 93%), they perform relatively poorly for acute‐phase sera (sensitivity of 38.5%52.7%).13 The high early false negative rate is believed to be a result of inadequate Leptospira antibody titers in the acute phase of the illness. Seroconversion or a 4‐fold rise between acute and convalescent‐phase antibody titers is the most definitive criterion for the diagnosis of leptospirosis. However, without paired sera samples, a single high microscopic agglutination test titer can be taken as diagnostic for leptospirosis depending on the degree of regional endemicity.14

Similarly, currently available serologic assays for ehrlichiosis produce negative results in most patients in the first week of illness, and it is important to obtain a convalescent phase serum specimen for confirmatory diagnosis of HME and HGA. Seroconversion or a 4‐fold increase in titer between acute and convalescent phase sera is considered diagnostic. The sensitivity of finding morulae (intracytoplasmic vacuolar microcolonies of Ehrlichia) on a peripheral smear is unknown, and data suggest that this finding is more common in cases of HGA compared to HME.15

Although doxycycline is the drug of choice for the treatment of ehrlichiosis, Leptospira is susceptible to a wide variety of antibiotics because it exhibits a double membrane surface architecture with components common to both gram‐negative and gram‐positive bacteria.1 Recommended treatment regimens for severe leptospirosis include the use of high‐dose intravenous penicillin or a third‐generation cephalosporin. Less severe cases can be treated with oral amoxicillin or doxycycline.16 The fact that this patient's clinical improvement appeared to lag after initiation of ceftriaxone does not necessarily indicate a lack of efficacy but perhaps a Jarisch‐Herxheimer reaction in response to appropriate antibiotic therapy.

If you wish to receive credit for this activity, please refer to the website: www.wileyblackwellcme.com.

Accreditation and Designation Statement

Blackwell Futura Media Services designates this journal‐based CME activity for a maximum of 1 AMA PRA Category 1 Credit.. Physicians should only claim credit commensurate with the extent of their participation in the activity.

Blackwell Futura Media Services is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

Educational Objectives

Upon completion of this educational activity, participants will be better able to:

• Illustrate the elements of a systematic approach to successful hospital smoking cessation programs.

• Describe the efficacy of a coordinated real world hospital smoking cessation program in a U.S. hospital.

• Evaluate the barriers to successful hospital smoking cessation programs.

This manuscript underwent peer review in line with the standards of editorial integrity and publication ethics maintained by Journal of Hospital Medicine. The peer reviewers have no relevant financial relationships. The peer review process for Journal of Hospital Medicine is blinded. As such, the identities of the reviewers are not disclosed in line with the standard accepted practices of medical journal peer review.

Conflicts of interest have been identified and resolved in accordance with Blackwell Futura Media Services's Policy on Activity Disclosure and Conflict of Interest. The primary resolution method used was peer review and review by a non‐conflicted expert.

Instructions on Receiving Credit

For information on applicability and acceptance of CME credit for this activity, please consult your professional licensing board.

This activity is designed to be completed within an hour; physicians should claim only those credits that reflect the time actually spent in the activity. To successfully earn credit, participants must complete the activity during the valid credit period, which is up to two years from initial publication.

Follow these steps to earn credit:

• Log on to www.wileyblackwellcme.com

• Read the target audience, learning objectives, and author disclosures.

• Read the article in print or online format.

• Reflect on the article.

• Access the CME Exam, and choose the best answer to each question.

• Complete the required evaluation component of the activity.

This activity will be available for CME credit for twelve months following its publication date. At that time, it will be reviewed and potentially updated and extended for an additional twelve months.

If you wish to receive credit for this activity, please refer to the website: www.wileyblackwellcme.com.

Accreditation and Designation Statement

Blackwell Futura Media Services designates this journal‐based CME activity for a maximum of 1 AMA PRA Category 1 Credit.. Physicians should only claim credit commensurate with the extent of their participation in the activity.

Blackwell Futura Media Services is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

Educational Objectives

Upon completion of this educational activity, participants will be better able to:

• Illustrate the elements of a systematic approach to successful hospital smoking cessation programs.

• Describe the efficacy of a coordinated real world hospital smoking cessation program in a U.S. hospital.

• Evaluate the barriers to successful hospital smoking cessation programs.

This manuscript underwent peer review in line with the standards of editorial integrity and publication ethics maintained by Journal of Hospital Medicine. The peer reviewers have no relevant financial relationships. The peer review process for Journal of Hospital Medicine is blinded. As such, the identities of the reviewers are not disclosed in line with the standard accepted practices of medical journal peer review.

Conflicts of interest have been identified and resolved in accordance with Blackwell Futura Media Services's Policy on Activity Disclosure and Conflict of Interest. The primary resolution method used was peer review and review by a non‐conflicted expert.

Instructions on Receiving Credit

For information on applicability and acceptance of CME credit for this activity, please consult your professional licensing board.

This activity is designed to be completed within an hour; physicians should claim only those credits that reflect the time actually spent in the activity. To successfully earn credit, participants must complete the activity during the valid credit period, which is up to two years from initial publication.

Follow these steps to earn credit:

• Log on to www.wileyblackwellcme.com

• Read the target audience, learning objectives, and author disclosures.

• Read the article in print or online format.

• Reflect on the article.

• Access the CME Exam, and choose the best answer to each question.

• Complete the required evaluation component of the activity.

This activity will be available for CME credit for twelve months following its publication date. At that time, it will be reviewed and potentially updated and extended for an additional twelve months.

If you wish to receive credit for this activity, please refer to the website: www.wileyblackwellcme.com.

Accreditation and Designation Statement

Blackwell Futura Media Services designates this journal‐based CME activity for a maximum of 1 AMA PRA Category 1 Credit.. Physicians should only claim credit commensurate with the extent of their participation in the activity.

Blackwell Futura Media Services is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

Educational Objectives

Upon completion of this educational activity, participants will be better able to:

• Illustrate the elements of a systematic approach to successful hospital smoking cessation programs.

• Describe the efficacy of a coordinated real world hospital smoking cessation program in a U.S. hospital.

• Evaluate the barriers to successful hospital smoking cessation programs.

This manuscript underwent peer review in line with the standards of editorial integrity and publication ethics maintained by Journal of Hospital Medicine. The peer reviewers have no relevant financial relationships. The peer review process for Journal of Hospital Medicine is blinded. As such, the identities of the reviewers are not disclosed in line with the standard accepted practices of medical journal peer review.

Conflicts of interest have been identified and resolved in accordance with Blackwell Futura Media Services's Policy on Activity Disclosure and Conflict of Interest. The primary resolution method used was peer review and review by a non‐conflicted expert.

Instructions on Receiving Credit

For information on applicability and acceptance of CME credit for this activity, please consult your professional licensing board.

This activity is designed to be completed within an hour; physicians should claim only those credits that reflect the time actually spent in the activity. To successfully earn credit, participants must complete the activity during the valid credit period, which is up to two years from initial publication.

Follow these steps to earn credit:

• Log on to www.wileyblackwellcme.com

• Read the target audience, learning objectives, and author disclosures.

• Read the article in print or online format.

• Reflect on the article.

• Access the CME Exam, and choose the best answer to each question.

• Complete the required evaluation component of the activity.

This activity will be available for CME credit for twelve months following its publication date. At that time, it will be reviewed and potentially updated and extended for an additional twelve months.

Communication and teamwork failures are the most frequently cited cause of adverse events.1, 2 Strategies to improve communication have focused on implementing formal teamwork training programs and/or teaching specific communication skills.36 For instance, many institutions have adopted SBAR (Situation‐Background‐Assessment‐Recommendation) as a method for providers to deliver critical clinical information in a structured format.7 SBAR focuses on the immediate and urgent event at hand and can occur between any 2 providers. The situation is a brief description of the event (eg, Hi Dr. Smith, this is Paul from 14‐Long, I'm calling about Mrs. Jones in 1427 who is in acute respiratory distress). The background describes details relevant to the situation (eg, She was admitted with a COPD exacerbation yesterday night, and, for the past couple hours, she appears in more distress. Her vital signs are). The assessment (eg, Her breath sounds are diminished and she's moving less air) and recommendation (eg, I'd like to call respiratory therapy and would like you to come assess her now) drive toward having an action defined at the end. Given the professional silos that exist in healthcare, the advent of a shared set of communication tools helps bridge existing gaps in training, experience, and teamwork between different providers.

Regulatory agencies have been heavily invested in attempts to standardize communication in healthcare settings. In 2003, the Joint Commission elevated the concerns for wrong‐site surgery by making its prevention a National Patient Safety Goal, and the following year required compliance with a Universal Protocol (UP).8 In addition to adequate preoperative identification of the patient and marking of their surgical site, the UP called for a time out (TO) just prior to the surgery or procedure. The UP states that a TO requires active communication among all members of the surgical/procedure team, consistently initiated by a designated member of the team, conducted in a fail‐safe mode, so that the planned procedure is not started if a member of the team has concerns.8 Simply, the TO provides an opportunity to clarify plans for care and discuss events anticipated during the procedure among all members of the team (eg, surgeons, anesthesiologists, nurses, technicians). This all‐important pause point ensures that each team member is on the same page.

Whereas a TO involves many high‐risk procedural settings, a significant proportion of hospital care occurs outside of procedures. Patients are often evaluated in an emergency department, admitted to a medical/surgical ward, treated without the need for a procedure, and ultimately discharged home or transferred to another healthcare facility (eg, skilled nursing or acute rehabilitation). In this paper, we introduce the concept of Critical Conversations, a form of nonprocedural time out, as a tool, intervention, and policy that promotes communication and teamwork at the most vulnerable junctures in a patient's hospitalization.

Rationale for Critical Conversations: a Case Scenario

An 82‐year‐old man with hypertension and chronic obstructive pulmonary disease (COPD) is admitted to the hospital with community‐acquired pneumonia and an exacerbation of his COPD. The admitting physician evaluates the patient in the emergency department and completes admission orders. The patient arrives on the medical/surgical unit and the unit clerk processes the orders, stimulating a cascade of downstream events for different providers.

Description of a Critical Conversation

In the hours that follow an admission, providers (and often the patients or their family as well) invariably exchange any number of inefficient calls or pages to clarify care plans, discuss a suspected diagnosis, anticipate concerns in the first night, and/or highlight which orders should be prioritized, such as medications or diagnostic studies. A Critical Conversation at time of admission does in this circumstance exactly what a TO attempts to provide before a procedure foster communication and teamwork as a patient is about to be placed at risk for adverse events. The exchange involves discussion of the following:

• Admitting diagnosis

• Immediate treatment plan

• Medications ordered (particularly those new to a patient to anticipate an adverse event)

• Priority for completing any admitting orders

• Guidelines for physician notification when a change in patient condition occurs.

At the other end of a hospitalization, with the known complications arising from a patient's discharge,11, 12 the same process is needed. Rather than having each discipline focus on an individual role or task in getting a patient safely discharged, Critical Conversations allow the entire team, including the patient,13 to ensure that concerns have been addressed. This might help clarify simple measures around follow‐up appointments, whom to call with questions after discharge, or symptoms to watch for that may warrant a repeat evaluation. Nurses anecdotally lament that they first learn about a planned discharge only when the discharge order is written in the chart or if a patient informs them. Both scenarios reflect poorly on the teamwork required to assure patients we're working together, and that key providers are on the same page with respect to discharge planning. The exchange at discharge involves discussion of these elements:

• Discharge diagnosis

• Follow‐up plans

• Need for education/training prior to discharge

• Necessary paperwork completed

• Anticipated time of discharge.

Finally, where many patients are admitted to a hospital, improve, and then return home, others develop acute changes during their hospitalization. For example, the patient in our case scenario could develop respiratory failure and require transfer to the intensive care unit (ICU). Or a different patient might have an acute change in mental status, a new fever, a new abnormal vital sign (eg, tachycardia or hypoxia), or an acute change re existing abdominal painall of which may require a battery of diagnostic tests. These circumstances define the third time for a Critical Conversation: a change in clinical condition. Such situations often require a change in the care plan, a change in priorities for delivering care at that time (for the patient in need and for other patients being cared for by the same nurse and physician), a need for additional resources (eg, respiratory therapist, phlebotomist, pharmacist), and, ultimately, a well‐orchestrated team effort to make it all happen. The specific item prompting the Critical Conversation may impact the nature of the exchange, which involves discussion of these components:

• Suspected diagnosis

• Immediate treatment plan

• Medications ordered (particularly those new to a patient to anticipate an adverse event)

• Priority for completing any new orders

• Guidelines for physician notification when a change in patient condition occurs.

In addition to the above checklist for each Critical Conversation, each exchange should also address two open‐ended questions: 1) what do you anticipate happening in the next 24 hours, and 2) what questions might the patient/family have?

One may ask, and we did, why not have a direct communication daily between a physician and a bedside nurse on each patient? Most physicians and nurses know the importance of direct communication, but there are also times when each is prioritizing work in competing fashions. Adopting Critical Conversations isn't meant to deter from communications that are vital to patient care; rather, it is intended to codify distinct times when a direct communication is required for patient safety.

Lessons Learned

Table 1 provides an example of a Critical Conversation using the sample case scenario. Table 2 lists the most frequent outcomes that resulted from providers engaging in Critical Conversations. These were captured from discussions with bedside nurses and internal medicine residents on our primary medical unit. Both tables highlight how these deliberate and direct communications can create a shared understanding of the patient's medical problems, can help prioritize what tasks should take place (eg, radiology study, medication administration, calling another provider), can improve communication between providers and patients, and potentially accomplish all of these goals in a more efficient manner.

Making Critical Conversations Happen

Integrating Critical Conversations into practice requires both buy‐in among providers and a plan for monitoring the interactions. We recommend beginning with educational efforts (eg, at a physician or nurse staff meeting) and reinforcing them with visual cues, such as posters on the unit (Figure 1). These actions promote awareness and generate expectations that this new clinical policy is being supported by clinical and hospital leadership. Our experiences have demonstrated tremendous learning, including numerous anecdotes about the value of Critical Conversations (Table 3). Our implementation efforts also raised a number of questions that ultimately led to improved clarity in later iterations.

Figure 1

Table 3.Provider Experiences Using Critical Conversations

Nothing is worse than meeting a patient for the first time at admission and not being able to answer the basic question of why they were admitted or what the plan is. It gives the impression that we don't talk to each other in caring for patients. [Critical Conversations] can really minimize that interaction and reassure patients, rather than make them worried about the apparent mixed messages or lack of communication and teamwork.Bedside Nurse
[Critical Conversations] seemed like an additional timely responsibility, and not always a part of my workflow, when sitting in the emergency department admitting patients. But, I found that the often 60 second conversations decreased the number of pages I would get for the same patientactually saving me time.Physician
I don't need to have direct communications for every order written. In fact, it would be inefficient for me and the doctors. On the other hand, being engaged in a Critical Conversation provides an opportunity for me to prioritize not only my tasks for the patient in need, but also in context of the other patients I'm caring for.Bedside Nurse
Late in the afternoon, there will often be several admissions coming to our unit simultaneously. Prioritizing what orders need to be processed or faxed is a typically blind task based on the way charts get organizedrather than someone telling me this is a priority.Unit Clerk
There are so many times when I'm trying to determine what the care plans are for a new admission, and simply having a quick conversation allows me to feel part of the team, and, more importantly, allows me to reinforce education and support for the patients and their family members.Bedside Nurse
Discharge always seems chaotic with everyone racing to fill out forms and meet their own tasks and requirements. Invariably, you get called to fix, change, or add new information to the discharge process that would have been easily averted by actually having a brief conversation with the bedside nurse or case manager. Every time I have [a Critical Conversation], I realize its importance for patient care.Physician

Communication and teamwork failures are the most frequently cited cause of adverse events.1, 2 Strategies to improve communication have focused on implementing formal teamwork training programs and/or teaching specific communication skills.36 For instance, many institutions have adopted SBAR (Situation‐Background‐Assessment‐Recommendation) as a method for providers to deliver critical clinical information in a structured format.7 SBAR focuses on the immediate and urgent event at hand and can occur between any 2 providers. The situation is a brief description of the event (eg, Hi Dr. Smith, this is Paul from 14‐Long, I'm calling about Mrs. Jones in 1427 who is in acute respiratory distress). The background describes details relevant to the situation (eg, She was admitted with a COPD exacerbation yesterday night, and, for the past couple hours, she appears in more distress. Her vital signs are). The assessment (eg, Her breath sounds are diminished and she's moving less air) and recommendation (eg, I'd like to call respiratory therapy and would like you to come assess her now) drive toward having an action defined at the end. Given the professional silos that exist in healthcare, the advent of a shared set of communication tools helps bridge existing gaps in training, experience, and teamwork between different providers.

Regulatory agencies have been heavily invested in attempts to standardize communication in healthcare settings. In 2003, the Joint Commission elevated the concerns for wrong‐site surgery by making its prevention a National Patient Safety Goal, and the following year required compliance with a Universal Protocol (UP).8 In addition to adequate preoperative identification of the patient and marking of their surgical site, the UP called for a time out (TO) just prior to the surgery or procedure. The UP states that a TO requires active communication among all members of the surgical/procedure team, consistently initiated by a designated member of the team, conducted in a fail‐safe mode, so that the planned procedure is not started if a member of the team has concerns.8 Simply, the TO provides an opportunity to clarify plans for care and discuss events anticipated during the procedure among all members of the team (eg, surgeons, anesthesiologists, nurses, technicians). This all‐important pause point ensures that each team member is on the same page.

Whereas a TO involves many high‐risk procedural settings, a significant proportion of hospital care occurs outside of procedures. Patients are often evaluated in an emergency department, admitted to a medical/surgical ward, treated without the need for a procedure, and ultimately discharged home or transferred to another healthcare facility (eg, skilled nursing or acute rehabilitation). In this paper, we introduce the concept of Critical Conversations, a form of nonprocedural time out, as a tool, intervention, and policy that promotes communication and teamwork at the most vulnerable junctures in a patient's hospitalization.

Rationale for Critical Conversations: a Case Scenario

An 82‐year‐old man with hypertension and chronic obstructive pulmonary disease (COPD) is admitted to the hospital with community‐acquired pneumonia and an exacerbation of his COPD. The admitting physician evaluates the patient in the emergency department and completes admission orders. The patient arrives on the medical/surgical unit and the unit clerk processes the orders, stimulating a cascade of downstream events for different providers.

Description of a Critical Conversation

In the hours that follow an admission, providers (and often the patients or their family as well) invariably exchange any number of inefficient calls or pages to clarify care plans, discuss a suspected diagnosis, anticipate concerns in the first night, and/or highlight which orders should be prioritized, such as medications or diagnostic studies. A Critical Conversation at time of admission does in this circumstance exactly what a TO attempts to provide before a procedure foster communication and teamwork as a patient is about to be placed at risk for adverse events. The exchange involves discussion of the following:

• Admitting diagnosis

• Immediate treatment plan

• Medications ordered (particularly those new to a patient to anticipate an adverse event)

• Priority for completing any admitting orders

• Guidelines for physician notification when a change in patient condition occurs.

At the other end of a hospitalization, with the known complications arising from a patient's discharge,11, 12 the same process is needed. Rather than having each discipline focus on an individual role or task in getting a patient safely discharged, Critical Conversations allow the entire team, including the patient,13 to ensure that concerns have been addressed. This might help clarify simple measures around follow‐up appointments, whom to call with questions after discharge, or symptoms to watch for that may warrant a repeat evaluation. Nurses anecdotally lament that they first learn about a planned discharge only when the discharge order is written in the chart or if a patient informs them. Both scenarios reflect poorly on the teamwork required to assure patients we're working together, and that key providers are on the same page with respect to discharge planning. The exchange at discharge involves discussion of these elements:

• Discharge diagnosis

• Follow‐up plans

• Need for education/training prior to discharge

• Necessary paperwork completed

• Anticipated time of discharge.

Finally, where many patients are admitted to a hospital, improve, and then return home, others develop acute changes during their hospitalization. For example, the patient in our case scenario could develop respiratory failure and require transfer to the intensive care unit (ICU). Or a different patient might have an acute change in mental status, a new fever, a new abnormal vital sign (eg, tachycardia or hypoxia), or an acute change re existing abdominal painall of which may require a battery of diagnostic tests. These circumstances define the third time for a Critical Conversation: a change in clinical condition. Such situations often require a change in the care plan, a change in priorities for delivering care at that time (for the patient in need and for other patients being cared for by the same nurse and physician), a need for additional resources (eg, respiratory therapist, phlebotomist, pharmacist), and, ultimately, a well‐orchestrated team effort to make it all happen. The specific item prompting the Critical Conversation may impact the nature of the exchange, which involves discussion of these components:

• Suspected diagnosis

• Immediate treatment plan

• Medications ordered (particularly those new to a patient to anticipate an adverse event)

• Priority for completing any new orders

• Guidelines for physician notification when a change in patient condition occurs.

In addition to the above checklist for each Critical Conversation, each exchange should also address two open‐ended questions: 1) what do you anticipate happening in the next 24 hours, and 2) what questions might the patient/family have?

One may ask, and we did, why not have a direct communication daily between a physician and a bedside nurse on each patient? Most physicians and nurses know the importance of direct communication, but there are also times when each is prioritizing work in competing fashions. Adopting Critical Conversations isn't meant to deter from communications that are vital to patient care; rather, it is intended to codify distinct times when a direct communication is required for patient safety.

Lessons Learned

Table 1 provides an example of a Critical Conversation using the sample case scenario. Table 2 lists the most frequent outcomes that resulted from providers engaging in Critical Conversations. These were captured from discussions with bedside nurses and internal medicine residents on our primary medical unit. Both tables highlight how these deliberate and direct communications can create a shared understanding of the patient's medical problems, can help prioritize what tasks should take place (eg, radiology study, medication administration, calling another provider), can improve communication between providers and patients, and potentially accomplish all of these goals in a more efficient manner.

Making Critical Conversations Happen

Integrating Critical Conversations into practice requires both buy‐in among providers and a plan for monitoring the interactions. We recommend beginning with educational efforts (eg, at a physician or nurse staff meeting) and reinforcing them with visual cues, such as posters on the unit (Figure 1). These actions promote awareness and generate expectations that this new clinical policy is being supported by clinical and hospital leadership. Our experiences have demonstrated tremendous learning, including numerous anecdotes about the value of Critical Conversations (Table 3). Our implementation efforts also raised a number of questions that ultimately led to improved clarity in later iterations.

Figure 1

Table 3.Provider Experiences Using Critical Conversations

Nothing is worse than meeting a patient for the first time at admission and not being able to answer the basic question of why they were admitted or what the plan is. It gives the impression that we don't talk to each other in caring for patients. [Critical Conversations] can really minimize that interaction and reassure patients, rather than make them worried about the apparent mixed messages or lack of communication and teamwork.Bedside Nurse
[Critical Conversations] seemed like an additional timely responsibility, and not always a part of my workflow, when sitting in the emergency department admitting patients. But, I found that the often 60 second conversations decreased the number of pages I would get for the same patientactually saving me time.Physician
I don't need to have direct communications for every order written. In fact, it would be inefficient for me and the doctors. On the other hand, being engaged in a Critical Conversation provides an opportunity for me to prioritize not only my tasks for the patient in need, but also in context of the other patients I'm caring for.Bedside Nurse
Late in the afternoon, there will often be several admissions coming to our unit simultaneously. Prioritizing what orders need to be processed or faxed is a typically blind task based on the way charts get organizedrather than someone telling me this is a priority.Unit Clerk
There are so many times when I'm trying to determine what the care plans are for a new admission, and simply having a quick conversation allows me to feel part of the team, and, more importantly, allows me to reinforce education and support for the patients and their family members.Bedside Nurse
Discharge always seems chaotic with everyone racing to fill out forms and meet their own tasks and requirements. Invariably, you get called to fix, change, or add new information to the discharge process that would have been easily averted by actually having a brief conversation with the bedside nurse or case manager. Every time I have [a Critical Conversation], I realize its importance for patient care.Physician

Communication and teamwork failures are the most frequently cited cause of adverse events.1, 2 Strategies to improve communication have focused on implementing formal teamwork training programs and/or teaching specific communication skills.36 For instance, many institutions have adopted SBAR (Situation‐Background‐Assessment‐Recommendation) as a method for providers to deliver critical clinical information in a structured format.7 SBAR focuses on the immediate and urgent event at hand and can occur between any 2 providers. The situation is a brief description of the event (eg, Hi Dr. Smith, this is Paul from 14‐Long, I'm calling about Mrs. Jones in 1427 who is in acute respiratory distress). The background describes details relevant to the situation (eg, She was admitted with a COPD exacerbation yesterday night, and, for the past couple hours, she appears in more distress. Her vital signs are). The assessment (eg, Her breath sounds are diminished and she's moving less air) and recommendation (eg, I'd like to call respiratory therapy and would like you to come assess her now) drive toward having an action defined at the end. Given the professional silos that exist in healthcare, the advent of a shared set of communication tools helps bridge existing gaps in training, experience, and teamwork between different providers.

Regulatory agencies have been heavily invested in attempts to standardize communication in healthcare settings. In 2003, the Joint Commission elevated the concerns for wrong‐site surgery by making its prevention a National Patient Safety Goal, and the following year required compliance with a Universal Protocol (UP).8 In addition to adequate preoperative identification of the patient and marking of their surgical site, the UP called for a time out (TO) just prior to the surgery or procedure. The UP states that a TO requires active communication among all members of the surgical/procedure team, consistently initiated by a designated member of the team, conducted in a fail‐safe mode, so that the planned procedure is not started if a member of the team has concerns.8 Simply, the TO provides an opportunity to clarify plans for care and discuss events anticipated during the procedure among all members of the team (eg, surgeons, anesthesiologists, nurses, technicians). This all‐important pause point ensures that each team member is on the same page.

Whereas a TO involves many high‐risk procedural settings, a significant proportion of hospital care occurs outside of procedures. Patients are often evaluated in an emergency department, admitted to a medical/surgical ward, treated without the need for a procedure, and ultimately discharged home or transferred to another healthcare facility (eg, skilled nursing or acute rehabilitation). In this paper, we introduce the concept of Critical Conversations, a form of nonprocedural time out, as a tool, intervention, and policy that promotes communication and teamwork at the most vulnerable junctures in a patient's hospitalization.

Rationale for Critical Conversations: a Case Scenario

An 82‐year‐old man with hypertension and chronic obstructive pulmonary disease (COPD) is admitted to the hospital with community‐acquired pneumonia and an exacerbation of his COPD. The admitting physician evaluates the patient in the emergency department and completes admission orders. The patient arrives on the medical/surgical unit and the unit clerk processes the orders, stimulating a cascade of downstream events for different providers.

Description of a Critical Conversation

In the hours that follow an admission, providers (and often the patients or their family as well) invariably exchange any number of inefficient calls or pages to clarify care plans, discuss a suspected diagnosis, anticipate concerns in the first night, and/or highlight which orders should be prioritized, such as medications or diagnostic studies. A Critical Conversation at time of admission does in this circumstance exactly what a TO attempts to provide before a procedure foster communication and teamwork as a patient is about to be placed at risk for adverse events. The exchange involves discussion of the following:

• Admitting diagnosis

• Immediate treatment plan

• Medications ordered (particularly those new to a patient to anticipate an adverse event)

• Priority for completing any admitting orders

• Guidelines for physician notification when a change in patient condition occurs.

At the other end of a hospitalization, with the known complications arising from a patient's discharge,11, 12 the same process is needed. Rather than having each discipline focus on an individual role or task in getting a patient safely discharged, Critical Conversations allow the entire team, including the patient,13 to ensure that concerns have been addressed. This might help clarify simple measures around follow‐up appointments, whom to call with questions after discharge, or symptoms to watch for that may warrant a repeat evaluation. Nurses anecdotally lament that they first learn about a planned discharge only when the discharge order is written in the chart or if a patient informs them. Both scenarios reflect poorly on the teamwork required to assure patients we're working together, and that key providers are on the same page with respect to discharge planning. The exchange at discharge involves discussion of these elements:

• Discharge diagnosis

• Follow‐up plans

• Need for education/training prior to discharge

• Necessary paperwork completed

• Anticipated time of discharge.

Finally, where many patients are admitted to a hospital, improve, and then return home, others develop acute changes during their hospitalization. For example, the patient in our case scenario could develop respiratory failure and require transfer to the intensive care unit (ICU). Or a different patient might have an acute change in mental status, a new fever, a new abnormal vital sign (eg, tachycardia or hypoxia), or an acute change re existing abdominal painall of which may require a battery of diagnostic tests. These circumstances define the third time for a Critical Conversation: a change in clinical condition. Such situations often require a change in the care plan, a change in priorities for delivering care at that time (for the patient in need and for other patients being cared for by the same nurse and physician), a need for additional resources (eg, respiratory therapist, phlebotomist, pharmacist), and, ultimately, a well‐orchestrated team effort to make it all happen. The specific item prompting the Critical Conversation may impact the nature of the exchange, which involves discussion of these components:

• Suspected diagnosis

• Immediate treatment plan

• Medications ordered (particularly those new to a patient to anticipate an adverse event)

• Priority for completing any new orders

• Guidelines for physician notification when a change in patient condition occurs.

In addition to the above checklist for each Critical Conversation, each exchange should also address two open‐ended questions: 1) what do you anticipate happening in the next 24 hours, and 2) what questions might the patient/family have?

One may ask, and we did, why not have a direct communication daily between a physician and a bedside nurse on each patient? Most physicians and nurses know the importance of direct communication, but there are also times when each is prioritizing work in competing fashions. Adopting Critical Conversations isn't meant to deter from communications that are vital to patient care; rather, it is intended to codify distinct times when a direct communication is required for patient safety.

Lessons Learned

Table 1 provides an example of a Critical Conversation using the sample case scenario. Table 2 lists the most frequent outcomes that resulted from providers engaging in Critical Conversations. These were captured from discussions with bedside nurses and internal medicine residents on our primary medical unit. Both tables highlight how these deliberate and direct communications can create a shared understanding of the patient's medical problems, can help prioritize what tasks should take place (eg, radiology study, medication administration, calling another provider), can improve communication between providers and patients, and potentially accomplish all of these goals in a more efficient manner.

Making Critical Conversations Happen

Integrating Critical Conversations into practice requires both buy‐in among providers and a plan for monitoring the interactions. We recommend beginning with educational efforts (eg, at a physician or nurse staff meeting) and reinforcing them with visual cues, such as posters on the unit (Figure 1). These actions promote awareness and generate expectations that this new clinical policy is being supported by clinical and hospital leadership. Our experiences have demonstrated tremendous learning, including numerous anecdotes about the value of Critical Conversations (Table 3). Our implementation efforts also raised a number of questions that ultimately led to improved clarity in later iterations.

Figure 1

Table 3.Provider Experiences Using Critical Conversations

Nothing is worse than meeting a patient for the first time at admission and not being able to answer the basic question of why they were admitted or what the plan is. It gives the impression that we don't talk to each other in caring for patients. [Critical Conversations] can really minimize that interaction and reassure patients, rather than make them worried about the apparent mixed messages or lack of communication and teamwork.Bedside Nurse
[Critical Conversations] seemed like an additional timely responsibility, and not always a part of my workflow, when sitting in the emergency department admitting patients. But, I found that the often 60 second conversations decreased the number of pages I would get for the same patientactually saving me time.Physician
I don't need to have direct communications for every order written. In fact, it would be inefficient for me and the doctors. On the other hand, being engaged in a Critical Conversation provides an opportunity for me to prioritize not only my tasks for the patient in need, but also in context of the other patients I'm caring for.Bedside Nurse
Late in the afternoon, there will often be several admissions coming to our unit simultaneously. Prioritizing what orders need to be processed or faxed is a typically blind task based on the way charts get organizedrather than someone telling me this is a priority.Unit Clerk
There are so many times when I'm trying to determine what the care plans are for a new admission, and simply having a quick conversation allows me to feel part of the team, and, more importantly, allows me to reinforce education and support for the patients and their family members.Bedside Nurse
Discharge always seems chaotic with everyone racing to fill out forms and meet their own tasks and requirements. Invariably, you get called to fix, change, or add new information to the discharge process that would have been easily averted by actually having a brief conversation with the bedside nurse or case manager. Every time I have [a Critical Conversation], I realize its importance for patient care.Physician