Andrew A. White, MD

CASE REPORT

Why You Might Think a Chest Radiograph is Helpful after Thoracentesis

Why a Routine Postprocedure Chest Radiograph is Not Helpful after Thoracentesis

Why PostProcedural CHEST RADIOGRAPHS Might be Helpful in Certain Circumstances

What You Should Do Instead

RECOMMENDATIONS:

CONCLUSION

CASE REPORT

Why You Might Think a Chest Radiograph is Helpful after Thoracentesis

Why a Routine Postprocedure Chest Radiograph is Not Helpful after Thoracentesis

Why PostProcedural CHEST RADIOGRAPHS Might be Helpful in Certain Circumstances

What You Should Do Instead

RECOMMENDATIONS:

CONCLUSION

CASE REPORT

Why You Might Think a Chest Radiograph is Helpful after Thoracentesis

Why a Routine Postprocedure Chest Radiograph is Not Helpful after Thoracentesis

Why PostProcedural CHEST RADIOGRAPHS Might be Helpful in Certain Circumstances

What You Should Do Instead

RECOMMENDATIONS:

CONCLUSION

DISCUSSION

TEACHING POINTS

DISCUSSION

TEACHING POINTS

DISCUSSION

TEACHING POINTS

Sitting while interacting with patients is standard in the outpatient setting and encouraged in the inpatient setting as a best practice.[1, 2] Michael W. Kahn defined etiquette‐based medicine as a set of easily taught behaviors that demonstrate respect for the patient; sitting at the bedside is included.[1] A prominent healthcare consulting group also recommends that physicians and nurses sit at the bedside, claiming that the patient will estimate you were in the room 3 times longer.[3] Previous studies suggest patients may perceive physicians who sit at the bedside as more compassionate and as spending more time with them, and may perceive the overall interaction as more positive when the physician sits.[4, 5, 6] Two small studies found that patients perceived the physician as having spent more time with them if he or she sat rather than stood.[5, 6] A study in the emergency department found no effect of posture on patient perception of physician communication skills, and a study of a single attending neurosurgeon found that patients reported a better understanding of their condition when the physician sat.[5, 6] The effect of physician posture on hospitalist physician‐patient communication has not been previously studied. Despite evidence that sitting in the inpatient setting may improve physician‐patient communication, studies suggest that physicians rarely sit at the bedside of inpatients.[7, 8]

We conducted a cluster‐randomized trial of the impact of hospitalist physician posture during morning rounds. We hypothesized that patients whose physician sat rather than stood would perceive that their physician spent more time with them and would rate the physician's communication skills more highly. We also hypothesized that sitting would not prolong the length of the patient‐physician encounter.

PATIENTS AND METHODS

We conducted a cluster‐randomized clinical trial with a crossover component randomizing physicians on the order of sit/stand within a consecutive 7‐day workweek. We enrolled patients being cared for by attending hospitalists on a resident‐uncovered general internal medicine service in an academic tertiary care hospital. We also enrolled the hospitalists and collected demographics and practice information. Wall‐mounted folding chairs (Figure 1) were installed in all rooms on two 28‐bed units for use by physicians. Eligible patients were newly admitted or transferred from the intensive care unit between June 2014 and June 2015, English speaking, and adults who consented to their own medical care. Physicians were randomly assigned to sit or stand during morning rounds for the first 3 days of their workweek. The last 4 days they provided care using the other posture. Blocks of 4 weeks were used to randomize the sit/stand order.

Figure 1

We measured the length of the physician‐patient interaction, asked both the physician and the patient to estimate the length of the interaction, and administered a written survey to the patient with questions about the physician's communication skills. Research assistants timed the interaction from outside the room and entered the room to consent patients and administer the survey after the physician departed. Survey questions were modeled on the physician communication questions from the Hospital Consumer Assessment of Healthcare Providers and Systems (HCAHPS) survey. We aggregated all answers other than the most positive answer because HCAHPS questions are analyzed according to a top box methodology. Adherence to the intervention was measured by asking the physician whether he or she actually sat or stood for each interaction. We administered a survey to physicians to collect demographics and feedback.

We estimated descriptive statistics for physician and patient participants using cross‐tabs and means. To estimate associations, we used logistic and linear regression that employed cluster‐adjusted t statistics and clustered patients within providers. This method optimizes estimation of standard errors (and corresponding confidence intervals and P values) when the number of clusters is small (16 physicians).[9] For our primary analysis, we analyzed as randomized using an intent‐to‐treat approach. In other words, those assigned to the standing group were analyzed in the standing group even if they actually sat (and vice versa). In a sensitivity analysis we used the same methods to analyze the data according actual provider posture as reported by the physician and not as randomized. We calculated the mean and range of the number of patients seen by physicians. We compared estimates of time spent between patients and providers and patients' satisfaction according to provider posture. We complied with the Consolidated Standards of Reporting Trials 2010 guidelines.[10] Our institutional review board approved this project. All participants provided written consent.

RESULTS

All 17 hospitalists attending on the service consented to participate; 1 did not see any patients involved in the study and was removed from the analysis. Sixty‐nine percent were female and 81% had been in practice for 3 years or less at the time of study enrollment; 94% reported standing when assigned to stand and 83% reported sitting when assigned to sit. We found 31% of physicians reported they routinely sat before participating in the study, and 81% said they would sit more after the study; this result approached statistical significance (exact McNemar P = 0.06). Of the 11 physicians who reported not routinely sitting before the study all, 7 cited not having a place to sit as a reason for not sitting. Other rationale provided included being too short to see the patient if seated, believing rounds would take more time if seated, and concerns about contact precautions. Comments in the postintervention survey regarding why providers planned to sit more centered around themes of having chairs available, thinking that sitting improves communication, and thinking that patients prefer providers to sit.

Two hundred eleven patients were assessed for eligibility. Fifty‐two were excluded (27 did not meet inclusion criteria and 25 declined to participate), leaving 159 participating patients. Seven patient‐physician pairs were inadvertently assigned the wrong intervention but were analyzed as randomized. There were no demographic differences between patient groups (Table 1). Physicians participating in the study saw an average of 13 study patients (range, 118) during the study. Mean time spent in the patient's room during rounds was 12:00 minutes for seated physicians and 12:10 for standing physicians (P = 0.84). Regardless of provider posture, patients overestimated the amount of time their physician spent in the room (mean difference 4:10 minutes, P = 0.01). Patients' estimates of the time the physician spent did not vary by posture (16:00 minutes for seated, 16:19 for standing, P = 0.86).

Patients whose physician sat on rounds were statistically significantly more likely to choose the answer always to the questions regarding their physician listening carefully to them (P = 0.02) and explaining things in a way that was easy to understand (P = 0.05, Table 2). There was no difference in the patients' response to questions about the physician interrupting the patient when talking or treating them with courtesy and respect. Nearly all patients chose just right when asked to rate the amount of time their physician had spent with them on rounds (Table 2). The results of our sensitivity analysis that classified physicians according to their actual posture yielded different results; none of the findings in that analysis including questions regarding the physician listening carefully or explaining things in a way that was easy to understand were statistically significant (see Supporting Information, Appendix 1, in the online version of this article).

DISCUSSION

In our study involving general medicine inpatients cared for by academic hospitalists, physicians did not spend more time in the room when seated, and were willing to adopt this practice. Patients perceived that seated compared to standing physicians listened more carefully and explained things in a way that was easy to understand when analyzed using an intent‐to‐treat approach. Patients did not perceive that seated physicians spent more time with them than standing physicians. To our knowledge, this is the first study showing the effects of hospitalist rounding posture on patient experience.

Our finding that patients rated seated physicians more highly on listening carefully and explaining things well indicates that training hospitalists to sit at the bedside may ultimately improve patient satisfaction. Our findings suggest seated interaction may improve satisfaction with communication without increasing time burden on physicians. However, given that these findings were not statistically significant when we analyzed our data according to actual behavior, larger studies should verify the impact of physician posture on patient experience.

Previous studies found that a minority of physicians sit in the inpatient setting, but did not study barriers to sitting while on rounds.[7, 8] A majority of physicians in our study sat when instructed to do so and when chairs were provided, and over 80% of physicians in our study said they planned to continue sitting while on rounds after the study was complete. A lack of chairs may be a major barrier to physicians adopting this facet of etiquette‐based medicine, and institutions wishing to promote this practice should consider providing chairs. Written comments from physician participants suggest physicians who are introduced to this practice enjoy sitting and think it improves physician‐patient communication. Further studies are needed to test our assumption that physicians continue sitting when chairs are provided.

Our work differs from previous studies. Johnson et al. studied interactions in the emergency room with a mean length of 8.6 minutes,[5] and Swayden et al. studied postoperative visits by a single neurosurgeon with a mean length of about 1 minute.[6] One explanation for the lack of a difference in time spent by posture might be that an average visit time of 12 minutes passes a threshold where patients make more accurate estimates of visit length or where factors other than posture more strongly influence perceptions of duration.

Limitations of our study include the relatively small sample size, single location, and limitation to English‐speaking patients able to consent themselves. Reasons for the limited sample size include that chairs were only installed in 2 units, and not all patients on the unit were under the care of participating physicians. Physician subjects were not blinded to their interactions being timed or to the fact that patients were surveyed about their communication skills. It is possible that factors that may have affected patients' responses such as severity of illness, number of consultants involved in their care, or prior experiences in the healthcare system were not equally distributed between our 2 groups. Additionally, our use of questions similar to those used in the HCAHPS instrument is not compliant with Centers for Medicare and Medicaid Services (CMS) policy. We caution others against using questions that might invalidate their hospital's participation in CMS payment programs.

Our study was limited to rounds involving 1 physician; our practice is that in a larger team the presenting member is encouraged to sit and others sit if there are additional chairs. Best practices on a teaching service are unclear and could be the subject of further study. The longer‐term sustainability of the practice of sitting on rounds is unclear. However, our physician subjects reported that they plan to continue to sit after the study, and we have shared the results with physicians in order to provide them with evidence supporting this practice. Not having a place to sit and thinking that sitting increases the amount of time spent on rounds were concerns provided in our preintervention survey, and we believe our study addresses these concerns.

Our study demonstrates the effects of a simple intervention on patient satisfaction without increasing burden on providers. Sitting at the bedside does not impact the amount of time spent with the patient, but may improve the patient's perception of the physician's communication skills and thus impact the patient experience. This simple intervention could improve patient satisfaction at little cost.

Sitting while interacting with patients is standard in the outpatient setting and encouraged in the inpatient setting as a best practice.[1, 2] Michael W. Kahn defined etiquette‐based medicine as a set of easily taught behaviors that demonstrate respect for the patient; sitting at the bedside is included.[1] A prominent healthcare consulting group also recommends that physicians and nurses sit at the bedside, claiming that the patient will estimate you were in the room 3 times longer.[3] Previous studies suggest patients may perceive physicians who sit at the bedside as more compassionate and as spending more time with them, and may perceive the overall interaction as more positive when the physician sits.[4, 5, 6] Two small studies found that patients perceived the physician as having spent more time with them if he or she sat rather than stood.[5, 6] A study in the emergency department found no effect of posture on patient perception of physician communication skills, and a study of a single attending neurosurgeon found that patients reported a better understanding of their condition when the physician sat.[5, 6] The effect of physician posture on hospitalist physician‐patient communication has not been previously studied. Despite evidence that sitting in the inpatient setting may improve physician‐patient communication, studies suggest that physicians rarely sit at the bedside of inpatients.[7, 8]

We conducted a cluster‐randomized trial of the impact of hospitalist physician posture during morning rounds. We hypothesized that patients whose physician sat rather than stood would perceive that their physician spent more time with them and would rate the physician's communication skills more highly. We also hypothesized that sitting would not prolong the length of the patient‐physician encounter.

PATIENTS AND METHODS

We conducted a cluster‐randomized clinical trial with a crossover component randomizing physicians on the order of sit/stand within a consecutive 7‐day workweek. We enrolled patients being cared for by attending hospitalists on a resident‐uncovered general internal medicine service in an academic tertiary care hospital. We also enrolled the hospitalists and collected demographics and practice information. Wall‐mounted folding chairs (Figure 1) were installed in all rooms on two 28‐bed units for use by physicians. Eligible patients were newly admitted or transferred from the intensive care unit between June 2014 and June 2015, English speaking, and adults who consented to their own medical care. Physicians were randomly assigned to sit or stand during morning rounds for the first 3 days of their workweek. The last 4 days they provided care using the other posture. Blocks of 4 weeks were used to randomize the sit/stand order.

Figure 1

We measured the length of the physician‐patient interaction, asked both the physician and the patient to estimate the length of the interaction, and administered a written survey to the patient with questions about the physician's communication skills. Research assistants timed the interaction from outside the room and entered the room to consent patients and administer the survey after the physician departed. Survey questions were modeled on the physician communication questions from the Hospital Consumer Assessment of Healthcare Providers and Systems (HCAHPS) survey. We aggregated all answers other than the most positive answer because HCAHPS questions are analyzed according to a top box methodology. Adherence to the intervention was measured by asking the physician whether he or she actually sat or stood for each interaction. We administered a survey to physicians to collect demographics and feedback.

We estimated descriptive statistics for physician and patient participants using cross‐tabs and means. To estimate associations, we used logistic and linear regression that employed cluster‐adjusted t statistics and clustered patients within providers. This method optimizes estimation of standard errors (and corresponding confidence intervals and P values) when the number of clusters is small (16 physicians).[9] For our primary analysis, we analyzed as randomized using an intent‐to‐treat approach. In other words, those assigned to the standing group were analyzed in the standing group even if they actually sat (and vice versa). In a sensitivity analysis we used the same methods to analyze the data according actual provider posture as reported by the physician and not as randomized. We calculated the mean and range of the number of patients seen by physicians. We compared estimates of time spent between patients and providers and patients' satisfaction according to provider posture. We complied with the Consolidated Standards of Reporting Trials 2010 guidelines.[10] Our institutional review board approved this project. All participants provided written consent.

RESULTS

All 17 hospitalists attending on the service consented to participate; 1 did not see any patients involved in the study and was removed from the analysis. Sixty‐nine percent were female and 81% had been in practice for 3 years or less at the time of study enrollment; 94% reported standing when assigned to stand and 83% reported sitting when assigned to sit. We found 31% of physicians reported they routinely sat before participating in the study, and 81% said they would sit more after the study; this result approached statistical significance (exact McNemar P = 0.06). Of the 11 physicians who reported not routinely sitting before the study all, 7 cited not having a place to sit as a reason for not sitting. Other rationale provided included being too short to see the patient if seated, believing rounds would take more time if seated, and concerns about contact precautions. Comments in the postintervention survey regarding why providers planned to sit more centered around themes of having chairs available, thinking that sitting improves communication, and thinking that patients prefer providers to sit.

Two hundred eleven patients were assessed for eligibility. Fifty‐two were excluded (27 did not meet inclusion criteria and 25 declined to participate), leaving 159 participating patients. Seven patient‐physician pairs were inadvertently assigned the wrong intervention but were analyzed as randomized. There were no demographic differences between patient groups (Table 1). Physicians participating in the study saw an average of 13 study patients (range, 118) during the study. Mean time spent in the patient's room during rounds was 12:00 minutes for seated physicians and 12:10 for standing physicians (P = 0.84). Regardless of provider posture, patients overestimated the amount of time their physician spent in the room (mean difference 4:10 minutes, P = 0.01). Patients' estimates of the time the physician spent did not vary by posture (16:00 minutes for seated, 16:19 for standing, P = 0.86).

Patients whose physician sat on rounds were statistically significantly more likely to choose the answer always to the questions regarding their physician listening carefully to them (P = 0.02) and explaining things in a way that was easy to understand (P = 0.05, Table 2). There was no difference in the patients' response to questions about the physician interrupting the patient when talking or treating them with courtesy and respect. Nearly all patients chose just right when asked to rate the amount of time their physician had spent with them on rounds (Table 2). The results of our sensitivity analysis that classified physicians according to their actual posture yielded different results; none of the findings in that analysis including questions regarding the physician listening carefully or explaining things in a way that was easy to understand were statistically significant (see Supporting Information, Appendix 1, in the online version of this article).

DISCUSSION

In our study involving general medicine inpatients cared for by academic hospitalists, physicians did not spend more time in the room when seated, and were willing to adopt this practice. Patients perceived that seated compared to standing physicians listened more carefully and explained things in a way that was easy to understand when analyzed using an intent‐to‐treat approach. Patients did not perceive that seated physicians spent more time with them than standing physicians. To our knowledge, this is the first study showing the effects of hospitalist rounding posture on patient experience.

Our finding that patients rated seated physicians more highly on listening carefully and explaining things well indicates that training hospitalists to sit at the bedside may ultimately improve patient satisfaction. Our findings suggest seated interaction may improve satisfaction with communication without increasing time burden on physicians. However, given that these findings were not statistically significant when we analyzed our data according to actual behavior, larger studies should verify the impact of physician posture on patient experience.

Previous studies found that a minority of physicians sit in the inpatient setting, but did not study barriers to sitting while on rounds.[7, 8] A majority of physicians in our study sat when instructed to do so and when chairs were provided, and over 80% of physicians in our study said they planned to continue sitting while on rounds after the study was complete. A lack of chairs may be a major barrier to physicians adopting this facet of etiquette‐based medicine, and institutions wishing to promote this practice should consider providing chairs. Written comments from physician participants suggest physicians who are introduced to this practice enjoy sitting and think it improves physician‐patient communication. Further studies are needed to test our assumption that physicians continue sitting when chairs are provided.

Our work differs from previous studies. Johnson et al. studied interactions in the emergency room with a mean length of 8.6 minutes,[5] and Swayden et al. studied postoperative visits by a single neurosurgeon with a mean length of about 1 minute.[6] One explanation for the lack of a difference in time spent by posture might be that an average visit time of 12 minutes passes a threshold where patients make more accurate estimates of visit length or where factors other than posture more strongly influence perceptions of duration.

Limitations of our study include the relatively small sample size, single location, and limitation to English‐speaking patients able to consent themselves. Reasons for the limited sample size include that chairs were only installed in 2 units, and not all patients on the unit were under the care of participating physicians. Physician subjects were not blinded to their interactions being timed or to the fact that patients were surveyed about their communication skills. It is possible that factors that may have affected patients' responses such as severity of illness, number of consultants involved in their care, or prior experiences in the healthcare system were not equally distributed between our 2 groups. Additionally, our use of questions similar to those used in the HCAHPS instrument is not compliant with Centers for Medicare and Medicaid Services (CMS) policy. We caution others against using questions that might invalidate their hospital's participation in CMS payment programs.

Our study was limited to rounds involving 1 physician; our practice is that in a larger team the presenting member is encouraged to sit and others sit if there are additional chairs. Best practices on a teaching service are unclear and could be the subject of further study. The longer‐term sustainability of the practice of sitting on rounds is unclear. However, our physician subjects reported that they plan to continue to sit after the study, and we have shared the results with physicians in order to provide them with evidence supporting this practice. Not having a place to sit and thinking that sitting increases the amount of time spent on rounds were concerns provided in our preintervention survey, and we believe our study addresses these concerns.

Our study demonstrates the effects of a simple intervention on patient satisfaction without increasing burden on providers. Sitting at the bedside does not impact the amount of time spent with the patient, but may improve the patient's perception of the physician's communication skills and thus impact the patient experience. This simple intervention could improve patient satisfaction at little cost.

Sitting while interacting with patients is standard in the outpatient setting and encouraged in the inpatient setting as a best practice.[1, 2] Michael W. Kahn defined etiquette‐based medicine as a set of easily taught behaviors that demonstrate respect for the patient; sitting at the bedside is included.[1] A prominent healthcare consulting group also recommends that physicians and nurses sit at the bedside, claiming that the patient will estimate you were in the room 3 times longer.[3] Previous studies suggest patients may perceive physicians who sit at the bedside as more compassionate and as spending more time with them, and may perceive the overall interaction as more positive when the physician sits.[4, 5, 6] Two small studies found that patients perceived the physician as having spent more time with them if he or she sat rather than stood.[5, 6] A study in the emergency department found no effect of posture on patient perception of physician communication skills, and a study of a single attending neurosurgeon found that patients reported a better understanding of their condition when the physician sat.[5, 6] The effect of physician posture on hospitalist physician‐patient communication has not been previously studied. Despite evidence that sitting in the inpatient setting may improve physician‐patient communication, studies suggest that physicians rarely sit at the bedside of inpatients.[7, 8]

We conducted a cluster‐randomized trial of the impact of hospitalist physician posture during morning rounds. We hypothesized that patients whose physician sat rather than stood would perceive that their physician spent more time with them and would rate the physician's communication skills more highly. We also hypothesized that sitting would not prolong the length of the patient‐physician encounter.

PATIENTS AND METHODS

We conducted a cluster‐randomized clinical trial with a crossover component randomizing physicians on the order of sit/stand within a consecutive 7‐day workweek. We enrolled patients being cared for by attending hospitalists on a resident‐uncovered general internal medicine service in an academic tertiary care hospital. We also enrolled the hospitalists and collected demographics and practice information. Wall‐mounted folding chairs (Figure 1) were installed in all rooms on two 28‐bed units for use by physicians. Eligible patients were newly admitted or transferred from the intensive care unit between June 2014 and June 2015, English speaking, and adults who consented to their own medical care. Physicians were randomly assigned to sit or stand during morning rounds for the first 3 days of their workweek. The last 4 days they provided care using the other posture. Blocks of 4 weeks were used to randomize the sit/stand order.

Figure 1

We measured the length of the physician‐patient interaction, asked both the physician and the patient to estimate the length of the interaction, and administered a written survey to the patient with questions about the physician's communication skills. Research assistants timed the interaction from outside the room and entered the room to consent patients and administer the survey after the physician departed. Survey questions were modeled on the physician communication questions from the Hospital Consumer Assessment of Healthcare Providers and Systems (HCAHPS) survey. We aggregated all answers other than the most positive answer because HCAHPS questions are analyzed according to a top box methodology. Adherence to the intervention was measured by asking the physician whether he or she actually sat or stood for each interaction. We administered a survey to physicians to collect demographics and feedback.

We estimated descriptive statistics for physician and patient participants using cross‐tabs and means. To estimate associations, we used logistic and linear regression that employed cluster‐adjusted t statistics and clustered patients within providers. This method optimizes estimation of standard errors (and corresponding confidence intervals and P values) when the number of clusters is small (16 physicians).[9] For our primary analysis, we analyzed as randomized using an intent‐to‐treat approach. In other words, those assigned to the standing group were analyzed in the standing group even if they actually sat (and vice versa). In a sensitivity analysis we used the same methods to analyze the data according actual provider posture as reported by the physician and not as randomized. We calculated the mean and range of the number of patients seen by physicians. We compared estimates of time spent between patients and providers and patients' satisfaction according to provider posture. We complied with the Consolidated Standards of Reporting Trials 2010 guidelines.[10] Our institutional review board approved this project. All participants provided written consent.

RESULTS

All 17 hospitalists attending on the service consented to participate; 1 did not see any patients involved in the study and was removed from the analysis. Sixty‐nine percent were female and 81% had been in practice for 3 years or less at the time of study enrollment; 94% reported standing when assigned to stand and 83% reported sitting when assigned to sit. We found 31% of physicians reported they routinely sat before participating in the study, and 81% said they would sit more after the study; this result approached statistical significance (exact McNemar P = 0.06). Of the 11 physicians who reported not routinely sitting before the study all, 7 cited not having a place to sit as a reason for not sitting. Other rationale provided included being too short to see the patient if seated, believing rounds would take more time if seated, and concerns about contact precautions. Comments in the postintervention survey regarding why providers planned to sit more centered around themes of having chairs available, thinking that sitting improves communication, and thinking that patients prefer providers to sit.

Two hundred eleven patients were assessed for eligibility. Fifty‐two were excluded (27 did not meet inclusion criteria and 25 declined to participate), leaving 159 participating patients. Seven patient‐physician pairs were inadvertently assigned the wrong intervention but were analyzed as randomized. There were no demographic differences between patient groups (Table 1). Physicians participating in the study saw an average of 13 study patients (range, 118) during the study. Mean time spent in the patient's room during rounds was 12:00 minutes for seated physicians and 12:10 for standing physicians (P = 0.84). Regardless of provider posture, patients overestimated the amount of time their physician spent in the room (mean difference 4:10 minutes, P = 0.01). Patients' estimates of the time the physician spent did not vary by posture (16:00 minutes for seated, 16:19 for standing, P = 0.86).

Patients whose physician sat on rounds were statistically significantly more likely to choose the answer always to the questions regarding their physician listening carefully to them (P = 0.02) and explaining things in a way that was easy to understand (P = 0.05, Table 2). There was no difference in the patients' response to questions about the physician interrupting the patient when talking or treating them with courtesy and respect. Nearly all patients chose just right when asked to rate the amount of time their physician had spent with them on rounds (Table 2). The results of our sensitivity analysis that classified physicians according to their actual posture yielded different results; none of the findings in that analysis including questions regarding the physician listening carefully or explaining things in a way that was easy to understand were statistically significant (see Supporting Information, Appendix 1, in the online version of this article).

DISCUSSION

In our study involving general medicine inpatients cared for by academic hospitalists, physicians did not spend more time in the room when seated, and were willing to adopt this practice. Patients perceived that seated compared to standing physicians listened more carefully and explained things in a way that was easy to understand when analyzed using an intent‐to‐treat approach. Patients did not perceive that seated physicians spent more time with them than standing physicians. To our knowledge, this is the first study showing the effects of hospitalist rounding posture on patient experience.

Our finding that patients rated seated physicians more highly on listening carefully and explaining things well indicates that training hospitalists to sit at the bedside may ultimately improve patient satisfaction. Our findings suggest seated interaction may improve satisfaction with communication without increasing time burden on physicians. However, given that these findings were not statistically significant when we analyzed our data according to actual behavior, larger studies should verify the impact of physician posture on patient experience.

Previous studies found that a minority of physicians sit in the inpatient setting, but did not study barriers to sitting while on rounds.[7, 8] A majority of physicians in our study sat when instructed to do so and when chairs were provided, and over 80% of physicians in our study said they planned to continue sitting while on rounds after the study was complete. A lack of chairs may be a major barrier to physicians adopting this facet of etiquette‐based medicine, and institutions wishing to promote this practice should consider providing chairs. Written comments from physician participants suggest physicians who are introduced to this practice enjoy sitting and think it improves physician‐patient communication. Further studies are needed to test our assumption that physicians continue sitting when chairs are provided.

Our work differs from previous studies. Johnson et al. studied interactions in the emergency room with a mean length of 8.6 minutes,[5] and Swayden et al. studied postoperative visits by a single neurosurgeon with a mean length of about 1 minute.[6] One explanation for the lack of a difference in time spent by posture might be that an average visit time of 12 minutes passes a threshold where patients make more accurate estimates of visit length or where factors other than posture more strongly influence perceptions of duration.

Limitations of our study include the relatively small sample size, single location, and limitation to English‐speaking patients able to consent themselves. Reasons for the limited sample size include that chairs were only installed in 2 units, and not all patients on the unit were under the care of participating physicians. Physician subjects were not blinded to their interactions being timed or to the fact that patients were surveyed about their communication skills. It is possible that factors that may have affected patients' responses such as severity of illness, number of consultants involved in their care, or prior experiences in the healthcare system were not equally distributed between our 2 groups. Additionally, our use of questions similar to those used in the HCAHPS instrument is not compliant with Centers for Medicare and Medicaid Services (CMS) policy. We caution others against using questions that might invalidate their hospital's participation in CMS payment programs.

Our study was limited to rounds involving 1 physician; our practice is that in a larger team the presenting member is encouraged to sit and others sit if there are additional chairs. Best practices on a teaching service are unclear and could be the subject of further study. The longer‐term sustainability of the practice of sitting on rounds is unclear. However, our physician subjects reported that they plan to continue to sit after the study, and we have shared the results with physicians in order to provide them with evidence supporting this practice. Not having a place to sit and thinking that sitting increases the amount of time spent on rounds were concerns provided in our preintervention survey, and we believe our study addresses these concerns.

Our study demonstrates the effects of a simple intervention on patient satisfaction without increasing burden on providers. Sitting at the bedside does not impact the amount of time spent with the patient, but may improve the patient's perception of the physician's communication skills and thus impact the patient experience. This simple intervention could improve patient satisfaction at little cost.

Interhospital transfers (IHTs) to academic medical centers (AMCs) or their affiliated hospitals may benefit patients who require unique specialty and procedural services. However, IHTs also introduce a potentially risky transition of care for patients suffering from complex or unstable medical problems.[1] Components of this risk include the dangers associated with transportation and the disrupted continuity of care that may lead to delays or errors in care.[2, 3] Furthermore, referring and accepting providers may face barriers to optimal handoffs including a lack of shared communication standards and difficulty accessing external medical records.[3, 4, 5] Although some authors have recommended the creation of formal guidelines for interhospital transfer processes for all patients to mitigate the risks of transfer, the available guidelines governing the IHT triage and communication process are limited to critically ill patients.[6]

A recent study of a diverse patient and hospital dataset demonstrated that interhospital transfer patients have a higher risk of mortality, increased length of stay (LOS), and increased risk of adverse events as compared with non‐transfer patients.[7] However, it is unknown if these findings persist in the population of patients transferred specifically to AMCs or their affiliated hospitals (the combination is hereafter referred to as academic health systems [AHSs]). AMCs provide a disproportionate share of IHT care for complex patients and have a vested interest in improving the outcomes of these transitions.[8] Prior single‐center studies of acute care adult medical patients accepted to AMCs have shown that IHT is associated with a longer LOS, increased in‐hospital mortality, and higher resource use.[9, 10] However, it is difficult to generalize from single‐center studies due to the variation in referral practices, geography, and network characteristics. Additionally, AMC referral systems, patient mix, and utilization of hospitalists have likely changed substantially in the nearly 2 decades since those reports were published.

Hospitalists and general internists often manage the transfer acceptance processes for internal medicine services at receiving hospitals, helping to triage and coordinate care for IHT patients. As a result, it is important for hospitalists to understand the characteristics and outcomes of the IHT population. In addition to informing the decision making around transfer for a given patient, such an understanding is the foundation for helping providers and institutions begin to systematically identify and mitigate peritransfer risks.

We conducted this large multicenter study to describe the characteristics and outcomes of a current, nationally representative IHT patient population discharged by hospitalists and general internists at AHSs. To identify unique features of the IHT population, we compared patients transferred from another hospital to an AHS to those admitted to the AHS directly from the AHS's emergency department (ED). Based on our anecdotal experiences and the prior single‐center study findings in adult medical populations,[9, 10] we hypothesized that the IHT population would be sicker, stay in the hospital and intensive care unit (ICU) longer, and have higher costs and in‐hospital mortality than ED patients. Although there may be fundamental differences between the 2 groups related to disease and patient condition, we hypothesized that outcome differences would persist even after adjusting for patient factors such as demographics, disease‐specific risk of mortality, and ICU utilization.

PATIENTS AND METHODS

We conducted a retrospective cohort study using data from the University HealthSystem Consortium (UHC) Clinical Database and Resource Manager (CDB/RM). UHC is an alliance of 120 academic medical centers and 300 of their affiliated hospitals for the purposes of collaboration on performance improvement. Each year, a subset of participating hospitals submits data on all of their inpatient discharges to the CDB/RM, which totals approximately 5 million records. The CDB/RM includes information from billing forms including demographics, diagnoses, and procedures as captured by International Classification of Diseases, Ninth Revision (ICD‐9) codes, discharge disposition, and line item charge detail for the type of bed (eg, floor, ICU). Most hospitals also provide detailed charge information including pharmacy, imaging, blood products, lab tests, and supplies. Some hospitals do not provide any charge data. The Beth Israel Deaconess Medical Center and University of Washington institutional review boards reviewed and approved the conduct of this study.

We included all inpatients discharged by hospitalists or general internal medicine physicians from UHC hospitals between April 1, 2011 and March 31, 2012. We excluded minors, pregnant patients, and prisoners. One hundred fifty‐eight adult academic medical centers and affiliated hospitals submitted data throughout this time period. Our primary independent variable, IHT status, was defined by patients whose admission source was another acute care institution. ED admissions were defined as patients admitted from the AHS ED whose source of origination was not another hospital or ambulatory surgery site.

RESULTS

DISCUSSION

Our study of IHT patients ultimately discharged by hospitalists and general internists at US academic referral centers found significantly increased average LOS, costs, and in‐hospital mortality compared with patients admitted from the ED. The increased risk of mortality persisted after adjustment for patient characteristics and variables representing endogenous risk of mortality, and in more homogeneous subgroups after stratification by presence and timing of ICU utilization. These data confirm findings from single‐center studies and suggest that observations about the difference between IHT and ED populations may be generalizable across US academic hospitals.

Our work builds on 2 single‐center studies that examined mixed medical and surgical academic IHT populations from the late 1980s and early 1990s,[9, 10] and 1 studying surgical ICU patients in 2013.[17] These studies demonstrated longer average LOS, higher costs, and higher mortality rates (in both adjusted and unadjusted analyses). Our work confirmed these findings utilizing a more current, multicenter large dataset of IHT patients ultimately discharged by hospitalists and general internists. Our work is unique from a larger, more recent study[7] in that it focuses on patients transferred to academic health systems, and therefore has particular relevance to those settings. In addition, we divided patients into subpopulations based on the timing of ICU utilization, and found that in each of these populations, IHT remained independently associated with in‐hospital mortality.

Our analysis does not explain why the outcomes of IHTs are worse, but plausible contributing factors include that (1) patients chosen for IHT are at higher risk of death in ways uncaptured by established mortality risk scores, (2) referring, transferring, or accepting providers and institutions have provided inadequate care, (3) the transfer process itself involves harm, (4) socioeconomic bias in selection for IHT,[18] or (5) some combination of the above. Regardless of the causes of the worse outcomes observed in these outside‐hospital transfers, as these patients are colloquially known at accepting hospitals, they present challenges to everyone involved. Referring providers may feel a sense of urgency as these patients' needs exceed their management capabilities. The process is often time consuming and burdensome for referring and accepting providers because of poorly developed systems.[19] The transfer often takes patients further from their home and may make it more difficult for family to participate in their care. The transfer may delay care if the accepting institution cannot immediately accept the patient or if the time in transport is prolonged, which could result in decompensation at a critical juncture. For providers inheriting such patients, the stress of caring for these patients is compounded by the difficulty obtaining records about the prior hospitalization.[20] This frustrating experience is often translated into unfounded judgment of the institution that referred the patient and the care provided there.[21] It is important for hospitalists making decisions throughout the transfer process and for hospital leaders who determine staffing levels, measure the quality of care, manage hospital networks, or write hospital policy to appreciate that the transfer process itself may contribute to the challenges and poor outcomes we observe. Furthermore, regardless of the cause for the increased mortality that we observed, our findings imply that IHT patients require careful evaluation, management, and treatment.

Many accepting institutions have transfer centers that facilitate these transitions, utilizing protocols and templates to standardize the process.[22, 23] Future research should focus on the characteristics of these centers to learn which practices are most efficacious. Interventions to mitigate the known challenges of transfer (including patient selection and triage, handoff communication, and information sharing) could be tested by randomized studies at referring and accepting institutions. There may be a role for health information exchange or the development of enhanced pretransfer evaluation processes using telemedicine models; there is evidence that information sharing may reduce redundant imaging.[24] Perhaps targeted review of IHTs admitted to a non‐ICU portion of the hospital and subsequently transferred to the ICU could identify opportunities to improve triaging protocols and thus avert some of the bad outcomes observed in this subpopulation. A related future direction could be to create protected forumsusing the patient safety organization framework[25]to facilitate the discussion of interhospital transfer outcomes among the referring, transporting, and receiving parties. Lastly, future work should investigate the reasons for the different proportions of black patients in the ED versus IHT cohorts. Our finding that black race was associated with lower risk of mortality has been previously reported but may also benefit from more investigation.[26]

There are several limitations of our work. First, despite extensive adjustment for patient characteristics, due to the observational nature of our study it is still possible that IHTs differ from ED admissions in ways that were unaccounted for in our analysis, and which could be associated with increased mortality independent of the transfer process itself. We are unable to characterize features of the transfer process, such as the reason for transfer, differences in transfer processes among hospitals, or the distance and mode of travel, which may influence outcomes.[27] Because we used administrative data, variations in coding could incorrectly estimate the complexity or severity of illness on admission, which is a previously described risk.[28] In addition, although our dataset was very large, it was limited by incomplete charge data, which limited our ability to measure ICU utilization in our full cohort. The hospitals missing ICU charge data are of variable sizes and are distributed around the country, limiting the chance of systematic bias. Finally, in some settings, hospitalists may serve as the discharging physician for patients admitted to other services such as the ICU, introducing heterogeneity and bias to the sample. We attempted to mitigate such bias through our subgroup analysis, which allowed for comparisons within more homogeneous patient groupings.

In conclusion, our large multicenter study of academic health systems confirms the findings of prior single‐center academic studies and a large general population study that interhospital transfer patients have an increased average LOS, costs, and adjusted in‐hospital mortality than patients admitted from the ED. This difference in mortality persisted even after controlling for several other predictors of mortality. Our findings emphasize the need for future studies designed to clarify the reason for the increased risk and identify targets for interventions to improve outcomes for the interhospital transfer population.

Interhospital transfers (IHTs) to academic medical centers (AMCs) or their affiliated hospitals may benefit patients who require unique specialty and procedural services. However, IHTs also introduce a potentially risky transition of care for patients suffering from complex or unstable medical problems.[1] Components of this risk include the dangers associated with transportation and the disrupted continuity of care that may lead to delays or errors in care.[2, 3] Furthermore, referring and accepting providers may face barriers to optimal handoffs including a lack of shared communication standards and difficulty accessing external medical records.[3, 4, 5] Although some authors have recommended the creation of formal guidelines for interhospital transfer processes for all patients to mitigate the risks of transfer, the available guidelines governing the IHT triage and communication process are limited to critically ill patients.[6]

A recent study of a diverse patient and hospital dataset demonstrated that interhospital transfer patients have a higher risk of mortality, increased length of stay (LOS), and increased risk of adverse events as compared with non‐transfer patients.[7] However, it is unknown if these findings persist in the population of patients transferred specifically to AMCs or their affiliated hospitals (the combination is hereafter referred to as academic health systems [AHSs]). AMCs provide a disproportionate share of IHT care for complex patients and have a vested interest in improving the outcomes of these transitions.[8] Prior single‐center studies of acute care adult medical patients accepted to AMCs have shown that IHT is associated with a longer LOS, increased in‐hospital mortality, and higher resource use.[9, 10] However, it is difficult to generalize from single‐center studies due to the variation in referral practices, geography, and network characteristics. Additionally, AMC referral systems, patient mix, and utilization of hospitalists have likely changed substantially in the nearly 2 decades since those reports were published.

Hospitalists and general internists often manage the transfer acceptance processes for internal medicine services at receiving hospitals, helping to triage and coordinate care for IHT patients. As a result, it is important for hospitalists to understand the characteristics and outcomes of the IHT population. In addition to informing the decision making around transfer for a given patient, such an understanding is the foundation for helping providers and institutions begin to systematically identify and mitigate peritransfer risks.

We conducted this large multicenter study to describe the characteristics and outcomes of a current, nationally representative IHT patient population discharged by hospitalists and general internists at AHSs. To identify unique features of the IHT population, we compared patients transferred from another hospital to an AHS to those admitted to the AHS directly from the AHS's emergency department (ED). Based on our anecdotal experiences and the prior single‐center study findings in adult medical populations,[9, 10] we hypothesized that the IHT population would be sicker, stay in the hospital and intensive care unit (ICU) longer, and have higher costs and in‐hospital mortality than ED patients. Although there may be fundamental differences between the 2 groups related to disease and patient condition, we hypothesized that outcome differences would persist even after adjusting for patient factors such as demographics, disease‐specific risk of mortality, and ICU utilization.

PATIENTS AND METHODS

We conducted a retrospective cohort study using data from the University HealthSystem Consortium (UHC) Clinical Database and Resource Manager (CDB/RM). UHC is an alliance of 120 academic medical centers and 300 of their affiliated hospitals for the purposes of collaboration on performance improvement. Each year, a subset of participating hospitals submits data on all of their inpatient discharges to the CDB/RM, which totals approximately 5 million records. The CDB/RM includes information from billing forms including demographics, diagnoses, and procedures as captured by International Classification of Diseases, Ninth Revision (ICD‐9) codes, discharge disposition, and line item charge detail for the type of bed (eg, floor, ICU). Most hospitals also provide detailed charge information including pharmacy, imaging, blood products, lab tests, and supplies. Some hospitals do not provide any charge data. The Beth Israel Deaconess Medical Center and University of Washington institutional review boards reviewed and approved the conduct of this study.

We included all inpatients discharged by hospitalists or general internal medicine physicians from UHC hospitals between April 1, 2011 and March 31, 2012. We excluded minors, pregnant patients, and prisoners. One hundred fifty‐eight adult academic medical centers and affiliated hospitals submitted data throughout this time period. Our primary independent variable, IHT status, was defined by patients whose admission source was another acute care institution. ED admissions were defined as patients admitted from the AHS ED whose source of origination was not another hospital or ambulatory surgery site.

RESULTS

DISCUSSION

Our study of IHT patients ultimately discharged by hospitalists and general internists at US academic referral centers found significantly increased average LOS, costs, and in‐hospital mortality compared with patients admitted from the ED. The increased risk of mortality persisted after adjustment for patient characteristics and variables representing endogenous risk of mortality, and in more homogeneous subgroups after stratification by presence and timing of ICU utilization. These data confirm findings from single‐center studies and suggest that observations about the difference between IHT and ED populations may be generalizable across US academic hospitals.

Our work builds on 2 single‐center studies that examined mixed medical and surgical academic IHT populations from the late 1980s and early 1990s,[9, 10] and 1 studying surgical ICU patients in 2013.[17] These studies demonstrated longer average LOS, higher costs, and higher mortality rates (in both adjusted and unadjusted analyses). Our work confirmed these findings utilizing a more current, multicenter large dataset of IHT patients ultimately discharged by hospitalists and general internists. Our work is unique from a larger, more recent study[7] in that it focuses on patients transferred to academic health systems, and therefore has particular relevance to those settings. In addition, we divided patients into subpopulations based on the timing of ICU utilization, and found that in each of these populations, IHT remained independently associated with in‐hospital mortality.

Our analysis does not explain why the outcomes of IHTs are worse, but plausible contributing factors include that (1) patients chosen for IHT are at higher risk of death in ways uncaptured by established mortality risk scores, (2) referring, transferring, or accepting providers and institutions have provided inadequate care, (3) the transfer process itself involves harm, (4) socioeconomic bias in selection for IHT,[18] or (5) some combination of the above. Regardless of the causes of the worse outcomes observed in these outside‐hospital transfers, as these patients are colloquially known at accepting hospitals, they present challenges to everyone involved. Referring providers may feel a sense of urgency as these patients' needs exceed their management capabilities. The process is often time consuming and burdensome for referring and accepting providers because of poorly developed systems.[19] The transfer often takes patients further from their home and may make it more difficult for family to participate in their care. The transfer may delay care if the accepting institution cannot immediately accept the patient or if the time in transport is prolonged, which could result in decompensation at a critical juncture. For providers inheriting such patients, the stress of caring for these patients is compounded by the difficulty obtaining records about the prior hospitalization.[20] This frustrating experience is often translated into unfounded judgment of the institution that referred the patient and the care provided there.[21] It is important for hospitalists making decisions throughout the transfer process and for hospital leaders who determine staffing levels, measure the quality of care, manage hospital networks, or write hospital policy to appreciate that the transfer process itself may contribute to the challenges and poor outcomes we observe. Furthermore, regardless of the cause for the increased mortality that we observed, our findings imply that IHT patients require careful evaluation, management, and treatment.

Many accepting institutions have transfer centers that facilitate these transitions, utilizing protocols and templates to standardize the process.[22, 23] Future research should focus on the characteristics of these centers to learn which practices are most efficacious. Interventions to mitigate the known challenges of transfer (including patient selection and triage, handoff communication, and information sharing) could be tested by randomized studies at referring and accepting institutions. There may be a role for health information exchange or the development of enhanced pretransfer evaluation processes using telemedicine models; there is evidence that information sharing may reduce redundant imaging.[24] Perhaps targeted review of IHTs admitted to a non‐ICU portion of the hospital and subsequently transferred to the ICU could identify opportunities to improve triaging protocols and thus avert some of the bad outcomes observed in this subpopulation. A related future direction could be to create protected forumsusing the patient safety organization framework[25]to facilitate the discussion of interhospital transfer outcomes among the referring, transporting, and receiving parties. Lastly, future work should investigate the reasons for the different proportions of black patients in the ED versus IHT cohorts. Our finding that black race was associated with lower risk of mortality has been previously reported but may also benefit from more investigation.[26]

There are several limitations of our work. First, despite extensive adjustment for patient characteristics, due to the observational nature of our study it is still possible that IHTs differ from ED admissions in ways that were unaccounted for in our analysis, and which could be associated with increased mortality independent of the transfer process itself. We are unable to characterize features of the transfer process, such as the reason for transfer, differences in transfer processes among hospitals, or the distance and mode of travel, which may influence outcomes.[27] Because we used administrative data, variations in coding could incorrectly estimate the complexity or severity of illness on admission, which is a previously described risk.[28] In addition, although our dataset was very large, it was limited by incomplete charge data, which limited our ability to measure ICU utilization in our full cohort. The hospitals missing ICU charge data are of variable sizes and are distributed around the country, limiting the chance of systematic bias. Finally, in some settings, hospitalists may serve as the discharging physician for patients admitted to other services such as the ICU, introducing heterogeneity and bias to the sample. We attempted to mitigate such bias through our subgroup analysis, which allowed for comparisons within more homogeneous patient groupings.

In conclusion, our large multicenter study of academic health systems confirms the findings of prior single‐center academic studies and a large general population study that interhospital transfer patients have an increased average LOS, costs, and adjusted in‐hospital mortality than patients admitted from the ED. This difference in mortality persisted even after controlling for several other predictors of mortality. Our findings emphasize the need for future studies designed to clarify the reason for the increased risk and identify targets for interventions to improve outcomes for the interhospital transfer population.

Interhospital transfers (IHTs) to academic medical centers (AMCs) or their affiliated hospitals may benefit patients who require unique specialty and procedural services. However, IHTs also introduce a potentially risky transition of care for patients suffering from complex or unstable medical problems.[1] Components of this risk include the dangers associated with transportation and the disrupted continuity of care that may lead to delays or errors in care.[2, 3] Furthermore, referring and accepting providers may face barriers to optimal handoffs including a lack of shared communication standards and difficulty accessing external medical records.[3, 4, 5] Although some authors have recommended the creation of formal guidelines for interhospital transfer processes for all patients to mitigate the risks of transfer, the available guidelines governing the IHT triage and communication process are limited to critically ill patients.[6]

A recent study of a diverse patient and hospital dataset demonstrated that interhospital transfer patients have a higher risk of mortality, increased length of stay (LOS), and increased risk of adverse events as compared with non‐transfer patients.[7] However, it is unknown if these findings persist in the population of patients transferred specifically to AMCs or their affiliated hospitals (the combination is hereafter referred to as academic health systems [AHSs]). AMCs provide a disproportionate share of IHT care for complex patients and have a vested interest in improving the outcomes of these transitions.[8] Prior single‐center studies of acute care adult medical patients accepted to AMCs have shown that IHT is associated with a longer LOS, increased in‐hospital mortality, and higher resource use.[9, 10] However, it is difficult to generalize from single‐center studies due to the variation in referral practices, geography, and network characteristics. Additionally, AMC referral systems, patient mix, and utilization of hospitalists have likely changed substantially in the nearly 2 decades since those reports were published.

Hospitalists and general internists often manage the transfer acceptance processes for internal medicine services at receiving hospitals, helping to triage and coordinate care for IHT patients. As a result, it is important for hospitalists to understand the characteristics and outcomes of the IHT population. In addition to informing the decision making around transfer for a given patient, such an understanding is the foundation for helping providers and institutions begin to systematically identify and mitigate peritransfer risks.

We conducted this large multicenter study to describe the characteristics and outcomes of a current, nationally representative IHT patient population discharged by hospitalists and general internists at AHSs. To identify unique features of the IHT population, we compared patients transferred from another hospital to an AHS to those admitted to the AHS directly from the AHS's emergency department (ED). Based on our anecdotal experiences and the prior single‐center study findings in adult medical populations,[9, 10] we hypothesized that the IHT population would be sicker, stay in the hospital and intensive care unit (ICU) longer, and have higher costs and in‐hospital mortality than ED patients. Although there may be fundamental differences between the 2 groups related to disease and patient condition, we hypothesized that outcome differences would persist even after adjusting for patient factors such as demographics, disease‐specific risk of mortality, and ICU utilization.

PATIENTS AND METHODS

We conducted a retrospective cohort study using data from the University HealthSystem Consortium (UHC) Clinical Database and Resource Manager (CDB/RM). UHC is an alliance of 120 academic medical centers and 300 of their affiliated hospitals for the purposes of collaboration on performance improvement. Each year, a subset of participating hospitals submits data on all of their inpatient discharges to the CDB/RM, which totals approximately 5 million records. The CDB/RM includes information from billing forms including demographics, diagnoses, and procedures as captured by International Classification of Diseases, Ninth Revision (ICD‐9) codes, discharge disposition, and line item charge detail for the type of bed (eg, floor, ICU). Most hospitals also provide detailed charge information including pharmacy, imaging, blood products, lab tests, and supplies. Some hospitals do not provide any charge data. The Beth Israel Deaconess Medical Center and University of Washington institutional review boards reviewed and approved the conduct of this study.

We included all inpatients discharged by hospitalists or general internal medicine physicians from UHC hospitals between April 1, 2011 and March 31, 2012. We excluded minors, pregnant patients, and prisoners. One hundred fifty‐eight adult academic medical centers and affiliated hospitals submitted data throughout this time period. Our primary independent variable, IHT status, was defined by patients whose admission source was another acute care institution. ED admissions were defined as patients admitted from the AHS ED whose source of origination was not another hospital or ambulatory surgery site.

RESULTS

DISCUSSION

Our study of IHT patients ultimately discharged by hospitalists and general internists at US academic referral centers found significantly increased average LOS, costs, and in‐hospital mortality compared with patients admitted from the ED. The increased risk of mortality persisted after adjustment for patient characteristics and variables representing endogenous risk of mortality, and in more homogeneous subgroups after stratification by presence and timing of ICU utilization. These data confirm findings from single‐center studies and suggest that observations about the difference between IHT and ED populations may be generalizable across US academic hospitals.

Our work builds on 2 single‐center studies that examined mixed medical and surgical academic IHT populations from the late 1980s and early 1990s,[9, 10] and 1 studying surgical ICU patients in 2013.[17] These studies demonstrated longer average LOS, higher costs, and higher mortality rates (in both adjusted and unadjusted analyses). Our work confirmed these findings utilizing a more current, multicenter large dataset of IHT patients ultimately discharged by hospitalists and general internists. Our work is unique from a larger, more recent study[7] in that it focuses on patients transferred to academic health systems, and therefore has particular relevance to those settings. In addition, we divided patients into subpopulations based on the timing of ICU utilization, and found that in each of these populations, IHT remained independently associated with in‐hospital mortality.

Our analysis does not explain why the outcomes of IHTs are worse, but plausible contributing factors include that (1) patients chosen for IHT are at higher risk of death in ways uncaptured by established mortality risk scores, (2) referring, transferring, or accepting providers and institutions have provided inadequate care, (3) the transfer process itself involves harm, (4) socioeconomic bias in selection for IHT,[18] or (5) some combination of the above. Regardless of the causes of the worse outcomes observed in these outside‐hospital transfers, as these patients are colloquially known at accepting hospitals, they present challenges to everyone involved. Referring providers may feel a sense of urgency as these patients' needs exceed their management capabilities. The process is often time consuming and burdensome for referring and accepting providers because of poorly developed systems.[19] The transfer often takes patients further from their home and may make it more difficult for family to participate in their care. The transfer may delay care if the accepting institution cannot immediately accept the patient or if the time in transport is prolonged, which could result in decompensation at a critical juncture. For providers inheriting such patients, the stress of caring for these patients is compounded by the difficulty obtaining records about the prior hospitalization.[20] This frustrating experience is often translated into unfounded judgment of the institution that referred the patient and the care provided there.[21] It is important for hospitalists making decisions throughout the transfer process and for hospital leaders who determine staffing levels, measure the quality of care, manage hospital networks, or write hospital policy to appreciate that the transfer process itself may contribute to the challenges and poor outcomes we observe. Furthermore, regardless of the cause for the increased mortality that we observed, our findings imply that IHT patients require careful evaluation, management, and treatment.

Many accepting institutions have transfer centers that facilitate these transitions, utilizing protocols and templates to standardize the process.[22, 23] Future research should focus on the characteristics of these centers to learn which practices are most efficacious. Interventions to mitigate the known challenges of transfer (including patient selection and triage, handoff communication, and information sharing) could be tested by randomized studies at referring and accepting institutions. There may be a role for health information exchange or the development of enhanced pretransfer evaluation processes using telemedicine models; there is evidence that information sharing may reduce redundant imaging.[24] Perhaps targeted review of IHTs admitted to a non‐ICU portion of the hospital and subsequently transferred to the ICU could identify opportunities to improve triaging protocols and thus avert some of the bad outcomes observed in this subpopulation. A related future direction could be to create protected forumsusing the patient safety organization framework[25]to facilitate the discussion of interhospital transfer outcomes among the referring, transporting, and receiving parties. Lastly, future work should investigate the reasons for the different proportions of black patients in the ED versus IHT cohorts. Our finding that black race was associated with lower risk of mortality has been previously reported but may also benefit from more investigation.[26]

There are several limitations of our work. First, despite extensive adjustment for patient characteristics, due to the observational nature of our study it is still possible that IHTs differ from ED admissions in ways that were unaccounted for in our analysis, and which could be associated with increased mortality independent of the transfer process itself. We are unable to characterize features of the transfer process, such as the reason for transfer, differences in transfer processes among hospitals, or the distance and mode of travel, which may influence outcomes.[27] Because we used administrative data, variations in coding could incorrectly estimate the complexity or severity of illness on admission, which is a previously described risk.[28] In addition, although our dataset was very large, it was limited by incomplete charge data, which limited our ability to measure ICU utilization in our full cohort. The hospitals missing ICU charge data are of variable sizes and are distributed around the country, limiting the chance of systematic bias. Finally, in some settings, hospitalists may serve as the discharging physician for patients admitted to other services such as the ICU, introducing heterogeneity and bias to the sample. We attempted to mitigate such bias through our subgroup analysis, which allowed for comparisons within more homogeneous patient groupings.

In conclusion, our large multicenter study of academic health systems confirms the findings of prior single‐center academic studies and a large general population study that interhospital transfer patients have an increased average LOS, costs, and adjusted in‐hospital mortality than patients admitted from the ED. This difference in mortality persisted even after controlling for several other predictors of mortality. Our findings emphasize the need for future studies designed to clarify the reason for the increased risk and identify targets for interventions to improve outcomes for the interhospital transfer population.

A 65‐year‐old man suffered a myocardial infarction (MI) while traveling in Thailand. After 7 days of recovery, the patient departed for his home in the United States. He developed substernal, nonexertional, inspiratory chest pain and shortness of breath during his return flight and presented directly to an emergency room after arrival.

Initially, the evaluation should focus on life‐threatening diagnoses and not be distracted by the travel history. The immediate diagnostic concerns are active cardiac ischemia, complications of MI, and pulmonary embolus. Other cardiac causes of dyspnea include ischemic mitral regurgitation, postinfarction pericarditis with or without pericardial effusion, and heart failure. Mechanical complications of infarction, such as left ventricular free wall rupture or rupture of the interventricular septum, can occur in this time frame and are associated with significant morbidity. Pneumothorax may be precipitated by air travel, especially in patients with underlying lung disease. The immobilization associated with long airline flights is a risk factor for thromboembolic disease, which is classically associated with pleuritic chest pain. Inspiratory chest pain is also associated with inflammatory processes involving the pericardium or pleura. If pneumonia, pericarditis, or pleural effusion is present, details of his travel history will become more important in his evaluation.

The patient elaborated that he spent 10 days in Thailand. On the third day of his trip he developed severe chest pain while hiking toward a waterfall in a rural northern district. He was transferred to a large private hospital, where he received a stent in the proximal left anterior descending coronary artery 4 hours after symptom onset. At discharge he was prescribed ticagrelor 90 mg twice daily and daily doses of losartan 50 mg, furosemide 20 mg, spironolactone 12.5 mg, aspirin 81 mg, ivabradine 2.5 mg, and pravastatin 40 mg. He had also been taking doxycycline for malaria prophylaxis since departing the United States.

His past medical history was notable for hypertension and hyperlipidemia. The patient was a lifelong nonsmoker, did not use illicit substances, and consumed no more than 2 alcoholic beverages per day. He denied cough, fevers, chills, diaphoresis, weight loss, recent upper respiratory infection, abdominal pain, hematuria, and nausea. However, he reported exertional dyspnea following his MI and nonbloody diarrhea that occurred a few days prior to his return flight and resolved without intervention.

The remainder of his past medical history confirms that he received appropriate post‐MI care, but does not substantially alter the high priority concerns in his differential diagnosis. Diarrhea may occur in up to 50% of international travelers, and is especially common when returning from Southeast Asia or the Indian subcontinent. Disease processes that may explain diarrhea and subsequent dyspnea include intestinal infections that spread to the lung (eg, ascariasis and Loeffler syndrome), infection that precipitates neuromuscular weakness (eg, Campylobacter and Guillain‐Barr syndrome), or infection that precipitates heart failure (eg, coxsackievirus, myocarditis).

On admission, his temperature was 36.2C, heart rate 91 beats per minute, blood pressure 135/81 mm Hg, respiratory rate 16 breaths per minute, and oxygen saturation 98% on room air. Cardiac exam revealed a regular rhythm without rubs, murmurs, or diastolic gallops. He had no jugular venous distention, and no lower extremity edema. His distal pulses were equal and palpable throughout. Pulmonary exam was notable for decreased breath sounds at both bases without wheezing, rhonchi, or crackles noted. He had no rashes, joint effusions, or jaundice. Abdominal and neurologic examinations were unremarkable.

Diminished breath sounds may suggest atelectasis or pleural effusion; the latter could account for the patient's inspiratory chest pain. A chest radiograph is essential to evaluate this finding further. The physical examination is not suggestive of decompensated heart failure; measurement of serum brain natriuretic peptide level would further exclude that diagnosis.

Laboratory evaluation revealed a leukocytosis of 16,000/L, with 76% polymorphonuclear cells and 12% lymphocytes without eosinophils or band forms; a hematocrit of 38%; and a platelet count of 363,000/L. The patient had a creatinine of 1.6 mg/dL, potassium of 2.7 mEq/L, and a troponin‐I of 1.0 ng/mL (normal <0.40 ng/mL), with the remainder of the routine serum chemistries within normal limits. An electrocardiogram (ECG) showed QS complexes in the anteroseptal leads, and a chest radiograph showed bibasilar consolidations and a left pleural effusion. A ventilation‐perfusion scan of the chest was performed to evaluate for pulmonary embolism, and was interpreted as low probability. Transthoracic echocardiography demonstrated severe left ventricular systolic dysfunction with anterior wall akinesis, and an aneurysmal left ventricle with an apical thrombus. No significant valvular pathology or other structural defects were noted.

The ECG and echocardiogram confirm the history of a large anteroseptal infarction with severe left ventricular dysfunction. Serial troponin testing would be reasonable. However, the absence of any acute ischemic ECG changes, typical angina symptoms, and a relatively normal troponin level all suggest his chest pain does not represent active ischemia. His low abnormal troponin‐I is consistent with slow resolution after a large ischemic event in the recent past, and his anterior wall akinesis is consistent with prior infarction in the territory of his culprit left anterior descending coronary artery.

Although acute cardiac conditions appear less likely, the brisk leukocytosis in a returned traveler prompts consideration of infection. His lung consolidations could represent either new or resolving pneumonia. The complete absence of cough and fever is unusual for pneumonia, yet clinical findings are not as sensitive as chest radiograph for this diagnosis. At this point, typical organisms as well as uncommon pathogens associated with diarrhea or his travel history should be included in the differential.

After 24 hours, the patient was discharged on warfarin to treat the apical thrombus and moxifloxacin for a presumed community‐acquired pneumonia. Eight days after discharge, the patient visited his primary care physician with improving, but not resolved, shortness of breath and pleuritic pain despite completing the 7‐day course of moxifloxacin. A chest radiograph showed a large posterior left basal pleural fluid collection, increased from previous.

In the setting of a recent infection, the symptoms and radiographic findings suggest a complicated parapneumonic effusion or empyema. Failure to drain a previously seeded fluid collection leaves bacterial pathogens susceptible to moxifloxacin on the differential, including Streptococcus pneumoniae, Staphylococcus aureus, Legionella species, and other enterobacteriaciae (eg, Klebsiella pneumoniae).

The indolent course should also prompt consideration of more unusual pathogens, including roundworms (such as Ascaris) or lung flukes (Paragonimus), either of which can cause a lung infection without traditional pneumonia symptoms. Tuberculosis tends to present months (or years) after exposure. Older adults may manifest primary pulmonary tuberculosis with lower lobe infiltrates, consistent with this presentation. However, moxifloxacin is quite active against tuberculosis, and although single drug therapy would not be expected to cure the patient, it would be surprising for him to progress this quickly on moxifloxacin.

In northern Thailand, Burkholderia pseudomallei is a common cause of bacteremic pneumonia. The organism often has high‐level resistance to fluoroquinolones, and may present in a more insidious fashion than other causes of community‐acquired pneumonia. Although infection with B pseudomallei (melioidosis) can occasionally mimic apical pulmonary tuberculosis and may present after a prolonged latent period, it most commonly manifests as an acute pneumonia.

The patient was prescribed 10 days of amoxicillin‐clavulanic acid and clindamycin, and decubitus films were ordered to assess the effusion. These films, obtained 5 days later, showed a persistent pleural effusion. Subsequent ultrasound demonstrated loculated fluid, but a thoracentesis was not performed at that time due to the patient's therapeutic international normalized ratio and dual antiplatelet therapy.

The loculation further suggests a complicated parapneumonic effusion or empyema. Clindamycin adds very little to amoxicillin‐clavulanate as far as coverage of oral anaerobes or common pneumonia pathogens and may add to the risk of antibiotic side effects. A susceptible organism might not clear because of failure to drain this collection; if undertreated bacterial infection is suspected, tube thoracentesis is the established standard of care. However, the protracted course of illness makes untreated pyogenic bacterial infections unlikely.

At this point, the top 2 diagnostic considerations are Paragonimus westermani and B pseudomallei. P westermani is initially ingested, usually from an undercooked freshwater crustacean. Infected patients may experience a brief diarrheal illness, as this patient reported. However, infected patients typically have a brisk peripheral eosinophilia.

Melioidosis is thus the leading concern. Amoxicillin‐clavulanate is active against many strains of B pseudomallei, so the failure of the patient to worsen could be seen as a partial treatment and supports this diagnosis. However, as prolonged therapy is necessary for complete eradication of B pseudomallei, a definitive, culture‐based diagnosis should be established before committing the patient to months of antibiotics.

After completing 10 days of clindamycin and amoxicillin‐clavulanate, the patient reported improvement of his pleuritic pain, and repeat physical exam suggested interval decrease in the size of the effusion. Two days later, the patient began experiencing dysuria that persisted despite 3 days of nitrofurantoin.

Melioidosis can also involve the genitourinary tract. Hematogenous spread of B pseudomallei can seed a number of visceral organs including the bladder, joints, and bones. Men with suspected urinary infection should be evaluated for the possibility of prostatitis, an infection with considerable morbidity that requires extended therapy. This gentleman should have a prostate exam, and blood and urine cultures should be collected if prostatitis is suspected. Empiric antibiotics are not recommended without culture in a patient with complicated urinary tract infection.

Prostate exam was unremarkable. A urine culture grew a gram‐negative rod identified as B pseudomallei. Because B pseudomallei can cause fulminant sepsis, the infectious disease consultant requested that he return for admission, further evaluation, and initiation of intravenous antibiotics. Computed tomography (CT) of the chest, abdomen, and pelvis revealed multiple pulmonary nodules, a persistent left pleural effusion, and a rim‐enhancing hypodensity in the prostate consistent with abscess (Figure 1). Blood and pleural fluid cultures were negative.

Figure 1

Initial treatment for a patient with severe or metastatic B pseudomallei infection requires high‐dose intravenous antibiotic therapy. Ceftazidime, imipenem, and meropenem are the best studied agents for this purpose. Surgical drainage should be considered for the abscess. Following the completion of intensive intravenous therapy, relapse rates are high unless a longer‐term, consolidation therapy is pursued. Trimethoprim‐sulfamethoxazole is the recommended agent.

The patient was treated with high‐dose ceftazidime for 2 weeks, followed by 6 months of high‐dose oral trimethoprim‐sulfamethoxazole. His symptoms resolved, and 7 months after presentation, he continued to feel well.

DISCUSSION

Melioidosis refers to any infection caused by B pseudomallei, a gram‐negative bacillus found in soil and water, most commonly in Southeast Asia and Australia.[1] It is an important cause of pneumonia in endemic regions; in Thailand, the incidence is as high as 12 cases per 100,000 people, and it is the third leading infectious cause of death, following human immunodeficiency virus and tuberculosis.[2] However, it occurs only as an imported infection in the United States and remains an unfamiliar infection for many US medical practitioners. Melioidosis should be considered in patients returning from endemic regions presenting with sepsis, pneumonia, urinary symptoms, or abscesses.

B pseudomallei can be transmitted to humans through exposure to contaminated soil or water via ingestion, inhalation, or percutaneous inoculation.[1] Outbreaks typically occur during the rainy season and after typhoons.[1, 3] Presumably, this patient's exposure to B pseudomallei occurred while hiking and wading in freshwater lakes and waterfalls. Although hospital‐acquired melioidosis has not been reported, and isolation precautions are not necessary, rare cases of disease acquired via laboratory exposure have been reported among US healthcare workers. Clinicians suspecting melioidosis should alert the receiving laboratory.[4]

The treatment course for melioidosis is lengthy and should involve consultation with an infectious disease specialist. B pseudomallei is known to be resistant to penicillin, first‐ and second‐generation cephalosporins, and moxifloxacin. The standard treatment includes 10 to 14 days of intravenous ceftazidime, meropenem, or imipenem, and then trimethoprim‐sulfamethoxazole for 3 to 6 months.[1] Treatment should be guided by culture susceptibility data when available. There are reports of B pseudomallei having different resistance patterns within the same host; clinicians should culture all drained fluid collections and tailor antibiotics to the most resistant strain recovered.[5, 6] Although melioidosis is a life‐threatening infection, previously healthy patients have an excellent prognosis assuming prompt diagnosis and treatment are provided.[3]

After excluding common causes of chest pain, the discussant identified the need to definitively establish a microbiologic diagnosis by obtaining pleural fluid. Although common clinical scenarios can often be treated with guideline‐supported empiric antibiotics, the use of serial courses of empiric antibiotics should be carefully questioned and is generally discouraged. Specific data to prove or disprove the presence of infection should be obtained before exposing a patient to the risks of multiple drugs or prolonged antibiotic therapy, as well as the risks of delayed (or missed) diagnosis. Unfortunately, a complete evaluation was delayed by clinical contraindications to diagnostic thoracentesis, and a definitive diagnosis was reached only after development of more widespread symptoms.

This patient's protean presentation is not surprising given his ultimate diagnosis. B pseudomallei has been termed the great mimicker, as disease presentation and organ involvement can vary from an indolent localized infection to acute severe sepsis.[7] Pneumonia and genitourinary infections are the most common manifestations, although skin infections, bacteremia, septic arthritis, and neurologic disease are also possible.[1, 3] In addition, melioidosis may develop after a lengthy incubation. In a case series, confirmed incubation periods ranged from 1 to 21 days (mean, 9 days); however, cases of chronic (>2 months) infection, mimicking tuberculosis, are estimated to occur in about 12% of cases.[4] B pseudomallei is also capable of causing reactivation disease, similar to tuberculosis. It was referred to as the Vietnamese time bomb when US Vietnam War veterans, exposed to the disease when helicopters aerosolized the bacteria in the soil, developed the disease only after their return to the United States.[8] Fortunately, only a tiny fraction of the quarter‐million soldiers with serologically confirmed exposure to the bacteria ultimately developed disease.

In The Adventure of the Dying Detective, Sherlock Holmes fakes a serious illness characterized by shortness of breath and weakness to trick an adversary into confessing to murder. The abrupt, crippling infection mimicked by Holmes is thought by some to be melioidosis.[9, 10] Conan Doyle's story was published in 1913, a year after melioidosis was first reported in the medical literature, and the exotic, protean infection may well have sparked Doyle's imagination. However, this patient's case of melioidosis proved stranger than fiction in its untimely concomitant development with an MI. Cracking our case required imagination and nimble thinking to avoid a number of cognitive pitfalls. The patient's recent MI anchored reasoning at his initial presentation, and the initial diagnosis of community‐acquired pneumonia raised the danger of premature closure. Reaching the correct diagnosis required an open mind, a detailed travel history, and firm microbiologic evidence. Hospitalists need not be expert in the health risks of travel to specific foreign destinations, but investigating those risks can hasten proper diagnosis and treatment.

TEACHING POINTS

• Melioidosis should be considered in patients returning from endemic regions who present with sepsis, pneumonia, urinary symptoms, or an abscess.
• For patients with a loculated parapneumonic effusion, tube thoracentesis for culture and drainage is the standard of care for diagnosis and treatment.
• Culture identification and antibiotic sensitivities are critical for management of B pseudomallei, because prolonged antibiotic treatment is needed.

Disclosure

Nothing to report.

A 65‐year‐old man suffered a myocardial infarction (MI) while traveling in Thailand. After 7 days of recovery, the patient departed for his home in the United States. He developed substernal, nonexertional, inspiratory chest pain and shortness of breath during his return flight and presented directly to an emergency room after arrival.

Initially, the evaluation should focus on life‐threatening diagnoses and not be distracted by the travel history. The immediate diagnostic concerns are active cardiac ischemia, complications of MI, and pulmonary embolus. Other cardiac causes of dyspnea include ischemic mitral regurgitation, postinfarction pericarditis with or without pericardial effusion, and heart failure. Mechanical complications of infarction, such as left ventricular free wall rupture or rupture of the interventricular septum, can occur in this time frame and are associated with significant morbidity. Pneumothorax may be precipitated by air travel, especially in patients with underlying lung disease. The immobilization associated with long airline flights is a risk factor for thromboembolic disease, which is classically associated with pleuritic chest pain. Inspiratory chest pain is also associated with inflammatory processes involving the pericardium or pleura. If pneumonia, pericarditis, or pleural effusion is present, details of his travel history will become more important in his evaluation.

The patient elaborated that he spent 10 days in Thailand. On the third day of his trip he developed severe chest pain while hiking toward a waterfall in a rural northern district. He was transferred to a large private hospital, where he received a stent in the proximal left anterior descending coronary artery 4 hours after symptom onset. At discharge he was prescribed ticagrelor 90 mg twice daily and daily doses of losartan 50 mg, furosemide 20 mg, spironolactone 12.5 mg, aspirin 81 mg, ivabradine 2.5 mg, and pravastatin 40 mg. He had also been taking doxycycline for malaria prophylaxis since departing the United States.

His past medical history was notable for hypertension and hyperlipidemia. The patient was a lifelong nonsmoker, did not use illicit substances, and consumed no more than 2 alcoholic beverages per day. He denied cough, fevers, chills, diaphoresis, weight loss, recent upper respiratory infection, abdominal pain, hematuria, and nausea. However, he reported exertional dyspnea following his MI and nonbloody diarrhea that occurred a few days prior to his return flight and resolved without intervention.

The remainder of his past medical history confirms that he received appropriate post‐MI care, but does not substantially alter the high priority concerns in his differential diagnosis. Diarrhea may occur in up to 50% of international travelers, and is especially common when returning from Southeast Asia or the Indian subcontinent. Disease processes that may explain diarrhea and subsequent dyspnea include intestinal infections that spread to the lung (eg, ascariasis and Loeffler syndrome), infection that precipitates neuromuscular weakness (eg, Campylobacter and Guillain‐Barr syndrome), or infection that precipitates heart failure (eg, coxsackievirus, myocarditis).

On admission, his temperature was 36.2C, heart rate 91 beats per minute, blood pressure 135/81 mm Hg, respiratory rate 16 breaths per minute, and oxygen saturation 98% on room air. Cardiac exam revealed a regular rhythm without rubs, murmurs, or diastolic gallops. He had no jugular venous distention, and no lower extremity edema. His distal pulses were equal and palpable throughout. Pulmonary exam was notable for decreased breath sounds at both bases without wheezing, rhonchi, or crackles noted. He had no rashes, joint effusions, or jaundice. Abdominal and neurologic examinations were unremarkable.

Diminished breath sounds may suggest atelectasis or pleural effusion; the latter could account for the patient's inspiratory chest pain. A chest radiograph is essential to evaluate this finding further. The physical examination is not suggestive of decompensated heart failure; measurement of serum brain natriuretic peptide level would further exclude that diagnosis.

Laboratory evaluation revealed a leukocytosis of 16,000/L, with 76% polymorphonuclear cells and 12% lymphocytes without eosinophils or band forms; a hematocrit of 38%; and a platelet count of 363,000/L. The patient had a creatinine of 1.6 mg/dL, potassium of 2.7 mEq/L, and a troponin‐I of 1.0 ng/mL (normal <0.40 ng/mL), with the remainder of the routine serum chemistries within normal limits. An electrocardiogram (ECG) showed QS complexes in the anteroseptal leads, and a chest radiograph showed bibasilar consolidations and a left pleural effusion. A ventilation‐perfusion scan of the chest was performed to evaluate for pulmonary embolism, and was interpreted as low probability. Transthoracic echocardiography demonstrated severe left ventricular systolic dysfunction with anterior wall akinesis, and an aneurysmal left ventricle with an apical thrombus. No significant valvular pathology or other structural defects were noted.

The ECG and echocardiogram confirm the history of a large anteroseptal infarction with severe left ventricular dysfunction. Serial troponin testing would be reasonable. However, the absence of any acute ischemic ECG changes, typical angina symptoms, and a relatively normal troponin level all suggest his chest pain does not represent active ischemia. His low abnormal troponin‐I is consistent with slow resolution after a large ischemic event in the recent past, and his anterior wall akinesis is consistent with prior infarction in the territory of his culprit left anterior descending coronary artery.

Although acute cardiac conditions appear less likely, the brisk leukocytosis in a returned traveler prompts consideration of infection. His lung consolidations could represent either new or resolving pneumonia. The complete absence of cough and fever is unusual for pneumonia, yet clinical findings are not as sensitive as chest radiograph for this diagnosis. At this point, typical organisms as well as uncommon pathogens associated with diarrhea or his travel history should be included in the differential.

After 24 hours, the patient was discharged on warfarin to treat the apical thrombus and moxifloxacin for a presumed community‐acquired pneumonia. Eight days after discharge, the patient visited his primary care physician with improving, but not resolved, shortness of breath and pleuritic pain despite completing the 7‐day course of moxifloxacin. A chest radiograph showed a large posterior left basal pleural fluid collection, increased from previous.

In the setting of a recent infection, the symptoms and radiographic findings suggest a complicated parapneumonic effusion or empyema. Failure to drain a previously seeded fluid collection leaves bacterial pathogens susceptible to moxifloxacin on the differential, including Streptococcus pneumoniae, Staphylococcus aureus, Legionella species, and other enterobacteriaciae (eg, Klebsiella pneumoniae).

The indolent course should also prompt consideration of more unusual pathogens, including roundworms (such as Ascaris) or lung flukes (Paragonimus), either of which can cause a lung infection without traditional pneumonia symptoms. Tuberculosis tends to present months (or years) after exposure. Older adults may manifest primary pulmonary tuberculosis with lower lobe infiltrates, consistent with this presentation. However, moxifloxacin is quite active against tuberculosis, and although single drug therapy would not be expected to cure the patient, it would be surprising for him to progress this quickly on moxifloxacin.

In northern Thailand, Burkholderia pseudomallei is a common cause of bacteremic pneumonia. The organism often has high‐level resistance to fluoroquinolones, and may present in a more insidious fashion than other causes of community‐acquired pneumonia. Although infection with B pseudomallei (melioidosis) can occasionally mimic apical pulmonary tuberculosis and may present after a prolonged latent period, it most commonly manifests as an acute pneumonia.

The patient was prescribed 10 days of amoxicillin‐clavulanic acid and clindamycin, and decubitus films were ordered to assess the effusion. These films, obtained 5 days later, showed a persistent pleural effusion. Subsequent ultrasound demonstrated loculated fluid, but a thoracentesis was not performed at that time due to the patient's therapeutic international normalized ratio and dual antiplatelet therapy.

The loculation further suggests a complicated parapneumonic effusion or empyema. Clindamycin adds very little to amoxicillin‐clavulanate as far as coverage of oral anaerobes or common pneumonia pathogens and may add to the risk of antibiotic side effects. A susceptible organism might not clear because of failure to drain this collection; if undertreated bacterial infection is suspected, tube thoracentesis is the established standard of care. However, the protracted course of illness makes untreated pyogenic bacterial infections unlikely.

At this point, the top 2 diagnostic considerations are Paragonimus westermani and B pseudomallei. P westermani is initially ingested, usually from an undercooked freshwater crustacean. Infected patients may experience a brief diarrheal illness, as this patient reported. However, infected patients typically have a brisk peripheral eosinophilia.

Melioidosis is thus the leading concern. Amoxicillin‐clavulanate is active against many strains of B pseudomallei, so the failure of the patient to worsen could be seen as a partial treatment and supports this diagnosis. However, as prolonged therapy is necessary for complete eradication of B pseudomallei, a definitive, culture‐based diagnosis should be established before committing the patient to months of antibiotics.

After completing 10 days of clindamycin and amoxicillin‐clavulanate, the patient reported improvement of his pleuritic pain, and repeat physical exam suggested interval decrease in the size of the effusion. Two days later, the patient began experiencing dysuria that persisted despite 3 days of nitrofurantoin.

Melioidosis can also involve the genitourinary tract. Hematogenous spread of B pseudomallei can seed a number of visceral organs including the bladder, joints, and bones. Men with suspected urinary infection should be evaluated for the possibility of prostatitis, an infection with considerable morbidity that requires extended therapy. This gentleman should have a prostate exam, and blood and urine cultures should be collected if prostatitis is suspected. Empiric antibiotics are not recommended without culture in a patient with complicated urinary tract infection.

Prostate exam was unremarkable. A urine culture grew a gram‐negative rod identified as B pseudomallei. Because B pseudomallei can cause fulminant sepsis, the infectious disease consultant requested that he return for admission, further evaluation, and initiation of intravenous antibiotics. Computed tomography (CT) of the chest, abdomen, and pelvis revealed multiple pulmonary nodules, a persistent left pleural effusion, and a rim‐enhancing hypodensity in the prostate consistent with abscess (Figure 1). Blood and pleural fluid cultures were negative.

Figure 1

Initial treatment for a patient with severe or metastatic B pseudomallei infection requires high‐dose intravenous antibiotic therapy. Ceftazidime, imipenem, and meropenem are the best studied agents for this purpose. Surgical drainage should be considered for the abscess. Following the completion of intensive intravenous therapy, relapse rates are high unless a longer‐term, consolidation therapy is pursued. Trimethoprim‐sulfamethoxazole is the recommended agent.

The patient was treated with high‐dose ceftazidime for 2 weeks, followed by 6 months of high‐dose oral trimethoprim‐sulfamethoxazole. His symptoms resolved, and 7 months after presentation, he continued to feel well.

DISCUSSION

Melioidosis refers to any infection caused by B pseudomallei, a gram‐negative bacillus found in soil and water, most commonly in Southeast Asia and Australia.[1] It is an important cause of pneumonia in endemic regions; in Thailand, the incidence is as high as 12 cases per 100,000 people, and it is the third leading infectious cause of death, following human immunodeficiency virus and tuberculosis.[2] However, it occurs only as an imported infection in the United States and remains an unfamiliar infection for many US medical practitioners. Melioidosis should be considered in patients returning from endemic regions presenting with sepsis, pneumonia, urinary symptoms, or abscesses.

B pseudomallei can be transmitted to humans through exposure to contaminated soil or water via ingestion, inhalation, or percutaneous inoculation.[1] Outbreaks typically occur during the rainy season and after typhoons.[1, 3] Presumably, this patient's exposure to B pseudomallei occurred while hiking and wading in freshwater lakes and waterfalls. Although hospital‐acquired melioidosis has not been reported, and isolation precautions are not necessary, rare cases of disease acquired via laboratory exposure have been reported among US healthcare workers. Clinicians suspecting melioidosis should alert the receiving laboratory.[4]

The treatment course for melioidosis is lengthy and should involve consultation with an infectious disease specialist. B pseudomallei is known to be resistant to penicillin, first‐ and second‐generation cephalosporins, and moxifloxacin. The standard treatment includes 10 to 14 days of intravenous ceftazidime, meropenem, or imipenem, and then trimethoprim‐sulfamethoxazole for 3 to 6 months.[1] Treatment should be guided by culture susceptibility data when available. There are reports of B pseudomallei having different resistance patterns within the same host; clinicians should culture all drained fluid collections and tailor antibiotics to the most resistant strain recovered.[5, 6] Although melioidosis is a life‐threatening infection, previously healthy patients have an excellent prognosis assuming prompt diagnosis and treatment are provided.[3]

After excluding common causes of chest pain, the discussant identified the need to definitively establish a microbiologic diagnosis by obtaining pleural fluid. Although common clinical scenarios can often be treated with guideline‐supported empiric antibiotics, the use of serial courses of empiric antibiotics should be carefully questioned and is generally discouraged. Specific data to prove or disprove the presence of infection should be obtained before exposing a patient to the risks of multiple drugs or prolonged antibiotic therapy, as well as the risks of delayed (or missed) diagnosis. Unfortunately, a complete evaluation was delayed by clinical contraindications to diagnostic thoracentesis, and a definitive diagnosis was reached only after development of more widespread symptoms.

This patient's protean presentation is not surprising given his ultimate diagnosis. B pseudomallei has been termed the great mimicker, as disease presentation and organ involvement can vary from an indolent localized infection to acute severe sepsis.[7] Pneumonia and genitourinary infections are the most common manifestations, although skin infections, bacteremia, septic arthritis, and neurologic disease are also possible.[1, 3] In addition, melioidosis may develop after a lengthy incubation. In a case series, confirmed incubation periods ranged from 1 to 21 days (mean, 9 days); however, cases of chronic (>2 months) infection, mimicking tuberculosis, are estimated to occur in about 12% of cases.[4] B pseudomallei is also capable of causing reactivation disease, similar to tuberculosis. It was referred to as the Vietnamese time bomb when US Vietnam War veterans, exposed to the disease when helicopters aerosolized the bacteria in the soil, developed the disease only after their return to the United States.[8] Fortunately, only a tiny fraction of the quarter‐million soldiers with serologically confirmed exposure to the bacteria ultimately developed disease.

In The Adventure of the Dying Detective, Sherlock Holmes fakes a serious illness characterized by shortness of breath and weakness to trick an adversary into confessing to murder. The abrupt, crippling infection mimicked by Holmes is thought by some to be melioidosis.[9, 10] Conan Doyle's story was published in 1913, a year after melioidosis was first reported in the medical literature, and the exotic, protean infection may well have sparked Doyle's imagination. However, this patient's case of melioidosis proved stranger than fiction in its untimely concomitant development with an MI. Cracking our case required imagination and nimble thinking to avoid a number of cognitive pitfalls. The patient's recent MI anchored reasoning at his initial presentation, and the initial diagnosis of community‐acquired pneumonia raised the danger of premature closure. Reaching the correct diagnosis required an open mind, a detailed travel history, and firm microbiologic evidence. Hospitalists need not be expert in the health risks of travel to specific foreign destinations, but investigating those risks can hasten proper diagnosis and treatment.

TEACHING POINTS

• Melioidosis should be considered in patients returning from endemic regions who present with sepsis, pneumonia, urinary symptoms, or an abscess.
• For patients with a loculated parapneumonic effusion, tube thoracentesis for culture and drainage is the standard of care for diagnosis and treatment.
• Culture identification and antibiotic sensitivities are critical for management of B pseudomallei, because prolonged antibiotic treatment is needed.

Disclosure

Nothing to report.

A 65‐year‐old man suffered a myocardial infarction (MI) while traveling in Thailand. After 7 days of recovery, the patient departed for his home in the United States. He developed substernal, nonexertional, inspiratory chest pain and shortness of breath during his return flight and presented directly to an emergency room after arrival.

Initially, the evaluation should focus on life‐threatening diagnoses and not be distracted by the travel history. The immediate diagnostic concerns are active cardiac ischemia, complications of MI, and pulmonary embolus. Other cardiac causes of dyspnea include ischemic mitral regurgitation, postinfarction pericarditis with or without pericardial effusion, and heart failure. Mechanical complications of infarction, such as left ventricular free wall rupture or rupture of the interventricular septum, can occur in this time frame and are associated with significant morbidity. Pneumothorax may be precipitated by air travel, especially in patients with underlying lung disease. The immobilization associated with long airline flights is a risk factor for thromboembolic disease, which is classically associated with pleuritic chest pain. Inspiratory chest pain is also associated with inflammatory processes involving the pericardium or pleura. If pneumonia, pericarditis, or pleural effusion is present, details of his travel history will become more important in his evaluation.

The patient elaborated that he spent 10 days in Thailand. On the third day of his trip he developed severe chest pain while hiking toward a waterfall in a rural northern district. He was transferred to a large private hospital, where he received a stent in the proximal left anterior descending coronary artery 4 hours after symptom onset. At discharge he was prescribed ticagrelor 90 mg twice daily and daily doses of losartan 50 mg, furosemide 20 mg, spironolactone 12.5 mg, aspirin 81 mg, ivabradine 2.5 mg, and pravastatin 40 mg. He had also been taking doxycycline for malaria prophylaxis since departing the United States.

His past medical history was notable for hypertension and hyperlipidemia. The patient was a lifelong nonsmoker, did not use illicit substances, and consumed no more than 2 alcoholic beverages per day. He denied cough, fevers, chills, diaphoresis, weight loss, recent upper respiratory infection, abdominal pain, hematuria, and nausea. However, he reported exertional dyspnea following his MI and nonbloody diarrhea that occurred a few days prior to his return flight and resolved without intervention.

The remainder of his past medical history confirms that he received appropriate post‐MI care, but does not substantially alter the high priority concerns in his differential diagnosis. Diarrhea may occur in up to 50% of international travelers, and is especially common when returning from Southeast Asia or the Indian subcontinent. Disease processes that may explain diarrhea and subsequent dyspnea include intestinal infections that spread to the lung (eg, ascariasis and Loeffler syndrome), infection that precipitates neuromuscular weakness (eg, Campylobacter and Guillain‐Barr syndrome), or infection that precipitates heart failure (eg, coxsackievirus, myocarditis).

On admission, his temperature was 36.2C, heart rate 91 beats per minute, blood pressure 135/81 mm Hg, respiratory rate 16 breaths per minute, and oxygen saturation 98% on room air. Cardiac exam revealed a regular rhythm without rubs, murmurs, or diastolic gallops. He had no jugular venous distention, and no lower extremity edema. His distal pulses were equal and palpable throughout. Pulmonary exam was notable for decreased breath sounds at both bases without wheezing, rhonchi, or crackles noted. He had no rashes, joint effusions, or jaundice. Abdominal and neurologic examinations were unremarkable.

Diminished breath sounds may suggest atelectasis or pleural effusion; the latter could account for the patient's inspiratory chest pain. A chest radiograph is essential to evaluate this finding further. The physical examination is not suggestive of decompensated heart failure; measurement of serum brain natriuretic peptide level would further exclude that diagnosis.

Laboratory evaluation revealed a leukocytosis of 16,000/L, with 76% polymorphonuclear cells and 12% lymphocytes without eosinophils or band forms; a hematocrit of 38%; and a platelet count of 363,000/L. The patient had a creatinine of 1.6 mg/dL, potassium of 2.7 mEq/L, and a troponin‐I of 1.0 ng/mL (normal <0.40 ng/mL), with the remainder of the routine serum chemistries within normal limits. An electrocardiogram (ECG) showed QS complexes in the anteroseptal leads, and a chest radiograph showed bibasilar consolidations and a left pleural effusion. A ventilation‐perfusion scan of the chest was performed to evaluate for pulmonary embolism, and was interpreted as low probability. Transthoracic echocardiography demonstrated severe left ventricular systolic dysfunction with anterior wall akinesis, and an aneurysmal left ventricle with an apical thrombus. No significant valvular pathology or other structural defects were noted.

The ECG and echocardiogram confirm the history of a large anteroseptal infarction with severe left ventricular dysfunction. Serial troponin testing would be reasonable. However, the absence of any acute ischemic ECG changes, typical angina symptoms, and a relatively normal troponin level all suggest his chest pain does not represent active ischemia. His low abnormal troponin‐I is consistent with slow resolution after a large ischemic event in the recent past, and his anterior wall akinesis is consistent with prior infarction in the territory of his culprit left anterior descending coronary artery.

Although acute cardiac conditions appear less likely, the brisk leukocytosis in a returned traveler prompts consideration of infection. His lung consolidations could represent either new or resolving pneumonia. The complete absence of cough and fever is unusual for pneumonia, yet clinical findings are not as sensitive as chest radiograph for this diagnosis. At this point, typical organisms as well as uncommon pathogens associated with diarrhea or his travel history should be included in the differential.

After 24 hours, the patient was discharged on warfarin to treat the apical thrombus and moxifloxacin for a presumed community‐acquired pneumonia. Eight days after discharge, the patient visited his primary care physician with improving, but not resolved, shortness of breath and pleuritic pain despite completing the 7‐day course of moxifloxacin. A chest radiograph showed a large posterior left basal pleural fluid collection, increased from previous.

In the setting of a recent infection, the symptoms and radiographic findings suggest a complicated parapneumonic effusion or empyema. Failure to drain a previously seeded fluid collection leaves bacterial pathogens susceptible to moxifloxacin on the differential, including Streptococcus pneumoniae, Staphylococcus aureus, Legionella species, and other enterobacteriaciae (eg, Klebsiella pneumoniae).

The indolent course should also prompt consideration of more unusual pathogens, including roundworms (such as Ascaris) or lung flukes (Paragonimus), either of which can cause a lung infection without traditional pneumonia symptoms. Tuberculosis tends to present months (or years) after exposure. Older adults may manifest primary pulmonary tuberculosis with lower lobe infiltrates, consistent with this presentation. However, moxifloxacin is quite active against tuberculosis, and although single drug therapy would not be expected to cure the patient, it would be surprising for him to progress this quickly on moxifloxacin.

In northern Thailand, Burkholderia pseudomallei is a common cause of bacteremic pneumonia. The organism often has high‐level resistance to fluoroquinolones, and may present in a more insidious fashion than other causes of community‐acquired pneumonia. Although infection with B pseudomallei (melioidosis) can occasionally mimic apical pulmonary tuberculosis and may present after a prolonged latent period, it most commonly manifests as an acute pneumonia.

The patient was prescribed 10 days of amoxicillin‐clavulanic acid and clindamycin, and decubitus films were ordered to assess the effusion. These films, obtained 5 days later, showed a persistent pleural effusion. Subsequent ultrasound demonstrated loculated fluid, but a thoracentesis was not performed at that time due to the patient's therapeutic international normalized ratio and dual antiplatelet therapy.

The loculation further suggests a complicated parapneumonic effusion or empyema. Clindamycin adds very little to amoxicillin‐clavulanate as far as coverage of oral anaerobes or common pneumonia pathogens and may add to the risk of antibiotic side effects. A susceptible organism might not clear because of failure to drain this collection; if undertreated bacterial infection is suspected, tube thoracentesis is the established standard of care. However, the protracted course of illness makes untreated pyogenic bacterial infections unlikely.

At this point, the top 2 diagnostic considerations are Paragonimus westermani and B pseudomallei. P westermani is initially ingested, usually from an undercooked freshwater crustacean. Infected patients may experience a brief diarrheal illness, as this patient reported. However, infected patients typically have a brisk peripheral eosinophilia.

Melioidosis is thus the leading concern. Amoxicillin‐clavulanate is active against many strains of B pseudomallei, so the failure of the patient to worsen could be seen as a partial treatment and supports this diagnosis. However, as prolonged therapy is necessary for complete eradication of B pseudomallei, a definitive, culture‐based diagnosis should be established before committing the patient to months of antibiotics.

After completing 10 days of clindamycin and amoxicillin‐clavulanate, the patient reported improvement of his pleuritic pain, and repeat physical exam suggested interval decrease in the size of the effusion. Two days later, the patient began experiencing dysuria that persisted despite 3 days of nitrofurantoin.

Melioidosis can also involve the genitourinary tract. Hematogenous spread of B pseudomallei can seed a number of visceral organs including the bladder, joints, and bones. Men with suspected urinary infection should be evaluated for the possibility of prostatitis, an infection with considerable morbidity that requires extended therapy. This gentleman should have a prostate exam, and blood and urine cultures should be collected if prostatitis is suspected. Empiric antibiotics are not recommended without culture in a patient with complicated urinary tract infection.

Prostate exam was unremarkable. A urine culture grew a gram‐negative rod identified as B pseudomallei. Because B pseudomallei can cause fulminant sepsis, the infectious disease consultant requested that he return for admission, further evaluation, and initiation of intravenous antibiotics. Computed tomography (CT) of the chest, abdomen, and pelvis revealed multiple pulmonary nodules, a persistent left pleural effusion, and a rim‐enhancing hypodensity in the prostate consistent with abscess (Figure 1). Blood and pleural fluid cultures were negative.

Figure 1

Initial treatment for a patient with severe or metastatic B pseudomallei infection requires high‐dose intravenous antibiotic therapy. Ceftazidime, imipenem, and meropenem are the best studied agents for this purpose. Surgical drainage should be considered for the abscess. Following the completion of intensive intravenous therapy, relapse rates are high unless a longer‐term, consolidation therapy is pursued. Trimethoprim‐sulfamethoxazole is the recommended agent.

The patient was treated with high‐dose ceftazidime for 2 weeks, followed by 6 months of high‐dose oral trimethoprim‐sulfamethoxazole. His symptoms resolved, and 7 months after presentation, he continued to feel well.

DISCUSSION

Melioidosis refers to any infection caused by B pseudomallei, a gram‐negative bacillus found in soil and water, most commonly in Southeast Asia and Australia.[1] It is an important cause of pneumonia in endemic regions; in Thailand, the incidence is as high as 12 cases per 100,000 people, and it is the third leading infectious cause of death, following human immunodeficiency virus and tuberculosis.[2] However, it occurs only as an imported infection in the United States and remains an unfamiliar infection for many US medical practitioners. Melioidosis should be considered in patients returning from endemic regions presenting with sepsis, pneumonia, urinary symptoms, or abscesses.

B pseudomallei can be transmitted to humans through exposure to contaminated soil or water via ingestion, inhalation, or percutaneous inoculation.[1] Outbreaks typically occur during the rainy season and after typhoons.[1, 3] Presumably, this patient's exposure to B pseudomallei occurred while hiking and wading in freshwater lakes and waterfalls. Although hospital‐acquired melioidosis has not been reported, and isolation precautions are not necessary, rare cases of disease acquired via laboratory exposure have been reported among US healthcare workers. Clinicians suspecting melioidosis should alert the receiving laboratory.[4]

The treatment course for melioidosis is lengthy and should involve consultation with an infectious disease specialist. B pseudomallei is known to be resistant to penicillin, first‐ and second‐generation cephalosporins, and moxifloxacin. The standard treatment includes 10 to 14 days of intravenous ceftazidime, meropenem, or imipenem, and then trimethoprim‐sulfamethoxazole for 3 to 6 months.[1] Treatment should be guided by culture susceptibility data when available. There are reports of B pseudomallei having different resistance patterns within the same host; clinicians should culture all drained fluid collections and tailor antibiotics to the most resistant strain recovered.[5, 6] Although melioidosis is a life‐threatening infection, previously healthy patients have an excellent prognosis assuming prompt diagnosis and treatment are provided.[3]

After excluding common causes of chest pain, the discussant identified the need to definitively establish a microbiologic diagnosis by obtaining pleural fluid. Although common clinical scenarios can often be treated with guideline‐supported empiric antibiotics, the use of serial courses of empiric antibiotics should be carefully questioned and is generally discouraged. Specific data to prove or disprove the presence of infection should be obtained before exposing a patient to the risks of multiple drugs or prolonged antibiotic therapy, as well as the risks of delayed (or missed) diagnosis. Unfortunately, a complete evaluation was delayed by clinical contraindications to diagnostic thoracentesis, and a definitive diagnosis was reached only after development of more widespread symptoms.

This patient's protean presentation is not surprising given his ultimate diagnosis. B pseudomallei has been termed the great mimicker, as disease presentation and organ involvement can vary from an indolent localized infection to acute severe sepsis.[7] Pneumonia and genitourinary infections are the most common manifestations, although skin infections, bacteremia, septic arthritis, and neurologic disease are also possible.[1, 3] In addition, melioidosis may develop after a lengthy incubation. In a case series, confirmed incubation periods ranged from 1 to 21 days (mean, 9 days); however, cases of chronic (>2 months) infection, mimicking tuberculosis, are estimated to occur in about 12% of cases.[4] B pseudomallei is also capable of causing reactivation disease, similar to tuberculosis. It was referred to as the Vietnamese time bomb when US Vietnam War veterans, exposed to the disease when helicopters aerosolized the bacteria in the soil, developed the disease only after their return to the United States.[8] Fortunately, only a tiny fraction of the quarter‐million soldiers with serologically confirmed exposure to the bacteria ultimately developed disease.

In The Adventure of the Dying Detective, Sherlock Holmes fakes a serious illness characterized by shortness of breath and weakness to trick an adversary into confessing to murder. The abrupt, crippling infection mimicked by Holmes is thought by some to be melioidosis.[9, 10] Conan Doyle's story was published in 1913, a year after melioidosis was first reported in the medical literature, and the exotic, protean infection may well have sparked Doyle's imagination. However, this patient's case of melioidosis proved stranger than fiction in its untimely concomitant development with an MI. Cracking our case required imagination and nimble thinking to avoid a number of cognitive pitfalls. The patient's recent MI anchored reasoning at his initial presentation, and the initial diagnosis of community‐acquired pneumonia raised the danger of premature closure. Reaching the correct diagnosis required an open mind, a detailed travel history, and firm microbiologic evidence. Hospitalists need not be expert in the health risks of travel to specific foreign destinations, but investigating those risks can hasten proper diagnosis and treatment.

TEACHING POINTS

• Melioidosis should be considered in patients returning from endemic regions who present with sepsis, pneumonia, urinary symptoms, or an abscess.
• For patients with a loculated parapneumonic effusion, tube thoracentesis for culture and drainage is the standard of care for diagnosis and treatment.
• Culture identification and antibiotic sensitivities are critical for management of B pseudomallei, because prolonged antibiotic treatment is needed.

Disclosure

Nothing to report.