736
Coleman et al
Discussion
22. Kandilov AM, Coomer NM, Dalton K. The impact of hospital-acquired conditions on Medicare program payments. Medicare Medicaid Res Rev 2014;4:E14eE17. 23. Kaafarani HM, Borzecki AM, Itani KM, et al. Validity of selected Patient Safety Indicators: opportunities and concerns. J Am Coll Surg 2011;212:924e934.
Discussion DR TIMOTHY C FABIAN (Memphis, TN): The authors highlight a potentially important and underappreciated complication after injury: early pulmonary embolism (PE). They acknowledge important limitations of the study in the manuscript. This retrospective review of registry data from 3 institutions could not provide the following important information: clinical indications for obtaining the diagnostic studies, clinical significance of the PEs, institutional differences in prophylaxis and screening protocols, and CT protocols and equipment. They appropriately note that Medicare and Agency for Healthcare Research and Quality (AHRQ) have focused on deep vein thrombosis (DVT) and PE as two Patient Safety Indicators, to aid internal quality improvement but increasingly used for hospital profiling and reimbursement. In this study, the authors may have let an opportunity pass to address that issue. They queried a fairly large database of nearly 55,000 trauma patients and noted a PE incidence of 0.24%. Their analysis was based around differences in early PE versus late PE. Interestingly, they found that timing of prophylaxis has no impact on early PE. I would suggest they should have also selected an injury matched cohort without PE among the 55,000 patients to compare with the 133 PE patients. Such an analysis would provide data relative to the validity of using DVT and PE as Patient Safety Indicators. Did the PEs have any impact on outcomes? The fact that timing of prophylaxis was shown to have no impact on early PE makes one wonder if the events should be considered complications. Perhaps they are simply another iteration of CT “incidentalomas” associated with obtaining chest CTs for follow-up of other problems. These patients are always multiply injured and you have demonstrated that early PEs are associated with long-bone fractures and severe extremity trauma. Sixty percent of PEs occurred within 4 days of admission, an interval in which many orthopaedic procedures are being done, and many orthopaedic surgeons are not terribly enthusiastic about heparin protocols at that juncture. How have the findings from this study influenced your current institutional approach to PE screening and prophylaxis? Should CT PE protocols be done routinely on the high-risk group within a day or two of admission? Since timing of prophylaxis did not seem to help, are you considering earlier or higher doses prophylaxis? I thank the authors for this early initiative studying PE after injury. I suspect it will lead to an interesting avenue of future work. DR ADDISON MAY (Nashville, TN): The authors are to be applauded for completing a multicenter retrospective analysis of
J Am Coll Surg
133 cases of post-traumatic PE in an attempt to identify factors associated with the early vs late diagnosis. The authors’ findings support those reported from recent single-center studies regarding the early diagnosis of PE and clearly conflict with older studies regarding the timing of post-traumatic PE. I have several questions for the authors: 1. Do you believe that the trauma registry ICD-9 documentation of PEs is real? One hundred thirty-three cases is a manageable size for further review. Have you done any chart review to confirm the accuracy of the data capture? 2. If you believe that the documented PEs are real, is the diagnosis of early PE just an epiphenomenon of the advancements in CT scanning technology? Can you go back to evaluate the severity, size, indication for imaging, etc, to advance your understanding of these 133 events? Did the PEs contribute directly to any of the 10 deaths in the group? The 24 cases documented on the first hospital day are particularly difficult for me to wrap my head around. Anecdotally, our center has documented filling defects in lobar pulmonary arteries, read by the radiologist as PE, that on a follow-up CT scan are nowhere to be found. Are these just small localized changes in flow in the pulmonary artery or small thrombi created at the time and site of injury that then embolize when flow increases again through the injured vein? Might these findings be analogous to those of fat emboli seen on transesophageal echocardiography during operative fixation of long bone fractures, in which patients may be totally asymptomatic? 3. Forty-two percent of patients in the early PE group received prophylaxis within 48 hours. Can you provide details about the type of prophylaxis? Was this in the form of sequential compression devices, unfractionated heparin, or fractionated heparin? Do you believe that even earlier prophylaxis would alter your PE rate, and are you planning to implement any changes in your practice? 4. If you use the 4-day vs the day definition for early PE, does the presence of long-bone fractures become significant in your model? If the incidence of early vs late PE has increased in the last 2 decades, can you hypothesize why? Finally, you mention in your discussion the use of thromboelastography (TEG) to evaluate patients at risk for PE. Do you have any preliminary data to suggest that TEG will actually identify patients at risk for early PE? DR KENNETH MATTOX (Houston, TX): I have concerns that this study was faulted from the onset due to drinking the Kool-Aid of coding confusion. The quality of CT on the pulmonary arteries is sufficient to show usually peripheral pulmonary arteriolar clot, most often caused by low flow states, especially in trauma patients, and most often occurring early. This condition, recognized by all of us, has no relationship or linkage to DVT. Heparin prophylaxis in this group of patients may actually be contraindicated. This condition is totally different from larger central thromboembolic clot most often from iliocaval sites to the main or central
Vol. 220, No. 4, April 2015
pulmonary arteries, which has been reported at this Association over the decades repeatedly, and is totally different from that of the peripheral ateriolars. These conditions have different etiologies, often different physiologic impact, and often different treatments, but have the very same ICD-9, and ICD-10, codes. So the question, for this case cohort selected by code identification, how did you separate these 2 distinctly different patient groups? Without such a mechanism, the interpretations, the treatments, the conclusions, and the recommendations are faulted, not only for past reports that are similar, but for this study and future best practice recommendations. Specifically, my question is, how did you differentiate the anatomic location and size of the pulmonary artery clot in your analysis? Or did you merely rely on the ICD-9 coding? DR NICK NAMIAS (Miami, FL): I will not be asking a question; I will be answering one because you asked if other centers can confirm your findings. Well, we are happy to announce in 2012 we confirmed them, that in a group of trauma patients who had the Greenfield risk-assessment profile applied, we found about 20% of those patients who were at high risk did in fact have a venous thromboembolic event early on, just as you described today. So the confirmatory process has begun. DR JEFF BENDER (Oklahoma City, OK): I would like to ask how you recommend we treat these patients. My colleagues and I have also noticed a small cluster of this, and we are very divided. Among us, the options are to fully anticoagulate them, place a filter even in the absence of a documented DVT, or, my approach, just to ignore the problem. DR KENNETH BRAYMAN (Charlottesville, VA): I found this study fascinating. It appears that you have a great opportunity to define differences between those who realize an embolic event and those who do not. Attempting to define differences in the 2 patient populations with genomic profiling to determine risk stratification to see who really is at risk for developing thromboembolic phenomena would be very insightful, and it may affect approaches in therapy. Do you have any thoughts about how to take your observation and move it forward to define actual risk? DR JAMIE JONES COLEMAN: On how we performed chart review: we used the ICD-9 code just to initially identify which patients we needed to go back and further review. You are right. The 133 patients is a manageable number. We did go back and review the charts individually and confirmed the clinical presence of a PE. There is a potential that we may have inadvertently not captured every patient with a PE at the 3 institutions if an incorrect ICD-9 code was used. However, given the significance of this particular complication and our awareness of this complication, we thought that this wouldn’t be as likely. To answer several of the questions relating to the increased incidence of blunt vascular injuries, splenic lacerations, and other
Coleman et al
Discussion
737
incidentalomas, we agree that this could be a manifestation of the popularity of the pan-CT scan. Every radiology report was reviewed by an attending radiologist. Since the PEs that were diagnosed within the first 24 hours of hospitalization were present in all 3 institutions, this did lead us to believe that these PEs were “real” and not just overcalls or flow artifacts. However, all these points are valid, that although these may seem to be real radiologic PEs on day 1, it begs the question, would they be real on day 3? Do they transform or will they ever become clinically significant if untreated? However, in our study, all patients who received a diagnosis of PE, regardless of the presence or absence of clinical symptoms, did undergo treatment. There were a total of 10 deaths in our study, and 3 of these were attributable PE. For the question about the type of prophylaxis, we were referring to chemical prophylaxis. However, unfortunately, one of the limitations of the study was that the drug and the dosage varied amongst the institutions. Even during the study period, or within the study period, all 3 hospitals did have changes in the protocols. Although we did not change the dosage, within the study period, the trend at our institution has been toward earlier and earlier initiation of chemical prophylaxis. Again, although there was no difference in the incidence of early PE among groups that did and did not have a delay in the initiation of chemical prophylaxis, and there is literature reporting the reduction of DVT and PE with chemical prophylaxis in general, there has been recent evidence in the literature that corresponds to our experience. After noting the relatively large number of PEs that were diagnosed on hospital day 4, we performed the same statistical analyses for PEs diagnosed within 3 hospital days and 4 hospital days. Of note, the same clinical factors remained statistically significant; that is that long-bone fractures and an increased extremity Abbreviated Injury Scale (AIS) score were associated with early formation of PE, while an increased head AIS was associated with late formation of PE. Although we do not have any preliminary TEG data, recent literature has shown a relative state of hypercoagulability on admission TEG studies done for trauma patients. Again, with Dr Fabian’s point, we completely agree that the study brings preventability into question, which then further begs the question, should the diagnosis of PE count against us in terms of quality scores and reimbursement, providing us another reason and area for future study. Again, although we are not really sure that the incidence of PE or early PE has actually changed in the past 20 years, but more that the increased use of CT, especially in our initial screening for trauma patients, has just raised our awareness of it. Dr Mattox, you are correct. We are unable to separate the 2 entities of patients you are describing. The focus of the study really was just to confirm the presence and the entity of early PE, which has been described in several smaller single-institution studies. Our analysis was limited because of that. In terms of how to treat, we fully treated all of our patients who were diagnosed with a PE.
Coleman et al
Discussion
22. Kandilov AM, Coomer NM, Dalton K. The impact of hospital-acquired conditions on Medicare program payments. Medicare Medicaid Res Rev 2014;4:E14eE17. 23. Kaafarani HM, Borzecki AM, Itani KM, et al. Validity of selected Patient Safety Indicators: opportunities and concerns. J Am Coll Surg 2011;212:924e934.
Discussion DR TIMOTHY C FABIAN (Memphis, TN): The authors highlight a potentially important and underappreciated complication after injury: early pulmonary embolism (PE). They acknowledge important limitations of the study in the manuscript. This retrospective review of registry data from 3 institutions could not provide the following important information: clinical indications for obtaining the diagnostic studies, clinical significance of the PEs, institutional differences in prophylaxis and screening protocols, and CT protocols and equipment. They appropriately note that Medicare and Agency for Healthcare Research and Quality (AHRQ) have focused on deep vein thrombosis (DVT) and PE as two Patient Safety Indicators, to aid internal quality improvement but increasingly used for hospital profiling and reimbursement. In this study, the authors may have let an opportunity pass to address that issue. They queried a fairly large database of nearly 55,000 trauma patients and noted a PE incidence of 0.24%. Their analysis was based around differences in early PE versus late PE. Interestingly, they found that timing of prophylaxis has no impact on early PE. I would suggest they should have also selected an injury matched cohort without PE among the 55,000 patients to compare with the 133 PE patients. Such an analysis would provide data relative to the validity of using DVT and PE as Patient Safety Indicators. Did the PEs have any impact on outcomes? The fact that timing of prophylaxis was shown to have no impact on early PE makes one wonder if the events should be considered complications. Perhaps they are simply another iteration of CT “incidentalomas” associated with obtaining chest CTs for follow-up of other problems. These patients are always multiply injured and you have demonstrated that early PEs are associated with long-bone fractures and severe extremity trauma. Sixty percent of PEs occurred within 4 days of admission, an interval in which many orthopaedic procedures are being done, and many orthopaedic surgeons are not terribly enthusiastic about heparin protocols at that juncture. How have the findings from this study influenced your current institutional approach to PE screening and prophylaxis? Should CT PE protocols be done routinely on the high-risk group within a day or two of admission? Since timing of prophylaxis did not seem to help, are you considering earlier or higher doses prophylaxis? I thank the authors for this early initiative studying PE after injury. I suspect it will lead to an interesting avenue of future work. DR ADDISON MAY (Nashville, TN): The authors are to be applauded for completing a multicenter retrospective analysis of
J Am Coll Surg
133 cases of post-traumatic PE in an attempt to identify factors associated with the early vs late diagnosis. The authors’ findings support those reported from recent single-center studies regarding the early diagnosis of PE and clearly conflict with older studies regarding the timing of post-traumatic PE. I have several questions for the authors: 1. Do you believe that the trauma registry ICD-9 documentation of PEs is real? One hundred thirty-three cases is a manageable size for further review. Have you done any chart review to confirm the accuracy of the data capture? 2. If you believe that the documented PEs are real, is the diagnosis of early PE just an epiphenomenon of the advancements in CT scanning technology? Can you go back to evaluate the severity, size, indication for imaging, etc, to advance your understanding of these 133 events? Did the PEs contribute directly to any of the 10 deaths in the group? The 24 cases documented on the first hospital day are particularly difficult for me to wrap my head around. Anecdotally, our center has documented filling defects in lobar pulmonary arteries, read by the radiologist as PE, that on a follow-up CT scan are nowhere to be found. Are these just small localized changes in flow in the pulmonary artery or small thrombi created at the time and site of injury that then embolize when flow increases again through the injured vein? Might these findings be analogous to those of fat emboli seen on transesophageal echocardiography during operative fixation of long bone fractures, in which patients may be totally asymptomatic? 3. Forty-two percent of patients in the early PE group received prophylaxis within 48 hours. Can you provide details about the type of prophylaxis? Was this in the form of sequential compression devices, unfractionated heparin, or fractionated heparin? Do you believe that even earlier prophylaxis would alter your PE rate, and are you planning to implement any changes in your practice? 4. If you use the 4-day vs the day definition for early PE, does the presence of long-bone fractures become significant in your model? If the incidence of early vs late PE has increased in the last 2 decades, can you hypothesize why? Finally, you mention in your discussion the use of thromboelastography (TEG) to evaluate patients at risk for PE. Do you have any preliminary data to suggest that TEG will actually identify patients at risk for early PE? DR KENNETH MATTOX (Houston, TX): I have concerns that this study was faulted from the onset due to drinking the Kool-Aid of coding confusion. The quality of CT on the pulmonary arteries is sufficient to show usually peripheral pulmonary arteriolar clot, most often caused by low flow states, especially in trauma patients, and most often occurring early. This condition, recognized by all of us, has no relationship or linkage to DVT. Heparin prophylaxis in this group of patients may actually be contraindicated. This condition is totally different from larger central thromboembolic clot most often from iliocaval sites to the main or central
Vol. 220, No. 4, April 2015
pulmonary arteries, which has been reported at this Association over the decades repeatedly, and is totally different from that of the peripheral ateriolars. These conditions have different etiologies, often different physiologic impact, and often different treatments, but have the very same ICD-9, and ICD-10, codes. So the question, for this case cohort selected by code identification, how did you separate these 2 distinctly different patient groups? Without such a mechanism, the interpretations, the treatments, the conclusions, and the recommendations are faulted, not only for past reports that are similar, but for this study and future best practice recommendations. Specifically, my question is, how did you differentiate the anatomic location and size of the pulmonary artery clot in your analysis? Or did you merely rely on the ICD-9 coding? DR NICK NAMIAS (Miami, FL): I will not be asking a question; I will be answering one because you asked if other centers can confirm your findings. Well, we are happy to announce in 2012 we confirmed them, that in a group of trauma patients who had the Greenfield risk-assessment profile applied, we found about 20% of those patients who were at high risk did in fact have a venous thromboembolic event early on, just as you described today. So the confirmatory process has begun. DR JEFF BENDER (Oklahoma City, OK): I would like to ask how you recommend we treat these patients. My colleagues and I have also noticed a small cluster of this, and we are very divided. Among us, the options are to fully anticoagulate them, place a filter even in the absence of a documented DVT, or, my approach, just to ignore the problem. DR KENNETH BRAYMAN (Charlottesville, VA): I found this study fascinating. It appears that you have a great opportunity to define differences between those who realize an embolic event and those who do not. Attempting to define differences in the 2 patient populations with genomic profiling to determine risk stratification to see who really is at risk for developing thromboembolic phenomena would be very insightful, and it may affect approaches in therapy. Do you have any thoughts about how to take your observation and move it forward to define actual risk? DR JAMIE JONES COLEMAN: On how we performed chart review: we used the ICD-9 code just to initially identify which patients we needed to go back and further review. You are right. The 133 patients is a manageable number. We did go back and review the charts individually and confirmed the clinical presence of a PE. There is a potential that we may have inadvertently not captured every patient with a PE at the 3 institutions if an incorrect ICD-9 code was used. However, given the significance of this particular complication and our awareness of this complication, we thought that this wouldn’t be as likely. To answer several of the questions relating to the increased incidence of blunt vascular injuries, splenic lacerations, and other
Coleman et al
Discussion
737
incidentalomas, we agree that this could be a manifestation of the popularity of the pan-CT scan. Every radiology report was reviewed by an attending radiologist. Since the PEs that were diagnosed within the first 24 hours of hospitalization were present in all 3 institutions, this did lead us to believe that these PEs were “real” and not just overcalls or flow artifacts. However, all these points are valid, that although these may seem to be real radiologic PEs on day 1, it begs the question, would they be real on day 3? Do they transform or will they ever become clinically significant if untreated? However, in our study, all patients who received a diagnosis of PE, regardless of the presence or absence of clinical symptoms, did undergo treatment. There were a total of 10 deaths in our study, and 3 of these were attributable PE. For the question about the type of prophylaxis, we were referring to chemical prophylaxis. However, unfortunately, one of the limitations of the study was that the drug and the dosage varied amongst the institutions. Even during the study period, or within the study period, all 3 hospitals did have changes in the protocols. Although we did not change the dosage, within the study period, the trend at our institution has been toward earlier and earlier initiation of chemical prophylaxis. Again, although there was no difference in the incidence of early PE among groups that did and did not have a delay in the initiation of chemical prophylaxis, and there is literature reporting the reduction of DVT and PE with chemical prophylaxis in general, there has been recent evidence in the literature that corresponds to our experience. After noting the relatively large number of PEs that were diagnosed on hospital day 4, we performed the same statistical analyses for PEs diagnosed within 3 hospital days and 4 hospital days. Of note, the same clinical factors remained statistically significant; that is that long-bone fractures and an increased extremity Abbreviated Injury Scale (AIS) score were associated with early formation of PE, while an increased head AIS was associated with late formation of PE. Although we do not have any preliminary TEG data, recent literature has shown a relative state of hypercoagulability on admission TEG studies done for trauma patients. Again, with Dr Fabian’s point, we completely agree that the study brings preventability into question, which then further begs the question, should the diagnosis of PE count against us in terms of quality scores and reimbursement, providing us another reason and area for future study. Again, although we are not really sure that the incidence of PE or early PE has actually changed in the past 20 years, but more that the increased use of CT, especially in our initial screening for trauma patients, has just raised our awareness of it. Dr Mattox, you are correct. We are unable to separate the 2 entities of patients you are describing. The focus of the study really was just to confirm the presence and the entity of early PE, which has been described in several smaller single-institution studies. Our analysis was limited because of that. In terms of how to treat, we fully treated all of our patients who were diagnosed with a PE.
