LETTERS
Traumatic brain injury is not associated with coagulopathy out of proportion to injury in other body regions To the Editor: t is with great interest that we read the recently published article by Lee et al.1 The question of what role traumatic brain injury (TBI) plays on the coagulopathy of severely injured trauma patients is very pertinent and has an immediate impact on treating the two leading causes of mortality. We applaud the authors of this multiinstitutional study for adding to the existing literature these disease processes and for bringing a counterpoint to the view that TBI causes a unique coagulopathic state. Upon review of the data provided however, we do not believe this counterpoint is fully supported. The foremost issue with making this conclusion, as the authors themselves point out, is the combining of injuries from different Abbreviated Injury Scale (AIS) body regions within the same group. We would state that separating groups solely by highest AIS score is flawed to the point of not being useful. The clinical application of AIS has primarily been used for prognostic equations and was not developed for the purpose of comparing physiologic dysfunction because of the subjectivity of scores in each region. When comparing brain injury patients with patients with injuries of other body regions, the addition of all AIS body groups adulterates the data. The authors do recognize this as a confounding factor and, to address it, perform a subgroup analysis where patients with only one body region are compared. The problem with this however is that there are too few patients in each body region (n = 3 for extremity, n = 3 for face, and n = 0 for external) to make any valid comparison. The authors do state that there are no significant differences; however, they do not show any data to illustrate potential trends between isolated body regions. This prevents us from surmising if the data show no significant difference simply because of lack of power. A second concern for this study is that the head AIS score includes injuries in the neck. There is no mention of excluding patients that have only neck and cervical spine injuries from the group where head was the dominant region of injury. This is an important population to exclude when examining coagulopathy caused by TBI
I
TO THE
EDITOR
because patients with neck injuries have never been associated with coagulopathy. The article eloquently states the different mechanisms of coagulopathy in trauma including acute traumatic coagulopathy and trauma-induced coagulopathy. The authors go on to state a purported mechanism of TBI-induced coagulopathy, the release of tissue factor. There may be other mechanisms that contribute to the differences between brain injuries and injuries to other body regions, such as the release of thrombospondin, and the change in platelet function seen in TBI.2 If this is to be considered, then neither conventional nor rapid TEG may pick up on these coagulation disorders, thereby rendering these groups incomparable. Last and certainly not the least, coagulopathy caused by trauma from body regions outside the brain is often caused by extensive blood loss. It is well-known however that bleeding inside the brain cannot cause a significant coagulopathy secondary to the volume of blood loss. These characteristics need to be teased out to have a meaningful discourse on comparing AIS body regions. If an isolated body region has an AIS score of 3 or greater, there should not be significant bleeding (in volume) to compare it with equivalent brain injury. One method to evaluate this could be to compare crush injuries with different body regions in anesthetized animals. Again, we would like to thank the authors for adding to the volume of literature and raising important questions in this evergrowing field.
*The authors declare no conflicts of interest. Matthew Edavettal, MD, PhD Ashley Vellucci Frederick B. Rogers, MD, MS, FACS Lancaster General Hospital Lancaster, PA
REFERENCES 1. Lee TH, Hampton DA, Diggs BS, et al. Traumatic brain injury is not associated with coagulopathy out of proportion to injury in other body regions. J Trauma Acute Care Surg. 2014;77(1):67Y72. 2. Castellino FJ, Chapman MP, Donahue DL, et al. Traumatic brain injury causes platelet adenosine diphosphate and arachidonic acid receptor inhibition independent of hemorrhagic show in humans and rats. J Trauma Acute Care Surg. 2014;76(5):1169Y1176.
Problems in analyzing helicopter emergency medical service accidents To the Editor: t is with great interest that we have read the article by Chesters et al.1 on a 26-year comparative review of UK helicopter emergency medical service (HEMS) crashes. We do appreciate this work, since research in this area is scarce and of extraordinary importance to improve flight safety in HEMS operations. We would like to add some important points to this article. Civil air rescue in the United Kingdom is a relatively young endeavor (started 1987) with a high number of providers and a low number of helicopters per Air Ambulance Service (range, 1Y3). This is in contrast to many other countries, for example, Germany, where three major operators provide HEMS services running approximately 85 stations nationwide. Therefore, the operational setting differs and makes comparisons difficult. As reported in a previous comparative review study, we found an accident rate of 0.4 to 3.05 per 10,000 missions.2 Four of five studies reported rates between 0.4 and 0.9, which is well in accordance with the present UK data.1 In addition, UK fatal accident rate was within the previously published ranges. In this context, it would be more accurate to use exact flying times and to access even more specific mission-associated parameters (e.g., helicopter model,3 location, flying conditions, and accident circumstances4) to calculate specific rates and risks. To calculate accidents risks, the authors used extrapolated/estimated mission numbers from Germany. According to this, their calculations may eventually be inaccurate. As the authors stated, there is no denominator data available for the United Kingdom. However, such data are essential to interpret accidents and the course of numbers. The general lack of denominator data is a known problem in most fields of aviation accident research5 in Germany and for other countries as well. The implementation of a valid database, for example, a national registry, with defined parameters for analysis, would be helpful and is required to further improve flight safety.
I
*The authors declare no conflicts of interest. Jochen Hinkelbein, MD, DESA, EDIC Department for Anaesthesiology and Intensive Care Medicine University Hospital Cologne Cologne, Germany
J Trauma Acute Care Surg Volume 77, Number 5
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
799
J Trauma Acute Care Surg Volume 77, Number 5
Letters to the Editor
Christopher Neuhaus, MD Department for Anaesthesiology University Hospital of Heidelberg Heidelberg, Germany
Stefan Braunecker, MD Department for Anaesthesiology and Intensive Care Medicine University Hospital Cologne Cologne, Germany
REFERENCES 1. Chesters A, Grieve PH, Hodgetts TJ. 26-year comparative review of United Kingdom helicopter emergency medical services crashes and serious incidents. J Trauma Acute Care Surg. 2014;76:1055Y1060. 2. Hinkelbein J, Schwalbe M, Genzwuerker HV. Comparison of Helicopter Emergency Medical Services (HEMS) accident rates in different international air rescue systems. Open Access Emerg Med. 2010;2:45Y49. 3. Hinkelbein J, Schwalbe M, Wetsch WA, et al. Helicopter type and accident severity in Helicopter Emergency Medical Services missions. Aviat Space Environ Med. 2011;82((12)):1148Y1152. 4. Hinkelbein J, Schwalbe M, Wetsch WA, et al. Application of the FIA score for German rescue helicopter accidents to predict fatalities in HEMS crashes. J Emerg Med. 2012;43(6):1014Y1019. 5. Hinkelbein J, Neuhaus C, Schwalbe M, et al. Significant lack of data in aviation accident analysis. Aviat Space Environ Med. 2010;81(1):77.
Delayed hemorrhagic complications in the nonoperative management of blunt splenic trauma To the Editor: have read the article by Leeper et al.1 with interest. I thought the study was well done and may have a significant clinical implication. I like the authors’ idea of repeating computed tomography (CT) within 48 hours to possibly help decrease the failure rate of nonoperative management, but I am not certain as a cost conscientious clinician that I like the idea of repeating CT on every grade injury for a mere 6% yield (29 of 453). I have the following comments and questions for the authors: 1. Can the authors provide us the denominator for the different splenic grade (Fig. 3 in their article) that had positive findings on a repeated CT? It would make more sense (economic sense anyway) to screen and repeat CT for those with high-grade injury first (IV and V). Some authors2
I
800
went further and advocated even more aggressive approach and performed angiography on everyone with high-grade injuries, but even that seemed so excessive. I realize the authors had commented that delayed arterial extravasation and splenic pseudoaneurysm (SPA) could still occur even in the low-grade injuries (I and II, 6 patients in their study), which leads me to my next question. 2. Can the authors elaborate in details on those six Grade I and II splenic injuries that had delayed arterial extravasation and SPA? Were these underappreciated injuries, or were these correctly graded? What did the authors actually see on the angiography? Was there anything unique about them, maybe an outlier that may be of interest that one can use to identify these individuals? Could this be the limitation of the CT scan used? They mentioned in their study that these six patients represented 20% of Grade I and II, which implied that their study only had 30 patients with Grade I and II splenic injuries. Was that correct? 3. As quoted in the article, Dr. Leeper and the group modeled the repeated CT algorithm after the Memphis group.3 In that original study, the rationale for repeating CT was to detect a missed or delayed SPA, which occurred at the rate of 5%. However, that was based on an earlier CT model (in that study by Weinberg et al., the CT used was Siemens Somatom Plus 4, which was a 4-slice CT). What CT scan did Dr. Leeper and the group use in their present study? Was the CT scan used different between the two eras? Do Dr. Leeper and the group think that with the more advanced CT (our institution uses a 64-slice CT), the incidence of missed or delayed SPA will diminish? Again, Dr. Leeper and the group had shown the decrease in the failure of nonoperative management from 12% to less than 1% after establishing the described management algorithm of routine repeated CT, which is quite remarkable, although half of that effect probably benefited from the advance in CT image quality that led to early aggressive angiography and intervention. I look forward to hear the authors’ reply and thank the group for their study endeavor. *The author declares no conflict of interest.
Narong Kulvatunyou, MD Division of Acute Care Surgery Department of Surgery University of Arizona Tucson, AZ
REFERENCES 1. Leeper WR, Leeper TJ, Ouellette D, et al. Delayed hemorrhagic complications in the nonoperative management of blunt splenic trauma: early screening leads to a decrease in failure rate. J Trauma Acute Care Surg. 2014;76:1349Y1353. 2. Bhullar IS, Frykberg ER, Tepas JJ, et al. At first blush: absence of computed tomography contrast extravasation in grade IV or V adult blunt splenic trauma should not preclude angioembolization. J Trauma Acute Care Surg. 2013;74:105Y112. 3. Weinberg JA, Magnotti LJ, Croce MA, et al. The utility of serial computed tomography imaging of blunt splenic injury: still worth a second look? J Trauma. 2007;62:1143Y1148.
Re: Delayed hemorrhagic complications in the nonoperative management of blunt splenic trauma In Reply: he authors thank Dr. Kulvatunyou for his interest in the article and his thoughtful comments. Each of his questions raised important points, and these have been addressed in the following sections:
T
1. Re: Clarification of the ‘‘denominator’’ for delayed computed tomographic (CT) findings Our current management protocol for splenic injury includes mandatory repeat CT imaging at 48 hours and splenic artery embolization whenever high-risk vascular lesions, splenic pseudoanuerysm (PSA), or arterial extravasation are identified. During the era of our current protocol, a total of 475 patients were treated initially with nonoperative management. Breakdown of these 475 patients by grade of injury and identification of high-risk vascular lesions on CT scan are given in the table online (Supplemental Digital Content [SDC] 1, http://links.lww.com/TA/A485). The development of delayed high-risk vascular lesions not seen on initial CT occurred in 21% of Grade 4 injuries (15 of 70), 8% of Grade 3 injuries (8 of 97), 4.5% of Grade 2 injuries (4 of 87), and 1% of Grade 1 injuries (2 of 189). If an argument is to be made concerning omission of mandatory repeat CT, Grade 1 injuries seem a logical place to start. Regarding the question raised by Dr. Kulvatunyou about the statement in the article that ‘‘20% of all delayed findings occurred in Grade I and II injuries,’’ this is true in that 6 * 2014 Lippincott Williams & Wilkins
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Traumatic brain injury is not associated with coagulopathy out of proportion to injury in other body regions To the Editor: t is with great interest that we read the recently published article by Lee et al.1 The question of what role traumatic brain injury (TBI) plays on the coagulopathy of severely injured trauma patients is very pertinent and has an immediate impact on treating the two leading causes of mortality. We applaud the authors of this multiinstitutional study for adding to the existing literature these disease processes and for bringing a counterpoint to the view that TBI causes a unique coagulopathic state. Upon review of the data provided however, we do not believe this counterpoint is fully supported. The foremost issue with making this conclusion, as the authors themselves point out, is the combining of injuries from different Abbreviated Injury Scale (AIS) body regions within the same group. We would state that separating groups solely by highest AIS score is flawed to the point of not being useful. The clinical application of AIS has primarily been used for prognostic equations and was not developed for the purpose of comparing physiologic dysfunction because of the subjectivity of scores in each region. When comparing brain injury patients with patients with injuries of other body regions, the addition of all AIS body groups adulterates the data. The authors do recognize this as a confounding factor and, to address it, perform a subgroup analysis where patients with only one body region are compared. The problem with this however is that there are too few patients in each body region (n = 3 for extremity, n = 3 for face, and n = 0 for external) to make any valid comparison. The authors do state that there are no significant differences; however, they do not show any data to illustrate potential trends between isolated body regions. This prevents us from surmising if the data show no significant difference simply because of lack of power. A second concern for this study is that the head AIS score includes injuries in the neck. There is no mention of excluding patients that have only neck and cervical spine injuries from the group where head was the dominant region of injury. This is an important population to exclude when examining coagulopathy caused by TBI
I
TO THE
EDITOR
because patients with neck injuries have never been associated with coagulopathy. The article eloquently states the different mechanisms of coagulopathy in trauma including acute traumatic coagulopathy and trauma-induced coagulopathy. The authors go on to state a purported mechanism of TBI-induced coagulopathy, the release of tissue factor. There may be other mechanisms that contribute to the differences between brain injuries and injuries to other body regions, such as the release of thrombospondin, and the change in platelet function seen in TBI.2 If this is to be considered, then neither conventional nor rapid TEG may pick up on these coagulation disorders, thereby rendering these groups incomparable. Last and certainly not the least, coagulopathy caused by trauma from body regions outside the brain is often caused by extensive blood loss. It is well-known however that bleeding inside the brain cannot cause a significant coagulopathy secondary to the volume of blood loss. These characteristics need to be teased out to have a meaningful discourse on comparing AIS body regions. If an isolated body region has an AIS score of 3 or greater, there should not be significant bleeding (in volume) to compare it with equivalent brain injury. One method to evaluate this could be to compare crush injuries with different body regions in anesthetized animals. Again, we would like to thank the authors for adding to the volume of literature and raising important questions in this evergrowing field.
*The authors declare no conflicts of interest. Matthew Edavettal, MD, PhD Ashley Vellucci Frederick B. Rogers, MD, MS, FACS Lancaster General Hospital Lancaster, PA
REFERENCES 1. Lee TH, Hampton DA, Diggs BS, et al. Traumatic brain injury is not associated with coagulopathy out of proportion to injury in other body regions. J Trauma Acute Care Surg. 2014;77(1):67Y72. 2. Castellino FJ, Chapman MP, Donahue DL, et al. Traumatic brain injury causes platelet adenosine diphosphate and arachidonic acid receptor inhibition independent of hemorrhagic show in humans and rats. J Trauma Acute Care Surg. 2014;76(5):1169Y1176.
Problems in analyzing helicopter emergency medical service accidents To the Editor: t is with great interest that we have read the article by Chesters et al.1 on a 26-year comparative review of UK helicopter emergency medical service (HEMS) crashes. We do appreciate this work, since research in this area is scarce and of extraordinary importance to improve flight safety in HEMS operations. We would like to add some important points to this article. Civil air rescue in the United Kingdom is a relatively young endeavor (started 1987) with a high number of providers and a low number of helicopters per Air Ambulance Service (range, 1Y3). This is in contrast to many other countries, for example, Germany, where three major operators provide HEMS services running approximately 85 stations nationwide. Therefore, the operational setting differs and makes comparisons difficult. As reported in a previous comparative review study, we found an accident rate of 0.4 to 3.05 per 10,000 missions.2 Four of five studies reported rates between 0.4 and 0.9, which is well in accordance with the present UK data.1 In addition, UK fatal accident rate was within the previously published ranges. In this context, it would be more accurate to use exact flying times and to access even more specific mission-associated parameters (e.g., helicopter model,3 location, flying conditions, and accident circumstances4) to calculate specific rates and risks. To calculate accidents risks, the authors used extrapolated/estimated mission numbers from Germany. According to this, their calculations may eventually be inaccurate. As the authors stated, there is no denominator data available for the United Kingdom. However, such data are essential to interpret accidents and the course of numbers. The general lack of denominator data is a known problem in most fields of aviation accident research5 in Germany and for other countries as well. The implementation of a valid database, for example, a national registry, with defined parameters for analysis, would be helpful and is required to further improve flight safety.
I
*The authors declare no conflicts of interest. Jochen Hinkelbein, MD, DESA, EDIC Department for Anaesthesiology and Intensive Care Medicine University Hospital Cologne Cologne, Germany
J Trauma Acute Care Surg Volume 77, Number 5
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
799
J Trauma Acute Care Surg Volume 77, Number 5
Letters to the Editor
Christopher Neuhaus, MD Department for Anaesthesiology University Hospital of Heidelberg Heidelberg, Germany
Stefan Braunecker, MD Department for Anaesthesiology and Intensive Care Medicine University Hospital Cologne Cologne, Germany
REFERENCES 1. Chesters A, Grieve PH, Hodgetts TJ. 26-year comparative review of United Kingdom helicopter emergency medical services crashes and serious incidents. J Trauma Acute Care Surg. 2014;76:1055Y1060. 2. Hinkelbein J, Schwalbe M, Genzwuerker HV. Comparison of Helicopter Emergency Medical Services (HEMS) accident rates in different international air rescue systems. Open Access Emerg Med. 2010;2:45Y49. 3. Hinkelbein J, Schwalbe M, Wetsch WA, et al. Helicopter type and accident severity in Helicopter Emergency Medical Services missions. Aviat Space Environ Med. 2011;82((12)):1148Y1152. 4. Hinkelbein J, Schwalbe M, Wetsch WA, et al. Application of the FIA score for German rescue helicopter accidents to predict fatalities in HEMS crashes. J Emerg Med. 2012;43(6):1014Y1019. 5. Hinkelbein J, Neuhaus C, Schwalbe M, et al. Significant lack of data in aviation accident analysis. Aviat Space Environ Med. 2010;81(1):77.
Delayed hemorrhagic complications in the nonoperative management of blunt splenic trauma To the Editor: have read the article by Leeper et al.1 with interest. I thought the study was well done and may have a significant clinical implication. I like the authors’ idea of repeating computed tomography (CT) within 48 hours to possibly help decrease the failure rate of nonoperative management, but I am not certain as a cost conscientious clinician that I like the idea of repeating CT on every grade injury for a mere 6% yield (29 of 453). I have the following comments and questions for the authors: 1. Can the authors provide us the denominator for the different splenic grade (Fig. 3 in their article) that had positive findings on a repeated CT? It would make more sense (economic sense anyway) to screen and repeat CT for those with high-grade injury first (IV and V). Some authors2
I
800
went further and advocated even more aggressive approach and performed angiography on everyone with high-grade injuries, but even that seemed so excessive. I realize the authors had commented that delayed arterial extravasation and splenic pseudoaneurysm (SPA) could still occur even in the low-grade injuries (I and II, 6 patients in their study), which leads me to my next question. 2. Can the authors elaborate in details on those six Grade I and II splenic injuries that had delayed arterial extravasation and SPA? Were these underappreciated injuries, or were these correctly graded? What did the authors actually see on the angiography? Was there anything unique about them, maybe an outlier that may be of interest that one can use to identify these individuals? Could this be the limitation of the CT scan used? They mentioned in their study that these six patients represented 20% of Grade I and II, which implied that their study only had 30 patients with Grade I and II splenic injuries. Was that correct? 3. As quoted in the article, Dr. Leeper and the group modeled the repeated CT algorithm after the Memphis group.3 In that original study, the rationale for repeating CT was to detect a missed or delayed SPA, which occurred at the rate of 5%. However, that was based on an earlier CT model (in that study by Weinberg et al., the CT used was Siemens Somatom Plus 4, which was a 4-slice CT). What CT scan did Dr. Leeper and the group use in their present study? Was the CT scan used different between the two eras? Do Dr. Leeper and the group think that with the more advanced CT (our institution uses a 64-slice CT), the incidence of missed or delayed SPA will diminish? Again, Dr. Leeper and the group had shown the decrease in the failure of nonoperative management from 12% to less than 1% after establishing the described management algorithm of routine repeated CT, which is quite remarkable, although half of that effect probably benefited from the advance in CT image quality that led to early aggressive angiography and intervention. I look forward to hear the authors’ reply and thank the group for their study endeavor. *The author declares no conflict of interest.
Narong Kulvatunyou, MD Division of Acute Care Surgery Department of Surgery University of Arizona Tucson, AZ
REFERENCES 1. Leeper WR, Leeper TJ, Ouellette D, et al. Delayed hemorrhagic complications in the nonoperative management of blunt splenic trauma: early screening leads to a decrease in failure rate. J Trauma Acute Care Surg. 2014;76:1349Y1353. 2. Bhullar IS, Frykberg ER, Tepas JJ, et al. At first blush: absence of computed tomography contrast extravasation in grade IV or V adult blunt splenic trauma should not preclude angioembolization. J Trauma Acute Care Surg. 2013;74:105Y112. 3. Weinberg JA, Magnotti LJ, Croce MA, et al. The utility of serial computed tomography imaging of blunt splenic injury: still worth a second look? J Trauma. 2007;62:1143Y1148.
Re: Delayed hemorrhagic complications in the nonoperative management of blunt splenic trauma In Reply: he authors thank Dr. Kulvatunyou for his interest in the article and his thoughtful comments. Each of his questions raised important points, and these have been addressed in the following sections:
T
1. Re: Clarification of the ‘‘denominator’’ for delayed computed tomographic (CT) findings Our current management protocol for splenic injury includes mandatory repeat CT imaging at 48 hours and splenic artery embolization whenever high-risk vascular lesions, splenic pseudoanuerysm (PSA), or arterial extravasation are identified. During the era of our current protocol, a total of 475 patients were treated initially with nonoperative management. Breakdown of these 475 patients by grade of injury and identification of high-risk vascular lesions on CT scan are given in the table online (Supplemental Digital Content [SDC] 1, http://links.lww.com/TA/A485). The development of delayed high-risk vascular lesions not seen on initial CT occurred in 21% of Grade 4 injuries (15 of 70), 8% of Grade 3 injuries (8 of 97), 4.5% of Grade 2 injuries (4 of 87), and 1% of Grade 1 injuries (2 of 189). If an argument is to be made concerning omission of mandatory repeat CT, Grade 1 injuries seem a logical place to start. Regarding the question raised by Dr. Kulvatunyou about the statement in the article that ‘‘20% of all delayed findings occurred in Grade I and II injuries,’’ this is true in that 6 * 2014 Lippincott Williams & Wilkins
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
