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 Table of Contents    
Year : 2011  |  Volume : 4  |  Issue : 4  |  Page : 450-454
Damage control in severely injured trauma patients - A ten-year experience

1 Department of Surgery, Hospital Uster, Switzerland
2 Department of Surgery, Division of Trauma and Critical Care, Los Angeles County + University of Southern California Medical Center, Los Angeles, CA, USA
3 Department of Surgery, Division of Trauma Surgery, University Hospital Zurich, Switzerland

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Date of Submission09-Aug-2010
Date of Acceptance05-Mar-2010
Date of Web Publication24-Oct-2011


Background : This study reviews our 10-year institutional experience with damage control management and investigates risk factors for early mortality. Materials and Methods : The trauma registry of our level I trauma centre was utilized to identify all patients from 01/96 through 12/05 who underwent initial damage control procedures. Demographics, clinical and physiological parameters, and outcomes were abstracted. Patients were categorized as either early survivors (surviving the first 72 hours after admission) or early deaths. Results : During the study period, 319 patients underwent damage control management. Overall, 52 patients (16.3%) died (early deaths) and 267 patients (83.7%) survived the first 72 hours (early survivors). Early deaths showed significantly deranged serum lactate (5.81±0.55 vs. 3.46±0.13 mmol/L; P<0.001), base deficit (10.10±0.95 vs. 4.90±0.28 mmol/L; P<0.001) and pH (7.16±0.03 vs. 7.29±0.01; P<0.001) levels compared to early survivors on hospital admission. An International Normalized Ratio >1.2, base deficit >3 mmol/L, head Abbreviated Injury Scale ≥3, body temperature <35°C, serum lactate >6 mmol/L, and hemoglobin <7 g/dL proved to be independent risk factors for early mortality on hospital admission. Conclusions : Several risk factors for early mortality such as severe head injury and the lethal triad (coagulopathy, acidosis and hypothermia) in patients undergoing damage control procedures were identified and should trigger the trauma surgeon to maintain aggressive resuscitation in the intensive care unit.

Keywords: Damage control surgery, mortality, risk factors, trauma

How to cite this article:
Frischknecht A, Lustenberger T, Bukur M, Turina M, Billeter A, Mica L, Keel M. Damage control in severely injured trauma patients - A ten-year experience. J Emerg Trauma Shock 2011;4:450-4

How to cite this URL:
Frischknecht A, Lustenberger T, Bukur M, Turina M, Billeter A, Mica L, Keel M. Damage control in severely injured trauma patients - A ten-year experience. J Emerg Trauma Shock [serial online] 2011 [cited 2020 Jul 10];4:450-4. Available from:

   Introduction Top

Damage control (DC) procedures for patients with major truncal or extremity trauma have evolved over the past 20 years and are recognized as major factors in decreasing morbidity and mortality in severely injured patients. [1] Early physiologic criteria, such as hypothermia, coagulopathy, and acidosis are used to select patients that would benefit from DC techniques. Injury severity scoring or the estimated time required to accomplish definitive repair of injuries are further useful parameters in determining the need for DC. [2]

Numerous studies have reported indications to perform DC operations in severely injured trauma patients. [2],[3],[4],[5],6] However, investigations evaluating predictors of poor outcome among the subset of trauma patients undergoing DC procedures are scarce. Thus, the objectives of this study were to review our institutional experience with DC management and to investigate risk factors for early mortality in patients undergoing DC procedures.

   Materials and Methods Top

After approval by the Institutional Review Board, the trauma registry of the Division of Trauma Surgery, University Hospital of Zurich, a verified Level I trauma centre, was reviewed to identify all severely injured patients [Injury Severity Score (ISS) ≥17] from January 1, 1996, through December 31, 2005 who underwent initial DC procedures. A DC management was defined by limited operations for control of hemorrhage and contamination, or temporary fixation of extremity injuries. This included management of solid organ injuries by packing, resection of gastrointestinal tract injuries without re-anastomosis, use of temporary closure techniques at a site of surgical exploration, or temporary stabilization of extremity and pelvic fractures.

Demographic and clinical information collected included age, sex, mechanism of injury (blunt vs. penetrating), systolic blood pressure, Glasgow Coma Score (GCS) upon admission, ISS, and Abbreviated Injury Scale (AIS) for each body area (head, chest, abdomen, and extremity). For the analysis, continuous variables were dichotomized using clinically relevant cut-points: GCS on admission (≤8 vs. >8), systolic blood pressure (SBP) on admission (≤90 mmHg vs. >90 mmHg) and ISS (≥25 vs. <25). Laboratory parameters including hemoglobin, hematocrit, lactate, base deficit (BD), and pH at hospital and intensive care unit (ICU) admission were also recorded.

Statistical analysis

Patients were categorized as early survivors (surviving the first 72 hours after admission) or early deaths (death within 72 hours after admission). The demographic and clinical characteristics between early survivors and early deaths were evaluated using bivariate analysis. The P values for categorical variables were derived from the Chi-square or two-sided Fisher's Exact test and continuous variables were evaluated with the Student's t-test or the Mann-Whitney test. Differences were considered significant at P<0.05.

To identify independent risk factors for early mortality, potential risk factors were examined by bivariate analysis. To explore critical thresholds for physiological and laboratory parameters associated with early mortality, a cut-off analysis was performed using repeated multivariate analysis. The highest R 2 value defined the best cut-off. All risk factors with P<0.2 were subsequently entered in a stepwise forward logistic regression model.

Values are reported as mean±standard error of the mean (SEM) for continuous variables and as percentages for categorical variables. All analyses were performed using the Statistical Package for Social Sciences (SPSS Windows͹ ), version 12.0 (SPSS Inc., Chicago, IL).

   Results Top

0During the 10-year study period, 1,144 patients with an ISS ≥17 were admitted to our trauma centre. Of those, 319 patients (27.9%) underwent initial DC procedures and constituted our study cohort mean age overall was 39.3±1.0 years, 71.8% were male and the mean ISS was 36.6±0.7. On admission, 8.7% (n=26) of the patients were hypotensive (SBP <90 mmHg), and 55.7% (n=176) had a GCS ≤8. Blunt trauma was responsible for the majority of injuries (n=291, 91.2%).

Overall, 74 patients (23.2%) died. Fifty-two patients (16.3%) died within the first 72 hours after admission (early deaths), with seven deaths occurring during the initial DC procedure. The cause of early deaths included hemorrhagic shock (n=18), head injury (n=28), and multiple organ failure (n=6). A total of 267 patients (83.7%) survived the first 72 hours (early survivors). Basic demographics and associated injuries of the two study groups are presented in [Table 1]. DC procedures performed are summarized in [Table 2].
Table 1: Comparison of clinical and demographic characteristics of early survivors and early deaths

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Table 2: Damage control procedures performed in 319 patients

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Laboratory parameters including serum lactate and BD level, pH, International Normalized Ratio (INR), hemoglobin, hematocrit, and platelet counts at hospital and ICU admission are delineated in [Table 3]. Early deaths showed significantly deranged serum lactate, BD and pH levels compared to early survivors on hospital and ICU admission. However, while hemoglobin and hematocrit levels were significantly lower in patients dying within 72 hours post admission, these values were similar upon admission to the ICU in both groups.
Table 3: Comparison of laboratory parameters in early survivors and early deaths

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Independent hospital admission predictors of early mortality in patients undergoing DC management

Various factors, potentially associated with early mortality in patients undergoing DC procedures, were identified using bivariate analysis. After stepwise logistic regression, an INR >1.2, BD >3 mmol/L, AIS head ≥3, body core temperature <35°C, lactate >6 mmol/L and hemoglobin <7 g/dL proved to be independent risk factors for early mortality (R 2 =0.453) [Table 4].
Table 4: Independent risk factors at hospital admission for early mortality in patients undergoing damage control management

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Independent ICU admission predictors of early mortality in patients undergoing DC management

For those patients admitted to the ICU (n=312), an arterial lactate level >4 mmol/L on admission to ICU and >10 Units PRBC transfused until ICU admission were found to be independent predictors of early mortality (R 2 =0.373) [Table 5].
Table 5: Independent risk factors at ICU admission for early mortality in patients undergoing damage control management

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Outcomes of early survivors

Intensive care unit length of stay for early survivors was 15.7±0.8 days and the mean hospital length of stay was 36.5±1.5 days. Overall, 59.6% (159 of 267) patients developed major in-hospital complications with the most frequent being sepsis (n=95, 35.6%), pneumonia (n=82, 30.7%), wound infection (n=64, 24.0%), intra-abdominal infection (n=17, 6.4%), and acute respiratory distress syndrome (ARDS) (n=12, 4.5%). Twenty-two early survivors (8.2%) died 22.5±5.3 days later due to multiple organ failure (n=16) or severe head injury (n=6).

   Discussion Top

Managing severely injured patients is a diagnostic and therapeutic challenge for every trauma team. During the last decade, several studies have shown that the DC concept for abdominal, thoracic, and orthopedic injuries improves outcome in blunt and penetrating trauma. [7],[8],[9],[10],[11] Johnson et al. recently demonstrated that the continued application of DC principles has led to improved survival in patients with penetrating abdominal injury by comparing a historical cohort with a current study population. In their study, overall survival improved from 58% to 90% with equivalent injury severity. They concluded that the early treatment of hypothermia and coagulopathy and the increasing experience with the open abdomen significantly contributed to improved survival. [7] For multiple injured patients with concomitant orthopedic trauma, it has been demonstrated that DC procedures significantly reduce the incidence of general systemic complications such as ARDS and multiple organ failure. [10] Likewise in our study cohort, although 84% of the 267 patients surviving the first 3 days presented with critical injuries (ISS ≥ 25), only 22 patients (8.2%) died in the later in-hospital course due to multiple organ failure or severe traumatic brain injury.

It is difficult to distinguish which patients qualify for DC management. Analysis of our data has identified several hospital and ICU admission parameters that predict early mortality in severely injured patients despite being managed with DC procedures. Among those variables, coagulopathy upon hospital admission was one of the strongest predictor of poor outcome. Early deaths presented with significantly deranged coagulation parameters including an elevated INR and lower platelet counts on hospital and ICU admission. An INR >1.2 on hospital admission represented the most important independent risk factor (adjusted odds ratio, 10.64) associated with early mortality. Likewise, in numerous previous studies, the development of coagulopathy in trauma patients has been associated with increased morbidity and a several-fold increased mortality. [12],[13],[14],[15],[16],17],[18],[ 19] In the study by MacLeod and colleagues, coagulation abnormalities upon admission, defined by a prothrombin time >14 seconds and a partial thromboplastin time >36 seconds, were independent predictors of in-hospital mortality with an adjusted odds ratio of 1.35 and 4.26, respectively. [13] In the analysis by Mitra et al., the presence of acute coagulopathy was independently associated with death within 24 hours of hospital admission (odds ratio, 8.77). [19] Additionally, coagulopathy is common following severe traumatic brain injury, mediated by the systemic release of tissue factor from the injured brain parenchyma, resulting in an unregulated activation of the extrinsic coagulation pathway. [17],[20],[21],[22],[23],[24] Talving et al. demonstrated that the development of traumatic brain injury-associated coagulopathy, defined by thrombocytopenia and/or elevated INR and/or activated thromboplastin time, is associated with longer ICU lengths of stay and an almost ten-fold increased risk of death. [17] Also, in a prospective study by Olson and colleagues, elevated fibrin degradation products and an increased consumptive coagulopathy at admission were identified as independent predictors of mortality after isolated head injury. [24] In our study, a significantly higher proportion of patients dying within the first 72 hours suffered severe traumatic brain injury compared to early survivors (71.2% vs. 43.1%, P<0.001), which may have further contributed to their impaired admission coagulation status and may explain their early detrimental outcome. In addition, the severity of brain injury (head AIS ≥3) itself remained an independent predictor of early mortality (Odds Ratio (OR) 4.27, 95% CI [1.55-11.76]).

In the present study, early deaths had significantly higher lactate and BD levels at hospital and ICU admission as compared to early survivors. Furthermore, an elevated BD >3 mmol/L, lactate level >6 mmol/L on hospital admission, and the inability to achieve a lactate level <4 mmol/L until ICU admission, indicating a decreased lactate clearance, were significant risk factors for early mortality in the current analysis. These findings are consistent with previously published results. [4],[5],[25],[26],[27],[28],[29],[30],[31],[32],[33],[34],[35] In the study by Smith and co-workers, lactate, BD, and the combination of the two were good predictors of morbidity and mortality in critically ill patients. [35] Furthermore, a recent retrospective analysis of 95 surgical ICU patients documented a stepwise increase of hospital mortality with increasing time to normal lactate levels (≤2.0 mmol/L). [32] In patients with major vascular injuries, initial emergency department acid-base variables such as pH, BD, and lactate were strongly associated with outcome. [29] Thus, serum lactate and BD levels are useful for estimating and monitoring the adequacy of surgical and resuscitative therapy and provide a means of predicting mortality in severely injured trauma patients.

Hypothermia on admission, defined as a core temperature lower than 35°C, has repeatedly been demonstrated to be a predictor of poor outcomes in severely injured trauma patients. [36],[37],[38],[39],[40],[41],[42],[43],[44],[45] In the present investigation, early deaths presented with significantly lower admission core temperature compared to early survivors. Moreover, admission hypothermia was independently associated with early mortality (adjusted OR, 3.68). In the study by Wang et al. admission hypothermia was likewise independently associated with an increased odds of death in both the full cohort of trauma patients (adjusted OR, 3.03) and the subset of patients with isolated severe head injury (adjusted OR, 2.21). [38] In another series of 71 severely injured trauma patients, a temperature below 32°C was associated with no survival. [36] Inaba et al. recently demonstrated that not only admission hypothermia, but also postoperative hypothermia after cavitary surgery represents an independent predictor of mortality. Compared to patients with a temperature of >35°C, the relative risk of death for patients with a temperature between 35°C and 33°C was 4.0, and that for patients with a temperature ≤33°C was 7.1. [46]

   Conclusion Top

We identified several risk factors present upon hospital and ICU admission for early mortality such as severe head injury and the lethal triad (coagulopathy, acidosis and hypothermia). These predictors of poor outcome should trigger the trauma surgeon to maintain aggressive resuscitation. However, when surviving the first 72 hours after injury, survival in severely injured trauma patients managed with damage control protocol exceeded 90%.

   References Top

1.Wyrzykowski AD, Feliciano DV. Trauma damage control. In: Feliciano DV, Mattox KL, Moore EE, editors. Trauma. 6 th ed. New York, Chicago, San Francisco: McGraw-Hill Companies; 2008. p. 851-70.  Back to cited text no. 1
2.Keel M, Labler L, Trentz O. "Damage control" in severely injured patients. Why, when, and how? Eur J Trauma Emerg Surg 2005;31:212-21.  Back to cited text no. 2
3.Cushman JG, Feliciano DV, Renz BM, Ingram WL, Ansley JD, Clark WS, et al. Iliac vessel injury: Operative physiology related to outcome. J Trauma 1997;42:1033-40.  Back to cited text no. 3
4.Davis JW, Kaups KL. Base deficit in the elderly: A marker of severe injury and death. J Trauma 1998;45:873-7.  Back to cited text no. 4
5.Abramson D, Scalea TM, Hitchcock R, Trooskin SZ, Henry SM, Greenspan J. Lactate clearance and survival following injury. J Trauma 1993;35:584-8.  Back to cited text no. 5
6.Moore EE, Burch JM, Franciose RJ, Offner PJ, Biffl WL. Staged physiologic restoration and damage control surgery. World J Surg 1998;22:1184-90.  Back to cited text no. 6
7.Johnson JW, Gracias VH, Schwab CW, Reilly PM, Kauder DR, Shapiro MB, et al. Evolution in damage control for exsanguinating penetrating abdominal injury. J Trauma 2001;51:261-9.  Back to cited text no. 7
8.Wall MJ Jr, Soltero E. Damage control for thoracic injuries. Surg Clin North Am 1997;77:863-78.  Back to cited text no. 8
9.Nicholas JM, Rix EP, Easley KA, Feliciano DV, Cava RA, Ingram WL, et al. Changing patterns in the management of penetrating abdominal trauma: The more things change, the more they stay the same. J Trauma 2003;55:1095-108.  Back to cited text no. 9
10.Pape HC, Hildebrand F, Pertschy S, Zelle B, Garapati R, Grimme K, et al. Changes in the management of femoral shaft fractures in polytrauma patients: From early total care to damage control orthopedic surgery. J Trauma 2002;53:452-61.  Back to cited text no. 10
11.Scalea TM, Boswell SA, Scott JD, Mitchell KA, Kramer ME, Pollak AN. External fixation as a bridge to intramedullary nailing for patients with multiple injuries and with femur fractures: Damage control orthopedics. J Trauma 2000;48:613-21.  Back to cited text no. 11
12.Brohi K, Singh J, Heron M, Coats T. Acute traumatic coagulopathy. J Trauma 2003;54:1127-1130.  Back to cited text no. 12
13.MacLeod JB, Lynn M, McKenney MG, Cohn SM, Murtha M. Early coagulopathy predicts mortality in trauma. J Trauma 2003;55:39-44.  Back to cited text no. 13
14.Maegele M. Frequency, risk stratification and therapeutic management of acute post-traumatic coagulopathy. Vox Sang 2009;97:39-49.  Back to cited text no. 14
15.Maegele M, Lefering R, Yucel N, Tjardes T, Rixen D, Paffrath T, et al. Early coagulopathy in multiple injury: An analysis from the german trauma registry on 8724 patients. Injury 2007;38:298-304.  Back to cited text no. 15
16.Niles SE, McLaughlin DF, Perkins JG, Wade CE, Li Y, Spinella PC, et al. Increased mortality associated with the early coagulopathy of trauma in combat casualties. J Trauma 2008;64:1459-63.  Back to cited text no. 16
17.Talving P, Benfield R, Hadjizacharia P, Inaba K, Chan LS, Demetriades D. Coagulopathy in severe traumatic brain injury: A prospective study. J Trauma 2009;66:55-61.  Back to cited text no. 17
18.Brohi K, Cohen MJ, Ganter MT, Matthay MA, Mackersie RC, Pittet JF. Acute traumatic coagulopathy: Initiated by hypoperfusion: Modulated through the protein C pathway? Ann Surg 2007;245:812-8.  Back to cited text no. 18
19.Mitra B, Cameron PA, Mori A, Fitzgerald M. Acute coagulopathy and early deaths post major trauma. Injury 2010 [In press].  Back to cited text no. 19
20.Stein SC, Smith DH. Coagulopathy in traumatic brain injury. Neurocrit Care 2004;1:479-88.  Back to cited text no. 20
21.Halpern CH, Reilly PM, Turtz AR, Stein SC. Traumatic coagulopathy: The effect of brain injury. J Neurotrauma 2008;25:997-1001.  Back to cited text no. 21
22.Harhangi BS, Kompanje EJ, Leebeek FW, Maas AI. Coagulation disorders after traumatic brain injury. Acta Neurochir (Wien) 2008;150:165-75.  Back to cited text no. 22
23.Kuo JR, Chou TJ, Chio CC. Coagulopathy as a parameter to predict the outcome in head injury patients - Analysis of 61 cases. J Clin Neurosci 2004;11:710-4.  Back to cited text no. 23
24.Olson JD, Kaufman HH, Moake J, O'Gorman TW, Hoots K, Wagner K. The incidence and significance of hemostatic abnormalities in patients with head injuries. Neurosurgery 1989;24:825-32.  Back to cited text no. 24
25.Callaway DW, Shapiro NI, Donnino MW, Baker C, Rosen CL. Serum lactate and base deficit as predictors of mortality in normotensive elderly blunt trauma patients. J Trauma 2009;66:1040-4.  Back to cited text no. 25
26.Cerovic O, Golubovic V, Spec-Marn A, Kremzar B, Vidmar G. Relationship between injury severity and lactate levels in severely injured patients. Intensive Care Med 2003;29:1300-5.  Back to cited text no. 26
27.Davis JW, Parks SN, Kaups KL, Gladen HE, O'Donnell-Nicol S. Admission base deficit predicts transfusion requirements and risk of complications. J Trauma 1996;41:769-74.  Back to cited text no. 27
28.Husain FA, Martin MJ, Mullenix PS, Steele SR, Elliott DC. Serum lactate and base deficit as predictors of mortality and morbidity. Am J Surg 2003;185:485-91.  Back to cited text no. 28
29.Kaplan LJ, Kellum JA. Initial pH, base deficit, lactate, anion gap, strong ion difference, and strong ion gap predict outcome from major vascular injury. Crit Care Med 2004;32:1120-4.  Back to cited text no. 29
30.Manikis P, Jankowski S, Zhang H, Kahn RJ, Vincent JL. Correlation of serial blood lactate levels to organ failure and mortality after trauma. Am J Emerg Med 1995;13:619-22.  Back to cited text no. 30
31.Martin MJ, FitzSullivan E, Salim A, Brown CV, Demetriades D, Long W. Discordance between lactate and base deficit in the surgical intensive care unit: Which one do you trust? Am J Surg 2006;191:625-30.  Back to cited text no. 31
32.McNelis J, Marini CP, Jurkiewicz A, Szomstein S, Simms HH, Ritter G, et al. Prolonged lactate clearance is associated with increased mortality in the surgical intensive care unit. Am J Surg 2001;182:481-5.  Back to cited text no. 32
33.Paladino L, Sinert R, Wallace D, Anderson T, Yadav K, Zehtabchi S. The utility of base deficit and arterial lactate in differentiating major from minor injury in trauma patients with normal vital signs. Resuscitation 2008;77:363-8.  Back to cited text no. 33
34.Rixen D, Raum M, Bouillon B, Neugebauer E. Base excess as prognostic indicator in patients with polytrauma. Anasthesiol Intensivmed Notfallmed Schmerzther 2002;37:347-9.  Back to cited text no. 34
35.Smith I, Kumar P, Molloy S, Rhodes A, Newman PJ, Grounds RM, et al. Base excess and lactate as prognostic indicators for patients admitted to intensive care. Intensive Care Med 2001;27:74-83.  Back to cited text no. 35
36.Jurkovich GJ, Greiser WB, Luterman A, Curreri PW. Hypothermia in trauma victims: An ominous predictor of survival. J Trauma 1987;27:1019-24.  Back to cited text no. 36
37.Shafi S, Elliott AC, Gentilello L. Is hypothermia simply a marker of shock and injury severity or an independent risk factor for mortality in trauma patients? Analysis of a large national trauma registry. J Trauma 2005;59:1081-5.  Back to cited text no. 37
38.Wang HE, Callaway CW, Peitzman AB, Tisherman SA. Admission hypothermia and outcome after major trauma. Crit Care Med 2005;33:1296-301.  Back to cited text no. 38
39.Arthurs Z, Cuadrado D, Beekley A, Grathwohl K, Perkins J, Rush R, et al. The impact of hypothermia on trauma care at the 31 st combat support hospital. Am J Surg 2006;191:610-4.  Back to cited text no. 39
40.Danzl DF, Pozos RS, Auerbach PS, Glazer S, Goetz W, Johnson E, et al. Multicenter hypothermia survey. Ann Emerg Med 1987;16:1042-55.  Back to cited text no. 40
41.Gentilello LM, Jurkovich GJ, Stark MS, Hassantash SA, O'Keefe GE. Is hypothermia in the victim of major trauma protective or harmful? A randomized, prospective study. Ann Surg 1997;226:439-47.  Back to cited text no. 41
42.Luna GK, Maier RV, Pavlin EG, Anardi D, Copass MK, Oreskovich MR. Incidence and effect of hypothermia in seriously injured patients. J Trauma 1987;27:1014-8.  Back to cited text no. 42
43.Martin RS, Kilgo PD, Miller PR, Hoth JJ, Meredith JW, Chang MC. Injury-associated hypothermia: An analysis of the 2004 national trauma data bank. Shock 2005;24:114-8.  Back to cited text no. 43
44.Steinemann S, Shackford SR, Davis JW. Implications of admission hypothermia in trauma patients. J Trauma 1990;30:200-2.  Back to cited text no. 44
45.Waibel BH, Schlitzkus LL, Newell MA, Durham CA, Sagraves SG, Rotondo MF. Impact of hypothermia (below 36 degrees C) in the rural trauma patient. J Am Coll Surg 2009;209:580-8.  Back to cited text no. 45
46.Inaba K, Teixeira PG, Rhee P, Brown C, Salim A, DuBose J, et al. Mortality impact of hypothermia after cavitary explorations in trauma. World J Surg 2009;33:864-9.  Back to cited text no. 46

Correspondence Address:
Thomas Lustenberger
Department of Surgery, Division of Trauma and Critical Care, Los Angeles County + University of Southern California Medical Center, Los Angeles, CA
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0974-2700.86627

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  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]

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