Damage control in severely injured trauma patients – A

advertisement
Damage control in severely injured trauma patients – A ten-year experiencehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214499/?report=printable
1 von 12
J Emerg Trauma Shock. 2011 Oct-Dec; 4(4): 450–454.
PMCID: PMC3214499
doi: 10.4103/0974-2700.86627
Damage control in severely injured trauma patients – A ten-year experience
Andreas Frischknecht, Thomas Lustenberger,1 Marko Bukur,1 Matthias Turina, Adrian Billeter, Ladislav Mica, and
Marius Keel2
Department of Surgery, Hospital Uster, Switzerland
1Department of Surgery, Division of Trauma and Critical Care, Los Angeles County + University of Southern California Medical Center, Los
Angeles, CA
2Department of Surgery, Division of Trauma Surgery, University Hospital Zurich, Switzerland
Address for correspondence: Dr. Thomas Lustenberger, E-mail: tom.lustenberg@gmail.com
Received August 9, 2010; Accepted March 5, 2011.
Copyright : © Journal of Emergencies, Trauma, and Shock
This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
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
INTRODUCTION
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
25.06.2012 14:16
Damage control in severely injured trauma patients – A ten-year experiencehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214499/?report=printable
2 von 12
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.[2–6] 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
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 R2 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
During 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
25.06.2012 14:16
Damage control in severely injured trauma patients – A ten-year experiencehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214499/?report=printable
3 von 12
(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.
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.
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 (R2=0.453) [Table 4].
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 (R2=0.373) [Table 5].
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
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.[7–11] 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.[12–19] In the study by
25.06.2012 14:16
Damage control in severely injured trauma patients – A ten-year experiencehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214499/?report=printable
4 von 12
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.[17,20–24]
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.[4,5,25–35] 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.[36–45] 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
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%.
Footnotes
25.06.2012 14:16
Damage control in severely injured trauma patients – A ten-year experiencehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214499/?report=printable
5 von 12
Source of Support: Nil.
Conflict of Interest: None declared.
REFERENCES
1. Wyrzykowski AD, Feliciano DV. Trauma damage control. In: Feliciano DV, Mattox KL, Moore EE,
editors. Trauma. 6th ed. New York Chicago San Francisco: McGraw-Hill Companies; 2008. pp.
851–70.
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.
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. [PubMed: 9210537]
4. Davis JW, Kaups KL. Base deficit in the elderly: A marker of severe injury and death. J Trauma.
1998;45:873–7. [PubMed: 9820695]
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. [PubMed: 8411283]
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. [PubMed: 9841741]
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.
[PubMed: 11493783]
8. Wall MJ, Jr, Soltero E. Damage control for thoracic injuries. Surg Clin North Am. 1997;77:863–78.
[PubMed: 9291987]
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. [PubMed: 14676657]
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. [PubMed: 12352480]
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. [PubMed: 10780592]
12. Brohi K, Singh J, Heron M, Coats T. Acute traumatic coagulopathy. J Trauma. 2003;54:1127–1130.
[PubMed: 12813333]
13. MacLeod JB, Lynn M, McKenney MG, Cohn SM, Murtha M. Early coagulopathy predicts mortality
in trauma. J Trauma. 2003;55:39–44. [PubMed: 12855879]
14. Maegele M. Frequency, risk stratification and therapeutic management of acute post-traumatic
coagulopathy. Vox Sang. 2009;97:39–49. [PubMed: 19392782]
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. [PubMed: 17214989]
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.
[PubMed: 18545109]
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. [PubMed: 19131806]
25.06.2012 14:16
Damage control in severely injured trauma patients – A ten-year experiencehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214499/?report=printable
6 von 12
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. [PMCID: PMC1877079] [PubMed: 17457176]
19. Mitra B, Cameron PA, Mori A, Fitzgerald M. Acute coagulopathy and early deaths post major
trauma. Injury. 2010 [In press]
20. Stein SC, Smith DH. Coagulopathy in traumatic brain injury. Neurocrit Care. 2004;1:479–88.
[PubMed: 16174954]
21. Halpern CH, Reilly PM, Turtz AR, Stein SC. Traumatic coagulopathy: The effect of brain injury. J
Neurotrauma. 2008;25:997–1001. [PubMed: 18687038]
22. Harhangi BS, Kompanje EJ, Leebeek FW, Maas AI. Coagulation disorders after traumatic brain
injury. Acta Neurochir (Wien) 2008;150:165–75. [PubMed: 18166989]
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. [PubMed: 15337130]
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. [PubMed: 2747858]
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.
[PubMed: 19359912]
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.
[PubMed: 12904861]
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. [PubMed: 8913202]
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. [PubMed: 12727572]
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.
[PubMed: 15190960]
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. [PubMed: 7575797]
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. [PubMed: 16647349]
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. [PubMed: 11754855]
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. [PubMed: 18367305]
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. [PubMed: 12063590]
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.
[PubMed: 11280677]
25.06.2012 14:16
Damage control in severely injured trauma patients – A ten-year experiencehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214499/?report=printable
7 von 12
36. Jurkovich GJ, Greiser WB, Luterman A, Curreri PW. Hypothermia in trauma victims: An ominous
predictor of survival. J Trauma. 1987;27:1019–24. [PubMed: 3656464]
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. [PubMed: 16385283]
38. Wang HE, Callaway CW, Peitzman AB, Tisherman SA. Admission hypothermia and outcome after
major trauma. Crit Care Med. 2005;33:1296–301. [PubMed: 15942347]
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.
[PubMed: 16647346]
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. [PubMed: 3631669]
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.
[PMCID: PMC1191057] [PubMed: 9351712]
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. [PubMed: 3656463]
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.
[PubMed: 16044080]
44. Steinemann S, Shackford SR, Davis JW. Implications of admission hypothermia in trauma
patients. J Trauma. 1990;30:200–2. [PubMed: 2304115]
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.
[PubMed: 19854397]
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. [PubMed: 19219493]
Figures and Tables
25.06.2012 14:16
Damage control in severely injured trauma patients – A ten-year experiencehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214499/?report=printable
8 von 12
Table 1
Comparison of clinical and demographic characteristics of early survivors and early deaths
25.06.2012 14:16
Damage control in severely injured trauma patients – A ten-year experiencehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214499/?report=printable
9 von 12
Table 2
Damage control procedures performed in 319 patients
25.06.2012 14:16
Damage control in severely injured trauma patients – A ten-year experiencehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214499/?report=printable
10 von 12
Table 3
Comparison of laboratory parameters in early survivors and early deaths
25.06.2012 14:16
Damage control in severely injured trauma patients – A ten-year experiencehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214499/?report=printable
11 von 12
Table 4
Independent risk factors at hospital admission for early mortality in patients undergoing damage
control management
25.06.2012 14:16
Damage control in severely injured trauma patients – A ten-year experiencehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214499/?report=printable
12 von 12
Table 5
Independent risk factors at ICU admission for early mortality in patients undergoing damage control
management
Articles from Journal of Emergencies, Trauma, and Shock are provided here courtesy of Medknow Publications
25.06.2012 14:16
Download