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 Table of Contents  
REVIEW ARTICLE
Year : 2015  |  Volume : 5  |  Issue : 3  |  Page : 131-136

Operability in polytrauma


Department of Orthopedics and Trauma Surgery, Ahmadu Bello University Teaching Hospital, Zaria, Kaduna State, Nigeria

Date of Web Publication19-Oct-2015

Correspondence Address:
Dr. Kenneth Ezenwa Amaefule
Department of Orthopedics and Trauma Surgery, Ahmadu Bello University Teaching Hospital, Zaria, Kaduna State
Nigeria
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2278-9596.167473

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  Abstract 

Trauma has been on the increase worldwide with significant morbidity and mortality, especially when it occurs in the form of polytrauma. The management of these patients has witnessed significant changes over the last decade with the better understanding of the pathophysiology of polytrauma and the recognition of the benefits of early fracture stabilization as part of the damage control orthopedics (DCO) surgical resuscitation of these patients. Inspite of these, the operability of the polytraumatized patients occasionally becomes contentious amongst the surgical trauma team. Available evidence, shows that the focus of polytrauma resuscitation in contemporary trauma surgical practice has now shifted to the operating room, to improve outcome in polytrauma management. An electronic search was done in the PubMed and EBSCO databases for relevant published articles on polytrauma. The terms "Polytrauma OR Multiple trauma" AND operability were entered. Only original articles on multiple trauma involving long bone(s) fractures and at least a thoracic injury not requiring intensive care treatment, or head injury with an initial Glasgow coma score ≥ 8 points or both, published in the last 2 decades were reviewed. In addition, the references from some of the retrieved articles were also reviewed to identify suitable articles.

Keywords: Damage control orthopedics, operability, polytrauma, surgical resuscitation


How to cite this article:
Amaefule KE, Lawal DI. Operability in polytrauma. Arch Int Surg 2015;5:131-6

How to cite this URL:
Amaefule KE, Lawal DI. Operability in polytrauma. Arch Int Surg [serial online] 2015 [cited 2024 Mar 29];5:131-6. Available from: https://www.archintsurg.org/text.asp?2015/5/3/131/167473


  Introduction Top


Trauma has been on the increase worldwide. This has been attributed to increase in urbanization, motorization, civil violence, wars, and criminal activities. [1] Major trauma, defined as trauma with Injury Severity Score (ISS) ≥ 16, [2] contribute significantly to overall morbidity, mortality, and long-term disabilities worldwide and usually occur in form of polytrauma (ISS > 18). Such trauma could be life-threatening and usually presents as an emergency requiring either early surgical intervention or intensive care or both.

The surgical world has over the past 2 decades been embroiled in the contentious issue of operability in polytrauma. That is, when can it be judged safe for a patient with polytrauma needing early surgical operation to successfully undergo such operation? The operability of such patients, no doubt, is mainly determined by the interaction between the magnitude of the operation and the pathophysiological derangements. A factor to be considered here is the benefit gained by performing the procedure early versus the consequences of not operating and vice versa, in the light of research evidences regarding the pathophysiology of trauma and the sequelae of early surgical interventions in such patients.

The concerns have largely been in the areas of pulmonary dysfunction, coagulopathy, fat embolism, and the systemic inflammatory response syndrome (SIRS). The patients in the midst of the controversy have been those with head injury, chest injury, and multiple long bone fractures. This has had significant impact on the management of the associated skeletal injuries and has led to the proposal of "damage control orthopedics" (DCO), a resuscitative interventional procedure, in the management of some of these patients. [3],[4],[5]

This controversy over the operability of some polytraumatized patients has often pitched the trauma surgeon, who sees himself as the chief caregiver in such instance (being the head of the trauma team), and hence the responsibility of deciding when to operate, against the anesthetist who often considers most surgeries, including some resuscitative interventional procedures in such patients as potentially hazardous, being the real "pilot of the surgical flight" (as the physiological well-being of the patient in the perioperative period rest largely on his shoulders). [6],[7]

Despite the available evidence-based information at our domain in recent years, this friction amongst the trauma team still continues in some of our trauma centers and often led to unnecessary postponement of some deserving early surgical procedures on account of inoperability, and this has had significant impact on the management of these patients.

This article, therefore aims to review the current knowledge of pathophysiological derangements in the polytraumatized patients and the possible sequelae and merits of early surgical interventions. We will then review, based on available evidences, the clinical predictors of adverse surgical outcome in such patients. This we hope will arouse the consciousness of care givers involved in the management of these patients, with regards to surgical timing, and avoid unnecessary postponement of some early surgeries that will impact positively on the management of the polytraumatized patients.


  Pathophysiology of Trauma Top


Trauma, even when localized, could spiral into a systemic disorder, affecting several body systems and organs. [8],[9]

Pulmonary dysfunction

Some level of pulmonary dysfunction could occur in the polytraumatized patients as a result of both direct and indirect mechanisms. One of the mechanisms is as a result of sequestration of activated neutrophils in the microvasculatures of the lungs and its effect on the endothelia cells with resultant increased capillary endothelia permeability and pulmonary interstitial edema which could lead to adult respiratory distress syndrome (ARDS) [10],[11],[12] in severely traumatized patients, especially with concomitant blunt chest trauma. Another mechanism is by lung contusion with resultant pulmonary edema in those with a concomitant chest trauma, which usually develops 2-3 days post-trauma. [13] A third mechanism the polytraumatized patient could develop pulmonary dysfunction is by fat embolism, in those with long bone fractures, [14],[15],[16] as some investigators have shown the presence of embolic fat globules in the circulation and lungs of a significant number of trauma patients with long bone and pelvic fractures. However, only a few of these patients develop clinical pulmonary symptoms. [14]

Fat embolism

As earlier stated, pulmonary fat embolism and fat embolism syndrome (FES) are uncommon complications of polytrauma with concomitant long-bone or unstable pelvic ring fractures. Gurd and Wilson showed that 67% of his trauma patients without any clinical evidence of FES had circulating fat globules. [14] While, Bulger et al., in a 10-year retrospective study at a level 1 trauma center, found a FES incidence of 0.9% among patients with long bone fractures. [15] In another 1 year prospective study of trauma patients with multiple femoral, tibia, and pelvic fractures; a FES incidence of 11% was found. [16] Indeed, the incidence rate is said to be higher in multiple long bone fractures or associated pelvic fracture than in patients with single long bone fracture.

Coagulopathy

Coagulopathy could occur in patients with major trauma. One way this could occur, is the release of tissue thromboplastin from injured tissue into the circulation with the resultant activation of the extrinsic coagulation pathway with consumption of platelets and clotting factors, commoner in concomitant head injured patients. [17],[18],[19],[20] Another pathway acute traumatic coagulopathy could occur, is via the protein C pathway in the presence of shock and tissue hypoperfusion. Tissue hypoperfusion, with resultant base-deficit is said to lead to increased thrombomodulin level with increased thrombin generation, producing a decrease in protein C concentration with anticoagulation. [21] A third way coagulopathy could result is by hemodilution in patients with multiple long bone and/or pelvic fractures with severe blood loss who have been resuscitated with large volume of intravenous fluid. [22] In general, six key initiators of trauma-induced coagulopathy, namely: Tissue trauma, shock, hemodilution, hypothermia, acidemia, and inflammation have been described. [17],[18],[19],[20],[21]

Systemic inflammatory response

Trauma initiates a local inflammatory response which involves cell signaling, cell migration, and the release of proinflammatory cytokines which may spill into the systemic circulation; the concentration of which correlates with the degree of tissue damage. [23],[24],[25],[26],[27],[28],[29] There is increased formation of activated neutrophils which release oxygen free radicals and proteases resulting in microvascular damage which contributes to increased capillary permeability leading to interstitial edema. [12],[26],[27],[28] This has been linked to the development of ARDS and multiple organ dysfunction syndrome (MODS).

Platelets are activated by several factors including exposed collagen. Activated platelets release mediators that serve as chemoattractant for neutrophils and monocytes. [26] Macrophages and monocytes are activated by products of tissue damage. Activated macrophages and monocytes produce cytokines, notable of which are interleukin-6 (IL-6), IL-1, and tumor necrosis factor (TNF). The blood level of IL-6 rises within an hour of trauma, and remains high between days 2 and 4 after trauma. IL-6 level remain elevated for more than 5 days in patients with a high ISS. [8],[26],[29],[30] It stimulates synthesis of B- and T-lymphocytes and acute phase proteins and also activates neutrophils which release proteases and reactive oxygen radicals which could cause tissue damage. The blood level of IL-6 correlate with severity of the trauma and its quantitative assay is being used as a major laboratory maker to determine when the immunomodulatory response of the polytrauma patient is safe for early surgical intervention. [29]

The pathophysiological derangements in a major trauma show a phasic course with respect to the immunomodulatory response. A surgical intervention is said to inflict a secondary trauma, and thus an additional burden (the second hit phenomenon). [31],[32] Depending on the inflammatory phase during which this second hit is inflicted, there may be a disturbance of homeostasis that could even lead to multiple organ failure. The chances of this happening, depends on the time and magnitude of the surgical operation.


  Associated High Risk Injuries Top


Certain injury patterns appear to be associated with higher morbidity and mortality rates following surgical intervention on the polytrauma patient.

Severe head injury

Severe head injury is said to have some impact on the overall host immune response. Research has demonstrated the ability of the central nervous system (CNS) to affect diverse systemic inflammatory response mechanisms. Neurohormonal signaling via binding of glucocorticoid, catecholamines, or adrenergic agonists to the corresponding receptors on immune cells is said to suppress cytokine production, and thus impair a competent immune regulatory cell-cell interaction. [33],[34],[35]

Chest Injury

The presence of clinically significant chest injuries, Abbreviated Injury Scale (AIS thorax ≥3) as an independent risk factor for surgical intervention associated complication in a polytrauma patient has been extensively studied, with contradicting results. O'Brien showed in his study that pulmonary function in polytrauma patients depends primarily on the initial lung injury sustained. [36] This was also the finding of Reynolds et al. [37] Parenchymal injury is more important for lung function than osseous injury. The challenge remains how best to determine early at the time of admission the severity of lung contusion of a patient with associated chest injury, as the resultant pulmonary edema usually develop 2-3 days post injury and the commonly done plain chest X-ray on admission is likely to underestimate the true severity.

The arterial blood gases estimation may also not be very useful in the early period of admission as it will also depend on a normal lung parenchyma, and hence will not be a useful early predictor of the development of pulmonary complications following thoracic injuries.

Multiple longbone fractures

Multiple long bone fracture is considered a risk factor for surgical intervention associated complication in the polytrauma patients. This is due to some factors such as the high incidence of pulmonary fat embolism which can occur post-trauma before surgical stabilization [14],[15],[16] or during reaming for intramedullary nailing of such fractures, especially femoral fractures. Another important factor is the higher incidence of coagulopathy either as a result of disseminated intravascular coagulation triggered by tissue thromboplastin via the extrinsic coagulation pathway or via the protein C pathway or dilutional in the course of resuscitation as previously stated. [17] A third factor for the high surgical intervention associated complications in these patients is the possibility of persistent hemodynamic instability on admission due to excessive hemorrhage with inadequate resuscitation.


  Merits and Demerits of Early Surgical Interventions Top


Orthopedic trauma patients have been classified into four categories of patients according to the severity of their injuries and their physiological state [Figure 1]. [3] A review of the literature, shows no disagreement on the operability of the stable patients in the early post-trauma period. The disagreement that existed previously, was regarding unstable, in extremis, and some "borderline" [Table 1] [3] patients; who are the patients damage control surgeries are now designed for. The role of DCO surgeries as part of the resuscitation of these patients has been extensively studied. [3],[38],[39]
Figure 1: Classification of polytrauma patients and their treatment algorithm. ICU = Intensive care unit, EX. FIX = External fixation, OR = Operating room, ABG = Arterial blood gases, IL = Interleukin, DCO = Damage control orthopedics, ETC = Early total care (Adapted from Pape et al.)

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Table 1: Clinical and Laboratory parameters used to define the "Borderline" patients


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Early surgical procedures in the polytraumatized patient could be for either of two reasons. It could be as part of resuscitative interventional measures (damage control surgery) or as a definitive procedure for such injuries which will also aid nursing care and the early physiological recovery of the injured part, which will ultimately translate to a better outcome in the stable patients.

As a damage control procedure, the aim is to do the minimum that will cause less additional trauma within a possible short time to stabilize and keep alive severely injured patients who otherwise will suffer a severe life-threatening complication. [40] A good example of this is the early skeletal stabilization usually with external fixators in the high risk class of polytrauma patients as proposed by Scalea et al., [5] and Pape et al., [3] [Figure 1]. One study showed that a delay of more than 24h in the stabilization of a major femoral fracture was associated with a fivefold increase in the incidence of ARDS and that the beneficial effect of early fracture stabilization became even more evident with increasing injuring severity. [41]

Though, some authors have reported neurological deterioration following early fixation of the associated long bone fractures in patients with significant primary brain injury and concluded in favor of delayed fracture fixation. [42],[43] It can be observed, however that the authors did not use the damage control protocol. Such conclusion could not be proved by the Eastern Association for the Surgery of Trauma (EAST) Practice Management Guidelines Work Group, in their review of published literature on the subject. [44] The EAST Work Group, revealed that there was no evidence that early long bone stabilization either enhances or worsens the outcome in patients with mild, moderate, or severe head injury.

Several studies have shown that early fracture fixation is not deleterious to the brain injured patient. [45],[46],[47],[48] One of such studies in Mississippi showed that a delay in fracture fixation did not protect the injured brain; the risk of CNS events being determined by the severity of the head injury. With regards to pulmonary complications in these high risk head injured patients, the same study showed that the risk of pulmonary complication was strongly influenced by the severity of injuries to the head and the chest, rather than the timing of the operations. [45] Early fracture fixation in patients with head injury, makes for easier patient care. Major head injured patients, no doubt, are very susceptible to the effects of hypotension, hypoxia, and raised intracranial pressure; which commonly occur following surgery and can compound the initial brain injury, but with close monitoring and proactive measures, such deleterious effect can be avoided.

Other benefits of early fracture fixation, include pain relief, early mobilization, reduced incidence of thromboembolism, prevents pressure sores, muscle wasting, and joint stiffness as well as operating on a patient in his optimum nutritional and immunologic state, [41],[49] as there are pronounce immunologic changes from day 2 to 4 post-trauma. Lastly, the benefit of operating on a patient who has not been colonized by resistant hospital organisms cannot be over emphasized.

While acknowledging the benefits of early surgical procedures in most of these patients, it has been shown that prolonged early surgical procedures lasting more than 6h are deleterious to most of those patients.


  Predictors of Adverse Surgical Outcome Top


Certain injury "personalities" and surgical interventions have been shown to have high perioperative mortality, and thus are of high surgical risk. The clinical difficulty in judging preoperatively which patients could suffer major postoperative complications, has led the Hanover trauma team to come up with some clinical indicators, from the German trauma registry, which should guide our decisions. This is probably the most popular [Table 2]. [50]
Table 2: Clinical parameters associated with adverse outcome in polytraumatized patients as reported in Hanover, Germany


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  Conclusion Top


With advances in emergency room resuscitation and supportive intensive care facilities, some deaths of polytraumatized patients who make it to the hospital, have been linked to delay in intervening surgically, as part of the resuscitative measures. The focus of polytrauma resuscitation in contemporary trauma surgical practice has therefore shifted to the operating room, and the best chance of salvage of these patients may well depend on the timing of the operating room interventions.[55]

 
  References Top

1.
Museru LM, Leshabari MT. Road traffic accidents in Tanzania. A 10-year epidemiological Appraisal. East Central African J Surg 2002;7:23-6.  Back to cited text no. 1
    
2.
Champion HR, Copes WS, Sacco WJ, Lawnick MM, Keast SL, Bain LW Jr, et al. The major trauma outcome study: Establishing national norms for trauma care. J Trauma 1990;30:1356-65.  Back to cited text no. 2
    
3.
Pape HC, Hilderbrand 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. 3
    
4.
Paper HC, Gianoudis P, Krettek C. The timing of fracture treatment in polytrauma patients: Relevance of damage control orthopedic surgery. Am J Surg 2002;183:622-9.  Back to cited text no. 4
    
5.
Scalea TM, Boswell SA, Scott JD, Mitchell KA, Kramer ME, Pollack AN. External fixation as a bridge to intramedullary nailing for patients with multiple injuries and with femur fractures: Damage control orthopaedics. J Trauma 2000;48:613-21.  Back to cited text no. 5
    
6.
Sarcevic A, Marsic I, Waterhouse LJ, Stockwell DC, Burd RS. Leadership structures in emergency care settings: A study of two trauma centers. Int J Med Inform 2011;80:227-38.  Back to cited text no. 6
    
7.
Courtney M, Nancarrow S, Dawson D. Interprofessional teamwork in trauma setting: A scoping review. Hum Resour Health 2013;11:57-5.  Back to cited text no. 7
    
8.
Pape HC, Schmidt RE, Rice J, Van Griensven M, das Gupta R, Krettek C, et al. Biochemical changes after trauma and Skeletal Surgery of the lower extremity: Quantification of the operative burden. Crit Care Med 2000;28:3441-8.  Back to cited text no. 8
    
9.
Hauser CJ, Zhou X, Joshi P, Cuchens MA, Kregor P, Devidas M, et al. The immune microenvironment of human fracture/soft-tissue haematomas and its relationship to systemic immunity. J Trauma 1997;42:895-903.  Back to cited text no. 9
    
10.
Patterson CE, Lum H. Update on pulmonary edema: The role and regulation of endothelial barrier function. Endothelium 2001;8:72-105.  Back to cited text no. 10
    
11.
Sturm JA, Wisner DH, Oestern HJ, Kant CJ, Tscherne H, Creutzig H. Increased lung capillary permeability after trauma: A prospective clinical study. J Trauma 1986;26;409-18.  Back to cited text no. 11
    
12.
McIntyre TM, Modur V, Prescott SM, Zimmermann GA. Molecular mechanisms of early inflammation. Thromb Heamost 1997;78:302-5.  Back to cited text no. 12
    
13.
Pinilla JC. Acute respiratory failure in severe blunt chest trauma. J Trauma 1982;22:221-6.  Back to cited text no. 13
[PUBMED]    
14.
Gurd AR, Wilson RI. The fat embolism syndrome. Br J Bone Joint Surg 1974;56:408-16.  Back to cited text no. 14
    
15.
Bulger EM, Smith DG, Majer RV, Jurkovich GJ. Fat embolism syndrome. A 10-year review. Arch Surg 1997;132:435-9.  Back to cited text no. 15
    
16.
Fabian TC, Hoots AV, Starnford DS, Patterson CR, Mangiante EC. Fat embolism syndrome: Prospective evaluations in 92 fracture patients. Crit Care Med 1990;18:42-6.  Back to cited text no. 16
    
17.
Brohi K, Singh J, Heron M, Coats T. Acute traumatic coagulopathy. J Trauma 2003;54:1127-30.  Back to cited text no. 17
    
18.
Cortiana M, Zagara G, Fava S, Seveso M. Coagulation abnormalities in patients with head injury. J Neurosurg Sci 1986;30:133-8.  Back to cited text no. 18
[PUBMED]    
19.
Hulka F, Mullins RJ, Frank EH. Blunt brain injury activates the coagulation process. Arch Surg 1996;131:923-7.  Back to cited text no. 19
    
20.
Preston FE, Malia RG, Sworn MJ, Timperley WR, Backburn EK. Disseminated intravascular coagulation as a consequence of cerebral damage. J Neurol Neurosurg Psychiatry 1974;37:241-8.  Back to cited text no. 20
    
21.
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. 21
    
22.
Shaz BH, Winkler AM, James AB, Hillyer CD, Macleod JB. Pathophysiology of early trauma induced coagulopathy: Emerging evidence for haemodilution and coagulation factor depletion. J Trauma 2011;70:1401-7.  Back to cited text no. 22
    
23.
Foex BA. Systemic responses to trauma. Br Med Bull 1999;55:726-43.  Back to cited text no. 23
    
24.
Giannoudis PV. Current concepts of the inflammatory response after major trauma: An update. Injury 2003;34:397-404.  Back to cited text no. 24
    
25.
Giannoudis PV, Smith RM, Banks RE, Windsor AC, Dickson RA, Guillou PJ, et al. Stimulation of inflammatory markers after blunt trauma. Br J Surg 1998;85:986-90.  Back to cited text no. 25
    
26.
Keel M, Trentz O. Pathophysiology of polytrauma. Injury 2005;36:691-709.  Back to cited text no. 26
    
27.
Cipolle MD, Pasquale MD, Cerra FB. Secondary Organ dysfunction. From clinical perspective to molecular mediator. Crit Care Clin 1993;9:261-98.  Back to cited text no. 27
    
28.
Anderson BO, Harken AH. Multiple Organ failures: Inflammatory priming and activation sequences promote autologous tissue injury. J Trauma 1990;30:S44-9.  Back to cited text no. 28
    
29.
Pape HC, Van Griensven M, Rice J, Ganssien A, Hilderbrand F, Zech S, et al. Major Secondary Surgery in blunt trauma patients and the perioperative cytokine liberation: Determination of the relevance of biochemical markers. J Trauma 2001;50:989-1000.  Back to cited text no. 29
    
30.
Gebhard F, Pfetsch H, Steinbach G, Strecker W, Kinzi L, Bruckner UB. Is interleukin-6 an early marker of injury severity following major trauma in humans? Arch Surg 2000;135:291-5.  Back to cited text no. 30
    
31.
Waydhas C, Nast-Kolb D, Trupka A, Zettle R, Kick M, Wiesholler J, et al. Posttraumatic inflammatory response, secondary operations, and late multiple organs failure. J Trauma 1996;40:624-31.  Back to cited text no. 31
    
32.
Giannoudis PV, Smith RM, Bellamy MC, Morrison JF, Dickson RA, Guillou PJ. Stimulation of the inflammatory system by reamed and unreamed nailing of femoral fractures. An analysis of second hit. J Bone Joint Surg Br 1999;81:356-61.  Back to cited text no. 32
    
33.
Celada A, Nathan C. Macrophage activation revisited. Immunol Today 1994;15:100-02.  Back to cited text no. 33
    
34.
Madden KS, Sanders VM, Felten DL. Catecholamine influences and sympathetic neural modulation of immune responsiveness. Annu Rev Pharmacol Toxicol 1995;35:417-48.  Back to cited text no. 34
    
35.
Pavlov VA, Wang H, Czura CJ, Friedman SG, Tracey KJ. The cholinergic anti-inflammatory pathway: A missing link in neuroimmunomodulation. Mol Med 2003;9:125-34.  Back to cited text no. 35
    
36.
O′Brien PJ. Fracture fixation in patients having multiple injuries. Can J Surg 2003;46:124-8.  Back to cited text no. 36
    
37.
Reynolds MA, Richardson JD, Spain DA, Seligson D, Wilson MA, Miller FB. Is the timing of fracture fixation important for the patient with multiple trauma? Ann Surg 1995;222:470-8.  Back to cited text no. 37
    
38.
Pape HC, Rixen D, Morley J, Husebye EE, Mueller M, Dumont C, et al; EPOFF Study Group. Impact of the method of initial stabilization of femoral shaft fractures in patients with multiple injuries at risk for complications (borderline patients). Ann Surg 2007;246:491-9.  Back to cited text no. 38
    
39.
Olson SA. Pulmonary aspect of treatment of long bone fractures in the ploytrauma patients. Clin Orthop Relat Res 2004;422:66-70.  Back to cited text no. 39
    
40.
Giannoudis PV. Surgical priorities in damage control in polytrauma. J Bone Joint Surg Br 2003;85:478-83.  Back to cited text no. 40
    
41.
Johnson KD, Cadambi A, Seibert GB. Incidence of adult respiratory distress syndrome in patients with multiple musculo-skeletal injuries. Effect of early operative stabilization of fractures. J Trauma 1985;25:375-84.  Back to cited text no. 41
[PUBMED]    
42.
Jaicks RR, Colin SM, Mollar BA. Early fracture fixation may be deleterious after head injury. J Trauma 1997;42:1-5.  Back to cited text no. 42
    
43.
Bhandari M, Guyatt GH, Khera V, Kulkami AV, Sprague S, Schemitsch EH. Operative management of lower extremity fractures in patients with head injuries. Clin Orthop Relat Res 2003;407:187-98.  Back to cited text no. 43
    
44.
Dunham CM, Bosse MJ, Clancy TV, Cole FJ Jr, Coles MJ, Knuth T, et al.; EAST Practice Management Guidelines Work Group. Practice guidelines for the optimal timing of longbone fracture Stabilization in Polytrauma Patient: The EAST Practice Management Guidelines work group. J Trauma 2001;50:958-67.  Back to cited text no. 44
    
45.
Poole GV, Miller JD, Agnew SG, Griswold JA. Lower extremely fracture fixation in head injured patients. J Trauma 1992;32:654-9.  Back to cited text no. 45
    
46.
Hofman PA, Goris RJ. Timing of osteosynthesis of major fractures in patients with severe brain injury. J Trauma 1991;31:261-3.  Back to cited text no. 46
    
47.
Smith J, Cunningham T. Timing of femur fracture fixation in patients with head injury. J OrthopTrauma 2000;14:125-33.  Back to cited text no. 47
    
48.
Brundage SI, McGhan R, Jurkovich GJ, Mack CD, Maier RV. Timing of femoral fracture fixation: Effects on the outcome in patients with thoracic and head injuries. J Trauma 2002;52:299-307.  Back to cited text no. 48
    
49.
Riska EB, von Bonsdoff H, HakkinenS, Jaroma H, Kiviluoto O, Paavilainen T. Primary operative fixation of long bone fractures in patients with multiple injuries. J Trauma 1977; 17:111-21.  Back to cited text no. 49
    
50.
Pape HC, Remmers D, Rice J, Ebisch M, Krettek C, Tscherne H. Appraisal of early evaluation of blunt chest trauma: Development of a standardized scoring system for initial clinical decision-making. J Trauma 2000;49:496-504.  Back to cited text no. 50
    
51.
Johnson EE, Simpson LA, Helfet DL. Delayed intramedullary nailing after failed external fixation of the tibia. Clin Orthop Relat Res 1990:251-7.  Back to cited text no. 51
    
52.
Cruickshank AM, Fraser WD, Burns HJ, Van Damme J, Shenkin A. Response of serum interleukin-6 in patients undergoing elective surgery of varying severity. Clin Sci 1990;79:161-5.  Back to cited text no. 52
    
53.
Roumen R, HendrijksT, vender Ven-Jongekrijk, Nieuwenhuijzen GA, Sauerwein RW, van der Meer JW, et al. Cytokine patterns in patients after major vascular surgery, haemorragic shock and severe blunt trauma. Ann Surg 1995;218:769-76.  Back to cited text no. 53
    
54.
Roumen R, Redl H, Schlag G, Zilow G, Sandtner W, Koller W, et al. Inflammatory mediators in relation to the development of multiple organ failure in patients after severe blunt trauma. Crit Care Med 1995;23:474-80.  Back to cited text no. 54
    
55.
Pape HC, Remmers D, Grotz M, Kotzerke J, von Glinski S, van Griensven M, et al. Reticulo-endothelial system activity and organ failure in multiply injured patients. Arch Surg 1999;134:421-7.  Back to cited text no. 55
    


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