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 Table of Contents  
Year : 2013  |  Volume : 6  |  Issue : 1  |  Page : 23-27

Damage control in orthopaedic patients

Department of Orthopaedics, All India Institute of Medical Sciences, Raipur, Chhattisgarh, India

Date of Web Publication23-Sep-2013

Correspondence Address:
Alok Chandra Agrawal
Department of Orthopaedics, All India Institute of Medical Sciences, Raipur - 492 099, Chhattisgarh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0975-7341.118742

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It has been found that many orthopaedic patients who have sustained multiple injuries benefit from the early total care of major bone fractures. However, early surgery has been found to be harmful to some multiply injured patients. Damage control orthopaedics is an approach that contains and stabilizes orthopaedic injuries so that the patient's overall physiology can improve. Its purpose is to avoid worsening of the patient's condition by the "second hit" of a major orthopaedic procedure and to delay definitive fracture repair until a time when the overall condition of the patient is optimized. The article deals with principles involve in damage control orthopaedics pertaining to diagnosis and management.

Keywords: Damage control, orthopaedics, polytrauma

How to cite this article:
Agrawal AC, Kalia RB. Damage control in orthopaedic patients. J Orthop Traumatol Rehabil 2013;6:23-7

How to cite this URL:
Agrawal AC, Kalia RB. Damage control in orthopaedic patients. J Orthop Traumatol Rehabil [serial online] 2013 [cited 2023 Mar 27];6:23-7. Available from: https://www.jotr.in/text.asp?2013/6/1/23/118742

  Introduction Top

Damage control in orthopedics is an approach based on the principle of limiting and minimizing the invasiveness of the operative procedure so that the procedure induced inflammatory response second hit is not detrimental to the patient. Many orthopedic patients with multiple injuries benefit from early total care (ETC) of major bone fractures. However, the strategy is not the best option and indeed might be harmful, for some multiply injured patients. Damage control focuses on control of hemorrhage, management of soft-tissue injury and achievement of provisional fracture stability may be by external fixation while avoiding additional insult to patient. [1],[2],[3],[4]

The physiological basis of damage control orthopedics (DCO) is that traumatic injury leads to systemic inflammation (systemic inflammatory response [SIR] syndrome) followed by a period of recovery mediated by a counter-regulatory anti-inflammatory response (AIR) [Figure 1]. Severe inflammation may lead to acute organ failure and early death after an injury [Figure 2]. A lesser inflammatory response followed by an excessive compensatory AIR syndrome may induce a prolonged immune-suppressed state that can be deleterious to the host. This conceptual framework may explain why multiple organ dysfunction syndrome (MODS) develops early after trauma in some patients and much later in others. [5],[6],[7],[8]
Figure 1: Schematic diagram showing that after trauma, there is a balance between the systemic inflammatory response and the counter regulatory anti-inflammatory response. SIR = Systemic inflammatory response, AIR = Anti-inflammatory response

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Figure 2: the two-hit theory is shown schematically. The first hit is the initial traumatic event and the second hit is the definitive orthopedic procedure, usually femoral nailing. MODS = Multiple organ dysfunction syndrome, ARDS = Adult respiratory distress syndrome

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Within this inflammatory process, there is a fine balance between the beneficial effects of inflammation and the potential for the process to cause and aggravate tissue injury leading to adult respiratory distress syndrome (ARDS) and MODS [Figure 2]. The key players in the host response appear to be the cytokines, the leukocytes, the endothelium and subsequent leukocyte-endothelial cell interactions. Reactive oxygen species, eicosanoids and microcirculatory disturbances also play pivotal roles. The development of this inflammatory response and its subsequent, often fatal consequences are part of the normal response to injury. [9],[10]

When the initial massive injury and shock give rise to an intense systemic inflammatory syndrome with the potential to cause remote organ injury, this "one hit" can cause an excessive inflammatory response that activates the innate immune system, including macrophages, leukocytes, natural killer cells and inflammatory cell migration enhanced by interleukin-8 (IL-8) production and complement components (C5a and C3a). When the stimulus is less intense and would normally resolve without consequence, patient is vulnerable to secondary inflammatory insults that can reactivate the SIR syndrome and precipitate late MODS. The second insult may take many forms as a result of a variety of circumstances, such as sepsis and surgical procedures and is the basis for the decision-making process regarding when and how much to do for a "borderline" multiply injured patient. Hyperstimulation of the inflammatory system by either single or multiple hits, is considered by many to be the key element in the pathogenesis of ARDS and MODS. [11],[12]

Some observations are as follows:

  1. Elevation in plasma concentrations of IL-6 and IL-8 in patients with an injury severity score (ISS) of 25 or more points.
  2. An immediate increase in expression of neutrophil L-selectin was reported in patients with an ISS of more than 16 points.
  3. A statistically significant (P < 0.05) increase in the expression of the integrin cluster of differentiation molecule 11B (CD11b) was noted in more severely injured patients. The development of MODS has also been associated with a persistent elevation of CD11b expression on both neutrophils and lymphocytes for 120 h, a finding that is suggestive of neutrophil activation in the early development of leukocyte mediated end-organ injury. [11],[12]

Several authors have demonstrated the immunosuppressive effect of trauma. Following trauma, the production of immunoglobulins and interferon (IFN) decreases and many patients become anergic as assessed with delayed hypersensitivity skin-testing and are thus exposed to an increased risk of post-traumatic sepsis. Defects in neutrophil chemotaxis, phagocytosis, lysosomal enzyme content, and respiratory burst have also been reported. Immunosuppression contributes to the etiology of infection and sepsis after trauma.

  Markers of Immune Reactivity Top

Inflammatory markers may hold the key to identifying patients at risk for the development of post-traumatic complications such as MODS. Common serum markers can be divided into markers of mediator activity such as C reactive protein, tumor necrosis factor-α (TNF-α), IL-1, IL-6, IL-8, IL-10 and procalcitonin and markers of cellular activity such as CD11b surface receptor on leukocytes, endothelial adhesion molecules (intercellular adhesion molecule-1 [ICAM-1] and e-selectin) and human leukocyte antigen (HLA-DR) class-II molecules on peripheral mononuclear cells. C-reactive proteins, procalcitonin, TNF-α, IL-1, and IL-8 have not been shown to be reliable markers 3. However, IL-6 correlates well with the degree of injury, appears to be a reliable index of the magnitude of systemic inflammation and correlates with the outcome. IL-10 inhibits the activity of TNF-α and

IL-1 and the levels detectable in the circulation correlate with the initial degree of injury. Persistently high levels of IL-10 also correlate with sepsis. However, its role in predicting outcome is still debatable. Regarding the markers of cellular activity, mixed results have been reported in the literature about the efficacy of endothelial adhesion molecules (ICAM-1 and e-selectin) and the CD11b receptor of leukocytes. HLA-DR class-II molecules mediate the processing of antigen to allow for cellular immunity. They are considered to be reliable markers of immune reactivity and a predictor of outcome following trauma.

Group examples of markers of immune reactivity:

  1. IL-IL-1-8, IL-10-13, IL-18
  2. TNF, lymphotoxin
  3. IFNs-IFN-alpha, IFN-beta, IFN-gamma
  4. Colony stimulating factors (CSF) G-CSF, M-CSF, GM-CSF.

It appears that, at present, only two markers, IL-6 and HLA-DR class-II molecules, accurately predict the clinical course and outcome after trauma. IL-6 measurement has already been implemented as a routine laboratory test in several trauma centers. Because of the additional laboratory processing required for tests of HLA-DR class-II molecules (antibody staining of cells and flow cytometric analysis), the use of such tests has not found great clinical acceptance. [10],[13],[14],[15]
"Borderline" patient for whom damage control orthopedics is often preferred:

  1. Polytrauma + injury severity score of >20 points and additional thoracic trauma (abbreviated injury score >2 points).
  2. Polytrauma with abdominal/pelvic trauma (Moore score >3 points) and hemorrhagic shock (initial blood pressure <90 mm Hg).
  3. Injury severity score of more than 40 points in the absence of additional thoracic injury. Radiographic findings of bilateral lung contusion.
  4. Initial mean pulmonary arterial pressure of >24 mm Hg. [5]
  5. Increase of >6 mm Hg in pulmonary arterial pressure during intramedullary nailing.

  Patient Selection for Damage Control Orthopedics Top

Because biochemical and genetic testing is currently not practical, it is a clinical decision when to shift from ETC to DCO. Which patient should be treated with DCO instead of ETC after trauma should be decided on the basis of the patient's overall physiological status and injury complexes. Many trauma scoring systems (e.g., the abbreviated injury scale, injury severity score, revised trauma score, anatomic profile and Glasgow coma scale) have been developed in an attempt to describe the overall condition of the trauma patient. However "there is no score that assists in decision-making

during the acute resuscitation phase." Therefore, one cannot rely exclusively on a scoring system. Patients who have sustained orthopedic trauma have been divided into four groups: stable, borderline, unstable and in extremis. Stable patients, unstable patients and patients in extremis are fairly easy to define. Stable patients should be treated with the local preferred method for managing their orthopedic injuries. Unstable patients and patients in extremis should be treated with DCO for their injuries. Borderline patients are more difficult to define. These may be patients with polytrauma and an injury severity score of >40 points in the absence of thoracic injury or an injury severity score of >20 points with thoracic injury (an abbreviated injury score of >2 points); polytrauma with abdominal trauma (a Moore score 75 of >3 points); a chest radiograph showing bilateral lung contusions; an initial mean pulmonary artery pressure of >24 mm Hg or an increase in pulmonary artery pressure of >6 mm Hg during nailing. [16],[17],[18]

Borderline trauma patients are probably best treated with DCO [Figure 3]. The term "borderline patient" describes a predisposition for deterioration. Among other factors, thoracic trauma appears to play a crucial role in this predisposition. However, whether the femoral fractures in patients with chest trauma should be treated with definitive stabilization or should be stabilized with a temporary external fixator remains a subject of debate. The clinical situation, including the presence or absence of a criterion indicating borderline status and factors associated with a high risk of adverse outcomes, should determine how the patient is treated. Some of the additional clinical criteria that we have used as a basis for shifting to DCO include a pH of <7.24, a temperature of <35°C, operative times of more than 90 min, coagulopathy and transfusion of more than ten units of packed red blood cells. Furthermore, certain specific orthopedic injury complexes appear to be more amenable to DCO; these include, for example, femoral fractures in a multiply injured patient, pelvic ring injuries with exsanguinating hemorrhage and polytrauma in a geriatric patient. [19],[20],[21],[22],[23]
Figure 3: The current treatment algorithm for the use of damage control orthopedics is based on a prompt and accurate determination of whether the patient is stable, borderline, unstable or in extremis. ER = Emergency room, ABG = Arterial blood gases, FAST = Focused assessment sonography for trauma, I/O ratio = Intake/output ratio, ABP = Arterial blood pressure, IL-6 = Interleukin-6, ETC = Early total care, OR = Operating room, DCO = Damage control orthopedics and ICU = Intensive care unit

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Clinical parameters associated with adverse outcomes in multiply injured patients:

  1. Unstable condition or resuscitation difficult (borderline patient).
  2. Coagulopathy (platelet count <90,000).
  3. Hypothermia (<32°C).
  4. Shock and >25 units of blood needed.
  5. Bilateral lung contusion on first plain radiograph.
  6. Multiple long-bone injuries and truncal injury; abbreviated injury score of 2 points or more.
  7. Presumed operation time >6 h.
  8. Arterial injury and hemodynamic instability (blood pressure <90 mm Hg).
  9. Exaggerated inflammatory response (e.g., IL-6 >800 pg/mL).

  Head Injury with Femur Fracture Top

In a study by Dunham et al. [24] it was concluded that patients with mild, moderate or severe brain injury who underwent long-bone stabilization within 48 h were similar to those treated with later stabilization with regard to the mortality rate, length of stay in the intensive care unit, need for mechanical ventilation and total length of stay in the hospital. The overall conclusion was that there was no compelling evidence that early long bone stabilization either enhances or worsens the outcome in patients with a mild, moderate or severe head injury. More recently, Recently it has been reported that there is no increase in morbidity or mortality in association with early intramedullary nailing (within 24 h) of femoral fractures in patients who had sustained blunt thoracic trauma. However, it is better to have a selective approach for patients with long-bone fractures and a chest injury. Defining the subgroup of patients for whom early nailing would increase the risk of early complications is the goal of damage control orthopedics. Treatment ought to be individualized. When early intramedullary nailing is not deemed to be the best alternative, damage control orthopedics, with short-term external fixation of the femur followed by staged conversion to an intramedullary nail in the 1 st week after an injury, can be utilized.

One of the most important issues in DCO is the timing of the secondary surgical procedures (definitive osteosynthesis). Days 2, 3 and 4 are not safe for performing definitive surgery. During this period, marked immune reactions are ongoing and increased generalized edema is observed. A recent prospective study demonstrated that multiply injured patients subjected to secondary definitive surgery between days 2 and 4 had a significantly (P < 0.0001) increased inflammatory response compared with that in patients operated on between days 6 and 8. It was concluded that in different post-traumatic periods, variable inflammatory responses to comparable stimuli are observed. This variation may contribute to the differences in clinical outcome (e.g., a higher incidence of multiple organ failure) that have been reported. In Hannover, Germany, all high-risk patients are being managed with a treatment plan that involves a re-evaluation of clinical and laboratory parameters in the emergency department after the primary diagnostic work-up. On the basis of this re-evaluation, specific recommendations can be made for specific groups of patients in the form of an algorithm. External fixation includes the use of an external fixation system that is user friendly and can be applied rapidly. Self-drilling pins, which can be manually inserted, can be applied quickly with a limited need for fluoroscopy. Operating time can be decreased by multiple operating teams working on opposite ends of the same limb or on different extremities. [25],[26],[27] External fixation systems that employ snap- and-click clamps can be assembled rapidly. In addition, a system that allows flexibility in pin placement is preferable so that areas of future incisions can be avoided.

  Current Concepts and Future Directions Top

DCO is ideal for an unstable patient or a patient in extremis and it has some utility for the borderline patient as well. Specific injury complexes for which DCO should be considered are femoral fractures (especially bilateral fractures), pelvic ring injuries with profound hemorrhage and multiple injuries in elderly patients. Specific subgroups of multiply injured orthopedic patients who may benefit from DCO are those with a head injury, chest trauma or a mangled limb. [28] A limited form of DCO (limb DCO) is a rational alternative for the treatment of isolated, complex limb injuries. [29]

As our understanding of the complex mechanisms that are triggered by polytrauma increase, in the future we may be able to device treatment modalities to alter or modulate the immunological response.

  References Top

1.Pape HC, Giannoudis 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. 1
2.Bradford DS, Foster RR, Nossel HL. Coagulation alterations, hypoxemia, and fat embolism in fracture patients. J Trauma 1970;10:307-21.  Back to cited text no. 2
3.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. 3
4.Bone LB, Johnson KD, Weigelt J, Scheinberg R. Early versus delayed stabilization of femoral fractures. A prospective randomized study. J Bone Joint Surg Am 1989;71:336-40.  Back to cited text no. 4
5.Granger DN, Kubes P. The microcirculation and inflammation: Modulation of leukocyte-endothelial cell adhesion. J Leukoc Biol 1994;55:662-75.  Back to cited text no. 5
6.Cipolle MD, Pasquale MD, Cerra FB. Secondary organ dysfunction. From clinical perspectives to molecular mediators. Crit Care Clin 1993;9:261-98.  Back to cited text no. 6
7.Anderson BO, Harken AH. Multiple organ failure: Inflammatory priming and activation sequences promote autologous tissue injury. J Trauma 1990;30:S44-9.  Back to cited text no. 7
8.Giannoudis PV, Smith RM, Ramsden CW, Sharples D, Dickson RA, Guillou PJ. Molecular mediators and trauma: Effects of accidental trauma on the production of plasma elastase, IL-6, sICAM-1, and s E selectin. Injury 1996;27:372.  Back to cited text no. 8
9.Giannoudis PV, Smith RM, Banks RE, Windsor AC, Dickson RA, Guillou PJ. Stimulation of inflammatory markers after blunt trauma. Br J Surg 1998;85:986-90.  Back to cited text no. 9
10.Giannoudis PV, Smith RM, Windsor AC, Bellamy MC, Guillou PJ. Monocyte human leukocyte antigen-DR expression correlates with intrapulmonary shunting after major trauma. Am J Surg 1999;177:454-9.  Back to cited text no. 10
11.Pape HC, Grimme K, Van Griensven M, Sott AH, Giannoudis P, Morley J, et al. Impact of intramedullary instrumentation versus damage control for femoral fractures on immunoinflammatory parameters: Prospective randomized analysis by the EPOFF Study Group. J Trauma 2003;55:7-13.  Back to cited text no. 11
12.Hoch RC, Rodriguez R, Manning T, Bishop M, Mead P, Shoemaker WC, et al. Effects of accidental trauma on cytokine and endotoxin production. Crit Care Med 1993;21:839-45.  Back to cited text no. 12
13.Cheadle WG, Hershman MJ, Wellhausen SR, Polk HC Jr. HLA-DR antigen expression on peripheral blood monocytes correlates with surgical infection. Am J Surg 1991;161:639-45.  Back to cited text no. 13
14.Napolitano LM, Ferrer T, McCarter RJ Jr, Scalea TM. Systemic inflammatory response syndrome score at admission independently predicts mortality and length of stay in trauma patients. J Trauma 2000;49:647-52.  Back to cited text no. 14
15.Taniguchi T, Koido Y, Aiboshi J, Yamashita T, Suzaki S, Kurokawa A. The ratio of interleukin-6 to interleukin-10 correlates with severity in patients with chest and abdominal trauma. Am J Emerg Med 1999;17:548-51.  Back to cited text no. 15
16.Baker SP, O'Neill B, Haddon W Jr, Long WB. The injury severity score: A method for describing patients with multiple injuries and evaluating emergency care. J Trauma 1974;14:187-96.  Back to cited text no. 16
17.Copes WS, Champion HR, Sacco WJ, Lawnick MM, Keast SL, Bain LW. The Injury Severity Score revisited. J Trauma 1988;28:69-77.  Back to cited text no. 17
18.Champion HR, Sacco WJ, Copes WS, Gann DS, Gennarelli TA, Flanagan ME. A revision of the Trauma Score. J Trauma 1989;29:623-9.  Back to cited text no. 18
19.Copes WS, Champion HR, Sacco WJ, Lawnick MM, Gann DS, Gennarelli T, et al. Progress in characterizing anatomic injury. J Trauma 1990;30:1200-7.  Back to cited text no. 19
20.Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet 1974;2:81-4.  Back to cited text no. 20
21.Bosse MJ, MacKenzie EJ, Riemer BL, Brumback RJ, McCarthy ML, Burgess AR, et al. Adult respiratory distress syndrome, pneumonia, and mortality following thoracic injury and a femoral fracture treated either with intramedullary nailing with reaming or with a plate. A comparative study. J Bone Joint Surg Am 1997;79:799-80.  Back to cited text no. 21
22.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. 22
23.Moore EE, Cogbill TH, Malangoni MA, Jurkovich GJ, Shackford SR, Champion HR, et al. Organ injury scaling. Surg Clin North Am 1995;75:293-30.  Back to cited text no. 23
24.Dunham CM, Bosse MJ, Clancy TV, Cole FJ Jr, Coles MJ, Knuth T, et al. Practice management guidelines for the optimal timing of long-bone fracture stabilization in polytrauma patients: The EAST Practice Management Guidelines Work Group. J Trauma 2001;50:958-67.  Back to cited text no. 24
25.Seibel R, LaDuca J, Hassett JM, Babikian G, Mills B, Border DO, et al. Blunt multiple trauma (ISS 36), femur traction, and the pulmonary failure-septic state. Ann Surg 1985;202:283-95.  Back to cited text no. 25
26.Rüedi T, Wolff G. Prevention of post-traumatic complications through immediate therapy in patients with multiple injuries and fractures. Helv Chir Acta 1975;42:507-12.  Back to cited text no. 26
27.Wilber MC, Evans EB. Fractures of the femoral shaft treated surgically. Comparative results of early and delayed operative stabilization. J Bone Joint Surg Am 1978;60:489-91.  Back to cited text no. 27
28.Wald SL, Shackford SR, Fenwick J. The effect of secondary insults on mortality and long-term disability after severe head injury in a rural region without a trauma system. J Trauma 1993;34:377-81.  Back to cited text no. 28
29.Pape H, Stalp M, v Griensven M, Weinberg A, Dahlweit M, Tscherne H. Optimal timing for secondary surgery in polytrauma patients: An evaluation of 4,314 serious-injury cases. Chirurg 1999;70:1287-93.  Back to cited text no. 29


  [Figure 1], [Figure 2], [Figure 3]


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