Skip to main content
SpringerLink
Log in

Local Inflammatory Changes Induced by Fractures and Soft Tissue Injuries

  • Chapter
  • First Online:
The Poly-Traumatized Patient with Fractures

  • 1800 Accesses

Abstract

Tissue trauma induces an inflammatory response in the host. Although the inflammatory response has beneficial effects at the site of injury including wound healing and the elimination of exogenous microorganisms, an exaggerated systemic inflammatory response may develop into acute respiratory distress syndrome (ARDS) and multiple organ failure (MOF). Various mediators and cell types are involved in the inflammatory response after trauma. In addition, the development of complications (ARDS, sepsis, and MOF) is regulated by the degree of injury, the type of injured tissue, age, gender, and physical condition. In this chapter, we describe various factors involved in the inflammatory changes after trauma, and aim to understand how these factors interact to progress to systemic inflammation, ARDS, and MOF.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Log in via an institution
Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 169.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

References

  1. Bone RC, Balk RA, Cerra FB, et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Chest. 1992;101:1644–55.

    Article  PubMed  CAS  Google Scholar 

  2. Bone RC. Toward a theory regarding the pathogenesis of the systemic inflammatory response syndrome: what we do and do not know about cytokine regulation. Crit Care Med. 1996;24:163–72.

    Article  PubMed  CAS  Google Scholar 

  3. Lin E, Calvano SE, Lowry SF. Inflammatory cytokines and cell response in surgery. Surgery. 2000;127:117–26.

    Article  PubMed  CAS  Google Scholar 

  4. Gruys E, Toussaint MJ, Niewold TA, et al. Acute phase reaction and acute phase proteins. J Zhejiang Univ Sci B. 2005;6:1045–56.

    Article  PubMed  CAS  Google Scholar 

  5. Keel M, Trentz O. Pathophysiology of polytrauma. Injury. 2005;36:691–709.

    Article  PubMed  Google Scholar 

  6. el Hassan BS, Peak JD, Whicher JT, et al. Acute phase protein levels as an index of severity of physical injury. Int J Oral Maxillofac Surg. 1990;19:346–9.

    Article  PubMed  Google Scholar 

  7. Castelli GP, Pognani C, Cita M, et al. Procalcitonin as a prognostic and diagnostic tool for septic complications after major trauma. Crit Care Med. 2009;37:1845–9.

    Article  PubMed  Google Scholar 

  8. Du Clos TW. Function of C-reactive protein. Ann Med. 2000;32:274–8.

    Article  PubMed  Google Scholar 

  9. Gosling P, Dickson GR. Serum c-reactive protein in patients with serious trauma. Injury. 1992;23:483–6.

    Article  PubMed  CAS  Google Scholar 

  10. Mimoz O, Benoist JF, Edouard AR, et al. Procalcitonin and C-reactive protein during the early posttraumatic systemic inflammatory response syndrome. Intensive Care Med. 1998;24:185–8.

    Article  PubMed  CAS  Google Scholar 

  11. Uzzan B, Cohen R, Nicolas P, et al. Procalcitonin as a diagnostic test for sepsis in critically ill adults and after surgery or trauma: a systematic review and meta-analysis. Crit Care Med. 2006;34:1996–2003.

    Article  PubMed  CAS  Google Scholar 

  12. Wanner GA, Keel M, Steckholzer U, et al. Relationship between procalcitonin plasma levels and severity of injury, sepsis, organ failure, and mortality in injured patients. Crit Care Med. 2000;28:950–7.

    Article  PubMed  CAS  Google Scholar 

  13. Lenz A, Franklin GA, Cheadle WG. Systemic inflammation after trauma. Injury. 2007;38:1336–45.

    Article  PubMed  Google Scholar 

  14. Pillay J, Hietbrink F, Koenderman L, et al. The systemic inflammatory response induced by trauma is reflected by multiple phenotypes of blood neutrophils. Injury. 2007;38:1365–72.

    Article  PubMed  CAS  Google Scholar 

  15. Trinchieri G. Interleukin-12 and the regulation of innate resistance and adaptive immunity. Nat Rev Immunol. 2003;3:133–46.

    Article  PubMed  CAS  Google Scholar 

  16. Watford WT, Moriguchi M, Morinobu A, et al. The biology of IL-12: coordinating innate and adaptive immune responses. Cytokine Growth Factor Rev. 2003;14:361–8.

    Article  PubMed  CAS  Google Scholar 

  17. Decker D, Schondorf M, Bidlingmaier F, et al. Surgical stress induces a shift in the type-1/type-2 T-helper cell balance, suggesting down-regulation of cell-mediated and up-regulation of antibody-mediated immunity commensurate to the trauma. Surgery. 1996;119:316–25.

    Article  PubMed  CAS  Google Scholar 

  18. O’Sullivan ST, Lederer JA, Horgan AF, et al. Major injury leads to predominance of the T helper-2 lymphocyte phenotype and diminished interleukin-12 production associated with decreased resistance to infection. Ann Surg. 1995;222:482–90; discussion 90–2.

    PubMed  Google Scholar 

  19. Spolarics Z, Siddiqi M, Siegel JH, et al. Depressed interleukin-12-producing activity by monocytes correlates with adverse clinical course and a shift toward Th2-type lymphocyte pattern in severely injured male trauma patients. Crit Care Med. 2003;31:1722–9.

    Article  PubMed  CAS  Google Scholar 

  20. Miller AC, Rashid RM, Elamin EM. The “T” in trauma: the helper T-cell response and the role of immunomodulation in trauma and burn patients. J Trauma. 2007;63:1407–17.

    Article  PubMed  CAS  Google Scholar 

  21. Heizmann O, Koeller M, Muhr G, et al. Th1- and Th2-type cytokines in plasma after major trauma. J Trauma. 2008;65:1374–8.

    Article  PubMed  CAS  Google Scholar 

  22. Wick M, Kollig E, Muhr G, et al. The potential pattern of circulating lymphocytes TH1/TH2 is not altered after multiple injuries. Arch Surg. 2000;135:1309–14.

    Article  PubMed  CAS  Google Scholar 

  23. Fosse E, Pillgram-Larsen J, Svennevig JL, et al. Complement activation in injured patients occurs immediately and is dependent on the severity of the trauma. Injury. 1998;29:509–14.

    Article  PubMed  CAS  Google Scholar 

  24. Mollnes TE, Fosse E. The complement system in trauma-related and ischemic tissue damage: a brief review. Shock. 1994;2:301–10.

    Article  PubMed  CAS  Google Scholar 

  25. Mastellos D, Lambris JD. Complement: more than a ‘guard’ against invading pathogens? Trends Immunol. 2002;23:485–91.

    Article  PubMed  CAS  Google Scholar 

  26. Hecke F, Schmidt U, Kola A, et al. Circulating complement proteins in multiple trauma patients – correlation with injury severity, development of sepsis, and outcome. Crit Care Med. 1997;25:2015–24.

    Article  PubMed  CAS  Google Scholar 

  27. Kapur MM, Jain P, Gidh M. The effect of trauma on serum C3 activation and its correlation with injury severity score in man. J Trauma. 1986;26:464–6.

    Article  PubMed  CAS  Google Scholar 

  28. Sharma DK, Sarda AK, Bhalla SA, et al. The effect of recent trauma on serum complement activation and serum C3 levels correlated with the injury severity score. Indian J Med Microbiol. 2004;22:147–52.

    PubMed  CAS  Google Scholar 

  29. Sugimoto K, Hirata M, Majima M, et al. Evidence for a role of kallikrein-P6nin system in patients with shock after blunt trauma. Am J Physiol. 1998;274:R1556–60.

    PubMed  CAS  Google Scholar 

  30. Joseph K, Kaplan AP. Formation of bradykinin: a major contributor to the innate inflammatory response. Adv Immunol. 2005;86:159–208.

    Article  PubMed  CAS  Google Scholar 

  31. Chu AJ. Blood coagulation as an intrinsic pathway for proinflammation: a mini review. Inflamm Allergy Drug Targets. 2009;9(1):32–44.

    Google Scholar 

  32. Abraham E. Coagulation abnormalities in acute lung injury and sepsis. Am J Respir Cell Mol Biol. 2000;22:401–4.

    PubMed  CAS  Google Scholar 

  33. Chu AJ. Tissue factor mediates inflammation. Arch Biochem Biophys. 2005;440:123–32.

    Article  PubMed  CAS  Google Scholar 

  34. Riddel Jr JP, Aouizerat BE, Miaskowski C, et al. Theories of blood coagulation. J Pediatr Oncol Nurs. 2007;24:123–31.

    Article  PubMed  Google Scholar 

  35. Rigby AC, Grant MA. Protein S: a conduit between anticoagulation and inflammation. Crit Care Med. 2004;32:S336–41.

    Article  PubMed  CAS  Google Scholar 

  36. Dinarello CA. Proinflammatory cytokines. Chest. 2000;118:503–8.

    Article  PubMed  CAS  Google Scholar 

  37. Kim PK, Deutschman CS. Inflammatory responses and mediators. Surg Clin North Am. 2000;80:885–94.

    Article  PubMed  CAS  Google Scholar 

  38. Ayala A, Perrin MM, Meldrum DR, et al. Hemorrhage induces an increase in serum TNF which is not associated with elevated levels of endotoxin. Cytokine. 1990;2:170–4.

    Article  PubMed  CAS  Google Scholar 

  39. Rabinovici R, John R, Esser KM, et al. Serum tumor necrosis factor-alpha profile in trauma patients. J Trauma. 1993;35:698–702.

    Article  PubMed  CAS  Google Scholar 

  40. Rhee P, Waxman K, Clark L, et al. Tumor necrosis factor and monocytes are released during hemorrhagic shock. Resusci­tation. 1993;25:249–55.

    Article  PubMed  CAS  Google Scholar 

  41. Roumen RM, Hendriks T, van der Ven-Jongekrijg J, et al. Cytokine patterns in patients after major vascular surgery, hemorrhagic shock, and severe blunt trauma. Relation with subsequent adult respiratory distress syndrome and multiple organ failure. Ann Surg. 1993;218:769–76.

    Article  PubMed  CAS  Google Scholar 

  42. Stylianos S, Wakabayashi G, Gelfand JA, et al. Experimental hemorrhage and blunt trauma do not increase circulating tumor necrosis factor. J Trauma. 1991;31:1063–7.

    PubMed  CAS  Google Scholar 

  43. Zingarelli B, Squadrito F, Altavilla D, et al. Role of tumor necrosis factor-alpha in acute hypovolemic hemorrhagic shock in rats. Am J Physiol. 1994;266:H1512–5.

    PubMed  CAS  Google Scholar 

  44. Biffl WL, Moore EE, Moore FA, et al. Interleukin-6 in the injured patient. Marker of injury or mediator of inflammation? Ann Surg. 1996;224:647–64.

    Article  PubMed  CAS  Google Scholar 

  45. Gebhard F, Pfetsch H, Steinbach G, et al. Is interleukin 6 an early marker of injury severity following major trauma in humans? Arch Surg. 2000;135:291–5.

    Article  PubMed  CAS  Google Scholar 

  46. Pape HC, Tsukamoto T, Kobbe P, et al. Assessment of the clinical course with inflammatory parameters. Injury. 2007;38:1358–64.

    Article  PubMed  Google Scholar 

  47. Partrick DA, Moore FA, Moore EE, et al. Jack A. Barney Resident Research Award winner. The inflammatory profile of interleukin-6, interleukin-8, and soluble intercellular adhesion molecule-1 in postinjury multiple organ failure. Am J Surg. 1996;172:425–9; discussion 9–31.

    Article  PubMed  CAS  Google Scholar 

  48. Pape HC, van Griensven M, Rice J, et al. Major secondary surgery in blunt trauma patients and perioperative cytokine liberation: determination of the clinical relevance of biochemical markers. J Trauma. 2001;50:989–1000.

    Article  PubMed  CAS  Google Scholar 

  49. DeLong Jr WG, Born CT. Cytokines in patients with polytrauma. Clin Orthop Relat Res. 2004;422:57–65.

    Article  PubMed  Google Scholar 

  50. Donnelly SC, Strieter RM, Kunkel SL, et al. Interleukin-8 and development of adult respiratory distress syndrome in at-risk patient groups. Lancet. 1993;341:643–7.

    Article  PubMed  CAS  Google Scholar 

  51. Pallister I, Dent C, Topley N. Increased neutrophil migratory activity after major trauma: a factor in the etiology of acute respiratory distress syndrome? Crit Care Med. 2002;30:1717–21.

    Article  PubMed  Google Scholar 

  52. Oswald IP, Wynn TA, Sher A, et al. Interleukin 10 inhibits macrophage microbicidal activity by blocking the endogenous production of tumor necrosis factor alpha required as a costimulatory factor for interferon gamma-induced activation. Proc Natl Acad Sci USA. 1992;89:8676–80.

    Article  PubMed  CAS  Google Scholar 

  53. Armstrong L, Millar AB. Relative production of tumour necrosis factor alpha and interleukin 10 in adult respiratory distress syndrome. Thorax. 1997;52:442–6.

    Article  PubMed  CAS  Google Scholar 

  54. Donnelly SC, Strieter RM, Reid PT, et al. The association between mortality rates and decreased concentrations of interleukin-10 and interleukin-1 receptor antagonist in the lung fluids of patients with the adult respiratory distress syndrome. Ann Intern Med. 1996;125:191–6.

    PubMed  CAS  Google Scholar 

  55. Giannoudis PV, Smith RM, Perry SL, et al. Immediate IL-10 expression following major orthopaedic trauma: relationship to anti-inflammatory response and subsequent development of sepsis. Intensive Care Med. 2000;26:1076–81.

    Article  PubMed  CAS  Google Scholar 

  56. Neidhardt R, Keel M, Steckholzer U, et al. Relationship of interleukin-10 plasma levels to severity of injury and clinical outcome in injured patients. J Trauma. 1997;42:863–70; discussion 70–1.

    Article  PubMed  CAS  Google Scholar 

  57. Pajkrt D, Camoglio L, Tiel-van Buul MC, et al. Attenuation of proinflammatory response by recombinant human IL-10 in human endotoxemia: effect of timing of recombinant human IL-10 administration. J Immunol. 1997;158:3971–7.

    PubMed  CAS  Google Scholar 

  58. Opal SM, DePalo VA. Anti-inflammatory cytokines. Chest. 2000;117:1162–72.

    Article  PubMed  CAS  Google Scholar 

  59. Phipps RP, Stein SH, Roper RL. A new view of prostaglandin E regulation of the immune response. Immunol Today. 1991;12:349–52.

    Article  PubMed  CAS  Google Scholar 

  60. Tilg H, Trehu E, Atkins MB, et al. Interleukin-6 (IL-6) as an anti-inflammatory cytokine: induction of circulating IL-1 receptor antagonist and soluble tumor necrosis factor receptor p55. Blood. 1994;83:113–8.

    PubMed  CAS  Google Scholar 

  61. Sasaki M, Joh T. Oxidative stress and ischemia-reperfusion injury in gastrointestinal tract and antioxidant, protective agents. J Clin Biochem Nutr. 2007;40:1–12.

    Article  PubMed  CAS  Google Scholar 

  62. Cristofori L, Tavazzi B, Gambin R, et al. Early onset of lipid peroxidation after human traumatic brain injury: a fatal limitation for the free radical scavenger pharmacological therapy? J Investig Med. 2001;49:450–8.

    Article  PubMed  CAS  Google Scholar 

  63. Kong SE, Blennerhassett LR, Heel KA, et al. Ischaemia-reperfusion injury to the intestine. Aust N Z J Surg. 1998;68:554–61.

    Article  PubMed  CAS  Google Scholar 

  64. Remick DG, Villarete L. Regulation of cytokine gene expression by reactive oxygen and reactive nitrogen intermediates. J Leukoc Biol. 1996;59:471–5.

    PubMed  CAS  Google Scholar 

  65. Schreck R, Rieber P, Baeuerle PA. Reactive oxygen intermediates as apparently widely used messengers in the activation of the NF-kappa B transcription factor and HIV-1. EMBO J. 1991;10:2247–58.

    PubMed  CAS  Google Scholar 

  66. Gasic AC, McGuire G, Krater S, et al. Hydrogen peroxide pretreatment of perfused canine vessels induces ICAM-1 and CD18-dependent neutrophil adherence. Circulation. 1991;84:2154–66.

    PubMed  CAS  Google Scholar 

  67. Villarete LH, Remick DG. Nitric oxide regulation of interleukin-8 gene expression. Shock. 1997;7:29–35.

    Article  PubMed  CAS  Google Scholar 

  68. Cirino G, Distrutti E, Wallace JL. Nitric oxide and inflammation. Inflamm Allergy Drug Targets. 2006;5:115–9.

    Article  PubMed  CAS  Google Scholar 

  69. Laroux FS, Pavlick KP, Hines IN, et al. Role of nitric oxide in inflammation. Acta Physiol Scand. 2001;173:113–8.

    Article  PubMed  CAS  Google Scholar 

  70. Srikrishna G, Freeze HH. Endogenous damage-associated molecular pattern molecules at the crossroads of inflammation and cancer. Neoplasia. 2009;11:615–28.

    PubMed  CAS  Google Scholar 

  71. Delneste Y, Beauvillain C, Jeannin P. Innate immunity: structure and function of TLRs. Med Sci (Paris). 2007;23:67–73.

    Article  Google Scholar 

  72. Bianchi ME. DAMPs, PAMPs and alarmins: all we need to know about danger. J Leukoc Biol. 2007;81:1–5.

    Article  PubMed  CAS  Google Scholar 

  73. Andersson U, Wang H, Palmblad K, et al. High mobility group 1 protein (HMG-1) stimulates proinflammatory cytokine synthesis in human monocytes. J Exp Med. 2000;192:565–70.

    Article  PubMed  CAS  Google Scholar 

  74. Fiuza C, Bustin M, Talwar S, et al. Inflammation-promoting activity of HMGB1 on human microvascular endothelial cells. Blood. 2003;101:2652–60.

    Article  PubMed  CAS  Google Scholar 

  75. Treutiger CJ, Mullins GE, Johansson AS, et al. High mobility group 1 B-box mediates activation of human endothelium. J Intern Med. 2003;254:375–85.

    Article  PubMed  CAS  Google Scholar 

  76. Wang H, Bloom O, Zhang M, et al. HMG-1 as a late mediator of endotoxin lethality in mice. Science. 1999;285:248–51.

    Article  PubMed  CAS  Google Scholar 

  77. Wang H, Vishnubhakat JM, Bloom O, et al. Proinflammatory cytokines (tumor necrosis factor and interleukin 1) stimulate release of high mobility group protein-1 by pituicytes. Surgery. 1999;126:389–92.

    Article  PubMed  CAS  Google Scholar 

  78. Fan J, Li Y, Levy RM, et al. Hemorrhagic shock induces NAD(P)H oxidase activation in neutrophils: role of HMGB1-TLR4 signaling. J Immunol. 2007;178:6573–80.

    PubMed  CAS  Google Scholar 

  79. Goldstein RS, Gallowitsch-Puerta M, Yang L, et al. Elevated high-mobility group box 1 levels in patients with cerebral and myocardial ischemia. Shock. 2006;25:571–4.

    Article  PubMed  CAS  Google Scholar 

  80. Kim JY, Park JS, Strassheim D, et al. HMGB1 contributes to the development of acute lung injury after hemorrhage. Am J Physiol Lung Cell Mol Physiol. 2005;288:L958–65.

    Article  PubMed  CAS  Google Scholar 

  81. Klune JR, Dhupar R, Cardinal J, et al. HMGB1: endogenous danger signaling. Mol Med. 2008;14:476–84.

    Article  PubMed  CAS  Google Scholar 

  82. Levy RM, Mollen KP, Prince JM, et al. Systemic inflammation and remote organ injury following trauma require HMGB1. Am J Physiol Regul Integr Comp Physiol. 2007;293:R1538–44.

    Article  PubMed  CAS  Google Scholar 

  83. Ombrellino M, Wang H, Ajemian MS, et al. Increased serum concentrations of high-mobility-group protein 1 in haemorrhagic shock. Lancet. 1999;354:1446–7.

    Article  PubMed  CAS  Google Scholar 

  84. Tsung A, Sahai R, Tanaka H, et al. The nuclear factor HMGB1 mediates hepatic injury after murine liver ischemia-reperfusion. J Exp Med. 2005;201:1135–43.

    Article  PubMed  CAS  Google Scholar 

  85. Yang R, Harada T, Mollen KP, et al. Anti-HMGB1 neutralizing antibody ameliorates gut barrier dysfunction and improves survival after hemorrhagic shock. Mol Med. 2006;12:105–14.

    Article  PubMed  CAS  Google Scholar 

  86. Botha AJ, Moore FA, Moore EE, et al. Postinjury neutrophil priming and activation: an early vulnerable window. Surgery. 1995;118:358–64; discussion 64–5.

    Article  PubMed  CAS  Google Scholar 

  87. Zallen G, Moore EE, Johnson JL, et al. Circulating postinjury neutrophils are primed for the release of proinflammatory cytokines. J Trauma. 1999;46:42–8.

    Article  PubMed  CAS  Google Scholar 

  88. Law MM, Cryer HG, Abraham E. Elevated levels of soluble ICAM-1 correlate with the development of multiple organ failure in severely injured trauma patients. J Trauma. 1994;37:100–9; discussion 9–10.

    Article  PubMed  CAS  Google Scholar 

  89. Seekamp A, Jochum M, Ziegler M, et al. Cytokines and adhesion molecules in elective and accidental trauma-related ischemia/reperfusion. J Trauma. 1998;44:874–82.

    Article  PubMed  CAS  Google Scholar 

  90. Simon SI, Green CE. Molecular mechanics and dynamics of leukocyte recruitment during inflammation. Annu Rev Biomed Eng. 2005;7:151–85.

    Article  PubMed  CAS  Google Scholar 

  91. Brochner AC, Toft P. Pathophysiology of the systemic inflammatory response after major accidental trauma. Scand J Trauma Resusc Emerg Med. 2009;17:43.

    Article  PubMed  Google Scholar 

  92. Endo S, Inada K, Kasai T, et al. Levels of soluble adhesion molecules and cytokines in patients with septic multiple organ failure. J Inflamm. 1995;46:212–9.

    PubMed  CAS  Google Scholar 

  93. Ayala A, Ertel W, Chaudry IH. Trauma-induced suppression of antigen presentation and expression of major histocompatibility class II antigen complex in leukocytes. Shock. 1996;5:79–90.

    Article  PubMed  CAS  Google Scholar 

  94. Ghirnikar RS, Lee YL, Eng LF. Inflammation in traumatic brain injury: role of cytokines and chemokines. Neurochem Res. 1998;23:329–40.

    Article  PubMed  CAS  Google Scholar 

  95. Morganti-Kossmann MC, Satgunaseelan L, Bye N, Kossmann T. Modulation of immune response by head injury. Injury. 2007;38:1392–400.

    Article  PubMed  Google Scholar 

  96. Schmidt OI, Heyde CE, Ertel W, et al. Closed head injury – an inflammatory disease? Brain Res Brain Res Rev. 2005;48:388–99.

    Article  PubMed  Google Scholar 

  97. Knoferl MW, Liener UC, Perl M, et al. Blunt chest trauma induces delayed splenic immunosuppression. Shock. 2004;22:51–6.

    Article  PubMed  CAS  Google Scholar 

  98. Perl M, Gebhard F, Bruckner UB, et al. Pulmonary contusion causes impairment of macrophage and lymphocyte immune functions and increases mortality associated with a subsequent septic challenge. Crit Care Med. 2005;33:1351–8.

    Article  PubMed  Google Scholar 

  99. Strecker W, Gebhard F, Perl M, et al. Biochemical characterization of individual injury pattern and injury severity. Injury. 2003;34:879–87.

    Article  PubMed  Google Scholar 

  100. Schirmer WJ, Schirmer JM, Townsend MC, Fry DE. Femur fracture with associated soft-tissue injury produces hepatic ischemia. Possible cause of hepatic dysfunction. Arch Surg. 1988;123:412–5.

    PubMed  CAS  Google Scholar 

  101. Giannoudis PV, Pape HC, Cohen AP, et al. Review: systemic effects of femoral nailing: from Kuntscher to the immune reactivity era. Clin Orthop Relat Res. 2002;404:378–86.

    Article  PubMed  Google Scholar 

  102. Hauser CJ, Joshi P, Zhou X, et al. Production of interleukin-10 in human fracture soft-tissue hematomas. Shock. 1996;6:3–6.

    Article  PubMed  CAS  Google Scholar 

  103. Hauser CJ, Zhou X, Joshi P, et al. The immune microenvironment of human fracture/soft-tissue hematomas and its relationship to systemic immunity. J Trauma. 1997;42:895–903; discussion 4.

    Article  PubMed  CAS  Google Scholar 

  104. Pape HC, Schmidt RE, Rice J, 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.

    Article  PubMed  CAS  Google Scholar 

  105. Perl M, Gebhard F, Knoferl MW, et al. The pattern of preformed cytokines in tissues frequently affected by blunt trauma. Shock. 2003;19:299–304.

    Article  PubMed  CAS  Google Scholar 

  106. Angele MK, Chaudry IH. Surgical trauma and immuno­suppression: pathophysiology and potential immunomodulatory approaches. Langenbecks Arch Surg. 2005;390:333–41.

    Article  PubMed  Google Scholar 

  107. Flohe S, Flohe SB, Schade FU, et al. Immune response of severely injured patients – influence of surgical intervention and therapeutic impact. Langenbecks Arch Surg. 2007;392:639–48.

    Article  PubMed  CAS  Google Scholar 

  108. Ni Choileain N, Redmond HP. Cell response to surgery. Arch Surg. 2006;141:1132–40.

    Article  PubMed  Google Scholar 

  109. Giannoudis PV, Smith RM, Bellamy MC, et al. Stimulation of the inflammatory system by reamed and unreamed nailing of femoral fractures. An analysis of the second hit. J Bone Joint Surg Br. 1999;81:356–61.

    Article  PubMed  CAS  Google Scholar 

  110. Smith RM, Giannoudis PV, Bellamy MC, et al. Interleukin-10 release and monocyte human leukocyte antigen-DR expression during femoral nailing. Clin Orthop Relat Res. 2000;373:233–40.

    Article  PubMed  Google Scholar 

  111. Malone DL, Dunne J, Tracy JK, et al. Blood transfusion, independent of shock severity, is associated with worse outcome in trauma. J Trauma. 2003;54:898–905; discussion 7.

    Article  PubMed  Google Scholar 

  112. Moore EE, Johnson JL, Cheng AM, et al. Insights from studies of blood substitutes in trauma. Shock. 2005;24:197–205.

    Article  PubMed  CAS  Google Scholar 

  113. Moore FA, Moore EE, Sauaia A. Blood transfusion. An independent risk factor for postinjury multiple organ failure. Arch Surg. 1997;132:620–4; discussion 4–5.

    PubMed  CAS  Google Scholar 

  114. Sauaia A, Moore FA, Moore EE, et al. Early predictors of postinjury multiple organ failure. Arch Surg. 1994;129:39–45.

    PubMed  CAS  Google Scholar 

  115. Shander A. Emerging risks and outcomes of blood transfusion in surgery. Semin Hematol. 2004;41:117–24.

    Article  PubMed  Google Scholar 

  116. Silliman CC, Moore EE, Johnson JL, et al. Transfusion of the injured patient: proceed with caution. Shock. 2004;21:291–9.

    Article  PubMed  Google Scholar 

  117. Nakao A, Kaczorowski DJ, Sugimoto R, et al. Application of heme oxygenase-1, carbon monoxide and biliverdin for the prevention of intestinal ischemia/reperfusion injury. J Clin Biochem Nutr. 2008;42:78–88.

    Article  PubMed  CAS  Google Scholar 

  118. Macintire DK, Bellhorn TL. Bacterial translocation: clinical implications and prevention. Vet Clin North Am Small Anim Pract. 2002;32:1165–78.

    Article  PubMed  Google Scholar 

  119. Fukushima R, Kobayashi S, Okinaga K. Bacterial translocation in multiple organ failure. Nippon Geka Gakkai Zasshi. 1998;99:497–503.

    PubMed  CAS  Google Scholar 

  120. Nieuwenhuijzen GA, Goris RJ. The gut: the ‘motor’ of multiple organ dysfunction syndrome? Curr Opin Clin Nutr Metab Care. 1999;2:399–404.

    Article  PubMed  CAS  Google Scholar 

  121. Lichtman SM. Bacterial [correction of baterial] translocation in humans. J Pediatr Gastroenterol Nutr. 2001;33:1–10.

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Department of Emergency and Critical Care Medicine, Nippon Medical School, 1-1-5 Sendagi Bunkyo-ku, Tokyo, Japan

    Takeshi Tsukamoto

Authors
  1. Takeshi Tsukamoto
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Takeshi Tsukamoto .

Editor information

Editors and Affiliations

  1. Klinik für Unfallchirurgie, Universitätsklinikum Aachen, Pauwelsstraße 30, Aachen, 52057, Germany

    Hans-Christoph Pape

  2. Florida Orthopaedic Institute, N. Telecom Parkway 13020, Temple Terrace, 33637, Florida, USA

    Roy Sanders

  3. Southwestern Medical Center at Dallas, University of Texas, Harry Hines Blvd. 5323, Dallas, 75390, Texas, USA

    Joseph Borrelli, Jr.

Rights and permissions

Reprints and permissions

Copyright information

© 2011 Springer-Verlag Berlin Heidelberg

About this chapter

Cite this chapter

Tsukamoto, T. (2011). Local Inflammatory Changes Induced by Fractures and Soft Tissue Injuries. In: Pape, HC., Sanders, R., Borrelli, Jr., J. (eds) The Poly-Traumatized Patient with Fractures. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-17986-0_4

Download citation

  • DOI: https://doi.org/10.1007/978-3-642-17986-0_4

  • Published:

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-17985-3

  • Online ISBN: 978-3-642-17986-0

  • eBook Packages: MedicineMedicine (R0)

Publish with us

Policies and ethics

Search

Navigation