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DOI: 10.1055/s-2006-933399
© Georg Thieme Verlag Stuttgart · New York
Shock - Good Things, Badly Out of Control
Publication History
Publication Date:
01 June 2006 (online)
![](https://www.thieme-connect.de/media/osteotrauma/200602/lookinside/thumbnails/10.1055-s-2006-933399-1.jpg)
Abstract
Shock occurs when the circulatory system fails to adequately nourish the body's cells and may arise from several causes including severe trauma. On the one hand, shock is associated with several good things, including rapid recognition of invading pathogens, immune stimulation and rapid activation of host defense, rapid immobilization of invading pathogens, rapid eradication of invading pathogens and many more, all meant to shield the body against the negative effects of malfunctioning circulation and to enhance host defense against pathogens. On the other hand, however, if shock remains untreated, good things get badly out of control, failing to de-activate host defense after eradication of invading pathogens, failing to activate host defense against remaining pathogens rapidly enough and eradicating invading pathogens at the host's expense. As a result, the patient is forced into a vicious cycle of immune overstimulation and multiple organ dysfunction, eventually leading to immune burn out, hypercatabolism and septic multiple organ failure. In the trauma patient, the stage for this vicious cycle is set immediately after trauma, during the first hours of hemorrhagic-traumatic shock. Therefore, shock should be treated as early as possible, before good things get badly out of control, driving the patient towards septic multiple organ failure and death.
Key words
trauma - hemorrhage - sepsis - systemic inflammatory response - mediators - translocation - multiple organ failure
References
- 1 Albelda S M, Smith C W, Ward P A. Adhesion molecules and inflammatory injury. FASEB J. 1994; 8 504-512
- 2 Adams H A, Baumann G, Gänsslen A, Janssens U, Knoefel W, Koch T, Marx G, Müller-Werdan U, Pape H C, Prange W, Roesner D, Standl T, Teske W, Werner G, Zander R, Schock I AG. Definition of shock types. Anasthesiol Intensivmed Notfallmed Schmerzther. 2001; 36 (Suppl 2) S140-S143
- 3 Bahrami S, Schlag G, Yao Y M, Redl H. Significance of translocation/endotoxin in the development of systemic sepsis following trauma and/or hemorrhage. Prog Clin Biol Res. 1995; 392 197-208
- 4 Bahrami S, Redl H, Yao Y M, Schlag G. Involvement of bacteria/endotoxin translocation in the development of multiple organ failure. Curr Top Microbiol Immunol. 1996; 216 239-258
- 5 Bahrami S, Yao Y M, Leichtfeld G, Redl H, Schlag G, Di Padova F E. Monoclonal antibody to endotoxin attenuates hemorrhage-induced lung injury and mortality in rats. Crit Care Med. 1997; 25 1030-1036
- 6 Bahrami S, Schlag G. Pathophysiology of trauma - Multiple organ failure. Acta Chir Austriaca. 1998; 6 325-331
- 7 Bahrami S, Redl H, Schlag G. Der Darm als Ursache von Sepsis und Multiorganversagen. Wien Klin Wochenschr. 1998; 10 (Suppl 1) 2-10
- 8 Baker J W, Deitch E A, Li M, Berg R D, Specan R D. Hemorrhagic shock induces bacterial translocation from the gut. J Trauma. 1988; 28 896-906
- 9 Bone R C. Modulators of coagulation: a critical appraisal of their role in sepsis. Arch Intern Med. 1992; 152 1381-1389
- 10 Bone R C, Balk R A, Cerra F B, Dellinger F P, Fein A M, Knaus W A, Schein R M, Sibbald W J. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine . Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Chest. 1992; 101 644-1655
- 11 Border J R, Hassett J, LaDuca J, Seibel R, Steinberg S, Mills B, Losi P, Border D. The gut origin septic states in blunt multiple trauma (ISS = 40) in the ICU. Ann Surg. 1987; 206 427-446
- 12 Christ F, Lackner C K. Präklinische Versorgung des Patienten mit Schock. Der Internist. 2004; 45 267-276
- 13 De Backer D, Creteur J, Presiser J C, Dubois M J, Vincent J L. Microvascular blood flow is altered in patients with sepsis. Am J Resp Crit Care Med. 2002; 166 98-104
- 14 Deitch E A, Mancini M C. Complement receptors in shock and transplantation. Arch Surg. 1993; 128 1222-1226
- 15 Deitch E A, Xu D, Franko L, Ayala A, Chaudry I H. Evidence favoring the role of the gut as a cytokine-generating organ in rats subjected to hemorrhagic shock. Shock. 1994; 1 141-146
- 16 Dellinger R P, Carlet J M, Masur H, Gerlach H, Calandra T, Cohen J, Gea-Banacloche J, Keh D, Marshall J C, Parker M M, Ramsay G, Zimmerman J L, Vincent J L, Levy M M. Surviving Sepsis Campaign Management Guidelines Committee . Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock. Crit Care Med. 2004; 32 858-873
- 17 Dutton R P, Mackenzie C F, Scalea T M. Hypotensive resuscitation during active hemorrhage: Impact on inhospital mortality. J Trauma. 2002; 52 1141-1146
- 18 Gillham M J, Parr M JA. Resuscitation for major trauma. Curr Opin Anaesthesiol. 2002; 15 167-172
- 19 Grimble I RF. Nutritional antioxidants and the modulation of inflammation: therapy and practice. New Horiz. 1994; 2 175-185
- 20 Hollenberg S M, Ahrens T S, Annane D, Astiz M E, Chalfin D B, Dasta J F, Heard S O, Martin C, Napolitano L M, Susla G M, Totaro R, Vincent J L, Zanotti-Cavazzoni S. Practice parameters for hemodynamic support of sepsis in adult patients: 2004 update. Crit Care Med. 2004; 32 1928-1948
- 21 Kneidinger R, Bahrami S, Redl H, Schlag G, Robinson M. Comparison of endothelial activation during endotoxic and posttraumatic conditions by serum analysis of soluble E-selectin in nonhuman primates. Lab Clin Med. 1996; 128 515-519
- 22 Koziol J M, Rush B F, Smith S M, Machiedo G W. Occurrence of bacteremia during and after hemorrhagic shock. J Trauma. 1988; 28 10-16
- 23 Mandell D C, King L G. Fluid therapy in shock. Vet Clinics of North America. 1998; 28 623-645
- 24 Nast-Kolb D, Waydhas C, Gippner-Steppert C, Schneider I, Trupka A, Ruchholtz S, Zettl R, Schweiberer L, Jochum M. Indicators of the posttraumatic inflammatory response correlate with organ failure in patients with multiple injuries. J Trauma. 1997; 42 446-455
- 25 Springer T A. Traffic signals for lymphocyte recirculation and leukocyte emigration: the multistep paradigm. Cell. 1994; 76 301-314
- 26 Voelckel W G, Goedecke A, Fries D, Krismer A C, Wenzel V, Lindner K H. Die Behandlung des hämorrhagischen Schocks. Der Anästhesist. 2004; 53 1151-1167
Univ.-Doz. Dr. med. L. E. Pelinka
Department of Anesthesiology and Intensive Care Medicine · Lorenz Böhler Trauma Center of the AUVA
Donaueschingenstraße 13
1200 Vienna
Austria
Phone: +43/1/33 11 00
Fax: +43/1/33 11 02 77
Email: lindapel@via.at