Zusammenfassung
Die Sepsis stellt ein Kontinuum von ineinander übergehenden pathophysiologischen Vorgängen unterschiedlicher Schweregrade dar, das von der Organdysfunktion bis zum Organversagen reicht und sowohl entzündungsfördernde als auch entzündungshemmende Komponenten einschließt. Klinisch erkennbare Stadien sind die unkomplizierte Sepsis, der septische Schock und das Multiorganversagen. Im klinischen Verlauf kann eine Infektion auch ohne die dazwischenliegende Phase des septischen Schocks zu einer schweren Sepsis mit den Zeichen der Gewebshypoxie und Organdysfunktion führen. Klinisch geht die Sepsis mit einer systemischen Entzündungsreaktion (“systemic inflammatory response syndrome„, SIRS) einher. Nicht die Infektion an sich ist Ursache für die Dysfunktion der Organe, sondern die Reaktion des Organismus auf die Infektion. Die Entzündungsreaktion wird durch die Aktivität endogener molekularer Substanzen vermittelt, deren Freisetzung einen systemischen Prozeß in Gang setzt. Ermöglichen die endogenen Mediatoren zu Beginn der Infektion noch eine an sich sinnvolle Abwehrreaktion, kommt es im weiteren Verlauf des Prozesses häufig zu einer überschießenden und damit pathogenen Abwehrreaktion des Organismus [14].
Chapter PDF
Literatur
Abe H, Okajima K, Okabe H, Takatsuki K, Binder BR (1994) Granulocyte protease and hydrogen peroxide synergistically inactivate thrombomodulin of endothelial cells in vitro. J Lab Clin Med 123: 874–881
Abildgaard CF, Corrigan JJ, Seeler RA (1967) Meningococcemia associated with intravascular coagulation. Pediatrics 40: 78–87
Abraham E, Wunderink R, Silverman H et al. (1995) Efficacy and safety of monoclonal antibody to human tumor necrosis factor a in patients with sepsis syndrome. JAMA 273: 934–941
Balk R, Bedrosian C, McCormick L, Baugham J (1995) Prospective double-blind, placebo-controlled trial of ATIII substitution in sepsis. In: Roussos C (ed): 8th European Congress of Intensive Care Medicine. Monduzzi, Bologna, pp 79611
Bauer KA, Cate H, ten, Barzegar S, Spriggs DR, Sherman ML, Rosenberg RD (1989) Tumor necrosis factor infusions have a procoagulant effect on the hemostatic mechanism of humans. Blood 74: 165–172
Bock RL (1994) Disseminated intravascular coagulation. Med Clin North Am 78: 511–543
Bick Rl (1995) Disseminated intravascular coagulation: Objective criteria for clinical and laboratory diagnosis and assessment of therapeutic response. Clin Appl Thrombosis/Hemostasis 1: 3–23
Blauhut B, Kramar H, Vinazzer H, Bergmann H (1985) Substitution of Antithrombin III in Shock and DIC: A randomized study. Thromb Res 29: 81–89
Bombeli T, Mueller M, Haeberli A (1997) Anticoagulant properties of the vascular endothelium. Thromb Haemost 77: 408–423
Bone RC (1991) A critical evaluation of new agents for the treatment of sepsis. JAMA 266: 1686–1691
Bone RC (1991) The pathogenesis of sepsis. Ann Intern Med 1115: 457–469
Bone RC (1992) Sepsis and coagulation. An important link. Chest 101: 594–596
Bone RC, Fisher CJ Jr., Clemmer TP, Slotman GJ, Metz CA, Balk RA (1989) Sepsis syndrome: A valid clinical entity. Crit Care Med 17: 389–393
Bone RC, Balk RA, Cerra FB (1992) Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Chest 101: 1644–1655
Cronberg S, Skansberg P, Nivenios-Larsson K (1973) Disseminated intravascular coagulation in septicemia caused by beta-hemolytic streptococci. Thromb Res 3: 405–414
Deventer SJH van, Buller HR, Cate JW, ten, Aarden LA, Hack CE, Sturk A (1990) Experimental endotoxemia in humans: Analysis of cytokine release and coagulation, fibrinolytic and complement pathways. Blood 76: 2520–2526
Dickneite G, Pques EP (1993) Reduction of mortality with antithrombin III in septicemic rats: A study of Klebsiella pneumoniae induced sepsis. Thromb and Haemost 69: 98–102
Dinarello CA (1991) The proinflammatory cytokines interleukin-1 and tumor necrosis factor and treatment of the septic shock syndrome: J Infect Dis 163: 1177–1184
Dinarello CA, Gelfand JA, Wolff SM (1993) Anticytokine strategies in the treatment of the systemic inflammatory response syndrome. JAMA 269: 1829–1835
Fisher CJ, Dhainaut JFA, Opal SM et al. (1994) Recombinant human Interleukin-1 receptor antagonist in the treatment of patients with sepsis syndrome. JAMA 271: 1836–1843
Fourrier F, Chopin C, Goudemand J et al. (1992) Septic shock multiple organ failure, and disseminated intravascular coagulation. Chest 101: 816–823
Fourrier F, Chopin C, Huart J, Runge I, Caron C, Goudemand J (1993) Double-blind, placebo-controlled trial of antithrombin III concentrates in septic shock with disseminated intravascular coagulation. Chest 104: 882–888
Greenman RL, Schein RMH, Martin MA et al. (1991) A controlled clinical trial of E5 murine monoclonal IgM antibody to endotoxin in the treatment of gram-negative sepsis. JAMA 266: 1097–1102
Guidice D, Galliolo G, Wolfler A et al. (1997) AT III in the ICU patient: A randomized double blind trial. In: Braschi A, Chiaranda M, Gattinoni L, Pesenti A, Raimondi F (eds) Simposio mostra anestesia rianimazione e terapia intensiva. Springer, Berlin Heidelberg New York Tokyo, pp 9–12
Hellgran M, Javelin L, Hägnevik K, Blombäck M, Meden-Britth G (1984) Antithrombin III concentrate as adjuvant in DIC treatment–a pilot study in 9 severely ill patients. Thromb Res 35: 459–466
Hinshaw LB (1996) Sepsis/septic shock: Participation of the microcirculation. Grit Care Med 24: 1072–1078
Horie S, Ishii H, Kazama M (1990) Heparin-like glycosaminoglycan is a receptor for antithrombin-III-dependent but not for thrombin-dependent prostacyclin production in human endothelial cells. Thromb Res 59: 895–904
Inthorn D, Hoffmann JN, Hartl WH, Mühlbayer D, Jochum M (1997) Antithrombin III supplementation in severe sepsis: beneficial effects on organ dysfunction. Shock 8: 328–334
Jochum M (1995) Influence of high-dose antithrombin concentrate therapy on the release of cellular proteinases. Cytokines, and soluble adhesion molecules in acute inflammation. Sem Hematol 32 [Suppl 2]: 19–33
Kirchmaier CM, Bender N, Oehm H, Breddin H (1987) Therapeutic use of antithrombin in septicaemia in adults. Biol Clin Hematol 9 /1: 113–119
Lamy M, Eisele B, Keinecke HO, Delvos U, Thijs LG (1996) Antithrombin III in Patients with Severe Sepsis. A randomized, placebo-controlled, double-blind multicenter trial. In: Bennett D (ed) 9th European Congress on Intensive Care Medicine. Monduzzi, Bologna, pp. 385–390
McCloskey RV, Straube RC, Sanders C, Smith SM, Smith CR (1994) Treatment of septic shock with human monoclonal antibody HA-1A. Ann Intern Med 121: 1–5
Okajima K, Uchiba M, Murakami K (1995) Antithrombin replacement in DIC and MOF. In: Vincent JL (ed) Yearbock of intensive care and emergency medicine. Springer, Berlin Heidelber New York Tokyo, pp. 457–464
Parrillo JE (1989) Septic shock in humans: clinical evaluation, pathophysiology and therapeutic approach. In: Shoemaker WC, Thompson WL, Holbrook P (eds) Textbook of critical care. 2nd edn. Saunders, Philadelphia, PA, pp. 1006–1023
Parrillo JE, Parker MM, Natanson C (1990) Septic shock in humans: advances in the understanding of pathogenesis, cardiovascular dysfunction and therapy. Ann Intern Med 113: 227–242
Piguet PF, Grau GE, Vassalli P (1990) Subcutaneous perfusion of tumor necrosis factor induces local proliferation of fibroblasts, capillaries, and epidermal cells, of massive tissue necrosis. Am J Pathol 136: 103–110
Pinner RV (1996) Trends in infectious disease mortality. JAMA 275: 189–193
Poll T van der, Buller HR, Cate H ten (1990) Activation of coagulation after administration of tumor necrosis factor to normal subjects. N Engl J Med 322: 1622–1627
Rao LVM, Nordfang 00, Hoang AD, Pendurthi UR (1995) Mechanism of antithrombin III inhibition of factor Vila/tissue factor activity on cell surfaces. Comparison with tissue factor pathway inhibitor/factor-Xa-induced inhibition of factor Vlla/tissue factor activity. Blood 85: 121–129
Remick DG, Kunkel RG, Larric JW, Kunkel SL (1987) Acute in vivo effects of human recombinant tumor necrosis factor. Lab Invest 56: 583–590
Rubenberg WL, Baker LR, McBride JA (1967) Intravascular coagulation in a case of clostridium perfringens septicemia. BMJ 3: 271–279
Schipper HG, Jenkins CSP, Kahl LH, Cate JW ten (1978) Antithrombin III transfusion in disseminated intravascular coagulation. Lancet I: 854–856
Schuster HP, Eisele B, Keinecke HO et al. (1998) S-AT III study: Antithrombin III in patients with sepsis. Intensive Care Med 24: (in print)
Seitz R, Wolf M, Egbring R, Havemann K (1989) The disturbance of haemostasis in septic shock: Role of neutrophil elastase and thrombin, effects of antithrombin III and plasma. Eur J Haematol 43: 22–28
Smith-Erichsen N, Aasen AO, Gallimore MJ, Amundsen E (1982) Studies of components of the coagulation systems in normal individuals and septic shock patients. Circ Shock 9: 491–497
Taylor FB, Emerson TE, Jordan R, Chang AK, Blick KE (1988) Antithrombin III prevents the lethal effects of escherichia coli infusion in baboons. Circ Shock 26: 227–235
Taylor FB, Chang ACK, Peer GT et al. (1991) DEGR-FXa blocks disseminated intravascular coagulation initiated by E. coli without preventing shock or organ damage. Blood 87: 364–368
Vinazzer H (1989) Therapeutic use of antithrombin III in shock and disseminated intravascular coagulation. Sem Thromb Hemost 15 /3: 347–352
Vinazzer H (1995) Antithrombin III in shock and disseminated intravascular coagulation. Clin Applied Thrombosis/Hemostasis 1: 62–65
Yamauchi T, Umeda F, Inogochi T (1989) Antithrombin-III-stimulated prostacyclin production by cultured aortic endothelial cells. Biochem Biophys Res Comm 29: 1404–1411
Ziegler EJ, Fisher CJ, Sprung CL et al. (1991) Treatment of gram-negative bacteremia and septic shock with HA-1A human monoclonal antibody against endotoxin. A randomized, double-blind, placebo-controlled trial. N Engl J Med 324: 429–436
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2000 Springer-Verlag Berlin Heidelberg
About this chapter
Cite this chapter
Schuster, HP., Knaub, S. (2000). Antithrombin III. In: Schuster, HP., Werdan, K. (eds) Intensivtherapie bei Sepsis und Multiorganversagen. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-07962-1_8
Download citation
DOI: https://doi.org/10.1007/978-3-662-07962-1_8
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-662-07963-8
Online ISBN: 978-3-662-07962-1
eBook Packages: Springer Book Archive